cardiology Flashcards

Question

Causes of a prolonged QT interval

Answer 1

Congenital Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel) Romano-Ward syndrome (no deafness) Drugs ``` amiodarone, sotalol, class 1a antiarrhythmic drugs tricyclic antidepressants, fluoxetine chloroquine terfenadine erythromycin ``` Other ``` electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia acute myocardial infarction myocarditis hypothermia subarachnoid haemorrhage ```

Answer 2

If the patient has adverse signs (systolic BP < 90 mmHg, chest pain, heart failure or rate > 150 beats/min) then immediate cardioversion is indicated. In the absence of such signs antiarrhythmics may be used. If these fail, then electrical cardioversion may be needed with synchronised DC shocks Drug therapy amiodarone: ideally administered through a central line lidocaine: use with caution in severe left ventricular impairment procainamide Verapamil should NOT be used in VT If drug therapy fails: ``` electrophysiological study (EPS) implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function ```

Answer 3

Agents used to control rate in patients with atrial fibrillation beta-blockers calcium channel blockers digoxin (not considered first-line anymore as they are less effective at controlling the heart rate during exercise. However, they are the preferred choice if the patient has coexistent heart failure) Agents used to maintain sinus rhythm in patients with a history of atrial fibrillation sotalol amiodarone flecainide others (less commonly used in UK): disopyramide, dofetilide, procainamide, propafenone, quinidine The table below indicates some of the factors which may be considered when considering either a rate control or rhythm control strategy: Factors favouring rate control: Older than 65 years History of ischaemic heart disease Factors favouring rhythm control: ``` Younger than 65 years Symptomatic First presentation Lone AF or AF secondary to a corrected precipitant (e.g. Alcohol) Congestive heart failure ```

Answer 4

Lifestyle advice should not be forgotten and is frequently tested in exams: a low salt diet is recommended, aiming for less than 6g/day, ideally 3g/day. The average adult in the UK consumes around 8-12g/day of salt. A recent BMJ paper* showed that lowering salt intake can have a significant effect on blood pressure. For example, reducing salt intake by 6g/day can lower systolic blood pressure by 10mmHg caffeine intake should be reduced the other general bits of advice remain: stop smoking, drink less alcohol, eat a balanced diet rich in fruit and vegetables, exercise more, lose weight ABPM/HBPM >= 135/85 mmHg (i.e. stage 1 hypertension) treat if < 80 years of age AND any of the following apply; target organ damage, established cardiovascular disease, renal disease, diabetes or a 10-year cardiovascular risk equivalent to 20% or greater ABPM/HBPM >= 150/95 mmHg (i.e. stage 2 hypertension) offer drug treatment regardless of age For patients < 40 years consider specialist referral to exclude secondary causes. Step 1 treatment: patients < 55-years-old: ACE inhibitor (A) patients > 55-years-old or of Afro-Caribbean origin: calcium channel blocker Step 2 treatment: ACE inhibitor + calcium channel blocker (A + C) Step 3 treatment: add a thiazide diuretic (D, i.e. A + C + D) NICE now advocate using either chlorthalidone (12.5-25.0 mg once daily) or indapamide (1.5 mg modified-release once daily or 2.5 mg once daily) in preference to a conventional thiazide diuretic such as bendroflumethiazide NICE define a clinic BP >= 140/90 mmHg after step 3 treatment with optimal or best tolerated doses as resistant hypertension. They suggest step 4 treatment or seeking expert advice Step 4 treatment: consider further diuretic treatment if potassium < 4.5 mmol/l add spironolactone 25mg od if potassium > 4.5 mmol/l add higher-dose thiazide-like diuretic treatment if further diuretic therapy is not tolerated, or is contraindicated or ineffective, consider an alpha- or beta-blocker Patients who fail to respond to step 4 measures should be referred to a specialist. NICE recommend: If blood pressure remains uncontrolled with the optimal or maximum tolerated doses of four drugs, seek expert advice if it has not yet been obtained. New drugs Direct renin inhibitors e.g. Aliskiren (branded as Rasilez) by inhibiting renin blocks the conversion of angiotensinogen to angiotensin I no trials have looked at mortality data yet. Trials have only investigated fall in blood pressure. Initial trials suggest aliskiren reduces blood pressure to a similar extent as angiotensin converting enzyme (ACE) inhibitors or angiotensin-II receptor antagonists adverse effects were uncommon in trials although diarrhoea was occasionally seen only current role would seem to be in patients who are intolerant of more established antihypertensive drugs

Answer 5

Clinic BP: Age < 80 years 140/90 mmHg Age > 80 years 150/90 mmHg ABPM / HBPM Age < 80 years 135/85 mmHg Age > 80 years 145/85 mmHg

Answer 6

The first heart sound (S1) is caused by closure of the mitral and tricuspid valves whilst the second heart sound (S2) is due to aortic and pulmonary valve closure

Answer 7

S1 closure of mitral and tricuspid valves soft if long PR or mitral regurgitation loud in mitral stenosis

Answer 8

S2 closure of aortic and pulmonary valves soft in aortic stenosis splitting during inspiration is normal

Answer 9

S3 (third heart sound) caused by diastolic filling of the ventricle considered normal if < 30 years old (may persist in women up to 50 years old) heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock)

Answer 10

S4 (fourth heart sound) may be heard in aortic stenosis, HOCM, hypertension caused by atrial contraction against a stiff ventricle in HOCM a double apical impulse may be felt as a result of a palpable S4

Answer 11

Whilst strictly speaking the term supraventricular tachycardia (SVT) refers to any tachycardia that is not ventricular in origin the term is generally used in the context of paroxysmal SVT. Episodes are characterised by the sudden onset of a narrow complex tachycardia, typically an atrioventricular nodal re-entry tachycardia (AVNRT). Other causes include atrioventricular re-entry tachycardias (AVRT) and junctional tachycardias.

Answer 12

Acute management vagal manoeuvres: e.g. Valsalva manoeuvre (The Valsalva maneuver or Valsalva manoeuvre is performed by moderately forceful attempted exhalation against a closed airway, usually done by closing one's mouth, pinching one's nose shut while pressing out as if blowing up a balloon.) intravenous adenosine 6mg → 12mg → 12mg: contraindicated in asthmatics - verapamil is a preferable option electrical cardioversion

Answer 13

Prevention of episodes beta-blockers radio-frequency ablation

Answer 14

These guidelines reiterate the need to offer primary PCI to patients who present within 12 hours of onset of symptoms, if it can be delivered within 120 minutes of the time when fibrinolysis could have been given. A practical example may be a patient who presents with a STEMI to a small district general hospital (DGH) which does not have facilities for PCI. If they cannot be transferred to a larger hospital for PCI within 120 minutes then fibrinolysis should be given. If the patient's ECG taken 90 minutes after fibrinolysis failed to show resolution of the ST elevation then they would then require transfer for PCI. Management of STEMI The 2008 British Thoracic Society oxygen therapy guidelines have now been widely adopted and oxygen should only be given if the oxygen saturations are < 94% Sublingual glyceryl trinitrate and intravenous morphine + metoclopramide should be given to help relieve the symptoms. Aspirin 300mg should be given to all patients (unless contraindicated). Following these initial steps there is a large amount of variation in practice in terms of which other medications are given prior to PCI. A second antiplatelet is normally given, usually ticagrelor, clopidogrel or prasurgel (all are antagonists of the P2Y12 adenosine diphosphate receptor). Other treatments that may be given include bivalirudin (a direct thrombin inhibitor, usually given alongside aspirin + clopidogrel) and a form of heparin (either low-molecular weight or unfractionated). → cath lab for primary PCI

Answer 15

One of the most common ways to remember the difference between LBBB and RBBB is WiLLiaM MaRRoW in LBBB there is a 'W' in V1 and a 'M' in V6 in RBBB there is a 'M' in V1 and a 'W' in V6

Answer 16

Causes of RBBB normal variant - more common with increasing age right ventricular hypertrophy chronically increased right ventricular pressure - e.g. cor pulmonale pulmonary embolism myocardial infarction atrial septal defect cardiomyopathy or myocarditis

Answer 17

55-120 umol/l

Answer 18

2.0-7 mmol/l

Answer 19

Acute myocardial infarction (MI) hyperacute T waves are often the first sign of MI but often only persists for a few minutes ST elevation may then develop the T waves typically become inverted within the first 24 hours. The inversion of the T waves can last for days to months pathological Q waves develop after several hours to days. This change usually persists indefinitely

Answer 20

new ST elevation at the J-point in two contiguous leads with the cut-off points: >=0.2 mV in men or >= 0.15 mV in women in leads V2-V3 and/or >= 0.1 mV in other leads

Answer 21

Atrial flutter is a form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves.

Answer 22

ECG findings 'sawtooth' appearance as the underlying atrial rate is often around 300/min the ventricular or heart rate is dependent on the degree of AV block. For example if there is 2:1 block the ventricular rate will be 150/min flutter waves may be visible following carotid sinus massage or adenosine

Answer 23

Management is similar to that of atrial fibrillation although mediction may be less effective atrial flutter is more sensitive to cardioversion however so lower energy levels may be used radiofrequency ablation of the tricuspid valve isthmus is curative for most patients

Answer 24

Anteroseptal - V1-V4 - Left anterior descending Inferior - II, III, aVF - Right coronary Anterolateral - V4-6, I, aVL - Left anterior descending or left circumflex Lateral - I, aVL +/- V5-6 - Left circumflex Posterior - Tall R waves V1-2 - Usually left circumflex, also right coronary

Answer 25

NICE produced guidelines in 2013 on the Secondary prevention in primary and secondary care for patients following a myocardial infarction management of unstable angina and non-ST elevation myocardial infarction (NSTEMI). These superceded the 2010 guidelines which advocated a risk-based approach to management which determined whether drugs such as clopidogrel were given. All patients should receive aspirin 300mg nitrates or morphine to relieve chest pain if required advise not giving oxygen unless the patient is hypoxic. Antithrombin treatment. Fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography within the next 24 hours. If angiography is likely within 24 hours or a patients creatinine is > 265 µmol/l unfractionated heparin should be given. Clopidogrel 300mg should be given to all patients and continued for 12 months. Intravenous glycoprotein IIb/IIIa receptor antagonists (eptifibatide or tirofiban) should be given to patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%), and who are scheduled to undergo angiography within 96 hours of hospital admission. Coronary angiography should be considered within 96 hours of first admission to hospital to patients who have a predicted 6-month mortality above 3.0%. It should also be performed as soon as possible in patients who are clinically unstable.

Answer 26

Antiplatelet - inhibits the production of thromboxane A2

Answer 27

Antiplatelet - inhibits ADP binding to its platelet receptor

Answer 28

Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa

Answer 29

Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa

Answer 30

Reversible direct thrombin inhibitor

Answer 31

hypertension - can drive unless treatment causes unacceptable side effects, no need to notify DVLA. If Group 2 Entitlement the disqualifies from driving if resting BP consistently 180 mmHg systolic or more and/or 100 mm Hg diastolic or more

Answer 32

angioplasty (elective) - 1 week off driving

Answer 33

CABG - 4 weeks off driving

Answer 34

acute coronary syndrome- 4 weeks off driving, 1 week if successfully treated by angioplasty

Answer 35

angina - driving must cease if symptoms occur at rest/at the wheel

Answer 36

pacemaker insertion - 1 week off driving

Answer 37

implantable cardioverter-defibrillator: if implanted for sustained ventricular arrhythmia: cease driving for 6 months. If implanted prophylatically then cease driving for 1 month

Answer 38

successful catheter ablation for an arrhythmia- 2 days off driving

Answer 39

aortic aneurysm of 6cm or more - notify DVLA. Licensing will be permitted subject to annual review. An aortic diameter of 6.5 cm or more disqualifies patients from driving

Answer 40

heart transplant: DVLA do not need to be notified

Answer 41

It is thought that between 5-10% of patients diagnosed with hypertension have primary hyperaldosteronism, including Conn's syndrome. This makes it the single most common cause of secondary hypertension.

Answer 42

Renal disease accounts for a large percentage of the other cases of secondary hypertension. Conditions which may increase the blood pressure include: glomerulonephritis pyelonephritis adult polycystic kidney disease renal artery stenosis

Answer 43

``` phaeochromocytoma Cushing's syndrome Liddle's syndrome congenital adrenal hyperplasia (11-beta hydroxylase deficiency) acromegaly ```

Answer 44

Other causes include: ``` NSAIDs pregnancy coarctation of the aorta the combined oral contraceptive pill steroids MAOI ```

Answer 45

Pericarditis is one of the differentials of any patient presenting with chest pain. Features chest pain: may be pleuritic. Is often relieved by sitting forwards other symptoms include non-productive cough, dyspnoea and flu-like symptoms pericardial rub tachypnoea tachycardia

Answer 46

Causes viral infections (Coxsackie) tuberculosis uraemia (causes 'fibrinous' pericarditis) trauma post-myocardial infarction, Dressler's syndrome connective tissue disease hypothyroidism

Answer 47

ECG changes widespread 'saddle-shaped' ST elevation PR depression: most specific ECG marker for pericarditis A modest rise in troponin is also seen in around one-third of patients with acute pericarditis. The widespread nature of the accompanying ECG changes (across coronary territories) points away from an ischaemic cause though.

Answer 48

Features of severe aortic stenosis ``` narrow pulse pressure slow rising pulse delayed ESM soft/absent S2 S4 thrill duration of murmur left ventricular hypertrophy or failure ```

Answer 49

Causes of aortic stenosis degenerative calcification (most common cause in older patients > 65 years) bicuspid aortic valve (most common cause in younger patients < 65 years) William's syndrome (supravalvular aortic stenosis) post-rheumatic disease subvalvular: HOCM

Answer 50

Management if asymptomatic then observe the patient is general rule if symptomatic then valve replacement if asymptomatic but valvular gradient > 50 mmHg and with features such as left ventricular systolic dysfunction then consider surgery balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement

Answer 51

Torsades de pointes ('twisting of the points') is a rare arrhythmia associated with a long QT interval. It may deteriorate into ventricular fibrillation and hence lead to sudden death

Answer 52

Causes of long QT interval congenital: Jervell-Lange-Nielsen syndrome, Romano-Ward syndrome antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs tricyclic antidepressants antipsychotics chloroquine terfenadine erythromycin electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia myocarditis hypothermia subarachnoid haemorrhage

Answer 53

IV magnesium sulphate

Answer 54

Hypertrophic obstructive cardiomyopathy (HOCM) is an autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins. The most common defects involve a mutation in the gene encoding β-myosin heavy chain protein or myosin binding protein C. The estimated prevalence is 1 in 500.

Answer 55

Hypertrophic obstructive cardiomyopathy (HOCM) is an autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins. The most common defects involve a mutation in the gene encoding β-myosin heavy chain protein or myosin binding protein C. The estimated prevalence is 1 in 500. Features often asymptomatic dyspnoea, angina, syncope sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure jerky pulse, large 'a' waves, double apex beat ejection systolic murmur: increases with Valsalva manoeuvre and decreases on squatting Associations Friedreich's ataxia Wolff-Parkinson White Echo - mnemonic - MR SAM ASH mitral regurgitation (MR) systolic anterior motion (SAM) of the anterior mitral valve leaflet asymmetric hypertrophy (ASH) ``` ECG left ventricular hypertrophy progressive T wave inversion deep Q waves atrial fibrillation may occasionally be seen ```

Answer 56

ECG left ventricular hypertrophy progressive T wave inversion deep Q waves atrial fibrillation may occasionally be seen

Answer 57

NICE issued updated guidelines on diagnosis and management in 2010. The choice of investigation is determined by whether the patient has previously had a myocardial infarction or not. Previous myocardial infarction arrange echocardiogram within 2 weeks No previous myocardial infarction measure serum natriuretic peptides (BNP) if levels are 'high' arrange echocardiogram within 2 weeks if levels are 'raised' arrange echocardiogram within 6 weeks

Answer 58

B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain. Very high levels are associated with a poor prognosis in heart failure

Answer 59

Normal levels < 100 pg/ml (29 pmol/litre) Raised levels 100-400 pg/ml (29-116 pmol/litre) High levels > 400 pg/ml (116 pmol/litre)

Answer 60

