Therapies of uncertain benefit in basic and advanced cardiac life support

INTRODUCTION — The modern approach to advanced cardiac life support (ACLS) reflects an increasingly rigorous approach to resuscitation science [1-3]. Nevertheless, while a few ACLS treatments are well supported by evidence, numerous controversies and uncertainties in the management of sudden cardiac arrest (SCA) persist.

Selected controversies related to the techniques and medications used in the performance of basic and advanced life support are discussed here. The performance of basic and advanced life support and the evidence supporting ACLS are reviewed separately. (See "Advanced cardiac life support (ACLS) in adults" and "Adult basic life support (BLS) for health care providers" and "Supportive data for advanced cardiac life support in adults with sudden cardiac arrest".)

MEDICATIONS USED DURING CARDIOPULMONARY RESUSCITATION — Medications commonly used in the management of cardiac arrest and life-threatening arrhythmias are reviewed separately; individual and combinations of medications of uncertain benefit or not commonly used but under investigation are discussed here. (See "Advanced cardiac life support (ACLS) in adults", section on 'Medications used during CPR'.)

Epinephrine: Dosing and long-term outcomes — We agree with the ACLS recommendation to administer standard-dose intravenous (IV)/intraosseous (IO) epinephrine, 1 mg every three to five minutes during cardiopulmonary resuscitation (CPR). There is no role for high-dose epinephrine.

Epinephrine is a potent vasoconstrictor that may improve coronary and cerebral perfusion and oxygen delivery, thereby promoting return of spontaneous circulation (ROSC) and minimizing hypoxic-ischemic brain injury in patients with sudden cardiac arrest (SCA).

Improved ROSC and survival to hospital admission after epinephrine administration must be followed by delivery of excellent post-arrest care to maximize the likelihood that these short-term benefits translate to long-term favorable recovery. (See "Initial assessment and management of the adult post-cardiac arrest patient" and "Intensive care unit management of the intubated post-cardiac arrest adult patient".)

The 1 mg dose of epinephrine recommended in ACLS is extrapolated from early animal models, with little evidence to support its superiority to other dosing regimens:

●A randomized controlled trial including 650 adults who suffered in- or out-of-hospital cardiac arrest compared standard-dose epinephrine (1 mg) with high-dose epinephrine (7 mg), each administered up to five times at five-minute intervals during CPR [4]. There was no difference in ROSC or survival to hospital discharge between arms, with worse outcomes in select subgroups of patients receiving high-dose epinephrine (eg, those with >10 minutes from collapse to medication administration).

●A randomized controlled trial including 816 adults resuscitated from out-of-hospital cardiac arrest compared standard-dose epinephrine (1 mg), high-dose epinephrine (15 mg), and high-dose norepinephrine (11 mg) [5]. High-dose epinephrine improved prehospital ROSC and survival to hospital admission compared with standard-dose epinephrine (13 versus 8 percent and 18 versus 10 percent, respectively). There was no difference in survival to hospital discharge, with a non-significant trend towards worse functional outcomes at hospital discharge in the high-dose epinephrine group.

Beyond the uncertainty about the optimal dose of epinephrine, it remains unclear whether any epinephrine administration improves long-term patient outcomes following SCA:

●The randomized controlled PARAMEDIC2 trial of 8014 adult patients with out-of-hospital cardiac arrest compared up to 10 doses of parenteral epinephrine versus placebo given every three to five minutes during standard ACLS [6]. Compared with placebo, epinephrine resulted in significantly better survival to hospital admission (24 versus 8 percent) and 30-day survival (3.2 versus 2.4 percent, p = 0.02) but did not improve functionally favorable survival at 30 days.

●A cost-effectiveness analysis of PARAMEDIC2 found improved survival to hospital admission in the epinephrine arm also increased the number of organs donated after in-hospital death and found epinephrine administration to be cost effective after accounting for this societal benefit [7].

●A systematic review and meta-analysis of five randomized controlled trials of epinephrine versus placebo during cardiac arrest found epinephrine to be associated with improved ROSC (odds ratio [OR]  3.1, 95% CI  2.16-4.45) and survival to hospital admission (OR 2.52, 95% CI  1.63-3.88) but not survival to discharge or neurological outcomes [8].

