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Medical Studies 1 > CVS Week 3 > Flashcards

CVS Week 3 Flashcards

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USMLE® Step 1 flashcards
1
Q

describe the histological structure of the pericardium outermost to innermost

A

OUTERMOST

fibrous pericardium - strong CT

serous parietal pericardium

pericardial fluid

serous visceral pericardium

adipose tissue

INNERMOST

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2
Q

what layers can the heart be divided into outermost to innermost

A

pericardium (mesothelium)

epicardium (adipose tissue, nerves, blood vessels)

myocardium (cardiomyocytes, conducting system)

endocardium (inner walls of ventricles + atria)

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3
Q

describe the histological structure of cardiomyocytes

A

myofilament arranged in sarcomeres

at the level of the Z-line, T-tubules penetrate the cells, forming direct contact with the sarcoplasmic reticulum to form structures known as Diads

numerous mitochondria to meet high energy demands

connected by intercalated discs which allow for synchronised contraction

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4
Q

explain how the contraction of cardiomyocytes are different to skeletal muscle contraction in terms of calcium

A

cardiomyocytes use calcium-induced calcium release for contraction

this is where extracellular calcium influx triggers further calcium release from the sarcoplasmic reticulum

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5
Q

describe sarcomeres

A

fundamental contractile units within cardiomyocytes which are separated by Z-lines

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6
Q

describe intercalated disks

A

specialised cell junctions that facilitate electrical and mechanical coupling

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7
Q

describe couplons

A

junctional complexes where T-tubules and sarcoplasmic reticulum meet, which is crucial for calcium signalling

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8
Q

describe axial tubules

A

intercellular tubules that assist in distributing calcium for excitation-contraction coupling within cardiomyocytes

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9
Q

describe the arrangement of cardiomyocytes that enable the heart to contract efficiently and in a twisting (wringing) motion

A

cardiac myocytes = arranged in helical arrangement around heart > facilitates efficient contraction / characteristic twisting or wringing motion during systole
this orientation > coordinated muscle contraction > enhanced ejection of blood from ventricles

longitudinal, transverse + oblique layers of muscle contribute to this complex motion > maximal Q as necessary

intercalated disks contain gap junctions + desmosomes > synchronise contraction + maintain structural integrity

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10
Q

describe the histological structure of the cardiac valves

A

trilaminar structure which contributes to the valves’ function and integrity - fibrosa, spongiosa, ventricularis/atrialis

almost avascular

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11
Q

describe the fibrosa layer of the cardiac valves

A

central layer composed predominantly of collagen fibres

provides structural integrity and rigidity to withstand mechanical stresses during valve closure

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12
Q

describe the spongiosa layer of the cardiac valves

A

middle layer with loose CT, rich in proteoglycans and glycosaminoglycans, acting as a shock absorber to facilitate smooth valve motion

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13
Q

describe the superficial (ventricularis/atrialis) layer of the cardiac valves

A

ventricularis = on the ventricular side

atrialis = on the atrial side

outermost layer with abundant elastic fibres (essential so they can adapt to varying pressure gradients), offering flexibility and resilience to accomodate pressure changes

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14
Q

if cardiac valves are almost avascular, how do they get nutrients and expel wastes

A

rely on simple diffusion from surrounding blood for nutrient and waste exchange

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15
Q

what are the 4 specific phases that occur during diastole

A

isovolumetric relaxation

rapid inflow into ventricles

diastasis (reduced inflow into ventricles)

atrial contraction

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16
Q

what are the 3 specific phases that occur during systole

A

irosvolumetric contraction

rapid ventricular ejection

reduced ventricular ejection

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17
Q

flow direction is governed by what

A

pressure gradients between chambers

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18
Q

outline the direction of flow in terms of pressure changes and valve openings/closings during diastole/systole

