This document provides an overview of acute myocardial infarction (MI or heart attack). It defines MI as diminished blood supply to the heart muscle leading to cell damage and death. Risk factors include age, family history, smoking, diabetes, hypertension, hyperlipidemia, obesity, and physical inactivity. Symptoms may include chest pain, nausea, sweating, and changes in vital signs. Diagnosis involves electrocardiograms and cardiac enzyme levels. Treatment aims to restore blood flow and includes medications, fibrinolytic therapy, angioplasty, and bypass surgery. Nursing focuses on monitoring for ischemia, controlling chest pain, educating patients, and modifying risk factors.
Aortic stenosis is a valvular heart disease resulting in reduction of blood flow to the body and making the heart work harder. The heart may weaken causing chest pain, fatigue and shortness of breath.
most common congenital cyanotic heart disease.one of the conotruncal family of heart lesions.. It accounts for 7 to 10% of all congenital heart abnormalities.
Aortic stenosis is a valvular heart disease resulting in reduction of blood flow to the body and making the heart work harder. The heart may weaken causing chest pain, fatigue and shortness of breath.
most common congenital cyanotic heart disease.one of the conotruncal family of heart lesions.. It accounts for 7 to 10% of all congenital heart abnormalities.
Post anesthesia care unit or , High Dependency unit is part of hospital for Post surgery/procedures recovery.Nursing, anesthesiologist, surgeons, hospital administration need to know about ideal conditions.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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
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
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
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.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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.
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
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
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
2. Definition
• Otherwise know as heart attack
• An MI occurs when there is a diminished
blood supply to the heart which leads to
myocardial cell damage and ischemia.
• Contractile function stops in the necrotic
areas of the heart.
• Ischemia usually occurs due to blockage
of the coronary vessels.
3. Definition cont.
• This blockage is often the result of
thrombus that is superimposed on an
ulcerated or unstable atherosclerotic
plaque formation in the coronary artery.
• MI’s are described by the area of
occurrence.
• Anterior, Inferior, Lateral or Posterior.
5. Coronary artery events
• Ischemia – Outer most area, source of
arrhythmias, viable if no further infarction.
• Injury – Viable tissue found between
ischemic and infarcted areas.
• Infarction/necrosis – Center area, dead
not viable tissue that turn into scar.
6.
7.
8. MI Classifications
• MI’s can be subcategorized by anatomy
and clinical diagnostic information.
Anatomic
• Transmural and Subendocardial
Diagnostic
• ST elevations (STEMI) and non ST
elevations (NSTEMI).
9. Epidemiology
• MI’s are the leading cause of death in the
United States, affecting one in five men
and one in six women.
• 450,000 people in the US die from
coronary disease each year.
• Incidence rates increase with age as do
mortality rates due to infarction.
10. Epidemiology
• The survival rate for those hospitalized
due to MI has reached approximately
95%.
• This is the result of the advancements
made in modern medical technology.
11. Risk Factors
• The presence of any risk factor is
associated with doubling the risk of an MI.
Non Modifiable
• Age
• Gender
• Family history
13. Smoking
• Tobacco use increases the risk of
coronary artery disease two to six times
more than non smokers.
• Nicotine increases platelet thrombus
adhesion and vessel inflammation.
14. Diabetes & Hypertension
• Diabetes not only increases the rate of
atherosclerotic formation in vascular
vessels but also at an earlier age.
• The constant stress of high blood
pressure has been associated with the
increased rate of plaque formation.
• Shearing Stress and inflammation of
endothelial lining begins the process.
15. Hyperlipidemia
• Elevated levels of cholesterol, LDL’s or
triglycerides are associated with the
increased risk of coronary plaque
formation and MI.
• Almost 50% of the
population has some
form of dyslipidemia.
16. Obesity and Physical Inactivity
• Mortality rate from CAD is higher in those
who are obese.
• Some evidence shows that those who
carry their weight in their abdomen have a
higher incidence of CAD
• Physically inactive people have lower HDL
levels with higher LDL levels and an
increase in clot formation.
17. Pathophysiology
• Ischemia develops when there is an
increased demand for oxygen or a
decreased supply of oxygen.
• Ischemia can develop within 10 seconds
and if it lasts longer than 20 minutes,
irreversible cell and tissue death occurs.
• Myocardial cell death begins at the
endocardium. The area most distal to the
arterial blood supply.
18. Pathophysiology
• As vessel occlusion continues cell death
spreads to the myocardium and eventually
to the epicardium.
• Severity of the MI depends on three
factors.
– Level of occlusion
– Length of time of occlusion
– Presence or absence of collateral circulation
19. Signs and Symptoms
• Signs and symptoms are unique to each
individual patient.
