Diseases & Management Flashcards
(80 cards)
1
Q
Describe Cheyne-Stokes, apneustic and Kussmaul breathing
A
Cheyne-Stokes:
- Seen in severe hypoxemia during sleep, or with neurologic injury
- Periods of apnea of 10-20s separated by equal periods of hyperventilation when tidal volume gradually waxes and wanes
Apneustic:
- Prolonged gasping inspiratory efforts punctuated by brief inefficient expiratory efforts
- Injury to apneustic center (pons)
Kussmaul breathing:
- Secondary to metabolic acidosis
- Deep and rapid respirations –> hyperventilation
2
Q
What percentage of MetHb is required to start having clinical signs
A
- 10-20%: mild symptoms (cyanosis, chocolate MM)
- 20-50%: dyspnea, dizziness, tachycardia
- > 50%: seizures, coma, arrhythmias, tachypnea
- > 70%: death
3
Q
In which category of patients (who would technically benefit from this) should transtracheal oxygen be used with caution?
A
Patients with upper airway obstruction –> pulmonary overdistention can occur from impaired exhalation
4
Q
Name 2 complications of oxygen therapy
A
- Oxygen toxicity
- Hypoventilation and respiratory failure in chronically hypercapnia patients secondary to depression of hypoxic respiratory drive
5
Q
What FiO2 can be provided by flow-by O2, face mask, O2 hood, nasal cannula, transtracheal oxygen?
A
Flow-by: 2-3L/min –> 25-40%
Face mask: 8-12L/min –> 50-60%
O2 hood: 0.5-1L/min –> 30-40%
Nasal cannula: 50-150 ml/kg/min –> 30-70% (200 mL/kg/min usually give 60% and starts causing discomfort)
Transtracheal O2 –> 50ml/kg/min –> 40-60%
6
Q
What is the affinity of Hb for CO compared to O2
A
200 times higher affinity for CO
7
Q
At what level should a transtracheal catheter be inserted
A
Between the 3rd and 5th tracheal rings
8
Q
Does hypoxemia from hypoventilation respond to oxygen therapy? Why?
A
Yes.
Hypoxemia from hypoventilation is due to the replacement of O2 by CO2 in alveoli (if PaCO2 is 80, PACO2 is going to be close to 80 mmHg, and so PAO2 will decrease from 100 mmHg to 60 mmHg). With oxygen therapy, nitrogen is replaced by oxygen in the alveoli and PAO2 is increased (if FiO2 is 100%, to ~600 mmHg), so even if PACO2 increases there will be plenty of oxygen left for oxygenation of blood.
9
Q
What are the different mechanisms of hypercapnia? List examples of etiologies
A
- Increased inspired CO2:
- Expired soda lime
- Faulty valves
(- Apparatus dead space) - Increases CO2 production (at fixed Vt):
- Hyperthermia
- Thyrotoxicosis
- Reperfusion injury
- Excessive nutritional support in ventilated patient
- Laparoscopy - Increased dead space ventilation:
- Physiologic dead space: general hypo perfusion (low CO, shock), pulmonary embolus, pulmonary bulla, alveolar overdistension
- Apparatus dead space: circuit, ET tube - Decreased minute ventilation
- Central neurological disease: sedatives, encephalitis, trauma, neoplasia, severe hypothermia, etc.
- Cervical spinal cord disease: IVDD, hemorrhage, fracture, neoplasia, MUE, etc.
- Lower motor neuron / neuromuscular disease: myasthenia gravis, botulism, polyradiculoneuritis, neuromuscular blockade, tick paralysis, etc.
