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352 SECTION 7: Cardiovascular Disease or are hemodynamically unstable as a means to bridge a patient’s stability en route to definitive treatment. SPECIAL POPULATIONS  POSTPROCEDURE CHEST PAIN Patients who present with symptoms of an ACS shortly after PCIs, such as angioplasty or stent placement, should be assumed to have had abrupt vessel closure, until proven otherwise . Subacute thrombotic occlusion after stent placement occurs in approximately 4% of patients 2 to 14 days after procedure. Bare metal stents are more likely to restenose in the short term. Drug-eluting stents are more likely to present with late stent thrombosis after cessation of daily clopidogrel, 9 to 12 months later. Treat patients aggressively for an ACS, and obtain emergent cardiology consultation. Patients with chest pain syndromes after coronary artery bypass grafting also may have abrupt vessel clo sure. However, symptoms of recurrent ischemia can be confused with post-AMI pericarditis, as discussed earlier.  COCAINE- AND AMPHETAMINE-INDUCED ACUTE CORONARY SYNDROME AMI occurs in approximately 6% of patients who present to the ED with chest pain after cocaine use. Cocaine-associated myocardial infarction occurs in younger patients, but over the past two decades, the average age has increased from 38 years 71 to 50 years,72 highlighting the increased use of cocaine in middle-age patients. The sensitivity, specificity, positive predictive value, and negative predictive value of the ECG to identify cocaine-associated MI are 36%, 89.9%, 17.9%, and 95.8%, respectively. Cardiac troponin is the most sensitive biomarker for cocaine-associated myocardial infarction. Aspirin, nitrates, and benzodiazepines are the mainstays of therapy for initial stabilization; β-blockers are contraindi cated in the first 24 hours. 73 Patients with cocaine-associated STEMI are best managed with PCI. 71 Antithrombotic and antiplatelet therapy may be given according to current guidelines for non–cocaine-related ACS. There are fewer cases of amphetamine-induced myocardial infarction to guide therapy and no care guidelines. The initial ECG may be unreliable in the setting of methamphetamine-related ACS, with false-positive ST-segment elevation prompting unneeded thrombolytic therapy. In one case series of 33 patients admitted for chest pain who were meth amphetamine positive, nine (25%) were diagnosed with ACS (positive markers or required revascularization). Three patients (8%; two ACS and one non-ACS) suffered cardiac complications (ventricular fibrilla tion, ventricular tachycardia, and supraventricular tachycardia, respec tively). Only one patient had Q-wave myocardial infarction treated with PCI. Medical management was the mainstay of therapy.  ACUTE MEDICAL DISORDERS ASSOCIATED WITH ACUTE CORONARY SYNDROME Those with GI bleeding, 72 stroke,73,74 and severe infection have a higher frequency of ACS 75; even those with disorders considered otherwise benign, such as acute anxiety or emotional upset, have a higher fre quency of myocardial infarction.76 In the case of stroke and GI bleeding, the primary disease process (which came first) is sometimes unclear or underdiagnosed until late in the patient’s course. In a group of patients admitted to the intensive care unit for GI bleeding, approximately 13% sustained myocardial infarction; however, this did not affect mortal ity in this intensive care unit population.

