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Lesley King, on faculty in small animal medicine
handout: approach to dyspneic animals

Respiration rate:
normal resp rate 20-30 bpm in dog and cat
should be nearly imperceptible. should look at animal and have to 
concentrate to see movement of chest wall. if you look at animal and 
visibly see respiration, you may have a problem. in clinic, spend lots of 
time counting respiratory rate as a way of monitoring respiratory 
function.

changes in respiration caused by three things:

1. pulmonary parenchymal dz eg lung dz, pneumonia, cancer, hemorrhage

2. upper airway obstruction/collapse - can't move air in/out - most 
commonly due to foreign bodies, tumors, laryngeal paralysis, tracheal 
collapse in little dogs

3. pleural dz - effusions, accumulations of fluid or air in pleural 
space. most common reason for air in pleural cavity (pneumothorax) is 
trauma, eg HBC. fluids commonly seen include blood, pus (pyelothorax), 
edema fluid, chyle

so we break down the problems into these three main areas. a problem with 
lung tissue itself, with the airway, or with the pleural space.

AND/OR...

changes in pattern/rate of respiration can occur due to:
pain, fear, stress, excercise, fever, heat, anemia, excessive fat 
limiting chest volume (Pickwickian syndrome - seen in obese little dogs), 
CNS dz (medulla controls respiration, remember), pressure from abdominal 
fluid or masses, metabolic dz eg acidosis, cardiovascular or 
musculoskeletal dz, etc. so you see the underlying problem could be 
totally unrelated to the respiratory 
tract itself.


Dyspnea == sensation of breathlessness. kind of a misnomer in veterinary 
medicine. term was taken from human medicine. feeling of not being able 
to catch your breath properly. but, when you see animal that seems to be 
struggling for air, you can say it is dyspneic.

Tachypnea == increased respiratory rate. doesn't necessarily imply dz. 
you will be tachypneic after a 4 mile run, but that is normal.

Orthopnea == this is pathological. difficulty breathing when recumbent. 
common in heart failure patients. dog will look uncomfortable at night, 
will cough when lying down, will get up a lot. often worse lying on side, 
better when sternal.

Stertorous or stridorous breathing: consider upper airway or laryngeal 
involvement. observing the patient, you may hear stertor or stridor (same 
thing) while sitting there looking at the animal. if you can hear a harsh 
sound without your stethoscope, that's a good clue that you have upper 
airway/laryngeal involvement. horses that are "roarers" will exhibit this 
sign.

restrictive lung disease: if you see shallow, rapid breathing, consider 
this. this is any kind of dz that prevents expansion of the lung. 
examples include: lung fibrosis (uncommon in dogs/cats), fluid in lungs, 
neoplasia, anything involving lung parenchyma, pneumonia, hemorrhage. 
also pleural effusions, diaphragmatic hernia - anything causing pleural 
cavity to swell/expand. tight chest bandage could have same effect.

obstructive disease: slower deeper breaths indicate this kind of problem. 
think about how you would breathe if you tried breathing through a straw 
(shades of RO's lab...). you'd have slow, prolonged, deep inspiration 
because you're trying to suck air in through narrow tube with increased 
resistance to flow. this prolonged, deep inspiratory phase is often seen 
in animals with upper airway obstructions eg neoplasia, foreign body, 
tracheal collapse, etc. exhalation is usually relatively normal in these 
patients.

PATTERNS OF RESPIRATION

during respiration, normal respiration at rest, primary muscles are 
intercostals and diaphragm. if someone jogs around the room, drive for 
respirationa nd oxygen demand increase, and as drive for respiration 
increases, there is recruitment of secondary muscles of respiration eg 
sternomastoids, sternohyoids, other muscles around ribs, etc. the alae 
nasae flare open the nostrils, etc. this isn't pathological if there is 
true need for increased respiratory drive, but if there is disease of 
respiratory tract, a resting animal may exhibit these signs as well. if 
you see an animal showing increased respiratory effort, it can be 
pathology, or can be normal.

respiratory muscle failure: paradoxical breathing. think about how 
chest/abd move during normal respiration - both move out together during 
inspiration, and in together during expiration. this makes sense - as you 
inhale, diaphragm contracts, pushes down into abdomen. when there is a 
lot of increased respiratory effort, we see animals that have abdomen 
collapse inward on inspiration, and outward on expiration. we may also 
see intercostal muscles collapse inwards on inspiration. this is a sign 
of very much increased respiratory effort, heading into muscle fatigue, 
and toward respiratory failure. this definitely indicates pathology of 
the respiratory tract

also look for

Changes in posture: postural adaptations are a very serious sign pointing 
toward true pathology of respiratory tract. can observe while talking to 
owner. all of the adaptations are designed to allow maximum movement of 
air into chest, with minimal resistance to airflow.
stretching out head and neck - whole head/neck extended to keep airway 
horizontal, maximizing opening of trachea.
extending elbows so that they don't get in the way of chest wall 
expansion
will sit or stand, or possibly lie sternal, but not lie on side. if you 
see an animal like this, do not restrain it in lateral recumbency!
dogs and cats will both openmouth breathe during respiratory distress. 
some cats won't ever do that unless they are actually dying. dogs do it 
more commonly. this minimizes resistance to airflow. if you see a cat 
doing this, you know it is having real trouble.

so dyspnea is true difficulty breathing that we need to address pretty 
quickly, really.

clinical evaluation of animal in respiratory distress:

1. history
2. observation for above signs
3. physical exam - find out more about what's going on
4. diagnostic tests if possible. but can get a lot of info from first 
three, and sometimes animal is too distressed to allow tests.

