D.A.

Gonzaga, SN
Acute Biologic Crisis of Cardiovascular System
Review of Anatomy and Physiology
Anatomy of the Heart
>> hollow, muscular organ
located in the center of the
thorax, where it occupies the
space between the lungs
(mediastinum) and rests on the
diaphragm.
>> It weighs approximately
300 g (10.6 oz); the weight and
size of the heart are influenced
by age, gender, body weight, extent of physical exercise and
conditioning,
and heart disease.
Left side of the heart, composed of the left atrium
and left ventricle, distributes oxygenated blood to the
remainder of the body via the aorta (systemic circulation).
- receives oxygenated blood from the pulmonary circulation
via four pulmonary veins.
Apical Impulse (also called the point
of maximal
impulse [PMI])
>> pulsation created during normal
ventricular contraction, called the
apical impulse. In the normal heart,
the PMI is located at the intersection
of the mid-clavicular line of the left chest wall and the fifth
intercostal space (Bickley, 2014).

Composed of 3 layers: Heart Valves

>> inner layer, or
ENDOCARDIUM, consists of
endothelial tissue and lines the
inside of the heart and valves.
>> middle layer, or
MYOCARDIUM, is made up of
muscle fibers and is responsible
for the pumping action.
>> exterior layer of the heart is
called
the EPICARDIUM
Heart Chambers
The four valves in the heart permit blood to flow in only one
direction.
>> composed of thin leaflets of fibrous tissue, open and
close in response to the movement of blood and pressure
changes within the
chambers.
2 types of valves:
Atrioventricular (AV) and Semilunar
AV VALVES (separate the
atria from the ventricles)
The tricuspid valve (three
cusps)- separates the right
atrium from the right
ventricle.

The pumping action of the heart is accomplished by the The mitral or

rhythmic relaxation and contraction of the muscular walls bicuspid (two cusps)
valve- lies between the left atrium
 Atria (2 top chambers)
and the left ventricle
 Ventricles (2 bottom chambers)
2 SEMILUNAR VALVES (composed of three leaflets,
 SYSTOLE refers to the events of the
which are shaped like half- moons)
heart during contraction of the atria and the ventricles. Atrial
1. Pulmonic Valve- valve between the right ventricle and the
systole occurs first, just at the end of diastole, followed by
pulmonary artery.
ventricular systole. This synchronization allows the
2. Aortic Valve- The valve between the
ventricles to fill completely prior to ejection of blood from
left ventricle and the aorta
these chambers
 DIASTOLE or period of ventricular filling
The semilunar valves are forced open during
(Relaxation phase: all 4 chambers relax simultaneously) –
ventricular systole as blood is ejected from the right and left
which allows the ventricles to fill in preparation for
ventricles into the pulmonary artery and aorta, respectively.
contraction
Coronary Arteries
Right side of the heart,
The left and right coronary
made up of the right atrium and
arteries and their
right ventricle, distributes venous
branches supply arterial
blood (deoxygenated blood) to the
blood to the heart.
lungs via the pulmonary artery
(pulmonary circulation) for
Perfused during diastole
oxygenation.
With a normal heart rate of
60 to 80 bpm, there is ample time during diastole for
myocardial perfusion. However, as heart rate increases,

diastolic time is shortened, which may not allow adequate
time for myocardial perfusion. As a result, patients are at risk
for myocardial ischemia (inadequate oxygen supply) during
tachycardia (heart rate greater than 100 bpm), especially
patients with CAD.
Coronary Arteries
>> Left Artery (3 branches)
>> Left main coronary artery-
from the point of origin to the
first major branch
a. Left anterior descending
artery (which
courses down the anterior wall of
the heart)
b. Circumflex artery (which
circles around to the lateral left wall of the heart)
>> The right side of the heart is supplied by the right coronary
artery.
>> Posterior descending artery (the posterior wall of the
heart receives its blood supply by an additional branch from
the right coronary artery)
Superficial to the coronary arteries are the coronary veins
Myocardium
>> middle,
muscular layer of
the atrial
and ventricular
walls
>> composed of
specialized cells
called myocytes
(which form an
interconnected
network of muscle
fibers). These fibers
encircle the heart in a figure-of-eight pattern, forming a spiral
from the base (top) of the heart to the apex (bottom)
Function of the Heart
Cardiac Electrophysiology
The cardiac conduction system generates and transmits
electrical impulses that stimulate contraction of the
myocardium.
3 physiologic characteristics of two types of specialized
electrical cells (nodal cells and the Purkinje cells) provide
this synchronization:
1. Automaticity: ability to
initiate an electrical impulse
2. Excitability: ability to
respond to an electrical impulse
3. Conductivity: ability to
transmit an electrical impulse
from one cell to another.
D.A.Gonzaga, SN
Sinoatrial (SA) node (the
primary pacemaker of the heart)
>> located at the junction of the
superior
vena cava and the right atrium
>> in a normal resting adult heart
has an inherent firing rate of 60 to
100 impulses per minute
The electrical impulses initiated
by the SA node are conducted along the myocardial cells of
the atria via specialized tracts called internodal pathways
Atrioventricular (AV) node
(the secondary pacemaker of
the heart)
>> coordinates the incoming
electrical impulses from the
atria and after a slight delay
(allowing the atria time to
contract and complete
ventricular filling) relays the
impulse to the ventricles.
>> Initially, the impulse is
conducted through a bundle of specialized conducting tissue,
referred to as the bundle of His, which then divides into the
right bundle branch (conducting impulses to the right
ventricle) and the left bundle branch (conducting impulses to
the left ventricle).
>> SA node has the highest inherent rate (60 to 100
impulses per minute)
>> AV node has the second-highest inherent rate (40 to 60
impulses per minute)
>> Ventricular pacemaker sites have the lowest inherent rate
(30 to 40 impulses per minute)
If the SA node malfunctions, the AV node generally takes over
the pacemaker function of the heart at its inherently lower
rate. Should both the SA and the AV nodes fail in their
pacemaker function, a pacemaker site in the ventricle will fire
at its inherent bradycardic rate of 30 to 40 impulses per
minute.
Cardiac Action Potential
The nodal and Purkinje cells (electrical cells) generate and
transmit impulses across the heart, stimulating the cardiac
myocytes (working cells) to contract.
>> Ions- Stimulation of the myocytes occurs due to the
exchange of electrically charged particles
>> The channels regulate the movement and speed of specific
ions: (enter and exit)
> SODIUM (primary extracellular ion)
> POTASSIUM (primary intracellular ion)
> CALCIUM
DEPOLARIZATION - this exchange of ions creates a
positively charged intracellular space and a negatively
charged extracellular space that characterizes the period.
REPOLARIZATION - once depolarization is complete, the
exchange of ions reverts to its resting state.
CARDIAC ACTION POTENTIAL- the repeated cycle
of depolarization and repolarization

