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Physiology > Cardiovascular Physiology > Flashcards

Cardiovascular Physiology Flashcards

1
Q

structure of blood vessels walls

A

3 layers (except capillaries)
-tunica intima
-basal membrane; fenestrated., endothelial cells protrude to tunica media and provides communication
-tunica media- SMC, 2 proteins elastin and collagen to protect against over stretch
-adventitia - more collagen, fibroblasts for more SMC production
-vasa vasorum - blood supply for vessel and nerve inn.

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2
Q

Elastic Arteries

A

25mm
eg aorta to accommodate SV pushed out by heart
elastin in walls to be able to stretch, walls push against it in elastic recoil
low compliance
aortic valve
elasticity maintains diastolic pressure in arterial system and contributes to after load of CO
pressures generated on RHS lower than pulmonary

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3
Q

conduit arteries

A

more muscular, feed blood to smalle arteries of organs
thick wall prevent compression
dense noradrenergic innervation of sympathetic vasoconstrictor fibres that cause VC when active

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4
Q

small arteries/arterioles

A

0.2-1.0mm
-resistance vessels where pressure falls sharply from one end to the other
-dense symp. noradrenergic inn that can effectively close off blood flow
-terminal arterioles determine no.of capillaries
-withdrawl of symp activity->vasodilation to reduce resistance to BF anf incr perfusion to cap beds
-has own basal tone and symp inn - blood pressure

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5
Q

capillaries

A

4-7uM
single layer of endothelium
exchange eg solutes and gases
little resistance to flow

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6
Q

describe filtration across capillaries

A

-balance on hydrostatic pressure in the capillary, tissue pressure in cap and tissue pressure surrounding, colloid osmotic pressures and extracellular forces
can be leaky therefore water moves into tissue - edema

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7
Q

infection and capillary role

A

infection in tissues - chemotaxins released from damaged tissues
chemicals diffuse across the endo that attract and activate WBCs
when activated, neutrophils stick to endo and separate neighbouring endothelial cells
podocytes extend through gap, neutrophils squeeze through to get to site of infection

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8
Q

venules

A

-intima, thin media and adventitia
-semilunar valves
-more than arterioles
-low resistance
-2/3 of BV - vary as they are distensible and sympathetic noradrenergic innervation
-when active venoconstriction can route a greater volume of blue back to heart/RA
- aided by muscle pump

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9
Q

left ventricular pressures

A

systole: 120mmHg
diastole: 80mmHg

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10
Q

pre capillary pressure

A

50mmHg

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11
Q

pulse pressure =

A

difference between systolic and diastolic pressures

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12
Q

mean arterial pressure =

A

=diastolic pressure + 1/3 pulse pressure (93mmHg)

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13
Q

what is larger systemic or pulmonary pressures

A

systemic, as resistance to flow in the pulmonary circulation is much lower than the systemic

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14
Q

innervation of Blood Vessels

A

sympathetic vasoconstrictor innervation that releases noradrenaline to cause vasoconstriction

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15
Q

features of vascular SM

A

-myosin and actin cross bridge and tension
-no sarcomeres as no Z line
-individual cells small. long and thin
-interconnected by gap junctions (electrical conduction and contract in sync)
-underlying rhythmical contractions (pacemaker cells)
-forces generated smaller than skeletal and maintained for longer

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16
Q

contraction of smooth muscle

A

relies on an increase in the intracellular concentration of Ca2+

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17
Q

Poiseuille’s Law

A

flow of a liquid is directly proportional to the viscosity of blood and length of vessel, inversely proportional to the 4th power of the radius of the vessel

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18
Q

the radius of vessel and resistance

A

resistance to flow is acutely sensitive to changes in radius
eg small decrease in radius - large increase in resistance, consequent reduction in flow

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19
Q

nervous activity and resistance

A

-highly influenced by sympathetic nerve activity
-release of NA causes SM contraction, increasing resistance and decreasing bloodflow
-symp withdrawl causes vasodilation and increased flow

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20
Q

arterial pressure =

A

(SV x HR) x TPR

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21
Q

arterial pressure equation shows….

A

driver pressure for flow across vascular beds is influenced by the resistance offered by all the blood vessels, especially the terminal arterioles of all the different tissues in the systemic circulation
alterations of individual contributions of the different tissues will alter the TPR and flow

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22
Q

extrinsic vascular control concept

A

balance between dilator and constrictor influences acting on vascular SM that alters resistanced and dlow
balance = basal tone

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23
Q

what are extrinsic vascular control influences

A

nervous control and circulating hormones
intercellular Ca

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24
Q

where does increase in Ca concentration come from

A

2 sources in smooth muscle
influx from surrounding extracellular fluid through receptor-operated and voltag operated calcium channel or from release from the internal stores of the SR

