Resp 2

Question 1

what is ventilation and what is it influenced by

Answer 1

-Ventilation is the movement of air into and out of the lungs (pulmonary ventilation) and alveoli (alveolar
ventilation).

-It is influenced by a number of physical and mechanical factors and processes that alter the physics of air flow and the forces that create that flow

Question 2

inspiration; what happens as thoracic cavity expands, what muscles contract, model of external intercostal muscle function

Answer 2

-The pleural space contains very little fluid. As the thoracic cavity expands,
the surfaces of the lungs are drawn outward with the thoracic wall,
increasing lung volume and drawing air inward as lung pressure decreases

-Inspiration begins with the contraction of the respiratory muscles:
* The diaphragm (innervated by the phrenic nerve)
* The external intercostal muscles (innervated by intercostal nerves)

-Upon contraction, thoracic wall is moved away from midline; thoracic volume increases

Question 3

expiration; what happens at end of inspiration, pressure, muscles of expiration,quiet vs active breathing

Answer 3

-At the end of inspiration, inspiratory muscles relax and the elastic recoil of the lungs and thoracic wall causes a decrease in volume
->this increases pressure within the lungs, causing air to flow outward

Quiet breathing
* Little to no muscle contraction involved in expiration
* A result of the elastic recoil of the lungs and the rib cage

Active breathing – elastic recoil plus:
* Internal intercostal muscles and the abdominal muscles (rectus abdominis; external & internal oblique; transversus abdominis) pull the thoracic cage inward and force air out of the lungs

Question 4

expiration; elastic recoil of the chest and thorax

Answer 4

-The thorax and lungs assume a resting shape which is determined by the elastic recoil of the lungs & thoracic wall

-Elastic recoil of the lungs is due to:
* Elastic tissue: 1/3 of elastic recoil forces of the lung
* Surface tension in alveoli is less than it would be without surfactant, but is still high, and would cause the alveoli to collapse if unopposed by the loose adherence of the lung
surface to the pleural lining of the chest

-Elastic recoil forces of the thorax come from musculoskeletal components

Question 5

ventilation compliance; refers to what, what is means, what conditions decrease compliance

Answer 5

-Refers to the distensibility of the lungs
–>measure of the ease with which lungs and thorax expand

-The greater the compliance, the easier it is for a change in pressure to cause expansion

-A lower-than-normal compliance means the lungs and thorax are harder to expand

Conditions that decrease compliance
include:
* Pulmonary fibrosis
* Pulmonary edema
* Respiratory distress syndrome (premature infants produce less surfactant)

Question 6

ventilation and gait

Answer 6

-Respiration rate may be synchronized with gait in some species
-In this figure, movement of the fore
& hind limbs away from the thorax helps to expand the thoracic cavity, facilitating inspiration

Question 7

effect of exercise at respiration;horse example at rest, walking, galloping

Answer 7

Horse at rest:
-VT ~5.5 L, minute ventilation ~80 L (~14 bpm)

Walking:
-VT ~5.8 L, minute ventilation ~320 L (~65 bpm) -> ~4 x resting rate

Galloping:
-VT ~13 L, minute ventilation ~1,600 L (~120 bpm) -> ~20 x resting rate

Question 8

pleura and pleural fluid; couples what, generation, absorption, total volume, accumulation

Answer 8

Pleural fluid couples movement of thoracic walls and lungs
* Generated by visceral & parietal pleura
* Absorbed by parietal pleura
* Total volume is tiny; pleural space is normally a virtual space
* Fluid accumulation (pleural effusion) -> dyspnea/partial lung collapse

Question 9

pleural pressure; what happens to it during inspiration and expiration

Answer 9

Ppl is subatmospheric (i.e. lower than
environmental air)
* Becomes more [-] during inspiration
* Becomes less [-] during expiration (even slightly [+] at end of expiration in dogs and horses)

Question 10

pleural pressure changes during quiet breathing (A,B,C,D)

Answer 10

A, Before the start of inhalation, slight negative pressure in pleural cavity to maintain slight lung inflation.

B, During inhalation, pressure in
pleural space becomes more
negative (-16 cm H2 O) as chest
expands away from lung. Negative
pressure initiates increased lung
inflation and airflow follows.

C, At the end of a tidal inhalation,
lung reaches maximal inflation for
that breath, and pleural pressure
becomes less negative.

D, During exhalation, chest wall
recoil begins to compress the
pleural space and the pressure
becomes close to zero, forcing the
lung to compress and expelling air
from alveoli and airways.

