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Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e

Chapter 50: Cardiogenic Shock Glass Casey; Manthey David

FIGURE 50-1.

INTRODUCTION AND EPIDEMIOLOGY

Cardiogenic shock is an acute state of decreased cardiac output resulting in inadequate tissue perfusiondespite adequate circulating volume. Cardiogenic shock is the leading cause of in-hospital death in patients

with acute myocardial infarction (AMI).1 The true incidence of cardiogenic shock is unknown because manypatients die before arrival and escape estimates. Cardiogenic shock is seen in 4% to 8% of patients with ST-

segment elevation myocardial infarction (STEMI).2,3 The incidence is declining in part as a result of the

increased use of percutaneous intervention for AMI.3,4,5,6 Cardiogenic shock occurs less frequently (2.5%) in

those with non–ST-segment elevation myocardial infarction (NSTEMI) compared with those with STEMI.7,8

Only ~10% of AMI patients who will develop cardiogenic shock have it at ED presentation, with the median

time of onset a�er arrival being approximately 6 hours.2,9 This underscores the therapeutic opportunity thatexists by thwarting ongoing myocardial ischemia.

During the past decade, a strategy of early revascularization by percutaneous coronary intervention orcoronary artery bypass surgery improved survival of cardiogenic shock patients with acute ischemia

compared to medical therapy alone.3,10,11,12 Despite these advances, the mortality remains high (~50%),

with half of the deaths occurring within the first 48 hours a�er presentation.3,13,14,15 Early recognition ofcardiogenic shock or ongoing myocardial ischemia is the key for emergency physicians. Prompt andsuccessful e�orts to restore perfusion optimize patient outcomes.

The more risk factors that are present (Table 50-1), the greater is the amount of vulnerable myocardium andthe greater is the likelihood of cardiogenic shock.

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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 le� anterior descending coronary artery occlusion

Anterior myocardial infarction

Multivessel coronary artery disease

Prior medical history:

Previous myocardial infarction

Congestive heart failure

Diabetes

PATHOPHYSIOLOGY

The most common cause of cardiogenic shock is extensive myocardial infarction that depresses myocardialcontractility. Additional causes are listed in Table 50-2. Regardless of the precipitating cause, cardiogenicshock is primarily "pump failure," which results in reduced cardiac output. The systolic blood pressure dropsdue to poor cardiac output, and vital organ perfusion is limited. Absent a rise in systemic vascular resistance,the diastolic blood pressure also drops, resulting in coronary artery hypoperfusion. This creates a cycle ofworsening myocardial ischemia and pump dysfunction, and eventual decompensation.

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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 insu�iciency (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

Le� atrial myxoma

Pericardial tamponade

Historically, many believed cardiogenic shock was associated with a reflex compensatory vasoconstrictionthat would increase systemic vascular resistance. Contemporary data refute this belief, showing the average

systemic vascular resistance was not elevated in cardiogenic shock patients, even with vasopressor use.16

Furthermore, the average le� ventricular ejection fraction (EF) was only moderately depressed (~30%),17 anddiastolic dysfunction was seen early and frequently, and was associated with greater depression of EF and an

increased need for mechanical support.18,19

A systemic inflammatory response syndrome occurs a�er AMI and in cardiogenic shock, due to complementsystem activation and release of systemic inflammatory mediators, including cytokines and inducible nitric

oxide synthase.20,21 The inflammatory response also depresses pump function, dilates the peripheral

vasculature, and increases the risk of death.22 However, targeting nitric oxide with tilarginine does not alter

mortality, although it improves blood pressure.23 The monoclonal c5 antibody pexelizumab has beenstudied as an adjunct to percutaneous intervention in an e�ort to blunt the activation of the complement

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cascade associated with infarction. The largest trial of pexelizumab failed to show a mortality benefit

compared to placebo.24

Resolution of severe ischemia, neurohormonal, and inflammatory abnormalities may explain the reversiblenature of cardiogenic shock in some patients. The wide variations in EF, ventricular size, and vascularresistance suggest that the pathophysiology of cardiogenic shock is diverse and poorly understood.

