Nursing Management: Respiratory Failure and Acute Respiratory Distress Syndrome



Nursing Management


Respiratory Failure and Acute Respiratory Distress Syndrome


Richard Arbour




Learning Outcomes



1. Compare the pathophysiologic mechanisms and clinical manifestations that result in hypoxemic and hypercapnic respiratory failure.


2. Differentiate between the nursing and collaborative management of the patient with hypoxemic or hypercapnic respiratory failure.


3. Relate the pathophysiologic mechanisms and the clinical manifestations associated with acute lung injury and acute respiratory distress syndrome (ARDS).


4. Select appropriate nursing and collaborative management strategies for the patient with ARDS.


5. Prioritize measures to prevent or reverse complications that may result from acute respiratory failure or ARDS.



Key Terms













Reviewed by Susan J. Eisel, RN, MSEd, Associate Professor of Nursing, Mercy College of Ohio, Toledo, Ohio; Eleanor Fitzpatrick, RN, MSN, CCRN, Clinical Nurse Specialist, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania; and Amanda Jones Moose, RN, BSN, Nursing Faculty, Caldwell Community College and Technical Institute, Taylorsville, North Carolina.


This chapter discusses the etiology, pathophysiology, and clinical manifestations of acute respiratory failure and acute respiratory distress syndrome (ARDS). Nursing and collaborative management of patients with respiratory failure and ARDS focuses on interventions to promote adequate oxygenation and ventilation while addressing the underlying causes.



Acute Respiratory Failure


The major function of the respiratory system is gas exchange. This involves the transfer of oxygen (O2) and carbon dioxide (CO2) between atmospheric air and circulating blood within the pulmonary capillary bed (Fig. 68-1). Respiratory failure results when one or both of these gas-exchanging functions are inadequate (e.g., insufficient O2 is transferred to the blood or inadequate CO2 is removed from the lungs). Diseases that interfere with adequate O2 transfer result in hypoxemia. This causes a decrease in arterial O2 (PaO2) and saturation (SaO2). Insufficient CO2 removal results in hypercapnia. This causes an increase in arterial CO2 (PaCO2).1–4


image
FIG. 68-1 Normal gas exchange unit in the lung.

Arterial blood gases (ABGs) are used to assess changes in pH, PaO2, PaCO2, bicarbonate, and SaO2. Pulse oximetry is used intermittently or continuously to assess arterial O2 saturation (SpO2).




image eNursing Care Plan 68-1   Patient With Acute Respiratory Failure




Patient Goal


Maintains adequate tissue oxygenation as indicated by normal or baseline arterial blood gases












Outcomes (NOC) Interventions (NIC) and Rationales








image




Patient Goals







Patient Goal


Demonstrates normal or baseline respiratory rate, rhythm, and depth of respirations












Outcomes (NOC) Interventions (NIC) and Rationales







image




Patient Goals







Patient Goals





ABGs, Arterial blood gases; CVP, central venous pressure; MAP, mean arterial pressure; PaCO2, partial pressure of carbon dioxide in arterial blood; PaO2, partial pressure of oxygen in arterial blood; PAP, pulmonary artery pressure; PAWP, pulmonary artery wedge pressure; SaO2, oxygen saturation in arterial blood measured by ABGs; ScvO2, central venous oxygen saturation; SpO2, oxygen saturation in arterial blood measured by pulse oximetry; SvO2, mixed venous oxygen saturation; SVV, stroke volume variation.


*Nursing diagnoses listed in order of priority.




