PHYSICAL

43 Respiratory Rate and PatternSHELDON R. BRAUN

Definition

Normal ventilation is an automatic, seemingly effortless in-spiratory expansion and expiratory contraction of the chestcage. This act of normal breathing has a relatively constantrate and inspiratory volume that together constitute normalrespiratory rhythm. The accessory muscles of inspiration(sternocleidomastoid and scalenes) and expiration (abdom-inal) are not normally used in the resting state. Abnormal-ities may occur in rate, rhythm, and in the effort of breathing .

Technique

The establishment of the tidal volume and pattern of res-piration in normal individuals is a complicated process . Rec-ognizing alterations in these factors is an important earlyclue of disease recognition . While frequently it is nonspe-cific, in many instances it can lead directly to a diagnosis .Careful observation of the respiratory rate and pattern is acrucial part of the physical examination .

Simple inspection of the respiratory cycle, observing rate,rhythm, inspiratory volume, and effort of breathing, is allthat is necessary. The rate is noted by observing the fre-quency of the inspiratory phase, since this phase is activeand easy to count. Record the number of breaths per min-ute; this is the respiratory rate . While observing the rate,note the inspiratory expansion of the chest cage . This ex-pansion should be the same during each cycle .

Normally, the accessory muscles of inspiration and ex-piration are not used . Their use should be observed and,if found, recorded as "use of accessory muscles on inspi-ration" and "expiration is active with abdominal musclecontraction."

Basic Science

The respiratory system's major functions are to provide anadequate oxygen (0 2 ) supply to meet the energy productionrequirements of the body and maintain a suitable acid-basestatus by removing carbon dioxide (CO 2 ) from the body .This is accomplished by moving varying volumes of air intoand out of the lungs . Ventilation, the process of air move-ment into the lungs, is a carefully controlled modality witha wide range of response that enables the markers of gasexchange adequacy (Pao 2 , Paco2 , and pH) to be kept withina relatively small physiologic range .

To maintain accurate control the respiratory system hasa central respiratory pacemaker located within the medullaof the brainstem . Neural output travels from this centerthrough the spinal cord to the muscles of respiration . Thechanges are effected through two groups of muscles, in-spiratory and expiratory, which contract and relax to pro-duce a rhythmic respiratory rate and pattern . In most

individuals with unchanging metabolic demand, the rateand pattern are surprisingly constant, only interrupted everyseveral minutes by a larger inspiratory effort or sigh . Ven-tilation at rest in most individuals requires only the inspi-ratory muscles . Expiration is usually passive and is secondaryto the respiratory system returning to its resting state .Therefore, with quiet breathing the inspiratory time is theperiod of active respiratory pacemaker output. Adjustingthe rate, length, and intensity of neural output from thepacemaker will lead to changes in the breaths per minuteand the volume of each inspiration or tidal volume . Thesefinal outputs of the respiratory pacemaker, the rate andtidal volume, are the two components of ventilation . Theexpiratory muscles begin to play a role with disease or in-creased ventilatory demands . When this occurs, the lengthof time it takes to empty the lungs adequately will also leadto changes in rate and tidal volume .

Minute ventilation is the product of rate and tidal vol-ume . It is important to differentiate between the effectchanges in rate and tidal volume have on gas exchange . Anygiven tidal volume is divided into two components . Onepart is the dead space . This is the portion of the volumemoved into the lungs during ventilation that does not comeinto contact with functioning pulmonary capillaries . An ex-ample is air at the end of inspiration, which reaches onlythe trachea or bronchi where there are no capillaries . Sincethere is no air-blood interface, 0 2 cannot reach the circu-lation nor can any CO 2 be removed. The other componentis called the alveolar volume . This is the part of a tidal breaththat enters the air spaces of the lung that are perfused byfunctioning capillaries . In normal individuals these air spacesare the terminal respiratory unit and include the respiratorybronchioles, alveolar ducts, alveolar sacs, and alveoli . Onlythe alveolar volume component of each tidal breath con-tributes to gas exchange ; the rest is really wasted ventilation .If minute ventilation is increased by making the tidal volumelarger, it will have a greater effect on gas exchange than ifthe same minute ventilation is reached by increasing therate .

Regulation of Pacemaker Output

The medullary respiratory control center, or pacemaker,receives three kinds of feedback . These impulses are inte-grated within the control center . The output from the res-piratory center is then altered in timing or intensity, leadingto changes in the rate and tidal volume . The three kinds offeedback are chemical, mechanical, and input from highercortical centers .

