You are on page 1of 18

Cardio Pulmonary Resuscitation

Internal and critical care medicine study notes

Dr. Ali Ragab


Critical Care Medicine
Damanhur Medical National Institute
Facebook (ali_ragab_ali@yahoo.com)
Cardio Pulmonary Resuscitation
Internal and critical care medicine study notes

Dr. Ali Ragab

Critical Care Medicine

Damanhur Medical National Institute

Facebook (ali_ragab_ali@yahoo.com)

Dr. Ali Ragab 2


Basic Life Support (BLS)

Commencement of cardiopulmonary resuscitation

The current BLS guidelines recommend that CPR be commenced if the victim is
unresponsive and not breathing normally
An appropriately trained ALS provider can check for a central pulse (e.g.
carotid) for up to 10 seconds during this period of assessment, but this should
not delay CPR
It is now recommended that CPR should start with compressions

External cardiac compression

Site of compression

The desired compression point for CPR in adults remains over the lower half
of the sternum
Compressions that are provided higher than this become less effective, and
compressions lower than this are also less effective and have an increased risk
of damage to intra abdominal organs

Rate of compression

It is recommended that chest compressions should be performed at a rate of


approximately 100 compressions/min
Lower rates (<80/min) were associated with worse outcomes
Higher rates (>120/min) were associated with more fatigue, and shallower
compressions

Depth of compression

The recommended compression depth for adults is now at least 5 cm; the chest
should be compressed approximately one-third of its depth

Dr. Ali Ragab 3


Minimise interruptions to compressions

Interruptions in chest compressions (hands-off time) are common, often


prolonged, and are associated with a decrease in coronary perfusion pressure
and a deceased likelihood of defibrillation success
These adverse effects commence within 10 seconds of stopping CPR, but appear
to be at least partially reversible with the recommencement of chest
compressions
It is recommended that chest compressions be commenced as soon as the
victim is confirmed to be unresponsive and not breathing normally
The frequency and duration of interruptions in compressions for rhythm
recognition or specific interventions (such as ventilations, charging the
defibrillator, defibrillation, or intubation) should be kept to a minimum

Compression/Ventilation ratio

A single compression/ventilation ratio of 30/2 remains recommended for adult


BLS before the airway is secured
The tidal breath should be delivered within 1 second
The desired tidal volume to be delivered is one that results in a visible chest rise

Monitoring the quality of CPR

Simple monitoring techniques include

Observing of the rate, depth and positioning of chest compressions


Observing the rate and depth of ventilation
Palpating central pulses
Waveform capnography should be considered for all arrests

Additional monitoring techniques that can be used include

Mechanical devices (e.g. For monitoring the depth of compressions)


Monitor/defibrillators (e.g. for monitoring the depth and rate of compressions
and ventilation)

Dr. Ali Ragab 4


Utility of end-tidal carbon dioxide monitoring during cardiac arrest

Cardiovascular (absolute value of ETCO2)

Falls immediately at the onset of cardiac arrest


Increases immediately with chest compressions
Provides a linear correlation with cardiac index
Allows early detection of ROSC (sudden increase)

Respiratory (ETCO2 waveform)

Allows assessment of endotracheal tube placement


Allows assessment of expiratory flow limitation

Prognosis (absolute value of ETCO2)

Predicts successful resuscitation

Compression-only CPR

Despite the limited data to support compression-only CPR, it is recommended


that if rescuers are unable, not trained, or unwilling to perform mouth-to-
mouth ventilation (rescue breathing) then they should perform compression
only CPR, as any attempt at resuscitation is better than no attempt

Defibrillation

Defibrillation remains the definitive treatment for shockable rhythms such as


pulseless ventricular tachycardia or ventricular fibrillation
Successful defibrillation requires an appropriate combination of defibrillator
waveform and energy level

