[PDF] FRACP Study Notes - Wellington ICU

39702_7FRACPStudyNotes.pdf

FRACP

Study Notes

Compiled by David Tripp

Volume 1

Cardiology 1

Endocrinology 45

Renal 101

Neurology 137

Respiratory 183

Immunology 223

Rheumatology 237

I am indebted to many people and sources, including but not limited to my study group (thanks Ben, Chris and Michelle) and the notes of a former group (thanks Matt, Travis and Phil), th Edition, physicians teaching the Wellington exam preparation programme, the DeltaMed Exam Preparation course, CMDT 2008, the BNF and a zillion journal articles. And special thanks to Helen, Laura and Esther, my lovely and long suffering wife and daughters. All profits from these notes are going to World Vision including helping build a maternity clinic in Rwanda currently 3 hours from any other health facility. The exam is hard, but others have an even rougher deal! Finding your way around: Page cross-references link to the page containing the heading of the section in which the cross referenced material occurs may be over the page Disclaimer: This document was an attempt to organise two metres of paper into a form I had some hope of studying from for the FRACP exam. It is shared with the hope that it will help you too. However, I accept no responsibility for mistakes it is your challenge to find them! This is also not intended as a guide to clinical practice your patients deserve something authoritative. God bless (He designed it so might also be a useful reference point!)

David Tripp

February 2009

David.Tripp@xtra.co.nz

FRACP

Study Notes

Compiled by David Tripp

Volume 2

Infectious Diseases 276

Gastroenterology 329

Oncology 375

Haematology 415

Dermatology 451

Pregnancy 459

Geriatric Medicine 467

Palliative Care 477

Psychiatric Medicine 479

Alcohol and Drug 485

Pharmacology 491

Critical and Perioperative Care 501

Genetics 505

Radiology 511

Statistics 513

Index 519

Cardiology 1

Cardiology

Physiology .................................................. 2 Examination ............................................... 2 ECG Interpretation ..................................... 3 Arrhythmias ............................................... 3 Atrial Fibrillation .................................. 3 Bradycardias ......................................... 6 Tachyarrhythmias ................................. 7 Valvular Heart Disease ............................ 11 Mitral Stenosis .................................... 11 Mitral Regurgitation ............................ 12 Mitral Valve Prolapse ......................... 13 Aortic Stenosis .................................... 13 Aortic Regurgitation ........................... 14 Tricuspid Valve ................................... 15 Pulmonary Valve ................................ 15 Congenital Heart Disease ......................... 15

Atrial Septal Defect/ASD.................... 15

Ventricular Septal Defects .................. 16

Tetralogy of Fallot .............................. 16

Transposition of the Great Arteries ..... 16

Patent Ductus Arteriosus ..................... 16 ................... 16 Aortic Coarctation ............................... 17 Hypertension ............................................ 17 Resistant Hypertension ....................... 18 Treatment ............................................ 19 Renal Vascular Disease ....................... 21

Malignant Hypertension ...................... 22

Ischaemic Heart Disease .......................... 23 Angina/Chest Pain .............................. 23 Myocardial Infarction ......................... 25 Stents ................................................... 29 Cardiomyopathy ....................................... 29 Heart Failure ............................................ 31 Cor Pulmonale .................................... 38 Aortic Disease .......................................... 39 Pericardial Disease ................................... 40 Pericarditis .......................................... 40 Pericardial Effusion ............................ 40

Pericardial Tamponade ....................... 41

Constrictive Pericarditis ...................... 41 Endocarditis ............................................. 41 Syncope .................................................... 43 Other ........................................................ 44

2 FRACP Study Notes

Physiology

Cardiac myocytes have a long action potential cf muscle cells (200 400 ms cf 1 5 ms) Most ion channels are voltage gated

Na (initially) & Ca (after Na) are the primary depolarising channels, K repolarisation hyperpolarises the

heart back to negative resting membrane potential Automaticity is usually caused by spontaneous phase 4 diastolic depolarisation autonomic tone important in modulating phase 4. extracellular K more positive diastolic potential increased rate of pacemaker cells Haemodynamic assessment: Cardiac output: Thermodilution: use Swann-Granz catheter with side hole in RA for injecting cooled 5% dextrose and thermistor distally calculations allow assessment of CO if no shunt Fick principle if shunts: Measure expired O2, O2 in aorta, (mixed venous O2), calculating the systemic A- Shunts: degree of shunt estimated by pulmonary:systemic flow ratio (Qp:Qs) Pulmonary Vascular Resistance: Pressure drop across pulmonary circulation, normal < 4 Woods

Units

VO2 Max: the maximum capacity of the CVS to deliver O2 to the exercising muscles. Is limited by maximum cardiac output during exercise. Maximal HR decreases as a function of age Antiarrhythmic drugs: Relegated to an ancillary role due to complexity and adverse effects Vaughan Williams classification: remember Some Block K C Class 1: local anaesthetic effect due to blockade of Na+ current Class II: interfere with -adrenergic receptor Class III: delay repolarisation due to inhibition of K+ current Class IV: interfere with Ca conduction Most drugs have actions across several classes Radiofrequency energy is used for catheter ablation

