Cardiac Arrest

Chapter: Cardiac Arrest
McMaster Section Editor(s): Deborah Cook, Roman Jaeschke
Section Editor(s) in Interna Szczeklika (Cardiovascular Diseases): Andrzej Budaj, Wiktoria Leśniak
Section Editor(s) in Interna Szczeklika (Critical Care): Miłosz Jankowski
McMaster Author(s): Craig Ainsworth, Andrew Gibson
Author(s) in Interna Szczeklika: Miłosz Jankowski, Grzegorz Cebula
Additional Information

Definition, etiology, pathogenesis Top

Cardiac arrest refers to the cessation of cardiac mechanical function characterized by the absence of palpable pulse, lack of the patient’s response to stimulation, and apnea or agonal respirations. If not rapidly reversed by cardiopulmonary resuscitation (CPR), defibrillation, cardioversion, or pacing, sudden cardiac arrest progresses to cardiac death.

Primary cardiac arrest is caused by or associated with a principal cardiac condition, such as the following:

1) Coronary artery disease (acute coronary syndrome/ischemic heart disease, coronary vasospasm, spontaneous coronary artery dissection).

2) Cardiomyopathies (ischemic cardiomyopathy, nonischemic dilated cardiomyopathy, hypertrophic cardiomyopathy, infiltrative disorders such as amyloidosis or sarcoidosis, arrhythmogenic right ventricular cardiomyopathy, ventricular noncompaction, myocarditis).

3) Congenital arrhythmogenic heart diseases (long QT syndrome, short QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, idiopathic ventricular fibrillation).

4) Structural heart disease (severe aortic stenosis, mitral valve prolapse, anomalous coronary artery circulation, Wolff-Parkinson-White syndrome, sinus node disturbances, atrioventricular conduction disturbances).

5) Other (cardiac tamponade, commotio cordis, aortic dissection).

Secondary cardiac arrest occurs due to noncardiac causes, such as pulmonary embolism, respiratory arrest, multisystem trauma, hemorrhage, acute intracerebral hemorrhage, intoxication, seizures, or near-drowning.

Rhythms in cardiac arrest:

1) Ventricular fibrillation or flutter (Figure 3.3-1).

2) Pulseless ventricular tachycardia (VT).

3) Asystole, that is, lack of electrical and mechanical activity of the heart (also diagnosed when the heart rate is <10 beats/min).

4) Pulseless electrical activity (PEA), that is, lack of a hemodynamically effective mechanical contraction of the heart despite preserved organized electrical activity.

Asystole and PEA commonly result from secondary cardiac arrest or more prolonged primary cardiac arrest (degenerated from ventricular fibrillation [VF] or pulseless VT) and therefore always require a search for reversible causes.

Management Top

Basic Life Support

Basic Life Support (BLS): Figure 3.3-2.

CPR refers to interventions (chest compressions and ventilation) aimed at maintaining the circulation and oxygenation of blood in an individual with cardiac arrest. The steps described below are followed in the course of BLS.

1. Make sure the patient and you (as well as other rescuers) are safe. Control possible hazards (as necessary, call the police, fire department, or other emergency agency for additional assistance).

2. Assess the patient’s consciousness. If the patient does not respond to voice and gentle shaking, assume that he or she is unconscious.

3. Shout or phone for help.

4. Clear the airway (Figure 3.3-3). Place the unconscious patient on the back. Then tilt the head backwards (this maneuver is contraindicated in individuals with suspected cervical spine injury) and examine the mouth, removing any visible foreign bodies. Proceed to chin lift or jaw thrust; these two maneuvers may be performed in patients with suspected cervical spine injury, provided that the head is stabilized in a neutral position without tilting.

