ARRHYTHMIAS for BSc Students HU.ppt

ARRHYTHMIAS
Critical Care I
BY AME M. (BSc, MSc)

By Ame M. (BSc, EMCCN)
 Know definition of arrhythmias
 Recognize key features of arrhythmias
 Identify different types of arrhythmias
 Recognize different types of arrhythmias on ECG
 Recognize key physical findings suggestive of arrhythmias
 Approach to Dx/Rx of arrhythmias.
Objectives

• The following conditions can interfere with normal heart
functioning:
• Disturbances of rate or rhythm
• Disorders of conductivity
• Enlarged heart chambers
• Presence of myocardial infarction
• Fluid and electrolyte imbalances.
• Trauma
• Endocrine disorders
• Other systemic disorders

ARRHYTHMIAS
• Dictionary definition of arrhythmia
– is an abnormal rate of muscle contractions in the heart.
• is an abnormal cardiac rhythm giving
– an abnormal heart beat which can be:
• fast or slow,
• regular or irregular
• is any rhythm that is not normal sinus rhythm with normal AV
conduction.

ARRHYTHMIAS …
CAUSES
• Idiopathic
• Ischemic heart disease
• Structural heart disease
• e.g. VHD, cardiomyopathy, myocarditis, RHD
• Electrolyte disturbance
– e.g. Hyper/hypo-kalemia
• Acid base disturbance
• Hypoxia
• Hyperthermia
• Others
– e.g. Thyrotoxicosis, raised ICP
• Drug toxicity
– Prescription drugs
• e.g. anti-arrhythmics, digoxin (especially in the presence of hypokalemia)
– Recreational
• e.g. Cocaine
– Intentional
• e.g. TCA overdose, Organophosphates

ARRHYTHMIAS …
• Arrhythmias can arise from problems in the:
1. Sinus Node
2. Atrial Cells
3. AV junction
4. Ventricular Cells

ARRHYTHMIAS …
1. Sinus Node
• Firing to slow = Sinus bradycardia
• Firing to fast = Sinus tachycardia
2. Atrial Cells
• Fire occasionally from a focus = Premature Atrial Contraction (PAC’s)
• Fire continuously due to a looping reentrant circuit = AF
• Fire continuously from multiple foci or fire continuously due to
multiple micro re-entrants = A Fib.

ARRHYTHMIAS …
3. AV junction
• Fire continuously due to a looping reentrant circuit = SVT
• Block impulses coming from the SA node = AV Junctional Block
4. Ventricular Cells
• Fire occasionally from 1 or more foci = Premature Ventricular
Contractions (PVC’s)
• Fire continuously from multiple foci = V Fib.
• Fire continuously due to a looping reentrant circuit = V Tach

Arrhythmias …
Classifications
• Origin: Defines acute and chronic treatment
– Supraventricular
– Ventricular
• Rates: Defines necessity for treatment
– Bradyarrhythmias
– Tachyarrhythmias
• Regularity: Helps classify arrhythmia
– Regularly, Irregular
– Irregularly, Irregular

Four questions to be raised
1. Is it sinus or not, If sinus, there is a p wave and every QRS is preceded by a p
wave.
2. Is this a Fast, slow or a normal rhythm.
3. Is this regular or irregular.
4. Is it narrow or Wide- reference QRS duration 0.12 sec.

Tachyarrhythmia
Wide complex
Narrow complex
Regular
Irregular
Regular
Irregular
Sinus tachy
SVT
Junctional tachy
Atrial flutter
Atrial fib
Multifocal atrial tachy
(MAT)
AF with variable block
V Tach:
(Monomorphic)
Polymorphic VT
V fib.
Torsade’s de pointe
Arrhythmia
Bradyarrhythmia

Tacyarrythimia
• Narrow Complex Tachycardia
– HR >100bpm
– Narrow QRS <0.12 sec
• Wide Complex Tachycardia
– HR >100bpm
– Wide QRS >0.12 sec

Narrow Complex regular Tachycardia
1. Sinus tachycardia
2. SVT
3. Junctional tachycardia
4. Atrial flutter (AF)

1. Sinus Tachycardia
• The impulse generating the heart beats
are normal, but they are occurring at a
faster pace than normal.
• Rhythm: Regular
• Rate: >100 bpm
• QRS Duration: Normal and Each QRS is
preceded by P wave
• P Wave: Visible before each QRS complex
• P-R Interval: Normal

1. Sinus Tachy …
• Causes:
– Due to sympathetic excess
– E.g.: Fever, anxiety, stress, illness, etc.
• Treatment:
– Treat underlying condition
– Treat only if symptomatic.

