Cardiovascular Flashcards

Question

what are the steps of leukocyte recruitment to vessel walls? what mediates this?

Answer 1

1. capture 2. rolling 3. slow rolling 4. firm adhesion 5. transmigration - selectins - integrins - chemoattractants

Answer 2

lipid-laden macrophages (foam cells) and T lymphocytes within the intimal layer of the vessel wall

Answer 3

layers of: - lipid laden macrophages (foam cells) - vascular smooth muscle cells - T lymphocytes - adhesion and aggregation of platelets to the vessel wall - isolated pools of extracellular lipid adhesion and aggregation of platelets to the vessel wall (aspirin inhibits platelet aggregation)

Answer 4

- impede blood flow - prone to rupture - covered by dense fibrous cap made of ECM proteins including collagen (strength) and elastin (flexibility) laid down by SMC that overlies lipid core and necrotic debris - may be calcified - contains smooth muscle cells, macrophages and foam cells and T lymphocytes

Answer 5

- constantly growing and receding | - fibrous cap has to be resorbed and redeposited in order to be maintained

Answer 6

- if balance shifted in favour of inflammatory conditions (increased enzyme activity), the cap becomes weak and plaque ruptures - basement membrane, collagen and necrotic tissue exposure as well as haemorrhage of vessels within the plaque - thrombus (clot) formation and vessel occlusion

Answer 7

- second most prevalent cause of coronary thrombosis - lesions tend to be small early lesions - fibrous cap doesn't disrupt - luminal surface underneath the clot may not have endothelium present, but is rich in smooth muscle cells - may be a prominent lipid core

Answer 8

exercise, alcohol in moderation, not smoking and lowered TG

Answer 9

statins - 24-30% reduction in mortality primary and secondary prevention - up to 50% reduction if dose of statin is titrated to achieve target LDL of <2.6mmol/L fibrates - reduction in CAD events in diabetics and patients with high TG and low HDL diet - Mediterranean diet leads to 75% reduction in CAD events in post MI patients

Answer 10

- patients with established CAD, PVD and cerebrovascular atherosclerotic disease - asymptomatic individuals who are at high risk of developing disease due to risk factors resulting in 10-year risk of 5% now for developing a fatal event (cholesterol >8mmol/L; LDL cholesterol >6mmol/L; BP>180/110mmHg) - all diabetics - close relatives of patients with early-onset atherosclerotic CV disease and asymptomatic individuals at high risk

Answer 11

- representation of the electrical events of the cardiac cycle - each event has a distinctive waveform - study of waveform can lead to greater insight into a patient's cardiac pathophysiology

Answer 12

- arrhythmias - myocardial ischaemia and infarction - pericarditis - chamber hypertrophy - electrolyte disturbances - drug toxicity (e.g. digoxin and drugs which prolong the QT interval)

Answer 13

- SA node: dominant pacemaker with an intrinsic rate of 60-100bpm - AV node: back up pacemaker with an intrinsic rate of 40-60bpm - ventricular cells: back up pacemaker with an intrinsic rate of 20-45bpm

Answer 14

25mm/s | 0.1 mV/mm

Answer 15

- impulse that travels towards the electrode produces an upright (positive) deflection - when a depolarisation wave spreads away from the lead, there is downwards (negative) deflection - shape of waveform in any lead depends on orientation of that lead to vector of depolarisation

Answer 16

SA node -> AV node -> bundle of His -> right and left bundle branches -> Purkinje fibres

Answer 17

atrial depolarisation - seen in every lead apart from aVR - 0.08-0.1s

Answer 18

- interval between the start of the P wave and the start of the QRS complex (whether this is a Q wave or an R wave) - time taken for excitation to pass from the sinus node, through the atrium, AV node and the His-Purkinje system to the ventricle - determines whether impulse transmission from atria to ventricles is normal - 0.12-0.22s

Answer 19

- the isoelectric (flat) line between the end of the P wave and the start of the QRS complex - baseline of the ECG curve - reference line or isoelectric line

Answer 20

- reflects depolarisation of the ventricles - <0.12s - short QRS complex implies that the ventricles are depolarised rapidly, and that the electrical conduction system functions normally - wide/broad QRS complexes indicate that ventricular depolarisation is slow

Answer 21

between end of the QRS complex and the start of the T wave | - interval between depolarisation and repolarisation

Answer 22

- ST segment depression implies that the ST segment is depressed below the level of the PR segment - ST segment elevation: ST segment elevated above the level of the PR segment - magnitude of deviation is measured as the height difference (mm) between the J point and the PR segment - PR segment is reference level

Answer 23

- measurement of ST-segment elevation and depression in most cases - where ST segment starts - point between QRS and ST segment

Answer 24

measurement of ST-segment depression in exercise stress testing

Answer 25

- reflects rapid repolarisation (recovery) of the ventricles - transition from ST segment to T wave should be smooth - normal T wave is somewhat asymmetric, with a steeper downward slope and first half more gradual - amplitude rarely exceeds 10mm

Answer 26

men: <0.44s | women <0.46s

Answer 27

- positive wave after the T wave; same direction as T wave - related to after-depolarisations which follow repolarisation - small, round, symmetrical and positive in lead II, amplitude <2mm - occurs occasionally on the ECG - its height (amplitude) is about 1/4th of the amplitude of the T wave - most often seen in leads V2, V3 and V4 - people with prominent T waves display U waves more often, and it's clearer during bradycardia

Answer 28

- total duration of ventricular depolarisation (activation) and repolarisation (recovery) - measured from start of QRS complex to end of T wave - QT interval increases at slower heart rates and vice versa - shorter at faster heart rates

Answer 29

horizontally: - one small box 0.04s - one large box 0.20s (5 x small boxes) (5mm wide) vertically: - one large box 0.5mV

Answer 30

measure the difference in electrical potential between two points - bipolar leads: two different points on the body - unipolar leads: one point on the body and a virtual reference point with 0 electrical potential, located in the centre of the heart

Answer 31

12 leads - 3 standard limb leads - 3 augmented limb leads - 6 precordial leads

Answer 32

I: negative (right arm) -> positive (left arm) II: negative (right arm) -> positive (left leg) III: negative (left arm) -> positive (left leg)

Answer 33

I: 0 II: +60 III: +120

Answer 34

aVL: -30 aVF: +90 aVR: -150

Answer 35

V1: fourth intercostal space, to right of sternum (septal) V2: fourth intercostal space, to left of sternum (septal) V3: between leads V2 and V3 (anterior) V4: fifth intercostal space in mid-clavicular line (anterior) V5: horizontally even with V4, in left anterior axillary line (lateral) V6: horizontally even with V4 and V5 in the mid-axillary line (lateral)

Answer 36

RA: white LA: black LL: red RL: green

Answer 37

- right side chest leads | - V7, V8 and V9 on posterior chest wall

Answer 38

row 1: I (lateral), aVR, V1 (septal), V4 (anterior) row 2: II (inferior), aVL (lateral), V2 (septal), V5 (lateral) row 3: III (inferior), aVF (inferior), V3 (anterior), V6 (lateral)

Answer 39

1. PR interval should be 120 to 200 milliseconds or 3 to 5 little squares 2. width of QRS complex should not exceed 110ms, less than 3 little squares 3. QRS complex should be dominantly upright in leads I and II 4. QRS and T waves tend to have the same direction in the limb leads 5. all waves are negative in lead aVR 6. R wave must grow from V1 to at least V4; S wave must grow from V1 to at least V3 and disappear in V6 7. ST segment should start isoelectric except in V1 and V2 where it may be elevated 8. P waves should be upright in I, II, and V2 to V6 9. there should be no Q wave or only a small less than 0.04s in width in I, II, V2 to V6 10. T wave must be upright in I, II, V2 to V6

Answer 40

- always positive in lead I and II - always negative in lead aVR - < 3 small squares in duration - < 2.5 small squares in amplitude - commonly biphasic in lead V1 - best seen in lead II

Answer 41

tall (>2.5mm), pointed P waves (P pulmonale)

Answer 42

notched/bifid P wave (P mitrale) in limb leads

Answer 43

Wolff-Parkinson-White syndrome - short PR interval (<0.2s) - accessory pathway (bundle of Kent) allows early activation of the ventricle (delta wave and short PR interval)

Answer 44

long PR interval (>0.2s)

Answer 45

short: Wolff-Parkinson-White syndrome long: first degree heart block

Answer 46

- non-pathological Q waves may present in I, III, aVL, V5 and V6; small and narrow - R wave in lead V6 is smaller than V5 - depth of S wave should not exceed 30mm - pathological Q wave: >2mm deep and >1mm wide or 25% amplitude of the subsequent R wave (except in aVR and V1); indicate MI

Answer 47

Sokolow and Lyon criteria - increases voltage-induced depolarisation of the free wall of the left ventricle - deep S waves (>30mm) in V1 and V2 - tall R waves (>25mm) in V5 or V6 - R wave of 11-13mm or more in lead aVL - sum of R wave in left ventricular leads and the S wave in the right ventricular leads exceeds 40mm - ST-segment depression - T wave flattening or inversion in left ventricular leads

Answer 48

symmetrical, tall, peaked, biphasic or inverted | - usually follows the direction of the QRS deflection

Answer 49

measured in lead aVL as this lead does not have prominent U waves

Answer 50

- total depolarisation and repolarisation of the ventricles - QT decreases when HR increases - for HR = 70bpm, QT <0.40s - should be 0.35-0.45s - should not be more than half of the interval between adjacent R waves (R-R)

Answer 51

- rule of 300/1500 | - 10 second rule

Answer 52

- represents overall direction of the heart's electrical activity - abnormalities hint at ventricular enlargement and conduction blocks (i.e. hemiblocks)

Answer 53

normal: -30 to +90 left axis deviation: -30 to -90 right axis deviation: +90 to +180

Answer 54

- quadrant approach | - equiphasic approach

Answer 55

imbalance between the heart's supply of oxygen (and other essential myocardial nutrients) and the myocardial demand for these substances

Answer 56

- atheroma - thrombosis - spasm - embolus - coronary ostial stenosis - coronary arteritis

Answer 57

- anaemia - carboxyhaemoglobulinaemia - hypotension causing decreased coronary perfusion pressure

Answer 58

increase in cardiac output (e.g. thyrotoxicosis) or myocardial hypertrophy (e.g. from aortic stenosis or hypertension) - aortic stenosis - valvular disease - arrhythmia

Answer 59

due to obstructive CAD in form of coronary atherosclerosis - variations in the tone of smooth muscle in the wall of a coronary artery may add another element of dynamic or variable obstruction

Answer 60

- largest single cause of death in the UK and many parts of the world - over the last decade, mortality in the UK has decreased - sudden cardiac death is a common feature of CAD - more common in men

Answer 61

- heavy, tight or gripping - pain is cental/retrosternal and may radiate to the jaw and/or arms - can range from a mild ache to a most severe pain that provokes sweating and fear

Answer 62

- constricting discomfort in the front of the chest, arms, neck, jaw - provoked by physical exertion, esp. after meals and in cold, windy weather or by anger or excitement - relieved (within minutes) with rest or glyceryl trinitrate - may disappear with continued exertion - pain may radiate to one or both arms, the neck, jaw or teeth - may be dyspnoea, nausea, sweatiness and faintness

Answer 63

typical angina: all three features of classical/exertional angina pectoris atypical angina: two out of three features of classical/exertional angina pectoris non-anginal chest pain: one or less features

Answer 64

when it is not a new symptom and when there is no change in the frequency or severity of attacks

Answer 65

angina of recent onset (<24hrs) or a deterioration in previous stable angina with symptoms frequently occurring at rest, i.e. acute coronary syndrome

Answer 66

patients with severe coronary disease in whom revascularisation is not possible and angina is not controlled by medical therapy

Answer 67

angina that occurs without provocation, usually at rest, due to coronary artery spasm - more frequent in women - ST elevation on ECG during pain - provocation tests may be needed for diagnosis

Answer 68

- refers to patients with good history of angina, positive exercise test and angiographically normal coronary arteries - heterogenous group - more common in women - good prognosis, symptomatic, difficult to treat - abnormal metabolic response to stress

Answer 69

- usually no abnormal findings in angina - 4th heart sound may be heard - signs to suggest anaemia, thyrotoxicosis, or hyperlipidaemia (e.g. lipid arcus, xanthelasma, tendon xanthoma should be sought - exclude aortic stenosis as possible cause - take BP

Answer 70

- to exclude an acute coronary syndrome - often normal between attacks - evidence of old MI, left ventricular hypertrophy or LBBB may be present - during an attack, transient ST depression, T wave inversion or other changes of the shape of the T wave may appear

Answer 71

clinical assessment alone or combined with anatomical (cardiac catheterisation or CT coronary angiography) or functional imaging (SPECT, stress-echocardiography, stress-MRI)

Answer 72

- information, lifestyle modification - short-acting nitrates - secondary prevention -> beta blocker or calcium channel blocker

Answer 73

- long acting nitrate (isosorbide mononitrate) - ivabradine (It current inhibitor ivabradine) - nicorandil (potassium channel activator) - ranolazine (sodium channel inhibitor)

Answer 74

consider revascularisation -> PCI or CABG PCI - single vessel disease - multi-vessel <65yrs - suitable anatomy CABG - unsuitable anatomy - multivessel >65yrs - diabetes

Answer 75

percutaneous coronary intervention - process of dilating a coronary artery stenosis using an inflatable balloon - metallic stent introduced into the arterial circulation via femoral, radial or brachial artery

Answer 76

discrete, soft lesion in a straight vessel without involving a bifurcation

Answer 77

occluded vessels, stenoses that are calcified, tortuous, long or involve a bifurcation

Answer 78

- bleeding - haematoma - dissection and pseudoaneurysm from the arterial puncture site (use of radial artery may reduce the risks) - acute MI (2%) - stroke (0.4%) - death (1%)

Answer 79

- use of heparin or direct thrombin inhibitor bivalrudin together with antiplatelet agents, aspirin and the thienopyridine clopidogrel - in high risk ACS or diabetic patients the antiplatelet GPIIb/IIIa antagonists (tirofiban, eptifibratide and abciximab) are used - coated stents lined with substances reducing coronary artery restenosis

