A Critical Examination of Therapeutic Procedures Used to

Provide Emergency Support for Dogs Presenting with Dyspnea:

Dennis T. (Tim) Crowe, Jr., DVM, DACVS - Emeritus, Charter DACVECC, FCCM,

Regional Institute for Veterinary Emergencies and Referrals, Chattanooga, TN

This presentation provides practical information to the emergency and general practice clinician on which procedures to perform to gain the best possible resolution for dogs presented with dyspnea based on their clinical presentation.

Recommendations made here were based on clinical outcome data that critically examined the effectiveness of these procedures. Criteria used to evaluate the effectiveness of the procedures examined included presenting signs (upper verses lower or mixed respiratory patterns), resolution of clinical signs such as decrease in work of breathing, level of oxygenation achieved, staff time and special devices or equipment required, ease of implementation, complications noted, and follow-up as prospectively studied in several busy emergency and critical care/ referral facilities. NOTE: The true complete definition of dyspnea is that of a symptom of a patient saying that they are having difficulty in breathing, but the expanded definition includes the clinical signs noted of difficult breathing as judged by the owner and / or clinical professionals.

ASSESSMENT:

Clinical assessment - By far and away the most important evaluation of the patient that is having difficulty breathing (*dyspnea) is a good observational assessment of signalment, history, and physical exam findings. Often the first few minutes of assessment and care determine the outcome if the patient”.breathing his or her last”” Because oxygen is 20 times less diffusible than carbon dioxide the immediate need for most patients to provide supplemental oxygen and often sedation. SUPPLEMENTAL OXYGEN IS PROVIDED WITH OXYGEN TUBING ATTACHED TO A 14 G IV CATHETER AND THE OXYGEN STEAM BLOWN TO THE PATIENTS FACE LIKE A WATER STEAM AIMED AT A FIRE. A CLEAR PASTIC BAG CAN ALSO BE PLACED OVER THE ANIMAL LIKE A PORTABLE OXYGEN TENT FILLED WITH O2 AND THEN ASSESSMENT CONTINUED:

A, THE PATTERN OF BREATHING IS ASSESSED and BREATH SOUNDS ARE CHARACTERIZED.

BLOW BY with CATHETER NOZZLE – to the face as the breathing pattern is noted:

Characterization of the breathing pattern:

Short Rapid Difficult Breaths = Restrictive Patterns = Lung can not expand – commonly associated with pneumothorax, pleural fluid buildup, diaphragmatic hernia, chylothorax, hemothorax – severe abdominal distension

Long slow breaths witb added effort to inhale (literally looking like the patient is sucking on a small straw) = Upper Airway Resistance Pattern. Seen with upper airway obstruction such as that seen with laryngeal collapse or tracheal stenosis or masses.

Longer slower breaths with additional force seen for exhalation = noted with lung parenchyma and small airways problems such as asthma or pneumonia

Characterization of the breathing generated sound from a distance:

Sounds normally are quiet and not obvious other than hard panting. If these added sounds (called adventitial sounds) they are characterized:

Low pitched guttural sounds heard on inhalation = pharyngeal obstruction

High pitched sibilant sounds heard on inhalation = laryngeal obstruction

Characterization of breath sounds on stethoscope auscultation: Then listen to the breath sounds bilaterally – pneumothorax does occur unilaterally initially. Breath sounds are generally quiet with a slightly more soft F sound on exhalation - Sounds other than these are adventitial sounds and are characterized:

Increased sounds on inhalation = generally associated with larger airway resistance as what might be seen with a tracheal injury and some stenosis

Increased sounds on exhalation = generally associated with increases in resistance in the small airways such as that associated with an increase in interstitial edema (as observed in early fluid overload) or inflammation (as is seen in very early pneumonia). These are called bronchovesicular sounds.

Musical adventitial exhalational sounds = those that are musical like wheezes indicate some bronchial constriction as occurs with asthma.

