Cardiology

Question 1

List the types of pneumothoraces

Answer 1

Primary (spontaneous) – no known underlying lung disease, more likely in young, tall, thin men (often have emphysematous bullae or blebs which rupture)

Secondary – underlying lung disease e.g. asthma, COPD, lung cancer, cystic fibrosis, Marfan’s

Tension – one-way valve, progressive accumulation of air leads to rapidly increasing thoracic pressure, causes mediastinal shift, impairment of cardiac output and death if not managed rapidly

Traumatic (often tension) – stab injury, fractured rib, iatrogenic e.g. central line insertion, mechanical ventilation

Question 2

Describe the presentation of pneumothoraces

Answer 2

Sudden onset shortness of breath – can be minor or severe depending on size and patient factors (underlying lung disease, physiological reserve)
Pleuritic chest pain
Rapid haemodynamic instability if tension
Can be asymptomatic if small

Signs:
Hyperresonance to percussion
Reduced air entry
Reduced chest expansion
Tracheal deviation away from side of pneumothorax
Tachycardia, tachypnoea, hypoxia, hypotension
May be penetrating injury through chest wall (tension), check back

Question 3

How are pneumothoraces assessed and managed?

Answer 3

A-E assessment

If tension suspected do not delay treatment – insert wide bore cannula into 2nd intercostal space, mid-clavicular line (just above 3rd rib to avoid neurovascular bundle), then insert chest drain when stable

If bilateral/haemodynamically unstable insert chest drain

If stable –
CXR – size of pneumothorax and symptoms determine treatment, size measured as interpleural distance at level of hilum

Primary –
Size over 2cm or breathless – aspirate less than 2.5L with 16-18G cannula
If improved (less than 2cm and breathing better) – consider discharge and review in 2-4 weeks as outpatient
If not improved insert chest drain and admit
If initially less than 2cm and not breathless can consider discharge and review as outpatient in 2-4 weeks

Secondary –
More than 2cm or breathless – insert chest drain
1-2cm – aspirate less than 2.5L with 16-18G cannula
If improved with aspiration (size less than 1cm) admit, give oxygen, observe for 24 hours
If not improved insert chest drain
If initial size less than 1cm admit, give oxygen, observe for 24 hours

Question 4

Where are chest drains inserted?

Answer 4

Triangle of safety – latissimus dorsi lateral edge (or mid-axillary line) laterally, anterior axillary line (or lateral edge of pectoris major) anteriorly, 5th intercostal line (nipple level) inferiorly

Question 5

What discharge advice should be given to patients who have had a pneumothorax?

Answer 5

Smoking cessation to reduce risk of recurrence
Avoid diving permanently (unless have undergone bilateral pleurectomy with normal lung function and CT chest post-op)
Avoid air travel until fully resolved – 1 week post X-ray if resolved
Return if increasing breathlessness
Follow-up for X-ray to check for resolution

Question 6

How are recurrent pneumothoraces managed?

Answer 6

High rate of recurrence

Indications for surgical intervention (first line)
2nd ipsilateral pneumothorax
1st contralateral
Synchronous bilateral spontaneous pneumothorax
Persistent air leak despite chest drain insertion (5-7 days)
Spontaneous haemothorax
Profession at risk – divers, pilots
Pregnant

Surgical options – open thoracotomy or video-assisted thoracotomy with pleurectomy, pleural abrasion
2nd line or patient unfit/unwilling to undergo surgery – chemical pleurodesis

Question 7

Describe the clinical presentation of lung cancer

Answer 7

Cough
Pleuritic chest pain
Dyspnoea
Haemoptysis
Finger clubbing
Recurrent LRTIs
Weight loss
Night sweats
Fever
Fatigue
Lymphadenopathy
Bone pain

Extra-pulmonary manifestations –
SCC – PTHrp secretion, causes hypercalcaemia
NSCLC – ADH and ACTH secretion, limbic encephalitis, Lambert-Eaton myasthenic syndrome
Mass effects – Horner’s syndrome, superior vena cava obstruction, recurrent laryngeal nerve palsy, phrenic nerve palsy

Question 8

What are the criteria for 2ww referral for suspected lung cancer?

Answer 8

2ww referral:
CXR findings suggestive of lung cancer
>40 with unexplained haemoptysis

Urgent X-ray (2ww):
>40 with two of (or one of if smoker) – cough, weight loss, appetite loss, dyspnoea, chest pain, fatigue

Question 9

How is lung cancer diagnosed and staged?

Answer 9

CXR – first line, signs e.g. opacity, hilar enlargement, pleural effusion, lobar collapse
CT chest is gold-standard imaging and CT CAP used for staging
Bronchoscopy and biopsy – required to make diagnosis, confirm subtype, presence of targetable mutations e.g., EGFR
May also use PET-CT for staging
Isotope bone scan for bone mets

U+Es – hypontraemia due to SIADH in SCLC
Calcium – hypernatraemia if bone mets or PTHrp secretion in SCC

Question 10

How is lung cancer managed?

Answer 10

Metastatic – chemotherapy +/- radiotherapy

Often prophylactic brain radiotherapy given for SCLC, usually have mets at diagnosis

Surgery – perform spirometry before to calculate likely post-op capacity and guide options
Curative, first-line in NSCLC
Lobectomy and mediastinal lymph node dissection is standard
Can also do pneumonectomy, wedge resection or sleeve resection

Targeted therapy – immune checkpoint inhibitors, used in NSCLC in patients with target mutations
EGFR – gefitinib, Osimertinib
ALK – alectinib
ROS1 – crizotinib

Question 11

List complications of lung cancer

Answer 11

Pancoast tumour (lung apex) – Horner’s syndrome (miosis, ptosis, anhidrosis, enophthalmos), superior vena cava obstruction (facial swelling, flushing, arm swelling, venous distention)
Recurrent laryngeal nerve palsy – hoarse voice
Phrenic nerve palsy – diaphragm paralysis, respiratory compromise

Paraneoplastic syndromes:
SCC – PTHrp secretion leading to hypercalcaemia
SCLC – ADH secretion (SIADH, hyponatraemia), ACTH secretion (Cushing’s), Limbic encephalitis (anti-Hu antibodies), Lambert Eaton myasthenic syndrome

Metastases – most commonly to local lymph nodes, brain, bones, liver

Question 12

Describe the cause, clinical consequences, and presentation of aortic stenosis

Answer 12

Cause:
Calcification with age – most common in over 65s
Congenital bicuspid aortic valve – most common in under 65s
Rheumatic fever

Consequences:
Reduced blood flow from left ventricle, increased pressure on left ventricle leading to hypertrophy to maintain stroke volume
Eventually decompensates leading to heart failure
Shearing forces degrade VWF, can cause coagulopathy e.g. GI bleeding
If calcified commonly have concurrent aortic regurgitation

Presentation:
Can be asymptomatic
Exertional dyspnoea
Angina – increased oxygen demand of LV
Syncope
Signs of heart failure

On examination –
Ejection systolic murmur, loudest in aortic region, radiates to carotids
Slow-rising pulse with narrow pulse pressure

ECG features – signs of LV hypertrophy (tall S in V1, tall R in V5/6 - over 35mm, ischaemic ST/T changes)

Question 13

How is aortic stenosis managed?