Answer 80

Cypher stent Xience V stent Taxus stent

Answer 81

sirolimus, which is an immunosuppressant agent that reduces cellular proliferation

Answer 82

everolimus, which is a derivative of sirolimus

Answer 83

paclitaxel, which is a mitotic inhibitor drug that inhibits neointima formation

Answer 84

exposure of thrombus stimulating surface when the patient discontinues clopidogrel therapy, leading to recommendation that patients take prolonged dual therapy (aspirin and clopidogrel) and avoid discontinuing therapy within 6-12 months of implantation

Answer 85

coronary artery bypass grafting - autologous veins or arteries are anastomosed to the ascending aorta and to the native coronary arteries distal to the area of stenosis

Answer 86

with in situ internal mammary and gastroepiploic arteries grafted onto the stenosed coronary artery

Answer 87

percutaneous transluminal coronary angioplasty - coronary angiography demonstrates occluded coronary artery - a soft wire passed through the guide catheter reopens the artery but a severe stenosis remains - balloon is inflated to dilate the stenosis - coronary artery is reopened with good antegrade flow

Answer 88

- coronary artery vein bypass grafting (CAVBG) | - internal mammary arterial implantation (IMA)

Answer 89

some patients remain symptomatic despite medication and are unsuitable for revascularisation; need a pain management programme

Answer 90

- vasodilators - beta blockers - calcium channel blockers - second line anti-anginal drugs - secondary prevention

Answer 91

- ST-elevation myocardial infarction (STEMI) - non-ST-elevation myocardial infarction (NSTEMI) - unstable angina (UA)

Answer 92

in NSTEMI, there is occluding thrombus, which leads to myocardial necrosis and a rise in serum troponins or CK-MB

Answer 93

when cardiac myocytes die due to prolonged myocardial ischaemia

Answer 94

- appropriate clinical history - 12 lead ECG - elevated biochemical markers: troponin I and T, CK-MB - three types of MIs

Answer 95

spontaneous MI with ischaemia due to a primary coronary event, e.g. plaque erosion/rupture, fissuring or dissection

Answer 96

Mi secondary to ischaemia due to increased oxygen demand or decreased supply, e.g. coronary spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension

Answer 97

diagnosis of MI in sudden cardiac death, after PCI and after CABG, respectively

Answer 98

- common mechanism to all ACS is rupture or erosion of the fibrous cap of a coronary artery plaque - leads to platelet aggregation and adhesion, localised thrombosis, vasoconstriction and distal thrombus embolisation - presence of a rich lipid pool within the plaque and a thin fibrous cap are associated with an increased risk of rupture - thrombus formation and the vasoconstriction produced by platelet release of serotonin and thromboxane A2, results in myocardial ischaemia due to reduction of coronary blood flow

Answer 99

leads to platelet aggregation and adhesion, localised thrombosis, vasoconstriction and distal thrombus embolisation

Answer 100

serotonin and thromboxane A2

Answer 101

- age >65 - more than three CAD risk factors: hypertension, hyperlipidaemia, family history, diabetes, smoking - known coronary artery disease (coronary angiography stenosis >50%) - aspirin use in last 7 days - severe angina (more than two episodes of rest pain in 24hrs) - ST elevation on ECG (horizontal ST depression or transient ST elevation >1mm) - elevated cardiac markers (CK-MB or troponin)

Answer 102

- new onset of chest pain - chest pain at rest - deterioration of pre-existing angina - atypical features e.g. indigestion, pleuritic chest pain or dyspnoea

Answer 103

- alternative diagnoses e.g. aortic dissection, PE or peptic ulceration - adverse clinical signs e.g. hypotension, basal crackles, fourth heart sounds and cardiac murmurs

Answer 104

- may be normal - ST depression and T wave inversion are highly suggestive for an ACS, esp. if associated with anginal chest pain - should be repeated when in pain - continuous ST-segment monitoring is recommended - STEMI: complete occlusion of coronary vessel results in persistent ST elevation or LBBB - transient ST elevation seen with coronary vasospasm of Prinzmetal's angina

Answer 105

- cardiac troponin complex - creatine-kinase-MB - myoglobin

Answer 106

- made up of three distinct proteins (I, T, C) situated with tropomyosin on thin actin filament - cardiac troponins are not detectable in normal people, so monoclonal antibody tests to cardiac specific troponin I and T are sensitive markers of myocyte necrosis - if initial troponin assay is negative, it should be repeated 6-12hrs after admission - serum levels increase within 3-12hrs from the onset of chest pain and peak at 24-48hrs - fall back to normal after 5-14days - can act as prognostic indicator

Answer 107

- troponin T binds the complex to tropomyosin and helps position it on actin, and together with the rest of the tropomyosin complex, modulates contraction of striated muscle - troponin C binds calcium during excitation-contraction coupling - troponin I inhibits the myosin binding site on the actin

Answer 108

- creatine-kinase-MB - previously the standard marker for myocyte death - there is presence of low levels of CK-MB in the serum of normal individuals and patients with skeletal muscle damage - can be used to determine to determine reinfarction as levels drop back to normal after 36-72hrs

Answer 109

- rapid diagnosis of an ACS as levels become elevated very early in MI - presence of myoglobin in skeletal muscle; poor specificity for ACS

Answer 110

oral aspirin, clopidogrel, beta blockers and nitrates

Answer 111

- exercise test (negative result has good prognosis and early positive test should lead to invasive strategy) - baseline ECG - dobutamine stress ECG - myocardial perfusion scintigraphy

Answer 112

- myocardial oxygenation - antiplatelet - antithrombin - glycoprotein IIb/IIIa inhibitors - analgesia (diamorphine or morphine) - myocardial energy consumption (atenolol and metoprolol) - coronary vasodilation (GTN) - plaque stabilisation/ventricular remodelling (HMG-CoA reductase inhibitors and ACEi)

Answer 113

- exposes circulating platelets to ADP, thromboxane A2, epinephrine, thrombin and collagen tissue factor - causes platelet activation, with thrombin as a potent stimulant - platelet activation stimulates the expression of glycoprotein IIb/IIIa receptors on platelet surface - receptors bridge fibrinogen between adjacent platelets, causing platelet aggregates

Answer 114

- blocks formation of thomboxane A2, and so prevents platelet aggregation - 150-300mg chewable or soluble aspirin, then 75-150mg orally daily - caution if active peptic ulceration - used in combination with ticagrelor

Answer 115

- thienopyridine - inhibits ADP-dependent activation of the GPIIb/IIIa complex that allows platelet aggregates to form - prodrug that requires conversion by hepatic CYP450 enzymes to an active moiety - active drug binds irreversibly to the P2Y12 receptor on platelet membranes and inhibits the ADP-dependent pathway of platelet activation - increased risk of bleeding - 300mg orally loading dose, then 75mg OD

Answer 116

- powerful inhibitors of platelet aggregation | - receptors usually bind to fibrinogen, initiating platelet aggregation

Answer 117

- monoclonal antibody that binds strongly and has a long half life - indicated if coronary intervention likely within 24hrs

Answer 118

- indicated in high-risk patients managed without coronary intervention or during PCI - cyclic peptide that selectively inhibits GPIIb/IIIa receptors - short half life, wears out in 2-4hrs

Answer 119

- small non-peptide that rapidly blocks the GPIIb/IIIa receptors - reversible in 4-6hrs - indicated in high-risk patients managed without coronary intervention or during PCI

Answer 120

- direct thrombin inhibitor that reversibly binds to thrombin and inhibits clot-bound thrombin

Answer 121

- synthetic pentasaccharide that selectively binds to antithrombin, which inactivates factor Xa resulting in strong inhibition of thrombin generation and clot formation - does not inactivate thrombin and has no effect on platelets

Answer 122

- risk of bleeding - factor Xa inhibitor - effective in reducing the risk of further cardiac events

Answer 123

- anti-ischaemia agents - for patients with no contraindications (asthma, AV-block, acute pulmonary oedema) - administered IV or orally - reduce myocardial ischaemia by blocking circulating catecholamines - reduce HR and BP, reducing myocardial oxygen consumption

Answer 124

- HMG-CoA reductase inhibitor drugs (statins) and ACE inhibitors - may produce plaque stabilisation, improve vascular and myocardial remodelling, and reduce future CV events - starting drugs whilst patient is still in hospital increases the likelihood of them receiving secondary drug therapy

Answer 125

- rupture or erosion of a vulnerable coronary artery plaque can produce a prolonged occlusion of a coronary artery leading to myocardial necrosis within 15-30 minutes - subendocardial myocardium is initially affected - with continued ischaemia the infarct zone extends through to the subepicardial myocardium, producing a transmural Q wave MI - early reperfusion may salvage regions of the myocardium, reducing future mortality and morbidity

Answer 126

- age >65yrs - age >75yrs - history of angina, hypertension or diabetes - systolic BP <100 - HR >100 - Killip II-IV - weight >67kg - anterior MI or LBBB - delay to treatment >4hrs

Answer 127

- any patient presenting with severe chest pain more than 20mins may have an MI - pain does not usually respond to sublingual GTN, and opiate analgesia is required - pain may radiate to left arm, neck or jaw - symptoms may be atypical and include dyspnoea, fatigue, pre-syncope or syncope (esp. in elderly/diabetics) - pale and clammy, marked sweating - thready pulse with significant hypotension, bradycardia or tachycardia - pain described as substernal pressure, squeezing, aching, burning or even sharp pain - breathlessness, fatigue, distress

Answer 128

- small: V3-V4 | - extensive: V2-V5

Answer 129

V4-V6, I, aVL

Answer 130

I, aVL, V5-V6

Answer 131

II, III, aVF

Answer 132

ST depression V1-V3 dominant R wave ST elevation V5-V6

Answer 133

first few minutes: T waves become tall, pointed and upright and there is ST segment elevation hours afterwards: T waves invert, R wave voltage decreases and Q waves develop days afterwards: ST segment returns to normal; T wave is still abnormal; Q wave remains weeks/months afterwards: T wave may return to upright but Q wave remains

Answer 134

- blood samples taken for cardiac troponin I or T levels (will be increased) - FBC, serum electrolytes. glucose and lipid profile - myoglobin (increased) - transthoracic ECG (TTE) may confirm an MI (wall motion abnormalities are detectable early in STEMI - TTE may detect alternative diagnoses e.g. aortic dissection, pericarditis or PE

Answer 135

- aspirin 150-300mg chewed and clopidogrel 300mg oral gel - sublingual GTN 0.3-1mg. repeat - nasal cannula 2-4L/min if hypoxia is present - brief history/risk factors, examination - IV access + blood for markers (+ FBC, biochemistry, lipids, glucose) - 12 lead ECG - IV opiate and antiemetic - beta blocker (if no contraindication) for ongoing chest pain, hypertension, tachycardia - if primary PCI available, give GPIIb/IIIa inhibitor; alternatively, give thrombolysis

Answer 136

enhance the breakdown of occlusive thromboses by activation of plasminogen to form plasmin - still used if PCI is unavailable

Answer 137

r-PA (reteplase), TNK-t-PA (tenecteplase), streptokinase

Answer 138

- haemorrhagic stroke or stroke of unknown origin at any time - ischaemic stroke in preceding 6 months - CNS damage or neoplasma - recent major trauma/surgery/head injury (within preceding 3 weeks) - GI bleeding within last month - known bleeding disorder - aortic dissection

Answer 139

- TIA in preceding 6 months - oral anticoagulant therapy - pregnancy or within 1 week postpartum - non-compressible punctures - traumatic resus - refractory hypertension (systolic >180) - advanced liver disease - infective endocarditis

Answer 140

- heart failure - myocardial rupture and aneurysmal dilatation - heart block - rupture of interventricular septum - pericarditis - thromboembolism - ventricular aneurysm - ventricular septal defect - mitral regurgitation - cardiac arrhythmias - conduction disturbances - post-MI pericarditis and Dressler's syndrome

Answer 141

used to assess patients with heart failure post-MI

Answer 142

Killip I: no crackles and no third heart sound Killip II: crackles in <50% of the lung fields or a third heart sound Killip III: crackles in >50% of the lung fields Killip IV: cardiogenic shock

Answer 143

- Mediterranean-style diet - >7g omega-3 fatty acids/week from oily fish or >1g daily of omega-3-acid ethyl esters - safe alcohol consumption - exercise 20-30mins a day - stop smoking - overweight and obese patients encouraged to get healthy - hypertension treated to 140/90 or 130/80 if CKD/diabetes - diabetics treated to maintain HbA1c <7%

Answer 144

- aspirin 75-100mg/day - second anti-platelet agent - beta blocker to maintain heart rate <60bpm - ACE inhibitors - high intensity statins - clopidogrel 75mg/day for 9-12 months in moderate-high-risk patients with NST-ACS - aldosterone antagonist for patients post-MI with clinical evidence of heart failure and left ventricular ejection fraction <40%

Answer 145

- age - male - smoking - family history - diabetes mellitus - hyperlipidaemia - hypertension - kidney disease - obesity - physical inactivity - stress - history of premature CHD/IHD

Answer 146

- anaemia - hypoxaemia - polycynthemia - hypothermia - hypovolaemia - hypervolaemia

Answer 147

- hypertension - tachyarrhythmia - valvular heart disease - hyperthyroidism - hypertrophic cardiomyopathy

Answer 148

- cold weather - heavy meals - emotional distress

Answer 149

1. impairment of blood flow by proximal arterial stenosis 2. increased distal resistance e.g. left ventricular hypertrophy 3. reduced oxygen-carrying capacity of blood e.g. anaemia

Answer 150

deltaP = (8uLQ)/(pi x r^4) - deltaP = pressure loss - L = length of pipe - u/mew = dynamic viscosity - Q = volumetric flow rate - r = radius - d = diameter

Answer 151

incidence - men 35/100000/yr - women 20/100000/yr prevalence - men 5% (5000/100000) - women 4 (4000/100000)

Answer 152

- personal details - presenting complaint - history of PC + risk factors - past medical history - drug history, allergies - family history - social history - systematic enquiry

Answer 153

- myocardial ischaemia - pericarditis/myocarditis - pulmonary embolism/pleurisy - chest infection/pleurisy - dissection of the aorta - GORD - musculoskeletal - psychological

