Cardiac CSC

A patient in cardiogenic shock is most likely to have which of the following he- modynamic profiles: A. Cardiac output = 6 L/min, CVP = 15 mmHg, PAOP = 26 mmHg, SVR = 1600 dynes/sec/cm-5. B. Cardiac output = 2.5 L/min, CVP = 4 mmHg, PAOP = 8 mmHg, SVR = 600 dynes/sec/cm-5. C. Cardiac output = 5 L/min, CVP = 8 mmHg , PAOP = 12 mmHg, SVR = 800 dynes/sec/cm-5. D.Cardiac output = 2.5 L/min, CVP = 15 mmHg, PAOP = 30 mmHg, SVR = 1800 dynes/sec/cm-5. A patient with a right ventricular infarction is likely to have which of the following hemodynamic profiles: A. Low cardiac output, high CVP, low PAOP, high SVR. B. High cardiac output, low CVP, low PAOP, high SVR. C. Low cardiac output, high CVP, high PAOP, low SVR. D. Low cardiac output, low SVR, low CVP, low PAOP. The hemodynamic profile most consistent with cardiogenic shock is: A. Decreased cardiac output, increased preload, decreased afterload and de- creased contractility. B. Decreased cardiac output, increased preload, increased afterload, and de- creased contractility. C. Decreased cardiac output, decreased preload, increased afterload, and de- creased contractility. D. Decreased cardiac output, increased D. In cardiogenic shock, cardiac contractility is decreased and filling pressures (CVP and PAOP) are high because the ventricles can't eject their contents ade- quately. SVR increases as compensatory vasoconstriction occurs in an attempt to support BP. A normal CO is 4-8 L/min; CVP is 2-6 mmHg, PAOP is 8-12 mmHg, and SVR is 800-1200 dynes/sec/cm-5. A. In right ventricular infarction right ventricular contractility is reduced, which causes RV pressure to rise (high CVP) and decreases forwards flow through the lungs and into the left ventricle, reducing LV filling pressure (low PAOP). SVR increases as peripheral vasoconstriction attempts to compensate for reduced left ventricular stroke volume in an effort to maintain BP. B. Cardiac output is decreased as a direct result of decreased contractility of the left ventricle in cardiogenic shock. Preload increases as a result of back- ward failure and afterload increases due to a compensatory vasoconstriction of the arterioles in an effort to support blood pressure