CARDIAC NOTES

Anatomy and Physiology Heart

 Three layers
o Endocardium (Inner layer) Ex (endocarditis is inflammation of inner layer)
o Myocardium (middle layer /muscular lining)
o Epicardium/pericardium (outer layer/ sac)
 Pericardium
The pericardium has 2 layers filled w/ fluid. When it gets inflamed and filled w/ more fluid
there is Pericardial friction rub
In order to distinguish a pericardial friction rub (heart) from pleural friction
rub (lungs) need to ask pt to hold respiration for few seconds

Four chambers
 Heart valves
o Atrioventricular (A-V) valves (S1/SYSTOLE)
o Semilunar valves (S2/DIASTOLE)
 Coronary arteries (Feed the heart)
 Cardiac conduction system
 Cardiac hemodynamics (pressure of blood/ fluid volume status)
Overview of Anatomy and Physiology – Heart
• Cardiac Cycle
• Systole (contraction)
• Diastole (relaxation)
• Cardiac Output= HR X SV
Anything that decreases cardiac output causes: dizziness, fatigue, LOC changes, and
shortness of breath
• HR
• SV
• Preload (diastole, relaxation, if there is a lot of fluid the preload will be increased and vice)
• Afterload (systole, contraction)
• Contractility
• Autonomic Nervous System (ANS)
• SNS (increase)
• PSNS (decrease)
Terms - Cardiac Output
• Stroke volume: amount of blood ejected with each heartbeat
• Cardiac output: amount of blood pumped by ventricle in liters per minute
• Preload: degree of stretch of cardiac muscle fibers at end of diastole
• Contractility: ability of cardiac muscle to shorten in response to electrical impulse
• After load: resistance to ejection of blood from ventricle
• Ejection fraction: percent of end diastolic volume ejected with each heart beat

CO = SV x HR
Control of heart rate
Autonomic nervous system, baroreceptors (located in aortic arch, right carotid, the
monitor pressure throughout the body, when the pressure is low, they send a
signal to speed the HR)
Control of stroke volume
Preload: Frank-Starling Law (AMOUNT THE HEART CAN STRETCH WHEN FILLING
UP)
After load: affected by systemic vascular resistance, pulmonary vascular resistance
 Contractility increased by catecholamines, SNS, some medications (Epinephrine,
dopamine)
Decreased by hypoxemia, acidosis, some medications

Cardiac Conduction System

Properties of the conduction system:
Automaticity (ability of stimulate on its own)
Excitability
Conductivity
Sinoatrial (SA) node
Internodal pathways
Atrioventricular (AV) node
Bundle of His
Bundle Branches
Purkinje fibers

Terms - Cardiac Action Potential

Depolarization: electrical activation of cell caused by influx of sodium into cell while
potassium exits cell
Repolarization: return of cell to resting state caused by re-entry of potassium into cell
while sodium exits
Refractory periods
Effective refractory period: phase in which cells are incapable of depolarizing
Relative refractory period: phase in which cells require stronger-than-normal stimulus to
depolarize
Assessment
Health history
Demographic information
Family/genetic history
-CAD
-DM (bc glucose damages the vessels, makes them hard, decrease blood flow, and
perfusion)
- HTN
Cultural/social factors (smoking, drinking, drugs, food)

Risk factors
Modifiable (diet, weight, drugs, smoking, exercises, stress management)
Nonmodifiable (age, gender, race, genetics)
Most Common Clinical Manifestations (MI, ANGINA, HF)
• Chest pain (due to lack of O2, hypovolemia or low BP, can also cause chest pain)
• Dyspnea (difficulty breathing)
• Peripheral edema, weight gain (retention of H2O.)
• Fatigue (not enough O2, pt gets tired)
• Dizziness, syncope, changes in level of consciousness
• Acute Coronary Syndrome (is prodromal(before) like S/S that there is a cardiac
problem.
-Shortness of breath
-Swell feet
- Tired
• Experience prodromal symptoms for a month to more prior to acute event
Assessment
Medications
Nutrition (Low Na, low cholesterol)
Elimination (avoid straining, to avoid increase pressure)
Activity, exercise
Sleep, rest
Self-perception, self-concept
Roles, relationships
Sexuality, reproduction
Coping, stress tolerance
Prevention strategies

Laboratory Tests
• Cardiac biomarkers
• Serum Enzymes:
- Creatinine Kinase (CK), CK-MB
Whenever there is injury to the heart muscle
• CK formerly known as (CPK)- elevation indicates muscle injury
• CK-MB: specific to myocardial muscle, rises within 6 hours of injury and peaks at 18 hours post
injury and returns to normal within 2-3 days.
• Useful in DX of MI
- Lactic dehydrogenase (LDH)
After an MI, LDH is always elevated. THIS TEST IS DONE AFTER TROPONIN I, AND CK-MB
• Found in many body tissues; elevation is detected within 24-72 hours after MI,
peaks in 3-4 days and returns to normal around 2 weeks.
• Useful for delayed DX of MI
- Troponin T and I (First to be drawn, bc is more specific)
Is released when there is damaged to cardiac muscle (is the most important to detect Heart attack,
mainly Troponin I which is specific for heart muscle, troponin T is heart muscle and skeletal muscle)
• Onset is before CK-MB in MI; peaks at 24 hours and returns to normal around 2 weeks; provides
early sensitivity
• More specific to cardiac injury for DX of MI

Laboratory Tests
Lipid profile: to determine risk factors of developing atherosclerosis (to determine what
build up of plaque)
Total serum lipids= 400-800 mg/dL
Triglycerides: lipids stored in fat tissue; normal 100-200 mg/dL
Cholesterol: main lipid associated with CAD; normal < 200mg/dL
Lipoproteins: proteins in the blood to transport cholesterol, triglycerides and other fats
HDL= 35-70 mg/dL (M); 35-85 mg/dL (F)
LDL= < 160 mg/dL

