eMedicine Specialties > Emergency Medicine > Cardiovascular
Myocardial Infarction: Treatment & Medication
Updated: Oct 5, 2009
- Overview
- Differential Diagnoses & Workup
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Treatment
Prehospital Care
- All patients being transported for chest pain should be managed as if the pain were ischemic in origin unless clear evidence to the contrary is established.
- If available, an ALS unit should transport patients with hemodynamic instability or respiratory difficulty.
- Prehospital notification by Emergency Medical Services (EMS) personnel should alert ED staff to the possibility of a patient with MI. EMS personnel should receive online medical advice for a patient with high-risk presentation.
- The American Heart Association (AHA) protocol can be adopted for use by prehospital emergency personnel. This protocol recommends empirical treatment of patients with suspected STEMI with morphine, oxygen, nitroglycerin, and aspirin.
- Specific prehospital care includes the following:
- Intravenous access, supplemental oxygen, pulse oximetry
- Immediate administration of aspirin en route
- Nitroglycerin for active chest pain, given sublingually or by spray
- Telemetry and prehospital ECG, if available
- Additionally, recently the AHA has published a statement on integrating prehospital ECGs into care for ACS patients (see AHA Publishes Statement on Integrating Prehospital ECGs Into Care for ACS Patients). Prehospital integration of ECG interpretation has been shown to decrease "door to balloon time," to allow paramedics to bypass non-PCI hospitals in favor of better equipped facilities, and to expedite care by allowing an emergency physician to activate the catheterization laboratory before patient arrival.
- Prehospital thrombolysis allows eligible patients to receive thrombolysis 30-60 minutes sooner than if treatment were given in the ED; however, prehospital thrombolysis is still under investigation.
Emergency Department Care
For purposes of determining appropriate treatment, viewing MI as part of a spectrum of coronary syndromes is helpful; this spectrum includes (1) STEMI, (2) NSTEMI, and (3) unstable angina. Patients with persistent ST elevation should be considered for reperfusion therapy (thrombolysis or primary PCI.) Those without ST elevation will be diagnosed with either NSTEMI if cardiac marker levels are elevated or with unstable angina if serum cardiac marker levels provide no evidence of myocardial injury. Patients presenting with no ST-segment elevation are not candidates for immediate thrombolytics but should receive anti-ischemic therapy and may be candidates for PCI urgently or during admission. Confirmation of the diagnosis of NSTEMI requires waiting for the results of cardiac markers. In the case of unstable angina, diagnosis may await further diagnostic studies such as coronary angiography or imaging studies to confirm the diagnosis and to distinguish it from noncoronary causes of chest pain.
The initial focus should be on identifying patients with STEMI. An ECG should be performed and shown to an experienced emergency medicine physician within 10 minutes of ED arrival. If STEMI is present, the decision as to whether the patient will be treated with thrombolysis or primary PCI should be made within the next 10 minutes. The goal for patients with STEMI should be to achieve a door-to-drug time of within 30 minutes and a door-to-balloon time of within 90 minutes. If STEMI is not present, then the workup should proceed looking for unstable angina or NSTEMI and for alternative diagnoses.
Rathore et al found that any delay in primary percutaneous coronary intervention after a patient with ST-elevation myocardial infarction (STEMI) arrives at hospital is associated with higher mortality.2 In a prospective cohort study of 43,801 patients enrolled in the American College of Cardiology National Cardiovascular Data Registry, 2005-2006, longer door-to-balloon times were associated with a higher adjusted risk of in-hospital mortality, in a continuous nonlinear fashion (30 min = 3%, 60 min = 3.5%, 90 min = 4.3%, 120 min = 5.6%, 150 min = 7%, 180 min = 8.4%, P<0.001). A reduction in door-to-balloon time from 90 minutes to 60 minutes was associated with 0.8% lower mortality, and a reduction from 60 minutes to 30 minutes was associated with a 0.5% lower mortality.
Treatment is aimed at (1) restoration of the balance between the oxygen supply and demand to prevent further ischemia, (2) pain relief, and (3) prevention and treatment of complications.