eTABLE 68-1


PREDISPOSING FACTORS FOR ACUTE RESPIRATORY FAILURE























































Predisposing Factors Mechanisms of Respiratory Failure
Airways and Alveoli
Acute respiratory distress syndrome
 Fluid enters the interstitial space and subsequently the alveoli, markedly impairing gas exchange. The result is an initial ↓ in PaO2 and later an ↑ in PaCO2. A low-flow state to pulmonary capillaries can result in ischemic injury to lung tissues with loss of integrity of the alveolar-capillary membrane.
Asthma Bronchospasm escalates in severity rather than responding to therapy. Bronchospasm, edema of the bronchial mucosa, and plugging of small airways with secretions greatly reduce airflow. Work of breathing increases, causing respiratory muscle fatigue. ↓ PaO2 and ↑ PaCO2.
Chronic obstructive pulmonary disease (COPD) Alveoli are destroyed by protease-antiprotease imbalance or respiratory infection. Exacerbation of COPD escalates in severity rather than responding to therapy. Secretions obstruct airflow. Work of breathing increases and causes respiratory muscle fatigue. ↓ PaO2 and ↑ PaCO2.
Cystic fibrosis Abnormal Na+ and Cl− transport produces secretions that are viscous, poorly cleared, and therefore foci for infection. Over time the airways become clogged with copious, purulent, often greenish-colored sputum. Secretions obstruct airflow. Repeated infections destroy alveoli. Work of breathing increases, causing respiratory muscle fatigue. ↓ PaO2 and ↑ PaCO2.
Central Nervous System
Opioid or other drug overdose with CNS depressant Respirations slowed by drug effect. Insufficient CO2 is excreted, resulting in ↑ PaCO2.
Brainstem infarction, head injury Medulla cannot alter respiratory rate in response to changes in PaCO2. Total loss of respiratory drive secondary to severe brainstem injury.
Massive inflammatory state from release of inflammatory mediators and cytokines from dead and/or dying brain tissue causes direct injury to lung tissue and interferes with gas exchange at alveolar-capillary interface.
Neurogenic pulmonary edema resulting from massive catecholamine release and shunting intravascular volume to central/pulmonary circulation Fluid entry into alveoli consequent to markedly elevated hydrostatic pressure, decreasing gas exchange and causing hypoxemia.
Chest Wall
Severe soft tissue injury, flail chest, rib fracture, pain Prevent normal rib cage expansion, resulting in inadequate gas exchange.
Kyphoscoliosis Change in spinal configuration compresses the lungs and prevents normal expansion of the chest wall.
Severe obesity Weight of the chest and abdominal contents prevents normal rib cage movement and excursion of diaphragm.
Neuromuscular Conditions
Cervical spinal cord injury, phrenic nerve injury Neural control is lost, preventing use of the diaphragm (major muscle of respiration). As a consequence, the patient inspires a smaller tidal volume, which predisposes to an ↑ in PaCO2. Diaphragm is innervated at C4 spinal cord level. With an injury at or above C4, risk for permanent ventilator dependence.
Amyotrophic lateral sclerosis (ALS), Guillain-Barré syndrome, muscular dystrophy, multiple sclerosis, poliomyelitis, myasthenia gravis, myopathy, critical illness polyneuropathy, prolonged effects of neuromuscular blocking agents Respiratory muscle weakness or paralysis occurs, preventing normal CO2 excretion. Dysfunction may be slowly progressive (e.g., muscular dystrophy, multiple sclerosis), progressive with no potential of recovery (e.g., ALS), rapid with good expectation of recovery (e.g., Guillain-Barré syndrome), or stable for extended periods of time (e.g., poliomyelitis, myasthenia gravis).
Toxin exposure: acetylcholinesterase inhibitors Prolonged cholinergic crisis, respiratory muscle weakness/paralysis and hypersecretory state. Lung ventilation impaired because of respiratory muscle weakness, as well as excessive lung secretions within airways and alveoli.


image


CNS, Central nervous system.


Respiratory failure is not a disease but a symptom of an underlying pathologic condition affecting lung function, O2 delivery, cardiac output (CO), or the baseline metabolic state. It is a condition that occurs because of one or more diseases involving the lungs or other body systems (Table 68-1 and eTable 68-1 [available on the website for this text]). Respiratory failure is classified as hypoxemic or hypercapnic (Fig. 68-2). Hypoxemic respiratory failure is also referred to as oxygenation failure because the primary problem is inadequate O2 transfer between the alveoli and the pulmonary capillaries. Although no universal definition exists, hypoxemic respiratory failure is commonly defined as a PaO2 less than 60 mm Hg when the patient is receiving an inspired O2 concentration of 60% or more. This definition incorporates two important concepts: (1) the PaO2 level indicates inadequate O2 saturation of hemoglobin, and (2) this PaO2 level exists despite administration of supplemental O2 at a percentage (60%) that is about three times that in room air (21%).5–7



image
FIG. 68-2 Classification of respiratory failure.

