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Phase 2a - Systems > Cardio 1 > Flashcards

Cardio 1 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

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.

53
Q

name 2 angiotensin receptor blockers (ARBs)?

A

losartan, candesartan

54
Q

how do angiotensin receptor blockers work?

A

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

55
Q

give 3 causes of mitral stenosis

A

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

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.

57
Q

give 3 symptoms of mitral stenosis

A

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

58
Q

what is the heart murmur heard in mitral stenosis?

A

rumbling mid-diastolic murmur

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.

60
Q

how would mitral stenosis be treated?

A

diuretics - decrease pre load.

balloon valvuloplasty / valve replacement.

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

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.

63
Q

give 3 symptoms of mitral regurgitation

A

dyspnoea, fatigue, palpitations, infective endocarditis

64
Q

what murmur is heard in mitral regurgitation?

A

pansystolic murmur

65
Q

what does a bifid P wave indicate on ECG?

A

bifid P waves = p mitrale - mitral valve disease

66
Q

what investigations would you perform in valvular heart disease?

A

ECG, CXR, echo ± cardiac catherization

67
Q

what would you see on CXR in mitral regurgitation?

A

enlarged LA and LV, mitral valve calcification, pulmonary oedema

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.

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.

70
Q

what is the classical triad of symptoms in aortic stenosis?

A

SAD:
Syncope
Angina
Dyspnoea - heart failure

71
Q

what murmur is heard in aortic stenosis?

A

ejection systolic murmur

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)

73
Q

what would you see on a CXR of a patient with aortic stenosis?

A

normal heart size, prominent ascending aorta, valvular calcification

74
Q

how would you treat aortic stenosis?

A

prompt valve replacement

75
Q

what are the most common causes of aortic regurgitation?

A

rheumatic fever and infective endocarditis

76
Q

give 3 causes of acute aortic regurgitation

A

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

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

78
Q

give 3 symptoms of aortic stenosis

A

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

79
Q

what murmur is heard in aortic regurgitation?

A

early diastolic murmur.

“at L sternal edge in 4th intercostal space”

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.

81
Q

how would you treat aortic regurgitation?

A

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

82
Q

what are the 3 main cardiomyopathies?

A

hypertrophic (HCM), dilated (DCM) and restrictive

83
Q

what is hypertrophic cardiomyopathy?

A

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

84
Q

what causes hypertrophic cardiomyopathy?

A 
50% = autosomal dominant 
50% = sporadic.
85
Q

what is the major consequence of hypertrophic cardiomyopathy?

A

sudden cardiac death in young people

86
Q

name 2 clinical features of hypertrophic cardiomyopathy

A

can be asymptomatic.

angina, syncope, sudden death, systolic thrill.

87
Q

what investigations might you carry out in cardiomyopathy?

A

CXR, ECG, echo.

cardiac MR.

88
Q

how would you treat hypertrophic cardiomyopathy?

A

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

89
Q

give 3 causes of dilated cardiomyopathy

A

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

90
Q

give 3 clinical features of dilated cardiomyopathy

A

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

91
Q

how would you treat dilated cardiomyopathy?

A

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

92
Q

what is restrictive cardiomyopathy?

A

rigid myocardium restricting diastolic ventricular filling.

93
Q

give 2 causes of restrictive cardiomyopathy

A

amyloidosis. haemachromatosis. sarcoidosis. scleroderma. idiopathic.

94
Q

give 3 clinical features of restrictive cardiomyopathy

A

constrictive pericarditis. raised JVP. oedema, ascites, features of RVH.

95
Q

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

A

cardiac catheterisation.

96
Q

what are the 2 causes of ventricular septal defect?

A

congenital.

acquired post-MI.

97
Q

how might a ventricular septal defect present?

A

severe heart failure in infancy.

OR - asymptomatic, detected later in life

98
Q

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

A

louder

99
Q

what murmur is heard in VSD?

A

harsh pansystolic murmur at left sternal edge, with systolic thrill

100
Q

give 2 complications of a ventricular septal defect

A

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

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.

102
Q

how would you manage a ventricular septal defect?

A

medical support until spontaneous closure.

OR - surgical patch repair or device closure.

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.

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.

105
Q

what investigations are used to diagnose most structural heart defects?

A

echo.

cardiac catheter.

106
Q

how would you treat an ASD?

A

transcatheter or surgical closure

107
Q

what genetic disorder is associated with atrioventricular septal defects?

A

Downs syndrome

108
Q

what structures are involved in an atrioventricular septal defect?

A

atrial septum, ventricular septum, mitral and tricuspid valve

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.

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.

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.

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

113
Q

how would you treat a PDA?

A

indometacin (prostaglandin) can stimulate closure.

if large - surgical or percutaneous closure.

114
Q

what is Eisenmenger’s syndrome?

A

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

115
Q

what is coarctation of the aorta?

A

congenital narrowing of the descending aorta

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.

117
Q

how would you treat coarctation of the aorta?

A

surgery or balloon dilation ± stenting

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.

119
Q

give some clinical features of pulmonary stenosis

A

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

120
Q

how would you treat pulmonary stenosis?

A

ballon valvuloplasty.

open vavlotomy.

121
Q

what are the 4 features of tetralogy of Fallot?

A

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

122
Q

what causes tetralogy of Fallot?

A

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

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.

124
Q

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

A

boot shaped heart

125
Q

how is tetralogy of Fallot managed?

A

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

Phase 2a - Systems (18 decks)

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