Nosim = 020 AM = < a 4 passmedicine.com HSaoOotrt © Passmedicine ee) BS Heart sounds ‘The first heart sound (t) is caused by closure ofthe mitral and tricuspid valvas whilst the second heart sound ($2) is due to aortic and pulmonary valve closure si ‘¢ closure of mitral and tricuspid valves “6 soft if ong PR or mitral regurgitation ‘© loud in miteal stenosis 82 ‘+ closure of aortic and pulmonary valves ++ soft in aortic stenosis 16 splitting dung inspiration is normal 83 (third heart sound) ‘© caused by diastole filing ofthe ventricle ‘© considered normal if < 30 years old (may persist in women up to 50 years ole) ‘+ heard in loft venticular failure (e.g, diated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mival reguigtstion 4 fourth heart sound) ‘* may be heard in aortic stonasis, HOCM, hypertension ‘© caused by alral contraction against astilf ventricle '* in HOOM a double apical impulse may be felt as a result cf a palpable S4 Sites of auscultation Valve Site Pulmonary valve Left second intercostal space, at the upper sternal border Aarti valve Right eocond intercostal space. at tho upper stemal border Mitral valve Left fith intercostal space, just modial to mid elavicular lino Tricuspid valve Left fourth intercostal space, at the lower loft steal border ‘The diagram below demonstrates where the various cardiac valves are best heard. emort Passmedicine a (Ganeral Mecical Counc Lab Values, Normal Adult Causes of a loud $2 “+ hypertension: systemic fous A2) ar pulmonary (luc P2) ‘+ hyperdynamic states: ‘+ vial soptal defect without pulmonary hypertension Causes of a soft $2 "+ aortic stenosis Causes of fixed split $2 ‘arial septal defect Causes of a widely spit S2 '¢ oop inspiration © PREB ‘+ pulmonary stenosis ‘¢severe mitral regurgitation Causes ofa reversed (paradoxica) spit $2 (P2 occurs before AZ) + Lp58 ‘sovere aortic stenosis fight ventricular pacing WPW type B (causes early P2) ‘© patent ductus arterioaus QcS soa > v8 am Prom) < a 4 passmedicine.com BO ot Passmetcine Corea eda! Comet | Gover Medel Oourci_| Lab Vos, Nomel A Atrial myxoma Overview # 75% occur inlet atrium ‘© more common in females Features * systomic: dyspnoea, fatigue, weight los, fever clubbing embol atria oritation mic-diastole murmur, tumour plop echo: pedunculated heterogeneous mass typically attached to the fossa ovale, region ofthe intoravial soptumoso aM na h @ passmedicine.com ¢€O@dt+ Pulses Pulsus paredoxus ‘© greater than the normal (10 mmHg) fallin systolic blood pressure during inspiration + faint or absent pulse in inspiration ‘+ severe asthma, cardiac tamponade Stowrising/plateau 1+ sorte stenosis Cotapsing * ‘orto regurgitation ‘+ patont ductus arteriosus ‘+ hyperkinatic (anaemia, thyrotoxic, fever, exerciso/pregnancy) Pulsus alternans 1+ regular altemation of the force ofthe arterial pulse 1» sovere LF Bisforions pulse ‘* ‘Couble pulse’ - two systole peaks (+ mixed aortic valve disease “Jerky? pulse ‘¢ hypertrophic obstructive cardiomyopathy’ “HOOM may occasionally be associated witha bisfeiens pulse Save my natesnam + weram me < nh & passmedicine.com HaoOot © Passmedicine ee) (General Medical Council | Lab Values, Normal Adu Jugular venous pulse ‘As well as providing information on right atrial pressure the jugular vein waveform may provide clues to underying valvular disease. A nonpulsatile JVP is seen in superior vena caval obstruction. Kussmaul's sign describes a paradoxical rise in JVP during inapiration acen in constrictive pericarditis. Ac y “a! wave « atrial eontraction ‘ largo if aval prossure 0.9. tricuspid stenosis, pulmonary stonosis, pulmonary hypertension ‘¢ absent if in atta fibrilation Cannon ‘* caused by atrial contractions against a closed tricuspid valve ‘¢ aro soon in complete hoart block, venticular tachycardivectopics, nodal mythm, singlo chambor ventvicular pacing 16 closure of ticuspic valve ‘© rot normally visible ‘* ue to passive filling of blood ino the avium against a closed Wiouspid valve ‘© Giant v waves in tricuspid regurcitaion ‘x! descent = fallin atrial pressure during ventricular systole 'y' descent = opening of tricuspid valve Brus Ay BBS Te Be wyJVP: cannon waves Caused by the right atrium contracting against a closed tricuspid valve. May be subdivided into regular or intermittent Regular cannon waves ‘© ventricular tachycardia (with 1:1 ventricular-atrial conduction) ** alrio-ventricular nodal re-entry tachycardia (AVNRT) Irregular cannon waves, = complete heart blockNosim = 10:06 AM ad < fh & passmedicine.com eM Ot Murmurs ection systolic "sorte stenosis ‘© pulmonary stenosis, HOOM '* ASD, Falot's Holosystolc (pansystotic) ‘© mitralvicuspid regurctalion (high-pitched and ‘blowing’ in character) ‘© VSD (‘harsh' in character) Late systolic 1 mitra valve prolapse ‘© coarctation of aorta Enly diastolic ‘© aortic rogurcitation (high-pitched and ‘blowing’ in charactor} {¢ Graharn-Stee! murmur (pLimonary regurgitation, again high-pitched and "blowing! in character) Micuiate diastolic ‘© rritral stenosis (rumbling’ in character) ‘© Auclin-Fnt murmur (sevore aortic regureitaion, again is "umbling' in charactor) Continuous machine-tike mumur ‘© patent ductus arteriosus HastNosim = 007 AM nD < a 4 passmedicine.com Boot {1st 2nd 3rd Atrial Normal Aortic stenosis 1 I I \ Mitral regurgitation f Aortic regurgitation I I 1 I Mitral stenosis I 1 Patent ductus f ! arteriosus \ oo Diastole! Systole ! Diastole 'SystoleAtrioventricular block In atrioventricular (AV) block, or heart block, there is impaired electrical conduction between the atria and ventricles. There are three types: First degree heart block © PRinterval > 0.2 seconds Second degree heart block: 1 type 1 (Mobit I, Wenckebach): progressive prolongation of the PR interval unt a dropped beat eccurs © type 2 (Mobi Il PR intervals constant but the P wave is often not followed by a QRS complex. Third degree (complete) heart block © there is no association betwaon the P waves and QRS complexes ECG: PR interval Causes of a prolonged PR interval ‘idiopathic ischaemic heart disease 4 passmedicine.com © Pmemeticine ‘General Medical Council ‘General Medical Counc ECG: left bundle branch block ‘The diagram below shows the