Familiar drug names appear in every resuscitation guide. Blindly following them does not save lives. What works in a noisy resus bay is a short, disciplined playbook for emergency cardiac drugs, applied with timing, situational judgement, and respect for physiology. This explainer sets out that playbook and keeps the focus on what to do, when to do it, and what to avoid.

Essential Emergency Cardiac Drugs

I think of the core set of emergency cardiac drugs as a compact toolkit. Each agent earns its place by changing a critical variable fast: vascular tone, rhythm, or conduction. The list below prioritises indication, practical administration, and key caveats.

Epinephrine (Adrenaline)

Epinephrine is the vasopressor that restores coronary and cerebral perfusion pressure during CPR. In practice, it is used early in non-shockable rhythms and after the second shock in shockable rhythms. For post-ROSC hypotension, low-dose infusions can stabilise vascular tone while causes are treated. Excess or premature dosing risks increased myocardial oxygen demand and arrhythmogenesis. Used well, it buys time. Misused, it raises lactate and afterload without benefit.

• Primary roles: vasoconstriction during CPR, vasopressor support post-ROSC.

• Do not let it delay high-quality chest compressions and defibrillation.

• Prepare for transient tachycardia and potential hypertension after ROSC.

For clarity, this discussion aligns with common practice for cardiac arrest medications while avoiding rote memorisation of numbers. I address epinephrine dosage in cardiac arrest in the dosing section, including timing nuances.

Amiodarone

Amiodarone is the default antiarrhythmic for shock-refractory ventricular fibrillation or pulseless ventricular tachycardia. It suppresses abnormal automaticity and prolongs repolarisation. For stable wide-complex tachycardia, an infusion may prevent degeneration. Monitor for hypotension during rapid boluses. In prolonged codes, cumulative dosing can complicate later haemodynamics, so I escalate deliberately and reassess rhythm response after each shock.

• Use after defibrillation attempts for refractory VF or pulseless VT.

• Watch for bradycardia and hypotension during loading.

Atropine

Atropine blocks vagal tone at the AV node and can improve symptomatic bradycardia with poor perfusion. It is less effective in high-grade blocks below the AV node. If the response is partial or absent, move to pacing and consider catecholamine support. I always pair atropine with planning for transcutaneous pacing when the clinical picture suggests an infranodal block.

Lidocaine

Lidocaine is a Class Ib agent with rapid sodium channel blockade that dampens ventricular excitability, particularly during ischaemia. It is a credible alternative when amiodarone is unavailable or poorly tolerated. As ANZCOR notes, it may replace amiodarone for shock-refractory VF or VT and can be given at 1 mg with repeat dosing based on response. Expect central nervous system signs if levels rise, and use an infusion to maintain effect after ROSC when indicated.

• Useful in ischaemia-driven ventricular arrhythmias.

• Consider a maintenance infusion to prevent recurrence.

• Monitor for neurological symptoms at higher cumulative doses.

Adenosine

Adenosine transiently blocks AV nodal conduction and is highly effective for AVNRT and many AVRT presentations. The half-life is extremely short, so it must be given as a rapid push with an immediate flush. As Mayo Clinic reports, its half-life is under **10 seconds**, which explains the need for brisk administration and close monitoring. Expect brief flushing or chest pressure. For irregular wide-complex tachycardia, avoid it and treat for possible atrial fibrillation with pre-excitation.

• Confirm regular narrow-complex tachycardia before use.

• Prepare for transient asystole and patient discomfort.

Magnesium Sulphate

Magnesium sulphate is the go-to agent for torsades de pointes and long QT-related polymorphic VT. It stabilises myocardial cells and shortens the QT over time in magnesium-deficient states. I use it in both pulseless and perfusing torsades, alongside correction of hypokalaemia and removal of QT-prolonging agents. Avoid over-rapid administration if the patient has a pulse to limit hypotension.

• Indicated in torsades and documented hypomagnesaemia with arrhythmia.

• Support with potassium optimisation and trigger removal.

Sodium Bicarbonate

Sodium bicarbonate is not a routine arrest drug. It becomes appropriate in select scenarios such as severe hyperkalaemia, tricyclic antidepressant toxicity, and prolonged resuscitation with significant acidaemia. As Medscape details, a common adult cardiac arrest dose is **1 mEq/kg** intravenously, with subsequent dosing guided by blood gases. Use with caution, because indiscriminate dosing can worsen intracellular acidosis and decrease oxygen unloading.

• Reserve for specific indications or documented severe acidaemia.

• Re-evaluate based on serial blood gas results.

Calcium Chloride

Calcium chloride enhances cardiac contractility and stabilises the myocardium in hyperkalaemia or calcium channel blocker toxicity. I prefer calcium chloride for its higher bioavailability through a central line, and calcium gluconate peripherally when central access is unavailable. In suspected hyperkalaemia arrest, give it early while preparing definitive potassium shifting and removal strategies.

