Study Material
Myocardial infarction (MI), commonly known as a heart attack. MI is a blockage of blood flow to the heart muscle. Myocardial infarction (MI) refers to tissue death (infarction) of the heart muscle (myocardium). It is a type of acute coronary syndrome, which describes a sudden or short-term change in symptoms related to blood flow to the heart. Myocardial infarction is a common presentation of coronary artery disease. The World Health Organization estimated in 2004, that 12.2% of worldwide deaths were from ischemic heart disease.
Study Material
Myocardial infarction (MI), commonly known as a heart attack. MI is a blockage of blood flow to the heart muscle. Myocardial infarction (MI) refers to tissue death (infarction) of the heart muscle (myocardium). It is a type of acute coronary syndrome, which describes a sudden or short-term change in symptoms related to blood flow to the heart. Myocardial infarction is a common presentation of coronary artery disease. The World Health Organization estimated in 2004, that 12.2% of worldwide deaths were from ischemic heart disease.
Coronary artery disease or Ischemic heart disease ANILKUMAR BR
Cardiovascular disease are becoming a leading cause of morbidity and mortality in developed countries and they are also emerging as prominent national health problem in developing countries.
Coronary artery disease has become the major cause of early death and disability in the population.
Coronary artery disease (CAD) can also be used interchangeably with the terms atherosclerotic heart disease or ischemic heart disease.
All of these terms imply insufficient perfusion of the coronary arteries from an abnormal narrowing of the vessels, leading to insufficient oxygen delivery to the myocardial tissue.
The term coronary heart disease, also known as coronary artery disease or Ischemic heart disease, is a condition refers to diseases of the heart that result from a decrease in blood supply to the heart muscle.
Non modifiable risk factors
Modifiable risk factors
Contributing risk factors
Coronary artery disease or Ischemic heart disease ANILKUMAR BR
Cardiovascular disease are becoming a leading cause of morbidity and mortality in developed countries and they are also emerging as prominent national health problem in developing countries.
Coronary artery disease has become the major cause of early death and disability in the population.
Coronary artery disease (CAD) can also be used interchangeably with the terms atherosclerotic heart disease or ischemic heart disease.
All of these terms imply insufficient perfusion of the coronary arteries from an abnormal narrowing of the vessels, leading to insufficient oxygen delivery to the myocardial tissue.
The term coronary heart disease, also known as coronary artery disease or Ischemic heart disease, is a condition refers to diseases of the heart that result from a decrease in blood supply to the heart muscle.
Non modifiable risk factors
Modifiable risk factors
Contributing risk factors
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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
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
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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
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
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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!
2. Myocardial Infarction (MI)
Introduction
• Commonly known as “Heart Attack”
results in death of heart muscle
• Occurs from partial or complete blockage
of coronary artery which decreases blood
supply to cells of heart
• Cardiac conduction, blood flow and
cardiac functions altered by MI
3. Definition
• It is necrosis of myocardium due to
insufficient oxygen and blood supply in the
myocardium leading to damage or death of
heart muscle tissue ( Myocardium).
4.
5. Etiology
• Reduced blood flow in coronary artery due
to atherosclerosis
• Complete occlusion of an artery by an
embolus or thrombus
• Sudden narrowing (vasospasm of coronary
artery)
• Acute coronary thrombosis
• Severe coronary artery disease
• Precipitate thrombus formation
• Spasm of coronary artery
• Coronary artery embolism
6. • Infectious disease causing arterial
inflammation, hypoxia
• Acute blood loss (anaemia)
• Severe exertion or stress on the heart
• Necrosis of heart muscle surrounding area.
• Inflammed and injured
• Intramural haemorrhage into atheromatous
plaques
7.
8. Risk Factors
Non-modifying factors
• Family History: Due to combination of
shared genetic, environmental and life style
factors
• Age and sex: MI is highest among white
and middle age men. However this gender
difference disappears rapidly after
menopause.
9. Risk Factors
Modifying factors
•Smoking: Nicotine in cigarette smoking causes
epinephrine and norepinephrine release
• Hypertension: Stress of constantly elevated
blood pressure increases rate of atherosclerotic
development
• Hypercholesterolemia: Risk of MI associated
with serum cholesterol level of >200mg/dl. Low
density lipoprotein (LDLs) contain more
cholesterol and have affinity for arterial wall
10. Risk Factors
• Diabetes Mellitus: Person with diabetes have
increased tendency of connective tissue
degeneration and this account for atheroma
development
• Physical Inactivity: Physically active people
have increased HDL levels and exercise enhances
fibrinolysis activity thus reducing risk of clot
formation
11. Risk Factors
• Obesity: Obese person are thought to produce
increased levels of LDL and triglycerides which
are strongly implicated in atherosclerosis
• Stress: Stress induced mechanism stimulate
sympathetic nervous system causing increased
release of epinephrine and norepinephrine. This
stimulation influences heart by increasing heart
rate and intensifying force of myocardial
contraction.
