Cardiac arrest, cardiopulmonary resuscitation (CPR) and advanced cardiac life support (ACLS)

 

Cardiac arrest, cardiopulmonary resuscitation (CPR) and advanced cardiac life support (ACLS)



Cardiac arrest is the cessation of effective circulation and is characterized by:

Unresponsiveness (the patient is unconscious and totally unresponsive)
Pulselessness (there is no palpable carotid or femoral pulse)
Little to no respiratory effort (the patient usually is not breathing at all, or has only ineffective agonal respirations, i.e. slow, irregular, shallow gasping respirations that may persist for a few minutes).

Note: Agonal breathing involves slow, irregular short gasps of air (“shallow half-breaths” which often sound like snoring or gasping) while the patient is unconscious and unresponsive. Agonal breathing occurs in approximately 40% of sudden cardiac arrest cases. It is caused by the lower brainstem getting deprived of oxygen and producing an involuntary breathing reflex as a result of this hypoxic stimulus. It is essential not to mistake agonal breathing for real breathing and respond promptly to cardiac arrest victims in need, by starting immediately basic life support (BLS).
Other emergencies that can cause agonal breathing include ischemic stroke involving the brainstem and hemorrhagic stroke. These situations involve restricting blood flow to the brain and this stimulates an involuntary agonal respiration reflex.

If corrective measures are not taken rapidly (such as cardiopulmonary resuscitation-CPR and defibrillation as early as possible in the presence of a shockable rhythm), sudden cardiac arrest progresses to sudden death.

Recognition of cardiac arrest 

By the lay rescuer: 
If a victim is unconscious and unresponsive,
with absent or abnormal breathing (ie, only gasping), the lay rescuer should assume the victim is in cardiac arrest ask for help (alert the emergency medical service) and begin CPR immediately
By a healthcare professional:  
If a victim is unconscious and unresponsive, with absent or abnormal breathing (ie, only gasping), the healthcare provider should check for a (carotid) pulse for 5-10 seconds (not more than 10 seconds). If no definite pulse is felt, the healthcare provider should assume the victim is in cardiac arrest, ask for help (alert the emergency medical service) and begin CPR immediately.

Epidemiology and prognosis of cardiac arrest

Epidemiology and prognosis: 60% of cardiac arrests occur out of the hospital and the overall mortality is 90% (10% survival rate) In the case of out-of-hospital cardiac arrests witnessed by bystanders capable of performing CPR survival rate is about 20%. In-hospital cardiac arrests have an overall survival rate of about 20-30%. The incidence of sudden cardiac arrest increases with age and it is more common in men (57% of the cases).

The cardiac rhythm on presentation is:
● A shockable rhythm in about 25 % of the cases (a cardiac rhythm that can respond to an electric shock delivered by a defibrillator, such as ventricular fibrillation-VF or ventricular tachycardia –VT). In this situation, the survival rate is > 30%.
● A non-shockable cardiac rhythm in about 75% of the cases, such as asystole or pulseless electrical activity (PEA). In these cases, the prognosis is much worse, with a survival rate of about 10%.

Cardiac rhythm in victims of cardiac arrest

Shockable cardiac rhythms include:
●Ventricular fibrillation (VF). VF is characterized by rapid and irregular ventricular electrical activity which renders the ventricles unable to contract in a synchronized manner, resulting in immediate loss of cardiac output. The ECG monitor shows chaotic irregular deflections of varying amplitude and no identifiable P waves, QRS complexes, or T waves. The amplitude of these fast and completely irregular waves decreases with duration (initial coarse VF with large waves progresses to fine VF with waves of small amplitude and ultimately the rhythm will degenerate into asystole, due to progressive depletion of myocardial energy stores).
                     
Coarse VF



                                                                                                                                         
Fine VF



●Pulseless ventricular tachycardia (pulseless VT)
Pulseless VT is a very rapid tachycardia with wide QRS complexes (> 120 milliseconds) that can be monomorphic (no variation of the QRS from beat to beat) or polymorphic ( QRS changes from beat to beat). The most common cause of pulseless ventricular tachycardia is cardiac ischemia. In pulseless VT the rapid ventricular contractions, result in a markedly decreased ventricular filling, leading to a dramatic decrease in cardiac output. As a result, a pulse is absent.