CLINICAL FEATURES

HISTORY

History can be di�icult to obtain if the patient is severely ill. EMS personnel, family, or the medical recordmay o�er additional historical information, notably of existing ischemic heart disease. Patients commonlycomplain of shortness of breath, chest pain, or weakness. Through history, try to exclude other causes ofshock, such as sepsis, massive pulmonary embolism, hemorrhage, or a viral prodrome suggestingmyocarditis. Ask about a history of preexisting valvular disease, recent illnesses, hypercoagulable states,substance abuse, or other risk factors for cardiogenic shock as outlined in Table 50-1. Assess for other causesof shock because treatment di�ers depending on the cause of cardiovascular system failure (Table 50-3).

TABLE 50-3

Cardiogenic Shock: A Limited Di�erential Diagnosis

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)

PHYSICAL EXAMINATION

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Cardiogenic shock is characterized by hypoperfusion; this is not always accompanied by hypotension.9

Systolic blood pressure is usually <90 mm Hg, although it can be higher with preexisting hypertension. Apulse pressure <20 mm Hg is another finding if systemic resistance has not plummeted, and sinustachycardia is common unless the patient is on medications that block a tachycardic response. Unless thepatient has advanced to the stage of respiratory fatigue or agonal respirations, tachypnea is common. Thelung examination demonstrates rales due to the presence of pulmonary edema, except in cases of isolatedright-sided failure. Jugular venous distention and a positive hepatojugular reflex are usually present. Patientsare usually pale or cyanotic and may have cool skin and mottled extremities or other signs of hypoperfusion.Peripheral edema suggests preexisting heart failure. Diaphoresis indicates activation of the sympatheticnervous system. Cerebral hypoperfusion may result in altered mental status, and renal hypoperfusion maydecrease urine output.

If the cardiac point of maximal impulse is normally located, shock is likely due to an acute event. If the pointof maximal impulse is laterally shi�ed and di�use from cardiac remodeling and enlargement, long-standingcardiac disease with acute decompensation can be presumed. About 10% of cardiogenic shock a�er AMI is

caused by mechanical complications.14 A new murmur may be the only physical exam finding of mechanicalcatastrophe; carefully seek any loud or new systolic murmurs. Acute mitral regurgitation can occur fromchordae tendineae rupture or papillary muscle dysfunction, accompanied by a so� holosystolic murmur atthe apex radiating to the axilla with rales. With papillary muscle dysfunction, the murmur starts with the firstheart sound but terminates before the second. An acute ventral septal defect is associated with a new loudholosystolic le� parasternal murmur, o�en with a palpable thrill, that decreases in intensity as theintraventricular pressures equalize. Acute aortic insu�iciency is characterized by a so� diastolic murmur anda so�er S1 sound.

DIAGNOSIS

Clinical signs of cardiogenic shock include evidence of poor cardiac output with tissue hypoperfusion(hypotension, mental status changes, cool mottled skin) and evidence of volume overload (dyspnea, rales,jugular venous distention). Hemodynamic criteria for cardiogenic shock include (1) sustained hypotension

(systolic blood pressure <90 mm Hg), (2) reduced cardiac index (<2.2 L/min/m2), and (3) an elevated (>18 mmHg) pulmonary artery occlusion pressure. The causes and di�erential diagnosis of cardiogenic shock arelisted in Tables 50-2 and 50-3.

LABORATORY TESTING

There are no laboratory markers specific for the diagnosis of cardiogenic shock. Cardiac biomarkers(primarily troponin) may not be elevated upon initial presentation from an acute myocardial ischemictriggering event, but will eventually elevate. A CBC excludes anemia, which can contribute to cardiacischemia. The clinical presentation guides the need for specific drug levels (e.g., digoxin, ethanol, or illicitdrugs). Hypoperfusion commonly results in an elevated serum lactate, so checking serum lactate may aid

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diagnosis when overt hypotension is absent. Serum electrolytes and renal and hepatic studies can identifyend-organ dysfunction.

