Clinical Skills Emergency Medicine & Critical Care

The Many Types of Shock

ARTICLE LAST UPDATED DECEMBER 2013 5 MIN READ PEER REVIEWED WEB-EXCLUSIVE

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Shock, a syndrome in which clinical deterioration can occur quickly, has many causes, each
one requiring careful analysis and rapid treatment. Broad definitions for shock include
inadequate cellular energy production or the inability of the body to supply cells and tissues
with oxygen and nutrients and remove waste products. Without rapid intervention, shock
ultimately leads to cell death. Although hypovolemic shock is the most common clinical form
of shock, other forms of shock include cardiogenic shock, distributive shock, obstructive
shock, hypoxic shock, and metabolic shock. Determining type of shock can be complicated,
as not only are there are many forms of shock, but their definitions overlap.

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Hypovolemic or Circulatory Shock
Hypovolemic or circulatory shock is the most common cause of shock seen in small animal
practice. Hypovolemic shock results from a decreased intravascular volume, and causes
commonly include hemorrhage, severe dehydration, and hypoproteinemia. Intraabdominal
hemorrhage (Figure 1) may occur as a result of a ruptured splenic or hepatic mass, a
coagulopathy, or trauma. Severe dehydration may be seen with prolonged fluid losses, as can
be seen with vomiting and/or diarrhea.

Figure 1. Ultrasound image: peritoneal effusion and splenic mass

Patients with hypovolemic shock present with such signs as pale mucous membranes (Figure
2), prolonged capillary refill time (CRT), tachycardia, and poor pulse quality. Treatment
includes rapid administration of IV fluids and may include isotonic crystalloids, hypertonic
crystalloids (eg, 7.5% NaCl), synthetic colloids, or blood products.

Figure 2. Triage examination with a concern for pale-white mucous membranes

Cardiogenic Shock
As compared with the decreased intravascular fluid volume in hypovolemic shock,
cardiogenic shock is a failure of the heart pump associated with a normal to increased
intravascular volume, leading to decreased cardiac output. Causes include congestive heart
failure, myocardial abnormalities (eg, dilated cardiomyopathy, hypertrophic
cardiomyopathy), or cardiac arrhythmias. Treatment (which typically does not include IV fluid
therapy) depends on the underlying disease process: β-agonist therapy for decreased
myocardial contractility (eg, dobutamine), diuretic therapy for excessive preload (eg,
furosemide), or therapy to reduce afterload in cases of severe valvular disease (eg,
nitroprusside). Patients with cardiogenic shock often have unique examination findings (eg,
tachypnea, dyspnea, auscultation of abnormal lung sounds [pulmonary crackles]) to help
differentiate this shock type from others.
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Distributive Shock
Distributive shock is often seen as a relative hypovolemia, resulting from a maldistribution of
blood flow despite adequate total body fluid volume. Causes of distributive shock include
Systemic Inflammatory Response Syndrome (SIRS), sepsis, and anaphylaxis. Treatment is
complex and warrants identification of the underlying disease process to provide goal-
directed therapy, which may include IV fluid therapy, vasopressors, and inotropic therapy.
Hemodynamic changes in distributive shock can be subdivided into early or late phases.
Examination findings in early distributive or septic shock are characterized by peripheral
vasodilation that causes bright (brick) red mucous membranes, a rapid (<1 second) CRT,
tachycardia, and hyperdynamic femoral pulses. In late distributive shock, peripheral vascular
paralysis results in hypoperfusion, characterized by pale mucous membranes, tachycardia,
and poor femoral pulse quality.

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Obstructive Shock
Obstructive shock is caused by any obstruction or maldistribution of blood flow that results in
a decreased preload and subsequent decreased cardiac output. Causes of obstructive shock
include gastric dilatation–volvulus (GDV), caval syndrome from heartworm disease, and
pericardial effusion (Figure 3). Therapy involves identification and correction of the
underlying cause of the obstruction—for example, stomach decompression in GDV or
pericardiocentesis for pericardial effusion. Similar to hypovolemic shock treatment, IV fluid
therapy can be beneficial for cases of obstructive shock.

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Figure 3. Ventrodorsal thoracic radiograph with severe, globoid cardiomegaly

Hypoxic Shock
Hypoxic shock is seen with normal tissue perfusion but decreased oxygen content of arterial
blood. The equation for oxygen content is:

CaO2 = Hb (gm/dl) x 1.34 ml O2/gm Hb x SaO2 + PaO2 x (.003 ml O2/mm Hg/dl)

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The value in understanding this equation and its relationship with hypoxic shock is that
tissues need a requisite amount of oxygen for normal metabolism. Neither the PaO2 nor the
SaO2 provide information on the number of oxygen molecules in the blood. Of the three
values used for assessing blood oxygen levels (ie, CaO2, PaO2, and SaO2), CaO2 is the only
value that has a measure of units, notably O2/dl. This is because CaO2 is the only value that
incorporates the hemoglobin content.

The most common causes of hypoxic shock include pulmonary disease resulting in a low
partial pressure of arterial oxygen and anemia resulting in low levels of hemoglobin,
impairing oxygen delivery to the tissues. Treatment often begins with oxygen therapy;
however, if severe anemia is present, oxygen therapy alone will not be sufficient to increase
the oxygen content of the blood. Patients with hypoxic shock as a result of severe anemia will
require a blood transfusion to improve the overall oxygen carrying capacity of the blood.

Related Article: Poor Perfusion: Stabilization & Fluid Resuscitation

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Metabolic Shock
Metabolic shock is seen when the tissues receive the appropriate perfusion, nutrients, and
oxygen delivery, but the cells are unable to utilize these fuel sources. Causes for metabolic
shock include cyanide toxicity, cytopathic hypoxia of sepsis (Figure 4), and hypoglycemia.
Diagnosis and treatment of the specific underlying cause will direct therapy. For example,
hypoglycemia can be rapidly diagnosed with a glucometer and quickly treated with dextrose
supplementation. Other forms of metabolic shock, including cyanide toxicity, are more
difficult to diagnose and treat.

Figure 4. Cytology: severe suppurative, neutrophilic effusion: 100X oil

Conclusion
The goals in diagnosis and treatment of shock are to decrease patient morbidity and
mortality by optimizing perfusion and oxygen delivery, improving the ability of cells to utilize
these nutrients.

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