Cardiovascular Flashcards

Question

Define aortic stenosis.

Answer 1

Narrowing of the left ventricular outflow at the level of the aortic valve.

Answer 2

1) Stenosis secondary to rheumatic heart diseas 2) Calcification of a congenital bicuspid aortic valve 3) Calcification and degeneration of a tricuspid aortic valve in the elderly Risk factors: - Age 60+years - Congenitally bicuspid aortic valve - Rheumatic heart disease - Chronic kidney disease

Answer 3

Prevalence in 3% of 75 year olds F>M Bicuspid aortic valve - may present earlier

Answer 4

- Initially asymptomatic - Angina - due to increased oxygen demand of the hypertrophied ventricles - Syncope or dizziness on exercise - Symptoms of heart failure - e.g. dyspnoea

Answer 5

- BP - narrow pulse pressure - Pulse - slow rising - Palpation - thrill in the aortic area, forceful sustained thrusting undisplaced apex beat - Auscultation - harsh ejection systolic murmer at aortic area, radiates to carotid artery and apex, 2nd heart sound softened or absent, ejection click due to bicuspid valve Distinguish from Aortic Sclerosis and Hypertorphic Obstructive Cardiomyopathy (HOCM). Aortic sclerosis - senile degernation with no left ventricular outflow tract obstruction (normal pulse character, no thrill, ejection systolic murmur radiates faintly, S2 heart sound normal)

Answer 6

1. ECG 2. CXR 3. Echocardigram 4. Cardiac angiography ECG - Signs of left ventricular hypertrophy, LBBB - Deep S wave in V1-2 - Tall R wave in V5-6 - Inverted T waves in I, AVL, V5-6 - Left axis deviation CXR - Post-stenotic enlargement of the ascending aorta - Calcification of aortic valve Echocardiogram - Visualises structual changes of the valves and level of stenosis - valvar, supravalvar, subvalvar - Estimation of the aortic valve area and pressure gradient across valev in systole and left ventricular function assessed Cardiac Angiography - Allows differentiation from other causes of angina - Assessment for concomitant coronary artery disease - 50% of patients

Answer 7

A localised area of damage and breakdown of skin due to inadequate aterial blood supply. Usually seen on the feet of patients with severe artheromatous narrowing of the arteries supplying the legs. [ischaemic ulcer]

Answer 8

Risk Factors: - Coronary heart disease - History of stroke or TIA - Diabetes mellitus - Peripheral aterial disease - e.g. intermittent claudication - Obesity - Immobility Cause: Lack of blood flow to the capillary beds of the lower extremities.

Answer 9

22% of leg ulcers Prevalence increases with age and obesity

Answer 10

- DISTAL - at the dosrum of the foot or between the toes over body prominences - Punched out appearance - Elliptical with clearly defined edges - sharp demarcation - Grey, granulation tissue - Night Pain - hallmark of arterial ulcers - e.g. at night, when legs are elevated, supine, relieved by dangling leg off the end of the bed

Answer 11

- Night Pain - Punched-out appearance - Hairlessness - Pale, cold skin - Absent pulses - Wasting of calf muscles - Dry necrotic base

Answer 12

1. Duplex ultrasonography of lower limbs - assess patency of arteries, potential for revascularisation or bypass surgery 2. ABPI - <0.8 3. Percutaneous angiography 4. ECG 5. Fasting serum lipids, fasting glucose, HbA1C 6. FBC - anaemia can worsen the ischaemia

Answer 13

Characterized by rapid, chaotic and ineffective atrial electrical conduction. Permanent, persistent, paroxysmal. Atrial flutter - characterized by atrial rate of 300/min, ventricular rate 150/min (2:1 heart block as the AV node conducts every second beat = saw tooth baseline Can be reversed by vagal maneouvres, IV adenosine (with cardiac monitoring) or chemical cardioversion.

Answer 14

May be no identifiable cause (lone AF) Secondary causes lead to abnormal atrial electircal pathways. Systemic - Thyrotoxicosis - Hypertension - Pneumonia - Alcohol Heart - Mitral valve disease - Ischaemic heart disease - Rheumatic heart disease - Cardiomyopathy - Pericarditis - Sick sinus syndrome - Atrial myxoma Lung - Bronchial carcinoma - Pulmonary embolism Risk Factors (Chornic): - Hypertension - CAD - CHF - Advancing age Risk Factors (Acute): - Increasing age - DM - Hypertension - CHF

Answer 15

Very common in the elderly - 5% of those >65 years | May be paroxysmal

Answer 16

- Asymptomatic - Palpitations - Syncope - Symptoms of the cause of AF

Answer 17

- Irregularly irregular pulse - Difference in apical beat and radial pulse - Look for thyroid disease - Look for valvular heart disease

Answer 18

1. ECG 2. Blood 3. Echocardiogram ECG - Uneven baseline (fibrillations) - Absent P waves - Irregular QRS complexes - Saw-tooth baseline - Consider atrial flutter Bloods - Cardiac enzymes - TFT - Lipid profile - U&E - Mg2+ - Ca2+ NB: Risk of digoxin toxicity increased with hypokalaemia, hypomagnesaemia or hypercalcaemia Echocardiogram - ?Mitral valve disease - ?Left atrial dilation - ?Left ventricular dysfunction - ?Structural abnormalities

Answer 19

- Treat reversible causes - e.g. thyrotoxicosis, chest infection 1) Rhythm Control - AF > 48 from onset, anticoagulate (3-4 weeks) before attempting cardioversion - DC cardioversion - synchronized DCshock (2x100J, 1x200J) - Chemical cardioversion - flecainide (contraindicated if IHD) or amiodarone - Prophylaxis against AF - sotalol, amiodarone, flecainide (pill in pocket strategy?) 2) Rate Control - Chronic AF - ventricular rate control with digoxin, verapamil and B-blockers (90/min rate aim) 3) Stroke Risk Stratification - Low risk - with aspirin - High risk - with anticoagulation with warfarin Risk Factors: - Previous TBE - Age 75 years+ - Hypertension - Diabetes - Vascular disease - Valve disease - Heart Failure - Impaired Left Ventricular Function

Answer 20

- TBE - 4% per year, increased risk with left atrial enlargement or left ventricular dysfunction - Worsens existing heart failure

Answer 21

Chronic AF in a diseasedheart does not usually return to sinus rhythm.

Answer 22

Acute cessation of cardiac function.

Answer 23

4 H's: - Hypoxia - Hypothermia - Hypovolaemia - Hypo or hyperkalaemia 4 T's: - Tamponade - Tension pneumothorax - Thromboembolism (TBE) - Toxins (drugs, therapeutic agents, sepsis)

Answer 24

Management precedes or is concurrent to history (e.g. from witnesses)

Answer 25

- Unconscious - Not breathing - Absent carotid pulses

Answer 26

1) Cardiac monitor - classifcation of rhythm directs management 2) Bloods - ABG, U&E, FBC, cross-match,clotting, toxicology screen, glucose

Answer 27

Safety - Approprach with caution - Cause of arrest may still pose a threat - Defibrillators and oxygen = hazards - Help summoned as soon as possible BLS - If arrest is witnessed and monitored, consider giving a precordial thump if no defibrillators avaliable - Clear and maintain airway with head tilt (if no spinal injury), jaw thrust and chin lift - Assess breathing by look, listen and feel - If not breathing, give 2 effective breaths immediately - Assess circulation at carotid pulse for 10s - If absent, give 30 chest compressions at a rate of 100/min - Continue cycles of 30 compressions for every two breaths - Proceed to advanced life support as soon as possible ALS - Attach cardiac monitor and defibrillator - Assess rhthym A) If pulseless ventricular tachycardia or ventricularfibrillation (SHOCKABLE) - Defibrillate once - 150-360J biphasic, 360J monophasic - Resume CPR immediately for 2 mins and then return to 2 - Administer adrenaline (1mg IV) after 2nd defibrillation and again every 3-5 mins - If SHOCKABLE persists, administer amiodarone 300mg IV bolus or lidocaine B) If pulseless electrical activity (PEA) or asystole: - CPR for 2 minutes then return to 2 - Administer adrenaline 1mg IV every 3-5 minutes - Atropine (3mg IV) if asystole or PEA with rate <60/min C) During CPR - Check electrodes, paddle positions and contacts - Secure the airway - e.g. attempt ET intubation, high-flow oxygen - Once airway secure, give continuous compresisons and breaths - Consider Mg, HCO3, external pacing - Stop CPR and check pulse only if change in rhythm or signs of life Treatment of Reversible Causes: - Hypothermia - warm slowly - Hypo/hyperkalaemia - correction of electrolytes - Hypovolaemia - IV colloids, crystalloids or blood products - Tamponade - pericardiocentesis under xiphisterum up and leftwards - Tension pneumothorax - needle into second intercostal space, mid-clavicular line

Answer 28

- Irreversible hypoxic brain damage | - Death

Answer 29

- Less successful outside hospital | - Duration of inadequate effective cardiac output is associated with poor prognosis

Answer 30

Inability of the cardiac output to meet the body's demands despite normal venous pressures.

Answer 31

LOW CARDIAC OUTPUT - Left heart failure - ischaemic heart disease, hypertesion, cardiomyopathy aortic valve disease, mitral regurgitation - Right heart failure - secondary to left heart failure, infarction, cardiomyopathy, pulmonary hypertension/embolus/valve disease, chronic lung disease, tricuspid regurgitation, constrictive pericarditis/pericardial tamponade - Biventricular failure - arrhythmia, cardiomyopathy (dilated or restirctive), myocarditis, drug toxicity HIGH DEMAND - Anaemia - Berberi - Pregnancy - Paget's disease - Hyperthyroidism - Arteriovenous malformation

Answer 32

10% of 65 year olds

Answer 33

Left - caused by pulmonary congestion - Dyspnoea - Orthopnea - Paroxysmal nocturnal dyspnoea - Fatigue Acute LVF - Dyspnoea - Wheeze - Cough - Pink frothy sputum Right - Swollen ankles - Fatigue - Increased weight - due to oedema - Reduced exercise tolerace - Anorexia - Nausea NB: New York Heart Association Classification 1. No dyspnoea 2. Dyspnoea or ordinary activities 3. Dyspnoea on less than ordinary activities 4. Dyspnoea at rest

Answer 34

Left - Tachycardia - Tachypnoea - Displaced apex beat - Bilateral basal crackles - 3rd heart sound - gallop rhythm, rapid ventricular filling - Pansystolic murmuer - functional mitral regurgitation Acute Left - Tachyhypnoea - Cyanosis - Tachycardia - Peripheral shutdown - Pulsus alternans - Gallop rhythm - Wheeze cardiac asthma - Fine crackles throughout the lung Right - High JVP - Hepatomegaly - Ascites - Ankle/sacral pitting - Oedema - Signs of functional tricuspid regurgitation

Answer 35

1. Bloods 2. CXR 3. ECF 4. Echocardiogram 5. Swan-Ganz Catheter Bloods - FBC - U&E - LFTs - CRP - Glucose - Lipids - TFTs - Acute LVF - ABG, troponin, brain natriuretic peptide (BNP) - High plasma BNP suggests cardiac failure CXR (Acute LVF) - Cardiomegaly - heart >50% of thoracic width - Prominent upper lobe vessels - Pleural effusion - Intestitial oedema - Kerley B lines - Perihilar shadowing - bat's wings - Fluid in fissures ECG - May be normal - Ischaemic changes - Arrhthmia - Left ventricular hypertrophy Echocardiogram - LVEF <40% = systolic dysfunction - Diastolic dysfunction - reduced compliance leading to a restrictive filling defect Swan-Ganz Catheter - Allows measurements of right atrial, right ventricular, pulonary artery, pulmonary wedge and left ventricular end-diastolic pressures

