cap PULMONOLOGY KAPLAN 2001 Kaplan Medical (800) 533-8850 or (949) 476-6282A. Pulmonary Function Tests 1. Spirometry Figure 10-1: Spirogram bf Posen dee Sh 0 leetes neuebane perme Hosq Aa oss FEV, fuse Table 1. Pulmonary Indices ‘Index Description Tidal Volume ee Volume exchanged during normal respiration ratory Reserve Volume ae 7 Ta aan ae cae. Reserve Volume lume maximally expired | eal sae ‘expiration fehl Volume: folume ‘remaining in lung after forced ration 3 Rees Capacity 225413.00197,ap Pulmonology * Symptomatology and Diagnosis, “ Folia fun” poltrrkind Vol is I 3 Figure 10-2: Flow volume I J *) Quek’ eeeite fim cutee Yo o7 detmae 15 ta tanga 6 tf) cee C%— 0.95 acthuan Volume increases to the felt a. Obstructive pattern 1) Decreased flows 2) TLC normal or increased 3) RVincreased 4) VC decreased secondary to markedly increased RV b. Restrictive pattern 1) Decreased volumes 2) TLC decreased 3) RV decreased 4) VC decreased 2. Forced Vital Capacity (FVC) a. Air contained in the fully inflated lungs is forcibly expelled into a spirometer b. To evaluate Total Lung Volume compare FVC with table of expected values 3. Forced Expiratory Volume (FEV) Measured as volume in liters at 1 second (FEV,) on a spirogram b. Ameasure of flow 4, FEVJFVC Ratio a, Evaluates obstruction b. Normal ratio range = 0.70-0.80 c. Obstructive disease 1) Ratio <0.70 2) FEV, is reduced, lowering the FEV/FVC ratio 3) <0.35 = severe d. Restrictive disease 1) Ratio is high or normal 2) Both FEV, and FVC are reduced but FEV, is not as low as in obstructive pattem 2 225413.00197>< ne an mponani Oy Content ot callolte level = 139 OIE Bieta FS 0031 x PA, ar’ “Pulmonology + Symptomatology and Diagnosis CED) © be wT yy thn ; ‘ ~ he ely py te hicbraly bey a pl tte tH 3 . Peak Flow nach bbe 2/0 AN “a 1 a. Easy way to assess obstruction, nerd 4 pt BU Prawee go \ ; b. Baseline value ee ares ¢. Comparison with tables of age/sex/height TSeLrsg nr d. Evaluation of acute exacerbation or response to treatment ey & oe sa 5 2 Figure 10-3: Spirograms in obstructive versus restrictive lung disease S NORMAL OBSTRUCTIVE RESTRICTIVE NORMAL | FEV, Fv FYC F | Sed . B. Disturbances in gas exchanges 1. Physiology = a. Diffusion of O, and co, b. Ventilation (V) and perfusion (Q) (poe ’ 2, Measurement of gas exchange y- 5-4. .tat ~f a. Arterial blood gases (ABG) eo 1) Alveolar arterial O, gradient (A-a) Pulse oximetry ¢. Diffusion capacity faov a Oy Ot Dee, fr he 6.08 pie RY oxy Ve vag Fu [ee 10 hye Gt wet id | p beg Laie vatuy 2050 me nell & Beh Asbechesis Abs tel p toss 1 225413.00197 lah F = 08 hs Cone ie te ® the oh gk ft esrqi 7 br CFE wae on oresapat wycenee > Atelecta: A. Definition 5 wy hte Fan tay fe Ye om be Galea - Lica on aesq A collapse of part or all of the lung. Itis most commonly seen in the immediate postoperative period secondary to poor inspiration and/or Jack of coughing. = Also caused by blockage from mucus plug, tumor, or foreign body. B. Signs and Symptoms 1 Acute ‘Tachycardia, dyspnea, fever, hypoxemia 2. Chronic ‘May be no symptoms other than x-ray abnormalities 3. X-ray a. Tracheal deviation to the affected side occurs in upper lobe atelectasis (volume loss) b. Lower lobe atelectasis may cause elevation of the corresponding part of the diaphragm. 4. Mediastinal shift to the involved side is seen with massive atelectasis 5. The atelectatic lobe is usually densely consolidated and smaller than the normal lobe. C. Treatment Postoperative atelectasis 1. Try to induce deep breathing and stimulate coughing. 2. Incentive spirometry, pulmonary toilet. 3. For spontaneous atelectasis, bronchoscopy with removal of mucus plug is the treatment of choice. saelerere ch ve Ghne other oh 2 seeking tah a na ole shen / 4 225413.00197A. Definition OP? 1. Asthma i Mo characterized by hyperreactivity of the respiratory wee to various stimuli, resulting in reversible airway obstruction 2. Bronchial obstruction is produced by a combination of mucosal inflammation, constriction of bronchial musculature, and an excessive secretion of viscous mucus which causes mucus plugs 3. Occurs at any age, nonimmunologic stimuli, such as infection, Attacks are severe; the prognosis is Tess favorable. 