Out-of-Hospital Cardiac Arrest Management

• Most out-of-hospital cardiac arrest cases are managed in the ED.
• Equipping first responders, non-traditional providers, and public venues with AEDs is increasingly common.
• Bystander CPR rates, including hands-only and dispatcher-assisted CPR, dramatically improve resuscitation rates.
• Failure to improve bystander CPR or AED use rates within the critical time window is less likely to increase survival rates.
• Paramedic units often have standing orders to follow advanced cardiac resuscitation protocols.
• In refractory cases, pronouncing the patient dead at the scene per protocols may occur.
• Transport to a comprehensive resuscitation center may be warranted if ECPR or PCI are available.
• Mechanical CPR during transport results in better chest compression quality and is safer for EMS providers.
• Mechanical CPR minimizes interruptions, eliminates rescuer fatigue, and delivers consistent compressions.
• AEDs enable first responders and bystanders to provide immediate defibrillation.
• AEDs significantly enhance survival rates when combined with effective CPR.
• Rapid CPR initiation is critical to maintain vital organ perfusion.
• CPR increases the likelihood of restoring spontaneous circulation and neurologic function.

History and Physical Examination

• Determining the cause of cardiac arrest at presentation can often be difficult.
• Key information is often unreliable or unavailable.
• Differential diagnosis can be narrowed by age, underlying diseases, and medications.
• Historical information from family, bystanders, and EMS personnel provides key insight regarding cause and prognosis.
• Information surrounding the event includes whether the arrest was witnessed, time of arrest, what the patient was doing, possibility of drug ingestion, whether bystander CPR was performed, time of initial CPR, initial electrocardiographic rhythm and interventions by EMS providers.
• Medical history includes: baseline health, previous heart, lung, or renal disease, malignancy, hemorrhage, infection, and risk factors for coronary artery disease and pulmonary embolism.
• Obtain information on patient medications and allergies if possible.
• Focused physical examination goals include: airway patency and ventilation adequacy, confirming cardiac arrest, finding the cause, and monitoring for complications.
• Examination occurs simultaneously with interventions, and is repeated frequently to assess therapy response and complications (Table 5.2).
• Physical examination may provide little evidence of arrest duration after the initial minutes.
• Pupils dilate within 1 minute but may constrict if CPR is initiated immediately and effectively.
• Dependent lividity and rigor mortis develop after hours of cardiac arrest.
• Temperature is an unreliable predictor, unaffected in the first hours but hypothermia may cause arrest or be caused by prolonged arrest.
• Historical details about a patient's activity prior to arrest, initial rhythm, and previous health conditions help guide diagnostic and treatment decisions.
• Priorities during the physical examination include: ensuring airway patency, confirming cardiac arrest diagnosis, evaluating potential causes, and monitoring for complications of interventions.
• The presence of dependent lividity and rigor mortis indicates a significant duration of cardiac arrest, impacting treatment decisions.
• Past medical history is crucial in assessing a cardiac arrest patient including knowledge of prior conditions, which helps guide clinicians in the differential diagnosis and follow-up care decisions after resuscitation.

Resuscitation

• Cardiac arrest management requires an orchestrated effort by a healthcare team.
• Interventions should be rapid and efficient to maximize neurologic outcome chances.
• Restoration of cardiac function is the defining factor of ROSC, but restoration of good neurologic function defines successful resuscitation.
• Likelihood of achieving these goals decreases with each minute spent in cardiac arrest.
• CPR maintains vital organ perfusion until ROSC.
• CPR quality is an underappreciated component of resuscitation.
• Quality performance measures include: compression rate (100-120/min), compression depth (5-6 cm), chest compression fraction (at least 80%), full chest recoil, and ventilation rate (10/min).
• Chest compression-only CPR is recommended for lay providers out-of-hospital setting.
• Trained providers who are willing and able to ventilate should do so.
• A 30:2 compression-to-ventilation ratio is recommended until an advanced airway is established.
• Either bag-mask ventilation or an advanced airway can be considered.
• Minimize CPR interruptions!
• Supraglottic airway placement can occur without interrupting CPR.
• Endotracheal intubation can be pursued in settings with high success rates.
• Once an advanced airway is secured, CPR should be continuous, without pausing for ventilation, while providing one ventilation every 6 seconds (10 ventilations/min).
• Avoid hyperventilation, reduces cardiac output during CPR.
• CPR should maintain a compression rate of 100-120 compressions/min and a compression depth of 5-6 cm.
• A 30:2 compression-to-ventilation ratio is advised for healthcare professionals until an advanced airway is established.
• Aim for a chest compression fraction of at least 80% to to ensure consistent blood flow to vital organs during the pulseless interval.
• Full chest recoil enables complete filling of the heart chambers, improving blood flow and perfusion during the next compression.
• Employ supraglottic airways allows for ventilation without ceasing chest compressions.
• Early CPR leads to improved outcomes, as successful resuscitation decreases with each passing minute of arrest.
• Primary goals are restoring spontaneous circulation and ensuring good neurologic outcomes.
• Once an advanced airway is in place, continuous chest compressions are advised with ventilation every 6 seconds (10 ventilations/min).
• Avoid hyperventilation, as it may reduce cardiac output.

