Distributive Shock

Updated October 2025 by Ashley L. Ayoob-Wagner, DVM, DACVECC, DACVIM; BluePearl Pet Hospital, Northfield, Illinois

You asked …

What is distributive shock, and how should it be treated?

The expert says …

Shock (ie, inadequate cellular energy production or the body’s inability to supply cells and tissues with oxygen and nutrients and remove waste products^1-3) can cause quick clinical deterioration and requires rapid identification and treatment. Distributive shock is a general classification for syndromes that cause massive maldistribution of blood flow. Conditions that cause loss of vascular tone with shifts in the vascular system and/or increased vascular permeability with volume loss from the intravascular space into the interstitium result in redistribution of the intravascular blood volume, effectively leading to a relative hypovolemia.⁴ Anaphylactic, neurogenic, and septic shock are common forms of distributive shock. Whether obstructive shock is a subclass of distributive shock or warrants a separate distinct type of shock is debated in the medical literature.⁴

Pathophysiology

Distributive shock is generally associated with altered vasomotor tone through the following pathways.^4-6

• Inappropriate vasodilation (eg, sepsis, systemic inflammatory response syndrome)

  • Excessive production of nitric oxide and cyclic guanosine monophosphate (cGMP)

  • Increased prostacyclin expression

  • Increased activity of adenosine triphosphate (ATP)-sensitive potassium channels

  • Desensitization and downregulation of alpha-adrenergic receptors

• Excessive vasoconstriction (eg, following trauma or anaphylaxis)

• Abnormalities in normal blood flow (eg, obstructive diseases [eg, gastric dilatation-volvulus [GDV], pericardial effusion]), resulting in maldistribution of blood flow

• Increased vascular permeability secondary to inflammatory mediator and cytokine release (most notable with septic shock)

The loss in systemic vascular resistance is often accompanied by a compensatory increase in cardiac output.

Septic Shock

Patients in septic shock experience uncontrolled vasodilation from inflammatory mediators and cytokine release in combination with increased vascular permeability. A full review of the pathophysiology, diagnosis, and treatment of septic shock is available.

Anaphylactic Shock

Anaphylactic shock is characterized by massive histamine-mediated vasodilation with maldistribution of the blood volume secondary to an intravascular to extravascular fluid shift. Anaphylaxis is immunoglobulin E-dependent, and anaphylactoid reactions are immunoglobulin E-independent physical, chemical, or osmotic (typically secondary to radiology contrast media) hypersensitivities.⁴ The main mediator of anaphylactic shock is histamine, in combination with bradykinins and leukotrienes. Histamine release from mast cells leads to upregulation in inducible nitric oxide synthase gene expression and an increase in nitric oxide leading to guanylyl cyclase-mediated vasodilation.⁶

Obstructive Shock

Obstructive shock occurs secondary to obstructions of the great vessels (eg, GDV, pericardial effusion, caval syndrome secondary to heartworm disease, thromboembolism). There is some debate in the medical literature as to whether obstructive shock is a subclass of distributive shock or whether it warrants a separate classfication.⁴ Obstruction to blood flow can occur secondary to mechanical, intravascular, extravascular, or luminal mechanisms, and the common clinical denominator in all causes of obstructive shock is a rapid and massive decrease in cardiac output and a resultant drop in blood pressure.⁴

Neurogenic Shock

Neurogenic shock is a critical condition characterized by organ tissue hypoperfusion due to a disruption in sympathetic mediated vasomotor tone and cardiac output. In humans, the most common cause of neurogenic shock occurs secondary to trauma of the thoracic spine with loss of communication between the bulbar regulator centers and spinal cord.⁴ Additional causes include brain stem trauma, cerebral embolism/ischemia, altered afferent signals to the medulla oblongata (fear, pain, stress, dysregulated vagal reflexes), drug mediated, meningitis, cerebral herniation, and (rarely) association with epileptic seizures. Neurogenic shock in veterinary patients is uncommon.

Additional uncommon etiologies of distributive shock include a chronic hypocortisolemic state (eg, critical illness-related corticosteroid insufficiency, hypoadrenocorticism) in which downregulation of arteriole alpha-1 receptor expression leads to vasoplegia, as well as calcium channel blocker toxicity with direct peripheral arterial vasodilation in combination with negative inotropic and chronotropic effects from inhibition of calcium influx into the myocardium leading to vasodilatory shock.⁷

Diagnostic Testing & Evaluation

Diagnostic testing for distributive shock depends on patient signalment, history, and physical examination findings. Although many diagnostics should be considered, physical examination is key.For example, a patient presented in an emergency situation following vaccine administration should indicate consideration of treatment for anaphylactic shock, whereas a large-breed dog presented with a distended abdomen and nonproductive retching is suggestive of GDV. Immediate point-of-care diagnostics and second- or third-tier diagnostics that are valuable but not immediately needed should be identified.

