Resp assessment and support March 25 2011

Respiratory Assessment and Respiratory Support Respiratory Assessment and Respiratory Support Dez Hughes BVSc, MRCVS, Dip. ACVECC

So this week we’re going to talk about the clinical assessment of the respiratory system and respiratory support. And next week we will put it all together when we cover the diagnostic approach to the dyspnoeic patient. Here you can see a picture of a very dyspnoeic cat who is also very not pleased! Fractious, dyspnoeic cats are a particular challenge because when you try to handle them they will commit Hari Kari (ritual suicide) and try to take you with them.

Outline Outline Anatomical levels of the respiratory tractMechanics of respirationPostural manifestations of dyspnoeaUsing respiratory pattern to localise the cause of dyspnoeaPulmonary auscultation and lung soundsOxygen supplementation

After reviewing the anatomical levels of the respiratory tract and the mechanics of respiration we’ll spend some time looking at the postural manifestations of dyspnoea and how we use these to assess the severity of respiratory distress. Then we’ll cover how you can sometimes use the respiratory pattern to localise the anatomical level of the respiratory tract that is affected. Next we’ll discuss pulmonary auscultation and lung sounds and finally we’ll skip through the different ways you can administer supplemental oxygen.

Anatomical Levels of the Respiratory Tract Anatomical Levels of the Respiratory Tract Upper airwaySmall airwaysPulmonary parenchymaPleural spaceChest wall and diaphragm

So to begin, let’s review the 5 levels of the respiratory tract. They are the upper airway (from nose to main stem bronchi), the small airways, the pulmonary parenchyma, the pleural space, and the chest wall and diaphragm. It is vitally important to work out which level is affected because the stabilisation, diagnostic approach, differential diagnoses, treatment and prognosis are so different for each group. It is actually possible to differentiate them largely on physical examination with a bit of practice. By the way, in my book, the upper airway extends all the way to the carina because there is no difference to the animal between an obstruction in the larynx and an obstruction of the distal trachea.

Mechanics of Respiration Inspirationnegative intrapleural pressurelung expansiondilation of intrathoracic tracheacollapse of extrathoracic airways Mechanics of Respiration

To understand what is happening during normal breathing, let’s consider the pressure changes occurring in the respiratory tract and the effects that they have on the system. As the animal breathes in the diaphragm moves caudally and the chest wall moves out a little. This expands the chest cavity and causes a drop in pressure in the pleural space. This then pulls the lung open. As the lung is expanded, the airways inside the lung are also pulled open and the pressure inside them drops. This low pressure in the intrathoracic airways then sucks air down the trachea and generates a lower pressure inside the upper airway in the neck and throat. But the pressure around the extrathoracic airway is atmospheric pressure (which is higher than the pressure inside) so this means that the upper airway outside the chest will collapse on inspiration. That is why animals have a muscle to keep their vocal folds open when they are inspiring (called cricoarytenoidalis dorsalis). If that muscle is not working (as in laryngeal paralysis) the vocal folds get pulled together on inspiration and cause an upper airway obstruction. If a dog has a collapsing trachea affecting the intrathoracic portion, then inspiration is fine cos the floppy dorsal membrane gets pulled open. But when he tries to breathe out, it all snaps shut and you get the classic “goose honk” cough. If the extrathoracic trachea is affected then the dog will have signs of an upper airway obstruction on inspiration. If both are affected then the dog will have trouble on both inspiration and expiration.

