Cardiac Arrest: Difference between revisions

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''Sébastien Krul, MD, Jonas de Jong, MD''
''Sébastien Krul, MD, Jonas de Jong, MD''


{{DevelopmentPhase}}
=Introduction=  
=Introduction=  
Survival of cardiac arrest continues to be very poor. In-hospital cardiac arrest has a survival to hospital discharge of 17,6% all rhythms<cite>Meaney</cite>. Out-of-hospital cardiac arrest has a worse survival with 10,7% survival to hospital discharge for all rhythms.<cite>Atwood</cite> Survival is dependent on the characteristics of the cardiac arrest (rhythm), on the patient’s medical history, and the time between the cardiac arrest en start of resuscitation.<cite>Waalewijn, Holmberg1, Holmberg2</cite> The introduction of the automated external defibrillator (AED) has dramatically increased survival of out-of-hospital cardiac arrest victims.<cite>ESC, Nolan1</cite> In this chapter we give an overview of basic life support (BLS) and advanced life support (ALS) based on the recommendation of the European Resuscitation Council Guidelines for Resuscitation 2010.
Survival of cardiac arrest continues to be very poor. In-hospital cardiac arrest has a survival to hospital discharge of 17,6% all rhythms<cite>Meaney</cite>. Out-of-hospital cardiac arrest has a worse survival with 10,7% survival to hospital discharge for all rhythms.<cite>Atwood</cite> Survival is dependent on the characteristics of the cardiac arrest (rhythm), on the patient’s medical history, and the time between the cardiac arrest en start of resuscitation.<cite>Waalewijn, Holmberg1, Holmberg2</cite> The introduction of the automated external defibrillator (AED) has dramatically increased survival of out-of-hospital cardiac arrest victims.<cite>ESC, Nolan1</cite> In this chapter we give an overview of basic life support (BLS) and advanced life support (ALS) based on the recommendation of the European Resuscitation Council Guidelines for Resuscitation 2010.
Line 15: Line 14:


====Foreign body airway obstruction====
====Foreign body airway obstruction====
An obstruction of the airway is uncommon, but reversible and adequate recognition can prevent cardiac arrest.<cite>Fingerhut</cite> Airway obstruction is usually related with eating. In a mild obstruction patients can cough and speak and only frequent reassessment is advised. Patients that have a severe obstruction are unable to speak and have problems breathing and coughing. If a patient is still conscious five back blows can be applied between the shoulder blades whilst the patient leans forward. Otherwise five abdominal thrusts can be applied by clenching a fist and grasping it with the other hand. Place the hands it between the rib-cage and the umbilicus and pull sharply inward and upward whilst standing behind the patients.<cite>Guildner, Ruben</cite> If the patient loses consciousness start BLS.<cite>Koster2</cite>
An obstruction of the airway is uncommon, but reversible and adequate recognition can prevent cardiac arrest.<cite>Fingerhut</cite> Airway obstruction is usually related to eating. In a mild obstruction patients can cough and speak and only frequent reassessment is advised. Patients that have a severe obstruction are unable to speak and have problems breathing and coughing. If a patient is still conscious five back blows can be applied between the shoulder blades whilst the patient leans forward. Otherwise five abdominal thrusts can be applied by clenching a fist and grasping it with the other hand. Place the hands it between the rib-cage and the umbilicus and pull sharply inward and upward whilst standing behind the patients.<cite>Guildner, Ruben</cite> If the patient loses consciousness start BLS.<cite>Koster2</cite>


====Basic life support in children====
====Basic life support in children====
Line 26: Line 25:


==Preventing in Hosptial Cardiac Arrest==
==Preventing in Hosptial Cardiac Arrest==
[[File:MEWS.svg|thumb|500px|right|'''Figure 2.''' An example of a MEWS<cite>IHI</cite>.]]
[[File:MEWS.svg|thumb|500px|right|'''Figure 2.''' An example of a MEWS. Adapted from: <cite>IHI</cite>.]]
The best way to prevent sudden death is to early detect deterioration of a patient and to act on early warning signs.<cite>Smith</cite> An early warning score (Figure 2) helps to create consensus among care providers about the sickness of a patient.<cite>Hodgetts, Hillman</cite> If the summed score is ≥ 3 a doctor should be notified. The notified doctor should assess the patient within 30 minutes and discuss a treatment plan. If the patient does not improve within 60 minutes a reassessment should follow with possible inclusion of a medical emergency team (MET) or intensive care specialist.<cite>Bellomo</cite>
The best way to prevent sudden death is to early detect deterioration of a patient and to act on early warning signs.<cite>Smith</cite> Cardiac arrest is rarely unpredictable and is precipitated by a slow deterioration.  An early warning score (Figure 2) helps to create consensus among care providers about the sickness of a patient.<cite>Hodgetts, Hillman</cite> If the summed score reached a certain threshold, a doctor should be notified. The notified doctor should assess the patient within 30 minutes and discuss a treatment plan. If the patient does not improve within 60 minutes a reassessment should follow with possible inclusion of a medical emergency team (MET) or intensive care specialist.<cite>Bellomo</cite>


