Flashcards in Lecture 15: Regulation of Cardiac Output (Hayward) Deck (27):
cardiac output =
flow. L/min CO = SV * HR ****MEMORIZE
parasympathetic or sympathetic input to heart is more quickly reversed?
Increases in HR are coupled with changes in :
Positive lusitropic effects --> HR and rate of relaxation
changes HR. Positive chronotropic effect = increased HR
lusotropic effect relates to
regulates myocardial performance.
Intrinsic regulation via cardiac muscle
Extrinsic regulation via external force (hormones, sympathetic innervation, pH, etc.)
Actin and myosin interact during
functional unit of a muscle
How does stretch in cardiac tissue prior to systole impact contractility?
SOME stretch increases capacity to generate force, but too much stretch generates less force
Active tension in cardiac muscle is dependent on:
starting length of the sarcomeres at the time of activation
Total tension +
passive + active tension
the stretch on the cardiac muscle that occurs during the relaxed state. Determines the force generated by the cardiac muscle for the subsequent contraction (length-tension relationship)
P in the outside of the system that heart must work against (i.e. aortic pressure)
volume load during diastole
relationship between muscle length and force generated. Uses the intrinsic properties of the muscle w/o any outside influence. Important mech. for equalizing outputs between R and L ventricles
main force ventricles have to overcome during volume ejection (isotonic contraction phase)
muscle shortens when total muscle force exceeds external load
increased aortic pressure --> stroke volume ?
end-systolic length of muscle after contraction is directly related to -->
AFTERLOAD and contractility (not preload!)
decreased aortic pressure --> stroke volume?
performance of the heart at a given preload and afterload. Determined by changes in intracellular Ca and rate of contractile protein interaction
inotropic changes ***
changes in contractility **
Increased NE --> contractility
increases (because more Ca is released) INOTROPIC EFFECT
lack of perfusion
Thyroid hormone ---> Ca reuptake and hypertrophy