Antidysrhythmics — We agree with ACLS recommendations that amiodarone or lidocaine may be reasonable treatments for shock-refractory ventricular tachycardia (VT)/ventricular fibrillation (VF), especially in patients with witnessed arrest, and may be administered to improve the chance of successful defibrillation [9]. Nevertheless, while study results suggest higher survival to hospital admission, evidence of improved functional outcomes among patients receiving these medications is lacking:

●A randomized trial compared amiodarone 300 mg IV versus placebo in 504 patients with shock-refractory VT/VF in Seattle and King County, Washington (United States) [10]. Survival to hospital admission was better in the amiodarone group than the placebo group (44 versus 34 percent). Bradycardia and hypotension were also more common in the amiodarone group, although it was unclear whether this was due primarily to the study drug or choice of diluent.

●A randomized trial compared amiodarone 5 mg/kg versus lidocaine 1.5mg/kg in 347 patients with shock-refractory VT/VF in out-of-hospital cardiac arrest [11]. Survival to hospital admission was better for patients receiving amiodarone compared with lidocaine (22.8 versus 12.0 percent).

●In a randomized trial of 3026 patients with shock-refractory out-of-hospital VT/VF arrest, survival to hospital admission was better in the groups treated with amiodarone or lidocaine compared with the placebo group (45.7 versus 47.0 versus 36.7 percent) [12]. However, survival to hospital discharge (primary outcome) and functionally favorable survival at discharge did not differ across treatment groups. Of the 1934 subjects with witnessed collapse (for whom time to drug administration was likely shorter), survival was better with either amiodarone or lidocaine compared with placebo (27.7 versus 27.8 versus 22.7 percent).

Vasopressin, glucocorticoid, and epinephrine — Studies of combinations of these medications or of glucocorticoid alone for the treatment of cardiac arrest have produced unclear results. Further study is needed before it is known whether such combination therapies have a justified role in clinical practice:

●A randomized trial of 268 consecutive cardiac arrest patients reported improved survival to hospital discharge with good neurologic status in patients treated initially with the combination of vasopressin, methylprednisolone, and epinephrine (VME) compared with those treated with placebo plus epinephrine, but only 25 patients achieved the primary outcome (18 out of 130 [13.9 percent] in the VME group versus 7 out of 138 [5.1 percent] in the placebo group (OR 3.28; 95 percent CI 1.17-9.20) [13].

●A trial of 501 patients randomly assigned to treatment with vasopressin and methylprednisolone or placebo reported an increased rate of ROSC in the intervention group but no difference in 30-day, six-month, or one-year survival rates or functionally favorable recovery [14,15]. A post hoc analysis found no difference in early post-arrest hemodynamics, vasopressor dependence, gas exchange, or lactate level between groups [16]. These patients were all inpatient cardiac arrests.

●A meta-analysis of 11 studies involving 2273 cardiac arrest patients found that treatment with glucocorticoid was not associated with improved neurologic outcomes (OR 1.13, 95% CI 0.81-1.58) or overall survival to hospital discharge (OR 1.29, 95% CI 0.74-2.26) [17].

Other medications

●Atropine – Atropine is a potent anticholinergic that reverses cholinergic-mediated bradycardia and conduction delays and is indicated for symptomatic bradycardia. We agree with ACLS recommendations that there is no role for atropine in the management of cardiac arrest. Intra-arrest atropine administration has not been evaluated in randomized trials. In 2010, a paucity of evidence supporting efficacy led the American Heart Association (AHA) to remove atropine from algorithms for resuscitation of pulseless electrical activity and asystole [18]. (See "Advanced cardiac life support (ACLS) in adults", section on 'Bradycardia'.)

●Sodium bicarbonate – Sodium bicarbonate expands circulating blood volume and can correct acidosis that develops during prolonged cardiac arrest. We agree with ACLS recommendations that sodium bicarbonate should not be administered routinely during cardiac arrest. At least four randomized trials and numerous observational studies have evaluated the effect of intra-arrest sodium bicarbonate administration on patient outcomes with conflicting results [19].

Sodium bicarbonate may benefit patients who sustain SCA due to hyperkalemia, acidosis, or overdose from medications such as tricyclic antidepressants, for which sodium bicarbonate is an indicated therapy. (See "Tricyclic antidepressant poisoning", section on 'Sodium bicarbonate for cardiac toxicity'.)

●Calcium – Calcium chloride is a vasopressor and inotrope. Calcium chloride should not be routinely administered during cardiac arrest but may be indicated in some special circumstances (eg, hyperkalemia, calcium channel blocker poisoning, hypocalcemia). (See "Treatment and prevention of hyperkalemia in adults" and "Calcium channel blocker poisoning".)

