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  /Title (copd.pdf)
  /Creator (Cheatography)
  /Author (xkissmekatex (kissmekate))
  /Subject (COPD Cheat Sheet)
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\noindent
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    {\parbox{\dimexpr\textwidth-2\fboxsep\relax}{\noindent
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    \vspace{-2pt}\large{\bf{\textcolor{DarkBackground}{\textrm{COPD Cheat Sheet}}}} \\
    \normalsize{by \textcolor{DarkBackground}{xkissmekatex (kissmekate)} via \textcolor{DarkBackground}{\uline{cheatography.com/33594/cs/10522/}}}
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  \mymulticolumn{2}{p{5.377cm}}{\bf\textcolor{white}{Cheatographer}}  \\
  \vspace{-2pt}xkissmekatex (kissmekate) \\
  \uline{cheatography.com/kissmekate} \\
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  \mymulticolumn{1}{p{5.377cm}}{\bf\textcolor{white}{Cheat Sheet}}  \\
   \vspace{-2pt}Published 13th January, 2017.\\
   Updated 16th January, 2017.\\
   Page {\thepage} of \pageref{LastPage}.
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  Measure your website readability!\\
  www.readability-score.com
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\begin{tabularx}{5.377cm}{x{1.89126 cm} x{3.08574 cm} }
\SetRowColor{DarkBackground}
\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{COPD (Obstructive Disease)}}  \tn
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COPD & Typical symptoms indicative of disease of large airways ({\bf{dyspnea, cough, and sputum}} production) with evidence of {\bf{irreversible airflow obstruction}} (FEV/FVC \textless{} 0.70). \tn 
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Symptoms & Can be asymptomatic. Any combination of cough, sputum, and dyspnea (on exertion or at rest depending on severity). Depends on relative contributions of chronic bronchitis and emphysema. {\bf{Most patients have MIXED features of both}}. \tn 
% Row Count 18 (+ 10)
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Risk Factors & Smoking (90\% of cases), alpha1-antitrypsin deficiency (risk is even worse with smoking), environmental factors (second hand smoke), and chronic asthma. \tn 
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Diagnosis & Get PFTs {\bf{(FEV/FVC \textless{} 0.70)}}, CXR, A1A level in patients with a personal or family history of premature emphysema (\textless{}50yo), and ABG (shows chronic pCO2 retention and decreased PO2).  {\bf{COPD leads to respiratory acidosis with metabolic alkalosis as compensation}}. \tn 
% Row Count 36 (+ 11)
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\begin{tabularx}{5.377cm}{x{1.89126 cm} x{3.08574 cm} }
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{COPD (Obstructive Disease) (cont)}}  \tn
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CXR & Low sensitivity for diagnosing COPD. Only severe, advanced shows {\bf{hyperinflation, flattened diaphragm, enlarged retrosternal space, and diminished vascular markings}}. \tn 
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Screening & Measure peak expiratory flow rate using peak flow meter. If \textless{}350L/min, get PFTs to test for obstruction. \tn 
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Pulmonary Function Tests & • Definitive diagnostic test. FEV1 (the amount of air that can be forced out of the lungs in 1s) is decreased. \{\{nl\}\}  • {\bf{TLC, RV, and FRV are increased (air trapping)}}. Although the TLC is increased, the air is not useful because it is RV (no gas exchange). Decreased vital capacity. \tn 
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FEV1 & • Best prognostic indicator for COPD\{\{nl\}\} • The best predictor of FEV1 is pack years of smoking\{\{nl\}\} • PaO2 falls when FEV1 is \textless{} 50\% \{\{nl\}\} • When FEV1 is \textless{} 25\% chronic retention of C02 occurs\{\{nl\}\} • Cor pulmonale occurs only after prolonged reduction in FEV1 (\textless{} 25\%) with severe, chronic hypoxemia. \tn 
% Row Count 38 (+ 13)
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{COPD (Obstructive Disease) (cont)}}  \tn
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Signs & • Prolonged forced expiratory time.\{\{nl\}\}     • {\bf{Timed full exhalation of VC \textgreater{}6sec.}} \{\{nl\}\}    • During auscultation, end-expiratory wheezes on forced expiration, decreased breath sounds, or inspiratory crackles. \{\{nl\}\}    • Tachypnea, tachycardia, cyanosis, use of accessory respiratory muscles, hyperresonance on percussion, and signs of cor pulmonale. \tn 