12. Pathophysiology
• Coronary artery embolism, coronary thrombosis,
coronary artery blockage, coronary artery disease
Decreased blood supply to the heart
Myocardial cells deprive of oxygen
Prolonged decreased blood supply lead to infraction
and than ischemia of myocardium muscles
13. Necrosis or death of cells
Myocardial Infraction
Chest pain, syncope, diaphoresis, Shortness
of breath, tachypnea and confusion
14. Clinical Manifestation
Chest pain:
• Severe immobilizing chest pain not relieved
by rest, position change or nitroglycerine
administration
• Persistent: Heaviness, pressure, burning,
constricting or crushing
• Sub sternal, retrosternal or Epigastric pain
• May radiate to neck, jaw, shoulders and inner
aspects upper arm usually left arm
• Duration: more than 30 min.
• Severity is more then angina
15.
16. Clinical Manifestation
Cardiovascular
• Increased Jugular Venous pressure
• Elevated blood pressure in sympathetic
stimulation or decreased blood pressure in
decreased myocardial contractility
• ECG may show tachycardia, bradycardia
or dysrhythmia
• Breathlessness/ Restlessness
• Syncope, collapse(arrhythmias)
18. Clinical Manifestation
Skin
• Cool, clammy skin, diaphoresis and pale due to
sympathetic stimulation
Neurologic
• Anxiety, restlessness and light headedness due to
decrease cerebral oxygenation
• Fear and anxiety of impending death
Psychological
• Disorientation
• Confusion
• Irritability
• Fainting marked weakness
19. Diagnostic Investigation
Patient History
• Patient history has two parts:
I. Description of presenting symptoms
II. History of previous illnesses and family history
Electrocardiogram (ECG)
• ECG should be obtained within 10 minutes from
time patient reports pain or arrives in emergency
department
20. Diagnostic Investigation
• As area of myocardial injury becomes
ischemic, myocardial repolarization is
altered and delayed causing the T wave to
invert
• Ischemic region may remain depolarized
while adjacent areas of myocardium return
to resting state
22. Diagnostic Investigation
• Injured myocardial cells depolarize normally but
repolarize more rapidly than normal cells,
causing ST segment to rise
• Elevation in ST segment in two contagious leads
is key diagnostic indicator of MI
24. Diagnostic Investigation
Cardiac Biochemical Markers:
Creatinine kinase and its isoenzymes (CK-MB).
Myoglobin
Troponin I and T
Lactic hydrogenous (LDH)
AST
Other Blood tests
Leucocytosis reaching peak on first day
Erythrocyte sedimentation rate (ESR) becomes raised
and remain so for several days
ABG
C-reactive protein (CRP) is elevated
25. Diagnostic Investigation
Cardiac angiography( Cardiac Catherization)
Chest X-Ray PA View
Echocardiogram
• Used to evaluate ventricular function
• Detect hypokinetic and akinetic wall motion and
can determine ejection fraction
26. Medical Treatment Guidelines
• Use rapid transit to hospital
• Obtain 12 lead ECG to be read within 10 minutes
• Obtain laboratory blood specimens of cardiac
biomarkers including troponin
• Obtain other diagnostics to clarify the diagnosis
Begin routine medical interventions
• Supplemental oxygen
• Nitroglycerin
• Morphine
• Aspirin
• Beta blockers
• Angiotensin converting enzyme inhibitor within 24
hours
27. Medical Treatment Guidelines
Evaluate for indications of reperfusion therapy
• Percutaneous coronary intervention
• Thrombolytic therapy
Continue Therapy as indicated
• Intravenous heparin
• Clopidrogel
• Bed rest for minimum of 12 to 24 hours
28. Thrombolytic
Purposes:
• To dissolve and lyse the thrombus in a coronary
artery (thrombolysis)
• To allow blood to flow through the coronary
artery (reperfusion)
• To minimize size of infarction
• To preserve ventricular function
29. Thrombolytic
Indication
• Chest pain for longer than 20 minutes,
unrelieved by nitroglycerin
• ST segment elevation in at least two ECG
leads
• Less than 6 hours from onset of chest pain
30. Thrombolytic
Thrombolytic Agents
• Streptokinase 1.5 million U in 100ml saline given
as intravenous infusion over 1 hour
• Alteplase, a tissue plasminogen activator (t-PA)
which activates plasminogen present on blood
clot, an IV blous is administered followed by
infusion
• Reteplase, a newer recombinant thrombolytic,
similar to alteplase, administered in two bolus
31. Thrombolytic
Nursing Consideration
• Minimize number of times the patient’s skin is
punctured
• Draw blood for laboratory test when starting IV
line
• Avoid continuous use of noninvasive blood
pressure cuff
• Check for signs of bleeding
32. Analgesics
• Morphine sulphate is administered to reduce pain
and anxiety
• It decreases workload of heart
• It relaxes bronchioles to enhance oxygenation
• Cardiovascular response should be monitored:
Blood pressure can decrease and respiratory rate
can be depressed
34. Anticoagulants
• Subcutaneous heparin (12500 U twice day)
may prevent reinfarction after successful
thrombolysis
• Intravenous heparin should be given for
48-72 hours following thrombolysis
36. Nitroglycerin
• Vasoactive agent that dilates veins causing venous
pooling of blood in body resulting in less blood
flow to heart
• IV infusion of nitroglycerin is not administered if
systolic blood pressure is <90 mm Hg
37. Medical Management
• MONATAS Or MONATAL
• M: Morphine 5-10 mg IV
• O: oxygen Therapy
• N: Nitroglycerine ( Nitrates) 300-500 mg
sublingually
• A: Aspirin 75-300 mg (Antiplatelet Therapy).
