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Table of Contents

I. Sudden Cardiac Arrest and CPR Awareness 3

II. The Chain of Survival 4

III. Steps in Basic Life Support for Healthcare Providers 5

IV. The New Step by Step Guide in CPR for Lay/Untrained Rescuers 7

V. The New Step by Step Guide in CPR for Trained Rescuers 7

VI. Algorithm Adult BLS Healthcare Providers 9

VII. Advanced Cardiac Life Support 10

VIII. Simple Approach to ECG Recognition of the Arrhythmias 11

During the ACLS

IX. Defibrillation 18

X. Cardiac Drugs 20

XI. Pulseless Cardiac Arrest Algorithm “Adult Cardiac Arrest” 25

XII. TachyCardia Algorithm 26

XIII. Bradycardia Algorithm 27

XIV. Post Cardiac Care Algorithm 28

XV. Acute Coronary Syndromes Algorithms 29

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SUDDEN CARDIAC ARREST AND CPR AWARENESS BACKGROUND Heart diseases are the number 1 killer in our country, accounting for close to 20% of all causes of death according to the latest Department of Health statistics. Approximately half of all deaths from cardiovascular disease occur as Sudden Cardiac Arrest. Sudden cardiac arrest

can happen at any time, to anyone, anywhere without warning

most common mode of death in patients with coronary artery disease

although pre-existing heart disease is a common cause, it may strike people with no history of cardiac disease or cardiac symptoms.

In sudden cardiac arrest or sudden cardiac death, the heart usually goes into a fatal arrhythmia called “Ventricular Fibrillation” (VF) wherein it suddenly goes into very irregular fast ineffective contractions, the heart stops beating, the victim loses consciousness, and if untreated, dies.

Despite advances in Emergency Medical Systems and in the technology of resuscitation, sudden cardiac arrest remains a major public health problem. It is associated with low survival rate, and major long term severe mental impairment due to delays in cardiopulmonary resuscitation (CPR) and treatment. Majority of cardiac arrests occur outside the hospital- at home, in the workplace, in public institutions. According to the American Heart Association, almost 80 percent of out-of-hospital cardiac arrests occur at home and are witnessed by a family member. Unfortunately, less than 10 percent of sudden cardiac arrest victims survive because majority of those witnessing the arrest are people who do not know how to perform CPR. CPR or cardiopulmonary resuscitation is an emergency procedure used when someone’s heart stops beating.

it is a simple inexpensive procedure that can be learned by anyone, and consists of a manual technique using repetitive pressing to the chest and breathing into the person's airways that keeps enough oxygen and blood flowing to the brain

requires no special medical skills and training is available for the ordinary person nationwide.

if effectively done immediately after cardiac arrest, it can double a victim’s chance of survival. Early CPR and defibrillation within the first 3–5 minutes after collapse, plus early advanced care can result in high (greater than 50 percent) long-term survival rates for witnessed ventricular fibrillation (VF).

If bystander CPR is not provided, a cardiac arrest victim’s chances of survival fall 7 % to 10 % for every minute of delay until defibrillation.

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THE CHAIN OF SURVIVAL

This is a concept which aims to improve the outcome for victims of cardiopulmonary arrest. It involves a series of events which are interconnected to each other like the links of a chain. The links in the Chain of Survival are described specifically as: (1) early access, (2) early CPR (3) early defibrillation, and (4) early ACLS. Recently, with the publication of the 2010 CPR Guidelines, a fifth link, (5) Integrated post-cardiac arrest care, has been added and emphasized. The First Link- Early Access

A well-informed person - key in the early access link. Recognition of signs of heart attack and respiratory failure Call for help immediately if needed Activate the Emergency Medical System

Second Link - Early CPR

Life saving technique for cardiac & respiratory arrest Chest compressions +/- Rescue breathing

Why is early CPR important?

CPR is the best treatment for cardiac arrest until the arrival of Advanced Life Support. prevents VF from deteriorating to asystole may increase the chance of defibrillation significantly improves survival

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STEPS IN BASIC LIFE SUPPORT FOR HEALTHCARE PROVIDERS

IF YOU SEE A PERSON DROP DEAD, OR LOSE CONSCIOUSNESS, WITH PRESUMED SUDDEN CARDIAC ARREST,

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THE NEW STEP BY STEP GUIDE IN CPR FOR LAY / UNTRAINED RESCUERS: IF A PATIENT/VICTIM SUDDENLY DROPS UNCONSCIOUS OR IS SEEN UNCONSCIOUS: 1. Survey the scene to see if it’s safe to do CPR.