- Chemoreceptor abnormalities: drugs (anesthetic agents), metabolic alkalosis, chronic CSF acidosis
- Abnormal respiratory mechanics: pulmonary fibrosis, fatigue, pleural space disease, poor chest wall compliance, loss of chest wall integrity
- Increased airway resistance: upper airway obstruction (BOAS, collapse, lar par, FB), bronchoconstriction, circuit resistance
10
Q
What are consequences of hypercapnia
A
- Acidosis -> decreased cardiac contractility, decreased vasomotor tone, altered mentation
- Cerebral vasodilation, increased intracranial pressure
- Constriction of renal afferent arteriole (-> AKI) + retention of Na, water, K
- Increased ACTH secretion
- Pulmonary vasoconstriction and bronchodilation
=> acidosis, altered mentation (narcosis when PaCO2 > 90), decreased UOP, electrolyte abnormalities
11
Q
Explain 3 mechanisms by which oxygen therapy can worsen hypercapnia
A
- Patients with chronic hypercapnia have buffers in their CSF bringing the pH to normal -> central chemoreceptors are no longer triggered by CO2 (unless gets much higher) and ventilation is dependent on peripheral chemoreceptors stimulated by hypoxemia. Oxygen therapy ->relieves hypoxemic drive
- Oxygen therapy relieves hypoxic pulmonary vasoconstriction -> perfuses hypoventilated alveoli -> worsens low V/Q mismatch (overall the alveolar ventilation of all perfused alveoli decreases)
- Oxyhemoglobin accepts protons less easily than deoxyhemoglobin -> oxyhemoglobin releases H+ (and so CO2) - Haldane effect (does not increase total CO2 content but increases PaCO2)
12
Q
Name respiratory stimulants and briefly describe their mechanism of action + adverse effects
A
- Doxapram: activates peripheral (and central at higher doses) chemoreceptors.
Also stimulates CNS and increases work of breathing leading to higher O2 demand and CO2 production. - Methylxanthines: stimulate central respiratory center directly + improve respiratory muscle contractility (+ bronchodilation)
Can cause tachycardia and arrhythmias
13
Q
What are the components of brachycephalic airway syndrome? What is thought to be primary / secondary?
A
Primary:
- Stenotic nares
- Elongated / thickened soft palate
(- Tracheal hypoplasia)
- Nasopharyngeal turbinates
Secondary:
- Eversed laryngeal saccules
- Eversed tonsils
- Laryngeal collapse
- Tracheal collapse
- Chronic GI signs (reflux, hiatal hernia)
14
Q
What is the recommended treatment for a nasopharyngeal polyp
A
Ventral bulla osteotomy (for cats) - can do traction and avulsion but 50% risk of recurrence (especially if in auditory canal)
- Main post-op risks of VBO:
- Horner’s syndrome (57% of cats) - resolves in up to 4 weeks
- Vestibular dysfunction
- Hypoglossal nerve paralysis
15
Q
What is the prevalence of aspiration pneumonia after unilateral arytenoid lateralization
A
8-33%
16
Q
What are the grades of laryngeal collapse? What breed is predisposed?
A
Grade I = eversion of laryngeal saccules
Grade II = medial positioning of cuneiform process and aryepiglottic collapse
Grade III = collapse of corniculate cartilage
Norwich Terriers are predisposed (part of the Norwich Terrier upper airway syndrome)
17
Q
What are the 2 types of tracheal collapse (based on etiology)
A
- Chrondromalacia
- Tracheal malformation (inversion of the tracheal rings ventrally)
18
Q
What are issues commonly associates with tracheal collapse which will result in failure of a stent to improve clinical signs
A
- Bronchial collapse (83% of dogs with cervical collapse)
- Laryngeal collapse (up to 30% of dogs with tracheal collapse)
19
Q
What are complications of tracheal stents? What predisposes to complications?
