By,
Dr. Arun Kumar MD
dept of Anesthesiology
YMC.
Moderator: Dr. Harish Hegde MD
 Hypoxemia resulting from respiratory
depression, airway obs, circulatory collapse is a
potential complication for any anesthetic
technique.
 However its also noted that during GA., an
additional cause of hypoxemia is noted i.e.
detioriation in the pulmonary exchange of
oxygen.
 First modern observation by Bradford and
Dean in 1894.
 Von Euler and Liljestrand 1946 recognized it as
the adaptive mechanism.
 They studied changes in the pulmonary
circulation of the cat in response to changes in
hypoxic mixtures.
 Relationship between PaO2 and hypoxic
segment of the lung was studied in animal
model (dogs).
 When hypoxic segments were small
(<30%), HPV had little effect on PaO2, because
shunt was small.
 When most lung is hypoxic no significant
normoxic region is seen to divert flow.
 When the lung is partially hypoxic (30-70%) as
in OLV, large difference between PaO2 to be
expected with normal HPV and in its absence.
 HPV brings the PaO2 from dangerously low
levels to acceptable levels.
 Current description is:
 The induction and maintenance of general
anesthesia results in.,
 Decrease in resting lung volume hence FRC
and the compliance of the lung and chest wall
reduces.
 These changes leads to atelectasis in the
dependant area of the lung.
 Pulmn shunting and perfusion of low V/Q
regions increases.
 HPV reduces blood flow to both atelectasis and
the low V/Q regions.
 Hence reducing the effects of the abnormalities
during the gas exchange.
 Redox theory.
 Pulmonary vascular smooth muscle
cells(pvsmc) and type 1 cells of the carotid
body.
 Hypoxia causes inhibition of outward
potassium current. Thus causing membrane
depol. and calcium entry through voltage gated
calcium channels.
 The general view is that the inhalational agents
inhibit HPV and intravenous agents do not.
 The studies done on the same, none are with
consistent results.
 But it is evident from these studies that both
inhalational and intravenous agents inhibit, but
inhibition is less in intravenous agents than in
inhalational.
 It is Observed that ketamine- no reduction in
FRC(adults), impaired O2 exchange(children).
 Thiopentone- (sheep, dogs) not assoc with dec
FRC, atelectasis or abnormal oxygen exchange.
 Inhibition:
 Trauma, vasodialator drugs(
nitroprusside, nitroglycerin, nitric
oxide, isoprenaline).
 Vasoconstrictors: which constrict the pulmn
vasculature (noradr, dopamine, histamine)
reduces the effectiveness of HPV.
 Indirect inhibitors: mitral stenosis, volume
overload, hypothermia, thromboembolism, larg
e hypoxic lung segment.
 Potentiator: Almitrine a respiratory stimulant
drug.
 Found to improve PaO2 in patients with COPD
and to have this effect in the absence of ventilatory
stimulation.
 It is tested in combination with nitric oxide to be
used in OLV.
 But till date the drug is not marketed outside of
france.
 Hypoxic pulmonary vasoconstriction is a
physiological, protective process occurring in a
non physiological settings.
 Helps in minimising the V/Q mismatch in a
hypoxic lung.
 It is abolished by factors causing pulmonary
vasodialatation, and also reduced by
vasoconstrictors.
 It is a process which makes OLV possible.
 During GA hypoxemia occurs due to atelectasis
or inhibition of HPV. Without these two events,
There wouldn’t have been increased shunt, and
hypoxemia would be a problem in every
patients, and OLV be difficult to manage
without additional measures to reduce blood
flow to collapse lung.
If hypoxemia occurs and extra pulm causes ruled
out, then its most probable cause is impairment
of HPV.
 What is hypoxia and hypoxemia?
 Why in OLV there is no saturation drop,
whereas in endobronchial intubation there is?
 Mechanism of HPV.
 V/Q mismatch.
 Factors affecting HPV.

