ACLS Special Considerations

Introduction

• Certain clinical conditions require important modifications to standard ACLS. The American Heart Association highlights special circumstances that can change both priorities and interventions during resuscitation, such as severe electrolyte disturbances, hyperthermia, opioid toxicity, high-risk respiratory pathogens, LVADs, and consideration for ECPR with parallels to ECMO.^1,2
• These scenarios often involve nonischemic or reversible causes (e.g., hyperkalemia) that require rapid, targeted treatment.^1,3
• Timely delivery of condition-specific therapies is crucial to reversing the underlying cause and restoring effective perfusion.^1,3
• Cardiac arrest in the setting of respiratory pathogens requires integrating infection-control measures, such as personal protective equipment (PPE), airway strategies, and team positioning, into the resuscitation effort.^1,3
• This summary focuses on ACLS considerations or modifications of six special circumstances: ECMO/ECPR, respiratory pathogens, hyperkalemia, hyperthermia, LVAD, and opioid-associated cardiac arrest.

ECMO

Role in ACLS

• ECPR is the use of venoarterial (VA) ECMO during ongoing cardiac arrest when conventional ACLS measures fail to achieve sustained return of spontaneous circulation (ROSC).^1,4
• VA-ECMO for ECPR is most commonly established via percutaneous cannulation of the femoral vein for drainage and the femoral artery for return.^1,4
• By providing continuous, nonpulsatile cardiac output and gas exchange, VA-ECMO can serve as a bridge to definitive therapy of underlying reversible causes such as acute coronary occlusion, massive PE, hypothermia, or severe poisoning.
  • For massive PE-related cardiac arrest, a study showed ICU survival of 26% with ECPR vs 5% with conventional CPR, and favorable neurologic survival of 21% vs 0%.^1,5

When To Consider ECPR

• ECPR is not a routine ACLS intervention; it is reserved for carefully selected patients with a reasonable chance of neurologically intact survival.^1,5
• Typical features of potential candidates include:
  • Refractory cardiac arrest despite high-quality ACLS ≥10–15 minutes without sustained ROSC.^1,4,5
  • Presumed reversible causes of arrest (acute coronary syndrome [ACS], pulmonary embolism [PE], hypothermia, toxin exposure) rather than end-stage chronic disease.^1,4,5
  • Favorable arrest characteristics, such as witnessed collapse, rapid initiation of CPR with a “no-flow” interval less than 5 minutes, and an arrest-to-ECMO “low-flow” interval ideally less than 60 minutes.^1,4,5
• Exclusion criteria typically include advanced, irreversible comorbidities, prolonged low-flow times beyond local protocol thresholds, or situations inconsistent with the patient’s goal of care.^1,5
• Conditions for which ECMO/ECPR can be used:
  • ACS, cardiac catheter lab arrest, or cardiac surgery with persistent cardiogenic shock or cardiac arrest despite defibrillation, vasopressors and inotropes.^1,4,5
  • Suspected or massive PE not responding to thrombolysis, standard ACLS, or patients who are poor candidates for systemic thrombolysis.
  • Severe poisoning/cardiotoxic drug overdose with refractory cardiogenic shock/arrest despite maximal medical therapy.^1,4,5
  • Severe hypothermia: ECMO allows controlled core rewarming.^1,4,5
  • Life-threatening asthma/status asthmaticus with refractory hypercapnic respiratory failure or arrest.^1,4,5
  • Anaphylaxis with no response to aggressive epinephrine, fluids, vasopressors, and standard ACLS.^1,4,5

Modifications to ACLS Protocol

• Conventional ACLS remains the foundation while ECPR candidacy is assessed and the ECMO team is activated. ECPR is not a replacement for standard ACLS.^1,2,4
• Early systems activation is crucial. Institutions that offer ECPR should have predefined inclusion criteria and activation pathways so that assessment and mobilizations occur within the first 10 to 20 minutes of refractory arrest.^1,4,5
• Phases of ECMO^1,5
  1) Selection: Identify refractory arrest/shock with a reversible cause and activate the ECMO/ECPR team if criteria are met.
  2) Cannulation/Initiation: Gain vascular access, start anticoagulation, and establish adequate ECMO flow.
• Continue chest compressions to maintain perfusion.
  3) Stabilization: Optimize flow, mean arterial pressures (MAP), oxygenation/ventilation, start sedation/analgesia.
  4) Maintenance/Recovery: Treat the underlying cause (percutaneous coronary intervention [PCI], embolectomy, rewarming, toxin clearance) while managing hemodynamics, anticoagulation, and organ support.
  5) Weaning/Decannulation: Gradually reduce ECMO support as native function recovers, decannulate when stable, and initiate postcardiac arrest care.

