BCLS, ACLS, & Cardiac Arrest Care

 

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Prehospital Stuff

BLS termination of resuscitation rule

 

ALS termination of resuscitation rule

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Basic Life Support

 

 

Sichuan Straddle

The quality of straddling external chest compression performed on a moving stretcher was as effective as standard external chest compression performed on the floor. By performing straddling external chest compression, time for transporting victims to the emergency department to get advanced life support may be shortened. Resuscitation. 2010 Nov;81(11):1562 from resus.me

 

Untrained Lay Rescuer

If a bystander is not trained in CPR, then the bystander should provide Hands-Only (chest compression only) CPR, with an emphasis on “push hard and fast,” or follow the directions of the emergency medical dispatcher. The rescuer should continue Hands-Only CPR until an AED arrives and is ready for use or healthcare providers take over care of the victim (Class IIa, LOE B).

Lay rescuers should assume cardiac arrest based on assessing unresponsiveness and absence of normal breathing (ie, the victim is not breathing or only gasping)

“Look, Listen, and Feel” was removed from the BLS algorithm Lay rescuers should not interrupt chest compressions to palpate pulses or check for ROSC (Class IIa, LOE C).

Trained Lay Rescuer

All lay rescuers should, at a minimum, provide chest compressions for victims of cardiac arrest. In addition, if the trained lay rescuer is able to perform rescue breaths, he or she should add rescue breaths in a ratio of 30 compressions to 2 breaths. The rescuer should continue CPR until an AED arrives and is ready for use or EMS providers take over care of the victim (Class I, LOE B).

 

Sequence change to chest compressions before rescue breaths (CAB rather than ABC)

Healthcare Providers

Optimally all healthcare providers should be trained in BLS. In this trained population it is reasonable for both EMS and in-hospital professional rescuers to provide chest compressions and rescue breaths for cardiac arrest victims (Class IIa, LOE B).

This should be performed in cycles of 30 compressions to 2 ventilations until an advanced airway is placed; then compressing rescuer should give continuous chest compressions at a rate of at least 100 per minute without pauses for ventilation (Class IIa, LOE B). The rescuer delivering ventilation can provide a breath every 6 to 8 seconds (which yields 8 to 10 breaths per minute). A compression-ventilation ratio of 30:2 is reasonable in adults, but further validation of this guideline is needed (Class IIb, LOE B).

 

Sequence change to chest compressions before rescue breaths (CAB rather than ABC)

Increased focus on methods to ensure that high-quality CPR (compressions of adequate rate and depth, allowing full chest recoil between compressions, minimizing interruptions in chest compressions and avoiding excessive ventilation) is performed

Recommendation of a simultaneous, choreographed approach for chest compressions, airway management, rescue breathing, rhythm detection, and shocks (if appropriate) by an integrated team of highly-trained rescuers in appropriate settings

The healthcare provider should take no more than 10 seconds to check for a pulse and, if the rescuer does not definitely feel a pulse within that time period, the rescuer should start chest compressions (Class IIa, LOE C).

 

Rescue Breaths • Deliver each rescue breath over 1 second (Class IIa, LOE C). • Give a sufficient tidal volume to produce visible chest rise (Class IIa, LOE C).55

 

Studies in anesthetized adults (with normal perfusion) suggest that a tidal volume of 8 to 10 mL/kg maintains normal oxygenation and elimination of CO2. During CPR, cardiac output is 25% to 33% of normal, so oxygen uptake from the lungs and CO2 delivery to the lungs are also reduced. As a result, a low minute ventilation (lower than normal tidal volume and respiratory rate) can maintain effective oxygenation and ventilation. For that reason during adult CPR tidal volumes of approximately 500 to 600 mL (6 to 7 mL/kg) should suffice (Class IIa, LOE B). This is consistent with a tidal volume that produces visible chest rise. In summary, rescuers should avoid excessive ventilation (too many breaths or too large a volume) during CPR (Class III, LOE B).

 

If an adult victim with spontaneous circulation (ie, strong and easily palpable pulses) requires support of ventilation, the healthcare provider should give rescue breaths at a rate of about 1 breath every 5 to 6 seconds, or about 10 to 12 breaths per minute (Class IIb, LOE C). Each breath should be given over 1 second regardless of whether an advanced airway is in place. Each breath should cause visible chest rise.

 

Cricoid Pressure

The routine use of cricoid pressure in adult cardiac arrest is not recommended (Class III, LOE B).

 

Compressions

Correct performance of chest compressions requires several essential skills. The adult sternum should be depressed at least 2 inches (5 cm) (Class IIa, LOE B), with chest compression and chest recoil/relaxation times approximately equal (Class IIb, LOE C). Allow the chest to completely recoil after each compression (Class IIa, LOE B). Although rescuers may not recognize that fatigue is present for 5 minutes. When 2 or more rescuers are available it is reasonable to switch chest compressors approximately every 2 minutes (or after about 5 cycles of compressions and ventilations at a ratio of 30:2) to prevent decreases in the quality of compressions (Class IIa, LOE B).

Healthcare providers should interrupt chest compressions as infrequently as possible and try to limit interruptions to no longer than 10 seconds, except for specific interventions such as insertion of an advanced airway or use of a defibrillator (Class IIa, LOE C). Because of difficulties with pulse assessments, interruptions in chest compressions for a pulse check should be minimized during the resuscitation, even to determine if ROSC has occurred.

Because of the difficulty in providing effective chest compressions while moving the patient during CPR, the resuscitation should generally be conducted where the patient is found (Class IIa, LOE C). This may not be possible if the environment is dangerous.

 

Electrical Therapies

After shock delivery, the rescuer should not delay resumption of chest compressions to recheck the rhythm or pulse. After about 5 cycles of CPR (about 2 minutes, although this time is not firm), ideally ending with compressions, the AED should then analyze the cardiac rhythm and deliver another shock if indicated (Class I, LOE B). If a nonshockable rhythm is detected, the AED should instruct the rescuer to resume CPR immediately, beginning with chest compressions (Class I, LOE B).

 

Shortening the interval between the last compression and the shock by even a few seconds can improve shock success (defibrillation and ROSC) Thus, it is reasonable for healthcare providers to practice efficient coordination between CPR and defibrillation to minimize the hands-off interval between stopping compression and administering shock (Class IIa, LOE C). For example, when 2 rescuers are present, the rescuer operating the AED should be prepared to deliver a shock as soon as the compressor removes his or her hands from the victim’s chest and all rescuers are “clear” of contact with the victim.

Biphasic waveforms are safe and have equivalent or higher efficacy for termination of VF when compared with monophasic waveforms. In the absence of biphasic defibrillators, monophasic defibrillators are acceptable (Class IIb, LOE B). Different biphasic waveforms have not been compared in humans with regard to efficacy. Therefore, for biphasic defibrillators, providers should use the manufacturer’s recommended energy dose (120 to 200 J) (Class I, LOE B). If the manufacturer’s recommended dose is not known, defibrillation at the maximal dose may be considered (Class IIb, LOE C).

Fixed and Escalating Energy It is not possible to make a definitive recommendation for the selected energy for subsequent biphasic defibrillation attempts. However, based on available evidence, we recommend that second and subsequent energy levels should be at least equivalent and higher energy levels may be considered, if available (Class IIb, LOE B).

Electrode Placement Data demonstrate that 4 pad positions (anterolateral, anteroposterior, anterior-left infrascapular, and anterior-right-infrascapular)are equally effective to treat atrial or ventricular arrhythmias. There are no studies directly pertaining to placement of pads/paddles for defibrillation success with the end point of ROSC. All 4 positions are equally effective in shock success. Any of the 4 pad positions is reasonable for defibrillation (Class IIa, LOE B). For ease of placement and education, anterolateral is a reasonable default electrode placement (Class IIa, LOE C). Ten studies indicated that larger pad/paddle size (8 to 12 cm diameter) lowers transthoracic impedance.

