Respiratory - S&H Flashcards
1
Q
What is the role of the medulla in respiration?
A
Respiratory center
Site responsible for the generation of the respiratory pattern and coordination of voluntary and involuntary input
2
Q
What is the central pattern generator?
A
A complex collection of neurons that form a pacemaker system for respiration
3
Q
Where are these pacemaker neurons predominantly concentrated in the medulla?
A
the Pre-Botzinger complex
4
Q
What are the three phases of the respiratory cycle?
A
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.
5
Q
Which neurotransmitters influence the CPG?
A
Glutamate (typically excitatory)
GABA and glycine (inhibitory)
6
Q
What is the role of the dorsal respiratory group neurons?
A
Generation of the respiratory pattern and coordination of respiratory activity.
Mostly inspiratory neurons.
7
Q
What is the role of the ventral respiratory group neurons?
A
The VRG neurons are inspiratory and expiratory neurons. The function depends on the specific sub group of neurons in this area.
8
Q
Where is the DRG located?
A
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.
9
Q
What are the four main collections of neurons within the VRG?
A
- Caudal ventral respiratory group (nucleus retroambigualis and nucleus paraambigualis) - expiratory function, governs forces of contraction of inspiratory muscles.
- Rostral ventral respiratory group (mostly composed of the nucleus ambiguous) - controls airway dilator functions of the larynx, pharynx, and tongue
- The pre-Botzinger complex - essential for pacemaker activity
- The Botzinger complex (within the nucleus retrofacialis) - extensive expiratory functions
10
Q
What is the pontine respiratory group?
A
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
11
Q
What does experimental disconnection of the apneustic center from the DRG result in?
A
Apneustic breathing pattern
12
Q
Which area of the brain controls voluntary breathing?
A
The cortex
13
Q
What does the suprapontine region control?
A
Involuntary breathing during actions such as coughing, sneezing, swallowing, chewing food
14
Q
What descending pathways does neural input follow after leaving the brain?
A
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
15
Q
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 ____
A
Cerebral blood flow
Brain metabolism
16
Q
Peripheral chemoreceptors respond rapidly, within ___ to ___ seconds, to a decline in PaO2, rise in PaCO2, rise in H+ concentration, or hypo perfusion
A
1-3 seconds
17
Q
How does the central chemoreceptor communicate with the CPG?
A
Connections to the nearby CPG
18
Q
What specific cell type in the peripheral chemoreceptors senses oxygen?
A
Glomus type I cells
19
Q
Information from the peripheral chemoreceptors is transmitted to the respiratory sinus via —–
A
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
20
Q
In the healthy individual, _____ is the most important factor affecting control of breathing
A
PCO2
21
Q
Central chemoreceptors have been attributed to account for approximately ___ - ___% of the response to CO2 (compared to peripheral chemoreceptors)
A
60-80%
22
Q
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.
A
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.
23
Q
Stretch receptors in the lungs communicate with the respiratory center (inspiratory area in the medulla and apneustic center in the pons) via __________
A
Large myelinated vagal fibers
24
Q
What is the Hering-Breuer inflation reflex?
A
When over-inflation stimulates stretch receptors, and the negative feedback is protective and slows respiratory rate down.
25
What is the deflation reflex?
The opposite response as the Hering-Breuer reflex, which stimulates inspiratory activity with deflation of the lungs.
26
Where are irritant receptors located?
Nasal mucosal epithelium
Epithelial mucosa of the upper airways, tracheobronchial tree, and possibly the alveoli
27
How do irritant receptors transmit information and what does activation of the irritant receptors result in?
Communicate with respiratory center via myelinated vagal afferent fibers.
Activation results in bronchoconstriction, cough, laryngospasm, mucus secretion, and increased rate/depth of breathing
28
What reflexes are involved in sneezing?
Aferrent pathways from the irritant receptors in the nasal mucosa send impulses via the trigeminal and olfactory tracts and leads to sneezing
29
J receptors (juxtacapillary receptors) are located where? What stimulates them?
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
30
What alterations can result in arterial baroreceptor influence over ventilation?
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
31
How do somatic receptors located in muscles, tendons, and joints impact ventilation?
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
32
How does pain and temperature affect ventilation?
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.
