Respiratory Flashcards
What are the conducting airways?
From trachea, main bronchi (R and L), then lobar bronchi then segmental bronchi.
This process continues down until terminal bronchioles - smallest airways without alveoli
Function of conducting airways
o To lead inspired air to the gas exchanging regions of the lung
o As the airways become smaller, the amount of cartilage decreases and smooth muscle increases - the very small distal airways are composer mostly of smooth muscle.
o Because there is no gas exchange, they constitute the anatomic dead space - areas with ventilation but no blood flow.
Anatomical dead space
Space of conducting airways where there is no gas exchange
About 150mL
What is the respiratory zone?
o The terminal bronchioles divide into respiratory bronchioles, which have occasional alveoli budding from their walls
o Then alveolar ducts, completely lined with alveoli
What is an acinus
Portion of the lung distal to a terminal bronchiole, forms an anatomical unit called acinus
Airways zones
Blood-gas interface
o Extremely thin (0.2-0.3um) over much of its area
o Big surface area of 50-100m2
What are the main 4 lung volumes?
Tidal volume
Inspiratory reserve volume
Expiratory reserve volume
Residual volume
Tidal volume
Volume inspired or expired with each breath
Inspiratory reserve volume (IRV)
o Is the volume that can be inspired over and above the tidal volume.
o Is used during exercise.
Expiratory reserve volume (ERV)
The volume that can be expired after the expiration of a tidal volume.
Residual volume (RV)
The volume that remains in the lungs after a maximal expiration. cannot be measured by spirometry.
What are the main lung capacities?
Inspiratory capacity
Functional residual capacity
Vital capacity
Total lung capacity
Inspiratory capacity (IC)
Sum of tidal volume and inspiratory residual volume
Functional residual capacity (FRC)
o Sum of expiratory reserve volume and residual volume
o Is the volume remaining in the lungs after a tidal volume is expired.
o Includes the RV, so it cannot be measured by spirometry.
Vital capacity (VC) (aka forced vital capacity - FVC)
o Is the sun of tidal volume, IRV, and ERV.
o Is the volume of air that can be forcibly expired after a maximal inspiration.
Total lung capacity (TLC)
o Is the sum of all four lung volumes.
o Is the volume in the lungs after a maximal inspiration.
o Includes RV, so it cannot be measured by spirometry.
Graph of lung capacities / volumes - draw
Physiologic dead space
o Is a functional measurement.
o Is defined as the volume of the lungs that does not participate in gas exchange.
o Is approximately equal to the anatomic dead space in normal lungs.
o May be greater than the anatomic dead space in lung diseases in which there are ventilation/perfusion (V/Q) defects.
Equation to calculate physiological dead space
Minute ventilation
Volume of gas inhaled or exhaled per minute
Minute ventilation = Vt x RR (bpm)
Alveolar ventilation - VA
VA = (VT - VD) x RR (bpm)
VT = tidal volume
VD = physiological dead space
A person with a tidal volume (VT) of 0.5 L is breathing at a rate of 15breaths/min. The PCO2 of his arterial blood is 40mmHg, and the PCO2 of his expired air is 36 mm Hg. What is his rate of alveolar ventilation?
Muscles of inspiration
- Diaphragm
o Is the most important muscle for inspiration.
o When the diaphragm contracts, the abdominal contents are pushed downward, and the ribs are lifted upward and outward, increasing the volume of the thoracic cavity.
- External intercostal and accessory muscles
o Not used for inspiration during normal quiet breathing.
o Used during exercise and in respiratory distress.
Muscles of expiration
o Expiration is normally passive.
o Because the lung-chest wall system is elastic, it returns to its resting position after inspiration.
o Expiratory muscles are used during exercise or when airway resistance is increased because of disease (e.g., asthma)
o Abdominal muscles -> compress the abdominal cavity, push the diaphragm up, and push air out of the lungs.
o Internal intercostal muscles -> pull the ribs downward and inward.
Compliance of the respiratory system
o Describes the distensibility of the lungs and chest wall.
o Is inversely related to elastance, which depends on the amount of elastic tissue
o Is inversely related to stiffness.
o Is the slope of the pressure-volume curve
o Is the change in volume for a given change in pressure. Pressure can refer to the pressure inside the lungs and airways or to transpulmonary pressure (i.e., the pressure difference across pulmonary structures).
Compliance equation
C = V / P
C = compliance (mL/mmHg)
V = volume (mL)
P = pressure (mmHg)
Transmural pressure
Alveolar pressure - intrapleural pressure
Compliance of the lungs
o When the pressure outside of the lungs (i.e., intrapleural pressure) is negative, the lungs expand and lung volume increases.
o When the pressure outside of the lungs is positive, the lungs collapse and lung volume decreases.
o In the air-filled lung, inflation (inspiration) follows a different curve than deflation
(expiration);
o This difference is called hysteresis and is due to the need to overcome surface tension forces at the air-liquid interface when inflating the lungs.
o In the middle range of pressures, compliance is greatest and the lungs are most distensible.
o At high expanding pressures, compliance is lowest, the lungs are least distensible, and the curve flattens.
Airway pressure Paw
Pressure in the upper airways
Unless pressure is applied at the airway opening, Paw is 0mmHg or 760mmHg (same as atmospheric pressure)
Intrapleural pressure (aka intrathoracic pressure)
o Pressure in the pleural space
o Normally about -4mmHg at the end of expiration - we compare all pressures with atmospheric, so if we consider atmospheric pressure 0mmHg, then intrapleural is -4mmHg
How can we measure intrapleural pressure?
Using the esophageal pressure, obtained placing a specially designed balloon in the esophagus
Intrapulmonary pressure (aka intraalveolar pressure)
o Pressure at the alveoli level
o Changes as the intrapleural pressure changes
How many pressure gradients do we normally use to describe normal ventilation?
Four
o Transairway pressure
o Transthoracic pressure
o Transpulmonary pressure
o Transrespiratory pressure
Transairway pressure - Pta
o Pressure difference between the airway opening and the alveolus
o Pta = Paw - Palv
o The pressure gradient required to produce airflow in the conductive airways.
o Pressure that must be generated to overcome airway resistance
Transthoracic pressure (Pw or Ptt)
o Pressure difference between the pleural space and the body surface (Pbs) (same as atmospheric)
o It represents the pressure required to expand or contract the lungs and the chest wall at the same time
o Ptt = Pintrapleural - Pbs = (-4mmHg - (0mmHg)) = -4mmHg
Transpulmonary pressure (PL or Ptp)
o AKA transalveolar pressure
o Pressure between alveolar space and pleural space
o Pressure required to maintain alveolar inflation and is sometimes called the alveolar distending pressure
o Ptp = Palveolar - Ppleural = (0mmHg - (-4mmHg)) = +4mmHg
Why is intrapleural pressure negative?
o Natural elasticity of the lungs - recoil, wanting to go back when stretched.
o Surface tension - tension due to water / air interaction, tries to collapse lung
o Elasticity of the chest wall
o The overall result of the interaction of these 3 factors is increasing thoracic cavity volume and maintain negative intrapleural pressure - based on Boyle’s law
Boyle’s law
o Pressure x volume is constant (at a constant temperature)
o As volume increases, the pressure of the gas decreases in proportion
o P1 x V1 = P2 x V2
Transrespiratory pressure
o Pressure difference between the alveolar pressure and the atmospheric pressure
o Ptr = Palv - Patm = 0 - 0 = 0
Summary of pressure gradients at rest
T/F During inspiration the thoracic cavity will increase in volume - same as the pleural space, therefore based in Boyle’s law, the intrapleural pressure will decrease. It decreases from -4mmHg at rest to -6mmHg during inspiration.
TRUE
T/F During inspiration, intrapulmonary pressure (or alveolar pressure) will also decrease as the lungs increase volume. It will decrease from 0mmHg at rest, to -1mmHg during inspiration
TRUE
Explain how will pressure gradients change with inspiration
o Transpulmonary pressure = alveolar - intrapleural = ((-1) - (-6)) = 5mmHg -> increases from +4 to +5 during inspiration.
o Transthoracic pressure = intrapleural - atmospheric = ((-6) - (0)) = -6mmHg -> chest is pulling outwards. It has decreased from -4mmHg at rest to -6mmHg during inspiration
o Transrespiratory pressure = intraalveolar - atmospheric = ((-1) - (0)) = -1mmHg -> has decreased from 0 to -1mmHg -> means that air is going from the atmospheric to the alveoli.
T/F During inspiration, the intrapulmonary pressure will decrease to -1mmHg, compared to 0mmHg of the atmospheric. The goal is to move air in from high pressure to low pressure, until it equals again the intrapulmonary with atmospheric.
TRUE
T/F Expiration is passive, no muscles involved. The stretch receptors will send signals to the respiratory centers to inhibit stimulus and muscles will relax.
TRUE
T/F During expiration, thoracic cavity volume decreases, therefore pressures increase
TRUE
Summary of pressure changes during inspiration and expiration
T/F During expiration, intrapulmonary pressure raises to +1mmHg, therefore air goes out as it is higher than atmospheric at 0mmHg
TRUE
T/F Forced expiration does involve muscles
TRUE - abdominal muscles and internal intercostals
Upper airways include
Nasal chambers
Larynx
Pharynx
Cranial trachea
Walls of nasal chambers and turbinates are covered in what?
Layer of ciliated columnar mucous membranes
Rich in capillaries and branches of olfactory nerve
Purpose: warm humidify and filter
Pharynx structure
o Muscular tube lined with mucous membranes
o Crossover point between respiratory and digestive system
How does the air moves through the nostrils when a dog breathes ?
Air comes in through the middle of their nose
Comes out through the alar fold
Can we affect that when we place nasal cannulas, HFO?? We don’t know
Vomeronasal organ
Sensory organ that detects pheromones picked up by a dog’s wet nose
Olfactory bulb
Brain region that processes signals from the olfactory epithelium
3 times larger than in humans
Structure of larynx
o Rigid box-like structure (cartilage and smooth muscle)
o Arytenoids, cricoid, thyroid and epiglottis
o Vocal folds, ventricles, saccules
Describe upper trachea
o Permanently open, flexible tube
o C-shaped rings of hyaline cartilage linked by smooth muscle and fibrous connective tissue
o Each rings open onto dorsal aspect of trachea
Lower respiratory tract
o Intrathoracic trachea - slightly right to the esophagus. Lined with ciliary columnar mucous membrane to trap dust/dirt, particles -> pharynx -> coughed out or swallowed and destroyed by stomach acid
o Bronchi - right and left main bronchi branch from trachea. Rings of cartilage are complete and smaller than trachea
o Each bronchus enters the root of each associated lung and divides into smaller secondary bronchi -> bronchioles.
o About 16 divisions before becoming respiratory zone
Describe anatomy of dog lungs
o Right: cranial, middle, caudal and accessory
o Left: cranial and caudal.
o Left: cranial LL has 2 portions -> cranial and caudal portions of the left cranial LL.
Describe cat lungs
o Right: cranial, middle, caudal and accessory
o Left: cranial, middle and caudal
Once we are in the bronchioles, how do the airways continue to divide?
Terminal bronchioles -> respiratory bronchioles -> each divides to form 2-11smaller alveolar ducts -> end in alveolar sacs with 2-4 alveoli.
Globet cells and club cells
o Globet cells and cilia along the respiratory tract from the trachea, but as we go down they decrease in number.
o Globet cells - secrete mucus and bring unwanted particles up from lower airways. No longer found in bronchioles.
o Club cells - important in making glycosaminoglycans to protect the bronchioles and also serve as stem cells to make more bronchial epithelium.
Is there muscle in the lungs?
No.
The ability to contract or expand is due to the presence of collagen and elastin from fibroblasts.
Alveoli structure
o 700 million alveoli in human lung
o 0.1-1.5 um thick
o 50-100 um radius -> tendency to collapse
o Pores of Kohn - allow for colateral ventilation between alveoli but also a bit of fluid, bacteria, cells to come in and out of alveoli. Tent to be next to cells that don’t actively participates in gas exchange.
o Three major type cells: pneumocystis type I, type II and macrophages
o Nitrogen skeleton, poorly soluble gas. Helps maintain the alveoli open.
o Pulmonary artery leads to the net of capillaries that surround the alveoli - covers about 70% of the surface area.
o Capillaries leave the alveoli and form pulmonary vein that goes to the left atrium
Describe function of the 3 major type of cells we can find in the alveoli
o Pneumocytes type I - thin, flat and make the structure of the alveoli, helps with functionality of gas exchange.
o Pneumocytes type II - cuboidal, responsible for making the surfactant to lower surface tension. Surfactant within lamellar bodies.
o Macrophages - clean up debris.
Arteries in the pulmonary vasculature are about ______ of the pressure compared to systemic circulation
1/6 th
Low pressure system
T/F The arteries within the pulmonary vasculature have a tunica media hall as thick as the arteries in the systemic circulation and have elastic / muscular tissue
TRUE
Arterioles in the pulmonary circulation have a diameter of ________ microns with no muscular tissue, similar to venues.
< 100 microns
T/F There are arteriovenous anastomosis in the pulmonary circulatory system that can open when CO decreases
FALSE - open only when CO increases - exercises, higher demands of O2 - body adjusts.
Capillaries in the pulmonary circulation
o They arise from metarterioles
o They create a dense network over alveoli that traverse multiple alveoli -> venule
Bronchial circulation
o Supplies conducting airways
o Provides heat to warm and humidify inspired air
Are there lymphatics in the lungs?
o Yes
o At junction between alveolar and extra alveolar spaces -> when they get dilated -> peribronchial coughing
What do the met arterioles pre capillary sphincters do?
o They open or close based on need for O2 / CO2 and potentially on what happens inside the alveoli itself
o Hypoxic vasoconstriction -> this sphincters are closed -> blood goes from terminal arteriole to the venule -> shunting blood
T/F The alveolar epithelium and capillary endothelium fuses their basement membranes in the areas of gas exchange, to facilitate it.
TRUE
Alveolar surface tension
o Forces of attraction between molecules of liquid lining the alveoli causing a centripetal pressure, therefore alveoli tend to collapse - the smaller the higher pressure for collapse.
o Elastic recoil of lungs largely due to surface tension of air-water interface.
o Pressure inside a bubble is always higher than the pressure of the surrounding gas, but the alveoli are connected with the atmospheric pressure.
o Surfactant will create repulsing forces that will opposing those of surface tension -> surfactant reduces surface tension, although radius of bubble is also important based on the Law of Laplace
Law of Laplace
P = 2T / r
P = collapsing pressure
T = surface tension
r = radius
Because of the collapsing pressures, air would tend to move from smaller to bigger alveoli.
When there is surfactant present, it reduces the surface tension therefore radius becomes a little less important and there is less tendency for air to move from small alveoli to larger alveoli.
Surfactant
o Produced in the lamellar bodies of the type II pneumocytes to decrease surface tension (by 28% compared to having only air/water interface)
o Surface tension tends to collapse alveoli and suck fluid into alveolar space from capillaries
o By reducing surface tension:
- Prevent transudation of fluid, small alveoli emptying, collapse of alveoli, decreases WOB, increases lung compliance.
o Made up of 90% lipid with a hydrophilic and hydrophobic ends - polar head + nonpolar tail.
o Remainder of surfactant made of proteins - A, B, C and D - immunologic function
What is the partial pressure of a gas?
o Pressure exerted independently by a gas within a mixture of gases.
o Partial pressure of each gas = total P x fractional composition of the gas in the mixture
Composition of dry air
Partial pressure of O2 and CO2 in the body
Diffusion of O2 and CO2 across concentration gradients is according ___________
Fick’s law
Fick’s law
o Diffusion of a gas is inversely proportional to the thickness and proportional to surface area
o A large, thin alveolar wall will enable more gas exchange than a short thick sheet
Diffusion = SA x D x (P1-P2) / T
SA = surface area
D = diffusion constant (different for each gas)
P1 - P2 = pressures at each side of the membrane
T = thickness of the membrane
Boyle’s law
P1 V1 = P2 V2
Dalton’s law
P total = P1 + P2 + P3 …
If partial pressure of one gas increases, another has to decrease to compensate
Henry’s law
o At a constant temperature, the concentration of a gas will be proportional to the pressure of the gas -> the amount of gas that dissolves in a liquid is directly proportional to the partial pressure -> more pressure, more concentration.
o Soda bottle - pressurized system - high concentration. If we open - pressure decrease as concentration decreases.
o Animal with SQ emphysema and we give 100% oxygen - trying to push out the nitrogen and put oxygen -> it will then move into the blood stream and be exhaled
How much oxygen contains each gram of hemoglobin when it is 100% saturated?
