Respiratory Flashcards
Upper Respiratory tract anatomy
#5
- Nostrils
- Nasal passages - contain Turbinates
- Pharynx -throat
- Larynx -voice box
- Trachea
Lower Respiratory Tract anatomy
#4
- Bronchi
- Bronchioles
- Alveolar ducts
- Alveoli
Primary Respiratory function
take in oxygen and remove carbon dioxide from the blood through the blood–gas barrier
Secondary Respiratory Functions
#4
- Physical defense against: inhaled particles, pathogens, immune functions
- Metabolizing of compounds
- Dissipating heat
- Serves as reservoir for blood
Respiratory Anatomy Zones
What % does each make up?
Two Zones:
Conducting = trachea branching → bronchi, segmental bronchi → terminal bronchioles, (none of which contain any alveoli) only serves to deliver air to the respiratory zone
– 5% of lung volume
Respiratory = Bronchioles and alveolar ducts; responsible for gas exchange
– 95% of lung volume
Anatomical Dead Space
Conductive airway
-Does not participate in gas exchange
Diaphragm Respiratory functions
–Contracts caudally to elongate the chest cavity longitudinally, and the intercostal muscles contract to enlarge the circumferential size of the chest cavity = creates negative pressure to pull air through conductive airway = ventilation
–Moves back cranially during passive exhalation process
Pulmonary Vasculature
–branches from pulmonary artery to pulmonary capillaries in alveoli
– then converge back to pulmonary vein/heart to circulate to the rest of the body
Alveoli blood-gas barrier
– capillary mesh network lines alveoli wall to allow for maximum efficieny of gas exchange
– Other side of barrier consists of vessels with circulating blood flow
– @ capillary level; single cell wall thickeness just large enough to allow RBCs to pass through
“Work of breathing”
Energy expended to created pressure gradient that allows airflow easily in and out of the lungs
– Air flows from high-pressure region (mouth/nouse) to low-pressure (lungs)
Lung inflation is dependent on what?
Compliance and resistance
Lung Compliance
– Ability of the lungs to expand
– determined by elasticity or tendancy of form to return to its original state
Respiratory system’s role with thermoregulation
– network of superficial blood vessels under epithelium in nasal passages help warm inhaled air before reaching lungs
–helps prevent hypothermia
– panting helps facilitate cooling with hyperthermia via increased evaporation of fluid from the lining of the respiratory passages and mouth → helps cool the blood circulating just beneath the epithelium
Respiratory system’s role with pH
contributes to acid–base control by its ability to influence the amount of CO2 in the blood
– inverse relation with pH, (high = low pH, low = high pH)
What does CO2 dissolve into?
CO2 dissolves in the plasma to form carbonic acid [H2CO3]
Anatomy/Function of nasal passages
#4
– pseudostratified columnar epithelium with cilia projecting from the cell surfaces
– layer of mucus that is secreted by many mucous glands and goblet cells
–houses the receptors for the sense of smell
– Responsible for warming, humidifying, and filtering inhaled air
Act of swallowing pathway
epiglottis covers the opening into the larynx →
move the material to be swallowed to the rear of the pharynx →
open the esophagus, and move the material into it
Once swallowing is complete, the opening of the larynx is uncovered and breathing resumes.
Common abnormalities with Brachycephalic breeds
- nostrils that are too narrow (stenotic nares)
- soft palate that is too long (elongated soft palate)
- trachea that is not wide enough (tracheal hypoplasia)
- breathing struggles can lead to gastrointestinal signs such as regurgitation and vomiting of material
Anatomy of the Larynx
- segments of cartilage connected to each other and the surrounding tissues by muscles
- supported in place by the hyoid bone
- Major cartilages include; single epiglottis, paired arytenoid cartilages (supports vocal cords), single thyroid cartilage, and single cricoid cartilage
Larynx role with breathing
#3
–Small adjustments aid the movement of air as the animal draws air into its lungs and blows it out
– protects airway from inhalation of material
–closes to build pressure before cough relfelx
Anatomy of Trachea
Type of muscle, epithelium present
– tube of fibrous tissue and smooth muscle held open by hyaline cartilage rings “C rings”
– lined by the same kind of ciliated epithelium that is present in the nasal passages
–mucous layer on its surface traps tiny particles of debris that made it further down respiratory tract
–cilia that project up into the mucous layer move the trapped material up toward the larynx to be coughed up and swallowed
Tracheal Collapse
How does it affect breathing?
– narrow space between the ends of several of the C-shaped tracheal rings is wider than normal
– with inhalation → widened area of smooth muscle gets sucked down into the lumen of the trachea and partially blocks it
–inspiratory dyspnea
2 benefits
Surfacant definition
thin layer of fluid that lines each alveolus
– helps reduce the surface tension (the attraction of water molecules to each other) of the fluid
–prevents alveoli from collapsing
Asthma
Disease that causes the bronchial tree to become overly sensitive to certain irritants
–Results in inflammation causing thickening of the lining of the air passageways, excess mucus production, and bronchoconstriction
– chronic disease of the small airways (bronchioles) within the lungs
Anatomy of Mediastinum
Area between the lungs
– contains rest of thoracic structures; heart, large blood vessels, nerves, trachea, esophagus, lymphatic vessels, and lymph nodes
Anatomy
Hilus definition
Medial side of the lung lobe where air, blood, lymph, and nerves enter and leave the lung
– only “fastened” area of the lung whereas the rest is “free” within the thorax
Anatomy
Pleura definition
Thin membrane that covers the organs and structures within the thorax
–divided into two layers; viseral and parietal
– smooth surfaces of the pleural membranes lubricated with the pleural fluid to ensure that the lungs, slide along the lining of the thorax smoothly during breathing
Anatomy
Visceral layer of the Pleura
Membrane covering organs and structures themselves
Anatomy
Parietal layer of Pleura
Layer that lines the body cavity in thorax
How does negative intrathoracic pressure facilitate breathing?
– System functions like a bellows, pulling air in and out of lungs
– Lungs follow passively as movements of the thoracic wall and diaphragm alternately enlarge and diminish the volume of the thorax
How does negative intrathoracic pressure help facilitate blood flow?
– aids the return of blood to the heart
–pulls blood into the large veins in mediastinum = cranial vena cava, caudal vena cava, and pulmonary veins
–pressure helps draw blood from the midsize veins into these large veins, which then dump the blood into the right and left atria (receiving chambers) of the heart
Pneumothorax
Air leaks into the pleural space (the space between the lungs and the thoracic wall) = negative pressure is lost
–Results in areas of the lung collapsing
Muscles involved with Inspiration
diaphragm and the external intercostal muscles
–external intercostal muscles located on the external spaces between the ribs
Muscles involved with Expiration
internal intercostal muscles and the abdominal muscles
– internal intercostal muscles located inbetween ribs
–abdominal muscles push contents onto caudal side of diaphram to push it forward and decrease thorax size
Tidal Volume
Tidal volume is the volume of air inspired and expired during one breath
Minute Volume
Minute volume is the volume of air inspired and expired during 1minute
Residual Volume
Residual volume is the volume of air remaining in the lungs after maximum expiration
– The lungs cannot be completely emptied of air; residual volume always remains.
