Cardiogenic shock



Background

Cardiogenic shock (CS) is a low-cardiac-output state resulting in critical end-organ hypoperfusion and hypoxia in the presence of euvolemia.

Acute myocardial infarction (AMI) is the leading cause of CS (accounting for 80% of patients with CS).

Cardiogenic shock is the leading cause of mortality in the setting of acute myocardial infarction (40-50%).

Definition

Low cardiac output(CO) state resulting in critical end organ hypoperfusion and hypoxia.

  • Persistent ↓BP despite fluid resusc.
  • Cold extremities
  • Oliguria
  • Altered mentation
  • Labs: ↑lactate, ↑creatinine, ↓pH

Pathophysiology

Cycle of myocardial contractility depression ⇒ ↓ cardiac output (CO) ⇒ ↓BP ⇒ further coronary insufficiency ⇒ further ↓CO.

A systemic inflammatory response is triggered by acute myocardial injury which may lead to pathological vasodilation. This leads to the release of nitric oxide synthase and peroxynitrite which have cardiotoxic inotropic effects. The reduction in cardiac index leads to severe tissue hypoxaemia.


Aetiology

Myocardial

  1. Acute MI
  2. Mechanical complication of AMI:
    1. Papillary muscle rupture
    2. Ventricular septal rupture
    3. Free wall rupture
  3. Acute decompensated heart failure:
    1. Chronic heart failure with decompensation
    2. Acute heart failure 1st presentation
      1. Chronic ischaemia
      2. Dilated cardiomyopathy
      3. Myocarditis
      4. Stress cardiomyopathy (Takotsubo)
      5. Pregnancy associated heart disease:
        1. Peri-partum cardiomyopathy
        2. Coronary artery dissection
      6. Endocrine (↑/↓ T4, pheochromocytoma)
    3. Post-cardiotomy shock
    4. Dynamic outflow tract obstruction
    5. Post cardiac arrest stunning
    6. Myocardial depression in septic shock/SIRS
    7. Myocardial contusion

Valvular

  1. Native valve
    1. Stenosis
    2. Acute regurgitation
    3. Valvular obstruction
  2. Prosthetic valve
    1. Valve obstruction
    2. Leaflet failure or restriction
    3. Mechanical failure
    4. Valve dehiscence

Electrical

  1. Atrial arrhythmia with rapid vent. rate
  2. Ventricular tachycardia
  3. Bradycardia

Extra-cardiac / obstructive

  1. Cardiac tamponade
  2. Constriction
  3. Pulmonary embolism

Other

  1. Toxidromes
  2. Hypothermic myocardial depression

Differential Dx

  • Hypovolemic shock (haemorrhage, internal fluid losses (3rd spacing), GI losses)
  • Distributive shock (sepsis, anaphylaxis)
  • Obstructive shock (PE, cardiac tamponade, tension pneumothorax)

Investigations

Labs

CXR

ECG / TTE

ECG

  • STEMI/NSTEMI, PE
  • Acute myocarditis
  • Electrolyte imbalances
  • Drug toxicity

Transthoracic echocardiogram

  • Haemodynamic status
  • Exclude mechanical complications (papillary/septal/wall rupture)

Management

Reperfusion and Revascularisation

Coronary reperfusion is the mainstay therapeutic intervention for patients with acute MI presenting cardiogenic shock.

Fibrinolytic Therapy

When early reperfusion cannot be completed in a timely fashion, fibrinolysis can be considered in CS with STEMI.

Stabilization and Resuscitation

Haemodynamic stabilization (volume expansion, vasopressors and inotropes).

Treat/prevent multi-organ failure:

  • Mechanical ventilation
  • Continuous renal replacement therapy
  • Mechanical circulatory support

Intravenous fluids

Fluid challenge should be considered unless there are signs of overt fluid overload.

Vasopressor support

Norepinephrine is the vasopressor of choice (fewer arrhythmias). Usual infusion dose: 0.05 – 0.4 mcg/kg/min.