Answer 36

Acute LVF - Cardiogenic shock - severe cardiac failure with low BP requires the use of inotropes (e.g. dopamine, dobutamine), manage in ITU - Pulmonary oedema - sit up patient, 60-10% oxygen, CPAP. - Monitor BP, respiatory rate, sats, urine output, ECG - Treat the cause - e.g. MI, arrythmia Also consider: diamorphine (venodilator and axiolytic), GTN infusion (reduce preload) IV furosemide if fluid overloaded (venodilator and diuretic) Chronic LVF - Treat the cause - e.g. hypertension - Treat exacerbating factors - e.g. anaemia - ACE inhibitors - e.g. enalapril, perindopril, ramipril - B-Blockers - e.g. bisprolol, carvidolol - Loop diuretics - e.g. furosemide - and dietary salt restritcion to correct fluid overload - Aldosterone Antagonists - e.g. spironolactone, eplerenone - Angiotensin Receptor Blokcers - e.g. candesartan - Hydralazine and Nitrate - Digoxin - N-3 Polyunsaturated Fatty Acids - Cardiac Resynchroniszation Therapy (CRT) - Avoid drugs that can adversely affect patients with heart failure due to systolic dysfunction - e.g. NSAIDs, non-dihydropyridine calcium channel blockers - e.g. diltiazem and verapamil.

Answer 37

- Respiratory failure - Cardiogenic shock - Death

Answer 38

50% of patients with severe heart failure die within 2 years.

Answer 39

- Inhibit intracardiac renin-angiotensin system that may contribute to myocardial hypertrophy and remodelling - Slow progression of heart failure and improves survival - Additive benefits of ACE inhibitors and beta-blockers

Answer 40

- Block the effects of chronically activated sympathetic system - Slows progresion of heart failure and improves survival - Additive benefits of ACE inhibitors + Beta-blockers

Answer 41

- Improve survival in patients with NYHA class II/IV symptoms and on standard therapy - Monitor K+ - may cause hyperkalaemia - Used to assist with management of diuretic induced hypokalaemia

Answer 42

- May be added in pateints with persistent symptoms despite ACE inhibitors and B-blockers - Monitor K+ - may cause hyperkalaemia

Answer 43

- May be added in patients (Afro-Carribeans) with persistent symptomsdespite therapy with ACE inhibitor and beta-blocker

Answer 44

- Positive ionotrope - Reduced hospitalisation - Does not improve survival

Answer 45

- Provide small beneficial advantage in terms of mortality

Answer 46

- Biventricular pacing - Improves symptoms and survival in patients with LVEF<35%, cardiac dyssynchrony (QRS>120msec) and moderate to severe symptoms despite optimal medical therapy - Most patients who meet these criteria are also candidates for implanatable cardiac defibrillator (ICD) and recieve combined device

Answer 47

Primary disease of the myocardium. | May be dilated, hypertrophic or restrictive.

Answer 48

Dilated - post-viral myocarditis, alcohol, drugs (doxorubicine, cocaine), familial (autosomal dominant), thyrotoxicosis, haemochromatosis, peripartum Hypertrophic - genetic (autosomal dominant) mutations in beta-myosin, troponin T or alpha-tropomyosin Restrictive - amyloidosis, sarcoidosis, haemachromatosis.

Answer 49

0.05-0.20% prevalence - dilated and hypertrophic | Restrictive cardiomyopaty is very rare

Answer 50

Dilated: - Symptoms of heart failure - Arrythmias - Thromboembolism - Family history of sudden death Hypertrophic: - Usually none - Syncope - Angina - Arrythmias - Family history of sudden death Restrictive: - Dyspnoea - Fatigue - Arrythmia - Ankle or abdominal swelling - Enquire about family history of sudden death

Answer 51

Dilated: - Raised JVP - Displaced apex beat - Functional mitral and tricuspid regurgitations - 3rd heart sound Hypertrophic - Jerky carotid pulse - Double apex beat - Ejection systolic murmur Restrictive - Raised JVP - Kussmaul's sign - further raised JVP on inspiration - Palpable apex beat - 3rd heart sound - Ascites - Ankle oedema - Hepatomegaly

Answer 52

1. CXR - show cardiomegaly, heart failure signs 2. ECG 3. Echocardiography 4. Cardiac catheterization - measure pressures 5. Endomyocardial biopsy - restrictive cardiomyopathy 6. Pedigree or Genetic Analysis - rare ECG: - All types --> non-specific ST changes, conduction defects, arrythmias - Hypertrophic --> left axis deviation, signs of left ventricular hypertrophy (aortic stenosis), Q waves in inferior and lateral leads - Restrictive - low voltage complexes Echocardiography: - Dilated --> dilated ventricles with global hyookinesia - Hypertrophic --> ventricular hypertrophy (disproportionate septal involvement) - Restritcive --> non-dilated non-hypertrophied ventricles, atrial enlargement, preserved systolic function, diastolic dysfunction, gradular or sparkling appearance of myocardium in amyloidosis

Answer 53

The heart is incased in a rigid pericardium.

Answer 54

Unknown. (UK) TB or after any pericarditis (elsewhere). Risk Factors: - 1% = idiopathic and viral pericarditis - 2-5% = autoimmune, immunemediated and neoplastic aetiology - 20-30% = bacterial aetiology (e.g. TB, purulent percarditis).

Answer 55

0. 76 cases per 1000 person-years after acute idiopathic or viral pericarditis. 31. 7 cases per 1000 person-years for acute tuberculous pericarditis. 52. 7 cases per 1000 person-years for purulent pericarditis.

Answer 56

- Difficulty breathing that develops slowly and becomes worse - Fatigue - Swollen abdomen - Chronic, severe swelling in legs and ankles - Weakness - Low grade fever - Chest pain

Answer 57

- Raised JVP - Kussmaul's sign - raised JVP paradoxically with inspiration - Soft, diffuse apex beat - Quiet heart signs - S3 - Diastolic percardial knock - Hepatosplenomegaly - Ascites - Oedema

Answer 58

1. CXR - small heart + pericardial calcification 2. CT/MRI - distinguish from restrictive cardiomyopathy 3. Echocardiography 4. Cardiac catheterisation

Answer 59

Coronary angiography - a procedure that uses contrast dye, usually containing iodine, and X-rays to detect blockages in the coronary arteries that are caused by plaque buildup. PCI = Percutaneous Coronary Intervention (Coronary Angioplasty) - a non-surgical procedure that improves blood flow to your heart, requiring cardiac catheterisation. Cardiac Catheterisation - the insertion of a catheter tube and injection of contrast dye (usually iodine-based) into your coronary arteries

Answer 60

Coronary angiography: - Symptoms of coronary artery disease - e.g. angina - Pain in your chest, jaw, neck or arm - New or increasing chest pain (unstable angina) - Unexplained congestive heart failure - Acute myocardial infarction with mechanical complications requiring cardiac surgery PCI: - Acute ST-elevated myocardial infarction (STEMI) - Non-ST-elevated acute coronary syndrome (NSTE-ACS) - Unstable angina - Stable angina - Anginal equivalent - e.g. dyspnea, arrythmia, dizziness, cyncope - High risk stress test findings

Answer 61

Coronary Angiography: - Heart attack - Stroke - Injury to catheterized artery - Arrhythmias - Allergic reactions to the dye or medications used during the procedure - Kidney damage - Excessive bleeding - Infection PCI: - Bleeding - Haematoma - Pseudoaneurysm at access site - Heart attack - Stroke

Answer 62

1. CXR - show cardiomegaly, heart failure signs 2. ECG 3. Echocardiography 4. Cardiac catheterization - measure pressures 5. Endomyocardial biopsy - restrictive cardiomyopathy 6. Pedigree or Genetic Analysis - rare ECG: - All types --> non-specific ST changes, conduction defects, arrythmias - Hypertrophic --> left axis deviation, signs of left ventricular hypertrophy (aortic stenosis), Q waves in inferior and lateral leads - Restrictive - low voltage complexes Echocardiography: - Dilated --> dilated ventricles with global hyookinesia - Hypertrophic --> ventricular hypertrophy (disproportionate septal involvement) - Restritcive --> non-dilated non-hypertrophied ventricles, atrial enlargement, preserved systolic function, diastolic dysfunction, gradular or sparkling appearance of myocardium in amyloidosis

Answer 63

The heart is incased in a rigid pericardium.

Answer 64

Unknown. (UK) TB or after any pericarditis (elsewhere). Risk Factors: - 1% = idiopathic and viral pericarditis - 2-5% = autoimmune, immunemediated and neoplastic aetiology - 20-30% = bacterial aetiology (e.g. TB, purulent percarditis).

Answer 65

0. 76 cases per 1000 person-years after acute idiopathic or viral pericarditis. 31. 7 cases per 1000 person-years for acute tuberculous pericarditis. 52. 7 cases per 1000 person-years for purulent pericarditis.

Answer 66

- Difficulty breathing that develops slowly and becomes worse - Fatigue - Swollen abdomen - Chronic, severe swelling in legs and ankles - Weakness - Low grade fever - Chest pain

Answer 67

- Dislodged blood clots - Abnormal heart rhythm dollowing the procedure - Skin burns - Ventricular fibrillation due to general anaesthetia or lack of synchronisation between DC shock and QRS - Thromboembolus - insufficient anticoagulant therapy - Non-sustained ventricular tachycardia - Atrial arrhthmia - Heart block - Bradycardia - Transient left bundle branch block - Myocardial necrosis - Myocardial dysfunction - Transient hypotension - Pulmonary oedema - Pain at application site

Answer 68

A healthy artery or vein from the body is grafted to the blocked coronary artery. The grafted artery or vein bypasses the blocked portion of the coronary artery, creating a new passage for oxygen-rich blood to be routed around the blockage to the heart muscle.

Answer 69

- Triple coronary vessel disease - Left main stem coronary artery disease - Two coronary vessel disease with a proximal left anterior descending artery lesion

Answer 70

- Stroke - Neurocognitie dysfunction - Intraoperative myocardial infarction - Temporary conduction abnormalities - Arrhythmias - e.g. atrial fibrillation - Pericardial effusion / tamponade - Haemorrhage - Mediastinitis - Steral wound infection - Renal dysfunction - Death

Answer 71

A procedure to convert an abnormal heart rhythm to a normal heart rhythm. Atrial fibrillation - most common arrhythmia Aim to completely depolarize the heart using a direct current.

Answer 72

To restore sinus rhythm if Ventricular Fibrillation / Ventricular Tachycardia, Atrial Fibrillation, Flutter, Supraventricular Tachycardias. If other treatments have failured or there is haemodynamic compromise. Emergency or electively. Emergency = VF, VT Electively = AF

Answer 73

Formation of a thrombus within the deep veins - most comonly of the calf or thigh.

