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7/31/2019 DYSPNEA Assessment& Management-ANIS
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Dyspnea
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Definition of dyspnea published byAmerican Thoracic Society (ATS):
Dyspnea, the subjective experience ofbreathing discomfort t, is the mostcommon that is comprised of qualitatively
distinct sensations that vary in intensity.
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The experience derives from
interactions among:-multiple physiological factor
-psychological
-social-environment
-may induce secondary physiological
& behavioral response
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Dyspnea - common complaint/symptom
shortness of breath or breathlessness
Defined as abnormal/uncomfortable
breathing
Multiple etiologies -
2/3 of cases - cardiac or pulmonaryetiology
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Standard of Care
1.Assessment
2. Diagnosis
3. Education
4. Treatment: Non-pharmacological
5. Treatment: Pharmacological
6. Crisis intervention
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Assessment of Dyspnea
Table 1:Dyspnea Assessment using Acronym O,P,Q,R,S,T,U and V
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Assessment: Physical examination
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Diagnosis
The most significant intervention in themanagement 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 benefitfrom management of the symptom using
education, energy conservation and breathcontrol, airflow and medications.
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Clues to diagnosis:
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Education
Providing information & education isfoundational 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 thatcan be managed.
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Develop the clear plan for the patient &
family to address the pattern ofShortness of Breath and the patientsway of coping.
Teach the purpose of each medication.Ensure an understanding of usingregular and breakthrough medications.
this is a key to effective management. Known COPD patient often use of
nebulizers & spacer. Ensure patients
compliance
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Treatment: Non-pharmacological
Energy conservation and breathcontrol
-Explain how to incorporate pacingand planning.
-Teach relaxation training and
breath control.
Air flow
-open window & air movement
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Environment
-Cool and humidify dry air, eliminate irritantsin air.
Positioning
-Avoid compression of abdomen or chestwhen positioning.
-Try placing in semi-Fowlers position.
Support
-Offer psychosocial support and/or counseling.
-Alternative therapies for relaxation include:massage, therapeutic touch, visualization, musictherapies.
-Acupuncture or acupressure.
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Treatment: Pharmacological
Opiods : 1st choice in palliation of dyspnea.
-Opioid naive protocol:
Consider hydromorphone in the elderly and if there isdecrease renal function.
Breakthrough of q4h dose (or 10% of TDD)ordered q1h p.r.n.
Morphine 2.5 to 5 mg PO q4h.Uselower dose in the elderly
Hydromorphone 0.5 to 1 mg PO q4h.Use lowerdose in the elderly.
Oxycodone 5mg PO. Titrate dose q4h.
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Oxygen
Canula2-4L
Non-rebreathing mask4-6L
Corticosteroids dexamethasone 8 to 24 mg PO or S.C.or I.V. dailydepending on
severity of dyspnea
Neuroleptics:adjuvant in chronicdyspnea
Methotrimeprazine 2.5 to 5 mg q8h andtitrate to effect.
Benzodiazepines:severe anxiety orrespiratory panicattacks
Lorazepam 0.5 to 2 mg SL q2-4hp.r.n.
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Crisis intervention
Treat aggressively with opioids as well assedatives 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 everythree 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 15min (for S.C.) If ineffective double dose as above.
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Use one of the following with opioid:midazolam 5 mg S.C. or I.V. q5 to15min. p.r.n., lorazepam 4 mg I.V. orS.C. q5 to 15 min. p.r.n.,methotrimeprazine 25 mg q5 to 15 min.
p.r.n., phenobarbital 90 to 120 mg q5to 15 min. p.r.n. or diazepam 5 to 10mg I.V. q5 to 15 min. p.r.n.
Use incremental titration until patientcomfortable, determined by subjectiveas well as objective means.