2. Check victim’s unresponsiveness. If unresponsive, roll victim on his/her back.

3. Call for help; activate the emergency medical services; call for an ambulance/doctor.

4. Start chest compressions. Place the heel of your hand on the center of the victim's chest. Put your other hand

on top of the first with your fingers interlaced.

5. Press down and compress the chest at least 2 inches in adults. Allow complete recoil after each compression.

Compress continuously with both hands at a rate of 100/minute or more (Compress to the tune of Bee Gee's

song "Stayin' Alive.")

6. For lay or untrained rescuers, continue this Hands Only CPR - do continuous chest compressions until help

arrives, an automated external defibrillator (AED) is available or the emergency personnel arrives, or the victim

is revived back to life.

THE NEW STEP BY STEP GUIDE IN CPR FOR TRAINED RESCUERS: IF A PATIENT/VICTIM SUDDENLY DROPS UNCONSCIOUS OR IS SEEN UNCONSCIOUS: 1. Survey the scene to see if it’s safe to do CPR.

2. Check victim’s unresponsiveness. If unresponsive, roll victim on his/her back.

3. Call for help; activate the emergency medical services; call for an ambulance/doctor.

4. Start chest compressions. Place the heel of your hand on the center of the victim's chest. Put your other hand

on top of the first with your fingers interlaced.

5. Press down and compress the chest at least 2 inches in adults. Allow complete recoil after each compression.

Compress 30 times with both hands at a rate of 100/minute or more (Compress to the tune of Bee Gee's song

"Stayin' Alive.").

6. After 30 compressions, you can now open the airway with a head tilt and chin lift.

7. Pinch to close the nose of the victim. Take a normal breath, cover the victim's mouth with yours to create an

airtight seal, and then give two, one-second breaths as you watch the chest rise.

8. Continue cycles of compressions and breaths -- 30 compressions, two breaths - until help arrives, until an

automated external defibrillator (AED) is available, until the victim is revived back to life, or until the emergency

medical personnel takes over.

If the rescuer is unsure or not confident or hesitant about doing mouth to mouth breathing, or does not have a barrier device for mouth to mouth, he may just do compression only, or Hands Only CPR: press hard and fast in the center of the chest by pressing down with two hands compressing the chest 2 inches at a rate of at least 100 per minute.

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Component

Adult

Children

Infants

Recognition

UNRESPONSIVE (for all ages)

No breathing or only gasping No pulse palpated within 10 secs. Only (HCP)

CPR Sequence

CAB

CAB

CAB

Compression Rate

At least 100/min

Compression Depth

At least 2 inches (5cm)

At least 1/3 AP depth, about 2 inches (5cm)

At least 1/3 AP depth,

about 1 1/2 inches (4cm)

Chest wall recoil

Allow complete recoil between compressions

HCPs rotate compression every 2 mins.

Compression Interruptions

Minimize interruptions in chest compressions. Attempt to limit interruptions to

less than 10 secs.

Airway

Head tilt-chin lift (HCP suspected trauma: Jaw thrust)

Compression to ventilation ratio (Until advanced airway

placed)

30:2

(1 or 2 rescuers)

30:2

(Single Rescuer) 15:2

(2 HCP Rescuers)

30:2

(Single Rescuer) 15:2

(2 HCP Rescuers)

Ventilations: When Rescuer Untrained or Trained but not

Proficient

Compressions only

Ventilations with Advanced

Airway

1 breath every 6-8 seconds (8-10 breaths/min)

Asynchronous with chest compressions About 1 second/breath

Visible chest rise

Abbreviations: HCP – healthcare provider. Table derived from 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science, Circulation vol 122, no. 18, supplement 3

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Figure reprinted from 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science, Circulation vol 122, no. 18, supplement 3

Unresponsiveness No breathing or no normal breathing

(ie, only gasping)

Activate emergency response system

Get AED/defibrillator or send second rescuer (if available) to do this

CHECK PULSE: DEFINITE PULSE

W/IN 10 SECS.?

Give 1 breath every 5 to 6 seconds

Recheck pulse every 2 minutes

Begin cycles of 30 COMPRESSIONS and 2 BREATHS

AED/defibrillator ARRIVES

CHECK RHYTHM: SHOCKABLE

RHYTHM?