Answer 13

Asymptomatic, valve gradient less than 40mmHg and no signs of left ventricular dysfunction – observe
Symptomatic or valve gradient more than 40mmHg or signs of left ventricular dysfunction – surgery

Surgery:
Open aortic valve replacement – young or low/medium risk
Transcatheter aortic valve replacement – high operative risk
Balloon valvuloplasty – children with no calcification, adults not fit for replacement

Question 14

Describe the cause and presentation of aortic regurgitation

Answer 14

Cause:
Calcification
Post-rheumatic fever – most common in developing world
Connective tissue disease e.g. RA, SLE, Marfan’s, Ehler-Danlos
Bicuspid aortic valve
Spondyloarthropathy e.g. AS
Hypertension
Syphilis
Acute – infective endocarditis, aortic dissection

Presentation:
Can be asymptomatic
Exertional dyspnoea
Features of LV hypertrophy then heart failure
Collapsing pulse – Corrigan’s pulse (distension and collapse of carotids)
Early diastolic murmur loudest over aortic area, louder sitting forward in expiration
Quinke’s sign – nailbed pulsation
De Musset’s sign – head bobbing
Mid-diastolic Austin-Flint murmur
Muller’s sign – uvular pulsation
Traube’s sign – pistol shot sound on auscultation of femoral arteries

ECG –
LV hypertrophy
LA enlargement (P wave abnormalities in II and V1)
T inversion
ST depression in chest leads

Question 15

How is aortic regurgitation managed?

Answer 15

Symptomatic or asymptomatic with LV systolic dysfunction – valve replacement

Question 16

Describe the cause, clinical consequences, and presentation of mitral stenosis

Answer 16

Cause:
Rheumatic fever – most common cause by far
Infective endocarditis

Causes increased pressure in LA, LA dilation leading to atrial fibrillation, reduced cardiac output, congestive heart failure

Presentation:
Heart failure
Atrial fibrillation
Haemoptysis – pink frothy sputum or sudden haemorrhage due to increased pulmonary pressure and vascular congestion
Low-pitched rumbling mid-diastolic murmur, loudest in mitral region in left lateral decubitus position
May have loud S1 or opening snap
Malar flush
Low volume pulse

Question 17

How is mitral stenosis managed?

Answer 17

AF – anticoagulation, warfarin if moderate/severe, DOAC if mild
Asymptomatic – monitor with regular echo
Symptomatic – percutaneous mitral balloon valvotomy, mitral valve surgery (commissurotomy or replacement)

Question 18

Describe the cause, clinical consequences, and presentation of mitral regurgitation

Answer 18

Cause:
Mitral valve prolapse due to myxomatous degeneration of valve leaflets and chordae tendinae
Rheumatic fever
Infective endocarditis
Papillary muscle rupture – MI
Congenital
Cardiomyopathy

Causes backflow of blood into left atrium which leads to reduced cardiac output, meaning left ventricle increases stroke volume to compensate
Eventually causes ventricular dilatation, reduced left ventricular ejection fraction and heart failure

Presentation:
Asymptomatic
Heart failure
Pansystolic murmur, best heard in mitral region with radiation to left axilla
3rd heart sound
Displaced, hyperdynamic apex beat

ECG – LA enlargement, LV hypertrophy +/- ischaemia

Question 19

How is mitral regurgitation managed?

Answer 19

Management of heart failure
Acute, severe regurgitation – surgical repair preferred over replacement when possible

Question 20

Describe the cause and presentation of tricuspid regurgitation

Answer 20

Causes:
RV enlargement secondary to pulmonary hypertension
Rheumatic fever
Infectious endocarditis – especially in IVDUs
Carcinoid syndrome
Congenital

Presentation:
Pansystolic murmur
Raised JVP
V waves in jugular veins
Hepatic pulsation
Ascites
Oedema

Question 21

Describe the cause and presentation of pulmonary regurgitation

Answer 21

Cause:
Pulmonary hypertension
Infective endocarditis
Congenital

Presentation:
Usually asymptomatic
Early diastolic murmur

Question 22

Describe the cause and presentation of tricuspid stenosis

Answer 22

Cause:
Rheumatic fever
Congenital
Infective endocarditis

Presentation:
Mid-diastolic murmur, usually inaudible
Raised JVP with big A waves
Peripheral oedema, ascites

Question 23

Describe the cause and presentation of pulmonary stenosis

Answer 23

Cause:
Tetralogy of Fallot
Turner’s syndrome
Noonan syndrome
William’s syndrome
Rheumatic fever
Carcinoid syndrome

Presentation:
Ejection systolic murmur
Raised JVP with A waves
RV heave
Right heart failure signs

Question 24

How is valvular disease assessed and managed?

Answer 24

Assessment – SCRIPT
S – site (where is it loudest?)
C – character
R – radiation
I – intensity (grade)
P – pitch
T – timing (systolic or diastolic)

Grading:
1 – difficult to hear
2 – quiet
3 – easy to hear
4 – easy to hear with palpable thrill
5 – can hear with stethoscope off chest
6 – can hear from across room

ECHO – transthoracic or transoesophageal

Management:
Catheter-based interventions
Transcatheter aortic valve implantation (TAVI) most common

Open surgery
Valve repair – mitral regurgitation
Valve replacement – mechanical or tissue valves

Mechanical are lifelong but require lifelong anticoagulation with heparin then warfarin, better for younger patients
Tissue have shorter lifespan but do not require anticoagulation, better for older patients

Question 25

Describe the mechanism of action of warfarin

Answer 25

Vitamin K antagonist to inhibit synthesis of vitamin K-dependent clotting factors – II, VII, IX, X, as well as proteins C and S

Question 26

Describe the indications for warfarin therapy

Answer 26

VTE prophylaxis in mechanical heart valves, rheumatic heart disease, valvular atrial fibrillation, symptomatic inherited thrombophilia 2nd line (after DOACs) for VTE, AF

Question 27

How are patients on warfarin monitored? What factors can impact the therapeutic effect of warfarin?

Answer 27

INR monitoring – ratio of patients PT to normal PT INR targets: 2-3 – VTE, AF, mitral valve disease, inherited symptomatic thrombophilia 2.5-3.5 – mechanical heart valves (targets vary) Long half-life, can take 5 days to achieve stable INR in therapeutic range Initially induces hypercoagulable state, if develop an acute VTE need heparin until INR is in therapeutic range Things which increase action of warfarin: CYP450 inhibitors – oral contraceptives, St John’s wort, cranberries Liver disease Acute illness Things which decrease action of warfarin: CYP450 inducers – alcohol, allopurinol, paracetamol, SSRIs, lipid-regulating drugs, influenza vaccine, foods high in vitamin K (e.g. leafy green vegetables) Many antibiotics/antivirals interact with warfarin – check before prescribing

Question 28

Describe the potential adverse effects of warfarin and reversal of warfarin

Answer 28

Adverse effects: Bleeding Teratogenic – can be used when breastfeeding Skin necrosis Procoagulant state when first started – concurrent heparin given Warfarin reversal – in order of least to most potent options: Withhold warfarin Vitamin K – oral or IV Prothrombin complex concentration – contains factor II, VII, IX, X If major bleeding – do all three (withhold warfarin, give vitamin K, give PCC) and give FFP INR >8 with minor bleeding – withhold warfarin and give vitamin K, restart when INR less than 5 INR >8 with no bleeding – withhold warfarin, give vitamin K, restart when INR less than 5 INR 5-8 with minor bleeding – withhold warfarin, give vitamin K, restart when INR less than 5 INR 5-8 with no bleeding – withhold 1 or 2 doses of warfarin, reduce subsequent maintenance dose

