This document provides an overview of acute coronary syndrome (ACS). It begins with a review of coronary artery anatomy and variations. It then discusses the presentations of ACS, including ischemic chest pain and equivalents. The main types of ACS - unstable angina, NSTEMI, and STEMI - are defined based on symptoms, electrocardiogram findings, and cardiac biomarker levels. Diagnosis and management strategies are outlined, including reperfusion therapies and drug treatments. Follow-up care after ACS and indications for procedures like cardiac catheterization and ICD placement are also summarized.
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.
Ventricular tachycardia (VT) is a broad complex tachycardia originating from a ventricular ectopic focus. It is defined as three or more ventricular extrasystoles in succession at a rate of more than 120 beats per minute (bpm). Accelerated idioventricular rhythm refers to ventricular rhythms with rates of 100-120 bpm
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.
Ventricular tachycardia (VT) is a broad complex tachycardia originating from a ventricular ectopic focus. It is defined as three or more ventricular extrasystoles in succession at a rate of more than 120 beats per minute (bpm). Accelerated idioventricular rhythm refers to ventricular rhythms with rates of 100-120 bpm
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
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 lecture details the science of sepsis care in 2015 with compliments to the multiple online sources used, some of which are other lectures on SlideShare.
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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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
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
2. Review of Coronary Anatomy
• Left Main
– Left Anterior
Descending (LAD)
– Circumflex (Cx)
• Right Coronary Artery
– Posterior Descending
Artery (PDA)
5. Anatomic Variations
• Be aware they exist, but this is beyond the
scope of today’s lecture
Ramus intermedius (RI) is a variant
coronary artery resulting from
trifurcation of the left main
coronary artery. It is present in
~20% (range 15-30%) of the
population
Single coronary artery: All
coronaries arise from the left cusp
with a single origin and there is a
retro-aortic (benign) course of the
RCA (RC)
Malignant LM: Axial MIP image
reveals a malignant LM taking origin
from the right cusp and coursing
between the aorta and the
pulmonary artery which can be
subjected to compression during
heavy exercise and cause sudden
death
6. Ischemic-Type Chest Pain
• Pressure sensation,
fullness or squeezing
retro-sternally
• Radiation of chest pain
into the jaw/teeth,
shoulder, arm, and/or
back
• Associated dyspnea or shortness of breath
• Associated epigastric discomfort with or
without nausea and vomiting
7. Presentations of Angina
• Among patients considered to have angina,
there are three presentations of angina
that suggest an ACS:
– Rest angina, which is usually more than 20
minutes in duration
– New onset angina that markedly limits
physical activity
– Increasing angina that is more frequent, longer
in duration, or occurs with less exertion than
previous angina
8. Anginal Equivalents
• Most commonly found in patient with
diabetes and in women
• Include
– Exertional dyspnea
– Fatigue
– Nausea
– Vomiting
9. What about Atypical Chest Pain?
• Reduces like likelihood that symptoms represent
myocardial ischemia or injury
• Per guidelines of the ACC and AHA, the following are not
characteristic of myocardial ischemia
– Pleuritic pain (sharp/knife-life pain associated with
respiration or cough)
– Primary or sole pain in the middle or lower abdomen
– Pain localized with one finger, particularly over the left
ventricular apex
– Pain reproduced with movement or palpation
– Constant pain persisting for many hours
– Very brief episodes of pain that last a few seconds or
less
10. What is Acute Coronary Syndrome (ACS)?
• Umbrella term for the clinical
signs and symptoms of myocardial
ischemia:
–Unstable angina
–Non–ST-segment elevation
myocardial infarction
–ST-segment elevation myocardial
infarction.
12. Unstable Angina
• Blood clots that block an artery partially or
totally are what causes unstable angina.
• Occurs at rest and usually lasting >20
minutes
• New onset angina that limits activity
• Increasing angina: Pain that occurs more
frequently, lasts longer periods or is
increasingly limiting the patients activity
14. ECG Paper
• Standardized paper
• Speed 25 mm/sec (1 small square = 0.04
seconds; large square = 0.2 seconds)
• Amplitude 1 mV (10 mm to 1 mV)
15. NSTEMI
• NSTEMI is a clinical syndrome with
symptoms of myocardial ischemia not in
association with persistent
electrocardiographic (ECG) ST elevation or
ST elevation equivalents. There may be ST
depressions or non-specific EKG changes.
This is subsequent release of biomarkers.