5. Assess respirations. Look for chest movements, listen at the patient’s mouth for the sounds of inspiration and expiration, place your cheek near the patient’s mouth to feel for air movement, and check for pulse at the carotid (or femoral) artery for a maximum of 10 seconds. The lack of chest movements, respiratory sounds, and perceptible air movement indicates apnea, which may be caused by a primary cardiac arrest or by complete airway obstruction, respiratory depression, or respiratory diseases. Agonal respirations (residual, single sighs) are treated as apnea. Other sounds accompanying respiration may indicate partial obstruction of the respiratory tract: (1) gurgling due to liquid or semiliquid content in the airways (ie, vomit, blood, respiratory tract secretions); (2) snoring due a partial closure of the throat by the tongue, palate, or a foreign body; (3) stridor due to obstruction or swelling at the level of the glottis.

In some cases it may be necessary to clear the airway. If the patient is breathing spontaneously, place him or her in the recovery position (Figure 3.3-4). If a pulse is definitely present in a patient who is not breathing spontaneously, deliver ventilations at the rate of 10 breaths/min without chest compressions (see below). Every 2 minutes check the pulse and look for signs of circulation. Absence of signs of circulation (ie, spontaneous movements, coughing, breathing) and of carotid pulse indicate a cardiac arrest and require immediate CPR. During CPR check for the signs of circulation and pulse every 2 minutes.

6. Call for help. If you are alone, immediately upon discovering apnea, grossly abnormal breathing, or lack of pulse call for expert assistance if at all practical, even if you have to briefly leave the patient for this purpose. When away from the hospital, call local emergency services. Hospitals should have an emergency extension or phone number known to and available for all employees. Exception: In the case of children and infants, before calling for help proceed with CPR for ~1 minute (perform 5 rescue breaths, then 15 sternal compressions, then another 2 breaths and 15 compressions).

7. Start chest compressions. Place the patient in the supine position on a hard surface and compress the center of the patient’s sternum. In adults compress from 5 to 6 cm deep at a rate of 100 to 120 compressions/min (~2 compressions/s), in children compress the sternum with one hand, and in infants compress with 2 fingers to one-third the depth of the sagittal dimension of the chest. To perform compressions in adults, place the heel of one hand in the center of the patient’s chest and the heel of your other hand on the top of the first hand, interlock the fingers of your hands, and keep your arms straight and your shoulders directly over the patient’s chest, all without leaning on the patient’s ribs. Completely release the pressure without taking your hands off the chest; the duration of a compression and a release should be identical. In adults start with 30 chest compressions followed by 2 rescue breaths, then continue with chest compressions and rescue breaths, maintaining a ratio of 30:2 (in nonintubated patients).

8. Continue ventilation giving mouth-to-mouth rescue breaths while pinching the patient’s nose if more than one responder is available. In infants perform mouth-to-mouth-and-nose rescue breaths. A lone rescuer should focus on compressions and should not interrupt compressions to provide rescue breaths. One breath should last ~1 second (2 rescue breaths [inspiration plus expiration] should last <5 seconds). Make sure the chest rises during inspiration and allow for its complete fall during exhalation. If the rescue breaths are ineffective (ie, the chest does not rise), change the position of the head and jaw and repeat a maximum of 2 ventilation attempts. In children start CPR from 5 rescue breaths; maintain a 15:2 ratio of chest compressions to rescue breaths (with a lone rescuer, a 30:2 ratio is acceptable).

9. Defibrillate using an automated external defibrillator (AED). Use an AED immediately when available. Switch on the AED and attach the electrodes to the chest (one below the right clavicle along the sternum and the other below and to the left of the left nipple in the midaxillary line: Figure 3.3-5). Keep away from the patient for the time the AED is assessing the rhythm and when the shock is being delivered. Charge the AED and trigger the shock whenever indicated by the AED. After 1 defibrillation, immediately start CPR and continue for 2 minutes before the AED reevaluates the heart rhythm.

Advanced Life Support or Advanced Cardiovascular Life Support

Advanced Life Support (ALS) or Advanced Cardiovascular Life Support (ACLS): Figure 3.3-6.