Answer 154

decreased HR (negative chronotropic) and decreased LV contractility (negative inotropic) -> decreased CO -> decreased O2 demand - decreased cardiac output - reduce force of contraction of heart - act on B1 receptors in the heart as part of the adrenergic sympathetic pathway - B1 activation -> Gs -> cAMP to ATP -> contraction

Answer 155

- tiredness, nightmares - erectile dysfunction - cold hands and feet - bradycardia

Answer 156

- severe bronchospasm; asthma - hypotension - bradyarrythmias - verapamil, diltiazem, amiodarone, digoxin - Prinzmetal's angina - untreated heart failure - severe heart block - excessive bradycardia

Answer 157

- venodilators - dilate arterioles -> decreased BP -> decreased afterload - dilates systemic veins -> decreased venous return -> decreased preload - coronary arteries dilate - reduced work of heart and O2 demand - profuse headache immediately after use

Answer 158

e. g. verapamil - dilate arteries -> flushing, postural hypotension and swollen ankles - decreased BP -> decreased afterload - coronary arteries dilate - decreased oxygen demand - decreased work (negative inotropic and decreased LV contraction) (negative chronotropic and decreased HR)

Answer 159

- less invasive - convenient - repeatable - acceptable - risk stent thrombosis - risk restenosis - can't deal with complex disease - dual antiplatelet therapy

Answer 160

- good prognosis - deals with complex disease - invasive - risk of stroke, bleeding - can't do if frail, comorbid - one time treatment - length of stay - time for recovery

Answer 161

- cardiac chest pain at rest - cardiac chest pain with crescendo pattern - new onset angina - diagnosis: history, ECG, troponin (no significant rise)

Answer 162

- coronary vasospasm without plaque rupture - drug abuse (amphetamines, cocaine) - dissection of coronary artery related to defects of the vessel connective tissue - thoracic aortic dissection

Answer 163

- Gram negative sepsis - pulmonary embolism - myocarditis - heart failure - arrhythmias - cytotoxic drugs

Answer 164

initial adhesion - GPIb/VWF rolling - GPIb/VWF - alpha2beta1/collagen stable adhesion and activation/aggregation - GPVI - GPIIb/IIIa

Answer 165

- PAR1 and PAR4 bind to thrombin - TPalpha binds to thromboxane A2 - GPVI binds to collagen - 5HT2A binds 5HT - P2Y1 binds ADP - P2X1 binds ATP

Answer 166

- shape change AND - alpha(IIb)beta(3) binds fibrinogen, which activates it and enhances adhesion and leads to platelet-platelet interactions - thrombin generation - alpha and dense granule secretion

Answer 167

coagulation and inflammation

Answer 168

- IGF1, PDGF, TGFbeta, platelet factor 4 - clotting proteins (e.g. thrombospondin, fibronectin, factor V, vWF) - P-selectin and CD63

Answer 169

contributes to platelet activation

Answer 170

ADP, ATP, ionised calcium, serotonin

Answer 171

- actual diagnosis not ACS - plaque rupture without significant stenosis and resolution of obstructive thrombus by time of angiography - stress induced (Tako-Tsubo) cardiomyopathy without obstructive CAD

Answer 172

- dose - age - weight - disease states including diabetes mellitus and CKD - drug-drug interactions e.g. omeprazole and strong CYP 3A inhibitors - CYP2C19 loss of function alleles

Answer 173

- inhibition of adenosine uptake via the ENT-1 pathway - adenosine -> vasodilation, cardioprotection, antiplatelet, immunomodulation - adenosine kinase catalyses AMP -> adenosine

Answer 174

- bleeding - rash - GI disturbance

Answer 175

an oral reversibly binding P2Y12 antagonist

Answer 176

- dyspnoea: usually mild and well tolerated, but if not it may require switching to prasugrel or clopidogrel - ventricular pauses: usually sinoatrial pauses, may resolve with continued treatment

Answer 177

leg and pelvis

Answer 178

- commonly involves saphenous veins and often associated with varicosities - axillary vein may be involved, due to trauma - local superficial inflammation of the vein wall, with secondary thrombosis - clinical picture: painful, tender cord-like structure with associated redness and swelling

Answer 179

rest, elevation of limb and analgesics

Answer 180

deep vein thrombosis - any inflammation of the vein wall is secondary to this - commonly occurs after immobilisation, but can occur in normal people - in 50% of patients after prostatectomy or after a cerebral vascular event - 10% of patients with an MI have DVT

Answer 181

- may be asymptomatic, presenting with features of PE - pain in the calf with swelling, redness and engorged superficial veins - warm - ankle oedema - calf tenderness - superficial venous distension - Homan's sign (pain in calf on dorsiflexion of foot) - complete occlusion -> cyanotic discolouration of limb and severe oedema, can lead to venous gangrene - PE more frequent from iliofemoral thrombosis and rare with thrombosis confined to veins below the knee

Answer 182

pain in calf on dorsiflexon of foot

Answer 183

- clinical diagnosis is unreliable - diagnosis sensitivity of 80% combined with D-dimer level - confirmation of iliofemoral thrombosis made with B mode venous compression, ultrasonography or Doppler ultrasound with a sensitivity and specificity over 90% - below knee thromboses detected reliably only by venography with non-invasive techniques, ultrasound, fibrinogen scanning and impedance plethysmography; sensitivity of 70% - venogram is performed by injecting a vein in foot with contrast, which detects all thrombi present

Answer 184

venogram is performed by injecting a vein in foot with contrast, which detects all thrombi present

Answer 185

to prevent PE; all patients with thrombi above the knee must be anticoagulated

Answer 186

- anticoagulation of below-knee thrombi recommended for 6 weeks, as 30% of patients have an extension of the clot proximally - bed rest advised until fully anticoagulated - mobilised, with elastic/compression stocking giving graduated pressure over the leg - low molecular weight heparin - thrombolytic therapy

Answer 187

- have replaced unfractioned heparin as they're more effective, do not require monitoring and less risk of bleeding - can be treated at home - warfarin started immediately and the heparin stopped when INR is in target range - 3 months warfarin - recurrent DVTs need permanent anticoagulents - target INR should be 2.5

Answer 188

occasionally used for patient with a large iliofemoral thrombosis

Answer 189

- active cancer or cancer treatment - age >60yrs - critical care admission - dehydration - known thrombophilias - obesity - comorbidities e.g. heart disease, metabolic, endocrine or respiratory pathologies, acute infectious diseases, inflammatory conditions - personal history or first-degree relative with a history of VTE - use of HRT or oestrogen containing oral contraceptive - varicose veins with phlebitis - pregnancy/childbirth - thrombophilia - plasminogen deficiency

Answer 190

- active bleeding - acquired bleeding disorders e.g. acute liver failure - concurrent use of anticoagulents - lumbar puncture/epidural/spinal anaesthesia within previous 4hrs or expected within 12hrs - acute stroke - thrombocytopenia - uncontrolled systolic hypertension - untreated inherited bleeding disorders

Answer 191

- destruction of deep vein valves produces clinically painful, swollen limb made worse by standing, accompanied by oedema and sometimes venous eczema - occurs in half of patients with clinically symptomatic DVT - elastic support stockings required for life

Answer 192

- all patients assessed on admission to hospital | - patients at risk if reduced mobility for >3 days or if mobility reduced and have a >1 risk factor for VTE

Answer 193

- surgical procedure with combined anaesthetic and surgery of >90min - if admitted with acute inflammatory or intraabdominal condition - if significantly reduced mobility - if >1 risk factor for CTE

Answer 194

- thombus, usually formed in systemic veins or rarely in the right heart, may disoldge and embolise into the pulmonary arterial system - common and potentially lethal condition

Answer 195

pelvic and abdominal veins, femoral DVT or axillary thrombosis (not as common)

Answer 196

three broad categories of factors that are throught to contribute to thrombosis: - stasis of blood flow - endothelial injury - hypercoagulability

Answer 197

tumour, fat (long bone fractures), amniotic fluid and foreign material during IV drug use

Answer 198

- antithrombin deficiency - protein C or S deficiency - factor V Leiden - resistance to activated protein C - prothrombin gene variant - hyperhomocysteinaemia - antiphospholipid antibody/lupus anticoagulant

Answer 199

a solid mass formed in the circulation from the constituents of the blood during life - fragments of thrombi (emboli) may break off and block vessel downstream

Answer 200

- tends to form at areas of turbulent blood flow e.g. bifurcation - platelets adhere to damaged vascular endothelium and aggregate in response to ADP and TXA2 to form white thrombus - growth of platelet thrombus is limited at its margins by PGI2 and NO - plaque rupture -> exposure of blood containing factor VIIa to tissue factor within the plaque, triggering blood coagulation and thrombus formation - > complete occlusion or embolisation

Answer 201

increased heart rate

Answer 202

decreased heart rate

Answer 203

heart on the right side of chest instead of left

Answer 204

ST segments are raised in anterior (V3-V4) and lateral (V5-V6) leads

Answer 205

ST segments are raised in inferior (II, III, aVF) leads

Answer 206

usually not evident on an ECG since it occurs at the same time as the QRS complex, so it's hidden

Answer 207

palpated in the 5th left intercostal space and mid-clavicular line, responsible for the apex beat

Answer 208

the volume of blood ejected from each ventricle during systole

Answer 209

the volume of blood each ventricle pumps as a function of time (litres per minute) - cardiac output (L/min) = stroke volume (L) x heart rate (bpm)

Answer 210

the total resistance to flow in systemic blood vessels from beginning of aorta to vena cava; arterioles provide the most resistance

Answer 211

the volume of blood in the left ventricle which stretches the cardiac myocytes before left ventricular contraction - how much blood is in the ventricles before it pumps (end-diastolic volume). - when veins dilate, it results in a decrease in preload (since by dilating veins the venous return decreases).

Answer 212

the pressure the left ventricle must overcome to eject blood during contraction - dilated arteries = decrease in afterload

Answer 213

- force of contraction and the change in fibre length; how hard the heart pumps - when muscle contracts myofibrils stay the same length but the sarcomere shortens; force of heart contraction that is independent of sarcomere length

Answer 214

myocardial ability to recover normal shape after systolic stress

Answer 215

the pressure required to fill the ventricle to the same | diastolic volume

Answer 216

how easily the heart chamber expands when filled with blood

Answer 217

- force of contraction is proportional to the end diastolic length of cardiac muscle fibre; the more the ventricle fills, the harder it contracts - at rest the cardiac muscle is not at optimal length; below optimal length means the force of contraction is decreased/inefficient

Answer 218

increased venous return -> increased end diastolic volume -> increased preload -> increased sarcomere stretch -> increased force of contraction thus -> increased stroke volume and force of contractions

Answer 219

- decreases venous return due to gravity thus, cardiac output decreases - causes a drop in blood pressure - stimulates baroreceptors to increase blood pressure

Answer 220

S1: mitral and tricuspid valve closure S2: aortic and pulmonary valve closure S3: in early diastole during rapid ventricular filling; normal in children and pregnant women; associated with mitral regurgitation and heart failure S4: gallop, in late diastole, produced by blood being forced into a stiff hypertrophic ventricle; associated with left ventricular hypertrophy

Answer 221

chest pain or discomfort as a result of reversible myocardial ischaemia - implies narrowing of one or more coronary arteries - exacerbated by exertion and relieved by rest

Answer 222

- plaque encroaches upon the lumen and runs the risk of haemorrhage or exposure of tissue HLA-DR antigens which might stimulate T cell accumulation - drives an inflammatory reaction against part of the plaque contents

Answer 223

ulceration, fissuring, calcification and aneurysm change

Answer 224

- acute occlusion due to thrombus - chronic narrowing of vessel lumen with healing of the local thrombus - aneurysm change - embolism of thrombus and/or plaque lipid content

Answer 225

* often normal * may show ST depression * flat or inverted T waves * look for signs of past MI

Answer 226

* put ECG on patient, then make them run on treadmill uphill * monitor how long patient is able to exercise for * if you see ST segment depression then this is a sign of late-stage ischaemia * many patients unsuitable e.g. can’t walk, very unfit, young females and bundle branch block

Answer 227

CT the heart and if there is atherosclerosis in the arteries then the calcium will light up white - if there is significant calcium then this indicates angina

Answer 228

* radio-labelled tracer injected into patient * it's taken up by the coronary arteries where there is good blood supply; this will light up * where there is little blood supply these areas will not light up * if there is no light after exercise then this is indicative of myocardial ischaemia

Answer 229

- antiplatelet effect in coronary arteries, thereby avoiding platelet thrombosis - COX inhibitor; reduces prostaglandin synthesis including thromboxane A2 -> reduced platelet aggregation - side effect: gastric ulceration - e.g. salicylate

Answer 230

- HMG-CoA reductase inhibitors; reduces cholesterol produced by the liver - reduce events and LDL-cholesterol - anti-atherosclerotic

Answer 231

- dilating coronary atheromatous obstructions by inflating balloon within it - insert balloon and stent, inflate balloon and remove it - stent persists and keeps artery patent - expanding plaque makes artery bigger

Answer 232

Left Internal Mammary Artery | - used to bypass proximal stenosis (narrowing) in LAD coronary artery

Answer 233

* occlusion of a coronary artery previously affected by atherosclerosis * this causes full thickness damage of heart muscle * can usually be diagnosed on ECG at presentation * will produce a pathological Q wave some time after MI so also known as Q-wave infarction

Answer 234

* angina of recent onset (less than 24hrs) or * cardiac chest pain with crescendo pattern * deterioration in previously stable angina, with symptoms frequently occurring at rest * angina of increasing frequency or severity, occurs on minimal exertion or even at rest - form of acute coronary syndrome

Answer 235

* occurs by developing a complete occlusion of a minor or a partial occlusion of a major coronary artery previously affected by atherosclerosis * is a retrospective diagnosis made after troponin results and sometimes other investigation results are available * this causes partial thickness damage of heart muscle * also known as a Non-Q wave infarction; will see ST depression and/or T wave inversion

