Presentation e acls aremt

Australasian Emergency Response
Specialists Pty Ltd

TASMANIA & PNG

A.E.R.S Emergency Response & Specialist Training Services

Advanced Cardiac Life Support
Craig Stevens
AREMT Instructor/Examiner
Bachelor of Health Science Paramedic

Version 1 June 2009

Scope of Training
• The ACLS course provides participants the
opportunity to learn and review the following key
components of advanced cardiac care:
– Arrhythmias
– Pharmacological therapy
– Electrical therapy
– Patient assessment and management

Certification

A wallet size reference card and A4 certificates will be issued on
successful completion of this course.
Valid for 2 years and then can be refreshed/recertified over a half –
1 day session after that.

Introduction

- Welcome!

- The course you are about to participate in will be
conducted over 2 days
- Day 1 Theory and Practical Rehearsals
- Day 2 Practical Stations & Examination

- Internationally recognised certification, with credits for
doctors and nurses in continuing education.

Cases
- There are 10 cases studied and the morphology
and management of these cases are covered in
depth.
- Acute Coronary Systems
- Asystole
- AED
- Bradycardia
- PEA
- Narrow Complex tachycardia
- Respiratory Arrest
- Stroke
- Ventricular Fibrillation
- Wide Complex Tachycardia

Conduct of Course
• Review of Cardiac Rhythms
• Pharmacologic and Electrical Therapy
• Patient Assessment and the Cardiac Patient
• Skills Practice and Remediation
• ACLS Practice Cases
• ACLS Practice Written Test and Remediation
• Final Skills Examination
• Final Written Examination

Chapter 1 – Review Cardiac
Rhythms

Cardiac Electrical Conduction
System
Revision:

System
As you recall the myocardium is different from every other
muscle.

It has an ability to produce it’s own electrical activity by a process
call “automaticity”

Specialised conduction system with impulses generated by pace
maker

The collection of nerve fibres sets the
inherent rate of electrical discharge

System
“SA” Sino-Atrial Node

Primary pacemaker is the “SA” Sino Atrial
Node

Located in superior aspect of right atrium and discharges at 60 – 100
beats per minute

Once initiated the SA node, impulse travels through right and left atria

Atria depolarises cells, the discharge stimulates atria muscle to
contract

System

“AV” Atrio-Ventricular Node

Impulse travels from “SA” Node to the “AV”
(Atrio-Ventricular Node)

Located in wall of right atrium

The impulse from the “AV” Node is delayed slightly, before entering
ventricles

This allows the Atria and ventricles to beat independently which
provides a double action pump

“AV” Node discharges at a rate of 40 – 60 impulses per minute

System
“Bundle of His” and
“Purkinje System”

“Bundle of His” is located partially in the
walls of the right atrium and inter-
ventricular septum

Accommodates the “right and left bundle branches”, terminating at the
“Purkinje Network”

The cells depolarise and cause the ventricles to contract at the
“Purkinje” level

“Purkinje Network” discharges at a rate of 20 – 40 beats per minute

System
Conduction Failure
If the “SA” Node is to fail the “AV”
Node picks up the pace requirement,
which fires at a delayed rate.

If the “AV” Node fails to capture the
“Bundle of His” and “Purkinje Network”
will take over with a considerable lower
rate of contractility

In both cases we see marked “Brady-cardia”

ECG Waveforms
Each event in the cardiac conduction system, produces a
specific waveform that can be analysed on the ECG.

ECG Waveforms
“P” wave is normally
upright, first waveform,
simultaneous
depolarisation of the
atria

“P-R” segment is the time
from “P” wave to
commencement of
“QRS” complex, which
represents the delay in
the “AV” node

The “PR” interval is from commencement of “P” wave to end of “QRS”
represents the entire depolarisation of the atria and the delay of the
“AV” node

Collectively the “QRS” segment is the entire depolarisation of the
ventricles

ECG Waveforms
The “Q” wave is the first
negative deflection
after the “P” wave,
may or may not be
present

The “R” wave is the first
positive deflection after
the “P” wave

The “S” wave is the first negative deflection after the “R” wave

ECG Waveforms
The “S-T” segment
represents time
between ventricular
depolarisation and
repolarisation

Should be “Iso-electric”
(Neutral, baseline for
ECG)

The “T” wave represents repolarisation of the ventricles, (ready to fire)

Normal Sinus Rhythm
We’ve look at the ECG representation, now let’s look at
the “Sinus Rhythm”

Normal Sinus Rhythm

The “Sinus Rhythm” indicates the “SA” node is the primary
pacemaker site and all components are intact and functioning
correctly.

ECG Markers of Acute Coronary
Syndrome
The “ST” segment represents depolarisation and
repolarisation, it should be “Isoelectric”.

Which identifies that the myocardium is electrically
“Neutral”

ECG Markers of Acute Coronary
Syndrome (ACS)
The “ST” segment “elevation” is commonly indicative of “Myocardial
Injury”
The “ST” segment “depression” is commonly indicative of
“Myocardial Ischemia”

These observations are only conclusive when seen in 2 or more
leads, therefore “MCL’s” or a 12 lead needs to be used to
confirm.

“T” Wave Inversion
The “T” wave represents the
repolarisation of the ventricles.

Should be in the same direction
as the “QRS” segment.

Again these need to be observed
in 2 or more leads to be
conclusive

Those patients however presenting with signs and symptoms of “ACS”
is clinically significant and to be treated as such until proven
otherwise.

The “Q” Wave
The “Q” wave is the first negative deflection after the “P” wave.

“Q” waves are insignificant in some leads, this is not a safe
assumption however in someone presenting with chest pain, and
showing them in multiple leads on a 12 lead ECG.

A significant pathologic “Q” wave is one that is seen to be deeper
than 1/3 of the “QRS” height or wider than 0.03 sec’s

The “Q” Wave
Pathologic “Q” waves represent “dead myocardium” and
are the ECG signature of a “Myocardial Infarction”.

Bradycardia

Bradycardia is defined, “by a heart rate of less than 60 beats per
minute”.
Can result in a decreased cardiac output, which would make the
patient clinically unstable.
“Absolute” bradycardia refers to any heart rate less than 60 beats per
minute

“Relative” bradycardia is when the heart rate is faster than expected,
(May be >60 bpm) and is accompanied by serious signs and
symptoms.

Eg: Hypotension, or Altered Mental Status

Sinus Bradycardia
“Sinus Bradycardia” Results from “excess vagal stimulation”,
which slows “SA” node discharge

Other causes include:
- Disease
- Damage to cardiac electrical conduction system
- Certain drugs (Beta – blockers)

***In well conditioned athletes sinus bradycardia may be present
and a normal finding.

Idioventricular Rhythm
Idioventricular Rhythm occurs when a “ventricular
focus” acts as the primary pacemaker of the heart

Idioventricular Rhythm

Origin:
This is evident by the wide and bizarre appearance of the “QRS” complexes,
and slow ventricular rate.
Because atrial activity is absent there are no discernable “P” waves.

