case study of myocardial infarction ppt

Myocardial Infarction (MI) Case Study (45 min)

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Definition of Myocardial Infarction (MI)

Myocardial infarction, commonly known as a heart attack, is a critical medical event that occurs when the blood supply to the heart muscle is severely reduced or completely blocked. It is a leading cause of death worldwide and a significant public health concern.

Introduction to Myocardial Infarction (MI)

This nursing case study aims to provide a comprehensive understanding of myocardial infarction by delving into its various aspects, including its pathophysiology, risk factors, clinical presentation, diagnostic methods, and management strategies. Through the exploration of a fictional patient’s journey, we will shed light on the intricate nature of this life-threatening condition and highlight the importance of early recognition and intervention.

Background and Significance of Myocardial Infarction

Myocardial infarction is a sudden and often catastrophic event that can have profound consequences on an individual’s health and well-being. Understanding its underlying mechanisms and risk factors is essential for healthcare professionals, as timely intervention can be life-saving. This case study not only serves as a learning tool but also emphasizes the critical role of medical practitioners in identifying and managing myocardial infarctions promptly.

Pathophysiology of Myocardial Infarction

A crucial aspect of comprehending myocardial infarction is exploring its pathophysiology. We will delve into the intricate details of how atherosclerosis, the buildup of plaque in coronary arteries, leads to the formation of blood clots and the subsequent interruption of blood flow to the heart muscle. This disruption in blood supply triggers a cascade of events, ultimately resulting in the death of cardiac cells.

Risk Factors of Myocardial Infarction

Understanding the risk factors associated with myocardial infarction is vital for prevention and early detection. This case study will examine both modifiable and non-modifiable risk factors, including age, gender, family history, smoking, high blood pressure, diabetes, and high cholesterol levels. Recognizing these risk factors is instrumental in developing effective strategies for prevention and risk reduction.

Clinical Presentation Myocardial Infarction

Recognizing the signs and symptoms of myocardial infarction is crucial for timely intervention. We will present a fictional patient’s experience, illustrating the typical clinical presentation, which often includes chest pain or discomfort, shortness of breath, nausea, lightheadedness, and diaphoresis. Through this patient’s journey, we will highlight the importance of accurate symptom assessment and prompt medical attention.

Diagnostic Methods for Myocardial Infarction

Modern medicine offers various diagnostic tools to confirm a myocardial infarction swiftly and accurately. This case study will explore these diagnostic methods, such as electrocardiography (ECG), cardiac biomarkers, and imaging techniques like coronary angiography. By understanding these diagnostic modalities, healthcare professionals can make informed decisions and initiate appropriate treatments promptly.

Management Strategies for Myocardial Infarction

The management of myocardial infarction involves a multidisciplinary approach, including medication, revascularization procedures, and lifestyle modifications. We will discuss the fictional patient’s treatment plan, emphasizing the importance of reestablishing blood flow to the affected heart muscle and preventing further complications.

Nursing Case Study for Myocardial Infarction (MI)

Having established a foundational understanding of myocardial infarction, we will now delve deeper into Mr. Salazar’s case, tracing his journey through diagnosis, treatment, and recovery. This in-depth examination will shed light on the real-world application of the principles discussed in the introduction, providing valuable insights into the clinical management of myocardial infarction and its impact on patient outcomes.

Mr. Salazar, a 57-year-old male, arrives at the Emergency Department (ED) with complaints of chest pain that began approximately one hour after dinner while he was working. He characterizes the discomfort as an intense “crushing pressure” located centrally in his chest, extending down his left arm and towards his back. He rates the pain’s severity as 4/10. Upon examination, Mr. Salazar exhibits diaphoresis and pallor, accompanied by shortness of breath (SOB).

What further nursing assessments need to be performed for Mr. Salazar?