A
- Stent fracture (especially if too big for the tracheal diameter)
- Stent migration (especially if too small)
- Infection (especially in the presence of areas of poor contact between stent and tracheal mucosa where mucus accumulates = “gutters”)
- Granulation tissue formation (especially with gutters)
20
Q
Where does bronchial collapse occur most commonly
A
Left mainstem bronchus (possibly due to compression between aorta and left atrium - especially for dogs with heart failure, but also in brachycephalic dogs)
21
Q
What is the difference between feline asthma and feline chronic bronchitis
A
- Asthma is a hyper-reactivity of airways causing a reversible bronchoconstriction (susp secondary to type I hypersensitivity)
- Chronic bronchitis is the thickening of airways with excessive mucus production
22
Q
What is the normal composition of a bronchoalveolar lavage fluid in dogs?
A
70-75% macrophages, 5-8% neutrophils / eosinophils / lymphocytes
23
Q
Why does hypoproteinemia rarely contribute to pulmonary edema
A
The protein reflection coefficient in the pulmonary capillaries is quite low (permeability for proteins is quite high), so the oncotic gradient plays little role in fluid flux
24
Q
What is the main actor in pulmonary edema drainage
A
The bronchial circulation (the lymphatics prevent the accumulation of interstitial fluid, but once edema is established it gets drained mostly by the bronchial circulation)
25
What is the mechanism for neurogenic pulmonary edema
- Increased in intracranial pressure (from trauma / seizures) -> catecholamine surge
- Catecholamines increase vascular resistance + venous return -> rise in capillary pressure -> increase in hydrostatic pressure + barotrauma causing increased permeability -> edema
- Catecholamines could also cause a direct insult to the pulmonary vasculature
26
What is the mechanism for negative pressure pulmonary edema
- Airway obstruction -> marked negative intrathoracic pressure
- Negative intrathoracic pressure -> increased venous return to right heart -> "overload" of right circulation causing increase in capillary hydrostatic pressure
- Negative intrathoracic pressure -> decreased interstitial pulmonary pressures
- Negative intrathoracic pressure -> increased left cardiac afterload (due to transmural pressure)
=> combination of these 3 effects causes edema
27
List common bacteria isolated in cases of pneumonia
- Pasteurella spp
- E Coli
- Streptococcus
- Staphylococcus
- Bordetella bronchiseptica
- Mycoplasma spp (often in coinfection)
28
List factors predisposing to pneumonia in dogs and cats
1. Impaired patient mobility
- Unconsciousness
- General anesthesia
- Paresis
2. Upper airway disorders
- Laryngeal mass / FB
- Laryngeal paralysis
- Laryngeal or pharyngeal dysfunction / surgery
3. Regurgitation syndromes
- Esophageal motility disorder
- Esophageal obstruction
- Megaesophagus (leading cause of aspiration pneumonia)
4. Other factors
- Bronchoesophageal fistula
- Cleft palate
- Crowded / unclean housing
- Force feeding
- Gastric intubation
- Immune compromise
- Inadequate vaccination
- Induced vomiting
- Seizures
- Tracheostomy
29
What viruses / bacteria are implicated in canine infectious respiratory disease (CIRD)
1. Viruses
- Canine adenovirus type-2
- Parainfluenza
- Distemper
- Respiratory coronavirus
- Influenza (H3N8, H3N2)
- Pneumovirus
- Herpesvirus
2. Bacteria
- Bordetella bronchiseptica
- Strep equi subs zooepidemicus
- Mycoplasma canis
30
Which lung lobes are most commonly affected by inhaled foreign bodies
- Accessory lung lobe
- Left caudal lung lobe
- Right caudal lung lobe
31
Discuss the use of bronchodilators in pneumonia
Indicated only if there is strong suspicion of bronchoconstriction (can happen just after aspiration event). No proven benefit otherwise.
- Argument that it can increase airflow, improve ciliary activity, mucokinetic properties vs suppress cough reflex, enhance spread of exudate, increase perfusion of poorly ventilated lung units
Beta-agonists could have an anti-inflammatory effect by decreasing mucosal edema and cytokine release.