Dr. Ali Ragab 5


Early defibrillation Vs CPR before defibrillation

The traditional approach to the treatment of a shockable rhythm during cardiac


arrest has been to perform defibrillation as soon as possible
In the scenario of recent-onset VF, and the best outcomes are associated with
defibrillation within 3 minutes (e.g. in electrophysiology labs or coronary care
units)
In situations where the VF has persisted for more than a few minutes, an initial
period of CPR could be considered before defibrillation

Waveform for defibrillation

No specific defibrillator waveform (either monophasic or biphasic) is


consistently associated with a greater incidence of return of spontaneous
circulation (ROSC) or increased hospital discharge rates from cardiac arrest due
to ventricular fibrillation
Defibrillation with biphasic waveforms using equal or lower energy levels,
appears at least as effective as monophasic waveforms for termination of VF

Energy levels

Recommendations for energy levels to be used for defibrillation vary according


to the type of defibrillator that the rescuers are using
The recommended energy level for defibrillation in adults where monophasic
defibrillators are used is 360 J for all shocks
When using biphasic waveforms, the energy level should be set at 200 J for all
shocks unless there exist relevant clinical data for the specific defibrillator
suggesting that an alternative energy level provides adequate shock success
There is no consistent evidence (e.g. survival benefit) to suggest that an
escalation of energy levels is required for subsequent shocks

Dr. Ali Ragab 6


Manual defibrillation or automated external defibrillator

Automated external defibrillators provide an opportunity for untrained


bystanders and BLS providers to defibrillate a shockable rhythm
In the hands of skilled healthcare providors, manual defibrillation should be
used whenever possible as the delays inherent in the use of an AED may be
detrimental

Single-shock technique

The use of a single-shock strategy for defibrillation is recommended (i.e.


delivers a single shock and then immediately commences CPR)
This strategy minimises the interruptions to chest compressions that occur
during defibrillation attempts
The Australian Resuscitation Council recommends the consideration of a
stacked shock strategy (up to three shocks as necessary) in specific
circumstances: patients with a perfusing rhythm who develop a shockable
rhythm, in a witnessed and monitored setting, where a manual defibrillator is
immediately available (e.g. first shock able to be delivered within 20 seconds)
and the time required for rhythm recognition and charging of the defibrillator
is short (e.g. <10 seconds). All subsequent shocks should be given using a
single-shock strategy

Pads or paddles

Self-adhesive defibrillation pads are safe and effective for defibrillation, can
facilitate pacing and allow charging during compressions
If there are concerns about contact or success of defibrillation, then paddles can
be used, but they require the use of conductive gel pads and the application of
sufficient firm pressure to maximise electrical contact

Dr. Ali Ragab 7


Advanced life support

Precordial thump

A precordial thump may be considered in a pulseless ventricular tachycardia if a


defibrillator is not immediately available
The technique should not delay defibrillation.
A precordial thump is no longer recommended for ventricular fibrillation

Chest compressions

Interruptions to chest compressions for definitive procedures or interventions


should be kept as brief as possible
Chest compressions should be continued up until defibrillation, including
during charging of the defibrillator
CPR should also be commenced again immediately following defibrillation
(without checking the rhythm), and continued for at least 2 minutes unless
signs of life return (the victim becomes responsive or starts breathing)
Even if defibrillation has successfully reverted the rhythm into one that could
generate a pulse, in the vast majority of cases this is not initially associated with
an output. Immediate compressions in these situations avoid the detrimental
effects of prolonged interruptions in compressions and maintain the coronary
perfusion
After each 2 minutes of CPR (or if signs of life return), the underlying rhythm
should be checked, and if a rhythm compatible with a return of spontaneous
circulation is observed at that time then a central pulse should also be checked

