Advanced cardiac life support: sudden cardiac arrest

I. Problem/Challenge.

Sudden cardiac arrest (SCA) refers to abrupt hemodynamic collapse due to a rapid degradation in the normal pump activity of the heart. It is accompanied by a loss of pulses and cessation of respiration. If SCA is not reversed (usually with cardioversion or defibrillation), it leads to sudden cardiac death (SCD). Despite recommendations by professional societies to carefully apply SCA and SCD terminology, it is still common for some clinicians to use the sudden cardiac death term to describe both SCA and true SCD.

SCA is a common and important clinical problem. In 2013, out of hospital SCA was seen in approximately 350,000 people in the United States with a survival rate of about 9.55% (with large regional variation). In-hospital cardiac arrest is estimated to occur at a rate of 1-5 events per every 1,000 hospital admissions. The published data from the National Registry of Cardiopulmonary Resuscitation shows a survival-to-discharge rate of only about 24% for in-hospital arrest.

However, the average survival rates vary immensely between patients presenting with different cardiac arrest rhythms. Sudden cardiac arrest is most often caused by ventricular fibrillation (VF) or ventricular tachycardia (VT) but pulseless electrical activity (PEA) and asystole can also be presenting rhythms during cardiac arrest. For in-hospital arrest, survival-to-discharge rates can be as high as 64% for patients presenting with VF/pulseless VT but only 1.2-14% for patients presenting with PEA or asystole.

Hospitalists are likely to participate in stabilizing patients resuscitated from out-of-hospital SCA by paramedics and emergency department staff. They are likely to be key players in performing a work-up in such patients to delineate the cause of the arrest. Hospitalists will also often be the first responders to medical emergencies and leaders of in-hospital resuscitations.

II. Identify the Goal Behavior.

The overall goals for hospitalists taking care of victims of SCA are straightforward.

III. Describe a Step-by-Step Approach/Method to This Problem.

Management of an ongoing cardiac arrest

Although one of the main goals of hospital medicine is to carefully monitor each patient’s clinical condition and anticipate changes in stability, some sudden cardiac arrests are not predictable.

A hospitalist is often called emergently to the bedside of a patient under “code blue” circumstances. If a physician is evaluating an unstable patient who becomes pulseless, it is almost always indicated to call for emergency assistance. In most hospitals, this entails activating a code blue via the internal or overhead paging system. Such action will provide the hospitalist with the multiple healthcare practitioners it will require to perform full ACLS.

The rhythm on the cardiac monitor should quickly be assessed. Next, chest compressions should be started immediately and continued with minimal interruptions during the resuscitation. It cannot be emphasized enough that the quality of cardiopulmonary resuscitation has a direct and significant impact on survival. The 2013 American Heart Association consensus statement takes a strong position on this by saying “poor-quality CPR should be considered a preventable harm.”

Five components of high quality CPR are described: compression rate, compression depth, chest recoil (leaning), chest compression fraction, and ventilation.

Chest compressions in adults should be performed at a rate of 100-120 compressions per minute and at a depth of 2-2.4 inches. Excessive depths should be avoided, and full recoil should be allowed between compressions. Chest compression fraction (CCF) describes the percentage of time that compressions are being performed during an arrest. A goal CCF of 60% is recommended in patients with an unprotected airway while higher rates are achievable in patients with an advanced airway.

Ventilation, whether by bag-mask, advanced airway, or other means should be performed in such a way to minimize the risk of impeding circulation. The positive intrathoracic pressure generated by positive pressure ventilation results in decreased venous return and thus decreased cardiac output. Breaths should be given at a rate of 10 breaths per minute and produce no more than minimal chest rise with each ventilation.

End tidal CO2 (ETCO2) is an important non-invasive means to monitor CPR quality. During a cardiac arrest, CO2 continues to be generated by cells but can no longer be transported to the lungs. In the absence of chest compressions, continued ventilation will result in a rapid decline in ETCO2 to near zero. High quality CPR should generate an ETCO2 of at least 10 mmHg with a goal ETCO2 of >20 mmHg. Some studies have suggested that maintaining an ETCO2 >20 mmHg during an arrest leads to better survival rates and more successful defibrillation. An abrupt, sustained rise in ETCO2 to 35-40 mmHg suggests return of spontaneous circulation, as even high quality CPR typically cannot generate the level of cardiac output to reach these levels.

