Heart failure

21 Heart failure




Overview/pathophysiology


Heart failure (HF) is a complex clinical syndrome in which the heart is unable to pump sufficient blood to meet the body’s metabolic demands. It is caused by any structural or functional cardiac disorder that impairs the ventricle’s ability to fill with or eject blood. HF is a chronic condition that is prone to acute exacerbations (termed acute decompensated heart failure [ADHF]). In most cases of ADHF, severe volume overload and pulmonary edema are present. Acute pulmonary edema is an emergency situation in which hydrostatic pressure in the pulmonary vessels is greater than the vascular colloid osmotic pressure that holds fluid in the vessels. As a result, fluid floods the alveoli. When the alveoli contain fluid, their ability to participate in gas exchange is reduced and hypoxia occurs. HF usually is a result of either systolic (previously known as left-sided HF) or diastolic (previously known as right-sided HF) cardiac dysfunction or a combination of both.




Systolic dysfunction:


Ventricular dilation and impaired ventricular contraction occur because of myocardial muscle injury or abnormality (see dilated cardiomyopathy, below). The initial injury or stressor to the heart muscle results in impaired cardiac output. This triggers a cascade of compensatory mechanisms, which together contribute to development and progression of HF.



Increased neurohormonal activation:


Activation of the sympathetic nervous system (SNS) and renin-angiotensin system (RAS) stimulates catecholamines and other neurohormones, causing increases in heart rate (HR) and blood pressure (BP), systemic vasoconstriction, decreased renal perfusion, and sodium and fluid retention in an effort to increase cardiac output.



Hemodynamic alterations:


Increase in left ventricular end-diastolic volume/pressure (preload) and thickening and elongation of the myofibrils (stretch) initially result in increased force of contraction (Frank-Starling law). The rise in myocardial oxygen demand further stimulates the neurohormonal response. Increases in preload and afterload (because of increased systemic resistance) add to left ventricular workload and cause excessive “stretch” of the myofibrils, thereby impairing ventricular contraction.



Remodeling:


The above mechanisms eventually lead to hypertrophy (enlargement and thickening of the left ventricular [LV] wall). The heart becomes more spherical (dilated) in shape because of lengthening of the myofibrils, cell slippage, fibrosis, and myocyte death. These progressive changes in size, shape, and structure of the heart muscle are termed remodeling.


The structural, hemodynamic, and neurohormonal alterations cause progressive deterioration in systolic function associated with decreased left ventricular ejection fraction (LVEF), increased intracardiac pressures, impaired valvular function, decreased forward flow to vital organs and tissues, and increased pulmonary pressures. This results in pulmonary (left-sided failure) and hepatic (right-sided failure) congestion, edema, renal impairment, and impaired oxygenation and metabolism. Ventricular and atrial dysrhythmias are common because of structural changes to the myocytes and increased myocardial oxygen demand and are a major cause of mortality for this population.



Diastolic dysfunction:


The ventricle becomes noncompliant and unable to accommodate increased preload and afterload (or decreased preload). These patients may have symptoms of HF because of volume overload without a reduction in systolic function as seen in individuals with long-standing hypertension, coronary artery disease (CAD), and hypertrophic and restrictive cardiomyopathies (see below).



Cardiomyopathies:


HF commonly occurs in the presence of an underlying cardiomyopathy (disorder of the heart muscle). Cardiomyopathies are classified according to underlying cause and abnormality in structure and function.



• Dilated cardiomyopathy (DCM):


Most prevalent type characterized by enlargement of one (usually left) or both ventricles and impaired contraction (systolic dysfunction). The most common form is ischemic cardiomyopathy caused by severe coronary (ischemic) heart disease and/or myocardial infarction. DCM also occurs secondary to hypertension, valvular heart disease, diabetes mellitus (DM), cardiotoxins, genetic causes, and metabolic, infectious, or systemic diseases. DCM is termed idiopathic when the cause cannot be identified. See “Systolic dysfunction,” earlier, for additional information.



• Hypertrophic cardiomyopathy:


Characterized by an abnormally enlarged left ventricle but without a concomitant increase in cavity size. Filling is restricted and may be associated with left ventricular outflow tract obstruction. Cardiac function can remain normal for varying periods before decompensation occurs. Symptoms are varied and include HF symptoms, chest pain, palpitations, dizziness, near-syncope, or syncope. Patients may be prone to ventricular dysrhythmias. Although it is theorized that hypertrophic cardiomyopathy has a strong hereditary link, etiology is unknown.