Ventricular Fibrillation and Pulseless Ventricular Tachycardia

• VF or pVT often has a primary cardiac origin.
• Treat VF and pVT identically.
• Therapy includes defibrillation, quality CPR, vasopressors and anti-dysrhythmic agents.
• Initiate chest compressions immediately until a defibrillator is available.
• Deliver a single countershock with minimal pause in chest compressions.
• Resume chest compressions for 2 minutes before rhythm check and additional defibrillation.
• Modify treatment to address specific rhythms if a patient is defibrillated into a different pulseless rhythm.
• Biphasic defibrillators have almost completely replaced monophasic defibrillators.
• Biphasic defibrillation requires lower energy for successful defibrillation, increasing initial defibrillation success and decreasing postcountershock myocardial dysfunction.
• Data are inadequate to conclude that a biphasic or monophasic waveform is superior in achieving ROSC or survival to hospital discharge.
• Follow device manufacturer's recommended countershock energies for biphasic defibrillators.
• The recommended energy for a single monophasic defibrillation is 360 J.
• Place defibrillation pads early in the resuscitation sequence and continue compressions while the defibrillator charges.
• Management includes immediate chest compressions, defibrillation, high-quality CPR, and vasopressors and anti-dysrhythmic agents.
• Biphasic defibrillation typically requires less energy and reduces post-countershock myocardial dysfunction compared to monophasic.

Pulseless Electrical Activity

• PEA is coordinated electrical activity (other than VF or pVT) without a palpable pulse.
• Electromechanical dissociation (EMD) is when no myocardial contractions occur.
• Pseudo-EMD is when myocardial contractions occur but are inadequate and no pulse can be palpated.
• Distinguishing EMD from pseudo-EMD may be useful in determining cause and guiding treatment.
• Initial assessment of PEA may include echocardiography to distinguish EMD from pseudo- EMD.
• Volume loading or continuous vasopressor infusions may be helpful in cases of pseudo- EMD.
• True EMD is a primary disorder of electromechanical coupling in myocardial cells.
• True EMD often is associated with abnormal automaticity and conduction, resulting in bradycardia and a wide QRS complex.
• Uncoupling is often associated with global myocardial energy depletion and acidosis resulting from ischemia or hypoxia.
• True EMD often occurs after defibrillation following prolonged VF and is associated with hyperkalemia, hypothermia, and drug overdose.
• Pseudo-EMD is typically a transient state in the progression to EMD.
• Cardiac causes of pseudo-EMD include papillary muscle and myocardial wall rupture, or primary supraventricular tachycardia.
• Extra-cardiac causes include: hypovolemia, tension pneumothorax, pericardial tamponade, and massive pulmonary embolism.
• Pseudo-EMD of extra-cardiac origin most often has narrow complex tachycardia initially, which can progress to bradycardia, with conduction abnormalities and QRS widening.
• Treatment of patients with PEA, including both EMD and pseudo-EMD, requires general resuscitation measures, including CPR, assisted ventilation, IV access, administration of vasopressors, and rapid diagnosis and treatment of the underlying cause.
• A mnemonic "4 H's and 4 T's" is often referenced to aid in rapidly identifying reversible etiologies of PEA arrest: hypoxia, hypovolemia, hypo/hyperkalemia, hypothermia, thrombosis (pulmonary embolism), tamponade (cardiac), toxins, and tension pneumothorax.
• History and physical examination may provide valuable clues to the underlying cause (Table 5.3).
• Diagnose hypoxia and hypovolemia based on response to empiric therapy, whereas other causes can be definitively diagnosed during resuscitation.
• EMD indicates a lack of myocardial contractions, while pseudo-EMD features inadequate contractions with no palpable pulse.
• Recognizing that EMD can signify advanced cardiovascular compromise which leads to swift interventions targeting underlying causes

Asystole

• Asystole represents complete cessation of myocardial electrical activity.
• Asystole generally represents the end-stage rhythm after prolonged cardiac arrest caused by VF, pVT, or PEA.
• Confirm asystole in at least two limb leads.
• Routine countershock of asystole has not been shown to improve survival.
• Treatment of asystole requires general resuscitation measures, including CPR, assisted ventilation, IV access, and repeated administration of vasopressors.
• Administration of atropine is not beneficial, and asystole in the out-of-hospital setting seldom responds to pacing.
• To be effective, pacing must occur within several minutes of arrest before progression to asystole.
• Management includes high-quality CPR, IV access, and vasopressors.
• Atropine is ineffective for asystole because it is typically not due to bradycardia.
• Rhythm confirmation should occur in at least two leads to help prevent misdiagnosing an organized rhythm for asystole.

