Catecholamine Vs. Non catecholamine Vasoactive agents

Catecholamine

Dopamine exerts its effects on both dopaminergic and adrenergic receptors. The meta-analysis from the Surviving Sepsis Campaign guidelines 2015 did not endorse the use of dopamine due to its association with increased mortality and arrhythmias when compared to norepinephrine. However, it may be considered as an alternative to norepinephrine in patients deemed to have a low risk of tachyarrhythmias, particularly in the presence of either absolute or relative bradycardia.

Norepinephrine is a leading endogenous catecholamine with significant inotropic properties. Its impact on cardiac output is minimal, as the increase in afterload due to alpha-1 stimulation often leads to reflex bradycardia. Nevertheless, the Surviving Sepsis Campaign guidelines firmly advocate for norepinephrine as the first-line vasopressor.

Epinephrine is known for its strong inotropic effects, serving as a second-line vasoactive agent in cases of septic shock. In skeletal muscle, it powerfully boosts glycolysis and glycogenolysis, leading to increased lactate production.

Phenylephrine is a potent and pure alpha 1-adrenergic receptor agonist with no binding affinity for beta receptors. It markedly enhances preload through venoconstriction and raises afterload via arterial constriction, leading to reflex bradycardia. This reflex bradycardia arises as a direct consequence of baroreceptor-mediated responses to rapid increases in mean arterial pressure (MAP). It is especially beneficial for patients experiencing severe hypotension and aortic stenosis.

Non catecholamine Vasoactive Agents

Vasopressin analogues serve to specifically target the V1 (vascular smooth muscle: markedly elevates intracellular calcium, resulting in significant vasoconstriction), V2 (kidney: vital for meticulous regulation of plasma volume and osmolality), and V3 (pituitary gland) receptors.

It is important to note that halting vasopressin administration prior to the introduction of norepinephrine may lead to heightened hypotension due to its brief half-life of less than 10 minutes. Furthermore, the simultaneous application of corticosteroids has been shown to effectively lessen these adverse effects.

Angiotensin II exerts direct vasoconstriction of peripheral vessels, contributes to cardiac remodeling, and enhances sympathetic stimulation. Numerous studies have demonstrated that elevated doses equivalent to norepinephrine correlate with increased mortality rates. In cases of refractory shock, the administration of non-catecholamine vasopressors may alleviate excessive catecholamine utilization while simultaneously increasing mean arterial pressure (MAP).

Names, dates, and personal identifying details have been changed throughout this website to comply with the Health Insurance Portability and Accountability Act (HIPAA). ** | This website runs on coffee. Thank you for supporting this journey!