Good

Morning
 ADULT
ADVANCED CARDIAC LIFE
SUPPORT
 Systematic approach

 The protocols are basically for non-experts to handle emergencies till expert
help arrives – so repetitions.

 If the patient appears unconscious, use the BLS survey for initial assessment

 After appropriate BLS, use ACLS survey for more advanced assessment &
treatment

 If the patient appears conscious, use the ACLS survey for initial assessment
BLS Approach safely
Check response
Check breathing
Shout for help
Call 6666
30 Chest compressions
Open airway
2 rescue breaths
Use AED
ACLS
 Scene safety
Start CPR
• Give /Mask
• Attach monitor/Defibrillator

ACLS Algorithm
ROSC
2 Mins Check Post Cardiac
rhythm Arrest Care

If VF/VT
Drug Therapy Shock
------------------- C
C
Advanced
Airway/ P
P
------------------- R
R
Treat Causes

Monitor CPR Quality

 Scene safety
Start CPR Non-shockable
• Give /Mask
• Attach monitor/Defibrillator
Asystole/PEA
Shockable
VF/VT

Patient Pulseless CPR 2 mins

CPR 2 mins
• IV/IO access
• Epinephrine Q 3-5 mins
• Advanced airway/

CPR 2 mins
• Epinephrine Q 3-5 mins
• Advanced airway/ CPR 2 mins
• Treat reversible causes

CPR 2 mins
• Amiodarone
• Treat reversible causes
 Case 1

 You arrive on the scene to find a 45 year old man with history of
severe distress with crushing central chest pain.

 You find him to be unresponsive & you call for help & start CPR.

 Help arrives & upon connecting the monitor you see,

 VT

Coarse VF

Fine VF
 VF and Defibrillation

 VF: rhythm causing “all” sudden cardiac arrest

 VF: useless quivering of heart  no blood flow

 VF treatment: only one therapy works  defibrillation

 Defibrillation success: chances drop every minute

 Defibrillation in VF/ Pulseless VT

 Approximately 50% survival after 5 100

80
minutes 60
Survival
40

 Survival reduced by 7% to 10% per 20

minute (if no CPR) 1 3 6 10

 Rapid defibrillation is key

Minutes: collapse to 1st shock
 CPR prolongs VF, slows
deterioration
 No Pulse

Any organised rhythm without detectable pulse is PEA

Asystole: agonal complexes too slow to make this rhythm “PEA”
Rhythms with pulse
 Stable
tachycardias
 Unstable
tachycardias
 Stable vs Unstable Tachycardia

 Hypotension

 Altered mental status

 Signs of shock

 Ischemic chest discomfort

 Acute heart failure

 Sinus tachycardia

 Sinus tachycardia is characterized by an increase in the rate of discharge of the

sinus node.
 Physiological response for the demand for a higher cardiac output.
 Normal looking QRS, rate >100 / min, regular rhythm
Supraventricular vs Ventricular
tachycardia
 Case 2

 You are an emergency physician. A 75 year old man, who is in town for a
wedding, was outside smoking a cigeratte during the reception when he
developed sudden onset palpitations. He continues to feel palpitations after
shifting to ER. He admits to drinking heavily for the previous 30 hrs.
• HR – 180/min
• RR – 24/min
• BP – 110/60 mm Hg
• Sp
• Temp - 37° C
Atrial fibrillation

Atrial flutter
 Delta wave

WPW syndrome: Sinus rhythm with delta wave (arrow) notching of positive upstroke of QRS
Orthodromic
Antidromic
 Inverted P after QRS

Junctional tachycardia: narrow QRS complexes at 130 bpm; P waves arise with QRS
Multifocal atrial tachycardia
SVT with aberration

Block
 Case 3

 You are a healthcare provider caring for a 71 year old man awaiting surgery
for a small bowel obstruction. He signals you with his bedside call light that
he is experiencing increasing shortness of breath, anxiety, and a feeling of
impending doom.

Unstable
Monomorphic ventricular tachycardia at rate of 150 bpm: wide QRS complexes with opposite
polarity T waves (arrow B)
Bradycardias
 Case 4

 You are treating a 62 year old man who had a syncopal episode.

 His skin is pale and he is diaphoretic. He is not following commands.

 There is no radial pulse but the carotid pulse is weak and slow.

 His BP is 78/42 mm Hg.

