Respiratory Distress and Failure

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Chapter 65 Respiratory Distress and Failure

The term respiratory distress is often used to indicate signs and symptoms of abnormal respiratory pattern. A child with nasal flaring, tachypnea, chest wall retractions, stridor, grunting, dyspnea, and wheezing is often judged as having respiratory distress. The magnitude of these findings is used to judge the clinical severity of respiratory distress. Although nasal flaring is a nonspecific sign, the other signs may be useful in localizing the site of pathology (Chapter 365). Respiratory failure is defined as inability of the lungs to provide sufficient oxygen (hypoxic respiratory failure) or remove carbon dioxide (ventilatory failure) to meet metabolic demands. Whereas respiratory distress is a clinical impression, the diagnosis of respiratory failure indicates inadequacy of oxygenation or ventilation or both. Respiratory distress can occur in patients without respiratory disease, and respiratory failure can occur in patients without respiratory distress.

Respiratory Distress

Nasal flaring is an extremely important sign of distress, especially in infants. It is indicative of discomfort, pain, fatigue, or breathing difficulty. The state of responsiveness is another crucial sign. Lethargy, disinterest in surroundings, and poor cry are suggestive of exhaustion, hypercarbia, and impending respiratory failure. Abnormalities of the rate and depth of respirations can occur with both pulmonary and nonpulmonary causes of respiratory distress. In diseases of decreased lung compliance, such as pneumonia and pulmonary edema, respirations are characteristically rapid and shallow (decreased tidal volume). In obstructive airway diseases, such as asthma and laryngotracheitis, respirations are deep (increased tidal volume) but less rapid. Rapid and deep respirations without other respiratory signs should alert the physician to the possibility of nonrespiratory causes of respiratory distress, such as response to metabolic acidosis (diabetic ketoacidosis, renal tubular acidosis) or stimulation of the respiratory center (encephalitis, ingestion of central nervous system [CNS] stimulants). Chest wall, suprasternal, and subcostal retractions are manifestations of increased inspiratory effort, weak chest wall, or both. Inspiratory stridor indicates airway obstruction above the thoracic inlet, whereas expiratory wheezing results from airway obstruction below the thoracic inlet. Grunting is most commonly heard in diseases with decreased functional residual capacity (e.g., pneumonia, pulmonary edema) and peripheral airway obstruction (e.g., bronchiolitis).

Respiratory Disease Manifesting as Respiratory Distress

Clinical examination is important in localizing the site of pathology (Chapter 365). Extrathoracic airway obstruction occurs anywhere above the thoracic inlet. Inspiratory stridor, suprasternal, chest wall, and subcostal retractions, and prolongation of inspiration are hallmarks of extrathoracic airway obstruction. By comparison, features of intrathoracic airway obstruction are prolongation of expiration and expiratory wheezing. Typical manifestations of alveolar interstitial pathology are rapid, shallow respirations, chest wall retractions, and grunting. The site of pathology can be localized and the differential diagnosis established on the basis of the clinical signs and symptoms (Tables 65-1 and 65-2).

Table 65-2 EXAMPLES OF ANATOMIC SITES OF LESIONS CAUSING RESPIRATORY FAILURE

LUNG RESPIRATORY PUMP
CENTRAL AIRWAY OBSTRUCTION THORACIC CAGE

PERIPHERAL AIRWAY OBSTRUCTION BRAINSTEM

Alveolar-Interstitial Disease Spinal Cord   NEUROMUSCULAR

ARDS, acute respiratory distress syndrome; CNS, central nervous system.

Respiratory Distress without Respiratory Disease

Although respiratory distress most commonly results from diseases of lungs, airways, and chest wall, pathology in other organ systems can manifest as “respiratory distress” and lead to misdiagnosis and inappropriate management (Table 65-3). Respiratory distress resulting from heart failure or diabetic ketoacidosis may be misdiagnosed as asthma and improperly treated with albuterol, resulting in worsened hemodynamic state or ketoacidosis.

