Cardiovascular Flashcards

Question

How can plaque erosion be detected?

Answer 1

These lesions are very difficult to detect with any kind of imaging so far. OCT is the best and the presence of luminal thrombus over an intact fibrous cap is indicative. OCT is intravascular tomography processing backscattering using infrared light.

Answer 2

PCI - Percutaneous Coronary Intervention Used to treat coronary artery disease 2 million + procedures / year worldwide More than 90% require stent implantation. Stents made out of stainless steel, cobalt chromium, metals that are cost-effective. Restenosis was a major limitation, no longer a problem.

Answer 3

The body wants to heal the area where the stent has been put in – smooth muscle cell proliferation. Used to happen after PCI. But drug eluting stents (with Taxol and Sirolimus) are so good now that restenosis is not a problem. These drugs work by reducing smooth muscle cell proliferation and in turn, this reduces regrowth after placement of the stent.

Answer 4

Patients will be given anti-platelet therapy before a stent. Aspirin – irreversible inhibitor of platelet cyclo-oxygenase Clopidogrel/Ticagrelor – inhibitors of the P2Y12 ADP receptor on platelets Statins – inhibit HMG CoA reductase, reducing cholesterol synthesis

Answer 5

New anti-inflammatory biologic (antibody) developed in 2017 to target IL-1 which acts as a major cytokine in atherosclerosis. Major clinical trial showed beneficial results.

Answer 6

A generic anti-inflammatory drug that lowers ischaemic events in patients with recent MI. Already used for gout and pericarditis. Given within 30 days of a heart attack.

Answer 7

Original deflections were labelled ABCD Mathematical convention dating back to Descartes using the second half of the alphabet; N has other meanings in mathematics and O was used for the origin of Cartesian coordinates. Einthoven chose the next letter of the alphabet!

Answer 8

Echo-cardiogram is a representation of the electrical events of the cardiac cycle. Each event has a distinctive wave form. The study of the waveform can give insight into the patient's cardiac pathophysiology.

Answer 9

``` Arrhythmia Myocardial ischemia and infarction Pericarditis Chamber hypertrophy Electrolyte disturbances - hyper/hypokalemia Drug toxicity ```

Answer 10

Contraction of any muscle associated with electrical changes is called depolarisation. The vast majority of the activity that we see on an ECG is depolarization, rather than repolarization.

Answer 11

SA Node - dominant pacemaker with an intrinsic rate of 60-100 bpm AV Node - back up pacemaker with an intrinsic rate of 40-60 bpm Ventricular cells - back up pacemaker with a intrinsic rate of 25-40 bpm

Answer 12

25mm/s 0.1mV/mm Electrical impulse that travels towards the electrode produces an upward 'positive' deflection.

Answer 13

``` Sinoatrial node AV node Bundle of His Bundle branches Purkinje fibres ```

Answer 14

P wave - atrial depolarisation QRS complex - ventricular depolarisation T wave - ventricular repolarisation We do have atrial repolarisation but it gets lost behind the QRS complex.

Answer 15

Atrial depolarisaton PLUS a delay in AV junction Delay allows for the atria to contract before the ventricles contract.

Answer 16

``` Horizontally One small box - 0.04 s One large box - 0.20 s Vertically One large box - 0.5 mV ```

Answer 17

They measure the difference in electrical potential between two different points. Bipolar leads: two different points on the body Unipolar leads: one point on the body and a virtual reference point with zero electrical potential located in the centre of the heart

Answer 18

``` VERTICAL PLANE 3 standard leads 3 augmented leads HORIZONTAL PLANE 6 precordial leads ```

Answer 19

``` Always positive in leads I and II Always negative in lead aVR Less than 3 small boxes in duration Less than 2.5 small boxes in amplitude Best seen in lead II ```

Answer 20

Right atrial enlargement: Tall (>2.5mm) and pointed P waves (P pulmonale) Left atrial enlargement: Notched/bifid M-shaped P wave in limb leads (P 'mitrale')

Answer 21

Short PR interval - Wolff Parkinson's White syndrome Accessory pathway allows for early activation of the ventricles Long PR interval - first degree heart block

Answer 22

ST segment is flat (isoelectric) Elevation or depression of the ST segment by 1mm or more "J" junction is the point between QRS and ST segment.

Answer 23

Normal T wave is asymmetrical, first half having a more gradual slope than the second. Rarely exceeds 10mm. Abnormal T waves are symmetrical, tall, peaked, biphasic or inverted. T waves follow the direction of the QRS deflection.

Answer 24

Total duration of the depolarisation and repolarisation QT interval decreases when heart rate increases Should be between 0.35-0.45 s Should not be more than half of the interval between adjacent R waves (R-R interval)

Answer 25

Afterdepolarisations that occur after repolarisation Small, round, symmetrical and positive in lead II with amplitude <2mm. U wave direction is the same as T wave. More prominent at slow heart rates.

Answer 26

Count the number of big boxes between two QRS complexes and divide this by 300 (1500 for smaller boxes).

Answer 27

ECGs record 10 seconds of rhythm per page Count the number of beats present on the ECG Multiple by 6.

Answer 28

Represents overall direction of the heart's electrical activity. Abnormalities hint at ventricular enlargement and conduction blocks. Normal QRS axis is from -30 to +90 -30 to -90 is referred to as left axis deviation (LAD) +90 to +180 is referred to as right axis deviation (RAD)

Answer 29

Involves a two stage electrical generated contraction Contraction initiated by depolarisation and changes to calcium concentration Removal of calcium (energy dependent) for relaxation to occur

Answer 30

Enlargement of the heart muscle Hypertrophic response triggered by angiotensin 2, ET-1 and insulin-like growth factor 1, TGF-β. Can be an adaptive process in pregnancy/athletes If you exceed stretch capability of sarcomeres then cardiac contraction force diminishes, there's only so far the heart can stretch before it goes into heart failure.

Answer 31

Left sided cardiac failure – pulmonary congestion and then overload of right side. Right sided cardiac failure with venous hypertension and congestion. Diastolic cardiac failure ~ Stiffer heart

Answer 32

The heart comprises a single chamber until the fifth week of gestation, then divided by intra-ventricular and intra-atrial septa from endocardial cushions. The muscular intra-ventricular septum grows upwards from the apex of the heart producing the four chambers and allowing valve development to occur.

Answer 33

Results from faulty embryonic development May complicate up to 1% of all live births. Misplaced structures or arrest of the progression of normal structure development. Ventricular and atrial septal defects are the most common.

Answer 34

Single genes associated = trisomy 21 (Downs), Turner Syndrome (XO) and di-George Syndrome. Homeobox genes particularly associated Infections – Rubella Drugs – Thalidomide, alcohol, Phenytoin, amphetamines, lithium, eostrogenic steroids Diabetes

Answer 35

Main features: - Pulmonary stenosis - Ventricular septal defect - Dextraposition/over-riding ventricular septal defect - Right ventricle hypertrophy Characteristic boot-shape on radiology and macroscopically. Often associated with other cardiac abnormalities. As a result of the pulmonary stenosis, right ventricle blood is shunted into the left heart producing cyanosis from birth. Surgical correction usually is performed during the first two years of life, as progressive cardiac debility and risk of cerebral thrombosis increases.

Answer 36

``` Systemic hypertension Cigarette smoking Diabetes mellitus Elevated cholesterol Also: obesity, increasing age, male sex, family history, oral contraceptive pill, sedentary life habit, personality features etc ```

