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Histology Spring 2020 > Respiratory System > Flashcards

Respiratory System Flashcards

1
Q

anticlinal vertebrea

A

11th thoracic vertebrae,, straight vertical, identifying landmark on radiographs

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2
Q

diagphragm

A

chief inspiratory muscle, innervated by C3-C5, (phrenic nerve)

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3
Q

thorax vs thoracic cavity

A

thorax is all structure from 1st to 13th rib, even those in the abdomen

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4
Q

What are the cranial and caudal boundaries of the diaphragm?

A

7th to 13th rib

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5
Q

significance of the cupula?

A

The pleural sac extends beyond the first rib and injury to this area can lead to collapse of the pleural cavity and collapse of lung

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6
Q

pleural cavity

A

potential space between visceral and parietal/costal pleura

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7
Q

directionality of the external and internal intercostal muscles

A

external intercostal is caudoventral internal intercostal is cranioventral

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8
Q

Muscles of expiration

A

expiration is normally passive but in disease cases the internal intercostal muscles can assist expiration (Heaves in horses, causing heaves line)

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9
Q

function of external intercostal muscle

A

inspiration

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10
Q

when should the thymus regress by?

A

6 months

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11
Q

boundaries for Auscultation of the lungs

A

triangle between 5th to 11th rib

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12
Q

Where is the proper location to tap for thoracocentesis?

A

7th to 10th intercostal space, cranial to ribs not caudal to avoid blood vessels, angle down towards body wall so you don’t hit the lungs

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13
Q

Components of the conducting portion of the respiratory system

A

nose and mouth, nasopharynx, larynx, trachea, bronchi, bronchiole, terminal bronchiole,

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14
Q

components of the respiratory portion of respiratory system

A

respiratory bronchiole, alveolar duct, alveolar sac, alveolus

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15
Q

significance of the conducting portion

A

contributes to dead space. When dead space is increased, gas exchange becomes more difficult

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16
Q

TRE on turbinate bones

A

coiled bones slows down the air to create laminar (slow) flow to warm it and add moisture
(air should be humidified with endotracheal tube)

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17
Q

TRE

A

typical respiratory epithelium: pseudostratified ciliated columnar epithelium
occupies bulk of the respiratory system

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18
Q

how might heartworms impact breathing?

A

Because the heart is closely associated with the lungs, heartworms can cause disrupted breathing

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19
Q

costodiaphragmatic recess

A

area where the longs will not go even when fully extended

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20
Q

line of pleural reflection

A

where the pleura turns back on itself, location differs depending on species

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21
Q

Cell Junctions

A

Tight junctions: seal
Adherens: attachment (contact inhibition)
Desmosomes: hold cells together (lightly)
Hemidesmosome: hold cells lightly to basal lamina

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22
Q

clinical significance of the cell junctions?

A

Pathogens and autoimmune diseases affect the cell junctions

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23
Q

contact inhibition

A

adherens junctions, cells grown in a lab will stop growing if they are touching

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24
Q

How do hydrogen sulfide and ammonia damage the epithelium?

A

disruption of tight junctions

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25
Q

5 cell types and functions in TRE

A 
goblet cells secrete mucus,
basal cells repair,
ciliated cells move mucus/ escalator,
neuroendocrine: sensing and growth
brush cells: connected with trigeminal nerve endings to activate sneezing and sense fumes
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26
Q

structure of goblet cells

A

mucus located toward apic side, nucleus pushed toward the basal side, microvilli present

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27
Q

neuroendocrine cells

A

no ducts, produce hormones transported by blood flow

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28
Q

how does goblet cell concentration change in response to an irritant (like smoking)?

A

Goblet cells increase for more mucus production

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29
Q

microscopic anatomy of nasal vestibule

A

keratinized stratified squamous epithelium with hair transitioning to non keratinized, hyaline cartilage, serous and sweat glands, hair follicles, few nerve fibers, blood vessels and immune cells in propria submucosa

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30
Q

microscopic anatomy of nasal cavity

A

(respiratory portion but no gas exchange) TRE responsible for humidification and warming with mucus secreting goblet cells,
thin walled veins and glands present
alpha adrenergic stimulation via sympathetic stimulation (constriction)
nerves, lymphatic nodules
P450 enzymes and detoxification (formalin)
Trigeminal and autonomic efferent innervation

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31
Q

microscopic anatomy of the olfactory region

A

thick high, pseudostratified epithelium
olfactory cells with bipolar neurons
supporting cells, basal cells (tight junctions),
20-30 cilia per cell longer than in TRE, nonmotile, have receptors for odorant molecules
Olfactory/ Bowman’s glands in propria submucosa
lipofuscin pigmentation makes this region darker
absence of goblet cells because mucous is antagonistic to olfaction,
serous glands in lamina propria, abundant olfactory nerves

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32
Q

supporting cells

A

sustentacular cells, protective, glial like, occluding/ tight junctions
oval shaped nuclei compared to rounder nuclei of olfactory cells

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33
Q

How is the olfactory anatomy different in dogs?

A

More olfactory epithelium, cribriform plate has more holes

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34
Q

Bowman’s gland

A

located in propria submucosa, initiates olfaction by producing watery secretion that solubilizes odorant molecules for the receptors on the cilia so the action potential can be initiated, these glands also cleanse the receptors for new smells

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35
Q

vomeronasal organ structure

A

joins the incisive duct and opens caudal to the central upper incisors, located in the mucosa of ventral portion of nasal septum, tubular blind-ended and paired structure
vomeronasal duct is crescent shaped
J-shaped hyaline cartilage support,
opens at incisive papilla,
medial epithelium containing neuro-sensory cells, sustentacular cells, basal cells,
vomeronasal gland,

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36
Q

Flehmen’s response

A

means bearing upper teeth in German to sense pheromones and urine particles in the air

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37
Q

functions of vomeronasal organ

A

chemoreception of liquid borne substances like pheromones, sexual behavior, maternal instinct, fetal interaction with amniotic fluid.

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38
Q

How does the mucociliary escalator work?

A

the cilia bend when moving backward so that the mucus moves in only one direction

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39
Q

structure of cilia

A 
9 doublets of microtubules surrounding a central doublet
Nexi protein binds tubules together
dynein arm (inner and outer) have sliding motion to propel cilia, fueled by ATP
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40
Q

primary ciliary dyskinesia

A

PCD, immotile ciliary syndrome/ Kartagener syndrome
Respiratory and middle ear infections, mucus gets in middle ear canal and causes ear infections, situs inversus totalis, situs ambiguous or heterotaxy syndrome, reproductive failures, rhino-sinusitis, bronchitis
defect in genes coding dynein protein seen in some dog breeds,
autosomal recessive genetic disorder
absence of dynein arm leads to defective or absent ciliary motility
diagnosed electron microscopy of bronchial biopsy
advise not to use in breeding because there is no effective treatment

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41
Q

diagnosis of situs inversus

A

auscultation and palpation

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42
Q

clinical conditions impacting the pharynx and larynx

A

collapse of pharynx, long soft palate of horses can cover the epiglottis in dorsal displacement of soft palate (DDSP), laryngeal hemiplegia

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43
Q

histology of nasopharynx and larynx

A

typical respiratory epithelium, propria submucosa: loose connective tissue, seromucous glands

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44
Q

histology of epiglottis and vocal folds

A

non keratinized stratified squamous transitioning to TRE at trachea, glands are absent, elastic cartilage

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45
Q

Why do the vocal folds have stratified squamous epithelium?

A

Because of the wear and tear that occurs in this area during vocalization

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46
Q

What type of epithelium is present at the alveoli?

A

simple squamous

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47
Q

Are goblet present in alveolar tissue?

A

No because mucus would inhibit respiration like during pulmonary edema, disappear in bronchioles

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48
Q

histology of trachea

A

TRE, C-shaped hyaline cartilages, trachealis muscle, longitudinal elastic fibers, most glands, seromucous glands, tunica adventitia (loose connective tissue), very little smooth muscle, goblet cells

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49
Q

trachealis muscle

A

allows flexibility as food moves along the esophagus next to it, supplies support, trachealis can be slightly inside or inside depending on species

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50
Q

composition of hyaline cartilage

A

chondrocytes, matrix, and type II collagen fibers

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51
Q

What happens when cartilage is defective?

A

tracheal collapse, presenting with goose honk coughing, common in toy breeds, but can occur in large dogs and cats, collapse inside thoracic cavity, 50% collapse of trachea increases airway resistance by 16 times the normal, medical management is temporary fix, surgical treatment is best option by placing a stent.

