L39: Respiratory Distress (Specht) Flashcards
(41 cards)
Steroids may predispose to PTE
HW prophylactics may –> thromboembolism
:)
INSPIRATORY distress or prolonged inspiratory phase often indicates:
EXTRA-THORACIC airway obstruction
-ie. Cervical tracheal collapse, lar par
EXPIRATORY distress or prolonged expiratory phase often indicates:
INTRA-thoracic airway obstruction:
- intra-thoracic tracheal collapse
- Chronic bronchitis
- Asthma
- pneumonia
True respiratory distress automatically localizes problem to (in the dog):**
Level of the larynx or lower
Reason: if it is nasal disease, dogs generally open their mouths. In cats, if YOU open the mouth and it is still in distress, this also localizes to below the larynx
Laryngeal or other upper airway dz is generally loud (stridor) with head/neck extension posturing and inspiratory component
Cardiac disease significant enough to cause distress usually associated with:
Tachycardia
Murmur
Pulse abnormalities
Expiratory effort with auscultable wheezes is highly suggestive of:
Bronchoconstrictive disease
Absence of lung sounds (esp. In vental or dorsal lung fields) in the face of tachypnea/dyspnea is suggestive of:
Pleural space disease (or PT)
5 basic mechs. Of hypoxemia**
1) decreased inspired O2 (ie. During anesthesia)
2) hypoventilation
3) diffusion abnormalities (usually not clinically sig.)
4) anatomic shunts
5) V/Q mismatch
Resp. Distress Ddx
Upper airway (lar par, tracheal collapse, obstructions) Lower airway (asthma, mainstem bronchi collapse, airway obstruction, infectious bronchitis)
Lungs (pneumonia, CHF, NCPE, PTE, neoplasia, hemorrhage, fibrosis, PHT)
Pleural space (air, fluid)
Other (anemia, smoke, drowning, aortic aneurism, resp. Paralysis)
Respiratory distress
Abnormal breathing rate or effort resulting in distress to the patient
- sign of ineffective oxygen delivery to tissues
- underlying cause may be a respiratory problem
CS of lar par
Resp. Distress Stridor Bark change Cyanosis Syncope
*exacerbated by increased resp. Effort
Dz associated with lar par
Hypothyroidism
Arytenoids close during ____ in lar par
Inspiration
Tx of lar par
- emergency airway mgmt PRN (O2, anxiolytic, anti-inflammatory, intubation or tracheostomy)
- address underlying dz if possible
- sx intervention (tie back
Components of brachycephalic syndrome
1) stenotic nares
2) elongated soft palate
3) everted laryngeal saccules
4) hypoplastic trachea (?)
5) +/- laryngeal collapse, laryngeal paralysis
Dx of brachy syndrome
- may be presumptive
- laryngoscopy and rads help with definitive characterization
Tx of brachy syndrome**
- emergency airway mgmt (as with lar par)
- sx correction (elongated soft palate, stenotic nares, and everted saccules can be fixed)
- hypoplastic trachea and laryngeal collapse CANNOT be corrected
Feline asthma char. By:
wheezing, coughing, dyspnea due to spontaneous bronchoconstriction
Factors that can contribute to feline bronchitis (Asthma)
- airway hypersensitivity –> bronchospasm
- bronchial smooth muscle or epithelial hypertrophy
- increased mucous production –> decreased clearance
- inflammation w/n airway walls
- exudate w/n lumen
- fibrosis
- emphysema
CS of feline bronchitis (Asthma)
- usually in younger cats
- sudden onset dyspnea +/- cough or wheeze
- increased expiratory effort with wheezes and crackles
- slowly progressive
- may be exacerbated by env. Changes
Dx of feline bronchitis (Asthma)*
- Hx/CS
- rads: bronchial pattern, hyperinflation, +/- aerophagia
- HW test and fecal to rule out other causes
**Definitive dx: airway wash cytology: eosinophilic, neutrophilic, or mixed inflammation
Tx of feline bronchitis (asthma)
- emergency airway mgmt with steroids
- short-acting bronchodilators if steroids don’t work
- env. Mod.
- long-term corticosteroids (oral or inhaled)
*sudden death always a possibility
2 classes of bronchodilators**
1) Sympathomimetics (B agonists)
- Terbutaline, Albuterol
- minimal cardiac effects
2) Methylxanthines
- long acting theophylline
*should not use bronchodilators without anti-inflammatories also on board
How is resp. Function affected by PTE?
- increased V/Q in non-perfused areas
- release of various humoral factors and stimulation of neurogenic reflexes –> decreased CO, increased PVR, bronchoconstriction, loss of surfactant, infarct, etc.
