18 American Nurse Today Volume 9, Number 11 www.AmericanNurseToday.com

RESPIRATORY FAILURE is one ofthe most common reasons for ad-mission to the intensive care unit(ICU) and a common comorbidityin patients admitted for acute care.What’s more, it’s the leading causeof death from pneumonia andchronic obstructive pulmonary dis-ease (COPD) in the United States.This article briefly reviews thephysiologic components of respira-tion, differentiates the main types ofrespiratory failure, and discussesmedical treatment and nursing carefor patients with respiratory failure.

Physiologic components ofventilation and respirationThe lung is highly elastic. Lung in-flation results from the partial pres-sure of inhaled gases and the diffu-sion-pressure gradient of thesegases across the alveolar-capillarymembrane. The lungs play a pas-sive role in breathing, but ventila-tion requires muscular effort. Whenthe diaphragm contracts, the tho-racic cavity enlarges, causing thelungs to inflate. During forced in-spiration when a large volume ofair is inspired, external intercostalmuscles act as a second set of in-spiratory muscles.

Accessory muscles in the neckand chest are the last group of in-spiratory muscles, used only fordeep and heavy breathing, such asduring intense exercise or respirato-ry failure. During expiration, the di-aphragm relaxes, decreasing tho-racic cavity size and causing the

lungs to deflate. With normalbreathing, expiration is purely pas-sive. But with exercise or forcedexpiration, expiratory muscles (in-cluding the abdominal wall and in-ternal intercostal muscles) becomeactive. These important muscles arenecessary for coughing.

Respiration—the process of ex-changing oxygen (O2) and carbondioxide (CO2)—involves ventilation,oxygenation, and gas transport; theventilation/perfusion (V/Q) relation-ship; and control of breathing. Res-piration is regulated by chemicaland neural control systems, includ-ing the brainstem, peripheral andcentral chemoreceptors, andmechanoreceptors in skeletal mus-cle and joints. (See Control ofbreathing.)

A dynamic process, ventilation isaffected by the respiratory rate (RR)and tidal volume—the amount ofair inhaled and exhaled with eachbreath. Pulmonary ventilation refersto the total volume of air inspiredor expired per minute.

Not all inspired air participates ingas exchange. Alveolar ventila-tion—the volume of air enteringalveoli taking part in gas ex-change—is the most important vari-able in gas exchange. Air that dis-tributes to the conducting airwaysis deemed dead space or wasted airbecause it’s not involved in gas ex-change. (See Oxygenation and gastransport.)

Ultimately, effective ventilationis measured by the partial pressureof CO2 in arterial blood (PaCO2).All expired CO2 comes from alveo-lar gas. During normal breathing,the breathing rate or depth adjuststo maintain a steady PaCO2 be-tween 35 and 45 mm Hg. Hyper-ventilation manifests as a low PaCO2; hypoventilation, as a high

Caring for patients in

respiratory failure Even if you don’t work in an ICU, you’re likely to

encounter patients in respiratory failure.

By Michelle Fournier, MN, RN, CCRN-K

LEARNING OBJECTIVES

1. Discuss the physiology of ventila-tion and respiration.

2. Differentiate the types of respirato-ry failure.

3. Describe the treatment of respira-tory failure.

The author and planners of this CNE activity havedisclosed no relevant financial relationships withany commercial companies pertaining to thisactivity. See the last page of the article to learnhow to earn CNE credit.

Expiration: 11/1/17

CNE1.32 contact hours

www.AmericanNurseToday.com November 2014 American Nurse Today 19

PaCO2. During exercise or certaindisease states, increasing breathingdepth is far more effective than in-creasing the RR in improving alve-olar ventilation.

Lung recoil and complianceThe lungs, airways, and vasculartrees are embedded in elastic tis-sue. To inflate, the lung muststretch to overcome these elasticcomponents. Elastic recoil—thelung’s ability to return to its origi-nal shape after stretching from in-halation—relates inversely to com-pliance. Lung compliance indirectlyreflects lung stiffness or resistanceto stretch. A stiff lung, as in pul-monary fibrosis, is less compliantthan a normal lung.

