INTRODUCTION TO ACLS

Introduction To ACLS,1 1 Sep 2006

EPIDEMIOLOGY • In Singapore, every year about 2,400 people suffer from an acute myocardial infarction. Of these about 900 die as a result of sudden cardiac arrest, 520 of them collapsing in the pre-hospital environment. • Heart disease is the second commonest cause of death in our country. Every year nearly 1000 people collapse out-ofhospital from heart disease. This amounts to nearly 3 persons per day. • The current survival of these is only about 4.5%. Introduction To ACLS,2 1 Sep 2006

Sudden Cardiac Death : Epidemiology • 50% of victims are < 75 years old • More than 80% of sudden cardiac deaths are due to Ventricular Arrhythmias

• About 80% of victims had Ischemic Heart Disease

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Terminal Arrhythmia 157 patients with SCD VT degenerated to VF Primary VF Torsade de pointes Bradyarrhythmias

62% 8% 13% 17%

Bayes deLuna, Ambulatory sudden cardiac death. Am Heart J, 1989

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Chain of Survival

Early Access

Early CPR

Early Defibrillation

Early Advanced Care

Sequence of events in emergency cardiac care is displayed schematically by “chain of survival” metaphor

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Role of ACLS in CPR • Last link in chain of survival Early access- early CPR - early defibrillation early ACLS

• However critical role in hospital resuscitation • ACLS is the most important treatment for potential lethal rhythms ie SVTs and VTs

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Cardiac Arrest From Abnormal Heart Rhythm Survival Rate and Promptness of CPR & ACLS Initiation of CPR (minutes)

Arrival of ACLS (minutes)

Survival Rate (%)

0-4

0-8

43

0-4

16 +

10

8 - 12

8 - 16

6

8 - 12

16 +

0

12 +

12 +

0

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Introduction To ACLS,8 1 Sep 2006

Introduction To ACLS,9 1 Sep 2006

Time is life

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Phase 1 • BCLS and ACLS need to be integrated • Basic foundation of BCLS is extremely important • Strong support needed for community skills in 9 CPR 9 Defibrillation • Public-access defibrillation • Early in-hospital defibrillation

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Phase 2 Entry 1. 2. 3. 4. 5.

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Entry vital signs Orderly transfer ABCD baseline measurements Concise history New vital signs

Team Organisation in ACLS • Team Leader • Assesses ABC • Endotracheal intubation • Identifies ECG rhythm • Gives order to defibrillate

D1

• Orders IV drugs • Speaks to relatives • Decides disposition of patient • Takes charge of debrief

D1 • Assists D1 in intubation. N1 • Documentation • Co-ordinates nursing action

LEGEND D1 = Doctor 1 D2 = Doctor 2 N1 = Nurse 1 N2 = Nurse 2 Introduction To ACLS,13 1 Sep 2006

N2

• Cardiac Monitor/Defibrillator • Performs CPR. • If pulse returns, monitors vital signs, prepares IV drip

• D2 • • •

Inserts IV line. Executes defibrillation. Gives IV drugs as instructed by D1. Alternates with N2 in performing cardiac compression. • Carries out procedures as instructed.

Phase 3 Resuscitation 1 2 3

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Focus on the primary and secondary ABCDs Decisive, professional, unflappable attitude One voice

Phase 4 Resuscitation 4

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Information supplied to the leader - Periodic and routine - Upon completion of procedure / medication - Clarification

Phase 5 Resuscitation 5

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Information supplied by the leader - Primary and secondary assessment information - Team leader’s observations

Phase 6 Transfer 1

Relinquish care to a team of equal or greater expertise

2

Provide complete, concise, and wellorganised information

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Phase 7 Critique

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1

A critical responsibility

2

Grieving process

3

Education

ACLS Course Present emphasis now is on case based scenarios so that when the doctor is faced with a critical life threatening case scenario, he/she is able to immediately react and provide life-saving measures within seconds to at most 1-2 minutes.

