Pathophysiology

Shock is now defined as circulatory insufficiency that creates an imbalance between tissue oxygen supply and oxygen demand. Global tissue hypoperfusion is associated with a decreased venous oxygen content and metabolic acidosis (lactic acidosis). Shock is classified into four categories by etiology: (1) hypovolemic (due to inadequate circulating volume), (2) cardiogenic (due to inadequate cardiac pump function), (3) distributive (maldistribution of blood flow), and (4) obstructive (extracardiac obstruction to blood flow). Clinically, shock may have a predominant cause, but as the shock state persists or progresses, other pathophysiologic mechanisms become operative.

Knowledge of the principles of oxygen transport and consumption is important to the understanding of shock. A maximum of four molecules of oxygen is loaded onto each molecule of hemoglobin as it passes through the lungs. If all available oxygen sites are occupied (four per molecule of hemoglobin), Sa o2 is 100 percent (see Table ^B-l for abbreviation definitions). The Cao2 is the amount of oxygen bound to hemoglobin plus a small amount dissolved in plasma (T.a.b,!®. .. .2.6.-2). Oxygen is delivered to the tissues by the pumping function of the heart. The D o2 is the product of the Cao2 and CO.

TABLE 26-1 Definitions of Abbreviations

TABLE 26-2 Oxygen Transport and Utilization Components

Do2 and Vo2 comprise a sensitive balance of supply and demand. Normally, 25 percent of the oxygen carried on hemoglobin is consumed by the tissues, and venous blood returning to the right heart is normally 75 percent saturated. When oxygen supply is insufficient to meet demands, the first compensatory mechanism is an increase in CO. If the increase in CO is insufficient, the amount of oxygen extracted from hemoglobin by the tissues increases, which decreases Smv o2.

When compensatory mechanisms have failed to correct the imbalance between tissue supply and demand, anaerobic metabolism occurs, resulting in the formation of lactic acid. Elevated lactic acid levels are associated with an Smv o2 of less than 50 percent. Most cases of lactic acidosis are due to inadequate oxygen delivery, as in cardiogenic shock, but lactic acidosis occasionally can develop from an excessively high oxygen demand (abnormally elevated V o2), for example, status epilepticus. Sometimes, lactic acidosis can occur because of an impairment of tissue oxygen utilization, as in septic shock and postresuscitation from cardiac arrest. 4 Elevated lactic acid and normal Smvo2 in the presence of adequate delivery indicate an impairment of tissue oxygen utilization. Lactic acid levels are markers of the severity of the tissue oxygen supply-to-demand imbalance and can be used in the triage, diagnosis, therapy, and prognosis of critically ill patients.

In addition to lactic acid, Smvo2 can be used as a measure of tissue oxygen supply and demand imbalance. Smvo2 is usually obtained from the pulmonary artery catheter, but similar information can be obtained by sampling the central venous blood through an internal jugular or subclavian catheter (Scv o2), which has been shown to correlate with Smvo2 and can be more easily obtained in the ED.

Shock is usually, but not always, associated with arterial hypotension: systolic blood pressure less than 80 or 90 mmHg. Since the product of flow and resistance determines pressure, blood pressure may not fall if, along with a marked reduction in flow, there is a corresponding increase in peripheral vascular resistance. MAP, CO, and SVR are related by the equation: MAP = CO * SVR. A marked reduction in CO may not be reflected by a decrease in MAP if SVR increases as a compensatory response. In this situation, the result will be global tissue hypoperfusion. The insensitivity of blood pressure to detect global tissue hypoperfusion has been repeatedly confirmed.5 Thus, shock may occur with a normal blood pressure, and hypotension may occur without shock.

The onset of shock induces autonomic responses, many which serve to maintain perfusion pressure to vital organs. Stimulation of the carotid baroreceptor stretch reflex activates the sympathetic nervous system leading to (1) arteriolar vasoconstriction, which overcomes local autoregulation and redistributes blood volume from the skin, skeletal muscle, kidneys, and splanchnic viscera; (2) an increase in heart rate and contractility that increases cardiac output; (3) constriction of venous capacitance vessels, which augments venous return; (4) release of the vasoactive hormones epinephrine, norepinephrine, dopamine, and cortisol to maintain arteriolar and venoconstriction; and (5) release of antidiuretic hormone and activation of the renin-angiotensin axis to enhance water and sodium conservation to maintain intravascular volume. These compensatory mechanisms attempt to maintain Do2 to the most critical organs: the coronary and cerebral circulation. In this process, blood flow to other organs such as the kidney and gastrointestinal tract may be compromised.

The cellular response to decreased Do2 is adenosine triphosphate depletion leading to ion-pump dysfunction, an influx of sodium, an efflux of potassium, and a reduction in membrane resting potential. Cellular edema occurs secondary to increased intracellular sodium while cellular membrane receptors become poorly responsive to the stress hormones insulin, glucagon, cortisol, and catecholamines. As shock progresses, lysosomal enzymes are released into the cells with subsequent hydrolysis of membranes, deoxyribonucleic acid, ribonucleic acid, and phosphate esters. As the cascade of shock continues, the loss of cellular integrity and the breakdown in cellular homeostasis result in cellular death. These pathologic events give rise to the clinical features of hyperkalemia, hyponatremia, metabolic acidosis, hyperglycemia, and lactic acidosis.

In the early phases of shock, these physiologic changes produce SIRS, defined as the presence of two or more of the following features: (1) temperature greater than 38°C or less than 36°C; (2) heart rate faster than 90 beats per minute; (3) respiratory rate faster than 20 breaths per minute; and (4) white blood cell count greater than 12.0 * 109/L, less than 4.0 * 109/L, or with greater than 10 percent immature forms or bands.6 If shock progresses, SIRS may be accompanied by MODS manifested by myocardial depression, adult respiratory distress syndrome, disseminated intravascular coagulation, hepatic failure, or renal failure. Inflammatory mediators or cytokines, which arise from endothelial cell disruption, have a significant pathogenic role in the progression from SIRS to MODS. How fulminant the progression is from SIRS to MODS is determined by the balance of these anti-inflammatory and proinflammatory mediators (Fig... i i i 26-1)7

FIG. 26-1. The pathophysiology of shock, SIRS, and MODS.

Global tissue hypoperfusion alone can independently activate SIRS or serve as a comorbid variable in the pathogenesis of other forms of shock. The progression from SIRS to MODS is frequently accompanied by cardiovascular insufficiency.8 The failure to diagnose and treat global tissue hypoperfusion in a timely manner leads to an accumulation of an oxygen debt; the magnitude of which correlates with increased mortality. 9

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