Cardoivascular Physiology - Lecture 5 Flashcards
Cardiac Output
The amount of blood moved per unit of time
CO = hear rate (HR) x stroke volume (SV)
Cardiac AV Valves structure
Fibrous skeletal rings that isolate the atrium and ventricles electrically
What is the “first heart sound”
AV valves closing
What is the “second heart sound”
Closure of the aortic and pulmonary vlaves
What are the different types of heart murmurs?
Stenosis = narrowing
Regurgitation = insufficiency - can lead to backflow
Other septal defects
Series
Components are connected end-to-end to form only one path for electrons/blood to flow through the circuit
The second component gets whatever electrons/blood is leftover
Parallel
Components are connected between the same two sets of electrically common points, creating multiple paths for electrons/blood to flow
Same amount of electrons go to each point
The systemic and pulmonary circulations are in what?
Series
So all of the blood going back to the heart will be oxygenated
Organs in the systemic circulation are in what?
Parallel
So every organ gets oxygenated blood
Flow
Volume per unit time
F = /\P/R
Systole
When ventricles are contracting
Diastole
When ventricles are relaxed
Study up on the Wigger’s diagram
Good job!
What would the Wigger’s diagram for the R side look like compared to the L?
Pressure for the R side won’t be as high
This is because the R side doesn’t have to pump the blood as far
What would the Cardiac Output be for a ventricle with a rate of 72 bpm, and ejects 70 mL of blood with each beat?
CO = HR x CV CO = 72 bpm x 0.07 L/beat CO = 5.0 L/min
How do parasympathetics effect HR?
Slow them down
How do sympathetics effect HR?
Speed them up
How does sympathetic stimulation increase HR?
It increases the Na influx at funny channels, allowing the cells to reach threshold and depolarize faster
How does parasympathetic stimulation decrease HR?
Acts on funny channels to decrease Na influx, causing threshold and depolarization to take longer to achieve
How do you increase HR?
Increase activity of sympathetics to the heart
Increase plasma epinephrine
Decrease activity of parasympathetics to the heart
What are the three factors that influence stroke volume?
Preload
The magnitude of sympathetic input to the ventricles
Afterload
Preload
The volume of blood in the ventricles just before contraction (end-diastolic volume)
Afterload
The pressure against which the ventricle pumps (Pressure in the aorta)
Increased afterload causes decreased stroke volume because the ventricle has to work harder to get the pressure up
What does the Frank-Starling mechanism say?
To increase the heart’s stroke volume, fill it more fully with blood - the stretch of the ventricle will align its actin and myosin in a more optimal pattern of overlap
How can you further increase stroke volume
Fill it more fully with blood (Frank-Starling mech.) -AND-
Deliver sympathetic signals (this will cause the ventricular cells to also relax more rapidly, allowing more time to refil)
What is the mechanism of sympathetic effects of cardiomyocyte contractility
1) Phosphorylate Ca channel - allowing more trigger Ca to enter the cell
2) Ca binds to Ryanodine receptor - PKA phosphorylates ryanodine to keep the channel open longer, releasing even more Ca into the cytoplasm
3 + 4) PKA phosphorylates myofilaments to increase kinetics - myofilaments produce more force due to increased Ca
5) More Ca is sucked up and stored in the SR
Effects of autonomics on the SA node
Symp = increased HR P-symp = decreased HR
Effects of autonomics on the ventricular muscle
Symp = increased contractility P-symp = no sig effect
To increase stroke volume, what could you increase?
End-diastolic volume
Norepinephrine delivery from symp neurons
Epinephrine delivery from the adrenal medulla
To increase HR, what could you increase?
Norepinephrine delivery from symp neurons
Epinephrine delivery from adrenal medulla
Reduce parasympathetic input
Can you increase HR without increasing stroke volume, and vice versa?
No - to increase one is to increase the other
Ejection fraction
Measurement of contractility
Defined as the ratio of the stroke volume minus end systolic volume to the end diastolic volume
EF = SV / EDV
SV = EDV - ESV
Hypertrophic cardiomyopathy
Increase in the heart wall thickness (particularly in the interventricular septum) which interferes with blood ejection
Happens with hypertensive patients - because the ventricle has to work harder, it gets bigger, which compensates preload volume
Can lead to angina, arrythmias, or sudden cardiac death
