Cardiovascular Flashcards

Question

Define aortic stenosis

Answer 1

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

Answer 2

* Stenosis can be secondary to rheumatic heart disease (MOST COMMON WORLDWIDE) * Calcification of a congenital bicuspid aortic valve * Calcification/degeneration of a tricuspid aortic valve in the elderly

Answer 3

* Present in 3% of 75 yr olds * More common in males * Those with bicuspid aortic valve present earlier

Answer 4

* May be ASYMPTOMATIC initially * Angina (due to increased oxygen demand of the hypertrophied left ventricle) * Syncope or dizziness on exercise (due to outflow obstruction) * Symptoms of heart failure (e.g. dyspnoea, orthopnoea)

Answer 5

* Narrow pulse pressure * Slow-rising pulse * Thrill in the aortic area (only if severe) * Forceful sustained thrusting undisplaced apex beat * Ejection systolic murmur at the aortic area, radiating to the carotid artery * Second heart sound may be softened or absent (due to calcification) * A bicuspid valve may produce an ejection click

Answer 6

• ECG o Signs of left ventricular hypertrophy • Deep S in V1/2 • Tall R in V5/6 • Inverted T waves in I, aVL and V5/6 • Left axis deviation o LBBB • CXR o Post-stenotic enlargement of ascending aorta o Calcification of aortic valve • Echocardiogram o Visualises structural changes of the valves and level of stenosis (valvar, supravalvar or subvalvar) o Estimation of aortic valve area and pressure gradient across the valve in systole o Assess left ventricular function • Cardiac angiography o Allows differentiation from other causes of angina (e.g. MI) o Allows assessment of concomitant coronary artery disease • NOTE: 50% of patients with severe aortic stenosis have significant coronary artery disease

Answer 7

• A localised area of damage and breakdown of skin due to inadequate arterial blood supply. Usually seen on the feet of patients with severe atheromatous narrowing of the arteries supplying the legs.

Answer 8

• The ulcers are caused by a lack of blood flow to the capillary beds of the lower extremities • Risk Factors o Coronary heart disease o History of stroke or TIA o Diabetes mellitus o Peripheral arterial disease (e.g. intermittent claudication) o Obesity and immobility

Answer 9

* 22% of leg ulcers | * Prevalence increases with age and obesity

Answer 10

• Often DISTAL - at the dorsum of the foot or between the toes • Punched-out appearance • Often elliptical with clearly defined edges • The ulcer base contains grey, granulation tissue • NIGHT PAIN - hallmark of arterial ulcers o Pain is worse when supine (because arterial blood flow is further reduced when supine) o Pain is relieved by dangling the affected leg off the end of the bed

Answer 11

* Night pain * Punched-out appearance * Hairlessness * Pale skin * Absent pulses * Nail dystrophy * Wasting of calf muscles

Answer 12

* Duplex ultrasonography of lower limbs - assess patency of arteries and potential for revascularisation or bypass surgery * ABPI * Percutaneous angiography * ECG * Fasting serum lipids, fasting blood glucose and HbA1c (diabetes is a major risk factor) * FBC - anaemia can worsen the ischaemia

Answer 13

• Characterised by rapid, chaotic and ineffective atrial electrical conduction. Often subdivided into: o Permanent o Persistent o Paroxysmal

Answer 14

``` • There may be no identifiable cause • Secondary causes lead to an abnormal atrial electrical pathway that results in AF • Systemic Causes o Thyrotoxicosis o Hypertension o Pneumonia o Alcohol • Heart Causes o Mitral valve disease o Ischaemic heart disease o Rheumatic heart disease o Cardiomyopathy o Pericarditis o Sick sinus syndrome o Atrial myxoma • Lung Causes o Bronchial carcinoma o PE ```

Answer 15

* VERY COMMON in the elderly * Present in 5% of those > 65 years * May be paroxysmal

Answer 16

* Often ASYMPTOMATIC * Palpitations * Syncope (if low output) * Symptoms of the cause of AF

Answer 17

* Irregularly irregular pulse * Difference in apical beat and radial pulse * Check for signs of thyroid disease and valvular disease

Answer 18

``` • ECG o Uneven baseline with absent p waves o Irregular intervals between QRS complexes o Atrial flutter = saw-tooth • Bloods o Cardiac enzymes o TFT o Lipid profile o U&Es, Mg2+ and Ca2+ • Because there is increased risk of digoxin toxicity with hypokalaemia, hypomagnesaemia and hypercalcaemia • Echocardiogram o May show: • Mitral valve disease • Left atrial dilatation • Left ventricular dysfunction • Structural abnormalities ```

Answer 19

First and foremost, try to treat any reversible causes (e.g. thyrotoxicosis, chest infection) There are TWO main components to AF management: • RHYTHM CONTROL o If > 48 hrs since onset of AF • Anticoagulate for 3-4 weeks before attempting cardioversion o If < 48 hrs since onset of AF • DC cardioversion (2 x 100 J, 1 x 200 J) • Chemical cardioversion: flecainide or amiodarone  NOTE: flecainide is contraindicated if there is a history of ischaemic heart disease o Prophylaxis against AF • Sotalol • Amiodarone • Flecainide • Consider pill-in-the-pocket (single dose of a cardioverting drug (e.g. flecainide) for patients with paroxysmal AF) strategy for suitable patients • RATE CONTROL o Chronic (Permanent) AF • Control ventricular rate with:  Digoxin  Verapamil  Beta-blockers • Aim for ventricular rate ~ 90 bpm • STROKE RISK STRATIFICATION o LOW RISK patients can be managed with aspirin o HIGH RISK patients require anticoagulation with warfarin o This is based on the CHADS-Vasc Score o Risk factors include: • Previous thromboembolic event • Age > 75 yrs • Hypertension • Diabetes • Vascular disease • Valvular disease • Heart failure • Impaired left ventricular function

Answer 20

• THROMBOEMBOLISM o Embolic stroke risk of 4% per year o Risk is increased with left atrial enlargement or left ventricular dysfunction • Worsening of existing heart failure

Answer 21

• Chronic AF in a disease heart does not usually return to sinus rhythm

Answer 22

• Acute cessation of cardiac function

Answer 23

``` The REVERSIBLE causes of cardiac arrest can be summarised as the 4 Hs and 4 Ts • FOUR Hs o Hypothermia o Hypoxia o Hypovolaemia o Hypokalaemia/Hyperkalaemia • FOUR Ts o Toxins (and other metabolic disorders (drugs, therapeutic agents, sepsis)) o Thromboembolic o Tamponade o Tension pneumothorax ```

Answer 24

• None available

Answer 25

* Management precedes or is concurrent to history | * Cardiac arrest is usually sudden but some symptoms that may preceded by fatigue, fainting, blackouts, dizziness

Answer 26

* Unconscious * Not breathing * Absent carotid pulses

Answer 27

``` • Cardiac Monitor o Allows classification of the rhythm • Bloods o ABG o U&E o FBC o X-match o Clotting o Toxicology screen o Blood glucose ```

Answer 28

• SAFETY IS IMPORTANT o Approach any arrest scene with caution o The cause of the arrest may pose a threat o Defibrillators and oxygen are hazards • Basic Life Support o If the arrest is witnessed and monitored, consider giving a precordial thump (thump the sternum of the patient with the ulnar aspect of your fist) o Clear and maintain the airway with head tilt, jaw thrust and chin lift o Assess breathing by look, listen and feel • If they are not breathing, give two rescue breaths o Assess circulation at carotid pulse for 10 seconds • If absent - give 30 chest compressions at around 100/min • Continue cycle of 30 chest compressions for every 2 rescue breaths o Proceed to advanced life support as soon as possible • Advanced Life Support o Attach cardiac monitor and defibrillator o Assess rhythm • If pulseless ventricular tachycardia or ventricular fibrillation (shockable rhythms)  Defibrillate once (150-360 J biphasic, 360 J monophasic) • Make sure no one is touching the patient or the bed  Resume CPR immediately for 2 minutes and then reassess rhythm, and shock again if still in pulseless VT or VF  Administer adrenaline (1 mg IV) after second defibrillation and again ever 3-5 mins  If shockable rhythm persists after 3rd shock - administer amiodarone 300 mg IV bolus (or lidocaine) • If pulseless electrical activity (PEA) or asystole (non-shockable rhythms)  CPR for 2, and then reassess rhythm  Administer adrenaline (1 mg IV) every 3-5 mins  Atropine (3 mg IV, once only) if asystole or PEA with rate < 60 bpm o During CPR: • Check electrodes, paddle positions and contacts • Secure airway  Once secure, give continuous compressions and breaths • Consider magnesium, bicarbonate and external pacing • Stop CPR and check pulse only if change in rhythm or signs of life • Treatment of REVERSIBLE causes o Hypothermia - warm slowly o Hypokalaemia and Hyperkalaemia - correction of electrolyte levels o Hypovolaemia - IV colloids, crystalloids and blood products o Tamponade - pericardiocentesis o Tension Pneumothorax - aspiration or chest drain o Thromboembolism - treat as PE or MI o Toxins - use antidote for given toxin

Answer 29

* Irreversible hypoxic brain damage | * Death

Answer 30

* Resuscitation is less successful if cardiac arrest happens outside the hospital * Increased duration of inadequate effective cardiac output --> poor prognosis

Answer 31

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

Answer 32

``` • LOW OUTPUT Cardiac Failure (reduced cardiac output) o Left Heart Failure • Ischaemic heart disease • Hypertension • Cardiomyopathy • Aortic valve disease • Mitral regurgitation o Right Heart Failure • Secondary to left heart failure (in which case it is called congestive cardiac failure) • Infarction • Cardiomyopathy • Pulmonary hypertension/embolus/valve disease • Chronic lung disease • Tricuspid regurgitation • Constrictive pericarditis/pericardial tamponade o Biventricular Failure • Arrhythmia • Cardiomyopathy (dilated or restrictive) • Myocarditis • Drug toxicity • HIGH OUTPUT Cardiac Failure (increased demand) o Anaemia o Beri beri o Pregnancy o Paget's disease o Hyperthyroidism o Arteriovenous malformation ```

Answer 33

• 10% > 65 yrs old

Answer 34

