15. Heart Failure

Heart failure, 428.9

I. Definition/general comments.

A. Heart failure (HF) is a syndrome, rather than a disease, caused by a variety of pathophysiologic processes in which the heart is unable to pump an adequate amount of blood to meet the metabolic demands of tissues.

B. HF usually develops over time and includes dysfunction of one or both ventricles characterized by the following:

1. Left ventricular dilatation or hypertrophy

2. Elevated cardiac filling pressure

3. Inadequate oxygen delivery caused by cardiac dysfunction

C. Most commonly, left-sided heart failure occurs first. After one side of the heart fails, the other may eventually fail because of increased strain and workload.

D. Other practice definitions of heart failure:

1. Myocardial remodeling—pathologic myocardial hypertrophy or dilatation

2. HF with reduced left ventricular ejection fraction (LVEF)

3. HF with a dilated left ventricle

4. HF with a preserved LVEF.

a. Most commonly associated with a nondilated left ventricle (LV)

b. May be caused by valvular disease or other conditions.

5. HF with a nondilated LV

6. Asymptomatic LV dysfunction (ALVD)—ejection fraction less than 40% but no clinical signs or symptoms of heart failure

II. Incidence/etiology/predisposing factors.

A. Affects more than 4.7 million persons in the U.S.

B. Estimated 400,000 new cases diagnosed each year

C. Most common inpatient diagnosis in patients older than age 65

D. Single largest Medicare hospitalization expenditure

E. CHF is more common in men than in women until age 75; at that time, incidence becomes approximately equal in both genders.

F. Estimated death rates among African Americans are 50% higher than among whites.

G. Left ventricular dysfunction from coronary artery disease is the most common cause; patients experiencing MI with atherosclerotic cardiovascular disease have an 8 to 10 times increased risk for subsequent HF.

H. Hypertension—risk is 3 times higher in patients with hypertension; leading risk factor for acute HF; coronary artery disease is the most common cause of chronic HF

J. Physical inactivity

L. Excessive alcohol intake

N. Other precipitating factors/disease states

1. Infections such as pericarditis, viral or bacterial systemic infections

2. Endocrine abnormalities such as hyperthyroidism, thyrotoxicosis, pheochromocytoma

3. Nutritional disorders such as beriberi (thiamine deficiency), kwashiorkor (protein deficiency)

4. Preeclampsia

5. Alcoholic cardiomyopathy

6. Musculoskeletal disorders such as muscular dystrophy, myasthenia gravis

7. Autoimmune disorders such as lupus erythematosus, sarcoidosis, amyloidosis

8. Genetic factors leading to hypertrophic cardiomyopathy

9. Valvular heart disease

10. Rheumatic or congenital heart disease

III. Compensatory mechanisms common with CHF.

A. Hypertrophy.

1. Cardiac wall thickens with increased muscle mass over time because of increased strain and workload.

2. Wall thickening leads to higher demand for oxygenation.

1. Chambers enlarge to compensate for increased blood volume.

2. Because of increased volume, muscle fibers are stretched to increase contractile force.

C. Sympathetic nervous system: Inadequate cardiac output activates the sympathetic nervous system to release epinephrine and norepinephrine. as a result, myocardial oxygen demands are increased.

D. Renal response (renin-angiotensin-aldosterone cascade).

1. Blood filtration in the kidneys decreases when cardiac output decreases.

2. The kidneys respond to a falsely decreased blood volume and release of renin.

3. Renin activates release of angiotensin I and II.

4. Angiotensin causes peripheral vasoconstriction and release of aldosterone.

5. Aldosterone causes sodium retention.

6. Sodium retention is detected by the pituitary, and antidiuretic hormone (ADH) is secreted.

7. ADH increases water absorption in the renal tubules; thus, water is retained.

IV. Right- vs left-sided heart failure: subjective and physical examination findings.

A. Right-sided heart failure: The right ventricle is impaired, and blood backs up into the right ventricle, the right atrium, and the systemic circulation

1. Increased central venous pressure

2. Jugular venous distention

3. Peripheral edema

4. Liver enlargement

6. S₃ and/or S₄ heart sounds

B. Left-sided heart failure: The left ventricle is impaired, and blood backs up into the left ventricle, left atrium, pulmonary veins, and lungs

1. Increased pulmonary capillary wedge pressure

2. Adventitious breath sounds (crackles)

4. Atrial fibrillation related to atrial distention

5. Pulsus alternans (every other pulse beat is diminished)

6. S₃ common and, rarely, S₄ heart sounds

V. General subjective and physical examination findings of CHF.

A. Fatigue—may be an early sign

B. Dyspnea—related to poor gas exchange associated with fluid retention

D. Paroxysmal nocturnal dyspnea (PND) or nocturnal cough

E. Tachycardia—related to the sympathetic nervous system response to decreased cardiac output

1. Legs (peripheral)

2. Liver (hepatomegaly)

3. Spleen (splenomegaly)

4. Abdominal cavity (ascites)

5. Lungs (pulmonary edema)

G. Nocturia—At night, when the body is in the supine position, fluid shifts from the interstitial spaces back into the intravascular space, resulting in increased renal blood flow and diuresis.

H. Skin changes—related to increased tissue capillary oxygen extraction. Thus, skin may look dusky and may also be diaphoretic.

I. Behavioral changes—related to impaired cerebral circulation, especially in the presence of atherosclerosis (e.g., unexplained fatigue, restlessness, confusion, delirium, decreased attention span, decreased memory)

J. Chest pain—In the presence of atherosclerosis, chest pain is related to decreased coronary perfusion.

VI. Laboratory and diagnostic testing

A. History and physical examination are very important for diagnosis and follow-up treatment.

B. Arterial blood gases (respiratory alkalosis due to compensatory hyperventilation is common)

C. B-type natriuretic peptide (BNP)—Elevated levels are strongly correlated with myocardial ischemia/damage and may serve to predict severity of current/future cardiac complications, including heart failure and mortality.

