Cardiogenic Shock, Emergency Medicine

Basics

Description

- Persistent hypotension and tissue hypoperfusion due to cardiac dysfunction in the presence of adequate intravascular volume and left ventricular (LV) filling pressure - Most common cause of death in hospitalized patients with acute MI (AMI) - Underlying mechanisms in AMI: - Pump failure: - ≥40% LV infarct - Infarct in pre-existing LV dysfunction - Reinfarction

- Mechanical complications: - Acute mitral regurgitation - Ventricular septal defect - LV rupture - Pericardial tamponade

- ABCs and vital signs: - Patent airway (early) - Labored breathing and tachypnea (early); respiratory failure (late) - Diffuse crackles or wheezing - Hypoxia - Hypotension: - Systolic BP <90 mm Hg - Decline by at least 30 mm Hg below baseline level

- General: - Cyanosis - Pallor - Diaphoresis - Dulled sensorium - Decrease in body temperature - Urine flow of <20 mL/hr

- Cardiac: - Ischemic chest pain - Systolic apical blowing murmur - Gallop rhythm: - S3 reflects severe myocardial dysfunction. - S4 is present in 80% patients in sinus rhythm with AMI.

- Emergent echocardiography: - Transthoracic echocardiography (TTE) with color Doppler - LV contractility looking for hypokinesis, akinesis, or dyskinesis - Acute mitral regurgitation or septal defects - RV dilatation, tricuspid insufficiency, high pulmonary artery and RV pressures suggest pulmonary embolism - RV hypokinesis or akinesis, RV dilatation, normal pulmonary pressures suggest RV infarction - Pericardial effusion, right atrium or RV diastolic collapse suggest cardiac tamponade

- Distributive shock: - Sepsis - Anaphylaxis - Addisonian crisis - Neurogenic shock

- Hypovolemic shock: - Hemorrhage - GI losses - Dehydration - Burns

- AMI: - Aspirin - Heparin - Thrombolysis if percutaneous coronary intervention or bypass surgery not available - GP IIb/IIIa inhibitors prior to percutaneous coronary intervention

Persistent hypotension and tissue hypoperfusion due to cardiac dysfunction in the presence of adequate intravascular volume and left ventricular (LV) filling pressure
Most common cause of death in hospitalized patients with acute MI (AMI)
Underlying mechanisms in AMI:Pump failure:≥40% LV infarctInfarct in pre-existing LV dysfunctionReinfarctionMechanical complications:Acute mitral regurgitationVentricular septal defectLV rupturePericardial tamponadeRight ventricular (RV) infarction
5-8% of patients with STEMI develop cardiogenic shock
Role for a systemic inflammatory response syndrome via excess nitric oxide in the pathophysiology of cardiogenic shock
Role of initial treatment with β-blockers, ACEI, and high-dose diuretics in cardiogenic shock development

Etiology

AMI
Sepsis
Myocarditis
Myocardial contusion
Valvular disease
Cardiomyopathy
Left atrial myxoma
Drug toxicity:β-blockerCalcium channel blockerAdriamycin

Diagnosis

Signs and Symptoms

ABCs and vital signs:Patent airway (early)Labored breathing and tachypnea (early); respiratory failure (late)Diffuse crackles or wheezingHypoxiaHypotension:Systolic BP <90 mm HgDecline by at least 30 mm Hg below baseline levelTachycardiaWeak pulses
General:CyanosisPallorDiaphoresisDulled sensoriumDecrease in body temperatureUrine flow of <20 mL/hr
Neck:Jugular venous distention
Cardiac:Ischemic chest painSystolic apical blowing murmurGallop rhythm:S3 reflects severe myocardial dysfunction.S4 is present in 80% patients in sinus rhythm with AMI.Systolic click:Suggests rupture of the chordae tendineae
Abdominal:Epigastric painNausea and vomiting
Neurologic:

History

Obtain history from patient, family, or EMS for clues to possible etiology
Medications history

Physical Exam

Perform rapid survey and stabilize ABCs
Distended neck veins and cool extremities distinguish cardiogenic shock from distributive and hypovolemic shock
Careful heart and lung exam

Essential Workup

Ancillary studies further define the type and degree of cardiac injury and determine the indications for emergent catheterization or surgical intervention.

