A 70-year-old woman presents to the emergency department with chest pain. An EKG shows ST segment elevation in leads V2-V4 indicating an anterior wall myocardial infarction. The most appropriate next step in management is to perform angioplasty, as it is associated with the greatest mortality benefit compared to other options such as thrombolytics, medications, or diagnostic tests. Aspirin should be administered as soon as possible to reduce mortality from acute coronary syndrome.
Contrast induced nephropathy (CIN) is agenerally reversible form of acute kidney injury (AKI) that occurs soon after the administration of radiocontrast media.
Contrast induced nephropathy (CIN) is agenerally reversible form of acute kidney injury (AKI) that occurs soon after the administration of radiocontrast media.
ECG In Ischemic Heart Disease - Dr Vivek Baliga ReviewDr Vivek Baliga
Dr Vivek Baliga Presentation on the role of ECG in the diagnosis of ischemic heart disease. Here, he covers the very basics in ECG diagnosis of heart disease. Suitable for medical students and physicians alike. For more health articles for patients, visit http://baligadiagnostics.com/category/dr-vivek-baliga/
What are anti-coagulants?
What are the difference between antiplatelet, anticoagulants and thrombolytics?
Coagulation cascade
Virchows Triad
Classification of anti-coagulants?
Indications of anti-coagulants?
Mechanism and site of action of different anti-coagulants?
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.
ECG In Ischemic Heart Disease - Dr Vivek Baliga ReviewDr Vivek Baliga
Dr Vivek Baliga Presentation on the role of ECG in the diagnosis of ischemic heart disease. Here, he covers the very basics in ECG diagnosis of heart disease. Suitable for medical students and physicians alike. For more health articles for patients, visit http://baligadiagnostics.com/category/dr-vivek-baliga/
What are anti-coagulants?
What are the difference between antiplatelet, anticoagulants and thrombolytics?
Coagulation cascade
Virchows Triad
Classification of anti-coagulants?
Indications of anti-coagulants?
Mechanism and site of action of different anti-coagulants?
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.
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.
"Спорные вопросы коррекции гипергликемии у больных с острым коронарным синдро...rnw-aspen
Доклад с XVI Межрегиональной научно-практической конференции "Искусственное питание и инфузионная терапия больных в медицине критических состояний" 21-22 апреля 2016 г.
The second edition of AIIMS Medicine Quiz was held on 11th September, 2021. This quiz was for residents currently pursuing MD/DNB in Medicine/ Geriatric Medicine/ Emergency Medicine and Infectious Diseases.
You can pass your CCNS Exam with our training kits and practice questions answers prepared by industry experts and professionals. For more info please visit here: https://www.certifyguide.com/exam/CCNS/
Café Au Lait Spot is A Marker for Pheochromocytoma in Hypertensive Crisis Wit...YasserMohammedHassan1
Café au lait Spot is a marker for pheochromocytoma in hypertensive crisis but with a wide-differential diagnosis. Labetalol may be chosen in hypertensive crisis due to pheochromocytoma.
EKG Worksheet Answer each question below. Use completeEvonCanales257
EKG Worksheet
Answer each question below. Use complete sentences when providing short answer responses.
1. You are the AGACNP in the emergency room. A 55-year-old Caucasian male with a past medical history of HTN, thyroid cancer, and diverticulitis presents with crushing chest pain. His chest pain developed one hour ago after eating a large steak and potato dinner. He states the pain is 10 out of 10 and is not relieved by antacids. He is also diaphoretic and anxious. You review his 12 lead EKG, as per below.
Using the EKG strip, answer questions A-D.
A. What part of the area of the heart is showing an evolving infarct?
a. Inferior
b. Anterior
c. Lateral
d. Posterior
B. Which leads show ST elevation?
a. II, III, AVL
b. V1-V3
c. II, III, AVF
d. II, III, AVR
C. Where would you expect to find reciprocal changes?
a. Reciprocal changes in at least AVL
b. Reciprocal changes in lead III
c. Reciprocal changes in lead IV and V
d. There are No reciprocal changes.