Assessing the Severity of Dyspnoea Assessing the Severity of Dyspnoea Respiratory rateRespiratory effortRespiratory patternRespiratory noiseAuscultationRate dyspnoea into moderate, severe or criticalCross-reference all the time

So, as we mentioned under major body system assessment, we initially look at the respiratory rate, effort and auscultation. We are going to expand that list a bit here to include respiratory pattern and respiratory noise. And we are always cross referencing to make sure that everything fits together. When you looking at a dyspnoeic animal always try to rate the severity of dyspnoea into moderate, severe or critical. I don’t have a mild category here because dyspnoea is always potentially life threatening and any dyspnoea is a very bad thing. One tip about rate here: the rate almost always increases as dyspnoea worsens. BUT in some very severe cases where there is a lot of work of breathing (like really stiff lungs) and especially if the animal also has respiratory muscle fatigue, there comes a point at which the respiratory rate can actually fall. This is a very serious sign and a marker of impending respiratory arrest. In most patients though, a fall in respiratory rate will mean an improvement.

Severity of Dyspnoea Increased abdominal movementAbdominal effortParadoxical abdominal movement Severity of Dyspnoea

At the start of this slide I would like to introduce you to our new colour scheme. If I need to make it clear how common something is: red means something that is relatively common, black means something that is less common and blue means something that is pretty rare. These are all common so they are all red. Anyway, as dyspnoea worsens the rate and effort increase, but initially the chest and abdomen will still move in and out together. I call this increased abdominal movement to differentiate it from abdominal effort and paradoxical abdominal movement. Abdominal effort is a push on expiration. Because inspiratory abdominal movement is passive, the only phase of respiration that abdominal muscle contraction can help with is expiration. A forced expiration means one of 3 things: small airway disease (which is asthma in cats), very stiff lungs or a fixed (as opposed to dynamic) upper airway obstruction (see later). In virtually all cases there will be increased inspiratory effort as well as the abdominal push. In contrast, paradoxical abdominal movement is when the abdomen goes in, instead of out, inspiration. Read on for more...

Paradoxical Abdominal Movement Paradoxical Abdominal Movement Upper airway obstruction Stiff lungs Diaphragm dysfunction Severe chronic pleural effusion in cats

In a normal animal, on inspiration the chest is moving out a little and the diaphragm is trying to move caudally. As dyspnoea worsens more chest movement will occur. Because the chest wall is a rigid bony structure, if the muscles of inspiration try to pull the chest out, then will pretty much always be successful in expanding the chest. The diaphragm though, is only a muscle attached around its periphery. If the chest wall expands but the lungs can’t expand for whatever reason then the diaphragm will get pulled cranially against its will and the abdomen will go in. Paradoxical abdominal movement is usually a sign of more severe dyspnoea. There are only really 4 things that cause paradoxical abdominal movement: upper airway obstruction, really stiff lungs, a diaphragm that is not working or has a hole in it or very severe pleural space disease, usually fluid. Pretty much any parenchymal disease will make the lungs stiffer or to use the correct terminology, less compliant. Observing the animal and listening with and without your stethoscope can be a real help in differentiating these 4 conditions and we will cover later in this Big Picture and next week. This is an old fella with very stiff lungs. Chest rads were very suggestive of diffuse neoplasia. Watch his chest move and count In, In, In with his inspirations. Then look replay the video and look at his abdomen as well and you can see that instead of going out on inspiration it is going in. A lot. I would class this as severe paradoxical abdominal movement and severe dyspnoea.

Severity of Dyspnoea Severity of Dyspnoea Extended neckAbducted elbowsOpen mouth breathingAnxious facial expression

An extended neck, abducted elbows, and open mouth breathing are all ways in which the animal tries to reduce the resistance to airflow to make it easier to breathe. Open mouth breathing means severe dyspnoea in either species but cats do it at a later stage of dyspnoea than dogs. By the time a cat is open mouth breathing things are getting grim. The anxious facial expression is common and a good cross reference point to see how distressed the animal is. Animals with chronic respiratory compromise may have marked chest excursions but a lesser degree of distress because they have had time to compensate. This Husky puppy has pulmonary haemorrhage from anticoagulant rodenticide toxicity.

