CR Flashcards
P wave
Atrial depolarisation
0.08-0.1s
QRS complex
Ventricular depolarisation
T wave
Ventricular repolarisation
PR interval
Delay at AVN
0.12-0.2s
QT interval
Time when all the ventricular muscle is contracting
0.35-0.43s
Physiology of AF
Atria experience chaotic signals and quiver
Only some APs pass through to ventricles giving irregular ventricular rhythm
Causes of AF
Hypertension Heart attacks Abnormal valves Hyperthyroid Sleep apnoea
Symptoms of AF
Palpitations Reduced ability to exercise Fatigue Dizziness Confusion Shortness of breath Chest pain
ECG evidence for AF
No distinct P wave
Irregular R-R intervals
Treatment for AF
Cardioversion to restore regular sinus rhythm
Thromboprophylaxis
Treatment of underlying cause if possible
Why is there an increased chance of clots with AF?
Pooling of blood in atria
Stagnant blood more likely to clot
Clots can dislodge and be pumped out of the heart
Can block arteries in the circulation
Can cause stroke if reach cerebral arteries
Rivaroxiban mode of action
Direct factor Xa inhibitor
Vitamin K antagonists
Warfarin
Prevent formation of some clotting factors
Heparins
Activate antithrombin III
Inhibits thrombin and factor Xa
Speed of action potential in different parts of the heart
Atria = 0.5m/s
AVN = 0.05m/s
Bundle of his and bundle branches = 2m/s
Purkinje fibres = 4m/s
Atrial contraction and exercise
10% of ventricular filling at rest
40% of ventricular filling in exercise
Less time for atrial filling in exercise
Atrial contractions needed to achieve maximum stroke volume
Normal cardiac output
- 9L/min for females
5. 6L/min for males
Normal stroke volume
70ml in 70kg male
Normal heart rate
60-100bpm
Normal MAP
65-110mmHg
Local mediators controlling vasodilation of arterioles supplying muscles
CO2, H+, K+, AMP, adenosine, NO, bradykinin
Blood distribution to muscles at rest and in exercise
21% at rest
85% in exercise
Mutation in Liddle syndrome
Mutation in C terminus of the ENaC channel
Inability for Nedd4-2 to bind
Channel cannot be marked for degradation
Increased activation of ENaC
Increased sodium retention
Increased water retention
Increased blood volume and therefore pressure
Symptoms of Liddle syndrome
Early onset hypertension
Metabolic alkalosis
Muscle wasting (low potassium)