D. What coronary artery is the likely cause?
a. The Right Coronary artery in most cases as it is usually dominant, however in some patients the left circumflex is dominant and thus the culprit for an inferior MI.
b. The left anterior descending
c. The septal artery
d. none of the above
2. A 67-year-old female is your established cardiology patient. She is following up with you regarding her uncomplicated mitral valve stenosis. During the visit, she happens to mention that she has suffered 9 hours of chest pain and sweating, which takes you by surprise. Your patient further describes the pain as both gnawing and intermittent. She thought she was experiencing heartburn, but admits that she has never experienced heartburn before, so she is not sure. You perform a 12-lead EKG immediately and call 911.
Interpret the EKG recording below.
What area of the heart is involved, what is your diagnosis, and which coronary artery is affected?
a. Anterior part of the heart; this is an ST elevation myocardial infarction (STEMI); and the Left anterior descending is affected
b. Inferior; this is a Non ST elevation MI (NSTEMI), and the right coronary artery is affected
c. Posterior; this is not an MI but does show ischemia, and the circumflex is involved
d. This simply pericarditis and thus the affected coronary arteries are not affected, the heart strain distribution is diffuse and global
3. What qualifies for “significant” ST elevation or depression in a 12 lead EKG- in the limb leads_(i)._____________? What is significant for the or the precordial leads_(ii)._____? These changes must be present in at least_(iii)___________consecutive leads in order to be considered diagnostic of myocardial pathology.
1. (i))1mm in a limb lead, (ii)1mm in precordial lead, (iii)and must be present 3 consecutive leads
1. (i)1mm in a limb lead, (ii)2mm in precordial lead, (iii)and must be present 2 consecutive leads
1. (i) 2mm in a limb lead; (ii)) 2 mm in a precordial lead, (iii) must be present in 3 consec ...
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
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.
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
2. Definition
• It is impossible to determine the precise etiology
of acute coronary syndromes (ACS) from history
and physical examination alone.
• The risk factors (e.g.,hypertension, diabetes
mellitus, tobacco) are the same as those
described previously for CAD.
3. A 70-year-old woman comes to the emergency department with
crushing substernal chest pain for the last hour. The pain radiates
to her left arm and is associated with anxiety, diaphoresis, and
nausea. She describes the pain as"sore" and "dull" and clenches
her fist in front of her chest. She has a history of hypertension.
Which of the following is most likely to be found in this patient?
a. >10 mm Hg decrease in blood pressure on inhalation
b. Increase in jugular venous pressure on inhalation
c. Triphasic scratchy sound on auscultation
d. Continuous "machinery" murmur
e. S4 gallop
f. Point of maximal impulse displaced towards the axilla
4. Answer: E. Acute coronary syndromes are associated with an S4 gallop
because of ischemia leading to noncompliance of the left ventricle. The
S4 gallop is the sound of atrial systole as blood is ejected from the
atrium into a stiff ventricle.
Incorrect answer:
• A. A decrease of blood pressure of greater than 10 mm Hg on
inspiration is a pulsus paradoxus and is associated with cardiac
tamponade.
• B. An increase in jugulovenous pressure on inhalation is the
Kussmaul sign and is most often associated with constrictive
pericarditis or restrictive cardiomyopathy.
• C. A triphasic "scratchy" sound is a pericardia! friction rub. Although
pericarditis can occur as a complication of myocardial infarction
(Dressler syndrome), this would not occur for several days after an MI
and is much rarer than simple ventricular ischemia.
5. • D. A continuous "machinery" murmur is what
would be found with a patent ductus arteriosus.
• F. A displaced point of maximal impulse (PMI) is
characteristic of left ventricular hypertrophy (LVH)
as well as dilated cardiomyopathy. A displaced
PMI is an anatomic abnormality that could not
possibly occur with an acute coronary syndrome.
• There are no specific physical findings to allow you
to answer a "most likely diagnosis" question in
terms of ST elevation or depression without an
EKG.
6. A 70-year-old woman comes to the emergency department with
crushing substernal chest pain for the last hour.
Which of the following EKG findings would be associated with
the worst prognosis?
a. ST elevation in leads II, Ill, aVF
b. PR interval >200 milliseconds
c. ST elevation in leads V2-V4
d. Frequent premature ventricular complexes (PVCs)
e. ST depression in leads V1 and V2
f. Right bundle branch block (RBBB)
Do not walk into your USMLE Step 2 CK exam
without knowing when you will expect each of
the cardiac physical findings described here.