Methylxanthines can increase mucociliary transport and increase diaphragmatic strength
32
What size do nebulized particles need to have to be able to reach the alveoli
0.5-5 um diameter
(particles <0.5 um get exhaled and particles > 5 um get trapped in nose or mouth)
33
What are mechanisms leading to pulmonary contusions
- Direct injury by the increased pressure (spalling effect) -> disrupts alveoli at the point of initial contact with shock waves
- Inertial effect because tissues accelerate at different rates -> mechanical tearing and laceration of lungs
- Implosion effect from overdistension of gas bubbles after shock wave passes -> tearing of parenchyma from excess distension
- Injury of the parenchyma by fractured ribs
34
What mechanisms contribute to pulmonary dysfunction with pulmonary contusions / hemorrhage
- Alveoli filled with blood -> low V/Q or shunt
- Decreased surfactant (caused by damage to pneumocystis II) -> alveolar collapse, worse V/Q
- Inflammatory reaction and increased capillary permeability leading to accumulation of protein-rich edema -> worse V/Q
- Possible capillary thrombosis from activation of inflammation and coagulation -> increases pathologic dead space
35
What is the prognosis for dogs with pulmonary contusions requiring mechanical ventilation
30% survival to discharge
36
List causes of atraumatic pulmonary hemorrhage
1. Infectious
- Bacterial (Lepto, Strep equi, E Coli)
- Parasitic (Angiostrongylus vasorum, Dirofilaria)
2. Coagulation abnormalities
- Primary coagulation: thrombocytopathia, thrombocytopenia
- Secondary coagulationL: rodenticide, hemophilia, vWD
- Thromboembolism
3. Cardiac
- Heart failure
- Pulmonary hypertension
4. Neoplasia
- Primary
- Metastatic
5. Anatomic: lung lobe torsion
6. Miscellaneous
- Exercise-induced pulmonary hemorrhage in racing Greyhounds
- Pulmonary-renal syndrome
- Post-seizure
7. Iatrogenic: lung FNA 1 biopsy
8. Toxic (envenomations): Eastern brown snake
37
What are the criteria for chest tube removal in a pyothorax
- Clinical improvement
- Fluid production < 2 mL/kg/day
- Resolution of infection on cytology
38
Name common micro-organisms causing pyothorax in cats and dogs
1. Aerobes
- Nocardia spp
- Streptococcus spp
- Corynebacterium spp
2. Facultative anaerobes
- E Coli
- Pasteurella spp
- Actinomyces spp
- Staphylococcus spp
3. Anaerobes
- Fusobacterium spp
- Bacteroides spp
- Clostridium spp
- Peptostreptococcus
- Prevotella spp
- Porphyromonas spp
4. Fungi
- Cryptococcus spp
- Candida albicans
- Blastomyces dermatitidis
39
List non-respiratory causes of respiratory distress
1. Non-respiratory decrease in O2 delivery
- Decreased CO
- Anemia
2. Metabolic derangements
- Metabolic acidosis
- HyperT4
- Hypoglycemia
3. Drugs
- Bicarbonates
- Opioids (alter thermoregulation)
4. Hyperthermia
5. Behavioral
6. Brain disease
40
What are breathing patterns seen with severe brain disease
- Cheyne-Stokes breathing: alternates between periods of high tidal volume and RR for a few breaths and periods of apnea
- Apneustic breathing: long periods of inhalation with short periods of exhalation
41
What are the mechanisms contributing to pulmonary hypertension in PTE
- Mechanical obstruction to blood flow by the emboli
- Reactive vasoconstriction (mediated by thromboxane, histamine, prostaglandins, endothelin)
- Hypoxic vasoconstriction
42
What type of V/Q mismatch contributes the most to hypoxemia in PTE
Low V/Q (areas that are hyper-perfused or under-ventilated)
43
What are radiographic findings associated with PTE
