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Cardiac output is the product of…
HR (heart rate) and SV (stroke volume)
The 3 major determinants of cardiac output
Preload
Afterload
Contractility
Preload
Stretch/tension on relaxed myocytes pre-contraction
Determined by end-diastolic volume and end-diastolic pressure
Afterload
Tension on myocytes during systole
Resistance that myocardium must overcome to push blood out of the ventricle
Muscle “feels” this load after it starts to contract
Determined by resistance of ventricular outflow tract + aorta and systemic vascular resistance
Approximated by mean arterial pressure
Contractility (inotropic state)
Intrinsic ability of heart to generate the force required to eject blood, independent of preload and afterload
Increased contractility (inotropy) = increased velocity and peak force of contraction (heart generates force faster and to a greater final degree)
The ______ system is the major way that the body regulates HR
Autonomic
Which tone dominates in a patient that is healthy and at rest?
Parasympathetic
Regulation of heart rate (reflex control)
As MAP increases the stretch and firing rate of arterial baroreceptors increases.
Signals are delivered to the vasomotor center which then decreases sympathetic flow and increases parasympathetic flow.
Results in a decreased HR
Intrinsic properties of stroke volume
Length-dependent activation (The Frank-Starling mechanism)
Response to changes in preload and afterload; important for beat-to-beat regulation
Extrinsic mechanisms of stroke volume
Effects of the autonomic nervous system and other hormones/substances
Allow adaptation to sustained/substantial hemodynamic challenges (exercise)
Frank-Starling Mechanism
The greater the stretch/tension on resting myocytes at end-diastole (greater the preload), the greater the force of contraction
Increased contractility = Increased stroke volume = increased cardiac output
When the amount of blood returning to the heart increases, this built-in mechanism allows it to adapt by matching output volume to input volume
Also explains how the heart adjusts to acute changes in afterload
Increases in afterload do not substantially reduce stroke volume and cardiac output, unless heart is diseased or afterload is severely increased.
Extrinsic myocardial regulation (sympathetic nervous system effects)
If greater increases in cardiac output are needed, the heart needs help
Sympathetic stimulation increases contractility = increases in stroke volume = increases in cardiac output = increase in preload