Question 11

what is pleural pressure affected by

Answer 11

Exercise
* As lung volume and/or air flow rate increase, Ppl becomes more [-] on inspiration

Lung compliance
* If lung compliance decreases (e.g. fibrosis), Ppl becomes more [-] on inspiration

Airway resistance
* If airway resistance increases (narrowed airways), Ppl becomes more [-] on inspiration (especially with upper airway obstruction), and more [+] on expiration (especially with lower airway obstruction)

Question 12

what is respiratory dead space, anatomic dead space, alveolar dead space, physiologic dead space

Answer 12

“Dead space” comprises all ventilated parts of the respiratory system where gas exchange does not occur

Anatomic Dead Space
-Air flows into the alveoli through the nares, nasal cavity, pharynx, larynx, trachea, bronchi, and bronchioles; these structures constitute the conducting airways
* Since gas exchange does not occur in these pathways, they are known as the “anatomic dead space”

Alveolar Dead Space
* Caused by ventilation of alveoli that are poorly perfused with blood, so that gas exchange cannot occur optimally

Anatomic Dead Space + Alveolar Dead Space = Physiologic dead space

Question 13

dead space ventilation, alveolar ventilation, what makes up minute ventilation here, implication

Answer 13

-A portion of each VT (tidal volume) and therefore VE (minute ventilation) ventilates the anatomic dead space

-The portion of each breath that participates in gas exchange is called alveolar ventilation (VA)

-The portion of each breath ventilates dead space is called dead-space ventilation (VD)

-Minute ventilation = Alveolar ventilation + Dead space ventilation

-This has significant implications for conditions where dead space increases because alveolar ventilation will often decrease as a result

Question 14

what happens to achieve adequate ventilation when you have increased dead space

Answer 14

If dead space is increased, tidal volume and/or respiratory rate and/or oxygen concentration in the
inspired gas must increase to achieve
adequate ventilation

MINIMIZE DEAD SPACE

Question 15

airway resistance; features of turbulent vs laminar flow

Answer 15

Features of Turbulent Flow
* Noisy, rapid air movement
* Occurs in larger airways

Features of Laminar Flow
* Silent, slow
* Streamlined, parabolic flow profile
* Occurs in smaller airways

-Normal healthy lungs are quiet when auscultated

-If turbulent flow develops in smaller airways, total gas movement is decreased and lung sounds increase

Question 16

where is most airway resistance in horses

Answer 16

50-70% in the nasal cavity, pharynx, larynx

Question 17

factors that interfrere with distribution of air

Answer 17

Factors that interfere with the distribution of air into the peripheral airways increase both the peripheral
resistance and the work of breathing. Airway “noise” and respiratory “effort” both increase

reasons:
-tissue growth, mucus plugs, bronchoconstriction, stiffened wall, thickened airway edema

Question 18

airway smooth muscle; promoting contraction vs relaxation

Answer 18

Promoting contraction ->constriction:
* Parasympathetic stimulation of muscarinic receptors by acetylcholine
* Inflammatory Mediators
* Histamine
* Leukotrienes
* Thromboxane a2
* Serotonin
* α-adrenergic agonists
* ↓ pCO2 in airways

Promoting relaxation-> dilation:
* Sympathetic stimulation of β2 receptors
* Circulating β2 agonists
* Nitric oxide
* ↑ Pco2 in airways
* ↓ Po2 in airways

Note that Β2 adrenoceptors are present in higher density than alpha receptors in airway smooth muscle, so NE release from adrenal glands causes airway smooth muscle relaxation

Question 19

what happens with upper airway obstrubtion and what causes it

Answer 19

-dyspnea on inspiration (physical narrowing = stenoic nares)

functional (dynamic) narrowing = dorsal displacement of the soft palate

Question 20

examples of combined physical and functional obstrubtion of upper airway, common causes of upper airway obstruction in large animals

Answer 20

• Laryngeal Hemiplegia (Horse) (e.g. left recurrent laryngeal nerve degeneration)
• Brachycephalic Syndrome (Dog)

Signs: Inspiratory dyspnea, upper airway inspiratory noise

Common causes for upper airway obstruction in large animals:
* Severe nasal edema, laryngeal edema or paralysis
* Retropharyngeal masses, guttural pouch tympany, pharyngeal paralysis and collapse

Question 21

lower airway obstruction; common causes, signs

Answer 21

-Some common causes of expiratory dyspnea:
-Physical Narrowing of intrathoracic airways caused by:
- accumulation of secretions and purulent material
- bronchoconstriction

-Dynamic Collapse of intrathoracic airways, including intrathoracic collapsed trachea

Signs:
* Expiratory dyspnea
* Shallow, rapid breathing (These signs are also seen in cases of pleural effusion or pneumothorax)