Contractility and Cardiac Output Flashcards
what physiological aspect of contractions does Cardiac Muscle rely on more than Skeletal muscle
Cardiac Muscle: More influence of adrenergic receptor inputs
and also relies more heavily on Sarcoplasmic Reticulum Calcium and its release
What are the functions of Cardiac Glycosides and what are their modes of action
they inhibit the Na/K+ ATPase binding site for K+
this then prevents the release of Na+ and increases its concentration
this then decreases the Ca+ efflux out of the cell through the Ca+/Na+ exchanger
then increases the Ca+ intracellular
leads to a positive inotropic effect
what is the equation for Cardiac output and its factors
CO= HR x SV
heart rate times stroke volume equals the cardiac output
What is the Length tension relationship and Cardiac output
Changes in cardiac output related to length-tension relationship
a positive ionotropic effect leads to an increase in Cardiac output
a negative ionotropic effect leads to a decrease in cardiac output
Generally proportional to the amount of calcium that is available to troponin on actin filaments of contractile apparatus
What is preload and what is it related too
Left Ventricle End Diastolic Volume (amount of blood ready to be pumped when diastole is over)
-wall tension in Left ventricle just before contraction
(fiber length at end of diastole from where it will contract)
it is related to the venous return (more venous return greater preload)
Frank-Starling Relationship
Volume of blood ejected by the ventricle depends on the volume present in the Ventricle at the end of diastole
therefore, more blood in ventricle means more stretch means more contraction
this relates length tension to functionality
what is afterload
Force opposing contraction or as the pressure required to eject the blood (open the aortic valve)
-essentially equal to the aortic or pulmonary pressure
Where is preload and afterload within the Cardiac cycle
Preload: Left ventricular End Diastolic volume
-end diastolic fiber length from where the muscle will begin its contraction
Afterload:
-for the left ventricle the aortic pressure (pressure needed to open the Aortic valve
What is the stroke Volume, Ejection fraction, and Cardiac output numerically
Stroke volume: volume of blood ejected by ventricle with each beat
SV= EDV-ESV (usually about 70 mL)
Ejection Fraction: Fraction of the EDV ejected in each stroke volume
- measure of efficiency and contractility
- EF% = SV/EDV (usually about 55%)
Cardiac Output: total volume of blood ejected by ventricle per minute
-CO=SVxHR (usually about 5 L/min)
if preload changes what happens to Cardiac Output
Preload increases = increase cardiac output and contractillity
Preload decreases = decrease in cardiac ouput and contractillity
if afterload changes what happens to Cardiac Output
Afterload increases = decrease in cardiac output
therefore body must increase contractillity or increase HR to overcome the afterload
How does Heart Rate effect Contractillity
Increased Heart Rate (positive chronotropic effect) increases contractillity (positive inotropic effect)
Positive staircase effect (bowditich staircase)
- more Ca+ enters cells and taken up into SR
- post-extrasystolic potention (arrythmia and extra beat)
What is the physiological effect sympathetics have on Cardiac output and mechanism
Positive inotropic effect: B-AR activation
- Phosphorylate the sarcolemmal Ca channels (increase intracellular ca+
- Phosphorylate of phospholamban (pump more Ca from SR)
- Phosphorylate to inhibit Troponin I (an inhibitor of troponin C
what is the physiological effect parasympathetics have on Cardiac output and its mechanism
Negative inotropic effect in Atria only!
- Muscarinic receptor activation
- decrease inward Ca+ current during pateau (phase 4 of SA)
- ACh increases outward K+ current via K+ ACh channel
in an Ventricular Pressure- Ventricular Volume Loop what is happening from 1 to 2?
1 is the preload
2 is the afterload
1 to 2: Isovolumetric contraction
- end of diastole and pressure is low
- must increase pressure to past afterload to eject blood and decrease volume
in an Ventricular Pressure- Ventricular Volume Loop what is happening from 2 to 3
2 to 3 is Ventricular ejection
pressure will reach a maximum point in middle
-if take starting volume and subtract to end volume will give you the stroke volume
aortic valve is open, AV valve closed
in an Ventricular Pressure- Ventricular Volume Loop what is happening from 3 to 4
Isovolumetric relaxation
- point 3 is systole ends and ventricle begins to relax (all valves are closed)
- Ventricular pressure falls quickly but volume remains the same
- pressure must fall below atria to allow for bicuspid valve to open (point 4)
in an Ventricular Pressure- Ventricular Volume Loop what is happening from 4 to 1
Ventricular filling
Aorta valve close, AV valve open
what is a dotted line on a Ventricular Pressure vs Volume loop
End-systolic pressure volume relation (ESPVR)
has to do with contractillity
what happens to Pressure volume loop of the ventricle as there is an increase of Preload
More venous return, and more blood volume, meaning greater EDV
Therefore, afterload stays the same and contractillity but there is an increase in stroke volume
what happens to Pressure volume loop of the ventricle as there is an increase in afterload
the increase afterload can be aortic stenosis, or hypertension
greater pressure needed to compensate
therefore a reduce in stroke volume and a reduced Ejection fraction %
what happens to Pressure volume loop of the ventricle as there is an increase in cpontractillity
may be caused by a adrenergic stimulation
increased stroke volume and increased Ejection fraction percentage
less blood left in the heart
what is Volume work, pressure work, minute work, stroke work
Volume work: cardiac output
Pressure work: aortic pressure
Minute work: Cardiac output x aortic pressure (volume work x pressure work)
Stroke work: (performed by the left ventricle) = stroke volume x aortic pressuure
-area within the pressure volume loop
where does the largest percentage of oxygen consumption go in the heart
goes to pressure work rather than volume work
this is because the left ventricle has to work harder than the right ventricle due to the fact the systemic pressure is greater than the pulmonary pressure
The fick Principle
Measurement of cardiac output
Cardiac output = O2 consumption/([O2] pulmonary vein- [O2]pulmonary artery)
what is the relationship between the CO and Venous return in the cardiac function and vascular function curve
x axis: Right atrial pressure
y axis: Cardiac output and venous return
Cardiac function curve: venous return increases and right atrial pressure increases
also end diastolic volume and end diastolic fiber length increases
Vascular function curve: gives the cardiac output in regards to the pressure of the right atrium
the mean systematic pressure will always be +7 or +8 when there is no cardiac output due to the vascular compliance and blood volume
what does it mean at the equilibrium of the Cardiac output and Venous return vs Right atrial pressure graph
at equilibrium the Cardiac output= the venous return and can only occur at specific preload
normal: CO 5L/min and PRA = +2mmhg
this is the point where the cardiac function and vascular function graph intersect
How is the cardiac function enhanced and depressed
enhanced:
increase in inotropy
increase in Heart rate
decrease in afterload
depressed:
decreasde in inotrophy
decrease in heart rate
increase in afterload
How does changes in Total peripheral resistance effect the CO and Venous return graph
increased TPR: decrease the equillibrium of cardiac output but not change the right atrial pressure
decreased TPR: will increase the equillibrium of cardiac output but not affect the right atrial pressure
how does changes in blood volume affect the CO and venous return graph
increase in Venous return graph in L/min and a increase in right atrial pressure
what occurs in the CO and venous return graph when there is cardiac failure
Decrease in intotropy
Decrease in vascular compliance
increase in blood volume
increase in SVR/TPR