Answer 74

Anticoagulation: - Heparin - whilst awaiting therapeutic INR from warfarin anti-coag - DVT below knee treated with anti-coagulation for 3 months - DVT above knee treated with anticoagulation for 6 months - Recurrent DVT - long term warfarin - If active anticoagulation is contraindicated and/or high risk of embolisation - place IVC filter by IVR to prevent embolus in lungs Prevention: - Use of graduated compression stockings - Mobilisation if possible - At-risk groups should have prophylactic heparin - e.g. low-molecular weight heparin if no contraindications

Answer 75

Of the disease: - PE - Damage to vein valves - Chornic venous insufficiency of the lower limb (pro-thrombotic syndrome) - Venous infarction - phlegmasia cerulea dolens Of the treatment: - Heparin-induced thrombocytopaenia - Bleeding

Answer 76

Depends on extent of DVT, below-knee DVTs lower risk of embolus. More proximal DVTs have higher risk of propagation and embolisation, which if large, may be fatal.

Answer 77

- Examine for swelling - Examine for calf tenderness - Severe leg oedema and cyanosis (phlegmasia cerulea dolens) is rare - Respiratory examination for signs of a PE Use Wells Clinical Prediction Score

Answer 78

1. Doppler ultrasound 2. Bloods 3. ECG, CXR, ABG - if PE? Doppler US - Gold standard - Good sensitivity for femoral veins - Less sensitive for calf veins Bloods - D-dimers = fibrinogen degradation products - sensitive but non-specific and only useful as a negative predictor in low-risk patinets - Thrombophilia screen, prior to starting anticoagulation - if recurrent episodes - FBC - platelet count prior to starting heparin - U&E - Clotting

Answer 79

Anticoagulation: - Heparin - whilst awaiting therapeutic INR from warfarin anti-coag - DVT below knee treated with anti-coagulation for 3 months - DVT above knee treated with anticoagulation for 6 months - Recurrent DVT - long term warfarin - If active anticoagulation is contraindicated and/or high risk of embolisation - place IVC filter by IVR to prevent embolus in lungs

Answer 80

Elevation of one or more plasma lipid fractions.

Answer 81

LDL accummulates in the intima of systemic arteries. Taken up by LDLR on macrophage = foam cell. HDL is a shuttle in periphery for transport of cholesterol esters back to the liver --> cardioprotective Primary - molecular genetic basis, some unknown - Familial hypercholesterolaemia - reduced functional hepatic LDLR - Familial hypertriglyceridaemia - unknown, autosomal dominant - Hypertriglyceridaemia - lipoprotein lipase or apo-CII deficiency - Familial combined hyperlipidaemia - unknown - Remnant hyperlipidaemia - apo-E2 genotype inheritance, accumulation of LDL remnants Secondary - subdivided depending on abnormality - HIGH CHOLESTEROL - hypothyroidism, nephrotic syndrome, cholestatic liver disease, anorexia nervosa - HIGH TRIGLYCERIDES - diabetes, drugs (e.g. B-blockers, thiazides, oestrogens), alcohol, obesty, chronic renal disease, hepatocellular disease

Answer 82

50% of UK population have a cholesterol level high enough to be a risk for CHD.

Answer 83

- Asymptomatic - Symptoms of complications Ask about other CVS risk factors: - Diabetes - Smoking - Hypertension - Family history

Answer 84

Usually normal - examine for secondary causes. Lipid deposits: - Xanthelasmas - around eyes - Corneal arcus - Tendons xanthomas - e.g. extensor tendons of the hands, Achilles, patella - Tuberous xanthomas on knees and elbows - Xanthomas in palmar creases - in remnant hyperlipidaemia - Eruptive xanthomas and lipidaemia retinalis (pale retinal vessels) - severe hypertriglyceridaemia Signs of Complications: - Reduced peripheral pulses - Carotid bruits - CVD risks - High BP

Answer 85

1. Bloods 2. Cardiovascular Risk Assessment Bloods - Fasting lipid profile - Exclude secondary causes - e.g. glucose, TFT, LFT, U&E CVD Risk Assessment - Algorithms - E.g. Framingham risk equation, QRISK, ASSIGN

Answer 86

Treat secondary causes. Advice - Exercise - Lose weight - Control BP - Control diabetes - Low alcohol - Dietary modification Lipid-lowering Drugs - Primary prevention - if multiple risk factors + no atherosclerosis + risk CHD >20% in 10 years - Secondary prevention - if established atherosclerosis (e.g. CHD, CAD, AA) - Target: total cholesterol <4mmol/L, LDL <2mmol/L Drugs for HIGH Total Cholesterol or HIGH LDL: - HMG-CoA Reductase Inhibitors - potently lowers mortality and CVS morbidity is demonstrated in numerous trials - high dose recommended as first line - e.g. 40mg simvastatin - Ezetimibe - inhibits cholesterol absorption in gut, used if statin not tolerated or as adjunctive agent Drugs for HIGH Triglycerides: - Fibrates - stimulates lipoprotein lipase activity via specific transcription factors - Fish oil - rich in omega-3 marine triglycerides, not recommended as can aggravate Others: - Anion-exchange resins - e.g. colestyramine, colestipol - binds bile acids and reduces reabsorption, increases hepatic cholesterol conversion to bile acids, increases LDLR on hepatocytes - Nicotinic acid - reduced hepatic VLDL release, reduces TG, reduces cholesterol, increases HDL, bad side effectes (PG-mediated vasodilation, flushing, dizziness, palpitations), increases glucose and urate.

Answer 87

- CAD - MI - PVD - Stroke - Hypertriglyceridaemia --> pancreatitis and retinal vein thrombosis - Complications of treatment - statins --> myositis

Answer 88

Depends on early diagnosis, treatment of hyperlipidaemia and control of other CVS risk factors. Lipid-lowering agents --> ?Reduce cerebrovascular accidents

Answer 89

Death of tissue from poor vascular supply. 2 main categories: - Infectious gangrene - e.g. necrotising fasciitis, gas gangrene - Ischaemia gangrene - e.g. arterial or venous obstruction

Answer 90

Due to: - Ischaemia - Infection - Trauma Risk factors: - Diabetes - Smoking - Atherosclerosis - Renal disease - Drug and alcohol abuse - Malignancy - Trauma - Abdominal surgery - Contaminated wounds - Malnutrition - Hyper-coagulable states - Prolonged use of tourniquets - Community-acquired MRSA

Answer 91

Fournier's gangrene = 1.6 cases per 100,0000. | Incidence peaks and remains steady after 50 years, at 3.3 cases per 100,000.

Answer 92

- Pain - Swelling - Fever - Chills

Answer 93

- Pain - Oedema - Swelling - Skin discolouration - Diminished pedal pulses and ankle-brachial index - e.g. ischaemic gangrene - Low-grade fever - e.g. infectious gangrene

Answer 94

- Bloods - FBC, serum LDH, coagulation panel, metabolic panel - Surgical exploration and skin biopsy - CT angiography - Magnetic resonance angiography (MRA) - CT chest and abdomen

Answer 95

Impairment of the AV node impulse conduction, as represented by the interval between P wave and QRS complex. 1st DEGREE: - Prolonged conduction through AV node (prolonged PR interval) 2nd DEGREE: MOBITZ TYPE I - progressive prolongation of AV node conduction culminating in one atrial impulse failing to be conducted through the AV node (cycle begins again - prolonged PR interval, longer and longer then skip). MOBITZ TYPE II - intermittent or regular failure of conduction through AV node (ratio!) 3rd DEGREE: - No relationship between atrial and ventricular contraction - Failure of conduction through the AV node leads to a ventricular contraction generated by a focus of depolarisation within the ventricle (ventricular escape)

Answer 96

- MI or IHD - Infection - e.g. rheumatic fever, infective endocarditis - Drugs - e.g. digoxin, B-blockers, Ca2+ channel antagonists - Metabolic - e.g. hyperkalaemia, cholestatic jaundice, hypothermia - Infiltration of conducting system - e.g. sarcoidosis, cardiac neoplasms, amyloidosis - Degeneration of the conducting system Risk Factors: - Age-related degenerative changes in the conduction system - Increased vagal tone - AV-nodal blocking agents - Chronic stable coronary artery disease (CAD) - Acute coronary syndrome - CHF - Hypertension - Cardiomyopathy - Left ventricular hypertrophy - Recent cardiac surgery - Acid-base or electrolyte disturbance - Neuromuscular disorders

Answer 97

250,000 pacemakers implanted annually for heart block

Answer 98

1st DEGREE - asymptomatic MOBITZ TYPE I - asymptomatic MOBITZ TYPE II & 3rd DEGREE: - Stokes-Adams attacks - syncope caused by ventricular asystole - Dizziness - Palpitations - Chest pain - Heart failure

Answer 99

Normal Examine for signs of the cause Complete Heart Block: - Slow large volume pulse - JVP may show cannon waves MOBITZ TYPE II & 3rd DEGREE - Reduced cardiac output - e.g. hypotension, heart failure

Answer 100

1) ECG (ambulatory Holter or 24h) 1st DEGREE - Prolonged PR interval >0.02s MOBITZ TYPE I - Progressively prolonged PR interval - Culminates in a P wave that is not followed by a QRS - Pattern begins again MOBITZ TYPE II - Intermittently a P wave is not followed by a QRS - Pattern begins again - May be a ratio - e.g. 2:1 block 3rd DEGREE - No relationship between P waves and QRS complexes - If QRS initiated by focus in bundle of His, then QRS is narrow - If QRS initiated distally, then QRS is wide and slow rate - 30bpm 2) CXR - cardiac enlargement, pulmonary oedema 3) Bloods - TFT, digoxin level, cardiac enzyme, troponin, potassium, calcium 4) Echocardiogram - wall motion abnormalities, aortic valve disease, vegetations

Answer 101

CHRONIC - Permanent pacemaker insertion (PPM) - If 3rd DEGREE , MOBITZ TYPE II, symptomatic MOBITZ TYPE I ACUTE - If associated with clinical deterioration - IV atropine - Temporary external pacemaker

Answer 102

- Asystole - Cardiac arrest - Heart failure - Complications of any pacemaker inserted

Answer 103

MOBITZ TYPE II and 3rd DEGREE --> serious underlying cardiac disease

Answer 104

SBP > 140mmHg DBP > 85mmHg Measured on 3 separate occasions Malignant hypertension - >200/130mmHg

Answer 105

Fibrotic intimal thickening of the arteries, reduplication of elastic lamina and smooth muscle hypertrophy. Arteriolar wall layers replaced by pink hyaline material with luminal narrowing (hyaline arteriosclerosis). Primary: - Essential or idiopathic = 90% cases Secondary: - Renal - renal artery stenosis, chronic glomerulonephritis, chronic pyelonephritis, polycystic kidney disease, chronic renal disease - Endocrine - DM, hyperthyroidism, Cushing's, Conn's, hyperparathyroidism, phaeochromocytoma, congenital adrenal hyperplasia, acromegaly - Cardiovascular - aortic coarctation, high intravascular volume - Drugs - sympathomimetics, corticosteroids, oral contraceptive pill - Pregnancy - pre-eclampsia Risk factors: - Obesity - Aerobic exercise <3 times a week - Moderate / high alcohol intake - Metabolic syndrome - DM - Black ancestry - Age > 60 years - Family history of hypertension or coronary artery disease - Sleep apnoea

Answer 106

10-20% of adults in Western world.