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52
Q

histology of bronchi

A

TRE, C shaped hyaline cartilage has broken into plates/pieces, goblet cells are present, many mixed glands, more smooth muscle, more associated blood vessel, pulmonary arteries and veins,

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53
Q

histology of bronchiole

A

simple columnar to simple cuboidal (ciliated and non ciliated), cartilage and glands absent, few goblet cells, most smooth muscle which is arranged in circular and oblique fascicles

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54
Q

Club cells

A

bronchiolar exocrine cells, club shaped, devoid of cilia, secrete glycosaminoglycan, metabolize xenobiotics like cytochrome P450, club cell secretory protein (similar to surfactant) is a biomarker/ marker for injury of these tissues, contain tryptase and activate hemagglutinin of Influenza A, act as stem cell for bronchiolar epithelium

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55
Q

surfacant

A

produced by type II alveolar cells

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56
Q

pulmonary trunk

A

from right ventricle dividing into right and left pulmonary artery and enter the lung at the hilus. Follows the branching of the major airways so visible in lung sections. Pulmonary veins go away from alveoli to heart
Pulmonary artery blood has low pressure from right side of heart but bronchial artery is from left side of heart has higher pressure like the systemic pressure

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57
Q

nutritional vs functional blood

A

Functional blood goes from right atrium and returns to left atrium
Nutritional blood includes bronchial artery to supply the cells of the major airways. Comes from bronchoesophageal artery from the aorta. then shunts to the pulmonary vein
Capillaries don’t need nutritional blood, they just use normal blood gas exchange

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58
Q

pulmonary artery

A

thin and carries deoxygenated blood. low pressure compared to systemic arteries, both internal and external elastic laminae

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59
Q

bronchial artery

A

thick walls, carries oxygenated blood, has only internal elastic laminae

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60
Q

pulmonary vein

A

carry oxygenated blood to left atrium, has only external elastic laminae and thinner tunica media
6 to 8 in number depending on the number of lung lobes

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61
Q

pulmonary arterial hypertension

A

can be due to chronic hypoxia or inflammation, seen in humans and animals, hypertension caused by effusion of pulmonary vessels and arteries become occluded.

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62
Q

importance of lymphatics

A

left atrioventricular valve defect could back up blood into pulmonary vein, lymphatic remove extra fluid, blood cells are not usually seen in lymphatics

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63
Q

terminal bronchiole

A

simple columnar (ciliated and nonciliated) no glands and no cartilages, smaller than normal bronchiole

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64
Q

respiratory bronchiole

A

simple cuboidal, few cilial and outpocketing of alveoli, continuation of terminal bronchiole, transitional portion between conducting and respiratory portion, both respiratory and conducting

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65
Q

alveoli

A

surrounded by capillaries, squamous (type 1) and cuboidal (type 2), alveolar macrophages

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66
Q

alveolar sac

A

several alveoli make one sac

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67
Q

pneumocytes

A

alveolar epithelial cells, type I is squamous and type II cuboidal

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68
Q

nucleated red blood cells

A

present in birds and reptiles, also in developing mammals and in cancer

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69
Q

blood gas exchange area

A

respiratory membrane, thickness of one hair

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70
Q

Type I Alveolar epithelial cells

A

squamous cells, only the nuclei are well seen, cover 95% of alveolar area, very thin blood-gas barrier, tight junctions hold them

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71
Q

Type II Alveolar epithelial cells

A

round and large cells, appear granular, produce surfactant, mostly in the corner of alveoli, cover 5% of the area, act as stem cells for Type I cells (most important ,function), can be phagocytic like macrophages

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72
Q

surfactant

A

produced by type II AEC, contained in osmiophilic lamellar bodies, disrupts surface tension to keep alveoli open

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73
Q

respiratory membrane

A

formed by fusion of basolamina of endothelial cells in capillaries and type I AEC
less than 1 micron thick, unless edema increases thickness and disrupts diffusion, thick in some areas and thin in others for support and for gas exchange

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74
Q

alveolar macrophages

A

found in the interstitial lumen, can have dark vacuoles with ingested toxins, can be viewed with a transtracheal wash/ lung labage, 20-80 microns in size, larger than type II AEC, do not confuse these, pulmonary intravascular macrophages are more inflamed compared to monocytes

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75
Q

pleura

A

thin, glistening, serous membrane, pleural cavity is very small with then film of fluid

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76
Q

pathologic conditions in pleura

A

pleuritis: inflammation, thoraco-abdominal or sholder pain), crackling noise as lungs rub against wall
pneumothorax and pleural effusion

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77
Q

primary vs secondary bronchi

A

secondary are within the lung

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78
Q

clinical significance of smooth muscle

A

causes heaves in horses, exploited for treatment of these conditions

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79
Q 
Name the corresponding physiological concept for each clinical condition:
Artificial ventilation
pneumoconiosis
lung fibrosis
lung function tests
gaseous anaesthetics
asthma/ heaves in horses
respiratory distress
diagnosis
sarcoidosis
A

Artificial ventilation: heat of vaporization
pneumoconiosis: turbulence
lung fibrosis: elasticity
lung function tests: gas laws
gaseous anaesthetics: vapor pressure
asthma/ heaves in horses: airway resistance
respiratory distress: surface tension/ surfactant
diagnosis: partial pressure
sarcoidosis: diffusion

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80
Q

respiration

A

O2 is acquired and CO2 is eliminated, involves forces to create a vacuum such as contraction of diaphragm and processes such as ventilation (movement of air), diffusion (blood gas exchange), transportation, and tissue delivery and return

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81
Q

What value can be used to assess if an endotracheal tube is placed correctly?

A

Use metabolism because all CO2 that is exhaled is a product of metabolism since there is none in the atmosphere

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82
Q

What is the atmospheric composition at sea level? Ames (1,000 ft above sea level)?

A

78% nitrogen, 21% oxygen, 0.93% argon, 0.04% CO2 and 1% H2O. These percentages are the same everywhere even though there is less total air at higher elevations

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83
Q

diffusion

A

blood-gas exchange, relies on concentration of gases across a membrane (concentration gradient) and the thickness of the membrane

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84
Q

hypoxia vs hypoxemia

A

hypoxia is less oxygen in the lungs or a particular region. Hypoxemia is less oxygen in the blood

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85
Q

path of upper respiratory tract

A

nares, nasal conchae, pharynx, larynx, trachea, principle bronchi

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86
Q

species with the most pliable nostrils

A

horse, helpful when exercising

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87
Q

Which anatomic feature is responsible for 90% of air humidification?

A

upper respiratory system

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88
Q

guttural pouches

A

extension of auditory tube in horses

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89
Q

what causes gunky eyes in the morning?

A

clogged nasolacrimal duct

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90
Q

Epithelium of epiglottis on oropharynx side vs tracheal side

A

stratified squamous epithelium (non-keratinized) on oral side and on the tip of the epiglottis. But epiglottis facing towards trachea is covered with TRE because of different locating needed different wear or breathing functions

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91
Q

inspiration

A

conduction of air, warm air to body temperature, add water vapor, saturate to 100% humidity, inhaled substances trapped in mucous

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92
Q

gutteral pouches

A

extension of auditory tube in horses

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93
Q

What causes gunky eyes in the morning?

A

clogged nasolacrimal duct

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94
Q

dry eye

A

can be caused by lost tears due to a nasolacrimal duct that is too large or open more

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95
Q

nasolacrimal duct

A

can be flushed

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96
Q

ways to improve respiration

A

mix oxygen with helium or nitrogen so the patient can breathe easier

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97
Q

surface area in airways

A

branching causes increased total surface area, and decreased resistance

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98
Q

blood supply to the alveoli

A

each alveolus is completely covered in capillaries

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99
Q

ventilation

A

Process of inhaling and exhaling so that the animal acquires O2 and eliminates CO2.
Involves: mechanical forces: respiratory muscles, pressure differences, negative and positive pressure ventilation

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100
Q

positive pressure ventilation

A

external force using a ventilator

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101
Q

tidal volume

A

volume of each breath, 0.5 L in humans

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102
Q

v (dot) E

A

minute ventilation, total volume of air breathed per minute

= tidal volume times respiratory frequency

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103
Q

respiratory frequency in humans

A

12-16 times per minute

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104
Q

dead space

A

VD, ventilation wasted, air that does not come in contact with the blood gas exchange area
1. equipment
2. Anatomic
3. Alveolar
Alveolar dead space adds to anatomic dead space
anatomic dead space can change eg. mucus
necessary so that air can be humidified but an increase in dead space ventilation is not desired
mixes fresh and used air so amount of oxygen delivered to the alveoli is less than that in the atmosphere, inhalation of old air so the concentrations of O2 and CO2 do not change very quickly
Assume that anatomic dead space is 150 mL

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105
Q

causes of alveolar dead space

A

hydrostatic pressure failure, embolus, emphysema, pre-capillary constriction due to tumor or foreign obstruction

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106
Q

emphysema

A

widening of alveoli and they don’t inflate and deflate properly, results in destroyed capillaries, can be caused by smoke, increased compliance

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107
Q

alveolar ventilation

A

not the same as minute volume/ minute ventilation

= total ventilation- dead space ventilation

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108
Q

physiologic (total) dead space

A

=anatomic dead space + alveolar dead space (functional dead space)

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109
Q

minute ventilation

A

=alveolar ventilation rate + dead space ventilation rate (important for thermoregulation)

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110
Q

tissue saturation of O2

A

can be represented by peripheral concentration of O2 in blood

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111
Q

rapid shallow breathing

A

ineffective because of less tidal volume and constantly reusing dead space air

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112
Q

v dot divided by q dot

A

ventilation- perfusion ratio

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113
Q

Ve

A

expired volume of gas

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114
Q

define these primary respiratory symbols:

P, V, S, F, Q, R, D

A 
P: Pressure, partial pressure, or tension of a gas
V: volume of gas
S: saturation of hemoglobin with O2
F: fractional concentration of a gas
Q: Blood volume
R: Resistance
D: Diffusing Capacity
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115
Q

bar above primary respiratory symbol

A

mean or mixed sample

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116
Q

prime sign after secondary symbol

A

end of a structure, eg. PE’CO2 refers to end tidal CO2

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117
Q

MRV

A

minute respiratory volume (total volume of gas moved in or out of airways and alveoli in 1 minute)

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118
Q

respiratory cycle

A

inspiration and expiration

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119
Q

respiratory pattern or waveform

A

smooth and symmetrical, horses have 2 phases of inspiration and 2 of expiration

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120
Q

complementary breathing cycle

A

sigh, deep rapid inspiration and expiration, not seen in horses, created using breathing bag

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121
Q

What happens to breathing pattern during peritonitis?

