The Code Crew: Medications That Save the Beat!

1. Pathophysiology of Cardiac Arrest:

Cardiac arrest arises from a failure of ventilation and perfusion. Hypoventilation leads to carbon dioxide retention, causing respiratory acidosis and systemic vasodilation, which compromise coronary perfusion pressure. This impairs oxygen delivery to the heart, increases myocardial irritability, and lowers the threshold for arrhythmias.

Simultaneously, decreased perfusion results in tissue hypoxia, driving lactic acidosis through anaerobic metabolism. This further contributes to multi-organ failure due to inadequate oxygenation^2-3.

The cornerstone of management is correcting these combined respiratory and metabolic derangements through:

1. Ensuring adequate ventilation
2. High-quality CPR to restore perfusion.
3. Early defibrillation to terminate arrhythmias.

2. Hyperkalemic Cardiac Arrest:

SB = Sodium Bicarbonate

Risk factors:

Let’s break down the risk factors into two categories: those specific to patients with end-stage renal disease (ESRD) and those that apply more generally. This overview is not exhaustive but highlights major considerations that inform bedside decision-making.

ESRD Risk Factors^4-5:

• Treatment non-adherence (e.g. high potassium diet, missed dialysis)
• Chronic hyperkalemia
• Medications (e.g. ACE inhibitors, angiotensin receptor blockers, spironolactone)
• Lower insulin states (e.g. patient is fasting for surgery)
• Under-dialyzed patients on peritoneal dialysis
  • In general, patients on peritoneal dialysis are at lower risk for hyperkalemia as they perform daily dialysis, have some residual kidney function and experience slower potassium shifts. However, they are at higher risk if their renal function declines without dialysis adjustments, they experience catheter dysfunction or are non-adherent to treatment.⁶

Overall, patients on dialysis face an exceptionally high risk of mortality from various causes, including cardiovascular disease, hyperkalemia, sepsis, and volume overload. Cardiovascular disease remains the leading cause of death in this population.⁷

While hemodialysis patients typically have a mild metabolic acidosis at baseline, they leave dialysis in an alkalotic state and gradually return to baseline before their next session. According to nephrologists at The Ottawa Hospital, acidosis is rarely the primary cause of cardiac arrest, even in patients who have missed a dialysis session. While correcting acidosis may be considered, prioritizing hyperkalemia treatment is critical, especially in patients with risk factors, abnormal labs, and/or ECG changes.

Notably, the highest-risk period for dialysis patients is early in the week — typically Monday or Tuesday — due to the longer interval between sessions and the resulting fluid and electrolyte shifts.⁸ Awareness of these patterns can help guide timely interventions and improve patient outcomes.

General Risk Factors^4-5:

• Tissue breakdown states (e.g. tumour lysis syndrome, rhabdomyolysis, trauma, burns, hemolysis, invasive group A strep infection)
• Diabetes
  • Lack of insulin
  • Hyperglycemia
• Medications
• Acute renal failure
• Metabolic acidosis
• Adrenal crisis

Hyperkalemic Arrest Management: “Stabilize and Shift” Approach

Adapted from ERC 2021¹² and AHA 2020¹³ guidelines, Ortiz et al⁵,Palmer et al⁹, Abuelo et al¹⁰, and Long et al¹¹.

I recommend against the use of salbutamol intra-arrest as we have already maximized our beta agonist effect with epinephrine and the onset of action is too long to be clinically useful.

Sodium bicarbonate is proposed to work through two mechanisms:^12,14

1. Promoting a transcellular potassium shift via H⁺/K⁺ exchange or HCO₃^–/K⁺ cotransport
2. Enhancing renal potassium excretion through alkalosis

However, transcellular shifts are largely ineffective without metabolic acidosis and patients with ESRD lack renal excretion. Hypertonic sodium bicarbonate may also be ineffective due to a “solute drag” where its high osmolarity pulls water and potassium out of cells, counteracting its intended purpose.^10,14

Overall, sodium bicarbonate should be the lowest priority in hyperkalemic cardiac arrests due to its unclear benefit and long onset of action. It may be considered in patients with ESRD to help counteract metabolic acidosis rather than to treat hyperkalemia.¹⁴

Potassium Elimination:

In low-flow states, interventions like furosemide (Lasix) or potassium binding resins (e.g. lokelma) have no role intra-arrest. If dialysis is significantly delayed, they may be considered, but only if residual renal and gastrointestinal function is adequate.⁹

Post-ROSC:

After achieving return of spontaneous circulation (ROSC), promptly obtain a STAT blood gas and ECG. If applicable at your site, activate a CODE ROSC (brings ICU and cardiology at the Ottawa Hospital), and page nephrology.

