Cardiac Output L10 Flashcards
What is the cardiac cycle?
All things that are associated with ONE heartbeat
Forces blood from areas of High pressure –> to areas of low pressure
What is the concept of Supply and Demand in Cardiac Output?
CO is supply
Metabolising Tissue, muscle and/or organs are the consumers which Demand energy and therefore demand O2, which is supplied by the heart’s blood
-their demand is due to their biochemical processes which need energy and therefore creates demand
The Heart’s supplying of this demand = CO
increased demand = increased HR
The hearts job is to supply (O2) based on/in response to demand (energy needs of metabolising tissue)
What is the job of the heart?
The heart’s job is to supply (O2) based on/in response to demand (energy needs of metabolising tissue)
What is CO supply or demand?
CO is the hearts supply (due to demand/controlled by metabolising tissue demand)
Why does metabolising tissue have demand?
Due to their biochemical processes which need energy, Therefore to get this energy they need O2 (demand) (and is supplied by the heart)
Why does the heart generate pressure?
To drive blood through the circuits and mediate flow into the aorta in particular
What is the equation for cardiac output?
CO = HR x SV CO(Lmin-1) = bpm x mLbeat-1
What is CO?
Cardiac output
The volume of blood ejected into the aorta(from the LV) per minute
Lmin-1
(-note: has to include LV and aorta, as we are talking about the genuine amount actually leaving the heart, not just being pumped - R is not systemic)
-effectively we pump out/our CO is just over our total blood volume (5L) every minute
–CO=HRxSV= 70bpm x 75mLbeat= 5.25Lmin-1
=supply is CO, and is based on demand
- Venous return is linked to CO
Venous return in the volume of blood returning from the vasculature, into the heart every minture
What is the rate of CO at rest?
approximately our entire blood volume (5L) get pumped right around out body every minute
CO = HR x SV = 70bpm x 75 mLbeat-1 = 5.25Lmin-1
because at rest CO is between 4-7 Lmin-1
What is CO cardiac output linked to?
Venous return
venous return is linked to CO
-venous return is the volume of blood returning form the vasculature, into the heart every mintue
What is venous return?
the volume of blood returning form the vasculature, into the heart every minute
-is linked to CO
Is cardiac output linked to anything?
Venous return
What is venous return linked to?
CO
Wha tis the volume of blood ejected into the aorta (From the LV) per minute?
Cardiac output
Lmin-1
(-note: has to include LV and aorta, as we are talking about the genuine amount actually leaving the heart, not just being pumped - R is not systemic)
What is the unit for CO?
Lmin-1
What is Lmin-1 the unit for?
Cardiac output
What is SV?
Stoke Volume
Lbeat-1
The volume of blood ejected by the ventricle during each contraction
SV=EDV-ESV
What is the unit for SV?
Lbeat-1
What is Lbeat-1 for?
SV
What is the volume of blood ejected by the ventricle during each contraction?
SV stroke volume
(each contraction=each beat)
Lbeat-1
What is the equation for SV?
EDV-ESV
What does EDV-ESV equal?
SV
SV = EDV-ESV
What is HR?
Heart Rate
beatsmin-1
the number of heart beats per minute
Increase in demand = increase in HR
What happens if there is an increase in demand?
Increase in HR
What is the unit for HR?
beatsmin-1
What is beatsmin-1 for?
HR
What are proprioceptors?
Joint receptors
sensory detectors on joint/muscle movement
Sends signals to CNS
they Forward project the increased Demand that will occur due to muscle movement/use
“anticipate increased supply of the heart and alerts CNS and therefore heart about it)
What sort of receptors are proprioceptors?
Joint receptors
What is special about the action of proprioceptors?
Forward projects the increased demand that demand due to muscle use/movement
What part of the body receives 20% of total CO?
Kidneys
about 1 L of blood per minute through the kidneys
This allows for the rapid filtering of waste and CO2 generated from other muscles being used, coming out of the bloodstream
-when exercising/during increase muscle use, remains at 20%/get more blood, and therefore filtration will be fast to get rid of the increase waste products used by the increased muscle activity
What is important about the relationship between the Kidneys and CO cardiac output.
Kidneys
about 1 L of blood per minute through the kidneys
This allows for the RAPID filtering of waste and CO2 generated from other muscles being used, coming out of the bloodstream
-when exercising/during increase muscle use, remains at 20%/get more blood, and therefore filtration will be fast to get rid of the increase waste products used by the increased muscle activity
How much blood do the kidney’s receive of CO (Lmin-1)
20% of CO Lmin-1
20% of 5L generated Lmin-1
1 L per min-1 is received by the kidneys
allows for RAPID FILTRATION of waste generated by used muscles
-when exercising/during increase muscle use, remains at 20%/get more blood, and therefore filtration will be fast to get rid of the increase waste products used by the increased muscle activity
Why is it imperative that the kidneys receive 20% of total CO ?(Lmin-1)
for the Rapid FILTRATION of waste products and CO2 generated by other muscles being used
-So when exercising/during increase muscle use, remains at 20%/get more blood, and therefore filtration will be fast to get rid of the increase waste products used by the increased muscle activity
Is the body a high or low flow system?
