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VTS ECC 2024 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Upper Respiratory tract anatomy

#5

A
  1. Nostrils
  2. Nasal passages - contain Turbinates
  3. Pharynx -throat
  4. Larynx -voice box
  5. Trachea
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2
Q

Lower Respiratory Tract anatomy

#4

A
  • Bronchi
  • Bronchioles
  • Alveolar ducts
  • Alveoli
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3
Q

Primary Respiratory function

A

take in oxygen and remove carbon dioxide from the blood through the blood–gas barrier

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4
Q

Secondary Respiratory Functions

#4

A
  1. Physical defense against: inhaled particles, pathogens, immune functions
  2. Metabolizing of compounds
  3. Dissipating heat
  4. Serves as reservoir for blood
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5
Q

Respiratory Anatomy Zones

What % does each make up?

A

Two Zones:
Conducting = trachea branching → bronchi, segmental bronchi → terminal bronchioles, (none of which contain any alveoli) only serves to deliver air to the respiratory zone
– 5% of lung volume
Respiratory = Bronchioles and alveolar ducts; responsible for gas exchange
– 95% of lung volume

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6
Q

Anatomical Dead Space

A

Conductive airway
-Does not participate in gas exchange

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7
Q

Diaphragm Respiratory functions

A

–Contracts caudally to elongate the chest cavity longitudinally, and the intercostal muscles contract to enlarge the circumferential size of the chest cavity = creates negative pressure to pull air through conductive airway = ventilation
–Moves back cranially during passive exhalation process

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8
Q

Pulmonary Vasculature

A

–branches from pulmonary artery to pulmonary capillaries in alveoli
– then converge back to pulmonary vein/heart to circulate to the rest of the body

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9
Q

Alveoli blood-gas barrier

A

– capillary mesh network lines alveoli wall to allow for maximum efficieny of gas exchange
– Other side of barrier consists of vessels with circulating blood flow
– @ capillary level; single cell wall thickeness just large enough to allow RBCs to pass through

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10
Q

“Work of breathing”

A

Energy expended to created pressure gradient that allows airflow easily in and out of the lungs
– Air flows from high-pressure region (mouth/nouse) to low-pressure (lungs)

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11
Q

Lung inflation is dependent on what?

A

Compliance and resistance

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12
Q

Lung Compliance

A

– Ability of the lungs to expand
– determined by elasticity or tendancy of form to return to its original state

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13
Q

Respiratory system’s role with thermoregulation

A

– network of superficial blood vessels under epithelium in nasal passages help warm inhaled air before reaching lungs
–helps prevent hypothermia
– panting helps facilitate cooling with hyperthermia via increased evaporation of fluid from the lining of the respiratory passages and mouth → helps cool the blood circulating just beneath the epithelium

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14
Q

Respiratory system’s role with pH

A

contributes to acid–base control by its ability to influence the amount of CO2 in the blood
– inverse relation with pH, (high = low pH, low = high pH)

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15
Q

What does CO2 dissolve into?

A

CO2 dissolves in the plasma to form carbonic acid [H2CO3]

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16
Q

Anatomy/Function of nasal passages

#4

A

– pseudostratified columnar epithelium with cilia projecting from the cell surfaces
– layer of mucus that is secreted by many mucous glands and goblet cells
–houses the receptors for the sense of smell
– Responsible for warming, humidifying, and filtering inhaled air

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17
Q

Act of swallowing pathway

A

epiglottis covers the opening into the larynx →
move the material to be swallowed to the rear of the pharynx →
open the esophagus, and move the material into it
Once swallowing is complete, the opening of the larynx is uncovered and breathing resumes.

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18
Q

Common abnormalities with Brachycephalic breeds

A
  1. nostrils that are too narrow (stenotic nares)
  2. soft palate that is too long (elongated soft palate)
  3. trachea that is not wide enough (tracheal hypoplasia)
  4. breathing struggles can lead to gastrointestinal signs such as regurgitation and vomiting of material
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19
Q

Anatomy of the Larynx

A
  • segments of cartilage connected to each other and the surrounding tissues by muscles
  • supported in place by the hyoid bone
  • Major cartilages include; single epiglottis, paired arytenoid cartilages (supports vocal cords), single thyroid cartilage, and single cricoid cartilage
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20
Q

Larynx role with breathing

#3

A

–Small adjustments aid the movement of air as the animal draws air into its lungs and blows it out
– protects airway from inhalation of material
–closes to build pressure before cough relfelx

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21
Q

Anatomy of Trachea

Type of muscle, epithelium present

A

– tube of fibrous tissue and smooth muscle held open by hyaline cartilage rings “C rings”
– lined by the same kind of ciliated epithelium that is present in the nasal passages
–mucous layer on its surface traps tiny particles of debris that made it further down respiratory tract
–cilia that project up into the mucous layer move the trapped material up toward the larynx to be coughed up and swallowed

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22
Q

Tracheal Collapse

How does it affect breathing?

A

– narrow space between the ends of several of the C-shaped tracheal rings is wider than normal
– with inhalation → widened area of smooth muscle gets sucked down into the lumen of the trachea and partially blocks it
–inspiratory dyspnea

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23
Q

2 benefits

Surfacant definition

A

thin layer of fluid that lines each alveolus
– helps reduce the surface tension (the attraction of water molecules to each other) of the fluid
–prevents alveoli from collapsing

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24
Q

Asthma

A

Disease that causes the bronchial tree to become overly sensitive to certain irritants
–Results in inflammation causing thickening of the lining of the air passageways, excess mucus production, and bronchoconstriction
– chronic disease of the small airways (bronchioles) within the lungs

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25
Q

Anatomy of Mediastinum

A

Area between the lungs
– contains rest of thoracic structures; heart, large blood vessels, nerves, trachea, esophagus, lymphatic vessels, and lymph nodes

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26
Q

Anatomy

Hilus definition

A

Medial side of the lung lobe where air, blood, lymph, and nerves enter and leave the lung
– only “fastened” area of the lung whereas the rest is “free” within the thorax

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27
Q

Anatomy

Pleura definition

A

Thin membrane that covers the organs and structures within the thorax
–divided into two layers; viseral and parietal
– smooth surfaces of the pleural membranes lubricated with the pleural fluid to ensure that the lungs, slide along the lining of the thorax smoothly during breathing

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28
Q

Anatomy

Visceral layer of the Pleura

A

Membrane covering organs and structures themselves

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29
Q

Anatomy

Parietal layer of Pleura

A

Layer that lines the body cavity in thorax

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30
Q

How does negative intrathoracic pressure facilitate breathing?

A

– System functions like a bellows, pulling air in and out of lungs
– Lungs follow passively as movements of the thoracic wall and diaphragm alternately enlarge and diminish the volume of the thorax

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31
Q

How does negative intrathoracic pressure help facilitate blood flow?

