Further measures: \212 \212 \212 \212 Wean off nitroglycerin (NTG) infusion when stabilized on oral drugs. Stop heparin when pain -free for 24 h, but give at least 3 \200\2235 d therapy. Check serial ECGs and cardiac enzy mes for 9 h. Address modifiable risk factors: Smoking, hypertension, hyperlipidemia, diabet es. Begin gentle mobilization. \212 If symptoms recur, refer to a cardiologist for urgent angiography and angio- plasty o r CABG . Prognosis Overall risk of death 1 \200\2232%, but 15% for refractory angina desp ite medical therapy. Risk stratification can help predict those most at risk and allow inte rvention to be targeted at those individuals. The following are associated with an increase d risk: \212 \212 \212 \212 \212 \212 Indications for consideration of invasive inter vention: \212 \212 \212 \212 Hemodynamic instability: Hypotension, pulmonary edema T-wave inversion or ST segment depres sion on resting ECG Previous MI Prolonged rest pain Older age Diabetes mellitus 752 Poor prognosis (e.g., pulmonary edema) Refractory symptoms Positive exercise tolerance test s (ETT)at low workload Non-Q wave MI. e n i c i d e m y c n e g r e m E Table 20.7 Acute management of ACS without ST-segment elevation Admit to a monitored setting \206\223 High-flow O 2 by face mask \206\223 Nitrates: NTG s pray or sublingual tablets as required \206\223 Analgesia: E.g., morphine mg IV + ondanset ron 4 mg IV \206\223 Aspirin: 160 \200\223325 mg if not given previously that day and no c ontraindi- cations reduces risk of mi and death \206\223 \222 -blocker: E.g., metoprolol 50 \200\223100 mg/8 h orally If \222 -blocker is contraindicated (asthma, COPD, left ventr icular function (LVF), bradycardia, coronary artery spasm), give rate-limiting calcium anta gonist (e.g., diltiazem 60 \200\223120 mg/8 h PO) \206\223 Low-molecular-weight heparin e. g., enoxaparin 1 mg/kg/12 h Alternatively: Unfractionated heparin 5,000 U IV bolus then iv infusion Check aPTT q6h. Alter IV rate to maintain aPTT at 1.5 \200\2232.5 \227 control \206\223 IV nitrate if pain continues titrate to pain, and maintain SBP at >100 mm Hg \206 \223 Record ECG while in pain \206\223 High-risk patients (persistent or recurrent ischemi a, st-depression, diabetes, \206\221 troponin) Infusion of a GPIIb/IIIa antagonist (e.g., tirofiban) and, ideally, urgent angiography. Addition of clopidogrel may also be useful \206\223 Optimize drugs: \222 -blocker; Ca 2+ channel antagonist; angiotensin-converting e nzyme (ACE)-inhibitor; nitrate Intensive statin regimens, starting at top dosages , may dec rease long- and short-term mortality/adverse events, e.g., by stabilizing plaques \206\223 If symptoms fail to improve, refer to a cardiologist for urgent angiography angioplasty or CABG Low-risk patients (no further pain, flat or inverted t-waves, or normal ecg, and n egative troponin) May be discharged if a repeat troponin (3, 6, and 9 h) is negative. Treat medically and arrange further investigation(e.g., stress test, angiogram) 753 Severe pulmonary edema Causes \212 Cardiovascular: Usually left ventricular (LV) failure \200\224post-MI \200\223or isch- emic heart disease. Also mitral stenosis, arrhythmias, and malignant hypertension Acute respira tory distress syndrome (ARDS) (Any cause (e.g., trauma, malaria, drugs); look for predispos ing factors (e.g., trauma, postop, sepsis). Is aspirin overdose or glue-sniffing/drug abuse likely ? Ask friends/relatives. Fluid overload Neurogenic (e.g., head injury) See X-RAY PL ATE 2 \212 \212 \212 \212 Differential diagnosis Asthma/COPD, pneumonia, and pulmonary edema are of ten hard to distinguish, especially in the elderly, in whom these may coexist. Do not hesit ate to treat all three simultaneously (e.g., with albuterol nebulizer, furosemide IV, morph ine, fluoroquinolone). Symptoms Dyspnea, orthopnea (e.g., paroxysmal), pink frothy sputum. NB: Drugs; other illnesses (recent MI/COPD)or pneumonia). Signs Distressed, pale, sweaty, p ulse \206\221 , tachypnea, pink frothy sputum, pulsus alternans, elevated JVP, fine lung c rackles, triple/gallop rhythm, wheeze (cardiac asthma). Usually sitting up and leaning forw ard. Quickly examine for possible causes. Investigations \212 CXR(X-RAY PLATE 2 : Cardiomegaly, signs of pulmonary edema. Look for shadowing (usually bil ateral), small effusions at costophrenic angles, fluid in the lung fissures, and Kerley B l ines (linear opacities). ECG: Signs of MI CMP; cardiac enzymes, arterial blood gasses (ABG) Consider echo \212 \212 \212 Management Begin treatment before investigations . See Table 20.8. Monito ring progress: BP, heart rate, cyanosis, respiratory rate, JVP, urine output, ABG. Once sta ble and