>> Cardiac action potential
has 5 phases:
Phase 0: Cellular
depolarization is initiated as
positive ions influx into the
cell.
Phase 1: Early cellular
repolarization begins during
this phase as potassium exits
the intracellular space.
Phase 2: This phase is called
the plateau phase because the
rate of repolarization slows.
Calcium ions enter the intracellular space.
Phase 3: This phase marks the completion of repolarization
and return of the cell to its resting state
Phase 4: This phase is considered the resting phase
before the next depolarization
Myocardial cells must completely repolarize before
they can depolarize again. During the repolarization process,
the cells are in a REFRACTORY PERIOD.
Two phases of the refractory period:
a. The Effective (Or Absolute) Refractory Period
o the cell is completely unresponsive to any electrical
stimulus
o it is incapable of initiating an early depolarization
o corresponds with the time in phase 0 to the middle
of phase 3 of the action potential.
b. Relative Refractory Period
o corresponds with the short time at the end of phase
3.
o if an electrical stimulus is stronger than normal, the
cell may depolarize prematurely
Cardiac Hemodynamics
An important determinant of blood flow in the cardiovascular
system is the principle that fluid flows from a region of higher
pressure to one of lower pressure. The pressures responsible
for blood flow in the normal circulation are generated during
systole and diastole.
Cardiac Cycle
refers to the events that occur in the heart from the
beginning of one heartbeat to the next.
Each cardiac cycle has three major sequential
events: diastole, atrial systole, & ventricular systole.
Atrial Systole increases the pressure inside the atria,
ejecting the remaining blood into the ventricles. Atrial systole
augments ventricular blood volume by 15% to 25% and is
sometimes referred to as the atrial kick (Woods et al., 2009).
At this point, ventricular systole begins in response
to propagation of the electrical impulse that began in the SA
node some milliseconds earlier, the pressure inside the
ventricles rapidly increases, forcing the AV valves to close.
As a result, blood ceases to flow from the atria into the
ventricles, and regurgitation (backflow) of blood into the atria
is prevented
The rapid increase in pressure inside the right and left
ventricles forces the pulmonic and aortic valves to open, and
blood is ejected into the pulmonary artery and aorta,
respectively. The exit of blood is at first rapid; then, as the
D.A.Gonzaga, SN
pressure in each ventricle and its corresponding artery
equalizes, the flow of blood gradually decreases.
At the end of systole, pressure within the right and left
ventricles rapidly decreases. As a result, pulmonary arterial
and aortic pressures decrease, causing closure of the
semilunar valves. These
events mark the onset of diastole, and the cardiac cycle is
repeated
Cardiac Output
- refers to the total amount of blood ejected by one of
the ventricles in liters per minute.
- in a resting adult is 4 to 6 L/min but varies greatly
depending on the metabolic needs of the body.
- computed by multiplying the stroke volume by the
heart rate.
Stroke volume is the amount of blood ejected from one of the
ventricles per heartbeat. The average resting stroke volume is
about 60 to 130 mL
(Woods et al., 2009).
Effect of Heart Rate on Cardiac Output
Cardiac Output
 responds to changes in the metabolic demands of the
tissues associated with stress, physical exercise, and
illness.
 is enhanced by increases in both stroke volume and
heart rate to compensate for these added demands
 Changes in heart rate are due to inhibition or
stimulation of the SA node mediated by the
parasympathetic and sympathetic divisions of the
autonomic nervous system.
 The balance between these two reflex control
systems normally determines the heart rate.
Branches of the parasympathetic nervous system
travel to the SA node by the vagus nerve.
>> Stimulation of the vagus nerve slows the heart rate. The
sympathetic nervous system increases heart rate by
innervation of the beta-1 receptor sites located within the SA
node.
>> The heart rate is increased by the sympathetic nervous
system through an increased level of circulating
catecholamines (secreted by the adrenal gland) and by excess
thyroid hormone, which produces a catecholamine Vlike
effect.
>> In addition, the heart rate is affected by central nervous
system and baroreceptor activity
Baroreceptors
- are specialized nerve cells located in the aortic arch
and in both right and left internal carotid arteries (at the point
of bifurcation from the common carotid arteries)
- sensitive to changes in blood pressure (BP)*
Hypertension- these cells increase their rate of discharge,
transmitting impulses to
the cerebral medulla.
This action initiates parasympathetic activity and inhibits
sympathetic response, lowering the heart rate and the BP.
Hypotension - Less baroreceptor stimulation during periods
of hypotension prompts a decrease in parasympathetic
activity and enhances sympathetic responses