The normal individual is able to keep Pao 2 , Paco 2 , andpH within narrow limits . In order to accomplish this levelof control, the respiratory center receives input from bothperipheral and central chemoreceptors . The major periph-eral receptors are located within the carotid bodies found

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in the bifurcation of each common carotid artery . Thereare also similar structures in the aorta, but less is knownabout these aortic bodies . The afferent limb of these re-ceptors responds to Pao 2 and pH changes . The efferentlimb produces changes in minute ventilation through therespiratory control center . The response to changing Pao 2levels can be detected as high as 550 mm Hg, but at thatPao2 level the resulting change in rate and volume is small .As the Pao2 drops to 55 to 60 mm Hg, there is a muchgreater and more important respiratory response with largeincreases in minute ventilation for each mm Hg change inPao2 . The carotid body also responds to small changes inpH, but approximately two-thirds of the response to pH isa result of the central chemoreceptors . The response of thecarotid bodies to Paco2 is secondary to changes in pH re-sulting from the Paco 2 change .

The medullary chemoreceptor is located on the ventralsurface of the medulla. This receptor responds to changesin pH and is the most important receptor regarding res-piratory changes to acid-base alterations . It responds tochanges in cerebrospinal fluid rather than blood and is verysensitive to very small changes in the hydrogen ion concen-tration in the cerebrospinal fluid . Since CO2 rapidly crossesthe blood-brain barrier, it rapidly alters the pH of the spinalfluid. An increase of 1 mm Hg of Pco 2 in the cerebrospinalfluid leads to an increased ventilation of 2 to 3 liters perminute. The medullary chemoreceptor also adjusts the res-piratory response to altered pH secondary to metabolic aci-dosis or alkalosis . With the slower equilibration of hydrogenor bicarbonate across the blood-brain barrier, however, thesechanges are not as quick as the rapid respiratory changesproduced by a change in Pco2 .

Another neural input to the respiratory pacemaker comesfrom receptors in the lung and is related to the mechanicalproperties of the lung . An individual who elected to breatheat a rate of 5 breaths per minute with a large tidal volumewould have efficient gas exchange because the ratio of deadspace to tidal volume would be low . The larger the inspi-ratory lung volume, however, the greater becomes the elas-tic recoil of the lung . At greater lung volumes, chest wallelasticity is also added and must be overcome. Therefore,the larger the inspiratory lung volume, the greater the in-spiratory pressure needed to overcome the elastic recoil andexpand the lung . The greater the inspiratory pressure, thegreater is the work of breathing by the respiratory muscles .The respiratory system appears to choose a rate that re-quires the least amount of mechanical work while main-taining adequate gas exchange . There is a wide range oftidal volumes before the mechanical limitation comes intoeffect, but there appear to be lower limits of rates that arenot tolerated because of the required increase in inspiratorywork .

Receptors in the lung itself appear to contribute to thisinspiratory limitation . One group is the stretch receptors .Efferents from these increase their neural output the largera given lung volume becomes . In some animals these re-flexes are very important, but in normal humans they ap-pear to be less important and can be easily overcome byother neural inputs. The output of these receptors can,however, limit the degree of inspiration by means of theHering-Breur reflex. Probably in disease states this reflexplays a more important role in limiting inspiration . Theother lung parenchymal receptors that may play a role inlimiting the size of each tidal volume are the juxtapulmona

ry capillary receptors, or J-receptors. These receptors firewhen pulmonary capillaries are distended .

A final modulator of the central respiratory drive is inputfrom higher centers . For example, the state of being awakeis associated with important neural inputs to the respiratorycenter that will play a large role in determining an individ-ual's respiratory rate and pattern. When an individual fallsasleep, the cortical input decreases, as does the respiratorycenter output . During nondreaming or non-rapid-eye-movement sleep, the input from the chemical receptors be-comes increasingly important. If absent, apnea may result .During sleep associated with rapid eye movements ordreaming, the breathing patterns may be related to thecontents of the dreams and again reflect input from highercortical centers . Higher center input also accounts for hy-perventilation associated with anxiety and other behavioralfactors .