With reduced compliance, morework is required to produce a nor-mal tidal volume. With extremelyhigh compliance, as in emphysemawhere there is loss of alveolar andelastic tissue, the lungs inflate ex-tremely easily. Someone with em-physema must expend a lot of ef-fort to get air out of the lungsbecause they don’t recoil back totheir normal position during expi-ration. In both pulmonary fibrosisand emphysema, inadequate lungventilation leads to hypercapnicrespiratory failure.

Respiratory failure Respiratory failure occurs whenone of the gas-exchange func-tions—oxygenation or CO2 elimina-tion—fails. A wide range of condi-tions can lead to acute respiratoryfailure, including drug overdose,respiratory infection, and exacerba-tion of chronic respiratory or car-diac disease.

Respiratory failure may beacute or chronic. In acute failure,life-threatening derangements inarterial blood gases (ABGs) andacid-base status occur, and pa-tients may need immediate intuba-tion. Respiratory failure also maybe classified as hypoxemic or hypercapnic.

Clinical indicators of acute respi-ratory failure include:• partial pressure of arterial oxy-

gen (PaO2) below 60 mm Hg, orarterial oxygen saturation asmeasured by pulse oximetry(SpO2) below 91% on room air

• PaCO2 above 50 mm Hg and pHbelow 7.35

• PaO2 decrease or PaCO2 increaseof 10 mm Hg from baseline inpatients with chronic lung dis-ease (who tend to have higherPaCO2 and lower PaO2 baselinevalues than other patients). In contrast, chronic respiratory

failure is a long-term condition thatdevelops over time, such as withCOPD. Manifestations of chronicrespiratory failure are less dramaticand less apparent than those ofacute failure.

Three main types of respiratoryfailureThe most common type of respira-tory failure is type 1, or hypoxemicrespiratory failure (failure to ex-change oxygen), indicated by aPaO2 value below 60 mm Hg witha normal or low PaCO2 value. InICU patients, the most commoncauses of type 1 respiratory failureare V/Q mismatching and shunts.

COPD exacerbation is a classic ex-ample of V/Q mismatching. Shunt-ing, which occurs in virtually allacute lung diseases, involves alveo-lar collapse or fluid-filled alveoli.Examples of type 1 respiratory fail-ure include pulmonary edema(both cardiogenic and noncardio-genic), pneumonia, influenza, andpulmonary hemorrhage. (See Ven-tilation and perfusion: A critical relationship.) Type 2, or hypercapnic, respira-

tory failure, is defined as failure toexchange or remove CO2, indicatedby PaCO2 above 50 mm Hg. Pa-tients with type 2 respiratory failurewho are breathing room air com-monly have hypoxemia. Blood pHdepends on the bicarbonate level,which is influenced by hypercapniaduration. Any disease that affectsalveolar ventilation can result intype 2 respiratory failure. Commoncauses include severe airway disor-ders (such as COPD), drug over-dose, chest-wall abnormalities, andneuromuscular disease.Type 3 respiratory failure (also

called perioperative respiratoryfailure) is a subtype of type 1 andresults from lung or alveolar at-electasis. General anesthesia cancause collapse of dependent lung

Control of breathingBreathing is controlled by carefully integrated neurologic, chemical, and mechani-cal processes. The neurologic respiratory center in the brain’s medulla is sensitive tocarbon dioxide (CO2) and hydrogen-ion concentrations in body fluids. It can com-pensate to changing conditions within seconds to minutes.

• Acidemia (decreased blood pH) or elevated partial pressure of arterial CO2 stim-ulates the respiratory center, which increases respiratory rate or depth. This, inturn, reduces the CO2 level and increases blood pH.

• Alkalemia (increased blood pH) inhibits the respiratory center, resulting in slow-er or more shallow breathing, CO2 retention, and reduced blood pH.

