Cardiovascular Assessment

11/18/2016

The volume of blood in the ventricles at the end of diastole, before the
next contraction, is called preload.
Preload can be increased by a number of conditions such as
myocardial infarction, aortic stenosis, and hypervolemia
Afterload is the peripheral resistance against which the left ventricle
must pump.
Afterload is affected by the size of the ventricle, wall tension, and
arterial blood pressure (BP)
o If the arterial BP is elevated, the ventricles meet increased
resistance to ejection of blood, increasing the work demand.
Eventually this results in ventricular hypertrophy, an
enlargement of the cardiac muscle tissue without an
increase in CO or the size of chambers
The ability to respond to numerous situations in health and illness
(e.g., exercise, stress, hypovolemia) is by altering CO is termed cardiac
reserve
hypovolaemia) noun Medicine
a decreased volume of circulating blood in the body.
The turbulent blood flow across the affected valve results in a murmur
Hypertension is not a normal consequence of aging, and should be
treated.
Postprandial hypotension (decrease in BP of at least 20 mm Hg that
occurs within 75 minutes after eating)
Paroxysmal nocturnal dyspnea (attacks of shortness of breath,
especially ones at night that awaken the patient)
Claudication, literally 'limping' (Latin) usually referring to impairment
in walking, or pain, discomfort or tiredness in the legs that occurs during
walking and is relieved by rest
Subjective Data Assessment

Important Health Information

History of Present Illness
o what problem has brought him or her to the health care
facility or provider
Past Health History
o Ask the patient about a history of chest pain, shortness of
breath, fatigue, alcohol and tobacco use, anemia, rheumatic
fever, streptococcal throat infections, congenital heart
disease, stroke, palpitations, dizziness with position changes,
syncope, hypertension, thrombophlebitis, intermittent
claudication, varicosities, and edema.
Medications
o Assess the patients current and past use of medications. This
includes over-the-counter (OTC) drugs, herbal supplements,
and prescription drugs.
Surgery or Other Treatments
o Ask the patient about specific treatments, past surgeries, or
hospital admissions related to car- diovascular problems.
Functional Health Patterns
Health PerceptionHealth Management Pattern
o Ask the patient about the presence of major cardiovascular
risk factors.
These include abnormal serum lipids, hypertension,
sedentary lifestyle, diabetes mellitus, obesity, tobacco
use, alcohol and recreational drugs
o Ask specifically about any allergic reaction to contrast media if
there is a chance that a cardiac catheterization may be
needed.
o Assess family history of cardiac problems
Including- CAD, peripheral vascular disease,
hypertension, bleeding, cardiac disorders, diabetes mellitus, atherosclerosis, and stroke
Nutritional-Metabolic Pattern
o Assess the patients weight history (e.g., over the past year)
o Determine the amount of salt and saturated fats in the
patients typical diet
Elimination Pattern
o Investigate any history of incontinence or constipation,
including any use of medications (prescribed and OTC) for
constipation.

to avoid straining during a bowel movement (Valsalva

maneuver)
Activity-Exercise Pattern
o Record the types of exercise done and the duration, intensity,
and frequency of each
Ask about and note the occur- rence of any symptoms
during exercise (e.g., chest pain, short- ness of breath,
claudication) that may indicate a cardiovascular
problem
Sleep-Rest Pattern
o Many patients with heart failure need to sleep with their head
elevated on pillows or in a chair
o Nocturia, sleep apnea are associated with heart problems
Cognitive-Perceptual Pattern
o problems with syncope(temporary loss of consciousness
caused by a fall in blood pressure), language, and memory
Self-PerceptionSelf-Concept Pattern
o If a cardiovascular event is acute, the patients self-perception
may be affected
Role-Relationship Pattern
o Assess the patients level of satisfaction or dis- satisfaction
with life roles, since this may alert you to possible areas of
stress or conflict
Sexuality-Reproductive Pattern
o Ask the patient about the effect of the cardiovascular

problem on sexual activity

o Erectile dysfunction (ED) may be a symptom of peripheral

vascular disease and/or a side effect of some medications
ED drugs are contraindicated if the patient is also taking
a nitrate because the combination of ED drugs and
nitrates can cause significant hypotension
o Women who smoke and use oral contraceptives are at
increased risk for blood clots
CopingStress Tolerance Pattern
o Ask the patient to identify areas that cause stress and the
usual methods of coping with stress
Values-Belief Pattern

o Individual values and beliefs, which are greatly affected by

culture, may play a significant role in the real or potential
conflict a patient faces when dealing with a diagnosis of CVD
Objective Data Assessment
Physical Examination
Vital signs
o Measure BP bilaterally. These readings normally vary

from 5 to 15 mm Hg. Use the arm with the highest BP for

subsequent BP measurements
o Take orthostatic (postural) BPs and HRs while the patient
is supine, sitting with legs dangling, and standing. SBP
should not decrease more than 20 mm Hg from the
supine to the standing position
Peripheral Vascular System

