Respiratory

Question 1

As systemic pressure or pulmonary blood flow increases, pulmonary vascular resistance ___. Why?

Answer 1

Decreases because recruitment of previously un-perfused vessels and distention of other vessels are employed

Question 2

Pulmonary arterial wedge pressure (PAWP) is a measure of:

Answer 2

Pulmonary venous pressure

Question 3

What 3 pressure systems drive pulmonary capillary perfusion?

Answer 3

• Pulmonary arterial pressure
• Pulmonary venous pressure
• Alveolar pressure

Question 4

The 3 different pressure systems that drive pulmonary capillary perfusion (pulmonary arterial pressure, pulmonary venous pressure, and alveolar pressure) define 3 gravitational dependent zones in the lungs.

• Which zone is used more during exercise?
• And which is used more during left sided heart failure?
• Which zone is throughout to not be present in quadrupeds?

Answer 4

• Zone 2 (middle) is used more during exercise because pulmonary arterial pressure will exceed alveolar and venous pressure
• Zone 3 (lowest) is used more during L-CHF because pulmonary arterial and pulmonary venous pressure will exceed pulmonary alveolar pressure
• Zone 1 where pulmonary alveolar pressure exceed arterial and venous pressure.

Question 5

As the lungs inflates, traction on the perivascular connective tissue of the extra alveolar vessels dilated, which causes these pulmonary vessels to ___, which decreased vascular resistance. However, at even further inflation, resistance is increased because ___.

Answer 5

• Dilate
• Flattening of alveolar capillaries occurs increasing vascular resistance

Question 6

During atelectasis, local blood blood flow is greatly ___ by what 2 things?

Answer 6

• Reduced
• By a combination of vessel closure as the lungs collapse but also vasoconstriction in response to local hypoxia

Question 7

Why does vasoconstriction occur under hypoxic conditions?

Answer 7

Because the lungs try to redistribute blood flow to perfused areas

Question 8

Do bronchiole arteries constrict?

Answer 8

No, under conditions of hypoxia the bronchiole arteries dilate.

Question 9

What are 2 different circulations supplying blood to the lung?

Answer 9

• Pulmonary
• Bronchial

Question 10

Where do the 2 different main bronchial arterial branches originate? And what do they supply?

Answer 10

• The bronchoesophageal artery, which branches off the ___ = supplies the airways and interlobular septa
• The right apical bronchial artery which branches off the bicarotid trunk = supplies the right apical lobe

Question 11

Do bronchial arteries and pulmonary vessels anastomoses? Why? Why is this nice?

Answer 11

Yes, it anastasmoses at the level of the capillaries and veins. Only very few anastasmoses occur between the bronchial arteries and pulmonary arteries. This is beneficial because if one system is obstructed then the other one can supply the lungs with blood.

Question 12

Where else the bronchial circulation drain?

Answer 12

Other than the pulmonary system, the bronchial system also drains the azygous vein.

Question 13

What is the tracheal disease often seen cranial to the carina and characterized by small intramural nodules protruding into the lumen?

Answer 13

Filaroides osleri

Question 14

The underlying etiology of ARDS complex is due to:

Answer 14

Vasculitis leading to increased permeability.

Multiple causes:

• infectious
• inflammatory
• toxic
• neoplastic
• electrocution
• drowning
• smoke
• DIC
• etc

Question 15

What are 2 possible causes for a patient with pituitary dependent hyperadrenocorticism to be hypoxic?

Answer 15

• Pulmonary mineralization
• PTE

Question 16

What imaging modality showed abnormalities 95% of the time with PTE?

Answer 16

Echocardiography

Question 17

The functional residual capacity of the lungs represents a balance between what 2 things?

Answer 17

• Outward elastic recoil of the chest wall
• Inward elastic recoil of the lungs

Question 18

What are 2 component of the inward elastic recoil of the lungs?

Answer 18

• Elastin and collagen fiber (~1/3)
• Surface tension (~2/3)

Question 19

What cell type in the lungs produce surfactant?

Answer 19

Type II cells, 10 % of alveolar surface

Question 20

How is air moved from the terminal bronchioles to the alveoli during resting inspiration?