``` Left ventricular hypertrophy Ischaemia Tachycardia Right ventricular overload Hypoxaemia (including pulmonary embolism) GFR < 60 ml/min Sepsis COPD Diabetes Age > 70 Liver cirrhosis ```

Answer 61

``` Obesity Diuretics ACE inhibitors Beta-blockers Angiotensin 2 receptor blockers Aldosterone antagonists ```

Answer 62

In the absence of contraindications, all patients should be given aspirin clopidogrel: the two major studies (CLARITY and COMMIT) both confirmed benefit but used different loading doses (300mg and 75mg respectively) low molecular weight heparin

Answer 63

NICE suggest the following in terms of oxygen therapy: do not routinely administer oxygen, but monitor oxygen saturation using pulse oximetry as soon as possible, ideally before hospital admission. Only offer supplemental oxygen to: people with oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic respiratory failure, aiming for SpO2 of 94-98% people with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to achieve a target SpO2 of 88-92% until blood gas analysis is available.

Answer 64

Primary percutaneous coronary intervention (PCI) has emerged as the gold-standard treatment for STEMI but is not available in all centres. Thrombolysis should be performed in patients without access to primary PCI With regards to thrombolysis: tissue plasminogen activator (tPA) has been shown to offer clear mortality benefits over streptokinase tenecteplase is easier to administer and has been shown to have non-inferior efficacy to alteplase with a similar adverse effect profile An ECG should be performed 90 minutes following thrombolysis to assess whether there has been a greater than 50% resolution in the ST elevation if there has not been adequate resolution then rescue PCI is superior to repeat thrombolysis for patients successfully treated with thrombolysis PCI has been shown to be beneficial. The optimal timing of this is still under investigation

Answer 65

Glycaemic control in patients with diabetes mellitus in 2011 NICE issued guidance on the management of hyperglycaemia in acute coronary syndromes it recommends using a dose-adjusted insulin infusion with regular monitoring of blood glucose levels to glucose below 11.0 mmol/l intensive insulin therapy (an intravenous infusion of insulin and glucose with or without potassium, sometimes referred to as 'DIGAMI') regimes are not recommended routinely

Answer 66

Onset < 48 hours If the atrial fibrillation (AF) is definitely of less than 48 hours onset patients should be heparinised. Patients who have risk factors for ischaemic stroke should be put on lifelong oral anticoagulation. Otherwise, patients may be cardioverted using either: electrical - 'DC cardioversion' pharmacology - amiodarone if structural heart disease, flecainide in those without structural heart disease Following electrical cardioversion if AF is confirmed as being less than 48 hours duration then further anticoagulation is unnecessary Onset > 48 hours If the patient has been in AF for more than 48 hours then anticoagulation should be given for at least 3 weeks prior to cardioversion. An alternative strategy is to perform a transoesophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus. If excluded patients may be heparinised and cardioverted immediately. If there is a high risk of cardioversion failure (e.g. Previous failure or AF recurrence) then it is recommend to have at least 4 weeks amiodarone or sotalol prior to electrical cardioversion Following electrical cardioversion patients should be anticoagulated for at least 4 weeks. After this time decisions about anticoagulation should be taken on an individual basis depending on the risk of recurrence

Answer 67

Overview acyanotic congenital heart defect connection between the pulmonary trunk and descending aorta more common in premature babies, born at high altitude or maternal rubella infection in the first trimester

Answer 68

Features ``` left subclavicular thrill continuous 'machinery' murmur large volume, bounding, collapsing pulse wide pulse pressure heaving apex beat ```

Answer 69

Management indomethacin closes the connection in the majority of cases if associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repair

Answer 70

glyceryl trinitrate aspirin 300mg. NICE do not recommend giving other antiplatelet agents (i.e. Clopidogrel) outside of hospital do not routinely give oxygen, only give if sats < 94%* perform an ECG as soon as possible but do not delay transfer to hospital. A normal ECG does not exclude ACS

Answer 71

Referral current chest pain or chest pain in the last 12 hours with an abnormal ECG: emergency admission chest pain 12-72 hours ago: refer to hospital the same-day for assessment chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement before deciding upon further action

Answer 72

1. constricting discomfort in the front of the chest, neck, shoulders, jaw or arms 2. precipitated by physical exertion 3. relieved by rest or GTN in about 5 minutes patients with all 3 features have typical angina patients with 2 of the above features have atypical angina patients with 1 or none of the above features have non-anginal chest pain

Answer 73

first estimate the likelihood of CAD in order to choose the appropriate diagnostic test. The risk tables are not reproduced here but can be found online via NICE. If patients have typical anginal symptoms and a risk of CAD is greater than 90% then no further diagnostic testing is required. It should be noted that all men over the age of 70 years who have typical anginal symptoms fall into this category. For patients with an estimated risk of 10-90% the following investigations are recommended. Note the absence of the exercise tolerance test: 61-90% - Coronary angiography 30-60% - Functional imaging, for example: myocardial perfusion scan with SPECT stress echocardiography first-pass contrast-enhanced magnetic resonance (MR) perfusion MR imaging for stress-induced wall motion abnormalities. 10-29% CT calcium scoring the risk of a patient having coronary artery disease (CAD) is calculated based on their symptoms (whether they have typical angina, atypical angina or non-anginal chest pain), age, gender and risk factors. USE THE GRACE SCORING SYSTEM the table is called = Percentage of people estimated to have coronary artery disease according to typicality of symptoms, age, sex and risk factors. stratifies by description of pain e.g. typical atypical non-angina, then by gender then by age then by presence of risk factors to give a percentage risk.

Answer 74

Pre-eclampsia is a condition seen after 20 weeks gestation characterised by pregnancy-induced hypertension in association with proteinuria (> 0.3g / 24 hours). Oedema used to be third element of the classic triad but is now often not included in the definition as it is not specific Pregnancy-induced hypertension in association with proteinuria (> 0.3g / 24 hours) Oedema may occur but is now less commonly used as a criteria Occurs in around 5% of pregnancies

Answer 75

Pre-eclampsia is important as it predisposes to the following problems fetal: prematurity, intrauterine growth retardation eclampsia haemorrhage: placental abruption, intra-abdominal, intra-cerebral cardiac failure multi-organ failure

Answer 76

Risk factors ``` > 40 years old nulliparity (or new partner) multiple pregnancy body mass index > 30 kg/m^2 diabetes mellitus pregnancy interval of more than 10 years family history of pre-eclampsia previous history of pre-eclampsia pre-existing vascular disease such as hypertension or renal disease ```

Answer 77

Features of severe pre-eclampsia hypertension: typically > 170/110 mmHg and proteinuria as above proteinuria: dipstick ++/+++ headache visual disturbance papilloedema RUQ/epigastric pain hyperreflexia platelet count < 100 * 106/l, abnormal liver enzymes or HELLP syndrome

Answer 78

Management consensus guidelines recommend treating blood pressure > 160/110 mmHg although many clinicians have a lower threshold oral labetalol is now first-line following the 2010 NICE guidelines. Nifedipine and hydralazine may also be used delivery of the baby is the most important and definitive management step. The timing depends on the individual clinical scenario

Answer 79

Features ``` syncope heart failure regular bradycardia (30-50 bpm) wide pulse pressure JVP: cannon waves in neck variable intensity of S1 ```

Answer 80

First degree heart block PR interval > 0.2 seconds

Answer 81

Second degree heart block type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex

Answer 82

Third degree (complete) heart block there is no association between the P waves and QRS complexes

Answer 83

Overdose of tricyclic antidepressants is a common presentation to emergency departments. Amitriptyline and dosulepin (dothiepin) are particularly dangerous in overdose. Early features relate to anticholinergic properties: dry mouth, dilated pupils, agitation, sinus tachycardia, blurred vision. ``` Features of severe poisoning include: arrhythmias seizures metabolic acidosis coma ``` ECG changes include: sinus tachycardia widening of QRS prolongation of QT interval Widening of QRS > 100ms is associated with an increased risk of seizures whilst QRS > 160ms is associated with ventricular arrhythmias

Answer 84

Management IV bicarbonate may reduce the risk of seizures and arrhythmias in severe toxicity arrhythmias: class 1a (e.g. Quinidine) and class Ic antiarrhythmics (e.g. Flecainide) are contraindicated as they prolong depolarisation. Class III drugs such as amiodarone should also be avoided as they prolong the QT interval. Response to lignocaine is variable and it should be emphasized that correction of acidosis is the first line in management of tricyclic induced arrhythmias dialysis is ineffective in removing tricyclics

Answer 85

Pacing spikes can be seen before the widened QRS complex, most clearly in V3-V6. The widened QRS complex means that ventricles are paced rather than the atria. Ventricular pacing tends to be on the right side giving the left bundle branch block like waveform seen here.

Answer 86

Pacemaker: permanent Indications for permanent pacemaker (PPM) insertion include: persistent symptomatic bradycardia e.g. sick sinus syndome complete heart block Mobitz type II AV block persistent AV block after myocardial infarction

Answer 87

Patients with bilateral renovascular disease (e.g. renal artery stenosis) may develop an acute kidney injury (AKI) if ACE inhibitors are administered. This is because elevated angiotensin II levels constrict the efferent arteriole more than the afferent arteriole within the kidney, which normally helps to maintain glomerular capillary pressure and filtration. Removing this constriction by blocking angiotensin II formation can cause an abrupt fall in glomerular filtration rate.

Answer 88

Side-effects: cough: occurs in around 15% of patients and may occur up to a year after starting treatment. Thought to be due to increased bradykinin levels angioedema: may occur up to a year after starting treatment hyperkalaemia first-dose hypotension: more common in patients taking diuretics also AKI

Answer 89

Cautions and contraindications pregnancy and breastfeeding - avoid renovascular disease - significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis aortic stenosis - may result in hypotension patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day) - significantly increases the risk of hypotension hereditary of idiopathic angioedema

Answer 90

Monitoring urea and electrolytes should be checked before treatment is initiated and after increasing the dose a rise in the creatinine and potassium may be expected after starting ACE inhibitors. Acceptable changes are an increase in serum creatinine, up to 30%* from baseline and an increase in potassium up to 5.5 mmol/l*. *Renal Association UK, Clinical Knowledge Summaries quote 50% which seems rather high. SIGN advise that the fall in eGFR should be less than 20%. The NICE CKD guidelines suggest that a decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable

Answer 91

Examples candesartan losartan irbesartan Like ACE inhibitors they should be used with caution in patients with renovascular disease. Side-effects include hypotension and hyperkalaemia.

Answer 92

Mechanism | block effects of angiotensin II at the AT1 receptor

Answer 93

Evidence base shown to reduce progression of renal disease in patients with diabetic nephropathy evidence base that losartan reduces CVA and IHD mortality in hypertensive patients

Answer 94

The 2010 Resuscitation Council (UK) guidelines have simplified the advice given for the management of peri-arrest tachycardias. Separate algorithms for the management of broad-complex tachycardia, narrow complex tachycardia and atrial fibrillation have been replaced by one unified treatment algorithm Following basic ABC assessment, patients are classified as being stable or unstable according to the presence of any adverse signs: shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness syncope myocardial ischaemia heart failure If any of the above adverse signs are present then synchronised DC shocks should be given Treatment following this is given according to whether the QRS complex is narrow or broad and whether the rhythm is regular or irregular.The full treatment algorithm can be found at the Resuscitation Council website, below is a very limited summary: Broad-complex tachycardia Regular assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block) loading dose of amiodarone followed by 24 hour infusion Irregular 1. AF with bundle branch block - treat as for narrow complex tachycardia 2. Polymorphic VT (e.g. Torsade de pointes) - IV magnesium Narrow-complex tachycardia Regular vagal manoeuvres followed by IV adenosine if above unsuccessful consider diagnosis of atrial flutter and control rate (e.g. Beta-blockers) Irregular probable atrial fibrillation if onset < 48 hr consider electrical or chemical cardioversion rate control (e.g. Beta-blocker or digoxin) and anticoagulation

Answer 95

shock: hypotension (systolic blood pressure < 90 mmHg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness

Answer 96

tachypnoea. Around 95% of patients with a PE have a respiratory rate > 16/min. Tachypnoea is not as common in any of the other diagnoses. A low-grade temperature is also an under appreciated sign of pulmonary embolism.

Answer 97

We know from experience that few patients (around 10%) present with the medical student textbook triad of pleuritic chest pain, dyspnoea and haemoptysis. Pulmonary embolism can be difficult to diagnose as it can present with virtually any cardiorespiratory symptom/sign depending on it's location and size.

Answer 98

The PIOPED study1 in 2007 looked at the frequency of different symptoms and signs in patients who were diagnosed with pulmonary embolism. The relative frequency of common clinical signs is shown below: Tachypnea (respiratory rate >16/min) - 96% Crackles - 58% Tachycardia (heart rate >100/min) - 44% Fever (temperature >37.8°C) - 43% It is interesting to note that the Well's criteria for diagnosing a PE use tachycardia rather than tachypnoea.

Answer 99

2012 NICE guidelines All patients with symptoms or signs suggestive of a PE should have a history taken, examination performed and a chest x-ray to exclude other pathology. If a PE is still suspected a two-level PE Wells score should be performed:

Answer 100

Clinical signs and symptoms of DVT (minimum of leg swelling and pain with palpation of the deep veins) 3 An alternative diagnosis is less likely than PE 3 Heart rate > 100 beats per minute 1.5 Immobilisation for more than 3 days or surgery in the previous 4 weeks 1.5 Previous DVT/PE 1.5 Haemoptysis 1 Malignancy (on treatment, treated in the last 6 months, or palliative) 1 Clinical probability simplified scores PE likely - more than 4 points PE unlikely - 4 points or less If a PE is 'likely' (more than 4 points) arrange an immediate computed tomography pulmonary angiogram (CTPA). If there is a delay in getting the CTPA then give low-molecular weight heparin until the scan is performed. If a PE is 'unlikely' (4 points or less) arranged a D-dimer test. If this is positive arrange an immediate computed tomography pulmonary angiogram (CTPA). If there is a delay in getting the CTPA then give low-molecular weight heparin until the scan is performed. If the patient has an allergy to contrast media or renal impairment a V/Q scan should be used instead of a CTPA.

Answer 101

The consensus view from the British Thoracic Society and NICE guidelines is as follows: computed tomographic pulmonary angiography (CTPA) is now the recommended initial lung-imaging modality for non-massive PE. Advantages compared to V/Q scans include speed, easier to perform out-of-hours, a reduced need for further imaging and the possibility of providing an alternative diagnosis if PE is excluded if the CTPA is negative then patients do not need further investigations or treatment for PE ventilation-perfusion scanning may be used initially if appropriate facilities exist, the chest x-ray is normal, and there is no significant symptomatic concurrent cardiopulmonary disease

Answer 102

ECG the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - 'S1Q3T3'. However this change is seen in no more than 20% of patients right bundle branch block and right axis deviation are also associated with PE sinus tachycardia may also be seen

Answer 103

The most common valves which need replacing are the aortic and mitral valve. There are two main options for replacement: biological (bioprosthetic) or mechanical.

Answer 104

Usually bovine or porcine in origin Major disadvantage is structural deterioration and calcification over time. Most older patients ( > 65 years for aortic valves and > 70 years for mitral valves) receive a bioprosthetic valve Long-term anticoagulation not usually needed. Warfarin may be given for the first 3 months depending on patient factors. Low-dose aspirin is given long-term.

Answer 105

The most common type now implanted is the bileaflet valve. Ball-and-cage valves are rarely used nowadays Mechanical valves have a low failure rate Major disadvantage is the increased risk of thrombosis meaning long-term anticoagulation is needed. Aspirin is normally given in addition unless there is a contraindication. Target INR aortic: 2.0-3.0 mitral: 2.5-3.5

Answer 106