 I degree

Benign
II degree Mobitz
type 1

II degree Mobitz
type 2

Malignant

III degree
AV dissociation
 Doses

Atropine
 First dose – 0.6 mg bolus
 Repeat Q 3-5 mins, Max dose: 3 mg
Dopamine IV infusion
 2 – 20 mcg/kg/min
Adrenaline
 2 – 10 mcg/min
Isoprenaline
 Not preferred – May cause severe hypotension due to profound action
Adenosine
 Antiarrhythmic doses

 Adenosine
 6mg rapid IV push & flush, 2nd dose 6 or 12 mg if required

 Amiodarone
 Cardiac arrest – 300 mg 1st dose & 150 mg 2nd dose
 Tachycardia with pulse – 150 mg over 10 mins, repeat SOS
 Follow with infusion 1 mg/min for 6 hrs & 0.5 mg/min for 18 hrs
 Establishing IV access & Drugs

 Important

 Should not interfere with CPR and delivery of shocks

 Drugs can be administered before or after shock delivery

 Drug doses should be prepared before the rhythm check

 Timing of drug delivery is less important than the need to minimize

interruptions in chest compressions
 Electrical Cardioversion

 Immediate electrical cardioversion is indicated for a patient with serious signs &
symptoms related to the tachycardia.

 Delivered energy should be synchronized with the cardiac cycle

 Synchronization searches for the peak of the QRS complex and delivers the shock
a few milliseconds after the highest part of R wave.

 This avoids the delivery of the shock during the vulnerable period of cardiac
repolarization(T wave) which can induce VF.
 When to synchronise?
 Synchronised shocks for

 Unstable SVT

 Unstable AF

 Unstable flutter

 Unstable regular monomorphic tachycardia with pulse

 Unsynchronised shocks for

 Pulseless VT/VF

 When you are unsure whether monomorphic or polymorphic VT

 Energy for shock?

 Narrow regular – 50 to 100 J synchronised

 Narrow irregular - 120 to 200 J biphasic or 200 J monophasic

 Wide regular - 100 J synchronised

 Wide irregular – Defibrillation dose

 Unstable AF

 Monophasic – 200 J synchronised

 Biphasic – 120 – 200 J synchronised

 A flutter & SVT – 50 to 100 J synchronised

 Monitors
1
Atleast 20 mm Hg
diastolic
2

Atleast 10 mm Hg
ROSC > 35 mm Hg

3
 Basic airway adjuncts

OPA NPA
 Advanced airway adjuncts

ET Tube LMA
 Advanced airway adjuncts

Combitube Laryngeal tube

Pregnancy
 Some misconceptions

 Adrenaline kick starts the heart during cardiac arrest

 Atropine should be given in asystole

 Any cardiac arrest patient has to be shocked

 Intubation is the first priority in a cardiac arrest situation

 Isolated myoclonic jerks are a poor prognostic indicator

 Absence of pupillary reactivity immediately after ROSC indicates poor

prognosis
Backup Slides
ECG Correlation
Normal Sinus Rhythm
 CPR before defibrillation
Cardiac arrest

Out of hospital In hospital

Unwitnessed Witnessed by
a healthcare worker

Give CPR for 2 min

(i.e. about 5 cycles at Do not delay
30:2) Do not delay defibrillation
defibrillation
Only then put on the
paddles
 Probability of Survival Is Related to 2 Intervals:
(1) Collapse to Defibrillation and (2) Collapse to CPR

Collapse to start of CPR: 1, 5, 10, 15 (min)

Probability of
survival to
hospital
discharge

Collapse to defibrillation interval (min)

 Most critical interventions during the first minutes of VF or pulseless VT are by immediate
bystander
 CPR with minimal interruption in chest compressions
 Defibrillation
Sinus bradycardia
First-degree AV block at rate of 37 bpm; PR interval 0.28 sec
Second-degree heart block type I. Note progressive lengthening of PR interval
until one P wave (arrow) is not followed by a QRS.
Type II (high block): regular PR-QRS intervals until 2 dropped beats occur;
borderline normal QRS complexes indicate high nodal or nodal block