A

– aids the return of blood to the heart
–pulls blood into the large veins in mediastinum = cranial vena cava, caudal vena cava, and pulmonary veins
–pressure helps draw blood from the midsize veins into these large veins, which then dump the blood into the right and left atria (receiving chambers) of the heart

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32
Q

Pneumothorax

A

Air leaks into the pleural space (the space between the lungs and the thoracic wall) = negative pressure is lost
–Results in areas of the lung collapsing

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33
Q

Muscles involved with Inspiration

A

diaphragm and the external intercostal muscles
–external intercostal muscles located on the external spaces between the ribs

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34
Q

Muscles involved with Expiration

A

internal intercostal muscles and the abdominal muscles
– internal intercostal muscles located inbetween ribs
–abdominal muscles push contents onto caudal side of diaphram to push it forward and decrease thorax size

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35
Q

Tidal Volume

A

Tidal volume is the volume of air inspired and expired during one breath

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36
Q

Minute Volume

A

Minute volume is the volume of air inspired and expired during 1minute

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37
Q

Residual Volume

A

Residual volume is the volume of air remaining in the lungs after maximum expiration
– The lungs cannot be completely emptied of air; residual volume always remains.

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38
Q

Pathway of Gas Exchange

A

Inspiration = Inhaled air contains a high level of oxygen and a low level of carbon dioxide
→ Blood entering the alveolar capillary contains a low level of oxygen and a high level of carbon dioxide.
Gas exchange = O2 diffuses from the air in the alveolus, high (into the blood in the alveolar capillary) to low. CO2 does the reverse, diffusing from the alveolar capillary into the alveolus
Expiration = Exhaled air contains less oxygen and more carbon dioxide than is present in room air. Next breath brings in a fresh supply of high-oxygen air.

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39
Q

Partial pressures of Gases

A

amount of a particular gas that dissolves in liquid exposed to a gaseous environment is determined by the partial pressure of the gas in the gaseous environment
– blood moving through the alveolar capillaries (the liquid) is affected by the partial pressures of O2 and CO2 in the alveolar air (the gaseous environment)

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40
Q

Control of Breathing

Respiratory center

A

Area in the medulla oblongata of the brainstem
– Contain individual control centers for functions such as inspiration, expiration, and breath holding

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41
Q

2 systems for Control of Breathing

A

Mechanical system : sets routine inspiration and expiration limits
Chemical system : monitors the levels of certain substances in the blood and directs adjustments in breathing

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42
Q

Control of Breathing

Mechanical control system

what does it utlize to operate?

A

Operates through stretch receptors in the lungs that set limits on routine breathing, resting, inspiration, and expiration
–Respiratory center sends out the appropriate nerve impulses to start and stop inspiratory/expiratory process.
–Senses preset inflation and deflation in lungs

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43
Q

Control of Breathing

Chemical Control system

A

Monitors the blood and only affects the breathing pattern if something gets out of balance
Chemical receptors in blood vessels constantly monitor various physical and chemical characteristics of the blood
* located in the Carotid artery/Aorta and in the brainstem
* CO2content, pH, and the O2content of the arterial blood important for Chemical response

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44
Q

Oxygen Toxicity

What can it cause?

A

Condition resulting from the harmful effects of breathing molecular oxygen at increased partial pressures
–can result in cellular damage affecting CNS, lungs and eyes

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45
Q

O2 molecule make up

A

Pair of O2 molecules bound w/ 2 electrons

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46
Q

Free Radicals

A

Unbound electrons that are highly reactive

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47
Q

Reactive Oxygen and Nitrogen Species

How does it lead to oxidative injury?

What is it a product of?

A

RONS
natural by products of normal O2 metabolism
–Important for cell signaling and homeostasis
–Excess accumulation of RONS taken care of by antioxidants
–Oxidative injury occurs when body’s capability to metabolize RONS becomes exhausted = dangerous levels of RONS (can be caused by endogenous or exogenous sources)

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48
Q

Endogenous Sources of oxidative injury

#6

A
  1. Aerobic exercise
  2. Excessive O2 in tissues compared to antioxidant defences
  3. Free electron production from NADPH in neutrophils/macrophages
  4. Ischemic reperfusion injury
  5. Iron/Copper
  6. Oxidation of Hb to Methemoglobin
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49
Q

Exogenous Sources of Oxidative Injury

#6

A
  1. Ionized Radiation
  2. Environmental background radiation
  3. Ultraviolet radiation
  4. Pollution
  5. Paraquat toxicity
  6. Bleomycin toxicity
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50
Q

Oxidative Injury

Superoxide Anion

A

When remaining O2 undergoes partial reduction and leaks into cytoplasm from oxidative injury → becomes O2-
–precursor to most Reactive Oxygen Species (ROS)
–O2- → H2O2 (highly toxic) → H2O via reaction catalyzed

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51
Q

Oxidative injury

Fenton/Haber-Weiss reaction

A

Most cytotoxic oxidative pathways
–dependent on availability of H2O2, Iron, and copper
– produces = OH free radical (one of the most toxic ROS

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52
Q

Oxidative injury

Myeloperoxidase Reaction

A

Hydrogen Peroxide can react w/ Cl- to form hypoclorus acid (HOCl → not ROS, precursor to free radicals)
–occurs with pahgocytic vesicles of neutrophils

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53
Q

Oxidative Injury

Reactive Nitrogen Species

A

NO (nitric oxide) potent endogenous vasodilator, celll messenger and platelet inhibitor
–can have cytotoxic efx in large quantities (ex. reperfusion injury)

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54
Q

Cellular Effect of Oxidative Injury

A

Lipid perioxidation: lipids most susceptible to oxidative injury
–Major source of of cellular injury = ↑ cell membrane permeability
* inhibits normal cellular enzyme process
* damage to proteins, intracellular membrane, capillaries, and alveoli
–Two main free radicals that initiate lipid perioxidation = OH and ONO2-

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55
Q

Oxidative Injury

Nucleic Acids

A

Oxidative stress causes DNA/RNA damage/mutations
–contributes to aging/carinogenesis

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56
Q

Protein damage from Oxidative Injury

A

Oxidative stress due to ↓ production 2nd to inhibition of ribosomal translation
–AA most susceptible
–Impairments of cellular signaling/metabolism

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57
Q

Role of Inflammation with Oxidative Injury

what is released?

A

–Necrosis/apoptosis
–relase DAMPs (damage associated molecular pattern molecules)
–DAMPs activate polymorphonuclear neutrophils = contribute to cytokine release, monocyte recruitment, stimulate inflammatory response,
–ultimately contribute further to RONS production = oxidative injury

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58
Q

Oxidative Injury

Ischemia-reperfusion Injury; early stages

how does it affect celluar metabolism?
Results in build up of?

A

Ischemia = anaerobic metabolism → accumulation of intracellular lactate and H+
–** less ATP available for ATP dependent pumps** = net efflux of K+ and influx of Na+/Ca++/Cl- = cell swelling
–High intracellular Ca++ associated with early IRI = cell apoptosis/necrosis and Xanthine oxidoreductase system

Ex; GDV with myocaridal injury, ATE

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59
Q

Oxidative Injury

How does Ischemia occur?

A

Depletion of NO = vasoconstriction, decrease perfusion and cellular injury

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60
Q

Oxidative Injury

What happens during reperfusion after ischemia?