Answer 37

``` Atherosclerosis Thrombosis Thromboemboli Artery spasm Collateral blood vessels Blood pressure/cardiac output/heart rate Arteritis Anaemia Altered oxygen dissociation curve Carbon monoxide Cyanide Increased demand from hypertension, valvular heart disease, hyperthyroidism, fever, thiamin (B1) deficiency, catecholamine stress. ```

Answer 38

Subendocardial/patchy infarction OR Transmural infarction Size and pattern of the infarction varies. Complications of infarcts differ according to which territory has compromised. Can date the infarct. The infarct can affect other areas of the heart - the immediate area may be ischaemic and there may be other areas which were already prone to infarction which will now be affected.

Answer 39

Reperfusion of completely infarcted tissue can produce significant haemorrhage - risks of problems downstream. The reperfusion allows oxygen delivery and a further degree of injury as a result of generation of superoxide radicals etc.

Answer 40

This is a dilation of part of the myocardial wall, usually associated with fibrosis and atrophy of myocytes. Variable fatty tissue replacement may also occur. The dilatation of the thin walled sac allows blood stasis and thrombosis. Risk of subsequent embolism of such material.

Answer 41

Reflects cardiac enlargement due to hypertension, and in the absence of other cause. Compensatory hypertrophy of the heart initially with increased myocyte size, squaring of the nuclei and slight increase of the interstitial fibrous tissue. Initially able to handle the increased workload, eventually the hypertrophy no longer compensates. Falling amount of oxygen delivery to cardiac myocytes produces further fibrosis and progressive contractile dysfunction. Often associated with coronary atheroma and ischaemic heart disease – aggravating situation.

Answer 42

Right ventricular hypertrophy and dilatation due to pulmonary hypertension. May reflect an acute event - causes problems with backstream pressure on the ventricular system. Classically disproportionate right ventricular hypertrophy as compared with the left. Progressive features of right side cardiac failure with venous overload, peripheral oedema and progressive hepatic congestion.

Answer 43

Group A β-haemolytic streptococcus infection usually in upper respiratory tract. Peak age of pathology 9-11 years, but can occur in adults. Seen commonly in those who have migrated to the UK and have not have antibiotics in childhood. Symptoms and features diminish after 3-6 months. Some patients die acutely and are shown to have granulomatous foci of inflammation (Aschoff body, Anitchkov cells and some giant cells). There may be pericarditis and endocarditis. Chronically scarring and deformity produces contracture of the valves (particularly the mitral and aortic valve) and chordae tendinae. These may subsequently calcify and distort blood flow allowing localised thrombosis. They also provide ideal settling sites for bacteria within the blood stream, and the development of infective endocarditis.

Answer 44

Clinical features include: carditis (cardiomegaly, murmurs, pericarditis and cardiac failure) polyarthritis, chorea, erythema marginatum and subcutaneous nodules. Minor criteria for diagnosis include: previous history of rheumatic fever, arthralgia, raised CRP, ESR and white cell count. Antibodies against group A streptococcal antigens, anti-streptolysin O, anti-DNAse B and anti-hyaluronidase.

Answer 45

Infection produces rapidly increasing cardiac valve distortion and disruption with acute cardiac dysfunction. Apart from the sudden development of cardiac failure and septic problems there are other consequences including generation of infected thromboemboli and damage to the kidneys (focal segmental glomerulonephritis FSGS). - Protean symptoms - Fever, anorexia, fatigue - Progressive splenomegaly, petechiae, clubbing - Neurological dysfunction due to mitotic emboli and aneurysms High morbidity and mortality rates.

Answer 46

In adults causes include rheumatic valvular heart, mitral valve prolapse, intravenous drug abuse, prosthetic valves, diabetes, the elderly and pregnancy. Characteristic organisms include streptococci and staphylococci although fungi and atypical bacteria are also recognised - will destroy the tissue and cause problems.

Answer 47

Nodular calcific deposits in cusps with progressive distortion of valves opening/closure. Obstruction to left ventricle outflow produces pressure overload and cardiac hypertrophy. Accelerated in bicuspid aortic valves. Risk of thrombosis and sudden cardiac death, as well as infective endocarditis.

Answer 48

Degenerative process which makes you prone to regurgitation. Calcification of the mitral valve annulus is usually asymptomatic and of no significance. It does not usually affect the mobile leaflets. However, calcification of the valves, following rheumatic valvular disease or previous inflammation/valvitis, is of significance with either mitral stenosis or regurgitant pathology.

Answer 49

Degeneration of the mitral valves such that the inner fibrosa layer becomes more loose and fragmentary with accumulation of mucopolysaccharide material. The valve cusp bow upwards and may not close adequately producing incompetence/regurgitation. Risk of sudden cardiac death and infective endocarditis.

Answer 50

Inflammation of the myocardium usually associated with muscle cell necrosis and degeneration. Can be caused by rheumatic fever or other causes. Viral myocarditis is the commonest. Direct viral toxicity with associated cell mediated immunity aggravating cell damage. Healing with scarring, but high risk of sudden death. Symptoms vary, often in association with an upper respiratory tract infection preceding.

Answer 51

Viruses – Coxsackie, Adeno-, Echo, Influenza Rickettsia – typhus Bacteria –diphtheria, staphylococcal, streptococcal, borrelia, leptospira Fungi and Protozoa parasites – toxoplasmosis, cryptococcus Metazoa - echinococcus Non-infective: Hypersensitivity/immune related diseases – rheumatic fever, SLE, scleroderma, drug reaction, rheumatoid arthritis Radiation Miscellaneous – sarcoid, uraemia

Answer 52

A very rare highly aggressive form of cardiac disease with areas of muscle cell death due to macrophage giant cells. Often fatal. Early treatment is transplantation but disease can often recur.

Answer 53

Various types ~ primary cardiac disease with contractile dysfunction and atypical morphology Dilated cardiomyopathy Hypertrophic cardiomyopathy Arrhythmogenic right ventricular cardiomyopathy Secondary dilated cardiomyopathy Rare forms

Answer 54

1/3 familial: Most autosomal dominant (AD) but some recessive and X-linked. Poorly generated contractile force leads to progressive dilation of heart with some diffuse interstitial fibrosis. May also follow a viral myocarditis or an inflammatory myocarditis/toxic myocarditis Enlarged, heavy and dilated heart, possibly cardiac weight up to 900 g. Histology shows variable atrophy and hypertrophy - increased interstitial tissue, occasional inflammatory cells Clinical progression slowly deteriorating cardiac failure, dysrrhythmias and ultimately death.

Answer 55

``` Alcohol Cobalt toxicity Catecholamines Micro-infarction Anthracyclines Cocaine Pregnancy. This may affect up to 1% of females, with an Afro-Caribbean bias. Many recover spontaneously, but one can be left with permanently damaged and dilated heart. ```

Answer 56

Muscle gene mutation - prone to cause bigger, thicker heart muscle. Bulge into the chambers affecting the valves. Related to defects in force degeneration/ energy usage allowing progressive sarcomeric dysfunction. Compensatory hypertrophy often occurs. Many mutations recognised involving β-myosin, myosin binding protein C, troponin T, titin etc. Asymmetric hypertrophy with distortion of a papillary architecture. Increased fibrosis in tissues. Ventricular outflow distortion. Myocyte disarray.

Answer 57

A degenerative condition with progressive dilatation of the right ventricle with fibrosis, lymphoid infiltrate and fatty tissue replacement. Particularly common in parts of Italy Familial inheritance pattern with genetic linkage chromosome 14,1 and 2. Sudden cardiac death.

Answer 58

This is a group of diseases in which poor dilation of the heart restricts the eventual ability of the heart to take on blood and pass it to the rest of the body. This can either be amyloid related to the heart (cardiac amyloid) or part of a systemic disorder (amyloidosis AL, AA). Firm enlarged and heavy heart with diffuse infiltration of the protein into the myocytes, blood vessels and valves. Progressive deterioration with right and left side failure.

Answer 59

Endomyocardial fibrosis, particularly in African settings and Löeffler endocarditis. This is a temporate region disorder with high grade eosinophilia , rash and progress endocarditis leading to cardiac failure. Characteristically grey-white layer of fibrous tissue extending of the endocardial surfaces of the ventricular cavities. Stiff and poorly compliant ventricle.

Answer 60

A chronic granulomatous disease with numerous granulomas of non-caseating giant cell type. May involve the heart producing widespread areas of fibrosis and compensatory hypertrophy. It can produce a restrictive disorder. If it involves the conduction system then this may be the prime pathology of the patients with the risk of sudden death.

Answer 61

Most common cardiac tumour At least 75% of cardiac tumours with bias towards atria. Rather jelly like proliferation of myxoid cells with abundant endothelial vascular channels. Usually produces obstructive symptoms but risk of embolisation.

Answer 62

These are rare and can show differentiation towards vascular, fibrous and muscle phenotypes. Almost invariably fatal - days or weeks. Cannot treat.

Answer 63

A degenerative condition of arteries characterised often by a fibrous and lipid rich plaque with variable inflammation, calcification and a tendency to thrombosis. Associated with ischaemic heart disease, myocardial infarction, stroke, peripheral vascular disease etc.

Answer 64

Initiation - Endothelial dysfunction and injury around sites of sheer and damage with subsequent lipid accumulation at sites of impaired endothelial barrier. Local cellular proliferation and incorporation of oxidised lipoproteins occurs. Mural thrombi on surface with subsequent healing and repeat of cycle. Adaptation - As plaque progresses to 50% of vascular lumen size the vessel can no longer compensate by re-modelling and becomes narrowed. This drives variable cell turnover within the plaque with new matrix surfaces and degradation of matrix. May progress to unstable plaque. Clinical stage - The plaque continues to encroach upon the lumen and runs the risk of haemorrhage of exposure of tissue HLA-DR antigens which may stimulate T cell accumulation. This drives an inflammatory reaction against part of the plaque contents.

Answer 65

Acute occlusion due to thrombus Chronic narrowing of vessel lumen with healing of the local thrombus Aneurysm change Embolism of thrombus +/- plaque lipid content - can break off and travel to other parts of the body

Answer 66

``` Hypertension Serum cholesterol level Tobacco smoking Diabetes Increasing age Male > female Inactive and stressful life patterns Homocysteine level CRP ```

Answer 67

Altered renin-angiotensin system elevates blood pressure by impairing sympathetic output increasing mineralocorticoid secretion and direct vaso-constriction. In effect the changes to auto-regulation produce an increase in peripheral resistance, that in normality would allow increased blood pressure, diuresis and restoration of normal pressure and volume.

Answer 68

Intermittent bilateral ischaemia of digits/extremities precipitated by motional cold temperature. Accelerated in cases of scleroderma and SLE. May produce distal atrophy and ulceration.

Answer 69

An inflammatory and variably necrotic process centred on the blood vessels that may involve arteries, veins or capillaries. Inflammation damaging the walls of the vessels.

Answer 70

Commonest type of vasculitis. Focal, chronic and granulomatous inflammation of temporal arteries mostly. Association with polymyalgia rheumatica. Can involve large arteries (aortic aneurysm/dissection). Average age 70+. Female bias. Feel stiff in the morning, painful head - temporal artery which supplies the scalp. Can go blind in a couple of hours.

Answer 71

Thickened blood vessel, often palpable. Granulomatous inflammation involving the full thickness of the wall with macrophages, lymphocytes, plasma cells, neutrophils and occasionally eosinophils. Giant cells tend to congregate around IEL. Variable necrosis. Old areas of inflammation show up as focal scars with fragmentation of elastic laminae. Thrombosis may occur.

Answer 72

An inflammatory disease of medium and small arteries affecting the distal limbs. Strong association with tobacco smoking. Cell mediated hypersensitivity to collagen II and III with impaired endothelium. Distal ischaemic symptoms and necrosis.

Answer 73

These are dilated areas of vasculature suggesting either congenital or acquired weakness of the wall of the vessels. The incidence rises with age. Described as fusiform, saccular, dissecting and arterio-venous. Prone to bulging off and travelling downstream or bursting.

Answer 74

>50% dilatation of aortic diameter Those greater than 5-6 cm diameter increased risk of aneurysm rupture. Prevalence rises with age, smoking, high blood pressure Strong association with atheromatous disease Familial clustering suggests a genetic component Local inflammatory changes can be profound and involve ureters and local nerves. Sudden shocking pain - death within minutes.

Answer 75

This rounded berry-like vascular dilatation is particularly common in the cerebral circulation. Consequence of long standing hypertension and/or focal area of weakness within the arterial substructure.

Answer 76

This is a haematoma within the arterial wall with blood entering under pressure from the lumenal surface and dissecting along the length of the media.

Answer 77

A varicose vein is an enlarged and torturous vein, principally affecting the superficial leg veins. Risk factors – age, female (pregnancy related), hereditary, posture, obesity Progressive incompetence of valves with further back pressure on venous circuit. Thinning and dilatation of vascular wall in places with patchy calcification. May produce stasis dermatitis with trophic changes to the skin.

Answer 78

This is a benign proliferation of blood vessel tissue, which varies in name and substructure depending on the site and age of the patient. Capillary haemangioma – birth marks, ruby spots Juvenile haemangioma – strawberry haemangioma Cavernous haemangioma – port wine stains Most are of no consequence.

Answer 79

A benign neoplasm involving the glomus body. Small lesion which is intensely painful. Composed of vascular channels with proliferation of the glomus cells (neuromyoarterial receptors) mainly affect the hands.

Answer 80

This is a highly aggressive malignant neoplasm of endothelial cells. Very difficult to control, often fatal. Commonly skin, soft tissue, breast, bone, live and spleen. Rapidly enlarging haemorrhagic tumour with rapid dissemination to other organs. Environmental carcinogens – arsenic and vinyl chloride.

Answer 81

Venous flow stasis from any cause (eg. cardiac failure, chronic venous insufficiency, post operative immobilisation, prolonged bed rest) Injury (trauma, surgery, child birth) Hypercoaguability (OCP), pregnancy, cancer, inherited thrombophilic disorders) Advanced age Sickle cell disease

Answer 82

The passage of material through the venous or arterial circulations. Commonest process is thrombo-embolus from a deep vein thrombosis. Post operative deep vein thrombosis occurs often following surgery or immobilisation following illness. Pulmonary emboli may be asymptomatic and small. May produce transient dyspnoea for relatively small emboli. May produce focal pulmonary infarction with chest pain, haemoptysis and secondary effusion (when lung tissue dies it can be painful). At a certain size, they can produce cardiovascular collapse and sudden death (saddle embolus).

Answer 83

Atherosclerotic plaques, mural thrombus in heart or vasculature Infective endocarditis Sites particularly vulnerable – brain, intestine, distal limbs, kidneys and coronary circulation

Answer 84

Mismatch of oxygen supply and demand Blockage of coronary arteries means that heart muscle cannot receive adequate oxygen Most common cause is ischemic heart disease

Answer 85

