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ACLS Case: Cardiac Arrest

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ACLS Case: Cardiac Arrest

Treating patients with cardiac arrest rhythms requires competency in BLS, ACLS, and post-cardiac arrest care. It is important to note that the fundamental ideas to the success of resuscitation are high-quality CPR and rapid defibrillation for shockable rhythms. Appropriate reasons for brief pauses in high-quality CPR include rhythm check, defibrillation, pulse check, or placing an advanced airway.

Key Takeaway

The rhythms associated with cardiac arrest are:

  • VF
  • pVT
  • PEA
  • Asystole

There are four rhythms of cardiac arrest: ventricular fibrillation (VF), pulseless ventricular tachycardia (pVT), pulseless electrical activity (PEA), and asystole. In VF, the ventricles are depolarizing and repolarizing in a completely disorganized fashion causing all pumping and ventricular function to fail. In pVT, there is an organized electrical activity of the myocardium that is ventricular in origin, as evidenced by wide QRS complexes in the ECG, which does not generate significant blood flow. In PEA, the electrical activity of the heart may represent normal tracing in ECG. However, there is a possible restriction of the heart, causing its mechanical function to fail. It can also be due to significant blood loss; hence, the ejection of blood is inadequate to generate a pulse.

The healthcare providers of ACLS must also have training in diagnosing and treating the reversible causes of cardiac arrest. Use the H’s and T’s <> as a guide to identifying the possible causes of cardiac arrest.

Post-cardiac arrest care begins once the patient achieves the return of spontaneous circulation (ROSC). Post-cardiac arrest care avoids re-arrest. It can also increase the chance of long-term survival and restore neurologic health.

The ACLS provider must understand the algorithms associated with cardiac arrest. The first algorithm below is the traditional linear format with the shockable rhythms (VF and pVT) on the left side and asystole and PEA on the right side. The second algorithm is a circular arrest algorithm introduced in 2015. Both algorithms are based on 5 cycles of compressions and ventilations or 2 minutes of continuous CPR.

Figure 5-2 Adult Cardiac Arrest Algorithm – Update

Adult Cardiac Arrest Circular Algorithm – Update

The ACLS provider must be able to recognize the rhythms of cardiac arrest on a cardiac monitor. Understanding the basics of these rhythms allows the user to identify them quickly.

Key Takeaway

ECG Characteristics of Shockable Cardiac Arrest Rhythms

  1. VF – shows as voltage fluctuations in the ECG strip. Amplitude is characterized as coarse (early VF) or fine (late VF).
  2. pVT – the patient does not exhibit a pulse. pVT shows a fast and usually regular rhythm with wide QRS complexes on ECG. No P waves.

ECG Characteristics of Shockable Cardiac Arrest Rhythms

  1. Asystole – ECG Characteristics of Non-Shockable Cardiac Arrest Rhythms
  2. PEA – depicted by an organized rhythm, but the patient fails to produce a pulse.

Box 1: Identify Cardiac Arrest and Start CPR

Ideally, the team performs rhythm-based management of cardiac arrest. The first provider is assigned to give high-quality CPR with chest compressions. If the patient is already attached to a cardiac monitor, the cardiac arrest rhythm can be diagnosed even before CPR is initiated. If the cardiac arrest is in-hospital, and oxygen is available, the patient should receive oxygen at 100% FiO2.

The second provider obtains a defibrillator or monitor, attaches the pads or electrodes to the cardiac arrest patient, and checks the rhythm. When the second provider checks the rhythm, it is necessary to pause chest compressions to prevent motion artifacts in the ECG tracing. Therefore, rhythm checks should be less than 10 seconds, anticipating a resumption of chest compressions as soon as possible. If the provider detects an organized rhythm, then the second provider checks for a pulse. If there is no pulse and the rhythm is shockable, the second provider commences the procedures for immediate defibrillation of the patient. Otherwise, for non-shockable cardiac arrest patients, high-quality CPR is resumed.

Box 2: Identify Shockable Rhythms: VF or pVT

If the rhythm is not shockable, the rescuer should proceed with treatment on the right side of the algorithm for asystole and PEA described in Box 9 below. VF and pVT are shockable rhythms.