Clinical Significance:
In an absence of atrial contraction, minimal volumes of blood are ejected, into
ventricles.
Ventricular rate is slow, cardiac output significantly reduced.

Heart Blocks

“First Degree AV Block”
Origin:
“First Degree AV” block is caused by an abnormal delay at the AV node which
prolongs the “P-R” interval > 0.20 sec
What can cause this cardiac rhythm:
- Vagal stimulation
- AV Nodal disease
- Certain medications

Heart Blocks

“First Degree AV Block”
Unlike higher blocks, 1st degree AV block is less likely to be associated
with Bradycardia
However if Bradycardia is present cardiac output can fall
1st degree AV block can be a variant in some people

Heart Blocks

“Second Degree AV Block Type 1”
Origin:
2nd degree AV block Type I is caused by “AV” nodal disease or vagal
stimulation.
Each complex progressively delayed at AV node until a “QRS” segment
is lost, leaving sole “P” wave with no associated QRS segment.

Heart Blocks

“Second Degree AV Block Type I”
Depends on AV block (2:1, 3:1, 4:1 etc) this rhythm can either present
as a “normal” or “bradycardic” rate.
If associated with Bradycardia, cardiac output may decrease.

Heart Blocks

“Second Degree AV Block Type II”
Origin:
2nd degree AV Block Type II occurs when the AV node intermittently
blocks some atrial complexes.
Results in some “P” waves not followed by any “QRS” complexes.

Heart Blocks

“Second Degree AV Block Type II”
2ND Degree AV Block Type II results from more severe AV nodal
disease, excessive vagal tone
Frequently associated with bradycardia and can decrease cardiac
output

Heart Blocks

“Third Degree AV Block”
Origin:
Occurs as a result of complete block at the “AV” node.

Complete blockage at AV node, prevents any atrial conducted
complexes to enter the ventricles

Ventricles respond with escape complexes producing wide “QRS”
complex.

Also referred to as “CHB or Complete Heart Block”

Heart Blocks

“Third Degree AV Block”

Atrial and Ventricle contractions are dissociated cardiac output is
significantly decreased and patient most always unstable.

A ventricular pacemaker occurs at an intrinsic rate of 20 – 40 bpm
with wide “QRS” complexes and severe bradycardia

Tachycardia’s
- Tachycardia is defined as,” heart rate that is >
100bpm”.

- Varying types, narrow or broad complex tachycardia’s
occur.

- If heart beats too fast, ventricles may not adequately fill.

- Decreases cardiac output, making clinically unstable
patient.

Tachycardia’s
Narrow QRS Complex

Sinus Tachycardia
Origin:
Sinus Tachycardia occurs when the SA node discharges faster than it’s
inherent rate of 60 – 100 impulses per minute.

This caused by, medication or required increased cardiac input.
(Shock, fever, hypoxemia, exercise)

Tachycardia’s (Narrow Complex)
Narrow QRS Complex

Sinus Tachycardia

Can result in a decreased cardiac output secondary to inadequate
ventricular filling.


Supra Ventricular Tachycardia (SVT)
SVT can manifest as:
- Atrial tachycardia
- Ectopic atrial tachycardia
- Rapid atrial fibrillation or flutter
- Junctional tachycardia
Defined as narrow complex tachycardia exceeds >150 bpm


Origin:
Occurs when a supraventricular pacemaker initiates the impulse. Not
necessarily the SA node
SVT can be caused by medications or situations requiring increased
cardiac output.
(Shock, fever, hypoxemia, exercise or SA node disease).



SVT can result in a decreased cardiac output, secondary to inadequate
ventricular filling,
More than sinus tachycardia


Atrial Fibrillation (AF)
Origin:
Result of multiple atrial pacemakers discharging chaotically.

No discernible “P” waves, only fibrillatory waves between “QRS”

No electrical pattern from Atria causes “irregularly irregular”
ventricular rhythm, from the AV node area


Atrial Fibrillation (AF)
Frequently in patients with “Congestive Heart Failure” (CHF)

Tendency to have blood stagnate, causing potential for, pulmonary,
coronary or cerebral embolism.

When >100bpm, cardiac output decreases, which is compounded by
decreased atrial kick from small volumes of blood delivered to
ventricles


Atrial Flutter
Origin:
Result of ectopic atrial pacemaker outside SA node

Commonly lower atrium, near AV node

SA node function suppressed by flutter

“P” waves present as “flutter” waves, as abnormal atrial depolarisation
occurs near AV node across atria in a retrograde direction


Atrial Flutter
Occurs in “CHF” and in those with SA node disease

Complications occur with inadequate ventricular filling especially when
accompanied by rapid ventricular rate

Cardiac output significantly decreased

Tachycardia’s (Wide Complex)

Monomorphic Ventricular Tachycardia (VT)
Origin:
Most common form of “VT”

Complexes are all same shape, size and direction

Caused by ectopic pacemaker in ventricle, overrides atrial activity

“P” waves may be seen but usually buried in wide “QRS” complexes


Monomorphic Ventricular Tachycardia (VT)

Can result from many underlying causes
Most commonly significant:
- “Coronary Artery Disease”
- “QT” interval prolongation
- Electrolyte imbalance, specifically potassium (K+)


Polymorphic Ventricular Tachycardia (VT)
Origin:
Complexes vary in size, shape and direction from complex to complex

Usually occurs when “QT” interval of underlying rhythm prolongs,
indicating severe delay in ventricular repolarisation

Ventricles become irritated and ectopic ventricular pacemaker overrides

Variant known as “TdP” - “Torsades De Pointes” or “Twisting of Points”


Polymorphic Ventricular Tachycardia (VT)
Prone to occur after administration of “Quinidine” or “Procainamide”
both drugs prolong the “QT” interval
Hypomagnesaemia (Low Magnesium) is also common cause
Atria do not contract regularly or adequately to fill ventricles before
they contract
Marked reduction in cardiac output
High potential to deteriorate to “Ventricular Fibrillation”

Cardiac Arrest Rhythms

Ventricular Fibrillation (VF)/ Pulseless Ventricular
Tachycardia
Origin:
Multiple ectopic ventricular pacemakers, which depolarise in a random,
chaotic fashion and spread throughout myocardium
Lethal arrhythmia
Uncontrolled quivering


Tachycardia
Does not produce a palpable pulse
Most common rhythm in cardiac arrest
Immediate defibrillation is critical
Coronary Artery Disease, leads to myocardial ischemia/infarction most
common cause
(Hypoxia, acidosis, early repolarisation, Eg: “R on T” phenomenon)


Tachycardia
Note:
“VT” covered earlier can be with cardiac output or pulseless

It can occur in patients in cardiac arrest

Not as common as “VF”, but in witnessed arrest may be present before
“VF”


Asystole
Origin:
All pacemaker sites fail to generate electrical impulse
Total absence of electrical and mechanical activity

Asystole does not produce a pulse,
It is commonly the result of untreated ventricular fibrillation (VF)
(Eg: Hypoxia, acidosis or electrolyte abnormalities)

Pulseless Electrical Activity (PEA)

“PEA” is not a particular cardiac rhythm, but rather any cardiac
arrhythmia that does not produce a palpable pulse.