Laboratory Tests
Brain (B-type) natriuretic peptide (BNP)
BNP, is secreted from the ventricules, it indicates, INCREASED PRELOAD, TOO
MUCH FLUID. IS TO RULE OUT CHF. If BNP is elevated then I need to look further
for CHF.
A neurohormone that helps regulate BP and fluid volume.
Secreted from the ventricles in response to increased preload with elevated ventricular
pressure
Useful in the diagnosis of HF
 Greater than 100 pg/mL
C-reactive protein (CRP)
A protein produced by the liver in response to inflammation. It is not specific for heart.
Anywhere where there is infection or injury to the body (Heart attack, plaque to heart, cut
in the toe anything that causes damage in the body elevates this protein)

Elevated CRP is increased risk for CAD (Coronary Artery Disease)

High: 3.0 mg/dl or greater
Moderate: 1.0-3.0 mg/dL
Low: less than 1.0 mg/dL

Laboratory Tests
Homocysteine (not specific for heart attack)
An amino acid linked to the development of atherosclerosis (deposit of plaque in
arteries) because it can damage the endothelial lining of the arteries and cause thrombus
formation
A 12 hour fast is necessary before drawing a blood sample for an accurate serum
measurement
Optimal: less than 12 mol/L
Borderline: 12-15 mol/L
High risk: above 15 mol/L

Myoglobin (not a primary heart test)

O2 binding protein found in heart and skeletal muscle. Found in the blood when released
following muscle injury.
Laboratory Tests
Coagulation Studies
Partial thromboplastin time (PTT): 60-70 (Heparin)
Activated partial thromboplastin time (APTT): 20-39
Prothrombin time (PT): 9.5-12 (Coumadin)
International normalized ratio (INR); 2-3.5
Hematologic Studies
Complete blood count (CBC)
Hematocrit: M 42-52% F 35-47%
Hemoglobin M 13-18 g/dL F 12-16 g/dL
Platelets: 150,000-450,000/ mm
White Blood Cells (WBC)
Drug Levels
Digoxin: Therapeutic range is 0.5-2 ng/mL
Digoxin has a narrow therapeutic range. Drop blood levels routinely
Quinidine: Therapeutic range is 2-6 mcg/mL
Laboratory Tests
Electrolytes: normal levels are essential for proper cardiac function
Potassium (K): 3.5-5.0
Hypo: ventricular dysrhythmias, flattened T wave or presence of U wave
Hyper: ventricular dysrhythmias, tall peaked T waves and asystole
Sodium (Na): 135-145
Hypo: intracellular osmotic fluid shift= brain edema
Hyper: increased BP, abnormal HR, seizures, neurological impairment
Calcium (Ca):
Low Ca = low HR
Hight Ca= tachycardia
Hypo: ventricular dysrhythmias, prolonged QT interval, and cardiac arrest
 Hyper: shorten the QT intervals and causes AV block, cardiac arrest

Magnesium (Mg):
High Mg=Bradycardia
Low Mg= Tachycardia
Hypo: ventricular tachycardia and fibrillation
Hyper: bradycardia, hypotension, prolonged PR and QRS intervals

Electrocardiography
12 lead ECG
Continuous monitoring: hardwire, telemetry
Signal-averaged electrocardiogram
Continuous ambulatory monitoring (HOLTER)
Transtelephonic monitoring
Wireless mobile monitoring
Cardiac stress testing
Exercise stress testing (how heart work in stress, exercises)
Pharmacologic stress testing (how pt response under certain meds)
Diagnostic Tests
Radionuclide imaging
Myocardial perfusion imaging (if heart is perfussing well)
Test of ventricular function, wall motion
Computed tomography CT (Looking at structures)
Positron emission tomography
Magnetic resonance angiography
Diagnostic Tests
Echocardiography (ultrasound of the heart)
US of heart to evaluate the structure and function of chambers and valves
Phonocardiography (recording w/ a simutaneos ECG)
Graphic recording of heart sounds with simultaneous ECG
Coronary Angiography/Arteriography
Invasive procedure where cardiologist injects dye into coronary arteries and
immediately takes a series of x-ray films to assess structure of arteries

Cardiac Catherization
Invasive procedure study used to measure cardiac chamber pressures, assess patency of
coronary arteries
Requires ECG, hemodynamic monitoring; emergency equipment must be available
Assessment prior to test; allergies, blood work (PT, PTT)
Assessment of patient post-procedure; circulation, potential for bleeding, potential for
dysrhythmias
Activity restrictions
Patient education pre-, post-procedure

Hemodynamic Monitoring
• Central Venous Pressure (CVP) (volume status)
High fluid or hypervolemia= Increased CVP and vice
CVP is looking at the right side of the heart
• Appropriate for clients who require accurate monitoring of fluid volume status but
are not candidates for the more invasive pulmonary artery pressure monitoring
• Done by a central catheter with the tip in the SVC to measure the R heart filling pressure
• Provides data about right ventricular preload. Not for left heart pressures
• Normal CVP 2-8 cm H2O or 2-6 mm Hg
• Decreased CVP= decreased circulating volume
 • Increased CVP= increased blood volume or right heart failure

Diagnostic Tests
• Pulmonary artery pressure (PAP)
PAP = left side of heart
High PAP = TOO MUCH FLUID and vice
• Appropriate for critically ill clients requiring more accurate assessments of left heart
pressures
• Pulmonary artery catheter (Swan-Ganz) has the tip in the pulmonary artery
• Pressure is obtained after the tip is wedged into a pulmonary capillary and is called
PCWP
• Good indicator of left ventricular preload also called left ventricular end diastolic pressure
(LVEDP)

