Acute coronary syndrome for critical care examDr fakhir Raza
This presentation is made to help students prepare for EDIC exam. this is board review for any exam for critical care examining acute MI, myocardial infarction, acute coronary syndrome.
ACS covering STEMI and NSTEMI. MI is the most common cause of death in the developed countries and it is important to have a basic information and reach doctor as soon as possible to avoid complications and sudden death.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
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.
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.
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We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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.
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.
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.
3. Hospitalizations in the U.S. Due to Acute
Coronary Syndromes (ACS)
Acute Coronary
Syndromes*
1.57 Million Hospital Admissions - ACS
UA/NSTEMI† STEMI
1.24 million
Admissions per year
.33 million
Admissions per year
Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69-171.
*Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA.
4. Acute Coronary Syndrome
Definition:
The spectrum of acute ischemia related syndromes ranging from UA to MI
with or without ST elevation that are secondary to acute plaque rupture or plaque
erosion.
[----UA---------NSTEMI----------STEMI----]
A constellation of symptoms related to obstruction of coronary arteries with
chest pain being the most common symptom in addition to nausea, vomiting,
diaphoresis etc.
5. Signs and symptoms of
ACS presentation
Symptoms may include:
• chest discomfort (tightness, pressure, heaviness) at rest or for a prolonged period
(> 10 minutes, not relieved by sublingual nitrates)
• recurrent chest discomfort
• discomfort associated with syncope/acute heart failure.
The pain may spread to other parts of the upper body, including:
• Back, neck, jaw, arm(s), shoulder(s) or epigastric pain.
The person may also experience:
• Dyspnoea (shortness of breath), diaphoresis (profuse perspiration), dizziness,
nausea or vomiting
• Recent research shows that women, the elderly and people with diabetes are
less likely to experience chest pain as a symptom.
6.
7. Anginal equivalent syndrome
• Patients who are experiencing ACS, yet do not complain of typical chest
pain; rather, these patients note atypical pain, dyspnea, weakness,
diaphoresis, or emesis—these complaints, in fact, are the manifestation of
the ACS event.
• Patients with altered cardiac pain perception e.g., the elderly or patients
with longstanding diabetes mellitus, are potentially at risk to present with
anginal equivalent syndromes.
• The most frequently encountered anginal equivalent chief complaint is
dyspnea, which is found in 10% to 30% of patients with AMI, often due to
pulmonary edema.
8. CHARACTERISTICS OF
TYPICAL ANGINAL CHEST PAIN
CHARACTERISTIC SUGGESTIVE OF ANGINA LESS SUGGESTIVE OF
ANGINA
TYPE OF PAIN DULL PRESSURE/CRUSHING
PAIN
SHARP/STABBING
DURATION 2-5 MIN, <20 MIN SECONDSTO
HOURS/CONTINUOUS
ONSET GRADUAL RAPID
LOCATION/CHEST WALL
TENDERNESS
SUBSTERNAL, NOT TENDER
TO PALP.
LATERAL CHEST
WALL/TENDER TO PALP.
REPRODUCIBALITY WITH EXERTION/ACTIVITY WITH BREATHING/MOVING
AUTONOMIC SYMPTOMS PRESENT USUALLY ABSENT
9. • STEMI: ST elevation, elevated cardiac enzymes
• NSTEMI: ST depression, T-wave inversion, elevated cardiac enzymes
• Unstable Angina: Non specific EKG changes, normal cardiac enzymes
Based on ECG and cardiac enzymes, ACS is classified into:
14. Unstable
Angina STEMINSTEMI
Non occlusive thrombus
Non specific ECG
Normal cardiac
enzymes
Non-occlusive thrombus
sufficient to cause
tissue damage & mild
myocardial necrosis
ST depression +/-
T wave inversion on
ECG
Elevated cardiac
enzymes
Complete thrombus
occlusion
ST elevations on ECG
or new LBBB
Elevated cardiac
enzymes
More severe symptoms
16. Gender Differences in MI
Females, when compared to males:
-present with MI later in life
-have poorer prognosis and high morbidity
-are 2x as likely to die in the first weeks
-are more likely to die from the first MI
-have higher rates of unrecognized MI
17. At least 2 of the following
• History ( angina or angina equivalent)
• Acute ischemic ECG changes
• Typical rise and fall of cardiac markers
• Absence of another identifiable etiology
Diagnosis of ACS
18. Diagnosis
Diagnosis requires a rise and/or fall in serum levels of cardiac markers
(preferably troponin) together with:
Defined clinically by patient history
ECG (new ST-T wave changes, new left bundle branch block or evolving
pathological Q waves)
Imaging evidence of new regional wall motion abnormality.