• Ranging from no symptoms to sudden
cardiac arrest.
20. Chest Pain
• The most common initial manifestation is
chest pain or discomfort.
• This is not relieved by rest, position
change or nitrate administration.
• Pain is described by heaviness, pressure,
fullness and crushing sensation.
• Not everyone experiences this sensation.
21. Chest Pain
• PQRST assessment for chest pain
• P- Precipitating events
• Q- Quality of pain
• R- Radiation of pain
• S- Severity of pain
• T- Timing
22. Nausea and Vomiting
• Not everyone will experience this.
• Vomiting results as a reflex from severe
pain.
• Vasovagal reflexes initiated from area of
ischemia.
23. Sympathetic Nervous System
Stimulation
• During an MI increased catecholamines
are released.
• This results in diaphoresis and
vasoconstriction of peripheral blood
vessels.
• “Cool Sweat” with a temperature increase
during the first 24 hours.
24. Cardiovascular Changes
• Initially the BP and pulse may be elevated.
• Later, BP will drop due to decreased
cardiac output.
• Urine output will decrease
• Lung sounds will change to crackles
• Jugular veins may become distended and
have obvious pulsations.
26. Within the first 10 minutes upon
arrival to the hospital:
• Check vital signs and evaluate oxygen
saturation
• Establish IV access
• Obtain and review 12-lead ECG
• Take a brief focused history and perform a
physical exam
• Obtain blood samples to evaluate initial cardiac
markers, electrolytes and coagulation
27. Diagnostics
• After collecting patient health history, a
series of EKG’s should be taken to rule
out or confirm MI.
• 12 lead EKG’s can help to distinguish
between ST-elevation MI’s and Non-ST-
elevation MI’s.
29. Angina
Stable
• Chest pain caused by the build up of lactic
acid and irritation to the myocardial nerve
fibers.
• Chest pain caused by the 4 E’s (Exertion,
Emotion, Exposure To Cold, Eating )
• Pain is usually relieved with rest, pain
meds and nitrates.
30. Variable/Prinzmetal/Spasm
• Transient ischemia that occurs
unpredictably and almost always at rest.
• Pain is caused by vasospasm of the
arteries.
• ST segment elevations will be noted.
31. Unstable
• Chest pain at rest or with exercise and
tends to last greater than 15 minutes.
• This results in reversible myocardial
ischemia but is a sign that an infarct is
soon to come.
• EKG will reveal ST segment depression
and T wave inversion.
32. STEMI
• ST segment elevations
• T wave changes
• Q wave development
• Enzyme elevations
• Reciprocals
33. NSTEMI
• ST segment depressions
• T wave changes
• No Q wave development
• Mild enzyme elevations
• No reciprocals
35. Phases of a STEMI
• Hyperacute Phase
– Occurs within the first few hours of MI onset.
– Leads facing the infarcted surface: ST
segment elevation.
– Leads facing the uninjured surface: ST
segment depression (reciprocals)
– T waves become tall, widened and might be
taller than the R wave.
36. Phases of a STEMI
• Fully Evolved Phase
– Q wave development
– ST elevation
– T waves start to become inverted in leads
facing the injury.
37. Phases of a STEMI
• Resolution phase
– Weeks after there will be a gradual return of
ST segments to baseline.
– T waves will gradually return to normal but are
the last to change back.
38. Serum Cardiac Markers
• Myocardial cells produce certain proteins
and enzymes associated with cellular
functions.
• When cell death occurs, these cellular
enzymes are released into the blood
stream.
• CPK and troponin
39. CPK
• Creatine Phosphokinase
• Begin to rise 3 to 12 hours after acute MI.
• Peak in 24 hours
• Return to normal in 2 to 3 days
40. Troponin
• Myocardial muscle protein released into
circulation after injury.
• These are highly specific indicators of MI.
• Troponin rises quickly like CK but will
continue to stay elevated for 2 weeks.
• Myoglobin-lacks cardiac specificity.
42. Treatment Options
• The immediate goal for any acute MI is to
restore normal coronary blood flow to
vessels and salvage myocardium.
• There are a variety of medical and
medicinal therapies to treat an MI.
43. General Treatment for the MI
patient
MONA
• Morphine
• Oxygen
• Nitroglycerin
• Aspirin
44. Fibrinolytic Therapy
• Indicated for patients with STEMI MI’s.
• Should be given within 12 hours of
symptom onset.
• Fibrinolytics will break down clots found
within the vessles
• Contraindications: post op surgical
patients, history of hemorrhagic stroke,
ulcer disease, pregnancy, ect.
