Adult, U.S.-first educational reference. This guide catalogs currently marketed cardiovascular agents plus guideline-referenced off-label, non-U.S., and withdrawn drugs that remain clinically or board relevant. Every card separates mechanism → typical adult dosing → guideline recommendation/COR/LOE → pivotal evidence → adverse effects → practical pearl. Dosing is a starting reference, not a substitute for the current label, a validated clinical pathway, the required renal method, or pharmacist verification.
Mechanism of Action AtlasTwenty-four class maps, two animated lessons and a licensed nephron illustration connect drug targets to physiology.
Open the visual atlas →
One canonical homeEach agent appears once under its primary clinical domain; cross-indications are carried inside the card and linked from the alphabetical index.
Indication-specific evidenceA drug is never simply “Class I.” The card names the population, use, guideline year, COR, and LOE - or explicitly states when none exists.
Label ≠ guideline ≠ trialNew approvals after a guideline carry a label/new-evidence badge, not a retrofitted recommendation grade. Surrogate and symptom effects stay separate from outcomes.
High-alert guardrailsHeparin nomograms, thrombolysis, infusions, antiarrhythmic loading, electrolyte replacement, and reversal require a current validated protocol.
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How to read a card
same six rows every time
MechanismTarget, channel, enzyme, or receptor → hemodynamic/electrophysiologic effect.
Adult doseMost common cardiology route, start/load, target, maximum, and key adjustment.
GuidelineExact indication and evidence framework; U.S. COR/LOE unless marked ESC/CHEST.
TrialNamed pivotal study, outcome direction, effect estimate, and key limitation when useful.
Safety + pearlCommon and serious adverse effects, hard stops, interactions, monitoring, and one clinical trap.
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Evidence badges
strength · provenance · status
COR 1 · A Strong guideline recommendationBenefit greatly exceeds risk; high-quality evidence. COR 2a = reasonable; 2b = may be considered; 3 = no benefit or harm.
NO COR/LOE Label, consensus, or legacy practiceCommon does not mean guideline graded. The evidence row states what kind of authority supports the use.
Status badgesU.S. RX current; NEW post-guideline; OFF-LABEL; NON-U.S.; WITHDRAWN.
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Fast safety map
pause before prescribing
| Trigger | Stop and verify | Why it matters |
|---|
| Kidney dysfunction | DOACs (use label-specified CrCl method), LMWH, fondaparinux, dofetilide, sotalol, digoxin, milrinone, colchicine | Accumulation causes bleeding, torsades, bradyarrhythmia, or toxicity; eGFR and Cockcroft-Gault are not interchangeable. |
| Pregnancy potential | ACEi/ARB/ARNI/aliskiren, MRAs, statins/new lipid agents, warfarin, ERAs, riociguat, myosin inhibitors | Fetal toxicity and contraceptive interactions are drug-specific; see P.45 and the current label. |
| Low EF / decompensated HF | Verapamil/diltiazem, dronedarone, cilostazol, thiazolidinediones, most class I antiarrhythmics, NSAIDs | Negative inotropy, fluid retention, or excess mortality can override an otherwise attractive mechanism. |
| Long QT / bradycardia | Dofetilide, sotalol, ibutilide, quinidine, procainamide, disopyramide; stacked AV-nodal blockers | Correct K/Mg, calculate CrCl, review interacting drugs, and use the required monitored initiation pathway. |
A-Z
All agents
generic first · grouped products named
Default ACS frame: aspirin plus a P2Y12 inhibitor for 12 months when bleeding risk is not high; personalize agent and duration around ischemic, bleeding, PCI, stroke, age, and weight features.
Not routine “more is better.” Cangrelor fills an oral-P2Y12 gap; GP IIb/IIIa inhibitors are chiefly bailout therapy for large thrombus/no-reflow and require renal/bleeding review.
Symptom drugs are not automatically prognosis drugs. Match the agent to BP, HR, LV function, vasospasm, and residual angina; never combine nitrates with PDE5 inhibitors or riociguat.
Four distinct roles: anti-inflammatory secondary prevention, claudication symptom therapy, no-benefit legacy therapy, and a rarely used platelet-pathway agent with major bleeding constraints.
Validated protocol required. Weight, indication, ACT/aPTT/anti-Xa method, renal function, timing of invasive procedures, and prior heparin exposure change the dose.
Do not borrow a dose from another indication. NVAF reduction rules, acute-VTE loading, extended therapy, vascular-dose therapy, and valve indications are different pathways.