Resume CPR Immediately for 2 minutes Check rhythm every 2 minutes; continue until ALS providesrs

take over or victim starts to move

Give 1 shock Resume CPR immediately

for 2 minutes

High Quality CPR

Rate at least 100/min

Compression depth at least 2 inches (5cm)

Allow complete check recoil after each compression

Minimize interruptions in chest compressions

Avoid excessive

ventilation

Note: The boxes bordered with dashed lines are performed by healthcare providers and not by lay rescuers © 2010 American Heart Association

Adult BLS Healthcare Providers

NOT SHOCKABLE SHOCKABLE

YES

NO

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ADVANCED CARDIAC LIFE SUPPORT ACLS includes 1. Basic Life Support (BLS) 2. The use of adjunctive equipment and special techniques for establishing and maintaining effective

ventilation and circulation. 3. Electrocardiographic (ECG) monitoring and arrhythmia recognition. 4. Establishment and maintenance of intravenous (IV) access. 5. Therapies for emergency treatment of patients with cardiac or respiratory arrests (including stabilization in

the post arrest phase) and, 6. Treatment for patients with suspected Acute Myocardial Infarction and stroke.

ACLS includes the ability to perform these skills, and the knowledge, training, and judgment about when and how to use them.

The Algorithm Approach to Emergency Cardiac Care (ECC) The following clinical recommendations apply to all treatment algorithms.

First, treat the patient not the monitor.

Algorithms for cardiac arrest presume that the condition under discussion continually persists, that the patient remains in cardiac arrest, and that CPR is always performed.

Apply different interventions whenever appropriate indications exist.

Adequate airway, ventilation, oxygenation, chest compressions, and defibrillation are more important than administration of medications and take precedence over initiating an intravenous line or injecting pharmacologic agents.

Several medications (epinephrine, lidocaine, and atropine) can be administered via the endotracheal tube, but the dose must be 2 – 2.5 times the intravenous dose. (Use a catheter or suction tip which should be passed beyond the tip of the endotracheal tube. Dilute with water instead of NSS for endotracheal route. )

With a few exceptions, intravenous medications should always be administered rapidly, in bolus method.

After each intravenous medication, give a 20-30 ml bolus of intravenous fluid and immediately elevate the extremity. This will enhance delivery of drugs to the central circulation, which may take 1-2 minutes.

Last, treat the patient, not the monitor.

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SIMPLE APPROACH TO ECG RECOGNITION OF THE ARRHYTHMIAS DURING ACLS

Steps in the Systematic ECG Interpretation of the ACLS Rhythms

Regularity? Is it regular or irregular?

Rate? Is it fast or slow or normal?

Rhythm? Is it Sinus?

Check the waveforms. Is there a P wave followed by a QRST?

Measure the Intervals: PR, QRS, QT

Is there a Rhythm abnormality?

Correlate clinically. SINUS RHYTHM

There is a P wave, followed by a QRS complex at a regular rhythm and rate of 60-100 bpm.

SR SINUS BRADYCARDIA

There is a regular P wave followed by a regularly occurring QRST, but the rate is < 60 bpm

SB SINUS TACHYCARDIA

There is a regular P wave followed by a regularly occurring QRST, but the rate is > 100 bpm

ST SLOW ACLS RHYTHMS- BRADYCARDIA

Sinus bradycardia Sinus pause Escape rhythms:

Junctional rhythm Idioventricular rhythm

Heart blocks 1

st degree AV block

2nd

degree AV block Mobitz I or Wenckebach Mobitz II

3rd

degree or complete AV block SINUS PAUSE (SINUS ARREST)

There is a P wave followed by a QRST, but at some point there is irregularity and slowing of the heart rate, and the ECG shows no P wave and no QRS. In other words, it simply PAUSED!

Pause

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JUNCTIONAL RHYTHM

This is an escape rhythm; Impulses come from the AV node

Usually a regular slow heart rate, < 60 bpm (rate is usually between 40-50 bpm). QRS are narrow. There are no discernible P waves (actually the P waves are inverted or buried w/in QRS or follows the QRS)

Junctional IDIOVENTRICULAR RHYTHM

Another escape rhythm; Impulse is ventricular in origin

Regular slow heart rate, < 40 bpm (usually between 20-40 bpm), wide QRS and no discernible P waves; QRS duration > 0.10 sec

Idioventricular FIRST DEGREE AV BLOCK

There is a normal regular P wave, followed by a regular QRS complex, but the PR interval is > 0.20 sec (>5 small squares in the ECG strip)

1st deg AV block

SECOND DEGREE AV BLOCK MOBITZ I (WENCKEBACH)

Progressive lengthening of the PR interval followed by intermittent dropped beats (a P wave NOT followed by a QRS)

2nd

deg AV block Mobitz I SECOND DEGREE AV BLOCK MOBITZ II

Fixed PR interval (NO progressive lengthening) w/ intermittent dropped beats .

