Ventilation/Perfusion Mismatch

There are regions in healthy lungs where ventilation and perfusion are not evenly matched, so it seems logical that this is the most common cause of hypoxemia. RTs are familiar with this concept through the work of West,⁵ which described a high ratio at the apex of the lungs and a low ratio at the bases. This concept can be oversimplified and stated as there being more air than blood at the apices and more blood than air at the bases.

Pathologic mismatch occurs when disease disrupts this balance, and hypoxemia results (Figure 41-1, A). Most commonly, areas of low ratio are seen in which ventilation is compromised despite adequate blood flow. Obstructive lung diseases are frequent causes. The bronchospasm, mucous plugging, inflammation, and premature airway closure that signal asthmatic or emphysematous exacerbations worsen ventilation and create mismatch. Infection, heart failure, and inhalation injury may lead to partially collapsed or fluid-filled alveoli, also resulting in decreased ventilation and reduced blood O₂ levels.

Shunt

Shunt is an extreme version of mismatch in which there is no ventilation to match perfusion ( = 0). About 2% to 3% of the blood supply is shunted via the bronchial and thebesian veins that feed the lungs and heart; this is normal anatomic shunt. Pathologic anatomic shunt occurs as a result of right-to-left blood flow through cardiac openings (e.g., atrial or ventricular septal defects) or in pulmonary arteriovenous malformations. Physiologic shunt leads to hypoxemia when alveoli collapse or are filled with fluid or exudate. Common etiologies of physiologic shunting include atelectasis, pulmonary edema, and pneumonia. In contrast to mismatch, shunt does not respond to supplemental O₂ because the gas exchange unit (the alveolus) is not open (Figure 41-2, A).

Alveolar Hypoventilation

Alveolar hypoventilation is discussed subsequently in the section on Hypercapnic Respiratory Failure (Type II).

Diffusion Impairment

Diffusion refers to movement of gas across the alveolar-capillary membrane secondary to a pressure gradient. Although diffusion is rarely a cause of significant hypoxemia at rest, its effects become more pronounced with exercise, which limits the time for gas exchange. This time limitation is normally not a problem, unless diffusion impairment is present, in which case hypoxemia results. Diffusion impairment in interstitial lung disease may contribute 20% to 30% of the widening in the alveolar-arterial O₂ gradient during exercise.⁷ Diffusion impairment most commonly manifests in patients with interstitial lung disease (e.g., pulmonary fibrosis, asbestosis, sarcoidosis) in which the thickening and scarring of the interstitium undermine normal gas exchange. Emphysema, with its inherent alveolar destruction, also has subnormal transfer of O₂ and CO₂ between the alveolus and the capillary. The reduced ventilation in both diseases implies that mismatch also plays a role in the resulting hypoxemia.

Pulmonary vascular abnormalities can also lead to diffusion impairment. Anemia, pulmonary hypertension, and pulmonary embolus all may reduce capillary blood flow, resulting in diminished gas transfer.

Perfusion/Diffusion Impairment

Perfusion/diffusion impairment is a rare cause of hypoxemia found in individuals with liver disease complicated by hepatopulmonary syndrome.⁶ In this condition, right-to-left intracardiac shunt combines with dilated pulmonary capillaries resulting in impaired gas exchange. Specifically, the normal alveolar partial pressures of O₂ may be insufficient to drive the O₂ molecules to the center of the dilated pulmonary vasculature. Cirrhosis is the most common liver disease, and portal hypertension is usually present. Although shunt is a component of the syndrome, significant supplemental O₂ can overcome the gas transfer reduction owing to the dilated vessels, so this is commonly called a perfusion/diffusion defect.

Decreased Inspired Oxygen

Also clinically uncommon, hypoxemia may develop when the inspired O₂ is less than body requirements. The most common situation is at high altitude, where barometric pressure decreases, which results in a decrease in the partial pressure of inspired O₂. Although airlines account for this decrease in barometric pressure by pressurizing their cabins, travelers with chronic hypoxemia may still need supplemental O₂.⁸ Similarly, mountain climbers sometimes require O₂ masks. Cases of patient-O₂ disconnects and delivery of an incorrect gas source, which, it is hoped, occur rarely, are also included in this category.