``` Age Cigarette smoking Family history Diabetes mellitus Hyperlipidemia Hypertension Kidney disease Obesity Physical inactivity Stress ```

Answer 86

``` Anemia Hypoxemia Polycythemia Hypothermia Hypovolaemia Hypervolaemia ```

Answer 87

``` Hypertension Tachyarrhythmia Valvular heart disease Hyperthyroidism Hypertrophic cardiomyopathy ```

Answer 88

Myocardial ischemia occurs when there is an imbalance between the heart's oxygen demand and supply, usually from an increase in demand (eg exercise) accompanied by limitation of supply: 1. Impairment of blood flow by proximal arterial stenosis 2. Increased distal resistance eg left ventricular hypertrophy 3. Reduced oxygen-carrying capacity of blood eg anemia

Answer 89

Prinzmetal’s angina (coronary spasm) Microvascular angina – left ventricular hypertrophy, older people, in diabetics Crescendo angina – no chest pain at rest, but now have an inability to perform physical activity Unstable angina – critical ischaemia but not quite enough to cause a MI

Answer 90

Chest pain Breathlessness May have other symptoms like fluid retention, palpitation, syncope or pre-syncope.

Answer 91

``` Onset Position (site) Quality (nature / character) Relationship (with exertion, posture, meals, breathing and with other symptoms) Radiation Relieving or aggravating factors Severity Timing Treatment ```

Answer 92

``` Myocardial ischemia Pericarditis/ myocarditis Pulmonary embolism/ pleurisy Chest infection/ pleurisy Dissection of the aorta Gastro-esophageal (reflux, spasm, ulceration) Musculo-skeletal Psychological ```

Answer 93

Reassure Lifestyle - stop smoking, lose weight, more exercise, improve diet Advice for emergency Medication - Aspirin, B blocker, statin, GTN Revascularisation

Answer 94

Routine bloods, lipids, ECG taken NICE recommends a CT Coronary Angiography for both typical and atypical presentations of angina (used more as a planning than diagnostic tool). Exercise testing with an ECG may also be used. Stress echocardiogram may be used - patient given a stimulant to look at the heart in ischemia (high-skill) Perfusion MRI

Answer 95

Negatively chronotropic - reduced heart rate Negatively inotropic - reduced force of contraction Reduced cardiac output Reduced oxygen demand Side-effects: tiredness, nightmares, erectile dysfunction, bradycardia, cold hands and feet DO NOT give to asthmatics

Answer 96

Very good at dilating coronary arteries and arterioles, reducing blood pressure and afterload, reducing venous return and preload. Most common side effect: headache

Answer 97

Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling. Afterload is the force or load against which the heart has to contract to eject the blood, the 'load' to which the heart must pump against.

Answer 98

Third-line treatment Coronary arteries dilate Negatively inotropic - reduced LV contraction Negatively chronotropic - reduced heart rate Reduced blood pressure Reduced afterload Side effects are flushing, postural hypotension, swollen ankles.

Answer 99

Aspirin is a derivative of salicylic acid - and is also known as acetylsalicylic acid. Cyclo-oxygenase inhibitor ↓ prostaglandin synthesis, incl. thromboxane ↓ platelet aggregation, antipyretic, anti-inflammatory, analgesic Most common side effect: gastric irritation

Answer 100

Angiotensin II as part of the renin-angiotensin system causes vasocontriction ACE inhibitors like ramipril block the angiotensin converting enzymes which convert angiotensin I to angiotensin II. Given to patients with IHD with high blood pressure or diabetes mellitus.

Answer 101

``` Aspirin GTN β Blocker – first-line Long acting nitrate – second-line Statin ACE inhibitor ``` If drugs aren’t successful in managing angina Revascularisation: PCI / CABG: MDT meeting Third-line Ca++ channel blocker Potassium channel opener Ivabradine

Answer 102

Percutaneous Coronary Intervention (PCI, formerly known as angioplasty with stent) is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by atherosclerosis.

Answer 103

Coronary Artery Bypass Grafting AKA Heart Bypass Surgery Used when coronary arteries are narrowed or blocked Blood vessels can be taken from your leg (saphenous vein), inside your chest (internal mammary artery - PREFERRED), or your arm (radial artery) to graft onto the coronary arteries to provide a alternative route around the blockage.

Answer 104

``` Pros Less invasive Convenient Repeatable Acceptable ``` ``` Cons Risk stent thrombosis Risk restenosis Can’t deal with complex disease Dual antiplatelet therapy ```

Answer 105

Pros Better prognosis Deals with complex disease ``` Cons Invasive Risk of stroke, bleeding Can’t do if frail, co-morbidities One time treatment Length of stay Time for recovery ```

Answer 106

Covers a spectrum of acute cardiac conditions from unstable angina to varying degrees of evolving myocardial infarction (MI)

Answer 107

Cardiac chest pain at rest Cardiac chest pain with crescendo pattern New onset angina Take history, ECG, troponin levels (no significant rise in unstable angina)

Answer 108

ST-elevation MI can usually be diagnosed on ECG at presentation Non-ST-elevation MI is a retrospective diagnosis made after troponin results and sometimes other investigation results are available. May also be defined retrospectively as non-Q wave or Q-wave (broader and deeper) MI on the basis of whether new pathological Q waves develop on the ECG. STEMI and MI with LBBB are more likely to develop pathological Q wave formation.

Answer 109

Cardiac chest pain that is: unremitting usually severe but may be mild or absent occuring at rest associated with sweating, breathlessness, nausea and/or vomiting one third occur in bed at night

Answer 110

Usually causes permanent heart muscle damage although this may not be detectable in small MIs. Higher risk associated with higher age, diabetes, renal failure, left ventricular systolic dysfunction (elevated NT-proBNP level) and other risk factors.

Answer 111

Get in to hospital quickly – 999 call Paramedics – if ST elevation, contact primary PCI centre for transfer Take aspirin 300mg immediately Pain relief – may be morphine (reduces pain and oxygen demand)