19. STEMI
• Compromised left ventricular (LV) function may result in pulmonary
edema with development of pulmonary bibasilar crackles and jugular
venous distention; a fourth heart sound can be present with small
infarcts or even mild ischemia, but a third heart sound is usually
indicative of more extensive damage. Pericardial rub may be heard.
20. • An ST-segment elevation myocardial infarction (STEMI) can be confirmed by an
ECG.
• A 12-lead ECG should be performed and interpreted expeditiously.
• STEMI is defined as presentation with clinical symptoms consistent with an ACS
with ECG features including any of:
Persistent ST-segment elevation ≥ 1 mm in two contiguous limb leads
ST-segment elevation ≥ 2 mm in two contiguous chest leads
New left bundle branch block (LBBB) pattern.
STEMI – what is it?
23. Serum cardiac markers
IDEAL MARKER:
• High concentration in
myocardium
• Myocardium specific
• Released early in injury
• Proportionate to injury
• Non expensive testing
24. Advantages
Myoglobin
1. High sensitivity
2. Useful in early detection of MI
3. Detection of reperfusion
4. Most useful in ruling out MI
CK-MB
1. Rapid, cost-efficient, accurate
assays
2. Ability to detect early
reinfarction
Troponins
1. Powerful for stratification
2. Greater sensitivity and specificity
than CK-MB
3. Detection of recent MI up to 2
weeks after onset
4. Useful for selection of therapy
5. Detection of reperfusion
25. Diadvantages
CK-MB
1. Lack of specificity with skeletal
muscle disease/injury
2. Low sensitivity during early MI
(<6 h) or late (>36 h) after
symptom onset and for minor
myocardial damage
Myoglobin
1. Very low specificity with
skeletal muscle injury or disease
2. Rapid return to normal
Troponins
1. Low sensitivity in early phase of
MI (<6 h after symptom onset)
2. Limited ability to detect late minor
re-infarction
26.
27. • Cardiac Imaging
2D ECHO may reveal wall motion abnormality and LV dysfunction. It may
also detect RV infarction, Ventricular aneurysms, pericardial effusion
and LV Thrombus.
Myocardial perfusion imaging with TI201 and Tc99m - sestamibi reveals
defect in most patient.
28. Time from symptom onset and likely outcome
< 1 hour
Aborted heart attack or only little heart muscle damage
1–2 hours
Minor heart muscle damage only
2–4 hours
Some heart muscle damage with moderate heart muscle salvage
4–6 hours
Significant heart muscle damage with only minor heart muscle salvage
6–12 hours
No heart muscle salvage (permanent loss) with potential infarct
healing benefit
> 12 hours
Reperfusion is not routinely recommended if the patient is
asymptomatic and haemodynamically stable
29. Therapy STEMI
• Once STEMI is suspected or diagnosed, the immediate concerns are to
ensure the patients stability and to intervene to limit infarct size by
restoring the blood flow to the infarct artery as soon as possible.
• Abolute and relative contraindication to therapies must be considered and
relative risk assessed. Choices may be limited for the availability of
specialized procedures, need to transport to another facility, significant co-
morbidities, bleeding risk,etc.
30. Early Therapy
• Patients presenting with suspected myocardial ischemia should undergo a rapid
evaluation, that is a 12 lead ECG, cardiac markers and related laboratory tests.
