PLT COLLEGE INC.

College of Nursing
Bayombong, Nueva Vizcaya

Nursing Care Management 103 (Care of the Clients with Cardiovascular & Hematologic
Diseases)

CARDIOVASCULAR DISEASES (Part 1)

1. ANGINA PECTORIS

Mr. Mabita is fond of eating in fast food joints. He likes the convenience and
the taste of the food they serve. This has gone for so many years until one day,
while he was walking the flight of stairs to his apartment, he felt a sudden,
crushing pain vibrating towards his neck and jaw. He sat down immediately when
he reached his room, and the pain was relieved. This episode occurred thrice that
week so he decided to visit a physician. The physician told him that he is
experiencing angina pectoris.

Angina pectoris is a clinical syndrome usually characterized by episodes or

paroxysms of pain or pressure in the anterior chest.
The cause is insufficient coronary blood flow, resulting in a decreased oxygen
supply when there is increased myocardial demand for oxygen in response to
physical exertion or emotional stress.

Classification
1. Stable angina. There is predictable and consistent pain that occurs on

SUFFER NOW AND BE A NURSE LATER…princerenerpera

exertion and is relieved by rest and/or nitroglycerin.
2. Unstable angina. The symptoms increase in frequency and severity and may
not be relieved with rest or nitroglycerin.
3. Intractable or refractory angina. There is severe incapacitating chest pain.
4. Variant angina. There is pain at rest, with reversible ST-segment elevation and
thought to be caused by coronary artery vasospasm.
5. Silent ischemia. There is objective evidence of ischemia but patient reports
no pain.

Pathophysiology
 Oxygen demands not met. Normally, the myocardium extracts a large
amount of oxygen from the coronary circulation to meet its continuous
demands.
 Increased demand. When there is an increase in demand, flow through the
coronary arteries needs to be increased.
 Ischemia. When there is blockage in a coronary artery, flow cannot be
increased, and ischemia results which may lead to necrosis or myocardial
infarction.

1
Causes

1. Physical exertion. This can precipitate an attack by increasing myocardial

oxygen demand.
2. Exposure to cold. This can cause vasoconstriction and elevated blood
pressure, with increased oxygen demand.
3. Eating a heavy meal. A heavy meal increases the blood flow to the
mesenteric area for digestion, thereby reducing the blood supply available
to the heart muscle; in a severely compromised heart, shunting of the blood
for digestion can be sufficient to induce anginal pain.
4. Stress. Stress causes the release of catecholamines, which increased blood
pressure, heart rate, and myocardial workload.

Clinical Manifestations

1. Chest pain. The pain is often felt deep in the chest behind the sternum and
may radiate to the neck, jaw, and shoulders.
2. Numbness. A feeling of weakness or numbness in the arms, wrists and hands.
3. Shortness of breath. An increase in oxygen demand could cause shortness of
breath.
4. Pallor. Inadequate blood supply to peripheral tissues cause pallor.

Gerontologic Considerations

 The elderly person with angina may not exhibit the typical pain profile
because of the diminished responses of neurotransmitters that occur with
aging.
 Often, the presenting symptom in the elderly is dyspnea.
 Sometimes, there are no symptoms (“silent” CAD), making recognition and
diagnosis a clinical challenge.

SUFFER NOW AND BE A NURSE LATER…princerenerpera

 Elderly patients should be encouraged to recognize their chest pain–like
symptom (eg, weakness) as an indication that they should rest or take
prescribed medications.

Complications

Myocardial infarction. Myocardial infarction is the end result of angina pectoris if

left untreated.
Cardiac arrest. The heart pumps more and more blood to compensate the
decreased oxygen supply, and the cardiac muscle would ultimately fail leading
to cardiac arrest.
Cardiogenic shock. MI also predisposes the patient to cardiogenic shock.

Assessment and Diagnostic Findings

ECG: Often normal when patient at rest or when pain-free; depression of the ST
segment or T wave inversion signifies ischemia. Dysrhythmias and heart block
may also be present. Significant Q waves are consistent with a prior MI.

2
24-hour ECG monitoring (Holter): Done to see whether pain episodes correlate
with or change during exercise or activity. ST depression without pain is highly
indicative of ischemia.
Exercise or pharmacological stress electrocardiography: Provides more
diagnostic information, such as duration and level of activity attained before
onset of angina. A markedly positive test is indicative of severe
Cardiac enzymes (AST, CPK, CK and CK-MB; LDH and isoenzymes LD1,
LD2): Usually within normal limits (WNL); elevation indicates myocardial damage.
Chest x-ray: Usually normal; however, infiltrates may be present, reflecting
cardiac decompensation or pulmonary complications.
Echocardiogram: May reveal abnormal valvular action as cause of chest pain.

Cardiac catheterization with angiography: Definitive test for CAD in patients with
known ischemic disease with angina or incapacitating chest pain, in patients
with cholesterolemia and familial heart disease who are experiencing chest pain,
and in patients with abnormal resting ECGs. Abnormal results are present in
valvular disease, altered contractility, ventricular failure, and circulatory
abnormalities. Note: Ten percent of patients with unstable angina have normal-
appearing coronary arteries.
Ergonovine (Ergotrate) injection: On occasion, may be used for patients who
have angina at rest to demonstrate hyperspastic coronary vessels. (Patients with
resting angina usually experience chest pain, ST elevation, or depression and/or
pronounced rise in left ventricular end-diastolic pressure [LVEDP], fall in systemic
systolic pressure, and/or high-grade coronary artery narrowing. Some patients
may also have severe ventricular dysrhythmias.)

