Mr. Harris, 44 years old with a history of hypertension, awakes with substernal chest pressure. En route to the ED, paramedics administer nitroglycerin spray 0.4 mg sublingual, aspirin 81 mg (four chewable tablets), and O2 at 4 L/min via nasal cannula. When Mr. Harris arrives at the ED, his vital signs are BP-172/90; T-99; P-74; R-18. His 12-lead ECG shows ST-segment elevation in leads II, III, and AVF with ST-segment depression in leads I and AVL. Creatine kinase (CK) is 620 with a creatine kinase-myocardial band (CK-MB) 47.5 and a relative index (RI) 7.7. Troponin I level is 40.5. Mr. Harris is started on IV nitroglycerin (Tridil) at 10 mcg/min to be titrated for pain. He receives metoprolol (Lopressor) 5 mg IV push. He also receives heparin 4,000 units IV push, and an infusion is started at 900 units/hr. He is evaluated for fibrinolysis treatment and receives reteplase (Retavase) 10 units IV push followed by another 10 units IV push 30 minutes later. Mr. Harris is transferred to the CCU.

What type of MI did Mr. Harris have, and what should the nurse do to evaluate his response to treatment? An estimated 565,000 new MIs and 300,000 recurrent MIs occur annually.¹ In 2003, an MI was an underlying or contributing cause of death for 221,000 patients.¹ The estimated direct and indirect cost for coronary heart disease in 2006 was $142.5 billion.¹

STEMI or not?

An MI can be classified as an ST-elevation myocardial infarction (STEMI) or a non-STEMI. A STEMI is due to an occlusion of a coronary artery and disruption of blood flow to the myocardium that can lead to cellular necrosis. RNs should be knowledgeable about STEMI since patients may be candidates for reperfusion therapy, which restores blood flow and preserves myocardium.

An MI diagnosis is based on a patient’s clinical presentation, proteins and enzymes released from the cells following myocardial injury (cardiac biomarkers), and a 12-lead ECG. The main symptom of myocardial ischemia is pain or discomfort that is typically substernal and may radiate to one (often the left) or both arms or to the throat, neck, jaw, and scapula. During a pain assessment, the nurse should question the patient about any pain or discomfort since many patients may not describe pain but rather a pressure, heaviness, tightness, fullness, squeezing, or ache. Some patients do not experience pain or discomfort in the chest; their ischemia may manifest as arm, throat, or back pain or discomfort.

Nurses should rate the severity of the pain or discomfort on a verbal 0-10 scale. If patients are nonverbal or have a cognitive impairment, RNs can use the FLACC (face, legs, activity, cry, consolability) scale. Each category of behaviors is assigned a score of 0 to 2 for a possible total score of 10 for the most pain possible.

Other symptoms of MI include dyspnea, diaphoresis, nausea, and vomiting. Women may present with atypical symptoms. Women experience prodromal symptoms more than a month before an MI.² Prodromal symptoms have been described as intermittent symptoms that appear before an MI or increase in frequency or severity before an MI and then disappear after an MI.² These symptoms include shortness of breath, unusual fatigue, sleep disturbance, indigestion, and anxiety, with chest discomfort reported less frequently.² Consequently, the classic symptom of chest pain or discomfort may be an unreliable indicator of myocardial ischemia in women, and women’s atypical presentation may lead to misdiagnosis.

The most common cardiac biomarkers used to diagnose MI are CK, CK-MB, myoglobin, and troponin T and I. CK is an enzyme that is released from skeletal muscle cells as a response to injury. A normal CK level is 25-200 units/L.³ Anything higher may indicate MI, but it’s nonspecific for myocardial ischemia since CK is released from any skeletal muscle. Clinicians need to also look at the CK-MB and RI because they are specific to myocardial cells.