==Advanced Life Support (ALS)==
==Advanced Life Support (ALS)==
Line 36: Line 35:


====Patient assessment====
====Patient assessment====
During a cardiac arrest a structured assessment of the patient is required to detect the effects of the resuscitation, return of spontaneous circulation, reversible causes. To facilitate this assessment, an ABCDE approach can be used.<br>
During a cardiac arrest a structured assessment of the patient is required to detect the effects of the resuscitation, return of spontaneous circulation, reversible causes. To facilitate this assessment, an ABCDE approach can be used.<cite>Thim, Guly</cite><br>
'''Airway:''' During the first step it is important to assess if the airway is clear. Airway obstruction can occur at any level. It can be caused by obstruction from the soft palate and epiglottis, blood, vomit and foreign bodies or airway oedema. It is important to look, listen and feel for airway obstruction. Look for chest and abdominal movements, listen and feel for airflow at the mouth and nose. In partial airway obstruction, the inspiration or expiration is usually noisy by an inspiratory stridor or expiratory wheeze.<br>
'''Airway:''' During the first step it is important to assess if the airway is clear. Airway obstruction can occur at any level. It can be caused by obstruction from the soft palate and epiglottis, blood, vomit and foreign bodies or airway oedema. It is important to look, listen and feel for airway obstruction. Look for chest and abdominal movements, listen and feel for airflow at the mouth and nose. In partial airway obstruction, the inspiration or expiration is usually noisy by an inspiratory stridor or expiratory wheeze.<br>
'''Breathing:''' Hypoxaemia is a reversible cause and after assessment and securing the airway, ventilation of the patient should be optimized. Arterial blood oxygen saturation can be monitored to assess hypoxaemia. If necessary tracheal intubation, sedation and controllered ventilation should be instituted.<br>  
'''Breathing:''' Hypoxaemia is a reversible cause and after assessment and securing the airway, ventilation of the patient should be optimized. The airway can be secured using a variety of devices and ventilation methods. Arterial blood oxygen saturation can be monitored to assess hypoxaemia. If necessary tracheal intubation, sedation and controllered ventilation should be instituted.<br>  
'''Circulation:''' Myocardial ischemia or infarction is a common cause of cardiac arrest. Furthermore before or after the cardiac arrest tachycardias or bradycardias may occur and acute management is indicated. <br>
'''Circulation:''' Myocardial ischemia or infarction is a common cause of cardiac arrest. Furthermore before or after the cardiac arrest tachycardias or bradycardias may occur and acute management is indicated. <br>
'''Disability:''' This step consist of determining the Glasgow Coma Scale of the patients and look for neurologic symptoms that might cause cardiac arrest. Furthermore it is important monitor glucose and temperature. <br>
'''Disability:''' This step consist of determining the Glasgow Coma Scale of the patients and look for neurologic symptoms that might cause cardiac arrest. Furthermore it is important monitor glucose and temperature. <br>
Line 44: Line 43:


====Shock protocol====
====Shock protocol====
When a shockable rhythm is detected, it is important to minimize the time between chest compressions and defibrillation. When the shock is delivered immediately resume with the chest compressions to minimize delay. Even after a successful shock the heart can be stunned and effective circulation can only be maintained through chest compressions. After the first round of shock and compressions reassess rhythm and act according to the protocol. After the third shock has been given, adrenaline 1mg and amiodarone 300mg can be administered intravenously. Further adrenaline 1mg can be administered every 3-5 minutes, there is no further indication for anti-arrhythmic drugs during resuscitation. Continuous monitoring is required for return of spontaneous circulation or for asystole and initiation of the no-shock protocol.
When a shockable rhythm is detected, it is important to minimize the time between chest compressions and defibrillation.<cite>Edelson, Eftestol</cite> When the shock is delivered immediately resume with the chest compressions to minimize delay. Even after a successful shock the heart can be stunned and effective circulation can only be maintained through chest compressions. After the first round of shock and compressions reassess rhythm and act according to the protocol. After the third shock has been given, adrenaline 1mg and amiodarone 300mg can be administered intravenously.<cite>Olasveengen, Dorian</cite> Further adrenaline 1mg can be administered every 3-5 minutes, there is no further indication for anti-arrhythmic drugs during resuscitation. Continuous monitoring is required for return of spontaneous circulation or for asystole and initiation of the no-shock protocol.


