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1 - Finals > Cardiology > Flashcards

Cardiology Flashcards

1
Q

what is angina?

A

chest pain/discomfort arising from the heart as a result of myocardial ischaemia - usually due to narrowing of lumen of CAD due to atherosclerosis/thrombosis

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2
Q

name 3 types of angina

A

classic/stable, unstable/crescendo, Prinzmetal’s. decibitus (lying down), nocturnal.

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3
Q

what are the differences between stable and unstable angina

A

stable angina is induced by effort + relieved by rest. unstable angina occurs at rest - treat as ACS.

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4
Q

what is Prinzmetal’s (variant) angina?

A

angina that occurs without provocation, usually at rest - due to coronary artery spasm.

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5
Q

what causes angina?

A

atheroma of coronary arteries leading to myocardial ischaemia

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6
Q

give 5 risk factors for angina

A

diabetes, smoking, hyperlipidaema, hypertension, family history, lack of exercise

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7
Q

list the differential diagnoses of central chest pain

A

angina, ACS, pericarditis, myocarditis, aortic dissection, massive PE, musculoskeletal, GORD

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8
Q

describe the presentation of angina

A

central, crushing, retrosternal chest pain - comes on with exertion, relieved by rest. may radiate to arms and neck

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9
Q

list some things that can exacerbate angina

A

exercise, cold weather, anger, excitement, heavy meals

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10
Q

give some clinical features, apart from pain, of angina

A

dyspnoea, nausea, sweating, faintess

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11
Q

what investigations would you carry out on a patient with angina? what would you find?

A

12 lead ECG - shows ischaemic changes at exercise stress test - FBC, glucose, LFT (pre-statin), U&E (renal func), TFT, lipids

functional scans - MRI perfusion scan etc.

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12
Q

how would you manage stable angina?

A

refer all suspected angina to rapid access chest pain clinic - within 2wks, for confirmation of Dx and severity assessment. - modify risk factors, patient education. - secondary prevention - aspirin 75mg or clopidogril, statins, treat HTN. - symptomatic treatment - GTN spray (and rest!) - first line = beta blockers (atenolol - low HR/BP, cold hands/feet, fatigue) or CCB (diltiazem/verapamil/amlodipine - ankle swelling, flushing) - second line = combo (must be dihydropyridine - if intolerant/CI - long acting nitrate or nicorandil or ivabradine.

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13
Q

how does aspirin work as a method of secondary prevention in angina?

A

inhibits COX2 and formation of thromboxane A2 - a platelet aggregating agent. reduces risk of coronary events.

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14
Q

name an alternative to aspirin in secondary prevention of coronary events.

A

clopidogrel

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15
Q

give some examples of beta-blockers

A

bisoprolol, atenolol, propranolol, metoprolol

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16
Q

describe the mechanism of action of beta blockers in improving symptoms of angina

A

by acting on beta1 receptors in the heart, they reduce the force of contraction and speed of conduction in the heart - relieves myocardial ischaemia by reducing cardiac work and oxygen demand

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17
Q

what is the major contra-indication of beta-blockers? why?

A

asthma - beta blockers also act on beta2-receptors which are found in the smooth muscles of airways - cause bronchoconstriction!

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18
Q

give some examples of calcium channel blockers

A

diltiazem, amlodipine, nifedipine, verapamil

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19
Q

describe the mechanism of action of calcium channel blockers in controlling symptoms of stable angina

A

they decrease calcium entry into vascular and cardiac cells. they reduce myocardial contractility and suppress cardiac conduction - reduce heart rate, contractility and afterload - reduces myocardial oxygen demand - prevents angina.

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20
Q

what are the major side effects of calcium channel blockers?

A

postural hypotension/dizziness, headache, ankle oedema - due to systemic vasodilation

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21
Q

describe the mechanism of action of short-acting (GTN) nitrates and long-acting nitrates in acute angina

A

Nitrates are converted to NO, which increases cGMP and reduces intracellular calcium in vascular smooth muscle cells - vasodilation of venous capacitance vessels reduces preload and LV filling. reduced cardiac work and myocardial oxygen demand - relieve angina

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22
Q

what interventions may be used in worsening angina, not resolved with drugs?

A

Percutaneous coronary intervention (PCI) - balloon used to dilate atheromatous arteries (stents can be placed) - via catheter. Coronary artery bypass grafting (CABG)

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23
Q

what is involved in a coronary artery bypass graft (CABG)?

A

internal mammary artery used to bypass stenosis in the LAD or RCA.

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24
Q

what does the term acute coronary syndromes (ACS) include?

A

unstable angina. NSTEMI. STEMI.

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25
Q

how would you differentiate between NSTEMI and unstable angina?

A

NSTEMI involves enough occlusion to cause myocardial damage - elevation of serum troponin and creatinine kinase. unstable angina doesn’t cause myocardial damage. *troponin rise is the key distinction*

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26
Q

describe the common pathology behind acute coronary syndromes

A

1) rupture/erosion of fibrous cap of an atheroma plaque in a coronary artery 2) platelet-rich clot forms 3) vasoconstriction due to chemicals released by platelets

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27
Q

name 3 non-modifiable risk factors for ACS

A

age. male gender. FHx of IHD

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28
Q

name 3 modifiable risk factors for ACS

A

smoking, hypertension, DM, hyperlipidaemia, obesity, sedentary lifestyle, cocaine use

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29
Q

list 3 symptoms and 3 signs of ACS

A

symptoms - central chest pain, sweating, dyspnoea, palpitations. signs - sweating, anxiety, tachycardia, pallor.

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30
Q

what biochemical markers would you test for in ACS?

A

cardiac enzymes = troponin T, troponin I, creatinine kinase (CK-MB) troponins most sensitive within 6hrs. hit max at 12-24hrs post infarct, persistently high 14 days - should test trops at 6 and 12 hours. CK-MB = cardiac specific, trops can also be raised by skeletal muscle injury

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31
Q

what would you expect to see on a 12 lead ECG in ACS?

A

hyperacute (tall) T waves ST elevation (STEMI) or ST depression (NSTEMI/unstable angina). new LBBB. after hrs-days - T wave inversion, Q waves.

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32
Q

what would be your immediate management of ACS?

A

ABCDE resus. - GTN + IV opioid w/antiemetic (morphine + metoclopramide) = pain control - dual antiplatelet: loading dose is 300mg aspirin + 180mg ticagrelor - give high flow O2 if sats <94% - monitor 12 lead ECG NSTEMI - fondaparinux/heparin (antithrombotic), coronary angiography/revascularisation if appropriate STEMI - immediately assess suitability for reperfusion (PCI or fibrinolysis) - offer coronary angiography + PCI if presents within *12hrs of onset + PCI can be delivered within 120mins - if beyond that + continuing ischaemia = coronary angiography - fibrinolysis if presenting <12hrs but PCI not available within 120mins = alteplase, streptokinase - then re-ECG and consider if PCI needed.

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33
Q

what drugs might a patient be put on after an ACS, for secondary prevention?

A

beta-blockers, ACE inhibitors, statins, dual antiplatelet therapy (aspirin + clopidogrel)

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34
Q

what might the non-medical management of ACS be?

A

PCI - percutaneous coronary intervention

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35
Q

list some possible complications following a MI

A

heart failure, rupture of interventricular septum, mitral regurg, arrhythmias, heart block, pericarditis, thromboembolism, ventricular aneurysm

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36
Q

give 3 causes of heart failure

A

mostly - IHD and HTN also - valvular disease; pericarditis; pericardial effusion; alcohol; cocaine; myocarditis; arrhythmias; cardiomyopathies; anaemia; pulmonary hypertension. high output = anaemia pregnancy, hyperthyroid, Paget’s disease of bone

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37
Q

what are the types of heart failure?

A

systolic/diastolic, low output/high output, left/right

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38
Q

what compensatory mechanisms are activated as the heart begins to fail?

A

sympathetic nervous system, RAAS, ventricular dilatation, ventricular remodelling

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39
Q

what causes the oedema and dyspnoea seen in heart failure?

A

activation of the RAAS by decreased renal perfusion (due to low CO) - salt/water retention - peripheral/pulmonary congestion

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40
Q

describe the ventricular remodelling seen in heart failure

A

initial dilatation. hypertrophy, loss of myocytes, increased interstitial fibrosis.

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41
Q

what is the difference between systolic and diastolic failure?

A

systolic = inability of ventricles to contract normally diastolic = inability of ventricles to relax and fill normally

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42
Q

give 3 symptoms of heart failure

A

exertional dypnoea, orthopnoea (SOB on lying down), paroxysmal nocturnal dyspnoea, fatigue, oedema, weight loss, wheeze

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43
Q

give 5 signs of heart failure

A

cold peripheries, cyanosis, displaced apex, wheeze, RV heave, valve disease, hypotension, pleural effusion, oedema, ascites

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44
Q

what are 5 features of heart failure seen on CXR?