                                 
monomorphic VT

                                               
                           Polymorphic VT torsade de pointes (French for "twisting of the points", a type of polymorphic Ventricular Tachycardia).
                                                                                           
                                                                            
A non-shockable rhythm is 
either
●Asystole ( absent cardiac electrical activity with a straight line displayed on the monitor)
or
●Pulseless electrical activity (PEA)
PEA ( previous term electromechanical dissociation) is characterized by unresponsiveness and the lack of a palpable carotid pulse in the presence of organized cardiac electrical activity. In PEA the monitor shows an organized cardiac rhythm which may be a supraventricular rhythm (sinus or non-sinus) or a ventricular rhythm (accelerated idioventricular rhythm or a ventricular escape rhythm) but there is no effective cardiac contraction and this results in the absence of effective circulation and thus the absence of a palpable pulse.
                                                

Factors affecting survival:

Initial rhythm
Time from the moment of cardiac arrest to the beginning of cardiopulmonary resuscitation-CPR)
Time to first defibrillation attempt (in the presence of a shockable cardiac rhythm)
Total time that the patient is in the state of cardiac arrest
Age of the victim and underlying cause of cardiac arrest

Causes of cardiac arrest:


●Coronary artery disease (the most common cause) 
Cardiac arrest may occur in acute myocardial ischemia (acute coronary syndrome) or in patients with chronic ischemic cardiomyopathy due to a previous myocardial infarction.

●Cardiomyopathies (hypertrophic cardiomyopathy, arrhythmogenic cardiomyopathy-ARVC, dilated cardiomyopathy)

●Valve disease (especially severe aortic stenosis/ very rarely mitral valve prolapse)

●Electrical conduction abnormalities (disorders of cardiac ion channels such as long QT syndrome, short QT syndrome, Brugada syndrome, catecholaminergic ventricular tachycardia/ Wolff- Parkinson- White syndrome due to the presence of an accessory pathway with the capability of rapid conduction between the atria and the ventricles)

●Cardiac tamponade

Non-cardiac etiologies of cardiac arrest:

●Metabolic disorders (especially severe electrolyte abnormalities)

●Toxic ingestions (ingestion of some toxic substances or drug overdose can induce cardiac arrest)

●Acute pulmonary embolism,

●Tension pneumothorax

●Severe infection (sepsis)

●Trauma with massive hemorrhage and circulatory shock

●Intracranial hemorrhage

●Hypothermia

● Electrocution

●Severe hypoxemia

●Primary respiratory arrest 
(Primary respiratory arrest can be due to a central nervous system disorder, adverse drug effect such as opioid overdose, upper airway obstruction due to a foreign body, unconsciousness, and loss of muscular tone leading to the displacement of the posterior portion of the tongue to occlude the oropharynx, pharyngolaryngeal inflammation in acute anaphylaxis, croup, epiglottitis, laryngeal trauma/ lower airway obstruction due to severe bronchospasm, airspace filling disorders (eg, pneumonia, pulmonary edema, pulmonary hemorrhage, drowning).

Respiratory arrest and cardiac arrest are conditions that without prompt and effective treatment, inevitably one will lead to the other.

Initial treatment (resuscitation) of the patient with cardiac arrest


If a person is unconscious with absent breathing or abnormal breathing, alert the emergency medical services (EMS) immediately. A lone bystander with a mobile phone should dial the EMS number, and use a hands-free option (such as the speaker) on the mobile phone and immediately start cardiopulmonary resuscitation (CPR).
Ensure that the scene is safe before approaching the patient.

Chest compressions should be started as soon as possible with the cardiac arrest victim lying on a firm surface whenever feasible. Chest compressions are delivered on the lower half of the sternum.
The heel of one hand is placed on the center of the patient’s chest ( on the lower half of the sternum) and the heel of the other hand
on top of the first. Thus, the hands are overlapped.
Compression depth should be at least 5 cm (2 inches) but not more than 6 cm and compression rate 100-120/ min, with as few interruptions as possible. Allow the chest to recoil completely after each compression. This will allow for the heart to adequately refill with blood between compressions. If possible, rotate the person providing chest compressions every 2-4 minutes (ideally every 2 minutes) to avoid fatigue. Rescuer fatigue could result in suboptimal depth and rate of the chest compressions delivered.