High flow system
as the body has demand requires quick delivery of O2 for energy
At rest what is CO?
about 5Lmin-1 CO=HR x SV CO= 75bpm x 7-mLbeat =5.25Lmin-1 Cellular metabolic need is reduced Workload has decrease Low demand
During exercise what is CO?
about 19.5Lmin-1 CO=HR x SV CO= 150bpm x 130mLbeat =19.5Lmin-1 Cellular metabolic need is increased Workload has increase Higher demand, therefore CO increases to compensate for sufficient suppl
What is the equation for CO at a rest?
about 5Lmin-1
CO=HR x SV
CO= 75bpm x 7-mLbeat
=5.25Lmin-1
What is the equation for CO during exercise?
about 19.5Lmin-1
CO=HR x SV
CO= 150bpm x 130mLbeat
=19.5Lmin-1
What is the relationship between CO at rest and CO during exercise?
4x increase
-is the concept of Cardiac Reserve
Overall what is the regulation of SV?
More in = More out
By increasing SV = SUPPLY the heart with more blood (more venous return) = more blood being pumped out per beat
-equalising and balancing the right and left sides of the ehart
What 2x Mechanisms is Stroke Volume regulated by?
- Intrinsic regulation
- intrinsic regulation of the FORCE on contraction
- is governed by the DEGREE OF STRETCH of the myocardial fibre at the END OF DIASTOLE (fully filled = fully stretched) - Extrinsic Regulation
- determined by the activity of the AUTONOMIC system, and the CIRCULATION of HORMONES
What is the Intrinsic Regulation of SV stroke volume?
Intrinsic regulation of the FORCE of contraction, governed by the DEGREE OF STRETCH at the END OF DIASTOLE
-the more fully filled = more fully stretched
What is the Extrinsic Regulation of SV stroke volume?
activity of AUTONOMIC system and the CIRCULATION of hormones
What sort of regulation does the circulation of hormones and the activity of the autonomic system have on SV?
Extrinsic regulation
What sort of regulation does the force of contraction(contractility/inotropy) due to the degree of stretch at the end of diastole have on SV?
Intrinsic regulation
When is the intrinsic regulation of SV regarding force of contraction, due to the degree of stretch of the myocytes evaluated?
at the end of diastole (filling)
fully filled = fully stretched
What are the 3x factors which Affect stroke volume?
- Preload
- Contractility
- Afterload
What is the difference between the regulation and affecting of Stroke volume?
Regulation (2x) of SV: via Mechanisms 1. Intrinsic Regulation 2. Extrinsic Regulation --- Affecting (3x) SV: Factors' influence 1. Preload 2. Contractility 3. Afterload
What does the factor of Preload have on SV?
Preload= the amount of blood flowing into the heart = venous return
STRETCH
Greater stretch allows more filling (big EDV)+ greater stretch more crossbridge formation/contraction (big SV)
The pressure of the blood returning into the heart
the STRETCH on the heart before the ventricle contracts (stretch at the End of diastole)
Increased stretch during Diastole
Diastole/filling is driven by the atria’s pumping
Stretching of the myocytes augments, stimulates and enhances the amount of cross bridge formation and contraction
Immediate effects 3x =
1. increase in EDV due to bigger stretch
2. increased volume of blood ejected out
3. increased SV
Increased pressure of major veins = Increased preload = increase stretch of myocytes to fill bigger volume of blood = increased preload/volume of blood entering ventricle =
augmentation of crossbridge formation/increased tension of heart that senses preload=
increased force of contraction
Increased stroke volume
What is another word for venous return?
Preload
What is another word for preload?
Venous return
What is the key word for Preload’s influence on SV?
STRETCH
=greater stretch allows more filling
-before the heart contracts (at the End of diastole/filling)
- more filling = more stretch = more/augmented cross bridge formation
What factor influencing SV has the key word STRETCH?
Preload
What happens when myocytes are stretched?
greater stretch allows more filling
+
Stretching of myocytes stimulates, enhances and augments the cross bridge formation and therefore force of contraction
What augments and enhances cross bridge formation?
Stretching of the myocytes
What are the 3x immediate effects of increased Preload?
1, Increased EDV, due to greater stretch to allow more filling
2, Increased volume of blood ejected out
3, increased SV
What is the flow on effect of increased preload?
Increased pressure of major veins = Increased preload = increase stretch of myocytes to fill bigger volume of blood = increased preload/volume of blood entering ventricle =
augmentation of crossbridge formation/increased tension of heart that senses preload=
increased force of contraction
Increased stroke volume
What are the two main points of Preload?
