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Respiratory II
Pulmonary Circulation
V/Q
Pulmonary Blood Volume
 This is about 10-20% of the blood volume
 Depends on posture, drugs and left heart
function
 Pulmonary circuit in parallel to the
systemic circuit
 Pulmonary blood flow is equal to the
cardiac output
PVR
 Resistance = driving pressure / blood flow
rate
 Factors:
 Autonomic control: sym mainly and some
parasym but the influence is less than the
systemic circuit
 Hypoxia, hypercarbia, chemicals and
drugs, physical factors
Hypoxia
 Hypoxic
vasoconstriction of
the pulmonary circuit
is important to divert
blood to areas that
have better
ventilation
Mixed Venous PO2
Hyper-oxia and capnia
 Hyperoxia has little effect on PVR in a
normal subject
 Hypercapnia has a slight pressor effect
and reinforces hypoxic vasoconstriction by
causing acidosis
Chemicals
 Ach relaxes smooth muscle -- PVR falls
 Adrenaline and dopamine increase in PVR
 PVR rises with serotonin, thromboxane A2,
PGF2, PGE2 and histamine (H1)
 PVR falls with PGI2, PGE1 and histamine
via H2 receptors
Receptors
Physical
 Recruitment and distension in the
pulmonary capillary bed eg when CO rises
 Lung inflation squeezes small vessels but
tethers open the large vessels and the
sum effect on PVR is minimal
 Collapsed lung tend to have closed vessels
(however this can be reversed by
vasodilators)
West’s Zones
 Zone 4 (Hughes et
al) reduced blood
flow in the lowest
part during low
volumes due to
compression of
larger blood
vessels by
interstitial fluid
Critical Closing Pressure
 This is close to the alveolar pressure
 Therefore during IPPV the pulmonary
vascular pressure rises by up to 8 mmHg
and beyond this there is an increase in the
dead space
Distribution of Ventilation
Ventilation L vs R Lung
 Slow inspiration
the compliance
is important
while at fast
rate the
resistance is
important
Time constant is the
compliance x
resistance
which is the time
required for inflation
to 63% of the final
volume attained if
inflation is prolonged
indefintely or the time
required for inflation
if the initial gas flow
rate were maintained
throughout inflation
The fast alveoli will take
in a higher proportion of
dead space gas as well
Distribution of Perfusion
V/Q
Posture and Perfusion
 Shown as per
alveoli but per
lung volume
then the
perfusion is
higher in the
bases since the
bases have
more but
smaller alveoli
V/Q
 Whole lung alveolar ventilation is about
4L/min and perfusion about 5L/min
therefore the V/Q is usually 0.8
V/Q
Shunt
Dead space
V/Q
V/Q
Dead Space
Dead Space
 Anatomical: the conducting airways
 Alveolar: ventilated but not perfussed
 Physiological: tidal volume that does not
participate in gas exchange
Bohr Equation
 For a single breath: CO2 exhaled (FECO2) x
tidal volume = CO2 exhaled from alveolar
volume x alveolar volume (FACO2) + CO2
from the dead space x dead space (FICO2)
 VD/VT = (PaCO2 -PECO2)/PaCO2

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physiology Resp IIa.ppt

  • 2. Pulmonary Blood Volume  This is about 10-20% of the blood volume  Depends on posture, drugs and left heart function  Pulmonary circuit in parallel to the systemic circuit  Pulmonary blood flow is equal to the cardiac output
  • 3. PVR  Resistance = driving pressure / blood flow rate  Factors:  Autonomic control: sym mainly and some parasym but the influence is less than the systemic circuit  Hypoxia, hypercarbia, chemicals and drugs, physical factors
  • 4. Hypoxia  Hypoxic vasoconstriction of the pulmonary circuit is important to divert blood to areas that have better ventilation Mixed Venous PO2
  • 5. Hyper-oxia and capnia  Hyperoxia has little effect on PVR in a normal subject  Hypercapnia has a slight pressor effect and reinforces hypoxic vasoconstriction by causing acidosis
  • 6. Chemicals  Ach relaxes smooth muscle -- PVR falls  Adrenaline and dopamine increase in PVR  PVR rises with serotonin, thromboxane A2, PGF2, PGE2 and histamine (H1)  PVR falls with PGI2, PGE1 and histamine via H2 receptors
  • 8. Physical  Recruitment and distension in the pulmonary capillary bed eg when CO rises  Lung inflation squeezes small vessels but tethers open the large vessels and the sum effect on PVR is minimal  Collapsed lung tend to have closed vessels (however this can be reversed by vasodilators)
  • 9. West’s Zones  Zone 4 (Hughes et al) reduced blood flow in the lowest part during low volumes due to compression of larger blood vessels by interstitial fluid
  • 10. Critical Closing Pressure  This is close to the alveolar pressure  Therefore during IPPV the pulmonary vascular pressure rises by up to 8 mmHg and beyond this there is an increase in the dead space
  • 13.  Slow inspiration the compliance is important while at fast rate the resistance is important
  • 14. Time constant is the compliance x resistance which is the time required for inflation to 63% of the final volume attained if inflation is prolonged indefintely or the time required for inflation if the initial gas flow rate were maintained throughout inflation
  • 15. The fast alveoli will take in a higher proportion of dead space gas as well
  • 17. Posture and Perfusion  Shown as per alveoli but per lung volume then the perfusion is higher in the bases since the bases have more but smaller alveoli
  • 18. V/Q  Whole lung alveolar ventilation is about 4L/min and perfusion about 5L/min therefore the V/Q is usually 0.8
  • 20. V/Q
  • 21. V/Q
  • 23. Dead Space  Anatomical: the conducting airways  Alveolar: ventilated but not perfussed  Physiological: tidal volume that does not participate in gas exchange
  • 24. Bohr Equation  For a single breath: CO2 exhaled (FECO2) x tidal volume = CO2 exhaled from alveolar volume x alveolar volume (FACO2) + CO2 from the dead space x dead space (FICO2)  VD/VT = (PaCO2 -PECO2)/PaCO2