Guidelines for cardiopulmonary resuscitation: Basic and advanced cardiovascular life support-II

Thursday, July 9, 2009

by Philip J Podrid, MD

This is a continuation of the discussion of the guidelines for cardiopulmonary resuscitation. (See "Guidelines for cardiopulmonary resuscitation: Basic and advanced cardiovascular life support-I").

ADVANCED CARDIAC LIFE SUPPORT – Advanced cardiovascular life support (ACLS) includes knowledge and skills necessary to provide appropriate early treatment for cardiopulmonary arrest and includes:

• Basic life support, as discussed above

• Use of advanced equipment and special techniques for establishing effective ventilation and circulation, including defibrillation; oxygenation, ventilation, and airway control; and devices to assist circulation

• ECG monitoring, 12-lead ECG interpretation, and arrhythmia recognition

• Establishment and maintenance of intravenous access

• Therapies for the treatment of patients with cardiac and respiratory arrest, including postarrest stabilization; this includes adequate knowledge about the antiarrhythmic agents and drugs for optimizing cardiac output and blood pressure

ILCOR Universal/International ACLS algorithm – The algorithm developed by the International Liaison Committee on Resuscitation (ILCOR) unifies and simplifies the essential information of adult ACLS (show algorithm 1) [1]. The steps include:

Basic life support algorithm – The basic life support algorithm, as discussed above includes (show algorithm 2):

• Check responsiveness

• Activate EMS response system

• Open the airway

• Check breathing

• Give two effective breaths

• Assess circulation

• Compress chest, if no signs of circulation detected

Attach defibrillator/monitor – Once the basic life support algorithm is activated, responders should attach a defibrillator and/or monitor to assess the rhythm (show algorithm 3).

• If the monitor displays VT or VF or the AED signal and voice prompts are for these arrhythmias, the rescuer should attempt defibrillation up to three times, as necessary. The current recommendation is up to three shocks using energies of 200, 200 to 300, and 360 joules when monophasic waveforms are delivered [2] or an equivalent amount of energy when machines delivering biphasic waveforms are utilized, ie, nonescalating 150 to 170 joules (class IIa recommendation) [3]. If available, a biphasic waveform defibrillator is preferable since the success rate for defibrillation is higher than with monophasic waveforms [4,5].

After three shocks, CPR should be resumed for at least one minute, allowing for a brief period of reoxygenation of blood and circulation of blood to the heart and brain; after this period, the rhythm should be reassessed and repeat shock delivered if appropriate. If VT/VF are refractory to defibrillation, additional interventions are necessary (see below).

• If an arrhythmia other than VT or VF, primarily asystole or pulseless electrical activity (PEA), are seen on the monitor or the AED signals "no shock therapy indicated", the responder should immediately check the pulse to determine if the nonshockable rhythm is producing a spontaneous circulation. If no pulse is detected, CPR is initiated and continued for approximately three minutes; the rhythm is then reassessed for the presence of VT or VF or spontaneous return of an organized rhythm in a beating heart. If an organized rhythm is not present, additional interventions are necessary.

Additional interventions – A number of additional interventions are often needed during CPR:

• Placement and confirmation of a tracheal tube; tube placement is primarily confirmed with physical examination and secondarily with a device that measures end-tidal CO2 or end-diastolic diameter (class IIa recommendation). Oxygenation and ventilation are confirmed with end-tidal CO2 oxygen saturation monitors.

The tracheal tube should be secured with special holders (class IIb indication) or tie and tape measures.

• Gaining intravenous access and starting an intravenous infusion

• Giving appropriate medications, including vasopressin, epinephrine, buffers, or antiarrhythmic drugs [6-13]. Vasopressin has hemodynamic effects that are similar to epinephrine, and some studies have suggested that it produces better outcomes [1,10-13]. However, a triple-blind randomized trial of 200 patients with an in-hospital cardiac arrest found no difference in one hour survival, survival to hospital discharge, and neurologic examination and performance between vasopressin and epinephrine therapy [14].

