ا.د/شريف مختار
Acute coronary syndrome management
المحاضرة التي قدمت يوم الاربعاء 9 ابريل 2014 في دار الحكمة بالقاهرة
من فعاليات مشروع اعداد طبيب حكيم ناجح بالتعاون مع معتمد باتحاد الاطباء العرب
و ضمن موديول الطوارئ و التخدير و العناية المركزة
Acute coronary syndrome result from a sudden blockage in a coronary artery. this blockage causes unstable angina or heart attack (MI), depending on the location and amount of blockage.
people who experience an ACS usually have chest pressure or ache, shortness of breath and fatigue.
People who think they are experiencing ACS should call for emergency help.
Doctors use ECG and blood test (troponin level) to determine whether a person is experiencing an ACS.
Treatment varies depending on the type of syndrome but usually include attempts to increase blood flow to affected area.
ا.د/شريف مختار
Acute coronary syndrome management
المحاضرة التي قدمت يوم الاربعاء 9 ابريل 2014 في دار الحكمة بالقاهرة
من فعاليات مشروع اعداد طبيب حكيم ناجح بالتعاون مع معتمد باتحاد الاطباء العرب
و ضمن موديول الطوارئ و التخدير و العناية المركزة
Acute coronary syndrome result from a sudden blockage in a coronary artery. this blockage causes unstable angina or heart attack (MI), depending on the location and amount of blockage.
people who experience an ACS usually have chest pressure or ache, shortness of breath and fatigue.
People who think they are experiencing ACS should call for emergency help.
Doctors use ECG and blood test (troponin level) to determine whether a person is experiencing an ACS.
Treatment varies depending on the type of syndrome but usually include attempts to increase blood flow to affected area.
Made by Ranjith R Thampi. This was a powerpoint I had made for a Cardiology Seminar during internship. Got it checked by cardiologists, all approved. Covers management of UA, NSTEMI and STEMI. This was my favorite topic. I think the flowcharts will be clear to the point. Kindly comment and let me know.
A presentatation on Acute coronary syndrome made while in Emergency Department. If you are making a presentation on ACS, you may want to add more on TIMI score as it is important. Some problems with display of pictures/diagrams due to ?conversion problems. Based on AHA Guidelines 2010 and from Harrison's 18th Ed.. Made using OpenOffice.
Made by Ranjith R Thampi. This was a powerpoint I had made for a Cardiology Seminar during internship. Got it checked by cardiologists, all approved. Covers management of UA, NSTEMI and STEMI. This was my favorite topic. I think the flowcharts will be clear to the point. Kindly comment and let me know.
A presentatation on Acute coronary syndrome made while in Emergency Department. If you are making a presentation on ACS, you may want to add more on TIMI score as it is important. Some problems with display of pictures/diagrams due to ?conversion problems. Based on AHA Guidelines 2010 and from Harrison's 18th Ed.. Made using OpenOffice.
this is a slide on myocardial infraction to figure you out what exactly it is !
though i have not mentioned the diet based causes ............etc.
so enjoy
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Antimicrobial stewardship to prevent antimicrobial resistanceGovindRankawat1
India is among the nations with the highest burden of bacterial infections.
India is one of the largest consumers of antibiotics worldwide.
India carries one of the largest burdens of drug‑resistant pathogens worldwide.
Highest burden of multidrug‑resistant tuberculosis,
Alarmingly high resistance among Gram‑negative and Gram‑positive bacteria even to newer antimicrobials such as carbapenems.
NDM‑1 ( New Delhi Metallo Beta lactamase 1, an enzyme which inactivates majority of Beta lactam antibiotics including carbapenems) was reported in 2008
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
Thyroid Gland- Gross Anatomy by Dr. Rabia Inam Gandapore.pptx
Management acute coronary syndrome
1. ACUTE CORONARY SYNDROME
The newest management
Nahar Taufiq
Jogja International Hospital
Yogyakarta
2. Atherothrombosis* is the
Leading Cause of Death Worldwide1
Pulmonary Disease 6.3
Injuries 9
AIDS 9.7
Cancer 12.6
Infectious Disease 19.3
Atherothrombosis* 22.3
0 5 10 15 20 25 30
Causes of Mortality (%)
*Atherothrombosis defined as ischemic heart disease and cerebrovascular disease.
1
The World Health Report 2001. Geneva: WHO; 2001.