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25
Q

what opens and closes Ca channels

A

membrane depolarisation - open
hyperpolarisation - close

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26
Q

sympathetic vasoconstrictor control

A

-most important element of BP control
-AP in postganglionic nerves can release NA along with other co-transmitters

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27
Q

describe the sympathetic neuroeffector junction

A

post ganglionic nerve branch as they reach the adventitia and varicosities are apparent that contain transmitter-filled vesicles
branches permeate outer layers of SM
no specialisations
adrenergic receptors are distributed all over SM so when transmitter is released it diffuses and interacts with receptors all around varicosities

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28
Q

sympathetic innervation

A

classic symp NTs - Ach @ symp ganglionic synapse and NA @ neuroeffector junction
-some act on PS synaptic memb of target tissue
-others act on symp nerve terminals they are released from
-2 main adrenergic receptor subtypes alpha and beta

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29
Q

adrenal medulla

A

releases adrenaline

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30
Q

circulation to an organ depends on:

A

intrinsic/local factors
autoregulation, mechanical compression
extrinsic/external factors - nervous and hormonal

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31
Q

autoregulation

A

ability of an organ to maintain blood flow despite changes in perfusion pressure
occurs in absence of extrinsic factors
intrinsic factors: myogenic, metabolic, endothelial

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32
Q

posture and circulation

A

affects BP
hydrostatic pressure
pooling in lower extremeties
reduce cerebral BF
normally compensated

33
Q

cardiac output =

A

CO= SV xHR

34
Q

how to measure CO in humans

A

Fick - uptake or relase of substance deoendnet on BF
Dye Dilution
Thermodilution
Doppler Flow ECG

35
Q

Pros and Cons of Fick Principle

A

-Good for low COs
-fairly invasive (cannula)
-tricuspid or pulmonary valve issues
-not very accurate or reliable

36
Q

describe thermodilution

A

small vol of chilled saline via catheter in RA
-temp gauge in pulmonary artery
-generates temp vs time curve
-temp equilibriates in 1 cardiac cycle
-less chance of adverse reaction
-invasive

37
Q

what was Frank’s finding

A

strength of ventricular contraction increased when the ventricle was stretched prior to contraction

38
Q

what was Starling’s finding

A

increasing VR -> increased SV

39
Q

what makes preload

A

VR stretches the ventricles and increases LVEDP

40
Q

starling’s heart-lung preparation

A

-allowed each factor to be changed independently so the authors could work out their relationships and importance in determining CO
-at rest SV low when Pra increased(incr VR) big change in vent volume
-more VR=EDV higher (more stretch on ventricular walls)
-heart responded by increasing contraction (increased SV) to eject more blood
-Pra reduced, EDV dropped, stretch lower, decr SV

41
Q

factors influencing venous return

A

Incr VR = Increased SV
increased SV = increased CO - factors increasing VR increase functionality of the heart
decr VR = devr SV
decreased CO decrease functionality of heart

42
Q

what is afterload

A

the ‘load’ that the heart must eject blood against

43
Q

what is afterload determined by

A

the level of constriction of the BVs into which the blood is flowing - determined by the TPR

44
Q

factors influencing CO

A

changes in TPR
shifts max CO but not mean central filling pressure
Pmc depends on vascular compliance which is mostly a product of venous tone rather than arterial
healthy heart compensates

45
Q

describe Laplace’s Law

A

afterload expressed as ventricular wall stress - while the TPR feeds back pressure into the systemic arteries and then the aorta - ultimately impacts on the pressure in the LV
incr TPR=incr DiaBP= incr ventricular diastolic pressure = increased vent wall stress
vent wall tension is proportional to pressure x radius / wall thickness

46
Q

describe nervous and humeral factors influencing cardiac output

A

chonotropic - enhance cardiac function by increasing HR
inotropic - length dependent activation of myocardial contractility eg by increasing ca2+ release

47
Q

inotropic effects on SV

A

positive; increase contraction by incr ca2+ entry or release. reduced afterload
negative; decreased contractility, drugs reduce workload, beta blockers, increased afterload

48
Q

what is the steady state operating point of the heart

A

point at which the heart functions most efficiently with the least effort

49
Q

effect of changes in inotropic mechanisms and steady-state operating point

A

can change it
eg if one trains and the inotropic state of the heart increases (more Ca enters or is releasded during excitation and the heart then contracts with more force)
CO curve is enhanced for any give Pra a higher SV results and more CO produced at steady state

50
Q

what other factors affect steady state operating

A

CO, VR can change dramatically and quite rapidly with vol changes in blood, vascular compliances and TPR so the ssop can shift quite quickly so the CO will demands of the body
eg start of exercise inotropic factors increase, TPR goes down, CO rises

51
Q

what are the 3 features of exercise

A

increase metabolites
increased nervous activity
increased muscle pump

52
Q

effect of increased metabolites in exercise and means of increase to CO

A

vasodilation - decrease TPR
chemoreceptors - increase nervous activity

53
Q

effect of increased nervous activity in exercise and means of increase to CO

A

incr sympathetic activity - incr HR and inotropic effect
decr parasympathetic activity - incr HR

