Cardiogenic shock in emergency medicine

Cardiogenic shock is characterized by a decreased pumping ability of the heart that causes a shocklike state (ie, global hypoperfusion). It most commonly occurs in association with, and as a direct result of, acute myocardial infarction (AMI).

Similar to other shock states, cardiogenic shock is considered to be a clinical diagnosis characterized by decreased urine output, altered mentation, and hypotension. Other clinical characteristics include jugular venous distension, cardiac gallop, and pulmonary edema. The most recent prospective study of cardiogenic shock defines cardiogenic shock as sustained hypotension (systolic blood pressure [BP] less than 90 mm Hg lasting more than 30 min).

Mortality/Morbidity

Cardiogenic shock is the leading cause of death in acute myocardial infarction (AMI).

The overall in-hospital mortality rate is 57%. For persons older than 75 years, the mortality rate is 64.1%. For those younger than 75 years, the mortality rate is 39.5%.

Outcomes significantly improve only when rapid revascularization can be achieved. The SHOCK trial demonstrated that overall mortality when revascularization occurs is 38%. When rapid revascularization is not attempted, mortality rates approach 70%.

Rates vary depending on the procedure (eg, percutaneous transluminal coronary angioplasty, stent placement, thrombolytic therapy), but they have been reported to be as low as 30-50%.

Mortality rates have declined over time. In the National Registry of Myocardial Infarction covering the period from 1995-2004, in-hospital mortality declined from 60.3% to 47.9%. This improvement has been attributed to the increasing frequency of the use percutaneous coronary intervention (PCI) and other revascularization procedures. Mortality rates attributable to cardiogenic shock are also thought to be due to the increased frequency of use of PCI, antiplatelet therapies, and lipid-lowering agents in patients with acute coronary syndromes. This has decreased the incidence of cardiogenic shock developing in the hospital due to acute coronary syndromes. The incidence of cardiogenic shock on arrival to the hospital has not changed significantly.

Physical

The physical examination findings are consistent with shock. Patients are in frank distress, are profoundly diaphoretic with mottled extremities, and are usually visibly dyspneic. Clinical assessment begins with attention to the ABCs and vital signs.

Although the patient may eventually require endotracheal intubation, the airway usually is patent initially.

Breathing may be labored, with audible coarse crackles or wheezing.

As in any shocklike state, circulation is markedly impaired. Tachycardia, delayed capillary refill, hypotension, diaphoresis, and poor peripheral pulses are frequent findings.

Other signs of end-organ dysfunction (eg, decreased mental function, urinary output) may be present.

Initial vital sign assessment should include BP measurements in both arms to evaluate possible thoracic aortic aneurysm or dissection. Vital signs should be regularly updated with continuous noninvasive physiologic monitoring.

Neck examination may reveal jugular venous distention, which may be prominent. This finding is evidence of RV failure.

LV dysfunction, characterized by florid pulmonary edema, can be auscultated as crackles with or without wheezing.

Careful cardiac examination may reveal mechanical causes of cardiogenic shock.

In children, hepatomegaly may also be present. Murmurs may be difficult to detect in children and in infants due to rapid heart rates.

Causes

The vast majority of cases of cardiogenic shock in adults are due to acute myocardial ischemia. Many cases of cardiogenic shock occurring after acute coronary syndromes may be due to medication administration. The use of beta-blockers and ACE inhibitors in acute coronary syndromes must be carefully timed and monitored.

In children, preceding viral infection may cause myocarditis. Children and infants may have unrecognized congenital structural heart defects that are well compensated until there is a stressor.

Risk factors for the development of cardiogenic shock include preexisting myocardial damage or disease (eg, diabetes, advanced age, previous AMI), AMI (eg, Q-wave, large or anterior wall AMIs), congenital heart disease, and dysrhythmia.

Prehospital care

Prehospital care is aimed at minimizing any further ischemia and shock.

All patients require intravenous access, high-flow oxygen administered by mask, and cardiac monitoring.

Twelve-lead electrocardiography performed in the field by appropriately trained paramedics may be useful in decreasing door to PCI times and/or thrombolytics because acute ST-segment elevation myocardial infarctions can be identified earlier. The ED, can thus be alerted, and may mobilize the appropriate resources.

Inotropic medications should be considered in systems with appropriately trained paramedical personnel.

When clinically necessary, positive pressure ventilation and endotracheal intubation should be performed.

Continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) support can be considered in appropriately equipped systems.