- Delays in administration of thrombolysis often occur because of delay in obtaining an ECG, interpretation, lack of immediate availability of thrombolytic agents, and outdated protocols requiring cardiology consultation before thrombolytic treatment.
- An ECG should be performed as soon as possible after the patient presents to the ED. The ECG should be hand-delivered to an experienced physician for timely review.
- All patients should be placed on telemetry.
- Two large-bore IVs should be inserted if the EMS has not already completed this.
- Pulse oximetry should be performed, and appropriate supplemental oxygen should be given (maintain oxygen saturation >90%).
- A chest radiograph should be obtained soon after arrival to screen for alternative causes of chest pain and identify possible contraindications to thrombolysis (eg, aortic dissection).
- Pharmacologic intervention is likely to include the following:
- Aspirin should be administered immediately if not already taken by the patient at home or administered by EMS before arrival. Aspirin has been shown to decrease mortality and reinfarction rates after MI. Use clopidogrel (Plavix) in case of aspirin allergy.
- Low-dose aspirin has shown substantial benefit for primary prevention of myocardial infarction and stroke, but its use must be weighed against the risk for hemorrhagic stroke and gastrointestinal bleeding. The Antithrombotic Trialists' (ATT) Collaboration conducted meta-analyses of serious vascular events, including myocardial infarction, stroke, and vascular death, and major bleeds in 6 primary prevention trials and in 16 secondary prevention trials that compared long-term aspirin versus control. The primary prevention trials included 95,000 individuals at low average risk, and the secondary prevention trials included 17,000 individuals at high average risk.3
- Aspirin was associated with significant reduction (12% proportional reduction) for serious vascular events (0.51% aspirin vs 0.57% control annually, p = 0.0001), but the net effect on stroke was not significant. This reduction was largely due to a 20% reduction in nonfatal myocardial infarction (0.18% vs 0.23% annually, p <0.0001).3 Aspirin increased risk for major gastrointestinal and extracranial bleeding. The use of aspirin for primary prevention must be advised in context with the patient's personal risks and history.
- Beta-blocker therapy for heart rate control and resultant decrease of myocardial oxygen demand if not contraindicated. Metoprolol (Lopressor) is the standard and is a selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. Beta-blockers reduce the rates of reinfarction and recurrent ischemia and may also reduce mortality.
- Morphine sulphate may be administered for relief of pain and anxiety.
- Nitrates are useful for preload reduction and symptomatic relief but have no apparent impact on mortality rate in MI. Systolic BP <90, HR <60 or >100, and RV infarction are a contraindications to nitrate use. Intravenous nitroglycerin is indicated for relief of ongoing ischemic discomfort, control of hypertension, or management of pulmonary congestion. Nitrates should not be administered to patients who have taken any phosphodiesterase inhibitor for erectile dysfunction within the last 24 hours (extend timeframe to 48 h for tadalafil).
- Thrombolytic therapy has been shown to improve survival rates in MI.
- Door-to-drug time should be no more than 30 minutes. Thrombolytic therapy administered within the first 2 hours can occasionally abort MI and dramatically reduce the mortality rate.
- The optimal approach is to administer thrombolytics as soon as possible after onset of symptoms (up to 12 h from symptom onset according to some authors) in patients with ST-segment elevation greater than 1 mm in 2 or more anatomically contiguous ECG leads, new or presumed new left bundle-branch block, or anterior ST depression where posterior infarction is suspected. With ST-segment elevation, the diagnosis is relatively secured; therefore, initiation of reperfusion therapy should not be delayed for the results of cardiac markers.
- Thrombolysis is generally preferred to PCI in cases where the time from symptom onset is less than 3 hours and if there would be a delay to PCI, greater than 1-2 additional hours to door-to-balloon time. A detailed list of contraindications and cautions for the use of fibrinolytic therapy is shown in Table 12 of the ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction—Executive Summary, at the American College of Cardiology.
- Administer a platelet glycoprotein (GP) IIb/IIIa-receptor antagonist (eptifibatide, tirofiban, or abciximab), in addition to aspirin and unfractionated heparin, to patients with continuing ischemia or with other high-risk features and to patients in whom PCI is planned. Studies suggest that the addition of intravenous platelet glycoprotein (GP) IIb/IIIa-receptor antagonists to aspirin and heparin improves both early and late outcomes, including mortality, Q-wave MI, need for revascularization procedures, and length of hospital stay.
