Porth's Essentials of Pathophysiology, 4e

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Heart Failure and Circulatory Shock

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the cellular and extracellular compartments, and lim- ited amounts of ATP are produced. Without sufficient energy production, normal cell function cannot be main- tained. The Na + /K + -ATPase membrane pump function is impaired, resulting in intracellular accumulation of sodium and loss of potassium. The increase in intracel- lular sodium results in cellular edema and increased cell membrane permeability. Mitochondrial activity becomes severely depressed and lysosomal membranes may rup- ture, resulting in the release of enzymes that cause fur- ther cellular destruction. This is followed by cell death and the release of intracellular contents into the extra- cellular space. The extent of the cell injury and organ dysfunction is primarily determined by the degree and duration of the shock state. Compensatory Mechanisms The clinical manifestations of shock are at least partly due to the body’s compensatory responses to hypoperfu- sion. The most immediate of the compensatory mecha- nisms are those of the sympathetic nervous system and the renin-angiotensin mechanism, which maintain car- diac output and blood pressure. Often blood is shunted from the kidneys to other vital organs. The sympathetic nervous system provides important reflexive mechanisms that are essential to the support of the circulatory system during shock, particularly hypo- volemic shock. 6 These reflexes increase heart rate and stimulate constriction of blood vessels throughout the body. There are two types of adrenergic receptors for the sympathetic nervous system: alpha ( α ) and beta ( β ). The β receptors which are further divided into subtypes β 1 and β 2 receptors. Stimulation of the α receptors causes vaso- constriction; stimulation of β 1 receptors cause an increase in heart rate and force of myocardial contraction; and of β 2 receptors, vasodilation of the skeletal muscle beds and relaxation of the bronchioles. In shock, there is an increase in sympathetic outflow that results in increased epinephrine and norepinephrine release and activation of both α and β receptors (Chapter 34). Thus, increases in heart rate and vasoconstriction occur in most types of shock (cardiac output = stroke × heart rate). The arteri- oles constrict in most parts of the systemic circulation, thereby increasing the peripheral vascular resistance, and the veins and venous reservoirs constrict, thereby helping to maintain adequate venous return to the heart. There also is an increase in renin release, leading to an increase in angiotensin II, which augments vasocon- striction and leads to an aldosterone-mediated increase in sodium and water retention by the kidneys. In addi- tion, there is a local release of vasoconstrictors as well as norepinephrine, angiotensin II, vasopressin, and endothelin, which contribute to arterial and venous vasoconstriction. The compensatory mechanisms that the body recruits cannot be sustained over the long term and become det- rimental when the shock state is prolonged. This intense vasoconstriction causes a decrease in tissue perfusion and insufficient supply of oxygen. Cellular metabolism is impaired, vasoactive inflammatory mediators such as

histamine are released, production of oxygen free radi- cals is increased, and excessive lactic acid and hydrogen ions result in intracellular acidity and accompanying metabolic acidosis. 6 Each of these factors promotes cellular dysfunction or death. If circulatory function is reestablished, whether the shock is irreversible or if the patient will survive is determined largely at the cellular level regardless of the type of shock. Types of Shock In general, shock states are distinguished by clinical signs and symptoms, history, and physical exam. Circulatory shock can be caused by a decrease in blood volume (hypovolemic shock), an alteration in cardiac function, obstruction of blood flow through the circulatory sys- tem (obstructive shock), or excessive vasodilation with maldistribution of blood flow (distributive shock). The main types of shock are summarized in Chart 20-1 and depicted in Figure 20-7. Hypovolemic Shock Hypovolemic shock occurs when there is an acute loss of 15% or more of the circulating blood volume. The decrease may be caused by a loss of whole blood, plasma, extracellular fluid or excessive dehydration (Chart 20-1). Hypovolemic shock also can result from an internal hemorrhage or from third-space losses, when extracellular fluid is shifted from the vascular compart- ment to the interstitial space. Hypovolemic shock, which has been the most widely studied type of shock, is often used as a prototype in Hypovolemic Loss of whole blood Loss of plasma Loss of extracellular fluid Cardiogenic Myocardial damage (myocardial infarction, contusion) Sustained arrhythmias Acute valve damage, ventricular septal defect Cardiac surgery Obstructive Inability of the heart to fill properly (cardiac tamponade) Obstruction to outflow from the heart (pulmonary embolus, cardiac myxoma, pneumothorax, or dissecting aneurysm) Distributive Loss of sympathetic vasomotor tone (neurogenic shock) Presence of vasodilating substances in the blood (anaphylactic shock) Presence of inflammatory mediators (septic shock) CHART 20-1 Classification of Circulatory Shock