Answer 107

- Asymptomatic - Symptoms of complications - Symptoms of the cause Accelerated or Malignant Hypertension - Scotomas (visual field loss) - Blurred vision - Headache - Seizures - Nausea - Vomiting - Acute heart failure

Answer 108

- Measure on 2-3 different occasions before diagnosing hypertension and record lowest reading - Loud 2nd heart sound, 4th heart sound - Examine for causes - e.g. radiofemoral delay (aortic coarctaction), renal artery bruit (renal artery stenosis) - Examine for end-organ damage - e.g. fundoscopy for retinopathy Keith-Wagner Classification of Retinopathy: (I) - Silver wiring (II) - + arteriovenous nipping (III) - + flame haemorrhages and cotton wool exudates (IV) - + papilloedema

Answer 109

1) Bloods 2) Urine dipstick 3) ECG 4) Ambulatory BP monitoring 5) Others Bloods - U&E - Glucose - Lipids Urine Dipstick - Blood - Protein ECG - Left ventricular hypertrophy - deep S waves in V1-2, tall R wave in V5-6, inverted T waves in I, AVL, V5-6, left axis devation - Ischaemia Ambulatory BP Monitoring - White coat hypertension - Allows monitoring of treatment response - Assesses preservation of nocturnal dip Others - Patients <35 years old - Suspected secondary cases

Answer 110

Assessment and modification of CVD risk factors. Conservative - Stop smoking - Lose weight - Reduced alcohol - Reduced dietary sodium Investigate for Secondary Causes - Young patients - Malignant hypertension - Poor response to treatment Medical - if SBP >160mmHg, DBP >100mmHg - Thiazide diuretics - 1st line if 55 years+, black patients (e.g. bendrofluamethiazide) - ACE Inhibitors (e.g. ramipril) or Angiotensin-II Antagonists (e.g. losartan) - 1st line <55 years, diabetics, HF, left ventricle dysfunction - Ca2+ channel Antagonists - 1st line for >60 years, black patients (e.g. amlodipine) - B-blockers - not preferred, younger patients, avoid combination with thiazides to avoid diabetes, increased risk of HF (e.g. atenolol) - alpha-blockers - 4th line, patients with prostatism Target BP: - Non-diabetic - <140/85 mmHg - Diabetic (no proteinuria) - <130/80mmHg - Diabetic (proteinuria) - <125/75mmHg Severe Hypertension (DBP >140mmHg) - atenolol (B-blocker) or nifedipine Acute Malignant Hypertension - IV B-blocker, labetolol or hydralazine sodium nitroprusside - avoid very rapid lowering due to cerebral infarction

Answer 111

- Heart failure - CAD - MI - CVA - PVD - DVT - PE - Retinopathy - Renal failure - Hypertensive encephalopathy - Posterior reversible encephalopathy syndrome (PRES) - Malignant hypertension

Answer 112

Good if BP controlled. Uncontrolled hypertension linked with increased mortality (6 x stroke risk, 3 x cardiac death risk). Treatment reduces incidence of renal damage, stroke and heart failure.

Answer 113

A device fitted surgically into the chest to send electrical pulses to the heart to keep it beating regularly and not too slowly.

Answer 114

- Arrhythmia - patients who have survived a 1st episode of life-threatening ventricular arrhythmias, to prevent further events - Heart failure - where symptoms and cardiac function can no longer be controlled by pharmacological treatment alone

Answer 115

- Infection at implant site - Allergic reaction to medications used during procedure - Swelling - Bleeding - Bruising - Damage to vein where the ICD leads are placed

Answer 116

Infection of intracardiac endocardial structures - mainly heart valves.

Answer 117

Vegetations form as a result of lodging of the organisms on the heart valves during a period of bacteraemia. - Made of platelets, fibrin, infective organisms - Poorly penetrated by immune system - Destroy valve leaflets - Invade myocardium - Invade aortic wall - Abscess cavities form - Activation of immune system also causes formation of immune complexes --> cutaneous vasculitis, glomerulonephritis, arthritis Endocardium can be colonized by virtually any organism, but most common are: 1) Streptococci (40%) - mainly alpha-haemolytic Streptococcus viridans or bovis 2) Staphylococci (35%) - aureus or epidermidis (IVDU) 3) Enterococci (20%) - faecalis 4) Others - e.g. Coxiella burnetti, histoplasma, HACEK - Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella Risk Factors: - Abnormal valves - e.g. congenital, post-rheumatic, calcification, degeneration - Prosthetic heart valves - Turbulant flow - e.g. patent ductus arteriosus or VSD - Recent dental work - Bacteraemia - S.bovis --> GI Malignancy

Answer 118

16-22 per million per year (UK)

Answer 119

- Fever - Sweats - Chills - Malaise - Arthralgia - Myalgia - Confusion - Skin lesions - Ask about recent dental surgery or IV drug use

Answer 120

- Pyrexia - Tachycardia - Signs of anaemia - Clubbing - if long-standing - New regurgitant murmur - Muffled heart sounds - Splenomegay NB: Right-sided lesions may imply IV drug use. Frequency: Mitral > Aortic > Tricuspid > Pulmonary Vasculitic Lesions: - Roth's spots - petechiae on retina - Petechiae (especially on pharyngeal and conjunctival mucosa) - Janeway lesions - painless palmar macules that blanch on pressure - Osler's nodes - tender nodules on finger / toe pads - Splinter haemorrhages - nail-bed haemorrhages

Answer 121

1) Bloods 2) Urinalysis 3) Blood culture 4) Echocardiography 5) Others Bloods - FBC - high neutrophils, normocytic anaemia - High ESR and CRP - U&E - Rheumatoid factor positive Urinalysis - Microscopic haematuria - Proteinuria Blood Culture - 3 sets 1 hour apart - Culture and sensitivity vital but start empirical treatment first - Culture negative 2-5% Echocardiography (Transthoracic) - Transoesophageal echocardiography more sensitive for endocarditis - Useful for detection of vegetations, valve abscess, diagnosis of prosthetic valve endocarditis, assessment of embolic risk Others: - ECG - conduction changes - CXR - septic pulmonary emboli : focal lung infiltrates, central cavitation - e.g. tricuspid valve endocarditis Duke's Classification (2 major, 1 major + 3 minor, all minor): - MAJOR - positive blood culture in 2 separate samples, positive echocardiogram - MINOR - high grade pyrexia >38 degrees, risk factors, positive blood culture (no major criteria), positive echocardiogram (not major), vascular signs +ve echocardiogram = vegetation, abscess, prosthetic valve dehiscence, new valve regurgitation Risk factors: - Abnormal valves - IV drug use - Dental surgery

Answer 122

Antibiotics for 4-6 weeks (at least 6 weeks for prosthetic valve endocarditis). On clinical suspicion: - Benzylpenicillin + Gentamycin - Gentamycin - dose adjusted for peak serum level of 3-4ug/ml, trough <1ug/ml STREPTOCOCCI - Continue Benzylpenicillin + Gentamycin - Alt - Ceftriaxone, Vancomycin STAPHYLOCOCCI - Flucloxacillin / Vancomycin + Gentamycin - Prosthetic - Vancomycin + Gentamicin + Rifampin ENTEROCOCCI - Ampicillin + Gentamycin HACEK - Ampicillin or Ceftriaxone + Gentamycin Culture Negative - Vancomycin + Gentamycin Surgery - If poor response or deterioration = urgent valve replacement - Replacement of prosthees - Kissing mitral valve vegetations - may be able to salvage Prophylaxis - If history of infective endocarditis + undergoing high risk procedures - High risk procedures - e.g. dental, incision or biopsy of respiratory mucosa, procedures in patients with GI/GU tract infection, procedures on infected skin or musculoskeletal tissue, prosthetic heart valve placement - Dental - 2g oral amoxicillin 30-60 mins before procedure

Answer 123

- Valve incompetence - Intracardiac fistulae or abscesses - Aneurysm formation - Heart failure - Renal failure - Glomerulonephritis - Arterial emboli from vegetations (brain, kidney, lungs, spleen)

Answer 124

Fatal if untreated. | When treated, 15-30% mortality.

Answer 125

Retrograde flow of blood from the left ventricle to the left atrium during systole.

Answer 126

Mitral valve damage or dysfunction: - Rheumatic heart disease - Infective endocarditis - Mitral valve prolapse - prolapse of the mitral valve leaflets into the left atrium during systole - Papillary muscle rupture or dysfunction - secondary to IHD or cardiomyopathy - Chordal rupture and floppy mitral valve associated with connective tissue diseases (e.g. psuedoxanthoma elasticum), osteogenesis imperfecta, Ehlers-Danlos syndrome, Marfan syndromes, SLE May also be secondary to left ventricular dilation.

Answer 127

5% of adults. Prolapse more common in young females.

Answer 128

Acute - Symptoms of left ventricular failure Chronic - Asymptomatic - Exertional dyspnoea - Palpitations if in AF and fatigue Mitral Valve Prolapse - Asymptomatic - Atypical chest pain - Palpitations

Answer 129

- Normal pulse or irregularly irregular (AF). - Apex beat laterally displaced and thrusting (left ventricular dilation) - Pansystolic murmur - Radiating to axilla - Palpable as a thrill - S1 is soft, S3 may be heard (rapid ventricular filling during early diastole) - Signs of left ventricular failure in acute mitral regurgitation Mitral Valve Prolapse - Mid-systolic click - Late systolic murmur - Click moves towards 1st heart sound on standing and moves away on lying down

Answer 130

1) ECG 2) CXR 3) Echocardiography ECG - Normal - AF - Broad bifid p wave - p mitrale - Delayed activation of left atrium due to enlargement CXR - Acute mitral regurgitation = left ventricular failure signs - Chronic mitral regurgitation = left atrial enlargement, cardiomegaly, left ventricular dilation, mitral valve calcification (rheumatic) Echocardiography - 6-12 months for moderate-sever MR to assess left-ventricular ejection fraction and end-systolic dimension

Answer 131

Mitral valve narrowing causing obstruction to blood flow from the left atrium to the ventricle.

Answer 132

- Rheumatic heart disease (90%) - Congenital mitral stenosis - SLE - Rheumatoid arthritis - Endocarditis - Atrial myxoma - rare cardiac tumour

Answer 133

Declining incidence in industrialised countries due to declining incidence of rheumatic fever.

Answer 134

- Asymptomatic - Fatigue - SOB on exertion - SOB on lying down - orthopnoea - Palpitations (due to AF) Rare: - Cough - Haemoptysis - Hoarseness due to compression of left laryngeal nerve by an enlarged left atrium

Answer 135

- Peripheral or facial cyanosis - malar flush - Pulse - thready, irregularly irregular (AF) - Palpation - apex beat undisplaced, tapping, parasternal heave (right ventricular hypertrophy, pulmonary hypertension) - Auscultation - loud 1st heart sound with opening snap, mid-diastolic murmur (presystolic accentuation if in sinus rhythm), pulmonary oedema (if decompensated)

Answer 136

1) ECG 2) CXR 3) Echocardiography 4) Cardiac catheterisation ECG - Normal - Broad bifid p wave (p mitrale) - due to left atrial hypertrophy - AF - Evidence of right ventricular hypertrophy in severe pulmonary hypertension CXR - Left atrial enlargement - Cardiac enlargement - Pulmonary congestion - Mitral valve calcified in rheumatic cases Echocardiography - Assess functional and structural impairments - Transoesophageal better valve visualisation Cardiac Catheterisation - Measures severity of heart failure

Answer 137

Acute inflammation and necrosis of cardiac muscle = myocardium.

