Answer: a, b, c Therapeutic adjustments of intravascular volume (preload) and systemic vascular resistance (afterload) form the basis of the treatment strategies for all forms of shock. Optimal volume resuscitation should precede measures to augment to contractile function of the heart. Inotropic agents are used in shock when there is inadequate cardiac output despite adequate circulating blood volume. Dopamine and dobutamine are often times first line agents in the pharmacologic treatment of shock. Dopamine, at low doses, stimulates dopaminergic receptors producing renal arteriolar vasodilatation with associated increases in renal blood flow, urine output, and sodium excretion. At moderate doses, stimulation of cardiac b-receptors produces increases in contractility and cardiac output with little effect on heart rate or blood pressure. At higher doses, peripheral vasoconstriction from increasing a activity becomes more pronounced, prompting significant increases in vascular resistance and blood pressure. Dobutamine’s predominant effect is an increasing cardiac contractility with lesser increases in heart rate. Some reduction of peripheral vascular resistance may also occur. When compared to dopamine, dobutamine produces less peripheral vasoconstriction and less chronotropic response. Norepinephrine exerts both a and b-adrenergic effects, with a effects being evident at lower infusion rates and a effects more prominent at high doses. The major use of norepinephrine in current practice is in the patient with hypotension that persists despite appropriate volume resuscitation and the use of inotropic agents. Renal and mesenteric vasoconstrictive effects of norephinepherine complicate its use, especially when support is needed for significant periods of time. Isoproterenol is a potent b-adrenergic agent. With isoproterenol, myocardial oxygen demand is increased and diastolic coronary feeling is limited by tachycardia or diminished diastolic pressure. Indications for the use of isoproterenol are fairly limited, because agents with fewer adverse effects have become available. Vasodilators are used to augment cardiac function through optimization of ventricular filling pressures (preload) and systemic vascular resistance (afterload) both of which reduce demands on the myocardium. Decreases in afterload prompt increases in cardiac output and venodilatation contributes to decreases in pulmonary venous pressure and central venous pressure. Hypotension, however, may develop therefore patients must have careful constant monitoring of arterial pressure and repeated hemodynamic measurements with a pulmonary artery catheter