Cardiovascular Notebook

Notebook
Care of the Patient with Cardiovascular

Disorders
Lesson 1: Cardiovascular Anatomy & Physiology
Lesson 2: Assessing the Cardiovascular System
Lesson 3: Management of Acute Coronary Syndromes
Lesson 4: Pathologic Conditions
Lesson 5: Cardiac Surgical Interventions
Lesson 6: Cardiac Pacemakers and AICD
Last Updated: November 2013
Inside:
• Module Outline
• Lesson Objectives
• Lesson Summary
• Lesson Resource Files
• Lesson Practice Pearls
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Module Outline
Module 2 - Care of the Patient with Cardiovascular Disorders
Lesson 1 - Cardiovascular Anatomy & Physiology

Topic 1: Structures and Functions
Topic 2: Conduction System
Topic 3: Blood Supply and Systemic Circulation
Topic 4: Electrophysiology And Cardiac Cycle
Topic 5: Cardiac Output, Stroke Volume, Preload, Afterload and Contractility
Topic 6: Autoregulation
Lesson 2 - Assessing the Cardiovascular System

Topic 1: Cardiovascular Assessment
Topic 2: Auscultation
Topic 3: Arterial Circulation Assessment
Topic 4: Blood Pressure Assessment
Topic 5: Venous System Assessment
Lesson 3- Management of Acute Coronary Syndromes

Topic 1: Assessment of Chest Pain
Topic 2: ACS Patient Management
Topic 3: ST Elevation MI
Topic 4: Non ST Elevation MI
Topic 5: Complications
Topic 6: Nursing Considerations
Topic 7: Invasive and Non-Invasive Cardiac Procedures
Lesson 4 - Pathologic Conditions

Topic 1: Heart Failure
Topic 2: Hypertension
Topic 3: Cardiomyopathy
Topic 4: Valvular Heart Disease
Topic 5: Aortic Aneurysm and Dissection
Lesson 5 - Cardiac Surgical Interventions

Topic 1: Coronary Artery Bypass
Topic 2: Off Pump Coronary Artery Bypass
Topic 3: Surgical Valve Replacement and Repair
Lesson 6 - Cardiac Pacemakers and AICD

Topic 1: Temporary Pacemakers
Topic 2: Permanent Pacemakers
Topic 3: Troubleshooting Pacemaker Malfunctions
Lesson 1
Cardiovascular Anatomy &
Physiology
Included in this Lesson:
• Structures and Functions
• Conduction System
• Blood Supply and Systemic Circulation
• Electrophysiology and Cardiac Cycle
• Cardiac Output, Stroke Volume, Preload, Afterload

and Contractility
• Autoregulation
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Lesson Objectives Module: Care of the Patient with Cardiovascular

Disease
Lesson: Cardiovascular Anatomy & Physiology
Upon completion of this lesson you will be able to:
• Identify the major anatomical structures and the associated physiology of

the cardiovascular system.
- Describe the structures and functions of the components of the

cardiovascular system
- Discuss the conduction system of the heart
- Describe cardiovascular blood flow
- Identify the electrophysiological properties of the cardiac muscles and

the phases of the cardiac cycle
- Define and discuss cardiac output, stroke volume, preload, afterload

and contractility
- Describe the neurohormonal regulation of the cardiac system

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Lesson Take-away – Cardiovascular Anatomy & Physiology
Topic One: Structures and Functions
Introduction
In this lesson, we will discuss the structures and functions of the heart. We will review the conduction system, the circulatory
system, electrophysiology of the heart, and the cardiac cycle. Finally, we'll discuss cardiac output and autoregulation.
Heart Muscle
• Has 3 layers (epicardium, myocardium, and endocardium) and a surrounding sac called the pericardium
• Location: In the mediastinum, above the diaphragm, and is surrounded on both sides by lung
• Shape: Resembling triangle, with base parallel to the right edge of the sternum
Heart Chambers
• The right side of the heart is a low pressure system and the left side is a high pressure system and each side has an atrium
and ventricle.
• Here is the Right Atrium (RA,) Right Ventricle (RV,) Left Atrium (LA,) Left Ventricle (LV,) and the Medial Wall separating the
RV and LV.
Valves
• The heart contains the two atrioventricular valves (AV) and two semilunar valves as well as the Chordae Tendineae and
the Papillary Muscles
• AV valves are Tricuspid Valve and Mitral Valve
• Semilunar valves are Pulmonic Valve and Aortic Valve
• Chordae Tendineae and Papillary Muscles work together to prevent valve leaflets from turning inside out.
Topic Two: Conduction System

Introduction
Here we will explore the tract of specialized tissue within the heart allowing it to conduct electrical impulses more rapidly
than normal cardiac tissue, thereby producing a coordinated atrial and ventricular contraction at a normal rate and regular
rhythm.
Cellular Electrophysiology of the Heart

• The fast, more organized tracts include the SA Node, AV junction (AV node and the Bundle of His,) and Purkinje fiber.
SA and AV Nodes
• SA Node is the major pacemaker of the heart. It keeps intrinsic heart rate at 60100 bpm
© 2008 American Association of Critical-Care Nurses (AACN). All rights reserved.

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• The AV Node receives impulse from atria and slows it down before sending to ventricles. This slowing is done in order to
allow time for ventricular filling from the atrial contraction. Is capable of generating its own impulse if doesn’t receive one
(Automaticity.) Intrinsic rate is 40-60 bpm.
Bundle of His
• Bundle of His is point where impulse divides into the right and left bundle branches and further proceeds on to the Purkinje
fibers
• A blockage in a bundle branch shows up on an ECG
• Bundle of His and Bundle Branches can together act as an escape pacemaker for the heart with an intrinsic rate of 20-40
bpm.
Topic Three: Blood Supply and Systemic Circulation

Introduction
In this topic we look at the coronary arteries. These supply oxygenated blood to the heart. We learn the importance of
knowing which arteries supply the different sections of the heart so that we can pull clues about potential complications if
and when they occur with a patient.
Coronary Arteries
• There are two main ones.
• They supply oxygenated blood to the heart.
• The main or “dominant” one of the two is usually the right coronary artery.
Right Coronary Artery

• Supplies blood to the right atria, the right ventricle, most of the conduction system, and to the inferior and posterior sections
of the left ventricle
• Occlusion can result in inferior or posterior MI, bradycardia-type dysrhythmias common with inferior MIs
Left Coronary Artery

• Divides into the left anterior descending (LAD) and circumflex artery
• Is the main blood supply to the left ventricle, septum, and anterior wall
• Occlusions of the LAD result in anterior MIs, associated with pump failure.
The Other Coronary Artery

• The Circumflex Artery supplies lateral portion of left ventricle.
• Occlusions of this artery result in lateral infarctions and, in some patients, a posterior MI.

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Coronary Venous
• Two thirds of coronary blood flow occurs during diastole.
• Coronary arteries dilate up to fourfold to increase the supply of oxygen if/when there is an increased need.
Cardiovascular Circulatory System

• Includes heart, arteries, and veins
• About 13% of blood volume is in the arteries.
• Autonomous nervous system innervates arterioles which constrict and dilate to regulate the amount of blood supplied to
tissues. The arterioles are largely responsible for systemic vascular resistance.
• Atherosclerotic plaque is the result of injury and can lead to coronary artery disease.
Capillaries
• Capillaries:
• Tiny, one-cell thick vessel networks
• Responsible for the exchange of cellular nutrients and the removal of cellular waste products
• Veins:
• Act as volume reservoirs to the circulatory system
• Return blood to the heart
• About 50% of blood volume is in the veins
Topic Four: Electrophysiology and Cardiac Cycle
Introduction
In this topic we look at myocardial cells, the contracting unit of the myocardium. We look at a single contraction from
beginning to end.
Myocardial Cells
• Myocardial cells are responsible for the contracting action of the heart.
• Cardiac muscle is composed of muscle fibers made up of myofibrils, each myofibril a series of sarcomeres. Sarcomeres
are made up of protein filaments myosin (thick) and actin (thin.)
• Contraction produced as myosin’s “cross bridges” reach out and pull actin in toward the sarcomere’s center.

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• Contraction produced as myosin’s “cross bridges” reach out and pull actin in toward the sarcomere’s center.
• The release of calcium at the beginning of a contraction, and the attaching of calcium to troponin, allow these cross bridges
to form and the contraction to occur. By contrast, the uptake of calcium then causes a relaxation of the cardiac muscle.
The Depolarization-Repolarization Cycle

• A contraction is an electrical event so understanding electrophysiology of the heart is important.
• Movement of electrical charges inside and outside the cell is the depolarization-repolarization cycle
• The cycle involves both positive ions (sodium, potassium, calcium, and magnesium) and negative ions (chloride and
phosphate.)
Electrophysiology of the Heart

• Requires an understanding of membrane potentials or the existing electrical differences between the inside of a cell and
the outside of a cell “at rest” or electrically inactive:
• The inside of the cell will have a high concentration of potassium and a low concentration of sodium
• The outside of the cell will have a low concentration of potassium and a high concentration of sodium. Result is that the
inside of the cell has a negative charge relative to the outside of the cell
• Depolarization is when things start to move and the cell is no longer at rest.
Depolarization and Repolarization

• Depolarization is when things start to move – ions flow across the cell membrane - and the cell is no longer at rest. Sodium
ions rush into the cell and potassium ions rush out. The net effect is that an electrical current is produced, followed by a
contraction.
• Depolarization is the electrical excitation of the cell membrane caused by the flow of ions across it.
• Repolarization is the return of the cell membrane to its resting state.
• Repolarization is a slower process that Depolarization.
• A Movement of ions across the cell membrane
• Generates a new action potential
• Occurs in 5 phases: Upstroke, Overshoot, Plateau, Repolarization, and Resting Membrane Potential

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Refractory Phases of Repolarization

• Within repolarization are 3 different refractory phases. These phases become important in antiarrhythmic therapies. The
phases are:
• Absolute refractory period: During this period, the cell will not depolarize no matter how strong the impulse
• Relative refractory period: During this period, the cell will depolarize only if it receives a strong stimulus
• Vulnerable refractory period: During this period, the cell responds to even a very weak stimulus
Phases of the Cardiac Cycle

• An ECG records the electrical events as the wave of electrical excitement (depolarization) spreads from the SA node
through the conduction system. Mechanical events – systole and diastole – result from, and follow the electrical events but
do not show up on the ECG tracing. However they can be seen can be seen on the wave patterns of an arterial catheter
monitor (arterial waveforms.)
• The mechanical event includes one complete mechanical cycle of heart beat
• Knowing the phases of the cardiac cycle is important for evaluating heart sounds and hemodynamic monitoring
results.
• The phases include early systole, late systole, onset of diastole, mid-diastole, and late diastole.
Topic Five: Components of Cardiac Output

Introduction
In this topic we look at Cardiac Output, the volume of blood ejected from the heart over a one-minute period.
Cardiac Output
• Is L/min of blood ejected from the heart over a single minute
• Normal range is 4-8 L/min
• Is heart rate times stroke volume
• Cardiac index is CO divided by the patient’s body surface area
Starling’s Law
• Describes the relationship between contractility and overall cardiac function
• The longer the stretch on the myocardium (the more you stretch a rubberband, for example,) the stronger the contraction
(the harder it snaps.)

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Starling’s Curve
• Describes the principle governing the balance between preload and afterload, the principle being the dependent
relationship between increased stretching and increased pressure of the myocardial fibers: The greater the stretch of the
muscle or cross bridging of the actin and myosin, the greater the force of contraction, up to the point of too much stretch,
then decompensation occurs. After the curve peaks, CO drops, the overworked heart yields, and a steady decline in the
curve occurs. Result is patients become fatigued with accompanying peripheral hypotension, dyspnea, pulmonary
congestion, and edema.
Stroke Volume
• The amount of blood (mL) pumped by the ventricle with every systolic contraction/beat
• Normal range is 50-100 mL/beat
• To understand the hemodynamics of the heart one must understand how SV is affected by preload, afterload, and
contractility
Preload
• Is the volume of blood in the ventricle at the end of diastole
• The most important component of SV
• Is affected by many things: absolute blood volume, how well the blood volume is distributed throughout the body, the atrial
contribution, ventricular function, and ventricular compliance.
• Right and left ventricular preloads are measured differently
Afterload
• Is the resistance to ventricular ejection; in other words, the tension or resistance in the arterial system that the ventricle
must overcome in order to eject the blood into the systemic circulation. Put even more simply, how hard the heart has to
work to pump the blood into the pulmonary or systemic circulation.
• Right and left ventricular afterloads are measured differently: PVR and SVR
• Is affected by many things from vascular volume to the presence of ventricular outflow obstructions
Contractility
• The ability of the heart to pump or the force with which the heart contracts
• Is determined by the vigor of the ventricular wall contraction

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Topic Six: Autoregulation
Introduction
In this topic we explore how the important role played by the autonomic nervous system in heart function. The autonomic
nervous system, which includes the sympathetic and parasympathetic nervous systems, controls the heart and blood
vessels. We also look at the roles played by chemoreceptors, baroreceptors, and the kidney in heart function.
Sympathetic Nervous System

• Has the greatest effect on the ventricles and blood vessels.
• Sympathetic fibers are adrenergic and are excitatory through the release of norepinephrine.
• Three types of sympathetic receptors: alpha-adrenergic, beta-adrenergic, and dopaminergic.
• "Fight or flight" response
Parasympathetic Nervous System

• Cardiac effects of parasympathetic stimulation are slowed heart rate, decreased speed of the conduction through the AV
node, and slight depression in contractility
• Originates in the medulla and is mediated by the vagus nerve
• Most of the fibers are cholinergic and secrete acetylcholine, which tends to be inhibitory in its actions
Chemoreceptors and Baroreceptors

• Reflexes which supplement the nervous system’s responses and serve as feedback mechanisms to the brain
• Chemoreceptors respond to changes in blood chemistry
• Baroreceptors respond to changes in blood pressure

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Renal Perfusion
• The kidneys play an important role in regulating blood pressure: If blood pressure drops, a decrease in perfusion of the
kidney occurs. This drop, in turn, stimulates the renin-angiotensin mechanism in order to restore adequate blood flow.
Ultimately, both blood pressure and blood flow to the kidneys are increased
• Playing a role in the restoration of blood pressure: renin, angiotensinogen, angiotensin I, angiotensin II, antidiuretic
hormone (ADH,) and aldosterone

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Coronary Arteries Lesson: Cardiovascular Anatomy & Physiology

Topic: Blood Supply and Systemic Circulation
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Myocardial Infarction Lesson: Cardiovascular Anatomy & Physiology

Indicative Reciprocal
Type Artery Complications Associated
Leads Leads
AV blocks, ↓ HR Papillary muscle
Inferior RCA II, III, aVf I, aVL, V5, V6 rupture, ↓ BP, N/V, hiccups
Septal LAD V1, V2 II, III, aVF VSD
2nd degree Type 2 block, RBBB, LAHB,
Anterior LAD V3, V4 II, III, aVF Complete Block
Lateral LCx, LAD I, aVL II, III, aVF Ventricular Aneurysm
Apical LAD, RCA, LCx V5, V6 II, III, aVF Ventricular Aneurysm
RVI RCA V3r, V4r RV failure, AV block
V1, V2
Posterior RCA, LCx None reciprocal AV blocks, bradychardia
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Phases of the Cardiac Cycle Lesson: Cardiovascular Anatomy & Physiology

Topic: Electrophysiology and Cardiac Cycle
Cardiac Cycle Left Ventricle

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Cardiac Output Lesson: Cardiovascular Anatomy & Physiology

Topic: Components of Cardiac Output
Cardiac output (CO) is defined as the volume of blood ejected from the heart over 1
minute, and is referred to in liters per minute. Normal CO ranges from 4 to 6 L/min.
Determinants of CO are heart rate and stroke volume. Stroke volume is the volume of
blood ejected from the left ventricle with each ventricular contraction. The equation is
CO = heart rate x stroke volume. Therefore, if either the heart rate or the stroke volume
increases or decreases on the right side of the equation, CO on the left side will
increase or decrease accordingly.
The cardiac index relates the cardiac output to the patient's body surface area. To
measure the cardiac index, divide CO by the patient’s body surface area.
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Autoregulation Lesson: Cardiovascular Anatomy & Physiology

Stimulates Adrenal
Glands
Stimulates Posterior
Pituitary
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Care of the Patient with Lesson: Cardiovascular Anatomy & Physiology

Cardiovascular Disorders Topic: Structures and Functions
Practice Pearls
Heart Muscle
Normally the cavity between the pericardial layers contains 10 – 30 mL of serous fluid.
A pericardial effusion occurs if additional blood or fluid collects in this space. If the
amount of fluid continues to increase and cardiac chamber filling is impeded, cardiac
tamponade results.
Valves
The valve leaflets form a parachute that helps prevent prolapse of the leaflets into the
atria during ventricular contraction. The closing of the valves produces the "lub-dub"
sounds heard when the heart is auscultated using a stethoscope.
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Cardiovascular Disorders Topic: Blood supply and systemic circulation
Coronary Venous
Patients with cardiovascular disease (CVD) or coronary artery disease (CAD) have fixed
lesions that cannot dilate to meet the increase demands. The disparity in supply and
demand can lead to angina, coronary dysfunction, and infarct.
Capillaries
In shock, the precapillary sphincters dilate and postcapillary sphincters constrict in an
attempt to supply cells with more needed nutrients due to reduced blood supply.
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Cardiovascular Disorders Topic: Electrophysiology and cardiac cycle
The Depolarization-Repolarization Cycle

Antiarrhythmic medications work on altering the movement of these ions across the cell
membrane. Disturbances in these electrolytes, especially potassium and magnesium
can lead to dysrhythmias.
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Cardiovascular Disorders Topic: Cardiac Output
Contractility
Two terms used to describe contractility are inotropy and inotropic state. Positive
inotropy strengthens the action of the heart muscle, whereas negative inotropy lessons
the contractility of the muscle.
Lesson 2
Assessing the Cardiovascular
System
• Cardiovascular Assessment
• Auscultation
• Arterial Circulation Assessment
• Blood Pressure Assessment
• Venous System Assessment

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Lesson Objectives Module: Care of the Patient With Cardiovascular

Disorders
Lesson: Assessing the Cardiovascular System

• Assess the cardiovascular status of the critically ill patient.
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Lesson Take-away – Assessing the Cardiovascular System
Topic One: Cardiovascular Assessment
Introduction
In this lesson we discuss assessing the cardiovascular system. Your accurate assessment of the critically ill patient’s
cardiovascular system allows you to quickly identify any alterations that may complicate the patient's recovery. A complete
assessment focuses not only on the heart—but on the arterial and venous systems as well—and includes an interview,
physical exam, and diagnostic testing.
Initial Interview
• Depth of interview depends on how critically ill patient is.
• Speaking patients should be asked for certain information.
• A family history may be helpful.
Symptoms
• Most common symptoms in cardiovascular system pathology include chest pain, shortness of breath, nocturia, cough,
fatigue, syncope, dependent edema and leg pain
• Your assessment becomes even more important in patients that cannot speak/communicate their symptoms to you.
Chest Pain
• The most frequent cardiovascular complaint
• Not just degree of pain but a detailed description of pain necessary
Causes of Chest Pain

• Can be variety of things – Aortic Dissection, Angina, Pericariditis, Gastric Reflux Pain, or Esophageal Spasm
• Asking questions is key for identifying
Symptoms Associated with the Origin of Chest Pain

• Symptoms indicating a cardiac origin: sweating, cool, clammy skin, light headedness or dizziness, shortness of breath,
nausea or vomiting, anxiety, palpitations or sensation that heart skipping a beat

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Dyspnea
• Can be indicative of cardiovascular problems or respiratory problems; important to identify the correct origin. This includes
questions about frequency and duration of episodes, what makes it worse, and accompanying symptoms.
Physical Assessment
• Provides objective data to confirm information obtained in interview
• Three modes of assessment: inspection, auscultation, and palpation
General Appearance
• The “assessment/physical assessment” portion looks at the patient’s general appearance.
• You’ll be examining / looking for acute distress, peripheral cyanosis, central cyanosis, pallor, consciousness, and posture
Cardiovascular Assessment
• After noting the patient’s general appearance, you now move to “cardiovascular assessment” where you focus on the
heart.
Precordial Movement
• Part of the cardiovascular assessment is to look for any precordial movement. This involves exposing and inspecting the
chest wall.
Palpation
• Next is palpation of the chest, done in order to locate the apical pulse as well as to assess for the presence of thrills, lifts,
or heaves.
• Needs to be done systematically such that the base, apex, precordium, and sternal borders are all included.

