eMedicine Specialties > Emergency Medicine > Cardiovascular

Myocardial Infarction: Follow-up

Author: Drew Evan Fenton, MD, Hospitalist, Our Health Care Consultants
Contributor Information and Disclosures

Updated: Oct 5, 2009

Follow-up

Further Inpatient Care

  • All patients with known or suspected MI should be admitted to an ICU.
  • Patients should continue to receive beta-blockers, nitrates, and heparin, as indicated.
  • ACE inhibitors have been shown to improve survival rates in patients who have experienced an MI. In the acute setting, afterload reduction from ACE inhibitors may reduce the risk of CHF and sudden death.
  • Lidocaine may be indicated for patients with ventricular ectopy that is complex or for patients with hemodynamically significant, nonsustained, or sustained ventricular tachycardia. Recall that the routine use of lidocaine as prophylaxis for ventricular arrhythmias is contraindicated.

Transfer

  • A recent study showed that the transfer of patients to an invasive-treatment center for primary PCI is superior to on-site fibrinolysis provided that the transfer can be accomplished within 2 hours. Transfer should be considered for those patients who are likely to benefit from PCI or cardiac surgery but who are in an institution where access to such interventions is not immediate. The benefits of transferring such a patient must outweigh the risks. Patients for whom transfer might be considered include the following:
    • Patients with new or worsening hemodynamically significant mitral regurgitant murmurs
    • Patients with known or suspected critical aortic stenosis and either ongoing ischemia or hemodynamic instability
    • Patients who have received thrombolysis and fail to reperfuse
    • Patients with significant LV dysfunction or cardiogenic shock
  • Cantor et al studied high-risk patients with ST-segment elevated myocardial infarction (STEMI) who received fibrinolytic therapy in hospitals that do not have percutaneous coronary intervention (PCI) capabilities.4
    • The patients (n=1059) were randomized to either standard treatment (ie, if needed, included rescue PCI, or delayed angiography) or immediate transfer to another hospital and PCI within 6 hours following fibrinolysis. All patients received aspirin, tenecteplase, and anticoagulation (heparin or enoxaparin), and clopidogrel was recommended.
    • The study’s primary endpoint was a composite of death, reinfarction, recurrent ischemia, new or worsening congestive heart failure, or cardiogenic shock within 30 days. The primary end point occurred in 11% of patients in the group that was immediately transferred compared with 17.2% of patients randomized to the standard treatment (P=0.004). A significant decrease in ischemic complications was observed in high-risk patients with STEMI who were treated with fibrinolysis and transferred for PCI within 6 hours following fibrinolysis.

Deterrence/Prevention

  • Patients should avoid risk factors when possible and act upon treatable risk factors.
  • Seeking medical attention or calling 911 with the first symptoms or signs of angina may initiate the cascade of interventions that will ultimately prevent or limit damage to the myocardium. All patients should be educated as to these symptoms and signs and when to call 911.
  • Daily low-dose aspirin may be helpful, but the decision to prescribe aspirin as a preventative measure for MI must be made considering his or her overall condition and risk-benefit ratio.

Complications

  • Monitoring and treatment of arrhythmias and conduction disturbances are an important part of the treatment of a post-MI patient within the first 48 hours. Conduction disturbances are most commonly observed in inferior MI but are more ominous when they occur with anterior MI.
  • Tachyarrhythmia
    • Sinus tachycardia is a poor prognostic sign that is indicative of ventricular dysfunction or failure.
    • PVCs - Simple (ie, <10/h), no need to treat
    • PVCs - Complex, NSVT/VT, lidocaine DOC
    • Accelerated idioventricular rhythm (AIVR) is the most common reperfusion arrhythmia, but it usually is well tolerated and does not require treatment.
  • Bradyarrhythmia
    • Type I second-degree heart block (ie, Wenckebach) is associated with inferior wall MI. Treat using temporary pacing or atropine only if it is hemodynamically significant.
    • Type II second-degree heart block is associated with anterior wall MI and may require a permanent pacemaker. Bundle branch blocks (BBB) that are new or preexisting with new second-degree heart block may also mandate consideration for a permanent pacemaker.
  • Cardiogenic shock
    • In the setting of an MI, cardiogenic shock is associated with an 80% in-hospital mortality rate.
    • Patients should undergo thrombolysis or PCI, placement of an intra-aortic balloon pump, or CABG.
  • Valvular insufficiency
    • This may occur acutely when ischemia or an infarct of the papillary muscle occurs resulting in mitral regurgitation. It usually presents as flash pulmonary edema and hypotension. Papillary muscle rupture may require valve repair.
    • Ischemia often responds to medical therapy and thrombolysis.
  • Congestive heart failure can be due to systolic or diastolic dysfunction in MI. The severity of the heart failure and systolic dysfunction depends on the extent of the infarct and the presence of any other complications, such as acute mitral regurgitation. Treatment may include nitrates, morphine, diuretics, and ACE inhibitors. Digoxin has no role in acute CHF due to ischemia.
  • Right ventricular infarct occurs in the setting of an inferior wall infarction. Because patients with an RV infarct are preload-dependent, they often are identified by profound hypotension with normal pulmonary auscultation, particularly after nitroglycerin therapy. They respond to volume loading. This can be diagnosed by ST-segment elevation in right-sided chest leads (ie, V4 R, V5 R).
  • Ventricular rupture occurs in the interventricular septum or the left ventricle free wall. Rupture represents a catastrophic event with mortality rates greater than 90%. Prompt recognition, stabilization, and surgical repair are crucial to any hope of survival. An echocardiogram usually defines the abnormality, and a right heart catheterization may show an oxygenation increase with septal rupture. It is more common in women, patients with hypertension, and those receiving NSAIDs or steroids.
  • Other complications include pericarditis, ventricular aneurysm, and mural thrombus.

