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Session 4
CIRCULATION & LUNG
PHYSIOLOGY I
M.A.S.T.E.R. Learning Program, UC Davis School of Medicine
Date Revised: Jan. 24, 2002
Revised by: Melissa Clark and Marc Hassid
1. What is the normal cardiac output for a resting man weighing 65kg? How is it distributed
among the major organs and tissues? How is it distributed during heavy exercise?
During resting periods, the normal CO is 6,000 ml/min and rises to 16,000 ml/min upon
heavy exercise. The greatest blood flow is located in the GI, and renal systems. Upon
exercising, there is a large transfer of blood flow to the skeletal muscles, heart and skin.
There is no change in blood flow to the brain and minimal change to the bones. (See chart on
Lec. 16/5.)
2. What are the exchange vessels? What are the factors which favor exchange in these vessels?
The capillaries and postcapillary venules are the exchange vessels. In these vessels, blood
velocity is slowest (<1 mm/sec) and surface area per unit mass of tissue highest (>100
cm2/g). In addition, capillary-to-cell distances are very short. All these factors favor
exchange of materials.
3. How are perfusion and blood pressure controlled in the exchange vessels?
The fraction of exchange vessels perfused is controlled by terminal arterioles (recruitment.)
When local metabolism increases, arteriolar dilation increases exchange surface area and
reduces blood-to-cell distances.
Blood pressure in exchange vessels is controlled by the ratio of pre-capillary resistance (in
arterioles) to post-capillary resistance (in muscular venules). Arteriolar vasodilation and
venular constriction increase capillary pressure, whereas arteriolar constriction and venular
dilation decrease capillary pressure.
4. What is the principal function of the sympathetic innervation to the skin of a resting, nude
man (or woman)?
Temperature regulation: Increases in temperature will cause a decrease in sympathetic tone
to the skin blood vessels. This results in increased blood flow through the arterioles and
increased arteriovenous shunting of blood to the venous plexus near the skin surface. (This
type of plexus is different than the nutritive capillary loops). The warm blood looses heat
through radiation and convection. Heat loss by evaporation depends on the activity of sweat
glands, which are innervated by the SNS. In the cold, sympathetic activity increases to the
blood vessels of the skin and there is a resulting vasoconstriction. This serves to conserve
heat by keeping it closer to the body core. Using a nude subject is standard experimental
practice because it limits the number of variables we have to worry about.
5. Of the three most important endothelial paracrines (EDRF-NO, Prostacyclin, Endothelin ) which of these mediates vasodilation through increased cGMP levels?
EDRF-NO, which is a locally active vasodilator. During exercise, it is released from
endothelium and has the potential to override any neurogenic tone.
6. Match mechanism of permeation through capillaries with the corresponding substance:
Oxygen
Through endothelial cells
Ions
Through tight junctions between endothelial cells
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Plasma proteins
Through large pores or through pinocytosis
7. Write the equation which describes the movement of small solute across exchange vessels.
J s  PsA  (Ccap  Cisf ) (Fick’s Law)
This equation describe how the rate of a solute out of a capillary (Js) can be increased by
increasing the permeability of the capillary (Ps), and/or increasing the surface area (A),
and/or increasing the capillary plasma concentration of solute(Ccap), which determines
oncotic pressure in the capillary, and/or decreasing the concentration of solute in the
interstitial fluid around the network(Cisf), which determines the oncotic pressure of the
interstitium.
8. Write the equation which describes bulk fluid across exchange vessels. Explain causes of
edema in this context.
J v  LpA[( Pcap  Pisf )   ( cap   isf )] Remember this equation from Cala’s lectures? He
used  instead of ..
Edema is the accumulation of excess fluid in the interstitial space. One cause of edema is
reduced concentrations of plasma protein, which reduce colloid osmotic pressure (cap).
This oncotic pressure problem can result from liver disease, since the liver normally
synthesizes many of the plasma proteins. Other causes of edema are increased capillary
permeability to proteins (decreased ) and increased capillary hydrostatic pressure (Pcap).
In all of these situations, Jv increases, and the tendency for fluid movement into the
interstitium is favored.
9. The most important mechanism by which coronary blood flow is regulated to match
myocardial oxygen requirements is:
Adenosine-mediated vasodilation. Adenosine is controlled by two mechanisms: 1) low pO2
and 2) increase metabolism; both of which are created by increased workload of the heart.
When ATP use increases, the relative concentration of ATP metabolites increases. Adenosine,
a potent vasodilator, is the final product of the breakdown of ATP to ADP and then AMP.
Adenosine mediated vasodilation results in increased coronary blood flow, and thus more
oxygen delivery and augmented washout of adenosine.
10. Diagram the following lung volumes: TLC, RV, VC, FRC, TV, IC, IRV, ERV, and MV in a
bar graph.
IC = Inspiratory Capacity
ERV = Expiratory Reserve Volume
IRV = Inspiratory Reserve Volume
RV = Residual Volume
VC = Vital Capacity
TV = Tidal Volume
FRC = Functional Residual Capacity
TLC = Total Lung Capacity
Note: Not shown on our graph-- MV is minimal volume, achieved
only when the lung collapses, as in a pneumothorax.