Answer 236

- rupture or erosion of the fibrous cap of a coronary artery plaque - leading to platelet aggregation and adhesion, localised thrombosis, vasoconstriction and distal thrombus embolisation - presence of a rich lipid pool within the plaque and a thin, fibrous cap is associated with an increased risk of rupture - thrombus formation and the vasoconstriction produced by platelet release of serotonin and thromboxane A2 result in myocardial ischaemia due to reduction of coronary blood flow

Answer 237

- in unstable angina the plaque has a necrotic centre and ulcerated cap and the thrombus results in partial occlusion - in myocardial infarction the plaque also has a necrotic centre but the thrombus results in total occlusion

Answer 238

* atheromatous plaque rupture results in platelets being exposed to ADP/thromboxaneA2/adrenaline/thrombin/collagen tissue factor * this results in platelet activation/aggregation via IIb/IIIa glycoproteins binding to fibrinogen (enables platelets to adhere to each other = aggregation) * then thrombin (already present in surroundings) is able to enzymatically convert fibrinogen to fibrin (insoluble) resulting in the formation of a fibrin mesh over platelet plug and the formation of a thrombotic clot

Answer 239

- aspirin - P2Y12 inhibitors (oral) - glycoprotein IIb/IIIa antagonists (IV)

Answer 240

clopidogrel, prasugrel and ticagrelor - side effects: neutropenia, thrombocytopenia, increased risk of bleeding - avoid if CABG planned

Answer 241

- only IV - e.g. abciximab, triofiban, eptifbatide - increases risk of major bleeding

Answer 242

simvastatin, pravastatin, atorvastatin

Answer 243

ramipril and lisonopril

Answer 244

ST depression and T wave inversion

Answer 245

stable angina, unstable angina, NSTEMI, pneumonia, pneumothorax, oesophageal spasm, GORD, acute gastritis, pancreatitis, MSK chest pain

Answer 246

- aspirin 300mg chewable - GTN (sublingual) - morphine

Answer 247

- IV morphine - oxygen if sats below 95% or breathless - beta blocker (atenolol) - P2Y12 inhibitor (clopidogrel)

Answer 248

- all patients who present with an acute STEMI who can be transferred to a primary PCI centre within 120 minutes of first medical contact - if not possible then give patient fibrinolysis and then transfer to PCI centre after infusion

Answer 249

enhances the breakdown of occlusive thromboses by the activation of plasminogen to form plasmin

Answer 250

- statins - aspirin long term - warfarin if large MI - beta blockers - ACE inhibitors

Answer 251

- sudden death - arrhythmias - persistent pain - heart failure - mitral incompetence - pericarditis - cardiac rupture - ventricular aneurysm

Answer 252

often within hours due to ventricular fibrillation

Answer 253

in first few days due to electrical instability following infarction, pump failure and excessive sympathetic stimulation

Answer 254

12 hours to a few days after due to progressive myocardial necrosis

Answer 255

- when CO is insufficient to meet the body's metabolic demands - due to ventricular dysfunction following muscle necrosis also resulting in arrhythmias

Answer 256

- in first few days or later | - due to myocardial scarring preventing valve closure

Answer 257

due to transmural infarct resulting in inflammation of pericardium, more common in STEMI

Answer 258

- early rupture: shearing between mobile and immobile myocardium - late rupture: due to weakening of wall following muscle necrosis and acute inflammation

Answer 259

due to stretching of newly formed collagenous scar tissue

Answer 260

- acts as a protective covering for the heart | - consists of an outer fibrous pericardial sac and an inner serous pericardium

Answer 261

pericardium, myocardium, endocardium

Answer 262

- inner visceral pericardium: single cell layer that’s adherent to the epicardium (myocytes), that lines the heart and great vessels, and its reflection - outer parietal pericardium: mainly collagen and elastin fibres, with no cells, that lines the fibrous sac - in between the layers is around 50ml of serous fluid that acts as a lubricant to allow the two surfaces to move over each other easily

Answer 263

in between the layers is around 50ml of serous fluid that acts as a lubricant to allow the two surfaces to move over each other easily

Answer 264

* great vessels lie in the pericardium; if the proximal segment (ascending) of the aorta is ruptured then it will bleed in into the pericardial space and result in a cardiac tamponade * left atrium is mainly outside the pericardium

Answer 265

if the proximal segment (ascending) of the aorta is ruptured then it will bleed in into the pericardial space and result in a cardiac tamponade

Answer 266

* it promotes cardiac efficiency by limiting dilation, maintaining ventricular compliance and distributing hydrostatic forces * aids atrial filling by creating a closed chamber, reduces external friction and acts as a barrier against infection and extension of malignancy * anatomically fixes the heart to the sternum, diaphragm and costal cartilages

Answer 267

initially stretchy but becomes stiff at higher tension, thus at low tension the pericardium has a small reserve volume

Answer 268

* if this volume is exceeded the pressure is translated to the cardiac chambers and thus puts pressure on the heart * small amount of volume added to this space has dramatic effects on filling e.g a cardiac tamponade

Answer 269

in a chronic pericardial effusion, the pericardium adapts slowly by laying down elastin and collagen and becomes more elastic so there is a much slower tamponade (thus there is no collapse of the right atrium) since the pressure equalises - but the entrance of fluid making up the effusion must be slow

Answer 270

acute inflammation of the pericardium; with or without effusion

Answer 271

- majority are idiopathic and most commonly seen in the young, previously healthy patient - occurs in men more than women - occurs in adults more than children

Answer 272

viral (common): • enteroviruses e.g. coxsackieviruses and echoviruses • adenoviruses • HIV bacterial: - Mycobacterium tuberculosis (other bacteria are rare) fungal (very rare): • Histoplasma spp. - most likely to be seen in immunocompromised patient

