Chapter 20. The Pathophysiology of the Circulation in Critical Illness

Lawrence D. H. Wood

Left ventricular (LV) stroke volume (SV) creates arterial pulse pressure (PP) by distending conducting vessels during systole, and systemic vascular resistance (SVR) preserves diastolic pressure (DP) by preventing SV from flowing through arterioles during diastole.
This coupling of ventricular and vascular elements allows rapid clinical separation of hypotensive patients into those with increased SV and cardiac output (Q̇T) demonstrating bounding pulses with large PP, low DP, and warm digits (low SVR, high Q̇T hypotension, or septic shock) from those who demonstrate thready pulses with small PP and cool digits signaling low SV and Q̇T with increased SVR, as in cardiogenic or hypovolemic shock.
LV pumping function is described by relating LV end-DP as estimated by pulmonary wedge pressure (Ppw) to SV; LV dysfunction is signaled by increased Ppw and decreased SV and may be due to systolic or diastolic dysfunction.
Systolic dysfunction, or decreased contractility, connotes increased LV end-systolic volume for a given LV end-systolic pressure that is approximately the mean blood pressure (BP); common causes of acute systolic dysfunction in critical illness are myocardial ischemia, hypoxia, acidosis, sepsis, intercurrent negative inotropic drugs (β or calcium blockers), and acute-on-chronic systolic dysfunction in cardiomyopathies.
Diastolic dysfunction connotes decreased LV end-diastolic volume despite increased Ppw because the heart cannot fill normally; common causes of diastolic dysfunction in critical illness are pericardial tamponade or constriction, positive end-expiratory pressure (PEEP), or other causes of increased pleural pressure as in pneumothorax, pleural effusion, or abdominal distention, ventricular interdependence in acute right heart syndromes, and chronic LV stiffness as in LV hypertrophy.
Early differentiation between diastolic and systolic dysfunctions in critical illness is aided by a questioning approach and dynamic imaging such as echocardiography; this avoids inappropriate and ineffective therapy for the wrong etiology of LV dysfunction.
Venous return (VR) to the right atrium is controlled by mechanical characteristics of the systemic vessels (unstressed volume, vascular capacitance, vascular volume); together these determine the mean systemic pressure responsible for driving VR back to the right atrium (Pra) through the resistance to VR.
For a given Pms, VR increases as Pra decreases to define the VR curve of the circulation, whereas SV and Q̇T from the heart increase as Pra and preload increase to define the cardiac function curve that intersects the VR curve at a unique value of Pra where VR = Q̇T.
When Q̇T is insufficient, volume infusion, baroreceptors, or metabolic receptors can increase mean systemic pressure to increase VR and Pra; this effect is mimicked by venoconstricting drugs such as dopamine or epinephrine; alternatively, VR can be increased by positive inotropic (dobutamine) or afterload-reducing (sodium nitroprusside) drugs that decrease Pra by enhancing cardiac function.
In hypovolemic shock, hemostasis and volume resuscitation are essential, whereas arteriolar constricting agents such as norepinephrine may be used briefly to provide a window of higher BP; in septic shock, considerable volume resuscitation is needed due to nitric oxide–mediated venodilation and decreased Pms, positive inotropic agents such as dobutamine treat ...