- Despite the traditional use of unfractionated heparin in ST elevation MI for decades, controversy regarding its role continues.
- In patients treated with fibrinolytic therapy, recommendations for heparin therapy depend on the fibrinolytic agent. Heparin has an established role as an adjunctive agent in patients receiving alteplase, reteplase, or tenecteplase but should not be used with nonselective fibrinolytic agents such as streptokinase and anistreplase.
- Heparin is also indicated in patients undergoing primary PCI. Data are scant with regard to heparin efficacy in patients not receiving thrombolytic therapy in the setting of MI; however, considerable rationale exists for ancillary heparin therapy to inhibit the coagulation cascade.
- Low-molecular-weight heparins (LMWH) are commonly used because of convenient dosing and reliable therapeutic levels, but there have been no definitive trials of LMWH in patients with STEMI to provide a firm basis for recommendations. Low-molecular-weight heparin should not be used as an alternative to unfractionated heparin as ancillary therapy to fibrinolytics in patients aged older than 75 years or in patients with significant renal dysfunction (serum creatinine level >2.5 mg/dL in men or >2 mg/dL in women).
- An ACE inhibitor (Captopril) should be given orally within the first 24 hours of STEMI to patients with anterior infarction, pulmonary congestion, or left ventricular ejection fraction (LVEF) less than 40% in the absence of hypotension.
- An angiotensin receptor blocker (valsartan or candesartan) should be administered to patients with STEMI who are intolerant of ACE inhibitors and who have either clinical or radiological signs of heart failure or LVEF less than 40%.
- Note that routine use of lidocaine as prophylaxis for ventricular arrhythmias in patients who have experienced an MI has been shown to increase mortality rates and its use is class indeterminate.
- Use of calcium channel blockers in the acute setting has come into question, with some randomized controlled trials and retrospective studies showing increased adverse effects. Diltiazem and verapamil should be avoided in patients with pulmonary edema or severe left ventricular (LV) dysfunction.
Consultations
Great differences in practice patterns and treatment outcomes exist in different hospital and geographic areas. This is due, at least in part, to the wide variation in the availability of PCI and emergency thoracotomy. One study showed that transferring patients to an invasive-treatment center for PCI is superior to on-site fibrinolysis provided that the transfer can be accomplished within 2 hours. Methods used for reperfusion/revascularization must be based on the resources available in a particular community, and protocols should be worked out in advance as a collaborative effort between emergency physicians, internists, cardiologists, and cardiothoracic surgeons.
- The decision to administer a thrombolytic agent may be made by the emergency physician, with or without the input of a cardiologist, depending on institutional protocol. In a center with the full range of treatment options, an expeditious phone consultation with a cardiologist would seem to be a wise choice to ascertain that the best possible option is chosen for the patient.
- A cardiologist should be consulted for the following:
- Patients who may benefit from PCI, including "rescue PCI," with transfer if required, for patients in whom thrombolysis for STEMI fails to achieve reperfusion
- Patients in cardiogenic shock
- Patients with hemodynamically significant new or worsening murmur
- Patients who are not candidates for thrombolytic intervention because of a contraindication
- Intractable angina despite medications
- Severe pulmonary congestion
- Late presentation (>3 h but no more than 12 h)
- Where the diagnosis is in doubt
- Note that PCI door-to-balloon time should be less than 90 minutes.
- Thoracotomy for coronary artery bypass graft may be indicated if PCI fails. Thoracotomy may also be necessary for valvular repair or in cases of mechanical complications such as LV rupture.
Medication
The main goals of ED medical therapy are rapid intravenous thrombolysis and/or rapid referral for PCI, optimizing oxygenation, decreasing cardiac workload, and controlling pain.
Antithrombotic agents
These agents prevent the formation of thrombus associated with myocardial infarction and inhibit platelet function by blocking cyclooxygenase and subsequent aggregation. Antiplatelet therapy has been shown to reduce mortality rates by reducing the risk of fatal myocardial infarctions, fatal strokes, and vascular death.
