Cardiovascular 2 Flashcards

Question

what can cause loss of blood in hypovolaemic shock?

Answer 1

- acute GI bleeding - trauma - peri/post-operative - splenic rupture

Answer 2

- dehydration - diarrhoea and vomiting - burns - heat damage increases the permeability of capillaries so plasma leaks - pancreatitis

Answer 3

heart doesn't pump • cardiac tamponade - blood in pericardial sack placing pressure on heart thereby limiting cardiac output • pulmonary embolism - flow of blood to lungs is blocked • acute MI • fluid overload • myocarditis

Answer 4

shock when an infection becomes out of control • referred to as a distributive shock • sepsis exists when a systemic inflammatory response is associated with an infection • septic shock exists when sepsis is complicated by persistent hypotension that is unresponsive to fluid resuscitation

Answer 5

release of IgE due to allergic response • intense allergic reaction • massive release of histamine and other vasoactive mediators causing haemodynamic collapse • accompanied by breathlessness and wheeze (due to bronchospasm)

Answer 6

Tennis score

Answer 7

* 15% blood loss * pulse below 100 bpm * BP normal * pulse pressure normal * resp rate; 14-20 * urine output greater than 30ml/hr * slightly anxious

Answer 8

* 15-30% blood loss * tachycardia * BP normal due to autonomic response (increased sympathetic activity) * pulse pressure decreased * resp rate; 20-30 * urine output: 20-30ml/hr * mental status: mildly anxious

Answer 9

* 30-40% blood loss * pulse above 120 bpm * BP decreased * pulse pressure decreased * resp rate; 30-40 * urine output: 5-15ml/hr * mental status: confused

Answer 10

- reduction in ventricular filling -> fall in BP and SV -> hypotension - leads to reduced stimulation of baroreceptors -> increased sympathetic activity with release of noradrenaline and adrenaline - vasoconstriction and increased contractility and heart rate helps restore BP and CO - reduced capillary BP -> greater level of net movement of fluid into vascular compartment - renin release -> Na and water retention - angiotensin II causes thirst - ADH release - release of cortisol causes fluid retention - release of glucagon raises blood sugar levels

Answer 11

``` • inadequate tissue perfusion: - skin: cold, pale, clammy, slate-grey, - brain: drowsiness and confusion • increased sympathetic tone • tachycardia - narrow pulse pressure and weak pulse • sweating • BP may be maintained initially but later hypotension • bradycardia ```

Answer 12

* signs of myocardial failure * raised jugular venous pressure (JVP) * gallop rhythm * basal crackles and pulmonary oedema

Answer 13

* pyrexia and rigors * nausea and vomiting * vasodilation with warm peripheries * bounding pulse

Answer 14

* signs of profound vasodilation * warm peripheries * low BP * tachycardia * bronchospasm * pulmonary oedema

Answer 15

- kidneys; acute tubular necrosis - lung; Acute Respiratory Distress Syndrome (ARDs) - heart; myocardial ischaemia and infarction - brain; confusion, irritability and coma

Answer 16

A: airway (ensure patency) B: breathing (give 100% O2) and correct immediately life threatening problems such as: - congestive cardiac failure - bronchospasm - tension pneumothorax C: circulation - establish secure IV access - give fluid quickly and blood if acute blood loss - ensure haemostasis i.e. stop bleeding

Answer 17

* Impaired oxygenation * bilateral pulmonary infiltrates * no cardiac failure * normal pulmonary arterial pressure (PAOP)

Answer 18

* shock of any cause * head injury * drug reaction * sepsis

Answer 19

* pneumonia * chemical pneumonitis * smoke inhalation * near drowning

Answer 20

- alveolar capillary membrane injury results in leakage of fluid into the alveolar spaces - there is resulting neutrophil invasion which attracts more neutrophils (exudative phase) - eventually fibroblasts come in and initiate healing (proliferative phase) - and make scar tissue (fibrotic phase) - results in severely stiff lungs and thus severe difficulty in ventilation and thus reduced O2 blood perfusion

Answer 21

- cyanosis - tachypnoea - tachycardia - peripheral vasodilation

Answer 22

* obstruction and narrowing of left ventricle inflow that prevents proper filling during diastole * mitral valve has 2 cusps

Answer 23

- normal mitral valve area is 4-6cm2, symptoms begin at areas less than 2cm2 - most common cause of mitral stenosis is rheumatic heart disease secondary to rheumatic fever - the condition is more common in men than women - prevalence and incidence is decreasing due to a reduction of rheumatic heart disease

Answer 24

most common cause of mitral stenosis is rheumatic heart disease secondary to rheumatic fever due to infection with group A beta-haemolytic streptococcus e.g. Streptococcus pyogenes

Answer 25

- inflammation due to rheumatic fever leads to commissural fusion and a reduction in mitral valve orifice area, causing the characteristic doming pattern seen on echocardiography - over many years, the condition progresses to valve thickening, cusp fusion, calcium deposition, a severely narrowed (stenotic) valve orifice and progressive immobility of the valve cusps

Answer 26

* infective endocarditis (3.3%) * mitral annular calcification (2.7%) - rarely leads to mitral stenosis if extensive, particularly in elderly patients and those with end-stage renal disease

Answer 27

- history of rheumatic fever | - untreated streptococcus infections

Answer 28

- thickening and immobility of the valve leads to obstruction of blood flow from the left atrium to the left ventricle - for cardiac output to be maintained, the left atrial pressure increases and left atrial hypertrophy and dilatation occur - pulmonary venous, pulmonary arterial and right heart pressures increase - the increase in pulmonary capillary pressure leads to development of pulmonary oedema; seen particularly when atrial fibrillation occurs, due to the elevation of left atrial pressure and dilatation, with tachycardia and loss of coordinated atrial contraction - partially countered by alveolar and capillary thickening and pulmonary arterial vasoconstriction - pulmonary vasoconstriction leads to pulmonary hypertension and eventually right ventricular hypertrophy, dilatation and failure with subsequent tricuspid regurgitation

Answer 29

- no symptoms until the valve orifice is moderately stenosed i.e. area is less than 2cm2 - usually doesn't occur until several decades after the first attack of rheumatic fever - progressive exertional dyspnoea - haemoptysis - atrial fibrillation leading to PE and abrupt deterioration - pulmonary hypertension leading to right heart failure with fatigue and lower limb oedema - systemic emboli - prominent “a” wave in jugular venous pulsations - mitral facies/malar flush

Answer 30

due to left atrial dilation resulting in pulmonary | congestion (reduced emptying), which is worse with exercise, fever, tachycardia and pregnancy

Answer 31

due to rupture of bronchial vessels due to the elevated | pulmonary pressure

Answer 32

due to the development of pulmonary hypertension with symptoms of weakness, fatigue and abdominal or lower limb swelling

Answer 33

due to left atrium dilation giving rise to palpitations

Answer 34

due to atrial fibrillation, most commonly in the cerebral | vessels

Answer 35

due to pulmonary hypertension and right ventricular hypertrophy

Answer 36

bilateral, cyanotic or dusky pink discolouration over the upper cheeks; pinkish-purple patches on the cheeks due to vasoconstriction in response to diminished cardiac output

Answer 37

- diastolic murmur - loud opening S1 snap - the apex beat is ‘tapping’ in quality due to combination of a palpable first heart sound and left ventricular backward displacement produced by an enlarging right ventricle. - auscultation at the apex reveals a loud first heart sound, an opening snap (when the mitral valve opens) in early diastole, followed by a rumbling mid-diastolic murmur. If the patient is in sinus rhythm the murmur becomes louder when atrial systole occurs (presystolic accentuation), as a result of increased flow across the narrowed valve.

Answer 38

- heard when blood flows over a valve - low-pitched diastolic rumble most prominent at the apex - heard best with patient lying on the left side in held expiration

Answer 39

- heard at apex when leaflets are still mobile - due to the abrupt halt in leaflet motion in early diastole, after a rapid initial opening, due to fusion at the leaflet tips - as the valve cusps become more immobile, the loud first heart sound softens and the opening snap disappears

Answer 40

``` CXR: • left atrial enlargement • pulmonary venous hypertension • pulmonary oedema/congestion in severe disease • occasionally calcified mitral valve ``` ECG: • atrial fibrillation • left atrial hypertrophy -> bifid P wave (P mitrale) • features of right ventricular hypertrophy in progressive disease Echocardiogram: • gold standard for diagnosis, assesses severity • assess mitral valve mobility, gradient and mitral valve area • valve area of <2cm2 indicates moderate stenosis, <1cm2 severe

Answer 41

- mitral stenosis is a mechanical problem and medical therapy does not prevent progression - beta-blockers and digoxin which control heart rate (for AF) and thus prolong diastole for improved diastolic filling - diuretics for fluid overload - anticoagulation in patients with AF to prevent clot formation and embolisation - percutaneous mitral balloon valvotomy - mitral valve replacement

Answer 42

* catheter is inserted into the right atrium via the femoral vein under local anaesthesia * the interatrial septum is punctured and the catheter advanced into the left atrium and across the mitral valve * the balloon is inflated and puts pressure on valve thereby separating the leaflets and increasing the size of the mitral valve opening, enabling more blood to flow from left atrium into left ventricle

Answer 43

• backflow of blood from the left ventricle to the left atrium during systole • mild physiological mitral regurgitation (MR) is seen in 80% of normal individuals - occurs due to abnormalities of the valve leaflets, chordae tendinae, papillary muscles or left ventricle

Answer 44

most frequent cause is myxomatous degeneration (MVP) (weakening of the chordae tendinae) resulting in a floppy mitral valve that prolapses

Answer 45

* ischaemic mitral valve * rheumatic heart disease * infective endocarditis * papillary muscle dysfunction/rupture * dilated cardiomyopathy * ruptured chordae tendineae * dilating left ventricle disease causing functional mitral regurgitation * hypertrophic cardiomyopathy * rarely: systemic lupus erythematosus, Marfan's syndrome * Ehlers-Danlos syndrome

Answer 46

- associated with females - lower BMI - advanced age - renal dysfunction - prior MI

Answer 47

- regurgitation into the left atrium produces left atrial dilatation but little increase in left atrial pressure if the regurgitation is longstanding, since the regurgitant flow is compensated for by the large left atrium - pure volume overload due to leakage of blood into left atrium during systole - circulatory changes depend on the speed of onset and severity of regurgitation - with acute mitral regurgitation there is a rise in left atrial pressure, resulting in an increase in pulmonary venous pressure and pulmonary oedema - left ventricle dilates, but more so with chronic regurgitation