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Topic Two: Auscultation
Introduction
Recall that the assessment of the patient includes three modes of assessment: inspection, auscultation, and palpation. In
this topic we look in detail at auscultation.
Auscultation
• Is an important cardiovascular assessment tool so it’s important to do it correctly. This includes:
• Eliminating noise
• Focusing on the sounds
• Using the right stethoscope
• Doing the auscultation directly on skin and not through a gown
• Doing the listening over several different patient positions
• Giving the patient specific breathing instructions
The Stethoscope
• Important to understand that wile some sounds are heard best with the diaphragm of the stethoscope, while others are
best heard best using the bell of the stethoscope.
• This doesn’t mean use one with one sound and the other with the other; rather, it serves as a reminder that to get the most
complete auscultation possible, you will use both – diaphragm and bell - in all areas of the precordium.
Auscultation Points
• Need to auscultate each of these areas/points:

• Aortic Area
• Pulmonic Area
• Tricuspid Area
• Mitral Area
• Erb’s Point
S1 S2 Heart Sounds
• The first heart sound (S1) results from the closing of the tricuspid and mitral valves (which separate the atria from the
ventricles) and is heard best at the fourth to fifth ICS to the left of the sternum and at the fifth ICS, left midclavicular line.
• The second heart sound (S2) results from closure of the pulmonic and aortic valves and is heard best at the second ICS to
the right and left of the sternum.

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S3 Heart Sounds
• S3 sounds, S4 sounds, and murmurs may be heard in patients with cardiovascular diseases. (S3 can also be heard in
children and adults under the age of 30 and may also occur during exercise, with anxiety, or in the presence of anemia.
However, if none of these are the case and you hear an S3 sound, consider it pathologic, and not simply physiologic.)
• The presence of an S4 heart sound is abnormal and is due to a noncompliant ventricle.
• This noncompliance may be due to ventricular wall hypertrophy, ischemic heart disease, infiltrative disease processes, or
an increase in ventricular volume.
S4 Heart Sounds
Summation Gallop
• The sound of a galloping horse, made when all 4 heart sounds are present. (The S3 and S4 sounds merge to create the
“gallop” sound.)
• Is often detected in the presence of heart failure.
Murmurs
• Produced by increased or turbulent blood flow
• Often implies significant disease of heart valves, great vessels, or septal defects
Murmur Classification
• Classified along many lines:
• Timing
• Pitch
• Quality
• Location
• Pattern
• Radiation
• Skill at identifying improves with time and exposure to patients with murmurs
Murmur Location
• Murmur location is done using the standard auscultatory landmarks.

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Differentiating Systolic and Diastolic Murmurs

• You palpate the carotid artery while listening to the murmur.
• If murmur heard when pulse is felt, it’s a systolic murmur
• If murmur heard when pulse is not felt, it’s a diastolic murmur
Murmur Intensity
• How loud the murmur is
• Graded from I (barely audile in a quiet room) to VI (very loud; audible even without stethoscope to the chest with palpable
and visible thrill)
Pericardial Friction Rubs

• A rough, scratching, squeaking sound or, like two pieces of hair or leather rubbing against each other
• Caused by inflammation of the pericardium. This occurs in up to 25% of myocardial infarctions.
• Sometimes sounds like a murmur
Identifying Abnormal Heart Sounds

• First, recognize that one is present and name the anatomical location
• Also, identify the presence of new “extra” heart sounds or murmurs
• Then, identify whether the sound is heard best in systole, heard best in diastole, or occurs all the time
Topic Three: Arterial Circulation Assessment
Introduction
Here we look at the assessment of arterial circulation.
Assessment
• Arterial Circulation is assessed by looking at the following:
• Palpation of pulses
• Skin color and temperature

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• Capillary refill and Sensation and motor function

• Blood Pressure
Palpating Pulses
• Palpation of pulses is the first step of Arterial Circulation assessment.
• Pulses may be palpated at a number of anatomical locations but in the critically ill patient, only upper and lower extremity
distal pulses, (radial, dorsalis pedis, and posterior tibial) are routinely evaluated.
Determining Heart Rate, Rhythm and Quality of the Pulse

• Pulses are palpated for the purposes of:
• Determining heart rate and rhythm
• Determining the quality of the pulse (pulse quality tells us about stroke volume)
• Allowing us to compare the apical and peripheral pulse rates; an important step
Abnormal Pulses
• Different types, each indicating something different:
• Thready pulses
• Bounding pulses
• Pulsus paradoxus
Palpating Locations
• When a pulse is not palpable in the radial and dorsalis pedis, it is important to systematically assess pulses beginning
distally and moving toward the central circulation until a pulse is palpable.
Carotid Pulse Palpation

• It is very important to remember these two points related to carotid pulse palpation:
• Never massage the artery while palpating.
• Never palpate both sides at the same time.
Skin Color, Temperature

• Looking at skin color and temperature is the second step of Arterial Circulation assessment.
• Inspect and palpate the extremities noting skin color and temperature, capillary refill, and sensation and motor function

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Capillary Refill, Sensation and Motor Function

• Looking at Capillary Refill and Sensation and Motor Function is the third step of Arterial Circulation assessment.
• Assessing capillary refill: Blanching should occur when you press on the ends of the fingers or nailbeds. When released,
color should return within 2-3 seconds.
• Diminished motor function (ability to wiggle fingers/toes) and diminished sensation can indicate cardiovascular disease.
Arterial Blockage
• A blocked artery is a medical emergency, requiring immediate intervention.
• Interventional cardiovascular procedures and surgeries place critically ill patients at risk for this.
• Signs/symptoms include the 4 Ps: Pulselessness, Pain, Pallor, and Paralysis
Ankle Brachial Index

• The Ankle Brachial Index is easy to take and a change in it can be a sign of inadequate peripheral perfusion.
• Notify physician if Ankle Brachial Index is not 80% or greater or if there is a decrease of over 15% from baseline.
Topic Four: Blood Pressure Assessment
Introduction
Here we explore blood pressure and learn about blood pressure’s importance in screening and trending cardiovascular
function as well as the importance of knowing the patient’s pre-illness blood pressure.
Blood Pressure Assessment

• Use the patient’s pre-illness blood pressure as a baseline for “normalizing” the patient’s blood pressure while hospitalized.
Blood Pressure Measurement

• Getting an accurate blood pressure depends on you understanding the effects of these elements on the blood pressure:
• Site – BP varies depending on site used
• Position
• MAP – Mean Arterial Pressure
• Symmetry
• Accuracy
Mean Arterial Pressure

• Should be utilized whenever possible to guide decisions such as titration or weaning of medications

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Topic Five: Venous System Assessment
Introduction
Here we look at the venous system; the final segment of our cardiovascular exam.
Venous System
• Although most assessment books and resources spend a great deal of time describing how to approximate central venous
pressure by visualizing the right internal jugular vein, this vein is often difficult to visualize.
Edema
• An abnormal accumulation of fluid in the interstitial spac which can be indicative of right-sided heart failure, renal failure,
low plasma albumin, or increased capillary permeability due to activation of the inflammatory response.
• Identify best spot for measurement and then mark it so that other caregivers are consistently using the same spot.
Pitting Edema
• An indentation that remains in the skin after pressure is applied to the edematous tissue
• Many methods for describing it exist but best is describing how long it takes for the tissue to return to baseline (i.e., “Skin
returned to baseline after one minute.”)

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Differential Diagnosis of Chest Pain Lesson: Assessing the Cardiovascular System

Topic: Cardiovascular Assessment
Diagnosis Type of Pain

Substernal chest, jaw, neck, arm, may radiate. Usually less
Angina
than 15 minutes. Relieved by O2 and NTG.
Same as above, lasts longer. Usually unrelieved by O2 and
MI
NTG.
Substernal chest, may radiate to back neck and legs. May
Dissecting
have different BP’s in each arm.
Esophageal/ Substernal orEpigastric, Increases when supine, ↑ eating, ↓
Peptic ulcer with antacids
Pericarditis Substernal, sharp, ↓ with leaning forward.
PE Sudden onset, sharp, SOB, ↑ with deep breath.
Muscle/skeletal Superficial, ↑ with palpation.
Pleuritic Substernal or on one side. Sharp and ↑ with coughing.
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Assessing Jugular Venous Lesson: Assessing the Cardiovascular System

Distention Topic: Venous System Assessment
Have the patient turn their head to the left side. As you look at the patient locate the top
of the clavicle where it intersects with the sternum. This is where the
sternocleidomastoid muscle attaches to the sternum and serves as an anterior
landmark for locating a soft tissue triangle within which the internal jugular vein lies. The
clavicle forms the bottom of this triangle.
Note the external jugular vein. It lies slightly posterior to the 3rd side of the soft tissue
triangle. Look for soft palpations within this triangle extending up towards the jaw. Make
sure you are not visualizing the carotid pulse which is located close by but is situated
more towards the front of the neck. Palpate the carotid if necessary to differentiate its
location.
Most textbooks describe a somewhat complex method of measuring the internal jugular
pressure using a centimeter ruler and straightedge to measure the height of the highest
pulsation. However, this type of assessment is not really feasible, especially in a critical
care setting. A simpler approach is to place the head of the bed at 30 degrees. Have the
patient turn their head to the opposite side, observe for the internal jugular pulsations
and determine if they extend more than 2-3 finger breaths above the clavicle. If so,
assess for other signs and symptoms of fluid volume overload.
If the JVD is absent when the patient is lying flat, they are hypovolemic. Tangential
lighting may be required to help visualize the internal jugular veins. The correct method
for utilizing tangential lighting to enhance visualization of the internal jugular vein is
demonstrated on the slide.
A comprehensive physical examination and clinical education site for medical students
and other health care professionals can be found at:
http://medicine.ucsd.edu/clinicalmed/heart.htm
34
Care of the Patient with Lesson: Assessing the Cardiovascular System

Cardiovascular Disorders Topic: Cardiovascular assessment
Practice Pearls
Initial Interview
The modifiable risk factors for cardiovascular disease are:
• Smoking
• High blood pressure
• High blood cholesterol
• Diabetes
• Being overweight or obese
• Physical inactivity
Palpation
Changes in apical impulse: Lateral and downward displacement results from left
ventricular enlargement. Upward displacement is seen with ascites, pregnancy, obesity,
and in short stature. Medial displacement, (meaning towards the midline of the body),
occurs in chronic obstructive pulmonary disease or with a mediastinal shift due to a left
pleural effusion or tension pneumothorax. It can also occur in tall, thin people.
35

Cardiovascular Disorders Topic: Auscultation
Auscultation
To ascultate the chest of a patient requiring an intra-aortic balloon pump, place the
pump on standby when auscultating as long as pausing the pump does not cause
hemodynamic stability or there are no other contraindications to doing so.
Auscultation Points
To locate the second ICS, find the sternal notch at the base of the neck. Move your
fingers downward until you feel a bump on the sternum. This is the angle of Louis. If you
slide your fingers slightly downward and to the left or right side of the stenum, you will
feel a hollow, which is the second ICS. Below that is a rib, then the third ICS, etc.
Murmur Classification
Systolic murmurs include: Mitral Regurgitation, Physiologic, and Aortic Stenosis:
Systolic. You can remember this with the acronym MR. PASS. Diastolic murmurs
include: Mitral Stenosis, Aortic Regurgitation: Diastolic, and can be remembered by the
acronym MS. ARD.
36

Cardiovascular Disorders Topic: Arterial Circulation Assessment
Carotid Pulse Palpation

During episodes of poor perfusion or during a code, if a femoral pulse is palpable, the
systolic pressure is at least 70 mmHg. If a radial pulse is palpable, the systolic pressure
is at least 80 mmHg. Palpation of a carotid pulse suggests a pressure of at least 60
mmHg systolic.
Skin Color, Temperature

It is important when changing caregivers that assessments be done together so that
continuity of care is maintained. The opportunity to ask questions will help qualify if any
problems identified are new findings or represent stabilization of a preexisting problem.
For example, if the tips of the patient’s toes are discolored after a femoral bypass
procedure, this information can be validated with the previous caregiver as having been
present since presentation to the critical care unit post operatively with full knowledge of
the physician. The degree of discoloration cannot fully be relayed verbally during report
but is easily qualified when both caregivers are present at the bedside.
37

Cardiovascular Disorders Topic: Blood Pressure Assessment
Blood Pressure Assessment

A rule of thumb related to adequate perfusion is that the patient should be warm from
their head to their toes and producing adequate amounts of urine that is not abnormally
concentrated.
Pitting Edema
Anasarca is generalized edema and is seen in severe heart failure, hepatic cirrhosis,
and nephritic syndrome.
Lesson 3
Management of Acute
Coronary Syndromes
• Assessment of Chest Pain
• ACS Patient Management
• ST Elevation MI
• Non ST Elevation MI
• Complications
• Nursing Considerations
• Invasive and Non-Invasive Cardiac Procedures

39

Disorders
Lesson: Management of Acute Coronary Syndromes
• Describe the etiology, pathophysiology, clinical presentation, and

management of patients with Acute coronary syndromes
- Discuss the approach to assessing chest pain
- Identify and describe the identification and management of patients

with the following:
• ST elevation MI
• Non-ST elevation MI
• Right Ventricular Infarction
- Identify indications for, complications of, and nursing management of

patients undergoing diagnostic and interventional coronary
angiography.
• Coronary Angiography
• PCI
• Valvuloplasty
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Lesson Take-away – Acute Coronary Syndrome
Topic One: Assessment of Chest Pain
Introduction
It is critical for you as a nurse to be able to recognize and respond to patients experiencing an acute coronary syndrome;
coronary heart disease being the leading cause of death in the United States. In this lesson we learn how to identify and
manage a patient with an acute coronary syndrome. Specifically we learn:
• How to assess chest pain

• How to manage patient care for someone experiencing an acute coronary syndrome
• How to differentiate between ST elevation myocardial infarctions and non-ST elevation myocardial infarctions and the
appropriate patient care approach for each
• Some of the common complications patients may experience as a result of a myocardial infarction
• The various invasive cardiac procedures such as a cardiac catheterization and PTCA
ACS Defined
• Acute Coronary Syndrome
• A term given to the spectrum of clinical symptoms compatible with acute myocardial ischemia of one of these sorts:
unstable angina, ST elevation MI, and non-ST elevation MI
• A generic/broad term used only in a prediagnostic setting; after medical evaluation/diagnosis it will defined further as one of
these: unstable angina, ST elevation MI (often called “STEMI”) or non-ST elevation MI (often called “NSTEMI.”)
Pathophysiology
• Primary mechanism of ACS is the development of atherosclerosis in which plaque is formed within the arterial lumen
Etiology
• An imbalance in myocardial oxygen supply and demand (specifically demand being higher than supply) can result in
symptoms of ACS. Elements affecting this supply and demand are:
• Preload • Contractility
• Afterload • Heart rate

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Oxygen Supply
• With CAD, atherosclerosis narrows the coronary artery lumen. As the occlusion increases, it will take less and less physical
activity by the patient to trigger pain. (This sensation of pain from physical activity usually begins once the lumen has
narrowed to only 50% its original size.)
Diagnosis
• A patient interview, physical exam, laboratory tests, CXR, and 12-lead ECG are used to determine whether it is unstable
angina, a non-ST elevation MI, or an ST elevation MI.
Presenting signs and symptoms

• Angina (chest discomfort) which is often increased by physical or emotional stress, exposure to cold weather, consuming a
heavy meal, smoking, cardiac dysrhythmias, anemia, fever, hypotension, hypoxemia, or valve dysfunction
Types of Angina
• There are many types, characterized by the duration and intensity
• Stable Angina • Anginal Equivalent
• Unstable Angina • Silent Ischemia
• Prinzmetal’s Angina • MI Associated Angina
Interview
• Important to use the right questions with patients in order to get the information you need to successfully differentiate
angina from noncardiac chest pain
• Anginal pain has certain symptoms:
• Onset that’s sudden
• Location in precordial or substernal areas
• Diffuse and may radiate to the arm, jaw, shoulders or back
• Often described as pressure, tightness, squeezing, heaviness, aching, or indigestion
Physical Exam
• May provide little information if the angina is stable
• More severe signs typically seen with unstable angina, NSTEMI, and STEMI

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Cardiac Injury Markers

• Blood work used to help determine the cause of the chest pain.
• Includes CBC, chemistries, and cardiac enzymes (aka cardiac biomarkers)
• Troponins most reliable biomarkers
Obtaining an ECG
• Should be obtained as soon as possible in patients presenting with symptoms. Standard of care for patients presenting to
the emergency department is to have an ECG completed and reviewed within 10 minutes of their arrival of ACS
• The ECG taken must be reliable; i.e., electrodes must be properly placed using standard anatomical locations. Follow 5-
step process.
ECG Leads
• Knowing the electrical activity recorded by each lead is helpful:
• Leads I, aVL, V5 and V6: Record the activity on the LV’s lateral surface
• Leads I and aVL: Record activity on LV’s high lateral surface
• Leads V5 and V6: Record activity on LV’s low lateral surface
• Leads II, III, and aVF: Record activity on the inferior surface of the left ventricle
• V1 and V2: Record activity of the interventricular septum
• V3 and V4: Record activity on the LV’s anterior surface
Reporting ECG Changes

• Monitor and report ECG changes as they occur, even if you are not sure which area of the myocardium is affected.
Identifying Ischemia, Injury, and Infarction

• The ST segment is the key to identifying
• Early identification of ST segment changes is helped by continuous 12 lead monitoring.
• If continuous 12 lead monitoring not available, can be done by obtaining serial ECGs every 5-10 minutes
Determining ST Segment Changes

• Before looking for ECG changes you want to establish a baseline against which these can be measured/ compared.
• The T to P interval provides a more accurate baseline than the more commonly-used PR interval.