Dr. Ali Ragab 8


Airway management during CPR

Endotracheal intubation remains the gold standard for airway maintenance


and airway protection during CPR
The endotracheal tube provides optimal isolation and patency of the airway,
allows suctioning of the airway and also provides access for the delivery of some
drugs (e.g. epinephrine (adrenaline), lidocaine and atropine)
Attempts at endotracheal intubation should not interrupt cardiac compressions
for more than 20 seconds
A large number of supraglottic airway devices have been trialled as
alternatives to the endotracheal tube

Ventilation during CPR

Before the airway is secured; a compression/ventilation ratio of 30/2 is


recommended
After the airway is secured; a ventilation rate of 810/minute is
recommended; one way to provide this, and to minimise interruptions to
compressions is to use a compression/ventilation ratio of 15/1 once the airway is
secured

Avoid hyperventilation

Hyperventilation during cardiac arrest is associated with increased


intrathoracic pressure, decreased coronary and cerebral perfusion
If there is a concern about potential gas trapping, a period of disconnection
from the ventilation circuit may be beneficial
The tidal volume recommended is one that results in a visible chest rise

Dr. Ali Ragab 9


Identification of reversible causes

Consider and correct

1. Hypoxia
2. Hypovolaemia
3. Hyper/hypokalaemia/metabolic disorders
4. Hypothermia/hyperthermia
5. Tension pneumothorax
6. Tamponade
7. Toxins
8. Thrombosis (pulmonary/coronary)

Diagnosis

A number of techniques are available to assist in the diagnosis and exclusion of


these conditions. These include a good history, a careful clinical examination,
and some specific investigations and interventions
Echocardiography can potentially diagnose (or help exclude) a number of
cardiac and non-cardiac reversible causes

Potentially useful diagnoses detectable by echocardiography

Hypovolaemia
Tamponade (pericardial)
Tension pneumothorax
Thrombosis (pulmonary)
Thrombosis (coronary) (regional or global wall motion abnormalities, including
lack of cardiac motion)
Pacemaker capture
Unexpected VF
Acute valvular insufficiency (e.g. papillary muscle rupture)
Ventricular rupture
Aortic dissection
Massive pleural effusion

Dr. Ali Ragab 10


Medications during CPR

Route of administration

The intraosseous route should be considered for administration of medications


if venous access is not immediately available

Vasopressors

The beneficial effect of vasopressors during cardiac arrest is to increase the


perfusion pressure to the heart and brain
Epinephrine remains the vasopressor of choice during the management of
cardiac arrest
The initial adult dose is 1 mg and this should be repeated approximately every
4 minutes

Anti-arrhythmics

Administration of amiodarone (300 mg or 5 mg/kg) for shock refractory


ventricular fibrillation
Either amiodarone or lidocaine (but not both) should be considered in those
patients still in ventricular fibrillation after repeated attempts at defibrillation
have failed (i.e. immediately after the third shock)

Dr. Ali Ragab 11


Cardiac arrest medications in specific circumstances

Medication Potential indications


Atropine Cholinergic/cardiac glycoside toxicity
Anti-venom Snake, funnel-web spider, box jellyfish venom
Benzodiazepines Sympathomimetic toxicity
Calcium Hypocalcaemia, hypermagnesaemia,
hyperkalaemia, beta-blocker/calcium channel
blocker toxicity
Digoxin-specific antibodies Cardiac glycoside toxicity
Flumazenil Benzodiazepine toxicity
Epinephrine Beta-blocker/calcium channel blocker toxicity
Glucagon Beta-blocker/calcium channel blocker toxicity
High-dose insulin/dextrose Beta-blocker/calcium channel blocker toxicity
Lipid emulsion Local anaesthetic agents
Magnesium Hypomagnesaemia, hypokalaemia,
hypercalcaemia, tricyclic antidepressant/cardiac
glycoside toxicity, torsade de pointes
Naloxone Opioid toxicity
Potassium Hypokalaemia
Pyridoxine Isoniazid toxicity
Sodium bicarbonate Hyperkalaemia, tricyclic antidepressant/sodium-
channel-blocker toxicity

