Transcript Cardiopulmonary Resuscitation

CARDIOPULMONARY
RESUSCITATION
Dr A. Anvaripour
Cardiac Anesthesiologist
 History of resuscitation back to 1966
 Standards for the performance of CPR
 Most recent recommendations Guidelines 2005
 New guidelines has undergone comprehensive evidencebased evaluation
BASIC LIFE SUPPORT
 Early recognition of medical emergencies
 Emergency response system (e.g., dialing 911 in the United
States)
 BLS assessments : Airway, breathing, and circulation performed
without equipment
 BLS interventions: breathing/Heimlich maneuver/application-
use of an automated external defibrillator (AED)/CPR
GOAL
supporting the circulation until restoration of spontaneous
circulation occurs after SCA
FOR THOSE PERFORMING
BLS INTERVENTIONS
Importance of prompt initiation and expert
these skills cannot be overemphasized
performance of
 Antegrade systemic arterial blood flow continues after
cardiac arrest until the pressure gradient between the aorta and
right heart structures reach equilibrium
 Similar process occurs during cardiac arrest with antegrade
pulmonary blood flow between the pulmonary artery and the
left atrium
 Arterial-venous pressure gradients dissipate left heart
becomes less filled/the right heart becomes more filled/venous
capacitance vessels become increasingly distended
CORONARY PERFUSION
AND CEREBRAL BLOOD
FLOW STOP
When arterial and venous pressure equilibrates (approximately
5 minutes after cardiac arrest)
 CPR is performed until return of spontaneous circulation occurs
 CPR is far less efficient than the native circulation , it can
provide coronary circulation and cerebral blood flow sufficient to
afford full recovery in many case
 Push hard and push fast
 chest compressions performed at a rate of 100/min until
generate a palpable carotid or femoral pulse are considered ideal.
CHEST COMPRESSIONS
Must not frequently interrupted
CURRENT
RECOMMENDATIONS
 Placing increased emphasis on limiting interruptions in
chest compressions
 single- and two-person CPR compression-ventilation ratios
of 30 : 2
“ CARDIAC PUMP
MECHANISM ”
 Blood is ejected
 Actual compression heart between the sternum and the
vertebral column
 Reduction in left and right ventricular volume
 Closure of the tricuspid and mitral valves
 Ejection of blood into the arterial system
COUGH CPR
 Forceful coughing sustain consciousness during
ventricular fibrillation (VF) 100 seconds
 Coughingarterial pressure pulseopens the aortic valve
THORACIC PUMP
MECHANISM
Increases in intrathoracic pressure generate forward blood flow
cardiac pump and thoracic pump mechanisms exist during
resuscitation
 Systemic, coronary, and cerebral blood flow during CPR is
dependent on effective chest compressions
 Modest increases in intrathoracic pressure will impair return of
venous blood reducing the chance of spontaneous circulation
 Cardiac output during effective CPR: 25% 30%
 oxygen content in the lungs at the time of cardiac arrest usually
sufficient for maintaining an acceptable arterial oxygen content
during the first several minutes of CPR
RESULT
Breaths are less important than initiating chest compressions
immediately after the onset of SCA
MONITORING DURING CPR
 palpation of the carotid or femoral
 observation of pupillary size
 Initial pupillary size and changes during CPR are of some
prognostic value
 1978, Kalenda described the use of capnography as a guide
to the effectiveness of external chest compressions
 Rapid decrease in PETCO2 with the onset of arrest
 Immediate increase with resuscitation
 Noninvasive guide to advanced life support interventions
during CPR
 Severe reductions in pulmonary blood flow acute failure of
delivery of O2 to the lungs very low PETCO2
 External chest compression & ventilaitonPETCO2
increased to 1.9% ± 0.3%,
 After successful defibrillation and 12 minutes of CPR 
PETCO2 immediate increase to 4.9% ± 0.3%
RESULT
Close correlation was found between changes in cardiac output
and PETCO2
MAJOR DETERMINANTS
OF P ETCO 2
 CO2 production
 Alveolar ventilation
 Pulmonary blood flow.