A randomized trial of calcium chloride versus placebo during resuscitation of out-of-hospital cardiac arrest patients was stopped early because of a trend towards reduced rates of ROSC in patients receiving calcium [20].

●Beta blocker – Sympathetic blockade using beta blockers has been suggested as a treatment for refractory VT/VF arrest when primary anti-arrhythmics and defibrillation are unsuccessful. Although some studies show benefit, more definitive research is needed to determine if rapid-acting agents, such as esmolol or propofol, are effective [21].

Fibrinolysis — We agree with the ACLS recommendation against routine use of fibrinolytics for patients in cardiac arrest. Thrombolytic therapy may have a role when pulmonary embolism is the presumed or likely cause of SCA, and it is used in some cases for management of acute coronary syndrome or stroke. These indications are reviewed separately. (See "Approach to thrombolytic (fibrinolytic) therapy in acute pulmonary embolism: Patient selection and administration" and "Acute ST-elevation myocardial infarction: The use of fibrinolytic therapy" and "Approach to reperfusion therapy for acute ischemic stroke".)

Acute coronary syndrome and pulmonary embolism account for an estimated 50 to 70 percent of cases of SCA that go on to autopsy after failed resuscitation [22-24]. Although fibrinolysis would seem to be a promising treatment for refractory SCA, studies have failed to demonstrate benefit [25]:

●A large, prospective multicenter trial (Thrombolysis in Cardiac Arrest, or TROICA, trial) was stopped early when preliminary analyses of 1050 patients failed to detect a difference between those receiving tenecteplase and those receiving placebo in the primary endpoint of 30-day survival [26]. There was also no significant difference in the secondary endpoints of hospital admission, ROSC, 24-hour survival, survival to hospital discharge, or neurologic outcome.

●Another randomized trial found no difference in survival to hospital discharge among patients with SCA and pulseless electrical activity treated with tissue plasminogen activator (t-PA) in addition to standard resuscitation (n = 117) compared with patients treated with standard resuscitation alone (n = 116) [27]. Patient characteristics in the two groups were similar.

●A prospective trial of 90 out-of-hospital SCA patients demonstrated a significant improvement in ROSC (68 versus 44 percent) and survival to intensive care unit (ICU) admission (48 versus 30 percent) in patients treated with recombinant t-PA compared with controls who received standard treatment, but no significant differences were noted in 24-hour survival or survival to hospital discharge [24].

Other studies have failed to find statistically significant benefit from fibrinolytic therapy in SCA [24,28,29].

Neuroprotective medications — Mechanisms of hypoxic-ischemic brain injury are complex and develop rapidly during cardiac arrest. There is interest in developing pharmacologic therapies that slow or prevent brain injury when administered during or shortly after cardiac arrest. Randomized trials have evaluated barbiturates, glucocorticoids, calcium channel blockers, benzodiazepines, and other drug classes [30-35]. As yet, no pharmacologic interventions providing effective neuroprotection have been identified.

Vascular and intraosseous access for medication administration — High-quality chest compressions and early defibrillation are cornerstones of effective CPR. Adjunctive medications including epinephrine, atropine, and antidysrhythmic have theoretical mechanistic benefits but a paucity of data, as reviewed above. It is unclear whether potential benefits outweigh adverse drug effects or the potential for establishing vascular access and medication administration to distract from high-quality CPR.

Routinely obtaining vascular access and intravascular medication administration during ACLS is of dubious benefit at the population level. The pathophysiology of SCA is heterogeneous, and it is likely that vascular access is beneficial in some patients but not others. As an example, patients with pulseless electrical activity due to hypovolemic or hemorrhagic shock are likely to benefit from intravascular volume expansion and transfusion, respectively. If pursued, establishing vascular access and medication administration must not distract from high-quality chest compressions and early defibrillation of shockable rhythms:

●A randomized trial of 851 adults treated by emergency medical service providers after out-of-hospital cardiac arrest compared ACLS with IV drug administration to ACLS without IV drug administration [36]. Medication administration improved rates of ROSC (40 versus 25 percent) and survival to ICU admission (30 versus 20 percent), but there was no difference in survival to hospital discharge (10.5 versus 9.2 percent), functionally favorable survival, or one-year survival.