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Essentials of ACLS • • • • • • • • •

Recognition of cardiac arrest and BCLS Adjuncts for airway control, ventilation and oxygenation ETT Defibrillation Arrhythmia recognition and management - Case Scenarios Intravenous techniques Cardiovascular pharmacology Emergency cardiac pacing Acute coronary syndromes and AMI Community approach to ECC: Prevention & Chain of survival

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An Organised Approach To Resuscitation • Primary Survey • Secondary Survey

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Preliminary First Actions performed before the “ A “ of the primary ABCD Survey • Assess responsiveness • Call for help fast • Appropriately position victim • Appropriately position rescuer

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Assess Responsiveness

• Non-traumatic cardiac arrest • ? Trauma

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Call For Help Fast • In a hospital • Outside a hospital Î with a second rescuer Î the lone rescuer Î the lone rescuer with an AED Î the lone rescuer with remote access to a telephone

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Appropriately Position The Victim • supine position • ? Cx spine injury

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Appropriately Position The Rescuer

• patient on the ground • patient on bed / trolley

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Primary Survey Focus on basic CPR and defibrillation First “A-B-C-D” • Airway

: open the airway

• Breathing

: provide positive - pressure ventilation

• Circulation

: give chest compressions

• Defibrillation : shock VF / pulseless VT

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Primary ABCD Survey A.

Open the Airway - head tilt, chin lift

- jaw thrust

- inspect for f.b., blood, vomitus - clear all foreign objects Introduction To ACLS,28 1 Sep 2006

B.

Assess Breathlessness look, listen, feel - if nil • What manoeuvre to check for obstructed airway • If obstructed - how to clear it? • If ventilations needed, what adjunts needed? • What rate and volume of ventilation required? • Are ventilations adequate?

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ABCD Survey

• nasopharyngeal airway

• Ventilate patient • oral airway

• bag mask ventilation

• pocket face mask

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Primary ABCD Survey C. Confirm Pulselessness – check carotid pulse • perform closed chest compression • attach ECG monitor • hunt for VF / VT D. Defibrillate, if appropriate

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Secondary Survey Focus on intubation, IV. Access, rhythms, drugs and reasons why cardiorespiratory arrest occurred Second “A-B-C-D” • Airway • Breathing • Circulation

: perform endotracheal intubation : assess bilateral chest rise & ventilation : gain iv. access, determine rhythm, give appropriate access • Differentials : search for, find and treat reversible causes

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Secondary Survey A.

Airway • Reassess adequacy of original airway opening techniques • Assess need for endotracheal intubation • Verify preparation for ETT done eg.- get tube of correct size - check ETT bulb - lubricate lower portion of ETT - ETT stylet - check laryngoscope - prepare suction • Intubate patient, if necessary

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Secondary Survey B.

Breathing • Check chest wall rises equally with ventilation • Check if breath sounds equal • Confirm ETT placement eg Esophageal detection device, ETCO2 • Add O2 - 100% • Chest X-Ray • Mechanical Ventilation

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Secondary Survey C. Circulation • Ante-cubital vein / external jugular vein • Infusion fluid : Normal saline Atropine

• Drugs administered via ETT: • Circulation time in cardiac arrest Introduction To ACLS,35 1 Sep 2006

Lignocaine Epinephrine (adrenaline)

Secondary Survey C.

Differential Diagnosis • What caused the arrest? • Are there any reversible causes - those that had a specific therapy? • Are there any complications of resuscitation that have an immediately remediable cause?

