Pulmonary Circulation Flashcards
Pulmonary Circulation
Largest vascular bed
Accommodates the entire cardiac output from the right heart
Rarely concerned with directing bloodflow
Bronchial Circulation
1-2% of cardiac output
Empties into pulmonary vein
Generates physiological shunt
With greater pathology –> greater amount is shunted (wasted volume)
Cardiac Output
Output of blood per minute
5L/min
R = to lungs
L = to body
In contrast to systemic circulation, in the lung….
- Rarely concerned with directing blood flow
- Much lower pressure
- Better clot filter
- Contains about 10% of total blood volume
Lower pressure in pulmonary circulation
Maintained by low resistance due to # of capillaries
Less smooth muscle than vessels in systemic circulation –> so changes diameter
Pulm. Circ. better clot filter
Can be bad with pulmonary embolism
Fibrinolytic substances are released from endothelium
Relationship btw. perfusion pressure and resistance unique in the lung
P = flow * resistance
Resistance is inversely related to diameter and pressure
As arterial pressure goes up, resistance goes down
As you increase cardiac output, what happens to flow, resistance and pressure
Increase flow
Increase pressure
Decrease resistance - alveoli are recruiting more capillaries and distend the ones that are already open
How does vascular resistance get so low?
- Recruitment
2. Distension
Recruitment
As you recruit more capillaries, pressure will drop
Fewer open capillaries at lung apex at rest
With increased CO2, the capillaries will open
As inc press, alveoli will recruit more and open up and keep resistance down
Distention
Inc CO2 stretches capillaries so they open more, pulmonary capillaries are thin and compliant
Benefits to vascular resistance being low
capillary recruitment and distension increase surface area for gas exchange
Decreases risk of pulmonary edema
- if had high pressure, there would be an inc in fluid leakage and edema
Resistance is affected by lung volume - inhalation
Alveolar vessels (pul cap) are exposed to expanding alveoli and are compressed Extraalveolar vessels are exposed to decreasing intrapleural pressure and expand Inhale = inc resistance
Resistance is affected by lung volume - exhalation
apposite occurs
Decrease resistance
Lower resistance does what to work of the heart
lowers the work
Resistance is lowest when>
FRC
Resistance affected by chemical mediators
Unique response to oxygen
Hypoxic Pulmonary VC = dec in O2 tension, Inc in pulmonary vascular resistance
Regional Hypoxia
due to bronchial obstruction
Diverts blood away from poorly ventilated areas
Constrict area with bad gas exchange and distribute blood to areas where gas exchange can occur
Generalized Hypoxia
Altitude –> widespread inc in pulmonary vascular resistance and pressure –> might lead to pulmonary hypertension and right heart hypertrophy
NE
Vasoconstriction
Bronchodilation
Hypoxic Pulmonary Vasoconstriction
Controls pulmonary blood flow distribution to better ventilated areas –> main mechanism for explaining sustained pulmonary hypertension
Hypoxic Pulmonary Vasoconstriction triggered by,…
- Airway obstruction
- Acute lung damage (pneumonia)
- Altitude
- Diseases like COPD
Pulmonary Arterioles Dec O2 vs. Inc O2
Dec = Vasoconstriction Inc = Vasodilation
Systemic Arterioles Dec O2 vs Inc O2
Dec = vasodilation Inc = vasoconstriction
Blood flow and air distribution in lung
More flow where?
More flow at base
More ventilation where?
