Labetalol

• •Acute hypertension perioperative (bolus or infusion)
• •Hypertensive emergency
• •Aortic dissection (with esmolol for HR control first)
• •Pheochromocytoma intraop crisis (after alpha blockade)
• •Pregnancy HTN (preeclampsia — first-line antihypertensive in OB)

Onset 5-10 min IV. Peak 5-15 min. Duration 2-6 h (much longer than esmolol). Hepatic glucuronidation, renal excretion (5% unchanged). Crosses placenta but minimal fetal effect — preferred OB antihypertensive.

↓HR (modest), ↓SVR, ↓BP. Beta-blockade prevents reflex tachycardia from alpha-blockade. Maintains cardiac output (minimal direct negative inotropy).

• !Bradycardia (additive with other beta-blockers)
• !Bronchospasm (less than non-selective due to combined mechanism but still risk)
• !Heart block (especially in AV node disease)
• !Hepatocellular injury rare with chronic use
• !Decompensation in heart failure

• ×Severe bradycardia, sick sinus syndrome
• ×Heart block 2nd/3rd degree
• ×Cardiogenic shock, decompensated heart failure
• ×Severe asthma (relative)
• ×Pheochromocytoma WITHOUT prior alpha blockade

• ★PREGNANCY first-line antihypertensive (preeclampsia) — preferred over hydralazine in many centers (smoother control, less tachycardia, less crystalloid loading needed).
• ★Postop HTN in PACU: 5-10 mg IV bolus is rapid + effective; longer duration than esmolol means less re-dosing.
• ★Bridging from esmolol to oral/longer-acting: labetalol IV → labetalol PO transition.
• ★Aortic dissection: combine with esmolol — esmolol controls HR first (beta-blockade limits reflex tachycardia), then labetalol or nicardipine for additional BP control.
• ★Pheochromocytoma + acute hypertensive crisis: ONLY after adequate alpha blockade (phenoxybenzamine ≥7 days) — labetalol's beta-blockade in unblocked patient produces unopposed alpha + lethal bradycardia.

• Epinephrine

  α1 (vasoconstriction), α2, β1 (inotropy + chronotropy), β2 (bronchodilation, vasodilation in skeletal muscle). Dose-dependent receptor preference: low-dose β-predominant, high-dose α-predominant.

• Norepinephrine

  Strong α1 → vasoconstriction. Mild β1 → modest inotropy. Minimal β2.

• Phenylephrine

  Pure α1 agonist → vasoconstriction. No β activity.

• Dexmedetomidine

  α2 agonist (locus coeruleus) → sedation + analgesia + anxiolysis without significant respiratory depression.

• Vasopressin

  Endogenous nonapeptide hormone. V1 receptor agonist on vascular smooth muscle (Gq → IP3 → Ca²⁺ → vasoconstriction). V2 on renal collecting ducts (Gs → cAMP → aquaporin insertion → water reabsorption). At pressor doses (0.01–0.04 U/min), V1 effects dominate.

• Esmolol

  Selective β1-adrenergic receptor antagonist. Decreases HR, contractility, conduction velocity, and AV node refractoriness. Selectivity for β1 over β2 reduces (does not eliminate) bronchospasm risk vs non-selective beta-blockers.

• Magnesium Sulfate

  Multiple mechanisms: (1) NMDA receptor antagonism (anticonvulsant, analgesic); (2) Voltage-gated calcium channel blockade in vascular + uterine smooth muscle (vasodilation, tocolysis); (3) Decreased ACh release at neuromuscular junction (NMB potentiation); (4) Membrane stabilization (antiarrhythmic, especially torsades).

• Amiodarone

  Multichannel blockade — primarily class III (K+ channel block → prolonged repolarization, increased refractory period), plus class I (Na+ block), class II (β-blocker), class IV (Ca²⁺ block) properties. Treats most supraventricular AND ventricular arrhythmias. Long elimination half-life (weeks–months) limits chronic use.

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