Learning Objectives
By the end of this section, you will be able to:
- Discuss the pathophysiology, risk factors, and clinical manifestations of myocardial infarction
- Describe the diagnostics and laboratory values of myocardial infarctions
- Apply nursing concepts and plan associated nursing care for the patient with myocardial infarction
- Evaluate the efficacy of nursing care for the patient with myocardial infarction
- Discuss the medical therapies that apply to the care of myocardial infarction
Coronary disease afflicts 7.1 percent of adults aged 45-65, 10.9 percent of adults aged 45 years and older, and 17 percent of adults 65 and older (CDC, 2019). Coronary heart disease (CHD) affects White people the most, followed by Black people, Hispanic people, and Asian and Pacific Islander people. Social determinants of prevalence include a lack of higher education, physical inactivity, smoking, and lack of disease surveillance. Patients with comorbid conditions such as diabetes, chronic kidney disease, chronic obstructive pulmonary disease, cerebrovascular disease, and peripheral artery disease have a 26 percent increased risk for mortality following myocardial infarction (MI) (Baechli et al., 2020).
Pathophysiology
The four major coronary vessels are the right coronary artery, the left main coronary artery, the left circumflex artery, and the left anterior descending artery (LAD) (Figure 12.22). The right coronary artery branches off the aorta, where oxygen-rich blood perfuses the right ventricle and assists with right ventricular contraction. It also perfuses the native sinoatrial node, which is the “pacemaker” of the heart. The left circumflex artery supplies blood to the left atrium, whereas the LAD perfuses the anterior wall. The LAD is not only solely responsible for perfusing the anterior wall of the heart but also perfuses other cardiac landmarks such as the septum and lateral anterior wall. Due to the high demand of the left atrium and left ventricle to perfuse the body, the left main coronary artery assists with perfusion to these chambers. Cardiac cells are sensitive to coronary perfusion, in that cells do not function properly under periods of blood flow deprivation or, in worse cases, myocyte death (infarction) with prolonged perfusion defects.
Clinical Manifestations
The clinical presentation of myocardial infarction can be very vague and not every clinical presentation is the same. Typically, patient interviews and clinical diagnostics cue the nurse for a high index of suspicion if a myocardial event has occurred or is occurring.
Age-related changes and lifestyle influences may influence the diameter and plaque occlusions of a diseased coronary artery. Initially, endothelial intimal thickening is compounded by plaque formation, whose composite is from high concentrations of low-density lipoprotein (LDL). Traveling platelets and red blood cells aggregate at the sites of plaque build-up and start to form a clot or a thrombus. Two physiological insults may happen. Under the first condition of physical duress, called ischemia, the coronary artery becomes constricted to the point where blood flow is temporarily stopped but resumes with medication or rest. If the same conditions occur, but blood flow to the myocardium is cut off completely, the cells die, called infarction. Symptom presentation and lethality may depend on the degree of infarction and which coronary artery is involved.
Clinical Safety and Procedures (QSEN)
Evidence-Based Practice: Intervention Time for Myocardial Infarction
- Note the onset of chest pain for a patient with a high suspicion of myocardial infarction.
- Patients who have no relief of chest pain after three doses of nitrates that are dosed at 5-minute intervals apart have a high risk of acute coronary syndrome.
- Evidence recommends activating the emergency medical system to assist with a 90-minute window from the onset of chest pain to angioplasty intervention to maximize perfusion outcomes from a myocardial infarction.
- Administer 325 mg aspirin for platelet aggregation.
Diagnostics and Laboratory Values
Chest pain or discomfort that occurs when blood flow to the heart is reduced is called angina. Stable angina is typically reversed with rest or pharmacological intervention, whereas unstable angina requires both rest and pharmacological support and can last several minutes. Classic symptoms include chest pain; pain radiating to the jaw, arms, neck, back, or stomach; shortness of breath; lightheadedness; and excessive sweating, also known as diaphoresis. A diagnostic workup entails the measurement of serum troponins and creatine kinase MB to rule out myocardial infarction. Serum troponin is a protein secreted when cardiac tissue is damaged, typically six to eight hours following a myocardial infarction (British Heart Foundation, 2024). The enzyme creatine kinase MB (CK-MB) is secreted in the presence of damaged cardiac tissue (Medline Plus, 2023). Its levels will peak in a few hours and decrease in two days. Most emergency departments will measure troponins every six to eight hours for three levels to fully rule out myocardial infarction.
