Respiratory Support for Neurologic Diseases
David B. Seder
Stephan A. Mayer
INTRODUCTION
Much of the high morbidity and mortality from acute neurologic disorders results from abnormalities of breathing. Respiratory abnormalities can themselves worsen neurologic injury, whereas neurologic abnormalities conversely predispose to aspiration, impaired airway clearance, atelectasis, and pneumonia. In stroke, traumatic brain injury, status epilepticus, Guillain-Barré syndrome, myasthenia gravis, and many other neurologic disorders, oropharyngeal and respiratory muscle weakness predispose to aspiration of secretions into the airways, mucus plugging, hypoventilation, atelectasis, and pneumonia. Accordingly, respiratory monitoring and support are among the most common indications for the admission of neurologic patients to an intensive care unit (ICU).
RESPIRATORY PHYSIOLOGY AND PATHOPHYSIOLOGY
PULMONARY GAS EXCHANGE
Hypoxemia is characterized by reduced oxygen content of the bloodstream. Hypoxemia is caused by five conditions: (1) a low inspired oxygen concentration, (2) alveolar hypoventilation, or impaired gas exchange within the lungs due to (3) ventilationperfusion (V/Q) mismatching, (4) transpulmonary or intracardiac right-to-left shunting, or (5) impaired diffusion of gases between the alveoli and the capillaries. It can also be caused by low mixed venous oxygen saturation.
Impaired gas exchange can be quantified by measuring the gradient between the partial pressure of oxygen in the alveoli and the arterial blood (the A/a gradient, which is normally <20 mm Hg) or the P/F ratio, which is the partial pressure of oxygen in the arterial blood (PaO2, normally 90 to 100 mm Hg) divided by the fraction of inspired oxygen (FiO2, normally 21% in room air). Alveolar oxygen tension (PaO2) can be calculated from the equation PaO2 = (FiO2 × 713) – (PaCO2/0.8), where PaCO2 is the arterial carbon dioxide tension.
The cause of impaired gas exchange leading to hypoxemia can be differentiated according to the response to supplemental oxygen. Shunting, defined as hypoxia unresponsive to oxygen supplementation, results from the direct transfer of deoxygenated venous blood into the arterial circulation through an intracardiac atrial septal defect, pulmonary arteriovenous malformation, or perfused but nonventilated lung parenchyma (i.e., dense airspace consolidation due to pneumonia). With V/Q mismatching, ventilation and perfusion relationships are heterogeneously deranged, but systemic oxygenation improves in response to a higher FiO2. Diffusion abnormalities are characterized by abnormalities of the intra-alveolar septae, which may be fibrotic (i.e., interstitial lung disease), reduced in number and surface area (i.e., emphysema), and inflamed or edematous (i.e., acute respiratory distress syndrome, congestive heart failure). Low inhaled FiO2 is typical of extreme altitude but can also result from equipment malfunction such as rebreathing of exhaled gases.
Hypercarbia results from impaired alveolar ventilation and is caused by some combination of inadequate “bellows function” of the lung (characterized by reduced minute ventilation, the product of the respiratory rate and tidal volume), increased carbon dioxide production, and impaired gas exchange. Hypoventilation can only be mechanism of hypoxia when concomitant hypercarbia is present.
RESPIRATORY FAILURE
The diagnosis of respiratory failure depends on arterial blood gas analysis and on the chronicity of the event. Three separate processes can contribute to the development of respiratory failure: (1) hypoxia, which results from impaired gas exchange in the lung; (2) ventilatory failure, which results from inadequate ability to move air into and out of the lungs; and (3) failure to protect the upper airway, which can result in airflow obstruction or aspiration of secretions, food, or gastric contents.