Emergency Department Care

ED care of cardiogenic shock is aimed at making the diagnosis, preventing further ischemia, and treating the underlying cause. Treatment of the underlying cause is directed in the case of acute myocardial infarction (AMI) at coronary artery reperfusion. This is best accomplished with rapid transfer of the patient to a cardiac catheterization laboratory.

Clinicians should be alert to the fact that the SHOCK trial demonstrated that percutaneous coronary intervention (PCI) or coronary artery bypass are the treatments of choice and that they have been shown to markedly decrease mortality rates at 1 year.

PCI should be initiated within 90 minutes of presentation; however, it remains helpful, as an acute intervention, within 12 hours of presentation. If such a facility is not immediately available, thrombolytics should be considered. However, this treatment is second best. An increased mortality is seen in situations where thrombolytics are used instead of PCI. This is due to the relative ineffectiveness of the thrombolytic medications to lyse clots in low blood pressure situations.

Treatment begins with assessment and management of the ABCs.

The airway should be assessed for patency and breathing evaluated for effectiveness and increased work of breathing. Endotracheal intubation and mechanical ventilation should be considered for patients with excessive work of breathing. Positive pressure ventilation may improve oxygenation but may also compromise venous return, preload, to the heart. In any event, the patient should be treated with high-flow oxygen. Recent studies in patients with acute cardiogenic pulmonary edema have shown noninvasive ventilation to improve hemodynamics and reduce the intubation rate. Mortality is, however, unaffected.

Other interventions are directed at supporting myocardial perfusion and maximizing cardiac output. Intravenous fluids should be provided to maintain adequate preload. The administration of such fluids should be guided by central venous pressure, pulmonary capillary wedge pressure monitoring, or sonographic assessment of IVC filling.

Anticoagulants and aspirin should be used as in other cases of acute myocardial infarctions. Care should be taken to ensure that the patient does not have myocardial wall rupture that is amenable to surgery before initiating therapy. There is no need to start clopidogrel until after angiography as this may determine a need for urgent coronary bypass.

Intravenous vasopressors provide inotropic support increasing perfusion of the ischemic myocardium and all body tissues. However, extreme heart rates should be avoided because they may increase myocardial oxygen consumption, increase infarct size, and further impair the pumping ability of the heart. No particular vasopressor has been shown to be superior to another. Carefully chosen combinations of pressors may be useful.

Dopamine may provide vasopressor support. With higher doses, it has the disadvantage of increasing the heart rate and myocardial oxygen consumption.

Dobutamine, inamrinone (formerly amrinone), or milrinone may provide inotropic support. In addition to their positive inotropic effects, inamrinone and milrinone have a beneficial vasodilator effect, which reduces preload and afterload.

Norepinephrine infusion can also be considered in refractory cardiogenic shock, though it significantly increases afterload.

Nitrates and/or morphine are advised for the management of pain; however, they must be used with caution because these patients are in shock, and excessive use of either of these agents can produce profound hypotension. Neither of these options has been shown to improve outcomes in cardiogenic shock.

Other supportive medications to be considered include nesiritide (Natrecor) and levosimendan.

Nesiritide (Natrecor) may be considered. Although nesiritide has been shown to increase mortality and renal dysfunction, it continues to be studied as a treatment of acute congestive heart failure and currently retains Food and Drug Administration (FDA) approval. It should be used with caution in the setting of cardiogenic shock because it has been shown to cause hypotension.

Levosimendan, though not approved for use in the United States, can be considered in conjunction with vasopressors. It should be used with caution as it can cause hypotension. Used with vasopressors, levosimendan may improve hemodynamics and improve coronary blood flow.

Mechanical device supports may be used to support patients in cardiogenic shock.

The use of an intra-aortic balloon pump (IABP) is recommended for cardiogenic shock not quickly reversed with pharmacologic therapy. It is also recommended as a stabilizing measure combined with thrombolytic therapy when angiography and revascularization are not readily available. Counterpulsation of the IABP reduces LV afterload and improves coronary artery blood flow.

Although this procedure is generally not performed in the ED, planning is essential, and early consultation with a cardiologist regarding this option is recommended. Although complications may occur in up to 30% of patients, extensive retrospective data support its use.

Left-ventricular assist devices (LVAD) may be used in selected patients with refractory shock as a bridge to cardiac transplantation. This is still controversial and requires the assistance of cardiologists and cardiac surgeons. LVADs have not been shown to be superior in terms of outcomes.