Severe or Critical Dyspnoea Open mouth breathingLateral recumbencyBeware of rapidly changing body position in cats!Pupillary dilation means resp. arrest Severe or Critical Dyspnoea

Open mouth breathing is one of the cut off points I use to classify dyspnoea as severe. An even worse sign for me is when the animals have a glazed look to their eyes and seem unaware of their surroundings. I am also really concerned when a dyspnoeic animal is in any body position that is NOT sternal recumbency. If they are past the point of being able to maintain the best position for themselves, then things are getting critical. If they spontaneously start moving around a lot (using up vital oxygen) then respiratory arrest may be imminent. Lateral recumbency is a bad sign in a dog but it is critical in a dyspnoeic cat. If you see the animal’s pupils begin to dilate then they are respiratory arresting in front of your eyes (eg this cat!).

Cyanosis Cyanosis

Cyanosis, when caused by hypoxia as opposed to circulatory abnormalities, always puts an animal into the critical group. It is always imminently life threatening and should be treated and fixed in seconds to minutes. When dealing with cyanosis due to hypoxia, you should NEVER look at an animal and say things like “He looks kinda cyanotic” or “Hmmm, I think she’s a bit blue?” Cyanosis caused by hypoxia is an absolute, degrees are irrelevant. Your response must be immediate and decisive: OXYGEN then a rapid analysis of which level of the respiratory tract is responsible then hopefully definitive stabilisation.

Critical Dyspnoea Critical Dyspnoea

But the main thing I look at when classifying the severity of respiratory distress is the amount of effort it is taking the animal to breathe. This dog that has been hit by a car and has severe pulmonary contusions. This is the worst that respiratory effort gets. His rate has actually slowed a bit due to the effort required to expand his blood filled lungs. This degree of effort means that respiratory arrest is imminent and this dog went into cardiopulmonary arrest only minutes after this video was taken.

Beware of Puppies! Beware of Puppies! Puppies lie to you!!!

Don’t be fooled by them: Puppies Lie To You!!! Seriously though, what I mean here is that puppies do not show the same degree of distress associated with difficulty breathing, either in their expressions of distress or their postural manifestations. They look like everything is not too bad when in fact it can be really, really bad. This Golden Retriever puppy had severe pulmonary contusions after being hit by a car. You can see that he only really has an anxious facial expression. On his chest rads though, you can see that there is a solid alveolar pattern in most of his lung lobes. He was dead a few hours after this picture was taken. Not looking sick when you really are is a protective evolutionary strategy in the wild. Puppies do it and cats do it. Don’t be fooled by it.

Respiratory Pattern Respiratory Pattern Inspiratory dyspnoeaupper airway obstruction (stertor or stridor)severe, chronic pleural effusion (no noise)Inspiratory dyspnoea with an expiratory pushFixed upper airway obstruction

By far the most important pattern to be able to recognise is the inspiratory dyspnoea that is associated with upper airway obstruction. When you watch an animal with an upper airway obstruction you will see that they spend much longer trying to breathe in compared to breathing out. Because of the obstruction they can only manage a very small inspiratory tidal volume so expiration is usually short. In all but the most severe cases you will hear a noise associated with inspiration that is either stertorous (snoring) or stridorous (wheezing). Rule of thumb: if you can hear the dog breathing on the other side of the room it has an upper airway obstruction til proven otherwise. Much less commonly, inspiratory dyspnoea can be due to large volume pleural space disease, usually a severe, chronic, pleural effusion. In this case your clue is that there will be no upper airway noise. Many upper airway obstructions are dynamic ie they can move in response to the pressure changes in the airways. Laryngeal paralysis is the classic one. With dynamic obstructions the dyspnoea only occurs on inspiration because there is no obstruction to expiration. Fixed upper airway obstructions are thankfully rare but when they do occur you will also see the animal struggle to exhale against the obstruction as well. In the most severe cases of fixed obstruction there may actually be little or no noise (because of the very small amount of air getting past the obstruction) but there will be a lot of chest movement as the animal struggles to get air in. These cases will always have paradoxical abdominal movement. One last word of caution for severe, upper airway obstructions that have come on gradually (like slow growing tumours): the animals will have learned not to move around much to compensate for their chronic hypoxia. These animals are sometimes NOT DYSPNOEIC at rest but on minimal stimulation they can go into respiratory arrest and die if you can’t perform an immediate tracheostomy. Learn from my mistakes: an emergency tracheostomy in a 16 year old cat is no fun at all. And especially not after 3 cups of coffee!!!!

