IV Cardiac Drips
Essential intravenous cardiac infusions — antiarrhythmics, vasopressors, inotropes, anticoagulation, sedation, and vasodilator drips with dosing protocols and clinical pearls.
Antiarrhythmic Infusions
Amiodarone IV
Amiodarone remains the most widely used intravenous antiarrhythmic for both ventricular and supraventricular arrhythmias. The standard loading protocol delivers approximately 1050 mg over the first 24 hours:
- Rapid loading: 150 mg IV over 10 minutes (15 mg/min)
- Slow loading: 1 mg/min × 6 hours (360 mg)
- Maintenance: 0.5 mg/min × 18 hours (540 mg)
- Breakthrough boluses: supplemental 150 mg IV over 10 min for recurrent VT/VF (may repeat every 10–15 min as needed)
- Maximum dose: 2.2 g in 24 hours
Central venous access is strongly preferred due to the high incidence of peripheral phlebitis (up to 30% with peripheral IVs). If a peripheral line must be used, choose a large-bore vein and limit infusion duration. Hypotension is the most common acute side effect (15–20%), primarily due to the polysorbate 80 solvent in the older formulation; the newer aqueous formulation (Nexterone) causes significantly less hypotension. Slow the infusion rate or administer IV fluids/vasopressors if hypotension develops.
Procainamide IV
Procainamide is the preferred antiarrhythmic for hemodynamically stable wide-complex tachycardia, particularly when WPW with atrial fibrillation is suspected (AV nodal blockers are contraindicated in this setting).
- Loading dose: 20–50 mg/min IV until arrhythmia terminates, hypotension occurs, QRS widens >50% from baseline, or maximum dose of 17 mg/kg (approximately 1–1.5 g in a 70 kg patient) is reached
- Maintenance infusion: 1–4 mg/min
- Stop loading if: QRS widens >50%, hypotension develops, arrhythmia terminates, or maximum dose reached
Continuous QRS and QT monitoring is mandatory. Procainamide prolongs the QT interval and can cause torsades de pointes. It also has significant negative inotropic and vasodilatory effects — hypotension risk is substantial during rapid loading. Preferred over amiodarone for stable monomorphic VT and pre-excited AF (WPW).
Ibutilide IV
Ibutilide is a Class III antiarrhythmic used exclusively for pharmacological cardioversion of atrial fibrillation or atrial flutter. It is not used for maintenance therapy.
- Dose: 1 mg IV over 10 minutes; may repeat ×1 after 10 minutes if arrhythmia persists
- Patients <60 kg: 0.01 mg/kg per dose
- Efficacy: 30–50% cardioversion for AF, 60–90% for atrial flutter
- QTc monitoring: continuous telemetry for at least 4–6 hours post-infusion
- TdP risk: approximately 4% (have defibrillator and IV magnesium at bedside)
Isoproterenol IV
Isoproterenol is a pure beta-adrenergic agonist (β1 and β2) with potent chronotropic and inotropic effects. It increases heart rate and shortens the QT interval, making it uniquely useful in specific arrhythmia scenarios:
- Dose: 1–10 mcg/min, titrate to target heart rate
- Brugada VF storm: increases heart rate, suppresses phase-2 reentry
- Torsades de pointes: shortens QT by increasing heart rate and accelerating repolarization
- Drug-induced bradycardia: temporizing measure while awaiting transvenous pacing
- EP lab use: provocation of VT, assessment of outflow tract arrhythmias
Lidocaine IV
Lidocaine is a Class IB antiarrhythmic with rapid onset and short duration. Its role has narrowed compared to amiodarone, but it remains useful in specific contexts:
- Loading: 1–1.5 mg/kg IV bolus (may repeat 0.5–0.75 mg/kg every 5–10 min, max 3 mg/kg)
