Dyspnea

Question 1

Prevalence of dyspnea

Answer 1

High.

Cancer (10-70%)
Lung cancer (75 - 87%)
COPD (90-95%)
CHF (60-88%)
Stroke (37%)
ALS (50%)
Dementia (70%)

Intensity tends to worsen towards EOL

May be breakthrough or constant

Question 2

Impact of dyspnea

Answer 2

Multidimensional stress to both patients and caregivers, with significant impact on QoL.

May cause anxiety, panic, hopelessness, loss of function, and social isolation.

Survival may be shortened in patients displaying dyspnea, used in Palliative Prognostic Scale.

Question 3

Investigations for dyspnea

Answer 3

Note that degree of dyspnea can only truly be measured by patient’s self report

Physical exam - look for red flags including stridor, tachypnea (RR > 30), tachycardia (HR >130), marked respiratory distress, altered LOC.

First line:
CBC (for Hb), O2 sats (note poor correlation between severity of hypoxia and dyspnea), CXR (if indicated).

Consider lung functions tests:

• Flow volume loop (upper airway obstruction)
• Maximum inspiratory presure or nasal sniff inspiratory pressure (inspiratory muscle weakness)

Consider echo and dopplers for investigation of pericardial/pleural effusions, CHF, DVT, or PE (note D-dimer has limited value in cancer).

May consider CT for PE, Major airway obstruction, SVC, and lymphangitic carcinomatosis

Question 4

Causes of dyspnea by system

Answer 4

Resp:
Airway obstruction, COPD, asthma, lung damage secondary to chemo/rads/surgery, PE, fibrosis, effusion, primary or metastatic tumour

Cardiac:
CHF, CAD, arrhythmias, pericardial effusion

Neuromuscular
ALS, CVA, poliomyelitis, myasthenia gravis

SVC syndrome (emergency)

Other
Anxiety, fatigue/deconditioning, weakness, pain, severe anemia, infection, carcinomatosis, hepatomegaly, phrenic nerve lesion, peritoneal effusion

Question 5

Principles of managing dyspnea

Answer 5

1. If not due to hypoxia, use other methods to provide fresh air
2. Anticipatory planning to promote self-care for respiratory distress
3. Relaxation, non-pharm treatment
4. Opioids are the cornerstone of pharmacologic treatment

Question 6

Non-pharm treatments for dyspnea

Answer 6

• Sit up right or forward leaning. When on side, position bad lung down
• Multidisciplinary approach
• In COPD, use exercise, walking aid, pulmonary rehab, and inspiratory muscle training (pursed lip breathing etc.)
• Airflow with room air if not hypoxic
• Fans (hand held or electric)
• Gait aid for forward leaning
• O2 if hypoxic, if non-hypoxic, may consider a limited trial of O2. In the community, there will be program criteria for home O2.
• Chest wall vibration in COPD and motor neuron patients

Weaker evidence:

• Elevate head of the bed by 15-45 degrees
• Provide supportive presence when distressed by the dyspnea
• Ask yes and no questions if talking worsens dyspnea
• relaxation techniques of guided imagery and therapeutic touch
• Anxiety management

Question 7

Treatment for Mild Dyspnea (e.g 1-3/10 severity)

Answer 7

-Bronchodilators (Salbutamol, ipratropium) for COPD or asthma
- PRN oral or parenteral opioids if dyspnea is only episodic (don’t forget bowel management)
If no previous opioids:
- Morphine 2.5mg PO q4H
- Hydromorphone 0.5mg PO q4h PRN

If previously on opioids - increment of 25% baseline dosage has been used in one study

• Consider trialling corticosteroids for major airway obstruction, lymphangitic carcinomatosis, radiation or drug-induced pneumonitis, or for endotracheal and bronchial lesions

Question 8

Pathophysiology of Dyspnea

Answer 8

1. Air hunger/unsatisfied inspiration:
   Mechanoreceptors and chemoreceptors in lungs/airways/chestwall transmit to sensory cortex and respiratory sensor in the medulla, then to sensory cortex (causing symptom). Signal is not matched by adequate ventilatory response by the motor cortex/respiratory muscles.
2. Work or effortful breathing:
   Likely due to combination of respiratory muscle afferents and perceived cortical motor command.
3. Tightness:
   Specific to bronchoconstriction, arises from pulmonary afferents through stimulation of airway receptors

Dyspnea is processed through cortico-limbic structures. Note multiple dimensions (similar to pain) - sensory dimension, immediate affective stage, and cognitive evaluative and emotional response that affects long term behaviour.

In summary, experience of dyspnea occurs when the sensory cortext perceives a mismatch between ventilatory demand and body’s ability to respond to that demand.