Increase stretch = increased filling (big EDV)
+
Increased stretch = increased crossbridge formation and contraction (big SV)
What does the factor Contractility have on SV?
Intrinsic regulation
The forcefullness of when the Left Ventricle contracts/squeezes down on the volume of blood in the LV
Inotropy: SV increases when there are positive inotropic agents are present (intrinsic contracting ability)
Determined by preload and afterload
Decreased ESV
Inotropy =/= chronotropy
Increased blood coming in = increased stretch of the wall = augmentation/stimulation of the cross fridge formation = muscles sense increased volume and respond by increased forcefullness of contractility = increase stroke volume
Immediate effets:
Increase SV as the contraction was more forceful,
More blood out
Decreased ESV as there is less blood left in the ventricles(due to the increased force of contraction)
Compounds which Enhance Ca2+ entry during Cardiac APs
Increased Ca2+ entry during action potentials in cardiac muscle INCREASES THE FORCE OF CONTRACTION
-therefore CONTRACTILITY/(inotropy!!!) is under INTRINSIC regulation
Heart failure results in some dead and damaged tissue
compounds containing positive inotropic agents which enhance Ca2+ entry, results in an increase in the force of contraction
this increase in contractility/inotropy by the inotropic agent, results in increased SV and therefore increase CO
-the stimulate the forcefullness of contraction
Negative Inotropic agent is: K+ potassium
1. Slows down HR
2. decreases the force of contraction/inotropy/intrinsically regulated contractility = decreased SV
Levels of Ca2+, Na+ and K+ need to be tightly controlled
Therefore small changes in there levels of calcium, sodium and potassium inside and outside cells will have large effects
-Levels of calcium, sodium and potassium are often the focus of Treating Heart failure and Hypertension
What is the key word for Contractility?
FORCE of contraction
INOTROPY
What factor influencing SV has the key word FORCE of contraction?
Contractility
What factor influencing SV has the key word INOTROPY?
contractility
-as is regarding the Force of contraction
What is Preload?
The amount of blood returning into the heart
(venous return)
increased stretch during diastole/filling
What is contractility?
The forcefulness that that LV contracts/squeezes down on the volume of blood in the LV
What happens to ESV during increased contractility?
Decreased ESV with increased contractility as More blood is being pushed out due to tis increased force
What is the flow on effect of increased contractility?
Increased blood coming in = increased stretch of the wall = augmentation/stimulation of the cross fridge formation = muscles sense increased volume and respond by increased forcefullness of contractility = increase stroke volume
What are the immediate effects of increased contractility?
Increase SV as the contraction was more forceful,
More blood out
Decreased ESV as there is less blood left in the
Are inotropy and Chronotropy the same thing?
NO
INOtropy are to do with SV
CHRONO = time = chronotropy is to do with HR
What is Chronotropy?
Chronotropy impacts HR HEART RATE
“chrono” = Time
What does “chrono-“ mean?
time
What is an example of a positive Inotropic agent?
Compounds which Enhance Ca2+ entry during Cardiac APs
Increased Ca2+ entry during action potentials in cardiac muscle INCREASES THE FORCE OF CONTRACTION
-therefore CONTRACTILITY/(inotropy!!!) is under INTRINSIC regulation
Heart failure results in some dead and damaged tissue
compounds containing positive inotropic agents which enhance Ca2+ entry, results in an increase in the force of contraction
this increase in contractility/inotropy by the inotropic agent, results in increased SV and therefore increase CO
-the stimulate the forcefullness of contraction
Negative Inotropic agent is: K+ potassium
1. Slows down HR
2. decreases the force of contraction/inotropy/intrinsically regulated contractility = decreased SV
Levels of Ca2+, Na+ and K+ need to be tightly controlled
Therefore small changes in there levels of calcium, sodium and potassium inside and outside cells will have large effects
-Levels of calcium, sodium and potassium are often the focus of Treating Heart failure and Hypertension
Why is enhanced Ca2+ entry a positive inotropy agent?
Increased Ca2+ entry during action potentials in cardiac muscle INCREASES THE FORCE OF CONTRACTION
- therefore CONTRACTILITY/(inotropy!!!) is under INTRINSIC regulation
- is a good treatment for when there has been heart failure which results in dead/weakened tissue, as it will increase SV and therefore increased CO
What is a good treatment for heart failure?
Heart failure results in some dead and damaged tissue
compounds containing positive inotropic agents which enhance Ca2+ entry, results in an increase in the force of contraction
this increase in contractility/inotropy by the inotropic agent, results in increased SV and therefore increase CO
What is an example of a negative inotropic agent?
K+ potassium
- Slows down HR
- decreases the force of contraction/inotropy/intrinsically regulated contractility = decreased SV
for what 2x reasons is K+ potassium a negative inotropic agent?