Reperfusion drug ≠ anticoagulant. Fibrinolysis requires a diagnosis-specific time window, contraindication checklist, BP control, weight-based dosing, and a plan for adjunct antithrombotics and rescue intervention.
Two opposite emergency lanes. Confirm whether the patient needs clot lysis or hemostatic reversal before reaching for a factor product; both carry thrombotic risk.
Andexanet alfa U.S. sales ended 22 December 2025. Current reversal should follow the specific anticoagulant, time since last dose, renal function, bleeding site, and a validated pathway.
First classify the CCB. Dihydropyridines lower vascular resistance; diltiazem/verapamil slow AV nodal conduction and are harmful in HFrEF.
Not a class-effect shortcut. Carvedilol, metoprolol succinate, and bisoprolol are the HFrEF outcome agents; atenolol is useful for BP/rate but is not HFrEF GDMT.
Short half-life is a safety feature. Esmolol is titratable for acute aortic/rate-control problems; labetalol is central to pregnancy and emergencies; propranolol spans thyrotoxicosis and channelopathies.
Never overlap with ARNI. Allow at least 36 hours when switching between an ACEi and sacubitril/valsartan in either direction. Avoid ACEi in pregnancy and bilateral renal-artery stenosis. HF guidance advises against ACEi with any angioedema history.
ARB selection is indication-specific. Candesartan, valsartan, and losartan have HFrEF evidence. Telmisartan has vascular-risk and BP evidence. Avoid dual ACEi/ARB/direct-renin blockade because toxicity increases without routine clinical benefit.
Core first-line treatment remains thiazide-like diuretic, ACEi/ARB, or long-acting DHP CCB. Central and alpha-blocking drugs usually enter for a specific comorbidity or later-line need.
Treat the emergency, not the number. The target and preferred infusion change for aortic dissection, pulmonary edema, stroke, pregnancy, catecholamine crisis, and renal failure.
Before adding: verify technique, adherence, long-acting triple therapy, diuretic adequacy, sodium/NSAIDs, OSA, kidney disease, and primary aldosteronism. Newer drugs may be FDA-approved but postdate the guideline.
Build the outcome stack early. In HFrEF, cover all four foundational classes; in higher EF, distinguish HF-event benefit from proven mortality benefit.
Different benefits: SGLT inhibitors reduce HF events; ivabradine is a sinus-rate/HF-admission drug; vericiguat is post-worsening-HF; digoxin is symptom/admission support with a narrow therapeutic margin.
Adjuncts solve specific barriers. They do not replace the foundational stack: treat iron deficiency, preserve RAAS/MRA therapy when possible, and use hydralazine-nitrate for the right population or intolerance pathway.
Loop diuretics relieve congestion; they are not proven mortality drugs. Dose to urine sodium/output, weight, symptoms, perfusion, kidney trajectory, and the lowest effective maintenance dose.
More urine can mean more harm. Combination therapy needs frequent electrolytes, creatinine, volume/perfusion assessment, and a plan to de-escalate once the resistance problem resolves.
Validated protocol required. Replacement concentration/rate, telemetry, IV access, acid-base state, renal function, and the cause of the abnormality determine safe dosing.
Wide + irregular is a pause signal. Pre-excited AF can deteriorate with AV-nodal blockade; synchronized cardioversion outranks drug experimentation when unstable.
Vaughan Williams is a mechanism map, not a prescription. Structural disease, ischemia/scar, conduction, QT, renal/hepatic clearance, and the target arrhythmia select the actual drug.
Class IC hard stop: prior MI or significant structural scar/disease. Pair flecainide/propafenone with AV-nodal protection when treating AF; amiodarone trades lower torsades risk for multi-organ toxicity.
Micrograms versus milligrams can kill. Dofetilide uses mcg and mandatory CrCl/QT-based monitored initiation; sotalol is renally cleared and also needs a QT-safe initiation pathway.
These are resuscitation pathways, not routine drug cards. Call poison control/toxicology early, manage airway/perfusion/electrolytes, and expect prolonged therapy or ECMO in refractory lipophilic cardiotoxic overdose.
Statins remain the foundation. Choose the intensity and molecule around the required LDL reduction, ASCVD risk, interactions, liver disease, pregnancy context, symptoms, and a structured rechallenge plan.
“Statin intolerant” is not one phenotype. Confirm timing, CK/thyroid/drug interactions, dechallenge/rechallenge, alternate statin/dosing, and the LDL gap that a nonstatin must close.
Choose by the LDL gap, outcomes evidence, and route. PCSK9 antibodies have completed cardiovascular outcomes trials; distinguish that evidence from the LDL-lowering data for siRNA and oral PCSK9 inhibition.