A

↑ in NO production = cytotoxic = severe nonresponsive vasodilation
–release of ROS
– NO and O2 combines into ONO2- = further cellular injury

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61
Q

Oxidative Injury

Xanthine oxidoreductase system

A

Causes significant cellular injury in IRI
–Intracellular Ca++ with reperfusion = start of XOS
–sudden ↑ in O2 delivery = combines with NAD = xanthine + uric acid production
* GI and endothelium highly susceptible to IRI

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62
Q

Oxidative injury

Clinical Signs with IRI

#4

A

HyperK+
myocaridal stunning
CNS changes
MODS

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63
Q

Oxidative Injury

“NO Flow” phenomenon

A

After resolution of occulsion theres a ↓ perfusion due to leukocyte adhesions; platelet-leukocyte aggregation and ↓ endothelium - dependent vasorelaxation

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64
Q

Oxidative Injury

Clinical Efx of Hyperoxia

#5

A

lungs → most affected due to high exposure levels
–causes apoptosis/necrosis of pul. parenchymal cells
–inflammation
– NCPE
– impaired gas exchange
–fibrosis

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65
Q

Efx of Hyperoxia on pneumocytes

A

Type I penumocytes of alveolar epithelium are lost → replaced with type II (surfactant secreting) that is resistant to O2
–contributes to thicker alveolar/capillaires
–diffusion impairment

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66
Q

Oxidative Injury

Alveolar collapse from Hyperoxia

What causes it?
This results in =

A

–Nitrogen displaced by 100% O2 = absorptive ateletasis
– ↑ alveolar O2 = rapid diffusion of O2 from alveoli to pul. circulation =contributes to atelectasis
–induces surfacant impairment

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67
Q

Oxidative Injury

How does Hyperoxia predipose pts to 2nd infections?

A

↓ mucociliary clearance and changes pulmonary microbial flora/immune function
–in people Hyperoxia from 3hrs on 100% O2 will cause ↓ mucociliary clearance

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68
Q

Oxidative Injury

CV effects of Hyperoxia

A

– ↑ SVR, vasoconstriction 2nd to ↓ NO bioavailability
– Vasoconstrictive efx cause baroreceptors to ↓ HR with no change in SV = ↓ CO
– ↓ perfusion to vital organs

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69
Q

Oxidative Injury

CNS effects of Hyperoxia

x3

A

↓ cerebral blood flow 2nd to hypoxic vasconstriction
–will also ↓ ICP
– may cause ↑ cerebral excitotoxicity

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70
Q

O2 targets with MV

A

PaO2 55-80
SpO2 88-92%

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71
Q

Hyperbaric O2 therapy

MOA, uses, possible complications

A

pressurized 100% O2 therapy
–Hb becomes completely saturated with O2 = further O2 diffusion into circulation = ↑ PaO2
–unbound O2 (not attached to Hb) diffuses much more readily into tissues and areas not accessible to Hb
–Used for; gas embolization, decompression sickness, carbon monoxide toxicity, severe crush injuries, burn injuries, compartment syndrome
–Complications: barotrauma, decompression sickeness, O2 toxicity, Sz (2nd to low cerebral metabolism

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72
Q

Oxidative Injury

Antioxidants

A

Any compound that can delay or prevent oxidation of a substance
–helps protect cells against oxidative injury/DNA mutations/malignant transformation/cell damage
–Depletion can occur with CKD, cardiac dz, hepatic dz, DM neoplasia
–3 categories: Endogenous enzyme, endogenous nonenzyme, exogenous

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73
Q

Oxidative Injury

Endogenous antioxidant enzymes

A

important for preventing oxidative injury
Superoxide dimustase (SOD) glutathione perioxidase

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74
Q

Oxidative Injury

Endogenous nonenzymatic Antioxidants

#8

A
  1. Albumin
  2. Glutathion
  3. Ferritin
  4. Bilirubin
  5. Uric acid
  6. COOq
  7. Vit C/Vit E
  8. Melatonin
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75
Q

Oxidative Injury

Exogenous Antioxidants

#6

A
  1. Vit C
  2. Vit E
  3. beta-carotene
  4. acetycyteine
  5. selenium
  6. zinc
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76
Q

Endothelial Surface layer (ESL)

important functions #4

A

Luminal side of ESL in blood vessels comprised of Glycocalyx with plasma layer
– important for blood-blood vessel and vessel - interstitium interfaces
– important for inflammation modulation, coagulation, vasomotor tone, permeability

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77
Q

Shedding of ESL in relation to oxidative injury

What is it affected by? #6

A

-affected by trauma, inflammation, hyperglycemia, hemodilution, hypovolemia
–Ischemia-reperfusion injury and oxidative stress = endothelial glyclocalyx shedding

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78
Q

Control of Breathing

Respiratory Center

A

Medulla
–neuronal network controls motor neuron activity that innervate respiratory muscles = chagnes to ventilation
–medulla initiates and coordinates control of breathing
–can be interrupted by voluntary control (cortex/hypothalamus)
–or involutary action interruption; swallowing, coughing, sneezing

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79
Q

Control of Breathing

Medulla Respiratory Center

Where is it located?
what is it made up of?

A

Located w/i brainstem
Complex collections form group “pacemaker” system = Central Pattern generator (CPG)
– Concentrated region of neurons w/i medually = pre-Botzinger Complex
* pacemaker neurons categorized based on shape - augmented, decrementing, constant-plateau

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80
Q

3 phases of Respiration: Phase 1

A
  1. Inspiration: sudden onset of activity of inspiratory neurons and augmenting neurons = motor discharge to inspiratory muscles and airway dictators
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81
Q

3 phases of Respiration: Phase 2

A
  1. Post-inspiratory phase (expiratory phase 1): declining motor discharge to inspiratory muscles and passive exhalation
    – expiratory decrementing neurons (in medulla) decrease in activity = mechanical brake to expiratory flow
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82
Q

3 phases of Respiration: Phase 3

Active or passive?
What structures are involved?

A
  1. Expiratory (expiratory II): no inspiratory muscle activity
    –passive with normal breathing
    –can be active (exercise) with expiratory augmenting neuron support (in medulla)
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83
Q

Spontaneous CPG activity

dependent on
similiar to
neurotransmitters involved

A

respiratory rhythmogensis
–dependent on intrinsic membrane properties/neurotransmitters
–similiar to cardiac pacemaker cells → Na+/K+/Ca++ ion channels required for membrane activity
* glutamate (excitatory), GABA/Glycine (inhibitory)
* Influenced by acetylcholine, neuropeptides

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84
Q

Two groups w/i Medulla Respiratory Center: Dorsal Respiratory Group

Primary responsibility
what do they carry?
Which cranial nerves are involved?

A

Dorsal Respiratory Group: primary function = timing of respiratory cycle
–Initiate phrenic nerves in diaphragm
–group terminates at visceral afferents from cranial nerves IX (glossopharyngeal) and X (vagus)
–Carry sensory info that influence Control of breathing (pH, PaCo2, PaO2 from carotid/aortic chemoreceptors)

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85
Q

Medulla Respiratory Center; Ventral Respiratory Group

x3 groups and their functions

A

Consists of inspiratory and expiratory neurons
1. caudal ventral group → expiratory function
* * 2. rostral ventral group → controls airway dilator functions of larynx/pharynx/tongue
3. Pre-Botzinger complex → pacemaker activity + CPG generation
4. Botzinger complex

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86
Q

Pontine Respiratory Group

A

collection of neurons located in the pons → fine tunes breathing pattern via synaptic connections in medulla resp. center
–influences timing of resp. phase/stablizes breathing pattern
–Afferent pathways connected to PRG = cortex, hypothalamus/ nuclease tractus solitarius

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87
Q

Apneusis

when is this typically seen?

