D.A.

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

Composed of 3 layers: Heart Valves

The four valves in the heart permit blood to flow in only one
>> inner layer, or direction.
ENDOCARDIUM, consists of >> composed of thin leaflets of fibrous tissue, open and
endothelial tissue and lines the close in response to the movement of blood and pressure
inside of the heart and valves. changes within the
chambers.
>> middle layer, or 2 types of valves:
MYOCARDIUM, is made up of Atrioventricular (AV) and Semilunar
muscle fibers and is responsible
for the pumping action. AV VALVES (separate the
atria from the ventricles)
>> exterior layer of the heart is
called The tricuspid valve (three
the EPICARDIUM cusps)- separates the right
atrium from the right
Heart Chambers 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,
 D.A.Gonzaga, SN
diastolic time is shortened, which may not allow adequate Sinoatrial (SA) node (the
time for myocardial perfusion. As a result, patients are at risk primary pacemaker of the heart)
for myocardial ischemia (inadequate oxygen supply) during >> located at the junction of the
tachycardia (heart rate greater than 100 bpm), especially superior
patients with CAD. vena cava and the right atrium
>> in a normal resting adult heart
Coronary Arteries has an inherent firing rate of 60 to
100 impulses per minute
>> Left Artery (3 branches) The electrical impulses initiated
>> Left main coronary artery- by the SA node are conducted along the myocardial cells of
from the point of origin to the the atria via specialized tracts called internodal pathways
first major branch
a. Left anterior descending Atrioventricular (AV) node
artery (which (the secondary pacemaker of
courses down the anterior wall of the heart)
the heart) >> coordinates the incoming
b. Circumflex artery (which electrical impulses from the
circles around to the lateral left wall of the heart) atria and after a slight delay
(allowing the atria time to
>> The right side of the heart is supplied by the right coronary contract and complete
artery. ventricular filling) relays the
>> Posterior descending artery (the posterior wall of the impulse to the ventricles.
heart receives its blood supply by an additional branch from
the right coronary artery) >> Initially, the impulse is
Superficial to the coronary arteries are the coronary veins conducted through a bundle of specialized conducting tissue,
referred to as the bundle of His, which then divides into the
Myocardium right bundle branch (conducting impulses to the right
ventricle) and the left bundle branch (conducting impulses to
>> middle, the left ventricle).
muscular layer of
the atrial >> SA node has the highest inherent rate (60 to 100
and ventricular impulses per minute)
walls >> AV node has the second-highest inherent rate (40 to 60
>> composed of impulses per minute)
specialized cells >> Ventricular pacemaker sites have the lowest inherent rate
called myocytes (30 to 40 impulses per minute)
(which form an If the SA node malfunctions, the AV node generally takes over
interconnected the pacemaker function of the heart at its inherently lower
network of muscle rate. Should both the SA and the AV nodes fail in their
fibers). These fibers pacemaker function, a pacemaker site in the ventricle will fire
encircle the heart in a figure-of-eight pattern, forming a spiral at its inherent bradycardic rate of 30 to 40 impulses per
from the base (top) of the heart to the apex (bottom) minute.

Cardiac Action Potential

Function of the Heart The nodal and Purkinje cells (electrical cells) generate and
Cardiac Electrophysiology transmit impulses across the heart, stimulating the cardiac
myocytes (working cells) to contract.
The cardiac conduction system generates and transmits >> Ions- Stimulation of the myocytes occurs due to the
electrical impulses that stimulate contraction of the exchange of electrically charged particles
myocardium. >> The channels regulate the movement and speed of specific
3 physiologic characteristics of two types of specialized ions: (enter and exit)
electrical cells (nodal cells and the Purkinje cells) provide > SODIUM (primary extracellular ion)
this synchronization: > POTASSIUM (primary intracellular ion)
1. Automaticity: ability to > CALCIUM
initiate an electrical impulse
2. Excitability: ability to DEPOLARIZATION - this exchange of ions creates a
respond to an electrical impulse positively charged intracellular space and a negatively
3. Conductivity: ability to charged extracellular space that characterizes the period.
transmit an electrical impulse REPOLARIZATION - once depolarization is complete, the
from one cell to another. exchange of ions reverts to its resting state.

