Respiratory - S&H

Question 1

What is the role of the medulla in respiration?

Answer 1

Respiratory center
Site responsible for the generation of the respiratory pattern and coordination of voluntary and involuntary input

Question 2

What is the central pattern generator?

Answer 2

A complex collection of neurons that form a pacemaker system for respiration

Question 3

Where are these pacemaker neurons predominantly concentrated in the medulla?

Answer 3

the Pre-Botzinger complex

Question 4

What are the three phases of the respiratory cycle?

Answer 4

1: inspiratory phase. Characterized by a sudden onset of activity of early inspiratory neurons and a ramp increase in inspiratory augmenting neurons, resulting in motor discharge to inspiratory muscles and airway dilators.

2: postinspiratory phase or expiratory phase I. Characterized by declining motor discharge to inspiratory muscles and passive exhalation. Expiratory decrementing neurons decrease in activity, resulting in a decline in laryngeal adductor muscle tone that functions as a mechanical brake to expiratory flow.

3: expiratory/expiratory phase II. There is no inspiratory muscle activity.

Question 5

Which neurotransmitters influence the CPG?

Answer 5

Glutamate (typically excitatory)
GABA and glycine (inhibitory)

Question 6

What is the role of the dorsal respiratory group neurons?

Answer 6

Generation of the respiratory pattern and coordination of respiratory activity.
Mostly inspiratory neurons.

Question 7

What is the role of the ventral respiratory group neurons?

Answer 7

The VRG neurons are inspiratory and expiratory neurons. The function depends on the specific sub group of neurons in this area.

Question 8

Where is the DRG located?

Answer 8

In close relation to the nucleus tractus solitaries at the termination of visceral afferents from CN IX and X. These nerves carry information that may influence control of breathing, including pH, arterial PO2/PCO2 (from carotid and aortic chemoreceptors) and systemic arterial blood pressure (from carotid/aortic baroreceptors). The vagus nerve also transmits stretch information from stretch receptors in the lungs.

Question 9

What are the four main collections of neurons within the VRG?

Answer 9

1. Caudal ventral respiratory group (nucleus retroambigualis and nucleus paraambigualis) - expiratory function, governs forces of contraction of inspiratory muscles.
2. Rostral ventral respiratory group (mostly composed of the nucleus ambiguous) - controls airway dilator functions of the larynx, pharynx, and tongue
3. The pre-Botzinger complex - essential for pacemaker activity
4. The Botzinger complex (within the nucleus retrofacialis) - extensive expiratory functions

Question 10

What is the pontine respiratory group?

Answer 10

A collection of neurons in the pons which functions to fine-tune the breathing pattern; previously called pneumotaxic center. Increased activity of neurons within this region can promote termination of inspiration, and experimental lesions in the PRG can lead to increase in the duration of inspiration

Question 11

What does experimental disconnection of the apneustic center from the DRG result in?

Answer 11

Apneustic breathing pattern

Question 12

Which area of the brain controls voluntary breathing?

Answer 12

The cortex

Question 13

What does the suprapontine region control?

Answer 13

Involuntary breathing during actions such as coughing, sneezing, swallowing, chewing food

Question 14

What descending pathways does neural input follow after leaving the brain?

Answer 14

They leave the brain etc. and travel through pathways in the white matter of the spinal cord to directly affect lower motor neurons to different groups of respiratory muscles

Question 15

Central chemoreceptors are sensitive to brain interstitial fluid pH, which mainly results from changes in PCO2 in the CSF, but can also be altered by ____ and ____

Answer 15

Cerebral blood flow
Brain metabolism

Question 16

Peripheral chemoreceptors respond rapidly, within ___ to ___ seconds, to a decline in PaO2, rise in PaCO2, rise in H+ concentration, or hypo perfusion

Answer 16

1-3 seconds

Question 17

How does the central chemoreceptor communicate with the CPG?

Answer 17

Connections to the nearby CPG

Question 18

What specific cell type in the peripheral chemoreceptors senses oxygen?

Answer 18

Glomus type I cells

Question 19

Information from the peripheral chemoreceptors is transmitted to the respiratory sinus via —–

Answer 19

Afferent information from the gloms cells is transmitted to the respiratory center via the carotid sinus nerves (branches of the glossopharyngeal nerve from the carotid body) and vagus nerve (from the aortic bodies) resulting in an increased rate and depth of breathing

Question 20

In the healthy individual, _____ is the most important factor affecting control of breathing

Answer 20

PCO2

Question 21

Central chemoreceptors have been attributed to account for approximately ___ - ___% of the response to CO2 (compared to peripheral chemoreceptors)

Answer 21

60-80%

Question 22

Central chemoreceptors are considered the monitors of steady-state arterial PaCO2, whereas the peripheral chemoreceptors detect and react to _____ and short-term changes in PaCO2, though the response to peripheral chemoreceptors results in ____ profound changes in ventilation.

Answer 22

Central chemoreceptors are considered the monitors of steady-state arterial PaCO2, whereas the peripheral chemoreceptors detect and react to RAPID and short-term changes in PaCO2, though the response to peripheral chemoreceptors results in LESS profound changes in ventilation.

Question 23

Stretch receptors in the lungs communicate with the respiratory center (inspiratory area in the medulla and apneustic center in the pons) via __________

Answer 23

Large myelinated vagal fibers

Question 24

What is the Hering-Breuer inflation reflex?

Answer 24

When over-inflation stimulates stretch receptors, and the negative feedback is protective and slows respiratory rate down.

Question 25

What is the deflation reflex?

Answer 25

The opposite response as the Hering-Breuer reflex, which stimulates inspiratory activity with deflation of the lungs.

Question 26

Where are irritant receptors located?

Answer 26

Nasal mucosal epithelium
Epithelial mucosa of the upper airways, tracheobronchial tree, and possibly the alveoli

Question 27

How do irritant receptors transmit information and what does activation of the irritant receptors result in?

Answer 27

Communicate with respiratory center via myelinated vagal afferent fibers.

Activation results in bronchoconstriction, cough, laryngospasm, mucus secretion, and increased rate/depth of breathing

Question 28

What reflexes are involved in sneezing?

Answer 28

Aferrent pathways from the irritant receptors in the nasal mucosa send impulses via the trigeminal and olfactory tracts and leads to sneezing

Question 29

J receptors (juxtacapillary receptors) are located where? What stimulates them?

