Myocardial ischemia occurs when heart muscle does not receive enough oxygen due to narrowing of the coronary arteries. The main causes are atherosclerosis and coronary thrombosis. Symptoms include chest pain known as angina. Diagnosis involves ECG, stress testing, and cardiac catheterization. Treatment aims to increase blood flow through medications like nitrates and calcium channel blockers, or procedures like angioplasty and bypass surgery. Myocardial infarction results from prolonged ischemia and cell death. It can cause complications like heart failure and arrhythmias. Treatment focuses on restoring blood flow, managing pain and arrhythmias, and preventing further damage.
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Some of the slides, i hide it from my real presentations for my own reference. Download to see all of them.
Arrhythmia is also known as irregular heart beats. If SA node is not the pacemaker, any other part of the heart such as atrial muscle, AV node and ventricular muscle becomes the pacemaker. the beats may be fast, slow or miss beats.
Definition of arrhythmia - background on cardiac physiology including conduction in heart - action potential - pathogensis of arrhythmia - causes and risk factors for arrhythmia- diagnosis of arrhythmia - symptoms of tachyarrhythmias and bradyarrhythmias - investigations for arrhythmia - treatment of arrhythmia - pharmacological and other modalities of therapy for arrhythmia - managment of different types of arrhythmias
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
Kindly leave your comment if you found this helpful ;)
Some of the slides, i hide it from my real presentations for my own reference. Download to see all of them.
Arrhythmia is also known as irregular heart beats. If SA node is not the pacemaker, any other part of the heart such as atrial muscle, AV node and ventricular muscle becomes the pacemaker. the beats may be fast, slow or miss beats.
Definition of arrhythmia - background on cardiac physiology including conduction in heart - action potential - pathogensis of arrhythmia - causes and risk factors for arrhythmia- diagnosis of arrhythmia - symptoms of tachyarrhythmias and bradyarrhythmias - investigations for arrhythmia - treatment of arrhythmia - pharmacological and other modalities of therapy for arrhythmia - managment of different types of arrhythmias
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
This presentation provides a knowledge about Ischemic heart Disease, Ischemia, Mechanism of Action, signs and symptoms, Causes of Ischemia, Ischemia in different body parts, Angina, Myocardial Infarction, Artherosclerosis, Drugs used to treat ischemia and recent discovery related to Cardiac ischemia. An assignment for the subject, Advanced Pharmacology-I, 1st year M.Pharm, 1st semester.
Comparing Evolved Extractive Text Summary Scores of Bidirectional Encoder Rep...University of Maribor
Slides from:
11th International Conference on Electrical, Electronics and Computer Engineering (IcETRAN), Niš, 3-6 June 2024
Track: Artificial Intelligence
https://www.etran.rs/2024/en/home-english/
DERIVATION OF MODIFIED BERNOULLI EQUATION WITH VISCOUS EFFECTS AND TERMINAL V...Wasswaderrick3
In this book, we use conservation of energy techniques on a fluid element to derive the Modified Bernoulli equation of flow with viscous or friction effects. We derive the general equation of flow/ velocity and then from this we derive the Pouiselle flow equation, the transition flow equation and the turbulent flow equation. In the situations where there are no viscous effects , the equation reduces to the Bernoulli equation. From experimental results, we are able to include other terms in the Bernoulli equation. We also look at cases where pressure gradients exist. We use the Modified Bernoulli equation to derive equations of flow rate for pipes of different cross sectional areas connected together. We also extend our techniques of energy conservation to a sphere falling in a viscous medium under the effect of gravity. We demonstrate Stokes equation of terminal velocity and turbulent flow equation. We look at a way of calculating the time taken for a body to fall in a viscous medium. We also look at the general equation of terminal velocity.
THE IMPORTANCE OF MARTIAN ATMOSPHERE SAMPLE RETURN.Sérgio Sacani
The return of a sample of near-surface atmosphere from Mars would facilitate answers to several first-order science questions surrounding the formation and evolution of the planet. One of the important aspects of terrestrial planet formation in general is the role that primary atmospheres played in influencing the chemistry and structure of the planets and their antecedents. Studies of the martian atmosphere can be used to investigate the role of a primary atmosphere in its history. Atmosphere samples would also inform our understanding of the near-surface chemistry of the planet, and ultimately the prospects for life. High-precision isotopic analyses of constituent gases are needed to address these questions, requiring that the analyses are made on returned samples rather than in situ.
