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