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Cardio Revision > Physiology > Flashcards

Physiology Flashcards

1
Q

Why are the baroreceptors important in the baroreflex located in the arterial system?

A

Not much increase in volume is required to produce a larger change in pressure (less compliance in arterial vessels)

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2
Q

What are the main baroreceptors and where are they located?

A

Carotid sinus in the internal carotid artery

Aortic baroreceptors in the aortic arch

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3
Q

Describe the carotid sinus

A

Thin-walled, highly innervated bulbous structure on the internal carotid artery

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4
Q

What changes to the CV system are caused by sympathetic activation?

A

Increased HR

Decreased SA and (mostly) AV conduction time

Increased contractility

Increased TPR

Increased venous tone (to push blood over to the arteries)

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5
Q

What changes to the CV system are caused by parasympathetic activation?

A

Decreased HR

Increased SA and (mostly) AV conduction time

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6
Q

What aspects of the CV system does the PNS have no effect on?

A

TPR (small arteries and arterioles are not innervated by PNS)

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7
Q

How quickly do baroreceptors respond to changes in pressure?

A

Within 1 cycle

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8
Q

What happens when MAP drops below 60mmHg?

A

Baroreceptors do not respond to changes in MAP <50-60mmHg and the brain instead receives information about blood flow from other receptors including chemoreceptors

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9
Q

How long does it take for the threshold for baroreceptor firing to reset to new pressure levels?

A

1-2 days

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10
Q

How is BP maintained in the acute setting?

A

By the baroreflex

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11
Q

How is BP maintained in the long term?

A

Predominantly RAAS

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12
Q

Where are the main chemoreceptors located?

A

Carotid and aortic bodies

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13
Q

When are chemoreceptors stimulated and by what kind of stimuli?

A

MAP <60mmHg

Respond to low O2, high CO2, low pH

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14
Q

Do men or women have higher BP on average?

A

Men

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15
Q

What changes occur to BP with age?

A

Systolic BP rises until and after 60 years

Diastolic BP rises until 60 years then decreases

Pulse pressure therefore increases

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16
Q

What causes the increase in pulse pressure with age?

A

Decreased large artery compliance

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17
Q

What is the relationship between BP and body size?

A

Bigger body = higher BP

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18
Q

Describe the diurnal variation of BP

A

Lower at night by ~20mmHg

Less variability at night

Less sympathetic activity (mostly maintained by RAAS)

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19
Q

How does BP vary between the seasons?

A

~3mmHg lower in summer compared to winter

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20
Q

Describe the population paradox

A

More deaths in the people at moderate risk (as there are more of these) than in the people at highest risk (as this is only a small number of people)

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21
Q

What is the formula for relative LV wall thickness?

A

LV wall thickness/LV chamber size (diameter)

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22
Q

Distinguish between remodelling, concentric hypertrophy, and eccentric hypertrophy

A

Remodelling: normal LV mass with increased relative wall thickness (heart gets smaller)

Concentric hypertrophy: increased LV mass and relative wall thickness but no increase in chamber size (so wall thickens)

Eccentric hypertrophy: increased LV mass but normal relative wall thickness - increased chamber size

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23
Q

What usually causes concentric hypertrophy?

A

Pressure overload

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24
Q

What usually causes eccentric hypertrophy?

A

Volume overload

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25
Q

What changes occur to cardiomyocytes to produce concentric hypertrophy?

A

More sarcomeres in parallel

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26
Q

What changes occur to cardiomyocytes to produce eccentric hypertrophy?

A

More sarcomeres in series (myocyte stretching)

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27
Q

What changes to the structure of the cardiac tissue occur with hypertrophy?

A

Increase myocardial cell size with more mitochondria, myofibrils and SR

Increased fibroendothelial cell numbers

Increased interstitial matrix

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28
Q

What changes occur with decompensation in hypertrophy?

