Cardiac Arrhythmias and ECG

Stimulation of the pacemaker of the heart causes tachycardia. Tachycardia >100 bpm

• Increased body temperature
• Sympathetic stimulation of the heart - 150 to 180 bpm
• Toxic conditions - digitalis toxicity

Vagal stimulation of the heart causes a decrease in heart rate.  Bradycardia <60 bpm. Parasympathetic system - acetylcholine.
Carotid sinus syndrome - an atherosclerotic process causes excessive sensitivity of the baroreceptors in the atrial wall. External pressure to the neck causes the atherosclerotic plaque in the carotid sinus to stimulate the baroreceptors, which then stimulate the vagus nerve and cause bradycardia.

Abnormal cardiac Rhythms that result from impulse conduction block. 

1. Rarely - Sinoatrial block - P waves are obsured by the QRS complex, and the ventricles pick up the rhythm originating from the atrioventricular node AV node
2. AV block inhibits or completely blocks impulses originating in the SA node. 
1. Ischemia of the AV node or AV bundle
2. Compression of the AV bundle - by scar tissue or calcified portions of the heart
3. Inflammation of the AV node or bundle, secondary to myocarditis, diphtheria, or rheumatic fever
4. Strong vagal stimuation of the heart
3. Types of AV block:
1. First degree heart block - Increase PR interval from 0.16 s to 0.20 s, and the heart beats at a normal rate.
2. Second degree heart block - PR interval increases to 0.25 to 0.45 s, only portion of the pulses pass through to the Ventricle -  "drop beats" of ventricle
3. Third degree heart block - This is a complete AV junction block, and a complete dissociation of the P waves to the QRS complex. The ventricles "escape" from the influence of the Sinoatrial pacemaker. A condition in which AV block comes and goes is called the Stokes-Adam's Syndrome

Premature Contractions

Most premature contractions (extrasystoles) result from ectopic foci that generate abnormal cardiac impulses. Causes:

1. Local Ischemia
2. Irritation of cardiac muscle as a result from pressure from a calcified cardiac plaque
3. Toxic irritation of the AV node, Purkinje system or myocardium by drugs, nicotine or caffeine.

Ectopic foci can cause premature contractions that originate in the atria, AV junction, or ventricle.

1. Premature atrial contraction - PR interval decreases - Premature atrial contraction causes premature ventricular beats and PULSE DEFICIT if ventricles do not have sufficient time to fill.
2. AV nodal or AV bundle premature contractions - The P wave is missing - P wave is superimposed on the QRS complex
3. Premature ventricular contractions (PVC) - ectopic foci orriginates in the ventricle, and the QRS complex is often prolonged because the impulse must pass through the muscle, which conducts at a much lower rate than the Purkinje system. The QRS voltage increases because one side of the heart depolarises before the other, causing a large electrical potential between the depolarised and polarised muscle. 

Paroxysmal Tachycardia

Cause of these foci is re-enterent pathways that set up local repeated self-excitation. The rapid rhythm of this area causes it to become the new pacemaker of the heart.  Paroxysmal tachycardia means that the heart rate bursts and after a few seconds to hours returns to normal. Rx: Qunidine  or Lignocain because they increase the sodium permeability of the cardiac muscle and thus block the rhythmic discharge of this irritable area. Two types:

1. Atrial paroxysmal tachycardia: Inverted P wave - SVT

Supraventricular tachycardia
Classification and external resources
Lead II electrocardiogram strip showing SVT with a heart rate of about 150.
ICD-10	I47.1

1. Ventricular paroxysmal tachycardia: This type of tachycardia usually does not occur unless significant ischemic changes is present in the ventricles - lethal fibrillation.

Ventricular tachycardia
Classification and external resources
ICD-10	I47.2

Ventricular Fibrillation

Ventricular fibrillation
Classification and external resources
ECG lead showing VF
ICD-10	I49.0

The ventricles contract and relax in an uncoordinated fashion, and form reentry circuits that stimulate themselves - circus movements
CIRCUS MOVEMENTS - 

1.  Increased pathway around the ventricle. By the time the impulses return to the originally stimulated muscle, it is no longer in the refractory state and the impulse will continue to 
2. Decreased velocity of conduction. By the time the slower impulse travels around the heart, the muscle is no longer refractory to new impulse and is stimulated again. This frequently occurs in the Purkinje system during ischemia of the cardiac muscle or during high blood potassium concentration - hyperkalemia 
3. Shortened refractory period of the muscle: This allows repeated stimulation as the impulse travels around the heart and occurs after epinepherine administration or repetitive cardiac electrical stimulation.

Defibrillation of the heart causes essentially all parts of the ventricles to refractory. 

ATRIAL FIBRILLATION

The atria and the ventricles are insulated from one another, therefore ventricular fibrillation can occur without atrial fibrillation and vice versa.

The causes of atrial fibrillation are the same as ventricular fibrillation: Increased pathway resistance, decreased velocity of conduction, shortened refractory period of muscle. 

Enlarged atria are caused by heart valve lesions, the atria do not pump if they are fibrillating, and the efficiency of the ventricular pumping decreases 20% to 30%. A person can live for years with atrial fibrillation and not know it.

ATRIAL FLUTTER: is different from atrial fibrillation in that a large single wave front travels around and around the atria. 250 to 300 bpm - volumes are small. 

1. Shortened refractory period of the muscles