• Use in hyperkalaemia, hypocalcaemia, and calcium antagonist overdose.

• Prefer central administration for calcium chloride due to local irritation risk.

Antiarrhythmic Drugs Classification and Clinical Applications

Classification helps thought, not dogma. In arrest and peri-arrest care, I translate class effects into expected clinical behaviour. Below is a concise antiarrhythmic drugs list by mechanism and common examples.

Class I Sodium Channel Blockers

In practice, lidocaine is the Class Ib drug with the most relevance in emergencies. It is quick on, quick off, and attenuates ischaemia-driven ventricular irritability. Class Ic agents are generally avoided in structural heart disease during acute care. When I am choosing among emergency cardiac drugs to suppress ventricular ectopy post-ROSC, lidocaine is often my first move if amiodarone is unsuitable.

Class II Beta-Blockers

Short-acting beta-blockers are valuable for rate control and for blunting adrenergic surges driving arrhythmias. They must be used carefully in hypotension or poor output states. I consider low-dose, titratable options once rhythm and perfusion are stabilised. Careful sequencing matters: stabilise circulation, then address triggers, then add a beta-blocker if the physiology allows.

Class III Potassium Channel Blockers

Amiodarone dominates this group in emergency care for VF or pulseless VT that resists shocks. Sotalol has a narrower role and is rarely used during a code. After ROSC, a controlled amiodarone infusion can reduce recurrence risk while the underlying cause is treated. The benefit is rhythm stability, but hypotension and bradycardia are credible trade-offs.

Class IV Calcium Channel Blockers

Verapamil and diltiazem slow AV nodal conduction and help terminate some re-entrant SVTs. For atrial fibrillation, they can control rate when haemodynamics are stable. I avoid them in suspected pre-excitation and in significant left ventricular dysfunction. In acute heart failure, I look to alternative rate control strategies first.

Unclassified Antiarrhythmic Agents

Adenosine is unique because it tests and treats AV node-dependent tachycardias in seconds. It also clarifies diagnoses when it transiently reveals atrial activity. Digoxin is slower and is not a frontline arrest drug, but it has a place in chronic atrial fibrillation with heart failure. When assembling emergency cardiac drugs for an SVT case, adenosine remains the initial lever if the rhythm is regular and narrow.

Dosage Guidelines and Administration Routes

Dose, route, and timing decide whether emergency cardiac drugs help or harm. I plan for the fastest reliable access, the cleanest line, and the shortest dwell between decision and delivery.

Epinephrine Dosage in Cardiac Arrest

Epinephrine dosage in cardiac arrest is less about memorising a number and more about rhythm-specific timing and consistent intervals. In non-shockable rhythms, give it early to support perfusion pressure. In shockable rhythms, prioritise defibrillation and place epinephrine after the second shock, maintaining regular cyclic dosing while compressions continue. I avoid stacking catecholamines during prolonged low-flow states without reassessment, because the physiological costs can outweigh benefits.

• Early use in asystole and PEA, timed use in VF or pulseless VT.

• Do not interrupt compressions for administration.

Weight-Based Paediatric Dosing

Paediatric dosing is weight based, often using a length-based tape for rapid estimates. For each agent, I align dosing and intervals with paediatric life support guidance and the child’s physiology. Many emergency cardiac drugs scale linearly, but distribution volume, hepatic clearance, and congenital substrates create exceptions. When there is uncertainty, I favour the lower end of ranges and reassess response closely.

Intravenous vs Intraosseous Administration

Intravenous access is preferred if it is immediately available and reliable. Intraosseous access offers near-equivalent delivery when IV attempts delay critical therapy. I place IO access early if two quick IV attempts fail or the veins are collapsed. The choice is not stylistic. It is a time and haemodynamics decision that determines how fast emergency cardiac drugs reach the central circulation.

• Use the shortest possible tubing and a brisk flush to speed delivery.

• Document the line used, time given, and clinical response.

Endotracheal Drug Administration

Endotracheal delivery is a fallback route when vascular access is not available and drug urgency is high. Only a limited subset of emergency cardiac drugs can be given this way. Doses are higher than intravenous to overcome dilution and variable absorption. The tube must be correctly placed, and the drug followed by a ventilatory cycle to disperse it. For neonates, specialist algorithms increase doses further to account for distinct airway and circulation physiology during resuscitation. In short, it is a bridge, not a destination.

Continuous Infusion Protocols

Infusions stabilise effect after a bolus, avoid peaks and troughs, and permit finer titration. Amiodarone, lidocaine, and vasopressors are common examples. I set a clear target: suppression of recurrent VF, maintenance of MAP, or control of ectopy. Infusion safety is basic discipline. Label lines, use smart pumps, and reassess at defined intervals to prevent drift into iatrogenic harm. Infusions extend benefit from emergency cardiac drugs beyond the initial push.