Table 65-3 NONPULMONARY CAUSES OF RESPIRATORY DISTRESS

  EXAMPLE(S) MECHANISM(S)
Cardiovascular

Central nervous system Stimulation of brainstem respiratory centers Metabolic Stimulation of central and peripheral chemoreceptors Renal Renal tubular acidosis Stimulation of central and peripheral chemoreceptors   Hypertension Left ventricular dysfunction → increased pulmonary blood/water content Sepsis

Cardiovascular Disease Manifesting as Respiratory Distress

A child with cardiovascular pathology may present with respiratory distress caused by 2 mechanisms: (1) decreased lung compliance and (2) cardiogenic shock (Table 65-4). Diseases that result in an increased pulmonary arterial blood flow (e.g., left-to-right shunts) or increased pulmonary venous pressure (e.g., left ventricular dysfunction from hypertension or myocarditis, obstructed total anomalous pulmonary venous return) cause an increase in pulmonary capillary pressure and transudation of fluid into the pulmonary interstitium and alveoli. The increased pulmonary blood and water content leads to decreased lung compliance and results in rapid shallow respirations.

Interstitial edema often results in small airway obstruction, manifesting as expiratory wheezing. Patients with cardiac lesions that result in a low cardiac output state, such as obstructive lesions of left side of the heart and acquired or congenital cardiomyopathy, often present in a state of shock with decreased tissue perfusion and metabolic acidosis. Such children demonstrate respiratory distress because of stimulation of chemoreceptors by metabolic acidosis and stimulation of baroreceptors by decreased blood pressure.

Neurologic Disease Manifesting as Respiratory Distress

CNS dysfunction can lead to alterations in respiratory patterns. Increased intracranial pressure (ICP) may manifest as respiratory distress. Early rise in ICP results in stimulation of respiratory centers, leading to increases in the rate (tachypnea) and depth (hyperpnea) of respiration. The resultant decrease in PaCO2 and elevation of cerebrospinal fluid pH lead to cerebral vasoconstriction and amelioration of intracranial hypertension. Cerebral hemispheric and midbrain lesions often result in hyperpnea as well as tachypnea. In such situations, blood gas measurements typically show respiratory alkalosis without hypoxemia. Pathology affecting the pons and medulla manifests as irregular breathing patterns such as apneustic breathing (prolonged inspiration with brief expiratory periods), Cheyne-Stokes breathing (alternate periods of rapid and slow breathing), and irregular, ineffective breathing or apnea. Level of consciousness is most often impaired when abnormal breathing pattern from a brainstem disorder is present. Along with respiratory changes, other manifestations of CNS dysfunction and increased ICP may be present, such as focal neurologic signs, pupillary changes, hypertension, and bradycardia (Chapter 63). Occasionally, severe CNS dysfunction can result in neurogenic pulmonary edema (NPE) and respiratory distress, which may be due to excessive sympathetic discharge resulting in increased pulmonary venous hydrostatic pressure as well as increased pulmonary capillary permeability. Central neurogenic hyperventilation is characteristically observed in CNS involvement by illnesses such as Reye syndrome and encephalitis. Bradycardia and apnea may be due to CNS-depressant medications, poisoning, prolonged hypoxia, trauma, or infection (see Table 65-2).

Respiratory Failure

Respiratory failure occurs when oxygenation and ventilation are insufficient to meet the metabolic demands of the body. Respiratory failure may result from an abnormality in (1) lung and airways, (2) chest wall and muscles of respiration, or (3) central and peripheral chemoreceptors (Fig. 65-1). Clinical manifestations depend largely on the site of pathology. Although respiratory failure is traditionally defined as respiratory dysfunction resulting in PaO2 < 60 torr with breathing of room air and PaCO2 > 50 torr resulting in acidosis, the patient’s general state, respiratory effort, and potential for impending exhaustion are more important indicators than blood gas values.