The sections below give specific recommendations about further actions based upon the presenting sudden cardiac arrest rhythm.

Ventricular fibrillation or pulseless ventricular tachycardia

Rapid defibrillation is the clear goal. If the presenting arrest rhythm is VF or pulseless VT, the defibrillator should be requested immediately. It will often take a brief period of time for the defibrillator to be brought into the room and for it to be charged. Chest compressions should be continued until as close to the moment of defibrillation as possible.

Both VF and pulseless VT are treated with unsynchronized high-energy shocks at defibrillation doses. This approach differs distinctly from unstable VT with pulses, which is treated with synchronized cardioversion. Defibrillation doses vary depending on the type of defibrillator used. The defibrillation dose for biphasic defibrillators is usually between 120 and 200 J. The recommended adult dose will often be noted on the energy selection dial. The defibrillation dose for a monophasic defibrillator is 360 J. Stacked shocks with escalating electrical doses are no longer recommended.

The patient in VF/pulseless VT should receive one shock at the recommended defibrillation dose, followed immediately by an uninterrupted 2 minutes of chest compressions. During those 2 minutes, additional intravenous or intraosseous access should be obtained if the patient does not have at least two secure vascular access sites.

After 2 minutes of compressions, the cardiac rhythm should be briefly reassessed. If the patient shows a viable rhythm, the pulse should be checked. If the patient is found to have a pulse (return of spontaneous circulation), focus should shift to post-cardiac arrest care (see below). If the patient remains in VF or pulseless VT, the patient should receive another unsynchronized shock at defibrillation dose. Chest compressions should be resumed, 1 mg of epinephrine should be given, and an advanced airway should be placed.

After 2 additional minutes of cardio-pulmonary resuscitation (CPR), there should be another brief pause for a rhythm and pulse check. If the patient remains in VF or pulseless VT, the patient should receive another single shock at a defibrillation dose, compressions should be resumed, and the patient should be given a 300 mg intravenous or intraosseous bolus of amiodarone for “shock-resistant” VF/VT.

After 2 additional minutes of CPR, a pulse and rhythm check should be performed again. If the patient still remains in VF or pulseless VT, additional 1mg doses of epinephrine can be given every 3 to 5 minutes, and a second bolus dose of amiodarone (this time at a dose of 150 mg) can be tried.

Every 2 minutes, the cardiac rhythm should be reassessed, and the patient should continue to be shocked with defibrillation doses of electricity until there is either a return of a perfusing sinus rhythm or the patient’s rhythm deteriorates into one that is not shockable (see management below).

Reversible causes of persistent arrhythmia should be sought. Some case reports have reported successful patient outcomes when coronary angiography with percutaneous coronary intervention was performed on patients undergoing CPR for refractory VF/VT in the setting of suspected acute coronary ischemia or myocardial infarction. However, fibrinolytics given during CPR for acute coronary occlusion do not appear to improve outcomes.

Asystole or pulseless electrical activity

These rhythms are not shockable. The hospitalist leading the resuscitation of a patient with one of these rhythms should focus on the provision of adequate chest compressions, placing an advanced airway, and looking for reversible causes of the patient’s clinical deterioration. Epinephrine at a dose of 1mg can be administered every 3 to 5 minutes. Routine administration of atropine is no longer recommended in the setting of asystole or PEA. Vasopressin, which could previously be used in place of the first or second dose of epinephrine, was removed from the 2015 guidelines for simplicity sake due to no evidence of superiority over epinephrine. However, it may be reasonable based on two randomized controlled trials to use a combination of epinephrine 1mg + vasopressin 20 units repeated every 3 to 5 minutes as well as methylprednisolone 40 mg x 1 with the first cycle.

Every 2 minutes, CPR can be paused briefly for a pulse and cardiac rhythm check. If a pulse returns (return of spontaneous circulation), next, focus on post-cardiac arrest care (see below). If the patient continues to be pulseless but converts to VF or VT, follow the algorithm detailed above.

Common reversible conditions include “the five H’s and the five T’s”:

The H’s: hypovolemia, hypoxia, hydrogen ions (acidosis), hypo/hyperkalemia, and hypothermia.

