Download COPD Tintinalli Chapter 69

COPD
Tintinalli Chapter 69
Dr. Batizy
Slides by
David R. Fisher, D.O.
September 20, 2005
1
Epidemiology
• 4th most common killer in US
• 3rd most common cause of hospitalization in the US
• Only leading cause of death increasing in prevalence
• 10% prevalence in 55-85 yrs
• Rare < 40 years old
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Epidemiology
• Men > Women
– Prevalence in women doubled in the past few decades
• Increased female smoking
• Prevalence highest in countries with most cigarette use
• Mortality of hospitalized is 5-14%
– ICU mortality is 24%
– If age > 65, one year mortality post ICU discharge is 59%
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COPD
• Consider diagnosis if:
– Chronic cough
– Sputum production
– Dyspnea
– Exposure to risk factors for disease
4
COPD
• 85% with chronic bronchitis primary
– Defined in clinical terms
– Productive cough for 3 months in 2 successive years
• Other causes of cough have been ruled out
• 15% with emphysema primary
– Defined by anatomic pathology
– Abnormal permanent enlargement of air spaces distal
to terminal bronchioles
• Accompanied by destruction of walls without obvious
fibrosis
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Risk factors
• Smoking
– 80-90% of those with COPD are smokers
– 15% of smokers develop clinically significant COPD
– Mortality increased
• Early starting age
• Total pack-years
• Current smoking status
• Other
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Respiratory infections
Occupational exposures
Ambient air pollution
Passive smoke exposure
α1-antitrypsin deficiency (1% of patients with COPD)
Diet
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Pathophysiology
• Insidious onset
– Early changes imperceptible clinically
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Small increase in peripheral airway resistance or lung compliance
Dyspnea and hypersecretion often requires decades of disease
Sedentary lifestyle prevents unmasking exertional dyspnea
May attribute symptoms to aging, poor conditioning, obesity or allergies
– Early abstinence of smoking from onset of disease:
• May eliminate symptoms and result in physiologic improvement
• Once disease established, abnormalities may persist and progress
despite cessation
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Pathophysiology
• Impedance to expiratory airflow
– Increased resistance or decreased caliber
• Throughout the small bronchi and bronchioles
– Airway inflammation
• Occurs in bronchioles and lung parenchyma
– Airflow obstruction
• Airway secretions
• Mucosal edema
• Bronchospasm and bronchoconstriction from impaired elasticity
– Exaggerated airway resistance
• Reduced total minute ventilation and increased respiratory work
• Alveolar hypoventilation results in hypoxemia and hypercarbia
8
Emphysema Pathophysiology
V/Q mismatch
– Destruction of alveolar architecture + vascular destruction
• Reduced matched alveolar and capillary surface area for diffusion of gas
• Resultant unmatched regions where ventilation is wasted
• Hypoxemia results
Aberrant neurochemical and proprioceptive ventilatory
responses in chronic airflow obstruction
– Ventilatory response to hypercarbia may be blunted during sleep
– Ventilatory drive and dyspnea exaggerated despite normal
pulmonary inflation
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Emphysema Pathophysiology
• Pulmonary arterial hypertension supervenes as
chronic airflow obstruction progresses
– Right ventricle hypertrophies and later dilates with the
evolution of overt cor pulmonale
– Low-output state of pulmonary circulation translates into low
left ventricular output
– Arterial hypoxemia increases as effects of right-to-left shunt
of poorly oxygenated mixed venous blood are exaggerated
– Right ventricular pressure overload associated with atrial
and ventricular arrhythmias
10
Clinical Findings of Chronic Compensated COPD
• Hallmark symptoms: exertional dyspnea and cough
• Chronic productive cough
• Minor hemoptysis frequent
• Clinical findings
– Tachypnea
– Accessory respiratory muscle use
– Pursed-lip exhalation
• Expiratory wheezing
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Clinical Findings of Chronic Compensated COPD
• Prolonged expiratory time
• Coarse crackles
– Uncleared secretions move about the central airways in dominantly
bronchitic disease
• Emphysematous disease
– Expansion of the thorax
– Impeded diaphragmatic motion
– Global diminution of breath sounds
• Weight loss frequent
– Poor dietary intake and excessive caloric expenditure for the work of
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breathing
Clinical Findings of Chronic Compensated COPD
• Plethora due to secondary polycythemia
• Hypercarbia in advanced disease
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Cyanosis
Tremor
Somnolence
Confusion
• Findings of secondary pulmonary hypertension with or without
