Pulmonary vascular resistance
What is a normal value for pulmonary vascular resistance? Outline physiological factors that influence pulmonary vascular resistance. (00A3)(02A4)
Normal value of pulmonary vascular resistance
Pulmonary vascular resistance (PVR) is about 1/8 to 1/10 of the systemic vascular resistance
Mean pulmonary blood pressure = 15
Left atrium blood pressure = 5
Pulmonary blood flow = 5~6
PVR = Pressure difference / blood flow
= (15-5)/5 or (15-5)/6
= about 1.7~2.0 mmHgL-1min
= about 100 dyne.sec.cm-5
Alternatively,
PVR = (Mean pulmonary artery pressure - mean pulmonary capillary wedge pressure) x 80 / cardiac output
= (in dyne.sec.cm-5)
All 3 of these variables can be measured with a Swan-Ganz catheter
Physiological factors influencing pulmonary vascular resistance
General factors
Factors that influence vascular resistance, both pulmonary and systemic:
- Blood viscosity
- (inversely proportional to 4th power of) vessel radius
Factors unique to lung
- pulmonary blood flow
- distension and recruitment
- lung volume
& its effect on alveolar and extra-alveolar vessels
- hypoxic pulmonary vasoconstriction
- others
=> include drugs, hormonal, pH, CO2
1. Pulmonary blood flow
As pulmonary blood flow increases, PVR drops because of:
- recruitment - some capillaries, which were closed or open but with no blood flow, begins to conduct blood
- distension - capillaries change from near flattened to more circular
Both mechanisms contribute, but:
- at low pulmonary arterial pressure, recruitment dominate
- at high pulmonary arterial pressure, distension dominate
2. Lung volume
At high lung volumes
Resistance is increased because:
stretching of alveolar walls
=> decreased caliber of alveolar capillary
=> increased resistance
At low lung volumes
Resistance is increased because:
- reduction in radial traction by lung parenchyma
=> decreased caliber of extra-alveolar capillary
=> increased resistance
- hypoxia-induced vasoconstriction in collapsed alveoli
Lowest PVR occurs at functional residual capacity.
3. Hypoxic pulmonary vasoconstriction (HPV)
- Occurs with decreased alveolar PO2 (PAO2)
- Locally mediated => smooth muscle contraction in arteriole
- Mechanism uncertain
=> ? inhibition of K channel
=> ? increased cytoplasmic [Ca2+]
=> contraction
NB: Hypoxia in all other tissues cause vasodilation not vasoconstriction.
NB: HPV reduces V/Q scatter, and responsible for pulmonary vascular redistribution to upper zones in cardiac failure
4. Others
Factors causing contraction of smooth muscles
(thus increasing PVR)
- (major effect) low PAO2 (i.e. HPV)
- acidosis (drop in pH)
- (weak effect) sympathetic stimulation
- serotonin
- histamine (H1)
- norepinephrine (alpha-1)
- arachidonic acid
- thromboxane A2, endothelin-1 (ET-1)
Factors causing relaxation of smooth muscles
(thus decreasing PVR)
- acetylcholine
(via release of endothelium-derived relaxing factor, mostly nitric oxide NO)
- isoproterenol
- histamine (H2)
- prostacycline
Additional notes
As per examiner's comment: Pulmonary vascular impendence is a more appropriate term for pulmonary circulation due to the relatively great pulsatility.
Hypoxic pulmonary vasoconstriction
Net effect - diverting blood away from poorly ventilated area
=> reduce V/Q scatter
Critical at birth
- during fetal life, pulmonary vascular resistance is high
- with breathing, PAO2 increase, and pulmonary resistance decrease (due to reverse of HPV as well as lung expansion)
=> blood flow increase.
Examiner's comment
- Need to state specific range of PVR, not just a value.
- Need to use the right unit (mmHg/L/min) or dyne/sec/cm5
- Even if exact value is not known, need to state that it is 1/8~1/10 of systemic vascular resistance
- Resistance is directly proportional to blood viscosity (influenced by haematocrits), and inversely proportional to 4th power of the radius (due to laminar flow)
- Other factors uniquely to lung: lung volume (and its effect of extra and intra-alveolar vessels), distension and recruitment (secondary to pulmonary arterial pressure), hypoxic pulmonary vasoconstriction
- Lowest PVR being at FRC
- (extra) effects of pH, CO2, endogenous vasodilator/vasoconstrictor (e.g. nitric oxide), effect of hormone (serotonin,histamine), autonomic factors, effect of posture
- Pulmonary vascular impendence is a more appropriate term for pulmonary circulation due to the relatively great pulsatility
- No need to have details discussion of West's zones, laminar flow vs turbulent flow, benefits of hypoxic vasoconstriction