• Heart Rate (HR): The number of heartbeats per minute.
• Blood Pressure (BP): The force of blood against the walls of the arteries, typically measured as systolic (during heartbeats) and diastolic (between heartbeats) pressure.
• Respiratory Rate (RR): The number of breaths a patient takes per minute.
• Body Temperature (Temp): The measurement of a patient’s internal body heat.
• Oxygen Saturation (SpO2): The percentage of oxygen in the blood.
• S1: The first heart sound, often described as “lub,” is caused by the closure of the mitral and tricuspid valves.
• S2: The second heart sound, known as “dub,” results from the closure of the aortic and pulmonic valves.
• These sounds provide important diagnostic information about the condition of the heart.
• Clear: Normal, healthy lung sounds with no added sounds.
• Crackles (Rales): Discontinuous, often high-pitched sounds are heard with conditions like pneumonia or heart failure.
• Wheezes: Whistling, musical sounds often associated with conditions like asthma or chronic obstructive pulmonary disease (COPD).
• Pulses refer to the rhythmic expansion and contraction of arteries with each heartbeat. Common pulse points for assessment include the radial artery (wrist), carotid artery (neck), and femoral artery (groin). Evaluating pulses helps assess the strength, regularity, and rate of blood flow.
• Edema is the abnormal accumulation of fluid in body tissues, leading to swelling. It can occur in various body parts and may indicate underlying conditions such as heart failure, kidney disease, or localized injury. Edema assessment involves evaluating the degree of swelling and its location.
• Skin condition (temperature, color, etc.)

What interventions do you anticipate being ordered by the provider?

• Oxygen therapy involves administering oxygen to a patient to increase the level of oxygen in their blood. It is used to treat conditions such as respiratory distress, and hypoxia (low oxygen levels), and to support patients with breathing difficulties.
• Nitroglycerin is a medication used to treat angina (chest pain) and to relieve symptoms of heart-related conditions. It works by relaxing and widening blood vessels, which improves blood flow to the heart, reducing chest pain.
• Aspirin is a common over-the-counter medication and antiplatelet drug. In the context of myocardial infarction (heart attack), it is often administered to reduce blood clot formation, potentially preventing further blockage in coronary arteries.
• A 12-lead EKG is a diagnostic test that records the electrical activity of the heart from 12 different angles. It provides information about the heart’s rhythm, rate, and any abnormalities, helping diagnose conditions like arrhythmias, heart attacks, and ischemia.
• Cardiac enzymes are proteins released into the bloodstream when heart muscle cells are damaged or die, typically during a heart attack. Measuring these enzymes, such as troponin and creatine kinase-MB (CK-MB), helps confirm a heart attack diagnosis and assess its severity.
• A chest X-ray is a diagnostic imaging procedure that creates images of the chest and its internal structures, including the heart and lungs. It is used to identify issues like lung infections, heart enlargement, fluid accumulation, or fractures in the chest area.
• Possibly an Echocardiogram

Upon conducting a comprehensive assessment, it was observed that the patient exhibited no signs of jugular vein distention (JVD) or edema. Auscultation revealed normal heart sounds with both S1 and S2 present, while the lungs remained clear, albeit with scattered wheezes. The patient’s vital signs were recorded as follows:

• BP 140/90 mmHg SpO 2 90% on Room Air
• HR 92 bpm and regular Ht 173 cm
• RR 32 bpm Wt 104 kg
• Temp 36.9°C

The 12-lead EKG repor t indicated the presence of “Normal sinus rhythm (NSR) with frequent premature ventricular contractions (PVCs) and three- to four-beat runs of ventricular tachycardia (VT).” Additionally, there was ST-segment elevation in leads I, aVL, and V2 through V6 (3-4mm), accompanied by ST-segment depression in leads III and aVF.

Cardiac enzyme levels were collected but were awaiting results at the time of assessment. A chest x-ray was also ordered to provide further diagnostic insights.

In response to the patient’s condition, the healthcare provider prescribed the following interventions:

• Aspirin: 324 mg administered orally once.
• Nitroglycerin: 0.4 mg administered sublingually (SL), with the option of repeating the dose every five minutes for a maximum of three doses.
• Morphine: 4 mg to be administered intravenously (IVP) as needed for unrelieved chest pain.
• Oxygen: To maintain oxygen saturation (SpO2) levels above 92%.