``` Features early diastolic murmur collapsing pulse wide pulse pressure mid-diastolic Austin-Flint murmur in severe AR - due to partial closure of the anterior mitral valve cusps caused by the regurgitation streams ```

Answer 107

``` Causes (due to valve disease) rheumatic fever infective endocarditis connective tissue diseases e.g. RA/SLE bicuspid aortic valve ```

Answer 108

``` Causes (due to aortic root disease) aortic dissection spondylarthropathies (e.g. ankylosing spondylitis) hypertension syphilis Marfan's, Ehler-Danlos syndrome ```

Answer 109

Pulsus parodoxus greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration severe asthma, cardiac tamponade

Answer 110

Slow-rising/plateau | aortic stenosis

Answer 111

Collapsing aortic regurgitation patent ductus arteriosus hyperkinetic (anaemia, thyrotoxic, fever, exercise/pregnancy)

Answer 112

Pulsus alternans regular alternation of the force of the arterial pulse severe LVF eg hocm

Answer 113

Bisferiens pulse 'double pulse' - two systolic peaks mixed aortic valve disease or HOCM

Answer 114

'Jerky' pulse | hypertrophic obstructive cardiomyopathy*

Answer 115

The first heart sound (S1) is caused by closure of the mitral and tricuspid valves whilst the second heart sound (S2) is due to aortic and pulmonary valve closure

Answer 116

S1 closure of mitral and tricuspid valves soft if long PR or mitral regurgitation loud in mitral stenosis

Answer 117

S2 closure of aortic and pulmonary valves soft in aortic stenosis splitting during inspiration is normal

Answer 118

S3 (third heart sound) caused by diastolic filling of the ventricle considered normal if < 30 years old (may persist in women up to 50 years old) heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock)

Answer 119

S4 (fourth heart sound) may be heard in aortic stenosis, HOCM, hypertension caused by atrial contraction against a stiff ventricle in HOCM a double apical impulse may be felt as a result of a palpable S4

Answer 120

Gallop rhythm (S3) is an early sign of LVF A gallop rhythm refers to a (usually abnormal) rhythm of the heart on auscultation.[1] It includes three or four sounds, thus resembling the sounds of a gallop. The normal heart rhythm contains two audible heart sounds called S1 and S2 that give the well-known "lub-dub" rhythm; they are caused by the closing of valves in the heart. A gallop rhythm contains another sound, called S3 or S4, dependent upon where in the cycle this added sound comes. Gallop rhythms may be heard in young or athletic people, but may also be a sign of serious cardiac problems like heart failure as well as pulmonary edema.

Answer 121

``` bradycardia 'J' wave - small hump at the end of the QRS complex first degree heart block long QT interval atrial and ventricular arrhythmias ```

Answer 122

Patients with aortic stenosis are at risk of profound hypotension with ACE inhibitors.

Answer 123

The New York Heart Association (NYHA) classification is widely used to classify the severity of heart failure: class 1, 2 , 3 and 4

Answer 124

The New York Heart Association (NYHA) classification is widely used to classify the severity of heart failure: NYHA Class I no symptoms no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations

Answer 125

The New York Heart Association (NYHA) classification is widely used to classify the severity of heart failure: NYHA Class II mild symptoms slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea

Answer 126

The New York Heart Association (NYHA) classification is widely used to classify the severity of heart failure: NYHA Class III moderate symptoms marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms

Answer 127

The New York Heart Association (NYHA) classification is widely used to classify the severity of heart failure: NYHA Class IV severe symptoms unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity

Answer 128

Ejection systolic aortic stenosis pulmonary stenosis, HOCM ASD, Fallot's

Answer 129

Holosystolic (pansystolic) mitral/tricuspid regurgitation (high-pitched and 'blowing' in character) VSD ('harsh' in character)

Answer 130

Late systolic mitral valve prolapse coarctation of aorta

Answer 131

Early diastolic ``` aortic regurgitation (high-pitched and 'blowing' in character) Graham-Steel murmur (pulmonary regurgitation, again high-pitched and 'blowing' in character) ```

Answer 132

Mid-late diastolic ``` mitral stenosis ('rumbling' in character) Austin-Flint murmur (severe aortic regurgitation, again is 'rumbling' in character) ```

Answer 133

Continuous machine-like mumur patent ductus arteriosus

Answer 134

Features ``` dyspnoea raised JVP, with an absent Y descent - this is due to the limited right ventricular filling tachycardia hypotension muffled heart sounds pulsus paradoxus Kussmaul's sign (much debate about this) ECG: electrical alternans ```

Answer 135

Causes of ST depression ``` secondary to abnormal QRS (LVH, LBBB, RBBB) ischaemia digoxin hypokalaemia syndrome X ```

Answer 136

ECG changes for thrombolysis or percutaneous intervention: ST elevation of > 2mm (2 small squares) in 2 or more consecutive anterior leads (V1-V6) OR ST elevation of greater than 1mm (1 small square) in greater than 2 consecutive inferior leads (II, III, avF, avL) OR New Left bundle branch block

Answer 137

Cardiac arrest This most commonly occurs due to patients developing ventricular fibrillation and is the most common cause of death following a MI. Patients are managed as per the ALS protocol with defibrillation.

Answer 138

``` 1- cardiac arrest 2 - cardiogenic shock 3 - chronic heart failure 4 - tachyarrhythmias 5 - bradyarrhythmias 6 - pericarditis 7 - ventricular aneurysm or free wall rupture 8 - ventricular septal defects 9 - acute mitral regurgitation ```

Answer 139

Pericarditis in the first 48 hours following a transmural MI is common (c. 10% of patients). The pain is typical for pericarditis (worse on lying flat etc), a pericardial rub may be heard and a pericardial effusion may be demonstrated with an echocardiogram.

Answer 140

Dressler's syndrome tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs.

Answer 141

Left ventricular aneurysm The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.

Answer 142

Left ventricular free wall rupture This is seen in around 3% of MIs and occurs around 1-2 weeks afterwards. Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required.

Answer 143

Isolated systolic hypertension (ISH) is common in the elderly, affecting around 50% of people older than 70 years old. The Systolic Hypertension in the Elderly Program (SHEP) back in 1991 established that treating ISH reduced both strokes and ischaemic heart disease. Drugs such as thiazides were recommended as first line agents. This approach is contradicated by the 2011 NICE guidelines which recommends treating ISH in the same stepwise fashion as standard hypertension.

Answer 144

Stanford classification type A - ascending aorta, 2/3 of cases type B - descending aorta, distal to left subclavian origin, 1/3 of cases DeBakey classification type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally type II - originates in and is confined to the ascending aorta type III - originates in descending aorta, rarely extends proximally but will extend distally

Answer 145

Type A surgical management, but blood pressure should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention Type B* conservative management bed rest reduce blood pressure IV labetalol to prevent progression

Answer 146

Coarctation of the aorta describes a congenital narrowing of the descending aorta. Overview more common in males (despite association with Turner's syndrome)

Answer 147

Features infancy: heart failure adult: hypertension radio-femoral delay mid systolic murmur, maximal over back apical click from the aortic valve notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children

Answer 148

Associations Turner's syndrome bicuspid aortic valve berry aneurysms neurofibromatosis

Answer 149

Digoxin is a cardiac glycoside now mainly used for rate control in the management of atrial fibrillation. As it has positive inotropic properties it is sometimes used for improving symptoms (but not mortality) in patients with heart failure. Mechanism of action decreases conduction through the atrioventricular node which slows the ventricular rate in atrial fibrillation and flutter increases the force of cardiac muscle contraction due to inhibition of the Na+/K+ ATPase pump. Also stimulates vagus nerve

Answer 150

Digoxin toxicity Plasma concentration alone does not determine whether a patient has developed digoxin toxicity. The BNF advises that the likelihood of toxicity increases progressively from 1.5 to 3 mcg/l. Features generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision arrhythmias (e.g. AV block, bradycardia)

Answer 151

Precipitating factors ``` classically: hypokalaemia* increasing age renal failure myocardial ischaemia hypomagnesaemia, hypercalcaemia, hypernatraemia, acidosis hypoalbuminaemia hypothermia hypothyroidism drugs: amiodarone, quinidine, verapamil, diltiazem, spironolactone (competes for secretion in distal convoluted tubule therefore reduce excretion), ciclosporin. Also drugs which cause hypokalaemia e.g. thiazides and loop diuretics ``` *hyperkalaemia may also worsen digoxin toxicity, although this is very small print

Answer 152

Management Digibind correct arrhythmias monitor potassium

Answer 153

Dilated cardiomyopathy (DCM) basics dilated heart leading to systolic (+/- diastolic) dysfunction all 4 chambers affected but LV more so than RV features include arrhythmias, emboli, mitral regurgitation absence of congenital, valvular or ischaemic heart disease

Answer 154

Causes often considered separate entities alcohol: may improve with thiamine postpartum hypertension Other causes inherited (see below) infections e.g. Coxsackie B, HIV, diphtheria, parasitic endocrine e.g. Hyperthyroidism infiltrative* e.g. Haemochromatosis, sarcoidosis neuromuscular e.g. Duchenne muscular dystrophy nutritional e.g. Kwashiorkor, pellagra, thiamine/selenium deficiency drugs e.g. Doxorubicin

Answer 155

Inherited dilated cardiomyopathy around a third of patients with DCM are thought to have a genetic predisposition a large number of heterogeneous defects have been identified the majority of defects are inherited in an autosomal dominant fashion although other patterns of inheritance are seen

Answer 156

Pericarditis Pericarditis is one of the differentials of any patient presenting with chest pain. Features chest pain: may be pleuritic. Is often relieved by sitting forwards other symptoms include non-productive cough, dyspnoea and flu-like symptoms pericardial rub tachypnoea tachycardia

Answer 157

Causes viral infections (Coxsackie) tuberculosis uraemia (causes 'fibrinous' pericarditis) trauma post-myocardial infarction, Dressler's syndrome connective tissue disease hypothyroidism

Answer 158

ECG changes widespread 'saddle-shaped' ST elevation PR depression: most specific ECG marker for pericarditis

Answer 159

The BNF warns that short-acting formulations of nifedipine are associated with large variations in blood pressure and may cause reflex tachycardia

Answer 160

Management if bradycardic then atropine in resistant cases glucagon may be used

Answer 161

Syncope may be defined as a transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery. Note how this definition excludes other causes of collapse such as epilepsy.

Answer 162

Reflex syncope (neurally mediated) vasovagal: triggered by emotion, pain or stress. Often referred to as 'fainting' situational: cough, micturition, gastrointestinal carotid sinus syncope Orthostatic syncope primary autonomic failure: Parkinson's disease, Lewy body dementia secondary autonomic failure: e.g. Diabetic neuropathy, amyloidosis, uraemia drug-induced: diuretics, alcohol, vasodilators volume depletion: haemorrhage, diarrhoea Cardiac syncope arrhythmias: bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular) structural: valvular, myocardial infarction, hypertrophic obstructive cardiomyopathy others: pulmonary embolism Reflex syncope is the most common cause in all age groups although orthostatic and cardiac causes become progressively more common in older patients.

