Advanced Cardiac Life Support (ACLS)

Function

The ACLS guidelines aim to improve outcomes in both out-of-hospital and in-hospital cardiac arrest by standardizing cardiac arrest management. The guidelines make cardiac arrest management accessible to prehospital and other healthcare providers based on the best available resuscitation science.

Recovery from cardiac arrest depends on an interprofessional system and an effective chain of survival for management. The process begins with immediate recognition of cardiac arrest, activation of the emergency response system (ERS) with immediate initiation of CPR, correction of life-threatening arrhythmias with defibrillation, care after return of spontaneous circulation (ROSC), and addressing underlying causes of cardiac arrest. This strategy is based on the assumption that most cardiac arrests are caused by underlying cardiac issues, such as myocardial infarction and electrical abnormalities. Arrests from other causes, such as respiratory failure, trauma, and toxicity, may require treatment for other reversible underlying causes and must be considered.[10]

ACLS providers must focus on fulfilling all these critical steps to improve outcomes. However, achieving a standard level of care for all patients experiencing cardiac arrest requires underlying infrastructure that provides training, resources, and an effective communication network to guarantee the best possible survival outcome for each patient.

Issues of Concern

Team Performance and Its Critical Impact on Resuscitation

Highly effective team performance is crucial for the success of resuscitation efforts. Resuscitation teams must execute their responsibilities with exceptional efficiency, leading to high performance and precise timing, which may increase the chances of survival for patients who experience cardiac arrest. To achieve these goals, high-performance teams rely on the dedication of each member to contribute to the team's optimal performance rather than merely executing commands. For optimal outcomes in patients experiencing cardiac arrest, a high-performance team must prioritize the following:

• Timing: Rapid initiation of compressions, early delivery of the first shock, maintenance of chest compression fraction above 80%, minimization of interruption time before delivering a shock, and rapid response times by EMS.
• Quality: Ensuring proper compression rate and depth, complete chest recoil, minimal interruptions, and regular rotation of compressors to avoid fatigue. In addition, preventing excessive ventilation and utilizing feedback devices for quality improvement.
• Coordination: Development of team dynamics where members collaborate fluidly toward a shared goal, each team member proficient in their respective roles.
• Administration: Implementing effective leadership, performance measurement, and ongoing quality improvement. In addition, managing the number of code team members.

The presence of a leader is essential in every high-performance team to coordinate the collective endeavors of the group. The team leader is pivotal in organizing the group, overseeing the individual performance of team members, and providing support when needed. The team leader must exemplify outstanding team behavior, serve as a mentor and coach, and facilitate clear understanding among members. The team leader's focus is always on delivering comprehensive patient care rather than procedures. In situations requiring an advanced procedure that other team members cannot perform, such as advanced airway placement, the team leader has the authority to temporarily delegate leadership responsibilities to another team member. This temporary delegation ensures that the team functions effectively, even while accomplishing complex tasks.[11][12]

Suggested positions for a 6-person high-performance team include the following:

• Resuscitation roles: Airway, compressor (alternates with monitor or defibrillator), and monitor or defibrillator (alternates with compressor)
• Leadership roles: Team leader, intravenous (IV) and intraosseous (IO) medication administration, and recorder

Each team member must be aware of their specific duties and obligations, as the contribution of every individual is crucial to the team's overall effectiveness. In situations where the team consists of fewer than 6 members, team leaders are responsible for determining the most critical tasks and delegating them to the available healthcare providers.

The team leader must clearly assign tasks. Team members should communicate their capacity to take on more tasks. The team leader should foster an environment where team members are engaged and contribute to the resuscitation rather than simply following orders.

In interactions with high-performance team members, the team leader should follow a structured approach to closed-loop communication. A direct message or task should be delivered to an individual team member, followed by clear acknowledgment through contact and a verbal response to verify that the order or message was received. The team leader should confirm that the task was completed before assigning the member a new one.[13]

Team members, including the team leader, should be aware of their capabilities and limitations. The team should feel confident in calling for backup when additional assistance is needed. During a code, team members must be prepared to intervene if an error is imminent or has already occurred. Mistakes should be addressed tactfully, without confrontation between team members. Interventions and analysis may be needed during debriefing to prevent future repetitive missteps.

Part of the team leader's critical responsibility includes ongoing monitoring and reassessment of the situation. The team leader must keep track of interventions, assessment results, and any changes in the patient's condition. Team leaders should communicate regularly with the team, providing updates and outlining upcoming interventions. Given that patient conditions can change, the management plan should adapt to the situation accordingly, staying open to modifying the resuscitation strategy.[14]

Recognition of Clinical Deterioration

Recognizing patients who are deteriorating clinically or facing impending cardiac arrest involves a systematic approach. The treatment of conscious patients begins with the primary assessment. The team should promptly assess airway, breathing, circulation, disability (neurological status), and exposure (the ABCDEs). Initial interventions may be started during the primary assessment, generally including opening the airway; placing the patient on cardiac, blood pressure, and pulse oximetry monitoring; and obtaining a 12-lead electrocardiogram (ECG). If hemodynamic instability is identified, patients may require immediate interventions without a complete workup.

Trained healthcare providers should use a systematic approach to assess and treat patients who are acutely ill or in cardiac arrest.[15] The approach begins with an initial survey of the scene, followed by a BLS assessment. ACLS management then builds on these principles with primary and secondary assessments.

Initial assessment: The initial assessment starts with ensuring scene safety, followed by evaluating the patient's general appearance to determine whether they are conscious or unconscious. Unconscious patients should undergo a BLS assessment, whereas conscious patients proceed directly to the primary assessment.

