Etiology and Pathophysiology

Hypertension and CAD are the primary risk factors for HF. Most patients with HF have a history of hypertension. The risk of HF increases with the severity of hypertension. Other factors, such as diabetes, advanced age, tobacco use, obesity, and high serum cholesterol, also contribute to the development of HF.

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, and (4) heart rate (HR). (Preload and afterload are discussed in Chapter 32.) Any changes in these factors can lead to decreased ventricular function and HF.

The major causes of HF may be divided into two subgroups: (1) primary causes (Table 35-1) and (2) precipitating causes (Table 35-2). Precipitating causes often increase the workload of the ventricles, resulting in an acute condition and decreased heart function.

 Genetic Link

Specific genes and gene mutations have been linked to the development of hypertension, CAD, and cardiomyopathy (weakening of the heart muscle) (see Chapters 33, 34, and 37). These cardiovascular diseases are known risk factors for HF. Knowledge of why some people with these diseases are at high risk for developing HF is incomplete. Future research into the effects of these gene mutations will most likely be related to the common causes of HF.⁴

Compensatory Mechanisms.

HF can have an abrupt onset as with acute MI, or it can be a subtle process resulting from slow, progressive changes. The overloaded heart uses compensatory mechanisms to try to maintain adequate CO. The main compensatory mechanisms include (1) sympathetic nervous system (SNS) activation, (2) neurohormonal responses, (3) ventricular dilation, and (4) ventricular hypertrophy.

Sympathetic Nervous System Activation.

SNS activation is often the first mechanism triggered in low-CO states. However, it is the least effective compensatory mechanism. In response to an inadequate stroke volume and CO, SNS activation increases, resulting in the increased release of catecholamines (epinephrine and norepinephrine). This results in increased HR, increased myocardial contractility, and peripheral vasoconstriction. Initially, this increase in HR and contractility improves CO. However, over time these factors are harmful, since they increase the already failing heart’s workload and need for oxygen. The vasoconstriction causes an immediate increase in preload, which may initially increase CO. However, an increase in venous return to the heart, which is already volume overloaded, actually worsens ventricular performance.

Neurohormonal Response.

As the CO falls, blood flow to the kidneys decreases. This is sensed by the juxtaglomerular apparatus in the kidneys as decreased volume. In response, the kidneys release renin, which converts angiotensinogen to angiotensin I (see Chapter 45 and Fig. 45-4). Angiotensin I is subsequently converted to angiotensin II by a converting enzyme made in the lungs. Angiotensin II causes (1) the adrenal cortex to release aldosterone, which results in sodium and water retention; and (2) increased peripheral vasoconstriction, which increases BP. This response is known as the renin-angiotensin-aldosterone system (RAAS).

Low CO causes a decrease in cerebral perfusion pressure. In response, the posterior pituitary gland secretes antidiuretic hormone (ADH), also called vasopressin. ADH increases water reabsorption in the kidneys, causing water retention. As a result, blood volume is increased in a person who is already volume overloaded.

Other factors also contribute to the development of HF. The production of endothelin, a potent vasoconstrictor produced by the vascular endothelial cells, is stimulated by ADH, catecholamines, and angiotensin II. Endothelin results in further arterial vasoconstriction and an increase in cardiac contractility and hypertrophy.

Locally, proinflammatory cytokines are released by heart cells in response to various forms of cardiac injury (e.g., MI). Two cytokines, tumor necrosis factor (TNF) and interleukin-1 (IL-1), further depress heart function by causing hypertrophy, contractile dysfunction, and cell death. Over time, a systemic inflammatory response also occurs. This accounts for the cardiac and skeletal muscle myopathy and fatigue that accompany advanced HF.