7. • Answer: C. Leads V2 to V4 correspond to the anterior
wall of the left ventricle. ST segment elevation most
often signifies an acute myocardial infarction.
• ST elevation in leads II, Ill, and aVF is also consistent
with an acute myocardial infarction,but of the inferior
wall. Untreated, the mortality associated with an
IWMI is less than 5% at 1 year after the event. With
an AWMI, mortality untreated is closer to 30%to40%.
• PR interval greater than 200 milliseconds is first-
degree atrioventricular (AV) block.First-degree AV
block has little pathologic potential and, when
isolated, requires no additional therapy.
8. • Ectopy such as PVCs and atrial premature complexes (APCs) are
associated with the later development of more severe arrhythmias,
but no additional therapy is needed for them if magnesium and
potassium levels are normal. We don't like to see PVCs, but their
presence does not require any changes in management. PVCs should
not be treated, even when associated with an acute infarction.
Treatment of PVCs only worsens outcome.
• ST depressions in leads V1 and V2 are suggestive of a posterior wall
myocardial infarction. These leads are read in the opposite direction
of the rest of the leads. In other words, ST depression in leads V1 and
V2 would be like ST elevation elsewhere-an acute infarction.
Infarctions of the posterior wall are associated with a very low
mortality, and again, there is no additional therapy to give because of
it.
• Right bundle branch block (RBBB) is relatively benign compared to a
new left bundle branch block(LBBB).
9. ECG localization of STEMI
INFARCT LOCATION LEADS WITH ST ELEVATIONS OR Q
WAVES
• Anteroseptal (LAD) V1–V2
• Anteroapical (distal LAD) V3–V4
• Anterolateral (LAD or LCX) V5–V6
• Lateral (LCX) I, aVL
• InFerior (RCA) II, III, aVF
• Posterior (PDA) V7–V9, ST depression in V1–V3
with tall R waves
10. A 70-year-old woman comes to the emergency
department with crushing substernal chest pain for the
last hour. An EKG shows ST segment elevation in V2 to
V4.What is the most appropriate next step in the
management of this patient?
a. CK-MB level
b. Oxygen
c. Nitroglycerin sublingual
d . Aspirin
e. Thrombolytics
f. Metoprolol
g . Atorvostatin
h . Angioplasty
i. Consult cardiology
j. Transfer the patient to the intensive care unit
k. Troponin level
I. Morphine
m. Angiography
n. Clopidogre
11. • Answer: D. Aspirin lowers mortality with acute coronary
syndromes, and it is critical to administer it as rapidly as
possible.
• With only 1 hour since the onset of pain, neither the CK-MB
level nor the troponin level would be elevated yet.
• Morphine, oxygen, and nitroglycerin should all be
administered, but they do not lower mortality and are
therefore not as important as aspirin.
• Aspirin should be given simultaneously with activating the
catheterization lab.
• Clopidogrel is indicated when the patient has an intolerance of
aspirin or has undergone angioplasty with stenting.
12. • The patient should be transferred to an intensive care unit
(ICU), but you must always initiate therapy and testing before
you simply move the patient to another part of the hospital. It
is much more important to start proper care than to move the
patient, even if it is a movement to an area of increased
observation and potential treatment.
• Thrombolytics or angioplasty should be done and it is critical
to do them quickly; however, aspirin is simply recommended
to be given first. Aspirin is then followed with another form of
acute revascularization .
• On USMLE Step 2 CK, consultation is almost never the correct
choice. Do everything yourself.
13. A 70-year-old woman comes to the emergency department
with crushing substernal chest pain for the last hour. An
EKG shows ST segment elevation in V2 to V4. Aspirin has
been given to the patient to chew. What is the most
appropriate next step in the management of this patient?
a. CK-MB level
b. Oxygen
c. Nitroglycerin sublingual
d . Morphine
e. Thrombolytics
f. Metoprolol
g. Atorvostatin
h. Angioplasty
i. Troponin level
j. Llsinopril
14. • Answer: H. Angioplasty is associated with the greatest mortality
benefit of all the steps listed in this question. All of the answers are
partially correct in that all of them should be done for the patient.
