Hypercapnia Respiratory Failure Definition Essay

Abstract

Acute respiratory failure (ARF) in patients over 65 years is common in emergency departments (EDs) and is one of the key symptoms of congestive heart failure (CHF) and respiratory disorders. Searches were conducted in MEDLINE for published studies in the English language between January 1980 and August 2007, using ‘acute dyspnea’, ‘acute respiratory failure (ARF)’, ‘heart failure’, ‘pneumonia’, ‘pulmonary embolism (PE)’ keywords and selecting articles concerning patients aged 65 or over. The age-related structural changes of the respiratory system, their consequences in clinical assessment and the pathophysiology of ARF are reviewed. CHF is the most common cause of ARF in the elderly. Inappropriate diagnosis that is frequent and inappropriate treatments in ED are associated with adverse outcomes. B-type natriuretic peptides (BNPs) help to determine an accurate diagnosis of CHF. We should consider non-invasive ventilation (NIV) in elderly patients hospitalised with CHF or acidotic chronic obstructive pulmonary disease (COPD) who do not improve with medical treatment. Further studies on ARF in elderly patients are warranted.

acute respiratory failure, elderly, pulmonary embolism, BNP, congestive heart failure

Introduction

Visits by older adults compose 12–21% of all emergency department (ED) encounters [1]. Furthermore, studies showed a progressive increase in the number of ED attendances and emergency admissions hospital of older patients in the last decade. Between 30 and 50% of all ED visits by older patients result in a hospital admission. Lastly when admitted, older emergency patients are more likely to require an ICU (intensive care unit) bed [2]. Acute respiratory failure (ARF) is a common complaint of elderly patients in ED, and the key clinical presentation of cardiac [congestive heart failure (CHF)] and respiratory disorders [3].

This article will summarise the age-related structural changes of the respiratory system and their consequences in clinical practice. It will also overview the causes, difficulties in diagnosis, treatment and the prognosis of ARF in elderly patients.

Searches were conducted in MEDLINE for published studies in the English language between January 1980 and August 2007, using ‘acute dyspnea’, ‘acute respiratory failure’, ‘heart failure’, ‘pneumonia’, ‘pulmonary embolism (PE)’ keywords and selecting articles concerning patients aged 65 or over.

Physiological changes according to age

Several changes related to ageing need to be taken into account before discussing ARF.

Pulmonary function

Chest wall compliance decreases progressively with age, presumably related to structural changes within the rib cage [4, 5].

Total lung capacity does not change with age, but the functional residual capacity and the residual volume both increase. There is an increased tendency in airway closure at small volumes (senile emphysema) related to the loss of supporting tissues around the airways [4]. Because a significant proportion of peripheral airways do not contribute to gas exchange (low V/Q ratio) zones, but also because of a reduced alveolar area, ageing was classically thought to be accompanied by a progressive decline in arterial oxygen tension (PaO2). Actually, recent studies have found no significant correlation between PaO2 and age [6]. Because of a decline in tests of forced expiration (i.e. increasing airway resistance), an obstructive pattern could exist even in women who are non-smokers. Furthermore, studies suggest that the ß-adrenoceptor dysfunction explains a less response to bronchodilation in older asthmatic patients [7].

Other common important changes include loss of diaphragmatic mass and strength with age [8]. Finally, as a consequence of poor nutritional status, decreased T-cell function, decline in mucociliary clearance, poor dentition with oropharyngeal colonisation, and swallowing dysfunction (Parkinson's disease, Alzheimer's disease and stroke), community-acquired (CAP) and aspiration pneumonia is exceedingly common in elderly patients [9].

Furthermore, decreased sensitivity of respiratory centres to hypoxaemia, hypercapnia, or added resistive loads will result in a diminished ventilatory response in cases of ARF; and could delay diagnosis because of the poor perception of the respiratory insults [4].

Cardiovascular changes

The physiological cardiovascular changes involve the decrease of myocyte number, intrinsic contractility, coronary flow reserve, ventricular compliance and ß-adrenoceptor-mediated modulation of inotropy.

The ageing heart increases cardiac output by increasing stroke volume rather than increasing heart rate. However, this compensatory mechanism is dependent on the effective atrial contribution to late diastolic filling (>30% in the elderly patient) [10]. This explains the frequency of CHF caused by rapid atrial fibrillation in the elderly.