Chronic respiratory failure is said to be present when a patient cannot maintain adequate oxygenation (PaO2 >59 mm Hg) or ventilation PCO2 <50 mm Hg) without supplemental oxygen or ventilatory assistance. In contrast, acute hypoxemic respiratory failure describes a state in which adequate oxygenation cannot be maintained despite supplemental oxygen delivery. In these patients, positive pressure ventilation and supplemental oxygen administered through an endotracheal tube or by noninvasive positive pressure ventilation are required to maintain normal oxygenation of arterial blood. In the hospital, hypoxemia can be easily and noninvasively diagnosed and monitored by measuring the percent oxygen saturation of hemoglobin in the blood (SpO2). The clinical hallmark of hypoxemic respiratory failure is cyanosis.
Hypercarbic respiratory failure may be clinically obvious, as seen when the accessory muscles of respiration are activated and the patient appears “working hard to breathe” or can be subtle, manifest only by decreased mental acuity, myoclonus, confusion, agitation, or lethargy. Acute hypercapnia leads to acidosis and cerebral vasodilatation, which in turn can cause depressed level of consciousness (“CO2 narcosis”), aggravation of elevated intracranial pressure (ICP), and blunted respiratory drive, leading to further hypoventilation. Arterial blood gas analysis is the most reliable method for diagnosing hypercarbic respiratory failure, but end-tidal carbon dioxide monitoring has gained popularity as a noninvasive method to monitor changes in alveolar carbon dioxide tension.
Failure of airway protection is diagnosed clinically when patients appear to be aspirating oral secretions, cannot maintain the upper airway open for gas exchange, have a rapid neurologic decline with a diminished gag and cough reflexes, or are experiencing repeated oxyhemoglobin desaturation due to intermittent plugging of the airways by secretions. Under unstable conditions, such as during a period of acute neurologic instability or during patient transport between hospitals or departments, it is advisable to intubate these patients and start mechanical ventilation to prevent sudden respiratory decompensation. Conversely, it may be safe to extubate
such patients later in their hospital course under controlled circumstances, despite significantly decreased mental status. There is no absolute measure of adequate upper airway protection, and unfortunately, such determinations remain for most part subjective.
such patients later in their hospital course under controlled circumstances, despite significantly decreased mental status. There is no absolute measure of adequate upper airway protection, and unfortunately, such determinations remain for most part subjective.
TABLE 116.1 Pullmonary Function Tests in Neuromuscular Respiratory Failure | ||||||||||||||||||||
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The pathophysiology of neuromuscular respiratory failure resembles a vicious cycle. Increased mucus production and/or weak cough leads to mucus plugging and atelectasis, which in turn cause decreased efficiency of ventilation. Hypoxemia usually precedes hypercapnia because atelectasis and V/Q mismatching are an early development. As fever and infection develop, carbon dioxide production increases, and ventilatory needs rise. The downward spiral of increasing carbon dioxide production, decreasing efficiency of ventilation, and progressive mucus plugging and atelectasis ultimately results in hypercarbia and respiratory failure. As ventilation fails, rapid shallow breathing and hypercapnia develop. At this stage, ventilatory reserves are exhausted, and there is the danger of sudden life-threatening hypoxemia, respiratory acidosis, or respiratory arrest.
EFFECTS OF RESPIRATORY COMPROMISE ON NEUROLOGIC INJURY
Many types of neurologic injury are exacerbated by respiratory compromise. Carbon dioxide and pH are powerful determinants of cerebral vascular tone, and the intended or unintended effects of hyperventilation (decreased cerebral blood flow, decreased intracranial blood volume, and decreased ICP) should be anticipated and monitored by clinicians. Conversely, hypoventilation and hypercapnia cause cerebral vasodilation and increased ICP. Hyperoxia is a potent exacerbant of reperfusion injury, whereas hypoxia is strongly associated with worse outcome in stroke, hypoxic-ischemic encephalopathy, and traumatic brain injury. Finally, when work of breathing is markedly increased, up to 50% of the cardiac output may be diverted to the respiratory muscles, driving metabolic stress, and potentially “stealing” blood flow from the ischemic brain or spinal cord. This metabolic stressor can be effectively managed by sedation, intubation, and initiation of full mechanical ventilatory support.