Answer 48

left arterial enlargement, left ventricle hypertrophy (since left ventricle must put in same effort to pump less blood due to regurgitation so needs to pump harder to maintain cardiac output and thus hypertrophy occurs to increase stroke volume) and increases contractility: * progressive left atrial dilatation and right ventricular dysfunction due to pulmonary hypertension * progressive left ventricular volume overload leads to dilatation and progressive heart failure

Answer 49

* soft S1 and a pansystolic murmur (palpated as a thrill) loudest at the apex radiating over the precordium and into the axilla * prominent third extra heart sound (S3) in congestive heart failure/left atrium overload, caused by rapid filling of the dilated left ventricle in early diastole * in chronic mitral regurgitation, the intensity of the murmur does not correlate with the severity

Answer 50

- exertion dysponea i.e. exercise intolerant - dysponea develops because of pulmonary venous hypertension that arises as a direct result of the mitral regurgitation and secondarily as a consequence of left ventricular failure - fatigue and lethargy due to reduced cardiac output - increased stroke volume is felt as a palpitation - symptoms of right heart failure and eventually lead to congestive cardiac failure - heart failure may coincide with increased haemodynamic burden e.g in pregnancy, infection or atrial fibrillation

Answer 51

- compensatory phase: 10-15 years - once patients ejection fraction becomes less than 60% and/or becomes symptomatic then mortality rises sharply - severe mitral regurgitation has a 5%/year mortality rate

Answer 52

ECG • may show left atrial enlargement, atrial fibrillation and left ventricle hypertrophy in severe MR (seen late in course of disease) • but not diagnostic CXR: • left atrial enlargement and central pulmonary artery enlargement Echocardiogram: • estimation of left atrium and left ventricle size and function • also gives valve structure assessment • transoesophageal is very helpful • can establish the aetiology and haemodynamic consequences of mitral regurgitation

Answer 53

* vasodilators such as ACE-inhibitors * heart rate control for atrial fibrillation with beta blockers, calcium channel blockers and digoxin * anticoagulation in atrial fibrillation and flutter * diuretics for fluid overload

Answer 54

• symptomatic severe mitral regurgitation - left ventricular fraction >30% and end-diastolic dimension of under 55mm • asymptomatic: - if ejection fraction is less than 60% - left ventricular dysfunction (end systolic dimension >45mm and/or ejection fraction of under 60%) - if new onset, atrial fibrillation, pulmonary hypertension

Answer 55

narrowing of the aortic valve resulting in obstruction to the left ventricular stroke volume, leading to symptoms of chest pain, breathlessness, syncope and fatigue

Answer 56

- normal aortic valve area is 3-4cm2 - symptoms occur when valve area is 1/4th of normal area - primarily a disease of ageing - congenital is the second most common cause - the most common type of valvular disease in the western world

Answer 57

* supravalvular e.g congenital fibrous diaphragm above the aortic valve * subvalvular e.g congenital condition in which a fibrous ridge or diaphragm is situated immediately below the aortic valve * valvular; most common

Answer 58

* calcific aortic valvular disease (CAVD) - essentially calcification and degeneration of the aortic valve resulting in stenosis, most commonly seen in elderly * calcification of a congenital bicuspid aortic valve (BAV) (valve has 2 leaflets instead of 3 due to genetic disease; this is the most common congenital heart disease) resulting in stenosis * rheumatic heart disease; rare now due to eradication

Answer 59

- congenital bicuspid aortic valve (BAV) predisposes to stenosis and regurgitation - congenital BAV is predominant in males

Answer 60

- due to narrowing there is obstructed left ventricular emptying and a pressure gradient develops between the left ventricle and the aorta resulting in increased afterload - results in increased left ventricular pressure and compensatory left ventricular hypertrophy - this results in relative ischaemia of the left ventricular myocardium (since hypertrophy results in increased blood demand), and consequent angina, arrhythmias and left ventricular failure - left ventricular systolic function is typically preserved in aortic stenosis - the obstruction to left ventricular emptying is relatively more severe on exercise; since exercise causes a many-fold increase in cardiac output, however due to severe narrowing of the aortic valve, the cardiac output can hardly increase; thus, the blood pressure falls, coronary ischaemia worsens, the myocardium fails and cardiac arrhythmias develop - when this compensatory mechanism is exhausted left ventricular function declines rapidly

Answer 61

- think aortic stenosis in any elderly person with chest pain, exertional dysponea or syncope - classic triad - sudden death - slow rising carotid pulse (pulsus tardus) and decreased pulse amplitude (pulsus parvus) - heart sounds

Answer 62

* syncope - usually exertional * angina (increases myocardial oxygen demand; with resulting demand/supply mismatch) * heart failure (usually after 60) * dysponea on exertion due to heart failure

Answer 63

* soft or absent second heart sound when the valve becomes immobile * carotid pulse is slow rising (plateau pulse) and the apex beat thrusting * harsh systolic ejection murmur (palpated as a thrill) at the right upper sternal border and radiating to the carotids * prominent 4th (S4) heart sound due to left ventricular hypertrophy * ejection systolic murmur crescendo-decrescendo character * loudness does not tell you anything about severity

Answer 64

- aortic regurgitation | - subacute bacterial endocarditis

Answer 65

Echocardiogram: • two measurements obtained are: - left ventricular size and function; left ventricular hypertrophy, dilation and ejection fraction - doppler derived gradient and valve area (AVA), allows for the assessment of the pressure gradient across the valve during systole ECG: • left ventricular hypertrophy • left atrial delay • left ventricular ‘strain’ pattern due to ‘pressure overload’ - depressed ST segments and T-wave inversion in leads orientated towards left ventricle i.e. I, AVL, V5 and 6 when disease is severe CXR: • left ventricular hypertrophy • calcified aortic valve • normal heart size, prominence of the ascending aorta

Answer 66

- rigorous dental hygiene/care due to the increased risk of infective endocarditis (IE) in anyone with valvular heart disease; consider IE prophylaxis in dental procedures - limited role for medication due to the fact that aortic stenosis is a mechanical problem - vasodilators are contraindicated in severe aortic stenosis because they may trigger hypotension and thus syncope - surgical aortic valve replacement (definitive treatment) - TAVI

Answer 67

surgical aortic valve replacement

Answer 68

- any symptomatic patients with severe aortic stenosis - any patient with decreasing ejection fraction - any patent undergoing CABG with moderate or severe aortic stenosis

Answer 69

Transcutaneous Aortic Valve Implantation • minimally invasive • pass catheter up the aorta then inflate balloon across the narrowed valve which will crack the calcification • then pass another catheter which leaves a stent with a valve = new aortic valve

Answer 70

- leakage of blood into the left ventricle from the aorta during diastole due to ineffective coaptation (bringing together) of the aortic cusps - reflux of blood from the aorta through the aortic valve into the left ventricle during diastole

Answer 71

- can be associated with aortic stenosis - main causes: • congenital bicuspid aortic valve (BAV) • rheumatic fever • infective endocarditis

Answer 72

- SLE - Marfan’s and Ehlers-Danlos syndrome; connective tissue disorders - aortic dilatation - infective endocarditis or aortic dissection

Answer 73

- if net cardiac output is to be maintained, the total volume of blood pumped into the aorta must increase and the left ventricular size must enlarge -> left ventricle dilatation and hypertrophy - progressive dilation leads to heart failure - the remaining blood in the root of the aorta supplies the coronary arteries via the coronary sinus during diastole; regurgitation causes diastolic blood pressure to fall and thus coronary perfusion decreases - the large left ventricular size is mechanically less efficient, so demand for oxygen is greater and cardiac ischaemia develops - stroke volume increases, leading to increased pulse pressure - contraction of the ventricle deteriorates -> left ventricular failure - adaptation to volume load entering left ventricle don't occur with acute regurgitation, leading to pulmonary oedema and reduced stroke volume

Answer 74

- in chronic regurgitation, patients remain asymptomatic for many years before symptoms develop - exertional dysponea - palpitations - angina - syncope - wide pulse pressure - apex beat displaced laterally - collapsing water hammer pulse (bounding and forceful, rapidly increasing and subsequently collapsing) - Quincke’s sign - capillary pulsation in the nail beds - de Musset’s sign - head nodding with each heart beat - pistol shot femoral - a sharp bang heard on auscultation

Answer 75

* early diastolic blowing murmur at the left sternal border in the 4th intercostal space; accentuated when patient sits forward with breath held in expiration * ejection systolic murmur; due to increased stoke volume leading to turbulent flow across the aortic valve * Austin Flint murmur: mid-diastolic murmur over the cardiac apex produced due to aortic jet impinging on the mitral valve, producing premature closure of the valve and physiological stenosis

Answer 76

- bounding and forceful pulse rapidly increasing and subsequently collapsing - seen in aortic regurgitation

Answer 77

- capillary perfusion in the nail beds | - seen in aortic regurgitation

Answer 78

- head nodding with each heart beat | - seen in aortic regurgitation

Answer 79

- a sharp bang heard on auscultation | - seen in aortic regurgitation

Answer 80

- heart failure - infective endocarditis - mitral regurgitation

Answer 81

echocardiogram: • evaluation of the aortic valve and aortic root • measurement of left ventricle dimensions and function • cornerstone for decision making and follow up evaluation CXR: • enlarged cardiac silhouette and aortic root enlargement • left ventricular enlargement ECG: • signs of left ventricular hypertrophy due to ‘volume overload’ - tall R waves and deeply inverted T waves in left-sided chest leads, and deep S waves in right-sided leads

Answer 82

- in general consider infective endocarditis prophylaxis - vasodilators and diuretics e.g ACE-inhibitors e.g. Ramipril will improve stroke volume and reduce afterload and regurgitation but only if patient is symptomatic or has hypertension - serial echocardiograms to monitor progression - surgery for valve replacement: • if symptoms are increasing, enlarging heart on CXR/ECHO, ECG deterioration (T wave inversion in lateral leads)

Answer 83

* an infection of the endocardium or vascular endothelium of the heart * known as subacute bacterial endocarditis (SBE) * may occur as a fulminating or acute infection

Answer 84

- valves with congenital or acquired defects (usually on the left side of the heart) - right sided endocarditis more common in IV drug addicts - normal valves with virulent organisms - prosthetic valves and pacemakers - in association with a ventricular septal defect or persistent ductus arteriosus

Answer 85

- more common in developing countries - disease of: • the elderly or those with prosthetic valves • the young IV drug user • the young with congenital heart disease - more common in males

Answer 86

* Staphylococcus aureus (IVDU, diabetes and surgery); most common cause * Pseudomonas aeruginosa * Streptococcus viridans (dental problems); gram positive, alpha haemolytic and optochin resistant (Strep. mutans, strep, sanguis, strep. milleri and strep. oralis) * enterococci * Coxiella burnetii, Chlamydia spp., Bartonella spp. and Legionella

