Cardiology COPY Flashcards

Question

Define Dressler's syndrome

Answer 1

* Post-MI syndrome, usually 2-3 weeks after * Caused by localised autoimmune response, pericarditis * Presentation * Fever * Pleuritic chest pain * Pericardial effusions * Anaemia * Raised ESR * Cardiomegaly on CXR * Pericardial rub on auscultation * ECG - global ST elevation and T wave inversion * Management - NSAIDs, steroids, pericardiocentesis? Usually self limiting

Answer 2

* Stop smoking * Reduce alcohol consumption * Mediterranean diet * Cardiac rehabilitation (a specific exercise regime for patients post MI) * Optimise treatment of other medical conditions (e.g. diabetes and hypertension)

Answer 3

Type 1: Traditional MI due to an acute coronary event Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension) Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event Type 4: MI associated with PCI / coronary stunting / CABG

Answer 4

* Manifestation of coronary artery disease (ischaemic heart disease) * Symptoms of insufficient blood supply to myocardium (ischaemia without infarct), brought on by exertion and relieved by GTN spray + rest * Differentiated from unstable angina - comes on at rest, not relieved by GTN/time

Answer 5

* Central or left sided chest discomfort - may radiate to jaw, arm * Can very from mild --\> severe * Tight/crushing nature * Dyspnoea * Usually brought on by exertion, relieved by rest * Duration - several minutes

Answer 6

* Same causes as ACS * Atheroma of coronary arteries * Aortic valve disease * Hypertrophic cardiomyopathy

Answer 7

* Physical examination - heart sounds, signs of HF * Bloods * ECG - rule out ACS, may have changes e.g. Q waves, ST depression, LBBB, T-wave flattening/inversion * FBC - anaemia * U&Es - prior to contrast in CT coronary angiography and other medications * LFTs * Lipid profile * TFTs * HbA1c and fasting glucose * Confirm diagnosis with imaging * CT coronary angiogram - gold-standard investigation * CXR - other causes of chest pain, signs of heart failure * Echo - left ventricular function + heart anatomy

Answer 8

* Refer to cardiology - urgently if unstable * Advise patient about diagnosis and when to call ambulance * Medical management * Immediate symptomatic relief - GTN * Long term symptomatic relief - beta-blocker or calcium channel blocker * Secondary prevention - aspirin (75mg once daily), statin (atorvastatin 80mg once daily), ACE inhibitor, beta-blocker (already on for symptomatic relief) * Procedural/surgical interventions * PCA with coronary angioplasty - offered to patients with proximal or extensive disease on CT coronary angiography * Coronary artery bypass graft (CABG) offered to patients with severe stenosis (midline sternotomy, associated with greater complications)

Answer 9

Clinical syndrome in which the heart is unable to pump adequate amounts of blood to meet the body's metabolic demand.

Answer 10

* Systolic HF - inability of the heart to contract efficiently to eject adequate volumes of blood to meet the bodies metabolic demand, most common * Diastolic HF - reduction in heart compliance resulting in compromised ventricular filling and therefore ejection * Left HF - inability of left ventricle to pump adequate amount of blood leading to pulmonary circulation congestion and pulmonary oedema * Ejection fraction of \<40% * Right HF - inability of right ventricle to pump adequate amount of blood leading to systemic venous congstion, therefore peripheral oedema and hepatic congestion * Most commonly due to respiratory disease e.g. COPD * Raised JVP and peripheral oedema indicate right HF * Congestive HF - failure of both right and left ventricles, common * Acute HF - acute onset of symptoms usually due to an acute event e.g. MI, ventricular aneurysm * Chronic HGF - slow symptom presentation usually due to slow progressive underlying disease * Acute-on-chronic - acute deterioration of a chronic condition usually following an acute event (infections, MI)

Answer 11

* Ischaemic heart disease - causes impaired ventricular function, reduced contractility * Myocardial ischaemia * Myocardial infarction * Hypertension - increases strain on heart, leads to hypertrophy which has risk of arrhythmia, heart gets too big for coronary system to perfuse * Valvular disease * Mitral/tricuspid regurgitation - volume overload * Aortic stenosis - pressure overload * Pericardial disease - pericarditis, pericardial effusion * Drugs * Beta-blocks, calcium channel blockers, anti-arrhythmics * Alcohol - AF, dilated cardiomyopathy * Cocaine * Arrhythmias * Bradycardia * Tachycardia - reduced ventricular filling, increased heart oxygen demand * AF - less ventricular filling * Cardiomyopathies * Congestive - weakening and dilation of ventricular wall leading to overstretching and reduced contractile efficiency * Hypertrophic - thickening of heart muscle wall leading to reduced compliance and reduced cardiac output * Restrictive - sarcoidosis, amyloidosis, haemochromatosis * Severe anaemia * Pulmonary hypertension - pulmonary pathologies e.g. COPD

Answer 12

* Age * Family history and genetics * Lifestyle - diet, smoking, cocaine use, alcohol, lack of physical activity * Serious lung disease * Obesity * HTN * Diabetes * CKD * Anaemia * Race/ethnicity - Afrocaribbean people more at risk * Sex - men develop at a younger age, more likely to have reduced ejection fraction (women have preserved ejection fraction more commonly, more symptomatic)

Answer 13

* Drop in cardiac output - reduced sensed volume * Increased vagal and sympathetic tone to increase heart contractility and rate therefore output * Vasoconstriction of veins and arteries * Release of adrenaline * Low kidney perfusion (due to reduced CO) stimulates RAS, angiotensin II causes vasoconstriction, aldosterone release and ADH causing sodium and waer retention by kidneys * These mechanisms are initially beneficial to increase blood volume, therefore venous return and CO, but chronically worsen the situation by increasing the workload and strain on the heart, increased oxygen demand on the heart and fluid retention * Fluid retention --\> movement of fluid into interstitial tissue causing peripheral and pulmonary oedema

Answer 14

* Dyspnoea - especially on exertion, due to pulmonary oedema and respiratory muscle weakness * Orthopnoea - breathlessness on lying flat * Paroxysmal nocturnal duspnoea - occurs lying down/sleeping causing sudden awakening * Fatigue, lethargy and exercise intolerance * Inability of heart to raise CO during exercise * Tissue hypoperfusion e.g. muscle * Peripheral oedema - swollen ankles * Weight loss * Wheeze * Cough - often worse at night, classic sign is pink frothy sputum

Answer 15

* Fluid overload * Peripheral oedema - ankles +/- sacrum, pitting oedema * Ascites * Elevated JVP * Hypotension * Tachycardia * Cardiac heave * Displaced apex beat - sign of cardiomegaly * Bilateral crepitations +/- wheeze * Cachexia * Hepatic tenderness/hepatomegaly

Answer 16

* Clinical presentation * Bloods - FBC (anaemia), U&Es (hyponatraemia due to dilution), LFTs (extent of liver congestion/damage), BNP (NT-proBNP), TFTs (rule out thyrotoxicosis), HbA1c (diabetes) * Echocardiogram * Reduced ejection fraction, structural/functional abnormalities of heart * ECG - may indicate cause of HF * MI * BBB * Ventricular hypertrophy * Pericardial disease * Arrhythmias * CXR - signs of pulmonary congestion * Angiography - assess extent of IHD

Answer 17

* Cardiomegaly - heart size \>1/2 thoracic cavity (cardiothoracic ratio \>0.5) * Must be PA X-ray to assess heart size * Kerley B lines - interstitial oedema * Pleural effusions * Upper zone vessel enlargement * Alveolar oedema (bat-wing opacities)

Answer 18

* New York Heart Association Classification (1 year mortality) * Grade I (5%) - no limitation on function * Grade II (10%) - slight limitation, moderate exertion causes symptoms, no symptoms at rest * Grade III (20%) - marked limitation, mild exertion causes symptoms, no marked symptoms at rest * Grade IV (50%) - severe limitation, any exertion causes symptoms, may also have symptoms at rest

Answer 19

* Muscle underperfusion - muscle weakness and atrophy causing fatigue, exercise intolerance and dyspnoea * Increased risk of thromboembolism and strokes due to blood stasis, arrhythmias and atheromas * Arrhythmias e.g. ventricular tachycardia in advanced HF --\> ventricular arrhythmias and cardiac arrest * Increased infection risk - can initiate acute on chronic event * Depression and impaired quality of life * Sudden cardiac death * Poor prognosis - 50% mortality within 5 years of diagnosis