Hypercapnic respiratory failure is also referred to as ventilatory failure because the primary problem is insufficient CO2 removal. Hypercapnic respiratory failure is commonly defined as a PaCO2 greater than 45 mm Hg in combination with acidemia (arterial pH less than 7.35). This definition incorporates three important concepts: (1) the PaCO2 is higher than normal, (2) there is evidence of the body’s inability to compensate for this increase (acidemia), and (3) the pH is at a level where a further decrease may lead to severe acid-base imbalance. (See Chapter 17 for a discussion of acid-base balance.) Numerous disorders can compromise lung ventilation and subsequent carbon dioxide removal (see Table 68-1 and eTable 68-1).


Many patients experience both hypoxemic and hypercapnic respiratory failure.6–9 Always interpret data within the context of your assessment findings and the patient’s baseline. For example, a person with chronic lung disease may have a baseline PaCO2 higher than “normal.”



Etiology and Pathophysiology


Hypoxemic Respiratory Failure.


Four physiologic mechanisms may cause hypoxemia and subsequent hypoxemic respiratory failure: (1) mismatch between ventilation (V) and perfusion (Q), commonly referred to as V/Q mismatch; (2) shunt; (3) diffusion limitation; and (4) alveolar hypoventilation. The most common causes are V/Q mismatch and shunt.



Ventilation-Perfusion Mismatch.

In normal lungs the volume of blood perfusing the lungs each minute (4 to 5 L) is approximately equal to the amount of gas that reaches the alveoli each minute (4 to 5 L). In a perfectly matched system, each portion of the lung would receive 1 mL of air (ventilation) for each 1 mL of blood flow (perfusion). This match of ventilation and perfusion would result in a V/Q ratio of 1:1, which is expressed as V/Q = 1. When the match is not 1:1, a V/Q mismatch occurs.


Although this example implies that ventilation and perfusion are ideally matched in all areas of the lung, this situation does not normally exist. In reality, some regional mismatch occurs. At the lung apex, V/Q ratios are greater than 1 (more ventilation than perfusion). At the lung base, V/Q ratios are less than 1 (less ventilation than perfusion). Because changes at the lung apex balance changes at the base, the net effect is a close overall match (Fig. 68-3).


image
FIG. 68-3 Regional V/Q differences in the normal lung. At the lung apex, the V/Q ratio is 3.3, at the midpoint 1.0, and at the base 0.63. This difference causes the PaO2 to be higher at the apex of the lung and lower at the base. Values for PaCO2 are the opposite (i.e., lower at the apex and higher at the base). Blood that exits the lung is a mixture of these values.

Many diseases and conditions cause V/Q mismatch (Fig. 68-4). The most common are those in which increased secretions are present in the airways (e.g., chronic obstructive pulmonary disease [COPD]) or alveoli (e.g., pneumonia), and in which bronchospasm is present (e.g., asthma).5–8 V/Q mismatch may also result from alveolar collapse (atelectasis) or as a result of pain. Pain interferes with chest and abdominal wall movement and compromises ventilation. Additionally, it increases muscle tension, producing generalized muscle rigidity. Pain also causes systemic vasoconstriction and activates the stress response. Finally, it increases O2 consumption and CO2 production.10 In this case, increased O2 demand and CO2 production may increase ventilation demands. All these conditions result in limited airflow (ventilation) to alveoli but have no effect on blood flow (perfusion) to the gas exchange units (see Fig. 68-1). The consequence of the imbalance is V/Q mismatch.


image
FIG. 68-4 Range of ventilation-to-perfusion (V/Q) relationships. A, Absolute shunt, no ventilation because of fluid filling the alveoli. B, V/Q mismatch, ventilation partially compromised by secretions in the airway. C, Normal lung unit. D, V/Q mismatch, perfusion partially compromised by emboli obstructing blood flow. E, Dead space, no perfusion because of obstruction of the pulmonary capillary.

A pulmonary embolus affects the perfusion portion of the V/Q relationship. The embolus limits blood flow but has no effect on airflow to the alveoli, again causing V/Q mismatch11 (see Fig. 68-4). If large enough, the embolus can cause hemodynamic compromise due to the blockage of a large pulmonary artery.


O2 therapy is an appropriate first step to reverse hypoxemia caused by V/Q mismatch because not all gas exchange units are affected. O2 therapy increases the PaO2 in blood leaving normal gas exchange units, thus causing a higher than normal PaO2. The well-oxygenated blood mixes with poorly oxygenated blood, raising the overall PaO2 of blood leaving the lungs. The optimal approach to treating hypoxemia caused by a V/Q mismatch is directed at the cause.



Shunt.