The only rhythm that is not classed as “PEA” is “Pulseless VT”
Can be caused by:
- Hypoxia
- Acidosis
- Pericardial tamponade
- Tension pneumothorax/haemothorax
- Hypolvolaemia

Summary
It is important to evaluate a cardiac rhythm of a patient with a cardiac-
related chief complaint.

Evaluation of the ECG of the patients signs and symptoms determines
the most appropriate treatment protocols.

More than one cardiac rhythm can be observed in a patient. The
clinician needs to be versatile enough to change the course of
management very quickly.

It is important to analyse and interpret, however a systemic assessment
is crucial in determining whether the cardiac rhythm is resulting in
haemodynamic compromise.

Pharmacologic and Electrical
Therapy
Introduction
This chapter reviews the most common pharmacologic and electrical
interventions used in ACLS to treat patients with a variety of
cardiovascular and respiratory system emergencies.

Therapy
Acute Coronary Syndrome – Pharmacology

Aspirin (Acetylsalicylic Acid, ASA)
Therapeutic Effects
- Blocks formation of thromboxane A2,
- Inhibiting platelet aggregation and vasoconstriction
- Reduces mortality from acute myocardial infarction, reduces
reinfarction and nonfatal stroke
Indications
- S & S suggestive of ACS such as chest pain or discomfort
- ECG changes consistent with ACS,
- ST Depression/Elevation
- T wave inversion

Therapy

Aspirin (Acetylsalicylic Acid, ASA)
Contra-Indications
- Known hypersensitivity
- Bleeding disorders
- Concomitant use of anti-coagulants
- Active ulcer, or recent GI Bleed
Adult Dose
- 160 – 325mg of chewable aspirin ASAP after onset of chest pain
- To achieve peak therapeutic plasma levels, instruct patient to chew
tablet before swallowing

Therapy

Fibrinolytic Therapy (Thrombolytics)
Therapeutic Effects
- Alteplase (Activase, tPA), Anistreplase (Eminase), Reteplase
(Retavase), Streptekinase, Tenectaplase

- Produce similar therapeutic effect, which is the conversion of
plasminogen to plasmin.

- Plasmin destroys fibrin and fibrinogen matrix of thrombus, destroying
clot obstructing the artery and re-establishing distal blood flow

Therapy

Indications:
- Acute Myocardial Infarction (AMI) in adults
- ST segment elevation > or equal to 1mm in 2 or more contiguous leads
- In S & S of AMI, no > than 12 hours from duration of onset (chest pain)
- Acute Ischaemic Stroke
- Sudden onset focal neurologic deficit (slurred speech, facial droop) or
alterations in mental status
- Absence of intracerebral/subarachnoid haemorrhage (rule out if
required)
- S & S not rapidly improving (TIA)
- S & S no > 3 hours in duration

Therapy
Contra-Indications:
- Active bleeding within 21 days, menses excluded
- History of intra-cerebral, intracranial, or intra-spinal event within 3
months
- Stroke
- Arteriovenous (AV) malformation
- Neoplasm
- Aneurism
- Trauma or surgery
- Major trauma or surgery in last 14 days
- Aortic dissection
- Severe uncontrolled hypertension
- Severe bleeding disorders

Therapy

Contra-Indications:
- History of intra-cerebral, intracranial, or intra-spinal event within 3
months cont…..
- History of prolonged CPR with evidence of thoracic trauma
- Lumbar puncture within 7 days
- Recent arterial puncture or non-compressible site
- Aspirin or heparin administered in last 24 hours after acute ischaemic
stroke

Therapy

Adult Dose:
- Variable depending on fibrinolytic agent used

Therapy

Morphine Sulphate (MSO4)
Therapeutic Effects:
- Narcotic analgesic that promotes, through it’s vasodilatory effects,
systemic venous pooling, reducing pre-load (venous return) as well
as systemic vascular resistance (after load)

- Reduces myocardial oxygen demand, and consumption

- Reduces chest pain and anxiety

Therapy

Indications:
- Chest pain in ACS that is not responsive totally to GTN
- Cardiogenic pulmonary oedema, (BP > 90mmHg)

Contra-Indications:
- Hypersensitivity to Morphine or opiate based medications
- Signs of CNS depression (Eg: respiratory depression, hypotension,
bradycardia)

Therapy


Adult Dose:
- 2 – 4mg via slow IV push, over 1 – 5 minutes,

- May be repeated every 5 – 30 minutes, to acquire the desired effect
- Should signs of CNS depression occur, including respiratory depression,
- Naloxone (Narcan) 0.4mg – 2.0mg should be administered IV or IMI to
reverse effects

Therapy

Glyceryl Trinitrate

- Smooth muscle relaxant, producing systemic venous pooling of blood
through it’s vasodilatory effects

- Reducing pre-load (venous return) as well as systemic vascular
resistance (after load)

- Reduces myocardial oxygen demand, and consumption

Therapy

Glyceryl Trinitrate
Indications:
- Chest pain suspected of cardiac in origin
- Cardiogenic pulmonary oedema to left sided CHF

Contra-Indications:
- Systolic BP <90mmHg
- Severe Bradycardia <50 bpm or Tachycardia >100bpm
- Use of “Viagra” in last 24 hours
- Or “Cialis” in last 48 hours

Therapy

Glyceryl Trinitrate
Adult Dose:
- Tablet
- 0.4mg sublingually
- If not had before or > 65 y/o give half tablet first
- Spray
- 0.4mg (1 spray) given every 5 minutes, up to maximum of 3 sprays
- IV Infusion
- 10-20mcg, titrated for effect,
- Frequently monitor BP to maintain >90mmHg

Therapy

Oxygen (O2)
Therapeutic effect:
- Increases haemoglobin saturation

- Enhances tissue oxygenation, provided that adequate ventilation and
circulation are maintained

- Increase oxygen surface tension in blood

Therapy

Oxygen (O2)
Indications:
- Any suspected, cardiovascular, cerebrovascular or respiratory system
emergency
- Chest pain
- Stroke
- Altered mental status
- SOB
- Anyone where it is felt it is needed!
Contra-Indications:
- None when given in emergency situations

Therapy

Oxygen (O2)
Dose/Method of Administration:
- Mild hypoxia with adequate breathing
- Nasal cannula @ 4lpm
- Severe hypoxia with adequate breathing
- Non re-breathing mask @ 15lpm
- Inadequate breathing or apnoea
- Bag valve mask resuscitator (BVM) and reservoir bag @ 15lpm

Therapy

Anti-Arrhythmics
Introduction:

Used to treat a variety of arrhythmia’s both supraventricular (narrow)
and ventricular (wide) in origin.
- Adenosine
- Amiodarone
- Lidocaine/Lignocaine
- Magnesium Sulphate
- Procainamide

Therapy

Adenosine
- Natural occurring endogenous nucleoside that is rapidly metabolised.
- Slows discharge rate of SA node and the conduction through the AV
node
- Restoring sinus rhythm in SVT

Indications:
- Narrow QRS supraventricular tachycardia’s
- SVT to slow the rate to determine underlying rhythm

Therapy

Adenosine
Contra-Indications:

- Toxin induced tachycardia’s (sepsis, crush injury)

- 2nd or 3rd degree AV block

- Atrial fibrillation or flutter

- Wide QRS VT

Therapy

Adenosine
Adult Dose:
- Initial Dose:
- 6mg rapid (1-3 seconds) IV push, with extremity elevated, followed by
20ml IV saline flush
- Repeat Dose:
- 12mg rapid IV push, 1-2 minutes after initial dose, further 12mg dose
may be repeated, 1-2 minutes later
- Up to a maximum of 30mg

Therapy

Amiodarone:
- Diverse anti-arrhythmic, blocks sodium, calcium and potassium, and
inhibits sympathetic nervous system stimulation.

