Alveolar Hypoventilation

Alveolar hypoventilation occurs when the amount of oxygen being brought into the alveoli is insufficient to meet the metabolic needs of the body.⁶ This can be the result of increasing metabolic oxygen needs or decreasing ventilation.⁵ Hypoxemia caused by alveolar hypoventilation is associated with hypercapnia and commonly results from extrapulmonary disorders.^1,2,7

Ventilation/Perfusion Mismatching

V/Q mismatching occurs when ventilation and blood flow are mismatched in various regions of the lung in excess of what is normal. Blood passes through alveoli that are underventilated for the given amount of perfusion, leaving these areas with a lower-than-normal amount of oxygen. V/Q mismatching is the most common cause of hypoxemia and is usually the result of alveoli that are partially collapsed or partially filled with fluid.^1,2,7

Intrapulmonary Shunting

The extreme form of V/Q mismatching, intrapulmonary shunting, occurs when blood reaches the arterial system without participating in gas exchange. The mixing of unoxygenated (shunted) blood and oxygenated blood lowers the average level of oxygen present in the blood. Intrapulmonary shunting occurs when blood passes through a portion of a lung that is not ventilated. This may be the result of 1) alveolar collapse secondary to atelectasis; or 2) alveolar flooding with pus, blood, or fluid.^1,2,7

If allowed to progress, hypoxemia can result in a deficit of oxygen at the cellular level. As the tissue demands for oxygen continue and the supply diminishes, an oxygen supply/demand imbalance occurs and tissue hypoxia develops. Decreased oxygen to the cells contributes to impaired tissue perfusion and the development of lactic acidosis and multiple organ dysfunction syndrome.⁸

Oxygenation

Actions to improve oxygenation include supplemental oxygen administration, either with a low flow system or a high flow system,¹¹ and the use of positive airway pressure.¹² The purpose of oxygen therapy is to correct hypoxemia, and although the absolute level of hypoxemia varies in each patient, most treatment approaches aim to keep the arterial hemoglobin oxygen saturation greater than 90%.⁹ The goal is to keep the tissues’ needs satisfied but not produce hypercapnia or oxygen toxicity.⁹ Supplemental oxygen administration is effective in treating hypoxemia related to alveolar hypoventilation and V/Q mismatching. When intrapulmonary shunting exists, supplemental oxygen alone is ineffective.¹¹ In this situation, positive pressure is necessary to open collapsed alveoli and facilitate their participation in gas exchange. Positive pressure is delivered via invasive and noninvasive mechanical ventilation. To avoid intubation, positive pressure is usually administered initially noninvasively via a mask.¹³ For further information on supplemental oxygen therapy and noninvasive ventilation, see Chapter 21.

Ventilation

Interventions to improve ventilation include the use of noninvasive and invasive mechanical ventilation. Depending on the underlying cause and the severity of the ALF, the patient may be treated initially with noninvasive ventilation.¹³ However, one study found that those patients with a pH of less than 7.25 at initial presentation had an increased likelihood of the need for invasive mechanical ventilation.¹⁴ The selection of ventilatory mode and settings depends on the patient’s underlying condition, severity of respiratory failure, and body size. Initially the patient is started on volume ventilation in the assist/control mode. In the patient with chronic hypercapnia, the settings should be adjusted to keep the ABG values within the parameters expected to be maintained by the patient after extubation.¹⁵ For further information on mechanical ventilation see Chapter 21.

Pharmacology

Medications to facilitate dilation of the airways may also be of benefit in the treatment of the patient with ALF. Bronchodilators, such as beta₂-agonists and anticholinergic agents, aid in smooth muscle relaxation and are of particular benefit to patients with airflow limitations. Methylxanthines, such as aminophylline, are no longer recommended because of their negative side effects. Steroids also are often administered to decrease airway inflammation and enhance the effects of the beta₂-agonists. Mucolytics and expectorants are also no longer used since they have been found to be of no benefit in this patient population.¹⁶

Sedation is necessary in many patients to assist with maintaining adequate ventilation. It can be used to comfort the patient and decrease the work of breathing, particularly if the patient is fighting the ventilator. Analgesics should be administered for pain control.^17,18 In some patients, sedation does not decrease spontaneous respiratory efforts enough to allow adequate ventilation. Neuromuscular paralysis may be necessary to facilitate optimal ventilation. Paralysis also may be necessary to decrease oxygen consumption in the severely compromised patient.¹⁸