- Slows HR
2. Decreases force of contraction/inotropy/intrinsically regulated contractility = decreased SV
Why is it important to have tight control over inotropic agents such as Ca2+, Na+ and K+?
Levels of Ca2+, Na+ and K+ need to be tightly controlled
Therefore small changes in there levels of calcium, sodium and potassium inside and outside cells will have large effects
-Levels of calcium, sodium and potassium are often the focus of Treating Heart failure and Hypertension
What is often the focus when treating Heart failure and Hypertension?
The levels of calcium, sodium and potassium inotropic agents
-small changes in their levels have large effects
Need to be tightly controlled
What sort of an effect can the potassium, calcium and sodium inotropic agent levels have on the body?
NEED TO BE TIGHTLY CONTROLLED
small changes in their levels inside and outside the cells have have Large Affects
What does the factor of Afterload have on contractility?
ARTERIAL/AORTA bp BLOOD PRESSURE, WORKING AGAINST, PUSHING
The pressure of the blood that the heart has to work against, in order to eject/pump blood out into the aorta
Arterial/aortic blood pressure MUST BE EXCEEDED in order for ejection to occur
Increased ESV
Decreased SV
Process of PUSHING
Immediate effects:
Increased afterload
Less blood ejected into the ventricles
Increased ESV
Decreased SV
MORE blood is still left in the ventricle at the end of systole (contraction)
What factor influencing SV has the key word WORKING AGINST?
Afterload
What is the relationship between ESV and increased afterload?
Increased ESV
as more blood remains in the ventricle at the end of systole
due to increased opposing pressure which the LV has to work against
What is a compulsory factor for Ventricular ejection to occur?
Arterial/aortic blood pressure MUST BE EXCEEDED BY VENTRICULAR PRESSURE in order for ejection to occur - blood flow DOWN the pressure gradient
Aortic P/Arterial P
What does the PRessure volume loop represent?
the amount of work in One single cardiac cycle
In which graphic manner is the amount of work in one single cardiac cycle represented?
Pressure - volume loop
What is on the Vertical axis in the pressure-volume loop?
ventricular Pressure 0-120mmHg
What is the range of the Vertical axis in the pressure-volume loop?
0 - 120mmHg
What is the Horizontal axis on the pressure-volume loop?
ventricular Volume
40-120
-starts at 40 as the ventricle is never fully emptied, some blood still remains in the ventricle after systole (40)
What is the range of the Horizontal axis in the pressure-volume loop?
40-120
-starts at 40 as the ventricle is never fully emptied, some blood still remains in the ventricle after systole (40)
How is stroke volume represented in the pressure-volume loop?
A-B
- not all the blood is pumped out with each cardiac cycle
- starts at 40 as the ventricle is never fully emptied, some blood still remains in the ventricle after systole (40)
What is the shape of the pressure volume loop?
- Inverse semi circle A-B 40-120 volume 20-7mmHg pressure down then up (0.55sec)
- Straight line up(no vol change) B(EDV)-C 20mmHg-80mmHg (0.05sec)
- Uneven upwards semicircle UP- DOWN C-D(ESV) 80-120-100mmHg, peak later 65 vol 120-40 volume backwards (0.25sec)
- Straight line down (no vol change) D (ESV)-A 80mmHg-20 mmHg (0.15sec)
What is the duration of the 4x periods of the pressure-volume loop?
- 0.55sec
- 0.05sec
- 0.25 sec
- 0.15 sec
What is the duration of the first period of the pressure-volume loop?
0.55sec
What is the duration of the second period of the pressure-volume loop?
0.05sec
What is the duration of the third period of the pressure-volume loop?
0.25sec
What is the duration of the fourth period of the pressure-volume loop?
0.15 sec
Where is EDV on the pressure-volume curve?
point B
Where is ESV on the pressure-volume curve?
point D
Where is their passive filling in the pressure-volume curve?
A-B
What does the area within the pressure-volume curve mean?
change in Pressure x change in volume
Area= total work carried out by the ventricle in a single cardiac cycle
=stroke work by the myocardium
Where is the total stroke work of the myocardium represented in a single cardiac cycle on the pressure-volume curve?
change in Pressure x change in Volume
= Area within the pressure-volume curve
What does point A-B on the pressure-volume curve represent?
0.55sec
Distance between = SV
Passive filling of ventricle
Pressure falls initially due to suction effects of the relaxing muscle
Later pressure rises passively as the Volume increases
Why does the pressure initially decrease in the pressure volume curve between points a-b?
Due to the suction of the relaxing muscle
What does the suction of the relaxing muscle during passive ventricular filling do to pressure?
Initial drop between points A-B in the pressure volume curve
Where does isovolumetric relaxation occur in the pressure-volume loop?
D-A