Answer 29

Pulmonary interstitium close to the pulmonary capillaries
Stimulated by pulmonary capillary distention, interstitial edema, chemicals in the pulmonary circulation; information transmitted to the respiratory center via slowly conducting non-myelinated C-fibers of the vagus nerve leading to rapid, shallow, breathing or even apnea if too much stimulation occurs

Question 30

What alterations can result in arterial baroreceptor influence over ventilation?

Answer 30

A marked decrease in arterial blood pressure sensed by the aortic and carotid sinus baroreceptors can result in reflex hyperventilation while a sustained INCREASE in blood pressure can cause hypoventilation

Question 31

How do somatic receptors located in muscles, tendons, and joints impact ventilation?

Answer 31

They provide feedback on lung volume and work of breathing (the ones located in the rib joints and muscles of breathing) and likely play a role in the hyperventilation occurring secondary to exercise

Question 32

How does pain and temperature affect ventilation?

Answer 32

Receptors that detect pain, temperature, touch and proprioception send information along ascending pathways of the spinal cord and can influence breathing.
Pain can initially cause apnea followed by hyperventilation. Hyperthermia in the skin can cause hyperventilation.

Question 33

Definition of hypoxia

Answer 33

Decrease in the oxygen supply to the tissues

Question 34

Definition of hypoxemia

Answer 34

Inadequate oxygenation of arterial blood, PaO2 < 80 mmHg at sea level (SpO2 <95%)

Question 35

Flow by oxygen therapy is effective if within ___ cm of the patient’s nostril

Answer 35

2 cm

Question 36

Flow by oxygen at 2-3 L/min can provide an FiO2 of ___ to ___%

Answer 36

25-40%

Question 37

A tight fitting face mask with flow rate of 8-12 L/min can provide an FiO2 of ___ to ___ %

Answer 37

50-60%

Question 38

Oxygen hoods with a rate of 0.5-1 L/min can provide an FiO2 of ___ to ___%

Answer 38

30-40%

Question 39

Oxygen cages can deliver ___ - ___ % FiO2

Answer 39

40-60%

Question 40

Placement of a nasal oxygen catheter- measure to where?

Answer 40

From the tip of the nose to the level of the LATERAL canthus of the eye

Question 41

Placement of a nasal oxygen catheter- what space are you entering in the sinus passages?

Answer 41

Ventral meatus

Question 42

Flow rates of 50-150 mL/kg/min via nasal catheter can provide ___ - ___ % FiO2

Answer 42

30-70%

Question 43

Where is the landmark to measure for placement of a nasopharyngeal tube?

Answer 43

The ramus of the mandible

Question 44

How can you facilitate passage of the tube ventrally and medially to the turbinates?

Answer 44

Pig nose (i.e. push lateral nostril medial and up.

Question 45

Transtracheal oxygen therapy should be used with caution (or only for short periods of time) in animals with upper airway obstruction because ______ and _____

Answer 45

They may not be able to exhale 100% and pulmonary over distention can occur.

Question 46

Which muscle do you pass through when inserting a percutaneous tracheal catheter?

Answer 46

Sternohyoideus muscle

Question 47

T/F: Transtracheal oxygen can provide some degree of CPAP, and allows for comparatively lower use of flow rate compared to nasal O2

Answer 47

True

Question 48

How much (%) does HBOT increase the percent of dissolved oxygen in the patient’s blood stream?

Answer 48

By 10-20%

Question 49

Hypoxemia defined as an arterial partial pressure of oxygen (PaO2) <80 mmHg OR an arterial blood hemoglobin saturation (SaO2 or SpO2) < _____ %

Answer 49

< 95 %

Question 50

What two wavelengths do pulse oximeters use?

Answer 50

660 nm and 940 nm - designed to measure only oxygenated hemoglobin

Question 51

What is the driving force for oxygen diffusion down to the mitochondria?

Answer 51

The partial pressure of oxygen in the plasma, NOT the hemoglobin saturation (i.e. it’s not the SpO2!!)

Question 52

Define severe hypoxemia

Answer 52

PaO2 <60 mmHg

Corresponds to a SpO2 of 90% or lower

Question 53

When does visible cyanosis develop?

Answer 53

It results when the deoxyhemoglobin exceeds 5.0 g/dL.

Question 54

T/F: SpO2 measurements cannot deter the difference between a PaO2 of 100 and 500.

Answer 54

True

Question 55

If a dog has a hemoglobin level of 15 g/dL, at what % saturation would cyanosis be visible?

Answer 55

15-5 g/dL = 10 g/dL
10 g/dL divided by 15 g/dL = 0.67 = SpO2 67%

–> equivalent to a PaO2 of 37 mmHg

Question 56

Would cyanosis be visible in a hypoxemic animal with a Hgb of 4 g/dL?

Answer 56

No, never.

Question 57

End-tidal CO2 is usually about ____ mmHg LOWER than PaCO2

Answer 57

5 mmHg

Question 58

Central venous PCO2 is usually about ____ mmHg HIGHER than PaCO2

Answer 58

5 mmHg

Question 59

Four gases of note within the alveoli

Answer 59

O2
CO2
Water vapor
Nitrogen

Question 60

Normal alveolar composition of gases when breathing room air at sea level

Answer 60

Water vapor- 50 mmHg (fixed)

CO2 ~ 40 mmHg (variable)

O2 - 105 mmHg

Nitrogen - 560 mmHg

Question 61

Alveolar air equation

Answer 61

PAO2 = (PB - PH2O)*FiO2- (PaCO2/RQ)

R = 0.8

Question 62

What is the respiratory quotient

Answer 62

The ratio of the CO2 produced to the O2 consumed in the body

Question 63

T/F: Hypoventilation is not a cause of hypoxemia in a patient who is being provided supplemental oxygen therapy

Answer 63

True- hypoventilation is a cause of hypoxemia in patients breathing room air, but not those who are receiving enriched oxygen

Question 64

PAO2 formula (*at sea level, breathing 21% FiO2)

Answer 64

PAO2 = 150 - PaCO2

Question 65

The PaCO2 + PaO2 added rule, or “the 120 rule”

(*only used with FiO2 21% at sea level)

Answer 65

A normal PaCO2 of 40 mmHg and a minimal PaO2 for normoxemia of 80 mmHg = 120 mmHg

Anything less than 120 mmHg indicates venous admixture; the greater the discrepancy, the worse the lung function

Ex: patient has a PaCO2 of 60 mmHg and a PaO2 of 60 mmHg as compared to baseline. Total is 120. One can assume that the hypoxia resulted from hypoventilation (CO2 also went up).

