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Pulmonary blood flow
Terms in this set (32)
What are the two sources of bronchial circulation?
2% output from left ventricle and 100% output from right ventricle
When are the connections or anastomoses between bronchial and pulmonary circulation most likely open?
if the circulation to one or the other is interfered with, so once again the bronchial circulation of the output of the left ventricle
heats and humidifies inspired air
Pressure is higher in systemic circulation than in pulmonary circulation because:
vessels are shorter in the pulmonary circulation, but mostly because pulmonary arteries are less muscular than systemic arterioles
systemic capillary blood flow is:
non-pulsatile; muscular systemic arterioles damp out the pulsatility before it gets to the capillaries
pulmonary capillary blood flow is:
What determines flow in systemic circulation?
In pulmonary circulation, what determines resistance?
Oxygen diffuses through the alveolus🡪 surfactant 🡪 capillary & alveolar epithelium🡪 interstitium 🡪 capillary endothelium🡪 through the plasma 🡪 through the PM of the RBC🡪 finds hemoglobin & mates with it in ~ a 50th of a second.
2 different groups of pulmonary blood vessels that contribute to PVR:
1. pulmonary capillaries (alveolar vessels)
2. extra-alveolar vessels
How does a change in lung volume affect the resistance to blood flow through the alveolar vessel and through the extra alveolar vessels?
Extra-alveolar resistance decreases, as alveoli expand (length increases & diameter decreases), resistance through alveolar vessels increases
lowest near FRC, and increases at both high and low lung volumes
Extra-alveolar vessels are stretched, their resistance decreases; alveolar vessels are lengthened, their resistance increases
If you go below FRC in a forced expiration:
The pressure outside the extra-alveolar vessels gets positive and squeezes them; EAV Resistance increases
Increased blood flow:
Passive influences on PVR:
decreased lung volume, increased lung volume, increased PAP, LAP, or CO, and gravity, increased interstitial pressure, PPV
Active influences that increase PVR:
SNS, NE, EPI, α-adrenergic agonists, some prostaglandins, Angiotensin, endothelin, histamine,
3 most important active influences that increase PVR and cause pulmonary vasoconstricion:
1. alveolar hypoxia, 2. alveolar hypercapnia, and 3. low pH of mixed venous blood; (these 3 together help maintain ventilation perfusion balance)
Active influences that decrease PVR:
PNS, ACh, β-adrenergic agonists, PGE1, PGI2, NO, bradikinin
Where arterial pressure = alveolar pressure:
there's no blood flow above that.
In zone 3:
the pressure gradient for blood flow is arterial - venous in lower most part of lung.
Pressures in zone 3:
Pa> PV > PA
In zone 2:
pressure gradient is arterial - alveolar
Pressures in zone 2:
Pa > PA> PV
In zone 1:
PA>Pa, so there's no blood flow
Pressures in zone 1:
PA> Pa> Pv
Hypoxemic Pulmonary Vasoconstriction
pulmonary arteries constrict in the presence of hypoxia → ↑PAP
What happens if airway obstruction & alveolus isn't being ventilated very well?
Hypoventilation; A O2 ↓, CO2 ↑, this sends mixed pulmonary venous blood to the left side of the circulation with ↓O2 and ↑CO2.→ shunt like state (Venous blood → arterial side)
How does hypoxic pulmonary vasoconstriction affect blood that goes to poorly ventilated alveoli:
It decreases the amount of shunted blood that goes to poorly ventilated alveoli
In the lungs, interstitial pressure:
is a little negative at the FRC
How would increasing venous return affect PVR?
It would decrease because recruitment and distention lower PVR
Factors predisposing to pulmonary edema:
↑ cap. permeability, ↑ Pc (cap. hydrostatic px), ↓interstitial hydro. px, ↓ colloid osmotic px, insufficient lymphatic drainage of lungs
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