Answer 112

``` Make diagnosis – history, ECG, troponin Bed rest Oxygen therapy if hypoxic Pain relief – narcotics/ nitrates Aspirin +/- P2Y12 inhibitor Consider beta-blocker Consider other antianginal therapy Consider urgent coronary angiography e.g. if troponin elevated or unstable angina refractory to medical therapy ```

Answer 113

Rupture of an atherosclerotic plaque and consequent arterial thrombosis is the cause in the majority of cases Uncommon causes include coronary vasospasm without plaque rupture, drug abuse (amphetamines, cocaine), dissection of the coronary artery related to defects of the vessel connective tissue, and thoracic aortic dissection

Answer 114

Protein complex regulates actin:myosin contraction in muscle Highly sensitive marker for cardiac muscle injury Not specific for acute coronary syndrome May not represent permanent muscle damage Positive in: gram negative sepsis, pulmonary embolism, myocarditis, heart failures, arrhythmias, cytotoxic drugs

Answer 115

Used in combination with aspirin in management of ACS = ‘dual antiplatelet therapy’ Three options: clopidogrel, prasugrel and ticagrelor Increase risk of bleeding so need to exclude serious bleeding prior to administration Without inhibition, P2Y12 acts to amplify platelet aggregation

Answer 116

Only intravenous drugs available Used in combination with aspirin and oral P2Y12 inhibitors in management of patients undergoing PCI for ACS Increase risk of major bleeding so used selectively Reducing use globally due to more effective oral antiplatelet therapy Still useful in STEMI patients undergoing primary PCI to cover delayed absorption of oral P2Y12 inhibitors in these patients (due to opiates delaying gastric emptying).

Answer 117

Used in addition to antiplatelet drugs Target formation and/or activity of thrombin Inhibit both fibrin formation and platelet activation Fondaparinux (a pentasaccharide) used in NSTE ACS prior to coronary angiography = safer than heparins as low level of anticoagulation used Full-dose anticoagulation used during PCI: options are heparins (usually unfractionated heparin; some centres use enoxaparin, a low-molecular-weight heparin) or the direct thrombin inhibitor bivalirudin (expensive, not used in Sheffield) High dose heparin used during cardiopulmonary bypass for CABG surgery

Answer 118

Dose Age Weight Disease states including diabetes mellitus and chronic kidney disease Drug-drug interactions e.g. omeprazole and strong cytochrome P450 (CYP) 3A inhibitors CYP2C19 loss-of-function (LOF) alleles

Answer 119

Prasugrel is a prodrug like Clopidogrel but it is more effectively converted to its active metabolite. More effective than Clopidogrel in ACS patients, but does increase bleeding.

Answer 120

Common to all P2Y12 inhibitors: Bleeding e.g. epistaxis, GI bleeds, haematuria Rash GI disturbance Idiosyncratic Dyspnoea: usually mild and well-tolerated, but occasionally not tolerated and requires switching to prasugrel or clopidogrel (which are not associated with the same adverse effect but do not have the same evidence for longterm mortality reduction) Ventricular pauses: usually sinoatrial pauses, may resolve with continued treatment

Answer 121

Signs: Tenderness, swelling, warmth and discolouration Symptoms and signs non specific, clinical diagnosis unreliable Unhelpful as it can have many differential diagnosis

Answer 122

Isolated distal DVT has no proximal component, is located below the knee, and is confined to the calf veins (peroneal, posterior, anterior tibial, and muscular veins). Proximal DVT is one that is located in the popliteal, femoral, or iliac veins. Can break off and travels to the IVC to the heart and then block off the pulmonary artery.

Answer 123

Ultrasound compression test for proximal veins - identifies whether there is a clot in the veins. Push with the probe to push the vein flat then it's empty and if it won't push flat then it's full of clot. D - dimer: Normal excludes diagnosis but a positive doesn't confirm diagnosis (Can be raised in malignancy, inflammation and infection as well as for DVT)

Answer 124

``` LMW Heparin straight away (reliable anticoag for quick therapeutic level, short half life) Oral warfarin (long half life - several days to build therapeutic dose. Stop LMW heparin at this level) DOAC - Start from outset, initially twice day, can cut down to once daily after a few weeks. Compression stockings ```

Answer 125

Underlying causes - Malignancy (1/3 of the elderly present with DVT's) and thrombophilia (Recurrent thrombosis from a young age - genetic predisposition) - Spontaneous DVT (No clear factor/out of the blue) - Provoked DVT (Injury means chances are higher) If spontaneous DVT or PE, then once treatment has stopped there is a higher chance of reoccurance.

Answer 126

Surgery, immobility, leg fracture/ daily prophalyxis Oral contraceptive/HRT/Pregnancy (High oestrogen states) Long haul flights/travel (Rare) - No increased risk of DVT if flying in Europe Inheritied thrombophillia (Runs in families)

Answer 127

Mechanical - Hydration and early mobilisation, compression stockings, foot pumps. Chemical - LMW Heparin (Prophylaxis given in hospital - Doesn't cause bleeding as low dose)

Answer 128

Pleuritic chest pain, shortness of breath, haemoptysis (Pulmonary infarct), non-specific. Differential diagnosis of chest pain and SOB. Consider also musculoskeletal, infection ,malignancy, pneumothorax, cardiac and gastro causes. Symptoms: Could have signs and symptoms of DVT

Answer 129

Small = Only one of the arteries or at the bifurcations Massive = Haemodynamically significant Can block both pulmonary arteries leading to death Near death experience/medical emergency

Answer 130

CXR (Usually normal) ECG (Sinus tachycardia) Blood gases (Type 1 resp failure, decreased CO2 and O2) Mainly to rule out alternatives D - dimer: Normal excludes diagnosis. Ventilation/Perfusion scan: Mismatch defects (Used in pregnancy) CTPA (Spiral CT with contrast, visualise major segmental thrombi, more invasive but quick and efficient, contraindicated in pregnancy)

Answer 131

Ensure normal Hb, platelets, renal function, baseline clotting. LMW Heparin IVC filter - Prevents clot moving and can be used if malignancy is suspected and needs investigations and have a high bleeding risk ie if need or had surgery.

Answer 132

Orally active tablet Prevents synthesis of active factors II, VII, IX and X Indirect anticoagulation Works in the liver. Antagonist of vitamin K Long half life (36 hours) Difficult to use (Old patients = small dose, Patient with lots of clots = higher dose) Affected by vit K (Can be affected by diet and lifestyle), constant blood tests)

Answer 133

Warfarin interferes with the vitamin K pathway Means vit K can be given to reverse warfarin (Allows them to start synthesise of active clotting factors but not quickly - Takes around 24 hours to work - Not good for patient who is bleeding so can be used for high INR with no bleeding)

Answer 134

``` Individual variation in dose Measure INR (International normalised ratio, derived from prothrombin time (Used with certain reagent and certain machine in each hospital - Different in different hospitals, therefore INR is a correction factor meaning the test can be done anywhere - Patients on warfarin want an increased prothrombin time) Usual target range 2 - 3. Higher range 3 - 4.5 (Artificial Heart Valves) ```

Answer 135

Direct Oral Anticoagulants Orally active Directly acting on factor II or X No blood tests or monitoring Shorter half-lives Dose can be weight adjusted and age adjusted and for renal function (but not constantly changing) Used for extended thromboprophylasis and treatment of AF and DVT/PE (Equivalent to INR 2-3, not higher so can't be used for heart valves/ patients with recurrent thrombosis that need high targets) Not used in pregnancy or breastfeeding (Small molecules so cross the placenta - Patients would usually inject with LMWH Heparin as warfarin is not used either)

Answer 136

Blood in vessels should be fluid. Thrombosis is blood coagulation inside a vessel. Veins = DVT or PE - Low pressure, fibrin rich - Anticoag (Warfarin and DOACs) Arteries = Heart attack or stroke - High pressure situation, tends to be difficult to clot so it's platelet rich - Anti platelet medications Not to be confused with appropriate coagulation when blood escapes a vessel, failure of coagulation in this situation leads to bleeding.

Answer 137

Coronary circulation = Myocardial infarction Cerebral circulation = cerebrovascular accident/stroke Peripheral circulation = Peripheral vascular disease, claudication, rest pain or gangrene.

Answer 138

MI - Aspirin, LMWH or Fondraparinuex, thrombolytic therapy (Streoptokinase tissue plasminogen activator) TPA generates plasmin that degrades fibrin. There is a narrow window to use in. This is narrower when used for strokes as opposed to MI. Stroke: Aspirin or clopidogrel, prasugrel, tiglacor: anti platelet.

Answer 139

Circumstantial causes: Surgery, Immobilisation, Oestrogens: Oral contraceptive pill, HRT, Malignancy, Long haul flights Genetic causes: Factor V Leiden, PT202107A (common) Antithrombin, Protein C or S deficiency (uncommon) Acquired causes: Anti phospholipid syndrome, Lupus anticoagulant, Hyperhomocysteinameia

Answer 140

Binds to antithrombin and increases it's activity. Indirect thrombin inhibitor Mointer with APTT, aim ratio 1.8 - 2.8 Given by continuous infusion (unfractionated - big so doesn't move into the vessel) Only really used in cardiothoracic theatres when patients are on bypass. Reversible with Protomean

Answer 141

Smaller molecules, less variation in dose and renal excretion. Not reversible with Protomean Weight adjusted once daily subcutaneous injection.

Answer 142

Inhibits cyclo - oxygenase irreversibly Act for lifetime of platelet so around 7 - 10 days. Stop aspirin, needs to be stopped a few days before hand. Inhibits thromboxane formation and hence platelet aggregation Used in arterial thrombosis form 75 (Daily) to 300 (MI) mg. Clopidogrel similar, but inhibits ADP induced platelet aggregation.

Answer 143

2 layers: - Visceral single cell layer adherent to epicardium - PERICARDIAL SPACE - Fibrous parietal layer 2mm thick – has fibrous attachments to fix the heart in the thorax – diapraghm Acellular collagen and elastin fibres 50ml of serous fluid Great vessels lie within the pericardium Left atrium is mainly outside the pericardium

Answer 144

Mechanical function restrains the filling volume of the heart. Initially stretchy but becomes stiff at higher tension. Thus pericardial sac has a small reserve volume. If this volume is exceeded the pressure is translated to the cardiac chambers. Small amount of volume added to space has dramatic effects on filling but so does removal of a small amount – Tamponade physiology Prolonged filling and stretch allows the pericardium to adapt.

Answer 145

Chronic accumulation allows adaptation of the parietal pericardium This compliance reduces the effect on diastolic filling of the chambers As a result very slowly accumulating effusions rarely cause tamponade

Answer 146

Acute pericarditis is an inflammatory pericardial syndrome with or without effusion Clinical diagnosis made with 2 of 4 from: Chest Pain (85-90%) Friction rub (33%) ECG changes (60%) Pericardial effusion (up to 60% usually mild)

Answer 147

Viral (common): Enteroviruses (coxsackieviruses, echoviruses), herpesviruses (EBV, CMV, HHV-6), adenoviruses, parvovirus B19 (possible overlap with aetiologic viral agents of myocarditis). Bacterial: Mycobacterium tuberculosis (other bacteria rare).

Answer 148

Autoimmune (common): Sjögren syndrome, rheumatoid arthritis, scleroderma, systemic vasculitides Neoplastic (secondary to viral causes): Secondary metastatic tumours (common, above all lung and breast cancer, lymphoma). Metabolic: Uraemia, myxoedema, ``` Traumatic and Iatrogenic: Early onset (rare): Direct injury (penetrating thoracic injury, oesophageal perforation). Indirect injury (non-penetrating thoracic injury, radiation injury). ``` Delayed onset: Pericardial injury syndromes (common) iatrogenic trauma (e.g.coronary percutaneous intervention, pacemaker lead insertion and radiofrequency ablation). Other: Amyloidosis, aortic dissection, pulmonary arterial hypertension and chronic heart failure.

Answer 149

Difficult to quantify 80-90% of all pericarditis idiopathic Seasonal with viral trends Higher in young, previously healthy patients

Answer 150

Chest pain: Severe, Sharp and pleuritic (without constricting crushing character of ischaemic pain) Rapid onset, Left anterior chest or epigastrium Radiates to arm more specifically trapezius ridge (co-innervation phrenic nerve) Relieved by sitting forward exacerbated by lying down Pretty common to have associated symptoms – viral infection that precedes the pericarditis ``` Dyspnoea Cough Hiccups (phrenic) Skin rash Joint pain ```

Answer 151

``` Clinical examination - Pericardial rub – pathognomonic, crunching snow - Sinus tachycardia - Fever - Signs of effusion (pulsus paradoxus, Kussmauls sign) ECG Bloods CXR Echocardiogram ```

Answer 152

Diffuse ST segment elevation Concave ST segment – may resemble acute injury pattern of STEMI No reciprocal ST depression Saddle shaped PR depression Mechanism is epicardial inflammation as adjacent to pericardium ( parietal is inert)

Answer 153

FBC: Modest increase in WCC, mild lympocytosis ESR & CRP: High ESR may suggest aetiology Antinuclear antibody test Troponin: Pericarditis in itself shouldn’t give a increased Troponin. But if the associate myocytes on the epicardium are damaged then there will be an increase in Troponin. CXR Often normal in idiopathic Pneumonia common with bacterial Modest enlargement of cardiac silhouette rule out effusion (>300ml to be detectable!)