A shunt occurs when blood exits the heart without having participated in gas exchange. A shunt can be viewed as an extreme V/Q mismatch (see Fig. 68-4). There are two types of shunt: anatomic and intrapulmonary. An anatomic shunt occurs when blood passes through an anatomic channel in the heart (e.g., a ventricular septal defect) and bypasses the lungs. An intrapulmonary shunt occurs when blood flows through the pulmonary capillaries without participating in gas exchange. Intrapulmonary shunt is seen in conditions in which the alveoli fill with fluid (e.g., acute respiratory distress syndrome [ARDS], pneumonia).


O2 therapy alone is often ineffective in increasing the PaO2 if hypoxemia is due to shunt. Patients with shunt are usually more hypoxemic than patients with V/Q mismatch. They often require mechanical ventilation and a high fraction of inspired O2 (FIO2) to improve gas exchange.



Diffusion Limitation.

Diffusion limitation occurs when gas exchange across the alveolar-capillary interface is compromised by a process that thickens, damages, or destroys the alveolar membrane or affects blood flow through the pulmonary capillaries (Fig. 68-5). Diffusion limitation is worsened by disease states affecting the pulmonary vascular bed such as severe COPD or recurrent pulmonary emboli. Some disease states cause the alveolar-capillary interface to become thicker (fibrotic), which slows gas transport. These include pulmonary fibrosis, interstitial lung disease, and ARDS.12,13


image
FIG. 68-5 Diffusion limitation. Exchange of CO2 and O2 cannot occur because of the thickened alveolar-capillary membrane.

The classic sign of diffusion limitation is hypoxemia that is present during exercise but not at rest. During exercise, blood moves more rapidly through the lungs, decreasing the time for diffusion of O2 across the alveolar-capillary interface. Diffusion limitation may also occur in a high CO state (e.g., hepatopulmonary syndrome) or other disease states (e.g., inflammatory response seen with pancreatitis or severe brain trauma) unrelated to lung tissue damage. In this situation, CO is markedly elevated and vascular resistance is low. Blood circulates through the pulmonary capillary bed rapidly, allowing less time for gas exchange to occur.14





Hypercapnic Respiratory Failure.

Hypercapnic respiratory failure results from an imbalance between ventilatory supply and ventilatory demand. Ventilatory supply is the maximum ventilation (gas flow in and out of the lungs) that the patient can sustain without developing respiratory muscle fatigue. Ventilatory demand is the amount of ventilation needed to keep the PaCO2 within normal limits. Normally, ventilatory supply far exceeds ventilatory demand. Therefore people with normal lung function can engage in strenuous exercise, which greatly increases CO2 production without an increase in PaCO2. Patients with lung disease such as severe COPD do not have this advantage and cannot effectively increase lung ventilation in response to exercise or metabolic demands.


Hypercapnia occurs when ventilatory demand exceeds ventilatory supply and PaCO2 cannot be sustained within normal limits. Hypercapnia reflects substantial lung dysfunction. Hypercapnic respiratory failure is sometimes called ventilatory failure because the primary problem is the respiratory system’s inability to remove sufficient CO2 to maintain a normal PaCO2. Hypercapnic respiratory failure is also described as acute or chronic respiratory failure. For example, an episode of respiratory failure may represent an acute decompensation in a patient whose underlying lung function has deteriorated to the point that some degree of decompensation is always present (chronic respiratory insufficiency).


Many different diseases can cause a limitation in ventilatory supply (see Table 68-1 and eTable 68-1). These diseases can be grouped into four categories: (1) abnormalities of the airways and alveoli, (2) abnormalities of the CNS, (3) abnormalities of the chest wall, and (4) neuromuscular conditions.16,17




Central Nervous System Abnormalities.

A variety of CNS problems may suppress the drive to breathe. A common example is an overdose of a respiratory depressant drug (e.g., opioids, benzodiazepines). In a dose-related manner, CNS depressants decrease CO2 reactivity in the brainstem. This allows arterial CO2 levels to rise. A brainstem infarction or severe head injury may also interfere with normal function of the respiratory center in the medulla. Patients with these conditions are at risk for respiratory failure because the medulla does not alter the respiratory rate in response to a change in PaCO2. CNS dysfunction may also include high-level spinal cord injuries that limit nerve supply to the respiratory muscles of the chest wall and diaphragm. Apart from direct brainstem dysfunction, metabolic or structural brain injury resulting in decreased or loss of consciousness may interfere with the patient’s ability to manage secretions or adequately protect his or her airway.