improving: \212 \212 \212 Daily weights; BP and pulse q6h. Repeat CXR. Change to oral furosemide or bumetanide. If on large doses of loop diuretic, consider the addition of a thiazide or metolazone 2.5 \200 \2235 mg/d PO. ACE-inhibitor if LV failure; also consider echo. If ACE-inhibitor is con- tr aindicated, consider hydralazine and nitrate. Also consider \222 -blocker and spironolacto ne. Is the patient suitable for cardiac transplantation? Consider digoxin warfarin, espe cially if AF. \212 \212 \212 \212 754 e n i c i d e m y c n e g r e m E Table 20.8 Management of heart failure Sit the patient upright \206\223 Oxygen 100% if no preexisting lung disease \206\223 IV a ccess and monitor ECG Treat any arrhythmias (e.g., atrial fib) \206\223 Investigations whi le continuing treatment \206\223 Furosemide 40 \200\22380 mg IV slowly Larger doses requir ed in renal failure \206\223 Nitroglycerin spray two puffs SL or 2 \227 0.3 mg tablets SL Don \200\231t give if systolic BP <90 mm Hg Necessary investigations, examination, and his tory \206\223 If systolic BP>100 mm Hg, start a nitrate infusion ( e.g., isosorbide dinitr ate 2 \200\22310 mg/h IV) keep systolic BP >90 mm Hg \206\223 If the patient is worsening: Further dose of furosemide 40 \200\22380 mg Consider ventilation (invasive or noninvasive; e.g., CPAP; get help)or increase nitrate infusion \206\223 If systolic BP <100 mm Hg, tre at as cardiogenic shock; i.e., consider a Swan \200\223Ganz catheter and inotropic support \206\223 If systolic BP is >180 mm Hg, consider treating for hypertensive LVF Cardiogenic shock This has a high mortality. Ask a senior physician \200\231s help both in formulating an exact diagnosis and in guiding treatment. Cardiogenic shock is caused primar ily by the failure of the heart to maintain the circulation. It may occur suddenly or after progressively worsening heart failure. Causes \212 \212 \212 \212 \212 \212 \212 \212 Arrhythmias Cardiac tamponade Tension pneumothorax MI Myocarditis; myocardial depression (d rugs, hypoxia, acidosis, sepsis) Valve destruction (endocarditis) Pulmonary embolus Aortic dissection 755 Management If the cause is MI, prompt revascularization (thrombolysis or acute angio- plast y) is vital; see MI section for indications and contraindications. \212 \212 \212 \212 Manage in coronary care unit, if possible. Investigation and treatment may need to be done concurrently. See Table 20.9 for details of management. ECG, CMP, CBC, CK, CK-MB, troponin, ABG, CXR, echo. Investigations: If indicated, CT thorax (aortic dissection) and ventilatio n/profusion scan or pulmonary angiogram for PE. \212Monitor CVP, BP, ABG, ECG, urine output. Do a 12-lead ECG every hour until the diagnos is is made. Consider a Swan \200\223Ganz catheter to assess pulmonary wedge pressure and ca rdiac output and an arterial line to monitor pressure. Catheterize for accurate urine outpu t. Cardiac tamponade Pericardial fluid collects \206\222 intrapericardial pressure rises \206\222 heart cannot fill \206\222 pumping stops Causes: Trauma, lung/breast cancer, peri carditis, myocardial infarct, bacteria (e.g., TB). Rarely : Urea \206\221 , radiation, myx edema, dissecting aorta, systemic lupus erythematosus (SLE). Signs: Falling BP, a rising JV P, and muffled heart sounds = Beck \200\231s triad; JVP \206\221 on inspiration (Kussmaul sign); pulsus paradoxus (pulse fades on inspira- tion). Echocardiography may be diagnostic. CXR: Globular heart; left heart border convex or straight; right cardiophrenic angle <90 d egrees. ECG: Electrical alternans. Management: Severe cases can be difficult to manage. Ear ly recognition is important. Ensure that proper backup is available including either cardio l- ogy or cardiac surgery. With luck, prompt pericardiocentesis brings swift relief. While awaiting this, give O 2 , monitor ECG, and set up IV. Draw blood. 756 e n i c i d e m y c n e g r e m E Table 20.9 Management of cardiogenic shock Oxygen Titrate to maintain adequate arterial saturations \206\223 Investigations and close monitoring \206\223 Correct arrhythmias, electrolyte abnormality, or acid \200\223base im balance \206\223 Optimize filling pressure; if available measure pulmonary capillary wedge pressure (PCWP) If PCWP <15 mm Hg fluid load (100mg every 15 min IV to PCWP 15 \200\22320) If PCWP > 15 mm Hg Inotropic support (e.g., dobutamine 2.5 \200\22310mcg/kg/min IV for a S BP >80 mm Hg \206\223 Consider intra-aortic balloon pump if you expect the underlying cond ition to improve or you need time awaiting surgery \206\223 Look for and treat any reversi ble cause (e.g., MI or PE; consider throm- bolysis; surgery for: Acute ventriculo-septal de fect (VSD), mitral, or aortic regurgitation) Wide complex tachycardia ECG shows rate of >100 bpm and QRS complexes >120 ms. Principles o f management If in doubt, treat as ventricular tachycardia (the most common cause). Identif y the underlying rhythm and treat accordingly. Differential \212 \212 \212 Ventricular tachycardia (VT) including torsade de pointes SVT with aberrant conduction (e.g ., AF, atrial flutter) Preexcited tachycardias (e.g., AF, atrial flutter, or AV reentry tac hycardia with accessory pathways such as underlying Wolff \200\223Parkinson \200\223White [ WPW] syndrome). NB: Ventricular ectopics should not cause confusion when occurring singly; but if >3 togeth er at a rate of >120, this constitutes VT. Identification of the underlying rhythm may be d ifficult; seek expert help. Diagnosis is based on the history: If heart disease/MI, the lik elihood of a ventricular arrhythmia is >95%. A 12-lead ECG and the lack of response to IV a denosine also helps to discover the underlying rhythm. ECG findings in favor of VT: \212 \212 \212 \212 \212 \212 Fusion beats or capture beats Positive QRS concordance in chest leads Marked left-axis devi ation or rightward axis AV dissociation (occurs in 25%) or 2:1 or 3:1 AV block QRS complex >160 ms Any atypical bundle branch block pattern 757 Management Give high-flow O 2 by mask and monitor O 2 saturations. \212 Connect patient to a cardiac monitor and have a defibrillator at hand. Assess CVS: Decreased consciousness, B P <90, oliguria, angina, pulmo- \212 nary edema Obtain 12-lead ECG(request CXR) and obtain IV access \212 If hemodynamically unstable: \212 Synchronized DC shock Correct any hypokalemia and hypomagnesemia: 20 \200\22340 mEq/h IV with car- \212 diac monitoring, 1 \200\2232 g IV ma gnesium sulfate over 30 min. Follow with amiodarone 150 mg IV over 10 min. For refractory c ases, procainamide or sotalol may be considered. \212 \212 If hemodynamically stable: \212 \212 \212 After correction of VT : \212 \212 Correct hypokalemia and hypomagnesemia, as above. Amiodarone 150 mg IV over 10 min If this fails, consider procainamide or sotalol or synchronized DC shock Establish the cause (via the history and tests above). Maintenance antiarrhythmic therapy m ay be required. If VT occurs after MI, give IV amiodarone; if 24 h after MI also start oral antiarrhythmic: e.g., amiodarone. Prevention of recurrent VT: Surgical isolation of the ar rhythmogenic area or implantation of tiny automatic defibrillators may help. \212 Ventricular Fibrillation Use nonsynchronized DC shock (there is no R wave to trigger defibr illation). Ventricular extrasystoles (ectopics) are the most common post-MI arrhyth- mias, but they are also seen in healthy people (often >10/h). Patients with frequent ectopics pos t-MI have a worse prognosis, but there is no evidence that antidysrhythmic drugs improve ou tcome; indeed they may increase mortality. Torsade de pointes: A form of VT with a constant ly varying axis, often in the setting of long-QT syndromes. This can be congenital or acqui red (e.g., from drugs, such as some antidysrhythmics, tricyclics, antimalarials, newer anti psychotics, and terfenadine). Give magnesium 1 \200\2232 g IV. Torsade in the setting of co ngenital long-QT syndromes can be treated with high doses of \222 -blockers. In acquired l ong-QT syndromes, stop all predisposing drugs, correct hypokalemia, and give magnesium 1 \200\2232 g IV. An alternative is overdrive pacing. 758 e n i c i d e m y c n e g r e m E Figure 20.2 AHA 2010 guidelines for advanced life support Management of tachycardia with a pulse Identify underlying cause, treat ABC \200\231s, place patient on monitor, BP, pulse ox, IV Is the patient unstable due to the tachyarrhythmia? (see below) Yes No Synchronized Cardioversion - Narrow regular 50-100 J - Narrow irregular 120-200 J biphasic or 200 J monophasic - Wide regular 100 J - Wide irregular defibrillation dose (not synchron ized) Wide QRS >/= 0.12 sec Yes No 12 - lead ECG * Consider adenosine only 12 - lead ECG * Vagal maneuver * Adenosine if if regular and monomorphic regular rhythm * -Blocker or * calcium channel Consider antiarrhythmic (see below) * Expert involvement blocker Expert involvement Unstable is defined as: (1) hypotension, (2) acute altered mental status, (3) signs of shoc k, (4) ischemic chest discomfort, or (5) acute heart failure. Antiarrhythmic infusions for stable wide complex tachycardia include: Procainamide IV 20 \200\22350 mg/min until arrhyth mia suppressed, hypoten- sion, QRS duration increases >50%, or max of 17 mg/kg given. Infus e at 1 \200\2234 mg/min. Avoid if prolonged QT or congestive heart failure (CHF). Amiodaron e IV dose is 150 mg over 10 min. Repeat as need if VT recurs. Infuse at 1 mg/min for first 6 h. Sotalol IV 100 mg (1.5 mg/kg) over 5 min. Avoid if prolonged QT. From 2010 American He art Association Guidelines for CPR and ECC. Circulation . 