Water like adventitial water like sounds = those associated with fluid or exudate within the bronchi which can be associated with pneumonia An older term was rales but these often are wet sounds and are heard with exudate within the airways. Rales are also seen with more advanced pulmonary edema, where fluid is accumulating into the small bronchial tubes. Rattles are more obvious and louder than rales and indicate an even more fluid accumulation within the small

Characterization of sounds heard and energy waves felt on percussion;

Percussion is difficult to do and interpret but can be useful in cases where air is accumulating rapidly as apposed to fluid that generally takes more time to do so. Immediate percussion done with one of the operators hands on the chest wall and the middle two fingers of the opposite hand used to thump the back of the opposite hand that is remaining on the chest wall. The operator does this procedure on both sides and compares the sound and the palpable characteristics of this thump. The sounds heard are then characterized:

Sounds same on both sides and are neither low base like or higher thud like = normal

Hollow sound like a base drum = air accumulation in the pleural space on that side

Dull thud like sound = fluid or solid mass or structure on that side

Auscultation of upper airway sounds generated with panting:

Similar to the physical test called “egophany” where the human patient is told to say the sound E and the stethoscope is used to hear the referred upper airway laryngeal sound E (termed Egophany) through the patent’s bronchi, the animal’s upper airway panting sounds are transferred through the bronchi and is used to detect blocked main sections of the bronchi. This diagnostic test I have termed “pantophany” is not difficult to do and does help in the detection of lung collapse and major bronchi blockage.

The NEW STETHOSCOPE = ULTRASOUND:

This is becoming the new stethoscope in practice. All animals with dyspnea on arrival, after supplemental oxygen is begun, are soaked with alcohol, applied to the lateral thoracic wall on both sides and the ultrasound probe is then applied and used to assess for pneumothorax, free pleural fluid, pulmonary parenchyma, pericardium, myocardium contractility and chamber size, and diaphragm:

Probe placed on the thoracic wall dorsally and thoracic structures visualized:

Examined for a glide sign – if not seen = pneumothorax,

Examine for lung rockets - If seen indicate increased pulmonary density as may be seen with pulmonary edema, pulmonary contusions, and pneumonia. Three or more lung rockets seen per field = indicate more increased water content than normal lungs

Examine for free fluid in the pleural space - seen as fluid between the parietal pleura and the visceral pleura = see with blood, chyle, or other types of free fluid; the US probe can be then used to aspitate some of this fluid if there enough that can be withdrawn safely. Occasionally pulmonary masses can also be observed.

Probe placed at midthoracic area (chest tube site) and structures visualized:

The same interpretations are made.

Probe placed at the ventral lung – pleural space area and structures visualized:

The same interpretations are made.

Probe placed over the heart, pericardium and diaphragm structures visualized;

Observe for pericardial fluid, or other– if seen is pericardial hemorrhage or fluid; Pericardial diaphragmatic hernia can be seen nicely with this technique. One case of dyspnea lead to acute cardiac arrest that occurred in our hospital lobby; jugular veins were distended – probe identified this possible reason for acute decompensation and immediate thoracotomy was completed and opening of the pericardium and CPR lead to a complete recovery with good neurological function

Observe cardiac contractility – provides aindex of cardiac output and possible cause of dyspnea and very useful in tracking response to fluid resuscitation, diuretic response, etc. Occasionally other reasons for the dyspnea will be detected, e.g., heart base mass.

Observe the diaphragm – provides a means of noting significant diaphragmatic hernia as often liver parenchyma is observed in these cases and this leads to the operator having a diagnosis or preliminary diagnosis within minutes of admission and without any added manipulation of the dyspnic patient. This can then lead to immediate intubation with a rapid induction and moving on to definitive repair as these patients can not be “stabilized” without rapid intervention.

Probe placed on the abdominal side of the diaphragm: - The cranial portion of the abdomen is visualized as an AFAST (a focused abdominal sound for trauma, tumors, etc). Some animals with abdominal conditions such as extreme sepsis will present with dyspnea and free fluid or an abdominal mass can be found. This would lead to a clinical workup for such.

