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186923 3 En Bookfrontmatter 1..20 2 CARDIOLOGY Section Editors: Dr. Mustafa Toma and Dr. Jason Andrade Aortic Dissection DIFFERENTIAL DIAGNOSIS PATHOPHYSIOLOGY (CONT’D) CARDIAC DEBAKEY—I ¼ ascending and at least aortic arch, MYOCARDIAL—myocardial infarction, angina II ¼ ascending only, III ¼ originates in descending VALVULAR—aortic stenosis, aortic regurgitation and extends proximally or distally PERICARDIAL—pericarditis RISK FACTORS VASCULAR—aortic dissection COMMON—hypertension, age, male RESPIRATORY VASCULITIS—Takayasu arteritis, giant cell arteritis, PARENCHYMAL—pneumonia, cancer rheumatoid arthritis, syphilitic aortitis PLEURAL—pneumothorax, pneumomediasti- COLLAGEN DISORDERS—Marfan syndrome, Ehlers– num, pleural effusion, pleuritis Danlos syndrome, cystic medial necrosis VASCULAR—pulmonary embolism, pulmonary VALVULAR—bicuspid aortic valve, aortic coarcta- hypertension tion, Turner syndrome, aortic valve replacement GI—esophagitis, esophageal cancer, GERD, peptic OTHERS—cocaine, trauma ulcer disease, Boerhaave’s, cholecystitis, pancreatitis CLINICAL FEATURES OTHERS—musculoskeletal, shingles, anxiety RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE AN ACUTE THORACIC PATHOPHYSIOLOGY AORTIC DISSECTION? ANATOMY—layers of aorta include intima, media, LR+ LRÀ and adventitia. Majority of tears found in ascending History aorta right lateral wall where the greatest shear force Hypertension 1.6 0.5 upon the artery wall is produced Sudden chest pain 1.6 0.3 AORTIC TEAR AND EXTENSION—aortic tear may Tearing or ripping pain 1.2–10.8 0.4–0.99 produce a tearing, ripping sudden chest pain radiat- Physical ing to the back. Aortic regurgitation can produce Pulse deficit 5.7 0.7 diastolic murmur. Pericardial tamponade may occur, Focal neurological deficit 6.6–33 0.71–0.87 leading to hypotension or syncope. Initial aortic tear Diastolic murmur 1.4 0.9 and subsequent extension of a false lumen along the CXR/ECG aorta may also occlude blood flow into any of the Enlarged aorta or wide 2.0 0.3 following vascular structures: mediastinum CORONARY—acute myocardial infarction (usually LVH on ECG 0.2–3.2 0.84–1.2 RCA) APPROACH—‘‘presence of tearing, ripping, or BRACHIOCEPHALIC, LEFT SUBCLAVIAN, DISTAL AORTA— migrating pain may suggest dissection. Pulse defi- absent or asymmetric peripheral pulse, limb cit or focal neurological deficits greatly increase ischemia likelihood of dissection. Absence of pain of sudden RENAL—anuria, renal failure onset decreases likelihood of dissection. Normal CAROTID—syncope/hemiplegia/death aorta and mediastinum on CXR help to exclude ANTERIOR SPINAL—paraplegia/quadriplegia, ante- diagnosis’’ rior cord syndrome JAMA 2002 287:17 CLASSIFICATION SYSTEMS STANFORD—A ¼ any ascending aorta involvement, B ¼ all others D. Hui, Approach to Internal Medicine, DOI 10.1007/978-1-4419-6505-9_2, 25 Ó Springer ScienceþBusiness Media, LLC 2006, 2007, 2011 26 Acute Coronary Syndrome INVESTIGATIONS DIAGNOSTIC AND PROGNOSTIC ISSUES (CONT’D) BASIC TYPE B—with aggressive hypertensive treatment, LABS—CBCD, lytes, urea, Cr, troponin/CK Â3, 1-month survival >90%, 10-year survival 56% glucose, AST, ALT, ALP, bilirubin, albumin, lipase, INR/PTT