A

use of costal breathing

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122
Q

What happens to breathing pattern during pleuritis?

A

Just abdominal breathing

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123
Q

Which breathing pattern is the predominant one?

A

abdominal breathing

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124
Q

Eupnea

A

normal breathing

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125
Q

apnea

A

temporary cessation of breathing, can result in headache

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126
Q

tachypnea

A

fast breathing

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127
Q

bradypnea

A

slow breathing

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128
Q

dyspnea

A

labored and difficult breathing

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129
Q

hypernea

A

increased depth and rate

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130
Q

polypnea

A

rapid, shallow breathing (panting)

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131
Q

respiratory frequency

A

number of respiratory cycles/minute, excellent indicator of health status, varies depending on certain conditions

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132
Q

factors that increase respiratory frequency

A

pregnancy, digestive tract fullness, lying down, diseases (usually)

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133
Q

factors that decrease frequency

A

low temperature, sleeping

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134
Q

breath sound

A

due to air movement through the tracheobronchial tree (turbulent air flow)

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135
Q

adventitious sound

A

extrinsic to normal breath sounds, abnormal sounds superimposed on breath sounds, could be due to pleural disease or lung parenchyma, crackles due to edema or exudates, wheezes due to airway narrowing

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136
Q

Can you hear the sound of air passing through bronchioles?

A

no because the bronchioles offer almost no resistance unless there is a disease condition

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137
Q

lung volumes

A

air within lung or breath. Tidal volumes, IRV, ERV can be measured and residual volume only assessed

138
Q

lung capacities

A

combination of volumes, inferred from measured values

139
Q

tidal volume

A

volume of each breath 0.5 L

140
Q

IRV

A

inspiratory reserve volume: extra volume that can still be inhaled after normal inspiration (tidal volume)

141
Q

ERV

A

expiratory reserve volume: extra volume that can still be expired after tidal volume

142
Q

residual volume

A

RV, amount of air remaining in the lung after most forceful expiration

143
Q

IC

A

inspiratory capacity: tidal volume plus IRV

144
Q

FRC

A

functional residual capacity: ERV plus RV,
acts as a windbag in a bagpipe, only source of O2 during apnea, affected by position, sex, physiological conditions (overweight animals have less FRC), lung diseases

145
Q

VC

A

vital capacity: IRV + tidal volume+ ERV

146
Q

TLC

A

total lung capacity: IRV + VT+ ERV+ RV
or VC + RV
or IRV+ VT + FRC

147
Q

Restrictive Lung Diseases

A

Parenchymal disease/ Fibrosis, Muscular diseases, sarcoidosis, chest wall deformities
cause restricted inspiration by decreasing VC, TLC, RV, and FRC

148
Q

Obstructive lung diseases

A

Inflammatory conditions: emphysema, chronic bronchitis, and asthma (heaves in horses),
Difficulty in expiration, VC is decreased and TLC, RV, and FRC, increased, inflammation in bronchioles, smooth muscle contraction upon expiration

149
Q

increases RV and FRC

A

not always a favorable condition if gas exchange has been inhibited

150
Q

Why does a patient with an underlying lung disease will experience difficulty in breathing when moved to higher elevation?

A

There is less total air at higher elevations and less oxygen availability, so pathologic conditions can combine with physical activity to cause difficult breathing

151
Q

atmospheric pressure in Ames

A

740 mmHg

152
Q

importance of atmospheric pressure

A

ambient pressure, impact respiration/diffusion

153
Q

gauge pressure

A

measured against local atmospheric pressure/ zero atmospheric pressure

154
Q

absolute prssure

A

best reference to use for comparison of pressures
= gauge pressure + atmospheric pressure,
can be achieved with absolute vacuum

155
Q

magdeburg experiment

A

used pump to remove air inside sphere, horses could not separate because the atmospheric pressure is more than the vacuum, could only open it when the air was added back into the sphere

156
Q

water pressure

A

1.35 cm H2O per 1 mm Hg,

Useful because density of blood is similar to water

157
Q

pressure in right ventricle

A

20 mm of Hg= 27.2 cm H2O or 10.7 inches H20

158
Q

Dalton’s Law of Partial Pressure

A

total pressure- sum of individual gases in a mixture

159
Q

ABG

A

arterial blood gas analysis

160
Q

PB

A

atmospheric pressure, 760 mm Hg equalized to 0 mm Hg

161
Q

Pressures in clinical medicine

A

If unable to perform arterial sampling in the field, can make approximations from a venous sample
Difference in partial pressures allows diffusion across blood gas membrane
Negative pressure in lungs causes inspiration and slightly positive pressure allows for expiration
Cap needle after taking blood to prevent outside air from impacting gases in the sample

162
Q

Paw

A

pressure within the airways, equals 0 in the phase between inspiration and expiration, Pressure in lungs is equalized to outside between inspiration and expiration

163
Q

Ppl

A

pleural pressure, -4 mm Hg (756 mm Hg)

164
Q

Boyle’s law

A

At constant temperature
P1V1= P2V2
Increase in pressure will lead to decrease in volume
Increase in volume will lead to decrease in pressure
Pressure and volume are inversely proportional

165
Q

Charle’s Law

A

Volume of a gas is directly proportional to the temperature at constant pressure
V1/T1=V2/T2
Decreased temperature causes decreased volume

166
Q

Ideal gas law

A

PV=nRT, At constant temperature and pressure, the volume of a sample of gas is directly proportional to the number of moles of gas in the sample
R= universal gas constant= 8.3145 J/mol K
Pressure directly proportional to moles and temperature of gas
Pressure inversely proportional to volume of gas

167
Q

why is intrapleural pressure negative?

A

Wall of lung and thoracic cavity slide against each other, lung is trying to recoil inwards and thoracic cavity moves outwards creating negative pressure

168
Q

Inspiration

A

diaphragm flattens and inspiratory muscle contracts, thoracic cavity expands, intrapleural pressure becomes more negative, alveolar transmural pressure increases, alveoli expand, airflow until Palv=0 mm Hg

169
Q

alveolar transmural pressure

A

difference in pressure between lung alveoli and pleural cavity

170
Q

Expiration

A

passive process normally, diaphragm returns to dome shape and inspiratory muscles relax, internal intercostal and abdominal muscles contract to aid in forced expiration (exercise or asthma), thoracic cavity goes back to normal size, intrapleural pressure becomes less negative, alveolar transmural pressure gradient decreases by going back to normal, alveoli return by elastic recoil, Palv=+1 mm Hg driving air out until =0 mm Hg

171
Q

time elapsed in one respiratory cycle

A

4 seconds

172
Q

Why do alveoli recoil?

A

elastin and collagen recoil, surface tension of alveolar fluid lining

173
Q

surfactant

A

hydrophilic and phobic moieties, breaks some of the hydrogen bonds, reduces surface tension, premature animals would not have enough surfactant to combat surface tension to keep the alveoli open and need a ventilator

174
Q

Law of LaPlace

A

P=2T/r the object with more surface tension has more pressure. Alveoli have different sizes and pressure is equalized by surfactant disrupting surface tension in the smaller alveoli

175
Q

alveolar interdependence

A

Collapsing alveoli could pull others inward, recoil effect of surrounding alveoli pull collapsing one back, Surrounding alveoli have enough surfactant but the central one does not
Altered by emphysema, if too many alveoli are damaged they cannot help each other
Infants die of surfactant deficiency, could occur in foals

176
Q

Compliance

A

= change in volume divided by change in pressure
opposite of elasticity, inspiration and expiration follow different paths, causing hysteresis
decreases during fibrosis
increases during emphysema

177
Q

hysteresis

A

occurs in substances that aren’t perfectly elastic causing difference in volume and pressure, impacted by surface tension but saline can disrupt this

178
Q

fibrosis

A

restrictive lung disease, paraquat found in pesticides, causes fibrosis, volume ore difficult to change, decreased compliance

179
Q

poiseuille’s law

A

laminar flow,
pressure difference divided by the airflow rate equals airway resistance
R= viscosityx lengthx8/ (pi r to 4th power)