Normal Values of Hemodynamic Readings

Diagnostic Tests
Intra-Arterial Blood Pressure Monitoring
To obtain direct and continuous BP measurements in critically ill patients who have
sever hyper or hypertension
Arterial catheters are useful when ABGs are needed frequently
Allen test completed prior to insertion of catheter.
Allen test is to check for perfusion in the hand
-Ask pt to make a fist
- Occlude both (ulnar and radial arteries)
- Ask pt to open hand
- Release ulnar artery and check for return of blood to hand (red/pink hand)

Common Cardiovascular Medications

Ace Inhibitors “ prils”
Angiotensin Receptor Blockers “sartans”
Beta Blockers: “olols”
Calcium Channel Blockers: “dipine”
Adrenergic Agonists (EPINEPHRINE, DOBUTAMINE)
Anticoagulants: Coumadin, Heparin
Cardiac Glycosides: Digoxin
Antidysrhythmics (Lidocaine, Quinidine) to correct fast dysrhythmias
Diuretics (eliminate excess fluid)
Antihyperlipedemia (niacin, statin, Lipitor)
Thrombolytics (clot busters, but you have to have a clot to give this)
Vasodilators (hydralazine )
Nitrates (vasodilation, for chest pain. Too much could aggravate angina
due to decrease perfussion)
Analgesics
Morphine
Oxygen
Nytroglicerine
Aspirin
Physical Assessment-Cardiac
General appearance
Inspection of skin
Blood Pressure
Arterial pulses
 Jugular venous pulsations
Heart inspection and palpation
Heart auscultation
Inspection of extremities
Assessment of other systems
Lungs
Abdomen
Cardiac Assessment- Auscultation
• Normal Heart Sounds
• S1: Tricuspid and mitral closure creates first sound
• Heard the loudest at the apical
• S2: closure of the pulmonic and aortic valves
• Heard loudest over the aortic and pulmonic areas
• Abnormal Heart Sounds
• S3: heard after S2
• Normal in children and adults up to 35 or 40 (physiological S3)
• Abnormally is due to overload of one or both ventricles (significant in HF)
• S4: heard before S1
• Generated during atrial CX as blood forcefully enters a noncompliant ventricle
• Caused by ventricular hypertrophy: HTN, CAD, cardiomyopathy, etc.

Cardiac Assessment- Auscultation

Systolic clicks:
Caused by opening of rigid and calcified aortic or pulmonic valve during
ventricular CX
Murmurs: (due to valvular problems)
Created by turbulent blood flow
Causes of the turbulence may be a critically narrowed or malfunctioning valve
Friction Rub: (two layer of pericardium friction
together)
Harsh grating sound that can be heard in both systole and diastole.
Caused by abrasion or inflamed pericardial surfaces from pericarditis

Cardiovascular Conditions:

1.Coronary Atherosclerosis
Homocysteine is a test specific for atheroesclerosis
Atherosclerosis is the abnormal accumulation of lipid deposits and fibrous tissue within
arterial walls and lumen.
In coronary atherosclerosis, blockages and narrowing of the coronary vessels
reduce blood flow to the myocardium.
Cardiovascular disease is the leading cause of death in the United States for men and
women of all racial and ethnic groups.
CAD, coronary artery disease, is the most prevalent cardiovascular disease in
adults.

Pathophysiology of Atherosclerosis
Inflammation (red and swollen area)
Coagulation (stop bleeding)
Bradikinin, which causes the pain

-Anywhere there is an ischemia the goal is to reperfuse

Risk Factors

Non-Modifiable
Family Hx of CAD
Older than 45 years old
Gender (men earlier than women)
Race

Modifiable
Hyperlipidemia
Smoking
HTN
DM
Obesity
Physical inactivity
Laboratory Tests
Lipid profile: to determine risk of developing atheroclerosis
Total serum lipids= 400-800 mg/dL
Triglycerides: lipids stored in fat tissue; normal 100-200 mg/dL
Cholesterol: main lipid associated with CAD; normal < 200mg/dL
Lipoproteins: proteins in the blood to transport cholesterol, triglycerides and other fats
HDL= 35-70 mg/dL (M); 35-85 mg/dL (F)
LDL= < 160 mg/dL
Medications
HMG-COA Reductase Inhibitors
“Statins”- Atorvastatin ( Lipitor)
Nicotinic Acids
“Niacins” (flushing, like a tomato)
Fibric Acids
Gemfibrozil ( Lopid)
Bile Acid Sequestrants
Cholestyramine ( Questran)
Cholesterol Absorption Inhibitors
Ezetimibe (Zetia)
Omega-3-acid
Fish oils
The main goal of all this categories is to lower cholesterol
The main side effect of this meds is
- Myalgia (muscle pain)
- GI – bloating, constipation, dispepcia (GERD)
- Myositis (inflammation of muscle)

Clinical Manifestations
Symptoms are due to myocardial ischemia
Symptoms and complications are related to the location and degree of vessel obstruction
-Angina pectoris (Ischemia)
-Myocardial infarction (if the ischemia wasn’t corrected then MI happens)
-Heart failure
-Sudden cardiac death (heart suddenly stops beating)
 Clinical Manifestations
The most common symptom of myocardial ischemia is chest pain; however, some
individuals may be asymptomatic or have atypical symptoms such as weakness, dyspnea,
and nausea.
Atypical symptoms are more common in women and in persons who are older,
or who have a history of heart failure or diabetes. (nausea, weight gain)

2. Angina Pectoris
CAD (the buildup of plaque in the arteries lead to angina pectoris)
• A syndrome characterized by episodes or paroxysmal pain or pressure in the anterior
chest caused by insufficient coronary blood flow.
• Physical exertion or emotional stress increases myocardial oxygen demand and the coronary
vessels are unable to supply sufficient blood flow to meet the oxygen demand.