Answer 20

* Refer to specialist (urgent if NT-proBNP \>2,000ng/L) * Heart failure specialist nurse input * Lifestyle measures * Stop smoking * Exercise if tolerated * Reduce salt * Fluid restriction * Reduce alcohol intake * Flu vaccination yearly * Medical management * ACE inhibitor e.g. ramipril titrated as tolerated up to 10mg once daily * Beta blocker e.g. bisoprolol titrated as tolerated up to 10mg once daily * Aldosterone antagonist when symptoms not controlled by ACEI/B-blocker (spironolactone or eplerenone) * Loop diuretics improves symptoms in acute fluid overload e.g. furosemide 40mg once daily * Other drugs used with specialist input e.g. digoxin, calcium channel blocker, (amlodipine) ivabridine, angiotensin receptor neprilysin inhibitor (ARNI) * Surgical intervention * Revascularisation in IHD - CABG or angioplasty * Valvular replacement * Implanted automatic cardiodefibrillator or pacemkaer * Heart transplant considered in end stages

Answer 21

* Usually presents with dyspnoea, anxiety and tachycardia * Sit upright, 100% oxygen flow * Do an ECG, FBC, U&Es, cardiac enzymes, ABG, CXR * Sublingual 2 puffs nitrates or oral to enhance myocardial perfusion * IV opiates to reduce anxiety and preload * IV furosemide 40-80mg to reduce fluid retention * If systolic \>90 give IV isosorbide dinitrate 2-10mg/h, if systolic \<90 treat as cardiogenic shock

Answer 22

* Improve prognosis * ACEi * B1 beta blockers e.g. bisoprolol, atenolol, carvedilol * Angiotensin-II receptor antagonists * Spironolactone * Improve symptoms * Loop diuretics * Digoxin * Vasodilators e.g. nitrates, hydralazine

Answer 23

* Diuretics - renal function monitored * ACE inhibitors - U&Es before treatment then after 1-2 weeks of treatment * Beta-blockers - monitor heart rate and BP when adjusting dose * ARBs - must have normal serum potassium and adequate renal function to commence

Answer 24

Infection of the endocardium by bacteria, or rarely fungi. Most commonly affects heart valves (natural or prosthetic), but can occur anywhere along the lining of the heart or blood vessels. Formation of vegetation, resulting in damage to endocardium.

Answer 25

1. Mitral valve 2. Aortic valve 3. Tricuspid valve - most common site in IVDU 4. Pulmonary valve (rare)

Answer 26

* Underlying valve abnormalities in 55-75% * Aortic stenosis * Mitral valve prolapse * Previous rheumatic heart disease * Age related valvular degeneration * Prosthetic valve - both mechanical and bioprostheses * IVDU - often tricuspid valve and right side of heart, can be multiple organisms, often more sub-acute insidious onset * No identifiable risk factors in 30%

Answer 27

* Endocardial damage occurs at areas of high haemodynamic pressure (higher shearing forces on endocardium) * Heart valves * Mostly left side (higher pressure blood flow) except IVDU * Thrombi form at damaged site, mainly made of platelets and fibrin, initially sterile ('sterile vegetations') * At times of transient bacteraemia (e.g. from poor oral hygiene, UTIs, other GU infections, IV drug injection, soft tissue infection, cannulae, cardiac surgery) bacteria can colonise the thrombi --\> vegetation * Vegetations can break off to form emboli and cause an obstruction, commonly affect CNS, lungs, spleen, kidneys, liver * Vegetation forms biofilm (especially on prosthetic valves) - difficult for antibiotics to penetrate and treat

Answer 28

* Native valve infection * Strep species - Strep viridans * Enterococci * IVDU * Staph. aureus * Higher incidence of gram negative organisms (HACEK, enterobacteriacaea, psuedomonas auerginosa) and fungal organisms * Prosthetic valve infections * Coagulative negative staphylococci - good at forming biofilm * Gram negative and fungal infection more common Streptococcal endocarditis, especially caused by viridans present more indolently - subacute endocarditis Staph. aureus, gram negative and fungal endocarditis present acutely, causing rapid valve destruction

Answer 29

1. Streptococcus pyogenes infection (e.g. strep throat) 2. Infection partially/not treated 3. Liberation of Streptolysin 'O' exotoxin 4. Anti-Streptolysin O antibodies produced against Streptolysin 5. Cross-reactivity of antibodies - cardiac valves have similar antigenic structure so antibodies attack valves 6. Stenosis or regurgitation of valves

Answer 30

* Classed as separate entity due to tendency to involve right-sided valves * Right sided due to: * Particulate induced endothelial damage to right-sided valves * Increased bacterial loads in these patients * Direct physiologic effects of injected drugs * Deficient immune response caused by IVDU * Tricuspid valve endocarditis more common than aortic or mitral (do occasionally occur) * Underlying valve normal in 75-93%, repeated bouts of IE in an IVDU will lead to gradual increase in structural abnormalities of the valve

Answer 31

* Acute - valve destruction and systemic infection developing over days to weeks * Subacute - presentation over weeks to months, rarely leads to systemic infection 1. Early manifestations of infection * Fever and new mumur - IE until proven otherwise * Fatigue and malaise 2. Embolic events * Can take days-weeks to occur * Seen earlier in acute endocarditis * Small emboli * Petechiae * Splinter haemorrhages * Janeway lesions - non-tender, small erythematous or haemorrhagic or nodular lesions on palm or sole due to septic emboli * Haematuria * Large emboli * CVA * Renal infarction * Right sided endocarditis - tricuspid valve involvement * Septic pulmonary emboli - pleuritic chest pain and classical CXR appearance 3. Long-term effects * Immunological reaction * Splenomegaly * Nephritis * Vasculitic lesions of skin and eye * Osler's nodes - painful palpable lesions on hands and feet * Clubbing * Tissue damage (seen more in acute endocarditis) * Valve destruction * Valve abscess - aortic root abscess, high mortality, need surgical intervention

Answer 32

* Local trauma * Crying - petechiae around eyes * Vasculitis e.g. IE * Thrombocytopaenia * Malignancy * Viral infection - particularly in children * Leukaemia * Typhus

Answer 33

Duke Criteria Major criteria * Positive blood culture for infective organism (on 2 separate tests if \>12 hours apart, or on 3/3 or 3/4 tests \>1 hour apart) * Evidence of IE from other tests * Echocardiogram shows - strictures, unusual blood flow, implanted/unusual material, abscesses * New valve regurgitation Minor criteria * Fever \>38 degrees * Risk factor for IE e.g. IVDU, congenital heart condition, prosthetic valve * Usual echo, but not findings stated above * Immunological factors present - Roth spots, Osler's nodes, glomerulonephritis, rheumatoid factor * Blood cultures positive but major criteria not satisfied * Vascular abnormalities, embolism, aneurysm, infarcts, conjunctival haemorrhage, intracranial haemorrhage etc. IE definitely present * 2 major criteria present OR * 1 major, 3 minor criteria OR * 5 minor criteria IE possibly present * 1-4 minor criteria AND * No other more likely diagnosis

Answer 34

* Blood cultures * Constant bacteraemia so no need to wait for fever * 3 sets of blood cultures required - if organism only found in one could be due to contamination * Volume most important factor in organism detection - 10mls/bottle required * Before antibiotics * Aseptic technique - reduce risk of contamination and risk of needle stick injury * Echocardiogram * Transthoracic - non-invasive, 50% sensitivity * Transoesophageal - invasive, 85-100% sensitivity * Transthoracic performed first, if negative and high clinical suspicious remains, transoesophageal indicated * Duke criteria * Other bloods * FBC - might have anaemia of chronic disease, raised WCC, thrombocytopaenia or thrombocytosis * U&Es - renal dysfunction common due to emboli * LFTs - ALP raied * Inflammatory markers - CRP and ESR likely raised * Urine - haematuria, proteinuria common * ECG - new AV block suggestive of abscess formation * CXR - evidence of heart failure, cardiomegaly, pulmonary emboli and/or abcesses (right sided)

Answer 35

* Medical - antimicrobial therapy * Surgical - valve replacement, partial valve repair

Answer 36

* Heart failure * Uncontrollable infection * Abscess, false aneurysm, enlarging vegetation (urgent) * Persisting fever and positive blood cultures \>7 days * Infection caused by multi-drug resistant organisms * Prevention of embolism * Large vegetations (\>10mm) and embolic episode