Acidosis

Acidosis may occur in the patient for a number of reasons. Hypoxemia causes impaired tissue perfusion, which leads to the production of lactic acid and the development of metabolic acidosis. Impaired ventilation leads to the accumulation of carbon dioxide and the development of respiratory acidosis. Once the patient is adequately oxygenated and ventilated, the acidosis should correct itself. The use of sodium bicarbonate to correct the acidosis has been shown to be of minimal benefit to the patient and thus is no longer recommended as first-line treatment. Bicarbonate therapy shifts the oxygen-hemoglobin dissociation curve to the left and can worsen tissue hypoxia. Sodium bicarbonate may be used if the acidosis is severe (pH less than 7.1), refractory to therapy, and causing dysrhythmias or hemodynamic instability.¹⁹

Nutrition Support

The initiation of nutrition support is of utmost importance in the management of the patient with ALF. The goals of nutrition support are to meet the overall nutritional needs of the patient while avoiding overfeeding, to prevent nutrition delivery-related complications, and to improve patient outcomes.²⁰ Failure to provide the patient with adequate nutrition support results in the development of malnutrition. Both malnutrition and overfeeding can interfere with the performance of the pulmonary system, further perpetuating ALF. Malnutrition decreases the patient’s ventilatory drive and muscle strength, whereas overfeeding increases carbon dioxide production, which then increases the patient’s ventilatory demand, resulting in respiratory muscle fatigue.²¹

The enteral route is the preferred method of nutrition administration. If the patient cannot tolerate enteral feedings or cannot receive enough nutrients enterally, he or she will be started on parenteral nutrition. Because the parenteral route is associated with a higher rate of complications, the goal is to switch to enteral feedings as soon as the patient can tolerate them.^20,21 Nutrition support should be initiated before the third day of mechanical ventilation for the well-nourished patient and within 24 hours for the malnourished patient.^20,21

Complications

The patient with ALF may experience a number of complications including ischemic-anoxic encephalopathy,²² cardiac dysrhythmias,²³ venous thromboembolism (VTE),²⁴ and gastrointestinal bleeding.²⁵ Ischemic-anoxic encephalopathy results from hypoxemia, hypercapnia, and acidosis.²² Dysrhythmias are precipitated by hypoxemia, acidosis, electrolyte imbalances, and the administration of beta₂-agonists.²³ Maintaining oxygenation, normalizing electrolytes, and monitoring medication levels will facilitate the prevention and treatment of encephalopathy and dysrhythmias.^22,23 VTE is precipitated by venous stasis resulting from immobility and can be prevented through the use of intermittent pneumatic compression devices and low-dose unfractionated heparin or low–molecular-weight heparin (LMWH).²⁴ Gastrointestinal bleeding can be prevented through the use of histamine receptor antagonists, cytoprotective agents, or proton pump inhibitors.²⁵ In addition, the patient is at risk for the complications associated with an artificial airway, mechanical ventilation, enteral and parenteral nutrition, and peripheral arterial cannulation.

Optimizing Oxygenation and Ventilation

Nursing interventions to optimize oxygenation and ventilation include positioning, preventing desaturation, and promoting secretion clearance.

Educating the Patient and Family

Early in the patient’s hospital stay, the patient and family should be taught about ALF, its etiologies, and its treatment. As the patient moves toward discharge, teaching should focus on the interventions necessary for preventing the reoccurrence of the precipitating disorder (Box 20-2). If the patient smokes, he or she should be encouraged to stop smoking and be referred to a smoking cessation program (Box 20-3). In addition, the importance of participating in a pulmonary rehabilitation program should be stressed.

Collaborative management of the patient with ALF is outlined in Box 20-4.

Exudative Phase

Within the first 72 hours after the initial insult, the exudative phase or acute phase ensues. Once released, the mediators cause injury to the pulmonary capillaries, resulting in increased capillary membrane permeability leading to the leakage of fluid filled with protein, blood cells, fibrin, and activated cellular and humoral mediators into the pulmonary interstitium. Damage to the pulmonary capillaries also causes the development of microthrombi and elevation of pulmonary artery pressures. As fluid enters the pulmonary interstitium, the lymphatics are overwhelmed and unable to drain all the accumulating fluid, resulting in the development of interstitial edema. Fluid is then forced from the interstitial space into the alveoli, resulting in alveolar edema. Pulmonary interstitial edema also causes compression of the alveoli and small airways. Alveolar edema causes swelling of the type I alveolar epithelial cells and flooding of the alveoli. Protein and fibrin in the edema fluid precipitate the formation of hyaline membranes over the alveoli. Eventually, the type II alveolar epithelial cells are also damaged, leading to impaired surfactant production. Injury to the alveolar epithelial cells and the loss of surfactant lead to further alveolar collapse.^38,39