Other diagnostic tools besides blood work are necessary to complete the workup. An EKG may demonstrate abnormalities with the T waves, in which the T waves will be flipped or the ST segment will be depressed (Figure 12.23). If a patient is asymptomatic, an echocardiogram may demonstrate ventricular wall motion abnormalities. Invasive procedures such as angiography may reveal coronary blockages, which will be further discussed.
In the acute phase of an anginal episode, nursing care focuses on maximizing the re-initiation of oxygenation to the blocked coronary vessel. Patients will have their chest pain managed, receive supplemental oxygen, and maintain bed rest. The nurse will monitor hemodynamics by applying telemetry monitoring.
An umbrella term, acute coronary syndrome (ACS) includes the following: non-ST-elevated myocardial infarction (NSTEMI), ST-elevated myocardial infarction (STEMI), and unstable angina (Figure 12.24). With an NSTEMI, there are no abnormal changes in the EKG; however, there would be a rise in the troponins and CK-MB levels. In contrast, with a STEMI, there are abnormal EKG changes with elevation of the ST segment in a 12-lead EKG with an upward trend in the troponins and CK-MB. Lastly, unstable angina presents with symptomatic chest pain that radiates to the jaw or down the left side with associated nausea, diaphoresis, dizziness, and fatigue that does not resolve with rest or with three doses of nitroglycerin administered five minutes apart. STEMIs require prompt, emergent intervention with angiography, as damage is more likely to extend deeper into the cardiac muscle.
Nursing Care of the Patient with Myocardial Infarction
The care of the patient experiencing an MI differs whether it is in the acute phase or post-recovery phase. The best outcomes occur when nurses recognize “muscle is time,” and prompt identification is the key. Rapid treatment will vary in the acute interventional phase compared to the post-recovery phase of myocardial injury.
Recognizing and Analyzing Cues
The very first assessment the nurse must initiate is a set of vital signs, noting any deviation from normal parameters. Findings will vary: a patient experiencing MI may be hypotensive or hypertensive or will have bradycardia or tachycardia. A low pulse oxygenation of < 92 percent will indicate the patient has hypoxia. The nurse will inspect the patient’s skin, noting any evidence of cyanosis or evidence of dyspnea. The patient’s capillary refill and a distal pulse assessment of the radials and dorsalis pedis are necessary to monitor distal perfusion and to obtain a baseline if the patient proceeds to angiography. Peripheral pulse assessments are required in the post-care of a patient undergoing angiography, and baseline assessment is required. A subjective assessment inquiring about chronic health conditions, lifestyle practices, and medication reconciliation is required.
Prioritizing Hypotheses, Generating Solutions, and Taking Action
Associated acute nursing care for the patient with MI includes the concepts of oxygenation, perfusion, and pain management. With oxygenation, the nurse must maintain pulse oximetry over 92 percent and apply telemetry with frequent hemodynamic monitoring to assess perfusion difficulties. The nurse promotes a quiet environment to decrease elevations in blood pressure and decrease oxygen demand. If the patient undergoes angiography, the patient must lie flat for a minimum of four to six hours post-procedure to reduce bleeding risk at the femoral artery puncture site. If the patient is experiencing any further chest pain, note the onset of chest pain, as ideal outcomes improve if the time from symptom onset to angiography is reduced. If the patient requires a coronary artery bypass graft (CABG) (Figure 12.25), a higher level of care in the intensive care unit level is required, as the patient is likely to be ventilated, have chest tubes, and require surgical incisional management.
Once stabilization of MI has been achieved, education is a core component of disease management. Education is directed at dietary adjustments (low saturated fat, low cholesterol, monitor processed foods), smoking cessation, and limiting/omitting alcohol. Following an MI event, the patient will participate in cardiac rehabilitation with a program to increase aerobic activity. Nurses must educate patients about sexual intimacy; often cardiologists will recommend safe resumption of intimacy if the patient can ascend a flight of stairs without chest pain, fatigue, or shortness of breath. Education should also include information about stress reduction strategies such as meditation, guided imagery, or yoga. Compliance with medications and follow-up with provider care are also necessary.