Usually, the lungs can compensate for respiratory and metabolic imbalances.But when lung dysfunction is severe or the metabolic imbalance is prolonged, thelungs can’t fully compensate and renal compensation is required. However, renalcompensation is slow, taking hours to days.

Interruption of or damage to respiratory structures or respiratory control mech-anism ultimately affects the ability to exchange gases effectively and can lead tosuch disorders as chronic obstructive pulmonary disease, interstitial lung disease,and respiratory failure.

20 American Nurse Today Volume 9, Number 11 www.AmericanNurseToday.com

alveoli. Patients most at risk fortype 3 respiratory failure are thosewith chronic lung conditions, ex-cessive airway secretions, obesity,immobility, and tobacco use, aswell as those who’ve had surgeryinvolving the upper abdomen.Type 3 respiratory failure alsomay occur in patients experienc-ing shock, from hypoperfusion ofrespiratory muscles. Normally, lessthan 5% of total cardiac outputflows to respiratory muscles. Butin pulmonary edema, lactic acido-sis, and anemia (conditions thatcommonly arise during shock),

up to 40% of cardiac output mayflow to the respiratory muscles.

Signs and symptoms ofrespiratory failurePatients with impending respiratoryfailure typically develop shortnessof breath and mental-status changes,which may present as anxiety, tach y - p nea, and decreased SpO2 despiteincreasing amounts of supplemen-tal oxygen.

Acute respiratory failure maycause tachycardia and tachypnea.Other signs and symptoms includeperiorbital or circumoral cyanosis,

diaphoresis, accessory muscle use,diminished lung sounds, inability tospeak in full sentences, an impend-ing sense of doom, and an alteredmental status. The patient may as-sume the tripod position in an at-tempt to further expand the chestduring the inspiratory phase of res-piration. In chronic respiratory fail-ure, the only consistent clinical in-dictor is protracted shortness ofbreath.

Be aware that pulse oximetrymeasures the percentage of hemo-globin saturated with oxygen, butit doesn’t give information about

Oxygenation and gas transportA gas consists of individual molecules in constant random mo-tion. These molecules bombard the walls of any vessel con-taining them, exerting pressure against the wall. The pressureexerted is proportional to gas temperature and concentration.

How gas exchange occursMovement of gases—oxygen (O2) and carbon dioxide(CO2)—into and out of the alveoli and cells occurs by simplediffusion, defined as passive movement of molecules from anarea of higher concentration to one of lower concentration.The distance across the capillary wall and the lubricating plas-ma layer measures about 1 micron—roughly 100 times small-er than a single human hair. This short distance allows quick,effective exchange of O2 and CO2 across the alveolar-capillarymembrane.

Hemoglobin (Hgb) transports O2 from the lungs to the tis-sues. Every 100 mL of blood that passes through the tissuesdelivers about 4 mL of O2. Where O2 pressure is high, oxygencombines loosely with the heme portion of hemoglobin in thelung, forming oxyhemoglobin. When oxyhemoglobin reachesthe tissues, where O2 pressure is low, hemoglobin releases O2.

The illustration below shows the basic process of gas exchange.

The oxyhemoglobin curve depicts O2 binding to Hgb inthe lung and O2 unloading in the tissues. Body temperature,blood acidity, and underlying conditions, such as anemia orchronic hypoxia, may influence the efficiency of this process.

Factors affecting gas diffusion across the respiratorymembraneThe following factors affect the rate of gas diffusion acrossthe respiratory (alveolar-capillary) membrane.• Membrane thickness. The diffusion rate is inversely propor-

tional to the thickness of the respiratory membrane. Suchconditions as pulmonary edema, excessive sputum, and fi-brosis thicken the membrane, lengthening the distance re-quired to cross the membrane.