Aspirin (Anacin, Bayer Buffered Aspirin, Ecotrin)
Administer as soon as possible. Inhibits cyclooxygenase, which produces thromboxane A2, a potent platelet activator. Early administration has been shown to reduce 35-d mortality rate by 23% compared with placebo. An added mortality benefit exists when used in combination with thrombolytics.
Adult
160-324 mg PO (chewed)
Pediatric
Not established
Effects may decrease with antacids and urinary alkalinizing agents; corticosteroids decrease salicylate serum levels; additive hypoprothrombinemic effects and increased bleeding time may occur with coadministration of anticoagulants; may antagonize uricosuric effects of probenecid and increase toxicity of phenytoin and valproic acid; doses >2 g/d may potentiate glucose-lowering effect of sulfonylurea drugs
Documented hypersensitivity; vitamin K deficiency; liver damage; hypoprothrombinemia; bleeding disorders; asthma; because of association of aspirin with Reye syndrome, do not use in children (<16 y) with influenza
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
May cause transient decrease in renal function and aggravate chronic kidney disease; caution in patients with severe anemia, in those with history of blood coagulation defects, or in those taking anticoagulants
Heparin
Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse preformed clot, but it is able to inhibit further thrombogenesis after thrombolysis. Heparin should be administered to patients undergoing PCI. Prevents reaccumulation of clot after spontaneous fibrinolysis. Benefit as adjunctive therapy for streptokinase not clear.
Adult
60 U/kg (max 4000 U) IV bolus; followed by a 12 U/kg/h (max 1000 U/h) maintenance infusion
Pediatric
Not established
Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase heparin toxicity
Documented hypersensitivity; subacute bacterial endocarditis, active bleeding; history of heparin-induced thrombocytopenia
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in severe hypotension and shock
Enoxaparin (Lovenox)
Produced by partial chemical or enzymatic depolymerization of unfractionated heparin (UFH). LMWH differs from UFH by having a higher ratio of antifactor Xa to antifactor IIa compared with UFH. Binds to antithrombin III, enhancing its therapeutic effect. The heparin-antithrombin III complex binds to and inactivates activated factor X (Xa) and factor II (thrombin). Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis.
Advantages include intermittent dosing and decreased requirement for monitoring. Heparin anti–factor Xa levels may be obtained if needed to establish adequate dosing. No utility in checking aPTT (drug has wide therapeutic window and aPTT does not correlate with anticoagulant effect).
Indicated for treatment of acute ST-segment elevation myocardial infarction (STEMI) managed medically or with subsequent percutaneous coronary intervention (PCI). Also indicated as prophylaxis of ischemic complications caused by unstable angina and non-Q-wave MI.
Adult
Treatment regimens include aspirin (75-325 mg/d) if not contraindicated
NSTEMI
1 mg/kg SC bid
CrCl <30 mL/min: 1 mg/kg SC qd
STEMI
<75 years: 30 mg IV single bolus plus 1 mg/kg SC, then 1 mg/kg SC q12h; not to exceed 100 mg/dose for first 2 SC doses
<75 years and CrCl <30 mL/min: 30 mg IV single bolus plus 1 mg/kg SC, then 1 mg/kg SC qd; not to exceed 100 mg/dose for first 2 SC doses
>75 years: 0.75 mg/kg SC q12h (no initial IV bolus administered), not to exceed 75 mg/dose for first 2 doses
>75 years and CrCl <30 mL/min: 1 mg/kg SC qd (no initial IV bolus administered)
With PCI: If last enoxaparin dose administered >8 h before balloon inflation, administer an additional IV bolus of 0.3 mg/kg
With thrombolytic agent: Give dose specified for age and renal function between 15 min before and 30 min after the start of fibrinolytic therapy
Pediatric
Not established
Platelet inhibitors or oral anticoagulants such as dipyridamole, salicylates, aspirin, NSAIDs, sulfinpyrazone, and ticlopidine may increase risk of bleeding
Documented hypersensitivity; major bleeding; thrombocytopenia
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Decrease dose if CrCl <30 mL/min; if thromboembolic event occurs despite LMWH prophylaxis, discontinue drug and initiate alternate therapy; elevation of hepatic transaminase levels may occur but is reversible; heparin-associated thrombocytopenia may occur with fractionated low-molecular-weight heparins; 1 mg of protamine sulfate reverses effect of approximately 1 mg of enoxaparin if significant bleeding complications develop; cases of epidural/spinal hematomas have been reported in adults receiving spinal or epidural anesthesia (holding 2 doses prior to LP or surgery is recommended); obtain hemostasis at puncture site before sheath removal after PCI
Vasodilators
These agents oppose coronary artery spasm, which augments coronary blood flow and reduces cardiac work by decreasing preload and afterload. It is effective in the management of symptoms in AMI and has no apparent impact on mortality rate. Nitroglycerin can be administered sublingually by tablet or spray, topically, or intravenously. In the setting of AMI, topical administration is a less desirable route because of unpredictable absorption and onset of clinical effects.