Hypoxemia occurs as a result of intrapulmonary shunting and V/Q mismatching secondary to compression, collapse, and flooding of the alveoli and small airways. Increased work of breathing occurs as a result of increased airway resistance, decreased functional residual capacity (FRC), and decreased lung compliance secondary to atelectasis and compression of the small airways. Hypoxemia and the increased work of breathing lead to patient fatigue and the development of alveolar hypoventilation. Pulmonary hypertension occurs as a result of damage to the pulmonary capillaries, microthrombi, and hypoxic vasoconstriction leading to the development of increased alveolar dead space and right ventricular afterload. Hypoxemia worsens as a result of alveolar hypoventilation and increased alveolar dead space. Right ventricular afterload increases and leads to right ventricular dysfunction and a decrease in cardiac output (CO).³⁸

Fibroproliferative Phase

This phase begins as disordered healing and starts in the lungs. Cellular granulation and collagen deposition occur within the alveolar-capillary membrane. The alveoli become enlarged and irregularly shaped (fibrotic) and the pulmonary capillaries become scarred and obliterated. This leads to further stiffening of the lungs, increasing pulmonary hypertension, and continued hypoxemia.^38,39

Resolution Phase

Recovery occurs over several weeks as structural and vascular remodeling take place to re-establish the alveolar-capillary membrane. The hyaline membranes are cleared and intra-alveolar fluid is transported out of the alveolus into the interstitium. The type II alveolar epithelial cells multiply, some of which differentiate to type I alveolar epithelial cells, facilitating the restoration of the alveolus. Alveolar macrophages remove cellular debris.^38,39

Low Tidal Volume. 

Low tidal volume ventilation uses smaller tidal volumes (6 mL/kg) to ventilate the patient, in an attempt to limit the effects of barotrauma and volutrauma. The goal is to provide the maximum tidal volume possible while maintaining end-inspiratory plateau pressure less than 30 cm H₂O. To allow for adequate carbon dioxide elimination, the respiratory rate is increased to 20 to 30 breaths/min.^42,43

Permissive Hypercapnia. 

Permissive hypercapnia uses low tidal volume ventilation in conjunction with normal respiratory rates, in an attempt to limit the effects of atelectrauma and biotrauma. Normally, to maintain normocapnia the patient’s respiratory rate would have to be increased to compensate for the small tidal volume. In ARDS though, increasing the respiratory rate can lead to worsening alveolar damage. Thus the patient’s carbon dioxide level is allowed to rise, and the patient becomes hypercapnic. As a general rule, the patient’s Paco₂ should not rise faster than 10 mm Hg per hour and overall should not exceed 80 to 100 mg Hg. Because of the negative cardiopulmonary effects of severe acidosis, the arterial pH is generally maintained at 7.20 or greater. To maintain the pH, the patient is given intravenous sodium bicarbonate or the respiratory rate and/or tidal volume are increased. Permissive hypercapnia is contraindicated in patients with increased intracranial pressure, pulmonary hypertension, seizures, and heart failure.⁴⁴

Pressure Control Ventilation. 

In pressure control ventilation (PCV) mode, each breath is delivered or augmented with a preset amount of inspiratory pressure as opposed to tidal volume, which is used in volume ventilation. Thus the actual tidal volume the patient receives varies from breath to breath. PCV is used to limit and control the amount of pressure in the lungs and decrease the incidence of volutrauma. The goal is to keep the patient’s plateau pressure (end-inspiratory static pressure) lower than 30 cm H₂O. A known problem with this mode of ventilation is that as the patient’s lungs get stiffer, it becomes harder and harder to maintain an adequate tidal volume and severe hypercapnia can occur.^42,43

Inverse Ratio Ventilation. 

Another alternative ventilatory mode that is used in managing the patient with ARDS is inverse ratio ventilation (IRV), either pressure controlled or volume controlled. IRV prolongs the inspiratory (I) time and shortens the expiratory (E) time, thus reversing the normal I : E ratio. The goal of IRV is to maintain a more constant mean airway pressure throughout the ventilatory cycle, which helps keep alveoli open and participating in gas exchange. It also increases FRC and decreases the work of breathing. In addition, as the breath is delivered over a longer period of time, the peak inspiratory pressure in the lungs is decreased. A major disadvantage to IRV is the development of auto–PEEP. As the expiratory phase of ventilation is shortened, air can become trapped in the lower airways, creating unintentional PEEP (or auto-PEEP), which can cause hemodynamic compromise and worsening gas exchange. Patients on IRV usually require heavy sedation with neuromuscular blockade to prevent them from fighting the ventilator.^42,43

High-Frequency Oscillatory Ventilation. 

Another alternative ventilatory mode that is used in patients who remain severely hypoxemic despite the treatments previously described is high-frequency oscillatory ventilation (HFOV). The goal of this method of ventilation is similar to that of IRV in that it uses a constant airway pressure to promote alveolar recruitment while avoiding overdistention of the alveoli. HFOV uses a piston pump to deliver very low tidal volumes at very high rates or oscillations (300 to 3000 breaths/min).⁴⁵

Positive End-Expiratory Pressure. 