- Suppressing SA node discharge, reducing heart rate

- Slows conduction through AV node

- Effective in slowing conduction in accessory pathways in WPW
syndrome.

Therapy

Amiodarone:
Indications:
- “V”-Fib and Pulseless VT that is refractory to defibrillation
- Polymorphic “V”-Tach and wide complex tachycardia of unknown
origin
- Stable “V”-Tach when cardioversion is unsuccessful
- Adjunct to synchronised cardioversion in supraventricular
tachycardia’s (Atrial Fibrillation)
- Termination of atrial tachycardia
- Rate control in atrial fibrillation and atrial flutter, when other
therapies have proven unsuccessful

Therapy

Amiodarone:
Contra-Indications:

- Sinus node disease with significant bradycardia

- 2nd and 3rd degree AV block

Therapy
Amiodarone:
Adult Dose:
- V Fib and Pulseless V Tach
- 300mg diluted in 20-30ml of D5W via rapid IV push
- May repeat 150mg diluted in 20-30ml of D5W via rapid IV push 3-5 min
intervals
- Stable V Tach, SVT and Atrial flutter/fibrillation
- 150mg diluted in 20-30ml of D5W via rapid IV push over 10 minutes
- May be repeated every 10 minutes as required
- 24 hour maintenance infusion
- 360mg via IV infusion over first 6 hours (1mg/min)
- 540mg over remaining 18 hours via IV infusion (0.5mg/min)
- Up to a maximum of 2.2 grams in 24 hours

Therapy

Lidocaine / Xylocard
- Blocks influx of sodium through fast channels of myocardium, decreasing
irritability in ischaemic areas
- Increases V-Fib threshold,
- Lidocaine decreases defibrillation threshold
Indications:
- V-Fib and Pulseless VT refractory to defibrillation
- Stable wide complex tachycardia’s (e.g. V-Tach, wide complex
tachycardia’s of uncertain origin)

Therapy

Contra-Indications:
- Known hypersensitivity to Lidocaine or any “cain” based medications
(e.g. Marcain etc)

- Sinus bradycardia

- AV Blocks

Therapy

Adult Dose:
- V-Fib and Pulseless V-Tach
- 1-1.5mg/kg via rapid IV push
- May be repeated at 0.5-0.75mg/kg every 5-10mins, to a maximum of
3mg/kg
- Stable V-Tach and wide complex tachycardia of unknown origin
- 1-1.5mg/kg via rapid IV push
- May be repeated at 0.5-0.75mg/kg every 5-10mins, to a maximum of
3mg/kg
- Maintenance Infusion
- 1-4mg per minute, titrated to desired effect

Therapy

Magnesium Sulphate
- Classified as an electrolyte, possesses an anti-arrhythmic type
property
- Slows SA node impulse rate, and suppresses automaticity in
partially depolarised cells
- Has CNS depressant properties
- Indications:
- Torsade de Pointes (TdP) with pulse
- Cardiac arrest only if Torsades or Hypomagnesaemia is present

Therapy

Magnesium Sulphate
Contra-Indications:
- CNS depression
- Hypomagnesaemia
- Hypocalcaemia
Adult Dose:
- Torsades with Pulse
- Loading dose of 1 -2 g mixed in 50-100ml of D5W given over 5-60 min
- Follow by 0.5-1g/hr IV, titrated to control Torsades de Pointes
- Cardiac Arrest (From Hypomagnesaemia or Torsades)
- 1-2g (2-4ml of 50% solution) diluted in 10ml of D5W given IV over 5-
20mins

Therapy

Procainamide (Pronestyl)
- Slows conduction of the atria, ventricles and “HIS” bundle,
- Prolonging P-R and Q-T intervals and refractory period of AV
node
- Slows refractory period within the atria
Indications:
- Recurrent V-Fib or Pulseless V-Tach
- Stable SVT uncontrolled by vagal manoeuvres or adenosine
- Atrial fibrillation with rapid ventricular rate in WPW

Therapy

Contra-Indications:
- Known hypersensitivity to procainamide or similar medications

- 3rd degree AV block (without artificial pacemaker)

- Digitalis toxicity (may exacerbate AV conduction depression)

- Pre-existing QRS and Q-T interval prolongation

Therapy

Adult Dose:
- Recurrent V-Fib and Pulseless V-Tach
- 20mg/min via IV infusion
- In urgent situations, up to 50mg/min may be administered,
- Use of procainamide in cardiac arrest is limited by need for slow IV
infusion and uncertain efficacy
- SVT, AF, and wide complex tachycardia of unknown origin
- 20mg/min via IV infusion
- Maintenance Infusion
- 1-4mg/min titrated to desired effect

Therapy

Adult Dose:
- Stop procainamide infusion if:
- Arrhythmia suppression
- Hypotension develops
- QRS complex widens > 50% of it’s pre-treatment width
- Maximum dose of 17mg/kg has been given

Therapy

Calcium Channel Blockers
Introduction:

- Calcium Channel Blockers are used in the treatment of stable narrow
complex tachycardia's

- As well as the rate control in atrial fibrillation and atrial flutter

Therapy
Diltiazem (Cardizem)
- Blocks movement of calcium ions, across cell membranes of
myocardium and smooth muscle

- Results in decreased myocardial contractility (negative inotropy)

- Slowing of conduction through AV node (negative dromotropy)

- Dilation of coronary arteries and peripheral vasculature, decreasing
myocardial oxygen demand

Therapy
Indications:
- Control of ventricular rate in atrial fibrillation and atrial flutter
- Adjunct to adenosine to treat stable narrow complex tachycardia’s
Contra-Indications:
- Wide complex tachycardia’s of unknown origin
- Poison or drug induced tachycardia’s
- Rapid AF and atrial flutter in WPW
- Sinus node disease
- AV block (without an artificial pacemaker)
- Concurrent use of beta blocking agents (e.g. Atenolol, Inderal)
- May precipitate significant hypotension

Therapy
Adult Dose:
- IV Bolus:
- 15-20mg (0.25mg/kg) IV over 2 minutes
- May be repeated 15 minutes later, at 20-25mg (0.35mg/kg) over
2 minutes
- Maintenance Infusion:
- 5-15mg/hour titrated to desired effect

Therapy
Verapamil (Calan, Isoptin)
- Blocks movement of calcium ions across cell membranes and smooth
muscle of vasculature