- Enlarged pulmonary arteries or loss of definition of pulmonary artery
- Alveolar infiltrates
- Hyperlucent areas
- Cardiomegaly (mostly right-sided)
- Pleural effusion
- Sometimes normal radiographs
44
What is the timing of D-dimer increase following PTE
Peak within 2h and are back to normal within 48h
45
How is the severity / probability of mortality assessed in patients with PTE
(In humans), based on:
- hemodynamic instability
- right ventricular dysfunction
- cardiac troponin
- score including demographics, history, RR. HR, T, SpO2, BP, mentation
46
What are the benefits of HFNC
H: heated and humidified gas delivery (improves comfort and mucus clearance)
I: inspiratory flow demands (meets demands of dogs with higher minute ventilation)
F: functional residual capacity (PEEP provided at > 1 L/kg/min)
L: light (compared to CPAP)
O: oxygen dilution (prevents dilution of O2 / gas administered by room air in dogs with high minute ventilation)
W: washout dead space (continuous fresh gas removes the 1/3 of Vt accumulated in airways with lower O2 and higher CO2)
+ reduces inspiratory resistance
47
How should the flow rate be set initially in HFNC
Ideally it should be equal to the patient's minute ventilation (in practice usually start at 1 L/kg/min and try to increase to 2 L/kg/min within 30 min - no benefit in going higher)
48
What is the recommendation (in Silverstein) for tracheostomy tube replacements
- Tubes with inner cannula: remove and clean inner cannula every 4h
- Tubes without inner cannula: change tube every 24h
- Suction every 4h or more
(!!)
49
What arteries should be avoided when doing a thoracocentesis for pleural effusion? Where are they located?
Internal thoracic arteries, located a few cm on each side of the sternum (parallel to it)
50
How to build a continuous suction (active drainage technique) for a chest tube
Three-chamber water seal suction apparatus:
- Empty chamber connected to patient and to 2nd chamber (closed to air) -> will fill with effusion
- Water trap with 2-3 cm water connected to 1st chamber (with end of tube submersed in the water) and to 3rd chamber (closed to air) -> will bubble in case of pneumothorax
- Suction control bottle filled with water connected to 2nd chamber and to suction + 1 tube open to air and submersed in the water (needs to have 10-20 cm in water to give the suction of -10 to -20 cmH2O)
51
At what pressure should continuous suction be kept for drainage of pneumothorax / pleural effusion
-10-20 cmH2O
52
Describe the pathophysiology of ARDS (phases, mechanisms, duration)
1. Acute exudative phase (1-7 days):
The innate immune system of the lung gets activated -> stimulation of macrophages + recruitment of neutrophils (neutrophils are the most important)
--> Release of inflammatory mediators (cytokines, ROS, eiconasoids)
--> Alveolar epithelial cell damage, surfactant dysfunction, dysfunction of Na/K ATPase to drain alveolar fluid
+ endothelial cell damage -> increased permeability + microthrombi
--> alveolar flooding with fluid, proteins, and leukocytes ("hyaline membrane = accumulated cell debris and proteins in alveoli) + alveolar collapse + heterogeneous perfusion --> major VQ mismatch
2. Fibroproliferative phase (weeks following, can begin as early as 48h):
- Proliferation of type II alveolar epithelial cells
- Interstitial fibrosis
--> decreased lung compliance and diffusion impairment
- Alveoli are still obliterated and microthrombi are still present
53
List common causes (risk factors) of ARDS in cats and dogs. What is the most common in dogs vs cats?