- Maintenance: 1–4 mg/min
- Primary indication: VT/VF in the setting of acute myocardial infarction
- Hepatic metabolism: reduce dose by 50% in liver disease, CHF, or advanced age (>70 years)
- Toxicity: perioral numbness, tinnitus, seizures (early signs mandate stopping infusion)
| Drug | Loading Dose | Maintenance | Key Monitoring | Clinical Pearls |
|---|---|---|---|---|
| Amiodarone | 150 mg IV over 10 min | 1 mg/min × 6h → 0.5 mg/min × 18h | BP, HR, QTc, liver/thyroid long-term | Central line preferred; max 2.2 g/24h; Nexterone = less hypotension |
| Procainamide | 20–50 mg/min (max 17 mg/kg) | 1–4 mg/min | QRS width, QTc, BP | Stop if QRS widens >50%; preferred for WPW + AF and stable VT |
| Ibutilide | 1 mg IV over 10 min (×1 repeat) | None (single use) | QTc × 4–6h post-dose | TdP risk ~4%; AF/flutter cardioversion only; have Mg2+ ready |
| Isoproterenol | None | 1–10 mcg/min | HR, BP, ischemia | Brugada VF storm, torsades, drug-induced bradycardia |
| Lidocaine | 1–1.5 mg/kg bolus | 1–4 mg/min | CNS toxicity, hepatic function | Reduce dose in liver disease/CHF; VT/VF in acute MI |
Vasopressors & Inotropes
Norepinephrine
Norepinephrine is the first-line vasopressor in both septic and cardiogenic shock per current guidelines. It acts primarily on α1 receptors (vasoconstriction) with moderate β1 activity (inotropy), resulting in increased SVR and MAP with modest augmentation of cardiac output.
- Dose: 0.1–0.5 mcg/kg/min (commonly started at 5–10 mcg/min in adults, titrated to MAP goal)
- Hemodynamic effect: ↑ SVR, ↑ MAP, ↑/↔ CO, ↔/↓ HR
Vasopressin
Vasopressin acts on V1 receptors (vascular smooth muscle vasoconstriction) independent of catecholamine pathways, making it a valuable adjunct to norepinephrine to reduce catecholamine requirements.
- Dose: 0.01–0.04 units/min (fixed, not titrated)
- Catecholamine-sparing: allows dose reduction of norepinephrine
- Note: does not directly increase cardiac output; avoid as sole agent in cardiogenic shock
Dopamine
Dopamine has dose-dependent receptor activation, though these ranges overlap significantly in clinical practice:
- Low dose (1–5 mcg/kg/min): dopaminergic (DA1) receptors — renal/mesenteric vasodilation (no proven renal protection)
- Moderate dose (5–10 mcg/kg/min): β1 receptors — increased contractility, heart rate, and cardiac output
- High dose (10–20 mcg/kg/min): α1 receptors — vasoconstriction, increased SVR
- Overall dose range: 2–20 mcg/kg/min
Dobutamine
Dobutamine is a synthetic catecholamine with predominant β1 agonist activity and mild β2 activity. It is the classic inotrope for acute decompensated heart failure.
- Dose: 2.5–20 mcg/kg/min
- Hemodynamic effect: ↑ CO, ↑ HR, ↓/↔ SVR, may ↓ BP (vasodilation from β2)
- Caution: may cause hypotension if SVR drops significantly; often combined with norepinephrine
Milrinone
Milrinone is a phosphodiesterase-3 (PDE3) inhibitor — an inodilator that increases contractility via cAMP accumulation independent of beta-receptor stimulation, while also causing vasodilation (reduced afterload and preload).
- Loading dose: 50 mcg/kg IV over 10 min (optional — often omitted in hypotension)
- Maintenance: 0.375–0.75 mcg/kg/min
- Renal dose adjustment: reduce dose in renal impairment (CrCl <50 mL/min)
- Advantages: effective in beta-blocker-treated patients (bypasses beta receptor); pulmonary vasodilation (useful in RV failure)
Epinephrine
Epinephrine is a potent α1, β1, and β2 agonist. At low doses, β effects predominate (inotropy, chronotropy); at higher doses, α1 vasoconstriction becomes dominant.