A

prolonged gasping inspiratory efforts punctuated by brief inefficient expiratory efforts

can be seen with brain injury in upper pons, possible stroke/trauma

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88
Q

Chemoreceptor

A

type of sensory receptor that responds to alterations in chemical composition of blood or fluid in the area it is immersed in

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89
Q

Central Chemoreceptors for respiration

location, responds to

A

Located in Medulla
–primarily responsible for response to CO2/pH changes in brain
–DOES NOT respond to PaO2 changes
– Interstial fluid in brain in contact with CSF = changes in pH of CSF/brain interstitial fluid affect ventilation
– 60-80% of response to CO2

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90
Q

Blood Brain Barrier relation with CO2

A

–impermeable to H+ and HCO3 ions
–CO2 can diffuse freely across BBB
–CSF/brain interstitium lack buffering system
– ↑ PaCo2 = ↑ H+ = ↓ pH of brain fluid = ↑ RR/depth to return PCO2 to normal

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91
Q

Peripheral Chemoreceptors

location, stimulants, effects

what do they respond to?

A

Located w/i carotid bodies and aoritc bodies
–carotid = primary respiratory response
–aortic = influence circulation
–fast response to change in PaO2/PaCO2/H+
–Responds to ↓ PaO2 rather than O2 content = little response from anemia/dyshemoglobinemia
– ↑ body temp = cause stimulation and enhance ventiltory responses to changes in O2 and CO2
–may result in bradycardia, hypertension/ ↑ bronchiolar tone and secretions of catecholamines

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92
Q

O2 sensing cells

A

Type I glomus
highly vascularized peripheral chemoreceptors

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93
Q

Chronic Respiratory Dz response to Hypercapnia

A

with chronic respiratory dz/hypercapnia
the response to elevated PCO2 becomes reduced
– leading to hypoxemia becoming primary stimulus for ventilation
– supplemental O2 for chronic hypercapnic pts depresses hypoxic respiratory drive = severe hypoventilation and resp. failure

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94
Q

Pulmonary Stretch Receptors

where are they found?
what does it stimulate?

A

slow adapting receptors present in smooth muscle of airway
–activate in response to excessive/sustained distention of lung
–transmits info to respiratory center (inspiratory center of medulla/PONS)
–stimulate protective feedback loop “Hering-Brever inflation Reflex”

95
Q

Lung Airway Receptors

A

Irritant receptors
J receptors

96
Q

Irritant Airway receptors

where are they located? what is it activated by? what do they cause?
which cranial nerves are involved?

A

located in epithelium of nasal mucousa, upper airways, tracheobronchial tree, alevoli
–activated by noxious gases inhaled dust, cold air, and chemical/mechanical things
–transmit info via myelinated vagal afferent fibers
–causes bronchoconstriction, cough, laryngeal spasm, mucous secretion, ↑ RR/depth
–afferent pathway in nasal mucosa signals trigeminal/olfactory tracts = sneezing

97
Q

J Airway receptors

located, stimulated by

which cranial nerves is involved?

A

Juxtacapillary receptors
–located in pulmonary interstitium close to capillaires
–stimulated by capillary distension/edema
–slow transmit via C fibers of vagus nerve = rapid shallow breathing pattern or apnea

98
Q

Arterial Airway baroreceptors

A

**primarily involved with circulation regulation
– hypotension sensed by aortic/carotid baroreceptors = reflex hyperventilation
– hypertension = hypoventilation

99
Q

Muscle/Joint/Tendon Respiratory receptors

A

Respiration muscle/rib joints respond to changes in lenth/tnesion = feedback regarding lung volume + WOB

100
Q

Pain/temperature receptors affecting airway

A

Proprioception receptors send info via ascending spinal cord pathways = influence breathing
–painful stimuli detected by nociceptors = initial apnea then hypoventilation

101
Q

Causes of Hypoxemia

#5

A
  1. Hypoventilation
  2. V/Q mistmatch
  3. Diffusion impairment
  4. Low FiO2
  5. Intrapulmonary shunt
102
Q

Arterial O2 Content

A

CaO2
depends on concentration of Hb and binding affinity of O2 saturation of Hb (SaO2) present
–majority of arterial O2 delievery to tissues is bound to Hb
–small fraction is dissolved or unbound = 0.003 x PaO2 in plasma

(1.34 x Hb x SaO2) + (PaO2 x 0.003)

103
Q

What section of trachea is tracheotomy performed?

A

between 3rd-5th tracheal ring

104
Q

How long should FiO2 levels > 50% be administered?

A

No longer than 24-72 hrs

105
Q

What do arterial blood gasses asses?

A

pulmonary function

106
Q

What do venous blood gases asses?

A

reflection of tissue function

107
Q

PaO2 definition

A

partial pressure (vapor pressure) of O2 dissolved in solution in plasma of arterial blood
– Ability of lungs to move O2 from atmosphere to blood @ sea level

108
Q

SpO2 definition

A

Red to infrared light oximeter measurement
Oxyhemoglobin (O2 + Hb) and deoxyHb (Hb not bound to O2) absorbs light @ different wavelengths
–amount absorbed measured with each wavelenth expressed as %
–2 waveforms = 660 and 940nm
–Poor perfusion can affect SpO2 = inaccuracy
–LATE indicator of hypoexmia
–CarboxyHb (carbon monoxide + Hb) = perfect SpO2 readings b/c Hb is occupied by CO BUT has no O2 carrying ability
–MetHb = falsely lowers SpO2
–anemia = may have N Spo2 but with significantly low O2 carrying capacity = low DO2

109
Q

Oxygen-hemoblobin Dissociation Curve

A

SO2/PO2 relationship
–degree of hemoglobin saturation w/ O2 determined by PO2 and relation to SO2
–small changes in SO2 (oxygen saturation) = large changes in PaO2 and vice versa
–affected by numerous physiological factors that can alter Hb’s affinity for O2

110
Q

Correlation of PaO2 and SaO2

A

Hyperoxemia = PaO2 > 125 = SaO2 100%
Normoxemia = PaO2 80-125 = SaO2 95-99%
Hypoxemia = PaO2 < 80 = SaO2 < 95%
Severe hypoxemia = PaO2 < 60 = SaO2 < 90%

111
Q

Severe Hypoxemia

A

PaO2 < 60 SaO2 = 90%
– level when Hb is still 90% saturated
–PaO2 (not Hb) Drives O2 diffusion into mitochondria
–PO2 (partial pressure of oxygen in blood) = driving force
– SO2 (Hb O2 saturation) = reservoir that prevents rapid ↓ in PO2

112
Q

Factors that affect O2/Hb Dissociation Curve

A

pH
Temp
PCO2
2,3 DPG

113
Q

Left shift in O2/Hb Dissociation Curve

#6

A

O2 has MORE attachment to Hb - less available for unloading to tissues
–HypOthermia, Alkalosis (H+↓, pH ↑), Carbon monoxide poisioning, hypOcapnia, ↓ 2,3 DPG

114
Q

Righ Shift in O2/Hb Dissociation Curve

#4

A

O2 has LESS attachment to Hb = greater ability to unload O2 into tissues
– HypERthermia, Acidcemia (H+ ↑ pH ), hyPERcapnia, upregulation of 2,3 DPG 2/ anemia