180
Q

pulmonary circulation

A

short, low resistance and low pressure system, dense capillary network around alveoli
Cardiac output is the same in the pulmonary trunk and aorta
1000 capillaries for every alveoli, pulmonary artery pressure is 1/6th of systemic arteries

181
Q

pulmonary vessels

A

negative pressure except forced cough, great dispensability and compliance, more capillaries than alveoli, thin sheet of blood surrounding alveoli

182
Q

response to hypoxia in pulmonary messels

A

vasoconstriction, need blood to go to the body instead of the lungs, could occur during exercise

183
Q

advantages of low pressure system

A

high pressure in the lungs would make the lungs burst, less work for heart, thin blood gas barrier is protected and prevents edema

184
Q

bronchial circulation

A

2% cardiac output, supplies tracheobronchial tree up to terminal bronchiole, supply hilar lymph nodes, visceral pleura, pulmonary artery, vein and vagus neve, and esophagus, provides nutritional blood,
venous return: either azygos or pulmonary veins,
communication between bronchial and pulmonary system (shunt)
Aa gradient created by deoxygenated blood from the bronchial vessels, increases in some patholgic conditions

185
Q

A-a gradient

A

alveolar arterial gradient, difference between alveolar and arterial pressure/ oxygen, (~5-10 mm Hg), increases in some diseases, created by deoxygenated blood from the bronchial vessels,
Increases with aging, VQ mismatches, shunt and diffusion impairment
Measured with;
Pulse oximetery (SpO2): peripheral O2 saturation, hard to get on animals with anemia, jaundice, or poor perfusion, use spectrometry,
Arterial Blood Gas (ABG) analysis (SaO2)
A-a equation: Aa=[PIO2-(PaCO2/0;8)]-PaO2

186
Q

PVR

A

Pulmonary Vascular Resistance, less than systemic circulation, calculate with poiseuille’s law, cannot be directly measured
=(MPAP-MLAP)/ pulmonary blood flow,
this is approximation because blood is not a Newtonion fluid, pulsatile pulmonary flow, pulmonary capillaries are distendable

187
Q

MPAP

A

mean pulmonary artery pressue

188
Q

MLAP

A

mean left atrial pressure

189
Q

Newtonian fluid

A

consistent viscosity and density

190
Q

Alveolar and extra-alveolar (corner) vessels

A

increase in diameter but small ones squeeze and decrease in diameter when lung expands
Increase in size of these vessels causes low resistance (radial traction effect)

191
Q

PVR at RV FRC and TLC

A

Reserve volume: high PVR since extra-alveolar vessels have low radius
FRC to TLC: alveolar capillaries have narrow radius and hence high PVR
Lowest total PVR is at FRC and flow is most favored
Alveolar and extra alveolar vessels experience opposing effect during change in lung volume

192
Q

exercise and PVR

A

cardiac output increases but without great increase in mean pulmonary artery pressure because of recruitment and distension
delta P=Flow x PVR so if cardiac output/ flow decreases PVR must also decrease for pressure to stay the same.
This is because not all capillaries are used normally, but when demand is high (exercise), they can be recruited or ones already being used can distend.

193
Q

vascular smooth muscle

A

causes contraction and relaxation, more smooth muscle, greater increase in pulmonary arterial pressure (hypoxia)
Cattle and pigs have more smooth muscle in pulmonary artery and more susceptible to hypoxic vasoconstriction, localized hypoxia lead to redistribution of pulmonary flow

194
Q

brisket disease/ edema

A

cattle experience hypoxia at high elevation, pulmonary arterial pressure increases (reversible),
Compensatory increase in RBC numbers, mild increase in cardiac output, without affecting left arterial pressure
Right ventricular hypertrophy due to pressure overload in pulmonary arteries and then dilation and failure, distension of system veins and edema of brisket region.
Low exercise intolerance, tachycardia and jugular pulse, Pulmonic 2nd heart sound
Recovery upon return to low elevation, treat with oxygen to relieve hypoxic stimulus helps

195
Q

EIPH

A

Exercise induced pulmonary hemorrhage, blood originating from blood gas exchange area, Normal Pa ~28 mm Hg, horses are obligate nose breathers with long soft palate, nasoincisive notch bridged by soft tissue, high vacuum created by large diaphragm and 18 ribs, high Pa 90-120, goes up with exercise
Because of high blood flow and increased demand, the capillary hydrostatic pressure increases and alveoli pulled to expand because of the vacuum. Force can cause breakage of alveolar epithelium and RBCs enter alveoli.
Damage from EIPh is healed by fibrosing which compromises gas exchange and horse cannot run as fast
Treatment options: nasal strips to hold soft tissue open and prevent collapse during respiration which reduces vacuum expect, furosemide reduces pressure in capillaries, diuretic, reduces blood volume

196
Q

obligate nose breathers

A

human babies and horses

197
Q

Modeling pulmonary blood flow

A

flow= upstream minus downstream pressure
When valve is open the collapsible tube needs to overcome pressure in the box as well. Blood flow needs to overcome alveolar pressure
hydrostatic pressure increases at lower heights due to gravity

198
Q

Differences in ventilation and perfusion in the zones

A

Lungs have gravity effect, different hydrostatic pressure to different zones of the lung
Zone 1: PA>Pa>PV, blood flow not usually seen unless in cases of severe blood loss causing Pa>PA, or positive pressure ventilation, the alveoli are pinching the vessels reducing flow
Zone 2: Pa>PA>PV, intermittent flow
Zone 3: Pa>PV>PA, continuous flow (capillaries distended)

199
Q

Pulmonary Fluid Clearance

A

Arteries have high hydrostatic pressure and veins lower hydrostatic pressure, some fluid leaks out, and oncotic pressure pushes it back, some lymph accumulates in extracellular space, Lymphatic vessels have valves for unidirectional blood flow
Fatty meal or cancer can make lymphatic vessels very big
normally no fluid accumulation
Interstitium has low compliance due to proteoglycans
Exercise and left side heart failure can cause increased capillary hydrostatic pressure,
fluid accumulation could be due to blockage of lymphatic vessels (parasite) loss of lumen or proteins, decreasing oncotic pressure,
Lung sounds can differ

200
Q

Starling’s Equation/Law

A

Qf= Kfx [(Pcap-Pif)- colloid reflection coefficient (picap- pi if)]= ~1 mm Hg causing lymph to flow out of vessels

201
Q

When does clinical edema develop?

A

Lymphatic capacity is exceeded, Proteoglycan bridges break (alveolar septa), then fluid enters alveoli and bronchioles

202
Q

Why does pulmonary edema fluid look foamy?

A

Pulmonary edema fluid is foamy since it is a mixture of air, edema fluid and surfactant molecules

203
Q

decreased plasma oncotic pressure

A

causes: hypoproteinemia (starvation, vigorous intravenous fluids), inflammatory lung diseases, increased vascular permeability, inflammation (fibrin deposition) Lymphatic obstruction, Lung edema can impede ventilation and oxygenation

204
Q

How is the fluid reabsorbed?

A

fluid originates from capillaries in the parietal pleura,
reabsorbed through stomata (holes) on parietal pleura, Lymphatics are dense in tendinous part of diaphragm and in the mediastinal part of pleural cavity

205
Q

Causes of hypoxemia

A

hypoventilation, diffusion impairment, Low PIO2/FIO2, shunt, ventilation perfusion mismatches

206
Q

impacts to oxygen cascade

A

hypoventilation, decreased respiratory rate, drops larger in cascade

207
Q

Alveolar gas equation

A

PAO2= FiO2 x PB- PH2O)- (PaCO2/R)
R=0.8 for most diets= Volume of CO2 made per unit time/ Volume of O2 consumed per unit time, can be changed by colling patient to reduce metabolism and R
PH20 is normally 47 mm Hg because air is 100% saturated with moisture
PaCO2 acquired from ABG because amount of CO2 in blood is the amount expired
FiO2 is normally 0.21

208
Q

impact of hypoventilation, how much O2 concentration needed to correct?

A 
CO2 builds up in the body, alveolar and arterial CO2 gradient is unchanged, because frequency and depth are changed but not the gas exchange area, PaO2 decreases and PaCO2 increases
eg. PaCO2=80 mm Hg PAO2=50 mm Hg
to bring PAO2 to 100
100=PIO2-80/0.8
PIO2=200=FIO2x713
FIO2=0.28= 28% O2 needed
Hypoventilation responds to O2 therapy
209
Q

Causes of hypoventilation

A

usually external to lung

  1. Respiratory Centre Depression/ Damage to CNS: Inflammation, Morphine, Barbiturates, trauma
  2. Peripheral Nerve Injury: chest wall injury, dislocation of vertebrae
  3. Neuromuscular diseases/ Damage to pump: muscle paralysis, trauma to chest, bloated abdomen
  4. Lung Resisting inflation: airway resistance/ obstruction, mucus, larger ETT, dense gas and deep diving, decreased lung compliance
210
Q

diffusion inpairment

A

caused by exercise (reduced contact time and hypoxemia because blood flow has increased), high altitude or low PiO2, lung pathologies (thickening of respiratory membrane)
Air spends 0.75 s in contact with the blood, majority of the diffusion is in the first 0.25 seconds/ first 1/3 PvO2 is 40 and PaO2 is 100
CO2 is highly diffusible so its diffusion is less of an issue
Responds to O2 therapy

211
Q

Why should thickness impact diffusion?