2nd

deg AV block Mobitz II Important point: 2

nd degree AV block is ALWAYS IRREGULAR and usually presents with GROUP

BEATING. 2:1 AV BLOCK

2 P waves for every 1 QRS complex (every other P wave is blocked)

2:1 AV block

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HIGH GRADE AV BLOCK

Atrio-ventricular conduction ratio is 3:1 or higher

3:1, 4:1, 5:1 AV block and anything higher is called High Grade AV block

High grade AV block THIRD DEGREE AV BLOCK OR COMPLETE HEART BLOCK

No recognizable consistent or meaningful relationship between atrial and ventricular activity (there is ATRIO-VENTRICULAR DISSOCIATION)

There are regularly occurring P waves, there are regularly occurring QRS complexes, but they are not related to each other (in other words, they are dissociated)

QRS morphology is constant; QRS rate constant (15-60 beats/min); atrial rate is usually faster than ventricular rate, but the atrial and ventricular rhythms are independent of each other; ventricular rhythm is maintained by a junctional or idioventricular escape rhythm or a ventricular pacemaker

CHB (upper arrows point to P waves; lower arrows point to QRS complexes)

CHB Complete heart block with a ventricular escape rhythm FAST ACLS RHYTHMS - TACHYCARDIA

Sinus tachycardia

Supraventricular tachycardia

Atrial fibrillation

Atrial flutter

Multifocal atrial tachycardia

Ventricular tachycardia TACHYCARDIA – divided into Narrow complex and Wide complex Tachycardia

Wide QRS Complex Tachycardia (QRS duration >0.12 secs )

Narrow QRS Complex Tachycardia (QRS duration < 0.12 secs)

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SUPRAVENTRICULAR TACHYCARDIA • Regular narrow QRS complex tachycardia, usually with sudden onset and termination, with a rate of 150-

250 beats/min • No discernible P waves

• P waves are generally buried in the QRS complex. Often, P wave is seen just prior to or just after the end of the QRS and causes a subtle alteration in the QRS complex that results in a pseudo-S or pseudo-r

SVT ATRIAL FIBRILLATION

Irregularly irregular narrow complex tachycardia with no discernible P waves

Chaotic irregular atrial fibrillatory waves

AF

AF

TACHYCARDIA

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ATRIAL FLUTTER

Narrow complex tachycardia, regularity and rate depends on the degree of AV conduction

Atrial rate = 220-350/min (P as flutter waves); Ventricular response usually 150-180 bpm

Look closely for your beautiful sawtooth flutter waves

Flutter

Flutter MULTIFOCAL ATRIAL TACHYCARDIA

Impulses originate irregularly and rapidly at different points in the atrium

Irregularly irregular narrow complex tachycardia with varying P wave, PR, PP and RR intervals, and 3 or more different P wave morphologies

MAT VENTRICULAR TACHYCARDIA

At least 3 consecutive PVC’s

Rapid, bizarre, wide QRS complexes firing in succession at a rate of >100 bpm; usually no discernible P wave

VT

VT ARREST RHYTHMS – there are only 4:

Asystole

Pulseless VT

Ventricular fibrillation

Pulseless electrical activity ASYSTOLE

The easiest rhythm to identify! There is no discernible electrical activity. ECG shows a flat line. The patient is in CARDIAC ARREST!

Asystole

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VENTRICULAR FIBRILLATION

Associated with coarse or fine chaotic undulations of the ECG baseline. There are no P waves and no true QRS complexes. The rate is indeterminate. The patient is in CARDIAC ARREST!

VF

VF PULSELESS VENTRICULAR TACHYCARDIA

Rapid, bizarre, wide QRS complexes firing in succession at a rate of >100 bpm, but the patient has NO PULSE and NO BLOOD PRESSURE. Patient is also in CARDIAC ARREST! Treat as VF!

VT PULSELESS ELECTRICAL ACTIVITY

ECG shows an organized electrical activity (NOT VF or pulseless VT); either a narrow QRS or wide QRS rhythm; fast (>100 beats/min) or slow (<60 beats/min).

There is organized cardiac electrical impulses but no effective myocardial contraction is produced (also known as “electromechanical dissociation”); patient has ZERO blood pressure and ZERO heart rate, in other words, PATIENT IS IN CARDIAC ARREST!