2. Supraventricular Tachycardia (SVT)
• is narrow complex tachycardia or atrial tachycardia,
• originates in the 'atria' but is not under direct
control of SA node.
• impulses stimulating the heart are not being
generated by the sinus node, but instead are
coming from a collection of tissue around and
involving the AV node.

2. SVT …
• Rhythm: Regular
• P waves or P wave often buried in preceding
T wave, ‘hidden’ or ‘retrograde’
• P-R Interval: - Depends on site of
supraventricular pacemaker.
• Rate: 160-200 bpm
• QRS interval: Normal

2. SVT …
• Signs and symptoms of SVT may include:
– Paroxysmal onset/offset
– A fluttering in your chest
– Rapid heartbeat (palpitations)
– Shortness of breath
– Lightheadedness or dizziness
– Sweating
– A pounding sensation in the neck
– Fainting (syncope) or near fainting
– Chest pain
• Treatment required!

2. SVT ….
Treatment
• Vagal maneuvers
– Carotid sinus massage
– Valsalva (90% success rate).
– Cold water immersion
• Adenosine 6mg rapid IVP
• AV nodal blocking agents
– Digoxin 0.5 mg IV (0.25 mg IV rpt. at 30 & 60 min)
– Diltiazem 0.25 mg/kg IV over 2 min; may rpt
– Metoprolol 5 mg IV Q5 min x 3 as needed
• Synchronized Cardio Version

3. Atrial Flutter(AF)

3. AF …
• occurs when a rapid impulse originates in the
atrial tissue.
• As with SVT the abnormal tissue generating the
rapid HR is also in the atria, however, the AV
node is not involved in this case.
• Has sawtooth pattern
• Flutter waves (atrial beats)
• Best seen in inferior leads II, III, aVF and in V1-V2

3. AF …
• Rhythm: Regular
• P waves: replaced with multiple flutter
waves (F), usually at a ratio of 2:1 (2F - 1QRS)
• Atrial Rate: 250-350 bpm
• Often 2:1 block with HR ~ 150 bpm
(ventricular rate) sometimes 3:1 block
• Usually signifies cardiac disease
• Requires Tx– rate or rhythm control

3. AF…
• Treatment:
• Focus on:
– Rate control
– Rhythm Control
• Based on the patients status whether:
– Stable: Rate control
– Unstable: Rhythm Control

3. AF…
Treatment
Stable:
• Rate Control
– Diltiazem IV
– Metoprolol IV
– Digoxin IV
• Slow AV conduction
• -blockers or CCB
• Digitalis (2nd line agent)
Unstable:
• Rhythm Control:
• Anticoagulation therapy before converting rhythm if
>48 hours
• Synchronized Cardioversion (@100 J) or
amiodarone to convert rhythm if less than 48 hours
• Also Class 1A agents (procainamide or quinidine
may be used).

Narrow Complex irregular Tachycardia
A. Atrial Fibrillation(A Fib)
B. Multifocal atrial tachycardia (MAT)
C. Atrial flutter with variable block

A. Atrial Fibrillation (A fib.)
• Multiple areas of atrial myocardium discharging
chaotically
• Loss of ‘atrial kick’
• Atrial rate >400 bpm
• Ventricular rate highly variable
• Ventricular rate irregularly irregular
• Fibrillatory waves best seen V1, 2, 3, aVF

A. A Fib. …
• Rhythm - Irregularly irregular
• Rate – Atrial rate ranges from 350-600 per min.
• The ventricular response is irregularly irregular
and may be fast or slow.
• QRS Duration - Usually normal
• P Wave - Not distinguishable as the atria are firing
off all over /No P waves.
• P-R Interval - Not measurable

A fib. …
• Commonly associated with four
disorders:
– RHD
– HTN
– Ischemic heart disease(MI)
– Thyrotoxicosis (hyperthyroidism)
• Other disorders
– Pulmonary embolism
– Pneumonia
– CHF
– Pericarditis/myocarditis
– Alcohol intoxication (ETOH)
– ASD(Atrial Septal Defect)

A. A fib. …
• Presentation:
– Syncope or dizziness
– Palpitations,
– SOB,
– Weakness
– Pulse rate changes,
– chest pain, or
– signs of heart failure, such as
• increasing dyspnea & peripheral
edema.