DIAGNOSTIC STUDIES OF CARDIOVASCULAR SYSTEM

Troponin is the biomarker of choice in the diagnosis of myocardial

infarction (MI)
cTnT and cTnI are detectable within hours (on average 4 to 6
hours) of myocardial injury, peak at 10 to 24 hours, and can be
detected for up to 10 to 14 days
Creatine kinase (CK)
CK-MB elevation is specific for myocardial injury or infarction. CKMB levels begin to rise 3 to 6 hours after symptom onset, peak in
12 to 24 hours, and return to baseline within 12 to 48 hours after
MI.

As BP increases, so does the risk of myocardial infarction (MI), heart

failure, stroke, and renal disease

 Key Terms

Blood pressure (BP) is the force exerted by the blood against

the walls of the blood vessel
Factors that effect BP

Sympathetic Nervous System

Baroreceptors
Vascular Endothelium
Renal System
o renin-angiotensin-aldosterone system (RAAS)
juxtaglomerular apparatus in the kidney secretes renin
Renin is an enzyme that converts angiotensinogen to
angiotensin I
Angiotensin-converting enzyme (ACE) converts
angiotensin I into angiotensin II (A-II)
o A-II is a potent vasoconstrictor and increases SVR
o A-II increases BP indirectly by stimulating the adrenal cortex
to secrete aldosterone
Aldosterone stimulates the kidneys to retain sodium and
water
o Prostaglandins (PGE2 and PGI2) secreted by the renal
medulla have a vasodilator effect on the systemic circulation.
Endocrine System
o Epinephrine and aldosterone

Etiology of HTN
Primary Hypertension. Primary (essential or idiopathic)
hypertension is elevated BP without an identified cause, and it accounts for
90% to 95% of all cases of hypertension
Contributing factors include increased SNS activity, overproduction
of sodium-retaining hormones and vasoconstricting substances,
increased sodium intake, greater- than-ideal body weight, diabetes
mellitus, tobacco use, and excessive alcohol consumption
Secondary Hypertension. Secondary hypertension is elevated BP
with a specific cause that often can be identified and corrected

 Risk Factors for primary hypertension

Clinical Manifestations
Hypertension is often called the silent killer because it is
frequently asymptomatic until it becomes severe and target organ
disease occurs
o Secondary symptoms include fatigue, dizziness, palpitations,
angina, and dyspnea
o Patients with hypertensive crisis may experience severe
headaches, dyspnea, anxiety, and nosebleeds
Complications

Hypertensive Heart Disease

Coronary Artery Disease- Hypertension is a major risk factor for
coronary artery disease (CAD)

o results in a stiff arterial wall with a narrowed lumen, and

accounts for a high rate of CAD, angina, and MI

Left Ventricular Hypertrophy. Sustained high BP increases
the cardiac workload and produces left ventricular hypertrophy
(LVH)

o Progressive LVH, especially in the presence of CAD, is

associated with the development of heart failure.
Heart Failure. Heart failure occurs when the hearts compensatory
mechanisms are overwhelmed and the heart can no longer pump
enough blood to meet the bodys demands

Cerebrovascular Disease- Atherosclerosis is the most common

cause of cerebrovascular disease

Peripheral Vascular Disease- Hypertension speeds up the

process of atherosclerosis in the peripheral blood vessels

Intermittent claudication (ischemic leg pain precipitated by

activity and relieved with rest) is a classic symptom of peripheral
vascular disease.