ALS or ACLS refers to the procedures performed by a team of appropriately equipped professional rescuers that are aimed at restoring spontaneous circulation using CPR, advanced airway management (eg, endotracheal intubation, laryngeal mask), defibrillation/cardioversion, and administration of medications.

1. Safety assessment (removal of threats) and diagnosis of cardiac arrest: see Basic Life Support, above.

2. Perform CPR: Figure 3.3-2. Minimize the time necessary for other activities (intubation performed as quickly as possible, preferably <10 seconds; defibrillation <5 seconds; continue CPR while charging the defibrillator below). If possible, the rescuers performing chest compressions should change every 2 minutes.

3. Assess the mechanism of cardiac arrest and defibrillate when indicated. If a defibrillator is immediately available and ready for discharge, and the cardiac arrest occurred in the presence of rescuers or in a hospital, defibrillation may be attempted before starting CPR. Connect a manual defibrillator and monitor the patient for arrhythmia eligible for defibrillation (VF or pulseless VT). After turning on the defibrillator, make sure that the lead selector is appropriately set to either paddles or standard electrodes (leads I, II, III). Then attach the 3 electrodes to the chest and connect them to the defibrillator (North American electrode placement: white on the right, red on the left lower chest, and black on the left upper chest; European electrode placement: red on the right shoulder, yellow on the left shoulder, green on the left midaxillary line at the costal margin). In the event of asystole on the monitor, check the connections of the defibrillator (monitor), settings of the signal amplification (gain), and readings from another lead. If in doubt whether the patient is in asystole or low-voltage VF, do not defibrillate and continue CPR. During CPR reassess the heart rhythm every 2 minutes.
Defibrillation using a manual defibrillator:

1) Apply gel (or defibrillation pads) on the skin of the chest where the paddles are to be placed or on the paddles themselves (self-adhesive defibrillation pads require no gel).

2) Apply the paddles with a force of ~10 kg or attach defibrillation pads to the chest (one below the right clavicle along the sternum and the other below and to the left of the left nipple: Figure 3.3-5).

3) Assess the rhythm on the defibrillator’s monitor (after applying the paddles or electrodes temporarily stop CPR). The indication for delivering a shock is VF or pulseless VT. Resume CPR while the defibrillator charges (remove the paddles from the chest for that time).

4) Set the shock energy:

a) In adults: When using biphasic defibrillators, providers should use the manufacturer’s recommended energy dose (ie, initial energy of 120-200 J). If the dose range is unknown, the provider may use a maximal dose of 200 J. The first shock is usually 150 J. The energy of subsequent shocks may be increased to a maximum of 200 J. In monophasic defibrillators the first and subsequent shocks are 360 J.

b) In children: 4 J/kg (first and subsequent shocks).

5) Charge the defibrillator (press “charge”).

6) Order all rescuers to move away and stay clear of the patient. Make sure no one is touching either the patient or any objects that are in contact with the patient. At this point, stop CPR; if using paddles, place them back in the areas of the chest previously covered with gel.

7) Deliver the shock (press and hold the “discharge” or “shock” button).

After delivering the shock, immediately restart CPR for 2 minutes; stop if signs of circulation appear (coughing, breathing, movements). Then reassess the rhythm and if the first shock has not been effective, deliver subsequent shocks every 2 minutes for shockable rhythms. Continue CPR between shocks. Next, establish vascular access (intravenous or intraosseous), intubate the patient when possible (if not done already), and administer medications (Figure 3.3-6). A series of 3 shocks at intervals shorter than 2 minutes may be used in the case of a cardiac arrest occurring during cardiac catheterization or shortly after a surgical cardiac procedure, or in the case of a witnessed cardiac arrest in a patient already connected to a manual defibrillator. Following the first 2 (American Heart Association [AHA] guidelines) or 3 (European Resuscitation Council [ERC] guidelines) ineffective shocks, administer IV epinephrine 1 mg. After 3 ineffective shocks, administer IV amiodarone 300 mg (see below) before delivering the fourth shock. Do not stop CPR for the time the drugs are being administered. If the fourth shock is also ineffective, deliver subsequent shocks every 2 minutes and administer epinephrine 1 mg every 3 to 5 minutes. Consider administration of another 150 mg of amiodarone and look for reversible causes of cardiac arrest (see below). Consider changing position of the defibrillator paddles to a front-to-back position (Figure 3.3-5) or to the opposite middle axillary lines.

