179: EKG SIGNS OF DISORDERED IMPULSE FORMATION OR CONDUCTION

Disorders of Impulse Formation

  • Disorders in SA node
  1. Sinus bradycardia

-Slow heart rate

-Features;

  1. Rate less than 60bpm (may be due to reduced automaticity of the sinus node or blocked conduction)
  2. P waves upright in lead II (source of impulse is SA node)
  3. One P wave for every QRS (no AV block)

-Causes;

  1. Athletics hearts
  2. Drug effects (e.g. beta blockers)
  3. Electrolyte imbalances
  4. Sleep
  5. Sick sinus syndrome
  1. Sinus tachycardia

-Fast heart rate

-Features;

  1. Rate more than 100bpm(may be due to increased automaticity of the SA node, or delayed repolarization, or re-entrant circuit)
  2. P waves upright in lead II (source of impulse is SA node)
  3. One P wave for every QRS (no AV block)

-Causes;

  1. Anaemia
  2. Drug effects (e.g. atropine)
  3. Exercise and stress
  4. Heart failure
  5. Fluid loss
  1. Sick sinus syndrome (SSS)

-Is caused by impaired sinus node activity leading to abnormalities in both impulse formation and conduction

-Features;

  1. Marked sinus bradycardia(may occur at rates in region of 30bpm)
  2. Sinoatrial block(is the intermittent failure of the sinus node to activate the atria resulting in a pause on the ECG)
  3. Sinus arrest (is the failure of the sinus node to activate the atria resulting in a pause on the ECG which bears no relationship to the predominant cycle length)
  4. Brady-tachy syndrome(is so called because the tachycardias often alternate with the bradycardia produced by sinus node dysfunction)
  5. Escape beats/rhythms (often seen following a prolonged pause and are a part of the heart’s “safety net” of subsidiary pacemakers)
  • Disorders not in SA node (heterotopic)
  • Active heterotopic impulse
  1. Extrasystoles
  • Also known as premature contraction, premature beat, or ectopic beat
  • Most premature contraction result from ectopic foci in the heart, which emits abnormal impulses at odd times during the cardiac rhythm. Possible causes of ectopic foci are;

a)Local areas of ischemia

b)Small calcified plaques at different points in the heart, which press against the adjacent cardiac muscle so that some of the fibres are irritated

c)Toxic irritation of the AV node, Purkinje system, or myocardium caused by drugs, nicotine, or caffeine

  • Atrial ectopics

a)When the atria are depolarised at any point other than at the sinus node an ectopic beat is produced demonstrating a P wave which looks different to the sinus P wave

b)Atrial ectopics are often of no clinical significance and occur in structurally normal hearts in small numbers

c)Causes;

  1. Atrial enlargement
  2. Digitalis toxicity
  3. Ischemic heart disease
  4. Hyperthyroidism

d) Features;

  1. P wave is abnormal in shape and occurs early (because the signal is not from SA node)
  2. Normal QRS conduction
  3. Compensatory pause
  • Ventricular ectopics

a)Arise from an irritable focus within the ventricular myocardium and are unmistakably broad and bizarre-looking(because the ventricular impulse is initiated at a point away from the specialised conduction tissue and hence the spread of depolarisation is slower)

b)Causes;

  1. Myocardial infarction
  2. Coronary artery disease
  3. Drug effects (e.g. digoxin)
  4. Electrolyte disturbances
  5. Caffeine and other stimulants

c)Features;

  1. Early ventricular beat with no associated P wave
  2. Broad and bizarre QRS
  3. Compensatory pause
  • AV nodal premature contraction

a)P wave is missing

b)Instead, the P wave is superimposed onto the QRS complex (because the cardiac impulse travelled backward into the atria at the same time that it travelled forward into the ventricles)

c)This P wave slightly distorts the QRS-T complex

  1. Atrial tachycardia
  • Is formed by a rapid succession of atrial ectopics
  • Causes are the same as for atrial ectopics
  • Features;

a)First beat occurs early

b)Abnormally shaped P waves(which may be upright in lead II)

c)Rate greater than 100bpm(but usually greater than 120bpm)

d)Compensatory pause

  1. Ventricular tachycardia
  • By definition ventricular tachycardia consists of five or more unifocal ventricular ectopics in a row at a rate in excess of 120-140bpm(also called monomorphic ventricular tachycardia)
  • Causes;

a)Acute causes (e.g. acute myocardial infarction, cardiac catheterisation, valvular heart disease and etc)

b)Predisposing conditions (e.g. long QT syndrome, cardiac surgery, arrhythmogenic right ventricular dysplasia and etc)

  • Features;

a)Broad complex QRS

b)QRS is regular

c)Rate greater than 120bpm

  • Polymorphic ventricular tachycardia is the result of rapidly discharging multifocal ventricular ectopics. Most often seen during acute myocardial infarction or ischemia and occurs in the presence of a normal QT interval
  1. Atrial flutter
  • Results from one of two mechanisms;

a)An atrial ectopic focus similar to atrial tachycardia but with a much faster atrial (P wave) rate

b)A self-perpetuating circular path of atrial depolarisation which typically forms a continuous circuit between the inferior and superior vena cavae within the right atrium

