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Pulmonary circulation
1.Ventilation
3.Diffusion
4.Transport O2
CO2
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Pulmonary Circulation
Unique circulation receives a volume of blood
similar to the entire circulation
pulmonary vascular bed = the systemic
circulation
exceptions - the walls of pulmonary artery &
large branches ~ 30% thickness of aortic wall
- small arterial vessels - endothelial tubes -
little muscle in their walls ; systemic arterioles
have more smooth muscle.
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Pulmonary Circulation
- walls of the post -
capillary vessels
contain smooth
muscle.
- pulmonary capillaries -
large, with multiple
anastomoses :. each
alveolus sits in a
capillary basket.
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Pulmonary Circulation
Major function :-
1. Supply of O2
2.Removal of CO2
3. Pulmonary veins
- Short
-carries Oxygenated blood
4. Bronchial vessels
- 1 2% of cardiac output
- carries Oxygenated blood
- provides nutrition to bronchi respiratory
bronchioles
- drains from pulmonary vessels
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Anatomy :-
1.Pulmonary arteries
- Short
- Thin walled
- Carries deoxygenated blood
- 15mmHg
Pulmonary Arterial pulse pressure:-
- Systolic press Diastolic press
- 16mmHg
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10 mm
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Special features of the pulmonary circulation cont.
Increased
Factors Predisposing to Pulmonary
capillary hydrostatic Oedema
pressure - Increased left atrial
pressure due to L V infarction / M Stenosis, Overload of I V fluids
Decreased interstitial hydrostatic pressure - Too rapid evacuation of
pneumothorax or hemothorax
Bronchopulmonary anastomosis
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4) Coronary veins drain direct into left side of heart
5) Bronchial veins (few) enter the pulmonary capillaries direct left
atrium
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Due to gravity
Intermittent flow :
Pulmonary arterial pressure in systole >alveolar pressure :. blood flows
Pulmonary arterial pressure low in diastole
<alveolar pressure no flow
water fall effect
As veins are compliant and takes the blood without causing an increase in
pressure ..
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Zone 3 :
Pressure at arteriolar end > alveolar pressure
Pressure at venous end > alveolar pressure
:. Capillaries open continuously continuous flow
Endothelin PGE1
Angiotensin Prostacycline
Rapid increase of
Pulmonary Art. Pressure
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=sustained elevation of pulmonary arterial pressure
- Def of endothelial NOS.
Occurs in : infants
Adults-mostly cause unknown
cocaine inhalers
Dexfenfluramine & other appetite suppressants
alter intracellular [serotonin]
leads to Rt Ht failure Death
Rx vasodilator Prostacyclin
vascular remodelling
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3. Defense Mechanism:
IgA- Bronchial Secretions
Pulmonary Alveolar Macrophage-PAM-Phagocytic
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Gas exchange
Removal of emboli
Immunological function
Synthesis of converting enzyme which converts angiotensin 1
angiotensin II
Acts as a blood reservoir
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Pulmonary Edema
Figure 20-11 shows a schematic diagram depicting the circulatory factors governing
the movement of edema ( E) between the pulmonary vessels and the lung
interstitial tissues; the Starling equation describing lung liquid flux is written
beneath the figure. The hydrostatic pressure in the microvessels of the lung (Pmv =
12 mm Hg) lies about halfway between Ppa (normally about 15 mm Hg) and LVEDP
(normally about 10 mm Hg). Hydrostatic pressure in the septal interstitial space (Pis
= 4 mm Hg) is subatmospheric, in part because it drains into the
peribronchovascular interstitium, which has a more negative pressure, and in part
because lymph vessels, valved like veins for unidirectional flow, actively remove
liquid from the interstitial spaces that have intrinsic structural stability to resist
collapse. 58 Accordingly, there is a positive hydrostatic pressure (Pmv Pis = 16 mm
Hg) driving edema across the microvascular endothelium to the lung septal
interstitium. The vascular wall presents a barrier to this bulk flow of liquid
characterized by its permeability to water (Kf; mL edema/min per mm Hg); Kf
includes surface area (S) and thus is heavily weighted by the characteristics of the
alveolar vessels, where so much S resides. 58 The microvascular membrane is also
characterized by its permeability to circulating proteins, dominated by albumin and
globulin. If these plasma proteins were completely reflected ( = 1), no protein
would pass from lung blood to the interstitium; in contrast, if the microvascular
membrane were freely permeable ( = 0), interstitial protein concentration (CL), as
measured in lung lymph, would equal that of plasma proteins (Cp). CL /Cp is about
0.6 in the normal steady-state edema flow in most mammals; when E, as
estimated from lung lymph flow ( L), is progressively increased by elevating Pmv,
CL /Cp decreases to a plateau value of about 0.3. This plateau value indicates the
microvascular protein reflection coefficient ( = 1 2 CL Cp = 0.7) measured in
conditions of high edema flow; at lower E levels, water diffuses from the
interstitium to the blood along the concentration gradient for water established by
Cp > CL. 58