The level of serum B-type natriuretic peptide (BNP) is an indicator of le� ventricular dysfunction. Because ofits high negative predictive value, a normal BNP level (<100 picograms/mL) eliminates cardiogenic shock asthe cause of hypoperfusion unless very early a�er onset or with isolated right heart failure. Conversely, an

elevated BNP does not diagnose cardiogenic shock.25,26

Although elevated inflammatory markers such as C-reactive protein have some prognostic value, these are

rarely needed in the acute phase of care.27 Arterial blood gas measurements help identify those at risk ofcarbon dioxide retention, quantify the presence and severity of acidosis, and determine the contribution ofmetabolic or respiratory components to acidosis.

IMAGING AND ANCILLARY STUDIES

Electrocardiogram

The ECG helps detect ischemia or STEMI, evaluates for rhythm abnormalities, and provides evidence ofelectrolytic abnormalities (e.g., hypokalemia) or drug toxicity (e.g., digoxin).

It is important to assess for right ventricle (RV) involvement whenever ischemia is considered because RV

infarction is associated with an increased risk for cardiogenic shock and death.28 RV infarction is bestevaluated by obtaining right-sided ECG leads (usually V4R and V5R) (Figure 50-1). RV infarction complicating

inferior myocardial infarction is detected by ST elevation in lead V1 with depression in V2.

FIGURE 50-1.

Right-sided leads demonstrating right ventricular infarction associated with inferior wall myocardialinfarction. Right sided leads have replaced the normal le�-sided V leads. In this example, the ST-segmentelevation is prominent in leads VR3-6.

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Chest Radiography

Obtain a portable chest radiograph in all patients. Chest x-ray typically shows pulmonary congestion oredema, alveolar infiltrates, and pleural e�usion. These findings may lag by hours, so their absence does notexclude cardiogenic shock. Another confounder to interpreting the chest radiograph is underlying preexistingcardiopulmonary disease; pulmonary edema is di�icult to detect on chest radiography in patients withsevere chronic obstructive lung disease or interstitial lung disease. Cardiomegaly is the end result of long-standing myocardial remodeling, and its presence may not explain the acute symptoms. The chestradiograph can suggest alternative or confounding diagnoses, such as pneumonia, pneumothorax, aorticdissection, or progressive pericardial e�usion (globular cardiac shape).

Bedside Echocardiography

In the setting of cardiogenic shock, emergency bedside echocardiography can help exclude alternativeetiologies of shock, identify some mechanical complications, and guide therapy. Assessment should includeevaluation of the inferior vena cava (IVC) to determine volume status and estimate right atrial pressure. Asubcostal four-chamber view is helpful to visualize pericardial e�usion and identify cardiac tamponade.When tamponade is present, there is a pericardial e�usion with associated dilation of the IVC and diastoliccollapse of the RV with systolic collapse of the right atrium. When cardiac rupture has occurred, there may bea visible clot in the pericardial space. Subcostal, parasternal, and apical views together can help estimate EFand cardiac contractility. An aortic root measurement greater than 3 cm is concerning for ascending aorticdissection, especially when associated with a pericardial e�usion. Also assess mitral valve morphology andmotion. Apical four-chamber views are helpful for evaluating chamber size. In cases of acute right heartfailure due to ischemia, the RV will be dilated and the le� ventricle (LV) will appear to be smaller than

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expected due to low filling pressures. In le� heart failure there will be dilation of the LV secondary todecreased cardiac output and increased filling pressure.

Bedside echocardiography is not a substitute for emergent formal transthoracic echocardiography. Formalechocardiography is better able to use color and spectral Doppler to identify mechanical complications andto characterize the nature of cardiac impairment. Echocardiography can detect regional wall motionabnormalities and identify a lack of compensatory hyperkinesis in uninvolved cardiac segments. Loss of RVcontractility, RV dilatation, and normal estimated pulmonary pressures occur more commonly with RVinfarction.

Color flow Doppler transthoracic echocardiography can identify mechanical causes of cardiogenic shock,such as acute mitral regurgitation or ventricular septal defect. Echocardiography can detect other causes ofdecreased cardiac output, notably pulmonary embolism. Acute RV dilatation, tricuspid insu�iciency,paradoxical systolic septal motion, and high estimated pulmonary artery and RV pressures suggestpulmonary hypertension from an acute pulmonary embolus.