- Results in decreased myocardial contractility,

- Slowing AV conduction through AV node and dilation of coronary
arteries and peripheral vasculature

- Decreases myocardial oxygen demand

Therapy
Indications:
- Control of ventricular rate in atrial fibrillation and atrial flutter and
ectopic atrial tachycardia
- Adjunct to adenosine to treat stable narrow complex tachycardia’s
Contra-Indications:
- Wide complex tachycardia’s of unknown origin
- Poison or drug induced tachycardia’s
- Rapid AF and atrial flutter in WPW
- Sinus node disease
- AV block (without an artificial pacemaker)
- Concurrent use of beta blocking agents (e.g. Atenolol, Inderal)
- May precipitate significant hypotension

Therapy
Verapamil (Calan, Isoptin)
Adult Dose:
- 2.5-5mg via IV push over 2 minutes
- May be repeated 5-10mg via IV push every 15-30 mins
- Maximum dose 20mg
- Alternative dosing regime
- 5mg via IV push every 15 minutes
- Maximum dose 30mg

Therapy
Electrical Therapy
Introduction
- Electrical therapy is frequently used

- Where serious S & S as a result of patients cardiac rhythm

- Patients with heart beat too fast or too slow, chaotic or pulseless

- Need prompt electrical therapy to stabilise their condition

Therapy
Defibrillation:

- Unsynchronised delivery of energy into myocardium

- To stop chaotic electrical activity by literally freezing the heart in
animation

- So an organised SA or AV pacemaker can dominate and restore a
perfusing rhythm

Therapy
Defibrillation:
Indications:
- V-Fib and Pulseless V-Tach
- Unstable polymorphic V-Tach
Contra-Indications:
- Asystole
- Routine defibrillation of asystole is not recommended, because it
may result in failure to identify and treat underlying cause of
asystole
- Regular cardiac rhythm with a pulse
- Other health care providers being in physical contact with the
patient
- Ensure no one is in contact with patient at time of defibrillation

Therapy
Defibrillation:
Adult Energy Settings:
- V-Fib or Pulseless V-Tach
- 360J (or biphasic equivalent) for first and subsequent shocks
- Follow each shock immediately with CPR
- Reassess after 2 minutes CPR
- If first defibrillation unsuccessful, defibrillate one time, as
needed, after every 2 minutes of CPR
- Unstable polymorphic V-Tach
- 360J (or biphasic equivalent) repeated as needed
- Be prepared to perform CPR if patient becomes pulseless

Therapy
Synchronised Cardioversion
- Timed delivery of energy into myocardium

- To correct rapid, regular cardiac rhythms, in patients who are
unstable as a result of cardiac rhythm

- An internal “synchroniser” times the shock to deliver when it senses
the “R” wave

- Avoids the shock during the refractory period (down slope of the “T”
wave) which may precipitate V-Fib

Therapy
Synchronised Cardioversion
Indications:
- Perfusing narrow and wide QRS complex tachycardia’s, >150bpm with
serious S & S linked to tachycardia
- Monomorphic V-Tach, SVT, AF, Atrial Flutter
Contra-Indications:
- V-Fib or pulseless VT (Requires Defibrillation)
- Poison or drug induced tachycardia
- Treat underlying problem with an antidote if available
- The serious symptoms are associated with poison or drug not
tachycardia
- Other health care providers being in physical contact with the patient
- Ensure no one is in contact with patient at time of defibrillation

Therapy
Defibrillation:
- Monomorphic V-Tach and AF
- Start with 100J (or biphasic equivalent)
- Repeat at 200J, 300J, 360J respectively if the rhythm is not corrected

- SVT and Atrial Flutter
- Start with 50J, (or biphasic equivalent)
- Repeat at 100J, 200J, 300J, 360J respectively if the rhythm is not
corrected

Therapy
Transcutaneous Cardiac Pacing:

- Uses an artificial electrical impulse to increase electrical discharge
rate of slow inherent pace maker in the heart

- Preferred initial cardiac pacing method in emergency cardiac care
because it is quickly initiated and relatively safe

Therapy
Transcutaneous Cardiac Pacing (TCP):
Indications:
- Symptomatic bradycardia, where S & S are related to bradycardia,
non reactive to atropine or if unavailable
- Rhythms that may require TCP:
- AV Blocks (Especially 2nd and 3rd degree)
- Bradycardia with ventricular escape beats (PVC’s)
Contra-Indications:
- Severe hypothermia
- Prolonged brady-asystolic cardiac arrest

Therapy
Defibrillation:
- Set pacing rate at 80bpm
- Symptomatic Bradycardia
- Increase output (mA) from minimum setting until consistent capture is
achieved
- Is evidenced by a widening QRS and broad “T” wave after each pacing
spike.
- Then increase by 2 mA as a safety margin to ensure positive capture

Therapy
Parasympatholytics:
Introduction:
- Referred to as parasympathetic blockers, vagolytic and
anticholinergic drugs
- Parasympatholytics block the parasympathetic nervous system, via
the vagus nerve
- Used to treat symptomatic bradycardia’s (absolute or relative)
caused by increased vagal tone

Therapy
Parasympatholytics:
Atropine Sulphate
Indications:
- Symptomatic bradycardia (absolute or relative)
- Asystole
- Bradycardic pulseless electrical activity (PEA)
Contra-Indications:
- Glaucoma (causes pupillary dilation)
- May not be effective in treating bradycardia associated with 2nd
degree type II and 3rd degree AV blocks
- Tachycardia
- Denervated (transplanted) hearts, use TCPM and catecholamine's
instead

Therapy
Sympathomimetics

Introduction:
- Mimic the effects of the sympathetic nervous system

- Increasing heart rate and blood pressure

- Synthetically produced

- Equivalent to endogenous bases that occurs in human body naturally

Therapy
Sympathomimetics:
Epinephrine (Adrenaline):
- Naturally occurring catecholamine, contains natural occurring Alpha
and Beta adrenergic effects

- Alpha effects result in vasoconstriction, increasing blood pressure

- Beta1 effects result in increased heart rate (positive chronotropy) and
increased myocardial contractility (positive inotropy)

- Beta2 effects cause relaxation of bronchial smooth muscle,
(bronchodilation)

Therapy
Sympathomimetics:
Indications:
- Cardiac Arrest
- V-Fib or Pulseless V-Tach
- Symptomatic Bradycardia
- After atropine and pacing
- Severe hypotension
- Treat with fluid boluses first
- Anaphylactic Shock
- Combined with fluid bolus, corticosteroids and antihistamines

Therapy
Sympathomimetics:
Contra- Indications:
- Tachycardia

- Hypertension

- Do not mix with alkaline solutions, (e.g. sodium bicarbonate)
deactivation will occur, as will, with all catecholamine's.