Point-of-care diagnostic testing may include a basic minimum database (ie, packed-cell volume, total protein, blood glucose, point-of-care qualitative dipstick test for elevated BUN, blood urea nitrogen/creatinine), followed by more advanced testing (eg, CBC with blood smear to assess WBCs for toxic changes and pathogens associated with leukocytes or erythrocytes, serum chemistry profile, urinalysis, coagulation parameters, serum lactate, blood pressure measurement).

Thoracic and abdominal radiography, as well as thoracic and abdominal ultrasonography, may also be indicated. Point-of-care ultrasound can be used to evaluate for the presence of pericardial effusion and to guide pericardiocentesis. In cases of anaphylactic shock, focused ultrasound may reveal an enlarged liver, gallbladder edema (ie, halo sign), and presence of abdominal effusion. Focused ultrasound can also be useful in the evaluation and collection of free abdominal or thoracic fluid in the case of septic abdomen or pyothorax.

A lactate test is important to assess tissue perfusion. With inadequate perfusion, patients in shock often develop hyperlactatemia caused by anaerobic metabolism. The normal lactate concentration in adult dogs and cats is <2.5 mmol/L.⁸ Several studies have highlighted that evaluation of traditional perfusion parameters alone may underdiagnose a state of persistent tissue hypoxia in up to 94% of critically ill patients.⁹ Lactate evaluation and shock index are both rapid point-of-care diagnostics that have clinical utility in the detection of occult hypoperfusion. Persistently elevated lactate concentrations in dogs may help predict mortality in specific diseases, notably GDV.^8,10-12 Although single lactate readings were initially used to predict mortality, trends in serial lactate concentration measurements (ie, lactime and lactate clearance) may be more beneficial during resuscitation and better predict outcome in dogs.^13-17 Shock index has been documented to be significantly higher in patients with ongoing tissue hypoxia and may identify occult hypoperfusion in both dogs and cats, with a suggested cutoff of >0.9 to be consistent with shock and values >1.4 to be consistent with severe shock; however, defined clinical cutoff points still need to be established.¹⁸

Treatment

Patients presented with presumptive distributive shock should undergo typical triage assessment, including ABC (airway, breathing, circulation) evaluation. If warranted, IV access and fluid resuscitation should be performed to correct hypoperfusion and hypotension. Isotonic crystalloids at shock doses of 90 mL/kg for dogs and 44 to 60 mL/kg for cats should be administered. The entire shock dose is not administered initially. An initial bolus of 20 to 25 mL/kg for dogs and 10 to 20 mL/kg for cats should be administered over 15 to 30 minutes, followed by patient reassessment (eg, heart rate, capillary refill time, mucous membrane color, core body temperature, blood pressure, lactate levels, shock index). These boluses can then be repeated until clinical resolution of hypoperfusion is obtained, the full shock dose has been administered, or other defined markers of end-point resuscitation are obtained. Supplemental oxygen should be administered via flow-by methods (50-150 mL/kg/minute) or nasal oxygen cannulas (50-100 mL/kg/minute) if needed.

Anaphylactic Shock

If anaphylaxis is suspected, epinephrine, a potent alpha- and beta-adrenergic agonist, is considered the treatment of choice. A loading dose of 2.5-5 micrograms/kg IV or 10 micrograms/kg IM, followed by a CRI of 0.05 micrograms/kg/minute has shown the best efficacy.^19,20 Stimulation of alpha-1 adrenergic receptors results in vasoconstriction, and activation of the cyclic adenosine monophosphate system results in inhibition of antigen-induced release of histamine and other anaphylactic mediators.²¹

Histamine (H₁)-receptor antagonists (eg, diphenhydramine, 2-4 mg/kg IM or SC) can also be considered to reduce pruritus, erythema, urticaria, hives, and angioedema. In conjunction with H₁-antagonists, histamine type 2 (H₂)-antagonists (eg, famotidine 1 mg/kg IV or IM) decrease erythema and gastric acid production. These medications do not prevent cardiovascular collapse and thus should be used adjunctively with, not substituted for, epinephrine.^20,22