• Should be treated with oxygen
• Sublingual Nitroglycerin (unless systolic pressure is <90 mm Hg), and Aspirin, 160
to 325 mg orally.
• Opiates relieve pain and also reduce anxiety, the salutary effects of which have
been known for decades and should not be underestimated.
31. Fibrinolytic therapy
• Early reperfusion of an occluded coronary artery is indicated for all
eligible candidates.
• Fibrinolytic agents administered early in the course of an acute MI
reduce infarct size, preserve LV function, and reduce short-term and
long-term mortality.
• Multiple studies conclude that greatest mortality benefit is seen if
fibrinolytics are administered within the first 12 hours of symptom
onset, but it is reasonable to administer fibrinolytics to patients
whose onset of symptoms exceeds 12 hours but who have continued
clinical or ECG evidence of ischemia.
33. • After administration of fibrinolytics for
STEMI, the patient should be monitored
for signs and symptoms of adequate
reperfusion within 90 minutes, as
indicated by relief of symptoms and/or
hemodynamic/ electrical instability
coupled with at least a 50% resolution of
the highest initial ST elevation.
• Patients who receive fibrinolytics for
STEMI and have at least one high-risk
feature should have cardiac
catheterization for risk stratification and
potential percutaneous revascularization,
even if this involves immediate transfer
from the presenting hospital to a PCI-
capable facility.
High-risk features include
• Extensive ST-segment elevation (>2 mm
ST elevation in two anterior leads),
• New-onset LBBB,
• Previous MI,
• Killip class 2 or 3 or Left ventricular
ejection fraction (LVEF) ≤ 35%,
• Systolic blood pressure ≤ 100 mm Hg,
• Heart rate ≥ 100 bpm, or
• Right ventricular involvement.
34. Fibrinolytic agents Used in ST elevation MI
Streptokinase 1.5 million intravenous over 30-60 mins
Alteplase (tPA) a 15-mg bolus, then 0.75 mg/kg (up to 50 mg) IV over the initial 30
minutes, and 0.5 mg/kg (up to 35 mg) over the next 60 minutes
Reteplase (rPA) two 10-U boluses 30 minutes apart
Tenecteplase (TNK-tPA) IV Bolus adjusted for weight
(30mg if < 60 kg; 35mg if 60-70 kg; 40 mg if 70-80 kg, 45mg if 80-90
kg; 50mg if > 90 kg)
35. Reperfusion Therapy
• It includes angioplasty, with or without deployment of an intracoronary Bare-
metal or Drug-eluting stent, with support of pharmacological measures to
prevent thrombosis.
i. Percutaneous coronary intervention
• Recent meta-analyses comparing direct PTCA with fibrinolytic therapy have
suggested lower rates of mortality and re-infarction among those receiving
direct PTCA. Thus direct angioplasty, if performed in a timely manner (ideally
within 60 minutes) by highly experienced personnel, may be the preferred
method of revascularization, since it offers more complete revascularization with
improved restoration of normal coronary blood flow and detailed information
about coronary anatomy.
36. There are certain subpopulations in which primary PCI is clearly preferred, and other
populations in which the data are suggestive of benefit.
37. Coronary Stents
• The use of coronary stents has been shown to reduce restenosis and adverse cardiac
outcomes in both routine and high-risk PCI.
• A large, randomized, multicenter trial involving 900 patients did not show a difference
in mortality at 6 months but did show improvement in ischemia driven target vessel
revascularization and less angina in the stented patients compared to balloon
angioplasty alone.
• Whether to use a bare metal stent or a drug-eluting stent in acute MI is a question that
has not yet been addressed definitively by clinical trials; selection is currently based on
both patient and angiographic characteristics.
38. • Early recognition and diagnosis of STEMI are key to achieving the
desired door-to-needle (or medical contact–to-needle) time for
initiation of fibrinolytic therapy of 30 minutes or door-to-balloon (or
medical contact–to balloon) time for PCI under 90 minutes.
