Lecture 14: Contractility and Cardiac Output Flashcards
What factors affect cardiac output?
Heart rate
Contractility
Preload
afterload
How is cardiac muscle contraction different from skeletal muscle contraction?
More responsive to adrenergic inputs and relies more heavily on Ca2+ since it allows heart to contract stronger
How are cardiac glycosides used to treat heart failure?
Blocks the Na/K ATPase and Ca/Na exchanger to keep Na and Ca inside the cell for depolarization and stronger contraction
What is the formula for cardiac output?
CO = HR x SV
How does length tension (stretching) relate to contraction?
The higher the length tension the stronger the contraction
What does preload mean? How is this measured?
How much blood is ready to be pumped into the system by the left ventricle (left ventricular end-diastolic volume). Measured by the tension (stretch) on the walls of the left ventricle
What is the Frank Starling relationship?
The LVEDV determines the volume pumped by the left ventricle
What is afterload?
Pressure needed to be overcome to open the valve and release the blood into the next vessel
What are the equations for calculating these? What are the normal numbers?
Stroke volume
Ejection fraction
Cardiac output
SV (70 mL) = EDV (120 mL) - ESV (50 mL)
EF% (55%)= SV / EDV
CO (5 mL/min) = SV x HR
If you increase preload, what happens to CO?
If you increase afterload, what happens to CO?
Increases (along with contractility)
Decreases (along with contractility)
How does the heart overcome decreased CO?
Increasing contractility and HR
How does HR affect contractility? What is this effect called?
Increased HR = increased Ca2+ stored in SR since there is no time to clear Ca2+ = stronger contraction.
Positive staircase effect
What are the characteristics of the positive staircase effect?
Since there are more Ca2+ stored in cardiac myocyte, the next contraction is much stronger
By which mechanism does activation of the sympathetic B-adrenergic receptors affect cardiac output?
Phosphorylation of Ca2+ channels, phospholamban and inhibitory troponin I produces a positive ionotropic effect
How does activation of parasympathetic muscarinic receptors affect cardiac output? Which type of cardiac myocytes do they mostly affect?
- Decreases influx of Ca2+ and increases efflux of K+ via K+-Ach channels
- Atrial myocytes
On the Ventricular pressure-volume loop, what happens at points 1-4? What represents the stroke volume?
- Isovolumetric contraction (pressure rises rapidly)
- Ventricle overcomes the pressure and ejects the blood
- Isovolumetric relaxation
- Ventricular filling
Distance between the vertical lines
What happens to the stroke volume (and thus the pressure-volume loop) when preload increases?
Increases EDV = increased stroke volume
What happens to stroke volume and the ejection fraction of the afterload is increased? What medical conditions does this happen?
- Increased pressure needed to open the valve = decreased stroke volume and ejection fraction
- Aortic stenosis, HTN
What happens to stroke volume and the ejection fraction if contractility is increased?
Increased SV and EF. Release more blood so less is left in the heart
What does Volume work mean?
Pressure work?
Minute work?
Stroke work?
Cardiac output
Aortic pressure
CO x aortic pressure
SV x aortic pressure
Why is increased aortic pressure (as in aortic stenosis or HTN) bad?
Higher pressure to overcome to pump the blood = decreases the stroke volume. Heart increases contractility and overworks itself to keep the stroke volume the same = hypertrophy of the heart
What is the Fick Principle equation?
O2 consumption = CO x [O2] in PV - [O2] in PA
What is the vascular function curve? What is the normal level?
Circulatory filling pressure when there is no blood flow (0 cardiac output)
+7-8 mmHg
What happens to cardiac and vascular function curves if you increase or decrease contractility?
Cardiac function curve:
Increase: Increases CO (y axis) and decreases RAP (x axis)
Decrease: decreases CO (y axis) and increases RAP (x axis)
Vascular function curve: no effect