BREATHING
 Breathing is indicated for a nontracheally intubated cardiac
arrest
 two 1-second breaths are delivered after the 30th compression
 Provide only enough force and volume to cause chest rise
 Excessive ventilation gastric inflation
 With tracheal tube 8 to 10 breaths per minute independent of
chest compressions
SCISSORS MANEUVER
“SNIFF“ POSITION
MACINTOSH
LARYNGOSCOPE IN
POSITION
SCHEMATIC VIEW OF THE
GLOTTIC OPENING
DURING DIRECT
LARYNGOSCOPY
SUPRAVENTRICULAR
TACHYARRHYTHMIA
 Atrial flutter
 Atrial fibrillation
 AV junctional tachycardia
 Multifocal atrial tachycardia
 Paroxysmal reentrant tachycardia
HEMODYNAMIC
COMPROMISE
 Paroxysmal supraventricular tachycardia (PSVT)
 Atrial fibrillation (or flutter) with rapid ventricular rates
 Multifocal atrial tachycardia
PSVT
PSVT
 With hemodynamic deterioration 
cardioversion
100 to 200 J if a monophasic defibrillator
100 to 120 J with a biphasic defibrilator
PSVT
Energy can be increased as needed if
is resistant to therapy
the arrhythmia
HEMODYNAMICALLY
STABLE PSVT
 vagal maneuvers (Valsalva ) before initiating pharmacologic
interventions
 terminate about 20% to 25%
 Adenosine (very effective in terminating PSVT)
ADENOSIN
 slows sinoatrial and AV nodal conduction
 prolongs refractoriness
 diagnostic usefulness with uncertain origin
AFTER INJECTION OF
6 MG ADENOSIN
 short half-life (<5 seconds) and short lived side effects
 Flushing
 Dyspnea
 chest pain
 tachyarrhythmia may recur
another drug
 necessitate the use of
VERAPAMIL
PSVT does not respond to adenosine or if it recurs
contraindicated in WPW syndrome
AF/AF
 Rate-related hemodynamic compromise  cardioversion
 100 to 200 J with monophasic
 100 J to 120 J with biphasic
 Escalation of energy doses for the second and subsequent
doses is indicated
AF/AF
 hemodynamically stable patients  pharmacologic
 Ibutilide
most rapid onset in restoring sinus rhythm
 Prolongs the action potential dration / effective refractory
 1 mg given over a 10-minute
 second dose can be administered 10 minutes after the first, if
necessary
 Conversion to sinus rhythm is more frequent with atrial
flutter than with atrial fibrillation (63% versus 31%)
IBUTILIDE SIDE EFFECTS
 Prolongation of the QT interval
 PVT (polymorphic v tach)
OPTIONS FOR THE
TREATMENT OF
SUPRAVENTRICULAR
ARRHYTHMIAS DRUGS
 Diltiazem
 Verapamil
 β-blocking medications
 Procainamide
 Amiodaron
MULTIFOCAL
(MULTIFORM) ATRIAL
TACHYCARDIA
 Often misdiagnosed as atrial fibrillation
 Increased automaticity in multiple atrial foci
 At least three morphologically different P waves in the same
lead with ventricular rate more rapid than 100/min
 occurring in patients with COPD, especially during
exacerbations, and ICU management
MAT OCCUR
 COPD, especially during exacerbations
 Hypokalemia
 Catecholamine administration
 Acute myocardial ischemia
TREATMENT
 underlying conditions
 Digitalization
 Cardioversion
 Calcium channel blockers
 β-adrenergic blockers
 Amiodarone
VENTRICULAR
BRADYARRHYTHMIA
 Urgent treatment is complete heart block
 Atropine can be tried
 Choice is external or transvenous pacing as soon as possible
VENTRICULAR
TACHYARRHYTHMIA
VT
 life-threatening and sometimes pre-arrest arrhythmias
 Urgent intervention
VT ETIOLOGY
 Hypoxemia
 Hypercapnia
 Hypokalemia
 Hypomagnesemia
 Digitalis toxicity
 Acid-base derangements
Stable and ventricular function preserved
Amiodaron
Procainamide and
cardioversion
AMIODARON
 150 mg / 100 cc over a 10-minute period
 Loading infusion of 1 mg/min for 6 hours and then a 0.5-
mg/min maintenance infusion over an 18-hour period, may be
effective
MAJOR ADVERSE EFFECTS
OF AMIODARONE
 Hypotension
 Bradycardia
can be prevented by slowing the rate of infusion
Unsatable patients,
systemic hypotension, pulmonary
edema
clinical or electrocardiographic
signs of acute myocardial
ischemia or infarction
Monophasic
energy doses
of 360 j
Biphasic
120 j
ATYPICAL VT (TWISTING
POINTS)
CHARACTERISTIC
long-short initiating sequence
This arrhythmia occurred in a patient after resuscitation from
cardiac arrest
TREATMENT
 Underlying correction ( esp. Hypokalemia)
 Pace
 Magnesium sulfate
 Without prolonged QT interval  similar to VT
MANAGEMENT OF