33
Definition of hypoxia
Decrease in the oxygen supply to the tissues
34
Definition of hypoxemia
Inadequate oxygenation of arterial blood, PaO2 < 80 mmHg at sea level (SpO2 <95%)
35
Flow by oxygen therapy is effective if within ___ cm of the patient's nostril
2 cm
36
Flow by oxygen at 2-3 L/min can provide an FiO2 of ___ to ___%
25-40%
37
A tight fitting face mask with flow rate of 8-12 L/min can provide an FiO2 of ___ to ___ %
50-60%
38
Oxygen hoods with a rate of 0.5-1 L/min can provide an FiO2 of ___ to ___%
30-40%
39
Oxygen cages can deliver ___ - ___ % FiO2
40-60%
40
Placement of a nasal oxygen catheter- measure to where?
From the tip of the nose to the level of the LATERAL canthus of the eye
41
Placement of a nasal oxygen catheter- what space are you entering in the sinus passages?
Ventral meatus
42
Flow rates of 50-150 mL/kg/min via nasal catheter can provide ___ - ___ % FiO2
30-70%
43
Where is the landmark to measure for placement of a nasopharyngeal tube?
The ramus of the mandible
44
How can you facilitate passage of the tube ventrally and medially to the turbinates?
Pig nose (i.e. push lateral nostril medial and up.
45
Transtracheal oxygen therapy should be used with caution (or only for short periods of time) in animals with upper airway obstruction because ______ and _____
They may not be able to exhale 100% and pulmonary over distention can occur.
46
Which muscle do you pass through when inserting a percutaneous tracheal catheter?
Sternohyoideus muscle
47
T/F: Transtracheal oxygen can provide some degree of CPAP, and allows for comparatively lower use of flow rate compared to nasal O2
True
48
How much (%) does HBOT increase the percent of dissolved oxygen in the patient's blood stream?
By 10-20%
49
Hypoxemia defined as an arterial partial pressure of oxygen (PaO2) <80 mmHg OR an arterial blood hemoglobin saturation (SaO2 or SpO2) < _____ %
< 95 %
50
What two wavelengths do pulse oximeters use?
660 nm and 940 nm - designed to measure only oxygenated hemoglobin
51
What is the driving force for oxygen diffusion down to the mitochondria?
The partial pressure of oxygen in the plasma, NOT the hemoglobin saturation (i.e. it's not the SpO2!!)
52
Define severe hypoxemia
PaO2 <60 mmHg
Corresponds to a SpO2 of 90% or lower
53
When does visible cyanosis develop?
It results when the deoxyhemoglobin exceeds 5.0 g/dL.
54
T/F: SpO2 measurements cannot deter the difference between a PaO2 of 100 and 500.
True
55
If a dog has a hemoglobin level of 15 g/dL, at what % saturation would cyanosis be visible?
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
56
Would cyanosis be visible in a hypoxemic animal with a Hgb of 4 g/dL?
No, never.
57
End-tidal CO2 is usually about ____ mmHg LOWER than PaCO2
5 mmHg
58
Central venous PCO2 is usually about ____ mmHg HIGHER than PaCO2
5 mmHg
59
Four gases of note within the alveoli
O2
CO2
Water vapor
Nitrogen
60
Normal alveolar composition of gases when breathing room air at sea level
Water vapor- 50 mmHg (fixed)
CO2 ~ 40 mmHg (variable)
O2 - 105 mmHg
Nitrogen - 560 mmHg
61
Alveolar air equation
PAO2 = (PB - PH2O)*FiO2- (PaCO2/RQ)
R = 0.8
62
What is the respiratory quotient
The ratio of the CO2 produced to the O2 consumed in the body
63
T/F: Hypoventilation is not a cause of hypoxemia in a patient who is being provided supplemental oxygen therapy
True- hypoventilation is a cause of hypoxemia in patients breathing room air, but not those who are receiving enriched oxygen
64
PAO2 formula (*at sea level, breathing 21% FiO2)
PAO2 = 150 - PaCO2
65
The PaCO2 + PaO2 added rule, or "the 120 rule"
(*only used with FiO2 21% at sea level)
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.
66
What two methods are recommended for use at ROOM AIR?
