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  • Left ventricular (LV) stroke volume (SV) creates arterial pulse pressure (PP) by distending elastic conducting vessels during systole, with energy stored in the form of pressure and volume and pulse pressure generated in proportion to the systemic vascular resistance (SVR). These same vessels contract during diastole, maintaining the forward flow of blood and the pressure throughout diastole.

  • This coupling of ventricular and vascular elements allows rapid clinical separation of hypotensive patients into those with increased SV and cardiac output (Q˙t) demonstrating bounding pulses with large PP, low diastolic pressure (DP), and warm digits (low SVR, high Q˙t hypotension, or septic shock) from those who demonstrate thready pulses with small PP and cool digits signaling low SV and Q˙t with increased SVR, as in cardiogenic or hypovolemic shock.

  • LV pumping function can be characterized in part by relating LV end-DP as estimated by pulmonary wedge pressure (Ppw) to SV; LV dysfunction is indicated by increased Ppw and decreased SV and may be due to systolic or diastolic dysfunction.

  • Systolic dysfunction, or decreased contractility, connotes decreased ejection fraction. Common causes of acute systolic dysfunction in critical illness are myocardial ischemia, hypoxia, sepsis, intercurrent negative inotropic drugs (β or calcium blockers), and acute-on-chronic systolic dysfunction.

  • Diastolic dysfunction connotes decreased LV end-diastolic volume despite increased Ppw; common causes of diastolic dysfunction in critical illness are LV hypertrophy, ischemia, or cardiomyopathy, positive end–expiratory pressure (PEEP), pericardial tamponade or constriction, or other causes of increased pleural pressure as in pneumothorax, pleural effusion, or abdominal distention, and ventricular interdependence in acute right heart syndromes.

  • Early differentiation between diastolic and systolic dysfunction in critical illness is aided by 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, principally those of venous circuit including the unstressed volume, vascular capacitance, and vascular volume. Together these determine the mean systemic pressure (Pms) that drives the VR against the right atrial pressure (Pra) to the right atrium through the resistance to VR.

  • For a given Pms, VR increases as Pra decreases (VR curve), whereas SV and Q˙t from the heart increase as Pra and preload increase (Starling curve). The superimposition of these two curves characterizes the circulation and generates a single point of intersection where VR=Q˙t.

  • When Q˙t is insufficient, Pms can be increased by volume infusion, baroreceptors, or metabolic receptors and thus increase VR and Pra. This same effect can be accomplished with venoconstricting drugs such as norepinephrine or phenylephrine. Alternatively, VR can be increased with positive inotropic (dobutamine) or afterload-reducing (sodium nitroprusside, fenoldopam) drugs that will decrease Pra by enhancing cardiac function.

  • In hypovolemic shock, hemostasis and volume resuscitation are essential. Arteriolar constricting agents such as phenylephrine or norepinephrine may be used ...

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