At resting lung volumes, what is the 1. ) Intra-alveolar pressure 2. ) Intrapleural pressure

1. ) 0 cm H2O 2. ) some negative value usually around -5 cm H2O

Pulmonary Physiology I Flashcards by Joel Glotfelty

What are the two vital purposes of the lungs?

) Gas exchange

2. ) Role of ventilation in controlling blood pH

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The exchange of O2 for CO2 occurs within structures called

Alveoli

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In order for air to reach the alveoli, which path does it have to travel?

Trachea, bronchi, bronchioles, terminal bronchioles, respiratory bronchioles, alveolar ducts, and finally alevoli

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Resistance to flow is inversely proportional to

Cross-sectional area of the vessel

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Airway resistance decreases as air approaches the

Alveoli

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The ducts which compromise the bronchial tree are ringed with

Smooth muscle (under autonomic control)

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We are negative pressure breathers. What this means is that under physiologic conditions, a negative pressure differential between the atmosphere and the alveoli allows for

Movement of air into the lungs

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There are opposing elastic recoil forces inherent to the

Chest wall and alveoli

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The chest wall wants to recoil

Outward (expand)

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The alveoli want to recoil

Inward (Collapse)

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Alveoli and the chest wall are separated by membranes which create an

Intrapleural space

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At resting lung volumes, what is the

) Intra-alveolar pressure
) Intrapleural pressure

) 0 cm H2O

2. ) some negative value usually around -5 cm H2O

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The difference between the intra-alveolar pressure and the intrapleural pressure creates the

Transpulmonary (transmural) pressure of 0 - (-5) = 5cm H2O

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The transpulmonary pressure is sufficient to provide a slight outward tug on the alveoli and keep them from

Collapsing

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Occurs as a result of chest wall expansion which causes the intrapleural pressure to become more negative, thereby increasing the transpulmonary pressure

Inspiration

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This pulls on the alveoli essentially from all directions, increasing alveolar diameter and dropping

Intra-alveolar pressure below zero

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Boyles law tells us that pressure is inversely proportional to

Volume

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By convention, we assume that unless told otherwise that the atmospheric pressure equals

Zero

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Thus a pressure gradient exists favoring the movement of air into the

Alveoli

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Inspiration is an active process that requires contraction of the

Diaphragm

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A normal non-stressed expiration is passive, owing to the relaxation of the

Diaphragm

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Chest wall collapse causes the intrapleural pressure to become

Less negative (or even very positive with a forced expiration)

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This alleviates the outward pull on the

Alveoli

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Alveolar diameter then decreases, thus elevating

Intra-alveolar pressure

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Once alveolar pressure supercedes that of atmospheric pressure, air moves

Outward (i.e. down the pressure gradient)

Keeps the lungs somewhat expanded during ventilation

Transpulmonary pressure

What happens if air is allowed to enter the intrapleural space?

Intrapleural pressure reaches or exceeds that of atmospheric pressure. Lung can collapse

Often caused by a chest wall trauma which creates open communication between the atmosphere and the intrapleural space

Simple pneumothorax

During a simple pneumothorax, as the chest wall expands during inhalation, the intrapleural pressure does not decrease in the affected

Hemithorax

Thus, the normal driving force for alveolar expansion (transpulmonary pressure) is not

Generated

Thus, as a result of the loss of the normal tug of war that exists between lung elastic recoil and chest wall expansion, we will eventually see

Lung collapse in the affected hemithorax

Results from some internal insult to the visceral or parietal pleura, or some region of the tracheobronchial tree

Tension pneumothorax

The nature of this damage is such that a one-way valve is created which enables

Air to enter but not exit the pleural space

Over time, intrapleural pressures rise which causes resistance to

Lung inflation

This will likely cause

collapse of lung ipsilateral to the region of injury

The pressure increase in the injured hemithorax can then cause deviation of the trachea toward the

Contralateral hemithorax

In addition to this deviation, we can also see compression of the

Heart, vena cava, and contralateral lung

If severe enough, venous return and cardiac output can be compromised so as to result in

Hypotension and hemodynamic instability

Defined as the change in lung volume (L) divided by the change in transpulmonary pressure (cm H2O)

Lung Compliance

An indicator of how efficiently the lung inflates and deflates (i.e. the work of breathing)

Lung compliance

When plotted using an X-Y graph, where the X-axis is transpulmonary pressure and the Y-axis represents lung volume, a very compliant lung is shown by a

Steep compliance curve (relative to normal)

In other words, in a very compliant lung, a large change in volume occurs with a

Small change in pressure

A steep compliance curve is clearly seen when dealing with

Emphysema -a manifestation of COPD

Why is too compliant of a lung a bad thing?