1. Normal BNP levels vary with age and sex, with women having slightly higher normal values.

2. Mean levels:

a. Ages 55 to 64 = 26 pg/ml

b. Ages 65 to 74 = 31 pg/ml

c. Ages 75 and older = 63 pg/ml

3. Expected levels associated with concurrent MI = 100 to 400 pg/ml.

4. Not recommended for routine evaluation of structural heart disease in patients at risk for but without signs or symptoms of HF

5. BNP or N-terminal-proBNP levels are recommended to be assessed in patients suspected of HF when the diagnosis is uncertain.

D. Erythrocyte sedimentation rate (decreased)

E. Electrolyte analyses

F. Urinalysis (may show renal dysfunction)

G. Chest x-ray (may reveal an enlarged heart)

H. ECG (used to detect old myocardial infarction)—may show small (reduced) ECG complex size

I. Echocardiogram (assesses valve and wall motion)

J. Exercise stress test (assesses baseline tolerance)

VII. Classification of HF

A. Systolic dysfunction—The major defect associated with this diagnosis is the inability of the heart to contract, leading to reduced ventricular emptying and insufficient cardiac output.

1. Associated with eccentric hypertrophy and therefore increased size of the heart

2. LVEF less than 40% denotes systolic dysfunction.

B. Diastolic dysfunction—Impairment in the ability of the heart to relax, resulting in impaired filling.

1. Leads to stiffening and thickening of the myocardial wall

2. Associated with concentric hypertrophy, with the heart’s size remaining basically normal (e.g., cardiothoracic ratio less than 55% on anteroposterior chest x-ray)

**TABLE 15-1** New York Heart Association Heart Failure Functional Classification
Data from www.hcoa.org/hcoacme/chf-cme/chf00070.htm. Accessed May 1, 2007.© 2007
Functional class	Patient description	Manifestations
Class I	No limitation of activities	Suffer no symptoms from ordinary activities
Class II	Slight, mild limitation of activity	Comfortable at rest or with mild exertion
Class III	Marked limitation of activity	Comfortable only at rest
Class IV	Should be at complete rest, confined to bed or chair	Any activity brings discomfort, and symptoms occur at rest.

VIII. Management considerations

A. Management of asymptomatic patients with reduced LVEF focuses on controlling cardiovascular risk factors and preventing/reducing ventricular modeling.

1. Regular exercise according to American College of Neuropsychopharmacology (ACNP) recommendations

2. Smoking cessation

3. Discourage alcohol consumption.

4. Aggressive blood pressure control

5. ACE inhibitor therapy is recommended for all with reduced LVEF less than 40%.

6. Angiotensin-receptor blockers (ARBs) are recommended for asymptomatic patients with reduced LVEF who cannot take ACE inhibitors because of cough or angioedema.

7. Beta blocker therapy is recommended for asymptomatic patients with reduced LVEF.

B. Nonpharmacologic management for patients with chronic heart disease.

1. Patients should receive carbohydrate and caloric restraint teaching.

2. Sodium restriction.

a. 2 to 3 g daily recommended for patients with the clinical syndrome of HF and preserved or depressed LVEF

b. Less than 2 g daily should be considered in moderate to severe HF

3. Fluid restriction: Less than 2 L is recommended for patients with severe hyponatremia (Na less than 130 mEq/L) and for all patients with fluid retention despite diuretic therapy.

4. Specifically monitor caloric intake, prealbumin, BUN for patients with unintentional weight loss/wasting.

5. Daily multivitamin recommended, especially for those on restricted diets or diuretic therapy.

6. Assess quality-of-life issues (e.g., depression, sexual dysfunction, impact on daily activities of living) at regular intervals.

7. Pneumococcal and annual flu vaccines

C. Basic management considerations for patients with LV systolic dysfunction (Table 15-2)

1. ACE inhibitors are recommended for symptomatic and asymptomatic patients with LVEF 40% or less, with doses titrated as tolerated during concomitant uptitration of beta blockers.

2. Substitute other therapies for ACE inhibitors in the following circumstances:

a. Patient cannot tolerate ACE inhibitors because of cough: ARBs are recommended. If patient cannot tolerate ARBs, the combination of hydralazine + oral nitrate may be considered.

b. Patient cannot tolerate ACE inhibitors because of hyperkalemia or renal insufficiency; similar response expected in terms of adverse effects as with ARBs: Combination of hydralazine + oral nitrate should be considered.

3. Beta blockers, along with ACE inhibitors, are established routine therapy in patients with LV systolic dysfunction. Further, this combination is recommended as routine therapy for asymptomatic patients with LVEF 40% or less.

a. Beta blockers are recommended for all patients with LVEF 40% or less.

b. Beta blockers are recommended in most patients and in those with LV systolic dysfunction, even if diabetes, chronic obstructive pulmonary disease (COPD), or peripheral vascular disease is present.

c. Beta blockers should be used with caution in patients with diabetes who have recurrent hypoglycemia, asthma, or resting limb ischemia; considerable caution is warranted in those with bradycardia or hypotension.

d. Beta blockers are not recommended in patients who have asthma with active bronchospasm

4. ARBs are recommended for routine therapy in asymptomatic and symptomatic patients with LVEF 40% or less who are intolerant to ACE inhibitors for reasons other than hyperkalemia or renal insufficiency

a. Individual ARBs rather than ACE inhibitors are considered initial therapy for the following patients:

i. Heart failure post MI

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Tags: Practice Guidelines for Acute Care Nurse Practitioners

Mar 3, 2017 | Posted by admin in NURSING | Comments Off

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