ary disease process (which came first) is sometimes unclear or underdiagnosed until late in the patient’s course. In a group of patients admitted to the intensive care unit for GI bleeding, approximately 13% sustained myocardial infarction; however, this did not affect mortal ity in this intensive care unit population. A case-control study found increased risk of death in patients with GI bleeding meeting criteria for myocardial infarction when compared with those with negative markers (33% vs. 8%). 72 In general, treatment of the GI bleed takes priority, which precludes the major treatments for AMI. For patients with acute ischemic stroke, 17% have positive troponin assessment, which is associated with 3.2 relative risk of death compared with patients with normal troponin. The risk of stroke complicating the course of AMI has been formerly reported as 2.4% to 3.5%, 77 but with improved treatments for AMI, the risk has dropped to 0.6% to 1.8%. Hospital mortality in patients with stroke after AMI is high (17% to 27%). ECG abnormalities are common in patients with subarachnoid hemorrhage, and elevated troponin levels occur in 28%, with over half of these demonstrating transient left ventricular dysfunction. However, simultaneous STEMI is not common with a subarachnoid hemorrhage. Approximately 50% of patients with severe sepsis and septic shock have impairment of left ventricular systolic function, frequently with an elevated troponin level. 76 AMI occurs in 5.3% of patients hospitalized with community-acquired pneumonia, with the risk increasing to 15% in those with severe pneumonia. For all patients with dual or multiple acute medical issues, individualize management and weigh the risks of AMI guideline therapies. When indicated, use PCI over thrombolysis to identify the lesion and need for additional therapy.  AFTER HOURS AND WEEKEND PRESENTATIONS The management of patients with ACS is time sensitive and intensive. Patients who present “after hours” and on weekends wait longer for interventions, with an adverse impact on outcome. Patients who pres ent when the ED is busy with other ill patients (e.g., trauma patients), patients who present in settings with increased health system dysfunc tion and high levels of ED boarding, and patients who are not expedi tiously transferred to an inpatient bed have worse outcomes. 79-81 Systems solutions to improve hospital flow for patients with ACS will help opti mize the care of patients with ACS. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Cardiogenic Shock David E. Manthey Bret A. Nicks INTRODUCTION AND EPIDEMIOLOGY Cardiogenic shock results from decreased cardiac output, leading to inadequate tissue perfusion despite adequate circulating volume, and it carries an in-hospital mortality rate of 27% to 51%. 1,2 The true incidence is unknown because many patients die before hospital arrival. Cardio genic shock occurs in 4% to 8% of patients with ST-segment elevation myocardial infarction (STEMI) and is the leading cause of in-hospital death in patients with acute myocardial infarction (AMI). 3-6 Cardiogenic shock occurs less frequently (2.5%) in those with non–ST-segment elevation myocardial infarction (NSTEMI). 7,8 Only approximately 10% of AMI patients who will develop cardiogenic shock have it at initial ED presentation, with the median time of onset after arrival being 6 hours. 9 This highlights the therapeutic opportunity possible with rapid treatment of myocardial ischemia. Over the past decade, a strategy of early revascularization by percutaneous coronary intervention or coronary artery bypass surgery has improved the survival of cardiogenic shock patients with acute ischemia compared to medical therapy alone.