120 rule
A-a gradient
67
Oxygenation index (OI) in ventilated patients
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
68
Oxygenation saturation index (OSI) in ventilated patients
Replaces PaO2 with SpO2
OSI = MAP x FiO2 x 100/SpO2
69
Formula for oxygen content of blood (mL/dL)
= (1.34 x Hgb x SO2) + (0.003 x PO2)
70
In the shunt formula, you solve for Qs/Qt, which represents what?
Qs = shunt fraction
Qt = cardiac output
Qs/Qt = the venous admixture expressed as a percent of cardiac output
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
<1%
72
Tidal volume = ____ + ____
Dead space ventilation (VD) plus alveolar ventilation (VA)
VA = VE -
VD
73
Alveolar ventilation
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
74
What are four divisions of dead space?
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
75
Bohr's method of measuring dead space measures -----
The volume of lung that does not eliminate CO2, i.e. it measures physiologic and not just anatomic dead space
76
T/F: Alveolar ventilation is decreased by an increase in dead space ventilation, regardless of the cause of the dead space.
True
77
T/F: Venous CO2 levels represent a combination of arterial PCO2, tissue metabolism, and blood flow
True
78
List cardiopulmonary effects of hypercapnia
Decreased cardiac contractility
Decreased systemic vascular resistance
Vasoconstriction of the pulmonary circulation
Bronchodilation
Decreased diaphragmatic contractility
79
In normal animals, venous CO2 is typically ___ - ___ mmHg higher than arterial CO2.
3-6 mmHg
80
Increased difference between venous PCO2 and arterial PCO2 has been associated with:
Decreased cardiac output
Shock
Poor perfusion
81
Normally, end tidal CO2 underestimates PaCO2 by ___ to ___ mmHg. This is a reflection of dead space ventilation.
2-6 mmHg
82
What mechanisms result in oxygen therapy causing a sudden worsening of hypercapnia in a chronically hypercapnic patient?
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)
83
Approximately ____% of the resistance to airflow during inspiration comes from the nares in normal dogs.
80%
84
Traction-avulsion of nasopharyngeal polyps may be associated with a recurrence rate of __-__% which is why VBO is recommended
40-50%
85
In normal dogs, the larynx accounts for only ___% of resistance to airflow during nasal breathing.
6%
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.
Recurrent laryngeal nerve
87
Surgical techniques for laryngeal paralysis are divided into three categories:
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)
88
Post-operative aspiration pneumonia is the most common complication following arytenoid lateralization, occurring in ___-___% of patients.
8-33%
89
Despite complications, ___% of patients experience improvement in respiratory status and stridor postoperatively.
90%
90
Stage/grade I laryngeal collapse
Eversion of the laryngeal saccules
91
Stage/grade II laryngeal collapse
Medial positioning of the cuneiform processes and aryepiglottic collapse
92
Stage/grade III laryngeal collapse
Collapse of the corniculate cartilages
93
Salvage procedure which can be performed for advanced laryngeal collapse (not a permanent tracheostomy)
Arytenoid laryngoplasty
94
Most common nasal neoplasm in dogs? Most common nasal neoplasm in cats?
Dogs: carcinomas/adenocarcinomas > sarcomas
Cats: lymphoma > carcinomas
95
Suspected mechanisms of tracheal collapse
Dorsal trachealis muscle flaccidity
Weakening of tracheal cartilages due to decreased glycosaminoglycan, chondroitin, and calcium content
96
With repeated mucosal contact, the tracheal mucosa undergoes _________ which results in loss of the mucociliary escalator.
Squamous metaplasia
97
Traditional grading of tracheal collapse (I-IV) has each grade resulting in a decrease in tracheal diameter by ___%.
25%
98
Grade IV tracheal collapse also has the additional feature of inversion of the _____ cartilages
Inversion of the ventral tracheal cartilages
99
Animals with tracheal collapse at the level of the ______ can have either/both inspiratory and expiratory signs.
Thoracic inlet
100
The "honking" heard during coughing/panting is classic for collapse/obstruction of the ____ and ____ trachea.
Cervical and thoracic inlet
101
Chrondromalacia tends to result in ___ clinical signs whereas obstructive malformations of the trachea result in ____ clinical signs.
