Cardiac Arrest - Agus Subagjo, MD, FIHA.pdf
Transcript of Cardiac Arrest - Agus Subagjo, MD, FIHA.pdf
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CARDIOVASCULAR EMERGENCIES COURSEBumi Surabaya Hotel, November 7-8th, 2015
Cardiac rrest
Dr. Agus Subagjo SpJP (K), FIHA
Tyagita Verdena
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Cardiac Arrest = Loss of cardiac function as resultant of :
1) Acute myocardial infarction, OR2) Ischemia without infarction, OR3) Structural alterations of heart
Priori et al, 2015
Definition
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Cardiac Arrest
360,000 people experience out-of-hospital cardiac arrest every year
in USA.
From 1000 px in Europe, 1-5 % suffered from cardiac arrest andonly 20% can survive and out from hospital.
Most die within an hour of the onset of acute symptoms
The majority of these deaths the presenting rhythm is Ventricular Fibrillation or pulseless Ventricular Tachycardia, (VF/ pulseless VT)
Sandroni, et al, 2007
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Risk Factors of Cardiac Arrest Fibrous scar tissue formation on cardiac muscle
Ischemia; chronic or acute
Cardiomyopathy
Drugs
Abnormality in conduction system
Abnormality in heart anatomy
Miscellaneous
Zipes et al, 2006
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Cardiac ArrestSign and Symptoms
Unresponsive
Gasping
Pulseless
Supporting Asessement
1. ECG
2. Examine 5H, 5T (Hypovolemia, Hypoxia, Hydrogen ion, Hypo-hyperkalema,Hypothermia, tension pneumothorax, tamponade cardiac, toxins, trombosispulmonary, thrombosis coronary)
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Pathology of Cardiac Arrest Cardiac arrest generally progresses through several
cardiac rhythm disburbances
V-Tachwithoutpulse
V-Fib
• Highsurvivalpotential!
Asystole/PEA
• Poor prognosisfor survival
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Chain of Survival
Management Cardiac Arrest
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Chain of Survival
Early Access
Early CPR
Early Defibrilation
Effective ACLS
Integrated post cardiac arrest care
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BLS algorithm2010 2015
Good
CPR
-30:2
-minimal
100x/m
-mimimal 5 cm
depth
- Not too fast,
max 120 bpm
- Not too deep,
max 5-6 cm
- 10 breath per
minute-CAB
Compression
only is not
endorsed for
trained provider
Opioid
intoxic
ation
naloxone
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Recognise sign and symptom of cardiac arrest
Call for help!
Don’t leave the victim
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CPR
1. Place both hands on the lower half of the sternum bone
2. With an upright body position, press the the victim’s chest wall bythe force of rescuers weight on a regular basis
Rate: 100 – 120/min
Depth: Between 2 in (5cm) and 2.5in (6cm)
Allow
full recoilof the chest between compressions
Minimize Interruptions
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Airway Check the airway
Open the airway, place one hand on the victimsforehead and gently tilt head back
Remove any visible obstruction from the victims mouth,including dislodged dentures.
DO NOT ATTEMPT ANY FINGER SWEEPS
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Breathing
Consists of two stages:
1. Ensuring adequate victim breathing / not breathing (not
exceed 10 seconds)
2. Provide assistance breath.
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Defibrilation
Use AED if out of hospital
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Often defibrillation only can restores the heart rhythm
But to sustain circulation, further advanced life support is
required
ACLS follow the rules of Circulation, Airway,
Breathing, Defibrilation.
C A B D
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ACLS 2010 vs 2015
Drugs 2010 2015
Vasopressin Considered asalternative theraphy
of epinefrin
Notrecomennded
Vasopressin : is out !
Equipment 2010 2015
Capnography
(ETCO2)
Less attention Considered as good
equipment in ACLS
2015
Echocardiography
during CPR
recommended
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ACLS Cardiac Arrest
Algorithm 2015
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CPR in ACLS
CPR is advised in patients with cardiac arrest (Class I, LOE B).
delay of a few seconds compression will reduce the success of
resuscitation.
The use of automatic CPR is not recommended, except in
circumstances where the rescuer to do CPR is less.
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ACLS: Airway and Breathing At the time the decision was made to install invasive
airway and breathing devices to patients, do not interfere
the process of CPR
in 2015 AHA recommendation emphasized for the use of
100% oxygen during resucitation.
