Caring For Patients In Respiratory Failure
Caring for patients inrespiratory failureEven if you don’t work in an ICU, you’re likely toencounter patients in respiratory failure.By Michelle Fournier, MN, RN, CCRN-KRESPIRATORYFAILURE is one ofthe most common reasons for admission 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 disease (COPD) in the United States.This article briefly reviews thephysiologic components of respiration, differentiates the main types ofrespiratory failure, and discussesmedical treatment and nursing carefor patients with respiratory failure.lungs to deflate. With normalbreathing, expiration is purely passive. But with exercise or forcedexpiration, expiratory muscles (including the abdominal wall and internal intercostal muscles) becomeactive. These important muscles arenecessary for coughing.Physiologic components ofventilation and respirationThe lung is highly elastic. Lung inflation results from the partial pressure of inhaled gases and the diffusion-pressure gradient of thesegases across the alveolar-capillarymembrane. The lungs play a passive role in breathing, but ventilation requires muscular effort. Whenthe diaphragm contracts, the thoracic cavity enlarges, causing thelungs to inflate. During forced inspiration when a large volume ofair is inspired, external intercostalmuscles act as a second set of inspiratory muscles.Accessory muscles in the neckand chest are the last group of inspiratory muscles, used only fordeep and heavy breathing, such asduring intense exercise or respiratory failure. During expiration, the diaphragm relaxes, decreasing thoracic cavity size and causing the18American Nurse TodayCNE1.32 contacthoursL EARNING O BJECTIVES1. Discuss the physiology of ventilation and respiration.2. Differentiate the types of respiratory failure.3. Describe the treatment of respiratory 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: 11/1/17Volume 9, Number 11Respiration—the process of exchanging oxygen (O2) and carbondioxide (CO2)—involves ventilation,oxygenation, and gas transport; theventilation/perfusion (V/Q) relationship; and control of breathing. Respiration is regulated by chemicaland neural control systems, including the brainstem, peripheral andcentral chemoreceptors, andmechanoreceptors in skeletal muscle 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 ventilation—the volume of air enteringalveoli taking part in gas exchange—is the most important variable in gas exchange. Air that distributes to the conducting airwaysis deemed dead space or wasted airbecause it’s not involved in gas exchange. (See Oxygenation and gastransport.)Ultimately, effective ventilationis measured by the partial pressureof CO2 in arterial blood (PaCO2).All expired CO2 comes from alveolar gas. During normal breathing,the breathing rate or depth adjuststo maintain a steady PaCO2 between 35 and 45 mm Hg. Hyperventilation manifests as a lowPaCO2; hypoventilation, as a highwww.AmericanNurseToday.com
PaCO2. During exercise or certaindisease states, increasing breathingdepth is far more effective than increasing the RR in improving alveolar ventilation.Control of breathingLung recoil and compliance Acidemia (decreased blood pH) or elevated partial pressure of arterial CO2 stim-The lungs, airways, and vasculartrees are embedded in elastic tissue. To inflate, the lung muststretch to overcome these elasticcomponents. Elastic recoil—thelung’s ability to return to its original shape after stretching from inhalation—relates inversely to compliance. Lung compliance indirectlyreflects lung stiffness or resistanceto stretch. A stiff lung, as in pulmonary fibrosis, is less compliantthan a normal lung.With reduced compliance, morework is required to produce a normal tidal volume. With extremelyhigh compliance, as in emphysemawhere there is loss of alveolar andelastic tissue, the lungs inflate extremely easily. Someone with emphysema must expend a lot of effort to get air out of the lungsbecause they don’t recoil back totheir normal position during expiration. In both pulmonary fibrosisand emphysema, inadequate lungventilation leads to hypercapnicrespiratory failure.Respiratory failureRespiratory failure occurs whenone of the gas-exchange functions—oxygenation or CO2 elimination—fails. A wide range of conditions can lead to acute respiratoryfailure, including drug overdose,respiratory infection, and exacerbation of chronic respiratory or cardiac disease.Respiratory failure may beacute or chronic. In acute failure,life-threatening derangements inarterial blood gases (ABGs) andacid-base status occur, and patients may need immediate intubation. Respiratory failure also maybe classified as hypoxemic orhypercapnic.www.AmericanNurseToday.comBreathing is controlled by carefully integrated neurologic, chemical, and mechanical processes. The neurologic respiratory center in the brain’s medulla is sensitive tocarbon dioxide (CO2) and hydrogen-ion concentrations in body fluids. It can compensate to changing conditions within seconds to minutes.