Pathway of Gas Exchange
Inspiration = Inhaled air contains a high level of oxygen and a low level of carbon dioxide
→ Blood entering the alveolar capillary contains a low level of oxygen and a high level of carbon dioxide.
Gas exchange = O2 diffuses from the air in the alveolus, high (into the blood in the alveolar capillary) to low. CO2 does the reverse, diffusing from the alveolar capillary into the alveolus
Expiration = Exhaled air contains less oxygen and more carbon dioxide than is present in room air. Next breath brings in a fresh supply of high-oxygen air.
Partial pressures of Gases
amount of a particular gas that dissolves in liquid exposed to a gaseous environment is determined by the partial pressure of the gas in the gaseous environment
– blood moving through the alveolar capillaries (the liquid) is affected by the partial pressures of O2 and CO2 in the alveolar air (the gaseous environment)
Control of Breathing
Respiratory center
Area in the medulla oblongata of the brainstem
– Contain individual control centers for functions such as inspiration, expiration, and breath holding
2 systems for Control of Breathing
Mechanical system : sets routine inspiration and expiration limits
Chemical system : monitors the levels of certain substances in the blood and directs adjustments in breathing
Control of Breathing
Mechanical control system
what does it utlize to operate?
Operates through stretch receptors in the lungs that set limits on routine breathing, resting, inspiration, and expiration
–Respiratory center sends out the appropriate nerve impulses to start and stop inspiratory/expiratory process.
–Senses preset inflation and deflation in lungs
Control of Breathing
Chemical Control system
Monitors the blood and only affects the breathing pattern if something gets out of balance
Chemical receptors in blood vessels constantly monitor various physical and chemical characteristics of the blood
* located in the Carotid artery/Aorta and in the brainstem
* CO2content, pH, and the O2content of the arterial blood important for Chemical response
Oxygen Toxicity
What can it cause?
Condition resulting from the harmful effects of breathing molecular oxygen at increased partial pressures
–can result in cellular damage affecting CNS, lungs and eyes
O2 molecule make up
Pair of O2 molecules bound w/ 2 electrons
Free Radicals
Unbound electrons that are highly reactive
Reactive Oxygen and Nitrogen Species
How does it lead to oxidative injury?
What is it a product of?
RONS
natural by products of normal O2 metabolism
–Important for cell signaling and homeostasis
–Excess accumulation of RONS taken care of by antioxidants
–Oxidative injury occurs when body’s capability to metabolize RONS becomes exhausted = dangerous levels of RONS (can be caused by endogenous or exogenous sources)
Endogenous Sources of oxidative injury
#6
- Aerobic exercise
- Excessive O2 in tissues compared to antioxidant defences
- Free electron production from NADPH in neutrophils/macrophages
- Ischemic reperfusion injury
- Iron/Copper
- Oxidation of Hb to Methemoglobin
Exogenous Sources of Oxidative Injury
#6
- Ionized Radiation
- Environmental background radiation
- Ultraviolet radiation
- Pollution
- Paraquat toxicity
- Bleomycin toxicity
Oxidative Injury
Superoxide Anion
When remaining O2 undergoes partial reduction and leaks into cytoplasm from oxidative injury → becomes O2-
–precursor to most Reactive Oxygen Species (ROS)
–O2- → H2O2 (highly toxic) → H2O via reaction catalyzed
Oxidative injury
Fenton/Haber-Weiss reaction
Most cytotoxic oxidative pathways
–dependent on availability of H2O2, Iron, and copper
– produces = OH free radical (one of the most toxic ROS
Oxidative injury
Myeloperoxidase Reaction
Hydrogen Peroxide can react w/ Cl- to form hypoclorus acid (HOCl → not ROS, precursor to free radicals)
–occurs with pahgocytic vesicles of neutrophils
Oxidative Injury
Reactive Nitrogen Species
NO (nitric oxide) potent endogenous vasodilator, celll messenger and platelet inhibitor
–can have cytotoxic efx in large quantities (ex. reperfusion injury)
Cellular Effect of Oxidative Injury
Lipid perioxidation: lipids most susceptible to oxidative injury
–Major source of of cellular injury = ↑ cell membrane permeability
* inhibits normal cellular enzyme process
* damage to proteins, intracellular membrane, capillaries, and alveoli
–Two main free radicals that initiate lipid perioxidation = OH and ONO2-
Oxidative Injury
Nucleic Acids
Oxidative stress causes DNA/RNA damage/mutations
–contributes to aging/carinogenesis
Protein damage from Oxidative Injury
Oxidative stress due to ↓ production 2nd to inhibition of ribosomal translation
–AA most susceptible
–Impairments of cellular signaling/metabolism
Role of Inflammation with Oxidative Injury
what is released?
–Necrosis/apoptosis
–relase DAMPs (damage associated molecular pattern molecules)
–DAMPs activate polymorphonuclear neutrophils = contribute to cytokine release, monocyte recruitment, stimulate inflammatory response,
–ultimately contribute further to RONS production = oxidative injury
Oxidative Injury
Ischemia-reperfusion Injury; early stages
how does it affect celluar metabolism?
Results in build up of?
Ischemia = anaerobic metabolism → accumulation of intracellular lactate and H+
–** less ATP available for ATP dependent pumps** = net efflux of K+ and influx of Na+/Ca++/Cl- = cell swelling
–High intracellular Ca++ associated with early IRI = cell apoptosis/necrosis and Xanthine oxidoreductase system
Ex; GDV with myocaridal injury, ATE
Oxidative Injury
How does Ischemia occur?
Depletion of NO = vasoconstriction, decrease perfusion and cellular injury
Oxidative Injury
What happens during reperfusion after ischemia?