Basic life support assessment: The BLS assessment is initiated by checking for responsiveness and activating the ERS. The next step is to check for breathing and a pulse, ensuring that both tasks are accomplished within 10 seconds. If no pulse is detected or confirmed, CPR should be initiated immediately. If indicated, defibrillation must be performed as soon as possible.

Primary assessment: During the primary assessment, high-performance teams should be able to evaluate the ABCDEs of an acutely ill patient simultaneously.[16] Patients should be placed on cardiac monitoring as quickly as possible to assess rhythm and guide further interventions.

Secondary assessment: The secondary assessment emphasizes identifying differential diagnosis, conducting a more focused assessment, and treating underlying causes, represented by the mnemonic "Hs and Ts." This mnemonic offers a simplified approach to remind healthcare professionals to consider reversible causes of deterioration and cardiac arrest during high-stress resuscitations. The Hs include hypovolemia, hypoxia, hydrogen ion (acidosis), hypokalemia or hyperkalemia, and hypothermia. The Ts include tension pneumothorax, cardiac tamponade, toxins, and thrombosis (pulmonary and coronary). Considering and addressing these underlying causes of deterioration may prevent cardiac arrest or, in cases of arrest, help achieve ROSC more quickly.

Signs of Clinical Deterioration

Signs of clinical deterioration include the following:

• Airway compromise
• Tachypnea greater than 30 breaths/min, bradypnea less than 6 breaths/min, or signs of respiratory distress
• Bradycardia less than 40 beats/min or tachycardia greater than 140 beats/min
• Hypotension with a systolic blood pressure less than 90 mm Hg
• Hypertension with signs and symptoms concerning a hypertensive emergency
• Decreased level of consciousness
• Agitation
• Seizure
• Decreased urine output

Prompt recognition of clinical deterioration is a key factor in team performance during resuscitation. A rapid response relies on sharp clinical observation and effective team communication.

Recognition and Initial Management of Cardiac Arrest

Lay rescuers must assume that unresponsive patients who are not breathing or have abnormal (agonal) respiration patterns are experiencing cardiac arrest. The ERS should be activated, and CPR should be started immediately. The benefit of performing CPR on a patient in cardiac arrest far outweighs the risk of injury to a patient not in cardiac arrest.[17][18] Trained healthcare professionals should check for a pulse for up to 10 seconds. If a pulse cannot be identified with absolute certainty, it should be assumed that the patient is in cardiac arrest, and CPR should be initiated immediately. Difficulties in detecting pulses during checks are common among responders and can result in delays in starting CPR.[19][20][21][22][23]

CPR quality is crucial, as it is the first intervention patients with cardiac arrest receive, significantly influencing outcomes. High-quality CPR is achieved as follows:

• Chest compressions should be performed with sufficient force, pushing down by at least 2 inches (5 cm), at a rate of 100 to 120 compressions/min, while ensuring complete chest recoil between each compression.
• Interruptions between chest compressions should be minimized. Continuous CPR has been shown to improve survival rates.
• Excessive ventilation should be avoided.
• Chest compressors should be rotated every 2 minutes or sooner if fatigued.
• A 30:2 compression-to-ventilation ratio should be maintained before advanced airway placement.
• Quantitative waveform capnography may be used to assess CPR quality. CPR quality should be reassessed, and corrective measures should be taken if end-tidal CO₂ (EtCO₂) is low or decreasing.

High-quality CPR and defibrillation are critical lifesaving interventions for cardiac arrest. Resuscitation should occur at the scene where the patient is found if the scene allows. The location should allow for the safe administration of high-quality CPR. Firm surfaces are preferred for CPR, with the patient in the supine position when possible. If the patient cannot be placed in the supine position, prone-position CPR techniques may be used alternatively in the hospital setting. Rescuers should place the heel of their dominant hand in the middle of the chest at the lower half of the sternum, with the heel of the nondominant hand on top of the first in an overlapping position. Metrics for high-quality CPR are constantly being researched and evolving with guideline updates over time.

Previous editions of the ACLS guidelines recommended an Airway-Breathing-Circulation approach to cardiac arrest. This recommendation was revised in 2010, prioritizing circulation as the primary focus in patients experiencing cardiac arrest. The change was made based on resuscitation research demonstrating that early initiation of CPR improved cardiac arrest outcomes compared to early airway management. Lone rescuers or healthcare providers should initiate chest compressions immediately and delay ventilation until additional providers are available to take over. The chest compressions-first strategy has been proven to result in faster initiation of chest compressions, shorter time to ventilation, and earlier completion of the first CPR cycle.[24][25][26][27]

Airway Management

Proper positioning is the first intervention that can improve oxygenation and ventilation in patients who can protect the airway and breathe spontaneously. Maneuvers include tilting the head and lifting the chin (head tilt-chin lift). If suspected trauma or cervical spine injury cannot be ruled out, the jaw thrust technique can open the airway without extending the head.

Supplemental oxygen should be administered to patients with signs and symptoms of respiratory distress and titrated to a saturation of 95% on pulse oximetry. Oxygenation goals may vary depending on the underlying cause of the presentation.

Respiratory distress may present as tachypnea, nasal flaring, accessory muscle use, increased breathing work, bradypnea, or poor respiratory effort. If left untreated, it may progress to respiratory failure, which is the inability to maintain adequate oxygenation and ventilation.

Respiratory failure may be detected clinically with basic monitoring devices, including pulse oximetry and capnography, or arterial blood gas analysis, which may indicate hypoxemia, hypercapnia, or a combination of both. If left untreated, prolonged respiratory failure can progress to cardiorespiratory arrest. Efforts should be made to open the airway, provide supplemental oxygen when needed, and treat the underlying cause of respiratory distress or failure.

