Arrhythmia,conduction

defects,ECG myocardial
infarction,hypertrophy
Dr.sanam
 OUTLINES???
• BASIC CONDUCTION SYSTEM
• NORMAL ECG
• WHAT IS ARRYTHMIA?
• TYPES OF ARRYTHMIA
• MI
• HEART HYPERTROPHY
 DEFINATION

Cardiac Arrhythmia is a condition in which

the heart beats with an irregular or
abnormal rhythm.
 ABNORMAL RHYTHM

CAN BE OF TWO EXTREME FORMS

1.Bradycardia - Cardiac beats below 60
beats per minute .
2.Tachycardia – Cardiac beat above 100
beats per minute.
 Arrhythmia Presentation
• Palpitation.
• Dizziness.
• Chest Pain.
• Dyspnea.
• Fainting.
• Sudden cardiac death.
 ETIOLOGY
• Coronary artery • Healing process after
disease. heart surgery.
• Electrolyte imbalances
in your blood (such as • Irregular heart rhythms
sodium or potassium). can also occur in
• Changes in your heart "normal, healthy"
muscle. hearts.
• Injury from a heart • Ischemic Heart Disease
attack.
• Drugs related
• Others
 Arrhythmia Assessment
• ECG
• 24h Holter monitor
• Echocardiogram
• Stress test
• Coronary angiography
• Electrophysiology study
 Mechanism of Arrhthmogensis
1. Disorder of impulse formation.
a) Automaticity.
b) Triggered Activity.
1) Early after depolarization.
2) Delayed after depolarization.
2. Disorder of impulse conduction.
a) Block – Reentry.
b) Reflection.
3. Combined disorder.
 SINUS TACHYCARDIA
• Rate: 101-160/min
• P wave: sinus
• QRS: normal
• Conduction: normal
• Rhythm: regular or slightly irregular
• It may be normal.
• Underlying causes include:
 increased circulating catecholamines
 CHF
 hypoxia
 PE
 increased temperature
 stress
 response to pain
• Treatment : the underlying cause and correction.
 SINUS BRADYCARDIA
• Rate: 40-59 bpm
• P wave: sinus
• QRS: Normal (.06-.12)
• Conduction: P-R normal or slightly prolonged at slower rates
• Rhythm: regular or slightly irregular

• This rhythm is normal variation in athletes, during sleep, or in response to

a vagal maneuver.

• Treatment includes:
 treat the underlying cause,
 atropine,
 isuprnol, or
 artificial pacing if patient is hemodynamically compromised.
 SINUS ARRHYTHIMIA
• Rate: 45-100/bpm
• P wave: sinus
• QRS: normal
• Conduction: normal
• Rhythm: regularly irregular

• The rate usually increases with inspiration and decreases with expiration.
• This rhythm is most commonly seen with respiration due to fluctuations in
vagal tone.

• The non respiratory form is present in diseased hearts and sometimes

confused with sinus arrset (also known as "sinus pause").

• Treatment is not usually required unless symptomatic bradycardia is

present.
PREAMATURE ATRIAL CONTRACTIONS
• Rate: normal or accelerated
• P wave: usually have a different morphology than sinus P waves because
they originate from an ectopic pacemaker
• QRS: normal
• Conduction: normal, however the ectopic beats may have a different P-R
interval.
• Rhythm: PAC's occur early in the cycle and they usually do not have a
complete compensatory pause.

• PAC's occur normally in a non diseased heart.

• They can also result from CHF, ischemia and COPD.
 SINUS PAUSE, ARREST
• Rate: normal
• P wave: those that are present are normal
• QRS: normal
• Conduction: normal
• Rhythm: The basic rhythm is regular. The length of the pause is not a
multiple of the sinus interval.

• Occur in individuals with healthy hearts,increased vagal tone, myocarditis,

MI, and digitalis toxicity.

• The treatment of this depends on the underlying cause.

 If the cause is due to increased vagal tone and the patient is symptomatic,
atropine may be indicated.
 ATRIAL FIBRILLATION
• Rate: atrial rate usually between 400-650/bpm.
• P wave: not present; wavy baseline is seen instead.
• QRS: normal
• Conduction: variable AV conduction; if untreated the ventricular response
is usually rapid.
• Rhythm: irregularly irregular. (This is the hallmark of this dysrhythmia).

• Atrial fibrillation may occur paroxysmally, but it often becomes chronic. It

is usually associated with COPD, CHF or other heart disease.