Central

inotropes
Agent Mechanism Effect Indications Considerations Usual infusion dose Preparation

Norepinephrine

α<β agonist Inotropy, chronotropy, dromotropy and vasoconstriction (↑↑SVR, ↑CO) Most common first line agent in shock Most benefits demonstrated in septic shock 0.05-0.4mcg/kg/min Norepinephrine Preparation

Epinephrine

Inotropy, chronotropy, dromotropy and vasoconstriction (↑↑SVR, ↑↑CO) 2nd line agent or 1st line in anaphylactic shock Sepsis Surviving sepsis guidelines support epinephrine as 2nd line agent 0.01-0.5mcg/kg/min Epinephrine preparation

Dobutamine

β1 and β2 Inotropy+, coronary perfusion ↑ Cardiogenic shock (low CO) Beware different "EM" (1mg/ml soln.) and "ITU" (2mg/ml soln.) dilutes 2.5-5 mcg/kg/min Dobutamine preparation

Peripheral

inotropes
Agent Mechanism Effect Indications Considerations Usual infusion dose Preparation

Metaraminol

α1 agonist, mild β1 agonist (&, indirect release endogenous noradrenaline) Vasoconstriction. Mild inotropic effect Short term Mx acute hypotension (before central line) Given via peripheral line. Agent of choice in initial resusc. 0.5 to 1mg (1 to 2mL of diluted solution) every 2–5 minutes as required Metaraminol preparation (await content)

Phenylephrine

α1 agonist Vasoconstriction (↑↑SVR) Various forms of shock Caution in cardiac dysfunction - ↑afterload 0.1-10mcg/kg/min Phenylephrine preparation

Oxygenation and ventilation

  • Continuous pulse oximetry to identify respiratory compromise early
  • NIV for pulmonary oedema should be considered if able to tolerate
  • Invasive ventilation with lung-protective settings if NIV is inadequate or airway protection is required

Be prepared for potential haemodynamic deterioration associated with induction, inappropriate ventilatory settings or vagal stimulation with endotracheal tube placement.

Continuous renal replacement therapy

Acute kidney injury (AKI) occurs 13 – 28% in patients with cardiogenic shock. Patients with cardiogenic shock are unable to tolerate fluid shifts associated with intermittent haemodialysis and therefore will require continuous renal replacement therapy.

Mechanical circulatory support

Intra-aortic balloon-pump: consider in patients with cardiogenic shock with mechanical complications of AMI (papillary muscle / septal / free wall rupture).



References

Management of cardiogenic shock complicating myocardial infarction: an update 2019. Holger Thiele,  E Magnus Ohman et. al. European Heart Journal, Volume 40, Issue 32, 21 August 2019, Pages 2671–2683, https://doi.org/10.1093/eurheartj/ehz363.

Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association. Sean van Diepen, Jason N. Katz et. al. Circulation.2017;136:e232-e268.

Cardiogenic Shock. Cyrus Vahdatpour, et. al. J Am Heart Assoc. 2019;8:011991.

Cardiogenic Shock. Semhar Z. Tewelde, Stanley S. Liu et.al. Cardiol Clin 36 (2018) 53-61.

Main Considerations of Cardiogenic Shock and Its Predictors: Systematic Review. Maria Christiane Valeria Braga Braile-Sternieri et. al. Cardiol Res. 2018 Apr;9(2):75-82. doi: 10.14740/cr715w. Epub 2018 Apr 25.

Intraaortic Balloon Support for Myocardial Infarction with Cardiogenic Shock. Holger Thiele, Uwe Zeymer et. al. N Engl J Med 2012;367:1287-1296.

Early revascularization in acute myocardial infarction complicated by cardiogenic shock. Judith S. Hochman, Lynn A et. al., for the shock investigators. N Engl J Med 1999;341:625-634. https://www.nejm.org/doi/pdf/10.1056/NEJM199908263410901.

Surviving Sepsis.


Content By Dr Arina Kruis, Dr Íomhar O' Sullivan 22/09/2020. Last review Dr ÍOS 11/06/21.