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38 Cards in this Set

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The volume of blood pumped by the heart per unit time
Cardiac output
The volume of blood ejected from the heart with each beat
Stroke volume
Cardiac output =
SV x HR

units ml/min or L/min
The ventricular volume at the moment diastole ends when the mitral valve has just closed
End diastolic volume
The ventricular volume after ventricular systole
End systolic volume
SV
EDV-ESV
The ventricular wall is made up of 3 layers
1. myocaridum
2. epicardium-outside heart and contains loose CT, nerves, and blood vessels
3. endocarium-layer on the inside of the heart (nearest to the blood)
The tissue that separates the atrial muscle from the ventricular muscle

Made up of dense fibrous CT, annulus fibrosis, the muscle of the heart inserts on this fibrous skeleton
Fibrous skeleton
Endothelium
-Innermost layer
-Simple squamous cells, continuous with vascular intima
Subendocarium
-contains the specialized conducting system called purkinje fibers
Characteristics of purkinje fibers
Do not have prominent striations (contractile proteins), have a lot of glycogen (not stained), larger than cardiac myocytes
Myocardium
-spiral layer
-attached to the cardiac skeleton
What are the factors that determine SV
1. preload
2. afterload
3. contractility
The force on the ventricular wall acting to stretch the ventricular muscles at the end of diastole

Stretching the muscle out as the ventricle fills
Preload
The force-length relationship in regards to preload.
As the preload increases, the muscle cell lengthens and the longer the cell lengthens the more forcefully they will contract.
What are other proxies for preload?
1. EDV
2. EDP
3. Ventricular filling
4. L atrial pressure
5. End diastolic wall tension
La Place's Law
The force acting on the ventricular wall is related to the ventricular pressure and the radius

T = Ventricular P x Ventricular radius
How is compliance related to preload?
The more compliant the ventricle is, the more the fibers will be stretched and the higher the EDV
What are the names given to the relationship between preload and SV?
Starlings Law of the Heart (heterometric autoregulation)
Preload has an effect on what?
End diastolic fiber length which is the core determinant of SV.
How is end diastolic fiber length related to SV?
Increased filling of the heart-->increased length of the sarcomeres-->increased force of contraction-->increases SV
Heart disease does what to compliance?
It dec complaince-->larager inc. in wall force-->larger inc. in EDP to get the same inc. in stretch to inc. muscle fiber length.
What is the best correlate of the degree of stretch of ventricular muscle?
The end diastolic volume because you don't have to worry about compliance unlike EDP.
The ability of cardiac muscle to develop contractile force at a given diastolic fiber length
Contractility
The relationship between SV and ED fiber length
Increased contractility is an incr. in stroke volume at a constant end-diastolic fiber length.
With increased contractility, there is increased?
1. Force of contraction
2. Speed of contraction
3. Rate of relaxation
Inc. contractility caused by inc. Epinephrine or NE
Both bidn to B adrenergic receptors-->inc. contractility-->inc. cytosolic Ca +2.
Increased HR has what effect on contracitlity?
Small effect bc there isn't enough time to clear out all the calcium between beats so the cytosolic Ca goes up a little more.
How does digitalis increase contractility?
Inhibits Na/K ATPase--> dec. NaATPAase--> inc. [Na]-->inc. [Ca]
Decreased contractility is caused by what physiologial mechansim?
Decreased SNS activation
Small effect of inc. PNS activation
What pharmacological mechanism causes decreased contractility?
1. Calcium antagonist
2. Beta adrenergic receptor antagonists
What other mechanisms cause decreased contractility?
1. Dec. supply of energy
2. Altered expression of cardiac muscle proteins
The force which ventricular muscle must develop in order to eject blood
Afterload
If the ventricular muscle has to develop more force to eject blood (afterload) it tends to eject more/less blood?
Less blood-->less SV

(throwing a heavy pen vs. light pen)
How can afterload be increased?
1. By an inc. in ventricular systolic pressure

2. Radius (think balloon example where the limpy part has less tension). The bigger the ventricle, the more force that must be developed to eject the bllod.
When inc. afterload dec. SV, how does the heart restore the SV?

Starling's Law (heterometric autoregulation)
less SV-->more bld left in ventricle-->heart starts o fill and the R heart will deliver the same volume that it delivered for the previous beat--> inc. in EDV-->inc. SV
Chronic inc. in afterload

Myocaridal hypertrophy (long arm)
Causes hypertrophy

Hypertrophy caused by activation of cell adhesion molecules
Another way to restore dec. SV caused by inc. afterload

Homeometric autoregulation
Increases contractility