1.36mL O2 / gram of Hb
Normal Hb is about ________, therefore 1dL of blood contains approximately ________ of O2 bound to Hb
15 grams / dL of blood
20mL (1.36 x 15)
T/F Amount of dissolved O2 is a linear function of PaO2
TRUE
0.003 mL / dL / mmHg PaO2
There is always a small physiologic shunt due to venous blood that bypasses pulmonary capillaries, therefore PaO2 is normally ______ mmHg and SpO2 ________%
97mmHg
97.5%
How much oxygen is normally removed in a resting state?
About 25%
Venous blood normally saturated to 75%, total O2 content of 15.2mL/dL
T/F - P50 is at what PaO2 the Hb is saturated 50% and it is species dependent
TRUE
Dogs 28.8mmHg
Cats 36mmHg - less affinity for Hb, more released to go into the tissues
Things that will shift Hb-O2 dissociation curve to the right
o Increased P50 (cats - decreased affinity)
o Increased temperature
o Increased CO2
o Increased 2,3-DGP
o Decreased pH
Things that will shift Hb-O2 dissociation curve to the left
o Decreased P50 (increased affinity for O2)
o Decreased temperature
o Decreased CO2
o Decreased 2,3-DGP
o Increased pH
Causes of hypoxemia
o Low FiO2
o Hypoventilation -> Dalton’s law (Total = P1 + P2 + P3…)
o Venous admixture: Low V/Q, no V/Q, diffusion impairment, shunt
Summary of partial pressures of gases in dead space, alveoli and blood
Causes of hypoxemia, PaO2, A-a gradient and responsiveness to O2
T/F - Breathing is controlled with respiratory centers in the medulla, but we can also control it voluntarily (cerebral cortex)
TRUE
Control of breathing
MEDULLA
o Ventral respiratory group (VRG) -> both inspiratory and expiratory neurons
- Pre-Botzinger complex -> central pattern generator (recently recognized as kind of the SA node for breathing, the pacemaker)
- Botzinger complex -> expiratory neurons
o Dorsal respiratory group (DRG) -> inspiratory neurons
PONS
o Apneustic center -> stimulate inspiratory neurons of DRG and VRG -> role in gasping breathing
o Pneumotaxic center -> regulates volume and rate, is like the off switch. For fine tunning
CORTEX, LIMBIC SYSTEM -> voluntary control, emotions
Central chemoreceptors in the medulla
o Retrotrapezoid nucleus in the brainstem
o Has pH sensors -> blood CO2 will diffuse into CSF and increase the concentration of protons, decreasing pH -> central mediated hyperventilation to eliminate CO2.
Peripheral chemoreceptors
o Bilaterally paired in carotid bodies (glomus type I cells), less in aortic bodies
o Hypoxemia (via oxygen sensitive K channels), hypercapnia, acidemia, or decreased in perfusion -> increased ventilation via glossopharyngeal nerve
o We also have baroreceptors -> mostly concerned with circulation, but severe hypotension will lead to hyperventilation.
Receptors within the lungs to control breathing
o Stretch receptors (usually inactive)
- Within airway smooth muscle -> stretch -> vagus nerve -> inhibits apneustic center
- Inhibits respiration / prevents overdistension (Hering Breuer reflex)
o Irritant receptors
- Between airway epithelial cells (noxious gases, cigarette smoke, dust, cold air)
- Causes bronchoconstriction and hyperpnea
o J receptors (juxtacapillary and in alveolar walls; aka C-fibers)
- Interstitial fluid or engorged pulmonary capillaries (PTE) -> stimulate rapid, shallow breathing
- Also in bronchi, larynx and nose
Summary control of respiration
T/F - Phrenic nerve controls diaphragmatic muscles and intercostal nerves travel from the spinal cord (C2-C3) to the intercostal muscles
TRUE
Why a patient that comes with cervical spinal cord injury might have breathing difficulties?
Interrupted connections between CNS and phrenic / intercostal nerves
T/F Atmospheric pressure increases with altitude
FALSE - decreases
760mmHg at sea level
T/F Intrapleural pressure changes from top to bottom of the lungs
TRUE
The lung is distorted by its own weight -> alveoli are stretched and expanded in the dorsal aspect, while they are compressed at the bottom by lung above
What makes air flow in and out of the lungs?
o Contraction and relaxation of diaphragm and intercostal muscles
o Lungs are passive participants -> due to adhesive nature of pleural fluid, lungs are pulled outward when thoracic wall expands
o Recoil of thoracic wall during exhalation causes compression of lungs
o Resistance -> force that will slow motion, slow flow of gases -> primarily dependent on diameter / size of airways -> ΔP / Flow
o Compliance -> ability to stretch while under pressure; aka distensibility. C = ΔV/ΔP
Compliance
o Varies with lung size -> decreases at high lung volumes
o When abnormally low -> lung is stiff. Difficult inhalation but easy exhalation.
o Increased compliance -> filling is easy, exhalation is difficult
Equation of motion
What is pendelluft
Movement of air within small airways; air pendulum
Why is it important to have an adequate inspiratory time and pause?
o Because we have fast and slow alveoli.
o If we deliver a very fast high velocity air into the airways we might be only filling the fast alveoli.
o Adequate inspiratory time and pause to allow equilibration of gases in the airways
T/F Lung compliance is the same during inspiration and exhalation
FALSE - at any given pressure, the lung volume will be less during inhalation than during exhalation
What is hysteresis? What causes the differences in compliance during inspiration and exhalation?
o The reluctance or delay of elastic structures to accept the deformation imposed by an applied stress.
o Is due to the surfactant - will change surface tension more rapidly during expansion than during compression
o Inhalation -> the lung becomes soon less compliant -> probably to avoid overdistension
o Exhalation -> the lung, as the volume decreases, becomes more compliant -> probably to allow collapsing of airways
How can we calculate resistance in a ventilated patient?
(PIP - Pplateau) / flow
Dynamic Compliance
Cdyn = ΔV / PIP - PEEP = mL/cmH2O
ΔV = tidal volume
PIP = peak inspiratory pressure
PEEP = positive end expiratory pressure
Static compliance
Cstat = ΔV / PIP - Pplateau = mL/cmH2O
ΔV = tidal volume
PIP = peak inspiratory pressure
Pplateau = plateau pressure
Relationship between tidal volume, inspiratory time and flow rate
Flow rate = Vt / Tins
Vt = tidal volume
Tins = inspiratory time
Changing things around we can also say:
Tins = Vt / Flow
Vt = Flow x Tins
Based on Bradbrook et al., 2013, which formulas did they come up with to calculate compliance and resistance based on body weight?
Crs = BW + 9
Rrs = (BW x (-0.1)) + 7
Crs = compliance of the respiratory system
Rrs = resistance of the respiratory system
T/F - There is more laminar flow within the small airways than within the trachea
TRUE
T/F Turbulent flow is more difficult to calculate as we don’t know exactly which gas with go from point A to point B, whereas with laminar flow it is easier, we just apply the formula
TRUE
T/F Due to gravity, the distribution of tidal volume is not the same between dorsal and ventral alveoli
TRUE
At FRC, dorsal alveoli are _______ and ________ to the plateau of their pressure/volume curve (cannot accept much more V) due to gravity pull
Large
Closer
Alveoli at the bottom are ________ on pressure/volume curve due to weight of lungs above and ______ accept more volume/change in pressure
lower
can
Why is there greater perfusion than ventilation in the bottom of the lungs?
Because blood is heavier compared to lungs, but both perfusion and ventilation increases in dependent regions of the lungs
T/F Increasing pressure ventrally distends vessels -> increases resistance to flow
FALSE - decreases resistance to flow
Ventilation (V) / Perfusion (Q)
o Non-dependent regions -> higher V/Q
o Dependent regions -> lower V/Q
o Pulmonary capillaries in non-dependent regions have increased O2 and decreased CO2
o Dependent regions suffer from atelectasis / edema + most greater influence on net blood ABG since they receive more blood flow -> prone position preferred if under GA.
West lung zones
In diseased lungs we have a zone 4 with increased interstitial pressure and reducing flow
TRUE
How is ventilation / perfusion normally controlled?
o Autoregulatory controls
o If low PAO2 -> constriction of terminal arteries -> shunt blood -> hypoxic pulmonary vasoconstriction
o If high PAO2 -> dilation of arterioles to increase blood flow
o If PaCO2 is high -> bronchioles will dilate to eliminate CO2
o End result: poorly ventilated areas with low PAO2 and high PaCO2 have vasoconstriction and bronchodilation to correct.
Dead space
How will the following diseases affect C / R?
Aspiration pneumonia
Feline asthma
Severe ascites
Tracheal collapse
Mainstem bronchus intubation
ARDS
Aspiration pneumonia -> decreased compliance
Feline asthma -> increased resistance
Severe ascites -> decreased compliance
Tracheal collapse -> increased resistance
Mainstem bronchus intubation -> decreased compliance - less volume per unit of change in pressure
ARDS -> decreased compliance
Pickwickian syndrome
Obesity hypoventilation syndrome, happens there is obesity and have hypoxemia and hypercapnia
Explain why with diseases that have decreased compliance we tend to see fast shallow breathing
o Lungs cannot expand well, needs higher pressures -> to get same minute ventilation as tidal volume is reduced, therefore they need to increase RR
o Also, J receptors in lungs activated -> will stimulate a rapid shallow breathing
Explain why with diseases that have increased resistance we tend to see slow deep breaths
We need to maintain a good minute ventilation -> takes longer to get an adequate tidal volume due to increased resistance -> we have to generate greater pressures to get air from point A to point B.
In which animals would we use the pulmonary function tests?
o In not very sick ones - exercise intolerance, cough or shortness of breath
o Or in patients that are on the vent
How would be a different way to classify respiratory diseases?
o Obstructive diseases (like COPD, air trapping) - big lungs
o Restrictive diseases (fibrosis) - small lungs
o In dogs / cats add upper airway / cervical obstruction
Forced expiratory volume / capacity
How much air you can breath out
o In 1 second - FEV
o Or completely (until getting to the residual volume) - forced vital capacity (FVC)
FVC / FEV in obstructive disease
o Hard to get the air out
o Small airway disease, inflammation, mucus plugs
FVC / FEV for restrictive disease
o Flow is not a problem, easy to get air out but capacity is reduced, they do not have more air to exhale
o Stiff lungs, they cannot inflate as much
If there is a patient with reversible obstruction to air flow and we give bronchodilators, what would we expect to occur to FEV/FVC?
Both would increase
Can be measured pre and post bronchodilator
T/F Dogs do not have airway reactivity and bronchoconstriction
TRUE
Causes of reduction of forced vital capacity
o Thoracic cage disease
o Neuromuscular disease
o Pleural space disease (pneumonia/effusion)
o Fibrosis
o Pulmonary edema
T/F Expiratory flow rates are limited by dynamic compression of airways during forced expiration, at some point you cannot increase anymore the rate
TRUE
What are challenges with pulmonary function testing in dogs?
o Cooperation
o Not possible to do effort breathing (maximal inspiration or exhalation)
Abnormalities in lung function testing
Rationale for lung function testing
What are veterinary options for pulmonary lung testing?
o TBFVL - tidal breathing flow volume loops
o Compliance and resistance
o 6 minute walk test
Tidal breathing flow volume loops
o Facemask connected to a pneumotachograph
o Measures flow, rate, and integrates to volume
o Changes in wave forms support obstructive diseases
Tidal breathing flow volume loops - upper airway obstruction
Tidal breathing flow volume loops - lower airway (feline asthma)
o Similar inspiratory flow
o Marked change in expiratory flow due to bronchoconstriction and mucus plug
T/F With tracheal collapse, if it is extrathoracic collapse they will have more inspiratory flow limitation vs intrathoracic collapse will curse with expiratory flow limitation
TRUE
Given this loop, what is the most likely disease?
o Most consistent with a fixed obstruction (tracheal mass)
o Light grey abnormal
What are lung mechanics governed by?
Flow rate - mL/sec
Driving pressure - cmH2O
Inspiratory time (occasionally expiratory time)
Resulting volume of air moved
T/F Higher flow rates require more pressure to generate
TRUE
For a given tidal volume, higher flow rates will result in _______ peak pressures over a short time
Higher
- Plateau pressure should be the same
T/F If there is a big difference between PIP and P-plateau it can be due to increased airway resistance but also due to a short inspiratory time (or both)
TRUE
Causes of increased lung resistance
o Primarily the upper / larger airways
o Lar par, BOAS
o Bronchoconstriction / lower airway dz
o Tracheal collapse
How can static compliance be measured under anesthesia?
o Having an anesthesia machine with pressure gauge and a hand held spirometer
o Inflate the lungs to 20cmH2O then measure exhaled volume
o Inflate the lungs to 10cmH2O then measure exhaled volume
o Measure static compliance (change in V / change in P)
Example of measuring static compliance in dogs under anesthesia
What is dynamic hyperinflation?
o Air trapping
o Intrinsic (auto) PEEP
o Most common in patients with intrinsic airway disease, with lower airway diseases
o Breathing without fully getting rid of the air -> chest cavity just expands and it becomes more difficult to move air.
Intrinsic (auto) PEEP
o Typically in ventilated patients
o Inadequate time for exhalation (may or may not be pathologic)
o Small airway disease /mucus
Negative effects of autoPEEP
o Worsening of cardiac pressure
o Barotrauma or hypoventilation if pressure limited ventilation
o Increased mean airway pressure
What is time constant?
o When pressure is applied to the lung, there is a time lag (very short, millisecond), until the volume change occurs
o The time point at which to inflate or deflate to 63% of tidal volume is called time constant
o Given also by compliance x resistance
Which disease would have the longest time constant?
ARDS
COPD
Pulmonary edema
Pneumonia
COPD - having hard time getting air out
What is an entrapped lung? and a trapped lung?
o Entrapped lung - unexpandable lung due to active process (like a pyothorax)
o Trapped lung - unexpandable lung due to long resolved process (resolved pyothorax 5 years later)
Six minutes walk test
PCO2 depends on?
Alveolar minute ventilation - Vt x RR
When we have a patient intubated, what properties of the respiratory system determines how much pressure reaches the alveoli?
Several factors:
o Resistance of the ET tube and airways
o Flow
o Airway pressure (at mouth point)
Palv = (Paw - (Ret + Raw)) x flow
In a patient in the vet, what property of the respiratory system determines how much volume reaches the alveoli?
Static compliance
What is static compliance?
o Overall compliance of the lungs and chest wall when there is no air flow
o Represents changes in compliance at the alveolar level
What is dynamic compliance?
o Compliance of the lungs during breathing
o Represents both airway and alveoli compliance
Name for each of these conditions which compliance would be affected, if static or dynamic
Asthma
Pneumonia
Pneumothorax
Tachypnea
ARDS
Pulmonary fibrosis
Pulmonary edema
Lung lobectomy
Emphysema
Bronchitis
Mucus plug/FB
o As dynamic compliance includes static compliance, secondarily it will also be affected
Driving pressure
Plateau pressure - PEEP
What processes can affect static compliance?
Parenchymal disease, chest wall stiffness (Pickwickian syndrome), pleural space disease, abdominal compartment syndrome
T/F - Dynamic compliance describes the overall effects of resistance of the airways and compliance of the lung and chest wall on the relationship between airway pressure and tidal volume
TRUE
How can we separate resistance and compliance effects?
o Stop flow
o With no flow, Paw an Palv become the same, so the pressure we measure at the airway would be the same as the driving pressure.
o On a ventilator -> do an inspiratory hold
T/F - The overall relationship between the pressure at the airway and the tidal volume delivered by the ventilator is summarized by dynamic compliance
TRUE
The dynamic compliance reflects two separate components
o The pressure drop from the airway to the level of the alveolus is due to the overall resistance and the inspiratory flow.
o The pressure available to provide alveolar ventilation is the driving pressure, which is the difference between the plateau pressure (the pressure in the alveolus after the tidal volume has been delivered and flow has stopped) and PEEP. This pressure is related to the tidal volume by the static compliance, which is the overall compliance of the lung and chest wall in the patient.