Question 29

Describe the mechanism of action, indications, and reversal of commonly used direct oral anticoagulants

Answer 29

Indications: Prevention of stroke in non-valvular AF (that meets risk factor requirements) Prevention of VTE following surgery (hip and knee) Treatment/prevention of DVT and PE Dagibatran Direct thrombin inhibitor Mostly renal excretion Reversal – idracizumab Rivaroxaban Direct factor Xa inhibitor Mostly hepatic excretion Reversal – andexanet alfa Apixaban Direct factor Xa inhibitor Mostly faecal excretion Reversal – andexanet alfa Edoxaban Direct factor Xa inhibitor Mostly faecal excretion No authorised reversal agent

Question 30

Describe the types of heparins, their mechanisms of action, side effects and monitoring requirements

Answer 30

Unfractionated (standard) heparin IV administration Short duration of action – useful for those at high risk of bleeding, can be terminated rapidly Mechanism of action – activates antithrombin III, forms a complex that inhibits thrombin, factors IXa, Xa, XIa and XIIa Side effects – bleeding, heparin-induced thrombocytopaenia, osteoporosis Monitoring – APTT Low molecular weight heparin e.g., dalteparin, enoxaparin Subcutaneous administration Longer duration of action Mechanism of action – activates antithrombin III, forms a complex that inhibits factor Xa Side effects – bleeding, lower risk of osteoporosis Monitoring not done routinely – can monitor anti-factor Xa Used for prophylaxis and treatment of DVT and PE, may be used for treatment of ACS but not first line

Question 31

Describe the types, mechanism of action, indications and side effects of antiplatelet drugs

Answer 31

Aspirin: Inhibits COX1 and 2, prevents thromboxane A2 formation in platelets which reduced platelet aggregation Indications – secondary prevention in cardiovascular disease, dual therapy for ACS if medically treated, PCI, second line for TIA, ischaemic stroke or peripheral arterial disease Side effects – bleeding, dyspepsia, Reye’s syndrome in children Thienopyridines – clopidogrel, ticagrelor, ticlopidine Antagonise P2Y12 adenosine diphosphate (ADP) receptor, inhibiting activation of platelets Indications – ticagrelor and aspirin for medical management of ACS, ticagrelor and aspirin for PCI, clopidogrel first line for TIA, ischaemic stroke, peripheral arterial disease Side effects – bleeding, GI upset, PPIs decrease efficacy

Question 32

Describe the management of anticoagulant drugs pre-operatively

Answer 32

Clopidogrel stopped 7 days prior to surgery Warfarin stopped 5 days prior to surgery, start on therapeutic dose LMWH if high risk for VTE (usually need INR less than 1.5 for surgery to go ahead) Aspirin usually continued Stop taking COCP 4 weeks before surgery

Question 33

Define acute coronary syndrome and describe how the subtypes are differentiated

Answer 33

Unstable angina – partial occlusion of coronary artery, cardiac chest pain not relieved by rest or GTN, no ST elevation/new LBBB, troponin normal NSTEMI – complete occlusion of coronary artery without infarction of myocardium, cardiac chest pain not relieved by rest or GTN, raised troponin, no ST elevation but may have other ECG changes present (ST depression, T wave inversion) STEMI – complete occlusion of coronary artery with full-thickness infarction of myocardium, cardiac chest pain not relieved by rest or GTN, lasting >20 minutes, raised troponin, ST elevation or new LBBB on ECG

Question 34

List the types of myocardial infarction

Answer 34

Type 1 – ischaemia due to coronary event, usually plaque rupture Type 2 – increased oxygen demand or reduced oxygen supply e.g. hypotension, hypovolaemia, anaemia Type 3 – sudden cardiac death Type 4 – associated with intervention e.g. PCI, stenting CABG

Question 35

Describe the presentation of acute coronary syndrome

Answer 35

Chest pain – central, crushing, radiating to left arm/jaw Associated symptoms – nausea, vomiting, sweating, SOB, palpitations Can have ‘silent’ MI – more common in diabetes, women, elderly, features such as dizziness, SOB more prominent

Question 36

Describe the initial assessment/management of acute coronary syndrome

Answer 36

A-E assessment, haemodynamic status ECG Troponin (+ routine bloods) History of pain CVD and risk factors Rule out other causes e.g. CXR Then can differentiate between unstable angina, NSTEMI, STEMI

Question 37

Describe the initial management of STEMIs

Answer 37

Determine when pain started – if within 12 hours onset and can get to PCI centre within 2 hours of presentation can get PCI If not get thrombolysis O2 if sats less than 94% If getting PCI: IV morphine + metoclopramide Oral aspirin 300mg + ticagrelor IV heparin (unless already had fondaparinux or enoxaparin) If getting thrombolysis: IV morphine + metoclopramide Oral aspirin 300mg IV heparin Oral clopidogrel (instead of ticagrelor) Tenecteplase (thrombolysis)

Question 38

Describe the initial management of NSTEMIs/unstable angina

Answer 38

IV morphine and metoclopramide Oral aspirin 300mg + ticagrelor IV heparin NSTEMI – use GRACE score to determine need for PCI (within 4 days of admission) Unstable angina – use GRACE score to determine whether to discharge or admit

Question 39

List important causes of raised troponin

Answer 39

ACS – NSTEMI or STEMI Sepsis Heart failure Aortic dissection Myocarditis PE CKD/AKI

Question 40

List contraindications to thrombolysis

Answer 40

Active bleeding Previous haemorrhagic stroke/intra-cerebral haemorrhage Cerebral neoplasm Major trauma/surgery within 3 weeks GI bleeding within month Known bleeding disorder Aortic dissection Ischaemic stroke within 6 months

Question 41

Describe the ongoing management of acute coronary syndrome following initial management

Answer 41

NSTEMI/STEMI – monitor in CCU for complications (arrhythmias, heart failure, myocardial rupture leading to cardiac tamponade, pericarditis, cardiogenic shock) Secondary prevention: Lifestyle ACEi (or ARB if not tolerated) Dual antiplatelet therapy – aspirin 75mg for life and ticagrelor for 3-6 months B-blocker – atenolol Atorvastatin Management of anginal symptoms: Calcium channel blockers – amlodipine or diltiazem (if not on B-blocker, don’t use with B-blocker) Nitrates – isosorbide mononitrate GTN spray for symptomatic relief B-blocker Procedural – PCI with coronary angioplasty or CABG if high-risk angina

Question 42

Describe the arteries which supply specific areas of the heart and the ECG changes they correspond with

Answer 42

Lateral - circumflex artery Anterior/septal - LCA Inferior - RCA

Question 43

Describe the cause, presentation, and management of Dressler’s syndrome

Answer 43

Cause – occurs post-MI (2-6 weeks), localised autoimmune response which causes pericarditis Presentation Fever Pleuritic chest pain Pericardial rub Increased ESR Cardiomegaly on CXR ECG – global ST elevation, T wave inversion Management Usually self-limiting 1st line – NSAIDs More severe – steroids ?Pericardiocentesis

Question 44

How is stable angina managed?

Answer 44

Immediate symptomatic relief – GTN spray Long-term symptomatic relief – calcium channel blockers, B-blocker, long acting nitrate (isosorbide nitrate) Secondary prevention – ACEi (or ARB), aspirin, atorvastatin, B-blocker Procedural – PCI with angioplasty or CABG if high risk/extensive ischaemic heart disease

Question 45

What is the gold-standard investigation for suspected coronary artery disease?