A

Fick’s Law of Diffusion of Gases: v dot gas=
[A D (P1-P2)]/ T
Diffusibility of gas directly proportional to (change in pressure, Area, S)/ [T sqrt (Molecular weight)]
If thickness increases (edema) diffusion goes down so you can give higher concentration of O2

212
Q

Physiologic shunts

A

normal shunts such as bronchial circulation, thebesian veins

arterial-venous anastomoses can be created in surgery

213
Q

Pathological Shunts

A

Arterial-venous anastomoses, absolute intra-pulmonary shunts/ true shunts, patent-ductus arteriosus, foramen ovale, intraventricular septal defects
Cannot be corrected with oxygen therapy, so if animal doesn’t respond to O2 suspect a pathologic shunt

214
Q

Thebesian veins

A

normal shunts, drain blood from myocardium into left ventricle and dilute the oxygenated blood

215
Q

impact of shunts

A

poor response to 100% O2 breathing to diagnose, shunt is blood bypassing gas exchange area, if size of shunt is large it causes hypoxemia
V/Q ratio is 0, airway occluded, O2=40 CO2=45, can’t eliminate CO2, low hemoglobin hypoxemia,

216
Q

oxygen dissociation curve

A

Max PAO2 is 100 mm Hg O2, beyond this the oxygen concentration has very little increase due to maximum saturation of hemoglobin, Also maximum concentration of hemoglobin in men is 15 mL/dL,
98.5% of O2 is transported by hemoglobin and the rest is dissolved in the blood, Maximum saturation of hemoglobin is 97.5%

217
Q

Ventilation-Perfusion

A

Ventilation has to match perfusion
Perfusion=Q= Cardiac output= ~5 L
V/Q: ventilation perfusion ratio
VT= 500 mL-150=350
350x12=4200 mL ~4 L
4L/5L= 0.8-1.2, normal range for ventilation perfusion ratio
eg. dead space, pulmonary embolism, same O2 as ambient , air, can’t eliminate CO2, V/Q ratio increases to infinity, one area does not get blood and all the other areas have V/Q mismatches, adding to hypoxemia

218
Q

Factors impacting V and Q

A

Top of lung: More negative intrapleural pressure, more of a transmural pressure gradient, larger alveoli (less compliance) less ventilation, poor Q (dead space)
Middle of Lung: optimal, ventilation match perfusion, blood going to left atrium will have optimal oxygenation because the regions are mixing unless there is a ventilation perfusion mismatch
Bottom of Lung: less negative intrapleural pressure, lesser transmural pressure gradient, smaller alveoli (more compliance), more ventilation, good blood supply, High Q (distended veins)
Va increases by 1.5-2 times going down, Q increases 3.5 times going down, ventilation perfusion ratio increases from 0.5 to 5 going up with middle 0.8-1.2.

219
Q

Compensation of V/Q mismatches

A

Well ventilated alveoli cannot compensate because of issues with perfusion,
Physiologic response: hypoxic vasoconstriction, Brisket desease in cattle, right side heart failure in chicken, COPD, asthma, pulmonary embolism, pneumonia
Clinical Intervention: anesthesia and VQ mismatches, O2 therapy helps, squeeze anesthesia bag, want to increase dissolved component of O2

220
Q

Barometric pressure measures in Ames IA at about 740 mm Hg. What will be the PIO2 of the moist (100%) inspired air in mmHg? Assume that oxygen saturation is 21% in Ames, and use the equation. you could round up your answer to the nearest digit? PIO2=FIO2x(PB-PH2O)

A

146 mm Hg

221
Q

external vs internal respiration

A

external respiration is gas exchange in alveoli and internal is the gas exchange in the tissues

222
Q

Changes in gas pressures during respiration

A

O2 diluted by humidifying in the nasal cavity, then gets mixed with the dead space air PO2 decreases, unable to rebreath because of high CO2 content, rebreathing used during hyperventilation to add CO2 back into the system

223
Q

diffusion of gases

A

involves diffusion and kinetic motion
Net movement is always from higher concentration towards lower concentration
Partial pressure determined by concentration and solubility of the gas
eg. nitrogen has high concentration but low solubility

224
Q

Does this kinetic motion cease?

A

Yes, at -273 degrees C (Charles’s law)

225
Q

Dalton’s Law of Partial Pressures

A

The pressure of a mixture of gases is the sum of the pressures of the individual components
Total pressure= sum of partial pressures
Partial pressure= concentration of dissolved gas/ solubility coefficient
Higher altitudes have lower total pressure (O2 always 21%)
Expired air has both O2 and CO2
vapor pressure reduces the the PO2

226
Q

differences in diffusion of CO2 and O2

A

CO2 24 times more soluble than O2
Higher pressure differences needed for O2
Diffusion of CO2 usually not a clinical problem as a result,
CO2 diffuses 20 times faster than O2 (Fick’s law)
Nitrogen used to make breathing easier during scuba diving, or helium can be used to make breathing easier to make the oxygen mixture lighter cause less airway resistance

227
Q

Henry’s Law of Gas Diffusion

A

Volume (quantity of gas) dissolved in water at equilibrium is not only affected by pressure of the gas but also by solubility coefficient
Concentration/Volume Cx= Px x Bx
Clinical application: scuba diving, N2 narcosis

228
Q

HBOT

A

Hyperbaric Oxygen Therapy, 3-4 atm to absorb more O2 (Henry’s and Fick’s Law
O2 diffuses and saturates to a high level of plasma
Indications: Anaerobic bacterial infections, Wound healing, stroke, heart conditions, CO poisoning, cerebral edema, gas embolism, bone infections

229
Q

Humidification of Air

A

Air is humidified for saturation, humification of air dilute the O2 content, vapor pressure increases with temperature increases then PIO2 goes down, When pressure is equal to atmospheric pressure, steam occurs
37 degrees C, PH2O=47 (normal temp)
39 degrees C, PH2O= 52 mm Hg

230
Q

respiratory membrane components

A 
Diffusion of O2 and CO2
Fluid lining
Alveolar epithelium
alveolar basement membrane
interstitial space
capillary basement membrane
capillary endothelium
plasm
RBC
231
Q

dissolved oxygen

A

depends on solubility and partial pressure of the gas (Henry’s law)
O2 solubility= 0.003 mL/dL mm Hg
For a PaO2 of 100 mm Hg, dissolved O2= ol3 mL/dL
Cardiac output during exercise: 30L/min
30x3=90 mL total O2/min but requirement is 3 L so hemoglobin is needed for transport
As gas tension of O2 rises, so does saturation of hemoglobin
1.5% of O2 is dissolved in plasma, concentration at 100 PO2 is 20 mL/100m:
PaO2 directly proportionate to dissolved O2 in plasma
HBOT

232
Q

hemoglobin

A

4 heme and 1 globin molecule
humans have ~10-15 g/dL of hemoglobin, animals 23 g/dL
Globin: amino acid sequence critical for O2 binding (2 alpha and 2 beta) Fetal Hb has 2 alpha and 2 gamma causing hypoxia in womb
Heme: one iron molecule per heme and one Fe bines one O2, 4 O2 molecules bind per Hb molecule, each molecule of O2 is 25% saturation of the hemoglobin
Clinical significance: nitrate poisoning causes changes valency of iron oxidation of iron making methemoglobin, which can not transport O2,
CO poisoning

233
Q

oxygen binding to hemoglobin

A

reversible, oxygen bound in the lungs and reaction reversed in tissues, law of mass action: proportion of products is in relation to the proportion of reactants, PO2 determines %Hb saturation,
allosteric (cooperativity), all or nothing response, once one O2 molecule binds the other three follow more easily
1 g of Hb combines with 1.34-139 ml O2 (fully saturated)
40 mm Hg PVO2 has 72% O2 saturation
60 mm Hg O2 has 85% saturation, below this is consider hypoxemia,
25 mm Hg O2 has 50% saturation
100 mm Hg has 97.5% saturation, maximum (note: this is different than the percentage of O2 transported with Hb)

234
Q

Total O2 calculation

A

If a patient’s Hb= 15 g/dL and PaO2=100 mm Hg, what is the CaO2? (assume Hb to be pure)
CaO2= O2 disolved in plasma + O2 bound to Hb= (0.003x100)+ (1.39x15x97.5/100)= 20.63 mL/dL ~21 mL/dL
CaO2: total oxygen content

235
Q

Factors Affecting hemoglobin’s affinity for O2

A

Oxygen unbinds from RBC and then diffuses out of blood into tissue,
pH, PCO2, temp, 2,3 DPG, type of Hb (fetal vs adult) and toxicities (nitrate poisoning, carbon monoxide)

236
Q

pH impact on O2 Hb binding

A

carbonic acid and lactic acid made in body,
drop in pH causes right shift, increase in pH causes left shift,
Carbonic anhydrase (CA) favors reaction of CO2 with water to form carbonic acid
PCO2 also dictates pH

237
Q

Bohr effect

A

increasing PCO2 or decrease in the blood pH reduces the affinity of Hb to O2, helps unload

238
Q

Impact of temperature on Hb O2 binding

A

increase in temperature causes right shift, metabolically active, could be due to exercising tissues, makes oxygen delivery easier

239
Q

impact of PCO2 on Hb O2 binding

A

CO2 can also bind to Hb, PCO2 similar to that of H+

Increased PCO2 causes right shift, decreased PCO2 causes left shift,

240
Q

Why does PCO2 change pH?