115
Q

2,3 DPG definition

A

a salt in RBCs that play role in liberating O2 from Hb in peripheral circulation

116
Q

Cyanosis

A

gray-bluish discoloration of mm signaling presence of deoxygenated Hb
–seen @ 5g/dl Hb concentration
– Late sign of severe hypoxemia ex: if pt is anemic pt will die of hypoxemia before cyanosis is ever seen

117
Q

Mechanisms of Hypoxemia

#4

A
  1. low inspired O2
  2. Hypoventilation
  3. Venous admixture
  4. Reduced venous O2 content 2nd to low CO and slow peripheral blood flow (shock) OR high O2 extraction (sz)
118
Q

Venous Admixture

A

way which venous blood can get from R side to L side of circulation w/o proper oxygenation

119
Q

Mechanisms of Venous admixture

x4 examples

A
  1. low V/Q regions = mod - severe diffuse lung dz (pneumonia/edema)
  2. No V/Q regions = Atelectasis
  3. Diffusion defects = mod-severe diffuse lung dz (O2 toxicity, smoke inhalation, ARDS)
  4. R → L PDA, intrapulmonary A-V anatomic shunts
120
Q

Low Alveolar O2 due to reduced O2 delivery to alveoli

examples

A

Low inspired O2 (ex. high altitude, or apparatus use)
Hypoventilation (ex: PaCO2 >45, low MV)

121
Q

Decreased efficiency of transport of O2 from Alveoli TO pulmonary capillaries

A

Low V/Q regions (ex: 2nd to airway narrowing or alveolar fluid accumulation)
Diffusion Impairment (ex: thickened resp. membrane, O2 toxicity, ARDS progression)
R to L Shunt(ex: congenital defects)

122
Q

Low Alveolar O2 due to ↑
extraction of O2 FROM Alveoli

A

Zero V/Q regions (ex: small airway, alveolar collapse from fluid accumulation)
Low venous O2 content

123
Q

4 gases in alveoli

A
  1. O2
  2. CO2
  3. Water vapor
  4. Nitrogen
124
Q

Regions of Low V/Q

x3 examples

A

– 2nd to small airway narrowing or alveolar fluid accumulation = impairs ventilation (some gas exchange maintained)
– High Q from pulmonary embolism
–bronchspasm, fluid accumulation in lower airways

125
Q

Regions of Zero V/Q

A

Small airway and alveolar collapse
–dz associated with transudate/exudate/blood fluid accumulation
– animals that may be recumbent for prolonged periods of time w/o deep breaths
–physiological shunt = blood bypasses all alveoli despite function
–Fixed with PPV or PEEP

126
Q

Diffusion Impairment

A

Interstitial fluid build up causes airway narrowing and ↑ alveolar surface tension
–low V/Q or Zero V/Q
–Diffusion defect = flate type I alveolar pneumocytes proliferate across surface of gas exchange site

127
Q

Alveolar - Arterial PO2 Gradient

A

Difference between calculated PAO2 and measured PaO2
–assess oxygen ability of lungs on room air
– N = 15 or less
– abnormal value = problem of O2 getting from alevoli into the blood

PAO2 - PaO2

128
Q

120 rule

A

@ 21% FiO2 @ sea level N PaCO2 = 40 and PaO2 = 80 = 120 mmHg
Hypoventilation = PaCO2 ↑ from 40 to 60 and PaO2 = 60
–conclusion is hypoxemia is from hypoventilation

129
Q

P/F Ratio

A

PaO2/FiO2
N= 500
(105/0.21)

130
Q

Oxygen Ratio

A

Evaluating oxygenation in ventilated patients
-account for Mean Airway Pressure (MAP)
– Lower # = better function

MAP x 100 x FiO2 / PaO2

131
Q

How is CO2 created?

A

Product of aerobic metabolism
–produced from internal cellular respiration primarily in mitochondria
–combines with H2O = carbonic acid → dissolves into H+ ion and Bicarbonate
– pulmonary capillaries where CO2 diffuses into alveoli

CO2 + H2O = H2CO3 = HCO3 + H

132
Q

Most common cause of hypercapnia?

A

Hypoventilation 2nd to Low MV

133
Q

Tidal Volume

A

Tidal volume is the volume of air inspired and expired during one breath
–dead space volume and volume of fresh gass entering alveoli for gas exchange

134
Q

“Dead Space” Definition

A

Portion of the tidal volume that does not participate in gas exchange
Characterized as:
1. Apparatus = circuit from the Y-piece to the nose of the patient comprises apparatus dead space
2. Anatomic = conducting airways from the nose to the level of the alveoli
3. Alveolar = alveoli that are ventilated but not perfused in pulmonary capillaries

135
Q

Physiological Dead Space

What parts are involved?
when does it become increased?

A

Anatomic + Alveolar dead space
–sum of portions that do not participate in gas exchange
–normally should be about the same as anatomic dead space however with V/Q inequality → PDS increases due to increase in alveolar dead space

136
Q

Fowlers Method

A

Used to measure dead space ventilation
–concentration of exhaled tracer gas (NO) over time following breath w/ 100% O2
– NO is in expired gas and ↑ with dead space

137
Q

Bohrs Method

A

Dead Space ventilation measurement
–measurement of physiologic dead space rather than anatomic
–principle that all CO2 exhaled w/ gas originates from alveolus

138
Q

Relation of PaCO2 measurement and ETCO2 and Central venous PCO2

A

ETCO2 usually about 5 mmHg lower than PaCO2
PCO2 usually about 5mmHg Higher than PaCO2

139
Q

Hypercapnia

What can cause it? x4 examples

A

Results when alveolar ventilation is inadequate to restore PaCO2 to normal range
– excess dead space, inadequate fresh gas flow, exhausted absorbent agents, faulty directional valves

140
Q

Elevated CO2 with Fixed MV

Causes; x5 examples

A

2nd to thyrotoxicosis, fever, sepsis, malignant hyperthermia, over exercise

141
Q

Causes of Impaired CO2 excretion from Hypoventilation

#6

A

Total MV = RR + TV( Vd + Va)
Vd = dead space vol
Va = Alveolar ventilation
– interferece w/ ability to achieve normal tidal breath → Neuro dz affecting Resp. Control Center
– Peripheral/Central chemoreceptor dysfunction
–Upper or Lower motor neuron dz
–Spinal Cord dz
–Neuromuscular dz
– elevated airway resistance

142
Q

Lower Motor Neuron Dz that affect MV

#8

A

Myasthenia gravis
Botulism
Tick paralysis
Demylination
Polyradicunuritis (coonhound paralysis)
Chemoreceptor abnormalities - drugs/anesthetics/ metabolic Alkalosis/ cerebral fluid acidosis

143
Q

Elevated Dead Space ventilation: High V/Q

x5 examples

A

increased physicological dead space
– low CO
– Shock
– Pulmonary embolus
– Pulmonary Hypotension
– Pulmonary bulla

144
Q

Increase in CO2 production with fixed TV

metabolic examples x5

A

Malignant hyperthermia
reperfusion injury
fever
Iatrogenic hyperthermia
thyrotoxicosis

145
Q

Central Respiratory Center role with hypercapnia

A

Responsible for 50% of hypercapnia’s ventilatory response

146
Q

Hypoventilation due to Neuromuscular dz

A

Due to low TV
–pts develop shallower breathing pattern = low TV
–compensate with ↑ in RR
– if MV normal with compensation in RR → alveolar ventilation will ↓ w/ pts taking shallow breaths due to greater Vd/TV = hypercapnia