Question 9

Measurement of Dyspnea

Answer 9

Three domains according to ATS:

1. Sensory-perceptual experience (intensity, frequency, duration, and sensory quality)
2. Affective distress
3. Symptom impact or burden (effect on behaviour, functions, QoL, health status)

Over 50 different rating scales. May consider combining rating of dyspnea intensity with assessment of the impact of dyspnea on a patient’s QoL.

NRS, modified BORG Scale (0 - 10 with ‘0.5’ for ‘just noticeable’, and Cancer dyspnea scale appear most suitable.

Question 10

Opioids for dyspnea - indications, dose

Answer 10

Clear evidence supporting use in advanced cancer and COPD without excessive respiratory depression.

CHF - evidence is conflicting and requires further study.

Motor neuron disease, ILD - anecdotal reports only

No clear starting dosage, but consider renal function, hepatic function, severity of pre-exsting Type II respiratory failure (e.g. chronic hypoxemia/hypercapnia), frailty, body size, and ability to monitor.

Morphine SR 10mg daily most studied

If already on opioids, use 25% of baseline dosage.

Use PRNs for episodic breathlessness.

Question 11

Oxygen for dyspnea (indications)

Answer 11

• Survival benefit in COPD (PaO2 55mmg Hg or less, SpO2 88% or less)
• May be some symptomatic benefit in patients with hypoxemia.

If patients are non-hypoxemic, there is no evidence that oxygen is better than medical air at relieving breathlessness and it should not be used routinely.

Question 12

Anxiolytics for dyspnea (indications, dose)

Answer 12

• Routine use not supported for dyspnea due to advanced cancer and COPD
• May be effective in decreasing dyspnea associated with anxiety

Question 13

Inhaled furosemide for dyspnea (indications)

Answer 13

• Thought to enhance pulmonary receptor activity, suppress pulmonary irritant activity and vasodilation.
• Studied in asthma, COPD and advanced cancer.
• May be helpful in COPD/airway disease but no proven benefit in cancer.

Question 14

Heliox for dyspnea (mechanism, indicatioN)

Answer 14

• Helium has a low density and is thought to reduce the work of breathing and improve alveolar ventilation
• May reduce dyspnea in people with lung cancer and COPD

Question 15

Palliative sedation for refractory dyspnea

Answer 15

• may be used for severe, refractory symptoms that have not been otherwise relieved by aggressive, symptoms specific palliation
• No association with hastened death (mean duration of 1 - 3.5 days)

Question 16

Palliative non-invasive ventilation (indications)

Answer 16

• Standard of care for motor neuron disease with respiratory insufficiency
• Labour intensive and requires a collaborative approach with advance care planning required, as well as the option to withdraw NIV (especially toward end of life)

In COPD or CHF, may reduce dyspnea and be used in management of an acute exacerbation while avoiding intubation.

Question 17

Treatment of dyspnea due to lung cancer

Answer 17

• Chemotherapy, molecular targeted therapy for EGFR+ lung ca
• Morphine (either SR or PRN for episodic breathlessness)
• Potentially oxygen, if hypoxic
• Non-pharm therapies

Question 18

Treatment of dyspnea secondary to pleural effusion

Answer 18

• Repeat thoracentesis (thoracoscopic more effective)
• Chemical pleurodesis (talc 90% efficacious)
• Indwelling pleural catheter (particularly for trapped lung)

Question 19

Treatment of dyspnea due to SVC

Answer 19

• Palliative emergency
• SVC stent by Interventional Radiology - 95% have relief, more rapid relief than chemo and rads
• Chemo and Rads (60% have response with NSCLC)
• Trial of steroids (if receiving rads and have severe airway obstruction not amenable to stenting OR if due to a steroid-responsive cancer such as thymoma or lymphoma. Do not use if dx not established as it may interfere with dx of lympoma)
• Trial of diuretics to avoid overhydration and decrease blood volume

Question 20

Treatment of dyspnea due to PE

Answer 20

• Dalteparin (note that LMWH has some anti-inflammatory properties that increase efficacy over warfarin, dose based on body weight - caution with CrCl < 30. If severe renal impairment, may discuss with Hematology about warfarin vs LMWH with anti-Xa levels vs empiric dose reduction)

May use a DOAC (edoxaban - preferred - with 5 days of LMWH first or rivaroxaban) IF:

• non-GI solid malignancy
• not at high risk of GI bleeding
• no relevant drug-drug interactions

DOACs have better or comparable efficacy, but come with 2-3x higher risk of significant bleeding (particularly UGIB) and there may be issues with oral absorption along with safety concerns with hepatic/renal impairment.

