0701 - Cardiac Output - RM Flashcards
What is cardiac output? How do you measure it?
Cardiac Output = ejected volume per unit-time = Stroke Volume (in L) times Heart Rate.
What is the ejection fraction? How do you manage it?
Ejection Fraction = ratio of SV to end-diastolic (full) volume (generally 120mL). Eg SV = 80mL, EDV = 120mL, EF=⅔
How is CO determined by HR?
As HR increases, filling time decreases significantly - there is a linear relationship. CO is maximal at ~130bpm, above this, there is insufficient filling time to compensate. CO is a function of the square of HR, thus there is a maximum - if you go beyond it, you’re not getting more CO even with a higher HR.
What is contractility? What are its determinants?
The force generation of each cardiac fibre. Depends on Ca++ (more = larger isometric force), SY activity, and preload (as well as HR and afterload). Can be modulated by drugs (Noreadrenaline increases, as does digitalis, beta-agonist, glucagon. Anaesthetics and toxins reduce), or disease states.
How does fibre thickness affect CO?
In healthy people (athletes), force increases with hypertrophy - more myofilaments per myocyte, thus produce bigger force - though this is reversible. In hypertrophic cardiomyopathy, hypertrophy can lead to decreased force production, as the remodeling is under beta-adrenergic control.
How are force production, sarcomere length, and shortening velocity related?
Both of these are as for preload - longer the sarcomere, better crossover, faster shortening velocity, bigger force.
What is preload? How does preload affect CO?
Preload - end diastolic pressure (or volume, doesn’t matter) - sets the sarcomere length. Up to a certain limit (two-fold), the bigger the preload, the larger the SV. As the sarcomere is longer (thus stronger), it has less effective load to push against (same load, but more cross-bridges, so less per cross-bridge), increasing shortening velocity, and thus ejection - this increases the stroke volume. It is a homeostatic measurement to match RV with LV output.
What is afterload? (Key Exam concept) How does afterload affect CO?
end-systolic pressure (approximately MAP NOT diastolic pressure - for exam). The average pressure against which the ventricle must contract to eject blood into the aorta - approximately equal to mean arterial pressure. the bigger the afterload, the smaller the SV, as there is a larger force the myocyte must push against, lowering shortening velocity - this is the problem in hypertension. Laplace’s law (tension force is proportional to radius) states that for a given afterload and myocardial thickness, a large ventricle requires more force to contract than a small one. There are clinical implications for dilated heart failure, as there’s a lot of force required to get the heart beating - maybe try to reduce afterload?
How can afterload influence preload?
If afterload is increased, stroke volume is decreased, and end-systolic volume is increased. This means that end-diastolic volume is increased slightly, which is an increase in preload, that offsets much of the loss in stroke volume.
In heart failure patients, EDV is already at maximum, so increasing afterload significantly reduces SV. You would want to reduce afterload (vasodilator) to increase SV.