Cardiac and respiratory systems are dependent. For example, (1) a bout of pneumonia is sufficient to trigger an acute exacerbation of heart failure, (2) a reduction in cardiac output accompanying septic shock is a cause of ARF caused by diaphragm hypoperfusion leading to alveolar hypoventilation, and respiratory arrest.

Other relevant changes

Decrease in glomerular filtration rate (approximately 45% by the age of 80) with ageing has important implications in terms of drug dosing, as most drugs are renally excreted [2].

Most studies have shown an imbalance between procoagulant/antifibrinolytic and anticoagulant factors, which could contribute to an increased incidence of PE.

Definition and pathophysiology of acute respiratory failure

The respiratory system consists of two parts: the lung, i.e. the gas-exchanging organ, and the pump [11]. The pump consists of the chest wall, including the respiratory muscles (essentially the diaphragm), the respiratory controllers in the central nervous system and the pathways that connect the central controllers with the respiratory muscles (spinal and peripheral nerves). ARF is a condition in which the respiratory system fails in one or both of its gas exchange functions, i.e. oxygenation (PaO2 <60 mmHg) of and/or elimination of carbon dioxide (arterial carbon dioxide tension (PaCO2) >45 mmHg) [11]. Both cut-off values simply serve as a general guide in combination with the history and clinical assessment of the patient. Thus, ARF could also be suspected by ‘simple’ clinical criteria: polypnea >30 per min, contraction of the accessory inspiratory muscles, abdominal respiration, orthopnea cyanosis, and asterixis. Orthopnea is frequently associated with all causes of ARF, and is neither a sensible nor specific predictor of CHF [3].

The four pathophysiological mechanisms related to hypoxaemic ARF (1) ventilation/perfusion inequality which is the main mechanisms in an emergency setting (CHF or pneumonia), (2) increased shunt (acute respiratory distress syndrome), (3) alveolar hypoventilation [chronic obstructive pulmonary disease (COPD)], and (4) diffusion impairment (pulmonary fibrosis) [11].

Failure of the pump (or ventilatory failure) results in alveolar hypoventilation with an increase in PaCO2 (Table 1). Mechanisms responsible are decreasing minute ventilation and increasing dead space. In elderly patients, the major cause is severe hyperinflation, with flattened diaphragm and reduced mechanical action of the inspiratory muscles (COPD exacerbation) [4].

Table 1

Principal causes of acute respiratory failure (adapted from [11])

Decreased central drive 
Morphine (or other drugs: sedatives) 
 Central nervous system diseases (encephalitis, stroke, trauma) 
Altered neural and neuromuscular transmission 
 Spinal cord trauma, transverse myelitis, tetanus, amyotrophic lateral sclerosis, poliomyelitis, Guillain–Barre’ syndrome 
 Myasthenia gravis, botulism 
Muscle abnormalities 
 Muscular dystrophy, disuse atrophy 
Chest wall and pleural abnormalities 
Kyphoscoliosis
 Chest wall trauma (flail chest, diaphragmatic rupture) 
Lung and airways diseases 
 Acute asthma 
Acute exacerbation of chronic obstructive pulmonary disease
Congestive heart failure and non-cardiogenic pulmonary oedema (acute respiratory distress syndrome) 
Pneumonia, tuberculosis 
 Upper airways obstruction 
Lung cancer, pulmonary fibrosis
 Pneumothorax, pleural effusion 
Bronchiectasis
Vascular diseases 
Pulmonary embolism
 Severe haemoptysis 
Other 
Severe sepsis or septic shock, other shock 
Decreased central drive 
Morphine (or other drugs: sedatives) 
 Central nervous system diseases (encephalitis, stroke, trauma) 
Altered neural and neuromuscular transmission 
 Spinal cord trauma, transverse myelitis, tetanus, amyotrophic lateral sclerosis, poliomyelitis, Guillain–Barre’ syndrome 
 Myasthenia gravis, botulism 
Muscle abnormalities 
 Muscular dystrophy, disuse atrophy 
Chest wall and pleural abnormalities 
Kyphoscoliosis
 Chest wall trauma (flail chest, diaphragmatic rupture) 
Lung and airways diseases 
 Acute asthma 
Acute exacerbation of chronic obstructive pulmonary disease
Congestive heart failure and non-cardiogenic pulmonary oedema (acute respiratory distress syndrome) 
Pneumonia, tuberculosis 
 Upper airways obstruction 
Lung cancer, pulmonary fibrosis
 Pneumothorax, pleural effusion 
Bronchiectasis
Vascular diseases 
Pulmonary embolism
 Severe haemoptysis 
Other 
Severe sepsis or septic shock, other shock 