Inspired O₂ less than 21% can be used diagnostically and therapeutically. The Hypoxia Altitude Simulation Test seeks to replicate inspired partial pressure of O₂ (PiO₂) during air travel by asking the potential traveler to inhale a hypoxic mixture. Inhaling at FiO₂ of 15% replicates the PiO₂ found at an altitude of 8000 feet (108 mm Hg). For a lower altitude of 5400 feet, an equivalent FiO₂ of 17% can be calculated.⁸ Infants with certain cyanotic congenital heart defects (e.g., hypoplastic left ventricle) may benefit from FiO₂ below room air level. In the preoperative state, low FiO₂ helps to prevent pulmonary dilation and the excessive pulmonary blood flow, which could flood the lungs.

Venous Admixture

A decrease in mixed venous O₂ increases the gradient by which O₂ needs to be stepped up as it passes through the lungs and can contribute to the development of hypoxemia. Congestive heart failure with low cardiac output is the most common cause of low mixed venous O₂, owing to increased peripheral extraction of O₂. Other causes include low hemoglobin concentration and increased O₂ consumption. A low mixed venous O₂ may have a significant effect on the ultimate arterial O₂ tension in the presence of lung disease. There may be other, more important coexisting determinants of hypoxemia, such as mismatch and shunting.³

Differentiating the Causes of Acute Hypoxemic Respiratory Failure

It is important to recognize the physiologic basis of each of the three main causes of hypoxemic respiratory failure (hypoventilation, mismatch, and shunt). Hypoventilation differs from the other causes in manifesting with a normal alveolar-to-arterial PO₂ difference [P(A − a)O₂] indicating normal lung parenchyma (Table 41-1). A clinical determination of this difference is made by subtracting PaO₂ from PAO₂ (partial pressure of alveolar O₂) derived from the alveolar air equation:

TABLE 41-1

Differentiating the Cause of Hypoxemia

Cause	P(a − a)O2	Response to Increased FiO2
Hypoventilation	Normal	Marked
Shunt	Increased	Minimal
mismatch	Increased	Marked

< ?xml:namespace prefix = "mml" />PAO2=FiO2(PB−PH2O)−PaCO2/R

where P_B is barometric pressure, P_H2O is water vapor tension, and R is the respiratory exchange ratio (0.8).

The P(A − a)O₂ ranges from 10 mm Hg in young patients to approximately 25 mm Hg in elderly patients while breathing room air (see the accompanying Rule of Thumb). In patients with hypoxemia caused by hypoventilation, treatment can be focused on improving ventilation because the hypoxemia is purely a result of alveolar displacement of O₂ by elevated CO₂.

 Rule of Thumb

The mean alveolar-to-arterial difference [P(A − a)O₂] in PO₂ increases slightly with age and can be estimated with the following equation:

Mean age-specific P(A−a)O2=(age/4)+4

Example: A 76-year-old person living at sea level:

P(A−a)O2=(76/4)+4=19+4=23 mm Hg

A mismatch and shunt both result in elevated P(A − a)O₂ levels, indicating that the resultant hypoxemia is due to an abnormality of lung tissue, requiring treatment to address that abnormality. When the RT encounters an increased P(A − a)O₂, a mismatch and shunt can be differentiated by means of O₂ administration (see Figures 41-1 and 41-2). A significant response to applying even small amounts of O₂ identifies mismatch as the cause of hypoxemia because altered P(A − a)O₂ has not been totally obliterated. True shunt shows little or no improvement in oxygenation even with 100% FiO₂ (see Table 41-1). As a result, treatment of intrapulmonary shunt must be directed toward opening collapsed alveoli or clearing fluid or exudative material before O₂ can be beneficial at below toxic levels. Testing to rule out anatomic shunt should be done in the right clinical setting (e.g., clear or black parenchyma on the chest radiograph).

Insidious Exposure

Although most cases of increased PaCO₂ are due to hypoventilation, an insidious exposure can occur in certain situations.

Increased Carbon Dioxide Production

Fever, agitation, exertion, shivering, hypermetabolism, and excess caloric intake all can result in an increase in , with consequent hypercapnia in patients with additional impairment in respiratory control and effector mechanisms.