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 slower 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 mechanism ultimately affects the ability to exchange gases effectively and can lead tosuch disorders as chronic obstructive pulmonary disease, interstitial lung disease,and respiratory failure.Clinical indicators of acute respiratory failure include: partial pressure of arterial oxygen (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 disease (who tend to have higherPaCO2 and lower PaO2 baselinevalues than other patients).In contrast, chronic respiratoryfailure 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 respiratory failure is type 1, or hypoxemicrespiratory failure (failure to exchange 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 example of V/Q mismatching. Shunting, which occurs in virtually allacute lung diseases, involves alveolar collapse or fluid-filled alveoli.Examples of type 1 respiratory failure include pulmonary edema(both cardiogenic and noncardiogenic), pneumonia, influenza, andpulmonary hemorrhage. (See Ventilation and perfusion: A criticalrelationship.)Type 2, or hypercapnic, respiratory failure, is defined as failure toexchange or remove CO2, indicatedby PaCO2 above 50 mm Hg. Patients with type 2 respiratory failurewho are breathing room air commonly 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 disorders (such as COPD), drug overdose, chest-wall abnormalities, andneuromuscular disease.Type 3 respiratory failure (alsocalled perioperative respiratoryfailure) is a subtype of type 1 andresults from lung or alveolar atelectasis. General anesthesia cancause collapse of dependent lungNovember 2014American Nurse Today19
Oxygenation and gas transportA gas consists of individual molecules in constant random motion. These molecules bombard the walls of any vessel containing them, exerting pressure against the wall. The pressureexerted is proportional to gas temperature and concentration.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.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 plasma layer measures about 1 micron—roughly 100 times smaller 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 tissues. 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 gasexchange.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 proportional to the thickness of the respiratory membrane. Suchconditions as pulmonary edema, excessive sputum, and fibrosis thicken the membrane, lengthening the distance required to cross the membrane. Surface area. The lung’s large surface area is influenced byalveolar size and inflation. Surface area is directly proportional to diffusion; a large surface area favors diffusion.Clinical conditions that reduce surface area include atelectasis and such procedures as lobectomy. Gas solubility and molecular weight. Each gas has an inherent solubility and molecular weight. The diffusion rateof a gas is directly proportional to its solubility and inversely proportional to its molecular weight. AlthoughCO2 weighs more than O2, it’s more soluble and diffuses20 times faster. Damage to the respiratory membrane impairs O2 diffusion capacity but may not affect CO2 diffusion. Therefore, in disease states, the partial pressure ofO2 in arterial blood (PaO2) decreases before the partialpressure of CO2 in arterial blood (PaCO2) changes. So patients with pulmonary diseases that interfere with diffusion develop problems related to hypoxemia before theystart retaining CO2. Driving pressure. In the lung, driving pressure is the gradient 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 increases driving pressure.alveoli. Patients most at risk fortype 3 respiratory failure are thosewith chronic lung conditions, excessive 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 experiencing shock, from hypoperfusion ofrespiratory muscles. Normally, lessthan 5% of total cardiac outputflows to respiratory muscles. Butin pulmonary edema, lactic acidosis, and anemia (conditions thatcommonly arise during shock),20American Nurse Todayup 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, tachypnea, and decreased SpO2 despiteincreasing amounts of supplemental oxygen.Acute respiratory failure maycause tachycardia and tachypnea.Other signs and symptoms includeperiorbital or circumoral cyanosis,Volume 9, Number 11diaphoresis, accessory muscle use,diminished lung sounds, inability tospeak in full sentences, an impending sense of doom, and an alteredmental status. The patient may assume the tripod position in an attempt to further expand the chestduring the inspiratory phase of respiration. In chronic respiratory failure, the only consistent clinical indictor is protracted shortness ofbreath.Be aware that pulse oximetrymeasures the percentage of hemoglobin saturated with oxygen, butit doesn’t give information aboutwww.AmericanNurseToday.com