Versus…

Animal has a PaCO2 of 60 mmHg and a PaO2 of 40 mmHg. The added value is 100 mmHg. Animal has lung dysfunction in addition to hypoventilation.

Question 66

What two methods are recommended for use at ROOM AIR?

Answer 66

120 rule
A-a gradient

Question 67

Oxygenation index (OI) in ventilated patients

Answer 67

Another means of evaluating oxygenation in ventilated patients

Takes into account mean airway pressure (MAP)

OI = MAP x FiO2 x 100/PaO2

A lower number indicates a better lung function

Question 68

Oxygenation saturation index (OSI) in ventilated patients

Answer 68

Replaces PaO2 with SpO2

OSI = MAP x FiO2 x 100/SpO2

Question 69

Formula for oxygen content of blood (mL/dL)

Answer 69

= (1.34 x Hgb x SO2) + (0.003 x PO2)

Question 70

In the shunt formula, you solve for Qs/Qt, which represents what?

Answer 70

Qs = shunt fraction
Qt = cardiac output
Qs/Qt = the venous admixture expressed as a percent of cardiac output

Question 71

The volume of air inhaled is usually slightly greater than the exhaled air because more oxygen is inhaled than CO2 exhaled. In health, this is less than ____% of the tidal volume

Answer 71

<1%

Question 72

Tidal volume = ____ + ____

Answer 72

Dead space ventilation (VD) plus alveolar ventilation (VA)

VA = VE -
VD

Question 73

Alveolar ventilation

Answer 73

The volume of fresh air (non dead space gas) available for gas exchange that enters the alveoli per minute , which is equivalent to the total gas exhaled per minute minus the air contained in the dead space per minute

Question 74

What are four divisions of dead space?

Answer 74

Anatomic: air that fills the upper airway, trachea, lower airways to the level of the terminal bronchioles

Alveolar: the portion of inspired gas that passes through the anatomic dead space, and mixes with gas in the alveoli but does not participate in gas exchange with the pulmonary capillaries

Physiologic: anatomic plus alveolar; the portion of the tidal volume that does not participate in gas exchange. In health, physiologic ~ anatomic dead space.

Apparatus: dead space contributed to by the breathing circuit

Question 75

Bohr’s method of measuring dead space measures —–

Answer 75

The volume of lung that does not eliminate CO2, i.e. it measures physiologic and not just anatomic dead space

Question 76

T/F: Alveolar ventilation is decreased by an increase in dead space ventilation, regardless of the cause of the dead space.

Answer 76

True

Question 77

T/F: Venous CO2 levels represent a combination of arterial PCO2, tissue metabolism, and blood flow

Answer 77

True

Question 78

List cardiopulmonary effects of hypercapnia

Answer 78

Decreased cardiac contractility
Decreased systemic vascular resistance
Vasoconstriction of the pulmonary circulation
Bronchodilation
Decreased diaphragmatic contractility

Question 79

In normal animals, venous CO2 is typically ___ - ___ mmHg higher than arterial CO2.

Answer 79

3-6 mmHg

Question 80

Increased difference between venous PCO2 and arterial PCO2 has been associated with:

Answer 80

Decreased cardiac output
Shock
Poor perfusion

Question 81

Normally, end tidal CO2 underestimates PaCO2 by ___ to ___ mmHg. This is a reflection of dead space ventilation.

Answer 81

2-6 mmHg

Question 82

What mechanisms result in oxygen therapy causing a sudden worsening of hypercapnia in a chronically hypercapnic patient?

Answer 82

1) Depression of hypoxia-driven chemoreceptors
2) Relief of hypoxic pulmonary vasoconstriction in poorly ventilated lung regions as local perfusion increases without a concomitant increase in ventilation
3) Significant correction of hypoxemia causes better saturation of hemoglobin so that previously buffered protons on deoxyhemoglobin are released with subsequent generation of new CO2 from stores (reverse-Haldane effect)

Question 83

Approximately ____% of the resistance to airflow during inspiration comes from the nares in normal dogs.

Answer 83

80%

Question 84

Traction-avulsion of nasopharyngeal polyps may be associated with a recurrence rate of __-__% which is why VBO is recommended

Answer 84

40-50%

Question 85

In normal dogs, the larynx accounts for only ___% of resistance to airflow during nasal breathing.

Answer 85

6%

Question 86

Laryngeal paralysis occurs with dysfunction of the ___ nerve, which impairs the normal contraction of the dorsal cricoarytenoideus muscle and subsequent abduction of the arytenoid cartilages.

Answer 86

Recurrent laryngeal nerve

Question 87

Surgical techniques for laryngeal paralysis are divided into three categories:

Answer 87

1. Widening of the dorsal glottis (unilateral or bilateral tie-back)
2. Widening of the ventral glottis (vocal fold resection, partial larygenctomy, modified castellated laryngofissure)
3. Widen the dorsal and ventral glottis (castellated laryngofissure combined with bilateral arytenoid lateralization)

Question 88

Post-operative aspiration pneumonia is the most common complication following arytenoid lateralization, occurring in ___-___% of patients.

Answer 88

8-33%

Question 89

Despite complications, ___% of patients experience improvement in respiratory status and stridor postoperatively.

Answer 89

90%

Question 90

Stage/grade I laryngeal collapse

Answer 90

Eversion of the laryngeal saccules

Question 91

Stage/grade II laryngeal collapse

Answer 91

Medial positioning of the cuneiform processes and aryepiglottic collapse

Question 92

Stage/grade III laryngeal collapse

Answer 92

Collapse of the corniculate cartilages

Question 93

Salvage procedure which can be performed for advanced laryngeal collapse (not a permanent tracheostomy)

Answer 93

Arytenoid laryngoplasty

Question 94

Most common nasal neoplasm in dogs? Most common nasal neoplasm in cats?

Answer 94

Dogs: carcinomas/adenocarcinomas > sarcomas

Cats: lymphoma > carcinomas

Question 95

Suspected mechanisms of tracheal collapse

Answer 95

Dorsal trachealis muscle flaccidity
Weakening of tracheal cartilages due to decreased glycosaminoglycan, chondroitin, and calcium content

Question 96

With repeated mucosal contact, the tracheal mucosa undergoes _________ which results in loss of the mucociliary escalator.