Multiple observational studies and several post hoc analyses of randomized trials have compared IV to interosseous (IO) vascular access during CPR with mixed results:

●In a secondary analysis of the Resuscitation Outcomes Consortium Continuous Chest Compression Trial including 3068 patients with attempted IO access and 16,663 patients with attempted IV access, IO access was independently associated with lower rates of ROSC (OR 0.80; 95% CI 0.71-0.89) but no difference in survival to hospital discharge or functionally favorable survival [37].

●In a secondary analysis of the Resuscitation Outcomes Consortium Amiodarone, Lidocaine or Placebo Study including 3019 patients, IV amiodarone and IV lidocaine resulted in significantly better risk-adjusted survival to hospital discharge compared with placebo (adjusted risk ratio 1.29 [95% CI 1.06-1.50] and 1.21 [95% CI 1.02-1.45], respectively). By contrast, neither amiodarone nor lidocaine administered by IO access improved risk-adjusted survival to hospital discharge compared with placebo [38].

●In a secondary analysis of the PARAMEDIC2 trial of epinephrine versus placebo for out-of-hospital cardiac arrest, including 7317 subjects of whom 2237 (30 percent) received the study drug via the IO route, there was no interaction detected between route of administration and treatment arm in models predicting ROSC at hospital arrival, survival at 30 days, or favorable functional status at 30 days post-arrest [39].

●A systematic review and meta-analysis of observational studies including 111,746 adult patients resuscitated from cardiac arrest found no difference in functionally favorable survival to hospital discharge in patients with IV versus IO vascular access [40].

MECHANICAL APPROACHES TO CARDIOPULMONARY RESUSCITATION — High-quality chest compressions optimize coronary and cerebral perfusion during cardiac arrest, promoting return of spontaneous circulation (ROSC) and minimizing hypoxic-ischemic brain injury. Multiple approaches to increase the benefits of closed-chest compression have been investigated, but none has demonstrated consistent benefit.

Inspiratory impedance threshold devices — The ACLS Guidelines state that routine use of an inspiratory impedance threshold device (ITD) during conventional cardiopulmonary resuscitation (CPR) is not recommended. When equipment and trained personnel are available, use of an ITD during active compression-decompression CPR (ACD-CPR) may be reasonable.

An ITD is designed to generate negative intrathoracic pressure during passive or active decompression of the chest wall, thereby increasing venous return to the heart (ie, preload) during CPR. The device is a plastic appliance with a silicone diaphragm placed between the airway and the bag ventilator. The ITD permits positive-pressure ventilation and exhalation but prevents the flow of air into the patient's airway during chest wall relaxation. Employing an ITD during active or passive decompression of the chest with CPR reduces intrathoracic pressures and improves both preload and myocardial perfusion.

The ITD is effective at generating negative intrathoracic pressures in patients ventilated using a bag-mask or invasive airway, but this has not been demonstrated to improve clinical outcomes [41]. When the ITD is used as part of bag-mask ventilation, it is crucial to maintain a good mask seal, and for this reason, a two-person ventilation technique is recommended. Regardless of the selected approach to airway management, ITD use should not affect standard CPR guidelines, such as the compression to ventilation ratio (30 to 2) or provision of high-quality CPR. (See "Basic airway management in adults".)

Clinical trials of ITDs have reported mixed results:

●In a multicenter trial in which 400 out-of-hospital cardiac arrest patients received treatment with ACD-CPR and were randomly assigned to ventilation incorporating either an active ITD or a sham device, survival at 24 hours (primary endpoint) was achieved in 32 percent of patients in the ITD group and 22 percent in the sham group (odds ratio [OR] 1.64; 95% CI 1.07-2.6) [42]. There was no difference in survival to hospital discharge (4 percent for the ITD group versus 5 percent for the sham group) or functionally favorable survival at discharge (3 percent for the ITD group versus 0.5 percent for the sham group).

●In a multicenter prospective trial of 8718 emergency medical services-treated patients resuscitated from out-of-hospital cardiac arrest and randomly assigned to treatment with an ITD or a sham device, no significant difference was found in functionally favorable survival (5.8 percent in the ITD group versus 6 percent in the sham group) [43]. In addition, there was no difference between groups in adverse events or in secondary outcomes, including ROSC on arrival or survival to hospital discharge.

Active compression-decompression CPR — ACD-CPR is a method of chest compression that uses a suction device to convert the passive recoil of the chest wall into active expansion, thereby enhancing venous return. According to the ACLS Guidelines, there is insufficient evidence to recommend for or against the use of ACD-CPR.