A

ABCDE: Aleveolar oedema (bats wings) Kerly B lines (interstitial oedema) Cardiomegaly Dilated upper lobe vessels pleural Effusion

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45
Q

list 2 major criteria on the Farmingham criteria for heart failure diagnosis

A

SAW PANIC S3 heart sound - gallop. Acute pulmonary oedema. Weight loss Paroxysmal nocturnal dyspnoea Abdominojugular reflux Neck vein distension Increased cardiac shadow on CXR (cardiomegaly) Crepitations (crackles heard in lungs)

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46
Q

list 2 minor criteria on the Farmingham criteria for heart failure diagnosis

A

HEART ViNo: Hepatomegaly Effusion, pleural Ankle oedema bilaterally exeRtional dyspnoea Tachycardia Vital capacity decrease by 1/3rd Nocturnal cough

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47
Q

describe the NHYA classification of heart failure

A

class I = no limitation class II = mild limitation (comfort at rest, fatigue and dyspnoea on normal physical activity) class III = marked limitation (comfort at rest, dyspnoea on gentle physical activity) class IV = symptomatic at rest, exacerbated by any physical activity

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48
Q

what investigations would you do in heart failure?

A

ECG - underlying cause. CXR. Bloods - BNP (B type natriuretic peptide - if normal, HF is unlikely). echocardiography.

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49
Q

describe the management of heart failure (not acute!)

A

1) lifestyle, pt education, cardiac rehab, inform DVLA, air travel likely fine unless needs O2 2) annual fluv vaccine, one off pneumococcal vaccine 3) manage comorbidities/cardiac RGs 4) Medical: - ACEi + beta blockers (ARB if can’t have ACEi, if can’t have either then hydralazine w/nitrate) - start low and titrate. - add aldosterone antagonist (spironolactone), ARB or hydralazine w/nitrate - 3rd line = digoxin or ivabradine - ICD if prev. vent arrhythmias. (I’m sure other diuretics get involved though…?)

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50
Q

name 2 ACE inhibitors

A

ramipril, lisinopril

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51
Q

what causes the common cough side effect of ACE inhibitors? what drug class are a good alternative?

A

increased levels of bradykinin, which is usually inactivated by ACE. ARBs

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52
Q

how do ACE inhibitors act?

A

prevent conversion of angiotensin I to angiotensin II. Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion - blocking this reuces afterload, lowering BP.

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53
Q

name 2 angiotensin receptor blockers (ARBs)?

A

losartan, candesartan

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54
Q

how do angiotensin receptor blockers work?

A

block action of angiotensin II on the AT1 receptor. similar effects as ACE inhibitors.

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55
Q

give 3 causes of mitral stenosis

A

rheumatic heart disease (most), congenital, cardial fibroelastosis, malignant carcinoid, prosthetic valve.

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56
Q

what is mitral stenosis?

A

thickening and immobility of valve leaflets - leads to obstruction of blood flow from left atrium to left ventricle. occurs due to: - structural abnormality of valve leading to increase LA pressure + pulmonary artery pressure - pulmonary HTN - RV failure

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57
Q

give 3 symptoms of mitral stenosis

A

aymptomatic for years then deteriorate - progressive breathlessess (SOBOE/orthopnoea/PND), palpitations from AF, systemic emboli (static blood flow in LA). hoarseness/dysphagia due to enlarge LA

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58
Q

what is the heart murmur heard in mitral stenosis? other examination findings?

A

rumbling mid-diastolic murmur best heard on left lateral position. loud S1 with opening snap. malar flush, raised JVP, displaced apex/RV heave (RVH), signs of RHF (hepatomegaly, ascites, peripheral oedema)

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59
Q

what diagnostic tests would you perform in mitral stenosis? what would you see?

A

ECG - AF, bifid P waves (p mitrale). RVH. CXR - LA enlargement, interstitial oedema (Kerley A/B lines - if RHF), prominent pulmonary vessels Echo - diagnostic.

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60
Q

how would mitral stenosis be treated?

A

yearly F/U for dyspnoea = diuretics - decrease pre load, or nitrates. for exercise tolerance = beta blockers, non-dihydropyridine CCBs surgery if severe/symptomatic = balloon valvuloplasty / valve replacement (percutaneous mitral commisurotomy, PMC)

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61
Q

give 2 complications of mitral stenosis

A

pulmonary hypertension. emboli (dilated LA). pressure from large LA on local structures e.g. hoarseness due to compression of L recurrent laryngeal

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62
Q

give 3 causes of mitral regurgitation

A

prolapsing mitral valve + rheumatic heart disease = most common (actually now it’s more commonly degenerative!) MI, CAD, IE, post mitral valve surgery, connective tissue disorders (Ehlers-Danos, Marfan’s). cardiomyopathy, congenital.

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63
Q

give 3 symptoms of mitral regurgitation

A

acute = rapid pulmonary oedema, needs surgery chronically = causes heart failure so - dyspnoea, fatigue, palpitations, infective endocarditis

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64
Q

what murmur is heard in mitral regurgitation?

A

pansystolic blowing murmur at apex, radiating to axilla. laterally displaced apex beat. S3 gallop.

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65
Q

what does a bifid P wave indicate on ECG?

A

bifid P waves = p mitrale - mitral valve disease

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66
Q

what investigations would you perform in valvular heart disease?

A

ECG, CXR, echo ± cardiac catherization

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67
Q

what would you see on CXR in mitral regurgitation? what about ECG?

A

enlarged LA and LV. ECG = enlarged LA, p mitrale, AF.

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68
Q

how would you treat mitral regurgitation?

A

asymptomatic = echo every 1-5yrs. anticoagulate with warfarin if - AF, hx of embolism, prosthetic valve, additional mitral stenosis. medical (acute) - diuretics, nitrates surgery if signs of LV dysfunction or AF, or acute/severe - valve replacement or repair.

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69
Q

give 3 causes of aortic stenosis

A

degeneration and calcification of normal valve (in the elderly). calcification of congenital biscuspid valve (middle age). rheumatic heart disease. CAD.

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70
Q

what is the classical triad of symptoms in aortic stenosis?

A

SAD: Syncope Angina Dyspnoea - heart failure also often SOBOE

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71
Q

what murmur is heard in aortic stenosis?

A

ejection systolic murmur other examination findings: slow rising pulse, narrow pulse pressure. apex thrill secondary to LVH.

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72
Q

what would you expect to see on an ECG in aortic stenosis?

A

p mitrale, LVH with strain pattern (depressed ST and T wave inversion in I, AVL, V5 and V6)

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73
Q

what would you see on a CXR of a patient with aortic stenosis? what type of imaging should be used for confirming diagnosis?

A

normal heart size (or cardiomegaly), prominent ascending aorta, calcification of aortic ring echo (transthoracic, TTE) = confirms presence/degree, LV function + thickness might also do Doppler echo to assess severity.

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74
Q

how would you treat aortic stenosis?

A

avoid exertion, modify IHD RFs if symptomatic - prompt valve replacement. not fit for surgery? balloon valvuloplasty, TAVI.

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75
Q

what are the most common causes of aortic regurgitation?

A

rheumatic fever and infective endocarditis associated with SLE, marfan’s, ehler-danos, Turner’s, ank spond (aortic dilatation)

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76
Q

give 3 causes of acute aortic regurgitation

A

infective endocarditis, acute rheumatic fever, dissection of the aorta, AAA dissection, prosthetic valve failure

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77
Q

give 3 causes of chronic aortic regurgitation

A

chronic rheumatic heart disease, syphilis, rheumatoid arthritis, severe hypertension, biscupid aortic valve, aortic endocarditis, Marfan’s, osteogenesis imperfecta

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78
Q

give 3 symptoms of aortic regurg

A

acute - cardiovascular collapse. chronic - SOBOE/ nonspecific, or symptoms of LH failure = orthopnoea, paroxysmal nocturnal dyspnoea

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79
Q

what murmur is heard in aortic regurgitation? other examination findings?

A

early diastolic murmur. “at L sternal edge in 4th intercostal space” other finds = collapsing water hammer pulse, wide pulse pressure. austin flint murmur.

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80
Q

what would you see on CXR/ECG in aortic regurgitation? what other investigations should be performed?

A

CXR - if heart failure: cardiomegaly and dilatation of the ascending aorta, pulmonary oedema. ECG - LVH. do a TTE and colour doppler.

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81
Q

how would you manage aortic regurgitation?

A

if acute and symptomatic = surgery. chronic = try to prevent heart failure. mild-mod = r/v yearly, 2 yearly echo. severe = monitor every 6/12. screen family if Marfan’s. surgical - valve replacement. medical - ACEi/ARB for HTN/HF. if Marfan’s - beta blocker helps slow aortic root dilatation.

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82
Q

what are the 3 main cardiomyopathies? what does cardiomyopathy actually mean?

A

dilated (DCM) = most common, left (or both) ventricle dilated with impaired contraction hypertrophic = 2nd most common, L/R ventricular hypertrophy restrictive = rare, reduced diastolic filling, near normal systolic function. cardiomyopathy = myocardial disorder in which heart muscle is structurally and functionally abnormal, without CAD, valvular diease, HTN or congenital abnormalities

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83
Q

what is hypertrophic cardiomyopathy?