Reprod.with permission from Cannon CP. Atherothrombosis slide compendium. Available at: www.theheart.org.
3. Atherothrombosis: A Generalized and
Progressive Disease
Atherothrombosis
Unstable
angina ACS
MI
Ischemic
stroke/TIA
Atherosclerosis Critical leg
ischemia
Intermittent
claudication
CV death
Stable angina/Intermittent claudication
MI = Myocardial infarction
ACS = Acute coronary syndromes
Adapted from Libby P. Circulation 2001; 104: 365–372
CV = Cardiovascular
8. P Ex ED Evaluation of Patients
Brief Physical Examination in the ED
1. Airway, Breathing, Circulation (ABC)
2. Vital signs, general observation
3. Presence or absence of jugular venous distension
4. Pulmonary auscultation for rales
5. Cardiac auscultation for murmurs and gallops
6. Presence or absence of stroke
7. Presence or absence of pulses
8. Presence or absence of systemic hypoperfusion (cool,
clammy, pale, ashen)
9. P Ex ED Evaluation of Patients
Differential Diagnosis of STEMI: Life-Threatening
Aortic dissection Tension pneumothorax
Pulmonary Boerhaave syndrome
embolus (esophageal rupture with
Perforating ulcer mediastinitis)
10. P Ex ED Evaluation of Patients
Differential Diagnosis of STEMI:
Other Cardiovascular and Nonischemic
Pericarditis LV hypertrophy with
Atypical angina strain
Early repolarization Brugada syndrome
Wolff-Parkinson-White
syndrome Myocarditis
Deeply inverted T- Hyperkalemia
waves suggestive of a Bundle-branch blocks
central nervous
system lesion or Vasospastic angina
apical hypertrophic Hypertrophic
cardiomyopathy cardiomyopathy
11. P Ex ED Evaluation of Patients
Differential Diagnosis of STEMI: Other Noncardiac
Gastroesophageal Cervical disc or
reflux (GERD) and neuropathic pain
spasm Biliary or pancreatic pain
Chest-wall pain Somatization and
Pleurisy psychogenic pain
disorder
Peptic ulcer disease
Panic attack
12. Dx Electrocardiogram
I IIa IIb III If the initial ECG is not diagnostic of STEMI,
serial ECGs or continuous ST-segment
monitoring should be performed in the patient
who remains symptomatic or if there is high
clinical suspicion for STEMI.
13. Dx Electrocardiogram
I IIa IIb III Show 12-lead ECG results to emergency
physician within 10 minutes of ED arrival in all
patients with chest discomfort (or anginal
equivalent) or other symptoms of STEMI.
I IIa IIb III In patients with inferior STEMI, ECG leads
should also be obtained to screen for right
ventricular infarction.
14. Dx Laboratory Examinations
I IIa IIb III Laboratory examinations should be performed as part
of the management of STEMI patients, but should not
delay the implementation of reperfusion therapy.
Serum biomarkers for cardiac damage
Complete blood count (CBC) with platelets
International normalized ratio (INR)
Activated partial thromboplastin time (aPTT)
Electrolytes and magnesium
Blood urea nitrogen (BUN)
Creatinine
Glucose
Complete lipid profile
15. Dx Biomarkers of Cardiac Damage
I IIa IIb III Cardiac-specific troponins should be used as
the optimum biomarkers for the evaluation of
patients with STEMI who have coexistent
skeletal muscle injury.
I IIa IIb III For patients with ST elevation on the 12-lead
ECG and symptoms of STEMI, reperfusion
therapy should be initiated as soon as
possible and is not contingent on a biomarker
assay.
16. Tx Oxygen
I IIa IIb III
Supplemental oxygen should be administered to
patients with arterial oxygen desaturation (SaO2
< 90%).
I IIa IIb III
It is reasonable to administer supplemental
oxygen to all patients with uncomplicated STEMI
during the first 6 hours.
17. Nitroglycerin
Tx
I IIa IIb III Patients with ongoing ischemic discomfort
should receive sublingual NTG (0.4 mg) every 5
minutes for a total of 3 doses, after which an
assessment should be made about the need for
intravenous NTG.
I IIa IIb III
Intravenous NTG is indicated for relief of ongoing
ischemic discomfort that responds to nitrate
therapy, control of hypertension, or management
of pulmonary congestion.