CARDIAC ARREST
Pulseless Ventricular Tachycardia
or Ventricular Fibrillation
 Most treatable arrhythmia
 In the hospital and out of the hospital
 Long-term survival
DEFINITIVE
INTERVENTION
Rapid Defibrillation
TERMINATION OF VF
 Amount of energy available from a defibrillator
 Resistance to flow of current
GUIDELINES
 Self-adhesive defibrillation pads
 Defibrillation should occur at the end of expiration to
minimize impedance
Momophasic
360 J
Biphasic
150-200 J
insufficient evidence that
escalation of energy is superior to
nonescalating energy shocks in
terminating recurrent VF
Witness
arrested
Unwitnes
arrested
Defebrilator
Chest
compression
VF recurs
after
successful
conversion
defibrillation
should be
repeated
IF THE DEFIBRILLATOR
IS IMMEDIATELY
AVAILABLE
Delay Enditracheal Intubation
No response
to 1st
Defebrilator
5 cycle CPR
30/2
second
defibrillatory
shock
pharmacologic interventions should accompany the
resuscitative efforts
CURRENTLY, ONLY TWO
MEDICATIONS
 Epinephrin
Vasopressin
EPINEPHRIN
 1 mg (1 : 10,000 solution)
 Every 3 to 5 minutes
 From tracheobronchial tree2-2.5 times IV routs
 Large doses of epinephrine (up to 0.2 mg/kg)
VASOPRESSIN
 Beneficial effects on perfusion of vital organs during cardiac
arrest
 High level of plasma concentration in stress situation
 Muscle V1 receptors  muscle constriction in the presence
of severe acidosis  maintain coronary perfusion
 Alternative to one dose of epinephrine during refractory VF
 One-time dose of 40 units intravenously or intraosseously
VF PERSISTS
 Amiodarone (preferred antiarrhythmic agent)
 Lidocaine
AMIODARON
 Initial amiodarone dose of 300 mg IV
 Can be followed by a single dose of 150 mg
AMIODARONE IN OUTOF-HOSPITAL
RESUSCITATION OF
REFRACTORY
SUSTAINED
VENTRICULAR
TACHYCARDIA (ARREST
 Out-of-hospital cardiac arrest
 Persistent VF
 Three attempts at defibrillation
 1 mg of intravenous epinephrine
300 mg Amiodartone
ALIVE STUDY
 demonstrated that amiodarone was superior to
lidocaine in terminating persistent VF in the outof-hospital setting
SODIUM BICARBONATE
cardiac arrest that does not respond
 Preexisting metabolic acidosis
 Severe metabolic acidosis documented during CPR
 Overdoses of tricyclic antidepressants
 Hyperkalemia
INJECTED DRUGS
 initial drug injection from IV rout  fluid bolus to propel
 typically require 1 to 2 minutes to resum central circulation
 Two minutes of CPR should be performed after drug
administration & before defebrilation
 Intraosseous cannulation
 Central circulation
FLUIDS
 Normal saline
 Lactated Ringer
 glucose-containing solutions not recommended
PULSELESS ELECTRICAL
ACTIVITY
 Hypovolemia
 Hypoxia
 Acidosis
 Hypo/Hyperkalemia
 Tamponade
 Tension pnemothorax
 Coronary thrombosis
 Pulmonary thrombosis
PEA TREATMENT
 Epinephrin 1 mg IV push  Q 3-5 min repeated
 Atropin 1 mg ( if rate of PEA is slow)  Q3-5 min repeared ,
total dose 0.04 mg/kg
CPCR
Cardiopulmonary cerebral rescucitation
POST CARDIAC ARREST
INDUCED HYPOTHERMIA
HYPOTHERMIA
 Intracellular PH increased significantly  ischemic tolerance
 Cerebral o2 consumption in profound hypothermia decreased
 CBF/CMRO2 = 75/1
normothermia = 20/1
METHODS
 Systemic ( Blanket)
 Topical (Ice application on head )
CONTRAVERSIES
Systemic hypothermia + topical hypothermia
Q10
predict safe time of arrest # 15 min /20 degree of c.
30 – 45 min Brain Tolerated
Therapeutic
Hypothermia
32 – 34 d of c. Induced with External cooling
12 – 24 hours After Resuscitation
Appears decreased neurological outcome in VF arrested patient
DHCA
Nasopharyngeal Temp 11- 14  max safe duration 30 min
Nasopharyngeal Temp 12.5 99.5% Electrocortical silence
OUTCOME AFTER IN HOSPITAL
RESUSCITATION
 Discharge survival rates 8-21 %
 Average survival rate of approximately 14%
 Intraoperative cardiac arrest survival 38%( Retrospective)
 Primary cardiac event was presumed to be causative in 50%
LIMIT SURVIVAL
VARIABLES
 Age
 Duration longer than 30 min
 Sepsis
 Cancer
 Pre- arrest hypotension
 Renal failure
 Unwitnessed arrest
MAJOR DETERMINANT
Age
AGE ALONE SHOULD NOT
PRECLUDE PATIENTS
FROM RECEIVING CPR
UNWARRANTED CPR
Sepsis or cancer in an elderly patient
Unwitnessed bradyarrhythmic arrested