In the case of a witnessed cardiac arrest—in particular during electrocardiography (ECG) monitoring that shows VF or pulseless VT—if a defibrillator ready to trigger off a discharge is not immediately available, you may hit the precordial area (sternum) with a clenched fist, delivering a precordial blow or “thump.” This is an attempt to defibrillate with low energy, which is sometimes effective within 30 seconds of the onset of VF or pulseless VT. However, the precordial thump should not delay CPR and defibrillation.

4. Clear the airway. Perform endotracheal intubation if the provider is sufficiently skilled in this procedure (this should be completed within 10 seconds). Note: CPR and prompt defibrillation have priority over intubation! If endotracheal intubation is unsuccessful, you may try an esophageal-tracheal tube (Combitube), laryngeal mask, or laryngeal tube. Alternatively, insert an oropharyngeal or nasopharyngeal airway.

5. Ventilate the patient using a self-inflating bag (with a valve) that is connected to a reservoir bag and high-flow oxygen (>10-15 L/min) to achieve the highest possible levels of oxygen in the inhaled air (close to 100%). Before the intubation (and also when an oropharyngeal or nasopharyngeal airway is used), ventilate the patient using a face mask, delivering 30 chest compressions followed by 2 rescue breaths. After successful intubation, ventilate the patient via the endotracheal tube at a rate of approximately 8 to 10 breaths/min; synchronization with chest compressions is not necessary. Asynchronous CPR may be also attempted once the airway has been secured using supraglottic airway devices. The ventilation volumes are 6-7 mL/kg (400-600 mL) over 1 second. If capnography (measurement of the end-expiratory CO2 levels) is available, it can be used to additionally confirm the endotracheal intubation, effectiveness of ventilation, presence of return of spontaneous circulation, and to assess the quality of chest compressions.

6. Look for and treat reversible causes of cardiac arrest, particularly in the event of asystole or PEA, but also in the case of VF or pulseless VT not responding to defibrillation. Take a history from witnesses and perform a quick targeted physical examination and diagnostic tests during CPR. Reversible causes can be remembered by H’s and T’s. If suspected or confirmed, reversible causes should be corrected immediately.
Reversible causes:

1) Hypoxia.

2) Hypovolemia (eg, hemorrhage, diarrhea).

3) Hydrogen ion or acidosis.

4) Hypothermia.

5) Hyperkalemia, hypokalemia, or other severe electrolyte disturbances (see Magnesium Disturbances, Calcium Disturbances, Phosphate Disturbances).

6) Tamponade (cardiac; see Pericardiocentesis).

7) Tension pneumothorax.

8) Thrombosis (see Pulmonary Embolism).

9) Thrombosis (myocardial infarction).

10) Toxins (eg, drug overdose, poisoning).

11) Trauma.

7. Administer medications: After every intravenous drug administration during CPR, use an additional 20 mL of 0.9% NaCl to flush the IV catheter. In patients without venous access, medications may be delivered via an intraosseous route.

1) Epinephrine. Indications: Asystole, PEA, VF, or pulseless VT not responding to the first 2 (AHA guidelines) or 3 (ERC guidelines) shocks. Dosage: 1 mg IV in 10 mL 0.9% NaCl (or nondiluted) every 3 to 5 minutes (in children 10 microg/kg).