Glucocorticoids are often administered for allergic or hypersensitivity reactions; however, in states of anaphylactic shock, glucocorticoids do not have immediate effect and are not a first-line therapy. Anti-inflammatory effects may not occur for 4 to 6 hours after administration. Glucocorticoids may help reduce the severity of a biphasic reaction but are not first-line therapy for anaphylaxis. If needed for inflammation or respiratory distress caused by oropharyngeal edema, dexamethasone sodium phosphate (0.05-0.1 mg/kg IV or IM every 12-24 hours) can be administered.¹⁹

A vasopressor or positive inotrope CRI may be required in patients unresponsive to fluid and epinephrine therapy. Potent vasoconstrictors (dopamine, dogs, 1-20 micrograms/kg/minute IV CRI; cats, 1-5 micrograms/kg/minute IV CRI; norepinephrine, 0.05-0.3 micrograms/kg/minute IV CRI) should be considered for hypotension refractory to fluids and epinephrine administration. Vasopressin (dogs, 0.01-0.04 units/kg/minute IV CRI; cats, 0.01-0.04 units/cat/minute IV CRI) may play a useful role in the treatment of anaphylaxis via vasoconstriction mediated through V1 receptors.

Several promising novel treatments for distributive shock include methylene blue and angiotensin-II.^5,6,23-26 Excessive production of nitric oxide and prostacyclin, heightened activity of ATP-sensitive potassium channels, and desensitization of alpha-adrenergic receptors that occur with distributive shock leads to a lack of response to catecholamine receptors in the endothelium and catecholamine-resistant hypoperfusion. High-dose adrenergic vasopressor therapy has an increased risk for adverse effects (eg, arrhythmias, tissue ischemia, necrosis, splanchnic vasoconstriction, immune dysfunction). Use of alternative therapies may thus help correct hypoperfusion in distributive shock with decreased risk to the patient. Angiotensin II has been shown to reduce catecholamine requirements in the treatment of vasopressor-resistant distributive shock in humans.^5,23,24 Methylene blue results in selective inhibition of the nitric oxide-cGMP pathway, which plays a significant role in histamine-induced hypotension. Caution should be used in patients receiving serotonergic drugs because of possible adverse drug reactions, and extreme caution should be used in cats due to the risk for Heinz body anemia. Angiotensin II and methylene blue have not proven a clear reduction in mortality in patients with distributive shock, but these treatments have shown a consistent decrease in vasopressor requirements, length of time in the intensive care unit, and length of hospitalization.^5,6,23-26 Experimental and clinical therapeutic benefits have been seen, but these therapies are not recommended as a first-line treatment because use remains controversial and dosage recommendations are needed.

Obstructive Shock

Obstructive shock occurs when there is an obstruction to flow (eg, GDV, pericardial effusion). Resolution is directed at correcting the cause of shock and requires immediate and causal treatment. Patients presented with presumptive obstructive shock should undergo typical triage assessment. If warranted, IV access and fluid resuscitation should be performed to correct hypoperfusion and hypotension. Isotonic crystalloids at a shock bolus rate (dogs, 20-25 mL/kg over 15-30 minutes; cats, 10-20 mL/kg over 15-30 minutes) should be administered. Supplemental oxygen should be administered with flow-by oxygen methods (50-150 mL/kg/minute) or nasal oxygen cannulas (50-100 mL/kg/minute).

In patients with GDV, gastric distension obstructs venous return in the caudal vena cava, leading to decreased cardiac preload and cardiac output. Poor perfusion is treated with IV fluid boluses given to effect, followed by gastric decompression and surgical return of the stomach to its normal position.

Pericardial effusion, another common cause of obstructive shock, can lead to pericardial tamponade resulting from increased intrapericardial pressure that equals or exceeds right atrial/ventricular pressure and results in decreased ventricular filling. Decreased ventricular filling then results in decreased stroke volume, leading to decreased cardiac output and decreased blood pressure. Poor perfusion is treated with IV fluid boluses given to effect, followed by pericardiocentesis and resolution of pericardial tamponade. The goal of treatment is to improve preload and reduce ischemia and reperfusion.

Conclusion

Distributive shock, whether anaphylactic or obstructive, should be carefully evaluated and quickly treated, as this condition often results in severe cardiovascular abnormalities, multiple organ failure, and/or death. Aggressive fluid resuscitation alone to promote adequate tissue perfusion may be unsuccessful, and additional therapy is often needed.