Advanced Cardiac Life Support. Basic Cardiac Life Support.

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Advanced Cardiac Life Support

Basic Cardiac Life Support

Definitions of death

Clinical death means that the heartbeat and breathing have stopped. This process is reversible.

Biological death is permanent, cellular damage due to lack of oxygen, the brain cells are the most sensitive to the lack of oxygen.

Brain damage occurs after 4 minute of cardio-respiratory arrest.

CPR It is the simple procedures which prevent

circulatory and/or respiratory arrest or insufficiency prompt intervention.

These simple procedures include: Open and clear airway Mouth to mouth breathing (through

a barrier) OR bag-mask ( Ambu-baging )

External cardiac compression

Basic knowledge

Basic knowledge External cardiac compression give 25% of

original Cardiac Output. It contract around 70 times/min, every

contraction ejects 70 ml of blood, so minute Cardiac Output is around 5 L/min. ( at rest).

Respiratory center is located in the brain which is stimulated by the level of the arterial carbon dioxide.

Adult respiratory rate is about 12-15 times/min.

Room air contain 21%O2 – our expiration contain 16% O2

To start CPR

The patient is Unresponsive Breathlessness Pulselessness

Chain Of Survival ( Sequences of action linked together too tightly with no gap )

Activate code blue Start CPR until Defibrillator and team

arrive Defibrillation if indicated Advanced cardiac life support actions

to be followed i.e. intubation, IV line for fluids and drugs etc….

Principles of Defibrillation Electric shock will terminate

ventricular fibrillation by transmural current flow

Entire myocardium is depolarised into refractoriness. The SA node, as the fastest pacemaker, may resume pacing function

Safe Defibrillation

To avoid accidental shocks to rescuer and patient injury

Safe environment, away from pooled water or metal surface under patient or rescuer

Apply conductive material Turn on defibrillator, select

energy and charge defibrillator Proper electrode placement Apply firm pressure on electrodes

Make sure no smearing of conductive gel

Remove transdermal patches Keep paddles >12 cm away from

implanted cardiac pacemakers Make sure no personnel are

directly in contact with the patient, clearing chant

Ensure VF or pulseless VT Depress both discharge buttons

simultaneously and deliver the electric shock

Defibrillation Energy

Adults200J 200/300J 360J 360J

thereafter (monophasic)Non-escalating 150J (biphasic)

Children2J/kg 2-4J/kg 4J/kg 4J/kg

thereafter

Some Determinants of Defibrillation Dose Chest impedance Electrode size and location Type of waveform Disease, drugs, metabolic

state of the subject

Factors Reducing Transthoracic Impedance Appropriate electrode size Coupling medium between

electrodes and chest wall Repeated shocks Expiratory phase of

respiration Electrode-chest wall contact

pressure (>10 kg) Post-cardiac surgery

Electrode Size

diameter of electrode impedance and defibrillation

thresholdIn animals:

8 cm : 71% defib success12.8 cm : 88% defib success

Very large electrodes impedance, but… in current density

defibrillation successInadequate contact with chest

Coupling Medium

Electrode paste (e.g. Redux paste)Electrode paste resulted in

significantly lower impedance than the disposable defibrillation pads. No difference in defibrillation success.

Beware of paste spread across the chest wall during CPR

Disposable coupling pads (e.g. Defib-Pads)

Adhesive pads

Self-adhesive pads

AdvantagesProphylactic placement in high

risk patientsLess interference with external

cardiac massageIncorrect coupling gel avoidedBetter operator safety

DisadvantagesSpecial connectionLack of firm pressureHigh impedanceHairy skin

Electrode Position

Proper polarity facilitates ECG interpretation. It does not affect success of defibrillation

Three acceptable positionsSternal-apicalLeft-anterior-posteriorApical –posterior

Sternal-apical

Below the outer right clavicle Cardiac apex

Left-anterior-posterior

Anterior apex just left of palpable cardiac apex

Back inferior to the left scapula

Apical–posterior

Left ventricular apex Back inferior to the left

scapula

If VF Persists:

Secure airway, ventilatory and circulatory support, IV access

Appropriate medications to maintain myocardial and cerebral viability

Detect and treat potentially reversible underlying causes

Resume defibrillation attempts After each minute of CPR, or after

each medication The best prospects for restoring a

perfusing rhythm still remain with defibrillation

Scope of ACLS

Basic life support ECG monitoring, interpretation and

arrhythmia recognition Advanced equipment and techniques

for ventilation and circulation Therapies for respiratory or cardiac

arrests Treatment of acute coronary

syndromes Treatment with tPA for eligible

stroke patients

Scope of ACLS

Basic life support ECG monitoring, interpretation and

arrhythmia recognition Advanced equipment and techniques

for ventilation and circulation Therapies for respiratory or cardiac

arrests Treatment of acute coronary

syndromes Treatment with tPA for eligible stroke

patients

International Guidelines 2005 Conference on Cardio-pulmonary Resuscitation and Emergency Cardiovascular Care