2. Extrinsic asthma (allergic, atopic) a. Results from sensitization Specific immunoglobulins of the Type IgE (type 1) class are produced and the total serum IgE. concentration is elevated. Positive family history of allergic disease. Precipitated by allergens Accounts for approximately 20% of asthmatics d. Other symptoms Allergic rhinitis, urticaria, eczema, acute and mild attacks. Good prognosis. 3. Many patients have features of both types. ting inhalants, cold air, exercise, and emotional upset. es C. Pathophysiology 1. There is narrowing of large and small airways due to hypertrophy and spasm of bronchial smooth muscle, edema and inflammation of the bronchial mucosa, and production of viscous mucus 2. Mediators released by the lung during an acute asthmatic attack are histamine and bradykinin, which cause bronchial constriction (and increased exocrine secretion), and eosinophil chemotactic factor of anaphylaxis. Brace be a. Slight tachypnea b. Tachycardia (increased respuratory rate) es c. Prolonged expirations “ 4. Mild, diffuse wheezing 2. Severe attack: a. Use of accessory muscles of respiration b. Diminished breath sounds c. Loud wheezing and hyperresonance (increased vocal fremitus) 4. Imtercostal retraction 3. Poor prognostic factors: a. Fatigue and diaphoresis b. Pulsus paradoxus (>20mmHg) ¢. Inaudible breath sounds and decreased wheezing | « d. Cyanosis e. Bradycardia 2341390197, 5aD Pulmonology + Asthma te Figure 10-4: Disorders of the respiratory system Is PAco, increased? Da Cay Hypoventilation Jinspired Re, IsPAg,Pao, increased? Is low Po, correctable with o,? 1. High altitude ves ves Flo, Hy oventilation V/Q Mismatch lus Another Shunt Mechanism ey 1. Alcor collapse 1, Aimays seas fashma, COPD) 2. Neuromuscular disease trelccas) 2. estan disease 2 Iralveolr ing < {Breumeria, pulmonary 3. Alveolar diseas®\ 4. Pulmonary vascular disease 3. intracardiac shunt Daa 4. Vascular shunt within lungs | Exam and Selected Abnormalities Inspection a Excursion b. Accessory muscles ¢. Movement of both sides Palpation a, Normal voice transmitted. (Vocal fremitus) b. No difference between both sides Percussion a. Normally resonant Auscultation a. Normal sounds are vesicular b. Some bronchial sounds are louder near large right bronchi. 2ase13.00197Plsselcortontall etal matt aret Pulmonology + Asthma EEED Table 2. Physical Diagnosis Findings in Selected Pulmonary Abnormalities Ascultation Palpation Percussion Diagnosis Increased-expiration phase, | Decreased fremitus Hyperresonant Asthma Wheezes Absent breath sounds: Decreased fremitus Dull Pleural effusion Wheezes, crackles, rhonchi__| Normal fremitus Normal Resonant Bronchitis Bronchial breath sounds Increased fremitus Dull Consolidation Decreased vesicular breath | Decreased or normal Hyperresonant Emphysema sotinds prolonged expiration | fremitus Bronchophony,. pectoriloquy | Increased fremitus Dull Pulmonary infarction ‘Absent breath’ sounds Absent fremitus “| Hyperresonant pneumothorax 5. Arterial blood gases. (#1) -75/29/s0 F. Diagnosis of Asthma > be may, hn 4, et 1. FEV, must show 15% reversibility at 5 and 20 minutes with the 2. Decreased peak expiratory flow (PEF) to 80% predicted a. Acute asthmatic 2shioo SF leds Barares Cie hie Decreased PaCO,, increased pH fidrmal PaO, : 7 b. Severe asthma/status asthmaticus Decreased P,O,, increased PaCO,, decreased pH (bicarbonate level usually will not be elevated in an acute setting, but becomes elevated in chronic obstructive pulmonary disease) ¢. Normal” pCO, is bad in tachypneic patient Chest X-ray Nonspecific in an asthmatic attack, May only be helpful for ruling out acute infection as the causative ‘agent of the acute attack. eee he 3. Decreased FVC 10 < 50% 4. Decreased FEV, <30% 5. Increased RV 6. Ina non-acute setting,when spirometry is normal a provocative challenge may be performed. (methacholine, cold air). In