Answer 87

- IV drug use - poor dental hygiene - skin and soft tissue infection - dental treatment - IV cannula - cardiac surgery - pacemaker

Answer 88

- a mass of fibrin, platelets and infectious organisms form vegetations along the edges of the valve - damaged endocardium promotes platelet and fibrin deposition, which allows organisms to adhere and grow, leading to an infected vegetation - aortic and mitral valves are most commonly involved; IV drug users are the exception since right-sided lesions are more common in them - virulent organisms destroy the valve they are on, leading to regurgitation and worsening heart failure

Answer 89

• new valve lesion/regurgitant murmur • embolic events of unknown origin • sepsis of unknown origin • haematuria, glomerulonephritis and suspected renal infarction • fever plus: - prosthetic material inside the heart - risk factor for infective endocarditis e.g. IV drug user - newly developed ventricular arrhythmias or conduction disturbances

Answer 90

- headache, fever, malaise, confusion, and night sweats - finger clubbing - if Staphylococcus aureus, then will develop very quickly; high fever and feel ill rapidly, with the other virulent ones you don't feel as ill - embolisation of vegetations e.g. stroke, pulmonary embolus, bone infections, kidney dysfunction and myocardial infarction - valve dysfunction results in in arrhythmia and heart failure - endocarditis should be excluded in any patient with a heart murmur and fever

Answer 91

* splinter haemorrhages on nail beds of fingers * embolic skin lesions; black spots on skin (infarcts caused by bits of infective vegetation blocking small capillaries) * Osler nodes; tender nodules in the digits * Janeway lesions; haemorrhages and nodules in the fingers * Roth spots; retinal haemorrhages with white or clear centres seen on fundoscopy * Petechiae; small red/purple spots caused by bleeds in the skin

Answer 92

black spots on skin (infarcts caused by bits of infective vegetation blocking small capillaries) - seen in infective endocarditis

Answer 93

painful, red, raised lesions found on the hands and feet | - seen in infective endocarditis

Answer 94

rare, non-tender, small erythematous or haemorrhagic macular, papular or nodular lesions on the palms or soles only a few millimeters in diameter - seen in infective endocarditis

Answer 95

retinal haemorrhages with white or clear centres seen on fundoscopy - seen in infective endocarditis

Answer 96

small red/purple spots caused by bleeds in the skin | - seen in infective endocarditis

Answer 97

- use Dukes criteria - blood cultures and tests - urinalysis (look for haematuria) - CXR: cardiomegaly, heart failure or septic emboli in right-sided endocarditis - ECG: long PR interval at regular intervals (may show MI or conduction defects) - echocardiogram - serum immunoglobulins are increased and complement levels are decreased due to immune complex formation

Answer 98

* 3 sets from different sites over 24 hours * take before starting antibiotics * identifies in 75% of cases

Answer 99

* CRP and ESR raised * normochromic, normocytic anaemia * neutrophilia

Answer 100

- transthoracic echo (TTE) | - tranoesophageal echo (TOE)

Answer 101

- safe, non invasive, no discomfort but often poor images so low sensitivity but can identify vegetations (if greater than 2mm); a negative TTE does not exclude the diagnosis of infective endocarditis - identifies vegetations and underlying valvular dysfunction - smaller vegetations may be missed

Answer 102

- more sensitive but very uncomfortable, is useful for visualising mitral lesions and possible development of aortic root abscess; better at diagnosing than TTE - used in cases of suspected prosthetic valve endocarditis

Answer 103

- antibiotic treatment for 4-6 weeks - if not staphylococcus then use penicillin, benzylpenicillin and gentamycin - if staphylococcus then use vancomycin and rifampicin (if MRSA) - treat complications - surgery - recommend good oral health and inform patients of symptoms

Answer 104

arrhythmia, heart failure, heart block, embolisation, stroke rehab and abscess

Answer 105

* operate if the infection cannot be cured with antibiotics * operate to remove infected devices * operate to remove large vegetations before they embolise

Answer 106

bicuspid aortic valve (1-2% of live births)

Answer 107

* most common form of congenital heart disease, occurring in 1-2% of live births * more common in males than females

Answer 108

* bicuspid aortic valve only has 2 cusps * these can work well at birth and go undetected but can be severely stenotic in infancy or childhood * degenerate quicker than normal valves * become regurgitant earlier than normal valves * are associated with coarctation and dilation of the ascending aorta * may eventually develop aortic stenosis (requiring valve replacement) with or without aortic regurgitation thereby predisposing to infective endocarditis * intense exercise may accelerate complications so do yearly echocardiograms on affected athletes

Answer 109

• often first diagnosed in adulthood and represents one third of congenital heart disease • more common in women than men

Answer 110

• abnormal connection between the two atria • a probe can be passed through the layers of the foramen ovale (called the primum and secundum) so is sometimes known as “Probe patent foramen ovale” • slightly higher pressure in the left atrium than the right atrium • shunt is left-to-right • thus not blue i.e. acyanotic • increased flow into the right heart and lungs

Answer 111

if left untreated develop right heart overload and dilatation; the right ventricle is compliant and easily dilates to accommodate the increased pulmonary flow. this can result in: - right ventricular hypertrophy - pulmonary hypertension - Eisenmenger’s reaction - increased risk of infective endocarditis

Answer 112

- dysponea - exercise intolerance - may develop atrial arrhythmias from right atrial dilatation - pulmonary flow murmur - fixed split second heart sound (delayed closure of the pulmonary valve because more blood has to get out)

Answer 113

CXR: • large pulmonary arteries • large heart ECG: • right bundle branch block (RBBB) due to right ventricle dilatation echocardiogram: • hypertrophy and dilation of right side of heart and pulmonary arteries

Answer 114

* abnormal connection between the two ventricles * many close spontaneously during childhood * common - 20% of all congenital heart defects * higher pressure in left ventricle than right ventricle * thus left-to-right shunt * thus does not go blue i.e. acyanotic * increased blood flow through the lung

Answer 115

* the large volumes of blood flowing through the pulmonary vasculature lead to pulmonary hypertension and eventual Eisenmenger’s complex, when right ventricular pressure becomes higher than the left, as a result blood starts to shunt right-to-left resulting in cyanosis * small breathless skinny baby * increased respiratory rate * tachycardia * CXR: big heart * murmur varies in intensity

Answer 116

* large systolic murmur * thrill (buzzing sensation) * well grown * normal heart rate * normal heart size

Answer 117

- medical initially since many will spontaneously close - surgical closure - if small then no intervention is required - prophylactic antibiotics - if moderately sized lesion; furosemide, ACE inhibitor and digoxin may suffice

Answer 118

• associated with Downs syndrome • basically a hole in the very centre of the heart • involves the ventricular septum, the atrial septum, the mitral and tricuspid valves • can be complete or partial • instead of two separate atrio-ventricular valves there is just one big malformed one which usually leaks

Answer 119

* breathlessness as neonate * poor weight gain and feeding * torrential pulmonary flow which can result in Eisenmenger’s resulting in cyanosis over time

Answer 120

* can present in late adulthood | * presents similar to ventricular/atrial septal defect e.g. dysponea, tachycardia, exercise intolerance etc.

Answer 121

- pulmonary artery banding if large defect in infancy; band reduces blood flow to lungs thereby reducing pulmonary hypertension and Eisenmenger’s syndrome - surgical repair is challenging - a partial defect may be left alone if there is no right heart dilatation

Answer 122

• affects girls more than boys • ductus arteriosus is a persistent communication between the proximal left pulmonary artery and the descending aorta

Answer 123

• in foetal life, pulmonary vascular resistance is high (since bronchioles are filled with fluid and vessels are vasoconstricted due to lack of O2) and the right heart pressure exceeds that of left; consequently flow is from right to left atrium through foramen ovale, and from pulmonary artery to aorta via the ductus arteriosus • normally, the ductus arteriosus closes within a few hours of birth in response to decreased pulmonary resistance; however in some cases e.g. in premature babies and in cases with maternal rubella, the ductus persists

Answer 124

- premature babies | - maternal rubella

Answer 125

• if it remains open, there is an abnormal left-to-right shunt (from aorta to pulmonary artery) and eventually means that the lung circulation is overloaded with pulmonary hypertension (leading to Eisenmenger syndrome) and right side cardiac failure (due to right ventricular hypertrophy in response to increased afterload) • also increases risk of infective endocarditis

Answer 126

- continuous ‘machinery’ murmus - bounding pulse - if large then large heart and breathlessness - Eisenmenger’s syndrome with differential cyanosis that is clubbed and blue toes but pink and not clubbed fingers - tachycardia

Answer 127

CXR: with large shunt the aorta and pulmonary arterial system may be prominent ECG: may demonstrate left atrial abnormality and left ventricular hypertrophy echocardiogram: may show dilated left atrium and left ventricle

Answer 128

- can be closed surgically or percutaneously - low risk of complications - venous approach may require an AV loop - Indometacin (prostaglandin inhibitor) can be given to stimulate duct closure

Answer 129

• a narrowing of the aorta at, or just distal to, the insertion of the ductus arteriosus (distal to the origin of the left subclavian artery) • the net result is a narrowing of the aorta just after the arch, with excessive blood flow being diverted through the carotid and subclavian vessels into systemic vascular shunts to supply the rest of the body, thus stronger perfusion to upper body compared to lower

Answer 130

resultant decreased renal perfusion leads to systemic hypertension that persists even after surgical correction

Answer 131

- more common in men than women | - associated with Turner syndrome, berry aneurysms and patent ductus arteriosus

Answer 132

- often asymptomatic for many years - right arm hypertension - bruits (buzzes) over the scapulae and back from collateral vessels - murmur - headaches and nose bleeds (due to hypertension) - hypertension in the upper limbs - discrepant blood pressure in the upper and lower body (will notice radial pulse before femoral pulse)

Answer 133

hypertension: - early coronary artery disease - early strokes - sub-arachnoid haemorrhage

Answer 134

CXR: dilated aorta indented at the site of the coarctation ECG: left ventricular hypertrophy CT: can accurately demonstrate the coarctation and quantify flow

Answer 135

* surgery * balloon dilatation (preferred for re-coarctation) and stenting * risk of aneurysm formation at the site of repair

Answer 136

Tetralogy of Fallot

Answer 137

• consists of: - a large, maligned Ventricular Septal Defect (VSD) - an overriding aorta - pulmonary valve stenosis - right ventricular hypertrophy * the stenosis of the right ventricle outflow leads to the right ventricle being at a higher pressure than the left * thus blue blood passes from the right ventricle to the left ventricle * the patients are blue/cyanotic

