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2a Systems🩺 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

what is angina pectoris?

A

chest pain arising from the heart as a result of myocardial ischaemia

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2
Q

name 3 types of angina

A

classic/stable, unstable/crescendo, Prinzmetal’s.
decibitus, 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.

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

A

exercise ECG test - ST depression, flat/inverted T waves

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12
Q

how would you manage stable angina?

A

modify risk factors.
secondary prevention - aspirin, statins.
symptomatic treatment - GTN spray, CCBs, beta blockers, nitrates.

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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?

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.

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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

troponin, creatinine kinase, myoglobin

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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

MONA:
Morphine, Oxygen, Nitrates, Aspirin
± clopidogrel/ticragelor

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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, aspirin

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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

ischaemic heart disease; valvular disease; pericarditis; pericardial effusion; alcohol; cocaine; myocarditis; arrhythmias; cardiomyopathies; anaemia; pulmonary hypertension

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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 excluded).
echocardiography.

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49
Q

describe the medical management of heart failure

A

loop diuretics (furosemide) ± spironolactone ± thiazide.
ACE inhibitors (or ARB).
beta blockers.
± digoxin, vasodilators (e.g. hydralazine)

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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.

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57
Q

give 3 symptoms of mitral stenosis

A

exertional dyspnoea, fatigue, palpitations, chest pain, systemic emboli, haemoptysis

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58
Q

what is the heart murmur heard in mitral stenosis?

A

rumbling mid-diastolic murmur

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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.
CXR - LA enlargement, pulmonary oedema, mitral valve calcification.
Echo - diagnostic.

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60
Q

how would mitral stenosis be treated?

A

diuretics - decrease pre load.
balloon valvuloplasty / valve replacement.

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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.
infective endocarditis, annular calcification, LV dilatation, ruptured chordae tendinae, papillary muscle rupture.
connective tissue disorders (Ehlers-Danos, Marfan’s).
cardiomyopathy, congenital.

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63
Q

give 3 symptoms of mitral regurgitation

A

dyspnoea, fatigue, palpitations, infective endocarditis

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64
Q

what murmur is heard in mitral regurgitation?

A

pansystolic murmur

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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?

A

enlarged LA and LV, mitral valve calcification, pulmonary oedema

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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.
diuretics.
surgery - 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.

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70
Q

what is the classical triad of symptoms in aortic stenosis?

A

SAD:
Syncope
Angina
Dyspnoea - heart failure

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71
Q

what murmur is heard in aortic stenosis?

A

ejection systolic murmur

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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?

A

normal heart size, prominent ascending aorta, valvular calcification

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74
Q

how would you treat aortic stenosis?

A

prompt valve replacement

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75
Q

what are the most common causes of aortic regurgitation?

A

rheumatic fever and infective endocarditis

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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 stenosis

A

exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, palpitations, angina, syncope, CCF

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79
Q

what murmur is heard in aortic regurgitation?

A

early diastolic murmur.

“at L sternal edge in 4th intercostal space”

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80
Q

what would you see on CXR/ECG in aortic regurgitation?

A

CXR - cardiomegaly and dilatation of the ascending aorta, pulmonary oedema.
ECG - LVH.

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81
Q

how would you treat aortic regurgitation?

A

reduce systolic hypertension - ACE inhibitors.
echo every 6-12/12.
valve replacement.

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82
Q

what are the 3 main cardiomyopathies?

A

hypertrophic (HCM), dilated (DCM) and restrictive

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83
Q

what is hypertrophic cardiomyopathy?

A

ventricular hypertrophy in absence of abnormal loading conditions - LV outflow tract obstruction.

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84
Q

what causes hypertrophic cardiomyopathy?

A

50% = autosomal dominant
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

can be asymptomatic.
angina, syncope, sudden death, systolic thrill.

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87
Q

what investigations might you carry out in cardiomyopathy?

A

CXR, ECG, echo.
cardiac MR.

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88
Q

how would you treat hypertrophic cardiomyopathy?

A

beta blockers/CCBs to control symptoms.
anticoagulate to prevent emboli.
implantable defib.

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89
Q

give 3 causes of dilated cardiomyopathy

A

alcohol, hypertension, haemachromatosis, viral infection, autoimmune, congenital.

