Revise Notes Cardio Flashcards

Question

Answer 1

ECG Underlying AF Pre-op CT/MRI angiography Only if time allows Can differentiate thrombosis from embolism Intra-arterial digital subtraction angiography Gold standard but rarely used

Answer 2

Post op (assessing cause): Echo Patent foramen ovale- venous embolism Ultrasound Aortic/femoral/popliteal arteries- arterial embolism

Answer 3

Initial management A to E assessment NBM Involve senior/vascular team early and urgently High flow oxygen Dual IV access (wide-bore) IV fluid whilst NBM Analgesia Morphine Anticoagulation IV heparin- bolus and infusion Monitor APTT (consult haematology, often aim 2-2.5x normal range

Answer 4

If thrombosis: Thrombolysis Angioplasty +/- stenting Emergency bypass/reconstruction If embolism: Embolectomy Anticoagulation If limb is not viable in either case: Amputation Post-op: Investigate for underlying cause i.e. echo Manage cardiovascular risk factors i.e. statin, anti-platelet, BP control

Answer 5

: Reperfusion injury Inflammation / oxidative damage when blood flow restores to tissue following prolonged period of reduced oxygen supply Can result in: Oedema Compartment syndrome Acidosis Arrhythmias (due to hyperkalaemia) ARDS GI oedema- can cause endotoxic shock Acute kidney injury- build up of toxic metabolites during the ischaemic episode which then re-enter blood stream Compartment syndrome See separate note

Answer 6

Useful links Rutherford Classification BMJ Best Practice - Peripheral arterial disease NICE CKS Peripheral arterial disease Geeky Medics- Rutherford Classification

Answer 7

Thrombosis: Slower onset (hours to days) Less severe as collaterals Claudication present Contralateral pulses often absent (as more likely acute on chronic) Thrombosis can be seen on angiography Management: Thrombolysis Bypass surgery

Answer 8

Embolism: Sudden onset Profound ischaemia (more severe) No claudication history Present collateral pulses More clinical diagnosis (investigations less useful) Management: Embolectomy Anticoagulation

Answer 9

Background The term angina describes the pain occurring secondary to cardiac ischaemia when coronary blood flow (and hence oxygen supply) does not meet cardiac demand. This is most commonly caused by atherosclerotic narrowing of the coronary arteries, and is precipitated by exertion and the associated increased oxygen requirement of the heart. Angina can be categorised as..

Answer 10

Stable - occurring in a stable, predictable pattern - precipitated by exertion and relieved by rest/GTN. Lasting < 10 minutes. Unstable - new onset angina/a deterioration in pre-existing anginal symptoms Requires urgent admission. Suspect UA if: Pain at rest or on minimal exertion Rapidly progressive/deteriorating anginal pain (e.g. increasing frequency)

Answer 11

Step 1: Categorise chest pain as typical, atypical or non-anginal according to the following clinical features: Constricting discomfort affecting the chest, arms or neck Symptoms precipitated by exertion Symptoms relieved within 5 minutes use of GTN or rest Typical chest pain – 3/3 features Atypical chest pain – 2/3 features Non-anginal chest pain – 1 or 0/3 If Non-anginal AND no significant risk factors – angina excluded If unable to rule out angina - i.e. atypical, typical history OR ECG changes OR risk factors - investigate as below (consider prescribing aspirin until diagnosis excluded)

Answer 12

Basic investigations for all patients: FBC + ECG +/- CXR if indicated 1st Line: CT coronary angiogram (CTCA) Diagnosis of significant coronary artery disease made if: 70% stenosis of 1 major coronary artery OR 50% stenosis of the left main coronary artery

Answer 13

2nd line: If CTCA is inconclusive/ patient already has a known diagnosis of CAD: Non-invasive functional imaging - to demonstrate reversible/inducible ischaemia Cardiac MRI (+ stress - dobutamine/exercise) Myocardial perfusion scan with SPECT Stress echocardiography Exercise ECG – only if known coronary artery disease

Answer 14

significant CAD on CTCA or.. Reversible myocardial ischaemia on non-invasive functional imaging

Answer 15

3rd line: Invasive coronary angiography

Answer 16

Basic Management All patients should be given Statin Aspirin 75mg OD for secondary prevention GTN – if angina persists despite 2 x doses – call 999 ACEi if any of - diabetes, HTN, HF, CKD or MI Consider SGLT2i if DM

Answer 17

1st line: B-blocker (bisoprolol) or calcium channel blocker (rate limiting CCBs (verapamil, diltiazem) are preferred to dihydropyridines) Titrate to the maximum tolerated dose Tip: Caution with B-blockers and asthma – in which case a RLCCB may be preferred due to risks of bronchospasm. 2nd line: B-blocker PLUS Calcium channel blocker If already taking a beta blocker: Add a long-acting dihydropyridine CCB (amlodipine, MR nifedipine/felodipine) If taking a dihydropyridine CCB: Add a beta-blocker

Answer 18

Do NOT co-prescribe B-blocker and rate limiting-CCB (risk of complete heart block, severe bradycardia and HF) - use a dihydropyridine instead (MR nifedipine, MR felodipine, amlodipine

Answer 19

Long acting nitrate - Isosorbide mononitrate (ISMN) Ivabradine Nicorandil Ranolazine

Answer 20

If the patient is on dual therapy (tolerating both BB and CCB), refer to cardiology for angiography +/- revascularisation if required (PCI/CABG) CABG is preferred over PCI if the patient is diabetic/ >65yrs/ has triple vessel disease - proven survival benefits Only consider adding a 3rd drug (from above list) whilst awaiting specialist review.

Answer 21

Mechanism of Action: Induce NO release by smooth muscle --> increased c. GMP --> Decreased intracellular calcium levels = vasodilation Side effects: Hypotension, tachycardia, flushing, headaches, reflux Tolerance: does NOT occur if we use modified release nitrates

Answer 22

Mechanism: Inhibits the funny (If) current channels in the sinoatrial node (SAN) --> reduced heart rate. Side effects: Luminous phenomena (halos/coloured bright lights/stars), bradycardia Tip: Funny current inhibitors - Funny vision Peripheral oedema/ankle swelling

Answer 23

Enoxaparin and fondaparinux – activates AT3 – inhibits factor Xa Bivalirudin – direct thrombin inhibitor References & Further Reading: National Institute for Health and Care Excellence [NICE] (2022). Angina. https://cks.nice.org.uk/topics/angina/ - Revised June 2023

Answer 24

Definition Abnormal localised dilatation of vessel of over 50% of normal diameter Aortic aneurysm = 3cm or above Pathophysiology A weakening of the aortic wall leads to bulging or dilation, predisposing to rupture All three layers of vessel involved (less = pseudo-aneurysm) Commonly involves the abdominal aorta (AAA) - most commonly infrarenal