  • Causes are the same as for atrial fibrillation
  • Features;

a)Sawtooth appearance of baseline

b)Atrial rate 250-350bpm(but typically 300bpm)

c)Presence of AV block

  1. Atrial fibrillation
  • The basis is multiple ectopic foci within the atria firing off at rates of up to 600times a minute
  • Causes;

a)Acute causes and precipitating conditions (acute myocardial infarction, alcohol intake, electrocution, hyperthyroidism and etc)

b)Cardiovascular disease associated with a high incidence of atrial fibrillation (cardiac tumours, cardiomyopathy, congestive heart failure, cor pulmonale and etc)

  • Features;

a)Ripple-like oscillations of the baseline (no discernible Pwaves)

b)QRS rate irregularly irregular

  1. Ventricular fibrillation
  • Causes;

a)Acute myocardial infarction

b)Cardiomyopathy

c)Drug toxicity

d)Long QT syndrome

e)Ischemic heart disease

  • Features;

a)Irregular, chaotic oscillations of the baseline

Disorders of Conduction

  • AV Block

-Conduction from the atria to the ventricles via the AV node may be either delayed (as in first degree AV block) or blocked

-Causes;

  1. Acute myocardial infarction
  2. Congenital heart disease
  3. Fibrosis and sclerosis of the conduction system
  4. Hyperkalemia
  5. Increased vagal tone
  6. Ischemic heart disease

-Types of block;

  1. First degree AV block (slow conduction)

a)Features;

PR interval >0.20 secs (and constant) as the impulse conducted slower than normal through the AV node

One P wave for every QRS

  1. Second degree AV block

a)Three types;

Mobitz type I

Mobitz type II

2:1 AV block

-Mobitz type I; often occurs during sleep or during periods of high vagal activity.

There is a cyclic prolongation of the PR interval starting with a normal PR interval which progressively lengthens until one P wave is not followed by a QRS complex and a pause ensues. The next beat demonstrates a normal PR interval and the cycle begins again

-Mobitz type II; characterised by occasional non-conducted P waves. The PR interval constant for conducted beats

-2:1 AV block; characterised by a fixed ratio of conducted to non-conducted P waves, where two P waves are seen for every one QRS complex. The PR interval constant for conducted beats and there is also constant P-P interval

  1. Third degree (Complete Heart Block (CHB))

-No conduction from the atria to the ventricles and the two therefore work entirely independently of each other

-The QRS complex may be either broad or narrow depending on whereabouts the escape rhythm is being generated. Impulse generated high up the conduction system (around the area of the His bundle or AV junction) will produce a narrow QRS with a faster escape heart rate and generally better tolerated by patients. Those generated further down (from the ventricular myocardium and Purkinje system) will more likely produce a broader complex with slower resultant heart rates

-The features are; no relationship between atrial and ventricular activity on the ECG, and PR interval appears variable

  • Bundle Branch Block (BBB)

-When a bundle branch or fascicle becomes injured (due to underlying heart disease, myocardial infarction, or cardiac surgery), it may cease to conduct electrical impulses appropriately. This results in altered pathways for ventricular depolarization. Since the electrical impulse can no longer use the preferred pathway across the bundle branch, it may move instead through muscle fibers in a way that both slows the electrical movement and changes the direction of the impulses. As a result, there is a loss of ventricular synchrony, ventricular depolarization is prolonged, and there may be a corresponding drop in cardiac output.

-Features of Right BBB;

  1. The heart rhythm must be supraventricular origin
  2. The QRS duration must be = or >120ms
  3. There should be a terminal R wave in lead V1 (e.g., R, rR', rsR', rSR' or qR)
  4. There should be a slurred S wave in leads I and V6

-Features of Left BBB;

  1. The heart rhythm must be supraventricular origin
  2. The QRS duration must be = or > 120ms
  3. There should be a QS or rS complex in lead V1
  4. There should be a monophasic R wave in leads I and V6
  • Increased conduction
  1. Wolff-Parkinson-White Syndrome (WPWS)

-Is a syndrome of pre-excitation of the ventricles of the heart due to an accessory pathway known as the bundle of Kent. This accessory pathway is an abnormal electrical communication from the atria to the ventricles.

-Both AV re-entry and AV nodal re-entry tachycardias require an additional conduction pathway. The mechanisms; they form a self-perpetuating circle of depolarisation either round and around the AV node or through the AV node and back to the atria via the additional pathway.

-Individuals with WPWS have an accessory pathway that connects the atria and the ventricles, in addition to the AV node. This accessory pathway is known as the bundle of Kent. This accessory pathway does not share the rate-slowing properties of the AV node, and may conduct electrical activity at a significantly higher rate than the AV node.

-Features on the EKG;

  1. It is manifested as a delta wave, which is a slurred upstroke in the QRS complex
  2. Ashort PR interval (The short PR interval and slurring of the QRS complex is actually the impulse making it through to the ventricles prematurely (across the accessory pathway) without the usual delay experienced in the AV node)
  3. Rate 130-250bpm

References:

  1. Wikipedia:
  1. ECG Complete (by Steven Bowbrick, Alex N. Borg)

PLAGIARISM SOURCES: 50%