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Cardiology Notes

This is a sample of our (approximately) 13 page long Cardiology notes, which we sell as part of the Medicine and Surgery Notes collection, a 2.1 package written at Bristol University in 2011 that contains (approximately) 143 page of notes across 7 different document.

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Cardiology Revision

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Medicine & Surgery Cardiology Essential anatomy
? Sinus node o Generates impulses automatically by spontaneous depolarisation of its membrane o Pacemaker o Influx of sodium controls the depolarisation

o The rate of depolarisation is controlled by: autonomic tone, stretch, temp, hypoxia, pH
? Atrial & ventricular myocyte action potentials o Different to sinus node cells o Arrival of AP opens Na channels resulting in a fast depolarisation Cardiac Cycle

Cardiac arrhythmias Bradycardia<60bpm Tachycardia>100bpm
? Supraventricular
? Ventricular Sinus rhythm

Mechanisms of arrhythmia production Sinus bradycardia - slow automacity Bradycadia due to AV block - abnormal conduction in the AV node
? Accelerated automacity o Reducing the threshold potential o Increasing the rate of diastolic depolarization
? Triggered activity o Myocardial damage can lead to oscillations in the transmembrane potential o These 'after depolarisations' may reach the threshold and produce an arrhythmia

Sinus bradycardia

Heart block Atrioventricular block First-degree block Prolonged PR interval by more than 0.22s Second-degree block Some p waves occur but others do not
? Mobitz I block (Wenckebach) o Progressive PR interval prolongation until P waves fail to conduct
? Mobitz II block o Every now and then, there is a dropped QRS

? 2:1or3:1 o Where every second or third P wave conducts the ventricles

3 rd degree (complete) block When all activity fails to conduct to the ventricles No relationship between P waves and QRS complexes P waves ~90/min QRS ~36/min

Bundle Branch Block Normal PR interval Widened QRS complex RBBB Late activation of the right ventricle MARROW Late activation of the left ventricle WILLIAM

LBBB

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