2) Amiodarone. Indications: VF or VT not responding to the first 3 shocks. Dosage: 300 mg in 20 mL of 5% glucose (dextrose) IV bolus (5 mg/kg in children). In the case of persistent VF or VT, an additional 150 mg may be administered; then consider 900 mg/d in a continuous IV infusion.

3) Sodium bicarbonate. Indications: Hyperkalemia and tricyclic antidepressant overdose. Outside of these indications, a routine use of sodium bicarbonate is not recommended. Dosage: 50 mmol (50 mL of 8.4% solution) IV; repeat as considered necessary according to the clinical condition and serial blood gas measurements.

4) Magnesium sulfate. Indications: Torsades de pointes (polymorphic VT with prolonged QT; Figure 3.3-1). Magnesium is not likely to be effective in terminating polymorphic VT with a normal QT interval. Dosage: 1 to 2 g diluted in 10 mL of 5% glucose IV over 1 to 2 minutes, repeat after 10 to 15 minutes if necessary.

5) Calcium chloride. Indications: Hyperkalemia, hypocalcemia, and overdose of calcium channel blockers. There are no data supporting beneficial effects of the use of calcium chloride in other causes of cardiac arrest; in some cases it may be harmful. Avoid calcium chloride in patients with suspected digoxin toxicity and severe hyperphosphatemia. Dosage: 10 mL of a 10% CaCl2 solution IV bolus; repeat as necessary.

6) Fibrinolysis. Fibrinolysis should not be used routinely in cardiac arrest. You may consider fibrinolytic therapy when the arrest was caused by proven or suspected pulmonary embolism in the absence of absolute contraindications (see Pulmonary Embolism). Consider continuation of CPR for 60 to 90 minutes following the administration of a fibrinolytic agent.

7) Other drugs:

a) IV glucose. Indications: Hypoglycemia.

b) IV glucagon. Indications: Hypoglycemia (1 mg) and overdose of beta-blockers or calcium channel blockers (5-10 mg).

c) Antihistamines (H1 and H2 antagonists) and IV glucocorticoids. Indications: see Anaphylaxis.

d) IV fluids. Indications: Hypovolemia, anaphylaxis, or undifferentiated shock.

e) Blood products (ie, red cells, frozen plasma, platelet concentrates). Indications: Hemorrhage (at the same time make attempts to stop the hemorrhage as soon as possible), coagulopathy.

f) Naloxone. Indications: Opioid poisoning.

g) Lipid emulsion therapy. Indications: Poisonings involving certain lipophilic medications (ie, overdoses of calcium channel blockers, beta-blockers, some tricyclic antidepressants, local anesthetics, and chlorpromazine). Before using lipid emulsion therapy, it is recommended to consult a poison control center or toxicologist. Dosage: 20% lipid emulsion (1-1.5 mL/kg bolus followed by a continuous IV infusion at 0.25-0.5 mL/kg/min). If cardiovascular stability has not been restored after 5 minutes, the 1.5 mL/kg bolus may be repeated a maximum of 2 times.

8. Cardiac pacing. Electrical pacing during cardiac arrest is generally considered ineffective and therefore is not recommended for routine use. Pacing may be considered for recurrent polymorphic VT when precipitated by bradycardia or pauses. Pacing can be done via transcutaneous pads or a temporary transvenous wire.

Management After Restoring Spontaneous Circulation

1. Placement of the unconscious patient with preserved spontaneous breathing in the recovery position (this does not apply to intubated patients; Figure 3.3-4) unless there is an immediate history of suspected trauma, particularly spine injury.

2. Prompt transfer to an intensive care unit (ICU) or a high acuity bed. The patient should be transported to a hospital by an ambulance with appropriate CPR equipment and CPR-competent personnel, and moved around the hospital when attended by a hospital resuscitation team, ideally with a connected defibrillator, continuous oxygen therapy, secured airway (in unconscious patients), and continued ventilation.