CARDIAC ACTION POTENTIAL- the repeated cycle

of depolarization and repolarization
 D.A.Gonzaga, SN
pressure in each ventricle and its corresponding artery
>> Cardiac action potential equalizes, the flow of blood gradually decreases.
has 5 phases: At the end of systole, pressure within the right and left
Phase 0: Cellular ventricles rapidly decreases. As a result, pulmonary arterial
depolarization is initiated as and aortic pressures decrease, causing closure of the
positive ions influx into the semilunar valves. These
cell. events mark the onset of diastole, and the cardiac cycle is
Phase 1: Early cellular repeated
repolarization begins during
this phase as potassium exits
the intracellular space. Cardiac Output
Phase 2: This phase is called - refers to the total amount of blood ejected by one of
the plateau phase because the the ventricles in liters per minute.
rate of repolarization slows. - in a resting adult is 4 to 6 L/min but varies greatly
Calcium ions enter the intracellular space. depending on the metabolic needs of the body.
Phase 3: This phase marks the completion of repolarization - computed by multiplying the stroke volume by the
and return of the cell to its resting state heart rate.
Phase 4: This phase is considered the resting phase Stroke volume is the amount of blood ejected from one of the
before the next depolarization ventricles per heartbeat. The average resting stroke volume is
about 60 to 130 mL
Myocardial cells must completely repolarize before (Woods et al., 2009).
they can depolarize again. During the repolarization process,
the cells are in a REFRACTORY PERIOD. Effect of Heart Rate on Cardiac Output
Two phases of the refractory period: Cardiac Output
a. The Effective (Or Absolute) Refractory Period  responds to changes in the metabolic demands of the
o the cell is completely unresponsive to any electrical tissues associated with stress, physical exercise, and
stimulus illness.
o it is incapable of initiating an early depolarization  is enhanced by increases in both stroke volume and
o corresponds with the time in phase 0 to the middle heart rate to compensate for these added demands
of phase 3 of the action potential.  Changes in heart rate are due to inhibition or
b. Relative Refractory Period stimulation of the SA node mediated by the
o corresponds with the short time at the end of phase parasympathetic and sympathetic divisions of the
3. autonomic nervous system.
o if an electrical stimulus is stronger than normal, the  The balance between these two reflex control
cell may depolarize prematurely systems normally determines the heart rate.
Branches of the parasympathetic nervous system
Cardiac Hemodynamics travel to the SA node by the vagus nerve.
An important determinant of blood flow in the cardiovascular >> Stimulation of the vagus nerve slows the heart rate. The
system is the principle that fluid flows from a region of higher sympathetic nervous system increases heart rate by
pressure to one of lower pressure. The pressures responsible innervation of the beta-1 receptor sites located within the SA
for blood flow in the normal circulation are generated during node.
systole and diastole. >> The heart rate is increased by the sympathetic nervous
Cardiac Cycle system through an increased level of circulating
refers to the events that occur in the heart from the catecholamines (secreted by the adrenal gland) and by excess
beginning of one heartbeat to the next. thyroid hormone, which produces a catecholamine Vlike
Each cardiac cycle has three major sequential effect.