Answer 138

Infection: - Viruses - e.g. Coxackie B, echovirus, EBV, CMV, adenovirus, influenza - Bacterial - e.g. post-streptococcal, tuberculosis, diptheria, Lyme disease - Fungal - e.g. candidiasis - Protozoal - e.g. trypanosomiasis (Chagas disease) - Helminths - e.g. thrichinosis Non-infective: - Systemic disorders - e.g. SLE, sarcoidosis, polymyositis - Hypersensitivity myocarditis - e.g. sulphonamides Drugs: - Chemotherapy agents - e.g. doxorubicin, streptomyocin - Cocaine abuse - Heavy metals - Radiation

Answer 139

Unknown. Many cases not detected at time of acute illness. Europe & USA - Coxsackie B virus SA - Chagas disease.

Answer 140

- Prodromal 'flu-like' illness - Fever - Malaise - Fatigue - Lethargy - Breathlessness - pericardial effusion, myocardial dysfunction - Sharp chest pain - suggesting associated pericarditis

Answer 141

Signs of concurrent pericarditis or complications - e.g. heart failure, arrhythmia.

Answer 142

1) Blood 2) ECG 3) CXR 4) Pericardial fluid drainage 5) Echocardiography 6) Myocardial biopsy Bloods - FBC - high WCC in infective causes - U&E - High ESR or CRP - Cardiac enzymes high - Antistreptolysin O titre, ANA, serum ACE, TFT - viral or bacterial serology ECG - Non-specific T wave and ST changes - Widespread saddle-shaped ST elevation in pericarditis CXR - Normal - Cardiomegaly - Pulmonary oedema Pericardial fluid drainage - Glucose - Protein - Cytology - Culture - Sensitivity Echocardiography - Systolic / diastolic function - Wall motion abnormalities - Pericardial effusion Myocardial Biopsy - Rarely required - Result does not influence management

Answer 143

Inflammation of the pericardium, may be acute, subacute or chronic.

Answer 144

- Idiopathic - Infective - commonly Coxsackie B, echovirus, mumps virus, streptococci, fungi, staphylococci, TB - Connective tissue disease - e.g. sarcoid, SLE, scleroderma - Post-myocardial infarction (24-72h) in up to 20% of patients - Dressler's Syndrome (weeks to months after acute MI) - Malignancy ( lung, breast, lymphoma, leukaemia, melanoma) - Metabolic (myxoedema, uraemia) - Radiotherapy - Thoracic surgery - Drugs - e.g. hydralazine, isoniazid

Answer 145

Uncommon Clinical incidence <1 in 100 hospital admissions. More common in males.

Answer 146

Chest pain: - Sharp - Central - Radiates to neck and shoulders - Aggravated by coughing, deep inspiration, lying flat - Relieved by sitting forward - Dyspnoea - Nausea

Answer 147

- Fever - Pericardial friction rub - best heard lower left sternal edge, with patient leaning forward in expiration - Heart sounds may be faint in the presence of an effusion Cardiac tamponade: - High JVP (Bell's Triad) - Low BP (^^) - Muffled heart sounds (^^) - Tachycardia - Pulsus paradoxus - Reduced SBP by >10mmHg on inspiration Constrictive Pericarditis (Chronic): - High JVP with inspiration - Kussmaul's sign - Pulsus paradoxus - Hepatomegaly - Ascites - Oedema - Pericardial knock - rapid ventricular filing - AF

Answer 148

1) ECG 2) Echocardiogram 3) Bloods 4) CXR ECG - Widespread ST elevation that is saddle shaped Echocardiogram - Assess pericardial effusion and cardiac function Bloods - FBC - U&E - ESR - CRP - Cardiac enzymes - normal - Blood cultures - ASO titres - ANA - Rheumatoid factor - TFT - Mantoux test - Viral serology CXR - Normal - globular heart shadow if 250mL effusion - Pericardial calcification can be seen in constrictive pericarditis - best seen on lateral CXR or CT

Answer 149

- Acute - cardiac tamponade treated by emergency pericardiocentesis - Medical - treat underlying cause, NSAIDs for relief of pain and fever - Recurrent - low-dose steroids, immunosuppressants or colchicine - Surgical - excision of pericardium in constrictive pericarditis

Answer 150

- Pericardial effusion - Cardiac tamponade - Cardiac arrhythmia

Answer 151

Depends on underlying cause Good prognosis in viral cases - recovery within 2 weeks Poor in malignant pericarditis Recurrent - particularly in those caused by thoracic surgery

Answer 152

Peripheral Vascular Disease - Insufficient tissue perfusion initiated by existing atherosclerosis acutely compounded by either emboli or thrombi. Peripheral Arterial Disease - A range of arterial syndromes that are caused by atherosclerotic obstruction of lower-extremity arteries Acute Limb Ischaemia - Sudden decrease in arterial blood flow to a limb that threatens its viability - Surgical emergency requiring revascularization in 4-6h to save the limb Chronic Limb Ischaemia - Peripheral arterial disease that results in a symptomatic reduced blood supply to the limbs typically caused by atherosclerosis and vasculitis, and affecting lower limbs

Answer 153

Caused by: - Atherosclerosis - Vasculitis - Emboli - due from heart (AF, mural thrombosis) or aneurysms Acute Limb Ischaemia - may be due to thrombus in situ, emboli, graft/angioplasty occlusion or trauma. Risk Factors: - Atherosclerosis - Smoking - Diabetes - Hypertension - Elevated CRP = inflammation - Hypertension - Hyperlipidaemia - Age 40years+ - History of coronary artery disease / cerebrovascular disease - Low levels of exercise

Answer 154

Acute Limb Ischaemia - 1.5 cases per 10,000 per year

Answer 155

Acute Limb Ischaemia - 6Ps - pale, pulseless, painful, paralysed, paraesthetic, perishingly cold - Asymptomatic - Intermittent claudication - Thigh or buttock pain with walking that is relieved with rest - Erectile dysfunction - Leg pain at rest - Gangrene - Non-healing wound / ulcer