2010;122 (suppl):729 \200\223767. 759 Narrow complex tachycardia ECG shows rate of >100 bpm and QRS complex duration of <120 ms. Differential diagnosis \212 \212 Sinus tachycardia: Normal p-wave followed by normal QRS. Atrial tachyarrhythmias: \212 \212 Rhythm arises in atria; Atrial fibrillation (AF): Absent Atrial flutter: Atrial rate 260 \200\223340 bpm. Saw-toot h baseline due to con- tinuous atrial electrical activity; ventricular rate is often 150 bp m (2:1 block) Atrial tachycardia: Abnormally shaped P-waves; may outnumber QRS Multifocal a trial tachycardia: \211 3 P-wave morphologies; irregular QRS complexes P -wave, irregular QRS complexes \212 \212 \212Junctional tachycardia: AV-node is part of the pathway; P-wave either bur- ied in QRS complex or occurring after QRS complex \212 \212 AV nodal reentry tachycardia AV reentry tachycardia, includes an accessory pathway (e.g., W PW). Principles of management See Figure 20.2. \212 \212 \212 If the patient is compromised, use DC cardioversion. Otherwise, identify the underlying rhy thm and treat accordingly. Vagal maneuvers (carotid sinus massage, Valsalva maneuver) trans iently increase AV block and may unmask an underlying atrial rhythm. If unsuccessful, give adenosine, which causes transient AV block. It has a short half-life (10 \200\22315 sec) an d works in two ways: \212 \212 \212 By transiently slowing ventricles to show the underlying atrial rhythm By cardioverting a j unctional tachycardia into sinus rhythm Give Adenosine 6 mg IV bolus into a large vein, followed by saline flush, while recording a rhythm strip. If unsuccessful, give 12 mg, then 12 mg again 2 min later if no response. Wa rn about : Transient chest tightness, dyspnea, headache, flushing. CI: Asthma, second-/thir d-degree AV block, or sinoa- trial disease (unless pacemaker). Interactions : Potentiated b y dipyridamole, antagonized by theophylline. Specifics Sinus tachycardia: Identify and trea t underlying cause. Supraventricular tachycardia: If adenosine fails, consider diltiazem (0 .25 mg/ kg or about 20 mg IV over 2 min. NB: When on a \222 -blocker, diltiazem should eit her be avoided or used with caution. Alternatives : Metoprolol 5 mg IV or amiodarone. If un successful, use DC cardioversion. Atrial Fibrillation/ \202 utter: Manage along standard l ines (see afib section). Atrial tachycardia: Rare; may be due to digoxin toxicity: Withdraw digoxin, consider digoxin-specific antibody fragments. Maintain K + at 4 \200\2235 mmol/L. Multifocal atrial tachycardia: Most commonly occurs in COPD. Correct hy- poxia and hyperca pnia. Consider Metoprolol or diltiazem if rate remains >110 bpm. Junctional tachycardia: Wh ere antegrade conduction through the AV node occurs, vagal maneuvers are worth trying. Aden osine will usually cardiovert a junctional rhythm into sinus rhythm. If it fails or recurs, \222 -blockers, dilti- azem ( not with \222 -blockers),or digoxin. If this does not cont rol symptoms, consider radiofrequency ablation. Wolff \200\223Parkinson \200\223White (WPW) syndrome Caused by congenital accessory conduction pathway between atria and ventricles. R esting ECG shows short P-R interval and widened QRS complex due to slurred upstroke or \200\234delta wave. \200\235 Two types: WPW type A(+ve QRS vector in V1), WPW type B( \200 \223ve QRS vector in V1). Patients present with SVT, which may be due to an AVRT preexcited AF, or preexcited atrial flutter. Risk of degeneration 760 to VF and sudden death. Consider Procainamide or amiodarone. Refer to cardiologist for elec trophysiology and ablation of the accessory pathway. e n i c i d e m y c n e g r e m E Acute severe asthma The severity of an attack is easily underestimated. An atmosphere of ca lm helps. Presentation Acute breathlessness and wheeze. History Ask about usual and recent treatment, previous acute episodes and their severity, and best peak expiratory flow rate ( PEFR). Has patient ever been admitted to ICU? or intubated, if so when? Differential diagno sis Acute infective exacerbation of COPD, pulmonary tract obstruction, pulmonary embolus, e dema, upper respiratory anaphylaxis. Investigations PEF \200\224but may be too ill, ABG, CX R (to exclude pneumothorax, infection), CBC,CMP. Assessing the severity of an acute asthmat ic attack Severe attack: \212 \212 \212 \212 Life-threatening attack: \212 \212 \212 \212 \212 Unable to complete sentences Respiratory rate >25/min Pulse rate >110 bpm PEF <50% of predi cted or