Although preliminary studies in swine and humans using this method reported increased cerebral and myocardial perfusion and improved stroke volume [44-46], the results of subsequent clinical trials have been mixed. A meta-analysis of 10 randomized and quasi-randomized trials (most involving out-of-hospital cardiac arrest) found no significant benefit from ACD-CPR compared with standard CPR in any patient-important outcome, including immediate mortality, survival to hospital discharge, and neurologic function [47]. In addition, the meta-analysis found no significant difference in major complications (eg, rib or sternal fractures, hemothorax, pneumothorax), although skin trauma and ecchymosis were more common in the ACD-CPR group.

One multicenter randomized trial of patients with out-of-hospital cardiac arrest, not included in the meta-analysis described above, reported that 75 of 849 patients (9 percent) treated with both ACD-CPR and an ITD survived to hospital discharge compared with 47 of 813 patients (6 percent) treated with standard CPR (OR 1.58; 95% CI 1.07-2.36) [48]. The trial was stopped early because of enrollment and funding difficulties. Other challenges with this trial include the difficulty of determining the impact of the device's metronome and force gauge (used only in the intervention arm) on the quality of CPR independent of ACD-CPR and the inability to control for the contribution of the ITD to the outcome.

Mechanical compression devices — Devices for mechanical chest compression do not improve patient-important outcomes and may be associated with complications [49,50]. Therefore, they should not be used routinely. In settings where it may be difficult or dangerous to perform or sustain high-quality chest compressions (eg, few rescuers, prolonged CPR, CPR during transport, CPR during cardiac catheterization [51,52]), these devices may be useful.

Researchers have developed mechanical devices that perform chest compressions and generate artificial circulation in much the same way as manually performed chest compressions. Two basic types of devices exist. One uses a load-distributing band wrapped around the chest that rhythmically squeezes the chest circumferentially. A second employs a piston placed on the sternum that compresses the chest in the anteroposterior plane. Both devices deliver closed chest compressions automatically, enabling rescuers to perform other interventions, minimizing interruptions in the performance of compressions, and eliminating the risk of decreased perfusion due to rescuer fatigue.

Three major randomized trials of these devices and a meta-analysis have been performed:

●A multicenter randomized trial reported no statistically significant differences between patients resuscitated with a piston-type mechanical chest compression device (n = 1300) compared with manual CPR (n = 1289) in survival at four hours (307 [23.6 percent] versus 305 [23.7 percent]) or functionally favorable survival at six months (98 [7.5 percent] versus 82 [6.4 percent]) [53]. Two issues that complicate the interpretation of the study results are the atypical resuscitation protocol used in the intervention arm and the additional training provided to participants.

●A multicenter randomized trial involving 4231 cardiac arrest patients compared the effectiveness of a load-distributing band mechanical compression device versus manual CPR and reported no statistically significant difference in survival to hospital admission or discharge [54].

●A randomized trial involving 4471 cardiac arrest patients reported no significant difference in 30-day survival between patients treated with a piston-type mechanical chest compression device and patients managed with manual CPR [55].

●A meta-analysis including 12,908 patients with cardiac arrest enrolled in one of seven randomized trials comparing mechanical CPR versus manual CPR found that patients who had received manual CPR had better survival to hospital discharge or 30 days (OR 1.40; 95% CI 1.09-1.94) and functionally favorable survival at discharge or 30 days (OR 1.51; 95% CI 1.06-2.39) [49]. Compared with load-distributing band mechanical compression, manual compressions had a lower risk of pneumothorax or hematoma formation.

Performance of interposed abdominal compression CPR — Preliminary data suggest that interposed abdominal compression cardiopulmonary resuscitation (IAC-CPR) when used in the in-hospital setting and performed by trained rescuers may be effective, and the ACLS Guidelines state that the technique may be used in this setting. However, the effectiveness of IAC-CPR for achieving improved survival without significant neurologic deficits remains unproven, and further study is needed.

IAC-CPR refers to the application of external chest compressions with interposed midabdominal compressions performed by a second rescuer during the upstroke of the chest compression. Multiple animal studies have shown that IAC-CPR can increase systolic and diastolic blood pressure, improving myocardial and cerebral perfusion [56].

A meta-analysis identified 38 peer-reviewed studies of IAC-CPR (25 were animal or mechanical model studies) of which 34 reported significant benefit over standard CPR based primarily on ROSC (a problematic endpoint); two found no difference in outcome, and two found IAC-CPR to be inferior to standard CPR [57]. The studies reported a single adverse event (case of likely traumatic pancreatitis) [58]. Of four randomized trials included, three were in-hospital studies, all of which found an increased rate of ROSC in the IAC-CPR arm [59,60], with one study reporting improved survival to discharge [61]. The lone prehospital study found no significant difference in ROSC [62].

