Respiratory Failure

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Chapter 3 Respiratory Failure

Mark D. Joffe, MD

1 Why is it so important to know about respiratory failure in children?

Children are at greater risk of respiratory failure than adults. Respiratory symptoms are one of the most common reasons children are taken to emergency departments (EDs) and the most frequent cause of cardiopulmonary arrest. The potential for progression of respiratory distress to respiratory failure necessitates prompt evaluation of children with respiratory symptoms. Much of the morbidity and mortality from respiratory disease in children can be prevented by competent pediatric emergency care.

2 Why are children at greater risk for respiratory failure?

Children have greater metabolic requirements and greater need for oxygen on a per-kilogram basis when compared to adults. Anatomic factors put infants, in particular, at high risk for respiratory failure. Infants breathe almost exclusively through their noses because the nasopharynx is in close proximity to the more cephalad glottis and the infant tongue fills most of the oropharynx. Nasal obstruction, therefore, can cause significant respiratory signs and symptoms in infants. The caliber of infant airways is small, so respiratory resistance is much higher in infants, especially when they have inflammation of the respiratory tree. Alveoli have less collateral ventilation in infants. Thus, obstruction of small, peripheral airways is more likely to lead to atelectasis and hypoxemia. A compliant chest wall facilitates passage through the birth canal but leads to respiratory problems when airway resistance is increased. The diaphragm of infants is weaker and more easily fatigued compared with the diaphragm of older children and adults. Also, the inability of younger children to verbalize their symptoms may cause delayed presentations of respiratory problems.

3 What are the clinical features of respiratory failure?

image Poor color (ashen or central cyanosis)

image Obtunded mental status

image Decreased chest wall movement, with or without signs of respiratory distress

image Bradypnea or marked tachypnea

American Heart Association, Subcommittee on Pediatric Resuscitation: Recognition of respiratory failure and shock. In Zritsky AL (ed): Pediatric Advanced Life Support Provider Manual, Dallas, American Heart Association, 2002, p 81.

4 Why does respiratory resistance increase so significantly with inflammation of the respiratory tree?

The resistance to laminar air flow through a tube is inversely related to the radius to the fourth power (Poiseuille’s law). Modest decreases in the radius of the lumen of the airway can lead to dramatic increases in respiratory resistance when airway caliber is small (Fig. 3-1).

image

Figure 3-1 Comparison of the effects of 1 mm of mucosal edema on airway resistance in an infant versus an adult. Resistance is inversely proportional to the fourth power of the radius for laminar flow and the fifth power for turbulent flow. Airway resistance increases sixteenfold in the infant for laminar flow. In a crying infant with turbulent air flow, resistance increases thirty-twofold.

From Cote CJ, Todres ID: The pediatric airway. In Cote CJ, Ryan JF, Todres ID, Groudsouzian NG [eds]: A Practice of Anesthesia for Infants and Children, 2nd ed. Philadelphia, W.B. Saunders, 1993.

5 Why do children get respiratory infections so frequently?

The immature immune system puts infants at risk for respiratory infections. Children have less immunologic memory, so exposure to a particular respiratory pathogen is more likely to be a child’s first. Young children playing together in a group tend to exchange contaminated respiratory secretions with particular aplomb. They do not know that frequent handwashing can dramatically reduce the spread of respiratory infections. Many adult caregivers do not recognize this as well.

6 Are there different types of respiratory failure?

Some clinicians divide respiratory failure into two categories. The first type is generally caused by mismatch of ventilation and perfusion resulting from problems in the lung. This type of respiratory failure is characterized by hypoxemia with normal or low PCO2. Other patients with respiratory failure have an overall decrease in alveolar ventilation that is usually the result of upper airway obstruction, neuromuscular disease, thoracic trauma, or muscle fatigue. These patients have relatively proportional decreases in PO2 and increases in PCO2. The physiology in most children with respiratory failure is a combination of these two types because one type often leads to the other. For instance, an infant with bronchiolitis initially may have hypoxemia from atelectasis and ventilation–perfusion mismatch, but may progress to inadequate alveolar ventilation when airway resistance is high and respiratory muscle fatigue supervenes.

7 How do I know which of the numerous children with respiratory symptoms will progress to respiratory failure?

Predicting the future is difficult, but many clinical skills can be employed. A detailed history can give information about the vulnerability of the child to respiratory decompensation. Children who are very young, were born prematurely, have chronic pulmonary or cardiac diseases, or have immunodeficiencies are at particular risk. Recent medical advances, including the development of home nursing capabilities, have resulted in many “graduates” of intensive care nurseries living in our communities. EDs are confronted with these medically fragile children more than ever before.