- 3 types of Angina
a) Stable angina: exertional (predictable response to increased activity)
With stable angina, the pt take the nitro, and pain goes away.

b) Unstable angina:(preinfarction) exertional- with exercise or stress

This one happens right before the MI
It is not relieve with med and rest. Need to go to ER IMMEDIATELY

c) Variant angina: (prinzmetals) spasms of coronary artery

Spasm means smaller (small blood vessel)
Often awakens pt from sleep. Treated with CCB

With angina the main med is nytroglicerin (1 SL) and if after 5 min if still hurts, go to ER
COSTOCHONDRIATIS (MUSCLE PAIN) is often confused with chest pain
(GERD, PNEUMONIA, PANIC ATTACKS) can be confused with heart attack
For Angina the main thing is re-perfuse !!!

Angina pain varies from mild to severe

May be described as tightness, choking, or a heavy sensation.
Frequently retrosternal and may radiate to neck, jaw, shoulders, back or arms (usually left
side).
Anxiety frequently accompanies the pain.
Other symptoms may occur: dyspnea/shortness of breath, dizziness, nausea, and
vomiting.
The pain of typical angina subsides with rest or Nitroglycerine.
Unstable angina is characterized by increased frequency and severity and is not relieved by
rest and NTG. Requires medical intervention!

Treatment
Treatment seeks to decrease myocardial oxygen demand and increase oxygen supply
Medications
-Beta-blockers & Ca Channel blocker (for long term/chronic angina) these 2 meds are also
used for HTN and Dysrhythmias.
- Nitrates (nitroglycerin) for acute/immediate angina
Oxygen
Reduce and control risk factors
Reperfusion therapy may also be done

Medications
Nitroglycerin
Beta-adrenergic blocking agents (to decrease the heart and the demand of O2)
Calcium channel blocking agents (to decrease the heart and the demand of O2)
Antiplatelet and anticoagulant medications
Aspirin
Clopidogrel and ticlopidine (Plavix)
Heparin
Glycoprotein IIB/IIIa agents

Treatment of Angina Pain

Treatment of angina pain is a priority nursing concern.
Patient is to stop all activity and sit or rest in bed.
Assess the patient while performing other necessary interventions. Assessment includes
VS, and observation for respiratory distress, and assessment of pain. In the hospital setting,
the ECG is assessed or obtained.
Administer oxygen.
Administer medications as ordered or by protocol, usually NTG.
Collaborative Problems
Acute pulmonary edema
Heart failure
Cardiogenic shock (shock is always related to lack of perfusion)
Dysrhythmias and cardiac arrest
Myocardial infarction

Patient Teaching
Lifestyle changes and reduction of risk factors
 Explore, recognize, and adapt behaviors to avoid to reduce the incidence of episodes of
ischemia
Teaching regarding disease process
Medications
Stress reduction (bc stress increase
SNS)
When to seek emergency care
Angina Pectoris Review
Warning sign of impending MI
Women and older adults present atypically
3 types
Stable angina: exertional
Unstable angina:( preinfarction) exertional- with exercise or stress
Variant angina: (prinzmetals) spasms of coronary artery
Pain unrelieved by rest or nitro and lasting more than 15 min differentiate
angina from MI
Precipitated by exertion or stress
Relieved by rest or nitro
Symptoms last < 15 min
Angina Review
Client education:
Stop activity and rest
Place nitro under tongue
Should be a bite to the med
3 in 15 minutes if not go to ER
HEADACHE is most common s/e of nitro
Encourage patient to sit and lie down slowly
Encourage smoking cessation
Diet and lifestyle modification
Get cholesterol and B/P checked regularly
Remain physically active

Angina- Nursing Diagnosis

Risk or decreased cardiac tissue perfusion
Anxiety related to cardiac symptoms and possible death
Deficient knowledge
Noncompliance

Myocardial Infarction
An area of the myocardium is permanently destroyed. Usually caused by reduced blood
flow in a coronary artery due to rupture of an atherosclerotic plaque and subsequent
occlusion of the artery by a thrombus.
In unstable angina, the plaque ruptures but the artery is not completely occluded.
Unstable angina and acute myocardial infarction are considered the same process but at
different point on the continuum.
The term acute coronary syndrome includes unstable angina and myocardial infarction.
Blockage of one or more of the coronary arteries
Causes:
Arteriosclerosis, emboli, thrombus, shock, hemorrhage, hypoxia leading to necrosis
Classic sign: substernal pain or feeling of heaviness on chest
Patients may report:
Substernal pain or pain over pericardium ↑ 15 min
Pain that is heavy and radiating down left arm
 Spontaneous pain not relived by nitro or rest
Pain that radiates to jaw
Pain accompanied by SOB, pallor, diaphoresis, N/V
↑HR, ↓ B/P, ↑ temp, ↑ RR

When the pain is not relieved by nitro, most probably is not an angina anymore
but an MI. This is when MONA comes into play

Mmorphine (to relieve the pain)

OOxygen (bc coronary arteries need to oxygenate)
NNitroglycerin (to vasodilation causing reperfusion)
AAspirin

Aspirin prophylactic: 81 mg
Aspirin Acute MI: 325-650 mg

Other causes of chest pain that may be confused with MI:

-GERD
-Anxiety
-Costochondriatis (inflammation of the cartilage that connects the ribs to sternum
and spine.)
-PE

