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
• 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

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.
• Exacerbated 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
 eg. 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:
1. PRELOAD (starling law)
2. AFTER LOAD
3. VIABLE MYOCARDIUM
4. AVAILABILITY OF INOTROPIC SUBSTANCES eg. Adr., N Adr., Ca2+
• Any derangement from NL ( mainly sudden / severe) can
cause PEA.

9. CAUSES :
6 H’s
Hypovolemia
Hypoxia
Hydrogen ion (acidosis)
Hypo-/Hyperkalemia
Hypoglycemia
Hypothermia
5 T’s
Toxins (TCA, DIGITALIS,
CCB, B-BLOCKER )
Tamponade
Thrombosis (coronary or
pulmonary)
Tension PTx
Trauma

10. Hypoxia 2ndary 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:
1. SEVERE HYPOVOLUMIA
2. PUMP FAILURE :
I. MASSIVE M.I.
II. POST A.M.I. MYOCARDIAL RUPTURE
III. SEVERE HEART FAILURE
3. OBSTRUCTION TO CIRCULATION:
I. TENSION PNEUMOTHORAX
II. CARDIAC TAMPONADE
III. MASSIVE PULMONARY EMBOLISM

12. 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

13. PEA - MORTALITY / MORBIDITY
• Only 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
– 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

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
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.

18. 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.

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
 Chest tube thoracostomy
 Emergent cardiac sx.

26. PREVENTION AFTER STABILIZATION :
• Prolonged 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

31. PEA / ASYSTOLE - Summary

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

33. 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

34. 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 CO2,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

38. * The Future???

39. THANK YOU
…….