 

Precordial Thump The precordial thump may be considered for termination of witnessed monitored unstable ventricular tachyarrhythmias when a defibrillator is not immediately ready for use (Class IIb, LOE B), but should not delay CPR and shock delivery. There is insufficient evidence to recommend for or against the use of the precordial thump for witnessed onset of asystole, and there is insufficient evidence to recommend percussion pacing during typical attempted resuscitation from cardiac arrest.

Supraventricular Tachycardias (Reentry Rhythms)

Biphasic

biphasic energy dose for cardioversion of adult atrial fibrillation is 120 to 200 J (Class IIa, LOE A). If the initial shock fails, providers should increase the dose in a stepwise fashion. Cardioversion of adult atrial flutter and other supraventricular tachycardias generally requires less energy; an initial energy of 50 J to 100 J is often sufficient. If the initial shock fails, providers should increase the dose in a stepwise fashion.Monophasic Adult cardioversion of atrial fibrillation with monophasic waveforms should begin at 200 J and increase in a stepwise fashion if not successful (Class IIa, LOE B).

Ventricular Tachycardia with Pulse

Biphasic & Monophasic

Adult monomorphic VT (regular form and rate) with a pulse responds well to monophasic or biphasic waveform cardioversion (synchronized) shocks at initial energies of 100 J. If there is no response to the first shock, it may be reasonable to increase the dose in a stepwise fashion. No studies were identified that addressed this issue. Thus, this recommendation represents expert opinion (Class IIb, LOE C).

Asystole

There was a worse outcome of ROSC and survival for those who received shocks. Thus, it is not useful to shock asystole (Class III, LOE B).

 

Pacing is not effective for asystolic cardiac arrest and may delay or interrupt the delivery of chest compressions. Pacing for patients in asystole is not recommended (Class III, LOE B).

Ventricular Fibrillation / Pulseless V-Tach

Biphasic

If a biphasic defibrillator is available, providers should use the manufacturer’s recommended energy dose (120 to 200 J) for terminating VF (Class I, LOE B). If the provider is unaware of the effective dose range, the provider may use the maximal dose (Class IIb, LOE C). Second and subsequent energy levels should be at least equivalent, and higher energy levels may be considered if available (Class IIb, LOE B).

Monophasic

If a monophasic defibrillator is used, providers should deliver an initial shock of 360 J and use that dose for all subsequent shocks. If VF is terminated by a shock but then recurs later in the arrest, deliver subsequent shocks at the previously successful energy level.

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Advanced Cardiac Life Support

Advanced Airway Management

During the first few minutes of witnessed cardiac arrest a lone rescuer should not interrupt chest compressions for ventilation. Advanced airway placement in cardiac arrest should not delay initial CPR and defibrillation for VF cardiac arrest (Class I, LOE C).

 

Empirical use of 100% inspired oxygen during CPR optimizes arterial oxyhemoglobin content and in turn oxygen delivery; therefore, use of 100% inspired oxygen (FIO2=1.0) as soon as it becomes available is reasonable during resuscitation from cardiac arrest (Class IIa, LOE C).

 

At this time there is insufficient evidence to support the removal of ventilations from CPR performed by ACLS providers or the use of passive oxygen delivery.

Bag-Mask Ventilation

BVM is most effective when performed by 2 trained and experienced providers. One provider opens the airway and seals the mask to the face while the other squeezes the bag. Bag-mask ventilation is particularly helpful when placement of an advanced airway is delayed or unsuccessful. approximately 600 mL of tidal volume sufficient to produce chest rise over 1 second.

Oropharyngeal Airways To facilitate delivery of ventilations with a bag-mask device, oropharyngeal airways can be used in unconscious (unresponsive) patients with no cough or gag reflex and should be inserted only by persons trained in their use (Class IIa, LOE C).

Nasopharyngeal Airways To facilitate delivery of ventilations with a bag-mask device, the nasopharyngeal airway can be used in patients with an obstructed airway. In the presence of known or suspected basal skull fracture or severe coagulopathy, an oral airway is preferred (Class IIa, LOE C).

Advanced Airway Placement

If advanced airway placement will interrupt chest compressions, providers may consider deferring insertion of the airway until the patient fails to respond to initial CPR and defibrillation attempts or demonstrates ROSC (Class IIb, LOE C).

Supraglottic Airways

During CPR performed by providers trained in its use, the supraglottic airway is a reasonable alternative to bag-mask ventilation (Class IIa, LOE B) and endotracheal intubation (Class IIa, LOE A). For healthcare professionals trained in its use, the esophageal-tracheal tube is an acceptable alternative to both bag-mask ventilation (Class IIa, LOE C) or endotracheal intubation (Class IIa, LOE A) for airway management in cardiac arrest. For healthcare professionals trained in its use, the laryngeal tube may be considered as an alternative to bag-mask ventilation (Class IIb, LOE C) or endotracheal intubation for airway management in cardiac arrest (Class IIb, LOE C). For healthcare professionals trained in its use, the laryngeal mask airway is an acceptable alternative to bag-mask ventilation (Class IIa, LOE B) or endotracheal intubation (Class IIa, LOE C) for airway management in cardiac arrest.

 

During CPR providers should minimize the number and duration of interruptions in chest compressions, with a goal to limit interruptions to no more than 10 seconds. If the initial intubation attempt is unsuccessful, a second attempt may be reasonable, but early consideration should be given to using a supraglottic airway.

 

Confirmation

Even when the endotracheal tube is seen to pass through the vocal cords and tube position is verified by chest expansion and auscultation during positive-pressure ventilation, providers should obtain additional confirmation of placement using waveform capnography or an exhaled CO2 or esophageal detector device (EDD). Continuous waveform capnography is recommended in addition to clinical assessment as the most reliable method of confirming and monitoring correct placement of an endotracheal tube (Class I, LOE A). If waveform capnography is not available, an EDD or nonwaveform exhaled CO2 monitor in addition to clinical assessment is reasonable (Class IIa, LOE B). Techniques to confirm endotracheal tube placement are further discussed below.

Continuous waveform capnography is recommended in addition to clinical assessment as the most reliable method of confirming and monitoring correct placement of an endotracheal tube (Class I, LOE A). Given the simplicity of colorimetric and nonwaveform exhaled CO2 detectors, these methods can be used in addition to clinical assessment as the initial method for confirming correct tube placement in a patient in cardiac arrest when waveform capnography is not available (Class IIa, LOE B).

 

EDDStudies of the syringe aspiration EDD and the self-inflating bulb EDD indicate that the accuracy of these devices does not exceed that of auscultation and direct visualization for confirming the tracheal position of an endotracheal tube in victims of cardiac arrest. Given the simplicity of the EDD, it can be used as the initial method for confirming correct tube placement in addition to clinical assessment in the victim of cardiac arrest when waveform capnography is not available (Class IIa, LOE B). The EDD may yield misleading results in patients with morbid obesity, late pregnancy, or status asthmaticus, or when there are copious endotracheal secretions because the trachea tends to collapse in the presence of these conditions.

 

Securing the ETT

The endotracheal tube should be secured with tape or a commercial device (Class I, LOE C). Devices and tape should be applied in a manner that avoids compression of the front and sides of the neck, which may impair venous return from the brain.

 

Vents during CPRDuring prolonged resuscitative efforts the use of an ATV (pneumatically powered and time- or pressure-cycled) may allow the EMS team to perform other tasks while providing adequate ventilation and oxygenation (Class IIb, LOE C). Providers should always have a bag-mask device available for backup.

