Control Of Cardiac Output Flashcards
After load
The load the heart must eject blood against (roughly equivalent to aortic pressure)
Preload
Amount the ventricles are stretched (filled) in diastole – related to the end diastolic volume or central venous pressure
Total peripheral resistance
sometimes referred to as systemic vascular resistance – resistance to blood flow offered by all the systemic vasculature
What happens to pressure of fluid in a tube as it encounters resistance:
The pressure that the blood exerts drops as it flows through ‘a resistance’
The arterioles offer the greatest resistance, have narrow lumen and have largest amount of muscle in tunica media
Constriction of the arterioles increases the resistance.
This will cause pressure in the capillaries and on the venous side to fall but will cause pressure on the arterial side to rise.
Pressure drops as you get to the venules and veins (makes sense as blood flows from hight pressure to low pressure)
Effects of changing total peripheral resistance
If TPR (total peripheral resistance) falls and CO us unchanged - this will lead to arterial pressure falling and venous pressure will increase - pressure drops on arterial side as easier to pass blood through capillaries - so more blood on venous side so pressure increases
If TPR increases and CO is unchanged - arterial pressure will increases and venous pressure will fall (vice versa to reason above)
If CO increases and TPR is unchanged, arterial pressure will increase and venous pressure will fall
If CO decreases and TPR is unchanged, arterial pressure will fall and venous pressure will increase
Changes in demand for blood
The heart must meet changes in demand for blood
If the tissues need more blood the arterioles and precapillary sphincters will dilate, Therefore peripheral resistance falls
The heart needs to pump more so that arterial pressure does not
fall and venous pressure doesn’t rise
The heart ‘sees’ changes in this demand as changes in arterial blood pressure (aBP) and central venous pressure (CVP)
The heart responds to changes in CVP and aBP by INTRINSIC (effects of myocardial cells)and EXTRINSIC (effects of NT and hormones) mechanisms
Cardiac output and stroke
Cardiac Output = Stroke Volume x Heart Rate
Stroke Volume = end diastolic volume – end systolic volume
SV = EDV - ESV
Typical stroke volume in ‘average text-book man at rest’ is about 70ml
This is about 67% of normal EDV (amount of blood in the heart at diastole)
Can increase SV by increasing EDV or decreasing ESV (blood left in the heart at the end of systole)
Ventricular filling
In diastole the ventricle communicates with the atrium and the veins but is isolated from the
outflow tract
The ventricle fills until the walls stretch enough to produces an intraventricular pressure equal to the venous pressure
The higher the venous pressure, the more the heart fills
The more the heart fills, the higher the left ventricular pressure
This relationship is the Ventricular Compliance Curve
Compliance can be increased or decreased in diseased states
When you increase the blood in the heart, so volume increases, but so does the pressure
Frank Starling law of the heart
Like skeletal muscle – if you stretch the fibres of the heart before contracting, it will contract harder
The more the heart fills, the harder it contracts (up to a limit)
This is the Frank – Starling Law of The Heart
The harder the heart contracts, the bigger the stroke volume
An increase in venous pressure will fill the heart more – How much the ventricles fill depends on the compliance
Otto Frank and Ernest Starling - Demonstrated that stretching the ventricles by increasing the filling of the heart increased the force of contractions
The starling curve
Increasing venous return leads to increased left ventricular end-diastolic pressure (LVEDP) and volume (‘increased preload’).
This causes an increase in stroke volume, so that the extra blood is pumped out of the ventricle.
The ‘normal’ operating point at rest is with an LVEDP around 8 mmHg and stroke volume of ~70 ml
Length tension curve for cardiac muscle
If sarcomeres length is too short, filaments overlap which interferes with contraction
In cardiac muscle you also get an increase in calcium sensitivity as the muscles fibers are stretched
Optimal sarcomeres length is 2.2um
Contractility and force of contraction
Contractility is the force of contraction for a given fibre length
SNS/ Noradrenaline will increase contractility
A change in contractility is seen as a change in the slope of the Starling Curve
An increase in contractility will increase the force of contraction
EXTRINSIC factors such as sympathetic stimulation and circulating adrenaline can increase contractility
Reducing sympathetic stimulation will reduce contractility
Effect of increasing arterial pressure on stroke volume
Effect of increasing arterial pressure on stroke volume
Afterload is the pressure that the heart has to pump against
This is the pressure in the aorta (aortic impedance)
Arterial (aortic) pressure is increased when the peripheral resistance is increased
– This makes it harder for the heart to pump out
Increased TPR also reduces venous pressure and therefore reduces filling of the heart
Over time you can get an inappropriate increase in arterial pressure - The heart will have to work harder
Factors determining cardiac output
How much the ventricle empties (end systolic volume) depends on:
- How hard it contracts -which is determined by the end diastolic volume (how much the heart fills) and contractility (increased by sympathetic drive)
- How hard it is to eject blood determined by aortic impedance (afterload) (roughly arterial pressure)
Cardiac Output = Stroke Volume x Heart Rate
Contractility and heart rate are controlled by the autonomic nervous system
A decrease in arterial BP (sensed by baroreceptors in the aortic arch and carotid body) will reduce parasympathetic NS activity and stimulate sympathetic NS increase heart rate and increase contractility
Demand led pumping
Eg. Of how the CVS responds
If the metabolism of the body increases, then TPR will fall to supply more blood
This will result in a fall in arterial pressure and an increase in venous pressure
The heart will respond by pumping more and stretching more,- drop in arterial pressure will be noticed by baroreceptors, and stimulate the SNS to stimulate the heart to “have” more CO
E.g. eating a meal
Get local vasodilation in the gut which leads to -
Drop in TPR, there for getting decrease in arterial pressure and increase in venous pressure, causing a increase in HR and SV, therefore increasing CO, therefore increasing arterial pressure and decreasing venous pressure
E.g. Standing up -
Standing up causes ‘pooling’ of blood in legs due to effect of gravity on a column of liquid
Causing a decrease Venous Pressure, causing a decrease in Cardiac Output causing a decrease in Arterial Pressure
Now both arterial and venous pressure have changed in the same direction
Cannot adjust by intrinsic mechanisms
Baroreceptor reflex and autonomic nervous system increase heart rate AND increase TPR
If reflexes don’t work you get postural hypotension
Exercise -
Initially muscle pumping and venoconstriction returns more blood to the heart
Later decreased TPR also increases venous return
Very early response of increased heart rate (decrease parasympathetic drive, increase sympathetic drive)
Increased contractility (increased sympathetic drive)
Note: increased venous pressure alone would move ventricular function to the top (flat) part of the Starling curve - wouldn’t be able to reach right to the top of the starling curve
An increase in Venous Pressure combined with an increase in Heart Rate and Contractility, help to increase Cardiac Output
