Respiratory disasters and how we managed them-Part 1 (Proceedings)

Recognizing and managing hypoventilation

Ventilation is the ability of the chest wall and diaphragm to move an adequate volume of air into the chest. The term "minute ventilation" refers to the volume of air moved into and out of the lung during a 60 second period. The volume of air is a product of the tidal volume (volume of a single breath), and the respiratory rate. For normal ventilation to occur, the animal must have a normal brain-stem respiratory control center, normal spinal cord function to the level of C3/C4, normal spinal and phrenic nerve function and neuromuscular transmission, normal muscle and chest wall integrity, absence of pleural disease, and a patent airway. If there is an abnormality of any of these functions, inadequate volumes of air may enter the body, resulting in hypoventilation. Thus, hypoventilation occurs if there is: neuromuscular disease affecting the chest wall and/or diaphragm, respiratory depressant drugs (eg anesthetics) which can suppress the central nervous system, or lesions such as flail chest or pleural effusion which affect the ability of the animal to move adequate quantities of air. Sometimes, severe pulmonary disease such as pneumonia can also lead to hypoventilation, but this is unusual.

Examples of the most common causes of hypercarbia include:

• neurologic disease or anesthesia affecting central medullary respiratory drive

• spinal cord dysfunction cranial to C4-C5

• phrenic nerve dysfunction

• chest wall injury

• respiratory muscle dysfunction

• airway obstruction

• pleural diseases: effusion, severe pneumothorax, diaphragmatic hernia

Because CO2 diffuses through tissues very easily (about 20x more soluble than O2), we use the amount of CO2 in arterial blood (PaCO2) as a measure of the extent of ventilation. Normally, if ventilation is adequate, then CO2 is "blown off" easily, and normal dogs have a PaCO2 of 35-45 mm Hg. If hypoventilation occurs, CO2 increases, leading to respiratory acidosis by formation of carbonic acid:

CO2 + H2O = H2CO3 = H+ + HCO3 -

As well as causing an increase in CO2, hypoventilation also leads to hypoxia, since there is less oxygen in the alveoli for gas exchange. Increased PaCO2 in hypoventilation is therefore accompanied by decreased PaO2. In a hypoventilating patient, oxygen supplementation will increase the PaO2, but will result in no change in PaCO2 values because it does not change the total volume of air moved into and out of the lungs per minute.

If PaCO2 is high, the animal experiences dyspnea. Profound respiratory acidosis may result from the hypercarbia, which can be life-threatening by causing decreased cardiac output, hypotension and neurologic depression due to carbon dioxide narcosis. Thus, if hypoventilation is found in clinical patients, the clinician must consider measures to improve ventilatory status by addressing the cause of hypoventilation. Hypoventilation can often be managed by treatment of the underlying problem eg thoracocentesis for a pleural effusion, reversing anesthetic drugs, or surgery for an airway obstruction. If conservative methods are not adequate for the management of the hypoventilating patient, then positive pressure ventilation is the only effective option.

The decision to initiate PPV is made based on the clinical condition of the animal and the degree of dyspnea, the arterial blood gas results and response to oxygen supplementation while spontaneously breathing, the prognosis, and the wishes of the owner. Animals with elevated PaCO2 (> 50 mmHg), those with PaO2 values less than 55mmHg on oxygen supplementation, or those with obvious ongoing respiratory distress or paradoxical respiration despite oxygen supplementation, are candidates for PPV. In general, we believe that better outcomes may be achieved if PPV is initiated early, rather than waiting until the animal is moribund before providing aggressive respiratory support. This decision is clearly a "judgement call", because PPV is invasive, labor intensive and expensive. Furthermore, PPV is not necessarily a benign procedure, as inappropriately delivered PPV can result in worsening of lung disease and hasten the death of the patient.

Pulmonary thromboembolism

Recognition and awareness of pulmonary thromboembolism has increased dramatically in the last few years. Thrombi may develop as a result of a combination of 2 or more of the following processes: 1) hypercoagulability, 2) vascular endothelial damage, 3) abnormal blood flow patterns or blood stasis.

Vascular endothelial damage is an integral part of sepsis as a sequela of SIRS. Diffuse vascular damage occurs frequently as a consequence of a variety of inflammatory disorders such as sepsis, pancreatitis, or immune-mediated diseases such as autoimmune hemolytic anemia. In each of these situations, various inflammatory mediators are activated, all of which can lead to endothelial damage. Once endothelial damage has occurred, activation of the coagulation cascade follows, contributing to the development of thrombi. Endothelial damage also occurs locally due to intravenous catheters, and infusion of irritating substances. Stasis of blood is a feature of many critical illnesses. Any condition that leads to poor perfusion or shock may predispose to pooling of blood in the periphery or in the splanchnic vasculature. This is particularly true of sepsis states. Other disorders that may be accompanied by blood stasis include vascular obstructive diseases and heart failure.

The diagnosis of pulmonary thromboembolism can be extremely challenging. Many animals with minor pulmonary showering by emboli may be completely asymptomatic, while those with major thromboembolic disease can develop profound respiratory distress and die acutely. Auscultation findings are very variable, ranging from normal, to harsh or even crackles.

Most clinically affected animals have significant hypoxia, which can be determined by clinical parameters, or by arterial blood gas analysis or pulse oximetry. Thoracic radiographs are variable, and often reveal normal to hyperlucent lung fields. Alternatively some animals with thromboembolism may have areas of alveolar disease or pleural effusion. Acute pulmonary thromboembolism is often accompanied by a sudden change in platelet count, which presumably is caused by platelet consumption. Definitive diagnosis of pulmonary thromboembolism is made by selective angiography. The finding of abnormal perfusion on scintigraphic ventilation/perfusion scanning is also strongly suggestive of thromboembolic disease.

If pulmonary thromboembolism is suspected, several potential therapies may be attempted. Aggressive supportive care, attention to tissue perfusion, oxygen supplementation, and treatment of the underlying disease remain priorities for management. If the size of the embolus is not excessive, the animal's own fibrinolytic system should be able to eventually break it down, and recanalize obstructed vessels. The time required for resolution in critically ill animals may vary from just a few days, to 2-3 weeks. "Clotbuster" drugs, such as tissue plasminogen activator, streptokinase, or urokinase, actively break down clots within the circulation.

If thromboembolic disease is suspected, prophylactic therapy with heparin seems to be helpful to prevent formation of more thrombi, but it has no effect to break down thrombi that are already present. We commonly use unfractionated heparin doses of 100-300 iu/kg SQ q 6 hours, or CRI 10-50 iu/kg/hr. Unfractionated heparin therapy must be monitored by daily measurement of PTT. We aim to cause prolongation of the PTT by 50% from the baseline. Heparin therapy must be gradually weaned, as rebound hypercoagulability may occur if it is suddenly withdrawn.

References Available on Request