Answer 273

``` - autoimmune (common): • sjorgrens syndrome • rheumatoid arthritis • SLE - neoplastic; secondary metastatic tumours (common, above all is lung or breast cancer, and also leukaemia and lymphoma) - dressler’s syndrome - post cardiac injury syndromes - traumatic and iatrogenic - uraemia ```

Answer 274

early onset (rare): - direct injury - penetrating thoracic injury or oesophageal perforation - indirect injury - non-penetrating thoracic injury or radiation delayed onset (common): - pericardial injury syndromes (common) - iatrogenic trauma e.g. coronary percutaneous intervention or pacemaker lead insertion

Answer 275

- pericardium becomes acutely inflamed, with pericardial vascularisation and infiltration with polymorphonuclear leukocytes - a fibrinous reaction frequently results in exudate and adhesions within the pericardial sac, and a serous or haemorrhagic effusion may develop

Answer 276

- sharp retrosternal chest pain which is characteristically relieved by leaning forward - pain may be worse on inspiration and radiate to the neck and shoulders - dysponea - cough - hiccups due to phrenic involvement - pericardial friction rub present on auscultation - fever and lymphocytosis (increase in lymphocytes) if due to virus or bacteria - tachycardia

Answer 277

- severe - sharp and pleuritic (without constricting crushing character of ischaemic pain) - rapid onset - worse on inspiration or lying flat; relieved by sitting forward - left anterior chest or epigastrium - radiates to arm, more specifically the trapezius ridge (has co-innervation with the phrenic nerve), whereas a STEMI would be arms, jaw and teeth

Answer 278

- angina - MI - pleuritic pain - pulmonary infarction - pneumonia, GI reflux, peritonitis and aortic dissection

Answer 279

- ECG is diagnostic - widespread concave (upwards) saddle shaped ST elevation - diffuse ST segment elevation - present in all leads (must exclude STEMI which would have ST segment elevation but will be limited to the infarcted area e.g. anterior or inferior) - return towards baseline as inflammation subsides - PR depression

Answer 280

- may demonstrate cardiomegaly in cases of effusion; if found then confirm with echocardiography - often normal in idiopathic - pneumonia is common with bacterial pericarditis

Answer 281

- slight increase in white cell count - anti Neutrophil Antibody in young females - SLE - troponin - elevation suggests myopericarditis

Answer 282

- restrict physical activity until resolution of symptoms and see improvement in ECG and CRP - treatment of underlying disorder - NSAID e.g ibuprofen for two weeks or aspirin for two weeks - systemic corticosteroids in resistant cases - colchicine for 3 weeks however is limited by nausea and diarrhoea but does reduce recurrence

Answer 283

- about 20% of cases of acute pericarditis go on to develop idiopathic relapsing pericarditis - this may occur within 6 weeks during weaning off NSAIDs or intermittently i.e. recurs more than 6 weeks after the initial presentation

Answer 284

- the first line treatment is oral NSAIDs e.g. ibuprofen - colchicine has been proven to be more effective than aspirin alone - in resistant cases, oral corticosteroids e.g. prednisolone may be effective, and in some patients, pericardiectomy (removal of part/most of the pericardium) may be appropriate

Answer 285

- a pericardial effusion is an accumulation of fluid within the potential space of the serous pericardial sac - it commonly accompanies an episode of acute pericarditis - can be caused by hypothyroidism which rarely compromises ventricular function

Answer 286

when a large volume of pericardial fluid collects in the potential space of the serous pericardial sac (often accumulated rapidly) leads to restricted diastolic ventricular filling, leading to marked reduction in the cardiac output/haemodynamic compromise

Answer 287

- symptoms of a pericardial effusion commonly reflect the underlying pericarditis - soft and distant heart sounds - apex beat obscured - raised jugular venous pressure - dysponea

Answer 288

- high pulse but low blood pressure - hypotension - tachycardia - high jugular venous pressure - muffled 1st and 2nd heart sounds - Kussmaul’s sign - rise in jugular venous pressure and increased neck vein distension during inspiration - pulsus paradoxus - an exaggeration in the normal variation in pulse pressure seen with inspiration, such that there is a drop in systolic blood pressure - reduced cardiac output

Answer 289

rise in jugular venous pressure and increased neck vein distension during inspiration - sign of cardiac tamponade

Answer 290

- a fall in BP of more than 10mmHg on inspiration - due to increased venous return to the right side of the heart during inspiration - increased right ventricular volume occupies more space within the rigid pericardium and impairs left ventricular filling - sign of cardiac tamponade

Answer 291

CXR: • large globular heart ECG: • low-voltage QRS complexes • sinus tachycardia Echocardiogram: • most useful for demonstrating effusion • echo-free zone surrounding heart

Answer 292

- falling blood pressure - rising jugular venous pressure - muffled heart sounds

Answer 293

CXR: • big globular heart Beck's triad ECG - low voltage QRS Echocardiogram: • is diagnostic • echo-free zone around heart • late diastolic collapse of right atrium (because most of left atrium is outside pericardium) • early diastolic collapse of right ventricle

Answer 294

- underlying cause should be sought and treated if possible - most pericardial effusions resolve spontaneously - pericardial effusions may re-accumulate most often due to malignancy - this may require a pericardial fenestration (a window in the pericardium is created to allow the slow release of fluid into the surrounding tissues)

Answer 295

a window in the pericardium is created to allow the slow release of fluid into the surrounding tissues - used in reccuring pleural effusion

Answer 296

- seek expert help - requires urgent drainage via pericardiocentesis which will drain the fluid to relieve the pressure on the heart - send fluid for culture, Ziehl-Nielsen stain and for cytology

Answer 297

- certain causes of pericarditis such as tuberculosis, bacterial infection and rheumatic heart disease result in the pericardium becoming thick, fibrous and calcified - cause is often unknown and can occur after any pericarditis - most cases are idiopathic or from intrapericardial haemorrhage during heart surgery

Answer 298

tuberculosis, bacterial infection and rheumatic heart disease

Answer 299

- in many cases, these pericardial changes do not cause any symptoms - heart becomes encased within a rigid fibrotic pericardial sac which prevents adequate diastolic filling of the ventricles

Answer 300

as these changes are chronic, allowing the body time to compensate, this condition is not as immediately life-threatening as in cardiac tamponade, in which the circulation is more acutely embarrassed

Answer 301

the sub-endocardial layers of myocardium may undergo fibrosis, atrophy and calcification

Answer 302

- Kussmaul’s sign - rise in jugular venous pressure and increased neck vein distension during inspiration - pulsus paradoxus - an exaggeration in the normal variation in pulse pressure seen with inspiration, such that there is a drop in systolic blood pressure - diffuse heart sounds - ascites - oedema - right heart failure signs - atrial dilatation - AF - pericardial knock on auscultation caused by rapid ventricular filling - jugular venous distension - hepatomegaly

Answer 303

CXR: • small/normal heart with/without pericardial calcification ECG: • low-voltage QRS Echocardiography: • thickened, calcified pericardium • small ventricular cavities with normal wall thickness

Answer 304

complete resection of the pericardium - risky with high complication rate

Answer 305

group of diseases of the myocardium that affect the mechanical (hypertrophic, arrhythmogenic right ventricular, dilated and restrictive cardiomyopathy) or electrical function (conduction system disease and ion channelopathies, e.g. long QT syndrome) of the heart

Answer 306

- all carry an arrhythmic risk - can occur at younger ages - restrictive cardiomyopathy is rare in childhood and has a poor outcome once symptoms develop - in general they are inherited genetic conditions although there are some acquired ones

Answer 307

- hypertrophic - dilated - primary restricted - arrythmogenic right ventricular

Answer 308

- family history of cardiomyopathy - high blood pressure - obesity - diabetes - previous MI

Answer 309

- hypertrophic cardiomyopathy (HCM) is characterised by marked ventricular hypertrophy in the absence of abnormal loading conditions such as hypertension and valvular disease - there is usually disproportionate involvement of the interventricular septum - the hypertrophic non-compliant ventricles impair diastolic filling, so that stroke volume is reduced - most cases are familial, autosomal dominant and caused by mutations in genes encoding sarcomeric proteins, e.g. troponin T and β-myosin - it is the most common cause of sudden cardiac death in young people.

Answer 310

* quite common, second most common cardiomyopathy (behind dilated) * 1/500 people have it * autosomal dominant - familial * may present at any age * most common cause of sudden cardiac death in the young * HCM refers to otherwise unexplained primary cardiac hypertrophy

Answer 311

* caused by sarcomeric protein gene mutations e.g troponin T and B-myosin * all in the absence of hypertension and valvular disease * the hypertrophic, non-compliant ventricles impair diastolic filling resulting in reduced stroke volume and thus cardiac output * another issue with thick powerful heart is that there is a disarray of cardiac myocytes so conduction is affected

Answer 312

* hypertrophy of the myocardium, particularly the intraventricular septum * sudden death may be the first manifestation * chest pain, angina, breathlessness, dysponea, dizziness, palpitations, syncope * left ventricular outflow obstruction may be a feature * cardiac arrhythmia * ejection systolic murmur * jerky carotid pulse * pansystolic murmur of functional mitral regurgitation

Answer 313

ECG is abnormal and shows signs of left ventricular hypertrophy with progressive T wave inversion and deep Q waves

Answer 314

shows ventricular hypertrophy and a small left ventricle cavity, and fibrosis

Answer 315

genetic analysis can confirm diagnosis since most cases are autosomal dominant and familial, and provide prognostic information

Answer 316

* amiodarone - anti-arrythmatic medication, if at high risk of arrhythmia then can place an implantable cardiac defibrillator * calcium channel blocker e.g. verampil * beta-blocker e.g. atenolol * vasodilators avoided because they may aggravate left ventricular outflow obstruction or cause refractory hypotension * outflow tract gradients can be reduced by surgical resection or alcohol ablation of the septum, or by dual-chamber pacing

Answer 317

dilated left ventricle which contracts poorly/has thin muscle

Answer 318

* most common cardiomyopathy * autosomal dominant - familial * can be caused by; ischaemia, alcohol, thyroid disorder or familial/genetic

Answer 319

ischaemia, alcohol, thyroid disorder, familial/genetic

Answer 320

* caused by cytoskeletal gene mutations * left ventricle or right ventricle or all 4 chamber dilatation and thus dysfunction * theory is that poorly generated contractile force leads to progressive dilatation of heart with some diffuse interstitial fibrosis

Answer 321

* shortness of breath at first and fatigue * dysponea * heart failure since heart can’t contract * arrhythmias * thromboembolism * sudden death * increased jugular venous pressure

Answer 322

• CXR: cardiac enlargement • ECG: tachycardia, arrhythmia and T wave flattening • echo: shows dilated ventricles with global hypokinesis - cardiac MR may show other aetiologies of left ventricular dysfunction, e.g. previous MI

Answer 323

- heart failure and AF are treated in a conventional way - cardiac resynchronisation therapy and ICDs are used in patients with NYHA III/IV grading - severe cardiomyopathy treated with cardiac transplantation

Answer 324

causes are amyloidosis, idiopathic, sarcoidosis, end-myocardial fibrosis

Answer 325

* there is normal or decreased volume of both ventricles with bi-atrial enlargement, normal wall thickness, normal cardiac valves and impaired ventricular filing * restrictive physiology * poor dilation of the heart restricts its the ability of the heart to take on blood and pass it to the rest of the body * rigid myocardium restricts diastolic ventricular filling

Answer 326

* similar to constrictive pericarditis * dysponea, fatigue and embolic symptoms * elevated jugular venous pressure with diastolic collapse and elevation of venous pressure with inspiration * hepatic enlargement, ascites and dependent oedema * third and fourth heart sounds

Answer 327

* CXR, echo and ECG are abnormal but non-specific * cardiac catheterisation helps to diagnose restrictive cardiomyopathy, and shows characteristic pressure changes * endomyocardial biopsy may be taken during catheter procedure, providing histological diagnosis

Answer 328

* no specific treatment with poor prognosis * patients die within a year * can consider cardiac transplantation

Answer 329

* progressive genetic cardiomyopathy characterised by progressive fatty and fibrous (fibro-adipose) replacement of right ventricular myocardium * cause is unknown * familial form is usually autosomal dominant with incomplete penetrance but can be recessive

Answer 330

progressive genetic cardiomyopathy characterised by progressive fatty and fibrous replacement of ventricular myocardium

Answer 331

* desmosome (normally holds cardiac cells together) gene mutation * right ventricle replaced by fat and fibrous tissue * muscle dies and replaced by fat as part of inflammatory process

Answer 332

* cardiac cells are held less together thus conduction issues * arrhythmia is most common feature * ventricular tachycardia * sudden death in a young man * syncope * in late stages may be signs of right heart failure

Answer 333

* ECG usually normal but may show T wave inversion * echo may also be normal but in advanced disease may show right ventricular dilation * genetic testing is the gold standard

Answer 334

* beta-blockers e.g. atenolol for patients with non-life-threatening arrhythmias * amiodarone for symptomatic arrhythmias * occasionally cardiac transplant indicated i.e. in cardiac failure or devastating arrhythmia

Answer 335

• 1% of all live births have some form of cardiac defect - common • vary from minor to incompatible with life ex-utero • there is an overall male predominance • although some individual lesions such as atrial septal defect and persistence ductus arteriosus occur more commonly in females • usually due to misplaced structures or the arrest of the progression of normal structure development

Answer 336

- one child with defect increases the chance of the second child having another defect - maternal prenatal rubella infection - persistent ductus arteriosus and pulmonary valvular and arterial stenosis - maternal alcohol misuse - septal defects - single genes associated e.g. Trisomy 21 (Down’s - septal, mitral and tricuspid valve defects) - drugs e.g. Thalidomide, Amphetamines and Lithium - diabetes of mother - genetic abnormalities e.g. the familial form of arterial spatial defect and congenital heart block

Answer 337

occurs because of right-left shunting of blood or because of complete mixing of systemic and pulmonary blood flow resulting in poorly oxygenated blood entering the systemic circulation

Answer 338

* results from large left-to-right shunts * the persistently raised pulmonary flow leads to the development of increased pulmonary artery vascular resistance and consequent pulmonary hypertension * this resistance is due to the thickening of the vascular walls of the pulmonary arteries in response to the higher pressure

Answer 339

- the increased pulmonary artery vascular resistance caused by pulmonary hypertension causes right ventricular pressure to increase and causes the reversal of a shunt to right-to-left resulting in the patient going blue i.e. cyanosis - known as Eisenmenger’s complex specifically in relation to a ventricular-septal defect

Answer 340

* common when severe right or left ventricular outflow tract obstruction is present * exertional syncope is associated with keeping central cyanosis and may occur in Fallot’s tetralogy

Answer 341

- central cyanosis - pulmonary hypertension - clubbing of the fingers (associated with prolonged cyanosis) - growth retardation - syncope - adolescents and adults present with specific common problems related to the longstanding structural nature of these conditions

Answer 342

* endocarditis - especially in small ventricular septal defects or bicuspid aortic valve * calcification and stenosis of congenitally deformed valves e.g. bicuspid aortic valve * atrial and ventricular arrhythmias * sudden cardiac death * right heart failure * end-stage heart failure

Answer 343

- acyanotic or cyanotic | - with or without shunts

Answer 344

- atrial septal defect - ventricular septal defect - patent ductus arteriosus - partial anomalous venous drainage

Answer 345

- coarctation of the aorta | - congenital aortic stenosis

Answer 346

- Fallot's tetralogy - transposition of the great vessels - severe Ebstein's anomaly

Answer 347

- severe pulmonary stenosis - tricuspid atresia - pulmonary atresia - hypoplastic left heart

Answer 348

- high BP - clinical BP of 140/90mmHg or higher, based on at least two readings on separate occasions - level of BP is abnormal when it is associated with a clear increase in morbidity and mortality from heart disease, stroke and renal failure; this level varies with age, sex, race and country

Answer 349

- stroke - ischaemic and haemorrhagic - myocardial infarction - heart failure - chronic renal disease - causes and is caused by hypertension - cognitive decline - premature death

Answer 350

increases the risk of atrial fibrillation which in turn increases the risk of stroke and emboli due to the fact that there is some stasis of blood in the fibrillating atria resulting in thrombus formation that can easily lead to emboli

Answer 351

people with suspected hypertension are offered ambulatory blood pressure monitoring (ABPM - over 24 hours) to confirm a diagnosis of hypertension

Answer 352

- cardiac output x Peripheral resistance = BP, can target peripheral resistance to alter BP - local vascular vasoconstrictor and vasodilator mediators - interplay between RAAS and sympathetic nervous system (noradrenaline)

Answer 353

- most drugs aim to block RAAS - kidney senses low BP and renin is released from the juxtaglomerular cells - renin converts angiotensinogen to angiotensin I - ACE from the lungs converts angiotensin I to angiotensin II - angiotensin II (extremely potent vasoconstrictor) stimulates aldosterone release resulting in increased Na+ and thus water reabsorption which leads to increased blood volume and thus blood pressure - thus angiotensin II increases peripheral resistance and inhibitors target this

Answer 354

- drop in BP also sends signals to the brain resulting in the release of noradrenaline resulting in vasoconstriction and increased contractility of the heart thus increasing peripheral resistance and cardiac output and thus BP - sympathetic nervous system also results in renin release

Answer 355

- increased peripheral resistance - increase cardiac output - vascular growth (hyperplasia and hypertrophy) - salt retention (aldosterone release and tubular sodium reabsorption)

Answer 356

- increased renin - increased peripheral resistance - increased cardiac output

Answer 357

- ramipril - enalapril - perindopril - lisinopril - trandolapril

Answer 358

- reduced angiotensin II formation | - increased kinin production

Answer 359

• first dose hypotension • acute renal failure: - if excess ACE inhibitor is given then kidney will detect drop and releases more renin and thus BP increases further which can lead to renal failure • hyperkalaemia • teratogenic effects in pregnancy - since angiotensin II is important for baby development • leucopenia • proteinuria

Answer 360

• dry chronic cough: - this is because ACE also breaks down bradykinin (inflammatory mediator) so if you inhibit it then there will be increased bradykinin resulting in cough • rash - due to increased bradykinin • anaphylactoid reaction - due to increased bradykinin

Answer 361

AT-1 receptor (angiotensin receptor): selectively block these

Answer 362

- candesartan - losartan - valsartan - irbesartan - telmisartan

Answer 363

- symptomatic hypotension (especially volume deplete patients e.g. dehydrated and severe blood loss) - hyperkalaemia - potential renal dysfunction - rash - angio-oedema - contraindicated in pregnancy - generally very well tolerated

Answer 364

- amlodipine - diltiazem - verapamil - nifedipine - felodipine - lacidipine

Answer 365

- vasodilators - dilatation of peripheral arterioles - diltiazem and verapamil have effects on electrical conductivity

Answer 366

dihydropyridines e.g. nifedipine, amlodipine, felodipine, lacidipine: - preferentially affect vascular smooth muscle - peripheral arterial vasodilators

Answer 367

phenylalkylamines e.g. verapamil: - main effect is on heart - reduce HR (negatively chronotropic) and force of contraction of the heart (negatively inotropic)

Answer 368

benzothiozepines e.g. diltiazem: | - intermediate heart/peripheral vascular effects

Answer 369

``` - due to peripheral vasodilation: • flushing • headache • oedema • palpitations - due to negatively chronotropic effects cardiac conduction defects: • bradycardia • atrioventricular block • postural hypotension - due to negatively inotropic effects: worsening of cardiac failure - verapamil causes constipation ```

Answer 370

- bisoprolol - carvedilol - propranolol - metoprolol - atenolol (antagonist at beta-1 adrenoceptor) - nadolol

Answer 371

use blockers smartly e.g. use selective B-1 (but note selectivity is linked to dose so best to avoid in asthma) in asthma since if non-selective used then will block B-2 resulting in airway constriction and thus the worsening of asthma

Answer 372

beta1 selective - metoprolol - bisoprolol middle - atenolol beta1/beta2 (non selective) - propranolol - nadolol - carvedilol

Answer 373

- fatigue - weakness - headache - sleep disturbance/nightmares - bradycardia - hypotension - cold peripheries - erectile dysfunction - bronchospasm

Answer 374

* asthma or COPD by inducing bronchospasm * PVD - claudication or raynauds * heart failure if given in standard dose or acutely - give blockers in small doses and increase slowly

Answer 375

- thiazides (cause Na+ and thus water loss in urine) and related drugs - act on distal tube - less potent, tend to end in ‘thiazide’ - loop diuretics (act on loop of Henle; more potent) - potassium sparing diuretics - aldosterone antagonists

Answer 376

- bendroflumethiazide - hydrochlorothiazide - chlorothalidone

Answer 377

- furosemide (blocks NKCC2 transporter) | - bumetanide

Answer 378

- spironolactone | - eplerenone

Answer 379

- hypovolaemia (mainly loop diuretics e.g. furosemide) - hypotension (mainly loop diuretics e.g. furosemide) - hypokalaemia - hyponatraemia - hypomagnesaemia - hypocalcaemia - hyperuricaemia - erectile dysfunction (mainly thiazides e.g. bendroflumethiazide) - impaired glucose tolerance i.e. diabetes (mainly thiazides e.g. bendroflumethiazide)

Answer 380

- alpha-1 adrenoceptor blockers - centrally acting anti-hypertensives (i.e. on the brain) - direct renin inhibitors

Answer 381

- moxonidine | - methyldopa (can be used in pregnancy)

Answer 382

under 55yrs: ACE-inhibitor or angiotensin II receptor blocker over 55yrs/Afro-Caribbean any age: calcium channel blocker

Answer 383

ACEi/ARB + CCB

Answer 384

ACEi/ARB + CCB + thiazide-like diuretic

Answer 385

resistant hypertension; consider addition of: - further diuretic therapy e.g. spironolactone - high dose thiazide-like diuretic - alpha blocker - beta blocker - others

Answer 386

diuretics, usually loop diuretics

Answer 387

* inhibition of RAAS e.g. ACE-inhibitors and ARB’s * inhibition of the sympathetic nervous system e.g. beta-blockers such as bisoprolol which are effective at blocking reflex sympathetic responses which stress the failing heart

Answer 388

* ACE inhibitors e.g. ramipril and beta-blocker e.g. bisoprolol * low dose and slow uptitration

Answer 389

* aldosterone antagonists * if ACE-inhibitor intolerant then give ARB’s (not as good as ACE-i) e.g. candesartan * if ACE-I and ARB intolerant then give hydralazine/nitrate combination (peripheral vasodilators)

Answer 390

- stretching of atrial and ventricular muscle cells - raised atrial or ventricular pressures - volume overload