best PEF <33% of predicted or best Silent chest, cyanosis, feeble respiratory effort Bradycardia or hypotension Exhaustion, confusion, or coma ABG: Normal/high <7.35. P a CO 2 >36 mm Hg; P a O 2 <60 mm Hg, low pH, e.g., Treatment Life-threatening or severe asthma, see Table 20.10. \212 Albuterol 5 mg nebulized, ipratropium bromide 500 mcg nebulized, with oxygen. If PEF remain s <75%, repeat albuterol and give prednisone 60 mg PO. Monitor oxygen saturation, heart rat e, and respiratory rate. \212 \212 Discharge Before discharge patients must have: \212 \212 \212 \212 \212 \212 Drugs used in acute asthma Albuterol: \222 -agonist. SE : Tachycardia, arrhythmias, t remor, K + \206\223 . Ipratropium bromide: Anticholinergic SE : Dry Mouth and Sedation Mag nesium: Smooth muscle relaxant SE : Hypotension with rapid infusion, in high doses muscle w eakness, absent reflexes, abnormal cardiac conduc- tion, respiratory depression Methylpredn isolone/prednisone: Steroid Had inhaler technique checked Peak flow rate >75% predicted or best with diurnal variabilit y <25% Steroid and bronchodilator therapy Instructed on use of PEF meter and management pla n Follow-up appointment within 1 wk Respiratory clinic appointment within 4 wks 761 Table 20.10 Immediate management of acute severe asthma Assess severity of attack (see above). Warn ICU if attack is severe. Start treatment immedi ately (prior to investigations). \212 \212 2 100% via non-rebreathing bag. \227 3 doses + ipratropium bromide 0.5 mg Sit patient up and give high-dose O Albuterol 5 mg every 20 min nebulized with O 2 . Methyl prednisolone 40 \200\22380 mg/d IV (If unable to tolerate PO) or pred- nisone 40 \200\22380 mg/d PO. CXR to exclude pneumothorax. \212 \212 If life-threatening features (above) present: \212 \212 \212 Inform ICU. Add magnesium sulfate (MgSO Give albuterol nebulizers every 15 min, or 10 mg co ntinuously per hour. 4 ) 1.2 \200\2232 g IV over 20 min. Further management If improving \212 40 \200\22360% O 2 \212 Consider oral prednisone 10 \200\22360 mg with taper. \212 Nebulized albuterol q4h Monitor peak flow and oxygen satura tions. \212 If patient not improving after 15 \200\22330 min \212 \212 2 and steroids. Continue 100% O Methylprednisolone 125 mg IV or prednisone 60 mg PO if not already given. G ive albuterol nebulizers every 15 min or 10 mg continuously per hour. Continue ipratropium 0.5 mg q4 \200\2236h. \212 \212 If patient still not improving \212 \212 \212 \212 Discuss with ICU staff. Repeat albuterol nebulizer every 15 min. MgSO If no improvement or life-threatening features are present, consider transfer to ICU, accompanied by a doctor pr epared to intubate; con- sider noninvasive ventilation (BIPAP). Monitoring the effects of t reatment \212 \212 \212 4 1.2 \200\2232g IV over 20 min, unless already given. Repeat PEF 15 \200\22330 min after initiating treatment. a O 2 >92%. Pulse oximeter monitor ing: Maintain S Check blood gasses within 2 h if: Initial initial P a O 2 <60 mm Hg or pati ent is deteriorating. Record PEF pre- and post- \222 -agonist in hospital. P a CO 2 was normal/raised or \212 Once patient is improving \212 \212 \212 Reduce nebulized albuterol and switch to inhaled \222 -agonist. Initiate inhaled steroids and stop oral steroids if possible. Continue to monitor PEF. Look for deterioration on redu ced treat- ment and beware early morning dips in PEF. Look for the cause of the acute exace rbation and admission. \212 762 Acute exacerbations of COPD Common medical emergency, especially in winter. May be triggere d by viral or bacterial infections. Presentation Increased cough, breathlessness, or wheeze . Decreased exercise capacity. History Ask about usual/recent treatments (especially home o xygen), smoking status, and exercise capacity (may influence a decision to ventilate the pa tient). Differential diagnosis Asthma, pulmonary edema, upper respiratory tract obstruction , pulmonary embolus, anaphylaxis. Investigations \212 \212 \212 \212 \212 \212 Manage ment \212 \212 \212 e n i c i d e m y c n e g r e m E PEF but patient may be too symptomatic to use) ABG CXR to exclude pneumothorax and infectio n CBC, CMP, blood cultures (if febrile) ECG Sending sputum for culture. Look for a cause (e.g., infection, pneumothorax) See Table 20.11 and 20.12 for acute manage ment. Prior to discharge, coordinate steroid reduction, home oxygen, smoking, pneumococcal and flu vaccinations. Treatment of stable COPD. Nonpharmacological: Stop smoking, encourage exercise, treat poor nutrition or obesity, influenza vaccination Pharmacological : Mild \212 \212 Short-acting \222 2 -agonist or ipratropium PRN. Regular short-acting \222 2 -agonist and /or