Dynamic
Static
102
Concurrent bronchial collapse has been documented in ___% of dogs with tracheal collapse
83%
103
Tracheal malformations most often occur at the level of the ______ and often appear as a ventral deviation of the tracheal margin on radiographs.
Thoracic inlet
104
Prosthetic tracheal ring placement success rate reported to be ___ - ___ %
75-85%
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.
Coughing
106
Tracheal stent diameter is ___-___% larger than the maximal tracheal diameter as determined under anesthesia.
10-20% larger
107
Collapse of the _____ lung lobe due to mucus plugging can be considered in cats with lower airway disease.
Right middle lung lobe
108
Greater than __% of eosinophils in cat lung wash fluid is abnormal.
>5%
109
Bronchomalacia is defined as >__% collapse of airway luminal diameter.
>50%
110
Cranial lung herniation may be seen in up to ___% of dogs with airway collapse.
70%
111
Normal BAL fluid
70-75% macrophages
5-8% neutrophils, eosinophils, and lymphocytes
112
Which drug can be beneficial in the first 24-48 hours following aspiration to minimize acid-related bronchoconstriction?
Terbutaline
113
Pulmonary hypertension is caused by what three mechanisms?
1) Increased pulmonary blood flow
2) Increased pulmonary vascular resistance
3) Increased pulmonary venous pressure
Or some combination of all three
114
Precapillary PH
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
115
Postcapillary PH
PH associated with increased pulmonary venous pressure (pulmonary venous hypertension) - secondary to increased left atrial pressure
116
Post capillary PH can be "passive" vs. "active" - describe
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.
117
Echocardiography can document which two findings to suggest PH
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
118
In the absence of a RVOTO, estimating systolic PAP on echo involves quantifying peak ________
Tricuspid regurgitation velocity
119
Simplified Bernoulli equation
Pressure gradient = 4 x velocity^2
120
Definition of PH in humans (PAP)
≥ 25 mmHg at rest measured invasively by right heart catheterization
121
PH classifications in veterinary medicine based on pressure gradient between the RA and RV during systole
Mild: 30-50 mmHg
Moderate: 50-75 mmHg
Severe: 75 mmHg
122
Clinically significant PH is unlikely unless clinical signs are present and a pressure gradient of at least ___ mmHg is present.
46 mmHg (flow of 3.4 m/s)
123
Six ACVIM classifications of PH
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
124
Why does documentation of LA enlargement have to be present for PH to be classified as being secondary to left heart disease?
Because LAE is a crude surrogate for documentation of chronically increased LA pressure (postcapillary PH)
125
How do phosphodiesterase 5 inhibitors work?
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
126
Why is PDE5i therapy potentially contraindicated in patients with PH secondary to left heart disease?
Because it can result in worsening of pulmonary edema. Will potentially cause acutely increased right heart cardiac output and thereby increase LA preload.
127
Two main pathophysiologic forms of pulmonary edema
1) High hydrostatic pressure edema (increased pulmonary capillary hydrostatic pressure)
2) Increased permeability edema (damage of the microvascular barrier and alveolar epithelium)
128
Mechanisms of the lung to prevent formation of pulmonary edema
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
129
Main determinant of the formation of pulmonary edema
Hydrostatic pressure
130
Pathway of fluid accumulation/development of edema
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
131
Increased permeability edema
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
132
Lymphatic system
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
133
Potential causes of NCPE
Seizures
Choking
Near drowning
Smoke inhalation
Electrocution
Head trauma
134
What proportion of cats with CHF may have no auscultable murmur?
20%
135
What % of cats with left-sided CHF will have pulmonary edema?
About 50%
136
Proposed mechanism of neurogenic pulmonary edema (NPE)
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
137
Negative pressure pulmonary edema (NPPE) i.e. edema secondary to upper airway obstruction
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.