• Surface area. The lung’s large surface area is influenced byalveolar size and inflation. Surface area is directly propor-tional to diffusion; a large surface area favors diffusion.Clinical conditions that reduce surface area include atelec-tasis and such procedures as lobectomy.

• Gas solubility and molecular weight. Each gas has an in-herent solubility and molecular weight. The diffusion rateof a gas is directly proportional to its solubility and in-versely proportional to its molecular weight. AlthoughCO2 weighs more than O2, it’s more soluble and diffuses20 times faster. Damage to the respiratory membrane im-pairs O2 diffusion capacity but may not affect CO2 diffu-sion. Therefore, in disease states, the partial pressure ofO2 in arterial blood (PaO2) decreases before the partialpressure of CO2 in arterial blood (PaCO2) changes. So pa-tients with pulmonary diseases that interfere with diffu-sion develop problems related to hypoxemia before theystart retaining CO2.

• Driving pressure. In the lung, driving pressure is the gradi-ent between PaO2 or PaCO2 in the alveoli and the pressureof these gases in the blood. In the tissues, driving pressureis the difference between PaO2 and PaCO2 in the capillariescompared to pressures in tissue cells. In the alveolus, O2driving pressure is 64 mm Hg; CO2 driving pressure is only5 mm Hg. Because CO2 is more soluble, it doesn’t need ahigh driving pressure. Administering supplemental O2 in-creases driving pressure.

www.AmericanNurseToday.com November 2014 American Nurse Today 21

For adequate organ and tissue oxygenation, ventilation (V, theamount of air reaching the alveoli) should match perfusion (Q,the amount of blood reaching the alveoli). Although ventila-tion and perfusion to the lungs aren’t distributed uniformly,they tend to match: Where ventilation is maximal, blood flowis maximal, and vice versa. The V/Q ratio reflects the matchingof these two components.

Because air rises, alveoli in the apex of each lung are alwayspartially inflated and thus don’t accommodate much furtherventilation. The lung bases, on the other hand, have a muchlower alveolar pressure and ventilate more readily than theapices. The low pulmonary arterial pressure is just enough topump blood to the top of the lung. Although all parts of thelung receive some perfusion, hydrostatic pressure in the vas-culature directs most of the blood flow through the lower (de-pendent) portion of the lung. So when a person sits or stands,blood flow to the lung bases exceeds blood flow to the apices.

Balancing ventilation and perfusionThe lung uses hypoxic vasoconstriction to balance ventilationand perfusion. When a lung region becomes hypoxic, small ar-teries feeding that region sense hypoxia in alveolar gas and con-strict in response. Constriction redirects blood away from thehypoxic region to better-oxygenated lung areas. When a V/Qmismatch or imbalance occurs, as from lung disease, hypoxemia

may result. Causes of extreme V/Q mismatching include:• shunting, in which alveolar perfusion is normal but venti-

lation is absent• dead space—portions of the respiratory tract where air

doesn’t participate in gas exchange • nonperfused lung areas.

A low V/Q ratio occurs when pulmonary gas exchange isimpaired—a situation that typically causes hypoxemia. Carbondioxide (CO2) excretion also is impaired, which can lead to in-creased partial pressure of CO2 in arterial blood (PaCO2). How-ever, this is rare because increased PaCO2 typically triggers res-piratory stimulation and increased alveolar ventilation, whichreturns PaCO2 to normal. This scenario is most common in pa-tients with chronic bronchitis, asthma, and acute pulmonaryedema.

On the other hand, a high V/Q ratio occurs when a well-ventilated lung area is poorly perfused; ventilation is wastedas it fails to oxygenate the blood. The most common cause ispulmonary embolism, which impairs blood flow. A high V/Qratio also may occur in emphysema due to air trapping.

These illustrations show what happens with a normal V/Qratio, a low V/Q ratio, a very low V/Q ratio (shunt), and a highV/Q ratio.