Therapy
Sympathomimetics:
Adult Dose:
- Cardiac Arrest:
- 1mg (10ml of 1:10,000) every 3-5mins, followed by 20ml flush of normal
saline
- No maximum dose when administered for persistent cardiac arrest

- Symptomatic bradycardia or severe hypotension
- 2-10mcg per minute
- Add 1mg Adrenaline (1ml of 1:1000) to 500ml normal saline and infuse at 1-
5mL/min

Therapy
Sympathomimetics:
Dopamine (Intropin):
- Naturally occurring catecholamine,
- Physiological effects vary with increasing doses
- At medium or “cardiac doses” (5-10mcg/kg/min), dopamine acts
directly on beta receptors
- Causing increased myocardial contractility, (increased inotropy), and
increased SA nodal discharge and increased heart rate (positive
chronotropy)
- Doses > 10mcg/kg/min (vasopressor dose) stimulate Alpha
receptors, increasing systemic vascular resistance (vasoconstriction)
- Dosing depends on patients condition

Therapy
Sympathomimetics:
Indications:

- Symptomatic Bradycardia:
- After atropine, pacing and adrenaline

- Hypotension (Systolic <70-100mmHg) with S & S of shock
- Consider fluid boluses first, dopamine should not be given when
hypovolaemic

Therapy
Sympathomimetics:
Contra-Indications:
- Hypolvolaemia
- Tachydysrhythmia’s or V-Fib
- Pheochromocytoma (Adrenal tumor producing adrenaline)
- Concurrent use of MOAI’s
- Do not mix with alkaline solutions, (e.g. sodium bicarbonate)
deactivation will occur, as will, with all catecholamine's.

Therapy
Sympathomimetics:

Adult Dose:
- As IV Infusion
- Mix 400mg-800mg of dopamine in 250ml of normal saline, D5W, or
Hartmann’s and titrate on patients clinical response

- Symptomatic bradycardia
- 2-10mcg/kg/min

- Profound hypotension (Non-hypovolaemic)
- 10-20mcg/kg/min

Therapy
Sympathomimetics:
Vasopressin (Pitressin Synthetic):

Introduction:
- Is an Anti-Diuretic Hormone (ADH) produced in the pituitary gland
- Binds to specific receptors, specifically vasopressin (V) receptors
- 2 receptors V1(V1a and V1b) and V2.
- V1a produces potent vasoconstriction
- V2 produces vasodilation
- Vasopressin possesses a greater vasoconstrictive effect, especially in
an acidotic or hypoxic environment (e.g. Cardiac Arrest)
- Does not increase myocardial oxygen consumption

Therapy
Sympathomimetics:

Indications:
- Used to replace the first and second dose of adrenaline for patients
in cardiac arrest from V-Fib/pulseless V-Tach, asystole and PEA
Contra-Indications:
- Known sensitivity to vasopressin
- Acute Coronary Syndrome
- Vasopressin may exacerbate hypertension because of it’s
vasoconstrictive effects

Therapy
Sympathomimetics:

Adult Dose:

- 40 units via IV push as a one off dose
- Wait approximately 10 minutes after vasopressin administration before
initiating/resuming adrenaline therapy

Assessment of Non-Cardiac
Arrest Patients
Introduction:
- Appropriate and prompt assessment and treatment of the patient
experiencing difficulties because of a cardiovascular or respiratory
related condition is imperative.

Arrest Patients
Introduction:
- You must perform a careful and systematic assessment aimed at
identifying serious S&S linked to the patient, or their cardiac rhythm.

Arrest Patients
Universal Treatment of the NON-Cardiac Arrest
Patient

- Certain interventions must be performed on all non cardiac arrest
patients, presenting with cardiovascular or respiratory related S&S.
- Oxygen
- IVT
- Pulse Oximetry
- 12 lead if available
- Cardiac monitoring

Arrest Patients
Summary:
- Patient presenting with S&S of Non cardiac related cardiovascular or
respiratory system emergencies needs a systematic assessment.
- Your findings will dictate the most appropriate treatment
- All patients require:
- Supplementary oxygen therapy
- Intravenous therapy
- The goal in managing these patients is preventing them from going
into cardiac arrest.

Assessment and treatment of
Cardiac Arrest Patients
Introduction:
- Successful management of a patient in cardiac arrest requires a
careful and systematic assessment, immediate identification of their
cardiac rhythm and selection of the appropriate treatment.

Assessing the Underlying causes of Cardiac Arrest
- Careful assessment needs to occur:
- Pm Hx – Past Medical History
- Hx - History
- Events leading to incident

- Management:
- Defibrillation, adrenaline and other pharmacological adjuncts will not be
effective until the underlying cause is identified and rectified.

- We use the 6 H’s and T’s to assess the underlying causes.

Universal Treatment of Cardiac Arrest
- Certain interventions must be carried out in all cases of cardiac
arrest regardless of the presenting cardiac rhythm.
- CPR
- Endotracheal intubation
- Vascular Access
- Vasopressors
- Circulation of cardiac drugs
- Identify and Correct underlying causes

Post Cardiac Arrest Treatment
- If a pulse and perfusing rhythm are successfully restored, you must
perform certain interventions to prevent the recurrence of cardiac
arrest.
- If the patient re-arrests, the chances of a second successful
resuscitation are much lower
- Prevention of recurrent cardiac arrest can be maximised by
performing appropriate management

Arrest Patients
Summary:
- You must focus on identifying and correcting the underlying cause of
cardiac arrest.
- Failure will significantly decrease the likelihood of successful
resuscitation
- Interventions must be performed regardless of underlying rhythm
- Interventions are aimed at maintaining effective ventilation and
circulation until the abnormal rhythm can be corrected

Case Review 1 - ACS
Introduction:
- Looks at a patient presenting with Acute Coronary Syndrome.
- Term used to describe unstable angina pectoris “Angina” or an acute
myocardial infarction (AMI).
- Most patients present with chest pain, discomfort, SOB, diaphoresis,
dyspnoea
- Advised to air on side of caution and suspect AMI

Case Review 1 - ACS
Signs & Symptoms:

Case Review 1 - ACS
Immediate Treatment & Management:

- In first 10 mins an immediate assessment and treatment regime
must occur

- Diagnosing patients problem, provide adequate treatment

- Mnemonic – “MONA”
- Morphine
- Oxygen
- Nitro-glycerine (GTN)
- Aspirin

Immediate Treatment & Management:

Case Review 1 - ACS
Targeted History for Fibrinolytic Therapy:
- In conjunction with 12 lead ECG
- Perform brief targeted history and physical examination targeted on
eligibility
- If administered within 12 hours of onset of symptoms, “clot busters”
can significantly reduce size of infarct, preserving myocardium
- The indications or “inclusion criteria” for therapy must be carefully
matched to contraindications “exclusion criteria”, if they are
administered to wrong patient, they can be lethal.

