pulseless electrical activity bradycardia Nov 2014

pulseless electrical activity bradycardia CPR

1. PULSELESS ELECTRICAL ACTIVITY & ASYSTOLE Mansoor Masjedi ; MD , FCCM Assistant professor of anesthesia & critical care Sums , Nov. 2014

2. DEFINITION : PEA : Unresponsiveness L ack of palpable pulse P resence of organized cardiac electrical activity P reviously , referred to as electromechanical dissociation ( EMD ) EMD may imply that there is little viable or functional myocardium Also known as ; Non- Perfusing Rhythm

3. 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)

4. MECHANISM: Presence of cardiac electrical rhythm without a proper response of the myocardial tissue and mechanical cardiac output

5. PATHO-PHYSIOLOGY: cardiovascular , respiratory or metabolic sudden changes in preload , afterload , or contractility often result in PEA. E xacerbated by worsening acidosis , hypoxia , and increasing vagal tone .

6. 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 e g . Hypovolemia ( dehydration, blood loss etc) massive pulmonary embolus pericardial tamponade Tension pneumothorax

7. 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.

8. DECREASED CONTRACTILITY: Optimal myocardial contractility depends on: PRELOAD (starling law) AFTER LOAD VIABLE MYOCARDIUM AVAILABILITY OF INOTROPIC SUBSTANCES eg . Adr ., N Adr ., Ca2+ Any derangement from N L ( mainly sudden / severe) can cause PEA.

9. CAUSES : 6 H’s H ypovolemia H ypoxia H ydrogen ion (acidosis) H ypo-/ H yperkalemia H ypoglycemia H ypothermia 5 T’s T oxins (TCA, DIGITALIS, CCB, B-BLOCKER ) T amponade T hrombosis (coronary or pulmonary) T ension PTx T rauma

10. Hypoxia 2 ndary to respiratory failure is probably the most common cause of PEA Resp. insufficiency ; 40-50% of PEA

11. The "3 and 3 rule’ ’ easy recall of the most common correctable causes: SEVERE HYPOVOLUMIA PUMP FAILURE : MASSIVE M.I. POST A.M.I. MYOCARDIAL RUPTURE SEVERE HEART FAILURE OBSTRUCTION TO CIRCULATION : TENSION PNEUMOTHORAX CARDIAC TAMPONADE MASSIVE PULMONARY EMBOLISM

12. SPECIAL ONE : POST DEFIBRILATION PEA : P resence 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

13. PEA - MORTALITY / MORBIDITY O nly 11.2% of PEA survived to hospital discharge rapid initiation of ACLS and identification of reversible cause, improve outcome

14. EVALUATION OF PATIENT PEA / ASYSTOLE

15. PEA - HISTORY prior medical conditions allows prompt identification and correction of reversible causes e g . Hx of : 1 . Severe d ysp . → Pul.Embli 2. MI 2 – 5 days back → cardiac rupture / re infarction 3. T rauma → hypovol . , ten. Pneumo . or pericardial tamp Drug hx . ( b-blocker, CCB ) is also very important

16. 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

17. Important clues : CONDITIONS CLUES HYPOVOLEMIA H/O Blood loss, Flat neck veins 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.

18. PEA - INVESTIGATIONS E mergent 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.

19. 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

20. TREATMENT PEA / ASYSTOLE

21. PEA - MEDICAL MANAGEMENT AHA-ACLS guidelines Initiate CPR Place an IV line Intubate the pt Oxygen 100%

22. 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

23. 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 -----------------

24. Defibrillator are not used as the problem lies in the response of the myocardial tissue to electrical impulses

25. PEA - Surgical Care lifesaving procedures in appropriate pts Pericardiocentesis C hest tube thoracostomy Emergent cardiac sx .

26. PREVENTION AFTER STABILIZATION : P rolonged bed rest → DVT prophylaxis Pts under ventilators → ? auto-PEEP Hypovol . → treat aggressively, esp. in active bleeding.

27. ASYSTOLE

28. Asystole Asystole end-stage rhythm that follows prolonged VF or PEA, and for this reason the prognosis is generally much worse

29. PEA / ASYSTOLE - Summary

30. PEA / ASYSTOLE - Summary The heart muscle looses its ability to contract even though electrical activity is preserved Also EMD & Non- Perfusing Rhythm

31. 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

32. PEA / ASYSTOLE Algorithm Includes 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 CO 2 ,ECG echocardiography, or arterial line Consider possible causes Hypovolemia (volume infusion) Drug overdoses - tricyclics , digitalis Hypoxia (ventilation) Beta-blockers, calcium channel blockers Cardiac tamponade ( pericardiocentesis ) Hyperkalemia Tension Pneumothorax Acidosis Hypothermia ( see hypothermia algorithm) Massive acute myocardial infarction Massive 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

33. The Future???

34. THANK YOU …….