Lecture #3 The Heart: Mechanics and Cardiac Output Flashcards
What is Systole?
Ventricular Systole starts when the AV valves close and the pressure within the ventricles begins to rise as the cardiac muscle fibers are depolarized and then contract.
What is Diastole?
Ventricular diastole starts with ventricular muscle repolarization, leading to a drop in ventricular pressure, and filling of the ventricle.
What is Atrial Systole?
Ventricular filling is largely passive.
What is Cardiac Output? (CO or Q)
Volume of blood pumped by the ventricles in a given unit of time
CO (L/min)=SV (L/beat) x HR (beats/min)
At rest, HR ~ 75 beat/min; Stroke Volume ~ 0.07 L/beat
CO=5.25 L/min
What affects Stoke Volume?
Aortic (or pulmonary valve) blood pressure or “afterload”
End-diastolic volume or “preload”
Contractility
What is afterload?
The ventricles cannot eject blood into the aorta or pulmonary artery until the pressure in the ventricle exceeds the pressure in the vessel–thus an increase in arterial pressure will have a major impact on the work of the heart and on stroke volume.
What is Preload? (End-Diastolic Volume)
The cardiac chambers are mechanical pumps, and therefore can pump only what is delivered to them (major impact on the stroke volume) stroke volume cannot increase unless the rate of cardiac filling also increases
What is contractility?
Contractility refers to the strength of cardiac muscle contraction
What are the two different types of contractility?
Active contractility: change in contractility due to stimulation of the sympathetic nervous input to the heart
Passive contractility: change in contractility due to changes in the length of cardiac muscle fibers (AKA Frank-Starling mechanism)
What is active contractility?
Actions of norepinephrine (or epinephrine) increases permeability of the cardiac muscle fibers to calcium
Increases rate of pacemaker activity/action potential invades the t-tubules and calcium is released from the sarcoplasmic reticulum
Increases force of cardiac muscle contraction/increases the number of actin/myosin crossbridge interactions
How does Norepinephrine (NE) alter active contractility?
SNS –> releases NE
Binds to Beta1 adrenergic receptor
Opens Ca2+ channel in membrane
Initiates cAMP second-messenger system
Activates PKA which extends Ca2+ channel opening phase
What is passive Contractility? (Frank-Starling mechanism)
The relationship between preload and stroke volume–if preload increases, stroke volume increase (even with no nerve supply)