Diagnosis
EKG
Angina= ST depression and/or T wave inversion (ischemia)
MI= T wave inversion (ischemia), ST elevation (injury), and abnormal Q wave
(necrosis)
When cardiac muscle suffers ischemic injury, cardiac enzymes are released into the blood
stream providing specific markers
Myoglobin
CK-MB
Troponin I
Troponin T
Thallium scans: (Look at the coronary arteries)
Cardiac Cath: evaluates blockage

Laboratory Tests
• Cardiac biomarkers
• Serum Enzymes:
• Creatinine Kinase (CK), CK-MB
• CK formerly known as (CPK)- elevation indicates muscle injury
• CK-MB: specific to myocardial muscle, rises within 6 hours of injury and peaks at 18
hours post injury and returns to normal within 2-3 days.
• Useful in DX of MI
• Lactic dehydrogenase (LDH)
• Found in many body tissues; elevation is detected within 24-72 hours after MI,
peaks in 3-4 days and returns to normal around 2 weeks.
• Useful for delayed DX of MI
• Troponin T and I
• Onset is before CK-MB in MI; peaks at 24 hours and returns to normal around 2 weeks;
provides early sensitivity
• More specific to cardiac injury for DX of MI
Management
 Monitoring
V/S q15 until stable (q 5min when the pt first come in)
EKG continuous monitoring (within 10 min in ER)
Location, severity, quality of pain
Hourly output (kidneys need O2 and fluid etc, if pt have decreased cardiac output, there is decreased
perfusion to kidneys and they don’t work, therefore there will be minimal output)
Labs
MONA
When B/P falls rapidly= dopamine
Thrombolytics= streptokinase, retavase
Promote energy conservation
Medications
Vasodilators (nitro, hydrolazine)
Nitroglycerin
Analgesics
Morphine
Beta-blockers/ Calcium Channel Blockers (to slow HR, decrease O2 demand)
Lopressor (Metoprolol), Norvasc (Amlodipine) Cardizem (Diltiazem)
Thrombolytic agents
-Streptokinase
Antiplatelet
-Aspirin, Clopidogrel
Anticoagulants
-Heparin, Lovenox
Glycoprotein inhibitors
Integrillin (blocks binding of fibrinogen=blocked platelet aggregation)

Surgical Interventions (invasive procedures)

Percutaneous transluminal coronary angioplasty (PTCA)
-Is a minimally invasive procedure to open up blocked coronary arteries, allowing blood to
circulate unobstructed to the heart muscle.
Coronary artery bypass graft (CABG)

Complications
Heart failure and cardiogenic shock
Ischemic mitral regurgitation
Ventricular aneurysm/rupture
Dysrhythmias

Collaborative Problems
Acute pulmonary edema
Heart failure
Cardiogenic shock (main problem is decreased BP, bc shock means low)
Dysrhythmias and cardiac arrest
Pericardial effusion and cardiac tamponade (right side failure)

Invasive Coronary Artery Procedures

AKA: Percutaneous Coronary Interventions (PCI)
Percutaneous Transluminal Coronary Angioplasty
A balloon tipped catheter is used to open blocked coronary vessels and resolve
ischemia
Purpose is to improve blood flow within the coronary artery by compressing and
“cracking” the atheroma
 Catheters are usually introduced into the femoral artery up to the aorta and into the
coronary arteries
Angiography is performed using dye to identify the blockage
Coronary Artery Stent
A metal mesh that provides structural support to a vessel at risk of acute closure
Atherectomy
An invasive interventional procedure that involves the removal of the atheroma,
or plaque from the coronary artery by cutting, shaving or grinding
Brachytherapy
Reduces the recurrence of obstruction, preventing vessel restenosis by inhibiting
smooth muscle cell proliferation
Complications of PCI (monitor for Bleeding)
• Complications during a PCI procedure
• Dissection
• Perforation
• Abrupt closure
• Vasospasm of coronary artery
• Acute MI
• Acute dysrhythmias
• Cardiac arrest
• Complications after PCI procedure
• Abrupt closure
• Bleeding at insertion site
• Retroperitoneal bleeding
• Hematoma
• Arterial occlusion
• Acute renal failure
• Coronary Artery Bypass Graft (CABG)
• A blood vessel is grafted to an occluded coronary artery so that blood can flow beyond
the occlusion
• Indications for CABG
• Alleviation of angina that cannot be controlled with medication or PCI
• Treatment of left main coronary artery stenosis or multivessel CAD
• Prevention and treatment of MI, dysrhythmias or heart failure
• Complications of CABG
• Hemorrhage
• Dysrhythmias
• MI
• Infection is not an acute (immediate) concern within 24 bc pt will receive prophylactic
antibiotic. So the first thing to worry wont be infection but HEMORRHAGE
Nursing Management-CABG
Pre-operative
Assessing the patient
Reducing the fear and anxiety
Monitoring and managing potential complications
Providing patient teaching

Postoperative
Assessing the patient
Monitoring for complications
Restoring cardiac output (BP, HR, I/O, Shortness of breath, increased energy. This shows pt
perfussess well)
Promoting adequate gas exchange
 Maintaining fluid and electrolyte balance (Na, K, Mg, Ca)
Relieving pain (watch for respiration !!)
Maintaining adequate tissue perfusion
Maintaining normal body temperature

Potential Complications of Cardiac SX

Hypovolemia
Persistent bleeding
Cardiac tamponade (right sided HF bc there is fluid buildup, increased pressure)
Fluid overload
HTN
Tachydysrhythmias
Bradycardia
Cardiac failure
MI
Hypothermia

Management of Patients With Complications From Heart Disease (Part 2)