Case Review 1 - ACS
- Inclusion criteria:

Case Review 1 - ACS
Other Perfusion Strategies:
- Depending on condition and haemodynamic status
- Other strategies may include:
- Percutaneous Coronary Interventions (PCI)
- (e.g. Coronary angioplasty with or without stent)
- Coronary Artery Bypass Grafting (CABG) (GAGS)

Case Review 1 - ACS
- Exclusion criteria:

Case Review 1 - ACS
Summary:
- Patient who presents with S & S of ACS, requires immediate
assessment within 10 minutes of presentation
- 12 lead ECG
- Cardiac serum markers
- Targeted history
- Emphasis on fibrinolytic therapy suitability

- Immediate management aimed at oxygenation and ventilation with
pharmacologic interventions to reduce pain and anxiety

- The adage “time is myocardium” definitely applies and should be
remembered and taken seriously in patients with ACS presentation

Case Review 2 - Asystole
Introduction:

- Asystole represents the absence of both cardiac electrical and
mechanical activity on a cardiac monitor

- Unfortunately asystole is rarely associated with a positive outcome

Treatment:
- Must be assessed in 2 or more leads, as it may be asystole in
appearance in one lead and fine V-Fib in another
- CPR
- Airway management
- Medications
- Assessment as to why the patient is presenting in this way

Treatment:

Summary:
- It should be considered to be the only true arrhythmia because it
represents a total absence of any electrical or mechanical activity of
the heart

- Unfortunately is associated with a poor prognosis

- There are potentially reversible causes of asystole, therefore
systematic assessment, and appropriate interventions will maximise
chances of successful resuscitation

Case Review 3 – Automated
External Defibrillation
Introduction:
- Most cardiac patients present with ventricular fibrillation (V-Fib) as
the initial dysrhythmia

- V-Fib does not produce a pulse, therefore blood is not circulated

- Pulseless V-Tach is less common but as lethal as V-Fib

- The single most effective treatment for V-Fib is defibrillation

- V-Fib is a transient rhythm and rapidly deteriorates

- The AED can provide rapid defibrillation and does not require an
ACLS operator to perform treatment

Assessment and Initial Treatment:

- A careful and systematic assessment is required for a patient in
cardiac arrest

- If arrest was witnessed by you, begin CPR and apply AED
immediately.

- If not witnessed perform 2 minutes of CPR prior to applying AED

- A return of spontaneous circulation (ROSC) occurs more often in V-
Fib or Pulseless V-Tach if 1 ½ - 3 minutes of CPR is conducted prior
to defibrillation

Cardiac Rhythm Analysis and Defibrillation:
- As soon as AED is available it must be attached

- For each minute in V-Fib and Pulseless V-Tach defibrillation is
delayed, the chance of survival is reduced by 10%

- If indicated the AED will deliver a single shock, after which CPR
should be continued

- After 2 minutes the AED will assess the patient’s rhythm and ask you
to check pulse, reanalyse and deliver a shock if indicated


Summary:
- A rapid assessment is required in order to confirm the presence of
cardiac arrest and begin the appropriate treatment ASAP.

Case Review 4 – Bradycardia
Introduction:
- A careful and systematic approach must occur to determine whether
serious S & S linked to bradycardia are present
- Bradycardia can take many forms
- Sinus bradycardia
- 1st, 2nd degree and complete heart blocks
- However the important concept to remember is that regardless of
the rhythm the rate is too slow and if the patient is symptomatic it
must be treated.

Absolute and Relative Bradycardia:
- Absolute bradycardia exists when the ventricular rate is less than 60
beats per minute, such occurs in sinus bradycardia

- Relative bradycardia exists when the patient’s heart rate is faster
than one would expect for his/her condition yet the patient is
unstable.

- E.G. A patient who has a heart rate of 65bpm, but a BP of
80/50mmHg may be experiencing “relative” bradycardia because the
pulse relative to BP is too slow

Treatment of Bradycardia:

- Treatment depends on the presence or absence of serious S & S.

- The asymptomatic patient may require little more than close
monitoring,

- However the unstable patient requires interventions aimed at
increasing the heart rate and improving perfusion.

Summary:
- A patient who is asymptomatic requires no more than observation

- However the patient presenting with serious S & S of inadequate
perfusion linked to bradycardia need immediate interventions

- Aimed at increasing the heart rate and preventing cardio-vascular
collapse

- Remember even though th4 patient may have a heart rate of 60-
70bpm, if the blood pressure is poor, the cardiac rate is bradycardic
and needs intervention rapidly

- “Absolute” or “relative” bradycardia needs rapid intervention to
ensure adequate oxygenation and perfusion

Case Review 5 – Narrow Complex
Tachycardia
Introduction:
- The term “Narrow Complex Tachycardia” refers to a rhythm in which
the QRS complex is less than 0.12 seconds or 3 small boxes on the
ECG,
- The ventricular rate is equal or > 100bpm
- SVT indicates that the origin of the cardiac rhythm is above (supra)
the ventricles
- SVT manifests as many other rhythms, atrial tachycardia, atrial
fibrillation, or flutter with rapid ventricular rate (RVR) and Junctional
tachycardia

Tachycardia
Treatment:
- Careful and systematic assessment must be performed so that the
most appropriate treatment can be provided to the patient.

- If the patient is not experiencing serious S & S linked to tachycardia,

- Initial treatment involves interventions aimed at decreasing the
ventricular rate and identifying the underlying cardiac rhythm

- If serious S & S are present synchronised cardioversion must be
performed without delay.

Tachycardia
Summary:
- Patient’s with narrow complex tachycardia requires careful and
systematic assessment
- All patient’s require:
- Supplemental oxygen
- IVT
- If the patient is stable, initial treatment is aimed at decreasing the
heart rate with a combination of vagal manoeuvres and
pharmacologic interventions
- Unstable patient’s require immediate synchronised cardioversion,
which in the conscious patient should be preceded with a sedative
agent

Case Review 6 – Pulseless Electrical Activity
(PEA)
Introduction:
- Patient's with Pulseless Electrical Activity (PEA) , is characterised by
a rhythm on the cardiac monitor when the patient does not have a
cardiac output
- Any rhythm can be seen with PEA
- Only exception is V-Fib and Pulseless V-Tach, both of which were
previously mentioned as requiring immediate defibrillation

(PEA)
Treatment:
- In addition to managing cardiac arrest, management focus is on
identifying the underlying cause

- Common causes of cardiac arrest, their clinical signs, their respective
treatments are in Table 3-14

- As a general rule, any rhythm that is slow indicates Hypoxia

- Any rhythm fast indicate Hypolvolaemia

(PEA)
Summary:
- PEA is a phenomenon that could be overlooked if you do not perform
a careful assessment
- Treatment of PEA involves treating cardiac arrest with:
- CPR
- Airway management
- IV Therapy
- And medications
- Ultimate goal is to rapidly identify and treat underlying cause(s)

Case Review 7 – Respiratory Arrest
Introduction:
- You must perform a rapid assessment and management regime in
patients with respiratory arrest

- Including patients with respiratory arrest as a result of a foreign
body airway obstruction (FBAO)

- Immediate positive pressure ventilations must be provided, while
maintaining airway patency

- Failure to recognise and immediately treat leads to cardiopulmonary
arrest and death within minutes

Assessment:
- Ensure airway is open and patent, clear of secretions, or obstructions

- In the non-injured patient, head tilt, chin lift manoeuvre or in the
patient with suspected spinal injury, the jaw thrust manoeuvre

