19 - Cardiac Output Flashcards
What is cardiac output?
- The volume of blood that is ejected from one ventricle in one minute
What assumptions are we making in determining the cardiac output this way?
- Left output equals right output
- Venous return equal cardiac output
There are two general methods for measuring cardiac output. What are they?
1 - Direct Fick method
2 - Dye dilution method
How does the direct Fick method measure cardiac output?
This method uses O2 content of arterial blood, mixed venous blood and O2 consumption
How does the dye dilution method measure cardiac output?
This method uses dyes, thermal dilution and radioisotope dilution
Where do you measure thermal dilution in the dye dilution method?
On the right side
Describe the Frank-Starling law of the heart
- Stretch and force contraction are linearly proportional to an upper limit
- As the ventricle fills to a greater degree, more stretch is produced prior to stimulation
- At stimulation, the increased stretch results in a more forceful contraction
Explain how the Frank-Starling law matches cardiac output to the venous system
- An increase in venous return will fill the ventricle to a greater degree
- The increased volume in the ventricle will then be pumped out to systemic circulation
Explain how the Frank-Starling law matches the cardiac output of the right side of the heart to the cardiac output of the left side of the heart
- A given volume of blood that is delivered to the right side of the heart will be pumped to the lungs
- From the lungs, this volume will be pumped back to the left side of the heart and delivered to systemic circulation
Explain how the Frank-Starling law compensates for slight variations in heart rate under resting conditions
- Increased heart rate results in a decreased stroke volume
- If the stroke volume had stayed the same, the cardiac output would have increased
Why are there numerous different Frank-Starling curves (Sarnoff) depending on the level of sympathetic or parasympathetic stimulation?
- The different neurotransmitters can either increase or decrease the force of contraction (not an increase in contractility) independent of left ventricle end diastolic volume (LVEDV)
- Depending on whether or not the neurotransmitter is a positive inotropic agent or a negative one - this can cause an infinite number of curves related to the level of stimulation by the ANS
What does it mean to be a negative inotropic agent?
This agent decreases the force of contraction
What is an example of a pathological reason that you would see a decrease in the force of contraction?
Congestive heart failure
What is an example of an agent that can decrease the force of contraction?
Acetylcholine
What does it mean to be a positive inotropic agent?
This agent increases the force of contraction
What are two positive inotropic agents?
Epinephrine
Norepinephrine
How does the left ventricle end diastolic volume (LVEDV) change during exercise?
The ventricle has less time to fill due to the increased heart rate
How does the left ventricle end systolic volume (LVESV) change during exercise?
During exercise, the heart contracts more forcefully so it empties more
How do you calculate the cardiac output from stroke volume and heart rate?
CO = SV x HR
CO = Cardiac output SV = Stroke volume HR = Heart rate
How would you calculate the cardiac output given an LVEDV=130 and LVESV=60 and HR=70?
SV = LVEDV-LVESV SV = 130 - 60 SV = 70
CO = SV x HR CO = 70 x 70 CO = 4900 mL/min CO = 4.9 L/min
How does cardiac output change with exercise?
Cardiac output increases with exercise, even though LVEDV decreases
What is the effect on diastolic and systolic during exercise?
Diastolic shortens while systolic remains the same
How is adenosine formed in the heart?
Adenosine is formed from the breakdown of ATP to AMP in hypoxic conditions in the heart
What dephosphorylates AMP to adenosine?
Cardiac enzymes within the heart
Once adenosine is formed in the cells, what does it do?
It diffuses out of the cell
What does adenosine cause in the coronary vessels?
Vasodilation
What is the result of adenosine causing vasodilation in the coronary vessels?
Increased blood flow to the heart to correct the hypoxia
Overall, what is the role of adenosine in controlling the coronary perfusion to account for metabolic needs?
Adenosine is formed in conditions of low oxygen, and its effect is one that dilates the coronary vessels, allows more blood to reach the heart tissue, and therefore helps the heart to adapt to conditions of differing metabolic needs, such as an increased need for oxygen
What is the effect of norepinephrine and epinephrine on heart rate?
The heart rate is INCREASED in the presence of norepinephrine and epinephrine
What is the effect of norepinephrine and epinephrine on glycogenolysis?
Glycogenolysis is INCREASED in the presence of norepinephrine and epinephrine
What is glycogenolysis again?
The breakdown of stored glycogen for energy…
the breakdown of glycogen (n) to glucose-1-phosphate and glycogen (n-1). Glycogen branches are catabolized by the sequential removal of glucose monomers via phosphorolysis, by the enzyme glycogen phosphorylase.
What is the effect of norepinephrine and epinephrine on membrane permeability to Ca++?
The membrane permeability to Ca++ is INCREASED in the presence of norepinephrine and epinephrine
What is effect of norepinephrine and epinethrine on contractility of cardiac muscle?
The contractility of cardiac muscle is INCREASED in the presence of norepinephrine and epinephrine
What is contractility again?
Myocardial contractility represents the intrinsic ability of the heart/myocardium to contract.
All of the effects of norepinephrine and epinephrine combine to __________ cardiac output
INCREASE cardiac output
What does norepinephrine do to the relaxation time in the cardiac cycle?
It decreases the time of relaxation
What does this do to the cardiac output?
It increases the cardiac output
What is the mechanism by which norepinephrine accomplishes this?
- Norepinephrine increases the rate at which Ca++ is pumped out of the cardiac cell
- This relates to a shorter relaxation time which corresponds to more efficient and faster filling of the ventricles
Why would an ischemic heart lead to diastolic failure?
An ischemic heart is stiffer than normal because it cannot actively pump calcium at a sufficient rates in order to relax properly
How does this change ventricular compliance?
The lack of relaxation of the ventricles does not allow for them to function properly
What is the mean systemic filling pressure?
Abbreviated Psf
- It is the average pressure in systemic circulation
- It is what determines the rate at which blood is returned to the heart
What are the three factors that alter the mean systemic filling pressure
1 - Change in blood volume (increase = increase in Psf)
2 - Change in sympathetic tone (increase = venoconstriction = increase in Psf)
3 - Massaging of veins by skeletal muscle (increase = increase in Psf)
Describe the relationship between venous return, mean systemic filling pressure and right atrial pressure
- Venous return is proportional to mean systemic filling pressure minus right atrial pressure
- Right atrial pressure is the pressure that must be overcome in order to return blood to the heart
- As right atrial pressure increases, cardiac output decreases
Describe a situation where the right atrial pressure would increase and cardiac output would decrease
Congestive heart failure
- This leads to the build up of blood in the lungs and increased right atrial pressure
- This therefore causes a decrease in cardiac output because venous return decreases and CO=VR
What is normal cardiac output?
5.0 L/min
What is the average atrial pressure during this cardiac output?
Zero
As the right atrial pressure increases, such as in congestive heart failure, the cardiac output will __________
Decrease
What happens to the sympathetic tone during exercise?
The sympathetic tone is increased
How does increased sympathetic tone affect the contractility of the heart?
Increased contractility
Does the normal right atrial pressure increase during exercise?
No, not too much
Assuming the atrial pressure did not change during exercise, what will be the result of increased contractility?
Increased cardiac output
