Stabilization of the Patient with Respiratory Distress

Chapter 8

Stabilization of the Patient with Respiratory Distress

Respiratory distress in small animals presents a therapeutic dilemma. By the time owners identify a problem, their animal may be so severely compromised that diagnostic testing and treatment could stress the pet to the point of respiratory and cardiac arrest. Thus diagnostic testing may be delayed or restricted to avoid placing the patient at further risk. In these circumstances, the clinician must quickly develop a rational list of differential diagnoses and treatments, while providing basic supportive care. Initial steps toward stabilization of the respiratory system, such as oxygen supplementation, thoracocentesis, and possibly airway control via endotracheal intubation or temporary tracheotomy, may be necessary before proceeding with diagnostics. This chapter reviews the pathophysiologic mechanisms behind respiratory distress and provides guidance on anatomic localization of the disease, recommendations for initial stabilization, and appropriate sequencing of diagnostic tests.

Pathophysiology of Respiratory Distress

Work of breathing, or the effort required for effective pulmonary gas exchange, depends mainly on two forces within the respiratory system: (1) airway resistance, which opposes airflow during inspiration and expiration and (2) elastic recoil, which is the tendency for the lungs to collapse following inspiration. In animals with respiratory tract pathology, additional energy and effort may be required to overcome these forces. The clinician who is faced with managing respiratory distress requires greater understanding of airway resistance and elastic recoil, as well as their contributions to overall work of breathing.

Airway resistance is the pressure difference between the alveoli and the mouth divided by flow rate. Airway caliber is critical in determining resistance. If the radius of the airway is halved, resistance increases sixteenfold; in comparison, doubling airway length only increases resistance by a factor of two. Therefore small changes in airway caliber can lead to noticeable clinical signs. The major site of airway resistance in healthy animals is the medium-sized bronchi. Airway resistance is determined by lung volume, bronchial smooth muscle tone, and dynamic airway compression. At reduced lung volumes, radial traction supporting the bronchi is lost and airway caliber is reduced. Similarly, bronchial muscle contraction narrows airways and increases resistance. Bronchoconstriction is mediated by reflex stimulation of irritant receptors in the upper airways or increased parasympathetic activity. Dynamic airway collapse is seen with forceful respiration. Sudden changes in intrathoracic pressure can affect the diameter of large airways. Intrathoracic and extrathoracic airway collapse, airway foreign bodies, and mass lesions also result in increased airway resistance.

The resting lung volume is a balance between the elastic properties of the lung (favoring alveolar collapse) and the elastic properties of the chest wall (favoring alveolar expansion). This resting lung volume, understood as the volume of air remaining in the lungs at the end of a normal breath, is called the functional residual capacity (FRC). At the normal FRC, the lung is very compliant. Compliance or stiffness is the change in lung volume for any given applied pressure. In a healthy state with compliant lungs, small changes in intrapleural pressure cause a large change in lung volume, subsequently drawing fresh air into the respiratory tract. A pressure-volume curve of the lung shows the change in the work of breathing at normal and reduced lung volumes (Figure 8-1). Most common pulmonary parenchymal diseases (e.g., pulmonary edema, pneumonia) increase FRC, flatten the pressure-volume curve, and decrease compliance. Significant pleural space disease resulting in lung collapse (e.g., pneumothorax, diaphragmatic hernia) produces similar changes in lung compliance and FRC.

Respiratory Failure

Impaired respiration occurs secondary to inadequate ventilation or inadequate gas exchange. If sufficiently severe, this impairment can progress to respiratory failure, a life-threatening situation that often necessitates aggressive intervention. Failure of ventilation is the inability to move fresh air into the pulmonary alveoli, resulting in high blood carbon dioxide levels (hypercarbia) and low blood oxygen levels (hypoxemia). Failure of gas exchange occurs at the level of the blood-air barrier, resulting in hypoxemia with or without hypercarbia. In cases of impaired gas exchange, the hypoxemic patient initially hyperventilates in an effort to improve oxygenation. This results in low blood carbon dioxide levels and a respiratory alkalosis. With progression of disease and onset of respiratory failure, effective exchange of both oxygen and carbon dioxide is lost, resulting in hypoxemia and hypercarbia. Appropriate differentiation of the type of respiratory failure is critical when moving forward with proper medical intervention. Close observation of respiratory pattern and physical examination findings are especially helpful in determining the likely cause and appropriate therapeutic interventions (Table 8-1).


Common Causes of Respiratory Distress in Dogs and Cats

Problem Phase Affected/Respiratory Pattern Emergency Treatment
Upper Airway Obstruction    
Laryngeal paralysis Inspiratory/Obstructive O2, sedation, antiinflammatory, +/− tracheostomy
Extrathoracic tracheal collapse Inspiratory/Obstructive O2, sedation, antitussive
Airway mass lesion Fixed/Obstructive O2, sedation, +/− tracheostomy
Airway foreign body Fixed/Obstructive O2, sedation, Heimlich maneuver
Laryngeal stenosis Fixed/Obstructive O2, sedation, +/− tracheostomy
Lower Airway Obstruction    
Intrathoracic tracheal collapse Expiratory/Obstructive O2, sedation, antitussive
Bronchitis Expiratory/Obstructive O2, sedation, antiinflammatory, bronchodilator
Airway mass lesion Fixed/Obstructive O2, sedation
Airway foreign body Fixed/Obstructive O2, sedation, Heimlich maneuver
Pulmonary Parenchymal Disease    
Pneumonia Inspiratory/Restrictive O2, IV fluids, antibiotic, physical therapy
Cardiogenic pulmonary edema Inspiratory/Restrictive O2, sedation, fluid restriction/diuretics
Noncardiogenic pulmonary edema Inspiratory/Restrictive O2, sedation
Pulmonary hemorrhage Inspiratory/Restrictive O2, sedation, FFP
Pulmonary neoplasia Inspiratory/Restrictive O2, sedation
Pleural Space Disease    
Chylothorax Inspiratory/Restrictive/Inverse O2, thoracocentesis
Pneumothorax Inspiratory/Restrictive/Inverse O2, thoracocentesis
Pyothorax Inspiratory/Restrictive/Inverse O2, thoracocentesis
Pleural hemorrhage Inspiratory/Restrictive/Inverse O2, FFP, thoracocentesis
Diaphragmatic hernia Inspiratory/Restrictive/Inverse O2, sedation, surgical correction
Pulmonary Thromboembolism Hyperventilation O2, sedation, thrombolytic, anticoagulation

Phase affected describes either inspiratory or expiratory dyspnea, with increased effort and time devoted to that phase of respiration. Fixed obstructive pattern will have increased effort during both phases of respiration. Obstructive pattern is generally deeper with a loud stridor. Restrictive pattern breathing is rapid and shallow.

O2, Oxygen supplemented by face mask, blow-by, nasal cannula, oxygen cage, oxygen tent, or positive pressure ventilation. FFP, fresh frozen plasma. Physical therapy consists of nebulization and coupage to loosen airway secretions.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Stabilization of the Patient with Respiratory Distress
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