The patient presented with symptoms of chest pain, shortness of breath, and sweating. ECG and blood tests showed elevated cardiac markers. This is consistent with a diagnosis of myocardial infarction (MI). MI occurs when blood flow to the heart is blocked, causing heart muscle cell death. On pathology, MI presents as areas of necrosis and inflammation. Laboratory tests for MI diagnosis include cardiac troponins, CK-MB, and myoglobin, which are more specific and sensitive than total CK or LDH. Together, the presentation and test results make the diagnosis of MI likely in this case.
this is a slide on myocardial infraction to figure you out what exactly it is !
though i have not mentioned the diet based causes ............etc.
so enjoy
this is a slide on myocardial infraction to figure you out what exactly it is !
though i have not mentioned the diet based causes ............etc.
so enjoy
Ischemia is defined as a condition of inadequate blood supply to an area of tissue.
Infarction- Localized area of ischemic necrosis in an organ or tissue resulting most often from reduction of arterial blood supply or occasionally its venous drainage
Public Health Significance- Long-term exposure to other lung irritants also is a risk factor for COPD leading to IHD. Examples of other lung irritants include secondhand smoke, air pollution, and chemical fumes and dust from the environment or workplace.
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
Cardiomyopathy, or heart muscle disease, is a type of progressive heart disease in which the heart is abnormally enlarged, thickened, and/or stiffened. As a result, the heart muscle's ability to pump blood is less efficient, often causing heart failure and the backup of blood into the lungs or rest of the body. The disease can also cause abnormal heart rhythms.
Ischemia is defined as a condition of inadequate blood supply to an area of tissue.
Infarction- Localized area of ischemic necrosis in an organ or tissue resulting most often from reduction of arterial blood supply or occasionally its venous drainage
Public Health Significance- Long-term exposure to other lung irritants also is a risk factor for COPD leading to IHD. Examples of other lung irritants include secondhand smoke, air pollution, and chemical fumes and dust from the environment or workplace.
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
Cardiomyopathy, or heart muscle disease, is a type of progressive heart disease in which the heart is abnormally enlarged, thickened, and/or stiffened. As a result, the heart muscle's ability to pump blood is less efficient, often causing heart failure and the backup of blood into the lungs or rest of the body. The disease can also cause abnormal heart rhythms.
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Myocardial infraction or Heart attack are terms used anonymously, but the preferred term is MI.
In an MI an area of the myocardium is permanently destroyed.
MI is usually caused by reduced or decreased blood flow in a coronary artery due to rupture of an atherosclerotic plaque and subsequent occlusion of the artery by a thrombus.
Myocardial infarction (MI) death of the cells of an area of the heart muscle (myocardium) as a result of oxygen deprivation, which in turn is caused by obstruction of the blood supply; commonly referred to as a “heart attack.”
MI refers to the processes by which myocardial tissue is destroyed in regions of the heart that are deprived of an adequate blood supply because of reduced coronary artery blood flow.
Eighty percent to 90% of all acute MI are secondary to thrombus formation. When thrombus develops , perfusion to the myocardium distal to the occlusion is halted, resulting in necrosis.The myocardium receives its blood supply from the two large coronary arteries and their branches.
Occlusion of one or more of these blood vessels (coronary occlusion) is one of the major causes of myocardial infarction.
The occlusion may result from the formation of a clot that develops suddenly when an athermanous plaque ruptures through the sub layers of a blood vessel, or when the narrow, roughened inner lining of a scleroses artery leads to complete thrombosis.
The acute MI process takes time. Cardiac cells can withstand in ischemic conditions for approximately 20 minutes before cellular death begins.
The earliest tissue to become ischemic is the sub endocardium (the innermost layer of tissue in the cardiac muscle)
If ischemia persists, it takes approximately 4 to 6 hours for the entire thickness if the heart muscle to become necrosis.
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.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
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
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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!
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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2. Case history:
• 50 yrs old hypertensive male came with
complaints of severe chest pain, dyspnoea
and sweating. On examination, pulse was
rapid and feeble. ECG- shows------------,
biochemical investigation shows elevated
cardiac markers like troponin and CK-MB .
• 1. what is your diagnosis
• 2. morphology of this disease
• 3. lab diagnosis
11. Chronic atheroscelerosis:
• More than 90% of patients with IHD have
atherosclerosis of one or more of the
epicardial coronary arteries.
• stenosis (“fixed” obstructions) , acute plaque
disruption with thrombosis.
• single major coronary epicardial trunk may be
affected, two or all three. 1. LAD, 2.LCX, and 3.
RCA.
12. Acute Plaque Change:
• Number, Distribution, Structure, and Degree
of obstruction of atheromatous plaques.
• Stable atherosclerotic plaque to an unstable
atherothrombotic lesion through rupture,
superficial erosion, ulceration, fissuring, or
deep hemorrhage.
