Pendidikan Profesi Apoteker Universitas Hasanuddin Angkatan 2010
Tuesday, September 28, 2010
Farmakoterapi dalam Pengelolaan Infark miokard akut
1 Farmakoterapi dalam Pengelolaan Infark miokard akut; Dasar Pemikiran & Pedoman Dr Ying-Sui Archie Lo, MD (Chicago), FRCP (Edin.), FRCP (Glasg.), FRCP (Kanada), F.H.K.C.P., F.H.K.A.M., F.A.C.C., F.A.C.P., Fellow American Heart Association Council on Kardiologi Klinis 7 Februari 2001 1:30 - 3:30 malam di Holiday Inn Golden Mile Tinjauan ini sebagian besar didasarkan pada panduan yang diterbitkan pada tahun 1999 & 2000 oleh gugus tugas dari American College of Cardiology dan American Heart Association. (Sirkulasi 1999; 100:1016; J Am Coll Cardiol 2000: 36:970). Penekanannya adalah pada alasan di balik penggunaan berbagai obat untuk pengobatan miokard akut infark. I. Pendahuluan Pengelolaan infark miokard akut (AMI) telah datang jauh sejak konsep perawatan koroner diperkenalkan beberapa dekade yang lalu. Defibrilasi, angioplasti koroner perkutan, trombolisis, obat baru lainnya, semuanya telah semua menyelamatkan jiwa kemajuan di bidang kedokteran. Sejumlah percobaan multi-berpusat besar telah selesai menambahkan informasi tak ternilai bagi pemahaman kita tentang ini-mengancam kehidupan kondisi berkenaan dengan baik pengobatan dan prognosis. II. Pendekatan awal kepada Manajemen Koroner Akut Sindroma Ketika seorang pasien menyajikan dengan nyeri dada dan sindrom koroner akut diduga, pendekatan awal harus terdiri dari sebagai berikut (J Am Coll Cardiol 2000: 36:970): 1) Tentukan kemungkinan iskemia akut yang disebabkan oleh CAD; 2) stratifikasi risiko berfokus pada gejala awal anginal, pemeriksaan fisik, EKG, dan biotanda cedera jantung; 3) Sebuah EKG 12-lead harus diperoleh segera (dalam waktu 10 menit) di pasien dengan ketidaknyamanan dada berkelanjutan; dan 4) a. Biomarker cedera jantung harus diukur pada semua pasien yang hadir dengan ketidaknyamanan dada konsisten dengan ACS; b. troponin jantung adalah penanda disukai; c. CK-MB juga diterima. Pada pasien dengan spidol jantung negatif dalam waktu 6 jam setelah onset nyeri, sampel lain harus ditarik dalam 6 - untuk jangka waktu 12-jam. III. Farmakoterapi dalam Pengelolaan AMI - Dasar Pemikiran & Pedoman 2 Setelah diagnosis AMI telah dibuat, ada daftar panjang obat yang akan perlu dipertimbangkan untuk administrasi. Berikut ini adalah ringkasan singkat dari utama obat untuk pengobatan AMI. 1. Aspirin aspirin itu mengurangi mortalitas di AMI telah ditunjukkan oleh beberapa studi. The meta-analisis penting dari percobaan terkontrol plasebo dengan aspirin oleh Antiplatelet Trialists Kolaborasi menunjukkan recution 25%> dalam risiko infark, stroke, atau kematian pembuluh darah di antara 70.000 pasien risiko tinggi. (1994 BMJ; 308:81) manfaat tambahan yang didokumentasikan dengan penambahan heparin dengan aspirin pada pasien dengan angina tidak stabil / non-ST elevasi MI (UA / NSTEMI) .. kombinasi mengurangi risiko kematian dan MI sebesar 48% dibandingkan dengan aspirin saja. (N ENGL Med1988 J; 319: 1105; Lancet 1990 336:. 827) Aspirin 160-320 mg harus diberikan kepada semua pasien pada hari 1 dari AMI kecuali ada kontraindikasi dan terus menerus pada secara harian. 2. Nitrogliserin Tidak ada manfaat kematian yang pasti telah ditunjukkan dengan terapi nitrat. (1996 JaCC; 27:337) nitrogliserin sublingual harus diberikan ketika pasien pertama disajikan dan sindrom koroner akut dianggap. Setelah diagnosis AMI telah dibuat, nitrat profilaksis tidak pernah terbukti berguna, walaupun mungkin nitrogliserin IV diberikan selama 24 sampai 48 jam pertama pada pasien dengan AMI dan CHF, anterior besar infark, iskemia persisten, atau hipertensi .. Hal ini tidak boleh digunakan pada pasien dengan tekanan darah sistolik kurang dari 90 mm Hg atau bradikardia berat (kurang dari 50 bpm). (Sirkulasi 1999; 100:1016). Setelah 24-48 jam pertama dari terapi IV, lisan atau patch transdermal dapat digunakan. Sebuah interval bebas nitrat 8-12 jam harus diberikan untuk mencegah toleransi nitrat. Ini mungkin diberikan untuk angina pasca infark. 3. B-blocker Terapi Pemberian pasca B-blocker-MI telah ditunjukkan oleh beberapa studi untuk menurunkan angka kematian, termasuk semua penyebab kematian, kematian jantung, menghidupkan kembali jantung penangkapan dan kematian arrhythmic. (Am 1994 Cardiol J; 74:674, JAMA 1993; 270: 1589; Sirkulasi 1999; 99:2268) Ketika diberikan dengan terapi trombolitik. itu menurunkan resiko perdarahan intraserebral. B-blocker umumnya kurang diatur dalam pengelolaan AMI dan ditandai dalam 1) pasien tanpa kontraindikasi untuk Bblocker terapi yang dapat diobati dalam waktu 12 jam onset infark, tanpa administrasi terapi trombolitik secara bersamaan atau kinerja primer angioplasty; 2) pasien dengan melanjutkan atau nyeri iskemik berulang; 3) pasien dengan tachyarrhythmias, seperti AF dengan respon ventrikel yang cepat. Hal ini kontraindikasi pada pasien dengan gagal LV parah. 4. Magnesium Sulfat Magnesium sulfat ditunjukkan dalam: 1) pasien dengan magnesium didokumentasikan (dan / atau kalium) defisit, terutama di Poin menerima diuretik sebelum timbulnya infark; 2) episode torsade VT pointes-tipe de dikaitkan dengan interval QT berkepanjangan. Ini dapat dipertimbangkan pada pasien beresiko tinggi seperti orang tua dan / atau mereka yang Terapi reperfusi tidak cocok. (Sirkulasi 1999; 100:1016) 5. ACE Inhibitor 3 Pada pasien post-MI, inhibitor ACE telah ditunjukkan oleh percobaan besar untuk mengurangi kematian (Lancet 95; 345:669; Lancet 94: 343: 1115). . Pada pasien dengan gangguan LV fungsi, inhibitor ACE meningkatkan fungsi LV, penurunan baik jangka pendek dan jangka panjang kematian, mengurangi resiko CHF, dan mungkin memiliki efek antiarrhythmic tidak langsung. Ini harus dipertimbangkan pada pasien dalam 24 jam pertama dari AMI yang dicurigai dengan STsegment elevasi dalam 2 sadapan prekordial atau dengan CHF klinis dalam ketiadaan hipotensi (tekanan darah sistolik <100 mm Hg) atau dikenal kontraindikasi untuk penggunaan ACE inhibitor. Pasien dengan AMI dan EF <40% atau pasien dengan CHF klinis harus juga menerima ACEI. (Sirkulasi 1999; 100:1016). 6. Calcium Channel Blockers Tidak blocker saluran kalsium telah terbukti menurunkan angka kematian setelah AMI. Dalam tertentu, dihydropyridines bertindak pendek seperti nifedipin adalah kontraindikasi pada AMI. Di sisi lain, baik verapamil atau diltiazem dapat diberikan kepada pasien di siapa ß-blocker tidak efektif atau kontraindikasi untuk menghilangkan iskemia berlangsung atau kontrol SDM yang cepat dengan AF setelah AMI dalam ketiadaan CHF, disfungsi LV, atau AV blok. Pasien dengan CHF umumnya harus tidak menerima calcium channel blockers. (Sirkulasi 1999; 100:1016). 