typical features of lft bundle branch block (LBBB): wv ks (One ofthe most common ways to remember tho difference botwoon LBBB and RBBB is WikLiaM MaRROW “¢ in LBBB there i a'W in Vt and "Min V6 (ein ERB there is @'M' in V4 and a Win VE EGA showing typical eaires of LAB Causes of LBBB ‘© lechaomic heart disease ‘+ hypertension 1+ aortic stenosis ‘© cardiomyopathy ‘rare: idiopathic frosts, digoxin toxicity, hyperkalaemia Now LBB is always pathological and may be a sign of a myocardial infarction. Diagnosing a myocardial infarction for patients with exsting LBBB js dificult. The Sgarbossa criteria can help wih this. Please see the link for more details, [ejija es [eles] me140 aM &@ passmedicine.com n= a0 a+ (Goveral Mecha Gaunt ‘Gane Medical Counc Lab Vaiues, Noval Adult Complete heart block Features ‘Types of heart block syncope heart falure regular bradyearcia (30-50 bpm) wide pulse pressure LIVP: cannon waves in neck variable intensity of $1 First dagrse heart block '* PR interval > 02 seconds Second degree heart block ‘* typo 1 (Mobitz |, Wonckobach): progressive prolongation ofthe PR interval until a dropped beat occurs ‘+ type 2 (Mobitz Ih: PR interval is constant but the P wave is often nat followed by 2 QRS complex ‘Third degree (complete) heart block “+ theve sna association between the P waves anc QRS complexes re s ECG showing third degree (complet) heat Hook s|im)-[s/e/e- 1 a la &ECG: normal variants ‘The following EGG changes are considered normal variants in an athlete: sinus bradycardia ‘© junctional rhythm + first degree heart block ‘+ Wenckebach phenomenon ECG: hypokalaemia ECG features of Fypokalaomia © Usaves ‘# small ocabsent T waves (occasionally inversion) {© prolong PR interval ST depression + long OT ‘The ECG below shows typical U waves. Note also the borderline PR interval (One registered user suggests the flloning shyme '¢ In Hypokalaemia, U have no Pot and no T, but long PR and a long QTECG: hypothermia ‘The folowing ECG changes may be seen in hypotherrnia bradycardia ‘+ J wave - small hump atthe end of the QRS complex «+ first degree heart block (© long GT inter ‘© vial and ventricular arhythemios ECG: ST elevation Causes of ST elevation ‘¢ myocardial infarction pericarditis Pormal variant - “high take-of loft venticular anouryern Prinzmetal's angina (coronary artery spasm) rare: subarachnoid haemnorrnage ECG: ST depression Causes of ST depression '¢ secondary o abnormal QRS (LVH, LBBB, RBBB) 1+ ischaemia ‘© digoxin ‘+ hypokalaomia ‘* syndrome X ais|a-le = a-|[n- astoon e oe one < fy 2 pasemedicine.com egoaoe+ © Anite a Ea] FS mE ECG: axis deviation Causes of left axia deviation (LAD) ‘loft anterior hamiblock left bundle branch block ‘Wolf-Pavkinson-White ayndcomet ~nght-sidad accessory pathivay ‘congenital: ostium primum ASD, tricuspid atrosia ‘+ hyperkalemia minor LAD in obese people (Causes of right axis deviation (RAD) “6 ight ventricular hypertrophy left posterior hemiblock. ‘chronic lung disoaso + cor pulmonale pulmonary embolism ‘stm secundum ASD ormal in infant < 1 years old minor RAD in tall people ‘Walt Parkinson White syndrome’ - left-sided accessory pathway ‘in the majority of eases, erin a question without qualification, Wolff-Parkinsen-White syndrome is associated with lett axis deviation Biijus|s ae ‘Save my notes via faeScoring systems ‘There are now numerous searing systems used in medicine. The table below lists some of the moce common ones: Scoring system CHA:DS2-VASe ascp2 NYHA pasza Child-Pugh classification Wolle score MMSE HAD PHO-9 GaD-7 Edinburgh Postnatal Depression Score SCOFF avoir CAGE Fast’ cuns.65, Epworth Sleepiness Seale Notes {sod to dotermino the noed to anticoaguiato a patont in atl illation Prognostic score for risk stratifying patients who've had a suspected TIA Heart faite severity scale Manaus of disease activity in suratoi artis [A scoring system used to assess the seventy of Iver cithosis Helps estimate tho risk of a pationt having a deop vein thrombosis Minimental stale examination - used to assess cognitive impairment Hospital Anxiety and Depression (HAD) scale - assesses severity of anxisty and depression symptoms Patient Health Questionnaire - essesses severity of depreasion symptoms Usod a.a screening tool and sovarity measure for gonoralisod anxity disorder Used to sereon for postnatal depression Questionnaire used to detect eating disorders and aid treatment ‘Neohol screening tool ‘Neohol screening tool ‘cohol screening tool Used to assess the prognosis ofa patient with pneumonia Used in the assessment of suspected obstructive sleep apnoeaBishop score Waterlow score FRAK Ranson ertoria ust International prostate symptom score Incieates prognosis in prostata cancer ‘Assesses the heath of rewoom immediatly ater bith UUsod te hola assess tho whether induction of labour wil be quired Assesses the risk ofa patient developing a pressure sore Fisk assessment tool developed by WHO which calculates a patients 10-year risk of developing an osteoporosis related fracture ‘Acute pancreatitis Malnattion “FAST aloo mnemonic to help patients/rlatves identiy the symptoms of a strokeosm = a0 pu omen < fh & passmedicine.com emoor © Passmedicine ee) (General Medical Council | Lab Values, Normal Adu Cardiac tamponade Fastnes ‘pepncen raised JVP, with an absent Y doscont- this fs duo tothe limited ight vertvoulr fing tachycardia bypotension muted heert sounds pulovs paradoxus Kusomaut's sign much debate about this) ECG: electrical altermans ‘The key diferences between constrictive pericaritis and cardiac tamponade are summarised inthe table below: Cardiac tamponade CConstrctive pericarditis ve Absent ¥ descent XY present Pulsus paradoxus Present Absent Kussmaul's sign oro Prosent Characteristic features Pericarial calcification on CXR A.commonly used mnemonic to remember the absent Y descent in cardiac tamponade is TAMponads = TaMpax Brus |S A+ BB By Te ae a & ‘Save my notesnom = exo pu > < nh & passmedicine.com Oemgoar Pasumedicia | Ganer Medical Go. | Goraral Medical Go.. | Lab Vas, Nomal.. | Walch Gxt Cae 0. © Constrictive pericarditis Causes ‘© any cause of pericarditis particularly TB Features + dyspnoea ‘Fight heart falure: elevated