138
Pneumonia characterized by
Infiltration of PMN leukocytes, edema fluid, erythrocytes, mononuclear cells, and fibrin into the lung
139
Lobar pneumonia
Typically encompasses an entire lung lobe
Spread is believed to be alveolus to alveolus and acinus to acinus through inter alveolar pores
140
Bronchopneumonia
Characterized by distal airway inflammation and alveolar disease
Through to spread through the airways rather than through adjacent alveoli/acini
141
Interstitial pneumonia
The inflammatory process initially occurs within the interstitium rather than alveolar spaces
142
The upper and lower airways provide a first line of defense against inhaled pathogens and contaminated particulate matter:
Anatomical barriers
Cough reflex
Mucociliary apparatus
Secretory IgA
Phagocytic dendritic cells within the basal layer of the respiratory mucosa
143
Particles smaller than ___ micrometers may bypass the upper respiratory tract defenses and get deposited into the alveoli
3 micrometers
144
The bronchoalveolar junction is a major site of all particle (___ to ___ micrometers) deposition and is especially vulnerable to damage.
0.5-3 micrometer
145
Presence of hypercapnia in the case of pneumonia suggests
Fatigue
Bronchoconstriction
Presence of severe pulmonary parenchymal diseases
146
Most common isolates found in dogs with pneumonia (wash samples)
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%)
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
<1.5
>2.4
148
Bacteria commonly cultured from companion animals with aspiration pneumonia
Enteric bacteria: E. coli, Klebsiella spp., Enterococcus spp.
Oropharyngeal Mycoplasma spp.
Primary respiratory pathogens: Pasteurella spp., Pseudomonas spp., Streptococcus spp.
Commensals such as Staph.
149
Viral organisms implicated in CIRD-C
Canine adenovirus 2
Parainfluenza
Canine distemper virus
Canine respiratory coronavirus
Canine influenza virus
Canine pneumovirus
Canine herpesvirus
150
Two important influenza strains in dogs
H3N8
H3N2
More likely to cause hemorrhagic bronchopneumonia than other influenza subtypes
151
Most common bacterial pathogens associated with CIRD-C
Bordetella bronchiseptica
Streptococcus equi subsp. zooepidemicus
Mycoplasma cynos
152
Most commonly isolated organisms associated with foreign body pneumonia
Strep
Pasteurella
Nocardia
Actinomyces
153
The major gas exhange surface of the alveolus is composed of _______ epithelial cells
Type I alveolar epithelial cells
Crucial role in maintaining the permeability function of the alveolar membrane
154
Inciting cause of ARDS
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
155
Explain the acute exudative phase of ARDS
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
156
Fibroproliferative phase of ARDS
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
157
Resolution of ARDS
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
158
Two phenotypes of ARDS
Hyperinflammatory: ~30% of patients, higher mortality rates; more often associated with shock and metabolic acidosis
Hypoinflammatory
159
Diagnostic criteria for ARDS (VetARDS)
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
160
Berlin criteria for ARDS
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
161
What are some lung-protective ventilator strategies and how do they help decrease VILI
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
162
How do contusions happen?
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.
163
Inertial effect
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
164
Spalling effect
A shearing or bursting phenomenon that occurs at gas-liquid interfaces; may disrupt the alveolus at the point of initial contact with shock waves
165
Implosion effect
Rebound or over-expansion of gas bubbles after a pressure wave passes --> tearing of the parenchyma due to over-distention
166
Main mechanism of hypoxia with contusions
Shunting (increased shunt fraction and dead space ventilation)
167
Two bacteria associated with pulmonary hemorrhage
E. coli and Streptococcus equi subs. zooepidemicus
168
T/F: The degree of hypoxemia correlates with the degree of embolization
False
169
Explain the V/Q mismatching that happens with PTE
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
170
Cor pulmonale definition
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.
171
Why is a positive D-dimer test more sensitive for fibrin formation than FDP's?
FDPs indicate either fibrin or fibrinogen degradation products, whereas D-dimers indicate breakdown of cross-linked fibrin.
172
Arterial blood gas analysis with PTE
Hypoxia
HyPOcapnia
173
Westermark sign
Focal peripheral hyperlucency secondary to oligemia resulting in a collapsed appearance of vessels distal to the occlusion
174
McConnell's sign
Akinesia of the right mid ventricular free wall with normal contractility at the apex - highly specific in humans for PTE
175
Drugs for treating VENOUS thromboembolism
Heparin (LMWH)
Direct factor Xa inhibitors (i.e. rivaroxaban)
176
Accessory inspiration muscles
Scalenes
External intercostals
Sternomastoids
177
What is the maximum number of ribs which can be resected surgically?