Heart Failure
• The inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen
and nutrients.
- (MI, HTN, Cardiac tamponade can lead to HF)
• A syndrome characterized by fluid overload or inadequate tissue perfusion.
• The term heart failure indicates myocardial disease, in which there is a problem with the
contraction of the heart (systolic failure) or filling of the heart (diastolic failure).
• Some cases are reversible.
• Most heart failure is a progressive, lifelong disorder managed with lifestyle changes and
medications.
Clinical Manifestations
• Right-sided failure
• RV cannot eject sufficient amounts of blood and blood backs up in the venous system.
This results in peripheral edema, hepatomegaly, ascites, anorexia, nausea,
weakness, and weight gain.
• Left-sided failure
• LV cannot pump blood effectively to the systemic circulation. Pulmonary venous pressures
increase and result in pulmonary congestion with dyspnea, cough, crackles, and
impaired oxygen exchange.
• Chronic heart failure is frequently biventricular. (Congestive HF)
Classification of Heart Failure (Once the heart is damage is difficult to go back)
• NYHA classification of heart failure
• Classification I: no symptoms w/activity
• Classification II: symptoms w/ordinary exertion
• Classification III: displays symptoms with minimal exertion
• Classification IV: symptoms at rest (means cardiac arrest is coming)
• Treatment guidelines are in place for each stage
Stages of Heart Failure
• ACC/AHA classification of heart failure
 • Stage A: high risk but no structural disease or S/S
• Stage B: LV dysfunction or heart disease no S/S
• Stage C: LVD or structural disease- prior S/S
Stage D: End stage HF requiring interventions (pt is waiting for transplant)
- In this stage pt is given Milrinone & Inamrinone (only used short term for end stage HF, have
the same function as Digoxin)

Medical Management of Heart Failure

• Eliminate or reduce etiologic or contributory factors. (obesity, HTN, High cholesterol)
• Reduce the workload of the heart by reducing afterload and preload. (r/t fluid)
• Optimize all therapeutic regimens.
• Prevent exacerbations of heart failure.
Medications are routinely prescribed for heart failure.

Common Medications
• Angiotensin Converting Enzyme Inhibitors (ACE Inhibitors)
• Angiotensin II Receptor Blockers (ARBS)
• Beta-blockers (decrease the HR, RELAX SMOOTH MUSCLE AROUND THE VEINS)
• Diuretics
• Digitalis (Digoxin, decrease HR, Increase contractility, slow conduction to AV)
• Hydralazine (vasodilator)
• Isosorbide Dinitrate (nitrate)

Lab and Diagnostics for Heart Failure

BNP (indicator of HF, send message that there is too much fluid)
– ↓100= no heart failure
– b/t 100-300= heart failure present
– ↑300= mild heart failure
– ↑600= moderate heart failure
– ↑900= severe heart failure

CVP (Central venous pressure)

(Right side of the heart. Pressure always means fluid)
– Elevated in Left sided and right sided

• PAP (Pulmornary arterial pressure)

(Left side of the heart)
– Elevated in L sided

• PAWP (pulmonary arterial wedge pressure)

– Elevated in L sided

• CO (Cardiac Output)
– Decreased

Assessment
• Health history
• Sleep and activity (Paroxismal Nocturnal Dyspnea)
Waking up at night and can’t breath
 • Knowledge and coping
• Physical exam
– Mental status
– Lung sounds: crackles and wheezes (Dyspnea, Orthopnea)
– Heart sounds: S3
– Fluid status/signs of fluid overload
• Daily weight (gain) and I&O (weight a pt at the same time, same scale, same
cloth, if gain 5 lb in 1 week is fluid retention)
• Assess responses to medications
• Lab test:
– Human B-type natriuretic peptides (hBNP): elevated in heart failure
– Used to differentiate dyspnea r/t heart failure versus respiratory problems
Collaborative Problems/Potential Complications
• Cardiogenic shock (heart not working, not perfusing, BP is on the floor)
• Dysrhythmias
• Thromboembolism (if the heart is not pumping well there is stasis of blood, and clot
forms)
• Pericardial effusion and cardiac tamponade (too much fluid in heart, accumulation, not
working)
Planning
• Goals may include
• Promoting activity and reducing fatigue.
• Relieving fluid overload symptoms.
• Decreasing anxiety or increasing the patient’s ability to manage anxiety.
• Encouraging the patient to make decisions and influence outcomes.
• Teaching the patient about the self-care program.
Activity Intolerance
• Bed rest for acute exacerbations
• Encourage regular physical activity; 30–45 minutes daily
• Exercise training
• Pacing of activities
• Wait 2 hours after eating for physical activity
• Avoid activities in extreme hot, cold, or humid weather
• Modify activities to conserve energy
• Positioning; elevation of the HOB to facilitate breathing and rest, support of arms

Fluid Volume Excess

• Assessment for symptoms of fluid overload
• Daily weight
• I&O
• Diuretic therapy; timing of meds
• Fluid intake; fluid restriction
• Maintenance of sodium restriction
Patient Teaching
• Medications
• Diet: low-sodium diet and fluid restriction
• Monitoring for signs of excess fluid, hypotension, and symptoms of disease
exacerbation, including daily weight
• Exercise and activity program
• Stress management
• Prevention of infection (when there is an infection, the HR goes up, fever
increases metabolism that’s not good for a failing heart)
 • Know how and when to contact health care provider

ASSESSMENT AND MANAGEMENT OF PATIENTS WITH HYPERTENSION

Hypertension
• High blood pressure
• Defined by the Seventh Report of the Joint National Commission on the Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) as a systolic pressure
greater than 140 mm Hg and a diastolic pressure greater than 90 mm Hg. based on
the average of two or more accurate blood pressure measurements taken during two or more
contacts with a health care provider

Classification of Blood Pressure for Adults Age 18 and Older

BP Classification Systolic Diastolic

(mmHg) (mmHg)
Normal < 120 <80
Prehypertension 120-139 80-89
Stage 1 Hypertension 140-159 90-99
Stage 2 Hypertension > 160 >100

Incidence of Hypertension— “The Silent Killer”

• Primary hypertension.
• Secondary hypertension. (due to kidney, CHF)
• 28–31% of the adult population of the U.S. has hypertension.
• 90–95% of this population with hypertension has primary hypertension.
• Incidence is greater in southeastern U.S. and among African-Americans.