Effect of Stroke Volume on Cardiac Output
Stroke volume is primarily determined by 3 factors:
PRELOAD
>> refers to the degree of stretch of the ventricular cardiac
muscle
fibers at the end of diastole
>> commonly referred to as left ventricular end-diastolic
pressure
>> decreased by a reduction in the volume of blood returning
to the ventricles by increasing the return of circulating blood
volume to the ventricles
Frank–Starling (or Starling) law of the heart - As the volume
of blood returning to the heart increases, muscle fiber stretch
also increases (increased preload), resulting in stronger
contraction and a greater stroke volume.
AFTERLOAD
>> or resistance to ejection of blood from the ventricle, is the
second determinant of stroke volume
>> The resistance of the systemic BP to left ventricular
ejection is called systemic vascular resistance.
>> The resistance of the pulmonary BP to right ventricular
ejection is called pulmonary vascular resistance
CONTRACTILITY
>> refers to the force generated by the contracting
myocardium
>> enhanced by circulating catecholamines, sympathetic
neuronal
activity, and certain medications (e.g., digoxin [Lanoxin],
dopamine, or dobutamine)
>> Increased contractility results in increased stroke volume.
>> Contractility is depressed by hypoxemia, acidosis, and
certain medications (e.g., beta-adrenergic blocking agents
such as metoprolol [Lopressor]).
The percentage of the end-diastolic blood volume that is
ejected with each heartbeat is called the ejection fraction (the
normal left ventricle is 55% to 65%, Woods et al., 2009); It is
used as a measure of myocardial contractility. An ejection
fraction of less than 40% indicates that the patient has
decreased left ventricular function and likely requires
treatment of HF
Gerontologic Considerations
o Changes in cardiac structure and function occur with
age. A loss of function of the cells throughout the
conduction system leads to a slower heart rate.
o The size of the heart increases due to hypertrophy
(thickening of the heart walls), which reduces the
volume of blood that the chambers can hold.
Hypertrophy also changes the structure of the
myocardium, reducing the strength of contraction.
The resulting backflow of blood creates heart
murmurs, a common finding in older adults
(Bickley, 2014; Woods et al., 2009).
o As a result of these age-related changes, the
cardiovascular system takes longer to compensate
from increased metabolic demands due to stress,
exercise, or illness.
D.A.Gonzaga, SN
Gender Considerations
o Structural differences between the hearts of men and
women have significant implications. The heart of a
woman tends to be smaller than that of a man. The
coronary arteries of a woman are also narrower in
diameter than a man’s arteries. When atherosclerosis
occurs, these differences make procedures such as
cardiac catheterization and angioplasty technically
more difficult.
o Women typically develop CAD 10 years later than
men, as women have the benefit of the female
hormone estrogen and its cardioprotective effects.
LEFT SIDED
RIGHT SIDED
HEART FAILURE
Heart Failure
It is a chronic, progressive condition in which the
heart muscle is unable to pump enough blood to meet the
body’s needs for blood and oxygen. Basically, the heart can’t
keep up with its workload. At first the heart tries to make up
for this by:
o Enlarging. The heart stretches to contract more
strongly and keep up with the demand to pump more
blood. Over time this causes the heart to become
enlarged.
o Developing more muscle mass. The increase in
muscle mass occurs because the contracting cells of
the heart get bigger. This lets the heart pump more
strongly, at least initially.
o Pumping faster. This helps increase the heart’s
output.
 The body also tries to compensate in other ways:
 The blood vessels narrow to keep blood pressure up,
trying to make up for the heart’s loss of power.
 The body diverts blood away from less important
tissues and organs (like the kidneys), the heart and
brain.
 These temporary measures mask the problem of
heart failure, but they don’t solve it. Heart failure
continues and worsens until these compensating
processes no longer work.
 Eventually the heart and body just can’t keep up, and
the person experiences the fatigue, breathing
problems or other symptoms that usually prompt a
trip to the doctor. Heart failure can involve the
heart’s left side, right side or both sides. However, it
usually affects the left side first.
Types of Heart Failure
Left sided heart failure
is the most common type of
heart failure. The left heart ventricle located in the bottom left
side of your heart.
This area pumps oxygen-rich blood to the rest of
your body. Left-sided heart failure occurs when the
left ventricle doesn’t pump efficiently. This prevents
your body from getting enough oxygen-rich blood.
The blood backs up into your lungs instead, which
causes shortness of breath and a buildup of fluid.

There are two types of left-sided heart failure. Drug
treatments are different for the two types.
1. Heart failure with reduced ejection
fraction (HFrEF), also called systolic failure: The left
ventricle loses its ability to contract normally. The
heart can't pump with enough force to push enough
blood into circulation.
2. Heart failure with preserved ejection fraction
(HFpEF), also called diastolic failure (or diastolic
dysfunction): The left ventricle loses its ability to
relax normally (because the muscle has become stiff).
The heart can't properly fill with blood during the
resting period between each beat.
Right Sided Heart Failure
is responsible for pumping blood to your lungs to
collect oxygen. Right-sided heart failure occurs when the
right side of your heart can’t perform its job effectively. It’s
usually triggered by left-sided heart failure.
 The accumulation of blood in the lungs caused
by left-sided heart failure makes the right ventricle work
harder. This can stress the right side of the heart and cause it
to fail.
 Right-sided heart failure can also occur as a
result of other conditions, such as lung disease. Right-sided
heart failure is marked by swelling of the lower extremities.
This swelling is caused by fluid backup in the legs, feet, and
abdomen.
Diastolic Heart Failure
It occurs when the heart muscle becomes stiffer than normal.
 The stiffness, which is usually due to heart
disease, means that your heart doesn’t fill with blood easily.
 This is known as diastolic dysfunction. It leads to
a lack of blood flow to the rest of the organs in your body.
Systolic Heart Failure
It occurs when the heart muscle loses its ability to contract.
 The contractions of the heart are necessary to
pump oxygen-rich blood out to the body.
 This problem is known as systolic dysfunction,
and it usually develops when your heart is weak and enlarged.
 Both diastolic and systolic heart failure can
occur on the left or right sides of the heart. You may have
either condition on both sides of the heart.
CAUSES:
 Heart failure is most often related to another
disease or illness. The most common cause of heart
failure is coronary artery disease (CAD), a disorder
that causes narrowing of the arteries that supply
blood and oxygen to the heart. Other conditions that
may increase your risk for developing heart failure
include:
- cardiomyopathy, a disorder of the heart muscle that causes
the heart to become weak
- a congenital heart defect
- a heart attack
- heart valve disease
- certain types of arrhythmias, or irregular heart rhythms
- high blood pressure
- emphysema, a disease of the lung
- Diabetes
- an overactive or underactive thyroid
- HIV
D.A.Gonzaga, SN
- AIDS
- severe forms of anemia
- certain cancer treatments, such as chemotherapy
- drug or alcohol misuse
RISK FACTORS:
People with diseases that damage the heart are also at an
increased risk. These diseases include:
o hyperthyroidism
o hypothyroidism
o emphysema
o anemia
Certain behaviors can also increase your risk of
developing heart failure, including:
o smoking
o eating foods high in fat or cholesterol
o living a sedentary lifestyle
o being overweight
CLINICAL MANIFESTATIONS OF LEFT SIDED
HEART FAILURE
Cough: A dry, hacking cough can be an early sign, which
occurs due to fluid build-up in the lungs. In later stages, the
sufferer can cough up white secretions that sometimes contain
blood.
Fatigue: This is due to the heart’s inability to pump enough
blood to other body parts. Arms and legs become weak.
During end-stage heart failure, patients find it hard to
participate in normal activities, such as walking or getting
dressed. People who are at this point tend to sleep a lot.
Chest discomfort: The heart can beat irregularly, causing
discomfort. The discomfort is described as fluttering, pain, or
pressure.
Confusion: The brain receives less oxygenated blood with
left-sided heart failure, so confusion or altered thinking can
occur. Memory loss may also be a problem.
Paroxysmal nocturnal dyspnea: This means that the person
is awakened from sleep with difficulty breathing.
S heart sound: This is a murmur due to a variation in blood
flow.
Cyanosis: A bluish discoloration of the skin called cyanosis
can occur as a result of poor circulation from inadequate
oxygenation of blood.
Elevated pulmonary capillary wedge pressure: This means
that the pressure in the small pulmonary arterial branch is
higher than it should be.
Decreased urine output: Since other parts of the body aren’t
receiving blood, the body has a tendency to want to hold on
to fluid.
Weight gain: When the body holds onto more fluid, overall
body weight increases.
RIGHT SIDED HEART FAILURE
Sleep apnea: Heavy and uncontrollable coughing and
breathlessness
Sudden and frequent shortness of breath: Having a hard
time focusing on tasks at hand
Anorexia induced by complete lack of appetite: Extreme
weakness felt throughout the body
Massive weight gain: Fainting
Chronic fatigue: Irregular heartbeat
Constant urge to urinate: Intense chest pain