Unfolding Case Study
COVID Complications: Part 2
Refer to COVID Complications: Part 1 for the first part of this patient’s medical history. He has now been transferred to the ICU.
| Nursing Notes | 2/20/2024, 12:30, Triage Assessment Patient presents to ICU. Increased agitation, increased VS, increased effort to breathe. Dry non-productive cough. Lung sounds with diminished bases and mid-lung field, with increasing crackles from baseline. Tachycardia, repeat ABG demonstrating respiratory acidosis with lower pH, decreased PO2, and increased PCO2 from baseline. Weak, bodily fidgeting has decreased. Not following all appropriate commands. Intervention Obtain coagulation profile Initiate isolation precautions for COVID Placed on ventilator per provider’s settings: positive end-expiratory pressure support of 5 cm/H2O IV rate of 75 ml/hr Continuous cardiac monitor and pulse oximetry Albuterol nebulizer ×1 via ET tube, administered by respiratory therapy Sputum culture obtained via ET tube ABG stat Acetaminophen 650 mg suppository PR for temperature > 100.7 Sedation, diprivan IV drip 1 mg/kg Labetalol 5 mg IV initial IV push dose for a BP > 160/90. May repeat 5 mg dose IV push ×2 administered every 10 minutes until the systolic blood pressure is within the desired range Notify provider if ineffective according to parameters provided Initiate hyperglycemic protocol as indicated Heparin drip IV 5,000 U bolus and heparin drip continuous at 1,000 U/hr Troponin Cardiac enzymes ×3 Cefazolin 1.5 mg IV every 6 hr Continuous reassessments VS: BP, HR, RR, temperature, O2 saturation Monitor blood sugars every 4 hr 02/20/24, 13:00, Assessment Physical Examination: HEENT: pupils equal and reactive to light, mucus membranes dry, no thyroid enlargement. Lymphatic: lymphatic nodes were not swollen or enlarged. Respiratory: increased agitation, increased VS, increasing effort to breathe. Lung sounds with diminished bases and mid-lung field, with increasing crackles from baseline. Cardiovascular: tachycardia, repeat ABG demonstrating respiratory acidosis with lower pH, decreased PO2, and increased PCO2 from baseline. Abdomen: soft, denies pain by shaking head no, not distended, bowel sounds present all four quadrants. Musculoskeletal: weak, bodily fidgeting has decreased. Not following all commands. Skin: pale, warm, and moist; patient sedated. 02/21/2024, 00:00 Patient sedated, remains on ventilator. Skin cool and moist. Hypotensive, initiate IV norepinephrine drip. ET tube suctioned with yellow secretions, remains febrile. 02/21/24, 04:00 Physical Examination: HEENT: pupils equal and reactive to light. Respiratory: increased agitation, remain on ventilator with positive end expiratory pressure lung sounds with diminished bases and mid-lung field, with increasing crackles from baseline Cardiovascular: tachycardia, repeat ABG demonstrating respiratory acidosis with lower pH, decreased PO2, and increased PCO2 from baseline. Abdomen: soft, denies pain by shaking head no, not distended, quiet bowel sounds present all four quadrants. Musculoskeletal: weak, bodily fidgeting has decreased. Not following all commands to move extremities. Skin: warm and moist. Renal: hourly urine output 5 ml past 3 hours Intervention Hemodynamic monitoring initiated with frequent hemodynamic monitoring to assess for perfusion difficulties. Quiet environment to decrease elevations in blood pressure and decrease oxygen demand. Continued monitoring of oxygenation, perfusion, and pain management, including hemodynamic values, VS. ABG to assure adequate tissue perfusion and oxygenation. Antiplatelet and/or anticoagulation therapy according to provider’s orders (based on lab reports). Increase IV rate to 125 ml/hr (fluid resuscitation). |