Answer 163

Evaluation ``` cardiovascular examination postural blood pressure readings: a symptomatic fall in systolic BP > 20 mmHg or diastolic BP > 10 mmHg or decrease in systolic BP < 90 mmHg is considered diagnostic ECG carotid sinus massage tilt table test 24 hour ECG ```

Answer 164

The following ECG changes are considered normal variants in an athlete: sinus bradycardia junctional rhythm first degree heart block Wenckebach phenomenon (progressive lengthening of conduction time in any cardiac tissue (most often the AV node or junction) with ultimate dropping of a beat (AV Wenckebach) or reversion to the initial conduction time (as in QRS Wenckebach))

Answer 165

Infective endocarditis diagnosed if pathological criteria positive, or 2 major criteria, or 1 major and 3 minor criteria, or 5 minor 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 Streptococcus 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 burnetii, Bartonella species or Chlamydia psittaci, 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 criteria predisposing heart condition or intravenous drug use microbiological evidence does not meet major criteria fever > 38ºC vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots

Answer 166

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 (99mTc) sestamibi: a coordination complex of the radioisotope technetium-99m with the ligand methoxyisobutyl isonitrile (MIBI), 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 (e.g. 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 cardiotoxic drugs are used

Answer 167

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 If these two techniques are combined cardiac CT has a very high negative predictive value for ischaemic heart disease.

Answer 168

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, determining right and left ventricular mass and differentiating forms 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.

Answer 169

Phaeochromocytoma is a rare catecholamine secreting tumour. About 10% are familial and may be associated with MEN type II, neurofibromatosis and von Hippel-Lindau syndrome Basics bilateral in 10% malignant in 10% extra-adrenal in 10% (most common site = organ of Zuckerkandl, adjacent to the bifurcation of the aorta)

Answer 170

Features are typically episodic ``` hypertension (around 90% of cases, may be sustained) headaches palpitations sweating anxiety ```

Answer 171

Tests 24 hr urinary collection of metanephrines (sensitivity 97%*) this has replaced a 24 hr urinary collection of catecholamines (sensitivity 86%)

Answer 172

Surgery is the definitive management. The patient must first however be stabilized with medical management: alpha-blocker (e.g. phenoxybenzamine), given before a beta-blocker (e.g. propranolol)

Answer 173

All patients should be offered the following drugs: dual antiplatelet therapy (aspirin plus a second antiplatelet agent) ACE inhibitor beta-blocker statin Some selected lifestyle points: diet: advise a Mediterranean style diet, switch butter and cheese for plant oil based products. Do not recommend omega-3 supplements or eating oily fish exercise: advise 20-30 mins a day until patients are 'slightly breathless' sexual activity may resume 4 weeks after an uncomplicated MI. Reassure patients that sex does not increase their likelihood of a further MI. PDE5 inhibitors (e.g, sildenafil) may be used 6 months after a MI. They should however be avoided in patient prescribed either nitrates or nicorandil Clopidogrel since clopidogrel came off patent it is now much more widely used post-MI STEMI: the European Society of Cardiology recommend dual antiplatelets for 12 months. In the UK this means aspirin + clopidogrel non-ST segment elevation myocardial infarction (NSTEMI): following the NICE 2013 Secondary prevention in primary and secondary care for patients following a myocardial infarction guidelines clopidogrel should be given for the first 12 months Aldosterone antagonists patients who have had an acute MI and who have symptoms and/or signs of heart failure and left ventricular systolic dysfunction, treatment with an aldosterone antagonist licensed for post-MI treatment (e.g. eplerenone) should be initiated within 3-14 days of the MI, preferably after ACE inhibitor therapy

Answer 174

Acute coronary syndrome (ACS) refers to a group of conditions due to decreased blood flow in the coronary arteries such that part of the heart muscle is unable to function properly or dies.[1] The most common symptom is chest pain, often radiating to the left arm or angle of the jaw, pressure-like in character, and associated with nausea and sweating. Acute coronary syndrome usually occurs as a result of one of three problems: ST elevation myocardial infarction (30%), non ST elevation myocardial infarction (25%), or unstable angina (38%)

Answer 175

ECG changes seen in hyperkalaemia include tall-tented T waves, small P waves, widened QRS leading to a sinusoidal pattern and asystole

Answer 176

Causes of hyperkalaemia: ``` acute renal failure drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin** metabolic acidosis Addison's rhabdomyolysis massive blood transfusion ``` *beta-blockers interfere with potassium transport into cells and can potentially cause hyperkalaemia in renal failure patients - remember beta-agonists, e.g. Salbutamol, are sometimes used as emergency treatment **both unfractionated and low-molecular weight heparin can cause hyperkalaemia. This is thought to be caused by inhibition of aldosterone secretion

Answer 177

Features may be picked up on routine ECG or following family screening Long QT1 - usually associated with exertional syncope, often swimming Long QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuli Long QT3 - events often occur at night or at rest sudden cardiac death

Answer 178

Management avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise) beta-blockers*** implantable cardioverter defibrillators in high risk cases

Answer 179

*the usual mechanism by which drugs prolong the QT interval is blockage of potassium channels

Answer 180

HbA1c | NICE do not advocate increasing treatment unless the HbA1c is >= 6.5%.

Answer 181

Poor prognostic factors Staph aureus infection (see below) prosthetic valve (especially 'early', acquired during surgery) culture negative endocarditis low complement levels Mortality according to organism staphylococci - 30% bowel organisms - 15% streptococci - 5%

Answer 182

Initial blind therapy: Native valve amoxicillin, consider adding low-dose gentamicin If penicillin allergic, MRSA or severe sepsis vancomycin + low-dose gentamicin If prosthetic valve vancomycin + rifampicin + low-dose gentamicin Native valve endocarditis caused by staphylococci: Flucloxacillin If penicillin allergic or MRSA vancomycin + rifampicin Prosthetic valve endocarditis caused by staphylococci: Flucloxacillin + rifampicin + low-dose gentamicin If penicillin allergic or MRSA vancomycin + rifampicin + low-dose gentamicin Endocarditis caused by fully-sensitive streptococci (e.g. viridans): Benzylpenicillin If penicillin allergic vancomycin + low-dose gentamicin Endocarditis caused by less sensitive streptococci: Benzylpenicillin + low-dose gentamicin If penicillin allergic vancomycin + low-dose gentamicin

Answer 183

Indications for surgery severe valvular incompetence aortic abscess (often indicated by a lengthening PR interval) infections resistant to antibiotics/fungal infections cardiac failure refractory to standard medical treatment recurrent emboli after antibiotic therapy

Answer 184

The ECG shows both right bundle branch block and left axis deviation indicating bifascicular block. Bifascicular block combination of RBBB with left anterior or posterior hemiblock e.g. RBBB with left axis deviation Trifascicular block features of bifascicular block as above + 1st degree heart block

Answer 185

Rheumatic fever develops following an immunological reaction to recent (2-6 weeks ago) Streptococcus pyogenes infection. Diagnosis is based on evidence of recent streptococcal infection accompanied by: 2 major criteria 1 major with 2 minor criteria Evidence of recent streptococcal infection ASOT > 200iu/mL history of scarlet fever positive throat swab increase in DNase B titre Major criteria ``` erythema marginatum Sydenham's chorea polyarthritis carditis (endo-, myo- or peri-) subcutaneous nodules ``` Minor criteria raised ESR or CRP pyrexia arthralgia (not if arthritis a major criteria) prolonged PR interval

Answer 186

Long QT syndrome (LQTS) is an inherited condition associated with delayed repolarization of the ventricles. It is important to recognise as it may lead to ventricular tachycardia and can therefore cause collapse/sudden death. The most common variants of LQTS (LQT1 & LQT2) are caused by defects in the alpha subunit of the slow delayed rectifier potassium channel. A normal corrected QT interval is less than 430 ms in males and 450 ms in females. An implantable cardioverter defibrillator is only required in high risk cases, for example if the patient has a QTc > 500ms or previous episodes of cardiac arrest.

Answer 187

Systemic inflammatory response syndrome (SIRS) at least 2 of the following body temperature less than 36°C or greater than 38.3°C heart rate greater than 90/min respiratory rate greater than 20 breaths per minute blood glucose > 7.7mmol/L in the absence of known diabetes white cell count less than 4 or greater than 12 SIRS may occur as a result of an infection (bacterial, viral or fungal) or in response to a non-infective inflammatory cause, for example burns or pancreatitis. Sepsis is defined as SIRS in response to a proven or presumed infection. The mortality rate of sepsis is around 10%.

Answer 188

Recently the Sepsis Trust have introduced the concept of 'red flag' sepsis. They recommend starting the 'sepsis six' if any 1 of the following are present: ``` Red flag signs: systolic blood pressure 40mmHg fall from baseline mean arterial pressure 131 per minute respiratory rate > 25 per minute* AVPU = V, P or U* ``` They also detail a number of laboratory findings which indicate severe sepsis. Severe sepsis sepsis with end organ dysfunction or hypoperfusion (indicated by hypotension, lactic acidosis or decreased urine output or others)

Answer 189

Septic shock severe sepsis with persistently low blood pressure which has failed to respond to the administration of intravenous fluids.

Answer 190

Management Clearly the underlying cause of the patients sepsis needs to be identified and treated and the patient supported regardless of the cause or severity. If however any of the red flags are present the 'sepsis six' should be started straight away: 1. Administer high flow oxygen. 2. Take blood cultures 3. Give broad spectrum antibiotics 4. Give intravenous fluid challenges 5. Measure serum lactate and haemoglobin 6. Measure accurate hourly urine output

Answer 191

ECG shows deep ST depression in leads V1-3 with tall T waves

Answer 192

Onset 48 hours If the patient has been in AF for more than 48 hours then anticoagulation should be given for at least 3 weeks prior to cardioversion. An alternative strategy is to perform a transoesophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus. If excluded patients may be heparinised and cardioverted immediately. If there is a high risk of cardioversion failure (e.g. Previous failure or AF recurrence) then it is recommend to have at least 4 weeks amiodarone or sotalol prior to electrical cardioversion Following electrical cardioversion patients should be anticoagulated for at least 4 weeks. After this time decisions about anticoagulation should be taken on an individual basis depending on the risk of recurrence

Answer 193

``` Management options in acute heart failure include: oxygen diuretics opiates vasodilators inotropic agents CPAP ultrafiltration mechanical circulatory assistance: e.g. intra-aortic balloon counterpulsation or ventricular assist devices ``` Consideration should be given to discontinuing beta-blockers in the short-term. The patient is suffering from severe pulmonary oedema with bilateral course crackles and cough productive of white sputum. The patient has signs of right sided heart failure with raised JVP and peripheral oedema. They also have a history of MI and hypertension that are two risk factors for heart failure. NICE guidance on Acute Heart Failure 2014 states that a patient who has failed medical management of pulmonary oedema with severe dyspnoea should be considered for CPAP. BIPAP is not used in acute pulmonary oedema.

Answer 194

greater than the normal (10 mmHg) fall in systolic blood pressure during inspiration → faint or absent pulse in inspiration severe asthma, cardiac tamponade

Answer 195

aortic stenosis

Answer 196

aortic regurgitation patent ductus arteriosus hyperkinetic (anaemia, thyrotoxic, fever, exercise/pregnancy)

Answer 197

regular alternation of the force of the arterial pulse | severe LVF

Answer 198

'double pulse' - two systolic peaks mixed aortic valve disease or HOCM

Answer 199

hypertrophic obstructive cardiomyopathy* *HOCM may occasionally be associated with a bisferiens pulse

Answer 200

The joint European Resuscitation Council and Resuscitation Council (UK) 2010 guidelines do not alter significantly from the 2005 guidelines. Please see the link for more details, below is only a very brief summary of key points / changes. Major points include: ratio of chest compressions to ventilation is 30:2 chest compressions are now continued while a defibrillator is charged during a VF/VT cardiac arrest, adrenaline 1 mg is given once chest compressions have restarted after the third shock and then every 3-5 minutes (during alternate cycles of CPR). In the 2005 guidelines, adrenaline was given just before the third shock. Amiodarone 300 mg is also given after the third shock atropine is no longer recommended for routine use in asystole or pulseless electrical activity (PEA). a single shock for VF/pulseless VT followed by 2 minutes of CPR, rather than a series of 3 shocks followed by 1 minute of CPR asystole/pulseless-electrical activity should be treated with 2 minutes of CPR, rather than 3, prior to reassessment of the rhythm delivery of drugs via a tracheal tube is no longer recommended following successful resuscitation oxygen should be titrated to achieve saturations of 94-98%. This is to address the potential harm caused by hyperoxaemia

Answer 201

Cardiac resynchronisation therapy: for patients with heart failure and wide QRS biventricular pacing improved symptoms and reduced hospitalisation in NYHA class III patients no reduction in mortality at present Exercise training: improves symptoms but not hospitalisation/mortality In symptomatic heart failure patients who are on optimal medical therapy, there are several treatment options to improve mortality. Cardiac resynchronisation therapy is indicated in patients with left ventricular dysfunction, ejection fracture 120ms. An Implantable cardiac defibrillator (ICD) is indicated in patients with previous sustained ventricular tachycardia, ejection fraction

Answer 202

LV failure or pleural effusion

Answer 203

apparently its a marker of poor prognosis

Answer 204

no but it can push the blood glucose up a little bit.

Answer 205

frusemide, vancomycin and gentamycin

Answer 206

Mg and K share a transporter and the body will preferentially uptake Mg so it is difficult to correct a hypokalaemia until a PT is Mg replete

Answer 207

it, along with other opiates i think, has a slight ventilatory effect

Answer 208

stroke volume/end diastolic volume ( i.e. the largest volume) normally about 60-65%

Answer 209

``` chemotherapy haemochromatosis alcohol thyrotoxicosis viral infection ```

Answer 210

systemic issue e.g. infection causes stress response and this easily triggers AF in them. treat by correcting the underlying issue.

Answer 211

1 - ACE inhibitors and ARBs, best. all of them 2 - beta blockers but only some - metoprolol, carvedilol and bisoprolol 3 - spironolactone digoxin only has symptomatic benefit

Answer 212

effectively a K sparing diuretic so can cause hyperkalamia can cause bad postural hypotension angioedema - lip swelling

Answer 213

weight loss stop smoking decrease salt intake water restriction is good for symptoms but doesn't affect prognosis

Answer 214

biventricular pacing cardiac transplant - v rare that eligible due to scarcity of hearts palliative care ultrafiltration - gets lots of volume off. intraaortic baloon pump is not a suitable option, its used occasionally to tide people over during flash pulmonary oedema but going out of fashion.

Answer 215

yes. heart failure with preserved ejection fraction HFPEF. diastolic dysfunction occurs. BNP will be really high but echo might appear normal. use a cardiac MRI to get more info. need to aggressively control BP in these PTs they tolerate AF really badly as they have bad diastolic function anyway and AF removes the atrial contribution to diastolic filling so will decompensate suddenly.

Answer 216

can infiltrate the myocardium, restrict the movement of the ventricle wall and cause heart failure.