Answer 25

Definition: 3cm or more dilation of all layers of vessel Commonly involves the abdominal aorta (AAA) - most commonly infrarenal Risk factors: Older men who have hypertension and smoke Symptoms: Often none until rupture, abdominal pain radiating to back Screening programme: One off scan for all men over 65 Management: If > 5.5cm or growing 1cm/yr or symptomatic- EVAR or open elective surgery Ruptured AAA confers 75% mortality and requires immediate resuscitation and open emergency surgery to repair

Answer 26

Stabilise if in shock- major haemorrhage protocol Portable USS (CT only if stable) Urgent surgical repair - usually open repair 75% mortality Other complications Embolisation- causes femoral artery thrash and acute limb ischaemia Direct pressure- compressed nearby structures including duodenem, ureters or IVC Useful links NICE guidelines- Abdominal aortic aneurysm: diagnosis and management

Answer 27

As per screening programme: Elective AAA repair EVAR preferred to open repair as lower post-op mortality and reduced length of stay If not fit for surgery: Control risk factors especially BP control

Answer 28

: Men > 65 can ask for one off abdominal US to assess AA size Men/women AAA size: - < 3cm= normal - 3-4.4cm= small- yearly scan (usually grow < 0.5cm/year) - 4.5-5.4cm= medium- 3 monthly scan - > 5.5cm or growth > 1 cm/yr or symptomatic need referral within 2 weeks for elective surgery (risk rupture > risk of surgery)

Answer 29

Rupture: Bedside focused USS can identify ruptured AAA in minutes CT angiography is gold standard Group and save and crossmatch 6 units Routine bloods including FBC, UE, LFT, coagulation

Answer 30

Based on imaging findings and clinical presentation. Emergency diagnosis and management of ruptured aneurysms is crucial.

Answer 31

History May be asympomtomatic until rupture- hence screening programme Abdominal pain radiating to back which may be sudden and severe if ruptured Examination Findings Palpable pulsatile mass in the abdomen Auscultation may reveal bruits over the aneurysm Signs of shock if ruptured ( hypotensive, tachycardic, cold and clammy, reduced GCS)

Answer 32

Epidemiology More prevalent in older adults, especially males Risk factors Smoking Hypertension Connective tissue disorders i.e. Marfan syndrome, Ehler's Danlos Family history aneurysms

Answer 33

Definition Abnormal localised dilatation of vessel of over 50% of normal diameter Aortic aneurysm = 3cm or above Pathophysiology A weakening of the aortic wall leads to bulging or dilation, predisposing to rupture All three layers of vessel involved (less = pseudo-aneurysm) Commonly involves the abdominal aorta (AAA) - most commonly infrarenal

Answer 34

Associated conditions Turners Syndrome Bicuspid aortic valve Clinical features Infancy – features of heart failure, failure to thrive Adulthood - uncontrolled hypertension Examination findings Radio-femoral delay A systolic murmur - left infraclavicular area and may be loudest below the left scapulae Apical click may be heard Investigations CXR: Notching of the inferior border of the ribs - Roesler sign

Answer 35

Aortic Dissection Pathology: tear within the tunica intima allows blood to flow between the layers of the aorta Risk factors Hypertension Marfans, Ehlers Danlos Turners syndrome / Noonan syndrome Clinical Features “Tearing” chest pain radiating into the back, between the scapulae Aortic regurgitation - early diastolic murmur

Answer 36

Diagnosis: CT angiogram Stanford Classification Type A – Dissection of the ascending aorta – most common Type B – Dissection of the descending aorta Management Type A Surgical management Permissive hypotension – target 100-120mmHg systolic BP (labetalol if req.) Type B Medical management – no surgery! Labetalol given to reduce BP which reduces progression of dissection

Answer 37

Epidemiology: Less common than venous ulcers; often in elderly with cardiovascular disease or diabetes. Causes: Primarily peripheral arterial disease (PAD); also embolism, thrombosis, or vasculitis. Clinical Features: Pain at rest/elevation; located on pressure points; deep, 'punched out' appearance. Examination Findings: Cool, pale skin; diminished pulses; delayed capillary refill; necrotic ulcer base. Investigations: ABPI < 0.8 indicates arterial insufficiency; < 0.5 suggests PAD-related ulceration. Utilise Doppler ultrasound and arterial duplex imaging. Management: Step-wise approach of lifestyle changes, pharmacological management (antiplatelets, statins) and surgical management (revascularisation/ wound debridement).

Answer 38

Pathophysiology Result from inadequate blood flow to the extremities, leading to tissue ischemia and subsequent ulceration Epidemiology Less common than venous ulcers Elderly individuals with underlying cardiovascular disease or diabetes. Causes Peripheral arterial disease (PAD) Other causes include embolism, thrombosis, or vasculitis. Clinical Features Painful, especially at rest or with elevation Tend to be located on pressure points including tips of toes, heels, or metatarsal heads

Answer 39

Arterial ulcers classically appear deep and 'punched out' Cool, pale, or cyanotic skin Diminished or absent pulses Delayed capillary refill The ulcer base may appear necrotic, with surrounding tissue exhibiting signs of ischemia.

Answer 40

Investigations Ankle-brachial pressure index (ABPI) measurement ABPI < 0.8= arterial insufficiency < 0.5 is suggestive of PAD-related ulceration. Doppler ultrasound, and arterial duplex imaging To assess arterial blood flow and identify any stenosis or occlusion.

Answer 41

Management Treatment aims to improve arterial perfusion 1) Lifestyle modifications (stop smoking, weight loss, exercise) 2) Medication (antiplatelets, statins) 3) Revascularization procedures (angioplasty, bypass surgery), wound debridement, and wound care. Complications Delayed healing Infection- can progress to osteomyelitis Progression to gangrene

Answer 42

Aspect Venous Ulcers Arterial Ulcers Diabetic Ulcers Pathophysiology Chronic venous insufficiency, leading to impaired venous return, venous hypertension, and tissue hypoxia Peripheral arterial disease (PAD), resulting in inadequate blood flow, tissue ischemia, and subsequent ulceration Neuropathy, microvascular disease, and impaired wound healing due to diabetes-related metabolic changes

Answer 43

Epidemiology Common, particularly in older adults and those with a history of deep vein thrombosis (DVT) or varicose veins Less common but often seen in elderly individuals with underlying cardiovascular disease or diabetes Common in diabetic patients, especially those with poor glycemic control or long-standing disease

Answer 44

Location of Ulcers Typically located on the lower legs, near the medial malleolus Commonly found on the toes, heels, or lateral ankle pressure points Predominantly affect the feet, particularly over pressure points such as the plantar surface

Answer 45

History - Painful - Worse on standing - Painful - Worse at night when legs elevated - Often painless - Report abnormal sensation