``` • Left Heart Failure - symptoms caused by pulmonary congestion o Dyspnoea - divided based on the New York Heart Association classification: • 1 - no dyspnoea • 2 - dyspnoea on ordinary activities • 3 - dyspnoea on less than ordinary activities • 4 - dyspnoea at rest o Orthopnoea o Paroxysmal nocturnal dyspnoea o Fatigue • Acute Left Ventricular Failure o Dyspnoea o Wheeze o Cough o Pink frothy sputum • Right Heart Failure o Swollen ankles o Fatigue o Increased weight (due to oedema) o Reduced exercise tolerance o Anorexia o Nausea ```

Answer 35

• Left Heart Failure o Tachycardia o Tachypnoea o Displaced apex beat o Bilateral basal crackles o S3 gallop (caused by rapid ventricular filling) o Pansystolic murmur (due to functional mitral regurgitation) • Acute Left Ventricular Failure o Tachypnoea o Cyanosis o Tachycardia o Peripheral shutdown o Pulsus alternans • Arterial pulse waveforms showing alternating strong and weak beats • Sign of left ventricular systolic impairment • Explanation:  In left ventricular dysfunction, ejection fraction significantly decreases leading to a reduction in stroke volume  This causes an increase in end-diastolic volume  This means that the left ventricle is stretched more for the next contraction  Due to Starling's Law, the increased stretch of the left ventricle caused by the increased end-diastolic volume following the previous beat leads to an increase in the strength of the myocardial contraction  This results in a stronger systolic pulse o Gallop rhythm o Wheeze (cardiac asthma) o Fine crackles throughout lung • Right Heart Failure o Raised JVP o Hepatomegaly o Ascites o Ankle/sacral pitting oedema o Signs of functional tricuspid regurgitation

Answer 36

``` • Bloods o FBC o U&E o LFTs o CRP o Glucose o Lipids o TFTs • In ACUTE Left Ventricular Failure o ABG o Troponin o BNP • Raised plasma BNP suggests diagnosis of cardiac failure • Low plasma BNP rules out cardiac failure (90% sensitivity) • CXR o Alveolar shadowing o Kerley B lines o Cardiomegaly o Upper Lobe Diversion o Pleural Effusion • ECG o May be normal o May show ischaemic changes (pathological q waves, t wave inversion) o May show arrhythmia or left ventricular hypertrophy • Echocardiogram o Assess ventricular contraction o Systolic dysfunction = LV ejection fraction < 40% o Diastolic dysfunction = decreased compliance of the myocardium leads to restrictive filling defect • Swan-Ganz Catheter o Allows measurement of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures ```

Answer 37

• Acute Left Ventricular Failure o Treating Cardiogenic Shock: • This is severe cardiac failure with low blood pressure • Requires the use of inotropes (e.g. dobutamine) • Managed in ITU o Treating Pulmonary Oedema: • Sit the patient up • 60-100% Oxygen (and consider CPAP) • Diamorphine (venodilator + anxiolytic) • GTN infusion (venodilator --> reduced preload) • IV furosemide (venodilator and later diuretic effect) • Monitor:  BP  Respiratory rate  Oxygen saturation  Urine output  ECG • TREAT THE CAUSE! (e.g. MI, arrhythmia) • Chronic Left Ventricular Failure o TREAT THE CAUSE (e.g. hypertension) o TREAT EXACERBATING FACTORS (e.g. anaemia) o ACE Inhibitors • Inhibits renin-angiotensin system and inhibits adverse cardiac remodelling • They slow down the progression of heart failure and improve survival o Beta-Blockers • Blocks the effects of a chronically activated sympathetic system • Slows progression of heart failure and improves survival • The benefits of ACE inhibitors and beta-blockers are additive o Loop Diuretics • Alongside dietary salt restriction, can correct fluid overload o Aldosterone Antagonists • Improves survival in patients with NYHA class III/IV symptoms on standard therapy • Monitor K+ (as these drugs may cause hyperkalaemia) o Angiotensin Receptor Blockers • May be added in patients with persistent symptoms despite the use of ACE inhibitors and beta-blockers • Monitor K+ (as these drugs may cause hyperkalaemia) o Hydralazine and a Nitrate • May be added in patients (particularly Afro-Caribbeans) with persistent symptoms despite the use of ACE inhibitors and beta-blockers o Digoxin • Positive inotrope • Reduces hospitalisation but does NOT improve survival o N-3 Polyunsaturated Fatty Acids • Provide a small beneficial advantage in terms of survival o Cardiac Resynchronisation Therapy • Biventricular pacing improves symptoms and survival in patients with a left ventricular ejection fraction < 35%, cardiac dyssynchrony (QRS > 120 msec) and moderate-severe symptoms • These patients are also candidates for implantable cardioverter defibrillator (ICD) • They may receive a combined device o CAUTION: avoid drugs that could adversely affect a patient with heart failure due to systolic dysfunction (e.g. NSAIDs, non-dihydropyridine CCBs)

Answer 38

* Respiratory failure * Cardiogenic shock * Death

Answer 39

• 50% with cardiac failure die within 2 years

Answer 40

• Primary disease of the myocardium. Cardiomyopathy may be: o Dilated o Hypertrophic o Restrictive

Answer 41

``` • The majority are IDIOPATHIC • Dilated Cardiomyopathy o Post-viral myocarditis o Alcohol o Drugs (e.g. doxorubicin, cocaine) o Familial o Thyrotoxicosis o Haemochromatosis o Peripartum • Hypertrophic Cardiomyopathy ``` o Up to 50% are genetic • Restrictive Cardiomyopathy o Amyloidosis o Sarcoidosis o Haemochromatosis

Answer 42

* Prevalence of dilated and hypertrophic cardiomyopathy is 0.05-0.20% * Restrictive is even rarer

Answer 43

``` • Dilated o Symptoms of heart failure o Arrhythmias o Thromboembolism o Family history of sudden death • Hypertrophic o Usually NO SYMPTOMS o Syncope o Angina o Arrhythmias o Family history of sudden death • Restrictive o Dyspnoea o Fatigue o Arrhythmias o Ankle or abdominal swelling o Family history of sudden death ```

Answer 44

``` • Dilated o Raised JVP o Displaced apex beat o Functional mitral and tricuspid regurgitations o Third heart sound • Hypertrophic o Jerky carotid pulse o Double apex beat o Ejection systolic murmur • Restrictive o Raised JVP • Kussmaul Sign - paradoxical rise in JVP on inspiration due to restricted filling of the ventricles o Palpable apex beat o Third heart sound o Ascites o Ankle oedema o Hepatomegaly ```

Answer 45

• CXR ``` o May show cardiomegaly o May show signs of heart failure • ECG o All Types • Non-specific ST changes • Conduction defects • Arrhythmias o Hypertrophic • Left-axis deviation • Signs of left ventricular hypertrophy • Q waves in inferior and lateral leads o Restrictive • Low voltage complexes • Echocardiography o Dilated • Dilated ventricles with global hypokinesia o Hypertrophic • Ventricular hypertrophy (asymmetrical septal hypertrophy) o Restrictive • Non-dilated non-hypertrophied ventricles • Atrial enlargement • Preserved systolic function • Diastolic dysfunction • Granular or sparkling appearance of myocardium in amyloidosis • Cardiac Catheterisation • Endomyocardial Biopsy • Pedigree or Genetic Analysis ```

Answer 46

• Chronic inflammation of the pericardium with thickening and scarring. It limits the ability of the heart to function normally.

Answer 47

``` • NOTE: it is often underdiagnosed because it is difficult to distinguish it from restrictive cardiomyopathy and other causes of right heart failure • Can occur after any pericardial disease process • More common causes of pericarditis: o Idiopathic o Virus o TB o Mediastinal irradiation o Post-surgical o Connective tissue disease ```

Answer 48

* RARE * Documented in all ages * 9% of patients with acute pericarditis will develop constrictive pericarditis * TB has the HIGHEST TOTAL INCIDENCE out of all causes * More common in MALES

Answer 49

• Gradual-onset of symptoms • EARLY - symptoms and signs may be very subtle • ADVANCED - jaundice, cachexia, muscle wasting • Right Heart Failure Signs o Dyspnoea o Peripheral oedema o Raised JVP o Kussmaul's sign (paradoxical rise in JVP on inspiration) o Pulsatile hepatomegaly

Answer 50

* CXR - may show calcification of the pericardium * Echocardiogram - usually diagnostic and helps distinguish from restrictive cardiomyopathy * MRI - allows assessment of thickness of pericardium * CT - same role as MRI * Pericardial biopsy - may be indicated (especially if suspected infective cause)

Answer 51

• Formation of a thrombus within the deep veins (most commonly in the calf or thigh)

Answer 52

``` • Deep veins in the legs are more prone to blood stasis, hence clots are more likely to form (look up Virchow's triad) • Risk Factors o COCP o Post-surgery o Prolonged immobility o Obesity o Pregnancy o Dehydration o Smoking o Polycythaemia o Thrombophilia (e.g. protein C deficiency) o Malignancy ```

Answer 53

* VERY COMMON | * Especially in hospitalised patients

Answer 54

* Swollen limb | * May be painless

Answer 55

• Examination of the Leg o Local erythema, warmth and swelling o Measure the leg circumference o Varicosities (swollen/tortuous vessels) o Skin colour changes o NOTE: Homan's Sign - forced passive dorsiflexion of the ankle causes deep calf pain • Risk is stratified using the WELLS CRITERIA (NOTE: this is different from the PE Wells criteria) o Score 2 or more = high risk • Examine for PE o Check respiratory rate, pulse oximetry and pulse rate