45. Cardiac Catheterization
• A diagnostic angiography which includes
angioplasty and possible stenting.
• Performed by an interventional
cardiologist with a cardiac surgeon on
stand by.
• Percutaneous procedure through the
femoral or brachial artery.
46. Cardiac Catheterization
• Upon arrival to the cath lab all actue MI
patients will receive:
– A bolus dose of plavix
– IV Integrelin
– Heparin dose either subcu or IV drip
– Angiomax : a DTI may be substituted for
heparin and integrelin.
47.
48. Coronary artery bypass graft
• Surgical treatment where saphenous vein
is harvested from the lower leg and used
to bypass the occluded vessels.
49.
50. Long Term Care
• Smoking Cessation and lifestyle
modifications.
• Aspirin, Beta Blockers and Clopidogrel will
be indefinite.
• Lipid lowering medication along with diet
modifications.
51. Nursing Management
• Nursing interventions of a patient with angina focus on:
• Early identification of myocardial ischemia.
• Assess immediately any complaints of chest pain using a
pain scale of 0 – 10, as pain (or pressure or heaviness) is an
indicator of myocardial ischemia. Immediate assessment is
important for early identification and treatment.
• Document vital signs, ECG, skin color, peripheral pulses,
level of consciousness, and overall tissue perfusion.
• Control of chest pain.
• Administer oxygen, nitrates, and analgesia as ordered.
• Use pulse oximetry to guide therapy and maintain
oxygen saturation above 90%.
52. • Nursing interventions of a patient with angina focus on
(Continued…):
• Patient and family education
• Educate your patient when his/ her condition has stabilised
(pain controlled).
• Teach the patient about the importance of avoiding the
Valsalva maneuver (bearing down when going to bath room).
This maneuver increases intrathoracic pressure that
decreases venous return to the right side of the heart which
is associated with hypotension and bradycardia.
• Teach the patient about risk factor modifications such as
decreasing fat intake, stopping smoking, reducing salt intake,
controlling hypertension, increasing physical activity as
tolerated, and achieving normal body weight.
• Provide information about medications; indications and side
effects.
• Teach the patient about the importance of follow up after
discharge and how to handle emotional stress and anger.
53. Nursing Management of MI
• Nursing interventions for a patient with acute MI
focus on:
– Achieving a balance between myocardial oxygen
supply and demand: This means that in the acute
phase, there is a need to increase myocardial oxygen
supply by oxygen administration to prevent tissue
hypoxia. Myocardial oxygen supply can be enhanced
by the administration of coronary artery vasodilators
(nitroglycerin).
– Prevention of complications: Nurses need to apply
cardiac monitoring of patient to detect early
ventricular dysrhythmias. In addition, nurses should
continue to assess for signs of ischemic pain.
54. Nursing Management of MI (Continued…)
– Health education: Nurses should focus on:
• Pathophysiology of acute MI.
• Description of signs and symptoms such as pain.
pressure, or heaviness in chest.
• Notification of nurses of any changes in chest pain
intensity.
• Avoidance of the Valsalva maneuver.
• Risk factors modification, including:
– Daily fat intake < 30% of total calories.
– Maintain serum cholesterol level < 200 mg/dL.
– Maintain LDL cholesterol to < 70 mg/dL.
– Stop smoking and reduce daily salt intake.
– Control hypertension and diabetes mellitus.
– Increase physical activity and reduce weight
–
55. Nursing Management of MI (Continued…)
– Health education (Continued…): Nurses should focus
on:
• Medication teaching: indications and side effects.
• Follow-up care after discharge.
56. Myocardial infarction
Nursing process
Assessment
• A careful history
• Description of symptoms (chest pain,
palpitation, dyspnea, syncope or
sweating). Each symptom must be
evaluated with regard to time, duration,
precipitating & relieving factors. In addition
complete physical assessment for:
*level of consciousness
58. Nursing diagnosis
– Chest pain related to reduced coronary blood flow.
– High risk for breathing pattern ineffective related to
fluid overload
– Anxiety related to fear from death
– High risk for tissue perfusion alteration related to
decreased cardiac output
– Health maintenance alteration related to no adherence
to therapeutic regimen
Nursing process (cont…)
59. Nursing process (cont…)
Patient's goals
• Report that pain is decreased
• Breath effectively
• Experience less anxiety level
• Have improved tissue perfusion
• Adhere to the self care program
60. Nursing process (cont…)
Nursing intervention
•Relief or control of chest pain
•Alleviate respiratory difficulties
•Reduce the anxiety level
•Maintain adequate tissue
perfusion
•Help the patient to adhere to the
self care program