Acute lung injury due to pneumonia, sepsis, aspiration, drowning, embolism, trauma, smoke inhalation, or drug overdose often leads to the acute respiratory distress syndrome (Table 65-5; Fig. 65-2).

image

Figure 65-2 Frontal portal chest radiograph showing diffuse bilateral infiltrates consistent with acute lung injury.

(From Wheeler AP, Bernard GR: Acute lung injury and the acute respiratory distress syndrome: a clinical review, Lancet 369:1553–1564, 2007.)

Pathophysiology of Respiratory Failure

Respiratory failure can be classified into 2 categories: (1) hypoxic respiratory failure (failure of oxygenation) and (2) hypercarbic respiratory failure (failure of ventilation). The two entities may coexist as a combined failure of oxygenation and ventilation. The main function of the respiratory system is to move atmospheric gases into the alveolar capillary units of the lung and to move alveolar gas back out into the atmosphere. Systemic venous (pulmonary arterial) blood is arterialized after mixing with the alveolar gas and being carried back to the heart by pulmonary veins. The arterial gas composition depends on the gas composition of the atmosphere and the effectiveness of alveolar ventilation, pulmonary capillary perfusion, and diffusion across the alveolar capillary membrane. Abnormality at any of these steps can result in respiratory failure.

Ventilation-Perfusion Mismatch, Venous Admixture, Intrapulmonary Shunt

For exchange of O2 and CO2 to occur, alveolar gas must be exposed to blood in pulmonary capillaries. Both ventilation and perfusion are lower in nondependent areas of the lung and higher in dependent areas of the lung. The difference in perfusion (image) is greater than the difference in ventilation (image). Perfusion in excess of ventilation results in incomplete “arterialization” of systemic venous (pulmonary arterial) blood and is referred to as venous admixture. Perfusion of unventilated areas is referred to as intrapulmonary shunting of systemic venous blood to systemic arterial circulation. Conversely, ventilation that is in excess of perfusion is “wasted”; that is, it does not contribute to gas exchange and is referred to as dead space ventilation. Dead space ventilation results in return of greater amounts of atmospheric gas (which has not participated in gas exchange and has negligible CO2) to the atmosphere during exhalation. The end result is a decrease in mixed expired PCO2 (PECO2) and an increase in the PaCO2-PECO2 gradient. The fraction of tidal volume that occupies dead space (VD/VT) is calculated as follows:

Normal VD/VT is around 0.33. VD/VT increases in states that result in decreased pulmonary perfusion, such as pulmonary hypertension, hypovolemia, and decreased cardiac output. Venous admixture and intrapulmonary shunting predominantly affect oxygenation, resulting in a PAO2-PaO2 (A-aO2) gradient without elevation in PaCO2. The reason is the greater ventilation of perfused areas, which is sufficient to normalize PaCO2 but not PaO2 because of their respective dissociation curves (Chapter 365). The relative straight-line relationship of hemoglobin-CO2 dissociation allows for averaging of PCO2 from hyperventilated and hypoventilated areas. Because the association between oxygen tension and hemoglobin saturation plateaus with increasing PaO2, the decreased hemoglobin-O2 saturation in poorly ventilated areas cannot be compensated for by well-ventilated areas where hemoglobin-O2 saturation has already reached near-maximum. This results in decreased SaO2 and PaO2. Elevation of PaCO2 in such situations is indicative of attendant alveolar hypoventilation. Examples of diseases leading to venous admixture include asthma and aspiration pneumonia, and those of intrapulmonary shunt include lobar pneumonia and acute respiratory distress syndrome.

Monitoring a Child in Respiratory Distress and Respiratory Failure

Clinical Examination

Clinical observation is the most important component of monitoring. The presence and magnitude of abnormal clinical findings, their progression with time, and their temporal relation to therapeutic interventions serve as guides to diagnosis and management (Chapter 365). The child with respiratory distress or failure should be observed in the position of greatest comfort and in the least threatening environment.