147
Q

Hypercapnia 2nd to pleural space dz

effects on TV

A

↓ TV due to decreased expansion
–MV stays N 2nd to ↑ RR
–Hypercapnia 2nd to ↓ alveolar ventilation from low TV and greater Vd/TV

148
Q

Hypercapnia 2nd to thromboembolic dz

A

Pulmonary capillary compression 2nd to overinflation and cardio shock
= hypercapnia from ↓ alveolar ventilation 2nd to ↑ alveolar dead space or poor perfusion in lungs

149
Q

Effects of Hypercapnia on CVS

#4

A

Hypercapnia + acidosis = ↓ myocaridal contractility and SVR
–compensated by SNS activation/catecholamine release 2nd to acute hypercapnia = ↑ HR and BP
–causes vasoconstriction in pulmonary circulation
–bronchodilation and ↓ diaphragmatic contractility

150
Q

Effects of Hypercapnia on Neuro system

#3

A

–Dependent on level, duration, and degree of hypoxemia
– Cerebral blood flow ↑ in response to ↑ PCO2 via vasodilation and ↑ systemic BP
– ↑ in cerebral blood flow = ↑ ICP

151
Q

Effects of Hypercapnia on Endocrine functions

#3

A

– Constricts renal afferent arterioles = acute kidney injury and low UOP
– may ↑ Na+/H2O retention and HyperK+
–↑ adrenocorticotropic hormone secretion from pituitary stimulation

152
Q

CO2 Blood gas analysis

PvCO2 vs PaCO2 vs CO2

A

PvCO2 = arterial CO2 inflow + local tissue CO2 production + tissue blood flow
PaCO2 = dependent on alveolar ventilation
CO2 = accumulates with decreased blood flow

153
Q

CO2 production with tissue hypoxia

A

CO2 produced as result of ↑ H+ production 2nd to lactate formation and hydrolysis of ATP
–buffered by HCO3- = ↑ CO2 production

154
Q

Stertorous respiration

A

low pitched snoring with inspiration/expiration

frenchie

155
Q

Stridorous respiration

A

High pitched noise associated with inspiration

Lar Par

156
Q

Causes of upper airway disease noises

A

collapse or obstruction of UpA rostral to thoracic inlet = create negative intrathoracic pressure with inspiration = negative transmural pressure/collapse
–prolongs inspiratory phase = noise for air/tissue reverberation

157
Q

Why are patients with Upper Airway dz more at risk for heat stroke?

A

–Pt with UpA dz = ↓ ability to efficiently ↑ MV for heat dissipation

158
Q

Upper Airway Obstruction

A

↑ WOB against obstruction = edema/inflammation/distress/progressive obstruction

159
Q

Paradoxical Laryngeal motion

A

Inward movement of arytenoids 2nd to negative pressure generated on inspiration

160
Q

BAS

A

Brachycephalic Syndrome
–stenotic nares, elongated soft palate, +/- tracheal hypoplasia and nasopharyngeal turbinates
–Chronic airflow resistance = everted laryngeal saccules, tonsil eversion
–Chronic GI signs

161
Q

Nasopharyngeal Polyps

A

common cause of UpA dz in cats
–benign inflammatory lesions coming from mucosa of auditory tube to middle ear → grow into nasopharynx/external ear canal

162
Q

Laryngeal Paralysis

A

Recurrent laryngeal nerve dysfunction = impairs arytenoid cartilage abduction during inspiration = respiratory stridor
–Congenital vs Acquired
–larynx accounts for 6% OF airflow resistance
–dysfunction of laryngeal nerve = atrophy of 1 or both dorsal muscles

163
Q

Laryngeal Collapse

What is another name for this?
what causes it?

A

2nd complication of BAS and Norwhich Terrier Upper Airway Syndrome
–Chronic ↑ of negative pressure in intraluminal airway = weakening of cartilages/loss of rim glottic diameter = ↑ WOB, inflammation, and airway obstruction

164
Q

Norwich Terrier Airway Syndrome

A

narrow infraglottic lumen of varys degrees of laryngeal collapse

165
Q

Grades of LC

3

A

-Grade 1 LC = eversion of laryngeal saccules
-Grade 2 LC = meidal positioning of cuneiform process
-Grade 3 = collapse of cornicilate cartilages

166
Q

Upper Airway Neoplasia

Dogs vs Cats

A

K9 = carcinomas or sarcomas, chondrosarcoma, melanoma, granular cell tumor
Cats = Lyphoma most common but sarcomas and carcinmoas and olfactory neuroblast reported

167
Q

O2/CO2 Transport

A

20% of CO2 Binds to Hb as carbaminoHb and is exchanged for O2 @ alveoli

168
Q

5 types of Hypoxia

A
  1. Hypoxemic hypoxia = inadequate O2 carrying capacity of blood 2nd to hypoxemia
  2. Hypemic hypoxemia (anemic Hypoxia) = anemia causes decrease in circulating Hb = reduced O2 carrying ability of Blood
  3. Stagnant of circulating hypoxia = decreased CO and poor perfusion
  4. Histiotoxic hypoxia = tissues unable to extract and utilize O2 appropriately
  5. Metabolic hypoxia = ↑ cellular consumption of O2 (VO2)
169
Q

Hypemic hypoxemia from hemoglobinopathy

A

caused by CarboxyHb (Carbon monoxide toxicity) and methemoglobinemia
–adequate amounts of Hb BUT Hb unavailable for O2 transport
– CarboxyHb has HIGH affinity for Hb (220xs O2) making them nonfunctional
– Methemoglobin 2nd to acetaminophen toxicity in cats
–both lead to Hypoxia and cause invalid SpO2 readings

170
Q

Dalton’s Law of Partial Pressure

A

hypoventiliation may result in hypoxemia b/c as CO2 ↑, it displaces O2 w/i alveoli = ↓ in PaO2

171
Q

R to L Shunt

A

= ↑ A-a gradient and responds poorly to O2 therapy
–deoxygenated blood (RS of heart) can enter systemic circulation (LS of heart) and may never reach lungs
–caused by vascular shunts w/i lungs or intrathoracic shunts → atrial septal defect, ventricular septal defect, Reverse PDA
–arteriovenous malformation = blood flow from pulmonary artery → pulmonary vein may occur w/o oxygenation @ alveoli cap. bed

172
Q

Cheyne Stokes breathing pattern

What can cause this?

A

respiration characterized by brief periods apnea followed by brief periods of hyperventilation

CNS disorder, ↑ ICP

173
Q

Kussmaul breathing pattern

What can cause this?