JVP, ascites, oedema, hepatomegaly ‘¢ AVP shows prominent x and y descent ‘+ povicardial knock - loud $3 ‘+ Kussmaul's sign is positive on “+ pericardial calefcation ‘The key differences between constrictive pericarcitis and cardiac tamponade are summarized inthe table below: Cardiac tamponade Constrctive pericarditis we ‘bsont Y daseont XY prosont Pulsus paradoxus Prosont Absont Kusemaul's sign’ ore Present Characteristic features Pencarcial caleionton on OXR A.commonly used mnemonic to remember the absent Y descent in cardiac tamponade is TAMponads = TAMpax *a paradoxical ise in JVP during inspiration Bijus|s wie ez ne ay [a] % Save mv notesnom = sem > < fq @ passmedicine.com go + (Goveral Mecha Gaunt General Medical Council | Lab Value, Nora Adult Acute pericarditis Poricarcitis is one of tho differontials of any pationt presonting with chest pain Features ‘¢ chest pain: may be pleuntic Is often rlieved by sting forwards «other symptoms include non-productive cough, dyspnoea and flu-like aymptome * poricardial rub + lechypnoea. 8 tachycardia Causes ‘¢ vial infections (Coxsackie) tubereulosis Uraemia (causes ibrinous' pericarditis) ‘trauma post-myocardial infarction, Dresses syndrome ‘connective tissue disease hhypothyreid'sm ECG changes '¢ wiclespread ‘saddie-shapad’ ST elavation '* PR depression: most specific ECG marker for pericarditis aac “Hein es eaeace Seed ateh aR EOG showing patcarsti, Nate the vadseoread nature ofthe ST tlovation and the PR depression Save my notesMyocarditis Causes Viral: coxsackie, HIV bacteria: diphtheria, clostridia spirochaetes: Lyme disease protozoa: Chagas’ disease, toxoplasmosis autoimmune drugs: doxorubicin Presentation usually young patient with acute history chest pain, SOB,Nosim = 1040 AM on < iil} & passmedicine.com Smo + ‘General Medical Counc General Mecical Council | Lab Values, Normal Aut: Qeestions [a [ [ede [non | Infective endocarditis: prophylaxis ‘Tne 2008 guidelines from NICE have radically changed the list of procedures for which antibiotic prophylaxis is recommended NICE recommends the following procedures do nat require prophylaxis: ‘* dental procedures ‘+ upper and lower gastrointestinal tract procedures ‘+ genitourinary tract; this includes urological, gynaecological and obstetric procedures and childbirth ‘+ upper and lower respiratory tract; this includes ear, nose and throat procedures and: bronchoscopy ‘The guidelines do however suggest: ‘+ any episodes of infection in people at risk of infective endocarditis should be investigated and treated promptly to reduce the risk of endocarditis developing ‘* Ifa person at risk of infective endocarditis Is receiving antimicrobial therapy because thoy are undergoing a gastrointestinal or genitourinary procedure at a site where there is a suspected infection they should be given an antibiotic that covers organisms that cause Infective endocarditis, Itis important to note that these recommendations are not in keeping with the American Heart Association/European Sociaty of Cardiology guidelines which still advocate antibiotic prophylaxis for high-risk patients who are undergoing dental procedures. BiaNosim = 15 PM ma < nh & passmedicine.com BO ot Confidentiality GMC | Ethical and legal duties of. | Lab Values, Normal Ad Qeestions Infective endocarditis: Modified Duke criteria Infective endocarditis diagnosed if ‘© pathological criteria positive, or ‘+ 2 major oriteria, or ‘¢ 1 mgjor and 8 minor criteria, oF + Sminer criteria Pathological criteria. Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery (valve tissue, vegetations, embolic fragments or intracardiac abscess content] Major criteria Positive blood cultures ‘+ two positive blood cultures showing typical organisms consistent with infective endocarditis, such as Streptococeus viridans and the HACEK group, or ‘+ persistent bacteraemia from two blood cultures taken > 12 hours apart or three or more positive blood cultures where the pathogen is less specific such as Staph aureus and Staph epidermidis, or '* positive serology for Coxiella bumetil, Bartonella species or Chiamyola psittact, or ‘+ positive molecular assays for specific gene targets Evidence of endocardial involvement + positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves), or ‘© new valvular regurgitation Minor eriteria ‘+ precisposing heart condition or intravenous drug use ‘+ microbiological evidence does not meet major criteria, # fever > 38°C ‘+ vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorchages, Janeway lesions, petechiae or purpura ‘+ immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots= oa < fy OEIoECeOSED © Passmedicine ee) a Infective endocarditis ‘The strangest risk factor for developing infective endocercits isa previous episode of endocereltis, The following types of patients are affected: ‘© proviously normal valves (60%. typically acute presentation) ‘* theumatie valve disease (30%) «© prosthetic valves ‘© congenital heat defects ‘ Intravenous drug users (VDUs, e.. typically causing tricuspid lesion] Causes '¢ Historically Steptococcus viridans was the most common cause of infective endocarditis, Ths is no longer the case, except in developing counties. Staphylococcus aureus is now the most common cause of infective endocarditis. Staphylococcus aureus i also particularly common in acute presentation and IVDUS ‘+ coagulaso-nogative Staphylococc’ such as Staphylococcus epidermials commonty colonize indwolling ino ‘and are the most cause of endocarditis in pationts following prosthetic valve surgery, usually the result of perioperative contamination. After 2 months the spectrum of organisms which cause endocarditis return to rrormal (ie. Staphylococcus aureus is the most common cause) '* Streptococcus viridans stil accounts for ound 20% of cases, Technically Streptococcus viridans is a psoudotaxonomie torm. roferring to vkidans stroptococsi rather than a particular organism. Tho two most notable viridans streplococci are Streptococcus mitis and Streptococcus sanguinis. They are beth ‘commonly foun! in the mouth and in particular clental plaque £0 endocarditis caused by these organisms is, linked with poor dental hygiene or following a dental