pulseless electrical activity bradycardia Nov 2014

PULSELESS ELECTRICAL ACTIVITY& ASYSTOLE

Mansoor Masjedi ; MD , FCCMAssistant professor of anesthesia & critical care

Sums , Nov. 2014

DEFINITION :

• PEA :• Unresponsiveness • Lack of palpable pulse • Presence of organized cardiac electrical activity

• Previously ,referred to as electromechanical dissociation (EMD) • EMD may imply that there is little viable or functional

myocardium

• Also known as ; Non-Perfusing Rhythm

• Pseudo-PEA :– Weak ventricular contractions / recordable aortic pressure

• True PEA : – Absent contractions + coordinated electrical activity

• Organized cardiac rhythms:– supraventricular rhythms (sinus versus non-sinus) or – ventricular rhythms (accelerated idioventricular or escape)

MECHANISM:

• Presence of cardiac electrical rhythm without a proper response of the myocardial tissue

and mechanical cardiac output

PATHO-PHYSIOLOGY:

• cardiovascular, respiratory or metabolic

• sudden changes in preload, afterload, or contractility often result in PEA.

• Exacerbated by worsening acidosis, hypoxia, and increasing vagal tone.

DECREASED PRELOAD:

• Cardiac sarcomeres require an optimal length (ie, preload) for an efficient contraction

• If unattainable , the left ventricle is unable to generate sufficient pressure to overcome its afterload

eg. Hypovolemia ( dehydration, blood loss etc) massive pulmonary embolus

pericardial tamponade Tension pneumothorax

DECREASED AFTERLOAD :

• Sudden ↓ afterload → ↓myocardial perfusion (before autoregulatory mechanism becomes active) & decreases contractility.

Eg . Hypovolumia vasodilator therapy

Shock etc.

Though very ↑↑↑ afterload can↓contractility but its rare cause of PEA.

DECREASED CONTRACTILITY:

• Optimal myocardial contractility depends on:1. PRELOAD (starling law)2. AFTER LOAD3. VIABLE MYOCARDIUM4. AVAILABILITY OF INOTROPIC SUBSTANCES eg. Adr., N Adr., Ca2+

• Any derangement from NL ( mainly sudden / severe) can cause PEA.

CAUSES :

6 H’sHypovolemiaHypoxiaHydrogen ion (acidosis)Hypo-/HyperkalemiaHypoglycemiaHypothermia

5 T’sToxins (TCA, DIGITALIS,

CCB, B-BLOCKER )TamponadeThrombosis (coronary or

pulmonary)Tension PTxTrauma

Hypoxia 2ndary to respiratory failure is probably the most common cause of PEA

Resp. insufficiency ; 40-50% of PEA

The "3 and 3 rule’’easy recall of the most common correctable causes:

1. SEVERE HYPOVOLUMIA 2. PUMP FAILURE :

I. MASSIVE M.I. II. POST A.M.I. MYOCARDIAL RUPTUREIII. SEVERE HEART FAILURE

3. OBSTRUCTION TO CIRCULATION:I. TENSION PNEUMOTHORAXII. CARDIAC TAMPONADEIII. MASSIVE PULMONARY EMBOLISM

SPECIAL ONE :

• POST DEFIBRILATION PEA : Presence of organized electrical activity, immediately after electrical

cardioversion in the absence of palpable pulse

Better prognosis than continued VF

Spontaneous return of pulse is likely

CPR should be continued for 2 min to allow spontaneous recovery

PEA - MORTALITY / MORBIDITY

• Only 11.2% of PEA survived to hospital discharge

• rapid initiation of ACLS and identification of reversible cause, improve outcome

EVALUATION OF PATIENTPEA / ASYSTOLE

PEA - HISTORY

• prior medical conditions allows prompt identification and correction of reversible causes– eg. Hx of : 1. Severe dysp. → Pul.Embli 2. MI 2 – 5 days back→ cardiac rupture / re infarction 3. Trauma → hypovol. , ten. Pneumo. or pericardial tamp

• Drug hx. ( b-blocker, CCB ) is also very important

PEA – Phys. Exam.

• No peripheral pulses

• Clues to aetiology : tracheal shift to opposite side & absent breath sound indicates

----------- Tension PTX

No respiratory finding with engorged JVP ------- pul. Embolism

Pulsus paradox. -------- pericardial tamp

Important clues :CONDITIONS CLUES

1. HYPOVOLEMIA H/O Blood loss, Flat neck veins

2. HYPOXIA Cyanosis, Airway Problem

3.CARDIAC TAMPONADE H/O Trauma, Renal failure, Thoracic Malignancy, Distended Neck Veins, Pulsus Paradoxus

4.TENSION PNEUMOTHORAX H/O ventilator used, trauma, COPD, tracheal deviation , absent breath sound

5. HYPOTHERMIA Low CORE Body Temperature

6. MASSIVE PUL. EMBOLUS NO RESP. FINDING in presence of sev dyspnoea & tachypnoea, distended JVP

7. DRUG OVERDOSE H/O drug intake, Bradycardia etc.

8.SEVERE ACIDOSIS H/O Renal Failure, DM; ACIDOTIC breathing.