Answer 154

Sedentary activity until resolution of symptoms and ECG/CRP NSAID: Ibuprofen or Aspirin Colchicine limited by nausea and diarrhoea, reduces recurrence

Answer 155

Major:Fever >38°C, Subacute onset, Large pericardial effusion, Cardiac tamponade, Lack of response to aspirin or NSAIDs after at least 1 week of therapy Minor: Myopericarditis, Immunosuppression, Trauma, Oral anticoagulant therapy

Answer 156

Most patients with acute pericarditis have a good long-term prognosis. Cardiac tamponade rarely occurs in patients with acute idiopathic pericarditis. Constrictive pericarditis may occur in 1% of patients with acute idiopathic pericarditis. The risk of developing constriction can be classified as: - low for idiopathic and presumed viral pericarditis - intermediate for autoimmune, immune- mediated and neoplastic aetiologies - high for bacterial aetiologies, especially with TB and purulent pericarditis 15 – 30% of patients with acute pericarditis will develop recurrence. Colchicine reduced recurrence rate by 50%

Answer 157

- Viral pericarditis: commonest cause in developed world - Purulent bacterial pericarditis and effusion Staph, strep and pneumococci (Pneumonia, empyema) Rare <1% Very sick, high mortality - Tuberculous effusion TB pericarditis 90% HIV +ve in developed countries. High mortality - Dressler's syndrome (Post cardiac injury syndromes) Late post MI 1-2 weeks post MI

Answer 158

``` HCM is a primary heart muscle disease and the most common. The enlargement of the thickened wall encroaches into the left ventricle.This increased thickened wall will make it hugely more powerful than the normal heart. But it is slower and less compliance in relaxation (diastolic dysfunction). Chaotic arrangement of myofibrils: myofibrillar disarray. Can be a cause of sudden death in otherwise healthy young people (18-25) – genetically passed through the family. Protein malfunction (due to genetic abnormality) in sarcomeres, the cytoskeleton and cell adhesion leads to cardiomyopathy. ```

Answer 159

Hypertrophic - muscle is thickened Dilated Arrhythmogenic - abnormality of structure which leads to rhythm disturbance

Answer 160

Wall of the heart is either normal or relatively thin. Present with heart failure - problems with contraction. Can have left ventricular dilatation, biventricular or all four chambers dilatation.

Answer 161

Any of the cardiomyopathies can cause rhythm disturbances but this one particular so. Death of myocytes and replacement with fibro-fatty tissue, cannot contract properly. Initially described in the right ventricle but can also occur in the left ventricle. Often get an abnormal ECG (particular V1-V3). Characteristic epsilon waves that can come and go. Disease of the desmosome (area between the cells). There are protein structures that cross this intracellular space. If there is an abnormality in any of these proteins, you start to lose the adhesion between the cells.

Answer 162

Patients with woolly hair and palmar plantar keratoderma also have arrhythmogenic cardiomyopathy. Primary problem of cell separation. Physical phenotype. Recessive disease.

Answer 163

Marfan’s syndrome - abnormality in fibrillin which is present all over the body, long arm span, long fingers, very tall, prone to aorta aneurysm or vascular aneurysm elsewhere. Familial Hypercholesterolaemia - 1 in 250/300, genetic mutation affecting the LDL receptor. LDL receptor would usually take up cholesterol from the circulation. Whereas, here there is very high amounts of cholesterol in the circulation. Very serious - causing 100x risk of a heart attack. Can get lipid deposition in the hands, tendons, eyes.

Answer 164

Important preventable cause of premature morbidity and mortality. ``` Major risk factor for: Stroke – ischaemic and haemorrhagic Myocardial infarction Heart failure Chronic renal disease Cognitive decline Premature death ```

Answer 165

Clinic BP 140/90 mmHg or higher

Answer 166

Stage 1 hypertension 140/90 and 135/85 (ABPM) Stage 2 hypertension 160/100 and 150/95 (ABPM) Severe hypertension SBP 180 or DBP 110

Answer 167

Primary (essential) hypertension (no obvious cause) - Lifestyle modification – weight, alcohol, smoking, salt intake - Antihypertensive drug therapy Consider secondary hypertension (underlying cause) eg young patient resistant BP symptoms/signs of underlying cause

Answer 168

People aged under 80 years with stage 1 hypertension who have one or more of the following: 1. Target organ damage e.g. eyes, heart, kidneys 2. Established cardiovascular disease 3. Renal disease 4. Diabetes 5. A 10-year cardiovascular risk of 20% or greater. OR people of any age with stage 2 hypertension.

Answer 169

Under 80 years < 140/90 < 135/85 (ABPM) | Over 80 years < 150/90 < 145/85 (ABPM)

Answer 170

- Cardiac output and Peripheral Resistance - Interplay between: a. Renin-Angiotensin-Aldosterone system b. Sympathetic nervous system (noradrenaline) - Local vascular vasoconstrictor and vasodilator mediators – also have an impact

Answer 171

ACE converts angiotensin I to angiotensin II. Angiotensin II is a powerful vasoconstrictor. Inhibiting this, reduce vasconstriction. Clinical indications: Hypertension, Heart failure, Diabetic nephropathy Ramipril, Enalapril, Perindopril, Trandolapril Main adverse effects - Related to reduced angiotensin II formation: Hypotension, Acute renal failure, Hyperkalaemia, Teratogenic effects in pregnancy - Related to increased kinin production: Cough – dry and persistant, Rash, Anaphylactoid reactions – allergic type reactions

Answer 172

Angiotensin II Receptor Blockers Blocks the receptor for Angiotensin II, reducing its vasoconstriction effect. Clinical indications: Hypertension, Diabetic nephropathy, Heart failure (when ACE-I contraindicated) Candesartan, Losartan, Valsartan, Irbesartan, Telmisartan Main adverse effects Symptomatic hypotension (especially volume deplete patients), Hyperkalaemia, Potential for renal dysfunction, Rash, Angio-oedema Contraindicated in pregnancy Generally very well tolerated

Answer 173

Vasodilators Reducing peripheral pressure Clinical indications: Hypertension, Ischaemic heart disease (IHD) – angina, Arrhythmia (tachycardia) Amlodipine, Nifedipine, Diltiazem, Felodipine, Lacidipine, Verapamil

Answer 174

1. Dihydropyridines: nifedipine, amlodipine, felodipine, lacidipine Preferentially affect vascular smooth muscle Peripheral arterial vasodilators 2. Phenylalkylamines: verapamil Main effects on the heart Negatively chronotropic, negatively inotropic 3. Benzothiazepines: diltiazem Intermediate heart/peripheral vascular effects

Answer 175

- Due to peripheral vasodilatation (mainly dihydropyridines): Flushing, Headache, Oedema – ankle swelling due to gravity, Palpitations – if you dilate peripheral vascularisation, your brain thinks that you are losing blood, so causes ventricular tachycardia. - Due to negatively chronotropic effects (mainly verapamil/diltiazem): Bradycardia, Atrioventricular block - Due to negatively inotropic effects (mainly verapamil): Worsening of cardiac failure - Verapamil causes constipation

Answer 176

Beta-adrenoreceptor antagonists act on the sympathetic nervous system Clinical indications: Ischaemic heart disease (IHD) – angina, Heart failure, Arrhythmia, Hypertension Bisoprolol, Carvedilol, Propanolol, Metoprolol, Atenolol, Nadolol

Answer 177

Selectivity is a spectrum: B1 selective (Metoprolol, Bisoprolol, in the middle (Atenolol), Non-selective (Propanolol, Nadolol, Carvedilol). The term “cardioselective” is often used to imply β-1 selectivity This is a misnomer since up to 40% of cardiac β-adrenoceptors are β-2

Answer 178

``` Fatigue Headache Sleep disturbance/nightmares – cross the blood brain barrier Bradycardia Hypotension Cold peripheries Erectile dysfunction ``` Worsening of: Asthma (may be severe) or COPD, PVD – Claudication or Raynaud’s, Heart failure – if given in standard dose or acutely

Answer 179

Clinical indications: Hypertension, Heart failure - Thiazides and related drugs (distal tubule) - Bendroflumethiazide, Hydrochlorothiazide, Chlorthalidone - Loop diuretics (loop of Henle) - Furosemide, Bumetanide - Potassium-sparing diuretics - Spironolactone, Eplerernone, Amiloride, Triamterine - Aldosterone antagonists

Answer 180

``` Hypovolaemia (mainly loop diuretics) Hypotension (mainly loop diuretics) Hypokalaemia Hyponatraemia Hypomagnesaemia Hypocalcaemia) Raised uric acid (hyperuricaemia – gout) Erectile dysfunction (mainly thiazides) Impaired glucose tolerance (mainly thiazides) ```

Answer 181

a-1 adrenoreceptor blockers: Doxazosin Centrally acting anti-hypertensives: Moxonidine, Methyldopa Direct renin inhibitors: Aliskiren

Answer 182