A. A fib …
Treatment
Unstable:
– Rhythm Control
– If unstable; or electively to re-
establish NSR if onset definitely
within 48 hrs
– Low energy cardio version (25-
50J)=converts>90%
– Cardio eversion @ 50-100J
Stable:
• Rate control
– if EF >40%:
• CCB
• B-blocker
– if EF <40%:
• Amiodarone
• Diltiazem
• Digoxin

Wide Complex Tachyarrhythmia
• In wide Complex Tachyarrhythmia
– Ventricular Rate >100 bpm.
– QRS duration > 0.12 seconds
• Can be:
– Regular;
• Monomorphic VT
– Irregular
• Polymorphic VT
• VF
• Torsade's de pointe

Wide Complex Tachyarrhythmia
Ventricular Tachycardia(VT)
• occurs when three or more PVCs occur in a row and the ventricular rate is >100
bpm.
• ventricles are essentially in a continuous contraction-relaxation pattern and
• no period of delay exists b/n depolarization (contraction).
• Can be
– Regular
• Monomorphic VT
– Irregular
• Polymorphic VT

Regular Ventricular Tachycardia:
Monomorphic VT
• Rhythm - Regular
• Rate - >120 bpm (usually 100-250)
• P wave: None or Not associated with QRS
• PR interval: None/Not seen/
• QRS: Wide (>0.12 seconds), Prolonged, bizarre appearance
have the same shape and amplitude
• It is important to confirm the presence or absence of pulses
– b/c monomorphic VT may be perfusing or nonperfusing
• monomorphic VT will probably deteriorate into VF or unstable
VT, if sustained & not treated.

Irregular Ventricular Tachycardia:
Polymorphic VT
• Rhythm –Irregular
• Rate - >120 bpm (usually 100-250)
• P wave: None or Not associated with QRS
• PR interval: None/Not seen/
• QRS: vary in shape & amplitude
• QT interval: normal or longer
• QRS: Wide (>0.12 seconds), bizarre appearance
• It is important to confirm the presence or absence of pulses b/c pulses
– b/c polymorphic VT may be perfusing or nonperfusing.
• Consider electrolyte abnormalities as possible etiology.

Monomorphic Vs. Polymorphic
VT

Wide Complex Tachyarrhythmia:
Ventricular Tachycardia
Treatment
• VT Treatment:
–Stable:
• Lidocaine 1mg/kg IV over 1 min
• Amiodarone 150 mg IV over 10 min
• Procainamide 1 gm IV at 50 mg/min
– Unstable:
• Immediate Synchronized Cardioversion @200 J

WIDE COMPLEX TACHY IS VT
UNTIL PROVEN OTHERWISE !!!

Torsade's de Pointe
• means “twisting about the points,”
• is a variant form of VT or a special form of polymorphic VT.
– with a rapid ventricular rate that varies 250 - 350 bpm.
• is is ‘Twisting’ wide complex tachy, irregular
• Occur in short ‘bursts’ 10-15 seconds long.
• The P wave is usually absent.
• Secondary to prolonged QT interval.
• Usually severe heart disease present.

Torsade's de Pointe
• results in an overall outline of the rhythm commonly described as spindle-shaped
• Ch’zed by QRS complexes that gradually change back & forth, with the amplitude
of each successive complex gradually increasing then decreasing.
• The hallmark ch’cs of this rhythm, are QRS complexes that rotate about the
baseline, deflecting downward and upward for several beats.

Torsade's …
Management
• Overdrive pacing at 90-120 bpm.
– shortens the QT interval to prevent recurrence.
• MgSO4 2 g IV over 60 secs then 2 g IV/hr.
• Synchronized cardio version, if sustained and resistant to other Tx.

