532 Journal of the Royal Society of Medicine Volume 81 September 1988

Hyperventilation -a therapist's point of view: discussion paper

Jenny C King DipCOT Cardiac Department, Charing Cross Hospital, London W6 8RF

Keywords: hyperventilation; buffer salts; arousal; performance; occupational therapy

Hyperventilation describes respiration that is inexcess of metabolic needs. Commonly it is rapidand arrhythmic with prominent upper chest move-ment and obvious sighing, but it can present asan almost imperceptible exaggeration of normalmovement and rate. The essence of it is the productionof inappropriately low levels of carbon dioxide,termed hypocarbia or hypocapnia, and measureddirectly by sampling arterial blood or indirectlyfrom the partial pressure of carbon dioxide inthe expired air. This paper describes the aspectsof hyperventilation that are important from thetherapist's point of view in everyday practice,namely its presentation as a primary disorder, butnot as a product of organic disease, altitude orhysterical overbreathing.The syndrome we now recognize as hyperventilation

was described in the medical literature by Da Costain 18711 from his study of soldiers who had beenmade incapable of further effort on the battlefieldby the physiological consequences of disorderedbreathing. Many good descriptions have come fromstudies made in wartime where the causes arerelatively violent and the responses acute anddramatic as compared with the more protracted andless intense conditions of peacetime. Apart fromDa Costa's syndrome, many other names have beengiven to the syndrome, e.g. soldier's heart2, neuro-circulatory asthenia3 and effort syndrome4. Lewis5is to be credited with the discovery of the metabolicbasis, an inadequate supply of buffer salts in theblood, and the recognition that the loss ofperformanceand disordered breathing patterns were not solely asoldier's malady but 'one ofthe commonest afflictionsof sedentary town dwellers'6. It was assumed thatthese town dwellers were neurotic7 until Lum madeit clear that the so-called neurosis was usuallyiatrogenic, the consequence of failure of recognitionand treatment8. Many cases today are given labelssuch as postviral syndrome or myalgic encephalo-myelitis.The clinical outcome of hyperventilation does not

depend solely upon the degree ofhypocapnia producedat a given moment because it is also affected by thefactors of chronicity and arousal.

0141-0768/88/090532-05/$02.00/0

1988The RoyalSociety ofMedicine

PathophysiologyChronicityThe transient hypocapnia of short-lived hyperventil-ation is buffered by the body and respiratory alkalosisdoes not occur. When the overbreathing is continued,the kidneys compensate for the respiratory alkalosisby excreting bicarbonate and reducing the body'salkaline reserves. Thus the chronic hyperventilator'spH regulation is finely balanced: diminished acid (theconsequence of hyperventilation) is balanced against

the low level ofblood bicarbonate maintained by renalexcretion. In this equilibrium small amounts of over-breathing induced by emotion can cause large fallsof carbon dioxide (PC2o) and, consequently, moresevere symptoms. In other words, the chronic hyper-ventilator lives closer to the threshold for hypocapniathan the normal person. The emotional arousal is notnecessarily fear or anxiety. It is commonly anger,and it may be laughter, pleasurable excitement orwatching television8.At the same time, the hypocapnia causes increased

adrenergic activity89 and decreased vagal activity8,and the subject's arousal level is increased. A viciouscircle is set up because increases of arousal stimulatethe breathing9. Thus the chronic hyperventilatoris abnormally vulnerable to changes of arousallevel.

ArousalArousal level expresses the position on a continuumfrom torpor or sleepiness at the lower end to conditionssuch as rage, terror, revulsion and ecstasy atthe higher. Kahneman1' defines it as the generalactivation or drive state of the mind which resultsfrom the person's interaction with his environment:what he is doing, the effort he is investing, thestress to which he is exposed and the way it affectshim.Figure 1, a performance/arousal curve12, illustrates

that there are levels of arousal (anabolic) which areconsistent with healthy function and higher levels(catabolic) that exhaust, generate illness or even causea breakdown when the individual loses the ability tocontinue to struggle with the demands made by hisenvironment.Health depends upon the ability of individuals