Answer 56

``` • Doppler Ultrasound - GOLD STANDARD • Impedance Plethysmography - changes in blood volume results in changes of electrical resistance • Bloods o D-dimer: can be used as a negative predictor o Thrombophilia screen if indicated • If PE suspected o ECG o CXR o ABG ```

Answer 57

• ANTICOAGULATION o Heparin whilst waiting for warfarin to increase INR to the target range of 2-3 o DVTs that do NOT extend above the knee may be observed and anticoagulated for 3 months o DVTs extending beyond the knee require anticoagulation for 6 months o Recurrent DVTs require long-term warfarin • IVC Filter o May be used if anticoagulation is contraindicated and there is a risk of embolisation • Prevention o Graduated compression stockings o Mobilisation o Prophylactic heparin (if high risk e.g. hospitalised patients)

Answer 58

* PE * Venous infarction (phlegmasia cerulea dolens) * Thrombophlebitis (results from recurrent DVT) * Chronic venous insufficiency

Answer 59

* Depends on extent of DVT * Below-knee DVTs have a GOOD prognosis * Proximal DVTs have a greater risk of embolisation

Answer 60

Dyslipidemia is an abnormal amount of lipids (e.g. triglycerides, cholesterol and/or fat phospholipids) in the blood.

Answer 61

Primary dyslipidemia Blood sample being tested by lab technician. Dyslipidemia can be diagnosed with a blood test. Genetic factors cause primary dyslipidemia, and it is inherited. Common causes of primary dyslipidemia include: Familial combined hyperlipidemia, which develops in teenagers and young adults and can lead to high cholesterol. Familial hyperapobetalipoproteinemia, a mutation in a group of LDL lipoproteins called apolipoproteins. Familial hypertriglyceridemia, which leads to high triglyceride levels. Homozygous familial or polygenic hypercholesterolemia, a mutation in LDL receptors. Secondary dyslipidemia Secondary dyslipidemia is caused by lifestyle factors or medical conditions that interfere with blood lipid levels over time. Common causes of secondary dyslipidemia include: obesity, especially excess weight around the waist diabetes hypothyroidism alcohol use disorder, also known as alcoholism polycystic ovary syndrome metabolic syndrome excessive consumption of fats, especially saturated and trans fats Cushing's syndrome inflammatory bowel disease, commonly known as IBS severe infections, such as HIV an abdominal aortic aneurysm Several factors are known to increase the chances of developing dyslipidemia and related conditions. These risk factors include: ``` obesity a sedentary lifestyle a lack of regular physical exercise alcohol use tobacco use use of illegal or illicit drugs sexually transmitted infections type 2 diabetes hypothyroidism chronic kidney or liver conditions digestive conditions older age a diet rich in saturated and trans fats a parent or grandparent with dyslipidemia female sex, as women tend to experience higher LDL levels after menopause ```

Answer 62

In high-income countries, over 50% of adults had raised total cholesterol; more than double the level of the low-income countries.

Answer 63

Unless it is severe, most people with dyslipidemia are unaware that they have it. A doctor will usually diagnose dyslipidemia during a routine blood test or a test for another condition. Severe or untreated dyslipidemia can lead to other conditions, including coronary artery disease (CAD) and peripheral artery disease (PAD). Both CAD and PAD can cause serious health complications, including heart attacks and strokes. Common symptoms of these conditions include: leg pain, especially when walking or standing chest pain tightness or pressure in the chest and shortness of breath pain, tightness, and pressure in the neck, jaw, shoulders, and back indigestion and heartburn sleep problems and daytime exhaustion dizziness heart palpitations cold sweats vomiting and nausea swelling in the legs, ankles, feet, stomach, and veins of the neck fainting These symptoms may get worse with activity or stress and get better when a person rests. Anyone who experiences severe chest pain, dizziness, and fainting, or problems breathing should seek emergency care.

Answer 64

The most common goals are: Total cholesterol: Below 200 mg/dL HDL cholesterol: Men - above 40 mg/dL; Women - above 50 mg/dL LDL cholesterol: Below 100 mg/dL; Below 70 mg/dL for people with diabetes or heart disease. Triglycerides: Below 150 mg/dL

Answer 65

A doctor will usually focus on lowering a person's levels of triglycerides and LDL. However, treatment can vary, depending on the underlying cause of dyslipidemia and how severe it is. Doctors may prescribe one or more lipid-modifying medications for people with very high total cholesterol levels of at least 200 milligrams per deciliter of blood. High cholesterol is usually treated with statins, which interfere with the production of cholesterol in the liver. If statins fail to lower LDL and triglyceride levels, a doctor may recommend additional medications, including: ``` ezetimibe niacin fibrates bile acid sequestrants evolocumab and alirocumab lomitapide and mipomersen Some lifestyle changes and supplements can help to encourage healthy blood lipid levels. ``` Natural treatments include: reducing the consumption of unhealthy fats, such as those found in red meats, full-fat dairy products, refined carbohydrates, chocolate, chips, and fried foods exercising regularly maintaining a healthy body weight, by losing weight if necessary reducing or avoiding alcohol consumption quitting smoking and other use of tobacco products avoiding sitting for long periods of time increasing consumption of healthy polyunsaturated fats, such as those found in nuts, seeds, legumes, fish, whole grains, and olive oil taking omega-3 oil, either as a liquid or in capsules eating plenty of dietary fiber from whole fruits, vegetables, and whole grains getting at least 6– 8 hours of sleep a night drinking plenty of water

Answer 66

People with minor dyslipidemia usually have no symptoms. They can often manage or resolve the condition by making lifestyle adjustments. People with dyslipidemia should contact a doctor if they experience symptoms relating to the heart or circulation, including: ``` chest pains or tightness dizziness heart palpitations exhaustion swelling of the ankles and feet trouble breathing cold sweats nausea and heartburn People who have severe dyslipidemia, especially those with other medical conditions, may need to manage their blood lipid levels with medication, in addition to making lifestyle changes. ```

Answer 67

Significantly reduced risk of CHD if managed well.

Answer 68

* Gangrene: tissue necrosis, either wet with superimposed infection, dry or gas gangrene * Necrotising Fasciitis: a life-threatening infection that spreads rapidly across fascial planes

Answer 69

``` o Tissue ischaemia and infarction o Physical trauma o Thermal injury o Gas gangrene is caused by Clostridia perfringens • Necrotising Fasciitis o Usually polymicrobial involving streptococci, staphylococci, bacterioides and coliforms • Risk Factors o Diabetes o Peripheral vascular disease o Leg ulcers o Malignancy o Immunosuppression o Steroid use o Puncture/surgical wounds ```

Answer 70

* Gangrene - relatively COMMON | * Necrotising fasciitis and gas gangrene - RARE

Answer 71

• Gangrene o Pain o Discolouration of affected area o Often affects extremities or areas subject to high pressure • Necrotising Fasciitis o Pain • Often seems SEVERE and out of proportion to the apparent physical signs o Predisposing event (e.g. trauma, ulcer, surgery)

Answer 72

• Gangrene o Painful area = erythematous region around gangrenous tissue o Gangrenous tissue = BLACK because of haemoglobin break down products o Wet Gangrene - tissue becomes boggy with associated pus and a strong odour caused by the activity of anaerobes o Gas Gangrene - spreading infection and destruction of tissues causes overlying oedema, discolouration and crepitus (due to gas formation by the infection) • Necrotising Fasciitis o Area of erythema and oedema o Haemorrhagic blisters may be present o Signs of systemic inflammatory response and sepsis (high/low temperature, tachypnoea, hypotension)

Answer 73

* Bloods - FBC, U&Es, glucose, CRP and blood culture * Wound Swab, Pus/Fluid Aspirate - MC&S * X-ray of affected area - may show gas produced in gas gangrene

Answer 74

• 1st Degree AV Block: prolonged conduction through the AV node • 2nd Degree AV Block: o Mobitz Type I (Wenckebach): progressive prolongation of AV node conduction culminating in one atrial impulse failing to be conducted through the AV node. The cycle ten begins again. o Mobitz Type II: intermittent or regular failure of conduction through the AV node. Also defined by the number of normal conductions per failed or abnormal one (e.g. 2:1 or 3:1) • 3rd Degree (Complete) AV Block: no relationship between atrial and ventricular contraction. Failure of conduction through the AV node leads to ventricular contraction generated by a focus of depolarisation within the ventricle

Answer 75

• 250,000 pacemakers are implanted every year and they are mostly for heart block

Answer 76

* MI or ischaemic heart disease (MOST COMMON) * Infection (e.g. rheumatic fever, infective endocarditis) * Drugs (e.g. digoxin) * Metabolic (e.g. hyperkalaemia) * Infiltration of conducting system (e.g. sarcoidosis) * Degeneration of the conducting system

Answer 77

• 1st Degree - asymptomatic • 2nd Degree - usually asymptomatic • Mobitz Type II and 3rd Degree - may cause Stokes-Adams Attacks (syncope caused by ventricular asystole) o May also cause dizziness, palpitations, chest pain and heart failure

Answer 78

• Often NORMAL • Check for signs of a potential cause of heart block • Complete Heart Block o Slow large volume pulse o JVP may show cannon a waves • Cannon A Waves: waves seen occasionally in the jugular vein of humans with certain cardiac arrhythmias. This occurs when the atria and ventricles contract simultaneously • Mobitz Type II and 3rd Degree Heart Block o Signs of reduced cardiac output (e.g. hypotension, heart failure)

