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Dyspnea

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

Dyspnea - common complaint/symptom


shortness of breath or breathlessness

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

Table 1:Dyspnea Assessment using Acronym O,P,Q,R,S,T,U and V

Assessment: Physical examination

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.

Oxygen Canula2-4L Non-rebreathing mask4-6L


Corticosteroids dexamethasone 8 to 24 mg PO or S.C. or I.V. daily depending on severity of dyspnea 2.5 to 5 mg q8h and titrate to effect. 0.5 to 2 mg SL q2-4h p.r.n.

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

Mixed Cardiac/Pulmonary Etiology


COPD with pulmonary HTN and/or cor pulmonale Deconditioning Chronic pulmonary emboli Pleural effusion

Noncardiac or Nonpulmonary Etiology


Metabolic conditions (e.g. acidosis) Pain Trauma Neuromuscular disorders Functional (anxiety,panic disorders,
hyperventilation)

Chemical exposure

Easily Performed Diagnostic Tests

Chest radiographs Electrocardiograph Screening spirometry

In cases where test results inconclusive


complete PFTs ABGs EKG Standard exercise treadmill testing/ or complete cardiopulmonary exercise testing Consultation with pulmonologist/cardiologist may be useful

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

Use of accessory muscles of inspiration diaphragmatic fatigue Paradoxical respirations


- reflect impending ventilatory failure

Altered mental status lethargy, exhaustion, agitation, confusion

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

Treatment Goals of Severe Asthma


Improve airway function rapidly Avoid hypoxemia Prevent respiratory failure and death

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 - Physical Findings


Tachypnea Accessory respiratory muscle use Pursed lip exhalation Weight loss due to poor dietary intake and excessive caloric expenditure for work of breathing

Dominant Clinical Forms of COPD


Pulmonary emphysema Chronic bronchitis

Most patients exhibit a mixture of symptoms and signs

COPD - Advanced Dx
secondary polycythemia cyanosis tremor somnolence and confusion due to hypercarbia Secondary pulmonary HTN w or w/o cor pulmonale

COPD Treatment Strategy


Elimination of extrinsic irritants bronchodilator & glucocorticoid therapy Antibiotics Mobilization of secretions respiratory vaccines Oxygen therapy - if oxygen saturation <90% at rest on room air

Spirometry

PNEUMONIA

6th leading cause of death in the US & Indonesia

Respiratory viruses & mycoplasma responsible for greater than 1/3 of cases

Common types of respiratory infections


Tracheobronchitis Pneumonia Effusions Empyema Abscess Cavitary lesions post-obstructive

Common Respiratory Viruses


Influenza A & B Parainfluenza 1& 3 Respiratory Syncytial Virus Adenovirus Cytomegalovirus Herpes Simplex & Zoster/varicella Hanta Virus Infection

Respiratory Syncytial Virus


Rapid diagnosis of Respiratory Syncytial Virus Infection by immunofluorescence of respiratory secretions

Classic Pneumonia Symptoms


Dyspnea, chills high fever, cough/sputum pleuritic chest pain

Viral Pneumonia - symptoms


Chest Pain Fever Dyspnea Prodrome - malaise, upper respiratory symptoms, and other GI symptoms

Viral pneumonia Clinical Findings


Minimal/variable Chest exam - may reveal wheezing Fine rales if heard can signify interstitial involvement Chest x-ray - patchy densities or interstitial involvement

Viral pneumonia Management /Prophylaxis


Supportive treatment - decrease severity of symptoms bed rest analgesics expectorants Patients w/
airway obstruction - treat w/bronchodilators secondary bacterial infection - antibiotics

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

Atypical Pneumonia Treatment


Antibiotics Macrolides fluroquinolones doxycycline

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

Pneumococcus pneumonia accounts for up to 90% of all bacterial pneumonias


Patients with a chronic Diagnosis are at an increased risk of contracting pneumonia

Bacterial pneumonia presentation


acute shaking - chills tachypnea tachycardia malaise anorexia myalgias flank or back pain vomiting

Lab Tests
WBC Chest X-ray Pulse Ox ABGs Sputum exam Blood cultures pleural fluid exam

Pneumothorax

Causes of Spontaneous Pneumothorax


Pleural blebs Bullae Emphysema Interstitial lung disease Alpha 1 antitrypsin deficiency

Traumatic and Iatrogenic Causes


Penetrating wounds Line placements Lung biopsies Mechanical ventilation

Two most common symptoms


Dyspnea Chest pain

Physical Examination
Decreased breath sounds hyperresonance to percussion decreased tactile fremitus
In patients with emphysema - clinical findings may be subtle

Chest X-ray to Confirm Dx


500ml of air required to visualize pneumothorax on x-ray
Characterized by hyperlucency and lack of lung markings at the periphery of the lung and appearance of fine line that represents the retraction of the visceral from the parietal pleura

Treatment Options
Observation - if pneumothorax involves < 15-20% of hemithorax and patient relatively asymptomatic Tube thoracostomy Simple Aspiration

Pulmonary Embolism (PE)

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

Classic triad of signs/symptoms

Hemoptysis Dyspnea Chest Pain

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%

Massive PE Diagnostic Studies


VQ scan Pulmonary angiography CT Echocardiography (TEE) Pulmonary artery catheterization Diagnostic algorithm D-dimer blood gases increased A-a gradient

A-a gradient
A-a gradient = predicted pO2 observed PO2
PAO2 = (FIO2 X 713) (PaCO2/0.8) at sealevel

PAO2 = 150-(PaCO2/0.8) at sealevel on room air


Normal range 10-15mm > 30 years of age Normal range 8mm < 30 years of age Increased A-aDO2=diffusion defect Right to left shunt V/Q mismatch

Treatment Strategies
Fluid administration anticoagulation Vena caval interruption Thrombolytics oxygen pulse ox

CHF

Left sided Failure


Blood/fluid back-up into the lungs result in
Shortness Of Breath Fatigue Cough (especially at night) Paroxymal Nocturnal Dyspnea orthopnea

Right sided Failure


Build-up of fluid in the veins Edema of feet, legs and ankles

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

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