Answer 217

Amyloidosis is a clinical disorder caused by extracellular and or intracellular deposition of insoluble abnormal amyloid fibrils that alter the normal function of tissues. Proteins that form amyloid fibrils differ in size, function, amino acid sequence and native structure but become insoluble aggregates that are similar in structure and in properties. really bad prognosis

Answer 218

the new bone is highly vascular and this causes a form of high output cardiac failure where the heart can't keep up

Answer 219

hydralazine is an arterial dilator and nitrates are a veno-dilator.

Answer 220

weight loss salt restriction reduce alcohol aerobic exercise. anything to reduce salt or long term vasomotor tone.

Answer 221

use methyldopa. SE = depression. all ACEI are teratogenic. They also made recommendations on reducing the risk of hypertensive disorders developing in the first place. Women who are at 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 chronic kidney disease autoimmune disorders such as SLE or antiphospholipid syndrome type 1 or 2 diabetes mellitus 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 1 - preexisting hypertension 2 - Pregnancy-induced hypertension (PIH, also known as gestational hypertension) 3 - Pre-eclampsia

Answer 222

labetalol hydralazine delivery

Answer 223

due to coronary artery spasm. pain usually occurs during rest, ECG during this will show ST elevation, this resolves as pain does. PTs usually don't have the CVD risk factors. Mx - CCB +- long acting nitrates. in this instance aspirin and beta blockers can make it worse.

Answer 224

1 - if known CAD and typical symptoms then none needed. if unstable angina then should admit to hospital. ``` then use a CAD likelihood chart to stratify likelihood of CAD. if 61-90% - angiography 30-60% - funcitonal imaging 10-29% CT less - reconsider diagnosis. ```

Answer 225

Cocaine is an alkaloid derived from the coca plant. It is widely used as a recreational stimulant. The price of cocaine has fallen sharply in the past decade resulting in cocaine toxicity becoming a much more frequent clinical problem. This increase has made cocaine a favourite topic of question writers. Mechanism of action cocaine blocks the uptake of dopamine, noradrenaline and serotonin The use of cocaine is associated with a wide variety of adverse effects: ``` Cardiovascular effects myocardial infarction both tachycardia and bradycardia may occur hypertension QRS widening and QT prolongation aortic dissection ``` ``` Neurological effects seizures mydriasis hypertonia hyperreflexia ``` Psychiatric effects agitation psychosis hallucinations Others hyperthermia metabolic acidosis rhabdomyolysis Management of cocaine toxicity in general benzodiazipines are generally first-line for most cocaine related problems chest pain: benzodiazipines + glyceryl trinitrate. If myocardial infarction develops then primary percutaneous coronary intervention hypertension: benzodiazipines + sodium nitroprusside the use of beta-blockers in cocaine-induced cardiovascular problems is a controversial issue. The American Heart Association issued a statement in 2008 warning against the use of beta-blockers (due to the risk of unopposed alpha-mediated coronary vasospasm) but many cardiologists since have questioned whether this is valid. If a reasonable alternative is given in an exam it is probably wise to choose it

Answer 226

Statins inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis Adverse effects myopathy: includes myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase. Risks factors for myopathy include advanced age, female sex, low body mass index and presence of multisystem disease such as diabetes mellitus. Myopathy is more common in lipophilic statins (simvastatin, atorvastatin) than relatively hydrophilic statins (rosuvastatin, pravastatin, fluvastatin) liver impairment: the 2014 NICE guidelines recommend checking LFTs at baseline, 3 months and 12 months. Treatment should be discontinued if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range there is some evidence that statins may increase the risk of intracerebral haemorrhage in patients who've previously had a stroke. This effect is not seen in primary prevention. For this reason the Royal College of Physicians recommend avoiding statins in patients with a history of intracerebral haemorrhage Who should receive a statin? all people with established cardiovascular disease (stroke, TIA, ischaemic heart disease, peripheral arterial disease) following the 2014 update, NICE recommend anyone with a 10-year cardiovascular risk >= 10% patients with type 2 diabetes mellitus should now be assessed using QRISK2 like other patients are, to determine whether they should be started on statins Statins should be taken at night as this is when the majority of cholesterol synthesis takes place. This is especially true for simvastatin which has a shorter half-life than other statins Current guidelines for lipid lowering* ``` Total cholesterol (mmol/l) LDL cholesterol Joint British Societies ```

Answer 227

In children and young adults the 2nd heart sound splits into two components during inspiration (lub da-dup) and comes together again in expiration. This is the result of minor changes in the stroke volume of L and R ventricles in respiration. Splitting of the second heart sound in expiration indicates an abnormality. During inspiration, venous return to the R side of the heart is increased, so R ventricular stroke volume is increased and closure of the pulmonary valve is delayed. At the same time, pooling of blood in the pulmonary veins reduces filling of the L ventricle and makes aortic valve closure slightly earlier than in expiration. The split may be widened by other factors that delay ventricular contraction, such as RBBB or pulmonary valve stenosis. 52 Conversely, anything that delays L ventricular contraction, such as LBBB or hypertrophic obstructive cardiomyopathy may so delay the aortic component of the 2nd heart sound that the normal relationship is reversed an there is increased splitting of the 2nd heart sound on expiration, with the sounds coming together on inspiration. Finally, in an atrial septal defect, there is a characteristically fixed splitting of the 2nd heart sound because the hole in the intra-atrial septum means that the L and R atrial pressure remains equal throughout the respiratory cycle

Answer 228

These are abnormal heart sounds that are heard in addition to the normal ones. The 3rd heart sound is a low-pitched, thudding sound that occurs in diastole and coincides with the end of the rapid phase of ventricular filling. 2 causes: Physiological – in young fit adults under circumstances of increased cardiac output (athletes/pregnancy). No pathological significance. Pathological – severe impairment of the L ventricle, eg. in dilated cardiac myopathy, after an MI, in massive PE. Patients with the pathological 3rd heart sound almost always have a tachycardia and the 1st and 2nd sounds are relatively quiet – ie. “da-da-boom, da-da-boom”. This called gallop rhythm. A 4th heart sound is an extra beat sound that coincides with atrial contraction. It is usually best heard in patients whose L atrium is hypertrophied but is NOT heard in mitral stenosis. A fourth sound sounds like “da-lub-dup, da-lub-dup”.

Answer 229

Ejection click This is a high-pitched ringing sound that usually follows very shortly after the 1st heart sound. It is a feature of aortic or pulmonary valve stenosis – it’s probably caused by the sudden opening of the deformed valve.

Answer 230

Opening snap This is a diastolic sound heard in mitral stenosis and associated with the tensing of the diaphragm formed by the stenosed valve. It is best heard to the L of the sternum and sounds a bit like the 2nd part of a widely split 2nd heart sound.

Answer 231

An artificial heart valve usually makes a noise both on opening and closing. The closing sound is usually louder than the opening sound, so an aortic prosthesis will have a soft opening click just after the 1st heart sound and a loud closing click that contributes to the 2nd heart sound. Conversely, a mitral valve will give a soft opening click in a similar position to the opening snap of mitral stenosis and a loud closing click that contributes to the first heart sound.

Answer 232

Systolic murmurs 3 causes: Leakage of blood through a structure that is usually closed during systole (mitral or tricuspid valves or the interventricular septum) Blood flow through a valve normally open in systole that has become abnormally narrowed (aortic or pulmonary stenosis) Increased blood flow through a normal valve (a flow murmur) Murmurs due to leakage of blood through an incompetent mitral or tricuspid valve or interventricular septum defect are usually of similar intensity throughout systole. They are called pansystolic murmurs. In mitral prolapse (where the valve is okay at the start of systole but then becomes incompetent) you get a mid or late systolic murmur. Murmurs that are due to blood being forced through a narrow aortic or pulmonary valve or to increased blood flow through a normal aortic or pulmonary valve tend to start quietly at the beginning of systole, rise to a crescendo in midsystole and then become quiet again. These are ejection systolic murmurs.

Answer 233

These can be divided into: Early diastolic murmurs – incompetence of the aortic or pulmonary valve. Maximal at beginning of diastole when aortic/pulmonary pressure is highest, and rapidly becomes quieter as pressure in the great vessel falls. It is described as a whispered letter ‘r’. Mid-diastolic murmurs – usually caused by blood flow through a narrowed mitral or tricuspid valve, or to increased flow through one of these (eg. children with atrial septal defect).

Answer 234

These are murmurs that are not associated with any structural abnormality or with haemodynamic disturbance. They are common in children and young adults. They are: always systolic, always quiet, usually best heard at the L sternal edge, not associated with ventricular hypertrophy.

Answer 235

Aortic stenosis Pulmonary stenosis Atrial septal defect L and R outflow tract obstruction

Answer 236

Mitral regurgitation Tricuspid regurgitation Ventricular septal defect

Answer 237

``` Innocent murmur Aortic stenosis Pulmonary stenosis Hypertrophic cardiomyopathy Flow murmurs (fever, athlete’s heart) ```

Answer 238

Mitral stenosis | Tricuspid stenosis

Answer 239

Aortic regurgitation | Pulmonary regurgitation

Answer 240

Patent ductus arteriosus | Aortic stenosis and regurgitation

Answer 241

``` HILT: Heaving Impalpable Laterally displaced Thrusting/ Tapping ``` DOPES: Dextrocardia Obesity Pericarditis/ Pericardial tamponade/ Pneumothorax Emphysema Sinus inversus/ Student incompetence/ Scoliosis/ Skeletal abnormalities (eg pectus excavatum)

Answer 242

``` PIRATES: Pulmonary: PE, COPD Iatrogenic Rheumatic heart: mirtral regurgitation Atherosclerotic: MI, CAD Thyroid: hyperthyroid Endocarditis Sick sinus syndrome ```

Answer 243

``` PULSE: Persistent chest pains Upset stomach Lightheadedness Shortness of breath Excessive sweating ```

Answer 244

``` MONAH: Morphine Oxygen Nitrogen Aspirin Heparin ```

Answer 245

"RILE": Right sided heart murmurs are louder on Inspiration. Left sided heart murmurs are loudest on Expiration.

Answer 246

``` CARDIAC RIND: Collagen vascular disease Aortic aneurysm Radiation Drugs (such as hydralazine) Infections Acute renal failure Cardiac infarction Rheumatic fever Injury Neoplasms Dressler's syndrome ```

Answer 247

PQRST (EKG waves): Pericardial effusion Quantity of fluid raised (fluid over load) Right heart failure Superior vena caval obstruction Tricuspid stenosis/ Tricuspid regurgitation/ Tamponade (cardiac)

Answer 248

``` HEAD HEART VESSELS: CNS causes include HEAD: Hypoxia/ Hypoglycemia Epilepsy Anxiety Dysfunctional brain stem (basivertebral TIA) ``` ``` Cardiac causes are HEART: Heart attack Embolism (PE) Aortic obstruction (IHSS, AS or myxoma) Rhythm disturbance, ventricular Tachycardia ``` ``` Vascular causes are VESSELS: Vasovagal Ectopic (reminds one of hypovolemia) Situational Subclavian steal ENT (glossopharyngeal neuralgia) Low systemic vascular resistance (Addison's, diabetic vascular neuropathy) Sensitive carotid sinus ```

Answer 249

``` CHAPS: Cushing's syndrome Hyperaldosteronism [aka Conn's syndrome] Aorta coarctation Phaeochromocytoma Stenosis of renal arteries Note: only 5% of hypertension cases are secondary, rest are primary ```