Factors that Influence the Development of Hypertension

• Increased sympathetic nervous system activity (Vasoconstriction increase BP)
• Increased reabsorption of sodium chloride and water by the kidneys
• Increased activity of the rennin-angiotensin system (Na and H2O reabsorption)
• Decreased vasodilatation
• Insulin resistance
Manifestations of Hypertension
BP needs to be taken twice in different situations to confirm HTN
• Usually NO symptoms other than elevated blood pressure
• Symptoms seen related to organ damage are seen late and are serious
• Peripheral edema (Fluid shift to extracellular spaces due to the pressure)
• There is another mechanism that push the fluid back in the vessels
(albumin/protein) and decrease peripheral edema, that is why need to check
the protein levels in HTN pts.
• Retinal and other eye changes
• Renal damage
• Myocardial infarction
• Cardiac hypertrophy (cardiac muscle is bigger bc is working harder, mainly the
left ventricule)
• S3 S4 sounds
• Stroke (BP is high, hemorrhagic stroke, due to the vessels in the brain can’t
 handle the pressure)
• HTN also causes aneurysm (creates bruit-turbulent blood flow). Main sign is
headache, diagnostic test is CT scan. Never palpate aneurysm bc it can rupture

Major Risk Factors

• Hypertension
• Smoking
• Excessive ETOH intake
• Obesity
• Physical inactivity
• Dyslipidemia
• Diabetes mellitus
• Microalbuminuria or GFR < 60
- Normal GFR (90-120). Less than 60 is a risk factor, that means the glomerulo is
not filtrating it out, so stays the toxins in the body. This is very caustic to RBC, so
they burst and release the K inside the cell and then Hyperkalemia happens.
• Older age
• Family history

Patient Assessment
• History and Physical
• Laboratory tests
• Urinalysis
- Protein
- Specific gravity if is high the urine will look concentrated and vice)
• Blood chemistry
• Cholesterol levels (the cholesterol accumulates in the lumen of the arteries
makes them narrow, increasing risk for HTN)
• Elevated BUN, Creatinine
- To determine kidney function, mainly Creatinine, bc BUN can change due to
dehydration or if the person workout for hours.
• Elevated glucose
• ECG: shows left ventricular hypertrophy (left ventricle working hard)
CXR: cardiomegaly (enlarged heart)

Lifestyle Modifications
• Weight loss
• Reduced alcohol intake
• Reduced sodium intake
• Regular physical activity
• Diet: high in fruits, vegetables, and low-fat dairy
• DASH diet (dietary approaches to stop hypertension) No Na, fat, low cholesterol.
Medication Treatment
• Usually initial medication treatment is a thiazide diuretic.
• Low doses are initiated and the medication dosage is increased gradually if blood pressure
does not reach target goal.
• Additional medications are added if needed.
• Multiple medications may be needed to control blood pressure.
Lifestyle changes initiated to control BP must be maintained
Medication Therapy for Hypertension
• Diuretic and related drugs
• Thiazide diuretics
 • Loop diuretics {Furosemide, bumex (is more potent than furosemide)}
• Potassium sparing diuretics (spironolactone, triamterene, amiloride, epleronone)
• Aldosterone receptors blockers
• Central alpha2-agonists and other centrally acting drugs (clonidine)
• Beta-blockers (HTN, ANGINA, DYSRHYTHMIAS)
• Beta-blockers with intrinsic sympathomimetic activity
• Alpha and beta blockers (ZOSIN)
• Vasodilators (HYDRALAZINE, NITROPRAZIDE)
• Angiotensin-converting enzyme (ACE) inhibitors
• Angiotenisin II antagonists (ARBS)
• Calcium channel blockers (HTN, ANGINA, DYSTHRYTHMIAS)
DON’T GIVE SPIRONOLACTONE WITH ACE INHIBITORS
CAN GIVE A SPARING AND A LOOP DIURETIC

Nursing History and Assessment

• History and risk factors
• Assess potential symptoms of target organ damage
• Angina, shortness of breath, altered speech, altered vision, nosebleeds,
headaches, dizziness, balance problems, nocturia
• Cardiovascular assessment: apical and peripheral pulses
• Personal, social, and financial factors that will influence the condition or its
treatment
Interventions
• Patient teaching (STRESS REDUCTION)
• Support adherence to the treatment regimen
• Consultation/collaboration (Nutritionist, case management)
• Follow-up care
• Emphasize control rather than cure (if is secondary due to kidney issues can be
reversible but if is primary then is a life long problem)
• Reinforce and support lifestyle changes
A lifelong process
Gerontologic Considerations
• Noncompliance (men in the 40’s the impotence is a reason for noncompliance)
• Include family
• Understanding of therapeutic regimen
• Reading instructions
• Monotherapy
Hypertensive Crises
• Hypertensive emergency
• Blood pressure > 180/120 and must be lowered immediately to prevent damage to target
organs
• Hypertensive urgency
• Blood pressure is very high but no evidence of immediate or progressive target organ
damage
Hypertensive Emergency
• Reduce BP 25% in first hour.
• Reduce to 160/100 over 6 hours. (If is done in less time then cause cardiovascular
collapse)
• Then gradual reduction to normal over a period of days.
• Exceptions are ischemic stroke and aortic dissection.
• Medications
• IV vasodilators: sodium nitroprusside, nicardipine, fenodopam mesylate,
 enalaprilat, nitrogylcerin
• Need very frequent monitoring of BP and cardiovascular status.