Answer 79

• ECG - GOLD STANDARD o First Degree - fixed prolonged PR interval (> 0.2 s) o Mobitz Type I (Wenckebach) - progressively prolonged PR interval, culminating in a P wave that is NOT followed by a QRS complex. The pattern then begins again. 'Going, going, gone'. o Mobitz Type II - intermittently a P wave is NOT followed by a QRS. There may be a regular pattern of P waves not followed by QRS (e.g. 2:1 or 3:1) o Complete Heart Block - no relationship between P waves and QRS complexes. If QRS is initiated in the: • Bundle of His - narrow complex • More distally - wide complex and slow rate (~ 30 bpm) ``` • CXR o Cardiac enlargement o Pulmonary oedema • Bloods o TFTs o Digoxin level o Cardiac enzymes o Troponin • Echocardiogram o Wall motion abnormalities o Aortic valve disease o Vegetations ```

Answer 80

``` • Chronic Block o Permanent pacemaker is recommended in: • Complete heart block • Advanced Mobitz Type II • Symptomatic Mobitz Type I • Acute Block o If associated with clinical deterioration use IV atropine o Consider temporary (external) pacemaker ```

Answer 81

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

Answer 82

• Mobitz Type II and 3rd degree block usually indicate serious underlying cardiac disease

Answer 83

* Systolic > 140 mm Hg and/or diastolic > 90 mm Hg measured on three separate occasions. * Malignant Hypertension: BP > 200/130 mm Hg

Answer 84

* VERY COMMON | * 10-20% of adults in the Western world

Answer 85

``` • Primary o Essential or idiopathic hypertension o Responsible for > 90% of cases • Secondary o Renal • Renal artery stenosis • Chronic glomerulonephritis • Chronic pyelonephritis • Polycystic kidney disease • Chronic renal failure o Endocrine • Diabetes mellitus • Hyperthyroidism • Cushing's syndrome • Conn's syndrome • Hyperparathyroidism • Phaeochromocytoma • Congenital adrenal hyperplasia • Acromegaly o Cardiovascular • Coarctation of the aorta • Increased intravascular volume o Drugs • Sympathomimetics • Corticosteroids • COCP o Pregnancy • Pre-eclampsia ```

Answer 86

``` • Often ASYMPTOMATIC • Symptoms of complications • Symptoms of the cause • Accelerated or Malignant Hypertension o Scotomas (visual field loss) o Blurred vision o Headache o Seizures o Nausea and vomiting o Acute heart failure ```

Answer 87

• Blood pressure should be measured on 2-3 different occasions before diagnosing hypertension • The lowest reading should be recorded • Examination may reveal information about causes: o Radiofemoral delay = coarctation of the aorta distal to the left subclavian artery o Renal artery bruit = renal artery stenosis o Fundoscopy to detect hypertensive retinopathy Keith-Wagner Classification of Hypertensive Retinopathy i. Silver wiring ii. As above + arteriovenous nipping iii. As above + flame haemorrhages + cotton wood exudates iv. As above + papilloedema Hypertensive retinopathy • Silver Wiring • Arteriovenous nipping • Flame Haemorrhages, Cotton Wool Exudates and Papilloedema

Answer 88

• Bloods: o U&Es o Glucose o Lipids • Urine Dipstick o Blood and protein (e.g. if glomerulonephritis) • ECG o May show signs of left ventricular hypertrophy or ischaemia • Ambulatory blood pressure monitoring o Excludes white coat hypertension • Other investigations may be performed if a secondary cause of the hypertension is suspected (e.g. renal angiogram)

Answer 89

• Conservative o Stop smoking o Lose weight o Reduce alcohol intake o Reduce dietary sodium • Investigate for secondary causes (mainly in young patients) • Medical - treatment recommended if systolic > 160 mm Hg and/or diastolic > 100 mm Hg, or if evidence of end-organ damage. Multiple drug therapies often needed. o ACE Inhibitors or Angiotensin Receptor Blockers - first line if: • < 55 yrs • Diabetic • Heart failure • Left ventricular dysfunction o CCBs - first line if: • > 55 yrs • Black • NOTE: thiazide diuretics can be used if CCBs are not tolerated o Beta-Blockers • Not preferred initial therapy • May be considered in younger patients • CAUTION: combining with thiazide diuretic may increase risk of developing diabetes • May increase risk of heart failure o Alpha-Blockers • 4th line • May be used in patients with prostate disease • Target BP o Non-Diabetic: < 140/90 mm Hg o Diabetes without proteinuria: < 130/80 mm Hg o Diabetes WITH proteinuria: < 125/75 mm Hg • Severe Hypertension Management (Diastolic > 140 mm Hg) o Atenolol o Nifedipine • Acute Malignant Hypertension Management: o IV beta-blocker (e.g. esmolol) o Labetolol o Hydralazine sodium nitroprusside o CAUTION: avoid rapid lowering of blood pressure because it can cause cerebral infarction • This is because the autoregulatory mechanisms within the brain for regulating blood flow will cause vasoconstriction of the vessels in the brain when blood pressure is very high • Lowering the blood pressure too rapidly would mean that the autoregulatory mechanisms do not adapt to the drop in blood pressure and so the vessels remain constricted • A rapid drop in blood pressure with constricted vessels will cause an infarction

Answer 90

* Heart failure * Coronary artery disease * Cerebrovascular accidents * Peripheral vascular disease * Emboli * Hypertensive retinopathy * Renal failure * Hypertensive encephalopathy * Posterior reversible encephalopathy syndrome (PRES) * Malignant hypertension

Answer 91

* Good prognosis if well controlled * Uncontrolled hypertension is associated with increased mortality * Treatment reduces incidence of renal damage, stroke and heart failure

Answer 92

• Infection of intracardiac endocardial structures (mainly heart valves)

Answer 93

• Most common organisms causing infective endocarditis: o Streptococci (40%) - mainly a-haemolytic S. viridans and S. bovis o Staphylococci (35%) - S. aureus and S. epidermidis o Enterococci (20%) - usually E. faecalis o Other organisms: • Haemophilus • Actinobacillus • Cardiobacterium • Coxiella burnetii • Histoplasma (fungal) • Pathophysiology o Vegetations form when organisms deposit on the heart valves during a period of bacteraemia o The vegetations are made up of platelets, fibrin and infective organisms o They destroy valve leaflets, invade the myocardium or aortic wall leading to abscess cavities o Activation of the immune system can lead to the formation of immune complexes --> vasculitis, glomerulonephritis, arthritis • Risk Factors o Abnormal valves (e.g. congenital, calcification, rheumatic heart disease) o Prosthetic heart valves o Turbulent blood flow (e.g. patent ductus arteriosus) o Recent dental work/poor dental hygiene (source of S. viridans)

Answer 94

• UK Incidence: 16-22/1 million per year

Answer 95

``` • Fever with sweats/chills/rigors o NOTE: this might be relapsing and remitting • Malaise • Arthralgia • Myalgia • Confusion • Skin lesions • Ask about recent dental surgery or IV drug use ```

Answer 96

``` • Pyrexia • Tachycardia • Signs of anaemia • Clubbing • New regurgitant murmur or muffled heart sounds • Frequency of heart murmurs: o Mitral > Aortic > Tricuspid > Pulmonary • Splenomegaly • Vasculitic Lesions o Roth spots on retina ``` o Petechiae on pharyngeal and conjunctival mucosa o Janeway lesions (painless macules on the palms which blanch on pressure) o Osler's nodes (tender nodules on finger/toe pads) o Splinter haemorrhages

Answer 97

• Bloods o FBC - high neutrophils, normocytic anaemia o High ESR/CRP o U&Es o NOTE: a lot of patients with infective endocarditis tend to be rheumatoid factor positive • Urinalysis o Microscopic haematuria o Proteinuria • Blood Culture o Do microscopy and sensitivities as well • Echocardiography o Transthoracic or transoesophageal (produces better image) • Duke's Classification - a method of diagnosing infective endocarditis based on the findings of the investigations and the symptoms/signs

Answer 98

``` • Antibiotics for 4-6 weeks • On clinical suspicion = EMPIRICAL TREATMENT o Benzylpenicillin o Gentamicin • Streptococci - continue the same as above • Staphylococci o Flucloxacillin/vancomycin o Gentamicin • Enterococci o Ampicillin o Gentamicin • Culture Negative o Vancomycin o Gentamicin • SURGERY - urgent valve replacement may be needed if there is a poor response to antibiotics ```

Answer 99

* Valve incompetence * Intracardiac fistulae or abscesses * Aneurysm * Heart failure * Renal failure * Glomerulonephritis * Arterial emboli from the vegetations shooting to the brain, kidneys, lungs and spleen

Answer 100

* FATAL if untreated | * 15-30% mortality even WITH treatment

Answer 101

• Characterised by decreased blood supply to the heart muscle resulting in chest pain (angina pectoris). May present as stable angina or acute coronary syndrome. • ACS can be further subdivided into: o Unstable angina - chest pain at rest due to ischaemia but without cardiac injury o NSTEMI o STEMI - ST elevation with transmural infarction o NOTE: MI = cardiac muscle necrosis resulting from ischaemia

Answer 102

* COMMON * Prevalence: > 2 % * More common in males * Annual incidence of MI in the UK ~ 5/1000

Answer 103

• Angina pectoris occurs when myocardial oxygen demand exceeds oxygen supply • This is usually due to atherosclerosis • Rarer causes of angina pectoris include coronary artery spasm (e.g. induced by cocaine), arteritis and emboli • Atherosclerosis pathophysiology o Endothelial injury leads to migration of monocytes into the subendothelial space o These monocytes differentiate into macrophages o Macrophages accumulate LDL lipids and become foam cells o These foam cells release growth factors that stimulate smooth muscle proliferation, production of collagen and proteoglycans o This leads to the formation of an atherosclerotic plaque • Risk Factors o Male o Diabetes mellitus o Family history o Hypertension o Hyperlipidaemia o Smoking