Nephrosclerosis- Hypertension is one of the leading causes of

chronic kidney disease, especially among African Americans.
Retinal Damage. The appearance of the retina provides
important information about the severity and duration of hypertension

Diagnostic Studies

Drug Therapy

Patient and Caregiver Teaching Related to Drug Therapy

A common side effect of several of these drugs is orthostatic

hypotension
Sexual problems may occur with many of the antihyperten- sive
drugs and can be a major reason that patients do not adhere to the
treatment plan

NURSING MANAGEMENT
PRIMARY HYPERTENSION

GERONTOLOGIC CONSIDERATIONS
The pathophysiology of hypertension in the older adult involves
the following age-related physical changes:
(1) loss of elasticity in large arteries from atherosclerosis,
(2) increased collagen content and stiffness of the
myocardium,
(3) increased peripheral vascular resistance,
(4) decreased adrenergic receptor sensitivity,
(5) blunting of baroreceptor reflexes,
(6) decreased renal function,
(7) decreased renin response to sodium and water depletion.
The recommended BP goals are less than 140/90 mm Hg for
people 65 to 79 years of age

SBP of 140 to 145 mmHg for those 80 years and older

Lower goals are recommended for older adults with diabetes
mellitus, kidney disease, or CAD

Reduce the likelihood of orthostatic hypotension

antihypertensive drugs should be started at low doses and
increased slowly. Measure BP and HR in the supine, sitting,
and standing positions at every visit
Avoid giving vasoactive medications with meals

CORONARY ARTERY DISEASE

Coronary artery disease (CAD) is a type of blood vessel dis- order
that is included in the general category of atherosclerosis

Etiology and Pathophysiology

It is characterized by deposits of lipids within the intima of the artery.
Endothelial injury and inflammation play a central role in the development of
atherosclerosis
The endothelium (the inner lining of the vessel wall) is normally
nonreactive to platelets and leukocytes, as well as coagulation,
fibrinolytic, and complement factors. However, the endothelial lining
can be injured as a result of tobacco use, hyperlipidemia,
hypertension, toxins, diabetes, hyperhomocys- teinemia, and
infection causing a local inflammatory response
C-reactive protein (CRP), a protein produced by the liver, is a
nonspecific marker of inflammation. It is increased in many patients with
CAD
Developmental Stages
Fatty streaks, the earliest lesions of atherosclerosis, are
characterized by lipid-filled smooth muscle cells

o Treatment that lowers LDL cholesterol may reverse this

process
The fibrous plaque stage is the beginning of progressive changes
in the endothelium of the arterial wall
o Normally the endothelium repairs itself immediately. This
does not happen in the individual with CAD. LDLs and growth
factors from platelets stimulate smooth muscle proliferation
and thickening of the arterial wall
Complicated Lesion. The final stage in the development of the
atherosclerotic lesion is the most dangerous
o As the fibrous plaque grows, continued inflammation can
result in plaque instability, ulceration, and rupture. Once the
integrity of the arterys inner wall is compromised, platelets
accumulate in large numbers, leading to a thrombus

Normally some arterial anastomoses or connections, termed

collateral circulation, exist within the coronary circulation. Two factors
contribute to the growth and extent of collateral circulation:
(1) the inherited predisposition to develop new blood vessels
(angiogenesis)
(2) the presence of chronic ischemia

Risk Factors for Coronary Artery Disease

AGINA

ACUTE CORONARY SYNDROME

ACS is associated with deterioration of a once stable atherosclerotic
plaque. The once stable plaque ruptures, exposing the intima to blood and
stimulating platelet aggregation and local vasoconstriction with thrombus
formation

UNSTABLE ANGINA

Unstable angina (UA) is chest pain that is new in onset, occurs at

rest, or has a worsening pattern. The patient with chronic stable angina may
develop UA, or UA may be the first clinical sign of CAD.
UA is unpredictable and is an emergency
These symptoms include fatigue, shortness of breath, indigestion,
and anxiety. Fatigue is the most prominent symptom.

MYOCARDIAL INFARCTION
A myocardial infarction (MI) occurs because of sustained ischemia,
causing irreversible myocardial cell death (necrosis)
MIs are usually described based on the location of damage (e.g.,
anterior, inferior, lateral, septal, or posterior wall infarction)
The degree of preexisting collateral circulation also influences the
severity of infarction
o This is one reason why a younger person may have a more
serious first MI than an older person with the same degree of
blockage