Answer 45

Coronary angiography

Question 46

Which vessels are most commonly used for coronary artery bypass grafting?

Answer 46

Great saphenous vein Radial artery Left internal mammary artery if LAD affected

Question 47

Define aortic dissection and describe the aetiology

Answer 47

Tear in the tunica intima of wall of aorta Strong association with hypertension Predisposition in – bicuspid aortic valve, coarctation of the aorta, aortic valve replacement, CABG, Ehlers-Danlos, Marfan’s

Question 47

Define aortic dissection and describe the aetiology

Answer 47

Tear in the tunica intima of wall of aorta Strong association with hypertension Predisposition in – bicuspid aortic valve, coarctation of the aorta, aortic valve replacement, CABG, Ehlers-Danlos, Marfan’s

Question 48

Describe the types of aortic dissections and the presentation of aortic dissections

Answer 48

Stanford classification Type A – ascending (2/3) Type B – descending, distal to origin of left subclavian DeBakey classification Type 1 – ascending aorta, extending to arch and possibly beyond Type 2 – ascending aorta only Type 3 – originates in descending aorta, rarely extends proximally, extends distally Presentation: Classically tearing pain in chest/back (chest more common in type A and back in type B) Weak or absent carotid, brachial or femoral pulse Difference in SBP (>20mmHg) between arms Aortic regurgitation Hypertension Focal neurological deficit Syncope Haemodynamic instability

Question 49

Describe the assessment and management of aortic dissections

Answer 49

Investigation of choice is CT angiography CAP (whole aorta) – findings include double lumen, entry tear, aortic dilatation, end-organ malperfusion Can use transoesophageal echo if too unstable for CT scan Management: A-E assessment Analgesia – IV morphine BP and HR control – minimise stress on aorta and limit spread of dissection, target HR 60-80, target SBP 100-120 (IV labetalol 1st line) Surgical management dependent on type: Type A usually need open resection of aorta and replacement with synthetic graft +/- aortic valve replacement (poor prognosis) Type B can be managed medically initially if uncomplicated, may need endovascular stent graft placement (thoracic endovascular aortic repair, TEVAR) acutely or in long-term to prevent worsening

Question 50

What are the potential complications of aortic dissection?

Answer 50

Acute aortic regurgitation MI Cardiac tamponade Aneurysmal dilatation Ischaemic stroke or paraplegia due to spinal artery dysfunction Acute limb ischaemia Renal failure Bowel ischaemia

Question 51

List causes of acute pericarditis

Answer 51

Viral infections – Coxsackie, HIV Tuberculosis Uraemia Post-MI – fibrinous pericarditis (early), Dressler’s syndrome (late) Radiotherapy Connective tissue disease – SLE, RA Hypothyroidism Malignancy – lung cancer, breast cancer Trauma Drug-induced – hydralazine

Question 52

Describe the presentation of pericarditis

Answer 52

Chest pain – retrosternal, can radiate to neck, shoulders (trapezius ridge classically) and arm Dyspnoea Pericardial rub Beck’s triad – hypotension, muffled heart sounds, raised JVP

Question 53

Describe the presentation of pericarditis

Answer 53

Chest pain – retrosternal, can radiate to neck, shoulders (trapezius ridge classically) and arm Dyspnoea Pericardial rub Beck’s triad – hypotension, muffled heart sounds, raised JVP ECG – Widespread concave/saddle-shaped ST elevation, PR depression, low-voltage QRS, electrical alternans

Question 54

How is pericarditis managed?

Answer 54

Usually self-limiting NSAIDs for symptomatic treatment (+PPI) Colchicine Steroids 2nd line

Question 55

Describe the cause and presentation of constrictive pericarditis

Answer 55

Presentation: Dyspnoea Right heart failure – elevated JVP, ascites, oedema, hepatomegaly Kussmaul’s sign – rise in JVP with inspiration CXR – pericardial calcification

Question 56

Describe the cause, presentation, management, and complications of myocarditis

Answer 56

Causes: Viral – Coxsackie, HIV Bacteria – diphtheria, clostridia Spirochetes – Lyme disease Protozoa – Chagas disease, toxoplasmosis Autoimmune Drugs – doxorubicin Presentation: Young patient with acute history Chest pain Dyspnoea Arrhythmias Raised inflammatory markers and cardiac enzymes, raised BNP ECG – tachycardia, arrhythmias, ST/T wave changes Management – treat underlying cause, supportive management of complications Complications – heart failure, arrhythmias (can cause sudden death), dilated cardiomyopathy

Question 57

Describe the causes of cardiomyopathy

Answer 57

Primary – Genetic: HOCM Arrhythmogenic right ventricular dysplasia Mixed Dilated (90% of cardiomyopathies) – alcohol, Coxsackie B, cocaine, doxorubicin Restrictive – amyloidosis, post-radiotherapy Acquired: Peripartum Takotsubo Secondary – Infective – Coxsackie B, Chagas disease Infiltrative – amyloidosis Storage – haemochromatosis Toxicity – doxorubicin Inflammatory – sarcoidosis Endocrine – diabetes, thyrotoxicosis, acromegaly Neuromuscular – Friedrich’s ataxia, Duchenne/Becker, myotonic dystrophy Nutritional deficiency – thiamine (Berberi) Autoimmune - SLE

Question 58

Describe the cause and clinical presentation of hypertrophic obstructive cardiomyopathy

Answer 58

Autosomal dominant disorder with defects in genes coding for contractile proteins – most commonly B-myosin heavy chain protein or myosin-binding protein C Causes mostly diastolic dysfunction, leading to left ventricular hypertrophy, decreased compliance, decreased cardiac output Presentation: Mostly asymptomatic Exertional dyspnoea Angina Syncope – exertional Sudden death usually due to ventricular arrhythmias Systolic murmur – ejection systolic due to left ventricular outflow tract obstruction, increases with Valsalva and decreases on squatting or pansystolic murmur due to mitral regurgitation

Question 59

Describe the investigation findings in hypertrophic obstructive cardiomyopathy

Answer 59

Echo – mitral regurgitation, systolic anterior motion of anterior mitral valve leaflet, asymmetric hypertrophy ECG – LVH, ST and T wave abnormalities, deep Q waves, sometimes AF

Question 60

How is hypertrophic obstructive cardiomyopathy managed?