If ongoing ECG changes indicate hyperkalemia:

• Administer another dose of calcium
• Consider repeat insulin therapy, with close glucose monitoring

If dialysis is delayed and the patient has residual kidney and gastrointestinal function, consider interim measures like furosemide and Lokelma via nasogastric tube, especially if the delay exceeds one hour, per Ottawa nephrologists’ local guidance.

Dialysis:

Emergent hemodialysis is the definitive treatment for patients who achieve ROSC and do not respond to standard medical interventions. Intermittent hemodialysis is typically the most effective approach. However, in hemodynamically unstable patients, sustained low-efficiency dialysis (SLED) is preferred.⁹

For patients on peritoneal dialysis, rapid cycling or acute peritoneal dialysis can be completed, but availability varies by institution. Understanding your hospital’s capabilities is essential when considering alternative dialysis strategies in the post-ROSC setting.

3. Drug Adjuncts:

1. Calcium:

A drug often debated in the context of cardiac arrest. Its powerful inotropic and vasopressor effects make it a tempting option in critical situations. But here’s the twist: during cardiac arrest, sodium–calcium exchanger may reverse, flooding cells with calcium and triggering hypercontraction of the heart — a phenomenon known “stone heart”. This overload can theoretically amplify cellular damage.¹⁵

 This raises a key question: In OHCA, does calcium administration meaningfully improve ROSC, or does it risk making outcomes worse?

Evidence Summary:

The COCA trial by Vallentin et al. is the most influential randomized controlled trial (RCT) informing current resuscitation guidelines. Although the study was terminated early, which can overestimate potential harms, it showed no benefit to empiric calcium use in OHCA, and point estimates consistently favoured harm. The primary outcome, sustained ROSC, occurred in 19% of the calcium group compared to 27% with placebo (RR 0.72, 95% CI 0.49–1.03; P = .09), a difference that was not statistically significant.¹⁵

This finding held true across pre-specified subgroups, including patients with ECG signs of hyperkalemia or ischemia, and remained consistent at 6 months and 1 year.^16,17

Earlier RCTs by Stueven et al. (1985) also showed no benefit, though they were small and methodologically limited.^18,19 The COCA trial provides the strongest evidence to date against the routine of calcium use during cardiac arrest.

Resuscitation Guideline Indications:

ILCOR & AHA 2023: Recommend against empiric use of calcium during cardiac arrest.^20-21Lower certainty of evidence for in-hospital cardiac arrest, given absence of RCTs in this population.

The AHA guidelines recommend calcium administration for:

• Severe hyperkalemia (K⁺>6.5 mmol/L)
• Hypocalcemia
  • Though a rare cause of cardiac arrest, hypocalcemia can occur in conditions associated with rapid cellular turnover, such as tumor lysis syndrome.
  • While treatment is generally indicated for serum calcium levels <2.1 mmol/L or ionized calcium <0.63 mmol/L, arrest is typically seen at much lower levels, though an exact threshold remains undefined.²²
• Hypermagnesemia
  • Particularly in obstetric patients receiving magnesium infusions
  • The ERC recommends calcium administration at magnesium levels ≥1.75 mmol/L, while earlier AHA guidelines associate cardiac arrest with levels between 6–10 mmol/L.^12,23
• Calcium channel and beta blocker overdoses

The thresholds above provide general guidance, but in acute care settings, calcium administration should be guided by clinical context, prior laboratory values, and ECG changes suggestive of electrolyte toxicity. 