Intro to Hypoxic pulmonary vasoconstriction

  • 1.
    By, Dr. Arun KumarMD dept of Anesthesiology YMC. Moderator: Dr. Harish Hegde MD
  • 2.
     Hypoxemia resultingfrom respiratory depression, airway obs, circulatory collapse is a potential complication for any anesthetic technique.  However its also noted that during GA., an additional cause of hypoxemia is noted i.e. detioriation in the pulmonary exchange of oxygen.
  • 3.
     First modernobservation by Bradford and Dean in 1894.  Von Euler and Liljestrand 1946 recognized it as the adaptive mechanism.  They studied changes in the pulmonary circulation of the cat in response to changes in hypoxic mixtures.  Relationship between PaO2 and hypoxic segment of the lung was studied in animal model (dogs).
  • 4.
     When hypoxicsegments were small (<30%), HPV had little effect on PaO2, because shunt was small.  When most lung is hypoxic no significant normoxic region is seen to divert flow.  When the lung is partially hypoxic (30-70%) as in OLV, large difference between PaO2 to be expected with normal HPV and in its absence.  HPV brings the PaO2 from dangerously low levels to acceptable levels.
  • 5.
     Current descriptionis:  The induction and maintenance of general anesthesia results in.,  Decrease in resting lung volume hence FRC and the compliance of the lung and chest wall reduces.  These changes leads to atelectasis in the dependant area of the lung.  Pulmn shunting and perfusion of low V/Q regions increases.
  • 6.
     HPV reducesblood flow to both atelectasis and the low V/Q regions.  Hence reducing the effects of the abnormalities during the gas exchange.
  • 7.
     Redox theory. Pulmonary vascular smooth muscle cells(pvsmc) and type 1 cells of the carotid body.  Hypoxia causes inhibition of outward potassium current. Thus causing membrane depol. and calcium entry through voltage gated calcium channels.
  • 8.
     The generalview is that the inhalational agents inhibit HPV and intravenous agents do not.  The studies done on the same, none are with consistent results.  But it is evident from these studies that both inhalational and intravenous agents inhibit, but inhibition is less in intravenous agents than in inhalational.
  • 9.
     It isObserved that ketamine- no reduction in FRC(adults), impaired O2 exchange(children).  Thiopentone- (sheep, dogs) not assoc with dec FRC, atelectasis or abnormal oxygen exchange.
  • 10.
     Inhibition:  Trauma,vasodialator drugs( nitroprusside, nitroglycerin, nitric oxide, isoprenaline).  Vasoconstrictors: which constrict the pulmn vasculature (noradr, dopamine, histamine) reduces the effectiveness of HPV.  Indirect inhibitors: mitral stenosis, volume overload, hypothermia, thromboembolism, larg e hypoxic lung segment.
  • 11.
     Potentiator: Almitrinea respiratory stimulant drug.  Found to improve PaO2 in patients with COPD and to have this effect in the absence of ventilatory stimulation.  It is tested in combination with nitric oxide to be used in OLV.  But till date the drug is not marketed outside of france.
  • 12.
     Hypoxic pulmonaryvasoconstriction is a physiological, protective process occurring in a non physiological settings.  Helps in minimising the V/Q mismatch in a hypoxic lung.  It is abolished by factors causing pulmonary vasodialatation, and also reduced by vasoconstrictors.  It is a process which makes OLV possible.
  • 13.
     During GAhypoxemia occurs due to atelectasis or inhibition of HPV. Without these two events, There wouldn’t have been increased shunt, and hypoxemia would be a problem in every patients, and OLV be difficult to manage without additional measures to reduce blood flow to collapse lung. If hypoxemia occurs and extra pulm causes ruled out, then its most probable cause is impairment of HPV.
  • 14.
     What ishypoxia and hypoxemia?  Why in OLV there is no saturation drop, whereas in endobronchial intubation there is?  Mechanism of HPV.  V/Q mismatch.  Factors affecting HPV.