Upper Airway Obstruction Upper Airway Obstruction

When you watch this Cavvy breathing and listen to the sound he is making as he breathes. you’ll be able to see that the dog is having difficulty on inspiration and that there is corresponding noise on inspiration and that there is paradoxical abdominal movement. Upper airway obstructions come in varying degrees of severity. When this video was taken, this Cavalier with brachycephalic occlusive syndrome had a moderate degree of obstruction. But if it opened its mouth it had virtually no obstruction at all! Which strongly suggests that the soft palate was the main component of this dogs problem.

Respiratory Pattern Respiratory Pattern Expiratory dyspnoeafeline asthma(COPD in horses)Short shallow respirationssome pleural space lesions

There is really only small airway disease that results a respiratory pattern where expiration is worse than inspiration. And that pretty much means asthma in cats and chronic obstructive pulmonary disease in horses. I can’t ever remember seeing a dog with allergic airway disease that had an expiratory push. I find that most asthmatic cats have a mixed dyspnoea and something like ½ - 2/3rds have an expiratory push. Short, shallow respirations may be associated with pleural space disease but lots of other things can cause a short, shallow pattern so it is not specific. Beware though that some animals with chronic pleural space disease that has accumulated gradually can have very large volume effusions or pneumothorax and only exhibit short shallow respirations.

Harsh Lung Sounds Harsh Lung Sounds

I classify abnormal lung sounds as either harsh (ie coarser and louder than normal) or crackles (which can be fine or coarse). There is a tendency to think that harsh lung sounds would be caused by “dry” lung disease and that crackles would be due to “wet” lung disease but this is not the case. Harsh lung sounds can be caused by any parenchymal or airway disease probably due to increased turbulence from airway narrowing. These radiographs are from a cat with severe interstitial lung disease, either chronic asthma or neoplasia. He had very harsh lung sounds in all fields. On the radiographs you can see that there is a very marked bronchointerstitial pattern throughout the lung lobes. Referred upper airway noise can also make the lung sounds sound louder than normal so have a quick listen over the trachea and mentally subtract any upper airway noise from what you are hearing in the chest.

Crackles Crackles

To hear crackles, the animal must be taking sufficiently deep breaths to inflate the lung. Consequently, they are usually loudest at the end of inspiration. Crackles can be either coarse or fine. Fine crackles are usually only heard at the very end of inspiration and are probably generated by the opening of collapsed small airways. Coarse crackles are usually associated with parenchymal disease but occasionally can be due to airway disease. Nevertheless, if you hear coarse crackles, it is most likely that the animal has a fluid build up of some sort in its lungs. But by auscultation you can’t tell what that fluid is. It could be blood, exudate from pneumonia, hydrostatic oedema from left heart failure or fluid overload, neoplasia related fluid, or neurogenic pulmonary oedema. These radiographs are from a dog with probable aspiration pneumonia. You can see that the middle lung lobe has a quite dense alveolar pattern and that is where you would hear harsh lung sounds or crackles or both.