Seminar of U.V. Spectroscopy by SAMIR PANDASAMIR PANDA
Spectroscopy is a branch of science dealing the study of interaction of electromagnetic radiation with matter.
Ultraviolet-visible spectroscopy refers to absorption spectroscopy or reflect spectroscopy in the UV-VIS spectral region.
Ultraviolet-visible spectroscopy is an analytical method that can measure the amount of light received by the analyte.
Toxic effects of heavy metals : Lead and Arsenicsanjana502982
Heavy metals are naturally occuring metallic chemical elements that have relatively high density, and are toxic at even low concentrations. All toxic metals are termed as heavy metals irrespective of their atomic mass and density, eg. arsenic, lead, mercury, cadmium, thallium, chromium, etc.
Richard's aventures in two entangled wonderlandsRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
Nutraceutical market, scope and growth: Herbal drug technologyLokesh Patil
As consumer awareness of health and wellness rises, the nutraceutical market—which includes goods like functional meals, drinks, and dietary supplements that provide health advantages beyond basic nutrition—is growing significantly. As healthcare expenses rise, the population ages, and people want natural and preventative health solutions more and more, this industry is increasing quickly. Further driving market expansion are product formulation innovations and the use of cutting-edge technology for customized nutrition. With its worldwide reach, the nutraceutical industry is expected to keep growing and provide significant chances for research and investment in a number of categories, including vitamins, minerals, probiotics, and herbal supplements.
Deep Behavioral Phenotyping in Systems Neuroscience for Functional Atlasing a...Ana Luísa Pinho
Functional Magnetic Resonance Imaging (fMRI) provides means to characterize brain activations in response to behavior. However, cognitive neuroscience has been limited to group-level effects referring to the performance of specific tasks. To obtain the functional profile of elementary cognitive mechanisms, the combination of brain responses to many tasks is required. Yet, to date, both structural atlases and parcellation-based activations do not fully account for cognitive function and still present several limitations. Further, they do not adapt overall to individual characteristics. In this talk, I will give an account of deep-behavioral phenotyping strategies, namely data-driven methods in large task-fMRI datasets, to optimize functional brain-data collection and improve inference of effects-of-interest related to mental processes. Key to this approach is the employment of fast multi-functional paradigms rich on features that can be well parametrized and, consequently, facilitate the creation of psycho-physiological constructs to be modelled with imaging data. Particular emphasis will be given to music stimuli when studying high-order cognitive mechanisms, due to their ecological nature and quality to enable complex behavior compounded by discrete entities. I will also discuss how deep-behavioral phenotyping and individualized models applied to neuroimaging data can better account for the subject-specific organization of domain-general cognitive systems in the human brain. Finally, the accumulation of functional brain signatures brings the possibility to clarify relationships among tasks and create a univocal link between brain systems and mental functions through: (1) the development of ontologies proposing an organization of cognitive processes; and (2) brain-network taxonomies describing functional specialization. To this end, tools to improve commensurability in cognitive science are necessary, such as public repositories, ontology-based platforms and automated meta-analysis tools. I will thus discuss some brain-atlasing resources currently under development, and their applicability in cognitive as well as clinical neuroscience.
(May 29th, 2024) Advancements in Intravital Microscopy- Insights for Preclini...Scintica Instrumentation
Intravital microscopy (IVM) is a powerful tool utilized to study cellular behavior over time and space in vivo. Much of our understanding of cell biology has been accomplished using various in vitro and ex vivo methods; however, these studies do not necessarily reflect the natural dynamics of biological processes. Unlike traditional cell culture or fixed tissue imaging, IVM allows for the ultra-fast high-resolution imaging of cellular processes over time and space and were studied in its natural environment. Real-time visualization of biological processes in the context of an intact organism helps maintain physiological relevance and provide insights into the progression of disease, response to treatments or developmental processes.
In this webinar we give an overview of advanced applications of the IVM system in preclinical research. IVIM technology is a provider of all-in-one intravital microscopy systems and solutions optimized for in vivo imaging of live animal models at sub-micron resolution. The system’s unique features and user-friendly software enables researchers to probe fast dynamic biological processes such as immune cell tracking, cell-cell interaction as well as vascularization and tumor metastasis with exceptional detail. This webinar will also give an overview of IVM being utilized in drug development, offering a view into the intricate interaction between drugs/nanoparticles and tissues in vivo and allows for the evaluation of therapeutic intervention in a variety of tissues and organs. This interdisciplinary collaboration continues to drive the advancements of novel therapeutic strategies.