therapeutic opportunity possible with rapid treatment of myocardial ischemia. Over the past decade, a strategy of early revascularization by percutaneous coronary intervention or coronary artery bypass surgery has improved the survival of cardiogenic shock patients with acute ischemia compared to medical therapy alone. 3,10-13 As more risk factors for cardiogenic shock exist (Table 50-1), a greater amount of vulnerable myocardium and greater likelihood of cardiogenic shock also exist. PATHOPHYSIOLOGY The most common cause of cardiogenic shock is extensive myocardial infarction that depresses myocardial contractility. Additional causes are listed in Table 50-2. Regardless of the precipitating cause, cardiogenic shock is primarily “pump failure, ” which results in reduced cardiac output. 14 The systolic blood pressure drops due to poor cardiac out put, causing hypoperfusion of vital organs. Without a rise in systemic CHAPTER Tintinalli_Sec07_p0329-0424.indd 352 8/2/19 6:42 PM

Regardless of the precipitating cause, cardiogenic shock is primarily “pump failure, ” which results in reduced cardiac output. 14 The systolic blood pressure drops due to poor cardiac out put, causing hypoperfusion of vital organs. Without a rise in systemic CHAPTER Tintinalli_Sec07_p0329-0424.indd 352 8/2/19 6:42 PM CHAPTER 50: Cardiogenic Shock 353 TABLE 50-1 Risk Factors for Cardiogenic Shock Elderly Female Acute or prior ischemic event associated with the following •  Impaired  ejection fraction •  Extensive  infarct (evidence of large myocellular leak) •  Proximal  left anterior descending coronary artery occlusion •  Anterior  myocardial infarction •  Multivessel  coronary artery disease Prior medical history •  Previous  myocardial infarction •  Congestive  heart failure •  Diabetes TABLE 50-2 Causes of Cardiogenic Shock Mechanical complications •   Acute mitral regurgitation secondary to papillary muscle dysfunction or chordal rupture •  Ventricular  septal defect •  Free  wall rupture •  Right  ventricular infarction •  Acute  aortic insufficiency (aortic dissection) Severe depression of cardiac contractility •  Acute  myocardial infarction •  Sepsis •  Myocarditis •  Myocardial  contusion •  Cardiomyopathy •  Medication  toxicity (e.g., β-blocker overdose, calcium channel–blocker overdose) •  Unstable  dysrhythmia Mechanical obstruction to forward blood flow •  Aortic  stenosis •  Hypertrophic  cardiomyopathy •  Mitral  stenosis •  Left  atrial myxoma •  Pericardial  tamponade TABLE 50-3 Shock With Pump Failure: A Limited Differential Diagnosis Cardiogenic Shock (see Table 50-2) Acute pulmonary decompensation •  Chronic  obstructive pulmonary disease exacerbation •  Cor  pulmonale •  Massive  pulmonary embolism Distributive shock •  Sepsis •  Anaphylaxis •  Neurogenic  shock (spinal cord injury) Hypovolemic shock •  Hemorrhage •  Severe  dehydration Dissociative shock •  Toxins/drugs  of abuse (cyanide)vascular resistance, the diastolic blood pressure drops, resulting in coronary artery hypoperfusion. This creates a cycle of worsening myocardial ischemia and pump dysfunction and eventual decompensation. Both increased afterload and systolic/diastolic dysfunction of the heart can lead to increased left ventricular end-diastolic pressures (LVEDP) and pulmonary edema. Pulmonary edema leads to hypoxia and hypoxemia, which worsens ischemia and causes progressive cardiac dysfunction. Decreased cardiac output due to decreased stroke volume leads to poor peripheral perfusion and vasoconstriction. Augmenting peripheral vasoconstriction may improve coronary artery and peripheral perfu sion, but the resultant increased afterload can decrease cardiac output. In addition, a cardiogenic shock triggers a systemic inflammatory response, with release of nitric oxide and other mediators, that has a negative inotropic effect and creates systemic vasodilation. 15-19 The inflammatory response depresses pump function, dilates the periph eral vasculature, and increases the risk of death. 20,21 Studies looking at directed interventions to blunt the inflammatory response, complement cascade, and vasodilation have to date failed to decrease mortality. 17,22 The classic and most common picture of acute cardiogenic shock is due to left ventricular (LV) infarction and is characterized by the physiologic triad of low cardiac index, high systemic vascular resis tance indices, and increased pulmonary capillary wedge pressure, with peripheral vasoconstriction and pulmonary edema. 23,24 When right ventricular (RV) infarction is the cause of cardiogenic shock, the RV filling pressures increase, and forward flow to the LV is decreased, resulting in lowered cardiac output.