Pulse oximetry is the most commonly utilized technique to monitor oxygenation. Noninvasive and safe, it is the standard of care in bedside monitoring of children during transport, procedural sedation, surgery, and critical illness. It indirectly measures arterial hemoglobin-O2 saturation by differentiating oxyhemoglobin from deoxygenated hemoglobin using their respective light absorption at wavelengths of 660 nm (red) and 940 nm (infrared). A pulsatile circulation is required to enable detection of oxygenated blood entering the capillary bed. Percentage of oxyhemoglobin is reported as arterial oxyhemoglobin saturation (SaO2); however, the correct description is oxyhemoglobin saturation as measured by pulse oximetry (SpO2). This is because SpO2 may not reflect SaO2 in certain situations. It is important to be familiar with the hemoglobin-O2 dissociation curve (Chapter 365) in order to estimate PaO2 at a given oxyhemoglobin saturation. Because of the shape of the hemoglobin-O2 dissociation curve, changes in PaO2 above 70 torr are not readily identified by pulse oximetry. Also, at the same PaO2 level, there may be a significant change in SpO2 at a different blood pH value. In most situations, an SpO2 value greater than 95% is a reasonable goal, especially in emergency situations. There are exceptions, such as in patients with single ventricle cardiac lesions, in whom the pulmonary and systemic circulations are receiving blood flow from the same ventricle (e.g., after Norwood procedure for hypoplastic left heart syndrome), or with large left-to-right shunts (e.g., ventriculoseptal defect [VSD] and patent ductus arteriosus). In these types of pathophysiologic situations, a lower SpO2 is desired to avoid excessive blood flow to the lungs and pulmonary edema from the pulmonary vasodilatory effects of oxygen, and, in the patient with a single ventricle, diverting blood flow away from the systemic circulation. Because pulse oximetry recognizes all types of hemoglobin as either oxyhemoglobin or deoxygenated hemoglobin, it provides inaccurate information in the presence of carboxyhemoglobin and methemoglobin. Percentage of oxyhemoglobin is overestimated in carbon monoxide poisoning and methemoglobinemia. It should be recognized that dangerous levels of hypercarbia may exist in patients with ventilatory failure, who have satisfactory SpO2 if they are receiving supplemental oxygen. Pulse oximetry should not be the only monitoring method in patients with primary ventilatory failure, such as neuromuscular weakness and CNS depression. It is also unreliable in patients with poor perfusion and poor pulsatile flow to the extremities. Despite these limitations, pulse oximetry is a noninvasive, easily applicable, and effective means of evaluating the percentage of oxyhemoglobin in most patients.

Capnography (end-tidal CO2 measurement) is helpful in determining the effectiveness of ventilation and pulmonary circulation. This method is especially useful for monitoring the level of ventilation in intubated patients. It should be kept in mind that diseases that increase dead space or decrease pulmonary blood flow lead to decreases in end-tidal CO2 and an overestimation of the adequacy of ventilation.

Assessment of Oxygenation and Ventilation Deficits

Indicators for following clinical progress and for determining the prognosis in patients with defects in oxygenation or ventilation include:

Management

The goal of management for respiratory distress and respiratory failure is to ensure a patent airway and provide necessary support for adequate oxygenation of the blood and removal of CO2. Compared with hypercapnia, hypoxemia is a life-threatening condition, initial therapy for which should be aimed at ensuring adequate oxygenation.

Oxygen Administration

Supplemental oxygen administration is the least invasive and most easily tolerated therapy for hypoxemic respiratory failure. Nasal cannula oxygen provides low levels of oxygen supplementation and is easy to administer. Oxygen is humidified in a bubble humidifier and delivered via nasal prongs inserted in to the nares. In children, a flow rate <5 L/min is most often used because of increasing nasal irritation with higher rates. A common formula for an estimation of the FIO2 during use of a nasal cannula in older children and adults is as follows:

The typical FIO2 value using this method is between 23 and 40%, although the fraction of inspired oxygen varies according to the size of the child, the respiratory rate, and the volume of air moved with each breath. In a young child, because typical nasal cannula flows are a greater percentage of total minute ventilation, significantly higher FIO2 may be provided. Alternately, a simple mask may be employed, which consists of a mask with open side ports and a valveless oxygen source. Variable amounts of room air are entrained through the ports and around the side of the mask, depending on the fit, size, and minute volume of the child. Oxygen flow rates vary from 5 to 10 L/min, yielding typical FIO2 values between 0.30 and 0.65. If more precise delivery of oxygen is desired, other mask devices should be used.

