Myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw.
Definition of heart failure - causes and types of heart failure - pathophysiology and risky factors for heart failure - Diagnosis clinical manifestations and investigations and classification of heart failure- treatment of chronic heart failure
Also Acute heart failure causes - clinical picture and treatment
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
Myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw.
Definition of heart failure - causes and types of heart failure - pathophysiology and risky factors for heart failure - Diagnosis clinical manifestations and investigations and classification of heart failure- treatment of chronic heart failure
Also Acute heart failure causes - clinical picture and treatment
definition of heart failure, classification of heart failure, risk factors for heart failure, clinical features, general physical examination findings in heart failure
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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
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The French Revolution, which began in 1789, was a period of radical social and political upheaval in France. It marked the decline of absolute monarchies, the rise of secular and democratic republics, and the eventual rise of Napoleon Bonaparte. This revolutionary period is crucial in understanding the transition from feudalism to modernity in Europe.
For more information, visit-www.vavaclasses.com
The Indian economy is classified into different sectors to simplify the analysis and understanding of economic activities. For Class 10, it's essential to grasp the sectors of the Indian economy, understand their characteristics, and recognize their importance. This guide will provide detailed notes on the Sectors of the Indian Economy Class 10, using specific long-tail keywords to enhance comprehension.
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http://sandymillin.wordpress.com/iateflwebinar2024
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Knowledge and skills frameworks, generally called competency frameworks, for ELT teachers, trainers and managers have existed for a few years now. However, until I created one for my MA dissertation, there wasn’t one drawing together what we need to know and do to be able to effectively produce language learning materials.
This webinar will introduce you to my framework, highlighting the key competencies I identified from my research. It will also show how anybody involved in language teaching (any language, not just English!), teacher training, managing schools or developing language learning materials can benefit from using the framework.
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Culturally, the Romans were eclectic, absorbing and adapting elements from the civilizations they encountered, particularly the Greeks. Roman art, literature, and philosophy reflected this synthesis, creating a rich cultural tapestry. Latin, the Roman language, became the lingua franca of the Western world, influencing numerous modern languages.
Roman architecture and engineering achievements were monumental. They perfected the arch, vault, and dome, constructing enduring structures like the Colosseum, Pantheon, and aqueducts. These engineering marvels not only showcased Roman ingenuity but also served practical purposes, from public entertainment to water supply.
4. 4
Introduction
Definiton:
Ischemic heart disease (IHD) is a condition in which there is
an inadequate supply of blood and oxygen to a portion of the
myocardium
Imbalance between myocardial oxygen supply and demand
Also known as Coronary Artery Disease (CAD)
5. 5
Introduction
Caused mainly by Atherosclerosis of
Coronary Artery
It includes
o Angina: Stable & Unstable
o Myocardial infarction
6. 6
Introduction
In 2015 CAD affected 110 million people and resulted in 8.9
million deaths.
It makes up 15.9% of all deaths making it the most common
cause of death globally.
The risk of death from CAD for a given age has decreased
between 1980 and 2010, especially in developed countries.
Rates are higher among men than women of a given age
8. 8
Atherosclerosis
Can affect any artery in the body
Heart: angina, MI and sudden
death
Brain: stroke and transient
ischaemic attack
Limbs: claudication and critical
limb ischaemia
9. 9
Atherosclerosis
Progressive inflammatory disorder of the arterial wall
characterized by focal lipid rich deposits of atheroma
Remain clinically asymptomatic until
o large enough to impair tissue perfusion,
o Ulceration and disruption of the lesion result in
thrombotic occlusion
o Distal embolization of the vessel.
Clinical manifestations depend upon the site of the
lesion and the vulnerability of the organ supplied
12. 12
Astherosclerosis
Relative Risk
o Smoking
o Hypertension
o Diabetes mellitus
o Hypercholesterolaemia
o Hemostatic factors.
o Obesity
o Physical in-activity
o Alcohol
14. 14
Angina
A type of chest pain
Not a disease, its a symptom of an underlying heart
problem specially IHD
Described as ‘heavy’, ‘tight’ or ‘gripping’.
Typically, central/retrosternal
Mild ache to most severe that provokes sweating
and fear
Associated breathlessness
15. 15
Classical or Exertional
Angina Pectoris
Characterized by
o constricting discomfort in the front of the chest,
arms,neck, jaw
o provoked by physical exertion, especially after meals and
in cold, windy weather or by anger or excitement
o relieved (usually within minutes) with rest or glyceryl
trinitrate. Occasionally, it disappears with continued
exertion (‘walking through the pain’).
16. 16
Classical or Exertional
Angina Pectoris
Typical angina: all three features,
Atypical angina: two out of the three,
Non-anginal chest pain: one or less of these features
17. 17
Types of Angina
I. Stable Angina:
episodic clinical syndrome where there is no change in
severity of attacks.
II. Unstable angina:
Deterioration(24 hrs) in previous stable angina with
symptoms frequently occurring at rest, i.e. acute
coronary syndrome
18. 18
Types of Angina
III. Refractory angina:
patients with severe coronary disease in whom
revascularization is not possible and angina is not
controlled by medical therapy.
