Tutor: Dr. Glenda Ogsimer Tagorda, M.D.

, FPCP

Group 1
 Output of the right
ventricle (~5 L/min in
a normal adult at rest)

Pulmonary
vasculature
 Thin-walled vessels of the
pulmonary arterial system -
provides little resistance to flow
and are capable of handling
large volume of blood at
perfusion pressures.
 The normal
mean aortic
pressure~95
mmHg

The normal
mean
pulmonary
artery
pressure is 15
mmHg
Regional blood flow in the
lung is dependent on:

vascular geometry

hydrostatic forces
In an upright person:
perfusion is least at the apex of the lung and greatest at
the base

When cardiac output increases (exercise)

pulmonary vasculature is capable of recruiting
previously unperfused vessels and distending
underperfused vessels, thus responding to the increase
in flow with a decrease in pulmonary vascular
resistance.

In consequence
increase in mean pulmonary arterial pressure, even
with a three- to fourfold increase in cardiac output, is
small.
Assessment
of pulmonary
circulatory vascular
function in
the pressures
pulmonary cardiac output
vasculature
 Measurements are commonly made in;
-intensive care units capable of invasive monitoring
-in cardiac catheterization laboratories

With a flow-directed pulmonary arterial catheter, PAP

and pulmonary capillary wedge pressure can be
measured directly, and cardiac output can be
obtained by the thermodilution method.
 PVR = 80(PAP PCW)/CO
Where:
PVR = pulmonary vascular resistance (dyn s/cm5)
PAP = mean pulmonary arterial pressure (mmHg)
PCW = pulmonary capillary wedge pressure (mmHg)
CO = cardiac output (L/min).

normal value = ~50150 dyn s/cm5

 Intraluminal thrombi or proliferation of
smooth muscle in vessel walls diminishes
the luminal cross-sectional area

Pulmonary Small pulmonary vessels

arterial and are destroyed, either by
arteriolar scarring or by loss of
vasoconstriction alveolar walls (chronic
(alveolar obstructive lung disease)
hypoxia)
Increase
PVR
 All diseases of the respiratory system causing
hypoxemia are potentially capable of
increasing PVR.
The more prolonged and intense the hypoxic
stimulus, the more likely it is that a significant
increase in PVR producing pulmonary
hypertension will result.
 chronic obstructive
lung disease
interstitial lung disease
chest wall disease
pulmonary
obesity hypertension
hypoventilationsleep
apnea syndrome

Patients with
hypoxemia
A decrease in the cross-sectional area of the pulmonary
vascular bed is primarily responsible for increased PVR

In the case of recurrent pulmonary emboli, parts of the

pulmonary arterial system are occluded by
intraluminal thrombi originating in the systemic
venous system.

With primary pulmonary hypertension or with

pulmonary vascular disease secondary to scleroderma,
the small pulmonary arteries and arterioles are affected
by a generalized obliterative process that narrows and
occludes these vessels. PVR increases and significant
pulmonary hypertension often results.