Application of Airway Pressure Therapy in Veterinary Critical Care: Part I: Respiratory Mechanics and Hypoxemia

Over the past several decades, recognition of acute respiratory failure as the cause of death in patients suffering from various clinical conditions has prompted aggressiv investigation into the area of respiratory physiology and supportive respiratory care. With the evolution of emergency medicine and critical care services in both human and veterinary medicine, many patients previously considered unsalvageable due to the severity of their underlying disease are now being resuscitated and successfully supported, creating a new population of critically ill patients. Where only a decade ago these patients would have succumbed to their underlying disease, they now survive long enough to manifest the complications of shock and tissue injury in the form of acute respiratory failure. Investigation into the pathophysiology and treatment of this acute respiratory distress syndrom (ARDS) has facilitated increased clinical application of respiratory theerapy and machanical ventilation.¹ The purpose of this paper is to provide a basic review of respiratory mechanics and the pathophysiology of hypoxemia as they relate to airway pressure therapy in veterinary patients and to review the use of airway pressure therapy in veterinary patients This paper is divided into two parts; part I reviews respiratory mechanics and hypoxemia as they apply to respiratory therapy, while part II deals specifically with airway pressure therapy andits use in clinical cases.     

Retrospective evaluation of sildenafil citrate as a therapy for pulmonary hypertension in dogs

Pulmonary arterial hypertension (PH) is a pathologic condition in dogs characterized by abnormally high pressures in the pulmonary circulation and has been associated with a poor outcome. Sildenafil is a type V phosphodiesterase inhibitor that produces nitric oxide mediated vasodilatation. Sildenafil treatment decreases pulmonary arterial pressure and pulmonary vascular resistance in people with PH. The purpose of this study was to describe the clinical characteristics and outcome of dogs with PH treated with sildenafil. The cardiology database was searched for dogs with PH treated with sildenafil. PH was defined as systolic pulmonary arterial pressure (PAPs) > or = 25 mmHg at rest. Medical records were reviewed for the following information: signalment, duration and type of clinical signs before treatment, underlying disease, estimated or measured PAPs, dosage and dosing interval of sildenafil, and the effect of treatment on clinical signs and pulmonary arterial pressure and survival time. Thirteen affected dogs were identified. Clinical signs included collapse, syncope, respiratory distress, and cough. Duration of clinical signs before presentation ranged from 3 days to 5 months. An underlying cause was identified in 8 dogs. The median sildenafil dosage was 1.9 mg/kg. Ten dogs received concurrent medications. Median PAPs was 90 mmHg; 8 dogs were reevaluated after therapy, and the median decrease in PAPs was 16.5 mmHg. The median survival time of all dogs was 91 days. Sildenafil appeared to be well tolerated in dogs with PH and was associated with decreased PAPs and amelioration of clinical signs in most. Sildenafil represents a reasonable treatment option for dogs with pulmonary hypertension.     

Pulmonary Thromboembolism in 29 Dogs: 1985–1995

Pulmonary thromboembolism (PTE) occurs as a complication to a number of commonly encountered clinical diseases. Antemortem recognition of this life-threatening disorder is hampered by nonspecificity of clinical signs. This retrospective study was performed to analyze clinical features, laboratory findings, imaging abnormalities, and concurrent postmortem diagnoses in 29 dogs with confirmed pulmonary embolism. A variety of clinicopathologic and radiographic abnormalities were noted but there were no pathognomonic findings for PTE. Arterial blood gas analyses were performed in 15 (52%) of 29 dogs; 12 (80%) of 15 exhibited hypoxemia and 15 (100%) of 15 had increased alveolar-arterial oxygen gradients. Response to supplemental O2 was variable and did not correlate with the presence or absence of additional pulmonary pathology on postmortem. At postmortem, 25 (86%) of 29 dogs had grossly visible emboli, 17 (59%) of 29 dogs had multiple disease processes, and 16 (55%) of 29 dogs had additional pulmonary pathology. PTE was suspected antemortem in 11 (38%) of 29 dogs. In dogs with respiratory signs consistent with PTE, the condition was a differential diagnosis in 11 of 17 animals; all had diseases previously reported to be associated with PTE. Neoplasia, systemic bacterial disease, and immune-mediated hemolytic anemia were diagnosed most frequently.     

A comparison of the effects of hydromorphone HCl and a novel extended release hydromorphone on arterial blood gas values in conscious healthy dogs

The purpose of this study was to evaluate arterial blood gases in dogs that were given hydromorphone or extended release liposome-encapsulated hydromorphone (LEH). Dogs were randomly administered LEH, n = 6, (2.0 mg kg⁻¹), hydromorphone, n = 6, (0.2 mg kg⁻¹) or a placebo of blank liposomes, n = 3, subcutaneously on separate occasions. Arterial blood samples were drawn at serial time points over a 6-h time period for blood gas analysis. There was no change from baseline values in P_aCO₂, P_aO₂, (HCO₃-), pH, and SBEc in the dogs that received the placebo. Administration of hydromorphone resulted in significant increases in P_aCO₂ (maximum (mean + SD] 44.4 + 1.1 mm of Hg) and significant decreases in P_aO₂ (minimum (mean + SD) 82.4 + 4.7 mm of Hg) and pH (minimum (mean + SD) 7.31 + 0.01) compared with baseline. Administration of LEH resulted in significant increases in P_aCO₂ (maximum (mean + SD) 44.6 + 0.9 mm of Hg) and significant decreases in P_aO₂ (minimum (mean + SD) 84.8 + 2.6 mm of Hg) and pH (minimum (mean + SD) 7.34 + 0.02) compared with baseline. There was no significant difference between these two groups at any time point. The changes observed in P_aCO₂, P_aO₂, and pH, however, were within clinically acceptable limits for healthy dogs. LEH was determined to cause moderate changes in arterial blood gas values similar to those caused by hydromorphone.     

Therapeutic strategies for COVID-19 based on its pathophysiological mechanisms

An outbreak of coronavirus disease 2019 (COVID-19) began in Wuhan, China in early December 2019, which dominated by pneumonia. As of March 11, 2020, the overall confirmed cases in China had reached 80 955. Part of them became seriously ill, such as acute respiratory distress syndrome, and was associated with ICU admission and high mortality. Therefore, how to prevent the patients from becoming serious is a key point in the treatment and control of COVID-19. This review provides an overview of pathophysiology of cytokine storm which was associated with COVID-19 severity, and proposes that anti-inflammation, antioxidation and oxygen-therapy at the early stage of disease are better therapeutic option to save COVID-19 patients.     

Potential pathophysiological mechanisms underlying COVID-19-induced myocardial injury

The outbreak of coronavirus disease 2019 (COVID-19) has rapidly spread to 99 countries and regions including China (update on March 9, 2020). Although patients with COVID-19 mainly manifest as pneumonia, some of them have clinical manifestations of myocardial injury. Recent histopathological results showed myocardial injury which is characterized by cardiomyocyte degeneration/necrosis, infiltration of monocytes, lymphocytes and/or neutrophils into the myocardial interstitium, endothelial cell detachment, intimal inflammation and microthrombus formation. These results indicate that the myocardium might be an important attack target of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes COVID-19. Therefore, investigation of the pathophysiological process of COVID-19-induced myocardial injury is of great significance to reduce the mortality and increase the cure rate of the patients. In this review, we focus on the current understanding of COVID-19-induced myocardial injury involving vasculitis and hypoxemia as well as their underlying potential mechanisms.