A

respiration w/ sustained ↑ depth of breathing w/ either a slow of faster rate in response to metabolic acidemia = body’s attempt to expire CO2 to correct acidosis

DKA, CKD

174
Q

Apneustic Respirations

A

respirations w/ deep inspiration w/ a pause @ full inspiration followed by brief expiration

Ex: ketamine administration or due to central neurological dz

175
Q

ARDS

x7

A

Acute Respiratory Distress Syndrome
–acute, diffuse, inflammatory leading to ↑ pulmonary vascular permeability
– ↑ lung weight
–loss of aerated lung tissue with hypoxemia
–bilateral CXR opacities
– associated with venous admixture
–↑ physiological dead space
– decrease lung compliance

176
Q

Diagnosis of ARDS

A

acute onset
CXR with bilat opacities consistent w/ pulmonary edema
P/F ratio < 300

177
Q

Lung protective MV setting for ARDS

#6

A

– Low TV = 6-8ml/kg
– Low Airway plateau pressure < 30 mmHg
– Higher RR = 35+ bpm
– Higher PEEP = > or = 5 cmH2o
– Permissive hypercapnia
– “Compatible with life” parameters = Sao2 = 88-95%, PaO2 55-80mmHg

178
Q

Tension Pneumothorax

A

Severe Pneumothorax
– life threatening impairment to both ventilation and blood circulation (venous return)
– 2nd to trauma →flap of tissue acts as one way valve = allows continuous influx of air into pleural cavity on inspiration but does not exit

179
Q

“Mixed cause” Pulmonary Edema

Results from =
2 examples

A

Combination of hydrostatic and increase in pulmonary edema
–Neurogenic pulmonary edema = following TBI, Sz, electrocution
–Negative pressure pulmonary Edema = UpA obstruction (BAS)

180
Q

Tracheal Collapse

A

Cause Unknown
–but contributed to dorsal trachealis flaccidity and loss of rigidity or tracheal cartilages
–possibly from ↓ glycosaminoglycen/chondroitin
–Grade I-IV = each grade approx. 25% progressive w/ reduction in tracheal diameter lumen/flattening

181
Q

Tracheal Collapse CS

A

Cervical (extrathoracic) TC = inspiratory dsypnea from inability of tracheal cartilages to withstand Neg airway pressure
– ↑ intrapleural pressure collapses intrathoracic trachea

182
Q

“Honkers” with Tracheal collapse

A

Prolonged Inspiratory with increased effort
ex: pectus excavatum, sinus arrhythmia, abducted elbows, orthopnea

183
Q

“Coughers” with Tracheal collapse

A

Respiratory effort on expiration
–expiratory abdominal push
–harsh expiratory lung sounds
–herniation of cranial lung lobes
–“heave” line

184
Q

Feline Bronchopulmonary Dz

A

Divided into “Feline Asthma” and Chronic Bronchitis

185
Q

Feline Asthma

type of hypersensitivity

A

Hyperactive airway w/ reversible bronchoconstriction (Type I hypersensitivity reaction)
–younger middle age cats
–lack b-lines
–diffuse bronchial/interstitial pattern on CXR

186
Q

Lower Airway Dz in Dogs

A

– Bronchomalacia can result in inspiratory and expiratory crackles
–Bronchitis associated with expiratory wheeze as air flows from alveolar region → glottis → narrow airways
–both can be seen with expiratory push or exaggerated abdominal effort

187
Q

What causes pulmonary edema

A

Hydrostatic pressure edema due to ↑ pulmonary capillary hydrostatic pressure
– increase in permeability = edema from damage to microvascular barrier and alveolar epithelium

188
Q

PathoPhys of Pulmonary edema

A

Normal = fluid fluxes determined by capillary/interstitial hydrostatic pressures, capillary COP
–↑ in interstitial hyrostatic pressures = ↑ driving pressures for lymphatic flow = protect lung against edema
– pulmonary ultrastructure designed to protect gaseous diffusion
– most fluid cleared via bronchial circulation
–Edema occurs when rate of interstitial fluid overwhelms protective fluid clearance mechanisms

189
Q

High hydrostatic pressure Edema

Example

A

–Cardiogenic Edema: most common form, results from LS-CHF (often chronic) esp. cats
–Compensatory mechanisms = fluid retention = worsening congestion

190
Q

Increased Permeability Edema

what is it synonymous with?

A

caused by direct injury to microvascular barrier, alveolar epithelium or both
–synonymous with ARDS

191
Q

Mixed cause Edema

Results from =
Examples

A

Combination of hydrostatic and ↑ permeability
–NPE following acute neuro event - surge in ICP = catecholamine surge = ↑ SVR = alveolar capillary leakage
–NPPE following UpA obstruction = ↑ negative intrathoracic pressure = ↑ venous return to RS < 3 = ↑ pulmonary venous pressures and interstitial hydrostatic pressure = movement of fluid from pulmonary capillaires into interstitium/alveoli

192
Q

Treatment for Pulmonary Edema

A

Reduce pulmonary capillary pressures by reducing Preload
= Diuretics and vasodilators
– furosemide → pumonary vasodilator/bronchodilator = COP ↑ 2nd to hemoconcentration = ↓ pulmonary hydrostatic pressure
–Vasodilators = nitroprusside/nitroglycerin

193
Q

Distribution Patterns to differentiate Pneumonia

3 types

A
  1. Lobar pneumonia pattern = entire lung lobe; dense consolidation
  2. Bronchopneumonia = distal airway inflammation and alveolar dz; patchy distribution
  3. Interstitial pneumonia = inflammation w/i interstitium rather than alveolar spaces
194
Q

PathoPhys of Pneumonia

what mechanisms are involved?

A

Infections occur when protective UpA mechanisms and humoral and cell mediated immunity become overwhelmed
–Inflammatory response from interactions between cell mediated/humoral immune system and elevated cytokines/chemokines

195
Q

Protective Airway defense mechanisms against pathogens/contaminants

x6

A
  • protective barriers
  • cough reflex
  • mucociliary apparatus w/ enzymes
  • Secretory immunoglobulin (IgA)
  • Phagocytic dendritic cells w/i basal layer of resp. tract
  • Surfacant/alveolar macrophages
196
Q

Types of Pneumonia

#7

A

Bacterial
Aspiration pneumonia
Pneumonia associated with CIRD
FB Pneumonia
Parasitic Pneumonia
Mycotic Pneumonia
Ventilator-associated Pneumonia

197
Q

Bacterial Pneumonia

gram neg and positive example

A

Bordetella
mycoplasma
Gram neg = pasturella, E. Coli
Gram Pos = Staph and Strept

198
Q

Aspiration Pneumonia

A

Bacterial Colonization of lungs after aspiration of acid/GI contents
–severe histologic damage caused by low pH < 1.5
– Common enteric bacteria cultured = E. Coli, Klebsiella, Enterococcus
–CXR typically show R middle lung lobe and ventral parts of lobe affected

199
Q

Pathogens that cause Pneumonia associated with CIRD

x7 examples

A

Viral pathogens = K9 adenovirus type 2, parainfluenza, distemper, resp. coronavirus, influenza, canine pneumovirus, herpevirus

200
Q

K9 Distemper

where does infection occur?