• Treatment includes:
 Digoxin to slow the AV conduction rate.
 Cardioversion may also be necessary to terminate this rhythm.
 FIRST DEGREE A-V HEART BLOCK
• Rate: variable
• P wave: normal
• QRS: normal
• Conduction: P-R interval is > 0.20 seconds.
• Rhythm: regular

• occurs in both healthy and diseased hearts.

• inferior MI,
• digitalis toxicity
• hyperkalemia
• increased vagal tone
• acute rheumatic fever
• myocarditis.

• Treat the underlying cause and observe.

 SECOND DEGREE A-V BLOCK MOBITZ TYPE I
(WENCKEBACK)
• Rate: variable
• P wave: normal morphology with constant P-P interval
• QRS: normal
• Conduction: the P-R interval is progressively longer until one P wave is
blocked; the cycle begins again following the blocked P wave.
• Rhythm: irregular
• Second degree AV block type I occurs in the AV node above the Bundle of
His.
• It is often transient , acute inferior MI or digitalis toxicity.

• Treatment is not indicated unless symptoms.

 SECOND DEGREE A-V BLOCK MOBITZ TYPE
II
• Rate: variable
• P wave: normal with constant P-P intervals
• QRS: usually widened because this is usually associated with a bundle
branch block.
• Conduction: P-R interval may be normal or prolonged, but it is constant
until one P wave is not conducted to the ventricles.
• Rhythm: usually regular when AV conduction ratios are constant

• This block usually occurs below the Bundle of His and may progress into a
higher degree block.

• Treatment is usually artificial pacing.

 THIRD DEGREE (COMPLETE)
A-V BLOCK
• Rate: atrial rate is usually normal; ventricular rate is usually less than 70/bpm.
The atrial rate is always faster than the ventricular rate.

• P wave: normal with constant P-P intervals, but not "married" to the QRS
complexes.

• QRS: may be normal or widened depending on where the escape pacemaker

is located in the conduction system

• Conduction: atrial and ventricular activities are unrelated due to the

complete blocking of the atrial impulses to the ventricles.

• Rhythm: irregular

• Treatment modalities include:

 external pacing and atropine for acute, symptomatic episodes and
 permanent pacing for chronic complete heart block.
Bundle Branch and Fascicular Blocks

• RBBB:
– ECD: Wide QRS, Abnormal QRS complexes in right precordical leads
(V1- V2) (rSR’). We know this.
– Incomplete RBBB
• RBBB block morphology with a normal QRS width
• Common finding in children and young adult
 LBBB

– ECG: Wide QRS.

– Abnormal morphology: RR’ or large wide R (I, V5,

V6) Anormal repol., QS or RS pattern in right
precordial leads (V1,V2)
LEFT BUNDLE BRUNCH BLOCK (LBBB)
• No Impulse conduction through Bundle Brunch
• Action Potential transferred through Right Ventricle
to Left Ventricle

RESULTS in Wide QRS complex

 VENTRICULAR TACHYCARDIA
• Rate: usually between 100 to 220/bpm, but can be as rapid as 250/bpm
• P wave: obscured and unrelated to the QRS complexes.
• QRS: wide and bizarre morphology
• Rhythm: three or more ventricular beats in a row; may be regular or
irregular.
• Ventricular tachycardia almost always occurs in diseased hearts.
• Patients are often symptomatic.

• Ventricular tachycardia can quickly deteriorate into ventricular fibrillation.

 Electrical countershock is the intervention of choice if the patient is

symptomatic and rapidly deteriorating.
 Some pharmacological interventions needed.
 TORSADE DE POINTES
• Rate: usually between 150 to 220/bpm,
• P wave: obscured if present
• QRS: wide and bizarre morphology
• Rhythm: Irregular
• Paroxysmal –starting and stopping suddenly
• Hallmark of this rhythm is the upward and downward deflection of the QRS
complexes around the baseline. The term Torsade de Pointes means
"twisting about the points."
• Consider it V-tach if it doesn’t respond to antiarrythmic therapy or
treatments

• Treatment:
 Synchronized cardioversion is indicated when the patient is unstable.
 IV magnesium
 IV Potassium to correct an electrolyte imbalance
 Overdrive pacing
 VENTRICULAR FIBRILLATION
• Rate: unattainable
• P wave: may be present, but obscured by ventricular waves
• QRS: not apparent
• Conduction: chaotic electrical activity
• Rhythm: chaotic electrical activity

• This dysrhythmia results in the absence of cardiac output.