MANAGEMENT IMAGING—CXR, echocardiogram (TEE), CT chest or ABC—O2 to keep sat >95%, IV, antihypertensive MRI chest (keep HR <60 and SBP <120 mmHg. Labetalol 2 mg/ ECG min IV loading drip, then 2–8 mg/min (target heart SPECIAL rate 55–60) or 20–80 mg IV q10min, maximum AORTOGRAPHY 300 mg, then 200–400 mg PO BID. If SBP still >100 mmHg, sodium nitroprusside 0.25–0.5 mg/kg/ DIAGNOSTIC AND PROGNOSTIC ISSUES min IV initially, then 0.25–10 mg/kg/min) CXR FINDINGS—wide mediastinum (>6cm TREAT UNDERLYING CAUSE—Type A (emergent [2.4 in.]), indistinct aortic knuckle, pleural cap, differ- surgical repair, endovascular stenting, long-term ence in diameter between ascending and descending blood pressure control). Type B (medical blood aorta, blurring of aortic margin secondary to local pressure control). Monitor over time with serial extravasation of blood, pleural effusion or massive CT/MR chest hemothorax, displaced calcification (separation of the intimal aortic calcification from the edge of the aortic Related Topics shadow >1 cm [0.4. in.]) Acute Coronary Syndrome (p. 26) PROGNOSIS Stroke (p. 299) TYPE A—with surgery, 1-month survival 75–80%, 10-year survival 55% Acute Coronary Syndrome ACC/AHA 2004 STEMI Guidelines ACC/AHA 2007 STEMI Focused Update ACC/AHA 2007 UA/NSTEMI Guidelines DIFFERENTIAL DIAGNOSIS OF CHEST PAIN DIFFERENTIAL DIAGNOSIS OF CHEST PAIN (CONT’D) CARDIAC PLEURAL—pneumothorax, pneumomediasti- MYOCARDIAL—myocardial infarction, angina num, pleural effusion, pleuritis (atherosclerosis, vasospasm) VASCULAR—pulmonary embolism VALVULAR—aortic stenosis GI—esophagitis, esophageal cancer, GERD, peptic PERICARDIAL—pericarditis ulcer disease, Boerhaave’s, cholecystitis, pancreatitis VASCULAR—aortic dissection OTHERS—musculoskeletal (costochondritis), shin- RESPIRATORY gles, anxiety PARENCHYMAL—pneumonia, cancer PATHOPHYSIOLOGY Pathologic changes Clinical presentation Pre-clinical Atherosclerosis Asymptomatic Angina Luminal narrowing Central chest discomfort; worsened by exertion, emotion, and eating; relieved by rest and nitroglycerine Unstable angina Plaque rupture or thrombus Worsening pattern or rest pain NSTEMI Partial occlusion Non-ST elevation MI STEMI Complete occlusion ST elevation MI PATHOPHYSIOLOGY (CONT’D) PATHOPHYSIOLOGY (CONT’D) UNIVERSAL DEFINITION OF MYOCARDIAL TYPE 3—MI associated with sudden unexpected INFARCTION (MI) cardiac death TYPE 1—spontaneous MI due to a primary coron- TYPE 4—MI associated with PCI (4A) or stent ary event (atherosclerotic plaque rupture or ero- thrombosis (4B) sion with acute thromboembolism) TYPE 5—MI associated with CABG TYPE 2—MI due to supply–demand mismatch Acute Coronary Syndrome 27 PATHOPHYSIOLOGY (CONT’D) CLINICAL FEATURES (CONT’D) RISK FACTORS LR+ MAJOR—diabetes, hypertension, dyslipidemia, Radiation to both arms 7.1 smoking, family history of premature CAD, Nausea or vomiting 1.9 advanced age, male gender Diaphoresis 2.0 ASSOCIATED—obesity, metabolic syndrome, seden- Pleuritic chest pain 0.2 tary lifestyle, high-fat diet Sharp or stabbing chest pain 0.3 EMERGING—lipoprotein abnormalities, inflamma- Positional chest pain 0.3 tion (" CRP), chronic infections, renal failure Chest pain reproducible by