Patients with respiratory arrest are unresponsive and have a palpable pulse but exhibit absent or inadequate respirations, making them unable to maintain oxygenation and ventilation. These patients need a complete systematic approach, which must include a BLS assessment before primary and secondary assessments. Cardiac arrest may be mistaken for respiratory arrest when a patient presents with agonal gasps instead of adequate respirations. Patients with true respiratory arrest rapidly develop cardiac arrest if adequate airway management is not provided immediately.

Management of respiratory arrest involves both BLS and advanced life support (ALS) interventions, including providing supplemental oxygen, opening the airway with opening techniques or airway adjuncts, and suctioning when indicated. Patients with respiratory arrest with a pulse should receive 100% oxygen and ventilatory support using bag-valve-mask ventilation (BVM) and, eventually, an advanced airway if they do not regain a spontaneous and adequate breathing pattern. Ventilatory support should be delivered at a rate of 1 breath every 6 seconds. The tidal volume provided should be 500 to 600 mL, or enough to produce chest rise, and should be delivered over 1 second.

Patients with cardiac arrest should receive rescue breaths using BVM or advanced airway along with 100% supplemental oxygen. Oropharyngeal or nasopharyngeal airways may be used as adjuncts during cardiac arrest to facilitate the delivery of rescue breaths through BVM. Both BVM and advanced airway devices are considered adequate for the resuscitation of these patients. Outcomes from both interventions are highly dependent on the individual experience and skills of each healthcare professional.[28] The provision of chest compressions for a prolonged period without assisted ventilation could worsen outcomes as circulating oxygen content decreases over time.[29]

Compression-to-ventilation ratio in cardiac arrest

The recommended compression-to-ventilation ratio before advanced airway management, such as through endotracheal intubation or supraglottic airway, is 30 compressions to 2 rescue breaths.[30] Experienced healthcare professionals can deliver 10 breaths/min (1 breath every 6 seconds), providing asynchronous ventilation while continuous chest compressions are performed before placing an advanced airway.[31][32][33] Once an advanced airway is in place, healthcare professionals should deliver 10 breaths/min while continuous chest compressions are performed.[34]

Rhythm Interpretation

The initial interpretation of cardiac rhythms follows a simplified approach. Skilled healthcare professionals identify the cardiac rhythm as fast or slow, the width of the QRS complex as wide or narrow, and the rhythm as regular or irregular. The cardiac rhythm should be assessed in the context of the overall hemodynamic stability and the presence or lack of a palpable pulse. These characteristics provide enough information to guide the initial resuscitation strategy.

Management of Pulseless Rhythms

Pulseless rhythms may be shockable or nonshockable. Shockable rhythms include pulseless ventricular tachycardia and ventricular fibrillation, whereas nonshockable rhythms encompass pulseless electrical activity (PEA) and asystole.

Shockable rhythms: Pulseless ventricular tachycardia and ventricular fibrillation are life-threatening arrhythmias that result in inadequate perfusion. Although ventricular tachycardia may lead to perfusion when stable, ventricular fibrillation is inherently nonperfusing due to its unstable nature. The management cornerstones for both pulseless ventricular tachycardia and ventricular fibrillation include rapid identification, high-quality CPR, and early defibrillation. Timely defibrillation increases the likelihood of survival by converting the arrhythmia to a perfusing rhythm.

Biphasic waveform defibrillators have largely replaced monophasic ones and are highly effective in terminating ventricular fibrillation and pulseless ventricular tachycardia. The optimal energy setting for biphasic defibrillation, whether fixed or escalating, has not been definitively determined and should follow the manufacturer's recommendations. If the specified energy setting is unknown, the maximum dose may be considered.

Studies indicate that escalating energy settings (200–300–360 J) lead to better conversion rates for patients requiring multiple shocks, although overall survival is similar to fixed energy settings. Both fixed and escalating approaches are effective, and the evidence does not show that one biphasic waveform is superior to another. For pulseless ventricular tachycardia or ventricular fibrillation that persists after the first shock, using an equivalent or higher energy setting for subsequent shocks is prudent. Immediate resumption of CPR after shock administration, bypassing a rhythm check, is deemed reasonable.

Patients experiencing a witnessed cardiac arrest in pulseless ventricular tachycardia or ventricular fibrillation, with pads already applied, can be defibrillated immediately. In contrast, individuals who cannot be defibrillated promptly should receive high-quality CPR until defibrillation is available, ideally as soon as possible. Patients who remain in pulseless ventricular tachycardia or ventricular fibrillation after defibrillation and 1 cycle of CPR should receive 1 mg of IV epinephrine every 3 to 5 minutes while high-quality CPR is ongoing. Amiodarone 300 mg IV or lidocaine 1 to 1.5 mg/kg IV should be administered if pulseless ventricular tachycardia or ventricular fibrillation persists despite defibrillation, epinephrine, and high-quality CPR.

Nonshockable rhythms: PEA consists of any organized or semi-organized ECG rhythm that fails to generate a detectable pulse. Asystole, on the other hand, is characterized by the complete absence of electrical and mechanical activity. Both rhythms fail to stimulate cardiac contractions with sufficient force to produce a pulse. The management of PEA and asystole involves rapid identification, high-quality CPR, IV epinephrine (1 mg every 3 to 5 minutes), and addressing potential underlying causes, commonly referred to as Hs and Ts.[35][36][37]

Monitoring During Cardiac Arrest

The ACLS guidelines emphasize the importance of clinical and physiological monitoring to improve CPR performance and detect ROSC. Continuous assessment, along with immediate feedback on chest compression rate and depth, chest recoil, and ventilation rate and force, is essential for effective CPR. Devices equipped with accelerometers, either integrated into defibrillator pads or used standalone, provide real-time metrics and feedback during compressions.