Ateplase 15 mg bolous, then followed by 0.75
mg/kg body weight over 30 min.
(Antithrombotics), Atenolol 5-10 mg IV than
oral for long term survival ( B-blocker).
38. • T: Thrombolytic agent ( Streptokinase 1.5
million unit in 100 ml NS over 1 hours.
• A: Anti coagulant, Subcutaneous heparin
(LMWH)
• S: Stool softener or L: Laxative
39.
40.
41. • Maintain ABCDE and give oxygen therapy
• Monitoring ECG contineously
• IV line should be open and collect blood sample
• Monitoring vital signs 2 hourly
• Pain control GTN 300- 500 mg sublingually
• Inj. Morphine 5-10 mg IV
• Inj. Ondecetron 4 mg IV before Morphine
administration
• Inj. Pantoprazole for stress ulcer
• Give low salt diet, low fat and low cholesteral
diet
• Patient should be connect with cardio monitoring
• Patient keep on Propped up position
44. Surgical Management
Advantages of PCI
• Provides an alternative to surgical intervention
• Performed with local anesthesia
• Patient is ambulatory 24 hours after procedure
• Length of hospital stay is approximately 1 to 3
days
• Rapid return to work (approximately 5 to 7 days
after PCI)
45. Life Style Modifications
• Do not smoke
• Maintain ideal body weight
• Take regular exercise (minimum of 20
minutes, three times a week)
• Eat diet containing fruits and vegetables
• Eat less cholesterol containing diet
• Achieve good control of hypertension
46. Nursing Diagnosis
• Acute chest pain related to imbalance between
oxygen supply and demand secondary to reduced
coronary blood flow
• Decreased cardiac output related to decreased
cardiac contractility and changes in heart rate
• Activity intolerance related to fatigue secondary
to insufficient oxygenation
47. Nursing Management
Nurses should obtain subjective data on:
Important Health information
• Past health history: Previous MI, diabetes,
hypertension, smoking
• Medications: Use of nitrates, calcium blockers,
antihypertensive medications
48. Nursing Management
Functional health pattern
• Family history of heart disease
• Nutritional-metabolic: Nausea, vomiting,
indigestion, heartburn
• Activity-exercise: Profound weakness, dyspnea
• Cognitive-perceptual: Severe sub sternal pain,
lasting more than 30 minutes
• Coping-stress tolerance: Persistent stress
49. Nursing Management
Chest pain documentation should include
following:
• Type, location and pain radiation to other areas of
body
• Vital signs, skin color and temperature
• Presence of dyspnea, labored respirations,
diaphoresis or nausea
51. Prognosis
• In almost one quarter of all cases of MI, death
occurs within a few minutes without medical
care.
• Half death occurs within 24 hours of onset of
symptoms
• 40% of all affected patients die within first month
• Prognosis of those who reach hospital is better
with 28 day survival of more than 80%
52. Prognosis
• Prognosis is worse for anterior wall infarction
than for inferior wall infarction
• Bundle branch block and high enzyme levels both
indicate extensive myocardial damage
• Old age, depression and social isolation are
associated with higher mortality
• Those who survive an acute attack more than 80%
live for a further year, 75% for 5 years, 50% for
10 years and 25% for 20 years.
53. Health Education
• Have regular blood pressure check ups and take
prescribed medications for BP control
• Reduce animal fat intake and adjust total caloric
intake to maintain ideal body weight
• Stop smoking
• Exercise regularly and maintain routine physical
activity that is done at least three or four times a
week
54. Health Education
• Alter patterns that are conducive to stress and
rushing (e.g. get up 30 minutes earlier so
breakfast is not eaten on the way to work)
• Avoid large and heavy meals
• For patient with diabetes mellitus monitor blood
glucose levels regularly and follow recommended
diet
• Gradually and progressively resume physical
activity