PEA ECG of a patient with PEA- may show either bradycardia (commonly idioventricular or junctional) or tachycardia (other than VT) but the patient has NO pulse and is in cardiac arrest. MISCELLANEOUS ACLS RHYTHMS WOLFF PARKINSON WHITE (WPW) ECG (PREEXCITATION)

ECG shows short PR interval (<0.12 secs), delta wave (upward slurring of the QRS complexes as indicated by arrows) and wide QRS complexes. These patients have an extra accessory pathway or bypass tract that may conduct impulses rapidly. They may present with supraventricular tachycardia (usual narrow QRS tachycardia) or with preexcited rapid atrial fibrillation which presents as irregular wide complex tachycardia (see below) and may be mistaken as VT or VF. In reality, such rapid preexcited AF may actually lead to VF and sudden death.

WPW

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PREEXCITED RAPID ATRIAL FIBRILLATION

Rapid atrial fibrillation in a patient with WPW syndrome presents as wide complex tachycardia that may look like VF/VT. Just remember the acronym F-B-I: Fast-Broad-Irregular for preexcited tachycardia. Important point to remember: DO NOT GIVE digoxin or calcium channel blockers because these may convert the arrhythmia into VF! What to do: either IV procainamide, IV amiodarone, or Cardiovert the patient!

WPW AF PACEMAKER RHYTHM

ECG of a patient with an artificial pacemaker which is inserted for significant bradycardia. Tracing shows a sharp pacemaker potential or spike (as indicated by the arrows) followed by a wide QRS complex which indicate “capture” of the ventricle.

Paced TORSADE POINTES

Polymorphic VT occurring in patients with long QT interval. ECG shows also irregular bizarre rapid wide QRS complexes, hence also Fast-Broad-Irregular (F-B-I). But take note that the QRS complexes seem to change from a positive to a negative axis around a certain point (twist around a point).Torsade pointes means “twisting of the points”.

TDP

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FOLLOW THE SIMPLE ALGORITHM BELOW FOR EASY AND RAPID RECOGNITION OF THE ACLS RHYTHMS

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DEFIBRILLATION

Defibrillation

therapeutic use of electric current delivered in large amounts over very brief periods of time.

temporarily “stuns” an irregularly beating heart and allows more coordinated contractile activity to resume.

termination of VF for at least 5 seconds following the shock Rapid defibrillation is the major determinant of survival in cardiac arrest due to ventricular fibrillation (VF). Early defibrillation is critical for several reasons: 1. Ventricullar fibrillation (VF)- most frequent initial rhythm in sudden cardiac arrest (SCA) 2. Treatment of VF is electrical defibrillation 3. Probability of successful defibrillation diminishes rapidly overtime 4. VF tends to deteriorate to asystole within a few minutes 5. CPR prolongs VF, delays the onset of asystole, and extends the window of time during which defibrillation can occur. In witnessed arrest, defibrillation should be applied immediately after the onset of VF, i.e. before the heart becomes anoxic and acidotic, which would make successful defibrillation and resumption of cardiac activity less likely. Defibrillation is accomplished by passage of sufficient electric current (amperes) through the heart. Current flows determined by the energy chosen (joules) and transthoracic impedance (ohms), a resistance to current flow. Factors that determine transthoracic impedance include:

1. energy selected 2. electrode size 3. paddle-skin coupling material (gel/cream or saline-solution gauze) 4. number and time interval of previous shocks 5. phase of ventilation 6. distance between electrodes (chest size) 7. paddle electrode pressure.

ELECTRODE POSITION Electrodes should be placed to maximize current flow through the myocardium. The standard placement is one electrode just to the upper part of the sternum below the clavicle and the other to the left of the nipple with the center of the electrode in the mid-axillary line.

Care should be taken that the electrodes are well separated and that paste or gel is not smeared between the paddles on the chest. Otherwise, current may flow preferentially along the chest wall, “missing” the heart

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ENERGY REQUIREMENTS The recommended energy for the first and succeeding defibrillation attempts is 360J monophasic or 200J biphasic. CPR should be continued immediately after defibrillation, for 2 minutes, followed by rhythm check. Biphasic waveform defibrillation with shocks of < 200J is safe and has equivalent or higher efficacy for termination of ventricular fibrillation (VF) compared with higher-energy monophasic – waveform shocks. SHOCK ENERGIES

The optimal energy for first shock biphasic waveform defibrillation has not been determined.