Post-ROSC Considerations

• Application of standard postcardiac arrest care:
  • Maintain MAP of at least 65 mmHg to ensure adequate perfusion pressures.^2,4
  • Use lung-protective ventilation (low tidal volume and pressures) and avoid hyperoxia.
  • Implement temperature management.^2,4
  • Neurologic monitoring.^2,4
• Identification and ongoing correction of the underlying cause.^1,5
• Continuation of systemic anticoagulation with close surveillance for bleeding at cannulation sites, surgical sites, and mucosal surfaces.^1,5

When To Consider Terminating Resuscitation with ECMO/ECPR

• No reversible causes are identified, low-flow duration far exceeds protocol limits, there are advanced, irreversible comorbidities, or there is catastrophic brain injury or poor neurologic prognosis.^1,5
• Follow local protocols and involve a multidisciplinary team when deciding to withhold ECPR or discontinue ECMO, balancing the likelihood of neurologically intact survival against the patient’s goals of care.^1,5

Respiratory Pathogens

Role in ACLS

• Many patients with high-consequence respiratory pathogens such as COVID-19, severe acute respiratory syndrome (SARS), or Middle East respiratory syndrome (MERS) can undergo cardiac arrest from profound hypoxemic respiratory failure or acute respiratory distress syndrome (ARDS), often after prolonged mechanical ventilation.^1,4
• Chest compressions, bag-mask ventilation, defibrillation, suctioning, and endotracheal intubation are all considered aerosol-generating procedures, posing a substantial transmission risk to rescuers if PPE is inadequate.^1,4
• The goal of ACLS in the presence of respiratory pathogens is to balance timely, effective resuscitation with preservation of healthcare provider safety.^1,4

Recognition

• Treat the arrest as high-risk when:
  • There are known or suspected SARS-CoV-2, SARS, MERS, avian/pandemic influenza, or other Centers for Disease Control and Prevention-designated high-consequence respiratory pathogens.^1,4
  • Patient is on airborne/contact precautions for severe pneumonia or ARDS of suspected infectious origin.^1,4

Modifications to ACLS Protocol

• Team protection and room setup:
  • Have all resuscitation team members wear appropriate PPE (N95/respirator, eye/face protection, gown, and gloves) when treating cardiac arrest in patients with confirmed or suspected respiratory pathogens.^1,4
  • Minimize the number of people in the room to those essential for effective resuscitation, and keep additional staff outside as back-up.^1,4
  • Whenever possible, use a negative-pressure room or closed doors to limit the spread of aerosols.^1,4
• Chest compressions and devices:
  • Initiate chest compressions promptly; however, a 30 to 60 second delay to put on PPE is an acceptable trade-off to reduce provider infection risk.^1,4
  • Mechanical CPR devices are reasonable to use to maintain high-quality compressions while reducing the number of personnel at the bedside.^1,4
• Airway and ventilation:
  • Whenever possible, include a high-efficiency particulate air filter on the exhalation limb of all ventilation devices to capture fugitive aerosols.^1,4
  • Endotracheal intubation is preferred over bag-mask ventilation to reduce aerosol generation.^1,4
  • Video laryngoscopy is preferred over direct laryngoscopy during intubation to increase first-pass success and allow personnel to remain slightly farther away from the airway.
  • Plan for rapid sequence intubation with full PPE.^1,4

Hyperkalemia

Role in ACLS

• Hyperkalemia is usually defined as K+ >5.0 mEq/L in adults and can cause arrythmias and cardiac arrest.^1,4
• In asystole or pulseless electric activity (PEA), hyperkalemia is one of the key reversible underlying causes that must be sought and treated rapidly.^1,2,4
  • In dialysis patients, severe renal dysfunction, or major tissue breakdown, assume hyperkalemia early and treat it in parallel with standard ACLS.^1,2,4
• In hyperkalemic arrest, standard ACLS alone may not be sufficient because the underlying membrane instability persists until potassium is shifted or removed.^1,4
• For this reason, ACLS requires targeted adjunctive therapy in parallel with standard algorithms.^1,2,4

Recognition

• Major risk factors include kidney dysfunction, potassium supplements, K-sparing diuretics, ACE inhibitors/ARBs, hemolysis, crush injury, and other high-cell-turnover states.^1,4
• Electrocardiogram interpretation may show peaked T waves, loss of P waves, PR prolongation, QRS widening, and sine-wave morphology.^1,4
• PEA/asystole in a high-risk patient without another obvious cause.^1,2,4
• Recognize that acidemia during arrest itself can transiently elevate K⁺, so lab values may confound whether hyperkalemia is the primary cause.^1,4

