Hemorrhage results in diminished venous return to the heart and decreased cardiac output. This is compensated by increased cardiac heart rate and contractility, as well as venous and arterial vasoconstriction. Stimulation of sympathetic fibers innervating the heart leads to activation of β 1 -adrenergic receptors that increase heart rate and contractility in this attempt to increase cardiac output. Increased myocardial O 2 consumption occurs as a result of the increased workload; thus, myocardial O 2 supply must be maintained or myocardial dysfunction will develop. The cardiovascular response in hemorrhage/hypovolemia differs from the responses elicited with the other etiologies of shock.