events: diastole, atrial systole, & ventricular systole. >> In addition, the heart rate is affected by central nervous
system and baroreceptor activity
Atrial Systole increases the pressure inside the atria,
ejecting the remaining blood into the ventricles. Atrial systole Baroreceptors
augments ventricular blood volume by 15% to 25% and is - are specialized nerve cells located in the aortic arch
sometimes referred to as the atrial kick (Woods et al., 2009). and in both right and left internal carotid arteries (at the point
At this point, ventricular systole begins in response of bifurcation from the common carotid arteries)
to propagation of the electrical impulse that began in the SA - sensitive to changes in blood pressure (BP)*
node some milliseconds earlier, the pressure inside the Hypertension- these cells increase their rate of discharge,
ventricles rapidly increases, forcing the AV valves to close. transmitting impulses to
As a result, blood ceases to flow from the atria into the the cerebral medulla.
ventricles, and regurgitation (backflow) of blood into the atria This action initiates parasympathetic activity and inhibits
is prevented sympathetic response, lowering the heart rate and the BP.
Hypotension - Less baroreceptor stimulation during periods
The rapid increase in pressure inside the right and left of hypotension prompts a decrease in parasympathetic
ventricles forces the pulmonic and aortic valves to open, and activity and enhances sympathetic responses
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
Effect of Stroke Volume on Cardiac Output Gender Considerations
Stroke volume is primarily determined by 3 factors: o Structural differences between the hearts of men and
PRELOAD women have significant implications. The heart of a
>> refers to the degree of stretch of the ventricular cardiac woman tends to be smaller than that of a man. The
muscle coronary arteries of a woman are also narrower in
fibers at the end of diastole diameter than a man’s arteries. When atherosclerosis
>> commonly referred to as left ventricular end-diastolic occurs, these differences make procedures such as
pressure cardiac catheterization and angioplasty technically
>> decreased by a reduction in the volume of blood returning more difficult.
to the ventricles by increasing the return of circulating blood
volume to the ventricles o Women typically develop CAD 10 years later than
men, as women have the benefit of the female
Frank–Starling (or Starling) law of the heart - As the volume hormone estrogen and its cardioprotective effects.
of blood returning to the heart increases, muscle fiber stretch
also increases (increased preload), resulting in stronger LEFT SIDED
contraction and a greater stroke volume. RIGHT SIDED
HEART FAILURE
AFTERLOAD Heart Failure
>> or resistance to ejection of blood from the ventricle, is the It is a chronic, progressive condition in which the
second determinant of stroke volume heart muscle is unable to pump enough blood to meet the
>> The resistance of the systemic BP to left ventricular body’s needs for blood and oxygen. Basically, the heart can’t
ejection is called systemic vascular resistance. keep up with its workload. At first the heart tries to make up
>> The resistance of the pulmonary BP to right ventricular for this by:
ejection is called pulmonary vascular resistance o Enlarging. The heart stretches to contract more
strongly and keep up with the demand to pump more
CONTRACTILITY blood. Over time this causes the heart to become
>> refers to the force generated by the contracting enlarged.
myocardium o Developing more muscle mass. The increase in
>> enhanced by circulating catecholamines, sympathetic muscle mass occurs because the contracting cells of
neuronal the heart get bigger. This lets the heart pump more
activity, and certain medications (e.g., digoxin [Lanoxin], strongly, at least initially.
dopamine, or dobutamine) o Pumping faster. This helps increase the heart’s
>> Increased contractility results in increased stroke volume. output.
>> Contractility is depressed by hypoxemia, acidosis, and
certain medications (e.g., beta-adrenergic blocking agents  The body also tries to compensate in other ways:
such as metoprolol [Lopressor]).  The blood vessels narrow to keep blood pressure up,
The percentage of the end-diastolic blood volume that is trying to make up for the heart’s loss of power.
ejected with each heartbeat is called the ejection fraction (the  The body diverts blood away from less important
normal left ventricle is 55% to 65%, Woods et al., 2009); It is tissues and organs (like the kidneys), the heart and
used as a measure of myocardial contractility. An ejection brain.
fraction of less than 40% indicates that the patient has  These temporary measures mask the problem of
decreased left ventricular function and likely requires heart failure, but they don’t solve it. Heart failure
treatment of HF continues and worsens until these compensating
processes no longer work.