• Almost always occurs with serious heart disease, especially acute MI.
•
• Treatment for ventricular fibrillation includes:
immediate defibrillation.
Identification and treatment of the underlying cause is also needed.
•
IDIOVENTRICULAR RHYTHM
Rate: 20 to 40 beats per minute
• P wave: Absent
• QRS: Widened
• Conduction: Failure of primary pacemaker
• Rhythm: Regular
• Absent P wave
Widened QRS > 0.12 sec.
Also called " dying heart" rhythm
Pacemaker will most likely be needed to re-establish a normal heart rate.
• Causes:
– Myocardial Infarction
– Pacemaker Failure
– Metabolic imbalance
– Myoardial Ischemia
• Treatment goals include measures to improve cardiac output and establish a
normal rhythm and rate.
• Options include:
– Atropine
– Pacing
• Caution: Supressing the ventricular rhythm is contraindicated because that rhythm
protects the heart from complete standstill.
VENTRICULAR STANDSTILL (ASYSTOLE)
• Rate: none
• P wave: may be seen, but there is no ventricular response
• QRS: none
• Conduction: none
• Rhythm: none
•
• Asystole of longer duration in the presence of acute MI and CAD is
frequently fatal.
• Interventions include:
 CPR,
 artificial pacing, and
 atropine.
 Bradydysrhythmia
• Sinus Bradycardia
– <60bpm, high vagal tone, medications,
hyothyroidism
– Signs and symptoms – generally asymptomatic, or
signs of hypoperfusion
– Rx: Direct towards degree of patient symptoms,
atropine, pacing, vasopressors.
 Bradydsyrhythmia
Simplified!
• Stable or Unstable?

• Wide or Narrow?

• Slow or VERY slow

 Bradydysrhythmia
• WHY IS THIS PATIENT BRADYCARDIC
–Ischemia
–Drugs
–Electrolytes
Myocardial infarction
 Definition
• Otherwise know as heart attack
• An MI occurs when there is a decreased blood
supply to the heart which leads to myocardial
cell damage and ischemia.
• Contractile function stops in that areas of the
heart.
• Ischemia usually occurs due to blockage of the
coronary vessels.
Ischemia – Outer most area, source of
arrhythmias, viable if no further infarction.
Injury – Viable tissue found between ischemic
and infarcted areas.
Infarction/necrosis – Center area, dead not viable
tissue that turn into scar.
 MI Classifications
• MI’s can be subcategorized by anatomy and
clinical diagnostic information.
Anatomic
• Transmural and Subendocardial
Diagnostic
• ST elevations (STEMI) and non ST
elevations (NSTEMI).
 Risk Factors
Non Modifiable Modifiable
• Age • Smoking
• Gender • Diabetes Control
• Family history • Hypertension
• Hyperlipidemia
• Obesity
• Physical Inactivity
 Within the first 10 minutes upon
arrival to the hospital:
• Check vital signs and evaluate oxygen saturation
• Establish IV access
• Obtain and review 12-lead ECG
• Take a brief focused history and perform a physical
exam
• Obtain blood samples to evaluate initial cardiac
markers, electrolytes and coagulation
Normal Sinus Rhythm
STEMI vs. NSTEMI
LEFT VENTRICULAR HYPERTROPHY

An increase in the mass of the left ventricle, which can be secondary to an

increase in wall thickness, an increase in cavity size, or both
• Causes:
• Hypertension
• Hypertrophic cardiomyopathy
• Aortic stenosis
• Athelitic training
 PATHOPHYSIOLOGY OF LVH
 High BP   LV wall stress
 Wall stress  1/ wall thickness
 LV wall thickening   wall stress
 Myocyte hypertrophy and  collagen matrix

Factors angiotensin II, norepinephrine, epinephrine, increased peripheral

and cardiac sympathetic drive and endothelin, promote both
hypertension and LVH.

LVH may be an inherited trait that predisposes to the development of

hypertension
 ECG
– To diagnose LVH you can use the following criteria*:
• R in V5 (or V6) + S in V1 (or V2) > 35 mm, or
• avL R > 13 mm
 RIGHT VENTRICULAR
HYPERTROPHY
enlargement of heart’s right ventricle
• RVH, is one of rare diseases of heart. Unlike LV, which tends to
overwork itself when it detects abnormalities, the RV dilutes itself. This is
the reason why LVH is way more common than RVH .CAUSES:
• Pulmonary hypertension
• Pulmonary valve stenosis
• Ventricular septal defect (VSD)
• High altitude
• Cardiac fibrosis
• Chronic obstructive pulmonary disease (COPD)
RIGHT VENTRICULAR HYPERTROPHY
ECG

To diagnose RVH you can use the following criteria:

• Right axis deviation, and
• V1 R wave > 7mm tall