The T’s: tension pneumothorax, tamponade (cardiac), toxins, thrombosis (pulmonary embolism [PE]), and thrombosis (coronary).

As noted above, percutaneous coronary intervention can be considered even in the midst of CPR if acute myocardial infarction is the suspected cause of the cardiac arrest. Administration of fibrinolytics while CPR is ongoing has not been effective in studies where it was given to unselected patients with PEA. However, some authors have reported success with administering fibrinolytics during CPR in patients with fulminant pulmonary embolism who are experiencing PEA or asystole.

The 2010 guidelines for cardiopulmonary resuscitation and emergency cardiovascular care do recommend to consider fibrinolytics if fulminant pulmonary embolism is thought to be the likely cause of a cardiac arrest. A hint that a massive PE may be the cause of PEA is a result suggestive of acute right ventricular strain on electrocardiogram or the cardiac monitor. There is no standardized dose for fibrinolytics in the setting of CPR for massive PE. AHA guidelines describe administration of alteplase 50mg IV bolus with option to repeat after 15 minutes, or weight based dose of tenecteplase. If PE is confirmed (not just suspected) as the cause of cardiac arrest, then other options including surgical and mechanical embolectomy can be considered. No evidence exists to support thrombolysis vs embolectomy.

Post-cardiac arrest care

Once spontaneous circulation has returned, the hospitalist should shift the focus to optimizing cardiopulmonary function and vital organ perfusion. Reversible causes of cardiac arrest should continue to be aggressively sought and treated. In particular, a rapid decision should be made as to whether a patient would benefit from an attempt at coronary artery reperfusion in the setting of probable ongoing myocardial ischemia. It is often necessary to provide maximum supportive care for ongoing shock or multiple organ injury.

A major goal after resuscitation is to maximize the patient’s chances for an acceptable neurologic recovery. To this end, randomized studies have shown improved neurologic outcomes (as well as improved survival) when patients who remain comatose after VF/VT arrest are treated with targeted temperature management. Target temperatures should be between 32-36 degrees Celsius.

Data thus far have not supported any benefit from treating patients resuscitated from PEA/asystole with current therapeutic mild hypothermia protocols. However, the AHA recommends that all adults without meaningful neurologic function after cardiac arrest be considered for targeted temperature management.

Work-up of the survivor of unanticipated sudden cardiac arrest

At times hospitalists are called upon to provide care to the patient who has been resuscitated from an unexpected sudden cardiac arrest that occurred in the outpatient setting. Such patients always require a thorough work-up to best determine the cause of their arrest and prevent a fatal recurrence. The patient should be evaluated and treated for standard reversible causes as discussed in the section on in-hospital cardiac arrest.

Next, nearly all patients who have experienced sudden cardiac arrest without an obvious precipitating cause should undergo diagnostic coronary angiography. Nearly all survivors of SCA should also undergo echocardiography. However, if possible, an official echocardiogram should be delayed for 48 hours after an arrest (or performed at the time of admission and repeated at 48 hours) due to myocardial stunning that can be seen in the peri-arrest period.

Echocardiography can suggest coronary heart disease (regional wall motion abnormalities), hypertrophic cardiomyopathy, myocarditis, and sometimes arrhythmogenic right ventricular cardiomyopathy. If there is strong suspicion for arrhythmogenic right ventricular cardiomyopathy, myocarditis or infiltrative diseases of the myocardium (including cardiac sarcoid) but no definitive proof is seen on an echocardiogram, consideration can be given to obtaining cardiac magnetic resonance imaging.

If no cause for SCA has been identified despite the work-up detailed above, electrophysiologic testing may be indicated. Special attention should be paid to any electrocardiographic findings that might suggest channelopathies such as Brugada syndrome (downward sloping elevated ST segments along with inverted T waves in V1 and V2) or long QT syndrome (familial or acquired prolongation of the corrected QT interval to greater than 450 ms).

Consulting a general cardiologist or cardiac electrophysiologist is often helpful for assistance with the work-up of electrical diseases that can cause SCA and with the decision of whether to place an implantable cardioverter defibrillator, which is often indicated with varied causes of SCA for secondary prevention against a deadly recurrence of arrhythmia.

