When you find someone without a pulse but then hook up the monitor and there is a rhythm, your first thought it probably “CRAP!” But as you start CPR, you need to be thinking about what caused it because not much will help the person except correcting the underlying problem.
So like most of medicine, there is a handy mnemonic for remembering the main causes: The 6 Hs and 5Ts
The 6 Hs
Hyperkalemia/Hypokalemia (potassium disturbances only get counted once)
The 5 Ts
(I’ll make a T doodle at a later date)
The other handy mnemonic for the Hs I learned from this video (so I take no credit for it): Diabetic crashing with a wide QRS
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.
>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.