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Universal / International ACLS Algorithm Adult AdultCardiac CardiacArrest Arrest

AA BB CC DD

Primary PrimaryABCD ABCDSurvey Survey Focus : basic CPR and Focus : basic CPR anddefibrillation defibrillation •Check •Checkresponsiveness responsiveness •Activate •Activateemergency emergencyresponse responsesystem system •Call for defibrillator •Call for defibrillator Airway Airway: :open openthe theairway airway Breathing : provide Breathing : providepositive-pressure positive-pressureventilations ventilations Circulation : check pulse, give chest compressions Circulation : check pulse, give chest compressions Defibrillation Defibrillation: :attach attachmonitor monitor/ /defibrillator defibrillator

Assess Assessrhythm rhythm

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Universal / International ACLS Algorithm

Assess Assessrhythm rhythm

VF/VT VF/VT

Attempt Attempt defibrillation defibrillationxx11 as asnecessary necessary

CPR CPR 11- -22minutes minutes

Secondary SecondaryABCD ABCDSurvey Survey Focus : more advanced assessments Focus : more advanced assessments&&treatments treatments AAAirway Airway • •place placeairway airwaydevice deviceas assoon soonas aspossible possible BBBreathing Breathing • •confirm confirmairway airwaydevice deviceplacement placementby byexamination examination (confirmation device is recommended) (confirmation device is recommended) • •secure secureairway airwaydevice device • •confirm effective confirm effectiveoxygenation oxygenationand andventilation ventilation CCCirculation Circulation • •establish establishIV IVaccess access • •identify & monitor identify & monitorrhythm rhythm • •administer drugs appropriate administer drugs appropriatefor forrhythm rhythm&&condition condition DDDifferential Diagnosis Differential Diagnosis • •search searchfor for&&treat treatidentified identifiedreversible reversiblecauses causes

Non-VF/VT Non-VF/VT

Consider Considercauses causesthat thatare arepotentially potentiallyreversible reversible ••Hypovolemia • “Tablets” (drug Hypovolemia • “Tablets” (drugOD, OD,accidents) accidents) ••Hypoxia • Tamponade, cardiac Hypoxia • Tamponade, cardiac ••Hydrogen ion acidosis • •Tension Tensionpneumothorax pneumothorax Introduction To ACLS,38 Hydrogen ion - acidosis ••Hyper-/hypokalemia, other metabolic • Thrombosis, 1 Sep 2006 Hyper-/hypokalemia, other metabolic • Thrombosis,coronary coronary(ACS) (ACS) ••Hypothermia • Thrombosis, pulmonary Hypothermia • Thrombosis, pulmonary(embolism) (embolism)

CPR CPR up to up to11- -22 minutes minutes

Basic ECG Reading

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ECG terminology

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Normal ECG Introduction To ACLS,42 1 Sep 2006

Approach to Interpretation of the ECG

• Rate • Regularity • Axis • PQRSTU

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Determining the Heart Rate • The number of large squares between 2 consecutive R waves = X

• Heart Rate = 300 / X

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1 small square = 0.04 s

5 large squares =1s 1 QRS per s Heart rate = 60 per min

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1 large square = 0.2 s

Count the number of large squares between 2 RR intervals and divide into 300

Is there any electrical activity? If there is no activity, Check - connections QRS gain In 2 other Leads, eg Lead I & II If still no activity - ASYSTOLE Introduction To ACLS,46 1 Sep 2006

Asystole • Complete absence of QRS • P waves may occur • If no organised QRS complex is seen and the patient has a pulse then the ECG is improperly connected, turned off or improperly calibrated • VF may masquerade as asystole; it is best always to check 2 leads perpendicular to each other to make sure that asystole is not VF

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Ventricular Fibrillation • Totally disorganised pattern • No distinguishable QRS complexes • Continuous erratic movement of the baseline • Rate is very rapid and too disorganised to count

Coarse VF vs Fine VF Management : Immediate defibrillation Introduction To ACLS,48 1 Sep 2006

Pulseless Electrical Activity

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Pulseless electrical activity

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What is the rhythm? Analyse P-QRS Assess: • P wave - present / absent • morphology • QRS morphology and width • Relation between P wave and QRS

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Complete heart block

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Sinus tachycardia

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What is the width of QRS?

