Intensive Care Medicine

Cardiogenic shock

Learning outcomes

  • The student defines cardiogenic shock.
  • The student understands the pathophysiological mechanisms of cardiogenic shock and its clinical manifestation
  • The student knows the basic diagnostic and therapeutic management of cardiogenic shock

Below is a summary of the chapter content. The topic is described in detail in the book Oxford Handbook of Critical Care, see below. This chapter is a review and will use your knowledge from previous courses.

Cardiogenic shock is covered in the Intensive Medicine curriculum as the first of the four types of shock, and it is also the first of four subsequent lessons that will address the issue of circulatory shock.

Circulatory shock

is a form of circulatory failure with generalized oxygen deficiency in the cells (tissues) of the human body.

There is a disparity between the actual oxygen supply by cardiovascular circulation and the required oxygen demand by the body.

Circulatory shock

very often leads to organ dysfunction, often affecting multiple organs, and is the most common global cause of death in ICU patients.

Types of shock according to the pathophysiological process leading to failure of oxygen delivery:

  • hypovolemic shock
  • cardiogenic shock
  • obstructive shock 
  • distribution shock

Each type will be described in more detail in the following chapters.

Cardiogenic Shock (CS)

is characterized by insufficient cardiac output and hypoperfusion of peripheral tissues. Cardiogenic shock is a life-threatening syndrome caused primarily by cardiac pump dysfunction.

Cardiogenic shock can be divided into:

  • predominant failure of left ventricle
  • predominant failure of right ventricle
  • biventricular failure

Common etiologies of CS

  • Primary myocardial dysfunction
    - ischemia/infarction, myocarditis, cardiomyopathy (septic, stress,...)
  • Valvular dysfunction
    - bacterial endocarditis (aortic, mitral) with acute regurgitation
    - papillary muscle rupture with acute mitral regurgitation
  • Arrhythmia
    - tachycardia, bradycardia
  • Other causes
    - negative inotropes, endocrinopathy

Signs and symptoms of CS

  • Common signs of tissue hypoperfusion
    more or less expressed in all types of shocks, in particular:
    • Skin changes
      - cold, clammy, mottling, acrocyanosis, prolonged CRT
    • Altered mental state
      - qualitative (agitation, confusion) 
      - quantitative (coma)
    • Oliguria/Anuria
      - diuresis < 0.5 (0.1) ml/kg/hod for 6 hours

  • Specific symptoms: angina, chest pain, palpitations, arrhythmias,   pulmonary oedema, peripheral oedema

Diagnostics of CS

  • Patient history
  • Clinical examination (see. Signs and symptoms)
  • Labs
    -     Markers of tissue hypoxia: lactate elevation (metabolic acidosis)
    -     Markers of myocardial injury and stress: elevation of troponin levels, natriuretic peptides (NT-pro BNP / BNP)
    - Markers of end-organs dysfunction: urea, creatinine, liver enzymes

  • EKG
    signs of Myocardial     ischemia: STEMI (ST-elevation myocardial infarction), NSTEMI (ST segment depression), new left bundle branch block (LBBB) 
    Arrhythmias (see. previous chapter)

  • Echocardiography
    - bedside information about cardiac structure and function
    - diagnosis of the underlying cause (systolic dysfunction - decreased contractility, diastolic dysfunction - elevated filling pressures, valvular pathology)
    - tool for evaluation of therapeutic intervention 

  • Invasive hemodynamic monitoring
    Basic hemodynamic monitoring
    - Arterial pressure (systolic; diastolic; pulse pressure - difference between systolic and diastolic; mean arterial pressure MAP = 1/3 of pulse pressure + diastolic pressure)
    - Central venous pressure
    Advanced haemodynamic monitoring
    - Transpulmonary dilution, pulmonary artery (Swan-Ganz) catheter

Management and therapy of CS

The goal of the therapy is to improve cardiac output and restore perfusion to vital organs.

The ABCDE procedure and the "treat-as-you-go" approach
e.g., the provision of oxygen therapy, ventilatory support, and correction of ions or acid-base disorders.

In addition, circulatory support, with the following steps:

  • Identification and treatment of the underlying cause
    - myocardial revascularization: percutaneous coronary intervention (PCI), coronary artery bypass grafting (CABG)
    - arrhythmia management
    - valvular disease management

  • Optimization of myocardial contractility - Inotropic support
  • - sympathomimetics (dobutamine, adrenaline)
  • - phosphodiesterase III inhibitors (milrinone) 
  • - calcium sensitizers (levosimendan)

  • Optimization of intravascular filling - Preload
  • - targeted and individualized fluid administration in specific cases
  • (e.g. LVOT obstruction in hypertrophic cardiomyopathy)
  • - diuretics or renal function replacement (IHD, CRRT) in volume overload
  • (tissue and organ congestion, pulmonary edema)

  • Optimization of systemic blood pressure - Afterload
  • - Vasopressors increase systemic vascular resistance and blood pressure
  • - Mean arterial pressure (MAP) is a macrohemodynamic determinant of organ perfusion
  • Mean arterial pressure (MAP)

    The recommended target MAP value is currently ≥ 65mmHg.
    The vasopressor of choice to maintain it is noradrenaline (norepinephrine).

  • Heart rate optimization: see previous chapter arrhythmias

Refractory cardiogenic shock

is persistent low cardiac output and hyperlactatemia despite adequate initial management. Its management often involves the implantation of temporary mechanical circulatory support (MCS) as a rescue procedure:
  • Intraaortic balloon counterpulsation (IABP)
  • Impella
  • VA ECMO
The issues surrounding these techniques are highly specialized, go beyond the required curriculum content, and belong to the intensivist or cardiologist's expertise.

Oxford Handbook of Critical Care. SINGER Mervyn, WEBB R. Andrew

  • Heart failure - assessment p. 392 and management p. 394

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