Monitor with weight, CBC, renal function q3 months

Optimal duration of therapy with either DOACs or LMWH unknown, but minimum of 3-6 months. Continue (R/A q3 months) if:
- on systemic chemotherapy
- metastatic disease
- progressive or relapsed disease
- other ongoing risk factors that increase the risk of recurrent thrombosis (e.g. central venous
catheter)

Question 21

Pericardial effusion

Answer 21

May occur due to malignant spread of non-pericardial tumours or mediastinal rads. Other causes include infection, idiopathic, renal failure with uremia, MI or cardiac surgery (more acute).

Presentation:

• Often asymptomatic unless in tamponade (then dyspnea, elevated JVP, edema, fatigue)
• Electrical alternans with sinus tach, low voltage QRS
• Hypotension with narrow pulse pressure
• Pulsus paradoxus
• Confirm with echo

Treatment:

• Pericardiocentesis
• Catheter drainage
• Pericardial window
• Pericardiotomy

Choice between pericardiocentesis and open surgical drainage based upon local preference and experience.

Indications for drainage:

• Hemodynamic compromise
• Need for sampling of effusion for diagnostic purposes if no clear etiology (non urgent)

Question 22

Treatment of Dyspnea related to major airway obstruction (etiology, presentation, diagnosis, treatment)

Answer 22

Etiology:

Presentation:

Diagnosis:

• Radiotherapy
• Bronchial stent
• Endobronchial treatment with laser, cryotherapy
• Trial of steroid

Question 23

Dyspnea related to lymphangitic carcinomatosis (etiology, presentation, diagnosis, treatment)

Answer 23

Etiology:

Presentation:

Diagnosis:

Treatment: trial of steroid

Question 24

Dyspnea related to radiation pneumonitis (etiology, presentation, diagnosis, treatment)

Answer 24

Etiology:

Presentation:

Diagnosis:

Treatment: Trial of steroid

Question 25

Dyspnea related to pneumonia

Answer 25

Treatment of CAP: Treatment of CAP: Outpatient Rx, health with no prior abx: Macrolide (+ amox for pneumococcal resistance) OR Doxy Outpatient Rx, comorbidities or prior abx in past 3 months: Resp FQ (levoflox) OR beta-lactam + macrolide (amox, amox/clav, cefuroxime + azithro) Inpatient (non-ICU): Resp FQ (levoflox) OR beta-lactam + macrolide (CTX + azithro) Inpatient (ICU): Beta-lactam + azithro OR resp FQ (levoflox) Inpatient (ICU with PCN allergy): Aztreonam + resp FQ (levoflox)

Question 26

Treatment of Dyspnea due to ascites

Answer 26

- Paracentesis

Question 27

Dyspnea due to hepatomegaly or hepatopulmonary syndrome

Answer 27

If simply hepatomegaly - sit patient up to lessen pressure on diaphragm. Patients with Hepatopulmonary syndrome present with dyspnea, platypnea, resting hypoxemia, progressive cyanosis, and orthodeoxia. Platypnea and orthodeoxia refer to dyspnea and desatting, respectively, that improve from the sitting to supine position, due to gravitational increase in blood flow and shunting through dilated vessels in the lung bases while in the seated position. Treatment is generally supplemental O2 and liver transplant (depending on cause)

Question 28

Treatment of COPD

Answer 28

COPD Staged Tx: Mild COPD: - SABA PRN + LAMA or LABA Low risk of AECOPD (one or less AECOPD in last year requiring meds but not hospital/ED) 1. LAMA or LABA 2. LAMA + LABA 3. LAMA + LABA + ICS High risk of AECOPD (one severe AECOPD in last year requiring hosp/ED, or two mod AECOPD in the last year requiring meds but no hosp/ED) 1. LAMA/LABA or ICS/LABA (if blood eos >300) 2. LAMA/LABA/ICS If triple therapy ineffective: - PDE4 inhibitors (roflumilast), unpleasant side effects but reduces exacerbation rate and improves lung function in those with bronchitis sx - Mucolytics (NAC 600mg PO) reduce exacerbation rate (recommended over azithro now!) - Daily azithro reduces exacerbation rate, but weaker evidence Regular PO steroids not recommended, risks > benefits PO theophylline not recommended, does not prevent AECOPD in patients on optimal long acting therapy.