procedure ‘+ Stroptococeus bovis is associated with colorectal cancar| ‘+ rominfective: systemic lupus erythematosus (Libman-Sacks), malignancy: marantic endocarditis Culture negative causes ‘prior antibiotic therapy Coxiella burnett Bartonella Brucella HACEK: Haemophilus, Actinobacilus, Caraiobacterium, Eikenells, Kingela) Lancet 2016; 987: 882-09 Infactive Endocarsitis Brus s w+ = Te a aw & ‘Save my natesNosim = oss aM aa < fh & passmedicine.com 9 mas © Passmedicine ee) ‘General Medical Council | Lab Values, Normal Adu Infective endocarditis: prognosis and management Poo prognostic factors ‘Staph aureus infection (see below) prosthetic vaive (especially early’, acquired during surgery) ‘culture negative endocarditis low comotemont lovols Mortality according to organism '# staphylococci - 30% 1+ bowel organisms - 1596 ‘© streptococci - 5% (Curent antibiotic guidelines (source: British National Formulary) Scenario ‘Suggested antibiotic therapy Initial blind therapy Native valve ‘¢ amoxicilin, consider adding low-dose gentamicin Ht penicilin allergic, MRSA or severe sepsis ‘© vancomycin + low-dose gentamicin I prosthetic valve “© vancomycin + rifampicin + low-dose gentamicin [Native valve endocarditis caused by staphylococci Flucloxacilin Hf penicilin allergic or MRSA, ‘© vancomycin + rifampicin Prosthetic vale endocarcitia caused by staphylacece! _-Flucloxacilin + rifamploin + low-dose gentamicin If penicilin allergic or MRSA ‘6 vancomycin + rifampicin + low-dose gentamicin Endocaritis caused by fully-sensitive streptococci (eg. Benzylpenieilin viridans)soon os ane < fy 2 passmedicine.com eogoaoe+ © Ameren aaa tne ama |p em | a i Wem aan Suggested anibiotc therapy iil bind ray Nate valve > emoxicn, consier adn ov dose gentamicin Native valve encocaltis caused by staphylococei Prosthetic valo endocarcite caused by staphylacece! Endocarditis caused by fuly-sensitve streptococci (e.9. viridans) Endocardilis caused by less sensitive streptococe! Indications fr curgery ‘¢ severe valvular incompetence Infections resistant to antibioticaungal infections, recurrent embol afer antibiotic therapy ‘cardiac failure rofractory to standard modicaltreatmont Hf penicilin allergic, MRSA or severe sepsis ‘© vancomycin + low-dose gentamicin I prosthetic valve ‘¢ vancomycin + rifampicin + low-dose gentamicin Flucloxacilin If ponicilin allorgic or MRSA ‘© vancomycin + rifampicin Flucloxacilin + rifampicin + low-dose gentamicin Hf penicilin allergic or MRSA, ‘© vancomycin + rifampicin + low-dose gentamicin Benzylpenicilin I penicilin allergic ‘© vancomycin + low-dase gentamicin Benzylpenicilin + low-dose gentamicin Ht penicilin allergic ‘© vancomycin + low-dose gentamicin sortic abscess (otten indicated by a lengthening PR interval)nam + vwatan me fi passmedicine.com ¢ [Buerger's disease (alse known as thromboangitis obkterans) i a small and macitum vessel \vascults that is strongly associated with amoking, Features ‘¢ extremity ischaemia: intermittent claudication, ischaemic ulcers ete ‘¢ superficial thrombophlebitis '* Raynaud's phenomenon ‘Save my notesNosim = 1010 AM a= h @ passmedicine.com €O@d+ Passmedicine ee) ‘General Medical Council | Lab Values, Normal Adu DVLA: cardiovascular disorders ‘The guidelines below relate to carfmotorcycle use unless specifically stated. For obvious reasons. the rules relating tod Speci vrs of heavy goods vohiclos tond to bo much stictor ic les hypertension - can drive unless treatment causes unacceptable side effects, no need to notity DVLA. f ‘Group 2 Enllement tho disqualifies from driving if resting BP coneistontly 180 mmHg systolic or more «and/or 100 mm Hg diastolic or more angioplasty (elective) - 1 week of diving CABG - 4 wooks off diving ‘acute coronary syndrome- 4 waoks off driving, 1 wook if succosstully treated by angioplasty angina - driving must cease if symptoms occur at resUat the vines! pacemaker insertion - 1 wask of diving implontable cardioverter definilator (ICD): if implanted for sustained ventricular arrhythmia: cease driving for ‘6 months. Ifimplantod prophyiatically then coase driving for 1 month. Having an ICD results in a pormanant bar for Group 2 drivers ‘¢successiul catheter ablation for an athythmia- 2 days off driving ‘aortic aneurysm of Gem or more - natty DVLA, Licensing willbe permitted subject to annual review. An ‘aortic diameter of 6.5 om or more disqualifies patients from driving hart ransplant: DVLA do not need to be notified PU # 8 Be eB BBY Te Be Bo Save my notesNogm = sazan n= Si hy 4 passmedicine.com SS Wess © Passmedicine General Meckcal Council (General Medical Council | Lab Values, Normal Adu Rheumatic fever: criteria Rheumatic fever develops following an immunological reaction to recent @-8 weeks age) Streptococcus pyogenes Infection, Diagnosis is baseei on evidence of tazent steptocoeeal infection accompanied by’ ‘* 2 major orteria ‘+ 1 major with 2 minor criteria Evidence of racont streptococcal infection ‘© ASOT > 200iu/ml. 1+ istory of scot fever postive thrast swab ‘increase in DNase B tite Majer eritoria ‘© erythema marginatum 1+ Sydenham's chorea polyarthritis ‘+ cards (endo-, myo- oF por) ‘¢ subouteneous nodules Minor extaria 1 raised ESR or CRP pyrexia ‘© arthralgia (not if arthritis a major eritria) ‘+ prolonged PR interval ~ Q Exthema marginatum 2 sn in arsund 10% of oleren with raumate fevor ear in acuteNosim = 0:0 AM a= < nh & passmedicine.com Soo t+ wwerpasemedi... | Ganeral Medica... | General Medica... | Lab Values, Nor... | Watch Cold Gas... | @ Panamedicine Anaphylaxis ‘Anaphylaxis may be defined as a severe, life-threatening, generalised or systemic hypersensitivity reaction, ‘Anaphylaxis one of the few times when you would not have time to ook up the dose of a medication, The osuscitation Council guidelines on anaphylaxis have recently been undated. Adrenaline is by far the most important drug in anaphylaxis and should be given as soon as possible, The recommended doses for adrenaline hydrocortisone and chlomphenamine are as follows: Adrenaline Hydrocortisone Chlorphenamine <6 months 180 micrograms (0.16mi 197,000) 25mg 250 microgramsvxg ‘Smonths -6 years 180 micrograms (0.16mi 1 in1,000 50mg 28m0 6412 yoars 300 