A

ventricular hypertrophy in absence of abnormal loading conditions - LV outflow tract obstruction. presents in 20s-30s –> most common cause of sudden cardiac death in young people/athletes (death due to arrhythmia or LV outflow tract obstruction). characterised by - LVH, mitral valve abnormalities, impaired diastolic filling, disorganised cardiac myocytes.

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84
Q

what causes hypertrophic cardiomyopathy?

A

50% = autosomal dominant, mutation in gene coding for beta-myosin or troponin. 50% = sporadic.

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85
Q

what is the major consequence of hypertrophic cardiomyopathy?

A

sudden cardiac death in young people

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86
Q

name 2 clinical features of hypertrophic cardiomyopathy

A

mainly asymptomatic. dyspnoea, chest pain, palpitations, syncope, sudden death, systolic thrill. O/E - forceful apex beat, harsh ejection systolic murmur

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87
Q

what investigations might you carry out in cardiomyopathy? what would they show?

A

ECG - LVH, ischaemia, LAD, AF. most common arrhythmias = premature ventricular complexes. echo = diagnostic. TTE shows asymmetrical septal hypertrophy >15mm. preserved systolic functioning. LV thickening. CXR = atrial enlargement if mitral regurg, variable cardiomegaly. genetic testing/counselling.

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88
Q

how would you treat hypertrophic cardiomyopathy?

A

beta blockers/CCBs to control symptoms. amiodarone or catheter ablation for rhythm control if AF (also anticoagulate) ICD if RFs for sudden death (e.g. Hx VFib, sustained tachy, unexplained syncope) genetic counselling avoid competitive sports

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89
Q

give 3 causes of dilated cardiomyopathy

A

characterised by ventricular chamber enlargement + contractile dysfunction w/normal LV wall thickness, due to biochemical abnormality of cardiac muscle. genetic (AD), *alcoholism, hypertension/IHD, thyrotoxicosis haemachromatosis, viral infection, autoimmune (SLE/RA), cocaine abuse

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90
Q

give 3 clinical features of dilated cardiomyopathy

A

often symptomless –> sudden death heart failure symps (L or R) dyspnoea, thromboemboli (stasis) or arrhythmia (AF or *VT), pleural effusion, oedema, jaundice, ascites O/E - displaced apex beat, S3 gallop.

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91
Q

how would you treat dilated cardiomyopathy?

A

bed rest. improve cardiac function by treating as for heart failure - diuretics, digoxin, ACE inhibitors, nitrates. biventricular pacing or ICDs. heart transplant.

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92
Q

what is restrictive cardiomyopathy?

A

rigid myocardium restricting diastolic ventricular filling –> increased atrial pressure

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93
Q

give 2 causes of restrictive cardiomyopathy

A

mostly old age, AF. weirder: amyloidosis. haemachromatosis. sarcoidosis. scleroderma. idiopathic.

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94
Q

give 3 clinical features of restrictive cardiomyopathy

A

constrictive pericarditis. raised JVP. oedema, ascites, features of RVH. usually present with heart failure, right sided mostly (as above). O/E - Kussmaul’s sign (increased JVP with inspiration), pulsus paradoxus (decreased pulse/BP on inspiration).

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95
Q

what investigation would you do in restrictive cardiomyopathy?

A

CXR = ABCDE of HF echo = non0dilated, non-hypertrophied ventricles, atrial enlargement (sparkling in amyloidosis) **cardiac catheterisation to assess pressures in different chambers - diagnostic. management is just as for heart failure and AF, mayyyybe transplant

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96
Q

what are the 2 causes of ventricular septal defect?

A

congenital. acquired post-MI.

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97
Q

how might a ventricular septal defect present?

A

severe heart failure in infancy. OR - asymptomatic, detected later in life

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98
Q

does a smaller ventricular septal defect produce louder or quieter murmurs?

A

louder

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99
Q

what murmur is heard in VSD?

A

harsh pansystolic murmur at left sternal edge

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100
Q

give 2 complications of a ventricular septal defect

A

aortic regurgitation, infundibular stenosis, IE, pulmonary hypertension, Eisenmenger’s complex.

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101
Q

what is seen on a CXR of someone with a ventricular septal defect?

A

Small VSD - normal sized heart ± enlarged pulmonary blood vessels. Large VSD - cardiomegaly, large pulmonary arteries, marked enlargement of pulmonary vessels.

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102
Q

how would you manage a ventricular septal defect?

A

medical support until spontaneous closure. OR - surgical patch repair or device closure.

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103
Q

what are the different types of atrial septal defect?

A

ostium secundum defects - most common - present in adulthood. ostium primum defects - associated with AV valve abnormalities - present early.

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104
Q

give 3 clinical features of an atrial septal defect - murmur?

A

pulmonary hypertension, cyanosis, arrhythmia, haemoptysis, chest pain, AF, raised JVP. pulmonary ejection systolic murmur.

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105
Q

what investigations are used to diagnose most structural heart defects?

A

echo. cardiac catheter.

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106
Q

how would you treat an ASD?

A

transcatheter or surgical closure

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107
Q

what genetic disorder is associated with atrioventricular septal defects?

A

Downs syndrome

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108
Q

what structures are involved in an atrioventricular septal defect?

A

atrial septum, ventricular septum, mitral and tricuspid valve

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109
Q

what are the clinical features and management of a complete AVSD?

A

breathless neonate, failure to thrive, poor feeding, torrential pulmonary blood flow. repair with PA band.

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110
Q

what are the clinical features and management of a partial AVSD?

A

presents in adulthood, similar to small ASD/VSD. treatment not necessary.

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111
Q

what is a patent ductus arteriosus?

A

persistent communication between left pulmonary artery and descending aorta - L to R shunt. normally the ductus arteriosus closes within hrs of birth.

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112
Q

what are the clinical features of a PDA? murmur?

A

3 classic signs: bounding pulse, ‘machinery murmur’, pulmonary hypertension. also - breathless, poor feeding, failure to thrive, Eisenmenger’s syndrome. murmur = continuous machinery murmur best heard across back

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113
Q

how would you treat a PDA?

A

indometacin (prostaglandin) can stimulate closure. if large - surgical or percutaneous closure.

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114
Q

what is Eisenmenger’s syndrome?

A

cyanosis - clubbed and blue toes, pink not clubbed fingers.

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115
Q

what is coarctation of the aorta?

A

congenital narrowing of the descending aorta

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116
Q

what are the clinical features of coarctation of the aorta? name 2 complications.

A

radiofemoral delay, weak femoral pulse, high BP, systolic murmur. heart failure + IE.

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117
Q

how would you treat coarctation of the aorta?

A

surgery or balloon dilation ± stenting

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118
Q

what are the consequences of a biscupid aortic valve?

A

go on to develop aortic stenosis - requiring valve replacement. higher risk of IE.

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119
Q

give some clinical features of pulmonary stenosis

A

RV failure as neonate. collapse. poor pulmonary blood flow. RVH. tricuspid regurg.

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120
Q

how would you treat pulmonary stenosis?

A

ballon valvuloplasty. open vavlotomy.

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121
Q

what are the 4 features of tetralogy of Fallot?

A

1 - VSD. 2 - pulmonary stenosis. 3 - RVH. 4 - aorta overriding the VSD

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122
Q

what causes tetralogy of Fallot?

A

abnormalities in separation of truncus arteriosus into the aorta and pulmonary arteries early in gestation

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123
Q

describe the presentation of tetralogy of Fallot

A

acyanotic at birth. gradually become cyanotic. Fallow (hypoxic) spells - go blue, restless, inconsolable crying - toddlers may squat.

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124
Q

what is the characteristic feature of a CXR in tetralogy of Fallot?

A

boot shaped heart

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125
Q

how is tetralogy of Fallot managed?

A

oxygen. knee-chest position. morphine. long-term beta blockers. surgery at less than 12 months.

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126
Q

outline the pathway of normal cardiac conduction

A
  • SA node initiates impulse, spread through atria via internodal pathways. - pause at AVN for depolarisation. then goes down bundle of His to right and left bundle branch. - Left splits into anterior and posterior hemifascicles as well.
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127
Q

what’s the equation for cardiac output?

A

CO = SV x HR

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128
Q

what’s the equation for blood pressure?

A

= SVR (systemic vascular resistance) x CO

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129
Q

briefly explain Starling’s law

A

preload (degree of stretch) = critical factor for SV. increased end-diastolic volume (EDV) leads to increased myocardial stretch. increased myocardial stretch leads to increased contracility, and increased SV –> decreases end systolic volume. so if blood loss, the reduced EDV = reduced CO

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130
Q

where on the chest should you be listening for murmurs?

A
  • mitral area = apex midclavicular line, 5th IC space - tricuspid = inferior right sternal area, 4th IC space - pulmonary = left 2nd IC space, next to sternum - aortic = right 2nd IC space next to sternum
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131
Q

how do you grade murmurs?