Answer 46

Examination Findings - Large shallow irregular ulcer - Granulating base with irregular edges - Associated oedema, hyperpigmentation, venous eczema, lipodermatosclerosis - Warm skin, normal pulses - Ulcers small, sharply defined - Deep and ‘punched out’ with necrotic base and surrounding ischemic tissue - Cool, pale, or cyanotic skin - Diminished or absent pulses, delayed capillary refill - Variable size/depth - Calluses - Signs of peripheral neuropathy -May have signs of infection - Warm skin - Normal pulses if no co-existing ischaemia

Answer 47

Investigations - Doppler ultrasound to assess venous reflux, venous duplex imaging, - Ankle-brachial pressure index (ABPI) typically > 0.8 - Doppler ultrasound/angiography - ABPI typically < 0.8 - Assessment of glycemic control (HbA1c) - Screening for neuropathy -ABPI > 0.8 -XR - exclude osteomyelitis

Answer 48

Management - Compression bandaging if excluded arterial insufficiency - Leg elevation - Wound care - Smoking cessation - Wound care - Antiplatelet therapy - Revascularization procedures (angioplasty, bypass surgery) - Optimize glycemic control - Wound debridement - - Offloading pressure areas - Wound care - Screening and management of diabetic complication

Answer 49

Complications Delayed healing, recurrent ulcers, cellulitis, venous stasis dermatitis, venous eczema Delayed healing, infection, gangrene, progression to limb ischemia, amputation Delayed healing, infection, progression to osteomyelitis, amputation, increased risk of recurrent ulcers

Answer 50

If there are any of the above life-threatening features treat as follows: Give atropine 500mcg IV Repeat step 1 every 3-5 minutes (up to total of 3mg atropine) If ineffective consider (a) transcutaneous pacing OR (b) second line medications: Isoprenaline Adrenaline Aminophyline – if bradycardia is secondary to spinal cord injury/recent inferior MI. Glucagon – if bradycardia is caused by beta-blocker or CCB If this fails consider transvenous cardiac pacing

Answer 51

1st degree block PR > 200ms 2nd degree HB Mobitz I (Wenkebach) – progressive PR prolongation until dropped QRS complex Mobitz II – Prolonged PR interval is constant with dropped QRS complexes More serious – higher risk of progressing to complete HB

Answer 52

3rd degree HB Complete dissociation between P waves and QRS complexes Examination findings: Cannon A waves (irregular) Wide pulse pressure Variable S1 intensity

Answer 53

Step 1: Identify adverse features Shock (e.g. Systolic < 90mmHg) Syncope Features of myocardial ischaemia – chest pain Symptoms of severe heart failure – hypoxia, crepitations etc. Risk factors for asystole including: Recent asystole Mobitz type 2 block Complete heart block with QRS > 120 Ventricular pause > 3 seconds

Answer 54

Key learning: See summary 2021 ALS guidelines below CPR 30 chest compressions : 2 breaths Assess rhythm: Shockable= VF (see ECG below)/pulseless VT If shockable give one shock, resume CPR and repeat rhythm check in 2 minutes, continue giving shocks if in shockable rhythm If given 3 shocks- give amiodarone Non-shockable= Pulseless electrical activity (PEA)/ asystole In both shockable and non-shockable- given adrenaline every 3-5 minutes

Answer 55

Identify reversible causes (4Hs and 4Ts): Hypoxia Hypovolaemia Hypo/hyperthermia Hypo/hyperkalaemia/other metabolic abnormalities Thrombosis- coronary or pulmonary (PE) Tension pneumothorax Tamponade (cardiac) Toxins (review drug chart/overdose history

Answer 56

Cardiac Tamponade Pathology Causes include: Trauma, MI, Cardiac surgery, malignancy Accumulation of fluid within the pericardium. Consequently, intrapericardial pressures > diastolic pressures This results in impaired diastolic filling of the heart –> reduced cardiac output.

Answer 57

Clinical features Shortness of breath Tachycardia Becks Triad – Hypotension, muffled heart sounds, raised JVP JVP – absent Y descent (due to limited right ventricular filling) Pulsus paradoxus Investigations ECG findings: Electrical alterans – alternation of QRS amplitude between each beat Management Urgent pericardiocentesis

Answer 58

Pathology: The ballooning of the myocardial apex due to severe hypokinesia, not caused by ischaemia. Causes: Severe emotional stress – bereavement, heartbreak Features: Chest pain, ST elevation but normal coronary arteries on angiogram Management: Supportive

Answer 59

Pathology: Reduced ventricular compliance leads to diastolic dysfunction with impaired ventricular filling. Causes Amyloidosis – AL (myeloma) Sarcoidosis, Haemochromatosis, Scleroderma ECG changes: Low voltage ECG complexes, bundle branch block

Answer 60

Causes Drugs: Alcohol, chemotherapy – esp. doxorubicin Myocarditis: (Coxsackie B) Peripartum, Duchenne MD CXR changes: “Balloon heart” On examination: 3rd heart sound

Answer 61

Inheritance: autosomal dominant Pathology: Mutation in genes encoding the B-myosin heavy chain or myosin binding protein C lead to left ventricular hypertrophy (LVH) and remodelling Clinical Features: Presentation: Syncope, angina, shortness of breath on exertion, SCD in a young patient Ejection systolic murmur due to ventricular outflow obstruction from LVH Jerky pulse, double apical pulse S4 heart sound Associations: Friedreich's ataxia and WPW Echocardiogram: Mitral regurgitation (MR) + systolic anterior motion (SAM) of the anterior valve leaflet with asymmetrical hypertrophy (ASH). Mnemonic: MR SAM ASH ECG changes: Deep Q waves, Progressive T wave inversion, LAD and LVH Management: ICD, dual chamber PM, amiodarone, beta blockers/RLCCBs

Answer 62

Associations: Friedreich's ataxia and WPW Echocardiogram: Mitral regurgitation (MR) + systolic anterior motion (SAM) of the anterior valve leaflet with asymmetrical hypertrophy (ASH). Mnemonic: MR SAM ASH ECG changes: Deep Q waves, Progressive T wave inversion, LAD and LVH Management: ICD, dual chamber PM, amiodarone, beta blockers/RLCCBs

Answer 63

Anacrotic pulse - slow-rising Aortic stenosis Collapsing pulse Aortic regurgitation, PDA Pulsus alterans - alternating strong then weak pulses Severe left ventricular failure (LVF) Jerky pulse HOCM Pulsus paradoxus - pulse becomes softer during inspiration due to a drop in SBP Cardiac tamponade Severe asthma attack

Answer 64

Aortic / pulmonary stenosis HOCM Tetralogy of fallot ASD

Answer 65

Mitral/tricuspid regurgitation – “high pitched/blowing” Ventricular septal defect – “Harsh” sound

