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Definition of dyspnea published by American Thoracic Society (ATS): Dyspnea, the subjective experience of breathing discomfort t, is the most common that is comprised of qualitatively distinct sensations that vary in intensity.
The experience derives from interactions among: -multiple physiological factor -psychological -social -environment -may induce secondary physiological & behavioral response
Defined as abnormal/uncomfortable breathing Multiple etiologies 2/3 of cases - cardiac or pulmonary etiology
Standard of Care
1. Assessment 2. Diagnosis 3. Education 4. Treatment: Non-pharmacological 5. Treatment: Pharmacological 6. Crisis intervention
Assessment of Dyspnea
Diagnosis
The most significant intervention in the management of dyspnea is identifying underlying cause(s) & treating as appropiate. Whether or not the underlying cause(s) can be relieved or treated, all patients will benefit from management of the symptom using education, energy conservation and breath control, airflow and medications.
Clues to diagnosis:
Education
Providing information & education is foundational to enhance the patient & familys ability to cope it: Explain to the patient & family about the multiple triggers of dyspnea. Reinforce that this is a symptom that can be managed.
Develop the clear plan for the patient & family to address the pattern of Shortness of Breath and the patients way of coping. Teach the purpose of each medication. Ensure an understanding of using regular and breakthrough medications. this is a key to effective management. Known COPD patient often use of nebulizers & spacer. Ensure patients compliance
Treatment: Non-pharmacological
Energy conservation and breath control -Explain how to incorporate pacing and planning. -Teach relaxation training and breath control. Air flow -open window & air movement
Environment -Cool and humidify dry air, eliminate irritants in air. Positioning -Avoid compression of abdomen or chest when positioning. -Try placing in semi-Fowlers position. Support -Offer psychosocial support and/or counseling. -Alternative therapies for relaxation include: massage, therapeutic touch, visualization, music therapies. -Acupuncture or acupressure.
Treatment: Pharmacological
Opiods : 1st choice in palliation of dyspnea. -Opioid naive protocol: Consider hydromorphone in the elderly and if there is decrease renal function. Breakthrough of q4h dose (or 10% of TDD) ordered q1h p.r.n.
Morphine Hydromorphone Oxycodone 2.5 to 5 mg PO q4h.Use lower dose in the elderly 0.5 to 1 mg PO q4h.Use lower dose in the elderly. 5mg PO. Titrate dose q4h.
Neuroleptics: adjuvant in chronic dyspnea Benzodiazepines: severe anxiety or respiratory panic attacks
Methotrimeprazine
Lorazepam
Crisis intervention
Treat aggressively with opioids as well as sedatives until comfort is achieved. Opioid naive use morphine 5 mg I.V. or S.C. bolus q5 to 10 min. Double dose if no effect every three doses. Opioid tolerant give full regular PO Q4h dose as S.C. or I.V. q5 to 10 min (for I.V.) or q10 to 15 min (for S.C.) If ineffective double dose as above.
Use one of the following with opioid: midazolam 5 mg S.C. or I.V. q5 to 15min. p.r.n., lorazepam 4 mg I.V. or S.C. q5 to 15 min. p.r.n., methotrimeprazine 25 mg q5 to 15 min. p.r.n., phenobarbital 90 to 120 mg q5 to 15 min. p.r.n. or diazepam 5 to 10 mg I.V. q5 to 15 min. p.r.n. Use incremental titration until patient comfortable, determined by subjective as well as objective means.
Differential Diagnosis
Composed of four general categories
Cardiac Pulmonary Mixed cardiac or pulmonary Non-cardiac or Non-pulmonary
Pulmonary Etiology
COPD Asthma Restrictive Lung Disorders Hereditary Lung Disorders Pneumonia Pneumothorax
Cardiac Etiology
CHF CAD MI (recent or past history) Cardiomyopathy Valvular dysfunction Left ventricular hypertrophy Pericarditis Arrhythmias
Chemical exposure
ABGs
Commonly used to evaluate acute dyspnea can provide information about altered pH, hypercapnia, hypocapnia or hypoxemia normal ABGs do not exclude cardiac/pulmonary dx as cause of dyspnea
Remember- ABGs may be normal even in cases of acute dyspnea - ABGs do not evaluate breathing
PULSE OX
Rapid, widely available, noninvasive means of assessment in most clinical situations insensitive (may be normal in acute dyspnea)
The % of Oxygen saturation does not always correspond to PaO2 The hemoglobin desaturation curve can be shifted depending on the pH, temperature or arterial carbon monoxide or carbon dioxide levels
ASTHMA
What is Asthma?