Gerontologic Considerations  Eventually the heart and body just can’t keep up, and
o Changes in cardiac structure and function occur with the person experiences the fatigue, breathing
age. A loss of function of the cells throughout the problems or other symptoms that usually prompt a
conduction system leads to a slower heart rate. trip to the doctor. Heart failure can involve the
heart’s left side, right side or both sides. However, it
o The size of the heart increases due to hypertrophy usually affects the left side first.
(thickening of the heart walls), which reduces the
volume of blood that the chambers can hold. Types of Heart Failure
Hypertrophy also changes the structure of the
myocardium, reducing the strength of contraction. Left sided heart failure
The resulting backflow of blood creates heart is the most common type of
murmurs, a common finding in older adults heart failure. The left heart ventricle located in the bottom left
(Bickley, 2014; Woods et al., 2009). side of your heart.
This area pumps oxygen-rich blood to the rest of
o As a result of these age-related changes, the your body. Left-sided heart failure occurs when the
cardiovascular system takes longer to compensate left ventricle doesn’t pump efficiently. This prevents
from increased metabolic demands due to stress, your body from getting enough oxygen-rich blood.
exercise, or illness. The blood backs up into your lungs instead, which
causes shortness of breath and a buildup of fluid.
 D.A.Gonzaga, SN
There are two types of left-sided heart failure. Drug - AIDS
treatments are different for the two types. - severe forms of anemia
1. Heart failure with reduced ejection - certain cancer treatments, such as chemotherapy
fraction (HFrEF), also called systolic failure: The left - drug or alcohol misuse
ventricle loses its ability to contract normally. The
heart can't pump with enough force to push enough RISK FACTORS:
blood into circulation. People with diseases that damage the heart are also at an
2. Heart failure with preserved ejection fraction increased risk. These diseases include:
(HFpEF), also called diastolic failure (or diastolic o hyperthyroidism
dysfunction): The left ventricle loses its ability to o hypothyroidism
relax normally (because the muscle has become stiff). o emphysema
The heart can't properly fill with blood during the o anemia
resting period between each beat.
Certain behaviors can also increase your risk of
Right Sided Heart Failure developing heart failure, including:
is responsible for pumping blood to your lungs to o smoking
collect oxygen. Right-sided heart failure occurs when the o eating foods high in fat or cholesterol
right side of your heart can’t perform its job effectively. It’s o living a sedentary lifestyle
usually triggered by left-sided heart failure. o being overweight
 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 CLINICAL MANIFESTATIONS OF LEFT SIDED
to fail. HEART FAILURE
 Right-sided heart failure can also occur as a Cough: A dry, hacking cough can be an early sign, which
result of other conditions, such as lung disease. Right-sided occurs due to fluid build-up in the lungs. In later stages, the
heart failure is marked by swelling of the lower extremities. sufferer can cough up white secretions that sometimes contain
This swelling is caused by fluid backup in the legs, feet, and blood.
abdomen. Fatigue: This is due to the heart’s inability to pump enough
blood to other body parts. Arms and legs become weak.
Diastolic Heart Failure During end-stage heart failure, patients find it hard to
It occurs when the heart muscle becomes stiffer than normal. participate in normal activities, such as walking or getting
 The stiffness, which is usually due to heart dressed. People who are at this point tend to sleep a lot.
disease, means that your heart doesn’t fill with blood easily. Chest discomfort: The heart can beat irregularly, causing
 This is known as diastolic dysfunction. It leads to discomfort. The discomfort is described as fluttering, pain, or
a lack of blood flow to the rest of the organs in your body. pressure.
Confusion: The brain receives less oxygenated blood with
Systolic Heart Failure left-sided heart failure, so confusion or altered thinking can
It occurs when the heart muscle loses its ability to contract. occur. Memory loss may also be a problem.
 The contractions of the heart are necessary to Paroxysmal nocturnal dyspnea: This means that the person
pump oxygen-rich blood out to the body. is awakened from sleep with difficulty breathing.