What is the equation of motion?
o The pressure available to generate a tidal volume is the sum of the the muscle pressure generated by the patient and the pressure applied by the vent.
o As the patient inspires, alveolar pressure decreases, so the net pressure applied to the alveolus and allows it to expand is the positive pressure from the vent PLUS the negative pressure generated by the muscles.
o Part of that net pressure is taken up from the resistive parts of the respiratory system multiplied by the inspiratory flow
o The rest of the pressure drop is from the static compliance of the respiratory system. The equation of motion is traditionally written using elastance which is just the inverse of compliance. Elastance as how much the lung wants to spring back when it’s stretched.
o The final term in the equation of motion is the residual pressure in the system, namely PEEP.
What are the control variables?
The physical variables that we can control on the vent
Volume, pressure, flow and time
What are phase variables?
Different phases of the breath governed by control variables
Trigger, limit, cycle and baseline
Trigger variable
Determines how inspiration is initiated
Time, flow, pressure and volume
Time triggered breath
Normally on mandatory modes where we decide an inspiration / expiration time and RR and the vent will deliver breaths.
Flow triggered breath
Patient will try to take a breath a cause a decrease in flow and trigger a breath
T/F In human medicine there is evidence that flow triggered breaths cause less work of breathing than pressure triggered breaths
TRUE.
Pressure triggered breath
Patient will try to take a breath and the vent will detect that drop in pressure and deliver a breath
Volume triggered breath
Same concept, vent will detect decrease in volume and deliver a breath
What is the limit variable
o A variable that cannot be exceeded during a breathing delivery. It does not stop the breath, that is the cycle variable.
o It can be flow, pressure or volume.
Flow limited scalar
Looks like a square
Volume control ventilation
o We set up a Tv and normally a flow limit
o The variable that will change is pressure - if there is a change in compliance and / or resistance
Pressure limited ventilation
o We set up a pressure that cannot be exceeded
o Typically associated with pressure control ventilation
Cycle variable
o Determines when the ventilator cycles into exhalation
o It can be time (after x seconds the breath stops), flow (after delivering x flow), volume (delivering a preset volume) or pressure (normally by setting the peak pressure alarm -> once the PIP reaches what we set up, the breath stops
Flow cycled breath
o Normally associated with pressure support
o We establish a specific level at which we want the breath to cycle off.
o Will reach a peak flow, then set a percentage at what point we want that breath to cycle off.
o Normally machines will automatically default to 25%
T/F Volume controlled ventilation is typically pressure limited and time cycled
TRUE
Ventilator modes
Pressure or volume control (control variable)
What determines the rest of the mode is how that breath is triggered
Controlled mandatory ventilation
o Time triggered - we decide, patient not doing anything
o Limit variable - pressure in PCV or flow in VCV
o Cycle - time (in PCV) or volume (in VCV)
Assist/controlled (A/C)
o Trigger can be time if it is controlled, or if it is assisted the patient can trigger (flow or pressure)
o Limit: pressure (PCV) or flow (VCV)
o Cycle - time (PCV) or volume (VCV)
Pressure support ventilation
o Trigger - always patient: flow or pressure
o Limit: pressure
o Cycle: flow
o Probably the most comfortable mode as the patient is determining how long, how much volume, small or bigger breath and the ventilator will give them what they want
Synchronized Intermittent Mandatory Ventilation (SIMV)
o Combined assisted control (PCV or VCV) and pressure support modes
o We set a RR - time triggered
o In between those breaths the patient can breath with pressure support breaths
What is patient ventilator asynchrony (PVA)?
When the ventilator gas delivery does not match the patient demands
It can be too much or too little
Indications for MV
Benefits of PEEP
PEEP and alveolar distension - at what PEEP there is increase in alveolar pressure but no more distension?
15cmH2O
What is auto-PEEP?
What is High Frequency Oscillatory Ventilation (HFOV)?
What is ventilator induced lung injury (VILI)?
PEEP and permissive hypercapnia
Contraindications for permissive hypercapnia
What is the normal spontaneous Tv
7-9mL/kg
T/F A breath in which the ventilator determines either the start or the end of inspiration is an assisted breath
FALSE - it is a mandatory breath
Decreased cardiac output is a potential detrimental effect of PEEP. Which mechanism is thought to be responsible?
The term “control” variable refers to
A
Fluffy is on a new mode of ventilation. Your mentor tells you this mode is time triggered. What does that mean?
A
What is the cycle variable in PSV?
Pressure
Your patient is on VCV-SIMV with PS. What type of breaths are possible?
Mainly A and C, but D would be correct too
a. CPAP
b. Pressure Support
c. SIMV
d. Assist/control
D - Assist/Control
A patient is on VCV-SIMV with PEEP. The clinician adds pressure support. What is the purpose of adding pressure support in this scenario?
a. Improve oxygenation
b. Decrease WOB
c. Prevent auto-PEEP
d. Protect against lung injury
B - Decrease WOB
Which of the following is thought to be most detrimental in a patient, an FiO2> 0.6 or a
PIP > 30cmH2O
PIP > 30cmH20
Define oxygen toxicity
Oxygen itself is a stable molecule with an indefinite Hal-life. However, excessive tissue oxygen can result in transformation of the stable O2 molecule to highly toxic substances, which is known as oxygen toxicity
Hyperoxia
An excess of oxygen supply
Hyperoxemia
A condition in which the PaO2 rises about normal values
Free radical
An especially reactive atom or group of atoms that has one or more unpaired electrons
Reactive oxygen species (ROS)
Chemically reactive chemical species containing oxygen
Reactive nitrogen species (RNS)
Chemically reactive chemical species containing nitrogen
Antioxidant
Compound that inhibits oxydation
What can be sources for oxygen toxicity?
Endogenous or exogenous
What are endogenous sources of oxygen toxicity?
Ionizing radiation procures
Environmental background radiation
UV radiation
Pollution
What are endogenous sources of oxygen toxicity?
Aerobic respiration
Excessive O2 in tissues compared to antioxidant defense mechanisms
Free electron production from NAPDH in neutrophils and macrophages during phagocytosis
Ischemic repercussion injury
Iron and copper
Oxidation of Hb to metHb
Toxicities including paraquat and bleomycin
T/F - ROS are natural by-products of normal oxygen metabolism and have important roles in cell signaling and homeostasis
TRUE
Why does ROS accumulation happens?
Because there is a limited capacity of the body to convert ROS into stable molecules via antioxidants.
T/F ROS does not contribute to RNS production
FALSE - ROS production can also contribute to RNS production which can be just as deleterious as ROS
What are the 3 stage reduction of O2?
Stage 1: reduction of molecular oxygen (O2) produces superoxide anion (O2-) -> precursor of most other ROS -> O2 + e- -> O2-
Stage 2: superoxide anion is stable itself but rapidly metabolized due to the presence of superoxide dismutase or glutathione peroxidase.
- Dismutation of O2- produces H2O2 -> not a ROS but it is a highly toxic molecule
2O2- + 2H+ -> H2O2 + O2
Stage 3: H2O2 can be reduced to water by the enzyme catalase
What is the Fenton / Haber-Weiss reaction?
o During the final stage of reducing H2O2 to water, hydrogen might be partially reduced to hydroxyl free radical (OH), which is the most toxic of ROS.
o Can be also reduced to hydroxyl anion (OH-) and singlet oxygen molecule (1O2)
o This reaction is canalized by iron or Cooper (pro-oxidants) -> that’s why they need to be tightly regulated in cells.
Myeloperoxidase reaction
o H2O2 can react with Cl to make hypochlorus acid (HOCl)
o It occurs in the phagocytic vesicle of the neutrophil
o Important in killing bacteria
Reactive nitrogen species
o NO can be beneficial in causing vasodilation
o In large quantities (like ischemic repercussion injury) can have cytotoxic effects and cause severe non-responsive vasodilation.
o NO can react with O2- (superoxide anion) to produce peroxynitrite (ONO2-) which can have deleterious effects to cells
With which molecules can free radicals interact and cause damage?
Lipids, proteins and nucleic acids
What can happen when free radicals interact with lipids?
o Lipid peroxidation
o Most susceptible to oxidation and free radical formation
o ROS reacts with lipids causing disruption of the lipid particles, and they also generate other ROS
o Lipid radical, peroxyl radical, lipid peroxide and ocoxyl radical
o Lipid peroxide is not a free radical but is damaging to the lipid membrane.
o Ocoxyl radical can lead to more radical formation.
What can happen when free radicals interact with proteins?
o Free radicals will interact with sulfhydryl-containing proteins
o Results in formation of disulphide bridges that will inactivate a whole range of proteins
What can happen when free radicals interact with nucleic acids?
o ROS can cause damage to DNA and RNA.
o If hydroxyl radical reacts with the base component -> DNA mutation
o If it reacts with the sugar component (ribose/desoxyribose) -> strand breakage, chromosome damage and mutation
What other effects can ROS cause?
o Can initiate the release of DAMPs - initiates inflammatory response.
o Release of cytokines and recruitment of neutrophils and monocytes will occur
o Vicious cycle of oxidative injury
T/F Hyperoxia during critical illness is associated with worse outcomes in people
TRUE
Which organ is the first target of oxidative injury and why?
o Lungs, due to continuous exposure to oxygen and its by-products.
o With prolonged exposure to O2 and during hyperbaric oxygen therapy (where partial pressure of O2 increases), there is increased O2 dissolved in plasma resulting in injury to other tissues and organs
What can oxygen toxicity lead to in the lungs?
Pulmonary parenchyma injury leading to pulmonary edema and impaired gas exchange.
What can happen when we administer 100% oxygen?
o Nitrogen displacement and wash out (maintains alveoli open) -> alveolar collapse
o Increased alveolar O2 concentration -> rapid diffusion of O2 in pulmonary circulation -> decreased alveolar volume, partial alveolar collapse and V/Q mismatch.
o Obstructive and adhesive atelectasis from poor mucociliary clearance and surfactant impairment
o Decreased immune response
o Alterations in microbial flora increasing the risk of secondary infections.
Name of the syndrome of oxygen toxicity in lungs in people
Lorrain Smith effect
Is there clear evidence that hyperemic therapies have positive benefits in outcomes of TBI?
No.
There are some proposed benefits of hyperopia including delayed cerebral ischemia and increased cerebral excitotoxcity after CVA, but no clear evidence
CNS and oxygen toxicity
o CNA is one of the first organs to be affected by O2 toxicity
o Syndrome in people is called Paul Bert effect
o Nausea, dizziness, headache, vision disturbances (retinal damage), neuropathies, paralysis and convulsions.
Oxygen toxicity and cardiovascular system
o Arterial hyperoxemia -> vasoconstriction -> increases SVR -> can impair perfusion, particularly coronary and cerebral circulation.
o Decreased HR, SV and CO have been documented with hyperoxia
o Potential beneficial effects of the vasoconstriction -> hemodynamic stabilization during shock and decrease ICP
Hyperoxia during MV
o High FiO2 associated with poor outcomes, due to all mechanisms discussed + VILI
o Even low levels of FiO2 40-60% -> linear association with pulmonary injury
o Imperative to decrease FiO2 asap.
o Target recommendations by ARDSnet group are SpO2 88-95%, PaO2 55-80mmHg
o The international consensus on MV -> minimum SaO2 of 90%
o Lower SpO2 targets (90-95%) associated with decreased pulmonary atelectasis, increased ventilator free days and lower mortality rates.
Hyperoxia during sepsis
o Can exacerbate the vicious cycle of hyperoxia and inflammation.
o Patients exposed to hyperoxia were associated with higher risk of mortality and serious adverse events, including ICU-acquired weakness and atelectasis.
Hyperoxia during cardiac arrest
o CPA can result in severe hypoxemia and repercussion injury after ROSC
o Several studies found association between hyperemia after CPR with mortality and worse neurological outcomes.
o Current recommendations are to target SpO2 of 94-96% in adults and 90-95% in neonates.
Hypoxemia and TBI
o Hyperoxia has some benefits to improve brain oxygen delivery and cerebral perfusion by causing vasoconstriction and decrease ICP
o FiO2 of 80% improved neurological outcomes compared to FiO2 of 50%
o Other studies found higher FiO2 to cause cerebral excitotoxicity and increase mortality.
o Currently no clear evidence for benefit of hyperoxia in TBI
What is hyperbaric oxygen therapy (HTO)
o Use of a pressurized 100% O2 above 2 atmospheres absolute (ATA) in a chamber.
o The increase in pressure reduces the volume of inert gas within the body -> dissolving gas bubbles back to the tissues
o High concentration gradient -> increases the rate of inert gas elimination which can treat decompression sickness
o Indications: gas embolization, CO toxicity, cyanide toxicity, ischemic injury, severe crush injuries, decompressive sickness, gas gangrene and compartment syndrome.
o Complications: barotrauma, decompression sickness, O2 induced seizures and pulmonary oxygen toxicity.
o Absolute contraindication: pneumothorax.
o Relative contraindications: bulla, pulmonary lesions, hx of thoracic or ear surgery, pyrexia, pregnancy and upper respiratory tract infections.
In which conditions has been ischemic repercussion injury (IRI) documented in veterinary medicine?
o Dogs: GDV, myocardial ischemia and cerebral injuries
o Cats: ATE
Why are the lungs and heart commonly injured during IRI? And the brain?
o Because they are the first organs to receive ROS from the portal blood system (injury to hepatocytes predominates during IRI).
o The brain has high concentrations of unsaturated fatty acids (a target for lipid per oxidation), a large iron store (resulting in hydroxyl radicals) and low antioxidant capacity.
What are the three areas of the lungs?
Upper, middle and lower
T/F Regardless of the lung position the lower area of the lung receives the most ventilation, followed by the middle, with the upper region having the last ventilation
TRUE
Hypoxia
Failure of oxygenation at the TISSUE oxygen
Hypoxemia
Arterial (BLOOD) oxygen tension (PaO2) below normal (80-100mmHg)
Types of hypoxia
Anemic hypoxia
Circulatory hypoxia
Histotoxic hypoxia
Hypoxemic hypoxia
Anemic hypoxia
o Low levels of hemoglobin - oxygen carrying capacity is reduced
o Supplemental oxygen will not increase the patient’s Hb concentration
o Treatment -> improve patients Hb concentration
Circulatory hypoxia
o Low CO causes reduction in blood flow (O2 delivery) to tissues.
o Decrease in PvO2 -> does not permit complete oxygenation during gas exchange.
o O2 supplementation will only benefit the patient if there is abnormal gas exchange.
o Treatments are aimed at increasing CO and tissue perfusion.
Histotoxic hypoxia
o The tissues (mitochondria) are unable to utilize the oxygen delivered to them.
o Delivering more oxygen will not improve mitochondrial dysfunction.
Hypoxemic hypoxia
o Low tissue oxygenation is a direct result of low arterial oxygen tension (hypoxemia).
o Supplemental oxygen will improve PaO2 therefore improve hypoxemia hypoxia.