Mechanical Catastrophe Diagnosis

If mechanical catastrophe is suspected, consult cardiothoracic surgery immediately while obtaining abedside echocardiogram. In the case of myocardial free wall rupture, death is probable unless apseudoaneurysm forms. Pseudoaneurysm is detected as an acute pericardial e�usion on echocardiography.An acute ventricular septal defect is confirmed by color Doppler echocardiography or right heartcatheterization demonstrating oxygen saturation step-up from the right atrium to the RV. Acute mitralregurgitation, from papillary muscle rupture or dysfunction, can complicate AMI.

Hemodynamic Monitoring

Patients in cardiogenic shock typically have low cardiac index (<2.2 L/min/m2) and elevated LV end-diastolic

pressure (pulmonary artery occlusion pressure >18 mm Hg).29 Invasive hemodynamic monitoring with a

pulmonary artery catheter can provide data and guide treatment but is unavailable in most EDs.29 Centralvenous pressure measurements can help guide fluid resuscitation, with the trend in venous pressures beingmore important than absolute values. Most patients will require continuous blood pressure monitoring, o�enwith an indwelling catheter.

TREATMENT

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 therapysuch as revascularization in the cardiac catheterization laboratory or surgical intervention for mechanicalcatastrophe. 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

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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 proceedsimultaneously.

AIRWAY

Give supplemental oxygen, and monitor closely for impending or acute respiratory failure that will requireimmediate mechanical ventilation. Continuous positive airway pressure or bilevel positive airway pressurecan provide temporary airway support, but these methods require a hemodynamically stable, cooperativepatient—a set of conditions rare in those with cardiogenic shock.

Endotracheal intubation is o�en necessary to maintain oxygenation and ventilation. However, the change topositive pressure ventilation may further decrease preload and cardiac output and worsen hypotension. Beprepared to administer a fluid bolus in the absence of pulmonary congestion, initiate an appropriateinotrope if congested with a compensated blood pressure, or start a vasopressor if hypotension exists.

STABILIZATION

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 monitorurine output in response to therapy.

In AMI, give aspirin early (if not already taking long term) unless there is an absolute contraindication.32 Ifblood pressure is >90 mm Hg systolic, chest pain may be relieved by careful use of IV nitroglycerin ormorphine. 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 othervasodilators.

HYPOTENSION

Initial therapy is guided by clinical findings. Give crystalloid fluid boluses (250 to 500 cc) for an RV infarct withhypotension, if pulmonary congestion is absent. If there is no improvement with the fluid bolus or ifpulmonary congestion develops, vasopressors or inotropes are indicated (Table 50-4).

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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 le� 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 isa mainstay of initial pharmacologic treatment. Dobutamine may increase cardiac contractility and should beconsidered as an individual agent if systolic blood pressure is ≥90 mm Hg without signs of overt shock ororgan dysfunction. Avoid the use of dobutamine alone when the systolic blood pressure is <90 mm Hgbecause of its vasodilatory potential. O�en, a vasoconstrictor is needed in addition to dobutamine.Dopamine may increase cardiac work by increasing heart rate and may also increase LV end-diastolicpressure by its β-agonist e�ect. Combination therapy with a vasopressor (dopamine) and an inotrope(dobutamine) may be more e�ective than either agent alone. Norepinephrine when combined withdobutamine may have more of an e�ect on peripheral vasoconstriction than dopamine when combined withdobutamine. If the systolic blood pressure is <70 mm Hg, norepinephrine is preferred over dobutamine due

to its antithrombotic e�ect.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

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Epinephrine is an alternative to norepinephrine/dobutamine when dobutamine is not available; however, itis 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 abetter choice. Milrinone (a selective phosphodiesterase inhibitor) can be substituted for the catecholamine ifdobutamine is ine�ective.

Pure vasoconstrictors and α1-adrenergic receptor agonists, such as phenylephrine, are contraindicated

because they increase cardiac a�erload without augmenting cardiac contractility.