Medical Management
Oxygen therapy. Oxygen therapy is usually initiated at the onset of chest pain in
an attempt to increase the amount of oxygen delivered to the myocardium and
reduce pain.

SUFFER NOW AND BE A NURSE LATER…princerenerpera

Pharmacologic Therapy
 Nitroglycerin gives long term and short term reduction of myocardial oxygen
consumption through selective vasodilation within three (3) minutes.
 Beta-blockers reduces myocardial oxygen consumption by blocking beta-
adrenergic stimulation of the heart.
 Calcium channel blockers have negative inotropic effects.
 Antiplatelet medications prevent platelet aggregation;
and anticoagulants prevent thrombus formation.

Nursing Management
The patient with angina pectoris should be managed by a cardiac nurse
specifically.

Nursing Assessment
In assessing the patient with angina, the nurse may ask regarding the following:
1. Location of pain.
2. Characteristics of pain.

3
 3. Health history.
4. Pain scale.
5. Onset of pain.
6. Cause of pain.
7. Measures that relieve pain.
8. Other symptoms that occur with pain.

Nursing Diagnosis
Based on the assessment data, major nursing diagnosis may include:
Ineffective cardiac tissue perfusion secondary to CAD as evidenced by
chest pain or other prodromal symptoms.
Death anxiety related to cardiac symptoms.
Deficient knowledge about the underlying disease and methods for
avoiding complication
Noncompliance, ineffective management of therapeutic regimen related
to failure to accept necessary lifestyle changes.

Nursing Care Planning and Goals

Immediate and appropriate treatment when angina occurs.
Prevention of angina.
Reduction of anxiety.
Awareness of the disease process and understanding pf the prescribed
care.
Adherence to the self-care program.
Absence of complications.

Nursing Interventions
Treating angina. The nurse should instruct the patient to stop all activities
and sit or rest in bed in a semi-Fowler’s position when they experience
angina, and administer nitroglycerin sublingually.

SUFFER NOW AND BE A NURSE LATER…princerenerpera

Reducing anxiety. Exploring implications that the diagnosis has for the
patient and providing information about the illness, its treatment, and
methods of preventing its progression are important nursing interventions.
Preventing pain. The nurse reviews the assessment findings, identifies the
level of activity that causes the patient’s pain, and plans the patient’s
activities accordingly.
Decreasing oxygen demand. Balancing activity and rest is an important
aspect of the educational plan for the patient and family.

Discharge and Home Care Guidelines

Reduce anginal attacks. Activities should be planned to minimize the
occurrence of angina episodes.
Follow-up monitoring. The patient may need reminders about follow-up
monitoring, including periodic blood laboratory testing and ECGs.
Adherence. The home care nurse may monitor the patient’s adherence
to dietary restrictions and to prescribed antianginal medications.

4
2. MYOCARDIAL INFARCTION

A patient was rushed to the emergency room because he was found in the men’s
public toilet sprawled on the floor, unconscious. ECG results show an inverted T
wave, an abnormal Q wave, and ST segment elevation. Upon waking up, the
patient narrated that he fell unconscious because of the unexplainable pain in the
chest that he felt. ER doctors diagnosed him with myocardial infarction.

Myocardial infarction (MI), is used synonymously with coronary occlusion and

heart attack, yet MI is the most preferred term as myocardial ischemia causes
acute coronary syndrome (ACS) that can result in myocardial death.
In an MI, an area of the myocardium is permanently destroyed
because plaque rupture and subsequent thrombus formation result in complete
occlusion of the artery.
The spectrum of ACS includes unstable angina, non-ST-segment elevation MI,
and ST-segment elevation MI.

Pathophysiology

In each case of MI, a profound imbalance exists between myocardial oxygen

supply and demand.

SUFFER NOW AND BE A NURSE LATER…princerenerpera

5
Unstable angina. There is reduced blood flow in a coronary artery, often due to
rupture of an atherosclerotic plaque, but the artery is not completely occluded.
Development of infarction. As the cells are deprived of oxygen, ischemia develops,
cellular injury occurs, and lack of oxygen leads to infarction or death of the cells.

Statistics and Epidemiology

“Time is muscle”; this is the reflection of the urgency of appropriate treatments to

improve patient outcome.
One fourth of the people with the disease die of MI.
Half of the people who die with acute MI never reach the hospital.

Causes

1. Vasospasm. This is the sudden constriction or narrowing of the coronary artery.

2. Decreased oxygen supply. The decrease in oxygen supply occurs from acute
blood loss, anemia, or low blood pressure.
3. Increased demand for oxygen. A rapid heart rate, thyrotoxicosis, or ingestion
of cocaine causes an increase in the demand for oxygen.

Clinical Manifestations

Some of the patients have prodromal symptoms or a previous diagnosis of CAD, but
about half report no previous symptoms.