| Flow Chart | 02/20/24, 12:30 Assessment Blood pressure: 100/98 Heart rate: 110 Respiratory rate: 16 per min rate per ventilator Temperature: 102.3 Oxygen saturation: 89 % on 4 Lpm Patient intubated on ventilator. Ventilator setting ordered per provider. 02/21/2024, 00:00 Vital signs: BP: 100/60 HR: 140 RR: 16 per ventilator-positive end expiratory pressure support of +10 cm/H2 (PEEP) Temp: 102.5 |
| Lab Results | 02/20/24, 13:00 ABG pH: 7.30 PCO2: 62 mm Hg PO2: 70 mm Hg HCO3: 30 mEq/L BS: 100 mg/dL Blood culture: positive for Pseudomonas aeruginosa Sputum culture: positive for Staphylococcus aureus Troponin elevated: 40 ng/l CK-MB-Cardiac enzymes elevated 02/20/24, 18:00 CBC with differential, pending WBC: 14.5 cells/mm3 Hgb: 15 g/dl Hct: 40% INR: 1.0 BUN: 19 mg/dl Creatinine: 1.09 mg/dl Lactic acid: 3 mmol/L Na: 140 mEq/L K+: 3.8 mEq/L Cl: 100 mEq/L Pulse oximetry: 92% ABG: pH: 7.31 PCO2: 55 mm/Hg PO2: 60 mm/Hg HCO3: 30mEq/L 02/21/24, 03:00 ABG: pH: 7.32 PCO2: 50 mm/Hg PO2: 75 mm/Hg HCO3: 22 mEq/L BS: 180 mg/dL Lactic acid: 4.0 mmol/L |
| Diagnostic Tests/Imaging Results | 02/20/24, 16:00 EKG: acute anterior lateral myocardial infarction CXR: profuse infiltrates and opacities Echocardiogram: left ventricular dysfunction (decreased wall motion and contractility) Ejection fraction: 40% Temperature: 102.5 02/21/24, 04:00 Echocardiogram: diffuse LV hypokinesis. Other findings included isolated right ventricular dysfunction. Ejection fraction: 40% CXR: bilateral peripheral and basal; multifocal air space and consolidation of increasing opacities (ground-glass) opacity |
| Provider’s Orders | 02/20/24, 16:00 Initiate isolation precautions for COVID On ventilator per provider’s settings IV started left antecubital, #20 gauge of Ringers Lactate rate of 125 ml/hr Continuous cardiac monitor and pulse oximetry Albuterol nebulizer ×1 via ET tube, administer by respiratory therapy Coagulation profile Coagulation profile, then begin repeat heparin 5,000 U IV bolus followed by 1,000 U/hr Troponin Cardiac enzymes ×3 Cefotaxime 1 mg IV every 12 hours Discontinue cefazolin 1.5 mg IV Sedation, diprivan IV drip 1 mg/kg Labetalol 5 mg IV initial IV push dose for a B/P > 160/90. May repeat 5 mg dose IV push ×2 administered every 10 minutes until the systolic blood pressure is within the desired range. Notify provider if ineffective according to parameters provided Initiate hyperglycemic protocol as indicated Continuous monitoring VS: BP, HR, RR, temperature, O2 saturation 02/21/24, 04:00 Insertion of hemodynamic monitoring. Following readings every 4 hours: Cardiac output Pulmonary wedge pressures Pulmonary arterial pressure Discontinue cefotaxime 1 mg IV every 12 hours Vancomycin 500 mg IV every 6 hours over a period of 60 minutes Vasopressin IV: 0.6-2.4 units/hr (0.6-2.4 mL/hr): consult critical care provider for dosing |
Evaluation of Nursing Care of the Patient with Myocardial Infarction
Patient recovery differs depending on the degree of damage from MI and the interventional treatment. Resumption of activities, returning to work, and restoration of stamina varies from person to person. The American Heart Association (2023) notes individuals will require several months to return to pre-disease levels with physical activity. All goals should be tailored to the patient’s physiological abilities.