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Ischemia
• Ischemia produces T-wave inversion and/or ST depression. This may occur transiently or may persist.
Myocardial Injury
• Myocardial injury results in ST-segment elevation.
• To be considered significant, the amount of elevation should be 1 mm or larger, and it should be this size in two leads
which look at the same area of the heart (i.e., Leads II and III, both of which look at the inferior surface of the left ventricle.)
• Early signs of ST elevation MI or STEMI:
• Hyperacute T waves
• Loss of the ST segment as the ST segment and the T wave become fused together
12 Lead ECG in Practice

• Lead II, Lead III, and the aVF Lead all look at the inferior surface of the left ventricle so an ST elevation of 1 mm or greater
in any two of these three leads would indicate myocardial injury.
Reciprocal Changes
• If - on an ECG showing some ST elevation – there is also an ST segment depression, you will need to do an angiogram to
determine whether the ST-segment depression is due simply to reciprocal changes or if it is due to an actual blockage and
occlusion of a coronary artery, resulting in ischemic changes.
Q Waves
• The first negative deflection of a QRS complex
• Produced by infarction
• May be seen in NSTEMI but more frequently result from STEMI
Systematic Review of 12 Lead

• Report any person with the following as suspicious for MI: Having signs/symptoms of ACS coupled with T wave inversion,
ST depression, hyperacute T waves, ST elevation, or new or developing Q waves.
• Important to have and use a systematic approach for your review of ECGs:
• Look for T wave inversion
• Look for ST depression (ischemia/NSTEMI)
• Look for hyperacute T waves
• Look for ST elevation (injury)
• Look for significant Q waves (injury moving to infarction or old infarct)

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Reviewing an ECG for Changes Related to ACS

• You might start first with a look at the lateral leads (leads I, aVL, V5, and V6) and do the 5 steps above (Look for T wave
inversion, then ST depression, etc.)
• You might then look at the inferior leads (leads II, III, and aVF) and do those same 5 steps again.
• You might then look at the anteroseptal leads (leads V1-V4) and do those same 5 steps again.
• You then would make an interpretation (i.e., “This patient is having ECG changes consistent with ACS, specifically a lateral
MI.”)
Topic Two: ACS Patient Management
Introduction
Here we explore the goals of therapy in ACS and look at the specific therapeutic interventions used.
Goals of Therapy
• The goals of therapy include:

• Reestablishing the balance between myocardial tissue supply and demand
• Relieving pain
• Preventing or limiting infarct size
• Preventing and treating complications
• Providing secondary prevention through risk factor management
• Therapeutic interventions:
• Restricting activity • Performing interventional therapies
• Administering pharmacologic agents • Educating the patient
Activity
• Activity restrictions are based around ischemic symptoms.
• Since immobility comes with its own set of complications, mobilization as early as reasonably possible is encouraged.

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Drug Therapy
• Paramount to caring for patients with ACS
• Includes:
• Oxygen
• Nitrates
• Anticoagulants, antiplatelets, antithrombins, and GP IIb IIIa platelet receptor inhibitors
• Beta blockers
• ACE Inhibitors or Angiotensin receptor blockers (ARBs)
• Calcium channel blockers (in select patients)
• Fibrinolytic agents (used only in the presence of STEMI)
Oxygen Therapy
• Supplemental oxygen used only in these cases:
• Arterial O2 saturation is less than 90%
• Patient is exhibiting respiratory distress
• Patient is at high risk for hypoxemia
• Need for continued oxygen therapy should be reevaluated six hours after patient presentation
Nitroglycerin
• A cornerstone of treatment for ischemic heart disease because it reduces preload and dilates coronary arteries
• First administered sublingually (spray or tablet) and if 3 doses like this don’t
relieve pain, continuous IV administration is considered Involves monitoring requirements
•There are certain steps to take to help patient avoid building up a tolerance.
• Nitrates in all forms should be avoided with these patients/situations:
• Patients with an initial systolic BP less than 90 mm HG or those who have had a drop in systolic BP of 30 mm Hg
or greater from their baseline
• Patients with marked bradycardia (less than 50 bpm) or tachycardia (greater than 100 bpm)
• Patients who have taken a phosphodiesterase inhibitor for erectile dysfunction within 24 hours (48 hours for
tadalafil)
• Patients suspected of having a right ventricular infarct
• When hypotension secondary to nitrates prohibits the administration of beta-blocking agents
Morphine Administration
• Morphine sulfate is the analgesic agent of choice for treating pain due to ST elevation MI.
• Is also used in treating pain related to unstable angina and non-ST elevation MI if ischemic symptoms persist or recur even
after anti-ischemic therapy.

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• In addition to controlling pain, also:

• Helps control preload in patients with heart failure secondary to ischemia
• Decreases anxiety (thereby helping to alleviate SNS factors like elevated heart rate and SVR)
• Is important to monitor the patient for hypotension and respiratory depression.
Platelet Activation
• Since a key contributor to ACS is thrombus formation, many of the pharmacologic agents used for ACS prevent platelet
aggregation.
• Different ones work in different phases of/on the clotting cascade (the cascade of events that makes up clotting) and
therefore several different antiplatelet and anticoagulant drugs are administered at the same time. Each of these does
something specific:
• Aspirin • Heparin 2 • GPIIb IIIa 1
• Clopidogrel 1 • Heparin 3 • GPIIb IIIa 2
• Clopidogrel 2 • LMW Heparin
• Heparin 1 • Bivalirudin
Other Medications
• Other medications used to manage patients with ACS are Beta Blockers, Calcium Channel Blocker, and ACE Inhibitors.
Mechanical Interventions
• Are interventions used to clear the involved coronary artery of occlusion
• Includes PTCA, stent placement, atherectomy, and rotablator
Topic Three: ST Elevation MI
Introduction
In this topic we will explore the fact that while some elements of caring for ACS patients are the same one patient to the
next, some elements are different.
Myocardial Infarction
• Is the irreversible death or necrosis of myocardial tissue due to an inadequate coronary blood supply

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• The amount of damage or necrosis (irreversible cell death) caused by an MI depends on several factors:
• Duration of the occlusion (i.e., necrosis begins within 20 minutes of the cessation of blood flow through the
coronary artery)
• Which coronary artery is blocked
• Degree of collateral blood flow to the affected area of the myocardium
Wavefront of Cellular Death

• Proceeds from the endocardium to the epicardium
• Zones of differing degrees of damage are produced from this wavefront (first, the zone of necrosis/death; second, zone of
injury; third, the zone of ischemia)
Standards of Care in the ER

• Many patients with symptoms of ACS are seen first in the Emergency Department
• Specific standards of care for the ER setting exist.
Fibrinolytic Therapy
Contraindications of Fibrinolytic Therapy
• Fibrinolytics (fibrinolytic therapies) work directly on the fibrin in a clot, causing it to lyse or break apart.
• Patients must be carefully screened before using these.
• There are many contraindications associated with fibrinolytic therapy.
True Posterior MI
• There are no leads directly monitoring the posterior wall of the left ventricle.
• Posterior MIs can be misinterpreted as anterior ischemia.
Posterior MI
• Be suspicious of posterior MI when leads V1-V3 and/or V4 show tall R waves with ST depression and an upright T wave.
Confirm that it is, in fact, posterior MI by using additional leads V7-V9 as well. ST segment elevation in leads V7V9 will
confirm posterior MI.

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Standard of Care for STEMI Patients

• There are specific standards of care for patients presenting with STEMI. They involve:
• Immediate Care • Reperfusion
• Medications • Ongoing Care
Topic Four: Non-ST Elevation MI
Introduction
In this topic we will explore the fact that while in many ways NSTEMI and Unstable Angina (UA) are closely related
conditions, in some ways they differ.
Differences Between NSTEMI and Unstable Angina (UA)

• The main way that NSTEMI and Unstable Angina (UA) differ is in their severity (i.e., whether the ischemia caused enough
myocardial damage to release detectable amounts of cardiac enzymes into the blood.)
• The patient is considered to have suffered from UA if no biomarkers are detected based on at least two blood
samples collected at least six hours apart with either transient or no ischemic changes on the ECG.
• The patient is considered to have suffered from NSTEMI if biomarkers are elevated.
ECG Interpretation / Evaluation

• Analyzing sample ECGs will give you practice at determining what the patient has suffered from.
Standard of Care for Non-STEMI

• Is similar to the Standards of Care for STEMI except that patients with Non-STEMI…
• Are generally not candidates for emergent reperfusion therapy
• May be taken immediately to the cath lab for angiography and possible angioplasty/stent, etc. when they have
ongoing, unrelieved chest pain, hemodynamic instability or rhythm disturbances
• Are stratified into early invasive or early conservative treatment pathways
• In Non-STEMI patients, fibinolytic therapy is contraindicated
Topic Five: Complications
Introduction
Here we will look at complications that can occur when caring for ACS patients, and the possible nursing interventions.

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Complications of MI
• Include, but are not limited to dysrhythmias, pump failure, infarct extension, thromboembolic phenomena, pericarditis, LV
aneurysm, ventricular septal defect, and valve malfunction
Dysrhythmias
• The most common complication of MI
• The use of beta-blockers as a standard of care decreases the risk of dysrhythmias due to SNS
Heart Failure
• Spans the continuum from mild dysfunction to cardiogenic shock
• Often due to the change in structure (and therefore in function) of the myocardial cells due to infarction
Thromboembolic Phenomenon
• May occur in patients with atrial fibrillation, mural wall thrombus, and akinetic wall segment
• May include the development DVT, PE, and ischemic stroke
Pericarditis
• The result when full thickness MI produces local pericardial inflammation with fluid, fibrin, and cellular exudates
• Anterior wall MIs are the most common culprit for early pericarditis.
Ventricular Free Wall Rupture

• Not often seen but can be fatal if occurs before being diagnosed and treated
• Patients with single vessel disease and no previous coronary artery disease are at greater risk

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Topic Six: Nursing Considerations
Introduction
Here we look at the nursing care for patients with MI.
Patient Management
• The 8 main aspects of caring for MI patients are:
• Assessment • Monitoring
• Heart Sounds • Oxygen Administration
• Chest Pain • Neurological
• Cardiac Monitoring • Bleeding Risk
Patient Management
• Nursing care for MI patients revolves around these 2 main elements:
• Ongoing focused clinical assessment • Use of appropriate interventions
• Patient care priorities for MI patients are:

• Activity: • Monitoring Labs:
• Fluid Balance: • Cardiac Enzymes:
• Constipation:
Patient Education
• Start should start as soon as the patient is stable
• Include the patient’s family or significant other
• Focus the education on evidence-based post STEMI and non-STEMI treatments such as the importance of:
• Smoking cessation
• Adhering to medication regimens
• Beginning an exercise program.
Topic Seven: Non-invasive and Invasive Cardiac Procedures
Introduction
Here we explore the elements of invasive and noninvasive cardiovascular procedures. Noninvasive procedures include
stress testing, stress echocardiography, myocardial perfusion imaging, and coronary CT scanning. Invasive procedures
include coronary arteriography, cardiac catheterization, PCI, pacemakers, and cardiac surgery.
Non-invasive Assessment of Heart Damage

• Some of the non-invasive or minimally invasive procedures for diagnosing the severity of ischemic heart disease and to
evaluate its effect on left ventricular function are as follows:
• Exercise Stress Test • Myocardial Perfusion Imaging

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• Dobutamine Stress Test • 64-Slice CT Scan

• Exercise Echo
Cardiac Catheterization
• Cardiac Catheterization with Angioplasty is one of the more invasive procedures for diagnosing the severity of heart
damage
• Because it provides direct visualization of the coronary artery anatomy, it is considered the gold standard for diagnosing
and localizing coronary artery disease.
PCI
• May be performed during the cardiac catheterization procedure if warranted
PTCA
• Percutaneous Transluminal Coronary Angioplasty (PTCA) and stent placement are commonly performed together to
improve the long-term patency of the artery.
Other Catheterization Laboratory Procedures

• Other procedures done in the catheterization laboratory to treat CAD are:
• Coronary Atherectomy • Transluminal Extraction Catheter • Balloon Valvuloplasty
• Rotational Atherectomy • Laser Angioplasty
Pre-procedure Preparations
• Taking a history • Cardiac and pulmonary assessments
• Review renal function tests • Medications
• Educate and prep the patient • Diabetic meds
• Pulse check

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Post-Procedure Care
• Includes vigilant monitoring of vital signs, access site, distal circulation, cardiac rhythm, and patient recovery from sedation
Vascular Access Site Assessment

• Observing for frank bleeding or oozing, hematoma formation, and palpation of a thrill or auscultation of a bruit
Circulation Checks
• Checking for presence and quality of pulses, extremity warmth and sensation, and motor function
Continuous Cardiac Monitoring

• Done to assess for ST segment changes, dysrhythmias, and vasovagal reactions when sheaths are pulled or pressure
held on groin access sites
IV Fluids
• Maintain IV fluid and pharmacologic infusions as ordered
• Fluid therapy important to prevent renal dysfunction and because contrast media acts as an osmotic diuretic.
Patient Education
• Activity restrictions
• The need to prevent undue stress on the access site
• After sheath removal, showing the patient how to hold pressure on the groin area (if utilized as the access site) if s/he
needs to cough
• Instructing the patient to report any chest pain or anginal equivalent immediately

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Complications
• Abrupt vessel closure • Pseudoaneurysm
• Restenosis • Vessel Occlusion
• Overt bleeding • Impaired renal function
• Covert bleeding

ECG Leads Lesson: Management of Acute Coronary Symptoms
Topic: Assessment of Chest Pain
• Leads I, aVL, V5 and V6 record electrical activity on the lateral surface of the left
ventricle.
• Leads I and aVL monitor the high lateral surface of the left ventricle, whereas Leads
V5 and V6 monitor the low lateral surface.
• Leads II, III, and aVF record the electrical activity on the inferior surface of the left
ventricle.
• V1 and V2 record electrical activity of the interventricular septum.
• V3 and V4 monitor the anterior surface of the left ventricle.
• Some sources include V1-V4 as anterior leads while others call all V leads anterior
leads.
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Indicative & Reciprocal Lesson: Management of Acute Coronary Syndromes

Changes Topic: Assessment of Chest Pain
Localization of a Myocardial Infarction

Indicative
changes (leads Reciprocal changes
facing affected (leads opposite
Location of MI area) affected area) Affected Coronary Artery
Anterior V3, V4 V7, V8, V9 Left coronary artery
• LAD: diagonal branch
Anteroseptal V1, V2, V3, V4 V7, V8, V9 Left coronary artery
• LAD: diagonal branch
• LAD: septal branch
Anterolateral I, aVL, V3, V4, II, III, aVF, V7, Left coronary artery
V5, V6 V8, V9 • LAD: diagonal branch and/or
• Circumflex branch
Inferior II, III, aVF I, aVL Right coronary artery (most
common): posterior descending
branch or
Left coronary artery: circumflex
branch
Lateral I, aVL, V5, V6 II, III aVF Left coronary artery
• LAD: diagonal branch and/or
• Circumflex branch
Right coronary artery
Septum V1, V2 V7, V8, V9 Left coronary artery
• LAD septal branch
Posterior V7, V8, V9 V1, V2, V3 Right coronary or left circumflex
artery
Right Ventricle V1R-V6R I, aVL Right coronary artery
• Proximal branches
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Myocardial Infarction Lesson: Management of Acute Coronary Syndromes

Topic: ST Elevation MI
Universal Definition of Myocardial Infarction

In October 2007, a joint the European Cardiology Society, the American College of
Cardiology, the American Heart Association, the World Heart Federation released a
joint definition for acute myocardial infarction. It is difficult to say whether this new
definition will be widely accepted in clinical practice. We wanted to include this
information for your reference should you begin to hear more about it.
Criteria for acute myocardial infarction
57
Clinical Classification of Myocardial Infarction

Clinically the various types of myocardial infarction can be classified as shown below in
Table 1. On occasion, patients may manifest more than one type of myocardial
infarction simultaneously or sequentially. It should also be noted that the term
myocardial infarction does not include myocardial cell death associated with mechanical
injury from coronary artery bypass grafting (CABG), for example ventricular venting, or
manipulation of the heart; nor does it include myocardial necrosis due to miscellaneous
causes, e.g. renal failure, heart failure, cardioversion, electrophysiological ablation,
sepsis, myocarditis, cardiac toxins, or infiltrative diseases.
For a more thorough look at this and more information go to :

http://circ.ahajournals.org/cgi/reprint/CIRCULATIONAHA.107.187397
58
Mr. Franks Results Lesson: Management of Acute Coronary Syndrome

Cumulative Summary – Cardiac Biomarkers
Study 6/1/09 6/2/09 6/2/09

2120 0450 1100
CK
740 615 442
(Normal: 35-230)
CK MB
54.1 25.8 20.8
(Normal: 0-7.9)
CK MB%
7.3% 4.2% 4.7%
(Normal: 0-1.9%)
Troponin I
9.44 4.02 3.78
(Normal: 0-0.3)
Franks, George M 72
Dr. Gail Hunter
Acct # 00045678349
MR 24-06-33
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Q-Waves Lesson: Management of Acute Coronary Syndromes