The technique of chest compressions in basic life support (BLS)



Rescue breaths 
Every 30 chest compressions should be followed by 2 rescue breaths and this sequence (30:2) is continued. Airway patency should be maintained using the head tilt-chin lift or the jaw thrust maneuver and any visible foreign bodies in the oral cavity should be removed. The head tilt-chin lift maneuver is used to maintain an open airway when trauma is not suspected, whereas if trauma is suspected use the jaw thrust maneuver to open the airway, in order to avoid moving the cervical spine. For a description of these maneuvers see chapter Emergency airway management and ventilation procedures.
To deliver rescue breaths use a bag-mask device (connected to an oxygen source if available), or a pocket mask, or mouth to mouth technique. When using a mask (a bag-mask device), an airway adjunct (eg, oropharyngeal and/or nasopharyngeal airway) in unconscious patients with no cough or gag reflex can be useful to maintain upper airway patency. An oral airway is preferred
compared with a nasopharyngeal airway when a basal skull fracture is suspected or in a patient with a significant coagulopathy.
 Each rescue breath should be delivered over 1 second with sufficient tidal volume to result in a visible chest rise. Note that you should provide a rescue breath until there is a visible chest rise avoiding over-ventilation (excessive ventilations), which can be harmful.
When providing CPR without an advanced airway, pause compressions (each time a sequence of 30 compressions has been completed) to deliver 2 breaths, each given over 1 second.

cardiopulmonary resuscitation  (CPR)- rescue breaths-emergency medicine book
Rescue breaths: Mouth to mask technique


If you are unable to provide ventilations, give only continuous chest compressions. Although ventilation with rescue breaths is important, not everyone is willing to perform mouth-to-mouth breathing due to concerns over infectious disease transmission. Chest compressions alone can be effective and should be performed even if rescue breaths are not being delivered.
If the cardiac arrest victim is not intubated, with a single rescuer or with two rescuers two ventilations (rescue breaths) should be given after every 30 compressions. 
In the case of a patient with an advanced airway in place (laryngeal mask airway-LMA or endotracheal tube) and two rescuers, ventilations should be given at a rate of 8 - 10 /minute, without interrupting chest compressions. (Approximately one breath every 6 seconds). Using quantitative waveform capnography during cardiopulmonary resuscitation in intubated patients is recommended by the  2020 AHA Guidelines for ACLS. The purpose of using waveform capnography is to monitor CPR quality (optimize the effectiveness of chest compressions), and also to detect the return of spontaneous circulation (ROSC) during chest compressions. For more information about capnography see Note 3, below.

If a defibrillator (either an automatic external defibrillator-AED, or a manual defibrillator) is available, use it promptly (after at least 1-2 minutes of CPR) to assess the underlying cardiac rhythm and to provide a shock (defibrillation) if a shockable rhythm (VF or pulseless VT) is identified.
 Turn on the defibrillator, connect the defibrillator pads, and the monitor to the patient and assess the patient’s cardiac rhythm. If there is a shockable rhythm, do not delay defibrillation to provide additional CPR once the defibrillator is ready. The general rule is that defibrillation should be performed as soon as possible in the case of a shockable rhythm. In this case, ensure that nobody touches the patient and give an asynchronous electric shock. The first shock should be of an energy 120-200 J if the defibrillator delivers a biphasic shock, or 360 J in the case of an older generation defibrillator that delivers a monophasic shock). Immediately resume CPR after defibrillation (don’t pause to check the cardiac rhythm).
After 2 minutes of CPR check the rhythm. Defibrillate again, if needed (if a shockable rhythm persists) using a higher energy level. When using a defibrillator, provide five cycles (or 2 min) of CPR between rhythm checks. Interruptions in chest compressions to check for the rhythm and for return of spontaneous breathing and carotic pulse should not last more than 10 seconds. Checking for the pulse should last not less than 5 seconds but also not more than 10 seconds, and at the same time (concomitantly) check for the return of spontaneous breathing.

Drug administration in cardiac arrest and advanced life support (ALS)

While CPR is continuously performed, another rescuer should establish a route for drug and fluid administration ( a peripheral –usually antecubital- intravenous catheter). If an intravenous (IV) line cannot be placed then the intraosseous (IO) route is used. New evidence suggests that the IO route may be less efficient compared with the IV route. Therefore, providers should first attempt establishing IV access for drug administration in cardiac arrest. The IO route may be considered if attempts at IV access are unsuccessful or not feasible. Drug administration by central venous access (by internal jugular, subclavian or femoral vein) may be considered
by skilled physicians (well trained and experienced in these techniques) when other access routes are not available. Although central venous access may achieve more rapidly, higher drug concentrations than peripheral IV, it takes more time and skill to perform. ( Also see chapter Peripheral and central venous cannulation technique ). Endotracheal drug administration may be used when all other access routes are not available but it is regarded as the least-preferred option because it is associated with lower drug concentrations.