Answer 66

Aortic regurgitation Pulmonary regurgitation

Answer 67

“Rumbling MDM” – mitral stenosis Tricuspid stenosis

Answer 68

PDA, associated with left subclavian thrill

Answer 69

Aortic– radiates into carotids Mitral – radiates into the axilla Left sided murmurs are heard with increased intensity on expiration (lEft = Expiration) – aortic / mitral Right sided murmurs are heard with increased intensity on inspiration (rIght – Inspiration)

Answer 70

Quiet S1: Mitral regurgitation Loud S1: Mitral stenosis

Answer 71

Quiet S2: Aortic stenosis Loud P2: Pulmonary hypertension

Answer 72

Fixed split: ASD

Answer 73

Causes of S3: Dilated cardiomyopathy, constrictive pericarditis, HF

Answer 74

Causes: Diastolic heart failure, HOCM

Answer 75

Aortic– radiates into carotids Mitral – radiates into the axilla Left sided murmurs are heard with increased intensity on expiration (lEft = Expiration) – aortic / mitral Right sided murmurs are heard with increased intensity on inspiration (rIght – Inspiration)

Answer 76

Ventricular Septal Defect Ventricular septal defect (VSD) is a congenital heart defect with an opening in the interventricular septum. This allows blood flow between the left and right ventricles, resulting in mixing of oxygen-rich blood from the left ventricle with deoxygenated blood in the right ventricle. The severity of symptoms depends on the size and location of the VSD. Causes Chromosomal disorders: Downs, Patau's syndrome Post-MI

Answer 77

Clinical features Failure to thrive Heart failure Hepatomegaly Tachypnoea Examination findings: Harsh pansystolic murmur loudest at the lower left sternal edge Complications

Answer 78

Harsh pansystolic murmur loudest at the lower left sternal edge Complications Eisenmenger’s syndrome The initial left to right shunt causes pulmonary hypertension Pulmonary HTN causes RVH with increased right heart pressures At a certain point the pressure generated by the right ventricle > left ventricle - the shunt reverses leading to a RIGHT TO LEFT shunt Signs: Cyanosis, clubbing Requires surgical management

Answer 79

Commonly identified in adulthood with Shortness of breath, esp. on exertion PHTN and RHF Arrhythmias - AF Stroke following DVT - classic exam q - the clot is able to pass through defect from RA to LA and into systemic circulation

Answer 80

Classification Ostium Primum ASD Defect of the atrial septum near the AV valve Commonly associated with Down’s syndrome Ostium Secundum ASD Defects of the superior atrial septum MOST COMMON form of ASD Examination findings Ejection systolic murmur Fixed splitting of S2 Holt-Oram syndrome: ASD + triphalangeal thumbs

Answer 81

Connection between the pulmonary trunk and the descending aorta. Usually closes when the neonate takes their first breath - increased pulmonary blood flow which results in prostaglandin clearance Incomplete closure causes PDA Risk factors: Prematurity, maternal rubella Examination findings Continuous 'machinery-like' murmur Left subclavicular thrill Bounding, collapsing pulse

Answer 82

Management INDOMETHACIN or ibuprofen - inhibit production of prostaglandins

Answer 83

Complications: The connection between the right and left heart mean that deep vein thrombosis / PEs can travel to the arterial circulation and cause stroke

Answer 84

Congenital heart disease (CHD) can be classified as cyanotic or acyanotic. Cyanotic CHD occurs when deoxygenated blood passes into the systemic circulation. This occurs in the context of a right-to-left shunt, where deoxygenated blood returns from the body to the right heart, then passes directly into the left heart, bypassing the pulmonary circulation/lungs, and therefore not having been re-oxygenated. Deoxygenated blood is then pumped from the left heart around the body, with resultant hypoxia and cyanosis.

Answer 85

Cyanotic CHDs include the 3 T’s Tetralogy of Fallot (TOF) – the most common cyanotic CHD (presents after approx. 1 month) Transposition of the Great Arteries (TGA) – most common cause of cyanosis at birth Tricuspid atresia Acyanotic CHDs include Ventricular septal defect – most common Atrial septal defect Coarctation of the aorta Patent ductus arteriosus

Answer 86

Cyanotic CHDs include the 3 T’s Tetralogy of Fallot (TOF) – the most common cyanotic CHD (presents after approx. 1 month) Transposition of the Great Arteries (TGA) – most common cause of cyanosis at birth Tricuspid atresia Acyanotic CHDs include Ventricular septal defect – most common Atrial septal defect Coarctation of the aorta Patent ductus arteriosus

Answer 87

. Defects 1.Ventricular septal defect 2.Pulmonary stenosis causing right ventricular outflow obstruction 3.Overriding aorta 4.Right ventricular hypertrophy Right heart pressure > left heart pressure due to the presence of pulmonary stenosis and right ventricular outflow obstruction The VSD allows the passage of blood from the right heart to the left, resulting in a RIGHT TO LEFT SHUNT, and cyanosis as described above.

Answer 88

Examination findings Ejection systolic murmur loudest in the pulmonary area, on inspiration – pulmonary stenosis Clubbing Investigations CXR - classically shows a ‘boot shaped’ heart due to RVH Echocardiogram - the investigation of choice Management Prostaglandin infusion in neonates - maintains the ductus arteriosus, which allows blood to flow from the aorta into the pulmonary arteries Definitive management - Total surgical repair (open heart surgery) Tet spells can be managed with beta blockers, morphine etc.

Answer 89

Clinical features If not diagnosed antenatally or at newborn check, may present 1-2 months postpartum with Cyanosis, dyspnoea Failure to thrive, poor feeding and poor weight gain Tet spells - acute worsening of cyanosis often precipitated by exertion/crying Tearful, irritable, agitated Dyspnoeic Squat to improve venous return

Answer 90

Right heart pressure > left heart pressure due to the presence of pulmonary stenosis and right ventricular outflow obstruction The VSD allows the passage of blood from the right heart to the left, resulting in a RIGHT TO LEFT SHUNT, and cyanosis as described above.

Answer 91

CXR: "egg on it's side" appearance Management PE1 (alprostadil) to maintain patency of the ductus arteriosus and allow mixing of oxygenated and deoxygenated blood Surgical management is required

Answer 92

Defects Absent tricuspid valve: No right atrium to right ventricle connection. Hypoplastic right ventricle: Underdeveloped right ventricle. Atrial septal defect (ASD): Allows blood to flow from right atrium to left atrium. Ventricular septal defect (VSD): Permits blood flow from the left ventricle to the pulmonary artery. Pulmonary stenosis or atresia: Often present, restricting pulmonary blood flow. Left ventricular hypertrophy: Increased workload on the left ventricle.

Answer 93

Examination Findings Cyanosis Tachypnoea Murmurs: Holosystolic (VSD) or ejection systolic (pulmonary stenosis) Clubbing (in chronic cases) Management Prostaglandin infusion: Maintains ductal patency for pulmonary blood flow. Surgical intervention: including Blalock-Taussig shunt, Glenn procedure, Fontan procedure.