Answer 60

Lifestyle advice – avoid dehydration and alcohol Angina – beta-blockers and CCB, nitrates only if LVOT obstruction excluded AF – avoid digoxin and flecainide, anticoagulation (warfarin), DC cardioversion if unstable, rate/rhythm control if stable Heart failure – B-blockers, CCBs, diuretics, RAAS inhibitors, cardiac transplantation considered Implantable cardioverter-defibrillator – secondary prevention if cardiac arrest or primary prevention if high risk for sudden cardiac death Septal reduction myomectomy or ablation if severe LVOT obstruction

Question 61

Describe the cause, presentation, and management of arrhythmogenic right ventricular cardiomyopathy

Answer 61

Autosomal dominant, most commonly mutation in genes coding for desmosomes Right ventricular myocardium replaced with fatty and fibrofatty tissue Presentation – palpitations, syncope, sudden cardiac death (second most common cause in young people) ECG – abnormalities in V1-3, typically T wave inversion ECHO – enlarged hypokinetic RV Management Sotalol – antiarrhythmic Catheter ablation to prevent ventricular tachycardia Implantable cardioverter defibrillator

Question 62

Describe causes and pathophysiology of chronic heart failure

Answer 62

Most common: Coronary artery disease Atrial fibrillation Valvular heart disease – most commonly aortic stenosis Hypertension Others: Endocrine disease – hypo/hyperthyroidism, diabetes, hypoadrenalism, Cushing’s Medications – calcium channel blockers, anti-arrhythmics, cytotoxic medication, beta-blockers Genetic – hypertrophic obstructive cardiomyopathy, dilated cardiomyopathy Volume overload – renal failure, hepatic failure Infiltrative – sarcoidosis, amyloidosis, haemochromatosis Decrease in cardiac output so that heart is unable to meet metabolic demands of body, due to: Decreased heart rate Decreased pre-load – reduced compliance (diastolic dysfunction) Decreased contractility (systolic dysfunction) Increased afterload

Question 63

Describe the presentation and clinical consequences of chronic heart failure

Answer 63

Left heart failure – Reduced systemic circulation – syncope/pre-syncope Pulmonary circulation congestion and oedema – dyspnoea, paroxysmal nocturnal dyspnoea, orthopnoea, crackles/wheeze Hypotension Raised JVP Displaced apex beat – left ventricular hypertrophy/dilatation Gallop rhythm Right heart failure – Systemic venous congestion – peripheral oedema, raised JVP, hepatic congestion (hepatomegaly, ascites) Cough – pink/white frothy sputum Weight loss Exercise intolerance

Question 64

How is chronic heart failure diagnosed?

Answer 64

ECG – previous MI (Q waves), arrhythmias, ventricular hypertrophy, tachycardia, AV block (prolonged PR) Urinalysis – protein FBC (anaemia), U&Es (renal disease, fluid overload), LFTs (hepatic congestion) Lipids, HbA1c – ischaemia risk N-terminal pro-B-type natriuretic peptide – level determines urgency of investigation/referral (>2000 urgent, 400-2000 routine, less than 400 unlikely to be HF) Echo CXR – alveolar oedema, Kerley B lines, cardiomegaly, upper lobe vessel enlargement, pleural effusions Cardiac MRI

Question 65

Describe the classification of chronic heart failure

Answer 65

New York Heart Association Class I – no symptoms, no limitation on physical exercise Class II – mild symptoms, slight limitation of physical activity (causes symptoms e.g. fatigue, palpitations, dyspnoea) Class III – moderate symptoms, marked limitation of physical activity Class IV – severe symptoms, unable to perform any physical activity without symptoms, symptoms present at rest

Question 66

Describe the management of chronic heart failure

Answer 66

Lifestyle – fluid and salt restriction, exercise, smoking cessation, reduce alcohol Vaccination – influenza and pneumococcal Medication: Stop any which may be harmful – CCB (verapamil, diltiazem), TCA, lithium, NSAIDs, steroids, QT prolonging Anticoagulation for AF ACEi (or ARB) B-blocker Mineralocorticoid receptor antagonists – if on ACEi/ARB, decreased ejection fraction, B-blocker and symptoms still not controlled Diuretics – loop, for relief of symptoms of volume overload SGLT2 inhibitors if LVEF less than 40% Specialist treatment: Ivabradine – inhibits SAN to slow heart rate Angiotenin receptor and neprilysin inhibitor (ARNI) Sacubatril valsartan Digoxin Amiodarone Procedural: Revascularisation e.g. CABG Valve repair/replacement Implantable cardiac defibrillator – if EF less than 30% Cardiac resynchronisation therapy and defibrillator – if EF less than 30% and QRS >130 Cardiac transplantation rarely

Question 67

What is the significance of ejection fraction in heart failure?

Answer 67

Reduced ejection fraction less than 35-40% - tends to be systolic dysfunction (IHD, dilated cardiomyopathy, arrhythmias) Preserved ejection fraction more than 40% - tends to be diastolic dysfunction (restrictive cardiomyopathy, cardiac tamponade, constrictive pericarditis, HOCM)

Question 68

List causes of high-output heart failure

Answer 68

Anaemia Pregnancy Thyrotoxicosis Paget’s disease

Question 69

Describe the causes of acute heart failure

Answer 69

New onset: Acute MI Acute valve dysfunction Arrhythmias Acute decompensation of CHF: Infection MI Uncontrolled hypertension Arrhythmias Worsening of chronic valve disease Change to medications

Question 70

Describe the presentation of acute (decompensated) heart failure

Answer 70

Dyspnoea – worse on exertion, worse lying flat, PND Reduced exercise tolerance Peripheral oedema Bibasal fine crepitations Raised JVP Hepatomegaly 3rd heart sound Cyanosis Cold, sweaty peripheries Type 1 respiratory failure – low oxygen, normal CO2 Tachypnoea, tachycardia

Question 71

Describe the assessment and management of acute (decompensated) heart failure

Answer 71

Oxygen to maintain sats 94-98% (88-92% in COPD) IV loop diuretic – 40mg furosemide, repeat if needed Nitrates (contraindicated in hypotension and aortic stenosis – glyceryl trinitrate Consider NIV (CPAP) if acidotic or poor response to initial therapy May need inotropic support if hypotensive (ICU) Consider slow IV opioids for chest pain/severe distress

Question 72

List causes of AF

Answer 72

Ischaemic heart disease Valve abnormality - particularly mitral (dilatation of left atrium) MI Hypertension Congenital heart disease Electrolyte abnormalities Hyperthyroidism Drugs Acute infection Inflammatory conditions – pericarditis, myocarditis Amyloidosis

Question 73

Describe the presentation of atrial fibrillation

Answer 73

Asymptomatic Palpitations Chest pain Syncope/pre-syncope Dyspnoea Irregularly irregular pulse

Question 74

How is atrial fibrillation investigated/diagnosed?

Answer 74

ECG – irregularly irregular, absent P waves, narrow QRS, tachycardia Ambulatory ECG – for paroxysmal AF diagnosis, using 24-hour ECH or Holter monitor for 7 days Assess for reversible causes – FBC, U&Es, TFTs, CRP ECHO – structural or valvular disease, left ventricular systolic dysfunction CXR – heart failure signs Coagulation – before giving anticoagulants

Question 75

Describe the principles of AF management

Answer 75

Emergency management if adverse features (syncope, shock, ischaemia, heart failure) – immediate synchronised DC cardioversion Anticoagulation to reduce risk of ischaemic stroke based on CHADVASc score Rate control – first line unless: Reversible cause New onset HF caused by AF New-onset AF Atrial flutter suitable for ablation Rhythm control used in these scenarios or if still symptomatic after adequate rate control New onset AF – cardioversion

Question 76

Describe the management of new-onset atrial fibrillation

Answer 76

Onset less than 48 hours: Heparinise Cardiovert – synchronised DC cardioversion or pharmacological (amiodarone if structural heart disease, flecainide or amiodarone if no structural heart disease) Onset more than 48 hours or uncertain time of onset: Must have anticoagulation for minimum 3 weeks before cardioversion, electrical cardioversion recommended Assess ischaemic stroke risk with CHADSVASc score to determine need for long term anticoagulation

Question 77

Describe anticoagulation in atrial fibrillation

Answer 77

Anticoagulation to reduce ischaemic stroke risk based on CHADVASc score: CHADSVASc 2 or more offer oral anticoagulant CHADSVASc = 1 in men consider oral anticoagulant CHADSVASc 1 or less in women or 0 in men do not offer anticoagulant (review if risk changes – age, CV comorbidities, diabetes) 1st line – DOAC (apixaban, dabigatran, edoxaban, rivaroxaban) 2nd line or if DOAC contraindicated/not tolerated – warfarin