7. Trombolisis Pasien dengan elevasi ST akut MI (STEMI) harus menerima terapi trombolitik dalam tidak adanya kontraindikasi. Sebaliknya, mereka yang non-ST elevasi akut (NSTEMI) seharusnya tidak menerima terapi trombolitik. (Sirkulasi 1999; 100:1016; J Am Coll Cardiol 2000: 36:970). Sebelumnya pasien STEMI menerima terapi, lebih tinggi kemungkinan mencapai patensi dari arteri infarct terkait. Sebelumnya perawatan, semakin tinggi jumlah nyawa diselamatkan dan semakin baik prognosis. Oleh karena itu, sekali diagnosis STEMI dibuat, langkah segera harus diambil untuk transfer pasien ke pusat di mana agen trombolisis dapat diberikan. The pilihan agen trombolisis tergantung pada biaya dan tarif patensi menyeimbangkan dengan stroke tarif. rTPA lebih efektif dibandingkan streptokinase dalam mencapai patensi arteri tetapi terkait dengan insiden yang lebih tinggi komplikasi stroke dibandingkan streptokinase. rTPA juga lebih mahal dari streptokinase. Jika rTPA lebih disukai, maka depan dimuat regimen harus digunakan. Dalam Trial-1 lahap, rTPA dikaitkan dengan 1% pengurangan absolut (6,3% dibandingkan 7,3%) dalam kematian dibandingkan dengan streptokinase. (N ENGL J Med 1993; 329:673) 8. Heparin Heparin diberikan dengan rTPA selama 24-48 jam; tidak jelas jika tingkat patensi yang ditingkatkan dengan memberikan heparin selama lebih dari 24 sampai 48 jam. Saat ini tidak ada data dukungan heparin rutin pada pasien yang menerima agen trombolitik non-fibrin-spesifik (Streptokinase, anistreplase, atau urokinase), selama aspirin diberikan; mungkin pengecualian termasuk pasien dengan anterior besar atau MI apikal, di dalam Dia mungkin heparin mengurangi risiko trombosis mural dan embolisasi sistemik. (Sirkulasi 1999; 100:1016) Pada pasien yang belum menerima terapi trombolitik, heparin mungkin nilai. heparins berat molekul rendah telah menjadi lebih populer dalam beberapa tahun terakhir sebagai akibat dari percobaan plasebo terkontrol menunjukkan perlindungan yang sama atau sedikit lebih baik dari heparin tak terpecah. Keuntungan Dari LMWH termasuk yang lebih menguntungkan farmakokinetik profil dengan suntikan dua kali sehari tapi tanpa laboratorium sering pemantauan (Lancet 2000; 355:1936). 4 9. Glikoprotein IIb / IIIa inhibitor Ini adalah produk dari bioteknologi modern. Percobaan dengan abciximab dengan tirofiban dan eptifibatide telah menunjukkan manfaat dan pengurangan tingkat kematian dan MI di pasien dengan angina tidak stabil atau NSTEMI. Manfaat juga terlihat dengan intervensi prosedur. (Lancet 1998; 352:87; Lancet 1997; 349: 1429; N ENGL J Med 1998; 338:1488). Namun, inhibitor lisan telah mengecewakan. Terutama itu digunakan pada pasien mengalami NSTEMI yang memiliki beberapa fitur berisiko tinggi dan / atau iskemia refrakter, asalkan mereka tidak memiliki kontraindikasi besar karena perdarahan risiko. 10. Antiarrhythmic Terapi Pasien dengan VT / VT harus defibrillated atau cardioverted segera dan ini adalah salah satu dari alasan utama mengapa unit perawatan koroner telah berhasil dalam menyelamatkan kehidupan .. Tidak ada indikasi untuk treament dari ketukan terisolasi prematur ventrikel, gurindam, berjalan ritme idioventricular dipercepat, dan VT nonsustained. Tidak ada indikasi untuk pemberian profilaksis terapi antiarrhythmic saat menggunakan agen trombolitik. (Sirkulasi 1999; 100:1016) IV. Kateterisasi jantung 1. Versus PTCA primer Trombolisis untuk STEMI Ada kontraindikasi untuk terapi trombolitik IV yang meliputi terbaru utama operasi, hipertensi yang tidak terkontrol, trauma atau perdarahan aktif dll Insiden stroke pada pasien lanjut usia yang menerima terapi trombolitik juga tinggi. Primer PTCA menawarkan alternatif yang menarik dalam pandangan hidup mengancam tingkat komplikasi dari 1-3% dengan laju patensi arteri hanya 50-80% dapat dicapai dengan agen trombolitik. PTCA primer menurunkan kejadian kematian dan reinfarction. (JACC 1999; 33:640) Dalam membandingkan PTCA primer dengan terapi invasif, analisis dikumpulkan dari 10 percobaan acak dengan 2.606 pasien menunjukkan manfaat kematian dengan PTCA primer atas bahwa dari trombolisis (JAMA 1997; 278: 2093). Glycoprotein IIb / IIIa inhibitor juga telah membuat lebih aman untuk melakukan prosedur intervensi segera setelah AMI. PTCA primer harus dipertimbangkan sebagai alternatif untuk terapi trombolitik. (Sirkulasi 1999; 100:1016) Pada pasien dengan AMI yang bisa menjalani angioplasti dari arteri infarct terkait dalam waktu 12 jam setelah di set gejala atau melebihi 12 jam jika gejala iskemik bertahan. Hal ini juga dapat dipertimbangkan pada pasien dengan syok kardiogenik, adalah <75 tahun tua dan yang dapat dilakukan revaskularisasi dalam waktu 18 jam setelah onset syok. Hal ini dapat digunakan untuk mencapai reperfusi ketika contraindicatinos untuk terapi trombolitik yang hadir. Harus ditekankan bahwa PTCA primer harus dilakukan hanya di pusat-pusat berpengalaman dalam prosedur ini. 2. Angiography + /-PTCA berikut Trombolisis Pasien dengan angina pasca infark spontan dan / atau iskemia dibuktikan diprovokasi dengan pengujian noninvasif harus dipertimbangkan untuk angiografi dengan maksud untuk PTCA melakukan atau BPK yang diperlukan. (Sirkulasi 1997; 96: 748, Sirkulasi 1998; 98:1860; Sirkulasi 1999; 100:1464) Sebuah kajian mendalam berada di luar ruang lingkup hari ini kuliah. Manajemen V. Post-MI Lipid 5 Beberapa percobaan pencegahan sekunder telah menunjukkan manfaat dari lipid menurunkan pada pasien dengan penyakit koroner. (Lancet 1994; 344:1383; N Eng J Med 1996; 335: 1001) Manfaat ini telah dibuktikan pada pasien pasca-MI dengan ditandai hiperkolesterolemia serta mereka dengan tinggi normal atau hanya lemak agak tinggi tingkat. Kemungkinan bahwa statin memiliki sifat anti-inflamasi serta efek menguntungkan pada fungsi endotel sangat menarik. The miokard Pengurangan iskemia dengan agresif Menurunkan Kolesterol (MIRACL) Studi (73 Sesi Ilmiah AHA, November 2000) menunjukkan bahwa inisiasi awal statin terapi mungkin memiliki manfaat kematian. Studi lain juga mendukung peran statin terapi setelah AMI. (Sirkulasi 1998; 98 (suppl 1): 1-45; N ENGL J Med 1998; 339:1349) Pedoman untuk Manajemen Lipid Pasien harus melakukan diet sama dengan diet AHA Langkah II, yang rendah lemak jenuh dan kolesterol (kurang dari 7% dari total kalori seperti lemak jenuh dan kurang dari 200 mg / d kolesterol). Pasien dengan kadar kolesterol LDL lebih besar dari 125 mg / dL meskipun diet Langkah AHA II harus ditempatkan pada terapi obat dengan tujuan mengurangi LDL hingga kurang dari 100 mg / dL. Pasien dengan kolesterol plasma normal tingkat yang memiliki high-density lipoprotein (HDL) tingkat kolesterol kurang dari 35 mg / dL harus menerima terapi nonpharmacological (misalnya, latihan) dirancang untuk meningkatkan itu. Terapi obat baik menggunakan niacin atau gemfibrozil dapat ditambahkan tanpa LDL dan tingkat HDL, ketika tingkat trigliserida adalah> 200 mg%. Statin menghasilkan terbesar penurunan kolesterol LDL. Niacin kurang efektif dalam mengurangi LDL meskipun lebih efektif dalam meningkatkan HDL. Resin jarang cukup efektif saja tetapi mereka dapat digunakan untuk supplemment niacin atau statin. Untuk menurunkan lipid, terapi statin umumnya disukai. Dosis statin harus dititrasi setiap empat sampai enam minggu untuk mencapai tingkat kolesterol LDL-90 sampai 100 mg / dL (2,3-2,6 mmol / L). Pasien statin harus memiliki s LFT mereka dan CPK secara berkala. Waktu untuk memulai terapi statin belum ditentukan tetapi data menyarankan bahwa mungkin perlu dimulai awal perjalanan AMI. VI. Predischarge noninvasif Pengujian untuk Identifikasi High- Pasien Risiko Echocardiography, 24 Holter monitoring, olahraga treadmill stress testing, miokard skintigrafi, rata-rata sinyal, variabilitas detak jantung semua alat invasif yang memberikan informasi prognostik. Sebuah tinjauan rinci adalah di luar lingkup hari ini kuliah.
Pharmacotherapy in the Management of Acute Myocardial Infarction
1
Pharmacotherapy in the
Management of Acute Myocardial Infarction;
Rationale & Guidelines
Dr. Ying-Sui Archie Lo,
M.D.(Chicago), F.R.C.P.(Edin.), F.R.C.P.(Glasg.), F.R.C.P.(Canada) ,
F.H.K.C.P., F.H.K.A.M., F.A.C.C., F.A.C.P.,
Fellow American Heart Association Council on Clinical Cardiology
7 February 2001
1:30 – 3:30 p.m.
at Holiday Inn Golden Mile
This review is based largely on guidelines published in 1999 & 2000 by task forces
from the American College of Cardiology and the American Heart Association.
