Regultion Of Cardiac Output Flashcards
CO =
SV * HR
SV =
EDV - ESV
heart rate is regulated by
The ratio of sympathetic vs parasympathetic inputs
Flow =
Liters/min
Cardiac output
Norepinephrine’s action
Positive chronotropic
Effect
Binds to beta-1 adrenergic receptors in SA node to increase phase 4 depolarization
Reuptake is relatively slow
Chronotropic effect
Increase in heart rate
Parasympathetic actions on heart rate
Ach binds to muscuricnisympathci receptors on pacemaker cells -modifying funny Na+ conductance - modifying K+ conductance -modifying Ca++ channel threshold Negative chronotropic effect
Typically increases in heart rate are coupled with changes in
Ventricular function
Positive lusitropic effects
Increased rate of relaxation
Intrinsic regulation
Mechanical properties of cardiac muscle
Extrinsic regulation
Effects of sympathetic innervation, hormonal, and alteration of blood gases and pH
The active tension is dependent upon the
Sharing length of the sarcoma refs at the time of activation.
Total tension =
Passive tension + active tension
External constraints include
EDV, aortic pressure
Preload
The stretch on the cardiac muscle that occurs during the relaxed state
Isometric force generation is dependent upon
The starting length
Frank - Starlng mechanisms important mechanism for
Equalizing outputs between right and left ventricles
Typically they heart operates to the left Lmax
Isotonic contractioase
Volume ejection
When total muscle force exceeds the external load the muscle begins to shorten
Afterload
When ventricular force (pressure) > the aortic pressure, the aortic alive opens
ESV of the muscle after contractio is directly related to
The afterload and contractility and not the preload
Increases in aortic pressure
Decrease stroke volume
Decrease in aortic pressure
Increase stroke volume
Contractility
The performance of the heart at a given preload and afterload
Reflects the activity taking place at the interacting cross bridges
Determined by changes in intracellular Ca++ and rate of contra lie protein interaction
Inotropic changes
Changes in contractility
Thyroid hormone
Enhance Ca++ reuptake and hypertrophy
Increases in CO2 and the associated decrease in cellular Ph cause a
Declines in myocardial performance
Myocardial ischemia that occurs during coronary occlusion contributes to
A rapid decline in myocardial force
Negative inotropic effects
Heart failure