Do not treat these as interchangeable add-ons. Bile-acid binders and niacin have major tolerability or outcomes limits; HoFH and severe-hypertriglyceridemia therapies have narrow specialty indications.
Match treatment to the outcome. Icosapent ethyl targets selected residual ASCVD risk. Severe-TG therapy targets pancreatitis risk, but direct prevention evidence differs by agent. Mixed fish oil is not interchangeable with purified EPA.
Weight loss alone is not the evidence claim. Name the product, population, cardiovascular indication, completed outcome trial, HF/CKD effects, and peri-procedure/sick-day issues.
Typical ICU ranges only. Concentration, weight convention, line/access, titration interval, arterial pressure monitoring, and extravasation rescue follow a validated infusion protocol.
Low output is not one physiology. Select around BP/SVR, RV versus LV failure, beta-blocker exposure, arrhythmia, renal function, pulmonary vascular load, and a bridge/escalation plan.
Never combine a PDE5 inhibitor with riociguat or any nitrate. PAH therapy should not be reflexively extrapolated to Group 2 or most Group 3 PH.
Never abruptly stop parenteral prostacyclin. Formulation, pump competence, backup supply, line infection, platelet count, pregnancy, and specialty-pharmacy continuity are part of the prescription.
Myosin inhibitors can cause systolic dysfunction. Current REMS/label echocardiography, LVEF/LVOT response, pregnancy prevention, and CYP interactions are part of treatment - not optional monitoring.
Treat confirmed ATTR-CM, not an isolated wrist deposit or equivocal scan. Tafamidis/acoramidis stabilize TTR; vutrisiran silences hepatic TTR; routine stabilizer-plus-silencer outcomes are not established.
Do not empirically immunosuppress routine presumed viral myocarditis. Steroid/steroid-sparing therapy belongs to defined immune-mediated phenotypes, specialist pathways, and infection exclusion.
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Never-miss combinations
hard stops and major hazards
Nitrate + sildenafil/tadalafil/riociguat → profound hypotension. Respect the product-specific nitrate washout; riociguat is also contraindicated with PDE5 inhibitors.
ACEi ↔ sacubitril/valsartan → allow at least 36 hours between doses in either direction. Never combine ARNI with an ACEi or a separate ARB.
Multiple AV-nodal blockers → beta blocker + verapamil/diltiazem ± digoxin/amiodarone can produce shock or high-grade block.
QT stack + low K/Mg + renal accumulation → dofetilide, sotalol, ibutilide, procainamide, quinidine, and disopyramide need a deliberate interaction/CrCl review.
Triple antithrombotic therapy → minimize aspirin duration when OAC + P2Y12 is required after PCI; use the AF/PCI pathway rather than an automatic 12-month triple regimen.
Dual RAAS or dual MRA therapy → ACEi + ARB + aliskiren and spironolactone + eplerenone/finerenone add renal/hyperkalemia harm without routine benefit.
Strong CYP/P-gp changes → review DOACs, ticagrelor, ranolazine, colchicine, statins, myosin inhibitors, and several antiarrhythmics before starting or stopping an inhibitor/inducer.
Volume depletion + fasting/illness → hold/assess SGLT inhibitors around major surgery, prolonged fasting, and acute illness because euglycemic ketoacidosis may occur with normal glucose.
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Renal and dosing equations
use the method named by the label
| Equation / check | Formula | Drug decisions |
|---|
| Cockcroft-Gault CrCl | [(140 − age in years) × weight (kg)] ÷ [72 × SCr (mg/dL)] × 0.85 if female | Use the label’s weight convention (actual weight for dofetilide). CrCl is in mL/min. Do not substitute indexed eGFR. |
| Corrected QT | QTcB = QT/√RR · QTcF = QT/∛RR | Use QT and RR in seconds, then convert QTc to ms. Follow the product protocol. Bazett overcorrects at fast HR and undercorrects at slow HR. |
| Apixaban NVAF reduction | Usual NVAF reduction to 2.5 mg BID when ≥2 of 3: age ≥80, weight ≤60 kg, SCr ≥1.5 mg/dL. | These criteria do not replace VTE dosing. Combined P-gp and strong CYP3A4 inhibitors require a separate dose check. The label exempts clarithromycin from dose adjustment. |
| UFH / LMWH | Weight-based protocol; anti-Xa/aPTT target and obesity/renal convention are protocol specific. | ACS, VTE, ECMO/MCS, pregnancy, and procedural anticoagulation are different protocols. |
| Electrolyte substrate | Set patient/protocol targets; reassess after replacement rather than “chasing” a single result. | QT-prolonging AADs, digoxin toxicity, torsades, diuresis, and renal failure need individualized K/Mg/Ca correction. |
See the ACE inhibitor–ARNI washout in motion →
UNITSRead the unit aloud: dofetilide is in micrograms; vasopressors/inotropes may be mcg/kg/min, mcg/min, ng/kg/min, or U/min; high-dose insulin for beta-blocker/CCB poisoning uses U/kg/h. A correct number with the wrong unit is still a lethal dose.
