Control of Cardiac Output Flashcards
afterload
preload
TPR
- load the heart must eject blood agaisnt (aortic pressure)
- amount the ventricles can be stretched (filled) diastole (Related to EDV or CVP central venous pressure)
- systemic pressure resistance to blood flow offered by all systemic vasculature
greatest difference in the pressure drop between vessels?
contraction fo arterioles?
- arteries and arterioles because arterioles have a lower lumen and thicken tunica media (smooth muscle) c increased resistance
- contractions causing increased resistance = increased pressure = decrease of flow
CO unchanged TPR decreases
= increase blood flow , lower AP, increase VP (heart pumps more so that AP doesnt fall and VP doesnt rise because rise in VPwill cause pulmonary oedema)
^ ABP = harder for bloodto be pumped around the body
TPR increases CO unchanged
= decreased VP decreases and AP increases
CO increaased TPR unchanged
- increased AP = TPR unchanged = decreased VP
decreased CO and TPR unchanged
decreased AP = unchanged TPR = increased VP
what do arterioles and x capillaires do to get more blood to tissues
how does heart respond to changes in CVP and aBP?
- x = precapillary sphincters -dilate
- intrinsic ( vasodilation, vasoconstriction)
- extrinsic ( SYM stimulation to cause vasoconstriction and increase aBP decrease CVP / PARASYM to caue vasodialtion decrease aBPand icrease CVP)
EDV?
ESV?
how does this relate ot SV and how do you increase SV?
- MAX volume of ventricle
- b left in the heart post systole (70ml 67% of normal EDV)
- SV = EDV- ESV
increase EDV or decreasing ESV
whats frank-starlings law of the heart?
if you stretch the heart before filling it it will contract harder up to a limit, and the harder the heart contracts the bigger the SV , an increase in VP will fill the heart up more
draw frank-starling curve?
what does increasing Venous return cause
image
- increase venous return increases EDV resulting in increase ventricular volume so increased preload so extra blood pumoed out the ventricle
- normal LVEDP is 8mmHg and SV = 70ml
what happens with the sacromere
it overlaps , alowing it to pull apart more allows more mysoin actin crossbridges and increased calcium sensitivity in cardaic muscles
what does starling law ensure?
ensures both sides of the heart pump maintain the same output since both pumps work in series makes sure pulmonary and systemic volume is the same
whats contractibility? and force of contraction?
graph
what can increase contraction
- contractability = force of contraction for given fibre length
- change in contractibility = chage starling cruve slope as increase in contractibility = ^ EDV = ^ SV
- sympatheti stimulation increased and with it increaes teh circulating adrenaline = increases contractibility rducing sympathetic stimualtion decreases contractibility
pressure in the aorta and agaisnt aorta?
increasing aBP affect on SV
against = afterload
oin = aortic impedence(resistance)
increaing ap makes it harder to blood to be pushed out of heart
- DECREASES IT becaue filling of heart decreases (diastole decreeases systole is always constat)
- increased TPR, decreased VP = decrease filling of heart
factors affecting CO
- how much ventricles empty(ESV); how hard it contracts which is determined by EDV and contractiblity
- how hard it is to ject the blood (aortic impedance (aBP)
- CO=SV x HR (contractibilitya dn HR controlled by ANS)
- decreae in aBP due to PSY causes the SYMP to come and increase HR and increase contracitbiltiy
describe this graph
a = atrial systole
c= closure of mitral valve
x = decrease in atrial pressure due to ventriular systole
v = filling of the atrium against the closed mitral valve
y = opening of the tricupsid valve
raised JVP but normal waveform
large a wave
absent a wave
cannon a wave
steep y wave
fluid overload or right sided heart failure
large a wave = pulmonary hypertension (due to. pul. emoblism) / pul. stenosis
absent a wave = artrial fibrillation
cannon a wave = heart block
steep y wave = tricupsid regurgitation