SUFFER NOW AND BE A NURSE LATER…princerenerpera

6
 Chest pain. This is the cardinal symptom of MI. Persistent and crushing substernal
pain that may radiate to the left arm, jaw, neck, or shoulder blades. Pain is
usually described as heavy, squeezing, or crushing and may persist for 12 hours
or more.
Shortness of breath. Because of increased oxygen demand and a decrease in
the supply of oxygen, shortness of breath occurs.
Indigestion. Indigestion is present as a result of the stimulation of the
sympathetic nervous system.
Tachycardia and tachypnea. To compensate for the decreased oxygen supply,
the heart rate and respiratory rate speed up.
Catecholamine responses. The patient may experience such as coolness in
extremities, perspiration, anxiety, and restlessness.
Fever. Unusually occurs at the onset of MI, but a low-grade temperature
elevation may develop during the next few days.

Prevention
Exercise. Exercising at least thrice a week could help lower cholesterol levels that
cause vasoconstriction of the blood vessels.
Balanced diet. Fruits, vegetables, meat and fish should be incorporated in the
patient’s daily diet to ensure that he or she gets the right amount of nutrients he or
she needs.
Smoking cessation. Nicotine causes vasoconstriction which can increase the
pressure of the blood and result in MI.

Assessment and Diagnostic Findings

Patient history. The patient history includes the description of the presenting
symptoms, the history of previous cardiac and other illnesses, and the family
history of heart diseases.
ECG. ST elevation signifying ischemia; peaked upright or inverted T wave
indicating injury; development of Q waves signifying prolonged ischemia or

SUFFER NOW AND BE A NURSE LATER…princerenerpera

necrosis.
Cardiac enzymes and isoenzymes. CPK-MB (isoenzyme in cardiac muscle):
Elevates within 4–8 hr, peaks in 12–20 hr, returns to normal in 48–72 hr.
LDH. Elevates within 8–24 hr, peaks within 72–144 hr, and may take as long as 14
days to return to normal. An LDH1 greater than LDH2 (flipped ratio) helps
confirm/diagnose MI if not detected in acute phase.
Troponins. Troponin I (cTnI) and troponin T (cTnT): Levels are elevated at 4–6 hr,
peak at 14–18 hr, and return to baseline over 6–7 days. These enzymes have
increased specificity for necrosis and are therefore useful in diagnosing
postoperative MI when MB-CPK may be elevated related to skeletal trauma.
Myoglobin. A heme protein of small molecular weight that is more rapidly
released from damaged muscle tissue with elevation within 2 hr after an acute
MI, and peak levels occurring in 3–15 hr.
Electrolytes. Imbalances of sodium and potassium can alter conduction and
compromise contractility.
WBC. Leukocytosis (10,000–20,000) usually appears on the second day after MI
because of the inflammatory process.
ESR. Rises on second or third day after MI, indicating inflammatory response.

7
 Chest x-ray. May be normal or show an enlarged cardiac shadow suggestive
of HF or ventricular aneurysm.
Two-dimensional echocardiogram. May be done to determine dimensions of
chambers, septal/ventricular wall motion, ejection fraction (blood flow), and
valve configuration/function.
Coronary angiography. Visualizes narrowing/occlusion of coronary arteries and
is usually done in conjunction with measurements of chamber pressures and
assessment of left ventricular function (ejection fraction). Procedure is not
usually done in acute phase of MI unless angioplasty or emergency
heart surgery is imminent.
Exercise stress test. Determines cardiovascular response to activity (often done
in conjunction with thallium imaging in the recovery phase).

Medical Management
The goals of medical management are to minimize myocardial damage, preserve
myocardial function, and prevent complications.

SUFFER NOW AND BE A NURSE LATER…princerenerpera

8
Pharmacologic Therapy
Morphine administered in IV boluses is used for MI to reduce pain and anxiety.
ACE Inhibitors. ACE inhibitors prevent the conversion of angiotensin I to
angiotensin II to decrease blood pressure and for the kidneys to secrete sodium
and fluid, decreasing the oxygen demand of the heart.
Thrombolytics. Thrombolytics dissolve the thrombus in the coronary
artery,allowing blood to flow through the coronary artery again, minimizing the
size of the infarction and preserving ventricular function.
Emergent Percutaneous Coronary Intervention. The procedure is used to open
the occluded coronary artery and promote reperfusion to the area that has
been deprived of oxygen.

Nursing Management
The nursing management involved in MI is critical and systematic, and efficiency is
needed to implement the care for a patient with MI.

Nursing Assessment
 Monitor vital signs, especially the blood pressure and pulse rate.
 Assess for presence of shortness of breath, dyspnea, tachypnea, and crackles.
 Assess for nausea and vomiting.
 Assess for decreased urinary output.
 Assess for the history of illnesses.
 Perform a precise and complete physical assessment to detect complications
and changes in the patient’s status.
 Assess IV sites frequently.

Diagnosis
Based on the clinical manifestations, history, and diagnostic assessment data,
major nursing diagnoses may include.
 Ineffective cardiac tissue perfusion related to reduced coronary blood flow.

SUFFER NOW AND BE A NURSE LATER…princerenerpera

 Risk for ineffective peripheral tissue perfusion related to decreased cardiac
output from left ventricular dysfunction.
 Deficient knowledge related to post-MI self-care.

Nursing Priorities
Relieve pain, anxiety.
Reduce myocardial workload.
Prevent/detect and assist in treatment of life-threatening dysrhythmias or
complications.
Promote cardiac health, self-care.