Question 78

Describe the scoring systems used for stroke risk and bleeding risk in anticoagulation for atrial fibrillation

Answer 78

Ischaemic stroke risk – CHADSVASc C – cardiac failure H – hypertension A2 – age >=75 D – diabetes S2 – stroke/TIA/thromboembolism history (2) V – peripheral vascular disease A – age 65-74 S – sex (female) ORBIT – bleeding risk Haemoglobin less than 130 in males, less than 120 in females (2) Age >74 Bleeding history – GI bleed, intracranial bleed, haemorrhagic stroke (2) Renal impairment (eGFR less than 60) Treatment with antiplatelet agents

Question 79

Describe rate and rhythm control for atrial fibrillation

Answer 79

Rate control: 1st line – beta-blocker (atenolol) or CCB (diltiazem) (consider digoxin if sedentary and can’t have other options) Aim for less than 110, if still symptomatic less than 80 If not controlled on monotherapy do two of beta-blocker, diltiazem or digoxin Rate control: Paroxysmal – consider ‘pill in pocket’ for infrequent paroxysms with flecainide (can’t use in structural or ischaemic heart disease) Persistent – electrical cardioversion (ensure sufficient anticoagulation before) beta-blockers, dronedarone, amiodarone (if coexisting heart failure) If drug treatment unsuccessful or not tolerated – left atrial radiofrequency ablation

Question 80

Describe the ECG findings and management of atrial flutter

Answer 80

ECG – sawtooth baseline, underlying atrial rate often 300/min, ventricular rate dependent on degree of AV block, commonly 2:1 so ventricular rate 150/min Management: Same management as AF – require anticoagulation as per CHADSVASc score Radiofrequency ablation of right atrium often curative but can still progress to atrial fibrillation

Question 81

List types of supraventricular tachycardias and describe their pathophysiology and ECG features

Answer 81

Any arrhythmia which arises from above the ventricles (above or within AV node) Usually refers to paroxysmal narrow-complex tachycardias – AV node re-entry tachycardia (AVNRT) or AV re-entry tachycardia (AVRT) Focal: Sinus tachycardia (origin is SA node) – regular, normal morphology Atrial tachycardia – abnormal P waves, regular, often in chronic lung disease (e.g. COPD) Multifocal atrial tachycardia – P waves with different morphologies beat to beat, regular Junctional rhythms (origin is AV node) – occurs in SA node dysfunction, P waves hidden as occur simultaneously with QRS Re-entry: Atrial flutter – single re-entry circuit, sawtooth baseline, constant rate of atrial contraction (usually 300:150) Atrial fibrillation – chaotic/disorganised contraction of atrium, absence of P waves, irregularly irregular AVNRT – re-entry circuit within the AV node, ventricles and atria activated almost simultaneously, P waves hidden, regular, tachycardia, pseudo R waves AVRT (including Wolff-Parkinson-White syndrome) – accessory pathway forms re-entry circuit (Bundle of Kent in WPW), prolonged PR, delta waves (slurred up-stroke of R wave), left axis deviation (if right-sided accessory pathway, which is most common)

Question 82

Describe the cause and management of sinus tachycardia

Answer 82

* Physiological - exercise, pregnancy * Infection * Dehydration * Pain * Hyperthyroidism * PE * Anxiety * Drugs - cocaine, amphetamines, salbutamol Management: If appropriate – leave alone, manage underlying trigger If inappropriate – ?slow using B-blockers or ivabradine

Question 83

Describe the acute management of supraventricular tachycardias (AVNRT and AVRT)

Answer 83

Life threatening features (shock, syncope, MI, severe heart failure) – synchronised DC shock, up to 3 attempts, with sedation/anaesthesia If unsuccessful IV amiodarone, repeat shock If no life-threatening features, narrow regular QRS Vagal manoeuvres – Valsalva (blow into syringe), carotid sinus massage If ineffective give adenosine IV (6mg, then 12mg, then 18mg) If ineffective give verapamil or beta-blocker If ineffective synchronised DC shock

Question 84

Describe the typical presentation of AVNRT

Answer 84

Young adults Female > male Triggers e.g. caffeine, drugs, fatigue Sudden onset regular fast palpitations

Question 85

Describe the mechanism of action, administration and contraindications to adenosine for acute SVT

Answer 85

Acts by slowing cardiac conduction through AV node, interrupts the re-entry circuit to reset back to sinus rhythm Given by rapid bolus Can cause brief asystole or bradycardia which should resolve quickly Avoid in asthma, COPD, heart failure, heart block, severe hypotension Warn patient about feeling of dying/impending doom

Question 86

How are SVTs (AVNRT and AVRT) managed long-term?

Answer 86

If recurrent episodes can give medication (rate/rhythm control) or radiofrequency ablation of accessory pathway

Question 87

Describe the ECG appearance and pathophysiology of Wolff-Parkinson-White syndrome

Answer 87

Accessory pathway – bundle of Kent ECG – Short PR (less than 0.12 seconds) Wide QRS (more than 0.12 seconds) Delta wave (slurred upstroke of QRS)

Question 88

What are the cardiac arrest rhythms? Which are shockable and which are not shockable?

Answer 88

Shockable: Ventricular tachycardia Ventricular fibrillation Non-shockable rhythms: Pulseless electrical activity – all electrical activity except VT/VF, including sinus rhythm Asystole – no significant electrical activity

Question 89

Describe the types of ventricular tachycardia and their causes

Answer 89

Tachycardia originating in the ventricles – broad QRS complex (>0.12 seconds) Sustained if >30 seconds Monomorphic – QRS looks the same throughout, usually >120 bpm, associated with MI Polymorphic – QRS has variable morphology (change amplitude and axis), HR tends to be >200 Torsades de pointes is a type of polymorphic VT precipitated by QT prolongation Predisposing conditions – Brugada syndrome, Wolff-Parkinson-White syndrome, QT prolongation (drugs, hypo/hyperkalaemia, hypomagnesaemia, hypocalcaemia, hypothermia), HOCM, congenital long QT

Question 90

How is ventricular tachycardia managed?

Answer 90

Adverse features (shock, syncope, myocardial ischaemia, severe heart failure) – synchronised DC shock up to 3 attempts, if unsuccessful amiodarone IV, repeat shock Broad QRS, regular: VT or uncertain rhythm – amiodarone IV If ineffective synchronised DC shock up to 3 attempts Torsades de pointes – IV magnesium, synchronised DC cardioversion if VT occurs Long-term management Avoid medications that prolong QT Correct electrolyte disturbances Beta-blockers Implantable cardioverter-defibrillator – especially if impaired LV function

Question 91

Describe the appearance of ventricular fibrillation on ECG

Answer 91

Irregular electrical activity with no pattern Coarse (more responsive to defibrillation) progressing to fine (less responsive)

Question 92

List causes and management of sinus bradycardia

Answer 92

Physiological in athletes Hypothyroidism Anorexia nervosa Electrolyte abnormalities Medications – beta-blockers, calcium channel blockers, digoxin, amiodarone, opiates, benzodiazepines Organophosphate poisoning If physiological does not require treatment Treat underlying cause