Infarction produces Q waves and may be seen in NSTEMI but more frequently result
from STEMI.
A Q wave is the first negative deflection of a QRS complex. Q waves are significant if
they become wider or if new Q waves appear where there were no Q waves in the past.
Q waves occur normally as an indication of septal depolarization in many leads
including I, aVL, V5, and V6. In some patients, small Q waves will also be seen in leads
II and aVF.
Normal Q waves are very small and very narrow. Pathologic Q waves, indicative of MI,
are generally at least 1 small box wide on the 12 lead ECG tracing.
Q waves seen in leads that did not have Q waves previously or leads where the Q wave
is widening or deepening is also indicative of an acute process. Q waves may occur in
the presence of ST elevation, which indicates that the infarction is acute.
Once present, pathological Q waves may remain and will be seen on subsequent ECG
tracings as a permanent reminder that infarction has occurred.
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Care of the Patient with Lesson: Management of Acute Coronary Syndromes

Cardiovascular Disorders Topic: Assessment of Chest Pain
Practice Pearls
Types of Angina
Unstable angina is not promptly relieved by rest or nitroglycerin.
Physical exam
If the patient has a pulmonary artery catheter in place, you may see giant "V" waves on
wedge tracings, indicating regurgitation of blood into the atrium with systole.
Cardiac Injury Markers

Until recently it was thought that Troponin levels did not provide good information
regarding reinfarction since they remain elevated for approximately 7-14 days.
The Consensus Statement on the Universal Definition of MI published in October of
2007states that data suggest that troponins provide similar information to that provided
by CK-MBs in patients where recurrent MI is suspected based on clinical signs and
symptoms. When reinfarction is suspected, two troponin blood samples should be
drawn 3-6 hours apart. If the troponin in the second sample is greater than or equal to
20% of the troponin drawn 3-6 hours earlier, recurrent infarction is diagnosed.
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Case Presentation
Reperfusion therapy is a general term used to describe any therapeutic intervention
aimed at removing the barrier to coronary artery blood flow and perfusion of the
myocardium with oxygenated blood. This can be accomplished with either the
administration of a Thrombolytic or with an Percutaneous Coronary Intervention (PCI).
Reperfusion therapy will be discussed a little later in the lesson.
Q Waves
You may see 12 lead ECGs printouts that say “infarct, age undetermined.” This usually
indicates the infarct is not acute and is sometimes referred to as an old MI.
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Cardiovascular Disorders Topic: ACS Patient Management
Nitroglycerin
When administering heparin and nitroglycerin concurrently, the nitroglycerin may block
some of the antithrombin effects of the heparin. Should the nitroglycerin be
discontinued, the effects of the heparin may be enhanced resulting in elevations in
aPTT and ACT values increasing the risk of bleeding.
ACS Patient Management

The administration of beta blockers to patients experiencing a STEMI is currently a
quality measure. All hospitals providing care to these patients must report their
compliance with the administration of a beta blocker within 24-hours of the patient’s
arrival to the hospital.
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Cardiovascular Disorders Topic: ST Elevation MI
Contraindications of Fibrinolytic Therapy

Locate and review your facility’s protocols for administration of fibrinolytics.
Posterior MI
Some ECG machines are equipped to record 15 lead ECGs, which include two
posterior leads. Check with your facility to determine if your equipment has this
capability.
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Cardiovascular Disorders Topic: Nursing Considerations
Patient Education
The American Heart Association is an excellent resource for current educational
materials related to ACS.
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Cardiovascular Disorders Topic: Management of a patient presenting with
Acute Coronary Syndrome (ACS).
Management of a patient presenting with Acute Coronary Syndrome (ACS)

Each facility has policies and procedures related to post cath monitoring procedures to
include site and distal perfusion checks as well as post sedation monitoring. Review
your unit/hospital specific policies.
Lesson 4
Pathologic Conditions

• Heart Failure
• Hypertension
• Cardiomyopathy
• Valvular Heart Disease
• Aortic Aneurysm and Dissection

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Disorders
Lesson: Cardiovascular Disease
• Describe the etiology, pathophysiology, clinical presentation, and

management of patients with other pathological cardiovascular conditions
- Discuss the clinical manifestations and management of patients in

hypertensive crisis
- Identify and discuss the the pathophysiology, clinical manifestations

and collaborative management of patients with heart failure
- Compare and contrast dilated, hypertrophic and restrictive

cardiomyopathy including the pathophysiology, hemodynamics and
treatment
- Compare and contrast the different types of valvular disease, their

causes and their clinical manifestations
- Discuss the locations, clinical presentation and management of

patients with aortic aneurysms
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Lesson Take-away – Pathologic Conditions
Topic One: Hypertension

Introduction
In this lesson we will discuss the pathological conditions of the cardiovascular system. We’ll look closely at some of the
cardiovascular diseases commonly encountered in the ICU.
Definitions, Classifications, and General Statistics

• Hypertension called the “silent killer” because thirty percent of people with high blood pressure don’t know they have it.
• Pre-hypertension and hypertension
• Two stages of hypertension
Consequences of Hypertension
• Is a major risk factor for coronary artery disease, myocardial infarction, heart failure, and stroke
• Can cause direct injury to the vascular system
• Can cause an increase in myocardial oxygen demand
• Increases the work of the left ventricle, causing left ventricular hypertrophy
• Left ventricular hypertrophy can cause myocardial ischemia and left ventricular diastolic dysfunction (a cause of
heart failure)
• Left ventricular hypertrophy, if left untreated, may lead to left ventricular dilatation and systolic dysfunction (a
cause of heart failure)
Systolic and Diastolic Blood Pressure

• In those over 50, an elevated (140 mmHg) systolic blood pressure is a more significant indicator of risk than an elevated
diastolic blood pressure
Primary/Essential Hypertension
• Three types of hypertension:
• Primary/Essential: No identifiable cause
• Secondary: Has an identifiable cause
• Resistant: Is not responding to treatment
Hypertensive Crisis: Consequences

• A life threatening elevation in blood pressure that occurs when blood pressure is not controlled
• Treatment needed within an hour
• Can produce encephalopathy

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Hypertensive Crisis: Causes

• Can result from these conditions:
• Uncontrolled hypertension • A postoperative complication
• Renal dysfunction • Pituitary tumor
• Preeclampsia • Adrenocortical hyperfunction
• Adrenergic crisis either caused by a drug reaction • Severe burns
or pheocromocytoma
Hypertensive Crisis: Signs and Symptoms

• A blood pressure elevated above 250/150 mmHg
• Neurological signs like a severe headache, altered level of consciousness, and seizures
• Vomiting
• Signs/symptoms of heart failure
Hypertensive Crisis: Treatment

• Lowering the mean arterial pressure no more than 25% in first 2 hours or to a blood pressure of 160/100 mmHg
• Continuous infusion of nitroprusside, a potent arterial dilator
• Nitroprusside is contraindicated in some situations such as pregnancy; use alternatives.
Topic Two: Heart Failure
Introduction
In this topic we will examine heart failure whereby the heart becomes unable to pump enough oxygenated blood to meet the
metabolic needs of the body. It is a complex clinical syndrome whereby the ventricle becomes impaired and can no longer
fill properly or eject optimally.
Statistics
• Patients with heart failure present with one or both of the following:
• Dyspnea and fatigue
• Extracellular fluid retention
• About 5 million Americans live with heart failure today.
• 550,000 new cases are diagnosed each year.
• 300,000 patients die each year of heart failure-related causes.
• 50% of those diagnosed with heart failure die within 5 years of their diagnosis.

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Mechanisms of Heart Failure

• Are directly related to preload, afterload, and contractility
• Ventricle becomes noncompliant because of continued overstretching
Preload, Afterload, and Heart Failure

• Patients with heart failure need to maintain the balance between optimal preload, afterload, and contractility.
Compensatory Mechanisms
• Activated to restore cardiac function to normal after acute heart failure (and the associated decrease in cardiac output and
in blood pressure)
• Includes activation of the sympathetic nervous system (SNS) and the renin-angiotensin system, ventricular hypertrophy,
and dilation.
• Knowledge of these is essential to adequately assess the patient and understand the goals of treatment.
Compensatory Mechanism Failure

• If the mechanism above fails to compensate for the overworked heart, then the following occurs:
• Increased preload • Increased LA pressure
• Increased afterload • Increased RV pressure
• Decreased contractility • Most common cause is left ventricular dysfunction
• Decreased ejection fraction
Common Causes of Heart Failure
Right and Left Sided Heart Failure

• Usually, right ventricular failure results from prolonged left ventricular failure. However it can also result from right
ventricular myocardial infarction, primary pulmonary hypertension, or acute or chronic lung disease.
Forward and Backward Failure

• In forward failure, ventricles fail to pump effectively in a forward direction.
• In backward failure, the pressure in the ventricle rises and that pressure is transmitted backward.

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Systolic Versus Diastolic Dysfunction

• Left ventricular dysfunction can range from predominantly diastolic dysfunction to predominantly systolic dysfunction.
• Patients with heart failure can also have a combination of systolic and diastolic dysfunction.
Other Classification Systems
• Heart failure can be classified as a progressive disorder by stages:

• Stage A:
• Stage B:
• Stage C:
• Stage D:
• It can also be classified with a functional classification:

• NY Class I
• NY Class II
• NY Class III
• NY Class IV
Clinical Presentation: Dyspnea/Fatigue/Exercise Intolerance
• Most patients with heart failure will present with a decreased exercise tolerance due to dyspnea or fatigue.
• The exercise intolerance could also be due to the fact that many heart failure patients also have coexisting conditions such
as pulmonary disease.
Clinical Presentation: Volume Overload

• As a resulting from backward failure, extracellular fluid overload is also common in patients with heart failure.
• Signs of right ventricular backward failure include jugular venous distention, abdominal swelling, and peripheral edema.

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Heart Failure Diagnosis
• Diagnostic tests that help determine the presence of heart failure include:
• Chest X-ray • Electrocardiogram
• Echocardiogram • Cardiac Catheterization
Ongoing Assessment in Heart Failure

• Key areas for the ongoing assessment of heart failure are:
• Functional status
• Fluid status
• Laboratory values
Fluid Status
• Functional status is assessed by the rating systems discussed earlier, so we now turn to fluid status. Extracellular fluid
volume status is difficult to assess, with the most reliable sign being jugular venous distention and others being edema,
organ congestion, and weight.
__________________________________________________________________________________________
__________________________________________________________________________________________
Laboratory Values
• Using lab values to monitor potassium levels is very important since
• Diuretics can cause hypokalemia which, in turn, can increase the risk of digoxin toxicity in patients also on digoxin
• Some of the other heart failure medications (like ACE inhibitors, angiotensin II receptor blockers, and aldosterone
antagonists) can predispose patients to hyperkalemia.
• Using lab values to monitor renal function and anemia is also important.
Key Nursing Assessments in Heart Failure

• Manage systolic blood pressure • Assess for fluid in lungs
• Auscultate heart sounds • Monitor the cardiac rhythm
• Assess lungs for adventitious sounds • Check for kidney failure and anemia
• Correct hypoxemia • Observe for any signs of activity intolerance

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Overview of Pharmacological Treatment of Active Heart Failure

• To interrupt the neurohormonal responses, slow disease progression, and improve survival, patients with active heart
failure are treated with Angiotensin Converting Enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARB) and beta
blockers.
• An aldosterone antagonist can help patients who experience symptoms at rest.
• Though they don’t improve survival, diuretics and digoxin may be used as well.
Nonpharmacological Treatment Options in Heart Failure

• Physical activity and exercise training
Dysynchrony
• Common in heart failure patients
• Cardiac Resynchronization Therapy (CRT) is helpful in patients with moderate to severe heart failure and in those with
bundle branch block (typically left bundle branch block) who are symptomatic despite optimal medical therapy.
Acute Decompensated Heart Failure

• Patients with Acute Decompensated Heart Failure (ADHF) commonly present with these signs, both of which exacerbate
heart failure and cause acute decompensation:
• Signs of fluid overload • Signs of hypoperfusion
BNP Levels in Acute Decompensated Heart Failure

• Blood levels of BNP can indicate left ventricular decompensation but BNP can’t be your only tool since elevated BNP levels
can be indicative of other things as well.
Diuretics in the Treatment of Acute Decompensated Heart Failure

• Help relieve symptoms of congestion while maintaining an adequate circulating volume

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Vasodilator Treatment of Acute Decompensated Heart Failure

• Patients in acute decompensated heart failure usually need vasodilator therapy to help reduce preload and afterload.
• One vasodilator is Nesiritide, a synthetic BNP that reduces both preload and afterload. Requires careful monitoring.
• Other vasodilators used are nitroglycerin and nitroprusside
Inotropes in the Treatment of Acute Decompensated Heart Failure

• Patients in acute decompensated heart failure may require IV administration of a positive inotrope.
• Vasodilator therapy should first be considered
• Inotropic therapy is not indicated unless filling pressures (central venous and pulmonary artery pressures) are known to be
elevated.
Topic Three: Cardiomyopathy
Introduction
In this lesson we discuss cardiomyopathy, a disease of the heart muscle that primarily affects the myocardial layer of the
heart.
Definition
Cardiomyopathy refers to a group of disorders which:
• Are associated with the mechanical and/or electrical dysfunction of the myocardium
• Are either confined to the heart or are part of a generalized systemic disorder
• Often lead to cardiovascular death or progressive heart failure-related disability
Classification of Cardiomyopathy
• Standard classifications equal primary and secondary however have evolved to also include mixed (genetic and
nongenetic) and acquired
• You can also classify cardiomyopathies in a functional manner, describing the ventricular changes:
• Dilated cardiomyopathy • Restrictive cardiomyopathy.
• Hypertrophic cardiomyopathy

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Dilated Cardiomyopathy: Overview

• Where cardiac chamber is enlarged and dilated
Dilated Cardiomyopathy: Pathophysiology

• Characterized by diffuse dilation of the ventricles without muscle hypertrophy
• An Ejection Fraction (EF) of 15% or less is common.
Dilated Cardiomyopathy: Clinical Presentation

• Has same signs/symptoms of heart failure including:
• Dyspnea on exertion • Palpitations
• Chronic fatigue • Dizziness
• Weakness • Syncope
• Orthopnea • Impotence
• Paroxysmal nocturnal dyspnea • Chest pain
• Cough • Insomnia
• Weight gain
Assessing Dilated Cardiomyopathy

• Various methods including:
• Chest X-ray • Cardiovascular assessment
• Echocardiogram • Pulmonary assessment
• Electrocardiogram
Dilated Cardiomyopathy: Patient Management

• Goals are to decrease the workload of the heart and relieve the patient’s symptoms. To do this we:
• Use drug therapies • Nutrition efforts
• Optimize activity levels • Surgical interventions

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Restrictive Cardiomyopathy: Overview

• The least common form of cardiomyopathy, accounting for a very small percent of those patients with cardiomyopathy
• Characterized by rigidity of the myocardial wall that causes a decreased ability of the chamber walls to expand during
ventricular filling
Restrictive Cardiomyopathy: Causes

• Has has both primary and secondary causes and in some cases, no cause can be determined
• Amyloidosis is responsible for 90% of cases of restrictive cardiomyopathy in North America
Restrictive Cardiomyopathy: Pathophysiology

• Ventricles are unable to stretch normally when receiving blood from the atria and therefore a smaller amount of blood
enters the ventricle than normal. Result is that there is a decreased amount of blood available for ejection during ventricular
systole (contraction); thereby decreased blood volume.
• Systolic function affected later in the disease process
• Blood backs up into the lungs (left-sided failure) and ultimately the venous circulation (right-sided failure), resulting in heart
failure.
• Both ventricles are usually involved
• Size of the ventricular cavity usually remains the same or may be slightly decreased
Restrictive Cardiomyopathy: Clinical Presentation

• Fatigue, weakness, and activity intolerance are usually the first signs
• The signs/symptoms of heart failure
Assessing Restrictive Cardiomyopathy

• Multiple tests exist for assessing:
• Echocardiogram • Endomyocardial biopsy
• Electrocardiogram • Cardiovascular assessment

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Restrictive Cardiomyopathy: Patient Management

• Supportive and aimed at the reduction of symptoms.
• Treatment focuses on:
• Reduction of diastolic dysfunction • Treatment of the underlying disease process
• Treatment of arrhythmias • Surgical treatment.
• Treatment of thromboembolic complications
Hypertrophic Cardiomyopathy: Overview

• Characterized by hypertrophy of the myocardium
• Some patients with HC end up having Hypertrophic Cardiomyopathy with Obstruction (called “Hypertrophic Obstructive
Cardiomyopathy” or HOCM.) Hypertrophic cardiomyopathy is found in one in every 500 people.
• Most common reason for sudden cardiac death in young adults
Hypertrophic Cardiomyopathy: Pathophysiology

• Complex and varies from patient to patient depending on whether the patient has the obstructive component or not
• Myocardial disarray
• Asymmetrical hypertrophy
• Diastolic dysfunction
Hypertrophic Cardiomyopathy: Clinical Presentation

• Many patients with HC remain asymptomatic for years and end up being identified during routine screening in relatives of a
patient with known HC.
• First sign of HC is often an episode of sudden cardiac death.
• Other symptoms are dyspnea, chest pain, and syncope.
Assessing Hypertrophic Cardiomyopathy

• There are two primary ways to assess HC:
• Echocardiogram
• Cardiovascular assessment

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Hypertrophic Cardiomyopathy: Patient Management

• Treatment aimed at relieving symptoms, preventing complications and/or reducing the risk of sudden cardiac death
• Treatment goals are:
• Increased ventricular filling • Reduction of any obstruction
• Maximizing of stroke volume
Hypertrophic Cardiomyopathy: Sudden Death

• The most serious complication of hypertrophic cardiomyopathy
• Is usually the event leading to diagnosis of hypertrophic cardiomyopathy
• Most literature agrees that ICDs should be placed in any patient with an episode of sudden cardiac death, sustained
ventricular tachycardia, or a family history of sudden cardiac death.
• In conjunction with the ICD, medications to treat the ventricular arrhythmias are used, Amiodarone being the drug of
choice.
Topic Four: Valvular Heart Disease
Introduction
In this lesson we look at valvular heart disease which affects about 5 million Americans.
General Assessment of Valve Disease

• Most valve disease is chronic with changes occuring over many years and in some cases decades before any symptoms
develop.
• The key to successful treatment is early recognition.
• There are many types of valve problems and here we will focus specifically on:
• Aortic stenosis • Mitral stenosis
• Acute and chronic aortic regurgitation • Acute and chronic mitral regurgitation
Abnormal Valve Function: Stenosis and Regurgitation

• Valve malfunction occurs 2 ways: Valve is stenotic or valve is regurgitant.
• End result of both types is decreased cardiac output
Aortic Stenosis: Overview and Classification

• When opening of the aortic valve narrows, impeding the normal flow of blood across the aortic valve during ventricular
systole
• Congenital or acquired

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Aortic Stenosis Pathophysiology

• LV hypertrophy, diastolic dysfunction, LV failure, and heart failure
• The compensatory mechanisms of left ventricular hypertrophy and increased contractility occurring with aortic stenosis
provide adequate cardiac output for many years and often decades before symptoms appear.
• Symptoms generally begin to appear when the valve opening is one-third its normal size.
Aortic Stenosis: Clinical Presentation
• Typically includes this trio of symptoms:

• Angina • Impeded blood flow • Arrhythmias
Evaluation of Aortic Stenosis
• Includes physical assessment and diagnostic studies; specifically:

• Echocardiogram • ECG
• Stress Test • Cardiovascular Assessment
• Cardiac Catheterization
Aortic Stenosis: Patient Management

• Medical treatment (beyond the occasional need for rate control for atrial fibrillation) is rarely needed early in the disease
process.
• Medications temporarily resolve heart failure but if valve not replaced, failure worsens and death is the end result.
• In severe aortic stenosis, there are certain medications that should be avoided.
Aortic Regurgitation: Overview

• Also called aortic insufficiency
• Occurs when the valve leaflets of the aortic valve do not close completely to form a tight seal, resulting in backward flow of
blood from the aorta to the left ventricle during ventricular diastole
• Classified as acute or chronic

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Chronic Aortic Regurgitation: Pathophysiology

• The chronic compensatory phase lasts for many years or even decades. Patients remain asymptomatic for years. As the
left ventricle continues to dilate the myocardium becomes overstretched and contractility decreases resulting in systolic
dysfunction.
Chronic Aortic Regurgitation: Clinical Presentation

• Exertional dyspnea and fatigue are the symptoms noted most frequently
• Complaints of paroxysmal nocturnal dyspnea and orthopnea with pulmonary edema not unusual
• Patient may become aware of his or her heartbeat
Evaluation of Chronic Aortic Regurgitation

• Echocardiogram • Cardiovascular Assessment
• Chest X-ray • Hyperdynamic Perfusion
• Cardiac Catheterization
Chronic Aortic Regurgitation: Patient Management

• Patient with no symptoms requires no treatment as long as LV function is normal.
• Surgical replacement is the treatment of choice once patient begins to show symptoms.
• Arterial Vasodilators treatment may be beneficial in easing the amount of regurgitation on a temporary basis.
Acute Aortic Regurgitation: Pathophysiology/Diagnosis

• There is a decrease in forward flow which the body attempts to compensate for by increasing heart rate and arterial
vasoconstriction. The increase in left ventricular afterload results in a worsening of the acute aortic regurgitation. The volume
overload is transferred backward to the left atrium and ultimately to the pulmonary veins, resulting in acute pulmonary
edema.
• The patient presents with signs of acute pulmonary edema and cardiogenic shock with tachycardia and hypotension.

