regulation of cardiac output and blood pressure Flashcards
(14 cards)
what is cardiac output, units of measurement and calc
- volume of blood pumped out of heart every minute
- millilitres or litres / min
- q = hr x sv
typical values of q, hr, sv
- rest
- peak exercise- 1- untrained, 2- trained, 3- elite
- q= 5.6 l/min, hr= 70bpm, sv= 80ml
1- q= 20 l/min, hr= 192 bpm, sv= 105 ml
2- q= 23 l/min, hr= 190 bpm, sv= 120 ml
3- q= 30 l/min, hr= 178 bpm, sv= 170 ml
relationship between q, hr, sv as exercise intensity increases
- increase intensity, all increase
- sv plateaus at sub max as not enough time to fill
- further increase in q due to increase hr
- at hr max, sv and therefore q falls slightly as theres very little filling time
control of hr
- 2 neural control
- 1 blood control
- parasympathetic nerve endings (vagus nerve) secrete acetylcholine into atria which decrease hr as its around sa and av nodes
- sympathetic fibres (cardiac nerves) release norepinephine supplying av and sa node increasing hr
- circulating epinephrine increase hr but takes longer to reach heart than neural
how sympathetic and parasympathetic stimulation impact hr
- parasympathetic stim of SAN cause hyperpolarisation so depolarisation drift and therefore hr slower as its further from threshold and slope shallower
- sympathetic stim of SAN cause more depolarisation so depolarisation drift and therefore hr faster as its closer to threshold and slope sharper. it also shortens AVN delay, shortens myocyte AP, increase speed of relaxation as well as contraction
control of sv
- 2 factors its regulated by
- 2 processes that regulate force of contraction
- explain each
- force heart contracts, arterial pressure against which they have to eject blood
- length tension properties of cardiac muscle cells and hormonal influences on contractility
- length tension relationship- frank starling mechanism, greater venous return leads togreater EDV, therefore SV as greater stretching of cardiac muscle fibres cause more forceful contraction
- sympathetic norepinephrine and circulating epinephrine increase force and speed of contractions
blood pressure
- what is it
- why must it be maintained
- bp in arteries vs veins
- is blood pressure different closer and further from heart
- what is the secondary pump and why important
- the driving force for the CVS (pressure difference between arteries and veins)
- high enough to create flow, not too high putting excessive stress on CVS
- arteries pulsatile, veins continuous
- higher closer to heart
- arteries stretch and recoil so flow is fairly consistent and it ensures blood keeps moving forward even in diastole
4 ways to measure bp
- direct cannulation
- cuff and stethoscope (tighten and listen)
- automated wrist/arm cuff monitor (shows values on screen)
- beat to beat bp monitor (finger cuff measuring changes of blood volume in finger)
impact of different cuff tightnesses
- looser than diastolic pressure- free flow no sound
- tighter than systolic pressure- no flow, no sound
- between systolic and diastolic pressure- no flow in diastole, flow in systole, so vessel opens and closes making tapping sound
how to calculate MAP and why we use that calc
-MAP= DBP + ((SBP-DBP) / 3)
- diastole is 2/3 of the cycle so MAP is closer to DBP value
BP normal values
SBP around 120 mmHg, DBP around 80mmHg, MAP around 93 mmHg for young adults of average build
3 factors affecting BP
- age- arteries stiffer as lose elasticity so BP increase
- BP higher in foot than head due to hydrostatic pressure
- gender- until menopause, women have lower bp than men due to female hormones
impact of dynamic and static exercise on BP, link to exercise prescription)
- dynamic (eg. walk, run, cycle, etc) keeps BP steady as systolic increase and diastolic decrease
- static (eg. lift weights) mean bp increase as bothb systolic and diastolic pressure increase (dangerous for cardiac patients who need to maintain bp)
determinants/calc for MAP
MAP= Q x TPR
-Q=HRxSV
-TPR is total resistance to blood flow in all tissues of body