Advanced Circulation Stuff

CPR Before Defibrillation

During treatment of VF/pulseless VT healthcare providers must ensure that coordination between CPR and shock delivery is efficient. When VF is present for more than a few minutes, the myocardium is depleted of oxygen and metabolic substrates. A brief period of chest compressions can deliver oxygen and energy substrates and “unload” the volume-overloaded right ventricle, increasing the likelihood that a perfusing rhythm will return after shock delivery At this time the benefit of delaying defibrillation to perform CPR before defibrillation is unclear (Class IIb, LOE B).

The value of VF waveform analysis to guide management of defibrillation in adults with in-hospital and out-of-hospital cardiac arrest is uncertain (Class IIb, LOE C).

Performing CPR while a defibrillator is readied for use is strongly recommended for all patients in cardiac arrest (Class I, LOE B).

Discovering ROSC

Pulse

Because there are no valves in the inferior vena cava, retrograde blood flow into the venous system may produce femoral vein pulsations. Thus, palpation of a pulse in the femoral triangle during compressions, may indicate venous rather than arterial blood flow. Carotid pulsations during CPR do not indicate the efficacy of myocardial or cerebral perfusion during CPR. Palpation of a pulse when chest compressions are paused is a reliable indicator of ROSC, but is potentially less sensitive than other physiologic measures discussed below and requires a lengthy pause without compressions.

End-Tidal CO2

With initiation of CPR, cardiac output is the major determinant of CO2 delivery to the lungs. If ventilation is relatively constant, PETCO2 correlates well with cardiac output during CPR.

 

The correlation between PETCO2 and cardiac output during CPR can be transiently altered by giving IV sodium bicarbonate. This is explained by the fact that the bicarbonate is converted to water and CO2, causing a transient increase in delivery of CO2 to the lungs. Therefore, a transient rise in PETCO2 after sodium bicarbonate therapy is expected and should not be misinterpreted as an improvement in quality of CPR or a sign of ROSC.

Animal and human studies have also shown that PETCO2 correlates with CPP and cerebral perfusion pressure during CPR. The correlation of PETCO2 with CPP during CPR can be altered by vasopressor therapy, especially at high doses (ie, >1 mg of epinephrine). Vasopressors cause increased afterload, which will increase blood pressure and myocardial blood flow during CPR but will also decrease cardiac output. Therefore, a small decrease in PETCO2 after vasopressor therapy may occur but should not be misinterpreted as a decrease in CPR quality.

 

Persistently low PETCO2 values (<10 mm Hg) during CPR in intubated patients suggest that ROSC is unlikely. Similar data using quantitative monitoring of PETCO2 are not available for patients with a supraglottic airway or those receiving bag-mask ventilation during CPR. Although a PETCO2 value of <10 mm Hg in intubated patients indicates that cardiac output is inadequate to achieve ROSC, a specific target PETCO2 value that optimizes the chance of ROSC has not been established. Therefore, it is reasonable to consider using quantitative waveform capnography in intubated patients to monitor CPR quality, optimize chest compressions, and detect ROSC during chest compressions or when rhythm check reveals an organized rhythm (Class IIb, LOE C).

If PETCO2 is <10 mm Hg, it is reasonable to consider trying to improve CPR quality by optimizing chest compression parameters (Class IIb, LOE C).

If PETCO2 abruptly increases to a normal value (35 to 40 mm Hg), it is reasonable to consider that this is an indicator of ROSC (Class IIa, LOE B).

 

 

 

Consequently, the rule of 10 mm Hg may be extended to include a sudden increase in continuously recorded PETCO2 by more than 10 mm Hg as an indicator of the possibility of ROSC. (JEM 2010;38(5):614)

Coronary Perfusion Pressure and Aortic Relaxation Pressure

CPP (coronary perfusion pressure=aortic relaxation [“diastolic”] pressure minus right atrial relaxation [“diastolic”] pressure) during CPR correlates with both myocardial blood flow and ROSC.Relaxation pressure during CPR is the trough of the pressure waveform during the relaxation phase of chest compressions and is analogous to diastolic pressure when the heart is beating. Increased CPP correlates with improved 24-hour survival rates in animal studies and is associated with improved myocardial blood flow and ROSC in animal studies of epinephrine, vasopressin, and angiotensin II. In one human study ROSC did not occur unless a CPP 15 mm Hg was achieved during CPR.However, monitoring of CPP during CPR is rarely available clinically because measurement and calculation require simultaneous recording of aortic and central venous pressure.

A reasonable surrogate for CPP during CPR is arterial relaxation (“diastolic”) pressure, which can be measured using a radial, brachial, or femoral artery catheter. These closely approximate aortic relaxation pressures during CPR in humans. The same study that identified a CPP threshold of 15 mm Hg for ROSC also reported that ROSC was not achieved if aortic relaxation “diastolic” pressure did not exceed 17 mm Hg during CPR. A specific target arterial relaxation pressure that optimizes the chance of ROSC has not been established. It is reasonable to consider using arterial relaxation “diastolic” pressure to monitor CPR quality, optimize chest compressions, and guide vasopressor therapy. (Class IIb, LOE C).

 

If the arterial relaxation “diastolic” pressure is <20 mm Hg, it is reasonable to consider trying to improve quality of CPR by optimizing chest compression parameters or giving a vasopressor or both (Class IIb, LOE C). Arterial pressure monitoring can also be used to detect ROSC during chest compressions or when a rhythm check reveals an organized rhythm (Class IIb, LOE C).

 

My own research would actually indicate an Aortic Diastolic pressure of 40 mm Hg is what you should shoot for. (JAMA 1990;263(8):1106)

 

Central Venous Oxygen Saturation

Therefore, when in place before cardiac arrest, it is reasonable to consider using continuous ScvO2 measurement to monitor quality of CPR, optimize chest compressions, and detect ROSC during chest compressions or when rhythm check reveals an organized rhythm (Class IIb, LOE C). If ScvO2 is <30%, it is reasonable to consider trying to improve the quality of CPR by optimizing chest compression parameters (Class IIb, LOE C).

Echocardiography

Transthoracic or transesophageal echocardiography may be considered to diagnose treatable causes of cardiac arrest and guide treatment decisions (Class IIb, LOE C). A beating heart may indicate ROSC.

 

Intravascular Access

It is reasonable for providers to establish IO access if IV access is not readily available (Class IIa, LOE C). Commercially available kits can facilitate IO access in adults.

The appropriately trained provider may consider placement of a central line (internal jugular or subclavian) during cardiac arrest, unless there are contraindications (Class IIb, LOE C). Central venous catheterization is a relative (but not absolute) contraindication for fibrinolytic therapy in patients with acute coronary syndromes.

VF/Pulseless VT

Check rhythm and defibrillate every 2 minutes

Vasopressors

A vasopressor can be given as soon as feasible with the primary goal of increasing myocardial and cerebral blood flow during CPR and achieving ROSC (see “Vasopressors” below for dosing) (Class IIb, LOE A).

 

It is reasonable to consider administering a 1 mg dose of IV/IO epinephrine every 3 to 5 minutes during adult cardiac arrest (Class IIb, LOE A). Higher doses can also be considered if guided by hemodynamic monitoring such as arterial relaxation “diastolic” pressure or CPP.

Vasopressin 40 units IV/IO may replace either the first or second dose of epinephrine in the treatment of cardiac arrest (Class IIb, LOE A).There are no alternative vasopressors (norepinephrine, phenylephrine) with proven survival benefit compared with epinephrine.268,281,282

When VF/pulseless VT persists after at least 1 shock and a 2-minute CPR period, a vasopressor can be given with the primary goal of increasing myocardial blood flow during CPR and achieving ROSC (see “Medications for Arrest Rhythms” below for dosing) (Class IIb, LOE A). However, if a shock results in a perfusing rhythm, a bolus dose of vasopressor at any time during the subsequent 2-minute period of CPR (before rhythm check) could theoretically have detrimental effects on cardiovascular stability. This may be avoided by using physiologic monitoring such as quantitative waveform capnography, intra-arterial pressure monitoring, and continuous central venous oxygen saturation monitoring to detect ROSC during chest compressions.