Biphasic: 120-200J (Class I LOE C)

If Manufacturer’s recommendation not known: Use maximal dose (Class IIb)

Monophasic: 360J PEDIATRIC

VF is uncommon in children

2-4 Joules/kg is recommended SYNCHRONIZED CARDIOVERSION Synchronized cardioversion is delivery of electrical shock timed to the peak of the QRS complex. Synchronization of delivered energy reduces the possibility of induction of VF, which can occur when a shock impinges on the relative refractory period of the cardiac electrical activity. Thus, synchronization is recommended for unstable supraventricular tachycardia, atrial fibrillation, atrial flutter, and monomorphic ventricular tachycardia. ENERGIES FOR SYNCHRONIZED CARDIOVERSION

Atrial flutter and SVT (narrow regular) - 50 J to 100 J (monophasic or biphasic)

Atrial fibrillation (narrow irregular) - 120J to 200J (biphasic) OR 200J (monophasic)

Monomorphic VT (wide regular) – 100J

Polymorphic VT (wide irregular) – defibrillation dose, NOT SYNCHRONIZED

TECHNIQUE FOR EXTERNAL ELECTRICAL DEFIBRILLATION 1. Turn the main power switch on. Turn the synchronize switch of the defibrillator off.

2. Set the energy to be delivered at 360J (for adults) or equivalent biphasic waveform shock at 200J.

3. Lubricate the paddle with electrode gel.

4. Charge paddles. Someone should continue CPR while you are charging the defibrillator.

5. Interrupt chest compressions (preferably 10 seconds, maximally 20 seconds) for the defibrillation. Place one

paddle just to the right of the upper sternum below the right clavicle, the other paddle just below and to the left

of the left nipple as indicated in the paddles.

6. Apply firm pressure with paddles against the chest to reduce lung volume and electric resistance.

7. Confirm ECG diagnostic of VT or VF (Pulseless ventricular tachycardia or ventricular fibrillation)

8. Clear the area with no one touching the patient. Shout: “I am going to shock the patient on three! One I’m

clear! Two you are clear! Three everybody clear!”

9. Discharge the defibrillator by pushing the appropriate triggers on the paddles simultaneously.

10. After defibrillation, immediately continue CPR.

11. Check rhythm after each 5 cycles (2mins) of CPR and proceed accordingly. (See VF/VT Algorithm)

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TO DO SYNCHRONIZED CARDIOVERSION, turn the “Synchronize” switch or “SYNC” ON and select the desired energy for cardioversion. Continue with steps 3 to 9 above. When discharging, place the paddles on the chest longer, and firmly. IMPORTANT NOTES:

Pulseless VT is treated as VF Defib!

Unstable monomorphic (regular) VT with pulse synchronized cardioversion (100J, increase dose if no

response to the 1st

shock)

Unstable polymorphic (irregular) VT w/ or w/o pulse- Defib!

If there is any doubt if monomorphic or polymorphic VT in unstable patient, DO NOT DELAY shock delivery,

provide high energy unsynchronized shocks (ie, defibrillation doses)

CARDIAC DRUGS

IMPORTANT PRINCIPLE: DURING A CARDIAC ARREST, DRUG INTERVENTION IS SECONDARY ONLY TO OTHER INTERVENTIONS. MOST IMPORTANT ASPECT IS STILL HIGH QUALITY CHEST COMPRESSIONS AND EARLY DEFIBRILLATION!

Epinephrine

MOA - Increases SVR, BP, HR, Contractility, automaticity Increases blood flow to heart & brain, AV conduction velocity Alpha-adrenergic effects can increase coronary & cerebral perfusion pressure during CPR Beta-adrenergic effects may increase myocardial work & reduce subendocardial perfusion

No evidence to show that it improves survival

Dose: 1 mg IV bolus every 3-5 mins

Vasopressin

MOA - Non-adrenergic peripheral vasoconstrictor that causes coronary & renal vasoconstriction Increases blood flow to heart & brain

Indications: Alternative to epinephrine for treatment of adult shock-refractory VF/pulseless VT, PEA and asystole

Hemodynamic support in vasodilatory shock

Dose: - 40U IV single dose to replace one dose of epinephrine (for cardiac arrest) - 0.02 – 0.04 U/min (for vasodilatory shock)

Norepinephrine

MOA - Naturally occurring potent vasoconstrictor and inotropic agent Usually induces renal and splanchnic vasoconstriction