A

hydration reaction produces H+ ion, reaction favored in RBCs because it is catalyzed by carbonic anhydrase, which is 5 times more prevalent in red blood cells than the rest of the body

241
Q

impact of 2,3 DPG on Hb O2 binding

A

2,3 DPG present in RBCs, erythrocytes don’t have a nucleus but still undergo glycolysis, producing 2,3 DPG that can bind with deoxygenated hemoglobin and favor unloading of oxygen, increase in 2,3 DPG causes right shift, decreased 2,3 DPG causes left shift,
Clinical significance: ascent to high altitude and anemia, 2,3 DPG levels decrease within the blood bank and need increased before delivery to the patient,
anemia causes high production of 2,3 DPG

242
Q

carbon monoxide

A

colorless, tasteless, and odorless gas, needs CO detector because CO-oximeters are expensive
CO binds to Hb to make carbonmonoxy or carboxy hemoglobin, CO occupies same site as O2, has 200x more affinity than O2, if you give too much O2 (100%) in ventilation the brain will shut down because it thinks breathing is not necessary, occurs in CO poisoning
treated with 100% O2 CO2 and fluids
poisoning treated with higher PO2 with 5% CO2, fluids and other support

243
Q

CO2 production

A

Glucose oxidized to CO2, H2O and ATP
higher metabolism causes increased CO2
Milk production, reproduction, exercise make more CO2

244
Q

Why should the CO2 be removed

A

CO2 is a waste by product, too much causes hypercapnia (hypercarbia) and acidosis (use bag breathing), if uncontrolled can lead to death,
Confusion, coma and death
CO2 is a vasodilator,

245
Q

carbon dioxide

A

part of bicarbonate buffer system,
~48 mL/dL compared to 20 mL/dL for O2 because solubility and diffusibility is very high for CO2 so only a small gradient is needed, By the time CO2 diffusion would be an issue the patient is already dead,
arterial CO2 is 92% of venous CO2 content,
Chemoreceptors highly sensitive to CO2,
Shunts don’t respond to additional O2, but removal of extra CO2 is good
Respiratory sensor in brain is very sensitive to CO2, stimulated H+ ions from hydration reaction,

246
Q

O2 delivery to tissue and CO2 pick up

A

Tissue has higher partial pressure of CO2, levels in artery and alveoli are the same, low pH, high temperature and low PO2, shifting curve to right to make oxygen delivery easier
Bohr effect

247
Q

CO2 transport modes

A

7% dissolved in plasma
Goes through hydration reaction with carbonic anhydrase to produce carbonic acid, reversible reaction, follows law of mass action, carbonate exits the cell and chloride ion enters to obtain electroneutrality, chloride shift, 70%
23%, H+ from hydration reaction is buffered by oxygen bound hemoglobin, O2 released because of right shift, hemoglobin becomes reduced and binds to CO2, forming carbaminohemoglobin that also binds oxygen, this part impacted by anemia
Influx of H20 causes RBC to swell

248
Q

carbonic anhydrase inhibitor

A

When animals are treated for glaucoma with acetazolamide, it is carbonic anhydrase inhibitor, need to monitor pCO2 with ABG, RBC swells from 7-8 microns to 9-10 microns but pulmonary capillaries are only 6-8 microns

249
Q

CO2 elimination in the lung

A

Lung is high PO2 and low pCO2, 7% of Co2 that is dissolved in plasma diffuses into alveoli
PACO2 is 40 mm Hg
PaCO2 is 45-46 mm Hg
other reactions reverse are carbonat enters cell and hydration reaction reverses

250
Q

Haldane effect

A

Removal of O2 allows more CO2 to be carried, addition of more O2 will knock off CO2, when hemoglobin is fully saturated with O2, it carries less CO2
mirror image of Bohr effect

251
Q

CO2 vs O2 dissociation curves

A

CO2 is steeper because it does not have cooperativity/ allosteric effect, O2 has plateau
CO2 can use small gradient, still has effective diffusion, range is 40-46 mm Hg,

252
Q

Homeostasis in the body

A

Relatively constant [H]+ due to acid-base balance

Regulation of H+ in the body fluid

253
Q

Sources of acids and bases

A

Physiological: food and cellular metabolism, lactic acid is week acid, does not completely dissociate
Pathological: metabolic disease, decreased ventilation, vomiting, diarrhea, renal insufficiency

254
Q

Is water an acid or base?

A

both

255
Q

Causes of acidosis

A

ethylene glycol (antifreeze) ingestion, sallicyte (aspirin), chronic kidney disease, diabetes mellitus, severe shock, hypoventilation due to disease

256
Q

causes of alkalosis

A

vomiting, consumption of bicarbonate, increased urinary loss of H+, hypoalbuminemia, kidney retention of HCO3-

257
Q

symptoms of acidosis

A

depression, rapid and deep breathing, diarrhea, confusion, fever

258
Q

symptoms of alkalosis

A

weakness, irregular heartbeats, Ileus, muscle twitching, dehydration, seizures (rare)

259
Q

Normal pH ranges

A

7.35-7.45

260
Q

acidosis vs acidemia

A

acidosis leads to acidemia
acidosis: all of the physical processes and chemical reactions that result in an abnormally low pH, May involve other body fluids
Acidemia: low blood pH, can not have acidemia without acidosis

261
Q

Factors affecting pH

A

pCO2 is normally 40 mm Hg
Strong Ion Difference (SID)
Atot: increased Atot causes increased metabolic acidosis, decreased Atot causes metabolic alkalosis,

262
Q

SID

A

strong ion difference: difference between the sums of concentrations of the strong cations and strong anions
Increase in SID is alkalinzing
Decrease in SID is acidifying

263
Q

Henderson-Hasselbalch Equation

A

pH=pK + Log( [HCO3-]/ (0.03 x PCO2))

6.1 is normal pK for buffers

264
Q

Chemical buffer system:

A

a mixture of a weak acid and its conjugate base, exchange a strong acid or base for a weak one
eg. Hemoglobin and other proteins can accept H+ ions

265
Q

bicarbonate buffer

A

NaHCO3) and carbonic acid (H2CO3), Maintain a 20:1 ratio: HCO3-: H2CO3

266
Q

Phosphate buffer

A

Major intracellular buffer
NaH2PO4 is weak acid and Na2HPO4 is conjugate base
concentration is 1/16th of bicarbonate buffer in ECF, Important in ICF (intra-cellular fluid),
can buffer tubular fluid effectively

267
Q

Protein buffer

A

Large number of acidic and basic groups, carboxyl gives up H+,
Amino group accepts H+, Plasma proteins are not significant buffers for blood,
hemoglobin has imidazole groups (38 Hist) that buffer H+, imidazole group donates H+ when oxygenated and accepts H+ when deoxygenated

268
Q

isohydric principle

A

buffers, buffer the buffer, helps maintain homeostasis as once the capacity of one buffer is exceeded, a different buffer system helps out

269
Q

Acid-Base Imbalance and Correction

A

1st Line of Defense: Chemical buffers, Bicarbonate buffer system, phosphate buffer system, protein buffer system, instant response
2nd line of defense: physiological buffers, lung excreting CO2 (minutes to hours), Kidneys excreting H+ (hours to days)

270
Q

levels of acidosis and alkalosis

A 
acidosis: pH <7.35
respiratory acidosis: PCO2 >40 mm Hg
Metabolic acidosis: [HCO3-]< 24 mM
Alkalosis: pH> 7.45
Respiratory alkalosis: PCO2<40 mm Hg
Metabolic alkalosis: [HCO3-]> 24 mM
271
Q

Anderson-Davenport Nomogram

A

PCO2 altered with ventilation and bicarb can be controlled with kidneys
If underlying cause is not removed, full problem can’t be corrected, only small adjustments
A. Respiratory alkalosis: decreased renal H+ excretion and decreased retention of HCO3-
B. Respiratory Acidosis: increase in both renal H+ excretion and increased retention of HCO3-
C. Metabolic Acidosis: decreased PaCO2 and subseq decrease in H+
D. metabolic Alkalosis: increased PaCO2 and increased H+

272
Q

Control of ventilation

A

We never forget to breathe, motor nerve endings reach into skeletal muscle, can alter contraction, diaphragm is mix of both smooth and skeletal muscle

273
Q

central controller

A

most is in pons and medulla
Four regions: DRG/ Dorsal respiratory group, VRG/ ventral respiratory group, AC/ apneustic center, PC/ Pneumotaxic center
Neurons have basic rhythmicity, similar to cardiomyocytes, override from higher brain centers: voluntary control of breathing, hold breath, neurons spread across small area, not a concentrated nucleus

