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MD3001 > cardiovascular disease > Flashcards

cardiovascular disease Flashcards

1
Q

what might you see on an ecg with angina

A

ST depression

due to sub endocardial ischaemia

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2
Q

what two mechanisms control coronary flow

A

autoregulation / myogenic

metabolic regulation

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3
Q

what is coronary flow reserve

A

maximum vasodilation - autoregulated flow

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4
Q

what determines myocardial oxygen consumption

A 
tension 
contractility
HR
basal  activity 
mass of tissue
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5
Q

what 4 types of drug are used in angina

A

B blockers
nitrates
ca channel blockers
Ikf channel inhibitors

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6
Q

what events increase the likelihood of mi

A 
time of day
inflammatory activity
infection
high BP 
catecholamines (adrenaline)
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7
Q

what preventative drugs would you give someone after a stemi

A

b blockers
ace inhibitors
statins

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8
Q

what are common complications of stemis

A 
arrhythmia
heart failure
rupture
mitral valve insufficiency
VSD
mural thrombus and embolism
LV dilation
recurrent MI
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9
Q

how would you treat a nstemi

A

antiplatelet
b blockers and nitrates
statin
ace inhibitors

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10
Q

describe age related vascular changes

A

fibrosis
accumulation of ground substances
fragmentation of elastic lamina

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11
Q

what are the 3 components of atheroma

A

lipid deposition
inflammation
fibrosis

also: neovascularisation, smooth muscle, macrophages, lymphocytes, collagen

necrotic core: cell debris, cholesterol crystals, foam cells, debris

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12
Q

where are atherosclerotic aneurysms usually found

A

abdominal aorta, distal to renal arteries

saccular or fusiform, may contain thrombi. often palpable or abdom bruits

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13
Q

where are the origins of dissecting aneurysms found

A

aortic valve

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14
Q

what is the most common cause of death in a dissecting aneurysm

A

dissection outward into the peritoneal, pleural or pericardial cavities

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15
Q

what might be the result of a berry aneurysm

A

sub arachnoid haemorrhage

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16
Q

what is a capillary microaneurysm

A

small aneurysm of the middle cerebral artery. may lead to intra cerebral haemorrhage

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17
Q

where are syphilitic microaneurysm normally found

A

thoracic aorta

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18
Q

what is a mycotic aneurysm

A

wall of artery is weakened often in the brain

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19
Q

what is giant cell arteritis

A

granulomatous inflammation of arteries, usually temporal, vertebral and opthalmic

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20
Q

what is takaysu arteritis

A

pulseless disease- (intermittent claudication of UL arteries)

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21
Q

what is polyarteritis nodosa

A

arteries of abdo organs

fibrinoid necrosis

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22
Q

what is kawasakis disease

A

very young children

fever , eye and mouth lesions

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23
Q

what are the type of vascular tumours (benign)

A 
angioma 
haemangioma
juvenile
capillary
cavernous
lymphangioma
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24
Q

what are some types of malignant tumours

A

angiosarcoma
kaposis sarcoma
angioproliferative tumour

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25
Q

what causes dysrhythmia

A

changes to heart cells

changes in conduction of the impulse

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26
Q

what are the 4 classes of arrhythmias

A

atrial/ SV
junctional (AVN)
ventricular
tachy/brady cardia

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27
Q

what are the 4 types of arrhythmia event

A

heart block
ectopic
delayed after depolarisation
circus re entry

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28
Q

what does a delayed after depolarisation cause

A

atrial or ventricular tachycardias

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29
Q

what usually causes heart block

A

ischaemia

usually affects AVN, slows or blocks impulses

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30
Q

describe the features of a first degree heart block

A

conduction is slowed
abnormally long PR interval
every p wave is passed to QRS

normal PR interval is 0.12- 0.2

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31
Q

describe a mobitz 2 heart block

A

some Ps don’t get through

constant PR interval except when there is missed QRS

32
Q

describe a wenkebach heart block

A

progressive lengthening of the PR Interval until a dropped QRS

33
Q

describe a 3rd degree heart block

A

complete block

ventricles depolarise at their inherent rate

34
Q

what are ectopic pacemakers

A 
when other areas of the heart develop pacemaker activity
eg due to 
damage
sympathetic activity
catecholamines
digoxin

ischaemic damage may cause cells to become leaky to Na
catecholamines (B1 rec) increase rate of depolarisation

35
Q

what is an early after depolarisation

A

occurs towards the end of phase 2

triggered by increase in Ca permeability
can set off self sustaining depolarisations - tachycardia

long QT

36
Q

what is a delayed after depolarisation

A

increase in Ca eg due to cardiac glycosides causes an after depolarisation

can become self perpetuating and trigger an AP

may be due to delayed repolarisation (long qt)

can lead to ventricular dysrhythmia

37
Q

what is circus reentry

A

an electrical impulse re enters a region of the heart after its refractory period
comes from an unusual direction and at the wrong time

no extinction by collision due to impulse dying out

may cause paroxysmal tachycardia

38
Q

what is wolf Parkinson white syndrome

A

due to an additional electrical connection between the atria and ventricles thereby passing the AVN
causes paroxysmal tachycardia and re entry
delta waves on the ecg
wide qrs
st changes