 This problem is known as systolic dysfunction, S heart sound: This is a murmur due to a variation in blood
and it usually develops when your heart is weak and enlarged. flow.
 Both diastolic and systolic heart failure can Cyanosis: A bluish discoloration of the skin called cyanosis
occur on the left or right sides of the heart. You may have can occur as a result of poor circulation from inadequate
either condition on both sides of the heart. oxygenation of blood.
CAUSES: Elevated pulmonary capillary wedge pressure: This means
 Heart failure is most often related to another that the pressure in the small pulmonary arterial branch is
disease or illness. The most common cause of heart higher than it should be.
failure is coronary artery disease (CAD), a disorder Decreased urine output: Since other parts of the body aren’t
that causes narrowing of the arteries that supply receiving blood, the body has a tendency to want to hold on
blood and oxygen to the heart. Other conditions that to fluid.
may increase your risk for developing heart failure Weight gain: When the body holds onto more fluid, overall
include: body weight increases.
- cardiomyopathy, a disorder of the heart muscle that causes
the heart to become weak RIGHT SIDED HEART FAILURE
- a congenital heart defect Sleep apnea: Heavy and uncontrollable coughing and
- a heart attack breathlessness
- heart valve disease Sudden and frequent shortness of breath: Having a hard
- certain types of arrhythmias, or irregular heart rhythms time focusing on tasks at hand
- high blood pressure Anorexia induced by complete lack of appetite: Extreme
- emphysema, a disease of the lung weakness felt throughout the body
- Diabetes Massive weight gain: Fainting
- an overactive or underactive thyroid Chronic fatigue: Irregular heartbeat
- HIV Constant urge to urinate: Intense chest pain
 D.A.Gonzaga, SN
Nausea and lightheadedness: Coughing pinkish-white
phlegm Surgical Management:
▪ Cardiac Resynchronization Therapy (CRT)
Diagnostic Procedure/S ▪ The procedure involves implanting a half-dollar
o Stress testing during exercise to determine whether sized pacemaker, usually just below the
the patient can exercise and raise their heart rate to a collarbone. Three wires (leads) connected to the
normal level for the level of activity they’re doing. device monitor the heart rate to detect heart rate
o Blood tests that look for specific substances that are irregularities and emit tiny pulses of electricity to
typically found in the bloodstream when a patient is correct them. In effect, it is "resynchronizing" the
suffering from right-sided heart failure while also heart.
checking other major organs for signs of
abnormality. Pacemakers
o Pulmonary function testing measures the quality of It is a small device with two parts — a generator and wires
your breath and how well your lungs are working as (leads, or electrodes) — that's placed under the skin in your
you breathe in and out of a tube that’s connected to chest to help control your heartbeat
a measuring device.
o Cardiac CT scans produce digital x-ray images of Implantable cardioverter-defibrillators (icds)
your heart so that your doctor can get a clear visual ▪An ICD is a battery-powered device placed under the skin
of what’s going on. that keeps track of your heart rate. Thin wires connect the ICD
o Myocardial biopsy is a procedure in which your to your heart. If an abnormal heart rhythm is detected the
doctor removes a portion of the heart muscle by device will deliver an electric shock to restore a normal
inserting a thin tube through an entry point on your heartbeat if your heart is beating chaotically and much too
body and attaching it to your heart. fast.
o Chest x-rays to examine the how the lungs and heart Coronary artery bypass grafting (CABG)
are functioning. Coronary bypass surgery redirects blood around a section of
o Coronary angiography involves your doctor a blocked or partially blocked artery in your heart to improve
injecting a blue dye into your arteries and heart blood flow to your heart muscle. The procedure involves
chambers so that your doctor can examine the way taking a healthy blood vessel from your leg, arm or chest and
in which blood flows through your heart and connecting it beyond the blocked arteries in your heart.
