Shock is a state in which the oxygen (O2) and metabolic demands of the body are not met by the cardiac output. When this process occurs in a single organ, rather than throughout the body, organ ischemia and infarction ensue. When shock occurs on a more global level, multiorgan dysfunction and failure are the consequence, ultimately leading to death if not corrected.

Shock is most often accompanied by hypotension, termed decompensated shock. However, shock may also occur with normal or elevated blood pressure. Examples include hypertensive emergency with compromised cardiac output, or carbon monoxide intoxication with the inability to deliver O2 despite normal hemodynamics. The approach to the patient in shock must proceed with the same urgency as the patient suffering from an acute myocardial infarction or cerebral vascular accident.

Classification
Shock states are classified according to the underlying physiologic derangement.

Hypovolemic shock:

  • Hemorrhage
  • Fluid loss/dehydration

Cardiogenic shock:

  • Pump failure
  • Valvular disorders
  • Cardiac dysrhythmia

Distributive shock:

  • Sepsis
  • Anaphylaxis
  • Intoxications

Neurogenic shock:

  • Spinal cord injury

Obstructive shock:

  • Tension pneumothorax
  • Pericardial tamponade/constrictive pericarditis
  • Massive pulmonary embolus
  • Severe pulmonary hypertension
  • Severe valvular stenosis

Differential diagnosis

Physical examination and right heart catheterization are useful in the determination of the etiology of the various shock states, but the latter is rarely immediately available in the emergency department (ED).

Hypovolemic shock

Hypovolemic shock is defined by the loss of intravascular volume. CVP, pulmonary artery occlusion pressure (PAOP), and cardiac output are low, while SVR is elevated. In the early compensated stages, the pulse pressure is narrowed due to vasoconstriction, but ultimately hypotension occurs with decompensation. The initial treatment of hypovolemic shock is aggressive volume expansion with crystalloid solution. Transfusion of blood products may be required if hemorrhage is the cause of hypovolemia.

Cardiogenic shock

The most common cause of cardiogenic shock is acute myocardial infarction, accounting for nearly half the cases. Low cardiac output and high SVR characterize cardiogenic shock. CVP and PAOP are most often elevated during acute exacerbations of CHF, but may be normal if the patient has received adequate diuresis. Suggested cardiac parameters for the diagnosis of cardiogenic shock include cardiac index (CI) 1.8L/min/m2, SBP 80mmHg, and PAOP 18cmH2O. The initial treatment of CHF includes preload and afterload reduction. When shock is present, addition of a cardiotonic vasopressor is required.

Strong evidence supporting selection of one vasopressor over another does not exist. Consensus committee (ACC/AHA) has recommended the use of dobutamine if SBP is greater than 90, dopamine if SBP is less than 90, and norepinephrine if hypotension is severe or refractory to dopamine infusion. An intra-aortic balloon pump (IABP) should be considered for patients who do not respond to vasopressor therapy. This technique employs placing an intra-aortic balloon that inflates during diastole, augmenting MABP and systemic perfusion, and deflates during systole, effectively diminishing afterload and improving cardiac output. Percutaneous coronary angioplasty and/or coronary artery bypass grafting should be strongly considered in patients with acute coronary ischemia complicated by shock.

Distributive shock

In early sepsis, SVR is elevated. However, as septic shock progresses, SVR drops precipitously. Cardiac output is increased in most cases, but a cytokine known as myocardial depressant factor is believed to be released from the pancreas, and may impair systolic function in later stages. Impaired cardiac perfusion will also adversely affect cardiac output. Vascular permeability is increased. Fluid shifts and increased insensible losses may lead to intravascular volume depletion and low CVP and PAOP. Early broad-spectrum antibiotic therapy and emergent surgical drainage or debridement, when indicated, are the cornerstones of treatment. Volume replacement should be guided by invasive monitoring of either CVP or PAOP.

Norepinephrine is the vasoactive agent of choice. Recently introduced to the US, activated protein C complex (Xigris®) may improve survival.

Anaphylactic shock is accompanied by the massive release of cytokines in an inflammatory cascade, with loss of vasomotor tone and increased vascular permeability. Epinephrine, steroids, and antihistamines are initial therapies. Persistent hypotension requires infusion of an agent that supports vasomotor tone. Again, norepinephrine makes the most sense physiologically.

Neurogenic shock

Neurogenic shock, classified by some as a type of distributive shock, is a consequence of injury to the sympathetic ganglion chain. Neurogenic shock characteristically manifests as hypotension and bradycardia. Since spinal cord injury is most prevalent in the young population, this entity usually occurs in patients with normal cardiac function.

It is of the utmost importance to rule out occult hemorrhage, and to use signs of organ perfusion to guide the initiation of pharmacologic therapy. Many of these patients perfuse their organs well at below-normal MABP. If signs of hypoperfusion develop, then selection of an agent that supports SVR (norepinephrine or neosynephrine) makes the most sense physiologically.

Obstructive shock

Two causes of obstructive shock, tension pneumothorax and cardiac tamponade, are reversible by surgical intervention. Support of the patient by volume loading is temporizing at best. Massive pulmonary embolus causes the release of vasoactive cytokines from the pulmonary vascular bed, obstruction of flow, and acute right ventricular dysfunction, collectively impairing left ventricular filling. Thrombectomy or thrombolysis can be life-saving interventions. Support of cardiac function with volume infusions and dobutamine may be a bridge to these interventions. Chronic pulmonary hypertension may also limit flow through the pulmonary vascular bed.

The onset of shock is an end-stage, pre-terminal event. Treatment with potent pulmonary vasodilators is hazardous in this shock state since hypotension from peripheral arterial dilation is a frequent side effect, mandating use of a pulmonary artery catheter.