``` 1) Under 55s: ACE-I, ARB Over 55s/Afro-Caribbean: CCB 2) ACE-I/ARB and CCB 3) Addition of thiazide-like diuretic 4) RESISTANT HYPERTENSION: Spironolactone, high dose thiazide-like diuretic, Alpha blocker, beta blocker, (others) ```

Answer 183

Heart failure is a complex clinical syndrome of symptoms and signs that suggest the efficiency of the heart as a pump is impaired. It is caused by structural or functional abnormalities of the heart. Can be acute or chronic. Most common cause is coronary artery disease Causes morbidity, mortality, hospital admissions and substantial cost - Heart failure due to left ventricular systolic dysfunction - LVSD - Heart failure with preserved ejection fraction (diastolic failure) – HFPEF Main benefit is with vasodilator therapy via neurohumoral blockade (RAAS - SNS) and not from LV stimulants

Answer 184

Symptomatic treatment of congestion: Diuretics (usually loop) Disease influencing therapy – neurohumoral blockade Inhibition of renin-angiotensin-aldosterone system Inhibition of the sympathetic nervous system a. First line: ACE inhibitors and beta blocker therapy (Low dose and slow uptitration) b. Aldosterone antagonists c. ACE-I intolerant: Angiotensin receptor blocker d. ACE-I and ARB intolerant: Hydralazine/nitrate combination e. Consider digoxin or ivabradine to slow heart rate down

Answer 185

Arterial and venous dilators Reduction of preload and afterload Lower BP Clinical indication: ischaemic heart disease (angina), heart failure Isosorbide mononitrate, GTN spray, GTN infusion (in ICU) Aren’t used as anti-hypertensive because they are not as effective and you can become tolerant to them. GTN syncope – lowers their BP and causes a throbbing headache

Answer 186

Chronic stable angina: Anginal chest pain, Predictable, Exertional, Infrequent, Stable Unstable angina / acute coronary syndrome (NSTEMI): Unpredictable, may be at rest, Frequent, Unstable ST elevation Myocardial Infarction (STEMI): Unpredictable, Rest pain, Persistent, Unstable

Answer 187

1) Antiplatelet therapy: Aspirin, Clopidogrel 2) Lipid-lowering therapy: Statins (simvastatin, atorvastatin, rosuvastatin, pravastatin) 3) Short acting nitrate: GTN spray for an attack 4) First-line: Beta-blocker, CCB 5) If intolerant, switch 6) If not controlled, combine 7) If intolerant/not controlled, consider monotherapy or combinations with long acting nitrates, Ivabradine, Nicorandil, Ranolazine

Answer 188

1) Pain relief: GTN spray, Opiates 2) Dual anti-platelet therapy: Aspirin plus ticagrelor or prasugrel or clopidogrel 3) Antithrombin therapy: Fondaparinux 4) Consider Glycoprotein IIb IIIa inhibitor (high risk cases): tirofiban, eptifibatide, abciximab 5) Background angina therapy: beta blocker, long acting nitrate, calcium channel blocker 6) Lipid lowering therapy: Statins 7) Therapy for LVSD/heart failure as required: ACE-I, beta blocker, aldosterone antagonist

Answer 189

Class I: Sodium channel blockers Ia - disopyramide, quinidine, procainamide Ib - lidocaine, mexilitene Ic - flecainide, propafenone Class II: Beta adrenceptor antagonists - propranolol, nadolol, carvedilol (non-selective) - bisoprolol, metoprolol (β1-selective) Class III: Prolong the action potential - amiodarone, sotalol Class IV: Calcium channel blockers - verapamil, diltiazem

Answer 190

Cardiac glycoside Inhibit Na/K pump Main effects are on the heart: Bradycardia (increased vagal tone) Slowing of atrioventricular conduction (increased vagal tone) Increased ectopic activity Increased force of contraction (by increased intracellular Ca) Narrow therapeutic range – can easily become toxic Nausea, vomiting, diarrhoea, confusion Difficult to diagnose Digoxin toxicity! Used in atrial fibrillation (AF) to reduce ventricular rate response Use in severe heart failure as positively inotropic

Answer 191

An inability of the heart to deliver enough blood (and O2) at a rate commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures. The syndrome of breathlessness, tiredness and fluid overload caused by a form of cardiac dysfunction

Answer 192

``` The commonest cause is myocardial dysfunction. This usually results from IHD. Other causes include: - Hypertension, - alcohol excess, - cardiomyopathy, - valvular, - endocardial, - pericardial causes ```

Answer 193

Higher in men - Men get heart failure earlier because they do not have the protective effects of oestrogen which protect against atherosclerosis. Incidence rises from the age of 55 and peaks in the over 80 years old

Answer 194

``` Breathlessness Tiredness Cold peripheries Leg swelling Increased weight ```

Answer 195

``` Tachycardia Displaced apex beat Raised JVP Added heart sounds/murmurs Hepatomegaly (eg pulsatile/tender) Peripheral/sacral oedema Ascites ```

Answer 196

Class I: No limitation (Asymptomatic) Class II: Slight limitation (mild HF) Class III: Marked limitation (Symptomatically moderate HF) Class IV: Inability to carry out any physical activity without discomfort (symptomatically severe HF)

Answer 197

You can check the NTproBNP but if it is positive it doesn’t mean that it is heart failure. It could be many other conditions too which have nothing to do with heart failure. 400-2000 72% chance of heart failure Above 2000 96% chance of heart failure

Answer 198

TTE to assess structural/functional abnormalities Not needed immediately (or at all) in those with established diagnosis of HF de Novo AHF require early TTE (within 48 h) Immediate TTE is only mandatory in patients with haemodynamic instability, and when acute life-threatening and potentially treatable abnormalities are expected. Repeat TTE is not recommended for its limited use

Answer 199

``` Acute coronary syndrome Tachyarrhythmias Excessive rise in BP Infection Non-adherence with salt/fluid intake or medications Bradyarrhythmias Toxic substances Drugs Exacerbation of COPD Pulmonary embolism Surgery and perioperative complications Increased sympathetic drive Metabolic hormonal dearrangements Cerebrovascular insult Acute mechanical cause ```

Answer 200

LEFT-SIDED Heart failure with reduced ejection fraction (HFrEF) (aka systolic failure) Left ventricle loses its ability to contract normally. The heart can't pump with enough force to push enough blood into circulation. Heart failure with preserved ejection fraction (HFpEF), aka diastolic failure (or diastolic dysfunction): The left ventricle loses its ability to relax normally (because the muscle has become stiff). The heart can't properly fill with blood during the resting period between each beat. Right-sided or right ventricular (RV) heart failure usually occurs as a result of left-sided failure. When the left ventricle fails, increased fluid pressure is, in effect, transferred back through the lungs, ultimately damaging the heart's right side.

Answer 201

``` Diuretics ACEI ARB Beta Blockers Mineralocorticoid receptor antagonists Ivabradine Tafamidis - reduces progression of the disease Sacubitril-Valsartan ```

Answer 202

Using multi-site pacemakers (right atrial, right ventricular and coronary sinus pacing leads), to simultaneously pace both sides of the LV, in patients with LBBB and significant dys-synchrony with QRS duration >130 m sec (ideally >150 m sec). These devices reduce morbidity and mortality.

Answer 203

HF differs from cancer in that the journey towards palliative care is an equilibrium of an excursion between active and palliative therapy, before the eventual event occurs.

Answer 204

Most strokes occur with people with normal blood pressure (just because there are more people with normal BP than high BP). Hypertensive patients have a 30-40% increased risk of a stroke.

Answer 205

Increased exercise, reduced salt intake, weight loss smoking, alcohol. WEIGHT, SALT, ALCOHOL are the main ones. Smoking itself doesn’t have a huge impact and smokers are often less likely to be obese, but it does increase the likelihood of other cardiovascular events.

Answer 206

Venlafaxine (a serotonin-noradrenaline reuptake inhibitor) which can increase blood pressure. NSAIDs can also increase blood pressure, along with the oral contraceptive pill, corticosteroids, cold cures.

Answer 207

``` Simple to perform Can provide information about range of conditions: Cardiac rhythm - Cardiac ischaemia Myocardial disease Electrolyte disturbances ```

Answer 208

Amplitude of deflection is related to mass of myocardium Width of deflection reflects speed of conduction Positive deflection is towards the lead/vector

Answer 209

Left axis deviation -30 to -90 degrees - Left anterior fascicular block - Left bundle branch block - Left ventricular hypertrophy Right axis deviation 90 to 180 degrees - Left posterior fascicular block - Right heart hypertrophy/strain