A

LV dilation

Increased LVEDV

Increased LVESV

Decreased EF

Decreased CO

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29
Q

What clinical signs are seen with LVH?

A

Forceful apex beat

S3

S4

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30
Q

What causes S3 and S4?

A

S3 - sound of the blood “sloshing” in the ventricles, heard with volume overload

S4 - blood being forced into a stiff/hypertrophic ventricle

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31
Q

What changes are seen on ECG with LVH?

A

Tall voltages

T wave inversion

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32
Q

List 3 causes of RVH, giving examples

A

Congenital

Pulmonary hypertension (e.g. in lung disease, PE, chronic LHF)

Right heart valves (e.g. stenosis/regurgitation)

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33
Q

What does hypertrophic cardiomyopathy increase the risk of?

A

Ventricular arrhythmias and sudden death

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34
Q

What changes occur in an athlete’s heart?

A

Eccentric hypertrophy with normal cardiac function (usually regresses)

Can cause enlargement especially of the RV (does not regress, may cause ventricular arrhythmias)

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35
Q

What cardiac changes occur in dehydration?

A

Decreased CO and BP

36
Q

How is RVEDP measured?

A

With a catheter inserted via a vein and placed across the tricuspid valve (measures RAEDP which is equal to JVP and RVEDP)

37
Q

How is LVEDP measured?

A

With a catheter inserted via an artery across the aortic valve (measures the LAEDP which is equal to LVEDP)

38
Q

What type of catheter is used for pressure tracing?

A

Swan-Ganz

39
Q

What is PA wedge pressure?

A

Catheter wedged into pulmonary artery

Measures pulmonary venous pressure (which is equal to LAP and LVEDP)

40
Q

How can one catheter be used to measure all the cardiac pressures?

A

Place catheter across tricuspid valve, measure R cardiac pressures

Measure PA wedge pressure

Provides a measure of preload for RV and LV

41
Q

Why doesn’t increased arterial pressure cause oedema?

A

Because the arterial pressure is “knocked off” by the arteriole before blood enters the capillaries

42
Q

What are the 4 causes of oedema?

A

Increased hydrostatic (venous) pressure

Decreased oncotic pressure

Blocked lymphatics

Increased capillary permeability

43
Q

What kind of oedema is caused by increased RVEDP? By increased LVEDP?

A

Increased RVEDP causes peripheral oedema

Increased LVEDP causes pulmonary oedema

44
Q

Describe the process whereby cardiac failure causes pulmonary congestion

A

Decreased contractility (due to a reduction in sensitivity to sympathetic drive, caused by downregulation and impaired coupling of B1-adrenoceptors) causes a drop in CO

In an attempt to sustain CO, the ventricles fill more (increased LVEDP) - also due to fluid retention

This increases PVP above threshold (~20-30mmHg) and causes fluid to leak out of the pulmonary capillaries

45
Q

What are the 3 main causes of cardiac failure?

A

Loss of myocardial muscle (e.g. IHD, cardiomyopathy)

Pressure overload (e.g. stenosis, hypertension)

Volume overload (e.g. regurgitation, shunts including septal defects)

46
Q

List 4 symptoms of LHF

A

SOB

Fatigue

Tachycardia

Lung crepitations (pulmonary oedema)

47
Q

What adaptations occur in cardiac failure?

A

Activation of RAAS due to decreased renal blood flow: causes fluid and Na+ retention with K+ loss, as well as vasoconstriction

SNS activation: causes increased contractility and vasoconstriction, can cause ventricular arrhythmias and have a direct toxic effect on the myocardium

48
Q

What is the purpose of fluid retention in cardiac failure? What complications does it cause?

A

To sustain CO by increasing LVEDP

Increased LVEDP causes pulmonary congestion, and the fluid retention also causes increased RVEDP which causes peripheral oedema and liver congestion

49
Q

What are the 3 main causes of RHF?