ipratro- Moderate pium. Consider corticosteroid trial. Either po or inhaled or both \212 Severe Combination therapy with regular short-acting \222 2 -agonist and ipratropium Consider corticosteroid trial. Either po or inhaled or both Assess for home nebulizers. +/ \200\223 macrolide antibiotic if evidence of infection More advanced disease: \212 \212 \212 Consider pulmonary rehabilitation in moderate/severe disease. Consider long-term oxygen the rapy if Indications for surgery: Recurrent pneumothoraces, isolated bullous dis- ease, lung volume reduction surgery (selected patients). Assess social circumstances and support requ ired. Identify and treat depression. P a O 2 <55 mm Hg. \212 763 Table 20.11 Management of acute copd Controlled oxygen therapy Start at 24 \200\22328%; vary according to ABG Aim for a P a O 2 >60 mm Hg with a rise in P a CO 2 <12 mm Hg \206\223 Nebulized bronchodilators: Albuterol 5 mg/20 min and ipratropium 500 mcg as first two doses \206\223 Steroids IV methylpredniso lone 125 mg/d or oral prednisone 40 \200\22380 mg/d \206\223 Antibiotics: Use if evidence of infection, e.g., macrolide \206\223 If no response: Repeat nebulizers \206\223 If no r esponse: 1. Consider biphasic positive airway pressure (BIPAP) if respiratory rate >30 or p H <7.35. \206\223 2. Consider intubation a & ventilation if pH <7.26 and P a CO 2 is risin g a A decision to ventilate will depend on the patient \200\231s premorbid state: Exercise capacity, home oxygen, and comorbidity. Ask about this information before you need to make this decision. Table 20.12 Oxygen therapy \212 The greatest danger is hypoxia, which probably accounts for more deaths than hypercapnia. D on \200\231t leave patients severely hypoxic. Therefore, care is required with O 2 , especi ally if there is evidence of CO 2 retention. Start with 24 \200\22328% O 2 in such patients . Reassess after 30 min. In patients without evidence of retention at baseline, use 28 \200 \22340% O 2 but still monitor and repeat ABG. \212 \212 764 Pneumothorax See X-RAY PLATE 6. Tension pneumothorax requires immediate relief (see below). Do not delay management by obtaining a CXR. Causes Often spontaneous (especially in young thin men) due to rupture of a subpleural bulla. Other causes: Asthma, COPD, TB, pneumonia, lung abscess, carcinoma, cystic fibrosis, lung fibrosis, sarcoidosis, connective tissue dis orders (Marfan \200\231s syndrome, Ehlers \200\223Danlos syndrome), trauma, iatrogenic (sub clavian CVP line insertion, pleural aspiration or biopsy, percutaneous liver biopsy, positi ve pressure ventilation). Clinical features Symptoms: There may be no symptoms (especially in fit young people with small pneumothoraces) or there may be sudden onset of dyspnea and/ or pleuritic chest pain. Patients with asthma or COPD may present with a sudden deteriorati on. Mechanically ventilated patients may present with hypoxia or an increase in ventilation pressures. Signs: Reduced expansion, hyperresonance to percussion, and diminished breath s ounds on the affected side. With a tension pneumothorax, the trachea can be deviated away f rom the affected side, and the patient may be very symptomatic. Investigations Immediate ne cessary treatment should not be delayed by a CXR. Otherwise, request an expiratory movie an d look for an area devoid of lung markings, peripheral to the edge of the collapsed lung (X -RAY PLATE 6 ). Ensure the suspected pneumothorax is not a large emphysematous bulla . Chec k ABG/VBG in dyspneic patients and those with chronic lung disease. Management Depends on w hether it is a primary or secondary (underlying lung disease) pneumothorax, size and sympto ms. \212 e n i c i d e m y c n e g r e m E Pneumothorax due to trauma or mechanical ventilation requires a chest tube. Aspiration of a pneumothorax (see below) Insertion and management of a chest tube \212 \212 Surgical backup should be arranged anytime a chest tube is being considered. Tension pneumothorax See X-RAY PLATE 6. This is a medical emergency . Essence: Air drawn in to the pleural space with each inspiration has no route of escape during expiration. The me diastinum is pushed over into the contra-lateral hemithorax, kinking and compressing the gr eat veins. Unless the air is rapidly removed, cardiorespiratory arrest will occur. Signs: R espiratory distress, tachycardia, hypotension, distended neck veins, trachea deviated away from side of pneumothorax. Increased percussion note, reduced air entry/breath sounds on th e affected side. Treatment: To remove the air, insert a large-bore (14 \200\22316F) needle into the second intercostal interspace in the midclavicular line on the side of the suspect ed pneumothorax. If