The most important intervention for ischemic-related cardiogenic shock is emergent revascularization.10,11,14,30 ED stabilization is a temporizing measure while arranging for definitive therapy such as revascularization in the cardiac catheterization laboratory or surgical intervention for mechanical catastrophe. In the prehospital setting, EMS should direct any suspected cardiogenic shock patient to a facility that has 24-hour emergency cardiac revascularization capability (i.e., cardiac bypass team).31
Initial management focuses on airway stability and improving myocardial pump function to maintain end-organ perfusion. Diagnosis, therapy, and arrangements for definitive cardiac care must proceed simultaneously.
Give supplemental oxygen, and monitor closely for impending or acute respiratory failure that will require immediate mechanical ventilation. Continuous positive airway pressure or bilevel positive airway pressure can provide temporary airway support, but these methods require a hemodynamically stable, cooperative patient—a set of conditions rare in those with cardiogenic shock.
Endotracheal intubation is often necessary to maintain oxygenation and ventilation. However, the change to positive pressure ventilation may further decrease preload and cardiac output and worsen hypotension. Be prepared to administer a fluid bolus in the absence of pulmonary congestion, initiate an appropriate inotrope if congested with a compensated blood pressure, or start a vasopressor if hypotension exists.
Cardiac monitoring and IV access are necessary. Correct any hypoxemia, hypovolemia, rhythm disturbances, electrolyte abnormalities, and acid-base alterations rapidly. Place a urinary drainage catheter to monitor urine output in response to therapy.
In AMI, give aspirin early (if not already taking long term) unless there is an absolute contraindication.32 If blood pressure is >90 mm Hg systolic, chest pain may be relieved by careful use of IV nitroglycerin or morphine. Do not use a-blockers in patients with myocardial infarction in cardiogenic shock or who are at risk for cardiogenic shock (Table 50-1).32 Withhold angiotensin-converting enzyme inhibitors or other vasodilators.
Initial therapy is guided by clinical findings. Give crystalloid fluid boluses (250 to 500 cc) for an RV infarct with hypotension, if pulmonary congestion is absent. If there is no improvement with the fluid bolus or if pulmonary congestion develops, vasopressors or inotropes are indicated (Table 50-4).
TABLE 50-4Inotropic Medications Used in Cardiogenic Shock ||Download (.pdf) TABLE 50-4 Inotropic Medications Used in Cardiogenic Shock
|Drug ||Dose ||Comments |
|Dobutamine ||2–5 micrograms/kg/min, titrated up to 20 micrograms/kg/min ||Inotrope and potential vasodilator; lowers blood pressure; give as individual agent as long as systolic blood pressure (SBP) ≥90. Can use with dopamine. |
|Dopamine ||3–5 micrograms/kg/min, titrated up to 20–50 micrograms/kg/min as needed ||Inotrope and vasoconstrictor; increases left ventricular end-diastolic pressure and causes tachycardia. Can use with dobutamine. |
|Norepinephrine ||2 micrograms/min, titrate to response ||Vasoconstrictor and inotrope; preferred as a single agent over dobutamine if SBP <70. Can use combined with dobutamine. |
|Epinephrine ||0.1–0.5 micrograms/kg/min ||Inotrope and vasoconstrictor; second-tier choice because it causes acidosis and dysrhythmias. |
|Milrinone ||0.5 micrograms/kg/min ||Inotrope and vasodilator; lowers blood pressure. Second tier to dobutamine. |
Inotropes do not change outcome alone but can temporize while ED personnel arrange interventions to restore coronary artery perfusion and LV function.33 In the absence of profound hypotension, dobutamine is a mainstay of initial pharmacologic treatment. Dobutamine may increase cardiac contractility and should be considered as an individual agent if systolic blood pressure is ≥90 mm Hg without signs of overt shock or organ dysfunction. Avoid the use of dobutamine alone when the systolic blood pressure is <90 mm Hg because of its vasodilatory potential. Often, a vasoconstrictor is needed in addition to dobutamine. Dopamine may increase cardiac work by increasing heart rate and may also increase LV end-diastolic pressure by its β-agonist effect. Combination therapy with a vasopressor (dopamine) and an inotrope (dobutamine) may be more effective than either agent alone. Norepinephrine when combined with dobutamine may have more of an effect on peripheral vasoconstriction than dopamine when combined with dobutamine. If the systolic blood pressure is <70 mm Hg, norepinephrine is preferred over dobutamine due to its antithrombotic effect.34 If shock persists despite use of these agents, an intra-aortic balloon pump is typically placed, although long-term evidence of benefit is lacking.25,35,36,37,38,39
Epinephrine is an alternative to norepinephrine/dobutamine when dobutamine is not available; however, it is associated with increased systemic acidosis, tachycardia, and dysrhythmias compared to the combination of norepinephrine and dobutamine.40
Patients on β-blocker therapy may have an attenuated response to dobutamine, making norepinephrine a better choice. Milrinone (a selective phosphodiesterase inhibitor) can be substituted for the catecholamine if dobutamine is ineffective.