- Dose: 0.01–0.5 mcg/kg/min
- Hemodynamic effect: ↑ HR, ↑ CO, ↑ SVR (dose-dependent), potent arrhythmogenicity
- Use: refractory cardiogenic shock, post-cardiotomy, anaphylaxis
Phenylephrine
Phenylephrine is a pure α1 agonist with no beta activity. It raises SVR and MAP without direct cardiac stimulation.
- Dose: 0.5–5 mcg/kg/min (infusion) or 100–200 mcg IV push for acute hypotension
- Hemodynamic effect: ↑ SVR, ↑ MAP, ↓/↔ HR (reflex bradycardia), ↓/↔ CO
- Caution: may reduce cardiac output by increasing afterload — avoid as sole agent in cardiogenic shock
| Agent | Dose Range | Receptors | HR | BP/MAP | CO | SVR |
|---|---|---|---|---|---|---|
| Norepinephrine | 0.1–0.5 mcg/kg/min | α1 >> β1 | ↔/↓ | ↑↑ | ↑/↔ | ↑↑ |
| Vasopressin | 0.01–0.04 U/min | V1 | ↔ | ↑ | ↔ | ↑ |
| Dopamine | 2–20 mcg/kg/min | DA / β1 / α1 | ↑↑ | ↑ | ↑ | ↑ (high dose) |
| Dobutamine | 2.5–20 mcg/kg/min | β1 > β2 | ↑ | ↔/↓ | ↑↑ | ↓ |
| Milrinone | 0.375–0.75 mcg/kg/min | PDE3 inhibitor | ↔/↑ | ↓ | ↑↑ | ↓↓ |
| Epinephrine | 0.01–0.5 mcg/kg/min | α1, β1, β2 | ↑↑ | ↑↑ | ↑↑ | ↑ (dose-dependent) |
| Phenylephrine | 0.5–5 mcg/kg/min | Pure α1 | ↓ (reflex) | ↑↑ | ↓/↔ | ↑↑↑ |
The SOAP II trial (De Backer et al., NEJM 2010) randomized 1679 patients in shock to norepinephrine vs dopamine as first-line vasopressor. While 28-day mortality did not differ overall, dopamine was associated with significantly more arrhythmic events (24.1% vs 12.4%, p <0.001), primarily sinus tachycardia and atrial fibrillation. In the pre-specified subgroup with cardiogenic shock, dopamine was associated with higher 28-day mortality (p = 0.03). This trial cemented norepinephrine as the preferred first-line vasopressor.
Anticoagulation Infusions
Unfractionated Heparin (UFH)
UFH remains the most widely used IV anticoagulant in acute cardiac care due to its short half-life, reversibility with protamine, and established monitoring protocols.
- Weight-based protocol: 80 units/kg IV bolus, then 18 units/kg/hr infusion
- aPTT target: 1.5–2.5 × control (typically 60–80 seconds, institution-dependent)
- Anti-Xa monitoring: alternative to aPTT, target 0.3–0.7 IU/mL; increasingly preferred as it is less affected by lupus anticoagulant, elevated factor VIII, and inflammation
- HIT monitoring: platelet count every 2–3 days for the first 14 days; drop >50% from baseline triggers HIT workup (4T score, serotonin release assay)
- Reversal: protamine sulfate (1 mg per 100 units of heparin given in the preceding 2–3 hours)
Bivalirudin
Bivalirudin is a direct thrombin inhibitor (DTI) with a short half-life of approximately 25 minutes, making it highly predictable and titratable. It is the preferred parenteral anticoagulant in patients with heparin-induced thrombocytopenia (HIT).
- PCI dosing: 0.75 mg/kg IV bolus, then 1.75 mg/kg/hr during procedure (may extend post-PCI at reduced rate)
- HIT dosing: 0.15–0.25 mg/kg/hr (no bolus), titrate to aPTT 1.5–2.5 × control
- No antidote: short half-life allows effect to dissipate rapidly with discontinuation
- Renal adjustment: reduce infusion rate if CrCl <30 mL/min; consider alternative if on dialysis
Argatroban
Argatroban is a direct thrombin inhibitor with hepatic metabolism, making it the preferred DTI in HIT patients with renal impairment (where bivalirudin may accumulate).