OTHER ASPECTS OF RESUSCITATION

Airway management — Airway management during cardiopulmonary resuscitation (CPR) should never interfere with provision of high-quality chest compressions and rapid defibrillation of shockable rhythms. Bag-valve-mask (BVM) ventilation or placement of a supraglottic airway are reasonable approaches to intra-arrest airway management and generally preferred to endotracheal intubation. If intubation is performed, it must be done by an experienced provider, ideally require less than 10 seconds to complete, be performed without interruption of chest compressions, and occur only after all other essential resuscitative maneuvers have been initiated. (See "Advanced cardiac life support (ACLS) in adults", section on 'Airway management'.)

Options for intra-arrest airway management include making no intervention, BVM ventilation, supraglottic airway insertion, and endotracheal intubation. The optimal approach remains uncertain:

●In a randomized trial of BVM ventilation (1020 patients) versus tracheal intubation (1023 patients) for prehospital management of out-of-hospital cardiac arrest in France and Belgium, functionally favorable survival at 28 days did not differ between groups (4.3 percent for BVM compared with 4.2 percent for tracheal intubation) [63]. The trial failed to meet the prespecified criteria for noninferiority. Ambulance teams in these countries include physicians with training in intubation.

●In a multicenter cluster randomized trial of a supraglottic airway device (4886 patients) versus tracheal intubation (4410 patients) for prehospital airway management of out-of-hospital cardiac arrest in England, functionally favorable survival at hospital discharge, 30 days, three months, and six months did not differ between groups [64]. However, initial ventilation success occurred more commonly in the supraglottic airway group (87 versus 79 percent).

●In a multicenter cluster-crossover trial of a laryngeal tube (1505 patients) versus tracheal intubation (1499 patients) for prehospital airway management of out-of-hospital cardiac arrest in the United States, 72-hour survival, survival to discharge, and functionally favorable survival were each better in the laryngeal tube group [65].

Use of transcutaneous pacing in asystole — We concur with the ACLS Guidelines, which state that transcutaneous pacing (TCP) is not recommended for management of asystole or pulseless electrical activity. The use of TCP for emergency treatment of symptomatic bradycardia is discussed separately. (See "Advanced cardiac life support (ACLS) in adults", section on 'Bradycardia'.)

TCP is the delivery of a rhythmic electrical current to induce electrical conduction and mechanical activity in the heart. The current is conducted between two electrodes placed on the skin in a manner that ensures the heart lies between them.

Multiple studies of TCP performed in the late 1980s found no significant survival benefit among patients in cardiac arrest from asystole or bradyasystole [66-70]. A larger, subsequent randomized trial of TCP in out-of-hospital asystolic cardiac arrest also found no benefit [71]. A systematic review found no evidence to support the use of TCP for out-of-hospital bradyasystolic arrest but found insufficient evidence to determine its role with symptomatic bradycardia [72].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Basic and advanced cardiac life support in adults".)

SUMMARY AND RECOMMENDATIONS

●Management of cardiac arrest – Standard management of patients in sudden cardiac arrest (SCA), cardiac arrhythmia, and related critical illness is thoroughly discussed in several UpToDate topic reviews:

•Advanced cardiac life support (ACLS) (see "Advanced cardiac life support (ACLS) in adults")

•Basic life support (BLS) (see "Adult basic life support (BLS) for health care providers")

•Post-cardiac arrest management (see "Initial assessment and management of the adult post-cardiac arrest patient" and "Intensive care unit management of the intubated post-cardiac arrest adult patient")

•Airway management (see "Basic airway management in adults" and "Extraglottic devices for emergency airway management in adults")

●Therapies and interventions of uncertain benefit – A number of potential therapies and interventions for patients with SCA continue to be the subject of clinical study. Such therapies include resuscitation techniques, mechanical devices, and medications. Therapies that are the subject of clinical research but are not generally accepted as part of standard resuscitation are reviewed above:

•Medications (see 'Medications used during cardiopulmonary resuscitation' above)

•Mechanical devices and approaches for cardiopulmonary resuscitation (CPR) (see 'Mechanical approaches to cardiopulmonary resuscitation' above)

•Airway management and other interventions (see 'Other aspects of resuscitation' above)