18. Tx Nitroglycerin
I IIa IIb III
Nitrates should not be administered to patients
with:
• systolic pressure < 90 mm Hg or ≥ to 30 mm
Hg below baseline
• severe bradycardia (< 50 bpm)
• tachycardia (> 100 bpm) or
• suspected RV infarction.
I IIa IIb III
Nitrates should not be administered to patients
who have received a phosphodiesterase inhibitor
for erectile dysfunction within the last 24 hours
(48
hours for tadalafil).
19. Tx Analgesia
Morphine sulfate (2 to 4 mg intravenously
I IIa IIb III
with increments of 2 to 8 mg intravenously
repeated at 5 to 15 minute intervals) is the
analgesic of choice for management of pain
associated with STEMI.
20. Tx Aspirin
I IIa IIb III
Aspirin should be chewed by patients who
have not taken aspirin before presentation
I IIa IIb III
with STEMI. The initial dose should be 162
mg (Level of Evidence: A) to 325 mg (Level of
Evidence: C)
Although some trials have used enteric-coated aspirin
for initial dosing, more rapid buccal absorption occurs
with non–enteric-coated formulations.
21. Tx Clopidogrel in Non STEMI
Cumulative events (myocardial infarction, stroke, or cardiovascular death)
Cumulative hazard rate
0.14 Placebo * (n =6,303)
20%
0.12
0.10
0.08 Clopidogrel * (n = 6,259)
0.06
p < 0.0001
0.04
0.02
0.00
0 3 6 9 12
Months of follow-up
*On top of standard therapy (including acetylsalicylic acid)
The CURE Trial Investigators. N Engl J Med 2001; 345: 494–502
22. Tx Clopidogrel in Non STEMI
1 0.9
Bleeding rate (%)
0.8 0.7
0.6
0.4
0.2
0.2 0.1
0
Fatal Intracranial Require surg Drop of Hb
interv > 5 g/dl
The CURE Investigators. N Engl J Med 2001;345:494-502
23. Tx Clopidogrel in Non STEMI
Primary endpoint ‡ ) during 24 hours
0.025
0.020 Placebo
Cumulative hazard
0.015
0.010
Clopidogrel
0.005 P=0.003
rates
0.0
0 2 4 6 8 10 12 14 16 18 20 22 24
Hours after randomization
‡ Cardiovascular death, myocardial infarction, stroke and severe ischemia
Yusuf S et al. Circulation 2003; 107: 966–972
24. Tx Clopidogrel in STEMI
Placebo (10.1%)
10
reinfarction or stroke before first
Proportion with death, 9
8 Clopidogrel (9.3%)
discharge (%)
7
6
RRR=9%
5
P=0.002
4
3
2
1
0
0 7 14 21 28
Time since randomization (days)
COMMIT= ClOpidogrel and Metoprolol in Myocardial Infarction Trial
COMMIT Collaborative Group. Lancet 2005;366:1607-21
25. CLARITY-TIMI 28: angka kejadian kumulative
dalam 30 hari
15
Placebo
20%
End point * (%)
10 Clopidogrel
5
P=0.03
0
0 5 10 20 25 30
Days
* Cardiovascular death, recurrent MI, or recurrent ischemia leading
to the need for urgent revascularization
Sabatine MS et al for the CLARITY-TIMI 28 Investigators. N Engl J Med 2005;352:1179-89
26. CLARITY-TIMI 28: Tingkat keamanan dalam 30
hari
ASA + CLO
ASA P=0.24
4
P=0.80 3.4
P=0.12
3
2.7
% of patients
2 1.9
1.7 1.6
1 0.9
0
Major bleeding Minor bleeding Major or minor
bleeding
27. Tx Onset of antiplatelet
Agent Dose Onset
Aspirin Dosis 80 - 320 mg1 15 - 30 minutes
Clopidogrel 75 mg maintenance dose2 Max at 3-7 days
300 mg loading dose3 Max at 24 to 48 h
600 mg loading dose4 Max at 2 h
900 mg loading same with 600 mg loading
dose3 dose
Ticlopidine 250 mg 2x perhari5 50% pada 5 hari dan
maksimum 8-11 hari
1 Dabaghi SF et al. Am J Cardiol 1994;74:720-3. 2. Savcic M et al. Semin Thromb Hemost 1999;25:15-19
3 Quinn MJ, Fitzgerald DJ. Circulation 1999;100:1667-72 4. Hochholzer W et al. Circulation
2005;111:2560-4 5. Lubbe DF, Berger PB. J Interv Cardiol
28. Tx Beta-Blockers
Oral beta-blocker therapy should be
I IIa IIb III
administered promptly to those patients without
a contraindication, irrespective of concomitant
fibrinolytic therapy or performance of primary
PCI.
