• Clinical science

Shock

Abstract

Content currently under development

Shock is a life-threatening circulatory disorder that leads to tissue hypoxia and a disturbance in microcirculation. There are many different causes of shock, which are classified into cardiogenic shock (e.g., as a result of acute heart failure or cardiac tamponade), hypovolemic shock (e.g., following massive blood or fluid loss), and shock due to a disturbance in the fluid distribution in the body (septic, anaphylactic, and neurogenic shock). The common clinical findings are hypotension and tachycardia, accompanied by specific symptoms related to the cause of shock. Hypoxia can result in organ damage and complex metabolic disorders such as kidney failure, DIC (disseminated intravascular coagulation), ARDS (acute respiratory distress syndrome), and circulatory collapse. Management of shock involves circulatory support and the treatment of the underlying cause. Shock is associated with a very high mortality rate.

Pathophysiology

Content currently under development

  • Shock is a life-threatening disorder of the circulatory system which results in inadequate organ perfusion
  • The causes for inadequate organ perfusion may differ, but they all ultimately result in tissue hypoxia:
  • Generalized tissue hypoxia causes life-threatening metabolic disturbances and ultimately irreversible organ damage

Stages of shock

  1. Non-progressive phase: (stage of compensation): activation of compensatory neurohumoral reflexes in order to maintain vital organ perfusion
    • Peripheral vasoconstriction → cold, clammy extremities and increased capillary refill time
      • Decreased capillary hydrostatic pressure; → increases absorption of interstitial fluids into intravascular space to help maintain blood pressure
    • Tachycardia
    • Oliguria
  2. Progressive phase
    • Worsening hypotension
    • Hypoperfusion of peripheral tissues → generalized tissue hypoxiaanaerobic metabolism in the underperfused organs → lactic acidosis
      • Worsening tachypnea
      • Precapillary dilation and postcapillary constriction of the blood vessels → pooling and stasis of blood in the capillary bed → decreased cardiac output and formation of microthrombi in the capillaries → DIC and further hypoxic injury to tissues
    • Acidosis, cerebral hypoperfusion → altered mental status
  3. Irreversible phase: (stage of decompensation): irreversible tissue damage sets in
    • Cerebral hypoxiaautonomic dysfunction → worsening of shock
    • Myocardial ischemiaacute coronary syndrome → decreased cardiac output → worsening of shock
    • Widespread cell necrosis
      • Release of lysosomal enzymes → further tissue injury → worsening of shock
      • Activation of the immune system → release of cytokinesDIC, further tissue damage → worsening of shock
    • Bowel ischemia → bacteremic sepsis → worsening of shock
    • The end result of these vicious cycles is a downward spiral from which there is no recovery (multiple organ failure)

These separate stages may not occur in the case of severe insults (e.g., severe hemorrhage from an abdominal aneurysm, cardiac tamponade). These stages may also not be very distinct in the case of septic shock.

Hypotension, oliguria, tachycardia, and altered mental status indicate that the patient is in shock!

Multiorgan dysfunction (MODS)

The prognosis is highly dependant on the cause as well as the time it takes to initiate treatment.

References:[1][2][3]

Hypovolemic shock

Content currently under development

Classification of hemorrhagic shock
Class I II III IV
Blood loss < 15% 15–30% 30–40% > 40%
Heart rate < 100 100–120 120–140 > 140
Systolic blood pressure Normal Normal
Pulse pressure Normal or ↑
Respiratory rate 14–20 20–30 30–40 > 35
Urine output > 30 mL/hr 20–30 mL/hr 5–15 mL/hr Absent
Mental status Anxious Mildly anxious Anxious, confused Confused, lethargic

Remember occult sites of hemorrhage in the case of trauma; blood on the floor (external hemorrhage) and four more, i.e., internal hemorrhage in the chest, abdomen (peritoneal cavity), pelvis (retroperitoneum), and thigh!

A patient can bleed and yet show a “normal” hemoglobin value (hyperacute bleeding without the compensatory “dilution effect”); in the case of hemorrhage, hemoglobin value will only start to drop after 8–12 hours, when the interstitial fluid shifts into the plasma. Continuous monitoring of the blood pressure and the heart rate is, therefore, more important in the acute setting!

Upon suspecting hemorrhage, perform blood grouping and cross-matching and have packed RBC concentrates at hand for transfusion!

References:[4][5][6]

Cardiogenic shock

Content currently under development

Unlike other causes of shock the administration of intravenous fluids in most cases of cardiogenic shock would worsen cardiogenic pulmonary edema!

The only accepted indication for fluid therapy in cardiogenic shock is right ventricular dysfunction with a normal RV afterload (e.g., following an inferior wall MI). Such a scenario is seen only in 5% of cases of cardiogenic shock. In such cases, carefully administered fluid boluses may be used to maintain the RV end-diastolic pressure (RV preload) in the optimal range of 8–12 mm Hg in order to maintain the cardiac output!

References:[4][5][7]

Distributive shock

Content currently under development

References:[8]

Septic shock

Content currently under development

References:[4][9]

Neurogenic shock

Content currently under development

In a patient who develops hypotension following high-energy trauma, neurogenic shock is a diagnosis of exclusion that is made after hypovolemic and obstructive cardiogenic shock have been ruled out!

References:[4][9][10]

Anaphylactic shock

Content currently under development

References:[11][12][13]

Diagnostics

Content currently under development

Differential diagnoses of shock
Type of shock Hypovolemic shock Cardiogenic shock Distributive shock
Septic shock Neurogenic shock Anaphylactic shock
Relative frequency 16% 18% 62% 2%
Cardiac output / Cardiac index
Heart rate
Central venous pressure ↔ or ↓ ↔ or ↑ ↔ or ↓ ↔ or ↓ ↔ or ↓
Pulmonary capillary wedge pressure (PCWP)
Left ventricular end-diastolic pressure (LVEDP)
Peripheral vascular resistance
Mixed venous oxygen saturation (SvO2)

More than one type of shock can occur simultaneously (e.g., with burns), which can make a specific classification impossible!

References:[5][11][14][15]

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  • 8. Lessnau KD. Distributive Shock. In: Pinsky MR. Distributive Shock. New York, NY: WebMD. https://emedicine.medscape.com/article/168689-overview. Updated January 5, 2018. Accessed February 27, 2018.
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  • 12. Mustafa SS, Kaliner MA. Anaphylaxis. In: Anaphylaxis. New York, NY: WebMD. http://emedicine.medscape.com/article/135065. Updated February 22, 2017. Accessed March 9, 2017.
  • 13. Campbell RL, Li JTC, Nicklas RA, Sadosty AT. Emergency department diagnosis and treatment of anaphylaxis: a practice parameter. Ann Allergy Asthma Immunol. 2014; 113(6): pp. 599–608. doi: 10.1016/j.anai.2014.10.007.
  • 14. Beachey W. Respiratory Care Anatomy and Physiology: Foundations for Clinical Practice. St. Louis, MO: Elsevier Mosby; 2013.
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  • Herold G. Internal Medicine. Cologne, Germany: Herold G; 2014.
last updated 06/21/2018
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