Because the hypoxemia that develops with ARDS is often refractory or unresponsive to oxygen therapy, it is necessary to facilitate oxygenation with PEEP. The purpose of using PEEP in the patient with ARDS is to improve oxygenation while reducing Fio₂ to less toxic levels. PEEP has several positive effects on the lungs, including opening collapsed alveoli, stabilizing flooded alveoli, and increasing FRC. Thus PEEP decreases intrapulmonary shunting and increases compliance. PEEP also has several negative effects including: 1) decreasing CO as a result of decreasing venous return secondary to increased intrathoracic pressure; and 2) barotrauma, as a result of gas escaping into the surrounding spaces secondary to alveolar rupture. The amount of PEEP a patient requires is determined by evaluating both arterial hemoglobin oxygen saturation and CO. In most cases, a PEEP of 10 to 15 cm H₂O is adequate. If PEEP is too high, it can result in overdistention of the alveoli, which can impede pulmonary capillary blood flow, decrease surfactant production, and worsen intrapulmonary shunting. If PEEP is too low, it allows the alveoli to collapse during expiration, which can result in more damage to alveoli.⁴²

Extracorporeal and Intracorporeal Gas Exchange. 

Extracorporeal and intracorporeal gas exchanges are last-resort techniques used in the treatment of severe ARDS when conventional therapy has failed. These methods allow the lungs to rest by facilitating the removal of carbon dioxide and providing oxygen external to the lungs by means of an “artificial lung,” or membrane/fiber oxygenator. Extracorporeal membrane oxygenation (ECMO), extracorporeal carbon dioxide removal (ECCO₂R), and intravascular oxygenation (IVOX) are three techniques that employ this type of technology. ECMO is similar to cardiopulmonary bypass in that blood is removed from the body and pumped through a membrane oxygenator, where CO₂ is removed and O₂ is added, and then returned to the body. ECCO₂R is a variation of ECMO in which the primary focus is removal of CO₂. IVOX facilitates oxygenation and ventilation with the use of a fiber oxygenator that is implanted in the inferior vena cava. All of these techniques pose serious bleeding problems to the patient, and none has been shown to improve patient outcome.^46,47

Prone Positioning. 

A number of studies have shown that prone positioning the patient with ARDS results in an improvement in oxygenation. Although a number of theories propose how prone positioning improves oxygenation, the discovery that with ARDS there is greater damage to the dependent areas of the lungs probably provides the best explanation. It was originally thought that ARDS was a diffuse homogenous disease that affected all areas of the lungs equally. It is now known that the dependent lung areas are more heavily damaged than the nondependent lung areas. Turning the patient prone improves perfusion to less damaged parts of lungs and improves V/Q matching and decreases intrapulmonary shunting. Prone positioning appears to be more effective when initiated during the early phases of ARDS.⁴⁹ For more information on prone positioning see Chapter 21.

Collaborative management of the patient with ARDS is outlined in Box 20-7.

Severe Community-Acquired Pneumonia

Pathogens that can cause severe CAP include Streptococcus pneumoniae, Legionella species, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus, Mycoplasma pneumoniae, respiratory viruses, Chlamydia pneumoniae, and Pseudomonas aeruginosa.⁵¹ A number of factors increase the risk for developing CAP, including alcoholism, chronic obstructive pulmonary disease (COPD), and comorbid conditions such as diabetes, malignancy, and coronary artery disease. Impaired swallowing and altered mental status also contribute to the development of CAP, because they result in an increased exposure to the various pathogens due to chronic aspiration of oropharyngeal secretions.⁵¹

Hospital-Acquired Pneumonia

Pathogens that can cause HAP include Escherichia coli, H. influenzae, methicillin-sensitive S. aureus, S. pneumoniae, P. aeruginosa, Acinetobacter baumannii, methicillin-resistant S. aureus (MRSA), Klebsiella spp., and Enterobacter spp. Two of the pathogens most frequently associated with VAP are S. aureus and P. aeruginosa. Risk factors for HAP can be categorized as host-related, treatment-related, and infection control-related (Box 20-8).⁵⁵

Health Care-Associated Pneumonia

Pathogens that can cause HCAP are similar to those causing both CAP and HAP with P. aeruginosa and MRSA being the most common in the United States.⁵⁴ Risk factors for HCAP include prior hospitalization (hospitalized for 2 or more days within the last 90 days), receiving hemodialysis, receiving intravenous antibiotic therapy, chemotherapy or wound care within 30 days, residing in a long-term care facility or with family member with multidrug-resistant infection, and an immunocompromised state. These patients are at a higher risk of developing multidrug-resistant organisms.⁵⁶

