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Cardiovascular Physiology Flashcards

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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
what opens and closes Ca channels
membrane depolarisation - open hyperpolarisation - close
26
sympathetic vasoconstrictor control
-most important element of BP control -AP in postganglionic nerves can release NA along with other co-transmitters
27
describe the sympathetic neuroeffector junction
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
28
sympathetic innervation
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
29
adrenal medulla
releases adrenaline
30
circulation to an organ depends on:
intrinsic/local factors autoregulation, mechanical compression extrinsic/external factors - nervous and hormonal
31
autoregulation
ability of an organ to maintain blood flow despite changes in perfusion pressure occurs in absence of extrinsic factors intrinsic factors: myogenic, metabolic, endothelial
32
posture and circulation
affects BP hydrostatic pressure pooling in lower extremeties reduce cerebral BF normally compensated
33
cardiac output =
CO= SV xHR
34
how to measure CO in humans
Fick - uptake or relase of substance deoendnet on BF Dye Dilution Thermodilution Doppler Flow ECG
35
Pros and Cons of Fick Principle
-Good for low COs -fairly invasive (cannula) -tricuspid or pulmonary valve issues -not very accurate or reliable
36
describe thermodilution
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
what was Frank's finding
strength of ventricular contraction increased when the ventricle was stretched prior to contraction
38
what was Starling's finding
increasing VR -> increased SV
39
what makes preload
VR stretches the ventricles and increases LVEDP
40
starling's heart-lung preparation
-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
factors influencing venous return
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
what is afterload
the 'load' that the heart must eject blood against
43
what is afterload determined by
the level of constriction of the BVs into which the blood is flowing - determined by the TPR
44
factors influencing CO
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
describe Laplace's Law
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
describe nervous and humeral factors influencing cardiac output
chonotropic - enhance cardiac function by increasing HR inotropic - length dependent activation of myocardial contractility eg by increasing ca2+ release
47
inotropic effects on SV
positive; increase contraction by incr ca2+ entry or release. reduced afterload negative; decreased contractility, drugs reduce workload, beta blockers, increased afterload
48
what is the steady state operating point of the heart
point at which the heart functions most efficiently with the least effort
49
effect of changes in inotropic mechanisms and steady-state operating point
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
what other factors affect steady state operating
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
what are the 3 features of exercise
increase metabolites increased nervous activity increased muscle pump
52
effect of increased metabolites in exercise and means of increase to CO
vasodilation - decrease TPR chemoreceptors - increase nervous activity
53
effect of increased nervous activity in exercise and means of increase to CO
incr sympathetic activity - incr HR and inotropic effect decr parasympathetic activity - incr HR
54
effect of increased muscles pump in exercise and means of increase to CO
increase VR -> increased SV/preload
55
pregnancy effect on heart
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
describe heart failure
-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
describe the effects of heart failure
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
what does ESPVR represent
inotropic state of the ventricle
59
describe intracellular volatage and current changes associated with excitation of the ventricle
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 4. more permeable to K at rest- free to move conc grad 5.at sufficient neg voltage K+ opposed. = equilibrium potential
60
describe atrial action potential
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
describe AV node Action Potential
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
arterial BP is directly related to:
Cardiac output TPR
63
Total peripheral resistance depends on
contractile state of smooth muscle in the arterioles depends on perfusion pressure level of vasodilation nervous inputs
64
Bainbridge Reflex
-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
ADH and BP
normal/raised BP inhibits supraoptic nerve and paraventricular nerve dependnent release of ASH
66
Renin and Blood pressure
-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
what does a rise in BP lead to
incr baroreceptor stimulation dcer renin released
68
what does a rise in BP drive
decr symp inotropic effects, decr LV contraction force decr symp VC decr HR decr ADH secretion and decr water reaborption
69
what does a rise in BP result in
decr CO, decr TPR, decr BP to normalise BP
70
what does a fall in BP lead to
decr barorecptor stimulation incr renin release
71
what does a fall in BP drive
incr symp inotropic effects, incr LV contraction force incr symp VC incr HR incr ADH and water reabosorption
72
what does fall in BP lead to
increased CO, TPR, BV normalisation of BP
73
Behold Jarisch Reflex
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
cushings reflex
cerebral ischaemic reflex compressive ischameia of CNS incr BP, initial tachycardia followed by bradycardia, then irregular breathing
75
chemoreceptor reflex
-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
3 factors of cardiac output
sympathetic loading and parasympathetic unloading hormones starling forces
77
ejection fraction =
SV/EDV
78
Vasodilation, perfusion and incr CO
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
BP and exercise demands
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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