6
178
Flail chest definition
Series of three or more rib fractures in a row, where both the dorsal and ventral aspects of the affected ribs are fractured
179
The main nerves that innervate muscles of respiration arise from cervical segments ___-___
C4-7P
180
Presynaptic neurotoxin in Elapid venom
Phospholipase A2 - prevent release of acetylcholine
181
Postsynaptic neurotoxin in Elapid venom
Antagonizes acetylcholine receptor
182
Acute pre-paralytic signs of Elapid envenomation in dogs
Vomiting
Hypersalivation
Nausea
Urination/defecation
183
T/F: Dogs with Campylobacter are more likely to develop acute polyradiculoneuritis
True - 9.4 times more likely
184
How does botulinum toxin result in paralysis?
Botulinum toxin inhibits acetylcholine release at the synaptic terminal by blocking presynaptic acetylcholine vesicle fusion with the terminal membrane
185
Are cranial nerve abnormalities present with botulism?
Yes- may help differentiate botulism from other LMN diseases
186
Animals with MG may present with respiratory distress for two reasons
1) Secondary to hypercapnia/hypoxemia from decreased chest wall excursions or aspiration pneumonia secondary to megaesophagus
2) Overdose of cholinesterase inhibitors
187
What is the average intrapleural pressure
-5 cm H2O
188
What percentage of cats may be normothermic or hypothermic on presentation and still have a pythorax?
50%
189
What is a glide sign
The visceral and parietal pleura moving past one another
190
What is a curtain sign
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
191
Suggested criteria for removal of chest tubes in patients with prothorax
Clinical improvement
Resolution of infection on cytology
<2 mL/kg/day fluid production
192
After how many days did infection develop in dogs with experimentally placed chest tubes?
4-6 days
193
Overall survival rates for dogs/cats with pyothorax
83% in dogs, 63% in cats
194
Pure transudate protein level vs. modified transudate/exudate protein level
Pure transudate <2.5 g/dL
Modified transudate/exudate ≥2.5 g/dL
195
Effusion triglyceride values compared to serum for chylous effusion
Often greater than 3:1 (effusion:serum), or ≥100 mg/dL in the effusion
196
How does rutin supposedly work?
Rutin is a benzopyrone that is theorized to increase lymphatic fluid uptake, reduce blood vessel permeability, and increase macrophage phagocytosis of protein in lymph
197
Hemothorax is defined as a pleural effusion with at least ___% of the PCV of the peripheral PCV
25%
198
What is one of the reasons effusions can develop with FIP?
Pyogranulomas form around venules
199
What ratio of pleural effusion to serum bilirubin is consistent with bilothorax?
>1:1
200
What ratio of pleural effusion to serum creatinine is consistent with urothorax?
>1:1
201
Most common cause of spontaneous pneumothorax in cats
Airway disease
202
Most common cause of traumatic pneumothorax in cats
High rise syndrome
Bite wounds
203
Six physiologic benefits of HFNO
H- Heated and humidified
I- Inspiratory flow demands
F- Functional reserve capacity
L- Lighter
O- Oxygen dilution
W- Wash out dead space
204
Preferred temperature of HFNO for comfort
31*C
205
Amount of PEEP provided by HFNO
Variable; may be more or less than the reported 1 mmHg PEEP for every 10 L/min
206
Equation of motion
Pvent + Pmuscles = Elastance x Volume x Resistance x Flow
*Elastance is the inverse of compliance
207
Resistance
The pressure required to generate a given flow
208
Compliance
The change in lung volume for a given change in pressure
= ΔV/ΔP = Vt/pressure required to achieve Vt
209
The three variables that the ventilator is responsible for
Pressure
Volume
Flow
210
Cycle variable
Terminates the breath
211
Limit variable
Parameter that the breath cannot exceed during inspiration - does not terminate the breath
212
Common/ideal I:E ratio
1:2
213
What is rise time?