ar resis tance indices, and increased pulmonary capillary wedge pressure, with peripheral vasoconstriction and pulmonary edema. 23,24 When right ventricular (RV) infarction is the cause of cardiogenic shock, the RV filling pressures increase, and forward flow to the LV is decreased, resulting in lowered cardiac output. Euvolemic cardiogenic shock occurs subacutely in patients with heart failure; normotensive cardiogenic shock is rare. CLINICAL FEATURES  HISTORY Patients commonly have shortness of breath, chest pain, or weakness. Be sure to ask about and consider other causes of shock or pump failure (Table 50-3). Ask about a history of preexisting valvular disease, congestive heart failure, reduced ejection fraction (EF), recent illnesses, hypercoagulable states, substance abuse, and other risk factors (Table 50-1).  PHYSICAL EXAMINATION Cardiogenic shock results in hypoperfusion due to a low cardiac index; this is not always accompanied by hypotension. 9 Systolic blood pres sure is usually <90 mm Hg, although it can be higher with preexisting hypertension or peripheral vasoconstriction response. A pulse pressure <20 mm Hg is another finding if systemic resistance has not plummeted, and sinus tachycardia is common unless the patient is on medications that block a tachycardic response. Until respiratory fatigue sets in, tachypnea is common. If there is LV compromise, chest examination demonstrates rales from pulmonary edema. Patients are usually pale or cyanotic and may have cool skin, mottled extremities, and/or other signs of hypoperfusion. Diaphoresis indicates activation of the sympathetic nervous system. Cerebral hypoperfusion may result in altered mental status, and renal hypoperfusion often creates low urine output. In isolated RV infarction, the lungs are spared and venous congestion occurs, presenting as increased jugular venous pressure, a rise in jugular venous pressure with inspiration (Kussmaul sign) or compression of the liver (hepatojugular reflux), an enlarged liver, peripheral edema, and a third heart sound (S 3) originating from the RV . About 10% of cardiogenic shock after AMI is caused by mechanical complications.23 A new murmur may be the only physical exam finding of mechanical catastrophe; carefully seek any loud or new systolic mur murs. Acute mitral regurgitation, characterized by a soft holosystolic murmur at the apex radiating to the axilla, can occur from chordae tendineae rupture or papillary muscle dysfunction. An acute ventral septal defect is associated with a new loud holosystolic left parasternal murmur, often with a palpable thrill, that decreases in intensity as the intraventricular pressures equalize. Suspect acute aortic insufficiency when you find a soft diastolic murmur and a softer S 1 sound. DIAGNOSIS Shock exists whenever there is evidence of tissue hypoperfusion (i.e., end-organ dysfunction/damage and a systolic blood pressure usually <90 mm Hg or mean arterial pressure <65 mm Hg). To identify the heart Tintinalli_Sec07_p0329-0424.indd 353 8/2/19 6:42 PM

nd a soft diastolic murmur and a softer S 1 sound. DIAGNOSIS Shock exists whenever there is evidence of tissue hypoperfusion (i.e., end-organ dysfunction/damage and a systolic blood pressure usually <90 mm Hg or mean arterial pressure <65 mm Hg). To identify the heart Tintinalli_Sec07_p0329-0424.indd 353 8/2/19 6:42 PM 354 SECTION 7: Cardiovascular Disease Evaluation: 1. Physical exam specifically for a. Rales b. Jugular venous distention/hepatojugular reflex/edema c. Murmurs 2. ECG a. Rule out STEMI b. Look for ischemic changes 3. Echocardiogram a. Ejection fraction b. Wall motion abnormality c. Dilated RV d. Pericardial fluid e. Valvular dysfunction f. Aortic root <3 cm g. Volume status of Inferior vena cava h. Lungs for B-lines Treatment (based on cause): If ECG shows STEMI: Emergent revascularization in cardiac catheterization lab If valvular failure, ventricular rupture, or aortic dissection: Emergent operative management If pulmonary embolism: Thrombolytics Treatment of Hypotension (SBP <90 mm Hg): 1. If no evidence of pulmonary congestion: a. Attempt fluid boluses of 250–500 mL and reassess. 2. If pulmonary congestion is present or develops: a. If blood pressure is <90 mm Hg, combine dobutamine with dopamine or norepinephrine. i. If on β-blockers, administer milrinone as inotrope. b. If blood pressure is <70 mm Hg, administer norepinephrine. FIGURE 50-1. Approach to patient with cardiogenic shock. RV = right ventricle; SBP = systolic blood pressure; STEMI = ST-segment elevation myocardial infarction. as the cause of the shock state, rapidly assess the heart with clinical exam (discussed earlier), ECG, and echocardiogram (Figure 50-1).  LABORATORY TESTING There are no laboratory markers specific for the diagnosis. Cardiac biomarkers (primarily troponin) may not be elevated upon initial pre sentation from an acute myocardial ischemic triggering event. A CBC identifies anemia, which can contribute to cardiac ischemia. Hypoperfusion may result in an elevated serum lactate, and serum electrolytes and renal and hepatic studies can identify end-organ dysfunction. Serum B-type natriuretic peptide is an indicator of LV dysfunction but does not identify the cause. Because of its high negative predic tive value, a normal B-type natriuretic peptide level (<100 picograms/ mL) eliminates cardiogenic shock as the cause of hypoperfusion unless very early after onset or with isolated right heart failure. Conversely, an elevated B-type natriuretic peptide does not diagnose cardiogenic shock. 