general be careful. be mehecbet aa chee Ge G. Treatment 2 oye sock jrlavrh| OP. 1. Acute attack Beal a A Bago (essa ‘ce enol, fnhalers 225413.00197 i) Mainstay of treatment in acute and chronic asthma therapy ii) Indicated for the relief of bronchospasm in patients with reversible obstructive airway disease and for prevention of exercise-induced bronchospasms iii) Used long-term as required (studies have shown that when used on a chronic basis and not as. required, a tachyphylaxis-type phenomenon develops and an increased mortality has been shown in these patients) iv) Syrup and tablets should not be used in the acute setting Vv) Must be used with caution in patients who have coexisting cardiovascular disorders, hyperthyroidism, diabetes mellitus, hypertension, and coronary insufficiency vi) Drug interactions ‘Must avoid concomitant use of tricyclic antidepressants and other sympathomimetic aerosol bronchodilators or epinephrine Vg mld 3 Abeeoe ed 7 Ve?) Ceane 7 ies (tad Hee, ot9e< not for salel > < ne ane mpe: EEED patmonotogy + Asthma H. Corticosteroids Mechanics of action 1. Non broncodilators useful in reducing airway inflammation 2. Inhaled corticosteroids are useful for chronic antiflammatory therapy; should be used before oral steroids for chronic therapy. 3. Systemic steroids: used acutely in short bursts and as last resort for chronic therapy. 4. Side effects of corticosteriods a, Oral candidiasis (inhaled corticosteriods) b. Weight gain, hypertension, glaucoma, cataracts, diabetes, muscle weakness, osteoporosis, decreased immunity with opportunistic infections, peptic ulcers, decreased wound healing, hypogonadism and adrenal insufficiency on withdrawal Mast cell stablilizers pp rel shlalara tt Cromolyn sodium 2. Nedocromil a. Similar to cromolyn in its effects used for prophylaxis (not acutely), b. Used only prophylactically in exercise and allergic asthma (better used in acute attacks). Aminophylline (ethylenediamine salt of theophylline) Not indicated for treatment of acute Asthma; even though frequently used. Maybe of benefit in chronic management. Mechanism of action: improves contractility of daiphragm, weak bronchi dilator. Poe elite Eas 4. teegtis F + Meat po! pos A 3 YP - Woe 225413.00197Aah = mam on samen seam ee ay acheckehtoe Lath bee ia = —— Sands eke 12-3 tes Pepin ctae eden oak le \ (..~ 1. Chronic Obstructive Pulmonary Disease (COPD) ind PD) ee patients with emphysema) and bronchitis. Emphysema and bronchitis must be identified and weated separately but most patients with COPD have characteristics of both conditions. sone 2 a. Chronic bronchitis C096 gw tte PE Leckes gobort Productive cough for most daysot a three-inonth: Fea ‘SF hrore for at least two consecutive years. b. Emphysema vi.,j Abnormal, permanent d cartilage. FF looks c. Causes of COPD 1). Cigarette smoking (10-15% of smokers develop COPD), 80-90% of COPD patients are cigarente smokers : > 2) Air pollution (Mainly for bronchitis) 3) Airway infections (Mainly for bronchitis) 4) Allergy (Mainly for bronchitis) 5) Hereditary factors (Emphysema) a), antitrypsin deficiency (autosomal Pecedneteaics 795 Q 4. Cigarette smoking is responsible for 80-90% of COPD patients. Also caused by air pollution, occupation, infection. €. The number of pack-years of smoking correlates to the reduction in the FEV, f. Only 15-20% develop severe disabling COPD (suggests other factors involved in the pathogenesis) tion of air spaces distal to the terminal bronchioles with destruction of We Tt Reep. Pete: HO REG 236/270 1-6 Ale : B. Pathophysiology 1, Decreased elastic recoil of the lungs (mainly emphysema). Increased airway resistance (mainly bronchitis/asthma). 