Widened QRS Complex (> 0.12s)

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Narrow QRS Complex

Irregular narrow complex tachycardia

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Narrow complex tachycardia

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Wide complex tachycardia

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Electrocardiogram of ACS • May be normal when pain free • Subtle features - Horizontality of the ST segment - Squaring of the ST-T wave angle • Ideal to do ECG at time of symptoms

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Ischaemia - ST depression

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Acute Ischemia

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Acute anteroseptal MI

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Evolved Anterior MI

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Acute Anterior MI

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Acute inferior + RV Mi

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Pericarditis

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69 years old female – Hyperkalemia

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Acute pulmonary embolism

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Pharmacological Modalities in ACLS

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Therapeutic Modalities Class I : definitely helpful Class IIa : acceptable, probably helpful Class IIb : acceptable, possibly helpful Class III: not indicated, may be harmful

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Adrenaline (Epinephrine) Endogenous Catecholamine Important Role in Cardiac Arrest, though little evidence to show improved outcome in humans α - Adrenergic Agonist Activity β - Adrenergic Agonist Activity Primary Beneficial Effect : 1. Peripheral Vasoconstriction Improve Cerebral & Coronary Blood Flow 2. Makes VF more Susceptible to DC

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Adrenergic Effects Receptor

Vascular

A1

Constriction

A2

Dilatation

β1 β2

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Dilatation (Bronchial, GIT, Uterus]

Inotropic

Chronotropic

+ ve

- ve

+ ve

+ ve

Adrenaline (Epinephrine) Indications : Cardiac Arrest from VF, Pulseless VT Unresponsive to Initial Counter Shock, Asystole, Pulseless Electrical Activity, or Profoundly Symptomatic Bradycardia

Dose : IV 1 mg (10 ml of 1:10,000) followed by 20 ml Flush, At Intervals of 3 - 5 min

Infusion : 1 mg (1 ml of 1:1000 Solution) Added to 500 ml N/S or 5% D/W, Titrate to 2 - 10 mcg/min

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Adrenaline (Epinephrine) Standard Dose Higher Dose

: 1 Mg I.V : no longer recommended

Given at Intervals of 3 - 5 min Followed by 20 ml Flush of IV Fluid Endotracheal Delivery at Dose 2 to 2.5 Times Peripheral IV Dose In Continuous Infusion : 2 to 10 mcg/min

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Adrenaline (Epinephrine) Precaution : Adrenaline should not be added to infusions that contain alkaline solution Can exacerbate Ischemia, induce Ventricular Ectopy

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High-dose Adrenaline • Not recommended for initial use since no improved long-term survival and neurological outcome has been demonstrated • May rarely be considered if standard 1 mg doses fail

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Sympathomimetic Amines Dosage

α

β

Adrenaline

0.5 - 1.0 mg 1 - 20 mcg / min

+ ++

++ +++

Noradrenaline

2 - 80 mcg / min

+++

++

Vasopressin

40 units IV bolus

+++

0

Dopamine

1 - 2 mcg/kg/min 2 - 10 mcg/kg/min 10 - 30 mcg/kg/min

+ ++ +++

+ ++ ++

Dobutamine

2 - 30 mcg/kg/min

+

+++

Isoprenalin

2 - 10 mcg/kg/min

+

+++

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Vasopressin • Naturally occurring antidiuretic hormone • A non-adrenergic peripheral vasoconstrictor • Acts by direct stimulation of smooth muscle V1 receptors • No longer in the main ACLS Algorithm

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Vasopressin Primary Beneficial Effect : • Intense Peripheral Vasoconstriction --> improved cerebral, renal and coronary blood flow • Has NO beta-adrenergic activity - no skeletal muscle vasodilatation or increased myocardial oxygen consumption during CPR

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Vasopressin Indications: • As an alternative to adrenaline in adult shockrefractory VF (Class Ilb) • For haemodynamic support in vasodilatory shock eg, septic shock / sepsis syndrome (Class Ilb) • Asystole / PEA (Insufficient evidence as yet)

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Vasopressin Dosage :

• 40 units IV bolus as a single dose (no dilution required)