Answer 250

``` "HEART MAy DIE": Hypertension Embolism Anemia Rheumatic heart disease Thyrotoxicosis (incl. pregnancy) Myocardial infarct Arrythmia Y Diet & lifestyle Infection Endocarditis ```

Answer 251

atrial tachy, AVN reentry tachy, AV reentry tachy. cf atrial fib and sinus tachy which are narrow complex but not counted as SVT.

Answer 252

these manœuvres transiently block the AVN so if the arrhythmia is dependent on it then they can reset the rhythm to normal sinus rhythm. Patients with AVNRT or AVRT may be able to terminate palpitations with vagal manoeuvres such as the Valsalva manoeuvre, breath holding, or coughing. AVNRT are more common and are due to having 2 distinct pathways in the region of the AVN, a fast one and a slow one. in AVRT there is an accessory pathway that bypasses the AVN, the most common type is WPW. Some patients can identify triggers such as caffeine or alcohol intake, which can initiate re-entrant tachycardia by increasing the frequency of extrasystoles. Sudden onset and offset of palpitations is typical for a re-entrant arrhythmia, while for sinus tachycardia onset and offset is usually gradual.

Answer 253

unlikely to affect a healthy individual if they don't have risk factors such as IVDU or dental surgery or replacement valves. v unwell, normal ECG, new heart murmur. cf pericarditis which can easily affect a previously healthy individual who just had a PMH of a mild infection . central chest pain, radiates to the back, makes them sit up and forwards to relieve. egg should support.

Answer 254

most commonly an inferior MI as in 60% of cases the RCA supplies the SAN. the LCA supplying it in the other 40%.

Answer 255

supplies right ventricle and 25% of the blood to the LV. AVN in 90%, SAN in 60%, posterior DA in 85% which supplies the inferior wall, ventricular septum and posteromedial papillary muscle.

Answer 256

main stem then LAD and L circumflex a. LAD = 2 thirds of the interventricualr septum, anterior part of the LV and apex. left marginal supplies left atrium, obtuse margin of the heart, posterior LV wall.

Answer 257

1 - cv uncompromised 2 - cv compromised 1 - amiodarone 300mg loading, then 900mg over 24hrs. 2 - eg chest pain, heart failure signs, systolic under 90, reduced consciousness - synchronised cardioversion.

Answer 258

causes LA enlargement, which via compression makes it difficult to clear bronchial secretions and compresses the recurrent laryngeal nerve .

Answer 259

HOCM. causes SIB, harsh ejection systolic murmur and double apex beat. and jerky pulse. can present with syncope or simply sudden death. half of cases have no family Hx and are usually due to sporadic mutations in the gene producing the beta-myosin heavy chain.

Answer 260

another term for a slow rising pulse as seen in aortic stenosis.

Answer 261

co2 liver failure sepsis narcosis.

Answer 262

atiral fib or regular pulse with multiple ectopics. do an ECG.

Answer 263

a barely palpable one as found in shock.

Answer 264

smooth, craggy (cloud), and nodular. | hard (bone), firm (cartilage), soft (muscle).

Answer 265

endothelial damage and rupture or fissuring of a plaque causes platelet aggregation and thrombus formation. vasospasm is induced by local inflam mediators causing further reduction in blood supply.

Answer 266

tall R waves and st segment depression in V1-3 and V6. caused by blockage in the left circumflex coronary artery.

Answer 267

after endoscopy if it diagnoses a peptide ulcer rather than say varices.

Answer 268

no. can also occur in myocarditis, pericarditis, PE, sepsis, renal failure.

Answer 269

2 types type 1 - wide PEF variability during the day despite intense therapy type 2 - sudden severe attacks on a background of apparently well controlled asthma

Answer 270

Score Anticoagulation 0 = No treatment 1 = Males: Consider anticoagulation Females: No treatment 2 or more = Offer anticoagulation Doctors have always thought carefully about the risk/benefit profile of starting someone on warfarin. A history of falls, old age, alcohol excess and a history of previous bleeding are common things that make us consider whether warfarinisation is in the best interests of the patient. NICE now recommend we formalise this risk assessment using the HASBLED scoring system.

Answer 271

H - Hypertension, uncontrolled, systolic BP > 160 mmHg = 1point A - Abnormal renal function (dialysis or creatinine > 200) = 1 point for any renal abnormalities Or Abnormal liver function (cirrhosis, bilirubin > 2 times normal, ALT/AST/ALP > 3 times normal = 1 point for any liver abnormalities S Stroke, history of =1 B Bleeding, history of bleeding or tendency to bleed =1 L Labile INRs (unstable/high INRs, time in therapeutic range 65 years) = 1 D Drugs Predisposing to Bleeding (Antiplatelet agents, NSAIDs) = 1 for drugs Or Alcohol Use (>8 drinks/week) = 1 for alcohol

Answer 272

Sildenafil is a phosphodiesterase type V inhibitor used in the treatment of impotence. Contraindications patients taking nitrates and related drugs such as nicorandil hypotension recent stroke or myocardial infarction (NICE recommend waiting 6 months) non-arteritic anterior ischaemic optic neuropathy ``` Side-effects visual disturbances e.g. blue discolouration, non-arteritic anterior ischaemic neuropathy nasal congestion flushing gastrointestinal side-effects headache ```

Answer 273

NICE produced guidelines on the management of patients following a myocardial infarction (MI) in 2013. Some key points are listed below All patients should be offered the following drugs: dual antiplatelet therapy (aspirin plus a second antiplatelet agent) ACE inhibitor beta-blocker statin Some selected lifestyle points: diet: advise a Mediterranean style diet, switch butter and cheese for plant oil based products. Do not recommend omega-3 supplements or eating oily fish exercise: advise 20-30 mins a day until patients are 'slightly breathless' sexual activity may resume 4 weeks after an uncomplicated MI. Reassure patients that sex does not increase their likelihood of a further MI. PDE5 inhibitors (e.g, sildenafil) may be used 6 months after a MI. They should however be avoided in patient prescribed either nitrates or nicorandil Clopidogrel since clopidogrel came off patent it is now much more widely used post-MI STEMI: the European Society of Cardiology recommend dual antiplatelets for 12 months. In the UK this means aspirin + clopidogrel non-ST segment elevation myocardial infarction (NSTEMI): following the NICE 2013 Secondary prevention in primary and secondary care for patients following a myocardial infarction guidelines clopidogrel should be given for the first 12 months Aldosterone antagonists patients who have had an acute MI and who have symptoms and/or signs of heart failure and left ventricular systolic dysfunction, treatment with an aldosterone antagonist licensed for post-MI treatment (e.g. eplerenone) should be initiated within 3-14 days of the MI, preferably after ACE inhibitor therapy

Answer 274

Electrical alternans is an electrocardiographic phenomenon of alternation of QRS complex amplitude or axis between beats and a possible wandering base-line. It is seen in cardiac tamponade and severe pericardial effusion and is thought to be related to changes in the ventricular electrical axis due to fluid in the pericardium, as the heart essentially wobbles in the fluid filled pericardial sac.[1] Generally electrical alternans can be seen with tamponade, and narrow AV junctional reenterant tachycardia with an accessory pathway (such as WPW syndrome). A similar phenomenon, pseudo-alternans, can be seen in bigeminal PVC in the PR interval, alternans pre-excitation, and alternans bundle branch block.[1] For the most part however, the most serious condition to rule out is tamponade. Electrical alternans with sinus tachycardia is a highly specific sign for large pericardial effusion. This is due to the swinging motion of the heart in the pericardial cavity causing a beat-to-beat variation in QRS axis and amplitude. Patients with cardiac tamponade and hemodynamic compromise should have emergency pericardiocentesis.

Answer 275

1 - diagnose heart failure due to left ventricular systolic dysfunction 2 - ACEI and beta blocker. ARB as alternative to ACEI 3 - specialist review 4 - if still symptomatic consider: aldosterone antagonist, ARB, hydralazine and nitrate esp if afrocarribean. 5 - if symptoms STILL persist - digoxin, cardiac resynchronisation therapy. on the side- (offer rehab, education and diuretics for fluid symptoms. )

Answer 276

Pregnancy-induced hypertension (PIH, also known as gestational hypertension) Hypertension (as defined above) occurring in the second half of pregnancy (i.e. after 20 weeks) No proteinuria, no oedema Occurs in around 5-7% of pregnancies Resolves following birth (typically after one month). Women with PIH are at increased risk of future pre-eclampsia or hypertension later in life

Answer 277

MONA be liberal with benzos, more so than other MI DO NOT use beta blockers or you get unopposed alpha action which will worsen.

Answer 278

NSAIDS or colchicine if NSAIDS are CI

Answer 279

atrial fibrillation. all the others are regular e.g. AVRT, AVNRT, atrial flutter, sinus tacky.

Answer 280

orthodromic is narrow complex, antidromic is broad.

Answer 281

put a syringe opening in their mouth and ask them to blow out the plunger

Answer 282

torsades (polymorphic vt) af with LBBB VF = pulseless

Answer 283

vt avrt antidromic SVT with BBB

Answer 284

sinus tachy avnrt avrt orthodromic atrial flutter

Answer 285

guaranteed to get SE if on it long enough, use sotalol in AF instead (an atypical beta blocker)

Answer 286

any beta blocker except sotalol as this is rhythm control. | if you can't use bb then use non dihydro CCB pref diltiazem

Answer 287

negatively chronotrophic positively inotropic so good in AF in heart failure.

Answer 288

in AF with mitral valve disease, their risk is automatically 20% so you anticoagulant.

Answer 289

1- adverse features ? if yes - atropine 500micrograms IV then assess for satisfactory response. if there is then move on as if there were no adverse features, if it fails to respond then move to interim measures. if no - is there a risk of asystole? (recent asystole, mobitz type 2, complete heart block with wide QRS, ventricular pause over 3secs) - if no then observe, if yes move to interim measures. - interim measures - 1- repeat IV atropine 500 micrograms up to 3g max. 2- isoprenaline 5micrograms per min IV 3- adrenaline 2-10 micrograms per min IV 4 - alternative drugs such as aminophylline, dopamine, glucagon (if beta blocker or CCB overdose), glycopyrrolate instead of atropine. alternatively - transcutaneous pacing. if all options fail seek expert help and arrange transvenous pacing

Answer 290

``` IV calcium (chloride or gluconate, whichever) second line is insulin, acts as positive inotrope. ```

Answer 291

Rupture is a potentially lethal consequence of an abdominal aortic aneurysm. The risk of rupture is generally considered to high once its diameter is > 5.5cm and so treatment is usually deferred until then when the risks of no surgery outweigh the risks of surgery. For aneurysms

Answer 292

Fever + Murmur = Infective Endocarditis until proven otherwise. causes: a) E.Faecalis is associated with genitourinary disease b) The HACEK group are gram negative coccobacilli and account for ~3% of the total cases of infective endocarditis. c) Staph. Aureas is common in IVDU users d) Iron Deficiency Anaemia + Weight Loss = Colon Cancer until proven otherwise. Streptococcus Bovis is associated with bowel cancer. e) Strep. Viridans is associated with dental procedures and Strep. epidermidis within the first year of valve replacements.

Answer 293

blocks or reduces AVN conduction .

Answer 294

The clues here are in the ECG and the fact that the tachycardia resolves with adenosine. Inverted P waves in the inferior leads are suggestive of retrograde atrial conduction. This phenomenon is common to junctional tachycardias, which would also fi t with the patient—the fact that she has had them before—and the fact that it resolves once the AV node is blocked by adenosine. Junctional tachycardias originate from the region of the AV node. They are either atrioventricular re-entrant tachycardias (AVRTs) or atrioventricular nodal re-entry tachycardias (AVNRTs). AVNRTs are the most common, usually aff ecting young, healthy individuals with no organic heart disease. They are caused by having two distinct pathways in the region of the AV node—a fast and a slow one. In AVRT, there is an accessory pathway that actually bypasses the AV node and activates the ventricles prematurely. The most common type is Wolff –Parkinson–White syndrome.