Earliest Galaxies in the JADES Origins Field: Luminosity Function and Cosmic ...Sérgio Sacani
We characterize the earliest galaxy population in the JADES Origins Field (JOF), the deepest
imaging field observed with JWST. We make use of the ancillary Hubble optical images (5 filters
spanning 0.4−0.9µm) and novel JWST images with 14 filters spanning 0.8−5µm, including 7 mediumband filters, and reaching total exposure times of up to 46 hours per filter. We combine all our data
at > 2.3µm to construct an ultradeep image, reaching as deep as ≈ 31.4 AB mag in the stack and
30.3-31.0 AB mag (5σ, r = 0.1” circular aperture) in individual filters. We measure photometric
redshifts and use robust selection criteria to identify a sample of eight galaxy candidates at redshifts
z = 11.5 − 15. These objects show compact half-light radii of R1/2 ∼ 50 − 200pc, stellar masses of
M⋆ ∼ 107−108M⊙, and star-formation rates of SFR ∼ 0.1−1 M⊙ yr−1
. Our search finds no candidates
at 15 < z < 20, placing upper limits at these redshifts. We develop a forward modeling approach to
infer the properties of the evolving luminosity function without binning in redshift or luminosity that
marginalizes over the photometric redshift uncertainty of our candidate galaxies and incorporates the
impact of non-detections. We find a z = 12 luminosity function in good agreement with prior results,
and that the luminosity function normalization and UV luminosity density decline by a factor of ∼ 2.5
from z = 12 to z = 14. We discuss the possible implications of our results in the context of theoretical
models for evolution of the dark matter halo mass function.
2. Myocardial Ischemia
• Myocardial ischemia occurs when the blood
flow demands of the heart exceed the blood
supplied by the coronary arteries.
• The leading cause of myocardial
ischemia is:
a) atherosclerosis or
b) Coronary thrombosis.
3. pathophysiology of myocardial
ischemia:
Under conditions of rest, myocardial oxygen supply and
delivery of nutrients through the coronary arteries should
match the metabolic requirements of the heart. When the
metabolic needs of the heart increase, the coronary blood
flow must increase accordingly.
The myocardial oxygen balance is affected by several factors
that :
a) will increase the oxygen and nutrient demand of the
myocardium as: exercise, stress and cold.
b) will increase coronary blood flow as cardiac metabolites and
nitric oxide.
4. With age and progressive occlusion of coronary arteries, smaller
collateral vessels may begin to carry a greater proportion of
blood and provide an alternate means of perfusion for an area
of myocardium. These collateral blood vessels may run parallel
to the larger coronary arteries and be connected to other small
coronary vessels by vascular connections called anastomoses.
Development of collateral circulation may reduce or delay the
occurrence of symptoms from myocardial ischemia until the
blockage is very progressed.
The presence of extensively developed collateral circulation
might also explain why many older individuals often survive
serious heart attacks when younger individuals, who have not
yet developed collateral circulation, often do not.
5. Manifestation of myocardial
ischemia:
• Angina pectoris
It is the major symptom of myocardial ischemia.
Angina pectoris most commonly presents as severe
pain the chest.
There are three types of Angina pectoris
1. Classic or stable angina
Pain is precipitated by increased workload on the heart. May be
caused by exercise, emotions, stress and cold exposure.
Symptoms may remain “stable” for a number of years or progress in
severity.
6. 2. Unstable angina
Angina that occurs at rest.
Also referred to as “pre-infarct” angina since it is usually
associated with extensive blockage of coronary arteries. Coronary
blood flow does not meet the needs of the heart even at rest.
Requires intensive treatment and evaluation.
3. Variant angina (vasospastic angina, Prinzmetal’s angina)
Caused by vasospasm of the coronary arteries.
Usually associated with coronary artery disease but may result
from excess sympathetic activity.
Frequently occurs at night, at rest or during minimal exercise.
May be precipitated by stress, cold exposure or smoking.
7. Silent ischemia
is a particularly dangerous form
of myocardial ischemia as there
is a lack of clinical symptoms,
i.e., ischemia without angina.
Usually diagnosed by exercise
stress testing or Holter
monitoring.
9. Rationale for treatment of myocardial
ischemia:
• Treatment of myocardial ischemia
and the resulting angina can
involve two strategies:
• 1. Increase coronary blood flow by
dilating coronary arteries.