• Again, morphine, oxygen, and nitrates should be given to the
patient immediately, but they do not clearly lower mortality.
• Enzyme tests should be done, but within the first 4 hours of the
onset of chest pain, they will certainly be normal. Even if they are
elevated, CK-MB and troponin levels would not alter the
management.
• Beta blockers are associated with a decrease in mortality, but they
are not critica lly dependent upon time. As long as the patient
receives metoprolol sometime during the hospital stay and at
discharge, she will derive benefit. The same is true of the use of
statins and ACE inhibitors.
15. The key issues in the management of acute
coronary syndromes are:
• Does the intervention/treatment lower
mortality?
• Which management is most important to
do first?
16. Diagnostic test
Test Time to becoming
abnormal
Duration of abnormalities
EKG Immediately at onset of
pain
ST elevation progresses to Q
waves over several days to
weeks
Myoglobin 1-4 hour 1-2days
CK-MB 4-6 hour 1-2 days
Troponin 4-6 hour 10-14 days
17. The use of the troponin level is not without its difficulties:
• Troponin cannot distinguish a reinfarction occurring several
days after the first event.
• Renal insufficiency can result in false positive tests since
troponin is excreted through the kidney.
Reinfarction
When a patient has a new episode of pain within a few days of
the first cardiac event, the management is:
1. Perform an EKG to detect new ST segment abnormalities.
2. Check CK-MB levels. After 2 days, the CK-MB level from the
initial infarction should have returned to normal. A CK-MB level
that is elevated several days after an initial myocardial infarction
is indicative of a new ischemic event
18. Intensive Care Unit Monitoring
After the initial management is put in place, the patient should be
monitored in an ICU.
Continuous rhythm monitoring is essential to an improved survival
and outcome.
Multiple factors contribute to the lowering of mortality through ICU
monitoring:
• The most common cause of death in the first several days after a
myocardial infarction is ventricular arrhythmia (ventricular
tachycardia, ventricular fibrillation)
.
• Rapid performance of electrical cardioversion or defibrillation is
available.
19. Treatment
• ST Segment Elevation Myocardial Infarction ACS
is best managed initially with aspirin, either
orally or chewed.
• Clopidogrel is often used if there is an allergy
to aspirin, but prasugrel is an alternative to
clopidogrel that seems to have superior benefit.
20. Angioplasty versus Thrombolytics
Angioplasty (PCI) is superior to thrombolytics in terms of:
• Survival and mortality benefit
• Fewer hemorrhagic complications
• Likelihood of developing complications of MI (less arrhythmia,
less CHF,fewer ruptures of septum, free wall [tamponade] and
papillary muscles [valve rupture])
The standard of care is that PCI is expected to be performed
within 90 minutes of the patient arriving in the emergency
department with chest pain.
21. Complications of PCI
Complications include:
• Rupture of the coronary artery on inflation of the balloon
• Restenosis (thrombosis) of the vessel after the angioplasty
• Hematoma at the site of entry into the artery (e.g., femoral
area hematoma)
Only 20% of U.S. hospitals are equipped to perform primary
angioplasty because many lack a catheterization laboratory. It is
important to have the ability to perform emergency cardiac
surgery to repair the vessel.
22. Which of the following is most important in decreasing the risk
of restenosis of the coronary artery after PCI?
a. Multistage procedure: i.e., doing 1 vessel at a time, with
multiple procedures
b. Use of heparin for 3- 6 months after the procedure
c. Warfarin use after the procedure
d. Placement of bare metal stent
e. Placement of drug-eluting stent (paclitaxel, sirolimus)
23. • Answer: E. The placement of drug-eluting stents that inhibit
the local T cell response has markedly reduced the rate of
restenosis.
• Heparin is used at the time of the procedure, but is not
continued long term.
• Warfarin has no place in the management of coronary disease.
Warfarin is useful for clots on the venous side of the
circulation such as DVT or pulmonary embolus.