Ventilation and perfusion: A critical relationship

22 American Nurse Today Volume 9, Number 11 www.AmericanNurseToday.com

oxygen delivery to the tissues orthe patient’s ventilatory function.So be sure to consider the patient’sentire clinical presentation. Com-pared to SpO2, an ABG study pro-vides more accurate informationon acid-base balance and bloodoxygen saturation. Capnography isanother tool used for monitoringpatients receiving anesthesia andin critical care units to assess a pa-tient’s respiratory status. It directlymonitors inhaled and exhaled con-centration of CO2 and indirectlymonitors PaCO2.

Treatment and managementIn acute respiratory failure, thehealthcare team treats the underly-ing cause while supporting the pa-tient’s respiratory status with sup-plemental oxygen, mechanicalventilation, and oxygen saturationmonitoring. Treatment of the un-derlying cause, such as pneumonia,COPD, or heart failure, may requirediligent administration of antibi-otics, diuretics, steroids, nebulizertreatments, and supplemental O2 asappropriate.

For chronic respiratory failure,despite the wide range of chronicor end-stage pathology present(such as COPD, heart failure, orsystemic lupus erythematosus withlung involvement), the mainstay oftreatment is continuous supplemen-tal O2, along with treatment of theunderlying cause.

Nursing careNursing care can have a tremen-dous impact in improving efficien-cy of the patient’s respiration andventilation and increasing thechance for recovery. To detectchanges in respiratory status early,assess the patient’s tissue oxygena-tion status regularly. Evaluate ABGresults and indices of end-organperfusion. Keep in mind that thebrain is extremely sensitive to O2

supply; decreased O2 can lead toan altered mental status. Also,know that angina signals inade-

quate coronary artery perfusion. Inaddition, stay alert for conditionsthat can impair O2 delivery, suchas elevated temperature, anemia,impaired cardiac output, acidosis,and sepsis.

As indicated, take steps to im-prove V/Q matching, which is cru-cial for improving respiratory effi-ciency. To enhance V/Q matching,turn the patient on a regular andtimely basis to rotate and maxi-mize lung zones. Because bloodflow and ventilation are distrib-uted preferentially to dependentlung zones, V/Q is maximized onthe side on which the patient islying.

Regular, effective use of incen-tive spirometry helps maximize dif-fusion and alveolar surface areaand can help prevent atelectasis.Regular rotation of V/Q lung zonesby patient turning and reposition-ing enhances diffusion by promot-ing a healthy, well-perfused alveo-lar surface. These actions, as wellas suctioning, help mobilize spu-tum or secretions.

Nutritional supportPatients in respiratory failure haveunique nutritional needs and con-siderations. Those with acute respi-ratory failure from primary lungdisease may be malnourished ini-tially or may become malnourishedfrom increased metabolic demandsor inadequate nutritional intake.Malnutrition can impair the func-tion of respiratory muscles, reduceventilatory drive, and decrease lung

defense mechanisms. Cliniciansshould consider nutritional supportand individualize such support toensure adequate caloric and pro-tein intake to meet the patient’srespiratory needs.

Patient and family educationProvide appropriate education tothe patient and family to promoteadherence with treatment and helpprevent the need for readmission.Explain the purpose of nursingmeasures, such as turning and in-centive spirometry, as well as med-ications. At discharge, teach pa-tients about pertinent risk factorsfor their specific respiratory condi-tion, when to return to the health-care provider for follow-up care,and home measures they can taketo promote and maximize respira-tory function. O

Selected referencesCooke CR, Erikson SE, Eisner MD, MartinGS. Trends in the incidence of noncardio-genic acute respiratory failure: the role ofrace. Crit Care Med. 2012;40(5):1532-8.

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

Kaynar AM. Respiratory failure treatment andmanagement. Updated August 14, 2014.http://emedicine.medscape.com/article/167981-treatment#aw2aab6b6b2. Accessed August23, 2014.

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

Pinson R. Revisiting respiratory failure, part1. ACP Hosp. 2013;Oct:5-6. www.acphospi-talist.org/archives/2013/10/coding.htm. Ac-cessed August 23, 2014.

