cardiac arrest

54
A&E(VINAYAKA) CARDIAC ARREST DR. PRAKASH MOHANASUNDARAM Emergency & Critical care Physician Vinayaka Mission University

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CARDIAC ARREST. DR. PRAKASH MOHANASUNDARAM Emergency & Critical care Physician Vinayaka Mission University SALEM. What is cardiac arrest?. Abrupt cessation of cardiac pump function which may be reversible by a prompt - PowerPoint PPT Presentation

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Page 1: CARDIAC ARREST

A&E(VINAYAKA)

CARDIAC ARREST

DR. PRAKASH MOHANASUNDARAM

Emergency & Critical care Physician Vinayaka Mission University SALEM

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What is cardiac arrest?

Abrupt cessation of cardiac pump function

which may be reversible by a prompt

intervention

but will lead to death in its absence

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NO Central Pulse

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Scenario 1

He was about to be shifted to the cathlab when he suddenly became drowsy and then unconscious

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CHECK FOR RESPONSE

OPEN THE AIRWAY

CALL FOR HELP

CHECK FOR BREATHING

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NO CENTRAL

PULSE

CHECK FOR CENTRAL PULSEGIVE 2 RESCUE BREATHS

NO BREATHING

KEEP DEFIB PADDLESCHECK RHYTHM

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Identify the rhythm

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What is VF?

Coarse fibrillatory waves

Chaotic electrical activity

If flatline increase gain - fine VF

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Identify the rhythm

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Ventricular tachycardia(VT)

QRS has a wide morphology

Rate is typically from 100-200 bpm

P waves are hidden if present

Can deteriorate rapidly to VF

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Polymorphic VT

The QRS morphology keeps varying

If preceded by a prolonged QT interval when in sinus rhythm – Torsades de pointes

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Primary ABCD Survey

Basic Life Support: Airway Breathing Circulation

Attach monitor/defibrillator

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Check rhythm

VF/VT Aystole/PEA

Shockable Not Shockable

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VF/Pulseless VT

Give 1 shockBiphasic: 120 to 200 JMonophasic: 360 J

Give the highest energy in that equipment

Resume CPR immediately

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PADDLE PLACEMENT

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Persistent VF/Pulseless VT

Give 1 shockResume CPRGive vasopressor

Epinephrine 1 mg IV repeat every 3 to 5 minutes

OR

Vasopressin 40 U IV

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If rhythm persists

Consider antiarrhythmics

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Amiodarone – Class II b

Na ,K and Ca channel blocker Also alpha and beta adrenergic effects

300 mg IV bolus followed by 1 dose of 150 mg IV

If perfusing rhythm achieved:1 mg/min for next 6 hrs0.5 mg for next 18 hrs

Preferred through central line

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Lidocaine – Class Indeterminate

The initial dose 1 to 1.5 mg/kg IV push

If VF / pulseless VT persists additional doses 0.5 to 0.75 mg/kg IV push 5 to 10min interval

Maximum dose of 3 mg/kg

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Magnesium – Class IIa

Polymorphic VT associated with prolonged QT interval (torsades de pointes)

1-2gm IV/IO in 10 ml of 5D over 5-20 mins

If with pulse same 1-2gm in 100ml of 5D over 20-60 mins

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Reduce interruptions as much as possible !!!!!!!

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Key points of CPR

Provide CPR while the defib is charging

Push hard and push fast

Allow chest recoil

Minimize interruption during chest compressions

Check rhythm only after delivery of 5 cycles / 2mins of CPR after shock delivery

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Vasopressor to be delivered only after 1 or 2 shocks

Palpate for pulse if organized rhythm appears.

If patient in hypothermic(< 30 deg C) with hold vasopressors until rewarmed.

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With advanced airway, compressions at 100/min ventilations at 8-10 breaths /min

Avoid fatigue by rotation

Drugs in peripheral lines- 20 ml chase fluids and elevate limb.

Rule out the 6Hs and 5Ts.

Page 26: CARDIAC ARREST

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Causes of pulseless arrest-6Hs

Hypo / hyperkalemia

Hypoxia

Hypothermia

H+ ion - acidosis

Hypoglycemia Hypovolemia

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5Ts

Toxins

Tamponade - cardiac Thrombosis

Tension Pneumothorax Trauma

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Scenario 2

A 65 year old male was admitted in the ICU with a diagnosis of hemorrhagic stroke, on ventilator support

Suddenly nurse noticed a fall in the GCS and alerted you

You find that there is no central pulse and the monitor shows this rhythm

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Pulseless Electrical Activity (PEA)

Pulseless patients with minimal electrical activityForce of contractions not enough to produce a perfusing rhythmOften caused by reversible conditionsTreat the cause(6Hs and 5Ts)

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What to do if you see this?