Answer 138

- central cyanosis - low birthweight and growth - dysponea on exertion - delayed puberty - systolic ejection murmurs - CXR: boot shaped heart

Answer 139

- full surgical treatment during first two years of life due to the progressive cardiac debility and cerebral thrombosis risk - often get pulmonary valve regurgitation in adulthood and require redo surgery

Answer 140

- narrowing of the outflow of the right ventricle | - valvar, sub-valvar or supra-valvar

Answer 141

- right ventricular failure as neonate - collapse - poor pulmonary blood flow - right ventricular hypertrophy - tricuspid regurgitation

Answer 142

- well tolerated for many years | - right ventricular hypertrophy

Answer 143

- balloon valvoplasty: place catheter with balloon through femoral vein then inflate balloon at stenosis to crush it but this can result in regurgitation - open valvotomy - shunt to bypass the blockage

Answer 144

* involves the aorta coming off the right ventricle and the pulmonary trunk coming off the left ventricle * two closed circulations result * more common in men and associated with diabetes

Answer 145

survival is only possible if there is communication between the two circuits and virtually all have some form of atrial septal defect with blood mixing

Answer 146

atrial switch operation, with good results

Answer 147

- heart points to the right side of the chest instead of to the left - associated with severe cardiovascular abnormalities

Answer 148

chest pain, breathlessness, palpitations, syncope, fatigue and peripheral oedema

Answer 149

cardiac status; severity of anginal pain, dyspnoea, palpitations or fatigue

Answer 150

Grade 1: uncompromised (no breathlessness) Grade 2: slightly compromised (on severe exertion) Grade 3: moderately compromised (on mild exertion) Grade 4: severely compromised (breathless at rest)

Answer 151

- chest pain or discomfort is a common presenting symptom of cardiovascular disease and must be differentiated from non-cardiac causes - the site of pain, its character, radiation and associated symptoms will often point to the cause

Answer 152

- angina pectoris - ACS - pericarditis - aortic dissection - massive PE - MSK pain - GORD

Answer 153

crushing pain on exercise, relieved by rest. may radiate to jaw or arms

Answer 154

similar in character to angina but more severe, occurs at rest, lasts longer

Answer 155

sharp pain aggravated by movement, respiration and changes in posture

Answer 156

severe tearing chest pain radiating through to the back

Answer 157

with dyspnoea, tachycardia and hypotension

Answer 158

tender to palpate over affected area

Answer 159

may be exacerbated by bending or lying down (at night). pain may radiate into the neck

Answer 160

when the patient is anxious, excited, exercising or lying on the left side

Answer 161

cardiac arrhythmia, commonly ectopic beats or a paroxysmal tachycardia

Answer 162

temporary impairment of consciousness due to inadequate cerebral blood flow - attacks occur suddenly and without warning - they last only 1 or 2 minutes, with complete recovery in seconds (compare with epilepsy, where complete recovery may be delayed for some hours)

Answer 163

- syncope - underlying structural cardiopulmonary disease, e.g. aortic stenosis, PE - arrhythmias - reflex – vasovagal (simple faint) - carotid sinus hypersensitivity - situational: cough, micturition, postexertional - postural (orthostatic) hypotension: autonomic failure, volume depletion - epilepsy - hypoglycaemia - psychogenic - panic attacks - hyperventilation - narcolepsy and cataplexy

Answer 164

- result of either very fast (e.g. ventricular tachycardia) or very slow heart rates (e.g. complete heart block) which are unable to maintain an adequate cardiac output - obstruction to ventricular outflow also causes syncope (e.g. aortic stenosis, hypertrophic cardiomyopathy), which occurs on exercise when the requirements for increased cardiac output cannot be met

Answer 165

a drop in systolic blood pressure (BP) of 20mmHg or more on standing up from a sitting or lying position

Answer 166

- pulmonary infarct - pneumonia - pneumothorax - MSK - lung carcinoma - herpes zoster

Answer 167

constant dull pain

Answer 168

burning unilateral pain corresponding to a dermatome that appears 2 to 3 days before the typical rash

Answer 169

a cardiothoracic ratio of greater than 50% on a PA film is abnormal and normally indicates cardiac dilatation or pericardial effusion

Answer 170

anterior superior division (anterior hemi-bundle) and a posterior inferior division (posterior hemi-bundle)

Answer 171

- broad and notched (> 0.12 s, i.e. three small squares) in left atrial enlargement (‘P mitrale’, e.g. mitral stenosis) - tall and peaked (> 2.5 mm) in right atrial enlargement (‘P pulmonale’, e.g. pulmonary hypertension) - replaced by flutter or fibrillation waves (p. 430) - absent in sinoatrial block

Answer 172

- ST elevation (>1mm above isoelectric line) occurs in early stages of MI and with acute pericarditis - ST depression (>0.5mm below the isoelectric line) indicates myocardial ischaemia

Answer 173

QTc = QT/square root of (R-R)

Answer 174

increased risk of torsades de pointes ventricular tachycardia and sudden death

Answer 175

overall direction of the wave of ventricular depolarisation in the vertical plane measured from a zero reference point

Answer 176

the normal range for the cardiac axis is between −30° and +90. an axis more negative than −30° is termed left axis deviation and an axis more positive than +90° is termed right axis deviation

Answer 177

an axis more negative than −30° is termed left axis deviation - block of anterior bundle of the main LBB, inferior MI and WPW syndrome

Answer 178

an axis more positive than +90° is termed right axis deviation - may be normal - right ventricular overload, dextrocardia, WPW and left posterior hemiblock

Answer 179

a simple method to calculate the axis is by inspection of the QRS complex in leads I, II and III. - the axis is normal if leads I and II are positive - there is right axis deviation if lead I is negative and lead III positive - there is left axis deviation if lead I is positive and leads II and III negative

Answer 180

lead I: normal QRS complex lead II: tall R wave lead III: small equal QRS complex

Answer 181

- unstable angina - severe hypertrophic cardiomyopathy - severe aortic stenosis - malignant hypertension

Answer 182

- chest pain - ST segment depression or elevation >1mm - fall in systolic BP >20mmHg - fall in HR despite and increase in workload - BP >240/110 - significant arrhythmias or increased frequency of ventricular ectopics

Answer 183

tilt testing is performed to investigate suspected neurocardiogenic (vasovagal) syncope in which patients give a history of repeated episodes of syncope which occur without warning and are followed by a rapid recovery

Answer 184

- transthoracic echo | - transoesophageal echo

Answer 185

transthoracic echo is the most common method and involves the placement of a handheld transducer on the chest wall. ultrasound pulses are emitted through various body tissues, and reflected waves are detected by the transducer as an echo

Answer 186

left ventricular function is assessed by the ejection fraction (percentage of blood ejected from the left ventricle with each heartbeat) – normally > 55%

Answer 187

transoesophageal echo uses miniaturized transducers incorporated into special endoscopes. it allows better visualization of some structures and pathology, e.g. aortic dissection, endocarditis

Answer 188

doppler echocardiography uses the Doppler principle to identify and assess the severity of valve lesions, estimate cardiac output and assess coronary blood flow.

Answer 189

- patients with adverse symptoms and signs (low cardiac output, chest pain, hypotension, impaired consciousness or severe pulmonary oedema) require urgent treatment of their arrhythmia - oxygen is given to all patients, intravenous access established and serum electrolyte abnormalities (potassium, magnesium, calcium) are corrected

Answer 190

- fluctuations of autonomic tone result in phasic changes in the sinus discharge rate - normal during sleep and in well-trained athletes

Answer 191

- drug therapy (beta blockers, digitalis and other antiarrhythmic drugs) - hypothyroidism - hypothermia - cholestatic jaundice - raised intracranial pressure

Answer 192

- acute ischaemia and infarction of the sinus node (as a complication of MI) - chronic degenerative changes e.g. fibrosis of the atrium and sinus node (sick sinus syndrome) occurring in elderly people

Answer 193

- patients with persistent symptomatic bradycardia are treated with a permanent cardiac pacemaker. - first-line treatment in the acute situation with adverse signs is atropine - temporary pacing (transcutaneous, or transvenous) is an alternative.

Answer 194

- bradycardia is caused by intermittent failure of sinus node depolarization (sinus arrest) or failure of the sinus impulse to propagate through the perinodal tissue to the atria (sinoatrial block) - the slow heart rate predisposes to ectopic pacemaker activity and tachyarrhythmias are common (tachy–brady syndrome)

Answer 195

the ECG shows severe sinus bradycardia or intermittent long pauses between consecutive P waves (> 2 s, dropped P waves)

Answer 196

- permanent pacemaker insertion - antiarrhythmic drugs are used to treat tachycardias. - thromboembolism is common in sinus node dysfunction and patients are anticoagulated unless there is a contraindication.

Answer 197

ventricular tachycardia is more likely than SVT with: - history of ischaemic heart disease - QRS interval > 140 ms - atrioventricular dissociation – P waves have no relationship to the QRS complexes - capture complexes – intermittent normal QRS complex - RS interval > 100 ms - bifid, upright QRS complex with a taller first peak in V1 - deep S wave in V6 - concordant QRS direction in leads V1–V6, i.e. all positive or all negative complexes

Answer 198

- adenosine (very short acting AV nodal blocking drug that will terminate most junctional tachycardias) - IV verapamil - beta blockers

Answer 199

- ischaemic heart disease, rheumatic heart disease, valvular heart disease - cardiomyopathy - lone atrial fibrillation (no cause identified) - Wolff–Parkinson–White syndrome - pericarditis, myocarditis - atrial septal defect, cardiac surgery

Answer 200

- pneumonia - PE - carcinoma of the bronchus - COPD

Answer 201

novel oral anticoagulants - direct thrombin inhibitors (e.g. Dabigatran) - oral direct factor Xa inhibitors (e.g. Rivaroxaban and Apixaban)

Answer 202

- block a single step in the coagulation cascade (thrombin or factor Xa inhibitors) - warfarin blocks several vitamin K dependent factors (II, VII, IX, X) - unlike warfarin, the NOACs have rapid onset of action, shorter half-life, fewer food and drug interactions and do not require INR testing - however, these agents require dose reduction or avoidance in patients with renal impairment, elderly patients or those with low body weight

Answer 203

- in cardiac arrest there is no effective cardiac output. the patient is unconscious and apnoeic with absent arterial pulses (best felt in the carotid artery in the neck) - irreversible brain damage occurs within 3 minutes if an adequate circulation is not established