palpation 0.2–0.4 POST–MI COMPLICATIONS—arrhythmia (VT/VF, bra- Physical dycardia), sudden death, papillary muscle rupture/dys- Hypotension 3.1 function, myocardial rupture (ventricular wall, interven- S3 3.2 tricular septum), ventricular aneurysm, valvular disease Pulmonary crackles 2.1 (especially acute mitral regurgitation), heart failure/car- ECG diogenic shock, pericarditis (Dressler’s syndrome) New ST elevation 1 mm 5.7–53.9 New Q wave 5.3–24.8 CLINICAL FEATURES Any ST elevation 11.2 CHEST PAIN EQUIVALENTS—dyspnea, syncope, New conduction defect 6.3 fatigue, particularly in patients with diabetic neuro- New ST depression 3.0–5.2 pathy who may not experience chest pain Any Q wave 3.9 NEW YORK HEART ASSOCIATION (NYHA) Any ST depression 3.2 CLASSIFICATION T wave peaking or inversion 1 mm 3.1 I ¼ no symptoms with ordinary physical activity New T wave inversion 2.4–2.8 II ¼ mild symptoms with normal activity (walking Any conduction defect 2.7 >2 blocks or 1 flight of stairs) APPROACH—‘‘radiation of chest pain, diaphor- III ¼ symptoms with minimal exertion esis, hypotension, and S3 suggest acute MI. IV ¼ symptoms at rest Chestpainthatispleuritic,sharporstabbing, CANADIAN CARDIOVASCULAR SOCIETY (CCS) positional or reproduced by palpation decreases CLASSIFICATION likelihood of acute MI. On ECG, any ST ",newQ I ¼ angina with strenuous activity waves, or new conduction D make acute MI II ¼ slight limitation, angina with meals/cold/stress very likely. Normal ECG is very powerful to III ¼ marked limitation, angina with walking <1–2 rule out MI’’ blocks or 1 flight of stairs JAMA 1998 280:14 IV ¼ unstable angina IVA ¼ unstable angina resolves with medical treatment INVESTIGATIONS IVB ¼ unstable angina on oral treatment, symp- BASIC toms improved but angina with minimal LABS—CBCD, lytes, urea, Cr, glucose, troponin/ provocation CK Â3 q8h, AST, ALT, ALP, bilirubin, INR/PTT, Mg, C IV ¼ unstable angina persists, not manageable Ca, PO4, albumin, lipase, fasting lipid profile, on oral treatment or hemodynamically HbA1C unstable IMAGING—CXR, echocardiogram (first 72 h), KILLIP CLASS CLASSIFICATION MIBI/thallium (>5 days later) I ¼ no evidence of heart failure ECG—q8h Â3 or with chest pain II ¼ mild to moderate heart failure (S3, lung rales less STRESS TESTS—ECG, echocardiogram, MIBI once than half way up, or jugular venous distension) stable (>48 h post-MI) III ¼ overt pulmonary edema CORONARY CATHETERIZATION IV ¼ cardiogenic shock DIAGNOSTIC AND PROGNOSTIC ISSUES RATIONAL CLINICAL EXAMINATION SERIES: RISK STRATIFICATION FOR STABLE CORONARY IS THIS PATIENT HAVING A MYOCARDIAL DISEASE INFARCTION? ECG EXERCISE STRESS TEST LR+ ABSOLUTE CONTRAINDICATIONS—recent myocardial History infarction (<4 days), unstable angina, severe Radiation to right shoulder 2.9 symptomatic LV dysfunction, life-threatening Radiation to left arm 2.3 28 Acute Coronary Syndrome DIAGNOSTIC AND PROGNOSTIC ISSUES (CONT’D) DIAGNOSTIC AND PROGNOSTIC ISSUES (CONT’D) arrhythmia, acute pericarditis, aortic dissection, CK/CKMB—rises within 4–6 h, peaks at 18–24 h, PE, severe symptomatic aortic stenosis remains elevated 3–4 days (sens 35–50% at pre- GOAL—keep on treadmill
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