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Actually, hypoxaemic ARF is a situation accompanied by increased work of breathing. However, energy availability is reduced due to hypoxaemia, resulting in muscle fatigue and ventilatory failure through imbalance between demand and supply [11].

ARF in elderly patients

Etiology of ARF

The EPIDASA study prospectively evaluated ARF in 514 patients (mean age of 80 years), presenting to the ED. CHF (43%), pneumonia (35%), COPD exacerbation (32%), and PE (18%) were the main causes [3]. Half of the patients had more than two diagnoses (CHF and CAP in 17%). Pneumothorax, lung cancer, severe sepsis and acute asthma were less frequent (<5%). An autopsy study of 234 elderly patients confirmed that the most common causes of death were CAP and CHF, both frequently underestimated [12]. Ely et al. reported the causes of being mechanically ventilated: CHF (16%), CAP (16%), COPD (14%), and sepsis (10%) [13].

Difficult diagnosis of ARF in the elderly

Ray et al. found that the sensitivity of the emergency physician was 86% for pneumonia, 75% for PE, and 71% for CHF [3]. In this study, the variables associated to a missed diagnosis were a final diagnosis of CHF, CAP or PE, highlighting the fact that frequent causes of ARF are very challenging to diagnose in the ED. Riquelme et al. demonstrated that the definite diagnosis of CAP was delayed for more than 72 h in 62% of patients [14]. The association of dyspnea, cough, and fever, was observed in only 32% of patients with CAP, and delirium at admission was very common (45%) [9, 14]. Atypical signs of CHF are frequent (confusion or leg swelling, or wheezing), and confusing [15, 16, 17]. Unfortunately, an inappropriate diagnosis is associated with an increased mortality (Figure 1a and b) [3, 18]. The difficulties of diagnosing CHF and PE [19, 20, 21, 22, 23, 24] are reported in Appendix 1 and Appendix 2 in the supplementary data on the journal's website http://www.ageing.oxfordjournals.org (Figure 2 and see Appendix 4 in the supplementary data on the journal's website http://www.ageing.oxfordjournals.org).

Figure 1

(a) Effects of an appropriate (black bars) or inappropriate (white bars) initial diagnosis in the emergency department on prognosis (used with permission from Ray P. [3]). (b) Effects of an appropriate (black bars) or inappropriate (white bars) initial treatments in the emergency department on prognosis (used with permission from Ray P. [3]).

Figure 1

(a) Effects of an appropriate (black bars) or inappropriate (white bars) initial diagnosis in the emergency department on prognosis (used with permission from Ray P. [3]). (b) Effects of an appropriate (black bars) or inappropriate (white bars) initial treatments in the emergency department on prognosis (used with permission from Ray P. [3]).

Figure 2

Diagnostic strategy based on B-type natriuretic peptide levels in elderly patients admitted for ARF in the emergency department. 1In the grey zone (BNP between 100 and 500 pg/ml), which represents less than a quarter of patients, further investigations are needed, and ER physicians should consider massive PE, CHE, severe exacerbation of COPD or severe pneumonia as possible diagnoses. 2Physicians should keep in mind that half of elderly patients with ARF has more than one diagnosis, i.e. a BNP greater than 500 pg/ml strongly suggests CHF, but other diagnosis that could have precipitated CHF. CXR: chest X-ray; EKG: electrocardiogram; ABG: arterial blood gas analysis; CHF: congestive heart failure; ACS: acute coronary syndrome; CT: computed tomography; IV: intravenous; NIV: non-invasive ventilation including continuous positive airway pressure; ACEi: angiotensin converting enzyme inhibitor; EC: echocardiography.