Answer 391

• increased renal excretion of sodium and water • relax vascular smooth muscle (except efferent arteriole of renal glomeruli to preserve filtration pressure in kidney whilst still removing Na+ and thus H2O thus no renal damage) • increased vascular permeability • inhibits the release or actions of: - aldosterone, angiotensin II, endothelin (most potent vasoconstrictor) and ADH • counter-regulatory system to RAAS

Answer 392

raised natriuretic peptides in serum blood

Answer 393

neural endopeptidase (NEP or neprilysin)

Answer 394

- sacubitril: neprilysin inhibitor - valsartan: ARB - entresto: combination of sacubitril and valsartan; very effective in heart failure

Answer 395

sacubitril and valsartan | - used in heart failure

Answer 396

- arterial and venous dilators - reduce preload and afterload - lower BP

Answer 397

ischaemic heart disease (angina) and heart failure

Answer 398

- isosorbide mononitrate (long acting) - GTN spray (sublingual spray, potent vasodilator, headache) - GTN infusion

Answer 399

headache and GTN spray syncope as well as potential tolerance to the drug

Answer 400

- simvastatin - atorvastatin - rosuvastatin - pravastatin

Answer 401

* beta blocker e.g. bisoprolol | * calcium channel blocker e.g. amlodipine

Answer 402

- ivabradine - nicorandil - ranolazine

Answer 403

- ticagrelor - prasugrel - clopidogrel

Answer 404

- tirofiban - eptifbatide - abciximab

Answer 405

sodium channel blocker e.g. flecainide

Answer 406

beta-adrenoceptor blockers

Answer 407

prolong the action potential - amiodarone - sotalol - potential for significant side effects

Answer 408

calcium channel blockers: • verapamil (more effective than amlodipine since it doesn't affect the calcium channel at rest) • dilatizem • amlodipine

Answer 409

- antiarrythmic drug - cardiac glycoside - inhibits the Na/K pump

Answer 410

- bradycardia (due to increased vagal parasympathetic tone) - increased ectopic activity - can trigger extra heartbeats i.e. minor arrhythmias - increased force of contraction (direct positive inotropic effect on heart muscle) by increased intracellular Ca2+ - slowing of AV conduction

Answer 411

narrow therapeutic range; need to have precise amount to have desired effects otherwise get side effects: - nausea, vomiting, diarrhoea and confusion

Answer 412

* used in atrial fibrillation to reduce ventricular rate response * used in severe heart failure as a positive inotropic (increases heart contractility)

Answer 413

- QT prolongation - polymorphic ventricular tachycardia - interstitial pneumonitis - abnormal liver function - hyperthyroidism/hypothyroidism - sun sensitivity - slate grey skin discolouration - optic neuropathy - effect optic nerve - multiple drug interactions - very large volume of distribution - gets into all tissues and can take up to 3 months to clear system

Answer 414

amiodarone and sotalol; can be fatal

Answer 415

* the inability of the heart to deliver blood and thus O2 at a rate that is commensurate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures * is a syndrome of breathlessness, tiredness and fluid overload caused by a form of cardiac dysfunction; not a diagnosis on its own * can result from any structural or functional cardiac disorder that impairs the hearts ability to function and meet the demands of supplying sufficient oxygen and nutrients to the metabolising body

Answer 416

- 25-50% of patients die within 5 years of diagnosis - 1-3% of the general population - around 10% in patients over 65yrs

Answer 417

* ischaemic heart disease (IHD) * cardiomyopathy * hypertension

Answer 418

- 65 and older - African descent - men - obesity - previous MI

Answer 419

- when the heart begins to fail, there are many systems involved that initiate physiological compensatory changes that try to maintain cardiac output and peripheral perfusion in order to negate the effects of the heart failure - as heart failure progresses, these mechanisms are overwhelmed and become pathophysiological also known as decompensation

Answer 420

- venous return (preload) - outflow resistance (afterload) - sympathetic system activation - RAAS

Answer 421

- breathlessness - tiredness - cold peripheries - leg swelling - increased weight - exertional dyspnoea - orthopnoea - paroxysmal nocturnal dyspnoea - fatigue

Answer 422

- tachycardia - displaced apex beat - raised JVP - added heart sounds/murmurs - cardiomegaly with a displaced apex beat, third and fourth heart sounds - bi-basal lung crackles - pleural effusion - ankle oedema - ascites - tender hepatomegaly

Answer 423

- myocardial failure leads to a reduction of the volume of blood ejected with each heart beat, and an increase in the volume of blood remaining after systole - this increased diastolic volume stretches the myocardial fibres and myocardial contraction is restored since the stretching of myocardial fibres will increase its force of contraction - in heart failure, the failing myocardium actually doesn't contract as much in response to increased preload meaning cardiac output cannot be maintained and may decrease

Answer 424

the load of resistance against which the ventricle contracts

Answer 425

* pulmonary and systemic resistance * physical characteristics of the vessel walls * the volume of blood that is ejected

Answer 426

- when there is an increase in afterload there is a increase in end-diastolic volume and a decrease in stroke volume and thus a decrease in cardiac output - this results in a increase of end-diastolic volume and dilatation of the ventricle itself (the more the ventricle is dilated the harder it must work i.e. the more resistance there is to contract against) which further exacerbates the problem of afterload

Answer 427

increases the force of contraction of the heart which increases stroke volume as well as heart rate - both resulting in an increase in cardiac output

Answer 428

- in heart failure there is chronic sympathetic activation which results in the receptors being acted on by the sympathetic system to down regulate - resulting in there being less receptors to act on so the effect of sympathetic activation is diminished and cardiac output stops increasing

Answer 429

- results in increased Na+ reabsorption and thus water reabsorption and release of ADH which stimulates water retention -> increased volume of the blood -> increased blood pressure and venous pressure which increases pre-load and increases the stretching of the heart and force of contraction, and stroke volume and cardiac output - fall in cardiac output and increased sympathetic tone -> diminished renal perfusion, activation of the RAAS and fluid retention - salt and water retention increases venous pressure and maintains stroke volume - peripheral and pulmonary congestion causes oedema and dyspnoea - with increased force of contraction the cardiac myocytes require more energy and more blood - in heart failure there will be no increase in blood and thus the cardiac myocytes will die resulting in decreased force of contraction and decreased stroke volume and cardiac output

Answer 430

* inability of the ventricle to contract normally resulting in a decrease in cardiac output * caused by ischaemic heart disease, myocardial infarction and cardiomyopathy

Answer 431

inability of the ventricles to relax and fill fully, thereby | decreasing stroke volume and cardiac output

Answer 432

- hypertrophy due to chronic hypertension of the ventricles and increased afterload, resulting in less space for blood to fill in and decreased cardiac output - aortic stenosis which increases afterload and decreases cardiac output

Answer 433

often used exclusively to mean new onset or decompensation of chronic heart failure characterised by pulmonary and/or peripheral oedema with or without signs of peripheral hypotension

Answer 434

SOB, fatigue and ankle swelling (non specific)

Answer 435

- three cardinal symptoms - dyspnoea especially when lying flat (orthopnoea) - cold peripheries - raised jugular venous pressure (JVP) - murmurs and displaced apex beat - cyanosis - hypotension - peripheral or pulmonary oedema due to back flow resulting from the decreased cardiac output - tachycardia - third and fourth heart sounds - ascites - bi-basal crackles

Answer 436

``` no limitation (asymptomatic) - exercise -> no fatigue, dyspnoea or palpitations ```

Answer 437

slight limitation (mild HF) - comfortable at rest - normal activity -> fatigue, dyspnoea and palpitations

Answer 438

marked limitation (moderate HF) - comfortable at rest - less gentle activity -> fatigue, dyspnoea and palpitations

Answer 439

inability to carry out any physical activity without discomfort (severe HF) - symptoms occur at rest - exacerbated by physical activity

Answer 440

brain natriuretic peptide (BNP) - increased in patients with heart failure - levels correlate with ventricular wall stress and the severity of heart failure - normal plasma concentrations (<100pg/mL exclude heart failure) FBC, liver biochemistry, blood glucose, U+E, thyroid function tests

Answer 441

* cardiac enlargement and features of left ventricular failure * alveolar oedema * cardiomegaly * dilated upper lobe vessels of lungs * effusions (pleural)

Answer 442

* shows underlying causes; ischaemia, left ventricular hypertrophy in hypertension or arrhythmia * if ECG and BNP normal then heart failure is unlikely * if both abnormal then go to echocardiogram

Answer 443

* assess ventricular systolic and diastolic function and may reveal the aetiology of heart failure * look for regional wall motion abnormalities, valvular disease and cardiomyopathies * look for sign of MI * ejection fraction of <0.45 is usually accepted as evidence for systolic dysfunction

Answer 444

- lifestyle changes - diuretics - ACE inhibitors - beta blockers - digoxin - inotropes - revascularisation (when some viable myocardium remains; PCI) - surgery (mitral valve repair, aortic or mitral valve replacement) - heart transplant in the young - cardiac resynchronisation

Answer 445

* promote sodium and thus water loss thereby reducing ventricular filling pressure (preload) decreasing systemic and pulmonary congestion * generally provide symptomatic relief * loop diuretic - furosemide * thiazide diuretic - bendroflumethiazide (inhibit sodium reabsorption in the distal convoluted tubule) * aldosterone antagonists

Answer 446

- often symptomless so screening is vital - major risk factor for CVD - remains under diagnosed, under treated and poorly controlled in the UK - prevalence is in those older than 35 - more common in men

Answer 447

- more than or equal to 140/90mmHg clinic BP - daytime average ambulatory blood pressure monitoring (ABPM - 24hr BP monitor) or home blood pressure monitoring (HBPM); greater than or equal to 135/85mmHg

Answer 448

- more than or equal to 160/100mmHg clinic BP | - daytime average ABPM or HBPM greater than or equal to 150/95mmHg

Answer 449

- clinical systolic BP greater than or equal to 180mmHg and/or diastolic BP greater than or equal to 110mmHg - start immediate anti-hypertensive drug treatment

Answer 450

- hypertension can be classified according to whether the cause is unknown ‘essential (primary or idiopathic) hypertension’ or is known ‘secondary hypertension’ - most cases are classified as essential

Answer 451

``` • primary cause unknown • accounts for the majority of cases • multifactorial involving: - genetic susceptibility - excessive sympathetic nervous system activity - abnormalities of Na+/K+ membrane transport - high salt intake - abnormalities in RAAS ```

Answer 452

- cause is known - commonly caused by renal disease or pregnancy - other potential underlying conditions include; endocrine causes, coarctation of the aorta and drug therapy

Answer 453

- Cushing's syndrome - Conn's syndrome - pheochromocytoma - adrenal hyperplasia - acromegaly

Answer 454

hypersecretion of corticosteroids (which enhance adrenalines resulting in a vasoconstrictive effect) is associated with systemic hypertension

Answer 455

adrenal tumour that secretescatecholamines (resulting in the stimulation of alpha-adrenergic receptors resulting in vasoconstriction, increased cardiac contractility and the stimulation of beta-adrenergic receptors resulting in an increase in heart rate and contractility) can cause hypertension

Answer 456

- raised blood pressure will be detected in either arm, but NOT in the legs - the femoral pulse is often delayed relative to the radial - undetected or untreated patients die from cardiac failure, hypertensive cerebral haemorrhage or dissecting aneurysm - hypertension due to decreased renal perfusion, delayed pulses in the legs, mid-late systolic murmur and rib notching on X ray

Answer 457

* corticosteroids e.g. prednisolone * cyclosporin * erythropoietin * some types of the contraceptive pill * NSAIDs * vasopressin alcohol, amphetamines, ecstasy and cocaine are also causes of hypertension

Answer 458

- age - risk increases as you age - race - hypertension is more common in blacks - family history - hypertension runs in families - overweight and obese - little exercise - smoking - too much salt in diet - alcohol - diabetes - stress

Answer 459

• hypertension accelerates atherosclerosis • also causes the thickening of the media of muscular arteries • smaller arteries and arterioles are especially affected in hypertension • the resulting endothelial cell dysfunction is associated with impaired nitric oxide-mediated vasodilatation and enhanced secretion of vasoconstrictors including endothelins and prostaglandins

Answer 460

kidney size is often reduced and small vessels show intimal thickening and medial hypertrophy and the numbers of sclerotic glomeruli are increased

Answer 461

• characteristic features are a markedly raised diastolic blood pressure, usually over 120mmHg and seen in progressive renal disease • quite rare • renal vascular changes are prominent and there is usually evidence of acute haemorrhage and papilloedema (optic disc swelling caused by increased intercranial pressure) • can occur in previously fit individuals, often black males in their 30s-40s

Answer 462

- cardiac failure with left ventricular hypertrophy and dilatation - blurred vision due to papilloedema and retinal haemorrhages - haematuria and renal failure due to fibrinoid necrosis of glomeruli - severe headache and cerebral haemorrhage - fibrinoid necrosis of the vessel wall -> end organ damage in the kidneys (haematuria, proteinuria, progressive kidney disease), brain (cerebral oedema and haemorrhage), retina (flame-shaped haemorrhages, cotton wool spots, hard exudates and papilloedema) and CVS (acute heart failure and aortic dissection)

Answer 463

urinalysis: • for protein, albumin:creatine ratio and haematuria ``` blood tests: • serum creatinine • eGFR • glucose (to assess diabetes risk) • UandE ``` fundoscopy/opthalmoscopy: • looking for retinal haemorrhage or papilloedema ECG - to detect left ventricular hypertrophy or myocardial ischaemia; use echo to further detect this serum lipids

Answer 464

A: ACE-inhibitor e.g. ramipril or enalapril, or ARB (use if ACEi is contraindicated e.g. due to cough) e.g. candesartan or losartan C: CCB e.g. nifedipine or amlodipine D: diuretics e.g. bendroflumethiazide (thiazide, distal tube; less potent) or furosemide (loop diuretic, loop of Henle; more potent) - beta blockers are not first line of treatment for hypertension but consider in young people if intolerant of ACEi/ARB - statins are also given to reduce the overall cardiovascular risk burden