determine whether there are any abnormalities. Percutaneous Coronary Intervention (PCI)
Cardiac catheterization: A thin flexible tube is threaded formerly known as angioplasty with stent, is a non- surgical
through a blood vessel and into the heart and accompanied procedure that uses a catheter (a thin flexible tube) to place a
with a contrast material so that an X-ray video can show heart small structure called a stent to open up blood vessels in the
functioning. heart that have been narrowed by plaque buildup, a condition
Echocardiogram: An ultrasound to take moving pictures of known as atherosclerosis.
heart chambers and valves. Transcatheter Aortic Valve Replacement (TAVR)
Electrocardiogram (EKG): A measurement of electrical is another type of minimally invasive aortic valve
activity of the heart, which can help determine if there is heart replacement that has a nonsurgical approach. It is also
enlargement or heart damage. capture moving images of the sometimes called transcatheter aortic valve implantation
heart to showcase the blood pressure and whether it’s (TAVI).
pumping as it should. Mechanical Valve Replacement
Electrophysiology: A test that records the heart’s electrical In a mechanical valve replacement, a mechanical valve
activity and pathways, which can detect heart rhythm replaces the damaged valve.
problems.
Radionuclide imaging: A radioactive isotope is injected into NURSING MANAGEMENT:
a vein and a special camera records it traveling through the Providing Oxygenation
heart. This helps highlight areas of heart damage.  Administer oxygen therapy per nasal cannula at 2-6
Treadmill exercise test: A measurement of a person’s LPM as ordered.
capacity to exercise and the amount of oxygen the heart  Evaluate ABG analysis results </li></ul><ul><li>
provides the muscles while in motion. This can indicate the  Semi-Fowler’s or High-Fowler’s position to
severity of left-sided heart failure and can help determine left- promote greater lung expansion
sided heart failure prognosis.  Promoting Rest and Activity
 Bed rest or limited activity may be necessary during
MEDICAL MANAGEMENT the acute phase
Non-pharmacologic therapies:  Provide an overbed table close to the patient to allow
 physical activity as appropriate; and resting the head and arms
 attention to weight gain.  Use pillows for added support when in High-
Pharmacologic therapies: Fowler’s position.
 the use of diuretics,  Administer Diazepam (Valium) 2-10 mg 3-4x a day
 vasodilators, as ordered to allay apprehension
 inotropic agents,  Gradual ambulation is encouraged to prevent risk of
 anticoagulants, venous thrombosis and embolism due to prolonged
 beta-blockers, and immobility
 digoxin.
 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 which heart has to pump (i.e., ↑’s afterload), and
cardiac output may therefore ↓ CO
 The greater the heart muscle fibers are stretched (b/c
of increases in volume), the greater their subsequent  Na AND WATER RETENTION: ↑’s fluid volume,
force of contraction – but only up to a point. Beyond which ↑’s preload. If too much “stretch” (d/t too
that point, fibers get over-stretched and the force of much fluid) → ↓ strength of contraction and ↓’s CO
contraction is reduced
 EXCESSIVE TACHYCARDIA → ↓’d diastolic
EXCESSIVE PRELOAD = excessive stretch → reduced filling time → ↓’d ventricular filling → ↓’d SV and
contraction → reduced SV/CO 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.
 D.A.Gonzaga, SN
 A transducer is attached, and pressures are measured insertion of the pulmonary artery catheter, the bedside
in millimeters of mercury monitor is observed
(mm Hg). for pressure and waveform changes, as well as dysrhythmias,
 The nurse monitors the as the catheter progresses through the right heart to the
patient for complications, pulmonary artery.