Nitroglycerin (Minitran, Nitrogard, Nitrol, Nitrolingual, Nitrostat, Nitro-Dur)
Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. Result is decrease in blood pressure.
Adult
400 mcg SL tab or spray q5min, repeated up to 3 times; if symptoms persist, infuse IV at a rate of 5-10 mcg/min; titrate dose to 10% reduction in MAP or limiting side effects of hypotension (>30% reduction in MAP or systolic BP <90), or severe headache
Pediatric
Not established
Aspirin may increase nitrate serum concentrations; marked symptomatic orthostatic hypotension may occur with coadministration of calcium channel blockers (dose adjustment of either agent may be necessary)
Documented hypersensitivity; severe anemia; shock; postural hypotension; head trauma; closed-angle glaucoma; cerebral hemorrhage; known right ventricular infarct
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in coronary artery disease and low systolic blood pressure
Beta-adrenergic blockers
These agents inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation and reduce blood pressure, which decreases myocardial oxygen demand. Short-term and long-term mortality rates are reduced in patients with AMI. Greatest benefit is achieved when given within 8 hours of symptom onset. Aim for a target heart rate of 60-90 beats per minute.
Metoprolol (Lopressor)
Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. During IV administration, carefully monitor blood pressure, heart rate, and ECG. Goal of treatment is to reduce heart rate to 60-90 bpm.
Adult
5 mg IV q5min 3 times; titrate to heart rate and SBP
Pediatric
Not established
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels of metoprolol, possibly resulting in decreased pharmacologic effects; toxicity of metoprolol may increase with coadministration of sparfloxacin, phenothiazines, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; metoprolol may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine
Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; asthma; cardiogenic shock; AV conduction abnormalities
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia and may decrease clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; monitor patient closely and withdraw the drug slowly; during IV administration, carefully monitor blood pressure, heart rate, and ECG
Esmolol (Brevibloc)
Excellent drug for use in patients at risk for complications from beta-blockade, particularly those with reactive airway disease, mild-to-moderate LV dysfunction, and/or peripheral vascular disease. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed.
Adult
Loading dose: 500 mcg/kg/min IV over 1 min
Optional loading dose: 0.5 mg/kg slow IV infusion
Maintenance dose: 0.1 mg/kg/min IV initially; titrate in increments of 0.05 mg/kg/min q10-15min to a total dose of 0.2 mg/kg/min
Average maintenance dose: 50 mcg/kg/min IV over 4 min
Pediatric
Not established
Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels of esmolol, possibly resulting in decreased pharmacologic effect; cardiotoxicity of esmolol may increase when administered concurrently with sparfloxacin, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity of esmolol increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents
Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities; cocaine-related ischemia
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Beta-adrenergic blockers may mask signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; symptoms of hyperthyroidism, including thyroid storm may worsen when medication is abruptly withdrawn (withdraw drug slowly and monitor patient closely); caution in patients on other negative inotropes, such as verapamil
Thrombolytic agents
These agents prevent recurrent thrombus formation and rapid restoration of hemodynamic disturbances. In addition, they remove pathologic intraluminal thrombus or embolus not yet dissolved by the endogenous fibrinolytic system. When given within 12 h of symptom onset, they restore patency of occluded arteries, salvage myocardium, and reduce morbidity and mortality rates of AMI. Thrombolytic treatment should be started within 30 min of arrival (door-drug time). Maximum benefit occurs when administered within 1-3 h of symptom onset.