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Asystole

Check the pulseCheck the leads first!Change the leadsIncrease the gain. Why?

PLEASE DON’T DELIVER SHOCK

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Evidence for no shock

In 1989 Losek- 49 children in asystole delivered shock with no positive results

1993 Nine city high dose epinephrine study group- “no benefit from shock for asystole”

CIRCULATION 2005

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PEA and Asystole

May give 1 dose of vasopressin 40IU to replace 1st or 2nd dose of

adrenaline

A,B,C, start CPR IV/IO give inj.adrenaline 1mg(repeat

every 3-5 mins)Atropine 1mg IV when slow PEA /

AsystoleMax 3 doses

Check rhythm after 5 cycles of CPR

PEA / Asystole Go to shockable

rhythm management

VF / VT

If NSR go to post resuscitation care

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Management of PEA / Asystole

Focus on high quality CPRAirway ASAPMinimize interruptions in chest compressionsDeliver IV/IO medications once CPR is startedEpinephrine every 3-5 minsAtropine is 1mg , max of 3 dosesVasopressin can replace adrenaline during the first or second dose

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Causes of Pulseless arrest

HypovolemiaHypoxiaHydrogen ionHypo/ hyperkalemiaHypoglycemiaHypothermia

ToxinsTamponade ,cardiacTension pneumothoraxThrombosis (coronary/pulmonary)Trauma

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The drugs in cardiac arrest

EpinephrineVasopressinAtropineAmiodarone Magnesium Lidocaine

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Classification of ACLS drugs

Class I Class II -a Class II - b Class -

Indeterminate Class III

Definitely usefulProbably usefulPossibly usefulNo supporting

evidenceHarmful

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Epinephrine – Class II b

Alpha adrenergic effects- beneficial

But Beta adrenergic effects increase myocardial oxygen demand and also reduces subendocardial perfusion

1mg IV/IO every 3-5 mins

If IO/IV unable to get, ET tube dose of 2-2.5mg

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Vasopressin – Class Indeterminate

Noradrenergic peripheral vasoconstrictor that also causes coronary and renal vasoconstriction

Benefit no better than epinephrine in survival

Significantly less neurological deficit

40 IU IV / IO

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Atropine – Class Indeterminate

Atropine reverses cholinergic mediated, decrease in heart rate

Asystole could be precipitated by excessive vagal tone

1 mg every 3-5 mins upto max of 3 mg

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Buffers

Adequate Oxygenation & Ventilation is the best buffer

Soda bicarb - only buffer authorised for use (Class II b)

Acidosis – accumulation of CO2 and lactate

No adequate tissue perfusion during prolonged CPR or late start

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How does it work

Corrects acidosis, improves vascular response

Decreases defibrillation threshold

Post resuscitation- increases myocardial contractility

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Cont…

Currently no evidence for empirical use!

Supported only in hyperkalemia(CRF), TCA overdose or preexisting metabolic acidosis

0.5-1 meq/kg over 10 mins or ABG guided.

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Pediatric arrest

2 rescuers 15 : 2

CPR technique

Drugs:No atropine in PEA/

Asystole

2 Joules / kg then 4 joules/ kg

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DRUGS

Adrenaline 0.01mg/kg IV/IO 0.1 mg/kg ET

Amiodarone 5mg/kg upto 15/mg/kg max of 300 mg.

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Neonate arrest

Start CPR when HR Less than 60 bpm

Ratio is 3 : 1

Turn the mask

Adrenaline 0.01mg/kg IV 0.1 mg/kg in

ET

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Definite NO NOs

Precordial thumpProcainamide in VFNor adrenaline - worse neurologic outcomesVolume expansion with IV fluids

Pacing in asystole

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Be prepared

Emergency drugs kitAirway kitRegular drillsTeam workDebriefing

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Summary

AnticipateRemember to change leads and increase gain in AsystoleBasics of CPRPlease don’t shock Asystole / PEAConstant update

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DEAD but STILL ALIVE

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Thank you !