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Organized Cardiac Rhythms Without Pulse
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
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.
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
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
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.
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