micrograms (0.ami1 4,000) 190mg 5g ‘Adult andl child > 12 years 500 micrograms (Smilin 1000) 200mg 40mg [Adrenaline can be repented every § minutes if necessary. The best site for IM injection is the anterolateral aspect of tho middie third ofthe thigh Common identified causes of anaphylaxis '* food (¢.9. Nuts) - the mast common eause in children + drugs ‘+ venom (eg. Wasp stn) ‘Sometimes itcan be dificult lo establish whether a pation! had a tue episode of anaphylaxis. Serum typtase levels re sometimes taken n such patients as they remain elevated for up to 12 hours following an acute episode of anaphylaxis Brusi|s we Te a 2% Save my natesNosim = 1021 PM xo < nh & passmedicine.com Boot a General Mecical Council | Lab Values, Normal Au: Qeestions Hypertension in pregnancy NICE published guidance in 2010 on the management of hypertension in pregnancy. They also made recommendations on reducing the risk of hypertensive disorders developing in the first place. Women who are al high risk of developing pre-eclampsia should take aspirin 75mg od from 12 weeks until the birth of the baby. High risk groups include: ‘+ hypertensive disease during previous pregnancies: ‘© chronie kidney disease ‘+ autoimmune disorders such as SLE or antiohospholipid syndrome # ype 1 or 2 diabetes mellitus ‘The classification of hypertension in pregnancy is complicated and varies. Remember, in normal pregnancy: ‘+ blood pressure usually falls in the first trimester (particularly the diastolic), and continues to fall until 20-24 weeks ‘+ after this time the blood pressure usually increases to pre-pregnancy levels by term Hypertension in pregnancy in usually defined as: ‘+ systolic > 140 mmbg or diastolic > 90 mmHg ‘+ or an increase above booking readings of > 30 mmHg systolic or > 15 mwnHg diastolic After establishing that the patient is hypertensive they should be categorised into one of the following groups Pregnancy-induced hypertension (PIH, also known as gestational Pre-existing hypertension _ hypertension) Pre-eclampsia Ahistory of hypertension Hypertension (as defined above) Pregnancy-induced before pregnancy or an occurring in the second half of hypertension in elevated blood pressure > pregnancy (ie. alter 20 weeks) association with 140/00 mmHg betore 20 proteinuria (> 0.39 / weeks gestation No proteinuria, no oedema 24 hours)Nosim = # < fy 1021 PM @ passmedicine.com xo e070 O+ © Ovestions Hypertension in pregnancy in usually defined as: ‘© systolic > 140 mmHg or diastolic > 90 mmHg + or an increase above booking readings of > 30 mmHg systolic or > 15 mmHg diastolic ‘After establishing that the patient is hypertensive they should be categorised into one of the following groups Pre-existing hypertension Ahistory of hypertension before pregnancy or an elevated blood pressure > 140/90 mmHg before 20, weeks gestation No proteinuria, no oedema Occurs in 3.5% of pregnancies and is more ‘common in older women Pregnancy-induced hypertension (PIH, also known as gestational hypertension) Hypertension (as defined above) courting in the second half of pregnancy (\2. after 20 weeks) No proteinuria, no oedema (Occurs in around 5-7% of pregnancies Resolves following birth (typically after one month). Women with PIM are at increased risk of future pre- ‘eclampsia or hypertension later in lite Pre-eclampsia Pregnancy-induced hypertension in association with proteinuria (> 0.89/ 24 hours) (Oedema may occur but is now less ‘commonly used as a criteria (Occurs in around 5% of pregnanciesPre-eclampsia Pro-oclampsia is a condition soon after 20 wooks gostation charactorisod by prognancy- induced hypertension in association with proteinuria (> 0:39 /24 hours). Oedema used to bs thie! elament of the classic triad but is now often not included in the definition as tis ot specific Pro-eclampsia is important as it predisposes tothe folowing problems. «fetal: prematurity, intauterine growth retardation eclampsia haemorrhage: placental abruption, intra-abdominal, itra-cerebral ‘cardia failure rmulti-organ failure NICE divide tsk factors into high anc moderate rile High risk factors ‘+ hypertensive disease in a previous pregnancy ‘© chronic kidnoy ciseaso ‘* aulcimmune disease, such as systemic lupus ‘enythematosus or antiphospholipid syndrome # type ortype2 diabetes ‘chronic hypertension Moderate risk factors first pregnancy © ago 40 yoars or older © pregnancy interval of, ‘more than 10 years ‘body mass index (BM of 35 kg/m? or more at first visit family history of pre eclampsia ‘mutipte pregnancyFoatures of sovere pre-eclampsia '¢ hypertension: typically > 170/410 mmHg and proteinuria as above proteinuria: dipstick +/+++ headache visual disturbance papilloedema RUQIepigastric pain hyperrefiexia platelet count < 100 10*/, abnormal liver enzymes or HELLP syndrome Management ‘consensus guidelines recommend treating blood pressure > 160/110 mmblg ‘although many cnicians have a lower threshold ‘ral labetall is now first-line following the 2010 NICE guidelines. Nifedipine and hydralazine may also be used 65 years for aortic valves and > 70 Major disadvantage is the increased risk of years for mitral valves) receive a _—_‘thrombosis meaning lang-term anticoagulation is, bioprosthetic valve needed. Following the 2017 European Society of. Cardiology guidelines, aspirin is only normally given Long-term anticoagulation not In addition if there is an additional indication, e.g usually needed. Warfarin may be ischaemic heart disease. given for the first 3 months depending on patient factors. Low- Target INR. dose aspirin is given long-term. * sortie: 3.0 © mitral: 3.5 Following the 2008 NICE guidalines for prophylaxis of endocarditis antibiotics are no longer recommended for common procedures such as dental workNosim = 4a PM m2 < nh & passmedicine.com Boot a General Mecical Council | Lab Values, Normal Au: Qeestions Primary pulmonary hypertension ‘The classification of pulmonary hypertension is currently changing with the term idiopathic pulmonary arterial hypertension (IPAH) becoming more widely used Primary pulmonary hypertension (PPH, now IPAH) ‘+ pulmonary arterial pressure > 25 mmbg at rest, > 30mmHg with exercise ‘+ PPH is diagnosed when no underlying