• 2. Reduce cardiac workload by
reducing heart rate and/or force of
contraction
10. The treatment regimen may include :
1. nonpharmacologic treatment
2. pharmacologic therapies.
Nonpharmacologic treatment
Pacing of physical activity.
• Avoidance of stress (emotional, physiologic, cold).
• Reduction of risk factors for ischemic heart disease,
(hyperlipidemia, obesity, hypertension, diabetes,
smoking, etc.)
11. Pharmacologic treatment
Organic Nitrates
Mechanism of action:
• Dilate coronary arteries and increase myocardial blood flow.
• Dilate peripheral arteries and reduce afterload.
• Dilate peripheral veins and reduce preload.
Examples
Amyl nitrate, nitroglycerine, isosorbide dinitrite
Route of administration : Inhalation, sublingual, oral, transdermal, intravenous
Long-acting forms such as isosorbide dinitrite used for prophylaxis of angina
Short-acting forms such as sublingual nitroglycerin may be used during angina
attacks
Major adverse effects :include headache, hypotension. Tolerance may develop
rapidly.
12. β-Adrenergic blockers
Mechanism of action:
Block myocardial β-adrenergic receptors.
Reduce heart rate and cardiac output (reduced
myocardial workload and oxygen demand).
Examples of β-Adrenergic Receptor Antagonists :
May be selective β1 (atenolol), or
nonselective β1 and β2 blockers (propranolol)
Major adverse effects :
include bradycardia, reduced cardiac output,
pacemaker
depression and bronchoconstriction with
nonspecific drugs
13. Calcium channel blockers
• Mechanism of action:
• Block calcium channels in vascular smooth muscle.
• Dilate coronary arteries and increase myocardial blood flow.
• Dilate peripheral arteries and reduce afterload.
Examples: Dihydropyridines (nifedipine), verapamil, diltiazem
Dihydropyridines have greater specificity for relaxing vascular smooth muscle
Verapmail and diltiazem have greater effects on cardiac pacemaker tissues
Major adverse effects include headache, hypotension, reflex tachycardia; risk of
heart block of cardiac failure particularly with verapamil or diltiazem
Also used for hypertension and arrhythmia
14. Aspirin
• Prevent platelet aggregation.
• Use for prophylaxis of blood clots particularly
in unstable angina.
15. Surgical treatment
• Coronary angioplasty
• Uses a balloon catheter to open occluded blood vessels
• Usually performed under local anesthetic
• 5% mortality, high rate of vessel re-occlusion
• Use of metal “stents” in opened vessel reduces rate of
occlusion
Coronary artery bypass graft
• Revascularization procedure in which a blood vessel is taken from
elsewhere in the body and surgically sutured around a blocked
coronary artery
• May involve multiple (one to five) blood vessels
• Re-occlusion of transplanted vessel is possible
16. Myocardial Infarction
• Myocardial infarction or “heart attack” is an irreversible injury to and
eventual death of myocardial tissue that results from ischemia and
hypoxia.
• Myocardial infarction is the leading killer of both men and women in
the United States.
• Most heart attacks are the direct result of occlusion of a coronary
blood vessel by a lipid deposit. These lipid deposits may accumulate
to the point where they completely block a coronary vessel or, more
commonly, accumulated lipid plaques may break off from the
vascular endothelium and act as a thrombus that blocks a coronary
artery at a narrower point downstream. Prolonged vasospasm might
also precipitate a myocardial infarction in certain individuals.
17. Coronary Arteries for the heart
The two main coronary arteries supplying the
myocardium are:
1. the left coronary artery (which subdivides into the
left anterior descending and circumflex branches) and
2. the right coronary artery
18. • The left anterior descending artery supplies blood to
the bulk of the anterior left ventricular wall, while the
left circumflex artery provides blood to the left atrium
and the posterior and lateral walls of the left ventricle.
The right coronary artery provides blood mainly to the
right atria and right ventricles.
• Nearly 50% of all myocardial infarctions involve the left
anterior descending artery that supplies blood to the
main pumping mass of the left ventricle.
• The next most common site for myocardial infarction is
the right coronary artery, followed by the left
circumflex.
19. A myocardial infarction may be:
a) transmural, meaning it involves the full thickness
of the ventricular wall, or
b) subendocardial, in which the inner one third to
one half of the ventricular wall is involved.
Transmural infarcts tend to have a greater effect on
cardiac function and pumping ability since a greater
mass of ventricular muscle is involved.