Adjuncts to CPR

Active-compression decompression (ACD) CPR is the most widely evaluated


technique
Mechanical devices (such as LUCAS or the load distributing band) may be
useful alternatives to manual CPR in situations where traditional CPR is
difficult or hazardous (e.g. during transport, or during interventions)

Dr. Ali Ragab 12


Management of the resuscitated post cardiac arrest patient

Pathophysiology

Post cardiac arrest brain injury

Accounts for a large portion of morbidity and mortality in resuscitated cardiac


arrest patients
The brain has limited tolerance to ischemia and has a unique response to
reperfusion
Much of the neurologic dysfunction that occurs after ROSC can be attributed to
cerebral edema, post ischemic neurodegeneration, and impaired
cerebrovascular autoregulation

Post cardiac arrest myocardial dysfunction

Patients can be hemodynamically unstable after ROSC because of a period of


global hypokinesis (myocardial stunning) that occurs or directly from the
precipitating pathology (e.g. myocardial infarction)
Myocardial stunning is usually reversible but can last up to 72 hours

Systemic ischemia/reperfusion response

After ROSC, a sepsis-like state has been described, in which there is a


significant systemic inflammatory response syndrome (SIRS) response,
impaired vasoregulation, increased coagulation, and adrenal suppression

Persistent precipitating pathology

The underlying cause of the arrest commonly contributes to and complicates


the pathophysiologic state of the patient, such as acute coronary syndrome,
pulmonary embolism, respiratory failure, electrolyte abnormalities, metabolic
abnormalities, environmental insults, toxic exposures, trauma, sepsis, and
others

Dr. Ali Ragab 13


Diagnosis

ECG should be performed as soon as possible post-ROSC to determine if an ST-


elevation myocardial infarction (STEMI) was the cause of the arrest
Chest x-ray should be performed to detect reversible causes of cardiac arrest
(i.e. pneumothorax) and to confirm position of supporting tubes and lines
A head CT should be performed when there is a suspicion that an intra cranial
event precipitated the cardiac arrest. Otherwise head CT is not mandatory and
should not delay further care
CT angiography of the chest if pulmonary embolism or aortic dissection is
suspected
Laboratory studies appropriate for critically ill patients should be obtained
including complete blood cell count, comprehensive metabolic panel, liver
function tests, cardiac enzymes, lactic acid, arterial blood gas, and toxin screen

Key factors to consider after resuscitation from cardiac arrest

Immediate tasks

Re-evaluate ABCDE
12-lead ECG
Treat precipitating causes
Re-evaluate oxygenation and ventilation
Temperature control (cool)

Early goals

Continue respiratory support


Maintain cerebral perfusion
Treat and prevent cardiac arrhythmias
Determine and treat the cause of the arrest

Dr. Ali Ragab 14


Specific tasks

Maintain MAP 65-100 mmHg


Maintain adequate oxygenation (SaO2 9496%)
Maintain normal pH and normocarbia (e.g. PaCO2 4045 mmHg)
Moderate glycemic control (144-200 mg/dL)
Consider therapeutic hypothermia (unless contraindicated)
Maintain appropriate sedation
Treat seizures
Continue search to identify underlying cause(s) and trauma related to
resuscitation
Consider specific treatment for underlying cause (e.g. percutaneous coronary
intervention, thrombolytics)
Consider prophylactic antiarrhythmics
Consider transfer to resuscitation centre

Therapeutic Hypothermia (TH)

Phases of TH

Induction(obtain target temperature <6 h of ROSC)

Obtain target temperature of 32C to 34C as soon as possible with cold saline
infusion followed by surface cooling systems or invasive cooling catheters
Shivering _ common during TH. Control with analgesics, sedatives, and
possibly neuromuscular blockade as shivering increases 02 consumption and
significantly decreases cooling rates

Maintenance (12-24 h)