Indications: Severe hypotension (SBP < 70mmHg) Low total peripheral resistance

Dose: - 0.1 – 0.5 mcg/kg/min infusion

Note: Not used for cardiac arrest

Do not administer in same IV line as Na Bicarbonate

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Dopamine

MOA - Catecholamine, alpha and beta-adrenergic receptor agonist and peripheral dopamine receptor agonist

Indications: Hypotension (SBP 70-100mmHg) Symptomatic significant bradycardia After ROSC (Return of Spontaneous Circulation)

Dose: - 2 – 20 mcg/kg/min infusion, titrate to patient response

Note: Do not administer in same IV line as Na Bicarbonate

Dobutamine

MOA - synthetic sympathomimetic amine with positive inotropic action and minimal positive chronotropic activity at low doses (2.5 ug/kg per min), but moderate chronotropic activity at higher doses

Indication: Severe systolic heart failure (SBP 70-100mmHg)

Dose : 2-20 ug/kg/min

Note: vasodilating activity precludes its use when a vasoconstrictor effect is required

Do not administer in same IV line as Na Bicarbonate

Buffers: Sodium Bicarbonate

Little data indicates that therapy with buffers improves outcome

Does not improve ability to defibrillate or improve survival rates in animals

Can compromise coronary perfusion pressure

May cause adverse effects due to extracellular alkalosis, including shifting the oxyhemoglobin saturation curve

May induce hyperosmolality and hypernatremia

Produce carbon dioxide

May inactivate simultaneously administered catecholamine

MOA : Reverses acidosis caused by global hypoperfusion

Indications: Hyperkalemia Tricyclic or phenobarbital overdose Patients with pre-existing metabolic acidosis ?After a protracted arrest or long resuscitative efforts

Dose: 1 mEq/kg

Diuretics: Furosemide

Potent diuretic

Direct venodilating effect in patients with acute pulmonary edema

Transient vasoconstrictor effect when heart failure is chronic

Onset of vascular effect is within 5 minutes

Dose: 0.5 – 1 mg/kg IV injected slowly

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Adenosine

MOA : Depresses AV node & sinus node activity

Half-life is < 5 seconds (degraded in the blood & periphery)

Indications: Should be used if SVT is suspected *Note : 2010 CPR Guideline

Recommended in the initial diagnosis & treatment of stable, undifferentiated regular, monomorphic wide-complex tachycardia

Dose: 6 mg rapid IV push in 2-3 seconds, followed by 20ml saline flush, raise the extremity for at least 30 seconds after push

If no response may give 2nd

dose: 12 mg after 1-2 minutes.May give a 3rd

dose: 12 mg if still no response

Calcium Channel Blockers

MOA : Slow conduction & increase refractoriness in the AV node

May also control ventricular response rate in patients with AF, Flutter, or MAT

Systemic vasodilation

Negative Inotropic effect

Verapamil

Indications: Effective in stable narrow complex PSVT Alternative drug after Adenosine

Contraindications Should not be given in patients with impaired ventricular function or heart failure Should not be given if hypotensive Dose: 2.5 – 5 mg IV given in 2 minutes. Administered every 15 – 30 mins to a max of 20 mg

B-Adrenergic Blockers

Indications: Class I in acute coronary syndromes To slow ventricular response (AF/ flutter,MAT) Also to convert SVT

Second line after adenosine

*Labetalol recommended for emergency anti-hypertensive therapy for hemorrhagic and acute ischemic stroke

Contraindications Hemodynamic instability 2

o and 3

o AV block

Asthma Cocaine-induced ACS

Labetalol Dose: 10 mg IV push (1-2mins), maybe repeated or doubled every 10 mins; max dose 150mg OR same initial bolus then infusion at 2-8mg/min

Esmolol Dose: 0.5 mg/ kg loading dose 50 mcg/ kg per minute maintenance infusion

2nd

bolus of 0.5 mg/ kg infused in 1 minute repeated every 4 minutes for a total maximum of 300 mcg/ kg per minute

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B-Adrenergic Blockers Class I in acute coronary syndromes

Metoprolol Dose: 5 mg IV every 5 minute interval for total of 15 mg (IV form not available locally)

Propranolol Dose: 0.1 mg/ kg IV every 2-3 minute interval (IV form not available locally)

Esmolol Dose: 0.5 mg/ kg loading dose 50 mcg/ kg per minute maintenance infusion

2nd

bolus of 0.5 mg/ kg infused in 1 minute repeated every 4 minutes for a total maximum of 300 mcg/ kg per minute