A

scale 1-6 (Levine’s scale) 2 = low intensity, everyone should be able to hear it though 3 = medium intensity, but no palpable thrill 4 = medium intensity with palpable thrill

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132
Q

what action in the heart does each heart sound correspond to?

A

S1 = closure of mitral and tricuspid valves (M1 + T1) S2 = closure of aortic and pulmonary valves (A2 + P2) - might split on deep inspiration due to delayed P2

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133
Q

give some causes of a third heart sound

A

might actually just be split S2 (delayed P2 in pulmonary HTN and pulmonary stenosis) in heart failure can 3rd heart sound = gallop rhythm systolic - can be innocent if pregnant/child - heard between S1 and S2 diastolic = always pathological, between S2 and S1

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134
Q

how do you best auscultate for mitral murmurs? what do they indicate?

A

best heard at apex ± radiate to axilla - left lateral position. mitral regurg = pansytolic murmur mitral stenosis = loud opening snap S1, mid-diastolic murmur

135
Q

what is an austin flint mumur?

A

head in aortic regurg = mid diastolic murmur at apex, as the aortic regurgitation vibrates the mitral valve

136
Q

how do you best auscultate for pulmonary murmurs? what do they indicate?

A

over left 2nd intercostal space pulmonary stenosis = crescendo-decrescendo systolic murmur that disappears on inspiration pulmonary regurg = early diastolic murmur

137
Q

how do you best auscultate for aortic murmurs? what do they indicate?

A

these get transmitted to the carotid. best to listen on breath hold. right 2nd intercostal space. aortic stenosis = crescendo-decrescendo systolic. aortic regurg = early diastolic murmur best heard when leaning forward and holding breath.

138
Q

what is a “flow murmur”?

A

murmur that’s heard when pt is in hyperdynamic state e.g. anaemia, thyrotoxicosis

139
Q

what are some possible complications of aortic stenosis?

A
  • predispose to IE - small emboli - decompenstion - increased pressure in pulmonary artery, can lead to CHF - need to anticoag mechanical heart valves (target INR 2.5-3.5 for aortic)
140
Q

what are the major and minor criteria for diagnosing rheumatic fever?

A

JONES (maj.) PEACE (min.) - dx if hx recent strep infection, plus 1maj+2min, or 2 major: Joints - large joint arthritis O - heart - carditis, valve damage Nodules Erythema marginatum (pale red macules/papules) Sydenham’s chorea PR interval prolongation ESR raised ++ Arthralgia (but not quite arthritis) CRP raised ++ Elevated temp (90% >39C!!)

141
Q

investigations for rheumatic fever?

A

look for evidence of strep - throat swab for culture, antistreptococcal antibodies (ASO, anti-DNase B) rise in first month (check 2/52 apart for this rise) ECG = PR prolonged, ST elevation (saddle shape) - suggests pericarditis CXR - ?heart failure FBC - for WCC, + ESR + CRP Doppler echo for carditis

142
Q

management of rheumatic fever?

A
  • strict bed rest till inflammatory markers normal - eradicate strep - single IV benpen then oral penicillin - treat any heart failure (HF) - diuretics, ACEi, digoxin - NSAIDs - for pain and suppresses inflammation - for chorea - self-limiting but haloperidol can help (caution re EPSE!)
143
Q

what would you find on investigation for dilated cardiomyopathy?

A

CXR = CHF (ABCDE) ECG = sinus tachy, LBBB or *non-specific T or ST change, or AF echo - marked dilatation of LV, reduced sys/dia function, MR or TR, mural thrombus. bloods - BNP for heart failure might biopsy if suspect amyloid/sarcoid

144
Q

what is myocarditis?

A

acute/chronic inflammation of myocardium. presents like an MI - but with fever. destruction of myocardium can lead to dilated cardiomyopathy or heart failure, it’s also a cause of unexplained cardiac death.

145
Q

what causes myocarditis?

A

usually viral (coxsackie). can be immune mediated - SLE, sarcoidosis, scleroderma. toxic - *alcohol, heavy metals

146
Q

what investigations should you do for myocarditis?

A

gold standard = endomyocardial biopsy - viral serology - FBC - WCC, raised ESR/CRP - cardiac enzymes (CK, TrI, TrT) - cardiac MRI can differentiate from infarction

147
Q

how do you treat myocarditis?

A
  • treat cause (viral = supportive + bed rest) - acute = ITU - +ve inotropes (e.g. phosphodiesterase inhibitors, dopamine) for symptomatic hypotension - anticoag if AF
148
Q

outline acute management of heart failure

A

1) O2 and IV furosemide ± non-invasive ventilation or invasive as needed 2) when stable = bisoprolol + ACEi (or ARB) + aldosterone antagonist 3) F/U in 2 wks with cardiology suspect acute heart failure if cardiogenic shock + low BP

149
Q

outline how you refer someone with newly detected ?heart failure according to investigation results

A
  • if previous MI then 2WW for specialist + doppler echo - no prev. MI = BNP (B type natriuretic hormone) measurement - >400 = 2WW, 100-400 = 6 week referral, <100 = heart failure unlikely also do - ECG, FBC, UE, Cr, LFT, glucose, fasting lipids, TFT, ?cardiac enzymes
150
Q

how do we determine who to prescribe statins to?

A

QRISK2 >10% 10yr risk - things like history of CVD, familial hypercholesterolaemia.

151
Q

what are the important side effects of statins? at what doses to we prescribe them? monitoring?

A

*myalgia! also stiffness, weakness, cramping SE onset usually at around 6 months. give atorvastatin 20mg for primary prevention, 80mg for secondary. monitor LFTs

152
Q

which ECG leads correspond to which coronary arteries/type of MI?

A

I, V5, V6 = circumflex artery, lateral II, III, aVF = right coronary artery, inferior V1-V4 = LAD, anterior

153
Q

list some possible complications post-MI

A

DEPARTS + fails: Death, dresslers syndrome Electrical = tachy/bradyarrhythmias Pericarditis Aneurysm (persistent ST elevation) Re-MI/Rupture (tamponade) Thrombus - stroke Shock - cardiogenic VSD heart failure - pulmonary oedema

154
Q

what is cardiac tamponade?

A
  • collection of blood/fluid/pus/gas in pericardial space - large vol. leads to reduced ventricular filling –> haemodynamic compromise MEDICAL EMERGENCY
155
Q

what is Beck’s triad?

A

seen O/E in acute cardiac tamponade - muffled heart sounds, hypotension, raised JVP if slower - pulsus paradoxus (as inspiration decreases intrathoracic pressure, so better flow to right heart)

156
Q

what do you see on ECG (and other Ix) in cardiac tamponade?

A

ECG = “low voltage” QRS complex - amplitude changes beat to beat. CXR = cardiomegaly, water-bottle shaped heart, calcification TTE = gold standard

157
Q

how do you manage cardiac tamponade?

A

O2, fluids, legs up, dobutamine (inotrope) –> immediate pericardiocentesis

158
Q

what is Brugada syndrome?

A

ECG abnormality with high incidence of sudden death in people with structurally normal hearts. due to mutation in cardiac sodium channel gene - sodium channelopathy.

159
Q

what are the criteria for diagnosing Brugada syndrome?

A

ECG change (Brugada sign) + clinical features: ECG = Coved (or saddleback I think) ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave. Clinical criteria (need 1): - Documented VF or polymorphic VT - FHx of sudden cardiac death at <45yo - coved-type ECGs in family members. - Inducibility of VT with programmed electrical stimulation . - Syncope. - Nocturnal agonal respiration. (all 3 “types” of Brugada syndrome/sign involve J point elevation in 1+ of V1-V3 - this was mentioned at ECG teaching)

160
Q

what management does someone with Brugada syndrome need?

A

need ICD. quinidine might help but ICD only proven option. bit of a debate over who needs one but if they actually have Brugada syndrome (rather than just ECG changes) they probs do - risk of SCD.

161
Q

list 3 viral causes of acute pericarditis

A

*Coxsackie B Influenza *EBV Mumps Varicella HIV

162
Q

list 3 bacterial causes of acute pericarditis

A

Pneumonia Rheumatic fever TB Streps Staphs

163
Q

list 5 causes, other than bacterial/viral infection, of acute pericarditis

A

Fungi, MI, uraemia, rheumatoid arthritis, *SLE, myxoedema, trauma, surgery, malignancy, radiotherapy, *sarcoidosis, idiopathic + drugs post MI (Dressler’s)

164
Q

describe the pain seen in acute pericarditis

A

sharp, central chest pain - worse on inspiration or lying flat, relieved by leaning forward

165
Q

what might be heard on auscultation of a patient with pericarditis?

A

pericardial friction rub tachypnoea/tachycardia/fever.

166
Q

what investigations would you carry out for acute pericarditis? what would you see?

A

ECG - concave upwards (saddle-shaped) ST segment elevation in all leads do serial ECGs. the above is stage 1, then stage 2 returns to normal, T waves flatten, stage 3 = T inversion, stage 4 = T wave normal CXR = globular heart bloods echo - if worried about effusion or tamponade

167
Q

how would you treat acute pericarditis?