A Venturi mask delivers preset fractions of oxygen through a mask and reservoir system by entraining precise amounts of room air into the reservoir with high-flow oxygen. The amount of room air entrainment and subsequent FIO2 are determined by the adapter at the end of each mask reservoir. The adapter can be chosen to provide between 30 and 50% oxygen concentrations. Oxygen flow rates of 5-10 L/min are recommended to achieve desired FIO2 and to prevent rebreathing. Partial rebreather and nonrebreather masks utilize a reservoir bag attached to a mask to provide higher fractions of oxygen. Partial rebreather masks have two open exhalation ports and contain a valveless oxygen reservoir bag. Some exhaled gas can mix with reservoir gas during exhalation, although most exits the mask via the exhalation ports. Through these ports, room air is also entrained during inspiration. A partial rebreather mask can provide up to 0.6 FIO2 as long as oxygen flow is adequate to keep the bag from collapsing (typically 10-15 L/min). As with nasal cannulas, smaller children with smaller tidal volumes entrain less room air, and their FIO2 values will be higher. Nonrebreather masks include two one-way valves, one between the oxygen reservoir bag and the mask and one on one of the two exhalation ports. This arrangement minimizes mixing of exhaled and fresh gas and entrainment of room air during inspiration. The second exhalation port has no valve, a safeguard to allow some room air to enter the mask in the event of disconnection from the oxygen source. A nonrebreather mask can provide up to 0.95 FIO2. The use of a nonrebreather mask in conjunction with an oxygen blender allows delivery of fractions of oxygen between 0.50 and 0.95. When supplemental oxygen alone is inadequate to improve oxygenation, or when ventilation problems coexist, additional therapies may be necessary.

Positive Pressure Respiratory Support

Noninvasive positive pressure respiratory support is useful in treating both hypoxemic and hypoventilatory respiratory failure. Positive airway pressure helps aerate partially atelectatic or filled alveoli, prevent alveolar collapse at end exhalation, and increase functional residual capacity (FRC). This improves pulmonary compliance and hypoxemia and decreases intrapulmonary shunt. In addition, positive pressure ventilation is useful in preventing collapse of extrathoracic airways by maintaining positive airway pressure during inspiration. Improving compliance and overcoming airway resistance also improves tidal volume and therefore ventilation. A high-flow nasal cannula delivers gas flow at 4-16 L/min, providing significant continuous positive airway pressure (CPAP). The amount of CPAP provided is not quantifiable and varies with each patient, depending on the percentage of total inspiratory flow that is delivered from the cannula, airway anatomy, and degree of mouth breathing. In small children, the relative amount of CPAP for a given flow is usually greater than in older children and may provide significant positive pressure. The FIO2 can be adjusted by provision of gas flow through an oxygen blender. For delivery of high-flow air or oxygen, adequate humidification is essential and is achieved with use of a separate heated humidification chamber. CPAP can also be provided through snugly fitting nasal prongs or a tight-fitting facial mask attached to a ventilator or other positive pressure device. Noninvasive CPAP is most useful in diseases of mildly decreased lung compliance and low FRC, such as atelectasis and pneumonia. Diseases of extrathoracic airway obstruction in which extrathoracic negative airway pressures during inspiration lead to airway narrowing (e.g., laryngotracheitis, obstructive sleep apnea, postextubation airway edema) may also benefit from CPAP.

Bilevel positive airway pressure (BiPAP)