Examination

Pressure waves in atria: a wave: atrial contraction at end of diastole atrial pressure. Coincides with first heart sound c point: bulging of AV valves into atria during systole atrial pressure. Not usually visible x descent: atrial relaxation between S1 and S2 v wave: End of atrial filling during systole venous inflow into atria with AV valve closed atrial pressure y descent: rapid ventricular filling following opening of the AV valve Differential: Causes of height: Right ventricular failure, tricuspid stenosis or regurgitation, pericardial effusion or constrictive pericarditis, SVC obstruction (no waves), fluid overload, hyperdynamic circulation Should normally fall on inspiration. If it rises then ?constrictive pericarditis Dominant a wave: tricuspid stenosis (also causes a slow descent), pulmonary stenosis, pulmonary hypertension Cannon a waves (nwave right atrium contracts against closed tricuspid valve): intermittently in complete heart block (two chambers beating independently), retrograde conduction Dominant v wave: tricuspid regurgitation (should never miss this, watch for movement of ear lobe) x descent: absent in AF, exaggerated in cardiac tamponade, constrictive pericarditis a c x v y

Cardiology 3

y descent: Sharp: severe tricuspid regurgitation, constrictive pericarditis, slow in tricuspid stenosis,

right atrial myxoma

ECG Interpretation

P Wave

RA enlargement: normal duration, amplitude inferiorly (II, II, aVL), +ive in V1 LA enlargement: duration, amplitude inferiorly, -ive in V1

LV Hypertrophy

S in V1 + R in V5 or V6 > 35 mm: Sokolow-Lyan Criteria (32% sensitive, 95% specific the other 5% are tall and thin) Other more sensitive criteria include: limb lead voltages, LA enlargement, LAD With ST change in lateral leads (I, aVL, V5, V6) = strain pattern

RV Hypertrophy

Prominent R in V1 (R > S with R > 5mm) but also happens in RBBB, Posterior MI, pre-excitation Deep S wave in V6 RAD RA enlargement With ST change in anterior leads (V1 V3) = RV strain

Ventricular Depolarisation

See diagnosis of STEMI, page 27 Septum depolarises L R. Initial upwards deflection in V1 BBB requires wide complexes (> 0.12 secs) and atrial pacing: LBBB: septum depolarises R L at the same time as RV depolarises, LV is bigger so still a +ive deflection in V1, followed by a late, slow depolarisation of the LV away from V1 So, to differentiate LBBB from RBBB look at the 2nd half of QRS in V1 if +ive then RBBB, if negative then LBBB Hemiblocks: if LBBB look at the electrical axis: If I is +ive and II is ive (LAD) then L anterior hemiblock If I is ive and II is +ive (RAD) then L posterior hemiblock Bifasicular block: RBBB + hemiblock Downward slopping ST segments consider digoxin toxicity (ask about appetite) U wave: hypokalaemia (also potentiates digoxin) If TWI in chest leads and no clinical suspicion of MI then think cardiomyopathy

Arrhythmias

See PMJ, 2006:82

Atrial Fibrillation

>5% over 70 May be triggered by other supraventricular tachycardias loss of atrial appendage contractility and emptying leading to risk of clot formation 3rd degree block + AF regular rhythm Causes: LA enlargement: can be 2nd to AF, LVF, HTN, valvular heart disease Surgery: CAGB: 30 60% (80% revert spontaneously within 24 hours), non-cardiac surgery 4 12% Acute Treatment:

Rate control with beta-blockers or Ca-channel blockers. Digoxin rarely used as stand alone in acute

setting Anticoagulate: Heparin till INR 1.8, then warfarin for 1 month Cardioversion: 200J biphasic shock conversion in 90%

4 FRACP Study Notes

Thromboembolic risk of acute reversion: No difference in TE risk with cardioversion vs drugs vs spontaneous has been demonstrated but lack of trial data. ACUTE study (JACC 2003) no difference in TE risk between 4 weeks of anticoagulation vs immediate TEE guided DCR Rhythm control: Amiodarone: Reasonable revering agent, best maintenance agent, no myocardial depression. Can be used in CHF (little negative inotropic effect), minimal effect on BP SE: Sun sensitivity Ocular toxicity: photosensitivity (50%), corneal deposits (90%), optic neuritis (1%) pulmonary fibrosis (1 17%): usually reversible with steroids and/or withdrawal Dose dependent abnormal LFTs in 25%, cirrhosis < 2% Thyroid toxicity: see page 82 Peripheral neuropathy on long term high doses Inhibits and is a substrate of 3A4. Doubles digoxin concentration (a p-glycoprotein effect, not CYP450) Prolongs Qt Disadvantages: long half life may take weeks or months to reach steady state. Very poor dose- response relationship between individuals drug monitoring not useful Sotalol: Primarily class III action + -blockade. Weak efficacy in reverting AF. Less effective than amiodarone at maintenance of AF Cessation in 15% due to fatigue, dyspnoea or bradycardia. Proarrhythmia: 2.5% Torsades at 6 months, QT prolongation Flecainide: 150 mg IV successful in 55 60% (better than sotalol and amiodarone)