A

treat underlying cause. rest, NSAIDs for analgesia. admit if - fever, evidence of tamponade, large effusion, on warfarin, trauma. if falling BP and shock - suspect tamponade, needs immediate pericardiocentesis with echo! chronic + symptomatic = pericardial resection recurrent = colchicine in addition to NSAIDs

168
Q

what is constrictive pericarditis?

A

heart is encased in a rigid fibrotic pericardium - prevents diastolic filling of ventricles.

169
Q

what causes constrictive pericarditis?

A

most common in UK = idiopathic. globally = TB. also occurs after any pericarditis.

170
Q

what are the clinical features of constrictive pericarditis?

A

those of right-sided heart failure - raised JVP, oedema, hepatomegaly, ascites, pulsus paradoxus, diffuse apex beat

171
Q

what two investigations would you carry out in constrictive pericarditis and what would you find?

A

CXR - normal/small heart + pericardial calcification. CT/MRI - pericardial thickening/calcification

172
Q

how would you treat constrictive pericarditis?

A

surgical excision of pericardium

173
Q

what is the definition of hypertension?

A

>140/90mmHg based on 2+ readings on separate occasions

174
Q

what are the criteria for treating hypertension?

A

ALL with sustained >160/100mmHg. those with sustained >140/90 that are at high risk of coronary events, have diabetes or end-organ damage

175
Q

list 3 causes of secondary hypertension

A

renal disease - diabetic nephropathy, chronic glomerulonephritis, PKD, chronic tubulointerstitial nephritis. endocrine disease - Conn’s, phaeochromocytoma, Cushing’s, acromegaly. Coarctation of the aorta. pregnancy. steroids. the Pill.

176
Q

give 3 risk factors for hypertension

A

age, FHx, male gender, African or Caribbean origin, high salt intake, sedentary lifestyle, overweight/obese, smoking, excess alcohol intake.

177
Q

what investigations would you carry out on a patient presenting with a high blood pressure reading?

A

take blood pressure again, on at least 1 other occasion. 24h ambulatory BP monitoring (ABPM) - exclude white coat effect

178
Q

give 3 examples of non-pharmacological measures you would encourage a patient with hypertension to take

A

weight reduction. Mediterranean diet - oily fish, low saturated fat, low salt. limit alcohol consumption. exercise. smoking cessation. increase fruit and veg intake.

179
Q

what drug would you prescribe for a 45yo caucasian patient with hypertension with no other medical history?

A

ACE inhibitor - ramipril. if CI (cough) - ARB - losartan

180
Q

what drug would you prescribe a 67yo Afro-Caribbean man with hypertension?

A

calcium channel blocker - amlodipine

181
Q

if first line treatment is failing to control a patient’s hypertension, what drug regime would you prescribe them? and if this fails?

A

ACE inhibitor + CCB or ACE inhibitor + thiazide. all 3 if a combination of 2 fails to control.

182
Q

how do calcium channel blockers work to reduce hypertension?

A

decrease calcium entry into vascular smooth muscle cells - vasodilation of arterial smooth muscle, lowering arterial pressure.

183
Q

what are the side effects of CCBs?

A

bradycardia, headaches, flushing

184
Q

what is the most common cardiac arrhythmia?

A

atrial fibrillation

185
Q

what is AF?

A

irregularly irregular atrial rhythm at 300-600bpm. AV node is conducting some of the atrial impulses - irregular ventricular response. irregularly irregular pulse.

186
Q

list 4 causes of atrial fibrillation

A

heart failure/ischaemia, hypertension, mitral valve disease, hyperthyroidism, caffeine, alcohol, hypokalaemia, hypomagnaesaemia. RFs - age, HTN, heart failure, CAD, valve disease, DM, CKD precipitants = alcohol, caffeine

187
Q

what ECG features would you see in atrial fibrillation?

A

absent P waves irregular QRS complexes atrial rate 300bpm. oscillating baseline = f waves.

188
Q

give 3 forms of treatment you would give a patient with atrial fibrillation

A

thromboprophylaxis e.g. warfarin, apixaban/rivaroxaban beta blockers/CCBs - rate control. Cardioversion - rhythm control.

189
Q

describe what you would see on an ECG trace in atrial flutter

A

saw tooth flutter waves between QRS complexes atrial rate 300 - absent p waves ventricular rate 150bpm (2:1 and 4:1 conduction comon)

190
Q

what is the difference between atrial fibrillation and atrial flutter?

A

atrial fibrillation = irregular ventricular conduction of atrial beats. atrial flutter = atrial rate of 300bpm (same as AF), but ventricles conduct every other atrial beat - 150bpm

191
Q

name some common causes of AV block

A

MI/ischaemia (esp. inferior), myocarditis, Lyme disease, SLE, endocarditis cardiomyopathy, fibrosis of conducting tissue, drugs (digoxin, beta blockers, CCB)

192
Q

what is first degree AV block? how does it appear on ECG?

A

delayed AV conduction. prolonged PR interval (>0.2s) - but PR constant, every P followed by QRS.

193
Q

how does Mobtiz type I (second degree) AV block appear on ECG? aka Wenckebach phenomenon

A

progressive PR interval prolongation until a P wave fails to conduct - PR interval then returns to normal, then begins to get longer again.

194
Q

how is Mobitz type II (second degree) AV block seen on ECG?

A

dropped QRS waves, prolonged but constant PR intervals.

195
Q

what is 2:1 or 3:1 advanced second degree AV block?

A

every second or third P wave conducts to ventricles subtype of Mobitz II heart block

196
Q

what is third degree AV block? how are ventricular contractions maintained?

A

all atrial activity is failing to conduct to ventricles - atrial and ventricular activity completely dissociated (so P and QRS waves appear totally independently). QRS narrow if block in/above His (nodal). QRS wide if block in/below His, plus rate <45bmp. ventricular contractions are being maintained by spontaneous escape rhythms from below site of block. causes = myocardial fibrosis

197
Q

describe the ECG features seen in RBBB - how does this relate to what’s actually happening.

A

depolarisation of RV is delayed, but LV depolarises normally - so initial bit of QRS is normal, then there’s slow spread L to R via non-specialised tissue. MarroW secondary R waves in V1, V2 (rSR - M shape!) deep wide slurred S in I, V5 and V6 associated T inversion in V1, V2

198
Q

list 2 causes of RBBB

A

Rheumatic heart disease RVH PE, IHD, cardiomyopathy idiopathic

199
Q

describe the ECG features seen in LBBB

A

opposite to RBBB - WilliaM wide QRS >0.12s absent Q in V5, V6 broad R waves in I, V5, V6. (W in V1) deep S in V1 and V2.

200
Q

list 2 causes of LBBB

A

coronary artery disease - LAD LVH, hypertensive heart disease, anterior infarction, aortic valve disease, post-op

201
Q

give 3 causes of sinus tachycardia - management if needed?

A

physiological - exercise/excitement. fever, anaemia, heart failure, thyrotoxicosis, acute PE, hypovolaemia, drugs. try vagal manoeuvres, beta blockers or non-dihydropyridine CCBs could help (diltiazem, verapamil)

202
Q

what causes atrioventricular junctional tachycardias?

A

re-entry circuits - two separate pathways for impulse conduction AVRT = atrioventricular re-entrant tachy AVNRT = atrioventricular nodal re-entrant tachy

203
Q

what are the ECG changes seen in supraventricular tachycardias?

A

absent or inverted P wave after (narrow) QRS HR > 100bpm may see atrial fibrillation, or flutter - or you get AV junctional tachycardias.

204
Q

name 2 things that may aggravate a supraventricular tachycardia

A

exertion, coffee, tea, alcohol

205
Q

what is the 1st line management of any narrow complex tachycardia?

A

vagal manoeuvres - breath holding, valsalva manoeuvre, carotid massage.

206
Q

general management of a narrow complex supraventricular tachycardia?

A

most narrow complex supraventricular tachys don’t need treatment - only Rx if needed for symptomatic relief or to prevent MI/HF etc - O2, IV access - if BP<90, chest pain (MI), heart failure, heart rate >200bpm = DC cardioversion with GA ± IV amiodarone (150mg IV over 10 mins) - if irregular (?AF) - IV beta blocker or IV digoxin if onset was within 48hrs, if not = IV amiodraone - regular = vagal manouevres then IV adenosine 6mg rapid bolus, then 12 mg every 1-2 mins if unsuccessful, up to max 3

207
Q

what are ventricular ectopic premature beats?

A

a premature beat arising from an ectopic focus in the ventricles - this focus depolarises before the SAN, leading to a premature and inefficient beat.

208
Q

describe the clinical and ECG features of a premature ventricular ectopic beat

A

broad, abnormal QRS complex before you would expect it. patient complains of extra/missed beats/heavy beats - palpitations

209
Q

how would you treat a symptomatic ventricular ectopic beat? what are patients with ventricular ectopic beats at a higher risk of?

A

beta blockers. ventricular fibrillation.

210
Q

what are the ECG features of a ventricular tachycardia?