Answer 210

``` Positive inferior leads Positive in lead I Negative in aVR Biphasic in V1 Normally <120 ms wide <0.3mV (3 small sq) tall ```

Answer 211

Low amplitude: Atrial fibrosis, obesity, hyperkalaemia High amplitude ‘Tall’: Right atrial enlargement Broad notched ‘Bifid’: Left atrial enlargement Alternative pacemaker foci: Focal atrial tacycardias

Answer 212

Consists of atrial depolarisation and conduction from atria to ventricles. Normally 120-200 ms Prolonged in disorders of AV node and specialised conducting tissue Shorter in younger patients or in pre-excitation (Wolf-Parkinson-White) P interval may lengthen if the AV node conduction is getting slower with age or due to an ectopic beat.

Answer 213

Ventricular depolarisation Normally <120ms Size of complexes related to myocardial mass Predominantly negative in V1, transitioning to postive by V6 Normal frontal axis -30 to +90 (positive in leads I, II)

Answer 214

Broad QRS: Ventricular conduction delay/bundle branch block Small QRS complexes: Obese patient, Pericardial effusion, Infiltrative cardiac disease Tall QRS complexes: Left ventricular hypertrophy, Thin patient – less tissue present

Answer 215

From start of QRS to end of T wave Represents ventricular depolarisation and repolarisation Corrected for heart rate (380 – 450ms) Excessively rapid or slow repolarisation can be arrhythmogenic “Long QT” or “Short QT” syndromes Congenital, drugs, electrolyte disturbances

Answer 216

From end of QRS (“J point”) to start of T wave Normally isoelectric Can be elevated in early repolarisation, myocardial infarction, pericarditis/myocarditis

Answer 217

Height of T wave normally less than QRS | Direction of deflection usually similar to QRS (in limb leads), but in opposite direction in bundle branch block

Answer 218

Atrial fibrillation, Atrial Flutter Supraventricular tachycardia Focal atrial tachycardia Ventricular tachycardia Ventricular fibrillation

Answer 219

Conduction tissue fibrosis Ischaemia Inflammation/infiltrative disease Drugs

Answer 220

In V1 and V6 Left bundle branch block - William (W shape) Right bundle branch block - Marrow (M shape)

Answer 221

Potassium Hyperkalaemia: Tall T waves, flattening of P waves, broadening of QRS Hypokalaemia: Flattening of T wave, QT prolongation Calcium Hypercalcaemia: QT shortening Hypocalcaemia: QT prolongation

Answer 222

Normal Aortic Valve Area: 3-4 cm2 Symptoms occur when valve area is 1/4th of normal. Types: Supravalvular, Subvalvular, Valvular

Answer 223

A pressure gradient develops between the left ventricle and the aorta. (increased afterload) LV function initially maintained by compensatory pressure hypertrophy When compensatory mechanisms exhausted, LV function declines.

Answer 224

Congenital: aortic stenosis or bicuspid valve, commonly associated with aortic coarctation, dissection or aneurysm. Acquired: degenerative calcification, rheumatic heart disease, rare causes. Adhesions and fusion of commissures and cusps. May be a result of infections/radiation.

Answer 225

Syncope: (exertional) 15% Angina: (increased myocardial oxygen demand; demand/supply mismatch) 35% Dyspnoea: on exertion due to heart failure (systolic and diastolic) 50% Sudden death <2%

Answer 226

Slow rising carotid pulse (pulsus tardus) & decreased pulse amplitude (pulsus parvus) Heart sounds- soft or absent second heart sound, S4 gallop due to LVH. Ejection systolic murmur- crescendo-decrescendo character. “Loudness” does NOT tell you anything about severity

Answer 227

Angina + AS: 50% survive for 5 years. Syncope + AS: 50% survive for 3 years, HF + AS mean survival is <2 years. Risk of sudden cardiac death in asymptomatic or minimally symptomatic patients is rare (<2%).

Answer 228

Echocardiography Two measurements obtained are: Left ventricular size and function: LVH, Dilation, and EF Doppler derived gradient and valve area (AVA)

Answer 229

Fastidious dental hygiene / care Medical - limited role since AS is a mechanical problem. Vasodilators are relatively contraindicated in severe AS Surgical Replacement: Definitive treatment TAVI – Transcatheter Aortic Valve Implantation

Answer 230

Guided wire through the femoral artery Blowing up a balloon to open up the narrowing (cracking it open) Put in a new valve where the old valve was (self-expanding/balloon expanding) Catheter guide wire removed

Answer 231

Any SYMPTOMATIC patient with severe AS (includes symptoms with exercise) Any patient with decreasing EF Any patient undergoing CABG with moderate or severe AS

Answer 232

Backflow of blood from the LV to the LA during systole | Mild (physiological) MR is seen in 80% of normal individuals.

Answer 233

Myxomatous degeneration (MVP) Ischemic MR – rupture or weakening Rheumatic heart disease Infective Endocarditis

Answer 234

Pure Volume Overload – blood going back to where it shouldn’t do Compensatory Mechanisms: Left atrial enlargement, LVH and increased contractility Progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension. Progressive left ventricular volume overload leads to dilatation and progressive heart failure.

Answer 235

Auscultation: pansystolic murmur at the apex radiating to the axilla In chronic MR, the intensity of the murmur does correlate with the severity. Displaced hyperdynamic apex beat Exertion Dyspnoea: ( exercise intolerance) Heart Failure: May coincide with increased hemodynamic burden e.g., pregnancy, infection or atrial fibrillation

Answer 236

Compensatory phase: 10-15 years Patients with asymptomatic severe MR have a 5%/year mortality rate Once the patient’s EF becomes <60% and/or becomes symptomatic, mortality rises sharply Mortality: From progressive dyspnoea and heart failure

Answer 237

ECG: May show, LA enlargement, atrial fibrillation and LV hypertrophy with severe MR CXR: LA enlargement, central pulmonary artery enlargement. ECHO: Estimation of LA, LV size and function. Valve structure assessment (TOE - transoesophageal echocardiography)

Answer 238

Vasodilator such as ACEI, hydralazine Rate control for atrial fibrillation with B-blockers, CCB, digoxin Anticoagulation in atrial fibrillation and flutter Diuretics for fluid overload Serial Echocardiography

Answer 239

ANY Symptoms at rest or exercise with (repair if feasible) Asymptomatic: If EF <60%, LVESD >45mm If new onset atrial fibrillation/raised PAP

Answer 240

Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps

Answer 241

Bicuspid aortic valve Rheumatic Infective endocarditis

Answer 242

Combined pressure AND volume overload | Compensatory Mechanisms: LV dilation, LVH. Progressive dilation leads to heart failure

Answer 243

Wide pulse pressure: most sensitive Hyperdynamic and displaced apical impulse Auscultation- Diastolic blowing murmur at the left sternal border Austin flint murmur (apex): Regurgitant jet impinges on anterior MVL causing it to vibrate Systolic ejection murmur: due to increased flow across the aortic valve

Answer 244

Asymptomatic until 4th or 5th decade Rate of Progression: 4-6% per year Progressive Symptoms include: - Dyspnoea: exertional, orthopnea, and paroxsymal nocturnal dyspnea - Palpitations: due to increased force of contraction and ectopics

Answer 245

CXR: enlarged cardiac silhouette and aortic root enlargement ECHO: Evaluation of the AV and aortic root with measurements of LV dimensions and function

Answer 246

General: consider infective endocarditis prophylaxis Medical: Vasodilators (ACEI’s improve stroke volume and reduce regurgitation only if pt symptomatic or hypertensive. Serial Echocardiograms: to monitor progression. Surgical Treatment: Definitive Tx

Answer 247

ANY Symptoms at rest or exercise Asymptomatic treatment if: EF drops below 50% or LV becomes dilated

Answer 248

Obstruction of LV inflow that prevents proper filling during diastole Normal MV Area: 4-6 cm2 Transmitral gradients and symptoms begin at areas less than 2 cm2 Rheumatic carditis is the predominant cause Prevalence and incidence: decreasing due to a reduction of rheumatic heart disease.

Answer 249

Rheumatic heart disease: 77-99% of all cases Infective endocarditis: 3.3% Mitral annular calcification: 2.7%

Answer 250

- Progressive Dyspnea (70%): LA dilation leads to pulmonary congestion (reduced emptying) worse with exercise, fever, tachycardia, and pregnancy - Increased Transmitral Pressures: Leads to left atrial enlargement and atrial fibrillation. - Right heart failure symptoms: due to Pulmonary venous hypertension - Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure

Answer 251

Disease of plateaus: Mild MS: 10 years after initial RHD insult Moderate: 10 years later Severe: 10 years later Mortality: Due to progressive pulmonary congestion, infection, and thromboembolism.

Answer 252

Prominent "a" wave in jugular venous pulsations: Due to pulmonary hypertension and right ventricular hypertrophy Signs of right-sided heart failure: in advanced disease Mitral facies: When MS is severe and the cardiac output is diminished, there is vasoconstriction, resulting in pinkish-purple patches on the cheeks

Answer 253

Diastolic murmur: Low-pitched diastolic rumble most prominent at the apex. Heard best with the patient lying on the left side in held expiration Intensity of the diastolic murmur does not correlate with the severity of the stenosis Loud Opening S1 snap: heard at the apex when leaflets are still mobile Due to the abrupt halt in leaflet motion in early diastole, after rapid initial rapid opening, due to fusion at the leaflet tips. A shorter S2 to opening snap interval indicates more severe disease.

Answer 254

ECG: may show atrial fibrillation and LA enlargement CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, gradient and mitral valve area

Answer 255

Serial echocardiography Medications: MS like AS is a mechanical problem and medical therapy does not prevent progression B-blockers, CCBs, Digoxin which control heart rate and hence prolong diastole for improved diastolic filling Diuretics for fluid overload Identify patient early who might benefit from percutaneous mitral balloon valvotomy.

Answer 256

ANY SYMPTOMATIC Patient with heart failure Class III (in activities in daily living) Asymptomatic moderate or Severe MS with a pliable valve suitable for percutaneous mitral balloon valvotomy

Answer 257

Infection of heart valve/s or other endocardial lined structures within the heart (such as septal defects, pacemaker leads, surgical patches, etc).

Answer 258

Left sided native IE (mitral or aortic) Left sided prosthetic IE Right sided IE (rarely prosthetic as rare to have PV or TV replaced) Device related IE (pacemakers, defibrillators, with or without valve IE) Prosthetic; can be Early (within year) or Late (after a year) post op

Answer 259

Have an abnormal valve; regurgitant or prosthetic valves are most likely to get infected. Introduce infectious material into the blood stream or directly onto the heart during surgery Have had IE previously

Answer 260

``` Used to be a disease of the young affected by rheumatic heart disease. Now it is a disease of: the elderly (in an ageing population) the young i.v. drug abusers the young with congenital heart disease. anyone with prosthetic heart valves ```

Answer 261

Incidence and mortality have not fallen over 30 years | 10 year survival 60-90%

Answer 262

Depends on site, organism, etc Signs of systemic infection (fever, sweats, etc) Embolisation; stroke, pulmonary embolus, bone infections, kidney dysfunction, myocardial infarction Valve dysfunction; heart failure, arrythmia New regurgitant heart murmur Embolic events of unknown origin Sepsis of unknown origin