Question 29

Treatment of AECOPD

Answer 29

Antibiotics for AECOPD: Systemic steroids x 5-7 days Antibiotics x 5 -7 days Simple = amox, doxy, or septra Complicated (FEV1 <50, 4 exacerbations per year, IHD, Home O2, chronic steroid use, antibiotics in last three months: - Same abx as above with oral steroids - Amox/clav - Levoflox or moxiflox GOLD Guidelines 2018: Still need 2/3 for GOLD guidelines (purulence, dyspnea, volume) or mechanical ventilation for antibiotics in AECOPD. Indications for BiPAP -AECOPD with hypercapnic acidosis (PaCO2 >45mmHg or pH <7.30

Question 30

Interventional Therapy in Stable COPD

Answer 30

- Lung volume reduction surgery (improves survival in severe emphysema patients, with upper lobe emphysema and low post-rehab exercise capacity) - Bullectomy (may decrease dyspnea, improve lung function and exercise tolerance) - Transplant - Bronchoscopic interventions (for advanced emphysema, less invasive than lung volume reduction surgery. Can do endobronchial valves for air trapping, lung coils, or vapor ablation)

Question 31

COPD - presentation, risk factors

Answer 31

One of the most common pulmonary diseases, categorized by cough, dyspnea, sputum production, and airflow obstruction. Risk factors: - Cigarette smoking (most important - 1ppd = 15% percent risk, 2 ppd = 25% risk) - Second hand (passive) smoking

Question 32

Abnormalities on chest xray with COPD

Answer 32

CXR - Increase in antero posterior diameter of the chest - flattening of the diaphragm secondary to hyperinflation

Question 33

Diagnosis of COPD

Answer 33

PFTs: - FEV1/FVC ≤70% predicted Moderate if FEV1 ≤50% Severe if FEV1 35-49% Very Severe ≤34% Reversibility noted if FEV1 increases >15% after bronchodilator

Question 34

Management goals in COPD

Answer 34

1. Improve symptoms (decreasing airflow obstruction and inflammation) 2. Prevent secondary complications (e.g. infection) 3. Maintain function 4. Improve patient's QOL

Question 35

Beta2 agonists in COPD (MOA)

Answer 35

- Bronchodilation via stimulation of B2 receptors in the air ways - SABAs used PRN (rapid onset, shorter half life)

Question 36

Anticholinergics in COPD

Answer 36

- Bronchodilation by inhibiting cholinergic mediated increases in bronchomotor tone and vagally mediated bronchoconstriction induced by airway irritants - Stronger bronchodilater effects than B2 agonists, longer half life, fewer side effects

Question 37

Role of pneumococcal and influenza vaccine in COPD

Answer 37

- All adults age 65 years of age or older or those with chronic lung disease, CKD, CLD, or malignancy should get a pneumococcal vaccine. - If underlying medical condition, patients should get a booster dose 5 years later - All adults should get an annual flu vaccine Patients with COPD at higher risk of pulmonary infections. Primary influenza can be fatal, but can also result in worsened lung status, functional status, and has associated risks of secondary bacterial pneumonia, MI, or stroke.

Question 38

Pulmonary rehabilitation in COPD (goals, components, outcomes)

Answer 38

- Optimize quality of life - Improve sense of control over symptoms Components include: - Inhaler use - Breathing and relaxation techniques - Energy conservation techniques - Nutritional guidance - Exercise programmes for aerobic training - Pursed lip breathing, tripod positioning Outcomes: - Decreased sensation of breathlessness - Improvement in exercise endurance - Improved QOL

Question 39

Tripod positioning in dyspnea - pathophys

Answer 39

- Improves dyspnea as it improves ventilatory efficiency by improving length tension dynamic of the diaphragm

Question 40

Pursed-lip breathing - pathophys

Answer 40

- Improves dyspnea by slowing respiratory rate, increasing intra-airway pressures (diminishing collapse of smaller airways)

Question 41

Parameters for Home O2

Answer 41

COPD and severe hypoxemia, home O2 for at least 15h/day: - PaO2 ≤55mmHg or SpO2 ≤88% at rest - PaO2 <60mmHg or SpO2 ≤89% at rest IF polycythemia, cor pulmonale, or pulm HTN Home O2 PRN for: - PaO2 ≤55mmHg or SpO2 ≤88% during exertion - PaO2 ≤55mmHg or SpO2 ≤88% during sleep Improves symptoms AND survival

Question 42

Consequences of malnutrition in COPD and interventions

Answer 42

- Respiratory muscle wasting and weakness may result from malnutrition in advanced COPD - Re-feeding, recondition, and anabolic steroids may improve exercise tolerance - Pulmonary rehab may improve respiratory muscle strength - Not unreasonable to attempt anti-cachexia measures in this population

Question 43

Prognosis of COPD

Answer 43

1 year survival of 30% in patients with FEV1 < 1L (worse than many cancers) FEV1 is a strong predictor of survival