274
Q

Sensors

A

Chemoreceptors (central and peripheral)
Lung,
Other receptors
carotid body, carotid sinus, upper respiratory tract

275
Q

Effectors

A

Respiratory muscles: External intercostal muscle, internal intercostal muscle, diaphragm

276
Q

DRG

A

Dorsal Respiratory Group, output primarily to diaphragm, dorsal medulla, inspiratory activity, basic rhythm of breathing
Output: phrenic nerve to diaphragm, C3-C5 spinal nerves
Input: vagus and glossopharyngeal nerve

277
Q

VRG

A

ventral respiratory group, ventral medulla, expiratory and some inspiratory, innervate muscles of intercostal and abdominal (auxiliary muscles of respiration)
VRG inactive during normal quiet breathing, expiration is passive
Output and Input: vagus nerve

278
Q

Pontine Respiratory Centers

A

modifies the output of medullary centers, includes apneustic and pneumotaxic center

279
Q

AC

A

stimulates the inspiratory neurons of the dorsal respiratory group and ventral respiratory group
Over stimulation causes apneusis

280
Q

apneusis

A

prolonged inspiration and then expiration, gasp for breath

281
Q

PC

A

Pneumotaxic center
inhibitory signals to inspiratory center (medulla)
Fine tunes inspiration and expiration
Increased signals increase respiratory rate

282
Q

Respiratory Centers

A

located in the pons and medulla, rhythmicity of inspiration and expiration
Receive input from: chemoreceptors, lung, other receptors, cortex
Output is to phrenic nerve and other respiratory muscles
vagus nerve gives negative feedback signals

283
Q

central chemoreceptors

A

Responds to pH of ECF
CO2 diffuses across blood brain barrier to CSF but not not H+ ions
Normal CSF pH is 7.32, does very little buffering and protein activity, bicarbonate in CSF is controlled by choroid plexus, CO2 diffusion stimulates chemoreceptors to increase ventilation and eliminate excess CO2
Bicarbonate and H+ are impermeable to blood brain barrier
Ependymal cells in choroid plexus produce CSF,

284
Q

carotid bodies

A

Peripheral Chemoreceptors, high arterial blood supply, Uses glossopharyngeal nerve,
Responds to PO2, PCO2, and pH (not CO),
more sensitive to O2 (hypoxia) than CO2, classified as fast acting receptors
Babies dead from SIDS had low levels of carotid body, forget to breathe
Type 1 (glomus) cell located in the center with type 2 cells surrounding, type 1 cells have dopamine, anesthetics depress dopaminergic receptors
Steep response when PaO2 is below 60 mm Hg
Bilateral carotid body resection: could occur in case of tumors, difficult to sense low O2 levels or low arterial pH

285
Q

baroreceptors

A

carotid sinus and aortic bodies, sense changes in blood pressure

286
Q

Pulmonary stretch receptors

A

lung receptors, slowly adapting, wait until break point to activate, don’t start firing signal right away, pulmonary stretch receptors, protective in nature
Hering Breuer reflex,: cannot manually inhale until lungs burst

287
Q

Irritant receptors

A

lung receptors, location in airway epithelium, rapidly-adapting pulmonary stretch receptors, cause bronchoconstriction (asthma)

288
Q

J receptors (juxtacapillary receptors)

A

lung receptors, endings of unmyelinated c fibers, response to injected materials in pulmonary circulation
role in lung edema, slow respiration to localize edema,(rapid shallow breathing with vagus nerve)
interstitial lung disease,

289
Q

Bronchial c fibers

A

lung receptors, similar to J receptors, supplied by bronchial circulation, rapid shallow breathing, bronchoconstriction and mucus

290
Q

nose and upper airway receptors

A

similar to lung irritant receptors, sneezing, coughing and bronchoconstriction
laryngeal spasm- ETT with insufficient local anesthetic

291
Q

joint and muscle

A

receptors stimulating ventilation

292
Q

gamma system

A

senses elongation of muscle (sense dyspnea) relaxation of muscle

293
Q

arterial baroreceptors

A

increase arterial blood pressure, reflex hypoventilation or apnea

294
Q

responses to pain and temperature

A

Pain: apnea followed by hyperventilation

Heat (skin): causes hyperventilation

295
Q

Ventilatory response to CO2

A

Arterial PCO2 is an important stimulator of ventilation, central chemoreceptors followed by peripheral receptors, even when PCO2 is low, the response to low PO2 is magnified

296
Q

Ventilatory response to PO2

A

no role under normotoxic conditions
Increased response if PCO2 is raised
High altitude and chronic lung disease

297
Q

Response to first ascent to high altitude

A

hyperventilation, decreased PaCO2, increased pH, ventilation remains elevated

298
Q

Short term acclimatization to high altitude

A

return of blood pH to normal, readjustment of CSF pH to normal, chemosensitivity of type I cells to hypoxia increases

299
Q

long term acclimatization to high altitude

A

increased RBC production, decreased affinity of hemoglobin for O2 due to increased 2,3 DpG, Increased pulmonary surface area, Increased capillary density in muscles
can acclimatize up to 6500 ft, need supplemental O2 above this level

300
Q

Response to exercise

A

increase in ventilation is rapid, moderate exercise-3 stimuli remain same (fall in PO2, rise in PCO2 or rise in pH), anaerobic exercise, lactic acid decreases pH and increases ventilation,
Other factors: Limb motion (brisk walk), increase in cardiac output, thermoregulatory, psychogenic (“Let’s go for walk”)
Race horses can only breathe one time per stride, can increase length of stride

301
Q

Fetal circulation

A

Lungs start functioning after birth, fetus has low O2 hypoxia, mixing of oxygenated and deoxygenated blood, prescence of shunts, ductus arteriosus connects pulmonary trunk and aorta, occurs after branches going to brain because of sensitivity to hypoxia, ductus venosus shunts blood to the liver, Lungs only have 7-8% of blood going through them, no mixing of fetal and adult blood,
2 umbilical arteries and one umbilical vein,

302
Q

placenta

A

functions as fetal lung, simple diffusion of simple molecules, passive carrier mediated transport of glucose, active transport of amino acids and ions
Transfer of O2 is problematic as it depends on uterine arterial PO2 levels,
receives 40% of cardiac output,

303
Q

compensations for hypoxia

A

uterine artery blood flow is increased, palpable on rectal exam
Fetal hemoglobin has higher affinity for O2 than adult hemoglobin,
Higher hemoglobin concentration in fetal blood (human, lambs and calves)
Relative to body mass, higher cardiac output (than adults)

304
Q

higher affinity of fetal hemoglobin for O2

A

Intrinsic property of hemoglobin (ruminants), inability to bind 2,3 DPG (primates), pigs and horses lack fetal hemoglobin (low 2,3 DPG)

305
Q

histology of developing lung

A

alveoli in pseudo glandular state, look more like cuboidal secretory cells, flatten out during development, cartilage more eosinophilic because proteoglycans can not be laid, not capable of supporting respiration, fetal lungs have amniotic fluid instead of air in the alveoli
surfactant production begins during 7th month of pregnancy, premature babies might not have enough surfactant, need supplemental

306
Q

Events shortly following birth

A
  1. hypoxia and hypercapnia, leads to drive for ventilation
  2. Cooling of fetus and evaporation of fetal fluids
  3. Sensory input (mother licking and nuzzling)
    First breath: great inspiratory effort, not all alveoli open first, surfactant is important
    carotid bodies in fetus and at birth, begin functioning in a few weeks,
    PVR decreases after lungs expand
    Rupture of umbilical vessels
    Loss of low resistance placental circulation, increases systemic vascular resistance, increases pressure on aorta, left ventricle and left atrium
    Aortic pressure greater than arterial pressure, left atrial pressure greater than right atrial pressure,
    blood flow through foramen ovale and ductus arteriosus reverses, foramen ovale closes and becomes fossa ovalis, O2 rich blood in ductus arteriosus causes smooth muscle contraction (arrest blood flow)
    now vasodilator PGE2 decreases (indomethacin inhibits prostaglandin synthesis)
    ductus arteriosus becomes ligamentum arteriosum, now fetal circulation is adult circulation, ductus venosus degenerates after birth and hepatic sinusoids open up
307
Q

Respiration in eggs

A 
Chorioallantois membrane (CAM), closely associated with inner membrane of shell- CaCO3 as cuticle thin, double soft membrane inside, pores in shell allowing gas diffusion, egg water loss and air cell
As surface area of CAM increases the efficiency of diffusion increases, inside O2 level is low and CO2 is high to rive diffusion gradient, as vascularity increases, blood flow/perfusion increases, increased cardiac output and hematocrit values,  increased O2 affinity for hemoglobin, 
Before hatching: air cell size (blunt end) increases to 12 mL, Chicks use beak and break open into air cell
308
Q

impact of heat stress and egg shell quality

A

hyperventilation and decreased PCO2, decreased HCO3-, shell weakens, leads to dehydration of egg, can impact the number of chicks hatched