Nausea and lightheadedness: Coughing pinkish-white
phlegm
Diagnostic Procedure/S
o Stress testing during exercise to determine whether
the patient can exercise and raise their heart rate to a
normal level for the level of activity they’re doing.
o Blood tests that look for specific substances that are
typically found in the bloodstream when a patient is
suffering from right-sided heart failure while also
checking other major organs for signs of
abnormality.
o Pulmonary function testing measures the quality of
your breath and how well your lungs are working as
you breathe in and out of a tube that’s connected to
a measuring device.
o Cardiac CT scans produce digital x-ray images of
your heart so that your doctor can get a clear visual
of what’s going on.
o Myocardial biopsy is a procedure in which your
doctor removes a portion of the heart muscle by
inserting a thin tube through an entry point on your
body and attaching it to your heart.
o Chest x-rays to examine the how the lungs and heart
are functioning.
o Coronary angiography involves your doctor
injecting a blue dye into your arteries and heart
chambers so that your doctor can examine the way
in which blood flows through your heart and
determine whether there are any abnormalities.
Cardiac catheterization: A thin flexible tube is threaded
through a blood vessel and into the heart and accompanied
with a contrast material so that an X-ray video can show heart
functioning.
Echocardiogram: An ultrasound to take moving pictures of
heart chambers and valves.
Electrocardiogram (EKG): A measurement of electrical
activity of the heart, which can help determine if there is heart
enlargement or heart damage. capture moving images of the
heart to showcase the blood pressure and whether it’s
pumping as it should.
Electrophysiology: A test that records the heart’s electrical
activity and pathways, which can detect heart rhythm
problems.
Radionuclide imaging: A radioactive isotope is injected into
a vein and a special camera records it traveling through the
heart. This helps highlight areas of heart damage.
Treadmill exercise test: A measurement of a person’s
capacity to exercise and the amount of oxygen the heart
provides the muscles while in motion. This can indicate the
severity of left-sided heart failure and can help determine left-
sided heart failure prognosis.
MEDICAL MANAGEMENT
Non-pharmacologic therapies:
 physical activity as appropriate; and
 attention to weight gain.
Pharmacologic therapies:
 the use of diuretics,
 vasodilators,
 inotropic agents,
 anticoagulants,
 beta-blockers, and
 digoxin.
D.A.Gonzaga, SN
Surgical Management:
▪ Cardiac Resynchronization Therapy (CRT)
▪ The procedure involves implanting a half-dollar
sized pacemaker, usually just below the
collarbone. Three wires (leads) connected to the
device monitor the heart rate to detect heart rate
irregularities and emit tiny pulses of electricity to
correct them. In effect, it is "resynchronizing" the
heart.
Pacemakers
It is a small device with two parts — a generator and wires
(leads, or electrodes) — that's placed under the skin in your
chest to help control your heartbeat
Implantable cardioverter-defibrillators (icds)
▪An ICD is a battery-powered device placed under the skin
that keeps track of your heart rate. Thin wires connect the ICD
to your heart. If an abnormal heart rhythm is detected the
device will deliver an electric shock to restore a normal
heartbeat if your heart is beating chaotically and much too
fast.
Coronary artery bypass grafting (CABG)
Coronary bypass surgery redirects blood around a section of
a blocked or partially blocked artery in your heart to improve
blood flow to your heart muscle. The procedure involves
taking a healthy blood vessel from your leg, arm or chest and
connecting it beyond the blocked arteries in your heart.
Percutaneous Coronary Intervention (PCI)
formerly known as angioplasty with stent, is a non- surgical
procedure that uses a catheter (a thin flexible tube) to place a
small structure called a stent to open up blood vessels in the
heart that have been narrowed by plaque buildup, a condition
known as atherosclerosis.
Transcatheter Aortic Valve Replacement (TAVR)
is another type of minimally invasive aortic valve
replacement that has a nonsurgical approach. It is also
sometimes called transcatheter aortic valve implantation
(TAVI).
Mechanical Valve Replacement
In a mechanical valve replacement, a mechanical valve
replaces the damaged valve.
NURSING MANAGEMENT:
Providing Oxygenation
 Administer oxygen therapy per nasal cannula at 2-6
LPM as ordered.
 Evaluate ABG analysis results </li></ul><ul><li>
 Semi-Fowler’s or High-Fowler’s position to
promote greater lung expansion
 Promoting Rest and Activity
 Bed rest or limited activity may be necessary during
the acute phase
 Provide an overbed table close to the patient to allow
resting the head and arms
 Use pillows for added support when in High-
Fowler’s position.
 Administer Diazepam (Valium) 2-10 mg 3-4x a day
as ordered to allay apprehension
 Gradual ambulation is encouraged to prevent risk of
venous thrombosis and embolism due to prolonged
immobility
 D.A.Gonzaga, SN
 Activities should progress through dangling, sitting Interventions:
up on a chair and then walking in increased distances > encourage patient to have adequate bed rest and sleep
under close supervision > assist the client in a side-lying position
 Assess for signs of activity intolerance (dyspnea, > elevate the head of the bed
fatigue and increased pulse rate that does not 3. Knowledge deficiency r/t to lack of
stabilize readily) understanding/misconceptions about
interrelatedness of cardiac disease
Decreasing Anxiety: Interventions:
▪ Allow verbalization of feelings > promote rest
▪ Identify strengths that can be used for coping > promote healthy nutrition
▪ Learn what can be done to decrease anxiety > educate regarding medication