These interventions were implemented to address the patient’s myocardial infarction (heart attack) and alleviate associated symptoms, with a focus on relieving chest pain, improving oxygenation, and closely monitoring vital signs pending further diagnostic results.

What intervention should you, as the nurse, perform right away? Why?

• Apply oxygen – this can be done quickly and easily and can help to prevent further complications from low oxygenation.
• Oxygen helps to improve oxygenation as well as to decrease myocardial oxygen demands.
• Often it takes a few minutes or more for medications to be available from the pharmacy, so it makes sense to take care of this intervention first.
• ABC’s – breathing/O 2 .

What medication should be the first one administered to this patient? Why? How often?

• Nitroglycerin 0.4mg SL – it is a vasodilator and works on the coronary arteries. The goal is to increase blood flow to the myocardium. If this is effective, the patient merely has angina. However, if it is not effective, the patient may have a myocardial infarction.
• Aspirin should also be given, but it is to decrease platelet aggregation and reduce mortality. While it can somewhat help prevent the worsening of the blockage, it does little for the current pain experienced by the patient.
• Morphine should only be given if the nitroglycerin and aspirin do not relieve the patient’s chest pain.

What is the significance of the ST-segment changes on Mr. Salazar's 12-lead EKG?

• ST-segment changes on a 12-lead EKG indicate ischemia (lack of oxygen/blood flow) or infarction (death of the muscle tissue) of the myocardium (heart muscle). 
• This indicates an emergent situation. The patient’s coronary arteries are blocked and need to be reopened by pharmacological (thrombolytic) or surgical (PCI) intervention.
• Time is tissue – the longer the coronary arteries stay blocked, the more of the patient’s myocardium that will die. Dead heart tissue doesn’t beat.

Mr. Salazar’s chest pain was unrelieved after three (3) doses of sublingual nitroglycerin (NTG). Morphine 5 mg intravenous push (IVP) was administered, as well as 324 mg chewable baby aspirin. His pain was still unrelieved at this point

Mr. Salazar’s cardiac enzyme results were as follows:

Troponin I 3.5 ng/mL

Based on the results of Mr. Salazar's labs and his response to medications, what is the next intervention you anticipate? Why?

• Mr. Salazar needs intervention. He will either receive thrombolytics or a heart catheterization (PCI).
• Based on the EKG changes, elevated Troponin level, and the fact that his symptoms are not subsiding, it’s possible the patient has a significant blockage in one or more of his coronary arteries. 
• It seems as though it may be an Anterior-Lateral MI because ST elevation is occurring in I, aVL, and V 2 -V 6 .

Mr. Salazar was taken immediately to the cath lab for a Percutaneous Coronary Intervention (PCI). The cardiologist found a 90% blockage in his left anterior descending (LAD) artery. A stent was inserted to keep the vessel open.

What is the purpose of Percutaneous Coronary Intervention (PCI), also known as a heart catheterization?

• A PCI serves to open up any coronary arteries that are blocked. First, they use contrast dye to determine where the blockage is, then they use a special balloon catheter to open the blocked vessels. 
• If that doesn’t work, they will place a cardiac stent in the vessel to keep it open.[ /faq]

[faq lesson="true" blooms="Application" question="What is the expected outcome of a PCI? What do you expect to see in your patient after they receive a heart catheterization?"]

• Blood flow will be restored to the myocardium with minimal residual damage.
• The patient should have baseline vital signs, relief of chest pain, normal oxygenation status, and absence of heart failure symptoms (above baseline).
• The patient should be able to ambulate without significant chest pain or SOB.
• The patient should be free from bleeding or hematoma at the site of catheterization (often femoral, but can also be radial or (rarely) carotid.

Mr. Salazar tolerated the PCI well and was admitted to the cardiac telemetry unit for observation overnight. Four (4) hours after the procedure, Mr. Salazar reports no chest pain. His vital signs are now as follows:

• BP 128/82 mmHg SpO 2 96% on 2L NC
• HR 76 bpm and regular RR 18 bpm
• Temp 37.1°C

Mr. Salazar will be discharged home 24 hours after his arrival to the ED and will follow up with his cardiologist next week. 

