Tag Archives: adrenaline vs noradrenaline

#EPINEPHRINE ( #Adrenaline) : Pharmacological Highlights

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🔻Epinephrine is an agonist of alpha 1, β1 , and β2 adrenoceptors. An intravenous infusion of epinephrine produces an increase in mean arterial pressure (MAP) characterized by selectively enhanced systolic pressure with no change in diastolic pressure. 
🔻Epinephrine exerts positive chronotropic and inotropic actions by stimulation of β1 adrenoceptors

🔻Epinephrine also increases the rate of myocardial relaxation and enhances early LV filling, thereby improving diastolic function. These combined effects result in a dramatic increase in cardiac output.

🔻Epinephrine (0.01–0.03 ug kg –1 min –1 ) has been shown to produce similar hemodynamic effects with less pronounced tachycardia than dobutamine (2.5–5.0 ug kg–1 min–1 ) in patients after coronary artery bypass graft (CABG) surgery

🔻Predictable increase in cardiac output, favours the use of epinephrine as the primary inotropic drug for the management of LV dysfunction after cardiopulmonary bypass

🔻Epinephrine causes direct positive dromotropic effects ( leading to increase in conduction velocity and reduction of the refractory period of the AV node, His bundle, Purkinje fibers, and ventricular muscle)

🔻This may contribute to detrimental increases in ventricular rate in patients with atrial flutter or fibrillation and the occurrence of ventricular arrhythmias

🔻The overall effect of epinephrine on blood flow to a specific organ depends on the relative balance of alpha 1 and β2 adrenoceptors located in the vasculature.

🔻β2 -Adrenoceptors are sensitive to lower doses of epinephrine and, as a result, peripheral vasodilation and modest reductions in arterial pressure are observed with such doses

🔻In contrast, the effects of epinephrine on alpha 1 -adrenoceptors predominate at greater doses with marked increases in systemic vascular resistance and arterial pressure.

🔻The intense vasoconstriction produced by high doses of epinephrine may adversely impede LV ejection by increasing after load after cardiopulmonary bypass. Thus, greater doses of epinephrine may be used in combination with arterial vasodilators such as sodium nitroprusside to optimize contractile performance in such situations .

🔻Adrenaline via alpha 1 receptors also mediates (1) venoconstriction & enhanced venous return (2) Pulmonary vasoconstriction and increases in pulmonary arterial pressures.

🔻 Pre-existing β-blockade by nonselective β-blocker propranolol abolishes the decrease in systemic vascular resistance from epinephrine-induced stimulation of β2 adrenoceptors and potentiates peripheral vasoconstriction mediated by unopposed alpha 1 adrenoceptors.

🔻The positive inotropic and chronotropic effects of epinephrine are also attenuated in the presence of pre-existing β-blockade and greater doses of epinephrine are required to overcome this competitive blockade

🔻Complete pharmacologic blockade of β1 and β2 adrenoceptors may theoretically make the hemodynamic effects of epinephrine indistinguishable from those of the pure alpha 1 adrenoceptor agonist phenylephrine.

#NorAdrenaline , #CriticalCare , #vasopressors , #TheLayMedicalMan , #IntensiveCare , #Pharmacology, #anesthesia , #anaesthesia, #drugs

(Reference: Paul S. Pagel and David C. Warltier, Essential drugs in anesthesia practice Positive inotropic drugs, Anesthetic Pharmacology, 2nd edition)

NORADRENALINE: PHARMACOLOGICAL HIGHLIGHTS & COMPARISON WITH ADRENALINE 

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Noradrenaline (Norepinephrine) is a directly and indirectly acting sympathomimetic amine which stimulates alpha 1 and β1 adrenoceptors, but, in contrast to Adrenaline (epinephrine), has little effect on β2 adrenoceptors.

🖍These actions produce positive inotropic effects, intense vasoconstriction, increases in arterial pressure, and relative maintenance of cardiac output.

🖍Noradrenaline increases arterial pressure while simultaneously enhancing contractile state and venous return by reductions in venous capacitance, thereby augmenting stroke volume and ejection fraction. In contrast, pure alpha 1 adrenoceptor agonists such as phenylephrine and methoxamine further compromise cardiac output in failing myocardium and contribute to peripheral hypoperfusion despite an increase in arterial pressure.

🖍In contrast to adrenaline, noradrenaline does not substantially affect heart rate because activation of baroreceptor reflexes resulting from arterial vasoconstriction usually counteracts β1 mediated, direct, positive, chronotropic effects.

🖍Its arrhythmogenic potential is considerably less than that of adrenaline. Thus, substitution of noradrenaline for adrenaline may be appropriate in the therapeutic management of cardiogenic shock when atrial or ventricular arrhythmias are present.

🖍Intravenous infusions of noradrenaline (0.03–0.90 mg kg –1 per minute) have been shown to increase arterial pressure, LV stroke work index, cardiac index, and urine output in septic patients with hypotension that was unresponsive to volume administration, dopamine or dobutamine

🖍Causes relatively greater increases in systemic vascular resistance and diastolic arterial pressure than adrenaline.

🖍The drug has a duration of action of 30–40 minutes; tachyphylaxis occurs with prolonged administration.

🖍The drug produces coronary vasodilatation, leading to a marked increase in coronary blood flow. However, as myocardial work may increase, the balance of myocardial oxygen consumption and delivery may lead to ischaemia on noradrenaline.

🖍Reflex vagal stimulation leads to a compensatory bradycardia

🖍The cerebral blood flow and oxygen consumption are decreased by the administration of noradrenaline; mydriasis also occurs

🖍The glomerular filtration rate is usually well maintained with noradrenaline; but it decreases the renal blood flow and this represents a major limitation on the prolonged use of high doses of norepinephrine.

🖍Noradrenaline increases the contractility of the pregnant uterus; this may lead to fetal bradycardia and asphyxia

🖍Noradrenaline may decrease insulin secretion, leading to hyperglycaemia

🖍The drug is pharmaceutically incompatible with barbiturates and sodium bicarbonate

(Reference: Paul S. Pagel and David C. Warltier, Essential drugs in anesthesia practice Positive inotropic drugs, Anesthetic Pharmacology, 2nd edition)