to adapt and cope in such a way as to maintain a

- Intended

tigue Brustion

! / %<;_ ~~~~~~~~~~~~~Actual

/eafthy tensionlI Breakdown

Arousal 4

Figure 1. Human function curve. A model illustrating thestations ofhealth as a continuum from healthy function andfatigue (upslope) to exhaustion and ill-health (downslope).P=point at which little extra arousal can precipitate abreakdown ofhealth. The dotted line indicates the patient'sintended level of activity and the solid line his actual levelofperformance, i.e. the general ability to cope with activitiesof daily living

PLerormac

Journal of the Royal Society of Medicine Volume 81 September 1988 533

stable and orderly internal milieu irrespective ofwhatis happening to him in his life'3.The level of arousal generated by meeting and

sustaining the challenges ofeveryday life varies fromindividual to individual and from time to time. Theamount that can be tolerated without ill effectdepends upon inheritance, education in its broadestsense, life events, psychological and social influences,the weight, rate and threat of challenges alreadypresented by the environment and the way theindividual perceives them - his self-talk.Some individuals are handicapped by low curves

and others, with higher curves, can cope better andkeep going longer, but no matter what the height ofthe individual's curve, stamina and endurance remainfinite qualities.

Healthy functionAt rest in healthy function on the upslope ofthe curve(Figure 1) breathing is an automatic unconsciousprocess, predominantly diaphragmatic, inspirationbeing the active phase and expiration a passive recoil.Its pattern follows the level of arousal in order toachieve proper oxygenation for the effort in hand, anda proper regulation of PCo2 upon which the orderlyfunction of the autonomic nervous system depends.In the face of danger, distress, excitement or beingtrapped for a moment by inability to see a satisfactorycourse to follow, the breathing of a healthy person

may shift from the basic mammalian diaphragmaticpattern to include prominent movement ofthe upperchest as part ofthe fight, flight or amatory response,

thus increasing the adrenergic drive and activatingthe sympathetic nervous system as vigilance riseswith the prospect of a challenge. Once the action hasbeen decided or the challenge has passed theprominent movement of the upper chest subsides.These transient changes of breathing pattern in

response to effort, challenge and threat, the promiseof reward or sexual activity are a part of healthyhuman function. However, ifthis pattern ofbreathingcauses the PCO2 level to fall too low for optimumautonomic function the individual is handicapped byloss of endurance through inadequately governedheart rate and blood pressure responses, unwantedor inappropriate emotional arousal, and loss ofpotential for effective action. For this reason studentsof the martial arts are taught to be aware and incontrol of their breathing in order to maintain a

proper condition of readiness for challenges.

Healthy fatigueIf the demands of daily life are high the individual

becomes reasonably tired, but, as can be seen on thehuman function curve (Figure 1) performance can

continue to increase with arousal. More effort isrequired to cope than at lower levels of arousal, andstimulants such as alcohol, coffee and cigarettesmay be increasingly used to enhance or sustainperformance'4. The breathing is more easily throwninto disorder as the limits of physiological toleranceare approached and so relatively little extra effort onexertion can cause breathlessness or other symptomsofhypocapnia such as giddiness. One individual mayrecognize fatigue and arrange to overcome it. Anothermight use hyperventilation to 'psyche' himself up,

generating an adrenergic overdrive which carrieshim over the top into an exhausted state. Theindividual who uses hyperventilation to over-ride

fatigue signals is vulnerable to exhaustion and illnessin ways that are not open to non-hyperventilators.