I IIa IIb III
It is reasonable to administer intravenous beta-
blockers promptly to STEMI patients without
contraindications, especially if a tachyarrhythmia
or hypertension is present.
29. Summary of Trials of Beta-Blocker Therapy
Phase of Total No. RR (95% CI)
Treatment Patients
Acute 28,970 0.87 (0.77-0.98)
treatment
Secondary 24,298 0.77 (0.70-0.84)
prevention
Overall 53,268 0.81 (0.75-0.87)
0.5 1 2
Relative risk (RR) of death
Beta blocker Placebo
better better
Antman E, Braunwald E. Acute Myocardial Infarction. In:
Braunwald E, Zipes DP, Libby P, eds. Heart Disease: A
textbook of Cardiovascular Medicine, 6th ed.,
Philadelphia, PA: W.B. Sanders, 2001, 1168.
30. Tx
Reperfusion Therapy and
Recommendations
STEMI
31. Tx Reperfusion
The medical system goal is to facilitate rapid
recognition and treatment of patients with STEMI
such that door-to- needle (or medical contact–to-
needle) time for initiation of fibrinolytic therapy
can be achieved within 30 minutes or that door-
to-balloon (or medical contact–to- balloon) time for
PCI can be kept within 90 minutes.
32. Treatment Delayed is Treatment Denied
Symptom Call to PreHospital ED-JIH Cath Lab
Recognition Medical System
Increasing Loss of Myocytes
Delay in Initiation of Reperfusion Therapy
33. Reperfusion Options for STEMI Patients
Select Reperfusion Treatment.
If presentation is < 3 hours and there is no delay to an invasive
strategy, there is no preference for either strategy.
Fibrinolysis generally preferred
Early presentation ( ≤ 3 hours from symptom
onset and delay to invasive strategy)
Invasive strategy not an option
Cath lab occupied or not available
Vascular access difficulties
No access to skilled PCI lab
Delay to invasive strategy
Prolonged transport
Door-to-balloon more than 90 minutes
> 1 hour vs fibrinolysis (fibrin-specific agent) now
34. Reperfusion Options for STEMI Patients
Select Reperfusion Treatment.
If presentation is < 3 hours and there is no delay to an invasive strategy,
there is no preference for either strategy.
Invasive strategy generally preferred
Skilled PCI lab available with surgical backup
Door-to-balloon < 90 minutes
• High Risk from STEMI
Cardiogenic shock, Killip class ≥ 3
Contraindications to fibrinolysis, including
increased risk of bleeding and ICH
Late presentation
> 3 hours from symptom onset
Diagnosis of STEMI is in doubt
36. Comparison of Heparin + ASA vs ASA Alone
Theroux
RISC
Cohen 1990
ATACS
Holdright
Gurfinkel
Summary Relative Risk
0.67 (0.44-0.1.02)
0.1 1 10
Heparin + ASA RR: ASA Alone
55/698=7.9% Death/MI 68/655=10.4%
ASA indicates acetylsalicylic acid; RISC, Research on InStability in Coronary artery disease; ATACS, Antithrombotic Therapy in Acute
Company Syndromes; RR, relative risk; and MI, myocardial infarction.
Data from Oler A, Whooley MA, Oler J, et al. Adding heparin to aspirin reduces the incidence of myocardial infarction and death in
patients with unstable angina: a meta-analysis. JAMA. 1996;276:811-815. Slide reproduced with permission from Cannon CP.
Atherothrombosis slide compendium. Available at: www.theheart.org.
38. TIMI 11B: Enoxaparin vs.
Heparin in NSTE-ACS
20 Unfractionated Heparin
16.7 %
Urgent Revascularization
Enoxaparin (Lovenox)
16
Death, MI or
12 14.2 %
8
p = 0.03
4 Relative Risk Reduction = 15%
0 2 4 6 8 10 12 14
Days
Adapted from Antman EM, et al. Circulation. 1999;100:1593-1601.