Clinical Manifestations of Myocardial Infarction

Pain. Severe, immobilizing chest pain not relieved by rest, position

change, or nitrate administration is the hallmark of an MI.
When epigastric pain is present, the patient may relate it to
indigestion and take antacids without relief.
It may occur while the patient is active or at rest, asleep or awake
commonly occurs in the early morning hours
o lasts for 20 minutes or longer and is more severe than usual
anginal pain
Patients with diabetes may experience silent (asymptomatic) MIs
because of cardiac neuropathy and may manifest atypical
symptoms (e.g., dyspnea)
older patient may experience a change in mental status (e.g.,
confusion), shortness of breath, pulmonary edema, dizziness, or a
dysrhythmia
Sympathetic Nervous System Stimulation. During the initial phase
of MI, the ischemic myocardial cells release catecholamines (norepinephrine
and epinephrine) that are normally found in these cells
Cardiovascular Manifestations. In response to the release of
catecholamines, BP and HR may be elevated initially. Later, the BP may drop
because of decreased cardiac output (CO)

Crackles, if present, may persist for several hours to several days,

suggesting left ventricular dysfunction.
Jugular venous distention, hepatic engorgement, and periph- eral
edema may indicate right ventricular dysfunction
Cardiac examination may reveal abnormal heart sounds that may
seem distant
o may indicate a septal defect, papillary muscle rupture, or
valve dysfunction

Nausea and Vomiting. The patient may experience nausea and

vomiting.
Fever. The temperature may increase within the first 24 hours up to
100.4 F (38 C) due to a systemic inflammatory process caused by
myocardial cell death
temperature elevation may last for as long as 1 week

*Healing Process

The bodys response to cell death is the inflammatory process.

Within 24 hours, leukocytes infiltrate the area
Catecholamine-mediated lipolysis and glycogenolysis occur. These
processes allow the increased plasma glucose and free fatty acids to
be used by the oxygen-depleted myocardium for anaerobic
metabolism.
o For this reason, serum glucose levels are frequently elevated
after MI
At 10 to 14 days after MI, the new scar tissue is still weak. The
myocardium is vulnerable to increased stress during this time
because of the unstable state of the healing heart wall so special
caution and assessment are necessary
By 6 weeks after MI, scar tissue has replaced necrotic tissue and
the injured area is considered healed.
o scarred area is often less compliant than the surrounding area
o changes in the infarcted muscle also cause changes in the
unaffected myocardium
In an attempt to compensate for the damaged muscle,
the normal myocardium hypertrophies and dilates. This
process is called ventricular remodeling
development of late HF

Complications of Myocardial Infarction

Dysrhythmias. The most common complication after an MI is

dysrhythmias
The intrinsic rhythm of the heart is disrupted. This can cause
tachycardia, bradycardia, or an irregular HR, all of which adversely
affect the ischemic myocardium
Heart Failure. Heart failure (HF) is a complication that occurs when
the hearts pumping action is reduced
Cardiogenic Shock. Cardiogenic shock occurs when oxygen and
nutrients supplied to the tissues are inadequate because of severe left
ventricular failure
Cardiogenic shock requires aggressive management.
o This includes control of dysrhythmias, intraaortic balloon
pump (IABP) therapy, and support of contractility with
vasoactive drugs.
o Goals of therapy are to maximize oxygen delivery, reduce
oxygen demand, and prevent complications (e.g., acute
kidney injury)
Papillary Muscle Dysfunction. Papillary muscle dysfunction may
occur if the infarcted area includes or is near the papillary muscle that
attaches to the mitral valve
should suspect papillary muscle dysfunction if you auscultate a new
murmur at the cardiac apex
Ventricular Aneurysm. Ventricular aneurysm results when the
infarcted myocardial wall is thin and bulges out during contraction
ventricular aneurysms harbor thrombi that can lead to an embolic
stroke
Pericarditis. Acute pericarditis, an inflammation of the visceral and/or
parietal pericardium, may result in cardiac tamponade(compression of the
heart by an accumulation of fluid in the pericardial sac), decreased
ventricular filling and emptying, and HF.
characterized by chest pain, which may vary from mild to severe
and is aggravated by inspiration, coughing, and movement of the
upper body
o Sitting in a forward position often relieves the pain

o Assess the patient with suspected pericarditis for the

presence of a friction rub over the pericardium. The sound
may be best heard with the diaphragm of the stethoscope at
the mid to lower left sternal border.
Dressler Syndrome. Dressler syndrome is pericarditis with effusion
and fever that develops 4 to 6 weeks after MI
It is thought to be caused by an antigen-antibody reaction to the
necrotic myocardium
o Laboratory findings include an elevated white blood cell count
and sedimentation rate.