Answer 37

* High dose antibiotics * Treatment tailored to organism susceptibility * Duration of therapy * Native valves - 4 weeks * Prosthetic valves - 6 weeks * IV therapy for duration in most cases - oral may not penetrate vegetations * Empirical therapy * Native - IV amoxicillin + IV flucloxicillin + IV gentamicin (vancomycin + gentamicin in penicillin/beta-lactam allergy) * Prosthetic - IV vancomycin + IV gentamicin

Answer 38

1. Benzylpenicillin +/- gentamicin 2. Amoxicillin or vancomycin +/- gentamicin 3. Flucloxacillin +/- gentamicin 4. Vancomycin +/- gentamicin 5. Vancomycin +/- gentamicin +/- rifampicin Organisms often intrinsically resistant to gentamicin, but pencillin/vancomycin act by destroying the bacterial cell wall, which allows the gentamicin to exert its effect --\> synergy

Answer 39

High BP BP \>140/90 in clinic or \>135/85 with ambulatory or home readings Mild (Grade 1) - SBP 140-159 or DBP 90-99 Moderate (Grade 2) - SBP 160-179 or DBP 100-109 Severe (Grade 3) - SBP \>180 or DBP \>110

Answer 40

* Majority of cases have no identifiable cause = essential/primary hypertension * Genetic influences + environmental factors * Defects in renal sodium haemostasis - inadequate sodium excretion --\> salt and water retention --\> increased plasma and extracellular fluid volume --\> increased cardiac output * Functional vasoconstriction + increased natriuretic hormone --\> increased vascular reactivity --\> increased total peripheral resistance * Defects in vascular smooth muscle growth and structure --\> increased vascular wall thickness --\> increased total peripheral resistance * Environmental factors * Obesity * Sleep apnoea * Alcohol intake * Sodium intake * Stress * Insulin intolerance * Due to identifiable disease process = secondary hypertension * Renal disease * Endocrine disease - Cushing's syndrome, Conn's syndrome, adrenal hyperplasia, phaeochromocytoma, acromegaly * Congenital disease - coarctation of the aorta * Neurological disease - raised intracranial pressure, brainstem lesions * Pregnancy - pre-eclampsia * Drugs - OCP, steroids, NSAIDs, EPO

Answer 41

* Increased peripheral vascular resistance * Atherosclerosis - endothelial damage * Microaneurysms in the brain (Charcot-Bouchard aneurysms) --\> haemorrhagic stroke * Cardiovascular events * Atherosclerosis * Aortic aneurysm * Cardiac failure * Atrial fibrillation * Cerebrovascular events i.e. haemorrhage or clot * Renal effects - renal failure and other renal problems * Eye effects * Visual disturbance due to papilloedema and retinal haemorrhages

Answer 42

* Non-modifiable * Age * Gender * Ethnicity * Genetic factors * Modifiable * Diet * Physical activity * Obesity * Alcohol in excess * Stress

Answer 43

* Usually asymptomatic and discovered incidentally * May have headaches * Epistaxis (nosebleeds) but very uncommon and only if BP is very high * Signs * Coarctation of aorta can cause radio-femoral delay * Renal artery bruits

Answer 44

* BP should be measured every 5 years to screen for hypertension, more in patients on the borderline for diagnosis (\>135/85 - annual review) and every year for patients with type 2 diabetes * Patients with clinical blood pressure between 140/90 and 180/20 should have 24 hour ambulatory blood pressure or home readings to confirm the diagnosis * Also should measure in both arms, if difference is more than 15mmHg use the reading from the arm with the higher pressure * Should be investigated for evidence of target organ damage * Bloods - HbA1c, U&Es, cholesterol * Urinalysis - haematuria, proteinuria * ECG - left ventricular hypertrophy * Check fundi for evidence of retinopathy * CXR if evidence of coarctation * Aldosterone for primary aldosteronism

Answer 45

Aim to get BP to less than 140/90, in high risk populations may benefit from lower (120/80) to reduce CV risk * If ambulatory or home BP \>135/85 and not high risk - lifestyle intervention and annual review * Ambulatory or home BP \>135/85 and high risk or 10 year CV risk \>20% - initiate drug treatment and lifestyle intervention * SBP 160-179 and/or DBP 100-109 (and unchanged on ambulatory or home monitoring) - initiate drug treatment and lifestyle intervention * Clinic SBP \>180 or DBP \>110 and no evidence of papilloedema or retinal exudates or haemorrhages - initiate drug treatment and lifestyle intervention * Clinic SBP \>180 or DBP \>110 and evidence of papilloedema or retinal exudates or haemorrhages - refer urgently

Answer 46

* Target organ damage * Known cardiovascular disease * Previous stroke or TIA * Renal disease * Diabetes mellitus

Answer 47

* Aim for healthy BMI * Exercise * Healthy diet * Reduce alcohol intake * Reduce salt intake * Stop smoking * Reduce caffeine intake

Answer 48

* \<55 years * Step 1 - ACE inhibitor (or ARB if intolerant to ACE inhibitor - usually dry cough) * Step 2 - ACEi (or ARB) + calcium channel blocker * Step 3 - ACEi (or ARB) + calcium channel blocker + thiazide-type diuretic * Add - further diuretic therapy (spironolactone 25 mg daily if K+ \<4.5mmol/L) or beta blocker * \>55 years or black patients (African or Carribbean) of any age * Step 1 - calcium channel blocker * Step 2 - ACEi (or ARB) + calcium channel blocker * Step 3 - ACEi (or ARB) + calcium channel blocker + thiazide type diuretic * Add - further diuretic therapy (spironolactone 25 mg daily if K+ \<4.5mmol/L) or beta blocker ACEi e.g. ramipril 1.25-10mg once daily ARB e.g. candesartan 8mg-32mg once daily Calcium channel blocker e.g. amlodipine 5-10mg once daily Thiazide diuretic e.g. indapamide 2.5mg once daily Beta blocker e.g. bisoprolol 5-20mg once daily

Answer 49

* Uncoordinated, rapid and irregularly contraction of the atria * Due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node * Disorganised electrical activity in the atria leads to irregular conduction of electrical impulses to the ventricles, resulting in * Irregularly irregular ventricular contractions * Tachycardia * Heart failure due to poor filling of the ventricles during diastole * Risk of stroke - disorgansed atrial contractions lead to clot formation, can embolise and travel to the brain, blocking the cerebral arteries

Answer 50

* Obesity * Hypertension * T2DM * Smoking * Obstructive sleep apnoea * Coronary artery disease * Valvular heart disease * Heart failure * CKD * Alcohol excess * Hyperthyroidism * Sepsis * Electrolyte abnormalities

Answer 51

* Cardiac * Heart failure * Heart ischaemia - MI * Hypertension * Mitral valve disease * Congenital heart disease * Pulmonary * PE * Pneumonia * Bronchocarcinoma * Other * Hyperthyroidism (fast AF) * Alcohol * Post-operatively * Sepsis * High caffeine intake * Antiarrhythmic drugs * Hypokalaemia * Hypermagnesaemia

Answer 52

* Often asymptomatic, incidentally discovered * Presenting symptoms * Palpitations * Shortness of breath * Syncope * Chest pain * Symptoms of associated conditions e.g. stroke, sepsis or thyrotoxicosis * Signs * Irregularly irregular pulse (also caused by ventricular ectopics, but these disappear above a certain heart rate, normal pulse when exercising)

Answer 53

* No p waves * Irregular baseline * Irregularly irregular QRS complexes * Tachycardia * Normal shape QRS - narrow (because conduction through the AV node is normal) * Normal T waves

Answer 54

* ECG * Bloods - U&Es, TFTs, cardiac enzymes, calcium, magnesium and phosphate * Consider ambulatory ECG * Echocardiogram to assess structural heart disease (transthoracic)

Answer 55

* Identify risk factors and reversible causes * Rate or rhythm control * Anticoagulation to prevent complications e.g. stroke

Answer 56

* Beneficial to reduce rate to allow proper ventricular filling and increase cardiac output * Rate control is first line unless * There is a revesible cause of AF * AF is now onset (with 48 hours) * AF is causing heart failure * Symptomatic despite effective rate control * Options * First-line: beta-blocker e.g. atenolol 50-100mg once daily * Calcium-channel blocker e.g. diltiazem (not preferable in HF) * Digoxin, only in sedentary people, needs monitoring and risk of toxicity

