Porth's Essentials of Pathophysiology, 4e

495

Heart Failure and Circulatory Shock

C h a p t e r 2 0

Acute Heart Failure Syndromes The acute heart failure syndromes (AHFS) are defined as “gradual or rapid change in heart failure signs and symptoms resulting in a need for urgent therapy.” 33 These signs and symptoms are primarily the result of severe pulmonary edema due to elevated left ventricu- lar filling pressures, with or without a low cardiac output. 33–35 The AHFS are among the most common disorders seen in emergency departments. A worsening of chronic heart failure, often complicated by episodes of acute decompensation, is the most common cause of the syndrome. The AHFS are thought to encompass three differ- ent types of conditions: (1) worsening of chronic sys- tolic or diastolic dysfunction that appears to respond to treatment; (2) new-onset acute heart failure that occurs secondary to a precipitating event such as a large myocardial infarction or a sudden increase in blood pressure superimposed on a noncompliant left ventricle; and (3) worsening of end-stage/advanced heart failure that is refractory to treatment, with pre- dominantly left ventricular systolic dysfunction associ- ated with a low-output state. 34 The difference between new-onset AHFS and AHFS caused by chronic heart failure is in the degree of physiologic response, which is more pronounced in the new-onset AHFS and more subtle in chronic heart failure because of the compen- satory pathophysiology. For example, with new-onset AHFS, the person will have a strong sympathetic response such as tachycardia with enhanced pulmo- nary vascular permeability causing rapid and dramatic symptoms of pulmonary edema. Because many com- pensatory mechanisms operate in persons with chronic heart failure, they tolerate higher pulmonary vascular pressures. Chronic changes in neurohormonal regu- lation lead to a strong activation of the angiotensin- aldosteronesystemwitharesultantvolumeoverload,and venous congestion in both the systemic and pulmonary circulations. 35 Acute pulmonary edema is the most dramatic symp- tom of AHFS. It is a life-threatening condition in which capillary fluid moves into the alveoli. 28 The accumulated fluid in the alveoli and airways causes lung stiffness, makes lung expansion more difficult, and impairs the gas exchange function of the lung. With the decreased ability of the lungs to oxygenate the blood, the hemo- globin leaves the pulmonary circulation without being fully oxygenated, resulting in shortness of breath and cyanosis. The person with severe pulmonary edema is usually seen sitting and gasping for air. The pulse is rapid, the skin is moist and cool, and the lips and nail beds are cyanotic. As the pulmonary edema worsens and oxy- gen supply to the brain drops, confusion and stupor appear. Dyspnea and air hunger are accompanied by a productive cough with frothy (resembling beaten egg whites) and often blood-tinged sputum—the effect of air mixing with the serum albumin and red blood cells that have moved into the alveoli. The movement of air through the alveolar fluid produces fine crepitant

failure of the left ventricle, cardiac output may fall to levels that are insufficient for providing the brain with adequate oxygen, causing cognitive impairment and disturbed behavior. Confusion, impairment of mem- ory, anxiety, restlessness, and insomnia are common in elderly persons with advanced heart failure, par- ticularly in those with cerebral atherosclerosis. These symptoms may confuse the diagnosis of heart failure in the elderly because of other possible causes associ- ated with aging. Cachexia and Malnutrition Cardiac cachexia is a condition of malnutrition and tis- sue wasting that occurs in persons with end-stage heart failure. 31 A number of factors probably contribute to its development, including fatigue and depression that interfere with food intake, and congestion of the liver and gastrointestinal structures that impairs digestion and absorption and produces feelings of fullness. Other factors are circulating toxins and mediators released from poorly perfused tissues that impair appetite and contribute to tissue wasting. Cyanosis Cyanosis, or a bluish discoloration of the skin and mucous membranes, is caused by excess desaturated hemoglobin in the blood. It is often a late sign of heart failure, and may be visible especially around the lips and in the peripheral parts of the extremities. Cyanosis may be central or peripheral. Central cya- nosis develops when impaired pulmonary gas exchange reduces oxygenation of the arterial blood in conditions such as pulmonary edema, left heart failure, or right- to-left cardiac shunting. Peripheral cyanosis develops as a consequence of venous desaturation resulting from extensive extraction of oxygen at the capillary level. It is caused by conditions such as low-output failure that result in delivery of poorly oxygenated blood to the peripheral tissues, or by conditions such as peripheral vasoconstriction that cause excessive removal of oxy- gen from the blood. Central cyanosis is best monitored by assessing the lips and mucous membranes because these areas are not subject to environmental condi- tions, such as cold temperatures, that cause peripheral constriction and cyanosis. Arrhythmias and Sudden Cardiac Death Both atrial and ventricular arrhythmias can occur in persons with heart failure. Atrial fibrillation is the most common arrhythmia (see Chapter 17). Manifestations associated with atrial fibrillation are related to loss of atrial contraction, tachycardia, irregular heart rate, and symptoms related to a drop in blood pressure. 32 There is also strong evidence that persons with heart failure are at increased risk for sudden cardiac arrest; that is, unwitnessed death or death that occurs within 1 hour of symptom onset. In persons with ventricular dysfunc- tion, sudden death is caused most commonly by ven- tricular tachycardia or ventricular fibrillation. 1