Answer 204

- this is defined as VT ≥ 5 consecutive beats but lasting <30s - common in patients with heart disease (and in a few individuals with normal hearts)

Answer 205

the treatments indicated are β-blockers in symptomatic patients or an ICD in patients with poor left ventricular function (ejection fraction < 30%) in whom it improves survival

Answer 206

• valvular heart disease e.g. aortic stenosis, aortic and mitral regurgitation, tricuspid • cardiomyopathy (hypertrophic, restrictive) • congenital heart disease (atrial septal defect, ventricular septal defect) • hyperdynamic circulation (anaemia, thyrotoxicosis, Paget's disease) • hypertension • alcohol and chemotherapy (e.g. imatinib, doxorubicin) • right heart failure (RV infarct, pulmonary hypertension, PE, cor pulmonale, COPD) • pericardial disease (constrictive pericarditis, pericardial effusion) • infections (Chagas' disease) • any factor that increases myocardial work e.g. anaemia, arrhythmias, hyperthyroidism, pregnancy and obesity - endocardial/pericardial causes

Answer 207

- ANP, BNP, C type pepide have diuretic, natiuretic and hypotensive properties - may lead to beneficial but inadequate compensatory response leading to reduced preload and afterload - N-terminal fragment released from pro-BNP and BNP itself correlate with severity of heart failure

Answer 208

- myocardial failure leads to a reduction of volume of blood ejected with each heartbeat, thus an increase in the volume of blood remaining after systole - increased diastolic volume stretches the myocardial fibres and myocardial contraction is restored - once heart failure is established, the compensatory effects of dilatation are limited by flattened contour of Starling's curve - increased venous pressure -> pulmonary and peripheral oedema - ventricular diameter increases and greater tension is needed to expel a given volume of blood, and oxygen requirements increase

Answer 209

- hypertrophy, loss of myocytes and increased interstitial fibrosis - leads to progressive and irreversible pump (contractile failure) - process is multifactorial and includes apoptosis of myocytes and changes in cardiac contractile gene expression (e.g. myosin)

Answer 210

- left ventricular systolic dysfunction (LVSD) - right ventricular systolic dysfunction (RVSD) - diastolic heart failure

Answer 211

- heart failure with normal ejection fraction - syndrome consisting of symptoms and sings of heart failure but with normal/near-normal left ventricular ejection fraction (above 45-50%) and evidence of diastolic dysfunction on echo - impairment of diastolic ventricular filling and decreased cardiac output

Answer 212

- cardiac catheterisation - thallium perfusion imaging - PET scanning - MRI - dobutamine stress echocardiography

Answer 213

a region of impaired myocardial contractility due to persistently impaired coronary blood flow

Answer 214

heart failure suspected due to symptoms and signs -> assess presence of cardiac disease by ECG, CXR and natriuretic peptides (normal BNP <100pg/mL -> abnormal -> imaging by echocardiography -> abnormal: assess aetiology, degree, precipitating factors, types of cardiac dysfunction

Answer 215

- ACEi (or ARA) - beta blockers - diuretic - spironolactone/eplerenone - digoxin - vasodilators - inotropic agents

Answer 216

- revascularisation - cardiac resynchronisation therapy (biventricular pacing) - implantable cardioverter-defibrillator - replacement of diseased valves - repair of congenital heart disease - cardiac transplantation - left ventricular assist device and artificial heart

Answer 217

- medical emergency, with left or right heart failure developing over minutes or hours - aetiology similar to chronic heart failure - initial investigations: ECG, CXR, blood tests, transthoracic echocardiogram - blood tests of serum troponin (for myocardial necrosis) and D-dimer (PE)

Answer 218

* acute decompensation of chronic heart failure * hypertensive heart failure – high BP, preserved left ventricular function, pulmonary oedema on chest X-ray * acute pulmonary oedema – acutely breathless, tachycardia, profuse sweating (sympathetic overactivity), wheezes and crackles throughout the chest, hypoxia, pulmonary oedema on chest X-ray * cardiogenic shock – hypotension, tachycardia, oliguria, cold extremities * high output cardiac failure – e.g. septic shock, warm peripheries, pulmonary congestion, BP may be low * right heart failure – low cardiac output, elevated jugular venous pressure, hepatomegaly, hypotension.

Answer 219

- high flow oxygen, CPAP sometimes indicated - furosemide IV 50mg - clinical evaluation of systolic blood pressure

Answer 220

- vasodilator e.g. GTN, nitroprusside, BNP - no response: consider mechanical assist devices, e.g. right or left ventricular assist devices - good response: oral therapy; furosemide and ACEi

Answer 221

- vasodilator and/or inotropic (dobutamine, PDE inhibitor) - no response: consider mechanical assist devices, e.g. right or left ventricular assist devices - good response: oral therapy; furosemide and ACEi

Answer 222

- volume loading? - inotropic and/or dopamine and/or noradrenaline - no response: consider mechanical assist devices, e.g. right or left ventricular assist devices - good response: oral therapy; furosemide and ACEi

Answer 223

- immediate investigations and treatment - reperfusion therapy or thrombolysis - metoprolol (5mg slow IV injection) if heart rate >100bpm (contraindicated if hypotension, heart failure, bradycardia, asthma) - insulin infusion - treat complications

Answer 224

* repeat ECG, serum cardiac markers and electrolytes at 24 and 48 hours after admission. * initiate secondary prevention therapy: aspirin, clopidogrel, statin, metoprolol, ACEI and modification of CAD risk factors (as for ACS). * transfer from CCU to medical ward after 48 hours. * mobilize gradually and discharge from hospital after 5 days. * submaximal exercise ECG test prior to discharge if primary angioplasty not performed. * refer to cardiac rehabilitation programme. * no driving for 1 month; special assessment is required for heavy goods or public service licence holder before driving. Usually return to work in 2 months.

Answer 225

* aspirin * a second anti-platelet agent * an oral β-blocker to maintain heart rate < 60 beats/min * ACEIs or angiotensin receptor blockers, particularly if left ventricular ejection fraction is below 40% * high-intensity statins with target low-density lipoprotein (LDL) cholesterol < 1.8 mmol/L * aldosterone antagonist – post-MI with clinical evidence of heart failure and left ventricular ejection fraction ≤ 40% if the serum creatinine is < 221 μmol/L (men) or < 177 μmol/L (women) and the serum potassium < 5.0 mEq/L.

Answer 226

- an inflammatory disease that usually has its first onset between 5 and 15 years of age as a result of infection with group A streptococci - It is a complication of less than 1% of streptococcal pharyngitis, developing 2–3 weeks after the onset of sore throat. - it is thought to develop because of an autoimmune reaction triggered by the streptococci rather than direct infection of the heart

Answer 227

- presents suddenly with fever, joint pains and loss of appetite - changing heart murmurs, mitral and aortic regurgitation, heart failure and chest pain, caused by carditis affecting all three layers of the heart - polyarthritis – fleeting and affecting the large joints, e.g. knees, ankles and elbows - skin manifestations – erythema marginatum (transient pink coalescent rings develop on the trunk) and small non-tender subcutaneous nodules which occur over tendons, joints and bony prominences - Sydenham’s chorea indicates involvement of the central nervous system and presents with ‘fidgety’ and spasmodic, unintentional movements.

Answer 228

erythema marginatum (transient pink coalescent rings develop on the trunk) and small non-tender subcutaneous nodules which occur over tendons, joints and bony prominences

Answer 229

leucocytosis and a raised ESR

Answer 230

- complete bed rest and high dose aspirin - penicillin to eradicate residual streptococcal infection - long term to patients with persistent cardiac damage

Answer 231

- loud second heart sound - parasternal heave - elevated JVP - peripheral oedema

Answer 232

systemic lupus erythematosus, Marfan's syndrome

Answer 233

rise in left atrial pressure, resulting in an increase in pulmonary venous pressure and pulmonary oedema

Answer 234

caused by rapid filling of the dilated left ventricle in early diastole

Answer 235

- common condition that occurs mainly in young women - one or more of the mitral valve leaflets prolapses back into the left atrium during ventricular systole, producing mitral regurgitation in a few cases

Answer 236

the cause is unknown, but it is associated with Marfan’s syndrome, hyperthyroidism and rheumatic or ischaemic heart disease

Answer 237

- most patients are asymptomatic - atypical chest pain is the most common symptom - some patients complain of palpitations caused by atrial and ventricular arrhythmias - the typical finding on examination is a mid-systolic click, which may be followed by a murmur - occasionally, there are features of mitral regurgitation

Answer 238

- chest pain and palpitations are treated with β-blockers - anticoagulation to prevent thromboembolism is indicated if there is significant mitral regurgitation and atrial fibrillation

Answer 239

- infective endocarditis - acute rheumatic fever - dissection of the aorta - ruptured sinus of Valsalva aneurysm - failure of prosthetic heart valve

Answer 240

- chronic rheumatic heart disease - bicuspid aortic valve - aortic endocarditis - arthritides: Reiter's syndrome, ankylosing spondylitis, rheumatoid arthritis - severe hypertension - Marfan's syndrome - syphilis - osteogenesis imperfecta

Answer 241

tricuspid stenosis is almost always the result of rheumatic fever and is frequently associated with mitral and aortic valve disease, which tends to dominate the clinical picture

Answer 242

- tricuspid regurgitation is usually functional and secondary to dilatation of the right ventricle (and hence tricuspid valve ring) in severe right ventricular failure - much less commonly it is caused by rheumatic heart disease, infective endocarditis or carcinoid syndrome - on examination there is a pansystolic murmur heard at the lower left sternal edge, the jugular venous pressure is elevated, with giant ‘v’ waves (produced by the regurgitant jet through the tricuspid valve in systole), and the liver is enlarged and pulsates in systole - there may be severe peripheral oedema and ascites - in functional tricuspid regurgitation these signs improve with diuretic therapy

Answer 243

- pulmonary regurgitation results from pulmonary hypertension and dilatation of the valve ring - occasionally it is the result of endocarditis (usually in intravenous drug abusers) - auscultation reveals an early diastolic murmur heard at the upper left sternal edge (Graham Steell murmur), similar to that of aortic regurgitation - usually there are no symptoms and treatment is rarely required - pulmonary stenosis is usually a congenital lesion but may present in adult life with fatigue, syncope and right ventricular failure

Answer 244

early diastolic murmur heard at the upper left sternal edge | - heard in pulmonary regurgitation