Answer 263

Definite IE 2 major, 1 major+3 minor, 5 minor Possible IE 1 major, 1 major+3 minor, 5 minor ``` Major Criteria Bugs grown from blood cultures evidence of endocarditis on echo, or new valve leak Minor Criteria Predisposing factors Fever Vascular phenomena Immune phenomena Equivocal blood cultures ```

Answer 264

Transthoracic echo (TTE). Safe, non-invasive, no discomfort, often poor images so lower sensitivity Transoesophageal (TOE/TEE). Excellent pictures as long as you don’t mind having a big tube pushed down your throat. Patients rarely want to have a second TOE. Generally safe but risk of perforation or aspiration. Easiest if ventilated (but never ventilate just for TOE)

Answer 265

Petechiae rash 10 to 15%, Splinter hemorrhages Osler’s nodes (small, tender, purple, erythematous subcutaneous nodules are usually found on the pulp of the digits) Janeway lesions are erythematous, macular, nontender lesions on the fingers, palm, or sole Roth spots on fundoscopy, soft exudates are also seen (retinal infarcts)

Answer 266

Cultures may remain negative in 2% to 5% of patients with IE. Certain organisms: cell media; special media or microbiological methods, or may require long incubtion 7-21/7. The most common cause for negative blood cultures in patients with IE is prior antimicrobial therapy. ``` ECG (ischemia or infarction, new appearance of heart block) Transthoracic echocardiography is of crucial importance in detecting a vegetation. Transoesophageal echo (TOE) has improved the rate of detection of vegetations on native valves to 90–95% A negative TTE/TOE does not eliminate the possibility that IE is present. ```

Answer 267

Antimicrobials; intravenous for around 6weeks; choice of agent/s based on culture sensitivities Treat complications; arrhythmia, heart failure, heart block, embolisation, stroke rehab, abscess drainage etc Surgery

Answer 268

The infection cannot be cured with antibiotics (ie recurs after treatment, or CRP doesn’t fall) Complications (aortic root abscess, severe valve damage to remove infected devices (always needed) To replace valve after infection cured (may be weeks/months/years later To remove large vegetations before they embolise

Answer 269

For years, patients with valve disease were given antibiotic prophylaxis during interventions (esp dental) NICE guidance in 2008 recommended not to give prophylaxis to anyone (and remains current) ESC guidance is to consider prophylaxis in high risk patients (prosthetic valves, previous IE, cyanotic heart disease)

Answer 270

Vary from minor problems to issues that incompatible with life ex-utero Many lesions used to have a very poor prognosis before cardiac childhood surgery The advent of surgery and interventional cardiology mean that >85% will survive to be > 18 years

Answer 271

Intellectual disability in 10% (Down's syndrome) Psychosocial issues Transition – mother’s care to independence can be difficult Explaining the lesion and the prognosis Building independence/ self reliance

Answer 272

Incidental, rather than genetic in most cases. However there are increased risks if you have a family history.

Answer 273

Pulmonary hypertension Severe left heart obstruction Systemic ventricular impairment (Ejection fraction < 30%) Marfans syndrome with aortic root diameter > 47 mm

Answer 274

4 DEFECTS: Ventricular septal defect, pulmonary stenosis, hypertrophy of right ventricle (boot sign), overriding aorta 10% of all congenital heart defects The stenosis of the right ventricle outflow leads to the right ventricle being at higher pressure than the left. Therefore de-oxygenated blood passes from the right ventricle to the left ventricle, sent round the body. The patients are BLUE (Fallot spells)

Answer 275

1986 first repair in infancy Now mostly repaired before the age of two years Mostly do very well Often get pulmonary valve regurgitation in adult life and require redo surgery

Answer 276

Abnormal connection between the two ventricles Common – 20% of all congenital heart defects Many close spontaneously during childhood High pressure LV Low pressure RV Blood flows from high pressure chamber to low pressure chamber - increased blood flow through the lungs

Answer 277

Very high pulmonary blood flow in infancy Breathless, poor feeding, failure to thrive Require fixing in infancy (PA band, complete repair) May lead to Eisenmengers syndrome Small breathless skinny baby Increased respiratory rate Tachycardia Big heart on chest X ray Murmur varies in intensity

Answer 278

``` Small increase in pulmonary blood flow only Asymptomatic Endocarditis risk Need no intervention Loud systolic murmur Thrill (buzzing sensation) Well grown Normal heart rate Normal heart size ```

Answer 279

High pressure pulmonary blood flow Damages to delicate pulmonary vasculature The resistance to blood flow through the lungs increases The RV pressure increases The shunt direction reverses The patient becomes BLUE

Answer 280

Abnormal connection between the two atria (primum, secundum, sinus venosus) Common Often present in adulthood Slightly higher pressure in the LA than the RA Shunt is left to right Therefore NOT blue Increased flow into right heart and lungs

Answer 281

Significant increased flow through the right heart and lungs in childhood Right heart dilatation Increased chest infections If any stretch on the right heart should be closed

Answer 282

``` Small increase in flow No right heart dilatation No symptoms Leave alone The shunt on small to moderate sized defects increases with age ```

Answer 283

Pulmonary flow murmur Fixed split second heart sound (delayed closure of PV because more blood has to get out) Big pulmonary arteries on CXR Big heart on chest X ray

Answer 284

Often Downs syndrome 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 AV valves there is one big malformed one It usually leaks to a greater or lesser degree

Answer 285

``` Breathless as neonate Poor weight gain Poor feeding Torrential pulmonary blood flow Needs repair or PA band in infancy Repair is surgically challenging ```

Answer 286

Can present in late adulthood Presents like a small VSD / ASD May be left alone if there is no right heart dilatation

Answer 287

A persistent opening between the pulmonary arteries and the aorta. The opening, called the ductus arteriosus, is a normal part of a baby's circulatory system before birth that usually closes shortly after birth.

Answer 288

Continuous ‘machinery’ murmur If large, big heart, breathless Eisenmenger’s syndrome Differential cyanosis (clubbed and blue toes, but pink not clubbed fingers)

Answer 289

Torrential flow from the aorta to the pulmonary arteries in infancy Breathless, poor feeding, failure to thrive More common in prem babies Need to be closed (surgically)

Answer 290

Little flow from the aorta to pulmonary arteries Usually asymptomatic Murmur found incidentally Endocarditis risk

Answer 291

Surgical or percutaneous Local anaesthetic Venous approach (sometimes requires an AV loop) Low risk of complications

Answer 292

Narrowing of the aorta at the site of insertion of the ductus arteriosus

Answer 293

Complete or almost complete obstruction to aortic flow Collapse with heart failure Needs urgent repair

Answer 294

Presents with hypertension Incidental murmur Should be repaired to try to prevent problems in the long term

Answer 295

Right arm hypertension Bruits (buzzes) over the scapulae and back from collateral vessels Murmur

Answer 296

``` Hypertension - Early coronary artery disease - Early strokes - Sub arachnoid haemorrhage Re-coarctation requiring repeat intervention Aneurysm formation at the site of repair ```

Answer 297

Normal AV has three cusps Bicuspid AVs are common 1-2% of the population (M>F) Can be severely stenotic in infancy or childhood Degenerate quicker than normal valves Become regurgitant earlier than normal valves Are associated with coarctation and dilatation of the ascending aorta

Answer 298

Narrowing of the outflow of the right ventricle Can be: valvar, sub valvar, supra valvar, branch 8-12 % of all congenital heart defects

Answer 299

Severe: Right ventricular failure as neonate, Collapse, Poor pulmonary blood flow, RV hypertrophy, Tricuspid regurgitation Mild: Well tolerated for many years, right ventricular hypertrophy

Answer 300

Balloon valvuloplasty Open valvotomy Open trans-annular patch Shunt (to bypass the blockage)

Answer 301

Legs - aorto-iliac, femoro-popliteal, tibial Brain - carotids, vertebrals Organs - coeliac , mesenterics, renals Arms - subclavian, axillary

Answer 302

``` Progression (increase in size) Haemorrhage Plaque rupture/fissure Overlying thrombosis Dissection Aneurysm ```

Answer 303

Stress-induced physiological malfunction - exercise induced angina, intermittent claudication Structural and functional breakdown - ischaemic cardiac failure, critical limb ischemia, vascular dementia Infarction - gangrene

Answer 304

Intermittent claudication - muscle cramps on walking (calf, thigh, buttock) Critical leg ischaemia - rest pain (particularly at night in bed), ulceration, gangrene Acute limb ischaemia (embolism or thrombosis) - 6Ps: pain, pale, paralysis, paraesthesia, perishing cold, pulseless 4-6 hours, may need to amputate rather than revascularize Carotid artery disease - stroke, transient ischaemic attack (resolves within 24 hours), amaurosis fugax Abdominal aortic aneurysm (AAA) - usually asymptomatic until rupture occurs

Answer 305

Intermittent claudication Moderate ischemia Anaerobic metabolism when O2 demand Critical ischaemia Blood supply barely adequate to allow basal metabolism No reserve available for increased demand

Answer 306

Most often atherosclerotic - medial thinning beneath the plaque Arteriomegaly - sometimes familial Collagen diseases - Marfan, vascular Ehlers Danlos Most common site: Infrarenal abdominal (6cm) - rupture risk 20% over 3 years

Answer 307

Investigate the pathophysiology - Blood glucose, Lipids, Vasculitic Screen, BP Image the vessels - Duplex (not very good quality if there is calcification), CT/MRA (gives good anatomical detail)

Answer 308

Risk factor modification Revascularization for ‘critical ischaemia’ - acute/chronic: open it up or bypass it Alternative is amputation If you have multiple risk factors - consider statins Antiplatelet agents Controlled blood pressure and diabetes

Answer 309

Prescribe walking exercise programme to treat PAD If that fails, bypass (femoral). Can use another vein or a prosthetic material. Carries risk. PCI preferred (balloon angioplasty/stents). If that fails, amputation.

Answer 310

Aim is to reduce risk of death from MI or stroke and relieve symptoms Exercise and weight reduction Control of hypertension, hyperlipidaemia, diabetes Antiplatelet therapy Smoking cessation