[2] Lecture 9: Cardiac Arrhythmias Flashcards
HR > 100bpm
And
Causes:
Tachycardia
Increased body temp.
Stimulation by sympathetic nerves
Toxic conditions of the heart
Endogenously mediated tachycardia:[exercise]
HR increase
CO increase
Filling time reduced but SV doesn’t decline
Sympathetic stimulation when exercising maintains SV how?
Increase contractility
Systolic interval reduced
Increase venous return
What are effects of pathologically mediated tachycardia?
HR increases
CO decreases
Why do the effects of pathological mediated tachycardia occur?
MAP decreases and activates sympathetic NS after the fact and is unable to compensate
No muscle pump to increase venous return
What is bradycardia and what causes it?
Respiratory type of sinus arrhythmia
Medullary resp. Center into vasomotor center during inspiratory /expiration cycles….increase/ decrease HR through sympathetic and vagus nerves to the heart
Sudden cessation of P waves- standstill of atria..ventricles pick up AV node rhythm. QRS pace is slower but not otherwise altered.
Sinoatrial block
Ischemia of AV node or AV bundles through coronary insufficiency
Compression of AV bundles by scar tissue
Inflammation of AV node/bundle
Extreme stimulation of the heart by the vagus nerve
Atrioventricular block
Extended PR interval:
Longer w/ slower HR
Shorter w/ faster HR
> .20s PR
1st degree AV block
Extended PR that results in dropped beats of the ventricle
2nd degree AV degree
No relation between the rate of the P waves and the rate of QRS-T complexes
Complete Atrioventricular block
Resumption of the ventricular beat may be due to parts of the purkinje system acting as ectopic pacemaker
Ventricular escape
Periodic fainting spells
Stokes-Adams syndrome
An alteration in the amplitude of P waves, QRS complexes, or T waves
Referred to as electrical alternans
Partial intraventricular block