A

rapid ventricular rhythm with broad abnormal QRS complexes

211
Q

list 3 causes of prolonged QT

A

congenital, hypokalaemia, hypocalcaemia, hypomagnesaemia, tricyclics, macrolides

212
Q

what causes Wolff-Parkinson-White?

A

congenital accessory conduction pathway between atria and ventricles

213
Q

what is an aneurysm? how might they cause symptoms?

A

permanent localised dilation of an artery. pressure effects on local structures, or vessel rupture. can be a source of emboli.

214
Q

how might an abdominal aortic aneurysm be discovered?

A

a pulsatile mass palpated on abdo exam. calcification on a plain XR. rupture. epigastric or back pain due to pressure effects.

215
Q

what is the difference between a true and false aneurysm?

A

true aneurysm has the wall of the artery forming a capsule around the aneursym. false aneurysm wall is made up of surrounding tissue.

216
Q

how would a ruptured AAA present?

A

sudden severe epigastric pain radiating to back leading to hypovolaemic shock - collapse

217
Q

initial management of ruptured AAA/aortic dissection? how would a ruptured AAA be repaired?

A

ABCDE, 2x large bore cannulas, group and crossmatch, order 4-6u blood/FFP/pt IMMEDIATE theatre - proximal aortic control, endovascular repair (EVAR) with stent insertion/prosthetic graft

218
Q

describe the pain of a dissecting aortic aneurysm

A

abrupt onset of severe, tearing central chest pain radiating through back

219
Q

how is a dissecting aortic aneurysm managed?

A

urgent BP control - lanetalol IV. surgical repair.

220
Q

give 3 risk factors for peripheral arterial disease

A

hypertension, smoking, diabetes, diet, sedentary lifestyle, obesity, hyperlipidaemia, age, male gender, FHx

221
Q

what causes peripheral artery disease?

A

atherosclerosis causing stenosis of arteries

222
Q

describe the clinical features of intermittent claudication

A

cramping pain in calf/thigh/buttock after walking a given distance (shorter=more severe) - relieved by rest

223
Q

describe the clinical features of critical ischaemia

A

ulceration, gangrene, pain at rest. burning foot pain at night relieved by hanging legs over the side of the bed

224
Q

what are the 4 stages in the Fontaine classification of peripheral artery disease?

A

asymptomatic - intermittent claudication - ischaemic rest pain - ulceration/gangrene (critical ischaemia)

225
Q

give 3 signs of peripheral artery disease

A

absent femoral, popliteal or foot pulses. cold, white leg(s), atrophic skin, punched out ulcers, postural colour change, capillary refill prolonged

226
Q

what are the 5 Ps of acute limb ischaemia?

A

Paraesthesia Perishingly cold Pallor Paralysis Pain need urgent hand-held doppler and urgent angiography - needs re-vascularisation in 4-6hrs with *immediate heparinisation!

227
Q

what diagnostic tests would be performed in peripheral artery disease?

A

doppler ultrasound to calculate Ankle-brachial pressure index (ABPI) - ratio of ankle and brachial (ankle/arm) systolic pressures - normal = 1, <0.9 = mild PAD, <0.8 = mod, <0.5 = ischaemic rest pain. MR/CT angiography.

228
Q

describe conservative treatment of limb ischaemia

A

exercise, quit smoking, lose weight, manage diabetes and hypertension. clopidogrel (antiplatelet) to prevent progression and reduce risk.

229
Q

how would intermittent claudication be managed, beyond conservative risk reduction treatments?

A

revascularisation - percutaneous transluminal angioplasty (PTA) or surgical reconstruction/arterial bypass graft.

230
Q

what are some risk factors for infective endocarditis?

A

congenital - valve defects, VSD, PDA. prosthetic valves. IVDU. poor dental hygiene. soft tissue infections.

231
Q

name the most common causative organism in infective endocarditis?

A

Streptococcus viridans

232
Q

give 3 organisms (apart from Strep viridans) that can cause infective endocarditis

A

enterococci, staph aureus/epidermidis, diphtheroids, Haemophilus, actinobacillus, Coxiella burnetii, chlamydia. fungi - Candida, aspergillus, histoplasma.

233
Q

what is an infective endocarditis patient at risk of?

A

stroke - vegetations. destruction of valve - regurgitation - worsening heart failure.

234
Q

give the important clinical features of infective endocarditis

A

FEVER + NEW MURMUR = ENDOCARDITIS TILL PROVEN OTHERWISE subacute = fatigue, low grade fever, polymyalgia, anorexia, wt loss etc acute = rapidly progressing infection *majority = fever + chills + poor appetite + wt loss

235
Q

what investigations should you carry out in suspected endocarditis?

A

3 sets of blood cultures, at different times (6hrs between) and sites. bloods - anaemia, neutrophilia, high ESR/CRP, rheumatoid factor. *transthoracic echocardiography (TTE) within 24hrs*

236
Q

describe the Duke criteria for diagnosis of IE

A

2 major or 1 maj + 3 min, or 5 min. Major criteria - persistently +ve blood culture. endocardium involvement seen on +ve echo, new murmur. Minor criteria - fever, vascular/immunological signs, +ve blood culture/echo that doesn’t meet major, predisposing factor (e.g. IVDU, heart condition)

237
Q

how would you treat infective endocarditis?

A

before results of culture - IV benpen + gentamicin (if native valve). then tailor to cultures and sensitivity. if severe sepsis = vancomycin + gentamicin. if confirmed staph = 4/52 IV fluclox (vanc. for MRSA) if confirmed strep = 4/52 IV benpen

238
Q

what is shock?

A

acute circulatory failure with inadequate or inappropriately distributed tissue perfusion - prolonged oxygen deprivation leads to necrosis, organ failure and death

239
Q

list the different types of shock

A

hypovolaemia, cardiogenic, sepsis, anaphylaxis, neurogenic shock

240
Q

give 3 causes of hypovolaemia shock

A

haemorrhages - GI bleed, trauma, AAA dissection etc. fluid loss - burns, diarrhoea, intestinal obstruction.

241
Q

give 3 causes of cardiogenic shock

A

(= pump faillure). ACS, arrhythmias, aortic dissection, PE, tension pneumothorax, cardiac tamponade, endocarditis

242
Q

give 3 signs of hypovolaemic shock

A

pale grey skin, slow capillary refill, sweating, weak pulse, tachycardia

243
Q

name 2 precipitating factors of anaphylactic shock

A

penicillin, contrast, latex, dairy, nuts, insect stings

244
Q

describe the clinical features of anaphylactic shock

A

onset within 5-60mins of exposure. warm peripheries, hypotension, urticarial, angio-oedema, wheezing, upper airway obstruction.

245
Q

how would you manage septic shock?

A

take blood cultures before abx - then co-amoxiclav and tazocin IV

246
Q

how would you manage anaphylactic shock?

A

remove cause. O2. IM adrenaline. IV chlorphenamine and hydrocotisone.

247
Q

how would you manage hypovolaemic shock?

A

raise legs. fluid bolus - repeat if shock improves.

248
Q

what risk score is used to determine stroke risk in AF patient?

A

CHA2DS2-VASc score: Congestive heart failure. Hypertension. Age >75yrs. (2 points, that’s why it’s A2). Diabetes mellitus. S2 - prior stroke (2pts). V - vascular disease Age - 65-74. Sex category - female sex.

249
Q

what is the enzyme that breaks down bradykinin?

A

angiotensin converting enzyme - excess bradykinin (since it’s not being broken down) is the reason why some patients on ACEi get a persistent dry cough

250
Q

explain how ACE inhibitors work

A

ACE inhibitors inhibit conversion of angiotensin I to angiotensin II in the lungs - this prevents it from acting on the adrenals to increase aldosterone secretion and thus cause water and sodium retention at the kidneys. angiotensin II is also a vasoconstrictor, so ACEi act as vasodilator, and causes sodium and water excretion - lower blood volume, lowers BP.

251
Q

how do angiotensin receptor blockers produce a similar effect to ACEi? give two examples of ARBs

A

by blocking angiotensin II receptors, so its actions cannot be exerted. losartan, candesartan.

252
Q

give 2 examples of ACEis

A

ramipril, lisinopril

253
Q

why do you get hyperkalaema as a side effect of angiotensin 2 receptor blockers?

A

ARBs cause a direct effect on aldosterone production in the adrenals - aldosterone works on the distal convoluted tubules of kidney by causing sodium to be reabsorbed in return for potassium excretion - ARBs reverse this transfer, so there’s potassium retention.

254
Q

calcium channel blockers are negatively inotropic and negatively chronotropic, what does this mean?

A

inotropic - reduces the contraction. chronotropic - lowers the heart rate.

255
Q

how do calcium channel blockers work? give some examples.

A

decrease calcium entry into vascular and cardiac cells. intracellular calcium is lower - relaxation and vasodilation of arterial smooth muscle. reduce myocardial contractility and suppress cardiac conduction, particularly at AV node. this reduces myocardial oxygen demand - important in angina. dihydropyridines (amlodipine, nifedipine) - selective for vasculature. non-dihydropyridines (diltiazem, verapamil)- selective for heart

256
Q

what clotting factors does warfarin work on?