Facilitating Fluid Balance: CORONARY ARTERY DISEASE

▪ Control of sodium intake is a condition in which plaque builds up inside the
▪ Administer diuretics and digitalis as prescribed coronary arteries. Coronary arteries are arteries that supply
▪ Monitor I and O, weight and V/S the heart muscle with oxygen rich blood.
▪ Dry phlebotomy (rotating tourniquets) The classic symptom is angina—pain* caused by loss of
▪ Providing Skin Care oxygen and nutrients to the myocardial tissue because of
▪ Edematous skin is poorly nourished and susceptible to inadequate coronary blood flow.
pressure sores Angina has three major forms:
▪ Change position at frequent intervals 1. STABLE: precipitated by effort, of short duration, and
▪ Assess the sacral area regularly easily relieved,
▪ Use protective devices to prevent pressure sores 2. UNSTABLE: longer lasting, more severe, may not be
relieved by rest or nitroglycerin; may also be new onset of
Promoting Nutrition: pain with exertion or recent acceleration in severity of pain.
 Provide bland, low-calorie, low-residue with 3. VARIANT: chest pain at rest with ECG changes due to
vitamin supplement during acute phase coronary artery spasm.
 Frequent small feedings minimize exertion and
reduce gastrointestinal blood requirements DUE TO ETIOLOGICAL FACTORS
⬇
Nursing Diagnoses for Left Sided Heart Failure: INJURY TO THE ENDOTHELIAL CELL THAT LINING THE
ARTERY
1. Decrease cardiac output r/t altered heart rate and
⬇
rhythm
INFLAMMATION AND IMMUNE REACTIONS
Interventions: ⬇
> assess for abnormal heart and lung sound ACCUMULATION OF LIPIDS IN THE INTIMA OF ARTERIAL
> monitor blood pressure and pulse WALL
> assess mental status and LOC ⬇
2. Excess fluid volume r/t decrease cardiac output of T LYMPHOCYTES AND MONOCYTES THAT BECOMES AS
sodium and water retention MACROPHAGES INFILTRATE
Interventions: ⬇
> monitor I&O every 4 hours THE AREA TO INGEST THE LIPIDS AND DIE
> assess for presence of peripheral edema ⬇
PROLIFERATION OF SMOOTH MUSCLEMCELLS WITH IN
> follow low-sodium diet and/or fluid restriction THE VESSEL
3. Ineffective tissue perfusion r/t decrease cardiac ⬇
output FORMATION OF FIBROUS CAP OVER DEAD FATTY CORE
Interventions: (ATHEROMA)
> elevate head of the bed ⬇
> monitor VS, especially BP and pulse every 5 minutes until PROTRUSION OF ATHEROMA IN TO THE LUMEN OF
the pain subsides VESSEL
> provide oxygen and monitor oxygen saturation via pulse ⬇
oximeter, as ordered. NARROWING AND OBSTRUCTION
⬇
IF CAP IS THIN THE LIPID CORE MAY GROW CAUSING IT
Nursing Diagnoses for Right Sided Heart Failure: TO RUPTURE
1. Ineffective breathing pattern r/t fatigue and ⬇
decreased lung expansion and pulmonary HEMORRHAGE INTO PLAQUE ALLOWING THROMBUS TO
congestion secondary to CHF. DEVELOP
Interventions: ⬇
> monitor VS THROMBUS AND OBSTRUCT THE BLOOD FLOW LEADING
> observe breathing pattern for SOB TO SUDDEN CARDIAC DEATH OF MYOCARDIAL
> assist patient to use relaxation techniques INFARCTION
⬇
ANGINA AND OTHER SYMPTOMS
2. Activity intolerance r/t imbalance 02 supply and
demand
 D.A.Gonzaga, SN
DIAGNOSIS: Nitrong, Nitro Cap T.D.), chewable tablets (Isordil,
> History collection Sorbitrate), patches, transmucosal ointment (Nitro-Dur,
> Physical examination Transderm-Nitro)
> Cardiac enzyme
> ELECTROCARDIOGRAMS (ECGS OR EKGS > Beta-blockers:
> ECG CHANGES  acebutolol (Sectral)
 atenolol (Tenormin)
DIAGNOSTIC:  nadolol (Corgard)
- Echocardiogram  metoprolol (Lopressor)
- Stress Test  propranolol (Inderal)
- Nuclear Cardiac Imaging > Calcium channel blockers:
- Angiogram  Bepridil (Vascor)
 Amlodipine (Norvasc)
SIGNS & SYMPTOMS:
 Nifedipine (Procardia)
✓ Chest pain (Angina pectoris)  Felodipine (Plendil)
✓ Myocardial infarction  Isradipine (DynaCirc)
✓ Diaphoresis  Diltiazem (Cardizem)
✓ ECG changes > Analgesics:
✓ Dysrhythmia  Acetaminophen (Tylenol)
✓ Chest heaviness > Morphine sulphate (MS)
✓ Dyspnea
✓ Fatigue SURGICAL INTERVENTION:
 ANGIOPLASTY
 STENTS
NURSING DIAGNOSIS:
 CORONARY ARTERY BYPASS GRAFTING
1. Acute Pain
(CABG)
2. Deficient Knowledge
 PTCA
3. Anxiety
4.Risk for Decreased Cardiac Output
PREVENTION:
1. CONTROLLING CHOLESTEROL ABNORMALITIES
NURSING INTERVENTION:
2. WEIGHT REDUCTION
 Instruct patient to notify nurse immediately when 3. Regular, moderate physical activity increases HDL levels
chest pain occurs. and reduces triglyceride levels,
 Assess and document patient response to 4. Cessation of Tobacco Use
medication.
 Identify precipitating event, if any: frequency,
duration, intensity, and location of pain. CONGESTIVE HEART FAILURE
 Observe for associated symptoms: dyspnea, nausea > Impaired cardiac pumping such that heart is unable to pump
and vomiting, dizziness, palpitations, desire to adequate amount of blood to meet metabolic needs
micturate. > Not a disease but a “syndrome”
 Evaluate reports of pain in jaw, neck, shoulder, arm, > Associated with long-standing HTN and CAD
or hand (typically on left side).
 Place patient at complete rest during anginal FACTORS AFFECTING CARDIAC OUTPUT
episodes.
 Monitor heart rate and rhythm.
 Monitor vital signs every 5 min during initial anginal
attack.
 Stay with patient who is experiencing pain or
appears anxious.
 Maintain quiet, comfortable environment. Restrict
visitors as necessary.
 Provide supplemental oxygen as indicated.
 Provide light meals. Have patient rest for 1 hr after
meals.
HEART RATE:
 Monitor serial ECG changes. > In general, the higher the heart rate, the lower the cardiac
output
PHARMACOLOGIC MANAGEMENT • E.g. HR x SV = CO
ADMINISTER: » 60/min x 80 ml = 4800 ml/min (4.8 L/min)
> Nitroglycerin: sublingual (Nitrostat), buccal, or oral » 70/min x 80 ml = 5600 ml/min (5.6 L/min)
tablets, metered-dose spray. > But only up to a point. With excessively high heart rates,
> Sublingual isosorbide dinitrate (Isordil) diastolic filling time begins to fall, thus causing stroke
> (Sustained-release tablets, caplets: volume and thus CO to fall
 D.A.Gonzaga, SN
PRELOAD:  Hormonal response: ↓’d renal perfusion
–The volume of blood/amount of fiber stretch in the interpreted by juxtaglomerular apparatus as
ventricles at the end of diastole (i.e., before the next hypovolemia. Thus:
contraction)  Kidneys release renin, which stimulates conversion
• PRELOAD INCREASES WITH: of angiotensin I → angiotensin II, which causes:
 Fluid volume increases o Aldosterone release → Na retention and
 Vasoconstriction (“squeezes” blood from vascular water retention (via ADH secretion)
system into heart) o Peripheral vasoconstriction

• PRELOAD DECREASES WITH:  Compensatory mechanisms may restore CO to near-

 Fluid volume losses normal.
Vasodilation (able to “hold” more blood, therefore  But, if excessive, the compensatory mechanisms
less returning toheart) can worsen heart failure because . . .