24. Rates of Restenosis within 6 Months of PCI
• No stenting: 30%-40%
• Bare metal stent: 15%-30%
• Drug-eluting stent: 10%
If there is a contraindication to the use of thrombolytics, the
patient should be transferred to a facility performing PCI.
Absolute Contraindications to Thrombolytics
• Major bleeding into the bowel (melena) or brain (any type
of CNS bleeding)
• Recent surgery (within the last 2 weeks)
• Severe hypertension (above 180/110)
• Nonhemorrhagic stroke within the last 6 months
Heme-positive brown
stool is not an absolute
contraindication to the use
of thrombolytics.
25. A patient comes to a small rural hospital without a
catheterization laboratory. The patient has chest pain and ST
segment elevation. What is the most appropriate next step in
the management of the patient?
a. Transfer for angioplasty
b. Administer thrombolytics now
c. Consult cardiology
26. • Answer: B. Immediate thrombolytics is far more beneficial to the
patient than angioplasty delayed by several hours. Remember
that consultation is almost never the right answer on USMLE
Step 2 CK.
• The mortality benefit of thrombolytics extends out to 12 hours
from the onset of chest pain.
• In other words, you can answer "thrombolytics" in any patient
with chest pain and ST segment elevation within the first 12
hours of the onset of chest pain.
• The mortality benefit is as much as a 50% relative risk reduction
within the first 2 hours of the onset of pain.
• This is why a patient with chest pain who arrives in the
emergency department should receive thrombolytics within 30
minutes of coming through the door.
• Time is muscle. Delay = death.
• "Door to needle time": under 30 minutes
27. Treatment indication and benefits
Therapy In what case effect greatest?
Aspirin Everyone, as the best initial therapy
Clopidogrel Aspirin not tolerated, those undergoing angioplasty
and stenting
Beta blockers Everyone, effect is not dependent on time; started
any time during admission
ACEi/ARB Everyone, benefit best with ejection fraction below 40%
Statins Everyone, benefit best with LDL > 1 00 mg/dl
Oxygen, nitrates Everyone, no clear mortality benefit
Heparin After thrombolytics/ PCI to prevent restenosis, initial
therapy with ST depression and other NON-ST elevation
events (unstable angina)
Calcium channel
blockers
Can't use beta blockers, cocaine-induced pain,
Prinzmetal or vasospastic variant angina
28. ST Segment Depression ACS
A man comes to the emergency department with chest pain for the
last hour that is crushing in quality and does not change with
respiration or the position of his body. An EKG shows ST segment
depression in leads V2 to V4. Aspirin has been given.
What is the most appropriate next step in the management of this
patient?
a. Low molecular-weight heparin
b. Thrombolytics
c. Glycoprotein lib/ lila inhibitor (abciximab)
d. Nitroglycerin
e. Morphine
f. Angioplasty
g. Metoprolol
29. • Answer: A. Heparin will prevent a clot from forming in the coronary
arteries. Heparin does not dissolve clots that have al ready formed .
When the patient has ACS and there is no ST segment elevation,
there is no benefit of thrombolytic therapy.
• Nitroglycerin, morphine, and oxygen are not associated with a clear
reduction in mortality.
• ACE inhibitors and statins are used, but the mortality benefit is,
again, based on either a low ejection fraction or increased LDL
respectively.
• Metoprolol should be used, but it has not been proven that it
matters whether we give the beta blockers immediately, or at any
time before hospital discharge. In other words, there is no urgency
in terms of time for metoprolol.
• There is tremendous urgency to give heparin immediately because
we want to prevent the clot from growing further and closing off
the coronary artery.
30. Glycoprotein lIb/lIla Inhibitors
(Abciximab, Tirofiban, Eptifibitlde)
• These agents (GPIIb/IIIa inhibitors) are used in acute coronary
syndromes in those who are to undergo angioplasty and stenting.
• They are not beneficial in acute ST elevation infarctions separate
from the use of angioplasty and stenting.
• GPIIb/IIIa inhibitors inhibit the aggregation of platelets.
• They lead to a reduction in mortality in those with ST depression,
particularly in patients whose troponin or CK-MB levels rise and who
then develop a myocardial infarction requiring PCI with stenting.