Answer 104

• ACS o Acute-onset chest pain o Central, heavy, tight, crushing pain o Radiates to the arms, neck, jaw or epigastrium o Occurs at rest o More severe and frequent pain that previously occurring stable angina o Associated symptoms: • Breathlessness • Sweating • Nausea and vomiting • SILENT INFARCTS occur in the elderly and diabetics • Stable Angina o Chest pain brought on by exertion and relieved by rest

Answer 105

``` • Stable Angina o Check for signs of risk factors • ACS o There may be NO CLINICAL SIGNS o Pale o Sweating o Restless o Low-grade pyrexia o Check both radial pulses to rule out aortic dissection o Arrhythmias o Disturbances of BP o New heart murmurs o Signs of complications (e.g. acute heart failure, cardiogenic shock) ```

Answer 106

• Bloods o FBC o U&Es o CRP o Glucose o Lipid profile o Cardiac enzymes (troponins and CK-MB) o Amylase (pancreatitis could mimic MI) o TFTs o AST and LDH (raised 24 and 48 hours post-MI, respectively) • ECG o Unstable Angina or NSTEMI: • May show ST depression or T wave inversion o STEMI: • Hyperacute T waves • ST elevation (> 1 mm in limb leads, > 2 mm in chest leads) • New-onset LBBB • Later changes:  T wave inversion  Pathological Q waves o Relationship between ECG leads and the side of the heart • Inferior: II, III, aVF • Anterior: V1-V5/6 • Lateral: I, aVL, V5/6 • Posterior: Tall R wave and ST depression in V1-3 • CXR o Check for signs of heart failure • Exercise ECG o Indications • Patients with troponin-negative ACS or stable angina with a high pretest probability of coronary heart disease • Pretest probability is based on characteristics of chest pain, cardiac risk factors, age and gender • NOTE: digoxin is associated with giving a false-positive result o Results: • Positive Test: > 1 mm horizontal or downsloping ST depression measured at 80 ms after the end of the QRS complex • Failed Test: failure to achieve at least 85% of the predicted maximal heart rate (220-age) and otherwise negative findings (no chest pain or ECG changes)  NOTE: beta-blockers reduce heart rate and so should be stopped before the test • Resting ECG Abnormalities: e.g. pre-excitation syndrome, > 1 mm ST depression, LBBB or pacemaker ventricular rhythm • Radionuclide Myocardial Perfusion Imaging (rMPI) o Uses Technetium-99m sestamibi or tetrofosmin o Can be performed under stress or at rest o Stress testing shows low uptake in ischaemic myocardium • Echocardiogram o Measures left ventricular ejection fraction o Exercise or dobutamine stress echo may detect regional wall motion abnormalities • Pharmacological Stress Testing o This is used in patients who are unable to exercise o Pharmacological agents can be used to induce a tachycardia, such as: • Dipyridamole • Adenosine • Dobutamine o These agents are used in conjunction with various imaging modalities (e.g. rMPI, echocardiography) to detect ischaemic myocardium o NOTE: Dypiridamole and adenosine are contraindicated in AV block and reactive airway disease • Cardiac Catheterisation/Angiography o Performed if ACS with positive troponin or if high risk on stress testing • Coronary Calcium Scoring o Uses specialised CT scan o May be useful in outpatients with atypical chest pain or in acute chest pain that isn't clearly due to ischaemia

Answer 107

• STABLE ANGINA o Minimise cardiac risk factors (e.g. blood pressure, hyperlipidaemia, diabetes) • All patients should receive aspirin 75 mg/day unless contraindicated o Immediate symptom relief (e.g. GTN spray) o Long-term management • Beta-blockers  Contraindicated in: • Acute heart failure • Cardiogenic shock • Bradycardia • Heart block • Asthma • Calcium channel blockers • Nitrates o Percutaneous coronary intervention (PCI) • Performed in patients with stable angina despite maximal tolerable medical therapy o Coronary artery bypass graft (CABG) • Occurs in more severe cases (e.g. three-vessel disease) • UNSTABLE ANGINA/NSTEMI o Admit to coronary care unit o Oxygen, IV access, monitor vital signs and serial ECG o GTN o Morphine o Metoclopramide (to counteract the nausea caused by morphine) o Aspirin (300 mg initially, followed by 75 mg indefinitely) o Clopidogrel (300 mg initially, followed by 75 mg for at least 1 year if troponin positive or high risk) o LMWH (e.g. enoxaparin) o Beta-blocker (e.g. metoprolol) o Glucose-insulin infusion if blood glucose > 11 mmol/L o GlpIIb/IIIa inhibitors may also be considered (e.g. tirofiban) in patients: • Undergoing PCI • At high risk of further cardiac events o If little improvement, consider urgent angiography with/without revascularisation o NOTE: the acute management of ACS can be remembered using the mnemonic MONABASH • Morphine • Oxygen • Nitrates • Anticoagulants (aspirin + clopidogrel) • Beta-blockers • ACE inhibitors • Statins • Heparin • STEMI o Same as UAP/NSTEMI management except: • Clopidogrel  600 mg if patient is going to PCI  300 mg if undergoing thrombolysis and < 75 yrs  75 mg if undergoing thrombolysis and > 75 yrs  MAINTENANCE: 75 mg daily for at least 1 year • If undergoing primary PCI:  IV heparin (plus GlpIIb/IIIa inhibitor)  Bivalirudin (antithrombin) o Primary PCI • Goal < 90 min if available o Thrombolysis • Uses fibrinolytics such as streptokinase and tissue plasminogen activator (e.g. alteplase) • Only considered if within 12 hours of chest pain with ECG changes and not contraindicated • Rescue PCI may be performed if continued chest pain or ST elevation after thrombolysis o Secondary Prevention • Dual antiplatelet therapy (aspirin + clopidogrel) • Beta-blockers • ACE inhibitors • Statins • Control risk factors o Advice • No driving for 1 month following MI o CABG • Considered in patients with left main stem or three-vessel disease

Answer 108

``` • Increased risk of MI and other vascular disease (e.g. stroke, PVD) • Cardiac injury from an MI can lead to heart failure and arrhythmias • Early Complications (within 24-72 hrs) o Death o Cardiogenic shock o Heart failure o Ventricular arrythmias o Heart block o Pericarditis o Myocardial rupture o Thromboembolism • Late Complications o Ventricular wall rupture o Valvular regurgitation o Ventricular aneurysms o Tamponade o Dressler's syndrome o Thromboembolism • MNEMONIC for Complications of MI o Death o Arrhythmias o Rupture o Tamponade o Heart failure o Valve disease o Aneurysm o Dressler's syndrome o Embolism ```

Answer 109

• TIMI score (0-7) can be used for risk stratification o NOTE: TIMI = thrombolysis in myocardial infarction o High scores are associated with high risk of cardiac events within 30 days of MI • Killip Classification of acute MI can also be used: o Class I: no evidence of heart failure o Class II: mild to moderate heart failure o Class III: over pulmonary oedema o Class IV: cardiogenic shock

Answer 110

• Retrograde flow of blood from left ventricle to left atrium during systole

Answer 111

* Affect ~5% of adults | * Mitral valve prolapse is common in young females

Answer 112

• Broadly speaking, it is caused by mitral valve damage or dysfunction, which, in turn could be caused by any of the following: o Rheumatic heart disease (MOST COMMON) o Infective endocarditis o Mitral valve prolapse o Papillary muscle rupture or dysfunction (secondary to IHD or cardiomyopathy) o Chordal rupture and floppy mitral valve associated with connective tissue disease (e.g. Ehlers-Danlos syndrome, Marfan's syndrome)

Answer 113

• Acute MR - may present with symptoms of left ventricular failure • Chronic MR - may be asymptomatic or present with: o Exertional dyspnoea o Palpitations if in AF o Fatigue • Mitral Valve Prolapse - asymptomatic or atypical chest pain or palpitations

Answer 114

• Pulse may be irregularly irregular (if in AF) • Laterally displaced apex beat with thrusting (due to left ventricular dilation) • Pansystolic murmur o Loudest at apex beat o Radiating to the axilla o Soft S1 o S3 may be heard due to rapid ventricular filling in early diastole • Signs of left ventricular failure in acute mitral regurgitation • Mitral Valve Prolapse o Mid-systolic click o Late systolic murmur o The click moves towards S1 when standing and away when lying down

Answer 115

• ECG o NORMAL o May show AF or p mitrale (indicates left atrial hypertrophy) • CXR o ACUTE mitral regurgitation may produce signs of left ventricular failure o CHRONIC mitral regurgitation shows: • Left atrial enlargement • Cardiomegaly (due to LV dilation) • Mitral valve calcification (if rheumatic heart disease is the cause) • Echocardiography o Performed every 6-12 months in moderate-severe MR o Allows assessment of LV ejection fraction and end-systolic dimension

Answer 116

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

Answer 117

• Incidence is declining because rheumatic fever is becoming more and more rare

Answer 118

``` • MAIN CAUSE: Rheumatic Heart Disease (90% of cases) • Rare causes of mitral stenosis: o Congenital mitral stenosis o SLE o Rheumatoid arthritis o Endocarditis o Atrial myxoma ```

Answer 119

``` • May be ASYMPTOMATIC • Fatigue • Shortness of breath on exertion • Orthopnoea • Palpitations (related to AF) • Rare symptoms: o Cough o Haemoptysis o Hoarseness caused by compression of left recurrent laryngeal nerve by an enlarged left atrium ```