Also note that Capacities (e.g. TLC) are composed of 2 or more
Volumes! (e.g. IC = TV + IRV, etc)
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11. Which values (TLC, RV, VC, FRC, TV, IC, IRV, ERV, and MV) cannot be measured via
spirometry?
RV, and thus FRC and TLC cannot be measured. These values cannot be assessed because
they are below forced tidal volume, which is the maximum that can be breathed out. (MV,
which is the volume of gas trapped in lung if it is removed from the thorax also cannot be
measured via spirometry.)
12. Contrast minimum volume with residual volume. Clinically, when would a patient’s lung be
at minimum volume?
Residual volume is the volume remaining after a maximal, forced expiration. At this
volume, the negative pressure exerted by the chest wall’s elasticity is so great that
positive alveolar pressure can no longer be generated to expire further. Minimal
volume is the volume remaining in the lung if no chest wall were present; thus, the
pressure generated by surface tension and elastic recoil is unopposed by any chest
wall pressure. This is what occurs in a pneumothorax, where the pleura is disrupted
and the parietal and visceral pleurae no longer contact.
13. What is transmural pressure?
Transmural pressures in the lung describe the pressure difference across a wall. It is defined
as the pressure inside a structure minus the pressure outside a structure.
14. Define transpulmonary (Lung) pressure (PL).
This is the transmural pressure across the lung with the airways and alveoli on the inside and
the pleura on the outside. Thus, PL = PA – PPL The pressure across the lung is equal to the
alveolar pressure (PA) minus the intrapleural pressure (PL) .
15. Define transthoracic pressure (PCW)
PCW = PPL – PB, and PB is always zero by definition. So, PCW = PPL.
16. Is the intraplural pressure (PPL) of a lung resting at FRC zero, negative, or positive?
Negative. When the lung is resting at FRC zero, air is not flowing (PA = PB = 0). The PPL
has to be negative, because the PL must be positive in order to prevent the alveoli from
collapsing. Another way to look at it—at FRC the chest wall tends to pull the pleura, and
thus the lungs outward. Since PCW is negative (spring outward), and PB is by definition zero,
then PPL must be negative.
17. Define Transrespiratory pressure (PRS). At FRC is the transrespiratory pressure (PRS) at zero,
negative, or positive?
PRS = PA - PB , so PRS = PL + PCW Why? Remember [PL = PA – PPL] and [PCW = PPL – PB].
The pressure across the respiratory system is equal to the pressure on the inside minus the
pressure on the outside: PRS = PA - PB . We can substitute PL + PCW for PA - PB , such that
PRS = PL + PCW . This basically states that the pressure across the respiratory system is
made up by pressures across the lung and the chest wall. Also, since barometric pressure is
zero, PRS = PA –0, and thus PRS = PA = PL + PCW. Any change in lung PL or PCW will affect
PA.
Since FRC is by definition the volume at which airflow stops (PA = zero) during passive
breathing with the glottis open, PRS must be zero.
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18. What would happen if the pleural space suddenly were equal to barometric pressure (as in a
pneumothorax)?
If PPL went to zero, then the PCW would not oppose the elastic recoil of the lung, and the lung
would collapse.
19. Is the pressure created by surface tension greater in smaller or larger alveoli? What is the
significance of this in the lung?
By the law of Laplace, [Pressure = 2 T/r], we can see that at any given tension, more
pressure is generated in an alveolus of smaller radius. This causes small alveoli to force
their air into larger alveoli and collapse. Compare this to the heart, where a small ventricle
generated more pressure than a diseased, dilated ventricle at any given amount of tension.
20. What are the functions of pulmonary surfactant?
Pulmonary surfactant decreases surface tension, offsetting the tendency for small alveoli to
collapse. It does so by decreasing surface tension more in small alveoli, allowing them to
remain expanded. Pulmonary surfactant also alters the compliance curve for the lung such
that it differs between expiration and inspiration, a phenomenon known as hysteresis.
21. Why doesn’t all of the tidal volume participate in gas exchange?
VT=VA+VD (ventilation of the alveoli plus ventilation of the dead space). The anatomical
dead space is the part of the conducting system that does not participate in gas exchange. In
addition to this there may be areas of the respiratory exchange apparatus which are not
perfused by blood. In these areas ventilation is ineffective, thus resulting in another form of
dead space. Total dead space (anatomical + other) is called the physiological dead space.
In a healthy individual the physiological dead pace should be equal to the anatomical dead
space.
Normal dead space may be approximated by body wt in pounds = # ml of dead space
22. What is the equation for alveolar ventilation expressed as a function of alveolar CO2?
VA= VCO2 X 863mm Hg / PACO2.
This equation shows that alveolar ventilation will be increased proportionally to the increase
in production of CO2. (We must assume that alveolar partial pressure is constant.)
23. Calculate the alveolar partial pressure of oxygen at sea level in a normal patient with good
humidification and normal respiratory quotient.
PAO2 = FIO2 (PB – PH2O) – PACO2 / R
= .21 (760 mm Hg – 47 mm Hg) – 40 mm Hg / 0.8
= 150 mm Hg – 50 mm Hg = 100 mm Hg
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