Antibiotic Therapy

Although bacteria-specific antibiotic therapy is the goal, this may not always be possible because of difficulties in identifying the organism and the seriousness of the patient’s condition. The time involved obtaining cultures should be balanced against the need to begin some treatment based on the patient’s condition. Empiric therapy has become a generally acceptable approach. In this approach, choice of antibiotic treatment is based on the most likely etiologic organism while avoiding toxicity, superinfection, and unnecessary cost. If available, Gram stain results should be used to guide choices of antibiotics. Antibiotics should be chosen that offer broad coverage of the usual pathogens in the hospital or community. Failure to respond to such therapy may indicate that the chosen antibiotic regimen does not appropriately cover all of the etiologic pathogens or that a new source of infection has developed.^51,55

Currently the Centers for Medicare and Medicaid Services (CMS) and The Joint Commission (TJC) standards for managing patients with CAP require that the first dose of antibiotics be administered within 6 hours of arrival to the hospital. This timeframe is very controversial and has been the subject of much debate. Those in favor of the standard believe that early antibiotic administration leads to improved outcomes while those not in favor of the standard believe it leads to the overuse of antibiotics. More research is needed to clarify the issue.⁵⁹

Independent Lung Ventilation

In patients with unilateral pneumonia or severely asymmetric pneumonia, this alternative mode of mechanical ventilation may be necessary to facilitate oxygenation. As the alveoli in the affected lung become flooded with pus, the lung becomes less compliant and difficult to ventilate. This results in a shifting of ventilation to the good lung without a concomitant shift in perfusion and thus an increase in V/Q mismatching. Independent lung ventilation (ILV) allows each lung to be ventilated separately, thus controlling the amount of flow, volume, and pressure each lung receives. A double-lumen endotracheal tube is inserted, and each lumen is usually attached to a separate mechanical ventilator. The ventilator settings are then customized to the needs of each lung to facilitate optimal oxygenation and ventilation.⁶⁰

Nursing Management

Nursing management of the patient with pneumonia incorporates a variety of nursing diagnoses (Box 20-9). Nursing interventions include optimizing oxygenation and ventilation, preventing the spread of infection, providing comfort and emotional support, and maintaining surveillance for complications. The patient’s response to the antibiotic therapy should be monitored for adverse effects.

Optimizing Oxygenation and Ventilation

Nursing interventions to optimize oxygenation and ventilation include positioning, preventing desaturation, and promoting secretion clearance. For further discussion on these interventions, see Nursing Management of Acute Lung Failure earlier in this chapter.

Preventing the Spread of Infection

Prevention should be directed at eradicating pathogens from the environment and interrupting the spread of organisms from person to person. Significant progress has been made in removing contaminants from the patient environment through proper disinfection of respiratory equipment and increased use of disposable supplies. Other possible environmental sources of pathogens include suctioning equipment and indwelling lines. These invasive tools must be given proper aseptic care.⁵⁵

Proper hand hygiene is the single most important measure available to prevent the spread of bacteria from person to person (Box 20-10). Hand hygiene should occur before and after touching a patient or their surroundings, before performing a procedure, and after exposure to any body fluids.⁶¹ In addition, meticulous oral care, including suctioning of the secretions pooling above the cuff of the artificial airway, is critical to decreasing the bacterial colonization of the oropharynx.⁵⁵ Oral care is further discussed in Chapter 21.

Collaborative management of the patient with pneumonia is outlined in Box 20-11.

Acid Liquid

The aspiration of acid (pH less than 2.5) liquid gastric contents results in the development of bronchospasm and atelectasis almost immediately. Over the next 4 hours, tracheal damage, bronchitis, bronchiolitis, alveolar-capillary breakdown, interstitial edema, and alveolar congestion and hemorrhage occur.⁶⁴ Severe hypoxemia develops as a result of intrapulmonary shunting and V/Q mismatching. As the disorder progresses, necrotic debris and fibrin fill the alveoli, hyaline membranes form, and hypoxic vasoconstriction occurs, resulting in elevated pulmonary artery pressures.^63,64 The clinical course will follow one of three patterns: 1) rapid improvement in 1 week; 2) initial improvement followed by deterioration and development of ARDS or pneumonia; or 3) rapid death from progressive ALF.⁶⁴

Acid Food Particles

The aspiration of acid (pH less than 2.5) nonobstructing food particles can produce the most severe pulmonary reaction because of extensive pulmonary damage. Severe hypoxemia, hypercapnia, and acidosis occur.^63,64

Nonacid Liquid

The aspiration of nonacid (pH greater than 2.5) liquid gastric contents is similar to acid liquid aspiration initially, but minimal structural damage occurs. Intrapulmonary shunting and V/Q mismatching usually start to reverse within 4 hours, and hypoxemia clears within 24 hours.^63,64

Nonacid Food Particles

The aspiration of nonacid (pH greater than 2.5) nonobstructing food particles is similar to acid aspiration initially, with significant edema and hemorrhage occurring within 6 hours. After the initial reaction, the response changes to a foreign-body-type reaction with granuloma formation occurring around the food particles within 1 to 5 days.⁶⁴ In addition to hypoxemia, hypercapnia and acidosis occur as a result of hypoventilation.^62,63

Optimizing Oxygenation and Ventilation

Nursing interventions to optimize oxygenation and ventilation include positioning, preventing desaturation, and promoting secretion clearance. For further discussion on these interventions, see Nursing Management of Acute Lung Failure earlier in this chapter.