EtCO₂ monitoring through continuous waveform capnography offers an estimate of cardiac output and CPR quality. EtCO₂ data are most reliable during cardiac arrest in intubated patients. Meanwhile, data supporting routine EtCO₂ monitoring in patients with supraglottic airways or BVM are currently lacking.

EtCO₂ levels persistently below 10 mm Hg indicate inadequate cardiac output, requiring improved CPR quality. A sudden, sustained increase in EtCO₂ above 10 mm Hg during CPR may indicate ROSC. EtCO₂ levels that are consistently below 10 mm Hg in a patient who recently experienced cardiac arrest and is intubated may indicate endotracheal tube (ETT) misplacement and should prompt further evaluation and management through laryngoscopy, chest x-ray, or reintubation. EtCO₂ levels that remain low after prolonged resuscitation attempts may indicate poor outcomes.[38][39]

Arterial catheters, when already placed or immediately available without interrupting CPR, can provide valuable feedback on CPR quality and ROSC. Diastolic pressure from arterial catheters may be used to estimate coronary perfusion pressure, with a recommended goal of greater than 25 mm Hg. Abrupt increases in diastolic pressure during CPR may indicate ROSC.[40][41]

Point-of-care ultrasound, when used by skilled operators, can help identify underlying issues, monitor resuscitation, and assess cardiac activity and recovery potential during cardiac arrest. However, the use of this tool should not interrupt high-quality CPR, especially since further research is needed to validate its effectiveness in this setting.[42][43]

Establishment of Vascular Access

The peripheral IV route remains the preferred initial approach for vascular access during resuscitation due to its accessibility and predictable drug response. IO access has gained popularity as a first-line alternative when IV access is unsuccessful. However, studies suggest better clinical outcomes with IV administration. Central venous access achieves faster drug delivery but is associated with higher morbidity and may interrupt CPR, making it less practical in emergencies. Endotracheal drug administration is the least preferred option due to its unpredictability and lower ROSC and survival rates. Further research is needed to compare the efficacy of IV and IO drug delivery and optimize resuscitation strategies.

Post-Cardiac Arrest Management

Post-cardiac arrest care is an integral part of the chain of survival, though the specifics of optimal hospital care for patients with ROSC after cardiac arrest remain unclear. Focus is growing on identifying and refining practices that could enhance patient outcomes. Ischemia-reperfusion injury from cardiac arrest and subsequent resuscitation affects multiple organ systems, necessitating comprehensive post-cardiac arrest care. This care involves hemodynamic support, mechanical ventilation, temperature management, and treatment of underlying causes and seizures. In addition, this strategy requires close monitoring for infections and management of the patient's critical condition.

A significant number of cardiac arrest survivors eventually succumb to the withdrawal of life-sustaining treatment, often due to neurological injury, particularly in out-of-hospital cardiac arrest cases but also frequently in in-hospital cardiac arrest cases. Therefore, minimizing brain injury is a major focus of post-cardiac arrest care. Strategies include optimizing cerebral perfusion pressure, managing oxygen and carbon dioxide levels, controlling core body temperature, and detecting and treating seizures. Given the complex nature of injuries from cardiac arrest, which can also lead to multiple organ dysfunction or shock, an interprofessional team with expertise in cardiac arrest care is essential. Developing interprofessional protocols is crucial for improving survival rates and neurological outcomes.

Observational studies on cardiac receiving centers suggest that a robust care system may be a crucial link between successful resuscitation and long-term survival. The post-cardiac arrest period can be divided into 2 phases—initial stabilization and continued management. The initial stabilization phase begins immediately after ROSC is obtained and is characterized by continued resuscitation. The continued management phase encompasses other early and emergent interventions for diagnosis and management in the post-cardiac arrest period.

Airway management should be prioritized during the initial stabilization phase, including early ETT placement if not already performed, followed by waveform capnography for continuous monitoring. Respiratory parameters should be adjusted to maintain a goal oxygen saturation (SpO₂) of 92% to 98% and an arterial carbon dioxide partial pressure (PaCO₂) of 35 to 45 mm Hg. Hemodynamic goals include a mean arterial blood pressure above 65 mm Hg or systolic blood pressure above 90 mm Hg. These targets may be achieved by administering IV fluids, vasopressors, or inotropic medications.

During the continued management phase, obtaining a 12-lead ECG is essential for guiding decisions on cardiac intervention. Achieving normoxia, normocapnia, and euglycemia is a key aspect of critical supportive care. Lung-protective ventilation should also be provided. At capable centers, continuous or intermittent electroencephalogram monitoring is recommended. Prompt identification and treatment of reversible causes of cardiac arrest and deterioration, such as the Hs and Ts, are essential, with early consultation of experts when necessary.

Current ACLS guidelines recommend initiating therapeutic hypothermia through targeted temperature management for patients who do not follow commands. Controlled cooling devices should be used to maintain a temperature between 32 °C and 36 °C. The guidelines continue to support active cooling protocols targeting hypothermia. However, recent evidence from the AHA that has not yet been reflected in the current ACLS guidelines suggests maintaining normothermia.