Answer 295

``` This man has had a myocardial infarction (MI) and is bradycardic. The most likely cause of bradycardia is an inferior MI as, in 60% of cases, the RCA supplies the sinoatrial (SA) node (the LCA supplying the other 40%). ```

Answer 296

The ECG shows a regular broad complex tachycardia. Guidelines state that if the patient is not cardiovascularly compromised—as in this case where he is maintaining a good blood pressure—the fi rst-line treatment is amiodarone 300mg as a loading dose, followed by 900mg over the course of the next 24h. In those that are compromised (chest pain, signs of heart failure, systolic BP

Answer 297

When the doctor receives the phone call from the ward about this patient, it is vital that he establishes immediately whether the palpitations are causing her haemodynamic compromise. He can do this by checking for the presence of any of the following four factors: 1. Systolic BP 150bpm If any are present, then he should be heading to the ward directly. It would also be wise to alert a senior doctor as the patient will certainly need treatment, possibly even sedation and direct current (DC) cardioversion.

Answer 298

A collapsing or ‘waterhammer’ pulse is found in aortic incompetence and is more likely to present with breathlessness or heart failure.

Answer 299

This describes atrial fi brillation or a regular output punctuated by multiple ectopics: an ECG would help to differentiate the two. This is the best diff erential diagnosis as it can present with faintness, but would be more likely also to cause palpitations.

Answer 300

The image shows corneal arcus, a sign—especially in those under 60—of hyperlipidaemia (in those over 60 it can be a normal fi nding). The key is finding the cause of the high lipid levels. If they are primary, then they will need treatment—initially with lifestyle measures and then with medications. However, it is important to fi rst rule out secondary causes of hyperlipidaemia, i.e. liver, kidney, and thyroid disease.

Answer 301

This can present with ascites and abdominal pain but symptoms and signs of liver failure including hepatomegaly would be expected.

Answer 302

This lady has cor pulmonale or right ventricular failure due to chronic hypoxic pulmonary vasoconstriction. Right ventricular hypertrophy, raised right atrial pressures (raised JVP), and raised systemic venous pressure can cause ascites and peripheral oedema. Peripheral oedema in someone with COPD should always prompt assessment of right heart function.

Answer 303

Treatment of complete heart block depends on the site of the block. When the atrial rhythm is not conducted, the ventricular rhythm that is seen is an ‘escape’ rhythm. The width of the QRS complex refl ects where the escape has been generated from. If it is from above the bundle of His, the complex is narrow, the escape rhythm coming from a junctional pacemaker at a rate of 45–60bpm. These patients are usually haemodynamically stable and may respond to medical therapy such as atropine. If the rhythm comes from below the bundle of His, the complex is wide at a rate of

Answer 304

This is symptomatic anaemia (Hb usually

Answer 305

Adenosine is used in atrial fl utter (depicted here with 2:1 block) as it causes a transient heart block at the AV node, slows the ventricles, and reveals the underlying atrial rhythm.

Answer 306

A 30-year-old man has been involved in a road traffi c accident. He has sustained injuries to the chest wall and is short of breath. A trauma series of X-rays suggests fl uid in the pleura and pericardium. This is confi rmed by a transthoracic echocardiogram. The JVP rises with inspiration. This paradoxical rise is Kussmaul’s sign. Anything—any sort of fl uid or an abnormal pericardium (in this case, a pericardial eff usion)—that stops the heart from expanding during inspiration also stops the jugular venous pulse from falling as it should

Answer 307

This is tricuspid regurgitation causing tender hepatomegaly. A pansystolic murmur is found with mitral and tricuspid regurgitation and ventricular septal defects. The ‘v’ wave occurs towards the end of the pulse and represents atrial fi lling against a closed tricuspid valve. RV heave is usually caused by RV hypertrophy and causes the examining hand to be forced off the chest wall during systole

Answer 308

The ‘a’ wave represents atrial systole and occurs just before the carotid pulsation. Prominence is seen in pulmonary hypertension/stenosis. A widely split S 2 is seen when A2 occurs early or P2 is delayed, as in this case where the most likely cause is pulmonary stenosis.

Answer 309

E A palpable fi rst heart sound and facies are typical of mitral stenosis.

Answer 310

In patients who have paroxysmal atrial fi brillation (AF), guidance is that a ‘pill in pocket’ strategy (i.e. a medicine to be taken as required) should be considered if the following criteria are met: There is no history of left ventricular dysfunction, or valvular or ischaemic heart disease. There are infrequent symptomatic episodes of paroxysmal AF. Systolic BP >100mmHg and resting HR >70bpm. Patients can understand how and when to take the medication. Flecainide is a class Ic anti-arrhythmic agent and can be used in this way due to its rapidity of action. Studies have shown that it is eff ective in 80% of arrhythmic episodes in those with paroxysmal AF and so reduces the need for hospitalization. A Amiodarone can be used if beta-blockers have been unable to suppress paroxysms in those with poor left ventricular function. B Digoxin is not used in paroxysmal AF but as a rate control in permanent AF for ‘sedentary’ patients. ``` D Metoprolol (or another ‘standard’ beta -blocker) would be the fi rst choice in paroxysmal AF where a pill-in-the-pocket strategy is not thought appropriate. ``` E Sotalol would be the next choice after a standard beta -blocker if suppression of symptoms has not been achieved

Answer 311

In severe hypertension, it is vital to establish whether the raised blood pressure is causing end-organ dysfunction, as, if it is, it will need emergency treatment. This is obvious in cases of myocardial infarction, pulmonary oedema, and aortic dissection, but can be present in rather more covert ways. One of these is hypertensive encephalopathy, which classically presents with a headache, change in consciousness, and some minor neurological dysfunction. In this case, therefore, the junior doctor should establish over the phone whether the patient has a headache: if she does, then he should head directly to the ward to perform an urgent assessment of her Glasgow Coma Scale (GCS) score, neurology, and fundi.

Answer 312

C The line tip is between the fi rst and third sternocostal joints This is a common task for the on-call junior doctor. A post-insertion X-ray should always be requested to check for two main things: (i) that there are no complications from the procedure and (ii) that the line is lying in the correct place for use. The most common immediate complication that can be screened for on an X-ray is a pneumothorax. If the junior doctor is happy that there are no intrapleural slivers of air and he or she can confi rm that the line tip lies between the fi rst and third sternocostal joints—i.e. in the superior vena cava—then he or she can say that there have been no immediate complications from the procedure and that the line is lying in the correct place ready for use.

Answer 313

The history recounts a series of Stokes–Adams attacks. These are transient bradycardias due to lack of conduction through the atrioventricular (AV) node causing decreased cardiac output and loss of consciousness. The ECG shows a lack of correlation between the P waves and the QRS complexes, and a ventricular rate of 25–30/min. Emergency treatment involves continuous cardiac monitoring and transcutaneous pacing with a view to the placement of a defi nitive transvenous pacemaker, even if the patient is asymptomatic.

Answer 314

This acts on the His–Purkinje system and is therefore used in the treatment of many supraventricular tachycardias.

Answer 315

Treating severe hypertension is a common but diffi cult clinical problem. The key to management is to appreciate the actual eff ect that the raised blood pressure is having. If the blood pressure is causing end-organ dysfunction, then it can be said to represent a hypertensive emergency; if it is not, then it is termed a hypertensive urgency. There are certain situations that are indicative of end-organ damage and, therefore, an emergency: Acute myocardial infarction/unstable angina Acute pulmonary oedema Acute renal failure Acute aortic dissection Hypertensive encephalopathy Eclampsia. The aim in emergencies is to stop ongoing end-organ damage. The most eff ective way of doing this (without dropping the blood pressure too quickly and adversely aff ecting cerebral perfusion) is via controlled IV therapy (labetalol is recommended), with the aim of reducing the diastolic blood pressure by 10–15%. A slower approach can be taken in urgencies with the aim of reducing the blood pressure gradually over a couple of days. The use of sublingual therapies such as nifedipine has been condemned due to the seriousness of adverse events reported due to the uncontrolled way in which it drops blood pressure.

Answer 316

Digoxin is cleared both renally and metabolically. Chronic cardiac failure and hypothyroidism reduce the effi cacy of clearance, leading to elevated levels. Drugs such as amiodarone, verapamil, and quinidine have the same eff ect and should prompt a reduction in digoxin dose once started to avoid precipitating toxic levels

Answer 317

If symptoms persist or even worsen, despite optimal medical therapy, then a cardiologist may consider the need for resynchronization therapy. This is essentially a biventricular pacemaker that co-ordinates the action of the right and left ventricles. There are various inclusion criteria, including the left ventricular ejection fraction and the width of the QRS complex.

Answer 318

A regular narrow complex tachycardia should initially be treated with a vagal manoeuvre. This increases vagal tone at the atrioventricular (AV) node in order to prevent conduction of impulses from the atria. In order of eff ectiveness these include the Valsalva manoeuvre, carotid sinus massage, and the ‘diving refl ex’, where the patient’s face is submerged in cold water or covered with a towel soaked in cold water

Answer 319

Regardless of the cause of the tachyarrhythmia, signs that the patient is unstable include: (i) chest pain; (ii) signs of heart failure; (iii) reduced consciousness level; and (iv) systolic BP

Answer 320

Thiazide diuretics can aff ect blood glucose control by decreasing both insulin secretion and peripheral insulin sensitivity. They can also lead to electrolyte imbalance, especially hypokalaemia, particularly in patients who have hepatic and renal impairment.

Answer 321

The management of stable angina comprises lifestyle changes, medication, percutaneous coronary intervention and surgery. NICE produced guidelines in 2011 covering the management of stable angina Medication all patients should receive aspirin and a statin in the absence of any contraindication sublingual glyceryl trinitrate to abort angina attacks NICE recommend using either a beta-blocker or a calicum channel blocker first-line based on 'comorbidities, contraindications and the person's preference' if a calcium channel blocker is used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used. If used in combination with a beta-blocker then use a long-acting dihydropyridine calcium-channel blocker (e.g. modified-release nifedipine). Remember that beta-blockers should not be prescribed concurrently with verapamil (risk of complete heart block) if there is a poor response to initial treatment then medication should be increased to the maximum tolerated dose (e.g. for atenolol 100mg od) if a patient is still symptomatic after monotherapy with a beta-blocker add a calcium channel blocker and vice versa if a patient is on monotherapy and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider one of the following drugs: a long-acting nitrate, ivabradine, nicorandil or ranolazine if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG Nitrate tolerance many patients who take nitrates develop tolerance and experience reduced efficacy the BNF advises that patients who develop tolerance should take the second dose of isosorbide mononitrate after 8 hours, rather than after 12 hours. This allows blood-nitrate levels to fall for 4 hours and maintains effectiveness this effect is not seen in patients who take modified release isosorbide mononitrate Ivabradine a new class of anti-anginal drug which works by reducing the heart rate acts on the If ('funny') ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity adverse effects: visual effects, particular luminous phenomena, are common. Bradycardia, due to the mechanism of action, may also be seen there is no evidence currently of superiority over existing treatments of stable angina

Answer 322

Both carvedilol and bisoprolol have been shown to reduce mortality in stable heart failure. The other beta-blockers have no evidence base to support their use. NICE recommend that all heart failure patients should take both an ACE-inhibitor and a beta-blocker.

Answer 323

Step 3 treatment add a thiazide diuretic (D, i.e. A + C + D) NICE now advocate using either chlorthalidone (12.5-25.0 mg once daily) or indapamide (1.5 mg modified-release once daily or 2.5 mg once daily) in preference to a conventional thiazide diuretic such as bendroflumethiazide thiazide-like

Answer 324

NICE define a clinic BP >= 140/90 mmHg after step 3 treatment with optimal or best tolerated doses as resistant hypertension. They suggest step 4 treatment or seeking expert advice Step 4 treatment consider further diuretic treatment if potassium 4.5 mmol/l add higher-dose thiazide-like diuretic treatment if further diuretic therapy is not tolerated, or is contraindicated or ineffective, consider an alpha- or beta-blocker Patients who fail to respond to step 4 measures should be referred to a specialist

Answer 325

As this gentleman is presenting with atrial fibrillation (as seen by palpitations and absent P waves on ECG), the options for management include rate or rhythm control, with the possibility of thromboprophylaxis. However, as he has an unmeasurable BP and signs of haemodynamic instability, he is acutely unwell and so his arrhythmia must be treated as soon as possible with DC cardioversion without delaying for thromboprophylaxis. Anticoagulation should be continued for 4 weeks after cardioversion however. If he was clinically stable and had atrial fibrillation of over 48 hours duration, the risk of stroke would mean parenteral anticoagulation would take precedence over cardioversion. (source: NICE, https://www.nice.org.uk/guidance/cg180) Peri-arrest rhythms: bradycardia The 2010 Resuscitation Council (UK) guidelines emphasise that the management of bradycardia depends on: 1. identifying the presence of signs indicating haemodynamic compromise - 'adverse signs' 2. identifying the potential risk of asystole Adverse signs The following factors indicate haemodynamic compromise and hence the need for treatment: shock: hypotension (systolic blood pressure 3 seconds If there is a delay in the provision of transvenous pacing the following interventions may be used: atropine, up to maximum of 3mg transcutaneous pacing adrenaline infusion titrated to response

Answer 326

Protamine sulfate is a drug that reverses the anticoagulant effects of heparin by binding to it.

Answer 327

``` ECG left ventricular hypertrophy progressive T wave inversion deep Q waves atrial fibrillation may occasionally be seen ``` Sudden death, unusual collapse in young person - ? HOCM In this age group hypertrophic obstructive cardiomyopathy would be a more common cause of the murmur/recurrent collapse than aortic stenosis.

Answer 328

Primary percutaneous coronary intervention (PCI) has emerged as the gold-standard treatment for STEMI but is not available in all centres. Thrombolysis should be performed in patients without access to primary PCI With regards to thrombolysis: tissue plasminogen activator (tPA) has been shown to offer clear mortality benefits over streptokinase tenecteplase is easier to administer and has been shown to have non-inferior efficacy to alteplase with a similar adverse effect profile An ECG should be performed 90 minutes following thrombolysis to assess whether there has been a greater than 50% resolution in the ST elevation if there has not been adequate resolution then rescue PCI is superior to repeat thrombolysis for patients successfully treated with thrombolysis PCI has been shown to be beneficial. The optimal timing of this is still under investigation

Answer 329

Deep ST depression in V1-V3 with tall T waves is a sign of a severe posterior myocardial infarction. These patients should be treated as a STEMI. If you were to place posterior leads on the back of the patient and re do the ECG you would see ST elevation. Therefore the patient should be treated with primary percutaneous coronary intervention.

Answer 330

All patients should receive: 1 - aspirin 300mg 2 - nitrates or morphine to relieve chest pain if required 3 - Antithrombin treatment. Fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography within the next 24 hours. If angiography is likely within 24 hours or a patients creatinine is > 265 µmol/l unfractionated heparin should be given. 4 - Clopidogrel 300mg should be given to all patients and continued for 12 months. 5 - Intravenous glycoprotein IIb/IIIa receptor antagonists (eptifibatide or tirofiban) should be given to patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%), and who are scheduled to undergo angiography within 96 hours of hospital admission. 6 - Coronary angiography should be considered within 96 hours of first admission to hospital to patients who have a predicted 6-month mortality above 3.0%. It should also be performed as soon as possible in patients who are clinically unstable. The 2008 British Thoracic Society oxygen therapy guidelines advise not giving oxygen unless the patient is hypoxic.

Answer 331

Overview acyanotic congenital heart defect connection between the pulmonary trunk and descending aorta more common in premature babies, born at high altitude or maternal rubella infection in the first trimester ``` Features left subclavicular thrill continuous 'machinery' murmur large volume, bounding, collapsing pulse wide pulse pressure heaving apex beat ```

Answer 332

Management indomethacin closes the connection in the majority of cases if associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repair

Answer 333

Brugada Syndrome is an ECG abnormality with a high incidence of sudden death in patients with structurally normal hearts. There’s really only one type of Brugada syndrome. Diagnosis depends on a characteristic ECG finding AND clinical criteria. Further risk stratification is controversial. Definitive treatment = ICD. Brugada sign in isolation is of questionable significance. In a nutshell, Brugada syndrome is due to a mutation in the cardiac sodium channel gene. This is often referred to as a sodium channelopathy. Over 60 different mutations have been described so far and at least 50% are spontaneous mutations, but familial clustering and autosomal dominant inheritance has been demonstrated. ECG changes can be transient with Brugada syndrome and can also be unmasked or augmented by multiple factors Type 1 (Coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave) is the only ECG abnormality that is potentially diagnostic. This has been referred to as Brugada sign This ECG abnormality must be associated with one of the following clinical criteria to make the diagnosis: Documented ventricular fibrillation (VF) or polymorphic ventricular tachycardia (VT). Family history of sudden cardiac death at

Answer 334

Management IV bicarbonate may reduce the risk of seizures and arrhythmias in severe toxicity arrhythmias: class 1a (e.g. Quinidine) and class Ic antiarrhythmics (e.g. Flecainide) are contraindicated as they prolong depolarisation. Class III drugs such as amiodarone should also be avoided as they prolong the QT interval. Response to lignocaine is variable and it should be emphasized that correction of acidosis is the first line in management of tricyclic induced arrhythmias intravenous lipid emulsion is increasingly used to bind free drug and reduce toxicity dialysis is ineffective in removing tricyclics

Answer 335

Prosthetic heart valves - antithrombotic therapy: bioprosthetic: aspirin mechanical: warfarin + aspirin

Answer 336

The patient is suffering from severe pulmonary oedema with bilateral course crackles and cough productive of white sputum. The patient has signs of right sided heart failure with raised JVP and peripheral oedema. They also have a history of MI and hypertension that are two risk factors for heart failure. NICE guidance on Acute Heart Failure 2014 states that a patient who has failed medical management of pulmonary oedema with severe dyspnoea should be considered for CPAP. BIPAP is not used in acute pulmonary oedema. Heart failure: acute management ``` Management options in acute heart failure include: oxygen diuretics opiates vasodilators inotropic agents CPAP ultrafiltration mechanical circulatory assistance: e.g. intra-aortic balloon counterpulsation or ventricular assist devices ``` Consideration should be given to discontinuing beta-blockers in the short-term.

Answer 337

'J' wave - small hump at the end of the QRS complex seen i hypothermia

Answer 338

Whilst some patients with acromegaly have mitral valve prolapse (MVP) it is not a common association. It should be remembered that the prevalence of MVP in a standard population is around 5-10% Mitral valve prolapse Mitral valve prolapse is common, occurring in around 5-10 % of the population. It is usually idiopathic but may be associated with a wide variety of cardiovascular disease and other conditions ``` Associations congenital heart disease: PDA, ASD cardiomyopathy Turner's syndrome Marfan's syndrome, Fragile X osteogenesis imperfecta pseudoxanthoma elasticum Wolff-Parkinson White syndrome long-QT syndrome Ehlers-Danlos Syndrome polycystic kidney disease ``` Features patients may complain of atypical chest pain or palpitations mid-systolic click (occurs later if patient squatting) late systolic murmur (longer if patient standing) complications: mitral regurgitation, arrhythmias (including long QT), emboli, sudden death

Answer 339

Thrombolytic drugs activate plasminogen to form plasmin. This in turn degrades fibrin and help breaks up thrombi. They in primarily used in patients who present with a ST elevation myocardial infarction. Other indications include acute ischaemic stroke and pulmonary embolism, although strict inclusion criteria apply.

Answer 340

In this situation NICE recommend either adding diltiazem or digoxin.

Answer 341

The correct answer is Papillary muscle rupture This patient has developed acute mitral regurgitation secondary to papillary muscle rupture. The differential diagnosis is ventricular septal rupture.