EARLY REVASCULARIZATION

In ischemic cardiogenic shock, early revascularization by percutaneous coronary intervention or coronaryartery bypass gra�ing is the treatment of choice. The greatest short-term benefit is reported in patients <75years 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 yearsold who have delayed or no revascularization, even though those >75 years old are less likely to receive

revascularization.41 Coronary artery bypass gra�ing requires extensive surgical and medical resources andposes operative risk for seriously ill patients. The cardiac surgeon will make an overall judgment, withoperative intervention chosen o�en for those with good prior functional status and less severe, earlypresentation 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 cuto� for percutaneous coronary

intervention.27,38,39,42

THROMBOLYTIC THERAPY

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 e�ective in establishingreperfusion in AMI with cardiogenic shock as it is in uncomplicated AMI. Survival from cardiogenic shock ishighest with emergency coronary intervention, followed by intra-aortic balloon pump combined withthrombolytic therapy; thrombolytic therapy alone is least e�ective in reducing mortality. Rescuepercutaneous 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 shockare available, if the hospital does not have a catheterization laboratory, or if there is prolonged transporttime for coronary intervention, thrombolytic therapy should be given to reduce mortality compared tosupportive treatment alone.

INTRA-AORTIC BALLOON PUMP COUNTERPULSATION

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Intra-aortic balloon pump counterpulsation provides hemodynamic support by decreasing a�erload (whichlowers myocardial oxygen consumption) and increasing diastolic blood pressure (which augments coronary

perfusion).38,42 Intra-aortic balloon pump improves survival a�er 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 le� ventricular assistdevice may augment cardiac output. This device is currently approved by the U.S. Food and DrugAdministration only as a bridge to transplantation, and most cardiogenic shock patients are not suchcandidates. Case studies have described successful support and weaning of patients su�ering from

cardiogenic shock in the setting of acute infarction.49,50,51,52,53 A recent meta-analysis failed to demonstratea mortality benefit for le� 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 maximummedical therapy has failed. The treating physician must consider the likelihood of recovery before institutingextracorporeal membrane oxygenation; patients with a very poor prognosis are not appropriate forextracorporeal membrane oxygenation. In the best cases, extracorporeal membrane oxygenation can providesupport until percutaneous coronary intervention can be performed or until the heart begins to recover a�erintervention. In other cases, it can provide a "bridge to decision" for transplant or permanent le� ventricularassist device placement.

DISPOSITION AND FOLLOW-UP

All patients with cardiogenic shock require admission to the intensive care unit at an institution with invasive

revascularization capability.10,30 In noncapable institutions, transfer should be accomplished as quickly as

possible.55,56 If no other definitive treatment modalities for cardiogenic shock are available, if the hospitaldoes not have a catheterization laboratory, or if there is prolonged transport time for coronary intervention,thrombolytic therapy should be given.

SPECIAL CONSIDERATIONS

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1. 

2. 

3. 

4. 

5. 

Compliance with guidelines for AMI has improved over the last two decades, although compliance in patients

with cardiogenic shock may be less.3,57,58 Some populations continue to face barriers to e�ective care,

especially the elderly and minorities.58,59 Compliance with recommended guidelines is needed in order toimprove outcomes. The most recent American College of Cardiology/American Heart Association guidelinesfrom 2011 recommend aggressive management of patients in cardiogenic shock. Class 1 recommendationsinclude percutaneous coronary intervention or coronary artery bypass gra� for STEMI patients in shock (levelof evidence B), percutaneous coronary intervention or coronary artery bypass gra� for NSTEMI patients inshock (level of evidence B), and transfer for rescue or facilitated percutaneous coronary intervention inpatients with persistent ischemia or shock despite lytic therapy (level of evidence B). European guidelines

reflect the same treatment priorities.60

Acknowledgment: We thank Jim Edward Weber and W. Frank Peacock for their contributions to the prioredition of this chapter.

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USEFUL WEB RESOURCES

American College of Cardiology Scientific Statements/http://www.cardiosource.org/science-and-quality/practice-guidelines-and-quality-standards.aspx.

Sonoguide: The Ultrasound Guide for Emergency Physicians—http://www.sonoguide.com/cardiac.html

For Patients: National Heart and Blood Institute Page on Cardiogenic Shock—http://www.nhlbi.nih.gov/health/dci/Diseases/shock/shock_what.html

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