Answer 465

ramipril/candesartan + nifedipine + bendroflumethiazide + furosemide

Answer 466

ramipril/candesartan + nifedipine + bendroflumethiazide + furosemide

Answer 467

an abnormality of the cardiac rhythm | - 24hr ambulatory ECG and event recorders are used to detect paryoxysmal arrhythmias

Answer 468

- sudden death - syncope - heart failure - chest pain - dizziness - palpitations - no symptoms at all

Answer 469

* heart rate is slow (less than 60bpm during the day and less than 50bpm at night) * usually asymptomatic unless the rate is very slow * slower heart rates are more likely to cause symptomatic arrhythmias * normal in athletes owing to increased vagal tone and thus parasympathetic activity

Answer 470

* heart rate is fast (more than 100bpm) | * more symptomatic when the arrhythmia is fast and sustained

Answer 471

- supraventricular tachycardias - arise from the atrium or the AV junction - ventricular tachycardias - arise from the ventricles

Answer 472

SAN → action potential → muscle cells of atria → depolarisation of the AVN → slow → interventricular septum → Bundle of His → right and left bundle branches → free walls of both ventricles → Purkinje cells → ventricular myocardial cells

Answer 473

at the junction between the SVC and right atrium

Answer 474

in the lower interatrial septum

Answer 475

to allow for the complete contraction of the atria before the ventricles are excited

Answer 476

- the normal cardiac pacemaker is the sinoatrial node and it depolarises spontaneously - the rate of SAN discharge is modulated by the autonomic nervous system - normally, the parasympathetic system predominates, resulting in slowing of the spontaneous discharge rate - a reduction of parasympathetic tone or an increase in sympathetic stimulation leads to tachycardia - conversely, increased parasympathetic tone or decreased sympathetic stimulation produces bradycardia - sinus rate in women is slightly faster than in men

Answer 477

P waves that are upright in leads I and II, but inverted in cavity leads aVR and V1

Answer 478

- fluctuations of autonomic tone result in changes of the sinus discharge rate - during inspiration: parasympathetic tone falls and the heart rate quickens - during expiration: parasympathetic tone increases and so heart rate falls - this variation is normal especially in children and young adults

Answer 479

a chaotic irregular atrial rhythm at 300-600bpm; the AV node responds intermittently, hence an irregular ventricular rate

Answer 480

- most common sustained cardiac arrhythmia - males more than females - around 5-15% of patients over age of 75 - can either be paroxysmal (stopping spontaneously within 7 days) or persistent (continues without intervention) - atrial activity is chaotic and mechanically ineffective

Answer 481

* acute: onset within the previous 48 hours * paroxysmal: stops spontaneously within 7 days * recurrent: two or more episodes * persistent: continuous for more than 7 days and not self terminating * permanent

Answer 482

* idiopathic (5-10%) * any condition that results in raised atrial pressure, increased atrial muscle mass, atrial fibrosis, or inflammation and infiltration of the atrium may cause atrial fibrillation * hypertension (most common in developed world) * heart failure (most common in developed world) * coronary artery disease * valvular heart disease; especially mitral stenosis * cardiac surgery (1/3rd of patients after surgery) * cardiomyopathy (rare cause) * rheumatic heart disease * acute excess alcohol intoxication

Answer 483

- older than 60 - diabetes - high blood pressure - coronary artery disease - prior MI - structural heart disease (valve problems or congenital defects)

Answer 484

- atrial fibrillation (AF) is maintained by continuous, rapid (300-600/min) activation of the atria by multiple meandering re-entry wavelets - these are often driven by rapidly depolarising automatic foci, located predominantly within the pulmonary veins - AV node conducts a proportion of the atrial impulses to produce an irregular ventricular response -> irregularly irregular pulse - the atria respond electrically at this rate but there is no coordinated mechanical depolarisation and only a proportion of the impulses are conducted to the ventricles - cardiac output drops by 10-20% as the ventricles are not primed reliably by the atria

Answer 485

- symptoms are highly variable - may be asymptomatic - palpitations - dyspnoea and or chest pains following the onset of atrial fibrillation - fatigue - apical pulse rate is greater than the radial rate - 1st heart sound is of variable intensity

Answer 486

- atrial flutter | - supraventricular tachyarrhythmias

Answer 487

- absent P waves, only a fine oscillation of the baseline (so-called fibrillation or f waves) - irregular and rapid QRS complex

Answer 488

- used in haemodynamically unstable patients - when AF is due to an acute precipitating event, such as alcohol toxicity, chest infection or hyperthyroidism, the provoking cause should be treated - immediate heparinisation - cardioversion with a synchronised DC shock - if cardioversion fails or AF recurs, IV amiodarone is given before another attempt - ventricular rate control (by drugs that block the AV node)

Answer 489

- rate control aims to reduce HR at rest and during exercise, but the patient remains in AF - AV nodal slowing agents plus oral anticoagulation - beta-blocker e.g. bisoprolol - calcium channel blocker e.g. verapamil or diltiazem - if above fails then try digoxin and then consider amiodarone

Answer 490

- for younger, <65yrs, highly symptomatic and physically active patients, with heart failure and recent onset AF (<48hrs) - cardioversion to sinus rhythm and use Beta-blockers e.g. bisoprolol to suppress arrhythmia - can use pharmacological cardioversion e.g. flecainide, sotalol, propafenone if no structural heart defect or use IV amiodarone instead if there is structural heart disease - appropriate anti-coagulation - catheter ablation techniques in patients not responding to antiarrhythmic drugs

Answer 491

CHA2DS2-VASc score

Answer 492

* congestive heart failure (1 point) * hypertension (1 point) * a2ge greater or equal to 75 (2 points) * diabetes mellitus (1 point) * s2troke/TIA/thromboembolism (2 points) * vascular disease (aorta, coronary or peripheral arteries) (1 point) * age 65-74 (1 point) * S(c)ex category: female (1 point) * If score is 1 then it merits consideration of anticoagulation and/or aspirin * If score is 2 and above then oral anticoagulation is required * score of 0 should not require any antithrombotic prophylaxis used to calculate stroke risk and need for anticoagulation in AF

Answer 493

usually an organised atrial rhythm with an atrial rate typically between 250-350bpm; ventricular rate of 150bpm

Answer 494

- often associated with atrial fibrillation and frequently require a similar initial therapeutic approach - either paroxysmal or persistent - much less common than atrial flutter - more common in men - prevalence increases with age

Answer 495

* idiopathic (30%) * coronary heart disease * obesity * hypertension * heart failure * COPD * pericarditis * acute excess alcohol intoxication

Answer 496

- palpitations - breathlessness - chest pain - dizziness - syncope - fatigue

Answer 497

- atrial fibrillation | - supraventricular tachyarrhythmias

Answer 498

• definitive diagnosis • regular sawtooth-like atrial flutter waves (F waves) between QRS complexes due to continuous atrial depolarisation • note if F waves are not visible then they may be able to be unmasked by by slowing atrioventricular conduction by carotid sinus massage or IV adenosine (AV nodal blocker)

Answer 499

- electrical cardioversion but anticoagulate before e.g low molecular weight heparin e.g. enoxaparin or dalteparin if acute, i.e. atrial flutter started less than 48 hours ago - catheter ablation; creating a conduction block to try an restore rhythm and block offending re-entrant wave - IV amiodarone to restore sinus rhythm and use a beta-blocker e.g. bisoprolol to suppress further arrhythmias - the treatment of atrial flutter is similar to AF, except that most cases of flutter can be cured by radiofrequency catheter ablation of the re-entry circuit

Answer 500

- first degree AV block - second degree AV block - third degree AV block

Answer 501

- this is prolongation of the PR interval to greater than 0.22 seconds on the ECG - no change in HR - every atrial depolarisation is followed by conduction to the ventricles but with delay - asymptomatic; no treatment

Answer 502

* hypokalaemia * myocarditis * inferior MI * atrioventricular node (AVN) blocking drugs e.g. beta blockers, calcium channel blockers and digoxin

Answer 503

- occurs when some P waves conduct and other do not - occurs when some atrial impulses fail to reach the ventricles - acute MI may produce second degree heart block - Mobitz I and II

Answer 504

* also known as the Wenckebach block phenomenon * caused by AV node block * a progressive PR interval prolongation until beat is ‘dropped’ and P wave fails to conduct i.e. excitation completely fails to pass through the AVN/bundle of His * absent QRS after the P wave * the PR interval before the blocked P wave is much longer than the PR interval after the blocked P wave * PR interval then returns to normal and cycle repeats itself

Answer 505

- atrioventricular node (AVN) blocking drugs e.g. beta blockers (Bisoprolol), calcium channel blockers (Verapamil) and Digoxin - inferior MI

Answer 506

* results in light headedness, dizziness and syncope | * does not require a pacemaker unless it's poorly tolerated

Answer 507

* due to a block at an infra-nodal level so the QRS is widened and QRS complexes are dropped without PR prolongation * PR interval is constant and QRS interval is dropped * failure of conduction through the His-Purkinje system * ratio of non-conducted P waves to QRS complexes is usually specified, e.g. 2:1 Mobitz II block is 2 P waves for every QRS complex

Answer 508

- anterior MI - mitral valve surgery - SLE and Lyme disease - rheumatic fever

Answer 509

* results in shortness of breath, postural hypotension and chest pain * high risk of developing sudden complete AV heart block and a pacemaker should be inserted

Answer 510

- complete AV block - complete heart block occurs when all atrial activity fails to conduct to the ventricles; complete dissociation between atrial and ventricular activity - ventricular contractions are sustained by spontaneous escape rhythm which originates below the block - P waves are completely independent of QRS complex

Answer 511

* structural heart disease e.g. transposition of great vessels * ischaemic heart disease e.g. acute MI * hypertension * endocarditis or Lyme disease

Answer 512

- narrow-complex escape rhythm | - broad complex escape rhythm

Answer 513

* QRS complex less than 0.12 seconds * implies block originates in the His bundle and thus the region of block lies more proximally in the AV node * recent-onset, narrow-complex AV block that has transient causes that may respond to IV atropine * chronic narrow-complex AV block requires permanent pacemaker if it is symptomatic

Answer 514

B = below His • QRS complex is greater than 0.12 seconds • implies block originates below the bundle of His and thus the region of block lies more distally in the His-Purkinje system • slow HR (<40 bpm) • unreliable • dizziness and blackouts often occur (Stokes-Adams attacks) • permanent pacemaker implantation is recommended

Answer 515

- depends on aetiology - one option is a permanent pacemaker - IV atropine

Answer 516

* usually asymptomatic * the His bundle gives rise to the right and left bundle branches * the left branch subdivides into the anterior and posterior divisions of the left bundle

Answer 517

bundle branch conduction delay results in the slight widening of the QRS complex (up to 0.11 seconds)

Answer 518

- associated with a wider QRS complex (larger than 0.12 seconds) with an abnormal pattern - usually asymptomatic - shape of the QRS depends on whether the right or the left bundle is blocked

Answer 519

- can occur in normal healthy individuals - pulmonary embolism - right ventricular hypertrophy - ischaemic heart disease - congenital heart disease e.g. atrial/ventricular septal defect and tetralogy of Fallot

Answer 520

* right bundle no longer conducts, meaning that the two ventricles do not get impulses at the same time, and instead spread from left to right * sequential spread of an impulse (i.e. first left ventricle and then the right) resulting in secondary R wave (RSR') in V1 and slurred S wave in V5 and V6; seen as deep S wave in leads V5 and V6 and as a tall late R wave in lead V1 * produces the late activation of the right ventricle

Answer 521

- looks like maRRow - maRRow = right bundle branch block - MarroW: • M - QRS looks like an M in lead V1 • W - QRS looks like W in V5 and V6 - seen as deep S wave in leads I, V1, V5 and V6 and as a tall late (slurred) R wave in lead V1 - causes wide physiological splitting of the second heart sound

Answer 522

- indicates underlying cardiac pathology - hypertension - severe CAD - ischaemic heart disease - aortic valve disease - following cardiac surgery

Answer 523

* produces the late activation of the left ventricle * secondary R wave (RSR') in left ventricular leads (I, AVL, V4, V5, V6) and a deep slurred S waves in V1 and V2 * since the left bundle branch conduction is normally responsible for the initial ventricular activation, left bundle branch block also produce abnormal Q waves

Answer 524

- looks like wiLLiam - wiLLiam = left bundle branch block - WilliaM: • W - QRS looks like a W in leads V1 and V2 • M - QRS looks like an M in leads V4-V6 - seen as deep S wave in lead V1 and a tall late R wave in leads I, aVL, V4, V5 and V6 - causes reverse splitting of the second heart sound

Answer 525

- fever - anaemia - anxiety - exercise - pain - heart failure - pulmonary embolism - thyrotoxicosis - hypovolaemia - drugs

Answer 526

- treating underlying causes | - beta blockers

Answer 527

AV nodal re-entrant tachycardia (AVNRT) and AV re-entrant tachycardia (AVRT)

Answer 528

- AV nodal re-entrant tachycardia (AVNRT) and AV re-entrant tachycardia (AVRT) are usually referred to as paroxysmal supraventricular tachycardias (SVTs) - they are often seen in young patients with no or little structural heart disease - first presentation is commonly between ages 12-30 - in these tachycardias the AV node is an essential component

Answer 529

- most common type of SVT - twice as common in women as in men - strikes suddenly without obvious provocation but there are some risk factors - an attack may stop spontaneously or may continue indefinitely until medical intervention

Answer 530

- exertion - emotional stress - coffee - tea - alcohol

Answer 531

2 • one has a short effective refractory period (the window of time where cells cannot be excited again after they have already been excited) and slow conduction • one has a longer effective refractory period and fast conduction

Answer 532

the window of time where cells cannot be excited again after they have already been excited

Answer 533

1. in sinus rhythm, the atrial impulse that depolarises the ventricles usually conducts through the fast pathway 2. if the atrial impulse occurs early e.g. atrial premature beat when the fast pathway is still refractory then the slow pathway takes over in propagating the atrial impulses to the ventricles 3. by the time the impulse has been propagated to the ventricles the fast pathway has finished its refractory period and is once again able to transmit impulses 4. the same impulse that was carried by the slow pathway can be transmitted to the ventricles but also travel back up the fast pathway which by that time would be out of its refractory period 5. by that time the slow pathway would have recovered from its refractory period so the signal will be able to go back down the slow pathway again 6. this sets up a reentrant loop at the AV node and the loop sends signals through the AV node at a much faster rate than a normal pacemaker would -> tachyarrhythmia with 100-250 bpm 7. it travels back through the fast pathway, which has already recovered its excitability, thereby initiating the slow-fast AVNRT in which the atria contract slowly in one cycle and then fast in the next