Pure vasoconstrictors and α1-adrenergic receptor agonists, such as phenylephrine, are contraindicated because they increase cardiac afterload without augmenting cardiac contractility.
In ischemic cardiogenic shock, early revascularization by percutaneous coronary intervention or coronary artery bypass grafting is the treatment of choice. The greatest short-term benefit is reported in patients <75 years old, those without previous myocardial infarction, and those treated within 6 hours of symptom onset. However, patients >75 years old who receive revascularization have improved survival over those >75 years old who have delayed or no revascularization, even though those >75 years old are less likely to receive revascularization.41 Coronary artery bypass grafting requires extensive surgical and medical resources and poses operative risk for seriously ill patients. The cardiac surgeon will make an overall judgment, with operative intervention chosen often for those with good prior functional status and less severe, early presentation of shock. Survival is higher in those receiving early revascularization compared with medical stabilization, even when elderly.41 Current guidelines do not have an age cutoff for percutaneous coronary intervention.27,38,39,42
Emergency coronary intervention in the catheterization laboratory or operating suite is the preferred definitive treatment for cardiogenic shock.43,44 Thrombolytic therapy is not as effective in establishing reperfusion in AMI with cardiogenic shock as it is in uncomplicated AMI. Survival from cardiogenic shock is highest with emergency coronary intervention, followed by intra-aortic balloon pump combined with thrombolytic therapy; thrombolytic therapy alone is least effective in reducing mortality. Rescue percutaneous coronary intervention does not convey the same mortality benefit as primary percutaneous coronary intervention for these patients.45 If no other definitive treatment modalities for cardiogenic shock are available, if the hospital does not have a catheterization laboratory, or if there is prolonged transport time for coronary intervention, thrombolytic therapy should be given to reduce mortality compared to supportive treatment alone.
INTRA-AORTIC BALLOON PUMP COUNTERPULSATION
Intra-aortic balloon pump counterpulsation provides hemodynamic support by decreasing afterload (which lowers myocardial oxygen consumption) and increasing diastolic blood pressure (which augments coronary perfusion).38,42 Intra-aortic balloon pump improves survival after thrombolytic therapy by augmenting diastolic perfusion pressure and unloading the LV.11,46,47 Outside of those receiving reperfusion, the long-term benefits of intra-aortic balloon pump use are not clear.36,37
Resolution of hemodynamic instability with intra-aortic balloon pump support has positive prognostic value.48 In hospitals without direct angioplasty capability, stabilization with intra-aortic balloon pump and thrombolysis followed by transfer to a tertiary care facility may be the best management option.38,42
PERCUTANEOUS LEFT VENTRICULAR ASSIST DEVICES
If cardiogenic shock persists despite revascularization and maximal medical therapy, a left ventricular assist device may augment cardiac output. This device is currently approved by the U.S. Food and Drug Administration only as a bridge to transplantation, and most cardiogenic shock patients are not such candidates. Case studies have described successful support and weaning of patients suffering from cardiogenic shock in the setting of acute infarction.49,50,51,52,53 A recent meta-analysis failed to demonstrate a mortality benefit for left ventricular assist devices compared with intra-aortic balloon pumps in patients with cardiogenic shock refractory to inotropic and vasopressor support.54
EXTRACORPOREAL MEMBRANE OXYGENATION
Extracorporeal membrane oxygenation can provide almost total circulatory support for a failing heart. Extracorporeal membrane oxygenation is typically instituted in emergency situations when maximum medical therapy has failed. The treating physician must consider the likelihood of recovery before instituting extracorporeal membrane oxygenation; patients with a very poor prognosis are not appropriate for extracorporeal membrane oxygenation. In the best cases, extracorporeal membrane oxygenation can provide support until percutaneous coronary intervention can be performed or until the heart begins to recover after intervention. In other cases, it can provide a "bridge to decision" for transplant or permanent left ventricular assist device placement.