cause can be found '* around 10% of cases are familial: autosomal dominant ‘+ endothelin thought to play a key role in pathogenesis ‘* associated with HIV, cocaine and anorexigens (e.g. fenfluramine) Features ‘+ more common in females, typically presents at 20-40 years old © progressive SOB cyanosis ‘+ right ventricular heave, loud P2, raised JVP with prominent 'a' waves, tricuspid regurgitation Investigation © echocardiography Management ‘+ diuretics i right heart failure: ‘* anticoagulation ‘+ vasodilator therapy: calcium channel blocker, lV prostaglandins, bosentan: endothelin-1 receptor antagonist «© eart-lung transplant BieNosim = ‘03 PM xo < nH & passmedicine.com Boot a General Mecical Council | Lab Values, Normal Au: Qeestions Pulmonary arterial hypertension: features and management Pulmonary arterial hypertension (PAH) may be defined as a sustained elevation in mean pulmonary arterial pressure of greater than 25 mmbg at rest or 80 mmHg after exercise. Features ‘+ exertional dyspnoea is the most frequent symptom ‘© chest pain and syncope may also occur + loud P2 ‘+ loft parasternal heave (due to right ventricular hypertrophy) Management should first involve treating any underlying conditions, for example with anticoagulants or oxygen. Following this, it has now been shown that acute vasodilator testing is central to deciding on the appropriate management strategy. Acute vasodilator testing aims to ‘decide which patients show a significant fallin pulmonary arterial pressure following the administration of vasodilators such as intravenous epoprostenol or inhaled nitric oxide If there is a positive response to acute vasodilator testing ‘© oral caleium channel blockers If there is a negative response to acute vasodilator testing ‘* prostacyclin analogues: treprostinl,iloprost '* endothelin receptor antagonists: bosentan ‘+ phosphodiesterase inhibitors: sildenalil Pent)Nosim = eae Pu m2 < nh & passmedicine.com Boost a General Mecical Council | Lab Values, Normal Au: Oeestions Exercise tolerance tests Exercise tolerance tests (ETT, also exercise ECG) are used for a variety of indications: ‘+ assessing patients with suspected angina - however the 2010 NICE Chest pain of recent onset guidelines do not support the use of ETT forall patients + risk stratifying pationts following a myocardial infarction ‘+ assessing exercise tolerance «+ Fisk stratifying patients with hypertrophic cardiomyopathy ETT has a sensitivity of around 80% and a specificity of 70% for ischaemic heart disease. Heart rate: ‘+ maximum predicted heart rate = 220 - patient's age + the target heart rate is at least 85% of maximum predicted to allow reasonable Interpretation of a test as low-risk or negative Contraindications ‘+ myocardial infarction less than 7 days ago © unstable angina ‘+ uncontrolled hypertension (systolic BP > 180 mmHg) or hypotension (aystolie BP < 90 mmHg) * aortic stenosis, ‘+ left bundle branch block: this would make the ECG very difficult to interpret Stop if ‘+ exhaustion / patient request ‘© ‘severe’, ‘limiting’ chest pain ‘+> 8mm ST depression ‘* > 2mm ST elevation Stop if rapid ST elev ‘+ systolic blood pressure > 230 mmHg ‘+ systolic blood pressure falling > 20 mmHg ‘+ altainment of maximum predicted heart rate ‘+ heart rate falling > 20% of starting rate ‘© arrhythmia developswos = + osm won < fh fa passmedicine.com ODd+ GemanesaiGorct) | ened ieciGomt| [awe Moma] © Cuero 6 BBB 2.000 | improv er Exercise: physiological changes Blood pressure ‘+ systolic increases, diastolic decreases ‘+ leads to increased pulse pressure ‘+ In healthy young people the increase in MABP is only slight Cardiac output ‘+ increase in cardiac output may be 3-5 fold ‘* results from venous constriction, vasodilation and increased myocardial contractibility, as, well as from the maintenance of right atrial pressure by an increase in venous return ‘+ heart rate up to 3-fold increase 1 stroke volume up to 1.5-fold increase Save my2:80 PM x 4 passmedicine.com eonoat (General Meckcal Council ab Values, Normal Aut... | Oumations Improve, Cardiac enzymes and protein markers Interpretation of the various cardiac enzymes has now largely been superceded by the Introduction of troponin T and I. Questions still however commonly appear in exams. Key points for the exam ‘* myoglobin is the first to rise ‘* CK-MB Is useful to look for reinfarction as it returns to normal after 2-3 days {troponin T remains elevated for up to 10 days) Myoglobin CK-MB cK TropT LDH Begins to rise 1-2 hours. 2-6 hours 4-8 hours 4-6 hours 12-24 hours 24-48 hours sak value 6-8 hours 16-20 hours 16-24 hours 12-24 hours 36-48 hours 72 hours Returns to normal 1-2 days 2-8 days 3-4 days 7-10 days 3-4 days 8-10 daysNosim = ea PM n= < nH & passmedicine.com HSoOort a General Mecical Council | Lab Values, Normal Au: B-type natriuretic peptide B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain, ‘Whilst heart failure is the most obvious cause of raised BNP levels any cause of left ventricular ‘dysfunction such as myocardial ischaemia or valvular disease may raise levels. Raised levels may also be seen due to reduced excretion in patients with chronic kidney disease. Factors ‘which reduce BNP levels include treatment with ACE inhibitors, angiotensin-2 receptor blockers and diuretics. Effects of BNP = vasodilator ‘© dluretic and natriuretic ‘+ suppresses both sympathetic tone and the renin-angiotensin-aldosterone system Clinical uses of BNP Diagnosing patients with acute dyspnoea ‘+ alow concentration of BNP(« 100pg/mi) makes a ciagnosis of heart fallure unlikely, but raised levels should prompt further investigation to confirm the diagnosis: ‘© NICE currently recommends BNP as a helpful test to rule out a diagn of heart failure Prognosis in patients with chronic heart failure «* inital evidence suggests BNP is an extremely useful marker of prognosis Guiding treatment in patients with chronic heart failure ‘+ cffective treatment lowers BNP levels Screening for cardiac dysfunction ‘+ not currently recommended for population screening,Nosim = + < iu 1250 AM &@ passmedicine.com el (Ganeral Mecical Council | Lab Values, Normal Ad: a= Oot © Questions Pulmonary capillary