The isoenzyme CK-MB is released from myocardial cells. A normal level is 1.5 ng/mL with a relative index (RI) of 1.0. A CK-MB of 4.5 ng/mL or greater and a RI of 2.5 or greater indicate myocardial cell injury, indicating MI.³ CK-MB levels can also be elevated due to surgery, trauma, intramuscular injections, exercise, CPR, and defibrillation. Myoglobin (an oxygen-carrying protein in muscles released in response to skeletal muscle injury and myocardial necrosis) and CK-MB are early markers for myocardial necrosis.⁴ Normal myoglobin is under 110 ng/mL. Levels over 110 ng/mL are consistent with an MI.³ Levels of myoglobin and CK-MB rise about one and three hours after the onset of cell injury and return to normal within 24 and 36 hours, respectively.⁴ CK-MB has been the gold standard in the diagnosis of MI, but troponin T and troponin I are the preferred biomarkers because of their greater sensitivity and specificity.⁴ Troponin I tests are more readily available.⁴

Troponin I is a highly sensitive and specific biomarker for myocardial cell damage, with a normal level of 0 to 0.1 ng/mL. Levels over 0.2 ng/mL indicate myocardial cell injury.³ Troponin I levels begin to rise within three to six hours after the onset of cell injury, peak in 14 to 20 hours, and return to normal in five to seven days. Troponin is a late marker for myocardial necrosis and helps diagnose MI in patients who seek treatment several days after the onset of symptoms, when myoglobin and CK-MB levels have returned to normal.⁴ Nurses should be aware that biomarker values may vary based on gender, race, and variation in lab assays.

Elevated levels of cardiac troponin not due to acute coronary syndromes have been reported in critically ill patients with hypotension, trauma, sepsis, pulmonary embolism, stroke, renal failure, and COPD.⁵ Nurses should not rely on a single diagnostic study for MI. The diagnosis should be based on a typical rise and fall of biochemical markers of myocardial necrosis and the presence of at least one of the following: signs and symptoms of ischemia, ECG signs of ischemia, or necrosis.⁵ In the critical care setting, clinicians often use a combination of elevated levels of cardiac troponin and ECG changes indicating ischemia in the diagnosis of MI.⁵

ECG is key

A 12-lead ECG should be performed and shown to a physician within 10 minutes of ED arrival for all patients with chest discomfort (or anginal equivalent).⁶ The 12-lead ECG is diagnostic of acute myocardial injury in STEMI. In a normal ECG, the ST segment is isoelectric (straight) and rests on the baseline of the ECG. Elevation of the ST segment is significant when it’s 1 mm or more above the isoelectric line in two or more contiguous leads (leads that transmit the electrical signal from a specific area of the myocardium).⁷ During a STEMI, the ST segments become elevated and reflect an acute myocardial injury, usually involving the left ventricle (LV). ST-segment elevation begins within minutes of the onset of STEMI and can persist for days.⁷ ST-segment elevation decreases sooner in patients who receive early reperfusion strategies (fibrinolytics or percutaneous coronary interventions, such as a percutaneous transluminal coronary angioplasty [PTCA]).⁷

ST-segment elevation in specific leads identifies the location of the myocardial injury: leads I, AVL and/or V5, V6 — lateral wall; leads II, III, AVF — inferior wall; V1, V2 — septum; V1, V2, V3, V4 — anterior/anteroseptal wall. Reciprocal ST-segment depression occurs in the wall opposite the site of injury. ST-elevation in leads I, AVL and/or V5, V6 would have ST-segment depression in leads II, III, AVF; ST elevation in leads II, III, AVF would have ST-segment depression in leads I, AVL and/or V5, V6; and ST elevation in leads V1, V2, V3, V4 would have ST-segment depression in leads II, III, AVF. The standard 12-lead ECG doesn’t allow the posterior wall to be assessed directly. A posterior MI would have tall R waves and ST depression in V1, V2 (a mirror image of an anterior MI). In addition, posterior leads V7, V8, and V9 (placed on the back) can be beneficial in diagnosing a posterior MI.