Preventing Aspiration

One of the most important interventions for preventing aspiration is identifying the patient at risk for aspiration (Box 20-13). Actions to prevent aspiration include confirming feeding tube placement, checking for signs and symptoms of feeding intolerance, elevating the head of the bed at least 30 to 45 degrees, feeding the patient via a small-bore feeding tube or gastrostomy tube, avoiding the use of a large-bore nasogastric tube, ensuring proper inflation of artificial airway cuffs, and frequent suctioning of the oropharynx of an intubated patient to prevent secretions from pooling above the cuff of the tube. For patients at risk for aspiration or intolerant of gastric feedings, the feeding tube should be placed in the small bowel.⁶⁵

Collaborative management of the patient with aspiration pneumonitis is outlined in Box 20-14.

Increased Dead Space

An increase in alveolar dead space occurs because an area of the lung is receiving ventilation without being perfused. The ventilation to this area is known as wasted ventilation, because it does not participate in gas exchange. This effect leads to alveolar dead space ventilation and an increase in the work of breathing. To limit the amount of dead space ventilation, localized bronchoconstriction occurs.⁷⁰

Bronchoconstriction

Bronchoconstriction develops as a result of alveolar hypocarbia, hypoxia, and the release of mediators. Alveolar hypocarbia occurs as a consequence of decreased carbon dioxide in the affected area and leads to constriction of the local airways, increased airway resistance, and redistribution of ventilation to perfused areas of the lungs. A variety of mediators are released from the site of the injury, either from the clot or the surrounding lung tissue, which further causes constriction of the airways. Bronchoconstriction promotes the development of atelectasis.⁷⁰

Compensatory Shunting

Compensatory shunting occurs as a result of the unaffected areas of the lungs having to accommodate the entire CO. This creates a situation in which perfusion exceeds ventilation and blood is returned to the left side of the heart without participating in gas exchange. This leads to the development of hypoxemia.⁷⁰

Hemodynamic Consequences

The major hemodynamic consequence of a PE is the development of pulmonary hypertension, which is part of the effect of a mechanical obstruction when more than 50% of the vascular bed is occluded. In addition, the mediators released at the injury site and the development of hypoxia cause pulmonary vasoconstriction, which further exacerbates pulmonary hypertension. As the pulmonary vascular resistance increases, so does the workload of the right ventricle as reflected by a rise in pulmonary artery (PA) pressures. Consequently, right ventricular failure occurs, which can lead to decreases in left ventricular preload, CO, and blood pressure, and shock.^67–70

Pulmonary Effects

As the diameter of the airways decreases, airway resistance increases, resulting in increased residual volume, hyperinflation of the lungs, increased work of breathing, and abnormal distribution of ventilation. V/Q mismatching occurs, which results in hypoxemia. Alveolar dead space also increases as hypoxic vasoconstriction occurs, resulting in hypercapnia.⁷⁵

Cardiovascular Effects

Inspiratory muscle force also increases in an attempt to ventilate the hyperinflated lungs. This results in a significant increase in negative intrapleural pressure, leading to an increase in venous return and pooling of blood in the right ventricle. The stretched right ventricle causes the intraventricular septum to shift, thereby impinging on the left ventricle. In addition, the left ventricle has to work harder to pump blood from the markedly negative pressure in the thorax to elevated pressure in systemic circulation. This leads to a decrease in CO and a fall in systolic blood pressure on inspiration (pulsus paradoxus).⁷⁵

Bronchodilators

Inhaled beta₂-agonists and anticholinergics are the bronchodilators of choice for status asthmaticus. Beta₂-agonists promote bronchodilation and can be administered by nebulizer or metered-dose inhaler (MDI). Usually larger and more frequent doses are given, and the medication is titrated to the patient’s response. Anticholinergics that inhibit bronchoconstriction are not very effective by themselves, but in conjunction with beta₂-agonists, they have a synergistic effect and produce a greater improvement in airflow. The routine use of xanthines is not recommended in the treatment of status asthmaticus because they have been shown to have no therapeutic benefit.^75–78