Impairment in Respiratory Control

Inspiratory muscles are innervated by the phrenic and intercostal nerves via spinal cord transmission from the CNS. Both central (medullary) and peripheral (aortic and carotid bodies) chemoreceptors responding to CO₂ tension and O₂ tension stimulate the drive to breathe.⁹ This ventilatory drive can be diminished by various factors, such as drugs (overdose or sedation), bilateral carotid endarterectomy with incidental resection of the carotid bodies, brainstem lesions, diseases of the CNS such as multiple sclerosis or Parkinson disease, hypothyroidism, morbid obesity (e.g., obesity-hypoventilation), and sleep apnea. Other, less common potential causes include metabolic alkalosis, malnutrition, and sleep deprivation.¹⁰ Patients with metabolic encephalopathy or elevated intracranial pressure (ICP) may develop a reduced drive to breathe. Patients at risk of having a decreased ventilatory drive usually can be identified by their clinical situation (e.g., CNS insult, overdose of sedative medications). Significantly, many causes of central depression are easily reversible with treatment, so the clinician should be attentive to reversible causes.

The lung is basically a pump that inhales and exhales under the guidance of the CNS. In some patients, the CNS signal does not reach its goal, resulting in neuromuscular dysfunction. Examples include spinal trauma, motor neuron disease in which lesions of the anterior horn cells may gradually lead to progressive ventilatory failure (e.g., amyotrophic lateral sclerosis or poliomyelitis), motor nerve disorders (including Guillain-Barré syndrome and Charcot-Marie-Tooth disease), disorders of the neuromuscular junction (e.g., myasthenia gravis and botulism), and muscular diseases (including muscular dystrophy, myositis, critical care myopathy, and metabolic disorders).¹² These diseases range from irreversible and usually terminal (e.g., amyotrophic lateral sclerosis) to reversible and usually self-limiting (e.g., myasthenia and Guillain-Barré syndrome).¹²

Acute-on-Chronic Respiratory Failure

Chronic respiratory failure can be complicated by acute setbacks that create acute-on-chronic respiratory failure. Patients with chronic hypercapnic respiratory failure (chronic ventilatory failure) are at significant risk for this condition, as indicated by the fact that COPD is now the fourth leading cause of death in the United States.¹⁸ Acute-on-chronic respiratory failure can also be the presenting manifestation of neuromuscular disease in the setting of a concurrent pulmonary infection.¹⁹ Most common precipitating factors include bacterial or viral infections, congestive heart failure, pulmonary embolus, chest wall dysfunction, and medical noncompliance.^19–21 In these patients, the presence of respiratory failure cannot be judged by the normal ABG criteria but by a significant change from the baseline PaCO₂ to a level having the potential for morbidity and mortality.

Treatment goals include normalizing pH (avoiding mechanical ventilation if possible), elevating SaO₂ to 90% (if hypoxemia is also present), improving airflow, treating infection, monitoring and maintaining fluid status, and preventing or treating complications as necessary.16,20,21 Optimally treated patients with acute-on-chronic respiratory failure have shown improving hospital mortality rates despite the overall stagnant rates for respiratory failure in general.^22,23 Higher death rates are associated with factors such as significant baseline disease, a severe precipitating illness, severity of acidosis, and presence of complications.²³ The use of advance directives regarding a patient’s desire for mechanical ventilation influences short-term mortality. Episodes of acute respiratory failure in these patients seem to have a significant long-term influence with mortality rates reaching 49% within 2 years of an acute exacerbation.²²

Patients with chronic hypoxemic respiratory failure (type I) are at similar risk for acute deterioration of hypoxemia. Infection and heart failure can result in worsening of the tenuous oxygenation status of patients with interstitial pulmonary fibrosis or primary pulmonary hypertension.

Complications of Acute Respiratory Failure

Although respiratory failure is life-threatening by itself, complications frequently arise that can add significantly to morbidity and mortality. Especially in patients with ARDS, more deaths are due to complications (e.g., sepsis, multiorgan failure) than to the primary disease.²⁴ Modern ICUs with sophisticated mechanical ventilation can prolong but may not preserve life. Pulmonary complications such as emboli, barotrauma, and infection may be secondary to treatment strategies such as catheters, mechanical ventilation, and endotracheal tubes. A wide array of nonpulmonary complications exists, ranging from cardiac disorders (e.g., arrhythmias, hypotension) to gastrointestinal ailments (e.g., hemorrhage, dysmotility) to renal disturbances (e.g., acute renal failure, positive fluid balance). Bacteremia, malnutrition, and psychosis secondary to prolonged ICU stays can also seriously complicate an episode of acute respiratory failure.²⁴