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Acute Aortic Regurgitation: Treatment

• Urgent surgical treatment is the therapy of choice.
• If the AAR is the result of infective endocarditis, 48 hours of antibiotics are preferred prior to surgery if the patient can
tolerate it (if the patient is hemodynamically stable.)
Acute Aortic Regurgitation: Patient Management
• These non-surgical treatment options in the time before surgery can be helpful:
• IV Medication • Beta Blockers
• Preload • Inotropic Support
• Contraindicated therapies in acute aortic regurgitation include:

• Intra-aortic balloon pumping • Arterial vasoconstrictors such as vasopressors
Mitral Valve Disease: Overview

• The mitral valve is a complex structure having an annular ring, valve leaflets, and the “mitral apparatus” which includes the
papillary muscles (which attach to the ventricular wall) as well as the chordae tendinea (which attach the valve leaflets to the
papillary muscles.)
Mitral Stenosis: Causes

• When an abnormality impedes the normal flow of blood across the mitral valve
• A constriction or narrowing of the mitral opening
• Most common cause is rheumatic heart disease, 60% of all patients presenting with mitral stenosis having a history of
rheumatic heart disease.
Mitral Stenosis: Pathophysiology

• Valve opening narrows, increased LA pressure transmitted to pulmonary vascular bed, LA dilates, and compensatory
system fails
Mitral Stenosis: Clinical Presentation

• Generally, valve area is less than half its normal size before any symptoms occur
• Development of symptoms could begin as long as 40 years after the development of rheumatic fever
• Once symptoms begin, they develop slowly and patients make adjustments in activity levels to compensate for the
changes, often without being aware that they are doing so.
• Most common symptom is dyspnea with exertion with no symptoms at rest.
• Conditions that increase heart rate (pregnancy, new-onset atrial fibrillation, hyperthyroidism, or fever) commonly result in
symptoms that alert the physician to the possibility of mitral stenosis.

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Evaluation of Mitral Stenosis

• Echocardiogram • Cardiovascular assessment
• Chest X-ray • RV Failure
• Cardiac Catheterization • Mitral Facies
Mitral Stenosis: Patient Management

• Treatment directed at alleviation of symptoms and include:
• Heart rate control
• Use of Beta blockers or calcium channel blockers in patients having exercise intolerance
• Use of Calcium channel blockers or beta blockers for treating atrial fibrillation and maintaining a ventricular rate of
less than 100 bpm if repeat cardioversion remains unsuccessful
• Use of anticoagulation in patients with atrial fibrillation and mitral stenosis
• Surgical options once valve area becomes less than 1.5 cm2
Mitral Regurgitation Overview

• Mitral regurgitation occurs when the cusps of the mitral valve do not close properly and therefore do not form a proper seal.
As a result, blood in the left ventricle returns to the left atrium during ventricular systole.
Chronic Mitral Regurgitation: Pathophysiology

• Provides a much different clinical picture than acute mitral regurgitation
• The compensatory mechanism that kicks in serves the patient for many years. Eventually, though, the myocardial fibers
are stretched beyond their limitations and systolic ventricular dysfunction develops.
Chronic Mitral Regurgitation: Clinical Presentation

• Patients are asymptomatic for many years
• When symptoms develop, they are most often fatigue and dyspnea. Later on they also may include paroxysmal nocturnal
dyspnea, orthopnea, and sometimes palpitations.
• Patients with mitral valve prolapse may report the following symptoms: tachycardia, orthostatic hypotension, and panic
attacks.

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Evaluation of Chronic Mitral Regurgitation

• Echocardiogram • Cardiac Catheterization
• Chest X-ray and ECG • Cardiovascular assessment
Chronic Mitral Regurgitation: Patient Management

• ACE inhibitors may be helpful if left ventricular dysfunction present
• Rhythm control important if atrial fibrillation present
• Exercise acceptable in some cases
• Once symptoms of heart failure develop, surgery should be considered.
Acute Mitral Regurgitation: Pathophysiology

• Can result from papillary muscle ischemia or when a papillary muscle tears away from the ventricular wall. Result is
decreased stroke volume and decreased cardiac output. Afterload increases as a compensatory mechanism. Systemic
vascular resistance increases causing even less forward flow and more regurgitant flow.
Acute Mitral Regurgitation: Signs and Symptoms/Diagnosis

• Pulmonary edema is a key assessment finding. • Time is critical in making the diagnosis so treatment can
• The echocardiogram is the key diagnostic tool. be rapidly implemented.
Acute Mitral Regurgitation: Patient Management

• Emergent surgical repair or replacement is the treatment of choice.
• Until the patient is taken to surgery, medical treatment is used with this goal:
• Decrease afterload in order to increase the forward flow and lessen the amount of mitral regurgitation (which, in
turn, decreases the amount of pulmonary congestion)
• Options for medical treatment include:

• Intra aortic balloon pump
• Sodium Nitroprusside (except if significant hypotension is present)
• Antibiotics (if the acute mitral regurgitation is the result of endocarditis)

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Topic Five: Aortic Aneurysm and Dissection
Introduction
In this lesson we look at Abdominal Aortic Aneurysms (AAA,) considered present when the anteroposterior diameter of the
aorta reaches 3 cm.
Abdominal Aortic Aneurysms (AAA): Definition

• Most common AAAs extend below the renal arteries and often extend to involve the common iliac arteries
• Risk factors for development of an AAA include: male gender, family history, advanced age, cigarette smoking, polycystic
kidney disease and other renal disease, other vascular disease, known popliteal aneurysms, and Marfan Syndrome.
AAA: Pathophysiology and Diagnosis

• Usually represents a degeneration of the medial layer of the aorta, along with destruction of the structural matrix proteins
such as elastin and collagen
• Patients with AAA:
• Are usually asymptomatic and discovered only during a diagnostic workup for another medical condition. When an
AAA is discovered, patients should be tested for more AAAs.
• Often have coexisting coronary artery disease
The majority of aortic dissections involve the ascending aorta. A smaller percentage involves the aortic arch
and descending thoracic aorta. Dissections of the abdominal aorta are rare
AAA: Complications
• Rupture or occlusion resulting from dissection • Compression of nearby anatomical structures such as
• Thromoembolic ischemic events the duodenum
AAA: Treatment
• Most important treatment goal is to prevent fatal rupture • Surgery
• Smoking cessation and blood pressure control
AAA: Surgical Repair

• Repair of an aneurysm can be performed transabdominally by an open procedure or else endovascularly.
Postoperative Nursing Care
• Patients having an open AAA repair will spend at least 24 hours in the intensive care unit.

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• The most common complications are:

• Bleeding from abdominal incision • Dysrhythmias
• Myocardial ischemia or infarction • Atelectasis
• Heart failure
Nursing Interventions
• Monitoring vital signs, oximetry, and ECG
• Reviewing lab values, especially hemoglobin and hematocrit, electrolytes, BUN, and Creatinine
• Managing the patient's pain
• Keeping blood pressure high enough to maintain perfusion through the graft but low enough to prevent rupture
• Monitoring the output from the NG tube and assessing bowel sounds for return of peristalsis
• In patients whose aorta was cross clamped during surgery, there are additional items to monitor for.
Surgical Treatments
• Thoracic aortic aneurysms are found in the ascending or descending thoracic aorta.
• Acute and Chronic
• “Acute” aortic dissections: Those diagnosed within two weeks of onset
• “Chronic” aortic dissections: Those diagnosed outside the two-week window
Aortic Dissection: Classifications

• Type A and Type B (the most current classification system; called the Stanford classification system)
• Type A dissections: Involve the ascending aorta • Type B dissections: Involve the descending thoracic aorta
Aortic Dissections: Complications

• All complications of aortic dissection are serious and potentially life threatening, yet there is a very high mortality rate for
untreated dissections.
• Complications include Regurgitation, MI, Cardiac Tamponade, Hemothorax, Bleeding, Stroke Paraplegia

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Aortic Dissection: Signs and Symptoms and Diagnosis

• Chest or back pain often described as a ripping or • Variation in upper extremity blood pressure
tearing • Others
Aortic Dissection Treatment

• Treatment depends on the type of dissection—Type A or B
• Dissections (acute or chronic) involving the ascending aorta (i.e.Type A dissections) require surgical repair.
• Dissections involving the descending thoracic aorta (i.e. Type B dissections) are usually treated medically.

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Treatment of Hypertension Lesson: Cardiovascular Disease

Topic: Hypertension
Treatment Goals
For patients with hypertension the blood pressure treatment goal should be < 140 mm
Hg systolic and < 90 mm Hg diastolic in all patients.
For patients with diabetes, heart failure, or chronic kidney disease, blood pressure
treatment goal should be lower at < 130 mm Hg systolic and < 80 mm Hg diastolic.
Importance of Effective Treatment

Thiazide diuretics can be used as first-line treatment in uncomplicated hypertension in
patients without diabetes, coronary artery disease or kidney disease. Two or more
medications are usually required to effectively treat hypertension in the majority of
patients. Effective treatment of blood pressure with medications has been shown to
protect against stroke, coronary events, heart failure, and the progression of kidney
disease. Untreated hypertension can lead to end organ damage. Organs affected by
hypertension include the heart, brain, kidneys, peripheral arteries, and eyes.
Lifestyle Interventions to Reduce Blood Pressure

In addition to medications, several lifestyle interventions have been shown to delay or
prevent the onset of hypertension. These lifestyle interventions include:
1) Weight Reduction: A body mass index of < 25 kg/mm2 is an effective strategy to
both prevent and treat high blood pressure. The greater the weight loss, the
greater reduction in blood pressure.
2) Increased Physical Activity: Patients should engage in aerobic activity most every
day for 30 to 45 minutes each day.
3) Sodium Restriction: Lowering sodium can be an effective strategy for both
preventing and treating hypertension. However, not all people have the same
blood pressure response to a decrease in sodium. Sodium reduction is generally
more effective in blacks, older adults, and in patients with hypertension, diabetes,
or chronic kidney disease. (When providing patient education it is important for
patients to understand that 75% of sodium intake comes from processed food,
not from added salt.)
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4) Increase in Potassium Intake: A higher potassium intake is associated with a

reduction in blood pressure. The recommended method for increasing potassium
intake is by eating fruits and vegetables rich in potassium. (In healthy people
excess potassium is excreted in the urine. However, an increased potassium
intake must be used cautiously in patients taking ACE inhibitors, angiotensin
receptor blockers, aldosterone blockers, and non-steroidal antiinflammatory
agents because these medications impair the excretion of potassium. Patients
with diabetes, renal disease, adrenal insufficiency, and advanced heart failure
will also have an impaired ability to excrete potassium.)
5) Whole Dietary Patterns: After weight loss, the DASH diet is the second most
effective lifestyle intervention to reduce blood pressure. DASH stands for Dietary
Approaches to Stop Hypertension. The DASH diet alters potassium, calcium, and
magnesium, while holding sodium constant. The DASH diet is high in fruits,
vegetables, and low-fat dairy products so it is rich in potassium and calcium. It is
low in both saturated fat and total fat. Vegetarian diets are also associated with
lower blood pressures.
6) Moderation of Alcohol Intake: Moderate alcohol intake is defined as no more than
two servings of alcohol per day for men, and no more than one serving per day
for women. A serving of alcohol is defined as 12 ounces of regular beer, 4 to 5
ounces of wine, or 1.5 ounces of 80 proof distilled spirits.
7) Additional lifestyle considerations include fish oil supplementation, high fiber
intake, and calcium and magnesium supplementation.
Special Considerations in the Elderly

Target blood pressure goals are the same for the elderly as for younger adults. Pseudo
hypertension may occur in the elderly due to excessive vascular stiffness. Assessment
for orthostatic hypotension is particularly important in elderly patients who are taking
antihypertensives. The elderly have a higher risk for orthostatic hypotension because
the percentage of water as body weight declines with aging.
Special Considerations in the African American

African-Americans have the highest prevalence and greatest severity of hypertension.
African-Americans produce less renin and are therefore not as receptive to beta
blockers or medications that block the renin angiotensin aldosterone system. Thiazide
diuretics, calcium channel blockers, or a combination of isosorbide dinitrate and
hydralazine hydrochloride are often used in treating this population.
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Special Considerations in Diabetes

In diabetic patients an ACE inhibitor or angiotensin II receptor blocker is usually the first-
line agent used to treat hypertension. Medications that interrupt the renin angiotensin
aldosterone system reduce microvascular and macrovascular complications in both type
I and type II diabetes. Diabetic patients commonly require two or more medications to
achieve the blood pressure goal of < 130/80 mm Hg.
Special Consideration in Kidney Disease

Patients with kidney disease generally require three or more antihypertensives to keep
blood pressure < 130/80 mm Hg. Medications that interrupt the renin angiotensin
aldosterone system are effective in reducing the progression of renal dysfunction in
patients with diabetic and nondiabetic kidney disease. Most patients with renal disease
also need to be on a loop diuretic.
Patient Education
Empowering patients with knowledge is an important part of hypertension management.
Patient's need education regarding:
• lifestyle modifications
• prescribed medications
• avoid over-the-counter medications such as decongestants.
• The risk of untreated hypertension.
Patient compliance is an important part of therapy; therefore, the costs and side effects
of medications are important considerations. Self-monitoring of blood pressure by
patients has been shown to improve compliance. Patients should have monthly follow-
up blood pressure checks, with medication adjustments, until target results are
achieved. More frequent follow-up is indicated for patients with stage 2 hypertension
and for those with cardiovascular disease, renal disease, or diabetes. After blood
pressure goals are achieved, follow-up should continue at 3- to 6-month intervals. Dose
reduction of medications should be attempted after 1 year of controlled therapy.
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Compensatory Mechanisms Lesson: Cardiovascular Diseases

Topic: Heart Failure
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Heart Failure Medications Lesson: Cardiovascular Disease

Key Considerations with ACE Inhibitors and Angiotensin II Receptor Blockers

ACE inhibitors interfere with the conversion of angiotensin I to angiotensin II in the renin
angiotensin aldosterone system. Benefits are seen in all stages of heart failure,
although it may take several weeks to months for the effects to be seen. ACE inhibitors
are used for mortality benefits, even when there is no symptom improvement.
ACE inhibitors should be used cautiously in the following situations:
• Systolic blood pressure < 80 mm Hg.
• Creatinine > 3 mg/dL.
• Bilateral renal artery stenosis.
• Elevated serum potassium.
ACE inhibitors are contraindicated in angioedema, pregnancy, and anuric kidney injury.
Angiotensin II receptor blockers directly block angiotensin II. Angiotensin II receptor
blockers are indicated in chronic heart failure patients who cannot tolerate an ACE
inhibitor due to cough or angioedema.
Key Considerations with Beta Blockers

Beta blockers are indicated in heart failure to block the neurohormonal responses of
chronic sympathetic nervous system stimulation and favorably impact ventricular
remodeling. Beta blockers can also decrease arrhythmias and ischemia by decreasing
heart rate and contractility, thereby decreasing myocardial oxygen consumption.
Patients who show signs of decompensation after a maintenance dose of beta blocker
therapy has been administered, generally do not have the beta blocker therapy
discontinued. Abrupt discontinuation of beta blockers should be avoided.
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End Stage Heart Failure Lesson: Cardiovascular Disease

End-stage heart failure patients often decompensate frequently and may need to be
admitted for intravenous inotropic or vasodilator therapy. Patients unable to be weaned
from intravenous inotropic support may be candidates for at-home continuous inotropic
support. This measure is a final option, used only for palliative relief in end-stage
disease. Because inotropic therapy is associated with an increased risk of sudden death
and there is a lack of research supporting the benefit, intermittent inotropic therapy is
not indicated in the management of chronic heart failure.
Physicians should discuss end-of-life care issues with patients with end-stage heart
failure while they are still able to participate in the decision-making process. Hospice
care is one option for end-stage disease management that is often underutilized.
Transplantation in Heart Failure