IV. Common Pitfalls.

Resuscitating a patient who does not want to be resuscitated

At times, a code blue will be activated by bedside staff who have either not received a proper sign-out on a patient’s goals of care or who panic when their patient has a sudden decompensation. When responding to a code blue activation on a patient who is not one of your primary patients, remember to verify that the patient is “full code” with the bedside nurse as you are beginning the resuscitation.

Failure to check blood glucose

Blood glucose should be checked early during any resuscitation. Especially in the setting of PEA or asystole, underlying severe hypoglycemia may have triggered a significant event (such as a seizure, or aspiration in the setting of alteration in mental status) that led to the patient’s decompensation.

Forgetting a backboard

A backboard will decrease mattress displacement, allowing more sternal force to be used to compress the chest. A backboard is particularly helpful for patients on softer intensive care unit (ICU) beds.

Failure to search for a cause of pulseless electrical activity

Identifying and treating the cause of PEA will likely be the only chance the arresting patient will have of a return of spontaneous circulation and, more importantly, surviving to discharge. Remember to work through the H’s and T’s.

Over-ventilating the patient in cardiac arrest

During the excitement of resuscitation, it is easy to squeeze the ambu bag too fast and too hard. Overventilation leads to increased intrathoracic pressure, which decreases venous return to the heart and, thus, diminishes cardiac output. Current ACLS guidelines recommend delivering approximately 600 mL of tidal volume to a patient during resuscitation.

Given that the average ambu bag holds 1600 mL, the bag may only need to be squeezed about one-third of the way to deliver sufficient volume. The recommended rate at which to manually ventilate a patient during an arrest situation is 10 breaths per minute.

Not recognizing when an endotracheal tube has become dislodged during a resuscitation

Due to this common error, the 2015 cardiopulmonary resuscitation guidelines now recommend the use of quantitative waveform capnography in addition to clinical assessment (auscultation of lungs and stomach) during ongoing resuscitations. Waveform capnography (or end tidal CO2) is superior to colorimetric devices for confirming initial airway placement and for ongoing monitoring.

Taking unnecessary pauses from chest compressions

Recent studies have confirmed that the rate, depth and continuity of chest compressions are inadequate in the majority of resuscitations. Minimize pauses in chest compression for rhythm checks. If continuous capnography is being used, a jump in end-tidal carbon dioxide (CO₂) can provide a tip that spontaneous circulation has returned even in the presence of ongoing compressions. The goal depth of chest compressions is 2-2.4 inches and the chest should be allowed to fully recoil between compressions. The goal rate of chest compressions is 100-120 per minute.

Creating a fire hazard

Avoid fires by not leaving the disconnected ventilator tubing directed so as to blow oxygen across the chest during defibrillation. Using self-adhesive defibrillation pads and ensuring good pad-chest-wall contact will minimize the risk of sparks and, thus, fire.

Failure to identify a code leader

If multiple physicians are present during resuscitation, all should be encouraged to share their thoughts and ideas (as should other participants such as nurses, respiratory therapists and pharmacists). However, one physician should clearly identify him or herself as the “code leader”. This leader should then give all official orders (for drugs, doses, etc.) during the resuscitation. This will minimize the confusion that can often ensue when physicians give conflicting or multiple simultaneous orders to nurses, pharmacists or respiratory therapists.

Failure of the code leader to verbalize his or her thoughts and elicit input

Working through a differential diagnosis out loud (even if the cause of an arrest is not entirely clear) can prompt other healthcare providers in the room to share their ideas. Such collaboration will often lead to less errors of omission. Although there should be one clear leader during a resuscitation (so team members know exactly where to look for orders), all healthcare providers in the room should be encouraged to speak out if they have ideas about a diagnosis or treatment modality that has not been considered or if they have concerns about the safety of any of the interventions being performed.

Missing special causes of sudden cardiac arrest

Although electrocardiographic findings suggestive of right bundle branch morphology or a true a right bundle branch block can be non-specific in many patients, very special attention should be paid to such abnormalities in a patient (particularly one of a younger age) who has had a sudden cardiac arrest. An acute right ventricular strain pattern can be seen in a patient with a fulminant pulmonary embolism. The downward-sloping ST segment elevations seen in electrocardiogram (EKG) leads V1 and V2 in Brugada syndrome can be confused with right bundle branch block. A right bundle block can be seen in arrhythmogenic right ventricular dysplasia due to the replacement of the right ventricular myocardium with fatty or fibrous tissue.