Box 3: Administer Shock

Prompts on the AED notify the providers to clear the patient and deliver a shock by pressing the shock button. After the AED announces that the shock was delivered, CPR must be resumed immediately for two minutes before performing the next rhythm check. The AED will prompt the providers to stop CPR to provide an opportunity for another rhythm check.

When using a manual defibrillator, the first provider must perform chest compressions while the defibrillator is charging. Once charged, stop chest compressions, and the second provider instructs everyone to clear the patient. Once everyone is clear of the patient, the second provider delivers a shock. Chest compressions immediately resume for two minutes before performing another rhythm check.

Studies show that biphasic manual defibrillators are preferred over monophasic defibrillators for the treatment of atrial and ventricular arrhythmias. Biphasic waveform defibrillators set to deliver 200 J or less for the first shock were efficacious.21 The first dose of shock delivery depends on the manufacturer’s recommended energy dose. If the provider does not know the manufacturer’s recommended dose, the clinician should consider the maximal dose.

The manufacturer’s recommendations should determine the choice between a fixed or escalating energy dose for subsequent shocks. If the provider does not know this information, escalating energies, or a subsequent shock with a higher energy dose is recommended. Studies have observed that a fixed energy dose of 150 J with a biphasic defibrillator can terminate initial and recurrent VF with high success rates.22 However, subsequent shocks demonstrate declined shock success.23 The single stacked strategy is preferred over stacked shocks for defibrillation.

Key Takeaway

Energy Dose for Shock

  • First Shock – refer to manufacturer’s recommendation or highest dose available
    (if the recommended shock is unknown)
  • Subsequent Shocks – refer to manufacturer’s recommendations or escalating energies (higher for second and subsequent shocks)

Box 4: Continue High-Quality CPR

After defibrillation, the heart undergoes a brief period of PEA or asystole with a delay in achieving a perfusing rhythm; hence, we must minimize the duration of interrupted CPR by immediately performing chest compressions after a shock. It is advisable that providers “switch out” performing chest compressions every two minutes, or when fatigued, as CPR quality diminishes when providers become physically tired. A good time to switch out compressors is when the AED or monitor is charging for another shock. It is not necessary to perform a pulse or rhythm check at this point unless the patient is showing signs of life, or there is ROSC as indicated by advanced monitoring. At this point in the algorithm, providers should obtain IV or IO (intraosseous) access in anticipation of drug delivery. Some non-AHA protocols call for continuous uninterrupted chest compressions and utilization of ETCO2.

Auto-compression devices

ETCO2 Monitoring

Box 5: Rhythm Check and Shock Administration

After two minutes of high-quality CPR, recheck the patient’s rhythm. If the rhythm continues as VF or pVT, prepare to administer another shock. The rhythm check should be as brief as possible, and the team should resume CPR immediately after. Again, as mentioned previously, the second and subsequent shocks should be at an equivalent or higher dose than the first shock. Follow the manufacturer’s recommendations. It is crucial to learn about the equipment in your workplace specifically, and preferably before needing to use it.

Box 6: Epinephrine and Consideration of Advanced Airway

Once the team delivers the shock, resume high-quality CPR immediately. At this point, two shocks were delivered, and vascular access is available. High-quality CPR is ongoing. It is now time to utilize drug therapy to restore a perfusing rhythm. The first-line medication for the treatment of VF or pVT is epinephrine.