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Vasopressin vs Adrenalin - a comparison Vasopressin • has no beta-adrenergic activity • has a longer half-life during cardiac arrest (10-20 mins) • is more effective in maintaining coronary perfusion above the critical threshold that correlates with successful ROSC • has a higher 24 hour survival rate (preliminary evidence), but NO advantage over adrenaline in survival to hospital discharge • is more expensive: cost per treatment for adrenalin < S$ 1 vasopressin S$ 34 - 40 Introduction To ACLS,81 1 Sep 2006

Lignocaine Reduces Automaticity, suppresses Ventricular Ectopy, elevates VF Threshold Indications : • Haemodynamically stable VT (Class IIb) • Refractory VF / pulseless VT (Class indeterminate) • Control of haemodynamically compromising PVCs (Class indeterminate) Note : Lignocaine is now a second choice behind other alternative agents in many of these circumstances

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Lignocaine Evidence no longer supports the use of lignocaine as a diagnostic discriminator between perfusing VT and wide-complex tachycardia of uncertain origin Lignocaine is NOT recommended for ventricular escape rhythm Lignocaine is no longer indicated to prophylactically suppress ventricular dysrhythmias associated with acute myocardial infarction and ischaemia (causes higher mortality) Introduction To ACLS,83 1 Sep 2006

Lignocaine Dosage : In Cardiac Arrest • 1 - 1.5 mg/kg (Given as bolus IV because of poor

blood flow & prolonged circulatory times) • May add a second bolus of 0.5 mg/kg

• After restoration of spontaneous circulation, Lignocaine IV Infusion 1 - 4 mg/min

• If dysrhythmia reappears during infusion of lignocaine : - give small IV bolus of 0.5 mg/kg - increase infusion rate in incremental doses to max rate of 4 mg/min

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Lignocaine Toxicity (Dose should not > 3 mg/kg bolus) Neurological Changes Drowsiness, Disorientation, Decreased Hearing Ability, Paresthesia, Muscle Twitching, Agitated, Fits Myocardial Depression Circulatory Depression

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Amiodarone • A complex antidysrhythmic agent: - effects on Na+, K+, and Ca++ channels - alpha-and beta-adrenergic blocking properties • Also alters conduction through accessory pathways

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Amiodarone Indications :

• pharmacological conversion of atrial fibrillation (Class IIa) • persistent VT or VF after defibrillation and adrenalin/vasopressin (Class IIb) • haemodynamically stable VT (Class IIb) • haemodynamically stable polymorphic VT (Class IIb) • haemodynamically stable wide-complex tachycardia of uncertain origin (Class IIb)

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Amiodarone Indications: • control of rapid ventricular rate in preexcitation supraventricular dysrhythmias due to accessory pathway conduction (Class Ilb) • as an adjunt to electrical cardioversion of refractory PSVTs/atrial tachycardias (Class IIb) • control of ventricular rate in SVTs with severely impaired LV function when digitalis has proved ineffective (Class Ilb)

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Amiodarone Adverse Effects: Hypotension and Bradycardia

• slow the rate of infusion • IV fluid challenge • pressors or positive chonotropic agents • temporary pacing

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Amiodarone Dosage: • in pulseless VT or VF - administer rapid infusion of 150 mg diluted in 20-30 ml saline or D5W, followed by an infusion of 1 mg/min, then 0.5 mg/min, to a daily maximum of 2g • In stable ventricular and supraventricular dysrhythmias administer IV 150 mg over 10 minutes (not to exceed 30 mg/min), followed by an infusion of 1 mg/min x 6 hours, then 0.5 mg/min Note: infusions > 2 hours must be administered in glass or polyolefin bottles due to amiodarone precipitating in plastic tubing Introduction To ACLS,90 1 Sep 2006

Magnesium • A cofactor in numerous enzymatic reactions • Essential for function of Na-K ATPase Pump • Mg deficiency associated with cardiac arrhythmia, sudden death, precipitates VF, hinders replenishment of intracellular K+

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Magnesium Indications : Proven hypomagnesaemia with or without dysrhythmias