====No-shock protocol====
====No-shock protocol====
When asystole or pulseless electrical activity is detected CPR should be started immediately simultaneously with 1mg intravenous adrenaline. Assess the rhythm after 2 minutes of chest compressions and continue according to the rhythm. Continue with adrenaline injections intravenously every 3-5 minutes if no return of spontaneous circulation has been achieved. There is no place for further medical intervention.  
When asystole or pulseless electrical activity is detected CPR should be started immediately simultaneously with 1mg intravenous adrenaline. Assess the rhythm after 2 minutes of chest compressions and continue according to the rhythm. Continue with adrenaline injections intravenously every 3-5 minutes if no return of spontaneous circulation has been achieved. There is no place for further medical intervention.


====Post-cardiac arrest treatment====
====Post-cardiac arrest treatment====
After cardiac arrest and return of spontaneous circulation the whole body ischemia/reperfusion affects all organ systems. Multiple organ failure, increased risk of infection, neurocognitive dysfunction and myocardial dysfunction are common problems encountered after a cardiac arrest which resembles the problems encountered with sepsis. After resuscitation strict control of oxygenation, cardiac output and glucose metabolism can improve outcome after cardiac arrest. Treatment of the underlying cause of the cardiac resuscitation, for instance a myocardial infarction should be considered. Studies have indicated that therapeutic hypothermia (32-34<sup>o</sup>C) during 12-24h after cardiac arrest can increase neurological outcome. This can be achieved by internal infusion or external cooling. Therapeutic hypothermia should be initiated in comatose patients quickly after return of circulation. When cooled the temperature should be maintained without to much fluctuations. Warming of the patient should occur very slowly (0.25<sup>o</sup>C to 0.5<sup>o</sup>C per hour) to prevent rapid plasma electrolyte concentration changes, intravascular volume and metabolic rate changes.
After cardiac arrest and return of spontaneous circulation the whole body ischemia/reperfusion affects all organ systems. Multiple organ failure, increased risk of infection, neurocognitive dysfunction and myocardial dysfunction are common problems encountered after a cardiac arrest which resembles the problems encountered with sepsis.<cite>Nolan5</cite> After resuscitation strict control of oxygenation, cardiac output and glucose metabolism can improve outcome after cardiac arrest.<cite>Balan,Nolan5,Padkin</cite> Treatment of the underlying cause of the cardiac resuscitation, for instance a myocardial infarction should be considered. Studies have indicated that therapeutic hypothermia (32-34<sup>o</sup>C) during 12-24h after cardiac arrest can increase neurological outcome.<cite>Froehler</cite> This can be achieved by internal infusion or external cooling. Therapeutic hypothermia should be initiated in comatose patients quickly after return of circulation. When cooled the temperature should be maintained without to much fluctuations.<cite>Polderman</cite> Warming of the patient should occur very slowly (0.25<sup>o</sup>C to 0.5<sup>o</sup>C per hour) to prevent rapid plasma electrolyte concentration changes, intravascular volume and metabolic rate changes.<cite>Arrich</cite>


