systemic circuit
pulmonic circuit
hematocrit
hematocrit and plasma proteins
3× at normal hematocrit, 10× at 70
in small vessels
Fahraeus-Lindqvist effect
rouleux formation
vessel clogging
plasma
about 7% protein
albumins
globulins
fibrinogen
Q = ΔP/R
laminar flow
parabolic velocity profile
turbulent flow
additional details on turbulent flow from Guyton’s Physiology
measurement of flow
ml/min
an account of pressure measurement written in 1733
standard units
mm Hg
1 mm Hg = 1.36 cm H2O
R = ΔP/Q
1 PRU = (1 mm Hg)/(1 ml/sec)
R (in dyne sec/cm5) = (1333 × mm Hg)/(ml/sec)
total pulmonary resistance
measure of blood flow for a given ΔP
conductance = 1/R
effect of vascular diameter
conductance ∝ diameter4
expresses the relationship of all factors in total blood flow 3
mean velocity v = (ΔPr2)/(8ηl)
Q = vπr2
substitute v, and Q = ( πΔPr4)/(8ηl)
solve for R
resistance of vessels in series: Rtotal = R1 + R2 + R3 + ...
resistance in parallel: start with conductances
Ctotal = C1 + C2 + C3 + ...
distensibility = (increase in volume)/((increase in pressure)×(original volume))
veins vs. arteries
compliance = (increase in volume)/(increase in pressure)
note that a vessel with a greater original volume will be more compliant
systole and diastole
relationship of the ECG 4 to the cardiac cycle
[ http://en.wikipedia.org/wiki/Image:SinusRhythmLabels.svg ]
cardiac cycle events
[ This file is licensed under the Creative Commons Attribution ShareAlike 2.5 License. ]
ventricles as pumps
ventricular filling
diastasis
isovolumic contraction
period of ejection
isovolumic relaxation
stroke volume output
role of preload and afterload
cardiac index
metabolism and exercise
|
Question: Why does one’s fitness level not have a direct correlation to cardiac output? The formula for cardiac output is CO=HR×SVO, so if you have a 55 kg marathoner whose resting heart rate is 50 bpm and a 140 kg extremely unfit person, whose resting heart rate is 85, does that not mean that the marathoner’s heart functions more efficiently with less effort? In other words does the 140 kg–unfit person’s heart have to work harder to accomplish the same task? |
|
One’s fitness (whatever that means) influences
how one achieves a given cardiac output.
CO=HR×SVO, as you noted, but there are many ways to get to CO.
The reason the athlete’s HR is only 50 bpm at rest is because her SVO is 100 ml/beat,
whereas the couch potato has a HR of 85 bpm at rest because his SVO is only 59 ml/beat.
Why the difference? There are many things that contribute to SVO; for the athlete,
contractility is undoubtedly better (as a result of her conditioning) and SVR
(systemic vascular resistance) is markedly decreased (again, her conditioning, resulting
in a lower BP) so the EDV is increased. While both the athlete and couch potato have the
same CO at rest, the difference shows up if they were to compete in an athletic event:
She might be able to increase her SVO to 200 ml/beat with a HR of 150 bpm (achieving a CO of
30.0 l/min), whereas he will get his HR up to 180 bpm but only be able to increase the SVO to
120 ml/beat, a CO of only [!] 21.6 l/min. So, at the extreme, fitness does affect CO, but not at
rest. This is why the totally diseased heart with an EF (ejection fraction) of only 20% can still
maintain a CO of 5.0 l/min. Explanation of previous statement: EF measures the percentage of SVO/EDV. So, if one has a SVO of 80 ml/beat and an EDV of 100 ml, then the EF is 80% [that’s very good for a human; cats have an EF of about 95%!]. If the patient has an EDV of 300 ml and an EF of 20% [possible in a very diseased heart], then a HR of 83 bpm will achieve a CO of 5.0 l/min. Dr Jack Wilmore has an interesting perspective on aerobic exercise and endurance. [Article from The Physician and Sports Medicine, 31(5), March 2003] |
age
control of cardiac output by venous return
permissive role of heart
sympathetic stimulation
role of total peripheral resistance
| Questions for thought | ||
|---|---|---|
| 1. | Describe the effects of sympathetic and parasympathetic stimulation on the heart. | |
| 2. | Describe the roles of the sinoatrial and atrioventricular nodes in the cardiac cycle. | |
| 3. | Karen is taking the medication verapamil, a drug belonging to a class called calcium-channel blockers. What effect should this have on Karen’s stroke volume output? | |
| 4. | Describe the significance of Poiseuille’s law. | |
| 5. | Draw and label a normal ECG pattern. Explain the significance of each deflection. | |
| 6. | Define blood pressure. Differentiate between systolic and diastolic pressures. Give a formula for calculating the mean blood pressure. | |
| 7. | Nicole the neonate needs surgery—she was born with a condition called transposition of the great vessels, in which the aorta arises from the R ventricle, and the pulmonary trunk arises from the L ventricle. Describe the physiological consequences of such a defect. What is her prognosis without surgery? | |
| Other questions to test your knowledge | ||
|
|
|
[ Anatomy & Physiology 2 syllabus ] [ Page created 1999-04-01 ][ Last updated 2008-07-22 ] [ Questions about this lecture? E-mail me ] |
|
[ http://webpages.charter.net/cfmoxey/lectures/cardiovascular_physiology_1.html ] [ xhtml validation ] |