↑ in NO production = cytotoxic = severe nonresponsive vasodilation
–release of ROS
– NO and O2 combines into ONO2- = further cellular injury
Oxidative Injury
Xanthine oxidoreductase system
Causes significant cellular injury in IRI
–Intracellular Ca++ with reperfusion = start of XOS
–sudden ↑ in O2 delivery = combines with NAD = xanthine + uric acid production
* GI and endothelium highly susceptible to IRI
Oxidative injury
Clinical Signs with IRI
#4
HyperK+
myocaridal stunning
CNS changes
MODS
Oxidative Injury
“NO Flow” phenomenon
After resolution of occulsion theres a ↓ perfusion due to leukocyte adhesions; platelet-leukocyte aggregation and ↓ endothelium - dependent vasorelaxation
Oxidative Injury
Clinical Efx of Hyperoxia
#5
lungs → most affected due to high exposure levels
–causes apoptosis/necrosis of pul. parenchymal cells
–inflammation
– NCPE
– impaired gas exchange
–fibrosis
Efx of Hyperoxia on pneumocytes
Type I penumocytes of alveolar epithelium are lost → replaced with type II (surfactant secreting) that is resistant to O2
–contributes to thicker alveolar/capillaires
–diffusion impairment
Oxidative Injury
Alveolar collapse from Hyperoxia
What causes it?
This results in =
–Nitrogen displaced by 100% O2 = absorptive ateletasis
– ↑ alveolar O2 = rapid diffusion of O2 from alveoli to pul. circulation =contributes to atelectasis
–induces surfacant impairment
Oxidative Injury
How does Hyperoxia predipose pts to 2nd infections?
↓ mucociliary clearance and changes pulmonary microbial flora/immune function
–in people Hyperoxia from 3hrs on 100% O2 will cause ↓ mucociliary clearance
Oxidative Injury
CV effects of Hyperoxia
– ↑ SVR, vasoconstriction 2nd to ↓ NO bioavailability
– Vasoconstrictive efx cause baroreceptors to ↓ HR with no change in SV = ↓ CO
– ↓ perfusion to vital organs
Oxidative Injury
CNS effects of Hyperoxia
x3
↓ cerebral blood flow 2nd to hypoxic vasconstriction
–will also ↓ ICP
– may cause ↑ cerebral excitotoxicity
O2 targets with MV
PaO2 55-80
SpO2 88-92%
Hyperbaric O2 therapy
MOA, uses, possible complications
pressurized 100% O2 therapy
–Hb becomes completely saturated with O2 = further O2 diffusion into circulation = ↑ PaO2
–unbound O2 (not attached to Hb) diffuses much more readily into tissues and areas not accessible to Hb
–Used for; gas embolization, decompression sickness, carbon monoxide toxicity, severe crush injuries, burn injuries, compartment syndrome
–Complications: barotrauma, decompression sickeness, O2 toxicity, Sz (2nd to low cerebral metabolism
Oxidative Injury
Antioxidants
Any compound that can delay or prevent oxidation of a substance
–helps protect cells against oxidative injury/DNA mutations/malignant transformation/cell damage
–Depletion can occur with CKD, cardiac dz, hepatic dz, DM neoplasia
–3 categories: Endogenous enzyme, endogenous nonenzyme, exogenous
Oxidative Injury
Endogenous antioxidant enzymes
important for preventing oxidative injury
Superoxide dimustase (SOD) glutathione perioxidase
Oxidative Injury
Endogenous nonenzymatic Antioxidants
#8
- Albumin
- Glutathion
- Ferritin
- Bilirubin
- Uric acid
- COOq
- Vit C/Vit E
- Melatonin
Oxidative Injury
Exogenous Antioxidants
#6
- Vit C
- Vit E
- beta-carotene
- acetycyteine
- selenium
- zinc
Endothelial Surface layer (ESL)
important functions #4
Luminal side of ESL in blood vessels comprised of Glycocalyx with plasma layer
– important for blood-blood vessel and vessel - interstitium interfaces
– important for inflammation modulation, coagulation, vasomotor tone, permeability
Shedding of ESL in relation to oxidative injury
What is it affected by? #6
-affected by trauma, inflammation, hyperglycemia, hemodilution, hypovolemia
–Ischemia-reperfusion injury and oxidative stress = endothelial glyclocalyx shedding
Control of Breathing
Respiratory Center
Medulla
–neuronal network controls motor neuron activity that innervate respiratory muscles = chagnes to ventilation
–medulla initiates and coordinates control of breathing
–can be interrupted by voluntary control (cortex/hypothalamus)
–or involutary action interruption; swallowing, coughing, sneezing
Control of Breathing
Medulla Respiratory Center
Where is it located?
what is it made up of?
Located w/i brainstem
Complex collections form group “pacemaker” system = Central Pattern generator (CPG)
– Concentrated region of neurons w/i medually = pre-Botzinger Complex
* pacemaker neurons categorized based on shape - augmented, decrementing, constant-plateau
3 phases of Respiration: Phase 1
- Inspiration: sudden onset of activity of inspiratory neurons and augmenting neurons = motor discharge to inspiratory muscles and airway dictators
3 phases of Respiration: Phase 2
- Post-inspiratory phase (expiratory phase 1): declining motor discharge to inspiratory muscles and passive exhalation
– expiratory decrementing neurons (in medulla) decrease in activity = mechanical brake to expiratory flow
3 phases of Respiration: Phase 3
Active or passive?
What structures are involved?
- Expiratory (expiratory II): no inspiratory muscle activity
–passive with normal breathing
–can be active (exercise) with expiratory augmenting neuron support (in medulla)
Spontaneous CPG activity
dependent on
similiar to
neurotransmitters involved
respiratory rhythmogensis
–dependent on intrinsic membrane properties/neurotransmitters
–similiar to cardiac pacemaker cells → Na+/K+/Ca++ ion channels required for membrane activity
* glutamate (excitatory), GABA/Glycine (inhibitory)
* Influenced by acetylcholine, neuropeptides
Two groups w/i Medulla Respiratory Center: Dorsal Respiratory Group
Primary responsibility
what do they carry?
Which cranial nerves are involved?
Dorsal Respiratory Group: primary function = timing of respiratory cycle
–Initiate phrenic nerves in diaphragm
–group terminates at visceral afferents from cranial nerves IX (glossopharyngeal) and X (vagus)
–Carry sensory info that influence Control of breathing (pH, PaCo2, PaO2 from carotid/aortic chemoreceptors)
Medulla Respiratory Center; Ventral Respiratory Group
x3 groups and their functions
Consists of inspiratory and expiratory neurons
1. caudal ventral group → expiratory function
* * 2. rostral ventral group → controls airway dilator functions of larynx/pharynx/tongue
3. Pre-Botzinger complex → pacemaker activity + CPG generation
4. Botzinger complex
Pontine Respiratory Group
collection of neurons located in the pons → fine tunes breathing pattern via synaptic connections in medulla resp. center
–influences timing of resp. phase/stablizes breathing pattern
–Afferent pathways connected to PRG = cortex, hypothalamus/ nuclease tractus solitarius
Apneusis
when is this typically seen?
prolonged gasping inspiratory efforts punctuated by brief inefficient expiratory efforts
can be seen with brain injury in upper pons, possible stroke/trauma
Chemoreceptor
type of sensory receptor that responds to alterations in chemical composition of blood or fluid in the area it is immersed in
Central Chemoreceptors for respiration
location, responds to
Located in Medulla
–primarily responsible for response to CO2/pH changes in brain
–DOES NOT respond to PaO2 changes
– Interstial fluid in brain in contact with CSF = changes in pH of CSF/brain interstitial fluid affect ventilation
– 60-80% of response to CO2
Blood Brain Barrier relation with CO2
–impermeable to H+ and HCO3 ions
–CO2 can diffuse freely across BBB
–CSF/brain interstitium lack buffering system
– ↑ PaCo2 = ↑ H+ = ↓ pH of brain fluid = ↑ RR/depth to return PCO2 to normal
Peripheral Chemoreceptors
location, stimulants, effects
what do they respond to?