====Prognosis after cardiac arrest====
====Prognosis after cardiac arrest====
Prognosis after cardiac arrest is difficult and cannot be fully predicted. Survival after cardiac arrest is poor, mainly due to neurological damage, and two out of three patients admitted to the ICU following cardiac arrest die from neurological injury. Most prognostic markers have been studied in the era before therapeutic hypothermia. Therefore their value in patients that are actively cooled is incompletely understood. It is not possible to predict outcome reliable within 24 hours after cardiac arrest. Clinical examination of the patient can give information on the prognosis of the patient 24 hours after cardiac arrest. After 72 hours the absence of both pupillary light and corneal reflex predict poor outcome. In patients that are not treated with therapeutic hypothermia absence of vestibulo-ocular reflexes at >24h and a Glasgow coma scale motor score of 2 or less >72 hours after return of spontaneous circulation are possible prognostic markers of a worse outcome. Furthermore myoclonal status is associated with poor outcome, but recovery can occur, and is therefore not useful in determining the prognosis. Electrophysiological studies measuring somatosensory evoked potentials (SSEP) after 24 hours, absence of bilateral N20 cortical response to median nerve stimulation predicts a poor outcome.
Prognosis after cardiac arrest is difficult and cannot be fully predicted. Survival after cardiac arrest is poor, mainly due to neurological damage, and two out of three patients admitted to the ICU following cardiac arrest die from neurological injury.<cite>Laver</cite> Most prognostic markers have been studied in the era before therapeutic hypothermia. Therefore their value in patients that are actively cooled is incompletely understood. It is not possible to predict outcome reliable within 24 hours after cardiac arrest. Clinical examination of the patient can give information on the prognosis of the patient 24 hours after cardiac arrest. After 72 hours the absence of both pupillary light and corneal reflex predict poor outcome.<cite>Zandbergen</cite> In patients that are not treated with therapeutic hypothermia absence of vestibulo-ocular reflexes at >24h and a Glasgow coma scale motor score of 2 or less >72 hours after return of spontaneous circulation are possible prognostic markers of a worse outcome.<cite>Zandbergen, Edgren</cite> Furthermore myoclonal status is associated with poor outcome, but recovery can occur, and is therefore not useful in determining the prognosis.<cite>English</cite> Electrophysiological studies measuring somatosensory evoked potentials (SSEP) after 24 hours, absence of bilateral N20 cortical response to median nerve stimulation predicts a poor outcome.<cite>Wijdicks</cite>


==Special circumstances==
==Special circumstances==
Line 71: Line 70:
=References=
=References=
<biblio>
<biblio>
# ESC isbn=9780199566990
#ESC isbn=9780199566990
# Nolan1 pmid=20956052
#Nolan1 pmid=20956052
# Koster2 pmid=20956051
#Koster2 pmid=20956051
# Deakin3 pmid=20956050
#Deakin3 pmid=20956050
# Deakin4 pmid=20956049
#Deakin4 pmid=20956049
# Soar8 pmid=20956045
#Soar8 pmid=20956045
# Atwood pmid=16199289
#Atwood pmid=16199289
# Meaney pmid=19770741
#Meaney pmid=19770741
# Waalewijn pmid=11719156
# Waalewijn pmid=11719156
# Holmberg1 pmid=11320981
# Holmberg1 pmid=11320981
# Holmberg2 pmid=9547841
# Holmberg2 pmid=9547841
# SOSKANTO pmid=17368153  
# SOSKANTO pmid=17368153
# White pmid=20026780
# White pmid=20026780
# Peberdy pmid=16784998
# Peberdy pmid=16784998
# Mejicano pmid=9841588
# Mejicano pmid=9841588
# Fingerhut pmid=10662354
# Fingerhut pmid=10662354
# Guildner pmid=1018395  
# Guildner pmid=1018395
# Ruben pmid=740619
# Ruben pmid=740619
# Niemann pmid=10381988
# Niemann pmid=10381988
Line 102: Line 101:
# Mattu pmid=12098179
# Mattu pmid=12098179
# Kornberger pmid=10488932
# Kornberger pmid=10488932
# Reuler pmid=358883  
# Reuler pmid=358883
# Zell pmid=3985447
# Zell pmid=3985447
# Pease pmid=12075060
# Pease pmid=12075060
Line 116: Line 115:
# Choo pmid=22513951
# Choo pmid=22513951
# Sheikh pmid=17620060
# Sheikh pmid=17620060
# Anthi pmid=9440561  
# Anthi pmid=9440561
# Pottle pmid=11886732
# Pottle pmid=11886732
# elBanayosy pmid=9713724
# elBanayosy pmid=9713724
Line 130: Line 129:
# Geddes pmid=3543629
# Geddes pmid=3543629
# Cooper pmid=8570929
# Cooper pmid=8570929
# Smith pmid=15071378
# Hodgetts pmid=12161291
# Bellomo pmid=20598425
# Hillman pmid=15964445
# Pellis pmid=19010581
# Glaeser pmid=8517560
# Olasveengen pmid=19934423
# Nolan5 pmid=18963350
# Thim pmid=22319249
# Guly pmid=12835350
# Balan pmid=17068310
# Padkin pmid=19460604
# Froehler pmid=17559883
# Polderman pmid=19237924
# Arrich pmid=17334257
# Laver pmid=15365608
# Zandbergen pmid=16401847
# Edgren pmid=3621954
# English pmid=19604197
# Wijdicks pmid=16864809
# Edelson pmid=16982127
# Eftestol pmid=12010909
# Dorian pmid=11907287
# IHI http://www.ihi.org/knowledge/Pages/ImprovementStories/HospitalatNightProgram.aspx
# IHI http://www.ihi.org/knowledge/Pages/ImprovementStories/HospitalatNightProgram.aspx
</biblio>

