Download - Cardiopulmonary Resuscitation
CARDIOPULMONARY RESUSCITATION
Dr A. Anvaripour
Cardiac Anesthesiologist
History of resuscitation back to 1966Standards for the performance of CPRMost recent recommendations Guidelines 2005New guidelines has undergone comprehensive evidence-based evaluation
BASIC LIFE SUPPORT
Early recognition of medical emergenciesEmergency response system (e.g., dialing 911 in the United States)BLS assessments : Airway, breathing, and circulation performed without equipmentBLS 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 performance of these skills cannot be overemphasized
Antegrade systemic arterial blood flow continues after cardiac arrest until the pressure gradient between the aorta and right heart structures reach equilibriumSimilar 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 occursCPR is far less efficient than the native circulation , it can provide coronary circulation and cerebral blood flow sufficient to afford full recovery in many casePush hard and push fastchest 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 compressionssingle- 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 columnReduction in left and right ventricular volumeClosure of the tricuspid and mitral valvesEjection of blood into the arterial system
COUGH CPR
Forceful coughing sustain consciousness during ventricular fibrillation (VF) 100 seconds
Coughingarterial pressure pulseopens 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 compressionsModest increases in intrathoracic pressure will impair return of venous blood reducing the chance of spontaneous circulationCardiac 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 value1978, 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 resuscitationNoninvasive 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 & ventilaitonPETCO2
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 ventilationPulmonary 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 riseExcessive ventilation gastric inflationWith tracheal tube 8 to 10 breaths per minute independent of chest compressions
SCISSORS MANEUVER
“SNIFF“ POSITION
MACINTOSH LARYNGOSCOPE IN POSITION
S C H E M AT I C V I E W O F T H E G L O TT I C O P E N I N G D U R I N G D I R E C T L A R Y N G O S C O P Y
SUPRAVENTRICULAR TACHYARRHYTHMIA
Atrial flutterAtrial fibrillationAV junctional tachycardiaMultifocal atrial tachycardiaParoxysmal reentrant tachycardia
HEMODYNAMIC COMPROMISE
Paroxysmal supraventricular tachycardia (PSVT)Atrial fibrillation (or flutter) with rapid ventricular ratesMultifocal 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
the arrhythmia is resistant to therapy
HEMODYNAMICALLY STABLE PSVT
vagal maneuvers (Valsalva ) before initiating pharmacologic interventionsterminate about 20% to 25%Adenosine (very effective in terminating PSVT)
ADENOSIN
slows sinoatrial and AV nodal conductionprolongs refractorinessdiagnostic usefulness with uncertain origin
AFTER INJECTION OF 6 MG ADENOSIN
short half-life (<5 seconds) and short lived side effectsFlushingDyspneachest pain
tachyarrhythmia may recur necessitate the use of another drug
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 monophasic100 J to 120 J with biphasicEscalation 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-minutesecond 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 intervalPVT (polymorphic v tach)
O P T I O N S F O R T H E T R E AT M E N T O F S U P R AV E N T R I C U L A R A R R H Y T H M I A S D R U G S
DiltiazemVerapamilβ-blocking medicationsProcainamideAmiodaron
MULTIFOCAL (MULTIFORM) ATRIAL TACHYCARDIA
Often misdiagnosed as atrial fibrillationIncreased automaticity in multiple atrial foci At least three morphologically different P waves in the same lead with ventricular rate more rapid than 100/minoccurring in patients with COPD, especially during exacerbations, and ICU management
MAT OCCUR
COPD, especially during exacerbationsHypokalemiaCatecholamine administrationAcute myocardial ischemia
TREATMENT
underlying conditions Digitalization CardioversionCalcium channel blockersβ-adrenergic blockersAmiodarone
VENTRICULAR BRADYARRHYTHMIA
Urgent treatment is complete heart block Atropine can be triedChoice is external or transvenous pacing as soon as possible
VENTRICULAR TACHYARRHYTHMIA
VT
life-threatening and sometimes pre-arrest arrhythmiasUrgent intervention
VT ETIOLOGY
HypoxemiaHypercapniaHypokalemia Hypomagnesemia Digitalis toxicityAcid-base derangements
Stable and ventricular function preserved
Procainamide and
cardioversion Amiodaron
AMIODARON
150 mg / 100 cc over a 10-minute periodLoading 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
HypotensionBradycardia
can be prevented by slowing the rate of infusion
Unsatable patients,systemic hypotension,
pulmonary edemaclinical 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 hospitalLong-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
Biphasic150-200 J
insufficient evidence that escalation of energy is
superior to nonescalating energy shocks in
terminating recurrent VF
Witness arrested
Defebrilator
Unwitnes arrested Chest
compression
VF recurs after
successful conversio
n
defibrillation
should be repeated
IF THE DEFIBRILLATOR IS IMMEDIATELY
AVAILABLE
Delay Enditracheal Intubation
No response
to 1st Defebrilato
r
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 tree2-2.5 times IV routsLarge doses of epinephrine (up to 0.2 mg/kg)
VASOPRESSIN
Beneficial effects on perfusion of vital organs during cardiac arrestHigh 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 VFOne-time dose of 40 units intravenously or intraosseously
VF PERSISTS
Amiodarone (preferred antiarrhythmic agent)Lidocaine
AMIODARON
Initial amiodarone dose of 300 mg IVCan be followed by a single dose of 150 mg
AMIODARONE IN OUT-OF-HOSPITAL
RESUSCITATION OF REFRACTORY SUSTAINED
VENTRICULAR TACHYCARDIA
(ARREST
Out-of-hospital cardiac arrestPersistent VFThree attempts at defibrillation1 mg of intravenous epinephrine
300 mg Amiodartone
ALIVE STUDY
demonstrated that amiodarone was
superior to lidocaine in terminating
persistent VF in the out-of-hospital setting
SODIUM BICARBONATE
cardiac arrest that does not respond
Preexisting metabolic acidosisSevere metabolic acidosis documented during CPROverdoses of tricyclic antidepressantsHyperkalemia
INJECTED DRUGS
initial drug injection from IV rout fluid bolus to propeltypically require 1 to 2 minutes to resum central circulationTwo minutes of CPR should be performed after drug administration & before defebrilationIntraosseous cannulationCentral 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