Neuromuscular Conditions.

Various types of neuromuscular diseases may result in respiratory muscle weakness or paralysis (see Table 68-1). For example, patients with Guillain-Barré syndrome, muscular dystrophy, myasthenia gravis (acute exacerbation), or multiple sclerosis are at risk for respiratory failure because the respiratory muscles are weakened or paralyzed as a result of the underlying neuromuscular condition. Therefore they are unable to maintain normal PaCO2 levels.15–17


Neuromuscular disorders may be acquired as a consequence of exposure to toxins (e.g., carbamate/organophosphate pesticides, chemical nerve agents) that interfere with the nerve supply to muscles and lung ventilation. Respiratory muscle weakness may also result from muscle wasting during a critical illness, peripheral nerve damage, and/or prolonged effects of neuromuscular blocking agents.


In summary, respiratory failure may occur in three of these categories (CNS, chest wall, neuromuscular conditions) despite the presence of normal lungs. Respiratory failure occurs because the medulla, chest wall, peripheral nerves, or respiratory muscles are not functioning normally. The patient may have no damage to lung tissue but may be unable to inspire a tidal volume sufficient to remove CO2 from the lungs.



Tissue Oxygen Needs.

Remember that even though PaO2 and PaCO2 determine the definition of respiratory failure, the major cause of respiratory failure is the lung’s inability to meet the O2 needs of the tissues. This failure may occur because of inadequate O2 delivery to the tissues or because the tissues cannot use the O2 delivered to them. It may also occur as a result of the stress response and dramatic increases in tissue O2 consumption.


Tissue O2 delivery is determined by cardiac output and the amount of O2 carried in the hemoglobin. Therefore respiratory failure places the patient at greater risk if there are coexisting heart problems or anemia. Failure of O2 use most commonly occurs in septic shock. Adequate O2 may be delivered to the tissues, but impaired O2 extraction or diffusion limitation exists at the cellular level. This results in an abnormally high amount of O2 returning in the venous blood because it is not used at the tissue level. (Chapter 67 discusses shock.) Acid-base alterations (e.g., alkalosis, acidosis) may also interfere with O2 delivery to peripheral tissues (see Chapter 17).



Clinical Manifestations


Respiratory failure may develop suddenly (minutes or hours) or gradually (several days or longer). A sudden decrease in PaO2 or a rapid rise in PaCO2 implies a serious condition, which can rapidly become a life-threatening emergency. An example is the patient with asthma who develops severe bronchospasm and a marked decrease in airflow, resulting in rapid respiratory muscle fatigue, acidemia, and respiratory failure.


A more gradual change in PaO2 and PaCO2 is better tolerated because compensation can occur. An example is the patient with COPD who develops a progressive increase in PaCO2 over several days after a respiratory tract infection. Because the change occurred over several days, there is time for renal compensation (e.g., retention of bicarbonate), which minimizes the change in arterial pH. The patient will have compensated respiratory acidosis.3,4 (See Chapter 17 for a discussion of renal compensation for acid-base disorders.)


Manifestations of respiratory failure are related to the extent of change in PaO2 or PaCO2, the rapidity of change (acute versus chronic), and the patient’s ability to compensate for this change. When the patient’s compensatory mechanisms fail, respiratory failure occurs. Because clinical manifestations vary, it is important to watch trends in ABGs, pulse oximetry, and assessment findings to fully evaluate the extent of change. Frequently, the first indication of respiratory failure is a change in the patient’s mental status. Mental status changes often occur early, before ABG results are obtained. This is because the brain is very sensitive to variations in O2 and CO2 levels and acid-base balance. Restlessness, confusion, agitation, and combative behavior suggest inadequate O2 delivery to the brain and should be fully investigated.


You may detect manifestations of respiratory failure that are specific (primary) (arising from the respiratory system) or nonspecific (secondary) (arising from other body systems) (Table 68-2). Understanding the significance of these manifestations is critical to your ability to detect the onset of respiratory failure and evaluate the effectiveness of treatment.



TABLE 68-2


MANIFESTATIONS OF HYPOXEMIA AND HYPERCAPNIA*


















Specific Nonspecific
Hypoxemia


Hypercapnia

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Nov 17, 2016 | Posted by in NURSING | Comments Off on Nursing Management: Respiratory Failure and Acute Respiratory Distress Syndrome

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