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CardioResp Block > Cardio Revision > Flashcards

Cardio Revision Flashcards

1
Q

cause of S1 (1st heart sound)?

A

vibrations through wall of heart as AV valves close during systole-mitral and tricuspid.

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2
Q

causes of a loud S1?

A

mitral stenosis- no gradual decrease in bflow in L ventricle at end of diastole so valves at their max. excursion at end and shut rapidly- the tapping apex- loud S1.

shortened diastolic filling time-AV valves more open at end of diastole as not had time to shut e.g. tachycardia, exercise, short PR interval e.g. WPW syndrome- accessory pathway conducts atrial depolarisation more quickly to the ventricles as no delay at the AVN.

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3
Q

causes of a soft S1?

A

prolonged diastolic filling time e.g. long PR interval e.g. hyperkalaemia, mitral incompetence.
HF- AV vales can’t open fully in diastole as ventricle still filled with blood after previous systole failed to eject out normal fraction, so valve is almost closed when systole starts.

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4
Q

causes of a soft S2?

A

aortic stenosis

pulmonary stenosis

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5
Q

causes of a loud S2?

A

loud aortic valve closure- HTN, tachycardia, transposition.

loud pulmonary valve closure- pulmonary HTN e.g. secondary to chronic lung disease e.g. COPD, or PE.

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6
Q

causes of a third heart sound?

A

rapid ventricular filling during early diastole, and the incoming blood rush is decelerated as a stiff or dilated ventricle suddenly reaches its elastic limit.

MI, HF, cardiomyopathy, HTN (pressure overload).

dilated LV with rapid ventricular filling e.g. mitral regurge, VSD, or poor LV function e.g. post MI or dilated cardiomyopathy. In elderly pts, indicates congestive heart failure.

normal in young pts- aged 30 or younger.

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7
Q

cause of a fourth heart sound which occurs just before S1?

A

this is always abnormal and represents atrial contraction against a stiff ventricle-may be hypertrophied or non-compliant e.g. due to aortic stenosis, or hypertensive heart disease which causes a thickened LV wall, or stiffness due to scar tissue e.g. with CHD.
low pitched

MI, HTN, HF, cardiomyopathy

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8
Q

cause of mid-systolic click?

A

mitral valve prolapse

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9
Q

timing on prosthetic mitral and aortic valve clicks?

A

S1 and S2 respectively

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10
Q

murmur in aortic stenosis?

A

ejection systolic, radiating to carotids
audible gap between murmur and S2
S2 quiet with severe stenosis
lub-whooshhh dub

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11
Q

murmur in aortic regurgitation?

A

early diastolic

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12
Q

murmur in mitral stenosis?

A

mid-diastolic rumbling, heard best in apex area with bell held lightly over apex and pt lying on the L side.

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13
Q

murmur in mitral regurgitation?

A

pansystolic, no gap between murmur and S2, S1 quiet

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14
Q

name given to an insulating layer that exists between the atrium and the ventricle?

A

annulus fibrosus

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15
Q

why do the coronary arteries fill during diastole?

A

when the heart is relaxed, the arteries are not occluded by valve cusps and are not squeezed by myocardial contraction.

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16
Q

origin of the R and L coronary arteries?

A

the R and L coronary sinuses respectively

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17
Q

describe how palpitations would be experienced by a pt with premature beats (ectopics)?

A

felt as a pause, followed by a forceful beat

as premature beat usually followed by a pause as heart resets itself before next normal beat, and then next beat more forceful as heart has had longer to relax and fill with more blood before this beat due to longer diastolic period.

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18
Q

how might the rhythm of the heart be described on auscultation if there is an S3 with a sinus tachycardia, or an S4 with a sinus tachycardia?

A

gallop rhythm
S3 and sinus tachycardia=ken-tucky rhythm
S4 and sinus tachycardia=tenne-ssee rhythm

if both occur in a tachycardia e.g. with a PE, they may summate and appear as a single sound-summation gallop.

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19
Q

when might an ejection systolic click be heard?

A

early in systole with bicuspid aortic valves, and if raised BP.

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20
Q

how many cusps do the AV and semilunar valves of the heart comprise normally?

A

AV: mitral=bicuspid, then tricuspid=3
semilunar: both aortic and pulmonary are tricuspid=3 cusps.

21
Q

when might an opening snap be heard?

A

precedes mid-diastolic murmur of mitral and tricuspid stenosis.
indicates a pliable (noncalcified) valve.

22
Q

how does the pitch of heart murmurs detected differ between the bell and diaphragm of the stethoscope?

A

bell-low-pitched e.g. mitral stenosis

diaphragm- high-pitched e.g. aortic regurge

23
Q

causes of diminished heart sounds?

A

emphysema
obesity
pericarditis-muffled

24
Q

causes of a split S2?

A

physiologic-max occurring at peak inspiration
paradoxical-max occurring at peak expiration e.g. aortic stenosis, LBBB, both causing a delay in aortic valve closure so it occurs after the pulmonic.

25
Q

cause of fixed splitting of S2?

A

atrial septal defect

26
Q

causes of ejection systolic murmurs (crescendo-decrescendo quality)?