• Achieving reperfusion in timely matter correlates with improvement
in ultimate infarct size, LV function, and survival.
• The ultimate goal is to restore adequate blood flow through the
infarct-related artery to the infarct zone, as well as to limit
microvascular damage and reperfusion injury.
• The latter is accomplished with adjunctive and ancillary treatments.
39.
40. Adjunctive therapy
1. Aspirin:
• Reduce mortality in acute infarction to the same degree as fibrinolytic
therapy, and its effects are additive to fibrinolytics. In addition, aspirin
reduces the risk of reinfarction.
• Unless contraindicated, all patients with a suspected ACS (STEMI,
NSTEMI, UA) should be given aspirin as soon as possible.
2. Thienopyridines:
• Clopidagrel
• Prasugrel
Patients presenting with MI should be considered
for a thienopyridine regardless of whether or not
they underwent reperfusion therapy. The duration
of thienopyridine use in this population has yet to
be defined.
41. 3. Anticoagulants:
Administration of full-dose heparin
after fibrinolytic therapy with tPA is
essential to diminish re-occlusion
after successful reperfusion.
4. Glycoprotein llb/IIIa Receptor
antagonist:
Role in STEMI uncertain. Not
routinely recommended.
42.
43. 5. Nitrates:
• They reduce myocardial oxygen demand by decreasing preload and
afterload, and they may also improve myocardial oxygen supply by
increasing sub-endocardial perfusion and collateral blood flow to the
ischemic region.
• Also reduce platelet aggregation.
• Nitrates are first-line agents for the symptomatic relief of angina
pectoris and when MI is complicated by congestive heart failure.
44. 6. β Blockers:
• Routine use of intravenous beta-blockers in the absence of systemic
hypertension is no longer recommended.
• Relative contraindications to oral beta-blockers include,
heart rate less than 60 bpm,
systolic arterial pressure less than 100 mm Hg,
moderate or severe LV failure,
signs of peripheral hypoperfusion,
shock,
PR interval greater than 0.24 second, second- or third-degree AV
block,
active asthma, or
reactive airway disease.
45. 7. ACE inhibitors
• Improve hemodynamic, functional capacity and symptoms, and
survival in patients with chronic congestive heart failure. Moreover,
ACE inhibitors prevent the development of congestive heart failure in
patients with asymptomatic LV dysfunction
8. Lipid Lowering agents
• All patients with ACS should be started on a statin prior to discharge
unless there is a contraindication
9. Calcium channel blockers
• May be useful for patients whose postinfarction course is
complicated by recurrent angina, because these agents not only
reduce myocardial oxygen demand but also inhibit coronary
vasoconstriction.
47. NTSEMI and Unstable angina
• Non-ST-elevation MI (NSTEMI) applies to patients with suspected MI in the
absence of other plausible causes of troponin elevation (e.g. sepsis,
pulmonary embolus).
• On physical examination, patients with NSTEMI may have a ‘normal’ ECG
reading, or show minor changes (occurs in up to 50% of patients).
• All patients with NSTEMI should have their risk stratified to direct
management decisions.
• The management of patients with NSTEACS requires evolving risk
stratification:
Clinical assessment, assessment of Cardiac biomarkers and Time.
48. ECG Changes
NSTEMI:
• ST depressions (0.5 mm at least) or T wave inversions ( 1.0 mm at
least) without Q waves in 2 contiguous leads with prominent R
wave or R/S ratio >1.
• Isolated T wave inversions:
• can correlate with increased risk for MI
• may represent Wellen’s syndrome:
• critical LAD stenosis
• >2mm inversions in anterior precordial leads
Unstable Angina:
• May present with nonspecific or transient ST segment depressions
or elevations
50. Evolving Risk Stratification
• Provides prognostic information
• Determines treatment and level of
intervention
Low risk patients ---> early discharge,
High risk ---> admission to high care
• Helps decongest the casualty and make
available medical resources to more
needy patients.