Answer 120

* Peripheral cyanosis * Malar flush (image) * Irregularly irregular pulse (if in AF) * Apex beat undisplaced and tapping * Parasternal heave (due to right ventricular hypertrophy secondary to pulmonary hypertension) * Loud S1 with opening snap * Mid-diastolic murmur * Evidence of pulmonary oedema on lung auscultation (if decompensated)

Answer 121

• ECG o May be NORMAL o May see p mitrale (broad bifid p wave caused by left atrial hypertrophy) o May see AF o Evidence of right ventricular hypertrophy may be seen if there is severe pulmonary hypertension • CXR o Left atrial enlargement o Cardiac enlargement o Pulmonary congestion o Mitral valve calcification (occurs in rheumatic cases) • Echocardiography o Assesses functional and structural impairments o Transoesophageal echocardiogram (TOE) gives a better view • Cardiac Catheterisation o Measures severity of heart failure

Answer 122

• Acute inflammation and necrosis of cardiac muscle (myocardium)

Answer 123

* Incidence is difficult to measure accurately * Coxsackie B virus is most common in Europe and USA * Chagas disease is most common in South America

Answer 124

``` • Usually IDIOPATHIC • Viruses o Coxsackie B o EBV o CMV o Adenovirus o Influenza • Bacteria o Post-streptococcal o Tuberculosis o Diphtheria • Fungal o Candidiasis • Protozoal o Trypanosomiasis (Chagas disease) • Helminths o Trichinosis • Non-infective o Systemic: SLE, sarcoidosis, polymyositis o Hypersensitivity myocarditis: sulphonamides • Drugs o Chemotherapy agents (e.g. doxorubicin, streptomycin) • Others o Cocaine, heavy metals, radiation ```

Answer 125

``` • Prodromal flu-like illness with: o Fever o Malaise o Fatigue o Lethargy • Breathlessness (due to pericardial effusion/myocardial dysfunction) • Palpitations • Sharp chest pain (suggesting there is also pericarditis) ```

Answer 126

* Signs of pericarditis | * Signs of complications (e.g. heart failure, arrhythmia)

Answer 127

``` • Bloods o FBC - raised WCC if infective cause o U&E o ESR/CRP - raised o Cardiac enzymes - may be raised o Tests to identify cause (e.g. viral/bacterial serology, ANA, TFT) • ECG o Non-specific T wave and ST changes o PERICARDITIS: widespread saddle-shaped ST elevation ``` ``` • CXR o May be NORMAL o May show cardiomegaly • Pericardial Fluid Drainage o Measure glucose, protein, cytology, culture and sensitivity o Helps identify causative organism • Echocardiography o Assesses systolic/diastolic function o Wall motion abnormalities o Pericardial effusions • Myocardial Biopsy o Rarely required ```

Answer 128

• Inflammation of the pericardium | o It may be acute, subacute or chronic

Answer 129

* UNCOMMON * < 1/100 hospital admissions * More common in males

Answer 130

``` • IDIOPATHIC • Infective Most common causative organisms: o Coxsackie B o Echovirus o Mumps o Streptococci o Fungi o Staphylococci o TB • Connective tissue disease (e.g. sarcoidosis, SLE, scleroderma) • Post-MI (within 24-72 hrs of MI - occurs in up to 20% of patients) • Dressler's Syndrome - pericarditis occurring weeks/months after acute MI • Malignancy - lung, breast, lymphoma, leukaemia, melanoma • Radiotherapy • Thoracic surgery • Drugs (e.g. hydralazine, isoniazid) ```

Answer 131

``` • CHEST PAIN o Sharp and central o May radiate to the neck or shoulders o Worse when coughing and deep inspiration (pleuritic pain) o Relieved by sitting forward • Dyspnoea • Nausea ```

Answer 132

``` • Fever • Pericardial friction rub o Heard best at lower left sternal edge, with patient leaning forward during expiration • Heart sounds may be faint due to a pericardial effusion • Cardiac Tamponade signs o Beck's Triad (signs associated with acute cardiac tamponade) • Raised JVP • Low Blood Pressure • Muffled Heart Sounds o Tachycardia o Pulsus paradoxus • Definition: an abnormally large decrease in SBP (> 10 mm Hg drop) and pulse wave amplitude during inspiration • Constrictive Pericarditis signs o Kussmaul's sign o Pulsus paradoxus o Hepatomegaly o Ascites o Oedema o Pericardial knock (due to rapid ventricular filling) o AF ```

Answer 133

• ECG - widespread saddle-shaped ST elevation • Echocardiogram - assesses pericardial effusion and cardiac function • Bloods o FBC o U&Es o ESR/CRP o Cardiac Enzymes (usually normal) o Other investigations for cause: blood cultures, ASO titres, ANA, rheumatoid factor • CXR o Usually normal o May be globular if there is a pericardial effusion

Answer 134

``` • Acute - cardiac tamponade is treated with emergency pericardiocentesis • Medical o Treat underlying cause o NSAIDs for pain and fever relief • Recurrent o Low-dose steroids o Immunosuppressants o Colchicine • Surgical o Pericardiectomy is performed in cases of constrictive pericarditis ```

Answer 135

* Pericardial effusion * Cardiac tamponade * Cardiac arrhythmias

Answer 136

* Depends on the underlying cause * Viral cases have a GOOD prognosis * Malignant pericarditis has a POOR prognosis

Answer 137

• Occurs due to atherosclerosis causing stenosis of arteries via a multifactorial process involving modifiable and non-modifiable risk factors

Answer 138

• Occurs due to ATHEROSCLEROSIS in peripheral arteries • Types of PVD include: o Intermittent claudication - calf pain on exercise o Critical limb ischaemia - pain at rest • NOTE: this is the MOST SEVERE manifestation of peripheral vascular disease o Acute limb ischaemia - a sudden decrease in arterial perfusion in a limb, due to thrombotic or embolic causes o Arterial ulcers o Gangrene • Risk Factors (same as the risk factors for any other atherosclerotic disease) o Smoking o Diabetes o Hypertension o Hyperlipidaemia o Physical inactivity o Obesity

Answer 139

* 55-70 yrs = 4-12% affected * 70+ yrs = 15-20% affected * More common in MALES * Incidence increases with AGE

Answer 140

``` • Intermittent claudication - cramping pain in the calf, thigh or buttock after walking for a given distance (claudication distance) and relieved by rest o Calf claudication = femoral disease o Buttock claudication = iliac disease • Features of Critical Limb Ischaemia o Ulcers o Gangrene o Rest pain o Night pain (relieved by dangling leg over the edge of the bed) • Leriche Syndrome (aortoiliac occlusive disease) o Buttock claudication o Impotence o Absent/weak distal pulses • Fontaine Classification of Peripheral Vascular Disease o Asymptomatic o Intermittent Claudication o Rest pain o Ulceration/gangrene ```

Answer 141

``` • Acute Limb Ischaemia - 6 Ps o Pain o Pale o Pulseless o Paralysis o Paraesthesia o Perishingly Cold • Other symptoms: o Atrophic skin o Hairless o Punched-out ulcers (often painful) o Colour change when raising leg (to Buerger's angle) ```

Answer 142

• Full cardiovascular risk assessment o Blood pressure o FBC - anaemia will worsen ischaemia o Fasting blood glucose o Lipid levels o ECG - check for pre-existing coronary artery disease o Thrombophilia screen - for patients < 50 yrs • Colour Duplex Ultrasound o FIRST-line o Shows site and degree of stenosis • MRI/CT o Assesses extent and location of stenoses • ABPI (Ankle-Brachial Pressure Index) o Marker of cardiovascular disease o ABPI < 0.8 = do NOT apply a pressure bandage because this will worsen ischaemia

Answer 143

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

Answer 144

``` Thrombus 95% arise from DVT in the lower limbs Rarely arises in the right atrium (in AF patients) Other causes of embolus: Amniotic fluid Air Fat Tumour Mycotic ``` ``` Risk Factors Surgical patients Immobility Obesity OCP Heart failure Malignanc ```

Answer 145

``` Relatively COMMON (especially in hospitalised patients) Occur in 10 - 20% of patients with confirmed proximal DVT ```

Answer 146

Depends on the SITE and SIZE of the embolus Small may be ASYMPTOMATIC ``` Moderate Sudden onset SOB Cough Haemoptysis Pleuritic chest pain ``` ``` Large (or proximal) As above and: Severe central pleuritic chest pain Shock Collapse Acute right heart failure Sudden death Multiple Small Recurrent Symptoms of pulmonary hypertension ```

Answer 147

Severity of PE can be assessed based on associated signs: Small often no clinical signs. There may be some tachycardia and tachypnoea ``` Moderate Tachypnoea Tachycardia Pleural rub Low O2 saturation ( despite O2 supplementation) ``` ``` Massive PE Shock Cyanosis Signs of right heart strain Raised JVP Left parasternal heave Accentuated S2 heart sound ``` Multiple Recurrent PE Signs of pulmonary hypertension Signs of right heart failure

Answer 148

``` The Well's Score is used to determine the best investigation for PE Low Probability (Wells 4 or less) - use D dimer High Probability (Wells > 4) required imaging (CTPA) ``` Additional investigations: Bloods - ABG, thrombophilia screen ECG May be normal May show tachycardia, right axis deviation or RBBB May show S1Q3T3 pattern CXR often NORMAL but helps exclude other diagnoses ``` Spiral CT Pulmonary Angiogram FIRST LINE INVESTIGATION Poor sensitivity for small emboli VERY sensitive for medium to large emboli ``` Ventilation - Perfusion (VQ) Scan Identifies areas of ventilation and perfusion mismatch, which would indicate an area of infarcted lung Pulmonary Angiography Invasive Rarely necessary Doppler US of Lower Limb allows assessment of venous thromboembolism Echocardiography may show right heart strain

Answer 149

Primary Prevention Compression stockings Heparin prophylaxis for those at risk Good mobilisation and adequate hydration ``` If haemodynamically stable O2 Anticoagulation with heparin or LMWH Switch over to oral warfarin for at least 3 months Maintain INR 2 - 3 Analgesia ``` If haemodynamically UNSTABLE (massive PE) Resuscitate O2 IV fluids Thrombolysis with tPA may be considered if cardiac arrest is imminent Surgical or radiological Embolectomy IVC filters sometimes used for recurrent PEs despite adequate anticoagulation or when anticoagulation is contraindicated

Answer 150

Death Pulmonary infarction Pulmonary hypertension Right heart failure

Answer 151

30% mortality in those left untreated 8% mortality with treatment Increased risk of future thromboembolic disease

Answer 152

• An increase in mean pulmonary arterial pressure which can be caused by or associated with a wide variety of other conditions.