Amiodarone

Class III anti-arrhythmic

MOA - Affects Na, K and Ca channels as well as alpha and beta adrenergic blocking properties Prolongs action potential duration, refractory period, decreases AV node conduction and sinus node function

Indications: After defibrillation and epinephrine in cardiac arrest with persistent pulseless VT or VF, stable/unstable VT Ventricular rate control of rapid atrial arrhythmias in severely impaired LV function Adjunct to electrical cardioversion in refractory PSVT’s, atrial tachycardia & pharmacologic cardioversion of AF

Side effects are hypotension and bradycardia

Dose: VT with pulse – 150mg IV over 10mins followed by 1mg/kg/min infusion for 6 hours, then 0.5mg/kg/min Pulseless VT/VF – 300mg IV push then 150mg IV - 2

nd dose if needed after another cycle of CPR

Lidocaine

Indications: VF/ pulseless VT that persist after defibrillation and administration of epinephrine Control of hemodynamically compromising PVC’s Hemodynamically stable VT Alternative if Amiodarone unavailable

Dose: Initial bolus of 1 – 1.5 mg/ kg IV. Additional bolus of 0.5 to 0.75mg/ kg can be given over 3 – 5 minutes for refractory VT/ VF.

Narrow toxic-to-therapeutic range

Routine use in AMI is not recommended

No proven short-term or long-term efficacy in cardiac arrest

CNS Toxicity: muscle twitching, slurred speech, resp. arrest, altered consciousness, seizures Magnesium

Effectively terminates torsades de pointes

Not effective in irregular/ polymorphic VT in patients with normal QT

Not recommended in cardiac arrest except when arrhythmias are suspected to be caused by magnesium deficiency

Dose: 1 – 2 gm (8-16meqs) mixed in 50 – 100 ml D5W given over 5 to 60 mins. Followed by 0.5 to 1gm IV infusion

1 to 2 gm diluted in 100 ml D5W administered over 1 – 2 mins in emergency situations Atropine

MOA : Parasympatholytic action: Accelerates rate of sinus node discharge Improves AV conduction Reverses cholinergic-mediated decreases in heart rate, systemic vascular resistance, & blood pressure

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Indications : Symptomatic sinus bradycardia (Class I) AV block Nodal level Use with caution in AMI Should not be relied fully in Mobitz type II block

Dose: 0.5 mg every 3 – 5 mins

A total dose of 3 mg (0.04 mg/kg) results in full vagal blockade in humans

*Note: 2010 CPR guideline changes Asystole & PEA indications have been deleted If atropine is not effective, may give epinephrine infusion for symptomatic bradycardia as an alternative to pacing (see Bradycardia algorithm) Epinephrine Dose : 2-10 mcg/min (1mg in 500cc of D5 W or normal saline by continuous infusion) titrate to patient’s response

Epinephrine

MOA - Increases SVR, BP, HR, Contractility, automaticity Increases blood flow to heart & brain, AV conduction velocity

Alpha-adrenergic effects can increase coronary & cerebral perfusion pressure during CPR

Dose: 2-10 mcg/min (1mg in 500cc of D5 W or normal saline by continuous infusion) - titrate to patient’s response

*Note: 2010 CPR guideline changes If atropine is not effective, may give epinephrine infusion for symptomatic bradycardia as an alternative to pacing

Digoxin

MOA: enhances central and peripheral vagal tone, slows SA node discharge rate, shortens atrial refractoriness, and prolongs AV nodal refractoriness through ANS effect

Indication: supraventricular arrhythmias (AF/flutter)

Peak effect - after 1.5 - 3 hours

Less effective than adenosine, verapamil, or beta blockers.

Dose : Acute loading dose 0.5 to 1.0 mg IV or PO o 0.004 to 0.006mg/kg initially over 5 min. o Then 0.002 to 0.003mg/kg at 4-8hr interval. o Total of 0.008 to 0.012mg/kg divided to 8 to 16hrs

Nitroglycerine

Decreases chest pain in ACS

Indication : ACS, CHF, Hypertensive urgency w/ ACS

MOA Increases venous dilation Decreases preload & O2 consumption Dilates Coronary Arteries Increases Collateral flow in MI

Tolerance may develop

IV bolus – 12.5 to 25 mcg (if no SL or spray given)

Infusion – 10mcg/min titrate to effect

Increase by 10 mcg /min every 3-5min until desired effect

Max dose 200mcg/min

Sublingual Tablet (0.3-0.4mg) 1 tab every 5min

Spray – 1-2 sprays for 0.5–1sec every 5min, Max of 3 doses

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