What patient education topics would need to be covered with Mr. Salazar?

• He should be taught any dietary and lifestyle changes that should be made.
• Diet – low sodium, low cholesterol, avoid sugar/soda, avoid fried/processed foods.
• Exercise – 30-45 minutes of moderate activity 5-7 days a week, u nless instructed otherwise by a cardiologist. This will be determined by the patient’s activity tolerance – how much can they do and still be able to breathe and be pain-free?
• Stop smoking and avoid caffeine and alcohol.
• Medication Instructions
• Nitroglycerin – take one SL tab at the onset of chest pain. If the pain does not subside after 5 minutes, call 911 and take a second dose. You can take a 3rd dose 5 minutes after the second if the pain does not subside. Do NOT take if you have taken Viagra in the last 24 hours.
• Aspirin – take 81 mg of baby aspirin daily
• Anticoagulant – the patient may be prescribed an anticoagulant if they had a stent placed.  They should be taught about bleeding risks.
• When to call the provider – CP unrelieved by nitroglycerin after 5 minutes. Syncope. Evidence of bleeding in stool or urine (if on anticoagulant). Palpitations, shortness of breath, or difficulty tolerating activities of daily living.

Linchpins for Myocardial Infarction Nursing Case Study

In summary, Mr. Salazar’s case highlights the urgency of recognizing and responding to myocardial infarction promptly. The application of vital signs, EKG, cardiac enzymes, and medications like aspirin, nitroglycerin, and morphine played a pivotal role in his care. Diagnostic tools like echocardiography and chest X-rays contributed to a comprehensive evaluation.

Nurses must remain vigilant and compassionate in such emergencies. This case study emphasizes the importance of adhering to best practices in the assessment, diagnosis, and management of myocardial infarction, with the ultimate goal of achieving favorable patient outcomes.

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Patient Case Presentation

Patient presentation.

Mr. Smith is a 60-year-old Caucasian male, who presents with 8/10 chest pain after working out. He just quit smoking and started a new workout and diet program after recently retiring. He has noticed some chest and shoulder discomfort with working out that usually resolves with rest, but decided to come to the emergency department because this episode was unrelenting and more severe. Mr. Smith describes his current pain as severe and sharp, and also complains of nausea and shortness of breath. Vital signs are HR: 110 BP: 150/90 RR: 30 Temp 97.6 O2 Sat: 92% on 2L nasal cannula, EKG shows ST segment elevation in leads II, III and AVf. Labs were drawn, including an elevated troponin (4.23 ng/ml), and slightly elevated white blood cell count (13.6 × 10 9 /L) .

Past Medical History

Type II diabetes (age 47), dyslipidemia (age 33), atherosclerosis (age 52), hypertension (age 49), obesity (age 33), viral pneumonia (age 29), hiatal hernia (age 28), peptic ulcer disease (age 41)

Family Medical History

Mother (deceased) – atrial fibrillation (diagnosed at age 45), died of MI (age 65)

Father (83) – obesity, type II diabetes (diagnosed at 50), COPD (diagnosed at 55)

Social History

Smoker (20 pack years), worked in an office sitting at a desk his whole career (35 years), recently began working out at his local gym since retiring this year.

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Case study 1: acute myocardial infarction

Published by Shanon Hunter Modified over 9 years ago

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Acute Myocardial Infarction

Oct 15, 2014

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Acute Myocardial Infarction. Willis E. Godin D.O., FACC. Acute Myocardial Infarction. Definition: Decreased delivery of oxygen and nutrients to the myocardium Myocardial tissue necrosis causing irreparable tissue/cell death. Pathophysiology.