the patient is in extremis, this procedure may be done before obtaining a chest x-ray. Then insert a chest tube. Chest tube drainage \212 \212 765 Use a small tube (10 \200\22314F) unless blood/pus is also present. Never clamp a bubbling tube. \212 Tubes may be removed 24 h after the lung has reexpanded and air leak has stopped (i.e., the tube stops bubbling). This is done during expiration or a Valsalva maneuver. If the lung f ails to reexpand within 48 h or if there is a persistent air leak, specialist advice should be obtained, as surgical intervention may be required. If suction is required, high-volume , low-pressure ( \200\22310 to \200\22320 cm H systems are required. \212 \212 2 O) Pneumonia See X-RAY PLATES 5 and 8 . An infection of the lung parenchyma. Incidence of comm unity-acquired pneumonia is 12:1,000 adults. Of these, one will require hospitalization, an d mortality in these patients is still 10%. Common organisms \212Streptococcus pneumoniae is the most common cause (60 \200\22375%). \212Mycoplasma pneumoniae (5 \200\22318%) \212 Staphylococcus aureus \212Haemophilus influenzae \212Legionella sp. and Chlamydia psittac i \212 Gram-negative bacilli, often hospital-acquired or in the immunocompro- mised (e.g., Pseudom onas , especially in those with COPD). Viruses including influenza account for up to 15%. \212 Symptoms \212 Fever, rigors, malaise, anorexia, dyspnea, cough, purulent sputum (classi- cally \200\234r usty \200\235 with pneumococcus), hemoptysis, and pleuritic chest pain. Signs \212 Fever, cyanosis, herpes labialis (pneumococcus), confusion, tachypnea, tachycardia, hypoten sion, signs of consolidation (diminished expansion, dull percussion note, \206\221 tactile vocal fremitus/vocal resonance, bronchial breathing), and a pleural rub. Investigations \212 \212 \212 \212 \212 \212 CXR(see X-RAY PLATES 5 and 8). Oxygen saturation, ABG if S CBC, CMP, LFT, CRP atypical sero logy Blood and sputum cultures Pleural fluid may be aspirated for culture Bronchoscopy and bronchoalveolar lavage if the patient is immunocom- promised or in ICU. a O 2 <92% or severe pneumonia Severity Core adverse features \200\234CURB \200\235 score: \212C onfusion \212B UN >20 mg/dL; \212R espiratory rate 30/min \212B P <90/60 mm Hg) A score >2 indicates severe p neumonia. Other features that increase the risk of death are age >50 yrs, coexisting diseas e, bilateral/multilobar involve- ment, P a O 2 <60 mm Hg or S a O 2 <92%. Management See Ta ble 20.13 Complications Pleural effusion, empyema, lung abscess, respiratory failure, septi cemia, pericarditis, myocarditis, cholestatic jaundice, renal failure. 766 e n i c i d e m y c n e g r e m E Table 20.13 Management of pneumonia Oxygen to maintain P a O 2 >60 mm Hg Caution if history of COPD \206\223 Treat hypotension and shock (p. 687) \206\223 Investigations \206\223 Antibiotics see Table 20.14 \206 \223 IV fluids may be required (anorexia, dehydration, shock) \206\223 Analgesia for pleur itic chest pain (e.g., acetaminophen 1 g/6 h or NSAID) \206\223 Some patients may need int ubation and a period of ventilatory support Table 20.14 Antibiotics Community-acquired Mild Doxycycline 100 mg/d PO, or Streptococcus Azithromycin 500 mg/d \227 3 d, 1 g then 500 mg/d \227 2 d or 2 g one time (all above pre ferred) or clarithromycin 1 g/d or 500 bid \227 7 d or levofloxacin 750 mg/d \227 7 d or moxifloxa- cin 400 mg/d \227 7 d pneumoniaeHae- mophilus influen- zaeMycoplasma pneumoniae Severe As above Levofloxacin 750 mg IV/PO or moxifloxacin 400 mg IV/PO q24h \227 7 \200\22310 days or (cef triax- one 1 g IV q24h or cefotaxime 1 g IV q8h each with azithromy- cin 500 mg/d IV/PO \227 3 days) Azithromycin 3 \200\2235 d or levofloxacin Atypical Legionella pneumophila Chlamydia species or moxifloxacin 7days Azithromycin or doxycycline 7 doxy 100 mg bid x High-dose co-trimoxazole Pneumocystis pneumoniae Hospital-acquired Gram +ve bacilli Pseudomonas Anaerobes If hospitalized >4 d, nursing home, ABX in last 90 d, immunosup- pression then vanc/linezol id for MRSA + antipseudomonal \222 -lactam + either (levoflox or Cipro) or (gent or tobra or amikacin). If none of the above features, then ceftriaxone 2 g/d IV or fluoroquinolone o r amp-sulbactam or ertapenem 767 (Continued) Table 20.14 (Continued) Aspiration Clindamycin q8h IV fluoroqui- Strep. pneumoniae nolone \227 10 d Anaerobes Massive pulmonary embolism Always suspect PE in sudden collapse 1 \200\2232 wks after surge ry. Mortality ranges from 0.7 to 6.0 per 100,000 persons. Mechanism Venous thrombi, usually from DVT, pass into the pulmonary circulation and block blood flow to lungs. The source is often occult. Risk factors \212 Malignancy \212 Surgery, especially pelvic \212 Immobil ity \212 Birth control pills (there is also a slight risk attached to HRT) \212 Previous thromboembolism and inherited thrombophilia Prevention Early postop mobilization is the sim plest method; consider: \212 \212 \212 \212 Antithromboembolic stockings Low-molecular-weight heparin prophylaxis SC Avoid contraceptiv e pill if at risk (e.g., major or orthopedic surgery). Recurrent PES may be prevented by an ticoagulation; vena caval filters are of limited use and should be combined with anticoagul ation. Signs and symptoms \212 \212 Acute dyspnea, pleuritic chest pain, hemoptysis, and syncope Hypotension, tachycardia, gall op rhythm, JVP heave, pleural rub, tachypnea, and cyanosis, AF \206\221 , loud P 2 , right ventricular Classically, PE presents 10 d postop with collapse and sudden breathlessness while strainin g at stool, but PE may occur after any period of immobility or with no predisposing factors . Breathlessness may be the only sign. Multiple small emboli may present less dramatically with pleuritic pain, hemoptysis, and gradually increasing breathlessness. Look for a source of emboli, especially DVT (is a leg swollen?). Investigations \212 \212 CBC, CMP, baseline clotting ECG(commonly normal or sinus tachycardia); right ventricular st rain pat- tern V1 \200\2233 (p. 95), right-axis deviation, RBBB, AF; may be deep S-waves in I, Q-waves in III, inverted T-waves in III ( \200\234S1 Q3 T3 \200\235) CXR is often norma l; increased vascular markings, small pleural effusion. Wedge-shaped area of infarction. \212 \212ABG: Hyperventilation + gas exchange \206\223 : P a O 2 \206\223 , P a CO 2 \206 \223 , pH often \206\221 \212 CT pulmonary angiography is sensitive and specific in determining if emboli are in pulmonar y arteries. If helical CT is unavailable, a ventilation \200\223 scan is equivocal, pul monary ) scan can aid diagnosis. If V perfusion (V angiography or bilateral lower ext ultra sound may help. D-dimer blood test, if low thrombosis absent. May help in excluding a PE. . /Q . /Q \212 768 e n i c i d e m y c n e g r e m E Table 20.15 Management of massive pulmonary embolism Oxygen, 100% \206\223 If critically ill, consider immediate surgery \206\223 IV access an d start heparin either unfractionated heparin 80 U/kg bolus then 18 U/kg/h IV as guided by aPTT or low-molecular-weight heparin (e.g., enoxaparin 1 mg/kg SC q12h) \206\223 What is t he systolic BP? <90 mm Hg Start rapid fluid resuscitation If BP still \206\223 after 500 mL colloid, dobut amine 2.5 \200\22310 mcg/kg/min IV; aim for systolic BP >90 mm Hg If BP still low, consider norepinephrine If the systolic BP <90 mm Hg after 30 \200\22360 min of standard treatment and signs of right ventricular dilation on echo, clinically definite PE and no CI, consider thrombolysis. >90 mm Hg Start warfarin10 mg/24 h PO Confirm diagnosis Management See Table 20.15 for immediate management. \212 \212 Try to prevent further thrombosis with compression stockings. Heparin should be given for 3 d and until International Normalized Ratio (INR) >2. Then transition to warfarin. If obvio us remedial cause, 6 wks treatment with warfarin may be suffi- cient. Otherwise, continue f or at least 3 \200\2236 months (long-term if recurrent emboli or underlying malignancy). Is there an underlying cause (e.g., thrombophilic tendency), malignancy [especially prostate, breast, or pelvic cancer], SLE, or polycythemia)? If good story and signs, make the diagno sis. Start treatment before definitive investigations. \212 \212 Acute upper GI bleeding Causes Common : Gastric/duodenal ulcer, gastritis, Mallory \200\223 Weiss tear (esophageal tear due to vomiting), esophageal varices, portal hypertensive gastr opathy, drugs (NSAIDS, aspirin, thrombolytics, anticoagulants). Rarer: Hemobilia, nose blee ds (swallowed blood), esophageal/gastric malig- nancy, esophagitis, angiodysplasia, hemangi omas, Ehlers \200\223Danlos or Peutz \200\223 Jeghers syndrome, bleeding disorders, aorto-e nteric fistula (in those with an aortic graft). 769 Signs and symptoms Hematemesis or melena, dizziness (especially postural), fainting, abdomi nal pain, dysphagia? Postural hypotension, hypotension, tachycardia (not if on \222 -block er), \206\223 urine output, cool and clammy, signs of chronic liver disease; telangiectasi a or purpura; jaundice (biliary colic + jaundice + melena suggests hemobilia). NB: Ask abou t previous GI problems, drug use, and alcohol intake. Management Assess whether patient is in shock: \212 Cool and clammy to touch (especially nose, toes, fingers); refill Pulse >100 bpm Systolic B P <100 mm Hg Postural drop Urine output <30 mL/h \206\223 capillary