Clinical Presentation

Clinically, a patient with respiratory muscle fatigue shows an initially increased respiratory rate followed by bradypnea (slowed respiratory rate) and apnea as fatigue ensues. Respiratory alternans, which is a phasic alteration between rib cage and abdominal breathing, may also occur. Opinions vary on the sensitivity and specificity of abdominal motion paradox in patients with respiratory muscle weakness, but at least some investigators suggest that respiratory muscle paradox is an early sign (see Chapter 15). When ventilatory failure is full-blown, ABG results show hypercapnia with acidosis. As mentioned earlier, the presence of hypercapnia with acidosis can also indicate that the respiratory center is not responding properly.²⁵

Tachypnea is the cardinal sign of increased work of breathing. Tachypnea occurs when the respiratory center increases breathing frequency in an attempt to lessen respiratory excursion and reduce the amount of work performed by the respiratory muscles.²⁶ Overall workload is reflected in the minute volume needed to maintain normocapnia.

Indications for Ventilatory Support

For each type of oxygenation and ventilatory failure, the goal of mechanical ventilation is either to support the patient until the underlying problem resolves or to maintain support of the patient with chronic ventilatory problems. These goals may be achieved by improving alveolar ventilation and arterial oxygenation, increasing lung volume, or reducing work of breathing.²⁷ This section discusses the indications for mechanical ventilation for hypoxemic (type I) and hypercapnic (type II) respiratory failure. Hypoxemic respiratory failure is divided into processes that require short-term and long-term ventilatory support. Hypercapnic respiratory failure is broken down into unstable ventilatory drive, muscle fatigue, excessive work of breathing, and alveolar hypoventilation. The relationship between work of breathing and the need for mechanical ventilation is discussed. Numerical indicators of the need for ventilatory support are reviewed. Management that is specific for each type of respiratory failure is described, including the indications for less commonly used modes of ventilation. Finally, the specific management of patients with obstructive lung disease and patients with head injury is discussed.

Parameters Indicating Need for Ventilatory Support

Although various measurements have been proposed to help decide if a patient needs mechanical ventilation, the clinical status of the patient is the most important criterion. Table 41-3 and the discussion that follows review common physiologic indicators for initiating support by the underlying cause of respiratory failure.

TABLE 41-3

Physiologic Indicators for Ventilatory Support, Classified by Mechanism Underlying Respiratory Failure

Mechanism	Normal Values	Support Indicated
Inadequate Alveolar Ventilation
PaCO2 (mm Hg)	35-45	>55
pH	7.35-7.45	<7.20
Inadequate Lung Expansion
Tidal volume (VT) ml/kg	5-8	<5
Vital capacity (VC) ml/kg	65-75	<10
Respiratory rate	12-20	>35
Inadequate Muscle Strength
Maximum inspiratory pressure (cm H2O)	−80-100	≥−20
Vital capacity (VC, ml/kg)	65-75	<10
Maximum voluntary ventilation (MVV, L/min)	120-180	<2× VE
Increased Work of Breathing
Minute ventilation ()	5-6	>10
VD/VT (%)	0.25-0.40	>0.6
Hypoxemia
P(A − a)O2 on 100% O2 (mm Hg)	25-65	>350
PaO2/FiO2	350-450	<200

VE, Minute ventilation.

Hypoxemic Respiratory Failure

Severe, refractory hypoxemia is a common indication for intubation and ventilator support. Table 41-3 lists different measures of hypoxemia that have been used to assess the need for ventilatory support. Most commonly, PaO₂ is compared with FiO₂ as with the PaO₂/FiO₂ ratio or the alveolar-arterial O₂ difference [P(A − a)O₂]. Indicators of profoundly impaired oxygenation suggesting the need for intubation, high inspired O₂ administration, and PEEP include P(A − a)O₂ value of 350 mm Hg on FiO₂ of 1.0 or a PaO₂/FiO₂ value of less than 200. These values are useful for all causes of hypoxemic respiratory failure (type I) but cannot help distinguish if the process is a readily reversible one, such as pulmonary edema or atelectasis, or a process, such as acute lung injury, that resolves more slowly. Frequently, patients have a combination of hypoxemic and hypercapnic respiratory failure.