Question 44

Clinical presentation of SVC syndrome

Answer 44

- Dyspnea, swelling of the face, neck, arms, orthopnea, cough - Facial flushing, hoarseness (laryngeal edema), headaches, stridor, nasal congestion - Later stages: cerebral edema and dizziness, syncope, confusion, coma Most symptoms exacerbated by laying down or bending forward. Less commonly: rhinorrhea, proptosis, mentation changes, elevated JVP

Question 45

Pathophysiology of SVC syndrome

Answer 45

Obstruction of the venous drainage of the head, neck, upper torso, and extremities - Formation of collatora venous pathways - Edema (including laryngeal edema, and in severe cases cerebral edema) Severity is dependent on speed of onset, degree of narrowing, and adequate of collaterals

Question 46

How quickly do symptoms of SVC syndrome devel

Answer 46

In one third of patients, symptoms develop over a period of two weeks

Question 47

Signs to assess in patients with SVC

Answer 47

- Swelling of the face (esp. periorbital edema), neck, or arms - Dilatation and tortuosity of the veins of the upper body - Plethora or cyanosis of the face

Question 48

Cause of SVC syndrome

Answer 48

Primary intrathoracic malignancies cause more than 90% of cases Most commonly: 1. NSCLC (50%) 2. Small cell lung ca (25%) 3. Lymphoma and metastatic lesions (10%)

Question 49

Most common metastatic cancer causing SVC syndrome

Answer 49

Breast CA

Question 50

Of patients with bronchogenic CA, how many develop SVCs?

Answer 50

3-15%

Question 51

What are non-malignant causes of SVCs?

Answer 51

Thrombosis (often due to intravascular devices like pacemakers or catheters). Can differentiate with contrast-enhanced CT imaging (extrinsic compression vs thrombosis)

Question 52

Investigation of suspected SVC

Answer 52

CXR - will often show abnormality, but may be normal Contrast-enhanced CT - most useful (differentiates between extrinsic compression and thrombosis) Venography - If an intervention such as stent placement or surgery is planned Tissue diagnosis - to confirm malignancy and guide treatment

Question 53

Biopsy options for malignancy causing SVC syndrome

Answer 53

- Peripheral biopsy site (e.g. enlarged supraclavicular node) - Percutaneous needle biopsy (lung primary, especially if peripherally located) - Bronchoscopy - Mediastinoscopy - Open lung biopsy

Question 54

Diagnostic yield of bronchoscopy for malignancy

Answer 54

50-70%

Question 55

Diagnostic yield of transthoracic needle aspiration biopsy for malignancy

Answer 55

75%

Question 56

Diagnostic yield of mediastinoscopy for malignancy

Answer 56

over 90%

Question 57

Management of SVC syndrome - overview

Answer 57

Simultaneous treatment of cancer and relief of obstructive symptoms

Question 58

Management of SVC syndrome - treatment of obstruction

Answer 58

- Short term, elevate patient's head and torso to decrease hydrostatic pressure and edema - O2 if hypoxemic - Fan for SOB if not hypoxemic - Dex 8mg PO or subcut qAM and qNoon (decreasing swelling around the tumour and enhaving venous return). Note not to give prior to dx as lymphoma can be very responsive to dex and it may make pathologic diagnosis difficult

Question 59

Diuretics in SVC syndrome

Answer 59

Avoid: - Decrease venous return, reduce preload, and can potentially cause hypotension and shock - May increase risk of thrombosis of SVC

Question 60

Management of SVC syndrome - treatment of malignant disease

Answer 60

Chemo, rads, or both. - No significant difference between the three in the RATE of relief from obstruction Rads: - majority of tumours that cause SVC syndrome are rads sensitive - Response usually seen in a few days, but may be delayed for 2-3 weeks Chemo - May provide complete relief of symptoms in around 80% of patients with SCLC or non-Hodgkin lymphoma - Preferred TX for small cell ca - Only about 40% of patients with NSCLC respond

Question 61

Endobronchial obstruction - Presentation

Answer 61

- Progressive SOB - Cough (common) - Hemoptysis (common - may be massive) - Hoarseness - Orthopnea - Chest discomfort - Dysphagia if concurrent esophageal compression

Question 62

Endobronchial obstruction - Pathophysiology

Answer 62

May be due to intrinsic (primary airway tumour - rare, e.g. endoluminal carcinoid) or extrinsic compression (often bronchogenic or NSCLC)

Question 63

Endobronchial obstruction - Findings

Answer 63

Auscultation - stridor - wheezing (generally not responsive to bronchodilators) - localized crackles