Answer 94

In tricuspid atresia, blood returns to the heart through the superior and inferior vena cava into the right atrium but cannot pass into the right ventricle due to the absence of the tricuspid valve, resulting in a hypoplastic right ventricle. A right-to-left shunt at the atrial level allows blood to mix in the left atrium, leading to variable oxygenation levels in the blood reaching the left ventricle and the systemic circulation.

Answer 95

Clinical Features Presentation typically within the first few days to weeks: Cyanosis Dyspnoea Failure to thrive Fatigue

Answer 96

Anteroseptal: Leads V1-V4 – supplied by the LAD Lateral – Leads 1, aVL, V5-6 – suppled by the left circumflex Inferior – Leads II, III, aVF – supplied by the RCA Note: ST depression in V1-3 can represent a posterior STEMI – confirm with V7-V9 lead placement (supplied by left circumflex)

Answer 97

Global PR depression (commonest) Saddle shaped ST elevation

Answer 98

Convex ST elevation followed by T wave inversion in V1-V3 Incomplete RBBB

Answer 99

Right ventricular hypertrophy – RAD, dominant R in V1 Right ventricular strain – T wave inversion in V1-V3 Epsilon waves – a small notch which follows QRS complex

Answer 100

Small QRS complexes Electrical alterans

Answer 101

Prolonged PR Down sloping ST depression T wave inversion Short QT Bradycardia Tip: Digoxin toxicity ECGs are said to have a ‘reverse Nike tick’ appearance with the down sloping of the ST and the T wave inversion.

Answer 102

Prolonged PR interval Long QTc J waves (Osborn waves) Bradycardic Tip: ECG slows down/gets frozen – slow rate, long pr, long qt Hypothermia including Osborn (J) wave Figure 109: Hypothermia including Osborn (J) wave.

Answer 103

Short PR interval Broad QRS complexes Delta wave - Slurred upstroke to the QRS Wolff Parkinson White Figure 110: Wolff Parkinson White. User Ksheka on en.wikipedia, Wolff-Parkinson-White syndrome 12 lead EKG, CC BY-SA 3.0

Answer 104

Flattened P waves Prolonged PR interval Tall Tented T waves Bradycardia Broad QRS Severe hyperkalaemia – sinusoidal pattern

Answer 105

U waves Flat/inverted T waves Prolongation of PR Long QTc ST depression Memory aid: U have no Pot and no T, but a long PR, a long QT and a depressed ST

Answer 106

Aetiology Coronary artery disease/ IHD is the most common cause Other causes include: Hypertension, Valvular heart disease (VHD), cardiomyopathy, CHD, arrhythmias (AF) etc.

Answer 107

Heart failure with reduced ejection fraction (HF-REF) if the LVEF is < 40% HF with mildly reduced EF (HFmrED) - EF 41-49% Heart failure with preserved ejection fraction (HF-PEF) Approximately 50% of patients Symptoms/signs of HF/ abnormalities in cardiac structure/pressures with LVEF > 50%

Answer 108

Class 1: No limitation Class 2: Slight limitation of ordinary activity Class 3: Significant limitation. Only comfortable at rest. Class 4: Severe limitations. Symptoms present at rest. Often bedbound.

Answer 109

Symptoms SOB - worse on exertion PND, orthopnoea Oedema - ankles, weight gain, abdominal distension Tired all the time (TATT) Elevated JVP

Answer 110

Step 1: Measure NT-Pro BNP NT-Pro BNP > 2000ng/L High - Specialist assessment and echocardiogram within 2 weeks NT-Pro BNP 400-2000ng/L Raised - Specialist assessment and echocardiogram within 6 weeks NT-Pro BNP < 400ng/L Normal – HF is unlikely Note: NT-Pro BNP may be falsely lowered by.. ACEi/ARBs/beta-blockers and aldosterone antagonists Obesity (BMI > 35) African-Carribean ethnicity Step 2: Echocardiogram

Answer 111

A: alveolar oedema (perihilar/bat-wing opacification) B: Kerley B lines (interstitial oedema) C: cardiomegaly (cardiothoracic ratio >50% on PA film) D: dilated upper lobe vessels E: effusions (pleural effusions – blunted costophrenic angles with meniscus sign)

Answer 112

Prescribe a combination of both ACE inhibitor AND a B-blocker Do not offer ACEi if suspected significant valve disease Switch to an ARB if unable to tolerate ACEi (e.g. due to cough) Step 2 If patient remains symptomatic - offer an MRA - e.g. spironolactone, eplerenone

Answer 113

1. Ivabradine – consider if ejection fraction (EF) < 35% AND in sinus rhythm with HR > 75bpm 2. Sacubitril-valsartan – consider if EF < 35% Stop the ACEi/ARB prescribed initially 3. SGLT-2 inhibitor - dapagliflozin, empagliflozin 4. Digoxin – consider in sinus or especially if co-existent AF 5. Hydralazine + Nitrate - consider especially if patient is of African-Caribbean family origin 6. Cardiac resynchronisation therapy (CRT) - consider for symptomatic benefit, especially if the patient has HF with a wide QRS consider biventricular pacing Improves symptoms but not mortality

Answer 114

The mainstay of management of HFpEF is with diuretics for symptomatic relief. There is no proven survival benefit associated with ACEi/B-blockers SGLT-2 inhibitors (dapagliflozin, empagliflozin) are now recommended by NICE

Answer 115

1. Symptomatic relief - Loop diuretics Furosemide, bumetanide, torasemide - symptomatic relief, no impact on mortality 2. Vaccinations Annual influenza vaccine One off pneumococcal vaccine Antiplatelets- if atherosclerotic arterial disease 3. Lipid modification - Statin 4. Cautions - avoid rate limiting CCBs (verapamil/diltiazem) in patients with heart failure References & Further Reading: National Institute for Health and Care Excellence [NICE] (2022). Heart Failure - Chronic. https://cks.nice.org.uk/topics/heart-failure-chronic/ - Revised October 2023

Answer 116

If clinic BP > 140/90 (but < 180/120) – perform ABPM or HBPM to confirm diagnosis If > 180/120 see below Stage 1 Hypertension Clinic BP > 140/90 Ambulatory blood pressure monitor (ABPM) > 135/85 Stage 2 Hypertension Clinic BP > 160/100 Ambulatory blood pressure monitor (ABPM) > 150/95 Severe hypertension Blood Pressure > 180/120 Accelerated hypertension: Stage 3 + Retinal haemorrhages/papilloedema - Admit

Answer 117

Admit if accelerated hypertension as above OR if there are features of a hypertensive emergency (chest pain, HF, acute renal failure). Consider investigating for secondary causes of hypertension (phaeochromocytoma etc.) If no indication for admission, perform urgent investigations to investigate for end organ damage: Bloods / ACR / ECG If there is evidence of end organ damage, initiate treatment immediately (before ABPM). If not, repeat clinic BP in 7 days

