Lecture 11 Flashcards by Taylor Dewall

Deoxygenated venous blood is the same as…
What is the PO2? The PCO2?

pulmonary arterial blood
PO2: 40mmHg
PCO2: 45mmHg

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What causes the difference between a PaO2 of 100mmHg in systemic circulation and a PAO2 of 104mmHg in the alveolar gas?

The pulmonary venous blood gets diluted with a bronchiolar mixture and empties into the left atrium which then equals a systemic PaO2 of 100mmHg.

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What is the anatomical dead space in a 500cc inspired breath?

The last portion of an inspired breath (150cc) won’t make it deep enough into the lungs for gas exchange, but is necessary to push gas into the lungs. 350cc makes it into the lungs for gas exchange.

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What is the second type of dead space?

This occurs in unhealthy or older lungs… alveolar dead space (portions of the lung that are ventilated but not perfused)

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What is physiological dead space?

Both anatomical dead space and alveolar dead space

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How do you calculate minute alveolar ventilation?

volume of ventilation in one breath x the number of breaths per minute = 350mL x 12 bpm = 4.2 L/min

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How do you calculate minute dead space ventilation?

volume of dead space ventilation x number of breaths per minute = 150mL x 12 bmp = 1.8 L/min

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How do you calculate total minute ventilation?
What else can you use to calculate total minute ventilation?

minute alveolar ventilation + minute dead space ventilation = total minute ventilation (VE) = 6L/min

Tidal volume (VT) x number of breaths per minute = 500mL x 12bpm = 6L/min

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What is the starling force for pulmonary capillary hydrostatic pressure?

7 mmHg

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What is the starling force for pulmonary blood oncotic pressure?

28 mmHg

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What is the starling force for the interstitial hydrostatic pressure?

-8 mmHg (lymphatics + more negative d/t negative pleural pressure)

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What is the starling force for the interstitial oncotic pressure?

14 mmHg

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What forces favor holding fluid in the pulmonary capillaries?

the pulmonary blood oncotic pressure (28mmHg)

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What forces favor filtration?

interstitial oncotic and hydrostatic pressures and the pulmonary capillary hydrostatic pressure (8+7+14 = 29mmHg)

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What is the net filtration pressure in the lungs? Does this favor filtration or absorption?

1mmHg. It favors filtration. The lymphatics are pretty active in the lungs so this is okay.

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How high can left atrial pressure go until pulmonary edema occurs?

Up to 23 mmHg (normal is 2mmHg)

Give an example of things that can cause pulmonary edema…

-increased capillary permeability (infections, too much oxygen and other toxins)
-increased capillary hydrostatic pressure (increased left atrial pressure d/t CHF, MI or mitral stenosis)
-decreased interstitial hydrostatic pressure
-decreased colloid osmotic pressure (too much IV fluid, marasmus, proteinuria)
-insufficient pulmonary lymphatic drainage (tumors, ILD/ fibrosis)
-HAPE
-Head injury (neurogenic)

What are two examples of what can cause a decreased interstitial hydrostatic pressure?

chest tube striping. Young healthy patients emerging too quickly. These patients can generate a tremendous force if they wake up and breathe against a closed circuit (obstruction) causing flash pulmonary edema.

What are a few examples of things that could disrupt lymphatic drainage in the lungs?

tumors blocking lymphatic drainage, high pressure vent settings, interstitial lung disease (scar tissue buildup on lymphatics)

On average the pleural pressure between breaths is -5cmH2O, however the lung is set up with a gradient… what is the pleural pressure above the hilum and below the hilum?

Pleural pressure towards the base… -1.5 cmH2O
Pleural pressure towards the apex… -8.5 cmH2O

What is significant about the pressure gradient in the pleural space?

It stretches the alveoli higher in the lung… more full with air and less compliant. At the bottom of the lung there is less pleural pressure pulling them open so the alveoli are more compliant here and readily fill up with fresh air when we take in a breath. This works out great since there is more blood flow in the lower part of the lung too!

What is hysteresis? Is the lung more compliant on an inspiration or expiration?

Hysteresis of the lungs means the lungs behave a little differently between deep inspiration and deep expiration. Expiring lungs are more compliant.

At FRC what is the transpulmonary pressure (distending pressure), the alveolar pressure and the intrapleural pressure at the top of the lung?

TP: 8.5 cmH2O
A: 0 cmH2O
IP: -8.5 cmH2O

At FRC what is the transpulmonary pressure (distending pressure), the alveolar pressure and the intrapleural pressure at the bottom of the lung?

TP: 1.5 cmH2O
A: 0 cmH2O
IP: -1.5 cmH2O

If the transpulmonary pressure at the top of the lung is 8.5 cmH2O and the TP pressure at the bottom of the lung is 1.5 cmH2O, where will air go first? (The conditions at FRC)

Air will flow into the bottom of the lung first, where pressure is lowest

At RV what is the transpulmonary pressure (distending pressure), the alveolar pressure and the intrapleural pressure at the top of the lung?

TP: 2.2 cmH2O A: 0 cmH2O IP: -2.2 cmH2O

At RV what is the transpulmonary pressure (distending pressure), the alveolar pressure and the intrapleural pressure at the top of the lung?

TP: -4.8 cmH2O A: 0 cmH2O IP: 4.8 cmH2O (positive number since you exerted force to expire ERV to get to RV)

If the transpulmonary pressure at the top of the lung is 2.2 cmH2O and the TP pressure at the bottom of the lung is -4.8 cmH2O, where will air go first? (The conditions at RV)

Air will go to the top of the lung first. At RV, top of the lung needs to expand first in order to open up bottom of the lung to accept volume. This is because the small airways in the bottom of the lung have collapsed d/t very negative transpulmonary pressures.

Where are the two set of smooth muscle in the lungs?

1. pulmonary blood vessel smooth muscle 2. airway smooth muscle

What happens during hypoxic pulmonary vasoconstriction (HPV)?

The pulmonary blood vessels respond by constricting if they sense an area of the lung with under ventilated alveoli. This helps divert blood to areas of the lung receiving more oxygen. (This is opposite from all other vascular beds in the body!)

What is another cause for vasoconstriction in an area of the lung that is under ventilated?

Hypoxic conditions will lead to a build up of CO2 which also causes vasoconstriction, but most of the pulmonary vasoconstriction is a function of low O2 (hypoxia) not the build up of CO2.

How do our general anesthetics affect HPV?

GA's open K+ channels in vascular smooth muscle causing it to relax, interfering with the body's ability to combat VQ mismatches by vasoconstriction. This is why we use so much supplemental oxygen.

Say you have a PE what happens to the PaO2? PCO2?

PaO2 will be closer to 150 mmHg and CO2 will be 0 mmHg (no perfusion is happening, so no blood for the air to mix with)

How does airway smooth muscle respond to VQ mismatching?

The airway smooth muscle will constrict and send the fresh air somewhere else (avoiding dead space ventilation).

What is a major problem that can occur with too much oxygenation for too long?

Too much oxygen for too long can cause airway reactivity and constriction making it harder to ventilate. Also, hyperoxia can be toxic to the the pulmonary blood vessels causing them to become leaky (more permeable).

What changes with our volumes/capacity when switching from an upright position to supine?

The FRC decreases as a product of the ERV shrinking. Vital capacity stays the same d/t an increase in IRV.

Lecture 11 Flashcards

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