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90
Q

give 3 clinical features of dilated cardiomyopathy

A

dyspnoea, emboli or arrhythmia, displaced apex beat, S3 gallop, pleural effusion, oedema, jaundice, ascites.

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91
Q

how would you treat dilated cardiomyopathy?

A

bed rest.
diuretics, digoxin, ACE inhibitors.
biventricular pacing/implantable cardiac defibs.
heart transplant.

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92
Q

what is restrictive cardiomyopathy?

A

rigid myocardium restricting diastolic ventricular filling.

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93
Q

give 2 causes of restrictive cardiomyopathy

A

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.

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95
Q

what investigation would you perform in order to diagnose restrictive cardiomyopathy?

A

cardiac catheterisation.

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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, with systolic thrill

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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

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?

A

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

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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

list 3 viral causes of acute pericarditis

A

Coxsackie B
Influenza
EBV
Mumps
Varicella
HIV

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127
Q

list 3 bacterial causes of acute pericarditis

A

Pneumonia
Rheumatic fever
TB
Streps
Staphs

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128
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

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129
Q

describe the pain seen in acute pericarditis

A

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

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130
Q

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

A

pericardial friction rub

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131
Q

what investigation would you carry out to diagnose acute pericarditis? what would you see?

A

ECG - concave upwards (saddle-shaped) ST segment elevation in all leads

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132
Q

how would you treat acute pericarditis?

A

treat underlying cause.
NSAIDs for analgesia.
colchicine if relapsing.

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133
Q

what is constrictive pericarditis?

A

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

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134
Q

what causes constrictive pericarditis?

A

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

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135
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

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136
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

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137
Q

how would you treat constrictive pericarditis?

A

surgical excision of pericardium

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138
Q

what is the definition of hypertension?

A

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

139
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

140
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.

141
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.

142
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

143
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.

144
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

145
Q

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

A

calcium channel blocker - amlodipine

146
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.

147
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.

148
Q

what are the side effects of CCBs?

A

bradycardia, headaches, flushing

149
Q

what is the most common cardiac arrhythmia?

A

atrial fibrillation

150
Q

what is AF?

A

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

151
Q

list 4 causes of atrial fibrillation

A

heart failure/ischaemia, hypertension, MI, PE, mitral valve disease, pneumonia, hyperthyroidism, caffeine, alcohol, hypokalaemia, hypomagnaesaemia

152
Q

what ECG features would you see in atrial fibrillation?

A

absent P waves
irregular QRS complexes
atrial rate 300bpm

153
Q

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

A

warfarin - anticoagulation.
beta blockers/CCBs - rate control.
Cardioversion - rhythm control.

154
Q

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

A

saw tooth flutter waves between QRS complexes

155
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

156
Q

name 2 common causes of heart block

A

coronary artery disease, cardiomyopathy, fibrosis of conducting tissue

157
Q

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

A

delayed AV conduction.
prolonged PR interval (>0.22s).

158
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.

159
Q

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

A

dropped QRS waves aren’t preceded by progressive PR prolongation. wide QRS complex.

160
Q

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

A

every second or third P wave conducts to ventricles

161
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 (shown in P and QRS waves).
ventricular contractions are being maintained by spontaneous escape rhythms from below site of block.

162
Q

describe the ECG features seen in RBBB

A

secondary R waves in V1.
slurred S in V5 and V6

163
Q

list 2 causes of RBBB

A

PE, RVH, IHD, congenital heart disease, idiopathic

164
Q

describe the ECG features seen in LBBB

A

opposite to RBBB.
secondary R waves in left ventricular leads (I, AVL, V4-V6).
slurred S in V1 and V2.

165
Q

list 2 causes of LBBB

A

IHD, LVH, aortic valve disease, post-op

166
Q

give 3 causes of sinus tachycardia

A

physiological - exercise/excitement.
fever, anaemia, heart failure, thyrotoxicosis, acute PE, hypovolaemia, drugs.

167
Q

what causes atrioventricular junctional tachycardias?

A

re-entry circuits - two separate pathways for impulse conduction

168
Q

what are the ECG changes seen in supraventricular tachycardia?

A

absent or inverted P wave after QRS

169
Q

name 2 things that may aggravate a supraventricular tachycardia

A

exertion, coffee, tea, alcohol

170
Q

what is the 1st line management of a supraventricular tachycardia?