Diagnosis Tests & Interpretation

ECG:

Normal ECG does not rule out AMI.
Findings of AMI (ST-elevations in 2 or more contiguous leads)
May occur in non-ST-elevation acute coronary syndrome
Dysrhythmias
LV hypertrophy

Lab

B-type natriuretic peptide (BNP):Diagnostic and prognostic value
Creatine kinase (CK), CK-MB, troponin
Electrolytes and renal function:Acute renal failure is a strong predictor of mortality.
CBC:Identify anemia or elevated WBC.
Drug levels (e.g., digoxin)

Imaging

CXR:Pulmonary congestionPleural effusionCardiomegalyPneumoniaPneumothoraxPericardial effusion
Emergent echocardiography:Transthoracic echocardiography (TTE) with color DopplerLV contractility looking for hypokinesis, akinesis, or dyskinesisAcute mitral regurgitation or septal defectsRV dilatation, tricuspid insufficiency, high pulmonary artery and RV pressures suggest pulmonary embolismRV hypokinesis or akinesis, RV dilatation, normal pulmonary pressures suggest RV infarctionPericardial effusion, right atrium or RV diastolic collapse suggest cardiac tamponade

Differential Diagnosis

Obstructive shock:Tension pneumothoraxCardiac tamponadePulmonary embolismSpontaneous esophageal ruptureAir embolus
Distributive shock:SepsisAnaphylaxisAddisonian crisisNeurogenic shock
Hypovolemic shock:HemorrhageGI lossesDehydrationBurns

Treatment

Pre-Hospital

ABCs, IV access, O2, monitor
Consider fluid bolus if no crackles
Aspirin
Nitroglycerin or morphine sulfate for chest pain in absence of hypotension
Transport AMI patients to facility with 24-hr cardiac revascularization capability

Initial Stabilization/Therapy

ABCs
2 large-bore peripheral IV lines
Cardiac monitor
Endotracheal intubation for airway compromise:Consider etomidate for induction (minimal effect on BP)
Fluid challenge (100-250 mL normal saline) in absence of pulmonary congestion
Foley catheter to monitor urine output

Ed Treatment/Procedures

AMI:AspirinHeparinThrombolysis if percutaneous coronary intervention or bypass surgery not availableGP IIb/IIIa inhibitors prior to percutaneous coronary intervention
Hypotension:Norepinephrine is 1st-line vasopressorConsider dopamine in absence of NE
Normotensive patient:Dobutamine may be used with NE or dopamine; combine with nitroprusside in acute mitral regurgitationMilrinone may be considered in conjunction with dobutamine or dopamine
Pulmonary edema:Nitroglycerin drip or furosemide in the normotensive patient
Prompt cardiology consultation is crucial for the initiation of the following therapies:IABP independently improves survival in experienced centersEarly revascularization is the single most important life-saving measure

Medication

Dobutamine: 3-5 Î¼g/kg/min, titrate to 20-50 Î¼g/kg/min as needed IV
Dopamine: 3-5 Î¼g/kg/min, titrate to 20-50 Î¼g/kg/min as needed IV
Furosemide: 40-80 mg/d (peds: 1 mg/kg IV or IM, not to exceed 6 mg/kg) IV or IM
Milrinone: 50 Î¼g/kg loading dose, 0.375-0.75 Î¼g/kg/min continuous infusion IV
Nitroglycerin: 10-20 Î¼g/min (peds: 0.1-1 Î¼g/kg/min) IV, USE NON-PVC tubing
Nitroprusside: 0.3 Î¼g/kg/min, titrate to a max. of 10 Î¼g/kg/min IV
Norepinephrine: 2 Î¼g/min, titrate up as needed IV

Follow-Up

Disposition

Admission Criteria

All patients in cardiogenic shock require admission to a critical care unit.

Pearls and Pitfalls

Cardiogenic shock is the leading cause of death in inpatient AMI.
Early recognition of preshock states is essential.
Early revascularization offers better outcomes.

Additional Reading

De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010;362:779-789.
Peacock WF, Weber JE. Cardiogenic shock. In: Tinitinalli JE, Stapczynski JS, eds. Emergency Medicine: A Comprehensive Study Guide. New York, NY: McGraw-Hill; 2010.
Reynolds HR, Hochman JS. Cardiogenic shock: Current concepts and improving outcomes. Circulation. 2008;117:686-697.
Topalian S, Ginsberg F, Parrillo JE. Cardiogenic shock. Crit Care Med. 2008;36:S66-S74.

Codes

ICD9

785.51 Cardiogenic shock

ICD10

R57.0 Cardiogenic shock

SNOMED

89138009 Cardiogenic shock (disorder)