Harder to expel air

Shows that a much greater change in pressure is required to move a given volume

Flat compliance curve

A flat compliance curve is clearly observed in

Lung fibrosis (a form of restrictive lung disease)

Abnormally high or abnormally low lung compliance both increase the work of

Breathing

The sound that is heard due to vibrations of the ventricular and large vessel walls due to recoil of arterial and ventricular blood against the semilunar valve leaflets

Normal conditions where A2-P2 are fused on expiration but split during inspiration

Physiologic splitting

Occurs due to the decreased intrathoracic pressure that is generated during inspiration

Physiologic splitting

Decreased intrathoracic pressure allows for increased venous return to the right atrium, which in fact prolongs

Diastolic filling of RV

This causes a lengthened systolic ejection from the RV and thus we see a delay in closure of th

Pulmonic valve

Also low intrathoracic pressure increases capitance of the

Pulmonary arteries and veins

Increased capitance of the pulmonary arteries and veins allows more blood to flow into the pulmonary system this also results in delayed closure of the

Pulmonic valve

As mentioned, the decrease in intrathoracic pressure lowers pulmonary vein pressure and reduces left heart diastolic filling. With less diastolic volume, we see faster closing of the

Aortic semilunar valve

Reduced left ventricular output during inspiration slightly lowers

Systolic BP

During expiration, we see an increase in

Intrathoracic pressure

The increase in intrathoracic pressure from expiration causes venous return to the right heart to be

Reduced

When venous return to the right atrium is reduced, we get quicker RV output and thus an earlier

The so-called respiratory centers are housed within the

Medulla

These respiratory centers consist of several regions that include the

Dorsal respiratory group (DRG) and Ventral respiratory group (VRG)

Largely responsible for coordinating inspiratory function

DRG

Assumes control over both inspiration and expiration

VRG

The rythm of respiration is due to the highly coordinated activation/inactivation of respiratory neurons within the

Pre-Bötzinger complex of the VRG

Axons from the DRG and VRG descend the spinal cord and activate neural tracts which ultimately innervate the

Muscles of respiraiton

Which motor neurons mediate inspiration?

Phrenic and external intercoastal

Contraction flattens and lowers the diaphragm, thus increasing the volume of the

Thoracic cavity

This is complemented by contraction of so-called accessory muscles which include the

External intercostals and sternocleidomastoid

Raise and enlarge the rib cage

External intercostals

Elevates the sternum

Sternocliedomastoid

Expiration is normally

Passive

However, contraction of the internal intercostals, rectus abdominis, internal and external obliques, and transversus abdominis muscles support

Forceful expiration

Bronchial smooth muscle is innervated by the

Vagus Nerve (X)

Vagal innervation of bronchial smooth muscle enables PARASYMPATHETIC nervous system dependent

Constriction of bronchial smooth muscle

Binds to the type 3 cholinergic-muscarinic receptors expressed in bronchial smooth muscle

Acetylcholine

In addition to type 3 cholinergic-muscarinic receptors, bronchial smooth muscle also expresses

Type B2 adrenergic receptors

Within bronchial smooth muscle, the activation of B2 adrenoreceptors induces

Dilation (opens airway)

Albuterol and salmeterol are B2 agonists that are used in the treatment of

Asthma and COPD

Since bronchial smooth muscle is not innervated by the SNS, SNS-dependent bronchiolar dilation relies upon

Circulating epinephrine

Responsible for obtaining atmospheric O2 and eliminating CO2

Lungs

This process is known as

Ventilation or respiration

Gas exchange within the lungs occurs at the level of the

Alveolus

A sac-like structure located within the respiratory zones of the lungs -the terminal point reached by inspired air

Alveolus

The alveoli are surrounded by

Capillaries

Capillary blood flow ot alveoli is known as

Perfusion (Q)

Air flwo to and from alveoli is known as

Ventilation (V)

The amount of air traversing the nose and/or mouth with each breath

Minute ventilation

Does the entire volume of air that is inspired with each breath reach the alveoli?

Thus, alveolar ventilation is less than the

Minute volume

For this reason, the conducting pathways (where gas exchange does not occur) are referred to as the

Anatomic dead space

The other type of dead space is known as the

Alveolar dead space

Any significant amount of alveolar dead space is pathologic. It develops when there are regions of

Ventilated but not perfused alveoli

A person with impaired cardiac output may be likely to develop significant

Alveolar dead space

Simply the sum of anatomic plus alveolar dead spaces

Physiologic dead space

A healthy adult has approximately how much dead space per pound of body weight?

1mL per pound

Transfer of gas across blood-gas barrier and blood-tissue barrier occur via diffusion as regulated by

Fick's Law

Fick's law shows that the amount of gas transferred is proportional to what three things?

1. ) Area of tissue layer 2. ) Diffusion constant 3. ) Difference in partial pressure (P1-P2)

Fick's law shows that the amount of gas transferred is inversely proportional to the

Tickness

Proportional to the gas solubility but inversely proportional to the square root of it's molecular weight

Diffusion constant

About 20 times more soluble in liquids than H2O

CO2