It should also be appreciated that what appears to be simple left ventricular hypertrophy on an electrocardiogram could represent hypertrophic cardiomyopathy.

V. National Standards, Core Indicators and Quality Measures.

Joint Commission standards mandate that all acute care hospitals have resuscitation equipment throughout the hospital based on the needs of the patient populations in each clinical area and that an evidence-based training program is used to train staff to recognize the need for and use of resuscitation equipment and techniques.

Of note, the Joint Commission does not require hospitals to create rapid response teams, but they do expect hospitals to develop written criteria for detecting early warning signs for a change in a patient’s condition, when to seek further assistance and assuring proper response in such situations.

Joint Commission standards on performance improvement do require that all acute care hospitals collect data on the results of resuscitation. Joint Commission standards also mandate that all staff that may be using restraint or seclusion for patients’ behavioral disturbances should be trained (and recertified regularly) in the use of cardiopulmonary resuscitation.

“Get With The Guidelines – Resuscitation”, formerly known as the National Registry of Cardio-Pulmonary Resuscitation (NRCPR), collects data on resuscitation events in multiple hospitals throughout the United States. This registry provides much of the observational data about epidemiology and outcomes in in-hospital resuscitation that is available. Published data from this registry can be useful if you are looking to benchmark the outcomes in your hospital.

If your hospital is a participant in “Get With The Guidelines – Resuscitation”, you have continuous access to the registry’s resuscitation event data, and it is possible to compare the performance of your hospital to that of similar facilities. If your hospital does not participate in “Get With The Guidelines – Resuscitation”, it is possible to purchase a subscription on their website.

VI. What's the Evidence?

CPR Statistics: CPR and Sudden Cardiac Arrest (SCA) Fact Sheet. 2012.

Sandroni, C. “In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival”. Intensive Care Med. vol. 33. 2007. pp. 237-245.

Get with the Guidelines – Resuscitation Overview. 2011.

2010.

Nishisaki, A, Maltese, MR, Niles, D, Sutton, RM, Urbano, J, Berg, RA, Nadkarni, VM. “CPR Backboard or No Backboard”. That is the Question! [Abstract] Circulation. vol. 122. 2010. pp. A247

Kurkciyan, I. “Pulmonary embolism as a cause of cardiac arrest: presentation and outcome”. Arch Intern Med. vol. 160. 2000. pp. 1529-1535.

Neumar, RW. “Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care”. Circulation. vol. 122. 2010. pp. S729-S767.

Neumar, RW. “Part 1: Executive Summary 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care”. Circulation. vol. 132. 2015. pp. S315-367. (Summary of the 2015 AHA update on resuscitation)

Link, MS. “Part 7: Adult Advanced Cardiovascular Life Support 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care”. Circulation. vol. 132. 2015. pp. S444-464. (ACLS section from the 2015 update)

Link, MS. “Part 6: Electrical Therapies: Automated External Defibrillators, Defibrillation, Cardioversion, and Pacing. 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care”. Circulation. vol. 122. 2010. pp. S706-S719.

Abu-Laban, RB, Christenson, JM, Innes, GD. “Tissue plasminogen activator in cardiac arrest with pulseless electrical activity”. N Engl J Med. vol. 346. 2002. pp. 1522-152.

Dumas, F. “Is hypothermia after cardiac arrest effective in both shockable and nonshockable patients? insights from a large registry”. Circulation. vol. 123. 2011. pp. 877-886.

Nielson, N. “Targeted temperature management at 33C versus 36C after cardiac arrest”. N Engl J Med. vol. 369. 2013. pp. 2197-2206. (Larger 2013 study comparing temperature targets for post resuscitation care. The change in the 2015 guidelines to allow for temperature range from 32-36 degrees is based on this study)

Mentzelopoulos, SD. “Vasopressin, steroids, and epinephrine and neurologically favorable survival after in-hospital cardiac arrest: a randomized clinical trial”. JAMA. vol. 310. 2013. pp. 270-27. (Larger study showing favorable outcomes with combination pressor of vaso+epi along with steroids. Mentioned in Part 7 2015 update as a reasonable option to try.)

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