16. STEMI
• STEMI is a clinical syndrome defined by
characteristic symptoms of myocardial
ischemia in association with persistent
electrocardiographic (ECG) ST elevation
and subsequent release of biomarkers of
myocardial necrosis.
18. Distinguishing Types
• The 12 lead EKG and serum biomarkers distinguish the
types of ACS
– Unstable angina: Normal cardiac biomarkers (troponin
and CK-MB) without characteristic EKG changes (non-
specific changes or normal)
– NSTEMI: Positive biomarkers without ST elevations or
ST-elevation equivalents (although ST depression and
non-specific changes can be seen)
– STEMI: Positive biomarkers and ST-segment elevation
in two or more contiguous leads; ST-elevation
equivalents including a new LBBB or a posterior MI
(tall R waves and ST depressions in V1-V3)
19. What Qualifies as ST elevation?
• The joint European Society of Cardiology,
American College of Cardiology Foundation, the
American Heart Association, and the World
Heart Federation (ESC/ACCF/AHA/WHF)
committee for the definition of MI established
specific ECG criteria for the diagnosis of ST
elevation MI:
– New ST segment elevation at the J point in
two contiguous leads with the cut-points: >0.1
mV in all leads other than leads V2-V3.
– For leads V2-V3, the following cut points
apply: ≥0.2 mV in men ≥40 years, ≥0.25 mV in
men <40 years, or ≥0.15 mV in women.
20. Don’t Be Tricked!
• Remember for real life and the boards
– STEMI is NOT the only cause of ST-elevation
segments.
– Consider acute pericarditis, left ventricular
aneurysm, takotsubo (stress) cardiomyopathy,
coronary vasospasm, or normal variant (early
repolarization)
25. ECG Evolution of Q-wave MI
• Usual ECG evolution of a Q-wave MI; not all of the
following patterns may be seen; the time from
onset of MI to the final pattern is quite variable
and related to the size of MI, the rapidity of
reperfusion (if any), and the location of the MI.
1. Normal ECG prior to MI
2. Hyperacute T wave changes - increased T wave
amplitude and width; may also see ST elevation
3. Marked ST elevation with hyperacute T wave
changes (transmural injury)
4. Pathologic Q waves, less ST elevation, terminal T
wave inversion (necrosis)
a. Pathologic Q waves are usually defined as
duration ≥ 0.04 s or ≥ 25% of R-wave
amplitude)
5. Pathologic Q waves, T wave inversion (necrosis and
fibrosis)
6. Pathologic Q waves, upright T waves (fibrosis)
26. Cardiac Biomarkers
• Troponin values within the normal range (using current
methodologies) likely come from a mixture of truly normal
individuals with detectable values and some with
comorbidities reflected by low but detectable values. (See
'Normal range' above.)
• Troponin elevations (above the 99th percentile) can be
due to structural heart disease in the absence of any
acute process.
• The diagnosis of an acute myocardial infarction depends
on observation of a rise and/or fall of blood biomarkers,
particularly troponins, with at least one value above the
99th percentile, in addition to clinical information or
electrocardiographic changes. The more sensitive the
assay, the more important it is to determine a change in
troponin level for confirmation of myocardial infarction.
27. Cardiac Biomarkers
• Cardiac troponins are recommended in preference to CK-MB for
diagnostic and prognostic purposes; it is unnecessary to obtain both
values. Cardiac troponins I and T are equally useful.
• For the diagnosis of myocardial infarction after coronary artery
bypass graft surgery (CABG), a 10-fold or greater increase from
baseline in biomarkers along with ancillary criteria, such as new Q
waves, is needed. Myocardial infarction after CABG is associated
with an increase in mortality.
• There is a delay in the rise of biomarkers after an acute myocardial
infarction (MI). In patients who have an acute ST elevation
myocardial infarction (STEMI), reperfusion therapy should not await
the results of cardiac biomarkers. In patients without diagnostic ST
segment elevation, serial biomarker testing is performed after four or
more hours if the initial values are indeterminate, the
electrocardiogram (ECG) remains nondiagnostic, and clinical
suspicion remains high.
30. Estimating Risk in UA and NSETMI
• Score 0-2
– Stress testing
and angiography
if testing shows
ischemia
• Score 3-4 or
recurrent angina,
elevated biomarkers
or previous
revascularization
– Early
angiography
• Score 5-7
– Early
angiography
31. Therapy
• With STEMI, PCI is preferred with a door-
to-balloon goal of <= 90 minutes
• Stent thrombosis may occur 24 hours to 1
year after placement and usually presents
as recurrent angina, sudden death, or MI.