Answer 156

``` Acute Limb Ischaemia - 6Ps - pale, pulseless, painful, paralysed, paraesthetic, perishingly cold - Fixed mottling = irreversibility Gangrene - Non-healing wound/ulcer ```

Answer 157

- Ankle-brachial index (ABI) - Toe-brachial index (TBI) - Segmental pressure examination - Pulse volume recording - Duplex ultrasound

Answer 158

Reduced blood supply to the heart muscle resulting in chest pain (angina pectoris). May present as stable angina or acute coronary syndrome. Acute coronary syndrome - divided into unstable angina (no cardiac injury), STEMI, NSTEMI. MI = cardiac muscle necrosis resulting from ischaemia. Atherosclerosis: - Endothelial injury - Migration of monocytes into sub-endothlial space - Differentiation into macrophages - Accumulation of LDL lipids insudated in subendothelium - Foam cells - Release of growth factors - Smooth muscle proliferation - Production of collagen and proteoglycans - Formation of atheromatous plaque

Answer 159

Angina pectoris = oxygen demand >> oxygen supply - Caused by atherosclerosis, spasm, arteritis, emboli MI - Caused by occlusion of a coronary artery due to rupture of an atheromatous plaque and thrombus formation Risk factors: - Male - DM - Family history - Hypertension - Hyperlipidaemia - Smoking - Previous history Atherosclerosis: - Endothelial injury - Migration of monocytes into sub-endothlial space - Differentiation into macrophages - Accumulation of LDL lipids insudated in subendothelium - Foam cells - Release of growth factors - Smooth muscle proliferation - Production of collagen and proteoglycans - Formation of atheromatous plaque

Answer 160

2% Common More common in males MI 5 in 1000 incidence UK

Answer 161

Acute Coronary Syndrome - Chest pain - Discomfort of acute onset - Central heavy tight gripping pain - Radiation to left arm, neck, jaw or epigastrum - Increase severity and frequency of previous stable angina - Breathlessness - Sweating - Nausea - Vomiting - Silent in elderly or patients with diabetes Stable Angina - Brought on by exertion - Relieved by rest

Answer 162

Acute Coronary Syndrome - No clinical signs - Pale - Sweating - Restless - Low-grade pyrexia - Check both radial pulses for aortic dissection - Arryhthmias - Disturbances of BP - New heart murmurs - e.g. pansystolic murmur of mitral regurgitation from papillary muscle rupture or ventricular septal defect - Signs of complications - e.g. acute heart failure, cardiogenic shock (hypotension, cold peripheries, oligura) Stable Angina - Look for signs of risk factors

Answer 163

1. Bloods 2. ECG 3. CXR 4. Exercise ECG Testing 5. Radionuclide Myocardial Perfusion Imaging (rMPI) 6. Echocardiogram 7. Pharmacologic Stress Testing 8. Cardiac catheterization / angiography 9. Coronary Calcium Scoring Bloods - FBC - U&E - CRP - Glucose - Lipid profile - Cardiac enzymes - CK-MB and troponin -T or I1 (high after 12h) - Amylase - pancreatitis mimics MI - TFTs - AST & LDH - high after 24-48h ECG - Unstable Angina or NSTEMI - ST depression, T-wave inversion, Q waves (may indicate old MI) - STEMI - ST elevation (>1mm in limb leads, >2mm in chest leads), hyperacute T-waves, new-onset LBBB, hours later T-wave invesion, days later Q waves Location of infarct: - Inferior walls --> II, III, AVF - Anterior wall --> Septum (V1-2), Apex (V3-4), Anterolateral Wall (V5-6) - Lateral wall --> I, AVL - Posterior infarct --> Tall R wave, ST depression in V1-3 CXR - Look for signs of heart failure - Look for differentials - e.g. aortic dissection Exercise ECG - treadmill test - Indications - troponin-negative ACS, stable angina with intermediate or high pretest probability of CHD - Not on digoxin - false-positive result - Take into account chest pain, cardiac risk factors, age, gender - Positive Test = >1mm horizontal or downsloping ST-segment depression measured 80ms after end of QRS - Failed Test = failure to achieve at least 85% of the predicted maximal heart rate (220-age), negative otherwise - B-blockers reduce maximal heart rate Radionuclide Myocardial Perfusion Imaging (rMPI) - Tc-99m sestamibi or tetrofosmin - Under stress (exercise or pharmacological) or at rest - Show low uptake in ischaemic myocardium during stress - Rest testing - used in patient with ACS, no previous MI but non-diagnostic troponin and ECGs Echocardiogram - Measure LVEF - myocardial stunning misleading in early measurements - Exercise or dobutamine stress - detect inducible wall motion abnormalities Pharmacologic Stress Testing - Patients who cannot exercise or if exercise test is inconclusive - E.g. Dipyridamole, adenosine, dobutamine induces tachycardia - Detect ischaemic myocardium - e.g. rMPI, echocardiography - Contraindicated in AV block and reactive airway disease (dipyridamole, adenosine) Cardiac Catheterisation / Angiography - ACS with positive troponin or TIMI score 5-7 or if high risk on stress testing - Use Duke treadmill score based on exercise time, maximum ST-segment deviation and exercise angina Coronary Calcium Scoring - Using specialized CT - Role in outpatieints with atypical chest pain or in acute chest pain that is not clearly due to ischaemia - e.g. absence of CAC exclusdes obstructive coornary artery disease

Answer 164

Stable Angina - Mimize cardiac risk factors - e.g. BP, hyperlipidaemia, diabetes, advice on smoking, exercise, weight loss, low-fat diet --> ASPIRIN 75mg/day - Immediate symptoms relief --> GTN as a spray or sublingually - Long-term --> B-BLOCKERS (e.g. atenolol), CALCIUM CHANNEL BLOCKERS ( e.g. verapamil, diltiazem), NITRATES (e.g. isosorbide dinrate) - Percutaneous Coronary Intervenion (PCI) - for localised areas of stenosis, in patients with angina not controlled by therapy, restenosis rate 25% at 6 months, drug-eluting coronary stents reduce rates (release sirolimus or paclitaxel) - Coronary Artery Bypass Graft (CABG) - for 3-vessel disease, rate of MI and survival similar betwen PCI and CABG NB: Contraindications of B-blockers - e.g. acute heart failure, cardiogenic shock, bradycardia, heart block, asthma, Unstable Angina / NSTEMI - Admit to CCU - Oxygen - IV access - Monitor vitals - Serial ECG - Analgesia - e.g. GTN, morphine sulphate / diamorphine, antiemetic (metoclopramide) - Aspirin - 300mg chewed, 75mg maintenance indefinite - Clopidogrel - 300mg, 75mg maintenance for 1 year if troponin positive or high risk - Low molecular weight heparin - e.g. enoxaparin, dalteparin - B-blocker - e.g. metoprolol - Glucose-insulin infusion if blood glucose >11 mmol/L - Glycoprotein IIb/IIIa inhibitors - e.g. tirofiban (initiated on presentation, continued for 48-72h or until PCI) --> for patients undergoing PCI, high risk for further cardiac events - Urgent angiography & revascularisation if no improvement High Risk for further cardiac events: - Troponin positive - TIMI risk score >4 - Continuing ischaemia STEMI - Admit to CCU - Oxygen - IV access - Monitor vitals - Serial ECG - Analgesia - GTN, morphine sulphate / diamorphine, antiemetic (metoclopramide) - Aspirin - 300mg chewed, 75mg maintenance indefinite - Clopidogrel - 600mg if patient going to primary PCI, 300mg if thrombolysis, <75yrs, 75mg if thrombolysis, >75yrs, 75mg maintenance for 1 year - B-Blocker - e.g. metoprolol - Primary PCI route - needs IV heparin + GP IIb/IIIa inhibitor OR bivalirudin (antithrombin) - Thrombolysis route with recobinant tissue plasminogen activator (rtPA) - IV heparin - Glucose-insulin infusion if blood glucose>11mmol/L NB: Primary PCI with goal <90 mins Thrombolysis with goal of 30 mins Rescue PCI if continued pain or elevation after thrombolysis of initial ST-segment elevation on follow up ECG 60-90min after fibrinolytic reaction Thrombolysis - Fibrinolytics - e.g. streptokinase, rtPA (alteplase, reteplase, tenecteplase) if within 12h of chest pain with ECG changes Secondary Prevention: - Antiplatelet agents - e.g. aspirin, clopidogrel - ACE inhibitors - B-Blockers - Statins - Control risk factors - e.g. smoking, diabetes, hypertension Advice - Do not drive for a month following MI - Education by cardiac rehabilitation team - Lifestyle changes - e.g. exercise, stop smoking, changing diet CABG - For patients with left main stem or three-vessel disease

Answer 165

At risk of MI and other vasuclar diseases - e.g. stroke, peripheral vascular disease Cardiac injury can lead secondarily to heart failure and arrhythmias Early Complications (24-72h) - Death - Cardiogenic shock - Heart failure - Ventricular arrythmias - Heart block - Pericarditis - Myocardial rupture - Thromboembolism Late Complications - Ventricular wall or septum rupture - Valvular regurgitation - Ventricula aneurysms - Tamponade - Dressler's syndrome (pericarditis) - Thromboembolism

Answer 166

Acute Coronary Sydnrome: - TIMI score used for risk stratification (0-7) - High score = high risk of cardiac events within 30 days 1) >65 yrs 2) Known CAD 3) Aspirin in last 7 days 4) Severe angina (>2 episodes in 24h) 5) ST deviation >1mm 6) Elevated troponin levels 7) >3 coronary artery disease risk factors - e.g. hypertension, hyperlipidaemia, family history, diabetes, smoking Killip Classification of Acute MI: - Class I - no evidence of acute heart failure - Class II - mild to moderate heart failure (S3, crepitations

Answer 167

Electronic devices that stimulate the heart with electrical impulses to maintain or restore a normal heartbeat. Most commonly accomplished through transvenous placement of leads to the endocardium (ie. right atrium or ventricle) or epicardium (i.e. to the left ventricular surface via the coronary sinus), which are subsequently connected to a pacing generator placed subcutaneously in the infraclavicular region.

Answer 168

- Sinus node dysfunction - Acquired AV block - Chronic bifascicular block - After acute phase of myocardial infarction - Neurocardiogenic syncope and hypersensitive carotid sinus syndrome - Post cardiac transplantation - Hypertrophic cardiomyopathy - Pacing to detect and terminate tachycardia - Cardiac resynchronization therapy in patients with severe systolic heart failure - Patients with congenital heart disease

Answer 169

- Infections - Haematoma formation - Pericardial effusion - Pericardial tamponade - Pneumothorax - Coronary sinus dissection - Perforation

Answer 170

Occlusion of pulmonary vessels, most commonly caused by a thrombus that has travelled to the vascular system from another site.

Answer 171

- Thrombus - 95% originate from DVT of lower limbs - Rarely from right atrium in patients with AF - Amniotic fluid embolus - Air embolus - Fat emboli - Tumour emboli - Mycotic emboli from right-sided endocarditis Risk factors: - Surgical patients - Immobility - Obesity - OCP - Heart failure - Malignancy

Answer 172

Fairly common, especially in hospitalized patients | Occur in 10-20% of those with a confirmed proximal DVT.

Answer 173

Depends on site and size. Small - may be asymptomatic Moderate - Sudden onset dyspnoea - Cough - Haemoptysis - Pleuritic chest pain Large - Sudden onset dyspnoea - Cough - Haemoptysis - Severe pleuritic chest pain - Shock - Collapse - Acute right heart failure - Sudden death Multiple Small Recurrent - Symptoms of pulmonary hypertension

Answer 174

Clinical Probability Assessment - Well's Score - >4 high probability, <3 probability ``` Clinically suspected DVT = 3.0 PE is most likely diagnosis = 3.0 Recent surgery (4 weeks) = 1.5 Immobilization = 1.5 Tachycardia = 1.5 History of DVT or PE = 1.5 Haemoptysis = 1 Malignancy = 1 ``` - Raised Geneva Score - >11 high probability, 4-10 intermediate probability, <3 low probability ``` >65 = 1 Recent surgery or fracture (28 days) = 2 Previous DVT / PE = 3 Active maliganancy = 2 Unilateral leg pain = 3 Haemoptysis = 2 Heart Rate > 75-94/min = 3 Heart Rate >85/min = 5 Unilateral leg oedema and tenderness = 4 ``` Small - No clinical signs - Tachycardia - Tachypnoea Moderate - Tachycardia - Tachypnoea - Pleural rub - Low O2 sats - despite O2 supplementation Large - Shock - Cyanosis - Signs of right heart strain - e.g. raised JVP, left parasternal heave, accentuated S2 heart sound Multiple Recurrent PE - Signs of pulmonary hypertension and right heart failure

Answer 175

Low Probability - D-dimer blood test - cross-linked fibrin degradation products - Highly sensitive - Poor specificity High Probability - Requires imaging Additional: - Bloods - ABG, thrombophilia screen - ECG - normal, tachycardia, right axis deviation, RBBB - CXR - exclude other differentials NB: Classic Si, QIII, TIII pattern uncommon. - Spiral CT Pulmonary Angiogram - 1st line, poor sensitivity for small emboli - Ventilation-Perfusion (VQ) Scan - administration of IV 99mTc macro-aggregated albumin and inhalation of 81 krypton gas to identify areas of ventilation and perfusion mismatch (If abnormal CXR or co-existing lung disease, do not use due to difficulty in interpretation) - Pulmonary angiography - gold standard, invasive though - Doppler USS of lower limb - to examine for VT - Echocardiogram - right heart strain shown