Lung sound distribution Lung sound distribution Cranioventral with pneumoniaCaudodorsal with mild/mod neurogenic oedemaPerihilar in some cases of L heart failureHarsh dorsal lung sounds with pleural effusionHarsh cranioventral sounds with pneumothoraxHarsh everywhere with feline asthma

Once you have detected abnormal lung sounds you should try to assess their distribution and this can sometimes tell you what the most likely causes are. For example, the previous radiographs in the dog with aspiration pneumonia the abnormal lung sounds would be cranioventral and on the side where the disease was located. Other useful distributions are perihilar in some cases of left heart failure (a tough call to make but possible) and dorsocaudal in mild or moderate neurogenic oedema. When you have pleural space disease, the lung sounds are quiet or absent where the fluid, air or mass is and normal or harsher harsher in the areas where the lungs are. With pleural space disease the lungs are often partially collapsed and the airways are narrower hence more turbulence.

Pneumothorax Auscultation Pneumothorax Auscultation

This is a moderate pneumothorax. You can see the cardinal sign which is the air ventral to the heart on a lateral radiograph. When a dog is sitting in sternal recumbency or standing the air will be located in the dorsocaudal part of the pleural space. The lungs will have moved ventrally so lung sounds will be quieter in the dorsocaudal chest. The lung sounds in the cranioventral chest will be normal or harsher than normal.

Pleural Effusion Auscultation Pleural Effusion Auscultation

In this radiograph of a dog with a pleural effusion you can see that the lungs are located in a more dorsal position than normal. This results in quieter or absent lung sounds in the ventral chest and harsh or normal lung sounds in the dorsocaudal region. Some textbooks say that the heart is muffled with pleural effusion but I can usually still hear it OK. In fact, I think it is sometimes easier to hear and can radiate over a greater area of the chest especially in cats (which may be due to sound carrying better through fluid than through air).

Methods of Oxygen Supplementation Methods of Oxygen Supplementation Flow-byMaskE collar and cling filmNasal catheter or prongsOxygen cageIntubation/ventilation

So these are the methods of oxygen administration in rough order of increasing inspired oxygen concentrations: flow-by is least followed by mask, collar and nasal catheter which can all be about the same. A good oxygen cage can give very high oxygen concentrations and then artificial ventilation which can obviously allow an inspired oxygen concentration of 100% if necessary.

Mask Oxygen Administration Mask Oxygen Administration Relatively low inspired oxygen concentrationStressful for some patientsEasy and cheapMay require restraintUseful when performing initial evaluation

With a mask, the oxygen concentration depends on how tight fitting the mask is. We often guesstimate that they allow about 40%. But with a large, tight fitting mask in a sedated dog you might actually get close to 60 or even 80%. Always remember that animals do not understand you are giving them oxygen. They may actually think that the mask is stopping them being able to breathe properly. I reckon that’s why some animals find it so stressful. And never use masks they can’t see through. If the animal starts to struggle DO NOT restrain them to keep their heads in the mask. Go for a less stressful method. By that way, that 200 ml of pus came out of that cat’s chest.

E Collar and Cling Film E Collar and Cling Film Variable inspired oxygen concentrationCan be higher if low venting of hoodPoorly ventilated hood will cause  CO2 temp and humidity

Using an E collar and cling film can work and, depending on the construction, you might get an inspired oxygen concentration of between 30 and 60%. But there is a trade off. Fewer leaks mean higher inspired O2, but you will also then get build up of CO2 and humidity and temperature all of which can be worsen respiratory distress in a patient that is already dyspnoeic.

Nasal Oxygen Catheter Nasal Oxygen Catheter Variable inspired oxygen concentrationNot tolerated by some patientsEasy and inexpensive

Nasal oxygen catheter are fairly straightforward to place and you can use unilateral or bilateral. But placement itself can be very stressful in some patients. Depending on the flow rates used relative to the size of the patient you may get inspired oxygen concentrations of 30-60%. I usually work out their expected minute volume to get an idea of what the highest rate I would use is. Tidal volume is ~10ml/kg and let’s say they are breathing at 40 breaths per minute. That gives a minute volume of 400 ml/kg so a 20 kg dog would get 8 litres a minute. If I don’t think that I need the full whack then I usually put them on about 100 ml/kg/min. I think that nasal tubing of any kind is potentially dangerous in head trauma patients because of the risk of sneezing, coughing or retching resulting in increases in intracranial pressure so I usually use an alternative administration method in these fellas. This pictures here are mainly to show you the two different ways of attaching them to the patient. In the fella on the left it is actually a nasogastric tube.