• Restrictive cardiomyopathy:


Least common in Western countries, it is characterized by inadequate compliance causing restriction of diastolic filling.



Other causes of heart failure


HF or acute pulmonary edema can occur secondary to other conditions that place excessive demands on cardiac output, such as hypertensive crisis, tachycardia due to hyperthyroidism, dysrhythmias, severe anemia, faulty heart valves, congenital heart defects, dysrhythmias, cardiomyopathy, myocarditis, trauma, infection, volume overload (i.e., caused by intravenous [IV] fluids, postoperative fluid shifts), pregnancy, and conditions that affect capillary permeability. In these cases, treatment/correction of the underlying cause is essential and may result in normalization or improvement of cardiac function.


Severe pulmonary diseases, including chronic obstructive pulmonary disease (COPD), pulmonary hypertension, and obstructive sleep apnea (OSA) can lead to diastolic HF (cor pulmonale). This is less likely to be reversible. Poorly compensated pulmonary disease, upper respiratory infection, and pneumonia can exacerbate all types of HF and need to be treated aggressively.



Health care setting


Primary care with possible hospitalization, including intensive care unit (ICU), resulting from complications. Note: Eighty percent of HF admissions are due to preventable factors.



Assessment



General



Signs and symptoms:


Dyspnea on exertion (DOE) or at rest, fatigue, decreased exercise tolerance, weakness, orthopnea (unable to lie flat; may need to sleep on pillows or sitting in a chair), paroxysmal nocturnal dyspnea, wheezing, cough, cyanosis, irregular or rapid HR, sudden weight gain from fluid retention, lower extremity edema, abdominal distention, nausea, early satiety, and nocturia. Associated indicators include chest/anginal pains, palpitations, near-syncope, syncope, and falls. Low-output symptoms include positional lightheadedness, weakness, mental status changes, and decreased urine output.



Physical assessment:


Decreased or elevated blood pressure (BP), dysrhythmias, tachycardia, tachypnea, increased venous pulsations, pulsus alternans (alternating strong and weak heart beats), increased central venous pressure (CVP), jugular venous distention, crackles (rales), wheezes, decreased breath sounds, cardiac gallop and/or murmur, hepatomegaly, ascites, and pitting edema in dependent areas (lower extremities, sacrum).



History/risk factors:


CAD, hypertension, DM, OSA or other pulmonary disease, recent IV fluid infusions, surgery, pregnancy, recent/current infectious illness, pneumonia, nonadherence to medication or diet regimen, obesity, hypercholesterolemia, and recent nonsteroidal antiinflammatory drug or COX-2 inhibitor use. In addition, see “Other causes of heart failure,” earlier.



Acute decompensated heart failure



Signs and symptoms:


Typified by marked severity of HF symptoms and deterioration of one or more New York Heart Association (NYHA) functional classes. Pulmonary edema and cardiogenic shock (see p. 143) may be present and, in more severe cases, renal dysfunction.



Acute pulmonary edema



Signs and symptoms:


Extreme dyspnea, anxiety, restlessness, frothy and blood-tinged sputum, severe orthopnea, and paroxysmal nocturnal dyspnea. Patient exhibits “air hunger” and may thrash about and describe a sensation of drowning.



Physical assessment:


Crackles (rales), wheezing, decreased breath sounds, tachycardia, tachypnea, engorged neck veins, and cardiac gallop/murmur.



Diagnostic tests




Chest x-ray examination:


May show cardiomegaly, engorged pulmonary vasculature, “Kerley-B lines” suggestive of HF, and pleural or pericardial effusions.



Electrocardiogram (ECG):


Changes may indicate CAD, acute myocardial ischemia, left ventricular hypertrophy (widened QRS), conduction defects, and dysrhythmias.



Left ventricular ejection fraction:


Percentage of blood ejected from the left ventricle during systole. Normal LVEF is 50%-70%. In systolic dysfunction, it is reduced. LVEF less than 35% is associated with increased risk for mortality-related HF and dysrhythmias. In hypertrophic cardiomyopathy, LVEF may be greater than 70%. LVEF assessment can be measured during echocardiogram, LV gram, magnetic resonance imaging (MRI), or radionuclide studies (multiple-gated acquisition scan, nuclear stress test [see below]).



Echocardiography:


Most commonly used means of evaluating ventricular function. It assesses left- and right-sided systolic function, LVEF, degree of ventricular dilation, wall thickness, abnormal wall and septal motion, valvular function, estimated pulmonary pressure, presence of thrombus, restriction, outflow tract obstruction, and pericardial effusion. Diastolic dysfunction may be evident. Tissue Doppler/three-dimensional echocardiography may reveal degree of ventricular synchrony and utility of cardiac resynchronization therapy.