 

However, adding an additional pause for rhythm and pulse check after shock delivery but before vasopressor therapy will decrease myocardial perfusion during the critical postshock period and could reduce the chance of achieving ROSC.

 

Antiarrhythmics

Amiodarone

Amiodarone is the first-line antiarrhythmic agent given during cardiac arrest because it has been clinically demonstrated to improve the rate of ROSC and hospital admission in adults with refractory VF/pulseless VT. Amiodarone may be considered when VF/VT is unresponsive to CPR, defibrillation, and vasopressor therapy (Class IIb, LOE A).

 

The adverse hemodynamic effects of the IV formulation of amiodarone are attributed to vasoactive solvents (polysorbate 80 and benzyl alcohol). When administered in the absence of these solvents, an analysis of the combined data of 4 prospective clinical trials of patients with VT (some hemodynamically unstable) showed that amiodarone produced no more hypotension than lidocaine. A formulation of IV amiodarone without these vasoactive solvents was approved for use in the United States.

 

Amiodarone may be considered for VF or pulseless VT unresponsive to CPR, defibrillation, and a vasopressor therapy (Class IIb, LOE B). An initial dose of 300 mg IV/IO can be followed by 1 dose of 150 mg IV/IO. Although anecdotally administered IO without known adverse effects, there is limited experience with amiodarone given by this route.

If amiodarone is unavailable, lidocaine may be considered, but in clinical studies lidocaine has not been demonstrated to improve rates of ROSC and hospital admission compared with amiodarone (Class IIb, LOE B).

 

Lidocaine Lidocaine may be considered if amiodarone is not available (Class IIb, LOE B). The initial dose is 1 to 1.5 mg/kg IV. If VF/pulseless VT persists, additional doses of 0.5 to 0.75 mg/kg IV push may be administered at 5- to 10-minute intervals to a maximum dose of 3 mg/kg.

Magnesium Sulfate Routine administration of magnesium sulfate in cardiac arrest is not recommended (Class III, LOE A) unless orsades de pointes is present. Magnesium sulfate should be considered only for torsades de pointes associated with a long QT interval (Class IIb, LOE B). PEA/Asystole

Aystole/PEA

A vasopressor can be given as soon as feasible with the primary goal of increasing myocardial and cerebral blood flow during CPR and achieving ROSC (see “Vasopressors” below for dosing) (Class IIb, LOE A).

 

Available evidence suggests that the routine use of atropine during PEA or asystole is unlikely to have a therapeutic benefit (Class IIb, LOE B). For this reason atropine has been removed from the cardiac arrest algorithm.

 

Electric pacing is not recommended for routine use in cardiac arrest (Class III, LOE B).

 

If available, echocardiography can be used to guide management of PEA because it provides useful information about intravascular volume status (assessing ventricular volume), cardiac tamponade, mass lesions (tumor, clot), left ventricular contractility, and regional wall motion.

Other Drugs

Sodium Bicarbonate In some special resuscitation situations, such as preexisting metabolic acidosis, hyperkalemia, or tricyclic antidepressant overdose, bicarbonate can be beneficial (see Part 12: “Cardiac Arrest in Special Situations”). However, routine use of sodium bicarbonate is not recommended for patients in cardiac arrest (Class III, LOE B).

 

CalciumRoutine administration of calcium for treatment of in-hospital and out-of-hospital cardiac arrest is not recommended (Class III, LOE B).

Fibrinolysis

Fibrinolytic therapy should not be routinely used in cardiac arrest (Class III, LOE B). When pulmonary embolism is presumed or known to be the cause of cardiac arrest, empirical fibrinolytic therapy can be considered (Class IIa, LOE B; see Part 12).

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Bradycardia

 

If bradycardia produces signs and symptoms of instability (eg, acutely altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or other signs of shock that persist despite adequate airway and breathing), the initial treatment is atropine (Class IIa, LOE B).

 

Atropine remains the first-line drug for acute symptomatic bradycardia (Class IIa, LOE B).The recommended atropine dose for bradycardia is 0.5 mg IV every 3 to 5 minutes to a maximum total dose of 3 mg. Doses of atropine sulfate of <0.5 mg may paradoxically result in further slowing of the heart rate. Atropine administration should not delay implementation of external pacing for patients with poor perfusion.

 

If bradycardia is unresponsive to atropine, intravenous (IV) infusion of B-adrenergic agonists with rate-accelerating effects (dopamine, epinephrine) or transcutaneous pacing (TCP) can be effective (Class IIa, LOE B) while the patient is prepared for emergent transvenous temporary pacing if required.

Pacing It is reasonable for healthcare providers to initiate TCP in unstable patients who do not respond to atropine (Class IIa, LOE B). Immediate pacing might be considered in unstable patients with high-degree AV block when IV access is not available (Class IIb, LOE C). If the patient does not respond to drugs or TCP, transvenous pacing is probably indicated (Class IIa, LOE C)

 

Alternative Drugs to Consider Dopamine infusion may be used for patients with symptomatic bradycardia, particularly if associated with hypotension, in whom atropine may be inappropriate or after atropine fails (Class IIb, LOE B). Begin dopamine infusion at 2 to 10 mcg/kg per minute and titrate to patient response.370Epinephrine infusion may be used for patients with symptomatic bradycardia, particularly if associated with hypotension, for whom atropine may be inappropriate or after atropine fails (Class IIb, LOE B). Begin the infusion at 2 to 10 mcg/min and titrate to patient response.

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Tachycardias

 

If the tachycardic patient is unstable with severe signs and symptoms related to a suspected arrhythmia (eg, acute altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or other signs of shock), immediate cardioversion should be performed (with prior sedation in the conscious patient) (Class I, LOE B). In select cases of regular narrow-complex tachycardia with unstable signs or symptoms, a trial of adenosine before cardioversion is reasonable to consider (Class IIb, LOE C).

 

Narrow-Complex Tachycardia

AdenosineIf PSVT does not respond to vagal maneuvers, give 6 mg of IV adenosine as a rapid IV push through a large (eg, antecubital) vein followed by a 20 mL saline flush (Class I, LOE B). If the rhythm does not convert within 1 to 2 minutes, give a 12 mg rapid IV push using the method above. Larger doses may be required for patients with a significant blood level of theophylline, caffeine, or theobromine. The initial dose should be reduced to 3 mg in patients taking dipyridamole or carbamazepine, those with transplanted hearts, or if given by central venous access.

 

Calcium Channel Blockers and B-Blockers. If adenosine or vagal maneuvers fail to convert PSVT, PSVT recurs after such treatment, or these treatments disclose a different form of SVT (such as atrial fibrillation or flutter), it is reasonable to use longer-acting AV nodal blocking agents, such as the nondihydropyridine calcium channel blockers (verapamil and diltiazem) (Class IIa, LOE B) or B-blockers (Class IIa, LOE C).

 

For verapamil, give a 2.5 mg to 5 mg IV bolus over 2 minutes (over 3 minutes in older patients). If there is no therapeutic response and no drug-induced adverse event, repeated doses of 5 mg to 10 mg may be administered every 15 to 30 minutes to a total dose of 20 mg. An alternative dosing regimen is to give a 5 mg bolus every 15 minutes to a total dose of 30 mg. Verapamil should be given only to patients with narrow-complex reentry SVT or arrhythmias known with certainty to be of supraventricular origin. Verapamil should not be given to patients with wide-complex tachycardias. It should not be given to patients with impaired ventricular function or heart failure.

