Contractile Properties of the Heart Flashcards
How do you increase the force of contraction of cardiac muscle?
Increase intracellular calcium
What effect does increasing stiffness of the heart have on compliance of the heart muscle?
increased stiffness decreases compliance
What is systolic dysfunction?
Alteration in myocardial contraction that is associated with pressure overload (due to increased afterload)
Cardiac muscle contraction is […] depenendent.
Calcium
Active tension in heart muscle is generated by […]
Cross bridge cycle between actin and myosin
What is the concept of concentric hypertrophy?
This occurs secondary to systolic dysfunction where the heart is working against increased afterload (resistance) in systemic circulation –> leads to increased stress on wall of left ventricle –> leads to increased oxygen demand of myocardium b/c heart has to work harder to pump blood –> leads to hypertrophy of left ventricle to generate enough force to pump blood against increased afterload but hypertrophy is due to increased wall thickness from parallel addition of new sarcomeres –> increased stress is now distributd across larger surface area –> ultimately heart muscle wears out and sarcomeric dysfunction occurs where the proteins that make up the sarcomeres stop working properly and the heart muscle cannot contract as much as it needs to leading to decreased EF and signs of heart failure (negative ionotropy)
What is the frank starling mechanism?
The more blood that is put into the chambers of the heart, the more passive tension is developed and the more blood the heart is able to pump out during systole.
What is lusitropy?
The rate and extent to which the heart relaxes during diastole
The End Diastolic P-V Relationship (EDPVR) is equivalent to […] and is shown by the lower dashed line in this image.
Compliance (stiffness)
The End Systolic P-V Relationship (ESPVR) is representative of […]. ESPVR is shown by the dashed line in the image below.
Contractility
- What would cause an increase in preload?
- What would cause a decrease in preload?
- What effect would increased or decreased preload have on the stroke volume of the heart?
- Increased venous return (IV and/or increased fluid intake)
- Decreased venous return (diuretics), diastolic dysfunction (increased stiffness)
- See image
The red line is the normal curve. What would cause an increase or decrease in the slope of this line, as is seen by the additional lines on the image?
New EDP vs. SV lines generated by changing afterload and/or ionotropy
If you look at a given EDP (let’s say 5mmHg), the stroke volume that is produced at that EDP increases if you decrease afterload or increase ionotropy (increased contractility - ex: increased sympathetic tone). The stroke volume that is produced at that EDP decreases if you increase afterload or decrease ionotropy (decreased contractility - ex: heart failure).
[…] is when the rate of ventricular pressure development is slower than normal.
Negative ionotropy
What is cardiac afterload?
The resistance against which the heart has to pump.
Negative ionotropy is seen in what cardiac disease?
Heart failure
- What increases afterload?
- What decreases afterload?
- What effect would increased or decreased afterload have on stroke volume?
- Aortic stenosis, hypertension
- Antihypertensive drugs that lower systemic resistance
- See image; right is decreased afterload
- What increases contractility?
- What decreases contractility?
- What effect does increasing or decreasing contractility (ionotropy) have on stroke volume?
- Increased sympathetic tone, positive ionotropic drugs (digoxin –> increases amount of intracellular Ca2+ leading to increased ionotropy)
- Increased parasympathetic tone
- See image
What effect does volume and end diastolic pressure have on the stroke volume?
Increasing left ventricular volume = increased SV
Increasing end diastolic pressure (volume) = increased SV
Below is a normal pressure-volume loop for the left ventricle. Explain what is happening at each point in this graph. Begin where diastole begins, with the closing of the aortic valve.
Starting with IV in image
- IV: AV closes, isovolumic drop in pressure in left ventricle. Blood from pulmonary vein begins entering left atrium.
- Point A: pressure from blood filling left atrium > pressure in left ventricle, so one way MV opens allowing blood from atrium to flow into left ventricle.
- I: Blood from left atrium fills left ventricle passively. At the end of this phase the AP from the SA node causes the atrium to contract (atrial kick) seen as little hump in phase I.
- Point B: Mitral valve closes S1 heart sound.
- II: No more blood fills the ventricle, but AP from AV node has propogated down the L/R branches to purkinje fibers and is causing left ventricle to contract, thus increasing the pressure in the left ventricle without an increase in volume.
- Point C: Pressure in left ventricle > pressure in aorta –> Aortic valve opens
- III: Blood is pushed out of left ventricle into aorta, this continues until pressure in aorta > pressure in ventricle
- Point D: Aortic valve closes S2 heart sound
Just looking at the points on the blue line, what would cause movement along the blue line?
Increasing preload
- Increase sympathetic tone (NE)
PSNS really only innervates the SA and AV nodes of the heart. The myocardium itself is innervated mostly by Sympathetic NS.
What impact does increasing or decreasing preload have on stroke volume?
The red line indicates […] compliance while the blue line indicates […] compliance.
Decreased
Increased
Frank-Starling relationship
- How is passive tension developed in a cardiac myocyte?
- What effect does this have on the force of contraction of the myocyte?
- As blood fills the atria and ventricles during diastole, the muscle is passively stretched by the volume of the fluid entering and filling the chamber. This generates a certain amount of passive tension.
- The more the fibers are stretched during diastole, the greater the force of contraction. This is true to a point, there is an optimal amount of passive tension, beyond which the sarcomere begins to become dysfunctional due to poor overlap between the actin and myosin filaments.
Preload is proporational to myocyte […] and determines how much […] the ventricle can develop during systole.
Length
Active tension
Describe the cross bridge cycle between actin and myosin in the cardiac myocyte.
1) Ca2+ binds to troponin, which is a protein on the actin (thin filaments). This exposes binding site for myosin heads on tropomyosin which are intertwined with actin filaments. At this point, ADP and Pi are bound to myosin and the myosin head is “cocked”.
2) ADP and Pi are released from myosin head leading to the “power stroke” where the myosin head bends and pulls on the tropomyosin/actin filament sliding the actin toward the M-line of the sarcomere.
3) ATP binds to the myosin head and this causes the myosin head to release the actin to stop the cross-bridge cycle.
4) ATP is hydrolyzed into ADP and Pi to restart the process with a “cocked” myosin head that is awaiting the opportunity to bind to a binding site on tropomyosin.