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Monitoring & {\bf{Serial FEV1 measurements}} have high predictive value. Watch pulse oximetry and exercise tolerance too. \tn 
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Complications & • acute exacerbations (most common causes are {\bf{infection, noncompliance and heart disease}}), secondary polycythemia (Hct\textgreater{}55\% in men or \textgreater{}47\% in women) compensating to chronic hypoxemia, cor pulmonale, pulmonary HTN. \tn 
% Row Count 31 (+ 10)
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\begin{tabularx}{5.377cm}{x{2.04057 cm} x{2.93643 cm} }
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Emphysema}}  \tn
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Define & • Permanent {\bf{enlargement of small airway spaces}} distal to terminal bronchioles due to {\bf{destruction of alveolar walls}}. \{\{nl\}\}  • Decreased elastic recoil means {\bf{increased compliance, increased TLC, RV (air trapping)}}, so the TC (or FVC) is decreased! \{\{nl\}\}   • Air trapping leads to {\bf{dynamic hyperinflation}} resulting in large auto-PEEP (intrinsic PEEP). \{\{nl\}\}  • Thin patients with severe dyspnea, hyperinflated chests, decreased vascular markings, moderate oxygen desaturation. \tn 
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Pathophysiology of Emphysema & • Destruction of alveolar walls (impaires gas exchange) due to relative {\bf{excess in protease (elastase) activity or relative deficiency of antiprotenase}} (alpha1-antitrypsin) activity in the lung. \{\{nl\}\}  • {\bf{Elastase is released from PMNs and macrophages and digests human lung. This is inhibited by alpha1-antitrypsin.}} \{\{nl\}\}  • Tobacco smoke increases the number of activated PMNs and macrophages, inhibits A1A, and increases oxidative stress on lung by free radical production. \tn 
% Row Count 44 (+ 22)
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Emphysema (cont)}}  \tn
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Pink Puffers & Tend to be thin due to increased energy expenditure during breathing. When sitting, they tend to lean forward, {\bf{barrel chest}} (increased AP diameter). Tachypnea with {\bf{prolonged expiration through pursed lips}}. Patient is distressed and uses accessory muscles (esp. strap muscles in the neck). \tn 
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Centrilobular Emphysema & most common type, typically seen in {\bf{smokers}}. Destruction is limited to respiratory bronchioles (proximal acini) with little changed distal acini. Predilection for {\bf{upper lung}} zones. \tn 
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Panlobular Emphysema & Panlobular Emphysema: seen in patients with {\bf{alpha1-antitrypsin deficiency}}. Destruction involves both proximal and distal acini. Predilection for {\bf{lung bases}}. \tn 
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\begin{tabularx}{5.377cm}{X}
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\mymulticolumn{1}{x{5.377cm}}{\bf\textcolor{white}{GOLD Criteria}}  \tn
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\mymulticolumn{1}{x{5.377cm}}{• GOLD I =mild: FEV1 \textless{}80\% predicted	\{\{nl\}\}   • GOLD 2 =moderate: FEV1 \textless{}50-{}-79\% predicted \{\{nl\}\}   • GOLD 3 =severe: FEV1 3  \textless{}9\% predicted\{\{nl\}\}   • GOLD 4=very severe: FEV1 \textless{} 30\% predicted\{\{nl\}\} Severity of symptoms\{\{nl\}\}   • A=fewer symptoms, low risk of exacerbations\{\{nl\}\}   • B = more symptoms, low risk\{\{nl\}\}   • C = fewer symptoms, high risk\{\{nl\}\}   • D =more symptoms, high risk} \tn 
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\mymulticolumn{1}{x{5.377cm}}{\bf\textcolor{white}{Treatment}}  \tn
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\mymulticolumn{1}{x{5.377cm}}{• SABAs as needed in all patients.} \tn 
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\mymulticolumn{1}{x{5.377cm}}{• LABAs in moderate-to-very severe stages (reduce exacerbations and hospitalizations) when SABAs fail to control.} \tn 
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\mymulticolumn{1}{x{5.377cm}}{• {\bf{ICS is recommended in patients with GOLD 3-4 disease (FEV1\textless{} 50\%)}}. Reduce exacerbations, improved lung function, QoL. But increased risk for PNA. Should be combined with LABAs.} \tn 
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\mymulticolumn{1}{x{5.377cm}}{• Combination LABA + ICS is more e effective at reducing exacerbations  associated with an increased risk of PNA.} \tn 
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\mymulticolumn{1}{x{5.377cm}}{• GOLD 3-4 patients may benefit from roflumilast, a phosphodiesterase-4 inhibitor for  bronchitis, not emphysema.} \tn 