1. Direct pulmonary causes
- Aspiration pneumonia / pneumonia
- Pulmonary contusions
- Mechanical ventilation
- Thoracic trauma
2. Indirect / extrapulmonary causes
- Sepsis
- SIRS
- Shock
- Pancreatitis
- Trauma
- AKI
- Multiple transfusions
3. Other causes
- Smoke inhalation
- Lung lobe torsion
- Bee envenomation
- Adverse drug reactions
- Paraquat intoxication
Most common in dogs = pneumonia
Most common in cats = indirect (sepsis, SIRS)
54
What is the Berlin definition of ARDS (in humans)
1. Resp distress within 1 week of know predisposing factors or new or worsening respiratory symptoms
2. Bilateral opacities on chest radiographs or CT not fully explained by effusions / collapse / nodule
3. Respiratory distress not fully explained by cardiac failure or fluid overload based on objective assessment (echo)
4. Hypoxemia:
Mild ARDS -> 200 < P:F ratio ≤ 300 with PEEP or CPAP ≥ 5 cmH2O
Moderate ARDS: 100 < P:F ratio ≤ 200 with PEEP ≥ 5 cmH2O
Severe ARDS: P:F ratio ≤ 100 with PEEP ≥ 5 cmH2O
55
What is the veterinary definition of ARDS (VetALI / VetARDS)
1. Acute onset of tachypnea and laboured breathing at rest (< 72h)
2. Known risk factors
3. Evidence of capillary leak without increased pulmonary capillary pressure:
- bilateral or diffuse infiltrates on thoracic radiographs
- OR bilateral dependent density on CT
- OR proteinaceous fluid within conduction airways
- OR increased extravascular lung water
- WITHOUT clinical or diagnostic evidence of left sided heart failure (including echo) or PAOP ≥ 18 mmHg
4. Evidence of inefficient gas exchange:
- Hypoxemia: P:F ratio ≤ 300 for VetALI or ≤ 200 for VetARDS (without PEEP) OR increased A-a gradient OR evidence of venous admixture
- OR increased dead space ventilation
5. Optional: Evidence of diffuse pulmonary inflammation:
- Neutrophilia on TTW / BAL
- OR biomarkers of inflammation on TTW / BAL
- OR evidence of inflammation on molecular imaging
56
List treatments that can be considered for ARDS. Which ones have a proven benefit in humans?
- Lung protective ventilation: Vt 4-6 mL/kg, Pplat<30cmH2O, permissive hypercapnia and hypoxemia (proven benefit)
- Prone positioning (proven benefit)
- Corticosteroids (proven benefit)
- Neuromuscular blockade (unclear benefit, not routinely recommended)
- Inhaled NO (no proven benefit)
57
What parameter determines occurrence of cyanosis
It is the absolute concentration of arterial deoxygenated hemoglobin (must be > 5 g/dL in arterial blood)
-> PaO2 around 40 mmHg in a patient with normal Hb, but an anemic patient might never become cyanotic
58
What is the venous admixture calculation
Qs/Qt = (CcO2 - CaO2) / (CcO2 - CvO2)
Qs = "shunt fraction"
Qt = cardiac output
(Qs/Qt = venous admixture)
CcO2 = oxygen content of end-capillary blood (calculated from PcO2 which is estimated to be the same as PAO2, needs to be calculated depending on FiO2 - ScO2 is then determined based on dissociation curve)
CaO2 = oxygen content of arterial blood
CvO2 = oxygen content of mixed venous blood (can be estimated with central venous blood)
Should be less than 5% ; greater than 10% indicates venous admixture issues (low V/Q or zero V/Q or anatomic shunt)
59
Briefly describe the Fowler's method vs Bohr's method to measure dead space
- Fowler's method is based on measurement of exhaled nitrogen over time following a breath at 100% O2 (the exhaled nitrogen comes from dead space getting washed out)
- Bohr's method is based on measurement of exhaled CO2 (= CO2 from the alveoli diluted in gas poor in CO2 coming from the dead space) compared to PaCO2 (which should be ~ equal to alveolar CO2)
60
Name 2 systemic diseases that have been associated with laryngeal paralysis.
Myasthenia gravis and hypothyroidism
61
Which breeds have been reported to have congenital laryngeal paralysis?
Bouvier des Flandres
Rottweilers
Dalmatians
Siberian Huskies
Bull Terriers
Pyrenean Mountain dogs
Leonburgers
62
What is an uncommon Ddx for tracheal narrowing?