Cardiac transplantation is the only established surgical treatment for refractory heart
failure. Evaluation for transplantation is indicated only for patients with refractory heart
failure who are not controlled, despite optimal medical therapy, device therapy, and
alternative surgical therapy. Candidates need to be otherwise healthy. The survival rate
at 1 year is approximately 85%. After transplantation, patients remain on lifelong
immunosuppression therapy, placing them at risk for further complications.
Left-ventricular Assist Devices

Left-ventricular assist devices can be used to provide hemodynamic support to failing
hearts for patients waiting for cardiac transplantation as well as those who are not
candidates for transplantation. Patients who are not transplant candidates will be
considered for surgically implanted assist devices. Complications with left-ventricular
assist devices are common and have the potential to be life threatening. For this
reason, the use of these devices is limited.
Sudden Death in Heart Failure

Patients with heart failure are at high risk for sudden cardiac death. They can also die
from progressive pump failure and congestion or end-organ failure from systemic
hypoperfusion.
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Interventions in heart failure to decrease the risk of sudden cardiac death include: beta
blockers, amiodarone, and implantable cardioverter-defibrillators (ICDs). Although not
routinely used due to its toxicity, amiodarone is one antiarrhythmic that can be tolerated
in heart failure patients if needed. ICDs are indicated in heart failure with suspected
survival and good functional status for at least one year who also meet one of the
following criteria:
• Survivors of cardiac arrest / sustained ventricular tachycardia / inducible
ventricular tachycardia on electrophysiology study.
• Ejection fraction less than 30% more than 40 days after an MI or less than
30% with no ischemic heart disease.
Patients with heart failure have an increased risk for ventricular arrhythmias and should
be assessed for exacerbating factors such as electrolyte abnormalities (low potassium
and low magnesium) and digitalis toxicity.
Additional Considerations in Heart Failure

Patients with advanced heart failure can develop cardiac cachexia. The support of a
nutritionist to help with caloric supplementation is beneficial.
Heart failure patients should be screened for depression at regular intervals. Selective
serotonin reuptake inhibitors are preferred over tricyclic anti-depressants in this
population. Tricyclic antidepressants are associated with ventricular arrhythmias. The
maintenance of employment or retraining for another employment opportunity should be
encouraged in heart failure patients whenever possible to avoid issues related to social
isolation.
Patient Education
Teaching the patient and family self-management strategies is key to the effective
management of heart failure. Patient education should include the following:
• Recognition of signs and symptoms
- Activity intolerance: An activity diary can provide an objective way for
patients or families to track activity tolerance.
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- Extracellular fluid retention: Patients should weigh themselves daily and

report a weight gain of two or more pounds in 24 hours or three or more
pounds in a week. Patients should weigh in the morning after voiding and
before eating. Assessment of a home scale should be part of discharge
planning.
• Medication compliance
- Review benefits of therapy.
- Provide wallet card with current medication list and instruct patient to carry
at all times.
- Assess for and eliminate barriers to accurate and consistent medication
administration.
- Encourage use of one consistent pharmacy.
• Sodium limitation
- Label reading: Patients should know how to determine the sodium content
per serving.
- Patients should be taught to avoid processed and canned foods.
• A physical activity plan to avoid deconditioning should be in place.
• A plan for social support should be in place to avoid social isolation.
• Pneumococcal vaccine and annual influenza vaccine should be a component
of each patient’s treatment plan.
• Patients need to understand the importance of keeping all scheduled
appointments with their heart failure provider, even when they are feeling
well.
• Printed educational resource materials should be provided or the patient can
be referred to www.hfsa.org for heart failure patient education modules.
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Care of the Patient with Lesson: Cardiac Pathological Conditions

Cardiovascular Disorders Topic: Hypertension
Practice Pearls
Hypertensive Crisis: Treatment

When the brain loses the ability to autoregulate as with hypertensive crisis, cerebral
blood flow depends on systemic blood pressure. Hypotension can result in inadequate
cerebral blood flow and therefore potential cerebral hypoxia. For this reason it is
important to lower blood pressure slowly and to avoid hypotension.
Thiocyanate toxicity is a potential side effect for patients on long-term nitroprusside
herapy greater than 48 hours or in those patients with renal insufficiency. Signs and
symptoms of thiocyanate toxicity include blurred vision, tinnitus, and seizures.
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Cardiovascular Disorders Topic: Heart Failure
Compensatory Mechanisms
Sinus tachycardia may be one of the earliest warning signs in heart failure.
Systolic Versus Diastolic Dysfunction

A fourth heart sound (S4) may be heard with diastolic dysfunction. S4 is a late diastolic
filling sound heard during active atrial contraction when the ventricle is noncompliant.
Patients with diastolic dysfunction can become symptomatic with exertion because their
heart rate is increased. With faster heart rates the ventricle has less time to fill. This
reduces left ventricular preload and therefore cardiac output is also reduced.
Flash pulmonary edema can develop if a patient becomes ischemic because ischemia
worsens the noncompliance of the ventricle.
Other Classification Systems

The New York Heart Association classification system is frequently used to assess
functional status. When assessing functional status it is important to assess if the
patient has decreased their level of activity to avoid dyspnea.
Clinical Presentation: Dyspnea/Fatigue/Exercise Intolerance

Symptom assessment is more difficult in elderly patients who often do not experience
exertional dyspnea because they have developed a more sedentary lifestyles to
compensate for their symptoms.
Clinical Presentation: Volume Overload

Many patients with left ventricular end stage heart failure have no signs of pulmonary
congestion because the lymphatic system is effective in removing excess volume from
the interstitial space before the volume enters the pulmonary alveoli.
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Fluid Status
Crackles may occur in the presence of rapid or acute left ventricular heart failure where
the lymph drainage system is not able to compensate for the rapid increase in volume.
Overview of Pharmacological Treatment of Active Heart Failure

Patients with chronic heart failure may have a blood pressure lower than normal and
therefore the hold criteria for these medications may be lower than in patients without
heart failure.
Beta blockers are not initiated when the patient is fluid overloaded or in a
decompensated state. Prior to initiating a beta blocker, the patient’s fluid status should
be optimized and the patient should not require intravenous diuretics or vasodilators.
Always assess creatinine and potassium levels prior to administering medications that
interrupt the renin angiotensin aldosterone system.
Acute Decompensated Heart Failure

Flu and pneumonia vaccines are an important part of the heart failure treatment regime
to prevent an episode of decompensation.
Acute decompensated heart failure has varying degrees of severity. At its most severe
state, you may hear this referred to as Pulmonary Edema.
Inotropes in the Treatment of Acute Decompensated Heart Failure

Other nursing considerations include:
• A fluid restriction of <2 liters/day should be initiated in patients not responsive to
diuretic therapy and in those with a sodium level <130 mEq/L.
• Ultrafiltration (mechanical diuresis) is another treatment option in acute
decompensated heart failure when congestion does not respond to loop
diuretics.
• The routine use of oxygen in the absence of hypoxemia is not indicated.
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Cardiovascular Disorders Topic: Cardiomyopathy
Restrictive Cardiomyopathy: Causes

Other much less common causes of restrictive cardiomyopathy include endomyocardial
fibrosis, radiation-induced myocardial fibrosis in patients who have undergone radiation
treatments, hemochromatosis, glycogen storage diseases and Fabry’s disease.
Restrictive Cardiomyopathy: Patient Management

Careful volume assessment is essential in patients with restrictive cardiomyopathy. Too
much volume results in fluid overload and symptoms of congestive heart failure,
however, an over reduction of volume will further decrease the already decreased
ventricular filling and stroke volume. Patients with restrictive cardiomyopathy have a
very narrow range of acceptable volume.
Hypertrophic Cardiomyopathy: Patient Management

Volume status is very important. Preload is already decreased due to the ventricle’s
inability to expand during filling. Any further loss of filling can result in a decrease in CO.
Many things decrease preload including increased heart rate, diuretics and venous
vasodilators (ACE Inhibitors and nitrates). In patients with hypertrophic OBSTRUCTIVE
cardiomyopathy (HOCM) any decrease in preload will INCREASE the obstruction.
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Cardiovascular Disorders Topic: Valvular Heart Disease
Abnormal Valve Function: Stenosis and Regurgitation

When listening to heart sounds and understanding the compensatory mechanisms that
occur with valve disease, keep in mind a stenotic valve is heard during the part of the
cardiac cycle when the valve is supposed to be open and a regurgitant or insufficient
valve is heard during the part of the cardiac cycle when the valve is supposed to be
closed.
Aortic Stenosis: Clinical Presentation

Patients with little or no coronary disease may still have angina as a result of a
thickened myocardial wall. These patients benefit from the same things that increase
supply to the myocardium in patients with coronary artery disease, such as oxygen and
adequate hemoglobin levels.
Medications that cause arterial vasodilation such as ACE inhibitors and high dose
nitroglycerine should be avoided in patients with severe aortic stenosis.
Aortic Stenosis: Patient Management

Fluid balance in patients with severe aortic stenosis is critical because the ventricular
chamber is no longer able to expand during filling. In order to produce an adequate
stroke volume, complete filling of the ventricular chamber is essential. Changes in
volume status with diuretics or fluids should occur gradually.
Chronic Aortic Regurgitation: Patient Management

The use of arterial vasoconstrictors or vasopressors such as Levophed or dopamine is
contraindicated in aortic regurgitation, as systemic vascular resistance will increase
causing an increase in the regurgitation.
The utilization of an intra-aortic balloon pump is an absolute contraindication in acute
aortic regurgitation and should be avoided in all patients with aortic regurgitation.
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Mitral Stenosis: Clinical Presentation

Atrial fibrillation occurs in over half of the patients with mitral stenosis. When a patient
presents with new onset atrial fibrillation or stroke, mitral stenosis should be ruled out.
Chronic Mitral Regurgitation: Pathophysiology

In patients with mitral regurgitation, an ejection fraction less than 60% is considered
abnormal because a calculated ejection fraction of 60% does not differentiate between
the amount of blood that is moving forward through the aortic valve and the amount of
blood that is moving retrograde through the abnormal mitral valve.
Chronic Mitral Regurgitation: Clinical Presentation

Frequently, the initial diagnosis of mitral regurgitation is made when patients present
with palpitation from new onset atrial fibrillation. Atrial fibrillation develops as a result of
atrial dilatation.
Chronic Mitral Regurgitation: Patient Management

Patients need to be educated regarding the importance of recognizing and reporting
symptoms. These symptoms include shortness of breath or a change in exercise
tolerance.
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Cardiovascular Disorders Topic: Aortic Aneurysm and Dissection
AAA: Surgical Repair

Patients with AAA often have coexisting coronary artery disease. Beta blockers are
used in the perioperative period to reduce mortality and cardiovascular complications.
Lesson 5
Cardiac Surgical Interventions

• Coronary Artery Bypass
• Off Pump Coronary Artery Bypass
• Surgical Valve Replacement and Repair

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Disorders
Lesson: Cardiac Surgery
• Discuss the different types of cardiac surgery and their indications
- Discuss the indications for and common complications of Coronary

Artery Bypass
- Discuss the indications for and common complications of Off-pump

Coronary artery bypass
- Discuss the indications for and common complications of surgical

repair or replacement of the aortic or mitral valve
- Discuss the indications for and common complications of valve

replacement or repair.
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Lesson Take-away – Cardiac Surgery
Topic One: CABG

Introduction
In this lesson we discuss cardiac surgery and the care of patients requiring some sort of cardiac surgery. Surgical
intervention is sometimes in more complicated cases of MI. We’ll look at the various types of surgery as well as the many
challenges of caring for the patient following cardiac surgery including traditional Coronary Artery Bypass Graft (CABG) and
Off Pump Coronary Artery Bypass (OPCAB.) CABG is one strategy for revascularization of coronary arteries when CAD is
present. Its goals include improving survival, minimizing complications of cardiac ischemia, and improving the quality of life.
Classifications
• The 4 classifications of cardiac surgery are:

• Reparative surgery: Used for closure of patent ducts, repair of atria or ventricular septal defects, and
valvotomy
• Reconstructive procedures: CABG, valve repair or replacement, and correction of Fallot’s tetralogy in
children
• Excisional procedures: Repair of ventricular aneurysms and removal of tumors
• Ablative surgery: Performed to eliminate dysrhythmias not responsive to more conventional therapies
Indications
• The decision to perform cardiac surgery is based on a number of factors, the most significant being severity of the cardiac
disease and the stability of the patient’s condition.
Contraindications
• CABG not recommended for patients who do not have adequate native vessels to use as a graft
• Patients with very small coronary arteries and atherosclerosis of the aorta are also challenges in CABG.
• Risks of surgery need to be weighed against benefits for each patient.
Preoperative Assessment
• The key to minimizing any postoperative complications is a thorough preoperative assessment. This includes:
• A thorough history and physical and detailed nursing assessment
• The completion of certain diagnostic studies as part of the preoperative evaluation

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Medications Prior to Surgery

• May need to discontinue certain medications prior to surgery while taking certain other ones right up to the time of surgery
DC aspirin 2-3 days a, DC clopidogrel 5-7 days a, tirofiban and eptifibadtide 4-6 hrs a, abciximab 12-14 hrs a
warfarin 4 days a, reg heparin doesn't need to be DC'd and lovenox 12-24 hrs a.
Preoperative Medications: Antiplatelets and Anticoagulants

• To reduce the incidence of postoperative bleeding, there are guidelines regarding Aspirin, Clopidogrel, Tirofiban and
Eptifibatide, Abciximab, Warfarin, and Heparin (both Unfractionated and Low Molecular Weight.)
Special Preoperative Considerations: Reducing Postoperative Pulmonary Complications

• COPD most common preoperative pulmonary dysfunction
• Preoperative steps to reduce postoperative complications include:
• Teaching all patients how to use the incentive spirometer and perform deep breathing exercises
• Resolving all pulmonary infectious processes
• Achieving optimal fluid status
Traditional CABG
• Intraoperatively, traditional CABG involves:

• General anesthesia • Cardiopulmonary bypass
• Median sternotomy • Myocardial protection
Conduits: Saphenous Vein Graft

• Conduit’s purpose: To create a bypass around the occluded section of the coronary artery
• Vein is most common conduit, especially the greater saphenous vein of the leg.
Conduit: Internal Mammary Artery Grafts

• The Internal Mammary Artery (IMA) another commonly used conduit
• Superior longevity to saphenous vein grafts
• Most CABG surgeries involve a combination of a left internal mammary artery graft and saphenous vein
grafts.
Additional Conduits
• Radial artery • Right gastroepiploic artery

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Cardiopulmonary Bypass Circuit

• Cardiopulmonary bypass used in order to allow the surgeon to operate on a still heart
• Blood is suctioned from the operative site and returned to the patient via the bypass pump, reducing the need for
exogenous blood.
Cardiopulmonary Bypass: Protective Measures

• To provide protection to all vital organs (especially the heart,) these 4 interventions are commonly used:
• Systemic hypothermia is created.
• Blood viscosity is reduced.
• Heparin is introduced into the pump system.
• A “cardioplegic” ("heart-paralyzing”) solution is administered periodically.
Systemic Effects of Cardiopulmonary Artery Bypass

• The effects are numerous, affecting every system throughout the body.
• You need to understand these in order to anticipate and treat postoperative problems quickly and efficiently.
• Effects on the endocrine system: Catecholamine release, RAS Activatio, and Insulin response
• There are also effects on electrolytes, the immune system, coagulation, and the myocardium as well as pulmonary effects
and neurological effects.
Post Operative Care: Blood Pressure and Cardiac Output

• Maintaining adequate cardiac output is of paramount importance during this postoperative period. Goal is a
cardiac index > 2.2 L/min/mm2.
• Monitor cardiac pressures with a central venous catheter, pulmonary artery catheter, or left atrial catheter.
• Try to achieve a MAP of at least 65-70 mm Hg.
• Keep systolic blood pressure between 90 mm Hg and 140 mm Hg
• Hypotension and rewarmng
• Capillary leak and fluid shifting into the interstitial space (third-spacing) might be present if fluid challenges fail to raise
preload. If capillary leak present, inotropes and vasopressors may be needed for hemodynamic support.

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Post Operative Care: Fluid Management

• Total body fluid is usually increased postoperatively.
• Fluid administration may be necessary to maintain circulating volume.
• When LV function is good, the excess fluid is mobilized to produce a large amount of urine.
• Excessive fluid administration however causes increased hemodilution and can adversely affect clotting factors.
Postoperative Care: Management of Hypothermia

• CPB is often accompanied by systemic hypothermia of 32º to 34º C, and the patient is rewarmed to a core
temperature of at least 36º.
• Tendency for afterdrop
• Make all efforts to avoid hypothermia and prevent shivering since there are adverse outcomes associated with
hypothermia.
Postoperative Care: Ventilation and Oxygenation

• Most patients return to the ICU intubated with mechanical ventilation for a minimum of 2 to 4 hours.
Postoperative Care: Epicardial Temporary Pacing Wires

• Postoperatively, some patients may require temporary cardiac pacing.
• Epicardial pacing wires are placed during surgery and removed after surgery. Cardiac tamponade may follow removal, so
patient should be closely monitored for signs/symptoms of cardiac tamponade.
Postoperative Care: Chest Tubes

• To prevent the accumulation of blood in the chest
• Mediastinal and Pleural
• Chest tubes removed when total drainage is < 100 ml for 8 hours

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Postoperative Care: Signs and Symptoms of Tamponade

• Rising filling pressures with a decreased cardiac output and hypotension. CVP,
• PAOP and PAD pressures that are equal
• Sudden drop/stop in previously significant mediastinal bleeding Narrowing of pulse pressure
• Tachycardia, dysrhythmias, and decreased ECG voltage
• Decrease in urine output from fall in cardiac output
Postoperative Care: Pain Control and Sedation

• Short acting narcotics and amnestic agents
Postoperative Care: Laboratory Testing

• Hemoglobin, hematocrit, and potassium levels • Glucose levels
• Coagulation study results
Topic Two: Off Pump CAB
Overview
Here we look at Off-Pump CABG (OPCAB,) an alternative method to performing CABG. This surgery is done without CPB
but does involve a full median sternotomy so that the surgeon has better visability to bypass the vessels that supply the
lateral and posterior walls of the left ventricle.
Advantages and Disadvantages

• Advantages of OPCAB (and avoiding CPB) are:
• Eliminates the need to clamp the aorta in patients with high-risk aortic atherosclerosis (the main advantage)
• Decreased need for blood transfusions
• Less myocardial enzyme release
• Less renal dysfunction
• Less early neurological dysfunction
• Disadvantages of OPCAB are:

• Decreased graft patency due to problems with anastomoses.

