Intrinsic control of cardiac output Flashcards
What is cardiac output?
Amount of blood the heart can circulate round the body in a set time: HR x SV = CO
What is Starlings law?
Stretch of the muscle fibres is set by a diastolic filling pressure and the increase in contractile energy with stretch is an intrinsic property called the Frank-Starling mechanism
What is the relationship between SV and preload?
Positively correlated with eachother, but plateau (hyperbolic).
What is the mechanism behind Starlings law?
Filaments get closer (lattice spacing hypothesis). Stretch reduces double overlap of thin actin filaments of sarcomeres. At the optimal sarcomere length (2.2 micrometers), at a given [Ca2+], the optimal number of cross bridges form and he greatest isometric active tension is developed.
Increased affinity of troponin C for calcium ions, more Ca2+ binds after CICR, increased disinhibition of actin filaments.
What happens when sarcomeres are too short?
When sarcomere length too short i.e. <2.0 micrometer, actin filaments extend beyond midline and onto other half of sarcomere, some myosin cross-bridges pulled in the wrong direction and reducing net tension generated
What happens when sarcomeres too long?
At very long length, actin and myosin fail to overlap, no cross bridges form
Why does the SV/pressure graph plateau?
More stretch, sarcomeres longer, actin and myosin dont overlap and less cross bridges form
Laplace’s Law limits the amount active wall tension can raise blood pressure. As the radius of the ventricle increases, the curvature of the wall decreases consequently, a smaller component of the wall tension is angled to the cavity reducing pressure exerted.
What is the importance of the Frank-Starling mechanism?
Heart can automatically accommodate changes in venous return, at any heart rate. Balances the outputs of the right and left ventricles: so that blood volume and flow in each circuit is equal.
How can Starlings law be modulated to affect SV, thus CO?
Change in the preload or afterload
What is the effect on increased preload on the EDV?
Increased
What is an example of increased preload increasing CO (by increasing SV)?
Exercise: peripheral venoconstriction occurs, dynamic exercise - skeletal muscle contraction (compress deep veins of legs), increased respiratory rate all contribute to increased CVP and SV.
In what individuals is Starlings laws influence on increased CO (by increasing SV) due to increased preload most important?
Heart transplant patients with denervated hearts who lose autonomic innervation, thus, Starling’s law compensates to increase stroke volume to increase CO, as HR cannot be increased extrinsically.
What is an example of a decrease in preload decreasing CO?
Standing 0.5 litre of blood pools in legs due to gravity.
Stand for too long-orthostatic intolerance and faint or haemorrhage, (reduced CO so less cerebral perfusion)
What does a decreases preload do to the EDV?
Decreases it
What volumes are determined by afterload?
EDV to stroke volume (the difference between them)
What is a pathological example that causes high afterload and how does it affect SV?
Aortic stenosis/systemic hypertension increase pressure gradient left ventricle must overcome to eject blood out of aorta), transiently decreases SV
What is a physiological example of cardiac adaptation to high afterload?
As SV decreases, EDV increases and so SV increases
Part of Anrep effect, sustained myocardial stretch increases myocardium contraction.
What is the mechanism behind the Anrep effect?
Sustained stretch activates tension dependent Na+/H+ exchangers, bringing Na+ ions into the sarcolemma.
This increase in Na+ in the sarcolemma reduces the Na+ gradient exploited by sodium-calcium exchanger (NCX) and stops them from working effectively.
Ca2+ ions accumulate inside the sarcolemma more taken into SR by SERCA for increased calcium induced calcium release (CICR) leads to positive inotropy