The right coronary artery (RCA) supplies the inferior wall of the LV and the right ventricle (RV). A thrombus in the RCA can involve both the RV and LV, and clinical signs and symptoms and treatment differ with RV involvement. Thus, patients with an inferior STEMI should have right precordial (chest) leads (V3R, V4R, and V5R) recorded to determine whether they have had a right ventricular infarction (RVI).⁸

Locating the leads

Leads are placed across the right side of the chest in a mirror image of the left side. Early diagnosis is crucial to avoid therapy that may be detrimental to patients with a RVI. ST-segment elevation in lead V4R is highly suggestive of RVI. A 1-mm ST-elevation in lead V4R is 70% sensitive and 100% specific for a RVI.⁸ Again, nurses should not rely on one diagnostic study, but consider the signs and symptoms suggestive of RVI: jugular venous distension, hypotension, and clear lung fields.⁸ Pericardial tamponade — an accumulation of fluid in the pericardial space — may share some of these symptoms and must be excluded.⁸ Constrictive pericarditis — an inflammation of the pericardium, causing pericardial thickening and preventing the heart chambers from filling — and a pulmonary embolism may mimic some of these symptoms.⁸ ST elevation in the posterior and right precordial leads is less pronounced (0.5 to 1.0 mm) and may return to baseline in 10 to 12 hours.⁸

Guidelines for the management of patients with STEMI include the following recommendations:

Prehospital: Teach patients discharged on sublingual nitroglycerin tablets to take one tablet for chest pain or discomfort. Advise patients to call 911 if the pain is unrelieved in five minutes.⁶ Paramedics should assess the patient and administer sublingual nitroglycerin spray as indicated. The spray preparation delivers a 0.4 mg/metered dose. Aspirin 162 to 325 mg (chewable tablets) should be administered, as well, unless contraindicated.⁶ A 12-lead ECG should be performed and transmitted to the nearest ED. If the patient is a candidate, a fibrinolytic (which degrades fibrin and lyses thrombi) may be administered en route to the hospital. (Only EMS personnel with special training should administer fibrinolytics, and a physician with experience in managing STEMI should be available by telephone.)⁶

ED/CCU: Patients may present to the ED with STEMI or experience signs and symptoms while hospitalized and be transferred to the CCU for emergency treatment. Management of STEMI includes relief of ischemic chest pain, reduction in myocardial oxygen demand, restoration of myocardial perfusion, and preservation of viable myocardium. Emergency and critical care nurses need to be knowledgeable about the drugs used and methods to evaluate the patient’s response to treatment. The following evidence-based recommendations should be part of the emergency management of patients with STEMI.

Aspirin: Aspirin inhibits platelet aggregation and interferes with the formation of thrombi. If a patient did not take aspirin at home — and didn’t receive it from EMS — he or she should receive an initial dose of 162 mg to 325 mg orally in the ED.⁶ All patients without an aspirin allergy should receive a maintenance dose of 75 mg to 162 mg indefinitely after STEMI.⁶ Adverse effects, including GI irritation,⁹ can be reduced by using enteric-coated aspirin.

Nitroglycerin: A venous and arterial vasodilator, nitroglycerin dilates the coronary arteries, increases blood flow to the myocardium, and relieves chest pain and discomfort. Patients with ischemic pain should receive sublingual nitroglycerin 0.4 mg every five minutes for a total of three doses.⁶ IV nitroglycerin can be administered for ischemic pain or discomfort, control of hypertension, and management of pulmonary congestion or heart failure.⁶ It’s beneficial in HF since venous vasodilatation reduces the amount of blood returning to the LV, and arterial vasodilatation reduces the resistance to LV contraction, reducing the workload on the failing LV. IV nitroglycerin is available as a premixed solution of 50 mg/250 mL of D5W (200 mcg/mL) and is initiated as a continuous infusion at 5 mcg/min to 10 mcg/min and titrated by 5 mcg/min to 10 mcg/min increments every three to five minutes until relief of pain or discomfort and while maintaining a systolic BP greater than 90 mmHg.⁹ The most common adverse effects are hypotension and headache.⁹ The nurse must monitor the BP after each increase in dosage. If the patient becomes hypotensive, the nurse should discontinue the infusion and notify the physician. The patient may be placed supine and fluid administered to support the BP. Once the BP is over 90 mmHg, the nurse may restart the infusion. Usually after the patient has been pain-free for 24 hours, the infusion is gradually weaned off, and the patient may be started on another nitrate preparation (topical, oral).