A

2, 7, 9, 10 by inhibiting vitamin K synthesis - so anticoagulates by inhibiting coagulation factor synthesis

257
Q

statins are given to correct hyperlipidaemia, what enzyme do they act on? name 2 statins.

A

HMG-CoA reductase - involved in making cholesterol. so they reduce the cholesterol production in liver and increase clearance of LDL-cholesterol from blood. simvastatin, atorvastatin, pravastatin.

258
Q

amiodarone is used for pharmacological cardioversion, but it also chemically resembles a hormone made naturally by the body - what is this and what can this cause?

A

thyroxine - can cause hyperthyroidism (or hypothyroid!)

259
Q

in supraventricular tachycardia, adenosine is administered IV to bring the heart back into normal rhythm, how does it work on the heart? what type of arrhythmias should it be used for?

A

it works via the A1 receptor, which reduces cAMP - so causes cell hyperpolarisation by pushing potassium out of the cell. also relaxes the smooth muscle of the heart causing vasodilation. only used for ventricular tachycardias.

260
Q

why do you need to warn the patient that they may get a sense of ‘impending doom’ after you administer adenosine?

A

because it induces transient heart block in the AV node so the heart stops for a beat or so

261
Q

atropine is derived from the deadly nightshade, but what heart arrhythmia is it used for and how does it help?

A

it is used for any severe bradycardia - it blocks the action of the vagus nerve/parasympathetic system by being a competitive antagonist of muscarinic ACh receptors. dilates pupils, increases heart rate and reduces salivation.

262
Q

if you have a patient that comes in with unstable angina but tells you he is allergic to aspirin, what is then your first line of treatment after giving GTN?

A

clopidogrel monotherapy

263
Q

give an example of a short and a long acting nitrate

A

short - glyceryl trinitrate (GTN). long - isosorbide mononitrate

264
Q

how do nitrates work to reduce the pain of angina?

A

converted to NO, which is a vasodilator - relaxation of capaticance vessels reduces cardiac preload + LV filling, which reduces cardiac work and myocardial oxygen demand.

265
Q

give 2 possible side effects of nitrates

A

flushing, headaches, light headedness, hypotension

266
Q

name 3 beta blockers

A

bisoprolol, atenolol, propranolol, metoprolol

267
Q

how do beta blockers work to improve symptoms of ischaemic heart disease?

A

they reduce force of contraction and speed of conduction in the heart via beta 1 receptors - reducing cardiac work and oxygen demand.

268
Q

how do beta blockers work as a treatment for AF?

A

slow the ventricular rate by prolonging the refractory period at the AV node

269
Q

list the indications for beta blockers

A

IHD - symptoms and improve prognosis. chronic heart failure. AF and other SVTs - reduce rate, maintain sinus rhythm. hypertension - only if other medicines are insufficient.

270
Q

how do beta blockers work as a treatment for hypertension?

A

reduce renin secretion from the kidney, which is mediated by beta1 receptors.

271
Q

give some possible SEs of beta blockers

A

fatigue, cold extremities, headache, nausea, sleep disturbance, ED in men.

272
Q

what major disease is a contraindication to the use of beta blockers?

A

ASTHMA - can cause life-threatening bronchospasm due to blockade of beta2 adrenoreceptors in airways

273
Q

name an aldosterone antagonist

A

spironolactone, epleronone

274
Q

what cardiac indication do aldosterone antagonists treat?

A

chronic heart failure - as an addition to beta blocker and ACEi/ARB

275
Q

name a LMWH. name a drug that is very similar to LMWHs

A

dalteparin, enoxaparin. similar drug - fondaparinux.

276
Q

how do LMWHs work?

A

inhibit factor Xa by inhibiting antithrombin

277
Q

how does fondaparinux work?

A

inhibits factor Xa.

278
Q

how does aspirin work in prevention of thrombosis?

A

it irreversibly inhibits cyclooxygenase (COX) to reduce production of pro-aggregation factor thromboxane from arachidonic acid - reduces platelet aggregation and risk of arterial occlusion.

279
Q

give some examples of antiplatelet drugs, apart from aspirin

A

clopidogrel, new oral anticoagulants, glycoprotein IIb/IIIa inhibitors

280
Q

how does clopidogrel work?

A

prevents platelet aggregation by binding irreversibly to adenosine diphosphate receptors on surface of platelets - independent of COX pathway, so can be taken with aspirin

281
Q

how do glycoprotein IIb/IIIa inhibitors work?

A

prevent platelet aggregation by inhibiting the GPIIb/IIIa receptor on platelet surface

282
Q

name 2 fibrinolytic (thrombolysis) drugs

A

alteplase, streptokinase

283
Q

how do fibrinolytic drugs work?

A

catalyse the conversion of plasminogen to plasmin which acts to dissolve fibrinous clots and re-canalise occluded vessels. - allows reperfusion of tissues, preventing/limiting tissue infarction.

284
Q

name a loop diuretic

A

furosemide, bumetanide

285
Q

give a cardiac indication of loop diuretics

A

symptomatic treatment of fluid overload in chronic heart failure

286
Q

describe the mechanism of loop diuretics

A

act on ascending limb of loop of Henle to inhibit the Na/K/2CL cotransporter that transports the ions into the cell - water follows these ions, so they have a potent diuretic effect. also - cause dilation of capaticance vessels - reduces preload + improves contractile function of the heart.

287
Q

what are potassium sparing diuretics used for? name an example.

A

used as part of combination therapy, to treat hypokalaemia arising from loop/thiazide diuretic use. amiloride.

288
Q

how do potassium sparing diuretics work?

A

weak diuretics. act on distal convoluted tubules in kidney - inhibit sodium and water reabsorption by acting on epithelial sodium channels - causes potassium retention.

289
Q

give an example of a thiazide/thiazide like diuretic

A

bendroflumethiazide, indapamide, chlortalidone

290
Q

describe the mechanism of action of thiazide diuretics

A

inhibit the Na/Cl cotransporter in the distal convoluted tubule of the nephron, preventing reabsorption of sodium and water. also cause vasodilation.

291
Q

how does digoxin work in AF/atrial flutter?

A

reduces heart rate and increases force of contraction (-vely chronotropic, +vely inotropic). works via indirect pathway - increased vagal tone, reduced contraction at AVN and preventing dome impulses travelling to the ventricles.

292
Q

for what cardiac problem might sildenafil be prescribed? what class of drug is this?

A

primary pulmonary hypertension. phosphodiesterase type 5 (PDE5) inhibitor

293
Q

how does sildenafil work as a treatment of pulmonary hypertension?

A

causes arterial vasodilation by increasing cGMP (normally broken down by PDE5).

294
Q

how do you define sinus bradycardia?

A

< 60bpm every P wave is followed by a QRS

295
Q

list some causes of sinus bradycardia

A
  • physiological: athletes, young people due to high resting vagal tone - pathological: acute MI, drugs (beta blockers, digoxin, amiodarone), hypothyroid, hypothermia, sick sinus syndrome
296
Q

what symptoms do you get with sinus bradycardia? how do you manage it, providing rate is >40bpm ish?

A

can get syncope, fatigue, dizziness, ischaemic chest pain, palpitations - depends on cause no treatment, just check for causes, stop drugs etc

297
Q

how do you treat a sinus bradycardia of <40 or a symptomatic sinus brady?

A

IV atropine temporary pacing wire

298
Q

what is sick sinus syndrome?

A

the result of a dysfunctional SA node, with impairment of ability to generate impulses. normally due to idiopathic fibrosis of the node, also associated with ischaemia and digoxin toxicity

299
Q

what ECG features would you see in sick sinus syndrome?

A

sinus bradycardia SA block = pause between P waves length of 2 or more PP intervals SA arrest = prolonged pause without P wave activity, unrelated to PP interval also can see escape rhythms - activity from an extra ‘pacemaker’ in atria/AV junct/ventricles. junctional = normal QRS shape, rate 40-60bpm ventricular = broad complex slow (15-40bpm!)

300
Q

how do you manage sick sinus syndrome?

A

“tachy-brady syndrome” - can get bursts of atrial tachycardia interspersed with bradycardia, or AF. brady - Rx with permanent atrial or dual chamber pacemaker tachy - give digoxin or verapamil

301
Q

when/how do you treat the different degrees of heart block?

A

first = benign and asymptomatic so leave it. Mobitz 1/Wenckebacks = treat if symptomatic or inferior MI; atropine won’t work as conduction is below AVN. Mobitz 2 = can progress to complete, consider pacemaker.