THERAPY REQUIRED:

This may range from oxygen supplementation (SEE BELOW) to nearly immediate resuscitative thoracotomy such as might occur with sudden cardiac arrest. This author has not seen very many patients in which closed chest CPR in the face of dyspnea has been successful. Yet with open chest CPR he has observed noted “saves” when a resuscitative thoracotomy and subsequent CPR with recognition and resolution of the reason for the arrest was accomplished.

Examples of Dyspnic Animals that required a Resuscitative Thoracotomy- the reason noted for the decompensation and resolution leading to a successful outcome:

Pericardial tamponade from a pericardial- diaphragmatic hernia

Severe tension pneumothorac from a ruptured pulmonary bulla

Severe tension pneumothorax from a dog bite associated lung/bronchus injury

Severe tension pneumomediastinum caused by a peritracheal wound

Severe tension pneumomedistainum following the creation of a tracheotomy that was required to be able to perform a partial arytenoidectiomy

Supplemental Oxygen - The first principle of resuscitative treatment of the dyspnic patient is to provide DtO2 to meet needs of all tissues of the Brain*, Heart, GI, etc. Therefore this commonly dictates the need for supplemental oxygen..* DtO2 is determined by FiO2 ~ pAO2~ paO2, [Hb], Q (t capillary), interstitial space. Since it is common to have VQ Mismatching in such conditions as shock, trauma, sepsis it is highly commended that supplemental O2 be provided in all critical patients especially if they exhibit dyspnea. The goal with supplemental oxygen therapy is to provide it as required to gain just enough increased FiO2 to allow for better tissue oxygenation to meet the metabolic oxygen demands for the cardiovascular, neurologic and gastrointestinal systems. The simplest and most clinically effective way to determine this initially is to observe the changes seen in both breathing rate and effort…. IF BREATING RATE AND EFFORT ARE BECOMING MORE NORMALIZED THESE OBSERVED SIGNS INDICATE that the supplemental oxygen is making a positive impact and should be continued as DO2 is at least getting close to satisfying the CNS VO2 (oxygen demand) and this includes the aortic arch.

Assessment may be also be enhanced through the attempted use of PULSE OXIMETRY as this provides a digital means of determining the need and results of treatment. Any SpO2 % above 94% is acceptable. HIGH FIDELETY SpO2 monitors like the Mosimo unit or those that provide nasal membrane oxygen placed saturation transducers may provide another means of oximetry. The common systems use transmissiveoximetry methods that involve the detection of the amount of oxygen saturation in the red blood cells using a photodetector that is placed on one side of the tissue being interrogated and the other side where the photon beams are being generated. The device passes two wavelengths of light through the body part to the photodector. The changes in absorbance at each of the near infrared wavelengths is measured. These differences in absorbance are due to pulsing arterial blood in the small arterioles. Reflectance pulse oximetry may also be used as an alternative. It does not require the light beams to be transmitted through the skin or membranes and is therefore more effective when interrogating the chest, feet, and forehead. This technology has recently been introduced into smartphone technology such as the Samsung Galaxy S5. For pulse oximetry to been effective and reliable the pulse wave MUST be able to be seen and assessed (Photoplethysmography) so that the accuracy can be determined. There must be a good wave form for clinical interpretation.

Unfortunately in many cases pulse oximetryis NOT able to be used initially due to the difficulty in applying the sensor anywhere. As many experienced clinicians have said “ These patients should not be messed with” and attempts to place a pulse oximeter, at least at the onset of therapy is contrainidicated. This also includes the procurement of blood samples for laboratory analysis and the procurement of radiographs.