IV. Variant (Prinzmetal’s) angina:
occurs without provocation, usually at rest, as a result of
coronary artery spasm, more frequently in women
19. 19
Stable Angina
Characterized by central chest pain, discomfort or
breathlessness that is precipitated by exertion or
other forms of stress and is promptly relieved by
rest
21. 21
Stable Angina
Activities precipitating angina
Common
o Physical exertion
o Cold exposure
o Heavy meals
o Intense emotion
Uncommon
o Lying flat (decubitus angina)
o Vivid dreams (nocturnal angina)
22. 22
Clinical Features
History is the most important factor in making the
diagnosis
Physical examination is unremarkable
Careful search for evidence of underlying
o valve disease - left ventricular dysfunction -
arterial disease
o unrelated conditions that may exacerbate angina
(anemia, thyrotoxicosis).
Important assessment of risk factors
23. 23
Investigations
Resting ECG
often normal
Reversible ST segment depression or
elevation, with or without T-wave
inversion, at the time the patient is
experiencing symptoms
24. 24
Investigations
Exercise ECG
Use standard treadmill or bicycle
while monitoring the patient’s
ECG, BP and general condition.
Planar or down-sloping ST
segment depression of ≥ 1mm is
indicative of ischemia
Up-sloping ST depression is less
specific and often occurs in
normal individuals
25. 25
Investigations
Coronary arteriography
detailed anatomical information about
the extent and nature of coronary artery
disease
indicated when non-invasive tests have
failed to establish the cause of atypical
chest pain
27. 27
Treatment
Management of angina pectoris involves:
careful assessment of the extent and severity of arterial
disease
identification and control of risk factors such as smoking,
hypertension and hyperlipidemia
use of measures to control symptoms
Identification of high-risk patients for treatment to improve
life expectancy.
28. 28
Medical Treatment
Antiplatelet therapy
Low-dose (75 mg) aspirin
o reduces the risk of adverse events such as MI
o prescribed for all patients with CAD indefinitely
Clopidogrel (75 mg daily)
o ALTERNATIVE if aspirin causes dyspepsia or other
side-effects
30. 30
Medical Treatment
1. Nitrates
act directly on vascular smooth muscle to produce venous and
arteriolar dilatation
reduction in myocardial oxygen demand
Increase in myocardial oxygen supply
prophylactically before taking exercise that is liable to provoke
symptoms.
Continuous nitrate therapy can cause pharmacological
tolerance
o avoided by a 6–8-hour nitrate-free period
o Nocturnal angina: long acting nitrates can be given at the end
of the day
31. 31
Medical Treatment
2. β-blockers
lower myocardial oxygen demand by reducing heart rate, BP
and myocardial contractility
May provoke bronchospasm in patients with asthma
3. Calcium antagonists
inhibit the slow inward current caused by the entry of
extracellular calcium through the cell membrane of excitable
cells
particularly cardiac and arteriolar smooth muscle
lower myocardial oxygen demand by reducing BP and
myocardial contractility
32. 32
Medical Treatment
4. Potassium channel activators
arterial and venous dilating properties
do not exhibit the tolerance seen with nitrates.
E.g Nicorandil
5. If channel antagonist
Ivabradine is the first of this class of drug
Induces bradycardia by modulating ion channels in the sinus
node
not have other cardiovascular effects
Safe to use in patients with heart failure
33. 33
Medical Treatment
It is conventional to start therapy with
o low-dose aspirin,
o a statin,
o sublingual GTN
o β-blocker,
And then add a calcium channel antagonist or a
long-acting nitrate later if needed
34. 34
Medical Treatment
goal is the control of angina with minimum side-
effects and the simplest possible drug regimen
little evidence that prescribing multiple anti-
anginal drugs is of benefit
Revascularisation : if an appropriate combination
of two or ore drugs fails to achieve an acceptable
symptomatic response
35. 35
Percutaneous Coronary
Intervention(PCI)
Passing a fine guide-wire across a coronary stenosis
under radiographic control
Balloon is placed and then inflated to dilate the stenosis
Then a coronary stent is deployed on a balloon
Mainly used in single or two-vessel disease
37. 37
Coronary artery bypass grafting
(CABG)
Stenosed artery is by-passed with
o internal mammary arteries
o radial arteries
o reversed segments of the patient’s own saphenous vein
Major surgery under cardiopulmonary bypass
40. 40
ACUTE CORONARY SYNDROMES
Myocardial Infarction: ST-elevation myocardial infarction
(STEMI) or Non-ST-elevation myocardial infarction
(NSTEMI)
o symptoms occur at rest
o evidence of myocardial necrosis - increased cardiac troponin or
Creatine kinase
Unstable angina (UA).
o new-onset or rapidly worsening angina (crescendo angina)
o angina on minimal exertion
o or angina at rest in the absence of myocardial damage
41. 41
ACUTE CORONARY SYNDROMES
Present as a new phenomenon or against a background
of chronic stable angina.