2. Cor pulmonale Signs of right heart failure secondary to COPD with absence of any left heart disease C. Diagnosis 1. Physical Examination in COPD a Emphysema shows distant breath sounds to auscultation b. Chronic bronchitis may show evidence of rhonchi and wheezes to auscultation ¢. May show signs and symptoms of right heart failure (cor pulmonale) d. Clubbing may be present 2. Chest x-ray Findings in COPD a, Emphysema b. Chronic bronchitis increased pulmonary markings Hyperinflation of bilateral lung fields with diaphragm flattening, small heart and an increase in the retrosternal space (mainly in emphysema) 3. Pulmonary Function Test a. FVC, FEY, and the FEV,: FVC ratio is reduced. b. Residual volume and total lung volume are usually increased in COPD. RV/TLV is increased. 225413.00197 9aD Pulmonology * Chronic Obstructive Pulmonary Disease D. Complications of Chronic Obstructive Pulmonary Disease 1 2. 3. Hypoxemia (nocturnal desaturation) in chronic bronchitis (mainly) Secondary erthyrocytosis as a result of chronically low PO, Cardiac Arrhythmias ‘The most common arrhythmias are supraventricular tachycardias (multifocal atrial tachycardia, which does not respond to digoxin, but may respond to verapamil) Pulmonary hypertension leading to cor pulmonale and subsequent right heart failure Chronic ventilary to failure (CO, retention) Spontaneous pneumothorax in emphysema patients Treatment of Chronic Obstructive Pulmonary Disease 2 Goal is to treat airway inflammation and bronchospasm and to reduce airway resistance and work of breathing, as well as improved gas exchange and V/Q mismatching Anticholinergic agents (ipratropium bromide, Atrovent) a. First-line drug in COPD SS Yen b. Control airway caliber and tone ¢. Usually given via metered dose inhaler d. When used with B, agonists, shows synergism in patients with COPD B, agonists (albuterol, terbutaline, metaproterenol) used as second-line drugs after anticholinergics a. The inhaled route is preferred b. Used as required due to down-regulation of the drug on the B, receptors (use chronically) 6. Indications and contsindications same as for use in asthma therapy Aminophylline * (vo! «- -« aug) Wet A obey Oral theophylline: used after B, agonists and anticholinergics 2. Hasa narrow therapeutic/toxic range Deiges b. Any COPD patients with coexisting cardiac disease necessitates close monitoring of aminophylline levels due to its proarthythmic potential ¢. Increased theophylline clearance is seen in patients with young age, smokers, rifampin, dilantin, phenobarbital, tegretol, hyperthyroidism, and a high-protein diet en el bey AA Heatly ae 4, Decreased theophylline clearance seen in old age, heart and liver disease, erythromy¢in, ciprofioxaci H, blockers (cimetidine, ranitidine), viral infections, and high-carbohydrate diet Corticosteroids Yi\eo Ae oqrany a. Systemic steroids i) Used as first line therapy for acute exacerbation and occasionally required for patients with severe chronic disease. ji) Side effects may be less with alternate day therapy. b. Inhaled steroids i) Used occasionally in patients with hyperresponsive airways and those with good response to systemic steroids. c. Side effects (see above) Human 0; proteinase inhibitor is available for patients with c,, antitrypsin deficiency. Its efficacy is still not known. ‘Home oxygen therapy a Given to patients with hypoxemia (pO, < 60) b. Patients with pulmonary hypertension, chronic cor pulmonale, erythrocytosis, impaired cognitive function, exercise imolerance, and morning headaches would receive maximum benefit from this therapy. 10 225413.00197Pulmonology * Chronic Obstructive Pulmonary Disease aD F._ Treatment of Complications of Chronic Obstructive Pulmonary Disease 1. Oxygen therapy a Goals are to maintain a PO, of 60, or arterial saturation of 90% or greater b. Oxygen therapy is used if 1) PO, acutely is less than 60 2) Home O, indication a) Stable COPD patient with a PO, < 55 or an O, saturation < 85 b) PO, 55-59 or an O, saturation 86—89 in a patient with cor pulmonale and/or right heart failure 3) Desaturation during exercise 4) Desaturation during sleep 5) Oxygen therapy and cessation of smoking are the only two things that have been shown to improve survival and quality of life in COPD patients 2. Antibiotics empirically for acute exacerbation of COPD should cover both influenzae and pneumococcus a. Azithromycin (zithromax) b. Quinotones c. Cephalosporins 4. Erythromycin €. Amoxicillin/ampicillin f Bactrim 3. Diuretics must be used cautiously in patients with cor pulmonale and/or right heart failure to avoid dehydration G_ Prognosis in Chronic Obstructive Pulmonary Disease 1. FEV, (after bronchodilator) is the best predictor of survival. The higher the FEV, the better the survival 2. Rate of FEV, decline Faster the decline, the worse the survival 3. Dyspnea at rest if FEV, < 25% predicted 4. Dyspnea on exercise if FEV, < 50% 5. Overall outlook is poor 6. Better for asthmatic bronchitis than emphysematous COPD 7. Smoking cessation is the only definite means of slowing the progression eleve \ acetate fo Qyenaly 7 of beeen A Cody: prenwo cers ‘225413 00197 Wbisss oe tceabapem pyeciaat > ———— CK APLAN) 7 ebm Cethtee bite on berate ycctan > é “rol, ptodut ie Gog EME a sy sheis seacee Gh ton phecce Defin ion and Etiology _ G8 Poti, | 2Pace Sevtae mba (TB step) 2 1. Dilatation of small-and-1 srpediur ‘sized bronchi resulting from i of bronchial elastic and muscular elements 2. Secondary to repeated pneumonic\ processes (like TB, fungal infectious, lung abscess, pneumonia) 3. Most common in third-world countries 4. Bronchiecitasis should be suspected in any patients with chronic cough, hemoptysis, foul-smelling sputum a production, and recurrent pulmonary infection (especially if associated with otitis media), sinusitis, immune deficiencies: T-cell deficient patients more often than f cells deficient patients are susceptible to infection with encapsulated bacteria, 5. May be difficdle to distinguish from chronic bronchitis 6._ Cystic fibrosis (defective chloride channel —> poor chloride permeability) is the most common cause of bronchiectasis in the first three decages of life 7. Immotile cilia syndrome (Kartagener’s syndrome) shows sinusitis, situs inversus, and male infertility 8. Other causes: * QL, antitrypsin deficiency plus smoking. Immunodeficiency, rheumatic disorders, obstruction from foreign body or tumor. 9. Should be suspected as an underlying cause for bronchiectasis if there is a positive family history, sweat:chloride ratio 260, and/or pancreatic insufficiency B. Signs and Symptoms athe promos Gamo), hee aplysrs 1. Patient has persistent cough with prevalent sputum production, wheezes, and/or crackles 2. Hypoxemia may occur causing secondary polycythemia, Anemia and weight loss is more common 3. Chest x-ray a. Early chest x-ray may be normal b. Chest x-ray in advanced cases may show 1-2 em cysts 4. Sputum culture and sensitivity usually of mixed flora ; (three-layered sputum in the specimen cup) ene 5. / CT scan of the chest is a s¢ ive way to detect bronchiectasis, bronchography has largely been replaced “By high resolution cut scan asthe test of choice. 17 bo) gt betes Citar ee C. Treatment < eho 4 een 1. Bronchodilators, chest physical therapy, and postural drainage to control and improve drainage of bronchial secretions 2. All patients require yearly vaccine for influenza 3. All patients require single vaccination for pneumococcal infection 4, Bronchoscopy may be needed to eliminate obstruction and evaluate atelectasis and hemoptysis 5. Recurrent pneumonic processes should be treated with antibiotics a. Amoxicillin and/or trimethoprim sulfamethoxazole b. Amoxicillin and/or tetracycline c. Amoxicillin/clavulanic acid (Augmentin) 6. Note: chest x-ray may show tracheal deviation and mediastinal shift to the affected side. 7. Surgery for patients with localized bronchiectasis with adequate ‘a functions and in-massive— hemoptysis Complications ae Te: Doble EF Amyloidosis, cor pulmonale, visceral abscesses (ye) au Gelenk f Newt bu inl peveglane #0 es | eae = nad coe ae y DD ErQ% PL hem, Tee Bheleing B Spine — Bot let wad totesPbored loses ells ter (Si RES dairy une 5 tox vei PE staat JS oe ven —> ap Malad Meroe ey fy He Sepselire/ fn BM PE cme fern! Phormeae vers ep) — Bt ide eas 6 A. Predisposing Factors ~ P ver ‘Venous stasis 2. Activation of blood coagulation pathway (hypercoaguable state, e.g., pregnancy, Antithrombin-I1I-deficiency, protein C deficiency, protein S deficiency), Anticardilipin Antibody Syndrome 3. Vascular damage 4 Concencer PS 4 immobiloetie ped of 2 HepBesazveble shy (hem Soke ng 5 Chnleoe 8 a cma as 5 ma i B. Etiology = A d 2 te é 90% of pulmonary embolisms come from deep leg veins. -— - mit" G be od i ee Cet BLE seep ene TES? oe C. Patients at High Risk of Postoperative Venous Thromboembolism a 1. General surgery patients older than 40 years with history of deep vein thrombosis (DVT) or pulmonary embolism 2. Extensive pelvic or abdominal surgery for malignant disease 3. Major orthopedic surgery of lower limbs D. EKG Changes Seen in Pulmonary Embolism 1. Right axis deviation 2. Deep S in Lead 1, Q wave Lead 3 and inverted T wave in Lead 3 (nonspecific) RV strain pattern 3. Sinus tachycardia (Most Common) Figure 10-5: Diagnosis of pulmonary embolism Suspect PE —— Diagnosed DVT mag. treat | “i | yest High | probatitity wt _ Spee prota | an re | No TX 225413.00197 13CKAPLAN) Male Fl S172 QnA ectnontet heer OB Pulmonology * Pulmonary Thromboembolism — + oc @ Re rae Pe fo — 7 ceRe me E. Diagnosis of Pulmonary Embolism ee heperen #6 Beatle, 1 Lung scan EC M4 Axes a. Abnormal perfusion scan may be due to decreased density ea pleural effusion, regional v»y- Tequction in ventilation seen in COPD and asthma) b. Ahigh-probability lung scan is when there is segmental or greater defects that are associated with a V/Q mismatch (86% of these patients have diagnosed pulmonary embolism by angiography and therapy with anticoagulants should be started) . “2 Venogram, if positive, warrants treatment for DVT 2. A negative study in a patient with shortness of breath does not rule out venous thromboembolism (30% of ; patients with documented pulmonary embolism have a negative venogram) ST & b. Compression U/S serially me one SVT yw Jes)\ > c. Radiofibrinogen for calves Ne 3. Macroaggregated albumin with xenon ‘Jus epee 2) Ve F. Patients Who Should be Treated for Pulmonary Embolism 1. High-probability scan 2. Abnormal scan with a positive DVT by venogram a, Any patient with an abnormal ventilation perfusion scan and negative venogram study should have an angiogram performed b. Angiogram is the definitive diagnostic test for pulmonary embolism G. isk Factors for Pulmonary Thromboembolism & «1. Prolonged immobilization 2 2. Trauma of the lower extremities A 3. Congestive heart failure 4. Pregnancy 5. Visceral cancer (lung, pancreas, genitourinary tract) 6. Trauma and burns 7. 8. x Obesity = 8, Advanced age ae) Hematologic disease (antithrombin-II-deficiency, protein C deficiency, protein $ S ficieey, lupus Anticoagulant , polycythemia vera, dysfibrinogenemia) paetvloble rhb ae y ~ 10. COPD ¢ on area T tey 1) 11 Diabetes mellitus 12. Risk Factors of deep vein thrombosis a, Surgical and nonsurgical tracma and immobilization ». Varicose veins ©. Obesity d. Estrogen therapy e. Previous history of DVT f. Age older than 40 years 2asen3.00097¢ nob for calal > < ua snc zpammx < maura oF Coremapelt pyccrn > Pulmonology * — Pulmonary Thromboembolism aD H. Clinical Manifestations of Thromboembolism ‘Sudden onset of dyspnea is the most common symptom with tachycardia Chest pain may be pleuritic or nonpleuritic Syncope (massive pulmonary embolism) Fever 5. Diaphoresis 6. Cough—blood hemoptysis (pulmonary infarction) aene Teal wT RE th same — bots I. Treatment of Pulmonary Embolism — 1. Massive pulmonary embolism — Patients who are hemodynamically unstable and have suspected massive pulmonary embolissWith no >’ contraindications may have thrombolytic agents administered. 