 

For diltiazem, give a dose of 15 mg to 20 mg (0.25 mg/kg) IV over 2 minutes; if needed, in 15 minutes give an additional IV dose of 20 mg to 25 mg (0.35 mg/kg). The maintenance infusion dose is 5 mg/hour to 15 mg/hour, titrated to heart rate.

 

Caution is advised when encountering pre-excited atrial fibrillation or flutter that conducts to the ventricles via both the AV node and an accessory pathway. Treatment with an AV nodal blocking agent (including adenosine, calcium blockers, ?-blockers, or digoxin) is unlikely to slow the ventricular rate and in some instances may accelerate the ventricular response. Therefore, AV nodal blocking drugs should not be used for pre-excited atrial fibrillation or flutter (Class III, LOE C).

 

Caution is also advised to avoid the combination of AV nodal blocking agents that have a longer duration of action. For example, the short elimination half-life of adenosine affords follow-up treatment, if required, with a calcium channel blocker or ?-blocker. Conversely the longer half-life of a calcium channel or ?-blocker means their effects will overlap; profound bradycardia can develop if they are given serially.

Wide-Complex Tachycardia

Precordial thump may be considered for patients with witnessed, monitored, unstable ventricular tachycardia if a defibrillator is not immediately ready for use (Class IIb, LOE C).

 

If the etiology of the rhythm cannot be determined, the rate is regular, and the QRS is monomorphic, recent evidence suggests that IV adenosine is relatively safe for both treatment and diagnosis(Class IIb, LOE B). However, adenosine should not be given for unstable or for irregular or polymorphic wide-complex tachycardias, as it may cause degeneration of the arrhythmia to VF (Class III, LOE C). If the wide-complex tachycardia proves to be SVT with aberrancy, it will likely be transiently slowed or converted by adenosine to sinus rhythm; if due to VT there will be no effect on rhythm (except in rare cases of idiopathic VT), and the brevity of the transient adenosine effect should be reasonably tolerated hemodynamically. Because close attention to these varying responses may help to diagnose the underlying rhythm, whenever possible, continuous ECG recording is strongly encouraged to provide such written documentation. This documentation can be invaluable in helping to establish a firm rhythm diagnosis even if after the fact. Typically, adenosine is administered in a manner similar to treatment of PSVT: as a 6 mg rapid IV push; providers may follow the first dose with a 12 mg bolus and a second 12 mg bolus if the rate fails to convert. When adenosine is given for undifferentiated wide-complex tachycardia, a defibrillator should be available.

Verapamil is contraindicated for wide-complex tachycardias unless known to be of supraventricular origin (Class III, LOE B). Adverse effects when the rhythm was due to VT were shown in 5 small case series. Profound hypotension was reported in 11 of 25 patients known to have VT treated with verapamil.

If IV antiarrhythmics are administered, procainamide (Class IIa, LOE B), amiodarone (Class IIb, LOE B), or sotalol (Class IIb, LOE B) can be considered. Procainamide and sotalol should be avoided in patients with prolonged QT. If one of these antiarrhythmic agents is given, a second agent should not be given without expert consultation (Class III, LOE B). If antiarrhythmic therapy is unsuccessful, cardioversion or expert consultation should be considered (Class IIa, LOE C).

IV sotalol (100 mg IV over 5 minutes) was found to be more effective than lidocaine (100 mg IV over 5 minutes) when administered to patients with spontaneous hemodynamically stable sustained monomorphic VT in a double-blind randomized trial within a hospital setting. In a separate study of 109 patients with a history of spontaneous and inducible sustained ventricular tachyarrhythmias, infusing 1.5 mg/kg of sotalol over 5 minutes was found to be relatively safe and effective, causing hypotension in only 2 patients, both of whom responded to IV fluid.Package insert recommends slow infusion, but the literature supports more rapid infusion of 1.5 mg/kg over 5 minutes or less. Sotalol should be avoided in patients with a prolonged QT interval.

 

Polymorphic VT

If a long QT interval is observed during sinus rhythm (ie, the VT is torsades de pointes), the first step is to stop medications known to prolong the QT interval. Correct electrolyte imbalance and other acute precipitants (eg, drug overdose or poisoning: see Part 12.7: “Cardiac Arrest Associated With Toxic Ingestions”). Although magnesium is commonly used to treat torsades de pointes VT (polymorphic VT associated with long QT interval), it is supported by only 2 observational studies that showed effectiveness in patients with prolonged QT interval.

One adult case series showed that isoproterenol or ventricular pacing can be effective in terminating torsades de pointes associated with bradycardia and drug-induced QT prolongation. Polymorphic VT associated with familial long QT syndrome may be treated with IV magnesium, pacing, and/or ?-blockers; isoproterenol should be avoided. Polymorphic VT associated with acquired long QT syndrome may be treated with IV magnesium. The addition of pacing or IV isoproterenol may be considered when polymorphic VT is accompanied by bradycardia or appears to be precipitated by pauses in rhythm.

In the absence of a prolonged QT interval, the most common cause of polymorphic VT is myocardial ischemia. In this situation IV amiodarone and B-blockers may reduce the frequency of arrhythmia recurrence (Class IIb, LOE C). Myocardial ischemia should be treated with B-blockers and consideration be given to expeditious cardiac catheterization with revascularization.

 

Magnesium is unlikely to be effective in preventing polymorphic VT in patients with a normal QT interval (Class IIb, LOE C), but amiodarone may be effective (Class IIb, LOE C).

Other causes of polymorphic VT apart from ischemia and long QT syndrome are catecholaminergic VT (which may be responsive to ?-blockers) and Brugada syndrome (which may be responsive to isoproterenol).

 

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Acute Coronary Syndromes

 

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Stroke

 

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Post-Rosc Stuff

 

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Pediatrics and Neonatal

 

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Special Situations

Cardiac Arrest in Pregnancy

The Importance of Timing With Emergency Cesarean Section The 5-minute window that providers have to determine if cardiac arrest can be reversed by BLS and ACLS was first described in 1986 and has been perpetuated in specialty guidelines.The rescue team is not required to wait 5 minutes before initiating emergency hysterotomy, and there are circumstances that support an earlier start. For instance, in an obvious nonsurvivable injury, when the maternal prognosis is grave and resuscitative efforts appear futile, moving straight to an emergency cesarean section may be appropriate, especially if the fetus is viable.

Many reports document long intervals between an urgent decision for hysterotomy and actual delivery of the infant, far exceeding the obstetric guideline of 30 minutes for patients not in arrest. Very few cases of perimortem cesarean section fall within the recommended 5-minute period. Survival of the mother has been reported with perimortem cesarean section performed up to 15 minutes after the onset of maternal cardiac arrest. If emergency cesarean section cannot be performed by the 5-minute mark, it may be advisable to prepare to evacuate the uterus while the resuscitation continues. (Class IIb, LOE C).

New Update

Based on the review of all extant lit (Resuscitation. 2012 Oct;83(10):1191-200), the 5 minute limit is way too strict. May consider proceeding even with longer times from arrest.

After Accidental Hypothermia

Unintentional or accidental hypothermia is a serious and preventable health problem. Severe hypothermia (body temperature <30°C [86°F]) is associated with marked depression of critical body functions, which may make the victim appear clinically dead during the initial assessment. Therefore, lifesaving procedures should be initiated unless the victim is obviously dead (eg, rigor mortis, decomposition, hemisection, decapitation). The victim should be transported as soon as possible to a center where aggressive rewarming during resuscitation is possible.

