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
    • Right 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-blocker
    • Calcium channel blocker
    • Adriamycin

Diagnosis

Signs and Symptoms

  • 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
    • Tachycardia
    • Weak pulses
  • General:
    • Cyanosis
    • Pallor
    • Diaphoresis
    • Dulled sensorium
    • Decrease in body temperature
    • Urine flow of <20 mL/hr
  • Neck:
    • Jugular venous distention
  • 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.
    • Systolic click:
      • Suggests rupture of the chordae tendineae
  • Abdominal:
    • Epigastric pain
    • Nausea and vomiting
  • Neurologic:
    • Obtundation

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.

Diagnostic Tests and 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 congestion
    • Pleural effusion
    • Cardiomegaly
    • Pneumonia
    • Pneumothorax
    • Pericardial effusion
  • 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

Differential Diagnosis

  • Obstructive shock:
    • Tension pneumothorax
    • Cardiac tamponade
    • Pulmonary embolism
    • Spontaneous esophageal rupture
    • Air embolus
  • Distributive shock:
    • Sepsis
    • Anaphylaxis
    • Addisonian crisis
    • Neurogenic shock
  • Hypovolemic shock:
    • Hemorrhage
    • GI losses
    • Dehydration
    • Burns

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:
    • Aspirin
    • Heparin
    • Thrombolysis if percutaneous coronary intervention or bypass surgery not available
    • GP IIb/IIIa inhibitors prior to percutaneous coronary intervention
  • Hypotension:
    • Norepinephrine is 1st-line vasopressor
    • Consider dopamine in absence of NE
  • Normotensive patient:
    • Dobutamine may be used with NE or dopamine; combine with nitroprusside in acute mitral regurgitation
    • Milrinone 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 centers
    • Early revascularization is the single most important life-saving measure

Medication

  • Dobutamine: 3–5 μg/kg/min, titrate to 20–50 μg/kg/min as needed IV
  • Dopamine: 3–5 μg/kg/min, titrate to 20–50 μg/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 μg/kg loading dose, 0.375–0.75 μg/kg/min continuous infusion IV
  • Nitroglycerin: 10–20 μg/min (peds: 0.1–1 μg/kg/min) IV, USE NON-PVC tubing
  • Nitroprusside: 0.3 μg/kg/min, titrate to a max. of 10 μg/kg/min IV
  • Norepinephrine: 2 μg/min, titrate up as needed IV

Ongoing Care

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.  [PMID:20200382]
  • 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.  [PMID:18250279]
  • Topalian S, Ginsberg F, Parrillo JE. Cardiogenic shock. Crit Care Med. 2008;36:S66–S74.  [PMID:18158480]

See Also

Shock; MI

Codes

ICD-9

785.51 Cardiogenic shock

ICD-10

Cardiogenic shock

SNOMED

  • 89138009 Cardiogenic shock (disorder)

Authors

Nadeem Alduaij


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