Recent findings from the Targeted Hypothermia Versus Targeted Normothermia After Out-of-Hospital Cardiac Arrest (TTM2) trial, which included 1861 patients, challenged the targeted hypothermia strategy. The trial showed no benefit from maintaining a temperature of 33 °C compared to normothermia at 36 °C to 37.5 °C with fever prevention. Fever should be avoided in post-cardiac arrest patients, with normothermia as the goal when therapeutic hypothermia is not part of the institutional protocol. Continuous monitoring of core temperature, whether esophageal, rectal, or bladder, remains essential.[44][45]

Rewarming post-cardiac arrest may occur during the initial temperature control phase or the transition to controlled normothermia. Patients with spontaneous hypothermia post-ROSC are at risk for secondary injury during rewarming. The optimal rewarming method—whether passive or controlled—remains unclear, but studies suggest controlled rewarming may offer benefits. Clinical trials, including the Target Temperature Management 33 °C versus 36 °C after Out-of-Hospital Cardiac Arrest (TTM) and Therapeutic Hypothermia after Cardiac Arrest in Nonshockable Rhythm (HYPERION), used controlled rewarming at rates of 0.25 °C/h to 0.5 °C/h to reach target temperatures. Based on available evidence, a rate of 0.25 °C/h to 0.5 °C/h is conservatively recommended, with faster rewarming considered in cases of severe trauma, bleeding, or bradycardia.[46]

Termination of Resuscitation Efforts

The BLS termination-of-resuscitation (TOR) rule recommends terminating resuscitation when 3 criteria are met before transport—the arrest was not witnessed by EMS providers or first responders, ROSC was not achieved, and no shocks were delivered. A meta-analysis of 7 studies involving 33,795 patients found that only 0.13% of patients meeting these criteria survived to hospital discharge.

The ALS TOR rule similarly advises TOR under specific conditions—the arrest was not witnessed, no bystander CPR was provided, no ROSC was achieved after full ALS care in the field, and no shocks were delivered. A meta-analysis of 2 studies involving 10,178 patients showed a survival rate to hospital discharge of only 0.01% for patients meeting the ALS termination criteria.

The BLS TOR rule, also known as the universal TOR rule, has been validated in combined BLS and ALS systems. Although the rule lacked adequate specificity after 6 minutes of resuscitation, specificity improved to over 99% after approximately 15 minutes, reducing the need for patient transportation by half. A retrospective analysis indicated that applying the universal TOR at 20 minutes could predict futility, correctly identifying over 99% of survivors and patients with favorable neurological outcomes.

For intubated patients, an EtCO₂ measurement below 10 mm Hg indicates low to no blood flow. Small studies have shown that an EtCO₂ below 10 mm Hg after 20 minutes of ALS resuscitation strongly predicts futility, though not with perfect accuracy. These studies are limited by a high risk of bias, and alternative EtCO₂ thresholds and time points have been proposed. Validation of EtCO₂ alone as a predictor of patient outcomes requires a large, prospective study.[47][48][49][50][51]

Management of Rhythms With a Pulse

Arrhythmias with a pulse require careful evaluation to determine the presence of hemodynamic instability and guide treatment. Management strategies depend on the type of arrhythmia and aim to stabilize the patient while addressing reversible causes.

Evaluation and Management of Symptomatic Bradycardia

Initial management of bradycardia follows the systematic approach described earlier—initial, BLS, and primary assessments with appropriate interventions at each stage of evaluation. Crucial measures include the following:

• A: Ensure airway patency.
• B: Provide assisted oxygenation and ventilation as needed, with pulse oximetry monitoring.
• C: Perform hemodynamic monitoring, obtain a 12-lead ECG, and establish IV access.
• D: Conduct a focused neurological examination.
• E: Perform a focused physical examination.

For ACLS assessment and management, bradycardia is defined as a heart rate below 50 beats/min.[52] Bradycardia itself does not always require intervention. Each patient should be assessed for signs and symptoms indicating hypoperfusion due to the slow heart rate. Patients may be asymptomatic or show symptoms suggestive of hypoperfusion, a state known as symptomatic bradycardia. These symptoms include altered mental status (AMS), ischemic chest discomfort or pain, acute heart failure, hypotension, and signs of shock.

Unconscious patients with bradycardia should be assessed for a pulse and spontaneous breathing. The absence of a pulse or spontaneous breathing warrants management as cardiac arrest or respiratory arrest, respectively. Hypoxemic patients with respiratory failure or respiratory arrest require emergent airway management concurrent with bradycardia interventions, as hypoxemia is a treatable cause of bradycardia.

The severity of bradycardia is closely related to its underlying cause, making identification critical for management decisions and acute outcomes. Patients with an acute onset of symptomatic bradycardia require thorough evaluation for reversible causes. However, symptomatic bradycardia associated with hemodynamic instability necessitates immediate intervention alongside diagnostic evaluation.

Atropine: The ACLS guidelines recommend 1 mg IV atropine as a first-line intervention to attempt increasing the heart rate. If the bradycardia does not improve after the initial dose, atropine can be re-administered every 3 to 5 minutes for a total maximum dose of 3 mg IV before considering alternative treatments.[53] Smaller doses of atropine are not recommended and may even paradoxically worsen the heart rate abnormality, especially if less than 0.5 mg is delivered.[54][55]

Symptomatic bradycardia may persist or recur until the underlying cause is addressed. Evaluation for potential underlying causes should proceed while initiating temporizing measures to achieve hemodynamic stability. If atropine fails to improve bradycardia, alternative pharmacological treatments or transcutaneous pacing may be necessary. Alternatives should be considered before reaching the maximum atropine dose, particularly in patients with second- or third-degree heart blocks. Heart blocks with wide QRS complexes often originate from intranodal tissue and are unlikely to respond to atropine.