A

vagal manoeuvres - breath holding, valsalva manoeuvre, carotid massage

171
Q

what drugs may be used to treat a supraventricular tachycardia?

A

IV adenosine.
if fails - verapamil/atenolol.

172
Q

what is the long-term management of a supraventricular tachycardia?

A

radiofrequency ablation of accessory pathway via catheter.

173
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.

174
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

175
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.

176
Q

what are the ECG features of a ventricular tachycardia?

A

rapid ventricular rhythm with broad abnormal QRS complexes

177
Q

list 3 causes of prolonged QT

A

congenital, hypokalaemia, hypocalcaemia, hypomagnesaemia, tricyclics, macrolides

178
Q

what causes Wolff-Parkinson-White?

A

congenital accessory conduction pathway between atria and ventricles

179
Q

describe the features of a resting ECG in a patient with WPW

A

short PR interval, wide QRS complex due to slurred upstroke (delta wave)

180
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.

181
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.

182
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.

183
Q

how would a ruptured AAA present?

A

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

184
Q

how would a ruptured AAA be repaired?

A

endovascular repair with stent insertion, or surgical replacement of aneurysmal section

185
Q

describe the pain of a dissecting aortic aneurysm

A

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

186
Q

how is a dissecting aortic aneurysm managed?

A

urgent BP control - lanetalol IV.
surgical repair.

187
Q

give 3 risk factors for peripheral arterial disease

A

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

188
Q

what causes peripheral artery disease?

A

atherosclerosis causing stenosis of arteries

189
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

190
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

191
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)

192
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

193
Q

what are the 5 Ps of acute limb ischaemia?

A

Paraesthesia
Perishingly cold
Pallor
Paralysis
Pain

194
Q

what diagnostic tests would be performed in peripheral artery disease?

A

Ankle-brachial pressure index (ABPI) - ratio of ankle and brachial systolic pressures.
colour duplex USS.
MR/CT angiography.

195
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.

196
Q

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

A

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

197
Q

what are some risk factors for infective endocarditis?

A

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

198
Q

name the most common causative organism in infective endocarditis?

A

Streptococcus viridans

199
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.

200
Q

what is an infective endocarditis patient at risk of?

A

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

201
Q

describe the clinical features of infective endocarditis

A

systemic features of infection - malaise, fever, night sweats, weight loss, anaemia.
heart failure + new murmurs.
vascular events - embolism ± metastatic abscesses.
immune complex deposition - petechial haemorrhages under skin, splinter haemorrhages under nails, Roth’s spots, arthrlagia, acute glomerulonephritis.

202
Q

what investigations should you carry out in suspected endocarditis?

A

3 sets of blood cultures, at different times and sites.
bloods - anaemia, neutrophilia, high ESR/CRP.

transthoracic echocardiography (TTE) - just standard echo.

203
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.

204
Q

how would you treat infective endocarditis?

A

before results of culture - IV benzylpenicillin + gentamicin.
then tailor to cultures and sensitivity.

205
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

206
Q

list the different types of shock

A

hypovolaemia, cardiogenic, sepsis, anaphylaxis, neurogenic shock

207
Q

give 3 causes of hypovolaemia shock

A

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

208
Q

give 3 causes of cardiogenic shock

A

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

209
Q

give 3 signs of hypovolaemic shock

A

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

210
Q

name 2 precipitating factors of anaphylactic shock

A

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

211
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.

212
Q

how would you manage septic shock?

A

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

213
Q

how would you manage anaphylactic shock?

A

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

214
Q

how would you manage hypovolaemic shock?

A

raise legs. fluid bolus - repeat if shock improves.

215
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.

216
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

217
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.

218
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.

219
Q

give 2 examples of ACEis

A

ramipril, lisinopril

220
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.

221
Q

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

A

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

222
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

223
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

224
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.

225
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

226
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.

227
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

228
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.

229
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

230
Q

give an example of a short and a long acting nitrate

A

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

231
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.

232
Q

give 2 possible side effects of nitrates

A

flushing, headaches, light headedness, hypotension

233
Q

name 3 beta blockers

A

bisoprolol, atenolol, propranolol, metoprolol

234
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.

235
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

236
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.

237
Q

how do beta blockers work as a treatment for hypertension?