Answer 57

* Used when rate control is not first line * Reversible cause of AF * New onset \<48 hours * AF causing HF * Symptomatic despite effective rate control * Aim to return patient to normal sinus rhythm - through single cardioversion event or long term medical rhythm control * Cardioversion - * Immediate if AF started 48 hours ago or are haemodynamically unstable * Delayed if AF present for more than 48 hours and they are stable * Should be anticoagulated for a minimum of 3 weeks prior - high risk of mobilising a blood clot with cardioversion * Should have rate control while waiting for cardioversion * Pharmacological cardioversion - flecainde, amiodarone (in structural heart disease) * Electrical cardioversion - cardiac defibrillator to deliver controlled shocks * Long term medical rhythm control * Beta blockers - first line * Dronedarone - maintain normal rhythm when patients have had successful cardioversion * Amiodarone - heart failure or LVD

Answer 58

* Use CHAD-VASc score to assess whether a patient with AF should be started on anticoagulation, score for risk factors * 0 = no anticoagulation * 1 = consider anticoagulation * \>1 = offer anticoagulation * Warfarin * Require INR monitoring and frequent dose adjustments to keep INR in range * Novel anticoagulants (NOACs) e.g. apixaban, dabigatran, rivaroxaban * More expensive than warfarin but don't require INR monitoring * Shorter half life than warfarin so reverse themselves quickly

Answer 59

CHA2DS2-VASc C - congestive heart failure H - hypertension A2 - age \>75 (scores 2) D - diabetes S2 - stroke or TIA previously (scores 2) V - vascular disease A - age 65-74 S - sex (female)

Answer 60

HAS-BLED H - hypertension A - abnormal renal and liver function S - stroke B - bleeding L - labile INRs (while on warfarin) E - elderly D - drugs or alcohol Usually in AF, risk of stroke usually outweights risk of bleeding

Answer 61

* When AF comes and goes in episodes, not usually lasting more than 48 hours * Patients still anticoagulated based on CHAD-VASc score * May be appropriate for 'pill in pocket' approach * Take flecanide to terminate AF when they feel symptoms of AF starting * Need to have infrequent episodes without underlying structural heart disease, and need to have awareness of when they are in AF

Answer 62

* Any tachycardia arisising from above the bundle of His * Usually caused by electrical signal re-entering the atria from the ventricles - causes fast narrow complex tachycardia * 3 main types * Atrioventricular nodal re-entrant tachycardia (AVNRT) - re-entry point through AV node * Atrioventricular nodal re-entrant tachycardia - re-entry point is accessory pathway (Wolff-Parkinson-White syndrome) * Atrial tachycardia - electrical activity originates in atria somewhere other than the SA node, caused by abnormally generated electrical activity in the atria

Answer 63

* Female gender * Occurs at any age and can be in otherwise fit and healthy patients * Precipitated by - caffeine, alcohol, exercise, drugs, beta-agonists, sympathomimetics (amphetamines, hyperthyroidism) * Often no cause identified

Answer 64

Sudden onset, regular palpitations May also have anxiety, shortness of breath

Answer 65

* Tachycardia rate 140-280bpm * Often no p waves as hidden by QRS complexes * Usually narrow QRS complexes * Regular * Sometimes ST depression

Answer 66

* Continuous ECG monitoring * Valsalva manoeuvre e.g. blow into syringe * Carotid sinus massage * Adenosine * Slows cardiac conduction through AV node, resets to sinus rhythm * Avoid if patient has asthma/COPD/heart failure/heart block/severe hypotension * Initially 6mg, then 12mg and further 12mg if no improvement * Alternative to adenosine - verapamil (calcium channel blocker) * Direct current cardioversion

Answer 67

* Medication - beta blockers, calcium channel blockers or amiodarone * Radiofrequency ablation

Answer 68

* Extra pathway connecting the atria and ventricles = Bundle of Kent * ECG * Short PR interval (\<0.12 seconds) * Wide QRS complex (\>0.12 seconds) * Delta wave - slurred upstroke on the QRS complex * Treatment - radiofrequency ablation of the accessory pathway

Answer 69

* Type of polymorphic ventricular tachycardia * Typical ECG characteristics - looks like QRS complex is twisting around the baseline (height gets smaller then larger etc.) * Depolarisations occuring before repolarisation has occurred - prolonged QT * Will either terminate spontaneously and revert to sinus rhythm or progress to ventricular tachycardia (can lead to cardiac arrest)

Answer 70

* Causes * Long QT syndrome (inherited) * Medications - antipsychotics, citalopram, flecanide, sotalol, amiodarone, macrolide antibiotics * Electrolyte disturbance - hypokalaemia, hypomagnesaemia, hypocalcaemia * Acute management of Torsades de pointes * Correct the cause e.g. electrolyte disturbands or medications * Magnesium infection (even if normal serum magnesium) * Defibrillation if VT occurs * Long term management of prolonged QT syndrome * Avoid medications that prolong the QT interval * Correct electrolyte disturbances * Beta blockers - not sotalol * Pacemaker or implantable defibrillator

Answer 71

* Arrhythmia caused by quivering of the ventricles due to disorganised electrical activity * Results in cardiac arrest with loss of consciousness and no pulse --\> cardiac arrest

Answer 72

* Mostly within patients with underlying heart disease e.g. IHD, cardiomyopathy, myocarditis * Electrolyte imbalance * Following near drowning or major trauma * Can also occur idiopathically

Answer 73

* Irregular, fibrillatory baseline, usually \>300bpm * Erratic undulations with indiscernible QRS complexes

Answer 74

CPR with defibrillation (shockable rhythm)

Answer 75

Regular rhythm, rate under 60 bpm

Answer 76

* Seen in healthy people, especially atheletes (due to increased vagal tone) * AV blocking medications - beta-blockers, calcium channel blockers, digoxin * Sick sinus syndrome * Hypothyroidism * Hypothermia * Obstructive sleep apnoea * Hypoglycaemia * Acute MI

Answer 77

* Often tolerated well, asymptomatic * Decreased CO --\> dizziness, hypotension, syncope, dyspnoea on exertion * Can lead to atrial, junctional or ventricular ectopic rhythms

Answer 78

Normal P wave before every QRS complex (sinus rhythm) with ventricular rate of less than 60 bpm

Answer 79

If well tolerated no treatment required If symptomatic e.g. sick sinus syndrome - pacemaker implantation can treat sinus node dysfunction

Answer 80

* First degree - P before every QRS, but PR interval longer than 0.2 seconds * Can be a sign of CAD, acute rheumatic carditis, digoxin toxicity or electrolyte disturbance, doesn't require treatment usually * Second degree - failure of one or more atrial impulses to conduct to the ventricles due to impaired conduction * Type 1 (Mobitz I/Wenckebach) - progressive prolongation of PR intervals followed by blocked P wave (no QRS complex after it), then cycle resets * Fixed number of P waves and QRS complexes per cycle * Almost always due to AV node disease * Type 2 (Mobitz II/Hay) - non-conducted P waves with no PR prolongation before/shortening after * Usually fixed number of non-conducted P waves for every conducted QRS complex * Can progress rapidly to complete heart block * Almost always disease of distal conduction system (His-Purkinje system) * Third degree (complete heart block) - no relationship between P waves and QRS complexes but both are present (more P than QRS complexes) * Causes - MI (acutely), chronic due to fibrosis around bundle of His, or bundle branch block of both branches * Always indicates underlying disease

Answer 81

* Break or tear in intima of aorta, allowing blood to collect between the intima and the media layers - creates a new arterial lumen * Lumen may be stable or rupture * Most commonly affects the ascending aorta and aortic arch, can affect any part * Specifically right lateral area of the ascending aorta - under the most stress from blood exiting the heart * Classification systems * Stanford system * Type A - ascending aorta, before the brachiocephalic artery * Type B - descending aorta, after left subclavian artery * DeBakey system * Type 1 - begins in ascending aorta, involves at least the aortic arch if not whole aorta * Type 2 - isolated to ascending aorta * Type 3a - begins in descending aorta, involves only section above diaphragm * Type 3b - begins in descending aorta, involves the aorta below the diaphragm

Answer 82

* Same as PAD - age, male, smoking, hypertension, poor diet, reduced physical activity, raised cholesterol * Can be triggered by events which cause increase in BP e.g. heavy weightlifting, cocaine use * Conditions/procedures that affect the aortia increase the risk of a dissection e.g. * Bicuspid aortic valve * Coarctation of the aorta * Aortic valve replacement * Coronart artery bypass graft * Conditions that affect connective tissues that increase the risk of a dissection * Ehlers-Danlos syndrome * Marfan's syndrome