Located w/i carotid bodies and aoritc bodies
–carotid = primary respiratory response
–aortic = influence circulation
–fast response to change in PaO2/PaCO2/H+
–Responds to ↓ PaO2 rather than O2 content = little response from anemia/dyshemoglobinemia
– ↑ body temp = cause stimulation and enhance ventiltory responses to changes in O2 and CO2
–may result in bradycardia, hypertension/ ↑ bronchiolar tone and secretions of catecholamines
O2 sensing cells
Type I glomus
highly vascularized peripheral chemoreceptors
Chronic Respiratory Dz response to Hypercapnia
with chronic respiratory dz/hypercapnia
the response to elevated PCO2 becomes reduced
– leading to hypoxemia becoming primary stimulus for ventilation
– supplemental O2 for chronic hypercapnic pts depresses hypoxic respiratory drive = severe hypoventilation and resp. failure
Pulmonary Stretch Receptors
where are they found?
what does it stimulate?
slow adapting receptors present in smooth muscle of airway
–activate in response to excessive/sustained distention of lung
–transmits info to respiratory center (inspiratory center of medulla/PONS)
–stimulate protective feedback loop “Hering-Brever inflation Reflex”
Lung Airway Receptors
Irritant receptors
J receptors
Irritant Airway receptors
where are they located? what is it activated by? what do they cause?
which cranial nerves are involved?
located in epithelium of nasal mucousa, upper airways, tracheobronchial tree, alevoli
–activated by noxious gases inhaled dust, cold air, and chemical/mechanical things
–transmit info via myelinated vagal afferent fibers
–causes bronchoconstriction, cough, laryngeal spasm, mucous secretion, ↑ RR/depth
–afferent pathway in nasal mucosa signals trigeminal/olfactory tracts = sneezing
J Airway receptors
located, stimulated by
which cranial nerves is involved?
Juxtacapillary receptors
–located in pulmonary interstitium close to capillaires
–stimulated by capillary distension/edema
–slow transmit via C fibers of vagus nerve = rapid shallow breathing pattern or apnea
Arterial Airway baroreceptors
**primarily involved with circulation regulation
– hypotension sensed by aortic/carotid baroreceptors = reflex hyperventilation
– hypertension = hypoventilation
Muscle/Joint/Tendon Respiratory receptors
Respiration muscle/rib joints respond to changes in lenth/tnesion = feedback regarding lung volume + WOB
Pain/temperature receptors affecting airway
Proprioception receptors send info via ascending spinal cord pathways = influence breathing
–painful stimuli detected by nociceptors = initial apnea then hypoventilation
Causes of Hypoxemia
#5
- Hypoventilation
- V/Q mistmatch
- Diffusion impairment
- Low FiO2
- Intrapulmonary shunt
Arterial O2 Content
CaO2
depends on concentration of Hb and binding affinity of O2 saturation of Hb (SaO2) present
–majority of arterial O2 delievery to tissues is bound to Hb
–small fraction is dissolved or unbound = 0.003 x PaO2 in plasma
(1.34 x Hb x SaO2) + (PaO2 x 0.003)
What section of trachea is tracheotomy performed?
between 3rd-5th tracheal ring
How long should FiO2 levels > 50% be administered?
No longer than 24-72 hrs
What do arterial blood gasses asses?
pulmonary function
What do venous blood gases asses?
reflection of tissue function
PaO2 definition
partial pressure (vapor pressure) of O2 dissolved in solution in plasma of arterial blood
– Ability of lungs to move O2 from atmosphere to blood @ sea level
SpO2 definition
Red to infrared light oximeter measurement
Oxyhemoglobin (O2 + Hb) and deoxyHb (Hb not bound to O2) absorbs light @ different wavelengths
–amount absorbed measured with each wavelenth expressed as %
–2 waveforms = 660 and 940nm
–Poor perfusion can affect SpO2 = inaccuracy
–LATE indicator of hypoexmia
–CarboxyHb (carbon monoxide + Hb) = perfect SpO2 readings b/c Hb is occupied by CO BUT has no O2 carrying ability
–MetHb = falsely lowers SpO2
–anemia = may have N Spo2 but with significantly low O2 carrying capacity = low DO2
Oxygen-hemoblobin Dissociation Curve
SO2/PO2 relationship
–degree of hemoglobin saturation w/ O2 determined by PO2 and relation to SO2
–small changes in SO2 (oxygen saturation) = large changes in PaO2 and vice versa
–affected by numerous physiological factors that can alter Hb’s affinity for O2
Correlation of PaO2 and SaO2
Hyperoxemia = PaO2 > 125 = SaO2 100%
Normoxemia = PaO2 80-125 = SaO2 95-99%
Hypoxemia = PaO2 < 80 = SaO2 < 95%
Severe hypoxemia = PaO2 < 60 = SaO2 < 90%
Severe Hypoxemia
PaO2 < 60 SaO2 = 90%
– level when Hb is still 90% saturated
–PaO2 (not Hb) Drives O2 diffusion into mitochondria
–PO2 (partial pressure of oxygen in blood) = driving force
– SO2 (Hb O2 saturation) = reservoir that prevents rapid ↓ in PO2
Factors that affect O2/Hb Dissociation Curve
pH
Temp
PCO2
2,3 DPG
Left shift in O2/Hb Dissociation Curve
#6
O2 has MORE attachment to Hb - less available for unloading to tissues
–HypOthermia, Alkalosis (H+↓, pH ↑), Carbon monoxide poisioning, hypOcapnia, ↓ 2,3 DPG
Righ Shift in O2/Hb Dissociation Curve
#4
O2 has LESS attachment to Hb = greater ability to unload O2 into tissues
– HypERthermia, Acidcemia (H+ ↑ pH ), hyPERcapnia, upregulation of 2,3 DPG 2/ anemia
2,3 DPG definition
a salt in RBCs that play role in liberating O2 from Hb in peripheral circulation
Cyanosis
gray-bluish discoloration of mm signaling presence of deoxygenated Hb
–seen @ 5g/dl Hb concentration
– Late sign of severe hypoxemia ex: if pt is anemic pt will die of hypoxemia before cyanosis is ever seen
Mechanisms of Hypoxemia
#4
- low inspired O2
- Hypoventilation