Nursing Interventions
Nursing interventions should be anchored on the goals in the nursing care plan.
Administer oxygen along with medication therapy to assist with relief of symptoms.
Encourage bed rest with the back rest elevated to help decrease chest discomfort
and dyspnea.
Encourage changing of positions frequently to help keep fluid from pooling in the
bases of the lungs.

9
Check skin temperature and peripheral pulses frequently to monitor tissue perfusion.
Provide information in an honest and supportive manner.
Monitor the patient closely for changes in cardiac rate and rhythm, heart sounds,
blood pressure, chest pain, respiratory status, urinary output, changes in skin color,
and laboratory values.

Discharge and Home Care Guidelines

Education. This is one of the priorities that the nurse must teach the patient about
heart-healthy living.
Home care. The home care nurse assists the patient with scheduling and keeping
up with the follow-up appointments and with adhering to the prescribed cardiac
rehabilitation management.
Follow-up monitoring. The patient may need reminders about follow-up monitoring
including periodic laboratory testing and ECGs, as well as general health screening.
Adherence. The nurse should also monitor the patient’s adherence to dietary
restrictions and prescribed medications.

3.HYPERTENSION
During Nurse Ofelia’s shift in a hospital hypertension clinic, a patient came in with
her daughter. The 85-year-old patient had her blood pressure taken, and Nurse
Maegan noted that it is 210/158 mmHg. The patient attributes the increase of her
blood pressure to her age.

 Hypertension is defined as a systolic blood pressure greater than 140

mmHg and a diastolic pressure of more than 90 mmHg.
 This is based on the average of two or more accurate blood pressure
measurements during two or more consultations with the healthcare provider.
 The definition is taken from the Seventh Report of the Joint National Committee
on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.

SUFFER NOW AND BE A NURSE LATER…princerenerpera

Classification

10
 Normal. The normal range for blood pressure is between, less than 120 mmHg and
less than 80 mmHg.
Elevated. Elevated stage starts from 120 mmHg to 129 mmHg for systolic blood
pressure and less than 80 mmHg for diastolic pressure.
Stage 1 hypertension. Stage 1 starts when the patient has a systolic pressure of 130
to 139 mmHg and a diastolic pressure of 80 to 89 mmHg.
Stage 2 hypertension. Stage 2 starts when the systolic pressure is already more than
or equal than 140 mmHg and the diastolic is more than or equal than 90 mmHg.

Pathophysiology

 When there is excess sodium intake, renal sodium retention occurs, which increases
fluid volume resulting in increased preload and increase in contractility.
 Obesity is also a factor in hypertension because hyperinsulinemia develops and
structural hypertrophy results leading to increased peripheral vascular resistance.
 Genetic alteration also plays a role in the development of hypertension because
when there is cell membrane alteration, functional constriction may follow and also
results in increased peripheral vascular resistance.

Epidemiology
Hypertension is slowly rising to the top as one of the primary causes of morbidity in the
world. Here are the current statistics of the status of hypertension in some of the leading
countries.
 African-Americans have the highest prevalence rate of 37%.
 In the total US population of persons with hypertension, 90% to 95% have primary
hypertension or high blood pressure from an unidentified cause.
 The remaining 5% to 10% of this group have secondary hypertension or high blood
pressure related to identified causes.
 Hypertension is also termed as the “silent killer” because 24% of people who had
pressures exceeding 140/90 mmHg were unaware that their blood pressures were

SUFFER NOW AND BE A NURSE LATER…princerenerpera

elevated.

Causes
 Increased sympathetic nervous system activity. Sympathetic nervous system
activity increases because there is dysfunction in the autonomic nervous system.
 Increase renal reabsorption. There is an increase reabsorption of sodium, chloride,
and water which is related to a genetic variation in the pathways by which the
kidneys handle sodium.
 Increased RAAS activity. The renin-angiotensin-aldosterone system increases its
activity leading to the expansion of extracellular fluid volume and increased
systemic vascular resistance.
 Decreased vasodilation of the arterioles. The vascular
endothelium is damaged because of the decrease in the vasodilation of the
arterioles.

Clinical Manifestations

11
Many people who have hypertension are asymptomatic at first. Physical examination
may reveal no abnormalities except for an elevated blood pressure, so one must be
prepared to recognize hypertension at its earliest.
1. Headache. The red blood cells carrying oxygen is having a hard time reaching the
brain because of constricted vessels, causing headache.
2. Dizziness occurs due to the low concentration of oxygen that reaches the brain.
3. Chest pain. Chest pain occurs also due to decreased oxygen levels.
4. Blurred vision. Blurred vision may occur later on because of too much constriction in
the blood vessels of the eye that red blood cells carrying oxygen cannot pass
through.

Prevention
Prevention of hypertension mainly relies on a healthy lifestyle and self-discipline.

Weight reduction. Maintenance of normal body weight can help prevent

hypertension.
Adopt DASH. DASH or the Dietary Approaches to Stop Hypertension includes
consummation of a diet rich in fruits, vegetable, and low-fat dairy.
Dietary sodium retention. Sodium contributes to an elevated blood pressure, so
reducing the dietary intake to no more than 2.4 g sodium per day can be really
helpful.
Physical activity. Engage in regular aerobic physical activity for 30 minutes thrice
every week.
Moderation of alcohol consumption. Limit alcohol consumption to no more than 2
drinks per day in men and one drink for women and people who are lighter in
weight.

Complications
If hypertension is left untreated, it could progress to complications of the different body
organs.