cor pulmonale may be present
• Physical signs of ventricular dysfunction
– Often disguised or underestimated
• Seemingly more overwhelming signs of respiratory disease
• Pulmonary hyperinflation prohibits adequate auscultation
13
Diagnosis of Chronic Compensated COPD
• Examination of:
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Lung mechanics
ABGs
Evaluation of ventilatory response patterns
Tests of respiratory muscle performance
Metabolic assessment
Non-invasive survey of hemodynamic reserve
• Most valuable tools for determining disease severity are PFTs
– Ratio of FEV1 to FVC used to diagnose mild COPD
• FEV1 < 80% predicted + FEV1/FVC <70%
• Once disease progresses, percentage of predicted FEV1 is better measure of
disease severity
14
Diagnosis of Chronic Compensated COPD
• ABGs
– Early stages of COPD:
• Mild to moderate hypoxemia
• No evidence of hypercapnia
– As disease progresses:
• Hypoxemia becomes more severe
• Hypercapnia becomes more evident
– Worse during:
• Exacerbations
• Exercise
• Sleep
15
Diagnosis of Chronic Compensated COPD
Radiographs
– Often misleading
– Mild chronic airflow obstruction not likely to be radiographically
apparent
– Right or left ventricular enlargement may not produce relative
enlargement of the cardiac silhouette
– Radiographs are valuable for complications such as
pneumothorax, pneumonia, pleural effusion and pulmonary
neoplasia
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Diagnosis of Chronic Compensated COPD
• Radiographs
– Bronchitic disease
• Associated with subtle or absent x-ray findings
– Emphysematous disease
• Associated with remarkable signs of hyperaeration:
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Increased AP diameter
Flattened diaphragms
Increased parenchymal lucency
Attenuation of pulmonary arterial vascular shadows despite only
mild-to-moderate physiologic alterations
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Treatment of Chronic Compensated COPD
• Healthy lifestyle
– Regular exercise
– Weight control
– Smoking cessation
• Only therapeutic intervention that can reduce the accelerated decline
in lung function
• Reduces COPD mortality along with long-term oxygen therapy
– Pulmonary rehab can improve exercise capacity and quality
of life
• Recommended in moderate to severe COPD
– Pneumococcal vaccine recommended
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Treatment of Chronic Compensated COPD
• Oxygen
– Primary goal of long-term oxygen therapy:
• Increase baseline PaO2 to 60 mm Hg or SaO2 to 90% at rest
– Use has been demonstrated to reduce mortality
– Start with patients with:
• ABG showing PaO2 of 55 mm Hg
• SaO2 below 88%
• PaO2 of 56-59 mm Hg with signs of:
– Pulmonary hypertension
– Cor pulmonale
– Polycythemia
– Home oxygenation 30% of all COPD related costs in US19
Treatment of Chronic Compensated COPD
• Pharmacotherapy
– No evidence it alters progression of COPD
– Does provide:
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Symptom relief
Control of exacerbations
Improved quality of life
Improved exercise performance
– Inhaled bronchodilators used:
• PRN for mild to moderately obstructed patients with intermittent
symptoms
• On a regular basis to prevent or decrease symptoms
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Treatment of Chronic Compensated COPD
• β2-agonists
– Relax smooth muscle
– Stimulates β2 -adrenergic receptors
– Long-acting β2 –agonists
• Salmeterol or formoterol
• May improve overall symptoms and health status
– Short-acting β2 –agonists
• May improve exercise capacity
• Less convenient to use
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Treatment of Chronic Compensated COPD
• Anticholinergics
– Facilitate bronchodilation
• Block acetylcholine on muscarinic-3 receptors
– Ipratropium bromide
• Drug of choice:
– Patients with persistent symptoms
» Refractory to β2-adrenergic agents
» Bothered by side effects of β2-adrenergic agents
– Regular use of inhaled ipratropium has been shown to
improve health status
22
Treatment of Chronic Compensated COPD
• Combination of β2 -agonists with ipratropium
may improve bronchodilation more than either
drug alone
• If symptoms increasing with optimization of the
above drugs, theophylline may be helpful
23
Treatment of Chronic Compensated COPD
• Systemic corticosteroids
– Evidence lacking for long-term use for all patients with COPD
– 20-30% of patients with COPD improve when given chronic
oral steroids
• Inhaled corticosteroids
– Indicated only if:
• Documented spirometric response to inhaled corticosteroids
• If FEV1 is <50%
• Those with predicted and recurrent exacerbations requiring antibiotic
treatment or systemic corticosteroids
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Treatment of Chronic Compensated COPD
• Mobilization of Secretions
– Generous oral fluid intake
– Atmospheric humidification
– Avoidance of antihistamine and decongestant agents
– Limitation of antitussives helps mobilize respiratory
