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Shock is “a syndrome resulting from failure of the cardiovascular system to maintain adequate tissue perfusion.”

Weil-Shubin Classification of Shock

1. Cardiogenic –  Poor cardiac function reduces forward blood flow.
2. Hypovolemic – Loss of intravascular volume caused by: hemorrhage, dehydration, third space loss, vomiting, diarrhea.
3. Obstructive – Impair cardiac filling due to external restriction. Caused by cardiac tamponade, tension pneumothorax, pulmonary embolus.
4. Distributive – Primarily characterized by loss of peripheral vascular tone. Caused by septic, anaphylactic, adrenal insufficiency, neurogenic, liver failure.

Adrenergic Receptors

• α1: Vasoconstriction
• α2: Inhibits norepinephrine release, decreases BP, sedative effects
• β1: Positive inoptrope (increases cardiac contractility and stroke volume)
• β2: Vasodilation, broncodilation

Vasoactive Drugs

Epinephrine

• Effects: Causes vasoconstriction and increases cardiac output. Inotrope effect predominates at low doses (< 4.0 mcg/min).
• Disadvantages: Associated with lactic acidosis, hyperglycemia, pulmonary hypertension, tachyarrythmias, and compromised hepatosplanchnic perfusion.
• Use: First-line agent for cardiac arrest and anaphylaxis. Second-line agent for vasopressor and inotrope effects, when other agents have failed.

Norepinephrine

• Effects: Potent vasoconstrictor. Causes a minor increase in stroke volume and cardiac output.
• Disadvantages: May decrease renal blood flow and increase myocardial oxygen demand. Extravasation at site of intravenous administration may lead to tissue necrosis.
• Use: First line therapy for maintenance of blood pressure.

Ephedrine

• Effects: Increases heart rate, cardiac output. Bronchodilator. Some anti-emetic effects. Longer duration than epinephrine. Has indirect actions on adrenergic system.
• Disadvantages: Epedrine losses effect with subsequent doses since part of its effect is indirect, by icreasing NE release, which becomes depleted
• Use: Common vasopressor during anesthesia, but only a temporizing agent in acute shock.

Dopamine

• Effects are dose-dependent:
  • < 5 mcg/kg/min – Acts at dopamine receptors only, with mild inotrope effect. Vasodilatory effects purported to improve perfusion through renal and mesenteric vessels; however, there is no clear clinical benefit of dopamine on organ function.
  • 5-10 mcg/kg/min – Predominantly β1 adrenergic effects. Increases cardiac contractility and heart rate.
  • >10 mcg/kg/min – Predominately α1 effects, causing arterial vasoconstriction and increased blood pressure. Overall decrease in renal and splanchnic blood flow at this dose.
• Disadvantages: Has a high propensity for tachycardia and dysrythmias. Potential for prolactin suppression and immunosuppression.
• Use: First line vasopressor for shock, but may be associated with more adverse outcomes than norepinephrine.

Dobutamine

• Effects: Racemic mixture. where the L-isomer acts at α1/β1 receptors and D-isomer acts at β1/β2 receptors. Increases cardiac output and decreases systemic/pulmonary cascular resistance. Can increase splanchnic blood flow and decrease endogenous glucose production.
• Disadvantages: May cause mismatch in myocardial oxygen delivery and requirement. Vasodilation undesirable in septic patients.
• Use: A ‘gold standard‘ inotropic agent in cardiogenic shock with low output and increased afterload. In sepsis, vasodilatory effects should be counteracted by co-administration with norepinephrine.

Dopexamine

• Effects: Acts at β2 and dopamine receptors. Causes vasodilation and decreased afterload. Has some positive inotrope effect. Bronchodilatory. Unlike dopamine, dopexamine is not associated with pituitary suppression.
• Disadvantages: Not widely accepted in practice.
• Use: Like dobutamine, useful for cardiogenic shock with decreased output and high afterload.

Phenylephrine

• Effects: Classic selective α1 agonist, causing vasoconstriction. Rapid onset and short duration.
• Disadvantages: Can reduce hepatosplanchnic perfusion. May cause significant reflex bradycardia.
• Use: Generally considered a temporary vasopressor until more definitive therapy is begun. Useful for vasdilated patients with adequate cardiac output, for whom other vasopressors present risk of tachyarrhythmias.

Dexmedetomidine/Clonidine

• Effects: Arousable sedation with preserved respiratory drive. Improved tissue perfusion and renal function. General sympathetic inhibition.
• Disadvantages: Bradycardia and hypotension.
• Use: Not used in acute shock setting, but may be useful in later critical care setting.

Vasopressin (not actually an adrenergic drug)

• Effects: Acts on V1 receptors to cause vasoconstriction. Increases vasculature response to catecholamines.
• Disadvantages: May cause tachycardia and tachyarrythmias. Excessive vasoconstriction can impair oxygen delivery and and cause limb ischemia.
• Use: May be used to augment norepinephrine or other agents. Not typically used alone.