Diseases have a natural history that must be considered. If a child is evaluated early in the course of respiratory infection, you can anticipate that the child is likely to worsen before improvement will be noted. Intervention may vary depending upon the stage in the natural history of the disease a child is in at the time of the visit. Children with significant respiratory distress may worsen as their disease process progresses or as they become fatigued.

Young children are more difficult to assess for respiratory problems. Histories are obtained secondhand, as the parent interprets behaviors and relays observations that have been made. Young children with significant respiratory distress may remain happy and playful until fatigue suddenly sets in. A careful clinical assessment of the current degree of respiratory distress is necessary to identify those sicker patients who are more likely to develop respiratory failure.

8 How do I assess respiration in a baby who screams every time I approach him?

“Stranger anxiety” normally develops in the second half of the first year of life. The child’s alertness to your presence is certainly a positive sign. Observing the child from across the room provides valuable information. General appearance, state of hydration, respiratory rate, nasal flaring, retractions, paradoxical respirations, and grunting can be appreciated without close proximity to the child. In many cases, the child is more cooperative if your approach is delayed, slow, and accompanied by soothing speech.

9 What are paradoxical respirations? Why do they occur?

Infants who have increased airway resistance need to generate high negative intrathoracic pressures to inflate their lungs. As the diaphragm moves downward and intrathoracic pressure becomes negative, the cartilaginous bones and weak intercostal musculature cannot maintain the thoracic circumference. As the abdomen moves outward, the chest collapses inward (rather than the normal expansion) on inspiration; hence the terms paradoxical respirations, thoracoabdominal asynchrony, or see-saw breathing. Paradoxical respirations are often a sign of impending respiratory failure.

10 How can one tell if the respiratory failure is caused by an upper airway disease or by lower airway disease?

Distinguishing upper from lower respiratory disease is a difficult but important part of clinical evaluation. Many children have disease processes that involve the upper and lower respiratory tracts simultaneously, for example, bronchiolitis caused by respiratory syncytial virus. In general, respiratory sounds reflecting upper airway inflammation are most prominent during inspiration, when negative intraluminal pressure causes upper airway narrowing. Conversely, intrathoracic (lower airway) processes produce wheezing and other sounds of airway obstruction primarily during expiration, when positive intrapleural pressure compresses intrathoracic airways. If breath sounds are more obstructed on inspiration, the upper airway is probably involved. Wheezing or other sounds more prominent during expiration suggests lower respiratory tract disease.

11 Is wheezing a reliable sign of severe lower airway disease?

No. Prominent wheezing requires significant airflow through narrowed small airways. Children with severe obstruction of small airways may have such great reduction of airflow that audible wheezing is not present. These children usually have decreased inspiratory breath sounds and increased work of breathing. Administration of bronchodilators to these patients will often increase wheezing because more air flows through the narrowed airways.

12 What is the value of a chest radiograph in evaluation of a child with suspected respiratory failure?

In previously normal children, respiratory failure is generally preceded by clinically identifiable respiratory distress. Young children with fever and tachypnea may benefit from a chest radiograph because bacterial pneumonia can be difficult to diagnose by history and physical examination alone. Foreign-body aspiration, pneumothorax/pneumomediastinum, and cardiac disease are a few of the diagnoses that can also be suspected on the basis of a chest radiograph. Children with minor respiratory illnesses generally do not need chest radiographs, even if they seek care in an ED. If there is concern about impending or existing respiratory failure, a chest radiograph can be very useful.

13 Why do some people call pulse oximetry the fifth vital sign?

Hypoxemia is not always obvious from the physical examination. “The fifth vital sign” is a phrase used by those who feel pulse oximetry should become routine in the assessment of pediatric patients. Most children who are hypoxemic from a respiratory illness have signs of respiratory distress, but in some cases hypoxemia may be clinically inapparent. Hypoxemia is a less potent stimulator of the respiratory center than is hypercarbia. Thus, the increase in minute ventilation that occurs with mild hypoxemia is modest, and may be difficult to detect by physical examination. Cyanosis requires 3–5 gm of unsaturated hemoglobin per deciliter to be visible. If a child has a total hemoglobin of 12 gm/dL, cyanosis is not apparent until the oxygen saturation drops below 75%. Most clinicians believe it is useful to be aware of hypoxemia before it is severe enough to cause visible cyanosis.

14 What’s the big deal if the oxygen saturation is 2–3% below normal?

The relationship between PO2 and saturation is not linear but sigmoidal. While there is little difference in PO2 between saturations of 99% and 96%, there is a much greater difference between 93% and 90%. In children with bronchiolitis, oxygen saturation below 95% during feeding was the most useful factor in identifying infants who would have a more severe course of illness. Sleeping children with respiratory illnesses often have transient periods of desaturation that require no intervention. Oxygen therapy and closer monitoring should be considered if the desaturation is persistent (Fig. 3-2).

image

Figure 3-2 As PO2 drops below 70 mmHg, oxygen saturation declines more precipitously.