A

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

238
Q

give some possible SEs of beta blockers

A

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

239
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

240
Q

name an aldosterone antagonist

A

spironolactone, epleronone

241
Q

what cardiac indication do aldosterone antagonists treat?

A

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

242
Q

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

A

dalteparin, enoxaparin.
similar drug - fondaparinux.

243
Q

how do LMWHs work?

A

inhibit factor Xa by inhibiting antithrombin

244
Q

how does fondaparinux work?

A

inhibits factor Xa.

245
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.

246
Q

give some examples of antiplatelet drugs, apart from aspirin

A

clopidogrel, new oral anticoagulants, glycoprotein IIb/IIIa inhibitors

247
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
248
Q

how do glycoprotein IIb/IIIa inhibitors work?

A

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

249
Q

name 2 fibrinolytic (thrombolysis) drugs

A

alteplase, streptokinase

250
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.

251
Q

name a loop diuretic

A

furosemide, bumetanide

252
Q

give a cardiac indication of loop diuretics

A

symptomatic treatment of fluid overload in chronic heart failure

253
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.

254
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.

255
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.

256
Q

give an example of a thiazide/thiazide like diuretic

A

bendroflumethiazide, indapamide, chlortalidone

257
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.

258
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.

259
Q

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

A

primary pulmonary hypertension.
phosphodiesterase type 5 (PDE5) inhibitor

260
Q

how does sildenafil work as a treatment of pulmonary hypertension?

A

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

261
Q

<p>What HR is considered sinus tachycardia?</p>

A

<p>>100bpm</p>

262
Q

<p>Name some causes of sinus tachycardia</p>

A

<p>Anxiety, dehydration, recent exercise, sepsis, pneumonia etc etc</p>

263
Q

<p>What lead(s) would you look in to assess sinus bradycardia/tachycardia?</p>

A

<p>any - rhythm strip is best</p>

264
Q

<p>What HR is considered sinus bradycardia?</p>

A

<p><60bpm</p>

265
Q

<p>List some causes of left axis deviation</p>

A

<p>left anterior hemiblock</p>

<p>WPW syndrome</p>

<p>inferior MI</p>

<p>ventricular tachycardia</p>

<p>LVH</p>

266
Q

<p>What is the most likely cause of right axis deviation? List any alternative causes</p>

A

<p>RVH is most likely</p>

<p>normal variant - tall thin people</p>

<p>lateral MI</p>

<p>WPW syndrome</p>

<p>dextrocardia or R/L arm lead switch</p>

<p>left posterior fascicular block</p>

267
Q

<p>How would you detect left axis deviation?</p>

A

<p>Look for lead I and II "Leaving" each other - small lead I, negative lead II and III</p>

268
Q

<p>What is a more likely cause of left axis deviation, conduction issues orLVH?</p>

A

<p>conduction issues</p>

269
Q

<p>What is the mechanism of atrial flutter?</p>

A

<p>a re-entry circuit within right atrium</p>

270
Q

<p>List some causes of AF</p>

A

<p>ischaemic heart disease</p>

<p>thyrotoxicosis (hyperthyroidosis)</p>

<p>sepsis</p>

<p>valvular heart disease</p>

<p>alcohol excess</p>

<p>PE</p>

<p>hypokalaemia/hpomagnesaemia</p>

271
Q

<p>What is the mechanism of atrial tachycardia?</p>

A

<p>A single ectopic focus, outside the SAN that's triggering rapid depolarisation of the atria</p>

272
Q

<p>List causes of atrial tachycardia</p>

A

<p>digoxin toxicity</p>

<p>atrial scarring</p>

<p>catecholamine excess</p>

<p>congenital abnormatlities</p>

273
Q

<p>What is the mechanism of junctional tachycardia?</p>

A

<p>AV junctional pacemaker rhythm exceeds that of SAN. There is increased automaticity in AVN coupled with decreased automaticity in SAN.</p>

274
Q

<p>List causes of first degree heart block</p>

A

<p>increased vagal tone</p>

<p>athletic training</p>

<p>inferior MI</p>

<p>mitral valve surgery</p>

<p>Myocarditis (Lyme disease)</p>

<p>electrolyte disturbances (e.g. hyperkalaemia)</p>

<p>AV nodal blocking drugs:</p>

<p>beta blockers</p>

<p>CCBs</p>

<p>digoxin</p>

<p>amiodarone</p>

275
Q

<p>Describe the ECG trace in Mobitz type I 2nd degree heart block (Wenckebach phenomenon)</p>