Epinephrine: Push-dose epinephrine or IV epinephrine infusion is a reasonable treatment strategy, particularly in the presence of concurrent hypotension.[56] Careful attention to epinephrine dosing is essential, as human error has been reported in managing hypotension and bradycardia with push-dose pressors.[57] Cardiac arrest dosing should be avoided when administering a push dose of epinephrine. Injecting a full 1-mg IV dose in this context may lead to severe hypertension and arrhythmias, potentially precipitating cardiac arrest.[58]

An IV bolus of 10 to 100 mcg of epinephrine is recommended when administering push-dose epinephrine in unstable symptomatic bradycardia. This dose may be escalated based on treatment response. Several methods are available to administer these doses, with the appropriate technique depending on the formulation of 1-mg epinephrine used, which may vary by institution and country. In the United States, epinephrine is commonly available as a premixed solution in a 1 mg/10 mL syringe, resulting in a concentration of 100 mcg/mL. In many other countries, epinephrine is commonly distributed in 1 mg/mL vials.

If the institution provides a 1 mg/10 mL syringe, 1 mL (100 mcg) should be drawn from this syringe and transferred into a 10-mL syringe containing 9 mL of 0.9% saline. The resulting solution should be labeled as 10 mcg/mL Epinephrine. Controlled administration of push doses of epinephrine can then be performed, with titration based on the patient's hemodynamic response.

When epinephrine is provided in 1 mg/mL vials, achieving a 10 mcg/mL concentration involves a similar process with an additional step. First, 1 mL is withdrawn from the 1 mg/mL vial and placed into a 10-mL syringe containing 9 mL of 0.9% saline. Then, 1 mL of this solution is transferred into another 10-mL syringe containing 9 mL of 0.9% saline. The final solution has a concentration of 10 mcg/mL epinephrine, suitable for administering controlled push doses.

Epinephrine infusion, when readily available, is a second-line treatment for patients who do not improve with atropine. This infusion should also be used for continuous hemodynamic support in patients who respond to push-dose epinephrine, as it increases heart rate, preload, afterload, and cardiac contractility. The effects of push-dose epinephrine are short-lived and provide only a temporizing measure. Reversal of treatable causes of bradycardia or continuous support is necessary beyond the initial stabilization period. The recommended initial dose for continuous IV epinephrine infusion in bradycardia is 2 to 10 mcg/min, titrated to the patient's hemodynamic response. 

Dopamine: IV dopamine infusion is recommended as a second-line drug for symptomatic bradycardia with signs of hypoperfusion, given at a rate between 5 and 20 mcg/kg/min titrated to hemodynamic response. The dose titration is typically 5 mcg/kg/min every 2 min until clinical improvement is observed.[59]

Transcutaneous pacing: Temporary transcutaneous cardiac pacing is a reasonable choice for second-line temporizing treatment of symptomatic bradycardia if readily available. Unstable patients with high-degree heart block without IV access are particularly suitable candidates for immediate pacing. This intervention may be considered immediately in patients who fail to respond to atropine.

After initiating pacing, electrical and mechanical capture should be confirmed, and the device should be configured to the lowest effective rate possible while titrating to clinical and hemodynamic response. Transcutaneous pacing can be uncomfortable; therefore, analgesia and sedation should be considered before initiation, if possible, or as soon as the patient is stabilized. Transcutaneous pacing should be used as a bridge to placing a temporary transvenous pacemaker, all while continuing workup and management of treatable causes of symptomatic bradycardia.

Pacemaker electrodes should be placed on the chest according to the manufacturer's instructions. The device should be activated, the demand rate set between 60 and 80 beats/min, and the electric current output adjusted to 2 mA above the level where consistent capture is observed on cardiac monitoring. The demand rate may then be titrated upward or downward based on clinical and hemodynamic response.

Other considerations when managing symptomatic bradycardia: After initial stabilization, patients may require placement of a temporary transvenous pacemaker while underlying causes are being addressed. In certain cases, permanent pacemaker placement may ultimately be necessary. During initial management and reassessment, possible causes of symptomatic bradycardia must be considered, including but not limited to demand ischemia, myocardial infarction; medication-induced reactions due to β-blockers, calcium channel blockers, or digoxin; hypoxemia; electrolyte abnormalities, such as hyperkalemia; and elevated intracranial pressure.[60][61][62] 

Evaluation and Management of Tachycardia

Tachycardia is defined as a heart rate greater than 100 beats/min. The initial assessment of tachycardia must include an evaluation of hemodynamic stability and appropriateness for the patient's clinical condition. Tachycardia may be an appropriate compensatory mechanism for clinical conditions, such as hypoxemia, hypovolemia, and sepsis, or it may be a pathological arrhythmia originating from a cardiac focus or other treatable causes. Cardiac tachyarrhythmias requiring treatment typically run over 150 beats/min.

Patients with tachycardia require a systematic approach for diagnosis and management, including initial, BLS, and primary assessments with appropriate interventions at each step. Key actions include the following:

• A: Maintaining airway patency
• B: Providing assisted oxygenation and ventilation as needed with pulse-oximetry monitoring 
• C: Performing hemodynamic monitoring, obtaining a 12-lead ECG, and establishing IV access
• D: Conducting a focused neurological examination
• E: Completing a focused physical examination

The ACLS guidelines recommend intervention for heart rates exceeding 150 beats/min, as rates above this threshold are more likely due to clinically significant arrhythmias that may affect hemodynamic stability. For patients with sinus tachycardia ranging from 100 to 150 beats/min, management should focus on identifying and addressing the underlying cause rather than targeting the heart rate alone.

The treatment of tachycardia depends on several critical factors, including the patient's clinical presentation, history, signs and symptoms, vital signs, and ECG results. Patients with unstable tachycardia are typically given electrical cardioversion. In contrast, stable patients are first treated using vagal maneuvers, followed by chemical cardioversion using medications tailored to the specific ECG findings. Individuals with stable tachycardia who fail several attempts of chemical cardioversion may require electrical cardioversion. Following a cardioversion attempt, patients should be frequently reassessed for changes in clinical status, including hemodynamic instability, which may require a different management approach.