309
Q

Trachea in birds

A

2.7 times longer and 1.29 times wider than mammal, but Resistance is the same as mammal (R=8nl/pi r ^4)
Complete and double ring appearance, not trachealis, rings telescope into each other, large tracheal dead space, volume 4.5 times greater,

310
Q

Factors reducing impact of large tracheal dead space in trachea

A
  1. 1/3 respiratory frequency
  2. VT, (birds), 1.7 time greater than mammals
    Equivalent to deep breathing with less frequency
  3. Large expansible volume
  4. Greater compliance of respiratory system (birds spend less energy overall)
311
Q

respiration in birds

A

lack epiglottis and alveoli, can intubate air sacs,
Parabronchi with their surrounding tissue in the basic gas exchange unit,
lack a diaphragm, use abdominal and chest cavity muscles, cross current flow

312
Q

Air sacs

A

expand instead of lungs, work like bellows, no gas exchange, 2 cervical, 1 clavicular, 2 cranial thoracic, 2 caudal thoracic, 2 abdominal
Pneumatic, light and strong

313
Q

inspiration and expiration in birds

A

neopulmonic parabronchi: 10 -12% of lung volume when present, meshwork
paleopulmonic parabronchi: present in all birds, parallel stacks, 90% of lung volume
Unidirectional air flow in paleopulmonic, two cycles of respiration, parabronchi always contact fresh air, high efficiency extraction and elimination,
Inspiration 1: air sacs expand and air flows into caudal air sacs
Inspiration 2: air goes toward cranial and caudal air saces
Experation 1: air flows out from caudal over Paleopulmonic parabronchi

314
Q

Air capillaries and blood capillaries

A

AC: air capillaries, similar to alveoli are surrounded by blood capillaries (BC)

315
Q

Blood gas barrier in birds

A

0.09 um in birds (thinnest), 0.56 um in ostritch
60% thinner compared to mammals, basement membrane has strength from type IVc collagen
Pulmonary capillary blood volume is 2.5-3 times mammals
Very high efficiency of gas exchange
Fick’s gas law: when thickness is decreased diffusion is favored

316
Q

Yak

A 
Bos grunniens
oxygen content 66-33% (high altitude)
Larger heart and lungs
Persistence of fetal hemoglobin
Other genes for hypoxia and metabolism
Do not do well below 10,000 ft
Do not tolerate above 59 degrees F
Hair is used for clothes, manure for fuel, and milk is thick
317
Q

Mammalian Diving Reflex

A

Dive to 1-1.5 miles
Present in all mammals
Bradycardia: seals 125 beats/min decreasing to 10 beats per minute
Peripheral vasoconstriction: diving pressure leads to vasoconstriction in extremities (toes, fingers, arms and legs), more blood being used by heart and brain
Blood shift: vasoconstriction pushes blood into lungs (intra alveolar gas pressure increases), after a certain point, risk of pulmonary edema
Can be used in pediatric ward: children with tachycardia put cold wet towel on face to cause mammalian diving reflex
Water into nose, slow/ cessation of breathing, bronchoconstriction
breathing reflex in the nose

318
Q

Problems faced by divers

A

Boyles law: As the pressure of a closed system increases, volume of the system decreases in direct proportion
combated in marine mammals by compliant chest and collapse of alveoli followed by terminal airways, push air from alveoli into dead space, prevent nitrogen narcosis
Specialized surfactants aid reinflation
Cavernous sinuses engorge and prevent middle ear squeeze, large middle ear size

319
Q

Histology of bronchi and bronchioles in mammals and seals

A

muscle extends almost to alveoli, cartilage in the bronchioles can collapse and reinflate alveoli and bronchioles

320
Q

Dealing with nitrogen narcosis

A

As pressure increases, concentration of dissolved gas increases (Henry’s law)
Dive and collapse lung, because air is in dead space, narcosis is avoided
Switch to anaerobic metabolism
Elastic aorta to keep blood pressure
Other adaptations: Aortic bulb and slender abdominal aorta, Large heart with glycogen store, Higer O2 in lung, muscle and blood, increased hematocrit values, large speen, increased muscle myoglobin, Lungs have great rigidity and elasticity, deep divers have small respiratory volume

321
Q

respiration in fish

A

counter current flow required because O2 in water is less than in the air

322
Q

Non Respiratory Function

A

Innate defense: anatomic arrangements, cells and soluble factors
Thermoregulations: absence of sweating, panting in dogs
Communication: sound production, smell (pheromones)
Metabolism: Angiotensin-converting enzyme (ACE)
Acid-base balance: ventilation

323
Q

Types of respiratory clearanc

A 
Upper respiratory clearance
Alveolar clearance (Lower respiratory tract clearance)
324
Q

3 physical forces causing respiratory clearance

A
  1. Gravitational setting/ Sedimentation: nasal cavity, tracheobronchial tree
  2. Inertial Forces: nasal cavity, pharynx, tracheobronchial tree
  3. Brownian Motion: submicron particles into small airway and alveoli
325
Q

Deposition

A

settlement of particles on respiratory membranes

326
Q

Particle size

A

> 10 micron is non respirable particle
<10 micron respirable size
<1-2 micron alveolar region
Particle deposition is least for 0.3-0.5 micron, suspended in alveolar air spaces, cocci bacteria are this same size
small airway/alveoli are <0.3 micron (Brownian Motion)

327
Q

daily intake of air

A

~10,000 L

328
Q

Upper Respiratory tract clearance

A

proximal/ cranial to alveolar duct, mucus blanket-towards pharynx, what pushes-ciliary beat (15 mm/min), particles consumed, Pharynx to GI to Feces

329
Q

Lower Respiratory tract clearance

A

Particles within alveoli,

  1. Absorptive site and lymphatics, near alveolar duct
  2. Fluid flow to bronchiolar epithelium and mucociliary escalator
  3. Phagocytosis, alveolar epithelial cells, macrophages
  4. Desquamation of cells, cells die then cleared
  5. lymph nodes
330
Q

factors inhibiting mucociliary escalator

A

dyskinesia, sliding of dynein arms create force to move cilia

331
Q

Panting

A

dogs, sheep, goat, gazelle and birds
Respiratory center reacting to core body temperature
Dead space ventilation is increased to cool off
Glandular secretions (nasal/ orbital) or vascular transudate
effective alveolar ventilation goes down, take breaks from panting to take deep breaths

332
Q

Lateral nasal glands

A

similar to sweat glands, one in each maxillary recess

25-40 degrees C: 40 times more secretion

333
Q

Panting patterns

A
  1. Inhalation and exhalation both through nose, least cooling, observed in resting dogs (ambient <26 degrees C), Running at slow speeds in cold temperatures
  2. Inhalation through nose, exhalation through nose and mouth, Rest quietly at >30 degrees C, exercise, Air through nose and out through moth- maximum cooling
  3. Inhalation and exhalation through nose and mouth, greater alveolar ventilation
334
Q

Purring

A

Activation of diaphragm and intrinsic laryngeal muscle, 25 time/second during inspiration and expiration, cats that roar do not purr

335
Q

three phases of purring

A
  1. Glottal closing
  2. Initiation of glottal opening and sound production
  3. Complege glottal opening (low resistance and high air flow)
336
Q

Why do cats purr?

A

Exact reason unknown, May be contented, sick, or sleeping
To provide better ventilation (shallow breathing)
Cats are better at healing, especially fractures
Drop in volume during sleep could cause atelectasis

337
Q

sneeze reflex

A

breathing reflex in the nose,
Foreign objects/ irritation of nasal mucosa (brush cells in TRE connected to trigeminal nerve), Strong inspiration and then vigorous expiration through nose, defensive

338
Q

aspiration or sniff reflex

A

reflex in the pharynx, foreign objects/ irritation of pharyngeal mucosa, series of inspiratory efforts (eg. reverse sneezing)
Closing nose to force mouth breathing helps

339
Q

swallowing reflex

A

reflexx in the pharynx, Food or drink pushes against soft palate, epiglottis bends upwards/backwards; closes larynx, once bolus is in esophagus, respiration continues, patients with neurological damage may not be able to swallow

340
Q

filtration

A

non respiratory functions of the lung, entire right ventricle output goes through lung, Filter particulate matter and blood clots, Some species have pulmonary intravascular macrophages
eg. horses, cattle, pig and cat are more susceptible to lung inflammation (sepsis)
Cat has more severe response to heartworm because of pulmonary intravascular macrophages

341
Q

Metabolism

A

non respiratory function of lung, arachidonic acid metabolites, major site of synthesis, metabolism, uptake, and release
ACE (Angiotensin converting Enzyme) from pulmonary endothelium converts Angiotensin I to Angiotensin II, Bradykin is inactivated by ACE, used to fight hypertension

342
Q

Defense mechanisms in lung

A

nonspecific immunity: surfactant proteins A&D, collectins, host defense peptides, mucociliary escalator, cough/sneezing, alveolar macrophages, toll like receptors
Specific immunity: surface Igs (IgA coats surface), Pulmonary dendritic and T cells, intranasal vaccines

Histology Spring 2020 (4 decks)

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