39. ACC/AHA Recommendations for
Antithrombin Therapy in Patients with
NSTE-ACS
• Class I
– Anticoagulation with subcutaneous LMWH or intravenous
UFH should be added to antiplatelet therapy
– Dose of UFH 60-70 U/kg (max 5000) IV followed by
infusion of 12-15 U/kg/hr (initial max 1000 U/hr) titrated
to aPTT 1.5-2.5 times control
– Dose of enoxaparin 1 mg/kg subcutaneously q12 hr; the
first dose may be preceded by a 30-mg IV bolus
• Class IIa
– Enoxaparin is preferable to UFH as an anticoagulant
unless CABG is planned within 24 hours
Available at: www.acc.org/clinical/guidelines/unstable/unstable.pdf.
43. Guidelines for the Use of Enoxaparin in Patients
with NSTE-ACS
• 1 mg/kg SQ q12 hours (actual body weight)
– An initial 30 mg IV dose can be considered
• Adjust dosing if CrCl <30 cc/min
– 1 mg/kg SQ q24 hours
• Do not follow PTT; do not adjust based on PTT
• Stop if platelets ↓ by 50% or below 100,000/mm3
• If patient to undergo PCI:
– 0-8 hours since last SQ dose: no additional
antithrombin therapy
– 8-12 hours since last SQ dose: 0.3 mg/kg IV
immediately prior to PCI
44. Applying Classification of
Recommendations and Level of Evidence
Class I Class IIa Class IIb Class III
Benefit >>> Risk Benefit >> Risk Benefit ≥ Risk Risk ≥ Benefit
Additional studies with Additional studies with No additional studies
focused objectives broad objectives needed; needed
needed Additional registry data
would be helpful Procedure/Treatment
Procedure/ Treatment IT IS REASONABLE to should NOT be
SHOULD be perform Procedure/Treatment performed/administered
performed/ procedure/administer MAY BE CONSIDERED SINCE IT IS NOT
administered treatment HELPFUL AND MAY BE
HARMFUL
should is reasonable may/might be considered is not recommended
is recommended can be useful/effective/ may/might be reasonable is not indicated
is indicated beneficial usefulness/effectiveness is should not
is useful/effective/ is probably recommended or unknown /unclear/uncertain is not
beneficial indicated or not well established useful/effective/beneficial
may be harmful
45. Applying Classification of
Recommendations and Level of Evidence
Level A Class I Class IIa Class IIb Class III
Multiple (3-5) • Recommen- • Recommen- • Recommen- • Recommen-
population risk dation that dation in favor dation’s dation that
strata evaluated procedure or of treatment or usefulness/ procedure or
treatment is procedure efficacy less treatment not
General useful/ being useful/ well useful/effective
consistency of effective effective established and may be
direction and • Sufficient • Some • Greater harmful
magnitude of evidence from conflicting conflicting • Sufficient
effect multiple evidence from evidence from evidence from
randomized multiple multiple multiple
trials or meta- randomized randomized randomized
analyses trials or meta- trials or meta- trials or meta-
analyses analyses analyses
46. Applying Classification of
Recommendations and Level of Evidence
Level B Class I Class IIa Class IIb Class III
Limited (2-3) • Recommen- • Recommen- • Recommen- • Recommen-
population risk dation that dation in favor dation’s dation that
strata evaluated procedure or of treatment or usefulness/ procedure or
treatment is procedure efficacy less treatment not
useful/effective being useful/ well established useful/effective
• Limited effective • Greater and may be
evidence from • Some conflicting harmful
single conflicting evidence from • Limited
randomized evidence from single evidence from
trial or non- single randomized trial single
randomized randomized or non- randomized trial
studies trial or non- randomized or non-
randomized studies randomized
studies studies
47. Applying Classification of
Recommendations and Level of Evidence
Level C Class I Class IIa Class IIb Class III
Very limited (1- • Recommen- • Recommen- • Recommen- • Recommend-
2) population dation that dation in favor dation’s ation that
risk strata procedure or of treatment or usefulness/ procedure or
evaluated treatment is procedure efficacy less treatment not
useful/ being well established useful/effective
effective useful/effective • Only diverging and may be
• Only expert • Only diverging expert opinion, harmful
opinion, case expert opinion, case studies, or • Only expert
studies, or case studies, or standard-of- opinion, case
standard-of- standard-of- care studies, or
care care standard-of-
care
48. Contraindications and Cautions
for Fibrinolysis in STEMI
Absolute • Any prior intracranial hemorrhage
Contraindications • Known structural cerebral vascular lesion
(e.g., arteriovenous malformation)
• Known malignant intracranial neoplasm
(primary or metastatic)
• Ischemic stroke within 3 months EXCEPT
acute ischemic stroke within 3 hours
NOTE: Age restriction for fibrinolysis has been removed
compared with prior guidelines.