A cardiac arrest patient may receive epinephrine when feasible after the placement of vascular access. Studies for IHCA patients show that there is an increased chance for ROSC if epinephrine is given within 1 to 3 minutes of cardiac arrest as opposed to epinephrine given after 3 minutes.24

For OHCA patients, studies show increased rates of ROSC if epinephrine is given 9 minutes or less from the onset of cardiac arrest as compared with patients given epinephrine later.25


Epinephrine 1: 10000 box

Medications for Arrest Rhythms

ACLS drug therapy aims to restore a perfusing spontaneous rhythm after successful resuscitation of cardiac arrest. Studies have shown increased rates of ROSC after high-quality CPR and drug therapy; however, long-term survival and good neurologic outcome seem to evade resuscitation science.26


Rescuer on far right preparing medication

Vasopressors in Cardiac Arrest

  1. Vasopressors in Cardiac Arrest: Standard-Dose Epinephrine

The recommendations are for epinephrine to treat cardiac arrest intravenously or via the intraosseous route with a preparation of 1:10,000 dilution, 1 mg every 3 to 5 minutes. Studies show that this standard dose is responsible for improved survival and ROSC. The addition of vasopressin does not show any advantage over using epinephrine alone; therefore, the AHA no longer recommends vasopressin as a treatment in cardiac arrest.
The effects of epinephrine include:

  • Vasoconstriction causes increased perfusion pressure to the heart and brain
  • An increased cardiac output that results in
  • Increased heart rate
  • Increased heart contractility
  • Increased conductivity of impulses through the AV node 

Key Takeaway

  • Recommendations no longer suggest vasopressin as a treatment choice in cardiac arrest.

Advanced Airways

In Box 6, in addition to administering epinephrine, providers are directed to consider the insertion of an advanced airway. An advanced airway is not always necessary if the patient is being ventilated adequately with a bag-valve-mask (BVM). Ideally, two rescuers are needed to ventilate effectively with a BVM. One provider obtains a tight seal with the mask over the patient’s mouth and nose. The second provider delivers each ventilation at the correct time in the CPR sequence (after 30 compressions 2 breaths are given), and at the correct volume to cause the chest to rise but avoiding excessive ventilation, essential components of high-quality CPR.

When you determine that an advanced airway is needed there are several essential points to remember:

  • Inserting an advanced airway can lead to unacceptable delays in the provision of CPR
  • Only those providers with expertise should attempt insertion of an advanced airway
  • Once inserted, determine proper placement by both physical confirmation (equal bilateral chest rise, air entry heard in all lung fields and no air auscultated over the epigastrium) and physiologic monitoring (waveform capnography monitoring)
  • Secure advanced airways in place, and check placement frequently to detect any complications, such as dislodgement
  • Once an advanced airway is in place, ventilation and compressions no longer need to be synchronous; the compressor provides continuous chest compressions while the ventilator provides one breath every 6 seconds

For more information on advanced airways and ventilation during cardiac arrest, see the chapter on adjuncts.

Box 7: Rhythm Check and Shock Administration

Once the initial dose of epinephrine has been given and two minutes have passed since the last shock, CPR pauses to perform another rhythm check. If the patient’s rhythm is unchanged or refractory (patient remains in VT or pVT), administer another shock. Once the team administers the shock, immediately resume CPR.

Box 8: Administer Antiarrhythmic and Consider Possible Causes

Antiarrhythmic Drugs During and Immediately After Cardiac Arrest

Administer amiodarone for VF or pVT refractory to defibrillation, CPR, and vasopressor therapy. Lidocaine is an alternative treatment for amiodarone. Give both drugs intravenously and via the intraosseous route.

Key Takeaway


Preparation of Antiarrhythmic Drugs in Cardiac Arrest

  • Amiodarone – 300 mg IV/IO push, first dose then 150 mg push IV/IO for succeeding dose
  • Lidocaine – 1.0 to 1.5 mg/kg IV/IO push, first dose then 0.5 to 0.75 mg/kg IV push succeeding for a maximum of 3 doses or a total of 3 mg/kg

Magnesium sulfate is recommended only in certain circumstances, such as torsades des pointes, or patients with low serum magnesium (i.e., alcoholic or undernourished patients). The patient’s chart may provide essential clues in identifying such individuals. Give magnesium as a loading dose of 1-2 g diluted in 10 mL of NS or D5W, given IV or IO slowly over 5 to 20 minutes.

Reversible Conditions of Cardiac Arrest

For any patient in cardiac arrest, it is crucial to consider why cardiac arrest occurred in the first place. The H’s and T’s allow providers to remember the possible reversible causes of cardiac arrest.

