1 COPD Tintinalli Chapter 69 Dr. Batizy Slides by David R. Fisher, D.O. September 20, 2005.

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COPD

Tintinalli Chapter 69

Dr. BatizySlides by

David R. Fisher, D.O.

September 20, 2005

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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

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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– 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

• 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

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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

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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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• 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

breathing

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• Plethora due to secondary polycythemia

• Hypercarbia in advanced disease– 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

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Diagnosis of Chronic Compensated COPD

• Examination of:– 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

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• 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

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• 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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• Radiographs

– Bronchitic disease• Associated with subtle or absent x-ray findings

– Emphysematous disease• Associated with remarkable signs of hyperaeration:

– 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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• 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 US

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• Pharmacotherapy – No evidence it alters progression of COPD

– Does provide:• 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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• 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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• 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

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• 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

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• 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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• 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• 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• 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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• Primary complaints dyspnea and orthopnea

• Intensified effort to ventilate is further dramatized by:– 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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• Complications may be neglected or minimized by the patient’s clinical distress:– Pneumonia– Pneumothorax– Pulmonary embolism– Acute abdomen

• Differential diagnosis:– 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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• 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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• 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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• 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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• 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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• 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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• ECGs– May reveal concurrent disease processes:

• 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– 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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• Oxygen– First goal is to alleviate hypoxemia with desired

PaO2 greater than 60 mm Hg or SaO2 of > 90 %

– May be accomplished by:• Nasal canula• Simple face mask• Venturi mask• Non-rebreather mask with reservoir and one-way valve

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• 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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• 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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• Anticholinergics

– First line COPD therapy

– Ipratropium and glycopyrrolate

– Similar short term improvements in airflow obstruction as β2-agonists

– 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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• 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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• 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 typical in studies

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• 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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• 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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• Assisted ventilation

– Patients who receive noninvasive positive pressure ventilation have better outcomes:

• Intubation rates• Short-term mortality rates• Symptomatic improvement• Length of hospitalization in patients with respiratory failure

– Disadvantages• 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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• Assisted ventilation– Contraindications

• 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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• 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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• 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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• Add corticosteroids– Oral or IV

• Consider antibiotics– Increased sputum volume– Change in sputum color– Fever– Suspicion of infectious etiology of exacerbation

• Consider noninvasive mechanical ventilation

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• Laboratory evaluation– CXR– CBC with differential – Electrolytes– ABG– ECG

• At all times:– Monitor fluid balance– Consider subcutaneous heparin (DVT prophylaxis)– Identify and treat associated conditions (CHF, arrhythmias)– Closely monitor condition of the patient

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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.

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V-Fib

• 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

– CAD– More common than Vtach in hypothermia

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V-Tach

• 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

– 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

1 COPD Tintinalli Chapter 69 Dr. Batizy Slides by David R. Fisher, D.O. September 20, 2005.

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