Activation of the SNS and the neurohormonal response lead to elevated levels of norepinephrine, angiotensin II, aldosterone, ADH, endothelin, and proinflammatory cytokines. Together, these factors result in an increase in cardiac workload, myocardial dysfunction, and ventricular remodeling. Remodeling involves hypertrophy of the ventricular myocytes, resulting in large, abnormally shaped contractile cells. This altered geometric shape of the ventricles eventually leads to increased ventricular mass, increased wall tension, increased oxygen consumption, and impaired contractility. Although the ventricles become larger, they become less effective pumps. Ventricular remodeling is a risk factor for life-threatening dysrhythmias and sudden cardiac death (SCD).

Dilation.

Dilation is an enlargement of the chambers of the heart (Fig. 35-1, A). It occurs when pressure in the heart chambers (usually the LV) is elevated over time. The heart muscle fibers stretch in response to the volume of blood in the heart at the end of diastole. The degree of stretch is directly related to the force of the contraction (systole) (this is the Frank-Starling law). This increased contraction initially leads to increased CO and maintenance of BP and perfusion. Dilation starts as an adaptive mechanism to cope with increasing blood volume. Eventually this mechanism becomes inadequate because the elastic elements of the muscle fibers are overstretched and can no longer contract effectively, thereby decreasing the CO.

Hypertrophy.

Hypertrophy is an increase in the muscle mass and cardiac wall thickness in response to overwork and strain (Fig. 35-1, B). It occurs slowly because it takes time for this increased muscle tissue to develop. Initially, the increased contractile power of the muscle fibers leads to an increase in CO and maintenance of tissue perfusion. Over time, hypertrophic heart muscle has poor contractility, requires more oxygen to perform work, has poor coronary artery circulation (tissue becomes ischemic more easily), and is prone to dysrhythmias.

Types of Heart Failure

HF is usually manifested by biventricular failure, although one ventricle may precede the other in dysfunction. Normally the pumping actions of the left and right sides of the heart are synchronized, producing a continuous flow of blood. However, as a result of pathologic conditions, one side may fail while the other side continues to function normally for a time. Because of the prolonged strain, both sides of the heart eventually fail, resulting in biventricular failure (Fig. 35-2).

Clinical Manifestations Acute Decompensated Heart Failure

In acute decompensated HF (ADHF), an increase in the pulmonary venous pressure is caused by failure of the LV. This results in engorgement of the pulmonary vascular system (Fig. 35-3, A and B). As a result, the lungs become less compliant, and there is increased resistance in the small airways. In addition, the lymphatic system increases its flow to help maintain a constant volume of the pulmonary extravascular fluid. This early stage is clinically associated with a mild increase in the respiratory rate and a decrease in partial pressure of oxygen in arterial blood (PaO₂).

If pulmonary venous pressure continues to increase, the increase in intravascular pressure causes more fluid to move into the interstitial space than the lymphatics can remove. Interstitial edema occurs at this point (Fig. 35-3, C). Tachypnea develops, and the patient becomes symptomatic (e.g., short of breath). If the pulmonary venous pressure increases further, the alveoli lining cells are disrupted and a fluid containing red blood cells (RBCs) moves into the alveoli (alveolar edema). As the disruption becomes worse from further increases in the pulmonary venous pressure, the alveoli and airways are flooded with fluid. This is accompanied by a worsening of the arterial blood gas values (i.e., lower PaO₂ and possible increased partial pressure of carbon dioxide in arterial blood [PaCO₂] and progressive respiratory acidemia).

ADHF can manifest as pulmonary edema. This is an acute, life-threatening situation in which the lung alveoli become filled with serosanguineous fluid (Fig. 35-3, D). The most common cause of pulmonary edema is left-sided HF secondary to CAD. (Other etiologic factors for pulmonary edema are listed in Table 28-25.)

Clinical manifestations of pulmonary edema are distinct. The patient is usually anxious, pale, and possibly cyanotic. The skin is clammy and cold from vasoconstriction caused by stimulation of the SNS. The patient has dyspnea (shortness of breath) and orthopnea (shortness of breath while lying down). Respiratory rate is often greater than 30 breaths/minute, and use of accessory muscles to breathe may be seen. There may be wheezing and coughing with the production of frothy, blood-tinged sputum. Auscultation of the lungs may reveal crackles, wheezes, and rhonchi throughout the lungs. The patient’s HR is rapid, and BP may be elevated or decreased depending on the severity of the HF.