- Critical the patient’s airway remains clear at all times

- Vomitus and other secretions in the airway require immediate
oropharyngeal suctioning

- Assess for spontaneous breathing, evident by rise and fall of the
chest and sounds of air exiting the chest, via nose and mouth

Management:
- Maintain patent airway, with a combination of manual positioning of
head and insertion of basic airway adjunct, OPA or NPA

- Positive pressure ventilations are then provided with a bag valve
mask (BVM) or a pocket mask at 10 -12 breaths per minute

- In order to deliver high concentrations of oxygen, you must ensure
supplemental oxygen is attached

Foreign Body Airway Obstruction (FBAO):
- May be food, can obstruct airway and prevent patient from moving
air
- Recognised in initial attempts to ventilate, you meet resistance
and/or do not see the chest rise and fall
- This needs to be rectified immediately
- Reposition patients head
- Attempt to re-ventilate, If both breaths do not produce visible chest
rise and fall,
- Perform chest compressions in an attempt to clear obstruction
- If compressions fail to dislodge airway obstruction, visualise vocal
chords with a laryngoscope (direct laryngoscopy) and remove the
obstruction with Magill Forceps

Endotracheal Intubation:
- In an adult patient Endotracheal intubation it is seen to be the “gold
standard” for airway management
- Patients in respiratory or cardiac arrest usually require prolonged
ventilatory support and are at extremely high risk for regurgitation
and aspiration of stomach contents
- The airway should be protected with an endotracheal tube

Alternate airway management:
- Alternate airway management tools include:
- LMA – Laryngeal mask Airway
- Oesophageal Combitube

Summary:
- Ensure airway is open and clear of obstructions

- Confirm absence of breathing, then ventilate with BVM for 2 breaths

- If initial ventilations unsuccessful, airway obstruction likely

- Clear obstruction, manually or by laryngoscopy

- Once airway is patent, continue positive pressure ventilation 10 – 12
breath per minute

- To secure airway, endotracheal intubation should be performed

Case Review 8 – Stroke
Introduction:
- An ischaemic stroke is the result of a blocked cerebral artery

- Common causes include formation of local thrombus or a thrombus
that breaks free (embolus) and travels to brain from another part of
the body

- Less common causes cerebral arterial vasospasm, and generalised
hypoperfusion (shock)

- All areas distal of the blocked artery are deprived of oxygen resulting
in varying degree’s of neurological impairment, ranging from:
- Limited mobility
- To total debilitation

Stroke Survival and Recovery:
- The goal is to begin therapy no longer than 60 minutes after the
arrival at the hospital door and within 3 hours of the initial onset
- This requires both pre-hospital and hospital providers to avoid delays
- Pivotal points represent survival and recovery

Assessment:
- After appropriate management of ABC’s a rapid assessment of
patient and a brief targeted history helps identify patient’s potential
for stroke enabling prompt treatment
- Warning signs of acute ischaemic stroke:
- Confusion
- Slurred speech
- Unilateral facial droop
- Unilateral weakness or paralysis
- Particularly important to determine when symptoms began
- If patient meets inclusion criteria fibrinolytic therapy can begin
- This must be accomplished within 3 hours of onset of symptoms

Cincinnati Pre-Hospital Stroke Scale:
- Allows identification of possible stroke
- Three tests, any abnormality in any one – STROKE suspected

Treatment:
- Mainly supportive and focuses on protecting the airway and
delivering supplemental oxygen
- Monitoring ECG and providing IV therapy
- Promptly transporting patient to facility that specialises in stroke care
where fibrinolytic therapy can be initiated

Fibrinolytic Therapy for Acute Ischaemic Stroke:
- If within 3 hours of onset, and meets inclusion criteria
- Fit the following criteria, therapy can commence

Summary:
- Can be a catastrophic event that can leave the patient with
permanent disabilities ranging from mild neurologic deficits to
complete incapacitation

- All patients require supplemental oxygen, IV therapy, cardiac
monitoring

- After assessment act quickly to identify as a candidate for therapy
and transfer for this critical intervention

Case Review 9 – Ventricular Fibrillation
Introduction:
- It is important to reiterate that for every minute in V-Fib and
Pulseless V-Tach persists the survivability is reduced by 10%
- The single most important treatment is immediate defibrillation,
monophasic or biphasic


Treatment of V-Fib or Pulseless V-Tach:

- The clinician must be prepared to change the treatment on the basis
of the patient’s clinical response to therapy.

- Remember to circulate all drugs with effective CPR for 2 minutes
followed by defibrillation in V-Fib or pulseless V-Tach persists

- Following defibrillation, immediately resume CPR and reassess in 2
minutes

Summary:
- V-Fib is most common initial dysrhythmia in cardiac arrest and if not
promptly treated will deteriorate to asystole
- Successful management requires rapid assessment to confirm
cardiac arrest
- If witnessed begin CPR ASAP
- If not witnessed perform CPR for 2 minutes and then apply cardiac
monitor and defibrillate
- Intubation, IVT and pharmacological interventions are mandatory
- Patient should be defibrillated with once off 360J or biphasic
equivalent then CPR for 2 minutes, reassess and defibrillate as
required

Case Review 10 – Wide Complex Tachycardia’s
Introduction:
- A wide complex tachycardia refers to a rhythm in which QRS
complexes are greater than 0.12 seconds in width and ventricular
rate is > 100bpm
- Approximately 90% of wide complex tachycardia’s are ventricular
tachycardia, indicating rhythm originated from an ectopic pacemaker
in the ventricles

Introduction:


Treatment of Wide Complex Tachycardia’s:
- Careful and systematic assessment

- If patient not experiencing serious S & S, pharmacologic
intervention, aimed at decreasing ventricular irritability, reducing
tachycardia

- If serious symptoms linked to tachycardia, synchronised
cardioversion needed without delay

- High risk of deterioration to V-Fib, be prepared to defibrillate if
patient becomes pulseless


Antiarrhythmic Maintenance Infusions:
- If terminated pharmacologically begin a maintenance infusion of
anti-arrhythmic agent that aided in the conversion

- If synchronised cardioversion was used with no pharmacological
agent, give anti-arrhythmic bolus and commence maintenance
infusion

- Important to maintain therapeutic blood levels of anti-arrhythmic
agent because this will prevent the recurrence of the wide complex
tachycardia


Summary:
- If a patient presents with a wide complex tachycardia you must
assume it is ventricular tachycardia until proven otherwise
- Continuous monitoring of the patient
- V-Tach can rapidly deteriorate to V-Fib
- Must have:
- Supplemental oxygen
- IVT
- Treatment is based on being unstable or stable in origin, therefore
systematic and careful assessment needs to occur, rapidly to
identify S & S associated with wide complex tachycardia

QUESTIONS?
That now concludes the theory component of the
“ADVANCED CARDIAC LIFE SUPPORT”
Course.

Thank you for your participation on behalf of
the…….

Australasian Emergency Response
Specialists Pty Ltd

TASMANIA & PNG

“FAILURE TO PREPARE IS TO
PREPARE TO FAIL”

Presentation e acls aremt

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