SUFFER NOW AND BE A NURSE LATER…princerenerpera

 Heart failure. With increased blood pressure, the heart pumps blood faster than
normal until the heart muscle goes weak from too much exertion.
 Myocardial infarction. Decreased oxygen due to constriction of blood vessels may
lead to MI.
 Impaired vision. Ineffective peripheral perfusion affects the eye, causing problems
in vision because of decreased oxygen.
 Renal failure. Blood carrying oxygen and nutrients could not reach the renal system
because of the constricted blood vessels.

Assessment and Diagnostic Findings

Assessment of the patient with hypertension must be detailed and thorough. There are
also diagnostic tests that can be performed to establish the diagnosis of hypertension.

Assessment
 Assess the patient’s health history
 Perform physical examination as appropriate.
 The retinas are examined to assess possible organ damage.
 Laboratory tests are also taken to check target organ damage.

12
Diagnostic Tests
1. Urinalysis is performed to check the concentration of sodium in the urine though
the specific gravity.
2. Blood chemistry (e.g. analysis of sodium, potassium, creatinine, fasting glucose,
and total and high density lipoprotein cholesterol levels). These tests are done to
determine the level of sodium and fat in the body.
3. 12-lead ECG. ECG needs to be performed to rule presence of cardiovascular
damage.
4. Echocardiography. Echocardiography assesses the presence of left ventricular
hypertrophy.
5. Creatinine clearance. Creatinine clearance is performed to check for the level of
BUN and creatinine that can determine if there is renal damage or not.
6. Renin level. Renin level should be assessed to determine how RAAS is coping.
7. Hemoglobin/hematocrit: Not diagnostic but assesses relationship of cells to fluid
volume (viscosity) and may indicate risk factors such as
hypercoagulability, anemia.
8. Blood urea nitrogen (BUN)/creatinine: Provides information about renal
perfusion/function.
9. Glucose: Hyperglycemia (diabetes mellitus is a precipitator of hypertension) may
result from elevated catecholamine levels (increases hypertension).
10. Serum potassium: Hypokalemia may indicate the presence of primary
aldosteronism (cause) or be a side effect of diuretic therapy.
11. Serum calcium: Imbalance may contribute to hypertension.
12. Lipid panel (total lipids, high-density lipoprotein [HDL], low-density lipoprotein
[LDL], cholesterol, triglycerides, phospholipids): Elevated level may indicate
predisposition for/presence of atheromatous plaques.
13. Thyroid studies: Hyperthyroidism may lead or contribute to vasoconstriction and
hypertension.
14. Serum/urine aldosterone level: May be done to assess for primary aldosteronism
(cause).

SUFFER NOW AND BE A NURSE LATER…princerenerpera

15. Urinalysis: May show blood, protein, or white blood cells; or glucose suggests renal
dysfunction and/or presence of diabetes.
16. Creatinine clearance: May be reduced, reflecting renal damage.
17. Uric acid: Hyperuricemia has been implicated as a risk factor for the development
of hypertension.
18. Renin: Elevated in renovascular and malignant hypertension, salt-wasting
disorders.
19. Kidney and renography nuclear scan: Evaluates renal status (TOD).
20. Excretory urography: May reveal renal atrophy, indicating chronic renal disease.
21. Chest x-ray: May demonstrate obstructing calcification in valve areas; deposits in
and/or notching of aorta; cardiac enlargement.
22. Computed tomography (CT) scan: Assesses for cerebral tumor, CVA, or
encephalopathy or to rule out pheochromocytoma.
23. Electrocardiogram (ECG): May demonstrate enlarged heart, strain patterns,
conduction disturbances. Note: Broad, notched P wave is one of the earliest signs
of hypertensive heart disease.

13
Medical Management
The goal of hypertensive treatment I to prevent complications and death by achieving
and maintaining the arterial blood pressure at 40/90 mmHg or lower.

Pharmacologic Therapy
 Thiazide diuretics decrease blood volume, renal blood flow, and cardiac output.
 ARBs are competitive inhibitors of aldosterone binding.
 Beta blockers block the sympathetic nervous system to produce a slower heart
rate and a lower blood pressure.
 ACE inhibitors inhibit the conversion of angiotensin I to angiotensin II and lowers
peripheral resistance.

Stage 1 Hypertension
Thiazide diuretic is recommended for most and angiotensin-converting enzyme-
1, aldosterone receptor blocker, beta blocker, or calcium channel blocker is
considered.

Stage 2 Hypertension
Two-drug combination is followed, usually including thiazide diuretic and angiotensin-
converting enzyme-1, or beta-blocker, or calcium channel blocker.

Nursing Management
The goal of nursing management is to help achieve a normal blood pressure through
independent and dependent interventions.

Nursing Assessment
Nursing assessment must involve careful monitoring of the blood pressure at frequent
and routinely scheduled intervals.
If patient is on antihypertensive medications, blood pressure is assessed to determine
the effectiveness and detect changes in the blood pressure.

SUFFER NOW AND BE A NURSE LATER…princerenerpera

Complete history should be obtained to assess for signs and symptoms that indicate
target organ damage.
Pay attention to the rate, rhythm, and character of the apical and peripheral pulses.