Answer 96

Squamous metaplasia

Question 97

Traditional grading of tracheal collapse (I-IV) has each grade resulting in a decrease in tracheal diameter by ___%.

Answer 97

25%

Question 98

Grade IV tracheal collapse also has the additional feature of inversion of the _____ cartilages

Answer 98

Inversion of the ventral tracheal cartilages

Question 99

Animals with tracheal collapse at the level of the ______ can have either/both inspiratory and expiratory signs.

Answer 99

Thoracic inlet

Question 100

The “honking” heard during coughing/panting is classic for collapse/obstruction of the ____ and ____ trachea.

Answer 100

Cervical and thoracic inlet

Question 101

Chrondromalacia tends to result in ___ clinical signs whereas obstructive malformations of the trachea result in ____ clinical signs.

Answer 101

Dynamic
Static

Question 102

Concurrent bronchial collapse has been documented in ___% of dogs with tracheal collapse

Answer 102

83%

Question 103

Tracheal malformations most often occur at the level of the ______ and often appear as a ventral deviation of the tracheal margin on radiographs.

Answer 103

Thoracic inlet

Question 104

Prosthetic tracheal ring placement success rate reported to be ___ - ___ %

Answer 104

75-85%

Question 105

Dogs with obstructive tracheal disease may benefit from tracheal stenting, versus dogs whose primary cause of distress is _____, which will likely not benefit from tracheal stenting.

Answer 105

Coughing

Question 106

Tracheal stent diameter is ___-___% larger than the maximal tracheal diameter as determined under anesthesia.

Answer 106

10-20% larger

Question 107

Collapse of the _____ lung lobe due to mucus plugging can be considered in cats with lower airway disease.

Answer 107

Right middle lung lobe

Question 108

Greater than __% of eosinophils in cat lung wash fluid is abnormal.

Answer 108

> 5%

Question 109

Bronchomalacia is defined as >__% collapse of airway luminal diameter.

Answer 109

> 50%

Question 110

Cranial lung herniation may be seen in up to ___% of dogs with airway collapse.

Answer 110

70%

Question 111

Normal BAL fluid

Answer 111

70-75% macrophages
5-8% neutrophils, eosinophils, and lymphocytes

Question 112

Which drug can be beneficial in the first 24-48 hours following aspiration to minimize acid-related bronchoconstriction?

Answer 112

Terbutaline

Question 113

Pulmonary hypertension is caused by what three mechanisms?

Answer 113

1) Increased pulmonary blood flow
2) Increased pulmonary vascular resistance
3) Increased pulmonary venous pressure

Or some combination of all three

Question 114

Precapillary PH

Answer 114

PH caused by increased pulmonary vascular resistance in the absence of increased pulmonary venous pressure

Typically the result of vasoconstriction, structural pulmonary arterial changes due to pulmonary vascular disease, or both

Question 115

Postcapillary PH

Answer 115

PH associated with increased pulmonary venous pressure (pulmonary venous hypertension) - secondary to increased left atrial pressure

Question 116

Post capillary PH can be “passive” vs. “active” - describe

Answer 116

Passive post capillary PH is passive when it is isolated, vs. reactive when it leads to pulmonary arterial vasoconstriction and pulmonary vascular disease

Reactive is due to reactive vasoconstriction, pulmonary vascular disease (wall stiffening, endothelial dysfunction, vascular inflammation and thrombosis, and fibrosis) or both.

Question 117

Echocardiography can document which two findings to suggest PH

Answer 117

1) Cardiac changes that occur secondary to PH (RV hypertrophy and systolic dysfunction, left ventricular underfilling, flattening of the IV septum; dilation and altered blood flow in the pulmonary artery)

2) Estimates of systolic pulmonary arterial pressure

Question 118

In the absence of a RVOTO, estimating systolic PAP on echo involves quantifying peak ________

Answer 118

Tricuspid regurgitation velocity

Question 119

Simplified Bernoulli equation

Answer 119

Pressure gradient = 4 x velocity^2

Question 120

Definition of PH in humans (PAP)

Answer 120

≥ 25 mmHg at rest measured invasively by right heart catheterization

Question 121

PH classifications in veterinary medicine based on pressure gradient between the RA and RV during systole

Answer 121

Mild: 30-50 mmHg
Moderate: 50-75 mmHg
Severe: 75 mmHg

Question 122

Clinically significant PH is unlikely unless clinical signs are present and a pressure gradient of at least ___ mmHg is present.

Answer 122

46 mmHg (flow of 3.4 m/s)

Question 123

Six ACVIM classifications of PH

Answer 123

1) Pulmonary arterial hypertension
2) PH secondary to left heart disease
3) PH secondary to respiratory disease, hypoxia or both
4) PH secondary to thromboembolic disease
5) PH secondary to parasitic disease (HW, angiostrongylous)
6) PH with multifactorial or unclear etiologies

Question 124

Why does documentation of LA enlargement have to be present for PH to be classified as being secondary to left heart disease?

Answer 124

Because LAE is a crude surrogate for documentation of chronically increased LA pressure (postcapillary PH)

Question 125

How do phosphodiesterase 5 inhibitors work?

Answer 125

Cause accumulation of cGMP in pulmonary vascular smooth muscle cells by inhibiting cGMP catabolism.

Accumulation of CGMP results in relaxation of vascular smooth muscle and inhibition of pulmonary arterial smooth muscle cell hypertrophy.

PDE5i drugs are generally effective at lowering PVR and potentially delaying remodeling of the pulmonary arteries.

REDUCES RH AFTERLOAD

Question 126

Why is PDE5i therapy potentially contraindicated in patients with PH secondary to left heart disease?

Answer 126

Because it can result in worsening of pulmonary edema. Will potentially cause acutely increased right heart cardiac output and thereby increase LA preload.