Question 64

Endobronchial obstruction - diagnosis

Answer 64

- CXR (not very sensitive. May show deviation of the trachea towards the side of collapse/obstruction due to tethering by the tumour and lymphadenopathy in the area.) - CT chest (most helpful to determine if there is an abnormality) - Bronchoscopy (for definitive diagnosis)

Question 65

Endobronchial obstruction - treatment

Answer 65

- External beam rads - Laster therapy - Electrocautery - Cryotherapy - Endobronchial irradiation - Tracheobronchial stents

Question 66

Pleural effusion - Clinical Presentation

Answer 66

- Dyspnea - Deviation of the trachea away from the effusion (fluid pushing the mediastinium outward) - Dullness to percusion - Tactile and vocal fremitus decreased

Question 67

Investigation of pleural effusion

Answer 67

- CXR to confirm dx | - Thoracentesis for diagnostic and therapeutic reasons

Question 68

What to order on thoracentesis

Answer 68

- Cell count - LDH - Protein and pH - cytology - C and S Also need serum protein, serum LDH

Question 69

Light's Criteria

Answer 69

Transudate vs Exudate: Light's Criteria (need one of three to define the fluid as an exudate) - Pleural fluid protein/serum protein ratio > 0.5 - Pleural fluid LDH/serum LDH ratio > 0.6 - Pleural fluid LDH > 2/3 ULN serum LDH

Question 70

Drainage of pleural effusion

Answer 70

- To help relieve SOB and for diagnosis - Do not remove more than 1.5 L at a time (may cause pulmonary edema) - Stop if dyspnea increases during the procedure - If significant improvement after, consider chest tube and subsequent pleurodesis

Question 71

Insertion of chest tube and pleurodesis

Answer 71

- Pre-mediate with parenteral opioid, if necessary a benzo - Once drainage is < 100ml/24 hrs, go to pleurodesis (injection of a sclerosing agent, like talc, to create inflammation and sticking together of pleural surfaces) - Give local anesthetic intrapleurally prior to sclerosisng agent and adequate analgesia after - May also consider a tunnelled pleural catheter for patients who decline pleurodesis or fail it

Question 72

Lymphangitic carcinomatosis

Answer 72

- Diffuse infiltration and obstruction of pulmonary parenchymal lymphatic channels by tumour

Question 73

Diagnosis of lymphangitic carcinomatosis

Answer 73

- Non-specific interstitial pattern on CXR, but symptoms on precede radiographic abnormalities - High res CT is diagnostic modality of choice

Question 74

Treatment of lymphangitic carcinomatosis

Answer 74

- Optimize underlying malignant process | - Steroids and diuretics (no RCTs to back up)

Question 75

Treatment of dyspnea when unable to treat underlying condition

Answer 75

- Oral or parenteral opioids to reduce the sensation of dyspnea (Cochrane) - No evidence to support use of nebulised opioids - No evidence to suggest opioids effect blood gas or O2 or impact oxygenation/carbon dioxide levels

Question 76

Mechanism of action of opioids to decrease dyspnea

Answer 76

- Change in the perception of breathlessness - Decreased consumption of O2 - Fall in ventilatory drive - reduced response to stimuli such as hypoxia and hypercapnea

Question 77

Factors influence whether opioid therapy causes hypoventilation

Answer 77

Clinically significant hypoventilation dependent on: - Previous exposure (tolerance) - Rate of dose increase - Possibly route of administration (give orally unless rapid control needed)

Question 78

Guidelines for supplemental O2 in dyspnea due to endstage malignancy

Answer 78

Hypoxic patients: - Supp O2 recommend for hypoxic patients experiencing dyspnea, but not if not hypoxic - If only mildly hypoxic, airflow via nasal cannula may be as effective Non-hypoxic patients: - Offer fan or humidifed air - If fan or humidified air are ineffective, consider a trial of humidified oxygen. If beneficial over several days, continue use

Question 79

Why does a fan improve dyspnea?

Answer 79

- Alleviates dyspnea by stimulation trigeminal nerve receptors

Question 80

Meds other than opioids for dyspnea?