Answer 245

- positive blood cultures for infective endocarditis - typical microorganism for infective endocarditis from two separate blood cultures in the absence of a primary focus - persistently positive blood cultures, defined as recovery of a microorganism consistent with infective endocarditis from blood cultures drawn more than 12 hours apart or all of three or the majority of four or more separate blood cultures, with first and last drawn at least 1 hour apart - single positive blood culture for Coxiella burnetii or antiphase IgG antibody titre - evidence for endocardial involvement - TTE (TOE in prosthetic valve) showing oscillating intracardiac mass on a valve or supporting structures, in the path of regurgitant jet or on implanted material, in the absence of an alternative anatomic explanation, or - abscess - new partial dehiscence of prosthetic valve - new valvular regurgitation

Answer 246

- predisposition, e.g. prosthetic valve, intravenous drug use - fever – 38°C - vascular phenomena (e.g. major arterial emboli, septic pulmonary infarcts) - immunological phenomena (e.g. Osler’s nodes, glomerulonephritis) - echocardiogram – findings consistent with infective endocarditis but not meeting major criteria - microbiological evidence – positive blood culture but not meeting major criteria

Answer 247

* systemic features of infection, such as malaise, fever, night sweats, weight loss and anaemia. slight splenomegaly is common. clubbing is rare and occurs late. * valve destruction, leading to heart failure and new or changing heart murmurs (in 90% of cases). * vascular phenomena due to embolization of vegetations and metastatic abscess formation in the brain, spleen and kidney. embolization from right-sided endocarditis causes pulmonary infarction and pneumonia. * immune complex deposition in blood vessels producing a vasculitis and petechial haemorrhages in the skin, under the nails (splinter haemorrhages) and in the retinae (Roth’s spots). Osler’s nodes (tender subcutaneous nodules in the fingers) and Janeway lesions (painless erythematous macules on the palms) are uncommon. * immune complex deposition in the joints causes arthralgia and, in the kidney, acute glomerulonephritis. microscopic haematuria occurs in 70% of cases but acute kidney injury is uncommon.

Answer 248

surgery to replace the valve should be considered when there is severe heart failure, early infection of prosthetic material, worsening renal failure and extensive damage to the valve.

Answer 249

one of the following: * direct evidence of infective endocarditis by histology or culture of organism, e.g. from a vegetation * two major (Dukes) criteria * one major and any three minor criteria * five minor criteria

Answer 250

if there is one major and one minor criterion or three minor (Dukes)

Answer 251

- the lung circulation offers a low resistance to flow compared to the systemic circulation and the normal mean pulmonary artery pressure (PAP) at rest is 10–14 mmHg (compared to mean systemic arterial pressure of about 90 mmHg) - pulmonary hypertension is characterized by an elevated PAP (> 25 mmHg at rest) and secondary right ventricular failure - occurs due to an increase in pulmonary vascular resistance or an increase in pulmonary blood flow

Answer 252

- idiopathic (no cause identified) - autoimmune rheumatic diseases, e.g. systemic sclerosis, systemic lupus erythematosus, rheumatoid arthritis - congenital heart disease with systemic-to-pulmonary communication (atrial septal defect, ventricular septal defect) - portal hypertension (portopulmonary hypertension) - drugs: long-term use of cocaine and amphetamines, dexfenfluramine - HIV infection - Hereditary - schistosomiasis - chronic haemolytic anaemia - pulmonary veno-occlusive disease

Answer 253

- left heart disease: valvular, systolic dysfunction, diastolic dysfunction - lung disease and/or hypoxia, e.g. chronic obstructive pulmonary disease, obstructive sleep apnoea, lung fibrosis - thromboembolic occlusion of proximal or distal pulmonary vasculature - multifactorial mechanisms: myeloproliferative disorders, sarcoidosis, glycogen storage disease

Answer 254

- exertional dyspnoea, lethargy and fatigue are the initial symptoms due to an inability to increase cardiac output with exercise. - as right ventricular failure develops there is peripheral oedema and abdominal pain from hepatic congestion. - on examination there is a loud pulmonary second sound, and a right parasternal heave (caused by right ventricular hypertrophy). - in advanced disease there are features of right heart failure (cor pulmonale): elevated jugular venous pressure with a prominent V wave if tricuspid regurgitation is present, hepatomegaly, a pulsatile liver, peripheral oedema, ascites and a pleural effusion. there are also features of the underlying disease.

Answer 255

chest X-ray shows enlarged proximal pulmonary arteries which taper distally. it may also reveal the underlying cause (e.g. emphysema, calcified mitral valve).

Answer 256

ventricular hypertrophy and P pulmonale

Answer 257

echocardiography shows right ventricular dilatation and/or hypertrophy and may also reveal the cause of pulmonary hypertension

Answer 258

right heart catheterization may be indicated to confirm the diagnosis (elevated PAP), to determine the pulmonary wedge pressure (PWP), to calculate the cardiac output and to assess for pulmonary vascular resistance and reactivity.

Answer 259

- oxygen - warfarin (due to higher risk of intrapulmonary thrombosis) - diuretics for oedema - oral calcium-channel blockers as pulmonary vasodilators - treatment of underlying cause

Answer 260

- aimed at decreasing pulmonary vascular resistance - oral endothelin receptor antagonists (bosentan, sitaxentan) - prostanoid analogues (inhaled iloprost, treprostinil, beraprost) - IV epoprostenol and oral sildenafil or tadalafil in primary pulmonary hypertension there is a progressive downhill course and many patients ultimately require heart and lung transplantation

Answer 261

- a massive embolism obstructs the right ventricular outflow tract and therefore suddenly increases pulmonary vascular resistance, causing acute right heart failure. - a small embolus impacts in a terminal, peripheral pulmonary vessel and may be clinically silent unless it causes pulmonary infarction. - lung tissue is ventilated but not perfused, resulting in impaired gas exchange. - it is important to consider PE in the differential diagnosis of chest pain with elevated troponin. the rise in troponin reflects right ventricular ischaemia and is associated with adverse outcomes.

Answer 262

- small/medium PEs present with breathlessness, pleuritic chest pain, and haemoptysis if there is pulmonary infarction. - on examination the patient may be tachypnoeic and have a pleural rub and an exudative (occasionally bloodstained) pleural effusion can develop.

Answer 263

- massive PE presents as a medical emergency: the patient has severe central chest pain and suddenly becomes shocked, pale and sweaty, with marked tachypnoea and tachycardia. - syncope and death may follow rapidly. - on examination the patient is shocked, with central cyanosis. - there is elevation of the jugular venous pressure, a right ventricular heave, accentuation of the second heart sound and a gallop rhythm (acute right heart failure).

Answer 264

- chest X-ray, ECG and blood gases may all be normal with small/medium emboli and any abnormalities with massive emboli are non-specific. - chest X-ray and ECG are useful to exclude other conditions that may present similarly. - CXR show decreased vascular markings and a raised hemidiaphragm (caused by loss of lung volume). with pulmonary infarction, a late feature is the development of a wedge-shaped opacity adjacent to the pleural edge, sometimes with a pleural effusion. - the most common ECG finding is sinus tachycardia or there may be new-onset atrial fibrillation. features of acute right heart strain may be seen: tall peaked P waves in lead II, right axis deviation and right bundle branch block. - ABGs show hypoxaemia and hypocapnia with massive emboli.

Answer 265

- plasma D-dimers are a subset of fibrinogen degradation products released into the circulation when a clot begins to dissolve. - D-dimers are, however, elevated in many other conditions (e.g. cancer, pregnancy, post-operatively) and a positive result is not diagnostic of thromboembolic disease. - the value of D-dimer testing is in patients with a low pre-test clinical probability score

Answer 266

subset of fibrinogen degradation products released into the circulation when a clot begins to dissolve

Answer 267

- spiral CT with intravenous contrast (CT pulmonary angiography, CTPA) images the pulmonary vessels directly and is highly sensitive for the detection of large proximal pulmonary emboli. - increasingly being used as the diagnostic test of choice for patients with suspected PE. - subsegmental emboli may be missed and occasionally patients may need further imaging

Answer 268

- ultrasound will detect clots in the pelvic or iliofemoral veins. - MRI gives similar results and is used if CT is contraindicated - Echocardiography is diagnostic in massive PE and can be performed at the bedside. it demonstrates proximal thrombus and right ventricular dilatation.

Answer 269

- age >65yrs (+1 point) - previous DVT or PE (+3) - surgery or fracture within 1 month (+2) - active malignancy (+2)

Answer 270

- unilateral leg pain (+3) | - haemoptysis (+2)

Answer 271

- HR 75-94 (+3 points) - HR >95 (+5 points) - pain on leg deep vein palpation and unilateral oedema (+4 points)

Answer 272

low: 0-3 intermediate: 4-10 high: >11

Answer 273

- determine pre test clinical probability of PE (Geneva) - low -> D-dimer - intermediate/high -> start LMWH -> CT pulmonary angiogram - positive D-dimer test -> CT pulmonary angiogram - PE present on CT pulmonary angiogram -> start warfarin

Answer 274

- only definitive indication for thrombolysis in acute massive embolism is persistent arterial hypotension - surgical embolectomy done if thrombolysis is contraindicated or ineffective - patients who are stable and with no other pathology can be treated at home - anticoagulation continued for 6 weeks to 6 months - lifelong treatment for recurrent emboli - insertion of a vena caval filter used to prevent further emboli

Answer 275

- occurs more frequently in pregnancy - leading cause of maternal death in the developed world - compression ultrasonography of legs is initial investigation - CT pulmonary angiography required if ultrasound is normal; delivers lower dose of radiation to fetus than other scans - warfarin is teratogenic - treated with LMWH

Answer 276

- the most common cause in the UK is viral, particularly Coxsackie virus infection - it may also occur with diphtheria, rheumatic fever, radiation injury and some drugs. - myocarditis in association with human immunodeficiency virus (HIV) infection is seen at postmortem in up to 20% of cases but causes clinical problems in less than 10% of cases.

Answer 277

- acute illness characterised by fever and varying degrees of biventricular failure - cardiac arrhythmias and pericarditis may also occur

Answer 278

- CXR may show cardiac enlargement - ECG shows non-specific T wave and ST changes and arrhythmias - the diagnosis is supported by demonstration of an increase in serum viral titres. cardiac biopsy is not usually performed as the findings rarely influence management. - cardiac enzymes are elevated.