Complex ulcerated or fissured atheromatous plaque
with adherent platelet rich thrombus and local coronary
artery spasm.
Without treatment, the infarct-related artery remains
permanently occluded in 20–30% of patients
42. 42
Myocardial Infarction (MI)
Evidence of myocardial necrosis in a clinical setting consistent
with myocardial ischemia, in which case any one of the
following meets the diagnosis for MI:
a) Detection of rise and/or fall of cardiac biomarkers (preferably
troponin)
b) ECG changes indicative of new ischemia (new ST-T changes
or new left bundle branch block)
c) Development of pathological Q waves
d) Imaging evidence of new loss of viable myocardium or new
regional wall motion abnormality
44. 44
Clinical features
Pain is the cardinal symptom
Prolonged cardiac pain: chest, throat, arms,
epigastrium or back
Anxiety and fear of impending death
Nausea and vomiting
Breathlessness
Collapse/syncope
45. 45
Investigations
Confirmatory diagnosis
difficult to interpret if there is bundle branch block
or previous MI.
Repeated ECGs are important:
o initial ECG may be normal or non-diagnostic in
one-third of cases
46. 46
Investigations
ECG
Non-ST segment elevation ACS
Partial occlusion of a major vessel or complete
occlusion of a minor vessel,
unstable angina or partial thickness (subendocardial)
MI.
o ST-segment depression and T-wave changes.
Presence of infarction: loss of R waves in the absence
of Q waves
47. 47
Investigations
ECG
ST segment elevation ACS
Myocardial infarction with presence of cardiac
biomarkers e.g creatine kinase (CK), a more sensitive
and cardiospecific isoform of this enzyme (CK-MB),
and the cardiospecific proteins, troponins T and I
49. 49
Investigations
Other blood tests:
erythrocyte sedimentation rate (ESR) and C-reactive
protein (CRP) are also elevated
Chest X-ray
pulmonary oedema that is not evident on clinical
examination
heart size is often normal but may be cardiomegaly due
to pre-existing myocardial damage
52. 52
Management
Early Medical treatment
Admitted urgently to hospital because of significant risk
of death or recurrent myocardial ischemia
Reduce the incidence by at least 60%
Oxygen : nasal cannula 2–4 L/min if hypoxia is present
53. 53
Management
Early Medical treatment
Brief history/risk factors and immediate
o Intravenous access + blood for markers
o 12-lead ECG
Aim of early management
Analgesia
Antithrombotic therapy
Anti-anginal therapy
Reperfusion therapy
54. 54
Anti-anginal Therapy
Sublingual glyceryl trinitrate :
o valuable first-aid measure
IV nitrates (GTN or isosorbide dinitrate ):
o left ventricular failure and the relief of recurrent or
persistent ischemic pain
55. 55
Analgesia
Essential to relieve distress and to lower adrenergic
drive
IV opiates:
o initially morphine sulphate 5–10mg
IV Antiemetics:
o initially metoclopramide 10mg
56. 56
Antithrombotic Therapy
Antiplatelet therapy
Aspirin: within the first 12 hour.
Aspirin + clopidogrel : early (within 12 hours
Ticagrelor: more effective than clopidogrel
Antiplatelet treatment with i.v. glycoprotein IIb/IIIa
inhibitors :
o reduces the combined endpoint of death or MI and used
in context of PCI
57. 57
Antithrombotic Therapy
Anticoagulants therapy
reduces the risk of thromboembolic complication
prevents reinfarction in the absence of reperfusion
therapy or after successful thrombolysis
Unfractionated heparin, fractioned (low molecular
weight) heparin.
Continued for 8 days or until discharge from hospital or
coronary revascularisation
58. 58
Reperfusion therapy
Depending on type of MI, outcome of reperfusion therapy
varies
o NSTEMI: No demonstrable benefit
o STEMI: restores coronary artery patency and preserves left
ventricular function and improves survival
Medium- to high-risk patients do benefit
Primary percutaneous coronary intervention (PCI)
59. 59
Reperfusion therapy
Thrombolysis
reduce hospital mortality by 25–50%
Alteplase (human tissue plasminogen activator)
o better survival rates than other thrombolytic agents, such as
streptokinase,
Analogues of tPA (tenecteplase and reteplase):
o longer plasma half-life than alteplase and can be given as an
intravenous bolus
60. 60
Late Management of MI
Risk stratification and further investigation lifestyle
modification
Cessation of smoking
Regular exercise
Diet (weight control, lipid-lowering)
61. 61
Late Management of MI
Secondary prevention drug therapy
Antiplatelet therapy (aspirin and/or clopidogrel)
β-blocker
ACE inhibitor
Statin
Additional therapy for control of diabetes and hypertension
Aldosterone receptor antagonist
Rehabilitation devices:
Implantable cardiac defibrillator (high-risk patients)
62. 62
Complications of Acute Coronary
Syndrome
Arrhythmias
Ischemia
Acute circulatory failure
Pericarditis
Mechanical complications e.g rupture of the ventricle
Embolism
Impaired ventricular function, remodeling and ventricular
aneurysm