Hypertensive Urgency
• Patient requires close monitoring of blood pressure and cardiovascular status.
• Assess for potential evidence of target organ damage.
• Medications
• Fast-acting oral agents: beta adrenergic blocker— labetalol; angiotensin-
converting enzyme inhibitor— captopril; or alpha2-agonist—clonidine (SL is very
fast)

Peripheral Disorders

Peripheral Arterial Disease (PAD)

Disorders that interrupt or impede arterial peripheral blood flow due to vessel compression,
vasospasm, and/or structural defects in the vessel wall
Primarily caused by atherosclerosis
May also be caused by:
Trauma, embolism, vasospasm, inflammation (edema constrict the lumen)
Femoral-popliteal are most common in nondiabetics
Diabetics are below the knee
Intermittent claudication (pain while walking bc the muscles in the area when walking need
O2 and stop at rest because they don’t need O2 and blood as much)
Ischemic muscle pain precipitated by a predictable amount of exercise and relieved by
rest
Due to chronic arterial obstruction leading to inadequate oxygenation of tissues

Risk Factors for Atherosclerosis and PVD

Nonmodifiable
• Age
• Gender
• Familial predisposition/genetics
Modifiable
• Nicotine
• Diet
• Hypertension
• Diabetes
• Obesity
• Stress
• Sedentary lifestyle
• C-reactive protein (for inflammation or any injury can cause elevation of the
CRP)
• Hyperhomcysteinemia
Peripheral Arterial Insufficiency—Assessment
Health history
Medications
Risk factors
Signs and symptoms of arterial insufficiency
Extremities are cool and pale with cyanotic color on elevation
Nails thick and opaque
Bruits may be auscultated
Claudication and rest pain
 Color changes (SHINY SKIN NOT ENOUGH OF HAIR)
Weak or absent pulses
Skin changes ( shiny with sparse hair) and skin breakdown (Ulcers)

Planning and Implementation

• Goal: adequate tissue perfusion
• Assess and record pulses (BILATERALLY - TOGETHER)
• Smoking cessation
• Change positions at least hourly and avoid crossing legs
• Encourage exercise and walk to the point of pain as this decreases claudication
Avoid restrictive clothing: girdles, garters and socks

Planning and Implementation

Goal: Intact healthy skin on extremities
Teach client skills in skin care and daily foot inspection
Teach client to always wear shoes/slippers and avoid trauma to the feet
Bath water should be checked with the hands not the feet
Teach client to have toenail care performed by a professional only
If an ulcer develops, healing will be slow unless arterial blood flow to the affected limb is
improved through a surgical revascularization procedure
Good nutrition, low-fat diet
Weight reduction as necessary

Medication Therapy (mainly antiplatelets)

• ASA inhibits platelet aggregation
• Pentoxifylline (Trental) decreases blood viscosity to increase blood flow to the
microcirculation and tissues of the extremities
• Cilostazol (Pletal) inhibits platelet aggregation and enhances vasodilation
• Clopidogrel (Plavix) inhibits platelet aggregation

Main side effect of these is bleeding

Aspirin (ASA) is ulcerative that is why it is ordered enteric coated.

Arterial Embolism
• Usually arise from thrombi that developed in the heart as a result of AFIB, MI,
prosthetic valves or CHF
• Assessment: 5 P’s
• Pain
• Pallor
• Pulselessness (↓ or absent)
• Parasthesias (altered local sensations)
• Paralysis (weakness or inability to move extremity)
• Poikilothermia ( body temp that varies with environment)

Arterial Embolism
• Medication therapy
• Thrombolytic therapy with streptokinase
• T-Pa
• Heparin
• Warfarin at home
 Arterial ulcer are usually dry and necrotic and in the upper part, the venous ulcers
are moist and in the lower part in the malleolar.

Venous Insufficiency
• Inadequate venous return over a long period of time that causes pathologic changes as
a result of ischemia in the vasculature, skin and supporting tissues
• Venous insufficiency occurs:
• After prolonged venous HTN-stretches the veins and damages the valves
preventing blood return
• After thrombus formation or when valves are not functioning correctly
• In time stasis results in edema of the lower limbs, discoloration to the skin of the legs and
feet and venous stasis ulcer

Venous Insufficiency-Assessment
• Past HX of thrombophlebitis, HTN, variscosities
• Past HX of long periods of sitting or standing
• Edema to lower legs, may extend to the knee
• Thick coarse, brownish skin around ankles and feet
• Stasis ulcers, usually in the malleolar area (ruddy base, uneven edges)
Venous Insufficiency
Increase blood return, decrease venous pressure
Bedrest
Keep legs elevated above heart
Avoid long periods of standing
Wear elastic support or compression stockings
Treat venous stasis ulcer(s)
Open lesions are treated with hydrocolloid dressings and compression wraps
May apply low-dose hydrocortisone, zinc or antifungal to area
Ulcers may be treated with an UNNA boot or other compression wrap that is changed
every 1-2 weeks and is usually applied over a base dressing
 May need surgical debridement

The wound bed need to be moist, the peri-wound dry.

Types of debridement
- Surgical debridement
- chemical debridement
- mechanical debridement
Unna Boot