- Venous admixture
- Reduced venous O2 content 2nd to low CO and slow peripheral blood flow (shock) OR high O2 extraction (sz)
Venous Admixture
way which venous blood can get from R side to L side of circulation w/o proper oxygenation
Mechanisms of Venous admixture
x4 examples
- low V/Q regions = mod - severe diffuse lung dz (pneumonia/edema)
- No V/Q regions = Atelectasis
- Diffusion defects = mod-severe diffuse lung dz (O2 toxicity, smoke inhalation, ARDS)
- R → L PDA, intrapulmonary A-V anatomic shunts
Low Alveolar O2 due to reduced O2 delivery to alveoli
examples
Low inspired O2 (ex. high altitude, or apparatus use)
Hypoventilation (ex: PaCO2 >45, low MV)
Decreased efficiency of transport of O2 from Alveoli TO pulmonary capillaries
Low V/Q regions (ex: 2nd to airway narrowing or alveolar fluid accumulation)
Diffusion Impairment (ex: thickened resp. membrane, O2 toxicity, ARDS progression)
R to L Shunt(ex: congenital defects)
Low Alveolar O2 due to ↑
extraction of O2 FROM Alveoli
Zero V/Q regions (ex: small airway, alveolar collapse from fluid accumulation)
Low venous O2 content
4 gases in alveoli
- O2
- CO2
- Water vapor
- Nitrogen
Regions of Low V/Q
x3 examples
– 2nd to small airway narrowing or alveolar fluid accumulation = impairs ventilation (some gas exchange maintained)
– High Q from pulmonary embolism
–bronchspasm, fluid accumulation in lower airways
Regions of Zero V/Q
Small airway and alveolar collapse
–dz associated with transudate/exudate/blood fluid accumulation
– animals that may be recumbent for prolonged periods of time w/o deep breaths
–physiological shunt = blood bypasses all alveoli despite function
–Fixed with PPV or PEEP
Diffusion Impairment
Interstitial fluid build up causes airway narrowing and ↑ alveolar surface tension
–low V/Q or Zero V/Q
–Diffusion defect = flate type I alveolar pneumocytes proliferate across surface of gas exchange site
Alveolar - Arterial PO2 Gradient
Difference between calculated PAO2 and measured PaO2
–assess oxygen ability of lungs on room air
– N = 15 or less
– abnormal value = problem of O2 getting from alevoli into the blood
PAO2 - PaO2
120 rule
@ 21% FiO2 @ sea level N PaCO2 = 40 and PaO2 = 80 = 120 mmHg
Hypoventilation = PaCO2 ↑ from 40 to 60 and PaO2 = 60
–conclusion is hypoxemia is from hypoventilation
P/F Ratio
PaO2/FiO2
N= 500
(105/0.21)
Oxygen Ratio
Evaluating oxygenation in ventilated patients
-account for Mean Airway Pressure (MAP)
– Lower # = better function
MAP x 100 x FiO2 / PaO2
How is CO2 created?
Product of aerobic metabolism
–produced from internal cellular respiration primarily in mitochondria
–combines with H2O = carbonic acid → dissolves into H+ ion and Bicarbonate
– pulmonary capillaries where CO2 diffuses into alveoli
CO2 + H2O = H2CO3 = HCO3 + H
Most common cause of hypercapnia?
Hypoventilation 2nd to Low MV
Tidal Volume
Tidal volume is the volume of air inspired and expired during one breath
–dead space volume and volume of fresh gass entering alveoli for gas exchange
“Dead Space” Definition
Portion of the tidal volume that does not participate in gas exchange
Characterized as:
1. Apparatus = circuit from the Y-piece to the nose of the patient comprises apparatus dead space
2. Anatomic = conducting airways from the nose to the level of the alveoli
3. Alveolar = alveoli that are ventilated but not perfused in pulmonary capillaries
Physiological Dead Space
What parts are involved?
when does it become increased?
Anatomic + Alveolar dead space
–sum of portions that do not participate in gas exchange
–normally should be about the same as anatomic dead space however with V/Q inequality → PDS increases due to increase in alveolar dead space
Fowlers Method
Used to measure dead space ventilation
–concentration of exhaled tracer gas (NO) over time following breath w/ 100% O2
– NO is in expired gas and ↑ with dead space
Bohrs Method
Dead Space ventilation measurement
–measurement of physiologic dead space rather than anatomic
–principle that all CO2 exhaled w/ gas originates from alveolus
Relation of PaCO2 measurement and ETCO2 and Central venous PCO2
ETCO2 usually about 5 mmHg lower than PaCO2
PCO2 usually about 5mmHg Higher than PaCO2
Hypercapnia
What can cause it? x4 examples
Results when alveolar ventilation is inadequate to restore PaCO2 to normal range
– excess dead space, inadequate fresh gas flow, exhausted absorbent agents, faulty directional valves
Elevated CO2 with Fixed MV
Causes; x5 examples
2nd to thyrotoxicosis, fever, sepsis, malignant hyperthermia, over exercise
Causes of Impaired CO2 excretion from Hypoventilation
#6
Total MV = RR + TV( Vd + Va)
Vd = dead space vol
Va = Alveolar ventilation
– interferece w/ ability to achieve normal tidal breath → Neuro dz affecting Resp. Control Center
– Peripheral/Central chemoreceptor dysfunction
–Upper or Lower motor neuron dz
–Spinal Cord dz
–Neuromuscular dz
– elevated airway resistance
Lower Motor Neuron Dz that affect MV
#8
Myasthenia gravis
Botulism
Tick paralysis
Demylination
Polyradicunuritis (coonhound paralysis)
Chemoreceptor abnormalities - drugs/anesthetics/ metabolic Alkalosis/ cerebral fluid acidosis
Elevated Dead Space ventilation: High V/Q
x5 examples
increased physicological dead space
– low CO
– Shock
– Pulmonary embolus
– Pulmonary Hypotension
– Pulmonary bulla
Increase in CO2 production with fixed TV
metabolic examples x5
Malignant hyperthermia
reperfusion injury
fever
Iatrogenic hyperthermia
thyrotoxicosis
Central Respiratory Center role with hypercapnia
Responsible for 50% of hypercapnia’s ventilatory response
