progressive dyspnea is an annoying symptom in cancer patients.

1. Samir A El Kafrawy
MD, Anaesthesia &Pain Relief
ElSahel Teaching hospital , Cairo, Egypt
Progressive Dyspnea in cancer patients

2.  Difficult, labored , uncomfortable breathing.
 A term used to characterize a subjective
experience of breathing discomfort that consists
of qualitatively distinct sensations that vary in
intensity.
Definition

3.  Depending on the type and stage of cancer,
21% - 90% of patients complain of dyspnea.
 Either due to pulmonary or non-pulmonary
causes.
Prevalence

4. Chemoreceptors
Central
peripheral
Peripheral
mechanoreceptors
Vagal afferents
Pulm.strech
Pulm.irritants
Alveolar C fibers
Cognitive/emotional
factors

5. Can be conceptually summarized in three
components:
 Work of breathing.
 Chemical component.
 Neuromechanical dissociation.
Pathophysiology

6. Work of breathing
 Also called “ abnormal ventilatory impedance”.
 Respiratory diseases as COPD and Asthma which cause
narrowing of the airway increase the airway resistance.
 Diseases of the lung parenchyma including interstitial
fibrosis and pulmonary fibrosis increase lung elasticity .
 Breathing with a diseased or fatigued muscle.
 The level of central respiratory motor output required to
achieve a given ventilation rises.

7. Chemical component
 Medullary chemoreceptors sense hypercarbia while
carotid and aortic body chemoreceptors sense
hypoxemia.
 It takes moderately sever levels of hypoxia to cause
dyspnea.
 Hypoxia and hypercarbia cause respiratory motor
activity to increase through these receptors.
 Chronic hypercarbia is compensated metabolically ,
so limits the ventilatory response.

8. Neuromuscular dissociation
 Mismatch between what the brain desires
for respiration and the sensory feedback it
recieves.

9.  “ patient self – report “ is the gold standard.
 Respiratory rate, oxygen saturation and ABGs neither
correlate with nor measure dyspnea.
 Functional assessment tools as Shuttle walking test and
reading aloud of umbers.
 Scales as visual analog and Borg .
 Questionnaires as chronic Respiratory disease, Saint
George , Pulmonary functional status.
 Practically, are impractical and burdensome.
Assessment of dyspnea

10. Causes of progressive dyspnea in cancer
patients

11. Etiologies
Co-morbidities Cancer
Treatment

12.  Primary/metastatic parenchymal lung involvement
 Airway obstruction (intrinsic or extrinsic tumor)
 Carcinomatous lymphangitis
 Pleural tumor
 Malignant pleural effusion
 Pericardial effusion
 Superior vena cava syndrome
 Tumor microemboli
 Phrenic nerve paralysis
 Atelectasis
 Tracheal esophageal fistula
 Chest-wall invasion (carcinoma en cuirasse)
 Pathologic chest-wall fractures
Directly related to cancer

13.  Pneumonia
 Cachexia
 Anemia
 Electrolyte abnormalities
 Pulmonary embolus
 Paraneoplastic syndromes
 Ascites
Indirectly related to cancer

14. Related to cancer therapy
 Surgery (postlobectomy/pneumonectomy)
 Radiation pneumonitis
 Chemotherapy-induced pulmonary fibrosis
 Chemotherapy-induced cardiomyopathy

15.  Chronic obstructive pulmonary disease
 Asthma
 Congestive heart failure
 Cardiac ischemia
 Arrhythmias
 Pulmonary vascular disease
 Obesity
 Neuromuscular disorders
 Aspiration
 Anxiety
 Pneumothorax
 Interstitial lung disease
 Psychosocial/spiritual pain
Unrelated to cancer

16.  The first step in the evaluation is to
establish the primary organ system
involved: pulmonary, cardiac, both, or
neither.
Evaluation of chronic dyspnea

17. Clues to Causes of Dyspnea
 Intermittent breathlessness;
triggering factors; allergic rhinitis;
nasal polyps; prolonged
expiration; wheezing
 Significant tobacco consumption;
barrel chest; prolonged expiration;
wheezing
 History of hypertension, coronary
artery disease, or diabetes
mellitus; orthopnea; paroxysmal
nocturnal dyspnea; pedal edema;
jugular vein distention; S3 gallop;
bibasilar rales; wheezing
 Asthma
 Chronic obstructive
pulmonary disease
 Congestive HF
Findings Clinical conditions