Latest revision as of 09:33, 1 November 2023

Sébastien Krul, MD, Jonas de Jong, MD

Introduction

Survival of cardiac arrest continues to be very poor. In-hospital cardiac arrest has a survival to hospital discharge of 17,6% all rhythms[1]. Out-of-hospital cardiac arrest has a worse survival with 10,7% survival to hospital discharge for all rhythms.[2] Survival is dependent on the characteristics of the cardiac arrest (rhythm), on the patient’s medical history, and the time between the cardiac arrest en start of resuscitation.[3, 4, 5] The introduction of the automated external defibrillator (AED) has dramatically increased survival of out-of-hospital cardiac arrest victims.[6, 7] In this chapter we give an overview of basic life support (BLS) and advanced life support (ALS) based on the recommendation of the European Resuscitation Council Guidelines for Resuscitation 2010.

Basic Life Support (BLS)

To increase survival after cardiac arrest it is vital to decrease the time to resuscitation.[3] The training of persons in BLS can increase bystander participation in performing cardiopulmonary resuscitation (CPR).[8] When non-arrest victims inadvertently receive CPR it is extremely rare to inflict serious harm (2% chance of a fracture)[9]. Furthermore the risk of disease transmission is extremely low, especially without high-risk activities as intravenous canulation.[10, 11] A straightforward protocol has been created to execute BLS (Figure 1).[12]



Figure 1. The basic life support algorithm.



If at any stage the patient is conscious, has normal ventilation or recovers consciousness a care provider should find out what is wrong with the person and get help if needed. Repeated reassessment is necessary to detected deterioration of the patient’s condition.

Foreign body airway obstruction

An obstruction of the airway is uncommon, but reversible and adequate recognition can prevent cardiac arrest.[13] Airway obstruction is usually related to eating. In a mild obstruction patients can cough and speak and only frequent reassessment is advised. Patients that have a severe obstruction are unable to speak and have problems breathing and coughing. If a patient is still conscious five back blows can be applied between the shoulder blades whilst the patient leans forward. Otherwise five abdominal thrusts can be applied by clenching a fist and grasping it with the other hand. Place the hands it between the rib-cage and the umbilicus and pull sharply inward and upward whilst standing behind the patients.[14, 15] If the patient loses consciousness start BLS.[12]

Basic life support in children

In general the BLS algorithm is similar in children. However, due to the differences in underlying pathology of cardiac arrest and the size of children, small changes must be incorporated. Firstly, as pulmonary causes for cardiac arrest are more frequent, the BLS can be started with 5 initial rescue breaths before starting with the chest compression. The chest compression should compress the chest at least one third of the depth. The chest compression can be performed with one or two hands for a child over 1 year and with 2 fingers for an infant under 1 year.[12]

Automatic external defibrillator (AED)

The AED is a complex device that analyses the rhythm of patients and delivers a shock to defibrillate patients. It detect whether a patient has ventricular fibrillation or a different arrhythmia. When it detects a shockable rhythm it advises the user to deliver the shock, all settings are automatically adjusted. It also remembers the course of events so that the tracing can be recovered and analysed after the resuscitation.

When the AED is attached during BLS let the AED assess the rhythm. Do not manipulate the person while the AED assesses the rhythm to prevent motion artefact disturbing the detection algorithm. Follow the instructions of the AED; this can be either a shock or no shock. After shock or non-shock immediately continue with chest compressions and rescue breaths. Continue the CPR until the AED rechecks the rhythm. Standard AED are usable for children older than 8 years, special paediatric pads and an AED paediatric mode should be used in younger children.[16]

Preventing in Hosptial Cardiac Arrest

Figure 2. An example of a MEWS. Adapted from: [17].

The best way to prevent sudden death is to early detect deterioration of a patient and to act on early warning signs.[18] Cardiac arrest is rarely unpredictable and is precipitated by a slow deterioration. An early warning score (Figure 2) helps to create consensus among care providers about the sickness of a patient.[19, 20] If the summed score reached a certain threshold, a doctor should be notified. The notified doctor should assess the patient within 30 minutes and discuss a treatment plan. If the patient does not improve within 60 minutes a reassessment should follow with possible inclusion of a medical emergency team (MET) or intensive care specialist.[21]

Advanced Life Support (ALS)

Figure 3. The advanced life support algorithm.