Type II (low block): regular PR-QRS intervals until dropped beats;

wide QRS complexes indicate infranodal block
Third-degree heart block: regular P waves at 50 to 55 bpm; regular ventricular “escape beats” at 35 to 40 bpm;
no relationship between P waves and escape beats
Cardiac action potential
Action potential of heart
Many factors can precipitate or exacerbate arrhythmias: ischemia, hypoxia, acidosis or alkalosis, electrolyte
abnormalities, excessive catecholamine exposure, autonomic influences, drug toxicity
(eg, digitalis or antiarrhythmic drugs), overstretching of cardiac fibers, and the presence of scarred or otherwise
diseased tissue.
However, all arrhythmias result from (1) disturbances in impulse formation, (2) disturbances in impulse conduction, or
(3) both.
Disturbances of Impulse Formation.The interval between depolarizations of a pacemaker cell is
the sum of the duration of the action potential and the duration of the diastolic interval. Shortening of either duration
results in an increase in pacemaker rate. The more important of the two,
diastolic interval, is determined primarily by the slope of phase 4 depolarization (pacemaker potential). Vagal
discharge and -receptor-blocking drugs slow normal pacemaker rate by reducing
the phase 4 slope (acetylcholine also makes the maximum diastolic potential more negative). Acceleration of
pacemaker discharge is often brought about by increased phase 4 depolarization
slope, which can be caused by hypokalemia,     -adrenoceptor stimulation, positive chronotropic drugs, fiber stretch,
acidosis, and partial depolarization by currents of injury.
Latent pacemakers (cells that show slow phase 4 depolarization even under normal conditions, eg, some Purkinje
fibers) are particularly prone to acceleration by the above mechanisms.
However, all cardiac cells, including normally quiescent atrial and ventricular cells, may show repetitive pacemaker
activity when depolarized under appropriate conditions, especially if hypokalemia is also present.
Afterdepolarizations (Figure 14–5) are depolarizations that interrupt phase 3 (early afterdepolarizations, EADs ) or
phase 4 (delayed afterdepolarizations, DADs ). EADs are usually exacerbated at slow heart rates and are thought
to contribute to the development of long QT-related arrhythmias.
DADs on the other hand, often occur when intracellular calcium is increased (see Chapter 13). They are exacerbated
by fast heart rates and are thought to be responsible for some arrhythmias related to digitalis excess, to
catecholamines, and to myocardial ischemia.
Disturbances of Impulse Conduction.
Severely depressed conduction may result in simple block, eg, atrioventricular nodal block or bundle branch block.
Because parasympathetic control of atrioventricular conduction is significant, partial atrioventricular block is
sometimes relieved by atropine. Another common abnormality of conduction is reentry (also known as "circus
movement"), in which one impulse reenters and excites areas of the heart more than once (Figure 14–6).
The path of the reentering impulse may be confined to very small areas, eg, within or near the atrioventricular node, or it may involve large portions of the atrial or
ventricular walls. Some forms of reentry are strictly anatomically determined; for example, in Wolff-Parkinson-White syndrome, the reentry circuit consists of atrial
tissue, the atrioventricular node, ventricular tissue, and an accessory atrioventricular connection (a bypass tract). In other cases (eg, atrial or ventricular fibrillation),
multiple reentry circuits, determined by the properties of the cardiac tissue, may meander through the heart in apparently random paths. Furthermore, the circulating
impulse often gives off "daughter impulses" that can spread to the rest of the heart. Depending on how many round trips through the pathway the impulse makes
before dying out, the arrhythmia may be manifest as one or a few extra beats or as a sustained tachycardia.
For reentry to occur, three conditions must coexist, as indicated in Figure 14–6. (1) There must be an obstacle (anatomic or physiologic) to homogeneous conduction,
thus establishing a circuit around which the reentrant wavefront can propagate. (2) There must be unidirectional block at some point in the circuit; that is, conduction
must die out in one direction but continue in the opposite direction (as shown in Figure 14–6, the impulse can gradually decrease as it invades progressively more
depolarized tissue until it finally blocks—a process known as decremental conduction). (3) Conduction time around the circuit must be long enough that the
retrograde impulse does not enter refractory tissue as it travels around the obstacle; that is, the conduction time must exceed the effective refractory period. It is
important to note that reentry depends on conduction that has been depressed by some critical amount, usually as a result of injury or ischemia. If conduction