• Formation of a superimposed thrombus that
partially or completely occludes the affected
artery.
13.
14.
15. Angina pectoris
• A symptom complex of IHD characterized
by paroxysmal attacks of chest pain,
usually substernal or precordial, caused
by myocardial ischemia that falls short of
inducing infarction. There are several
patterns
16. Variants of Angina
• 1. Stable angina (typical) - paroxysms of pain
related to exertion and relieved by rest or
vasodilators. subendocardial ischemia with ST-
segment depression
• 2. Variant or Prinzmetal's angina - angina that
classically occurs at rest and is caused by reversible
spasm in normal to severely atherosclerotic
coronary arteries. ST-segment elevation or
depression maybe seen during attacks.
17. Variants of Angina
• 3. Unstable angina - prolonged pain, pain at rest in
a person with stable angina, or worsening of pain in
stable angina. ST-segment depression (usually) and
ST-segment elevation.
• .
20. Pathogenesis-MI
• Coronary artery occlusion-
• Sudden change in the morphology of the plaque
• Adhesion,aggregation, activation and release of
potent platelet aggregators including thromboxane
A2,serotonin,platelet factor 3 & 4
• Vasospasm
• Activation of extrinsic pathway of coagulation
• Thrombus completely occludes vessel lumen
21. Pathogenesis (contd)
• Other mechanisms-
• Emboli-from lt. atrium,paradoxical emboli
• Unexplained-diseases of small intra-mural
coronary vessels like
vasculitis,haemoglobinopathies,amyloid
deposition in vessel walls,other unusual
disorders like vascular dissection and
inadequate protection during cardiac surgery.
22. Pathogenesis -contd
• Myocardial response-Coronary artery
occlusion leads to loss of critical blood supply
to the myocardium,producing profound
functional,biologic and morphologic
consequences.
• Results in cell death in the area of supply,seen
in sub-endocardium.Outcome depends on
duration and severity of flow deprivation
23. Pathogenesis -contd
• Early biochemical change-switch from aerobic to anaerobic
glycolysis within seconds→inadequate production of high
energy phosphates(creatine phosphate and adenosine
triphosphate)
• Accumulation of lactic acid
• Within 60 secs of onset of ischaemia-loss of contractility
occurs→acute heart failure(myofibrillar relaxation,glycogen
deposition,cell and mitochondrial swelling)
• These changes are reversible and cell death is not immediate
24. Pathogenesis -contd
• Severe ischaemia lasting 20-40 mins leads to
irreversible necrosis of some cardiomyocytes(primary
structural defects in sarcolemmal membrane)
• With prolonged ischemia injury to micro-vasculature
follows
• Arrhythmias occur through poorly understood
mechanism
• Sudden cardiac death
• “Wavefront”of myocardial ischaemia
25. Gross morphology -MI
Patterns include:
• Transmural infarct - involving the entire thickness
of the left ventricular wall from endocardium to
epicardium, usually the anterior free wall and
posterior free wall and septum with extension into
the RV wall in 15-30%. Isolated infarcts of RV and
right atrium are extremely rare.
• Subendocardial infarct - multifocal areas of
necrosis confined to the inner 1/3-1/2 of the left
ventricular wall. These do not show the same
evolution of changes seen in a transmural MI.
Global hypotension-sub-endocardial infarcts are usually circumferential.
29. Irreversible injury
Time Gross features Light microscopy
½–4 hr None Usually none; variable waviness of fibers at border
4-12 hrs Dark mottling
(occasional)
Early coagulation necrosis; edema; hemorrhage
12–24 hr Dark mottling Ongoing coagulation necrosis; pyknosis of nuclei;
myocyte hypereosinophilia; marginal contraction band
necrosis; early neutrophilic infiltrate
1–3 days Mottling with yellow-tan
infarct center
Coagulation necrosis, with loss of nuclei and
striations; brisk interstitial infiltrate of neutrophils
3–7 days Hyperemic border;
central yellow-tan
softening
Beginning disintegration of dead myofibers, with dying
neutrophils; early phagocytosis of dead cells by
macrophages at infarct border
30. Time Gross features Light microscopy
7–10 days Maximally yellow-tan and soft,
with depressed red-tan margins
Well-developed phagocytosis of dead
cells; early formation of fibrovascular
granulation tissue at margins
10–14 days Red-gray depressed infarct
borders
Well-established granulation tissue
with new blood vessels and collagen
deposition
2–8 wk Gray-white scar, progressive from
border toward core of infarct
Increased collagen deposition, with
decreased cellularity
>2 mo Scarring complete Dense collagenous scar
37. Diagnosis Of MI
• Clinical features-diaphoresis,dyspnoea,pulmonary
congestion and oedema
• Clinical laboratory-CK-MB
Elevated at 2-4 hrs, lasts 72hrs
Troponin I 2-4 hrs & lasts 7-10 days
Troponin T
• ECG
• Radiologic (angiography)
38. Creatine Kinase -Total
• The total CK is a simple and inexpensive test
that is readily available using many laboratory
instruments.