Answer 279

due to left ventricular outflow obstruction

Answer 280

- persistent effusion - purulent, tuberculous or malignant effusion is suspected - if effusion is not known to be secondary to an underlying illness

Answer 281

- pericardiocentesis (aspiration of fluid under echo guidance) - pericardial biopsy for culture - cytology/histology - PCR

Answer 282

* genetic component * low birthweight * obesity * excess alcohol intake * high salt intake * the metabolic syndrome

Answer 283

- renal disease - endocrine disease - pre-eclampsia - drugs

Answer 284

- diabetic nephropathy - chronic glomerulonephritis - adult polycystic kidneys - chronic tubulointerstital nephritis - renovascular disease

Answer 285

a congenital narrowing of the aorta at, or just distal to, the insertion of the ductus arteriosus

Answer 286

grade 1: increased tortuosity and reflectiveness of the retinal arteries (silver wiring) grade 2: grade 1 plus arteriovenous nipping grade 3: grade 2 plus flame shaped haemorrhages and soft cotton wool exudates grade 4: grade 3 plus papilloedema

Answer 287

block the conversion of angiotensin I to angiotensin II, which is a potent vasoconstrictor, and block degradation of bradykinin, which is a vasodilator

Answer 288

increase renal sodium and water excretion and directly dilate arterioles

Answer 289

- younger patients - intolerance or contraindication to ACEi and angiotensin-II receptor blockers - women of child bearing potential - patients with evidence of increased sympathetic drive

Answer 290

- the β-adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas and liver are blocked. - they decrease heart rate, reduce the force of cardiac contraction and lower BP. - these effects reduce myocardial oxygen demand and give more time for coronary perfusion. β-Blockers improve functional status and reduce cardiovascular morbidity and mortality in patients with heart failure.

Answer 291

- alpha blocking agents e.g. doxazosin - hydralazine - aldosterone antagonist (spironolactone) - centrally acting agents (clonidine, moxonidine)

Answer 292

offer treatment to everyone under 80yrs old with at least one of the following risk factors: - target organ damage - cardiovascular disease - renal disease - diabetes - 10 year cardiovascular risk >20%

Answer 293

- oral antihypertensives, e.g. atenolol or amlodipine - sublingual and IV hypertensives not recommended because they may produce a precipitous fall in BP, leading to cerebral infarction - when rapid control of BP is required, the agent of choice is sodium nitroprusside (starting dose 0.3 μg/kg/min, i.e. 100 mg nitroprusside in 250 mL saline at 2–5 mL/h) or labetalol

Answer 294

- consists of intermittent spasm in the arteries supplying the fingers and toes - usually precipitated by cold and relieved by heat - initial pallor (resulting from vasoconstriction) followed by cyanosis and finally, redness from hyperaemia

Answer 295

no underlying disorder causing Raynaud's phenomenon

Answer 296

- keeping hands and feet warm - stopping smoking - stopping beta blockers - oral Nifedipine - occasionally prostacyclin infusions - lumbar sympathectomy may help lower limb symptoms

Answer 297

- inflammation of a vein near the surface of the skin (usually a varicose vein) caused by a blood clot - vein is painful, tender adn hard, with overlying redness - treatment with simple analgesia, e.g. NSAIDs - anticoagulation with fondaparinux can limit the extension of superficial thrombosis - thromboembolic events are uncommon

Answer 298

- PE - post-thrombotic syndrome (permanent pain, swelling, oedema and sometimes venous eczema may result from destruction of deep-vein valves) - recurrence of thrombosis

Answer 299

- hospital-acquired venous thromboembolism is largely preventable. - all patients should be assessed on admission to hospital and those at risk should be considered for pharmacological prophylaxis (fondaparinux, LMWH or unfractionated heparin if renal impairment) unless they have a risk factor for bleeding.

Answer 300

- lower limb trauma or surgery or immobilisation in a plaster cast (+1) - bedridden for more than 3 days or surgery within the last 4 weeks (+1) - malignancy (including treatment up to 6 months previously) (+1) - tenderness along deep venous system (+1)

Answer 301

- entire limb swollen (+1) - calf swelling more than 3cm compared to asymptomatic side, measured at 10cm below tibial tuberosity (+1) - pitting oedema (greater in symptomatic leg) (+1) - dilated collateral superficial veins (non-varicose) (+1)

Answer 302

alternative diagnosis (e.g. musculoskeletal injury, haematoma, chronic oedema, cellulitis of the leg, arthritis of the leg, Baker’s cyst) as likely or greater than that of DVT (-2)

Answer 303

- MSK injury - haematoma - chronic oedema - cellulitis of the leg - arthritis of the leg - Baker's cyst