Question 127

Two main pathophysiologic forms of pulmonary edema

Answer 127

1) High hydrostatic pressure edema (increased pulmonary capillary hydrostatic pressure)
2) Increased permeability edema (damage of the microvascular barrier and alveolar epithelium)

Question 128

Mechanisms of the lung to prevent formation of pulmonary edema

Answer 128

Relatively non-distensible intersitium, increased interstitial hydrostatic pressures and increased driving pressure for lymphatic flow
The pulmonary capillary microvascular barrier is relatively permeable to protein compared with other tissues, so this lymphatic flow is largely responsible for protecting the lung against edema, and the decreased role of the COP gradient is largely why hypoproteinemia alone doesn’t result in pulmonary edema

Question 129

Main determinant of the formation of pulmonary edema

Answer 129

Hydrostatic pressure

Question 130

Pathway of fluid accumulation/development of edema

Answer 130

Fluid initially flows toward the peribronchovascular interstitium, then distends all parts of the pulmonary interstitium, then spills over into the airspaces at the junction of the alveolar and airway epithelia

Question 131

Increased permeability edema

Answer 131

Damage to the microvascular barrier and alveolar epithelium –> extravasation of high protein fluid –> interstitial fluid develops at even low hydrostatic pressures because the oncotic pressure gradient is in favor of continued fluid extravasation –> can progress rapidly to alveolar flooding

Question 132

Lymphatic system

Answer 132

Plays a major role in limiting interstitial fluid accumulation
Only has a minor role in clearance of pulmonary edema
Most edema fluid is cleated via the bronchial circulation

Question 133

Potential causes of NCPE

Answer 133

Seizures
Choking
Near drowning
Smoke inhalation
Electrocution
Head trauma

Question 134

What proportion of cats with CHF may have no auscultable murmur?

Answer 134

20%

Question 135

What % of cats with left-sided CHF will have pulmonary edema?

Answer 135

About 50%

Question 136

Proposed mechanism of neurogenic pulmonary edema (NPE)

Answer 136

Surge in intracranial pressure results in catecholamine surge –> increased systemic vascular resistance –> increased capillary hydrostatic pressure –> capillary leakage of fluid

Blast theory: acute transient rise in capillary pressure resulting in barotrauma and damage to the capillary alveolar membrane

Tends to develop within 24 hours, takes about 48 hours to resolve

Question 137

Negative pressure pulmonary edema (NPPE) i.e. edema secondary to upper airway obstruction

Answer 137

Negative intrathoracic pressure thought to cause the pathophysiologic cascade resulting in pulmonary edema

Negative intrathoracic pressure increases venous return to the right side of the heart, leading to increased pulmonary venous pressures and decreased perivascular interstitial hydrostatic pressure. There is also increased left ventricular after load due to transmural pressure across the cardiac wall. Fluid moves from the capillaries to the interstitium. Tends to be acute onset and resolve within 48 hours.

Question 138

Pneumonia characterized by

Answer 138

Infiltration of PMN leukocytes, edema fluid, erythrocytes, mononuclear cells, and fibrin into the lung

Question 139

Lobar pneumonia

Answer 139

Typically encompasses an entire lung lobe
Spread is believed to be alveolus to alveolus and acinus to acinus through inter alveolar pores

Question 140

Bronchopneumonia

Answer 140

Characterized by distal airway inflammation and alveolar disease
Through to spread through the airways rather than through adjacent alveoli/acini

Question 141

Interstitial pneumonia

Answer 141

The inflammatory process initially occurs within the interstitium rather than alveolar spaces

Question 142

The upper and lower airways provide a first line of defense against inhaled pathogens and contaminated particulate matter:

Answer 142

Anatomical barriers
Cough reflex
Mucociliary apparatus
Secretory IgA
Phagocytic dendritic cells within the basal layer of the respiratory mucosa

Question 143

Particles smaller than ___ micrometers may bypass the upper respiratory tract defenses and get deposited into the alveoli

Answer 143

3 micrometers

Question 144

The bronchoalveolar junction is a major site of all particle (___ to ___ micrometers) deposition and is especially vulnerable to damage.

Answer 144

0.5-3 micrometer

Question 145

Presence of hypercapnia in the case of pneumonia suggests

Answer 145

Fatigue
Bronchoconstriction
Presence of severe pulmonary parenchymal diseases

Question 146

Most common isolates found in dogs with pneumonia (wash samples)

Answer 146

Pasteurella (22-28%)
Enterobacteria such as E. coli (17-46%)
Gram positive cocci such as Staph (10-16%) and Strep (14-21%)
Anaerobes isolated in 10-21% of cases (should prompt evaluation for abscess)

Mycoplasma detected commonly, either as a sole organism (8%) or co infection with other bacteria (62%)

In puppies with pneumonia, Bordatella bronchiseptica most common (49%)

Question 147

Severe histological damage from aspiration results when contents are a pH of ____ ; minimal damage occurs if the pH is greater than ____ unless there is particulate matter present

Answer 147

<1.5
>2.4

Question 148

Bacteria commonly cultured from companion animals with aspiration pneumonia

Answer 148

Enteric bacteria: E. coli, Klebsiella spp., Enterococcus spp.
Oropharyngeal Mycoplasma spp.
Primary respiratory pathogens: Pasteurella spp., Pseudomonas spp., Streptococcus spp.
Commensals such as Staph.

Question 149

Viral organisms implicated in CIRD-C

Answer 149

Canine adenovirus 2
Parainfluenza
Canine distemper virus
Canine respiratory coronavirus
Canine influenza virus
Canine pneumovirus
Canine herpesvirus

Question 150

Two important influenza strains in dogs

Answer 150

H3N8
H3N2

More likely to cause hemorrhagic bronchopneumonia than other influenza subtypes

Question 151

Most common bacterial pathogens associated with CIRD-C

Answer 151

Bordetella bronchiseptica
Streptococcus equi subsp. zooepidemicus
Mycoplasma cynos

Question 152

Most commonly isolated organisms associated with foreign body pneumonia

Answer 152

Strep
Pasteurella
Nocardia
Actinomyces

Question 153

The major gas exhange surface of the alveolus is composed of _______ epithelial cells

Answer 153

Type I alveolar epithelial cells

Crucial role in maintaining the permeability function of the alveolar membrane

Question 154

Inciting cause of ARDS

Answer 154

Inflammatory insult that damages either the alveolar epithelial cells or the pulmonary capillary endothelial cells –> impaired barrier function/increased permeability –> flooding of the interstitium and alveoli with protein rich fluid and inflammatory cells –> surfactant issues –> atelectasis
Also impaired gas exchange via diffusion impairment and venous admixture from intrapulmonary shunting and VQ mismatch

Question 155

Explain the acute exudative phase of ARDS

Answer 155

The first 1-7 days of ARDS
Diffuse alveolar damage with hyaline membrane formation and neutrophil influx
Alveolar flooding with fluid, protein, WBC, RBC secondary to injury of the alveolar epithelial cell:capillary endothelial cell boundary

Innate immune system becomes activated

Stimulation of alveolar macrophages and recruitment of neutrophils/circulating macrophages to the lung

Widespread release of inflammatory mediators including cytokines, ROS, and eicosanoids

–> continued alveolar epithelial cell damage, protein degradation, surfactant dysfunction, increased permeability of endothelial:epithelial barrier, and local micro thrombi development

**Neutrophils considered to play a central role in this response

Question 156

Fibroproliferative phase of ARDS

Answer 156

In the weeks following the exudative phase, there is a proliferation of type II alveolar cells, interstitial fibrosis, and organization of the exudate.