Answer 176

A consistently increased pulmonary arterial pressure (>20mmHg) under resting conditions.

Answer 177

Primary - Idiopathic Secondary - Left heart disease - mitral valve disease, left ventricular failure, left atrial myxoma/thrombosis - Chronic lung disease - COPD - Recurrent pulmonary emboli - Increased pulmonary blood flow - ASD, VSD, patent ductus arteriosus - Connective tissue disease - SLE, systemic sclerosis Drugs - e.g. amiodarone

Answer 178

Primary pulmonary hypertension - young females.

Answer 179

- Dyspnoea - on exertion - Chest pain - Syncope - Tiredness - Symptoms of the underlying cause - e.g. chronic cough

Answer 180

- Raised JVP - prominent a wave in the JVP waveform - Left parasternal heave - right ventricular hypertrophy - Loud pulmonary component of S2 (S3/S4 may be heard) - Early diastolic murmur - Graham Steell murmur (caused by pulmonary regurgitation if tricuspid regurgitation develops - large CV wave, pansystolic murmur) - Signs of underlying condition - Right heart failure signs in severe cases

Answer 181

1. CXR 2. ECG 3. Echocardiography 4. Lung function test 5. VQ Scan 6. Cardiac catheterization 7. High-Resolution CT-Thorax 8. Lung Biopsy CXR - Cardiomegaly - right ventricular enlargement, right atrial dilation - Prominent main pulmonary arteries - taper rapidly - Signs of the cause - e.g. COPD, calcified mitral valves ECG - Right ventricular hypertrophy - right-axis deviation

Answer 182

1. CXR 2. ECG 3. Echocardiography 4. Lung function test 5. VQ Scan 6. Cardiac catheterization 7. High-Resolution CT-Thorax 8. Lung Biopsy CXR - Cardiomegaly - right ventricular enlargement, right atrial dilation - Prominent main pulmonary arteries - taper rapidly - Signs of the cause - e.g. COPD, calcified mitral valves ECG - Right ventricular hypertrophy - right-axis deviation, prominant R wave in V1, T inversion in V1-2 - Right atrial enlargement - peaked P wave in II (P pulmonale) - Limb leads exhibit low voltage (R < 5mm) in COPD Echocardiography - Visualise right ventricular hypertrophy or dilation - Possible underlying cause Lung Function Tests - Assess for chronic lung disease VQ Scan - Assess for PE Cardiac Catheterisation - Assess severity, right heart pressures, response to vasodilators High Resolution CT-Thorax - Images pulmonary arteries - Diagnose lung disease Lung Biopsy - Assess structural lung changes

Answer 183

An inflammatory multisystem disorder, occurring following group A B-haemolytic streptococci (GAS) infection.

Answer 184

Unknown. Streptococcal pharyngeal infection required. Genetic susceptibility. Molecular mimicry - role in the initiation of tissue injury - e.g. antibodies directed against GAS antigens cross-react with host antigens

Answer 185

5-15 years - peak incidence Far East, Middle East, Easter Europe, South America Mean incidence 19/100,000 . Reduction in incidence in West, non-Western countries incidence is relatively high.

Answer 186

- 2-5 weeks after GAS infection - Fever - Malaise - Anorexia - Painful, swollen joints - Reduced movement and function - Breathlessness - Chest pain - Palpitations

Answer 187

- Duckett Jones Criteria - positive diagnosis if at least 2 major criteria, or one major plus 2 minor criteria Major Criteria: - Arthritis - migratory or fleeting polyarthritis with swelling, redness, tenderness of large joints - Carditis - new murmur (Carey Coombs murmur - mid-diastolic murmur due to mitral valvulitis), pericarditis, pericardial effusion or rub, cardiomegaly, cardiac failure, ECG changes - Chorea - rapid, involuntary, irregular movements with flowing or dancing quality, slurred speech (more common in females) - Nodules - small, firm, painless, subcutaneous nodules on extensor surfaces, joints and tendons - Erythema Marginatum (20%) - transient erythematous rash with raised edges, seen on trunk and proximal limbs (cresent or ring-shaped patches) Minor Criteria - Pyrexia - Previous rheumatic fever - Arthralgia - only if arthritis is not present as major criteria - Recent streptococcal infection - supported by positive throat cultures or high antitreptolysin O titre - High ESR, CRP orWCC - High PR and QT intervals on ECG - if carditis not present as major criteria

Answer 188

1. Bloods 2. Throat swab 3. ECG 4. Echocardiogram Bloods - FBC - raised WCC - ESR/CRP - raised ESR, CRP - Raised antitreptolysin O titre Throat Swab - Culture for GAS - Rapid streptococcal antigen test ECG - Saddle shaped ST elevation - PR segment depression - Arrhythmias (signs of pericarditis) Echocardiogram - Pericardial effusion - Myocardial thickening or dysfunction - Valvular dysfunction

Answer 189

A dysrhythmia originating at or above the atrioventricular node, and if defined by a narrow complex (QRS < 120ms) at a rate >100bpm. Atrioventricular nodal reentrant tachycardia (AVNRT) = paroxysmal SVT - defined as intermittent SVT without provoking factors, presenting with a ventricular rhythm of 160 bpm.

Answer 190

Most common cause is orthodromic re-entry phenomenon - when the tachycardia is secondary to normal anterograde electrical conduction from the atria to the AV node to the ventricles, with the retrograde conduction via an accessory pathway form the ventricles back to the atria. Children <12 - accessory AV pathways causes re-entry tachycardia Narrow QRS complex indicates ventricles are being activated superior to the bundle of His - implies the arrythmia originates from the SA node, atrial myometrium, AV node or within His bundle. Rarer - anti-dromic conduction passing from atria to ventricles via accessory pathway and then returns retrograde through AV node to atria. Differential diagnosis: - Sinus tachycardia - Atrial tachycardia - Junctional tachycardia - Atrial fibrillation - Atrial flutter - Multi atrial tachycardia In patients susceptible, triggers can be: - Caffeine - Alcohol - Physical stress - Emotional stress - Cigarette smoking Risk Factors: - Children with congenital heart disease

Answer 191

AVNRT: 35 per 100,000 - most common non-sinus tachydysrhythmia in young adults M:F 2:1 Old:Young 5:1 SVT: Most common symptomatic dysrhymthmia in infants and children.

Answer 192

- Anxiety - Palpitations - Chest discomfort - Light-headedness - Syncope - Dyspnea - Shock

Answer 193

- Hypotension - Signs of heart failure - e.g. bibasilar crackles, 3rd heart sound, JVP raised - Exercise intolerance - Tachycardia Check for Haemodynamic Instability: - Hypotension - Hypoxia - SOB - Chest pain - Shock - Evidence of poor end-organ perfusion - Altered mental status

Answer 194

- ECG - narrow complex, regular tachycardia (180-220bpm), no detectable P waves (if P waves are detectable, consider sinus tachycardia, atrial fibrillation, atrial flutter) - Bloods - check electrolyte abnormalities, anaemia, hyperthyroidism, digoxin levels

Answer 195

Step 1 - Give O2 if SaO2 < 90% - Get IV access - 12-lead ECG Step 2 - Check for haemodynamic instability - shock, chest pain, ischaemia on ECG, heart failure, syncope Step 3 - If Haemodynamic Instability - Get expert help - Sedation - Up to 3 synchronized DC shocks - 70-120J for first (if AF 120-150J) then 120-360J - Check and correct K+, Mg2+,Ca2+ Step 3 - if Haemodynamically Stable -

Answer 196

Step 1 - Give O2 if SaO2 < 90% - Get IV access - 12-lead ECG Step 2 - Check for haemodynamic instability - shock, chest pain, ischaemia on ECG, heart failure, syncope Step 3 - If Haemodynamic Instability - Get expert help - Sedation - Up to 3 synchronized DC shocks - 70-120J for first (if AF 120-150J) then 120-360J - Check and correct K+, Mg2+,Ca2+ Step 3 - if Haemodynamically Stable - Ask is the rhythm regular? Step 4 - Rhythm is NOT REGULAR - Start continuous ECG trace - Perform vagal manoeuvres (Valsalva Manouvre) but take care if possible digoxin toxicity, acute ischaemia, carotid bruit - Step 4 - Rhythm is REGULAR - Treat as AF - Control rate with B-blocker - e.g. metoprolol 1-10mg IV, small increments to slow rate - Control rate with rate-limiting Ca2+ channel blocker - verapamil 5-10mg IV - Control rate with digoxin (if heart failure - e.g. load with 500mcg PO then 500mcg PO after 8h and further 250mcg PO after 8h - Control rate with amiodarine - Anticoagulation with warfarin or NOAC to reduce risk of stroke - If onset <48h or effectively anti-coagulated for >3 weeks, consider cardioversion under sedation with DC or chemical cardioversion - Chemical cardioversion - e.g. flecanide 300mg PO (if no structural heart damage) or amiodarone 300mg IVI over 20-60mins, then 900mg over 24h

Answer 197

- Haematoma - Pseudoaneurysm of the artery - Bleeding - Myocardial infarction - Heart block and the need for a pacemaker - Stroke - Death

Answer 198

- Good outcome - Small risk of sudden death - Depends on the severity of the defect - Pregnancy - higher risk of death if unrepaired heart defect

Answer 199

Backflow of blood from the right ventricle to the right atrium during systole.

Answer 200

Congenital - Ebstein anomaly = malpositioned tricuspid valve - Cleft valve in ostium primum defect Functional - Consequence of right ventricular dilation - e.g. pulmonary hypertension - Valve prolapse Rheumatic Heart Disease - Associated with valvular disease Infective Endocarditis - Common in IV drug users - Usually staphylococcal Others - Carcinoid syndrome - Trauma - Cirrhosis - long-standing - Iatrogenic - e.g. radiotherapy to the thorax

Answer 201

Differs with various causes | Infective endocarditis probably most common cause

Answer 202

- Fatigue - Breathlessness - Palpitations - Headaches - Nausea - Anorexia - Epigastric pain made worse by exercise - Jaundice - Lower limb swelling

Answer 203

- Irregular pulse - due to AF, right atrial enlargement - Raised JVP with giant v waves that may oscillate the earlobe - caused by the transmission of right ventricular pressure (may also be giant a wave if in sinus rhythm) - Parasternal heave - Pansystolic murmur best heart at the left lower sternal edge, louder on inspiration (Carvallo sign), loud P2 component of second heart sound - Pleural effusion - Causes of pulmonary hypertension - e.g. emphysema - Palpable liver - tender, smooth, pulsatile - Ascites - Pitting oedema

Answer 204

1. Bloods 2. ECG 3. CXR 4. Echocardiogram 5. Right Heart Catheterization Bloods - FBC - LFT - Cardiac enzymes - Blood cultures ECG - Tall P wave - right atrial hypertrophy if in sinus rhythm - Changes indicative of other cardiac disease CXR - Right-sided enlargement of cardiac shadow Echocardiography - Extent of regurgitation estimated by colour flow Doppler - May be able to detect tricuspid valve abnormality - e.g. prolapse - Right ventricular dilation Right Heart Catheterization - Rarely necessary - Assess pulmonary artery pressure

Answer 205

Long, tortuous and dilated veins of the superficial venous system.

Answer 206

Blood from superficial veins of the leg passess into deep veins via perforator veins (perforate deep fascia) and at the saphenofemoral and saphenopopliteal junctions. Valves prevent blood from passing from deep to superficial veins. If they become incompetent there is venous hypertension and silatation of the superficial veins occurs. Risk Factors: - Prolonged standing - Obesity - Pregnancy - Family history - Contraceptive pill Causes: - Primary mechanical factors (95%) - Secondary to obstruction (DVT, foetus, pelvic tumour), arteriovenous malformations, overactive muscle pumps (e.g. cyclists), rarely congenital valve absence

Answer 207

Reports of prevalence of chronic venous insufficiency vary from < 1% to 40% in females and from < 1% to 17% in males. Prevalence estimates for varicose veins are higher, <1% to 73% in females and 2% to 56% in males.

Answer 208

- My legs are ugly - Pain - Cramps - Tingling - Heaviness - Restless legs

Answer 209

- Oedema - Eczema - Ulcers - Haemosiderin - Haemorrhage - Phlebitis - Atrophie blanche - white scarring at the site of a previous, healed ulcer - Lipodermatosclerosis - skin hardness from subcutaneous fibrosis caused by chronic inflammation and fat necrosis - VVs don't caused DVTs on their own - except possibly proximally spreading thrombophlebitis of the long sapheneous veins

Answer 210

- Duplex ultrasound - assesses for reversed flow

Answer 211