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The 3 Unequivocally Effective Interventions Basic cardiopulmonary

resuscitation Oxygenation and ventilation

of the lungs through a patent secure airway

Defibrillation for ventricular fibrillation or pulseless ventricular tachycardia

Advanced Equipment & Techniques for Ventilation

& Circulation

Airway Adjuncts

Oropharyngeal airways Nasopharyngeal airways Laryngeal mask airway

64-100% success Combitube

69-100% success Cuffed oropharyngeal

airways (COPA) Suction devices

Combitube

Endotracheal Intubation

Optimal airwaySecure and clear airwayProtect airwayNo gastric inflationDrugBronchial toilet

Need 3 minutes of preoxygenation Ventilation should not be

interrupted for > 30 seconds Cricoid pressure Use of stylet or gum elastic bougie Confirm and secure tube position

Breathing

FiO2 of 1.0 Manual resuscitators or

ventilators 12-15 breaths/minute Tidal Volume

10-12 ml/kg, if intubated6-7 ml/kg, if not

unintubated

Circulation

Closed chest compression at 100/minute

Open chest CPR should be restricted to operating theatre and selected instances of penetrating thoracic injury

Specific Drug Therapy

Meticulous, systematic review reveals that relevant, valid, and credible evidence to confirm a benefit due to these agents simply does

NOT exist.

Routes of Drug Administration Peripheral veins Central veins Tracheal Intraosseous Intracardiac

Peripheral Venous Route

Peak effect 1.5-3 min. after injection at antecubital fossa

IV push20 ml NS flush after drug

injection circulation time by 40% Comparable to drug delivery

through a central vein

Central Venous Route

Faster, higher peak concentration and more potent effect compared to peripheral injection

Should be used if it is already in situ

Inserting a central line is associated with problems of interrupting CPR, bleeding arterial puncture and air embolism

Tracheal Route

Second line route due to impaired absorption and unpredictable pharmacodynamics

Need 2-3 times the IV dose, diluted to at least 10 ml in 0.9% NS

Non-ionic drugs only:adrenalin, atropine, lignocaine and

naloxone NEVER calcium or sodium

bicarbonate

Intracardiac Route

NOT recommended May produce pneumothorax,

injury to a coronary artery and prolonged interruption of cardiac massage.

Inadvertent injection into the myocardium may produce intractable arrhythmias

Drugs for Resuscitation

VasopressorsAdrenalineVasopressin

Other AgentsAtropineBuffer agentsCalcium

Adrenaline

Adrenaline 1 mg (10 ml of 1:10,000 dilution) IV boluses every three minutes until pulse returns

Short half life of 3-5 minutes -effect (vasoconstriction)

aortic pressure to maintain myocardial and cerebral blood flow

Cautions: solvent abuse, cocaine and other sympathomimetic drugs

Vasopressin

40 U IV: powerful vasoconstriction V1 receptors in smooth muscle Longer half-life of 10-20 minutes If there is no response 10-20 min.

after 40 U of IV vasopressin, resume epinephrine 1 mg IV push every 3 to 5 minutes

Used in VF/VT ? role in asystole or PEA

Antiarrhythmic DrugsDrug Fibrillatio

n threshold

Defibrillation threshold

Proarrhythmo-genicity

Quinidine ++ +++ +

Procainamide

++ 0 +

Flecainide ++ +++ +

Lignocaine ++ + +

Bretylium ++ - +

Amiodarone ++ - 0/+

Verapamil + ++ 0

Diltiazem + ++ 0

Nifedipine + 0 0

Adrenergic agents

Beta-blockers

++ + 0

Sotolol + - +

Antiarrhythmic DrugsDrug Fibrillatio

n threshold

Defibrillation threshold

Proarrhythmo-genicity

Quinidine ++ +++ +

Procainamide

++ 0 +

Flecainide ++ +++ +

Lignocaine ++ + +

Bretylium ++ - +

Amiodarone ++ - 0/+

Verapamil + ++ 0

Diltiazem + ++ 0

Nifedipine + 0 0

Adrenergic agents

Beta-blockers

++ + 0

Sotolol + - +

Drugs for Persistent VF

AmiodaroneClass IIbRapid infusion of 300 mg in 20-

30 ml NS IV push (cardiac arrest dose)

If VF/pulseless VT recurs, Supplementary doses of 150 mg

IV by rapid infusionFollowed by 1 mg/min for 6 hours

and then 0.5 mg/minMaximum daily dose of 2 g

Lignocaine Class indeterminate Initial bolus of 1.0-1.5 mg/kgAdditional bolus of 0.5-0.75 mg/kg Maximum total of 3 mg/kgMaintenance infusion of 1-4 mg/min

Magnesium sulphate1-2 g diluted in 100 ml D5 over

1-2 minutesClass IIb in torsades de pointes or

suspected hypomagnesaemia or severe refractory VF

Atropine

Good for haemodynamically significant bradycardia from high vagal tone, hypoxia or nodal ischaemia

? For asystole or PEA 1 mg up to 3 doses or

single dose of 3 mg will produce a fully vagolytic effect

Buffer Agents

8.4% sodium bicarbonate solution

Initial dose of 1 mEq/kg Problems

Left shift of Hb dissociation curveParadoxical intracerebral acidosisHigh osmolality and Na loadInactivate simultaneously

administered catecholamines

Indications of NaHCO3

Class I Preexisting hyperkalemiaPexisting bicarbonate-responsive

acidosis

Alkaline diuresis; overdose of tricyclic antidepressant, aspirin, etc.