302
Q

outline general investigation and management of bradycardias

A

Ix = 12 lead ECG, bloods for electrolyte imbalance Rx = only if symptomatic (syncope, hypotension, heart failure) or <40bpm: - resus, IV access, bloods, treat causes etc - IV atropine 0.5mg, can repeat up to 3mg - poor response = transcutaneous pacing - can try glycopyrrolate, glucagon helps if due to beta blocker/CCB - temporary or permanent pacing

303
Q

explain the mechanism of AVNRTs

A

(most common cause of paroxysmal narrow complex tachys - onset in late teens/early 20s) - they’ve got 2 pathways in AV node, with a joined common pathway lower in AVN and into bundle of His - one path fast with long refractory period, one slow with quick refractory period - normally (sinus) impulse goes down the fast pathway to ventricles, still goes down the slow path but the common bit is still in refractory period. - AVNRT initiated if a premature atrial beat happens at critical point when fast pathway is refractory, but slow recovered = goes down slow, then back UP fast - re-entry circuit initiated. ** suden onset palpitations ± chest pain ± SOB ± syncope **

304
Q

what is seen on ECG for AVNRT? management?

A
  • regular, narrow QRS, rate 130-250 - retrograde atrial conduction shows up as inverted P waves in II, III, aVF (inferior leads) - P waves get buried in QRS as often depolarising together! first line rx = vagal manoeuvres second line = adenosine (but feels like they’re gonna die!!) prophylaxis - digoxin, diltiazem, verapamil, fleicanide, beta blockers curative - radiofrequency ablation
305
Q

what’s the mechanism behind AVRT/wolff parkinson white

A
  • anatomically separate AV connection, outside of AVN, that allows atrial impulse to bypass AVN and activate ventricles prematurely = ventricular pre-excitation - WPW = accessory pathway (bundle of Kent) connects atria directly to ventricles (congenital) - can be broad or narrow QRS depending on whether the AVN or the accessory pathway is used for anterograde condution
306
Q

what is seen on ECG in WPW / AVRT?

A

in sinus rhythm: - shortened PR interval (early depolaristion) - delta wave = slurred upstroke in the QRS in tachycardia: - P hidden in the QRS so can appear absent - narrow QRS

307
Q

what are the different types of WPW?

A

type A = delta wave and QRS predominantly upright in precordial leads - dominant R in V1 can be mistaken for RBBB type B = delta and QRS predominantly negative in V1 + V2 - resembles LBBB

308
Q

management for WPW?

A
  • vagal manoeuvres ± adenosine - prophylactic drugs for AVN and accessory = fleicanide or sotalol - curative = radiofrequency ablation
309
Q

explain how AF puts you at increased risk of stroke

A

rapid chaotic atrial firing causes stagnation of the blood in atria –> thrombus formation –> risk of embolism, so risk of stroke reduced CO can also lead to heart failure

310
Q

what are the different types of AF?

A
  • paroxysmal = spontaneous termination within 7 days, but normally <48hrs - recurrent = 2+ episodes - persistent = lasts longer than 7 days - permanent = long-standing AF not successfully terminated by cardioversion
311
Q

what investigations would you order for someone with AF?

A
  • ECG ± 24h ECG if paroxysmal - TFT, FBC, U&E, renal function, LFT/coag - might do TTE if heart murmur/considering valvular disease
312
Q

who would you consider managing with rhythm control for AF?

A

if rate control hasn’t worked well enough if persisting over 48hrs you might DC cardiovert might use amiodarone 4 weeks before, and 12 months after cardioversion. drug rhythm control = beta blockers (anything but sotalol), dronedarone, amiodarone.

313
Q

what drugs are used for rate control in AF?

A

standrad beta blocker or rate-limiting CCB (diltiazem, verapamil) for dual therapy can either add digoxin, or combine two of the above (ONLY combine diltiazem w/beta blocker)

314
Q

what risk score should you use to determine need for thromboprophylaxis in someone with AF?

A

CHA2DS2Vasc HASBLED also determines bleeding risk in people being started on anticoagulants

315
Q

what treatment options are there if drug management of AF fails?

A
  • left atrial catheter ablation if paroxysmal - pace and ablate if permanent
316
Q

what are the criteria used in CHA2DS2VASc?

A

CHF (1) HTN >140/90 (1) Age >75 (2) DM (1) prior stroke/TIA (2) vasc dis: MI, PVD (1) Age 65-75 (1) Female (1)

317
Q

what are the criteria for the HASBLED score?

A

HTN (>160) (1) abnormal liver or renal function (1 or 2) stroke (1) bleeding Hx or predisp e.g. anaemia (1) labile INR (1) elderly >65 (1) drugs (alcohol, NSAIDs, antipt) (1 or 2)

318
Q

using CHA2DS2Vasc, who would you offer anti-coagulation to in AF? warfarin targets?

A

males scoring >1 or anyone scoring >2 offer warfarin or NOAC. target INR = 2-3 if poor warfarin control switch to NOAC (poor control = 2xINR >5 or one >8 last 6/12, or 2xINR <1.5)

319
Q

management for atrial flutter?

A

similar Ix as for AF - rhythm control w/ cardioversion or IV amiodarone/sotalol/fleicanide - if recurrent = radiofrequency catheter ablation - consider need for anticoagulation

320
Q

what are the different types of broad complex tachycardia?

A

either ventricular conduction system not work (BBB) or not using AVN correctly: - ventricular tachycardia: may be regular (monomorphic vent. tachy, RV outflow tract tachy, fascicular tachy) or irregular (torsades de points, polymorphic vent. tachy) - supraventricular - aberrant conduction (LBBB or RBBB), WPW, AF with atrioventricular re-entry loop

321
Q

what ECG changes will you see in broad complex ventricular tachycardias?

A
  • monomorphic (broad) QRS complexes - if conduction starting in L ventricle you’re getting RBBB, if in R then you get LBBB - ventricular rate 120-300, usually regular - independent atrial activity indicated by: capture beats, fusion beats, concordance in chest leads (all QRS predominantly +ve or -ve in chest leads)
322
Q

management for broad complex ventricular tachycardia?

A
  • support ABC, O2, venous access - monitor ECG, BP, sats - identify and treat reversible causes e.g. potassium - if unstable/reduced CO (pulseless VT) - synchronised DC shock (up to 3 attempts) - then amiodarone 300mg IV over 10-20mins and repeat shock, then 900mg over 24hrs if refractory - if irregular/stable - if polymorphic VT give magnesium 2g over 10 mins - if regular/stable - VT amiodarone as above, consider adenosine
323
Q

what are the shockable rhythms?

A

VF pulseless VT

324
Q

what is torsades de points? ECG features?

A

polymorphic VT in which cardiac axis rotates over series of 5-20 points - so trace gets taller then shorter then taller again (think arctic monkeys album cover) ECG - varied axis and varies amplitude QRS associated with anything that prolongs QT, can be transient in MI risk is it may deteriorate to VF

325
Q

how do you manage torsades de pointes?

A

IV magnesium sulphate (2g) can try sotalol/amioderone check for electrolyte disturbance as cause.

326
Q

what is ventricular fibrillation and why do we care about it?

A
  • cause of cardiac arrest and sudden death - ventricular fibres start contracting randomly causing ventricular function to fail - shockable rhythm!
327
Q

what are the 2 non-shockable cardiac arrest arrhythmias?

A

asystole pulseless electrical activity

328
Q

what is seen on ECG in VF? management?

A

chaotic, varying amplitudes no identifiable P, QRS or T rate 150-500 amplitude decreases with duration (coarse AF to fine AF) Rx = defibrillation!! might need beta blockers or implantable cardioverter defibrillator (ICD) long term.

329
Q

what is Brugada syndrome? ECG/Rx?

A

genetically inherited condition characterised by abnormal ECG and increased risk of sudden death - autosomal dominant, to do with sodium channels. - ECG = cover ST segment elevation in V1-V3 followed by -ve T wave (Brugada sign) + document VF, pVT - FHx of sudden death <45yrs Rx = ICD

330
Q

what ECG changes are seen in a PE?

A
  • sinus tachy = main finding - S1Q3T3 = deep S in I, deep Q wave in III, T wave in III = only actually seen in 10% - RBBB can be associated
331
Q

how does amiodarone work? important SEs?

A

blacks Na/K/Ca channels, antagonist to alpha and beta adrenergic receptors - reduces automaticity, slows conduction, increases AVN refractory period. can cause hypotension during IV infusion chronic use = pneumonitis, AV block, hepatitis, grey discolouration of skin does weird stuff to thyroid cos it’s got lots of iodine in and is similar to levothyroxine.

332
Q

what are some symptoms of digoxin toxicity? what plasma concentrations are you aiming for?

A

nausea, vomiting, diarrhoea, dyspnoea, confusion, dizziness, headache, blurred vision - low therapeutic index so be careful!! target 1.0-1.5nmol/L > 2.0 suggests toxicity

333
Q

list the different examination findings you might see in infective endocarditis

A

FROM JANE: Fevere >38, tachycardia Roth’s spots - retinal haemorrhage w/pale centre Osler’s nodes - painful red blisters on ends of fingers/toes Murmur - tricuspid, but any new murmur Janeway lesions - painless red maculae on thenar eminence Anaemia/arhtritis Nail haemorrhage - splinter Embolic things - STROKE

334
Q

**more detailed HTN cards in GP deck from 3a**

A

see GP deck

1 - Finals (15 decks)

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