Modifications to ACLS Protocol

• Continue standard ACLS (high-quality compressions, epinephrine, defibrillation as indicated), and add targeted therapy when hyperkalemia is strongly suspected.^1,2,4
• Three goals of hyperkalemia management:
  1. Stabilize the myocardium: 1 g intravenous (IV) calcium chloride while continuing ACLS. Effectiveness of administration is not well established but reasonable to give.^1,4
  2. Shift potassium into cells: 10 units regular insulin IV + 50 g IV dextrose over 15-30 minutes with glucose monitoring.^1,4
  3. Correct acidosis/further K+ shift: Sodium bicarbonate (50-100 mEq IV) is reasonable when there is strong suspicion or evidence of metabolic acidosis or hyperkalemia, however routine bicarbonate during CPR does not improve outcomes.^1,2,4

Considerations

• Avoid succinylcholine in high-risk patients (which can transiently raise free K+ ions in circulation), use nondepolarizing neuromuscular blockers.
• If hyperkalemia is refractory, urgent dialysis may be required.^1,4

Hyperthermia

Role in ACLS

• Severe hyperthermia (more than 40-40.5°C with central nervous system [CNS] dysfunction) drives a hypermetabolic state (tachycardia, hypercarbia, vasodilation, volume depletion), coagulopathy/disseminated intravascular coagulation (DIC), rhabdomyolysis with hyperkalemia, and myocardial dysfunction.¹
• It can rapidly cause multi-organ failure, arrhythmias, and cardiac arrest from heat stroke, drug toxicity, or malignant hyperthermia.¹
• Rapid recognition and aggressive cooling are as important as standard ACLS in determining outcomes, as hyperthermia can worsen CPR quality and defibrillation success.¹
• For hyperthermic arrest, high-quality CPR and defibrillation proceed as usual, but active, aggressive cooling and treatment of the underlying cause are integral parts of resuscitation.¹

Recognition

• Core temperature is usually more than 40°C in addition to an altered mental status or other CNS dysfunction (agitation, delirium, seizures, coma).¹
• Clinical contexts of environmental or exertional heat stroke (outdoor work, exercise, heat wave, confined hot spaces, drug/anesthetic-induced hyperthermia (sympathomimetic/stimulant toxicity or malignant hyperthermia in the operating room or postanesthesia care unit).¹

Modifications to ACLS Protocol

• Continue ACLS and add immediate, aggressive cooling as part of primary resuscitation:
  • Strip the patient and move them to a cool environment.¹
  • Full-body ice water immersion is the fastest and preferred method.¹
  • Use active external cooling by applying cool water or wet towels with fanning and ice packs to the groin/axilla/neck if immersion is not feasible.¹
  • Give cold isotonic crystalloid boluses (4-10°C normal saline or lactated Ringer’s) unless contraindicated by volume overload.¹
• Use a core probe as soon as possible, aiming to cool to approximately 38-39°C, then stop active cooling to avoid overshooting hypothermia.¹
• If it is stimulant or sympathomimetic drug-induced hyperthermia (cocaine, amphetamines, 3,4-methylenedioxymethamphetamine, etc.)
  • Initiate standard ACLS with active cooling. Benzodiazepines may be used post-ROSC to reduce agitation and muscle activity.¹
• If due to malignant hyperthermia
  • Initiate standard ACLS with active cooling, stop the underlying agent (volatile agents and/or succinylcholine), and administer IV dantrolene promptly.¹
  • Treat any underlying hyperkalemia, acidosis, and arrhythmia secondary to the cause.¹
• Neuroleptic malignant syndrome (NMS) or serotonin syndrome (SS)
  • NMS is a life-threatening hyperthermic reaction to dopamine-receptor antagonists characterized by muscle rigidity, altered mental status, and autonomic instability.⁷
  • SS is a potentially life-threatening drug-induced toxidrome that is caused by excess serotonergic activity, presenting with mental status changes, autonomic instability, and neuromuscular hyperactivity.⁶
  • For both conditions, initiate standard ACLS with active cooling and stop the underlying offending drug. Benzodiazepines may be used once perfusion is restored to reduce muscle activity and autonomic storm.^6,7
  • Administer syndrome-specific therapy once ROSC is achieved (dantrolene/bromocriptine for NMS, cyproheptadine for SS).^6,7