PULMONARY FUNCTION TESTING
Pulmonary function testing should be routinely used to monitor respiratory function in patients with neuromuscular respiratory compromise (Table 116.1). Arterial blood gases and end-tidal carbon dioxide monitoring are helpful, but abnormalities of gas exchange usually develop later in the cycle of respiratory decompensation and are therefore insensitive for early detection of ventilatory decline. Forced vital capacity (FVC), the volume of air exhaled after maximal inspiration and exhalation, normally ranges from 40 to 70 mL/kg. Reduction in vital capacity to 30 mL/kg is associated with a weak cough, accumulation of oropharyngeal secretions, atelectasis, and nocturnal hypoxemia. FVC below 15 mL/kg (1 L in a 70-kg person) is the level at which invasive or noninvasive ventilatory support should be considered (Table 116.2). Maximal inspiratory pressure (MIP), normally more than 80 cm H2O, measures the strength of the diaphragm and other muscles of inspiration and generally reflects the ability to maintain normal lung expansion and avoid atelectasis, whereas maximal expiratory pressure (MEP), normally more than 140 cm H2O, measures the strength of the muscles of expiration and correlates with cough and the ability to clear secretions from the airway.
MANAGEMENT OF RESPIRATORY FAILURE
EXAMINATION
The initial management of the patient with impending respiratory failure is directed toward assessing the adequacy of oxygenation and ventilation, workload and stability of breathing, and assessment of the airway. In patients with fulminant respiratory failure, intubation can be lifesaving and is preferentially performed under safe, controlled circumstances well before the threat of impending cardiopulmonary arrest.
The patient’s overall comfort and anxiety levels and the rate of progression of respiratory compromise should be assessed. Hypoxia is usually easy to diagnose with pulse oximetry and arterial blood gas analysis. Hypoventilation and hypercarbia may be present without distress or increased work of breathing if central respiratory drive is compromised, whereas increased respiratory
effort with intact respiratory drive manifests as respiratory alkalosis. Sidestream end-tidal carbon dioxide monitoring, less well established than oximetry but effective, is increasingly used to provide early warning of hypoventilation in patients at risk. Rapid, shallow breathing, the use of accessory muscles of the neck and the shoulder, and visible gulping or gasping with inability to generate adequate tidal volumes are signs of respiratory muscle fatigue and impending collapse, although such signs may be absent when central respiratory drive is impaired. Diaphragmatic strength can be estimated by palpating for normal outward movement of the abdomen with inspiration; with severe diaphragmatic paralysis, inspiration is associated with spontaneous inward movement of the diaphragm (abdominal paradox). Activation of respiratory muscles during the expiratory phase often indicates airflow obstruction.
effort with intact respiratory drive manifests as respiratory alkalosis. Sidestream end-tidal carbon dioxide monitoring, less well established than oximetry but effective, is increasingly used to provide early warning of hypoventilation in patients at risk. Rapid, shallow breathing, the use of accessory muscles of the neck and the shoulder, and visible gulping or gasping with inability to generate adequate tidal volumes are signs of respiratory muscle fatigue and impending collapse, although such signs may be absent when central respiratory drive is impaired. Diaphragmatic strength can be estimated by palpating for normal outward movement of the abdomen with inspiration; with severe diaphragmatic paralysis, inspiration is associated with spontaneous inward movement of the diaphragm (abdominal paradox). Activation of respiratory muscles during the expiratory phase often indicates airflow obstruction.
TABLE 116.2 Criteria for Intubation and Mechanical Ventilation | |||||||
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When neuromuscular weakness is present, ventilatory reserves can be assessed by checking the patient’s ability to count from 1 to 20 in a single breath. The strength of the patient’s cough should be noted. A wet gurgled voice and pooled oropharyngeal secretions are clinical signs of dysphagia and ongoing aspiration. When severe, weakness of the glottic and oropharyngeal muscles can lead to stridor, which indicates possibly life-threatening obstruction of the upper airway.
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