Answer 534

- rapid regular palpitations with abrupt onset and sudden termination - chest pain and breathlessness - neck pulsations - polyuria (due to the realise of atrial natriuretic peptide in response to increased atrial pressures during the tachycardia)

Answer 535

* QRS complex is usually of normal shape because the ventricles are activated in the normal way * sometimes the QRS complex is wide, due to a rate-related BBB, and it may be difficult to distinguish from ventricular tachycardia * P waves are either not visible or are seen immediately before (normal) or after the QRS complex due to simultaneous atrial and ventricular activation

Answer 536

- large circuit involving the AV node, the bundle of His, the ventricle and an abnormal connection of myocardial fibres from the ventricle back to the atrium - this ‘abnormal connection’ is called the accessory pathway or bypass tract and results from an incomplete separation of the atria and the ventricles during fetal development - connects the atria and ventricles and is capable of antegrade or retrograde conduction or both - each part of the circuit is activated sequentially, so atrial activation occurs after ventricular activation and the P wave is clearly seen between the QRS and T wave

Answer 537

normal AV circuit and accessory circuit which both transmit impulses from the atria and the ventricles

Answer 538

impulse can travel from atria to ventricle (anterograde) or from ventricle back to atria (retrograde)

Answer 539

Wolff-Parkinson-White (WPW) syndrome; an aberrant pathway syndrome

Answer 540

- atrial activation occurs after ventricular activation | - patients are prone to atrial fibrillations and sometime ventricular fibrillation

Answer 541

* there is normal AV conduction but also an accessory pathway * so when the SAN depolarises the impulse can travel to the AVN via the atria as well as to the accessory pathway * if the accessory pathway conducts from the atrium to the ventricle during sinus rhythm, the electrical impulse can conduct quickly over this abnormal connection to depolarise part of the ventricles abnormally; this is pre-excitation

Answer 542

- short PR interval - wide QRS complex that begins as a slurred start to the QRS, known as a delta wave - QRS is narrow

Answer 543

- normal AV conduction and an accessory pathway - SAN depolarises -> impulse travels to AVN via atria and to the accessory pathway - pre-excitation - pre-excitation does not result in AVRT and doesn't result in tachyarrhythmia - premature beat from SAN will travel -> AVN and if accessory pathway is in refractory period it can't transmit the signal - impulse travels down via AVN, down interventricular septum through the bundle of His and LBB/RBB and into free walls of both ventricles via Purkinje cells until it meets the accessory pathway - accessory pathway is out of its refractory period and can conduct the impulse back to the atria - once in the atria the impulse can travel back to the AVN, setting up a reentry circuit; the signal goes around and around -> tachycardia

Answer 544

if the accessory pathway conducts from the atrium to the ventricle during sinus rhythm, the electrical impulse can conduct QUICKLY over this abnormal connection to depolarise part of the ventricles ABNORMALLY; this is known as pre-excitation

Answer 545

- rapid regular palpitations - severe dizziness - dysponea - central chest pain - syncope - exertion, coffee, tea or alcohol may aggravate the arrhythmia

Answer 546

- patients presenting with haemodynamic instability (hypotension and pulmonary oedema) require emergency cardioversion - if stable then vagal manoeuvres - if manoeuvres unsuccessful then IV adenosine; causes complete heart block for a fraction of a second and is highly effective at terminating AVNRT and AVRT - surgery

Answer 547

increases vagal stimulation of the sinus node • breath-holding • right carotid sinus massage (contraindicated in carotid bruit) • Valsalva manoeuvre - several seconds after the release of the strain, the resulting intense vagal effect may terminate the AVNRT or AVRT

Answer 548

* radiofrequency catheter ablation of the accessory pathway in AVRT, successful in 95% of cases * modification of the slow pathway in AVNRT

Answer 549

- ventricular ectopics - ventricular tachycardia - sustained ventricular tachycardia (SVT) - ventricular fibrillation - some of these conditions are cardiac channelopathies; these are congenital disorders that are caused by mutations that affect the function of cardiac ion channels and hence the electrical activity of the heart, these include: • long QT syndrome

Answer 550

congenital disorders that are caused by mutations that affect the function of cardiac ion channels and hence the electrical activity of the heart - e.g. long QT syndrome

Answer 551

- premature ventricular contraction | - these are asymptomatic or patients complain of extra beats, missed beats or heavy beats

Answer 552

- patient complains of extra beats, missed beats or heavy beats - if the ectopics are frequent then left ventricular dysfunction may develop - these premature beats have a broad (greater than 0.12 seconds) and bizarre QRS complex because they arise from an abnormal (ectopic) site in the ventricular myocardium - following a premature beat, there is usually a complete compensatory pause because the AV node or ventricle is refractory to the next sinus impulse; resulting in missed beat - can provoke ventricular fibrillation; potentially fatal

Answer 553

- may be uncomfortable especially when frequent - pulse is irregular owing to the premature beats - usually are asymptomatic - can feel faint or dizzy

Answer 554

widened QRS complex with a bizarre configuration; greater than 0.12 seconds

Answer 555

- reassure patient | - give beta-blockers e.g. Bisoprolol if symptomatic

Answer 556

pulse of more than 100bpm with a least 3 irregular heart beats in row

Answer 557

commonly found in patients with structurally normal hearts (known as idiopathic ventricular tachycardia), in these cases it is usually a benign condition with an excellent long-term prognosis • occasionally it is pathological and known as Gallavardin’s tachycardia and if untreated may lead to cardiomyopathy

Answer 558

* there is rapid ventricular beating leading to inadequate filling of ventricles since there is less time to fill * results in decreased cardiac output and thus a decrease in the amount of oxygenated blood that is circulated around the body

Answer 559

- breathlessness (lack of lung perfusion) - chest pain (lack of heart perfusion) - palpitations - light headed or dizzy (lack of brain perfusion)

Answer 560

ventricular tachycardia for longer than 30 seconds

Answer 561

- dizziness (pre-syncope) - syncope - hypotension - cardiac arrest - pulse rate between 120-220 bpm

Answer 562

- rapid ventricular rhythm - broad and abnormal QRS complex (greater than 0.14 seconds) - with BBB, there is a broad complex tachycardia, which can be differentiated from VT on ECG criteria

Answer 563

- haemodynamically unstable (e.g. hypotensive or pulmonary oedema): emergency electrical cardioversion - stable: IV beta blocker e.g. Esmolol and IV Amiodarone - prevented by use of beta blockers and implantable cardiac defibrillator

Answer 564

involves very rapid and irregular ventricular activation with no mechanical effect i.e no CO

Answer 565

* patient is pulseless and becomes unconscious and respiration ceases * ECG shows shapeless, rapid oscillations and there is no hint of organised complexes * usually caused by a ventricular ectopic beat

Answer 566

* only effective treatment is electrical defibrillaton * survivors are at increased risk of sudden death so long term, implantable cardioverter-defibrillators are the first-line therapy

Answer 567

describes an ECG where the ventricular repolarisation/QT interval is greatly prolonged

Answer 568

* Jervell-Lange-Nielsen syndrome (autosomal recessive); mutation in cardiac potassium and sodium-channel genes * Romano-Ward syndrome (autosomal dominant)

Answer 569

- hypokalaemia - hypocalcaemia - hypomagnesamia - drugs; Amiodarone and Tricyclic antidepressants e.g. Amitriptyline, phenothiazines and macrolide antibiotics - bradycardia - acute MI - diabetes

Answer 570

- syncope - palpitations - due to polymorphic ventricular tachycardia that usually terminate spontaneously but may degenerate to ventricular fibrillation - polymorphic VT: torsades de pointes, rapid irregular sharp QRS complexes that continuously change from an upright to an inverted position on the ECG - ECG shows prolonged QT interval

Answer 571

- treat underlying cause | - if acquired long QT then give IV isoprenaline (contraindicated for congenital long QT)

Answer 572

an aneurysm is defined if there is a permanent localised dilatation of the artery to twice the normal diameter

Answer 573

- abnormal dilatations that involve all layers of the arterial wall - types: saccular and fusiform - arteries most frequently involved are: • abdominal aorta (most common) • iliac, popliteal and femoral arteries • thoracic aorta

Answer 574

around 2cm; increases with age

Answer 575

- also known as pseudoaneurysm - involves the collection of blood in the outer layer only (adventitia) which communicates with the lumen e.g after trauma from a femoral artery puncture

Answer 576

- most commonly occur BELOW the renal arteries (infra-renal) - incidence increases with age - AAA’s are present in 5% of the population above 60 - more common in men than women - most result from a degenerative process and present in elderly men - some are due to connective tissue disease

Answer 577

- classified as an aortic diameter exceeding 3cm | - most commonly occur below the renal arteries (intra-renal)

Answer 578

* most have no specific identifiable causes * severe atherosclerotic damage * family history * tobacco smoking * male * increasing age * hypertension * COPD * trauma * hyperlipidaemia

Answer 579

- degradation of the elastic lamellae resulting in leukocyte infiltrate causing enhanced proteolysis and smooth muscle cell loss - the dilatation affects all three layers of the vascular tunic - if it doesn't then it is a pseudoaneurysm

Answer 580

* often asymptomatic and only picked up via a routing abdominal examination or plain X-ray * pain in abdomen, back, loin or groin * pulsatile abdominal swelling (less pronounced)

Answer 581

* rupture is more likely if there is; increased BP, female, smoker, strong family history * intermittent or continuous abdominal pain (radiates to the back, iliac fossas or groin) * pulsatile abdominal swelling (more pronounced) * collapse * hypotension * tachycardia * profound anaemia * sudden death

Answer 582

- increased BP - female - smoker - strong family history

Answer 583

- GI bleed - ischaemic bowel - MSK pain - perforated GI ulcer - pyelonephritis - appendicitis

Answer 584

- abdominal ultrasound - can assess aorta to degree of 3mm | - CT and/or MRI angiography scans

Answer 585

- small aneurysms below 5.5cm are generally just monitored - treat underlying causes - modify risk factors e.g. smoking and diet - smoking cessation - vigorous BP control - lowering of lipid in blood - surgical replacement of the aneurysmal segment with a prosthetic graft indicated for a symptomatic aneurysm or large asymptomatic aneurysm (>5.5cm) - in patients who are poor surgical risks, endovascular repair with insertion of an aortic stent is being increasingly employed

Answer 586

* patients tend to do better if aneurysm is symptomatic, larger than 5.5cm and expanding yearly * open surgical repair * endovascular repair - stent inserted via femoral or iliac arteries

Answer 587

- the ascending, arch or descending thoracic aorta may become aneurysmal - ascending thoraco-abdominal aneurysms occur most commonly in patients with Marfan syndrome or hypertension - descending or arch TAAs occur secondary to atherosclerosis and are now rarely due to syphilis

Answer 588

• genetic link; in some families it is an autosomal dominant trait • usual causes are cystic medial necrosis and atherosclerosis • certain connective tissue disorders: - Marfan’s syndrome - Ehlers-danlos syndrome - Loeys-dietz syndrome • mycotic aneurysm is endocarditis • aortic dissection • weight lifting, cocaine and amphetamine use; perhaps due to the large rise in BP when undertaking these activities

Answer 589

- Marfan’s syndrome - Ehlers-danlos syndrome - Loeys-dietz syndrome

Answer 590

- hypertension - increasing age - smoking - bicuspid or unicuspid aortic valves - atherosclerosis - COPD - renal failure - previous aortic aneurysm repair

Answer 591

- involves inflammation, proteolysis and reduced survival of the smooth muscle cells in the aortic wall - once the aorta reaches a crucial diameter (around 6cm in the ascending and 7cm in the descending) it loses all distensibility so that a rise in BP to around 200mmHg can exceed the arterial wall strength and may trigger dissection or rupture

Answer 592

- most TAA’s are asymptomatic - may be diagnosed incidentally e.g. on routing CXR or cardiological investigation or if complicated by dissection, rupture or other complications - pain in chest, neck, upper back, mid-back or epigastrium - cause pressure on local structures (causing back pain, dysphagia and cough) - aortic regurgitation - fever if there is infective cause - symptoms due to compression of local structures - acute pain - collapse, shock and sudden death - cardiac tamponade - haemoptysis

Answer 593

- thoracic back pain - arterial ischaemia - collapse - MI

Answer 594

- CT or MRI used for assessment of TAA - aortography may be helpful for assessing the position of the key branches in relation to the aneurysm - transoesophageal echocardiography can be useful for identifying aortic dissection - ultrasound

Answer 595

- immediate urgent surgery is required for ruptured TAA - symptomatic TAA’s merit surgery regardless of size - regular monitoring by CT or MRI every 6 months - rigorous BP control using beta-blockers e.g. Bisoprolol - smoking cessation - treat underlying cause

Answer 596

- aortic dissection begins with a tear in the intima (inner wall) - blood then penetrates the diseased medial layer and flows between the layers of the aorta, forcing the layers apart resulting in dissection; creates a false lumen - a medical emergency that can lead to death

Answer 597

- most common emergency affecting the aorta - affects men more than females - most common between the ages of 50-70 and is rare below 40 - very rare in children

Answer 598

can be classified according to the timing of diagnosis from the origin of symptoms: • acute - less than 2 weeks • subacute - 2-8 weeks • chronic - more than 8 weeks

Answer 599

- inherited - degenerative - atherosclerotic - inflammatory - trauma e.g. shearing stresses in a road traffic accident (RTA)

Answer 600

look at the heart in a horizontal plane

Answer 601

look at the heart in a vertical plane

Answer 602

aVR, aVL, aVF

Answer 603

I, II and III

Answer 604

tall R waves in right ventricular leads

Answer 605

- sudden death - atrial and ventricular arrhythmias - thromboembolism - infective endocarditis - heart failure

Cardiovascular Flashcards

(637 cards)