Pulmonary Circulation Flashcards
lung as a filter
clears small emboli (has protesases) and particles associated with recreational drugs
lung as a metabolic clearance organ
- Angiotensin I- Converted to angiotensin II in one pass
- Angiotensin II- Untouched
- Bradykinin- 80% removed in one pass
- 5-Hydroxytryptamine (serotonin)- 90% removed in one pass
- Epinephrine- Not affected
- Norepinephrine- Up to 30% removed
pulmonary arterial pressure
pulsitile, 25/8 (systolic over diastolic, units of mm Hg).
mean pressure = 15mmHg
does not increase with exercise bc resistance decreases with cardiac output
Mean pulmonary venous pressure
2 mm Hg and is virtually the same as left atrial pressure.
pulmonary capillary pressure
highly pulsitile (unlike systemic)
contribute significantly to the total pulmonary (circulatory) resistance
arteries and arterioles
carry little pressure, they do not have considerable smooth muscle tissue around the walls
pulmonary resistance
If the mean arterial pressure is about 15 mm Hg, the mean venous pressure is about 2 mm Hg, and the cardiac output is about 5 L/min, the resistance is therefore (15-2)/5 or around 2 to 3 mm Hg per (L/min). This is about 10 fold less than the systemic circulation
decreases with increasing cardiac output
decrease in pulmonary resistance
passive phenomenon. It is due to
1) distension of vessels that are already well-perfused
2) recruitment (opening up) of vessels not perfused
Hypoxic vasoconstriction
unique to the pulmonary arterial bed
acute- caused by blockage in small airways -> blood flow is “re-routed” to regions of the lung which have better ventilation
generalized- vasoconstriction throughout the entire lung -> resistance of the entire pulmonary vasculature is increased -> pulmonary arterial pressure rises -> “pulmonary hypertension”
pulmonary hypertension
change in right ventricular structure and function, and that is named Cor Pulmonale
Cor Pulmonale
a dilation, or hypertrophy, of the right ventricle due to this increase in the resistance of the pulmonary vasculature
Regional differences in ventilation and perfusion
In an upright individual, there is less ventilation and less perfusion in the top, or apex, of the lung, than there is at the base of the lung
West Zones
“three zone model” of lung perfusion
Zone1: PA>Pa>Pv
Zone2: Pa>PA>Pv
Zone3: Pa>Pv>PA
Zone1
lung apex
no perfusion due to gravity
PA>Pa>Pv -> capillary collapses
Zone2
middle lung
some perfusion
Pa>PA>Pv -> capillary open on arterial side, constriction on venous side
Zone3
lung base
Pa>Pv>PA -> no vessel constriction
RQ
respiratory quotient is the ratio of CO2 produced to oxygen consumed
RQ= V(.)CO2/V(.)O2
Or, = (Cv(CO2)-Ca(CO2))/(Cv(O2)-Ca(O2))
normally ~ .8
Glucose metabolism:
C6H12O6 + 6 O2 = 6 CO2 + 6 H2O
RQ= 6/6 = 1
Fat metabolism
RQ <1 ~.7
alveolar air equation
If RQ =1.0 or FI(O2)=100%O2:
PA(O2) = PI(O2) - Pa(CO2)
If RQ =.8 and or FI(O2)=21%O2:
PA(O2) = PI(O2) - 1.2*Pa(CO2)
Because RQ<1 lowers the PA(O2) because more oxygen is consumed than CO2 produced so the alveoli restores atmospheric pressure by drawing in air that is 2partsO2 and 8parts N
alveolar ventilation equation
V(.)A = V(.)(CO2)/Pa(CO2) x 863
units of L/min
shunt
a pathway by which blood flows from the venous circulation to the arterial circulation without participating in gas exchange
different from poorly ventilated regions
- > substantial A-a O2 diff
dx: breathe 100% O2, if there is a A-a diff then there is a shunt
ventilation-perfusion mismatching
can be corrected by breathing high oxygen mixtures
Blood traversing poorly ventilated regions can be oxygenated if the inspired oxygen partial pressure is raised to sufficiently high levels
people with mild to moderate Q/V mismatching have a near normal PaCO2 and below normal PaO2. This is because a well ventilated region of the lung can compensate for a poorly ventilated region of the lung with respect to CO2 gas exchange BUT cannot compensate with respect to O2 gas exchange due to the oxyhemoglobin dissociation curve.
ventilation perfusion ration
V(.)A/Q(.)
=0 = shunt, lung is not ventilated but well perfused
-> The gases in this alveolar region will come into equilibrium with the mixed venous blood
= infinity = physiological dead space -> alveolar gases will come into equilibrium with the inspired gases
ventilation-perfusion line
describes different ventilation-perfusion ratios on the gamut from shunts to dead space
the lung regulates ventilation to keep PA(CO2) in a narrow range
c’
end-capillary blood
poorly ventilated
low V/Q
-> PA(O2) lower and PA(CO2) higher
well ventilated
high V/Q
-> PA(O2) highe and PA(CO2) lower
central chemoreceptor
regulates spontaneous respiration
ventral lateral surface of medulla
monitors the partial pressure of CO2 but responds to H+
can only respond to changes in PaCO2 because dissolved carbon dioxide (but not bicarbonate nor hydrogen ion) can diffuse rapidly across the blood-brain barrier into the cerebrospinal fluid (CSF)
in CSF:
CO2 + H2O HCO3- + H+
carotid bodies
located at the bifurcation of the common carotid arteries
send signals through the glossopharyngeal nerve
only structure responsible for the ventilatory response to hypoxia
principal sensor responsible for the ventilatory response to non-carbonic acids (metabolic acidosis)
aortic bodies
in man, no ventilatory role for the aortic bodies can be assigned
set point
partial pressure of carbon dioxide which we try to maintain in the arterial circulation
35-40mm Hg CO2
as PACO2 increases, rate of ventilation V(.)E increases
hypercapnia
increased PI(CO2)
hyperoxia
elevated partial pressures of oxygen in the inspired air)
no ventilatory response
hypoxia
decreased partial pressures of oxygen in the inspired air)
ventilatory response is hyperbolic in relationship to decreased PAO2 and linear with hemoglobin saturation
Response to metabolic acidosis
ex: lactate (anaerobic exercise) and various acids (diabetic ketoacidosis)
increase in ventilation is due to stimuli coming from the carotid bodies
Acute vs. chronic hypoxia/acidosis
acute: a minor increase in ventilatory rate but the PaCO2 drops and the brain reduces ventilatory rate
chronic: pH of the cerebrospinal fluid is adjusted. The alkaline CSF pH value, brought about by the hypoxia, changes to a more normal pH -> higher ventilatory rate is then observed chronically