BLS the cornerstone to the treatment of cardiac arrest. Early and high quality CPR is critical to survival. In the hospital setting trained experts and technical equipment can facilitate cardiac arrest management. In case of a witnessed cardiac arrest caused by VT/VF in a monitored setting, three successive shocks followed by immediate CPR may be considered. If no defibrillation options are available and a precordial thump can be given in the first few seconds after the cardiac arrest.[22] It can not cause delay of the resuscitation attempt. The only intervention besides proper BLS and early defibrillation to increase survival is the administration of adrenaline.[23] The ALS protocol deviates into two strategies encountered in the setting of cardiac arrest; a shock protocol and no-shock protocol (Figure 3). During both protocols it is important to establish intravascular access as soon as possible, as an alternative intraosseous injection of drugs can be performed.[24] Furthermore assessment of airway management and ventilation is essential. Oxygen should be administered as soon as possible and be titrated to the arterial blood oxygen saturation. Tracheal intubation is the optimal method of providing and maintaining a clear and secure airway. Intubation should be performed by experienced personnel to reduce complications and delay between intubation and chest compressions. When there is return of spontaneous circulation the resuscitation team should stabilize the patient to prevent recurrence of cardiac arrest.[25, 26]

Patient assessment

During a cardiac arrest a structured assessment of the patient is required to detect the effects of the resuscitation, return of spontaneous circulation, reversible causes. To facilitate this assessment, an ABCDE approach can be used.[27, 28]
Airway: During the first step it is important to assess if the airway is clear. Airway obstruction can occur at any level. It can be caused by obstruction from the soft palate and epiglottis, blood, vomit and foreign bodies or airway oedema. It is important to look, listen and feel for airway obstruction. Look for chest and abdominal movements, listen and feel for airflow at the mouth and nose. In partial airway obstruction, the inspiration or expiration is usually noisy by an inspiratory stridor or expiratory wheeze.
Breathing: Hypoxaemia is a reversible cause and after assessment and securing the airway, ventilation of the patient should be optimized. The airway can be secured using a variety of devices and ventilation methods. Arterial blood oxygen saturation can be monitored to assess hypoxaemia. If necessary tracheal intubation, sedation and controllered ventilation should be instituted.
Circulation: Myocardial ischemia or infarction is a common cause of cardiac arrest. Furthermore before or after the cardiac arrest tachycardias or bradycardias may occur and acute management is indicated.
Disability: This step consist of determining the Glasgow Coma Scale of the patients and look for neurologic symptoms that might cause cardiac arrest. Furthermore it is important monitor glucose and temperature.
Environment: In an out of hospital cardiac arrest setting it is important to secure the environment of the cardiac arrest. There should be a safe environment for both the caregiver and the patient. The patient and environment itself might show the cause of the cardiac arrest e.g. chemical or electrical burns, drowning, anaphylactic shock, illicit drugs.

Shock protocol

When a shockable rhythm is detected, it is important to minimize the time between chest compressions and defibrillation.[29, 30] When the shock is delivered immediately resume with the chest compressions to minimize delay. Even after a successful shock the heart can be stunned and effective circulation can only be maintained through chest compressions. After the first round of shock and compressions reassess rhythm and act according to the protocol. After the third shock has been given, adrenaline 1mg and amiodarone 300mg can be administered intravenously.[23, 31] Further adrenaline 1mg can be administered every 3-5 minutes, there is no further indication for anti-arrhythmic drugs during resuscitation. Continuous monitoring is required for return of spontaneous circulation or for asystole and initiation of the no-shock protocol.

No-shock protocol

When asystole or pulseless electrical activity is detected CPR should be started immediately simultaneously with 1mg intravenous adrenaline. Assess the rhythm after 2 minutes of chest compressions and continue according to the rhythm. Continue with adrenaline injections intravenously every 3-5 minutes if no return of spontaneous circulation has been achieved. There is no place for further medical intervention.

Post-cardiac arrest treatment

After cardiac arrest and return of spontaneous circulation the whole body ischemia/reperfusion affects all organ systems. Multiple organ failure, increased risk of infection, neurocognitive dysfunction and myocardial dysfunction are common problems encountered after a cardiac arrest which resembles the problems encountered with sepsis.[26] After resuscitation strict control of oxygenation, cardiac output and glucose metabolism can improve outcome after cardiac arrest.[26, 32, 33] Treatment of the underlying cause of the cardiac resuscitation, for instance a myocardial infarction should be considered. Studies have indicated that therapeutic hypothermia (32-34oC) during 12-24h after cardiac arrest can increase neurological outcome.[34] This can be achieved by internal infusion or external cooling. Therapeutic hypothermia should be initiated in comatose patients quickly after return of circulation. When cooled the temperature should be maintained without to much fluctuations.[35] Warming of the patient should occur very slowly (0.25oC to 0.5oC per hour) to prevent rapid plasma electrolyte concentration changes, intravascular volume and metabolic rate changes.[36]