2. Continuous heparin therapy for at least five days to prolong the partial thromboplastin time (PTD) to 1.5-2 times normal sine when hepaBed COT) is Patep ardor - 3. Long-term treatment carried out with warfarin therapy started on Day 1 or 2 and given in a dose to prolong the prothrombin time 1.3-1.5 times baseline for eee 4. If thrombolytics and anticoagulants are contraindicated (GI bleeding, recent CNS surgery, recent trauma) or if the patient is hypotensive (secondary tormassive pulmonary embolism) and refractive to medical therapy, acute embolectomy is indicated. These patiénts and others with recurrent pulmonary embolism despite adequate anticoagulant therapy will need vena(caval interupdon with a Greenfield vena caval filter or ligation ee BS Er Feo VL st 3 PT J. Pregnancy and Pulmonary Embolism yaa Patients will require adjusted dose of subcutaneous heparin = ed bone 1 eye, “A 2. Indefinite anticoagulant therapy is required in patients with protein C deficiency, antithrombin-Ill-deficiency, l and protem S deficiency, (Warfarin is contraindicated in pregnant women.) ' Ecce Cutie pt TPE» Ts pee ‘s PS Coase gece ze 1. Adverse effects of ee we aps a ae @ Veg Bleeding occurs in 5-10% of patients 3] ibocytopenia in 4% of patients (usually 7-10 days after treatment is started) Antiplatelet antibodies 2° £0. 2/ 20h; Fo Weemiee Increased incidence of thrombocytopenia with beef heparin (rather than pork) c. Hypersensitivity 4. Antidote to heparin toxicity is protamine sulfate (give slowly due to hypotensive effect) 2. Coumadin a. Vitamin K antagonist (blocks factors 2, 7, 9 and 10) b. Requires 36-72 hours to reach adequate levels for anticoagulant effect (time for normal clotting factors to be cleared from the hepatic system) c. Inhibits the vitamin K-dependent synthesis of protein C d. Activated protein C inhibits activated factors 5 and 8 ce. Even though the PT is prolonged after 2-3 days on coumadin therapy, heparin should be continued for at least five days (maximal antithrombotic effect of coumadin takes five days to work) f. Side effects of coumadin 1) Bleeding 2) Skin necrosis (protein C deficiency) 3) Teratogenic effects (do not use in the sixth to twelfth week of gestation), associated with skeletal defects in second or third trimester or CNS toxicity K. Drug Therapy 2a5a13.00187 15 af 9 ed Sepa vig: eaeEBD paimonotogy = pulmonary thictbocmbclsee” °°" ” Figure 10-6: Management of diagnosed pulmonary embolism Diagnosed Pulmonary Embolism Hemegynamicaly Hemodyrarical stable Unable” Anticoagulation Aticoagulation Contoindieated Thrombolnic Coninsicnted ‘Therapy W Heparin 2 Interop neon a Paulo Vena Cova entelecery Interrupt rir IW Heparin & Ora aoe ‘anicoapulation “3 ays Oral Anticoagulation S months, 225413.001972. Almost any organ system may be inyd{ved (pulmonary most common, visual, dermatologic, myocardial, theumatologic, GI, neurologic) clipes lo pa iv guka dead? C. Diagnosis 1, Chest x-ray 2. Shows three or four stage’ of disease (the stages are not progressive) 2. Bilateral hilar adenopathies b. Hila adenopathy with reticulonodular parenchyma cc, Without adenopathies reticulonodular parenchyma d. Honeycombing of bilateral lung fields with fibrosis 3. ‘Hypercalcemia, hypercalciuria - due to increased circulating Vitamin D - produced by macrophage 4. Skin anergy 7 5. Elevation and angiotensin converting enzyme (ACE) in 60% of patients with sarcoidosis. ACE is useful in following the course of the disease (nonspecific) 6. Abnormalities of liver function test 30% liver involvement (90%) often asymptomatic 7. All patients with suspected sarcoidosis should have an ophthalmalogic examination (uveitis and conjunctivitis are found in over 25% of cases) 8. PFTs may be normal or may show a restrictive pattern 9. Definitive diagnosis of sarcoidosis rests on biopsy of suspected tissues (if no tissues are available for biopsy, transbronchial biopsy is the procedure of choice) D. Prognosis 1. 80% of patients remain stable or spontaneously resolve 2. _20% develop progressive disease with evidence of end-organ compromise E. Treatment 1, No evidence that therapy alters the course of the disease 2. In the setting of serious organ impairment, a trial of steroids may be used—high dose for two months— tapered over three months 3. Parameters to follow while on steroids (Chest x-ray, PFTs, angiotensin converting enzyme levels Ody tof eyes Y by pee > $eek Ty Cole 225413.00197 WwW