Thus far, we have discussed the treatment of patients with a shockable rhythm (VF or pVT), following the left side of the cardiac arrest algorithm. On the right side of the algorithm, we consider patients who have an organized or semi-organized rhythm but no pulse (PEA), or patients who have no electrical activity at all (“flatline”) and no pulse (asystole).

Boxes 9, 10, and 11 of the Adult Cardiac Arrest Algorithm, outline the steps for providers to take in when treating patients in a non-shockable rhythm. Again, high-quality CPR is of utmost importance. In this branch of the algorithm, epinephrine should be given as soon as possible. Rather than a focus on defibrillation, as with shockable rhythms, the focus is on the H’s and T’s and attempting to reverse any process that may have led to cardiac arrest. As hypoxia is a common cause of PEA, providers may consider an advanced airway sooner rather than later. Hypovolemia is also a common cause of PEA, thus obtaining IV or IO access and providing fluids may be helpful. The only drug you should give to patients in PEA or asystole is epinephrine. As in the shockable rhythms, epinephrine may be given every 3 to 5 minutes at a dose of 1 mg (1:10,000 solution).

If at any time the patient regains a pulse and an organized rhythm (ROSC), providers should begin post-cardiac arrest care.

Prognostication During CPR: End-Tidal CO2

Use end-tidal carbon dioxide (ETCO2) levels as a prognostication tool in considering when to end resuscitative efforts in intubated patients. Cardiac arrest patients that fail to attain an ETCO2 greater than 10 mmHg via waveform capnography after 20 minutes of CPR exhibits poor prognosis. The team should not use ETCO2 for prognostication of cardiac arrest in the non-intubated patient.

During cardiac arrest, ETCO2 levels reflect cardiac output generated by chest compression; hence, lower values indicate poor chest compression quality or low cardiac output. Low ETCO2 values may also indicate that there is bronchospasm, kinking of the ET tube, or mucus plugging of the ET tube.

Extracorporeal CPR

ECPR is a clinical intervention that utilizes venoatrial extracorporeal membrane oxygenation during cardiac arrest. It is not a recommended treatment for cardiac arrest, but the clinician should consider ECPR in hospital settings where they can perform the procedure immediately. Consider ECPR for selected patients in cardiac arrest, where the suspected etiology may be reversible. (see pages 145-147)

Interventions Not Recommended During Cardiac Arrest

Atropine

Studies report that there is no therapeutic benefit of atropine for routine use in cardiac arrest patients with PEA or asystole.

Sodium Bicarbonate

AHA no longer recommends sodium bicarbonate for patients in cardiac arrest. High-quality CPR provides ventilation and perfusion to the surrounding tissues to restore the acid-base balance during cardiac arrest. During cardiac arrest, tissue acidosis ensues because of anaerobic metabolism. Hence, sodium bicarbonate aims to return the physiologic pH. However, studies have shown that sodium bicarbonate does not improve survival rates.

Also, sodium bicarbonate causes adverse effects when used during CPR, such as compromising cerebral perfusion pressure by reducing systemic vascular resistance.29

Key Takeaway


Medications NOT recommended in cardiac arrest:

  • Atropine
  • Sodium bicarbonate
  • Calcium
  • Fibrinolysis

Calcium

Current recommendations do not include routine use of calcium for the treatment of IHCA and OHCA. Studies fail to show the association of calcium treatment with ROSC or survival.30

Fibrinolysis

Fibrinolytic therapy is not routinely used in cardiac arrest. Current recommendations include fibrinolytic therapy for patients with acute coronary syndrome or pulmonary embolism. Some studies show promising results with the use of fibrinolytic therapy for the treatment of cardiac arrest patients unresponsive to standard therapy.31 However, other clinical trials fail to show good outcomes with the routine use of fibrinolytic therapy during CPR.32,33

Terminating Resuscitation Efforts

As important as it is to know how to resuscitate a patient, it is equally important to know when to terminate resuscitation efforts. Unfortunately, the answer to this question is not always clear-cut. Before terminating resuscitation efforts, consider the physical, psychological, social, and ethical aspects of this decision. Some principles that can help guide this decision include:

  • Medical futility or the belief that prolonged resuscitation does not change the outcome. That is, even with resuscitation efforts, the patient is likely to die. This concept is important when dealing with a pre-hospital arrest in which no one witnessed the arrest, there was no prehospital ROSC, or EMS identified an initial unshockable rhythm. Any of these conditions would predict a > 99% chance of inferior outcome or medical futility.
  • Autonomy or the patient’s right to refuse treatment. Does the patient have a “do not resuscitate” order, or is the family informed of the patient’s DNR status?
  • Beneficence or what is in the best interest of the patient. If we attempt prolonged resuscitation on this 95-year old, are we doing them a favor?
  • Benefit versus a burden. If we continue medical treatment, will the benefits for the patient be higher than the burden?

Ultimately, there must be guidelines in place that help to direct EMS and in-hospital personnel about decisions to terminate treatment. The hospital Ethics Committee is a valuable resource when making these sorts of decisions.


21 Morrison LJ, Henry RM, Ku V, Nolan JP, Morley P, Deakin CD. Single-shock defibrillation success in adult cardiac arrest: a sys- tematic review. Resuscitation. 2013;84:1480–1486. doi: 10.1016/j. resuscitation.2013.07.008.

22Hess EP, Russell JK, Liu PY, White RD. A high peak current 150-J fixed-energy defibrillation protocol treats recurrent ventricular fibrilla- tion (VF) as effectively as initial VF. Resuscitation. 2008;79:28–33. doi: 10.1016/j.resuscitation.2008.04.028.

23GKoster RW, Walker RG, Chapman FW. Recurrent ventricular fibril- lation during advanced life support care of patients with prehospi- tal cardiac arrest. Resuscitation. 2008;78:252–257. doi: 10.1016/j. resuscitation.2008.03.231.

24 Donnino MW, Salciccioli JD, Howell MD, Cocchi MN, Giberson B, Berg K, Gautam S, Callaway C; American Heart Association’s Get With The Guidelines-Resuscitation Investigators. Time to administration of epinephrine and outcome after in-hospital cardiac arrest with non-shock- able rhythms: retrospective analysis of large in-hospital data registry. BMJ. 2014;348:g3028.

25Goto Y, Maeda T, Goto Y. Effects of prehospital epinephrine during out- of-hospital cardiac arrest with initial non-shockable rhythm: an observa- tional cohort study. Crit Care. 2013;17:R188. doi: 10.1186/cc12872.

26Olasveengen TM, Sunde K, Brunborg C, Thowsen J, Steen PA, Wik L. Intravenous drug administration during out-of-hospital cardiac arrest: a randomized trial. JAMA. 2009;302:2222–2229.

27Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL. Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial. Resuscitation. 2011;82:1138– 1143. doi: 10.1016/j.resuscitation.2011.06.029.

28Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL. Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial. Resuscitation. 2011;82:1138– 1143. doi: 10.1016/j.resuscitation.2011.06.029.

29 Kette F, Weil MH, Gazmuri RJ. Buffer solutions may compromise cardiac resuscitation by reducing coronary perfusion pressure. JAMA. 1991;266:2121–2126.

30Harrison EE, Amey BD. The use of calcium in cardiac resuscitation. Am J Emerg Med. 1983;1:267–273.

31Fatovich DM, Dobb GJ, Clugston RA. A pilot randomised trial of thrombolysis in cardiac arrest (the TICA trial). Resuscitation. 2004;61:309–313.

32 Bottiger BW, Arntz HR, Chamberlain DA, et al. Thrombolysis during resuscitation for out-of-hospital cardiac arrest. N Engl J Med. 2008;359:2651–2662.

33Abu-Laban RB, Christenson JM, Innes GD, van Beek CA, Wanger KP, McKnight RD, MacPhail IA, Puskaric J, Sadowski RP, Singer J, Schechter MT, Wood VM. Tissue plasminogen activator in cardiac arrest with pulseless electrical activity. N Engl J Med. 2002;346:1522–1528.

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