velocity is too slow, bidirectional block rather than unidirectional block occurs; if the reentering impulse is too weak, conduction may fail, or the impulse may arrive
so late that it collides with the next regular impulse. On the other hand, if conduction is too rapid—ie almost normal—bidirectional conduction rather than
unidirectional block will occur. Even in the presence of unidirectional block, if the impulse travels around the obstacle too rapidly, it will reach tissue that is still
refractory.
Slowing of conduction may be due to depression of sodium current, depression of calcium current (the latter especially in the atrioventricular node), or both. Drugs
that abolish reentry usually work by further slowing depressed conduction (by blocking the sodium or calcium current) and causing bidirectional block. In theory,
accelerating conduction (by increasing sodium or calcium current) would also be effective, but only under unusual circumstances does this mechanism explain the
action of any available drug.
Lengthening (or shortening) of the refractory period may also make reentry less likely. The longer the refractory period in tissue near the site of block, the greater the
chance that the tissue will still be refractory when reentry is attempted. (Alternatively, the shorter the refractory period in the depressed region, the less likely it is that
unidirectional block will occur.) Thus, increased dispersion of refractoriness is one contributor to reentry, and drugs may suppress arrhythmias by reducing such
dispersion.
1.Class 1 action is sodium channel blockade.
Subclasses of this action reflect effects on the
action potential duration (APD) and the kinetics of sodium channel blockade.
Drugs with class 1A action prolong the APD and dissociate from the channel
with intermediate kinetics; drugs with class 1B action shorten the APD in
some tissues of the heart and dissociate from the channel with rapid kinetics;
and drugs with class 1C action have minimal effects on the APD and dissociate
from the channel with slow kinetics.
2.Class 2 action is sympatholytic. Drugs with this action reduce -adrenergic
activity in the heart.
3.Class 3 action manifests as prolongation of the APD. Most drugs with
this action block the rapid component of the delayed rectifier potassium current, I Kr.
4.Class 4 action is blockade of the cardiac calcium current.
5.This action slows conduction in regions where the action potential upstroke is
6.calcium dependent, eg, the sinoatrial and atrioventricular nodes.
 Not witnessed out-of-hospital arrest the provider
 Give 5 cycles of CPR before attempting defibrillation
 In prolonged arrest - shock delivery may be more successful after a period of effective chest
compressions
 Witnessed arrest with a defibrillator on-site
 Deliver 2 rescue breaths
 Provider should check for a pulse
 NO PULSE within 10 seconds – defibrillator
 Place adhesive pads or paddles and check the rhythm
 If VF/pulseless VT is present - deliver 1 shock
 360 J mono
 150 – 200 J biphasic
 1 shock rather than the 3 successive
 first-shock success rate for biphasic defibrillators is high
 it is important to minimize interruptions in chest compressions
 compelling evidence that interruption of chest compressions reduces coronary perfusion
pressure
 Provide CPR while the defibrillator charges
 until it is time to “clear” the victim for shock delivery
 Immediately after shock delivery
 Resume CPR without delay – 30:2
 5 cycles
 about 2 minutes if an advanced airway is in place
 Once an advanced airway is in place
 Compressions need not be interrupted for ventilation
 Compressing rescuer should deliver 100 compressions per minute continuously
 The rescuer delivering the ventilations should give 10 breaths per minute
 Check the rhythm only after 2 minutes
 Next shock
 Pulse and rhythm checks are limited
 Not recommended immediately after shock delivery
 Compression should be interrupted only for
 ventilation (until an advanced airway is placed)
 rhythm check
 shock delivery
 Drug therapy
 Inadequate evidence - Expert consensus
 If VF/VT persists after delivery of 1 or 2 shocks plus CPR
 Vasopressor
 Repeat every 3 to 5 minutes
 Should be administered during CPR and as soon as possible after the rhythm is checked
 When VF/pulseless VT persists after 2 to 3 shocks plus CPR and administration of a
vasopressor
 Consider administering an antiarrhythmic such as amiodarone
 Give Amiodarone – 300 mg after 3rd shock, repeat 150 mg after 5th shock if rhythm remains the
same.
 Rhythm checks should be brief
 Pulse checks should generally be performed only if an
organized rhythm is observed
 Look for causes
 H’s and T’s to identify a factor that may have caused the arrest or
may be complicating the resuscitative effort
 If the patient has ROSC, begin postresuscitation care
Hs