31. Summary of different
treatments btw cardiac events
Stable angine Unstable angina/Non
ST elevation MI
ST elevation MI
Aspirin Yes Yes Yes
Beta blockers Yes Yes Yes
Nitrates Yes Yes Yes
Heparin No Yes Yes ,but only after
thrombolytics
GpIIb/IIIa No Yes No
Thrombolytics No No Yes ,but not good as
PCI
CCB No No No
Warfarin No No No
32. Bottom Line:
1. tPA (thrombolytics) are beneficial only with ST
elevation MI.
2. Heparin is best for non-ST elevation MI.
3. GP lIb/lIla inhibitors are best for non-ST
elevation Ml and those undergoing PCI and
stenting.
• Calcium channel blockers and warfarin have no
clear mortality benefit in ACS.
• Low molecular-weight heparin is superior to
unfractionated heparin in terms of mortality
benefit.
33. In non-ST elevation ACS, when all medications have
been given, and the patient is not better, urgent
angiography and possibly angioplasty (PCI) should be
done. "Not better" means:
• Persistent pain
• S3 gallop or CHF developing
• Worse EKG changes or sustained ventricular
tachycardia
• Rising troponin levels
34. Complications of Acute
Myocardial Infarction
• Complications of acute myocardial infarction are an
excellent source of "What is the most likely diagnosis?"
questions, the most common type of question on USMLE
Step 2 CK.
• All the complications of myocardial infarction can result in
hypotension, so the presence of hypotension will not help
you determine the diagnosis.
• Starving hearts have ventricular tachycardia open it fast
with PCI!
35. Bradycardia
• Heart rate is key to establishing the diagnosis.
• Sinus bradycardia is very common in association with MI because
of vascular insufficiency of the sinoatrial (SA) node.
• Third-degree (complete) AV block will have cannon A waves.
• They are the best way to distinguish third-degree AV block from
sinus bradycardia before you obtain an EKG.
• Cannon A waves are produced by atrial systole against a closed
tricuspid valve. The tricuspid valve is closed because the very
essence of third-degree block is that the atria and ventricles are
contracting separately and out of coordination with each other.
• The cannon is the bounding jugulovenous wave bouncing up into
the neck. Look for an association with right ventricular infarction
and third-degree AV block.
• All symptomatic bradycardias are treated first with atropine and
then by placing a pacemaker if the atropine is not effective.
36. Tachycardia
Right Ventricular Infarction
Look for the association with a new inferior wall MI and clear lungs
on auscultation.
You cannot get blood into the lungs if the blood cannot get into the
heart. You can diagnose by flipping the EKG leads from the usual left
side of the chest to the right side of the chest. ST elevation in RV4 is
the most specific finding.
The right coronary artery supplies:
• Right ventricle (RV)
• AV node
• Inferior wall of the heart
This is why up to 40% of those with an inferior wall myocardial
infarction (IWMI) will have a right ventricular infarction. Treat RV
infarctions with high-volume fluid replacement. Avoid nitroglycerin
to RV infarctions. They markedly worsen cardiac filling.
37. Tamponade/ Free Wall Rupture
• It usually takes several days after an infarction for the
wall to scar and weaken enough for it to rupture.
• Look for "sudden loss of pulse" in the case. Lungs are
clear. It is a cause of pulseless electrical activity.
• You can diagnose with emergency echocardiography.
• Emergency pericardiacentesis is done on the way into
the operating room to repair it.
38. Ventricular Tachycardia/ Ventricular Fibrillation
• Both ventricular tachycardia and ventricular fibrillation can cause
sudden death and there is no way to distinguish them without an EKG
if they cause loss of pulse.
• Both are treated with emergency electrical shock (cardioversion/
defibrillation).
Valve or Septal Rupture
• Both valve rupture and septal rupture present with new onset of a
murmur and pulmonary congestion.
• Mitral regurgitation murmur is best heard at the apex with radiation
to the axilla.
• Ventricular septal rupture is best heard at the lower left sternal
border.
39. • These complications are the reason patients with acute Ml are
monitored in an ICU for the first several days after the
infarction.
• Look for a step-up In oxygen saturation as you go from the
right atrium to the right ventricle to hand you the diagnosis of
septal rupture.