21,25 Blood gas measurements help identify those at risk of acute respira tory failure/carbon dioxide retention, quantify the presence and severity of acidosis, and determine the contribution of metabolic or respiratory components to acidosis.  IMAGING AND ANCILLARY STUDIES Electrocardiogram The ECG may identify ischemia, STEMI, or rhythm abnormalities and give evidence of cardiac response to identify electrolytic abnormalities (e.g., hypokalemia) or drug toxicity (e.g., digoxin). Obtain right-sided ECGs to identify RV infarction accompanying inferior infarction, looking for ST elevation in lead V 1 and ST-segment elevation in leads V3R to V6R; this finding elevates the shortterm risk of death26,27 (Figure 50-2). FIGURE 50-2. Right-sided leads demonstrating right ventricular infarction associated with inferior wall myocardial infarction. Right-sided leads have replaced the normal left-sided V leads. In this example, the STsegment elevation is prominent in leads VR 3-6. III aVR aVL aVF V1r V2 V3 V4 V5 V6r III aVR aVL aVF V1r V2 V3 V4 V5 V6r Tintinalli_Sec07_p0329-0424.indd 354 8/2/19 6:42 PM

nfarction associated with inferior wall myocardial infarction. Right-sided leads have replaced the normal left-sided V leads. In this example, the STsegment elevation is prominent in leads VR 3-6. III aVR aVL aVF V1r V2 V3 V4 V5 V6r III aVR aVL aVF V1r V2 V3 V4 V5 V6r Tintinalli_Sec07_p0329-0424.indd 354 8/2/19 6:42 PM CHAPTER 50: Cardiogenic Shock 355 Chest Radiography Obtain a portable chest radiograph, seeking pulmonary congestion or edema, alveolar infiltrates, and pleural effu sion. Such findings may lag by hours, so their absence does not exclude cardiogenic shock. Preexisting disease can confound the radiographic appearance, with pulmonary edema difficult to detect in patients with severe chronic obstructive lung disease or interstitial lung disease. Car diomegaly is the result of long-standing myocardial remodeling, and its presence may not explain the acute symptoms. The chest radiograph can suggest alternative or confounding diagnoses, such as pneumonia, pneumothorax, aortic dissection, or progressive pericardial effusion. Bedside Point of Care Ultrasound POCUS can help exclude alter native etiologies of shock, identify mechanical concerns, and guide therapy. Assessment should include a volume status evaluation of the inferior vena cava and estimation of right atrial pressure. A subcostal four-chamber view visualizes pericardial effusion and cardiac tamponade. When tamponade exists, there is a pericardial effusion, dilation of the inferior vena cava, and diastolic collapse of the RV with systolic collapse of the right atrium. When cardiac rupture occurs, there may be a visible clot in the pericardial space. Subcostal, parasternal, and apical views together can help estimate EF and cardiac contractility. An aortic root >3 cm is concerning for ascending aortic dissection, especially when associated with a pericardial effusion. Assess the valves for appropriate motion and flow characteristics, specifically the mitral valve. Apical four-chamber views are helpful for evaluating chamber size. In cases of acute right heart failure due to ischemia, the RV will be dilated and the LV will appear to be smaller than expected due to low filling pressures. In left heart failure, there will be dilation of the LV secondary to decreased cardiac output and increased filling pressure. 28 On lung assessment, B-lines (three B-lines in two bilateral lung zones) are the US equivalent of the Kerley B-lines found on chest radiograph and are commonly present with interstitial edema. 29 The line will traverse the entire US screen in a vertical manner as well as cross any present A-lines. 29 Bedside echocardiography is an adjunct, not replacement, for emer gent formal transthoracic echocardiography. Formal echocardiography uses color and spectral Doppler to identify mechanical complications and to characterize the nature of cardiac impairment. Echocardiography detects regional wall motion abnormalities and a lack of compensatory hyperkinesis in uninvolved cardiac segments. Loss of RV contractility, RV dilatation, and normal estimated pulmonary pressures occur more commonly with RV infarction. Color flow Doppler transthoracic echocardiography identifies mechanical causes of cardiogenic shock, such as acute mitral regurgita tion or ventricular septal defect. Echocardiography detects other causes of decreased cardiac output, notably pulmonary embolism. Acute RV dilatation, tricuspid insufficiency, paradoxical systolic septal motion, and high estimated pulmonary artery and RV pressures suggest pulmonary hypertension from an acute pulmonary embolus. Mechanical Catastrophe Diagnosis When suspecting a mechani cal catastrophe, consult a cardiothoracic surgeon immediately while obtaining a bedside echocardiogram.