3. Hospitalization in the ICU or an equivalent unit for a period of time deemed necessary, usually at least for 24 hours.

1) Continuous monitoring of ECG, pulse oximetry, blood pressure, and urine output, when deemed necessary supplemented with the use of the central line as well as hemodynamic monitoring with an intra-arterial line.

2) Treatment of arrhythmias (eg, ventricular and supraventricular tachycardias, bradycardia), shock, heart failure, acute coronary syndrome (ACS), respiratory failure.

3) Determination of the cause of cardiac arrest and further diagnostic workup and treatment:

a) A repeated broader history and physical examination (if the patient cannot provide information on his or her own, ask the rescuers, witnesses of the cardiac arrest, family, and other persons living with or close to the patient, and use the available medical records).

b) 12-lead ECG, other diagnostic tests of ACS (cardiac troponin and echocardiography, when necessary), and appropriate treatment if the diagnosis of ACS is established (including revascularization and medical therapies).

c) Chest radiographs looking for evidence of various conditions as dictated by clinical situation, for example, pneumothorax, pneumonia, atelectases, pericardial or pleural effusion, or venous congestion. Verify the positioning of the endotracheal tube, gastric tube, and intravenous catheters.

d) Arterial blood gas measurements and treatment of acid-base disturbances and respiratory insufficiency (administer oxygen when necessary to maintain the arterial hemoglobin oxygen saturation 94%-98%). Note: Hyperoxia (PaO2 above 200 or 300 mm Hg) may be harmful.Evidence 1Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to indirectness to patient-important outcomes in the randomized controlled trial, imprecision, and observational nature of evidence. Wang CH, Huang CH, Chang WT, et al. Association between early arterial blood gas tensions and neurologic outcome in adult patients following in-hospital cardiac arrest. Resuscitation. 2015 Apr;89:1-7. doi: 10.1016/j.resuscitation.2015.01.003. Epub 2015 Jan 17. PubMed PMID: 25600183. Kuisma M, Boyd J, Voipio V, Alaspää A, Roine RO, Rosenberg P. Comparison of 30 and the 100% inspired oxygen concentrations during early post-resuscitation period: a randomised controlled pilot study. Resuscitation. 2006 May;69(2):199-206. Epub 2006 Feb 24. PubMed PMID: 16500018.

e) Measurements of serum electrolyte levels and treatment of electrolyte disturbances. Measurements of blood glucose levels (if >10 mmol/L [180 mg/dL], administer continuous IV insulin).

f) Looking for signs of active bleeding (particularly gastrointestinal bleeding; start appropriate prophylaxis), complete blood count measurements (look for anemia and transfuse packed red blood cells when necessary).

g) Kidney and liver function tests.

h) Basic coagulation tests.

i) Toxicology tests in the case of suspected poisoning, appropriate treatment when indicated.

j) Other investigations to assess for the cause of the arrest as dictated by the clinical situation (eg, chest computed tomography [CT] for suspected pulmonary embolism, echocardiogram for suspected ACS or pericardial effusion).

4) Consider bronchoscopy to clear the airway in patients with suspected or documented aspiration.

5) Consider imaging studies of the head in unconscious patients or those with neurologic symptoms to assess for intracranial hemorrhage, ischemic stroke, cerebral edema, or other significant intracranial pathology.