(Circulation 1999; 100:1016; J Am Coll Cardiol 2000: 36:970). The emphasis is on
the rationale behind the use of various drugs for the treatment of acute myocardial
infarction.
I. Introduction
The management of acute myocardial infarction (AMI) has come a long way since the
concept of coronary care was introduced several decades ago. Defibrillation,
percutaneous coronary angioplasty, thrombolysis, other new drugs, have all been all
life-saving advances in medicine. Numerous large multi-centered trials have been
completed adding invaluable information to our understanding of this life-threatening
condition with regard to both treatment and prognosis.
II. Initial Approach to the Management of Acute Coronary
Syndrome
When a patient presents with chest pain and acute coronary syndrome is suspected,
the initial approach should consist of the following (J Am Coll Cardiol 2000: 36:970):
1) Determine the likelihood of acute ischemia caused by CAD;
2) Early risk stratification focuses on anginal symptoms, physical exam, ECG,
and biomarkers of cardiac injury;
3) A 12-lead ECG should be obtained immediately (within 10 minutes) in
patients with ongoing chest discomfort ; and
4) a. Biomarkers of cardiac injury should be measured in all patients who
present with chest discomfort consistent with ACS;
b. Cardiac troponin is the preferred marker; c. CK-MB is also acceptable.
In patients with negative cardiac markers within 6 hours of the onset of pain,
another sample should be drawn in the 6- to 12-hr time frame.
III. Pharmacotherapy in the Management of AMI - Rationale &
Guidelines
2
Once the diagnosis of AMI has been made, there is a long list of medications that will
need to be considered for administration. The following is a brief summary of the
major drugs for the treatment of AMI.
1. Aspirin
That aspirin reduces mortality in AMI has been shown by multiple studies. The
important meta-analysis of the placebo-controlled trials with aspirin by the
Antiplatelet Trialists Collaboration showed a >25% recution in the risk of infarction,
stroke, or vascular death among 70,000 high risk patients. (BMJ 1994; 308:81)
Additional benefit was documented by the addition of heparin to aspirin in patients
with unstable angina/non-ST elevation MI (UA/NSTEMI)..The combination reduces
the risk of death and MI by 48% compared with aspirin alone. (N Engl J Med1988;
319: 1105; Lancet 1990 336: 827.) Aspirin 160-320 mg should be given to all patients
on day 1 of AMI unless there are contraindications and continued indefinitely on a
daily basis.
2. Nitroglycerin
No definite mortality benefits have been shown with nitrate therapy. (JACC 1996;
27:337) Sublingual nitroglycerin should be given when the patient first presented and
acute coronary syndrome is considered. Once the diagnosis of AMI has been made,
prophylactic nitrates have never shown to be useful, although IV nitroglycerin may be
given during the first 24 to 48 hours in patients with AMI and CHF, large anterior
infarction, persistent ischemia, or hypertension.. It should not be used in patients with
systolic blood pressure less than 90 mm Hg or severe bradycardia (less than 50 bpm).
(Circulation 1999; 100:1016). After the first 24-48 hours of IV therapy, oral or
transdermal patches may be used. A nitrate free interval of 8-12 hours should be
given to prevent nitrate tolerance. It may be given for post-infarction angina.
3. B-blocker Therapy
The administration of B-blockers post-MI have been shown by multiple studies to
reduce mortality, including all cause mortality, cardiac death, resuscitated cardiac
arrest and arrhythmic death. (Am J Cardiol 1994; 74:674; JAMA 1993; 270: 1589;
Circulation 1999; 99:2268) When given with thrombolytic therapy. it lowers the risk
of intracerebral hemorrhage. B-blockers are generally under-prescribed in the
management of AMI and is indicated in 1) patients without a contraindication to Bblocker
therapy who can be treated within 12 hours of onset of infarction, irrespective
of administration of concomitant thrombolytic therapy or performance of primary
angioplasty; 2) patients with continuing or recurrent ischemic pain; 3) patients with
tachyarrhythmias, such as AF with a rapid ventricular response. It is contraindicated
in patients with severe LV failure.
4. Magnesium Sulfate
Magnesium sulfate is indicated in: 1) patients with documented magnesium (and/or
potassium) deficits, especially in pts receiving diuretics before onset of infarction; 2)
episodes of torsade de pointes–type VT associated with a prolonged QT interval. It
may be considered in high-risk patients such as the elderly and/or those for whom
reperfusion therapy is not suitable. (Circulation 1999; 100:1016)
5. ACE Inhibitors
3
In post-MI patients, ACE inhibitors have been shown by large trials to reduce
mortality (Lancet 95; 345:669; Lancet 94: 343: 1115). . In patients with impaired LV
function, ACE inhibitors improve LV function, decrease both short and long term
mortality, decrease the risk of CHF, and may have an indirect antiarrhythmic effect. It
should be considered in patients within the first 24 hrs of suspected AMI with STsegment
elevation in 2 precordial leads or with clinical CHF in the absence of
hypotension (systolic BP <100 mm Hg) or known contraindications to use of ACE
inhibitors. Patients with AMI and EF<40% or patients with clinical CHF should
also receive ACEI. (Circulation 1999; 100:1016).
6. Calcium Channel Blockers
No calcium channel blocker has been shown to decrease mortality after AMI. In
particular, short acting dihydropyridines such as nifedipine are contraindicated in
AMI. On the other hand, both verapamil or diltiazem may be given to patients in
whom ß-blockers are ineffective or contraindicated for relief of ongoing ischemia or
control of a rapid HR with AF after AMI in the absence of CHF, LV dysfunction, or
AV block. Patients with CHF should generally not receive calcium channel blockers.
(Circulation 1999; 100:1016).
7. Thrombolysis
Patients with acute ST elevation MI (STEMI) should receive thrombolytic therapy in
the absence of contraindications. In contrast, those with acute non-ST elevation
(NSTEMI) should not receive thrombolytic therapy. (Circulation 1999; 100:1016; J
Am Coll Cardiol 2000: 36:970). The earlier the STEMI patient receives therapy, the
higher the likelihood of achieving patency of the infarct-related artery. The earlier
the treatment, the higher the number of lives saved and the better the prognosis.
Therefore, once the diagnosis of STEMI is made, immediate steps should be taken to
transfer the patient to a center where a thrombolytic agent can be administered. The
choice of thrombolytic agent depends on cost and balancing patency rates with stroke
rates. rTPA is more effective than streptokinase in achieving artery patency but is
associated with a higher incidence of stroke complication than streptokinase. rTPA
is also more expensive than streptokinase. If rTPA is preferred, then the front loaded
regimen should be used. In the GUSTO-1 Trial, rTPA is associated with a 1%
absolute reduction (6.3% versus 7.3%) in mortality compared with streptokinase. (N
Engl J Med 1993; 329:673)
8. Heparin
Heparin is given with rTPA for 24-48 hours; it is unclear if patency rates are enhanced
by giving heparin for more than 24 to 48 hours. Currently there are no data to
support routine heparin in patients receiving non-fibrin-specific thrombolytic agents
(streptokinase, anistreplase, or urokinase), as long as aspirin is given; possible
exceptions include patients with a large anterior or apical MI, in whom heparin may
reduce risk of mural thrombosis and systemic embolization. (Circulation 1999;
100:1016) In patients who have not received thrombolytic therapy, heparin may be
of value. Low molecular weight heparins have become more popular in recent years
as a result of placebo controlled trials showing similar or slightly better protection
than unfractionated heparin. Advantages Of LMWH include a more favorable
pharmacokinetic profile with twice daily injection but without frequent laboratory
monitoring .(Lancet 2000; 355:1936)
4
9. Glycoprotein IIb/IIIa inhibitor
These are products of modern biotechnology. Trials with abciximab with tirofiban
and eptifibatide have shown a benefit and reduction in the rates of death and MI in
patients with unstable angina or NSTEMI. Benefits are also seen with interventional
procedures. (Lancet 1998; 352:87; Lancet 1997; 349: 1429; N Engl J Med 1998;
338:1488). However, the oral inhibitors have been disappointing. Primarily it is
used in patients experiencing NSTEMI who have some high-risk features and/or
refractory ischemia, provided they do not have a major contraindication due to a
bleeding risk.
10. Antiarrhythmic Therapy
Patients with VT/VT should be defibrillated or cardioverted promptly and this is one
of the main reason why coronary care units have been successful in saving lives..