15 What causes pulse oximeter readings to be inaccurate?

The most common problem is the oximeter probe not consistently registering the pulsatile arterial flow through the skin. This is often caused by movement, poor perfusion of the skin, or bright ambient light. Careful attention to the graphical display of pulsatile flow on the pulse oximeter can almost always distinguish a falsely low saturation due to poor signal capture from true hypoxemia. Occasionally, hemoglobin is abnormal. Carboxyhemoglobinemia will cause a falsely elevated measurement of oxygen saturation by pulse oximetry; methemoglobinemia in significant concentrations will cause a modest lowering.

Lee WW, Mayberry K, Crapo R, et al: The accuracy of pulse oximetry in the emergency department. Am J Emerg Med 18:427, 2000.

16 Why are some children with severe respiratory distress well saturated, while others who look comfortable are hypoxemic?

In most cases, hypoxemia is due to a mismatch of ventilation and perfusion, not to alveolar hypoventilation. As long as unventilated areas of the lung are not perfused because of hypoxic pulmonary vasoconstriction, systemic oxygen saturation may remain normal. Many children with respiratory distress have hypoxemia and hypocarbia, suggesting ventilation–perfusion mismatch despite alveolar hyperventilation. The absence of hypoxemia is not, by itself, reassurance that the child’s respirations are adequate.

17 Why do some patients with wheezing have a reduction in their oxygen saturation after bronchodilator treatment when they otherwise appear to be improving?

Albuterol and other bronchodilators are β-adrenergic agents that are somewhat β2 selective. β2 receptor stimulation causes vasodilation as well as bronchodilation. One explanation for decreases in oxygen saturation noted after treatment with bronchodilators is that the agents cause some pulmonary vasodilation, resulting in increased perfusion of poorly ventilated areas of the lung and thereby worsening ventilation–perfusion matching. This is seen in a minority of patients; is usually a transient phenomenon; and is not a contraindication to continued, aggressive bronchodilator therapy in children with severe lower airway disease.

18 Can respiratory failure be present without respiratory distress?

Absolutely. Children may hypoventilate because of reduced level of consciousness (ingestion, metabolic derangements, head trauma) or neuromuscular dysfunction. After prolonged respiratory distress, children may become fatigued, and their work of breathing may appear normal in the presence of significant hypoventilation. Elevation of the PCO2 may signal the presence of fatigue and hypoventilation.

19 What is ARDS in children? Doesn’t the “A” stand for ADULT?

Acute respiratory distress syndrome (ARDS) occurs in children, so the “A” was changed from adult to acute. It is a common cause of respiratory failure at all ages. ARDS is a diffuse pulmonary process that develops after another condition injures the lung. Some causes of ARDS that are treated in EDs include sepsis, hypotension, pneumonia, aspiration of gastric contents, smoke or other inhalation injury, near drowning, and chest trauma with pulmonary contusion. Chest radiographs show diffuse, bilateral infiltrates that resemble left-sided congestive heart failure, but left atrial pressures must be normal for the diagnosis of ARDS. The diagnostic criteria for ARDS are as follows:

image Acute onset

image Severe hypoxemia (PO2 < 200 mmHg regardless of fraction of inspired oxygen and positive end-expiratory pressure)

image Diffuse bilateral infiltrates on chest radiography

image Normal left atrial pressure

Bernard GR: Acute respiratory distress syndrome: A historical perspective. Am J Respir Crit Care Med 172:798, 2005.

20 How is respiratory failure defined? When does respiratory distress become respiratory failure?

A general definition of respiratory failure is inadequate oxygenation to meet metabolic needs and/or inadequate excretion of CO2. Many specific definitions have been proposed, but the best clinicians individualize their decisions about therapy according to the particulars of the case. One definition is PO2 <60 mmHg or O2 saturation <93% on >60% oxygen, PCO2 >60 mmHg and rising, or clinical apnea.

21 Why are some patients who meet the definition for respiratory failure not intubated and mechanically ventilated to normalize their blood gases?

Children tolerate hypercarbia better than adults do. If oxygenation is adequate, and hypercarbia is likely to be reversed in the near future, some intensivists permit the hypercarbia to persist for a period of time. So-called permissive hypercarbia reduces barotrauma to the lungs that results from mechanical ventilation. In patients with reactive airway disease or asthma, positive-pressure ventilation is fraught with risk of pneumomediastinum and pneumothorax. Since there are effective medications to reverse airway obstruction in a relatively short period of time, some patients can be closely monitored without endotracheal intubation and mechanical ventilation, despite levels of CO2 that define respiratory failure.