 

Cardiogenic shock in emergency medicine

Cardiogenic shock is characterized by a decreased pumping ability of the heart that causes a shocklike state (ie, global hypoperfusion). It most commonly occurs in association with, and as a direct result of, acute myocardial infarction (AMI). Similar to other shock states, cardiogenic shock is considered to be a clinical diagnosis characterized by decreased urine output, altered mentation, and hypotension. Other clinical characteristics include jugular venous distension, cardiac gallop, and pulmonary edema. The most recent prospective study of cardiogenic shock defines cardiogenic shock as sustained hypotension (systolic blood pressure [BP] less than 90 mm Hg lasting more than 30 min). Mortality/Morbidity Cardiogenic shock is the leading cause of death in acute myocardial infarction (AMI). The overall in-hospital mortality rate is 57%. For persons older than 75 years, the mortality rate is 64.1%. For those younger than 75 years, the mortality rate is 39.5%. Outcomes significantly improve only when rapid revascularization can be achieved. The SHOCK trial demonstrated that overall mortality when revascularization occurs is 38%. When rapid revascularization is not attempted, mortality rates approach 70%. Rates vary depending on the procedure (eg, percutaneous transluminal coronary angioplasty, stent placement, thrombolytic therapy), but they have been reported to be as low as 30-50%. Mortality rates have declined over time. In the National Registry of Myocardial Infarction covering the period from 1995-2004, in-hospital mortality declined from 60.3% to 47.9%. This improvement has been attributed to the increasing frequency of the use percutaneous coronary intervention (PCI) and other revascularization procedures. Mortality rates attributable to cardiogenic shock are also thought to be due to the increased frequency of use of PCI, antiplatelet therapies, and lipid-lowering agents in patients with acute coronary syndromes. This has decreased the incidence of cardiogenic shock developing in the hospital due to acute coronary syndromes. The incidence of cardiogenic shock on arrival to the hospital has not changed significantly. Physical The physical examination findings are consistent with shock. Patients are in frank distress, are profoundly diaphoretic with mottled extremities, and are usually visibly dyspneic. Clinical assessment begins with attention to the ABCs and vital signs. Although the patient may eventually require endotracheal intubation, the airway usually is patent initially. Breathing may be labored, with audible coarse crackles or wheezing. As in any shocklike state, circulation is markedly impaired. Tachycardia, delayed capillary refill, hypotension, diaphoresis, and poor peripheral pulses are frequent findings. Other signs of end-organ dysfunction (eg, decreased mental function, urinary output) may be present. Initial vital sign assessment should include BP measurements in both arms to evaluate possible thoracic aortic aneurysm or dissection. Vital signs should be regularly updated with continuous noninvasive physiologic monitoring. Neck examination may reveal jugular venous distention, which may be prominent. This finding is evidence of RV failure. LV dysfunction, characterized by florid pulmonary edema, can be auscultated as crackles with or without wheezing. Careful cardiac examination may reveal mechanical causes of cardiogenic shock. In children, hepatomegaly may also be present. Murmurs may be difficult to detect in children and in infants due to rapid heart rates. Causes The vast majority of cases of cardiogenic shock in adults are due to acute myocardial ischemia. Many cases of cardiogenic shock occurring after acute coronary syndromes may be due to medication administration. The use of beta-blockers and ACE inhibitors in acute coronary syndromes must be carefully timed and monitored. In children, preceding viral infection may cause myocarditis. Children and infants may have unrecognized congenital structural heart defects that are well compensated until there is a stressor. Risk factors for the development of cardiogenic shock include preexisting myocardial damage or disease (eg, diabetes, advanced age, previous AMI), AMI (eg, Q-wave, large or anterior wall AMIs), congenital heart disease, and dysrhythmia. Prehospital care Prehospital care is aimed at minimizing any further ischemia and shock. All patients require intravenous access, high-flow oxygen administered by mask, and cardiac monitoring. Twelve-lead electrocardiography performed in the field by appropriately trained paramedics may be useful in decreasing door to PCI times and/or thrombolytics because acute ST-segment elevation myocardial infarctions can be identified earlier. The ED, can thus be alerted, and may mobilize the appropriate resources. Inotropic medications should be considered in systems with appropriately trained paramedical personnel. When clinically necessary, positive pressure ventilation and endotracheal intubation should be performed. Continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) support can be considered in appropriately equipped systems. Emergency Department Care ED care of cardiogenic shock is aimed at making the diagnosis, preventing further ischemia, and treating the underlying