There is no indication for treament of isolated ventricular premature beats, couplets,
runs of accelerated idioventricular rhythm, and nonsustained VT. There is no
indication for prophylactic administration of antiarrhythmic therapy when using
thrombolytic agents. (Circulation 1999; 100:1016)
IV. Cardiac Catheterisation
1. Primary PTCA versus Thrombolysis for STEMI
There are contraindications to IV thrombolytic therapy which include recent major
surgery, uncontrolled hypertension, trauma or active bleeding etc. The incidence of
stroke in elderly patients receiving thrombolytic therapy is also high. Primary PTCA
offers an attractive alternative in view of life threatening complication rates of 1-3 %
with a artery patency rate of only 50-80% achievable with thrombolytic agents.
Primary PTCA decreases incidence of death and reinfarction. (JACC 1999; 33:640) In
comparing primary PTCA with noninvasive therapy, a pooled analysis of 10
randomised trials with 2606 patients showed mortality benefits with primary PTCA
over that of thrombolysis.( JAMA 1997; 278: 2093) Glycoprotein IIb/IIIa inhibitors
have also made it safer to perform interventional procedures soon after AMI.
Primary PTCA should be considered as an alternative to thrombolytic therapy.
(Circulation 1999; 100:1016) In patients with AMI who can undergo angioplasty of
the infarct-related artery within 12 hours of the on set of symptoms or beyond 12
hours if ischemic symptoms persist. It may also be considered in patients with
cardiogenic shock, are <75 yr old and in whom revascularisation can be performed
within 18 hours of the onset of shock. It can be used to achieve reperfusion when
contraindicatinos to thrombolytic therapy are present. It should be emphasized that
primary PTCA should be performed only in centers experienced in this procedure.
2. Angiography +/-PTCA following Thrombolysis
Patients with spontaneous post-infarction angina and/or demonstrable ischemia
provoked by noninvasive testing should be considered for angiography with a view to
performing PTCA or CABG as needed. (Circulation 1997; 96: 748; Circulation 1998;
98:1860; Circulation 1999; 100:1464) An in-depth review is beyond the scope of
today’s lecture.
V. Post-MI Lipid Management
5
Multiple secondary prevention trials have demonstrated the benefit of lipid lowering
in patients with coronary disease. (Lancet 1994; 344:1383; N Eng J Med 1996; 335:
1001) This benefit has been demonstrated in post-MI patients with marked
hypercholesterolemia as well as those with high normal or only mildly elevated lipid
levels. The possibility that statins have anti-inflammatory properties as well as
favorable effects on endothelial function are especially intriguing. The Myocardial
Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) Study (73rd
AHA Scientific Session, November 2000) suggested that early initiation of statin
therapy may have mortality benefits. Other studies also support a role for statin
therapy after AMI. (Circulation 1998; 98(suppl 1): 1-45; N Engl J Med 1998;
339:1349)
Guidelines to Lipid Management
The patient should go on a diet similar to the AHA Step II diet, which is low in
saturated fat and cholesterol (less than 7% of total calories as saturated fat and less
than 200 mg/d cholesterol). Patients with LDL cholesterol levels greater than 125
mg/dL despite the AHA Step II diet should be placed on drug therapy with the goal of
reducing LDL to less than 100 mg/dL. Patients with normal plasma cholesterol
levels who have a high-density lipoprotein (HDL) cholesterol level less than 35
mg/dL should receive nonpharmacological therapy (eg, exercise) designed to raise it.
Drug therapy using either niacin or gemfibrozil can be added regardless of the LDL
and HDL levels, when the triglyceride level is > 200 mg%. Statin produces the
greatest reduction in LDL cholesterol. Niacin is less effective in reducing LDL
although it is more effective in raising HDL. Resins are rarely sufficiently effective
alone but they can be used to supplemment niacin or statins. For lipid lowering,
statin therapy is generally preferred. The statin dosage should be titrated every four
to six weeks to achieve an LDL-cholesterol level of 90 to 100 mg/dL (2.3 to 2.6
mmol/L). Patients on statins should have their LFT’ s and CPK at regular intervals.
The timing for the initiation of statin therapy has yet to be determined but data
suggest that it may need to be started early in the course of AMI.
VI. Predischarge Noninvasive Testing for the Identification of High-
Risk Patients
Echocardiography, 24 Holter monitoring, treadmill exercise stress testing, myocardial
scintigraphy, signal averaging, heart rate variability are all noninvasive tools that
provide prognostic information. A detailed review is beyond the scope of today’s
lecture.
Pharmacotherapy in the
Management of Acute Myocardial Infarction;
Rationale & Guidelines
Dr. Ying-Sui Archie Lo,
M.D.(Chicago), F.R.C.P.(Edin.), F.R.C.P.(Glasg.), F.R.C.P.(Canada) ,
F.H.K.C.P., F.H.K.A.M., F.A.C.C., F.A.C.P.,
Fellow American Heart Association Council on Clinical Cardiology
7 February 2001
1:30 – 3:30 p.m.
at Holiday Inn Golden Mile
This review is based largely on guidelines published in 1999 & 2000 by task forces
from the American College of Cardiology and the American Heart Association.
(Circulation 1999; 100:1016; J Am Coll Cardiol 2000: 36:970). The emphasis is on
the rationale behind the use of various drugs for the treatment of acute myocardial
infarction.
I. Introduction
The management of acute myocardial infarction (AMI) has come a long way since the
concept of coronary care was introduced several decades ago. Defibrillation,
percutaneous coronary angioplasty, thrombolysis, other new drugs, have all been all
life-saving advances in medicine. Numerous large multi-centered trials have been
completed adding invaluable information to our understanding of this life-threatening
condition with regard to both treatment and prognosis.
II. Initial Approach to the Management of Acute Coronary
Syndrome
When a patient presents with chest pain and acute coronary syndrome is suspected,
the initial approach should consist of the following (J Am Coll Cardiol 2000: 36:970):
1) Determine the likelihood of acute ischemia caused by CAD;
2) Early risk stratification focuses on anginal symptoms, physical exam, ECG,
and biomarkers of cardiac injury;
3) A 12-lead ECG should be obtained immediately (within 10 minutes) in
patients with ongoing chest discomfort ; and
4) a. Biomarkers of cardiac injury should be measured in all patients who
present with chest discomfort consistent with ACS;
b. Cardiac troponin is the preferred marker; c. CK-MB is also acceptable.
In patients with negative cardiac markers within 6 hours of the onset of pain,
another sample should be drawn in the 6- to 12-hr time frame.
III. Pharmacotherapy in the Management of AMI - Rationale &
Guidelines
2
Once the diagnosis of AMI has been made, there is a long list of medications that will
need to be considered for administration. The following is a brief summary of the
major drugs for the treatment of AMI.
1. Aspirin
That aspirin reduces mortality in AMI has been shown by multiple studies. The
important meta-analysis of the placebo-controlled trials with aspirin by the
Antiplatelet Trialists Collaboration showed a >25% recution in the risk of infarction,
stroke, or vascular death among 70,000 high risk patients. (BMJ 1994; 308:81)
Additional benefit was documented by the addition of heparin to aspirin in patients
with unstable angina/non-ST elevation MI (UA/NSTEMI)..The combination reduces
the risk of death and MI by 48% compared with aspirin alone. (N Engl J Med1988;
319: 1105; Lancet 1990 336: 827.) Aspirin 160-320 mg should be given to all patients
on day 1 of AMI unless there are contraindications and continued indefinitely on a
daily basis.
2. Nitroglycerin
No definite mortality benefits have been shown with nitrate therapy. (JACC 1996;
27:337) Sublingual nitroglycerin should be given when the patient first presented and
acute coronary syndrome is considered. Once the diagnosis of AMI has been made,
prophylactic nitrates have never shown to be useful, although IV nitroglycerin may be
given during the first 24 to 48 hours in patients with AMI and CHF, large anterior
infarction, persistent ischemia, or hypertension.. It should not be used in patients with
systolic blood pressure less than 90 mm Hg or severe bradycardia (less than 50 bpm).
(Circulation 1999; 100:1016). After the first 24-48 hours of IV therapy, oral or
transdermal patches may be used. A nitrate free interval of 8-12 hours should be
given to prevent nitrate tolerance. It may be given for post-infarction angina.
3. B-blocker Therapy
The administration of B-blockers post-MI have been shown by multiple studies to
reduce mortality, including all cause mortality, cardiac death, resuscitated cardiac
arrest and arrhythmic death. (Am J Cardiol 1994; 74:674; JAMA 1993; 270: 1589;
Circulation 1999; 99:2268) When given with thrombolytic therapy. it lowers the risk
of intracerebral hemorrhage. B-blockers are generally under-prescribed in the
management of AMI and is indicated in 1) patients without a contraindication to Bblocker
therapy who can be treated within 12 hours of onset of infarction, irrespective
of administration of concomitant thrombolytic therapy or performance of primary
angioplasty; 2) patients with continuing or recurrent ischemic pain; 3) patients with
tachyarrhythmias, such as AF with a rapid ventricular response. It is contraindicated
in patients with severe LV failure.