Diagnosis
Based on the assessment data, nursing diagnoses may include the following:
Deficient knowledge regarding the relation between the treatment regimen and
control of the disease process.
Noncompliance with the therapeutic regimen related to side effects of the prescribed
therapy.
Risk for activity intolerance related to imbalance between oxygen supply and
demand.
Risk-prone health behavior related to condition requiring change in lifestyle.

Nursing Care Plan and Goals

Understanding of the disease process and its treatment.
Participation in a self-care program.
Absence of complications.

14
 BP within acceptable limits for individual.
Cardiovascular and systemic complications prevented/minimized.
Disease process/prognosis and therapeutic regimen understood.
Necessary lifestyle/behavioral changes initiated.
Plan in place to meet needs after discharge.

Nursing Priorities
Maintain/enhance cardiovascular functioning.
Prevent complications.
Provide information about disease process/prognosis and treatment regimen.
Support active patient control of condition.
Nursing Interventions
Encourage the patient to consult a dietitian to help develop a plan for improving
nutrient intake or for weight loss.
Encourage restriction of sodium and fat
Emphasize increase intake of fruits and vegetables.
Implement regular physical activity.
Advise patient to limit alcohol consumption and avoidance of tobacco.
Assist the patient to develop and adhere to an appropriate exercise regimen.

4.HEART FAILURE

Mrs. Malabanan is a retired school teacher who has been experiencing dyspnea
for the past few weeks, along with cough. At night, she has difficulty of sleeping at
night because of shortness of breath. When she visited her physician, she was
diagnosed with heart failure stage 2.

 Heart failure, also known as congestive heart failure, is recognized as a clinical

syndrome characterized by signs and symptoms of fluid overload or of

SUFFER NOW AND BE A NURSE LATER…princerenerpera

inadequate tissue perfusion.
 Heart failure is the inability of the heart to pump sufficient blood to meet the
needs of the tissues for oxygen and nutrients.
 The term heart failure indicates myocardial disease in which there is a problem
with contraction of the heart (systolic dysfunction) or filling of the heart (diastolic
dysfunction) that may or may not cause pulmonary or systemic congestion.
 Heart failure is most often a progressive, life-long condition that is managed with
lifestyle changes and medications to prevent episodes of acute
decompensated heart failure.

Classification
Heart failure is classified into two types: left-sided heart failure and right-sided heart
failure.

Left-Sided Heart Failure

Left-sided heart failure or left ventricular failure have different manifestations with
right-sided heart failure.

15
 Pulmonary congestion occurs when the left ventricle cannot effectively pump
blood out of the ventricle into the aorta and the systemic circulation.
 Pulmonary venous blood volume and pressure increase, forcing fluid from the
pulmonary capillaries into the pulmonary tissues and alveoli, causing pulmonary
interstitial edema and impaired gas exchange.

Right-Sided Heart Failure

When the right ventricle fails, congestion in the peripheral tissues and the viscera
predominates.
The right side of the heart cannot eject blood and cannot accommodate all the
blood that normally returns to it from the venous circulation.
Increased venous pressure leads to JVD and increased capillary hydrostatic pressure
throughout the venous system.

The American College of Cardiology and American Heart Association have

classifications of heart failure.
Stage A. Patients at high risk for developing left ventricular dysfunction but without
structural heart disease or symptoms of heart failure.
Stage B. Patients with left ventricular dysfunction or structural heart disease that has
not developed symptoms of heart failure.
Stage C. Patients with left ventricular dysfunction or structural heart disease with
current or prior symptoms of heart failure.
Stage D. Patients with refractory end-stage heart failure requiring specialized
interventions.

Pathophysiology
 Heart failure results from a variety of cardiovascular conditions, including
chronic hypertension, coronary artery disease, and valvular disease.
 As HF develops, the body activates neuro-hormonal compensatory mechanisms.
 Systolic HF results in decreased blood volume being ejected from the ventricle.

SUFFER NOW AND BE A NURSE LATER…princerenerpera

 The sympathetic nervous system is then stimulated to
release epinephrine and norepinephrine.
 Decrease in renal perfusion causes renin release, and then promotes the
formation of angiotensin I.
 Angiotensin I is converted to angiotensin II by ACE which constricts the blood
vessels and stimulates aldosterone release that causes sodium and fluid
retention.
 There is a reduction in the contractility of the muscle fibers of the heart as the
workload increases.
 Compensation. The heart compensates for the increased workload by increasing
the thickness of the heart muscle.

Statistics
 Just like coronary artery disease, the incidence of HF increases with age.
 There are 550, 000 cases of HF diagnosed each year according to the American
Heart Association.
 HF is most common among people older than 75 years of age.

16
 HF is the most common reason
for hospitalization of people older
than 65 years of age.

It is also the second most

common reason for visits to the
physician’s office.

The estimated economic burden

caused by HF is more than $33
billion annually in direct and
indirect costs and is still expected
to increase

Incidences
Heart failure can affect both
women and men, although the
mortality is higher among
women.
There are also racial differences;
at all ages death rates are higher
in African American than in non-
Hispanic whites.
Heart failure is primarily a disease
of older adults, affecting 6% to
10% of those older than 65.
It is also the leading cause of
hospitalization in older people.