22 Is endotracheal intubation the only way to manage an airway in respiratory distress?

No. In fact, bag-valve-mask ventilation is adequate for many children with transient, reversible airway problems. Positioning the child with some extension of the neck and moving the mandible forward by lifting the angles of the jaw pulls the tongue off the posterior pharynx, often relieving airway obstruction. Oral or nasal airways can be used to maintain the patency of the upper airway in selected patients. All children should receive effective bag-valve-mask ventilation with 100% oxygen prior to intubation.

American Heart Association: 2005 Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 11: Pediatric Basic Life Support. Circulation 112:156–166, 2005.

KEY POINTS: INDICATIONS FOR ENDOTRACHEAL INTUBATION

1 Progressive respiratory exhaustion—unlikely to reverse quickly

2 Apnea, hypoventilation that requires mechanical ventilation

3 Need for airway protection (upper airway obstruction, loss of protective airway reflexes)

4 Shock

5 Need to improve pulmonary toilet

23 What are the indications to intubate the trachea of a child?

image Respiratory failure that is unlikely to be reversed quickly, especially if hypoxemia is present despite >60% oxygen administration

image Apnea, hypoventilation, or progressive respiratory exhaustion that requires ongoing mechanical ventilation

image Need for airway protection for children who have upper airway obstruction or an inability to protect their airway from aspiration

image Desire to decrease the work of breathing for patients in shock (under normal circumstances, work of breathing requires less than 5% of the total energy expenditure, but with respiratory distress it can demand up to 50%; in a shock state, energy can be better utilized for other essential body functions)

image Therapeutic interventions, such as tracheal administration of medications and suctioning for pulmonary toilet (mechanical ventilation is also required)

KEY POINTS: STEPS TO PERFORM ENDOTRACHEAL INTUBATION

1 Preoxygenate with 100% oxygen by bag-valve-mask device.
2 Prepare equipment (e.g., suction, endotracheal tubes, laryngoscopes).
3 Confirm functioning IV line.
4 Apply cricoid pressure (Sellick maneuver).
5 Administer medications (atropine, sedative, paralytic agent).
6 Intubate the trachea, observing the tube pass through the vocal cords.
7 Verify proper placement—auscultate the chest, check for CO2 by capnometry, chest radiograph.
8 Secure the endotracheal tube.

24 What are the steps for emergency endotracheal intubation of a child?

Bag-valve-mask ventilation with 100% oxygen should begin as soon as the need for positive-pressure ventilation is identified. Emergency endotracheal intubations are generally treated as “full-stomach” intubations. The steps for a rapid sequence intubation are:

1 Preoxygenate with bag-valve-mask ventilation with 100% oxygen.

2 Prepare all equipment, including suction, endotracheal tubes, and laryngoscopes.

3 Make certain an IV catheter is functioning well.

4 Apply cricoid pressure (Sellick maneuver) to prevent passive regurgitation and aspiration. (Keep applying pressure until endotracheal tube is known to be in the trachea.)

5 Administer atropine (for younger children), followed by a sedative agent and then a paralytic agent.

6 Perform laryngoscopy once paralysis is complete, and watch the endotracheal tube go through the vocal cords into the trachea.

7 Auscultate for equal breath sounds, and check for gurgling over the stomach, which suggests esophageal intubation. Observe symmetric chest expansion, misting in the tube with exhalation, improvement in oxygen saturation by pulse oximetry, and presence of CO2 by capnometry.

8 Release cricoid pressure.

9 Secure the tube with tape.

10 Obtain chest radiograph to check position of the tube and adjust accordingly.

American Heart Association: 2005 Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 12: Pediatric Advanced Life Support. Circulation 112:167–187, 2005.

King C, Stayer SA: Emergent endotracheal intubation. In Henretig FM, King C (eds): Textbook of Pediatric Emergency Procedures. Baltimore, Williams & Wilkins, 1997.

25 Can a difficult endotracheal intubation be predicted?

Not always, so it is important to have people experienced with airway management available, especially when a difficult intubation is anticipated. The following conditions often result in difficult intubations:

Congenital Acquired
Micrognathia Hoarseness/stridor/drooling
Macroglossia Facial burns/singed facial hairs
Cleft or high-arched palate Facial fractures/oral trauma
Protruding upper incisors Foreign body
Small mouth
Limited mobility of temporomandibular joint

26 What should you consider if a patient deteriorates after endotracheal intubation?

If an intubated patient’s condition deteriorates after endotracheal intubation, consider DOPE:

image Displacement of the endotracheal tube—no longer in the trachea

image Obstruction of the tube—perhaps by mucus

image Pneumothorax

image Equipment failure—perhaps the ventilator is malfunctioning or perhaps you are not actually delivering 100% oxygen as you thought

American Heart Association: 2005 Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 12: Pediatric Advanced Life Support. Circulation 112:167–187, 2005.

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