STARLING’S LAW  VASOCONSTRICTION: ↑’s the resistance against

 Describes the relationship between preload and
cardiac output
 The greater the heart muscle fibers are stretched (b/c
of increases in volume), the greater their subsequent
force of contraction – but only up to a point. Beyond
that point, fibers get over-stretched and the force of
contraction is reduced
EXCESSIVE PRELOAD = excessive stretch → reduced
contraction → reduced SV/CO
which heart has to pump (i.e., ↑’s afterload), and
may therefore ↓ CO
 Na AND WATER RETENTION: ↑’s fluid volume,
which ↑’s preload. If too much “stretch” (d/t too
much fluid) → ↓ strength of contraction and ↓’s CO
 EXCESSIVE TACHYCARDIA → ↓’d diastolic
filling time → ↓’d ventricular filling → ↓’d SV and
CO

AFTERLOAD RISK FACTORS:

 The resistance against which the ventricle must  CAD
pump. Excessive afterload = difficult to pump blood  Age
→ reduced CO/SV  HPN
 Afterload increased with:  Obesity
 Hypertension  Cigarette smoking
 Vasoconstriction  Diabetes mellitus
 High cholesterol
 Afterload decreased with:  African descent
 Vasodilation
ETIOLOGY:
CONTRACTILITY • May be caused by any interference with normal
 Ability of the heart muscle to contract; relates mechanisms regulating cardiac output (CO)
to the strength of contraction. • Common causes:
Contractility decreased with:  HTN
 infarcted tissue – no contractile strength  Myocardial infarction
 ischemic tissue – reduced contractile strength.  Dysrhythmias
 Electrolyte/acid-base imbalance  Valvular disorders
 Negative inotropes (medications that decrease
 contractility, such as beta blockers). TYPES OF CONGESTIVE HEART FAILURE
Contractility increased with:  Left-sided failure
 Sympathetic stimulation (effects of epinephrine)  Most common form
 Positive inotropes (medications that increase  Blood backs up through the left atrium into the
 contractility, such as digoxin, sympathomimmetics) pulmonary veins
 Pulmonary congestion and edema
PATHOPHYSIOLOGY OF CHF – Eventually leads to biventricular failure
 Pump fails → decreased stroke volume /CO.
 Compensatory mechanisms kick in to increase Left-sided failure most common cause:
CO  HTN
 SNS stimulation → release of  Cardiomyopathy
epinephrine/norepinephrine
 Valvular disorders
o Increase HR
 CAD (myocardial infarction)
o Increase contractility
o Peripheral vasoconstriction (increases
 Right-sided failure
afterload)
 Myocardial hypertrophy: walls of heart thicken to  Results from diseased right ventricle
provide more muscle mass → stronger contractions  Blood backs up into right atrium and venous
circulation
 D.A.Gonzaga, SN
 Causes:
 LVF DIAGNOSTIC STUDIES:
 Cor pulmonale • Primary goal is to determine underlying cause
 RV infarction > Physical exam
 Right-sided failure > Chest x-ray
 Venous congestion > ECG
 Peripheral edema > Hemodynamic assessment
 Hepatomegaly
 Splenomegaly
 Jugular venous distension

 Right-sided failure
 Primary cause is left-sided failure
 Cor pulmonale
 RV dilation and hypertrophy caused by
pulmonary pathology

Acute Congestive Heart Failure

Clinical Manifestations:
 Pulmonary edema (what will you hear?)
 Agitation
 Pale or cyanotic
> Echocardiogram (Uses ultrasound to visualize myocardial
 Cold, clammy skin structures and movement, calculate EF)
 Severe dyspnea > Cardiac catheterization
 Tachypnea
 Pink, frothy sputum Acute Congestive Heart Failure
Nursing And Collaborative
Chronic Congestive Heart Failure Management
Clinical Manifestations:  Primary goal is to improve LV function by:
 Fatigue  Decreasing intravascular volume
 Dyspnea  Decreasing venous return
 Paroxysmal nocturnal dyspnea (PND)  Decreasing afterload
 Tachycardia  Improving gas exchange and oxygenation
 Edema – (lung, liver, abdomen, legs)  Improving cardiac function
 Nocturia  Reducing anxiety
 Behavioral changes
 Restlessness, confusion, ↓ attention span  Decreasing intravascular volume
 Chest pain (d/t ↓ CO and ↑ myocardial work)  Improves LV function by reducing venous return
 Weight changes (r/t fluid retention)  Loop diuretic: drug of choice
 Skin changes  Reduces preload
 Dusky appearance  High Fowler’s position
CONGESTIVE HEART FAILURE  Decreasing Afterload
CLASSIFICATION Drug therapy:
Based on the person’s tolerance to physical activity  vasodilation, ACE inhibitors
 Class 1: No limitation of physical activity  Decreases pulmonary congestion
 Class 2: Slight limitation  Improving cardiac function
 Class 3: Marked limitation  Positive inotropes
 Class 4: Inability to carry on any physical activity  Improving gas exchange and oxygenation
without discomfort  Administer oxygen, sometimes intubate and
CLASSIFICATION OF HEART FAILURE ventilate
 Reducing anxiety
 Morphine- cause sedation=relax

Chronic Congestive Heart Failure

Collaborative Care
 Treat underlying cause
 Maximize CO
 Alleviate symptoms
 Oxygen treatment
 Rest
 D.A.Gonzaga, SN
DRUG THERAPY:  Establishment of quality-of-life goals
 ACE inhibitors  Symptom management
 Diuretics  Conservation of physical/emotional energy
 Inotropic drugs (i.e. Digitalis; IV: Dobutamine)  Support systems are essential
 Vasodilators
 β-Adrenergic blockers OTHER INTERVENTIONS:
 Hydralazine and Isosorbide Dinitrate (Alternative Heart Failure
for ACE inhibitor)  Supplemental Oxygen
 Coronary Artery Revascularization or CABG (Patients
with CAD)
 An implantable cardioverter defibrillator (ICD) is
used for heart-failure treatment when the person is
considered to be a high risk of dying from an abnormal
heart rhythm -- called sudden cardiac death. It is a small
device that is implanted in the chest and continually
monitors the heart's rhythm.
 Cardiac Resynchronization Therapy (CRT)