Class IIbLong arrest interval

In intubated and ventilated patientsOn return of circulation

Class IIIHypercarbic acidosis

Calcium

Only used in hypocalcaemia, hyperkalaemia and calcium antagonist overdose

10% CaCl2 at 2-4 mg/kg repeated as necessary at 10-minute intervals

Worries regarding the role of Ca++ in ischaemic cell damage during reperfusion to the heart and the brain

UniversalAdvanced

Life Support

Algorithm

The Universal Advanced Life Support Algorithm Two arrest rhythms

VF/Pulseless VT Ventricular fibrillationPulseless ventricular

tachycardiaNon-VF/VT

Pulseless electrical activityAsystole

VF / Pulseless VT

VF: commonest primary arrest rhythm

VF/VT: 85% to 95% of the survivors from cardiac arrest

Pulseless VT deteriorates rapidly to VF and treatment is identical to that of VF

Management of VF / Pulseless VT Electrical defibrillation is the

most effective treatment for VF

CPR unlikely to convert VF Speed of defibrillation is the

major determinant of success of VF treatment Survival rates after VF arrest

7-10 %/min

In-hospital Cardiac Arrest

• 1325 Resuscitation attempts using 1997 Guidelines• Updated from: Gwinnutt C et al. Resuscitation 1998; 37: S64

VF/VT EMD/Asystole

Number 422 (32%) 903 (68%)

ROSC 298 (71%) 344 (38%)

Survive discharge

179 (42%) 58 (6%)

Cardiac Arrest Time before Defibrillation

Yakaitis et al. Crit Care Med 1982;8:157-163.

Balance between electrical injury and efficiency of defibrillation

Damage related to the peak current, not the energy delivered

Weaver et al. N Engl J Med 1982;307:1101

Morbidity & Mortality

Dahl et al. Circulation 50:956. Ehsani et al. Am J Cardiol 37:12.Warner et al. Arch Pathol 99:55.

Transthoracic Impedance

70-80 (range 15-143) impedance current Current-based defibrillation

30-40A MDS

(sec)Duration*(ohms)Resistance(joules)Energy

Current

Defibrillation vs. Cardioversion

Defibrillation

Electric shock delivered without synchronization with ECG activity

Used in VF or pulseless VT

Synchronized Cardio-version

Electric shock delivered with synchronization with R wave to avoid the R on T phenomenon

Used in unstable tachyarrhytmias other than VF or pulseless VT

Non-VF/VT

RhythmsUniversalAdvanced

Life Support Algorithm

Non-VF/VT Rhythms

Defibrillation is NOT indicated Prognosis much poorer than VF/VT Secure basic life support, airway,

oxygen, ventilation, IV access Detect and treat potentially

reversible conditions Consider:

Atropine: 3 mg bolus given once or 1 mg bolus to a maximum of 3 mg

Pacing if P waves are present

Pulseless Electrical Activity (PEA) Absence or undetectable mechanical

activity in the presence of coordinated electrical activity

Includes Pseudo-EMD Idioventricular rhythmsVentricular escape rhythmsPostdefibrillation idioventricular rhythmsBradyasystolic rhythms

Rhythm of survival if a reversible cause of PEA is identified and treated appropriately

Possible Underlying Reversible Causes

H’s Hypovolemia Hypoxia Hydrogen ion

(acidosis) Hyperkalemia/

hypokalemia/ metabolic disorders

Hypothermia/ hyperthermia

T’s Toxins/tablets

(drug overdose)

Tamponade, cardiac

Tension pneumothorax

Thrombosis, coronary

Thrombosis, pulmonary

Asystole

Primary rhythm in up to 25% inhospital arrests

Most commonly seen in outpatients with VF who have not been resuscitated successfully

Low survival rate 1-2 out of 100 cardiac arrests

Identify and treat a reversible cause

Consider “not starting” and “when to stop”

Post-resuscitation Care

CNS is most vulnerable for ischaemic-hypoxic damage during cardiac arrest

ICU or CCU admission Avoid and correct hypotension,

hypoxia, hypercarbia, electrolyte imbalance, hypoglycaemia and hyperglycaemia

Control convulsions with anticonvulsants

No drugs have been demonstrated to reduce cerebral complications

In Summary

Perform CPR at all times for pulseless patients

Defibrillate VF/VT until it is no longer present

Gain airway control and provide adequate oxygenation and ventilation

Give IV boluses of epinephrine

Correct reversible causes