- Dose: 2 mcg/kg/min continuous infusion (no bolus for HIT)
- Hepatic adjustment: start at 0.5 mcg/kg/min in hepatic impairment (Child-Pugh B or C)
- aPTT target: 1.5–3 × baseline (check at 2 hours, then adjust)
- INR interaction: argatroban elevates INR, complicating warfarin transition. Overlap for ≥5 days, and verify INR >4 on argatroban before stopping (true INR will be ~2–3)
Cangrelor
Cangrelor is an intravenous P2Y12 receptor antagonist with an ultra-short half-life (3–6 minutes), providing rapid-onset, rapidly reversible platelet inhibition — the only IV antiplatelet with this profile.
- Dose: 30 mcg/kg IV bolus, then 4 mcg/kg/min infusion
- Indications: bridge antiplatelet therapy during PCI in patients not pre-treated with oral P2Y12 inhibitors, or when oral agents cannot be administered
- Transition to oral P2Y12: administer ticagrelor or prasugrel immediately upon discontinuation of cangrelor (no interaction). Clopidogrel must be given after cangrelor is stopped (competitive binding reduces clopidogrel effect if co-administered)
| Agent | Bolus | Infusion Rate | Monitoring | Half-Life | Key Consideration |
|---|---|---|---|---|---|
| UFH | 80 U/kg | 18 U/kg/hr | aPTT or anti-Xa | 60–90 min | Protamine reversal; HIT risk |
| Bivalirudin | 0.75 mg/kg (PCI) | 1.75 mg/kg/hr (PCI); 0.15–0.25 mg/kg/hr (HIT) | ACT (PCI); aPTT (HIT) | 25 min | Preferred in HIT; renal adjustment |
| Argatroban | None (for HIT) | 2 mcg/kg/min | aPTT | 39–51 min | Hepatic metabolism; elevates INR |
| Cangrelor | 30 mcg/kg | 4 mcg/kg/min | Platelet function (if available) | 3–6 min | Give clopidogrel only after stopping infusion |
Sedation & Procedural Infusions (EP Lab)
Propofol
Propofol provides rapid-onset, rapidly-titratable deep sedation with a quick recovery profile, making it the most commonly used agent for prolonged EP procedures such as AF ablation.
- Induction: 0.5–1 mg/kg IV bolus (titrated)
- Maintenance: 25–75 mcg/kg/min (150–300 mcg/kg/min for general anesthesia)
- Adverse effects: hypotension (dose-dependent vasodilation and myocardial depression), respiratory depression/apnea, propofol infusion syndrome (rare, prolonged high-dose use in ICU)
- EP lab consideration: may suppress arrhythmia inducibility — relevant during VT ablation and EP studies
Dexmedetomidine
Dexmedetomidine is a highly selective α2-adrenergic agonist providing sedation with minimal respiratory depression — a key advantage over propofol and benzodiazepines.
- Loading: 0.5–1 mcg/kg IV over 10–20 min (optional; often omitted in EP lab to avoid acute hemodynamic changes)
- Maintenance: 0.2–0.7 mcg/kg/hr
- Bradycardia risk: sympatholytic effect can cause significant sinus bradycardia and AV block — particularly relevant in EP procedures where baseline conduction is being assessed
- Advantages: patients remain arousable ("cooperative sedation"), airway reflexes preserved
Midazolam + Fentanyl (Moderate Sedation)
The combination of midazolam and fentanyl provides effective moderate (conscious) sedation for shorter EP procedures including device implantation and diagnostic EP studies.