Answer 304

``` <0 = 3% (low) 1-2 = 17% (moderate) >3 = 75% (high) ```

Answer 305

- adenosine is a purine nucleotide. - it acts on adenosine receptors and enhances the flow of potassium out of myocardial cells; it produces hyperpolarization of the cell membrane and stabilizes the cell membrane. - it has potent effects on the sinus (SA) node, causing complete heart block for a fraction of a second after i.v. administration and producing sinus bradycardia.

Answer 306

the main indication is reversion to sinus rhythm of atrioventricular junctional tachycardia.

Answer 307

- 3mg/mL - by rapid i.v. injection into a central or large peripheral vein, 6 mg over 2 seconds with cardiac monitoring and resuscitation equipment available; if necessary, followed by 12 mg after 1–2 minutes, and then 12 mg after a further 1–2 minutes; increments should not be given if high-level AV block develops at any dose.

Answer 308

unwanted effects are common; however, they are usually transient. patients should be warned before drug administration of side effects usually lasting less than 1 minute: - bradycardia and AV block - facial flushing, headache, chest pain or tightness - bronchospasm, sense of impending doom

Answer 309

contraindicated in asthma, second- or third-degree AV block and sick sinus syndrome (unless pacemaker fitted).

Answer 310

class III (Vaughan Williams’ classification) drug action, which prolongs the duration of the action potential, thus increasing the absolute refractory period. inhibits the potassium channels involved in repolarization.

Answer 311

- intravenous injection of amiodarone is used in cardiopulmonary resuscitation for ventricular fibrillation or pulseless tachycardia unresponsive to other interventions. - oral and i.v. amiodarone is used in the treatment of arrhythmias - in the non-emergency setting it should only be initiated under specialist supervision. - amiodarone causes little or no myocardial depression.

Answer 312

tablets: 100 mg, 200 mg. Injection: 30 mg/mL or concentrate 50 mg/mL. - oral administration is 200 mg three times daily for 1 week reduced to 200 mg twice daily for a further week - IV administration is via central line catheter, initially 5 mg/kg in 250 mL glucose 5% over 20–120 minutes with ECG monitoring. This may be repeated if necessary to a maximum of 1.2 g in 24 hours in 500 mL. as soon as an adequate response has been obtained, oral therapy should be initiated and the i.v. therapy phased out.

Answer 313

- amiodarone therapy can be proarrhythmogenic in patients with significant structural heart disease. - amiodarone contains iodine and can cause both hypothyroidism and hyperthyroidism. - liver toxicity can also occur - other side effects are reversible corneal microdeposits, phototoxic skin reactions, slate-grey skin pigmentation, pneumonitis and peripheral neuropathy.

Answer 314

- it is contraindicated in sinus bradycardia or sinoatrial heart block, unless pacemaker fitted, iodine sensitivity and thyroid dysfunction. - many drugs interact with amiodarone, including warfarin and digoxin. it has a very long half-life (extending to several weeks) and months may be required to achieve steady-state concentrations

Answer 315

- class Ic (Vaughan Williams’ classification) antiarrhythmic drug. it is a membrane-depressant drug that reduces the rate of entry of sodium into the cell (sodium channel blocker). - this may slow conduction, delay recovery or reduce the spontaneous discharge rate of myocardial cells.

Answer 316

- AV nodal reciprocating tachycardia, arrhythmias associated with accessory conducting pathways, paroxysmal atrial fibrillation. - occasionally it is used in ventricular tachyarrhythmias resistant to other treatments.

Answer 317

- SVT – 50 mg twice daily, increased to maximum 300 mg daily. - ‘on demand’ treatment for AF – 200 mg or 300 mg if weight greater than 70 kg, at the onset of paroxysm.

Answer 318

- include dizziness, visual disturbances, dyspnoea, palpitations, proarrhythmic effects, headache, fatigue and nausea - rarely, bronchospasm, heart block, bone marrow suppression and increased ventricular rate in AF/flutter are seen.

Answer 319

- class Ic agents increase mortality in post-MI patients with ventricular ectopy and should be reserved for patients who do not have significant coronary artery disease, left ventricular dysfunction, or other forms of significant structural heart disease. - interactions with other drugs, including β-blockers and calcium-channel blockers, can occur

Answer 320

- this drug blocks AV conduction and reduces heart rate by enhancing vagal nerve activity and inhibiting sympathetic activity. - it is positively inotropic (enhancing strength of cardiac contraction) by inhibition of Na+/K+-ATPase and secondary activation of the Na+/Ca2 + membrane exchange pump, thereby increasing intracellular calcium levels.

Answer 321

- digoxin is used in heart failure with atrial fibrillation or patients in sinus rhythm who remain symptomatic despite ACEI, β-blocker and diuretic uses. - it is also used for rate control in sedentary patients with atrial fibrillation/flutter.

Answer 322

tablets: 62.5, 125 and 250 μg. Injection: 250 μg/mL. - check renal function and electrolytes before starting therapy; reduce dose in the elderly and in renal impairment. - oral: rapid digitalization for atrial fibrillation/flutter 0.75–1.5 mg in divided doses over 24 hours and then maintenance of 125–250 μg once daily according to heart rate and renal function - IV infusion: intravenous infusion for emergency loading dose for atrial fibrillation or flutter 0.75–1 mg over at least 2 hours and then maintenance dose the next day by mouth.

Answer 323

- side effects include nausea, vomiting, diarrhoea, conduction disturbances, blurred or yellow vision and ventricular arrhythmias. - hypokalaemia and renal impairment (reduce dose) increase the risk of toxicity. - plasma digoxin concentrations should be measured if toxicity is suspected; concentrations of > 2 mmol/L usually suggest toxicity. In severe toxicity, give anti-digoxin antibodies.

Answer 324

- contraindicated in arrhythmias associated with accessory conduction pathways because the accessory pathway is not affected. - blocking the normal pathway can increase the speed of conduction in the abnormal pathway and lead to ventricular arrhythmias. - caution should be demonstrated in left ventricular outflow tract obstruction. - diltiazem, verapamil, spironolactone and amiodarone inhibit renal excretion of digoxin; avoid with amiodarone and measure plasma levels with other drugs - tetracycline, erythromycin and possibly other macrolides enhance the effect of digoxin. Rifampicin reduces serum concentrations.

Answer 325

- angina - MI - arrhythmias - stable heart failure - hypertension - alleviation of symptoms of anxiety - prophylaxis of migraine - prevention of variceal bleeding - symptomatic treatment of hyperthyroidism

Answer 326

- atenolol and metoprolol are used in angina - stoalol in management of supraventricular and ventricular arrhythmias - propanolol in treatment of hyperthyroidism, prevention of variceal bleeding and prophylaxis of migraine (usually) - bisoprolol and carvedilol in the management of heart failure (usually specialist initiated) - nebivolol in the treatment of stable mild–moderate heart failure in patients over 70 years old.

Answer 327

- portal hypertension: initially 40 mg twice daily, increased according to heart rate; maximum 160 mg twice daily - angina: initially 40 mg two to three times daily; maintenance dose 120–240 mg daily - arrhythmias: anxiety, hyperthyroidism, migraine prophylaxis, essential tremor, 10–40 mg three times daily - hypertension: initially 80 mg twice daily, increased at weekly intervals as required; maintenance 160–320 mg daily. - intravenous: arrhythmias and thyrotoxic crisis: 1 mg over 1 minute; if necessary, repeat at 2-minute intervals; maximum 10 mg.

Answer 328

* angina: 25–100 mg daily in one or two doses * after MI: 25–100 mg daily * hypertension: 25–50 mg daily. intravenous - for arrhythmias: 2.5 mg at a rate of 1 mg/min, repeated at 5-minute intervals to a maximum of 10 mg, or by infusion 150 μg/kg over 20 minutes, repeated every 12 hours if required.

Answer 329

Tablets: 1.25 mg, 2.5 mg, 3.75 mg, 5 mg, 7.5 mg, 10 mg. - hypertension and angina, usually 5–10 mg once daily; maximum 20 mg daily - heart failure, initially 1.25 mg daily titrated up at weekly intervals over 8–10 weeks to maximum 10 mg daily.

Answer 330

Tablets: 50 mg, 100 mg. Injection: 1 mg/mL. - after MI: 100 mg twice daily - angina, arrhythmias, anxiety, thyrotoxicosis, migraine prophylaxis, essential tremor: 50–100 mg two to three times daily - hypertension: 50–100 mg twice daily. intravenous - for arrhythmias: up to 5 mg at a rate of 1–2 mg/min, repeated after 5 minutes to a maximum of 10–15 mg.

Answer 331

Tablets: 40 mg, 80 mg, 160 mg, Injection: 10 mg/mL. - sotalol use is limited to the treatment of ventricular arrhythmias or the prevention of supraventricular arrhythmias. - oral: 80 mg daily in one to two divided doses, increased gradually at intervals of 2–3 days to usual dose of 160–320 mg daily. - IV: over 10 minutes: 20–120 mg with ECG monitoring repeated at 6-hourly intervals if necessary.

Answer 332

- bradycardia - exacerbation of intermittent claudication - lethargy - nightmares - hallucinations - deterioration of glucose tolerance and interference with metabolic and autonomic responses to hypoglycaemia in diabetics.

Answer 333

- asthma - severe peripheral arterial disease - second- or third-degree heart block - marked bradycardia - hypotension - phaeochromocytoma (apart from specific use with α-blockers).

Answer 334

these drugs inhibit the conversion of angiotensin I to angiotensin II and reduce angiotensin II-mediated vasoconstriction.

Answer 335

- ACEIs improve symptoms and significantly improve survival in all grades of heart failure. - recommended in patients at risk of developing heart failure (e.g. ischaemic heart disease). - other indications are hypertension and diabetic nephropathy.

Answer 336

Tablets: 2 mg, 4 mg, 8 mg. - hypertension, initially 4 mg once daily, subsequently adjusted according to response to maximum 8 mg daily - heart failure: initially 2 mg once daily, increased after at least 2 weeks to maintenance usually 4 mg daily - ischaemic heart disease, diabetic nephropathy: 4 mg daily increased after 2 weeks to 8 mg daily.

Answer 337

Tablets: 2.5 mg, 5 mg, 10 mg, 20 mg. - hypertension: initially 10 mg once daily, usual maintenance 20 mg daily, maximum 80 mg daily - heart failure: initially 2.5 mg once daily, increased by 10 mg every 2 weeks if tolerated to maintenance 35 mg daily - ischaemic heart disease, diabetic nephropathy: 5–10 mg daily. Immediately post-STEMI start at 2.5 mg if systolic BP 100–120 mmHg and gradually increase to maintenance dose of 5–10 mg. Do not give if systolic BP < 100 mmHg.

Answer 338

Tablets: 1.25 mg, 2.5 mg, 5 mg, 10 mg. - hypertension: initially 1.25 mg daily, increased weekly to maintenance 2.5–5 mg daily, maximum 10 mg once daily - heart failure: initially 1.25 mg daily, increased if necessary to maximum 10 mg daily - ischaemic heart disease, diabetic nephropathy: 2.5 mg twice daily, maintenance 2.5–5 mg daily.

Answer 339

after the first dose, side effects can include hypotension in heart failure and patients taking diuretics, dry cough, hyperkalaemia, sudden deterioration in renal function in patients with renal artery stenosis and in patients taking NSAIDs, loss of taste, rashes and hypersensitivity reactions.

Answer 340

- bilateral renal artery stenosis - pregnancy - angio-oedema - severe renal failure - severe or symptomatic mitral or aortic stenosis - hypertrophic obstructive cardiomyopathy (risk of hypotension)

Answer 341

- hypertension - heart failure - diabetic nephropathy in patients intolerant to ACE inhibitors due to cough

Answer 342

Tablets: 2 mg, 4 mg, 8 mg, 16 mg, 32 mg. - hypertension: initially 8 mg daily, increased as necessary to 32 mg daily - heart failure: initially 4 mg once daily increased at intervals of at least 2 weeks to target dose of 32 mg.

Answer 343

Capsules: 40 mg, 80 mg, 160 mg. - hypertension: 80 mg once daily and increased if necessary after 4 weeks to 160 mg daily - ischaemic heart disease: 20 mg twice daily increased gradually to 160 mg twice daily.

Answer 344

- postural hypotension - rash - abnormalities in liver biochemistry - hyperkalaemia

Answer 345

- lower doses should be given in liver and renal impairment, patients taking high-dose diuretics and the elderly (over 75 years). - caution should be applied in renal artery stenosis, aortic or mitral valve stenosis and in obstructive hypertrophic cardiomyopathy.

Answer 346

have a vasodilating effect, leading to a reduction in venous return, which reduces left ventricular work and dilatation of the coronary circulation

Answer 347

- an increase in cyclic guanosine monophosphate (cGMP) in vascular smooth muscle cells causes a decrease in intracellular calcium levels and smooth muscle relaxation with dilatation of veins and arteries, including the coronary circulation. - nitrates reduce venous return, which reduces left ventricular work.

Answer 348

prophylaxis for and in the treatment of angina, as an adjunct in congestive heart failure and intravenously in the treatment of acute heart failure and acute coronary syndrome

Answer 349

sublingual tablets: 300 μg, 500 μg, 600 μg. spray: 400 μg/dose. - angina: one or two tablets or sprays under the tongue repeated as required. more effective if taken before exertion known to precipitate angina.

Answer 350

Tablets: 10 mg, 20 mg, 40 mg. - 10–40 mg twice daily, 8 hours apart rather than 12 to prevent nitrate tolerance.

Answer 351

- mainly due to vasodilating properties and are minimised by initiating therapy with a low dose - flushing - headache - postural hypotension - methaemoglobulinaemia

Answer 352

- hypotension and hypovolaemia, hypertrophic obstructive cardiomyopathy, aortic stenosis, mitral stenosis, cardiac tamponade and constrictive pericarditis. - nitrates potentiate the effect of other vasodilators and hypotensive drugs. - sildenafil is contraindicated in patients taking nitrates.

Answer 353

- block calcium channels and modify calcium uptake into myocardium and vascular smooth muscle cells. - dihydropyridine calcium-channel blockers (e.g. amlodipine, nifedipine, nimodipine) are potent vasodilators with little effect on cardiac contractility or conduction. - verapamil, and to a lesser extent diltiazem, are weak vasodilators but depress cardiac conduction and contractility.

Answer 354

- hypertension and prophylaxis for angina - verapamil used in treatment of some arrhythmias - nimodipine for prevention of ischaemic neurological deficits following aneurysmal subarachnoid haemorrhage

Answer 355

Tablets: 5 mg, 10 mg. - 5–10 mg once daily.

Answer 356

Tablets: 40 mg, 80 mg, 120 mg, 160 mg. Oral solution: 40 mg/5 mL. - angina: 80–120 mg three times daily. - hypertension: 240–480 mg daily in two to three divided doses. - supraventricular arrhythmias: oral 40–120 mg three times daily

Answer 357

Adalat LA tablets: 20 mg, 30 mg, 60 mg. - angina: initially 30 mg once daily, increased if necessary to 90 mg once daily - hypertension: initially 20 mg once daily, increased if necessary.

Answer 358

Tablets: 60 mg. - angina: 60 mg three times daily.

Answer 359

Capsules for twice daily use: 90 mg, 120 mg, 180 mg. Capsules for once daily use: 120 mg, 180 mg, 240 mg, 300 mg. - hypertension: 120 mg twice daily - angina: 90 mg twice daily - angina and hypertension: 240 mg once daily,

Answer 360

- these are mainly due to vasodilator properties: flushing, dizziness, tachycardia, hypotension, ankle swelling and headache. - side effects are minimized by starting with a low dose and increasing slowly. - constipation occurs with verapamil. - worsening heart failure can be seen with verapamil and diltiazem.

Answer 361

- the major contraindication is aortic stenosis. - verapamil and diltiazem diminish cardiac contractility and slow cardiac conduction; thus they are relatively contraindicated in patients taking β-blockers, left ventricular failure, sick sinus syndrome and heart failure. - verapamil is contraindicated for treatment of arrhythmias complicating Wolff–Parkinson–White syndrome. - short-acting calcium antagonists increase mortality and are contraindicated immediately after MI.

Answer 362

- the mechanism of action here is a hybrid of nitrates and calcium-channel blockers. - potassium-channel activators cause an increase in potassium flow into the cell, which indirectly leads to calcium-channel blockade and arterial dilatation.

Answer 363

use is indicated in cases of refractory angina in patients who are uncontrolled on standard regimens of aspirin, beta-blockers, nitrates, calcium antagonists and statins

Answer 364

- nicorandil - tablets: 10mg, 20mg - 5-30mg twice daily

Answer 365

- headache - flushing - nausea - vomiting - dizziness - hypotension - tachycardia

Answer 366

- contraindicated in left ventricular failure and cardiogenic shock - sildenafil is contraindicated in patients taking nicorandil

Cardiovascular 2 Flashcards

(390 cards)