• Pacing, if indicated

• Search for and correction of reversible causes

Ventricular fibrillation/pulseless ventricular tachycardia – The algorithm for VF or pulseless VT considered the specifics of the ACLS recommendations for these arrhythmias. Since the ILCOR Universal algorithm assumes that all adult cardiac arrests are due to VF or pulseless VT, the initial part of the algorithm, including basic life support, defibrillation, and therapy of persistent or recurrent VT/VF, is the same and places a strong emphasis on the immediate recognition and treatment of these arrhythmias (show algorithm 4) [1].

Drug therapy – The use of drugs, including sympathomimetic agents, antiarrhythmic drugs, and buffers has been relegated to a secondary role since there is little evidence that these agents are of benefit; there use is considered indeterminate or class IIb [1,15,16]. (See "Controversies in cardiopulmonary resuscitation" and see "Acute therapy and outcome of sudden cardiac death").

• Epinephrine is administered as 1 mg intravenously every three to five minutes; a higher dose (0.2 mg/kg) is acceptable, but not recommended, if the lower dose is ineffective [17,18]. An acceptable alternative is vasopressin, which is recommended only for VT or VF; there is no evidence to support its use in asystole or PEA [1,13,19]. A single intravenous dose of 40 U is given once (since the half life is 10 to 20 minutes compared to 3 to 5 minutes with epinephrine). The potential value of vasopressin was illustrated in a controlled trial of patients with out-of-hospital VF who received either vasopressin or epinephrine; those treated with vasopressin had higher rates of survival to hospital admission (70 versus 35 percent, p = 0.06) and survival at 24 hours (60 versus 20 percent, p = 0.02) [13].

A repeat dose does not appear to be of value and it is uncertain what the best approach is if there is no response. An acceptable approach if there is no response after 5 to 10 minutes is the administration of epinephrine (1 mg every three to five five minutes).

• The use of one of the following antiarrhythmic agents is acceptable, although there is only fair evidence supporting their benefit for shock-refractory VT/VF [15,20,21].

- Amiodarone is administered as 300 mg intravenous push. If VF or pulseless VT recurs, the administration of a second 150 mg dose can be considered. The maximum cumulative dose is 2.2 grams over 24 hours [22-26].

- Lidocaine is administered at a dose of 1 to 1.5 mg/kg as an intravenous push. This dose can be repeated every 3 to 5 minutes up a maximum dose of 3 mg/kg [27-30].

- Procainamide, administered at a dose of 30 mg/min intravenously up to a maximum dose of 17 mg/kg is acceptable but not recommended since the prolonged time for administration is unsuitable for a cardiac arrest [29].

- Magnesium sulfate, 1 to 2 grams intravenously is recommended for the treatment of polymorphic VT (torsade de pointes) and suspected hypomagnesemic states [31,32].

• Sodium bicarbonate, 1 meq/kg intravenously, is indicated for severe conditions known to provoke sudden death, such as hyperkalemia, preexisting metabolic acidosis, or certain drug overdoses [8,9]. (See "Pulseless electrical activity" below).

Defibrillation, using energy levels discussed above, should be attempted after each medication is administered or after each minute of CPR.

Pulseless electrical activity – Pulseless electrical activity (previously called electromechanical dissociation) is defined by the presence of some type of electrical activity other than VT or VF in the absence of a detectable pulse. PEA is often often associated with specific clinical states that can be reversed when identified early and effectively treated (show algorithm 5).

Survival is poor when electrical activity is wide and slow; these rhythms often represent the last electrical activity of a dying myocardium or may be associated with hyperkalemia, hypothermia, hypoxia, preexisting acidosis, or a variety of drug overdoses (eg, tricyclic antidepressants, beta blockers, calcium channel blockers, digoxin) (show table 1A-1B). (See "Treatment of hyperkalemia" and see "Basic approach to arrhythmias due to digitalis toxicity").

Electrical activity that is narrow complex and wide indicates a relatively normal heart that is responding as it should; causes include hypovolemia, infection, pulmonary embolism, or cardiac tamponade (show table 1A-1B). (See "Massive pulmonary embolism" and see "Pericardial compressive syndromes").