A

aortic stenosis and sclerosis
pulmonary stenosis
hypertrophic obstructive cardiomyopathy (HCM)

high output states e.g. pregnancy, tachycardia

27
Q

causes of pansystolic murmurs?

A

mitral regurge
tricuspid regurge
VSD

28
Q

causes of radio-femoral delay?

A

coarctation of aorta

29
Q

causes of radio-radial delay?

A

aortic arch aneurysm

30
Q

causes of angina pectoris OTHER than coronary heart disease?

A

aortic stenosis

hypertrophic cardiomyopathy-increased myocardial O2 demand due to increased LV afterload.

31
Q

when might pain be absent in a pt with an MI?

A

elderly

presence of diabetes mellitus-autonomic neuropathy

32
Q

how are R sided heart murmurs heard best?

A 
during Inspiration (rIght)
as increased venous return to R side of heart
33
Q

how can murmurs be graded?

A

1-6
1=very faint
2=soft
3=heard easily
4= loud, with a palpable thrill
5=very loud, with thrill. may be heard when stethoscope is partly off the chest.
6=very loud, with thrill. may be heard with stethoscope entirely off the chest.

34
Q

HF classification?

A 
New York Heart Association (NYHA), based on symptoms
class 1- no limitation of physical activity
class 2- slight limitation of physical activity (symptomatically mild HF)
class 3- marked limitation of physical activity (moderate HF)
class 4- symptoms at rest (severe HF)
35
Q

normal left ventricular ejection fraction (LVEF)?

A

55-70%

36
Q

what LVEF may classify as mild LV systolic dysfunction?

A

between 40-45 and 55%

37
Q

what LVEF may classify as moderate LV systolic dysfunction?

A

35-40/45%

38
Q

what LVEF may classify as severe LV systolic dysfunction?

A

less than 35%

39
Q

causes of mitral stenosis?

A

50% have history of rheumatic fever or chorea- this is the 3rd most common manifestation of rheumatic fever, and may occur in isolation or alongside other features of the disease e.g. joint pain, and rheumatic mitral stenosis is much more common in women.
old age and calcification

40
Q

signs of mitral stenosis o/e and why?

A

pulse-irregularly irregular- AF, due to high LA pressure
malar flush
tapping apex beat on palpation due to palpable S1
auscultation: loud S1- valve remains open until late in diastole as no reduction in b.flow towards the end, with continuous high LA pressure.
L parasternal heave due to RV hypertrophy as PA HTN from LA pressure back up.
‘opening snap’=high pitched sound must after S2, with high LA pressure. if severe, AP increases and mitral valve opens earlier in ventricular diastole, so shorter gap between S2 (dub) and ‘opening snap’.
RUMBLING MID-DIASTOLIC murmur, best heard at apex with bell held lightly and pt lying on their L side. LUB De Derrr.

41
Q

mitral stenosis indication with investgations?

A

CXR: LA enlargement
signs of pulmonary oedema: bilateral increased lung marking-perihilar ‘bats wing’ shadowing, septal (kerley B) lines- fluid accumulation between the seconday lobules of the lung.

ECG: AF- irregularly irregular rhythm, absent P waves, irregular baseline
bifid P wave- L atrial hypertrophy-L atrial delay
R axis deviation and tall R waves in V1 and V2 due to RV hypertrophy.

42
Q

define pulmonary oedema

A

excess fluid in the lung interstitium and alveoli, due to leakage from the pulmonary capillary network, and with fluid filtration exceeding the ability of the lymphatics to clear the fluid.

43
Q

2 main types of pulmonary oedema?

A

cardiogenic- raised pulmonary capillary hydrostatic pressure due to LHF
noncardiogenic- often minimal elevation of pulmonary capillary pressure except in oliguric renal failure causing vol. overload. May be altered alveolar-capillary membrane permeability e.g. ARDS, or lymphatic insufficiency e.g. following lung transplant or lymphangitic carcinomatosis. May be lowered oncotic pressure e.g. nephrotic syndrome, liver cirrhosis and protein-losing enteropathy.
May be neurogenic e.g. following status epilepticus.

44
Q

causes of mitral regurge?

A

mitral valve prolapse
ruptured papillary muscles following MI
rheumatic mitral regurge- shrunken and fibrotic cuffs
cardiomyopathy
CT disorders e.g. Marfan’s, Ehlers Danlos and osteogenesis imperfecta.

45
Q

ECG in mitral regurge?

A

bifid P wave-LA hypertrophy
tall R wave in V5 and V6- LV hypertrophy: Sokolow-Lyon voltage criteria- S wave in V1 and R wave in V5 and V6 which is more than 35mm or 3.5 large squares.

46
Q

ECG pattern of aortic stenosis?

A

LV hypertrophy- S wave V1 and tall R wave V5 and V6

LV strain pattern- depressed ST segments and T wave inversion in leads orientated towards LV e.g. I, aVL, V5 and V6.

47
Q

signs of aortic stenosis?

A

pulse-slow rising character, volume= low with narrow pulse pressure
forceful apex beat
ejection systolic murmur radiating to carotids.

48
Q

the apex of the ventricle refers to which location?

A

the bottom of the ventricle

contraction is from apex to base*

49
Q

the apex of the ventricle refers to which location?

A

the bottom of the ventricle

contraction is from apex to base*

CardioResp Block (11 decks)

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