Initial Care for Victims of Accidental Hypothermia When the victim is extremely cold but has maintained a perfusing rhythm, the rescuer should focus on interventions that prevent further loss of heat and begin to rewarm the victim immediately. Additional interventions include the following:• Preventing additional evaporative heat loss by removing wet garments and insulating the victim from further environmental exposures. Passive rewarming is generally adequate for patients with mild hypothermia (temperature >34°C [93.2°F]). • For patients with moderate (30°C to 34°C [86°F to 93.2°F]) hypothermia with a perfusing rhythm, external warming techniques are appropriate. Passive rewarming alone will be inadequate for these patients.• For patients with severe hypothermia (<30°C [86°F]) with a perfusing rhythm, core rewarming is often used, although some have reported successful rewarming with active external warming techniques.Active external warming techniques include forced air or other efficient surface-warming devices. • Patients with severe hypothermia and cardiac arrest can be rewarmed most rapidly with cardiopulmonary bypass. Alternative effective core rewarming techniques include warm-water lavage of the thoracic cavity and extracorporeal blood warming with partial bypass.• Adjunctive core rewarming techniques include warmed IV or intraosseous (IO) fluids and warm humidified oxygen. Heat transfer with these measures is not rapid, and should be considered supplementary to active warming techniques. • Do not delay urgent procedures such as airway management and insertion of vascular catheters. Although these patients may exhibit cardiac irritability, this concern should not delay necessary interventions.

 

Beyond these critical initial steps, the treatment of severe hypothermia (temperature <30°C [86°F]) in the field remains controversial. Many providers do not have the time or equipment to assess core body temperature or to institute aggressive rewarming techniques, although these methods should be initiated when available.

BLS Modifications When the victim is hypothermic, pulse and respiratory rates may be slow or difficult to detect,and the ECG may even show asystole. If the hypothermic victim has no signs of life, begin CPR without delay. If the victim is not breathing, start rescue breathing immediately. The temperature at which defibrillation should first be attempted in the severely hypothermic patient and the number of defibrillation attempts that should be made have not been established. There are case reports of refractory ventricular arrhythmias with severe hypothermia; however, in a recent animal model it was found that an animal with a temperature of as low as 30°C had a better response to defibrillation than did normothermic animals in arrest. If VT or VF is present, defibrillation should be attempted. If VT or VF persists after a single shock, the value of deferring subsequent defibrillations until a target temperature is achieved is uncertain. It may be reasonable to perform further defibrillation attempts according to the standard BLS algorithm concurrent with rewarming strategies (Class IIb, LOE C).

ACLS Modifications For unresponsive patients or those in arrest, advanced airway insertion is appropriate as recommended in the standard ACLS guidelines. Advanced airway management enables effective ventilation with warm, humidified oxygen and reduces the likelihood of aspiration in patients in periarrest. ACLS management of cardiac arrest due to hypothermia focuses on aggressive active core rewarming techniques as the primary therapeutic modality. Conventional wisdom indicates that the hypothermic heart may be unresponsive to cardiovascular drugs, pacemaker stimulation, and defibrillation; however, the data to support this are essentially theoretical. In addition, drug metabolism may be reduced, and there is a theoretical concern that medications could accumulate to toxic levels in the peripheral circulation if given repeatedly to the severely hypothermic victim. For these reasons, previous guidelines suggest withholding IV drugs if the victim’s core body temperature is <30°C (86°F).

It may be reasonable to consider administration of a vasopressor during cardiac arrest according to the standard ACLS algorithm concurrent with rewarming strategies (Class IIb, LOE C).

After ROSC After ROSC, patients should continue to be warmed to a goal temperature of approximately 32° to 34°C; this can be maintained according to standard postarrest guidelines for mild to moderate hypothermia in patients for whom induced hypothermia is appropriate. For those with contraindications to induced hypothermia, rewarming can continue to normal temperatures. Because severe hypothermia is frequently preceded by other disorders (eg, drug overdose, alcohol use, or trauma), the clinician must look for and treat these underlying conditions while simultaneously treating hypothermia.

Withholding and Cessation of Resuscitative Efforts Multiple case reports indicate survival from accidental hypothermia even with prolonged CPR and downtimes. Thus, patients with severe accidental hypothermia and cardiac arrest may benefit from resuscitation even in cases of prolonged downtime and prolonged CPR. Low serum potassium may indicate hypothermia, and not hypoxemia, as the primary cause of the arrest. Patients should not be considered dead before warming has been provided.

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Non-ACLS Course Cardiac Arrest Topics

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In-Hospital Cardiac Arrest

Continue in-house resuscitation longer and more patients survive neurologically intact (Lancet 2012 Sept. 4 [doi:10.1016/S0140-6736(12)60862-9]).

 

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  Review Articles

• Incredible Review (DM=Disease-A-Month 1997;July:433) by the man himself, WeilBobrow’s ReviewMcMAID Approach to initial management
• Still to be Edited and Added Back In
• CPR Airway Breathing CPR/Capnography Defib Echo Myocardial blood flow is 25% normal, cerebral blood flow is 50% normal during well performed CPRbecause outflow is low, much smaller amounts of ventilation are needed to maintain normal V/Q ratios. Emphasis should always be on consistent compressions with a de-emphasis on breathing Huge difference in the PaCO2 and PvCO2. alkalemic in arteries and hypercarbic in veinsPalpating pulses during CPR has poor correlation with actual flow, it just represents pressure transmission to the arteries (DM)A complete balloon occlusion of aorta still allows pulses to be palpated. ETCO2 or amplitude of V-Fib are more predictive (DM) As CPR goes on, it becomes less effective due to changes in heart and chest complianceETCO2 predictive of success (Crit Care Med 1985, 13:907)>10 indicates potential survival (NEJM 1988 318:607 & JAMA 1989 262:1347 & Ann Emerg Med 1995;25:762-767)ETCO2 <10 at 20 minutes in a PEA code–no chance of survival (NEJM 1997;337:301-6)If arrest time is <6 minutes then code for 30 minutes; If arrest time is >6 minutes, code for 15 minutes (Crit Care Med 1985,13:930-931)Pulse with compressions is not helpful (Circ 2000 102:I86)Get Venous Blood Gas, not arterial as this is more representative of systemic oxygenation (Marino)The prohibition against shocking asystole may not be evidence-based (AJEM 2008;26:618)Thrombolytics“There is insufficient evidence to recommend for or against the routine use of fibrinolysis for cardiac arrest. It may be considered on a case-by-case basis when pulmonary embolus is suspected (Class IIa). ”
  

  New Metaanalysis

  Resus 2006;70:31

  8 papers

  Lytics increased ROSC, 24 hr survival, discharge, neuro function, and severe bleeds. All bleeds were treatable. Since the bleeding rate was only recorded in survivors, it may just be that rate is the same in both groups but only treatment bleeds seen.

   

  Impedance Threshold Device (ITD)

  Although increased long-term survival rates have not been documented, when the impedance threshold device (ResQValve, Advanced Circulatory Systems) is used by trained personnel as an adjunct to CPR in intubated adult cardiac arrest patients, it can improve hemodynamic parameters and ROSC (Class IIa).

   

  

  Inspiratory Impedence Threshold Valves (ITVs) are devices attached to resuscitation breathing circuits that prevent passive indrawing of air during chest recoil/decompression following chest compression as part of CPR. In doing so the ITV enhances the period of negative intrathoracic pressure thereby augmenting venous return and so improving CPR-generated cardiac output.92 ITVs are particularly effective when combined with active compression–decompression CPR (ACD CPR) but also provide some benefit during conventional CPR.93 and 94 In order for the ITV to be effective a negative intrathoracic pressure must be maintained.

   

  The ITV contains pressure-sensitive valves and is designed to selectively impede the gas influx through the airway during chest-wall decompression. During chest decompression, pressure in the upper airways decreases, inducing the closure of the valve and preventing the gases from entering the lungs. Coupled with ACD, the ITV will thereby augment the amplitude and the duration of the vacuum within the thorax during active decompression [28], enhancing venous return and cardiac preload. The increase in cardiac filling during decompression will result in an increase in cardiac output during the next compression. The cracking pressure, defined as the inspiratory pressure needed to allow gases to flow inwards through the valve, usually varies from -7 to -16 cmH2O. Current evidence supports the use of ITV with a cracking pressure of -7 cmH2O for standard CPR and -15 cmH2O for ACD CPR.