Answer 83

* Typical - sudden onset, severe, 'ripping' or 'tearing' chest pain * Anterior chest if ascending aorta affected, back if descending aorta is affected * Pain may migrate over time * May not have any chest pain * Other features * Hypertension * Differences in BP between the arms (\>20mmHg) * Radial pulse deficit - decreased in one arm or absent and does not match apex beat * Diastolic murmur * Focal neurological deficit e.g. limb weakness or paraesthesia * Chest and abdominal pain * Syncope * Hypotension as dissection progresses

Answer 84

* ECG and CXR used to exclude other causes e.g. MI - may be normal * MI can occur in combination with aortic dissection, and treatment of MI can cause fatal progression of aortic dissection * CT angiogram usually initial investigation to confirm the diagnosis * MRI angiogram provides greater detail, help to plan management, takes longer to perform * Often clinical diagnosis - mortality increases rapidly with time elapsed since initial dissection

Answer 85

* Surgical emergency, need immediate involvement of vascular surgeons, anaesthetists and ICU/HDU * Analgesia e.g. morphine to manage pain * BP/HR need to be well controlled to reduce stress on aortic walls - usually involves B-blockers * Type A - open surgery (midline sternotomy) to remove section of aorta with defect and replace with synthetic graft, may also need to remove aortic valve * Type B - thoracic endovascular aortic repair, catheter inserted via femoral artery inserting a stent graft into affected section of aorta, complicated cases may require open surgery

Answer 86

* MI * Stroke * Paraplegia * Cardiac tamponade * Aortic valve regurgitation * Death

Answer 87

* QRISK3 * Requires * Age * Sex * Ethnicity * Smoking status * Diabetes status * Heart degree in 1st degree relative \<60 * CKD * Atrial fibrillation * BP medication * Rheumatoid arthritis * Measures - cholesterol/HDL ratio, SBP, height, weight (for BMI calculation) * Based on UK patient cohort

Answer 88

* Broad term which includes conditions e.g. hypercholesterolaemia, hyperlipidaemia, mixed dyslipidaemia * Disturbances in fat metabolism which alters the concentration of lipids in the blood * Hypercholesterolaemia can be: * High total cholesterol * High low-density lipoprotein (in comparison to high-density lipoprotein - 'good' cholesterol) * Can also have elevated triglycerides, low HDL, qualitative lipid abnormalities

Answer 89

* Mostly (poly)genetic/lifestyle factors but can be due to specific causes e.g. * Hypercholesterolaemia caused by high LDL: * Drugs e.g. sertraline * Hypothyroidism * Nephrotic syndrome * Cholestasis * Familial hypercholesterolaemia * Anabolic steroids * Hypercholesterolaemia due to triglyceride * T2DM/obesity * Alcohol excess * Pregnancy * Drugs e.g. risperidone * Familial combined hyperlipidaemia * Hypothyroidism * End stage renal disease

Answer 90

* Usually discovered incidentally on screening (asymptomatic) * Recommended for those \>40 who are obese, known to have high cholesterol, family history of CVD, or other risks e.g. HTN, T2DM * Lipid profile * Total cholesterol (\<5.5 if no CVD, \<4 if known CVD) * Triglyceride * HDL * LDL (\<4 if no CVD, \<2 if known CVD) * May also have - VLDL, total cholesterol:HDL, LDL:HDL * Total cholesterol high may be due to high HDL, which is not bad - LDL level and LDL:HDL more important * If patient is hypercholesterolaemic should also have: * Fasting blood glucose, HbA1c * U&Es * LFTs - statin may be contraindicated if AST high * TFTs

Answer 91

* Isolated hypercholesterolaemia may not need treatment, use QRISK to determine overall CVD risk * Lifestyle - exercise, smoking cessation, reduce alcohol intake, weight loss, minimise processed foods and animal products * Statins first choice for hypercholesterolaemia and moderate hypertriglyceridaemia * Low intensity e.g. simvastatin 10mg, pravastatin 10-40mg, fluvastatin 20/40mg * Medium intensity e.g. atorvastatin 10mg, simvastatin 20/40mg * High intensity e.g. simvastatin 80mg, atorvastatin 20-80mg * Risk of myopathy with high dose (80mg) simvastatin, only use in patients with severe hypercholesterolaemia and high risk CVD who have not achieved treatment goals on lower doses * Alternative agents e.g. ezetimibe, bile acid binding agents, fibrates used if statins not working

Answer 92

* Xanthomata - cholesterol deposits in palm, tendons of wrist and elbow * Corneal arcus (in under 50s) - hazy white, grey or blue opaque ring in peripheral cornea * Xanthelasma - cholesterol deposits around eyes

Answer 93

* Cardiovascular disease * Atherosclerotic disease - ACS, CVA, PAD

Answer 94

* Ensure blood flows in one direction only * 4 valves * Two atrioventricular - tricuspid and mitral (bicuspid) valve, between the atria and corresponding ventricle * Two semilunar valves - pulmonary valve and aortic valve, between the ventricles and corresponding artery, regulate flow of blood leaving the heart * AV valves - close during ventricular contraction (systole), first heart sound * Tricuspid - between right atrium and right ventricle, three cusps (anterior, septal and posterior) * Mitral - between left atrium and left ventricle, two cusps (anterior and postierior) * Supported by chordae tendinae from free edges of valve cusps to papillary muscles on interior surface of ventricles, contract to prevent prolapse of valves into atria * Semilunar valves - close during ventricular relaxation (distole), second heart sound * Pulmonary valve - between right ventricle and pulmonary artery, three cusps (left, right and anterior) * Aortic valve - between left ventricle and ascending aorta, three cusps (right, left and posterior) * Sides of valve leaflets attached to wall of vessel, slightly dilated to form a sinus, at the beginning of diastole blood flows back towards the heart, filling the sinuses and pushing the valve closed

Answer 95

* Valve leaflets * Calcification - occurs with age, e.g. aortic stenosis * Thickening * Degeneration * Infection - endocarditis * Prolapse - volume overload, leads to leakage * Apparatus/annulus * Annular dilation * Annular calcification * Apparatus tethering/thickening/rupture * Regional wall motion abnormality

Answer 96

* Rheumatic valve disease - inflammation and fibrosis of heart valve following untreated streptoccocal URTI, most commonly affects mitral valve * Endocarditis - vegetation formation on valve leaflets * Congenital valve disease - most commonly bicuspid aortic valve * Aging - calcification * Systemic connective tissue disease * Marfan's * Ehlers Danlos * Ankylosing spondylitis * SLE * Secondary to cardiovascular disease * Volume/pressure overload - heart failure, pulmonary hypertension * Atrial fibrillation * LV or RV dilatation

Answer 97

* Narrowing of mitral orifice due fusion of commissures and shortened, thickened chordae tendinae * Cause * Rheumatic heart disease - most common * Infective endocarditis * Congenital defects * SLE * Can coexist with mitral regurgitation if valve cannot properly close

Answer 98

* Mitral stenosis - narrowing of mitral orifice, less blood able to move through from left atrium to left ventricle * To maintain cardiac output the left atrial size and pressure progressively increase to push blood through narrower mitral orifice * This causes pulmonary venous and capillary pressures to increase and may cause secondary pulmonary hypertension, which in turn leads to right ventricular heart failure, tricuspid regurgitation and pulmonic regurgitation * LA enlargement predisposes to atrial fibrillation, increases risk of VTE

Answer 99

* Symptoms - often asymptomatic until complications develop * Right heart failure symptoms * Exertional dyspnoea * Orthopnoea * Paroxysmal noctural dyspnoea * Fatigue * Atrial fibrillation - SOB, palpitations, embolic event e.g. stroke * Pulmonary vessel disease - haemoptysis, hoarseness (left laryngeal nerve compression) * Signs * Malar flush - plum-red discolouration of cheeks due to CO2 retention --\> vasodilation * Pulmonary hypertension * Palpable second heart beat at upper L sternal border * Heave at left sternal border * Raised JVP * Loud 1st heart sound, early diastolic opening snap, low-pitched descrescendo-crescendo rumbling diastolic murmur best heard at apex * Loudest in left lateral decubitus position on expiration * Low-volume pulse which may be irregularly iregular (AF) * May have coexisting aortic regurgitation (early diastolic murmur)