Question 93

Describe the ECG criteria for right bundle branch block and list causes of RBBB

Answer 93

QRS >120 RSR pattern in V1-3 Wide slurred S wave in lateral leads – I, aVL, V5-6 MaRRoW M in V1 W in V6 Causes: Normal variant – more common with increasing age RV hypertrophy Increased RV pressure e.g. cor pulmonale PE MI Atrial septal defect Cardiomyopathy or myocarditis

Question 94

Describe the ECG criteria for left bundle branch block and list causes of LBBB

Answer 94

QRS >120 Dominant S wave in V1 Broad monophasic R in lateral leads Absence of Q waves in lateral leads Prolonged R wave >60ms in leads V5/6 WiLLiaM W in V1 M in V6 Left bundle branch splits into anterior and posterior fascicles, anterior block can cause left axis deviation (common), posterior can cause right axis deviation (uncommon) NEW LBBB IS ALWAYS PATHOLOGICAL Causes: MI Hypertension Aortic stenosis Cardiomyopathy Digoxin toxicity

Question 95

List causes of first-degree AV block and ECG features

Answer 95

Causes: Athletes – normal variant Post-MI Lyme’s disease, SLE, myocarditis Congenital Electrolyte derangement Drugs – AV blocking e.g., beta-blockers, CCB, digoxin ECG findings: Regular P waves always present and followed by QRS PR prolonged, >0.2 seconds, 5 small squares QRS normal, narrow

Question 96

How does first-degree heart block present? How is it managed?

Answer 96

Usually asymptomatic Stop AV blocking drugs No intervention if asymptomatic, if symptomatic consider pacemaker Does not usually progress to higher degree block

Question 97

Describe the cause and ECG features of second-degree heart block

Answer 97

Mobitz type 1 (Wenckebach phenomenon) Causes – Athletes Drugs – beta-blockers, CCBs, digoxin, amiodarone Inferior MI Myocarditis ECG – Irregular All P waves present but not always followed by QRS Progressive prolongation of PR interval then QRS dropped Normal QRS Mobitz type II Causes – MI Cardiac surgery Inflammatory disease – rheumatic fever, myocarditis, Lyme’s Autoimmune – SLE Infiltrative – amyloidosis, haemochromatosis, sarcoidosis Drugs – beta-blockers, CCBs, digoxin, amiodarone ECG – Irregular – may be regularly irregular with 3:1 or 4:1 block P waves present, more Ps than QRS PR interval consistent and normal with intermittently dropped QRS complexes QRS normal or broad

Question 98

Describe the clinical presentation and management of second-degree heart block

Answer 98

Type 1 – usually asymptomatic, can develop symptomatic bradycardia with pre-syncope/syncope Management – stop AV blocking drugs, if symptomatic consider pacemaker Type 2 – palpitations, pre-syncope/syncope Risk of progression to complete AV block, should be on cardiac monitor Temporary pacing or isoprenaline if haemodynamic compromise Permanent pacemaker if cause not reversible

Question 99

Describe the cause and ECG features of complete heart block

Answer 99

Causes – Congenital IHD – MI, ischaemic cardiomyopathy Valve disease Dilated cardiomyopathy Iatrogenic – post-pacemaker insertion, post-cardiac surgery Drugs – digoxin, B-blockers, CCBs, amiodarone Infection – endocarditis, Lyme, Chagas Autoimmune – SLE, RA Thyroid ECG: Variable rhythm P wave present but not associated with QRS complexes PR interval absent – AV dissociation QRS narrow or broad depending on site of escape rhythm

Question 100

Describe the presentation and management of complete heart block

Answer 100

Presentation – palpitations, pre-syncope/syncope, SOB, chest pain, haemodynamic compromise, sudden cardiac death Management Cardiac monitoring Transcutaneous pacing/temporary pacing wire or isoprenaline infusion May response to atropine Usually require permanent pacemaker

Question 101

Describe the acute management of bradycardia

Answer 101

A-E assessment Give oxygen if appropriate, obtain IV access Monitor ECG, BP, SpO2 Identify and treat reversible causes e.g. electrolyte abnormalities Evidence of life-threatening signs (shock, syncope, MI, heart failure) – atropine 500mcg IV If good response and not at risk of asystole observe If no life-threatening signs but risk of asystole or inadequate response to atropine Atropine 500mcg IV (repeat to max 3mg) Isoprenaline IV Adrenaline IV OR transcutaneous pacing

Question 102

List causes of pleural effusions

Answer 102

Transudate: Heart failure Liver failure Hypoalbuminaemia Nephrotic syndrome Peritoneal dialysis Hypothyroidism Meig’s syndrome (rare) Exudate: Infection Malignancy Pulmonary infarction Autoimmune disease e.g. rheumatoid arthritis Pancreatitis Post-MI – Dressler’s syndrome Post-CABG Asbestos Other: Haemothorax Empyema Chylothorax

Question 103

List symptoms of pleural effusion

Answer 103

Dyspnoea Cough Pleuritic chest pain Tracheal deviation away from affected side Reduced chest expansion on affected side Stony dullness to percussion Reduced breath sounds and vocal resonance

Question 104

How should pleural effusions be assessed?

Answer 104

CXR first-line CT or US chest to assess further Echo – signs of heart failure or right heart strain (PE) If unilateral and thought to be exudate – pleural aspiration under US guidance Pleural fluid sent for biochemistry (protein, LDH, glucose), gram stain, culture, cytology Serum protein, LDH

Question 105

Describe analysis of pleural fluid

Answer 105

Transudate – protein <30g/L (if normal serum protein) Exudate – protein >30g/L Light’s criteria more accurate for diagnosis of exudative effusions, considered exudate if: Ratio of pleural fluid to serum protein >0.5 Ratio of pleural fluid to serum LDH >0.6 Pleural fluid LDH greater than 2/3 upper limit of normal serum value Also assess: Colour Glucose pH Amylase WBC Cholesterol and triglycerides

Question 106

Describe the uses and procedure of cardiac catheterisation

Answer 106

Local anaesthetic, needle makes hole, catheter inserted into artery/vein in neck, arm, groin (most commonly femoral or radial), fed through major blood vessels into heart chambers/coronary arteries Takes 40-60 minutes Can be used for coronary angiography, percutaneous coronary intervention (balloon inflated to open narrowed coronary arteries), valvuloplasty, valve replacement

Question 107

What considerations should be taken in valve replacements for women of childbearing age?

Answer 107

Should get tissue valves – warfarin is teratogenic so mechanical valves not suitable

Question 108

What are the potential complications of cardiac catheterisation?

Answer 108

Not usually uncomfortable, can usually go home shortly after procedure If stent inserted need overnight stay in hospital Contrast agent can cause tachycardia and hypotension, rarely causes bradycardia or asystole briefly Coughing usually resolves this Mild complications – nausea, vomiting, coughing Serious complications – shock, seizures, kidney injury, cardiac arrest (rare) Radiopaque contrast – AKI, anaphylaxis Complication risk higher in older people

Question 109

List the indications for heart transplantation

Answer 109

Refractory cardiogenic shock requiring left ventricular assist device, continuous IV inotropic therapy NYHA III or IV despite optimised medical and resynchronisation therapy Recurrent life-threatening left ventricular arrhythmias despite implantable cardiac fibrillatory, antiarrhythmic therapy, catheter-based ablation End-stage congenital HF with no pulmonary hypertension Refractory angina without medical or surgical therapeutic options

Question 110

What are the contraindications to heart transplant?

