Integrated CV response 1

Question 1

Why blood continues to flow when standing

Answer 1

pump pressure is higher than outflow pressure. Arterial pressure always higher than venous pressure

Question 2

Supine mean capilary pressure

Answer 2

30mmHg

Question 3

What happens to foot BP when standing

Answer 3

rise by around 90mmHg. Foot capillary pressure rises, increases filtration, feet swell

Question 4

How orthostasis challenges CV system

Answer 4

Fall in cardiac output=veins are distensible so when the valves shut, CO output momentarily exceeds flow to heart->vein contain more blood->pressure in vein rises but CVP still falls thus CO falls
Plasma vol lost: hydrostatic pressure in feet rises but onccotic doesn’t so plasma lost to interstitium causing oedema

Question 5

Mechanisms limiting effects of orthostasis

Answer 5

1. upon standing and blood distribution to lower body, decrease stroke volume and CO, decrease blood flow to brain, decrease MABP in upper body->activate baro and volume receptors->increase HR, increase vasoconstriction, increase TPR->change minimised or reversed
2. Arteriolar constriction by reflex sympathetic vasoconstriction via baroreceptors and a local sympathetic axon reflex to reduce blood flow on standing
3. skeletal muscle pumping aiding venous return

Question 6

sketch graph of time vs venous pressure in foot for healthy and valve failure

Answer 6

ref. notes, venous pressure=chronic high pressures

Question 7

Venous pressures above heart on standing

Answer 7

Pressure in veins above heart falls. Veins outside the crainium collapses a few cm above the heart to prevent internal pressures from falling below 0. Blood still flow through margins of collapsed veins. Veins in cranium don’t fall and is about -10mmHg. Cerebral blood flow can decrease by 20%

Question 8

Why fainting after prolonged standing

Answer 8

Barorecpetor reflex becomes less effective, blood continues to pool as pressure gradient driving flow through veins decrease+fall in pulse pressure+rise in HR and TPR–>MABP falls->fall in TPR->fall in BP and cerebral blood flow–>faint->horizontal, venous return restored

Question 9

Why veins within cranium don’t collapse

Answer 9

Downward displacement of CSF within subarachnoid space->creates negative intracranial pressure which prevents veins within the cranium from collapsing.

Question 10

Supine to upright, what happens to the following: central blood vol, CVP, stroke volume, heart rate, contractility, cardiac output, limb+splanchnic flow, TPR, cerebral flow

Answer 10

central blood vol=decrease 400ml, CVP=decrease 3mmHg, stroke volume=decrease 40%, heart rate increases 25%, contractility increases, cardiac output decreases 25%,
(limb+splanchnic flow=decreases 25% , TPR=increases 25%,) so only transient fall in blood pressure
cerebral flow=decreases 25%

Question 11

Sketch graph of relative energy potential against time

Answer 11

ref. notes. Immediate=due to muscle ATp and phosphocreatine which are depleted very quickly
Non oxidative=anaerobic glycolyysis muscle glycogen->glucose->lactate falls rapidly with time
Oxidative=aerobic metabolism using glucose, lactate and FA entering from blood. Is ssustained, requires increased O2 delivery to working muscle

Question 12

sketch graph of muscle work against O2 consumption

Answer 12

linear starting 0.25 and plateaus at VO2 max

Question 13

O2 consumption equation

Answer 13

O2 consumption=Cardiac Output(arterial-mixed venous O2 content)

Question 14

Basal and max work O2 consumption values

Answer 14

Basal: around 0.25lmin-1
Maax: around 5lmin^-1

Question 15

Arterial O2 content equation and does exercise affect this

Answer 15

Arterial O2 content=[Hb]xarterial O2 saturationx1.34)

unaffected by exercise or physical fitness

Question 16

Effect of exercise on venous O2 content

Answer 16

Falls progressively as exercise intensity increases and is limited by the need to maintain a capiillary PO2 sufficient to drive diffusion. Similar in fit and unfit but improves with training as increase in capillary density and reduces diffusion distance

Question 17

Effect of exercise on cardiac output

Answer 17

Increases

Question 18

What determines max O2 consumption

Answer 18

Cardiac output

Question 19

Cardiovascular adjustment flow chart draw

Answer 19

ref. notes

Question 20

Control of regional blood flow with exercise

Answer 20

Active muscle: vasodilation and capillary recruitment due to local metabolites e.g. increase PCO2, decrease PO2, increase H_, increase adenosisne
Inactive muscle and ssplanchnic circulation: sympathetic vasoconstriction
Skin: Initial vasoconstriction (increase smpathetic) followed by vasodilation (decrease sympathetic) due to temp rise. At max exercise, vasoconstriction dominates
Net effect: fall in TPR

Question 21

How to increase muscle blood flow

Answer 21

redistribution of blood flow not enough, increase CO. Mostly due to increase in heart rate but stroke vol also increase because enhanced filling of the heart (increase filling pressure) due to increase in CVP+increase in skeletal muscle pump->Frank Starling mechanism and enhanced emptying
NB increased SV occurs even thouh reduced time for filling

Question 22

What happens to CO and TPR at exercise and changes associated with MABP

Answer 22

CO increases, TPR falls, MABP increases

systolic increases, diastolic doesn’t change much

Question 23

Effects of isometric exercise

Answer 23

progressive rise in BP and HR, systolic and diastolic pressures both increase. For any given O2 consumption BP rise is greater than in dynamic exercise and fails to plateau

Question 24

Why BP rise is higher in static than dynamic exercise

Answer 24

TPR falls in dynamic whereas it falls less, if not rises in static