Pulmonary Circulation- Scharf Flashcards
Comparison picture of pulmonary and systemic circulations
What is the difference between alveoli and capillary pressure between the apex and the base?
Alveolar pressure is > capillary pressure at the apex so the capillaries will collapse. High dead space with no gas exchange and infinite V/Q so no flow.
What are the two mechanisms in which increased pulmonary pressures can decrease pulmonary resistance?
Recruitment (more common in the base than the apex), distension.
How does the total peripheral resistance/vascular resistance respond to increased lung volume (graph)?
Start at RV, Intraalveolar resistance goes up with lung volume and extraalveolar goes down until TLC, so least resistance is the intersection between them-FRC.
What are the pulmonary vasoconstrictors?
Norepinephrine (sympathetic stimulation), serotonin, Angiotensin 1 and 2, hypoxia, histamine, endothelin-1
What are the pulmonary vasodilators?
Acetylcholine, beta agonists, NO (used therapeutically), Ca++ channel blockers (e.g. nifedipine), nitrates, epoprostenol,high O2
Fick principle for pulmonary blood flow
Blood flow is cardiac output. Cardiac output = oxygen flow / (Arterial - venous oxygen content)
Three ways to measure pulmonary flow through dye dilution
- Fick principle
- Dye dilution or saline injected into right atrium and measured in the pulmonary artery.
- Inject xenon in blood and scan the lung.
Blood flow in distance on lung with different postures
Total blood flow decreases from bottom to top.
Starling experiment of resistors
Vascular waterfalls: rigid tubes on either side of a flexible tube (Ps- surrounding pressure), Po is outflow pressure, Pi is inflow pressure. When Ps is greatest, flow is zero. When Pi is highest and Po is lowest, flow is Pi-Ps. When Pi is highest and Ps is lowest, flow is Pi - Po.
Starling resistors applied to the lungs
In zone 1, no flow when alveolar is highest.
In zone 2: flow is Ps-Pa / R
Zone 3 is the classic model: flow is Pa-Pv / R
Possible candidates for mediators of hypoxia-induces pulmonary vasoconstriction
Endothelin-1, K+ (smooth muscle), lack of NO
Prolonged effects of Hypoxia
Vascular remodeling
Release of mediators and growth factors with prolonged hypoxia
Leads to pulmonary hypertension and cor pulmonale
At least partially reversible with elimination of hypoxia
(Thickening of smooth muscularis, Thickening of intima, Medial necrosis)
Starling’s Law for Fluid Exchange between capillary and interstitium
J = K [(Pc – Pi) – (πc – πi)]
J is fluid flux, net tendency for fluid. Tendency is flow into capillary from interstitium. Pcap is positive, Pi is negative, Osmotic capillary is positive, interstial is negave.
What are the stages of edema in the interstitial area?
Pe4rivascular cuffing (interstitial pressure is more negative in peribronchilar and perivascular space in the alveolar walls so fluid leaks into interstitium. Tendency to move around artery and bronchi-promotes migration of fluid. When these fluids are overwhelmed it creates pulmonary edema.