Cardiac catheterization:


Rules out underlying ischemic heart disease and assesses hemodynamics (left- and right-sided filling pressures, cardiac output, and systemic and pulmonary vascular resistance).



Left ventriculography:


Provides assessment of LV function and LVEF.



Endomyocardial biopsy:


May be obtained during right heart catheterization. Usually it is reserved for severe, refractory HF in nonelderly patients to assist in identifying pathologic agent and reversible causes.



Radionuclide stress test, stress echocardiogram:


To assess for underlying ischemic heart disease and reversible or fixed ischemic defects.



Pulmonary function tests:


Useful in differentiating causes of shortness of breath and other HF symptoms. Pulmonary function tests (PFTs) may reveal underlying COPD or reactive airways disease (asthma).



Oximetry/arterial blood gas (ABG) values:


Will reveal hypoxemia. Desaturations may be noted with activity. Overnight (sleep) oximetry may reveal OSA.



Serum blood urea nitrogen (BUN), creatinine:


Elevated in renal insufficiency and chronic kidney disease due to low cardiac output and hypotension, possibly related to treatment with diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), or aldosterone antagonists.



Serum electrolytes:


May reveal hyperkalemia due to renal dysfunction or ACE inhibitor/ARB or aldosterone antagonist use. Hypokalemia may occur as a result of diuretic use. The presence of hyponatremia is a poor prognostic indicator in advanced HF.



Serum enzymes:


Mild elevation in cardiac troponins (with normal creatinine kinase [CK]) is not uncommon in patients with chronic HF or chronic kidney disease. Cardiac troponin elevation in the presence of elevated CK may indicate acute coronary syndrome.



Liver function tests, including serum aspartate aminotransferase and serum bilirubin:


May be elevated in patients with hepatic congestion.



Brain natriuretic peptide (BNP):


Released from the ventricles in response to wall stress. This test is useful in differentiating HF from other causes of dyspnea, including pulmonary disease. Negative BNP (less than 100 pg/mL) suggests non-HF etiology. When used in conjunction with standard clinical assessment, elevated BNP may support diagnosis of HF and evaluate patient’s response to treatment.



Digoxin level:


The goal in HF is a level less than 1.0 ng/mL. Hypokalemia and impaired renal function can predispose patient to digoxin toxicity.



Complete blood count (CBC):


May reveal decreased hemoglobin (Hb) and hematocrit (Hct) in the presence of anemia.



Thyroid-stimulating hormone level:


To rule out hyperthyroidism or hypothyroidism, either of which may contribute to HF and dysrhythmias.





Nursing diagnosis:


Impaired gas exchange

related to alveolar-capillary membrane changes (fluid accumulation in the alveoli)


Desired Outcome: Within 30 min of treatment/intervention, patient has adequate gas exchange as evidenced by normal breath sounds and skin color, presence of eupnea, HR 100 bpm or less, Pao2 80 mm Hg or higher, and Paco2 45 mm Hg or less.

























ASSESSMENT/INTERVENTIONS RATIONALES
Assess all lung fields for breath sounds. The presence of crackles (rales) may signal alveolar fluid congestion and systolic dysfunctional (left-sided) HF. Decreased breath sounds signify fluid overload or decreased ventilation. Wheezing may signify associated bronchitis or asthma.
Monitor oximetry and ABG values and report significant findings. Oximetry of 92% or less and the presence of hypoxemia (decreased Pao2) and hypercapnia (increased Paco2) signify decreased oxygenation.
Assess respiratory rate (RR), lung excursion, use of accessory muscles, air hunger, mental status changes, cyanosis, and changes in HR or BP. Report significant changes. These are signs of increasing respiratory distress that require prompt intervention.
Assist patient into high Fowler’s position with head of bed (HOB) up 90 degrees. This position decreases work of breathing, reduces cardiac workload, and promotes gas exchange.
Teach patient to take slow, deep breaths. Administer O2 as prescribed. Taking deep breaths increases oxygenation to the myocardium and improves prognosis. Hypoxia adds stress to the already distressed myocardium.
Deliver oxygen with humidity.
In ADHF/pulmonary edema, high-flow O2 may be given either by non-rebreathing mask, positive airway pressure devices, or endotracheal intubation and mechanical ventilation. Once stabilized, O2 is titrated to keep pulse oximetry readings higher than 92%.
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Jul 18, 2016 | Posted by in NURSING | Comments Off on Heart failure

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