18.  History of generalized
anxiety disorder, post-
traumatic stress
disorder, obsessive-
compulsive disorder,
panic disorder;
intermittent symptoms;
sighing breathing
 Postprandial dyspnea
 Recurrent pneumonia
 Drug exposure
 Anxiety disorder;
hyperventilation
 GORD; aspiration; food allergy
 Br.C ; bronchiectasis; aspiration
 Beta blockers:COPD
Amiodarone ,nitrofurantoin:Pn.
Methotrexate :IPF
Findings Clinical conditions

19.  History of
immunosuppression
 Exposure to inorganic dust,
asbestos, or volatile
chemicals
 Organic exposure to dust
(birds, mushrooms)
 Accentuated P2; right
ventricular heave; murmurs
 Abnormal inspiratory or
expiratory sounds heard
best
over the trachea
 Localized, decreased, or
absent breath sounds
 Opportunistic infections:
 Pneumoconiosis; silicosis;
berylliosis; coal workers lung;
asbestosis
 Hypersensitivity pneumonitis
(bird fancier's lung)
 Pulmonary hypertension
 Central airway obstruction; vocal
cord paralysis; laryngeal tumor;
tracheal stenosis
 Pleural effusion; atelectasis;
pneumothorax
Findings Clinical conditions

20. Clinical Evaluation of Chronic Dyspnea

21. Patient with Ch.
Dyspnea
H&Ex
Inv. (level one)
Is diagnosis
evident?
Asthma
COPD
Pleural effusion
CHF
Anaemia
Conduct
Inv. (level two)
Conduct
Inv. (level Three)
CHF,CAD,Valv.D
Pericardialdisease
Arrhythmia
IPF,Ch. PE
GORD
CAD
1ry PH
psychogenic
Y
e
s
n
o
N
o
Level 3:
Cardiac Cath.
Cardiopul. Ex
Esophageal PH
Bronchoscopy
Lung biopsy
Level 2:
Echo
Cardiac Enz.
PFT
ABG
HRCT
Holter
Radionuclide S
V/Q scan
Level 1:
CBC
X ray
ECG
Spirometry
Pulse oximetry
Metabolic profile

22.  In advanced cancer: usually multifactorial
 Majority of underlying causes irreversible
 Palliative treatments partially successful
 Important to reverse what is reversible
 Relatively small improvement in different
parameters may give significant relief
Things to be remembered

23. What makes dyspnea progressive?
Dyspne
a
Reduced
activity
Deconditioni
ng

24. Management of dyspneic cancer
patient.

25. Investigate
 Should be investigated
 Certain causes easily identifiable and reversible
 Minimal intervention
 Rapid symptom improvement

26. Whatever the cause , elevating the head of the bed
, keeping air moving using fans and open windows,
and reducing environmental irritants are likely to be
helpful.
Then move to either pharmacological or non-
pharmacological intervention.

27.  Reduce ventilatory demand.
 Reduce ventilatory impedance.
 Strengthen the weakened inspiratory
muscle.
 Alter central perception of dyspnea.
General approach

28. Interventions and their tie to pathophysiology
pathophysiology Therapeutic intervention
Reduce ventilatory demand
Reduce metabolic load
Decrease central drive
Exercise training: co2 elimination
Supplemental O2 therapy
Supplemental O2 therapy
• Pharmacological therapy:
Opiates therapy
Anxiolytic therapy
• Alter pulmonary afferent
information:
Vibration
Ventilator settings
Inhaled pharmacologic therapy
Fans
• Improve efficiency of Co2
elimination:
Altered breathing pattern

29. Reduce ventilatory impedance:
Reduce/counterbalance lung
hyperinflation
Reduce resistive load
Surgical volume reduction
• Continuous positive airway
pressure
Pharmacological therapy
Improve inspiratory muscle function Nutrition
Inspiratory muscle training
Positioning
Partial ventilatory support
Minimizing use of steroids
Alter central perception Education
Cognitive-behavioral approaches
Desensitization
Pharmacological therapy
Thomas J and Gunten C, Management of dyspnea . J Supportive
Oncology2003;1:23-34

30. Opioid Therapy for Dyspneic cancer
patient

31.  Bruera et al., were the first to study the use of
opioids for controlling dyspnea in cancer
patients.
 functional brain imaging has identified cortical
areas putatively involved with the perception
and modulation of dyspnea.
 Opioid receptors have also been identified
throughout the tracheobronchial tree specially
alveolar walls.

