Ahmedzai-Hjelmeland Sam

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171www.onk.ns.ac.yu/Archive    October 1, 2004Evaluation and management of dyspnoeaSam Hjelmeland AhmedzaiKEY WORDS: Dyspnoea; Medical Oncology; Neoplasms; Palliative CareAcademic Palliative Medicine Unit, The University ofSheffield, Royal Hallamshire Hospital, Sheffield, UK;Address correspondence to: Sam Hjelmeland AhmedzaiMD, FRCP, Professor of Palliative Medicine, AcademicPalliative Medicine Unit, The University of Sheffield, RoyalHallamshire Hospital, Sheffield S10 2JF, UK; The manu-script was received: 15.08.2004, Accepted for publication:15.09.2004© 2004, Institute of Oncology  Sremska Kamenica, Serbia &MontenegroArch Oncol 2004;12(3):171-2.SYMPOSIUM ARTICLEUDC: 616-052:616-006:504.06Dyspnoea is one of the commonest symptoms experienced by patients with cancer -both as a feature of the disease and also as a consequence of its treatments.  In arecent Canadian series of nearly 1000 cancer out-patients, 46% reported dyspnoea (1).The Medical Research Council (MRC) of the UK has found that of lung cancer patientsentering its trials, dyspnoea was a presenting complaint in 87% of small cell cancer and in86% of non-small cell cancer patients.  In advanced cancer, 33% of patients entering aJapanese hospice reported dyspnoea but that rose to 66% near to death (2).CAUSATIONDyspnoea is the end result of many discrete but overlapping potential pathways of patho-physiological change that can occur in patients with cancer.  These are modified and maybe amplified by :- Co-morbidities (especially COPD, other chronic lung diseases and heart disease);- De-conditioning associated with immobility and cancer cachexia;- Effects of ageing;In any single patient, several of these factors could be involved, to produce a symptom leveland an effect on functioning and quality of life.  Thus, the assessment and management ofdyspnoea requires a good understanding of the underlying mechanisms.  However, the clin-ical features displayed by patients with dyspnoea are often non-specific and this oftenmakes it difficult -even with laboratory testing and medical imaging - to differentiatebetween different pathophysiological causes.  There are three basic dimensions of the sensation of dyspnoea: (1) Air hunger - theunpleasant sensation of the need to breathe harder, but being unable to actually increaseventilation; (2) Effort of breathing - the physical discomfort and tiredness associated withprolonged hard breathing; (3) Chest tightness - the feeling of constriction in the chest walland the inability to breathe in or out.There are several validated questionnaires, which have been developed to capture thesedimensions of dyspnoea and their impact on functioning and quality of life (3).In broad terms, the main causes of dyspnoea are :- Increased chemical or neurological drive to breathe- Increased work of breathing- Decreased neuromuscular power to ventilate.Often in cancer patients, especially those with cachexia, there is a combination of these fac-tors.  Identifying which of these mechanisms are at work in an individual patient can behelpful for planning rational treatment.The major neurochemical drives, which control normal breathing and can influence dysp-noea, are the response to hypercapnia and to hypoxia.   Usually the hypercapnic drive isstronger and is mainly responsible for the sensation of air hunger.  Hypercapnia results fromsevere airflow obstruction or restrictive lung disease.  Hypoventilation can also arise fromrestriction of chest movement by pleural effusion and ascites.  Very small increases inPCO2 can give measurable change in the sensation of dyspnoea.Hypoxia can be caused by loss of alveoli or small air-conducting bronchioles, leading toreduced or turbulent airflow.  It can arise in bronchopneumonia, airflow obstruction, pul-monary congestion and lung collapse.  Ventilation-perfusion mismatching, e.g., with pul-monary thromboembolism, can also cause hypoxia.Besides the neurochemical drives to respiration, the other important mechanisms thatimpact on dyspnoea are the mechanoreceptors and the ergoreceptors (also called meta-boreceptors) (4).  These are responsible for the increased ventilation seen in pulmonarycongestion (via J-receptors) and the generation of dyspnoea in muscle wasting conditions.Increased work of breathing arises when the "ventilatory pump" is working against a signif-icant strain, e.g., in pneumonia, pulmonary fibrosis, pleural effusion, lymphangitis carcino-matosa, upper airway obstruction, and emphysema.  