Causes of hypoxemia
Hypoventilation
Diffusion impairment
V/Q mismatch
Shunt
Low inspired FiO2
Hypoventilation
o Upon reaching the pulmonary capillaries, CO2 diffuse into the alveolus, where a balance between CO2 production and alveolar ventilation determines its concentration.
o If CO2 production is constant, the arterial CO2 serves as a surrogate for alveolar ventilation
o Changes in alveolar ventilation will decrease the rate of CO2 removal and cause hypercapnia.
o Hypercapnia can be caused by hypoventilation, increased CO2 production, increased in dead space ventilation or increased inspired CO2.
o Most common cause of hypercapnia is hypoventilation due to decreased minute ventilation.
o Dalton’s law -> increases in CO2 will decrease O2
Diffusion impairement
Uncommon in SA
When alveolar membrane is thickened
Governed by Fick’s law
Shunt
o Refers to blood that enters the arterial system without traveling through ventilated areas of the lungs.
o In healthy animals small shunts are present -> bronchial artery blood is collected by pulmonary veins. Coronary venous blood drains into the left ventricle by way of the thebesian veins.
o The fraction of blood going through a shunt is expressed by the shunt equation:
Qs/Qt = Cc’O2 - CaO2 / Cc’O2 - CvO2
o If hypoxemia is caused by a shunt, oxygen supplementation will do very little to improve CaO2
Shunt equation 1 - terms for flow and oxygen content
Shunt equation 2 - origin of the equation
Inspired air PO2 and CO2
150mmHg
0mmHg
Alveolar PO2 and PCO2 in steady state
PO2 100mmHg
CO2 40mmHg
Mixed venous PO2 and CO2 content
40mmHg
45mmHg
If only 0.3% of oxygen is dissolved why do we recommend PPV when the PaO2 measures 60mmHg?
o Oxygen-Hb dissociation curve -> at a PaO2 of 60mmHg the SpO2 is <90% despite O2 supplementation
Oxygen nasal canulas, how much FiO2 can they deliver?
o 100mL/kg/min can increase FiO2 to about 40%
o 200mL/kg/min up to 80%
T/F Despite their widespread use, bubble humidifiers rarely increase the humidity of the oxygen passing through it.
TRUE
How much flow can accommodate the nasal cannulas of the HFOT?
o Small cannulas are limited to 8L/min
o Larger cannulas up to 40L/min
How should we chose the cannula size for HFOT?
Diameter of cannula should not be more than 50% of the diameter of the nares
What happens if we use a nasal cannula much larger than 50% of the nare diameter when providing HFOT?
Risk of barotrauma due to a lack of “pressure release”
Why is providing a heated and humidified gas with HFOT beneficial?
o Better tolerated
o Minimize nasal complications - desiccation, mucosal erosions, hemorrhage, propensity for opportunistic infections due to impaired local immunity
o Decrease airway inflammation, maintain mucociliary function and improve mucus clearance
What are initial HFOT flow rates recommendations?
o Between 150-200mL/kg/min
o However, in for example a 20kg patient with hypoxemia, a RR of 60bpm -> has a minute ventilation of 18L/min -> 250mL/kg/min (in this case that would be 5L/min flow) will not improve oxygenation as much.
How much PEEP can we gain with HFOT, if any?
o In people, about 1mmHg of PEEP for every 10L/min
o In healthy dogs, some degree of PEEP but not well established.
T/F - To deliver high amounts of FiO2 effectively with HFOT, flow rate should at least match, if not exceed, the patient minute ventilation to minimize oxygen dilution
TRUE
T/F - During a normal breath cycle, about 1/3 of the previous expired Tv is re-breathed
TRUE
o Because 1/3 of the exhaled breath remains in the upper airways.
o When the next inspiration occurs, this low oxygen concentration gas mixes with fresh atmospheric gas as it travels to the alveoli.
T/F In patients with acute respiratory failure the percentage of gas rebreathed ___________ as they draw breath from the upper airway
TRUE
o Dead space increases
o HFOT washes out the low oxygen concentration gas mixes
How are heart-lung interactions mediated?
By modifications in lung volume, intrathoracic pressure and gas exchange
T/F Venous return varies during the respiratory cycle due to the change in intrathoracic pressure
TRUE
What happens during spontaneous inspiration wit the intrathoracic pressure and venous return?
o The intrathoracic pressure falls to sub-atmospheric pressure, and right atrial pressure decreases too
o That increases the pressure gradient -> increased venous return
o Diaphragm moves caudally, increasing intraabdominal pressure -> mobilizes blood towards the RA
T/F Intrathoracic pressure only affects the R side of the heart
FALSE - it also influences LV afterload
T/F Decreased intrathoracic pressure causes _____________ LV afterload
Increased
Describe what happens with RV and LV volumes during inspiration
o RV diastolic volume increases due to increased venous return
o Due to ventricular interdependence, RV will cause a decreased LV diastolic volume, therefore a decrease in SV
o The combination of decreased LV diastolic volume and increased LV afterload, will lead to a decrease in CO during inspiration.
T/F The effect of spontaneous expiration on ventricular performance is the inverse of the inspiratory effects
TRUE
What can happen in patients with respiratory disease and the intrathoracic pressure?
o Larger variation in ITP during breathing could amplify the cycle of variations in LV stroke volume and arterial pressure.
o Profound reduction in intrathoracic pressure (ITP) during inspiration, like with upper airway obstruction, causes more dramatically increases in LV afterload and decreases LV stroke volume, and venous return would be augmented due to a decreased RAP secondary to a decreased ITP.
The small pulmonary vessels are sensitive to __________ pressure and are called intra-alveolar vessels. The larger (extra-alveolar) pulmonary vessels are affected more by __________ pressure.
Alveolar
Interstitial
T/F Right ventricular afterload is highly dependent on the distribution of blood flow in the lung
TRUE
What immediate effects can have the respiratory cycle on the heart rate?
o Alterations on autonomic tone due to altered lung volume.
o Spontaneous inspiration with normal Tv and decreased intrathoracic pressure induces vagal ton withdrawal, leading to increased HR.
o Spontaneous expiration with reduced lung volume and increased ITP induces vagal tone leading to decreased heart rate.
o This is the respiratory sinus arrhythmia.
T/F - Hypoxic pulmonary vasoconstriction (HPV) reduces V/Q mismatch by reducing pulmonary blood flow to poorly ventilated areas. However, it can cause an overall increase in pulmonary vascular resistance and decrease pulmonary blood flow
TRUE
T/F During MV with PPV, intrathoracic pressure rises in proportion to chest wall compliance and tidal volume
TRUE
o That will lead to decreased right atrial pressure and drop on venous return.
What are the consequences of PEEP on cardiovascular function?
Generally decreases LV stroke volume due to decreased venous return with increased venous resistance (caused by focal compression of the intrathoracic veins), and increased RAP that reduces pressure gradient (therefore less venous return).
For these reasons, patients under MV, especially if hypovolemic, could have significant reductions in CO and hypotension.
T/F Patients with PPV can develop RV dysfunction due to elevated pulmonary vasculature resistance and RV afterload with increased alveolar pressure
TRUE
Reduction in intrathoracic pressure causes ____________ venous return and _________ LV afterload
Increased
Increased
Why can WOB be a problem when we transition a patient from PPV to spontaneous ventilation?
Because the oxygen consumption is drastically increased in respiratory and cardiac muscles.
Is sympathetic tone increased or decreased during the weaning process
Increased due to stress, hypercapnia and hypoxia - elevates LV afterload due to increased SVR-
RAP and PVR ______________ during PPV inspiration and ___________ during PPV expiration.
Increase
Decrease
Venous return and RV stroke volume _________ during PPV inspiration and ________ during expiration
Decrease
Increase
T/F - Variations in RV preload and SV causes variations in LV preload and stroke volume, but with a time delay due to the pulmonary circulation
TRUE
o The variation of LV stroke volume leads to pulse pressure and stroke volume variations during PPV that are accentuated during hypovolemia (steep part of Starling curve).
Can we trust pulse pressure variation and stroke volume variation during spontaneous breathing?
No, they become unreliable due to the influence of variable tidal volume and lung compliance.
What is the RV preload reserve
The right ventricle’s ability to handle the changing volume loads
How can the RV preload reserve be estimated?
o It can be indirectly determined by dynamic changes in caudal vena cava diameters during a respiratory cycle using US.
o Collapse of CVC might be seen during spontaneous inspiration and PPV expiration
o Distension of CVC is seen during spontaneous expiration and PPV inspiration.
ISCAID - What is the feline upper respiratory tract disease
o Is a syndrome consisting of clinical signs that can include serous to mucopurulent ocular and nasal discharges, epistaxis, sneezing, and conjunctivitis.
o Clinical signs can be acute (≤10 days) or chronic (>10 days). The term “upper respiratory infection (URI)” is reserved for cats with clinical signs of URTD.
o The majority of cats with acute clinical signs of URTD have feline herpesvirus 1 (FHV-1)- or calicivirus (FCV)-associated URI.
o Some cats can develop secondary bacterial infections with Staphylococcus spp., Streptococcus spp., Pasteurella multocida, Escherichia coli, and anaerobes.
o Several bacterial species, including Chlamydia felis, Bordetella bronchiseptica, Streptococcus canis, Streptococcus equi subspp. zooepidemicus, and Mycoplasma spp., have been isolated or detected by molecular techniques (PCR) from cats with URTD without the presence of pathogenic viruses, suggesting a primary role in some cats.
ISCAID - Diagnosis of acute bacterial upper respiratory infection (≤10 days duration)
o All cats with suspected bacterial URI be evaluated for the FIV / FeLV.
o They do not cause respiratory disease directly, but both have been associated with lymphoma (which could cause URTD) and both can cause immunosuppression that could predispose to severe viral and bacterial URIs.
o There is limited benefit to performing cytology of nasal discharges to diagnose bacterial infection and guide the antimicrobial choice.
o If nasal discharges are serous and lack a mucopurulent or purulent component, antimicrobial treatment is not recommended because of the likelihood of uncomplicated viral infection.
ISCAID - T/F If acute bacterial URI in cats is suspected based on purulent or mucopurulent discharge, in the absence of evidence of the cause of URTD based on history and physical examination findings, it is recommended a period of observation without immediate use of an antimicrobial drug.
TRUE
ISCAID - When is it recommended to start antibiotics in humans for URTI?
o If clinical signs have not improved after 10 days
o If clinical signs have worsened after 5-7 days
ISCAID - Why are aerobic bacterial culture and susceptibility from nasal discharges difficult to interpret?
o Because some pathogenic organisms, like Chlamydia or Mycoplasma cannot be cultured on standard media.
o Positive culture might not be associated with bacterial infection due to growth of comensal organisms.
ISCAID - Treatment of suspected acute (<10 days) bacterial upper respiratory infection in cats
o Some cats with mucopurulent nasal discharge maintain normal appetite and attitude and experience spontaneous resolution of illness within 10 days without antimicrobial treatment.
o Antimicrobial treatment be considered within the 10-day observation period only if fever, lethargy, or anorexia is present concurrently with mucopurulent nasal discharge.
o If antibiotic is started, optimal duration unknown
o It is recommended empirical administration of doxycycline for 7– 10 days to cats with suspected acute bacterial URI as the first-line antimicrobial option.
o Most B. bronchiseptica isolates from cats are susceptible to doxycycline in vitro and is effective in vivo for the treatment of cats with C. felis infections and Mycoplasma spp. infections.
o Doxycycline also has activity against many opportunistic bacterial pathogens that are components of the normal microbiota of the respiratory tract.
ISCAID - What are cats prone when given tablets and why?
o Due to delayed esophageal transit time for capsules and tablets, cats are prone to drug-induced esophagitis and resultant esophageal strictures.
o Any table or capsule could cause this problem, but doxycycline tablets and clindamycin hydrochloride capsules have been reported most frequently to cause problems.
o Tablets and capsules should be given coated with a lubricating substance, followed by water, administered in a pill treat, concurrently with at least 2 mL of a liquid, or followed by a small amount of food.
ISCAID - What other antibiotic could be used for URTI in cats other than doxycycline?
o Amoxicillin -> for the treatment of acute bacterial URI when C. felis and Mycoplasma are not highly suspected.
o Based on evidence that cats administered amoxicillin for the treatment of suspected secondary bacterial infections in shelter cats with acute bacterial URI often have apparent clinical responses.
o Amoxicillin + clavulanate could be considered as an alternative to doxycycline in regions where a high prevalence of beta-lactamase-producing organisms has been identified (based on regional antibiograms).
o
ISCAID - Monitoring treatment for acute URTI in cats
o Most cats will rapidly improve within 10 days with or without antibiotics.
o If an antibiotic was prescribed and was ineffective and bacterial infection is still suspected after the first 7–10 days of administration, a more extensive diagnostic workup should be offered to the owner.
o An alternate antibiotic with a different spectrum should be considered only if the owner refuses a diagnostic workup and careful re-evaluation of the cat still supports the presence of a bacterial infection without an obvious underlying cause
ISCAID - Diagnosis of chronic bacterial upper respiratory infection (>10 days duration)
o A more extensive diagnostic workup should be considered for cats with URTD of >10 days of duration, particularly in the face of therapeutic failure after treatment of suspected acute bacterial URI.
o The diagnostic workup should evaluate other causes including Cuterebra spp. and fungal diseases as well as noninfectious causes of URTD including allergic diseases, neoplasia, foreign bodies, nasopharyngeal stenosis, oronasal fistulas, nasopharyngeal polyps, and trauma.
o If other treatable causes of URTD are not identified, a nasal lavage or brushings (for cytology, aerobic bacterial culture and antimicrobial susceptibility testing, Mycoplasma spp. culture or PCR, and fungal culture) and nasal tissue biopsy for histopathological examination with or without cultures (if not evaluated by lavage) should be performed.
ISCAID - T/F - Multidrug-resistant bacteria can colonize and be grown from the nasal passages in the absence of infection.
TRUE
ISCAID - What is the purpose of culture and sensitivity testing in cats with chronic bacterial URTI?
To identify the antimicrobial susceptibility of severe secondary bacterial infections that occur secondary to an untreatable underlying cause (eg, idiopathic inflammatory rhinitis)
ISCAID - Treatment of chronic (>10 days) bacterial upper respiratory infection in cats - 1
o The antimicrobial agent should be selected on the basis of culture and antimicrobial susceptibility test results if available.
o If an organism with resistance against a previously prescribed antimicrobial agent is identified and the clinical response is poor, an alternate drug should be substituted
o Because of concerns about the emergence of resistance to fluoroquinolones and third-generation cephalosporins, these drugs should be reserved for situations where culture and susceptibility results indicate potential efficacy and when other antimicrobial agents (eg, doxycycline, amoxicillin) are not viable options.
o There is no clinical evidence indicating that fluoroquinolones and third-generation cephalosporins are superior to doxycycline and amoxicillin in the treatment of chronic bacterial URI in cats.
o Azithromycin should be reserved for situations when chlamydiosis is not likely and when other antimicrobial agents (eg, doxycycline, amoxicillin) are not viable options.
ISCAID - Treatment of chronic (>10 days) bacterial upper respiratory infection in cats - 2
o If Pseudomonas aeruginosa is isolated in culture and believed to be the cause of a secondary infection, extensive flushing of the nasal cavity under anesthesia should be performed to remove loculated secretions.
o The use of drug combinations (such as a fluoroquinolone combined with a beta-lactam) has been recommended to treat P. aeruginosa infections.
o Because of the tendency of this organism to rapidly develop resistance, monotherapy is accepted.
o Antimicrobials be selected on the basis of culture and susceptibility testing
o Optimal duration of the treatment of chronic bacterial URI in cats with no other underlying disease is unknown.
o Recommended to administer the chosen antimicrobial for at least 7 days and if the drug is tolerated and showing a positive clinical effect, the drug should be continued as long as there is progressive clinical improvement and for at least 1 week past clinical resolution of nasal disease or plateau in response to treatment.
However, stopping treatment sooner might also be effective in some cats.
ISCAID - Treatment of chronic (>10 days) bacterial upper respiratory infection in cats - 3
o If mucopurulent discharge with or without sneezing recurs after treatment in a cat that has had a thorough diagnostic evaluation, the previously effective antimicrobial agent is usually prescribed empirically again, for at least 7–10 days, to assess for the treatment response.
o Switch to a different drug class or a more active drug within the class if treatment is ineffective after a minimum of 48 hours. Collection of specimens for culture and susceptibility is recommended if neither of these approaches is successful.
o There is no evidence to support the use of topical (intranasal) antiseptic or antimicrobial administration for the treatment of acute or chronic bacterial URI.
o However, topical administration of 0.9% saline solution is believed to have a mild mucolytic effect and might be effective in clearing nasal secretions in some cats.
ISCAID - T/F Many cats with chronic URTD have complete diagnostic evaluations performed and the only finding is lymphocytic–plasmacytic or mixed inflammation identified on histopathological evaluation without a known underlying cause (idiopathic feline rhinosinusitis).
TRUE
ISCAID - Monitoring treatment for chronic URTI in cats
o Usually based on clinical signs of disease.