 Hypoxia (CNS events)

 Hypokalemia/hyperkalemia
(and other electrolytes)
 Hypothermia/hyperthermia
 Hypoglycemia/hyperglycemia
 Hypovolemia (tank/anaphylaxis, gravid)
Ts

 Trauma
 Tamponade
 Thrombosis (pulmonary)
 Thrombosis (coronary)
 Tablets (ODs, drugs, etc)
 Tension (pneumothorax, asthma)
Case 3

 A 55-year-old man walks into the ED complaining of severe chest and

abdominal pains
 He is placed on a stretcher and begins to remove his clothes
 Just as the nurse starts to attach the monitor leads, he falls back unconscious on the
stretcher
Non shockable rhythms

 Survival rate from cardiac arrest with asystole/PAE is dismal

 Often caused by reversible conditions
 In both PEA & asystole
 hope for resuscitation is to identify and treat a reversible cause
 Their treatment has been combined
 If there is a doubt of very fine VF vs asystole continue with this arm of CPR
Primary ABCD Survey

A = Airway: open the airway

B = Breathing: provide
positive-pressure ventilations
C = Circulation: give chest compressions
D = Defibrillation: Not indicated
 Secondary ABCD Survey
Focus: more advanced assessments and treatments

A - Airway: place airway device as soon as possible

B - Breathing: confirm airway device placement by exam plus
confirmation device
B - Breathing: secure airway device; purpose-made tube holders preferred
B - Breathing: confirm effective oxygenation and ventilation
C - Circulation: establish IV access
C - Circulation: identify rhythm  monitor
C - Circulation: administer drugs appropriate for rhythm and condition
C - Circulation: assess for occult blood flow (“pseudo-EMD”)
D - Differential Diagnosis: search for and treat identified reversible causes
 Will not benefit from defibrillation attempts
 Focus on resuscitation – For 2 minutes
 perform high-quality CPR with minimal interruptions
 identify reversible causes or complicating factors
 CPR – 30 : 2 (5 cycles)
 Insert an advanced airway
 2 rescuers
 Compressing rescuer should give continuous chest
compressions at a rate of 100 per minute without pauses for
ventilation
 The rescuer delivering ventilation provides 10 breaths per
minute
 Minimize interruptions in chest compressions
 inserting the airway
 establishing IV
 At end of 2 minutes
 Rhythm check
 PEA/asystole
 Resume CPR immediately – for 2 minutes
 Drugs
 Vasopressor – repeat every 3 – 5 minutes
 Atropine
 Keep looking for correctable causes – Hs & Ts
 Continue CPR – vasopressor sequence until rhythm chnanges
 Assess appropriateness for
Bradycardia clinical condition
HR < 50/min

Identify & treat cause

• Maintain airway/
• Monitor – Rhythm, BP, SP
• IV access
• 12 – lead ECG if possible

Symptoms? / ? Well perfused Transcutaneous Pacing

• Hypotension • IV Benzodiazepine for
• Alt. mental status anxiety/muscle contractions
Monitor & Observe • IV Narcotic for analgesia
• Shock
• Ischemic chest discomfort
• Acute heart failure

Atropine
If ineffective
Consider expert consultation
• Transcutaneous pacing
Transvenous pacing
• Dopamine infusion
• Adrenaline infusion
 Assess appropriateness for
Tachycardia clinical condition
HR < 50/min

Identify & treat cause

• Maintain airway/
• Monitor – Rhythm, BP, SP
• IV access
• 12 – lead ECG if possible
Synchronised cardioversion
• Consider sedation
Symptoms? / ? Well perfused • If regular narrow complex
Wide QRS? > 0.12 sec • Hypotension consider Adenosine
• Alt. mental status
• Shock
• IV access/ 12 lead ECG
• Ischemic chest discomfort
• Adenosine only if regular &
• Acute heart failure
monomorphic
• • Consider antiarrhythmic
IV access/ 12 lead ECG
• Vagal maneuvers infusion
• • Consider expert consultation
Adenosine (if regular)
• β-blocker, Ca. channel blocker
• Consider expert consultation
Antiarrhythmic infusion

 Page 127
 Avoid AV nodal blockers like Adenosine, Ca channel blockers, Digoxin & possibly β-
blockers in pre-excitation AF.
Tachycardia
Stable tachycardia

Unstable Tachycardia
Pt. displays serious symptoms

 Shortness of breath
 Chest pain
 Dyspnea
 Altered mental status
Objective


At the end one should be able to recognize:
 Type

 Unstable

 Cardioversion
 Classification

1. Narrow-complex tachycardia
 Paroxysmal supraventricular tachycardia
(PSVT)
 Junctional tachycardia
 Multifocal atrial tachycardia
 Atrial fibrillation/flutter
4. Ventricular tachycardia
 Monomorphic VT
 Polymorphic VT
 Torsades de pointes
Ventricular Tachycardia
 Ventricular Tachycardia

 Defined as three or more beats of ventricular origin in succession at a rate greater than 100
beats per minute
Ventricular Tachycardia

 Monomorphic VT

All QRS of same shape

 Polymorphic VT

Varying QRS morphology

 ECG Criteria
 No normal looking QRS complexes
 Rate :
100 – 220 beats / minute
 Rhythm :
Usually regular but may be irregular
 P :
Usually not recognizable
 ECG Criteria