which include local
obstruction with distal
ischemia, external It is important to note that the pulmonary artery wedge
hemorrhage, massive pressure is achieved by inflating the balloon tip, which causes
ecchymosis, dissection, air it to float more distally into a smaller portion of the
embolism, blood loss, pain, pulmonary artery until it is wedged into position. This is an
arteriospasm, and occlusive maneuver that impedes blood flow through that
infection. segment of the pulmonary artery. Therefore, the wedge
pressure is measured immediately and the balloon deflated
Pulmonary Artery Pressure Monitoring promptly to restore blood flow.
used in critical care for assessing left ventricular
function, diagnosing the etiology of shock, and evaluating the Pulmonary Artery Pressure Monitoring
patient’s response to medical interventions (e.g., fluid NURSING INTERVENTIONS:
administration, vasoactive medications).  Catheter site care is essentially the same as for
a CVP catheter. Similar to CVP measurement,
A variety of catheters are available for cardiac the transducer must be positioned at the
pacing, oximetry, cardiac output measurement, or a phlebostatic axis to ensure accurate readings.
combination of functions. The distal lumen has a port that Serious complications include pulmonary artery
opens into the pulmonary artery. Once connected by its hub rupture, pulmonary thromboembolism,
to the pressure monitoring system, it is used to continuously pulmonary infarction, catheter kinking,
measure pulmonary artery pressures. The proximal lumen dysrhythmias, and air embolism.
has a port that opens into the right atrium. It is used to
administer IV medications and fluids or to monitor right atrial Left Atrial Pressure Monitoring
pressures (i.e., CVP). Each catheter has a balloon inflation  ❑ Left atrial pressure (LAP) monitoring is
hub and valve. A syringe is connected to the hub, which is performed to obtain hemodynamic insight into
used to inflate or deflate the balloon with air (1.5-mL left-sided cardiac structures.
capacity). The valve opens and closes the balloon inflation  LAP may provide value when there is concern for
lumen. 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-
 The pulmonary artery catheter, covered with a sterile sided structures following a two-ventricle repair,
sleeve, is inserted into a large vein, preferably the mitral valve repair, and acutely following LV
subclavian, through a sheath. As noted previously, assist device placement.
the femoral vein is avoided; insertion techniques and  ❑ Patients at risk for right heart failure or
protocols mirror those used for inserting a CVP vulnerable to pulmonary hypertensive crisis may
catheter. benefit from LAP monitoring because an acute
 The sheath is equipped with a side port for infusing decrease in LAP can signify loss of LV preload.
IV fluids and medications.  ❑ Given the risk of introducing thromboemboli to
 The catheter is then passed into the vena cava and the systemic circulation, the risk of bleeding, and the
right atrium. In the right atrium, the balloon tip is potential for catheter retention at the time of
inflated, and the catheter is carried rapidly by the removal, caution has been taken in limiting routine
flow of blood through the tricuspid valve into the placement of these catheters and emphasis directed
right ventricle, through the pulmonic valve, and into to early removal.
a branch of the pulmonary artery. When the catheter
 ❑ Increased left atrial pressure resulting from
reaches the pulmonary artery, the balloon is deflated
reduced left ventricular contractility or compliance,
and the catheter is secured with sutures.
pulmonary venous obstruction, mitral valve disease,
pericardial disease, or hypervolemia causes
Fluoroscopy may be used during insertion to visualize the
pulmonary edema and affects lung mechanics and
progression of the
gas exchange
catheter through the right heart chambers to the pulmonary
artery. During
 D.A.Gonzaga, SN
Direct measurement of left atrial pressure  Normal ScvO2 (from an internal jugular or
 is indicated when pulmonary artery catheter subclavian vein) is >70%.
monitoring is technically difficult or  ATP (energy) is needed for all cell function and
 when the patient's anatomy or clinical condition survival. Tissues require oxygen in order to make
makes the use of a pulmonary artery catheter ATP (energy). If the amount of oxygen being
impossible. received by the tissues falls below the amount of
oxygen required (because of an increased need, or
Such conditions exist with decreased supply), the body attempts to compensate
tricuspid stenosis or atresia, as follows:
pulmonary stenosis or atresia, 1. First Compensation: Cardiac Output increases
severe pulmonary 2. Second Compensation: Tissue oxygen extraction
hypertension, and right heart increases.