ISCAID - What is the canine infectious respiratory disease complex?
o The clinical syndrome associated with CIRDC is generally characterized by an acute onset of cough with or without sneezing.
o Nasal and ocular discharges can also occur depending on the infectious agent that is involved.
o Fever is uncommon but can be present.
o The virus that have been implicated are canine adenovirus 2, canine distemper virus, canine respiratory coronavirus, canine influenza virus, canine herpesvirus, canine pneumoniavirus and canine parainfluenza.
o Bacteria implicated as primary pathogens in this complex include B. bronchiseptica, Streptococcus equi subspecies zooepidemicus, and Mycoplasma spp
ISCAID - Canine distemper and ocular / nasal discharge
o Dogs with canine distemper virus infection often have diarrhea and can have mucopurulent ocular and nasal discharge that might be confused with mucopurulent discharges caused by primary bacterial pathogens.
o Because of its significance to the health of other dogs and for prognosis, the possibility of underlying distemper virus infection should always be considered in young dogs with mucopurulent ocular and nasal discharges, even when other signs of distemper are absent.
ISCAID - CIRDC and co-infections
o Co-infections with multiple respiratory pathogens are common in dogs with CIRDC and each of the agents can be harbored by dogs with no clinical signs.
o Vaccines are available for some of the causes of CIRDC in some countries and include canine parainfluenza virus, canine adenovirus 2, canine distemper virus, H3N8 canine influenza virus, H3N2 influenza virus, and B. bronchiseptica.
o With the exception of canine distemper virus, the immunity induced by vaccination does not prevent colonization and shedding of the organisms and clinical signs of disease can develop in vaccinated dogs.
o Morbidity is generally decreased in vaccinated dogs compared with dogs that are not vaccinated when exposed to the pathogens.
ISCAID - Diagnosis of bacterial causes of CIRDC
o Many diagnostic tests could be performed to assess for evidence of primary or secondary bacterial CIRDC.
o There is limited benefit to performing cytology of nasal discharges to diagnose bacterial infection and guide the antimicrobial choice.
o Each of the organisms involved can be grown or detected by molecular methods from healthy and diseased dogs and vaccine strains of the organisms can be amplified by molecular diagnostic assays.
o Molecular assays might also be of limited sensitivity by the time dogs are presented for examination because viral shedding rates tend to peak very early in disease.
o Molecular tests not recommended for single cases with typical clinical presentations, no evidence of pneumonia, and when high-risk populations (eg, breeding kennels) are not involved.
o If an outbreak of CIRDC is suspected in populations of dogs like in shelters, breeding kennels, boarding facilities, or multiple dog households, molecular assays might be indicated, along with bacterial culture and serological testing for viral pathogens, particularly if poor response to treatment or severe clinical disease is occurring.
o If clinical signs consistent with pneumonia develop, a more extensive diagnostic evaluation is indicated.
ISCAID - Treatment of suspected bacterial CIRDC
o The majority of cases of CIRDC are currently believed to be viral in etiology and so antimicrobial administration is often not indicated.
o Most dogs with clinical signs of CIRDC including mucopurulent nasal discharge maintain normal appetite and attitude and might resolve spontaneously within 10 days without antimicrobial treatment.
o Antimicrobial treatment be considered within the 10-day observation period only if fever, lethargy, or inappetence is present together with mucopurulent discharges.
o If bacterial CIRDC is suspected in dogs with mucopurulent nasal discharge, fever, lethargy, or inappetence but no clinical evidence of pneumonia, it is recommended the administration of doxycycline empirically for 7–10 days as the first-line antimicrobial option.
o Optimal duration unknown.
o Amoxicillin or amoxicillin + clavulanate can be used as alternate first-line antimicrobials for the treatment of secondary bacterial infections in this syndrome if treatment with doxycycline fails or is not possible - some B. bronchiseptica isolates and all mycoplasmas are resistant to amoxicillin–clavulanate.
ISCAID - Monitoring treatment for bacterial CIRDC
o Usually self-limited or responds quickly to antimicrobial treatment.
o Primary or repeated diagnostic tests are rarely needed unless pneumonia is suspected.
o CIRDC has not been associated with chronic upper respiratory disease in the dogs.
o If the first drug chosen is ineffective and bacterial disease is still suspected after the first 7 days, a more extensive diagnostic workup should be considered before considering use of other drug classes like fluoroquinolones or azithromycin.
ISCAID - Bacterial bronchitis in dogs and cats
o Inflammation of the bronchi in dogs and cats is associated with many different conditions including inhaled irritants; infections by bacteria, viruses, Dirofilaria immitis, respiratory parasites (tissue migration of Toxocara canis); pharyngeal or esophageal dysfunction; and allergies.
o Acute inflammation of the bronchi can occur secondary to the primary infectious disease agents that can cause acute and chronic URI in cats and CIRDC in dogs.
o Clinical manifestations, diagnostic plan, and treatment plan would be the same as for URTI / CIRDC
o Some dogs and cats infected with the primary bacterial pathogens B. bronchiseptica and Mycoplasma spp. can develop chronic bronchitis or bronchopneumonia.
o Dogs and cats with other inflammatory diseases of the bronchi or anatomic defects of the larynx and trachea (eg, laryngeal paralysis, collapsing airways) might develop secondary bacterial bronchitis.
o Many dogs with chronic bronchitis do not have large numbers of bacteria cultured after bronchoalveolar lavage and so the syndrome is not always associated with bacterial infection
o The source of those bacteria is thought to be the natural oral microbiota.
ISCAID - Diagnosis of suspected bacterial bronchitis
o The primary clinical manifestation of bacterial bronchitis in dogs and cats is cough, with or without signs of respiratory distress.
o Thoracic radiographs should be made on full inspiration to evaluate for pulmonary and cardiac changes that could be associated with cough.
o In dogs, radiographs should include the cervical and intrathoracic trachea and both inspiratory and expiratory radiographs can be performed to identify collapsing airways (or fluoroscopy if available).
o Some dogs and cats with bacterial bronchitis have radiographic evidence of thickened bronchi, but others have normal radiographs even though inflammation exists on cytology of airway washings.
o CT can also be used to determine the extent of disease.
o Other causes of bronchial inflammation should be explored (D. immitis serology, fecal flotation, fecal sedimentation, Baermann test, laryngeal function evaluation) as indicated by the history.
o If radiographic evidence of bronchial disease is present or suspected based on clinical findings, airway washings for cytological examination are indicated to determine the type of inflammation that is present and to obtain materials for Mycoplasma spp. culture and aerobic bacterial culture and antimicrobial susceptibility testing.
o The presence of neutrophilic inflammation, intracellular bacteria, and positive bacterial culture with characteristic radiographic findings suggests primary or secondary bacterial bronchitis. However, the trachea is not sterile in normal dogs and low numbers of bacteria cultured in the absence of cytological evidence of intracellular bacteria might not imply bacterial infection.
ISCAID - Treatment of suspected bacterial bronchitis
o While waiting for results of culture and antimicrobial susceptibility testing, either no antimicrobial treatment or, if the clinical disease is severe, empirical administration of doxycycline for 7–10 days.
o Recommended based on its in vitro activity against B. bronchiseptica isolates from dogs and cats, reports of positive clinical responses to doxycycline in cats with respiratory Mycoplasma infections, and a low rate of adverse effects.
o If a positive response is obtained in the first 7–10 days, treatment should be continued to 1 week past resolution of clinical signs of disease. Optimal duration of treatment for this syndrome is unknown.
o Dogs that fail to respond to antimicrobial treatment are likely to have primary chronic (noninfectious) bronchitis.
o Antimicrobial choices for dogs with suspected or proven Mycoplasma-associated bronchitis are often made empirically. Doxycycline or minocycline are commonly used for this syndrome and is likely to have a therapeutic effect for pets with suspected Mycoplasma spp. bronchitis.
o Fluoroquinolones and azithromycin are other drugs that might be effective for the treatment of Mycoplasma spp. infections.
ISCAID - Monitoring treatment for bacterial bronchitis
o If bronchitis is associated with Mycoplasma spp. or B. bronchiseptica, clinical resolution might be obtained with 1 course of antimicrobial treatment.
o In some cases, prolonged antimicrobial treatment might be needed.
o In the event that another primary cause of inflammation such as allergic bronchitis exists and secondary bacterial infections are occurring, recurrent treatment might be required.
o Repeated thoracic radiographs can be taken to follow bronchial changes, but this is of limited sensitivity.
o In some cases, repeated cytology and culture might be indicated.
ISCAID - Pneumonia in dogs and cats
o In dogs and cats, although uncommon, primary bacterial pneumonia can occur after infection with B. bronchiseptica, Mycoplasma spp., S. equi zooepidemicus, S. canis, and Yersinia pestis.
o In dogs and cats, although uncommon, primary bacterial pneumonia can occur after infection with B. bronchiseptica, Mycoplasma spp., S. equi zooepidemicus, S. canis, and Yersinia pestis.
o Of 65 puppies <1 year of age with “community acquired” pneumonia in the US, 49% were infected with B. bronchiseptica.
o Most cases of bacterial pneumonia in dogs and cats are secondary to other primary inflammatory events like viral infections or aspiration of oral, esophageal, or gastric contents during vomiting or regurgitation (commonly associated with megaesophagus), after aspiration because of pharyngeal or laryngeal function abnormalities, during anesthesia recovery, and after inhalation of foreign bodies.
o Bacterial pneumonia can develop in the presence of immunodeficiency syndromes.
o Secondary bacterial pneumonia potentially could develop as a result of other pulmonary or airway diseases like neoplasia, ciliary dyskinesia, bronchiectasis, and collapsing airways.
ISCAID - Diagnosis for bacterial pneumonia - 1
o Dogs and cats that develop cough that is associated with fever, lethargy, inappetence, or tachypnea should be evaluated for the presence of pneumonia.
o Full physical examination, complete blood cell count, and thoracic radiographs.
o If clinicopathologic findings and thoracic radiological findings support a diagnosis of bacterial pneumonia, collection of a transtracheal, endotracheal, or a bronchoalveolar lavage specimen for cytologic examination, aerobic bacterial culture, and antimicrobial susceptibility and Mycoplasma spp. culture is recommended.
o Culture and susceptibility testing should be recommended to the client and performed before starting antimicrobial drug treatment, provided that the animal is sufficiently stable.
o However, antimicrobial treatment should not be unduly delayed.
o Antimicrobial treatment should be initiated as soon as possible and within 1–2 hours if clinical signs of sepsis exist.
ISCAID - Diagnosis for bacterial pneumonia - 2
o Not all cases of aspiration pneumonia require antimicrobial treatment, because clinical disease might be primarily or solely chemical pneumonitis from aspirated materials.
o Anaerobic bacteria are sometimes associated with pneumonia, particularly if there is a history of aspiration, or grass awn foreign bodies are present.
o In cases with probable aspiration pneumonia, multiple bacteria are often cultured making it difficult to determine which is involved with continued inflammation.
o It is recommended consulting with a clinical microbiologist or specialist with expertise with infectious diseases or pulmonology for interpretation of culture and antimicrobial susceptibility results from endotracheal or bronchoalveolar lavage specimens.
o In cats and dogs that have life-threatening bacterial pneumonia or are oxygen dependent, airway sampling might not be feasible.
o Consider blood cultures in these animals before starting empirical antimicrobial drug treatment as an alternative way to obtain isolates for targeted antimicrobial susceptibility to guide long-term management.
o Empirical antimicrobial treatment should not be delayed in an effort to stabilize affected animals and obtain a pre-antimicrobial airway sample.
ISCAID - Treatment of suspected bacterial pneumonia -1
o Not all clients can afford diagnostic procedures and pneumonia can be a life- threatening disease -> provide empirical antimicrobial treatment while waiting for test results with potential for deescalation of treatment based on antimicrobial susceptibility testing.
o While hospitalized, parenteral antimicrobial treatment is generally recommended, regardless of the severity. Once discharged, PO can be continued.
o Doxycycline is a reasonable empiric choice for dogs or cats with mild pneumonia that is suspected to be from infection with B. bronchiseptica or Mycoplasma spp. (eg, the animal is from a shelter or boarding environment) and no other systemic signs of disease like fever, dehydration, lethargy, or respiratory distress are present.
o Not all dogs or cats with acute aspiration pneumonia have a bacterial infection. However, aspirated bacteria can cause infection secondary to the chemical inflammation associated with aspiration.
o If the patient is acutely affected and has no evidence of systemic sepsis -> either no treatment or parenteral administration of a beta-lactam antimicrobial like ampicillin, ampicillin-sulbactam, or the first-generation cephalosporin cefazolin might be sufficient.
o Oral medications could be adequate for this syndrome. However, if megaesophagus or other esophageal motility disorders exist, parenteral administration of the antimicrobial drug is indicated.
ISCAID - Treatment of suspected bacterial pneumonia - 2
o If signs of sepsis -> concurrent parenteral administration of either enrofloxacin or marbofloxacin combined with a drug with Gram-positive and anaerobic spectra until bacterial culture and antimicrobial susceptibility testing results return.
o Common options for Gram-positive and anaerobic bacteria include ampicillin or clindamycin administered parenterally
o if Bacteroides spp. were present, clindamycin could be ineffective and that metronidazole could be considered another option.
o If culture and antimicrobial susceptibility testing was not performed, the antimicrobial drug class or classes that were initially prescribed and associated with clinical response is/are chosen for continued oral treatment.
o Further data are needed from dogs and cats before a definitive recommendation can be made in regard to the use of systemic or inhaled glucocorticoids, which have the potential to contribute to adverse outcomes due to immunosuppression.
ISCAID - Monitoring treatment of bacterial pneumonia
o The current recommendation is to treat bacterial pneumonia for 4–6 weeks, but evidence to support this duration of treatment is lacking.
o Re-evaluation of animals with pneumonia no later than 10–14 days after starting treatment.
o At that point, decisions to extend treatment should be based on clinical, hematological, and radiographic findings.
ISCAID - Bacterias isolated in cats with pyothorax
o Most commonly a mixture of oropharyngeal anaerobes including Fusobacterium, Prevotella, Porphyromonas, Bacteroides, Peptostreptococcus, Clostridium, Actinomyces, and Filifactor villosus.
o Pasteurella spp, Streptococcus spp., and Mycoplasma spp. have also been isolated.
o Less commonly, Staphylococcus spp., Gram-negative bacteria other than Pasteurella, and organisms such as Nocardia spp. and Rhodococcus equi have been isolated.
o Wounds resulting from cat fights and URI are risk factors for pyothorax in cats.
ISCAID - Bacterias isolated in dogs with pyothorax
o Most commonly mixed anaerobes (Prevotella spp., Peptostreptococcus spp., Propionibacterium acnes, Clostridium spp., Bacteroides spp., Fusobacterium spp.) and Enterobacteriaceae, especially E. coli and Klebsiella pneumoniae.
o Streptococcus canis, Staphylococcus spp, Enterococcus spp., Corynebacterium spp., Bacillus spp., Trueperella (formerly Arcanobacterium) pyogenes, Pasteurella, Acinetobacter, Capnocytophaga spp., Enterobacter spp., Stenotrophomonas maltophila, Aeromonas hydrophila, Achromobacter xylosoxidans, Serratia marcescens and Pseudomonas spp. Actinomyces spp. and to a lesser extent Nocardia spp. and Streptomyces spp. have been implicated in canine pyothorax.
o Commonly results from migrating plant foreign bodies or trauma but can also result from bite wound inoculation.
ISCAID - Diagnosis of pyothorax in dogs and cats
o Thoracic radiographs -> evaluate for the presence of lung consolidation in the dog or cat after therapeutic thoracocentesis.
o Pleural fluid should be submitted for cytologic analysis, aerobic bacterial culture, and antimicrobial susceptibility testing, as well as culture for anaerobic bacteria and Myco- plasma spp. (cats) if available.
o Performance of Gram stain and acid-fast stains might provide addition information.
o Detection of actinomycetes and Mycoplasma spp. requires specialized growth conditions and prolonged incubation, and so the laboratory should be informed that Actinomyces spp., Nocardia spp., or Mycoplasma spp. are differential diagnoses.