 QRS :
Width of QRS is 0.12 seconds or more
Morphology – Bizarre & notching
 ST segment & T waves:
Usually opposite in polarity to the QRS
Polymorphic Ventricular Tachycardia
 Unstable, malignant, "ugly" form of VT that often degenerates to VF

 Look similar to VF
 Some identifiable QRS complexes and T waves
Monomorphic Polymorphic VT
VT
Torsades de pointes

 Form of VT
 QRS appears to be constantly changing.
 Electrical activity appears to be twisted like a helix.
Supraventricular Tachycardia

 Narrow complex
 Regular Rate 140 to 220 / minute
Multi Focal Tachycardia

 Three or more consecutive P waves of different morphologies at rates greater than 100
beats per minute.

Rate 100-250/bpm

Two or more ectopic P waves

P wave
with different morphologies

QRS Normal
Conduction P-R intervals vary

Rhythm Irregular
Juctional Tachycardia
P Waves may vary in location and will be inverted if visible.

Atria Depolarized
Before the Ventricles

Simultaneous
Depolarization of
Atria and Ventricles

Ventricles
Depolarized Before
the atria
 AF
 Definition:

Atrial Fibrillation may result from multiple areas of reentry within the
atria or from multiple ectopic foci.
A&E(SRMC)
 ECG

 Is there a P wave
 Rate: Atrial / Vent.
 Rhythm:
Fibrillatory waves
QRS
Atrial fibrillation
Atrial Flutter

 P waves
 Characteristic ‘ sawtooth appearence’ - atrial flutter.
Atrial Flutter
Atrial Rate = 250 bpm, Ventricular Rate = 125bpm
Synchronized Cardioversion

 Premedication if appropriate

Sedatives Analgesics
 Midazolam
 Barbiturates
• Fentanyl
• Morphine
• Meperidine
Synchronized Cardioversion - Procedure

1. Attach monitor leads to patient

2. Apply conductive material

3. Turn on defibrillator
Procedure (cont’d)

4. Turn on synchronization mode

5. Verify synchronization signal
on screen
6. Select energy level
7. Place defibrillator paddles on
chest and apply pressure
Procedure (cont’d)
8. Charge defibrillator
9. “CLEAR!”
 Check yourself
 Check patient
 Check bed/stretcher

10.Press both buttons until discharge occurs

 Energy selection
 PSVT: 50 J,100 J, 200 J

 Atrial fibrillation: 100 J, 200 J

 Atrial flutter: Start with 50 J

 Energy selection

 VT: 100 J, 200 J

 Polymorphic VT (treat like VF) 200J

 ELECTROCARDIOGRAM
“5” steps approach to arrhythmias
Step1: Is there a “QRS”
Step2: Is there a “P” Wave
Step3: What is the relationship between the
P waves and the QRS complexes?
Step4: Calculate rate
Step5:Miscellaneous
 1) Is there a “QRS”
(No pulse)

YES NO

NARROW WIDE CHAOTIC FLAT LINE

PEA VT VF Asystole
No “QRS” & Chaotic
No QRS & Flat line
Wide QRS
Wide QRS
Wide QRS & Polymorphic
 2) Is there a “P” Wave

YES NO

RR Interval
RATE MORPHOLOGY

VARY CONSTANT
Inverted
220 to 350
AF JUNCTIONAL
JUNCTIONAL
Atrial Flutter
A&E(SRMC)
No “P” & Varying “RR” interval
A&E(SRMC)
3)What is the relationship between the P
waves and the QRS complexes?
 HEART BLOCK
n“P” = n“QRS” ?
Yes No
PR interval PR interval
< 0.2 > 0.2 Constant ?

Normal Io AVB No Yes

Type2 IIo
RR interval
Constant?
Yes No
IIIo AVB Type1 IIo
1st Degree block
(AV Nodal Delay)
 P-R Interval

IST Degree heart block

n“P” = n“QRS” ?
P-R interval is >0.2 Sec
 HEART BLOCK
n“P” = n“QRS” ?
Yes No
PR interval PR interval
< 0.2 > 0.2 Constant ?

Normal Io AVB No Yes

Type2 IIo
RR interval
Constant ?
Yes No
IIIo AVB Type1 IIo
n“P” is not equal to n“QRS”?
PR interval is constant
A&E(SRMC)
 HEART BLOCK
n“P” = n“QRS” ?
Yes No
PR interval PR interval
< 0.2 > 0.2 Constant ?