Answer 342

Conn's syndrome is the likely diagnosis - a renin:aldosterone ratio would be an appropriate first-line investigation. A normal clinical examination makes a diagnosis of Cushing's syndrome less likely Primary hyperaldosteronism Primary hyperaldosteronism was previously thought to be most commonly caused by an adrenal adenoma, termed Conn's syndrome. However, recent studies have shown that bilateral idiopathic adrenal hyperplasia is the cause in up to 70% of cases. Differentiating between the two is important as this determines treatment. Adrenal carcinoma is an extremely rare cause of primary hyperaldosteronism Features hypertension hypokalaemia (e.g. muscle weakness) alkalosis ``` Investigations high serum aldosterone low serum renin high-resolution CT abdomen adrenal vein sampling ``` Management adrenal adenoma: surgery bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone

Answer 343

This patient has developed ankle oedema after being started on amlodipine. Oedema is listed as one of the most common side-effects of amlodipine in the BNF. In this situation NICE advise ' If a calcium channel blocker is not suitable, for example because of oedema or intolerance, or if there is evidence of heart failure or a high risk of heart failure, offer a thiazide-like diuretic.' eg indapamide

Answer 344

NICE guidelines recommend adding a calcium channel blocker for angina which is not adequately controlled with beta-blocker monotherapy. Verapamil is contraindicated whilst taking a beta-blocker and diltiazem should be used with caution due to the risk of bradycardia.

Answer 345

Clinic BP ABPM / HBPM | Age 80 years 150/90 mmHg 145/85 mmHg

Answer 346

The T waves in V2 + V3 are very large or 'hyperacute' to use the cardiology lingo. This is often the first change seen with myocardial ischaemia. This patients ECG 30 minutes later is shown below: STEMI basically this person had hyper acute T waves and i missed that. the just looked really big and in one vessel territory. should have admitted to hospital

Answer 347

if the are out of hospital. give them the aspirin and GTN but NICE say no clopidogrel until in hospital

Answer 348

Firstly, exam technique - we can discount verapamil - this lady has heart failure and would not be prescribed a drug which has such strong negative inotropic effects. The above ECG shows slow atrial fibrillation. A beta-blocker overdose may explain the bradycardia but not give the characteristic ECG changes seen here - 'scooped' or 'reverse tick' ST depression in I and aVL and a short QTc interval. ECG: digoxin ``` ECG features down-sloping ST depression ('reverse tick') flattened/inverted T waves short QT interval arrhythmias e.g. AV block, bradycardia ```

Answer 349

NICE now only recommend diagnosing people over the age of 80 years as hypertensive if they have stage 2 hypertension (ABPM daytime average or HBPM average BP >= 150/95 mmHg).

Answer 350

NICE issued guidelines on atrial fibrillation (AF) in 2006. They included advice on the management of patients with AF who develop a stroke or transient-ischaemic attack (TIA). Recommendations include: following a stroke or TIA warfarin should be given as the anticoagulant of choice. Aspirin/dipyridamole should only be given if needed for the treatment of other comorbidities in acute stroke patients, in the absence of haemorrhage, anticoagulation therapy should be commenced after 2 weeks. If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed

Answer 351

The administration of adenosine is contraindicated by her history of asthma. Verapamil should therefore be given.

Answer 352

Aortic dissection type A - ascending aorta - control BP(IV labetalol) + surgery type B - descending aorta - control BP(IV labetalol)

Answer 353

Myocarditis is an acute inflammatory condition of the heart which often occurs in patients with no underlying cardiac disease. Clinical features include chest pain (usually due to co-existant pericarditis), acute heart failure and arrhythmias. While the most common aetiology in Europe is viral, the most common cause worldwide is Trypanosoma cruzi (Chaga's disease). 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

Answer 354

Cardiac tamponade Constrictive pericarditis JVP: Absent Y descent X + Y present Pulsus paradoxus: Present Absent Kussmaul's sign: Rare Present Characteristic features : none, Pericardial calcification on CXR

Answer 355

Flash pulmonary oedema, U&Es worse on ACE inhibitor, asymmetrical kidneys → renal artery stenosis - do MR angiography Renal artery stenosis may cause sudden onset or 'flash' pulmonary oedema. A myocardial infarction is unlikely given the normal ECG and cardiac enzymes. Chest pain would also be expected in a 55-year-old patient with no history of diabetes. Fibromuscular dysplasia is generally seen in young woman. Renal vascular disease Renal vascular disease is most commonly due to atherosclerosis (> 95% of patients). It is associated with risk factors such as smoking and hypertension that cause atheroma elsewhere in the body. It may present as hypertension, chronic renal failure or 'flash' pulmonary oedema. In younger patients however fibromuscular dysplasia (FMD) needs to be considered. FMD is more common in young women and characteristically has a 'string of beads' appearance on angiography. Patients respond well to balloon angioplasty Investigation MR angiography is now the investigation of choice CT angiography conventional renal angiography is less commonly performed used nowadays, but may still have a role when planning surgery

Answer 356

NICE NSTEMI/unstable angina guidelines are based on 6 month mortality risk: if > 1.5% clopidogrel for 12 months if > 3% angiography within 96 hours

Answer 357

All patients should be offered the following drugs: dual antiplatelet therapy (aspirin plus a second antiplatelet agent) ACE inhibitor beta-blocker statin Some selected lifestyle points: diet: advise a Mediterranean style diet, switch butter and cheese for plant oil based products. Do not recommend omega-3 supplements or eating oily fish exercise: advise 20-30 mins a day until patients are 'slightly breathless' sexual activity may resume 4 weeks after an uncomplicated MI. Reassure patients that sex does not increase their likelihood of a further MI. PDE5 inhibitors (e.g, sildenafil) may be used 6 months after a MI. They should however be avoided in patient prescribed either nitrates or nicorandil Clopidogrel since clopidogrel came off patent it is now much more widely used post-MI STEMI: the European Society of Cardiology recommend dual antiplatelets for 12 months. In the UK this means aspirin + clopidogrel non-ST segment elevation myocardial infarction (NSTEMI): following the NICE 2013 Secondary prevention in primary and secondary care for patients following a myocardial infarction guidelines clopidogrel should be given for the first 12 months Aldosterone antagonists patients who have had an acute MI and who have symptoms and/or signs of heart failure and left ventricular systolic dysfunction, treatment with an aldosterone antagonist licensed for post-MI treatment (e.g. eplerenone) should be initiated within 3-14 days of the MI, preferably after ACE inhibitor therapy

Answer 358

A baseline chest x-ray is required due to the risk of pulmonary fibrosis / pneumonitis in patients treated with amiodarone. Urea and electrolytes are suggested by the BNF to detect hypokalaemia which may increase the risk of arrhythmias developing. Amiodarone Amiodarone is a class III antiarrhythmic agent used in the treatment of atrial, nodal and ventricular tachycardias. The main mechanism of action is by blocking potassium channels which inhibits repolarisation and hence prolongs the action potential. Amiodarone also has other actions such as blocking sodium channels (a class I effect) The use of amiodarone is limited by a number of factors long half-life (20-100 days) should ideally be given into central veins (causes thrombophlebitis) has proarrhythmic effects due to lengthening of the QT interval interacts with drugs commonly used concurrently e.g. Decreases metabolism of warfarin numerous long-term adverse effects (see below) Monitoring of patients taking amiodarone TFT, LFT, U&E, CXR prior to treatment TFT, LFT every 6 months ``` Adverse effects of amiodarone use thyroid dysfunction corneal deposits pulmonary fibrosis/pneumonitis liver fibrosis/hepatitis peripheral neuropathy, myopathy photosensitivity 'slate-grey' appearance thrombophlebitis and injection site reactions bradycardia ```

Answer 359

Verapamil and digoxin should be avoided in patients with Wolff-Parkinson White as they may precipitate VT or VF

Answer 360

The ECG shows both right bundle branch block and left axis deviation indicating bifascicular block. ECG: bi/tri-fascicular block Bifascicular block combination of RBBB with left anterior or posterior hemiblock e.g. RBBB with left axis deviation Trifascicular block features of bifascicular block as above + 1st degree heart block

Answer 361

Rheumatic fever develops following an immunological reaction to recent (2-6 weeks ago) Streptococcus pyogenes infection. Diagnosis is based on evidence of recent streptococcal infection accompanied by: 2 major criteria 1 major with 2 minor criteria ``` Evidence of recent streptococcal infection ASOT > 200iu/mL history of scarlet fever positive throat swab increase in DNase B titre ``` ``` Major criteria erythema marginatum Sydenham's chorea polyarthritis carditis (endo-, myo- or peri-) subcutaneous nodules ``` ``` Minor criteria raised ESR or CRP pyrexia arthralgia (not if arthritis a major criteria) prolonged PR interval ```

Answer 362

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 cardiotoxic drugs are used

Answer 363

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 diuretic and natriuretic suppresses both sympathetic tone and the renin-angiotensin-aldosterone system Clinical uses of BNP Diagnosing patients with acute dyspnoea a low concentration of BNP(400) carry poor prognosis. In these cases 2 week wait for urgent echocardiography and specialist assessment is advised. Although elevated levels of BNP do not confirm the diagnosis of heart failure, normal levels rule the diagnosis out (highly sensitivity but varying specificity). NICE suggest that BNP measurements are not necessary in people with suspected heart failure who have had a previous myocardial infarction. These patients require urgent referral, echocardiography and specialist assessment because if heart failure is present this carries a poor prognosis. Increased BNP levels (>400) are not on their own diagnostic of heart failure, and may be elevated as a result of left ventricular hypertrophy, myocardial ischaemia, atrial fibrillation, pulmonary hypertension, hypoxia, pulmonary embolism, right ventricular strain, chronic obstructive pulmonary disease, liver failure, sepsis, diabetes, and renal impairment. In addition, levels tend to be higher in women, and in people older than 70. Heart failure is unlikely if BNP levels are low (

Answer 364

Causes of a loud S2 hypertension: systemic (loud A2) or pulmonary (loud P2) hyperdynamic states atrial septal defect without pulmonary hypertension

Answer 365

Causes of a soft S2 | aortic stenosis

Answer 366

Causes of fixed split S2 | atrial septal defect

Answer 367

``` Causes of a widely split S2 deep inspiration RBBB pulmonary stenosis severe mitral regurgitation ```

Answer 368

``` Causes of a reversed (paradoxical) split S2 (P2 occurs before A2) LBBB severe aortic stenosis right ventricular pacing WPW type B (causes early P2) patent ductus arteriosus ```

Answer 369

If patients have typical anginal symptoms and a risk of CAD is greater than 90% then no further diagnostic testing is required. It should be noted that all men over the age of 70 years who have typical anginal symptoms fall into this category.

Answer 370

ACE inhibitors are first-line for hypertension in diabetics, irrespective of the patients age This patient has stage 1 hypertension as defined by NICE. He should however be treated because he has underlying diabetes. The first-line treatment for a patient aged > 55 years is a calcium channel blocker. However, in patients with diabetes ACE inhibitors are used first-line due to their renoprotective effect. Diabetes mellitus: hypertension management NICE recommend the following blood pressure targets for type 2 diabetics: if end-organ damage (e.g. renal disease, retinopathy)

Answer 371

The association between angiodysplasia and aortic stenosis is thought to be caused by von Willebrand factor (vWF) being proteolysed in the turbulent blood flow around the aortic valve vWF is most active in vascular beds with high shear stress, such as angiodysplasia, and deficiency of vWF increases the bleeding risk from such lesions Angiodysplasia Angiodysplasia is a vascular deformity of the gastrointestinal tract which predisposes to bleeding and iron deficiency anaemia. There is thought to be an association with aortic stenosis, although this is debated. Angiodysplasia is generally seen in elderly patients Diagnosis colonoscopy mesenteric angiography if acutely bleeding Management endoscopic cautery or argon plasma coagulation antifibrinolytics e.g. Tranexamic acid oestrogens may also be used

Answer 372

Causes of long QT syndrome: 1. Genetic: LQT1 / LQT2 (potassium channel mutation); LQT3 (sodium channel mutation) Jervell and Lange-Nielsen syndrome (associated with deafness) Romano-Ward syndrome 2. Electrolytes: Hypocalcaemia Hypomagnesaemia Hypokalaemia 3. Drugs: Antiarrhythmics (e.g. amioderone, sotalol) Antibiotics (e.g. erythromycin, clarithromycin, ciprofloxacin) Psychotropic drugs (e.g. serotonin reuptake inhibitors, tricyclic antidepressants, neuroleptic agents)

Answer 373

If a patient is suspected of having a DVT a two-level DVT Wells score should be performed: Clinical probability simplified score DVT likely: 2 points or more DVT unlikely: 1 point or less If a DVT is 'likely' (2 points or more) a proximal leg vein ultrasound scan should be carried out within 4 hours and, if the result is negative, a D-dimer test if a proximal leg vein ultrasound scan cannot be carried out within 4 hours a D-dimer test should be performed and low-molecular weight heparin administered whilst waiting for the proximal leg vein ultrasound scan (which should be performed within 24 hours) If a DVT is 'unlikely' (1 point or less) perform a D-dimer test and if it is positive arrange: a proximal leg vein ultrasound scan within 4 hours if a proximal leg vein ultrasound scan cannot be carried out within 4 hours low-molecular weight heparin should be administered whilst waiting for the proximal leg vein ultrasound scan (which should be performed within 24 hours)

Answer 374

Management Low molecular weight heparin (LMWH) or fondaparinux should be given initially after a DVT is diagnosed. a vitamin K antagonist (i.e. 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 or fondaparinux is given at the same time as warfarin until the INR is in the therapeutic range warfarin should be continued for at least 3 months. At 3 months, NICE advise that clinicians should 'assess the risks and benefits of extending treatment' NICE add 'consider extending warfarin beyond 3 months for patients with unprovoked proximal DVT if their risk of VTE recurrence is high and there is no additional risk of major bleeding'. 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 3 months. In practice most clinicians give 6 months of warfarin for patients with an unprovoked DVT/PE for patients with active cancer NICE recommend using LMWH for 6 months

Answer 375

Further investigations and thrombophilia screening As both malignancy and thrombophilia are obvious risk factors for deep vein thrombosis NICE make recommendations on how to investigate patients with unprovoked clots. Offer all patients diagnosed with unprovoked DVT or PE who are not already known to have cancer the following investigations for cancer: a physical examination (guided by the patient's full history) and a chest X-ray and blood tests (full blood count, serum calcium and liver function tests) and urinalysis. Consider further investigations for cancer with an abdomino-pelvic CT scan (and a mammogram for women) in all patients aged over 40 years with a first unprovoked DVT or PE Thrombophilia screening not offered if patients will be on lifelong warfarin (i.e. won't alter management) consider testing for antiphospholipid antibodies if unprovoked DVT or PE consider testing for hereditary thrombophilia in patients who have had unprovoked DVT or PE and who have a first-degree relative who has had DVT or PE