ISCAID - Treatment of pyothorax in dogs and cats
o Intravenous fluid administration and critically, drainage of pus after placement of chest tubes with intermittent or preferably continuous suction with or without lavage.
o Surgical debridement might be required in some cases.
o Not recommended the administration of antimicrobial drugs into the pleural space.
o Parenteral administration of enrofloxacin or marbofloxacin (when available in parenteral form) with a penicillin or clindamycin combined with therapeutic drainage of the pleural space with or without lavage for the initial treatment or canine and feline pyothorax pending the results of culture and antimicrobial susceptibility testing.
o Treatment with an antimicrobial drug with activity against anaerobes should be continued regardless of culture results because fastidious anaerobic bacteria could be present.
o If combination treatment was initiated and the bacterial isolates are susceptible to both drugs in the initial treatment regime, then either of the treatment drugs could be discontinued.
o If organisms are grown that are resistant to one of the drugs and clinical improvement is not noted, that antimicrobial agent should be discontinued. A second drug to which the iso- late is susceptible should be substituted if the animal has not responded sufficiently.
o If organisms are grown that are resistant to both antimicrobials or clinical evidence of improvement is not evident, antimicrobial treatment should be changed to a drug to which the organisms are susceptible in vitro.
o Consultation with a specialist is recommended when multidrug-resistant organisms are isolated.
ISCAID - Monitoring treatment of pyothorax
o It has been recommended that cats with pyothorax be treated for a minimum of 3 weeks and ideally 4– 6 weeks.
o Serial thoracic radiography might be useful to determine whether antimicrobial treatment needs to be continued -> further study is also required to determine whether persistent radiographic abnormalities correlate with the need for additional antimicrobial drug treatment.
o At a minimum, follow-up radiography should be performed for 10–14 days after starting treatment and at completion of treatment.
o If the pyothorax persists or reoccurs after cessation of antimicrobials, repeated thoracocentesis should be performed for cytological assessment and for culture and antimicrobial susceptibility testing.
Hemoglobin extinction curves and SpO2
When is oxygen therapy indicated?
PaO2 less than 70 mmHg/ SpO2 less than 93% on room air
Why is humidifcation of oxygen important in longer term oxygen supplementation?
To avoid drying of the airway mucosa, which can lead to increased risk of infection and decreased mucociliary clearance
For flow by oxygen, how close to the patient’snostrils does the oxygen hose have to be?
No further than 2 cm.
What FiO2 can you achieve with a flow rate of 2-3 L/min (flow by)?
25-40%
Nasal oxygen flow rates and associated tracheal FiO2
With a tight-fitting face mask, what Fio2 can be achieved with what flow rates?
Flow rates of 8-12 L/min can achieve an FiO2of 50-60%.
What is a disadvantage of tight-fitting masks?
CO2 rebreathing
What FiO2 can you achieve with an oxygen hood?
Once the oxygen hood has been flooded with oxygen (1 to 2 L/min), oxygen flow rates of 0.5 to 1 L/min typically will deliver an FiO2 of 30% to 40%.
What are the measuring landmarks for a nasal oxygen catheter?
Tip of the nose to lateral canthus of the eye
With nasal catheters, what FiO2 can you achieve with what flow rates?
Flow rates: 50-150 ml/kg/min -> FiO2 of 30-70%
Why is there such a large variability in FiO2 with nasal catheters?
Panting, open mouth breathing, respiratory rate, seize of the animal
What are the landmarks for a nasopharyngeal oxygen catheter?
Tip of the nose to ramus of the mandible
What is the advantage of a nasopharyngeal catheter of a nasal catheter?
Less likely to sneeze
Describe 2 ways of applying tranctracheal oxygen
a. Percutaneously with a large bore through the needle catheter (aseptic technique, secure with white tape) – careful: ventroflexion or excessive skin can cause kinking of the catheter. Can do mattress suture on the dorsal aspect o the neck to reduce skin folds. Rates: 50-150 ml/kg/min
b. Temporary tracheostomy – like, with the exception that you use a catheter (just larger bore than in technique a) -> might as well place an actual tracheostomy tube.
By how much can hyperbaric oxygen therapy increase a patient’s PaO2?
10-20%
What is HBOT used for?
CO intoxication
Certain wounds -> higher dissolved oxygen content helps oxygen dissolve into tissues even if they don’t have great circulation
Risks of HBOT
Pneumothorax, ruptured tympanic membrane
Chamber can’t be opened without slowly decreasing the pressure complications cannot be readily addressed
What are complications of oxygen therapy?
a. Oxygen toxicity (FIO2 of 50% or higher for more than 24-72 h)
b. Depressed hypoxic drive for ventilation in patients with chronic hypercapnia (“blue bloater” syndrome, e.g. COPD in humans)
c. Depletion of N2 in the lung -> atelectasis
Describe the 5 phases of oxygen toxicity
a. Initiation phase: ROS cause damage to pulmonary epithelium: within 24-72 h of 100% oxygen
b. Inflammatory phase: recruitment of activated inflammatory cells -> increased vascular permeability -> pulmonary edema
c. Destruction phase: high mortality
d. Proliferation stage: type II pneumocytes and monocytes proliferate
e. Fibrotic stage: Collagen deposition, interstitial fibrosis
What is a complication of oxygen treatment in neonates?
Retrolental fibroplasia (retinal damage)
Define hypoxemia
Decreased oxygen partial pressure (leading to decreased oxygen saturation)
PaO2 less than 80 mmHg or SpO2/SaO2 less than 95%
What are the main causes of hypoxemia?
a. Decreased inspired oxygen concentration
b. Hypoventilation
c. Venous admixture
* V/Q mismatch (severe grades; that is low V/Q ratios)
* Anatomic shunts
* Diffusion impairment
* Atelectasis -> that’s an extreme of V/Q mismatch (zero v/Q ratio)
d. Decreased venous oxygen content
Which pulse oximeter wavelengths measures oxyhemoglobin versus de-oxyhemoglobin:
O2Hb: 940 nm
HHb: 660 nm
Which one of the 2 (PaO2or SaO2) determines the diffusion of oxygen into the mitochondria?
PaO2
At what SpO2 can cyanosis be seen and why?
SPo2 of 67%.
A normal Hgb level is approximately 15g/dL.
It takes 5 g/dL of deoxygenated blood to see cyanosis.
How can reduced venous oxygen content cause a low PaO2?
During states of shock the venous oxygen saturation will be low because less oxygen is delivered to the tissues in the first place.
During states of increased oxygen extraction (i.e.seizures), the venous oxygen saturation is also lower.
In these situations, it takes more time for the blood to take up enough oxygen in the lung to generate normal PaO2/SaO2 -> if this is not accomplished, the arterial oxygen saturation is lower than normal.
What is the P50 and how much is it for dogs and cats, respectively?
The P50 is the PaO2 at which 50% of the Hg is saturated.
Dog: 28.7 mmHg (my dissertation sources say between 28.3-30) -> depends on the breed! Boxer:25.9, hunting dogs 35.8
Cats: 34.1mmHg
What characteristic of Hg does the P50 describe?
Oxygen affinity -> the further to the right, the lower the oxygen affinity
The relationship of PaO2 = 80 mmHg corresponding to an SaO2 of 95% and PaO2 of 60mmHg corresponding to an SaO2 of 90% is derived from the human hemoglobin dissociation curve. What does this mean for dogs and cats in terms of SaO2 representing hypoxemic states?
It means that the SaO2 cut off for hypoxemia and severe hypoxemia are lower.
Meaning that an SpO2 of 95 does not really indicate hypoxemia.
Name causes for low inspired oxygen content
Defective oxygen cage, oxygen mask, anesthesia circuit etc.
High altitude
What is the relationship between PaCO2, PvCO2 and etCO2?
etCO2 < PaCO2 < PvCO2 (by 5 mmHg each)
What are the only 4 gases of importance in the alveoli?
O2, CO2, N2, water vapor
Which of these causes of hypoxemia are responsive to oxygen?
a. Low inspired oxygen: Responsive
b. Hypoventilation: responsive
c. Low V/Q: responsive
d. Anatomic shunt: Not responsive
e. Diffusion impairment: responsive (partially)
f. Atelectasis: Not responsive (but responsive to PPV)
g. Decreased venous O2: responsive
Why is diffusion impairment rare and under which circumstances can it occur?
It is rare because of compensatory mechanisms that prevent fluid accumulation in the lung interstitium, such as a pressure gradient from the alveolar interstitium to the interseptal instertitium, as well as lymphatics.
Diffusion impairment can occur when type I pneumocytes are damaged and type II pneumocytes proliferate (they are more plump).
Examples: oxygen toxicity, ARDS. Technically though, purely interstitial stages of cardiogenic edema can also cause this.
Explain the rule of 120.
At roomair at sea level, in a normal lung, the additive values of paCo2 and PaO2 will be 120.
If the value is less than 120, there is concern for venous admixture
Only at near-sea level and Fio2 of 21%
What is an advantage and a disadvantage of the Aa gradient?
(+) With the full formula, it can be used at any sea level and any Fio2
(-) The normal Aa gradient increases with increasing FiO2 (can be as high as 100-150 mmHg at 100% oxygen) -> easier to evaluate on room air.
What is an advantage and a disadvantage of the P/F ratio?
(+) It can be used easily at any FiO2
(-) It cannot account for hypoventilation. However, this is less relevant at higher FiO2s -> on room air the impact of PaCO2 on PaO2 is much higher -> recommend to use the rule of 120!
Write the formula for the venous admixture or shunt fraction.
Qs/Qt = (CcO2 - CaO2)/(CcO2-CvO2)
Qs/Qt = shunt fraction or venous admixture expressed as a % of cardiac output
Qs = Shunt flow
Qt = total flow
CcO2 = capillary oxygen content
CaO2 = arterial oxygen content
CvO2 = mixed venous oxygen content
Shunt fraction is the term when the patient is breathing supplemental oxygen, because under these circumstances, the V/Q mismatch does not contribute much to venous admixture, which leaves anatomic and physiologic shunts (i.e. 0 V/Q states/atelectasis)
What degree of venous admixture is normal?
<5%
What is minute ventilation and what is its formula?
a. Total volume of gas exhaled per minute
b. V = VT x RR
Explain what is tidal volume and its formula
a. Volume of air delivered to the lungs with each breath
b. VT = VD + VA
c. Where VD is the portion of tidal volume that is in the dead space, it does not participate in gas exchange and VA is the portion of fresh gas entering the alveoli.
What is alveolar ventilation and its formula
a. Volume of fresh inspired air available for gas exchange that enters the alveoli per minute
b. VA = VT - VD
How can we subdivide dead space?
Anatomic, alveolar, physiologic and apparatus
What is anatomic dead space
The volume of gas filling the upper airway, trachea and lower airways to the level of the terminal bronchiole
What is alveolar dead space
The portion of inspired gas that passes through the anatomic dead space and mixes with gas in the alveoli but does not participate in gas exchange with the pulmonary capillaries.
What is physiologic dead space?
a. Anatomic + alveolar
b. The sum of all portions of the tidal volume that do not participate in gas exchange
When does the physiologic dead space increases?
In VQ mismatch – portion of tidal volume ventilates alveoli that are not perfused.
What are the two ways of calculating dead space?
Fowler’s method and Bohr’s method
Explain Fowler’s method:
Measures the concentration of an exhaled tracer gas, normally nitrogen, over time, and displaying its concentration against the volume exhaled.
Explain Bohr’s method:
a. Uses the principle that all of the CO2 in the exhaled gas originates from the alveolus.
b. Concentration of CO2 in exhaled gas comprises alveolar CO2, that is diluted by air free of CO2 in conducting airways and in the airways that are poorly perfused
c. Assuming alveolar and arterial PCO2 are equal: VD / VT = PaCO2 – PECO2/PaCO2
What does Bohr method measure mainly?
The volume of lung that does not eliminate CO2 => physiologic dead space rather than anatomic dead space
What are normal values for PaCO2 in dogs and cats?
a. Dogs: 30-42mmHg
b. Cats: 25-36mmHg
What are values that will indicate hyperventilation or hypoventilation?
a. Hyperventilation < 30-35mmHg
b. Hypoventilation > 40-45mmHg
How high are the venous CO2 values compared to the arterial?
a. 3-6mmHg higher
What are the main factors controlling alveolar minute ventilation?
a. Central and peripheral neural control
b. Central and peripheral chemoreceptors
c. Neuromuscular junctions
d. Respiratory mechanics/muscles
Where is the respiratory control center in the nervous system?
Brainstem
What are the three main groups of neurons in the respiratory control center?
a. Medullary respiratory center
b. Apneustic center
c. Pneumotaxic center
Which area is the responsible for inspiration?
Dorsal respiratory group in the region of the nucleus tractus solitarius
What does the ventral respiratory group controls mainly?
Voluntary forced exhalation
What is the main function of the apneustic center?
Speed of inhalation / exhalation
What is the main function of the pneumotaxic center?
Terminates inspiration, thereby regulates inspiratory volume and respiratory rate
These nerve fibers converge on the phrenic motor neurons in the ventral horns from…
C3-C5
And the external intercostal motor neurons in the ventral horns of…
T2-T12
Where are mainly the peripheral chemoreceptors located?
Carotid and aortic bodies, and airway and lung receptors
How does the levels of CO2 in blood regulate ventilation?
Through the changes in pH of the CSF
How fast can are carotid bodies able to sense changes in arterial blood gas and respond?
1-3 seconds
How does hypoxemia stimulates ventilation?
Primary through peripheral chemoreceptors, it has no action on central chemoreceptors
What is the Hering-Breuer inflation reflex?
Pulmonary stretch receptors present in the smooth muscle of the airways respond to excessive stretching of the lung during large inspirations, inhibiting inspiration: it slows respiratory frequency by increasing the expiratory time.
What are the irritant receptors? And the J receptors?
a. Irritant: stimulated by noxious gases, cold, and inhaled dust. They lead to bronchoconstriction and increased RR
b. J receptors: respond to chemicals in pulmonary circulation, distention of pulmonary capillary walls and accumulation of interstitial fluid. Leads to rapid and shallow breathing. Play a role in dyspnea due to L-CHF. Also in PTE.
What are the main muscles involved in normal breaths?
a. Pharyngeal and laryngeal muscles, the diaphragm, rib cage, spine and neck muscles play a role in inspiration
b. Muscles of the abdominal wall, rib cage and spine on active expiration
What are the 2 main sources of impedance to gas flow that the muscles have to overcome
a. The elastic recoil of the lungs and chest wall
b. Resistance to gas flow, mainly in upper airways
What are the 4 main causes of hypercapnia and what are the 2 most common:
a. Hypoventilation
b. Increased dead space ventilation
c. Increased CO2 production with a fixed minute ventilation
d. Increased inspired CO2
e. Most common: a, b, or a combination of both
What are the main causes of hypoventilation?
a. Central neurological disease
b. Peripheral or central chemoreceptor dysfunction
c. LMN disease
d. Neuromuscular disease
e. Abnormal respiratory mechanics
f. Increased airway resistance
In which situations patients can be hypercapnic despite an increase in minute ventilation?
PTE with increased physiologic dead space and CO2 retention
What are systemic effects of hypercapnia and respiratory acidosis?
a. Directly decreases myocardial contractility and systemic vascular resistance
b. Tachyarrhythmias and prolonged QT interval
c. Constriction of renal afferent arteriole – AKI, decreased urine output
d. Increased Na and H2O retention and hyperkalemia
e. Increased ACTH secretion by anterior pituitary
What happens to the cerebral blood flow with hypercapnia?
Increases – vasodilation of cerebral vasculature and increased systemic BP
When is carbon dioxide narcosis seen?
With PCO2 > 90mmHg
What is venous CO2 a reflection of?
Arterial CO2 inflow, local tissue CO2 production and tissue blood flow
When will the venous-arterial PCO2 gradient increase? With what has been correlated with?
a. With decreased tissue perfusion
b. Correlated with decreased CO
c. Correlated with ROSC in animal models of CPA
Name other methods for continuous, noninvasive monitoring of PaCO2
a. ETCO2
b. Transcutaneous devices
Is ETCO2 higher or lower than PaCO2 in healthy patients? By how much?