Answer 118

For Stage 2 HTN (clinic 160/100 or ABPM > 150/95) Offer antihypertensive drug treatment For Stage 1 HTN (clinic 140/90 or ABOM 135/85) If < 80 years - start antihypertensive drug treatment if any one of the following: Evidence of EOD Cardiovascular disease or QRISK > 10% Comorbidities - CKD or diabetes “consider” antihypertensive drugs if < 60 yrs and QRISK < 10% “consider” antihypertensive drugs if If > 80 years and clinic BP > 150/90

Answer 119

Age < 80 – aim for… Clinic BP < 140/90 ABPM < 135/85 Age > 80 - add 10 to systolic - aim for… Clinic BP < 150/90 ABPM < 145/85 In patients with CKD and diabetes or if urine albumin to creatinine ratio (ACR) >70 mg/mmol) A blood pressure below 130/80 mmHg is advised i

Answer 120

STEP 1: ACE inhibitor Used in diabetics regardless of age due to renoprotection benefits Trial ARB if the ACEi not tolerated (e.g. due to cough) Step 2: Continue ACEi/ARB Add either a CCB OR a thiazide like diuretic (TLD) Step 3: ACEi + CCB + TLD Step 4: Resistant hypertension - See below

Answer 121

Step 1: CCB Step 2: Continue CCB Add either a ACEi/ARB OR a thiazide like diuretic (TLD) Step 3: CCB + ACEi + TLD Step 4: Resistant hypertension - See below

Answer 122

’ If the potassium is < 4.5 – commence low dose spironolactone Remember - side effect of mineralocorticoid receptor antagonists - hyperkalaemia If the potassium is > 4.5 – commence alpha or beta blocker

Answer 123

Nb. Thiazide-like diuretics Indapamide is the TLD recommended by NICE Alternatives include chlortalidone, metolazone

Answer 124

References & Further Reading: National Institute for Health and Care Excellence [NICE] (2019). Hypertension in adults: diagnosis and management [NG136]. https://www.nice.org.uk/guidan...

Answer 125

Infective endocarditis describes inflammation of the endocardium, most commonly of infectious aetiology. Causative organisms Staphylococcus Aureus The most common organism Staphylococcus Epidermis The most common post-valve surgery (for the first 2 months post op) Can also colonise indwelling lines Streptococcus Viridans Include Streptococcus Mitis and Streptococcus Sanguinis Common following dental work or in patients with poor dental hygiene Streptococcus Bovis Subtypes include Streptococcus Gallolyticus Most common in patients with colorectal cancer Therefore, consider a colonoscopy if gallolyticus positive Other ‘culture negative’ causes of infective endocarditis include: 1.The B’s: coxiella Burnetti, Brucella, Bartonella 2. HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

Answer 126

The modified Duke criteria can be used to aid the diagnosis of infective endocarditis. Pathological features: Positive histopathology from cardiac surgery/autopsy Major features: Positive blood cultures or serology Evidence of endocardial involvement – new valvular regurgitation / positive echocardiogram

Answer 127

History of cardiovascular conditions or IVDU – predisposing factors Pyrexia > 38 degrees Vascular phenomena - septic emboli, Janeway lesions Immunological phenomena – Osler nodes, Roth spots, Glomerulonephritis

Answer 128

Janeway lesions - irregular, nontender haemorrhagic macules, present on the palms of hands and soles of feet. Osler nodes - tender, red-purple lesions, located most commonly in the pulp of the fingers/toes Roth spots - white-centred retinal haemorrhages

Answer 129

TTE is often used as the initial investigation of choice, due to its less invasive nature However, TOE is more sensitive and specific and therefore is of value if High clinical suspicion remains despite a negative TTE Results of the TTE are equivocal Prosthetic valve Positive TTE - but suspected complication/virulent organism

Answer 130

❤️Prophylaxis NOT recommend for common procedures e.g. dental work / GI surgery ❤️Blind therapy Native valve: Amoxicillin (+ consider gentamicin) Prosthetic valve: Vancomycin + gentamicin + rifampicin ❤️Staphylococci Native valve: Flucloxacillin Prosthetic valve: Flucloxacillin + gentamicin + rifampicin ❤️Streptococci Benzylpenicillin is 1st line

Answer 131

Severe valvular incompetence Cardiac failure which is refractory to medical management/diuretics etc. Presence of an aortic abscess Suggested by prolongation of the PR interval on ECG

Answer 132

Inheritance: Autosomal dominant Pathology: Mutation in ryanodine receptor (RYR2) in the myocardial sarcoplasmic reticulum Presentation: Emotional stimuli/exertion causes PVT presenting with syncope or SCD Management: Beta blockers/ ICD

Answer 133

Inheritance: Autosomal dominant Subtypes: LQT1 – typical presentation = exertional syncope (e.g. whilst swimming) LQT2 – present with syncope following auditory stimuli/ emotional stress Pathology: Defect of the alpha subunit of the slow cardiac potassium channel. Management: ICD, avoid drugs which prolong the QTC.

Answer 134

Inheritance: Autosomal dominant Presentation: Sudden cardiac death (SCD) - mean age of death is 41 yrs More common in Asian ethnicities, especially SE Asia including the Phillipines Pathology: SCN5a gene mutation (Na+ channel in myocardium) 50% of cases are inherted, in an autosomal dominant fashion There may be no FHx in the other 50%, which result from a new spontaneous mutation ECG changes: Convex ST elevation > 2mm in more than 1 of V1, V2 or V3 followed by negative T wave Partial RBBB Investigation: Flecainide or Ajmaline provocation test - ECG changes become more obvious Management: ICD

Answer 135

The second most common cause of sudden cardiac death. Inheritance: Autosomal dominant Pathology: Abnormal cardiac desmosomes. Right ventricular myocardium is replaced by fibrous and fatty tissue ECG changes: T wave inversion in V1, V2, V3 Epsilon wave (a terminal notch seen after the QRS complex) Management: Sotalol, ICD, Catheter ablation to reduce risk of VT Naxos disease = ARVC + palmoplantar keratosis + woolly hair

Answer 136

) The commonest cause of sudden cardiac death. Inheritance: autosomal dominant Pathology: Mutation in genes encoding the B-myosin heavy chain or myosin binding protein C lead to left ventricular hypertrophy (LVH) and remodelling Clinical Features: Presentation: Syncope, angina, shortness of breath on exertion, SCD in a young patient Ejection systolic murmur due to ventricular outflow obstruction from LVH Jerky pulse, double apical pulse S4 heart sound