Pinson R. Revisiting respiratory failure, part2. ACP Hosp. 2013;Nov:7-8. www.acphospi-talist.org/archives/2013/11/coding.htm. Ac-cessed October 3, 2014.

Schraufnagel D. Breathing in America: Dis-eases, Progress, and Hope. American Tho-racic Society; 2010.

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

To detect changes inrespiratory statusearly, assess the patient’s

tissue oxygenationstatus regularly.

www.AmericanNurseToday.com November 2014 American Nurse Today 23

Please mark the correct answeronline.

1. Which statement about therespiratory center’s response to changesin carbon dioxide (CO2) and hydrogen-ionconcentration is correct?

a. The respiratory center can compen-sate for changes in hours or days.

b. The respiratory center can compen-sate for changes in seconds or minutes.

c. Alkalemia stimulates the respiratorycenter.

d. Acidemia inhibits the respiratory cen-ter.

2. The most important variable in gasexchange is:

a. amount of wasted air.b. amount of dead space.c. bronchial ventilation.d. alveolar ventilation.

3. Which statement about lungcompliance is correct?

a. Compliance is not related to the workit takes to breathe.

b. High compliance is associated withless work required to breathe.

c. Elastic recoil relates inversely tocompliance.

d. Elastic recoil relates directly tocompliance.

4. Which of the following clinicalfindings indicate acute respiratoryfailure?

a. Partial pressure of CO2 in arterial blood(PaCO2) above 50 mm Hg and pHbelow 7.35

b. PaCO2 below 50 mm Hg and pH above7.35

c. Partial pressure of arterial oxygen(PaO2) increase of 10 mm Hg frombaseline in patients with chronic lungdisease

d. PaCO2 decrease of 10 mm Hg frombaseline in patients with chronic lungdisease

5. Which statement about ventilationand perfusion is correct?

a. When a lung region becomes hypoxic,small arteries constrict in response.

b. When a lung region becomes hypoxic,small arteries dilate in response.

c. A high ventilation/perfusion (V/Q) ratiooccurs when pulmonary gas exchangeis impaired.

d. A low V/Q ratio occurs when a well-ventilated lung area is poorly perfused.

6. In which type of respiratory failure dopatients who are breathing room aircommonly have hypoxemia?

a. Type 1b. Type 2c. Type 3d. Type 4

7. Shunting and V/Q mismatching arecommon causes of which type ofrespiratory failure?

a. Postoperativeb. Perioperativec. Hypercapnicd. Hypoxemic

8. Which type of respiratory failureresults from lung or alveolar atelectasis?

a. Postoperativeb. Perioperativec. Hypercapnicd. Hypoxemic

9. Signs and symptoms of impendingrespiratory failure include:

a. bradypnea.b. tachypnea.c. bradycardia.d. increased SpO2.

10. Which statement about pulmonarycare for patients with respiratory failure isaccurate?

a. V/Q matching is minimized on the sideon which the patient is lying.

b. Incentive spirometry should be usedsparingly.

c. Regular turning helps improve V/Qmatching.

d. Slight decreases in temperature canimpair O2 delivery.

11. Which statement about the nutritionalneeds of patients with respiratory failure iscorrect?

a. Malnutrition can increase ventilatorydrive.

b. Malnourishment typically is not aproblem.

c. Nutritional support requirements areuniversal.

d. Increased metabolic demands cancause malnourishment.

POST-TEST • Caring for patients in respiratory failure Earn contact hour credit online at www.AmericanNurseToday.com/ContinuingEducation.aspx

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Contact hours: 1.32

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PURPOSE/GOAL

To provide nurses with information on how to better care forpatients in respiratory failure.

LEARNING OBJECTIVES

1. Discuss the physiology of ventilation and respiration.2. Differentiate the types of respiratory failure.3. Describe the treatment of respiratory failure.

CNE: 1.32 contact hours

CNE