Non-guideline Indication:

• Hemorrhagic shock
  • Hypocalcaemia in hemorrhagic arrest may result from calcium binding during the coagulation cascade and chelation by citrate in transfused blood products. However, source control and timely administration of blood products, including clotting factors, remain the primary priorities in management.²⁴

*Dosing based on guidelines and local expert consensus

2. Sodium Bicarbonate:

Sodium bicarbonate has a long history in resuscitation medicine, dating back to the 1976 ACLS guidelines. Its use was initially driven by concerns that severe acidosis during cardiac arrest could:

• Reduce myocardial contractility
• Cause peripheral vasodilation
• Decrease responsiveness to endogenous and exogenous catecholamines

Advocates have argued that sodium bicarbonate administration could buffer this acidosis, potentially improving hemodynamics.³

Physiologic Concerns:

In most Canadian emergency departments, it’s available as a 50 mL pre-filled syringe of 8.4% NaHCO₃, a hypertonic, hypernatremic solution. While it can transiently raise serum pH by buffering hydrogen ions, this reaction produces carbon dioxide as a byproduct. Carbon dioxide rapidly diffuses across cell membranes, potentially worsening intracellular acidosis, particularly in the myocardium and brain.

The accompanying extracellular alkalosis introduces additional concerns. Alkalemia shifts the oxyhemoglobin dissociation curve to the left, impairing oxygen release to tissues. It can also blunt acidemia-driven cerebral vasodilation, potentially reducing cerebral perfusion at a time when it is most critical.

Beyond acid-base effects, sodium bicarbonate administration can lead to:

• Hypernatremia and osmotic fluid shifts, potentially exacerbating cerebral edema
• Hypokalemia and hypocalcaemia, which impair cardiac conduction and contractility
• Suppressed respiratory drive, as respiratory alkalosis decreases central chemoreceptor stimulation

While theoretical, these mechanisms may explain why sodium bicarbonate has shown no clear benefit in cardiac arrest.²⁵

Evidence Summary:

Three randomized controlled trials have evaluated the use of sodium bicarbonate in OHCA.^26-28 None demonstrated a statistically significant benefit in either short- or long-term survival. However, these studies are limited by methodological constraints, including small sample sizes and their completion prior to major resuscitation guideline updates.

In addition, several propensity score–matched observational studies have also explored this question.^29-31 While larger in scale, these studies carry a critical risk of bias, particularly due to resuscitation time bias — the phenomenon where sodium bicarbonate is more likely to be administered in prolonged arrests, confounding outcome interpretation. Importantly, no consistent survival benefit has been demonstrated in this literature either.

Resuscitation Guideline Indications:

AHA 2023: Recommend against routine administration of sodium bicarbonate during cardiac arrest.²¹

The AHA guidelines recommend sodium bicarbonate for:

• Hyperkalemia
  • Its benefit is debatable (as discussed above)
• Sodium channel blocker toxicity
  • Supported by case reports, animal studies, observational data, and toxicology consensus.¹³
  • Here are some of the sodium channel blockers you are most likely to encounter in the ED:
• Carbamazepine
• Citalopram
• Cocaine
• Dimenhydrinate
• Diphenhydramine
• Escitalopram
• Fluoxetine (supported by single case report)
• Hydroxychloroquine
• Lamotrigine
• Local anesthetics
• Procainamide
• Propranolol
• Tricyclic antidepressants
• Venlafaxine

Non-guideline Indications:

In discussion with local experts at TOH, consider sodium bicarbonate in the following cases:

 Non-anion gap metabolic acidosis (NAGMA): In the absence of strong RCT data, sodium bicarbonate replacement may be reasonable in critical NAGMA from gastrointestinal or renal losses, though it’s rarely an isolated cause of arrest.³

 ESRD with suspected metabolic acidosis: May be appropriate if supported by VBG findings, though significant acidosis is uncommon, even after missed dialysis. Other causes of arrest should be explored.⁷

 Toxicologic arrest and pre-arrest metabolic acidosis: Its use is most strongly supported in poisonings involving sodium channel blockers, salicylates, and toxic alcohols, where evidence suggests a clear benefit. For most other toxins, the impact on patient outcomes remains less certain.³²

*Dosing based on guidelines and local expert consensus

3. Magnesium:

Magnesium is a key mineral and vasodilator, essential for regulating sodium, potassium, and calcium flow across cell membranes. Magnesium stabilizes excitable membranes, is vital for correcting intracellular potassium deficiency, and plays a role in managing atrial and ventricular arrhythmias.³³

Evidence Summary:

Between 1997 and 2002, four RCTs evaluated the use of magnesium in cardiac arrest.^34-37 ILCOR conducted a comprehensive review in 2018 and found no new evidence since then.³⁸ Consistently, research has demonstrated no significant benefit of magnesium for achieving ROSC, survival, or favorable neurological outcomes, regardless of the presenting rhythm, including shock-refractory ventricular fibrillation and pulseless ventricular tachycardia (VF/pVT) arrests or polymorphic VT with a normal QT interval.^13,38

Resuscitation Guideline Indications:

ILCOR 2024: Recommend against the routine use of magnesium in shock-refractory VF/pVT.³⁸

The AHA guidelines recommend magnesium for:

• Torsades de Pointes
  • Defined as polymorphic ventricular tachycardia with prolonged QT interval, typically when the corrected QT interval exceeds 500 milliseconds.
  • Usually presents as self-terminating episodes of hemodynamic instability but can progress to ventricular fibrillation, requiring immediate intervention.
    • Defibrillation may be needed but does not prevent recurrence.
  • Rather than directly terminating the arrhythmia, magnesium stabilizes myocardial action potentials and suppresses early afterdepolarizations, lowering the risk of recurrence.
    • Supported by anecdotal evidence and small case series.¹³
  • Hypomagnesemia (<0.65 mmol/L).²³

Non-Guideline Indication:

 Severe hypokalemia (<2.5 mmol/L)²²: While potassium replacement is the primary goal, magnesium is a critical cofactor for maintaining intracellular potassium balance. Without correcting hypomagnesemia, potassium repletion may be ineffective, resulting in persistent arrhythmias and refractory hypokalemia.

*Dosing based on guidelines and local expert consensus

4. Amiodarone vs. Lidocaine

Last, we discuss which antiarrhythmic has the strongest supporting evidence in shock-refractory VF/pVT arrests.

Evidence Summary:

The ROC-ALPS trial by Kudenchuk et al. (2016) remains the most recent randomized controlled trial informing current practice. In this study of OHCA patients with shock-refractory VF/pVT (≥1 shock), neither amiodarone nor lidocaine significantly improved survival to hospital discharge or favorable neurological outcomes compared to placebo. However, amiodarone was associated with a 3% absolute survival benefit, which may be clinically meaningful.³⁹

Consistent with earlier RCTs,^40-41 both amiodarone and lidocaine improved survival to hospital admission. Notably, higher survival rates were observed with amiodarone in EMS- and bystander-witnessed arrests, and with lidocaine in bystander-witnessed arrests, suggesting a potential benefit with earlier drug administration.³⁹ 

A subsequent Bayesian reanalysis of ROC-ALPS further supported a survival advantage, demonstrating a high probability that amiodarone improves both survival and neurological outcomes compared to placebo.⁴²

Resuscitation Guideline Indications:

ILCOR 2024: Use either amiodarone or lidocaine in adults with shock-refractory VF/pVT.³⁸

• There were insufficient studies on other agents for ILCOR to make additional recommendations, allowing us to keep management simple in the emergency department

Expert Opinion Cardio-Intensivist at the University of Ottawa Heart Institute:

1. Use amiodarone first line for all causes of VF/pVT.
2. Administer it as soon as it becomes available during the resuscitation.

Non-Guideline Indication:

 Consider administering lidocaine as a secondary agent in VF/pVT arrest with strong suspicion of acute coronary ischemia as the precipitating cause, given lidocaine’s effectiveness on ischemic tissue.⁴³

• Dose to remember: 100 mg IV push. This aligns with the ACLS-recommended dosing range of 1–1.5 mg/kg for most adults.

Post-ROSC antiarrhythmics:

ILCOR 2024: “The confidence in effect estimates is currently too low to support an ALS Task Force recommendation regarding the prophylactic use of antiarrhythmic drugs immediately after ROSC in adults with VF/pVT cardiac arrest”.³⁸

Three observational studies have specifically addressed the prophylactic use of lidocaine and amiodarone following OHCA, and do not provide sufficient evidence to support this intervention.^44-46

Overall, this decision can be deferred to cardiology and/or intensive care as there is no clear evidence to guide this practice, and it is frequently influenced by individual provider preference.

References:

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