Lung re-organization results in significant decrease in compliance

Proliferation of type II alveolar cells, interstitial thickening, and obliteration of alveoli and capillary networks

**Fibrosis can begin as early as 48 hours after onset of ARDS

Question 157

Resolution of ARDS

Answer 157

Requires apoptosis of neutrophils, differentiation of type II –> type I alveolar epithelial cells, termination of the fibroproliferative response, and reabsorption of alveolar edema and the provisional matrix

Question 158

Two phenotypes of ARDS

Answer 158

Hyperinflammatory: ~30% of patients, higher mortality rates; more often associated with shock and metabolic acidosis

Hypoinflammatory

Question 159

Diagnostic criteria for ARDS (VetARDS)

Answer 159

Acute onset (<72h) dyspnea at rest

Known risk factors

Evidence of pulmonary capillary leak without increased pulmonary capillary pressure (any one of the following):
–> Bilateral/diffuse infiltrate on thoracic radiographs (more than 1 lobe/quadrant)
–> Bilateral dependent density on CT
–> Proteinaceous fluid within conducting airways
–> Increased extravascular lung water

Evidence of inefficient gas exchange (one or more of the following):
–> Hypoxemia without CPAP or PEEP and known FiO2
–>P:F ratio ≤ 300 mmHg for Vet ALI, ≤ 200 mmHg for VetARDS
–> Increased A-a gradient
–> Venous admixture (non cardiac shunt)
–> Increased dead space ventilation

Evidence of diffuse pulmonary inflammation
–> Neutrophilic BAL sample
–> BAL biomarkers of inflammation
–> PET scan

Question 160

Berlin criteria for ARDS

Answer 160

Within 1 week of known clinical insult or new/worsening respiratory signs

Respiratory failure not fully explained by cardiac failure or fluid overload (absence of left atrial hypertension, PAWP ≤ 18 mmHg)

Bilateral opacities in the lungs not fully explained by effusions, lobar/lung collapse, or nodules

Mild: 200 mmHg < P:F ≤ 300 mmHg with PEEP or CPAP ≥ 5 cm H2O

Moderate: 100 mmHg < P:F ≤ 200 mmHg with PEEP or CPAP ≥ 5 cm H2O

Severe: PF ≤ 100 mmHg with PEEP ≥ 5 cm H2O

Question 161

What are some lung-protective ventilator strategies and how do they help decrease VILI

Answer 161

Low-volume (4-6 mL/kg) and end-inspiratory plateau pressures <30 cm H2O + use of PEEP

Preventing alveolar over-distention helps preserve the epithelial:endothelial boundary

Question 162

How do contusions happen?

Answer 162

Acute compression then subsequent expansion of the lungs leads to transmission of mechanical forces and energy to the pulmonary parenchyma. This happens via the spalling effect, inertial effect, and implosion effect.

Question 163

Inertial effect

Answer 163

Occurs when low density alveolar tissue is stripped from heavier hilar structures as they accelerate at different rates –> mechanical tearing and laceration of the lungs

Question 164

Spalling effect

Answer 164

A shearing or bursting phenomenon that occurs at gas-liquid interfaces; may disrupt the alveolus at the point of initial contact with shock waves

Question 165

Implosion effect

Answer 165

Rebound or over-expansion of gas bubbles after a pressure wave passes –> tearing of the parenchyma due to over-distention

Question 166

Main mechanism of hypoxia with contusions

Answer 166

Shunting (increased shunt fraction and dead space ventilation)

Question 167

Two bacteria associated with pulmonary hemorrhage

Answer 167

E. coli and Streptococcus equi subs. zooepidemicus

Question 168

T/F: The degree of hypoxemia correlates with the degree of embolization

Answer 168

False

Question 169

Explain the V/Q mismatching that happens with PTE

Answer 169

Low V/Q –> potentially more important actually than its counterpart; since blood isn’t going to the area downstream from the thrombus, more is getting directed to other areas, and therefore the flow is increasing while the ventilation remains the same.

High V/Q –> there is no flow downstream from the thrombus, but those lung lobes are still ventilating; dead space ventilation

Question 170

Cor pulmonale definition

Answer 170

Pulmonary heart disease, also known as cor pulmonale, is the enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance or high blood pressure in the lungs.

Question 171

Why is a positive D-dimer test more sensitive for fibrin formation than FDP’s?

Answer 171

FDPs indicate either fibrin or fibrinogen degradation products, whereas D-dimers indicate breakdown of cross-linked fibrin.

Question 172

Arterial blood gas analysis with PTE

Answer 172

Hypoxia
HyPOcapnia

Question 173

Westermark sign

Answer 173

Focal peripheral hyperlucency secondary to oligemia resulting in a collapsed appearance of vessels distal to the occlusion

Question 174

McConnell’s sign

Answer 174

Akinesia of the right mid ventricular free wall with normal contractility at the apex - highly specific in humans for PTE

Question 175

Drugs for treating VENOUS thromboembolism

Answer 175

Heparin (LMWH)
Direct factor Xa inhibitors (i.e. rivaroxaban)

Question 176

Accessory inspiration muscles

Answer 176

Scalenes
External intercostals
Sternomastoids

Question 177

What is the maximum number of ribs which can be resected surgically?

Answer 177

6

Question 178

Flail chest definition

Answer 178

Series of three or more rib fractures in a row, where both the dorsal and ventral aspects of the affected ribs are fractured

Question 179

The main nerves that innervate muscles of respiration arise from cervical segments ___-___

Answer 179

C4-7P

Question 180

Presynaptic neurotoxin in Elapid venom

Answer 180

Phospholipase A2 - prevent release of acetylcholine

Question 181

Postsynaptic neurotoxin in Elapid venom

Answer 181

Antagonizes acetylcholine receptor

Question 182

Acute pre-paralytic signs of Elapid envenomation in dogs

Answer 182

Vomiting
Hypersalivation
Nausea
Urination/defecation

Question 183

T/F: Dogs with Campylobacter are more likely to develop acute polyradiculoneuritis

Answer 183

True - 9.4 times more likely

Question 184

How does botulinum toxin result in paralysis?