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Differential Diagnosis
Composed of four general categories
Cardiac
Pulmonary
Mixed cardiac or pulmonary
Non-cardiac or Non-pulmonary
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Pulmonary Etiology
COPD
Asthma
Restrictive Lung Disorders
Hereditary Lung Disorders
Pneumonia
Pneumothorax
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Cardiac Etiology CHF
CAD
MI (recent or past history) Cardiomyopathy
Valvular dysfunction
Left ventricular hypertrophy Pericarditis
Arrhythmias
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Mixed Cardiac/PulmonaryEtiology
COPD with pulmonary HTN and/or corpulmonale
Deconditioning
Chronic pulmonary emboli
Pleural effusion
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Noncardiac or NonpulmonaryEtiology
Metabolic conditions (e.g. acidosis)
Pain
Trauma
Neuromuscular disorders
Functional (anxiety,panic disorders,hyperventilation)
Chemical exposure
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Easily Performed DiagnosticTests
Chest radiographs
Electrocardiograph
Screening spirometry
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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
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Commonly used to evaluate acute dyspnea
can provide information about altered pH,hypercapnia, hypocapnia or hypoxemia
normal ABGs do not excludecardiac/pulmonary dx as cause of dyspnea
Remember- ABGs may be normal even in cases
of acute dyspnea - ABGs do not evaluatebreathing
ABGs
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Rapid, widely available, noninvasivemeans of assessment in most clinical
situations- insensitive (may be normal in acute dyspnea)
The % of Oxygen saturation does notalways correspond to PaO2
The hemoglobin desaturation curve can beshifted depending on the pH, temperatureor arterial carbon monoxide or carbon
dioxide levels
PULSE OX
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ASTHMA
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What is Asthma?
A Chronic disease of the airways thatmay cause:
Wheezing Breathlessness
Chest tightness
Nighttime or early morning coughing
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The bronchospasm characteristic of theacute asthmatic attack is typically
reversible. It improves spontaneouslyor within minutes to hours of treatment
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Asthma can exist by itself or coexistwith chronic bronchitis, emphysema, or
bronchiectasis
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Symptoms/Chief Complaint
Progressive dyspnea
Cough
Chest tightness
Wheezing/coughing
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The rapidly reversible airflowobstruction of asthma is mainly due to
bronchial smooth muscle contraction
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Focus of Therapy
Pharmacologic manipulation of airway smoothmuscle
Do not overlook physiologic impairment caused bymucous production and mucosal edema
Bronchospasm can be reversed in minutes
Airflow obstruction due to mucous plugging and
inflammatory changes in bronchial walls may notresolve for days/weeks -
may lead to atelectasis, infectious bronchitis,pneumonitis
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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
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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
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Patient Exam
Hypersonance to percussion
decreased intensity of breath sounds
prolongation of expiratory phase w orw/o wheezing
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Patient Exam
The intensity of the wheeze may notcorrelate with the severity of airflow
obstruction
quiet chest- very severe airflow
obstruction
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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
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Treatment Goals of Severe Asthma
Improve airway function rapidly
Avoid hypoxemia
Prevent respiratory failure and death
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COPD
Hallmark symptom - Dyspnea
Chronic productive cough
Minor hemoptysis
pink puffer
blue bloater
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COPD- pulmonary hyperinflation- the diaphragms are at the levelof the eleventh posterior ribs and appear flat.
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COPD - Physical Findings
Tachypnea
Accessory respiratory muscle use
Pursed lip exhalation
Weight loss due to poor dietary intakeand excessive caloric expenditure for
work of breathing
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D i t Cli i l F f
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Dominant Clinical Forms ofCOPD
Pulmonary emphysema
Chronic bronchitis
Most patients exhibit a mixture of
symptoms and signs
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COPD - Advanced Dx
secondary polycythemia
cyanosis
tremor
somnolence and confusion due tohypercarbia
Secondary pulmonary HTN w or w/o corpulmonale
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COPD Treatment Strategy
Elimination of extrinsic irritants
bronchodilator & glucocorticoid therapy
Antibiotics
Mobilization of secretions
respiratory vaccines
Oxygen therapy - if oxygen saturation
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Spirometry
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6th leading cause of death in the US &Indonesia
Respiratory viruses & mycoplasma
responsible for greater than 1/3 ofcases
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Common types of respiratoryinfections
Tracheobronchitis
Pneumonia
Effusions
Empyema
Abscess
Cavitary lesions
post-obstructive
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Common Respiratory Viruses
Influenza A & B
Parainfluenza 1& 3
Respiratory Syncytial Virus
Adenovirus
Cytomegalovirus
Herpes Simplex & Zoster/varicella
Hanta Virus Infection
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Respiratory Syncytial Virus
Rapid diagnosis of RespiratorySyncytial Virus Infection by
immunofluorescence of respiratorysecretions
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Classic Pneumonia Symptoms
