Shock is “a syndrome resulting from failure of the cardiovascular system to maintain adequate tissue perfusion.”
Weil-Shubin Classification of Shock
- Cardiogenic – Poor cardiac function reduces forward blood flow.
- Hypovolemic – Loss of intravascular volume caused by: hemorrhage, dehydration, third space loss, vomiting, diarrhea.
- Obstructive – Impair cardiac filling due to external restriction. Caused by cardiac tamponade, tension pneumothorax, pulmonary embolus.
- Distributive – Primarily characterized by loss of peripheral vascular tone. Caused by septic, anaphylactic, adrenal insufficiency, neurogenic, liver failure.
- α1: Vasoconstriction
- α2: Inhibits norepinephrine release, decreases BP, sedative effects
- β1: Positive inoptrope (increases cardiac contractility and stroke volume)
- β2: Vasodilation, broncodilation
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.