Hypoventilation due to Neuromuscular dz
Due to low TV
–pts develop shallower breathing pattern = low TV
–compensate with ↑ in RR
– if MV normal with compensation in RR → alveolar ventilation will ↓ w/ pts taking shallow breaths due to greater Vd/TV = hypercapnia
Hypercapnia 2nd to pleural space dz
effects on TV
↓ TV due to decreased expansion
–MV stays N 2nd to ↑ RR
–Hypercapnia 2nd to ↓ alveolar ventilation from low TV and greater Vd/TV
Hypercapnia 2nd to thromboembolic dz
Pulmonary capillary compression 2nd to overinflation and cardio shock
= hypercapnia from ↓ alveolar ventilation 2nd to ↑ alveolar dead space or poor perfusion in lungs
Effects of Hypercapnia on CVS
#4
Hypercapnia + acidosis = ↓ myocaridal contractility and SVR
–compensated by SNS activation/catecholamine release 2nd to acute hypercapnia = ↑ HR and BP
–causes vasoconstriction in pulmonary circulation
–bronchodilation and ↓ diaphragmatic contractility
Effects of Hypercapnia on Neuro system
#3
–Dependent on level, duration, and degree of hypoxemia
– Cerebral blood flow ↑ in response to ↑ PCO2 via vasodilation and ↑ systemic BP
– ↑ in cerebral blood flow = ↑ ICP
Effects of Hypercapnia on Endocrine functions
#3
– Constricts renal afferent arterioles = acute kidney injury and low UOP
– may ↑ Na+/H2O retention and HyperK+
–↑ adrenocorticotropic hormone secretion from pituitary stimulation
CO2 Blood gas analysis
PvCO2 vs PaCO2 vs CO2
PvCO2 = arterial CO2 inflow + local tissue CO2 production + tissue blood flow
PaCO2 = dependent on alveolar ventilation
CO2 = accumulates with decreased blood flow
CO2 production with tissue hypoxia
CO2 produced as result of ↑ H+ production 2nd to lactate formation and hydrolysis of ATP
–buffered by HCO3- = ↑ CO2 production
Stertorous respiration
low pitched snoring with inspiration/expiration
frenchie
Stridorous respiration
High pitched noise associated with inspiration
Lar Par
Causes of upper airway disease noises
collapse or obstruction of UpA rostral to thoracic inlet = create negative intrathoracic pressure with inspiration = negative transmural pressure/collapse
–prolongs inspiratory phase = noise for air/tissue reverberation
Why are patients with Upper Airway dz more at risk for heat stroke?
–Pt with UpA dz = ↓ ability to efficiently ↑ MV for heat dissipation
Upper Airway Obstruction
↑ WOB against obstruction = edema/inflammation/distress/progressive obstruction
Paradoxical Laryngeal motion
Inward movement of arytenoids 2nd to negative pressure generated on inspiration
BAS
Brachycephalic Syndrome
–stenotic nares, elongated soft palate, +/- tracheal hypoplasia and nasopharyngeal turbinates
–Chronic airflow resistance = everted laryngeal saccules, tonsil eversion
–Chronic GI signs
Nasopharyngeal Polyps
common cause of UpA dz in cats
–benign inflammatory lesions coming from mucosa of auditory tube to middle ear → grow into nasopharynx/external ear canal
Laryngeal Paralysis
Recurrent laryngeal nerve dysfunction = impairs arytenoid cartilage abduction during inspiration = respiratory stridor
–Congenital vs Acquired
–larynx accounts for 6% OF airflow resistance
–dysfunction of laryngeal nerve = atrophy of 1 or both dorsal muscles
Laryngeal Collapse
What is another name for this?
what causes it?
2nd complication of BAS and Norwhich Terrier Upper Airway Syndrome
–Chronic ↑ of negative pressure in intraluminal airway = weakening of cartilages/loss of rim glottic diameter = ↑ WOB, inflammation, and airway obstruction
Norwich Terrier Airway Syndrome
narrow infraglottic lumen of varys degrees of laryngeal collapse
Grades of LC
3
-Grade 1 LC = eversion of laryngeal saccules
-Grade 2 LC = meidal positioning of cuneiform process
-Grade 3 = collapse of cornicilate cartilages
Upper Airway Neoplasia
Dogs vs Cats
K9 = carcinomas or sarcomas, chondrosarcoma, melanoma, granular cell tumor
Cats = Lyphoma most common but sarcomas and carcinmoas and olfactory neuroblast reported
O2/CO2 Transport
20% of CO2 Binds to Hb as carbaminoHb and is exchanged for O2 @ alveoli
5 types of Hypoxia
- Hypoxemic hypoxia = inadequate O2 carrying capacity of blood 2nd to hypoxemia
- Hypemic hypoxemia (anemic Hypoxia) = anemia causes decrease in circulating Hb = reduced O2 carrying ability of Blood
- Stagnant of circulating hypoxia = decreased CO and poor perfusion
- Histiotoxic hypoxia = tissues unable to extract and utilize O2 appropriately
- Metabolic hypoxia = ↑ cellular consumption of O2 (VO2)
Hypemic hypoxemia from hemoglobinopathy
caused by CarboxyHb (Carbon monoxide toxicity) and methemoglobinemia
–adequate amounts of Hb BUT Hb unavailable for O2 transport
– CarboxyHb has HIGH affinity for Hb (220xs O2) making them nonfunctional
– Methemoglobin 2nd to acetaminophen toxicity in cats
–both lead to Hypoxia and cause invalid SpO2 readings
Dalton’s Law of Partial Pressure
hypoventiliation may result in hypoxemia b/c as CO2 ↑, it displaces O2 w/i alveoli = ↓ in PaO2
R to L Shunt
= ↑ A-a gradient and responds poorly to O2 therapy
–deoxygenated blood (RS of heart) can enter systemic circulation (LS of heart) and may never reach lungs
–caused by vascular shunts w/i lungs or intrathoracic shunts → atrial septal defect, ventricular septal defect, Reverse PDA
–arteriovenous malformation = blood flow from pulmonary artery → pulmonary vein may occur w/o oxygenation @ alveoli cap. bed
Cheyne Stokes breathing pattern
What can cause this?
respiration characterized by brief periods apnea followed by brief periods of hyperventilation
CNS disorder, ↑ ICP
Kussmaul breathing pattern
What can cause this?