ncy, paradoxical systolic septal motion, and high estimated pulmonary artery and RV pressures suggest pulmonary hypertension from an acute pulmonary embolus. Mechanical Catastrophe Diagnosis When suspecting a mechani cal catastrophe, consult a cardiothoracic surgeon immediately while obtaining a bedside echocardiogram. In the case of myocardial free wall rupture, death is likely unless a pseudoaneurysm forms, which may present as an acute pericardial effusion on echocardiography. An acute ventricular septal defect appears on color Doppler echocar diography or right heart catheterization by showing oxygen satura tion flow or step-up from the right atrium to the RV . 28 Acute mitral regurgitation, from papillary muscle rupture or dysfunction, can complicate AMI. Hemodynamic Monitoring Patients in cardiogenic shock require continuous monitoring of blood pressure and other hemodynamic measures. Typically, patients with cardiogenic shock have a low car diac index (<2.2 L/min/m 2) and elevated LVEDP (pulmonary artery occlusion pressure >15 mm Hg). 9,12,14 Cardiac output measurement via pulmonary artery catheterization provides continuous measurements of pulmonary artery occlusion pressure, vascular resistances, ventricular work, and other hemodynamic parameters. 30,31 Although numerous trials have assessed the value of pulmonary artery catherization in intensive care patients, most have demonstrated no harm, but also no benefit.31 Noninvasive blood pressure measurements may underesti mate systolic pressure by >30 mm Hg; however, mean arterial pressure varies by only 1 to 2 mm Hg whether central or peripheral. 32 Arterial blood pressure monitoring allows accurate assessment of cardiovascular instability during resuscitation and is particularly useful when giving vasoactive medications. Central venous pressure, an indirect indicator of central blood volume, can aid assessment of global volume status, but isolated values outside extremes to guide resuscitation in critically ill patients are less helpful (see “Hemodynamic Monitoring”). ED TREATMENT AND STABILIZATION The most important definitive intervention for acute ischemiarelated cardiogenic shock is emergent revascularization. 8,11,14,15,23,34 In anticipation of the need for revascularization, EMS should direct any suspected cardiogenic shock patient to a facility that has 24-hour full-service emergency cardiac revascularization capability (including a cardiac bypass team). Initial ED management focuses on airway stability and improving myocardial pump function to maintain end-organ perfusion while arranging definitive care.  AIRWAY Give supplemental oxygen to keep saturations >91%, and monitor closely for impending or acute respiratory failure that will require immediate mechanical ventilation. Noninvasive ventilation using continuous positive airway pressure, bilevel positive airway pressure, or high-flow nasal cannula can provide temporary airway support. 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 hypo tension. Be prepared to administer a fluid bolus in the absence of severe pulmonary congestion and in the presence of RV infarction, while also considering the use of push dose pressors (small discrete doses of vaso pressors) to mitigate the potential hypotensive effects of intubation. Keep end-expiratory pressures and tidal volumes as low as possible (see Chapter 29B, “Mechanical Ventilation”) to avoid impairing preload. Recognize that patients may need additional vasopressor support after positive-pressure ventilation.  STABILIZATION Continuous cardiac monitoring and IV access are necessary.