Hypercapnic Respiratory Failure (Ventilatory Failure)

As previously discussed, hypercapnic (type II) respiratory failure or ventilatory failure can be caused by increased ventilatory dead space, increased CO₂ production, or decreased alveolar ventilation. All of these processes cause an increase in PaCO₂.²⁵ Assessment of the pH allows a determination of whether the problem is acute or chronic. Chronic hypoventilation is compensated by the kidneys’ retention of bicarbonate, although this response requires several days. The following example shows the importance of pH in interpreting the significance of elevated PaCO₂.

	Patient A	Patient B
PaCO2	60 mm Hg	60 mm Hg
Serum HCO3−	25 mEq/L	36 mEq/L
pH	7.25	7.38

Although both patients in this example have the same level of hypercapnia, only patient A exhibits acute ventilatory failure with an elevated PaCO₂ but normal serum bicarbonate (25 mEq/L). Patient B has a compensated respiratory acidosis from chronic hypercapnic respiratory failure, as indicated by the normal pH and elevated serum bicarbonate (36 mEq/L). This condition is also known as chronic ventilatory failure. The distinction between acute and chronic ventilatory failure is very important in respiratory care and emphasizes the need to use both PaCO₂ and pH as indicators for ventilatory support. The trend in pH and PaCO₂ values is also useful in assessing the effects of therapies in correcting acute ventilatory failure.

Significance of Elevated Alveolar Partial Pressure of Carbon Dioxide

Because elevated PaCO₂ increases ventilatory drive in healthy subjects, the existence of hypoventilation suggests other problems with the respiratory apparatus. Specifically, the presence of acute respiratory acidosis indicates one of three major problems: (1) The respiratory center is not responding normally to elevated PaCO₂; (2) the respiratory center is responding normally, but the signal is not getting through to the respiratory muscles; or (3) despite normal neurologic response mechanisms, the lungs and chest bellows are incapable of providing adequate ventilation because of parenchymal lung disease or muscular weakness.²⁸

Respiratory Muscle Fatigue

Fatigue is usually defined as a condition in which there is loss of the capacity to develop force or velocity of a muscle resulting from muscle activity under load, which is reversible by rest.³² Fatigue can be assessed by measuring the loss of force in response to repeated stimulations. It can be caused by both specific demands placed on the muscle and reduced supply of necessary nutrients. The demand on a muscle is increased by increased work of breathing, increased strength of muscle contraction, and decreased muscle efficiency. Hypoxemia, decreased inspiratory muscle blood flow, poor nutrition, and inability of a muscle to extract energy from supplied substrates can lead to fatigue as well.²⁹

There are three types of respiratory muscle fatigue. (1) Central muscle fatigue is an exertion-induced, reversible decrease in central respiratory drive; (2) transmission muscle fatigue is an exertion-induced, reversible impairment in the transmission of neural impulses; and (3) contractile muscle fatigue is a reversible impairment in the contractile response to a neural impulse in an overloaded muscle.²⁸

Respiratory Failure

Respiratory failure is an unfavorable imbalance between a respiratory workload, on the one hand, and ventilatory muscle strength and endurance, on the other hand. The tension-time index takes into account the fact that respiratory muscle endurance depends both on the size of the respiratory load in relation to respiratory strength (P_di/P_dimax) and on the duration of the inspiratory effort in relation to total breath time (the duty cycle, or T_i/T_tot). This index (P_di/P_dimax) × (T_i/T_tot) determines whether a respiratory load can be tolerated without development of failure: Values less than 0.15 are generally tolerated for a long period, whereas indices greater than 0.18 usually result in fatigue and respiratory failure within 45 minutes.³³ Comparing the spontaneous minute ventilation with MVV is also a helpful index because fatigue and failure are both likely to occur if the minute ventilation exceeds 60% of MVV.³⁴

These closely related concepts of weakness, fatigue, and failure usually overlap and can result in acute or chronic respiratory failure. Respiratory muscle weakness can predispose to ventilatory muscle fatigue. Whether fatigue consistently leads to failure has historically been the subject of much debate.³⁵ In one study, weaning failure was not accompanied by fatigue of the diaphragm despite the presence of diaphragm weakness.³⁶ Alternatively, fatigue of the diaphragm lasting for 24 hours is reliably present after hyperventilation at 60% of MVV or greater until task failure.^34,37