A

<p>progressive lengthening of PR interval, followed by absent QRS (a non-conducted P wave), then cycle repeats</p>

<p>PR interval is longest just before dropped beat, and shortest just after</p>

276
Q

<p>What is the mechanism of Mobitz I 2nd degree heart block?</p>

A

<p>usually due to reversible conduction block at AVN - malfunctioning AVN cells progressively fatigue until they fail to conduct an impulse (dropped beat)</p>

277
Q

<p>List causes of Mobitz I 2nd degree heart block</p>

A

<p>Drugs: beta blockers CCBs digoxin amiodarone</p>

<p>Increased vagal tone (e.g. athletes)</p>

<p>inferior MI</p>

<p>myocarditis</p>

<p>cardiac surgery</p>

278
Q

<p>Describe the ECG trace in Mobitz type II 2nd degree heart block</p>

A

<p>intermittent non-conducted P waves without progressive prolongation of PR interval</p>

<p>P waves 'march through' at constant rate</p>

279
Q

<p>What is the mechanism of Mobitz II 2nd degree heartblock?</p>

A

<p>usually due to failure of conduction at His-Purkinje system</p>

<p>generally due to structural damage to conducting system "all-or-nothing"</p>

<p>- no progressive fatigue like in Mobitz I, instead His-Purkinje cells suddenly and unexpectedly fail to conduct</p>

280
Q

<p>List causes of Mobitz II 2nd degree heart block</p>

A

<p>Anterior MI (septal infarction wiht necrosis of bundle branches)</p>

<p>Idiopathic fibrosis of conducting system</p>

<p>cardiac surgery</p>

<p>inflammatory conditions (rheumatic fever, myocarditis, Lyme disease)</p>

<p>autoimmune (SLE, systemic sclerosis)</p>

<p>infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis)</p>

<p>hyperkalaemia</p>

<p>Drugs: beta blockers CCBs digoxin amiodarone</p>

281
Q

<p>List causes of complete heart block</p>

A

<p>inferior MI</p>

<p>AVN blocking drugs - CCBs, beta blockers, digoxin</p>

<p>Idiopathic degeneration of conducting system</p>

282
Q

<p>In what lead(s) is complete heart block best seen?</p>

A

<p>II and V1</p>

283
Q

<p>What is the mechanism of complete heart block?</p>

A

<p>there is complete absence of AV conduction - end point of second degree heart block.</p>

<p>Either progressive fatigue of AVN cells (mobitz I) or due to sudden onset of complete conduction throughout His-Purkinje system (mobitz II)</p>

284
Q

<p>What is the clinical significance of complete heart block? How would it be treated?</p>

A

<p>high risk of sudden cardiac death - urgent admission for cardiac monitoring, backup temporary pacing followed by permanent pacemaker insertion</p>

285
Q

<p>Describe what is seen:</p>

A

<p><strong>Complete heart block.</strong></p>

<p>atrial rate is 60bpm</p>

<p>ventricular rate is 27bpm</p>

<p>slow ventricular escape rhythm</p>

286
Q

<p>Describe what is seen:</p>

A

<p>2:1 heart block</p>

287
Q

<p>Describe what is seen:</p>

A

<p>3:1 heart block</p>

288
Q

<p>Describe what is seen:</p>

A

<p>Mobitz II second degree heart block</p>

<p>Intermittent P waves without progressive lengthening of PR interval</p>

289
Q

<p>Describe what is seen:</p>

A

<p>Mobitz I second degree heart block</p>

<p>aka Weckebach phenomenon</p>

<p>progressive lengthening of PR interval until a QRS fails to conduct (dropped beat)</p>

