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Try it - forever07
#1
68-year-old hypertensive man undergoes successful repair of a ruptured abdominal aortic aneurysm. He receives 9 L Ringer™s lactate solution and 4 units of whole blood during the operation. Two hours after transfer to the surgical intensive care unit, the following hemodynamic parameters are obtained:

¢ Systemic blood pressure (BP): 90/60 mm Hg
¢ Pulse rate: 110 beats/min
¢ Central venous pressure (CVP): 7 mm Hg
¢ Pulmonary artery pressure: 28/10 mm Hg
¢ Pulmonary capillary wedge pressure: 8 mm Hg
¢ Cardiac output: 1.9 L/min
¢ Systemic vascular resistance: 35 Woods units (normal is 24“30 Woods units)
¢ PaO2: 140 kPa (FiO2: 0.45)
¢ Urine output: 15 mL/h (specific gravity: 1.029)
¢ Hematocrit: 35%
Administration of a fluid challenge to increase urine output was done. The patient then has an improvement in all hemodynamic parameters. However, 6 h later he develops ST segment depression, and a 12-lead cardiogram shows anterolateral ischemia. New hemodynamic parameters are obtained:
¢ Systemic BP: 70/40 mm Hg
¢ Pulse rate: 100 beats/min
¢ Central venous pressure (CVP): 18 cm H2O
¢ Pulmonary capillary wedge pressure (PCWP): 25 mm Hg
¢ Cardiac output: 1.5 L/min
¢ Systemic vascular resistance: 25 Woods units
The single best pharmacologic intervention would be ?



Options:

1. Sublingual nitroglycerin
2. Intravenous nitroglycerin
3. A short-acting beta blocker
4. Sodium nitroprusside
5. Dobutamine
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#2
5? cardiogenic shock?
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#3
5....
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#4
yea cardio shock...PCWP>18
5
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#5
whats correct answer?
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#6
5,pt was in cardiogenic shock initially but is no longer in shock from d 2nd stem bcos SVR has normalized but still hypotensive,so give dobutamine or dopamine
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#7
The Correct Answer is: Dobutamine
Explanation:



This patient has developed pump failure due to a combination of preexisting coronary artery occlusive disease and high preload following a fluid challenge; afterload remains moderately high as well because of systemic vasoconstriction in the presence of cardiogenic shock. Poor myocardial performance is reflected in the low cardiac output and high pulmonary capillary wedge pressure. Therapy must be directed at increasing cardiac output without creating too high a myocardial oxygen demand on the already failing heart. Administration of nitroglycerin could be expected to reduce both preload and afterload, but if it is given without an inotrope it would create unacceptable hypotension. Nitroprusside similarly would achieve afterload reduction but would result in hypotension if not accompanied by an inotropic agent. A beta blocker would act deleteriously by reducing cardiac contractility and slowing the heart rate in a setting in which cardiac output is likely to be rate dependent. Dobutamine is a synthetic catecholamine that is becoming the inotropic agent of choice in cardiogenic shock. As a β1-adrenergic agonist, it improves cardiac performance in pump failure both by positive inotropy and peripheral vasodilation. With minimal chronotropic effect, dobutamine only marginally increases myocardial oxygen demand.


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