Answer 20

Diffusion

Question 21

What is the pressure difference between alveolar and pleural spaces during inspiration and expiration? What is it called?

Answer 21

Transpulmonary pressure:

• Pleural -4 to -6 cm H2O
• Lung -1 to +1 cm H2O
  
  • • 1 cm H20 at inspiration so gas diffuse into the lungs
  • • 1 cm H2O at expiration so gas diffuse out of the lungs

Question 22

What does the trans pulmonary pressure represent?

Answer 22

Elastic recoil of the lungs

Question 23

What are the normal pressures of oxygen and carbon dioxide in arterial and venous blood?

Answer 23

• O₂ 104 mmHg and 40 mmHg
• CO₂ 40 mmHg and 45 mmHg

Question 24

How does hemoglobin help oxygen and carbon dioxide exchange?

Answer 24

Oxygen binds reversibly with hemoglobin, better when high pressures (lungs) and less when low pressures (tissue). It also binds with carbon dioxide as carbaminohemoglobin more when low oxygen binding (tissue) and less when high oxygen binding (lungs). When bound to oxygen it is more acidic reducing carbaminohemoglobin and producing hydrogen ions which cause bicarbonate to become CO2 and diffuse out of blood.

Question 25

Define minute ventilation

Answer 25

Minute ventilation= tidal volume x respiratory frequency…either can increase if oxygen demands increase

Changes in Ventilation:

• Conducting airways = nares, nasal cavity, pharynx, larynx, trachea, bronchi, bronchioles
• No gas exchange so called anatomic dead space
• Physiologic Dead Space = Anatomic Dead Space + Alveolar Dead Space
• Alveolar dead space = air in poorly perfused alveoli
• Tidal Volume = Gas in alveoli + dead space gas
• Minute ventilation = alveolar ventilation + dead space ventilation but the volume of anatomic dead space is constant so can still change ventilation with tidal volume or frequency
• If heated, animals increase frequency of respiration to lose heat
• If cold stressed, metabolic demands are higer and they increase tidal volume but not frequency to get more oxygen without losing heat

Question 26

What is funtional residual capacity?

Answer 26

Functional Residual Capacity = the air remaining in the lung after exhalation (pressue is 5 cm H2O below atm)

Question 27

What determines pulmonary vascular resistence?

Answer 27

Pulmonary vascular resistance = (mean pulmonary arterial pressure – left atrial pressure) / cardiac output

** generally low**

Question 28

What affects diffusion of gasses?

Answer 28

Diffusion of gasses – movement down a concentration gradient

Diffusion of gasses = D x A x (PAO2 – PcapO2) / x

Rate of gas exchange between alveolus and blood depends on:

• Physical properties of the gas (D)
• Surface area available for diffusion (A)
  
  • Depends on perfusion of capillaries, increases with exercise
• Thickness of the barrier (x)
  
  • Includes surfactant, epithelial layer, basement membrane, interstitum, endolthelium- all < 1 micron
  • Diseased lung makes this thicker
• Pressure gradient (PAO2= alveolar, PcapO2= capillary)
  
  • Usually PAO2= 100mmHg, PcapO2=40 mmHg so rapid diffusion occurs
  • Hb takes up the O2 that crosses the barrier and keeps PcapO2 low
  • If thick lung, other problems can increase PAO2 to overcome it
• For CO2, there is little pressure gradient (46 mmHg in capillaries, 40 mmHG in alveolus) but diffusion is still rapid because it is 20x more soluble than O2

Question 29

Describe ventilation/perfusion and how certain diseases affect it?

Answer 29

V/Q: ventilation and perfusion theoretically should always be matched – never really happens but gets a lot worse with disease

• With over-perfusion and under-ventilation you end up with blood returning to the heart that is low in oxygen and high in carbon dioxide…common in disease as there is poor ventilation (airway obstruction, inflammation)
• With under-perfusion (pulmonary hypertension, PTE) you have blood that is high in oxygen and low in carbon dioxide (but there is less of it??)
• V/Q mismatch has a large effect on oxygen exchange, less on carbon dioxide exchange (hypercapnia is rare) - over ventilation of oxygen does not make up for underventilation because of the oxyhemoglobin disassociation curve.