Dyspnea, chills
high fever, cough/sputum
pleuritic chest pain
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Viral Pneumonia - symptoms
Chest Pain
Fever
Dyspnea
Prodrome - malaise, upper respiratorysymptoms, and other GI symptoms
Viral pneumonia
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Viral pneumonia -Clinical Findings
Minimal/variable
Chest exam - may reveal wheezing
Fine rales if heard can signify interstitialinvolvement
Chest x-ray - patchy densities or
interstitial involvement
Viral pneumonia
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Viral pneumoniaManagement /Prophylaxis
Supportive treatment - decreaseseverity of symptoms
bed rest analgesics
expectorants
Patients w/
airway obstruction - treatw/bronchodilators
secondary bacterial infection - antibiotics
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Atypical Pneumonia
Accounts for 25% of communityacquired 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
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Atypical PneumoniaTreatment
Antibiotics
Macrolides
fluroquinolones
doxycycline
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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 pneumococcalfollowed by haemophilus influenza
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Pneumococcus pneumonia accounts forup to 90% of all bacterial pneumonias
Patients with a chronic Diagnosis are atan increased risk of contracting
pneumonia
Bacterial pneumonia
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Bacterial pneumoniapresentation
acute shaking - chills
tachypnea
tachycardia malaise
anorexia
myalgias flank or back pain
vomiting
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Lab Tests
WBC
Chest X-ray
Pulse Ox
ABGs
Sputum exam
Blood cultures
pleural fluid exam
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Pneumothorax
Causes of Spontaneous
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Causes of SpontaneousPneumothorax
Pleural blebs
Bullae Emphysema
Interstitial lung disease
Alpha 1 antitrypsin deficiency
Traumatic and Iatrogenic
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Traumatic and IatrogenicCauses
Penetrating wounds
Line placements
Lung biopsies
Mechanical ventilation
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Two most common symptoms
Dyspnea
Chest pain
http://images.google.com/imgres?imgurl=http://pain.health-info.org/pictures/chest.bi.jpg&imgrefurl=http://pain.health-info.org/Pain%20Pages/Chest.Pain.and.Chest.Discomfort.htm&h=1157&w=1170&sz=182&tbnid=NKrFmpN03-e-oM:&tbnh=148&tbnw=150&hl=en&start=1&prev=/images?q=+chest+pain&svnum=10&hl=en&lr=7/31/2019 DYSPNEA Assessment& Management-ANIS
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Physical Examination
Decreased breath sounds
hyperresonance to percussion
decreased tactile fremitus
In patients with emphysema - clinical
findings may be subtle
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Chest X-ray to Confirm Dx
500ml of air required to visualizepneumothorax on x-ray
Characterized by -
hyperlucency and lack of lung markings at
the periphery of the lung and appearanceof fine line that represents the retraction ofthe visceral from the parietal pleura
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Treatment Options
Observation - if pneumothorax involves< 15-20% of hemithorax and patient
relatively asymptomatic Tube thoracostomy
Simple Aspiration
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Pulmonary Embolism (PE)
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PE History
PE is so common and deadly that thediagnosis should be considered in any
patient who presents with chestsymptoms that cannot be proven tohave another cause
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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
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Classic triad ofsigns/symptoms
These symptoms are not sensitive orspecific and occur in fewer than 20% ofpatients diagnosed with PE
Hemoptysis
Dyspnea
Chest Pain
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PE Physical Exam
Massive PE causes hypotension due toacute cor pulmonale
Physical findings in early submassive PEmay be completely normal
Initially, abnomal findings are absent in
most patients with PE
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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%
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Massive PE Diagnostic Studies
VQ scan
Pulmonary angiography
CT
Echocardiography (TEE)
Pulmonary artery catheterization
Diagnostic algorithm
D-dimer
blood gases increased A-a gradient
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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 ageNormal range 8mm < 30 years of age
Increased A-aDO2=diffusion defectRight to left shuntV/Q mismatch
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Treatment Strategies
Fluid administration
anticoagulation
Vena caval interruption Thrombolytics
oxygen
pulse ox
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CHF
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Left sided Failure
Blood/fluid back-up into the lungs -result in
Shortness Of Breath Fatigue
Cough (especially at night)
Paroxymal Nocturnal Dyspnea orthopnea
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Right sided Failure
Build-up of fluid in the veins -
Edema of feet, legs and ankles
may effect liver/portal circulation and 3rdspacing into soft tissue/ascites/pleuraleffusion
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Causes of CHF
Variety of cardiac diseases
Most common cause of CHF - CAD
other causes - valvular heart dx,
HTN,cardiomyopathies, myocarditis, renaldx,fluid overload,liver dx w/loss of proteinand osmotic forces,high altitude and manyothers
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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
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Diagnostic Work-Up
History
Physical exam
EKG Echo
Chest x-ray
BNP
ABG/pulse ox
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Treatment
Diuretics
Digitalis
Peripheral vasodilators/NTG Positive inotropic agents
ACE inhibitors
Beta blockers Oxygen
MS04