Considerations

• Watch for secondary complications like rhabdomyolysis, hyperkalemia, acute kidney injury, hepatic injury, and coagulopathy/DIC, as these can trigger recurrent arrests if unrecognized.¹
• Do not use antipyretics instead of cooling, as acetaminophen/nonsteroidal anti-inflammatory drugs have no meaningful role in resuscitation and can worsen hepatic injury.¹

LVADs

Role in ACLS

• Patients with LVADs present unique challenges in ACLS as they have no palpable pulse, noninvasive monitors can be unreliable, and cardiac arrest may result from device malfunction, inadequate flow, or right-ventricular failure rather than a primary arrhythmia.¹
• Current guidelines emphasize early chest compressions for unresponsive LVAD patients with a second provider who can simultaneously troubleshoot the device.¹

Recognition

• Assume possible arrest in any unresponsive LVAD patient with signs of poor perfusion, such as abnormal skin color/temperature, delayed capillary refill, MAP less than 50 mmHg (from Doppler or arterial line), or EtCO₂ less than 20 mmHg.¹

Modifications to ACLS Protocol

• If the patient is unresponsive and there is evidence of impaired perfusion, then start the LVAD emergency algorithm and standard ACLS.¹
• Start high-quality chest compressions and attach a monitor/defibrillator while a second rescuer immediately initiates the assessment of device-related reversible causes in parallel.¹
• Chest compressions are considered reasonable despite theoretical risks of device dislodgement or retrograde flow.¹
• Second rescuer checks for a pump “hum,” controller alarms, driveline disconnection/fracture, and power supply problems.¹
• Use perfusion indicators from skin findings, Doppler/arterial line, or end-tidal CO₂ (EtCO₂) rather than pulse alone to decide whether to continue compressions and to assess response to resuscitation.¹

Considerations

• Once perfusion is restored, point-of-care echo would be reasonable to assess left ventricular size, right ventricular function, cannula position, suction, and volume status.¹
• If the pump is running but perfusion is poor, think about low-flow causes from poor preload, afterload, right ventricle function, or rhythm.¹

Opioid Overdose

Role in ACLS

• Opioid overdose is common and progresses from CNS and respiratory depression to respiratory and cardiac arrest.^1,3,4
• Though naloxone can restore breathing and prevent deterioration to cardiac arrest, the benefit is uncertain in true cardiac arrest.^1,2,4
• With opioid overdose and cardiac arrest, high-quality CPR and standard ACLS remain the priority.^1,2,4

Recognition

• Opioid-associated emergencies are suspected when there is unresponsiveness with slow, shallow, or absent breathing, miosis, drug paraphernalia, or known opioid use.^1,3,4
• Differentiate as best you can:
  • Respiratory depression/respiratory arrest with a definite pulse, then a life-threatening opioid overdose, not yet cardiac arrest.^1,3
  • No definite pulse/agonal or no breathing, then treat as cardiac arrest, even if opioid overdose is suspected.^1,3

Modifications to ACLS Protocol

• If suspected opioid overdose with respiratory arrest/severe respiratory depression with a present pulse:
  • Open the airway and provide breaths/bag-mask ventilation. This alone may prevent progression to cardiac arrest.^1,3,4
  • Administer naloxone as soon as possible.^1,3,4
  • Do not delay ventilations or emergency medical service activation while preparing or giving naloxone.^1,3,4
• If suspected opioid overdose with cardiac arrest: follow standard ACLS and administer naloxone if it does not delay compressions, ventilation, or shocks.^1,2,4

Considerations

• People reversed with naloxone are at risk for recurrent respiratory depression, especially with long-acting or sustained-release opioids.^1,4
• Recurrent respiratory depression is managed with repeat naloxone doses or an IV infusion with a longer observation period.^1,4

Summary

• ACLS always starts with high-quality CPR, early defibrillation, and rapid treatment of reversible causes.
• ECMO/ECPR offers a rescue strategy for carefully selected patients with refractory arrest from potentially reversible etiologies, serving as a bridge to definitive interventions rather than a replacement for standard ACLS.
• High-consequence respiratory pathogens require strict PPE, aerosol-aware airway management, and team minimization to protect rescuers.
• Hyperkalemia and hyperthermia need adjunct therapy in parallel with ACLS.
• LVAD patients challenge traditional pulse- and cuff-based assessments, prompting clinicians to focus on perfusion indicators and to troubleshoot devices simultaneously.
• Opioid-associated emergencies emphasize that ventilations and naloxone are lifesaving before arrest. Still, once cardiac arrest occurs, high-quality CPR and standard ACLS remain the central priorities, with opioid antagonists as optional adjuncts.