Answer 110

Advanced irreversible renal failure, liver disease, pulmonary parenchymal disease or arterial hypertension History of malignancy within past 5 years Relative – severe peripheral vascular or cerebrovascular disease, obesity, advanced age, diabetes with end-organ damage

Question 111

Describe the cause of hypertension

Answer 111

Primary (idiopathic) Secondary: Phaeochromocytoma Conn’s syndrome Cushing’s Hyperthyroidism Acromegaly Renal artery stenosis Coarctation of the aorta Chronic kidney disease – glomerulonephritis, PKD, obstructive uropathy, diabetic nephropathy Obstructive sleep apnoea Pre-eclampsia

Question 112

What is malignant hypertension? How does it present?

Answer 112

BP >180/120 Headache Visual disturbance Seizures Nausea and vomiting Chest pain

Question 113

How is hypertension diagnosed? Describe the staging.

Answer 113

Clinic reading >=140/90 Offer ambulatory BP monitoring or home BP monitoring If 180/120 or more and retinal haemorrhage, papilloedema, life-threatening symptoms, symptoms of phaeochromocytoma refer for specialist assessment If 150/95 or more treat regardless of age If 135/85 or more assess cardiovascular risk and end-organ damage If less than 135/85 not hypertensive, monitor Assess cardiovascular risk using QRISK (if more than 10% should treat) Assess for end-organ damage – urine dip for protein/blood, albumin:creatinine, U&Es, fundoscopy, ECG Other CV risk factors – HbA1c, lipids

Question 114

Describe management of hypertension

Answer 114

Lifestyle intervention Low salt – less than 6g/day, ideally less than 3g/day Reduce caffeine Smoking cessation, reduce alcohol, balanced diet, exercise, weight loss Step 1: Under 55 or T2DM – ACEi or ARB Over 55 or African-Caribbean – calcium channel blocker Step 2: If already taking ACEi/ARB add calcium channel blocker or thiazide-like diuretic If already taking calcium channel blocker add ACEi or ARB (ARB better if Afro-Caribbean) or thiazide-like diuretic Step 3: Triple therapy with ACEi/ARB, calcium channel blocker and thiazide diuretic Step 4: If potassium less than 4.5 add spironolactone If potassium more than 4.5 add alpha/beta-blocker Refer to specialist Targets: Under 80 – aim for less than 140/90 clinic or 135/85 home Over 80 aim for less than 150/90 clinic or 145/85 home

Question 115

Side effects, contraindications and monitoring required for ACE inhibitors

Answer 115

Side effects: Cough Angioedema Hyperkalaemia Contraindications: Pregnancy, breastfeeding Renal artery stenosis Aortic stenosis Hyperkalaemia Monitoring: U+Es before treatment and after dose increases – acceptable to have 30% increase in creatinine and K up to 5.5

Question 116

Side effects, contraindications and monitoring required for angiotensin receptor blockers

Answer 116

Side effects: Renal impairment Hyperkalaemia Angioedema Hypotension Contraindications: Diabetes eGFR less than 60 Pregnant, breastfeeding Monitoring: U+Es BP

Question 117

Side effects, contraindications and monitoring required for calcium channel blockers

Answer 117

Side effects: Flushing Headaches Erectile dysfunction Palpitations Contraindications: Heart failure – left ventricular failure diltiazem and verapamil contraindicated Cardiac outflow obstruction e.g. aortic stenosis AV block Recent MI, unstable angina Hepatic/renal impairment Pregnancy and breastfeeding Monitor BP

Question 118

Side effects of and contraindications to thiazide-like diuretics

Answer 118

Side effects: Postural hypotension Hypokalaemia, hyponatraemia, hypercalcaemia Gout Impaired glucose tolerance Rare – thrombocytopaenia, agranulocytosis, pancreatitis Contraindications: Hypokalaemia Hyponatraemia Hypercalcaemia Addison’s Severe liver/renal impairment Pregnant women

Question 119

Side effects of and contraindications to spironolactone

Answer 119

Side effects: AKI Hyperkalaemia, hyponatraemia Gynaecomastia Contraindications: Addison’s AKI Hyperkalaemia

Question 120

Side effects of and contraindications to beta-blockers

Answer 120

Side effects: Bradycardia Bronchospasm Cold extremities, paraesthesia, numbness, exacerbation of Raynaud’s Erectile dysfunction Contraindications: History of obstructive airway disease – asthma, COPD Phaeochromocytoma 2nd or 3rd degree heart block Severe peripheral arterial disease Uncontrolled heart failure

Question 121

Give examples of antihypertensives of each class

Answer 121

ACEi – end in -pril Ramipril Lisinopril ARB – end in -sartan Candesartan Losartan CCB Amlodipine Nifedipine Diltiazem Verapamil Thiazide-like diuretics Indapamide Potassium-sparing diuretics Spironolactone Beta-blockers – end in -lol Atenolol Bisoprolol Carvedilol Labetolol

Question 122

List risk factors for venous thromboembolism

Answer 122

Age FHx Pregnancy – post-partum especially Immobilisation – hospitalisation, long-haul flight Surgery – especially lower limb Central venous catheter – femoral > subclavian Malignancy Inherited thrombophilia Antiphospholipid syndrome Polycythaemia Nephrotic syndrome Sickle cell disease Medication – COCP, HRT (combined), raloxifene, tamoxifen, antipsychotics

Question 123

Describe the presentation of a pulmonary embolism

Answer 123

Chest pain – pleuritic Dyspnoea Cough +/- haemoptysis Haemodynamic instability – tachypnoea, tachycardia, hypotension Low-grade fever Hypoxia Syncope Signs of DVT – red, swollen, tender calf

Question 124

Describe the initial assessment of a pulmonary embolism

Answer 124

Pulmonary embolism rule-out criteria (PERC) – if ALL are absent probability of PE less than 2% 50 or younger HR 100 or more SpO2 94 or less Previous DVT or PE Surgery or trauma in past 4 weeks Haemoptysis Unilateral leg swelling Oestrogen use – HRT, COCP Wells score then used: PE likely – more than 4 points PE unlikely – 4 points or less If likely – arrange immediate CTPA (if delay give therapeutic anticoagulation until scan – DOAC) If CTPA positive PE diagnosed If CTPA negative consider proximal leg vein US if DVT suspected If unlikely – measure D-dimer If positive CTPA If negative PE unlikely, stop anticoagulation and consider alternative diagnosis ECG – classic changes are S1Q3T3 (big S in I, big Q in III, inverted T in III) RBBB and right axis deviation Sinus tachycardia is most common

Question 125

When is a V/Q scan used in diagnosis of pulmonary embolism?

Answer 125

If CXR normal, no significant concurrent cardiopulmonary disease Renal impairment (no contrast)

Question 126

Describe the Well’s score

Answer 126

Question 127

Describe the Well’s score

Answer 127

Question 128

How are pulmonary embolisms managed?

Answer 128

Oxygen as required Analgesia Low-risk (based on Pulmonary Embolism Severity Index) – outpatient management DOAC first line for treatment – apixaban or rivaroxaban If contraindicated give LMWH then dabigatran or edoxaban or LWMH then warfarin If renal impairment – LMWH then warfarin Antiphospholipid syndrome – LMWH then warfarin All should be anticoagulated for at least 3 months Provoked VTE – stop after 3 months Unprovoked VTE – continue for additional 3 months (6 months in total) Massive PE with haemodynamic instability – thrombolysis Repeat PE despite anticoagulation – consider inferior vena cava filter