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\begin{tabularx}{5.377cm}{x{2.38896 cm} x{2.58804 cm} }
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\mymulticolumn{2}{x{5.377cm}}{\bf\textcolor{white}{Chronic Bronchitis}}  \tn
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Define & • Chronic cough productive of sputum for at least 3 months per year for at least 2 consecutive years. \{\{nl\}\} • Due to {\bf{hypersecretion of mucus}} and {\bf{structural changes}} in the {\bf{large \seqsplit{airway/tracheobronchial} tree }}\{\{nl\}\} • Bronchovascular markings, flattened diaphragm, and normal DLCO. \tn 
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Pathophysiology of Chronic Bronchitis & Excess mucus production narrows the airways. Productive cough. {\bf{Inflammation and scarring in airways, enlargement in mucous glands, and smooth muscle hyperplasia}} lead to obstruction. \tn 
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Blue Bloaters & • Predominantly {\bf{chronic bronchitis, overweight and cyanotic}} (secondary to hypercapnia and hypoxemia).\{\{nl\}\} • Chronic cough and sputum production. \{\{nl\}\} • Signs of cor pulmonale may be present in severe or long-standing disease.\{\{nl\}\}  • Respiratory rate is normal or slightly increased, no apparent distress, no use of accessory muscles. \tn 
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\begin{tabularx}{5.377cm}{X}
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\mymulticolumn{1}{x{5.377cm}}{\bf\textcolor{white}{Acute Exacerbation}}  \tn
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\mymulticolumn{1}{x{5.377cm}}{Define} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}• Persistent increase in {\bf{dyspnea not relieved with bronchodilators}}. Increased sputum production and cough are common.\{\{nl\}\}    • Can lead to acute respiratory failure requiring hospitalization and possibly mechanical ventilation. • \{\{nl\}\}   • {\bf{Pulmonary infection}} is one of the main precipitants. \{\{nl\}\}   • CXR shows {\bf{hyperinflation}}. ABG shows {\bf{hypoxia, hypercarbia}}, and {\bf{respiratory acidosis}}.} \tn 
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\mymulticolumn{1}{x{5.377cm}}{Treatment of Acute Exacerbation} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}• bronchodilators (beta agonist and/or anticholinergics), {\bf{systemic corticosteroids (methylprednisolone)}} when hospitalized, {\bf{antibiotics (azithromycin or levofloxacin)}}, supplemental oxygen, noninvasive positive pressure ventilation (BIPAP or CPAP), and intubation if necessary (only severe CO2 retention). {\bf{NO INHALED CORTICOSTEROIDS}}.} \tn 
% Row Count 19 (+ 9)
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\begin{tabularx}{5.377cm}{X}
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\mymulticolumn{1}{x{5.377cm}}{\bf\textcolor{white}{Oxygen Therapy}}  \tn
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\mymulticolumn{1}{x{5.377cm}}{• Improves survival and quality of life in patients. Some need continuous oxygen, while others only require it during exertion or sleep. {\bf{Get ABG to determine need}}. \{\{nl\}\}   • Criteria: {\bf{PaO2 55, SaO2\textless{}88\%, or PaO2 55-59}} plus {\bf{polycythemia or cor pulmonale}}. \{\{nl\}\}   • Long standing hypoxemia may lead to {\bf{pulmonary HTN and cor pulmonale}}. \{\{nl\}\}   • Continuous oxygen {\bf{therapy for \textgreater{}18 hr/day}} has been shown to reduce mortality\{\{nl\}\}   • Hypoxemia is due to {\bf{V/Q mismatching}} therefore responsive to low flow oxygen (2-3L/min). If {\bf{not responsive to oxygen, consider shunt}}.} \tn 
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\begin{tabularx}{5.377cm}{X}
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\mymulticolumn{1}{x{5.377cm}}{\bf\textcolor{white}{Smoking Cessation}}  \tn
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\mymulticolumn{1}{x{5.377cm}}{• {\bf{Most important intervention}}. \{\{nl\}\}   • Disease progression is accelerated by continued smoking and can be greatly slowed by its cessation. Around age 35, FEV1 decreases approximate 25-30mL/yr. In smokers, the decline is faster (3-4x). If a smoker quits, the rate of decline slows to normal. \{\{nl\}\}   • Smoking does not completely reverse. Respiratory symptoms improve within 1 year of quitting. \{\{nl\}\}    • {\bf{Smoking cessation and oxygen therapy}} are the only interventions shown to {\bf{reduce mortality}}.} \tn 
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% That's all folks
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