respiration w/ sustained ↑ depth of breathing w/ either a slow of faster rate in response to metabolic acidemia = body’s attempt to expire CO2 to correct acidosis
DKA, CKD
Apneustic Respirations
respirations w/ deep inspiration w/ a pause @ full inspiration followed by brief expiration
Ex: ketamine administration or due to central neurological dz
ARDS
x7
Acute Respiratory Distress Syndrome
–acute, diffuse, inflammatory leading to ↑ pulmonary vascular permeability
– ↑ lung weight
–loss of aerated lung tissue with hypoxemia
–bilateral CXR opacities
– associated with venous admixture
–↑ physiological dead space
– decrease lung compliance
Diagnosis of ARDS
acute onset
CXR with bilat opacities consistent w/ pulmonary edema
P/F ratio < 300
Lung protective MV setting for ARDS
#6
– Low TV = 6-8ml/kg
– Low Airway plateau pressure < 30 mmHg
– Higher RR = 35+ bpm
– Higher PEEP = > or = 5 cmH2o
– Permissive hypercapnia
– “Compatible with life” parameters = Sao2 = 88-95%, PaO2 55-80mmHg
Tension Pneumothorax
Severe Pneumothorax
– life threatening impairment to both ventilation and blood circulation (venous return)
– 2nd to trauma →flap of tissue acts as one way valve = allows continuous influx of air into pleural cavity on inspiration but does not exit
“Mixed cause” Pulmonary Edema
Results from =
2 examples
Combination of hydrostatic and increase in pulmonary edema
–Neurogenic pulmonary edema = following TBI, Sz, electrocution
–Negative pressure pulmonary Edema = UpA obstruction (BAS)
Tracheal Collapse
Cause Unknown
–but contributed to dorsal trachealis flaccidity and loss of rigidity or tracheal cartilages
–possibly from ↓ glycosaminoglycen/chondroitin
–Grade I-IV = each grade approx. 25% progressive w/ reduction in tracheal diameter lumen/flattening
Tracheal Collapse CS
Cervical (extrathoracic) TC = inspiratory dsypnea from inability of tracheal cartilages to withstand Neg airway pressure
– ↑ intrapleural pressure collapses intrathoracic trachea
“Honkers” with Tracheal collapse
Prolonged Inspiratory with increased effort
ex: pectus excavatum, sinus arrhythmia, abducted elbows, orthopnea
“Coughers” with Tracheal collapse
Respiratory effort on expiration
–expiratory abdominal push
–harsh expiratory lung sounds
–herniation of cranial lung lobes
–“heave” line
Feline Bronchopulmonary Dz
Divided into “Feline Asthma” and Chronic Bronchitis
Feline Asthma
type of hypersensitivity
Hyperactive airway w/ reversible bronchoconstriction (Type I hypersensitivity reaction)
–younger middle age cats
–lack b-lines
–diffuse bronchial/interstitial pattern on CXR
Lower Airway Dz in Dogs
– Bronchomalacia can result in inspiratory and expiratory crackles
–Bronchitis associated with expiratory wheeze as air flows from alveolar region → glottis → narrow airways
–both can be seen with expiratory push or exaggerated abdominal effort
What causes pulmonary edema
Hydrostatic pressure edema due to ↑ pulmonary capillary hydrostatic pressure
– increase in permeability = edema from damage to microvascular barrier and alveolar epithelium
PathoPhys of Pulmonary edema
Normal = fluid fluxes determined by capillary/interstitial hydrostatic pressures, capillary COP
–↑ in interstitial hyrostatic pressures = ↑ driving pressures for lymphatic flow = protect lung against edema
– pulmonary ultrastructure designed to protect gaseous diffusion
– most fluid cleared via bronchial circulation
–Edema occurs when rate of interstitial fluid overwhelms protective fluid clearance mechanisms
High hydrostatic pressure Edema
Example
–Cardiogenic Edema: most common form, results from LS-CHF (often chronic) esp. cats
–Compensatory mechanisms = fluid retention = worsening congestion
Increased Permeability Edema
what is it synonymous with?
caused by direct injury to microvascular barrier, alveolar epithelium or both
–synonymous with ARDS
Mixed cause Edema
Results from =
Examples
Combination of hydrostatic and ↑ permeability
–NPE following acute neuro event - surge in ICP = catecholamine surge = ↑ SVR = alveolar capillary leakage
–NPPE following UpA obstruction = ↑ negative intrathoracic pressure = ↑ venous return to RS < 3 = ↑ pulmonary venous pressures and interstitial hydrostatic pressure = movement of fluid from pulmonary capillaires into interstitium/alveoli
Treatment for Pulmonary Edema
Reduce pulmonary capillary pressures by reducing Preload
= Diuretics and vasodilators
– furosemide → pumonary vasodilator/bronchodilator = COP ↑ 2nd to hemoconcentration = ↓ pulmonary hydrostatic pressure
–Vasodilators = nitroprusside/nitroglycerin
Distribution Patterns to differentiate Pneumonia
3 types
- Lobar pneumonia pattern = entire lung lobe; dense consolidation
- Bronchopneumonia = distal airway inflammation and alveolar dz; patchy distribution
- Interstitial pneumonia = inflammation w/i interstitium rather than alveolar spaces
PathoPhys of Pneumonia
what mechanisms are involved?
Infections occur when protective UpA mechanisms and humoral and cell mediated immunity become overwhelmed
–Inflammatory response from interactions between cell mediated/humoral immune system and elevated cytokines/chemokines
Protective Airway defense mechanisms against pathogens/contaminants
x6
- protective barriers
- cough reflex
- mucociliary apparatus w/ enzymes
- Secretory immunoglobulin (IgA)
- Phagocytic dendritic cells w/i basal layer of resp. tract
- Surfacant/alveolar macrophages
Types of Pneumonia
#7
Bacterial
Aspiration pneumonia
Pneumonia associated with CIRD
FB Pneumonia
Parasitic Pneumonia
Mycotic Pneumonia
Ventilator-associated Pneumonia
Bacterial Pneumonia
gram neg and positive example
Bordetella
mycoplasma
Gram neg = pasturella, E. Coli
Gram Pos = Staph and Strept
Aspiration Pneumonia
Bacterial Colonization of lungs after aspiration of acid/GI contents
–severe histologic damage caused by low pH < 1.5
– Common enteric bacteria cultured = E. Coli, Klebsiella, Enterococcus
–CXR typically show R middle lung lobe and ventral parts of lobe affected
Pathogens that cause Pneumonia associated with CIRD
x7 examples
Viral pathogens = K9 adenovirus type 2, parainfluenza, distemper, resp. coronavirus, influenza, canine pneumovirus, herpevirus
K9 Distemper
where does infection occur?