Prognosis after cardiac arrest

Prognosis after cardiac arrest is difficult and cannot be fully predicted. Survival after cardiac arrest is poor, mainly due to neurological damage, and two out of three patients admitted to the ICU following cardiac arrest die from neurological injury.[37] Most prognostic markers have been studied in the era before therapeutic hypothermia. Therefore their value in patients that are actively cooled is incompletely understood. It is not possible to predict outcome reliable within 24 hours after cardiac arrest. Clinical examination of the patient can give information on the prognosis of the patient 24 hours after cardiac arrest. After 72 hours the absence of both pupillary light and corneal reflex predict poor outcome.[38] In patients that are not treated with therapeutic hypothermia absence of vestibulo-ocular reflexes at >24h and a Glasgow coma scale motor score of 2 or less >72 hours after return of spontaneous circulation are possible prognostic markers of a worse outcome.[38, 39] Furthermore myoclonal status is associated with poor outcome, but recovery can occur, and is therefore not useful in determining the prognosis.[40] Electrophysiological studies measuring somatosensory evoked potentials (SSEP) after 24 hours, absence of bilateral N20 cortical response to median nerve stimulation predicts a poor outcome.[41]

Special circumstances

In all circumstances the normal protocol for BLS and ALS is the cornerstone in the treatment of cardiac arrest. However some conditions encountered during resuscitation or as a cause of cardiac arrest, can affect the procedure.[42]