ExhaustionThe human function curve is drawn with a peak toemphasize the watershed between legitimate fatigueand the exhaustion which sets up vicious circles fromwhich the individual can neither recover spontan-eously nor keep up the level of performance needed.The vicious circles of exhaustion promote hyper-ventilation and sleep deprivation, loss of insight andjudgement, social and behavioural deterioration,disorganization of surveillance and self-defence, andhigh levels of anger and despair15.On the downslope of the curve (Figure 1), the

individual naturally struggles to close the gapbetween what he can do and what he thinks isintended of him, but the effort is self-defeating:performance decreases and arousal-induced metabolicdisorders increase. The emotional changes areparticularly important. Struggle with anger oranxiety is linked with activation of the sympatho-adrenomedullary system, and the feelings of despairor the prospect of defeat with stimulation of thepituitary-adrenocortical system'6. Hyperventilationis commonly adopted as a displacement activity whenthe emotions are bottled up, and heightens adrenergicdrive9.The nature and intensity of these products of high

arousal, their aggravation by disordered breathing,and their persistence through failure of habituationand adaptation'7"18 shift the individual downwardsand to the right, widen the gap, reduce performanceand further degrade the organization of the internalmilieu. Loss of sleep is one of the most importantconsequences as it accelerates and aggravates thetransition from an anabolic mode of metabolism to acatabolic mode'9'20.

Ill-healthIn this catabolic mode the internal self-regulatinghomeostatic mechanisms lose their abfihty to maintaina stable and orderly internal milieu and the individualbegins to experience symptoms of ill-health associatedwith the hyperventilation syndrome. Unfortunatelythe individual can rarely see the downhill course andtake effective action to escape because denial removesinsight.The earlier symptoms are unspecific and distributed

among all the body's systems. They have been docu-mented by Lum8. Among the diagnoses commonlypresented to us are angina pectoris with or withoutangiographic abnormality, vasomotor instability,chest pain, syncope and tachyarrhythmia, hypo-glycaemia, hiatus hernia, irritable bowel, ill-defmeddisorders of immunity, migraine, multiple sclerosis,neurological disorders with paraesthesiae, tinnitusand hyperacussis and musculoskeletal aches andpains, anxiety states, phobic disorders, panic attacks,asthma, myalgia and non-pecific arthralgia assocatedwith sleeplessness2l.The major cardiovascular consequences of hyper-

ventilation and exhaustion ofthe buffer reserves havebeen described (Figure 2).

BreakdownThe concept of myocardial infarction and suddencoronary death as a sudden failure of homeostasis,riggred by hyperventilation-induced coronary arterial

534 Journal of the Royal Society of Medicine Volume 81 September 1988

HYPERVENTILATION -__-- hypocapnia

Extracellular alkalosis t catecholamine release

t sympathetic activity

4 vagal activity

4 oxygen uptake (Bohr)

4 potassium

Intracellular alkalosis _ Increased Ca++- o

myocardium

coronary vessels

E.C.G.

Thromboxane A2

systolic contraction

4 diastolic relaxation

4 compliance

Constriction and spasm

Arrhythmia

ST, T abnormality

Vasoconstriction andthrombosis.

Figure 2. Some effects ofhyperventilation-induced respiratoryalkalosis on the cardiovascular system

spasm, with or without atherosclerotic disease, aftera long period of failure of adapting and copinge23provides for creation of strategies for anticipation andprevention that are not conceivable if the death isthought to be from accident or chance.

DiagnosisThe diagnosis ofhyperventilation-linked illness firstdepends upon the doctor's being aware of hyper-ventilation and on the lookout for it, especially amongpatients who complain of fatigue, unspecific illnessand failure ofcoping(effort syndrome). Masse ofclinicalcase notes revealing a multitude of fruitless investi-gations for specific disease may provide advancewarning. The simple questionnaire prepared byGrossman and de Swart24 is a useful pointer to thediagnosis. In the interview, it is important to pay

attention not only to what the patient says, but alsothe way in which the verbal message is delivered:changes ofbreathing patterns may provide the mostuseful information about the way a patient perceivesand copes with his or her environment25. Shortperiods of hyperventilation might highlight topicswith a high but unacknowledged emotional charge.A mindless repetition of questions and answers withincreasingly disordered breathing may indicate thatthe patient is trapped by inability to cope withproblems but too exhausted to assimilate theinformation and answers given by the doctor.The disorders ofbreathing include frequent breaks