Answer 137

Associations: Friedreich's ataxia and WPW Echocardiogram: Mitral regurgitation (MR) + systolic anterior motion (SAM) of the anterior valve leaflet with asymmetrical hypertrophy (ASH). Mnemonic: MR SAM ASH ECG changes: Deep Q waves, Progressive T wave inversion, LAD and LVH Management: ICD, dual chamber PM, amiodarone, beta blockers/RLCCBs

Answer 138

Pathophysiology The pericardium becomes thickened and fibrotic forming a ‘non-compliant shell’ which impairs filling and causes diastolic dysfunction Causes The same causes as listed above for pericarditis, especially TB Post cardiac surgery, radiotherapy Clinical Features Symptoms - Shortness of breath

Answer 139

. Causes Viral – Coxsackie B, influenza, covid-19 Autoimmune - Rheumatoid arthritis Tuberculosis Uraemia / renal failure Post MI pericarditis Dressler’s syndrome Clinical features Pleuritic chest pain, positional – relieved leaning forwards, worse when lying down Flu-like symptoms Fever

Answer 140

Examination findings Pericardial rub over the left sternal border - a ‘grating’ like sound which occurs as layers of inflamed pericardium slide over one another. Investigations ECG: Global changes - PR depression, Saddle shaped (convex) ST elevation Management 1st Line: NSAIDs plus colchicine

Answer 141

Clinical Features A history of recent viral symptoms (fever, myalgia, headache, sore throat, arthralgia etc). Chest pain Shortness of breath Arrhythmias, palpitations, Investigations ECG: ST segment elevation, T wave inversion Bloods: Elevated CRP + Troponins Management Treat the cause, supportive measures Complications Dilated cardiomyopathy Arrhythmias Heart failure

Answer 142

Clinical features Weight loss Pyrexia of unknown origin Clubbing Fatigue Shortness of breath Examination findings: Mid-diastolic murmur with a tumour plop Investigations Echocardiogram: “A pedunculated mass” Figure 192: Atrial Myxoma. The myxoma is the light mass.(arrows) (In this view, the heart is "upside down" - the apex of the heart is at the top and the left atrium is on the bottom left

Answer 143

Key learning Commonly results from atherosclerosis in vessels causing reduced perfusion of limbs Risk factors as for all cardiovascular disease Symptoms progress from intermittent claudication to rest pain to tissue loss ABPI and US arterial duplex identify severity and site of disease Management involves conservatively and pharmacologically modifying cardiovascular risk factors and surgery if above fails All patients given atorvastatin and clopidogrel for life Critical limb ischaemia managed as urgent surgical emergency

Answer 144

Fontaine classification outlines natural progression (and symptom severity) Asymptomatic (< 50% stenosis) Intermittent claudication Ischaemic rest pain Tissue loss (ulcers/gangrene)

Answer 145

Re-thrombosis Compartment syndrome Reperfusion injury If amputation: Phantom limb pain- manage with gabapentin

Answer 146

Causes Most common- atherosclerosis Buerger’s disease - acute inflammation and thrombosis of lower limb veins/arteries Risk factors- heavy smoking Fibromuscular dysplasia- non-inflammatory artery wall thickening

Answer 147

Critical limb ischaemia - urgent to prevent limb loss, give IV heparin Pain at rest/night Tissue loss Failed medical management or symptoms limiting lifestyle Surgical options: Endovascular revascularisation (percutaneous transluminal angioplasty +/- stenting) Useful if short stenosis in big vessels Bypass surgery More extensive disease Amputation Last resort Often if gangrene Level of amputation high enough to ensure healing Above knee amputation has worse rehab outcomes than below knee

Answer 148

Medical: Optimise BP, lipids and DM control All patients with symptomatic PVD: Atorvastatin 80mg OD Clopidogrel 75mg OD If tissue loss Tissue viability to debride/dress Consider antibiotics if wet gangrene

Answer 149

Smoking Cessation Pharmacological management options for smoking cessation include: Nicotine replacement therapy Varenicline Mechanism: Nicotine receptor partial agonist Contraindications: Suicidal ideation, depression, pregnancy or breastfeeding Bupropion Mechanism: Nicotinic antagonist, dopamine reuptake inhibitor Adverse effects: Seizures (1/1000) Contraindications: Epilepsy, pregnancy or breast feeding

Answer 150

Type 1 DM with any of: Age > 40 DM for more than 10 years Established nephropathy Any other RFs for CVD CKD Familial hypercholesterolaemia Lipid modification 1st Line - Atorvastatin 20mg ON If a reduction in non-HDL cholesterol of 40% is not achieved, consider increasing the dose

Answer 151

Dietary Advice General dietary guidance includes the following.. Fat should contribute to < 30% of total calories 2+ fish per week (1 oily) Salt < 6g 5+ fruit /veg 4-5 portions of unsalted nuts / seeds

Answer 152

Lipid Modification Qrisk A validated risk stratification tool to calculate a patient's risk of having a heart attack/stroke in the next 10 years https://qrisk.org/ Note - QRISK is not appropriate if there is a history of: Cardiovascular disease CKD Type 1 diabetes mellitus Familial hypercholesterolaemia Age > 85 Qrisk < 10% - Give lifestyle advice and reassess in 5 years Qrisk > 10% - Commence lipid modification (atorvastatin 20mg) + give lifestyle advice

Answer 153

Pharmacological management Positive response to AVT (minority) – CCBs - nifedipine Negative response to AVT – management options include: Prostacyclin analogues – Iloprost Endothelin receptor antagonists – Bosentan/ ambrisentan Phosphodiesterase inhibitors: Sildenafil Other recommendations Pregnancy is contraindicated in pulmonary hypertension due to a mortality rate of 30-50 %

Answer 154

Examination findings Right (left parasternal) ventricular heave Loud P2 Raised JVP with large A waves Tricuspid regurgitation - Pansystolic murmur (loudest on inspiration) Investigations Echocardiogram Right heart catheterisation to confirm diagnosis

Answer 155

Causes & Classification Group 1 PH: Idiopathic – familial pulmonary HTN, HIV, Persistent pulmonary hypertension of the newborn Group 2 PH: PAH with Left sided heart disease Group 3 PH: Respiratory disease – COPD, ILD, OSA Group 4 PH: thromboembolic disease – e.g. PE Group 5 PH: Miscellaneous – sarcoidosis, carcinomatosis etc.

Answer 156

Assessment Step 1: A-E assessment – identify life threatening features: Shock (e.g. Systolic < 90mmHg) Syncope Features of myocardial ischaemia – chest pain Symptoms of severe heart failure – hypoxia, crepitations

Answer 157

If any life-threatening features are present - perform synchronised DC cardioversion (up to 3 attempts). If unsuccessful, prescribe amiodarone 300mg over 20 minutes and repeat the shock.