A

Global heart disease

Specific RH disease

LHF

50
Q

List 5 specific RH diseases which can cause RHF

A

RV cardiomyopathy

Right-sided valves, shunts

Pericardial disease

Pulmonary hypertension (arterial; caused by cor pulmonale or PE)

51
Q

How does LHF cause RHF?

A

LHF causes pulmonary congestion (via pulmonary venous hypertension)

Pulmonary congestion causes chronic hypoxia of the lungs

Lungs respond via release of endothelin and angiopoietin to produce pulmonary vasoconstriction

Widespread pulmonary vasoconstriction causes pulmonary arterial hypertension

Sustained PA hypertension causes RHF

52
Q

What is diastolic HF?

A

Normal systolic function but reduced LV compliance (due to scar from infarct or chronic hypertension/hypertrophy) causes increased LVEDP and therefore PVP (causes pulmonary congestion)

53
Q

Why is the pressure gradient across the valve increased in aortic stenosis?

A

Because the LV needs to achieve higher pressures to push open the valve and empty into the aorta (normally it just needs to equal the pressure in the aorta, so emptying occurs once the gradient reaches 0, but in severe stenosis the gradient can be as high as 50mmHg)

This means that if MAP is measured as 120/80, the pressure in the ventricle is actually 170/80

54
Q

What type of valve dysfunction causes pressure overload?

A

Stenosis

55
Q

What type of valve dysfunction causes volume overload?

A

Regurgitation/incompetence

56
Q

What causes aortic stenosis?

A

Fibrosis/calcification (common in ageing)

57
Q

What is the LV response to aortic stenosis?

A

Pressure overload causes concentric hypertrophy

Less compliant LV walls require increased atrial contraction to produce adequate LV filling

Changes reverse after surgery

58
Q

What are some possible causes of aortic regurgitation? Give examples of each

A

Damaged leaflets (e.g. endocarditis, RHD)

Dilated leaflets (e.g. Marfan’s syndrome, aortic dissection)

59
Q

What cardiac pathologies can be caused by RHD?

A

Aortic regurgitation

Mitral regurgitation

Mitral stenosis (most characteristic)

60
Q

What is the LV response to AR?

A

Part of each SV leaks back into LV during diastole

To compensate, LV pumps an increased SV and EF (this requires an increased EDV)

End systolic volume is normal (the same amount of blood is left over in the heart but more is ejected, to compensate for the amount that will leak back during diastole)

Pulse pressure is increased

61
Q

What causes the increased pulse pressure in AR?

A

“Bounding” and “collapsing” pulse, due to increased EF entering the aorta (causing an increased systolic pressure), and then reduced aortic diastolic pressure following the leaking of blood back into the LV

62
Q

What findings will be present in AR on auscultation?

A

Decrescendo diastolic murmur (murmur replaces 2nd heart sound; due to the leaking of blood back across the valve in diastole)

63
Q

What are the symptoms of AR?

A

Asymptomatic if mild or moderate

Severe will cause acute pulmonary oedema (due to increased LVEDP and LAP) and cardiogenic shock

64
Q

What changes occur with decompensation in prolonged severe AR?

A

LV diastolic volume increases markedly (increased LVEDP)

LV function decreases (and therefore EF and contraction)

LV systolic volume increases (due to reduced EF)

These are IRREVERSIBLE changes

65
Q

List 7 possible causes of MR

A

Myxomatous degeneration (causes prolapse)

Ruptured chordae tendinae (flail leaflet)

Infective endocarditis

Myocardial infarct leading to rupture of a papillary muscle

RHD

Collagen vascular disease

Cardiomyopathy

66
Q

How does cardiomyopathy cause MR?

A

Change in ventricular shape causes change in the geometry of the valve leaflets

67
Q

What cardiac changes occur with MR?

A

Portion of SV ejected into LA (increased LAV, LAP)

LV must pump greater SV to maintain CO, which requires a greater EDV and therefore EF

ESV is normal

68
Q

What LV changes occur with decompensation in prolonged severe MR?