Ventricular Fibrillation(VF)
• is chaotic asynchronous electrical activity within the ventricular tissue.
• is the absence of organized electrical activity.
• is chaotic in appearance
• is the quivering of entire myocardium
• VF is the commonest initial rhythm leading to cardiac arrest, particularly in
pts with CHD.
• Fibrillating, chaotic, and ineffective ventricular contractions.

VF …
• Always pulseless.
• No effective pumping activity.
• Severe cardiac ischemia with or without MI.
• Can be primary or secondary.
– Sudden onset (Primary VF)
– Gradual deterioration (Secondary VF):
• sepsis, trauma, Digoxin, quinidine, lytes

VF …
• Rhythm: Irregular (disorganized).
• Rate: >300 bpm
• QRS duration: Not recognizable
• P Wave: Not seen
• Treatment: required !
• This patient needs to be defibrillated!! QUICKLY
• Follow ACLS protocol

Approach to Tachycardia:
4 KEY QUESTIONS
1. Is my patient stable or unstable?
2. Is the rhythm narrow or wide?
3. Is the rhythm regular or irregular?
4. Is there a potential to degenerate to a more dangerous rhythm.

Stable vs. Unstable
• Stable patients are ~ asymptomatic
• Unstable patients exhibit signs and symptoms of hypo
perfusion/circulatory compromise;
– Altered mental status
– Ongoing chest pain
– Dyspnea/Tachypnea
– Hypotension
• Rate-related symptoms uncommon at <150 bpm.

Stable vs. Unstable
• STABLE = DRUGS
UNSTABLE = ELECTRICITY

Brady arrhythmias

Mechanism of Conduction Blocks
• Intrinsic AV nodal disease
• Enhanced vagal tone
• Acute MI (inferior, anterior)
• Myocarditis
• Diphtheria
• Electrolyte disturbances
• Drugs (anti-arrhythmic, digoxin)
• RHD, Infective Endocarditis
Athletes have physiologically
increased vagal tone

Causes of bradycardia
• Drugs
– Beta-blockers
– Calcium-channel blockers
– Clonidine
– Digoxin
– Opiates
– Quinine
• Electrolytes
– Hypocalcaemia
– Hyperkalemia
– Hypo/hypermagnesemia
• Ischemic Causes
– Acute inferior MI
– Acute anterior MI -
damages infranodal
conduction system)

Sinus Bradycardia
• Looking at the ECG you'll see that:
– Rhythm: Regular
– Rate: < 60 bpm
– QRS Duration: Normal
– P Wave: Visible before each QRS complex
– P-R Interval: Normal
– Usually benign and often caused by patients on β-blockers

Sinus Bradycardia…
• Heart rate < 60 bpm
• Identify underlying cause
• DDx
– Hypothermia
– Hypothyroidism
– Advanced liver disease
– Severe hypoxia, hypercapnia or acidemia
– Amyloidosis
– Myocarditis
– High vagal tone

Simplified Approach to Bradycardia:
4 Steps
1. Is my patient stable or unstable?
2. Look at the PR interval
3. Treat the patient, not the rhythm!
4. Consider “DIE”
– Drugs
– Ischemia
– Electrolytes

Stable vs. Unstable
• Stable patients are ~ asymptomatic
• Unstable patients exhibit signs and symptoms of hypo-perfusion/circulatory
compromise;
– Altered mental status
– Ongoing chest pain
– Dyspnea/Tachypnea
– Hypotension

Stable vs. Unstable
STABLE = DRUGS
UNSTABLE = ELECTRICITY

Classification of Conduction Blocks
• 1st degree AV block
• 2nd degree AV block
– Mobitz I (Wenckebach)
– Mobitz II (Classical heart block)
• 3rd degree AV block — complete heart block.

Causes of AV block
• Causes of temporary block
– Myocardial infarction (MI), usually
inferior wall MI
– Digoxin (Lanoxin) toxicity
– Acute myocarditis
– Calcium channel blockers
– Beta-adrenergic blockers
– Cardiac surgery
• Causes of permanent block
– Changes associated with aging
– Congenital abnormalities
– MI, usually anteroseptal MI
– Cardiomyopathy
– Cardiac surgery
 AV blocks can be temporary or permanent.