A number of studies have focused on the bronchodilator abilities of magnesium. Although it has been demonstrated that magnesium is inferior to beta₂-agonists as a bronchodilator, in patients who are refractory to conventional treatment, magnesium may be beneficial. A bolus of 1 to 4 g of intravenous magnesium given over 10 to 40 minutes has been reported to produce desirable effects.^75,76,78

A number of other studies are evaluating the effects of leukotriene inhibitors such as zafirlukast, montelukast, and zileuton in the treatment of status asthmaticus. Leukotrienes are inflammatory mediators known to cause bronchoconstriction and airway inflammation. Research suggests that these agents may be beneficial as bronchodilators in those patients who are refractory to beta₂-agonists.⁷⁸

Systemic Corticosteroids

Intravenous or oral corticosteroids also are used in the treatment of status asthmaticus. Their anti-inflammatory effects limit mucosal edema, decrease mucus production, and potentiate beta₂-agonists. It usually takes 6 to 8 hours for the effects of the corticosteroids to become evident.⁷⁶ The use of inhaled corticosteroids for the treatment of status asthmaticus remains undecided at this time.^75,76 Initial studies indicate they may be beneficial in certain patient populations.⁷⁶

Oxygen Therapy

Initial treatment of hypoxemia is with supplemental oxygen. High-flow oxygen therapy is administered to keep the patient’s Spo₂ greater than 92%.⁷⁵ Another therapy currently under investigation is the use of heliox. A mixture of helium and oxygen, heliox has a lower density and higher viscosity than an oxygen and air mixture. Heliox is believed to reduce the work of breathing and improve gas exchange because it flows more easily through constricted areas. Studies have shown that it reduces air trapping and carbon dioxide and helps relieve respiratory acidosis.⁷⁵

Intubation and Mechanical Ventilation

Indications for mechanical ventilation include cardiac or respiratory arrest, disorientation, failure to respond to bronchodilator therapy, and exhaustion.^75,77,78 A large endotracheal tube (8 mm) should be used to decrease airway resistance and to facilitate suctioning of secretions. Ventilating the patient with status asthmaticus can be very difficult. High inflation pressures should be avoided because they can result in barotrauma. The use of PEEP should be monitored closely because the patient is prone to developing air trapping. Patient–ventilator asynchrony also can be a major problem. Sedation and neuromuscular paralysis may be necessary to allow for adequate ventilation of the patient.^75,77

Optimizing Oxygenation and Ventilation

Nursing interventions to optimize oxygenation and ventilation include positioning, preventing desaturation, and promoting secretion clearance. For further discussion on these interventions, see Nursing Management of Acute Lung Failure earlier in this chapter.

Educating the Patient and Family

Early in the patient’s hospital stay, the patient and family should be taught about asthma, its triggers, and its treatment (Box 20-21). As the patient moves toward discharge, teaching should focus on the interventions necessary for preventing the recurrence of status asthmaticus, early warning signs of worsening airflow obstruction, correct use of an inhaler and a peak flowmeter, measures to prevent pulmonary infections, and signs and symptoms of a pulmonary infection. If the patient smokes, he or she should be encouraged to stop smoking and be referred to a smoking cessation program. In addition, the importance of participating in a pulmonary rehabilitation program should be stressed.

Collaborative management of the patient with status asthmaticus is outlined in Box 20-22.

Pneumothorax

Regardless of the cause, the entry of air into the pleural space compresses the affected lung. As the lung collapses, the alveoli become underventilated, causing V/Q mismatching and intrapulmonary shunting. If the pneumothorax is large, hypoxemia ensues and ALF quickly develops. Increased pressure within the chest can lead to shifting of the mediastinum, compression of the great vessels, and decreased CO.^79,80

Barotrauma

After air enters the interstitial space, it travels though the pulmonary interstitium (pulmonary interstitial emphysema), out through the hilum, and into the mediastinum (pneumomediastinum), pleural space (pneumothorax), subcutaneous tissues (subcutaneous emphysema), pericardium (pneumopericardium), peritoneum (pneumoperitoneum), and retroperitoneum (pneumoretroperitoneum).⁸¹ Except for pneumothorax, the resultant disorders are usually fairly benign. Pneumomediastinum has been associated with decreased venous return and upper airway obstruction,⁸² and pneumopericardium has been associated with cardiac tamponade.⁸³

Tension Pneumothorax

A tension pneumothorax develops when air enters the pleural space on inhalation and cannot exit on exhalation. As pressure inside the pleural space increases, it results in collapse of the lung and shifting of the mediastinum and trachea to the unaffected side (see Fig. 20-6). The resultant effect is decreased venous return and compression of the unaffected lung. Clinical signs include diminished breath sounds, hyperresonance to percussion, tachycardia, and hypotension. Treatment comprises administration of supplemental oxygen and insertion of a large-bore needle or catheter into the second intercostal space at the midclavicular line of the affected side. This action relieves the pressure within the chest. The needle should remain in place until the patient is stabilized and a chest tube is inserted.^79,86

Tension Pneumopericardium

A tension pneumopericardium develops when air enters the pericardial space and has no outlet for exiting. As pressure inside the pericardium increases, it results in compression of the heart and the development of cardiac tamponade. A pericardiocentesis should be performed immediately to relieve the pressure within the pericardial sac.⁸³

Optimizing Oxygenation and Ventilation

Nursing interventions to optimize oxygenation and ventilation include positioning, preventing desaturation, and promoting secretion clearance. For further discussion on these interventions, see Nursing Management of Acute Lung Failure earlier in this chapter.

