Diltiazem
Cardizem
Non-dihydropyridine calcium channel blocker (class IV antiarrhythmic)
L-type Ca²⁺ blocker — AV-nodal slowing with less myocardial depression than verapamil; some vasodilation.
Indications
- •Rate control in AF/flutter (common IV choice)
- •SVT
- •Angina/coronary vasospasm
- •HTN
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| Rate control | 0.25 mg/kg IV over 2 min (~15–20 mg); repeat 0.35 mg/kg after 15 min; infusion 5–15 mg/hr | — |
Pharmacokinetics
Onset 2–5 min IV. Hepatic CYP3A4.
Hemodynamic effects
Hypotension + bradycardia (less negative inotropy than verapamil).
Side effects
- !Bradycardia, AV block, hypotension
- !Worsens HFrEF (less than verapamil)
- !Raises some drug levels (CYP3A4)
Contraindications
- ×Pre-excited AF (WPW)
- ×2nd/3rd-degree block
- ×HFrEF
- ×Wide-complex tachycardia of uncertain origin
Clinical pearls
- ★Preferred non-DHP for AF rate control in the OR/ICU — less myocardial depression than verapamil.
- ★Calcium + glucagon reverse toxicity (as with all CCBs).
Other drugs in Cardiac / BP
- 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.
Browse all classes: /reference/drugs
Suggested reading
- •Stoelting & Hines, Pharmacology & Physiology in Anesthetic Practice, 6e
- •Miller's Anesthesia, 9e
- •FDA package insert