Answer 80

- Phenothiazines (oral promethazine, not parenteral) have been assessed in small studies only - May consider trial of methotrimeprazine (oral or subcut) if dyspnea persists, or palliative sedation

Question 81

Noisy respirations at end of life

Answer 81

- Occurs due to loss of ability to swallow and independently clear secretions - Results in secretions pooling in the oropharynx and bronchi, with air moving over them and turbulence producing noisy ventilation - May be distressing for family members Management: - Reassure that he is not choking on secretions - Reposition patient on side to allow postural drainage - May consider gentle suctioning (but not deep or frequent as it may be uncomfortable or distressing) - Anticholinergics (glycopurrolate or hyoscine hydrobromide/scopolamine) can lessen the noise - Note that Scopolamine crosses the blood brain barrier and is associated with a higher risk of neuro toxicity - Evidence does not necessarily suggest this is distressing to the patient, but may be difficult for family members

Question 82

Role of theophyllines in COPD

Answer 82

- LABAs and LAMAs are more effective as bronchodilators - Theophylline should not be used in COPD - insufficient evidence that it provides any additional benefit to LAMA/LABA mono or dual therapy in improving dyspnea, functional status, or health status (CTS guidelines 2019) - Side effects: Nausea, vomiting, poor appetite, palps and tremors - Requires bloodwork to monitor levels

Question 83

PDE4 inhibitors in COPD

Answer 83

- Used in patients at high risk of AECOPD who fail triple therapy if they have a chronic bronchitis phenotype - Side effects: Nausea, diarrhea, HA, weight loss - Use with caution in cachectic patients

Question 84

Treatment of mild COPD

Answer 84

Mild COPD: | - SABA PRN + LAMA or LABA

Question 85

Treatment of Mod/Severe COPD at low risk of AECOPD

Answer 85

Low risk of AECOPD (one or less AECOPD in last year requiring meds but not hospital/ED) 1. LAMA or LABA 2. LAMA + LABA 3. LAMA + LABA + ICS

Question 86

Treatment of Mod/Severe COPD at high risk of AECOPD

Answer 86

High risk of AECOPD (one severe AECOPD in last year requiring hosp/ED, or two mod AECOPD in the last year requiring meds but no hosp/ED) 1. LAMA/LABA or ICS/LABA (if blood eos >300) 2. LAMA/LABA/ICS If triple therapy ineffective: - PDE4 inhibitors (roflumilast), unpleasant side effects but reduces exacerbation rate and improves lung function in those with bronchitis sx - Mucolytics (NAC 600mg PO) reduce exacerbation rate (recommended over azithro now!) - Daily azithro reduces exacerbation rate, but weaker evidence Regular PO steroids not recommended, risks > benefits PO theophylline not recommended, does not prevent AECOPD in patients on optimal long acting therapy.

Question 87

Definition of high versus low risk of AECOPD

Answer 87

Low risk of AECOPD (one or less AECOPD in last year requiring meds but not hospital/ED) High risk of AECOPD (one severe AECOPD in last year requiring hosp/ED, or two mod AECOPD in the last year requiring meds but no hosp/ED)

Question 88

Treatment if triple therapy in effective in mod/severe COPD with high risk of AECOPD:

Answer 88

If triple therapy ineffective: - PDE4 inhibitors (roflumilast), unpleasant side effects but reduces exacerbation rate and improves lung function in those with bronchitis sx - Mucolytics (NAC 600mg PO) reduce exacerbation rate (recommended over azithro now!) - Daily azithro reduces exacerbation rate, but weaker evidence Regular PO steroids not recommended, risks > benefits PO theophylline not recommended, does not prevent AECOPD in patients on optimal long acting therapy.

Question 89

O2 therapy during AECOPD

Answer 89

- Risk of death with uncontrolled oxygen, risks associated with excess O2 - Safest to use a venturi max to target SpO2 of 88-89% Inappropriately high FiO2 (especially a risk with nasal prongs in CO2 retainers) can further increase PaCO2 In general, AECOPD hypoxemia is easily corrected with low FIO2 (e.g. 28%). If it does not, consider other causes (PE, ARDS, pulm edema, severe pna)

Question 90

Longterm O2 therapy in AECOPD

Answer 90

- Reduces morbidity and mortality - May impact mobility and quality of life COPD and severe hypoxemia, home O2 for at least 15h/day: - PaO2 ≤55mmHg or SpO2 ≤88% at rest - PaO2 <60mmHg or SpO2 ≤89% at rest IF polycythemia, cor pulmonale, or pulm HTN Home O2 PRN if patients have persistent dyspnea for: - PaO2 ≤55mmHg or SpO2 ≤88% during exertion - PaO2 ≤55mmHg or SpO2 ≤88% during sleep

Question 91

AECOPD definition, impact

Answer 91

AECOPD is a sustained worsening of respiratory symptoms beyond normal day to day variations - Associated with accelerated decline in lung function, impaired quality of life, increased mortality - As COPD worsens, exacerbations become more frequent and severe

Question 92

Presentation of AECOPD

Answer 92

- Worsening SOB - Increased cough (with or without increased sputum production) - Increased sputum purulence - Wheeze, chest tightness, fatigue, decreased appetite