9. HYPERKALEMIA H/O CKD, Dialysis, tall T wave/ absent P wave/ wide QRS complex in ECG

10. Acute MI Relevant History, ECG changes, cardiac enzymes.

PEA - INVESTIGATIONS

• Emergent nature of the problem • Labs; not likely to be helpful in the immediate management of

the pt.

• If available rapidly ; ABG, electrolytes & glucose ( to determine pH, oxygenation, serum potassium and glucose.

PEA - INVESTIGATIONS - Contd……..

• Imaging : Bedside Echo. / Sono.

• Other Tests : 12 lead ECG( difficult to obtain during ongoing resuscitation)

– ↑K– AMI– HYPOTHERMIA (Osborne wave)– Drug overdose (TCA : QT prongation)– Pul embolism : Rt. Axis daviation

Procedures : arterial line in pts with a very low BP

TREATMENTPEA / ASYSTOLE

PEA - MEDICAL MANAGEMENTAHA-ACLS guidelines

Initiate CPRPlace an IV lineIntubate the ptOxygen 100%

PEA - MEDICAL MANAGEMENT – Cont….

Then reversible causes should be sought and corrected :

Hypovolemia -Volume infusion Hypoxia - Ventilation Cardiac Tamponade - Pericardiocentesis Tension Pneumothorax - Needle decompression Hypothermia - Hypothermia correction Massive pulmonary embolism - surgery, thrombolytics Drug overdose - Appropriate therapies Hyperkalemia - Sodium bicarbonate Massive AMI – AMI rx

Resuscitative pharmacology DRUGS INDICATION DOSES AD/DISVANTAGE

1. EPINEPHRINE •PEA arrest•B-blocker/ CCB overdose

1 mg IV q3-5min No improvement in outcome in most. In CCB/B-blocker overdose its very effective

2.VASOPRESSIN may replace either the first or second dose of epinephrine

40 U IV ------------

3. ATROPINE bradycardia (ie, heart rate <60 bpm) associated with hypotension.

0.5-1 mg IV q 3-5 min Total vagolytic dose is 3 mg

total vagolytic dose, SO HIGHER DOSE IS INEFFECTIVE.

4. Na- bicarb. Acidosis hyperkalemia

1 mEq/kg IV depending on ABG Additional 0.5 mEq/kg may be given every 10 min

-----------------

• Defibrillator are not used as the problem lies in the response of the

myocardial tissue to electrical impulses

PEA - Surgical Care

lifesaving procedures in appropriate pts Pericardiocentesis Chest tube thoracostomy Emergent cardiac sx.

PREVENTION AFTER STABILIZATION :

• Prolonged bed rest → DVT prophylaxis

• Pts under ventilators → ?auto-PEEP

• Hypovol.→ treat aggressively, esp. in active bleeding.

ASYSTOLE

Asystole

• Asystole – end-stage rhythm that follows prolonged VF

or PEA, and for this reason the – prognosis is generally much worse

PEA / ASYSTOLE - Summary

PEA / ASYSTOLE - Summary

• The heart muscle looses its ability to contract even though electrical activity is preserved

• Also EMD & Non-Perfusing Rhythm

PEA / ASYSTOLE - Summary

• ECG shows organised electrical activity• Unable to palpate a pulse• Unable to measure blood pressure• Signs of progressive/irreversible stage of shock

PEA / ASYSTOLE AlgorithmIncludes

EMD Postdefibrillation idioventricular rhythm Pseudo - EMD Bradyasystolic rhythms Idioventricular rhythms Ventricular escape rhythms

• Continue CPR / Intubate at once / Obtain IV Access• Assess blood flow using Doppler ultrasound, endtidal CO2,ECG echocardiography, or arterial line

Consider possible causesHypovolemia (volume infusion) Drug overdoses - tricyclics, digitalisHypoxia (ventilation) Beta-blockers, calcium channel blockersCardiac tamponade (pericardiocentesis) HyperkalemiaTension Pneumothorax AcidosisHypothermia ( see hypothermia algorithm) Massive acute myocardial infarctionMassive pulmonary embolism (surgery, lysine) Massive acute MI (go to Fig 9)

Epinephrine 1 mg IV push,a,c repeat q 3 - 5 min• If absolute bradycardia (< 60 BPM) or relative bradycardia• give atropine 1 mg IV• Repeat q 3 -5 min to a total of 0.03 - 0.04 mg/kg

* The Future???

THANK YOU …….