Note : The routine prophylactic use of magnesium in patients with AMI is no longer recommended There is no clear cut evidence to support the use of magnesium in Torsades de Pointes, UNLESS, the patient is in cardiac arrest with a classic ECG rhythm

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Magnesium Dosage : • 1 - 2 g magnesium sulfate (2 - 4 ml of 50% soln) • Diluted in 100 ml of 5% D/W over 1 - 2 min, may give up to 5 - 10 G • Give I.V push if patient in VF

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Magnesium Side Effects : • Flushing, Sweating, Mild Bradycardia, Hypotension, Asystole • Hypermagnesemia may produce Depressed reflexes, Flaccid paralysis, Circulatory collapse, Resp paralysis, Diarrhoea • Rapid administration of magnesium may cause clinically significant hypotension or asystole

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Procainamide Suppresses both atrial and ventricular dysrhythmias Indications : Acceptable as a second line drug for • Conversion of A fib and A flutter to sinus rhythm (Class IIa) • Control of rapid ventricular rate due to accessory pathway conduction in preexcitation atrial dysrhythmias (Class IIb) • Differentiation of wide-complex tachycardias (Class IIb) Introduction To ACLS,95 1 Sep 2006

Procainamide Dosage: Slow infusion of 20 mg/min until • dysrhythmia is suppressed • hypotension ensues • QRS complex prolonged by 50% from its original duration • total of 17 mg/kg of the drug has been administered • Maintenance infusion of 1-4 mg/min

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Procainamide Note: • Reduce dose in renal failure • Continuous monitoring of ECG and BP is essential since administration of procainamide can result in toxic concentrations

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Procainamide Precautions : • Reduce the dose in renal failure • Avoid in patients with prolonged QT intervals • Avoid in Torsades de Pointes

The need to infuse slowly limits use of this drug in life-threatening conditions

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Bretylium Tosylate Following a review of the evidence, bretylium has been removed from the ACLS treatment algorithms and guidelines because : • High occurrence of side effects • Availability of safer agents at least as efficacious • Limited supply and availability of the drug

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Atropine • Parasympatholytic Agent • Enhances Sinus Node Automaticity & AV Conduction via Direct Vagolytic Action Indications : • Symptomatic sinus bradycardia (Class I) • First degree and type I AV block (at nodal level) (Class IIa) • Brady-asystolic arrest after adrenaline has been given • use with caution in type II AV block and new third degree AV block with wide QRS complexes (Class IIb) Introduction To ACLS,100 1 Sep 2006

Atropine Dosage : • I.V 0.6 - 1.2 mg, may be repeated at 5 min intervals (to max 2 - 3 mg) • If asystolic arrest : 2.4 mg IV push

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Atropine Atropine may be administered Endotracheally, if no I.V access

Dosage : 1.2 - 2.4 mg diluted to 10 ml of sterile water or normal saline solution

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Atropine Precautions : May induce Tachycardia, VF Over-dosage symptoms : Tachycardia, Delirum, Coma, Flushed & hot skin, Ataxia, Blurred vision < 0.6 mg IV may produce paradoxical Bradycardia & precipitate VF

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Verapamil/Diltiazem Calcium Channel Blockers Potent Direct Negative Chronotropic & Negative Inotropic Effects

Primary Beneficial Effect : • Both slow conduction and increase refractoriness in the AV node • Diltiazem produces less myocardial depression than verapamil, but is equipotent as a negative chonotrope

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Verapamil/Diltiazem Indications : • Treatment of PSVT • Slow down Ventricular response in Atrial Flutter & Fibrillation (But not for AF with WPW)

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Verapamil / Diltiazem Dosage of Verapamil : • I.V 1 mg/min •Maximum 20 mg in total dose Dosage of Diltiazem : • I.V 0.24 mg/kg (approx 20 mg) over 2 min • May repeat 0.35 mg/kg 15 min later • Infusion 5 - 15 mg/hr titrate to heart rate for control of Ventricular Response in AF

