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Medical Studies 1 > CVS Week 3 > Flashcards

CVS Week 3 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
what is the frank starling mechanism
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
26
what constitutes pre load
central venous pressure ie venous return
27
what constitutes afterload
aortic pressure and properties of arterial system
28
what is afterload
resistance against which heart must pump in order to eject blood from LV
29
describe the effect of the sympathetic nervous system when faced with a physiological stressor such as exercise
release of adrenaline and noradrenaline leads to increased positive inotropy and positive chronotropy, which results in more efficient circulation of oxygenated blood
30
describe the effect of vasodilation in skeletal muscle arterioles when faced with a physiological stressor such as exercise
vasodilation reduces systemic vascular resistance and optimises tissue perfusion
31
describe the effect of increased venous return when faced with a physiological stressor such as exercise
increased venous return > increase preload > increase stroke volume according to frank starling mechanism
32
what are 3 mechanisms that work to increase HR/SV during times of physiological stress e.g exercise
sympathetic nervous system activation increased venous return vasodilation in skeletal muscle arterioles
33
arterial pressure is regulated by, in the short term by...
control of systemic vascular resistance control of cardiac output
34
describe the baroreceptor reflex
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
outline vagal stimulation of baroreflex
parasympathetic brief but rapid change in HR, acting via the SA and AV nodes
36
outline sympathetic stimulation of baroreflex
much slower change than parasympathetic (vagal) stimulation
37
what does pressure diuresis mean
increases fluid output due to increased BP
38
what does pressure natriuresis mean
increase in Na+ excretion w increased BP
39
how does angiotensin ll contribute to fluid and salt retention
direct effect - vasoconstriction of renal artery which reduces renal flow leading to increased fluid reabsorption indirect effect - release of aldosterone
40
what are 5 metabolic 'needs' that allow for changes in local blood flow
O2 delivery CO2 removal nutrient delivery H+ removal hormone transport
41
how does increased need for O2 delivery affect local blood flow
triggers vasodilation through release of vasodilators like adenosine and NO > increased blood flow to deliver more O2
42
how does increased need for CO2 removal affect local blood flow
increased CO2 > vasodilation > increase blood flow > remove excess CO2
43
how does increased need for H+ removal affect local blood flow
accumulation of H+ > lowers blood pH > local vasodilation > increase blood flow > removal of H+
44
how does increased need for hormone transport affect local blood flow
increased demand for hormone > stimulate release of hormones that regulate vascular tone + flow > efficient transport of hormones
45
how does increased need for nutrient transport affect local blood flow
high demand for nutrients > blood flow redirected to GI tract or growing tissues via vasodilation > increased nutrient delivery + absorption
46
describe autoregulation of cerebral flow
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
what are 6 causes of heart failure
CAD HTN valvular disease arrhythmias inherited/acquired cardiomyopathies infiltrative disease
48
what is HFrEF
heart failure w reduced ejection fraction LVEF of equal to or less than 40%
49
what is HFpEF
heart failure w preserved ejection fraction LVEF of equal to or greater than 50%
50
what is LVEF and how is it calculated
left ventricular ejection fraction LVEF = SV / LV EDV
51
what is normal LVEF
greater than 60%
52
describe the development of HFrEF
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
describe neurohormonal activation as a result of reduction in pumping capacity in HF
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
what are natriuretic peptides
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
describe early pathological remodelling of the heart following an ischemic event such as MI
<72 hrs after wall thinning, chamber dilation, increased wall stress
56
describe late remodelling of the heart following an ischemic event such as MI
>72 hrs after myocardial hypertrophy > increased fibrosis driven by increased wall stress and activation of RAAS/SNS
57
describe HFpEF
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
what does diagnosis of HFpEF rely on
signs/symptoms CV imaging demonstrating impaired diastolic function increased BNP raised LV filling pressures during catheterisation
59
describe how a primary myocardial disease leads to HF through a reduced LV systolic reserve
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
describe how a primary myocardial disease leads to HF through a reduced LV diastolic reserve
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
describe how comorbidities lead to HF through a reduced LV systolic reserve
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
describe how comorbidities lead to HF through a reduced LV diastolic reserve
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
what are 4 symptoms of HF
dyspnea at rest or upon exertion orthopnea ankle swelling exercise intolerance
64
how is dyspnea caused in HF
reduced LV output or elevated end diastolic pressure leads to increased pulmonary pressures and pulmonary edema
65
how is orthopnea caused in HF
supine position results in blood displaced from extremities to thoracic compartment low LV output increases pulmonary pressure
66
how is ankle swelling caused in HF
peripheral edema caused by congestion due to low LV output
67
how is exercise intolerance caused in HF
low Q ventilation-cardiac output mismatching within pulmonary circulation skeletal muscle dysfunction
68
describe the role of echocardiography in diagnosing HF
helps assess LVEF, chamber sizes, and diastolic function to determine the extent of cardiac impairment
69
describe the role of echocardiography in diagnosing valvular disease
enables the detailed examination of valve morphology, function, and presence of regurgitation or stenosis
70
describe the diagnostic approach used in cases of suspected heart failure
comprehensive history physical examination echo and ECG blood markers e.g BNP, ANP etc
71
describe acute management of heart failure
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
describe long term management of heart failure
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
what are 6 key differentials for dyspnea
COPD asthma HF PE pneumonia interstitial lung disease
74
what are 5 exacerbating factors of HF and brief outline of how they make it worse
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
what are 5 complications of HF and brief outline of each
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
what are two main types of valvular dysfunction
regurgitation stenosis
77
what is valvular disease
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
what are 8 causes of valvular disease
congenital heart defects rheumatic fever degenerative changes infective endocarditis connective tissue disorders radiation therapy medications trauma/injury
79
what are 4 major types of left sided valvular pathology and briefly describe the outcome of each
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
untreated valvular disease can lead to ...
kindey failure liver failure HTN HF
81
valve lesions can lead to what 6 symptoms and brief outline of how
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 (16 decks)

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