Figure 2

Diagnostic strategy based on B-type natriuretic peptide levels in elderly patients admitted for ARF in the emergency department. 1In the grey zone (BNP between 100 and 500 pg/ml), which represents less than a quarter of patients, further investigations are needed, and ER physicians should consider massive PE, CHE, severe exacerbation of COPD or severe pneumonia as possible diagnoses. 2Physicians should keep in mind that half of elderly patients with ARF has more than one diagnosis, i.e. a BNP greater than 500 pg/ml strongly suggests CHF, but other diagnosis that could have precipitated CHF. CXR: chest X-ray; EKG: electrocardiogram; ABG: arterial blood gas analysis; CHF: congestive heart failure; ACS: acute coronary syndrome; CT: computed tomography; IV: intravenous; NIV: non-invasive ventilation including continuous positive airway pressure; ACEi: angiotensin converting enzyme inhibitor; EC: echocardiography.

Outcomes

The mortality rate associated with ARF in the elderly varies according to the etiology. In a study, the crude mortality of CAP requiring hospitalisation was 26%, and age by itself was not a significant factor related to prognosis [14]. CHF has an in-hospital mortality, ranging from 13 to 29%, with a rate of early re-hospitalisation from 29 to 47% within 3–6 months of the initial discharge, and a 1 year survival of 50% [3, 16, 25}, 26]. In the EPIDASA study, 29% of patients were admitted to an ICU, and 16% died in hospital. The five variables associated to death were: inappropriate initial treatment, hypercapnia >45 mmHg, creatinine clearance <50 ml/min, elevated B-type natriuretic peptides (BNP and NT-proBNP), and clinical signs of ARF. Age was not significantly associated with mortality.

Prognosis of elderly admitted in an ICU

Age is included in several scores of severity such as the APACHE II, Fine's score for CAP [27], and Aujesky's score for PE [2, 28]. However, the large majority of the studies indicate that acute physiology disturbances and diagnosis have larger relative contributions to prognosis than age [2]. Kaarlola et al. reported that the cumulative 3-year mortality rate among the elderly patients was lower than that among the controls (40% versus 57%). However, 88% of the elderly survivors assessed their present health state as satisfactory [29].

Ethical considerations

The decision to admit a patient to the ICU from the ED is challenging, as physicians must decide in a short time. When a patient potentially requiring ICU care is admitted to the ED, emergency physicians take the first decision as to whether to propose the patient to the ICU. Thus, intensivists are involved only if an ICU admission is requested for the patient. Age over 85 years seems to be an independent predictor of ICU refusal [30]. Actually, the decision to admit an elderly patient to an ICU should be based on the patients’ co-morbidities, acuity of illness, pre-hospital functional status and the patient's preferences [2].

How could we improve outcomes of ARF in elderly patients?

Studies suggested that an inappropriate diagnosis and treatment were associated with an increased mortality rate [Figure 1(b)] [3, 18]. Usual tools used to differentiate CHF from respiratory disorders are not very accurate, even the chest X-ray (CXR) in CHF [31] or the classical hypocapnia in PE [32]. Thus valid diagnostic tools for differentiating CHF from other etiologies of ARF could aid clinicians.

Usefulness of transthoracic echocardiography

Echocardiography (EC) should be encouraged because the diagnosis of systolic CHF can be easily confirmed by the emergency physician [33, 34]. However non-systolic CHF is more difficult to evaluate by EC, and needs Doppler and myocardial tissue imaging (see Appendix 1 in the supplementary data on the journal's website http://www.ageing.oxfordjournals.org) [35].

Role of B-type natriuretic peptides

BNP is a polypeptide, released by ventricular myocytes directly proportional to wall tension, for lowering renin-angiotensin-aldosterone activation. In the blood, the cleavage of a precursor protein produces BNP and the biologically inactive NT-proBNP. For diagnosing CHF, both BNP and NT-proBNP have similar accuracy [36, 37] (see Appendix 1 in the supplementary data on the journal's website http://www.ageing.oxfordjournals.org). However, threshold values are higher than in middle-aged population. A study demonstrated that the use of BNP in patients >70 years early in the ED reduced the time to discharge, total treatment cost, and 30-day mortality. Figure 2 shows a diagnostic strategy based on BNP in elderly patients admitted for ARF in the ED [38, 39]

