CVS 5 - Control of Cardiac Output Flashcards
Define the following terms:
- After-load
- Preload
- Central Venous Pressure (CVP)
- Arterial Pressure
- Total Peripheral Resistance (TPR)
- Afterload = The load the heart must eject blood against (roughly aortic pressure)
- Preload = Amount the ventricles are stretched/filled - related to EDV
- CVP = The pressure in the large veins draining into the heart
- Arterial Pressure = The pressure in large arteries
- TPR = Resistance to blood flow offered by all systemic vasculature
How does constriction of arterioles affect resistance and the pressure in the venous + arterial side of capillaries?
- Constriction of arterioles causes an increase in resistance.
- This causes a decrease in pressure on the venous side and an increase in pressure on the arteriole side
What are the effects of the following scenarios on arterial and venous pressure …
1) TPR falls, CO unchanged
2) TPR rises, CO unchanged
3) CO falls, TPR unchanged
4) CO rises, TPR unchanges
1) Arterial pressure decreases, venous rises - as blood flows through vessels more easily towards the venous side causing pressure increase.
2) Arterial pressure rises, venous decreases - vice versa of scenario 1.
3) Arterial pressure decreases, venous rises - as more blood left in heart after contraction, so venous pressure increases
4) Arterial pressure rises, venous decreases - More blood being pumped from heart so refills more easily, causing venous pressure to drop.
How does the systemic circulation and heart respond to an increased demand for blood in tissues?
- Arterioles and pre-capillary sphincters dilate, decreasing TPR.
- The heart needs to pump more so that arterial pressure doesn’t fall and venous pressure doesn’t rise.
- The heart responds to changes in arterial bp (aBP) and CVP via intrinsic and extrinsic mechanisms.
NB:
- Intrinsic = Starling’s Law
- Extrinsic = ANS control
How is CO and SV calculated and what are the typical values?
How can you increase SV?
- CO = HR x SV (5L/min)
- SV = EDV - ESV (70mL) - or 67% of EDV
- By increasing EDV or decreasing ESV
What is the relationship between venous pressure, ventricular filling and LV pressure during diastole?
- Higher venous pressure = more ventricular filling
- higher ventricular filling = higher LV pressure
What is the Frank-Starling law of the heart?
What is the Starling curve essentially telling us?
- The more the heart fills, the more the fibres are stretched, the harder it will contract.
- The harder it contracts, the larger the SV. An increase in stretch will be caused by an increase in venous pressure
- How much the ventricle fill depends on compliance
- Starling curve is telling us that increased venous return = increased LVEDP and LV volume (pre-load) = causing increased contraction = increased SV.
What is the “length-tension relationship” for cardiac muscle fibres?
What does the Starling law of the heart ensure?
If you increase the sarcomere length via stretching, there is an increase in Ca2+ sensitivity and therefore cross-bridge formation. Upto an optimum sarcomere length of 2.2um.
Starling law of the heart is an INTRINSIC control mechanism, ensuring both sides of the heart maintain the same output. Same volume of blood pumped to the body must also be pumped to the lungs.
What extrinsic factors can increase contractility?
- Sympathetic Stimulation + Circulating Adrenaline
What is the effect of increasing arterial pressure on SV?
- This increases afterload, which is a result of increased TPR
- Therefore harder for the heart to pump blood out, decreasing SV.
- This increased TPR also reduces venous pressure and therefore reduces filling (EDV) and therefore SV.
What 2 factors determine CO + what are they determined by?
1) How hard it contracts - determined by EDV + contractility. (NB: contractility + HR controlled by ANS)
2) How hard it is to eject blood (determined by afterload)
How does the CVS respond to local vasodilation in the gut caused by eating a meal?
1) TPR falls as a result of dilation, leading to decreased aBP and increased vBP
2) The heart responds by increasing HR + SV, which work to increase CO.
3) This increases aBP and decreases vBP back to typical values
What are the consequences and responses of the CVS to standing up?
1) Standing up causes pooling of blood in legs due to gravity, causing decreased vBP, therefore decreased CO and decreased aBP.
2) As aBP and vBP have both decreased, the CVS cannot adjust via an intrinsic mechanism.
3) Baroreceptor reflex + ANS increase HR, contractility and TPR, so postural hypotension is avoided (see later lecture)
How does the CVS system respond to exercise to increase CO?
1) Calf muscle pumping + vasoconstriction increase venous pressure
2) Increased sympathetic and decreases PS drive increase HR
3) Increased sympathetic drive increases contractility
- All together work to increase CO.
What is jugular venous pulse (JVP)?
What kind of conditions increase JVP?
- Biphasic pulse measure in right internal jugular vein - a direct column of blood connected to RA. Also measured with central line inserted into jugular vein.
- Those that affect right side pumping or those that affect filling of the heart.