Patients with ADHF can be categorized into one of four groups based on hemodynamic and clinical status: dry-warm, dry-cold, wet-warm, and wet-cold¹ (Table 35-3). The most common presentation is the warm and wet patient. This patient has adequate perfusion (warm) but has volume overload (e.g., congestion, dyspnea, edema).

Clinical Manifestations Chronic Heart Failure

Chronic HF is characterized as a progressive worsening of ventricular function and chronic neurohormonal activation that results in ventricular remodeling. This process involves changes in the size, shape, and mechanical performance of the ventricle. The clinical manifestations of chronic HF depend on the patient’s age, the underlying type and extent of heart disease, and which ventricle is failing to pump effectively. Table 35-4 lists the manifestations of right-sided and left-sided chronic HF. The patient with chronic HF usually has manifestations of biventricular failure. The Heart Failure Society of America (HFSA) developed the acronym FACES (Fatigue, limitation of Activities, chest Congestion/cough, Edema, and Shortness of breath) to help teach patients to identify HF symptoms⁷ (see eTable 35-1 on the website for this chapter).

Pleural effusion results from increasing pressure in the pleural capillaries. A transudation of fluid occurs from these capillaries into the pleural space. (Pleural effusion is discussed in Chapter 28.)

Classification of Heart Failure

In 1964 the New York Heart Association (NYHA) developed functional guidelines for classifying people with heart disease based on tolerance to physical activity. Because this system only reflected exercise capacity, the American College of Cardiology Foundation/AHA (ACCF/AHA) developed a staging system that identified disease progression and treatment strategies.¹ This system allows for identification of people at risk for developing HF but who do not currently have heart disease. The ACCF/AHA system encourages clinicians to actively address the patient’s risk factors and treat any existing conditions to prevent further disease progression. This may help reduce the growing number of HF patients. The two systems are compared in Table 35-5.

Diagnostic Studies

Diagnosing HF is often difficult, since neither patient signs nor symptoms are highly specific, and both may mimic those associated with many other medical conditions (e.g., anemia, lung disease). Diagnostic tests for ADHF and chronic HF are presented in Table 35-6. A primary goal in diagnosis is to find the underlying cause of HF.

An endomyocardial biopsy (EMB) may be done in patients who develop unexplained, new-onset HF that is unresponsive to usual care.⁸ EF is used to differentiate systolic and diastolic HF. This distinction is important to make in the early treatment of HF. EF is measured using echocardiography and/or nuclear imaging studies (see Table 32-6). Other useful diagnostic tests include electrocardiogram (ECG), chest x-ray, and heart catheterization.

Laboratory studies also aid in the diagnosis of HF. In general, BNP levels correlate positively with the degree of left ventricular failure. Many laboratories routinely measure the N-terminal prohormone of BNP (NT-proBNP). This is a more precise assay to aid in the diagnosis of HF (see Table 32-6). Levels are temporarily higher in patients receiving nesiritide (Natrecor) and may be high in patients with chronic, stable HF. Increases in BNP or NT-proBNP levels can be caused by conditions other than HF. These conditions include pulmonary embolism, renal failure, and acute coronary syndrome.

Collaborative Care Acute Decompensated Heart Failure

With the addition of new drugs and device therapies, the management of HF has dramatically changed in the past few years. Because of the large number of patients and the high cost of care related to hospital readmissions, strategies to improve outcomes have been developed. One example is the use of guideline-directed medical therapy as defined by the AACF/AHA.¹ Another example is specialized HF inpatient units with transitional programs to the outpatient setting to help manage these patients. These units are staffed with multidisciplinary HF teams, including nurses who are educated in the care of these patients. Table 35-6 lists the collaborative therapy for the patient with ADHF.