  (Crit Care Med 2007;35:1145) experimental study on impedance threshold device to improve BP in central hypovolemia

   

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  Is This Patient Dead, Vegetative, or Severely Neurologically Impaired?

  (Jama Vol. 291 No. 7, February 18, 2004)

  Physical Examination Maneuvers

  In addition to the GCS, various brainstem reflexes are used in the physical examination of comatose patients.10, 12 The pupillary reflex involves cranial nerves II and III. Shining a penlight into one eye and then the other tests the patient’s pupillary light response; the examiner observes the direct and consensual response (constriction of the opposite eye). The corneal reflex involves cranial nerves V and VII. Touching the cornea with a piece of cotton or tissue should cause both eyes to blink. The gag and cough reflexes test cranial nerves IX and X. To elicit a gag, apply a tongue depressor to the posterior pharynx. The soft palate should rise symmetrically. In patients who are intubated, assess the cough (or carinal) reflex by applying deep suction through the endotracheal tube to the carina. The suction will produce a gasp followed by several rapid coughs. Vestibular signs are also commonly examined in the comatose patient. The oculocephalic (or “Doll’s eye”) reflex involves observing the patient’s eyes during passive rotation of the skull. In a comatose patient with intact midbrain and vestibular reflexes, the eyes will move in a direction opposite to that in which the head is moved. If this reflex is lost, the globes will remain fixed within the head and the eyes will continue to stare in whatever direction the head is pointed. This reflex should not be tested in cases of suspected cervical trauma. Cold water caloric testing (oculovestibular reflex) also tests the vestibular and oculomotor systems. To perform the test, first examine the tympanic membrane to ensure there is no perforation or impacted cerumen. With the head 30° higher than the horizontal, irrigate up to 120 mL of ice cold water into the auditory canal. In the unconscious patient with intact brainstem function, there will be slow tonic deviation of eyes towards the irrigated ear. It is also important to note the presence of seizures or myoclonus when examining the comatose patient, for some clinicians believe they may be useful in prognosis of comatose survivors of cardiac arrest. Seizures may be generalized or focal. Myoclonus refers to isolated sudden muscular contractions and may be either focal or generalized contractions of axial and limb musculature. In patients with seizures, the physical examination should be repeated after the postictal period. Finally, mechanically ventilated patients are frequently sedated and/or paralyzed. Accordingly, when performing a detailed neurological examination it is crucial that these medications be at least temporarily discontinued.

  Summary

  Summary measures for clinical variables that were assessed in at least 3 studies are presented in Table 5. Five pooled variables were found to have a 95% CI lying entirely above 1. The clinical signs at 24 hours with the highest LRs were absent corneal reflexes (LR, 12.9; 95% CI, 2.0-68.7), absent pupillary reflexes (LR, 10.2; 95% CI, 1.8-48.6), absent motor response (LR, 4.9; 95% CI, 1.6-13.0), and absent withdrawal to pain (LR, 4.7; 95% CI, 2.2-9.8). At 72 hours after cardiac arrest, absent motor response was found to accurately predict death or poor neurological outcome (LR, 9.2; 95% CI, 2.1-49.4). No clinical findings were found to accurately predict good neurological outcome (ie, no useful negative LRs).

   

  Rescuers hyperventilate patients and this leads to poorer outcomes (CCM Volume 32(9) September 2004)

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  Thrombolytics

  Thrombolysis for MI. Gave all patients without pulse TNKase. 36 ABI in ROSC (Resus 2004;61:309-313)

  Review (Emerg Med J 2006;23:747)

   

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  MIs need cath after cardiac arrest

  8 P. Garot, T. Lefevre and H. Eltchaninoff et al., Six-month outcome of emergency percutaneous coronary intervention in resuscitated patients after cardiac arrest complicating ST-elevation myocardial infarction, Circulation 115 (2007), pp. 1354–1362. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (0) 9 V. Gorjup, P. Radsel, S.T. Kocjancic, D. Erzen and M. Noc, Acute ST-elevation myocardial infarction after successful cardiopulmonary resuscitation, Resuscitation 72 (2007), pp. 379–385. SummaryPlus | Full Text + Links | PDF (109 K) | View Record in Scopus | Cited By in Scopus (2)

   

   

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  Mechanical Devices

  impedance threshold device-

  An impedence threshold device (ITD) is a device added into the respiratory circuit (between the endotracheal tube or mask and bag-valve) to impede the influx of respiratory gases into the chest during the chest wall recoil phase of cardiopulmonary resuscitation (CPR).

   

  Adverse effects of positive pressure ventilation include an increase in intrathoracic pressure, and the inability to develop a negative intrathoracic pressure during the release phase of chest compression. Positive pressure ventilation inhibits venous return to the thorax and right heart and thus results in decreased coronary and cerebral pressures. Another aspect of hyperventilation and increased intrathoracic pressure is its adverse effect on intracranial pressure and cerebral perfusion pressure [22,23]. These adverse effects are compounded by the fact that ventilation rates by physicians as well as paramedic rescuers are often much faster than the rate recommended by the guidelines, and unfortunately are still significantly above those recommended even after extensive retraining [20,21]. During cardiac arrest, faster ventilation rates increase the mean intra thoracic pressure and further impede forward blood flow.

   

  predictors of outcome in cardiopulmonary resuscitation: systematic review (Emerg. Med. J. 2005;22;700-705)

   

  We have no idea what people really die of in the ED (Emerg. Med. J. 2005;22;718-721)

   

  Chest Compression in first 5 minutes of code with and without ventilations; no change in outcomes. NEJM 2000;342(21):1546

   

  Chest compression efficacy not reflected by pulse, ETCO2 is the way to tell

   

  Open Chest massage is better ([Benson DM, O’Neil BO, Kakish E, Erpelding J, et al: Open chest CPR improves survival and neurologic outcome following cardiac arrest. RESUSCITATION 2005; 64: 209-217.])

   

   

  review of lytics in arrest (Minerva anestesiol 2005;71:291)

   

  Survival for in-hopsital arrest in adults is ~18% (JAMA 2006;295 50-57)

   

   

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  Haemodynamics of Arrest

  Curr Opin Crit Care 2006;12:198

   

  CPP=Ao-RA

  Coronary perfusion pressure is the most important determinant for successful defib

  takes up 12 beats to build up aortic pressure

   

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  Time sensitive Model of Arrest

  JAMA 2002;288(23):3035

  3 phase model

  Electrical Phase 0-4 minutes

  easy to shock out

  Circulatory Phase 4-10 minutes

  need compressions before shock

  Metabolic Phase >10 minutes

  hypothermia attenuates injury

   

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  Predicting Outcome

  (Neurology 2006;67:203)

  

   

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  Percussion Pacing

  percussion pacing (Br J of Anaes 2007;98(4):429) at left sternal border 70-80 times per minute

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  Suspended animation

  suspended animation article (Crit Care Med 1996;24(2S):24S)

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  History of Resuscitation

  history of resuscitation (Crit Care Med 1996;24(Supp):S3)

   

  Compression rate is obviously suboptimal in the hospital (Circulation 2005;111(4):428)

   

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  End Tidal CO2

  Can cardiac sonography and capnography be used independently and in combination to predict resuscitation outcomes?