Answer 184

Botulinum toxin inhibits acetylcholine release at the synaptic terminal by blocking presynaptic acetylcholine vesicle fusion with the terminal membrane

Question 185

Are cranial nerve abnormalities present with botulism?

Answer 185

Yes- may help differentiate botulism from other LMN diseases

Question 186

Animals with MG may present with respiratory distress for two reasons

Answer 186

1) Secondary to hypercapnia/hypoxemia from decreased chest wall excursions or aspiration pneumonia secondary to megaesophagus

2) Overdose of cholinesterase inhibitors

Question 187

What is the average intrapleural pressure

Answer 187

-5 cm H2O

Question 188

What percentage of cats may be normothermic or hypothermic on presentation and still have a pythorax?

Answer 188

50%

Question 189

What is a glide sign

Answer 189

The visceral and parietal pleura moving past one another

Question 190

What is a curtain sign

Answer 190

The demarcated vertical edge separating the lung from abdominal contents

May be asynchronous (i.e. vertical edge moves in opposite direction of abdominal contents) with pneumothorax

Question 191

Suggested criteria for removal of chest tubes in patients with prothorax

Answer 191

Clinical improvement
Resolution of infection on cytology
<2 mL/kg/day fluid production

Question 192

After how many days did infection develop in dogs with experimentally placed chest tubes?

Answer 192

4-6 days

Question 193

Overall survival rates for dogs/cats with pyothorax

Answer 193

83% in dogs, 63% in cats

Question 194

Pure transudate protein level vs. modified transudate/exudate protein level

Answer 194

Pure transudate <2.5 g/dL
Modified transudate/exudate ≥2.5 g/dL

Question 195

Effusion triglyceride values compared to serum for chylous effusion

Answer 195

Often greater than 3:1 (effusion:serum), or ≥100 mg/dL in the effusion

Question 196

How does rutin supposedly work?

Answer 196

Rutin is a benzopyrone that is theorized to increase lymphatic fluid uptake, reduce blood vessel permeability, and increase macrophage phagocytosis of protein in lymph

Question 197

Hemothorax is defined as a pleural effusion with at least ___% of the PCV of the peripheral PCV

Answer 197

25%

Question 198

What is one of the reasons effusions can develop with FIP?

Answer 198

Pyogranulomas form around venules

Question 199

What ratio of pleural effusion to serum bilirubin is consistent with bilothorax?

Answer 199

> 1:1

Question 200

What ratio of pleural effusion to serum creatinine is consistent with urothorax?

Answer 200

> 1:1

Question 201

Most common cause of spontaneous pneumothorax in cats

Answer 201

Airway disease

Question 202

Most common cause of traumatic pneumothorax in cats

Answer 202

High rise syndrome
Bite wounds

Question 203

Six physiologic benefits of HFNO

Answer 203

H- Heated and humidified
I- Inspiratory flow demands
F- Functional reserve capacity
L- Lighter
O- Oxygen dilution
W- Wash out dead space

Question 204

Preferred temperature of HFNO for comfort

Answer 204

31*C

Question 205

Amount of PEEP provided by HFNO

Answer 205

Variable; may be more or less than the reported 1 mmHg PEEP for every 10 L/min

Question 206

Equation of motion

Answer 206

Pvent + Pmuscles = Elastance x Volume x Resistance x Flow

*Elastance is the inverse of compliance

Question 207

Resistance

Answer 207

The pressure required to generate a given flow

Question 208

Compliance

Answer 208

The change in lung volume for a given change in pressure

= ΔV/ΔP = Vt/pressure required to achieve Vt

Question 209

The three variables that the ventilator is responsible for

Answer 209

Pressure
Volume
Flow

Question 210

Cycle variable

Answer 210

Terminates the breath

Question 211

Limit variable

Answer 211

Parameter that the breath cannot exceed during inspiration - does not terminate the breath

Question 212

Common/ideal I:E ratio

Answer 212

1:2

Question 213

What is rise time?

Answer 213

The time in which the airway pressure increases from baseline to peak pressure

Question 214

Low tidal volume decreases which aspects of VILI

Answer 214

Barotrama
Volutrama
Biotrama

Question 215

Five main components of smoke inhalation injury

Answer 215

Upper airway injury
Lower airway injury
Pulmonary parenchymal injury
Systemic injury
Systemic toxicity

Question 216

Upper airway injury in smoke inhalation

Answer 216

Temperature (can exceed 300*F)
Direct thermal injury –> edema and inflammation (usually peaks 24 hours post exposure)

Question 217

Pulmonary parenchymal injury

Answer 217

Classically delayed
Increased transvascular fluid efflux, lack of surfactant and loss of hypoxic pulmonary vasoconstriction result in impaired oxygenation

Question 218

Lower airway injury in smoke inhalation

Answer 218

Not usually direct thermal injury
Chemical inhalation –> irritant receptors –> release of neuropeptides/severe inflammatory response –> bronchoconstriction, pulmonary vasoconstriction, airway fluid accumulation and development of casts which further obstruct air flow

Increased NO levels impair pulmonary hypoxic vasoconstriction

Question 219

Systemic injury

Answer 219

Corneal injury
Hypercoagulability
Left ventricular dysfunction
Hypotension (especially if CO present)

Most toxic compounds present in smoke are carbon monoxide and cyanide

Question 220

Carbon monoxide

Answer 220

Most frequent cause of immediate death following smoke inhalation in humans
High affinity for Hgb (200-250 times stronger than oxygen)
Cellular hypoxia
Brain and heart have higher oxygen extraction and as a consequence are majorly affected during COHb circulation
CO causes a left shift on the dissociation curve
Cytochrome oxidase systems inhibited by CO, resulting in intracellular inability to use oxygen
Cardiac and neuro dysfunction

Question 221

Hydrogen cyanide

Answer 221

Physiologically converted to thiocyanate in the liver under normal circumstances
During intoxication, the liver may not be able to handle large amounts and the primary toxic effect is at the level of the mitochondria- it inhibits the electron transport chain, impairing cellular ATP production

Neurotoxicity, tachypnea, arrhythmias and death

Question 222

Cherry red MM

Answer 222

High levels of COHb

Question 223

Hyperlactatemia and smoke inhalation

Answer 223

Hyperlactatemia in a patient with otherwise adequate perfusion raises concern for CO

Question 224

Pulse oximetry and smoke inhalation

Answer 224

Regular pulse ox cannot differentiate oxyhemoglobin from COhemoglobin

Question 225

CO half life and effect of oxygen on half life

Answer 225

Normal CO half life 320 minutes in a patient breathing room air; goes down to 70 minutes if breathing 100% oxygen.