Clinical clues, which help to identifythis factor, include the patient favouring the upright position, or stridor.Decreased neuromuscular power is seen in patients with neurological impairment, e.g.,phrenic nerve palsy, cachexia and other wasting disorders (including steroid-inducedmyopathy).  The maximal inspiratory pressure (MIP) is a useful pulmonary function labora-tory method of determining neuromuscular power.ASSESSMENTPut together, the signals from the peripheral and medullary receptors to the brain process-ing areas form the "feed-back" system, while the neurogenic flow from the brain to the res-piratory muscles are the "feed-forward" system.  When an imbalance forms between thesetwo information flows, the resulting ’error signal’ is a key factor in the generation of the sen-sation of dyspnoea4.It is important to be aware of non-respiratory causes of dyspnoea, e.g., anaemia, heart fail-ure and pulmonary thromboembolism.  With normal ageing, several changes take place -- Decreased lung elasticity- Decreased respiratory muscle strength- Reduced forced vital capacity and peak flow rate- Increased air-trapping- Deterioration in gas exchange- Reduced ventilatory response to hypoxia and hypercapnia- Increased ventilatory response to exercise.Bedside assessment of the breathless patient therefore requires several clinical measures:- Observation of the patient’s position and behaviour- Clinical examination of the chest and heart- Pulse oximetry- Simple exercise testing.Further investigations that may be helpful include -- Medical imaging (chest radiograph; ultrasound; CT for mediastinal features)- Response in dynamic lung volumes to bronchodilator- Flow-volume loop if upper airway obstruction is suspected- MIPMANAGEMENTWith the preceding grounding in respiratory physiology and understanding of the patholog-ical mechanisms, it is possible to prepare a rational multimodal plan for management.  First,treatable factors should be tackled, e.g., pleural effusion, heart failure, anaemia, andreversible airflow obstruction.  If anti-cancer treatments are still feasible (radiation orchemotherapy) then these should be started sooner rather than later.  Agents, which modify the neurochemical drives, are most helpful for symptomatic pallia-tion.  These include the opioids, benzodiazepines and oxygen.  Systematic review favoursoral or subcutaneous morphine but other opioids may have advantages (5).  The additionof helium to oxygen (heliox) gives significant improvement to exercise-related dyspnoea inlung cancer (6).   Novel approaches, e.g., nebulised frusemide, need further evaluation (7).Non-pharmacological approaches are nearly always helpful, particularly in the early stages.These include psychological therapies, breathing training and acupuncture (8).   However,in the terminal stage, the management of dyspnoea requires sensitive use of sedation-inducing drugs, oxygen and nursing care.REFERENCES1. Dudgeon DJ, Kristjanson L, Sloan JA, Lertzman M, Clement K.Morit. Dyspnea in cancer patients:prevalence and associated factors. J Pain Symptom Manage 2001;21(2):95-102.2. Hoskins P, Ahmedzai SH.  In: Ahmedzai SH, Muers M, editors. Supportive care in respiratory dis-ease. Chapter 30. Assessment and management of respiratory symptoms of malignant disease.Oxford: Oxford University Press (in press)3. Bruera E, Neumann CM.  In: Ahmedzai SH, Muers M, editors. Supportive care in respiratory dis-ease. Chapter 7. Assessment of dyspnoea in clinical practice and audit. Oxford: Oxford UniversityPress (in press)4. Gillette MA, Schwartzstein RM.  In: Ahmedzai SH, Muers M, editors.  Supportive care in respira-tory disease. Chapter 6. Mechanisms of dyspnoea. Oxford: Oxford University Press (in press)5. Jennings AL, Davies AN, Higgins JP, Gibbs JS, Broadley KE. A systematic review of the use ofopioids in the management of dyspnoea. Thorax 2002;57(11):939-44.6. Ahmedzai SH, Laude E, Robertson A, Troy G, Vora V. A double-blind, randomised, controlledPhase II trial of Heliox28 gas mixture in lung cancer patients with dyspnoea on exertion. Br JCancer. 2004;90(2):366-71.7. Nishino T, Ide T, Sudo T, Sato J. Inhaled furosemide greatly alleviates the sensation of experi-mentally induced dyspnea. Am J Respir Crit Care Med 2000;161(6):1963-7.8. MacLeod R.  In: Ahmedzai SH, Muers M, editors. Supportive care in respiratory disease.  Chapter12. Psychosocial therapies. Oxford: Oxford University Press (in press)Ahmedzai H.S.172www.onk.ns.ac.yu/Archive/   October 1, 2004

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