BIOL 208 Lecture Notes - Lecture 9: Carotid Sinus, Stroke Volume, Cardiac Output
Cardiac output (CO)
***CO is the measure/amount of the blood pumped by each ventricle per minute***
● the actual amount is 5.25 liters
● cardiac output is equal to stroke volume (SV) X heart rate (HR)
● **stroke volume is amount of blood ejected when ventricle contracts
● if SV is 70ml and HR is 75 BPM, cardiac output is 5,250
Cardiac reserve
***is the maximal amount that the cardiac output can increase above normal***
● as it turns out its been determined under normal circumstances the cardiac reserve is 7
Stroke volume
● 3 components
● 1) endogenous (aka intrinsic)
● theres something within heart playing a role in controlling stroke volume
● the blood coming into right atrium continues to flow and lot flows into ventricle, and the
ventricle even at start of diastole will expand. after that, atrial kick, actual contraction, artial
systole, and more blood inject, so now you come to end volume is end diastolic volume.
point is theres 2 factors that really determine end diastolic volume, but they can vary
depending on 2 factors
● resting end diastolic volume is determined by 2 factors
● 1) incoming venous pressure - greater venous pressure, more blood flows in, more blood
coming into atrium and the ventricle, meaning there may end up being a larger than normal
end diastolic volume due to this
● 2) length of ventricular diastole - longer than normal heart beat, more and more blood flowing
into the ventricle, ventricular walls stretch more and more
● the more blood comes in, walls stretch greater. brings about the certain law of the heart,
starlings law, frank starlings law
Cardiac output (review)
● the cardiac output is equal to the stroke volume X HR
● standard number for SV is 70ml X HR (75) = 5,250ml (5.25L)
● factors that control these things
● factors that control stroke volume;
Frank Starling’s law of the heart
***within limits the greater the length of stretched ventricular fibers the stronger the contraction (like
a rubber band)***
Stroke volume
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● *** stroke volume is the amount of blood ejected from the left ventricle into the aorta each
time the ventricle contracts (SV = 70ml)
● 3 components
● 1) endogenous (aka intrinsic)
● theres something within heart playing a role in controlling stroke volume
● the blood coming into right atrium continues to flow and lot flows into ventricle, and the
ventricle even at start of diastole will expand. after that, atrial kick, actual contraction, artial
systole, and more blood inject, so now you come to end volume is end diastolic volume.
point is theres 2 factors that really determine end diastolic volume, but they can vary
depending on 2 factors
● resting end diastolic volume is determined by 2 factors
● 1) incoming venous pressure - greater venous pressure, more blood flows in, more blood
coming into atrium and the ventricle, meaning there may end up being a larger than normal
end diastolic volume due to this
● 2) length of ventricular diastole - longer than normal heart beat, more and more blood flowing
into the ventricle, ventricular walls stretch more and more
● the more blood comes in, walls stretch greater. brings about the certain law of the heart,
starlings law, frank starlings law
Control of Stroke Volume (cont.)
2) Exogenous (extrinsic) component
● discussed in influence in heart rate. same for heart rate and SV
3) transmural pressure component
● respiratory pump
● when you inhale, pressure around major veins in chest diminishes and allows for slight
expansion of walls due to less pressure and allows for more blood to come up
● same pump works around heart, because heart is in same area
● every time breathing, especially during exercise and breathing heavy, what happens is
pressure around heart wall is less, diminishes for small period of time so heart wall naturally
expands
● as this happens, the internal lumen of the ventricle expands so more blood can get inside
● facilitates the stroke volume in the end
● walls stretch more, therefore contraction will be stronger - starlings law
Heart rate
***the changing HR is the principle mechanism of short term control over both the CO and therefore
the BP***
● if all of a sudden you need to increase BP, CO increase rate of heart beat is quickest way to
get to it
Endogenous (intrinsic) factors that control heart rate
● nodes, nodal system
● AV node, SA node, AV bundle, branches, purkinjie fibers etc.
Exogenous (extrinsic) factors that control heart rate
● most of these effect heart rate also effect stroke volume (above)
1) nervous system control
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● ANS - sympathetic (accelerates) and parasympathetic (slows down) - these fibers leave the
brain and do this
● these are all EFFERENT fibers. they're called effectors. they are coming from the brain/CNS
to go bring their effect
● Tachycardia - rapid heart rate, above normal. 125, 130 BPM
● Bradycardia - slowing down of heart rate
● 2 centers that control HR/overall heart activity (review);
● CAC - cardioacceletory center. sympathetic fibers leave here, accelerate the rate function of
the heart
● CIC - cardioinhibitory center. parasympatheticic fibers, will slow down the heart rate when
stimulated
Reflex pathways
● play role in the overall control of the heart rate or stroke volume so appropriate amount of
blood can leave heart and travel
● 1) carotid sinus reflex - Marey’s law of the heart (MLOH)
● at the very base of internal carotid are special presso-receptors, they monitor pressure. also
known as baro-receptors.
● these constantly monitor BP
● BP is too high or too low, they send off impulses from receptors to the brain center, the
cardiac center
● these are afferent fibers
● these are called sensory fibers
● the internal carotid supplies the brain
● monitor blood pressure going to the brain
● ***MLOH defines the inverse relationship (concept) between A) the BP of the vessels taking
blood to the brain and B) the HR***
● keyword is inverse, meaning if the rate is increased, something else will go down
● for example, lets say BP in carotid artery is lower than normal, automatically sends receptors
in the sinus, the baro-receptors pick up drop and send impulses to the CAC to activate
sympathetic impulses going to the heart
● if the pressure going to the brain is too high, you will have the impulses leaving the sinus and
it will stimulate the CIC to active parasympathetic impulses going to the heart, HR will go
down
● changing HR is quickest way to change CO. both effect SV
● 2) aortic sinus reflex
● does same thing MLOH does, carotid does
● EXCEPT doesn't monitor blood to brain, monitors blood to the rest of the body
● found in aortic arch
● if theres abnormal pressure in aortic arch, sufficient blood not to rest of body, receptors fire
afferent impulses to CAC increasing HR, pushing more blood to that area
● another example of inverse relationship
● 3) right heart (atrial) reflex - bainbridge reflex
● this is NOT inverse, but a DIRECT relationship
● if theres an increase in amount of blood flowing into right atrium, pressure in right atrium
increases
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Document Summary
***co is the measure/amount of the blood pumped by each ventricle per minute*** the actual amount is 5. 25 liters. Cardiac output is equal to stroke volume (sv) x heart rate (hr) **stroke volume is amount of blood ejected when ventricle contracts if sv is 70ml and hr is 75 bpm, cardiac output is 5,250. ***is the maximal amount that the cardiac output can increase above normal*** As it turns out its been determined under normal circumstances the cardiac reserve is 7. Cardiac output (review) the cardiac output is equal to the stroke volume x hr. Standard number for sv is 70ml x hr (75) = 5,250ml (5. 25l) factors that control these things factors that control stroke volume; ***within limits the greater the length of stretched ventricular fibers the stronger the contraction (like a rubber band)*** *** stroke volume is the amount of blood ejected from the left ventricle into the aorta each time the ventricle contracts (sv = 70ml)