Causes

SUFFER NOW AND BE A NURSE LATER…princerenerpera

Systemic diseases are usually one
of the most common causes of heart failure.
Coronary artery disease. Atherosclerosis of the coronary arteries is the primary cause
of HF, and coronary artery disease is found in more than 60% of the patients with HF.
Ischemia. Ischemia deprives heart cells of oxygen and leads to acidosis from the
accumulation of lactic acid.
Cardiomyopathy. HF due to cardiomyopathy is usually chronic and progressive.
Systemic or pulmonary hypertension. Increase in afterload results from hypertension,
which increases the workload of the heart and leads to hypertrophy of myocardial
muscle fibers.
Valvular heart disease. Blood has increasing difficulty moving forward, increasing
pressure within the heart and increasing cardiac workload.

Clinical Manifestations

The clinical manifestations produced y the different types of HF are similar and
therefore do not assist in differentiating the types of HF. The signs and symptoms can
be related to the ventricle affected.

17
Left-sided HF
Dyspnea or shortness of breath may be precipitated by minimal to moderate
activity.
Cough. The cough associated with left ventricular failure is
initially dry and nonproductive.
Pulmonary crackles. Bibasilar crackles are detected earlier and as it worsens,
crackles can be auscultated across all lung fields.
Low oxygen saturation
levels. Oxygen saturation
may decrease because of
increased pulmonary
pressures.

Right-sided HF
Enlargement of the liver
result from venous
engorgement of the liver.
Accumulation of fluid in the
peritoneal cavity may
increase pressure on
the stomach and intestines
and cause gastrointestinal
distress.
Loss of appetite results from
venous engorgement and
venous stasis within the
abdominal organs.

Prevention

SUFFER NOW AND BE A NURSE LATER…princerenerpera

Prevention of heart failure
mainly lies in lifestyle
management.
Healthy diet. Avoiding
intake of fatty and salty
foods greatly improves the
cardiovascular health of an
individual.
Engaging in cardiovascular
exercises thrice a
week could keep the cardiovascular system up and running smoothly.
Smoking cessation. Nicotine causes vasoconstriction that increases the pressure
along the vessels.

Complications

Many potential problems associated with HF therapy relate to the use of diuretics.
Hypokalemia. Excessive and repeated dieresis can lead to hypokalemia.

18
Hyperkalemia. Hyperkalemia may occur with the use of ACE inhibitors, ARBs, or
spironolactone.
Prolonged diuretic therapy might lead to hyponatremia and result in
disorientation, fatigue, apprehension, weakness, and muscle cramps.
Dehydration and hypotension. Volume depletion from excessive fluid loss may lead
to dehydration and hypotension.

Assessment and Diagnostic Findings

HF may go undetected until the patient presents with signs and symptoms of
pulmonary and peripheral edema.

 ECG: Ventricular or atrial hypertrophy, axis deviation, ischemia, and damage

patterns may be present. Dysrhythmias, e.g., tachycardia, atrial fibrillation,
conduction delays, especially left bundle branch block, frequent premature
ventricular contractions (PVCs) may be present. Persistent ST-T segment
abnormalities and decreased QRS amplitude may be present.
 Chest x-ray: May show enlarged cardiac shadow, reflecting chamber
dilation/hypertrophy, or changes in blood vessels, reflecting increased pulmonary
pressure. Abnormal contour, e.g., bulging of left cardiac border, may suggest
ventricular aneurysm.
 Heart scan (multigated acquisition [MUGA]): Measures cardiac volume during
both systole and diastole, measures ejection fraction, and estimates wall motion.
 Exercise or pharmacological stress myocardial perfusion (e.g., Persantine or
Thallium scan):Determines presence of myocardial ischemia and wall motion
abnormalities.
 Positron emission tomography (PET) scan: Sensitive test for evaluation of
myocardial ischemia/detecting viable myocardium.
 Cardiac catheterization: Abnormal pressures are indicative and help differentiate
right- versus left-sided heart failure, as well as valve stenosis or insufficiency. Also
assesses patency of coronary arteries. Contrast injected into the ventricles reveals

SUFFER NOW AND BE A NURSE LATER…princerenerpera

abnormal size and ejection fraction/altered contractility. Transvenous
endomyocardial biopsy may be useful in some patients to determine the
underlying disorder, such as myocarditis or amyloidosis.
 Digoxin and other cardiac drug levels: Determine therapeutic range and
correlate with patient response.
 Bleeding and clotting times: Determine therapeutic range; identify those at risk for
excessive clot formation.
 Electrolytes: May be altered because of fluid shifts/decreased renal function,
diuretic therapy.
 Pulse oximetry: Oxygen saturation may be low, especially when acute HF is
imposed on chronic obstructive pulmonary disease (COPD) or chronic HF.
 Arterial blood gases (ABGs): Left ventricular failure is characterized by mild
respiratory alkalosis (early) or hypoxemia with an increased Pco2 (late).
 BUN/creatinine: Elevated BUN suggests decreased renal perfusion. Elevation of
both BUN and creatinine is indicative of renal failure.
 Serum albumin/transferrin: May be decreased as a result of reduced protein
intake or reduced protein synthesis in congested liver.

19
 Complete blood count (CBC): May reveal anemia, polycythemia, or dilutional
changes indicating water retention. Levels of white blood cells (WBCs) may be
elevated, reflecting recent/acute MI, pericarditis, or other inflammatory or
infectious states.
 ESR: May be elevated, indicating acute inflammatory reaction.
 Thyroid studies: Increased thyroid activity suggests thyroid hyperactivity as
precipitator of HF.

