đCall Girls In Amritsar đŻAnvi đ˛đ8725944379đAmritsar Call Girl Nođ°Advance Cash...
Â
pulseless electrical activity bradycardia Nov 2014
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
ďą eg. Hypovolemia ( dehydration, blood loss etc)
massive pulmonary embolus
pericardial tamponade
Tension pneumothorax
7. DECREASED AFTERLOAD :
⢠Sudden â afterload â âmyocardial perfusion (before
autoregulatory mechanism becomes active) & decreases
contractility.
ďą Eg . Hypovolumia
vasodilator therapy
Shock etc.
Though very âââ afterload canâcontractility 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 ruleââeasy 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 :
ď Presence of organized electrical activity, immediately after electrical
cardioversion in the absence of palpable pulse
ď Better prognosis than continued VF
ď 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
â eg. Hx of :
1. Severe dysp. â Pul.Embli
2. MI 2 â 5 days backâ cardiac rupture / re infarction
3. Trauma â hypovol. , ten. Pneumo. or pericardial tamp
⢠Drug hx. ( b-blocker, CCB ) is also very important
16. PEA â Phys. Exam.
⢠No peripheral pulses
⢠Clues to aetiology :
ď tracheal shift to opposite side & absent breath sound indicates ------
----- Tension PTX
ď No respiratory finding with engorged JVP ------- pul. Embolism
ď 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 - ContdâŚâŚ..
⢠Imaging : Bedside Echo. / Sono.
⢠Other Tests : 12 lead ECG( difficult to obtain during ongoing
resuscitation)
â âK
â AMI
â HYPOTHERMIA (Osborne wave)
â Drug overdose (TCA : QT prongation)
â Pul embolism : Rt. Axis daviation
ď Procedures : arterial line in pts with a very low BP
21. PEA - MEDICAL MANAGEMENT
AHA-ACLS guidelines
ďInitiate CPR
ďPlace an IV line
ďIntubate the pt
ďOxygen 100%
22. PEA - MEDICAL MANAGEMENT â ContâŚ.
Then reversible causes should be sought and corrected :
ď§ Hypovolemia -Volume infusion
ď§ Hypoxia - Ventilation
ď§ Cardiac Tamponade - Pericardiocentesis
ď§ Tension Pneumothorax - Needle decompression
ď§ Hypothermia - Hypothermia correction
ď§ Massive pulmonary embolism - surgery, thrombolytics
ď§ Drug overdose - Appropriate therapies
ď§ Hyperkalemia - Sodium bicarbonate
ď§ Massive AMI â AMI rx
23. Resuscitative pharmacology
DRUGS INDICATION DOSES AD/DISVANTAGE
1. EPINEPHRINE â˘PEA arrest
â˘B-blocker/ CCB
overdose
1 mg IV q3-5min ď No improvement
in outcome in most.
ď 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.
ď 0.5-1 mg IV q 3-5
min
ď Total vagolytic
dose is 3 mg
ď total vagolytic
dose, SO HIGHER
DOSE IS
INEFFECTIVE.
4. Na- bicarb. ď Acidosis
ď hyperkalemia
ď 1 mEq/kg IV
depending on
ABG
ď 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
ď Pericardiocentesis
ď Chest tube thoracostomy
ď Emergent cardiac sx.
26. PREVENTION AFTER STABILIZATION :
⢠Prolonged bed rest â DVT prophylaxis
⢠Pts under ventilators â ?auto-PEEP
⢠Hypovol.â 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