290
Q

<p>Describe what is seen:</p>

A

<p>First degree heart block</p>

<p>PR >0.2s (5 small squares)</p>

291
Q

<p>Describe what is seen:</p>

A

<p><strong>R</strong>ight axis deviation</p>

<p>leads I and II <strong>r</strong>eaching towards each other</p>

292
Q

<p>Describe what is seen:</p>

A

<p><strong>L</strong>eft axis deviation</p>

<p>Leads I and II are <strong>l</strong>eaving each other</p>

293
Q

<p>Describe what is seen:</p>

A

<p>atrial fibrillation</p>

<p>irregularly irregular, absent P waves</p>

294
Q

<p>Describe what is seen:</p>

A

<p>Atrial fibrillation</p>

<p>irregularly irregular</p>

<p>absent P waves</p>

295
Q

<p>Describe what is seen:</p>

A

<p>Atrial flutter</p>

<p>"saw tooth P waves" at c300bpm</p>

<p></p>

296
Q

<p>Describe what is seen:</p>

A

<p>atrial tachycardia</p>

<p>narrow complex tachycardia at 120bpm</p>

<p>each QRS is preceded by an abnormal p wave</p>

297
Q

<p>Describe what is seen:</p>

A

<p>junctional tachycardia</p>

<p>narrow QRS</p>

<p>retrograde P waves before, during or after QRS</p>

<p></p>

298
Q

<p>Describe what is seen:</p>

A

<p>RBBB</p>

<p>broad QRS</p>

<p>M complex in V1-3</p>

<p>W complex in V6 (slurred S waves)</p>

299
Q

<p>Describe what is seen</p>

A

<p>LBBB</p>

<p>broad QRS</p>

<p>dominant S in V1 - W</p>

<p>broad R in lateral leads- M</p>

300
Q

<p>Describe what is seen:</p>

A

<p>ST elevation in I and aVL (high lateral leads)</p>

<p>reciprocal ST depression in III and aVF (inferior leads)</p>

<p></p>

<p>acute MI localised to superior part of lateral wall -</p>

<p><strong>high lateral STEMI</strong></p>

<p>occluded first branch of LAD</p>

301
Q

<p>Describe what is seen</p>

A

<p>ST elevation in inferior (II, III, aVF) leads and lateral (I, V5-V6) leads</p>

<p>ST depression in V1-V3 suggests associated posterior infarction</p>

<p><strong>acute anterolateral STEMI with posterior extension</strong></p>

<p>occlusion of proximal circumflex</p>

302
Q

<p>Describe the ECG changes seen in right bundle branch block</p>

A

<p>broad QRS >120ms</p>

<p>RSR pattern in V1-3 ('m' shaped complex)</p>

<p>wide, slurred S waves in lateral leads (I, aVL, V5-6) giving a 'W' shaped complex in V6</p>

<p>(MarroW - M in V1, W in V6, rr = right)</p>

<p>possible ST depression in precordial leads (V1-3)</p>

303
Q

<p>Describe what is seen:</p>

A

<p>ST elevation in leads II, III and aVF</p>

<p>Q-wave formation in III and aVF</p>

<p>reciprocal ST depression and T wave inversion in aVL</p>

<p><strong>inferior STEMI</strong></p>

<p>circumflex occlusion - ST elevation in lead II = lead III</p>

304
Q

<p>Describe what is seen:</p>

A

<p>marked ST elevation in leads II, III and aVF</p>

<p>reciprocal changes in aVL</p>

<p><strong>inferior STEMI</strong></p>

<p>RCA occlusion as ST elevation in lead III> lead II</p>

305
Q

<p>What is the mechanism in RBBB?</p>

A

<p>activation of R ventricle is delayed as depolarisation has to spread across septum from left ventricle due to blockage of R bundle of Purkinje fibres</p>

<p></p>

<p>left ventricle is activated normally, so early part of QRS is unchanged, but delayed R ventricle activation produces a secondary R wave in V1-3 and a slurred S wave in lateral leads</p>