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Technical Considerations
• During OPCAB, hemodynamics are controlled by the patient’s heart; not by the CPB system.
• Patients who have persistent instability are converted to on-pump surgery, and those requiring return to on-pump surgery
have a higher risk of mortality and other complications.
• To allow for suturing on a beating heart, medications such as beta blockers or
adenosine can be given to slow or temporarily stop the heart.
• Patient’s temperature is kept as close to normothermic as possible to prevent arrhythmias, bleeding, and postoperative
shivering.
Topic Three: Surgical Valve Replacement and Repair
Introduction
Here we discuss heart valve operations, about 99,000 performed each year in the U.S., most done to repair or replace the
mitral or aortic valves. Some patients have more than 1 valve that is damaged and in need of repair or replacement.
Valve Prosthetics: Overview

• There are 2 types of valve prosthetics; type chosen depends on patient’s anticipated longevity and his/her ability to take
long-term anticoagulants:
• Mechanical valves
• Tissue (bioprosthetic) valves
Mechanical Valves
• More durable than tissue valves, but require life-long anticoagulation with warfarin.
• Are indicated in young patients with no contraindications to anticoagulation.
• 3 primary types:
• Ball and cage
• Single leaflet tilting disc
• Bileaflet valve
Bioprosthetic valves
• Also called tissue valves
• Lower rate of mechanical failure compared to mechanical valves
• Warfarin is not required with tissue valves, but the patient will take a daily aspirin
• Particularly beneficial in
• Older patients who are not already on warfarin for another indication
• Women of child bearing age
• 2 primary types:
• Homograft (allograft)

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• Heterograft (xenograft)
Valve Surgery in Aortic Stenosis: Overview

• The valve surgery may be for either of these:
• Regurgitation (also called insufficiency or incompetence:) A valve isn’t closing properly and blood is leaking
backward instead of moving in the proper one-way direction.
• Stenosis: Leaflets are not opening wide enough and only a small amount of blood is able to flow through the
valve. The narrowed valve means that the heart must work harder to move blood through the body. With stenosis,
valve replacement needed.
Valve Surgery in Aortic Regurgitation: Overview

• Once patients with aortic regurgitation begin to have symptoms, patients should be evaluated for surgical repair or
replacement of the aortic valve.
• Both mechanical and bioprosthetic valves are used.
• Repair is becoming an acceptable alternative to replacement if the cause of the regurgitation involves the valve annulus
and not calcification or stiffness of the valve leaflets. Symptom relief should be the most important guide in making the
decision.
• Age is not a contraindication for surgery.
Valve Surgery in Mitral Regurgitation: Overview

• Mitral regurgitation will lead to symptoms of heart failure at which point surgery should be considered and done as soon as
possible; before significant damage ensues.
• Elderly patients 75 and older have a higher mortality rate with mitral valve surgery than the same age group having aortic
valve surgery.
• Repair is recommended over replacement for the majority of patients with severe chronic MR who require surgery.
Valve Surgery in Mitral Regurgitation: Mitral Valve Repair
• This is the surgery of choice if the valve is suitable for repair.

• Is a technically complex surgery and the patient may require longer cardiopulmonary bypass time.

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Mitral Valve Repair or Replacement

• Mitral valve replacement surgery can be done in a way that preserves part or all of the mitral apparatus. This produces
better postoperative valve compliance than complete replacement does. Complete replacement of the mitral apparatus is
required if the apparatus is damaged beyond repair as is often the case in rheumatic heart disease and severe calcification.
Valve Surgery in Acute Mitral Regurgitation

• Surgery for repair or replacement is the treatment of choice in acute mitral regurgitation.
• Patients having acute mitral regurgitation as a complication of acute MIs have a very high surgical risk.
Valve Surgery in Mitral Valve Stenosis: Overview

• Consider surgery when the valve area becomes less than 1.5 cm2, the point at which most patients begin to experience
symptoms impacting quality of life.
• There are several options for surgery.
Valve Surgery in Mitral Stenosis: Postoperative Care And Summary of Nursing Care in Valve Surgery
• Patients experience excellent short- and long-term outcomes. Improvements felt shortly after surgery.
• For echocardiogram results to be reliable, perform it no sooner than 72 hours after surgery.

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Care of the Patient with Lesson: Cardiac Surgery

Cardiovascular Disorders Topic: CABG
Practice Pearls
Medications Prior to Surgery

Continued administration of antianginals, antihypertensives and heart failure
medications is important to avoid any preoperative myocardial ischemia.
Special Preoperative Considerations: Reducing Postoperative Pulmonary

Complications
It is important to perform preoperative incentive spirometry and deep breathing teaching
even in-patients without lung disease, because postoperative sedation and pain
interfere with the patient’s ability to learn during the early postoperative period.
Traditional CABG
While cardiopulmonary bypass has made it possible to perform surgery on a non-
beating heart, it is not without complications. The two most clinically important
complications of cardiopulmonary bypass are:
• Initiation of systemic inflammatory response
• Development of coagulapathies
Conduits: Saphenous Vein Graft

Patients with hypotension are at increased risk for acute vein graft closure. Aspirin
should be administered as soon as possible after extubation in the postoperative period
to prevent vein graft closure.
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Conduit: Internal Mammary Artery Grafts

If bilateral internal mammary arteries are used, the patient will have a decrease in
sternal blood flow and therefore an increased risk for sternal wound infection. This is a
particular concern in diabetic patients.
Additional Conduits
The Allen’s test must be done to assess for patency of the ulnar artery before the radial
artery can be harvested.
When a radial artery is used as a graft, intravenous nitrates and calcium channel
blockers are used during the perioperative period to reduce the risk of spasm. Oral
medications are continued for a period of time after discharge.
Post Operative Care: Blood Pressure and Cardiac Output

Patients with longer CPB times are at greater risk for capillary leak. In these patients a
large amount of fluid is required to maintain adequate circulating volume.
Left atrial lines are not encountered very often because they are placed by a
transthoracic approach. They require special care and handling.
Postoperative Care: Management of Hypothermia

Gradual rewarming can be accomplished by using a warm forced air warming unit.
Shivering may be stopped by administering IV morphine or thorazine.
Postoperative Care: Ventilation and Oxygenation

Early extubation has been shown to improve patient outcomes.
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Postoperative Care: Chest Tubes

Signs of undrained blood in the pleural space or mediastinum include: decreased breath
sounds, increased inspiratory pressures on the ventilator, or widening of the
mediastinum on chest x-ray.
Dumping of blood with a position change may indicate an acute onset of bleeding.
However, if the blood is dark in color and there is minimal additional drainage, then an
acute problem can be ruled out.
Postoperative Care: Pain Control and Sedation

Elderly patients or those with hepatic disease may take longer to wake up after
anesthesia. If a patient does not wake up in 24 to 36 hours, the differential diagnoses of
stroke or encephalopathy must be considered.
Postoperative Care: Laboratory Testing

Serum potassium should be maintained at 4.5 ± 0.5 mEq/L and magnesium at > 2.0
mEq/L to decrease incidence of cardiac arrhythmia. New transfusion guidelines
recommend transfusion at a Hgb < 6.0 g/dL as a life saving strategy. It is considered
reasonable to transfuse most patients at a Hgb < 7.0 g/dL. It may also be reasonable to
transfuse patients with higher hemoglobin levels who are exhibiting signs of end organ
ischemia.
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Care of the Patient with Lesson: Cardiac Surgery

Cardiovascular Disorders Topic: Surgical Valve Replacement and Repair
Bioprosthetic valves
Antibiotic Prophylaxis Against Infective Endocarditis After Valve Surgery
Endocarditis prophylaxis is appropriate for all patients with a prosthetic valve.
Procedures requiring endocarditis prophylaxis include all dental procedures that involve
manipulation of the gingival tissue or the periapical region of teeth or perforation of the
oral mucosa.
Endocarditis prophylaxis may be used for patients with a prosthetic valve who have an
invasive procedure of the respiratory tract involving an incision or biopsy of the
respiratory mucosa. This does not include standard endoscopic procedures.
Endocarditis prophylaxis is no longer recommended for patients with a prosthetic valve
undergoing a GU or GI procedure.
Valve Surgery in Aortic Regurgitation: Overview

Although reducing systemic vascular resistance is a key treatment strategy in
symptomatic aortic regurgitation, it is important to remember that intra aortic balloon
pumping which is a therapy that can be used to reduce systemic vascular resistance is
contraindicated in aortic regurgitation.
Valve Surgery in Mitral Regurgitation: Mitral Valve Repair

A long cardiopulmonary bypass (CPB) time will predispose the patient to the same
complications of cardiopulmonary bypass as discussed in the lesson on CABG. The
patient will be prone to coagulopathies as well as complications resulting from
prolonged activation of systemic inflammatory response.
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Valve Surgery in Acute Mitral Regurgitation

Patients with an acute MI involving the posterior wall of the left ventricle are at high risk
for papillary muscle ischemia or rupture which can result in acute mitral regurgitation. It
is important to listen to heart sounds in patients with acute MI to detect the presence of
a new holosystolic murmur. Acute mitral regurgitation will present with a new
holosystolic murmur.
Lesson 6
Cardiac Pacemakers and
AICD
• Temporary Pacemakers
• Permanent Pacemakers
• Troubleshooting Pacemaker Malfunctions

118

Disorders
Lesson: Cardiac Pacemakers
• Discuss the type and components of temporary and permanent

pacemakers.
• Define the indications for temporary and permanent pacemakers, potential

problems and treatment of problems related to pacing.
- Identify the indications for initiating temporary pacemakers.
- Identify the components of cardiac pacing systems and the various

settings.
- Describe the types of temporary pacemakers.
- Identify the indications for permanent pacemaker insertion.
- Compare and contrast different common pacing modes.
- Identify and troubleshoot the common complications of cardiac pacing.

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Lesson Take-away - Cardiac Pacemakers
Topic One: Temporary Pacemakers

Introduction
In this lesson we’ll discuss cardiac pacemakers and pacemaker therapy including temporary pacemakers and permanent
pacemakers. We’ll learn the basics of pacing equipment, pacemaker terminology, types of temporary pacemakers, and how
to analyze pacemaker function and troubleshoot malfunctions. Pacemaker therapy often plays an important role in the care
of patients with cardiac disorders, pacemakers providing an artificial stimulus to the atria and/or ventricles in order to either
assist or override the patient’s native/intrinsic cardiac activity.
Pacing
• There are 3 basic indications for pacing (though others exist):
• Bradyarrhythmias
• Tachyarrhythmias
• Situations where they are placed prophylactically
Components
• Temporary pacemaker components include the temporary pacemaker, bridging cables, and electrodes.
Types of Temporary Pacemaker Generators

• The 2 types of temporary pacemaker generators are single chamber (one port) and dual chamber (2 ports.)
Single and Dual Chamber Pacemakers

• Each type allows the clinician to set certain aspects.
Temporary Pacemaker Electrodes

• There are 4 types: transcutaneous, epicardial, transthoracic, and transvenous
• It is important to remember that in reference to pacemaker therapy, the words “leads” and “electrodes” are often used
interchangeably.

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Transcutaneous External Electrodes

• Also called external electrodes
• Transcutaneous means through the skin.
• Deliver the electrical stimulus to the heart via two large patches placed on the chest wall. Directions for pad placement are
generally found on the surface of the pacing pads.
Epicardial Electrodes
• Pacing wires placed by a cardiovascular surgeon during cardiac surgery
• Some surgeons attach only one wire to the atrium and one to the ventricle; others attach two wires to the atrium and/or two
wires to the ventricle.
• Important to know which method each surgeon uses so that you will be best able to utilize pacing therapy should it become
necessary
Transvenous Electrodes
• Pacing via one or two electrodes advanced into the right atrium/ventricle through a peripheral or central vein
• Generally have the negative pacing electrode labeled. It is sometimes referred to as the distal electrode.
Transthoracic Electrodes
• Transthoracic means through the thorax • Is usually attempted only when other temporary pacing
• Are used for ventricular pacing methods have failed
Bridging Cable
• Serves as a bridge between the pacing generator and the electrodes
• The bridging cable and the end of the pacemaker generator have negative (distal) and positive (proximal) ports labeled.
Pacing
• “Pacing” is the firing of electrical energy by the pacemaker generator.

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• “Pacemaker firing” is when electrical energy is fired. The pacing light on the pacing generator will illuminate.
• “Pacing Spikes” will be visible on your EKG tracing.
• “Pacemaker Output” is the energy or electricity fired by the pacemaker. It is measured in milliamps or mA.
Capture
• To have capture, the pacemaker generator must fire electricity, the electrode must deliver the electrical impulse to the
atrium or ventricle, and the chamber must respond to the electrical stimulus.
Stimulation Threshold
• The lowest amount of energy or the lowest amount of output (milliamps) required to cause the heart to respond each time
an electrical impulse is fired by the pacemaker
• When pacing, it is important to use the least amount of energy or output required to capture the targeted chamber.
Sensitivity
• The ability of the pacemaker to see or sense the patient’s intrinsically generated (native) cardiac activity
• The clinician is responsible for setting the sensitivity for each chamber being paced. This is done by performing a
sensitivity threshold.
Demand vs. Asynchronus Pacing

• In “demand” pacing, the clinician sets the sensitivity so that the pacemaker only generates pacing when the patient’s own
heart fails to do so after a set interval of time.
• In “asynchronous” pacing, the sensitivity is set so that the pacemaker cannot see intrinsic cardiac activity and delivers
output (mA) at a set rate.
AV Interval
• Is only available for dual chamber pacing

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Basic Temporary Pacemaker Setup

• You need to know how to set up temporary pacemaker therapy emergently and electively.
• Basic directions:
• In transcutanous pacemakers, generally used emergently, only the ventricle is paced and you need only to set the
rate and output.
• Turn up the current until you obtain capture of the ventricle each time the pacemaker stimulates the myocardium.
• Once capture is obtained, double the mA to provide an adequate margin of safety which allows pacing with
capture to continue should patient’s condition change.
• Because you are pacing through the skin, the mA setting will be much higher than what you would need utilizing
the other three temporary pacing electrodes.
Transvenous, Transthoracic and Epicardial Pacemaker Function

• You need to know how to set up transvenous, transthoracic, and epicardial temporary pacemakers as well.
• Basic directions:
• Set the rate at 80-100 bpm.
• Turn up the mA until you have capture.
• Set the sensitivity.
• Note that some pacemaker generators have an emergency button that when depressed initiates pacemaker
therapy at predetermined default settings.
• Once the patient stabilizes, alternative pacing parameters may be ordered specifically for the patient and
sensitivity and stimulation thresholds can be done.
• Note that when pacing nonemergently, the reason for pacing, patient condition, and physician preference will
dictate pacemaker settings.
Topic Two: Permanent Pacemakers
Introduction
Here we take a look at permanent pacemakers.
Permanent Pacemaker
• Are similar to temporary pacemakers
• Have implanted generators consisting of a lithium battery which lasts 8-10 years and electrical micro circuitry encased in
titanium
• Endocardial or transvenous placement of pacemaker leads is the most common approach for electrode/lead insertion.

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Indications for Permanent Pacing

• Symptomatic bradycardia • Hypersensitive carotid sinus disease
• Acquired atrioventricular block • Congenital anomalies
• Chronic bifasicular or trifasicular block • Nonreversible drug toxicity
• Sinus node dysfunction • Heart failure
• Conduction system injury due to trauma or cardiac
surgery
Pacemaker Modes
• The possible modes for a temporary pacemaker are:

• Fixed
• Demand
• AV Sequential
• The possible modes for a permanent pacemaker are:

• Fixed • AV Sequential
• Demand • Programmable
Pacemaker 5-letter Identifying Code

• The development of a five-letter generic code used to describe any type of pacemaker from any company was
necessitated by the advanced made greatly increasing the capabilities of pacemakers.
Pacemaker Code Positions

• The first letter in the pacemaker identification code indicates the chamber or chambers paced.
• The second letter indicates which chamber or chambers are sensed.
• The third letter indicates the response to sensing.
• The fourth letter refers to programmability of the pacemaker.
• The fifth letter in the designation describes the pacemaker’s antitachycardia function.

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Topic Three: Troubleshooting Pacemaker Malfunctions
Introduction
Here we discuss potential pacemaker complications.
Pacemaker Complications
• Failure to pace (Failure to fire) • Undersensing
• Failure to capture • Oversensing
Failure to Pace
• When the pacemaker fails to deliver an electrical • Is often equipment related
stimulus at the preprogrammed interval • Can also be related to a sensing problem
Failure to Pace Strip

• A pause occurring where a pacemaker spike should have occurred
• Requires replacing the battery, validating the rate setting, checking/tightening lead connections, and performing a
sensitivity threshold
Failure to Capture
• When the pacemaker delivers the pacing stimulus at the appropriate timing interval but it does not result in a depolarization
of the paced chamber
• On an ECG tracing, this would be seen as the absence of a P wave during atrial pacing or the absence of a QRS complex
during ventricular pacing immediately following the pacing spike.
• Both equipment and physiologic causes possible
• Requires assessing and supporting the patient, replacing the battery, increasing the mA, checking/tightening the lead
connections, and attending to identified physiologic alterations.

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Failure to Capture Strip

• When the ECG tracing shows pauses in the rhythm with a pacemaker spike but no P wave or QRS following the spike
Sensing Malfunctions
• There are 2 types of sensing malfunctions:
• Undersensing (failure to sense): The pacemaker is not sensitive to or does not SEE intrinsic cardiac activity and
sends out pacing energy even though the patient’s heart is generating P waves and QRSs at adequate intervals
• Oversensing: The pacemaker interprets noncardiac activity as intrinsic cardiac activity, causing the pacemaker to
inhibit pacing.
Not Sensing Patient’s Intrinsic Rhythm

• If the pacemaker is not sensing the patient’s intrinsic rhythm, the ECG tracing will show pacemaker spikes in inappropriate
locations.
Oversensing
• When the pacemaker interprets noncardiac activity as intrinsic cardiac activity, causing the pacemaker to inhibit pacing.
• Requires changing the battery and checking electrodes and connections, as with other malfunctions. Also requires treating
physiologic causes, unplugging unnecessary electrical equipment and removing it from the room, and doing a sensitivity
threshold.
Pacemaker Interpreting Noncardiac Activity

• If the pacemaker is interpreting noncardiac activity as intrinsically generated, there will be pauses longer than the pacing
interval on the ECG tracing.