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Verapamil • Transient Hypotension due to peripheral vasodilation may occur • I.V calcium chloride 5 - 10 ml of 10% solution will restore arterial pressure, without affecting the electrophysiological properties of verapamil

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Verapamil / Diltiazem Precautions : • May cause hypotension • Not to use with I.V Beta Blocker • Avoid in sick sinus syndrome, AV Block or Heart Failure • Diltiazem IV is incompatible with simultaneous IV Frusemide

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Adenosine • An endogenous purine nucleoside that slows conduction through AV node • Interrupts AV nodal re-entry pathways • Restores normal sinus rhythm in PSVT (including PSVT associated with WPW) • Short-lived pharmacologic response • Half-life of free adenosine 5-10 sec (sequestrated by circulating RBCs)

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Adenosine Indications : • Termination of PSVT (Re-entry type) • Diagnosis of SVT

Dosage : • 6 mg bolus over 1 - 3 sec, followed immediately by 20ml saline flush • If unsuccessful, give 12 mg bolus (may be repeated once to a total dose of 30 mg) Note : preferably administer via antecubital or central IV line Introduction To ACLS,110 1 Sep 2006

Adenosine Precaution : • Side effects are transient: • Flushing, Dyspnea, Chest Pain, Transient Bradycardia, Asystole • Drug Interaction with Theophylline & related xanthines - block effect of adenosine Dipyridamole potentiates effect of adenosine • Relatively C/I in asthma Introduction To ACLS,111 1 Sep 2006

Calcium Chloride Indications : • Hyperkalemia • Hypocalcemia • Hypotension or Arrhythmia from calcium blocker overdose • Prophylactic use before I.V calcium blocker (2 ml of 10% soln) not routinely used in cardiac arrest, not to mix with Na HCO3

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Sodium Bicarbonate Continuous CO2 production & release

At Tissue Level CO2 Accumulation

Clearance of CO2 by adequate perfusion & blood flow Introduction To ACLS,113 1 Sep 2006

Sodium Bicarbonate • Continuous CO2 release from anaerobic metabolism of ischemic tissues • Dissociation of endogenous bicarbonate At Tissue Level CO2 Accumulation

Reduced clearance of CO2 due to low blood flow Introduction To ACLS,114 1 Sep 2006

Sodium Bicarbonate

CPR generates only 25 - 30 % of normal cardiac output Hence, results in limited organ perfusion & oxygen delivery

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Sodium Bicarbonate

H+ + HCO3Anaerobically generated hydrogen ions

H2CO3

H2O + CO2

Reduced clearance of CO2 due to low blood flow

Hypercarbic Venous Acidemia Hypocarbic Arterial Alkalemia Lactic Acidemia Introduction To ACLS,116 1 Sep 2006

H+ + HCO3-

H2CO3

H2O + CO2

• CO2 freely diffused across cell membranes, resulting in tissue & intracellular hypercarbic acidosis • Reduces myocardial contractility & resuscitability • Alkalemia, plasma hyperosmolality, hypernatremia • Intracerebral H’rage • NaHCO3 induces left shift of oxyhb dissociation curve

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Sodium Bicarbonate NaHCO3 when used during CPR does not improve defibrillation success or increase survival rates Adequate alveolar ventilation is central for control of acid-base balance during cardiac arrest and the post arrest period

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Sodium Bicarbonate Therapy Class I (Definitely Helpful) Known preexisting Hyperkalemia Class II a (Acceptable, Probably Helpful) Known preexisting HCO3 responsive acidosis Tricyclic antidepressant overdose To alkalinize urine in drug overdoses Class II b (Acceptable, Possibly Helpful) Intubated & long arrest interval Upon return of spontaneous circulation After long arrest interval Class III (May be Harmful) Hypoxic Lactic Acidosis Introduction To ACLS,119 1 Sep 2006

Sodium Bicarbonate Dosage : • 1 mEq/kg IV bolus as initial dose • Then, 0.5 mEq/kg every 10 min • Continuous infusion with 5% NaHCO3 Solution • Guided by blood gas monitoring

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