Usually the most stable phase of TH


Avoid major temperature fluctuations

Dr. Ali Ragab 15


Rewarming (0.25C/h to 0.5C/h)

Rewarm slowly at a rate of 0.25C/h to 0.5C/h to avoid rebound hyperrhermia,


which can lead to unstable hemodynamics and further neurologic damage
Monitor electrolyte as rewarming precipitates hypoglycemia and hyperkalemia

Normothermia

Maintain normothermia after TH, as hyperthermia post-ROSC has been shown


to be associated with worse outcomes

Relative contraindications

Relative contraindications for TH include traumatic arrest, sepsis as the


etiology of arrest, coma for other reasons, uncontrolled bleeding, prolonged
duration of resuscitation (>60 minutes), or severe intracranial hemorrhage

Oxygenation

Initially during resuscitation, it is common to use 100% oxygen to avoid hypoxia


Wean FIO2 as low as possible for goal SaO2 of 94%-96%

Ventilation

Goal PaCO2 of high normal (40-45 mmHg) should be targeted


Avoid hyperventilation with hypocapnia to prevent cerebral vasoconstriction
and auto-PEEP
Target a tidal volume of 6-8 mL/kg of ideal body weight to prevent lung damage
from alveolar over distension

Hemodynamics

Hypotension is common secondary to relative volume depletion, vasodilation


from the severe SIRS response, and cardiac depression from myocardial
stunning or infarct

Dr. Ali Ragab 16


Early goal-directed therapy

Initial volume resuscitation to optimize preload


If still hypotensive, add vasopressors for a goal MAP between 65-100 mmHg
Echocardiography or invasive hemodynamic monitoring may guide use of
inotropes (e.g. dobutamine or milrinone) for hypotension secondary to
myocardial depression
Consider mechanical support devices like intra aortic balloon pump, ventricular
assist devices, or extracorporeal membrane oxygenation (ECMO) for
persistently hemodynamically unstable patients
Goal to achieve Scv02 >70% and lactate clearance

Glucose control

TH can cause insulin resistance and hyperglycemia


Moderate glycemic control (144-200 mg/dL) should be employed

Coronary revascularization

Electrocardiogram _ Obtain immediately post-ROSC to determine if ST


elevations are present, which should prompt immediate consideration for
reperfusion, ideally primary PCI
lschemia without STEMI may also precipitate cardiac arrest, so that even in the
absence of STEMI, it may be reasonable to consider angiography
Coronary angiography should not delay TH

Treatment of seizures

Obtain early and ideally continuous EEG monitoring, as it is common to have


non convulsive status epilepticus in this setting, in particular, for patients who
are paralyzed
It is reasonable to institute prompt and aggressive treatment of seizures

Dr. Ali Ragab 17


Antiarrhythmic drug

It may be reasonable to continue an infusion of an antiarrhythmic drug that


successfully restored a stable rhythm during resuscitation (e.g. lidocaine 24
mg/min or amiodarone 0.6 mg/kg/h for 1224 hours)

Neuroprognostication

Neuroprognostication is extremely difficult in the post arrest period


There are no post arrest physical exam findings or diagnostic tests that can
accurately predict poor outcome during the first 24 hours
At 72 hours, incomplete recovery of brainstem reflexes, myoclonus, extension
posturing or absent motor response to pain, and bilaterally absent
somatosensory cortical evoked potentials (N20) were associated with a 0% false
positive rate for poor outcome. These observations were made in patients who
did not undergo TH
TH and the accompanying use of sedative, analgesic, and paralytic medication
can delay neurologic recovery. In the setting of TH, traditional prognostic
features should be interpreted with caution so as to avoid premature
documentation of poor prognosis leading to inappropriate withdrawal of care in
patients
Until further investigations are conducted, we recommend attempts to provide
neuroprognostication be held at least until 72 hours after patients have been
rewarmed

Dr. Ali Ragab 18

You might also like