Inflammatory markers

Diagnosing CAP is difficult and urgent because it requires prompt antibiotics [40]. Thus, biological markers such as C-reactive protein (CRP) and procalcitonin (PCT) may be useful to suggest bacterial infection [41]. PCT seems to be more sensitive and specific than CRP, with an additional prognostic value [42]. Several studies suggested that, in a middle-aged population with suspected CAP or COPD exacerbation, PCT guidance of antibiotherapy reduced antibiotic use without adverse effect [43]. However, in elderly patients Strucker et al. have found that it had a low sensitivity (24%) for infection [44].

Potential usefulness of thoracic imaging

When PE is suspected, throcacic computed tomography (CT) is now one of the first line investigations (see Appendix 2 in the supplementary data on the journal's website http://www.ageing.oxfordjournals.org, Figure 2) [45

Respiratory failure is one of the most common reasons for admission to the intensive care unit (ICU) and a common comorbidity in patients admitted for acute care. What’s more, it’s the leading cause of death from pneumonia and chronic obstructive pulmonary disease (COPD) in the United States. This article briefly reviews the physiologic components of respiration, differentiates the main types of respiratory failure, and discusses medical treatment and nursing care for patients with respiratory failure.

Physiologic components of ventilation and respiration

The lung is highly elastic. Lung inflation results from the partial pressure of inhaled gases and the diffusion-pressure gradient of these gases across the alveolar-capillary membrane. The lungs play a passive role in breathing, but ventilation requires muscular effort. When the diaphragm contracts, the thoracic cavity enlarges, causing the lungs to inflate. During forced inspiration when a large volume of air is inspired, external intercostal muscles act as a second set of inspiratory muscles.

Accessory muscles in the neck and chest are the last group of inspiratory muscles, used only for deep and heavy breathing, such as during intense exercise or respiratory failure. During expiration, the diaphragm relaxes, decreasing thoracic cavity size and causing the lungs to deflate. With normal breathing, expiration is purely passive. But with exercise or forced expiration, expiratory muscles (including the abdominal wall and internal intercostal muscles) become active. These important muscles are necessary for coughing.

Respiration—the process of exchanging oxygen (O2) and carbon dioxide (CO2)—involves ventilation, oxygenation, and gas transport; the ventilation/perfusion (V/Q) relationship; and control of breathing. Respiration is regulated by chemical and neural control systems, including the brainstem, peripheral and central chemoreceptors, and mechanoreceptors in skeletal muscle and joints. (See Control of breathing.)

A dynamic process, ventilation is affected by the respiratory rate (RR) and tidal volume—the amount of air inhaled and exhaled with each breath. Pulmonary ventilation refers to the total volume of air inspired or expired per minute.

Not all inspired air participates in gas exchange. Alveolar ventilation—the volume of air entering alveoli taking part in gas exchange—is the most important variable in gas exchange. Air that distributes to the conducting airways is deemed dead space or wasted air because it’s not involved in gas exchange. (See Oxygenation and gas transport.)

Ultimately, effective ventilation is measured by the partial pressure of CO2 in arterial blood (Paco2). All expired CO2 comes from alveolar gas. During normal breathing, the breathing rate or depth adjusts to maintain a steady Paco2 between 35 and 45 mm Hg. Hyperventilation manifests as a low Paco2; hypoventilation, as a high Paco2. During exercise or certain disease states, increasing breathing depth is far more effective than increasing the RR in improving alveolar ventilation.

Lung recoil and compliance

The lungs, airways, and vascular trees are embedded in elastic tissue. To inflate, the lung must stretch to overcome these elastic components. Elastic recoil—the lung’s ability to return to its original shape after stretching from inhalation—relates inversely to compliance. Lung compliance indirectly reflects lung stiffness or resistance to stretch. A stiff lung, as in pulmonary fibrosis, is less compliant than a normal lung.

With reduced compliance, more work is required to produce a normal tidal volume. With extremely high compliance, as in emphysema where there is loss of alveolar and elastic tissue, the lungs inflate extremely easily. Someone with emphysema must expend a lot of effort to get air out of the lungs because they don’t recoil back to their normal position during expiration. In both pulmonary fibrosis and emphysema, inadequate lung ventilation leads to hypercapnic respiratory failure.