tion. Keep end-expiratory pressures and tidal volumes as low as possible (see Chapter 29B, “Mechanical Ventilation”) to avoid impairing preload. Recognize that patients may need additional vasopressor support after positive-pressure ventilation.  STABILIZATION Continuous cardiac monitoring and IV access are necessary. Correct any hypoxemia, hypovolemia, rhythm disturbances, electrolyte abnormali ties, and acid-base alterations rapidly. Although not needed immediately, many benefit from a urinary drainage catheter to follow renal output. In AMI, give aspirin early (if not already taking long term) unless there is an absolute contraindication. 37 If blood pressure is >90 mm Hg systolic, you may use IV nitroglycerin. Do not use α-blockers in patients with myocardial infarction in cardiogenic shock or who are at risk for cardiogenic shock (Table 50-1). 37 Withhold angiotensinconverting enzyme inhibitors or other vasodilators.  HYPOTENSION Guide initial therapy by the clinical findings. Give crystalloid fluid boluses (250 to 500 mL, and repeat after assessing benefit or harm) if pulmonary congestion is absent or for an RV infarct with hypotension. If there is no improvement with the fluid bolus or if pulmonary congestion develops, use vasopressors (for hypotension) or inotropes (for conges tion without profound hypotension) (Table 50-4). Inotropes do not change outcome alone but can temporize while ED personnel arrange interventions to restore coronary artery perfusion and LV function. 38 In the absence of profound hypotension, dobutamine is a mainstay of initial pharmacologic treatment. Dobutamine increases cardiac contractility and is most effective if the systolic blood pressure is ≥90 mm Hg. Avoid the use of dobutamine alone when the systolic Tintinalli_Sec07_p0329-0424.indd 355 8/2/19 6:42 PM

n. 38 In the absence of profound hypotension, dobutamine is a mainstay of initial pharmacologic treatment. Dobutamine increases cardiac contractility and is most effective if the systolic blood pressure is ≥90 mm Hg. Avoid the use of dobutamine alone when the systolic Tintinalli_Sec07_p0329-0424.indd 355 8/2/19 6:42 PM 356 SECTION 7: Cardiovascular Disease 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 mm Hg. Can use with dopamine or norepinephrine. Avoid if on β-blocker. 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. Increased risk of dysrhythmia. Norepinephrine 2 micrograms/min, titrate to response Vasoconstrictor and inotrope; preferred as a single agent over dopamine if SBP <70 mm Hg. Can use combined with dobutamine. Epinephrine 0.1–0.5 microgram/kg/min Inotrope and vasoconstrictor; second-tier choice because it causes acidosis and dysrhythmias. Milrinone 0.5 microgram/kg/min Inotrope and vasodilator; lowers blood pressure. Second tier to dobutamine. Use if on β-blocker. blood pressure is <90 mm Hg because of its vasodilatory potential. Often, a vasoconstrictor added to dobutamine is helpful, but only when the blood pressure allows this dual therapy. Dopamine is a vasopressor with some inotropic effect, but it may increase cardiac work by increas ing heart rate and may also increase LVEDP by its β-agonist effect. Combination therapy with a vasopressor (dopamine or norepinephrine) and an inotrope (dobutamine) may be more effective than either agent alone. Norepinephrine, when combined with dobutamine, has a more profound effect on peripheral vasoconstriction than dopamine alone or when combined with dobutamine. If the systolic blood pressure is <70 mm Hg, most prefer norepinephrine rather than dobutamine. 39 If shock persists despite use of these agents, consider an intra-aortic balloon pump or other assist device. Epinephrine is associated with more systemic acidosis, tachycardia, and dysrhythmias compared to the combination of norepinephrine and dobutamine. 38,39,41 Patients on β-blocker therapy may have an attenuated response to dobutamine, making milrinone a better choice. Milrinone (a selective phosphodiesterase-3 inhibitor) can be substituted for the catecholamine if dobutamine is ineffective. Pure vasoconstrictors and 1-adrenergic receptor agonists, such as phenylephrine (often a push dose drug), are contraindicated because they increase cardiac afterload without augmenting cardiac contractility. DEFINITIVE MANAGEMENT  EARLY REVASCULARIZATION In ischemic cardiogenic shock, early revascularization by percutane ous coronary intervention or coronary artery bypass grafting is the treatment of choice. 42,43 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. Survival is higher in those receiving early revascularization compared with medical stabilization, even in the elderly. 44 Current guidelines do not have an age cutoff for percutaneous coronary intervention.42,43,45,46  THROMBOLYTIC THERAPY Emergency coronary intervention in the catheterization laboratory or operating suite is the preferred definitive treatment for cardio genic shock. 42-45 Thrombolytic therapy is not as effective in establishing reperfusion in AMI with cardiogenic shock as it is in uncomplicated AMI.