4. Magnesium Sulfate
Magnesium sulfate is indicated in: 1) patients with documented magnesium (and/or
potassium) deficits, especially in pts receiving diuretics before onset of infarction; 2)
episodes of torsade de pointes–type VT associated with a prolonged QT interval. It
may be considered in high-risk patients such as the elderly and/or those for whom
reperfusion therapy is not suitable. (Circulation 1999; 100:1016)
5. ACE Inhibitors
3
In post-MI patients, ACE inhibitors have been shown by large trials to reduce
mortality (Lancet 95; 345:669; Lancet 94: 343: 1115). . In patients with impaired LV
function, ACE inhibitors improve LV function, decrease both short and long term
mortality, decrease the risk of CHF, and may have an indirect antiarrhythmic effect. It
should be considered in patients within the first 24 hrs of suspected AMI with STsegment
elevation in 2 precordial leads or with clinical CHF in the absence of
hypotension (systolic BP <100 mm Hg) or known contraindications to use of ACE
inhibitors. Patients with AMI and EF<40% or patients with clinical CHF should
also receive ACEI. (Circulation 1999; 100:1016).
6. Calcium Channel Blockers
No calcium channel blocker has been shown to decrease mortality after AMI. In
particular, short acting dihydropyridines such as nifedipine are contraindicated in
AMI. On the other hand, both verapamil or diltiazem may be given to patients in
whom ß-blockers are ineffective or contraindicated for relief of ongoing ischemia or
control of a rapid HR with AF after AMI in the absence of CHF, LV dysfunction, or
AV block. Patients with CHF should generally not receive calcium channel blockers.
(Circulation 1999; 100:1016).
7. Thrombolysis
Patients with acute ST elevation MI (STEMI) should receive thrombolytic therapy in
the absence of contraindications. In contrast, those with acute non-ST elevation
(NSTEMI) should not receive thrombolytic therapy. (Circulation 1999; 100:1016; J
Am Coll Cardiol 2000: 36:970). The earlier the STEMI patient receives therapy, the
higher the likelihood of achieving patency of the infarct-related artery. The earlier
the treatment, the higher the number of lives saved and the better the prognosis.
Therefore, once the diagnosis of STEMI is made, immediate steps should be taken to
transfer the patient to a center where a thrombolytic agent can be administered. The
choice of thrombolytic agent depends on cost and balancing patency rates with stroke
rates. rTPA is more effective than streptokinase in achieving artery patency but is
associated with a higher incidence of stroke complication than streptokinase. rTPA
is also more expensive than streptokinase. If rTPA is preferred, then the front loaded
regimen should be used. In the GUSTO-1 Trial, rTPA is associated with a 1%
absolute reduction (6.3% versus 7.3%) in mortality compared with streptokinase. (N
Engl J Med 1993; 329:673)
8. Heparin
Heparin is given with rTPA for 24-48 hours; it is unclear if patency rates are enhanced
by giving heparin for more than 24 to 48 hours. Currently there are no data to
support routine heparin in patients receiving non-fibrin-specific thrombolytic agents
(streptokinase, anistreplase, or urokinase), as long as aspirin is given; possible
exceptions include patients with a large anterior or apical MI, in whom heparin may
reduce risk of mural thrombosis and systemic embolization. (Circulation 1999;
100:1016) In patients who have not received thrombolytic therapy, heparin may be
of value. Low molecular weight heparins have become more popular in recent years
as a result of placebo controlled trials showing similar or slightly better protection
than unfractionated heparin. Advantages Of LMWH include a more favorable
pharmacokinetic profile with twice daily injection but without frequent laboratory
monitoring .(Lancet 2000; 355:1936)
4
9. Glycoprotein IIb/IIIa inhibitor
These are products of modern biotechnology. Trials with abciximab with tirofiban
and eptifibatide have shown a benefit and reduction in the rates of death and MI in
patients with unstable angina or NSTEMI. Benefits are also seen with interventional
procedures. (Lancet 1998; 352:87; Lancet 1997; 349: 1429; N Engl J Med 1998;
338:1488). However, the oral inhibitors have been disappointing. Primarily it is
used in patients experiencing NSTEMI who have some high-risk features and/or
refractory ischemia, provided they do not have a major contraindication due to a
bleeding risk.
10. Antiarrhythmic Therapy
Patients with VT/VT should be defibrillated or cardioverted promptly and this is one
of the main reason why coronary care units have been successful in saving lives..
There is no indication for treament of isolated ventricular premature beats, couplets,
runs of accelerated idioventricular rhythm, and nonsustained VT. There is no
indication for prophylactic administration of antiarrhythmic therapy when using
thrombolytic agents. (Circulation 1999; 100:1016)
IV. Cardiac Catheterisation
1. Primary PTCA versus Thrombolysis for STEMI
There are contraindications to IV thrombolytic therapy which include recent major
surgery, uncontrolled hypertension, trauma or active bleeding etc. The incidence of
stroke in elderly patients receiving thrombolytic therapy is also high. Primary PTCA
offers an attractive alternative in view of life threatening complication rates of 1-3 %
with a artery patency rate of only 50-80% achievable with thrombolytic agents.
Primary PTCA decreases incidence of death and reinfarction. (JACC 1999; 33:640) In
comparing primary PTCA with noninvasive therapy, a pooled analysis of 10
randomised trials with 2606 patients showed mortality benefits with primary PTCA
over that of thrombolysis.( JAMA 1997; 278: 2093) Glycoprotein IIb/IIIa inhibitors
have also made it safer to perform interventional procedures soon after AMI.
Primary PTCA should be considered as an alternative to thrombolytic therapy.
(Circulation 1999; 100:1016) In patients with AMI who can undergo angioplasty of
the infarct-related artery within 12 hours of the on set of symptoms or beyond 12
hours if ischemic symptoms persist. It may also be considered in patients with
cardiogenic shock, are <75 yr old and in whom revascularisation can be performed
within 18 hours of the onset of shock. It can be used to achieve reperfusion when
contraindicatinos to thrombolytic therapy are present. It should be emphasized that
primary PTCA should be performed only in centers experienced in this procedure.
2. Angiography +/-PTCA following Thrombolysis
Patients with spontaneous post-infarction angina and/or demonstrable ischemia
provoked by noninvasive testing should be considered for angiography with a view to
performing PTCA or CABG as needed. (Circulation 1997; 96: 748; Circulation 1998;
98:1860; Circulation 1999; 100:1464) An in-depth review is beyond the scope of
today’s lecture.
V. Post-MI Lipid Management
5
Multiple secondary prevention trials have demonstrated the benefit of lipid lowering
in patients with coronary disease. (Lancet 1994; 344:1383; N Eng J Med 1996; 335:
1001) This benefit has been demonstrated in post-MI patients with marked
hypercholesterolemia as well as those with high normal or only mildly elevated lipid
levels. The possibility that statins have anti-inflammatory properties as well as
favorable effects on endothelial function are especially intriguing. The Myocardial
Ischemia Reduction with Aggressive Cholesterol Lowering (MIRACL) Study (73rd
AHA Scientific Session, November 2000) suggested that early initiation of statin
therapy may have mortality benefits. Other studies also support a role for statin
therapy after AMI. (Circulation 1998; 98(suppl 1): 1-45; N Engl J Med 1998;
339:1349)
Guidelines to Lipid Management
The patient should go on a diet similar to the AHA Step II diet, which is low in
saturated fat and cholesterol (less than 7% of total calories as saturated fat and less
than 200 mg/d cholesterol). Patients with LDL cholesterol levels greater than 125
mg/dL despite the AHA Step II diet should be placed on drug therapy with the goal of
reducing LDL to less than 100 mg/dL. Patients with normal plasma cholesterol
levels who have a high-density lipoprotein (HDL) cholesterol level less than 35
mg/dL should receive nonpharmacological therapy (eg, exercise) designed to raise it.
Drug therapy using either niacin or gemfibrozil can be added regardless of the LDL
and HDL levels, when the triglyceride level is > 200 mg%. Statin produces the
greatest reduction in LDL cholesterol. Niacin is less effective in reducing LDL
although it is more effective in raising HDL. Resins are rarely sufficiently effective
alone but they can be used to supplemment niacin or statins. For lipid lowering,
statin therapy is generally preferred. The statin dosage should be titrated every four
to six weeks to achieve an LDL-cholesterol level of 90 to 100 mg/dL (2.3 to 2.6
mmol/L). Patients on statins should have their LFT’ s and CPK at regular intervals.
The timing for the initiation of statin therapy has yet to be determined but data
suggest that it may need to be started early in the course of AMI.
VI. Predischarge Noninvasive Testing for the Identification of High-
Risk Patients
Echocardiography, 24 Holter monitoring, treadmill exercise stress testing, myocardial
scintigraphy, signal averaging, heart rate variability are all noninvasive tools that
provide prognostic information. A detailed review is beyond the scope of today’s
lecture.