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Presentation Transcript

Acute Myocardial Infarction Willis E. Godin D.O., FACC

Acute Myocardial Infarction • Definition: • Decreased delivery of oxygen and nutrients to the myocardium • Myocardial tissue necrosis causing irreparable tissue/cell death

Pathophysiology • The most frequent cause of an acute MI is a disruption in the vascular endothelium that is associated with myocardial plaque • Plaque occurs over a period of years to decades • This combination causes the development of an intra-coronary thrombus, which causes the coronary artery to occlude • Within 20-40 minutes of an occlusion, irreversible myocardial cell damage/death occurs

Pathophysiology • 2 primary characteristics of plaque development are 1) a fibromuscular cap and 2) an underlying lipid rich core. • The overall loss of structural stability of the plaque usually occurs at the junction between the fibromuscular cap and the vessel wall (shoulder region) • Thrombus develops (due to the platelet-mediated activation of the coagulation cascade) and partial or complete occlusion occurs causing an acute myocardial infarction.

Pathophysiology • The severity of an MI depends on three factors • 1) The level of the occlusion in the coronary artery • Generally, the more proximal the coronary occlusion, the more extensive the amount of myocardium that will be at risk of necrosis • 2) The length of time of the occlusion • The longer the period of vessel occlusion, the greater the chances of irreversible myocardial damage distal to the occlusion • 3) The presence or absence of collateral circulation

Pathophysiology • STEMI • “complete” blockage of a coronary artery • NSTEMI • “near-complete” blockage of a coronary artery

Pathophysiology • Left Coronary Artery • Left Anterior Descending Artery (LAD) • “widow maker” • Anterior MI • Lateral MI • Left Circumflex Artery (LCx) • Lateral MI • Posterior MI • Right Coronary Artery • Inferior MI • RV MI

Prevalence • Myocardial Infarction is the leading cause of death in the United States • Approximately 450,000 people in the US die from coronary disease per year • 50% of all acute MI’s in the US occur in people under the age of 65 • No longer considered a “disease of the elderly”

Risk Factors • Dyslipidemia • Diabetes Mellitus • Hypertension • Tobacco use • Family History • Male gender

Diagnosis • Symptoms (gained by an accurate history) • Electrocardiogram (ECG) • Laboratory Tests • CK • CK-MB • Troponin • Echocardiogram

Symptoms • Chest pain described as a pressure sensation, fullness, or squeezing in the midportion of the thorax • Radiation of chest pain into the jaw or teeth, shoulder, arm, and/or back • Associated dyspnea or shortness of breath • Associated epigastric discomfort with or without nausea and vomiting • Associated diaphoresis or sweating • Syncope or near syncope without other cause • Impairment of cognitive function without other cause

Electrocardiogram • ST elevation myocardial infarction (STEMI) • > 1mm ST elevations in contiguous leads • Non-ST elevation myocardial infarction (NSTEMI) • ST depression • T wave inversions • No obvious ECG changes

ECG - STEMI

ECG -NSTEMI

ECG - NSTEMI

Cardiac Enzymes • Serial blood draws • Every 4 hours x 4 sets • Myoglobin peaks first (detectable in 1-4 hrs) • Troponin • peaks last (detectable in 3-12 hrs) • most specific • remains detectable in serum the longest

Cardiac Enzymes

Imaging (Echocardiography) • An echocardiogram can be performed to assess areas of the left ventricle that are not contracting normally as compared to areas that are contracting normally • After normal blood flow is interrupted, the area of the myocardium affected by the occluded artery will not function normally. • This abnormal wall motion can be detected by echocardiography

Treatment • Antiplatelets • Supplemental oxygen • Nitrates • Pain control • Beta Blockers • Statin Therapy • Heparin (unfractionated / low-molecular-weight heparin) • Fibrinolytics • Angiotensin-Converting Enyme Inhibitors / Angiotensin Receptor Blockers • Glycoprotein Iib/IIIa Antagonists • Aldosterone Antagonists

Other Treatment Options • Percutaneous Coronary Intervention • PCI / coronary stenting • Surgical Revascularization • CABG • Implantable Cardiac Defibrillators • AICD

Treatment Outcomes • Long-term medications • Smoking cessation • Cardiac Rehabilitation