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Pregnancy and lactation: rapid frame
card-level label still governs
| Commonly used when indicated | Avoid / contraindicated | Nuance |
|---|
| Labetalol, nifedipine ER, methyldopa; IV labetalol or hydralazine, or oral immediate-release nifedipine, for acute severe pregnancy hypertension; LMWH for many anticoagulation indications | ACEi, ARB, ARNI, aliskiren; ERAs and riociguat; warfarin for most pregnancy contexts; myosin inhibitors; most novel lipid agents | Mechanical valves, PAH, arrhythmia, acute thrombosis, and severe hypertension require maternal-fetal medicine plus disease specialists; trimester and breastfeeding status matter. |
| Selected beta blockers, digoxin, adenosine, flecainide/sotalol in expert pathways; low-dose aspirin for preeclampsia prevention when indicated | Amiodarone unless life-threatening/refractory; spironolactone generally avoided; statins usually stopped though the FDA removed the blanket strongest warning | Most pregnant patients stop statins. Patients who need ongoing statin therapy should not breastfeed. Specialist exceptions require an explicit risk–benefit decision. |
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Monitoring cadence by toxicity domain
baseline → early check → longitudinal
| Domain | Baseline / after change | Longitudinal triggers |
|---|
| RAAS / MRA / diuretics | BP/volume, K, Na, Mg and SCr/eGFR. Use drug-specific timing after initiation/titration: spironolactone K within 1 week, finerenone K at 4 weeks with eGFR in HF. | Check earlier or more often with AKI, intensive diuresis, poor intake, hypotension or new NSAID/K exposure. Continue the label-based longitudinal schedule. |
| Anticoagulation | Indication, weight, CBC, renal/hepatic function, interacting drugs, adherence, procedure/pregnancy plan | Bleeding, thrombosis, weight/renal change, new antiplatelet, falls/frailty, surgery, refill interruption |
| Antiarrhythmics | 12-lead ECG/QTc/QRS/PR, rhythm, K/Mg, kidney/liver, EF/scar, full interaction list | Illness/AKI, bradycardia, syncope, new QT drug, dose change; thyroid/liver/lung/eye surveillance for amiodarone |
| Lipid / cardiometabolic | Lipid panel, secondary causes, liver/muscle history, diabetes/weight/renal status, pregnancy plans | 4-12-week lipid response after change; symptoms/interactions; pancreatitis/gallbladder, retinopathy, or dehydration/ketosis risks by agent |
| Specialty cardiomyopathy / PAH | Confirm phenotype/indication; echo/hemodynamics, CBC/LFT, pregnancy test, specialty access, REMS/formulation training | LVEF or symptoms, line/pump interruption, anemia/thrombocytopenia, vitamin A symptoms, CYP changes, coverage gaps |
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Primary evidence map
original evidence set · 9 Aug 2026
ACC/AHA clinical practice guidelines
2025 ACS and High BP; 2026 Dyslipidemia, CKM, and Acute PE; 2023 AF/CCD; 2024 HCM/PAD; 2022 HF and Aortic Disease.
ESC / specialty guidance
2025 Pregnancy and Myocarditis/Pericarditis, 2024 AF and peripheral/aortic, 2022 ESC/ERS PH plus the 2026 ERS PAH treatment update, and current CHEST/ASH VTE guidance.
Regulatory and trial evidence
Current Drugs@FDA/DailyMed labels, safety withdrawals, and pivotal randomized trials. New post-guideline approvals are labeled rather than assigned invented COR/LOE.
USEBefore clinical use: identify the indication → scan mechanism and dose → apply the card’s COR/LOE to that exact population → check the trial limitation → run safety/interaction/renal/pregnancy gates → verify the current label and a validated clinical protocol.
REVIEWEducational reference. Exact doses, mixing/titration, renal thresholds, contraindications, and availability require current-label and pharmacy/cardiology verification before clinical use. Original evidence set: 9 August 2026. Prior targeted review: 5 September 2026. All-chapter editorial and source review: 17 October 2026.