secretions
– Effect of expectorants questionable
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Acute Exacerbations of COPD
• Decompensation usually due to worsening of airflow obstruction from:
– Superimposed respiratory infection
– Increased bronchospasm
– Respiratory pathology
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Pulmonary embolism
Interference with respiratory drive
Cardiovascular deterioration
Smoking
Non-compliance with medications
Noxious environmental exposures
Uses of medications that prevent bronchorrhea
Adverse response to medication
– Disordered ventilatory drive
• Misuse of oxygen therapy, hypnotics or tranquilizers
• Metabolic disturbances and inadequate oxygen delivery independent of respiratory
function may cause decompensated COPD
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Acute Exacerbations of COPD
• Frequently result in progressive hypoxemia
– Signs
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Tachypnea
Tachycardia
Systemic hypertension
Cyanosis
Change in mental status
– Most life threatening complication is hypoxemia
• Arterial saturation less than 90%
• Increased work of breathing increases muscle production of CO2
• Alveolar ventilation is often unable to increase to prevent CO2 retention
and respiratory acidosis
• Signs of hypercapnea include mental status changes and hypopnea
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Acute Exacerbations of COPD
• Primary complaints dyspnea and orthopnea
• Intensified effort to ventilate is further dramatized by:
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Sitting-up-and-forward position
Pursed-lip exhalation
Accessory muscle use
Diaphoresis
• Pulsus paradoxus may be noted during blood pressure
recording
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Acute Exacerbations of COPD
• Complications may be neglected or minimized by the patient’s
clinical distress:
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Pneumonia
Pneumothorax
Pulmonary embolism
Acute abdomen
• Differential diagnosis:
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Asthma
CHF
Pneumonia
PE
TB
Metabolic disturbances
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Diagnosis of Acute Exacerbations of COPD
• Medical history
• COPD history
• Assessment of oxygenation
• Physical examination
• Bedside PFTs if available
• Assessment of sputum
• Chest X-ray
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Diagnosis of Acute Exacerbations of COPD
• Oxygenation
– Pulse oximetry may identify hypoxemia
• Cannot identify hypercapnia or acid-base disturbances
– No correlation between FEV1 and oxygenation
– PaO2 of less than 60 mm Hg or SaO2 of less than 90 % in
room air indicates respiratory failure
– Hypercapnia or pH of less than 7.30
• Likely experiencing a life-threatening episode of ventilatory failure
• Need intensive management in the ED and ICU
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Diagnosis of Acute Exacerbations of COPD
• Bedside PFTs
– May provide rapid objective assessment of therapy
– Patient cooperation is essential
• Patients commonly too dyspneic to do
– Not recommended during an acute exacerbation
– If able to cooperate:
• Peak expiratory flow rate less than 100 L/minute or FEV1 less than
1.00 L in a patient without chronic severe obstruction indicates a
severe exacerbation
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Diagnosis of Acute Exacerbations of COPD
• Bedside PFTs
– Sequential measurements can be very helpful in
determining response to therapy
– Signs on physical examination and physician
estimates of pulmonary function are inaccurate
– Measurement of FEV1 is preferred to PEFR
• Allows comparison with baseline studies and published
guidelines
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Diagnosis of Acute Exacerbations of COPD
• Assessment of sputum
– Changes in volume and color
• Especially increase in purulence
• Suggests a bacterial etiology for the exacerbation
• Indicates need for antibiotics
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Diagnosis of Acute Exacerbations of COPD
• Radiographic abnormalities common in COPD
exacerbations
– May elucidate underlying etiology of exacerbation
• Pneumonia
– May identify an alternative diagnosis such as CHF
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Diagnosis of Acute Exacerbations of COPD
• ECGs
– May reveal concurrent disease processes:
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Ischemia
MI
Cor pulmonale
Arrhythmias such as MAT
• Theophylline level if taking
• Other
– Order based on clinical picture
• CBC, lytes, βNP, CTA chest, D-dimer
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Treatment of Acute Exacerbations of COPD
• Goals of treatment
– Correct tissue oxygenation
– Alleviate reversible bronchospasm
– Treat underlying etiology of exacerbation
• Factors influencing therapy
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Patient’s mental status