Work of Breathing

Work of breathing is the amount of pressure needed to move a given volume into the lung with a relaxed chest wall. Excessive work of breathing is the most common cause of respiratory muscle fatigue. Work of breathing is due to physiologic work and imposed work. Physiologic work involves overcoming the elastic forces during inspiration and overcoming the resistance of the airways and lung tissue. Normal work of breathing is 0.3 to 0.6 J/L. Airway and pulmonary parenchymal abnormalities can increase the physiologic work of breathing. In intubated patients, sources of imposed work of breathing include the endotracheal tube, ventilator circuit, and auto-PEEP secondary to dynamic hyperinflation with airflow obstruction, as is commonly seen in a patient with COPD.²⁶ Increased work of breathing can also be an impediment to weaning.³⁸ Measurement of work of breathing with an esophageal balloon catheter and a flow transducer has been used to determine work of breathing and break it down into physiologic and imposed components.³⁸ Kirton and colleagues³⁹ showed that 96% of patients with a physiologic work of breathing less than 0.8 J/L were successfully weaned and extubated from ventilatory support.

Noninvasive Ventilation

A consensus report supports the use of noninvasive support of ventilation to reduce the morbidity and possibly the mortality of both hypoxemic and hypercarbic respiratory failure.⁴⁰ In this context, noninvasive ventilation (NIV) can be defined as any mode of ventilatory support that is provided without endotracheal intubation, encompassing continuous positive airway pressure (CPAP) alone or in combination with any mode of pressure-limited or volume-limited ventilation.⁴⁰ NIV can improve hypoxemia and hypercarbia via several mechanisms including but not limited to (1) compensating for the inspiratory threshold load imposed by intrinsic PEEP,⁴¹ (2) supplementing a reduced tidal volume,⁴² (3) partial or complete unloading of the respiratory muscles,⁴² (4) reducing venous return and left ventricular afterload,^43,44 (5) alveolar recruitment,⁴⁵ (6) preventing intermittent narrowing and collapse in patients with concomitant obstructive sleep apnea hypopnea syndrome by acting as a pneumatic splint during sleep,⁴⁶ and (7) improving lung function (particularly functional residual capacity) and daytime gas exchange in obstructive sleep apnea hypopnea syndrome.⁴⁷ NIV currently has indications in both acute⁴⁸ and chronic⁴⁹ respiratory failure.

NIV is considered to be a standard of care practice in patients with exacerbations of COPD.⁵⁰ A meta-analysis of eight randomized controlled trials showed that NIV combined with usual care in exacerbations of COPD resulted in a lower relative risk (RR) of treatment failure (defined as mortality, need for intubation, or intolerance) of 0.51 in favor of NIV (number needed to treat [NNT] to prevent 1 treatment failure was 5), reduced risk of intubation (RR 0.43, NNT = 5), reduction in mortality (RR 0.41, NNT = 8), reduced risk of complications (RR 032, NNT = 3), and reduced hospital length of stay by about 3 days.⁵⁰

Current recommendations are to initiate NIV before the development of severe acidosis in the course of a COPD exacerbation with PaCO₂ greater than 45 mm Hg.⁵⁰ Otherwise, in patients with mild COPD exacerbations (pH > 7.35), NIV was no more effective than standard medical therapy in preventing the occurrence of acute respiratory failure, improving mortality, or reducing length of hospitalization.⁵¹ Nearly 50% of the patients did not tolerate NIV.⁵¹

Obesity-hypoventilation syndrome refers to the presence of daytime hypercapnia (PaCO₂ > 45 mm Hg) in obese individuals when no other cause of hypoventilation is present. In a meta-analysis, factors associated with daytime hypercapnia included body mass index, the presence of nocturnal apnea hypopnea, mean overnight O₂ saturation, and severity of restrictive pulmonary function.⁶¹ In a study of patients with obesity-hypoventilation syndrome who failed initial CPAP treatment, average volume-assured pressure support, a form of NIV in which pressure support is automatically adjusted to reach a set tidal volume, was found to lower PaCO₂ compared with bilevel positive airway pressure alone but without improving oxygenation, sleep quality, or quality of life.⁶²

Neuromuscular Diseases and Thoracic Cage Abnormalities

This condition most commonly applies to chronic neuromuscular disease, with several studies showing that even in progressive neuromuscular disorders, NIV can prolong survival, improve quality of life, enhance cognitive function, and reduce pneumonia and hospitalization rates.¹² Other NIV techniques using rocking beds, pneumobelts, and negative pressure ventilation are much less frequently used and are becoming less easily available.