• However, an elevation in total CK is not
specific for myocardial injury,
• because most CK is located in skeletal muscle,
and elevations are possible from a variety of
non-cardiac conditions.
39. Creatine Kinase
• Three isoenzymes
– CK – MM (heart & skeletal muscle)
– CK – BB (brain, lung & other tissues)
– CK – MB (Principally myocardium, variable
amounts in skeletal muscle)
• CK – MB rises within 2 – 8 hours of MI, peaks
at 18 hours and disappears by 48 to 72 hours
• An absence of a change in levels in CK – MB
during the first 2 days of chest pain essentially
excludes MI
40. CK-MB
• Is a very good marker for acute myocardial injury, because
of its excellent specificity, and it rises in serum within 2 to 8
hours of onset of acute myocardial infarction.
• Serial measurements every 2 to 4 hours for a period of 9 to
12 hours after the patient is first seen will provide a pattern
to determine whether the CK-MB is rising, indicative of
myocardial injury.
• The CK-MB is also useful for diagnosis of reinfarction or
extension of an MI because it begins to fall after a day,
dissipating in 1 to 3 days, so subsequent elevations are
indicative of another event.
41. Troponin I and T
• Troponin I and T are structural components of cardiac muscle.
• They are released into the bloodstream with myocardial
injury.
• They are highly specific for myocardial injury – more so than
CK-MB – and help to exclude elevations of CK with skeletal
muscle trauma.
• Troponins will begin to increase following MI within 2 to 12
hours, about the same time frame as CK-MB. However, the
rate of rise for early infarction may not be as dramatic as for
CK-MB.
42. Troponins
• Troponins will remain elevated longer than CK--up to 5 to
9 days for troponin I and up to 2 weeks for troponin T.
• This makes troponins a superior marker for diagnosing
myocardial infarction in the recent past--better than
lactate dehydrogenase (LDH).
• However, this continued elevation has the disadvantage
of making it more difficult to diagnose reinfarction or
extension of infarction in a patient who has already
suffered an initial MI.
• Troponin T lacks some specificity because elevations can
appear with skeletal myopathies and with renal failure.
43. Myoglobin
• Is a protein found in skeletal and cardiac muscle
which binds oxygen.
• It is a very sensitive indicator of muscle injury.
The rise in myoglobin can help to determine the
size of an infarction.
• A negative myoglobin can help to rule out
myocardial infarction. It is elevated even before
CK-MB.
• However, it is not specific for cardiac muscle, and
can be elevated with any form of injury to skeletal
muscle.
44. LDH
• The LDH has been supplanted by other tests. It begins to
rise in 12 to 24 hours following MI, and peaks in 2 to 3
days, gradually dissipating in 5 to 14 days.
• Measurement of LDH isoenzymes is necessary for
greater specificity for cardiac injury.
• There are 5 isoenzymes (1 through 5). Ordinarily,
isoenzyme 2 is greater than 1, but with myocardial
injury, this pattern is "flipped" and 1 is higher than 2.
• LDH-5 from liver may be increased with centrilobular
necrosis from passive congestion with congestive heart
failure following ischemic myocardial injury.
45. Infarct modification by reperfusion
• Restoration of coronary flow→salvage ischaemic
myocardium.To be established in 3-4 hrs.Within 15-
20 mins-prevents all necrosis
• Contraction bands-occurs in lethally injured cells on
reperfusion
• Reperfusion injury-Leukocytes in the reperfused
blood→apoptosis of myocytes and microvascular
injury→haemorrhage,endothelial
swelling→occludes capillaries→prevents local
reperfusion-no reflow
46. Complications
Complicated(80%)
• Contractile dysfunction,pump failure,cardiogenic shock(15%)
• >40% ventricular wall involved
• Arrhythmias and conduction defects, with possible "sudden
death" (85%)
• Myocardial rupture-3-7 days,mid-ventricular wall
• Risk factors-female gender,older than 60 yrs,pre-existing
hypertension,lack of lt ventr hypertrophy
• Myocardial wall rupture, with possible tamponade (1-2%)
• Papillary muscle rupture, with possible valvular insufficiency
• Rupture of Ventricular septum-L→R shunt(1-2%)
47. • Extension of infarction, or re-infarction
• Congestive heart failure (pulmonary edema) (60%)
• Pericarditis-2-3 days
• Right ventricular infarction
• Infarct expansion-Stretching,thinning and dilatation
of infarct region as with mural thrombus
• Mural thrombosis, with possible embolization (30%)
• Ventricular aneurysm formation-late
complication,rarely undergoes rupture
• Papillary muscle dysfunction
• Progressive late heart failure
• Uncomplicated (20%)