wedge pressure Pulmonary capillary wedge pressure (PCWP) is measured using a balloon tipped Swan-Ganz ‘catheter which is inserted into the pulmonary artery. The pressure measured is similar to that of the left atrium (normally 6-12 mmHg). One of the main uses of measuring the PCWP is determining whether pulmonary oedema is ‘caused by either heart failure or acute respiratory distress syndrome, In many modern ITU departments PCWP measurement has been replaced by non-invasive techniques. © Save my notes ‘SearchNosim = #: 028 AM = < nh & passmedicine.com Boot a General Mecical Council | Lab Values, Normal Au: Qeestions Cardiac imaging: non-invasive techniques excluding echocardiography ‘The ability to image the heart using non-invasive techniques such as MRI, CT and radionuclides has evolved rapidly over recent years. Nuclear imaging ‘These techniques use radiotracers which are extracted by normal myocardium. Examples Include: © thallium ‘+ technetium @9mTe) sestamibi: a coordination complex of the radioisotope technetium: 99m with the ligand methoxyisobutylisonitile (MIB), used in 'MIBI' or cardiac Single Photon Emission Computed Tomography (SPECT) scans ++ fluorodeoxyglucose (FDG): used in Positron Emission Tomography (PET) scans ‘The primary role of SPECT is to assess myocardial perfusion and myocardial viability. Two sets of images are usually acquired. First the myocardium at rest followed by images of the myocardium during stress (either exercise or following adenosine / dipyridamole). By comparing the rest with stress images any areas of ischaemia can classified as reversible or fixed (2.9. Following a myocardial infarction). Cardiac PET is predominately a research tool at the current time MUGA, ‘+ Multi Gated Acquisition Scan, also known as radionuclide angiography ‘# radionuclide (technetium-99m) is injected intravenously ‘+ the patient is placed under a gamma camera ‘+ may be performed as a stress test ‘+ can accurately measure left ventricular ejection fraction. Typically used before and after cardictoxic drugs are used Cardiac Computed Tomography (CT) Cardiac CT is useful for assessing suspected ischaemic heart disease, using two main methods: ‘+ calcium score: there is known to be a correlation between the amount of atherosclerotic pplaque calcium and the risk of future ischaemic events. Cardiac GT ean quantify theNosim = *: 028 AM = < fu & passmedicine.com Ongar eee eel General Mecical Council | Lab Values, Normal Au: Qeestions cardiotoxic drugs are used Cardiac Computed Tomography (CT) Cardiac CT is useful for assessing suspected ischaemic heart disease, using two main methods: ‘+ calcium score: there is known to be a correlation between the amount of atherosclerotic plaque calcium and the risk of future ischaemic events. Cardiac CT can quantify the ‘amount of calcium producing a ‘calcium score’ ‘+ contrast enhanced CT: allows visualisation of the coronary artery lumen Hf these two techniques are combined cardiac CT has a very high negative predictive value for Ischaemic heart disease, Cardiac MRI Cardiac MRI (commonly termed CMR) has become the gold standard for providing structural images of the heart. It is particularly useful when assessing congenital heart disease, atermining right and lett ventricular mass and differentiating farms of cardiomyopathy. Myocardial perfusion can also be assessed following the administration of gadolinium, Currently CMR provides limited data on the extent of coronary artery disease. Please also see the British Heart Foundiation link for an excellent summary.Nosim = 0:90 AM a < fh & passmedicine.com aoOort ey General Mecical Council | Lab Values, Nocmal Aut: Qeestions Reduction in intrathoracic pressure Valsalva manoeuvre ‘The Valsalva manoeuvre describes a forced expiration against a closed glottis. This leads to increased intrathoracic pressure which in turn has a number of effects on the cardiovascular system. Uses ‘* to terminate an episode of supraventricular tachycardia, ‘+ normalizing middle-ear pressures: Stages of the Valsalva manoeuvre ‘+ 1. Increased intrathoracic pressure ‘+ 2, Resultant increase in venous and right atrial pressure reduces venous return ‘+ 3. The reduced preload leads to a fallin the cardiac output (Frank-Starling mechanism) ‘+4. When the pressure is released there is a further slight fall in cardiac output due to Increased aortic volume ‘+5, Return of normal cardiac outputNosim = 145 PM < th @ passmedicine.com Confdanialty-GMC | Ethical and legal dui of.. | Lab Vals, Normal Adu Pulmonary embolism: management ‘The NICE guidelines of 2012 provided some clarity on how long patients should be anticoagulated for after a pulmonary embolism (PE). Selected points are listed below. Low molecular weight heparin (LMWH) or fondaparinux should be given intially after a PE is diagnosed. An exception to this is for patients with a massive PE where thrombolysis is being considered. In such a situation unfractionated heparin should be used, + avitamin K antagonist (.<. warfarin) should be given within 24 hours of the diagnosis ‘¢ the LMWH or fondaparinux should be continued for at least 5 days or until the international normalised ratio (INR) is 2.0 or above for at least 24 hours, whichever is longer, i.e. LMWH. co fondaparinux is given at the same time as warfarin unti the INR is in the therapeutic range ‘* warfarin should be continued for at least 3 months. At 3 months, NICE advise that linicians should ‘assess the risks and benefits of extending treatment’ ‘+ NICE advise extending warfarin beyond 3 months for patients with unprovoked PE. This essentially means that if there was no obvious cause or provoking factor (surgery, trauma, significant immobility) it may imply the patient has a tendency to thrombosis and should be given treatment longer than the norm of $ months, ‘+ for patients with active cancer NICE recommend using LMWH for 6 months Thrombolysis ‘+ thrombolysis is now recommended as the first-line treatment for massive PE where there is, circulatory failure (e.g. hypotension). Other invasive approaches should be considered Where appropriate facilties existNos = yea PM eo < hy @ passmedicine.com eOodt Passmedicine ar (General Mecfcal Counc! | Lab Values, Normal Ad Adenosine ‘The effects of adenosine are enhanced by dipyridamole (arti-platelet agent) and blocked by theophylines. it should 'be avoided in asthmatios due to possible bronchospasm. ‘Mechanism of action ‘+ causes transient haart block in the AV node ‘¢ agonist of the At receptor which inhibits adenylyl oyclase thus reducing cAMP and causing hyperpolarization by increasing outward potassium flux ‘+ adenosine has a very short hal-lfe of about 8-10 seconds '¢ bronchospasm ‘+ can enhance conduction down accessory pathways, resulting in increased ventricular rate (.g. WW syndrome) Bee oT 8 2% Save my notesNo sim = sox AM om < ri @ passmedicine.com @emgoaort+ Passmedicine ar (General Mecfcal Council | Lab Values, Normal Ad Amiodarone Amiodarone is a class Ill antiarhythmic agent used inthe treatment of stra, nodal and ventricular tachyearhas. ‘The main mechanism of action is by blocking potassium channels which inhibits repolaisetion and henee prolongs tho action potential, Amiodarone alse has other actions euch as blocking sodium channels (a clase | effect) ‘The use of amiodarone is limited by a number of factors ‘ong hat-ife (20-100 days) ‘* should ideally be given into central veins (causes thrombophlebitis) ‘+ has proarthythmie effects due to lengthening of the QT interval «interacts with drugs commonly used concurrent e.g. Decreases metabolism of warfarin ‘+ numerous long-term adverse effects (sa= below) Monitoring of patients taking amiodarone ‘¢ TFT, LFT, UBE, CXR prior to troatment (© TFT, LET every 6 months Adverse effects of amiodarone use “+ thyroid dysfunction '¢ comeal deposits ‘© pulmonary fbrosis/pnoumorits + liver fibrosisihepatiis ‘peripheral newopathy, myopathy ‘+ photosensitivity ‘ ‘slate-grey’ anpearance ‘+ thrombophlebitis and injection cite reactions: 1+ bradycardia BIoUs $ A+ Se @ ee Te ae a 8 Save my notesNo sim = wear M, 24465 < ri & passmedicine.com SMO ad+ Warfarin: management of high INR ‘The following is based on the EINF guidelines, which in tum take into account the British ‘Committee for Standards in Haematology (ECSH) guidelines, A 2005 update of the BCSH guidolins emphasised tho preference of prothrombin commplax concontrato over FFP in ‘major bleeding, Situation Management Major Stop warfarin bleeding Give intravenous vitamin K mg Prothrombin complex concontrato- f not available thon FFP* Stop warfarin Give intravenous vitamin K 1-mg Repeat dose of vitamin K ifINF stil too high after 24 hours Restart warfarin when INR < 5.0 Stop warfarin Give vitamin K 1-5mg by mouth, using the intravencus preparation rally Repeat dose of vitamin K if INF stil too high after 24 hours ostart when INF < 5.0 INR6.0-8.0 Stop warfarin Give intravenous vitamin K 1-8mg Restart when INR < 5.0 INR5.0-8.0 —_Withhold 1 oF 2 doses of warfarin No ble Roduce subsoquent maintenanco dose ‘as FFP can take tine ta defrost prothrombin complex concentrate should be considaree In cases of intracranial haemorrhage Save my notesNo sim = osc aM nD th @ passmedicine.com eO ort Warfarin Warfarin an oral anticoagulant which inhibits the tection of vitamin K to is active hydroquinone form, which in turn acts as a cofactor inthe carboxylation of clotting factor 1, Vl, and x (mnemonic = 1972} and protein C. Indications venous thromboembolism: target INR = 2.5, recurrent 3.5 atrial fbilation. target INF = 2.6 ‘mechanical hart valves, target INR dopends on the valve type and location. Mitral valves generally require a higher INR than aortic valves. Patients on warterin are monitored using the INR international narmalised cation), the ratio fof the prothrombin time forthe patient over the normal prottvombia time. Warfarin has a long half-ife and achieving a stable INF may take several days. There a variety of loading regimes and computer software is now often used to alter the dose. Factors that may potentiate warfarin * Iver disease ‘+ 450 enzyme inhibitors, e.g. amiodarone, ciprofloxacin cranberry juice Crags which displace warfarin from plasma albumin, @.g. NSAIDS Inhibit platelet function: NSAIDS Side-effecto haomonhage teratogenic, although can be used in breast-feeding mothers ‘kin necrosis: when warfarin is frst started biosynthesis of protein © is rcuced ‘This results in a temporary procoagulant state ater intially starting warfarin, rnoxmally avoided by concurrent hoparin administration. Thrombosis may occur in venules leading to skin necrosis purple toes, Save my natesNosim = 2:00 PM ae < nH & passmedicine.com BOodst Confdentilty-GMC | Ethical and loga dios Lab Values, Normal Adult... | @ Questions Dabigatran Dabigatcan is an oral anticoagulant that works by being a direct thrombin inhibitor. It is one of the drugs developed over the past 10-15 years as an alternative to warfarin, with the advantage that it does not require regular monitoring, ‘What is dabigatran used for? Dabigatcan is currently used for two main indications. Firstly it is an option in the prophylaxis of venous thromboembolism following hip or knee replacement surgery Secondly i is also licensed in the UK for prevention of stroke in patients with non-valvular atrial {ibzilation who have one or more of the following risk factors present: ‘+ previous stroke, transient ischaemic attack or systemic embolism ‘+ [oft ventricular ejection fraction below 40% ‘+ symptomatic heart failure of New York Heart Association (NYHA) class 2 or above 1+ age 75 years or olcer '* age 65 years or older with one of the following: diabetes mellitus, coronary artery disease or hypertension What are the known side-effects of dabigatran? Unsurprisingly haemorthage is the major adverse effect, Doses should be reduced in chronic kidney disease and dabigatran should not be prescribed if ‘the creatinine clearance is < 30 ml/min Drug Safety Update 2013 ‘The RE-ALIGN study showed significantly higher bleeding and thrambotic events in patients with recent mechanical heart valve replacement using dabigatran compared with warfarin. Previously there had been no guidance to support the use of dabigatran in patients with prosthetic heart valves but the advice has now changed to dabigatran being contraindicated in such patients.