  OBJECTIVE: To measure the ability of cardiac sonography and capnography to predict survival of cardiac arrest patients in the emergency department (ED). METHODS: Nonconsecutive cardiac arrest patients prospectively underwent either cardiac ultrasonography alone or in conjunction with capnography during cardiopulmonary resuscitation at two community hospital EDs with emergency medicine residency programs. Cardiac ultrasonography was carried out using the subxiphoid view during pauses for central pulse evaluation and end-tidal carbon dioxide (ETCO(2)) levels were monitored by a mainstream capnograph. A post-resuscitation data collection form was completed by each of the participating clinicians in order to assess their impressions of the facility of performance and benefit of cardiac sonography during nontraumatic cardiac resuscitation. RESULTS: One hundred two patients were enrolled over a 12-month period. All patients underwent cardiac sonographic evaluation, ranging from one to five scans, during the cardiac resuscitation. Fifty-three patients also had capnography measurements recorded. The presence of sonographically identified cardiac activity at any point during the resuscitation was associated with survival to hospital admission, 11/41 or 27%, in contrast to those without cardiac activity, 2/61 or 3% (p < 0.001). Higher median ETCO(2) levels, 35 torr, were associated with improved chances of survival than the median ETCO(2) levels for nonsurvivors, 13.7 torr (p < 0.01). The multivariate logistic regression model, which evaluated the combination of cardiac ultrasonography and capnography, was able to correctly classify 92.4% of the subjects; however, of the two diagnostic tests, only capnography was a significant predictor of survival. The stepwise logistic regression model, summarized by the area under the receiver operator curve of 0.9, furthermore demonstrated that capnography is an outstanding predictor of survival. CONCLUSIONS: Both the sonographic detection of cardiac activity and ETCO(2) levels higher than 16 torr were significantly associated with survival from ED resuscitation; however, logistic regression analysis demonstrated that prediction of survival using capnography was not enhanced by the addition of cardiac sonography.(Acad Emerg Med. 2001 Jun;8(6):610-5.)

   

  Late values (20 minutes from onset of ACLS) of <10 = no survival (NEJM 1997;337:301)

   

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  Hands Off?

  Hands-On Defibrillation

  Brief interruptions in chest compressions reduce the efficacy of resuscitation from cardiac arrest. Interruptions of this type are inevitable during hands-off periods for shock delivery to treat ventricular tachyarrhythmias. A recent trial revealed that while compressing the chests of patients receiving external biphasic shocks, in no cases were shocks perceptible to the rescuer. It should be noted that in addition to using a biphasic defibrillator, the rescuers wore gloves and the shocks were delivered through self-adhesive pre-gelled pad electrodes.

  The authors also measured the average leakage of current flow through the rescuer’s body for each phase of the waveform and found it to be well below the allowable standards used for household and business equipment and also below the usual threshold for human perception.

  The accompanying editorial suggests that the AHA should consider a modification of current when gloves, self-adhesive pad electrodes, and biphasic defibrillation is available.

  We are grateful to Dr. Amal Mattu for developing this clinical pearl

  References: (1) Lloyd MS, et al. Hands-On Defibrillation: An Analysis of Electrical Current Flow Through Rescuers in Direct Contact With Patients During Biphasic External DefibrillationCirculation 2008;117:2510-2514. (2) Kerber, RE. “I’m Clear, You’re Clear, Everybody’s Clear”: A Tradition No Longer Necessary for Defibrillation? Circulation 2008;117:2435-2436.

   

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  Progression to shockable rhythm = better outcome

  (Resuscitation Volume 80, Issue 1, January 2009, Pages 24-29)

  Progressing from initial non-shockable rhythms to a shockable rhythm is associated with improved outcome after out-of-hospital cardiac arrest

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  Vaso + Steroids Study

  pts received 20 IU of vaso in addition to epi Q 3 minutes for 5 cycles, on the 5th cycle, they received solumedrol 40 mg and then hydrocortisone 100 mg tid for 7 days and then taper. Stat. sig for ROSC and mortality (Arch Intern Med 2009;169(1):15)

   

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  IV Drugs

  IV Drugs seem to have no outcome difference in prehospital setting

  JAMA. 2009;302(20):2222-2229.

  Conclusion  Compared with patients who received ACLS withoutintravenous drug administration following out-of-hospital cardiacarrest, patients with intravenous access and drug administrationhad higher rates of short-term survival with no statisticallysignificant improvement in survival to hospital discharge, qualityof CPR, or long-term survival.

  Study from down under shows no stat sig benefit to Epi, but it would probably have had the exact opposite results if a bunch of services did not fall prey to ridiculous equipoise bias and refused to enroll patients (Resuscitation. 2011 Sep;82(9):1138-43. Epub 2011 Jul 2. Effect of adrenaline on survival in out-of-hospital cardiac arrest: A randomised double-blind placebo-controlled trial. Jacobs IG, Finn JC, Jelinek GA, Oxer HF, Thompson PL.)

  Japanese trial showed no survival benefit from hospital or neurologic improvement (JAMA.
  
  
  2012;307(11):1161-1168)

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  Atropine can give Extended Pupillary Dilation

  3mg of atropine gave 12-24 hours of pupil dilation when given IV during code (Resuscitation 82 (2011) 232) in a case report

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  Nitroprusside

  CCM 2011; :1269

  may open the microcirculation

  .

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  Airway Management

  yet another study showing 48 sec for ETT and 13 sec or less for SGA (Resuscitation Volume 82, Issue 8, August 2011, Pages 1060-1063) and another showing the benefits (Critical Care 2011, 15:R236)

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Metronome Use

 

4 R.A. Berg, A.B. Sanders and M. Milander, et al. Efficacy of audio-prompted rate guidance in improving resuscitator performance of cardiopulmonary resuscitation on children. Acad Emerg Med,  1 1 (1994), pp. 35–40

5 W.C. Chiang, W.J. Chen and S.Y. Chen, et al. Better adherence to the guidelines during cardiopulmonary resuscitation through the provision of audio-prompts. Resuscitation,  64 3 (2005), pp. 297–301

6 D. Fletcher, R. Galloway and D. Chamberlain, et al. Basics in advanced life support: a role for download audit and metronomes. Resuscitation,  78 2 (2008), pp. 127–134

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Double Down for Refractory VT/VF

from clic-em

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Automated External Compression Devices

neurologically intact survival increase with auto-pulse (Crit Care 2012;16:R144)

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Advanced Airways – Not helpful

Association of Prehospital Advanced Airway Management With Neurologic Outcome and Survival in Patients With Out-of-Hospital Cardiac Arrest JAMA 2013;309(3):257-66

If one person is doing airway, shocks, IV, etc. then any advanced airway led to worse outcome

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Peri-Compressions Realization of ROSC

From Dan Davis (Resuscitation 2013;84:25)

Pre-pause HR >=40 and ETCO2 >20

Pause ETCO2 stays >20 No precip drop in ETCO2 (>=10 in 10 sec)

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Lidocaine Resurgence

“Prophylactic lidocaine for post resuscitation care of patients with out-of-hospital ventricular fibrillation cardiac arrest”
www.ncbi.nlm.nih.gov/pubmed/23743237‎

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Vasopressin Epi And Steroids

Vasopressin, Steroids, and Epinephrine and Neurologically Favorable Survival After In-Hospital Cardiac ArrestA Randomized Clinical Trial (JAMA. 2013;310(3):270-279)

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Meta-Analysis of Mechanical CPR Devices

Shows benefit for both LUCAS and Band-Device (Crit Care Med 2013;41:1782)

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Hemodynamic Goal CPR

In swine, goal of CPP of 20 and SBP>100 showed increased benefit over ACLS (Resuscitation 84 (2013) 696– 701)

And another pig study (Crit Care Med 2013;41:2698)

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ETCO2 is not Prognostic

Resuscitation. 2013 Nov;84(11):1470-9

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Linc Trial

No benefit or harm from mechanical CPR devices (JAMA. 2014;311(1):53-61. doi:10.1001/jama.2013.282538)

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More about avoiding Hands-On Defib

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