PULMONARY

VASCULAR
RESISTANCE (PVR)
◦ Pulmonary vascular resistance (PVR) is the difference between the mean pulmonary
arterial pressure (mPAP/P1) and mean left atrial pressure (mLAP/P2) divided by the
PBF (PBF/Q), i.e., PVR = P1−P2/Q. PVR is directly proportional to mPAP and inversely
proportional to mLAP and blood flow
Technique for measurement of left
atrial pressure
Parameters that determine PVR
Passive factors such as :
◦ gravity,
◦ position of the body,
◦ transmural pressure difference,
◦ lung volume, and
◦ CO and

Active factors such as :

◦ hormonal-catecholamines,
◦ histamine,
◦ prostaglandins,
◦ nitric oxide,
◦ isoproterenol,
◦ hypoxia and hypercapnia, and
◦ autonomic nervous system for vessels >30 microns 
◦ And another conditions like…
◦ High lung volumes result in a stretching/elongation of the alveolar vessels resulting
in an increased PVR
◦ The extra-alveolar vessels are subject to radial traction and negative pleural
pressure resulting in a decreased PVR
◦ Mechanical ventilation with positive end expiratory pressure (PEEP) results in
increased alveolar pressure as well as intrapleural pressure, and therefore
increases PVR at both alveolar and extra-alveolar levels throughout the
respiratory cycle
Pathophysiology and clinical correlation

◦ Exercise
Pulmonary arterial pressure demonstrates only slight increase with exercise in normal
individuals secondary to decrease in PVR from additional arterial recruitment and
arterial distension

◦ High altitude/hypoventilation
Generalized hypoxic vasoconstriction secondary to decreased PO 2 results in increased
arterial pressure and recruitment/distension of alveolar capillaries for better gaseous
exchange. However, increased pulmonary arterial pressure also increases capillary
hydrostatic pressure and thereby resulting in pulmonary edema. Increased PVR and
right heart work load can present as right heart failure 
Airway obstruction or atelectasis
◦ Decreased PO2 (possible contributions from low pH and increased PCO2) results in a
not so robust hypoxic precapillary vasoconstriction and locally increased PVR (at the
level of small arteries and arterioles) with shunting of blood to better ventilated
areas.
Pulmonary arterial hypertension (PAH)
◦ A mPAP >25 mmHg is defined as PAH, and can be primary from pulmonary
vasculature involvement or secondary to lung disease. Increased pulmonary arterial
pressure could be due to increased PVR, left atrial pressure (pulmonary venous
hypertension) or PBF
◦ Hypoxia should be avoided (for example, air travel) due to concern for hypoxemic
pulmonary vasoconstriction and sudden increase in PVR
◦ Calcium channel blockers, endothelin receptor antagonists, phosphodiesterase
inhibitors, and prostanoid treatments decrease the PVR and PAH, forming the main
stay of medical treatment 
◦ Pulmonary embolism
Pulmonary embolism is secondary to venous thromboembolic disease from venous
stasis, endothelial injury, and hypercoagulable state (Virchow’s triad)
◦ Small and chronic emboli result in gradual increase of PVR and PAH.
Closing
◦ Changes in PVR, pressure and blood flow predominantly determine the physiologic
response to various respiratory and metabolic demands as well as contribute to
pathological disease states.
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