Question 93

Managing AECOPDs

Answer 93

- Ensure patients have a written COPD action plan In general: - SABA or SAMA to treat wheeze and dyspnea, continue other inhalers - Prednisone 25-50mg PO daily x 10 days if mod/severe COPD Antibiotics - FEV1 >50%: PO Doxy - FEV1 <50%; >3 AECOPD/year, IHD, home O2, abx in the last 3 months: Levofloxacin (PO or IV)

Question 94

Dyspnea in COPD

Answer 94

- 'Total dyspnea' - physical, emotional, social, spiritual, existential suffering - May be a significant source of disability and impact quality of life - May put patients at risk for social isolation

Question 95

Pathophysiology of dyspnea

Answer 95

- Dyspnea and fear often coxist in advanced COPD | - Anxiolytics often unhelpful, but treating coexisting anxiety may be prevent anxiety symptoms from worsening dyspnea

Question 96

Dyspnea crisis definition

Answer 96

"Sustained and severe resting breathing discomfort in patients with advanced, often life-limiting illness and overwhelmes the patient and caregivers' ability to achieve symptom relief"

Question 97

Approach to dyspnea in advanced COPD overall

Answer 97

1. Initiate and optimise pharmacologic therapies (SABAs, LABA/LAMAs, ICS, PO meds, O2 if hypoxemic) 2. Initiate and optimise non-pharm therapies (exercise, pursed-lip breathing, walking aid, chest wall vibration, neuromuscular electrical stimulation) 3. Initiate and optimize opioid tx (short and long acting, start low and go slow)

Question 98

CTS recommendations for dyspnea:

Answer 98

- Do not routinely use anxioulytics or antidepressants in the management of dyspnea in patients with advanced COPD - Recommend oral (not nebulized) opioids be used for the treatment of refractory dyspnea in the individual patient with advanced COPD - neuromuscular electrical stimulation (over 4-6 weeks) and chest wall vibration are helpful in reducing dyspnea in patients with COPD - Use of walking aids may improve dyspnea - Pursed lip breathing can be an effective strategy for relief of dyspnea and patients with advanced COPD should be instructed in its use

Question 99

Suggested protocol for introduction of opioids in advanced COPD (CTS)

Answer 99

- Initiate with immediate release oral morphine syrup, titrate weekly - Start at 0.5mg PO BID x 2 days, then 0.5mg PO q4h while awake for remainder of week one - Increase morphine to 1mg PO q4H in week two - Increase by 25%/week until lowest effective dose appropriately managing the dyspnea is achieved Once stable dosage achieved (e.g. over two weeks), convert to SR If significant side effects, consider rotation to HM Ensure patients are prescribed a bowel protocol Note comparatively lower doses are needed than for pain

Question 100

Role of pulmonary rehab in COPD

Answer 100

- May improve dyspnea and enhance exercise tolerance, functional capacity, and QoL - May reduce healthcare utilization - May interrupt the 'spiral of disability' Ensure early referral. Typically 6 - 12 weeks of exercise training, self-management education, nutritional counselling, and psychosocial support.

Question 101

Integrated care systems in COPD

Answer 101

Eg INSPIRED program - home based education and support including disease self-management education, advance care planning, healthcare navigation, allied health, and AECOPD action plans Reduces hospitalizations and length of hospital stay for those admitted.

Question 102

Advance care planning topics in COPD

Answer 102

- Discuss CPR, NIVPP (e.g. BiPAP), intubation, mechanical ventilation, life-sustaining medications, IVF, nutrition, meaning of comfort measures - Emphasise the teams commitment to ongoing care and non-abandoment of the patient and family

Question 103

Signs of worsening COPD that should prompt advance care planning

Answer 103

- FEV1 <30% - O2 dependency - one or more hospitalisations for AECOPD in the last year - Weight loss/cachexia - Decreasing functional status - Increasing dependence - Age >70 - Lack of additional therapeutic options

Question 104

Enabling activity for dyspneic patients (OT)

Answer 104

1. Prioritize - Consider which activities are important and conserve energy for them 2. Plan - Organize activities to make them as efficient as possible, and consider time of day and spacing through the week 3. Pace - Balance periods of activity with rest 4. Position - Find a position that is comfortable during dyspnea and practise this 5. Permission - Patient needs to give oneself permission to NOT do activities that result in breathlessness

Question 105

Personal plan for coping with dyspnea

Answer 105

- Breathing control - What to do when breathless (oxygen, rest, puffers, relaxation) - Positions to use when breathless (upright and leaning forward, laying on side, etc.) - Exercise (what level of gentle exercise will help - Breath control during ambulation - Management of ADLs - Equipment (wheelchair for energy conservation, four wheel walker for dyspnea, etc.)