Pharmacology

• Obtain IV or IO access for an ongoing resuscitation that fails to abort following CPR and defibrillation.
• Epinephrine 1 mg every 3 to 5 minutes is recommended, based on improved survival and ROSC.
• Vasopressin offers no advantage as a substitute for epinephrine in cardiac arrest.
• High-dose epinephrine is not recommended for routine use.
• Administer epinephrine as soon as feasible for patients with non-shockable rhythms.
• Administer epinephrine after initial defibrillation attempts have failed in those with shockable rhythms.
• Hemodynamic directed resuscitation titrates chest compressions and vasopressor therapy rather than a one-size-fits-all approach.
• Titrate compressions and vasopressors to maintain systolic blood pressure of 90 mm Hg and a coronary perfusion pressure (CPP) of 20 mm Hg during CPR.
• CPP during CPR = the difference between aortic and right atrial pressures during relaxation (CPR diastole).
• Titrate vasopressors to an arterial relaxation pressure of at least 20 to 25 mm Hg.
• Administer anti-dysrhythmics for VF or pVT refractory to defibrillation.
• Recommended first-line agents include: amiodarone (first dose: 300 mg IV/IO; second dose: 150 mg IV/IO) or lidocaine (first dose: 1-1.5 mg/kg IV/IO; second dose: 0.5-0.75 mg/kg IV/IO).
• Only lidocaine resulted in an increased rate of ROSC, although neither therapy resulted in statistically significant improvements in survival.
• Other medications that may be valuable in special cases include: Magnesium sulfate in torsades de pointes (2-4g IV), calcium in hyperkalemia (1 g calcium chloride IV or 3 g calcium gluconate IV), sodium bicarbonate in tricyclic antidepressant overdose (1-2 mEq/kg), and dextrose in hypoglycemia (25-50g IV).
• Routine administration of atropine outside the setting of bradycardia is not beneficial.
• Epinephrine 1 mg should be administered every 3-5 minutes during resuscitation efforts.
• Vasopressin may be used at a dose of 40 IV push but does not replace epinephrine.
• Sodium bicarbonate should be administered at 1 to 2 mEq/kg in tricyclic antidepressant overdose.
• Magnesium sulfate is used in torsades de pointes at doses of 2 to 4 g IV.
• Calcium is given for hyperkalemia, with doses of 1 g calcium chloride IV or 3 g calcium gluconate IV.
• Dextrose should be administered at a dose of 25 to 50 g IV to address hypoglycemia.
• Early administration of epinephrine (1 mg every 3-5 minutes) is critical, particularly in non-shockable rhythms.
• Dosage decisions should consider patient weight, response to initial doses, and specific arrhythmia management protocols.
• Routine use of high-dose epinephrine is not advised.
• Monitoring of hemodynamic status, rhythm, and response to medications is critical when administering IV medications.
• In severe hyperkalemia, beta-agonists, insulin with glucose, and sodium bicarbonate can complement administration.
• Aim to maintain systolic blood pressure of 90 mm Hg and coronary perfusion pressure of at least 20 mm Hg when titrating vasopressors during CPR.
• Be aware of potential medication interactions.
• Prior history of cardiac conditions can guide specific drug dosing and choice.
• Monitor for hypertension, tachycardia, and ischemic complications when using epinephrine.
• Providers should undergo regular training for drug administration, including dosage calculations, administration routes, drug interactions, and monitoring patient responses.
• Knowledge of how drugs work informs timing, dosing, and anticipation of interactions.

System Considerations

• Accurate records of initial rhythms and interventions inform treatment, assess response, and contribute to quality improvement.
• Prolonged cardiac arrest may lead to acidosis and electrolyte imbalances.
• Advanced life support protocols should be implemented promptly.
• Availability of interventions guides transport decisions.
• Regular refreshers ensure preparedness.
• Clear communication helps family members understand the situation and cope better.
• Be cautious with fluid administration to avoid exacerbating conditions like tension pneumothorax or congestive heart failure.
• Consider transport to centers offering ECPR based on patient's response and the nature of arrest.