The time in which the airway pressure increases from baseline to peak pressure
214
Low tidal volume decreases which aspects of VILI
Barotrama
Volutrama
Biotrama
215
Five main components of smoke inhalation injury
Upper airway injury
Lower airway injury
Pulmonary parenchymal injury
Systemic injury
Systemic toxicity
216
Upper airway injury in smoke inhalation
Temperature (can exceed 300*F)
Direct thermal injury --> edema and inflammation (usually peaks 24 hours post exposure)
217
Pulmonary parenchymal injury
Classically delayed
Increased transvascular fluid efflux, lack of surfactant and loss of hypoxic pulmonary vasoconstriction result in impaired oxygenation
218
Lower airway injury in smoke inhalation
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
219
Systemic injury
Corneal injury
Hypercoagulability
Left ventricular dysfunction
Hypotension (especially if CO present)
Most toxic compounds present in smoke are carbon monoxide and cyanide
220
Carbon monoxide
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
221
Hydrogen cyanide
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
222
Cherry red MM
High levels of COHb
223
Hyperlactatemia and smoke inhalation
Hyperlactatemia in a patient with otherwise adequate perfusion raises concern for CO
224
Pulse oximetry and smoke inhalation
Regular pulse ox cannot differentiate oxyhemoglobin from COhemoglobin
225
CO half life and effect of oxygen on half life
Normal CO half life 320 minutes in a patient breathing room air; goes down to 70 minutes if breathing 100% oxygen.
226
Antidotes to cyanide
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
227
Drowning definition
A process resulting in primary respiratory impairment from submersion or immersion in a liquid medium. Liquid is present in the victim's airway.
228
Dry drowning definition
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
229
Most survivors of drowning in human medicine are thought to have aspirated less than __ mL/kg of fluid
<22 mL/kg
230
Hypoxemia in drowning victims results from _____
Intrapulmonary shunting
231
In humans, about ___% of all victims experience severe neurologic effects.
10%
232
Submersion in ice cold water <___*F increases the chances of survival due to the ____ reflex.
<41*F
Diving reflex
233
Diving reflex
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
234
Three factors associated with 100% mortality in human drowning victims under the age of 20
1) Submersion duration longer than 25 minutes
2) Resuscitation duration longer than 25 minutes
3) Pulseless cardiac arrest on presentation to the ED
235
What percentage of trauma-induced upper airway rupture dogs had SQ emphysema at presentation to the ER?
80%
236
What percentage of cats with pneumomediastinum had SQ emphysema?
66%
237
T/F: In dogs and cats the mediastinum is usually fenestrated
True
238
The Macklin effect
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
239
How can provision of oxygen therapy hasten recovery of pneumomediastinum and SQ emphysema?
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.
240
The mass median diameter (MMD) of a particle must be less than ___ µm to reach the small bronchioles and alveoli
< 5 µm
241
Particles larger than ___ µm are deposited in the larynx and nasal turbinates.
>10 µm
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.
2-3%
243
Feline hemoglobin has a lower/higher affinity for oxygen compared to dog and human blood.
LOWER (P50 is 34-36 mmHg compared to dogs which is 28-31 mmHg)
244
What is the Beer-Lambert law?
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.
245
What is the main technological method for pulse oximetry?
Spectrophotometry
246
What species of hemoglobin do co-oximeters detect?
Oxyhemoglobin
Deoxyhemoglobin
Carboxyhemoglobin
Methemoglobin
247
Which two wavelengths of light does a pulse oximeter emanate?
660 nm - red light
940 nm - infrared light
248
What basic property of the functional hemoglobins does a pulse oximeter detect
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.
249
Above what point does the oxygen hemoglobin dissociation curve flatten out?
Above SpO2 97%
250
How does methemoglobin affect pulse ox reading?
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
251
The ligament you incise when making a tracheostomy is called _____
The annular ligament (exists between the rings)
252
Tracheostomy site should account for no more than ____% of the tracheal diameter
50%
253
What is a long-term consequence of performing a vertical incision for tracheostomy?
Long term segmental tracheal collapse
254
How often should tracheostomy tubes without an inner canula be changed?
Every 24 hours
255
Using a three-bottle suction technique, which chamber determines the suction pressure?
The third one- fill the water to the desired pressure
256
Chest tube removal criteria
Ideally, no air should be removed for 24 hours prior to removal
Ideally less than 2 mL/kg/day fluid production x 24 hours
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
Decrease in partial pressure