- Midazolam: 0.5–2 mg IV initial bolus, then 0.5–1 mg IV every 5–15 min as needed (max ~5–10 mg total)
- Fentanyl: 25–100 mcg IV initial bolus, then 25–50 mcg IV every 5–15 min as needed (max ~250–500 mcg total)
- Reversal: flumazenil (0.2 mg IV for midazolam), naloxone (0.4 mg IV for fentanyl)
- Monitoring: continuous pulse oximetry, capnography, BP every 5 min
Atropine
Atropine is a muscarinic antagonist used in the EP lab primarily for vagal-mediated bradycardia and as a pre-treatment before certain EP maneuvers.
- Dose: 0.5–1 mg IV push (may repeat every 3–5 min, max 3 mg total)
- EP lab use: pre-treatment before EP study to eliminate vagal tone and unmask intrinsic conduction disease; reversal of vasovagal episodes during catheter manipulation
- Caution: doses <0.5 mg may paradoxically worsen bradycardia (central vagal stimulation)
Phenylephrine Bolus
Phenylephrine push-dose boluses are a cornerstone of acute hypotension management in the EP lab, particularly during sedation or post-cardioversion.
- Dose: 100–200 mcg IV push every 1–3 min as needed
- Preparation: dilute 10 mg in 100 mL NS (100 mcg/mL) for easy bolus dosing
- Onset: immediate (seconds); duration 5–10 minutes
- Mechanism: pure α1 vasoconstriction increases SVR and MAP without direct cardiac stimulation
The choice between monitored anesthesia care (MAC) and deep sedation/general anesthesia (GA) for AF ablation has significant practical implications. GA with endotracheal intubation allows controlled ventilation, eliminates patient movement (critical for 3D mapping accuracy), and enables high-frequency jet ventilation to minimize catheter excursion. Multiple studies, including the GENERAL-AF trial, have demonstrated that GA is associated with higher single-procedure success rates compared to conscious sedation. Most high-volume centers now use GA with controlled ventilation as the standard approach for AF ablation. However, MAC remains appropriate for shorter EP procedures, device implantation, and diagnostic studies where deep sedation is unnecessary.
Vasodilators & Special Infusions
Nitroprusside
Sodium nitroprusside is a potent arterial and venous vasodilator that reduces both preload and afterload. It has the fastest onset and most predictable dose-response of any IV vasodilator.
- Dose: 0.3–5 mcg/kg/min (start low, titrate every 5 min)
- Indications: hypertensive emergency, acute afterload reduction (severe MR, acute HF), aortic dissection (with beta-blocker first)
- Cyanide toxicity: risk increases with doses >2 mcg/kg/min or duration >48 hours. Monitor lactate, mixed venous O2. Treat with sodium thiosulfate, hydroxocobalamin.
- Light sensitivity: wrap infusion bag in opaque cover
Nitroglycerin IV
IV nitroglycerin is a predominantly venodilator at low doses (reducing preload) with additional arterial vasodilation at higher doses.
- Dose: 5–200 mcg/min, titrate by 5–10 mcg/min every 3–5 min
- Indications: ACS (reduces ischemia, preload), acute decompensated HF, hypertensive emergency with pulmonary edema
- Tolerance: tachyphylaxis develops within 24–48 hours of continuous infusion; consider nitrate-free intervals
- Contraindications: PDE5 inhibitor use within 24–48 hours, severe aortic stenosis, right ventricular infarction
Nicardipine
Nicardipine is a dihydropyridine calcium channel blocker providing potent, titratable arterial vasodilation with minimal negative inotropic effect.
- Dose: 5 mg/hr initial, increase by 2.5 mg/hr every 5–15 min to maximum 15 mg/hr
- Indications: perioperative hypertension, aortic dissection (alternative to esmolol), hypertensive emergency, acute stroke
- Advantages: predictable dose-response, no cyanide toxicity, long duration of action after discontinuation (4–6 hours to fully wear off)
Esmolol
Esmolol is an ultra-short-acting cardioselective β1 blocker (half-life ~9 minutes) with rapid onset and offset, ideal for acute rate and blood pressure control.