on.42,43,45,46  THROMBOLYTIC THERAPY Emergency coronary intervention in the catheterization laboratory or operating suite is the preferred definitive treatment for cardio genic shock. 42-45 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. 44,46 Rescue percutaneous coronary intervention does not convey the same mortality benefit as primary percutaneous coronary intervention for these patients. 47,48 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, thrombolytics should be considered, but do not delay access to percutaneous coronary intervention. 14,15,48  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 aug ments coronary perfusion). 40,49 Intra-aortic balloon pump improves survival after thrombolytic therapy by augmenting diastolic perfusion pressure and unloading the LV . 50,51 Outside of those receiving reperfu sion, the long-term benefits of intra-aortic balloon pump use are not clear. 50-53 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 in severe car diogenic shock. 50,53,54  VENTRICULAR ASSIST DEVICES When cardiogenic shock is refractory to medical therapy, engage experts to assess for percutaneous mechanical circulatory support (cardiogenic shock) candidacy, which usually consists of a team of intensivists, cardiologists, and cardiothoracic surgeons. Acute cardiogenic shock devices range from intra-aortic balloon pumps to percutaneous ventricular assist devices to extracorporeal membrane oxygenation, and can aid, maintain, or restore adequate tissue perfusion. Current percutaneous ventricular assist devices include nonpulsatile (e.g., Impella ® , Tandem- Heart® ) and pulsatile versions (e.g., iV AC ® , HeartMate ® ) designed to provide LV unloading. 55-59 Although the degree of hemodynamic sup port varies, they can effectively serve as a bridge to long-term devices, such as an LV assist device and/or heart transplantation. (See Video: Left Ventricular Assist Device.) Current LV assist devices are continuous-flow pumps with non contact bearings (magnetic levitation) to enhance rotation without friction or wear and decrease pump thrombosis and stroke. Increas ingly, case studies and small cohort studies have described successful ventricular assist device support and weaning of patients suffering from cardiogenic shock in the setting of acute infarction. 56-60 However, despite current device improvements, there are no data demonstrating a mortality benefit for LV assist devices compared with intra-aortic balloon pumps in patients with cardiogenic shock refractory to inotro pic and vasopressor support; either is a stabilizing bridge to potential transplantation. 58-61 Complications, including pump thrombosis, stroke, bleeding events, and driveline infection, remain a concern with these interventions.  EXTRACORPOREAL MEMBRANE OXYGENATION Extracorporeal membrane oxygenation can provide almost total circulatory support for a failing heart. Extracorporeal membrane oxygenation usually follows emergency situations when maximum medical therapy has failed.

nd driveline infection, remain a concern with these interventions.  EXTRACORPOREAL MEMBRANE OXYGENATION Extracorporeal membrane oxygenation can provide almost total circulatory support for a failing heart. Extracorporeal membrane oxygenation usually follows emergency situations when maximum medical therapy has failed. The Survival After Veno-arterial Extracorporeal Membrane Oxygenation score can predict survival in patients receiving extracor poreal membrane oxygenation for refractory cardiogenic shock 62 (www .save-score.com). In the best cases, extracorporeal membrane oxygen ation provides support until percutaneous coronary intervention or Tintinalli_Sec07_p0329-0424.indd 356 8/2/19 6:42 PM