Normal Io AVB No Yes

Type2 IIo
RR interval
Constant ?
Yes No
IIIo AVB Type1 IIo
A&E(SRMC)
IInd Degree Type-I heart block
n“P” is not equal to n“QRS” ?
Both PR and RR intervals
are not constant

PROGRESSIVE PROLONGATION OF ‘P-R’

INTERVAL

DROPPED ‘QRS’ COMPLEX

 HEART BLOCK
n“P” = n“QRS” ?
Yes No
PR interval PR interval
< 0.2 > 0.2 Constant ?

Normal Io AVB No Yes

Type2 IIo
RR interval
Constant ?
Yes No
IIIo AVB Type1 IIo
A&E(SRMC)
 IIIrd Degree heart block

n“P” is not equal to n“QRS”?

PR intervals are not constant
RR intervals are constant
4)Calculating Heart Rates

A Count the number of R waves in a

6-second strip and multiply by 10.(especially
for irregular rhythm)
•Not very accurate
•Used only with very quick estimate
Calculating Heart Rates(cont..)

B Count the number of large squares between two

consecutive R waves and 300 / Big squares

•Very quick
•Not very accurate with fast rates
•Used only with regular rhythms
Calculating Heart Rates (cont..)

C Count the number of small squares between two

consecutive R waves and or 1500 / small squares.
.

•Most accurate
•Used only with regular rhythms
•Time consuming
Calculating Heart Rates (cont..)

D Count the number of BIG squares between two

consecutive R waves in descending order as
300,150,100,75,60,50...

•Not very accurate

•Used only with regular rhythms
•Time saving
A&E(SRMC)
A&E(SRMC)
A&E(SRMC)
A&E(SRMC)
A&E(SRMC)
 Objectives

 To understand the indications, doses and actions of drugs used in

Resuscitation & Peri-arrest arrhythmias
 Classification of ACLS drugs

 Class I  Definitely useful

 Class II -a  Probably useful
 Class II - b  Possibly useful
 Class - Indeterminate  No supporting evidence
 Class III  Harmful
Adrenaline / Vasopressin

 Class – Indeterminate
Asystole
Pulseless electrical activity
 Atropine

 Symptomatic bradycardia – Class I

 Pulseless electrical activity - Class II b

 Asystole - Class II b
 A 55 year old patient is admitted to the ER with an acute MI .The monitor alarm sounds &
the doctor responding to the cardiac monitor finds the patient unresponsive.
Monitor shows
Epinephrine
 Epinephrine
Actions of Epinephrine
 agonist - arterial vasoconstriction
  systemic vascular resistance
  cerebral and coronary blood flow
 agonist -  heart rate/CO
 force of contraction
 myocardial O2 demand (may increase
ischaemia)
Indications
PEA / Bradycardia PulselessVT

VF Asystole
 Special circumstances

 Anaphylaxis

 Bronchial asthma
Recommended Dose

 1.0 mg of 1:1000,administered iv every 3 to 5 minutes – Arrest

 3-5 ml 1:10,000 i.v - Anaphylaxis

 1:1000 - 1ml =1mg
 S.C – 0.3 to 0.5ml – severe asthma, Anaphylaxis
 I.M – 0.3ml – Severe asthma, Anaphylaxis
 1ml(1:1000) + 9ml NS = 10ml – 1:10,000(1ml=100mics)

 IV 300 – 500 mics – Severe asthma,severe anaphylaxis

 1ml(1:10,000) + 9ml NS = 10ml – 1:1,00,000(1ml = 10mics)
 Mainly used in paediatric resuscitation
 Dose –10mics/kg
 ET dose – 100mics/kg
 25 yrs old female came to ER with history of breathlessness,sweating after
taking IV tramadol for pain abdomen, her vitals were stable.
 ABC
 Inj.avil, hydrocortisone 200mg IV given, there was no improvement
What is your response?

 Start IV fluids

 Inj.adrenaline IM 0.3 ml given, patient felt much better

Vasopressin
Indications

 Used as an alternative pressor to epinephrine in refractory VF

 Asystole and PEA
 May be useful for hemodynamic support in septic shock.
 Dose

 40 U Single IV bolus (Cardiac arrest)

 Precautions:
- May provoke cardiac ischemia and angina,Bronchial constriction
 64 year old women was brought to ER after she collapsed in the hospital car parking.
Monitor shows
 CPR initiated
 Adrenaline 1mg I.V .
Atropine
Mechanism of Action

 Parasympathetic blocking (vagolytic) agent.

  heart rate, A-V conduction
 May restore cardiac rhythm in asystole if due to

parasympathetic tone.
Paradoxical bradycardia

 Doses smaller than 0.2mg may enhance bradycardia and should not be used.
 Atropine is no longer indicated in Second Degree Type II or Third Degree AV Blocks!
Indications

 Asystole
 Symptomatic bradycardias
 PEA (rate < 60 beats min)
 May be beneficial in presence of AV block at the nodal level.
Dose

 1.0 mg IV every 3 to 5 minutes for asystolic cardiac arrest.