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Pacemaker Override
• When a permanent pacemaker is malfunctioning, you can try this as a temporary fix to maintain the patient until the
pacemaker can be assessed and reprogrammed:
• Place a magnet over the implanted generator to stop malfunctions and override the pacemaker. Generally this
puts pacemaker into an asynchronous mode at a predetermined rate of usually 100 bpm. This will stop the
malfunction and help to maintain the patient until the pacemaker can be assessed.
• This rule applies to pacemakers and not AICDs

Stimulation Thresholds Lesson: Cardiac Pacemakers
Topic: Temporary Pacemakers
Pacing Thresholds
Stimulation Thresholds
Determine the stimulation threshold (for each chamber as necessary):
• Set the pacing rate to approximately 10 beats above the patient's intrinsic rate.
• Gradually decrease the output until capture is lost.
• Gradually increase the mA until 1:1 capture is established. This is the stimulation
threshold.
• Set the mAs at least two times higher than the stimulation threshold. This output
setting is sometimes referred to as the maintenance threshold.
Assess the cardiac rhythm for appropriate pacemaker function:

• Capture: Is there a QRS complex for every ventricular pacing stimulus? Is there
also a P wave for every atrial pacing stimulus?
• Rate: Is the rate at or above the pacemaker rate if in the demand mode?
• Sensing: Does the sensitivity light indicate that every QRS complex is sensed?
128
Setting Sensitivity Lesson: Cardiac Pacemakers

Topic: Temporary Pacemakers
Pacing Thresholds
Setting Sensitivity
Determine the sensitivity threshold (for each chamber as appropriate).
• Gradually turn the sensitivity dial counterclockwise (or to a higher numeric
setting), and observe the pace indicator light for flashing,
• Slowly turn the sensitivity dial clockwise (or to a lower numeric setting) until the
sense indicator light flashes with each complex, and the pace indicator light
stops. This value is the sensing threshold.
• Set the sensitivity dial to the number that was half the sensing threshold to
provide a 2:1 safety margin.
Assess the cardiac rhythm for appropriate pacemaker function:
• Capture: Is there a QRS complex for every ventricular pacing stimulus? Is there
also a P wave for every atrial pacing stimulus?
• Rate: Is the rate at or above the pacemaker rate if in the demand mode?
• Sensing: Does the sensitivity light indicate that every QRS complex is sensed?
129
Care of the Patient with Lesson: Cardiac Pacemakers

Cardiovascular Disorders Topic: Temporary pacemakers
Practice Pearls
Epicardial electrodes
By convention, wires exiting to the right of the sternum are atrial electrodes and those
exiting the left side of the sternum are ventricular electrodes. Some surgeons place the
ground lead beneath the sternal incision. Others make one lead longer than the other.
Anytime you are uncertain of electrode location, ask for clarification.
When not in use, epicardial pacing wires should be grounded and taped to the chest
wall. The ends of epicardial pacing wires can be placed in a glove finger, finger cot,
empty needle sheath or commercially available lead protector and secured to the
patient's chest wall with tape. Anytime epicardial wires are handled, gloves should be
worn to prevent unintentional microshock.
Capture
When atrial pacing occurs, the QRS complex is narrow (unless the patient has a
preexisting bundle branch block or other interventricular conduction defect) because
conduction occurs quickly down the normal conduction pathways. With ventricular
pacing, the QRS is wide due to cell to cell conduction which occurs much more slowly
than using the heart’s electrical conduction system.
Stimulation Threshold
The pacemaker you use may look different than these examples. Please refer to your
hospital policy and procedure manual for information on your specific temporary
pacemaker.
130
Demand vs. Asynchronus Pacing

PVCs and PJCs are interpreted correctly as intrinsic activity in patients utilizing
pacemaker technology.
AV interval
Fusion beats: There will be times when the pacemaker initiates pacing at the same time
the patient initiates their own cardiac activity. On the EKG tracing, the paced beat will
look different than if the patient generated their own cardiac activity and it will look
different than the other paced beats. It will be a blend of these two complexes.
131
Care of the Patient with Lesson: Cardiac Pacemakers

Cardiovascular Disorders Topic: Lesson Review
Lesson Summary
If all else fails, support the patient pharmacologically and with an external
transcutaneous pacemaker and/or CPR if needed.
132
Care of the Patient with

Cardiovascular Disorders Glossary
Absolute refractory period where the cell will not depolarize no matter how strong the
period impulse
Afterload the force that a ventricle must overcome to eject contents,

primarily determined by systemic vascular resistance (SVR.)
Increased SVR requires the left ventricle to create higher pressures
to open the aortic valve. This increased workload consumes more
oxygen. An imbalance in the supply and demand ratio of oxygen
results when an increase in demand exceeds the supply or when a
decrease in supply fails to meet the demand. This imbalance leads
to myocardial ischemia.
Akinesis complete loss of movement. Occurs when there is tissue death

such as in a myocardial infarction. The myocardium cannot move.
Allograft from a human
Angiotensin I See Renin-angiotensin-aldosterone system
Angiotensin II: See Renin-angiotensin-aldosterone system
Angiotensinogen See Renin-angiotensin-aldosterone system
Atrial kick the atrial contraction forcing blood from the atriums into the
ventricles. Seventy percent of blood flows passively into the
ventricles. The additional thirty percent of blood flowing into the
ventricles is referred to as the atrial kick.
Automaticity the ability of the cardiac cells to spontaneously depolarize

133
Baroreceptors located in the aortic arch and carotid sinus, these receptors respond
to changes in blood pressure. For example, when the arterial walls
are stretched by an increase in blood pressure, the vasomotor
center in the brain is inhibited resulting in vasodilation. The
baroreceptors also stimulate a decrease in heart rate via the vagus
nerve and the net effect is a decrease in blood pressure.
Bovine an organ from a cow
Cachexic state of wasting, malnutrition, and poor health
Cardiac enzymes also known as markers, these are proteins that are released as a
result of cardiac cell injury or death. They are sensitive and reliable
in indicating the degree of myocardial damage. They include
creatinine kinase (CK,) myoglobin, lactate dehydrogenase or LDH,
troponin I, and troponin T.
Cardiac Output the volume of blood ejected from the heart over 1 minute.
(CO) Measured in liters per minute. Normal CO ranges from 4 to 6 L/min.
Determinants of CO are heart rate and stroke volume. The equation
is as follows: CO=heart rate times stroke volume. Therefore, a
change in either heart rate or the stroke volume affects CO.
Cardiac tamponade when there is an accumulation of fluid in the pericardial sac which
progresses until the point in which it causes the compression of the
atria and ventricles. As the accumulations continues, there is a
decrease in cardiac filling pressures and a decrease in venous
return.
Cardiomegaly hypertrophy or increase in the size of the heart
Cardiomyopathy a disease process of the cardiac muscle; specifically the

myocardium. May be the result of infection, exposure to toxins,
connective tissue disease, or infiltrative disorders or it may be
idiopathic (of unknown cause.)
Catecholamine neurotransmitter epinephrine and norepinephrine
Chemoreceptors receptors located in the bifurcation of the common carotid artery

and along the aortic arch. These receptors respond to changes in
the chemistry of the blood such as oxygen, carbon dioxide, and
hydrogen ion concentrations, particularly to acidosis.
134
Chordae tendendea strong fibrous cords that connect the valve leaflet to the papillary
muscles
CO See Cardiac output
Conductivity ability of the cardiac cells to transmit the depolarization from cell to
cell
Contractility ability of the myocardial muscle tissue to contract and relax after an
electrical stimulus
Depolarization when there is a change in the membrane potential of a cell allowing

sodium to move into and potassium to move out of the cell,
resulting in the cell becoming more positively charged
Diastole also known as filling stage, this is the relaxation of the atriums or
ventricles. It usually refers to the ventricles.
Dysknesis occurrence of uneven or disorganized muscle movement or

contraction of the myocardium
Dysphagia difficulty swallowing
Dyspnea See Dyspnic
Dyspnic shortness of breath
Electrical potential is generated by the capacity to restrict the movement of ions

between the extracellular and intracellular compartments
Electrophysiology The heart has a track of specialized tissue capable of rhythmic

electrical impulses. This track can conduct impulses much more
rapidly than normal cardiac tissue. The tracks are responsible for
the generation and orderly spread of electrical impulses throughout
the heart, producing a coordinated atrial and ventricular contraction
at a normal rate and regular rhythm.
Excitability ability of the cardiac cells to depolarize
Hemoptysis coughing up blood

135
Hypertrophic See Cardiomyopathy

cardiomyopathy:
Hypertrophy the increase in the size of an organ not related to a tumor. In

stenosis, the valve has a narrowed opening, which impedes blood
flow. Insufficiency (also called regurgitation) indicates a valve that
does not close completely.
Hypokinesis a decrease in the ability of the muscle to move. In the area of the
hypokinesis there will be less contraction of the myocardial muscle.
Idiopathic diseases in which the cause is unknown
Injury occurs to the heart muscle whenever there is a shortage in the

supply of oxygenated blood to the heart because there is a decrease
in cellular metabolism and function. It is reversible.
Inotrope anything that increases the strength of contraction of the heart.
Inotropic agents used in reference to various drugs that affect the strength of
contraction of heart muscle (myocardial contractility.)
Insufficiency characterizes valve disease, a situation where the valve has a

narrowed opening which impedes blood flow
Ischemia due to a shortage in the supply of oxygenated blood to the heart,

there is a decrease in the cellular metabolism and function that is
temporary and reversible.
Isoelectric line This line is also referred to as the baseline and is represented by a
dotted line. Any wave above the line is called a positive deflection;
any wave below the line is called a negative deflection (or may be
referred to as inverted.)
Myocardial See Ischemia

ischemia
Necrosis when the shortage in the supply of oxygenated blood becomes so

great that there is tissue death. It is irreversible.
136
Orthopnea shortness of breath related to lying down. It is better when the

person is sitting up. Assess by asking the patient how many pillows
they have to use to be able to breath while lying down.
Papillary muscles are attached to the ventricular wall and work together with the
chordae tendinae to prevent valve leaflets from turning inside out.
The valves open and close in response to pressure changes within
the chambers.
Parasympathetic See Parasympathetic nervous system
Parasympathetic originates in the medulla and is mediated by the vagus nerve. Most
nervous system of the fibers are cholinergic and secrete acetylcholine, which tends
to be inhibitory in its actions. The cardiac effects of parasympathetic
stimulation include a slowing of heart rate, decrease in the speed of
the conduction through the AV node, and slight depression in
contractility.
Paroxysmal periodic episodes of nighttime shortness of breath

nocturnal dyspnea
Pericardial effusion the accumulation of fluid in the pericardial sac
Pericardiocentesis the removal of fluid from the pericardial sac through a needle
Pericarditis inflammation of the pericardial sac
Pheochromocytoma a tumor of the adrenal system that produces catecholamines
Porcine from a pig
Preload the volume of blood in the ventricle at the end of diastole. It is

dependent on venous return and total blood volume, cardiac output,
and length of the diastolic phase of the cardiac cycle.
Proarrythmic causing dysrhythmias or extra heart beats
Pulmonary edema the result of severe pulmonary congestion due to excess fluid in the
interstitial and/or alveolar spaces
137
Pulse pressure the pressure exerted by the blood flow during cardiac contraction. It
is reflective of stroke volume, systemic vascular resistance, and
vessel distensibility.
Pulmonary the resistance to blood flow offered by the vasculature of the lungs.
Vascular Vasoconstriction increases SVR, whereas vasodilation decreases
Resistance (PVR) SVR.
Pulsus alternans produces alternating smaller and larger pulse waves. The variability
in waveforms is a result of inconsistent stroke volume from heart
beat to heart beat.
Pulsus paradoxus produces alternating pattern of blood pressure decreases and

increases associated with altered venous return related to
inspiration and expiration
RAS See Renin-angiotensin-aldosterone system
Regurgitation due to valvular dysfunction resulting in retrograde or the backwards

flow of blood
Relative refractory the cell will depolarize only if it receives a strong stimulus
period
Renin See Renin-angiotensin-aldosterone system

138
Renin-angiotensin- The renin-angiotensin mechanism is activated when there is a drop

aldosterone system in renal perfusion; a decrease in perfusion of the kidneys. This
(RAS) decrease results from blood pressure dropping, illustrating the
kidneys’ important role in regulating blood pressure. The renin-
angiotensin mechanism is stimulated in an attempt to restore
adequate blood flow. The process goes like this: specialized cells in
the distal convoluted tubule release renin. Renin combines with
angiotensinogen to create angiotensin I. Converting enzymes
transform angiotensin I into angiotensin II, an extremely powerful
agent causing generalized vasoconstriction. Conversely, constriction
of the renal arterioles results in a decrease in blood flow to the
kidney, stimulating the posterior pituitary gland to release
antidiuretic hormone which causes conservation of water.
Simultaneously, angiotensin II also stimulates the adrenal glands to
secrete aldosterone which acts on the renal tubules to increase
sodium and water retention. The net effect of the activation of the
RAS is increased blood pressure and blood flow to the kidneys.
Repolarization the return of the membrane potential to its resting state. Potassium
moves into the cell and sodium moves out of the cell.
Sinus dysrhythmia Sinus dysrythmia occurs when the sinus node discharges
irregularly. It occurs frequently as a normal phenomenon and is
commonly associated with the phases of respiration. During
inspiration, the sinus node fires faster; during expiration, it slows.
Starling’s Law first hypothesized in 1914, this law states that, “The greater the
stretch exerted on the ventricle by the EDV, the more forceful the
heart’s contraction.”
Stroke Volume the amount of blood pumped by the ventricle with every systolic
(SV) contraction. A healthy heart will eject more than half the total
ventricular blood volume. Normal stroke volume is 60 to 130
mL/beat.
SV See Stroke volume
SVR See Systemic vascular resistance
Sympathetic See Sympathetic nervous system

139
Sympathetic innervates all parts of the heart, including the atria, ventricles, the
nervous system SA and AV nodes, and all of the blood vessels. The sympathetic
fibers are adrenergic and tend to be excitatory through the release
of norepinephrine. There are three types of sympathetic receptors:
alpha-adrenergic, beta-adrenergic, and dopaminergic.
Sympathomimetic medications that mimic the sympathetic nervous system response

drugs such as epinephrine and norepinephrine
Systemic Vascular the resistance to blood flow offered by the peripheral circulation.
Resistance (SVR) Also referred to as the total peripheral resistance. Vasoconstriction
increases SVR, whereas vasodilation decreases SVR.
Systole contraction of the atriums or ventricles. This contraction propels

blood out of the chambers into the pulmonary circulation for the
atria and out to the aorta and body for the ventricles.
Systolic contraction of the atriums or ventricles. This propels blood out of

the chambers into the pulmonary circulation for the atria and out to
the aorta and body for the ventricles.
Tamponade See Cardiac tamponade
Trabeculae See Chordae tendinae
Tropomyosin Around the actin fibril are interwoven protein rods of troponin and
tropomyosin. They inhibit the ability of actin to connect with
myosin. At the beginning of a contraction, calcium is released and
attaches to troponin, allowing cross bridges on the myosin to attach
to the actin.
Troponin Around the actin fibril are interwoven protein rods of troponin and
tropomyosin. They inhibit the ability of actin to connect with
myosin. At the beginning of a contraction, calcium is released and
attaches to troponin, allowing cross bridges on the myosin to attach
to the actin.
Valsalva’s This maneuver may be done by inhaling and tightening the

maneuver diaphragm and chest muscles while bearing down as if to try to
have a bowel movement. It causes a reflex parasympathetic
response resulting in a slowing down of the heart rate.
140
Vasodepressor fainting due to stimulation of the vagas nerve. It is the result of

synchope parasympathetic vasodilation, which reduces cerebral blood flow.

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Care of the Patient with Cardiovascular

Lesson 1 - Cardiovascular Anatomy & Physiology

Lesson 2 - Assessing the Cardiovascular System

Lesson 3- Management of Acute Coronary Syndromes

Lesson 4 - Pathologic Conditions

Lesson 5 - Cardiac Surgical Interventions

Lesson 6 - Cardiac Pacemakers and AICD

• Blood Supply and Systemic Circulation

• Electrophysiology and Cardiac Cycle

• Cardiac Output, Stroke Volume, Preload, Afterload

Lesson Objectives Module: Care of the Patient with Cardiovascular

Upon completion of this lesson you will be able to:

• Identify the major anatomical structures and the associated physiology of

- Describe the structures and functions of the components of the

- Discuss the conduction system of the heart

- Describe cardiovascular blood flow

- Identify the electrophysiological properties of the cardiac muscles and

- Define and discuss cardiac output, stroke volume, preload, afterload

- Describe the neurohormonal regulation of the cardiac system

Lesson Take-away – Cardiovascular Anatomy & Physiology

Topic One: Structures and Functions

Topic Two: Conduction System

Cellular Electrophysiology of the Heart

© 2008 American Association of Critical-Care Nurses (AACN). All rights reserved.

Topic Three: Blood Supply and Systemic Circulation

Right Coronary Artery

Left Coronary Artery

The Other Coronary Artery

© 2008 American Association of Critical-Care Nurses (AACN). All rights reserved.

Cardiovascular Circulatory System

Topic Four: Electrophysiology and Cardiac Cycle

© 2008 American Association of Critical-Care Nurses (AACN). All rights reserved.

The Depolarization-Repolarization Cycle

Electrophysiology of the Heart

Depolarization and Repolarization

© 2008 American Association of Critical-Care Nurses (AACN). All rights reserved.

Refractory Phases of Repolarization

Phases of the Cardiac Cycle

Topic Five: Components of Cardiac Output

© 2008 American Association of Critical-Care Nurses (AACN). All rights reserved.

© 2008 American Association of Critical-Care Nurses (AACN). All rights reserved.

Topic Six: Autoregulation

Sympathetic Nervous System

Parasympathetic Nervous System

Chemoreceptors and Baroreceptors

© 2008 American Association of Critical-Care Nurses (AACN). All rights reserved.

© 2008 American Association of Critical-Care Nurses (AACN). All rights reserved.

Coronary Arteries Lesson: Cardiovascular Anatomy & Physiology

Myocardial Infarction Lesson: Cardiovascular Anatomy & Physiology

Phases of the Cardiac Cycle Lesson: Cardiovascular Anatomy & Physiology

Cardiac Cycle Left Ventricle

Cardiac Output Lesson: Cardiovascular Anatomy & Physiology

Autoregulation Lesson: Cardiovascular Anatomy & Physiology

Care of the Patient with Lesson: Cardiovascular Anatomy & Physiology

Care of the Patient with Lesson: Cardiovascular Anatomy & Physiology

Care of the Patient with Lesson: Cardiovascular Anatomy & Physiology

The Depolarization-Repolarization Cycle

Care of the Patient with Lesson: Cardiovascular Anatomy & Physiology

• Arterial Circulation Assessment

• Blood Pressure Assessment

• Venous System Assessment

Lesson Objectives Module: Care of the Patient With Cardiovascular