Question 30

What causes the oxygen dissociation curve to shift to the right?

Answer 30

Dissociation curve shift to the right = less affinity to oxygen

“CADET, face RIGHT!”

• C - CO2
• A - Acidity
• D - DPG
• E - Exercise
• T - Temperature Rise in all these shifts the curve to right.

Question 31

What are the normal blood gas values?

Answer 31

NORMAL BLOOD GAS VALUES

• pH: 7.36-7.44
• PaO2: 90-100 mmHg
• PaCO2: 36-40 mmHg
• HCO3: 20-24 mEq/L
• BE: 4 mEq/L

Question 32

What is the 120 rule?

Answer 32

This assessment of hypoxemia only works for an animal at sea level breathing room air. If a normal PaO2 is 80 – 100 mmHg and a normal PCO2 is 35 – 45 mmHg, the sum of PaO2 and PCO2 should be approximately 130 – 140 mmHg. If the PCO2 and PaO2 do not equal AT LEAST 120, the animal has primary lung disease (i.e., the hypoxemia could not be attributed solely to hypoventilation if present).

Question 33

What are some causes of acid base disturbances?

Answer 33

Respiratory acidosis:

• Caused by alveolar hypoventilation
• Incomplete removal of CO2 by the lungs causes blood PCO2 to increase
• ↑PaCO2, ↓pH, minor ↑ HCO3-, no change in base excess
• Base excess: an increase (excess/positive) or decrease (deficit/negative) of the total available blood buffers
  
  • Increased PaCO2 and decreased pH causes increased H+ and NH3 production in the kidneys, increasing H+ excretion in the urine and generation of new HCO3- (compensatory metabolic alkalosis); develops base excess

Respiratory alkalosis:

• Caused by alveolar hyperventilation, usu due to stim of chemoreceptors in response to hypoxia
• ↓PaCO2, ↑pH, minor ↓ HCO3- (replaced by other buffers), no change in base excess
• Over time, decreased PaCO2 and increased pH causes decreased H+ and NH3 production in the kidneys; filtered HCO3- is not reabsorbed and is lost in the urine (compensatory metabolic acidosis); develops a base deficit

Metabolic acidosis:

• Most common acid-base abnormality; accumulation of “fixed” acids or loss of buffer base
• Caused by protein catabolism, ketone production, anaerobic metabolism, diarrhea (loss of excessive bicarbonate in the feces); rumen acidosis in ruminants (too much CHO’s)
• ↓pH, ↓ HCO3-, negative base excess (i.e. base deficit)
• Stimulates increased ventilation causing ↓PaCO2 and helping restore pH close to normal (compensatory respiratory alkalosis)

Metabolic alkalosis:

• Most common cause is vomiting (loss of H+); also caused by hypokalemia (H+ in the blood is exchanged for K+ in the cells to try to restore normal plasma [K+]; H+ are subsequently lost in the urine instead of K+)
• ↑pH, ↑ HCO3-, positive base excess
• Reduces drive to ventilate causing ↑PaCO2 helping to restore blood pH (compensatory respiratory acidosis)

Question 34

Choanal restriction or Artresia

Answer 34

The choana forms the junction between the nasal and nasopharyngeal airways. Choanal restriction is uncommon. Congenital total obstruction of the choanae may occur unilaterally or bilaterally, due to a bone or membranous septum, resulting in an abnormal respiratory noise, severe dyspnea or death in a neonatal foal. A bone septum may be visible in a VD radiographic image. If an obstructive membranous septum is suspected from endoscopic examination, it can be confirmed radiographically by observing blockage of radiodense contrast medium placed in the nasal cavities.

Narrowing of the caudal aspect of one or both nasal airways can occur, with or without deviation of the nasal septum, resulting in respiratory noise. Carefully positioned VS radiographic images are required to document narrowing, with comparison may between the two sides of the head and with horses of similar breed, age and size.