RACP Divisional Written Exam · FRACP

Cardiology for the written exam

Everything Physify has for Cardiology: short lessons written to Australian guidance, exam-style questions with a worked explanation for each, and Bedside, our AI tutor, under every one. Try a question below, no sign-up.

courses: 35courses
lessons: 157lessons
exam-style questions: 1,094exam-style questions
figures in the lessons: 32figures in the lessons

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Cardiology

A 55-year-old woman has LDL 2.9 mmol/L, HDL 1.6 mmol/L, triglycerides 1.1 mmol/L and lipoprotein(a) 180 nmol/L, measured after her mother's myocardial infarction at 61. BP is 126/78 mmHg, she has never smoked and her 5-year risk is 6 per cent. After discussion she has started atorvastatin 20 mg. How should the lipoprotein(a) be managed?

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What's covered

35 courses, each a set of lessons with a quiz after them. The bar shows how many questions each has. Open a course to see its lesson outline.

From the lessons

32 figures sit in the Cardiology lessons: ECGs, diagrams, films and clinical images, each with what to look for. Here are 4. Tap one to enlarge it.

Schematic left ventricular pressure-volume loop, volume on the x axis and pressure on the y axis, running anticlockwise. Mitral closure at end-diastole (about 120 mL) starts isovolumic contraction up the right side; the aortic valve opens at about 80 mmHg; ejection runs along the top, peaking near 120 mmHg; the aortic valve closes at end-systole (about 50 mL, about 100 mmHg); isovolumic relaxation falls down the left side; the mitral valve opens and filling runs along the bottom. The width of the loop is the stroke volume, about 70 mL; ejection fraction is stroke volume divided by end-diastolic volume and the area inside the loop is stroke work. A dashed straight end-systolic pressure-volume relation (contractility) touches the end-systolic corner, and a dashed exponential end-diastolic relation (passive stiffness) runs along the filling limb. Four smaller panels compare abnormal loops with the normal one: aortic stenosis, a tall loop with very high systolic pressure, a normal or small stroke volume and a steeper filling curve; chronic mitral regurgitation, a large end-diastolic volume and ejection into the atrium from the start, so no true isovolumic contraction or relaxation; chronic aortic regurgitation, a very large end-diastolic volume and very wide loop with filling from the aorta during relaxation, so no true isovolumic relaxation; and diastolic dysfunction, a steeper end-diastolic relation giving a higher filling pressure at the same or a smaller volume. — Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Ventricular Mechanics, Coronary Flow and Oxygen Transport” in Cardiovascular Physiology

Schematic of the conduction system: sinus node, AV node, His bundle, right bundle, and the left bundle dividing into anterior and posterior fascicles, labelled with the block that occurs at each site. — Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Bundle Branch and Fascicular Block” in Bradycardia and Conduction Disease

12-lead ECG recorded during chest pain, with upright, near-normal anterior T waves and a lead II rhythm strip. — A near-normal tracing recorded during chest pain. ECG: James Heilman, MD, CC BY-SA 3.0, via Wikimedia Commons; resized. Original. Tap the image to zoom.

From the lesson “Mimics and Hidden Signs: Repolarisation, Electrolytes, Ischaemia and Inherited Disease” in Reading the 12-Lead ECG: Real Tracings

Schematic ventricular myocyte action potential, membrane potential in mV against time. Phase 4: the inward rectifier IK1 holds a stable resting potential of about minus 85 to minus 90 mV. Phase 0: rapid upstroke from fast sodium entry (INa); class I drugs block the sodium channel and slow phase 0. Phase 1: a brief notch from the transient outward potassium current Ito. Phase 2: the plateau, with L-type calcium entry balanced by potassium exit through IKr and IKs. Phase 3: repolarisation by potassium exit through IKr and IKs, then IK1; class III drugs block potassium channels, and a dashed trace shows the longer phase 3 and so the longer QT. A second panel shows a sinoatrial or atrioventricular nodal cell: slow phase 4 depolarisation from about minus 60 mV (funny current If and T-type calcium) to threshold, a slow phase 0 upstroke carried by L-type calcium, and phase 3 repolarisation by potassium exit. Class II beta blockers flatten phase 4 (a dashed trace reaches threshold later) and slow the atrioventricular node; class IV verapamil and diltiazem block the L-type calcium channel and slow the nodal upstroke. A key lists the class I subclasses: Ia (quinidine, procainamide, disopyramide) widen the QRS and prolong the action potential and QT, with additional potassium channel block; Ib (lidocaine, mexiletine, phenytoin) leave the QRS unchanged and shorten the action potential and QT; Ic (flecainide, propafenone) widen the QRS with use dependence and have little effect on repolarisation. Class III amiodarone and sotalol act mainly on the rapid delayed rectifier IKr. Outside the scheme: ivabradine (If), digoxin, adenosine and magnesium. — Physify teaching diagram (schematic). Tap the image to zoom.

From the lesson “Antiarrhythmics and Rate-Controlling Agents” in Cardiovascular Pharmacology

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10 free Cardiology questions

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Cardiology high-yield summary

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Cardiology in the clinical exam

25 interactive short cases and 6 long cases for the RACP Divisional Clinical Exam: you examine, present and are marked on the five RACP domains.

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Cardiology on the blog

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