In the immediate, acute, and tertiary phase of treatment of MI, the nurse must implement pharmacological therapies and prepare the patient for medical or surgical intervention for revascularization. Overall goals include optimizing oxygenation, relieving chest pain, stabilizing dysrhythmias, and preserving myocardial tissue. Once the patient is stabilized, the goals will be directed more toward discharge and cardiac rehabilitation:
- demonstrating adequate oxygenation by maintaining SPO2 > 92%
- hemodynamic stability with normal parameters for pulse and blood pressure
- resolution of chest pain
- employing rest periods with activities of daily living to conserve oxygen demands
- demonstrating understanding of adherence to medication therapy
Evaluating Outcomes
The nurse must reinforce the importance of staying on a full dose of aspirin and/or antiplatelet therapy as prescribed. Patients recovering from MIs must continue with beta-blockers to reduce the risk of reinfarction. Having the patient verbalize understanding and teach back are effective methods to evaluate understanding. The nurse will monitor the patient’s willingness to make lifestyle modifications through smoking cessation and reduction of alcohol intake.
Survival from MI has increased greatly over the years with the advancement of pharmacological and interventional methods. Acceptance of this diagnosis will be life-changing for the patient and family members. The nurse should approach the care of the family unit with a nonjudgmental approach. Interprofessional referral for social services, nutrition, and case management will be considered in the planning of nursing care.
Medical Therapies and Related Care
Medical and surgical interventions include angiography and coronary artery bypass graft. In angiography, a catheter is threaded into the femoral artery and fluoroscopy dye is injected into the patient’s coronary arteries to assess the presence of coronary blockages. If deemed safe by the provider, a stent, which resembles a coil, will be deployed following an opening of the blockage with ballooning equipment. Angiography is preferred, as the patient will be under monitored anesthesia care and it is the least invasive. Major risks associated with the procedure include dislodging any clots proximal to the blockage elsewhere, dysrhythmia, or bleeding (Malik & Tivakaran, 2023).
If there are multiple blockages, cardiothoracic surgeons will perform surgical revascularization through coronary artery bypass graft (CABG), a more aggressive form of restoring perfusion, as the patient will require general anesthesia and a higher level of care (Figure 12.25). A CABG is a surgical procedure that relocates vasculature from other vessels in the body, such as the saphenous vein in the leg, into the cardiac vasculature to restore perfusion to the heart muscle. These bypasses may be single, double, triple, or quadruple, depending upon how widespread the blockages are that need to be bypassed.
Acute pharmacological therapies may include antiplatelets/anticoagulants, nitrates, and beta-blockers. The most common antiplatelet therapy is aspirin 325 mg. Another antiplatelet, clopidogrel 75 mg, reduces the aggregation of a thrombus. Nursing interventions include monitoring for gastrointestinal upset, excessive bruising, and blood in the urine or stool. Anticoagulants, such as heparin, may be administered intravenously as a bolus and continuous drip. Titration of anticoagulants is weight-based and assists with thrombus reduction. The nurse is responsible for monitoring for bleeding and monitoring serum/PTT/anti-factor Xa heparin (institution specific).
Nitrates cause coronary vasodilation which helps to maximize coronary perfusion and reduce ischemia. These medications can be administered via a spray into the mouth, wearable patch paste, or sublingual pills. Nursing assessments include monitoring for hypotension, headache, and response of chest pain resolution. The nurse must use gloves when administering nitro paste to avoid undue side effects.
Beta-blockers are critical to reducing infarct involvement by reducing oxygen demand and lowering heart rate, blood pressure, and contractility, and ideally, improving myocardial oxygenation. The nurse must monitor hemodynamics closely and withhold in cases of symptomatic bradycardia (less than 50 bpm or at the provider’s discretion) or low blood pressure (less than 90/50 mm Hg or at the provider’s discretion).
Chronic medication therapies include antiplatelets, beta-blockers, and statins. Anti-hyperlipidemic agents are indicated to reduce endothelial inflammation and reduce plaque formation. The nurse must educate a patient taking statins about the importance of avoiding grapefruit juice due to food-drug interaction. The patient must be monitored for hepatotoxicity and educated that myalgias are a common side effect. A month following an MI, an echocardiogram will be completed to assess the left ventricular ejection fraction (EF). If the patient has a depressed EF (less than 40%), ACE inhibitors/ARBs will be initiated to reduce the risk of congestive heart failure.
Lastly, morphine, oxygen, nitrates, and aspirin were previously a therapy for ACS but are no longer practiced. Morphine is not endorsed by the American Heart Association and American College of Cardiology. Oxygen therapy and aspirin are recommended for both NSTEMI and STEMI, but nitrates are only effective for NSTEMI.