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Cardiology Notes

Medicine Notes > Medicine and Surgery Notes

This is an extract of our Cardiology document, which we sell as part of our Medicine and Surgery Notes collection written by the top tier of Bristol University students.

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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


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