Dyspnea Flashcards
Prevalence of dyspnea
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
Impact of dyspnea
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.
Investigations for dyspnea
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
Causes of dyspnea by system
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
Principles of managing dyspnea
- If not due to hypoxia, use other methods to provide fresh air
- Anticipatory planning to promote self-care for respiratory distress
- Relaxation, non-pharm treatment
- Opioids are the cornerstone of pharmacologic treatment
Non-pharm treatments for dyspnea
- 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
Treatment for Mild Dyspnea (e.g 1-3/10 severity)
-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
Pathophysiology of Dyspnea
- 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. - Work or effortful breathing:
Likely due to combination of respiratory muscle afferents and perceived cortical motor command. - 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.
Measurement of Dyspnea
Three domains according to ATS:
- Sensory-perceptual experience (intensity, frequency, duration, and sensory quality)
- Affective distress
- 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.
Opioids for dyspnea - indications, dose
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.
Oxygen for dyspnea (indications)
- 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.
Anxiolytics for dyspnea (indications, dose)
- Routine use not supported for dyspnea due to advanced cancer and COPD
- May be effective in decreasing dyspnea associated with anxiety
Inhaled furosemide for dyspnea (indications)
- 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.
Heliox for dyspnea (mechanism, indicatioN)
- 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
Palliative sedation for refractory dyspnea
- 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)
Palliative non-invasive ventilation (indications)
- 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.
Treatment of dyspnea due to lung cancer
- Chemotherapy, molecular targeted therapy for EGFR+ lung ca
- Morphine (either SR or PRN for episodic breathlessness)
- Potentially oxygen, if hypoxic
- Non-pharm therapies
Treatment of dyspnea secondary to pleural effusion
- Repeat thoracentesis (thoracoscopic more effective)
- Chemical pleurodesis (talc 90% efficacious)
- Indwelling pleural catheter (particularly for trapped lung)
Treatment of dyspnea due to SVC
- 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
Treatment of dyspnea due to PE
- 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)
Pericardial effusion
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)
Treatment of Dyspnea related to major airway obstruction (etiology, presentation, diagnosis, treatment)
Etiology:
Presentation:
Diagnosis:
- Radiotherapy
- Bronchial stent
- Endobronchial treatment with laser, cryotherapy
- Trial of steroid
Dyspnea related to lymphangitic carcinomatosis (etiology, presentation, diagnosis, treatment)
Etiology:
Presentation:
Diagnosis:
Treatment: trial of steroid
Dyspnea related to radiation pneumonitis (etiology, presentation, diagnosis, treatment)
Etiology:
Presentation:
Diagnosis:
Treatment: Trial of steroid
Dyspnea related to pneumonia
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)
Treatment of Dyspnea due to ascites
- Paracentesis
Dyspnea due to hepatomegaly or hepatopulmonary syndrome
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)
Treatment of COPD
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)
- LAMA or LABA
- LAMA + LABA
- 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)
- LAMA/LABA or ICS/LABA (if blood eos >300)
- 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.
Treatment of AECOPD
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
Interventional Therapy in Stable COPD
- 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)
COPD - presentation, risk factors
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
Abnormalities on chest xray with COPD
CXR
- Increase in antero posterior diameter of the chest
- flattening of the diaphragm secondary to hyperinflation
Diagnosis of COPD
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
Management goals in COPD
- Improve symptoms (decreasing airflow obstruction and inflammation)
- Prevent secondary complications (e.g. infection)
- Maintain function
- Improve patient’s QOL
Beta2 agonists in COPD (MOA)
- Bronchodilation via stimulation of B2 receptors in the air ways
- SABAs used PRN (rapid onset, shorter half life)
Anticholinergics in COPD
- 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
Role of pneumococcal and influenza vaccine in COPD
- 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.
Pulmonary rehabilitation in COPD (goals, components, outcomes)
- 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
Tripod positioning in dyspnea - pathophys
- Improves dyspnea as it improves ventilatory efficiency by improving length tension dynamic of the diaphragm
Pursed-lip breathing - pathophys
- Improves dyspnea by slowing respiratory rate, increasing intra-airway pressures (diminishing collapse of smaller airways)
Parameters for Home O2
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
Consequences of malnutrition in COPD and interventions
- 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