Alterations in Rate and Tidal Volume

All three types of input are integrated in the medullaryrespiratory center and lead to changes in the minute ven-tilation . These changes are seen as changes in rate, volume,or both. Table 43 .1 demonstrates how these factors mayinterrelate in normal individuals . If the ventilation duringa minute (minute ventilation) was 6 liters and was done ata rate of 60 breaths with a tidal volume of 100 cc each, therewould be no alveolar ventilation at all . This is because thenormal dead space consisting of the trachea and some bron-chi is about 150 cc. Even if the rate was slowed to 30 breathsper minute, the result would be an alveolar ventilation ofonly 1 .50 L. This would be inadequate to meet CO 2 pro-duction and would lead to an elevation of the Paco 2 and alowering of the pH . Both the central and peripheral chemo-receptors would be stimulated . There might also be a con-comitant fall in Pao2 , which would lead to increased neuraloutput from the carotid bodies . The result of the increaseof input to the central center would be an alteration in therate and pattern of breathing .

Table 43 .1The Effect of Changes of Respiratory Rate and Tidal Volume on Alveolar Ventilation

Minute

Respiratoryventilation (L)

rateTidal

volume (L)Dead space°

(L/min)Alveolar ventilation

(L/min)

6.0 60 0 .1 6 .0 06 .0 30 0.2 4 .5 1 .56 .0 15 0 .4 2.25 3 .756 .0 2 3 .0 0 .3 5 .7

'A dead space of 150 ml/breath is assumed .

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A third breathing alternative would be choosing a res-piratory rate of 2 per minute . This would give an extremelyefficient breath with very little wasted as dead space . Theproblem with the large volume is it would require increasedwork of breathing and stimulate stretch receptors . There-fore, unless a constant conscious effort was maintained, therespiratory central center would inhibit inspiratory effectbefore reaching tidal volumes of 3 liters . Furthermore, thevery efficient gas exchange could lead to a lowered Paco 2 .The resulting increased pH would produce less drive tobreathe and lower minute ventilation. The best alternativein a normal individual would be to choose an intermediaterate of 10 to 20 breaths per minute . The example of 15breaths per minute would meet metabolic needs effectively .

In normal individuals, multiple factors affect the respi-ratory rate and pattern at rest . Normal people also mustadjust to changing metabolic demands, as seen with exer-cise. Using the input from various receptors, the respiratorycenter finely adjusts both rate and pattern to keep Pao 2 andpH within a relatively small range in spite of increased meta-bolic demands of 15 or more times the needs at rest .

Clinical Significance

Abnormal Central Respiratory Control

Altered respiratory rate and pattern often accompany avariety of disease states . These diseases frequently lead toalterations in one of the three kinds of feedback to thecentral respiratory control center or in the control centeritself. For example, pathological conditions altering Pao2,Paco2, or pH can obviously alter the input from both thecarotid body and the medullary chemoreceptors . The usualresponse to any altered chemoreceptor input is, first, achange in tidal volume, followed by change in respiratoryrate. Therefore, lung diseases that cause acute hypoxemiato a level lower than 55 to 60 mm Hg will usually produceincreased ventilation . The response to increasing Paco 2 andlowered pH can produce rapid changes in minute ventila-tion also by stimulating the chemoreceptors . The elevationof Paco 2 is not always associated with the expected increasein minute ventilation, however . Elevation of PaCO2 can leadto CO 2 narcosis and depression of the respiratory center .Metabolic acidosis, in contrast, will most likely increase theventilation predominantly by increasing the tidal volume .Kussmaul respiration, the classic pattern seen in diabeticketoacidosis, consists of slow, deep breaths that reflect theincreased tidal volume and actual slowing of rate . The oc-currence of respiratory compensation for a metabolic changemay be slowed because cerebrospinal fluid changes lag be-hind blood changes . An acute pH drop in the blood willstimulate the peripheral chemoreceptors, leading to hyper-ventilation and acutely lowering the Paco2 . This will leadto a lowered Pco 2 in the cerebrospinal fluid . Since the hy-drogen ion associated with the metabolic acidosis does notcross the blood-brain barrier immediately, the medullarychemoreceptors may initially reduce respiration because thereduced Pco 2 will make the cerebrospinal fluid alkalotic . Ina matter of hours the spinal fluid pH is decreased, and theappropriate response will occur . Ventilation will also beslowed with metabolic alkalosis. This change may not bedetectable on routine physical examination . Nevertheless,it can also lead to enough slowing that the Paco 2 becomesmarkedly elevated .