Replicates in lymphoid cells of resp. tract before spreading to epithelial cells of other organs (including CNS)
–CS = nasal/ocular d/c, resp. distress, V/D, hyperkeratosis of paw pads, progressive neuro dysfunction
K9 Respiratory Coronavirus
↓ mucociliary clearance that leads to infection
H3N8 and H3N2 influenza strains
Can result in =
Unique to transmit between dogs
–can lead to hemmorhagic broncopneumonia
Parasitic Pneumonia
Nemoatodes and Trematodes migrate thru lung
–cats → aeluerostrongylus abstrucsus
Mycotic Pneumonia
Infection from Fungal agents
–typically geographical
–Blastomyces dermatitides
–Histoplasma capsulatam
Pneumonia POCUS signs
– early pneumonia → Patchy areas of fluid filled alveoli surrounded by aerated lung = numberous B lines
– Progressive pneumonia → lung consolidation w/ evidence of air bronchograms + shred sign
POCUS
Air bronchograms
Air filled bronchi surrounded by consolidated tissue
appear as bright hyperechoic lines
POCUS
Shred sign
–consolidation creates deep jagged hyperechoic border between two areas
– irregular interface between area of consolidated lung and area of aerated lung
POCUS
Curtain Sign
caudal border of lungs contact w/ chest wall
–sharply divided vertical line separated aerated lung from abdominal contents
–can be used to orient sonographer to define caudal thoracic border
Feline inflammatory bronchial diseases
asthma and chronic bronchitis
– common lower respiratory diseases in cats that are characterized by recurrent episodes of coughing, wheezing, and/or labored breathing
– associated with airway inflammation, hyperreactivity, and airway remodeling
– tx: β2-adrenergic receptor agonists (albuterol, salmeterol)
inhaled β2-agonists
– Stimulation of the β2-receptor causes an increase in intracellular levels of adenylate cyclase, which decreases intracellular calcium levels and subsequently causes smooth muscle relaxation of the bronchial wall.
(albuterol, salmeterol)
Canine inflammatory bronchial diseases
x4
- chronic bronchitis
- eosinophilic bronchopneumopathy
- eosinophilic bronchitis
- eosinophilic granuloma
– idiopathic inflammatory bronchial diseases that typically are characterized by either coughing, wheezing, nasal discharge, and/or labored breathing
Canine infectious tracheobronchitis
gram negative or positive?
– most common pathogen = Bordetella bronchiseptica
– Gram-negative bacterium is predominantly extracellular and has several characteristics that allow the organism to attach to the tracheal cilia
Cricothyroidotomy
needle cricothyroidotomy, oxygen can be provided via a large-gauge needle or catheter inserted through the cricothyroid membrane or through the tracheal wall
– temporary adjunct used for minutes because ventilation will not be effective.
Surgical tracheostomy placement
between the third and fourth or fourth and fifth tracheal rings
Thoracocentesis indications
pneumothorax and pleural effusions
Thoracocentesis location
Blind thoracocentesis is performed between the seventh and ninth intercostal spaces
– Fluid may be best aspirated in the lower third of the chest
– ventral thoracocentesis is performed, care must be taken to avoid the internal thoracic arteries, which run along the ventral thorax a few centimeters to either side of the sternum
Seldinger technique for small-bore thoracostomy tubes
– specialized atraumatic guidewire and matching thoracostomy tube
–chest tube to be inserted in the thorax should be first determined by estimating the distance from the insertion site to the second rib.
– over-the-needle catheter (or hypodermic needle) is inserted through a small skin incision over the7th, 8th, or 9th intercostal space, angled cranioventral in the direction desired for the chest tube
– Seldinger technique has the advantage of requiring a smaller incision using a small-bore tube; it is likely to be less painful and leakage is less likely.
Pleural ports
Vascular access ports connected to a Jackson-Pratt drain have been successfully used for treatment of recurrent pleural effusion and pneumothorax
– allow connection of the drain to the subcutaneously located access port.
Active drainage techniques
Continuous suction may also allow sustained lung expansion and better healing of leaks by pleural adhesion
– A suction pressure of 10 to 20 cm H2O is used
Thoracostomy tubes Removal
– Decision to remove a chest tube depends on the rate of fluid production or air accumulation in the pleural space
– no air should be retrieved for 24 hours before tube removal
– fluid production falls to less than 2 ml/kg/day
– Exceptions are patients with septic exudates and those in which the thoracostomy tube is used for lavage
How long are chest tubes in place for spontaneous pneumo?
dogs with spontaneous pneumothorax that require chest tubes, the tubes are left in for an average of 4.5 days (range, 1 to 8 days)
carbon monoxide toxicity
Smoke inhalation associated with fires can result in pulmonary dysfunction and upper airway edema due to inhalation of hot and noxious gases
– can result in carboxyhemoglobinemia
What is Carbon Monoxide? (CO)
– colorless, odorless, nonirritating gas that is produced by incomplete combustion of hydrocarbons in fires
– produced endogenously as an end product of erythrocyte and heme catabolism and in the CNS as a neurotransmitter
CS of CO toxicity
classic sign
– delayed neurological injury, including altered level of consciousness, anxiety, vocalization, agitation, ataxia, and seizures, can develop following carbon monoxide toxicity
– cherry red mucous membranes
Pathophysiology of carbon monoxide toxicity
2 main mechainsms
– CO rapidly absorbed in alveoar
– amount absorbed dependent on exposure duration and concentration in air
– CO toxicity involves two main mechanisms: impaired oxygen delivery to tissues (hypoxia via dyshemoglobinemia) and direct cellular toxicity.
CO affinity for Hb
What type of O2/Hb dissplacement shift does it cause?
– CO displaces oxygen from Hb and causes an hindrance of oxygen release from Hb to the tissues
– Carbon monoxide competes with oxygen for Hb binding sites with 200–240 times the affinity
– CO binds two of the four available heme groups in each molecule of Hb, causing a decrease in the oxygen carrying capacity of 50%
Left/low shift on O2/Hb curve
Direct cellular toxicity from CO toxicity
– disrupts oxidative metabolism, potentially causing the generation of oxygen free radicals and impaired cellular respiration
– Binding to myoglobin can cause myocardial hypoxia, depression, and arrhythmias as well as direct skeletal muscle toxicity and rhabdomyolysis
Indirect cellular toxicity from CO toxicity
– occurs through sequestration of leukocytes
– increased nitric oxide production
– reperfusion injury
– lipid peroxidation
– direct neurotoxicity from CO as a neurotransmitter
Carboxyhemoglobinemia
causes which type of hypoxia?
tx for CarboxyHb
– hemoglobinopathy that occurs when carbon monoxide preferentially binds to hemoglobin,
– hemoglobin is not able to effectively transport oxygen
– hypemic hypoxia ensues
– Oxygen therapy dramatically decreases the half‐life of carbon monoxide
What influences O2 offloading into tissues ability?
pH,
CO2,
2,3-diphosphoglycerate [2,3-DPG] concentration.
** O2 dissociative curve **
What is the O2 extration ratio?
– oxygen extraction ratio is about 25%
– Under normal physiological conditions, DO2 is about four times greater than actual tissue requirements
Hypoxemia with N A-a gradient
Extrapulmonary: Hypoventilation, Low Atm O2 (fire, elevation)
Hypoxemia with Elevated A-a gradient
x3 examples
Intrapulmonary:
1. V/Q mismatch (pneumonia, PTE)
1. Diffusion impairment (pulmonary edema, interstitial lung dz)
1. R to L shunting (Tetralogy of Fallot)