• Risk stratification should be ongoing – at
admission, 6-8 hrs, 24hrs, discharge
51. Evolving risk stratification…
Admit to coronary care unit or high
dependency unit:
• Estimate ischemic risk,
estimate bleeding risk, choose
augmented antithrombotic
therapy
→ refer for angiography to
determine surgery/PCI, or
medical therapy.
53. Evolving risk stratification…
Intermediate-risk NSTEACS
Recurrent ischemia or elevated troponin?
YES
• admit to CCU or high dependency unit:
estimate ischemic risk, estimate
bleeding risk, choose augmented
antithrombotic therapy
→refer for angiography to determine
surgery/PCI, or medical therapy.
NO
• undertake stress test (e.g. exercise ECG):
→positive – refer for angiography to determine
surgery/PCI, or medical therapy
→negative – proceed to discharge patient with
urgent cardiac follow-up (on upgraded medical
therapy) according to long-term management
after control of myocardial ischemia.
54. Evolving risk stratification…
Appropriate period of
observation. Consider if
stress test (e.g. exercise
ECG) needed?
Stress test (e.g. exercise ECG)
using treadmill.
YES
Proceed to discharge patient with urgent
cardiac follow-up (on upgraded medical
therapy) according to long-term
management after control of myocardial
ischemia.
NO
55. • Age ≥ 65 years =1 point
• At least 3 risk factors for CAD =1 point
• Prior coronary stenosis of ≥ 50% =1 point
• ST-segment deviation on ECG presentation =1 point
• At least 2 anginal events in prior 24 hours =1 point
• Use of aspirin in prior 7 days =1 point
• Elevated serum cardiac biomarkers =1 point
Variables Used in the TIMI Risk Score
57. GRACE Risk Score
Variable Odds ratio
Older age 1.7 per 10 y
Killip class 2.0 per class
Systolic BP 1.4 per 20 mm Hg ↑
ST-segment deviation 2.4
Cardiac arrest during presentation 4.3
Serum creatinine level 1.2 per 1-mg/dL ↑
Positive initial cardiac biomarkers 1.6
Heart rate 1.3 per 30-beat/min
↑
58. Management
• It Includes increasing myocardial oxygen demand delivery by improving
perfusion and decreasing myocardial oxygen demand.
• Reversing myocardial ischemia and confirming the diagnosis of ACS is
essential priority.
• Oxygen should be administered to patients with dyspnea, hypoxemia or
evidence of heart failure or shock.
• If precipitating reversible causes such as fever, anemia, hypoxemia,
infection, hypertension, anxiety, hyperthyroidism, arrhythmias or any drug
ingestion (eg cocaine, ephedrine) can be identified, they should be treated
aggressively.
• Further management includes relief of pain and anti- ischemic therepy,
therepy for platelet aggregation/thrombosis, ongoing risk stratification
and consideration of invasive reperfusion procedures.
60. 2. Antiplatelet therapy
• The current guidelines recommend a loading dose of 300 to 600mg
of clopidogrel in patients of UA/NSTEMI, followed by 75 mg daily.
The duration of clopidogrel may depend upon whether or not the
patient has received stent.
3. Anti thrombin therapy
Recommendation
Low risk : Aspirin + Anticoagulant + either a glycoprotein IIb/IIIa inhibitor or a
thienopyridine
High Risk: Aspirin + Anticoagulant + a glycoprotein IIb/IIIa inhibitor + a
thienopyridine
61. Interventional Management
In patients with High Risk, following treatment with anti-ischemic and
antithrombotic agents, coronary arteriography is carried out within ~ 48 h of
admission, followed by coronary revascularization (PCI or coronary artery
bypass grafting), depending on the coronary anatomy.
In low-risk patients, the outcomes from an
invasive strategy are similar to those
obtained from a conservative strategy,
which consists of anti-ischemic and
antithrombotic therapy followed by
“watchful waiting,” and in which coronary
arteriography is carried out only if rest pain
or ST-segment changes recur or there is
evidence of ischemia on a stress test.