22.3.1 Which Pharmacologic Agents Would You Select for This Case?
Drug selection in individuals who are moribund is particularly important, especially medications that have significant cardiopulmonary side effects.
18.104.22.168 Neuromuscular Blocking Agent
Recalling that circulation times in cardiogenic shock are prolonged, the muscle relaxant of choice for intubation is the one with the most rapid onset, succinylcholine, unless there is a contraindication. In the face of metabolic acidosis, as is almost certainly the case in this patient, the potassium may be elevated, but this ought not deter the use of succinylcholine. Longer-acting neuromuscular blocking agents, such as pancuronium, vecuronium, and rocuronium, may be employed postintubation to maintain paralysis. The relative sympathomimetic side effects of pancuronium may be of some benefit in this patient, although the degree of sympathetic activation that is evident indicates that this would be of marginal value.
22.214.171.124 Sedative/Induction Agent
The selection of an induction agent is more difficult. However, in this patient, one is more interested in amnesia than induction of anesthesia. Recognizing this as the goal, small doses of ketamine (10-20 mg) and midazolam (1-2 mg) are clearly preferable to the other induction agents. Small doses of etomidate may be used, although the amnestic effects of etomidate may be less intense than with those already mentioned. Agents such as thiopental or propofol may cause further deterioration in this patient's hemodynamic status and should not be used.
126.96.36.199 Cardiovascular Pressure Support
This patient is hypotensive, and it is likely that intubation and positive pressure ventilation will acutely worsen his hypotension. Therefore, vasopressors should be prepared and immediately available, recognizing that balanced α/β adrenergic agonists (epinephrine, norepinephrine, vasopressin) are preferable to α-agonists alone, particularly in a catecholamine-depleted heart, as in this patient.
Inotropic support should theoretically improve outcomes in patients who present with CPE. However, they can also cause tachycardia, dysrhythmias, increase myocardial oxygen demand, and myocardial ischemia, all of which may increase mortality. These medications should be used judiciously. There are two common inotropic classes, catecholamines and phosphodiesterase inhibitors (PDEIs). The catecholamine class includes dopamine, dobutamine, and norepinephrine. Dopamine and norepinephrine may provide blood pressure support by increasing systemic vascular resistance, which can actually worsen cardiac output. Dobutamine, while inducing some mild preload and afterload reductions, may also further lower the blood pressure. Catecholamines work through the adenoreceptors, which are often saturated with endogenous catecholamines due to the patient's condition. Therefore, higher than normal dosages may be needed in the CPE patient, and unfortunately these dosages are associated with a higher rate of adverse effects. Regarding vasopressin, one experimental study comparing dobutamine (DOB) to dobutamine-norepinephrine combination to arginine vasopressin (AVP) demonstrated that AVP further worsened shock by decreasing the cardiac output and systemic vascular resistance compared with DOB alone.7
PDEIs work by increasing intracellular cyclic-AMP, which produces a positive inotropic effect on the heart, induces peripheral vasodilation, and reduces pulmonary vascular resistance. Together, these effects produce preload, afterload, and cardiac output improvement.8 Studies comparing milrinone to dobutamine in patients with severe CPE did not show any improvement in hospital length of stay or mortality.9,10
"Calcium sensitizer" levosimendan has been suggested and studied recently as an alternative to dobutamine for CPE.11,12 In one study comparing the two agents, levosimendan produced greater improvement in cardiac output and pulmonary vascular pressures and a reduced 180-day mortality rate (26% vs 38%).13 However, in the SURVIVE trial there was no decrease in 180-day mortality. There was significant reduction in B-type natriuretic peptide in the levosimendan group.14