Degree of reversible bronchospasm
Recent medication usage and evidence of potential toxicity
Prior history of exacerbation courses, hospitalizations and intubation
Presence of contraindications to any drug or class of drugs
Specific causes or complications related to the exacerbation
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Treatment of Acute Exacerbations of COPD
• Oxygen
– First goal is to alleviate hypoxemia with desired
PaO2 greater than 60 mm Hg or SaO2 of > 90 %
– May be accomplished by:
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Nasal canula
Simple face mask
Venturi mask
Non-rebreather mask with reservoir and one-way valve
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Treatment of Acute Exacerbations of COPD
• Oxygen
– Need to increase PaO2 must be balanced against the
possibility of producing hypercapnia
• Monitoring of oxygenation and CO2 levels with ABGs is imperative
– Improvement after administration of supplemental oxygen
may take 20-30 minutes to achieve a steady state
– If adequate oxygenation is not achieved or respiratory
acidosis ensues, assisted ventilation may be required
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Treatment of Acute Exacerbations of COPD
• β2-Adrenergic agonists
– First line agent in management of acute, severe COPD
– Aerosolized forms preferred due to minimized systemic
toxicity
– May give q 30-60 minutes prn as tolerated
– Side effects include tremors, anxiety and palpitations
– Should have monitor if suspected or known heart disease
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Treatment of Acute Exacerbations of COPD
• Anticholinergics
– First line COPD therapy
– Ipratropium and glycopyrrolate
– Similar short term improvements in airflow obstruction as β2agonists
– Repeat dose timing not well studied
– Side effects minimal but include dry mouth and metallic taste
– Efficacy of combination with β2-agonists evidence conflicting
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Treatment of Acute Exacerbations of COPD
• Corticosteroids
– Short course of 7-14 days of systemic steroids
improves FEV1 in acute exacerbations of COPD
– Optimal effective dose is 1-3 times the maximal
physiologic adrenal secretion rate
• Equivalent to 60-180 mg prednisone daily
– Hyperglycemia is the most common adverse effect
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Treatment of Acute Exacerbations of COPD
• Antibiotics
– All guidelines recommend concurrent antibiotic treatment in
COPD exacerbations if evidence of infection
– Studies show small benefit in resolution of obstruction and
symptoms
– Benefits more apparent in severe exacerbations
– Direct antibiotic choices at S. pneumoniae, H. influenzae
and M. catarrhalis
– Little evidence regarding duration of treatment but 3-14 days
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typical in studies
Treatment of Acute Exacerbations of COPD
• Methylxanthines
– Role of theophylline and aminophylline controversial
– Routine use not supported unless little relief with other
medications or in those already using with sub-therapeutic
levels
– Formulas for loading doses and IV maintenance dose
infusions
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Indications for Invasive Mechanical Ventilation
• Severe dyspnea with:
– Use of accessory muscles
– Paradoxical abdominal motion
• Respiratory frequency > 35 bpm
• Life-threatening hypoxemia:
– PaO2 < 50 mm Hg or PaO2/FIO2 <200 mm Hg
• Severe acidosis (ph<7.25) and hypercapnia (PaCO2 >
60 mm Hg)
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Indications for Invasive Mechanical Ventilation
• Respiratory arrest
• Somnolence, impaired mental status
• Cardiovascular complications
– Hypotension
– Shock
– Heart failure
• Noninvasive positive pressure ventilation failure
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Treatment of Acute Exacerbations of COPD
• Assisted ventilation
– Main goals to rest ventilatory muscles and to
restore gas exchange to a stable baseline
– Noninvasive positive pressure ventilation can be
delivered via a nasal mask, full face mask or
mouthpiece
– No mode has been shown to be superior
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Treatment of Acute Exacerbations of COPD
• Assisted ventilation
– Patients who receive noninvasive positive pressure
ventilation have better outcomes:
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Intubation rates
Short-term mortality rates
Symptomatic improvement
Length of hospitalization in patients with respiratory failure
– Disadvantages
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Slower correction of gas-exchange abnormalities
Risk of aspiration
Inability to control airway secretions directly
Possible complications of gastric distension and skin necrosis
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Treatment of Acute Exacerbations of COPD
• Assisted ventilation
– Contraindications