Answer 158

Narrow complex tachycardia: Irregular? Probable atrial fibrillation - treat with b-blocker (bisoprolol) or rate limiting calcium channel blocker (Diltiazem) Consider amiodarone or digoxin if there is evidence of HF

Answer 159

Regular? Step 1: vagal manoeuvres (Valsalva or carotid massage) Step 2: Next give adenosine 6mg Step 3: Then adenosine 12mg Step 4: Then adenosine 18mg Step 5: verapamil or beta blocker

Answer 160

Probable atrial fibrillation with bundle branch block - b-blocker (bisoprolol) or rate limiting calcium channel blocker (Diltiazem).

Answer 161

Regular? Probable VT with pulse – amiodarone 300mg over 10-60 minutes If ineffective perform synchronised DC cardioversion

Answer 162

VT can be differentiated into: Monomorphic - commonly caused by an MI Polymorphic – including torsades de pointes

Answer 163

Causes: Atrioventricular nodal re-entry tachycardia (AVNRT) functional re-entry within AV node Atrioventricular re-entry tachycardia (AVRT) anatomical re-entry circuit - e.g. bundle of kent Management: As per ALS guidelines. If recurrent consider b-blockers or radiofrequency ablation.

Answer 164

Management Rate control– b-blocker/RL-CCB Anticoagulation – as per atrial fibrillation (see below) Definitive management – radiofrequency ablation (most commonly of the tricuspid valve isthmus

Answer 165

Rate control NICE most commonly advocate using a rate control strategy with certain exceptions. 1st line: Beta-blocker (bisoprolol) or RL-CCB (verapamil/diltiazem) Remember to be cautious with B-Bs in asthmatic patients 2nd line: Add a B-blocker/RL-CCB or Digoxin (esp. if HF) Avoid combining bisoprolol with RL-CCB – risk of inducing complete heart block. Rhythm control Indications for consideration of rhythm control strategy: First detected episode Clear and reversible trigger (e.g. pneumonia) Worsening features of HF. Rhythm control of AF can be achieved by pharmacological means or with synchronised (to R wave) electrical cardioversion, with the aim of reverting the patient into sinus rhythm.

Answer 166

CCF = 1 Hypertension = 1 Age of 75years or more = 2 Diabetes = 1 Previous stroke / TIA or thromboembolism = 2 Vascular disease = 1 Age 65-74 = 1 Sex – Female = 1

Answer 167

Use ORBIT bleeding risk score (replaced hasbled) – a score of 3 or more suggests “high risk of bleeding”

Answer 168

Definition: irregular tachycardia caused by electrical impulses originating from 3 or more different sites in the atria (hence multifocal..). This is identified on the ECG by the presence of 3 morphologically distinct P waves. Management: RL-CCB 1st line

Answer 169

ECG: rapid, irregular QRS complexes, appear to be rotating around the ECG baseline Causes of long QTc include: Inherited cardiac disease – long QT syndrome Drugs: antihistamines (Terfenadine), Macrolides – erythromycin/clari, Tricyclic antidepressants (TCAs), Chloroquine Electrolyte abnormalities: Hypocalcaemia, hypokalaemia, hypomagnesaemia Management of TDP: IV Magnesium Sulfate 2g push

Answer 170

ECG changes: Short PR interval (<120ms) Wide QRS (>110ms) Delta wave – describes a slurred, slow-rising QRS upstroke Management: Radiofrequency ablation of the accessory pathway

Answer 171

Age > 65 years – degenerative calcification of the aortic valve - most common Age < 65 years – bicuspid aortic valve is the most common Causes include Turner’s syndrome Other causes: Williams Syndrome – supravalvular AS Hypertrophic obstructive cardiomyopathy (HOCM) Examination findings Ejection systolic murmur radiating to the carotids Narrow pulse pressure Slow rising (anacrotic) pulse Soft S2 Management Indications: symptomatic or valvular gradient > 40 – consider valve replacement If not fit enough - consider balloon valvuloplasty or TAVI.

Answer 172

Valve disease – bicuspid aortic valve, rheumatic heart disease, infective endocarditis Aortic root disease – Marfans, Ehlers Danlos, aortic dissection Examination findings Early diastolic murmur Collapsing pulse Wide pulse pressure De Musset’s (head bobbing), Quinke’s (nailbed pulsation)

Answer 173

Causes Rheumatic fever, rheumatic fever, rheumatic fever Clinical Features SOB, pink frothy haemoptysis Examination findings Mid diastolic murmur Opening snap Loud S1 malar flush ECG findings P Mitrale - broad bifid P wave in lead II

Answer 174

Ischaemic heart disease/post MI MV prolapse, rheumatic fever Examination findings Pansystolic "blowing" murmur which radiates into the axilla Quiet S1 Severe MR - widely split S2 Left ventricular failure

Answer 175

Associated conditions: ADPKD, Marfans Examination findings: Late systolic murmur with mid systolic click

Answer 176

Examination findings: Harsh ejection systolic murmur which is loudest on inspiration Associated conditions: Carcinoid cancer (flushing, diarrhoea, weight loss)

Answer 177

Causes Pulmonary hypertension Infective endocarditis (especially in IVDUs) Examination findings Pansystolic murmur (loudest on inspiration) Left parasternal heave (RVH) JVP: Prominent A waves

Answer 178

Advantages: Long term anticoagulation is NOT needed Lifelong aspirin should be given Disadvantages: Susceptible to degeneration and calcification Hence used in more elderly patients with fewer remaining years of life (> 65yrs)

Answer 179

Advantages: ‘hard-wearing’ – so less likely to need replacement/repeat surgery Disadvantages: Increased risk of thrombosis – lifelong warfarin is required Aortic valve – target INR 3.0 Mitral valve – INR 3.5

Answer 180

Bleeding- highest risk in large veins over bony prominences subjected to trauma Superficial vein thrombosis- hard and tender over vein DVT Skin ulcers Psychological - low mood due to appearance of varicose veins

Answer 181

Refer to vascular surgery if: Associated pain, swelling, itching Lower limb skin changes Superficial vein thrombosis Active ulceration Interventional options: Endothermal ablation Foam Sclerotherapy Surgery- ligation or stripping of vein

Answer 182

Risk factors Family history Pregnancy Prolonged sitting or standing History of DVT Examination findings 1.Examine standing and lying down 2,Varicose veins- 3mm + in diameter when standing 3.Assess for chronic venous insufficiency- skin hyperpigmentation, venous eczema, lipodermatosclerosis, atrophie blanche 4.Assess for complications- see below Investigations Further imaging only if concerned: USS for DVT

Answer 183

Varicose Veins Key learning Dilated, tortuous superficial veins Most commonly cosmetic concern but can cause symptoms and complications Indicate venous insufficiency Risk factors include obesity, pregnancy and prolonged standing/sitting Clinical diagnosis Referral to vascular surgeons only if causing symptoms or complications (skin changes, ulcers, superficial vein thrombosis)