6) In patients who remain comatose (Glasgow Coma Scale <8 [see Table 10.3-2] or inability to respond to verbal commands) following the return of spontaneous circulation from ventricular fibrillation or pulseless VT arrest, it is recommended to initiate a targeted temperature management to help improve the neurologic prognosis, including improved survival with a good neurologic outcome.Evidence 2Strong recommendation (benefits clearly outweigh downsides; right action for all or almost all patients). Moderate Quality of Evidence (moderate confidence that we know true effects of intervention). Quality of Evidence lowered due to some indirectness (no temperature control in the control group) and expected lack of blinding. Arrich J, Holzer M, Havel C, Müllner M, Herkner H. Hypothermia for neuroprotection in adults after cardiopulmonary resuscitation. Cochrane Database Syst Rev. 2012 Sep 12;9:CD004128. doi: 10.1002/14651858.CD004128.pub3. Review. PubMed PMID: 22972067. Vargas M, Servillo G, Sutherasan Y, Rodríguez-González R, Brunetti I, Pelosi P. Effects of in-hospital low targeted temperature after out of hospital cardiac arrest: A systematic review with meta-analysis of randomized clinical trials. Resuscitation. 2015 Jun;91:8-18. doi: 10.1016/j.resuscitation.2015.02.038. Epub 2015 Mar 20. Review. PubMed PMID: 25796995. Lower-level evidence exists for the use of the targeted treatment management in cardiac arrest survivors of nonshockable rhythms.Evidence 3Low Quality of Evidence (low confidence that we know true effects of the intervention). Quality of Evidence lowered due to imprecision of subgroup analysis and lack of blinding. Arrich J, Holzer M, Havel C, Müllner M, Herkner H. Hypothermia for neuroprotection in adults after cardiopulmonary resuscitation. Cochrane Database Syst Rev. 2012 Sep 12;9:CD004128. doi: 10.1002/14651858.CD004128.pub3. Review. PubMed PMID: 22972067. The International Liaison Committee on Resuscitation recommends cooling to 32 to 34 degrees Celsius for 12 to 24 hours (most centers continue cooling for 24 hours) using ice packs or specialized equipment (eg, cooling blankets, intravascular devices). As an adjunct, an infusion of up to 30 mL/kg of cold (4 degrees Celsius) 0.9% NaCl or Ringer lactate may be considered to lower the body temperature, initially by up to 1.5 degrees Celsius. After the cooling period, rewarm the patient’s body temperature slowly (0.25-0.5 degrees Celsius/h). There is a strong suggestion of similar effects of cooling to 33 and 36 degrees CelsiusEvidence 4Moderate Quality of Evidence (moderate confidence that we know true effects of intervention). Quality of Evidence lowered due to imprecision and lack of blinding. Nielsen N, Wetterslev J, Cronberg T, et al; TTM Trial Investigators. Targeted temperature management at 33 degrees Celsius versus 36 degrees Celsius after cardiac arrest. N Engl J Med. 2013 Dec 5;369(23):2197-206. doi: 10.1056/NEJMoa1310519. Epub 2013 Nov 17. PubMed PMID: 24237006. Vargas M, Servillo G, Sutherasan Y, Rodríguez-González R, Brunetti I, Pelosi P. Effects of in-hospital low targeted temperature after out of hospital cardiac arrest: A systematic review with meta-analysis of randomized clinical trials. Resuscitation. 2015 Jun;91:8-18. doi: 10.1016/j.resuscitation.2015.02.038. Epub 2015 Mar 20. Review. PubMed PMID: 25796995. and no benefits of cooling with a cold saline infusion before arrival to the hospital. A formal consensus and updated guidelines on temperature targets are pending. Our own practice is generally to cool to 36 degrees Celsius for 24 hours; however, there is room in our protocol for physicians to choose a cooler temperature based on the patient factors or personal preference.


Figure 3.3-1. Ventricular arrhythmia. A, monomorphic ventricular tachycardia. B, ventricular flutter. C, polymorphic ventricular tachycardia. D, ventricular fibrillation.

Figure 3.3-2. Basic Life Support algorithm. Adapted from the 2010 European Resuscitation Council guidelines.

Figure 3.3-3. Clearing the airway.

Figure 3.3-5. Recommended placement of the electrodes for defibrillation. Location on the front (red), side (green), and back (blue) of the chest.

Figure 3.3-6. Advanced Life Support algorithm. Based on the 2010 European Resuscitation Council guidelines.

Figure 3.3-4. Placing an unconscious patient in the recovery position.

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