Haematology Lab Normal Value
Normal Laboratory Values - Patient Test Charts
In the following tables, normal haematology reference values for commonly requested laboratory tests are listed in traditional units and in SI units. The tables are a guideline only. Values are method dependent and
normal lab values may vary between laboratories. | Determination | Normal Reference Value | |||||||||||||||||||||||||||||||
| Conventional units | SI units | |||||||||||||||||||||||||||||||
| Blood, Plasma or Serum | ||||||||||||||||||||||||||||||||
| Ammonia (NH3) - diffusion | 20-120 mcg/dl | 12-70 mcmol/L | ||||||||||||||||||||||||||||||
| Ammonia Nitrogen | 15-45 µg/dl | 11-32 µmol/L | ||||||||||||||||||||||||||||||
| Amylase | 35-118 IU/L | 0.58-1.97 mckat/L | ||||||||||||||||||||||||||||||
| Anion gap (Na+-[Cl - + HCO3- ]) (P) | 7-16 mEq/L | 7-16 mmol/L | ||||||||||||||||||||||||||||||
| Antithrombin III (AT III) | 80–120 U/dl | 800–1200 U/L | ||||||||||||||||||||||||||||||
| Bicarbonate | ||||||||||||||||||||||||||||||||
| Arterial | 21–28 mEq/L | 21–28 mmol/L | ||||||||||||||||||||||||||||||
| Venous | 22–29 mEq/L | 22–29 mmol/L | ||||||||||||||||||||||||||||||
| Bilirubin | ||||||||||||||||||||||||||||||||
| Conjugated (direct) Total | £ 0.2 mg/dl & 0.1–1 mg/dl | £ 4 mcmol/L & 2–18 mcmol/L | ||||||||||||||||||||||||||||||
| Calcitonin | < 100 pg/ml | < 100 ng/L | ||||||||||||||||||||||||||||||
| Calcium | ||||||||||||||||||||||||||||||||
| Total | 8.6–10.3 mg/dl | 2.2–2.74 mmol/L | ||||||||||||||||||||||||||||||
| Ionized | 4.4–5.1 mg/dl | 1–1.3 mmol/L | ||||||||||||||||||||||||||||||
| Carbon dioxide content (plasma) | 21–32 mmol/L | 21–32 mmol/L | ||||||||||||||||||||||||||||||
| Carcinoembryonic antigen | < 3 ng/ml | < 3 mcg/L | ||||||||||||||||||||||||||||||
| Chloride | 95–110 mEq/L | 95–110 mmol/L | ||||||||||||||||||||||||||||||
| Coagulation screen | ||||||||||||||||||||||||||||||||
| Bleeding time | 3–9.5 min | 180–570 sec | ||||||||||||||||||||||||||||||
| Prothrombin time | 10–13 sec | 10–13 sec | ||||||||||||||||||||||||||||||
| Partial thromboplastin time (activated) | 22–37 sec | 22–37 sec | ||||||||||||||||||||||||||||||
| Protein C | 0.7–1.4 µ/ml | 700–1400 U/ml | ||||||||||||||||||||||||||||||
| Protein S | 0.7–1.4 µ/ml | 700–1400 U/ml | ||||||||||||||||||||||||||||||
| Copper, total | 70–160 mcg/dl | 11–25 mcmol/L | ||||||||||||||||||||||||||||||
| Corticotropin (ACTH adrenocorticotropic hormone) - 0800 hr | < 60 pg/ml | < 13.2 pmol/L | ||||||||||||||||||||||||||||||
| Cortisol | ||||||||||||||||||||||||||||||||
| 0800 hr | 5–30 mcg/dl | 138–810 nmol/L | ||||||||||||||||||||||||||||||
| 1800 hr | 2–15 mcg/dl | 50–410 nmol/L | ||||||||||||||||||||||||||||||
| 2000 hr | £ 50% of 0800 hr | £ 50% of 0800 hr | ||||||||||||||||||||||||||||||
| Creatine kinase | ||||||||||||||||||||||||||||||||
| Female | 20–170 IU/L | 0.33–2.83 mckat/L | ||||||||||||||||||||||||||||||
| Male | 30–220 IU/L | 0.5–3.67 mckat/L | ||||||||||||||||||||||||||||||
| Creatinine kinase isoenzymes, MB fraction | 0–12 IU/L | 0–0.2 mckat/L | ||||||||||||||||||||||||||||||
| Creatinine | 0.5–1.7 mg/dl | 44–150 mcmol/L | ||||||||||||||||||||||||||||||
| Fibrinogen (coagulation factor I) | 150–360 mg/dl | 1.5–3.6 g/L | ||||||||||||||||||||||||||||||
| Follicle-stimulating hormone (FSH) | ||||||||||||||||||||||||||||||||
| Female | 2–13 mlU/ml | 2–13 IU/L | ||||||||||||||||||||||||||||||
| Midcycle | 5–22 mlU/ml | 5–22 IU/L | ||||||||||||||||||||||||||||||
| Male | 1–8 mlU/ml | 1–8 IU/L | ||||||||||||||||||||||||||||||
| Glucose, fasting | 65–115 mg/dl | 3.6–6.3 mmol/L | ||||||||||||||||||||||||||||||
| Glucose Tolerance Test (Oral) | ||||||||||||||||||||||||||||||||
| ||||||||||||||||||||||||||||||||
| (g) - Glutamyltransferase (GGT) | ||||||||||||||||||||||||||||||||
| Male | 9–50 units/L | 9–50 units/L | ||||||||||||||||||||||||||||||
| Female | 8–40 units/L | 8–40 units/L | ||||||||||||||||||||||||||||||
| Haptoglobin | 44–303 mg/dl | 0.44–3.03 g/L | ||||||||||||||||||||||||||||||
| Hematologic Tests | ||||||||||||||||||||||||||||||||
| Fibrinogen | 200–400 mg/dl | 2–4 g/L | ||||||||||||||||||||||||||||||
| Hematocrit (Hct) | ||||||||||||||||||||||||||||||||
| female | 36%-44.6% | 0.36–0.446 fraction of 1 | ||||||||||||||||||||||||||||||
| male | 40.7%-50.3% | 0.4–0.503 fraction of 1 | ||||||||||||||||||||||||||||||
| Hemoglobin A 1C | 5.3%-7.5% of total Hgb | 0.053–0.075 | ||||||||||||||||||||||||||||||
| Hemoglobin (Hb) | ||||||||||||||||||||||||||||||||
| female | 12.1–15.3 g/dl | 121–153 g/L | ||||||||||||||||||||||||||||||
| male | 13.8–17.5 g/dl | 138–175 g/L | ||||||||||||||||||||||||||||||
| Leukocyte count (WBC) | 3800–9800/mcl | 3.8–9.8 x 109/L | ||||||||||||||||||||||||||||||
| Erythrocyte count (RBC) | ||||||||||||||||||||||||||||||||
| female | 3.5–5 x 106/mcl | 3.5–5 x 1012/L | ||||||||||||||||||||||||||||||
| male | 4.3–5.9 x 106/mcl | 4.3–5.9 x 1012/L | ||||||||||||||||||||||||||||||
| Mean corpuscular volume (MCV) | 80–97.6 mcm3 | 80–97.6 fl | ||||||||||||||||||||||||||||||
| Mean corpuscular hemoglobin (MCH) | 27–33 pg/cell | 1.66–2.09 fmol/cell | ||||||||||||||||||||||||||||||
| Mean corpuscular hemoglobin concentrate (MCHC) | 33–36 g/dl | 20.3–22 mmol/L | ||||||||||||||||||||||||||||||
| Erythrocyte sedimentation rate (sedrate, ESR) | £30 mm/hr | £30 mm/hr | ||||||||||||||||||||||||||||||
| Erythrocyte enzymes | ||||||||||||||||||||||||||||||||
| Glucose-6 - Pphosphate dehydrognase (G-6-PD) | 250–5000 units/106 cells | 250–5000 mcunits/cell | ||||||||||||||||||||||||||||||
| Determination | Reference Value | |||||||||||||||||||||||||
| (Conventional units) | (SI units) | |||||||||||||||||||||||||
| Blood, Plasma or Serum: Ammonia (NH3) - diffusion | 20–120 mcg/dl | 12–70 mcmol/L | ||||||||||||||||||||||||
| Ammonia Nitrogen | 15–45 µg/dl | 11–32 µmol/L | ||||||||||||||||||||||||
| Amylase | 35–118 IU/L | 0.58–1.97 mckat/L | ||||||||||||||||||||||||
| Anion gap (Na+-[Cl - + HCO3-]) (P) | 7–16 mEq/L | 7–16 mmol/L | ||||||||||||||||||||||||
| Antithrombin III (AT III) | 80–120 U/dl | 800–1200 U/L | ||||||||||||||||||||||||
| 21–28 mEq/L 22–29 mEq/L | 21–28 mmol/L 22–29 mmol/L | ||||||||||||||||||||||||