  • Anaphylaxis: Anaphylaxis is a life-threatening hypersensitivity reaction and can be accompanied by airway/breathing/circulation problems due to swelling of the mucosa.[43] The cause of the anaphylaxis should be identified and can be a broad range of triggers (food, insects, drugs etc.).[44] Anaphylaxis rapidly develops after exposure to the trigger, usually within minutes. Patients should receive intramuscular adrenaline before an intravenous route is established and anti-inflammatory drugs (steroids, anti-histamines) should be initiated.[44, 45, 46, 47] Oxygen en fluids should be administered as swelling of the airway can result impair breathing and due to fluid loss is out of the circulation hypovolaemia can develop.
  • Asthma: Patients with asthma who experience a cardiac arrest usually have a long period of hypoxaemia, however cardiac arrest is not necessarily related to asthma severity.[48] Patients with acute severe asthma require oxygen, aggressive medical therapy and should be admitted to the critical care area. The main troubles encountered in the resuscitation of patients with asthma relates to the underlying lung disease. In general increased lung resistance makes ventilation of these patients difficult and can increase the risk of gastric inflation.[49] Early intubation is indicated in these patients during the ALS setting. Due to the hyperinflation of the lungs more energy might be required in defibrillating these patients, as the heart is isolated by air.[50]
  • Cardiac arrest after cardiac surgery: Cardiac arrest after cardiac surgery is usually caused by specific causes related as a consequence of the cardiac surgery, such as tamponade, hypovolaemia, myocardial ischaemia, tension pneumothorax, or pacing failure.[51] Early resternotomy can be the key to survival, especially after repeated defibrillation has failed or if asystole is observed.[52, 53, 54] When the sternum is opened internal cardioversion (output of 5-20J) and cardiac compression can be applied across the ventricles.
  • Drowning: Drowning is a common cause of accidental death.[55] There are no differences between victims of salt water and fresh water drowning. Correction of hypoxia is critical in the outcome of these victims as cardiac arrest is a consequence of the hypoxia. Care should be taken to start immediate resuscitation and restore oxygenation, ventilation and perfusion. During BLS it is recommended to start the BLS with 5 rescue breaths.[56] Rescue breathing is difficult after drowning due tot the presence of fluid in the airway and the high inflation pressure required after drowning. Furthermore regurgitation is common and removal of the regurgitated material during resuscitation is required.[57] It is common for hypothermia to be present in victims of drowning, complicating the resuscitation attempt. After return of spontaneous circulation, pneumonia is common and patients are prone to develop acute respiratory distress syndrome (ARDS).[58, 59]
  • Electrocution: Electrocution can result in multi-system injury and usually occur in the workspace in adult or at home in children. The direct effects of an electric shock on tissues, for instance paralysis of the respiratory system or muscles, VF in the myocardium, ischemia due to coronary artery spasm or asystole can result in a cardiac arrest.[60] Electrical burns can complicate the resuscitation and care should be taken to avoid further complications resulting from these burns. Adequate fluid therapy is required if there is significant tissue destruction. Due to electrical burns around the neck and muscular paralysis early intubation and prolonged ventilatory support may be required.[61]
  • Electrolyte disorder: Electrolyte abnormalities are among the most common causes of cardiac arrhythmias. Potassium disorders are commonly seen, especially hyperkalaemia has a high risk of malignant arrhythmias.[62] During cardiac arrest treatment of these abnormalities is no different than in the normal clinical setting, and aggressive treatment of the electrolyte disorder should be initiated.[63, 64]
  • Hyperthermia: Exogenous or endogenous hyperthermia can result in heat stress, progressing to heat exhaustion and results in heat stroke.[65] Heat stress can provoke edema, syncope and cramps and is treated with rest, cooling and oral rehydration and salt replacement. Heat exhaustion is a systemic reaction to prolonged heat exposure and is accompanied by headaches, dizziness, nausea, vomiting, tachycardia, hypotension, muscle pain, weakness and cramps. Treatment is similar as in a heat stroke, but active cooling might be required in severe cases with ice packs or cold intravenous fluids. Heat stroke is a systemic inflammatory response with a core temperature above 40,6oC. It can lead to varying levels of organ dysfunction accompanied by mental changes.[66] It can occur during high environmental temperatures or during strenuous physical exercise in high environmental temperatures. Rapid cooling of the victim should occur as soon as possible.[67] Patients with heat-stroke usually have electrolyte abnormalities and hypovolaemia.
  • Hypothermia: In hypothermia (<35oC) it is difficult to detect signs of life. Therefore resuscitation should proceed according to standard protocols until the patient has reached normothermia. Second to resuscitation, warming of the body temperature by passive or active external and internal methods should be started. Examples of passive rewarming are drying and insulation of the body, whilst examples of active rewarming are infusion of warmed intravenous fluids or forced air rewarming.[68, 69, 70] As a result of rewarming vasodilatation occurs and fluid administration may be required. Resuscitation during hypothermia is difficult, the thorax is stiff and the heart is less responsive to medication and defibrillation. Furthermore drug metabolism is slowed, resulting in increased plasma levels of medication.[71] Medication should be administered at double intervals in patients <35oC and withheld in patient <30oC. Rhythm disturbances usually seen at rewarming after hypothermia are bradycardia, atrial fibrillation, VF and asystole. Bradycardia and atrial fibrillation revert to normal sinus rhythm as the core body temperature increases.[72]
  • Poisoning: Accidental poisoning in children or by therapeutic or recreational drugs in adults are the main causes of poisoning, however rarely causes cardiac arrest.[73] It is important to identify the poison to start antidote treatment or decontamination.[74] During the BLS and ALS care should be taken when performing mount-to-mouth ventilation in the presence of certain chemical types of poisoning. Respiratory arrest and airway depression is more common after poisoning.[75] Early intubation can prevent cardiac arrest and pulmonary aspiration. When confronted with a poisoning in an ALS setting, temperature should be monitored as hypo- or hyperthermia my occur after drug overdose. Furthermore, due to the slow metabolization or excretion of certain poisons the resuscitation can continue for a long period.
  • Pregnancy: If a cardiac arrest occurs during pregnancy the safety of the fetus should always be considered. Due to the growth of the uterus compression of the inferior vena cava can occur and as a result venous return and cardiac output is compromised. During CPR displace the uterus to the left or apply a left lateral tilt of the surface the patient is lying upon to minimize compression from the uterus.[76] Furthermore the increased abdominal pressure can increase the risk of pulmonary aspiration and can hamper proper ventilation; therefore early intubation can lower risks and ease cardiopulmonary resuscitation. During ALS normal defibrillator shock energies can be used.[77] An emergency hysterotomy or cesarean section needs to be considered, if gestational age is after 20 weeks.[78] After 20 weeks the size of the uterus is large enough to compromise cardiac output, however fetal viability begins at approximately 24-25 weeks.[79]
  • Traumatic Cardiorespiratory Arrest: Cardiac arrest caused by trauma has low chance of survival.[80] Blunt trauma can cause commotio cordis if there is an impact to the chest wall over the heart.[81] This impact can cause arrhythmias (usually ventricular fibrillation) and occurs often during sports.[82] Penetrating trauma can be cause for an emergency thoracotomy. Emergency thoracotomy has to be performed early after onset of CPR.[83] It is important to manage the resuscitation according to protocol and treat reversible causes.

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