A Chronic disease of the airways that may cause:
Wheezing Breathlessness Chest tightness Nighttime or early morning coughing
The bronchospasm characteristic of the acute asthmatic attack is typically reversible. It improves spontaneously or within minutes to hours of treatment
Asthma can exist by itself or coexist with chronic bronchitis, emphysema, or bronchiectasis
Symptoms/Chief Complaint
Progressive dyspnea Cough Chest tightness Wheezing/coughing
The rapidly reversible airflow obstruction of asthma is mainly due to bronchial smooth muscle contraction
Focus of Therapy
Pharmacologic manipulation of airway smooth muscle Do not overlook physiologic impairment caused by mucous production and mucosal edema Bronchospasm can be reversed in minutes Airflow obstruction due to mucous plugging and inflammatory changes in bronchial walls may not resolve for days/weeks may lead to atelectasis, infectious bronchitis, pneumonitis
Asthma Triggers
Immunologic reaction Viral respiratory/sinus infections change in temperature/humidity Drugs/Chemicals aspirin, NSAIDS
Exercise GE reflux Laughing/coughing Environmental factors strong odors, pollutants, dust, fumes
Patient Exam
Wheezing
may be audible w/o stethoscope
Patient Exam
Hypersonance to percussion decreased intensity of breath sounds prolongation of expiratory phase w or w/o wheezing
Patient Exam
The intensity of the wheeze may not correlate with the severity of airflow obstruction
quiet chest - very severe airflow obstruction
Asthma Treatment
Nebulized B-adrenergic drugs Corticosteroids Nebulized anticholinergics Magnesium sulfate Oxygen Long acting beta-agonists Inhaled steroids
Managing Asthma:
Indications of a severe attack:
Breathless at rest hunched forward talking in words rather than sentences Agitated Peak flow rate less than 60% of normal
COPD
COPD
Hallmark symptom - Dyspnea Chronic productive cough Minor hemoptysis pink puffer blue bloater
COPD- pulmonary hyperinflation- the diaphragms are at the level of the eleventh posterior ribs and appear flat.
COPD - Advanced Dx
secondary polycythemia cyanosis tremor somnolence and confusion due to hypercarbia Secondary pulmonary HTN w or w/o cor pulmonale
Spirometry
PNEUMONIA
Respiratory viruses & mycoplasma responsible for greater than 1/3 of cases
Atypical Pneumonia
Accounts for 25% of community acquired pneumonias Mycoplasma/chlamyda/legionella can case extrapulmonary manifestations meningitis, encephalitis, pericarditis, hepatitis, hemolytic anemia typically bilateral infiltrates on chest x-ray primarily effects younger persons
Bacterial pneumonia
3.3 million cases yearly in US responsible for 10% of hospital admissions unilateral infiltrate on x-ray high mortality in elderly population most common cause pneumococcal followed by haemophilus influenza
Lab Tests
WBC Chest X-ray Pulse Ox ABGs Sputum exam Blood cultures pleural fluid exam
Pneumothorax
Physical Examination
Decreased breath sounds hyperresonance to percussion decreased tactile fremitus
In patients with emphysema - clinical findings may be subtle
Treatment Options
Observation - if pneumothorax involves < 15-20% of hemithorax and patient relatively asymptomatic Tube thoracostomy Simple Aspiration
PE History
PE is so common and deadly that the diagnosis should be considered in any patient who presents with chest symptoms that cannot be proven to have another cause
PE Risk Markers
Hypercoagulable states Prior history of DVT or PE Recent surgery or pregnancy Prolonged immobolization Underlying malignancy smoking birth control pills trauma
These symptoms are not sensitive or specific and occur in fewer than 20% of patients diagnosed with PE
PE Physical Exam
Massive PE causes hypotension due to acute cor pulmonale Physical findings in early submassive PE may be completely normal Initially, abnomal findings are absent in most patients with PE
Massive PE - Signs/Symptoms
Tachypnea -96% Rales - 58% Accentuated second heart sound - 53% Tachycardia - 44% Fever - 43% S3 or S4 gallop - 34% signs/symptoms suggestive of thrombophlebitis - 32% Lower extremity edema - 24% Cardiac murmur - 23% Cyanosis - 19%
A-a gradient
A-a gradient = predicted pO2 observed PO2
PAO2 = (FIO2 X 713) (PaCO2/0.8) at sealevel
Treatment Strategies
Fluid administration anticoagulation Vena caval interruption Thrombolytics oxygen pulse ox
CHF
may effect liver/portal circulation and 3rd spacing into soft tissue/ascites/pleural effusion
Causes of CHF
Variety of cardiac diseases
Most common cause of CHF - CAD
other causes - valvular heart dx, HTN,cardiomyopathies, myocarditis, renal dx,fluid overload,liver dx w/loss of protein and osmotic forces,high altitude and many others
Physical Findings
Peripheral edema JVD tachycardia tachypnea, using accessory muscles of respiration Skin - diaphoretic/cold/gray/cyanotic Wheezing/rales on ausculation Apical impulse displaced laterally ascites hepatosplenomegaly
Diagnostic Work-Up
History Physical exam EKG Echo Chest x-ray BNP ABG/pulse ox
Treatment
Diuretics Digitalis Peripheral vasodilators/NTG Positive inotropic agents ACE inhibitors Beta blockers Oxygen MS04 BNP