Patients with ADHF need continuous monitoring and assessment. This may be done in an intensive care unit (ICU) if the patient is unstable. 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). If a pulmonary artery catheter is placed, evaluate CO and pulmonary artery wedge pressure (PAWP). Therapy is titrated to maximize CO and reduce PAWP. A normal PAWP is generally between 8 and 12 mm Hg. Patients with ADHF may have a PAWP as high as 30 mm Hg. (Hemodynamic monitoring is discussed in Chapter 66.)

Supplemental oxygen helps increase the percentage of oxygen in inspired air. (Oxygen therapy is discussed in Chapter 29.) In severe pulmonary edema the patient may need noninvasive ventilatory support (e.g., bilevel positive airway pressure [BiPAP]) or intubation and mechanical ventilation. BiPAP is also effective in decreasing preload. (Ventilatory support is discussed in Chapter 66.)

Some patients with ADHF require hospitalization but are more stable. They are often admitted to a telemetry or stepdown unit for treatment. Assess these patients every 4 hours (e.g., vital signs, pulse oximetry) for adequate oxygenation. Record intake and output and daily weights to evaluate fluid status.

If the patient is dyspneic, place in a high Fowler’s position with the feet horizontal in the bed or dangling at the bedside. This position helps decrease venous return because of the pooling of blood in the extremities. This position also increases the thoracic capacity, allowing for improved breathing.

Ultrafiltration (UF), or aquapheresis, is an option for the patient with volume overload.⁹ It is a process to remove excess salt and water from the patient’s blood. UF can rapidly remove intravascular fluid volume while maintaining hemodynamic stability. The ideal patients for UF are those with major pulmonary or systemic volume overload who have shown resistance to diuretics and are hemodynamically stable. UF also may be an appropriate adjunctive therapy for patients with HF and coexisting renal failure. (UF is discussed in Chapter 47.) Once the patient is more stable, determination of the cause of ADHF and pulmonary edema is important. Diagnosis of systolic or diastolic HF will then direct further management protocols.

Circulatory assist devices are used to manage patients with worsening HF. The intraaortic balloon pump (IABP) is a device that increases coronary blood flow to the heart muscle and decreases the heart’s workload through a process called counterpulsation. It is useful in hemodynamically unstable patients because it decreases SVR, PAWP, and PAP, leading to improved CO. Ventricular assist devices (VADs) can be used to maintain the pumping action of a heart that cannot effectively contract by itself. A VAD is a battery-operated, mechanical pump that is surgically implanted. (IABPs and VADs are discussed in Chapter 66.)

Coexisting psychologic disorders, especially depression and anxiety, contribute to an increased risk of mortality and higher readmission rates and health care costs in patients with HF.¹⁰ In addition, patients with psychologic disorders have poorer adherence to treatment and self-care.¹¹ Assess patients with HF for depression and anxiety and, if appropriate, initiate treatment plans.

Drug Therapy.

Drug therapy is essential in treating ADHF (Table 35-7).

TABLE 35-7

DRUG THERAPY
Heart Failure

Drug	Mechanism of Action
Diuretics (see Table 33-7)
Loop Diuretics	• Decrease fluid volume • Decrease preload • Decrease pulmonary venous pressure • Relieve symptoms of heart failure (e.g., edema) Only gold members can continue reading. Log In or Register to continue Share this: Click to share on Twitter (Opens in new window) Click to share on Facebook (Opens in new window) Related Related posts: Introduction Nursing Management: Sexually Transmitted Infections Nursing Assessment: Cardiovascular System Nursing Management: Musculoskeletal Problems Stay updated, free articles. Join our Telegram channel Join Tags: Medical-Surgical Nursing Assessment and Management of Clinical P Nov 17, 2016 | Posted by admin in NURSING | Comments Off on Nursing Management: Heart Failure Full access? Get Clinical Tree Get Clinical Tree app for offline access Get Clinical Tree app for offline access