Long-Term Medications • Most oral medications instituted in the hospital at the time of acute MI will be continued long term • Aspirin, beta blockade, and statin therapy is continued indefinitely in all patients • ACE inhibitors are continued indefinitely in patients with CHF, left ventricular dysfunction, hypertension, or diabetes • Diet modification, regular exercise

Smoking Cessation • Smoking is a major risk factor for coronary artery disease and MI • For patients who have undergone an MI, smoking cessation is essential to recovery, long-term health, and prevention of re-infarction • In one study, the risk of recurrent MI decreased by 50% after 1 year of smoking cessation

Smoking Cessation • All STEMI and NSTEMI patients with a history of smoking should be advised to quit and offered smoking cessation resources • Nicotine replacement therapy • Pharmacologic therapy • Referral to behavioral counseling or support groups • Smoking cessation counseling should begin in the hospital, at discharge, and during follow up

Cardiac Rehabilitation • Provides a venue for continued education, reinforcement of lifestyle modification, and adherence to a comprehensive prescription of therapies for recovery from MI including exercise training • Participation in cardiac rehabilitation programs after MI is associated with decreases in subsequent cardiac morbidity and mortality • Other benefits include improvements in quality of life, functional capacity, and social support

Summary • MI results from myocardial ischemia and cell death, most often because of an intra-arterial thrombus superimposed on an ulcerated or unstable atherosclerotic plaque • Despite advances in therapy, MI remains the leading cause of death in the United States. • MI risk factors include hyperlipidemia, diabetes, hypertension, male gender, and tobacco use. • Diagnosis is based on the clinical history, ECG, and blood test results, especially creatinephosphokinase (CK), CK-MB fraction, and troponin I and T levels.

Summary • Outcome following an MI is determined by the infarct size and location, and by timely medical intervention. • Aspirin, nitrates, and beta blockers are critically important early in the course of MI for all patients. • Post-discharge management requires ongoing pharmacotherapy and lifestyle modification.

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Safer Healthcare Now! Acute Myocardial Infarction. Presented by Amanda Thompson, Safer Healthcare Now Facilitator. Safer Healthcare Now! Background. Largest patient safety initiative in Canadian history Adopted form IHI Over 600 teams registered across Canada

519 views • 32 slides

SGD 1: Acute Myocardial Infarction

SGD 1: Acute Myocardial Infarction. PATHOLOGY. Chest Pain. An unpleasant sensation in the anterior wall of the thorax actual or potential tissue damage mediated by specific nerve fiber to the brain - conscious appreciation may be modified by various factors.

906 views • 19 slides

Arrhythmias Complicating Acute Myocardial Infarction

Arrhythmias Complicating Acute Myocardial Infarction. Sinus Bradycardia. Most common arrhythmia occurring during the early hours after MI and may occur in up to 40% of inferior and posterior infarcts. May be related to autonomic imbalance or to atrial and sinus node ischemia or both.

441 views • 27 slides

Improved Acute Myocardial Infarction (AMI) Guidelines

ICD-10-CM implementation brought several significant changes to the OCG (Official Guidelines for Coding and Reporting) with regard to Chapter 9 (Diseases of the Circulatory System) I.C.9.e Acute myocardial infarction (AMI). Preparing yourself for coding updates based on MI type is not sufficient. You also must learn how to apply these new codes using OGC for Coding and Reporting.

56 views • 3 slides

Practical Electrocardiography – Myocardial Ischemia and Acute Myocardial Infarction

Practical Electrocardiography – Myocardial Ischemia and Acute Myocardial Infarction. Scott Ewing, D.O. Cardiology Fellow August 30, 2006. Assess Initial 12-Lead ECG Findings. Classify patients with acute ischemic chest pain. ST elevation or new or presumably new LBBB:

578 views • 49 slides

Practical Electrocardiography – Myocardial Ischemia and Acute Myocardial Infarction. Scott Ewing, D.O. Cardiology Fellow August 30, 2006. Assess Initial 12-Lead EKG Findings. Classify patients with acute ischemic chest pain. ST elevation or new or presumably new LBBB:

637 views • 49 slides