Shock is a state of severe systemic reduction in tissue perfusion characterized by decreased cellular oxygen delivery and utilization as well as decreased removal of waste byproducts of metabolism. Hypotension, although common in shock, is not synonymous to shock. One can have hypotension and normal perfusion, or shock without hypotension in a patient who is usually very hypertensive. Shock is the final preterminal event in many diseases. Progressive tissue hypoxia results in loss of cellular membrane integrity, a reversion to a catabolic state of anaerobic metabolism, and a loss of energy-dependent ion pumps and chemical and electrical gradients. Mitochondrial energy production begins to fail. Multiple organ dysfunction follows localized cellular death, and organism death follows. Despite recent advances in treatment, mortality remains high: > 50% in cardiogenic shock and > 35% in septic shock.
Blood pressure is determined by the formula BP = systemic vascular resistance (SVR) × cardiac output (CO), where CO = heart rate (HR) × stroke volume (SV). SV = end diastolic volume (EDV) minus end systolic volume (ESV). EDV is the filled ventricular volume prior to systolic contraction averaging about 100 cc in many adults. ESV is residual blood left in the ventricle after emptying during systole averaging about 40 cc. Therefore, the determinants of blood pressure are vascular resistance, HR, preload volume, and contractility (see Figure 11–1). SVR is the vascular “tone” and is a large determinant of diastolic blood pressure. EDV is largely determined by preload volume that augments SV via Frank–Starling curves where increases in diastolic filling volumes increase CO. ESV is determined largely by cardiac contractility and it decreases as the heart ejects a greater percentage of its diastolic volume. For example, one can increase SV by increasing preload (EDV) with volume or decreasing ESV with increased contractility. The ejection fraction ((EDV – ESV)/EDV) thus increases.
Determinants of blood pressure.
The initial derangement precipitating a state of shock might be (1) vasodilation (causing a decreased SVR) from sepsis, anaphylaxis, drugs, or cervical cord lesion, (2) extremes of HR, (3) loss of preload volume (causing decreased EDV) from blood or volume loss, or (4) loss of contractility (increasing the ESV) from heart failure. Compensatory mechanisms come into play and provide many of the clinical clues to early shock.
The initial compensatory mechanisms depend on the initial insult. (1) Vasodilation with loss of SVR generally causes a compensatory tachycardia and thirst. Despite systemic tissue hypoxemia, the skin remains perfused and is warm initially. (2) Blood or fluid loss (decreasing EDV) causes a reflex increase in SVR, which increases diastolic BP, narrowing the pulse pressure, increases sympathetic cholinergic sweating and makes the patient pale, thirsty, and cool. As volume loss increases, tachycardia and hypotension ensue. (3) Loss of contractility also is compensated by increases in SVR to maintain blood pressure with similar symptoms.