DIAGNOSTIC STUDIESACUTE CORONARY

SYNDROME
The primary diagnostic studies used to determine whether a person
has UA or an MI include an ECG and serum cardiac markers

Electrocardiogram Findings
The ECG is one of the primary tools to diagnose UA or an MI
ECG often reveals the time sequence of ischemia, injury, infarction,
and resolution of the infarction

Serum Cardiac Markers

Serum cardiac markers are proteins released into the blood from
necrotic heart muscle after an MI
Cardiac-specific troponin has two subtypes: cardiac-specific
troponin T (cTnT) and cardiac-specific troponin I (cTnI)
o Highly specific indicators of MI and have greater sensitivity
and specificity for myocardial injury than creatine kinase (CK)
MB (CK-MB)
o Serum levels of cTnI and cTnT increase 4 to 6 hours after the
onset of MI, peak at 10 to 24 hours, and return to baseline
over 10 to 14 days
CK levels begin to rise about 6 hours after an MI, peak at about 18
hours, and return to normal within 24 to 36 hours
Myoglobin is released into the circulation within 2 hours after an MI
and peaks in 3 to 15 hours
o Lacks cardiac specificity, Its role in diagnosing MI is limited

Coronary Angiography

Guidelines suggest that it is reasonable to do coronary angiography on

stable but high-risk patients with UA or NSTEMI
Coronary angiography is the only way to confirm the diagnosis of
Prinzmetals angina

Other Measures
Exercise or pharmacologic stress testing and echocardiogram are used
when a patient has an abnormal but nondiagnostic baseline ECG
COLLABORATIVE

CAREACUTE CORONARY

SYNDROME
Initial Nursing Interventions

Obtain a 12-lead ECG and start continuous ECG monitoring.

Position the patient in an upright position unless contraindicated,
and initiate oxygen by nasal cannula to keep oxygen saturation
above 93%.
Establish an IV route to provide an access for emergency drug
therapy.
Give SL NTG and aspirin (chewable) if not given before arrival at
the ED.
Morphine sulfate is given for pain unrelieved by NTG.
Monitor vital signs, including pulse oximetry, frequently during the
first few hours after admission and closely thereafter.
Maintain bed rest and limit activity for 12 to 24 hours, with a
gradual increase in activity unless contraindicated.
For patients with STEMI or NSTEMI with positive cardiac markers,
reperfusion therapy is initiated
o Reperfusion therapy can include emergent PCI for STEMI and
NSTEMI or thrombolytic (fibrinolytic) therapy for STEMI

Emergent PCI (Balloon Angioplasty)

Emergent percutaneous coronary intervention (PCI) is the first
line of treatment for patients with confirmed MI (i.e., definitive ECG changes
and/or positive cardiac markers)
The goal is to open the blocked artery within 90 minutes
the patient undergoes a cardiac catheterization to locate the
blockage(s), assess the severity of the blockage(s), determine the
presence of collateral circulation, and evaluate left ventricular
function.

Less invasive, the patient is able to go home sooner than CABG

surgery

Thrombolytic Therapy
Thrombolytic therapy is given as soon as possible, ideally within the
first hour and preferably within the first 6 hours after the onset of symptoms
Procedure- Each hospital has a protocol for giving thrombolytic
therapy, but several factors are common.
Draw blood to obtain baseline laboratory values and start two or
three lines for IV therapy.
All other invasive procedures are done before the thrombolytic
agent is given to reduce the possibility of bleeding
Evaluate heart rhythm, vital signs, and pulse oximetry and assess
the heart and lungs frequently to evaluate the patients response to
therapy.
Regularly assess for changes in neurologic status, since this may
indicate a cerebral bleed.
If signs and symptoms of major bleeding occur (e.g., drop in BP, an
increase in HR, a sudden change in the patients level of consciousness, blood in the urine or stool), stop the therapy and notify the
physician.

Coronary Surgical Revascularization

Coronary Artery Bypass Graft Surgery

The long-term patency rate for internal mammary artery (IMA)

grafts is greater than 90% after 10 years.
Patency rates of saphenous vein grafts are 50% to 60% at 10 years

Transmyocardial Laser Revascularization

Used for patients with advanced CAD who are not candidates for
traditional CABG surgery and who have persistent angina after
maximum medical therapy

Drug Therapy
IV Nitroglycerin

Because hypotension is a common side effect, closely monitor BP

during this time.
o Patients who do become hypotensive are often volume
depleted and can benefit from an IV fluid bolus.

Morphine Sulfate

Morphine sulfate is the drug of choice for chest pain that is

unrelieved by NTG
Monitor patients for signs of bradypnea (abnormally slow breathing
rate) or hypotension, conditions to avoid in myocardial ischemia
and infarction

-Adrenergic Blockers

-Adrenergic blockers decrease myocardial oxygen demand by

reducing HR, BP, and contractility.