Criteria for specialist referral of patients with VVs should be: Pain, Bleeding, Ulceration, Superficial Thrombophlebitis, Severe Impact on Quality of Life - Treat underlying cause - Education - avoid prolonged standing, elevate legs whenever possible, support stockings, lose weight, regular walks (calf muscle action aids venous return) - Endovascular Treatment Endovascualr Treatment - Radiofrequency ablation - catether inserted into vein, heated to 120 degree, destoys endothelium, closes vein, as good as surgery at 3 months - Endovenous laser ablation - similar to above, uses laser, similar outcome to surgery at 2 years - Infection Sclerotherapy - A) Liquid sclerosant is indicated for varicosities below the knee if there is no gross saphenofemoral incompetence, injected at multiple sites, vein compressed for a few weeks to avoid thrombosis (intravascular granulation tissue obliterates lumen). B) Foam sclerosant injected under ultrasound guidance (prevents spread of foam to femoral vein) at single site, spreads rapidly throughout veins, damage endothelium - Surgery - depends on vein anatomy and surgical preference - e.g. saphenofemoral ligation, multiple avulsions, stripping from groin to upper calf, bandage legs elevated after surgery

Answer 212

- Bruising - Swelling - Skin discolouration - Pain - Infection - Blood clots - e.g. thrombophlebitis, DVT, PE - Scarring

Answer 213

Although varicose veins and venous insufficiency are chronic diseases, their prognosis is essentially benign in the great majority of cases, even without intervention. However, good self-care is especially important in order to decrease the discomfort, complications, and progression.

Answer 214

Fainting when your body overreacts to certain triggers, such as the sight of blood, extreme emotional distress. The vasovagal syncope trigger causes your heart rate and blood pressure to drop suddenly.

Answer 215

Occurs due to reflex bradycardia with/without peripheral vasodilation provoked by emotion, pain or standing too long (cannot occur when you're lying down). Onset is over seconds (not instantaneous) and is often preceded by pre-syncopal symptoms - e.g. nausea, pallor, sweating, narrowing of visual fields. Brief clonic jerking of the limbs may occur due to cerebral hypoperfusion, but there is no tonic/clonic sequence. Urinary incontinence is uncommon, there is no tongue biting. Unconsciousness usually lasts for 2 mins, and recovery is rapid.

Answer 216

In the general population, the annual number episodes are 18.1–39.7 per 1000 patients, with similar incidence between genders, and with high prevalence between 10 and 30 years of age, mainly of vasovagal syncope (Moya et al., 2009).

Answer 217

- Collapse - Loss of consciousness - Nausea - Pallor - Sweating - Narrowing of visual fields - Clonic jerking of the limbs - No tonic/clonic sequence - No urinary incontinence - No tongue-biting

Answer 218

- Collapse - Loss of consciousness - Nausea - Pallor - Sweating - Narrowing of visual fields - Clonic jerking of the limbs - No tonic/clonic sequence - No urinary incontinence - No tongue-biting

Answer 219

- Cardiovascular examination - Neurological examination - Measure BP lying and standing

Answer 220

- Cardiovascular examination - Neurological examination - Measure BP lying and standing - ECG & 24h ECG - Bloods - U&E, FBC, Mg2+, Ca2+, Glucose - Tilt table test - EEG - Sleep EEG - Echocardiogram - CT MRI brain - ABG if practical

Answer 221

Short PR interval and delta-wave on ECG predisposing to supraventricular tachycardias (SVT). ``` 2 Types : Type A - +ve delta wave in V1 Type B - -ve delta wave in V1 ```

Answer 222

Congenital accessory pathway (bundle of Kent) bypasses the atrioventricular node causing ventricular pre-excitation. Risk Factors: - Ebstein's anomaly - Hypertrophic cardiomyopathy - Mitral valve prolapse - Atrial septal defect

Answer 223

Peak incidence has been reported in individuals between 30 and 40 years old in otherwise healthy adults. Some reports suggest that WPW syndrome occurs in males more often than females. The disorder's estimated prevalence is . 1-3.1 per 1,000 people in the United States.

Answer 224

- Asymptomatic - Atrioventricular re-entrant tachycardia - Atrial fibrillation - Sudden cardiac death - Palpitations - Dizziness - Shortness of breath - Chest pain

Answer 225

- Asymptomatic - Atrioventricular re-entrant tachycardia - Atrial fibrillation - Sudden cardiac death - Palpitations - Dizziness - Shortness of breath - Chest pain

Answer 226

Wounds that are thought to occur due to improper functioning of venous valves, usually of the legs.

Answer 227

The main cause of venous leg ulcers is faulty valves inside the leg veins. These valves normally allow the blood to flow up the leg towards the heart, and they also prevent backward flow down the leg. If the valves are faulty, backward flow is not prevented and pressure builds up inside the veins. Develops after minor injury, where persistently high pressure in the veins of the legs damages the skin. Risk factors: - Varicose veins - History of DVT - Blockage of the lymph vessels - causes fluid to build up in the legs - Older age - Female - Tall height - Family history of venous insufficiency - Obesity - Pregnancy - Smoking - Osteoarthritis - Leg injury - Paralysis

Answer 228

70-90% of leg ulcer cases caused by venous valve dysfunction. 1 in 500 people in the UK Become more common with age 1 in 50 people >80 yrs.

Answer 229

- Heavy feeling in the legs - Aching in the legs - Itchy skin on legs - Pain - Fever

Answer 230

- Pedal oedema - Discolouration and darkening of the skin around the ulcer = hyperpigmentation - Hardened skin around the ulcer = lipodermatosclerosis - Varicose eczema - red, flaky, scaley skin on legs - Enlarged veins on the legs (varicose veins) - Unpleasant and foul-smelling discharge from ulcer

Answer 231

1) Duplex ultrasound - Demonstrates retrograde or reversed flow - Valve closure time >0.5 seconds indicates venous insufficiency 2) Ascending phlebography - evaluate treatment options for complex cases, as identifies obstruction site and level, presence and location of collaterals 3) CT venography - reveals detailed venous anatomy 4) MR Venography - reveals detailed venous anatomy 5) CT CAP - rule out extrinsic compression for iliac vein compressions (e.g. pelvic or abdominal mass) 6) Intravascular ultrasound - in specialised centres as secondary test to identify iliac vein obstruction 7) Air Plethysmography - identifies reflux and obstruction

Answer 232

Prevention - Graded compression stockings - for CVI-related oedema, stasis dermatitis, small venous leg ulcers In general, there are three classes of compression stockings: class 1 stockings (light compression) control oedema; class 2 (medium compression) and class 3 (high compression) are usually required for more advanced CVI. Patients with severe CVI or previous ulcers generally require lifelong graded compression stockings of at least 30 to 40 mmHg. - Moisturisers - to combat skin dryness and flaking - Pentoxifylline - 400mg orally QDS - Diosmin - consult specialist With Superficial Venous Reflux: - Endovenous ablation or saphenectomy With Angiomata and Varicosities: - Endovenous ablation or injection sclerotherapy With Perforating Vein Incompetence: - Endovenous ablation With Iliac Vein Obstruction: - Percutaneous iliac angioplasty and stenting With Deep Venous Reflux : - Venous valvular reconstruction - for patients whose conventional therapy has failed With Leg Pain: - Horse chesnut seed extract

Answer 233

- Osetomyelitis - Septicaemia - Cellulitis - Venous Eczema - Malignancy

Answer 234

The healing was worst for patients with venous ulcers, only 44% had healed their original ulcers without recurrence. The 5 year survival was 52%, significantly lower than for age- and sex-matched controls (68%) (p = 0.0002).

Answer 235

Irregular, rapid ventricular activation with no cardiac output.

Answer 236

The most common cause is a problem in the electrical impulses traveling through your heart after a first heart attack or problems resulting from a scar in your heart's muscle tissue from a previous heart attack. Some cases of ventricular fibrillation begin as a rapid heartbeat called ventricular tachycardia (VT). This rapid but regular beating of the heart is caused by abnormal electrical impulses that start in the ventricles. Most VT occurs in people with a heart-related problem, such as scars or damage from a heart attack. Sometimes VT can last less than 30 seconds (nonsustained) and may not cause symptoms. But VT may be a sign of more-serious heart problems. If VT lasts more than 30 seconds, it will usually lead to palpitations, dizziness or fainting. Untreated VT will often lead to ventricular fibrillation. Risk Factors: - Previous episode of ventricular fibrillation - Previous heart attack - Congenital heart disease - Cardiomyopathy - Injuries that cause damage to heart muscle - e.g. electrocution - Cocaine or Methamphetamine use - Electrolyte abnormalities - e.g. potassium, magnesium

Answer 237

In the pediatric and adolescent age groups, VF occurs with an annual incidence of 1.3-8.5 cases per 100,000 persons, accounting for approximately 5% of all deaths in this group. VF is often the first expression of coronary artery disease (CAD) and is responsible for approximately 50% of deaths from CAD.

Answer 238

- Chest pain - Dizziness - Nausea - Rapid, fluttering heartbeat - Shortness of breath - Fainting

Answer 239

- Loss of consciousness | - Rapid, fluttering heart beat

Answer 240

- Cardiac Monitor - classification of the rhythm | - Bloods - ABG, U&E, FBC, cross-match, clotting, toxicology screen, glucose

Answer 241

BLS. If pulseless Ventricular Tachycardia or Ventricular Fibrillation = Shockable Rhythm: - Defibrillate once - 150-360J biphasic, 360J monophasic - Resume CPR immediately for 2 min, then return to assess rhythm again - Administer adrenaline (1mg IV) after second defibrillation and again ever 3-5 minutes - If shockable rhythm persists after third shock, administer amiodarone 300mg IV bolus or lidocaine.

Answer 242

- Sudden cardiac death - Coma - Loss of nerve function - Changes in mental function

Answer 243

Overall survival to 1 month was only 1.6% for patients with non-shockable rhythms and 9.5% for patients found in VF. With increasing time to defibrillation, the survival rate fell rapidly from approximately 50% with a minimal delay to 5% at 15 min.

Answer 244

>3 Successive ventricular extrasystoles (broad QRS complexes >120ms) at a rate of >12- bpm Patients at high risk of recurrent VT should be considered for implantable defibrillator which has been shown to be more effective than amiodarone.

Answer 245

- MI - Congenital heart defect - Hypertrophic or dilated cardiomyopathy - Myocarditis - Ischaemic heart disease - Heart failure Risk Factors: - Age - Heart condition - Previous MI - Family history of VT - inherited catecholaminergic polymorphic ventricular tachycardia or arrhythmogenic right ventricular dysplasia

Answer 246

The prevalence of VT was 16% in men and 15% in women with CAD, 9% in men and 8% in women with hypertension, valvular disease, or cardiomyopathy without CAD, and 3% in men and 2% in women with no cardiovascular disease.

Answer 247

- Lightheadedness - Dizziness - Palpitations - Fatigue - Chest pressure or pain - Shortness of breath - Fainting spells

Answer 248

- Lightheadedness - Dizziness - Palpitations - Fatigue - Chest pressure or pain - Shortness of breath - Fainting spells

Answer 249

- Cardiac monitor - classification of rhythm - Bloods - ABG, U&E, FBC, cross-match, clotting, toxicology screen, glucose - ECG - Transoesophageal echocardiogram - ultrasound probe inserted into oesophagus - Cardiac MRI - Cardiac CT - Coronary angiogram - CXR - Stress echocardiogram

Answer 250

If sustained ventricular tachycardia with haemodynamic stability: - Amiodarone hydrochloride - Flecainide acetate - propafenone hydrochloride - Lidocaine hydrochloride - If sinus rhythm not restored, then DC cardioversion or pacing considered - Catheter ablation option if cessation of arrhythmia is not urgent If non-sustained ventricular tachycardia with haemodynamic stability: - Treat with beta-blocker If unstable sustained Ventricular Tachycardia: - Watch for deterioration with signs of hypotension or reduced cardiac ouput - DC cardioversion to restore sinus rhythm - IV amiodarone hydrochloride and repeat DC cardioversion If pulseless Ventricular Tachycardia or Ventricular Fibrillation = Shockable Rhythm: - Defibrillate once - 150-360J biphasic, 360J monophasic - Resume CPR immediately for 2 min, then return to assess rhythm again - Administer adrenaline (1mg IV) after second defibrillation and again ever 3-5 minutes - If shockable rhythm persists after third shock, administer amiodarone 300mg IV bolus or lidocaine. Maintenance Therapy: - Implantable cardioverter-defibrillator - Beta-blockers - Sotalol hydrochloride - in place of standard beta-blocker - Amiodarone hydrochloride

Answer 251

At higher risk of ventricular fibrillation.

Cardiovascular Flashcards

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