CARDIAC ARREST

-Dr.Praveen Kumar
Moderater- Dr.Viju Wilben
 56 yr old male h/o breathlessness fallowed by
unresponsiveness ,with ? One episode of seizure
On Primary survey
Airway- patent
Breathing-tachypnic , spo2 86%
Circulation- PR-140, BP -80/50
Disability-E2V2M5
Adjuvents- ABG - metabolic acidosis ,lactate -5
ECG
 SVT with abberancy
● Stable vs unstable
● Adenosine ,B blocker, CCB
● Amiodarone , procainamide, sotalol
CARDIAC ARREST is an abrupt cessation of
cardiac pump function that may be
reversible but will progress to death without
prompt intervention
 KEY POINTS

The four rhythms that produce pulseless

cardiac arrest are ventricular fibrillation,
pulseless ventricular tachycardia , asystole,
and PEA
● Sudden cardiac arrest is usually due to
underlying heart disease; ventricular
fibrillation is the most common initial rhythm
● In ventricular fibrillation, loss of
consciousness occurs within 15 seconds,
but agonal gasping may persist for around
60 seconds following collapse. Brief seizure
may occur, caused by cessation of cerebral
blood flow
● PEA is continued electrical activity of the
heart without effective mechanical
contractions, and it often results from
reversible causes ,5H and 5T
● Asystole is often a preterminal rhythm, and
the rate of survival is extremely poor
● Cardiac arrest secondary to respiratory
arrest causes loss of consciousness,
bradycardia, and absent pulse within 5
minutes
● Cardiac arrest in the pediatric patient is
usually the result of progressive respiratory
failure or shock; a primary cardiac event is
much less common
● Outcome is influenced by several factors,
the most important of these being time from
arrest to CPR and defibrillation.
Other factors include the following
● Underlying rhythm: Patients with ventricular
tachycardia and ventricular fibrillation have a
better prognosis than those with asystole
● Blood pressure on return of spontaneous
circulation: Greater than 90 mm Hg systolic
indicates a better chance of survival
● Any coexisting cardiac or other disease
CONCLUSION:
Witnessed arrests, early initiation of CPR by
bystanders, CPR duration ≤20 minutes, initial
presenting shockable rhythm, OHCA with
non-cardiac etiology are associated with a
good outcome
 Monitoring during CPR
● Rhythm assesment
● ABG
● Et CO2
● PETCO2 is measured using a waveform
capnogram and provides a reliable indicator
of cardiac output during CPR
● It is also recommended as an adjunct to
direct visualization and auscultation to
confirm endotracheal tube placement
● It is listed as a Class I recommendation in the
AHA's 2010 advanced cardiac life support
(ACLS) guidelines
● PETCO2 less than 10 mm Hg indicates that
cardiac output is not adequate to achieve return
of spontaneous circulation
● PETCO2 monitoring can be used to titrate
compression force and rate
● High quality CPR
● The AHA algorithm for pulseless cardiac arrest
divides into two treatment pathways, depending
on whether the monitored rhythm is ventricular
fibrillation/ventricular tachycardia or
asystole/PEA
● Early defibrillation
● Biphasic shock waves are more effective in
initial shock than monophasic.
● Amiodarone
● Lignocaine
● Mgso4
● Routine use of sodium bicarbonate for the
treatment of cardiac arrest is not recommended. It
may be beneficial in a small select group of
patients, including those with tricyclic
antidepressant overdose, severe cocaine toxicity ,
hyperkalemia , and pre-existing acidosis
Post ROSC Management tachyarrhytmia and
Bradyarrhytmia
● A 12-lead ECG should be obtained as soon as
possible after ROSC to determine whether acute
ST elevation is present. (Class I, LOE B)
● Coronary angiography should be performed
emergently (rather than later in the hospital stay
or not at all) for OHCA patients with suspected
cardiac etiology of arrest and ST elevation on
ECG. (Class I, LOE B-NR)
● Emergency coronary angiography is
reasonable for select (eg, electrically or
hemodynamically unstable) adult patients
who are comatose after OHCA of suspected
cardiac origin but without ST elevation on
ECG. (Class IIa, LOE B-NR)
● Immediate per- cutaneous coronary intervention is
associated with better survival after out-of-hospital
cardiac arrest: from the PROCAT (Parisian Region Out
of hospital Cardiac ArresT) registry.
● in which consecutive post–cardiac arrest patients
with suspected cardiovascular cause were taken to
coronary angiography, a coronary artery lesion
amenable to emergency treatement was found in 96%
of patients with ST elevation and in 58% of patients
without ST elevation.
● Avoiding and immediately correcting
hypotension (systolic blood pressure less
than 90 mm Hg, MAP less than 65 mm Hg)
during postresuscitation care may be
reasonable. (Class IIb, LOE C-LD)
● Vasoactive drugs may be administered after
ROSC to support cardiac output
● Brain injury is the cause of death in 68% of
patients after out-of-hospital cardiac arrest
and in 23% after in-hospital cardiac arrest
● Seizure management
● TTM
● An EEG for the diagnosis of seizure should be
promptly performed and interpreted, and then
should be monitored frequently or continuously
in comatose patients after ROSC. (Class I, LOE
C-LD)
● The same anticonvulsant regimens for the
treatment of status epilepticus caused by other
etiologies may be considered after cardiac
arrest. (Class IIb, LOE C-LD)
● We recommend that comatose adult patients
with ROSC after cardiac arrest have TTM
(Class I, for VF/pVT OHCA; for non-VF/pVT
(ie, “nonshockable”) and in-hospital cardiac
arrest). (Class I)
● We recommend selecting and maintaining a
constant temperature between 32ºC and 36ºC
during TTM. (Class I)
● It is reasonable that TTM be maintained for
at least 24 hours after achieving target
temperature. (Class IIa, LOE C-EO)
● It may be reasonable to actively prevent
fever in comatose patients after TTM.
(Class IIb, LOE C-LD)
● It is reasonable to consider the titrated use
of sedation and analgesia in critically ill
patients who require mechanical
ventilation or shivering suppression during
induced hypothermia after cardiac arrest.
(Class IIb, LOE C)
● Maintaining the Paco2 within a normal
physiological range, taking into account any
temperature correction, may be reasonable.
(Class IIb)
● To avoid hypoxia in adults with ROSC after
cardiac arrest, maintain spo2 >94% (Class IIa)
 TIMING OF OUTCOME PREDICTION
● The earliest time for prognostication using
clinical examination in patients treated with TTM,
where sedation or paralysis could be a
confounder, may be 72 hours after return to
normothermia. (Class IIb)
● The earliest time to prognosticate a poor
neurologic outcome using clinical examination in
patients not treated with TTM is 72 hours after
cardiac arrest. (Class I )
● This time until prognostication can be even
longer than 72 hours after cardiac arrest if the
residual effect of sedation or paralysis confounds
the clinical examination. (Class IIa )
Useful clinical findings that are associated with
poor Neurolocal outcome
● Absence of pupillary reflex to light at 72 hours or
more after cardiac arrest
● Presence of status myoclonus during the first 72
hours after cardiac arrest
● Absence of the N20 somatosensory evoked potential
cortical wave 24 to 72 hours after cardiac arrest or
after rewarming
● Presence of a marked reduction of the gray-white
ratio on brain CT obtained within 2 hours after
cardiac arrest
● Extensive restriction of diffusion on brain MRI at 2
to 6 days after cardiac arrest
● Persistent absence of EEG reactivity to external
stimuli at 72 hours after cardiac arrest
● Persistent burst suppression or intractable status
epilepticus on EEG after rewarming