Special Considerations and Contraindications

No drug is context free. The same ampoule can rescue or derail the case. The following considerations reduce surprises and improve the odds of meaningful recovery.

Drug Interactions in Emergency Settings

Watch for QT-prolonging combinations when giving amiodarone or certain antipsychotics. Beware additive AV nodal block when combining beta-blockers and non-dihydropyridine calcium channel blockers. Calcium can antagonise some antidotes, while bicarbonate can alter drug ionisation. I use a simple discipline: before pushing another ampoule, state the last three drugs with doses to the team. It prevents silent interactions and duplication.

• QT risk: combine long QT agents only with a clear indication.

• AV block risk: avoid dual nodal blockade unless planned and monitored.

Age-Specific Considerations

Paediatric patients have different distribution volumes and receptor sensitivities. Older adults have reduced renal and hepatic clearance and more polypharmacy. I lower thresholds for electrolyte correction in both extremes of age. For fragile patients, titration beats repeated bolusing. The goal is the same rhythm outcome with less physiological collateral.

Pregnancy and Cardiac Emergencies

During pregnancy, maternal resuscitation takes precedence and supports the foetus. Positioning to relieve aortocaval compression matters. Many emergency cardiac drugs remain indicated, but dosing and timing must consider altered volume of distribution and placental transfer. Early involvement of obstetrics is not optional. It shortens time to definitive decisions if ROSC is delayed.

Post-Resuscitation Drug Management

After ROSC, the drug strategy simplifies to three aims: maintain perfusion, prevent recurrent arrhythmia, and avoid secondary injury. I titrate vasopressors to MAP targets and wean as causes are fixed. If amiodarone or lidocaine suppressed VF, an infusion may continue while electrolytes and ischaemia are addressed. Sedation must support ventilation and neuroprotection, not obscure deterioration. Consistency matters, because emergency cardiac drugs that rescued the patient can hinder recovery if not de-escalated.

Key Takeaways on Emergency Cardiac Medications

• Start with cause and timing. The right emergency cardiac drugs, given at the right moment, change outcomes.

• Defibrillation and compressions come first for shockable rhythms. Drugs support, they do not replace fundamentals.

• Use amiodarone or lidocaine for refractory VF or pulseless VT, with clear reassessment after each intervention.

• Reserve sodium bicarbonate for specific indications or documented severe acidaemia.

• Prefer IV, move to IO early if access delays therapy. Endotracheal dosing is a temporary bridge.

• Infusions maintain effect after ROSC and limit peaks and troughs.

• Check interactions, especially QT and dual nodal blockade risks.

• Paediatric and geriatric physiology change drug handling. Adjust thoughtfully.

The habit worth keeping: decide the intent of a drug, state it aloud, and confirm the effect within minutes. Precision beats volume.

Frequently Asked Questions

What is the first drug given during cardiac arrest?

Epinephrine is typically the first-line drug in non-shockable rhythms, given early to support perfusion pressure. In shockable rhythms, defibrillation takes priority, and epinephrine follows after the second shock. The exact sequence depends on rhythm recognition and team readiness. Emergency cardiac drugs work best when aligned to those rhythm paths.

How quickly should epinephrine be administered in cardiac arrest?

Administer epinephrine without delaying compressions. In asystole or PEA, give it promptly once access is available. For VF or pulseless VT, defibrillate first, then incorporate epinephrine after the second shock and maintain consistent intervals. Timely, not frantic, is the standard.

Can emergency cardiac drugs be given through an IV cannula?

Yes. Intravenous delivery is preferred when immediately available. If IV access is not obtainable within moments, intraosseous access offers comparable speed and effect for emergency cardiac drugs. The priority is rapid, reliable delivery without interrupting CPR or defibrillation.

What are the most common side effects of antiarrhythmic drugs?

Expect hypotension and bradycardia with many antiarrhythmics, particularly during loading. Adenosine can cause brief flushing and chest pressure. Lidocaine may produce neurological symptoms at higher levels. These effects are manageable with preparation, careful dosing, and reassessment.

How long do emergency cardiac drugs remain effective after administration?

Onset and duration vary. Adenosine acts for seconds. Lidocaine and amiodarone have longer and clinically useful effects that support rhythm stability post-ROSC. Vasopressors require titration because effect fluctuates with intravascular volume, pH, and receptor sensitivity. Duration is not a fixed number. It is a relationship with the patient’s physiology.

Which cardiac arrest medications can be given via endotracheal tube?

Only a limited group is suitable for endotracheal administration. Epinephrine is the most relevant in modern algorithms. Doses are higher than IV because of unpredictable absorption, and the approach is considered a temporary measure until vascular access is secured. I switch to IV or IO as soon as possible.