A

LV filling occurs when LA pressure > LV pressure

as LV fills, LV pressure > LA pressure which forces the mitral valve to close

the initation of LV contraction leads to increased LV pressure

as LV pressure > aortic pressure, the aortic valve opens

with ongoing LV contraction, both LV pressure and aortic pressure increase

as LV empties, LV pressure decreases and diastole begins

the aortic valve closes once LV pressure < aortic pressure

once LV pressure < LA pressure, the mitral valve opens

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19
Q

what creates heart sound 1

A

mitral and tricuspid valves closing

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20
Q

what creates heart sound 2

A

aortic and pulmonary valves closing

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21
Q

what creates heart sound 3

A

ventricular filling

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22
Q

what creates heart sound 4

A

vibration of ventricular wall during atrial contraction

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23
Q

outline the splitting of heart sounds

A

S1 and S2 can be split due to differences in timing between valves ie left vs right side

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24
Q

what is pre load

A

tension applied to cardiac muscle, due to filling of ventricles, that passively stretches it to a new length

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25
Q

what is the frank starling mechanism

A

describes the relationship b/w LV end-diastolic volume and LV output

that is, increased venous return leads to increase LV EDV which leads to increase in stroke volume leading to increased cardiac output

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26
Q

what constitutes pre load

A

central venous pressure ie venous return

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27
Q

what constitutes afterload

A

aortic pressure and properties of arterial system

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28
Q

what is afterload

A

resistance against which heart must pump in order to eject blood from LV

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29
Q

describe the effect of the sympathetic nervous system when faced with a physiological stressor such as exercise

A

release of adrenaline and noradrenaline leads to increased positive inotropy and positive chronotropy, which results in more efficient circulation of oxygenated blood

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30
Q

describe the effect of vasodilation in skeletal muscle arterioles when faced with a physiological stressor such as exercise

A

vasodilation reduces systemic vascular resistance and optimises tissue perfusion

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31
Q

describe the effect of increased venous return when faced with a physiological stressor such as exercise

A

increased venous return > increase preload > increase stroke volume according to frank starling mechanism

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32
Q

what are 3 mechanisms that work to increase HR/SV during times of physiological stress e.g exercise

A

sympathetic nervous system activation

increased venous return

vasodilation in skeletal muscle arterioles

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33
Q

arterial pressure is regulated by, in the short term by…

A

control of systemic vascular resistance

control of cardiac output

34
Q

describe the baroreceptor reflex

A

short term control of arterial pressure

involves mechanosensitive afferent nerve endings sensitive to arterial stretch in the carotid sinuses and aortic arch

pressure signal processed within medullary CV control centre

response mediated by both sympathetic and parasympathetic efferent pathways

35
Q

outline vagal stimulation of baroreflex

A

parasympathetic

brief but rapid change in HR, acting via the SA and AV nodes

36
Q

outline sympathetic stimulation of baroreflex

A

much slower change than parasympathetic (vagal) stimulation

37
Q

what does pressure diuresis mean

A

increases fluid output due to increased BP

38
Q

what does pressure natriuresis mean

A

increase in Na+ excretion w increased BP

39
Q

how does angiotensin ll contribute to fluid and salt retention

A

direct effect - vasoconstriction of renal artery which reduces renal flow leading to increased fluid reabsorption

indirect effect - release of aldosterone

40
Q

what are 5 metabolic ‘needs’ that allow for changes in local blood flow

A

O2 delivery

CO2 removal

nutrient delivery

H+ removal

hormone transport

41
Q

how does increased need for O2 delivery affect local blood flow

A

triggers vasodilation through release of vasodilators like adenosine and NO > increased blood flow to deliver more O2

42
Q

how does increased need for CO2 removal affect local blood flow

A

increased CO2 > vasodilation > increase blood flow > remove excess CO2

43
Q

how does increased need for H+ removal affect local blood flow

A

accumulation of H+ > lowers blood pH > local vasodilation > increase blood flow > removal of H+

44
Q

how does increased need for hormone transport affect local blood flow

A

increased demand for hormone > stimulate release of hormones that regulate vascular tone + flow > efficient transport of hormones

45
Q

how does increased need for nutrient transport affect local blood flow

A

high demand for nutrients > blood flow redirected to GI tract or growing tissues via vasodilation > increased nutrient delivery + absorption

46
Q

describe autoregulation of cerebral flow

A

ensures brain receives consistent supply of oxygen and glucose via blood

this is mediated through myogenic respone - cerebral blood vessels constrict in response to increased intravascular pressure to prevent excessive blood flow, and vice versa