Question 226

Antidotes to cyanide

Answer 226

Amyl nitrate and sodium thiosulfate –> convert hemoglobin to methemoglobin which CN binds preferentially to, but causes decrease oxygen carrying capacity

Hydroxocobalamin (B12a) binds cyanide to form cyanocobalamin which is excreted by the kidneys; way safer

Question 227

Drowning definition

Answer 227

A process resulting in primary respiratory impairment from submersion or immersion in a liquid medium. Liquid is present in the victim’s airway.

Question 228

Dry drowning definition

Answer 228

Dry drowning is when liquid is not aspirated into the lungs, whereas wet drowning refers to aspiration of liquid. Victims of dry drowning do suffer mortality due to laryngospasm

Question 229

Most survivors of drowning in human medicine are thought to have aspirated less than __ mL/kg of fluid

Answer 229

<22 mL/kg

Question 230

Hypoxemia in drowning victims results from _____

Answer 230

Intrapulmonary shunting

Question 231

In humans, about ___% of all victims experience severe neurologic effects.

Answer 231

10%

Question 232

Submersion in ice cold water <___*F increases the chances of survival due to the ____ reflex.

Answer 232

<41*F
Diving reflex

Question 233

Diving reflex

Answer 233

Within seconds of the face touching ice cold water, the trigeminal nerve signals to the CNS that cause bradycardia, hypertension, and preferential shunting of blood to the cerebral and coronary circulations

Question 234

Three factors associated with 100% mortality in human drowning victims under the age of 20

Answer 234

1) Submersion duration longer than 25 minutes
2) Resuscitation duration longer than 25 minutes
3) Pulseless cardiac arrest on presentation to the ED

Question 235

What percentage of trauma-induced upper airway rupture dogs had SQ emphysema at presentation to the ER?

Answer 235

80%

Question 236

What percentage of cats with pneumomediastinum had SQ emphysema?

Answer 236

66%

Question 237

T/F: In dogs and cats the mediastinum is usually fenestrated

Answer 237

True

Question 238

The Macklin effect

Answer 238

The Macklin effect relates to a three-step pathophysiologic process: blunt traumatic alveolar ruptures, air dissection along bronchovascular sheaths, and spreading of this blunt pulmonary interstitial emphysema into the mediastinum and pleural space

Question 239

How can provision of oxygen therapy hasten recovery of pneumomediastinum and SQ emphysema?

Answer 239

The administration of oxygen in patients with a pneumothorax should theoretically hasten the re-expansion of the collapsed lung, by washing out nitrogen from the arterial blood and should therefore increase the absorption gradient between blood and air in the pleural cavity.

Question 240

The mass median diameter (MMD) of a particle must be less than ___ µm to reach the small bronchioles and alveoli

Answer 240

< 5 µm

Question 241

Particles larger than ___ µm are deposited in the larynx and nasal turbinates.

Answer 241

> 10 µm

Question 242

The dissolved portion of oxygen, measured as the partial pressure of oxygen (PO2), makes up only ____-____% of total oxygen content of blood in health.

Answer 242

2-3%

Question 243

Feline hemoglobin has a lower/higher affinity for oxygen compared to dog and human blood.

Answer 243

LOWER (P50 is 34-36 mmHg compared to dogs which is 28-31 mmHg)

Question 244

What is the Beer-Lambert law?

Answer 244

States that the concentration of a substance can be determined by its ability to transmit light.
Oxygen binding to hemoglobin changes its structure and therefore its ability to absorb light.

Question 245

What is the main technological method for pulse oximetry?

Answer 245

Spectrophotometry

Question 246

What species of hemoglobin do co-oximeters detect?

Answer 246

Oxyhemoglobin
Deoxyhemoglobin
Carboxyhemoglobin
Methemoglobin

Question 247

Which two wavelengths of light does a pulse oximeter emanate?

Answer 247

660 nm - red light
940 nm - infrared light

Question 248

What basic property of the functional hemoglobins does a pulse oximeter detect

Answer 248

Pulse oximetry differentiates oxyhemoglobin from deoxyhemoglobin based on the light characteristics of the two in tissue.
It emits two wavelengths of light from the probe’s diodes, and the light absorption in the patient’s tissue is recorded by a photodetector. Oxyhemoglobin dissolves more INFRARED light and deoxyhemoglobin absorbs more RED light. The pulse oximeter microprocessing unit then determines the proportion of oxygenated hemoglobin present.

Because other tissues absorb light, the pulse ox evaluates only pulsatile (arterial) wavelength absorption in the calculations, based on an optical technique known as photoplethysmography.

Question 249

Above what point does the oxygen hemoglobin dissociation curve flatten out?

Answer 249

Above SpO2 97%

Question 250

How does methemoglobin affect pulse ox reading?

Answer 250

The presence of methemoglobin will cause lower than normal SpO2 readings, and when methemoglobin levels approach 30%, it will cause the SpO2 to plateau at approximately 85% regardless of the true level of oxygen saturation

Question 251

The ligament you incise when making a tracheostomy is called _____

Answer 251

The annular ligament (exists between the rings)

Question 252

Tracheostomy site should account for no more than ____% of the tracheal diameter

Answer 252

50%

Question 253

What is a long-term consequence of performing a vertical incision for tracheostomy?

Answer 253

Long term segmental tracheal collapse

Question 254

How often should tracheostomy tubes without an inner canula be changed?

Answer 254

Every 24 hours

Question 255

Using a three-bottle suction technique, which chamber determines the suction pressure?

Answer 255

The third one- fill the water to the desired pressure

Question 256

Chest tube removal criteria

Answer 256

Ideally, no air should be removed for 24 hours prior to removal
Ideally less than 2 mL/kg/day fluid production x 24 hours

Question 257

According to Henry’s law, blood temperature decrease should lead to a _____ in partial pressure of CO2/oxygen and subsequently a decrease in values in vivo

Answer 257

Decrease in partial pressure