20. Manifestations of myocardial
infarction
1. Severe chest pain and discomfort : Pressing or crushing
sensation often accompanied by nausea, vomiting, sweating
and weakness due to hypotension. A significant percentage of
myocardial infarctions are “silent” and have no symptoms.
2. Irreversible cellular injury: Generally occurs 20 to 30 minutes
after the onset of complete ischemia.
3. Release of myocardial enzymes such as creatine
phosphokinase (CPK) and lactate dehydrogenase (LDH) into
circulation from myocardial damaged cells.
21. 4.Electrocardiogram changes : Inversion of T wave, ST
elevation, pronounced Q waves.
5.Inflammatory response from the injured myocardium :
Leukocyte infiltration, increased white blood cell
counts, fever.
6. Coagulative necrosis of the area of the myocardium
affected by the infarction.
7. Repair of damaged areas occurs by replacement with
scar tissue and not functional muscle tissue; therefore,
some alteration in function is inevitable
22. Complications of myocardial
infarction
Depending on the extent of the area involved in a myocardial
infarction, a number of complications might arise, including:
1. Rupture of weakened myocardial wall. Bleeding into pericardium
may cause cardiac tamponade and further impair cardiac pumping
function. This is most likely to occur with a transmural infarction.
Rupture of the septum between the ventricles might also occur if
the septal wall is involved in the infarction.
2. Formation of a thromboembolism from pooling of blood in the
ventricles.
3. Pericarditis : Inflammation due to pericardial friction rub. Often
occurs 1 to 2 days after the infarction.
4. Arrhythmia : Common as a result of hypoxia, acidosis and altered
electrical conduction through damaged and necrotic areas of the
myocardium. May be life-threatening and lead to fibrillation.
23. 5. Reduced cardiac function : Typically presents with reduced
myocardial contractility, reduced wall compliance, decreased
stroke volume and increased left ventricular end diastolic
volume.
6. Congestive heart failure: may result if a large enough area of
the myocardium has been damaged such that the heart no
longer pumps effectively.
7. Cardiogenic shock : Marked hypotension that can result from
extensive damage to the left ventricle. The resulting
hypotension will trigger cardiovascular compensatory
mechanisms that will further tax the damaged myocardium
and exacerbate impaired function. Cardiogenic shock is
associated with a mortality rate of 80% or greater.
24. Compensatory mechanisms of
myocardial infarction
As a result of the hypotension and hemodynamic changes that accompany a
myocardial infarction, the cardiovascular system initiates a number of
reflex compensatory mechanisms designed to maintain cardiac output
and adequate tissue perfusion :
1.Catecholamine release : Increases heart rate, force of contraction and
peripheral resistance.
2. Sodium and water retention.
3. Activation of renin–angiotensin system leading to peripheral
vasoconstriction.
4. Ventricular hypertrophy.
Unfortunately, these compensatory changes may increase oxygen demand and
workload on the infarcted heart and worsen overall cardiac function.
25. Treatment for myocardial infarction
1. Oxygen : Used to maintain blood oxygenation as well as
tissue and cardiac O2 levels.
2. Aspirin : If administered when myocardial infarction is
detected, the antiplatelet properties of aspirin may reduce
the overall size of the infarction.
3. Thrombolytic therapy :If employed in the first 1 to 4 hours
following the onset of a myocardial infarction, these drugs
may dissolve clots in coronary blood vessels and re-
establish blood flow.
4. Vasodilator drugs : Intravenous nitroglycerin can increase
blood flow to the myocardium and reduce myocardial work.
26. 5.β -Blockers : Blunt the effect of catecholamine release on the
myocardium, reduce heart rate and myocardial work.
6. Pain management : Sublingual nitroglycerin, morphine if
necessary
7. Antiarrhythmic drugs : To treat and prevent a number of
potentially life-threatening arrhythmias that might arise
following a myocardial infarction.
8. ACE inhibitors : the negative effects of vasoconstriction and
salt and water retention on the myocardium.
27. Thrombolytic Agents Used Clinically
a. Streptokinase : Derived from β -hemolytic streptococcus
bacteria; involved in the activation of plasmin
b. Anistreplase (APSAC) : Complex of human lys-plasminogen
and streptokinase; Administered as a prodrug
c. Alteplase (TPA): Recombinant tissue plasminogen activator
d. Urokinase : Endogenous human enzyme that converts
plasminogen to active plasmin
e. Routes of administration : Intravenous. for all of the above
f. Major unwanted effects : Internal bleeding,
gastrointestinal bleeding, stroke, allergic reactions