Respiratory failure

Respiratory failure occurs when one of the gas-exchange functions—oxygenation or CO2 elimination—fails. A wide range of conditions can lead to acute respiratory failure, including drug overdose, respiratory infection, and exacerbation of chronic respiratory or cardiac disease.

Respiratory failure may be acute or chronic. In acute failure, life-threatening derangements in arterial blood gases (ABGs) and acid-base status occur, and patients may need immediate intubation. Respiratory failure also may be classified as hypoxemic or hypercapnic.

Clinical indicators of acute respiratory failure include:

  • partial pressure of arterial oxygen (Pao2) below 60 mm Hg, or arterial oxygen saturation as measured by pulse oximetry (Spo2) below 91% on room air
  • Paco2 above 50 mm Hg and pH below 7.35
  • Pao2 decrease or Paco2 increase of 10 mm Hg from baseline in patients with chronic lung disease (who tend to have higher Paco2 and lower PaO2 baseline values than other patients).

In contrast, chronic respiratory failure is a long-term condition that develops over time, such as with COPD. Manifestations of chronic respiratory failure are less dramatic and less apparent than those of acute failure.

Three main types of respiratory failure

The most common type of respiratory failure is type 1, or hypoxemic respiratory failure (failure to exchange oxygen), indicated by a Pao2 value below 60 mm Hg with a normal or low Paco2 value. In ICU patients, the most common causes of type 1 respiratory failure are V/Q mismatching and shunts. COPD exacerbation is a classic example of V/Q mismatching. Shunting, which occurs in virtually all acute lung diseases, involves alveolar collapse or fluid-filled alveoli. Examples of type 1 respiratory failure include pulmonary edema (both cardiogenic and noncardiogenic), pneumonia, influenza, and pulmonary hemorrhage. (See Ventilation and perfusion: A critical relationship.)

Type 2, or hypercapnic, respiratory failure, is defined as failure to exchange or remove CO2, indicated by Paco2 above 50 mm Hg. Patients with type 2 respiratory failure who are breathing room air commonly have hypoxemia. Blood pH depends on the bicarbonate level, which is influenced by hypercapnia duration. Any disease that affects alveolar ventilation can result in type 2 respiratory failure. Common causes include severe airway disorders (such as COPD), drug overdose, chest-wall abnormalities, and neuromuscular disease.

Type 3 respiratory failure (also called perioperative respiratory failure) is a subtype of type 1 and results from lung or alveolar atelectasis. General anesthesia can cause collapse of dependent lung alveoli. Patients most at risk for type 3 respiratory failure are those with chronic lung conditions, excessive airway secretions, obesity, immobility, and tobacco use, as well as those who’ve had surgery involving the upper abdomen. Type 3 respiratory failure also may occur in patients experiencing shock, from hypoperfusion of respiratory muscles. Normally, less than 5% of total cardiac output flows to respiratory muscles. But in pulmonary edema, lactic acidosis, and anemia (conditions that commonly arise during shock), up to 40% of cardiac output may flow to the respiratory muscles.

Signs and symptoms of respiratory failure

Patients with impending respiratory failure typically develop shortness of breath and mental-status changes, which may present as anxiety, tach­­y­­p­nea, and decreased Spo2 despite increasing amounts of supplemental oxygen.

Acute respiratory failure may cause tachycardia and tachypnea. Other signs and symptoms include periorbital or circumoral cyanosis, diaphoresis, accessory muscle use, diminished lung sounds, inability to speak in full sentences, an impending sense of doom, and an altered mental status. The patient may assume the tripod position in an attempt to further expand the chest during the inspiratory phase of respiration. In chronic respiratory failure, the only consistent clinical indictor is protracted shortness of breath.

Be aware that pulse oximetry measures the percentage of hemoglobin saturated with oxygen, but it doesn’t give information about oxygen delivery to the tissues or the patient’s ventilatory function. So be sure to consider the patient’s entire clinical presentation. Compared to SpO2, an ABG study provides more accurate information on acid-base balance and blood oxygen saturation. Capnography is another tool used for monitoring patients receiving anesthesia and in critical care units to assess a patient’s respiratory status. It directly monitors inhaled and exhaled concentration of CO2 and indirectly monitors Paco2.

