Treatment Guidelinesfor Medicine and PrimaryCare
2004 Edition
New
NMS
Practice Parameters
Paul D. Chan, MDMargaret T. Johnson, MD
Current Clinical Strategies Pub- lishing
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Copyright © 2004 by Current Clinical Strategies Publish-ing. All rights reserved. This book, or any parts thereof,may not be reproduced or stored in an informationretrieval network without the permission of the publisher.Current Clinical Strategies is a registered trademark of Current Clinical Strategies Publishing Inc. The reader isadvised to consult the drug package insert and other references before using any therapeutic agent. Nowarranty exists, expressed or implied, for errors andomissions in this text.Current Clinical Strategies Publishing27071 Cabot RoadLaguna Hills, California 92653Phone: 800-331-8227 or 949-348-8404Fax: 800-965-9420 or 949-348-8405E-mail: info@ccspublishing.comwww.ccspublishing.com/ccs
Cardiovascular Disorders
Acute Coronary Syndromes(Acute Myocardial Infarction andUnstable Angina)
Acute myocardial infarction (AMI) and unstable
anginaare part of a spectrum known as the acute coronarysyndromes (ACS), which have
in common a rupturedatheromatous plaque.
These syndromes include unstableangina, non–Q-wave MI,
and Q-wave MI. The ECGpresentation of ACS includes ST-segment
elevationinfarction, ST-segment depression (including non–Q-wave
MI and unstable angina), and nondiagnostic ST-segment and T-wave abnormalities.
Patients with ST-segment elevation will usually develop
Q-wave MI.Patients with ischemic chest discomfort who do not haveST-segment elevation will develop Q-wave
MI andnon–Q-wave MI or unstable angina.
I.Clinical evaluation of chest pain and acute coro-nary syndromesA.History.
Chest pain is present in 69% of patientswith AMI. The pain may be characterized as aconstricting or squeezing sensation in the chest.Pain can radiate to the upper abdomen, back,either arm, either shoulder, neck, or jaw. Atypicalpain presentations in AMI include pleuritic, sharpor burning chest pain. Dyspnea, nausea, vomiting,palpitations, or syncope may be the only com-plaints.
B.Cardiac Risk factors
include hypertension,hyperlipidemia, diabetes, smoking, and a strongfamily history (coronary artery disease in early or
mid-adulthood in a first-degree relative).
C.Physical examination
may reveal tachycardia or bradycardia, hyper- or hypotension, or tachypnea.Inspiratory rales and an S3 gallop are associatedwith left-sided failure. Jugulovenous distention(JVD), hepatojugular reflux, and peripheral edemasuggest right-sided failure. A systolic murmur mayindicate ischemic mitral regurgitation or ventricular septal defect.
II.Laboratory evaluation of chest pain and acutecoronary syndromesA.Electrocardiogram (ECG)1.
The hallmark of Q-wave infarction is acuteST-segment elevation in association with severechest pain. Significant ST-segment elevation isdefined as 0.10 mV or more measured 0.02second after the J point in two contiguous leads,from the following combinations: (1) leads II, III,or aVF (inferior infarction), (2) leads V
1
throughV
6
(anterior or anterolateral infarction), or (3)leads I and aVL (lateral infarction). Abnormal Qwaves usually develop within 8 to 12 up to 24 to48 hours after the onset of symptoms. AbnormalQ waves are at least 30 msec wide and 0.20 mVdeep in at least two leads.
2.
Complete left bundle branch block with acute,severe chest pain should be managed as acutemyocardial infarction pending cardiac marker analysis. It is usually not possible to definitivelydiagnose acute myocardial infarction by theECG alone in the setting of left bundle branchblock.
B.Laboratory markers1.Creatine phosphokinase
(CPK) enzyme isfound in the brain, muscle, and heart. Thecardiac-specific dimer, CK-MB, however, ispresent almost exclusively in myocardium.
Common Markers for Acute Myocardial Infarc-tionMarkerInitialEleva-tion Af-ter MIMeanTime toPeakEleva-tionsTime toReturnto Base-line
Myoglobin1-4 h6-7 h18-24 hCTnl3-12 h10-24 h3-10 dCTnT3-12 h12-48 h5-14 dCKMB4-12 h10-24 h48-72 hCKMBiso2-6 h12 h38 hCTnI, CTnT = troponins of cardiac myofibrils; CPK-MB, MM= tissue isoforms of creatine kinase.
2.CK-MB subunits.
Subunits of CK, CK-MB, -MM, and -BB, are markers associated with arelease into the blood from damaged cells.Elevated CK-MB enzyme levels are observedin the serum 2-6 hours after MI, but may not bedetected until up to 12 hours after the onset of symptoms.
3.Cardiac-specific troponin T (cTnT)
is aqualitative assay and cardiac troponin I (cTnI)is a quantitative assay. The cTnT level remainselevated in serum up to 14 days and cTnI for 3-7 days after infarction.
4.Myoglobin
is the first cardiac enzyme to bereleased. It appears earlier but is less specificfor MI than other markers. Myoglobin is mostuseful for ruling out myocardial infarction in thefirst few hours.
Differential diagnosis of severe or prolongedchest pain
Myocardial infarctionUnstable anginaAortic dissectionGastrointestinal disease (esophagitis, esophageal spasm,peptic ulcer disease, biliary colic, pancreatitis)PericarditisChest-wall pain (musculoskeletal or neurologic)Pulmonary disease (pulmonary embolism, pneumonia,pleurisy, pneumothorax)Psychogenic hyperventilation syndrome
III.Initial treatment of acute coronary syndromesA.Continuous cardiac monitoring and IV access
should be initiated.
Morphine, oxygen, nitroglyc-erin, and aspirin
("MONA")
should be adminis-tered to patients with ischemic-type chest painunless contraindicated.
B.Morphine
is indicated for continuing
pain unre-sponsive to nitrates. Morphine reduces ventricular preload and
oxygen requirements by venodilation.Administer morphine sulfate 2-4 mg IV every 5-10minutes prn for pain or anxiety.
C.Oxygen
should be administered to all patients withischemic-type
chest discomfort and suspectedACS for at least 2 to 3 hours.
D.Nitroglycerin1.
Nitroglycerin is an
analgesic for ischemic-typechest discomfort. Nitroglycerin is indicated for the initial management of pain
and ischemiaunless contraindicated by hypotension (SBP<90 mm Hg) or RV infarction. Continued use of nitroglycerin beyond
48 hours is only indicatedfor recurrent angina or pulmonary congestion.
2.
Initially, give up to three doses of 0.4 mgsublingual NTG every five minutes or nitroglyc-erine aerosol, 1 spray sublingually every 5minutes. An infusion of intravenous NTG maybe started at 10-20 mcg/min, titrating upwardby 5-10 mcg/min every 5-10 minutes (maxi-mum, 3 mcg/kg/min). Titrate to decrease themean arterial pressure by 10% in normotensivepatients and by 30% in those with hyperten-sion. Slow or stop the infusion if the SBP dropsbelow 100 mm Hg.
E.Aspirin1.
Aspirin should be given as soon as possible toall patients with suspected ACS unless thepatient is allergic
to it. Aspirin therapy reducesmortality after MI by 25%.
2.
A dose of 325 mg of aspirin should be chewedand swallowed on day 1 and continued POdaily thereafter at a dose of 80 to 325 mg
.Clopidogrel (Plavix) may be used in patientswho are allergic to aspirin as an initial dose of 75 to 300 mg, followed by a daily dose of 75mg.
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Treatment Guidelines
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