in the rhythm such as heaving sighs or inspirationsdeeper than required for the physical effort of theconversation. In the middle or end of a sentence theair is released as an expiratory sigh that is not readilynoticed unless the clinican is on the look-out for it.The PC02 of the expired air can be recorded by

means of a capnograph26 which analyses the airdrawn contin-uously through a fine bore plastic tubefom the nostril. The end-tidal level (Pet coo) closelyreflects the arterial partial pressure when the peakexpiratory flow rate is normal. A reading of30 mmHgor less fis the suspicion of significant hypocapniaat rest. This is especially useful where hypocapnia isnot produced by the usual arrhythmic upper chestbreathing but an undramatic, small and persistentincrease of rate and depth of a normal rhythm ofrespiration.When the Pet C02 is normal at rest a challenge is

required to test the patient's ability to remain belowthe threshold for frank hypocapnia and symptomproduction.

The Hardonk and Beumer forced hyperventilationprovocation test27 is in standard use today. Thepatient overbreathes deeply and quickly for 3 min.Normally the Pet Co2 returns to a level above two-thirds of the resting level within 3 min of the end ofthe test, whereas there is a delay in the return amonghyperventilators. This test may make the patienthighly sensitive to emotional stimuli, and so thesecond challenge is to record the Pet Co2 during therecall of symptoms and circumstances of emotionallycharged events such as admission to a coronary careunit28. A variation of this test is to use the challengeof recall during hypnosis29. The third challenge isexercise30: in the normal case the Pet c02 rises duringexercise, but in the hyperventilator the effort isbrought to an end by hypocapnia. The symptoms maysuggest angina pectoris and the ECG may showischaemic-looking ST depression.Another useful diagnostic trait of chronic hyper-

ventilators is their insensitivity to hypocapnia: levelsof Pet CO2 less than 50% of normal may be regardedas normal (data to be published).

ManagementRecovery from hyperventilation-induced symptomscannot be achieved by tackling the breathing disorderalone; the hyperarousal, the failure ofperformance andthe other downslope disorders must also be considered.On the downslope the patients' denial and infor-

mation input overloading make them incapable ofassimilating the information and executing thechanges needed for recovery. Struggling fruitlesslyto change a habit as deeply rooted as hyperventilationis likely to increase the arousal and move the patientsfurther down the human function curve. They needto be led from illness to health through the twotraditional phases of intervention2'6'31-33.The first phase is the one in which the patients rest

and sleep well enough to recover from the exhaustionof the mind and the degradation of the homeostaticsystems. In the second, patients learn to understandtheir condition, to recover healthy function and toreorganize their life against relapse.

Homeostatic recoveryExcept for the mild and transient overbreathingattacks that can be overcome by rebreathing from apaper bag, the most important step towards homeo-static recovery is the speedy reduction of arousal toa level where the patient can take control and reducethe rate and volume of respiration to a proper level.This reduction can be achieved by the judicious useof diazepam 2-5 mg-chewed and swallowed with adrink ofwater, but only while the patient is acquiringthe confidence and skill to take charge, relax, andovercome the breathing problem.After this the patient must rest and sleep well. A

few days offwork might be required for the recoveryof healthy function. Sleep and the reduction ofvigilance foster the recovery of autonomic stability,the reduction of hyperventilation, the recovery ofthebody's buffering systems and the essential switch froma catabolic to an anabolic mode of metabolism19.In heavier cases, those who have shifted from

exhaustion to ill-health or close to breakdown, a muchlonger period away from duty may be needed. Thepatient is usually reluctant to accept what is required:resenting imprisonment in inactivity, feeling angryand frustrated because the escape into exhausting