Base
Ventilation Perfusion Mismatch -
Ideal match when ratio is 1, typically is .8 throughout the lung though
At base there is more
Flow than ventilation
More flow and ventilation though compared to apex
At apex there is more
Ventilation than flow
But both still lower at apex compared to base
Arterial pressure inc from…
apex to base
Alveolar pressure inc from
equal at apex and base
Transmural pressure
Talking blood vessels now…
Inc from apex to base, inc capillary distension and dec resistance from apex to base
Burly Alveoli
Get more ventilation than flow (apex)
Weakling Alveoli
More flow than ventilation (base)
Ventilation Perfusion Ratio
Mismatching of ventilation and blood flow is responsible for most defective gas exchange in pulmonary diseases
Global, at rest, ratio is…
0.8
Regional Differences - Apex
Too much ventilation for given blood flow (3)
Lots of O2 in alveolus (favorable for bacteria)
CO2 low in alveolus
Regional Differences - Base
Too much perfusion for the level of ventilation (0.6)
Some blood is not adequately oxygenated
Lower PO2 and higher PCO2 of blood leaving alveolar capillaries from here
When perfusion (blood flow) is greater than airflow - too much CO2
Base
Too much CO2 = Dilation of airway, decreases airway resistance, inc airflow
When perfusion (flow) is greater than airflow - too little O2
Constriction of blood vessels, Inc vascular resistance, dec blood flow
When ventilation is greater then flow - Too little CO2
Bronchoconstriction –> Inc airway resistance, Dec airflow
When ventilation is greater than flow - too much O2
Vasodilation –> dec vascular resis –> inc blood flow
Zone 1
More ventilation than flow
Alveolar presure is higher than arterial or venous press
No blood flow through here - dead space
nonexistent in healthy
Zone 2
alveolar is higher than venous but lower than arterial
Alveolar press is determining how much flow is going through
Zone 3
More blood flow than ventilation
Arterial and venous are higher than alveolar
Amount of flow depends on diff btw art and venous
Anatomical Dead Space
wasted air
150mL
happens normally
Alveolar Dead Space
Ventilation to alveolus but no flow to meet it
wasted air
Venous admixture
Wasted blood
Have blood coming in, but no air to diffuse into, getting less oxygen in
More likely to get dead space
Apex
More likely to get venous admixture
Base
Dead Space
Anatomic + Alveolar
Anatomic = air remaining in conducting zone
Alveolar = alveoli that don’t participate in gas exchange
Embolism
Air coming into alveoli but no flow to meet it so now you have inc. alveolar dead space
Embolism Compensation
Vessels go through hypoxic vasoconstriction to redirect blood to areas of good ventilation so arterial press will inc and work load will inc too
Can lead to heart failure
What happens to CO2 with embolist
CO2 gets mroe diluted, end title CO2 dec.
Causes of alveolar dead space
- Hydrostatic Pressure Failure (gravity effect)
- Normal
- Emobolus
- Emphysema - destruction of walls and elastic tissue, more air going in that wont participate in gas exchange, destroys surface area
- Pre-capillary constriction
Causes of venous admixture
- Anatomical shunts
2. Low regional ventilation perfusion ratio
Anatomical Shunts
blood that doesn’t get to ventilated areas of the lung
Atrial of ventricular septal defect
Direct connection of pulmonary artery to vein
Some bronchial venous blood dumps directly into pulmonary veins (normal)
Low regional ventilation perfusion ratio
Insufficient alveolar ventilation to adequately oxygenate blood in a region of the lung
Occurs at base of lung under normal conditions (weakling alveoli)
Partially restricted airway –> regional hypoventilation
Physiological Shunt
Total amount of wasted blood = venous admixture = anatomic shunt + low perfusion ratio
Normally 1-2% of cardiac output (higher with COPD)
Bronchial Circulation
Suplies blood to conducting airways and supportin tissues
Capable of angiogenesis (new vessel formation)
Routes for bronchial circulation
Bronchial Veins - Carry about 50% of bronchial blood flow directly to atrium
Bronchopulmonary Anastomoses - Connect bronchial blood flow to pulmonary veins, Contributes to Venous Admixture
Pulmonary Embolus
Dead Space
Wasted Air
Normal Apex Ratio
High V/Q
Burly Alveoli
Normal Base Ratio
Low V/Q
Weakling Alveoli
Limiting factor is ventilation
Airway Obstruction
Shunt
Ratio = 0
Wasted Blood/Venous Admixture - flow but no air to meet it
Pulmonary Embolism - what is it
Inc in alveolar dead space
Most commonly caused by thrombi from a leg or pelvic vein
Pulmonary Embolism - Clinical Picture
Severe respiratory distress - chest pain
Right ventricular failure
Hypoxemia
Hypotension
What is hypoxemia in pulmonary embolism caused by
Right to left shunting in areas of partial or complete atelectasis
What is the low BP in pulmonary embolidm caused by
You are inc press upstream of your embolist so this will make your right heart work a lot
downstream from the clot though there is not as much flow so not as much going into the left side so the pressure goes down
Interalveolar Connection
Pores of Kohn
Pores of Kohn
Pores btw. adjacent alveoli
Functions as means of collateral ventilation
If lung is partially deflated, ventilation can occur to some extent through the pores
Hydrostatic Pressure
Promotes fluid loss from capillaries
Fluid moves from capillaries into the interstitial space (edema)
Alveolar Surface Tension
Inward pressure on alveoli favors fluid loss from capillaries
Fluid moves from capillaries into interstitial space
Colloid Osmotic Pressure
Created by plasma proteins - inhibits fluid leakage from capillaries
From space into capillaries
Alveolar Pressure
Compresses interstiium and increases interstital pressure
From space into capillaries
Pulmonary Edema
Small net fluid efflux from pulmonary capillaries to interstitium
- lymphatics picks up the excess fluid
Excess fluid accumulation in interstitium is pulm edema
Causes of pulmonary edema
Increased capillary hydrostatic pressure
Increased capillary permeability
Loss of surfactant –> inc surface tension –> dec interstitial press
Starvation –> Loss of plasma proteins –> dec in osmotic press