| Bilirubin: Conjugated (direct) Total | £ 0.2 mg/dl (0.1–1 mg/dl) | £ 4 mcmol/L (2–18 mcmol/L) | ||||||||||||||||||||||||
| Calcitonin | < 100 pg/ml | < 100 ng/L | ||||||||||||||||||||||||
| 8.6–10.3 mg/dl 4.4–5.1 mg/dl | 2.2–2.74 mmol/L 1–1.3 mmol/L | ||||||||||||||||||||||||
| Carbon dioxide content (plasma) | 21–32 mmol/L | 21–32 mmol/L | ||||||||||||||||||||||||
| Carcinoembryonic antigen | < 3 ng/ml | < 3 mcg/L | ||||||||||||||||||||||||
| Chloride | 95–110 mEq/L | 95–110 mmol/L | ||||||||||||||||||||||||
| Coagulation screen: Bleeding time Prothrombin time Partial thromboplastin time (activated) Protein C Protein S | 3–9.5 min 10–13 sec 22–37 sec 0.7–1.4 µ/ml 0.7–1.4 µ/ml | 180–570 sec 10–13 sec 22–37 sec 700–1400 U/ml 700–1400 U/ml | ||||||||||||||||||||||||
| Copper, total | 70–160 mcg/dl | 11–25 mcmol/L | ||||||||||||||||||||||||
| Corticotropin (ACTH adrenocorticotropic hormone) - 0800 hr | < 60 pg/ml | < 13.2 pmol/L | ||||||||||||||||||||||||
| 5–30 mcg/dl 2–15 mcg/dl £ 50% of 0800 hr | 138–810 nmol/L 50–410 nmol/L £ 50% of 0800 hr | ||||||||||||||||||||||||
| 20–170 IU/L 30–220 IU/L | 0.33–2.83 mckat/L 0.5–3.67 mckat/L | ||||||||||||||||||||||||
| Creatinine kinase isoenzymes, MB fraction | 0–12 IU/L | 0–0.2 mckat/L | ||||||||||||||||||||||||
| Creatinine | 0.5–1.7 mg/dl | 44–150 mcmol/L | ||||||||||||||||||||||||
| Fibrinogen (coagulation factor I) | 150–360 mg/dl | 1.5–3.6 g/L | ||||||||||||||||||||||||
| Follicle-stimulating hormone (FSH): Female Midcycle Male | 2–13 mlU/ml 5–22 mlU/ml 1–8 mlU/ml | 2–13 IU/L 5–22 IU/L 1–8 IU/L | ||||||||||||||||||||||||
| Glucose, fasting | 65–115 mg/dl | 3.6–6.3 mmol/L | ||||||||||||||||||||||||
| Glucose Tolerance Test (Oral) Fasting 60 min 90 min 120 min |
|
| ||||||||||||||||||||||||
| (g) -Glutamyltransferase (GGT): Male Female | 9–50 units/L 8–40 units/L | 9–50 units/L 8–40 units/L | ||||||||||||||||||||||||
| Haptoglobin | 44–303 mg/dl | 0.44–3.03 g/L | ||||||||||||||||||||||||
| Determination | Reference Value | |||||||||||||||||||||||||
| Conventional units | SI units | |||||||||||||||||||||||||
| Hematologic tests: Fibrinogen Hematocrit (Hct), female male Hemoglobin A 1C Hemoglobin (Hb), female male Leukocyte count (WBC) Erythrocyte count (RBC): female male Mean corpuscular volume (MCV) Mean corpuscular hemoglobin (MCH) Mean corpuscular hemoglobin concentrate (MCHC) Erythrocyte sedimentation rate (sedrate, ESR) | 200–400 mg/dl 36%-44.6% 40.7%-50.3% 5.3%-7.5% of total Hgb 12.1–15.3 g/dl 13.8–17.5 g/dl 3800–9800/mcl 3.5–5 x 106/mcl 4.3–5.9 x 106/mcl 80–97.6 mcm3 27–33 pg/cell 33–36 g/dl £30 mm/hr | 2–4 g/L 0.36–0.446 fraction of 1 0.4–0.503 fraction of 1 0.053–0.075 121–153 g/L 138–175 g/L 3.8–9.8 x 109/L 3.5–5 x 1012/L 4.3–5.9 x 1012/L 80–97.6 fl 1.66–2.09 fmol/cell 20.3–22 mmol/L £ 30 mm/hr | ||||||||||||||||||||||||
| Erythrocyte enzymes: Glucose-6 - Pphosphate dehydrognase (G-6-PD) Ferritin Folic acid: normal Platelet count Reticulocytes Vitamin B12 | 250–5000 units/106 cells 10–383 ng/ml >3.1–12.4 ng/ml 150–450 x 103/mcl 0.5%-1.5% of erythrocytes 223–1132 pg/ml | 250–5000 mcunits/cell 23–862 pmol/L 7–28.1 nmol/L 150–450 x 109/L 0.005–0.015 165–835 pmol/L | ||||||||||||||||||||||||
| 30–160 mcg/dl 45–160 mcg/dl | 5.4–31.3 mcmol/L 8.1–31.3 mcmol/L | ||||||||||||||||||||||||
| Iron binding capacity | 220–420 mcg/dl | 39.4–75.2 mcmol/L | ||||||||||||||||||||||||
| Isocitrate dehydrogenase | 1.2–7 units/L | 1.2–7 units/L | ||||||||||||||||||||||||
| Isoenzymes Fraction 1 Fraction 2 Fraction 3 Fraction 4 Fraction 5 | 14%-26% of total 29%-39% of total 20%-26% of total 8%-16% of total 6%-16% of total | 0.14–0.26 fraction of total 0.29–0.39 fraction of total 0.20–0.26 fraction of total 0.08–0.16 fraction of total 0.06–0.16 fraction of total | ||||||||||||||||||||||||
| Lactate dehydrogenase | 100–250 IU/L | 1.67–4.17 mckat/L | ||||||||||||||||||||||||
| Lactic acid (lactate) | 6–19 mg/dl | 0.7–2.1 mmol/L | ||||||||||||||||||||||||
| Lead | £ 50 mcg/dl | £ 2.41 mcmol/L | ||||||||||||||||||||||||
| Lipase | 10–150 units/L | 10–150 units/L | ||||||||||||||||||||||||
| Lipids: Total Cholesterol Desirable Borderline-high High LDL Desirable Borderline-high High HDL (low) Triglycerides Desirable Borderline-high High Very high | < 200 mg/dl 200–239 mg/dl > 239 mg/dl < 130 mg/dl 130–159 mg/dl > 159 mg/dl < 35 mg/dl < 200 mg/dl 200–400 mg/dl 400–1000 mg/dl > 1000 mg/dl | < 5.2 mmol/L < 5.2–6.2 mmol/L > 6.2 mmol/L < 3.36 mmol/L 3.36–4.11 mmol/L > 4.11 mmol/L < 0.91 mmol/L < 2.26 mmol/L 2.26–4.52 mmol/L 4.52–11.3 mmol/L > 11.3 mmol/L | ||||||||||||||||||||||||
| Magnesium | 1.3–2.2 mEq/L | 0.65–1.1 mmol/L | ||||||||||||||||||||||||
| Osmolality | 280–300 mOsm/kg | 280–300 mmol/kg | ||||||||||||||||||||||||
| Oxygen saturation (arterial) | 94%-100% | 0.94 - fraction of 1 | ||||||||||||||||||||||||
| PCO2, arterial | 35–45 mm Hg | 4.7–6 kPa | ||||||||||||||||||||||||
| pH, arterial | 7.35–7.45 | 7.35–7.45 | ||||||||||||||||||||||||
| Determination | Reference Value | |||||||||||||||||||||||||
| Conventional units | SI units | |||||||||||||||||||||||||
| PO, arterial: Breathing room air On 100% O | 80–105 mm Hg > 500 mm Hg | 10.6–14 kPa | ||||||||||||||||||||||||
| Phosphatase (acid), total at 37°C | 0.13–0.63 IU/L | 2.2–10.5 IU/L or 2.2–10.5 mckat/L | ||||||||||||||||||||||||
| Phosphatase alkaline | 20–130 IU/L | 20–130 IU/L or 0.33–2.17 mckat/L | ||||||||||||||||||||||||
| Phosphorus, inorganic, (phosphate) | 2.5–5 mg/dl | 0.8–1.6 mmol/L | ||||||||||||||||||||||||
| Potassium | 3.5–5 mEq/L | 3.5–5 mmol/L | ||||||||||||||||||||||||
| Progesterone Female Follicular phase Luteal phase Male | 0.1–1.5 ng/ml 0.1–1.5 ng/ml 2.5–28 ng/ml < 0.5 ng/ml | 0.32–4.8 nmol/L 0.32–4.8 nmol/L 8–89 nmol/L < 1.6 nmol/L | ||||||||||||||||||||||||
| Prolactin | 1.4–24.2 ng/ml | 1.4–24.2 mcg/L | ||||||||||||||||||||||||
| Prostate specific antigen Protein: Total Albumin Globulin | 0–4 ng/ml 6–8 g/dl 3.6–5 g/dl 2.3–3.5 g/dl | 0–4 ng/ml 60–80 g/L 36–50 g/L 23–35 g/L | ||||||||||||||||||||||||
| Rheumatoid factor | < 60 IU/ml | < 60 kIU/L | ||||||||||||||||||||||||
| Sodium | 135–147 mEq/L | 135–147 mmol/L | ||||||||||||||||||||||||
| Testosterone: Female Male | 6–86 ng/dl 270–1070 ng/dl | 0.21–3 nmol/L 9.3–37 nmol/L | ||||||||||||||||||||||||