Answer 100

* Echocardiogram, can grade severity * ECG * LA enlargement - long P wave with negative deflection in terminal component * Right axis QRS deviation and tall R waves in V1 - RV hypertrophy * CXR - straightening of left cardiac border due to dilated LA and widening of carina, dilated pulmonary vessels

Answer 101

* Risk factors for death - atrial fibrillation, pulmonary hypertension * Causes of death * Heart failure * Pulmonary or cerebrovascular embolism

Answer 102

* Asymptomatic - appropriate prophylaxis against recurrent group A streptoccocal infection * Surveillance with serial echo for RV enlargement --\> pulmonary hypertension * Mild symptoms * Diuretics * If sinus tachycardia or AF - beta blockers or calcium channel blockers to control rate * Anticoagulation (warfarin) to prevent VTE if AF, embolism or left atrial clot * Moderate/severe stenosis * Percutaneous balloon commissurotomy - balloon inflated to separate fused mitral valve commissures * Surgical commissurotomy - via thoracotomy or sternotomy * Valve replacement - often high risk due to older, comorbid patients

Answer 103

* Narrowing of aortic valve, obstructing blood flow from left ventricle to ascending aorta * Causes * In older patients usually developes from aortic sclerosis due to fibrosis and calcification * Bicuspid aortic valve (congenital) * Rheumatic fever

Answer 104

* May have coexisting aortic regurgitation due to inability of aortic valve to close properly, mitral regurgitation is also common with calcification of valves * Aortic stenosis - increased pressure in left ventricle as more difficult for blood to pass out into aorta * Left ventricular hypertrophy, eventually without enlargement of cavity then leading to CV cavity enlargement, reduced ejection fraction, decreased cardiac output * Elevated shear across stenosed aortic valve degrades von Willebrand factor multimers - results in coagulopathy with may cause GI bleeding in patients with angiodysplasia

Answer 105

* Exertional syncope - cardiac output cannot increase enough to meet demands of physical activity * Angina * Dyspnoea * Symptoms of heart failure - peripheral oedema, orthopnoea, paroxysmal noctural dyspnoea * Arrhythmias - palpitations, ventricular fibrillation leading to sudden death * Signs * Ejection systolic mumur loudest over aortic area, radiates to carotid arteries, loudest on expiration when patient is sitting forwards * Slow rising pulse with narrow pulse pressure * Non-displaced, heaving apex beat (LV hypertrophy) * Reduced or absent S2 * Reverse splitting of S2 - aortic valve closes after pulmonary valve

Answer 106

* Echocardiography * ECG - LV hypertrophy with or without ischaemic ST and T-wave pattern * CXR - calcification of aortic cusps and evidence of heart failure, heart size normal or mildly enlarged

Answer 107

* In children and young adults with congenital AS - balloon valvotomy * Older patients not fit for surgery - balloon valvuloplasty * Only temporary relief * Surgical aortic valve replacement - mechanical or bioprosthetic valve * Can use pulmonic valve, then replace pulmonic with bioprosthesis (less stress on pulmonic valve so prosthesis less likely to fail) * Transcatheter aortic valve implantation (TAVI) * Surgical preferred for patients \<65 * TAVI \>80 or life expectancy \<10 years * Shorter hospital stay, less pain, quicker recovery, but increased risk vascular complications and regurgitation

Answer 108

* Incompetency of aortic valve causing backflow from the aorta into the left ventricle during diastole * Acute aortic regurgitation (rare) * Dissection of ascending aorta * Infective endocarditis * Chronic aortic regurgitation * Degeneration of aortic valve and root (with or without bicuspid valve) * Infective endocarditis * Myxomatous degeneration * Rheumatic fever * Thoracic aortic aneurysm * Trauma * Ventricular septal defect - aortic valve prolapse in children * Seronegative spondyloarthropathies * Connective tissue diseases - Marfan's syndrome, Ehlers-Danlos syndrome

Answer 109

* Volume overload in left ventricle due to regurgitated blood from the aorta during ventricular diastole * Chronic - left ventricular dilation, hypertrophy, eventually decompensation with arrhythmias, LV impairment and heart failure * Acute - not enough time for left ventricle to dilate, rapid increase in left ventricular pressure, pulmonary oedema, decreased cardiac output

Answer 110

* Symptoms of heart failure - dyspnoea, fatigue, oedema * Cardiogenic shock - especially in acute, hypotension with resultant multisystem organ damage * Chronic typically asymptomatic for years, progressive exertional dyspnoea, orthopnoea, PND, palpitations develop insidiously * Symptoms of endocarditis - fever, weight loss, embolic phenomena, anaemia * Signs * Descrescendo early diastolic murmur, loudest at left sternal edge sometimes loudest over aortic area * Austin Flint murmur - low pitched rumbling mid-diastolic murmur heard at apex, caused by regurgitated blood through aortic valve mixing with blood from left atrium during contraction, sign of severe aortic regurgitation * Collapsing pulse - 'water hammer pulse' with wide pulse pressure * Displaced, hyperdynamic apex beat * Eponymous signs * Corrigan’s sign: visible distention and collapse of carotid arteries in the neck * De Musset’s sign: head bobbing with each heartbeat * Quincke’s sign: pulsations are seen in the nail bed with each heartbeat when the nail bed is lightly compressed * Traube’s sign: ‘pistol shot’ sound heard when stethoscope placed over the femoral artery during systole and diastole * Muller’s sign: uvula pulsations are seen with each heartbeat

Answer 111

* Echocardiography - aortic regurgitation and severity of pulmonary hypertension secondary to LV failure, detect vegetations or pericardial effusions (e.g. in aortic dissection) * ECG - axis deviation, LV hypertrophy, LA enlargement, T-wave inversion with ST-segment depression in precordial leads * CXR - cardiomegaly, prominent aortic root in chronic progressive aortic regurgitation, if severe can show HF e.g. pulmonary oedema

Answer 112

* ARBs can slow aortic root dilatation * Surgical aortic valve replacement or repair * Anticoagulation following valve replacement - Warfarin * Bioprosthetic - 3-6 months * Mechanical - lifetime * If not a surgical candidate can benefit from medical management of HF - diuretics, vasodilators, nitrates

Answer 113

* Billowing of mitral valve leaflets into left atrium during systole * Most often caused by myxomatous degeneration of mitral valve leaflets and chordae tendinae * Idiopathic * Inherited - autosomal dominant or X-linked * Connective tissue disorders - Marfan's, Ehlers-Danlos, polycystic kidney disease, SLE * More common in those with Grave's, von Willebrand disease, sickle cell disease, rheumatic heart disease * Mitral regurgitation is most common complication --\> heart failure, AF, VTE

Answer 114

* Asymptomatic usually * Non-specific symptoms - chest pain, dyspnoea, palpitations, syncope * Can present with mitral regurgitation * Signs * Crisp mid-systolic click best heard over left apex when patient is in left lateral decubitus position * Prolapse and regurgitation - click with late-systolic murmur

Answer 115

* Usually benign and does not require treatment but can lead to regurgitation * Beta-blockers can be used to relieve symptoms of excess sympathetic tone (e.g. palpitations, dizziness) and to reduce risk of tachyarrhythmias * Treatment of complications e.g. AF, regurgitation

Answer 116

* Incompetency of mitral valve causing flow from left ventricle to left atrium during ventricular systole * Can be acute or chronic, primary or secondary causes * Infective endocarditis * Acute MI with rupture or papillary muscles * Rheumatic heart disease * Congenital defects of mitral valve * Cardiomyopathy

Answer 117

* Acute - pulmonary oedema and cardiogenic shock or sudden cardiac death * Chronic * Gradual enlargement of left atrium, left ventricular enlargement and eccentric for hypertrophy which initially compensates for regurgitant flow (preserving stroke volume) but eventually decompensates * AF --\> thromboembolism

Answer 118

* Acute - heart failure (dyspnoea, fatigue, weakness, oedema) and cardiogenic shock (hypotension with multisystem organ damage) * Chronic * Initially asymptomatic * Symptoms develop insidiously as LA enlarges, pulmonary artery pressure and venous pressure increase and LV compensation fails * Dyspnoea * Fatigue * Orthopnoea * Palpitations - AF * Signs * Pansystolic murmur loudest over mitral area, using bell of stethoscopy, on expiration in left lateral decubitus position * Radiation of murmur to axilla * Displaced, hyperdynamic apex beat