Prognosis

  • MI may be associated with a mortality rate as high as 30%, with more than half of deaths occurring in the prehospital setting. Prognosis is highly variable and depends on a number of factors related to the timing and nature of intervention, success of the intervention (ie, infarct size), and post-MI management.
  • Better prognosis is associated with factors including the following:
    • Successful early reperfusion
    • Preserved LV function
    • Short-term and long-term treatment with beta-blockers, aspirin, and ACE inhibitors
  • Poorer prognosis is associated with the following:
    • Delayed or unsuccessful reperfusion
    • LV function is the strongest predictor of outcome in the post-MI patient.
  • Ventricular dysrhythmias
    • Recent experience with amiodarone suggests that it may improve long-term mortality in survivors of MI with ectopy and ventricular tachycardia.

Patient Education

  • For excellent patient education resources, see eMedicine's Cholesterol Center. Also, visit eMedicine's patient education articles Chest Pain, Coronary Heart Disease, and Heart Attack.
  • All patients must be educated on the need to call 911 for symptoms and signs of ACS or MI.
  • All patients must be aggressively encouraged to quit smoking.

Miscellaneous

Medicolegal Pitfalls

  • Failure to diagnose MI can result in costly litigation. In most studies, this diagnosis accounts for the largest sum of dollars paid out. The often-grim outcome also adds a major emotional cost for clinicians involved in litigation.
  • Attribution of epigastric or chest symptoms from myocardial ischemia to a GI source may lead to litigation. Often, this is done despite the presence of dyspnea or diaphoresis, symptoms that are difficult to attribute to the GI system. Additionally, patients with myocardial ischemia may report relief or improvement with GI remedies (eg, antacids). Remember that even myocardial ischemia can worsen with recumbency (eg, angina decubitus) because of an increase in venous return and a temporary greater workload.
  • Attribution of the discomfort of myocardial ischemia to a musculoskeletal etiology may lead to litigation. Tenderness of the chest wall is reported in as many as 5% of patients who prove to have an MI. If no injury or event is defined that could have led to a soft tissue injury, the clinician should be reluctant to render a diagnosis of musculoskeletal chest pain.
  • Aortic dissection can also be a pitfall if a retrograde dissection is present. The dissection may extend to the pericardial sac and produce cardiac tamponade or disrupt the origin of a coronary artery producing STEMI as a complication of dissection. Thrombolytics administration to such a patient could produce disastrous results.
  • Younger patients are overly represented in cases of missed MI. Most likely, this is because of the inherent bias that this is a disease of those who are late middle-aged and older. Approach each patient with chest symptoms as an individual who could have the disease.
  • ECG misinterpretation
    • Unfortunately, in a series of missed MI, the failure to recognize ischemic changes is frequent. The inferior leads, in particular, must be scrutinized carefully for any evidence of ST-segment elevation by using a straight edge across the T-P segments.
    • Another common error is to recognize ischemic changes and then discharge the patient without definitively proving that the changes were pre-existent. Nonischemic causes of ST-segment elevation include LVH, pericarditis, ventricular-paced rhythms, hypothermia, hyperkalemia, and LV aneurysm. Nonischemic causes may lead to over treatment.
  • Failure to diagnose an MI in the setting of a left bundle-branch block may lead to litigation. Criteria for the diagnosis are as follows:

1.      ST-segment elevation greater than 1 mm and concordant with QRS complex

2.      ST-segment depression greater than 1 mm in lead V1, V2, or V3

3.      ST-segment elevation greater than 5 mm and discordant with QRS complex

These criteria have been assigned a score from 1-5. A score of 3 is necessary for a specificity for MI of 90%. The first criterion is scored a 5, the second is scored a 3, and the third is scored a 2.

  • Delays or failure to administer thrombolytics or to initiate PCI may lead to litigation.
    • This is usually because of delays in ECG performance, interpretation, and decision-making, and it is also affected by the availability of thrombolytics in ED.
    • Excluding patients based on age alone will deny some the significant benefit of thrombolysis.
 


More on Myocardial Infarction

Overview: Myocardial Infarction
Differential Diagnoses & Workup: Myocardial Infarction
Treatment & Medication: Myocardial Infarction
Follow-up: Myocardial Infarction
Multimedia: Myocardial Infarction
References
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References

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Further Reading

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Keywords

signs of myocardial infarction, symptoms of myocardial infarction, non stemi myocardial infarction, MI, acute myocardial infarction, AMI, heart attack, chest pain, hypertension, mitral regurgitation, dysrhythmias, acute valvular dysfunction, congestive heart failure, CHF, third heart sound, fourth heart sound, heart block, emboli, right ventricular failure, cannon jugular venous a waves, left ventricular hypertrophy, coronary artery vasospasm, acute coronary syndrome

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Contributor Information and Disclosures

Author

Drew Evan Fenton, MD, Hospitalist, Our Health Care Consultants
Drew Evan Fenton, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Robert M McNamara, MD, FAAEM, Chair and Professor, Department of Emergency Medicine, Temple University School of Medicine
Robert M McNamara, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, Pennsylvania Medical Society, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Gary Setnik, MD, Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School
Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD, Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

 
 
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