Mechanical properties also are altered by diseases . In-terstitial disease probably enhances the stretch receptor re-sponse, leading to rapid shallow ventilation . This is efficientbecause the lung with interstitial disease is less compliant,requiring more distending pressure per unit of volume thannormal. By breathing at lower tidal volumes, the work ofbreathing is diminished . Congestive heart failure can pro-duce a similar effect . This is partly related to the reducedcompliance, but also may be a result of stimulation of theJ-receptors, which lie right next to the capillaries .

The respiratory center feedback from the higher corticalcenters can also be modulated with diseases . Anxiety canincrease the respiratory rate and pattern . The acute hy-perventilation syndrome is an example where drive fromhigher centers can maintain a high minute ventilation inface of an elevated pH . Increased intracranial pressure leadsto a rapid and deep breathing pattern . This pattern is fre-quently seen with head trauma . Pain contributes to a rapidrespiratory rate. A fractured rib produces pain on inspi-ration and therefore leads to a low-volume, rapid-rate pat-tern. Tachypnea is commonly part of any chest pain and ispartly modulated through higher cortical input .

The central controlling center can be affected directly .Any central nervous system depressing drug will reduce therespiratory rate and pattern. It will also blunt the responseto other neural inputs . The patient with obstructive lungdisease who receives a narcotic frequently will elevate thePaco 2 even further. The same is true for many drug ov-erdoses. If the central nervous system is depressed by drugs,the depression of the respiratory center leads to CO 2 re-tention .

Central Nervous System Abnormalities

The changing rate and pattern of respiration can oftensuggest localization of CNS changes . Understanding of theareas of the brain involved with specific patterns have comefrom animal studies . Lesions or cuts made in various partsof the brain lead to specific breathing patterns . Transectionof the pons will not affect normal breathing if the vagi areintact. If vagi are cut, however, larger tidal volumes with aslower rate are observed . A midpons transection will leadto maintenance of spontaneous breathing but with a slowand regular pattern . If the vagi are cut, apneustic breathingoccurs. This is sustained inspiratory spasm . Pontomedullaryjunction transection will lead to an irregular, ataxic breath-ing pattern .

Abnormal Respiratory Patterns

Cheyne-Stokes breathing is a classic breathing pattern seen inboth normal individuals at altitude and individuals withsevere neurological or cardiac disease. The pattern (Figure43.1) demonstrates periods of hyperventilation alternatingwith periods of apnea . The apneic spells can last as long as45 seconds . The abnormality appears to be related to a slowfeedback loop and an enhanced response to Paco 2 . Duringperiods of hyperventilation, the Paco2 is at its highest, whilethe Pao, is at its lowest . As ventilation slows, the Paco 2 dropsand reaches its lowest level during apnea . It is important toobserve that Paco 2 levels do not exceed the normal rangeduring any part of the cycle .

43 . RESPIRATORY RATE AND PATTERN

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Figure 43.1Cheyne-Stokes breathing .

There are several probable causes of this abnormalbreathing pattern . Many cases have diffuse cerebral dam-age, whereas some individuals are in congestive heart fail-ure. It is seen in normal individuals during sleep at altitude .It has been shown in dogs that a markedly prolonged cir-culation time from the left ventricle back to the brain canalso induce Cheyne-Stokes respiration . In individuals witheither neurological or cardiac disease it frequently is a poorprognostic sign . Treatment is usually improvement of theunderlying disease, but aminophylline has been effective insome cases .

A Cheyne-Stokes respiratory pattern can also be seen inindividuals with much more severe neurological depression .These individuals have a low pontine or upper medullarylesion. Unlike the more classic Cheyne-Stokes respiration,these individuals are cyanotic and have CO 2 retention. Theyhave reduced sensitivity to CO 2 . Oxygen will enhance thispattern, while it may reduce the more classic picture .

Biot respiration, or cluster breathing, is also periodic innature but does not have the crescendo-decrescendo pat-tern seen with Cheyne-Stokes respiration . It is clusters ofirregular breaths that alternate with periods of apnea . Thisbreathing pattern is seen in individuals with pontine lesions .Ataxic breathing is one of varying tidal volumes and rates .

These individuals can frequently keep their rate morerhythmic if they try consciously . The abnormality is in themedullary chemoreceptor or the medullary respiratory con-trol center .