39
Q

how might you diagnose a left anterior fascicular hemiblock

A

left axis deviation

40
Q

how might you diagnose a left posterior fascicular hemiblock

A

right axis deviation

41
Q

what might cause a bradycardia

A 
b blockers
diltiazem (Ca channel blocker)
hypothyroidism
sinus node disease
electrolyte abnormalities

you might treat with a pace maker

42
Q

how do you diagnose a right bundle branch block

A

widened qrs complex

two r waves

43
Q

how do you diagnose a left bundle branch block

A

widening of QRS complex

a notch in the qrs

44
Q

what is a narrow complex tachycardia

A

superventricular
atrial/junctional/re-entry
usually no p waves

45
Q

what is a broad complex tachycardia

A

usually ventricular

46
Q

how would you treat an AV node tachycardia eg avnrt or avrt

A

adenosine

causes transient AV block

47
Q

how would you treat AF

A

diltazem, verapamil, b blocker

48
Q

what is polymorphic ventricular tachycardia also known as

A

torsade de points

must also have QT prolongation. associated with early after depolarisations

sudden cardiac death after adrenergic setting

49
Q

what might cause secondary hypertension

A

renal disease, phaeochromocytoma, cushings, diabetes, coarctation, eclampsia
drugs eg illegal drugs and contraceptive pill

50
Q

what is stage 1 hypertension

A

140/90 in the clinic

135/85 ambulatory

51
Q

what is stage 2 hypertension

A

160/100

52
Q

what is severe hypertension

A

180 syst
or 110 diastolic

may have left axis deviation and inverted t waves on the ecg
albinuria

53
Q

what can cause an increase in TPR

A

sympathetic nerve activity

increased vascular reactivity

54
Q

what are the effects of hypertension on the body

A

accelerated atherosclerosis and narrowing
retinopathy
renal failure
dilatation

55
Q

what is stenosis

A

narrowing of the valve outlet caused by thickening of valve cusps, increased rigidity or scarring

56
Q

what is valve incompetence

A

an incomplete seal allowing blood to flow backwards

57
Q

what are common causes of valve disease

A

congenital heart disease
cardiomyopathy
acquired - rheumatic fever, MI, age, calcific stenosis, endocarditis

58
Q

what might result from aortic stenosis

A 
RVH
syncope
sudden cardiac death 
dyspnoea
angina
59
Q

what are causes of aortic incompetence

A

marfan’s
rheumatic fever
infective endocarditis(may causes perforation)

may have calcification of a congenital bicuspid valve

60
Q

what is the most common cause of mitral incompetence or stenosis

A

rheumatic fever

leads to pulmonary hypertension and RVH due to back pressure
may cause atrial fibrillation

61
Q

what is infective endocarditis

A

infection of the valve with thrombotic vegetations

62
Q

what are the risk factors for infective endocarditis

A

valve damage
dental
catheterisation
immunosuppression

63
Q

what is rheumatic fever

A

3 weeks post streptococcal infection (usually pharyngitis)
immune mediated
occurs in children
multisystem disease

64
Q

what might be found in a vegetation

A

group D strep
gut commensals
skin strep

65
Q

what are the complications of endocarditis

A 
splinter haemorrhages
clubbing 
emboli
renal infarcts
pneumonia 
osler's nodes and janaway lesion
66
Q

what is acute on chronic heart failure

A

chronic failure becomes decompensated by an acute event

67
Q

what is systolic failure

A

failure to pump blood in systole
reduced ejection fraction

may be caused by 
reduced contractility
volume overload
pressure overload (stenosis/hypertension)
regurgitation
dilated cardiomyopathy 
severe hypertension 
increased preload (EDV) dilation and increased tension
68
Q

what is diastolic failure

A

failure of the ventricle wall to relax
restrictive, stiff ventricle (cardiomyopathy)
may be caused by scaring or amyloidosis
also may be increased wall thickness( hypertrophy)
or delayed relaxation or increased heart rate
tamponade
normal ejection fraction but impaired filling

69
Q

what are the causes of heart failure

A 
coronary heart disease
hypertension
cardiomyopathies
drugs
toxins
endocrine
nutritional 
infiltrative
70
Q

what is backward heart failure

A

increased venous pressure

increased heart filling pressures

71
Q

what is forward failure

A

reduced tissue perfusion

usually advanced failure

72
Q

what do cardiac glycosides inhibit

A

Na/ Ca exchange

73
Q

what is the NYHA classification of heart failure

A

1 no limitation
2 slight limitation on physical activity
3 marked limitation
4 unable to carry out physical activity, discomfort at rest

74
Q

what are the compensatory mechanisms in heart failure

A

frank starling
sympathetic activity
renin angiotensin

75
Q

what is the problem with RAAS as compensation for heart failure

A

increased renin release and angiotensin and aldosterone

vasoconstriction, water reabsorption, increased preload
inflammatory response leading to fibroblast deposition

76
Q

what is the problem with sympathetic activity as compensation for heart failure

A

tachycardia, vasoconstriction, decreased tissue perfusion, increases the heart workload
desensitisation of b receptors

77
Q

what is the problem with the frank starling mechanism in heart failure

A

pulmonary congestion

increased muscle stretch and O2 consumption

MD3001 (33 decks)

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