| Thyroid Hormone Function Tests: Thyroid-stimulating hormone (TSH) Thyroxine-binding globulin capacity Total triiodothyronine (T3) Total thyroxine by RIA (T4) T3 resin uptake | 0.35–6.2 mcU/ml 10–26 mcg/dl 75–220 ng/dl 4–11 mcg/dl 25%-38% | 0.35–6.2 mU/L 100–260 mcg/L 1.2–3.4 nmol/L 51–142 nmol/L 0.25–0.38 fraction of 1 | ||||||||||||||||||||||||
| Transaminase, AST (aspartate aminotransferase, SGOT) | 11–47 IU/L | 0.18–0.78 mckat/L | ||||||||||||||||||||||||
| Transaminase, ALT (alanine aminotransferase, SGPT) | 7–53 IU/L | 0.12–0.88 mckat/L | ||||||||||||||||||||||||
| Transferrin | 220–400 mg/dL | 2.20–4.00 g/L | ||||||||||||||||||||||||
| Urea nitrogen (BUN) | 8–25 mg/dl | 2.9–8.9 mmol/L | ||||||||||||||||||||||||
| Uric acid | 3–8 mg/dl | 179–476 mcmol/L | ||||||||||||||||||||||||
| Vitamin A (retinol) | 15–60 mcg/dl | 0.52–2.09 mcmol/L | ||||||||||||||||||||||||
| Zinc | 50–150 mcg/dl | 7.7–23 mcmol/L | ||||||||||||||||||||||||
2 Infants and adolescents up to 104 U/L
3 Infants in the first year up to 6 mg/dl
| Urine | ||
| Determination | Reference Value | |
| Conventional units | SI units | |
| Calcium | 50–250 mcg/day | 1.25–6.25 mmol/day |
| Catecholamines: Epinephrine Norepinephrine | < 20 mcg/day < 100 mcg/day | < 109 nmol/day < 590 nmol/day |
| Catecholamines, 24-hr | < 110 µg | < 650 nmol |
| Copper | 15–60 mcg/day | 0.24–0.95 mcmol/day |
| Creatinine: Child Adolescent Female Male | 8–22 mg/kg 8–30 mg/kg 0.6–1.5 g/day 0.8–1.8 g/day | 71–195 µmol/kg 71–265 µmol/kg 5.3–13.3 mmol/day 7.1–15.9 mmol/day |
| pH | 4.5–8 | 4.5–8 |
| Phosphate | 0.9–1.3 g/day | 29–42 mmol/day |
| Potassium | 25–100 mEq/day | 25–100 mmol/day |
| Protein Total At rest | 1–14 mg/dL 50–80 mg/day | 10–140 mg/L 50–80 mg/day |
| Protein, quantitative | < 150 mg/day | < 0.15 g/day |
| Sodium | 100–250 mEq/day | 100–250 mmol/day |
| Specific gravity, random | 1.002–1.030 | 1.002–1.030 |
| Uric acid, 24-hr | 250–750 mg | 1.48–4.43 mmol |
| Drug Levels* | |||
| Drug Determination | Reference Value | ||
| Conventional units | SI units | ||
| Aminoglycosides | Amikacin (trough) (peak) | 1–8 mcg/ml 1.7–13.7 mcmol/L | 20–30 mcg/ml 34–51 mcmol/L |
| Gentamicin (trough) (peak) | 0.5–2 mcg/ml 6–10 mcg/ml | 1–4.2 mcmol/L 12.5–20.9 mcmol/L | |
| Kanamycin (trough) (peak) | 5–10 mcg/ml 20–25 mcg/ml | nd nd | |
| Netilimicin (trough) (peak) | 0.5–2 mcg/ml 6–10 mcg/ml | nd nd | |
| Streptomycin (trough) (peak) | < 5 mcg/ml 5–20 mcg/ml | nd nd | |
| Tobramycin (trough) (peak) | 0.5–2 mcg/ml 5–20 mcg/ml | 1.1–4.3 mcmol/L 12.8–21.8 mcmol/L | |
| Drug Determination | Reference Value | ||
| Conventional units | SI units | ||
| Antiarrhythmics | Amiodarone | 0.5–2.5 mcg/ml | 1.5–4 mcmol/L |
| Bretylium | 0.5–1.5 mcg/ml | nd | |
| Digitoxin | 9–25 mcg/L | 11.8–32.8 nmol/L | |
| Digoxin | 0.8–2 ng/ml | 0.9–2.5 nmol/L | |
| Disopyramide | 2–8 mcg/ml | 6–18 mcmol/L | |
| Flecainide | 0.2–1 mcg/ml | nd | |
| Lidocaine | 1.5–6 mcg/ml | 4.5–21.5 mcmol/L | |
| Mexiletine | 0.5–2 mcg/ml | nd | |
| Procainamide | 4–8 mcg/ml | 17–34 mcmol/ml | |
| Propranolol | 50–200 ng/ml | 190–770 nmol/L | |
| Quinidine | 2–6 mcg/ml | 4.6–9.2 mcmol/L | |
| Tocainide | 4–10 mcg/ml | nd | |
| Verapamil | 0.08–0.3 mcg/ml | nd | |
| Anticonvulsants | Carbamazepine | 4–12 mcg/ml | 17–51 mcmol/L |
| Phenobarbital | 10–40 mcg/ml | 43–172 mcmol/L | |
| Phenytoin | 10–20 mcg/ml | 40–80 mcmol/L | |
| Primidone | 4–12 mcg/ml | 18–55 mcmol/L | |
| Valproic Acid | 40–100 mcg/ml | 280–700 mcmol/L | |
| Antidepressants | Amitriptyline | 110–250 ng/ml | 500–900 nmol/L |
| Amoxapine | 200–500 ng/ml | nd | |
| Bupropion | 25–100 ng/ml | nd | |
| Clomipramine | 80–100 ng/ml | nd | |
| Desipramine | 115–300 ng/ml | nd | |
| Doxepin | 110–250 ng/ml | nd | |
| Imipramine | 225–350 ng/ml | nd | |
| Maprotiline | 200–300 ng/ml | nd | |
| Nortriptyline | 50–150 ng/ml | nd | |
| Protriptyline | 70–250 ng/ml | nd | |
| Trazodone | 800–1600 ng/ml | nd | |
| Antipsychotics | Chlorpromazine | 50–300 ng/ml | 150–950 nmol/L |
| Fluphenazine | 0.13–2.8 ng/ml | nd | |
| Haloperidol | 5–20 ng/ml | nd | |
| Perphenazine | 0.8–1.2 ng/ml | nd | |
| Thiothixene | 2–57 ng/ml | nd | |
| Drug Determination | Reference Value | ||
| Conventional units | SI units | ||
| Miscellaneous | Amantadine Amrinone | 300 ng/ml 3.7 mcg/ml | nd nd |
| Chloramphenicol | 10–20 mcg/ml | 31–62 mcmol/L | |
| Cyclosporine | 250–800 ng/ml (whole blood, RIA) 50–300 ng/ml (plasma, RIA) | nd nd | |
| Ethanol | 0 mg/dl | 0 mmol/L | |
| Hydralazine | 100 ng/ml | nd | |
| Lithium | 0.6–1.2 mEq/L | 0.6–1.2 mmol/L | |
| Salicylate | 100–300 mg/L | 724–2172 mcmol/L | |
| Sulfonamide | 5–15 mg/dl | nd | |
| Terbutaline | 0.5–4.1 ng/ml | nd | |
| Theophylline | 10–20 mcg/ml | 55–110 mcmol/L | |
| Vancomycin (trough) (peak) | 5–15 ng/ml 20–40 mcg/ml | nd nd | |
1 nd = No data available.
2 Parent drug plus N-desmethyl metabolite.
3 24–hour trough values.
4 Toxic: 50–100 mg/dl (10.9–21.7 mmol/L).
The following table is adopted from the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, National Institutes of Health.
| Classification of Blood Pressure * | |||
| Category | Reference value | ||
| Systolic (mm Hg) | Diastolic (mm Hg) | ||
| Optimal | < 120 | and | < 80 |
| Normal | < 130 | and | < 85 |
| High-normal | 130–139 | or | 85–89 |
| Hypertension Stage 1 Stage 2 Stage 3 | 140–159 160–179 ³ 180 | or or or | 90–99 100–109 ³ 110 |
* For adults age 18 and older who are not taking antihypertensive drugs and not acutely ill. When systolic and diastolic blood pressures fall into different categories, the higher category should be selected to classify the individual's blood pressure status. In addition to classifying stages of hypertension on the basis of average blood pressure levels, clinicians should specify presence or absence of target organ disease and additional risk factors.
1 Optimal blood pressure with respect to cardiovascular risk is below 120/88 m Hg. However, unusually low readings should be evaluated for clinical significance.
2 Based on the average of two or more readings taken at each of two or more visits after an initial screening.
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