Answer 153

• Pulmonary hypertension has a variety of causes o Idiopathic o Problems with smaller branches of the pulmonary arteries o Left ventricular failure o Lung disease (e.g. COPD, interstitial lung disease) o Thromboses/Emboli in the lungs

Answer 154

* Idiopathic pulmonary hypertension is RARE | * More common in severe respiratory and cardiac disease

Answer 155

* Progressive breathlessness * Weakness/tiredness * Exertional dizziness and syncope * LATE STAGE - oedema and ascites * Angina and tachyarrhythmia

Answer 156

* Right ventricular heave * Loud pulmonary second heart sound * Murmur - pulmonary regurgitation * Tricuspid regurgitation * Raised JVP * Peripheral oedema * Ascites

Answer 157

* CXR - exclude other lung diseases * ECG - right ventricular hypertrophy and strain * Pulmonary function tests * LFTs - liver damage --> portal hypertension * Lung biopsy - interstitial lung disease * Echocardiography - assess right ventricular function * Right Heart Catheterisation - directly measure pulmonary pressure and confirm the diagnosis

Answer 158

Rheumatic fever is an inflammatory disease that can develop as a complication of inadequately treated strep throat or scarlet fever. Strep throat and scarlet fever are caused by an infection with streptococcus bacteria.

Answer 159

Rheumatic fever is most common in 5- to 15-year-old children, though it can develop in younger children and adults. Family history. Some people carry a gene or genes that might make them more likely to develop rheumatic fever. Type of strep bacteria. Certain strains of strep bacteria are more likely to contribute to rheumatic fever than are other strains. Environmental factors. A greater risk of rheumatic fever is associated with overcrowding, poor sanitation and other conditions that can easily result in the rapid transmission or multiple exposures to strep bacteria.

Answer 160

Rare in developed countries

Answer 161

Fever Painful and tender joints — most often in the knees, ankles, elbows and wrists Pain in one joint that migrates to another joint Red, hot or swollen joints Small, painless bumps (nodules) beneath the skin Chest pain Heart murmur Fatigue Flat or slightly raised, painless rash with a ragged edge (erythema marginatum) Jerky, uncontrollable body movements (Sydenham chorea, or St. Vitus' dance) — most often in the hands, feet and face Outbursts of unusual behavior, such as crying or inappropriate laughing, that accompanies Sydenham chorea

Answer 162

Valve stenosis. This narrowing of the valve decreases blood flow. Valve regurgitation. This leak in the valve allows blood to flow in the wrong direction. Damage to heart muscle. The inflammation associated with rheumatic fever can weaken the heart muscle, affecting its ability to pump. An irregular and chaotic beating of the upper chambers of the heart (atrial fibrillation) An inability of the heart to pump enough blood to the body (heart failure)

Answer 163

Major signs and symptoms are strongly associated with ARF and include carditis (swelling of the heart), arthritis (pain, redness and swelling of one or more joints), Sydenham’s chorea (strange movements of the body and face), erythema marginatum (painless skin pigmentation), and subcutaneous nodules (small lumps under the skin). Minor signs and symptoms are used to help support the diagnosis. These include fever, arthralgia (generalised joint aches), blood tests that suggest general illness, and changes seen on heart electrocardiogram. A combination of these signs and symptoms, plus a positive test for recent group A streptococcus infection is required to confirm ARF diagnosis.

Answer 164

• A regular narrow-complex tachycardia (> 100 bpm) with no p waves and a supraventricular origin. o AF technically counts as a type of SVT o However, SVT generally refers to: • Atrioventricular Nodal Re-entry Tachycardia (AVNRT) • Atrioventricular Re-entry Tachycardia (AVRT)

Answer 165

``` • AVNRT o A localised re-entry circuit forms around the AV node • AVRT o A re-entry circuit forms between the atria and ventricles due to the presence of an accessory pathway (Bundle of Kent) • Risk Factors o Nicotine o Alcohol o Caffeine o Previous MI o Digoxin toxicity ```

Answer 166

* VERY COMMON | * 2 x more common in FEMALES

Answer 167

* May have minimal symptoms or may present with syncope * Symptoms vary depending on rate and duration of SVT * Palpitations * Light-headedness * Abrupt onset and termination of symptoms * Other symptoms: fatigue, chest discomfort, dyspnoea, syncope

Answer 168

• AVNRT - normal except tachycardia • Wolff-Parkinson-White o Tachycardia o Secondary cardiomyopathy (S3 gallop, RV heave, displaced apex beat)

Answer 169

• ECG o Differentiating between AVNRT and AVRT - once the SVT has been terminated and normal rate and rhythm are re-established: • AVNRT - appears normal • AVRT - delta-waves (slurred upstroke of the QRS complex) o 24 hr ECG monitoring - will be required in patients with paroxysmal palpitations • Cardiac Enzymes o Check for features of MI (especially if there is chest pain) • Electrolytes - can cause arrhythmia • TFTs - can cause arrhythmia • Digoxin Level - for patients on digoxin • Echocardiogram - check for structural heart disease

Answer 170

• If Haemodynamically UNSTABLE o DC cardioversion • If Haemodynamically STABLE --> vagal monouevres + chemical cardioversion o Vagal manoeuvres (e.g. Valsalva, carotid massage) • Carotid massage could dislodge atherosclerotic plaques, so is only performed in young patients If Vagal manoeuvres fail: o Adenosine 6 mg bolus (can increase to 12 mg) • Contraindicated in ASTHMA as it can cause bronchospasm o Can give verapamil 2.5 - 5 mg if unsuccessful/adenosine contraindicated due to asthma o Alternatives: atenolol, amiodarone • If unresponsive to chemical cardioversion or tachycardia > 250 bpm or adverse signs (low BP, heart failure, low consciousness) o Sedate and synchronised DC cardioversion o Amiodarone • Ongoing management of SVT o AVNRT • Radiofrequency ablation of slow pathway • Beta-blockers • Alternatives: fleicanide, propafenone, verapamil o AVRT • Radiofrequency ablation o Sinus Tachycardia • Exclude secondary cause (e.g. hyperthyroidism) • Beta-blocker or rate-limiting CCB

Answer 171

* Haemodynamic collapse * DVT * Systemic embolism * Cardiac tamponade

Answer 172

* Dependent on the presence of underlying structural heart disease * If structurally normal heart - GOOD PROGNOSIS * People with pre-excitation have a small risk of sudden death

Answer 173

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

Answer 174

• Congenital o Ebstein's anomaly (malpositioned tricuspid valve) o Cleft valve in ostium primum • Functional o Consequence of right ventricular dilation (e.g. due to pulmonary hypertension) o Valve prolapse • Rheumatic Heart Disease • Infective Endocarditis • Other: carcinoid syndrome, trauma, cirrhosis, iatrogenic

Answer 175

* Differs based on cause | * Infective endocarditis is the MOST COMMON cause

Answer 176

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

Answer 177

• Pulse - irregularly irregular if AF • Inspection o Raised JVP with giant V waves (which may oscillate the earlobes) o This is caused by transmission of high right ventricular pressures into the great veins o Giant A waves may also be present • Palpation - parasternal heave • Auscultation o Pansystolic murmur - heard best at lower left sternal edge o Louder on inspiration (Carvallo sign) o Loud P2 component of second heart sound • Chest Examination may show signs of: o Pleural effusion o Causes of pulmonary hypertension • Abdominal Examination may show: o Palpable liver (tender, smooth and pulsatile) o Ascites • Legs - pitting oedema

Answer 178

• Bloods o FBC o LFT o Cardiac enzymes o Blood cultures • ECG o P pulmonale - due to right atrial hypertrophy • CXR o Right-sided enlargement of cardiac shadow • Echocardiography o Extent of regurgitation can be estimated using Doppler ultrasound o May show valve prolapse and right ventricular dilation • Right Heart Catheterisation o Rarely necessary but may be useful for assessing pulmonary artery pressure

Answer 179

• Veins that become prominently elongated, dilated and tortuous, most commonly the superficial veins of the lower limbs.

Answer 180

``` • Primary o Due to genetic or developmental weakness in the vein wall o Results in increased elasticity, dilatation and valvular incompetence • Secondary o Due to venous outflow obstruction • Pregnancy • Pelvic malignancy • Ovarian cysts • Ascites • Lymphadenopathy • Retroperitoneal fibrosis o Due to valve damage (e.g. after DVT) o Due to high flow (e.g. arteriovenous fistula) • RISK FACTORS o Age o Female o Family history o Caucasian o Obesity ```

Answer 181

* COMMON * Incidence increases with age * 10-15% of men * 20-25% of women

Answer 182

* Patients may complain about the cosmetic appearance * Aching in the legs * Aching is worse towards the end of the day of after standing for long periods of time * Swelling * Itching * Bleeding * Infection * Ulceration