Unstable tachycardia: The management of unstable tachycardia with a pulse requires immediate cardioversion. Unstable tachycardia often presents with hypotension, signs of shock, ischemic chest pain, acute-onset heart failure, and AMS.

Unstable wide and narrow complex tachycardia are treated with synchronized cardioversion.[63] If the tachycardia is refractory to synchronized cardioversion, increasing the energy level, adding antiarrhythmic drugs, and obtaining expert consultation should be considered. Adenosine may be administered for regular narrow complex tachycardia.

Unstable polymorphic ventricular tachycardia is managed with unsynchronized cardioversion (defibrillation). This approach is indicated regardless of the presence of a pulse, as polymorphic wide complex tachycardia cannot be reliably synchronized due to variability in each QRS complex. After cardioversion, further treatment with sodium channel blockers or β-blockers may be necessary to address recurrent arrhythmias.[64] Sedation and analgesia should be considered before cardioversion if feasible. Suitable sedative options include midazolam, etomidate, and propofol, whereas fentanyl and morphine may be used for analgesia. Cardioversion should not be delayed to obtain a 12-lead ECG in unstable patients, as the cardiac monitor and rhythm strip provide sufficient information to make emergent treatment decisions.

Stable tachycardia: Stable tachycardia refers to tachycardia with a pulse but without signs suggestive of hemodynamic instability, particularly hypotension, shock, AMS, ischemic chest pain, and acute heart failure. The treatment of choice is determined based on whether wide or narrow complex tachycardia is present on cardiac monitoring and if the accompanying rhythm is regular or irregular.

For regular narrow complex tachycardia, vagal maneuvers may be attempted as first-line treatment. If ineffective, adenosine 6 mg IV can be administered for chemical cardioversion. If tachycardia persists and conversion to sinus rhythm is not achieved, adenosine should be attempted again before exploring other treatments but at a dose of 12 mg IV. Other treatment options include adding other types of antiarrhythmic medications and performing elective electrical cardioversion.

Stable narrow complex irregular tachycardia is likely due to underlying atrial fibrillation. Acute rate control may be achieved with calcium channel blockers, β-blockers, amiodarone, or digoxin.[65]

Calcium channel blocker choices include diltiazem and verapamil. Diltiazem may be given as an IV bolus of 0.25 mg/kg over 2 min, followed by an infusion at a rate of 5 to 10 mg/h. Verapamil is administered as an IV bolus of 0.075 to 0.15 mg/kg over 2 min, followed by a continuous infusion at a rate of 0.005 mg/kg/min. Calcium channel blockers should be avoided in decompensated heart failure.

Common β-blockers used in the management of atrial fibrillation include metoprolol and esmolol. Metoprolol is typically given in doses of 2.5 to 5 mg IV over 2 min for up to 3 doses until rate control or improvement is achieved. This medication can bridge the patient into oral rate control therapies. Esmolol is typically administered as a continuous infusion. A loading dose of 500 μg/kg IV over 1 min is required, followed by an infusion of 50 to 300 μg/kg/min until rate control is achieved.

Amiodarone may be considered in decompensated heart failure but should be avoided in moderate-to-severe left ventricular dysfunction. Amiodarone is dosed as 300 mg IV over 1 h, followed by an infusion of 10 to 50 mg/h over the next 24 h. A variety of dosing schemes exist in the literature for amiodarone and may be institution-dependent.

Digoxin may be used as an adjunct to other therapies and is a reasonable option for patients with decompensated heart failure. The typical dosing of digoxin in the acute setting is 0.25 mg IV, repeated to a maximum dose of 1.5 mg IV within 24 h.

Regular wide complex tachycardia should be presumed to be ventricular or supraventricular tachycardia with aberrancy. Several treatment options are available for wide complex tachycardia in stable patients, including, but not limited to, procainamide, sotalol, amiodarone, adenosine, and, in refractory cases, elective electrical cardioversion.

Procainamide is administered as an IV infusion of 20 to 50 mg/min up to a maximum of 16 mg/kg. The initial dose should be continued until arrhythmia is suppressed, and the medication should be discontinued if the patient develops signs of hypotension or further QRS widening or has received the maximum dose. Once arrhythmia suppression is achieved, a maintenance IV infusion should be started at a rate of 1 to 4 mg/min. Procainamide should be avoided in patients with QTc prolongation or heart failure.

Sotalol is administered as a 100-mg bolus dose over 5 min. Alternatively, the dose may be calculated based on weight at 1.5 mg/kg. Similar to procainamide, sotalol should be avoided in patients with QTc prolongation.

Amiodarone is typically administered at a loading dose of 150 mg IV over 10 min, which may be repeated as needed for recurrent or breakthrough arrhythmias. The initial loading dose is followed by a 1 mg/min continuous infusion for approximately 6 h, though protocols are institution-dependent. 

Adenosine is also considered safe in stable patients with monomorphic regular wide complex tachycardia if the etiology is unknown. This drug may also aid in diagnosing the underlying cause and specific etiology of arrhythmia.

