3. HPV Flashcards

1
Q

Definition

A

HPV is a mechanism that diverts blood flow away

from areas of the lung where the alveolar oxygen tension is low,

shunting it to better ventilated zones and
improving the ventilation–perfusion ratio.

(Elsewhere in the circulatory system,
hypoxia always results in the vasodilatation of vascular beds.)

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2
Q

Significance:

A

HPV is of little importance in health, but it is more significant in
disease. It explains, for example, the upper lobe diversion characteristic of left
ventricular failure, as blood in the congested and hypoxaemic lower parts of the
lung is diverted away. It is significant during one-lung anaesthesia

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3
Q

Response:

A

this occurs via the constriction of small arterioles;
it is not neurally mediated.
- in denervated lungs (following transplantation).

Nor is it mediated by humoral vasoconstrictors
but rather by pulmonary mixed venous oxygenation and,

more importantly, by alveolar oxygenation.

Larger blood vessels may be affected globally,
as in the fetal pulmonary circulation in which the
low PaO2 reduces pulmonary blood flow to
about 15% of the cardiac output.

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4
Q

Onset:

A

Onset: this is within seconds of the decrease in PaO2, and lobar blood flow may
halve within minutes from its value during normoxia.

The phenomenon is biphasic,
with the vascular resistance returning
almost to baseline before the onset of a
second phase of slower and sustained
vasoconstriction that reaches a plateau at 40 minutes

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5
Q

Mediators

A

Mediators: the mechanisms have not been fully identified.

  1. Nitric oxide
  2. Endothelin
  3. O2 sensitive K channel

The pulmonary vasculature is maintained in a state of active vasodilatation to which nitric oxide may contribute,
and so suppression of endothelial nitric oxide production
will lead to vasoconstriction.

In addition, hypoxia stimulates production of the peptide endothelin,
which is the most potent vasoconstrictor yet identified in humans.

It is also known that pulmonary blood vessels have oxygen-sensitive potassium channels such that the membrane potential alters in response to hypoxia,
with opening of calcium channels and smooth muscle contraction. This phenomenon is not seen in the
systemic vasculature.

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6
Q

Influences

A

Influences: acidosis and hypercarbia potentiate HPV, while alkalosis either attenuates
or abolishes it and causes pulmonary vasodilatation.

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7
Q

The Influence of Anaesthesia on HPV

A

all inhalational anaesthetics inhibit HPV.

The effect is dose-dependent and is similar for all the agents apart from nitrous oxide, whose action is less potent.

The dose–response curve is of typical sigmoid shape; the ED50 is just under 2 MAC,
and the ED90 is around 3 MAC. At 1.3 MAC,

HPV is diminished by around 30%.

Intravenous induction agents have little effect

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8
Q

Oxygen

A

Oxygen: a high FiO2 may inhibit HPV by maintaining higher PaO2 even in underventilated
alveoli

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9
Q

Cardiac output:

A

Cardiac output: any factor which depresses cardiac output will reduce mixed venous
PO2 and so may enhance HPV.

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10
Q

Drug effects

A

Drug effects: drugs such as calcium-channel blockers, sodium nitroprusside, glyceryl
trinitrate, bronchodilators, nitric oxide and dobutamine all attenuate HPV.

It is potentiated by cyclo-oxygenase inhibitors,

propranolol and by the respiratory stimulant almitrine.

(Although not used in the UK, it acts by stimulating carotid body
chemoreceptors. It also enhances the effect of HPV in situations in which it is
deficient

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