How Am I Supposed to Breathe with No Air? Nikki Lewis, CVT, VTS (ECC) 2016 ISVMA Conference Proceedings
Total Page:16
File Type:pdf, Size:1020Kb
How am I supposed to breathe with no air? Nikki Lewis, CVT, VTS (ECC) 2016 ISVMA Conference Proceedings When the respiratory center begins to fail, functions such as oxygenation and elimination of carbon dioxide are compromised. This results in hypercapnia and hypoxemia. The major components of gas exchange are the lungs and the respiratory muscles which provide a force or pump to the lungs. If either one of these primary functions are compromised it can result in respiratory failure. Assessment of oxygenation and ventilation To accurately define respiratory failure, you must evaluate arterial blood gasses. A partial pressure of oxygen (PaO2) that’s less than 60mmHg and a partial pressure of carbon dioxide (PaCO2) of greater than 50mmHg define respiratory failure. The term partial pressure refers to the total pressure exerted by a single molecule of this gas. There are several molecules all combined in a cell; however, the partial pressure is the single gas’ pressure. Pulse oximetry is another method of quantifying oxygenation, although not as precise as arterial blood gasses. This is an indirect measurement of PaO2. A pulse oximetry measurement of 91-100% typically reflects a PaO2 of 80-100mmHg, which is a normal value. If the pulse oximetry falls below 91% this results in a rapid drop of the PaO2. Several factors can make the pulse oximetry reading false. These include pigmented tissues, motion and methemoglobinemia. Lastly, the measurement of end-tidal CO2 (ETCO2) will evaluate proper gas exchange. This is done by intubating the patient and using capnography. Capnography measures the expired CO2. Normal ETCO2 range is 35-45mmHg. An increase in ETCO2 is indicative of hypoventilation or increased dead space and a decrease in ETCO2 is indicative of hyperventilation. Hypoxemia or hypoxemic respiratory failure Hypoxemia is defined as a decreased delivery of oxygen to tissues. There are 5 main causes of hypoxemia: 1. V/Q mismatch = ventilation perfusion mismatch occurs when ventilation is not equal to the blood flow to the lungs. Examples of this include pulmonary thromboembolism (PTE), bronchitis and chronic obstructive pulmonary disease (COPD). 2. Decreased fraction of inspired air (FiO2) = percentage of air that is inspired has been decreased or compromised. This is commonly seen in acute respiratory distress syndrome (ARDS) and carbon monoxide poisoning. 3. Shunting = there are three types of shunts that can be characterized. An anatomic shunt occurs when blood enters the left side of the heart without passing through the lungs, therefore decreasing oxygen carrying capacity. A capillary shunt is defined as blood that passes through the lungs, however it does not get oxygenated because it does not respire with the alveolar gas. This is commonly seen in atelectasis. Lastly venous admixture occurs when the alveoli fill with fluid such as cardiogenic/noncardiogenic edema, pneumonia or coagulopathies. The impairment of alveolar function prohibits oxygenation. 4. Hypoventilation = decrease in respiratory rate, therefore a decrease in oxygenation and an increase in levels of carbon dioxide (CO2). 5. Diffusion impairment = this occurs when the blood-gas barrier becomes thickened and oxygen cannot exchange within the red blood cells. Hypercapnic respiratory failure Hypercapnia is defined as an elevation of CO2 in the blood and is an indication of hypoventilation. Ventilation is driven by the respiratory pump. The respiratory pump is comprised of the respiratory muscles, spinal cord, neuromuscular junction and peripheral nerves. Any disorders of this pump will result in hypercapnic failure. Respiratory fatigue will also cause hypercapnia simply because the muscles tire out from excessive work. The energy that is exerted does not equal the energy that is taken in, which causes decreased energy supply to the muscles. This is seen with decreased lung compliance. Examples of decreased lung compliance include pulmonary edema, bronchoconstrictive pneumonia and ARDS. In the aforementioned examples, the lungs are not able to expand to their full capacity, reducing the amount of inspired air and retention of CO2. Treatment of respiratory failure Any patient with respiratory distress, dysfunction or failure should be treated with supplemental oxygen. It is important to first assess the ventilation status to determine the appropriate oxygen delivery method. This assessment may be done by obtaining pulse oximetry (SPO2) and, if it can be done safely, arterial blood gases (ABG). todaysveterinarypractice.navc.com A normal SPO2 should be 95% or higher. An SPO2 that is read at approximately 90% is equivalent to a PO2 of 60-70mmHg, which indicates the need to begin oxygen therapy. To define respiratory failure using ABG sampling the PO2 must be <60-80mmHg and the PCO2 must be >50mmHg. There are many ways to deliver oxygen. It is extremely important to ensure that all methods of oxygen delivery are humidified to prevent drying of the mucous membranes, respiratory epithelial damage and decreased mucociliary clearance which put the patient at risk for infection. Beginning with the least, or noninvasive method to the most invasive method of delivery, oxygen can be delivered as follows: 1. Flow-by oxygen = this is done by placing oxygen tubing near or around the nose and mouth. It is not appropriate for patients with significant respiratory dysfunction. A flow rate of 2-3L/min should be used. 2. Face mask = an appropriate size mask must be selected to provide a “seal”. A flow rate of 2- 10L/min should be used. The down side to this method is rebreathing expired CO2, since the fit of the mask doesn’t allow the CO2 to escape completely. 3. Oxygen hood or portable oxygen device (POD) = this is done by using supplies such as a large e-collar and plastic wrap. Roughly 75% of the e-collar is covered and the other 25% is left open to allow the CO2 to escape. A flow rate of 0.5-1L/min is used. The downside to this method is the patient may become hot, being closed inside the device. 4. Oxygen cage = the benefits to using an oxygen cage are temperature, O2 percentage and humidity control. The largest disadvantage most professionals have is the separation between themselves and the patient, resulting in a feeling of helplessness. 5. Nasal cannula = If oxygen is needed for more than 24 hours, or the patient is too large for an oxygen cage, cannulas should be placed. This is achieved by using a red rubber catheter measured to the TMJ joint, fed into the nares and secured using a finger trap method. A flow rate of 50-150ml/kg/min is used. Complications of this method include epistaxis and nasopharyngeal irritation. 6. Endotracheal intubation = this should be done in cases where other methods of delivery fail to provide sufficient O2. The patient must be sedated, unless they are obtunded or unconscious. The down sides to this method of delivery include tracheal irritation, oxygen toxicity and prolonged sedation. While respiratory failure is a serious, sometimes dire situation, there are times where a “hands off” approach is necessary. If a patient is in physiologic distress it can be extremely anxious which can contribute to the respiratory dysfunction. In these cases, the patients can be put in the oxygen cage to help them relax prior to starting any treatment. Medication such as butorphanol may be used to aid in the anxiety and is noted to be “respiratory friendly”. Even if you do not have a confirmed diagnosis, this is almost always an appropriate treatment. Now you can breathe easy when you have a respiratory patient because you know how to safely provide supplemental oxygen. References available on request. .