49. Contraindications and Cautions
for Fibrinolysis in STEMI
Absolute • Suspected aortic dissection
Contraindications
• Active bleeding or bleeding diathesis
(excluding menses)
• Significant closed-head or facial trauma
within 3 months
50. Contraindications and Cautions
for Fibrinolysis in STEMI
Relative • History of chronic, severe, poorly controlled
Contraindications hypertension
• Severe uncontrolled hypertension on
presentation (SBP > 180 mm Hg or DBP >
110 mm Hg)
• History of prior ischemic stroke greater than
3 months, dementia, or known intracranial
pathology not covered in contraindications
• Traumatic or prolonged (> 10 minutes) CPR
or major surgery (< 3 weeks)
51. Contraindications and Cautions
for Fibrinolysis in STEMI
Relative • Recent (< 2 to 4 weeks) internal bleeding
Contraindications • Noncompressible vascular punctures
• For streptokinase/anistreplase: prior
exposure (> 5 days ago) or prior allergic
reaction to these agents
• Pregnancy
• Active peptic ulcer
• Current use of anticoagulants: the higher the
INR, the higher the risk of bleeding
Editor's Notes
Atherothrombosis is leading cause of death worldwide.
Atherosclerosis is an ongoing process affecting mainly large- and medium-sized arteries; it can begin in childhood and progresses throughout a person’s lifetime. 1 Stable atherosclerotic plaques may encroach on the lumen of the artery and cause chronic ischemia, resulting in (stable) angina pectoris or intermittent claudication, depending on the vascular bed affected. Unstable atherosclerotic plaques may rupture, leading to the formation of a platelet-rich thrombus that partially or completely occludes the artery and causes acute ischemic symptoms. 2 A large rupture typically results in the formation of a large thrombus that completely occludes the vessel, resulting in an acute vascular event. A smaller rupture may result in a mural thrombus that partially or transiently occludes the artery, causing acute ischemia and, in the long term, contributing to progression of atherothrombosis. References Jager A, Stehouwer CDA. Early detection of diabetic and non-diabetic subjects with increased cardiovascular risk: new risk indicators. Heart and Metabolism . Available at: www.heartandmetabolism.org/HMScardiac_metabolism.htm. (Last accessed 3 March, 2003). Rauch U et al . Ann Intern Med. 2001; 134: 224 – 238.
Patients who present with ST segment depression have at least as great a six-month risk of mortality as those who present with ST-segment-elevation ACS, emphasizing the importance of aggressive in-hospital and post-discharge therapy.
Individual studies and cumulative data strongly suggest the additional benefit of risk reduction in patients with unstable angina when unfractionated heparin is added to treatment with aspirin.
The ESSENCE study was the first major study to demonstrate a reduction in major adverse cardiac events in patients with NSTE-ACS randomized to treatment with the low molecular weight heparin enoxaparin.
In TIMI 11B, patients with NSTE-ACS were randomized to treatment with either the low-molecular-weight heparin enoxaparin (30 mg IV then 1 mg/kg SC q 12 hrs) or unfractionated heparin. At 14 days, the composite primary ischemic endpoint was statistically significantly lower in those treated with enoxaparin, similar to what was observed in the ESSENCE study.
The ACC/AHA Guidelines Update for the Management of Patients with Unstable Angina and Non-ST-Segment Elevation Myocardial Infarction make several recommendations regarding antithrombin therapy in patients with NSTE-ACS. The use of either unfractionated heparin (UFH) or a low molecular weight heparin (LMWH) is a class I recommendation. Based primarily on the ESSENCE and TIMI 11B studies, a class IIa recommendation was that enoxaparin was preferable to UFH. Whether this preferential recommendation changes as a result of the SYNERY study remains to be determined.
Guidelines for the use of enoxaparin in patients with NSTE-ACS.