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RESUSCITATION
Wiwi Jaya
SMF Anesthesiology & Intensive
Treatment
RS Saiful Anwar Malang - East Java
CARDIAC ARREST
Abrupt loss of consciousness caused
by lack of adequate cerebral blood
flow due to failure of cardiac pump
function.
CARDIAC ARREST
Survival depends on
The setting in which arrest occurs
Electrical mechanisms
Underlying clinical status
Electrical mechanisms
Ventricular fibrillation
Pulseless VT
Asystole
Pulseless electrical activity
PHASES OF VF
ELECTRICAL (0-4 min)
o adequate myocardial ATP store
o defibrillation alone restore perfusing
o rhythm(without chest compressions)
o duration of this phase can be
prolonged
by bystander CPR.
PHASES OF VF
Circulatory phase(4-10 min)
depletion of ATP store, lactic acidosis
defibrillation without chest
compression
rarely successful, may result in PEA
ECG fine fibrillatory wave.
PHASES OF VF
Metabolic phase(>10 min)
terminal phase
irreversible damage
less chance of successful
defibrillation
mild therapeutic hypothermia delay
the
onset.
Hypoxia
Hypovolemia
Hydrogen ion(acidosis)
Hypo/hyperkalemia
Hypothermia.
TS
Toxins
Tamponade
Tension pneumothorax
Thrombosis(pulmonar
y)
Thrombosis(coronary)
Asystole
No cardiac electrical and mechanical
activity of heart.
Terminal rhythm in non intervened
PEA or VF
Same causes of PEA can also
sometimes present initially as
asystole
Chain
Chain of
of Survival
Survival
Early CPR
Chest
Compressions
Chest compressions consist of forceful rhythmic
applications of pressure over the lower half of the
sternum.
These compressions create blood flow by
increasing intrathoracic pressure and directly
compressing the heart.
This generates blood flow and oxygen delivery to
the myocardium and brain.
Rescue Breaths
by mouth-to-mouth or bag-mask
Deliver each rescue breath over 1
second
Give a sufficient tidal volume to
produce visible chest rise.
Use a compression to ventilation
ratio of 30:2
Ventilation
When an advanced airway (ie, endotracheal
tube, combitube,or laryngeal mask airway
[LMA]) is in place during 2-person CPR,
give 1 breath every 6 to 8 seconds without
attempting to synchronize breaths between
compressions
This will result in delivery of 8 to 10
breaths/minute
There should be no pause in chest
compressions for delivery of ventilations
Cricoid Pressure
Applying pressure to the victims cricoid
cartilage to push the trachea posteriorly
and compress the esophagus against
the cervical vertebrae
Used in a few special circumstances (eg,
to aid in viewing the vocal cords during
tracheal intubation,
The routine use of cricoid pressure in
adult cardiac arrest is not recommended
Advanced airways
Advantages
Improved ventillation and
oxygenation
Eliminate pauses in chest
compressions
1 breath every 6-8 sec(8-10
breath/min)
Reduce risk of aspiration
Supraglotic airways
Laryngeal mask airways
regurgitation less
when ET is difficult
neck injury
positioning of patient is difficult for ET
Provides equivalent ventillation comp.
ET.
Esophageal tracheal tube
Laryngeal tube
DEFIBRILLATION
Initial shock
360j for monophasic , same dose for
subsequent shocks
120-200j for biphasic defibrillator,
subsequent dose same or higher.
If VF recurs use previously successful
energy level
Vasopressin
Non adrenergic
Coronary vasoconstrictor
Dose:40 units IV/IO
ANTI ARRYTHMICS
AMIODARONE
For VF/Pulseless VT unresponsive to
CPR,
defibrillation ,vasopressor
Initial 300mg IV/IO can be followed
by 150mg
Lidocaine
if amiodarone not available
initial dose 1 to 1.5 mg/kg IV
addl. Dose 0.5 to 0.75 mg/kg if not
responding
Magnesium sulphate
Used in torsades de pointes
Dose 1-2gm diluted in 5% D
Induced hypothermia
In comatose (lack of meaningful
response to verbal commands) adult
patients
With ROSC after out of hospital VF
arrest
(class 1)
In hospital arrest with any rhythm
(class2 b)
Cooled to 32-340C for 12 -24 hrs
Cooling blanket
Ice packs
Direct immersion in ice water
IV ice-cold fluids (500 ml to 30 ml/kg
NS or Ringers lactate)
Monitor with esophageal
thermometer
or bladder catheters in nonanuric
patients
THANK
U
THANK U
3) Therapeutic hypothermia
a)32-34
b)30-32
c)27-30
d)35