One other aspect of respiratory pattern must be consid-ered. This is the coordination between the chest wall andabdomen. Normal individuals contract both the diaphragmand external intercostal muscles during inspiration . Onphysical examination the action of both inspiratory muscleactions can be determined . The diaphragm, when contract-ing normally, moves the abdominal contents downward andoutward. In Figure 43 .2 this is represented by an upwarddeflection of the abdominal curve . On physical examinationit is felt as an anterior movement of the abdomen . Theother major groups of inspiratory muscles, the external in-tercostals, move the chest wall outward . This can also bedetermined by feeling an anterior movement of the chestwall during inspiration and is reflected in the figure as anupward deflection . In normal persons, therefore, there isa coordinated movement of the chest wall and abdomenmoving outward on inspiration and inward on expiration .Alterations in this pattern will allow diagnosis of changingrespiratory muscle contribution to the tidal breath .

Paralysis of the intercostals results from cervical spinalcord injury. In this group of patients on physical exam thereis a paradoxical movement of the chest wall inward and theabdomen outward during inspiration (Figure 43 .2). Thisreflects the passive movement of the chest wall. The patternresults from the tidal breath being produced by diaphrag-matic contraction . Diaphragmatic paralysis can be diagnosedor suggested by an inward movement of the diaphragmduring inspiration. This movement is accentuated in thesupine position . In that position, diaphragmatic contractionproduces approximately two-thirds of the inspiratory vol-ume as compared to one-third in the upright position .

Diaphragmatic dysfunction can also be diagnosed withthe finding of the same paradoxical inward abdominal

Figure 43 .2Chest wall and abdominal coordination during tidal breathing .

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movement during inspiration . This pattern of respirationis seen in some individuals with severe emphysema and airtrapping. The air trapping leads to a low, flat diaphragm.The diaphragm no longer can contract effectively . Thisinability to contract is demonstrated by the inward inspi-ratory movement of the abdomen. The movement resultsfrom the ineffective diaphragm being pulled into the thoraxduring inspiration . This breathing pattern has been re-ported to have a predictive value for impending respiratoryfailure .

Another value of determining changes in chest wall ab-dominal breathing patterns has been seen in individualsbeing weaned from mechanical ventilation . They developa respiratory alternans pattern. A series of tidal breaths al-ternates between a short period of abdominal inward move-ment during inspiration followed by a period of chest wallinward movement during inspiration. This has been dem-onstrated to be associated with fatigue and indicates wean-ing should be stopped .

Other Applications of Respiratory Rate and Pattern

Understanding respiratory rate and pattern is a very im-portant addition in dealing with many respiratory, cardiac,and neurological diseases . Nevertheless, understanding therole of rate and tidal volume is also essential in managingindividuals requiring mechanical ventilation . This is oneclinical situation where the physician can directly manipu-late the respiratory rate and pattern to produce the appro-priate arterial blood gases . The sum of each alveolar volume

over one minute is the alveolar ventilation and is inverselyrelated to the Paco 2 . Hyperventilation reduces Paco 2 , lead-ing to decreased respiratory drive and a patient who doesnot "trigger" the ventilator . Hypoventilation produces CO 2retention and increased respiratory drive by the patient .This leads to either rapid ventilation rates triggered by thepatient or a patient demonstrating marked discomfort . Con-sideration of dead space is important. Diseases can increasethe dead space by reducing the capillary bed . Therefore,larger tidal volumes may be necessary to get adequate gasexchange. Finally, volumes that are too large lead to asy-chrony by the patient who tries to start the next breathbefore the ventilator is ready . This may relate to stretchreceptor responses, but is a fatiguing and inefficient modeof gas exchange .

References

Brown HW, Plum F . The neurological basis of Cheyne-Stokes res-piration. Am J Med 1961 ;30:849-86.

Cohen CA, Zagelbaum G, Gross D, Roussos CH, Macklen PT . Clin-ical manifestation of inspiratory muscle fatigue . Am J Med1982;73:308-16 .

Kryger MH. Abnormal control of breathing . In : Kryger MH, ed .Pathophysiology of respiration . New York : Wiley, 1981 ;103-22 .

Mead J. Control of respiratory frequency . J Appl Physiol 1960 ;12:882-87 .

Tobin MJ, Snyder JV . Cheyne-Stokes respiration revisited : con-troversies and implications . Crit Care Med 1984 ;12 :882-87 .