Research has proven that supplemental oxygen might be a means of care that provides a buffer between catastrophic decompensation and getting by while the history and exam (as best as can be done safety) are completed

Research papers supporting supplemental oxygen: Head injury swine model supplemental O2 reduced the edema and improved outcome…. “ The MOST important treatment for all head injured” Geoff Manley MD 2003; Chief Neuro-Trauma, Univ. California San Francisco, San Francisco General Hospital: 0% mortality w/ 100% O2 verses 71% mortality w/ 20% O2 in hemorrhagic shock pigs partially fluid resuscitated w/ hetastarch. .Meier J, et al: Hyperoxic ventilation reduces 6 hour mortality after partial fluid resuscitation from hemorrhagic shock. Shock 2004 Sept 22(3):240-247

NOTE ABOUT SUPPLEMENTAL OXYGEN: Please refer to the manuscript entitled:

ACritical Look at Supplemental Oxygen Delivery Methods - What is the evidence. And a look at a new method: Using a High Flow Humidified Oxygen Cannula-This presentation reviews all the current means of providing supplemental oxygen (blow by, cages of various types, open mask, sealed mask with BVM and reservoir, hood, collar, boat, nasal catheter, nasal cannula, bilateral nasal catheter, nasopharyngeal, bilateral nasopharyngeal, nasotracheal) and relatively new method involving a nasal cannula fitted to deliver higher flow humidified oxygen. These methods are compared regarding ease of use, patient acceptance, equipment/supplies needed and FiO2 achievable over given amounts of time, and oxygen flow rate required.(further information is provided that addresses these modalities is written in the proceedings entitled: A Critical Look at Supplemental Oxygen Delivery Methods

Sedation as a critical therapy:

This is one of the most important therapies that should be completed for the patient having difficult breathing. If anyone has ever had a respiratory crisis it is commonly remembered as one of the most frightening times in his or her entire life. Although we can not truly know what our animal patients are sensing or thinking I have noted in their eyes a look of panic and fright. This appeared to be greatly heightened as their breathing effort increased. This often becomes more exaggerated as they arrive at the very place (veterinary hospital) were they might remember other visits were they were subjected to examinations, vaccinations, blood draws, etc., that were associated with a sense of fright. THEREFORE, as many other authors have recommended – these animals need substantial and very early treatment for their physiologically induced PANIC.

Protocols that have been critically examined and found to be effective in decreasing patient panic. I have not found any clinically reproducible studies that will fit every patient however. Each patient will need a protocol that is tailored to their needed and the response observed to assure as much clinically safety and effectiveness as possible:

Butorphenol 0.2 mg/kg IM with either Acepromazine 0.01 mg.kg IM or Midazolam 0.2 mg/kg IM – acupuncture point LI-11, GV -20 and the calming point located behind the mastoid process – each activated with either pressure, red photonic light, low level laser or needed. I prefer the use of the photonic “torch” as it very quickly activates the AC point and attendant light based meridian. NOTE: This protocol can then be supplemented with added doses once an IV catheter is placed.

Hydromorphone 0.1 mg/kg with either Acepromazine 0.01 mg/kg or Midazolam 0.2 mg/kg IM along with acupuncture points as well – Of course these protocols can be used without the ACPs but the effect is enhanced by their use and in some cases the can be used along. IV doses of these combinations will also work well in most cases as long as they are not given rapidly and it is recommended that only half doses are given initially.

Ketamine 2-4 mg/kg, butorphenol 0.1-0.2 mg/kg, and acepromazine 0.01-0.04 mg/kg mixture in the same syringe given IM in the epaxial muscles (if IV access is not already available).

Anesthesia Induction, Intubated and Positive Pressure Breathing Instituted:

Anesthesia Induction with IV doses of these drugs with a small dose of propofol may also be needed for the very critical difficult breathing patient on occasion. This may be indicated when the dog or cat is literally “breathing their last” Blow by oxygen is given until the IV hydromorphone and Midazolam are on board and then a bag valve mask is added and assist ventilation is given. Then a small amount of propofol is provided (generally 1-4 mg/kg starting with the lower end of the dose. The trachea is intubated with the assistance of a laryngoscope (if available – which is especially helpful in cats and those dogs with airway compromises such as those that are brachycephalic. Positive pressure ventilation will then be instituted while other diagnostics and therapy such as chest taps , chest tube placement, or thoracic surgery such as what might be needed for a small dog that was attached by a large dog and sustaining injury to both the right and left thoracic wall and lung tissue, those with severe pulmonary edema from congestive heart failure, or centroneurogenic pulmonary edema from a choking episode.