failure. Infants with pulmonary 3. Third Compensation: Anaerobic Metabolism
hypertension may benefit from increases
simultaneous measurement of Mixed Venous Oxygen Saturation Monitoring
pulmonary artery and left atrial  measures the end result of O2 consumption and
pressures via transthoracic delivery
lines USES:
 ❑ It is important to note that the left atrial catheter  measurement of oxygenation saturation from mixed
must be placed surgically and has the serious venous blood (SvO2) in the pulmonary artery
disadvantage of being a possible site for air entry  requires Pulmonary Artery Catheter insertion in
into the left side of the heart. most clinical settings
 ❑ The consequences of air or clot embolism on the
left (systemic) circulation may be profound: USEFULNESS:
 with potential neurologic or coronary vascular  it can be used as a marker of how well O2 is being
occlusion delivered to the peripheral tissues by extrapolation
 possibly devastating consequences (if SvO2 low and patient in multiorgan failure then
 bleeding can also occur with removal of the left we can add a inotrope to help increase cardiac output
atrial line ie. in severe sepsis)
 its surrogate ScvO2 has used as a treatment goal in
Low left atrial pressure, particularly with low right atrial severe sepsis and has been shown to decrease
pressure (CVP), is suggestive of volume depletion mortality and morbidity (Rivers study)
High left atrial pressure is suggestive of left ventricular  continuous measurement obtained once inputting
dysfunction, volume overload, tamponade, or mitral valve data about patient (thus can see trends with changes
regurgitation. in therapy – fluid, inotropes, vasodilators, dialysis)
Mixed venous oxygen saturation (SvO2)
 is the percentage of oxygen bound to PROBLEMS:
hemoglobin in blood returning to the right side 1. Must be measured from a PAC thus patient exposed
of the heart. to risks associated with pulmonary artery
 this reflects the amount of oxygen "left over" catheterization (arrhythmia, pulmonary infarction,
after the tissues remove what they need. It is embolism, bleeding, pneumothorax, line sepsis)
used to help us to recognize when a patient's 2. Blood taken from a normal central line to estimate
body is extracting more oxygen than normally. SvO2 (referred to as ScvO2 not true result and not
An increase in extraction is the bodies way to as accurate and may mainly be blood from SVC
meet tissue oxygen needs when the amount of which has a different O2 saturation than SvO2 -
oxygen reaching the tissues is less than needed. 3. used as a treatment goal in severe sepsis and has
 A true mixed venous sample (called SvO2) is drawn been shown to decrease mortality and morbidity
from the tip of the pulmonary artery catheter, and (Rivers))
includes all of the venous blood returning from the 4. Can be high in a number of situations (sepsis, liver
head and arms (via superior vena cava), the gut and failure, wedged PAC, administration of high FiO2)
lower extremities (via the inferior vena cava) and the 5. Can be low in a number of situation (multiple organ
coronary veins (via the coronary sinus). By the time failure, cardiac arrest)
the blood reaches the pulmonary artery, all venous 6. Requires calibration for changing haematocrit
blood has "mixed" to reflect the average amount of 7. Gattinoni RCT showed no benefit from SvO2
oxygen remaining after all tissues in the body have monitoring
removed oxygen from the hemoglobin. The mixed
venous sample also captures the blood before it is INTERPRETATION:
re-oxygenated in the pulmonary capillary.  High Sv02
 Mixed venous oxygen saturation (SvO2) can help to  increased O2 delivery (increased FiO2, hyperoxia,
determine whether the cardiac output and oxygen hyperbaric oxygen)
delivery is high enough to meet a patient's needs.  decreased O2 demand (hypothermia, anaesthesia,
NORMAL VALUES neuromuscular blockade)
 Normal SvO2 60-80%. \  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