Lower, ETCO2 underestimates PaCO2 by 2-6mmHg
Which conditions can decrease the ETCO2 and increase the PaCO2-PETCO2 gradient?
a. Low VQ
b. Hypoperfused lung portions
What is the only way to decrease arterial PCO2?
Increasing effective alveolar ventilation
What are the main steps to decrease arterial PCO2 and increase effective alveolar ventilation?
a. Airway patency – supplemental oxygen if needed
b. Hemodynamic stability
c. Underlying cause of hypoventilation: drugs: use reversals
d. Chemical stimulation of breathing: doxapram, caffeine, methylxanthines
Is sodium bicarbonate indicated in the treatment of correction of acidemia secondary to respiratory acidosis?
No
What is the most effective treatment for hypoventilation?
MV
What are the parts of the upper airways?
Nasal passages and choanae, nasopharynx and oropharynx, larynx and trachea
When do upper airway dynamic or static sings occur?
a. Dynamic signs occur during inspiration or expiration, depending on the location of the obstruction, or with stress, anxiety and activity that will precipitate obstruction
b. Static signs occur with fixed intraluminal or extraluminal obstructions.
What is the main clinical signs of tracheal, mainstem and laryngeal disease and from what do we have to differentiate it?
a. Cough
b. Differentiate from lower airway, pulmonary parenchymal and cardiac disease.
How is the cough that results from upper airway disease different from lower airway or pulmonary parenchyma cough?
Upper airway is dry and nonproductive, whereas the other is moist and productive cough.
How can we differentiate if it is upper airway disease cranial or caudal to the thoracic inlet?
a. When there is upper airway disease rostral to the thoracic inlet trachea, patients tend to have loud, noisy breathing and increased inspiratory time. There is a collapse of the airways cranial to the thoracic inlet trachea because generation of negative intrathoracic pressure upon inspiration collapses the weakened airway structure into the lumen.
b. Increased intrapleural pressure upon expiration collapses the upper airway caudal to the thoracic inlet and results in prolonged expiration, expiratory dyspnea and lower airway sounds (wheezes) on auscultation.
What are possible lung parenchyma complications associated with upper airway disease / obstruction?
NCPE / Aspiration pneumonia
Describe how we can stabilize upper airway disease patients in emergency, the main treatments
a. Oxygen – with a cage is the best method – one disadvantage? We cannot hear them if they worsen
b. Control of anxiety: if cardiovascular stable we can give acepromazine (low dose), butorphanol.
c. Airway access if needed: intubation, tracheostomy
d. Steroids to decrease airway inflammation. Consider risks on hypovolemic patients, previously on NSAIDs or with suspected neoplasia that steroids could mask its diagnosis.
What will we normally see on ABG of an upper airway obstruction?
a. Respiratory acidosis due to increased PCO2
b. If chronic: there will be a metabolic compensation with increased HCO3, improve acidemia and negative BE, but CO2 will still be mild elevated.
What diagnostics can we perform that will help us tailor better the origin of the upper airway disease process?
a. Thoracic radiographs (3 views): NCPE, pneumonia, intrathoracic tracheal collapse, mainstem collapse, airway/pulmonary neoplasia.
b. Cervical radiographs: laryngeal and pharyngeal masses, extra thoracic tracheal collapse and foreign bodies.
c. Fluoroscopy: preferable as it is dynamic assessment of all airways
d. Skull CT for nasal passages, nasopharynx and bulla.
e. Sedated laryngeal exam
f. Endoscopy
g. Bronchoscopy and lavage (cytology and culture)
What are the main disease of the upper airway tract?
a. BAS
b. Nasopharyngeal polyps
c. Nasopharyngeal stenosis
d. Congenital choanal atresia
e. Nasopharyngeal FB and infection
f. Laryngeal paralysis
g. Inflammatory laryngeal disease
h. Tracheal collapse
i. Tracheal stenosis/stricture
j. Tracheal FB
k. Upper airway neoplasia
What are main the changes we see in BOAS?
a. Stenotic nares
b. Nasopharyngeal turbinate
c. Prolonged soft palate
d. Tracheal hypoplasia
e. Tongue base thickness
And the secondary changes associated with the primary disease?
a. Everted laryngeal saccules
b. Tonsillar eversion
c. Laryngeal collapse
d. Tracheal collapse
e. Chronic GI signs
f. Syncope
Where is mainly the resistance to airflow during inspiration in normal dogs?
80% in the nose
How many dogs with BOAS presented for surgery had at bronchoscopy some degree of collapse or stenosis?
87%
Does worsening of GI signs correlate with worsen respiratory signs in BAOS dogs?
Yes
Why is cardiac troponin I elevated in BAS patients?
Myocardial injury from chronic hypoxemia
Why do we think there is minimal systemic inflammation in BOAS patients?
Because the C-reactive protein and haptoglobin levels are not increased.
What is the first line management for BOAS?
a. Weight loss
b. Control of excitement/anxiety
c. Medical management of GI signs
d. Treating if there is any underlying lung parenchyma disease
What is the most important part of the BAS surgical correction?
The nares: many of the other airway changes are considered to be secondary to stenotic nares.
Which specie is more prone to nasopharyngeal polyps? What is a nasopharyngeal polyp?
Cats
Benign inflammatory lesions that arise from the mucosa of the auditory tube or middle ear and grow into the nasopharynx or external ear canal.
Is medical management successful for nasopharyngeal polyps?
No.
Traction-avulsion of the polyp is a simple method, but, is there an associated chance of recurrence?
Yes, 40-50%
What are possible post-operative complications of ventral bulla osteotomy?
a. Horner’s syndrome
b. Vestibular dysfunction
c. Facial and hypoglossal nerve paralysis
What is nasopharyngeal stenosis?
a. Partial or complete narrowing of the nasopharynx by a membrane caudal to the choanae and rostral to the caudal aspect of the soft palate.
b. Can be congenital or secondary to chronic rhinitis, trauma and neoplasia
Is congenital choanal atresia unilateral or bilateral?
Can be both
What are examples of nasopharyngeal fungal infectious agents?
Cryptococcosis
Blastomycosis
What is the cause of the laryngeal paralysis?
Recurrent laryngeal nerve dysfunction
What are the main causes of recurrent laryngeal nerve dysfunction?
Congenital, denervation, trauma, iatrogenic, idiopathic, neoplastic and associated with diffuse neuromuscular disease (myasthenia gravis, hypothyroidism)
Name a few breeds that are predisposed to congenital laryngeal paralysis
Rottweilers, Dalmatians, Siberian Huskies, Bull Terriers
What is commonly associated with laryngeal paralysis that will worsen gastrointestinal signs?
Esophageal dysmotility
Medical management for lar par?
a. Weight loss
b. Stress/anxiety management
c. Heat and humidity management
d. Medications for GI support
e. Treat underlying condition
What are normally the three main procedural outcome goal categories?
a. Widen the dorsal glottis
b. Widen the ventral glottis
c. Widen both
Which surgery has more post-operative complications, unilateral or bilateral arytenoid lateralization?
Bilateral
What is the most common PO complication? Percentage seen?
Aspiration pneumonia, 8-33%
What are potential causes of inflammatory laryngeal disease in dogs and cats?
Feline respiratory viruses, bacterial infection, endotracheal intubation, previous FB and secondary to laryngeal surgery.
What is tracheal collapse?
Progressive, degenerative disease of the tracheal cartilages commonly seen in older toy and small breed dogs (Yorki!!)
How are radiographs to localize tracheal collapse?
Some benefit but they are static images, fluoroscopy is better.
Can laryngeal paralysis happen together with tracheal collapse?
Yes, ideally always do a laryngeal exam too.
Main treatment of tracheal collapse?
Cough control.
Other therapies:
a. Steroids
b. Bronchodilators
c. Harness
d. Weight loss
What are the main post-operative complications of prosthetic extraluminal rings?
Infection, laryngeal paralysis, tracheal necrosis and progressive tracheal collapse
When should we consider endoluminal tracheal stenting?
In patients with respiratory crisis that do not respond to medical management.
What is the most common upper airway neoplasia in cats?
Lymphoma
What is the sleep apnea-hypopnea syndrome in humans?
a. Repeat upper airway collapse during sleep
b. Patients are challenged by repeated hemoglobin desaturation episodes during their sleep.
Has the SAHS been seen in veterinary medicine?
a. Yes, a small group of brachycephalic dogs confirmed night-time desaturation in these dogs compared to the control group
b. SpO2 below 90% during 32% of the time spent in REM
What systemic complications is SAHS associated with in humans?
Arrhythmias, thrombosis, systemic inflammation
What is the consequence of overcoming increased upper airway resistance?
Greater sub atmospheric pleural pressures on inspiration => creates more strain on intrathoracic tissues
What can lead to repeat increases in sub atmospheric pleural pressure?
Weakening of the lower airways
What are common ABG abnormalities seen in brachycephalic breeds?
Lower PaO2, normal A-a gradient and increased PaCO2
Is the outcome of brachycephalic dogs undergoing MV different than non-BD?
No
How is the percentage of Bulldogs having GI issues, low, moderate or high?
High, around 97%, even if there are no clinical manifestations of GI disorders
Which parts of the GI tract are most commonly affected on BOAS dogs?
Esophagus, stomach and duodenum
When is there a favorable response in respiratory and GI sings in BOAS dogs?
If medical management is associated with BOAS corrective surgery
What are the main causes of tracheal trauma?
a. Projectile injuries, bite wounds, endotracheal tube damage and blunt trauma
The amount of damage depends on what on projectile injuries?
Size and mass of the projectile, its velocity and the amount of kinetic energy transferred to the tissues
There is a tracheal perforation. Where is the air going to go?
a. Cranial mediastinum and even retroperitoneal space.
b. If pneumomediastinum ruptures it will cause a pneumothorax
Where is normally the tracheal trauma associated with hit by car in cats?
Intrathoracic, because the carina is fixed, trachea ruptures cranial to it.
The onset of dyspnea due to tracheal damage following blunt trauma, is acute or chronic?
a. It can be both, can take days to weeks to develop
Why does the endotracheal tube causes damage to the trachea? Which kind of cuffs?
a. Mainly for overinflation of the ET cuff
b. Other causes: improper tube placement, injury from using a stylet, failure to deflate the cuff before repositioning or removing the tube.
c. Low-volume, high pressure cuffs
What are clinical signs associated with tracheal damage?
a. Increased RR and effort, cyanosis, exercise intolerance, open-mouth breathing…
b. SQ emphysema
c. If due to trauma: shock and hypovolemia signs, wounds and injuries in other parts of the body, signs of SIRS and sepsis.
What else can cause SQ emphysema after an anesthetic procedure apart from a tracheal tear?
Barotrauma
What are other conditions with similar clinical signs like tracheal trauma?
Intrathoracic tracheal compression by esophageal FB or mediastinal tumors, abscesses or hematomas. Pneumothorax, pleura effusion and diaphragmatic hernia.
What are some diagnostic tests we can do to diagnose a tracheal trauma?
Thoracic radiographs, fluoroscopy, CT, endoscopy, positive contrast tracheography
What should be avoided during anesthesia when there is a tracheal tear because it could acutely worsen our patient status?
PPV
How will we approach a cervical tracheal tear?
a. Through ventral midline cervical incision
And how do we approach a tracheal tear it if it is intrathoracic?
Right lateral thoracotomy, 3rd or 4th intercostal space.
How much is the percentage of trachea that can be resected?
20% in young dogs
25-50% in mature dogs
Which technique will be used in medium and large breed dogs for tracheal anastomosis? Why?
a. Split cartilage technique
b. It results in better alignment
Which technique will be used in small dogs and cats for tracheal anastomosis?
a. The trachea will be resected incising the annular ligament between cartilage rings.
Does conservative management work for tracheal tears and injuries?
Yes
A part from stricture resection, what other technique could be done for tracheal stricture?
Balloon dilation
What is the prognosis for tracheal trauma?
If trachea is repaired successfully is good.
Is stenosis after a tracheal resection a common complication?
No
Which pressures should be used in the ET cuff to avoid tracheal tears?
20-30mmHg to provide a seal without compromising tracheal mucosal perfusion.
Which diseases are considered allergic diseases in dogs and cats?
Parasitic allergic airway disease
Eosinophilic bronchopneumonia
Feline asthma
Pulmonary infiltrates with eosinophils
What are the main clinical signs associated with allergic airway disease?
Labored breathing, rapid shallow breathing, increased expiratory effort and coughing.
What does the term hyperreactivity describes?
The ease with which the airways narrow in response to a variety of stimuli
Explain the human asthma pathogenesis:
a. Large number of IgE => crosslink to mast cells in the submucosa of the bronchi and bronchioles => mast cell degranulation => release of inflammatory mediators => airway constriction and late phase inflammatory response.
b. Inflammatory mediators: pulmonary mucosal edema, smooth muscle hypertrophy of bronchi and bronchioles, accumulation of pulmonary secretions and airway narrowing
Why is functional residual capacity increased in asthmatic patients (humans)?
Because of air trapping
Is it very well known the pathogenesis in SA as well as in humans?
No
Name the main canine parasites that can cause allergic airway disease:
Parasites that migrate through lungs:
i. Toxocara canis
ii. Ancylostoma caninum
iii. Strongyloides stercolaris
Primary lung parasites:
i. Paragonimus kellicotti
ii. Capillaria aerophile
iii. Filaroides hirthi
iv. Dirofilaria immitis (HW) can cause allergic inflammation when large numbers of antimicrofilarial antibodies entrap microfilariae within the pulmonary capillaries
Name the main feline parasites that can cause allergic airway disease:
Parasites that migrate through lungs:
i. Strongyloides stercolaris
Primary lung parasites:
i. Paragonimus kellicotti
ii. Aleurostrongylus abstrusus
iii. Capillaria aerophile
iv. Filaroides hirthi
v. Dirofilaria immitis (HW) can cause allergic inflammation when large numbers of antimicrofilarial antibodies entrap microfilariae within the pulmonary capillaries
How can A. caninum and T. canis be detected? And Strongyloides stercolaris?
a. With a routine fecal flotation technique
b. Strongyloides better with Baermann
What is the treatment for parasitic allergic airway disease?
Anthelminthic treatment and anti-inflammatory dose of steroids to help decrease the inflammation associated in moderate to severe cases.
What is Canine allergic bronchitis and what other name is it known by?
a. Is pulmonary hypersensitivity with eosinophilic infiltration of lung and bronchial mucosa
b. AKA eosinophilic bronchopneumopathy
What is the signalment for canine allergic bronchitis? Any predisposed breeds?
a. Younger animals (mean 3.3 years +/- 2)
b. Siberian Huskies and Alaskan Malamutes are overrepresented
How often do we find peripheral eosinophilia in canine allergic bronchitis?
In about 60% of the cases
What are the common cytologic findings of the BAL or ETW of canine allergic bronchitis? Main treatment?
o More than 50% eosinophils in about 87% of the dogs, between 20-50% eosinophils in 13% of the dogs
o Steroids long term
What is pulmonary infiltrates with eosinophils (PIE)?
Umbrella term to describe a spectrum of diseases that involve a type I hypersensitivity reaction occurring in the pulmonary parenchyma.
What are stimuli that can cause PIE?
a. Pulmonary or migrating parasites, heartworm, drugs or inhaled allergens
What are the symptoms of PIE?
a. Symptoms of parenchymal disease: respiratory distress, rapid and shallow breathing, coughing and possible cyanosis
What will we see radiographically on PIE?
a. Diffuse, interstitial, bronchial o alveolar pattern, many dogs also have hilar lymphadenopathy.
What is feline bronchopulmonary disease?
a. Another broad term to describe several diseases process, some of them allergic in origin and some not.
What are the main 2 factors responsible for feline bronchopulmonary disease?
The cellular inflammatory response and the lower airway hyperreactivity
What are the most common clinical sings?
Coughing, respiratory distress with increased expiratory effort, rapid, shallow breathing, open-mouth breathing.
Which breed is overrepresented for feline lower airway disease?
Siamese
Feline lower airway disease - do they normally have peripheral eosinophilia?
a. No, normally CBC, chem and UA are pretty unremarkable.
What are the 2 main diagnostic tests we can do to diagnose feline lower airway disease?