– To prevent this, start ASA and a
thienopyridine (clopidogrel or prasugrel),
continue dual therapy for 1-12 months with a
bare-metal stent with ASA afterward
– DES – Clopidogrel for 12 months or longer.
41. What if PCI is not available?
• Administer tPA for large MI or previous
streptokinase use (90 minute patency better with tPA
than SK; roughly equal at 24 hours)
• Contraindications or cautions:
– Previous ICH (absolute contraindication)
– Ischemic stroke within the last 3 months except acute ischemic
stroke within 3 hours (absolute contraindication)
– Malignant intracranial neoplasm (absolute contraindication)
– Aortic dissection or active bleeding excluding menses (absolute
contraindication)
– Major surgery within 3 weeks (relative contraindication)
– BP >180/110 (relative contraindication)
– Pregnancy (relative contraindication)
– Concurrent warfarin therapy (relative contraindication)
– Active peptic ulcer disease (relative contraindication)
42. When is CABG the answer?
• STEMI in the presence of:
– Failure of fibrinolysis or PCI
– Cardiogenic shock
– Left main or left main equivalent disease
– Two- or three-vessel disease involving the LAD
and a reduced LVEF
43. Remember for Exams
• Choose transfer for PCI instead of thrombolytic therapy for
STEMI only if transfer and PCI can be done within 90 minutes
– Real world: The Danish DANAMI-2 trial (2003) suggested
that transferring patients for primary PCI is associated
with better outcomes than local thrombolysis if the transfer
time is less than three hours
• Do not choose thrombolytic therapy for patients with NSTEMI
or for asymptomatic patient with onset of pain <24 hours
• Reperfusion arrhythmias following thrombolytic therapy,
typically manifested as transient accelerated idioventricular
arrhythmia, do not require additional antiarrhythmic therapy
– AIVR appears similar to ventricular tachycardia with wide
QRS complexes (QRS >120) and a regular rhythm. It can
most easily be distinguished from VT in that the rate is less
than 120 and usually less than 100 bpm.
44. Drug Therapy
Therapy
Aspirin If CI, use clopidogrel, except if CABG is likely
Clopidogrel Use for UA, NSTEMI, and STEMI, and for PCI with stent placement
IV Beta blockers for acute care Decreased mortality evident by day 1; Avoid in pulmonary edema and/or
cardiogenic shock, SBP <90, HR <50, or second degree AV block
Calcium Channel Blockers (not
nifedipine)
Use in patient with contraindications to B-blockers and in those with continued
angina despite B-blockers and nitrates
IV Nitroglycerin Pain due to ongoing ischemia relived with nitro; routine recommendation for most
MI’s 24-48 hours; Use except with suspected RV infarction
LMWH or UFH Use for all cases of ACS
Bivalrudin Alternative to UFH/LMWH, especially in patients undergoing PCI
Fondaparinux Alternative to UFH/LMWH
Glycoprotein IIb/IIIa antagonists Considerations
ACE Inhibitors Within 24 hours of MI or MI + CHF with EF <40%; Can use ARBs as an alternative
Statins Prognosis improves in post-MI; Use within 24-96 hours
Cardioselective B-blockers Use within 3-21 days, continue indefinitely
Eplerenone Use for severe LV dysfunction after MI; Do not select spironolactone as its
effectiveness in patients with acute MI is unknown
46. Follow-up Care
• Mechanical complications (VSD, papillary muscle
rupture, LV free wall rupture) may occur 2-7 days
after an MI.
– Emergency echocardiography is the initial
diagnostic study
– Patients with VSD or papillary muscle rupture develop
abrupt pulmonary edema or hypotension and a loud
holosystolic murmur
– LV free wall rupture causes sudden hypotension or
cardiac death associated with PEA
47. Follow-up Care
• Cardiac catheterization is indicated for
patients with postinfarction angina or the
following post-MI stress test results:
– Exercise-induced ST-segment depressions or
elevations
– Inability to achieve 5 METs during testing
– Inability to increase systolic BP by 10-30
mmHg
– Inability to exercise (arthritis)
48. When To Place an ICD?
• ICDs are indicated in patients meeting the
following criteria:
– >40 days since MI
– >3 months since PCI or CABG
– EF <30%