47
Q

what are 6 causes of heart failure

A

CAD

HTN

valvular disease

arrhythmias

inherited/acquired cardiomyopathies

infiltrative disease

48
Q

what is HFrEF

A

heart failure w reduced ejection fraction

LVEF of equal to or less than 40%

49
Q

what is HFpEF

A

heart failure w preserved ejection fraction

LVEF of equal to or greater than 50%

50
Q

what is LVEF and how is it calculated

A

left ventricular ejection fraction

LVEF = SV / LV EDV

51
Q

what is normal LVEF

A

greater than 60%

52
Q

describe the development of HFrEF

A

typically initiative by an index event e.g MI

this leads to decreased LVEF which decreases Q

as a result of this early reduction in pumping capacity, a series of compensatory mechanisms partially restore function, such as sympathetic activation and neurohormonal activation

over time, there is secondary end organ damage, including progressive LV remodelling

53
Q

describe neurohormonal activation as a result of reduction in pumping capacity in HF

A

decreased SV > sympathetic innervation > positive chronotropic effect of heart and positive inotropic effect of LV

renal hypoperfusion and sympathetic stimulation activates RAAS (provides short term circulatory support but long term adverse effects e.g cardiac fibrosis)

54
Q

what are natriuretic peptides

A

released in response to myocardial volume overload and stretch

atrial natriuretic peptide (ANP) is released from atria

brain natriuretic peptide (BNP) is released from ventricles

it effects in opposition to RAAS (ANP decrease blood pressure and cardiac hypertrophy while BNP acts locally to reduce ventricular fibrosis)

BNP (or NT-ProBNP) is used as diagnostic marker for HF

55
Q

describe early pathological remodelling of the heart following an ischemic event such as MI

A

<72 hrs after

wall thinning, chamber dilation, increased wall stress

56
Q

describe late remodelling of the heart following an ischemic event such as MI

A

> 72 hrs after

myocardial hypertrophy > increased fibrosis

driven by increased wall stress and activation of RAAS/SNS

57
Q

describe HFpEF

A

typically considered to be those w raised LV end-diastolic pressure ie LV diastolic dysfunction due to things like ventricular hypertrophy or slowed relaxation of the ventricle etc

~50% of patients w signs/symptoms of HF have HFpEF

58
Q

what does diagnosis of HFpEF rely on

A

signs/symptoms

CV imaging demonstrating impaired diastolic function

increased BNP

raised LV filling pressures during catheterisation

59
Q

describe how a primary myocardial disease leads to HF through a reduced LV systolic reserve

A

primary myocardial disease e.g cardiomyopathy

then, primary myocardial injury

then, LV concentric remodelling, hypertrophy, fibrosis

then, decreased LV systolic reserve

then, decreased Q

60
Q

describe how a primary myocardial disease leads to HF through a reduced LV diastolic reserve

A

primary myocardial disease e.g cardiomyopathy

then, primary myocardial injury

then, LV concentric remodelling, hypertrophy, fibrosis

then, decreased LV diastolic reserve

then, increased LV filling pressures

then, increased LA pressure

then, LA remodelling dysfunction

then, A-fib or pulmonary HTN

then, RV dysfunction

then, systemic venous congestion

then, renal dysfunction

61
Q

describe how comorbidities lead to HF through a reduced LV systolic reserve

A

comorbidity e.g HTN or diabetes

then, systemic microvascular dysfunction and decreased NO signalling

then, secondary myocardial injury

then, LV concentric remodelling, hypertrophy, fibrosis

then, decreased LV systolic reserve

then, decreased Q

62
Q

describe how comorbidities lead to HF through a reduced LV diastolic reserve

A

comorbidity e.g HTN or diabetes

then, systemic microvascular dysfunction and decreased NO signalling

then, secondary myocardial injury

then, LV concentric remodelling, hypertrophy, fibrosis

then, decreased LV diastolic reserve

then, increased LV filling pressures

then, increased LA pressure

then, LA remodelling dysfunction

then, A-fib or pulmonary HTN

then, RV dysfunction

then, systemic venous congestion

then, renal dysfunction

63
Q

what are 4 symptoms of HF

A

dyspnea at rest or upon exertion

orthopnea

ankle swelling

exercise intolerance

64
Q

how is dyspnea caused in HF

A

reduced LV output or elevated end diastolic pressure leads to increased pulmonary pressures and pulmonary edema