Mini Clini

Indications for Continuous Positive Airway Pressure versus Continuous Mechanical Ventilation With Positive End Expiratory Pressure

 Problem

A patient in the ICU is severely tachypneic and hypoxemic. The respiratory rate is 30 breaths/min. On approximately 50% O₂ by mask at sea level, PaO₂ is 50 mm Hg, PaCO₂ is 30 mm Hg, pH is 7.51, and HCO₃⁻ is 23 mEq/L. The patient is in distress but alert and able to cooperate and follow instructions.

1. What is this patient’s P(A − a)O₂?

2. What type of respiratory failure is this?

3. What is the appropriate initial therapy?

Discussion

This patient does not have hypercapnic respiratory failure, as is confirmed by PaCO₂ of 30 mm Hg. The patient does have a serious oxygenation defect, as confirmed by P(A − a)O₂.

PAO2=0.50 (713)−30/0.8=318 mm Hg

P(A−a)O2=318−50=268 mm Hg

The elevated P(A − a)O₂ indicates the presence of severe intrapulmonary shunt. Shunts this severe can occur only when significant airway closure and atelectasis are present. The mode of therapy should be aimed at reinflating collapsed alveoli and keeping the alveoli open throughout the breathing cycle. In this patient, alveolar ventilation is not impaired (PaCO₂ = 30 mm Hg). CPAP alone may be effective in reducing shunt. (CPAP does not ventilate the patient; all breaths are patient-initiated and spontaneous.) CPAP may be applied noninvasively via face mask, as would be indicated in this alert, cooperative patient. If hypercapnia and acidemia develop, mechanical ventilation with PEEP would be indicated.

Invasive Ventilatory Support

Patients with profound hypoxemia from a process that is expected to resolve slowly, such as acute lung injury, usually require intubation and mechanical ventilation. Other indications for intubation include conditions where NIV may be poorly tolerated or even deleterious, such as the presence of upper airway obstruction, inability to clear secretions and protect airway, inability to achieve a proper mask fit, and intolerance of the intervention. Both hypoxemic and hypercarbic types of respiratory failure can be managed effectively by invasive mechanical ventilation.

Mini Clini

Acute Hypercapnic Respiratory Failure

 Problem

A patient with COPD presents to the emergency department in moderate respiratory distress. He is alert and cooperative. Respiratory rate is 26 breaths/min. Lung examination shows poor air entry with expiratory wheezing. Room air ABGs show pH 7.24, PaCO₂ 60 mm Hg, and PaO₂ 60 mm Hg.

1. What type of respiratory failure is this?

2. How should the patient be managed?

Discussion

ABGs show an acute respiratory acidosis with normal PaO₂ − PaO₂ gradient.

PAO2=0.21 (713)−60/0.8=74

P(A−a)O2=74−60=14 mm Hg

This patient has hypercapnic respiratory failure related to obstructive lung disease, also known as ventilatory failure. In addition to bronchodilators and corticosteroids, the RT should aim to improve ventilation to reverse the respiratory acidosis. In this patient, who is alert and cooperative, NIV via face mask may be tried. Initial mask ventilation can start in the pressure support ventilation mode with a level of support of 10 cm H₂O and 5 cm H₂O PEEP. Tidal volume should be maintained at approximately 6 to 8 ml/kg. If this patient deteriorates despite therapy, he would need to be intubated and mechanically ventilated.

There are several ventilator variables, some independently set by the operators and others that are dependent on the set variables. Independent and dependent variables vary with the mode of ventilation. FiO₂ and PEEP are independently set variables regardless of mode of ventilation used to manage hypoxemia. In volume-controlled or flow-controlled ventilation, tidal volume, flow, and respiratory rate are independently set variables. In pressure control ventilation, driving pressure, inspiratory time, and respiratory rate are independently set variables. Other modes and strategies include inverse ratio ventilation, liquid ventilation, prone positioning, airway pressure release ventilation, and high-frequency ventilation. Considerations in selected cases of respiratory failure requiring invasive ventilatory support are briefly reviewed.