32. Mild dyspnea
• Hydrocodone 5 mg PO q4h or codeine 30 mg PO q4h
• For breakthrough symptom management, give an
equivalent dose q1–2h, as needed
Severe dyspnea
• Morphine sulfate 5 mg PO q4h, oxycodone 5 mg PO
q4h, or hydromorphone 1 mg PO q4h
• For breakthrough symptom management, give an
equivalent dose q1–2h, as needed
• Titrate up in increments of 50%–100% every 24
hours, as needed.
Note: For patients with severe pulmonary disease, such
as COPD, start at 50% of the above doses and titrate
more conservatively, with increments of 25% every 24
hours, as needed.
Opioid-naïve patients

33. Increase baseline opioid dose by 25%–50% and titrate
as above.
Opioid-tolerant patients
Except for constipation, patients become pharmacologically
tolerant to all of the adverse effects of opioids, such as
sedation and nausea, within 1–2 weeks.
Bruera E, Macmillan K, Hanson J, et al. The cognitive effects of the administration of narcotic
analgesics in patients with cancer pain. Pain1989;39:13–16.

34. Interrelationship Between Dyspnea and Anxiety

35. Phenothiazines and benzodiazepines
 No randomized controlled trials
 Phenothiazines preferred- less resp depression
 beneficial effects of morphine in controlling baseline
levels of dyspnea could be improved with the addition
of midazolam to the treatment.
 morphine (2.5 mg Q4hrs for opioid-naïve or a 25%
increment over daily dose for pts receiving baseline
opioids) plus midazolam (5 mg Q4hrs) with morphine
rescue doses (2.5 mg)
J Pain Symptom Manage. 2006 Jan;31(1):38-47.

36. Lorazepam
• 0.5–1 mg PO q1h until dyspnea is settled, then dose
• routinely q4–6h to keep settled
Diazepam
• 5–10 mg PO q1h until dyspnea is settled, then dose
• routinely q6–8h
Clonazepam
• 0.25–2 mg PO q12h
Midazolam
• 0.5 mg IV every 15 min until dyspnea is settled, then
• give by continuous SC or IV infusion
Anxiolytic Therapy for Dyspnea

37.  Mechanism uncertain
 Correction of hypoxemia may not alleviate
dyspnea
 May be activation trigeminal nerve.
 Randomized trials suggest that both O2 and
air can reduce dyspnea in cancer patients.
Oxygen

38. Heliox
 Less dense than air When mixed with O2,
reduces turbulent flow in narrowed airways
Reduces work of reathing and improves
alveolar ventilation.
 One randomized controlled trial, Heliox
increased exercise capacity and SaO2 at rest
and exertion.
Br J Cancer. 2004 Jan 26;90(2):366-71.

39. Scopolamine
0.2–0.4 mg SC q4h or 1.5 mg transdermal patch 1–3
q72h or 0.1–1 mg/h via continuous IV or SC infusion
Glycopyrrolate
0.2 mg SC q4–6h or 0.4–1.2 mg/d via continuous IV or
SC infusion
Anticholinergic Therapy for
Dyspnea

40. Rapid shallow breathing, periods of apnea, and a Cheyne-
Stokes respiratory pattern are common end-of-life breathing
patterns
As death approaches, the gag reflex and reflexive clearing of
the oropharynx decline and secretions accumulate. Air
passing through these accumulated secretions can create
gurgling or crackling sounds colloquially termed the “death
rattle.”
Terminal care of dyspnea

41. Refractory dyspnea
Sedating medications, such as benzodiazepines,
neuroleptics, barbiturates,or propofol (Diprivan), may be
titrated to sedation.
Opioids alone are unreliable sedatives.
Doses should be titrated to provide the desired degree of
sedation.