Pulmonary Circulation Flashcards
PAPs
25/10 mean 15
Where do pulmonary vessels branch of into?
Alveolar vessels- closely related to acini, can become compressed with high PEEP
Extra alveolar- Larger and thicker, do not compress with high PEEP,
Vascular resistance / lung volume graph
“J” shape, high resistance at low volumes, low resistance at medium volumes, high resistance at high volumes
How are alveolar dimensions controlled?
Not by autonomic or hormone control
Alveolar capillaries contribute to 40% resistance
Alveolar arterioles contribute to 50% of resistance (compared to 75% of SVR)
How is blood flow directed to the lungs?
With increased CO, lungs RECRUIT mainly
Recuit- opens more vessels as any muscle does during work out
Also distend to a smaller amount
Functional Capillary volume
70ml (1ml/kg) at rest
200ml maximal volume during exercise
How fast does gas exchange occur?
.25 seconds, but stays in network for .75 seconds
How much blood is in the lungs
500 ml- 50% of weight of lungs
More than any other organ
Capacitance resevoir of lungs
can alter from 50% to 200% of resting volume
Prevents change in blood return to RV from affected LV filling pressures of 2-3 cardiac cycles
Chief mechanism of fall in PVR during exercise
Recruitment
Distension
Internal vessel pressure rises and opens capillary beds
Elevated LA pressure extends capillary beds (mitral regurg, LV failure)
Leads to lung congestions and ultimately HF
Seen at high vascular pressures
Pleural pressure during inspiration
Volumes in RV and LV
More negative than -5mm H2)
Lower pressure allows for more venous return to right heart
Higher RV pressure
LV ejects less blood
Pleural pressure on expiration
Pleural pressure less negative than -5mm H2O
Higher pressures decrease venous return
Less RV ejection pressure
What increases PVR?
Higher and lower lung volumes
How do extra alveolar and alveoli react during breathing?
Extra alveolar dilate on inspiration
Alveolar compress during inspirating
How does mechanical ventilation effect alveolar pressure?
Increases alveolar pressure- can decrease CO or increase VQ mistmatch
- Increase amount of ZONE 2
- Increase in resistance to ZONE 2
Where does bronchial blood circulation return to?
RA via azygos vein
Conducting airways to terminal bronchioles, & pleura, interlobar spaces, pulmonary arteries and veins
1-2% of cardiac output
The rest of the bronchial blood exits lung by small anastomeses with pulmonary veins to contribute to normal venous mixture (R to L shunt)
How much fluid do the lymphatic system remove?
20 ml/hr
Hydrostatic forces (slightly negative) are responsible
VO2 at rest
Oxygen consumption/ minute
300 ml/min
CO= O2 Consumption (VO2)/ AV O2 differences
Fick principle
One method of determining CO, blood flow thru lungs
Indicator dilution principles
Dye injected into venous circulation
Diluted concentration measured on arterial side
Thermodilution technique also commonly used to measure CO
Blood flow at different levels
Top lung- low
Middle lung- higher
Bottom lung- Peaks but drops at very bottom
Pressure gradient from gravity on systemic BP
0.74mm Hg/cm
In supine position- arterial pressure is higher in feet than in head
What are the two zero reference points for hydrostatic pressure
RA
Middle lung
Zone 1 formula
PA> Pa> Pv
High pressure in alveoli
No blood flow- capillaries are collapsed by alveolar pressure
Zone 2 formula
Pa> PA> Pv
Moderate bloow flow
Waterfall effect
Zone 3 formula
Pa> Pv> PA
Most blood flow
Hydrostatic pressure causes distention and recruitment, which decrease resistance
What does pressure in the alveoli depend on?
Hydrostatic pressure
Gravity
Transmural compressive pressure
Lung volume
What does blood flow (PVR) depend on?
Pressures in the pulmonary vessels relative to alveolar pressure
Zone 4
Abnormal condition of reduced blood flow
High PVR
Causes- LV failure, MV stenosis
Pulmonary edema
What expands zone 1?
Decreased PAP- shock, hypovolemia
Increased PA- high PEEP
Occlusion of blood vessels- PE
What reduces Zone 1?
Increased PAP- infusion or bolus
Reduced hydrostatic effect- standing to supine, change in pt position
Regulation of pulmonary blood flow is ___
Active- altering vascular smooth muscle tone in pulmonary arterioles
What is active regulation of pulmonary vessels mediated by?
Local metabolic influences
What does an increase in sympathetic outflow cause in pulmonary vasculature
Stiffening of PV walls- vasoconstriction
PVR vasoconstrictors
Reduced PaO2
Increased PCO2
Histamines
Levo
Thromboxane A2
PVR Vasodilators
Increased PaO2
NO
Prostaglandin I2
Thromboxane A2
Potent vasoconstrictor
Product of cell membrane arachidonic acid metabolism
Constricts pulmonary arterial and venous smooth muscle
When is Thromboxane A2 produced?
Acute lung injury by macrophages, leukocytes, endothelial cells
Effect localized because of short half time of seconds
Prostacyclin (Prostaglandin I2)
Potent vasodilator
Inhibitor of platelet activation
How is prostaglandin I2 made?
By endothelial cells as a product of arachidonic acid metabolism
NO
Potent endogenous dilator
Localized effect
Toxic at high concentrations- binds to HGB 200000x more than oxygen
How is NO formed?
From L arginine which causes smooth muscle relaxation through synthesis of cyclic GMP
NO activates guanylyl cyclase and increases cGMP
How do NTG and sodium nitroprusside work?
Same as NO
From L arginine which causes smooth muscle relaxation through synthesis of cyclic GMP
NO activates guanylyl cyclase and increases cGMP
PAO2 effect on blood flow
Low PAO2 causes vasoconstriction
High PAO2 causes vasodilation
PH causes ______ in the body
Increase in hypoxia
High PVR
Hypoventilation
Low inspired PO2
High PCO2
Pain
Histamine release
RV hypertrophy/ cor pulmonale
Tricuspid regurgitation
PH
Serious condition
Transplant only effective treatment
What causes non uniform and regional ventilation?
Airway resistance Compliance
Hydrostatic effects
The distribution of ventilation in the lung is _____
Nonuniform caused by gravity/ hydrostatic pressure
Bottom receives more ventilation due to increased compliance
Decreased compliance ___ lung volumes
reduces
A-a PO2 levels
Alveolar arterial differences
Normal- 10-15mmHg
What causes high Aa gradients?
Intrinsic pulmonary disease- shunting
Most common cause of inefficient O2/CO2 exhange
Mismatch V/Q ratio
Shunt
Perfused but not ventilated (think alveoli shrinks up)
Small shunts are normal
True anatomical (R-L) shunts
Bronchopulmonary venous anastomoses
Intracardiac thesbian veins
Mediastinal veins
Pleural veins
Venous admixture of blood
“Wasted ventilation”
R-L shunt
L-R shunt
Does not affect systemic arterial oxygen tension
Oxygen in R heart increased
R-L shunt
Pulmonary venous admixture
A portion of CO does not participate in gas exchange
HPV
Hypoxic pulmonary constriction
Blood diverts to better ventilated areas
HPV causes/ enhancements
Hypoxia
Hypercapnia & acidosis