Neonatal Incubator Neonatal Incubator High inspired oxygen concentrationsStress free environmentInexpensiveLimited access

You can often get these for a reasonable price from local hospitals or from medical suppliers of refurbished equipment. Depending on how leaky they are and how much oxygen you pump in you can get high inspired oxygen concentrations. Now that I think of it, an oxygen sensor is a good bit of kit to have if you use oxygen cages with any frequency. They are fairly inexpensive and that way you can actually measure what you are giving rather than guessing. So neonatal incubators are pretty good for cats and small dogs and can usually be heated which is good for warming cold patients (even if they are not dyspnoeic).

Oxygen cage Oxygen cage

Oxygen cages range from solid cage fronts to purpose built ones with full environmental control. The solid cage fronts have all the same problems as E collars with cling film. The purpose built ones are expensive (up to $40, 000) but they allow you to give near to 100% oxygen, they have soda lime to remove CO2 and they also allow control of humidity and can heat or cool the patients. Being able to cool a dog with an upper airway obstruction while giving them 100% oxygen is a real boon. The cages shown here can take large dogs (up to 40 kg reasonably comfortably). If you need to put bigger ones in there you can. It’s a tight fit, but I’ve used them for giant breeds when I had no choice and they can still be kept cool. And one use that is dead handy is for flippin’ barking dogs (like seizuring patients that are now normal but still need observation). The cages are soundproofed so you just set the cage to use room air and close the front door and Hey Presto! It’s quiet!

Artificial Ventilation Artificial Ventilation Allows 100% inspired oxygen concentrationFull control of ventilation and oxygenationRequires prolonged anaesthesiaExpensive and very labour intensivePoor survival rates for severe lung disease

If you put an animal on a ventilator then you can control all aspects of its ventilation and oxygenation. But it requires at least heavy sedation and usually anaesthesia. And you then become an essential part of the animal’s major body systems! You now have control of its life. Usually this means that there must be someone with the animal 100% of the time. And you have to know how to ventilate and as importantly how to troubleshoot when problems occur like leaks, blockages, fighting the ventilator, or the dreaded ventilator induced lung injury, pneumonia and pneumothorax . Even with the best planning and oversight, problems usually do occur in some shape or form. If you are ventilating an animal because it has respiratory paralysis (eg snake bites) then survival rates can be very good. But if you are forced to ventilate an animal because it has severe lung disease and hypoxia that doesn’t respond to oxygen supplementation then you are looking at poor survival rates, something like 10-20%. So while ventilation is a very doable part of critical care, the decision to ventilate a veterinary patient should not be taken lightly.

Sternal Recumbency Sternal Recumbency Much better gas exchange vs. lateralPaO2 may rise by 20-30 mmHg or moreCheap and easy

Sometimes the simple things are just as important as the difficult ones! Putting an animal into sternal recumbency is one of the most effective ways of improving their gas exchange. Sometimes the improvement in arterial oxygen concentration when the animal is moved into sternal recumbency can be life saving. I’ve seen a PaO2 of 40mmHg on oxygen (ie imminently life threatening) go up to 70 (safe) with nothing other than sticking the dog in sternal recumbency.

That’s All Folks! That’s All Folks!

Well that’s the lot for this week’s Big Picture. I hope that you have found it useful. Respiratory distress is one of my very favourite topics because you can get so much more from your assessment and make a real difference to your survival rates with a bit of effort and a healthy dose common sense and logic. I’ll leave you with one of my favourite videos. I was asked to come into ICU to look at this dog because it was collapsing. It’s a very rare condition but you’ll never forget it once you’ve seen it!