Beta-blockers: Oral beta-blockers, such as metoprolol, should be administered promptly to patients without a contraindication (second- or third-degree heart block, cardiogenic shock, or severe bradycardia).⁶ Beta-blockers blunt the effect of catecholamines, decreasing the heart rate (HR) and contractility and reducing the workload on the ventricle.¹⁰ IV beta-blockers may be administered if a tachydysrhythmia or hypertension is present. IV metoprolol can be administered as a 5 mg bolus times three doses (a total of 15 mg).⁹ In patients who tolerate the full dose, metoprolol 50 mg orally every six hours times 48 hours can be administered 15 minutes after the last IV dose.⁹ Adverse effects are hypotension, bradycardia, and fatigue.⁹ Thus, nurses should monitor BP and HR. Physicians may write orders to hold beta-blockers (i.e., when systolic BP is under 90 or 100 mmHg or HR is under 50/min).¹⁰ RNs should contact the physician for any concerns about BP, HR, or beta-blocker administration.

Focus on the LV

Angiotensin converting enzyme (ACE) inhibitors: All STEMI patients should have an echocardiogram to assess LV function.⁶ An oral ACE inhibitor, such as enalapril (Vasotec), should be initiated within 24 hours of STEMI in patients with an anterior infarction, pulmonary congestion, or an LV ejection fraction less than 0.40.6 (The EF is the percent of blood ejected from the ventricle with each heartbeat.) ACE inhibitors block the conversion of angiotensin I to angiotensin II, producing vasodilatation.¹⁰ For HF, enalapril should be started as a 2.5 mg dose with a recommended dosing range between 5 mg/day and 20 mg/day in two divided doses.⁹ It should be titrated up as tolerated over a few days or weeks. ACE inhibitors increase levels of bradykinin, a vasodilator with some effects similar to those of histamine. The increased levels may produce a cough, which some patients may not tolerate.¹⁰

Patients intolerant of ACE inhibitors should receive an angiotensin receptor blocker (ARB), such as valsartan (Diovan) and candesartan (Atacand).^6,10 ACE inhibitors and ARBs can cause hypotension and hyperkalemia.¹⁰ Nurses should monitor BP and potassium levels. Physicians may write orders to hold ACE inhibitors or ARBs, such as in the case of systolic BP less than 90 or 100 mmHg.¹⁰ Nurses should contact the physician if they have concerns about the patient’s BP or the administration of ACE inhibitors and ARBs.

Fibrinolytics: All patients with STEMI should be evaluated for reperfusion therapy to restore blood flow to the myocardium.⁶ Fibrinolytic drugs are the pharmacological method for reperfusion, and several are available, including reteplase, tenecteplase (TNKase), and alteplase (Activase). Among the contraindications are a history of intracranial hemorrhage (ICH), closed head or facial trauma in the previous three months, uncontrolled hypertension, or ischemic stroke in the previous three months.⁶ Fibrinolytic therapy should be administered to STEMI patients with an onset of symptoms within the prior 12 hours and ST elevation over 0.1 millivolt (mV) in at least two contiguous precordial leads or in at in least two adjacent limb leads.⁶ On the ECG paper, 1 millimeter vertically represents 0.1 mV. Door-to-drug time should be 30 minutes or less.⁶

Reteplase activates plasmin, which degrades the fibrin thrombus. Reteplase is administered as a 10-unit IV bolus over two minutes followed by a second 10-unit IV bolus 30 minutes after the first dose.⁹

The major adverse effect is bleeding.⁹ Nurses must monitor the patient’s vital signs, LOC, chest pain or discomfort, and dysrhythmias. Findings suggesting reperfusion include resolution of symptoms, maintenance or restoration of hemodynamic or electrical stability, and a decrease of at least 50% of the initial ST elevation on a follow-up 12-lead ECG 60 to 90 minutes after the start of therapy. A change in neurological status during or after fibrinolytic therapy may indicate an ICH.⁶ Fibrinolytic, antiplatelet, and anticoagulant therapy should be stopped until a CT scan shows no evidence of ICH.⁶

