Stroke Volume - created from Mind Map

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Preload

Afterload

Contractility

is the degree of stretch of heart muscle cells just before they contract

Increasing the length of the cardiac muscle cells (i.e, stretching them) can produce dramatic increases in contractile force.

The important factors stretching cardiac muscles are:

Venous Return

EDV

is the amount of blood returned to the heart

Factors that increase VR also increase EDV and SV and force of contraction

Factors that decrease VR also decrease EDV causing the heart to beat less forcefully and the SV drops

Slow Heart Rate

Exercise

Severe Blood Loss

Extremely Rapid HR

is back pressure exerted by blood in the large arteries leaving the heart

normal afterload doesn't affect the SV

the pressure must be overcome for the ventricle to eject blood from the heart

except: in the case of uncontrolled hypertension or valve stenosis

the increased afterload may lead to hypertrophy of the ventricle and eventually heart failure

is cardiac fiber contractile force that is due to factors other than EDV

The more vigorous contractions are a direct consequence of a greater Ca++ influx into the cytoplasm from extracellular matrix and sarcoplasmic reticulum

Enhanced Contractility:

Results in:

+ve inotropic agents

-ve inotropic agents

Lower ESV

Greater SV

Increased sympathetic stimulation

Hormones

Ions

drugs

releases norepinephrine or epinephrine which increase Ca++ entry and promote ventricular contractility

e.g. thyroxine

Increased Ca++

Hypercalcemia

digitalis

acidosis

hyperkalemia

is high K+ in the blood