65
Q

how is orthopnea caused in HF

A

supine position results in blood displaced from extremities to thoracic compartment

low LV output increases pulmonary pressure

66
Q

how is ankle swelling caused in HF

A

peripheral edema caused by congestion due to low LV output

67
Q

how is exercise intolerance caused in HF

A

low Q

ventilation-cardiac output mismatching within pulmonary circulation

skeletal muscle dysfunction

68
Q

describe the role of echocardiography in diagnosing HF

A

helps assess LVEF, chamber sizes, and diastolic function to determine the extent of cardiac impairment

69
Q

describe the role of echocardiography in diagnosing valvular disease

A

enables the detailed examination of valve morphology, function, and presence of regurgitation or stenosis

70
Q

describe the diagnostic approach used in cases of suspected heart failure

A

comprehensive history

physical examination

echo and ECG

blood markers e.g BNP, ANP etc

71
Q

describe acute management of heart failure

A

involves prompt stabilisation of patient and relief of symptoms

initial Rx involves furosemide (diuretic) which reduces volume overload and pulmonary congestion, GTN (vasodilator) which lowers systemic vascular resistance, dobutamine (inotropic agent) which improves myocardial contractility, and monitoring/supportive care

72
Q

describe long term management of heart failure

A

beta blockers are used to reduce HR by reducing SNS activity

calcium channel blockers are used to manage HTN and angina

ACE inhibitors are used to lower BP

ARBs are used for similar benefits as ACE but in patients who are intolerant to ACE

73
Q

what are 6 key differentials for dyspnea

A

COPD

asthma

HF

PE

pneumonia

interstitial lung disease

74
Q

what are 5 exacerbating factors of HF and brief outline of how they make it worse

A

non-compliance (w meds) - inadequate control of HF symptoms

diet - high Na diet leads to increased fluid retention which increases workload for heart

infection - increase body’s O2 demand meaning heart has to work harder

sedentary life - deconditioning + muscle weakness > harder for heart to pump good

stress/anxiety - increase HR and BP

75
Q

what are 5 complications of HF and brief outline of each

A

pulmonary oedema - fluid in lungs > severe dyspnea and deoxygenation

cardiac arrhythmias - e.g AF > increased risk of stroke

renal impairment - fluid retention and electrolyte imbalance

hepatic congestion - liver dysfunction and elevated liver enzymes

thromboembolic events - e.g DVT and PE

76
Q

what are two main types of valvular dysfunction

A

regurgitation

stenosis

77
Q

what is valvular disease

A

group of conditions in which one or multiple of the heart’s valves do not function properly, leading to disrupted blood flow within the heart

78
Q

what are 8 causes of valvular disease

A

congenital heart defects

rheumatic fever

degenerative changes

infective endocarditis

connective tissue disorders

radiation therapy

medications

trauma/injury

79
Q

what are 4 major types of left sided valvular pathology and briefly describe the outcome of each

A

aortic stenosis - results in increased ventricular pressure and reduced Q

mitral stenosis - results in volume overload and LV dilation

aortic regurgitation - results in elevated atrial pressure + pulmonary congestion

mitral regurgitation - results in atrial enlargement and volume overload

80
Q

untreated valvular disease can lead to …

A

kindey failure

liver failure

HTN

HF

81
Q

valve lesions can lead to what 6 symptoms and brief outline of how

A

dyspnea - back pressure/reduced forward flow > reduced O2 supply > breathless

chest pain - obstructed flow + increased pressure in heart > chest pain

fatigue - lesions > inefficient pumping > heart pump harder > fatigue

palpitations - irregular blood flow + turbulence (esp in regurgitant valves)

oedema - increased pressure in heart chambers > fluid retention + pulmonary edema

syncope - reduced Q > fainting episodes due to inadequate blood supply to brain

Medical Studies 1 (11 decks)

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