A

LV diastolic volume increases markedly (increased LVEDP)

LV function decreases (and therefore EF and contraction)

LV systolic volume increases (due to reduced EF)

These are IRREVERSIBLE changes

69
Q

What LA changes occur in MR and what are some possible sequelae of these?

A

LAP and LAV increase (risk of AF)

AF can cause thrombus production and embolism (esp to brain or kidney)

Increased PVP causes pulmonary congestion, oedema and hypoxia

Hypoxia leads to widespread vasoconstriction, causing increase PAP (pulmonary hypertension) - this may cause RHF

70
Q

Define cardiac failure

A

CO < body needs (usually systolic failure due to loss of contractility)

71
Q

What cardiac changes occur with MS?

A

Pressure gradient across the mitral valve

Reduced filling of LV Increased LAP and LAV

72
Q

What LA changes occur in MS and what are some possible sequelae of these?

A

As in MR:

LAP and LAV increase (risk of AF) AF can cause thrombus production and embolism (esp to brain or kidney)

Increased PVP causes pulmonary congestion, oedema and hypoxia

Hypoxia leads to widespread vasoconstriction, causing increase PAP (pulmonary hypertension) - this may cause RHF)

73
Q

What in MS serves as a trigger for intervention?

A

Development of symptoms (including pulmonary hypertension)

74
Q

What interventions are used to treat MS?

A

Valvotomy (surgical or balloon dilatation

Valve replacement

75
Q

What compensatory changes occur in AS, AR, MR and MS, respectively?

A

AS: LV concentric hypertrophy

AR and MR: LV eccentric hypertrophy/dilation

MS: LA dilation and increased pressure

76
Q

Draw and describe the SA node pacemaker potential

A

Phase 4: unstable membrane potential (~-60mV to +20mV), spontaneous depolarisation, Na+ and Ca2+ in

Phase 0: depolarisation, Ca2+ in

Phase 3: repolarisation, K+ out

77
Q

Draw and describe the ventricular AP

A

Phase 0: depolarisation, Na+ in

Phase 1: rapid repolarisation, K+ out

Phase 2: plateau, Ca2+ in, K+ out

Phase 3: repolariation, K+ out

Phase 4: RMP (~-90mV)

78
Q

How does the PNS cause bradycardia?

A

ACh acts on M2 receptors; signalling cascade decreases cAMP

Decreased cAMP leads to K+ channel opening

K+ efflux slows Na+ and Ca+ influx

Slowed phase 4 and therefore rate of conduction

79
Q

How does the SNS cause tachycardia?

A

NA and adrenaline act on B1-adrenoceptors; signalling cascades increases cAMP

Increased cAMP leads to Ca2+ channel opening

Increased Ca2+ influx increases the slope of phase 4 depolarisation to increase rate of firing in the SA node, and speed of conduction in the AV node

Also increases contraction in myocardial cells

80
Q

List 4 symptoms of dysrhythmia

A

SOB

Fainting

Fatigue

Chest pain

81
Q

What 3 factors (other than ANS innervation) can alter cardiac rate and rhythm, and potentially cause dysrhythmias?

A

Ionic balance (Na+, Ca2+, K+)

Myocardial integrity (compromised by ischaemia, infarct or fibrosis)

Drugs

82
Q

What are the 3 main mechanisms underlying dysrhythmias?

A

Altered impulse formation

Altered impulse conduction

Triggered activity (early or late after-depolarisations)

83
Q

Give 2 examples of mechanisms underlying altered impulse formation

A

Automaticity of pacemaker cells

Abnormal generation of APs at sites other than the SA node

84
Q

Give 2 examples of mechanisms underlying altered impulse conduction

A

Conduction block (ventricles adopt own slower rate)

Re-entry (extra beats increase rate)

85
Q

Formula for CO

A

CO = HR x SV

86
Q

Formula for MAP

A

MAP = CO x TPR

Cardio Revision (6 decks)

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