Radiographs and BAL
What are the main radiographic changes that will be seen with feline bronchopulmonary disease?
Bronchial pattern (doughnuts and tram lines), increased in interstitial marking, alveolar patter or hyperinflation of the lungs with flattening of the diaphragm
Does the severity of the radiographic changes correlate with clinical sings of feline bronchopulmonary disease?
No
What are the most predominant cells found in the BAL of a cat with lower airway disease?
a. Neutrophils and eosinophils
What are the main treatments of Feline bronchopulmonary disease?
Steroids
Bronchodilators
Antihelmintic
Which kind of bronchodilators can we administer for feline bronchopulmonary disease?
o Methylxanthines (theophylline, aminophylline)
o Selective B2-receptor agonists (terbutaline or albuterol).
What are some secondary effects of the selective B2-receptor agonists and why do we need to be careful?
They can cause tachycardia / tachyarrhythmias therefore ideally to rule out cardiac disease before administering them.
Mention other experimental therapies for feline bronchopulmonary disease
Cyclosporine, leukotriene receptor blockers, cyproheptadine
What are the two main forms of pulmonary edema (pathogenesis wise)?
High pressure edema and permeability edema
What does the reflection coefficient of a tissue indicate?
The degree to which proteins are reflected across a capillary surface. 1 = 100% reflected, i.e. impermeable to protein; 0 = completely permeable to protein.
Name a few safety factors that protect tissues against ongoing edema formation.
a. Protein poor fluid that is filtered into the interstitium dilutes the interstitial proteins -> COP gradient between capillary and interstitium becomes larger, which opposed fluid filtration
b. Fluid filtration into non-distensible tissues causes an increase in interstitial hydrostatic pressure, which opposes fluid filtration
c. Increased driving pressure for lymphatic flow due to increase in interstitial pressure after fluid filtration
Why is hypoproteinemia alone rarely a cause of pulmonary edema?
Because the reflection coefficient in pulmonary capillaries is les tan in most tissues (0.7-0.95, this is from another source), and as such, there is less of a COP gradient between capillary and interstitium)
What is the main protective factor against edema in the lung?
Increased lymphatic blood flow
How fast can protein poor versus protein rich fluid be reabsorbed?
Protein poor: minutes
Protein rich: hours to days
What is the characteristic of high permeability edema (in terms of what structures are damaged?)
Pulmonary endothelium, epithelium or both
Name a few risk factors for VetALI
Inflammation, sepsis, SIRS, trauma, multiple blood transfusions, smoke inhalation, submersion injury, aspiration pneumonia, drugs, toxins
Other than VetALI, what are causes for high permeability edema?
PTE, toxic pneumonitis (inhalation of hydrocarbons etc), VILI
Name 2 forms of mixed etiology pulmonary edema.
NPE, NPPE
What is the blast theory?
o NPE is believed to be a consequence of fulminant neuronal sympathetic activation secondary to a neurologic insult
o Increase in SVR -> systemic hypertension -> increased afterload for the left ventricle -> increased pulmonary capillary hydrostatic pressure. Additionally, due to systemic arterial and venous hypertension, the blood is shifted to the pulmonary vasculature -> increase in capillary hydrostatic pressure. Due to the acute rise in capillary hydrostatic pressure -> endothelial damage (“stress failure”) -> protein leak
What is the presumed pathophysiology behind NPPE?
o Airway obstruction -> inspiration against closed glottis -> negative intrathoracic pressure -> negative pressure in pulmonary interstitium, increased venous return to right heart -> increased intravascular pressure -> combination of decreased interstitial hydrostatic pressure and increased capillary hydrostatic pressure causes edema. Additionally, this increase in hydrostatic pressure could cause stress failure -> protein leakage
o Sympathetic stimulation due to hypoxia may also play a role -> pathophysiology mechanism similar to NPE
What are potential causes for re-expansion pulmonary edema?
Decrease in interstitial hydrostatic pressure and increase in capillary hydrostatic pressure after re-expansion, reperfusion injury, surfactant depletion, mechanical disruption of endothelium
What are the mainstays of treating CPE?
Oxygen supplementation, diuretics, vasodilators, positive inotropes
What are the effects of furosemide on CPE?
Loop diuretic -> decrease in hydrostatic pressure, additionally it is a pulmonary venodilator and bronchodilator -> this is why it may be beneficial in treating edema forms other than CPE
What vasodilators can be used in CPE?
NO donors: Nitroprusside (arterial and venous dilation), nitroglycerin (venous dilation)
What medical options are experimentally investigated for NCPE?
Alpha antagonists, beta 2 agonists
What is a potential effect of colloid treatment in high permeability edema?
Due to the lower reflection coefficient, the edema may worsen due to accumulation of the colloid in the interstitium
Why can necropsy confirmation of PTE can be difficult?
o Thrombi undergo 50% reduction in clot volume in the first 3 hours postmortem because of fibrinolytic dissolution.
o With heparin administration, clot volume is further reduced as a result of inhibition of clot formation.
What are conditions in dogs and cats that have increased risk of PTE?
Dogs: immune-mediated hemolytic anemia, sepsis, neoplasia, amyloidosis, hyperadrenocorticism, and dilated cardiomyopathy
Cats: neoplasia and cardiomyopathy.
Unlike the systemic circulation, the pulmonary circulation is ______ (able/unable) to accommodate substantial changes in blood flow without ________ (increases/decreases) in pulmonary vascular pressure as a result of distention and recruitment of pulmonary vessels.
Able
Increases
Vascular obstruction from embolization results in both ________ _________ of the vasculature and reactive ______________ because of the release of vasoactive mediators.
Mechanical obstruction
Vasoconstriction
When there is a PTE, there will be a vascular obstruction and reactive vasoconstriction. What will happen with the cross-sectional area of the pulmonary vasculature? What are the consequences?
It is reduced. It will increase pulmonary vasculature resistance and in moderate to severe cases, increases in pulmonary arterial pressure.
Why are the main causes of hypoxemia with a PTE?
o Mainly decreased V/Q
o Physiologic shunting and reduced diffusion capacity also contribute to reduced CaO2
The severity of hypoxemia in a PTE will be impacted by
The presence of underlying cardiopulmonary disease, reflex bronchoconstriction, and atelectasis.
How much is the normal V/Q in a healthy patient?
1
What does PTE to the redistribution of flow?
o PTE causes a redistribution of blood flow, resulting in a wide spectrum of high, normal, and low V/Q units.
o Low V/Q units are the most important contributors to hypoxemia.
o As the degree of vascular obstruction exceeds 50% of the surface area of the circulatory bed, intrapulmonary shunting (areas of no V/Q) occurs, leading to venous admixture
When V = 4L/min and CO = 0, what is the V/Q?
Infinite
When V= 0L/min and CO = 4L/min, how much is the V/Q?
0
In which situation there is no V and no Q?
CPA
Ventilation is controlled by the interaction between the sensors, which are activated by __________ in the central nervous system and decreased _________ in the periphery, with the responders (respiratory muscles).
Elevated CO2
PaO2
What are potential causes of hyperventilation with PTE?
o Hypoxemia could drive hyperventilation.
o Platelet aggregation with release of humoral mediators and cytokines could activate C fibers and irritant receptors to cause breathlessness.
o Embolization of additional organs often occurs with PTE, therefore vascular obstruction in the CNS could also affect ventilatory control.
What are the changes in lung mechanisms after a PTE?
o Changes in lung mechanics are likely important contributors to tachypnea because increased resistance and decreased compliance greatly affect the work of breathing.
o Experimental studies in dogs have documented increased airway resistance after PTE; 5-hydroxytryptamine (serotonin) likely mediates this bronchoconstriction.
o Lung compliance is reduced in PTE because of pulmonary edema and atelectasis.
o Pulmonary edema appears to result from increased hydrostatic pressure associated with increased blood flow to nonembolized lung regions and from release of humoral factors that increase microvascular permeability.
Clinical signs associated with PTE?
o Labored breathing, tachypnea, lethargy, and altered neurologic status.
o Cough, syncope, and hemoptysis.
o Altered mental state is reported in 20% of human patients with PTE and might be related to transient hypoxemia or cerebral ischemia.
o In a report in dogs, abnormal neurologic status was recorded in more than one third of affected animals and thus might be a common finding with PTE.
o Obvious respiratory distress and tachypnea can be absent in some dogs or cats that have pulmonary embolization documented at necropsy.
Thoracic auscultation findings in patients with PTE?
o Harsh or abnormal lung sounds such as crackles or wheezes.
o Alternately, lung and heart sounds may be dampened because of pleural effusion.
o Cardiac murmurs are not uncommon in affected dogs or cats because of the presence of underlying cardiac pathology (particularly cardiomyopathy in cats) or development of pulmonary hypertension.
T/F Proving the presence of PTE antemortem is simple
FALSE - it is challenging
What has been suggestive of PTE in dogs with IMHA?
o Hyperbilirrubinemia
o Negative Coombs test
Why can hypoalbuminemia should raise the suspicion for PTE?
o Due to loss of antithrombin III
What concentrations of antithrombin III are suspicious for hypercoagulability and have an increased risk of PTE?
o Less than 50% to 75% of normal
When there is hypoalbuminemia and hypoglobulinemia, what should we consider?
o PLE.
o Low vitamin B12 serum levels are supportive of intestinal dysfunction.
o Hypercoagulability has been documented by TEG in dogs with PLE.
What does TEG evaluate? And PT/PTT?
o Evaluates the kinetics and efficiency of clot formation. Provides a dynamic assessment of clot construction and strength and can identify both hypocoagulable and hypercoagulable states.
o Evaluates the time required to form a clot.
How can D dimers be helpful in a patient suspected to have a PTE?
o Assessment of d-dimer concentration has been recommended as a way to exclude PTE when the test is negative or to increase the likelihood that embolization is present when a high titer is detected.
o D-dimer is a degradation product of fibrin that has undergone cross- linkage, and a positive test is more specific for fibrin formation than the fibrin degradation product test (FDP) because the FDP detects both fibrin and fibrinogen breakdown products.
o Unfortunately, many diseases in veterinary medicine result in elevation of d-dimer, and a negative test does not exclusively rule out thromboembolism.
o A study in human medicine evaluating the accuracy of d-dimer testing vs location of embolus reported that a negative d-dimer could be used to rule out the majority (93%) of large pulmonary emboli but only half of the subsegmental emboli.
What will most likely an ABG show on a PTE patient?
o Hypoxemia
o Hypocapnia
o Increased A-a gradient
If we have a patient suspected PTE and its oxygen levels improve with oxygen, what does that mean? And if it doesn’t?
o A positive response to exogenous oxygen supplementation suggests that low V/Q regions are the primary pathophysiologic mechanism for hypoxemia.
o A negative response suggests that intrapulmonary shunting (zero V/Q regions) or pulmonary infarction could be present.
o Although patients with PTE are classically described as being oxygen responsive, this is not always the case and response to oxygen therapy cannot be used as a definitive diagnostic test.
What is a normal P/F ratio
> 450
The lower, the more severe the pulmonary disease
What are radiographic abnormalities that we might see in a PTE?
o Pleural effusion, loss of definition of the pulmonary artery, alveolar infiltrates, cardiomegaly, hyperlucent lung regions, and enlargement of the main pulmonary artery.
o Interstitial or alveolar infiltrates can represent focal or diffuse edema associated with overperfusion or atelectasis.
o Normal thoracic radiographs do not rule out the possibility of PTE, and in a patient with dramatic tachypnea and respiratory distress should be considered highly suspicious for PTE.
What information can give us on a suspected PTE patient an echocardiography?
o Noninvasive assessment of major pulmonary vessels -> thrombi can occasionally be seen in pulmonary arteries or in the right atrium.
o Signs of acute right ventricular overload may be evident, such as right ventricular hypokinesis or dilation, abnormal septal motion, or tricuspid regurgitation.
o In human medicine, echocardiographic changes of RV dilation, paradoxical septal motion, and increased velocity of tricuspid regurgitant jet are evident in the majority of patients with clinically relevant PTE.
PTE treatment
o Treatment and stabilization of the underlying condition should be initiated to limit further thrombus formation and subsequent embolization.
o Oxygen therapy is essential to reverse hypoxemia associated with V/Q mismatching and diffusion impairment.
o The degree of improvement in PaO2 in response to exogenous oxygen supplementation will depend on the percentage of the vascular bed that is obstructed, the concentration of inspired O2 administered, the distribution of V/Q mismatching across the lung, and the degree of shunting that is present.
o Thrombolytics - tPA used experimentally. Streptokinase - successful but limited availability.
o Anticoagulant therapy - aimed at decreasing the thrombus size and avoid the formation of further thrombi.
Human recommendations on PTE treatment
o Recommend thrombolysis for massive pulmonary embolism, defined as pulmonary embolism with hypotension or cardiogenic shock.
o Thrombolysis is also recommended for pulmonary embolism associated with right ventricular enlargement or hypokinesis (submassive pulmonary embolism).
o In less severe cases, the risk for hemorrhage is considered to outweigh the benefits.
o Thrombolysis is performed using tissue plasminogen activator (tPA) to cause direct fibrinolysis at the site of the clot. It can be delivered systemically or in a catheter-directed approach.
o Anticoagulant therapy is recommended for use in all human patients with PTE. The duration of anticoagulant therapy recommended depends on various underlying risk factors, with 3 months of therapy as a minimum in most scenarios
Define ARDS
o It is not a disease itself, it is a syndrome
o Severe inflammatory process at the level of the lung
o Occurs secondary to a catastrophic event - pulmonary or extra-pulmonary in origin
o Can be seen as a maladaptative response to an initial insult
Berlin Definition of ARDS
T/F Many ARDS patients will have elevated PAOP
TRUE
T/F Up to 20% of patients do not have risk factors for ARDS identified
TRUE
Risk factors for ARDS
ARDS phases
Exudative phase of ARDS
Picture damaged alveoli in ARDS
Pathogenesis of exudative phase of ARDS
Proliferative phase of ARDS
o From day 7 to 21 - most patients recover during this phase
o Some will progress into fibroproliferative phase
o Gradual clinical & radiographic resolution of ARDS
What will the pneumocytes type II do during the proliferative phase?
o Reabsorb the protein rich fluid
o Produce surfactant
o Differentiate in pneumocytes type I
Fibrotic phase of ARDS
o Not all patients, but some will develop fibrosis
o Worsening lung condition.
o Histologically - fibrosis with chronic inflammatory cell infiltrate & filling of the alveoli with mesenchymal cells
Define volutrauma
o Overdistension of healthy alveoli
o Can lead to injury of the capillary endothelium & epithelium
o Increase leak of proteinaceous material -> atelectasis & alveolar instability
Atelectrauma (aka shearing injury)
o Repetitive open and closure of alveoli
o Amplify lung strain & denature surfactant
o Risk of pneumothorax
o Use PEEP, low plateau pressures
Biotrauma
o Inflammatory reaction to volu / atelectrauma
o Can lead to MODS
Findings of this paper
o Most substantial mortality benefit ever demonstrated for any therapeutic intervention in ARDS patients
Permissive hypercapnia in ARDS
Is there anything we can do to improve hypercapnia before accepting increased values in an ARDS patient?
Beneficial effects of PEEP
Detrimental effects of PEEP
Use of PEEP in ARDS patients
What is a recruitment maneuver?
Transient sustained increase in trans pulmonary pressure in an attempt to open previously collapsed alveoli -> the goal is to increase lung compliance and improve gas exchange
How do we perform a recruitment maneuver?
What factors do we have to consider when adjusting PEEP and looking at our PV loops?
Another method to guide PEEP?
ARDS Netwrok PEEP / FiO2
Indications for prone position in humans
Neuromuscular blockers
ARDS recommendations on NM blockade
T/F ARDS patients are at high risk for fluid overload
TRUE
Lung protective strategies ARDS net
Risk factors to develop ARDS in vet medicine
Definition of VetALI / VetARDS
What are the most common causes of ARDS in vetmed?
o Bacterial pneumonia
o Aspiration pneumonia
o Sepsis /shock
Veterinary clinical signs of ARDS
If we perform a BAL on ARDS patients, what will be the most common finding on cytology?
Severe neutrophilic inflammation
How should we treat veterinary ARDS patients?
