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IV. The New Step by Step Guide in CPR for Lay/Untrained Rescuers 7
IX. Defibrillation 18
X. Cardiac Drugs 20
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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.
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 someones 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 victims chance of survival.
Early CPR and defibrillation within the first 35 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 victims 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.
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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 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
Compression Depth At least 2 inches (5cm) At least 1/3 AP depth, At least 1/3 AP depth,
about 2 inches (5cm) about 1 1/2 inches
(4cm)
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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Adult BLS Healthcare Providers
YES
CHECK PULSE: Give 1 breath every 5 to 6
DEFINITE PULSE seconds
W/IN 10 SECS.? Recheck pulse every 2 minutes
NO
Begin cycles of 30 COMPRESSIONS and 2 BREATHS
AED/defibrillator ARRIVES
Note: The boxes bordered with dashed lines are performed by healthcare providers and not by lay rescuers 2010 American Heart Association
Figure reprinted 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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ADVANCED CARDIAC LIFE SUPPORT
ACLS includes
ACLS includes the ability to perform these skills, and the knowledge, training, and judgment about when
and how to use them.
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.
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.
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SIMPLE APPROACH TO ECG RECOGNITION OF THE ARRHYTHMIAS DURING ACLS
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
st
1 degree AV block
nd
2 degree AV block
Mobitz I or Wenckebach
Mobitz II
rd
3 degree or complete AV block
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
st
1 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)
nd
2 deg AV block Mobitz I
SECOND DEGREE AV BLOCK MOBITZ II
Fixed PR interval (NO progressive lengthening) w/ intermittent dropped beats .
nd
2 deg AV block Mobitz II
nd
Important point: 2 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
CHB
(upper arrows point to P waves; lower arrows point to QRS complexes)
CHB
Complete heart block with a ventricular escape rhythm
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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
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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
MAT
VENTRICULAR TACHYCARDIA
At least 3 consecutive PVCs
Rapid, bizarre, wide QRS complexes firing in succession at a rate of >100 bpm; usually no discernible P
wave
VT
VT
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
VT
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.
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).
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 Manufacturers 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.
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 Im
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
st
response to the 1 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
Epinephrine
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
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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
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
response
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
o o
2 and 3 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
nd
2 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
nd
2 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
Lidocaine
Indications:
VF/ pulseless VT that persist after defibrillation and administration of epinephrine
Control of hemodynamically compromising PVCs
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
Atropine
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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 patients response
Epinephrine
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
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