Journal of the Royal Society of Medicine Volume 81 September 1988 535

displacement activity is now denied, and feeling guiltybecause he is not working to close the gap betweenwhat he can achieve and what he sees as intendedof him. If the exhaustion is generated at work, aperiod of leave may allow recovery to take place, butwithdrawal is much harder to organize when theexhausting influences are at home.In severe cases, where the patient appears to be

heading towards a catastrophic breakdown such asunstable angina or a recurrence of myocardialinfarction, it may be necessary to admit him tohospital in spite ofthe risk that admissions to hospitalin general and coronary care units in particular canincrease arousal by promoting anxiety, anger, help-lessness, depersonalization and sleep-loss and so pushthe patient further down towards breakdown insteadof rescuing him from it3. Nurses who understandthese factors provide comfort and take care of theneeds for security, confidence and dignity. Their skillsreduce arousal and lead the patient through denial,rage, bargaining and despair into acceptance andreadiness for the second phase of training.The first phase ends when the patient is well rested

and calm, and able to accept the predicament insteadof denying it. A useful clinical sign of this is thepatient being seen to waken and face the worldwithout hyperventilating.

Second phaseBy the end of the first phase many patients, perhapsthe majority, have reached a vantage point fromwhich they can look back, see the psychosocial originsof their illness and correct them spontaneously. It issuggested that this is because they have recovered theproper balance offunction ofthe cerebral hemispheresinstead of being handicapped by a disproportionateoutput from one side'7'35The patients who do not recover spontaneously need

time and help in coming to terms with their illness:without accepting their predicament they cannotlearn how to go back to their environment and adaptand cope in a healthy way. They appear to be handi-capped by alexithymia 6'3, that is to say they seeminsensitive to the somatic effects of exhaustion anddistress: they tend to be unaware of their breathingpatterns, oblivious of fatigue, incapable of choosinga tolerable balance ofrest and effort. Repeated failurekeeps them highly aroused, incompetent and low inself-esteem. The occupational therapist is trained todeal with these handicaps and to spot what the patientrequires for healthy function. The therapist acts asa trainer, helping the patient to become aware ofstrengths and weaknesses and to outwit the problemsthat previously he allowed to overload and underminehim37'38. The rate of progression is usually governedby the patient's ability to recognize and outwitthe temptations to recreate exhaustion and hyper-ventilation by doing too much too soon.In high arousal states and severe chronic hyper-

ventilation, extreme care mustbe taken with breathingand relaxation exercises because the body's bufferingreserves are diminished: reducing the respiratoryr rateand volume may cause distressing acidosis, andreducing the production of co2 by relaxing the limbscan trigger severe hypocapnia39.

ConclusionHyperventilation causes hypocapnia which inducesautonomic instability and a wide variety of bio-

chemical and metabolic changes. These, in turn, producefatigue, inability to sustain effort, unspecific illnessand symptoms mimicking a host of clinical disorders.The outcome of hyperventilation is governed by theindividual's arousal level and his loss ofperformanceat adapting and coping, and it is not usually possiblefor recovery to take place without alleviation ofthesefactors. Although the condition is extremely commonthe diagnosis is rarely made except in the case ofhysterical overbreathers who comprise about 1% ofthe total8. Cases presenting to hospital commonly goundiagnosed for years on end (Fat Folder syndrome)and may be subjected to extravagant and prolongedinvestigations for non-existent specific disease. Anegative coronary arteriogram is commonplace incardiovascular practice. Large numbers grow frustratedand drift away from conventional medicine. Theyprobably make up the bulk of alternative practice.Diagnostic technology is unavailable to most practising

clinicians and the general index of suspicion is low.The purpose of this paper is to increase awareness ofthe condition, to highlight the need for close clinicalobservations in diagnosis and to emphasize the fact thatmanagement requires a biopsychosocial approach4041:palliative treatment is ineffective because it neitheraddresses the problems ofadapting and coping nor thedisability caused by the inappropriate breathing. Theoccupational therapist is trained in the biopsycho-social approach. Herjob is to work with these patientsand teach them how to outwit the psychological andsocial origins of the hyperventilation, and the chronic,relapsing disability that it causes.

Acknowledgments: I would like to thank Dr Peter Nixon forthe opportunity to work in a teaching hospital departmentwhere the biopsychosocial approach is employed. I also thankthe Rayne Foundation and Smith's charity for their support.

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(Accepted 28 March 1988)