54
Q

effect of increased muscles pump in exercise and means of increase to CO

A

increase VR -> increased SV/preload

55
Q

pregnancy effect on heart

A

changes in BP and volume and inotropic changes due to hormones enhance CO and move the steady state operating point up
ensures higher metabolic demands are met

56
Q

describe heart failure

A

-clincial syndrome arising from any structural and functional cardiac disorder that impairs ability of the heart to function as a pump to meet the demands of tissues

57
Q

describe the effects of heart failure

A

results in symptoms of fatigue or dyspnoea
-inadequate CO for a given filling pressure
-reduced entropy is compensated for by incr BV and decreased venous compliance-increased VR
-increases work of the heart as more blood to pump

58
Q

what does ESPVR represent

A

inotropic state of the ventricle

59
Q

describe intracellular volatage and current changes associated with excitation of the ventricle

A
  1. PM selective membrane,
    2.Xtracellular environ set by kidney - Na high K low. NaK-ATPase umps K in and Na out
    3.3Na out for every 2K; gets more negative inside so neg proteins trapped in
  2. more permeable to K at rest- free to move conc grad
    5.at sufficient neg voltage K+ opposed. = equilibrium potential
60
Q

describe atrial action potential

A

APs in atria v short duration comapred to ventricle and a less defined plateau
due to expression of v powerful and fast acting K channel which activates rapidly after depolarisation and acts as a transient outward current causing the atria to repolarise much earlier than ventricles

61
Q

describe AV node Action Potential

A

less depended on IF
upstroke of AP is a little faster than SA due to increased expression of L-type Ca channels in AV compared to SA node

62
Q

arterial BP is directly related to:

A

Cardiac output
TPR

63
Q

Total peripheral resistance depends on

A

contractile state of smooth muscle in the arterioles
depends on perfusion pressure
level of vasodilation
nervous inputs

64
Q

Bainbridge Reflex

A

-stretch receptors in the junction of the RA and VC/pulmonary vein and LA respond to changes in volume
-fibres in the vagus n signal to the medulla
-inhibition of vagus outlaw to SA node increases HR
-or intrinsic effect on the pacemaker current
-mechanosensor still not positively identified

65
Q

ADH and BP

A

normal/raised BP inhibits supraoptic nerve and paraventricular nerve dependnent release of ASH

66
Q

Renin and Blood pressure

A

-JG cells sensitive to BP
-incr afferent arteriole pressure activates TRPV4-ca2+ influx inhibits adenylate cyclase V
-decr cAMP reduces renin release from JG
-decr aff art press decr activation of TRPV4 - increases renin release

67
Q

what does a rise in BP lead to

A

incr baroreceptor stimulation
dcer renin released

68
Q

what does a rise in BP drive

A

decr symp inotropic effects, decr LV contraction force
decr symp VC
decr HR
decr ADH secretion and decr water reaborption

69
Q

what does a rise in BP result in

A

decr CO, decr TPR, decr BP
to normalise BP

70
Q

what does a fall in BP lead to

A

decr barorecptor stimulation
incr renin release

71
Q

what does a fall in BP drive

A

incr symp inotropic effects, incr LV contraction force
incr symp VC
incr HR
incr ADH and water reabosorption

72
Q

what does fall in BP lead to

A

increased CO, TPR, BV
normalisation of BP

73
Q

Behold Jarisch Reflex

A

CV an neurological process which causes hypopnea
pressure receptors on LV wall sense and activate C-fibre afferent to trigger paradoxial bradycardia, decr contractility and arterial hypotension
prolonged stanfin
vasovagal syncope

74
Q

cushings reflex

A

cerebral ischaemic reflex
compressive ischameia of CNS
incr BP, initial tachycardia followed by bradycardia, then irregular breathing

75
Q

chemoreceptor reflex

A

-peripheral chemoreceptors (carotid bodies)
-sense decr po2, pH and incr pCO2
-signals to NTS and RVLM
circulatoryu effects:
incr symp outflow, vasoconstriction, decr vagal n outflow, incr HR CO and BP
incr BF to lungs
also incr resp rate

76
Q

3 factors of cardiac output

A

sympathetic loading and parasympathetic unloading
hormones
starling forces

77
Q

ejection fraction =

A

SV/EDV

78
Q

Vasodilation, perfusion and incr CO

A

in metaboliclaly active muscle
via metabolites
K+, pH, adenosine, Pi, head Endo derived relaxing factor
CO must also be increased to maintain perfusion in face of opening vessels

79
Q

BP and exercise demands

A

CO incr necessary to sustain incr perfusion
opening one large vascular bed - decr TPR, reduce BP in spite of CO increase
generalised vasoconstriction

Physiology (4 decks)

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