HEMODYNAMIC MONITORING
 Critically ill patients require continuous assessment
of their cardiovascular system to diagnose and
manage their complex medical conditions.
 This type of assessment is achieved by the use of
direct pressure monitoring systems, referred to as
NUTRITIONAL THERAPY: Hemodynamic Monitoring.
 Fluid restrictions not commonly prescribed  Patients requiring hemodynamic monitoring are
 Sodium restriction cared for in critical care units. Some progressive
 2 g sodium diet care units also admit stable patients with CVP or
 Daily weights intra-arterial BP monitoring.
 Same time each day
 Wearing same type of clothing Hemodynamic Monitoring
To perform hemodynamic monitoring, a CVP,
NURSING DIAGNOSES: pulmonary artery, or arterial catheter is introduced into the
1. Activity intolerance appropriate blood vessel or heart chamber. It is connected to
2. Excess fluid volume a pressure monitoring system that has several components,
3. Disturbed sleep pattern including:
4. Impaired gas exchange  A disposable flush system, composed of IV normal
5. Anxiety saline solution (which may include heparin), tubing,
stopcocks, and a flush device, which provides
PLANNING continuous and manual flushing of the system.
 Overall goals:  A pressure bag placed around the flush solution that
 ↓ Peripheral edema is maintained at 300 mm Hg of pressure. The
 ↓ Shortness of breath pressurized flush system delivers 3 to 5 mL of
solution per hour through the catheter to prevent
 ↑ Exercise tolerance
clotting and backflow of blood into the pressure
 Drug compliance
monitoring system.
 No complications

NURSING IMPLEMENTATION:
 Acute intervention
 D.A.Gonzaga, SN
a. PNEUMOTHORAX (The nurse observes for signs of
pneumothorax during the insertion of catheters using a central
venous approach (CVP and pulmonary artery catheters)
b. INFECTION (The longer any of these catheters are left in
place (after 72 to 96 hours), the greater the risk of infection)
c. AIR EMBOLISM (can be introduced into the vascular
system if the stopcocks attached to the pressure transducers
are mishandled during blood drawing, administration of
medications, or other procedures that require opening the
system to air)

Intra-Arterial Bp Monitoring
 Used to obtain direct and continuous BP
measurements in critically ill patients who have
severe hypertension or hypotension. Arterial
catheters are also useful when arterial blood gas
measurements and blood samples need to be
obtained frequently.
Radial artery is the usual site selected
 However, placement of a catheter into the radial
artery can further impede perfusion to an area that
has poor circulation. As a result, the tissue distal to
the cannulated artery can become ischemic or
necrotic .
STOPCOCK
Traditionally, collateral circulation to the involved extremity
was assessed by using the Allen test.

 To perform the Allen test, the hand is elevated, and

Hemodynamic Monitoring
the patient is asked to make a fist for 30 seconds. The
 A transducer to convert the pressure coming from
nurse compresses the radial and ulnar arteries
the artery or heart chamber into an electrical signal
simultaneously, causing the hand to blanch. After the
 An amplifier or monitor, which increases the size of
patient opens the fist, the nurse releases the pressure
the electrical signal for display on an oscilloscope
on the ulnar artery. If blood flow is restored (hand
turns pink) within 6 seconds, the circulation to the
Nurses caring for patients who require hemodynamic
hand may be adequate enough to tolerate placement
monitoring receive training prior to using this sophisticated
of a radial artery catheter.
technology.

The nurse helps ensure safe and effective care by adhering

to the following guidelines:
1. Ensuring that the system is set up and maintained
properly (free of air bubbles)
2. Checking that the stopcock of the transducer is
positioned at the level of the atrium before the
system is used to obtain pressure measurements
(uses a marker to identify this level on the chest wall,
which provides a stable reference point for
subsequent pressure readings)
3. Establishing the zero-reference point in order to
ensure that the system is properly functioning at
atmospheric pressure (placing the stopcock of the
transducer at the phlebostatic axis, opening the
transducer to air, and activating the zero-function
key on the bedside monitor)

Measurements of CVP, BP, and pulmonary artery pressures

can be made with the head of the bed elevated up to 60°;
however, the system must be repositioned to the phlebostatic
axis to ensure an accurate reading (Urden, Stacy, & Lough,
2014).

NURSING INTERVENTIONS:
Complications from the use of hemodynamic monitoring  The catheter flush solution is the same as for
systems are uncommon and can include: pulmonary artery catheters.

 A transducer is attached, and pressures are measured
in millimeters of mercury
(mm Hg).
 The nurse monitors the
patient for complications,
which include local
obstruction with distal
ischemia, external
hemorrhage, massive
ecchymosis, dissection, air
embolism, blood loss, pain,
arteriospasm, and
infection.
Pulmonary Artery Pressure Monitoring
used in critical care for assessing left ventricular
function, diagnosing the etiology of shock, and evaluating the
patient’s response to medical interventions (e.g., fluid
administration, vasoactive medications).
A variety of catheters are available for cardiac
pacing, oximetry, cardiac output measurement, or a
combination of functions. The distal lumen has a port that
opens into the pulmonary artery. Once connected by its hub
to the pressure monitoring system, it is used to continuously
measure pulmonary artery pressures. The proximal lumen
has a port that opens into the right atrium. It is used to
administer IV medications and fluids or to monitor right atrial
pressures (i.e., CVP). Each catheter has a balloon inflation
hub and valve. A syringe is connected to the hub, which is
used to inflate or deflate the balloon with air (1.5-mL
capacity). The valve opens and closes the balloon inflation
lumen.
 The pulmonary artery catheter, covered with a sterile
sleeve, is inserted into a large vein, preferably the
subclavian, through a sheath. As noted previously,
the femoral vein is avoided; insertion techniques and
protocols mirror those used for inserting a CVP
catheter.
 The sheath is equipped with a side port for infusing
IV fluids and medications.
 The catheter is then passed into the vena cava and
right atrium. In the right atrium, the balloon tip is
inflated, and the catheter is carried rapidly by the
flow of blood through the tricuspid valve into the
right ventricle, through the pulmonic valve, and into
a branch of the pulmonary artery. When the catheter
reaches the pulmonary artery, the balloon is deflated
and the catheter is secured with sutures.
Fluoroscopy may be used during insertion to visualize the
progression of the
catheter through the right heart chambers to the pulmonary
artery. During
D.A.Gonzaga, SN
insertion of the pulmonary artery catheter, the bedside
monitor is observed
for pressure and waveform changes, as well as dysrhythmias,
as the catheter progresses through the right heart to the
pulmonary artery.
It is important to note that the pulmonary artery wedge
pressure is achieved by inflating the balloon tip, which causes
it to float more distally into a smaller portion of the
pulmonary artery until it is wedged into position. This is an
occlusive maneuver that impedes blood flow through that
segment of the pulmonary artery. Therefore, the wedge
pressure is measured immediately and the balloon deflated
promptly to restore blood flow.
Pulmonary Artery Pressure Monitoring
NURSING INTERVENTIONS:
 Catheter site care is essentially the same as for
a CVP catheter. Similar to CVP measurement,
the transducer must be positioned at the
phlebostatic axis to ensure accurate readings.
Serious complications include pulmonary artery
rupture, pulmonary thromboembolism,
pulmonary infarction, catheter kinking,
dysrhythmias, and air embolism.
Left Atrial Pressure Monitoring
 ❑ Left atrial pressure (LAP) monitoring is
performed to obtain hemodynamic insight into
left-sided cardiac structures.
 LAP may provide value when there is concern for
LV function (systolic and diastolic), left atrial
hypertension, or concern for LV preload (acute right
heart failure, pulmonary hypertension).
 ❑ Access to left atrial pressures can be acquired via
the transthoracic route or via the transseptal route.
 ❑ LAP monitoring can impact management in
patients when apprehension exists in regard to LV
function, such as when separating from CPB,
following heart transplantation, and in neonates with
arterial switch procedures. Left atrial hypertension
is a typical concern in patients with diminutive left-
sided structures following a two-ventricle repair,
mitral valve repair, and acutely following LV
assist device placement.
 ❑ Patients at risk for right heart failure or
vulnerable to pulmonary hypertensive crisis may
benefit from LAP monitoring because an acute
decrease in LAP can signify loss of LV preload.
 ❑ Given the risk of introducing thromboemboli to
the systemic circulation, the risk of bleeding, and the
potential for catheter retention at the time of
removal, caution has been taken in limiting routine
placement of these catheters and emphasis directed
to early removal.
 ❑ Increased left atrial pressure resulting from
reduced left ventricular contractility or compliance,
pulmonary venous obstruction, mitral valve disease,
pericardial disease, or hypervolemia causes
pulmonary edema and affects lung mechanics and
gas exchange