Maintaining the Chest Tube System

Maintaining the chest tube system involves careful attention to the suction applied and to maintenance of unobstructed drainage tubes. Kinks and large loops of tubing should be avoided, because they impede drainage and air evacuation, which may prevent timely lung re-expansion or may result in a tension pneumothorax. Retained drainage also becomes an excellent medium for bacterial growth. The water-seal chamber must routinely be observed for unexpected bubbling caused by an air leak in the system.⁸⁸

If unexpected bubbling is present, the source must be identified. To determine whether the source is within the system or within the patient, systematic brief clamping of the drainage tube should be performed. The nurse should place a padded clamp on the drainage tubing as close to the occlusive dressing as possible. If the air bubbling stops, the air leak is located between the patient and the clamp. The leak can be within the patient or at the insertion site. The clamp should then be removed and the chest tube site exposed. The tube should be inspected at the site where it enters the chest to ensure that all the eyelets are within the patient. If an eyelet port is outside the chest, it can be a source of an air leak and must be occluded, which may require the attention of the physician. After the insertion site has been eliminated as a leakage source, the chest dressing should be reapplied, completely and securely covering the site. If the air bubbling does not stop when a clamp is placed on the chest tube, the leak must be located between the clamp and the drainage collector. It can be found by releasing the clamp and moving it down the tubing a few inches at a time until the bubbling stops. After the area of the leak is located, it can be taped to re-establish a seal, or the system can be replaced.⁸⁸

A sterile occlusive dressing and a bottle of sterile water should be available at the patient’s bedside at all times. If the chest tube system is inadvertently interrupted, the tube should be placed a few centimeters into the bottle of water while the drainage system is re-established. A sterile occlusive dressing is applied to the chest wall if the chest tube is accidentally removed. Immediate implementation of these techniques minimizes or prevents the formation of a pneumothorax and avoids greater complications.

Throughout the duration of chest tube placement, the patient should be assessed periodically for re-expansion of the lung and for complications of chest tube drainage. The nurse should assess the thorax and lungs, paying particular attention to any tracheal deviation, asymmetry of chest movement, presence of subcutaneous emphysema, characteristics of breathing, quality of lung sounds, and presence of tympany or percussion sounds, which are indicative of pneumothorax.

Collaborative management of the patient with an air leak disorder is outlined in Box 20-24.

Preweaning Stage

For the long-term ventilator-dependent patient, the preweaning phase consists of resolving the precipitating event that necessitated ventilatory assistance and preventing the physiologic and psychologic factors that can interfere with weaning. Before any attempts at weaning, the patient should be assessed for weaning readiness, an approach should be determined, and a method should be selected.^92,93

Weaning Approach. 

Although weaning the patient requiring short-term mechanical ventilation is a relatively simple process that can usually be accomplished with a nurse and respiratory therapist, weaning the patient with LTMVD is a much more complex process that usually requires a multidisciplinary team approach. Multidisciplinary weaning teams that use a coordinated and collaborative approach to weaning have demonstrated improved patient outcomes and decreased weaning times. The team should consist of a physician; a nurse; a respiratory therapist; a dietitian; a physical therapist; and a case manager, a clinical outcomes manager, or a clinical nurse specialist. Additional members, if possible, should include an occupational therapist, a speech therapist, a discharge planner, and a social worker. Working together, the team members should develop a comprehensive plan of care for the patient that is efficient, consistent, progressive, and cost effective.⁹⁷ Several studies have demonstrated successful weaning through the use of nurse and respiratory therapist-managed protocols.⁹⁸

Collaborative management of the patient requiring long-term mechanical ventilation is outlined in Fig. 20-9.

Weaning Process Stage

For the long-term ventilator patient, the weaning process phase consists of initiating the weaning method selected and minimizing the physiologic and psychologic factors that can interfere with weaning.^91,92 It is imperative that the patient not become exhausted during this phase, because this can result in a setback in the weaning process.⁹⁵ During this phase, the patient is assessed for weaning progress and signs of weaning intolerance.⁹³

Weaning Outcome Stage

Two outcomes are possible for a patient with LTMVD: weaning completed and incomplete weaning.⁹³