Answer 119

* Echo - cause and severity of regurgitation, presence and extent of annular calcification, size and function of LV and LA, detect pulmonary hypertension * ECG - LA enlargement and LV hypertrophy with or without ischaemia * CXR - pulmonary oedema, can't usually see cardiac silhouette abnormalities unless chronic (LA and LV enlargement), pulmonary vascular congestion and pulmonary oedema with heart failure

Answer 120

* If LV dilation or dysfunction - ARB, neprilysin inhibitor (e.g. sacubitril), aldosterone antagonist and/or vasodilating beta-blocker * If ECG shows BBB - biventricular pacing may be beneficial * Loop diuretics to reduce HF symptoms * Digoxin and anticoagulation in AF * Surgical intervention * Mitral valve replacement or repair

Answer 121

* Causes * Right ventricular dilatation e.g. secondary to pulmonary stenosis or pulmonary hypertension * Rheumatic fever * Infective endocarditis, especially in IVDU * Carcinoid syndrome * Congenital * Pansystolic mumur, loudest over tricuspid region, loudest during inspiration * Other clinical features (movement of blood back into systemic venous system) * V-waves in jugular veins, right atrial filling with blood against closed tricuspid valve * Visible/palpable hepatic pulsations * Signs of right-sided heart failure - right ventricular heave, peripheral oedema, hepatomegaly, ascites

Answer 122

* Causes * Pulmonary hypertension * Infective endocarditis * Congenital valvular heart disease * Usually asymptomatic * Early diastolic decrescendo mumur loudest over left sternal edge, loudest during inspiration * Usually due to pulmonary hypertension

Answer 123

* Causes * Rheumatic fever (most common) * Congenital disease * Infective endocarditis * Presentation * Soft mid-diastolic murmur, rarely audible, loudest at 3rd-4th intercostal space at left sternal edge, during inspiration * Raised JVP with giant A waves * Peripheral oedema, ascites

Answer 124

* Causes * Congenital: Turner’s, Noonan’s and Williams syndromes. Tetralogy of Fallot (pulmonary stenosis, right ventricular hypertrophy, ventricular septal defect and an overriding aorta). * Rheumatic fever * Carcinoid syndrome * Presentation * Ejection systolic murmur loudest over pulmonary area, loudest during inspiration * Radiates to left shoulder/left infraclavicular region * If severe murmur is longer and may obscure sound of S2 * Prominant 'a waves' in jugular veins * Right ventricular heave, tricuspid regurgitatio and peripheral signs of right heart failure due to right ventricular dilatation

Answer 125

* Heart muscle disorder * Types * Dilated cardiomyopathy * Hypertrophic cardiomyopathy * Restrictive cardiomyopathy

Answer 126

* Enlarged ventricular size with normal ventricular wall thickness, systolic dysfunction * Usually affects left or both ventricles * Causes - often a combination of risk factors * Ischaemic heart disease * Alcohol * Cocaine use * Thyroid disorder * Valvular disease * Genetic cause * Idiopathic * Infective * Bacterial * HIV * Viral e.g. coxsackie, viral myocarditis * Autoimmune, connective tissue and granulomatous disorders * Drugs * Peripartum

Answer 127

* Heart failure * Dyspnoea, especially on exertion * Fatigue * Peripheral oedema * Raised JVP, especially if right ventricle involved * Arrhythmia * Thromboembolism - stroke or PE * Acute myocarditis

Answer 128

* ECG * Sinus tachycardia * T wave inversion and Q waves (even without previous MI) * ST-depression (non-specific pattern) * LBBB * CXR - cardiomegaly, heart failure signs * Echo * Dilated, hypokinetic chambers * Useful to rule out primary valve disorders

Answer 129

* Treat reversible causes * Infectious * Haemochromatosis * Thyrotoxicosis * Prophylactic anticoagulation - warfarin or NOAC * Consider pacemaker for AV node block * Treat as for heart failure * ACEI (or ARB if intolerant) * +/- Beta-blockers * Diuretics * Nitrates * Consider implantable cardioverter defibrillator - high risk for arrhythmia * Heart transplant * Very poor prognosis - often death due to thrombus or arrhythmia

Answer 130

* Hypertrophy of left ventricle, causes left ventricular outflow obstruction, mitral valve problems, myocardial ischaemia and increased risk of tachyarrhythmias * Most common cause of sudden cardiac death in young people * Autosomal dominant genetic disorder - genetic defects in genes that code for cardiac proteins e.g. troponin

Answer 131

* Most asymptomatic * Dyspnoea * Chest pain * Syncope - especially exercising, risk factor for sudden death * Palpitations * Sudden death - arrhythmia or outflow tract obstruction * Signs * Forceful apex beat * Late ejection systolic murmur, does not radiate to neck, best heard at left sternal edge * Abnormal blood pressure response to exercise - does not rise or falls * AF in 20%

Answer 132

* ECG - non-specific changes to ST, T wave * Echo - standard diagnostic test * Asymmetric septal hypertrophy \>15mm * Normal systolic function * Absence of valvular disease * CXR - often normal, heart size may be normal or enlarged * Myocardial biopsy can rule out other conditions

Answer 133

* If arrhythmia present * Control with anti-arrhythmic drugs * Anticoagulation in AF * Reduce outflow obstruction, improve diastolic filling - beta-blockers, verapamil * Beware drugs that reduce preload e.g. ACEI, ARBs, nitrites, diuretics * Implantable defibrillator if risk of sudden death * Avoid competitive sports and strenuous exercise * Sudden death typically in young patients with few or no symptoms, annual mortality risk 1-3%

Answer 134

* Least common cardiomyopathy * Reduced compliance of ventricular walls during diastolic filling, two types * Infiltration of myocardium by invasive substance e.g amyloid plaques, sarcoidosis, iron in haemochromatosis * Fibrotic myocardium without external invasive substance * Most commonly affects L ventricle, can affect both

Answer 135

* Signs of heart failure * Dyspnoea - especially exertional * Orthopnoea * Fatigue * Pulmonary oedema * Heart size normal or enlarged * Features of right ventricular failure - raised JVP, hepatomegaly, oedema, ascites * AF in 75%, other arrhythmias

Answer 136

* ECG - non-specific T and ST changes, pathological Q waves, left ventricular hypertrophy * CXR - heart size normal or small, may be enlarged in amyloidosis or haemochromatosis * Echo - normal systolic function, dilated atria, myocardial hypertrophy may be present

Answer 137

* Treat underlying cause * Poor prognosis - often no effective treatments that alter cause of disease * Beware diuretics, digoxin, nitrites * Endocardial resection? * Heart transplant

Answer 138

* Oxygenated blood supply from placenta - umbilical vein through ductus venous in liver to inferior vena cava * Lungs not fully formed, vascular resistance in the pulmonary arteries is high, therefore blood from IVC takes path of least resistance and passes from right atrium through foramen ovale directly into left atrium then out through aorta * Any blood that passes into the pulmonary artery goes through ductus arteriosus to the aorta * Two shunts (foramen ovale and ductus arteriosus) that allow mixing of oxygenated and deoxygenated blood after birth if not closed properly

Answer 139

* Acyanotic * L to R shunts * VSD 30% * Persistent ductus arteriosus 12% * ASD 10% * Outflow obstruction * Pulmonary stenosis 7% * Aortic stenosis 5% * Coarctation of the aorta 5% * Cyanotic * Tetralogy of the Fallot 5% * Transposition of the great arteries 5% * Atrioventricular septal defect (complete) 2%

Answer 140

* Hole in wall between L and R atria - higher pressure in L atria creates L --\> R shunt * Different types depending on position of hole * Primum - opening between atria near AV vales, more complex * Secundum - most common, hole between atria in middle of septal wall * Common atrium (no septum between atria) * Patent foramen ovale is not an atrial septal defect, embryological remnant

Answer 141

* Shunt L --\> R * Right heart volume overload - RA and RV dilate to accommodate extra volume * Can have no symptoms early in life, often diagnosed in adulthood * Dilatation of RA - arrhythmias, present with palpitations, SOB, embolic stroke * On examination * Pulmonary flow murmur * Fixed, split second heart sound * May lead to * RV failure * Tricuspid regurgitation * Atrial arrhythmias * Pulmonary hypertension * Eisenmenger syndrome - higher pressure in RA over time leads to R --\> L shunt (cyanotic) * Only need treatment if signs of strain on heart * Surgical repair with sternotomy or through groin with transcatheter device