Ventilation and perfusion: A critical relationshipFor 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 ventilation 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 vasculature directs most of the blood flow through the lower (dependent) 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 arteries feeding that region sense hypoxia in alveolar gas and constrict 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, hypoxemiawww.AmericanNurseToday.commay result. Causes of extreme V/Q mismatching include: shunting, in which alveolar perfusion is normal but ventilation is absent dead space—portions of the respiratory tract where airdoesn’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 increased partial pressure of CO2 in arterial blood (PaCO2). However, this is rare because increased PaCO2 typically triggers respiratory stimulation and increased alveolar ventilation, whichreturns PaCO2 to normal. This scenario is most common in patients with chronic bronchitis, asthma, and acute pulmonaryedema.On the other hand, a high V/Q ratio occurs when a wellventilated 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.November 2014American Nurse Today21
oxygen delivery to the tissues orthe patient’s ventilatory function.So be sure to consider the patient’sentire clinical presentation. Compared to SpO2, an ABG study provides more accurate informationon acid-base balance and bloodoxygen saturation. Capnography isanother tool used for monitoringpatients receiving anesthesia andin critical care units to assess a patient’s respiratory status. It directlymonitors inhaled and exhaled concentration of CO2 and indirectlymonitors PaCO2.Treatment and managementIn acute respiratory failure, thehealthcare team treats the underlying cause while supporting the patient’s respiratory status with supplemental oxygen, mechanicalventilation, and oxygen saturationmonitoring. Treatment of the underlying cause, such as pneumonia,COPD, or heart failure, may requirediligent administration of antibiotics, 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 supplemental O2, along with treatment of theunderlying cause.Nursing careNursing care can have a tremendous impact in improving efficiency of the patient’s respiration andventilation and increasing thechance for recovery. To detectchanges in respiratory status early,assess the patient’s tissue oxygenation status regularly. Evaluate ABGresults and indices of end-organperfusion. Keep in mind that thebrain is extremely sensitive to O2supply; decreased O2 can lead toan altered mental status. Also,know that angina signals inade22American Nurse TodayTo detect changes inrespiratory statusearly, assess the patient’stissue oxygenationstatus regularly.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 improve V/Q matching, which is crucial for improving respiratory efficiency. To enhance V/Q matching,turn the patient on a regular andtimely basis to rotate and maximize lung zones. Because bloodflow and ventilation are distributed preferentially to dependentlung zones, V/Q is maximized onthe side on which the patient islying.Regular, effective use of incentive spirometry helps maximize diffusion and alveolar surface areaand can help prevent atelectasis.Regular rotation of V/Q lung zonesby patient turning and repositioning enhances diffusion by promoting a healthy, well-perfused alveolar surface. These actions, as wellas suctioning, help mobilize sputum or secretions.Nutritional supportPatients in respiratory failure haveunique nutritional needs and considerations. Those with acute respiratory failure from primary lungdisease may be malnourished initially or may become malnourishedfrom increased metabolic demandsor inadequate nutritional intake.Malnutrition can impair the function of respiratory muscles, reduceventilatory drive, and decrease lungVolume 9, Number 11defense mechanisms. Cliniciansshould consider nutritional supportand individualize such support toensure adequate caloric and protein 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 incentive spirometry, as well as medications. At discharge, teach patients about pertinent risk factorsfor their specific respiratory condition, when to return to the healthcare provider for follow-up care,and home measures they can taketo promote and maximize respiraOtory function.Selected referencesCooke CR, Erikson SE, Eisner MD, MartinGS. Trends in the incidence of noncardiogenic acute respiratory failure: the role ofrace. Crit Care Med. 2012;40(5):1532-8.Gehlbach BK, Hall JB. Respiratory failureand mechanical ve
acute failure. Three main types of respiratory failure The most common type of respira - tory failure is type 1, or hypoxemic respiratory failure (failure to ex - change oxygen), indicated by a Pa O2 value below 60 mm Hg with a normal or low Pa CO 2 value. In ICU patients, the most common cau
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