Irregular wide complex tachycardia is a complicated rhythm that may require early expert consultation for management. The underlying rhythm causing this presentation may be atrial fibrillation with aberrancy, preexcited atrial fibrillation (with accessory pathway), polymorphic ventricular tachycardia, or torsades de pointes. Correct rhythm identification is of utmost importance for drug selection and appropriate treatment. Adenosine should be avoided in irregularly irregular and polymorphic wide complex tachycardias.[66]

Preexcited atrial fibrillation should be considered when the ECG reveals an irregularly irregular wide complex tachycardia with monomorphic QRS complexes. Atrial fibrillation with aberrancy should be considered when the ECG shows changes in the configuration of QRS complexes from beat to beat. Both arrhythmias can present in patients with accessory conduction pathways, such as in Wolff-Parkinson-White (WPW) syndrome. Atrioventricular node-blocking drugs should be avoided as they may cause conduction to preferentially follow the accessory pathway, leading to further rhythm derangements.

Acute management includes procainamide as an IV infusion of 20 to 50 mg/min up to a maximum of 16 mg/kg. The initial dose should be continued until the arrhythmia is suppressed. The medication should be discontinued if the patient shows signs of hypotension or further QRS widening or has been given the maximum dose. Once arrhythmia suppression is achieved, a maintenance IV infusion should be started at a rate of 1 to 4 mg/min. Procainamide should be avoided in patients with QTc prolongation or heart failure. Other sodium channel blockers, such as lidocaine, have been used in the past but are not currently recommended as first-line treatment.

Polymorphic ventricular tachycardia is an inherently unstable rhythm that either spontaneously terminates or degenerates into ventricular fibrillation, leading to cardiac arrest. Patients presenting with this rhythm may develop syncopal episodes, warranting the initiation of the unstable tachycardia algorithm. In rare instances when patients present with runs of polymorphic ventricular tachycardia and remain stable, magnesium sulfate may be administered empirically as an IV bolus while efforts are made to identify and correct the underlying cause.

Possible etiologies include electrolyte abnormalities that can lead to long QT syndrome; organic heart diseases, such as ischemia; genetic channelopathies, such as Brugada or short QT syndrome; and exercise-induced catecholaminergic ventricular tachycardia. Long QT-induced polymorphic ventricular tachycardia is managed emergently with magnesium sulfate given as a 2-g IV bolus, which may be repeated as long as hypermagnesemia is avoided. Magnesium decreases the length of the QT interval and helps prevent recurrence. β-blockers may be considered in refractory cases.

In patients with normal baseline QT intervals, polymorphic ventricular tachycardia is most likely due to myocardial ischemia. β-blockers may be used if blood pressure remains within tolerable limits. Amiodarone may also be used acutely to prevent recurrent episodes. Magnesium is less likely to be effective in underlying myocardial ischemia but may also be trialed, especially if underlying electrolyte abnormalities exist. An urgent cardiology consultation is recommended for further workup and possible angiography.

During the initial workup and management of arrhythmias with a pulse, reversible causes of tachyarrhythmia and bradyarrhythmia should be identified and corrected, whereas rate and rhythm should be controlled when indicated. Affected individuals require close monitoring after the initial resuscitation period, as they face a high risk of deterioration and hemodynamic instability. Many patients require frequent reassessment and admission to units with telemetry capability for detecting arrhythmias and evaluating treatment response.

Clinical Significance

Studies have validated the standardization of initial resuscitation management. Establishing clear guidelines for this process allows for cognitive offloading and better adherence to evidence-based practices.[67] By understanding and implementing the latest guidelines and algorithms, all team members know their roles in a resuscitation attempt, contributing to optimal patient care.

The impact of ACLS training on cardiac arrest outcomes is profound. Research shows that healthcare professionals well-trained in ALS protocols perform life-saving interventions more proficiently, leading to improved survival rates and better neurological outcomes. This training equips clinicians with the necessary skills to make rapid, evidence-based decisions during critical situations, which is essential for effective cardiac emergency management. Regular ACLS recertification ensures healthcare professionals remain proficient and up-to-date with evolving best practices and guidelines, thereby enhancing overall care quality.[68]

Incorporating ACLS training into the routine education of healthcare professionals significantly improves patient outcomes. Hospitals and medical institutions that prioritize ACLS training often report faster response times and more efficient management of cardiovascular emergencies. These improvements not only increase survival chances but also reduce the risk of long-term complications by ensuring patients receive prompt and appropriate treatment. ACLS training is a vital component of emergency medical education, directly impacting the preparedness and effectiveness of healthcare systems in managing life-threatening cardiovascular events.[69]

Enhancing Healthcare Team Outcomes

The ACLS guidelines developed by the AHA aim to improve the management of severe cardiovascular emergencies, including cardiac arrest, stroke, and acute coronary syndromes. These guidelines encompass advanced medical procedures, medications, and techniques to stabilize patients and improve survival rates. Key components of ACLS include high-quality CPR, arrhythmia management, defibrillation, advanced airway placement, and IV medication administration. The structured algorithms provided in ACLS training enable healthcare professionals to make rapid, evidence-based decisions during critical situations, ensuring each step aims to optimize patient outcomes.

The successful implementation of ACLS protocols relies heavily on the collaboration of an interprofessional team. Emergency medicine clinicians, paramedics, pharmacists, and other healthcare providers must collaborate to provide timely and coordinated care. Each team member brings unique expertise and skills, contributing to a comprehensive approach to patient care. This collaborative effort, supported by clear communication and shared decision-making, enhances patient safety, reduces errors, and ultimately improves patient outcomes.

Effective interprofessional communication is paramount in ACLS administration, allowing for seamless information exchange and collaborative decision-making among team members. Regular training and simulations help reinforce these communication skills and ensure that all team members are familiar with the latest ACLS protocols and procedures. By fostering a culture of continuous learning and mutual respect, healthcare teams can better coordinate care, address any challenges that arise during emergencies, and provide high-quality, patient-centered care. This team-based approach not only improves patient outcomes but also enhances the overall performance and efficiency of the healthcare system in managing cardiovascular emergencies.