Medical Management
The overall goals of management of HF are to relieve patient symptoms, to improve
functional status and quality of life, and to extend survival.
from

Pharmacologic Therapy
ACE Inhibitors. ACE inhibitors slow the progression of HF, improve exercise tolerance,
decrease the number of hospitalizations for HF, and promote vasodilation and
diuresis by decreasing afterload and preload.
Angiotensin II Receptor Blockers. ARBs block the conversion of angiotensin I at the
angiotensin II receptor and cause decreased blood pressure, decreased systemic
vascular resistance, and improved cardiac output.
Beta Blockers. Beta blockers reduce the adverse effects from the constant
stimulation of the sympathetic nervous system.
Diuretics. Diuretics are prescribed to remove excess extracellular fluid by increasing
the rate of urine produced in patients with signs and symptoms of fluid overload.
Calcium Channel Blockers. CCBs cause vasodilation, reducing systemic vascular
resistance but contraindicated in patients with systolic HF.

Nutritional Therapy
Sodium restriction. A low sodium diet of 2 to 3g/day reduces fluid retention and the
symptoms of peripheral and pulmonary congestion, and decrease the amount of

SUFFER NOW AND BE A NURSE LATER…princerenerpera

circulating blood volume, which decreases myocardial work.
Patient compliance. Patient compliance is important because dietary indiscretions
may result in severe exacerbations of HF requiring hospitalizations.

Additional Therapy
Supplemental Oxygen. The need for supplemental oxygen is based on the degree of
pulmonary congestion and resulting hypoxia.
Cardiac Resynchronization Therapy. CRT involves the use of a
biventricular pacemaker to treat electrical conduction defects.
Ultrafiltration. Ultrafiltration is an alternative intervention for patients with severe fluid
overload.
Cardiac Transplant. For some patients with end-stage heart failure, cardiac
transplant is the only option for long term survival.

Nursing Management
Despite advances in the treatment of HF, morbidity and mortality remains high.
Nurses have a major impact on outcomes for patients with HF.

20
Nursing Assessment
The nursing assessment for the patient with HF focuses on observing for the
effectiveness of therapy and for the patient’s ability to understand and implement
self-management strategies.

Health History
Assess the signs and symptoms such as dyspnea, shortness of breath, fatigue, and
edema.
Assess for sleep disturbances, especially sleep suddenly interrupted by shortness of
breath.
Explore the patient’s understanding of HF, self-management strategies, and the
ability and willingness to adhere to those strategies.

Physical Examination
Auscultate the lungs for presence of crackles and wheezes.
Auscultate the heart for the presence of an S3 heart sound.
Assess JVD for presence of distention.
Evaluate the sensorium and level of consciousness.
Assess the dependent parts of the patient’s body for perfusion and edema.
Assess the liver for hepatojugular reflux.
Measure the urinary output carefully to establish a baseline against which to assess
the effectiveness of diuretic therapy.
Weigh the patient daily in the hospital or at home.

Diagnosis
 Activity intolerance related to decrease CO.
 Excess fluid volume related to the HF syndrome.
 Anxiety related to breathlessness from inadequate oxygenation.
 Powerlessness related to chronic illness and hospitalizations.
 Ineffective therapeutic regimen management related to lack of knowledge.

SUFFER NOW AND BE A NURSE LATER…princerenerpera

Planning & Goals
Promoting physical activities.
Reducing fatigue.
Relieving fluid overload symptoms.
Decreasing anxiety.
Increasing the patient’s ability to manage anxiety.
Encouraging the patient to verbalize his or her ability to make decisions and
influence outcome.
Teaching the patient about self-care program.

Nursing Interventions
Nursing interventions for a patient with HF focuses on management of the patient’s
activities and fluid intake.
1. Promoting activity tolerance. A total of 30 minutes of physical activity every
day should be encouraged, and the nurse and the physician should
collaborate to develop a schedule that promotes pacing and prioritization of
activities.

21
 2. Managing fluid volume. The patient’s fluid status should be monitored closely,
auscultating the lungs, monitoring daily body weight, and assisting the patient
to adhere to a low sodium diet.
3. Controlling anxiety. When the patient exhibits anxiety, the nurse should
promote physical comfort and provide psychological support, and begin
teaching ways to control anxiety and avoid anxiety-provoking situations.
4. Minimizing powerlessness. Encourage the patient to verbalize their concerns
and provide the patient with decision-making opportunities.

Nursing Priorities
 Improve myocardial contractility/systemic perfusion.
 Reduce fluid volume overload.
 Prevent complications.
 Provide information about disease/prognosis, therapy needs, and prevention
of recurrences.
Evaluation
 Demonstration of tolerance for increased activity.
 Maintenance of fluid balance.
 Less anxiety.
 Decides soundly regarding care and treatment.
 Adherence to self-care regimen.

Discharge and Home Care Guidelines

The nurse should provide education and involve the patient in the therapeutic
regimen.

Discharge Goals
 Cardiac output adequate for individual needs.
 Complications prevented/resolved.
 Optimum level of activity/functioning attained.

SUFFER NOW AND BE A NURSE LATER…princerenerpera

 Disease process/prognosis and therapeutic regimen understood.
 Plan in place to meet needs after discharge.

“You Learn More From Failure Than From Success.

Don’t Let It Stop You.
Failure Builds Character.”

22