Intraluminal tracheal hemorrhage from rodenticide toxicity and tracheal hematoma
63
What are the common nasal neoplasms in dogs and cats?
Dogs:
- Carcinomas (adenocarcinoma, squamous cell carcinoma)
- Sarcomas (fibrosarcoma, osteosarcoma, chondrosarcoma)
Cats:
- Lymphoma +++
- Sarcomas
- Carcinomas
- olfactory neuroblastomas
64
What are the 2 categories of tracheal collapse regarding reclassification?
Traditional condromalacia & tracheal malformations
65
Which anti-epileptic drug has been associated with cough and respiratory disease in cats and should be discontinued in the face or respiratory disease?
Potassium bromide
66
Which lung lobe is most commonly collapsed due to mucus plug in cats with asthma?
Right middle
67
List 10 disorders associated with PTE
- IMHA
- Corticosteroid adminsitration
- Hyperadrenocorticism
- Pancreatitis
- PLN/PLE
- Central catheter use
- Trauma
- Cardiac disease
- Sepsis
- Neoplasia
68
What is the McConnell's sign (highly specific for Dx of acute PTE in people)?
Akinesia of right mid ventricular free wall with normal contractility of the apex
69
Mechanical ventilation considerations in dogs with PTE
Avoid high levels of PEEP or mean airway pressure --> reduction in venous return can impair CO in patients with RV dysfunction
70
71
Name 5 neuromuscular diseases that can impair chest wall movement
1. Elapid snake envenomation - presynaptic (phospholipase A2) and post-synaptic toxins
2. Tick paralysis
3. Acute idiopathic polyradiculoneuritis - neuronal demyelination and degeneration of axones
4. Botulism
5. Myasthenia gravis
72
Classification of effusions
1. Pure transudate
- protein: < 2.5g/dl
- nucleated cell count: < 1000 cells/ul
2. Modified transudate
- protein: >= 2.5g/dl
- nucleated cell count: 1000-5000 cells/ul
3. Exudate
- protein: >= 2.5g/dl
- nucleated cell count: > 5000 cells/ul
73
What is the triglyceride cutoff for diagnosis of chylothorax?
Effusion: serum ratio of > 3:1 OR effusion triglyceride concentration of >= 100 mg/dl
74
What is a unique radiographic finding with angiostrongylus vasorum?
Peripheral alveolar pattern
75
Why is N-Acetylcystein sometimes considered in management of pneumonia?
Mucolytic properties --> breakdown of the disulphide bonds in thick airway mucus + precursor to glutathione, a free radical scavenger
76
Prognosis for survival of aspiration pneumonia in academic institutions?
77-82%
77
What is the ideal tracheal cuff pressure for ETT?
Not defined but 19-24 mmHg in recent vet studies
20-30 cmH2O in humans
78
List 3 methods of appropriate ETT placement verification
1. Direct visualization
2. Measurement of exhaled CO2 (caution in CPA)
3. Transtracheal ultrasound
79
List 6 complications of tracheostomy tubes
1. Tube occlucion
2. Tube dislodgement
3. SC emphysema
4. Pneumothorax
5. Aspiration of fluid or FB
6. Pneumonia
80
Describe the surgical technique for a temporary tracheostomy
1. Patient is anesthetized and placed in dorsal recumbency
2. Routine surgical preparation of the ventral cervical region is performed
3. 2-5 cm incision is performed on midline from the cricoid cartilage towards the sternum
4. Sternohyoid muscles are separated along midline with blunt dissection and retracted laterally
5. Peritracheal connective tissue is removed
** Avoid dissection lateral to the trachea to prevent injury to the left recurrent laryngeal nerve and tracheal blood supply
6. Incise horizontally annular ligament between 3rd and 4th tracheal rings. Do not exceed more than 50% of tracheal circumference
7. Long loops of suture are placed around the tracheal rings adjacent to the incision
8. ETT is slowly pulled out as the tracheostomy tube is placed