306
Q

<p>What does this V2 lead trace suggest?</p>

A

<p>posterior MI</p>

<p>horizontal ST depression</p>

<p>upright T wave</p>

<p>dominant R wave (R/S ratio >1)</p>

307
Q

<p>List causes of RBBB</p>

A

<p>RVH / cor pulmonale</p>

<p>PE</p>

<p>IHD</p>

<p>rheumatic heart disease</p>

<p>myocarditis or cardiomyopathy</p>

<p>degenerative disease of conduction system</p>

<p>congenital heart disease</p>

308
Q

<p>Describe the ECG changes seen in left bundle branch block</p>

A

<p>broad QRS >120ms</p>

<p>dominant S wave in V1 - W</p>

<p>broad, notched R wave in V6 - M</p>

<p>(WilliaM - W in V1, M in V6, ll = left)</p>

<p>no Q waves in lateral leads (I, V5-6, small Q waves in aVL)</p>

<p>prolonged R wave peak time >60ms in V5-6</p>

309
Q

<p>List causes of LBBB</p>

A

<p>aortic stenosis</p>

<p>ischaemic heart disease</p>

<p>dilated cardiomyopathy</p>

<p>anterior MI</p>

<p>primary degnerative disease (fibrosis) of the conducting system</p>

<p>hyperkalaemia</p>

<p>digoxin toxicity</p>

310
Q

<p>Describe the mechanisms in LBBB?</p>

A

<p>septum is activated R to L instead of L to R</p>

<p>spreads via right bundle branch, and then via septum to left bundle branch</p>

<p>this extends the QRS duration and removes Q waves in lateral leads</p>

<p>as the venrticles are activated sequentially, broad R waves are produced</p>

311
Q

<p>Describe what is seen:</p>

A

<p>ST elevation is maximal in anteroseptal leads (v1-V4)</p>

<p>Q waves present in septal leads (V1-2)</p>

<p>hyperacute (peaked) T waves in (V2-4)</p>

<p><strong>hyperactute anteroseptal STEMI</strong></p>

312
Q

<p>Describe what is seen:</p>

A

<p>ST elevation in V1-6 + I and aVL</p>

<p>minimal reciprocal depression in III and aVF</p>

<p><strong>anterior STEMI</strong></p>

313
Q

<p>Describe the ECG changes seen in junctional escape rhythms</p>

A

<p>no p waves, or p waves completely unrelated to QRS</p>

<p>normal QRS, maybe slightly narrow</p>

<p>slow HR</p>

<p></p>

314
Q

<p>What is the mechanism of junctional escape rhythms?</p>

A

<p>there are pacemaker cells at various points in the conduction system</p>

<p>junctional escape rhythm occurs when the rate of AV node depolarisation is less than the intrinsic rate of an ectopic pacemaker</p>

315
Q

<p>list causes of junctional escape rhythms</p>

A

<p>severe sinus bradycardia</p>

<p>sinus arrest</p>

<p>sino-atrial exit block</p>

<p>high-grade second degreeheart block (4:1, 5:1 etc)</p>

<p>complete heart block</p>

<p>hyperkalaemia</p>

<p>drugs:</p>

<p>beta blockers</p>

<p>CCBs</p>

<p>digoxin poisoning</p>

316
Q

<p>Describe the ECG changes seen in a ventricular escape rhythm</p>

A

<p>ventricular rhythm of 20-40bpm</p>

<p>broad QRS complexes, possibly with a LBBB or RBBB morphology</p>

317
Q

<p>Describe what is seen:</p>

A

<p>ventricular fibrillation</p>

318
Q

<p>what arteries are likely to be blocked in a lateral STEMI</p>

A

<p>LAD and LCx</p>

319
Q

<p>Describe what is seen:</p>

A

<p>sinus rhythm</p>

<p>broad QRS with slurred upstroke - delta wave</p>

<p>dominant R wave in V1</p>

<p><strong>Wolff-Parkinson-White</strong></p>

320
Q

<p>Describe the ECG changes seen in a lateral STEMI</p>

A

<p>ST elevation in the lateral leads</p>

<p>(I, aVL, V5-6)</p>

<p>reciprocal ST depression in inferior leads (III and aVF)</p>

321
Q

<p>Describe what is seen</p>

A

<p><strong>Digoxin effect</strong></p>

<p>"sagging" ST segements</p>

<p>hockey stick T waves</p>

322
Q

<p>Describe the ECG changes seen in an inferior MI</p>

A

<p>ST elevation in II, III and aVF</p>

<p>progressive development of Q waves in II, III and aVF</p>

<p>reciprocal depression in aVL (±lead I)</p>

<p></p>

323
Q

<p>Describe what is seen:</p>

A

<p><strong>pericarditis</strong></p>

<p>widespread concave ST elevation and PR depression throughout V2-V6 and I, II, aVL, aVF</p>