Answer 183

• Inspection o Inspect when the patient is standing • Palpation o May feel fascial defects along the veins o Cough impulse may be felt over the saphenofemoral junction o Tap Test - tapping over the saphenofemoral junction will lead to an impulse felt distally (this would not happen if the valves were competent) o Palpation of a thrill or auscultation of a bruit would suggest an AV fistula • Trendelenburg Test o Allows localisation of the sites of valvular incompetence o Leg is elevated and the veins are emptied o A hand is placed over the saphenofemoral junction o The leg is put back down and filling of the veins is observed before and after the hand is released from the saphenofemoral junction o A Doppler ultrasound can be used to show saphenofemoral incompetence • Rectal or Pelvic Examination o If secondary causes are suspected • Signs of Venous Insufficiency o Varicose eczema o Haemosiderin staining o Atrophie blanche o Lipodermatosclerosis o Oedema o Ulceration

Answer 184

• Duplex Ultrasound o Locates sites of incompetence or reflux o Allows exclusion of DVT

Answer 185

``` • Conservative o Exercise - improves skeletal muscle pump o Elevation of legs at rest o Support stockings • Venous Telangiectasia and Reticular Veins o Laser sclerotherapy o Microinjection sclerotherapy • Surgical o Saphenofemoral ligation o Stripping of the long saphenous vein ``` o Avulsion of varicosities o NOTE: short saphenous vein isn't stripped because of the risk of damaging the sural nerve

Answer 186

``` • Venous pigmentation • Eczema • Lipodermatosclerosis • Superficial thrombophlebitis • Venous ulceration • Complications of Treatment o Sclerotherapy - skin staining, local scarring o Surgery - haemorrhage, infection, recurrence, paraesthesia, peroneal nerve injury ```

Answer 187

* Slowly progressive | * High recurrence rates

Answer 188

• Loss of consciousness due to a transient drop in blood flow to the brain caused by excessive vagal discharge.

Answer 189

``` • Vasovagal syncope is a very common cause of fainting • Can be precipitated by: o Emotions (e.g. fear, severe pain, blood phobia) o Orthostatic stress (e.g. prolonged standing, hot weather) ```

Answer 190

* VERY COMMON | * Syncope (of all causes) affects 40% of people

Answer 191

* Loss of consciousness lasting a short time * Patients may experience vagal symptoms (sweating, dizziness, light-headedness) before passing out * There may be some twitching of limbs during the blackout * Recovery is normally very quick

Answer 192

• Usually NO SIGNS

Answer 193

• Investigations are involved with checking for other causes of syncope o ECG - check for arrhythmia o Echocardiogram - check for outflow obstruction o Lying/standing blood pressure - check for orthostatic hypotension o Fasting blood glucose - check for DM/hypoglycaemia

Answer 194

• Large, shallow, sometimes painful ulcers usually found superior to the medial malleoli. They are caused by incompetent valves in the lower limbs leading to venous stasis and ulceration.

Answer 195

``` • They are caused by incompetent valves in the lower limbs • Valve incompetence leads to venous stasis and increased venous pressure • This results in ulceration • Risk Factors o Obesity o Immobility o Recurrent DVT o Varicose veins o Previous injury/surgery to the leg o Age ```

Answer 196

* VERY COMMON | * Increases with age

Answer 197

``` • Large, shallow, relatively painless ulcer with an irregular margin situated above the medial malleoli (most of the time) • Features of the history: o Varicose veins o DVT o Phlebitis o Fracture, trauma or surgery o Family history o Other symptoms of venous insufficiency: • Swelling • Itching • Aching ```

Answer 198

``` • Described above • Other signs of venous ulcers: o Stasis eczema o Lipodermatosclerosis (inverted champagne bottle sign if SEVERE) o Haemosiderin deposition (dark colour) ```

Answer 199

• ABPI o Exclude arterial ulcer o If ABPI < 0.8 - do NOT apply a pressure bandage as this could worsen the ulcer • Measure surface area of ulcer - allows monitoring of progression • Swabs for microbiology - if signs of infection • Biopsy - if possibility of Marjolin's ulcer

Answer 200

• Graduated compression (reduced venous stasis) o NOTE: must exclude diabetes, neuropathy and PVD before this is attempted • Debridement and cleaning • Antibiotics - if infected • Topical steroids - may help with surrounding dermatitis

Answer 201

* Recurrence | * Infection

Answer 202

* GOOD | * Results are better if patients are mobile with few comorbidities

Answer 203

• An irregular broad-complex tachycardia that can cause cardiac arrest and sudden cardiac death

Answer 204

``` • The ventricular fibres contract randomly causing complete failure of ventricular function • Most cases occur in patients with underlying heart disease • Risk Factors o Coronary artery disease o AF o Hypoxia o Ischaemia o Pre-excitation syndrome ```

Answer 205

* The MOST COMMON arrhythmia identified in cardiac arrest patients * Incidence of VF parallels the incidence of ischaemic heart disease

Answer 206

``` • History of: o Chest pain o Fatigue o Palpitations • There may be known pre-existing conditions: o Coronary artery disease o Cardiomyopathy o Valvular heart disease o Long QT syndrome o Wolff-Parkinson-White syndrome o Brugada syndrome ```

Answer 207

* ECG * Cardiac enzymes (e.g. troponins) - check for recent ischaemic event * Electrolytes - derangement can cause arrhythmias, including VF * Drug levels and toxicology screen - anti-arrhythmics can (ironically) cause arrhythmia, as can various recreational drugs (e.g. cocaine) * TFTs - hyperthyroidism can cause tachyarrhythmias * Coronary angiography - if patient survives VF, to check the integrity of coronary arteries

Answer 208

* VF requires urgent defibrillation and cardioversion * Patients who survive need full assessment of left ventricular function, myocardial perfusion and electrophysiological stability * Most survivors will need an implantable cardioverter defibrillator (ICD) * Empirical beta-blockers * Some patients may be treated with radiofrequency ablation (RFA)

Answer 209

* Ischaemic brain injury due to loss of cardiac output * Myocardial injury * Post-defibrillation arrhythmias * Aspiration pneumonia * Skin burns * Death

Answer 210

* Depends on the time between onset of VF and medical intervention * Early defibrillation is essential (ideally within 4-6 mins) * Anoxic encephalopathy is a major outcome of VF

Answer 211

• A regular broad-complex tachycardia originating from a ventricular ectopic focus. The rate is usually > 120 bpm.

Answer 212

• Electrical impulses arise from a ventricular ectopic focus • Risk Factors o Coronary heart disease o Structural heart disease o Electrolyte deficiencies (e.g. hypokalaemia, hypocalcaemia, hypomagnesaemia) o Use of stimulant drugs (e.g. caffeine, cocaine)

Answer 213

* Fairly common * It is one of the shockable rhythms that is seen in cardiac arrest patients * VT incidence peaks in the middle decades of life

Answer 214

``` • Symptoms of ischaemic heart disease or haemodynamic compromise due to poor perfusion • Symptoms: o Chest pain o Palpitations o Dyspnoea o Syncope ```

Answer 215

``` • Signs are dependent on the degree of haemodynamic instability o Respiratory distress o Bibasal crackles o Raised JVP o Hypotension o Anxiety o Agitation o Lethargy o Coma ```

Answer 216

• ECG o It can sometimes be difficult to distinguish between VT and SVT with aberrant conduction o If in doubt, treat as a VT o ECG Features: • Rate > 100 bpm • Broad QRS complexes • AV dissociation • Electrolytes - derangement can cause arrhythmias • Drug levels - e.g. check for digoxin toxicity • Cardiac enzymes - e.g. troponins to check for recent ischaemic event

Answer 217

• ABC approach • CHECK WHETHER THE PATIENT HAS A PULSE OR NOT • Pulseless VT - follow advanced life support algorithm • Unstable VT - reduced cardiac output o NOTE: VF and pulseless VT require defibrillation (unsynchronised), but other VTs can be treated with synchronised cardioversion o Correct electrolyte abnormalities o Amiodarone • Stable VT o These patients DO NOT experience symptoms of haemodynamic compromise o Correct electrolyte abnormalities o Amiodarone o Synchronised DC shock (if steps above are unsuccessful) • Implantable Cardioverter Defibrillator (ICD) o ICD is considered if: • Sustained VT causing syncope • Sustained VT with ejection fraction < 35% • Previous cardiac arrest due to VT or VF • MI complicated by non-sustained VT

Answer 218

* Congestive cardiac failure * Cardiogenic shock * VT may deteriorate into VF

Answer 219

* GOOD if treated RAPIDLY | * Long-term prognosis depends on the underlying cause

Answer 220

• A congenital abnormality which can result in supraventricular tachycardias that use an accessory pathway. It is a pre-excitation syndrome.

Answer 221

• The accessory pathway (bundle of Kent) is likely to be congenital • Associations: o Congenital cardiac defects o Ebstein's anomaly (congenital malformation of the heart characterised by displacement of septal and posterior tricuspid leaflets) o Mitral valve prolapse o Cardiomyopathies (e.g. HOCM)

Answer 222

* Relatively COMMON * Most common of the ventricular pre-excitation syndromes * Found in ALL AGES * More common in the YOUNG * Prevalence decreases with age

Answer 223

• SVT may occur in early childhood • Often ASYMPTOMATIC - may be an incidental finding of an ECG • Symptoms: o Palpitations o Light-headedness o Syncope • Paroxysmal SVT may be followed by a period of polyuria, due to atrial dilatation and release of ANP • Sudden death - if SVT deteriorates into VF • Clinical features of associated cardiac defects (e.g. mitral valve prolapse, cardiomyopathy)

Answer 224

• ECG may be normal if the conduction speed of the impulse along the accessory pathway matches the conduction speed down the bundle of His • Classic ECG findings: o Short PR interval o Broad QRS complex o Slurred upstroke producing a delta wave • Patient may be in SVT (AVRT) • Bloods - check for other causes of arrhythmia • Echocardiogram - check for structural heart defects