Sodium bicarbonate – Sodium bicarbonate (1 meq/kg) has a role in the treatment of PEA when due to specific causes:

• It has a class I indication for patient who has known preexisting hyperkalemia.

• The use of bicarbonate is acceptable (class IIa indication) when a known, preexisting bicarbonate-responsive acidosis is present; for treatment of tricyclic antidepressant overdose; and to alkalinize the urine in aspirin or other drug overdoses. It is not routinely used for the acute lactic acidosis associated with CPR, but may be given if the initial interventions (defibrillation, ventilation, cardiac compression, and vasopressor therapy) have been ineffective. (See "Bicarbonate therapy in lactic acidosis").

• The use of bicarbonate is acceptable in intubated and ventilated patients with a long arrest interval or upon return of circulation after a long arrest interval; however, there is only fair evidence for its efficacy in these settings.

• The use of bicarbonate is harmful and not indicated for respiratory (hypercapnic) acidosis.

Epinephrine – The efficacy of epinephrine (1 mg intravenous push every three to five minutes) for PEA is uncertain (class indeterminate). If this dose of epinephrine fails, higher doses (up to 0.2 mg/kg) may be used, but are not recommended. There is no evidence to support the routine use of vasopressin for PEA.

Atropine – The administration of atropine (1 mg every three to five minutes) is possibly helpful for PEA when the rate is slow, ie, absolute bradycardia with a rate <60 beats/min or a relative bradycardia (rate less than expected relative to the underlying condition).

Asystole – Patients with asystole on a cardiac monitor have a dismal rate of survival, as low as 1 or 2 percent; however, true asystole should be confirmed by checking lead and cable connections, making certain that the monitor is on and that the gain in turned up, and checking another lead for asystole (show algorithm 6).

During CPR, brief periods of an organized QRS complex may appear that usually represents an "agonal" rhythm. CPR should not be initiated if the patient has any objective evidence of a do not resuscitate status (DNR) or has any indication that resuscitation attempts are not indicated, eg, signs of death.

Drugs – The indications for the use of sodium bicarbonate, epinephrine, vasopressin, and atropine are the same as discussed above under PEA.

Transcutaneous pacing – Transcutaneous pacing may be effective if performed early and when combined with drug therapy. However, there is no evidence to support the routine use of pacing. (See "Temporary cardiac pacing").

Persistent asystole – When asystole persists, the decision about ceasing further CPR efforts must be made; consideration is given to the quality and duration of CPR.

• Was tracheal intubation performed?

• Was effective ventilation achieved?

• Was VF, if present, adequately shocked?

• Was intravenous access obtained?

• Were intravenous epinephrine and atropine given?

• Was a reversible cause ruled out or corrected, if identified?

• Was asystole continuously documented for more than 5 to 10 minutes after all of the above were accomplished?

Bradycardia – Bradycardia may be the cause of cardiac arrest but it is more often associated with signs and symptoms of a low cardiac output (show algorithm 7). These include chest pain, shortness of breath, decreased level of consciousness, low blood pressure, shock, pulmonary congestion, or heart failure.

Atropine is effective for treating symptomatic sinus bradycardia (class I recommendation); it may be beneficial in the presence of AV block at the nodal level (class IIa recommendation) or ventricular asystole, but should not be used when infranodal (Mobitz type II block) is suspected.

If the patient is symptomatic, atropine is given as the initial drug therapy (0.5 to 1 mg every three to five minutes up to a total of 0.03 to 0.04 mg/kg); however, transcutaneous pacing should not be delayed while awaiting intravenous access or for atropine to take effect (class I indication). Patients who have had a heart transplant and have a denervated heart will not respond to atropine; as a result, pacing and/or catecholamine infusion should be used initially.

A transvenous pacemaker should be inserted if second or third degree heart block is present or bradycardia persists after atropine and/or catecholamine infusion; transcutaneous pacing may be used prior to the insertion of a transvenous pacemaker (class I indication). Antiarrhythmic drugs, particularly lidocaine, should not be used in patients with third degree heart block. (See "Third degree (complete) atrioventricular block").


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