Answer 142

* Narrowing of the aorta, typically at insertion point of ductus arteriosus * LV has to generate higher pressure to push blood through --\> LV hypertension, hypertrophy, can progress to LV failure * Collateral vessels develop to allow blood to reach the descending aorta * Highly variable severity * Severe narrowing presents early in life with complications of poor lower limb perfusion e.g. cold feet, claudication of legs, abdominal angina * Complications of increased systemic pressure proximal to coarctation e.g. headaches and nosebleeds * Discrepancies in limb BP - lower \> upper * Radio-femoral delay on palpation * Complications - upper body hypertension, berry aneurysms, claudication, renal insufficiency

Answer 143

* Often associated with other congenital heart defects e.g. bicuspid aorta, need to screen for them * Surgical or transcatheter repair * Surgical repair via thoracotomy * Non-surgical - balloon passed through and inflated to stretch narrow artery

Answer 144

* Aorta and pulmonary artery switched, aorta connected to right ventricle and pulmonary artery connected to left ventricle * Creates 2 separate circulation systems * In the systemic circulation deoxygenated blood returns to RA via the SVC and IVC, passes through tricuspid valve and into RV, then pumped through aortic valve into the aorta and around the body without being oxygenated * In the pulmonary circulation the oxygenated blood passes into the left atrium via the pulmonary veins, through the mitral valve into the left ventricle, then pumped back into the pulmonary artery via the pulmonary valve * Without mixing the oxygenated and deoxygenated blood there is profound cyanosis - foetal circulation allows for oxygenation of blood * When baby breaths after birth, foramen ovale and ductus arteriosus close within a few hours * Loss of shunts is catastrophic for baby so delay closing * Signs * Cyanotic spells * Ejection systolic murmur at upper left sternal edge * Single 2nd heart sounds * Clubbing

Answer 145

* Use prostaglandins after birth to delay closure of foetal shunts, buys time to perform surgery * Atrial switch - no longer used * Redirect venous blood to appropriate side of heart, create a channel for deoxygenated venous blood to pass into pulmonary artery via the left ventricle and atrial septum is removed to allow oxygenated venous blood to pass throgh the RA and into the aorta via the LV * Problem because RV becomes main systemic pump - results in right ventricular failure eventually, tricuspid valve regurgitation * Aterial switch * Disconnect aorta and pulmonary artery, switch them and sew them back on - aorta above LV and pulmonary artery above RV * Coronary arteries need to be reconnected to the aorta carefully - risk of MI or sudden death post-op

Answer 146

* 4 components * Ventricular septal defect * Right ventricular outflow tract obstruction - stenosis below pulmonary valve due to large muscle mass * Overriding aorta - aortic valve enlarged and appears to arise from both left and right ventricles * Right ventricular hypertrophy * Severity varies with each patient from mild sub-pulmonary stenosis to complete absence of pulmonary valve, and from slight deviation of aorta to predominantly overlying right ventricle * RVOT - restricted flow into pulmonary arteries, mostly passes through VSD to systemic circulation via aorta --\> mixing of blood and drop in saturation

Answer 147

* BT shunt * Connect carotid or subclavian artery directly onto pulmonary artery - more long-term circulation to pulmonary system * Improves chance of survival before definitive corrective surgery * Complete repair * Within a few days of birth * Close VSD with patch, resection of RVOT obstruction, enlargement of pulmonary arteries

Answer 148

* Significant pulmonary regurgitations * Leads to RV overload, RV dilation and eventually RV failure * Will often need pulmonary valve replacement later on in life * Arrhythmia * Increase in RV pressure causes rise in RA pressure, subsequently dilates and can trigger arrhythmias (more likely to be atrial flutter) * Particularly ventricular tachycardia (SVT with RBBB can be similar) * Can be treated with anti-arrhythmic agents such as amiodarone or beta-blockers * Pulmonary arterial/branch pulmonary artery stenosis * Will contribute to rising RV pressure with dilation and failure, can be improved with transcutaneous stenting

Answer 149

* One effective pumping ventricle, caused by many kinds of CHD * Cause e.g. tricuspid atresia, hypoplastic left heart syndrome, double inlet left ventricle * Foetal circulation relies on patent foramen ovale/ductus arteriosus for mixing oxygenated and deoxygenated blood

Answer 150

* Formation of a Fontan circulation * Single functional ventricle used to support systemic circulation by disconnecting it from the pulmonary valve and artery * IVC and SVC disconnected and attached to pulmonary ateries, bypassing heart * Deoxygenated blood flows up IVC into pulmonary arteries without passing through any valves, blood oxygenated in lungs and flows back to left atrium, through mitral valve, into single ventricle, through aortic valve into aorta * Stages to formation of Fontan circulation * BT shunts - subclavian to pulmonary artery * Norwood procedure 1st week of life * Bi-directional Glenn - 3-6 months * Fontan completion - 2-3 years

Answer 151

* No functioning RV, pulmonary circulation is dependent on high systemic venous pressure and low pulmonary vascular resistance * Anything that causes imbalance can cause catastrophic haemodynamic compromise * PE - increases pulmonary vascular resistance (majority of patients require anticoagulation) * Arrhythmia - reduce systemic circulation and systemic venous pressure crashes (require cardioversion) * Dehydration - reduce venous pressure, keep hydrated with IV fluids if fasting * Bleeding - reduced venous pressure, low threshold for transfusion

Answer 152

* Excess fluid within pericardial sac * Can be acute or chronic * Can fill entire pericardial cavity or only a localised section * Effusion can be * Transudate - low protein content * Exudates - inflammation * Blood * Pus * Gas - bacterial infections

Answer 153

* Pericardium - membrane that surrounds the heart * Two layers with a small amount of fluid between (\<50ml), providing lubirication for movement as the heart beats * Potential space between layers called the pericardial cavity * Pericardial effusion when potential space of the pericardial cavity fills with fluid, creates an inwards pressure on the heart, making it more difficult to expand during diastole * Pericardial tamponade occurs whn pericardial effusion is large enough to raise the intra-pericardial pressure, this squeezes the heart and affects its ability to function --\> reduced filling during diastole --\> decreased cardiac output during systole * Emergency - requires immediate drainage to relieve pressure

Answer 154

* Transudative effusion - increased venous pressure can reduce drainage from pericardial cavity * Congestive heart failure * Pulmonary hypertension * Exudative effusion - any inflammatory process (pericarditis) * Infection e.g. tuberculosis, HIV, coxsackievirus, Epstein-Barr virus etc. * Autoimmune and inflammatory conditions e.g. SLE, RA * Injury to pericardium e.g. MI, open heart surgery or trauma * Uraemia secondary to renal impairment * Cancer * Medications e.g. methotrexate * Rupture of heart or aorta can cause bleeding into pericardial cavity, resulting in rapid-onset cardiac tamponade * MI * Trauma * Aortic dissection (type A)

Answer 155

* Speed of onset depends on how quickly the effusion develops * Rapidly collecting effusion with cardiac tamponade - rapid haemodynamic compromise and collapse * Slowly developing, chronic effusions - * Initially asymptomatic * Chest pain * Shortness of breath * Feeling of fullness in the chest * Orthopnoea * Compression of surrounding structures * Phrenic nerve - hiccups * Oesophageal compression - dysphagia * Recurrent laryngeal nerve - hoarseness * Signs * Quiet heart sounds * Pulsus paradoxus - abnormally large fall in BP during inspiration * Hypotension * Raised JVP * Fever - pericarditis * Pericardial rub - pericarditis

Answer 156

* Echo * Diagnose pericardial effusion * Assess size of effusion * Assess effect on heart function - haemodynamic effect * Fluid analysis of pericardial effusion fluid * Protein content - distinguish between transudative or exudative * Bacterial culture * Viral PCR * Cytology and tumour markers (for cancer) * Bloods - WCC and ESR/CRP raised in pericarditis with bacterial/viral infection * ECG - * Saddle-shaped ST elevation across inferior and anterior leads * PR depression * Later - T wave inversion

Answer 157

* Treatment of underlying cause e.g. infection * Inflammatory pericarditis management - aspirin, NSAIDs, colchinine, steroids * Drainage of effusion where required * Needle pericardiocentesis - echo guided * Surgical drainage * Pericardial window - portion of pericardium removed, allows fluid to drain from pericardial cavity into pleural or peritoneal cavity * Pericardiectomy - surgical removal or pericardium in recurrent cases

Cardiology COPY Flashcards

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