<p>reciprocal ST depression and PR elevation in aVR</p>

324
Q

<p>Which artery most commonly causes an inferior STEMI?</p>

A

<p>right coronary artery</p>

<p>(more ST elevation in lead III than II)</p>

<p>LCx can cause it less commonly</p>

<p>(ST elevation in lead II = lead III)</p>

<p></p>

325
Q

<p>Describe the ECG changes seen in posterior MI</p>

A

<p>In V1-V3:</p>

<p>horizontal ST depression</p>

<p>tall, broad R waves</p>

<p>upright T waves</p>

<p>dominant R wave in V2</p>

326
Q

<p>Occlusion of what artery causes an anterior STEMI?</p>

A

<p>LAD</p>

327
Q

<p>Describe the ECG changes seen in anterior STEMI</p>

A

<p>ST elevation with Q wave formation in the precordial leads (V1-6) ± the high lateral leads (I and aVL)</p>

<p>reciprocal ST depression in the inferior leads (mainly III and aVF)</p>

328
Q

<p>In what leads would ST elevation be maximal in a septal STEMI?</p>

A

<p>V1-2</p>

329
Q

<p>In what leads would ST elevation be maximal in an anterior STEMI?</p>

A

<p>V2-5</p>

330
Q

<p>In what leads would ST elevation be maximal in an anteroseptal STEMI?</p>

A

<p>V1-4</p>

331
Q

<p>In what leads would ST elevation be maximal in an anterolateral STEMI?</p>

A

<p>V3-6, I + aVL</p>

332
Q

<p>What is seen in an NSTEMI?</p>

A

<p>pathological Q waves only</p>

333
Q

<p>Describe the ECG changes that may be seen in a ventricular tachycardia</p>

A

<p>very broad QRS (>160ms)</p>

<p>no p waves</p>

<p>T waves difficult to identify</p>

<p>rate > 200bpm</p>

<p></p>

334
Q

<p>Describe the ECG changes seen in ventricular fibrillation</p>

A

<p>chaotic irregular deflections of varying amplitude</p>

<p>no identifiable P waves, QRS complexes or T waves</p>

<p>rate 150-500bpm</p>

<p></p>

335
Q

<p>Causes of VF</p>

A

<p>myocardial iscahemia/infarction</p>

<p>electrolyte abnormalities</p>

<p>cardiomyopathy (dilated, hypertrophic, restrictive)</p>

<p>Long QT</p>

<p>Brugada syndrome</p>

<p>Drugs</p>

<p>environmental - electrical shock, drowing, hypothermia</p>

<p>PE</p>

<p>cardiac tampnoade</p>

<p>blunt trauma</p>

<p></p>

336
Q

<p>Describe the ECG changes seen in Wolff-Parkinson-White syndrome</p>

A

<p>sinus rhythm</p>

<p>right axis deviation</p>

<p>short PR interval</p>

<p>sluured upstroke of the QRS complex, best seen in V3 and V4 - wide QRS due to this delta wave</p>

<p>dominant R wave in V1</p>

<p></p>

337
Q

<p>what is the mechanism in Wolff-Parkinson-White?</p>

A

<p>accessory pathway, usually from left atria, allows direct transmission of signal, bypassing AVN (hence short PR)</p>

<p></p>

<p></p>

338
Q

<p>Describe the "digoxin effect"</p>

A

<p>downsloping ST depression with "sagging" appearance</p>

<p>flattened, inverted or biphasic T waves - hockey stick</p>

<p>shortened QT</p>

339
Q

<p>What is the mechanism behind the digoxin effect?</p>

A

<p>shortening of atrial and ventricular refractory periods - producing short QT</p>

<p>increased vagal effects at AVN - prolonged PR interval</p>

340
Q

<p>Describe the ECG changes seen in pericarditis</p>

A

<p>widespread concave ST elevation and PR depression</p>

<p>Reciprocal ST depression and PR elevation in aVR</p>

<p></p>

341
Q

<p>What is P Pulmonale?</p>

A

<p>peaked P waves</p>

342
Q

<p>What is seen in p mitrale?</p>

A

<p>bifid p waves</p>

343
Q

<p>list causes of p pulmonale</p>

A

<p>anything that cause right atrial enlargement</p>

<p>e.g. tricuspid stenosis, pulomnary hypertension</p>

2a Systems🩺 (12 decks)

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