Treatment and management

In acute respiratory failure, the healthcare team treats the underlying cause while supporting the patient’s respiratory status with supplemental oxygen, mechanical ventilation, and oxygen saturation monitoring. Treatment of the underlying cause, such as pneumonia, COPD, or heart failure, may require diligent administration of antibiotics, diuretics, steroids, nebulizer treatments, and supplemental O2 as appropriate.

For chronic respiratory failure, despite the wide range of chronic or end-stage pathology present (such as COPD, heart failure, or systemic lupus erythematosus with lung involvement), the mainstay of treatment is continuous supplemental O2, along with treatment of the underlying cause.

Nursing care

Nursing care can have a tremendous impact in improving efficiency of the patient’s respiration and ventilation and increasing the chance for recovery. To detect changes in respiratory status early, assess the patient’s tissue oxygenation status regularly. Evaluate ABG results and indices of end-organ perfusion. Keep in mind that the brain is extremely sensitive to O2 supply; decreased O2 can lead to an altered mental status. Also, know that angina signals inadequate coronary artery perfusion. In addition, stay alert for conditions that can impair O2 delivery, such as elevated temperature, anemia, impaired cardiac output, acidosis, and sepsis.

As indicated, take steps to improve V/Q matching, which is crucial for improving respiratory efficiency. To enhance V/Q matching, turn the patient on a regular and timely basis to rotate and maximize lung zones. Because blood flow and ventilation are distributed preferentially to dependent lung zones, V/Q is maximized on the side on which the patient is lying.

Regular, effective use of incentive spirometry helps maximize diffusion and alveolar surface area and can help prevent atelectasis. Regular rotation of V/Q lung zones by patient turning and repositioning enhances diffusion by promoting a healthy, well-perfused alveolar surface. These actions, as well as suctioning, help mobilize sputum or secretions.

Nutritional support

Patients in respiratory failure have unique nutritional needs and considerations. Those with acute respiratory failure from primary lung disease may be malnourished initially or may become malnourished from increased metabolic demands or inadequate nutritional intake. Malnutrition can impair the function of respiratory muscles, reduce ventilatory drive, and decrease lung defense mechanisms. Clinicians should consider nutritional support and individualize such support to ensure adequate caloric and protein intake to meet the patient’s respiratory needs.

Patient and family education

Provide appropriate education to the patient and family to promote adherence with treatment and help prevent the need for readmission. Explain the purpose of nursing measures, such as turning and incentive spirometry, as well as medications. At discharge, teach patients about pertinent risk factors for their specific respiratory condition, when to return to the healthcare provider for follow-up care, and home measures they can take to promote and maximize respiratory function.

Selected references
Cooke CR, Erikson SE, Eisner MD, Martin GS. Trends in the incidence of noncardiogenic acute respiratory failure: the role of race. Crit Care Med. 2012;40(5):1532-8.

Gehlbach BK, Hall JB. Respiratory failure and mechanical ventilation. In Porter RS, ed. The Merck Manual. 19th ed. West Point, PA; Merck Sharp & Dohme Corp.; 2011.

Kaynar AM. Respiratory failure treatment and management. Updated August 14, 2014. http://emedicine.medscape.com/article/167981-treatment#aw2aab6b6b2. Accessed August 23, 2014.

Kress JP, Hall JB: Approach to the patient with critical illness. In Longo DL, Fauci AS, Kasper DL, et al., eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill Professional; 2012.

Pinson R. Revisiting respiratory failure, part 1. ACP Hosp. 2013;Oct:5-6. www.acphospitalist.org/archives/2013/10/coding.htm. Accessed August 23, 2014.

Pinson R. Revisiting respiratory failure, part 2. ACP Hosp. 2013;Nov:7-8. www.acphospitalist.org/archives/2013/11/coding.htm. Accessed October 3, 2014.

Schraufnagel D. Breathing in America: Diseases, Progress, and Hope. American Thoracic Society; 2010.

Michelle Fournier is director of clinical consulting with Nuance/J.A. Thomas & Associates in Atlanta, Georgia.

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