cause. Treatment of the underlying cause is directed in the case of acute myocardial infarction (AMI) at coronary artery reperfusion. This is best accomplished with rapid transfer of the patient to a cardiac catheterization laboratory. Clinicians should be alert to the fact that the SHOCK trial demonstrated that percutaneous coronary intervention (PCI) or coronary artery bypass are the treatments of choice and that they have been shown to markedly decrease mortality rates at 1 year. PCI should be initiated within 90 minutes of presentation; however, it remains helpful, as an acute intervention, within 12 hours of presentation. If such a facility is not immediately available, thrombolytics should be considered. However, this treatment is second best. An increased mortality is seen in situations where thrombolytics are used instead of PCI. This is due to the relative ineffectiveness of the thrombolytic medications to lyse clots in low blood pressure situations. Treatment begins with assessment and management of the ABCs. The airway should be assessed for patency and breathing evaluated for effectiveness and increased work of breathing. Endotracheal intubation and mechanical ventilation should be considered for patients with excessive work of breathing. Positive pressure ventilation may improve oxygenation but may also compromise venous return, preload, to the heart. In any event, the patient should be treated with high-flow oxygen. Recent studies in patients with acute cardiogenic pulmonary edema have shown noninvasive ventilation to improve hemodynamics and reduce the intubation rate. Mortality is, however, unaffected. Other interventions are directed at supporting myocardial perfusion and maximizing cardiac output. Intravenous fluids should be provided to maintain adequate preload. The administration of such fluids should be guided by central venous pressure, pulmonary capillary wedge pressure monitoring, or sonographic assessment of IVC filling. Anticoagulants and aspirin should be used as in other cases of acute myocardial infarctions. Care should be taken to ensure that the patient does not have myocardial wall rupture that is amenable to surgery before initiating therapy. There is no need to start clopidogrel until after angiography as this may determine a need for urgent coronary bypass. Intravenous vasopressors provide inotropic support increasing perfusion of the ischemic myocardium and all body tissues. However, extreme heart rates should be avoided because they may increase myocardial oxygen consumption, increase infarct size, and further impair the pumping ability of the heart. No particular vasopressor has been shown to be superior to another. Carefully chosen combinations of pressors may be useful. Dopamine may provide vasopressor support. With higher doses, it has the disadvantage of increasing the heart rate and myocardial oxygen consumption. Dobutamine, inamrinone (formerly amrinone), or milrinone may provide inotropic support. In addition to their positive inotropic effects, inamrinone and milrinone have a beneficial vasodilator effect, which reduces preload and afterload. Norepinephrine infusion can also be considered in refractory cardiogenic shock, though it significantly increases afterload. Nitrates and/or morphine are advised for the management of pain; however, they must be used with caution because these patients are in shock, and excessive use of either of these agents can produce profound hypotension. Neither of these options has been shown to improve outcomes in cardiogenic shock. Other supportive medications to be considered include nesiritide (Natrecor) and levosimendan. Nesiritide (Natrecor) may be considered. Although nesiritide has been shown to increase mortality and renal dysfunction, it continues to be studied as a treatment of acute congestive heart failure and currently retains Food and Drug Administration (FDA) approval. It should be used with caution in the setting of cardiogenic shock because it has been shown to cause hypotension. Levosimendan, though not approved for use in the United States, can be considered in conjunction with vasopressors. It should be used with caution as it can cause hypotension. Used with vasopressors, levosimendan may improve hemodynamics and improve coronary blood flow. Mechanical device supports may be used to support patients in cardiogenic shock. The use of an intra-aortic balloon pump (IABP) is recommended for cardiogenic shock not quickly reversed with pharmacologic therapy. It is also recommended as a stabilizing measure combined with thrombolytic therapy when angiography and revascularization are not readily available. Counterpulsation of the IABP reduces LV afterload and improves coronary artery blood flow. Although this procedure is generally not performed in the ED, planning is essential, and early consultation with a cardiologist regarding this option is recommended. Although complications may occur in up to 30% of patients, extensive retrospective data support its use. Left-ventricular assist devices (LVAD) may be used in selected patients with refractory shock as a bridge to cardiac transplantation. This is still controversial and requires the assistance of cardiologists and cardiac surgeons. LVADs have not been shown to be superior in terms of outcomes.