CASES:

Buffy: 4 yo Fs k9x
assumed postural adaptations, has increased respiratory effort 
came into ER. 
V/D 6 weeks prior to episode
coughing x 1 month
gradual onset weakness, lethargy, anorexia x 1 week

at presentation, had increased respiratory effort, with an abdominal 
component (auxillary muscle recruitment), rapid, shallow breathing, 
refused to lie down, open mouthed breathing, productive cough.

thoughts about where to start looking? well, this is a restrictive 
pattern.

PE: temp = 104, RR = 60, pulse 140. mm pink, pulses weak, thready. 
prominent submand LNs, crackles on auscultation of chest. (like crinkling 
up a plastic bag sound. indicates fluid in alveoli.) also harsh air 
sounds in all lung fields.

what kind of fluid is in there, then? an exudate due to aspiration 
pneumonia? that's fairly likely. what other causes? heart failure is 
possible - her HR is elevated, pulses are weak. those are top two 
differentials. also could be hemorrhage or neoplastic situation. 

buffy had clear evidence of true lung dz. there was evidence of 
recruitment of secondary muscles of respiration and postural adaptation 
as well as the crackles. so we know from looking at her that there's 
probably some hypoxia.
normal Pa02 should be 90-100 mmHg

decreased PaO2 may be due to one or more of:

inadequate diffusion - due to alveolar thickening or inflammation

shunt or ventilation-perfusion mismatch - area of lung where there is 
mismatch of air coming in and blood coming in. area where alveoli full of 
fluid is heavily perfused due to inflammation, but that blood doesn't get 
oxygenated.
so less of the blood is oxygenated with each breath. this is probably the 
biggest reason we see hypoxia - alveoli full of fluid, or abscess, or 
tumor, or whatever, causing perfusion without ventilation.

hypoventilation

decreased Fl02


Tentative Dx:
aspiration pneumonia: fever, no heart murmur, history.
R/O heart disease.

Plan:
IV catheter, IV fluids, pursue diagnostics

Diagnostics:
CBC, Chemscreen, UA, Chest rads, transtracheal wash w/ C&S.

in Radiology, acute onset cyanosis, severe respiratory distress while 
taking radiographs. RR 120, HR 220, Temp 105. she severely decompensated 
during attempted restraint. they got films quick then rushed back to O2 
cage. 

why did this happen? 
by stressing her and preventing her from assuming postural adaptations by 
trying to restrain her, we greatly reduced her airflow.

Treatment: fluids, O2, rest.
she improved.

chest rads show obscured cardiac sillouhette due to increased opacity in 
ventral lung fields. can see air bronchograms due to background clouding. 
think of aspiration pneumonia, since the opacity is in the ventral 
fields. the DV view shows one side of her heart showing up, but the other 
side is obscured and the whole lung field is cloudy. this is severe 
aspiration pneumonia.

O2/Hb dissociation curve: very clinically relevant. this shows us the 
relationship between amt O2 in blood and amt attached to RBC (O2sat). 
normal animals have PO2 about 90-100 and are fully saturated. in a normal 
dog, even if the PO2 goes down to about 70 or 80, the O2 sat remains at 
about 90.
but if your PO2 is down around 60 like Buffy's was when she came into the 
ER, the O2 sat is still near 90. but if you stress this animal, the PO2 
drops, and if it goes down below 60, you start seeing rapid desaturation. 
a drop to 45 will drop you down to about 60% desaturation. as soon as you 
see desaturation and cyanosis you are in a crisis situation. this is 
really important, remember it.

Hypoxemia:
mm color is a crude estimate of hypoxia, PaO2 must be less than about 60 
mmHg for us to see cyanosis of the mms. 

desaturation can be caused by eating, drinking, walking, sleeping, taking 
blood, taking radiographs. these animals may not be able to stop 
breathing long enough to eat or drink, or even to sleep. many of these 
animals will try to sleep sitting up, and then wake up as they fall down, 
and really go for days without actually sleeping because they can't lie 
down. 

mucoous membrane color depends on amount of O2 attaching to Hb, also on 
amount of blood flowing through tissues - animal in shock w/pale mms may 
also be cyanotic but you can't tell, because there's no blood flow. also 
Hb concentration. if animal is very anemic, may not appreciate cyanosis.

transtracheal wash: very useful, easy to do. important diagnostic 
procedure. must know what bacteria is in there to treat correctly. if 
animal very sick, can't do this right away, so treat for a couple of days 
then do it. you clip a spot under the chin, put needle through skin about 
half way down trachea, into the airway, then advance a catheter through 
needle down into the lung - down to bifurcation of trachea. inject about 
10 ml saline, and then suck it back up. usually only get about 1 cc back, 
but in buffy, can see the fluid coming back is very purulent exudate. 
then we culture that fluid and do a sensitivity. also look under 
microscope for abnormal cells, etc.

found: many PMNs, alveolar macrophages, intracellular and extracellular 
bacteria.

treated with fluids and abx, nebulization and coupage, nasal O2.
need animal to cough and move the fluid and stuff out of lungs. to 
maximize opportunity for dog to do this, you need to keep the exudate 
thin, liquidy. if dry, sticky due to dehydration etc, is harder to get 
rid of. so keep animal well hydrated and use nebulization ("breathing 
treatments" to keep inside of lungs moist) and coupage (hitting chest 
wall with cupped hand, stimulates increased tidal volume and coughing).

improved over next two weeks. discharged on clavamox, had complete 
recovery.

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