The administration of adrenaline (epinephrine) is important in cardiac arrest because, in 2 randomized clinical trials, epinephrine increased return of spontaneous circulation (ROSC) and survival.
For adult patients in cardiac arrest with a shockable rhythm administer adrenaline (epinephrine) 1 mg IV (or IO) after the third shock. ( 1 amp of 1 mg adrenaline is drawn into a syringe and normal saline is added so that the total volume of the solution is 10 ml -1:10.000 adrenaline solution). Immediately after giving IV adrenaline also administer a 20 ml IV push of normal saline.
During continued advanced life support (ALS) repeat adrenaline 1 mg IV (or IO) every 3-5 minutes. 
Give amiodarone 300 mg IV (or IO) for adult patients in cardiac arrest who are still in ventricular fibrillation (VF) or pulseless ventricular tachycardia (pulseless VT) after three shocks have been administered. Amiodarone should only be used after defibrillation and adrenaline (epinephrine) have failed to convert VT or VF.
A further dose of amiodarone 150 mg IV (or IO) should be administered to adult patients in cardiac arrest who are in VF or pVT after five shocks have been administered.

For adult patients in cardiac arrest with a non-shockable rhythm, adrenaline should be administered as soon as possible 1 mg IV ( or IO) as soon as possible and repeated (1 mg adrenaline IV or IO) every 3-5 minutes. Studies indicate that the administration of adrenaline with concurrent high-quality CPR improves survival, particularly in patients with non-shockable rhythms.
In patients with a non-shockable rhythm besides CPR and adrenaline administration, also identification and treatment of any correctable cause of cardiac arrest is essential. In these cases, cardiac arrest generally results from a major cardiovascular, respiratory, or metabolic derangement. Such causes include hypovolemia, hypothermia, hypoxia, hypokalemia,  hyperkalemia, acidosis, severe hypoglycemia, tension pneumothorax, cardiac tamponade, thrombosis (pulmonary embolism or acute myocardial infarction), toxins, trauma.
For the treatment of cardiac arrest, routine administration of calcium, sodium bicarbonate, or magnesium is not recommended.


Note: 1
During CPR, interruptions of chest compressions should be minimal (about 5-10 seconds when checking for the carotid pulse and for return of spontaneous respiration). For the delivery of a defibrillator shock, the pause should also be minimized, at about 5 seconds, and this is achieved by continuing chest compressions while charging the defibrillator, stopping compressions to deliver the shock, and starting again the compressions immediately after.

Note 2. 
Airway management in ACLS
After the initiation of CPR and the ALS sequence, if possible consider the progression from simple airway management (head tilt-chin lift or jaw thrust maneuver often with the placement of an oropharyngeal/ and or nasopharyngeal airway with bag-mask ventilation combined with the administration of oxygen) to more advanced airway management (such as a laryngeal mask airway -LMA or an endotracheal tube). (For techniques of airway management see chapter Emergency airway management and ventilation procedures.)  This can be considered when a rescue team member, trained and experienced with these techniques is present. In an attempt for endotracheal intubation (performed only by a well-trained and experienced rescuer) do not interrupt chest compressions for more than 10 seconds.

Note 3. 
The 2020 AHA Guidelines for ACLS recommend using quantitative waveform capnography in intubated patients during CPR. Waveform capnography along with clinical assessment is the preferred method for confirming and monitoring correct placement of an endotracheal tube. It also aids in the assessment of CPR quality (optimization of chest compressions), and detect ROSC (return of spontaneous circulation) during chest compressions. Capnography is a technique that measures expired carbon dioxide (CO2) which is a metabolic product transferred to the lungs via blood perfusion. The inhaled and exhaled carbon dioxide is graphically displayed on the monitor as a waveform along with its corresponding numerical measurement. The measurement obtained is end-tidal carbon dioxide (ETCOor PetCO2). ETCO2is the level of carbon dioxide that is released at the end of an exhalation. ETCO2 levels reflect the adequacy with which carbon dioxide (CO2) is carried in the blood back to the lungs and also the adequacy with which it is exhaled by the lungs. For this reason, capnography can directly assess ventilation in the lungs, and it also indirectly measures metabolism and circulation. For example, a decrease in perfusion (cardiac output) will lower the delivery of carbon dioxide to the lungs. This will cause a decrease in the ETCO2 (end-tidal CO2). A decrease in ventilation will cause a reduction in the ability of the lungs to exhale CO2 also resulting in a decrease in the ETCO2Normal ETCO2 in the adult is 35-45 mmHg.
During CPR in an intubated patient, a low ETCO2 value (< 10 mmHg) is an indication that the quality of chest compressions needs improvement. High-quality chest compressions are achieved when the ETCOvalue during CPR is at least 10-20 mmHg.
When ROSC occurs, this will cause a significant increase in the ETCO2 (35-45 mmHg). This is due to a drastic improvement in blood flow (more COis delivered to the lungs by the circulation).

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