Direct measurement of left atrial pressure
 is indicated when pulmonary artery catheter
monitoring is technically difficult or
 when the patient's anatomy or clinical condition
makes the use of a pulmonary artery catheter
impossible.
Such conditions exist with
tricuspid stenosis or atresia,
pulmonary stenosis or atresia,
severe pulmonary
hypertension, and right heart
failure. Infants with pulmonary
hypertension may benefit from
simultaneous measurement of
pulmonary artery and left atrial
pressures via transthoracic
lines
 ❑ It is important to note that the left atrial catheter
must be placed surgically and has the serious
disadvantage of being a possible site for air entry
into the left side of the heart.
 ❑ The consequences of air or clot embolism on the
left (systemic) circulation may be profound:
 with potential neurologic or coronary vascular
occlusion
 possibly devastating consequences
 bleeding can also occur with removal of the left
atrial line
Low left atrial pressure, particularly with low right atrial
pressure (CVP), is suggestive of volume depletion
High left atrial pressure is suggestive of left ventricular
dysfunction, volume overload, tamponade, or mitral valve
regurgitation.
Mixed venous oxygen saturation (SvO2)
 is the percentage of oxygen bound to
hemoglobin in blood returning to the right side
of the heart.
 this reflects the amount of oxygen "left over"
after the tissues remove what they need. It is
used to help us to recognize when a patient's
body is extracting more oxygen than normally.
An increase in extraction is the bodies way to
meet tissue oxygen needs when the amount of
oxygen reaching the tissues is less than needed.
 A true mixed venous sample (called SvO2) is drawn
from the tip of the pulmonary artery catheter, and
includes all of the venous blood returning from the
head and arms (via superior vena cava), the gut and
lower extremities (via the inferior vena cava) and the
coronary veins (via the coronary sinus). By the time
the blood reaches the pulmonary artery, all venous
blood has "mixed" to reflect the average amount of
oxygen remaining after all tissues in the body have
removed oxygen from the hemoglobin. The mixed
venous sample also captures the blood before it is
re-oxygenated in the pulmonary capillary.
 Mixed venous oxygen saturation (SvO2) can help to
determine whether the cardiac output and oxygen
delivery is high enough to meet a patient's needs.
NORMAL VALUES
 Normal SvO2 60-80%. \
D.A.Gonzaga, SN
 Normal ScvO2 (from an internal jugular or
subclavian vein) is >70%.
 ATP (energy) is needed for all cell function and
survival. Tissues require oxygen in order to make
ATP (energy). If the amount of oxygen being
received by the tissues falls below the amount of
oxygen required (because of an increased need, or
decreased supply), the body attempts to compensate
as follows:
1. First Compensation: Cardiac Output increases
2. Second Compensation: Tissue oxygen extraction
increases.
3. Third Compensation: Anaerobic Metabolism
increases
Mixed Venous Oxygen Saturation Monitoring
 measures the end result of O2 consumption and
delivery
USES:
 measurement of oxygenation saturation from mixed
venous blood (SvO2) in the pulmonary artery
 requires Pulmonary Artery Catheter insertion in
most clinical settings
USEFULNESS:
 it can be used as a marker of how well O2 is being
delivered to the peripheral tissues by extrapolation
(if SvO2 low and patient in multiorgan failure then
we can add a inotrope to help increase cardiac output
ie. in severe sepsis)
 its surrogate ScvO2 has used as a treatment goal in
severe sepsis and has been shown to decrease
mortality and morbidity (Rivers study)
 continuous measurement obtained once inputting
data about patient (thus can see trends with changes
in therapy – fluid, inotropes, vasodilators, dialysis)
PROBLEMS:
1. Must be measured from a PAC thus patient exposed
to risks associated with pulmonary artery
catheterization (arrhythmia, pulmonary infarction,
embolism, bleeding, pneumothorax, line sepsis)
2. Blood taken from a normal central line to estimate
SvO2 (referred to as ScvO2 not true result and not
as accurate and may mainly be blood from SVC
which has a different O2 saturation than SvO2 -
3. used as a treatment goal in severe sepsis and has
been shown to decrease mortality and morbidity
(Rivers))
4. Can be high in a number of situations (sepsis, liver
failure, wedged PAC, administration of high FiO2)
5. Can be low in a number of situation (multiple organ
failure, cardiac arrest)
6. Requires calibration for changing haematocrit
7. Gattinoni RCT showed no benefit from SvO2
monitoring
INTERPRETATION:
 High Sv02
 increased O2 delivery (increased FiO2, hyperoxia,
hyperbaric oxygen)
 decreased O2 demand (hypothermia, anaesthesia,
neuromuscular blockade)
 high flow states: sepsis, hyperthyroidism, severe
liver disease
 D.A.Gonzaga, SN
 Low Sv02
 decreased O2 delivery:
1. decreased Hb (anaemia, haemorrhage, dilution)
2. decreased SaO2 (hypoxaemia)
3. decreased Q (any form of shock, arrhythmia)
4. increased O2 demand (hyperthermia, shivering,
pain, seizures)

Causes of High SvO2 despite evidence of End-organ

Hypoxia:
 microvascular shunting (e.g. sepsis)
 histotoxic hypoxia (e.g. cyanide poisoning)
 abnormalities in distribution of blood flow