Angiotensin-Converting Enzyme Inhibitors

Antidysrhythmic Drugs
Lipid-Lowering Drugs

A fasting lipid panel is obtained on all patients admitted with ACS

Stool Softeners

This prevents straining and the resultant vagal stimulation from the
Valsalva maneuver producing bradycardia which can provoke
dysrhythmias.

ACUTE INTERVENTION
If your patient experiences angina, institute the following measures:
(1) position patient upright unless contraindicated and administer
supplemental oxygen,
(2) assess vital signs,
(3) obtain a 12-lead ECG,
(4) provide prompt pain relief first with a nitrate followed by an
opioid analgesic if needed, and
(5) auscultate heart and breath sounds

Ask the patient to describe the pain and to rate it on a scale of 0 to

10 before and after treatment to evaluate the effectiveness of the
interventions
Assess for other manifestations of pain, such as restlessness; ECG
changes; elevated HR, respiratory rate, or BP; clutching of the bed
linens; or other nonverbal cues
Priorities for nursing interventions in the initial phase of ACS include
(1) pain assessment and relief,
(2) physiologic monitoring,

(3) promotion of rest and comfort,

(4) alleviation of stress and anxiety,
(5) understanding of the patients emotional and behavioral
reactions

AMBULATORY AND HOME CARE

Provide the patient with information regarding CAD, angina,
precipitating factors for angina, risk factor reduction, and
medications
Assist the patient to identify factors that precipitate angina
Assist the patient to identify personal risk factors for CAD

HF may be caused by any interference with the normal mechanisms

regulating cardiac output (CO). CO depends on
(1) preload,
(2) afterload,
(3) myocardial contractility,
(4) heart rate (HR)

Pathophysiology of Ventricular Failure. HF is classified as systolic

or diastolic failure (or dysfunction). Patients can have isolated systolic or
diastolic failure or a combination of both.
Systolic Failure. Systolic failure results from an inability of the
heart to pump blood effectively
o The hallmark of systolic failure is a decrease in the left
ventricular ejection fraction (EF)
Normal EF is 55% to 60%. Patients with systolic HF
generally have an EF less than 45%. It can be as low as
10%.
Diastolic Failure. Diastolic failure is the inability of the ventricles
to relax and fill during diastole
o Diastolic failure is often referred to as HF with normal EF.
Mixed Systolic and Diastolic Failure. Mixed systolic and diastolic
failure is seen in disease states such as dilated cardiomyopathy
(DCM)
BNP and ANP significance
Natriuretic peptides (atrial natriuretic peptide [ANP] and brain, or btype, natriuretic peptide [BNP]) are hor- mones produced by the heart
muscle
ANP is released from the atria
BNP is released from the ventricles in response to increased blood
volume in the heart
The natriuretic peptides have renal, cardiovascular, and hormonal
effects.
o Renal effects include (1) increased glomerular filtration rate
and diuresis and (2) excretion of sodium (natriuresis).
o Cardiovascular effects include vasodilation and decreased BP.
o Hormonal effects include (1) inhibition of aldosterone and
renin secretion and (2) interference with ADH release.
o The combined effects of ANP and BNP help to counter the
adverse effects of the SNS and RAAS in patients with HF

Types of Heart Failure

Left-Sided Heart Failure

This prevents normal, forward blood flow and causes blood to back
up into the left atrium and pulmonary veins.
The increased pulmonary pressure causes fluid leakage from the
pulmonary capillary bed into the interstitium and then the alveoli.
o This manifests as pulmonary congestion and edema

Right-Sided Heart Failure

occurs when the right ventricle (RV) fails to contract effectively

Right-sided HF causes a backup of blood into the right atrium and
venous circulation.
o Venous congestion in the systemic circulation results in
jugular venous distention, hepatomegaly, splenomegaly,
vascular congestion of the gastrointestinal tract, and
peripheral edema

Interventions
In the ICU, you will monitor ECG and oxygen saturation
continuously.

Assess vital signs and urine output at least every hour.

The patient may have hemodynamic monitoring, including
intraarterial BP and pulmonary artery pressures (PAPs)

Interventions
Administration of oxygen improves saturation and assists in
meeting tissue oxygen needs.
Instruct the patient to participate in prescribed activities with
adequate recovery periods