First Degree AV Block
• ECG findings will show that:
– Rhythm – Regular
– Rate – Normal
– QRS Duration – Normal
– P Wave - Ratio 1:1
– P Wave rate – Normal
– P-R Interval - Prolonged (>5 small squares)
> 0.2 seconds
– 1.6 % in younger patients
– 9% in highly trained athletes
– Increases with age

2nd Degree AV Block
• Two types:
– Mobitz Type I (Wenkebach)
• LENGTHENING PR INTERVAL
• Delay usually in AV node (narrow QRS)
• Often transient.
– Mobitz Type II (Classical heart block)
• CONSTANT PR INTERVAL
• Pattern of conducted and skipped beats, commonly 2:1 or 3:1.
• Delay commonly BELOW AV node (wide QRS)
• Often permanent

2nd Degree AV Block Type I
(Wenckebach)
– Rhythm - Regularly irregular
– Rate - Normal or Slow
– QRS Duration - Normal
– P Wave –
• Ratio 1:1 for 2, 3 or 4 cycles then 1:0.
– P Wave rate –
• Normal but faster than QRS rate.
– P-R Interval –
• Progressive lengthening of P-R interval until QRS complex is dropped.

2nd Degree AV Block Type 2
– Rhythm - Regular
– Rate –
• Normal or Slow (d/t atrial & ventricular rate)
– QRS Duration - Prolonged
– P Wave - Ratio 2:1, 3:1
– Every third P wave is not followed by a QRS
complex(dropped beat)
– P Wave rate –
• Normal but faster than QRS rate
– P-R Interval –
• Normal or prolonged but constant

2nd Degree AV Block Type II
Mangement
• Look for reversible causes:
– Electrolytes, Ca++, Mg++ levels
– Digoxin level
– Myocarditis serology
– Cardiac enzymes
• Symptomatic Mobitz I or any Mobitz II – requires monitoring +/- pacing.
• Atropine not likely to be effective if block at or below Bundle of His
(therefore Mobitz 2 or CHB)

Third Degree AV Block
Complete Heart Block (CHB)
• Atria and ventricles do not communicate
• Atrial contractions may be normal
• Heart generates junctional or ventricular
escape beats at 20–60 bpm
• VARIABLE PR interval

3rd Degree/CHB …
• ECG will show that:
– Rhythm - Regular
– Rate - Slow
– P Wave –
• appear at regular intervals as QRS complexes but
have nothing to do with one another (Unrelated)
– P Wave rate – Normal but faster than QRS rate
– P-R Interval – Variation
– QRS Duration –
• Prolonged/wide, implying a ventricular origin
– No atrial impulses pass through AV node & the
ventricles generate their own rhythm

CHB…
Management
• Think about “DIE” and correct reversible causes
– Drugs
– Ischemia
– Electrolytes: hyper K, hyper Mg
– Other causes of CHB include:
• myocarditis,
• Lyme disease,
• acute renal failure (hyperkalemia)
• Transcutaneous pacing
• Pressors as needed
• Early consultation!
• Definitive pacemaker

Asystole
• is absence of ventricular activity and depolarization.
• No electrical activity is present in the myocardium
• is called “the straight or flat line” of rhythms
• Rhythm - Flat
• Rate - 0 bpm
• QRS Duration - None
• P Wave - None
• Carry out CPR !!!

Asystole
• Ventricular standstill, no electrical activity, no cardiac output
• Occurs in cardiac arrest, may follow VF or PEA
• Remember! No defibrillation with Asystole
• Treatment:
– Epinephrine and Atropine,
– consider causes
• pulmonary embolism, acidosis, tension pneumothorax, hypo/hyperkalemia,
hypoxia, cardiac tamponade, hypothermia, drug overdose, MI
• Rate: absent due to absence of ventricular activity.
• Occasional P wave may be identified.
• Patient will not have a pulse.

SUMMARY ARRHYTHMIA MANAGEMENT
• Initial Stabilization
– Position patient
– Airway
– Breathing
– Circulation
– Consider immediate Synchronised
Cardioversion where indicated
– Consider Atropine if bradycardia is
present
– Record GCS and pupil response
– Monitor ECG, SaO2, BP
• Directed History and Examination
– Ask about
• Event
• Symptoms
• Past History
– Interpretation of ECG
• Rate: slow or fast?
• Rhythm regular or irregular?
• QRS complex wide or narrow?

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