A

Replicates in lymphoid cells of resp. tract before spreading to epithelial cells of other organs (including CNS)
–CS = nasal/ocular d/c, resp. distress, V/D, hyperkeratosis of paw pads, progressive neuro dysfunction

201
Q

K9 Respiratory Coronavirus

A

↓ mucociliary clearance that leads to infection

202
Q

H3N8 and H3N2 influenza strains

Can result in =

A

Unique to transmit between dogs
–can lead to hemmorhagic broncopneumonia

203
Q

Parasitic Pneumonia

A

Nemoatodes and Trematodes migrate thru lung
–cats → aeluerostrongylus abstrucsus

204
Q

Mycotic Pneumonia

A

Infection from Fungal agents
–typically geographical
–Blastomyces dermatitides
–Histoplasma capsulatam

205
Q

Pneumonia POCUS signs

A

– early pneumonia → Patchy areas of fluid filled alveoli surrounded by aerated lung = numberous B lines
– Progressive pneumonia → lung consolidation w/ evidence of air bronchograms + shred sign

206
Q

POCUS

Air bronchograms

A

Air filled bronchi surrounded by consolidated tissue
appear as bright hyperechoic lines

207
Q

POCUS

Shred sign

A

–consolidation creates deep jagged hyperechoic border between two areas
– irregular interface between area of consolidated lung and area of aerated lung

208
Q

POCUS

Curtain Sign

A

caudal border of lungs contact w/ chest wall
–sharply divided vertical line separated aerated lung from abdominal contents
–can be used to orient sonographer to define caudal thoracic border

209
Q

Feline inflammatory bronchial diseases

A

asthma and chronic bronchitis
– common lower respiratory diseases in cats that are characterized by recurrent episodes of coughing, wheezing, and/or labored breathing
– associated with airway inflammation, hyperreactivity, and airway remodeling
– tx: β2-adrenergic receptor agonists (albuterol, salmeterol)

210
Q

inhaled β2-agonists

A

– Stimulation of the β2-receptor causes an increase in intracellular levels of adenylate cyclase, which decreases intracellular calcium levels and subsequently causes smooth muscle relaxation of the bronchial wall.

(albuterol, salmeterol)

211
Q

Canine inflammatory bronchial diseases

x4

A
  1. chronic bronchitis
  2. eosinophilic bronchopneumopathy
  3. eosinophilic bronchitis
  4. eosinophilic granuloma
    – idiopathic inflammatory bronchial diseases that typically are characterized by either coughing, wheezing, nasal discharge, and/or labored breathing
212
Q

Canine infectious tracheobronchitis

gram negative or positive?

A

– most common pathogen = Bordetella bronchiseptica
– Gram-negative bacterium is predominantly extracellular and has several characteristics that allow the organism to attach to the tracheal cilia

213
Q

Cricothyroidotomy

A

needle cricothyroidotomy, oxygen can be provided via a large-gauge needle or catheter inserted through the cricothyroid membrane or through the tracheal wall
– temporary adjunct used for minutes because ventilation will not be effective.

214
Q

Surgical tracheostomy placement

A

between the third and fourth or fourth and fifth tracheal rings

215
Q

Thoracocentesis indications

A

pneumothorax and pleural effusions

216
Q

Thoracocentesis location

A

Blind thoracocentesis is performed between the seventh and ninth intercostal spaces
– Fluid may be best aspirated in the lower third of the chest
– ventral thoracocentesis is performed, care must be taken to avoid the internal thoracic arteries, which run along the ventral thorax a few centimeters to either side of the sternum

217
Q

Seldinger technique for small-bore thoracostomy tubes

A

– specialized atraumatic guidewire and matching thoracostomy tube
–chest tube to be inserted in the thorax should be first determined by estimating the distance from the insertion site to the second rib.
– over-the-needle catheter (or hypodermic needle) is inserted through a small skin incision over the7th, 8th, or 9th intercostal space, angled cranioventral in the direction desired for the chest tube
– Seldinger technique has the advantage of requiring a smaller incision using a small-bore tube; it is likely to be less painful and leakage is less likely.

218
Q

Pleural ports

A

Vascular access ports connected to a Jackson-Pratt drain have been successfully used for treatment of recurrent pleural effusion and pneumothorax
– allow connection of the drain to the subcutaneously located access port.

219
Q

Active drainage techniques

A

Continuous suction may also allow sustained lung expansion and better healing of leaks by pleural adhesion
– A suction pressure of 10 to 20 cm H2O is used

220
Q

Thoracostomy tubes Removal

A

– Decision to remove a chest tube depends on the rate of fluid production or air accumulation in the pleural space
– no air should be retrieved for 24 hours before tube removal
– fluid production falls to less than 2 ml/kg/day
– Exceptions are patients with septic exudates and those in which the thoracostomy tube is used for lavage

221
Q

How long are chest tubes in place for spontaneous pneumo?

A

dogs with spontaneous pneumothorax that require chest tubes, the tubes are left in for an average of 4.5 days (range, 1 to 8 days)

222
Q

carbon monoxide toxicity

A

Smoke inhalation associated with fires can result in pulmonary dysfunction and upper airway edema due to inhalation of hot and noxious gases
– can result in carboxyhemoglobinemia

223
Q

What is Carbon Monoxide? (CO)

A

– colorless, odorless, nonirritating gas that is produced by incomplete combustion of hydrocarbons in fires
– produced endogenously as an end product of erythrocyte and heme catabolism and in the CNS as a neurotransmitter

223
Q

CS of CO toxicity

classic sign

A

– delayed neurological injury, including altered level of consciousness, anxiety, vocalization, agitation, ataxia, and seizures, can develop following carbon monoxide toxicity
– cherry red mucous membranes

224
Q

Pathophysiology of carbon monoxide toxicity

2 main mechainsms

A

– CO rapidly absorbed in alveoar
– amount absorbed dependent on exposure duration and concentration in air
– CO toxicity involves two main mechanisms: impaired oxygen delivery to tissues (hypoxia via dyshemoglobinemia) and direct cellular toxicity.

225
Q

CO affinity for Hb

What type of O2/Hb dissplacement shift does it cause?

A

– CO displaces oxygen from Hb and causes an hindrance of oxygen release from Hb to the tissues
– Carbon monoxide competes with oxygen for Hb binding sites with 200–240 times the affinity
– CO binds two of the four available heme groups in each molecule of Hb, causing a decrease in the oxygen carrying capacity of 50%

Left/low shift on O2/Hb curve

226
Q

Direct cellular toxicity from CO toxicity

A

– disrupts oxidative metabolism, potentially causing the generation of oxygen free radicals and impaired cellular respiration
– Binding to myoglobin can cause myocardial hypoxia, depression, and arrhythmias as well as direct skeletal muscle toxicity and rhabdomyolysis

227
Q

Indirect cellular toxicity from CO toxicity

A

– occurs through sequestration of leukocytes
– increased nitric oxide production
– reperfusion injury
– lipid peroxidation
– direct neurotoxicity from CO as a neurotransmitter

228
Q

Carboxyhemoglobinemia

causes which type of hypoxia?
tx for CarboxyHb

A

– hemoglobinopathy that occurs when carbon monoxide preferentially binds to hemoglobin,
– hemoglobin is not able to effectively transport oxygen
– hypemic hypoxia ensues
– Oxygen therapy dramatically decreases the half‐life of carbon monoxide

229
Q

What influences O2 offloading into tissues ability?

A

pH,
CO2,
2,3-diphosphoglycerate [2,3-DPG] concentration.

** O2 dissociative curve **

230
Q

What is the O2 extration ratio?

A

– oxygen extraction ratio is about 25%
– Under normal physiological conditions, DO2 is about four times greater than actual tissue requirements

231
Q

Hypoxemia with N A-a gradient

A

Extrapulmonary: Hypoventilation, Low Atm O2 (fire, elevation)

232
Q

Hypoxemia with Elevated A-a gradient

x3 examples

A

Intrapulmonary:
1. V/Q mismatch (pneumonia, PTE)
1. Diffusion impairment (pulmonary edema, interstitial lung dz)
1. R to L shunting (Tetralogy of Fallot)

VTS ECC 2024 (17 decks)

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