- Loading: 500 mcg/kg IV over 1 min
- Maintenance: 50–200 mcg/kg/min (titrate by 50 mcg/kg/min every 4–5 min)
- Indications: aortic dissection (first-line for rate/BP control), SVT, perioperative tachycardia/hypertension, thyroid storm
- Advantage: ultra-short half-life makes it ideal when negative inotropic tolerance is uncertain
Diltiazem IV
IV diltiazem is the most commonly used non-dihydropyridine CCB for acute rate control in atrial fibrillation and atrial flutter.
- Loading: 0.25 mg/kg IV bolus over 2 min (~15–20 mg); may repeat at 0.35 mg/kg after 15 min if inadequate response
- Maintenance: 5–15 mg/hr continuous infusion
- Onset: 2–7 minutes (IV bolus)
- Caution: avoid in HFrEF (negative inotropy), pre-excited AF (WPW), and concurrent IV beta-blocker use (risk of severe bradycardia/heart block)
Clevidipine
Clevidipine is an ultra-short-acting IV dihydropyridine CCB (half-life ~1 minute) metabolized by blood esterases, providing extremely rapid onset and offset.
- Dose: 1–2 mg/hr initial, double every 90 seconds until approaching goal, then increase by <2 mg/hr; maximum 32 mg/hr (21 mg/hr for >24 hours)
- Indications: perioperative hypertension (FDA-approved), acute hypertension requiring precise titration
- Lipid formulation: soybean oil emulsion — contraindicated in soy/egg allergy; contributes 2 kcal/mL (factor into TPN/nutrition calculations)
- Advantages: organ-independent metabolism, no dose adjustment for renal/hepatic impairment
| Agent | Dose Range | Onset | Primary Indication | Key Consideration |
|---|---|---|---|---|
| Nitroprusside | 0.3–5 mcg/kg/min | Seconds | Hypertensive emergency, afterload reduction | Cyanide risk >48h; light-sensitive |
| Nitroglycerin | 5–200 mcg/min | 1–2 min | ACS, acute HF, pulmonary edema | Tolerance in 24–48h; avoid with PDE5i |
| Nicardipine | 5–15 mg/hr | 5–15 min | Periop HTN, aortic dissection | Prolonged offset (4–6h); no cyanide risk |
| Esmolol | 50–200 mcg/kg/min | 60 seconds | Aortic dissection, SVT, periop | Ultra-short t½ (~9 min); loading 500 mcg/kg |
| Diltiazem IV | 5–15 mg/hr | 2–7 min | AF/flutter rate control | Avoid in HFrEF, WPW; bolus 0.25 mg/kg |
| Clevidipine | 1–32 mg/hr | 1–2 min | Periop HTN, acute HTN | t½ ~1 min; lipid emulsion (soy/egg allergy) |
Key References
- De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010;362(9):779–789. DOI: 10.1056/NEJMoa0907118
- Levy B, Clere-Jehl R, Legras A, et al. Epinephrine versus norepinephrine for cardiogenic shock after acute myocardial infarction. J Am Coll Cardiol. 2018;72(2):173–182. DOI: 10.1016/j.jacc.2018.04.051
- Cuker A, Arepally GM, Chong BH, et al. American Society of Hematology 2018 guidelines for management of venous thromboembolism: heparin-induced thrombocytopenia. Blood Adv. 2018;2(22):3360–3392. DOI: 10.1182/bloodadvances.2018024489
- Kowey PR, Marinchak RA, Rials SJ, Bharucha D. Intravenous amiodarone. J Am Coll Cardiol. 1997;29(6):1190–1198. DOI: 10.1016/S0735-1097(97)00068-3
- Di Biase L, Saenz LC, Burkhardt DJ, et al. Esophageal capsule endoscopy after radiofrequency catheter ablation for atrial fibrillation: documented higher risk of luminal esophageal damage with general anesthesia as compared with conscious sedation. Circ Arrhythm Electrophysiol. 2009;2(2):108–112. DOI: 10.1161/CIRCEP.108.815266