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Uncooperative or obtunded patient
Inability of patient to clear airway secretions
Hemodynamic instability
Respiratory arrest
Recent facial or gastroesophageal surgery
Burns
Poor mask fit
Extreme obesity
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Treatment of Acute Exacerbations of COPD
• Assisted ventilation
– Invasive ventilation should be considered in
patients with ventilatory or respiratory failure who
do not qualify for noninvasive positive pressure
ventilation
– Adverse events include pneumonia, barotrauma
and failure to wean
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Treatment of Acute Exacerbations of COPD
• Other Options
– Little evidence to support use of mixture of helium
and oxygen or magnesium in the treatment of acute
COPD exacerbation
– Factors underlying the exacerbation, comorbidities
and other etiologies of dyspnea should be identified
and treated
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ED Management of Exacerbations of COPD
• Assess severity of symptoms
– Administer controlled oxygen therapy
– Perform ABG measurement after 20-30 minutes if SaO2
remains < 90 % or if concerned about symptomatic
hypercapnia
• Administer bronchodilators
– β2-agonists and/or anticholinergic agents by nebulization or
MDI with spacer
• Consider adding IV methylxanthine if needed
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ED Management of Exacerbations of COPD
• Add corticosteroids
– Oral or IV
• Consider antibiotics
– Increased sputum volume
– Change in sputum color
– Fever
– Suspicion of infectious etiology of exacerbation
• Consider noninvasive mechanical ventilation53
ED Management of Exacerbations of COPD
• Laboratory evaluation
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CXR
CBC with differential
Electrolytes
ABG
ECG
• At all times:
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Monitor fluid balance
Consider subcutaneous heparin (DVT prophylaxis)
Identify and treat associated conditions (CHF, arrhythmias)
Closely monitor condition of the patient
54
Hospitalize for Acute Exacerbation of COPD
• Marked increase in intensity of symptoms such as
sudden development of resting dyspnea
• Severe background of COPD
• Onset of new physical signs
– Cyanosis, peripheral edema
• Failure of exacerbation to respond to initial medical
management
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Hospitalize for Acute Exacerbation of COPD
• Significant comorbidities
• Newly occurring arrhythmias
• Diagnostic uncertainty
• Older age
• Insufficient home support
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If stable to be discharged home:
• Arrange adequate supply of home oxygen if
needed
• Arrange adequate and appropriate
bronchodilator treatment
• Consider short course of oral corticosteroids
• Arrange for follow-up with their PCP
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True/False Questions:
• 1. Chronic bronchitis is defined in clinical terms wheras emphysema is
defined by anatomic pathology.
• 2. Patients who receive noninvasive positive pressure ventilation have better
outcomes in terms of future intubation rate, short-term mortality rate, symptomatic
improvement and length of hospitalization in patients with respiratory failure.
• 3. Radiographic findings of patients with emphysematous disease are
associated with remarkable signs of hyperaeration including increased AP
diameter, flattened diaphragms and increased parenchymal lucency.
• 4. Complications that may be neglected or minimized in examining a patient
with COPD include pneumonia, pneumothorax, pulmonary embolism and
acute abdomen.
• 5. Risk factors for COPD include smoking, respiratory infections,
occupational exposures, ambient air pollution, passive smoke exposure
and α1-antitrypsin deficiency.
58
•
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The squiggly line
Totally disorganized depolarization and contraction of ventricular myocardium
No effective ventricular activity
Absence of QRS complexes and P waves
May have coarse vs. fine VFib
Clinically associated with absent pulse and blood pressure
Etiology
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CAD
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More common than Vtach in hypothermia
V-Fib
59
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Three or more consecutive PVCs
Wide bizarre appearing QRS Complex (0.12 s or greater)
Most common rate 150-200
Usually regular, may be slightly irregular
Fusion beats may be present, representing a combination of normally conducted sinus beats and ventricular ectopic
beats
VT may occur in paroxysms or sustained
Etiology
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V-Tach
Rare in patients without underlying heart disease
Most common causes are ischemic heart disease, especially post MI
Cardiomyopathy, MVP, drug toxicity, electrolyte imbalance and sympathomimetics are other causes
60