• Most accurate test: Echocardiogram for both valve rupture
and septal rupture .
• You can't always depend on buzzwords like "step-up" for
oxygenation.Often, the numbers are simply presented to you:
"42% oxygen saturation is found on a sample of blood from
the right atrium. 85% saturation is found on the right
ventricular sample."
40. lntraaortic Balloon Pump
• Intraaortic balloon pump (IABP) is the answer
when there is acute pump failure from an
anatomic problem that can be fixed in the
operating room.
• IABP contracts and relaxes in sync with natural
heartbeat. It helps give a "push“ forward to the
blood .
TIP
• IABP is never a permanent device. It serves as a
bridge to surgery for valve replacement or
transplant for 24 to 48 hours.
41.
42. Extension of the
lnfarction/Reinfarction
• When a patient presents with either an inferior or
anterior infarction, it is common for a second event to
infarct a second geographic area of the heart.
• Look for recurrence of pain, new rales on exam, a new
bump up in CK-MBs, and even sudden onset of
pulmonary edema.
• Repeat the EKG and re-treat with angioplasty and
sometimes thrombolytics in addition to the usual
medications (aspirin, metoprolol, nitrates, ACE, statins).
43. Aneurysm/Mural Thrombus
• Aneurysm or mural thrombus is detected
with echocardiography.
• Most aneurysms do not need specific
therapy.
• Mural thrombi, like all thrombi, are
treated with heparin followed by warfarin
44. What is the most likely diagnosis
Diagnosis Key feature
Third degree AV block Bradycardia, cannon A wave
Sinus bradycardia No cannon A wave
Tamponade/wall rupture Sudden loss of pulse/jugulovenous
distension
RV infarction IWMI in history, clear lungs,tachycardia,
hypotension with nitroglycerin
Valve rupture New murmur, rales/congestion
Septal rupture New murmur, increase in oxygen saturation
on entering the right Ventricle
Ventricular fibrillation Loss of pulse, need EKG to answer question
45. Preparation for Discharge from
Hospital
• Detection of Persistent Ischemia
• Everyone gets a stress test prior to discharge. The stress test
determines if angiography is needed. Angiography determines the
need for revascularization such as angioplasty or bypass surgery .
TIP
• Do not do a stress test if the patient remains symptomatic. These
people clearly need angiography.
• Do not do angiography if reversible signs of myocardial ischemia are
absent.
• There is no point in revascularizing to myocardium that is dead
(infarcted)
46. Post-MI Stress Test
• Identify those with residual ischemia prior to leaving the
hospital. Do not just cath (angiography) everyone.
Postinfarction Routine Medications
Everyone should go home on:
• Aspirin
• Beta blockers (metoprolol)
• Statins
• ACE inhibitors - ACE inhibitors are best for anterior wall
infarctions because of the high likelihood of developing systolic
dysfunction.
• Clopidogrel: those intolerant of aspirin or post-stenting
• ARBs : those with a cough on ACE inhibitor
• Ticlopidine : the rare person intolerant of both aspirin and
clopidogrel
47. • Dipyridamole is never the right choice for
coronary artery disease.
• Prophylactic antiarrhythmic medications:
-Do not use amiodarone, flecainide, or any
rhythm-controlling medication to prevent the
development of ventricular tachycardia or
fibrillation. Do not be fooled by the question
describing "frequent PVCs and ectopy."
Prophylactic antiarrhythmics increase mortality.
48. Sexual Issues Postinfarction
This is a very frequently tested subject. The 4 most commonly tested facts
are:
1. Do not combine nitrates with sildenafil; hypotension can result
because they are both vasodilators.
2. Erectile dysfunction postinfarction is most commonly from anxiety;
however, of all the medications that cause erectile dysfunction, the most
common is beta blockers.
3. The patient does not have to wait after an MI to reengage in sexual
activity. If the patient is symptom-free, sexual activity may begin
immediately. This is because sexual activity usually does not last long
enough to constitute an excessive increase in myocardial oxygen
consumption.
4. If the post-MI stress test is described as normal, the patient can
reengage in any form of exercise program as tolerated, including sex.