Lecture 9: Cardiac arrhythmias Flashcards
Endogenously mediated tachycardia
Heart rate increases
Cardiac output increases
Filling time is reduced by stroke volume does not fall
Sympathetic stimulation contracts veins and increases venous return to help maintain ventricular filling
First-degree incomplete AV block
Normal P-R time interval is 0.16 sec
When P-R interval increases to greater than 0.20 seconds, the patient has a first degree incomplete heart block
Fibrillation occurs a result of
Circus movements
Pathologically mediated tachycardia
Heart rate increases
Cardiac output decrease
Mean atrial pressure decreases and activates sympathetic nervous system, which occurs after the fact and is unable to compensate
Spillover signals
Related to respiratory sinus arrhythmia
These signals alternately increase and decrease number of impulses transmitted through sympathetic and vagus nerves to the heart
Causes of Atrial fibrillation
Enlargement of the atria (due to valve lesions)
Inadequate emptying of the ventricles, causing blood to back up into the atria
What causes conduction velocity to be slowed down
Blockage of the Purkinje system
Ischemia
High potassium levels
Sinoatrial block characteristics
Sudden cessation of P waves
Resultant standstill of atria
Ventricles pick up a new rhythm, usually originating in AV node
Rate of QRS is slowed
What can shorten the refractory period
Response to drugs such as epinephrine
Repepitive electrical stimulation
Paroxysmal tachycardia
Heart becomes rapid in paroxysms
Paroxysm begins suddenly and last for variable amounts of time, then ends suddenly
Pacemaker of heart shifts back to sinus node
Premature contraction causes
Most are result of ectopic foci:
- Local ischemic areas
- Calcified plaques
- Irritation of the conduction system or nodes
Causes of Tachycardia
Increased body temperature
Stimulation of heart by sympathetic nerves (due to loss of blood/state of shock)
Toxic conditions of heart (results in weakening of myocardium)
Complete AV block
Ventricles establish their own signal (usually AV node)
No relation between rate of P waves and QRS-T complex
Fibrillation
Twitching of individual muscle fibers in the atria or ventricles and also in recently denervated skeletal muscle fibers
Stokes-adams syndrome
Periodic fainting spells due to complete AV block
Partial intraventricular block
Referred to as “electrical alternans”
Term refers to an alternation in the amplitude of P waves, QRS complexes or T waves
Causes of AV block
Ischemia of AV node or AV bundle fibers
Compression of AV bundle by scar tissue
Inflammation of AV node/bundle
Extreme stimulation of the heart by vagus nerves
Second-degree incomplete AV block
When P-R time interval increases to 0.25–>0.45 seconds
Atrial P wave is present but QRS-T wave may be missing, resulting in dropped beats of the ventricle
2:1 rhythm or other variations may develop
Tachycardia
Fast heart rate (>100 beats/min)
Causes of Bradycardia
Athletic heart
Vagal stimulation
Extremely sensitive carotid baroreceptors in carotid sinus syndrome
Three conditions that cause the impulse to travel around the circle (circus movements)
The pathway around the circle is too long
The length of the pathway remains constant but the velocity of conduction slows down
The refractory period of the muscle might become greatly shortened
What happens when pathway is too long
If the heart is dilated (making pathway too long) impulse takes longer to get back to starting point and the muscle is no longer in its refractory period, allowing for another depolarization
Ventricular escape
Resumption of ventricular beat in complete AV block-may be due to parts of purkinje system acting as ectopic pacemaker
Bradycardia
Slow heart rate (<60 beats/min)