 0.5 to 1.0 mg IV every 3 to 5 minutes for bradycardia.
Maximum dose

 Upto a total dose of 0.04mg/kg.

(asystolic cardiac arrest)

 Upto a total dose of 0.03mg/kg.

(Bradycardia)
 55 year old man know case of hypertension,DM & CAD presents to ER with sudden onset
of palpitations.
Monitor shows
Amiodarone
Indications

 Refractory VF / Pulseless VT
 Haemodynamically stable VT
 Atrial & Ventricular tachyarrythmias
Dose

 Refractory VF / Pulseless VT
 300 mg i.v bolus followed by 150 mg IV if necessary.
 1mg/min for 6 hrs,0.5 mg/min for 18hrs - Infusion
 Max. 2.2 gms over 24 hours.
 Stable tachyarrhythmias
 Bolus: 150 mg in 20 ml 5% dextrose over 10 mins
 Maintenance: 1mg/min for next 6hrs and 0.5mg/min, for remaining 18hrs.
Suppose

 Amiodarone is not available

Monitor shows
Lidocaine
 Actions

 Suppresses ventricular ectopy

 Decrease excitability in ischemic tissue
 Blunts oropharyngeal reflex
 chances of VF
 Indications

 Refractory VF / Pulseless VT
 when amiodarone is unavailable
 Haemodynamically stable VT
 as an alternative to amiodarone
 Dose

 Refractory VF / Pulseless VT
 1 to 1.5 mg/kg as bolus and ½ the dose incrementally up to max of 3 mg/kg.
 Infusion – 2mg/min
 A 25 year old women presents to ED saying “I am having another episode of
PSVT”.HR:180 bpm. Vagal maneuvers have no effect.How will you proceed ?
Adenosine
 Indications
 Paroxysmal supraventricular tachycardia
 Broad complex tachycardia of uncertain etiology
 Actions

 Decreases the sinus rate

 Slows conduction across the AV node
 Half- life is <5 seconds

Must be used only in a monitored

environment
Dose

 6 mg by rapid I.V push.

 If necessary, two further doses of 12 mg each can be administered every 1–2 mins(saline
chase)
Contra indications

 Bronchial asthma

 Congestive cardiac failure

 Severe hypotension.
 A 60 year old man with the H/O chronic alcoholism presents to you with the H/O
tachycardia. HR: 160, BP: 90 / 70
Monitor shows
 Torsade de pointes
Magnesium
 Actions

 Depresses neurological and myocardial function

 Acts as a physiological calcium blocker, alpha blocker.

Indications
 Torsades de pointes

 Shock refractory VF (with possible hypomagnesaemia)

 Ventricular tachyarrhythmias(with possible hypomagnesaemia)
Dose

Shock Refractory VF
 1 to 2 g IV over 10 to 20 mins.
Other situations
 45 year old female known case of Hypertension & diabetic nephropathy on native line of
treatment presents to you with breathlessness.Her ECG shows
Sodium Bicarbonate
Actions

 Alkalinizing agent (increases pH)

 Indications
 Severe metabolic acidosis (pH < 7.1)
 Hyperkalaemia
 Special circumstance
 Tricyclic antidepressant poisoning
 Sodium Bicarbonate

 Pre existing hyperkalemia - Class I

 Tricyclic overdose – Class II a
 Aspirin overdose – Class II a
 Long arrest with intubation & ventilation - Class
II b
 ROSC after prolonged arrest – Class II b
 Lactic acidosis – Class III
Dose

 1 - 2 mmols / Kg i.v.
Caution

 carbon dioxide load

 inhibits release of oxygen to tissues (shifts ODC curve to left)
 impairs myocardial contractility
 Hypernatremia.
How will you proceed

 You are examining a patient in the ER,while the attender near by collapses.You have
started your CPR, & established definitive airway & breathing.But you are not able to get
an I.V. access.
 After IV, the next preferred route is IO.
 If IO is not possible, then ET route