cardiac arrest - agus subagjo, md, fiha.pdf

8/18/2019 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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cardiac arrest - agus subagjo, md, fiha.pdf

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