In the airway and breathing resuscitation suggested
giving artificial breath as much as 10x/min.
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Defibrilation Strategy inACLS
Type of Waves and Energy:
If the type of biphasic defibrillator is available:
recommended dose of electric shock is 120 to 200 Jto cope with ventricular fibrillation (Class I, LOE B).
If defibrillation is needed again, it is advisable to use
the maximum power of 200 joules (class IIb, LOE B).
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If available monophasic defibrillator
Use 360 J and the dose can be repeated on
The 2015 AHA recommendations:
The succes rate of biphasic defibrillator defibrillation in the first shockis higher than monophasic defibrillation, as well as side effects post-
shock myocardial dysfunction are lower than monophasic defibrillator.
The success of defibrillation assessed if VF / VT without pulse gone 5seconds after defribrilation.
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Drugs in Cardiac Arrest LifeSupport
1. Vasopressor
2. Antiarhytmic
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Vasopressor Epinephrine• Epinephrine work on α-adrenergic receptor that serves as a
vasoconstrictor
increase cerebral perfusion pressure during
resuscitation.
• Epinephrine have side effects increase miocard contraction anddecrease myocardial perfusion subendocardium.
• The AHA recommendations dose of epinephrine in cardiac arrest
recommended is 1 mg IV / intraosteal every 3-5 minutes (class IIb, LOE
A).
• If venous access / osteal not available, can be administered
endotracheal dose of 2 to 2.5 mg5.
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Other vasopressors
No other vasopressors (eg, norepinephrine) that may indicate increase life
expectancy with equivalent results with epinefrin
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Antiarrhytmia Amiodarone• Intravenous amiodarone affects:
• sodium channel
• potassium channel
• Calcium channel
• has the effect of α and β-adrenergic blocker
• Amiodarone may be considered on the condition of VF or VT without
pulse that is not a response to CPR, defibrillation, and vasopressors
(class IIb, LOE B).
• The administration of amiodarone at a dose of 300 mg or 5 mg / kg
followed by 150 mg IV / IO reduce the time of hospitalization whencompared with placebo or 1.5mg / kg lidokain.
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Lidocaine
• The initial dose is 1 to 1.5 mg / kg IV, with a repeat dose is 0.5 to 0.75
mg / kg every 5 to 10 minutes with a maximum dose of 3 mg / kg.
• Lidocaine can be given on the condition:• stable monomorphic VT with ventricular function is still good
• stable polymorphic VT with a normal QT interval when ischemia
condition
• electrolyte abnormalities have been overcome
• stable polymorphic VT with prolongation of the QT interval.
Lidocaine no longer used as first choice drug in arrhytmia
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Magnesium Sulfate
• Magnesium sulfate give good therapeutic effect on:
• the condition of torsades de pointes (irregular / polymorphic VT with
prolongation of the QT interval): administered IV / IO bolus of 1 to 2 g
diluted in 10 cc D5 (class IIb, LOE C)
Magnesium sulfate can not stop polymorphic VT with a normal QT interval.
Magnesium sulfate can provide hypotensive effects.
Administration of magnesium sulfate on condition of impaired renal functionshould be cautious.
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Post cardiac arrest care
If the cardiacarrest victims
can survive
further thecomprehensive
treatment
prevent cardiacarrest reset
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Prognostic
Cardiac Arrest prognostic depends on former condition
before arrest: Age (elderly or infancy)
Race
Chronic illness (diabetes mellitus, CKD, sepsis,
stroke)
Quality of chain survival
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Stopping the life support
The chances of survival fallrapidly with time
There is no absolute cut off
when mortality becomes zero Resuscitation attempts
requiring longer than 20minutes of CPR have a veryhigh mortality rate
We recommend stopping ataround 20 minutes unless there
is a clinical reason to continuefor longer
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Stopping the life support
(cont)
CPR can be stopped in some conditions like
the signs of death present: rigor mortis asystole persisting more than 10 minutes
there is a demand from the nuclear family
the patient will
terminal illness
Resucitation harm the rescuer
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Conclusion
Cardiac Arrest unexpected event
Cardiac arrest could be a reversible moment
Good quality of the “chain of survival” is the key of
an successful resusitation
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