UFH — promptly

Heparin: Along with fibrinolytics, the patient receives unfractionated (naturally occurring) heparin (UFH) to prevent thrombi.⁶ Heparin interferes with the clotting cascade and prevents the conversion of prothrombin to thrombin. UFH is administered as a weight-based IV bolus of 60 units/kg (maximum 4,000 units) followed by an initial infusion of 12 units/kg per hour (maximum 1,000 units/hr) and adjusted to maintain the aPTT at about 50 to 70 seconds.⁶ UFH should be started promptly, even before a decision is made on administrating fibrinolytics.⁶ The most common complication is bleeding.⁹ The nurse should monitor for signs and symptoms of bleeding as well as monitoring the aPTT, H&H, and platelet count.

About 1% to 5% of patients on heparin develop heparin-induced thrombocytopenia.¹¹ In HIT, thrombocytopenia is a result of platelets being activated by an immune complex, causing them to release platelet factor 4 and prothrombotic microparticles. In place of bleeding problems, HIT is associated with thrombosis.¹¹ Clinical studies have described HIT as a fall in platelet count between 30% and 50% of baseline or to less than 150,000/uL.¹¹ HIT usually occurs five to 14 days after heparin therapy is started. With any unexplained drop in platelet count, the nurse should consider HIT. All heparin is stopped immediately.¹¹ HIT can occur in patients receiving heparin SC or IV, heparin flushes, or heparin-coated catheters.¹¹ Another measure of anticoagulation must be started to prevent thrombosis. Treatment modalities include direct thrombin inhibitors, such as lepirudin (Refludan) and argatroban.¹¹

Percutaneous coronary intervention: If available, PCI should be performed in patients with STEMI (including true posterior MI) or MI with new or presumably new left bundle branch block.⁶ PCI should be performed quickly, with a goal of a door-to-balloon time within 90 minutes.⁶

PCI includes PTCA and stenting. PTCA involves passing a balloon-tipped catheter through the femoral artery up the aorta to the coronary artery. The catheter is advanced into the coronary artery to the area of stenosis (narrowing). The balloon is inflated, which presses the plaque up against the arterial walls and reestablishes perfusion to the myocardium. Another balloon-tipped catheter with a stent can be advanced into the coronary artery. The balloon is inflated, and the stent keeps the vessel open. Complications may include abrupt closure of the coronary artery, bleeding, and hematoma.

The nurse must frequently monitor vital signs, the access site, and distal pulses. The ST segment should be monitored continuously to detect abrupt closure of the coronary artery,⁷ which usually occurs in the first six hours after PTCA.⁷ The RN should ascertain which lead identifies the patient’s “fingerprint,” the lead with the maximum ST-segment elevation during balloon inflation.⁷ The RN should pay special attention to that lead and if the ST segment is elevated, notify the cardiologist immediately. Emergency PCI may be required.

The antiplatelet drug clopidogrel (Plavix) should be started and continued for at least a month if a bare metal stent is implanted, for several months after implantation of a drug-eluting stent (a stent coated with a drug that interferes with restenosis), and up to 12 months for patients with a DES who are not at high risk for bleeding.⁶ A recent study found that patients with a DES who were no longer on clopidogrel at six or 12 months had a significantly higher risk for death or MI during 24 months of follow-up than patients still on clopidogrel at these time points.¹² In December, an FDA panel¹³ recommended that DES labeling reference guidelines on the duration of antiplatelet therapy from the American College of Cardiology, American Heart Association, and Society for Cardiovascular Angiography and Interventions. (See www.acc.org/quallityandscience/clinical/guidelines/percutaneous/update/index_summaryupdate.pdf.)

What happened to Mr. Harris?

Mr. Harris is admitted to the CCU with an inferior STEMI. He has a diagnostic cardiac catheterization with a mid-left anterior descending artery stenosis of 50% and a mid-RCA stenosis of 80%. LV EF is 0.48. He receives IV heparin and clopidogrel postcardiac catheterization and is transferred to a tertiary care facility for a PCI.