Alteplase (Activase)
Fibrin-specific agent with a brief half-life of 5 min. Adjunctive therapy with IV heparin is necessary to maintain patency of arteries recanalized by tPA, especially during the first 24-48 h. Heparin may be administered during tPA infusion.
Adult
15 mg IV bolus; 0.75 mg/kg IV over 30 min; not to exceed 50 mg; followed by 0.5 mg/kg over 60 min, up to 35 mg; not to exceed 100 mg
Pediatric
Not established
Drugs that alter platelet function (aspirin, dipyridamole, abciximab) may increase risk of bleeding prior to, during, or after therapy; may give heparin with, and after, alteplase infusions to reduce risk of rethrombosis; either heparin or alteplase may cause bleeding complications
Documented hypersensitivity; stroke within last 2 mo; intracranial or intraspinal surgery or trauma; intracranial hemorrhage on pretreatment evaluation; active internal bleeding; intracranial neoplasm; arteriovenous malformation or aneurysm; bleeding diathesis; severe uncontrolled hypertension; suspicion of subarachnoid hemorrhage
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Monitor for bleeding, especially at arterial puncture sites, with coadministration of vitamin K antagonists; control and monitor blood pressure frequently during and following therapy (when managing acute ischemic stroke); caution in cardiovascular arrhythmias, hypotension, and perfusion arrhythmias
Do not use >0.9 mg/kg alteplase to manage acute ischemic stroke; doses >0.9 mg/kg may cause ICH
Tenecteplase (TNKase)
Modified version of alteplase (tPA) made by substituting 3 amino acids of alteplase. Can be given as single bolus over 5-second infusion instead of 90 min with alteplase. Appears to cause less nonintracranial bleeding but has similar risk of intracranial bleeding and stroke as alteplase. Base the dose using patient weight. Initiate treatment as soon as possible after onset of AMI symptoms. Because tenecteplase contains no antibacterial preservatives, reconstitute immediately before use.
Adult
Give IV bolus over 5 s using body weight; not to exceed 50 mg
<60 kg: 30 mg (6 mL)
60-70 kg: 35 mg (7 mL)
70-80 kg: 40 mg (8 mL)
80-90 kg: 45 mg (9 mL)
>90 kg: 50 mg (10 mL)
Pediatric
Not established
Heparin and vitamin K antagonists, acetylsalicylic acid, dipyridamole, and GP IIb/IIIa inhibitors may increase risk of bleeding if coadministered with tenecteplase therapy
Documented hypersensitivity; active internal bleeding; intracranial neoplasm; known bleeding diathesis; severe uncontrolled hypertension; arteriovenous malformation or aneurysm; history of stroke; intracranial or intraspinal surgery or trauma within 2 mo
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution if readministering to patients who have received prior plasminogen activator therapy (may develop immunity); coronary thrombolysis may result in arrhythmias associated with reperfusion but not different from those often observed in ordinary course of AMI (may be managed with standard antiarrhythmic measures); in elderly patients, weigh benefits of tenecteplase on mortality against risk of increased adverse events, including bleeding; cholesterol embolism is associated with all types of thrombolytic agents but true incidence is unknown
Anistreplase (Eminase)
Recently approved for use in AMI. Nonfibrin specific agent with a half-life of 90 min. Activates the conversion of plasminogen to plasmin, which is capable of degrading fibrin, fibrinogen, and other procoagulant proteins into soluble fragments. These effects result in thrombolysis. Has no survival benefit over streptokinase and higher rate of allergic and bleeding complications. Easier to administer than tPA, has a lower cost ($1500), and does not require heparinization.
Adult
30 U IV over 2-5 min
Pediatric
Not established
Increases bleeding potential of heparin, warfarin, and aspirin
Documented hypersensitivity; history of stroke; intracranial neoplasm; active internal bleeding; recent intracranial surgery; severe uncontrolled hypertension; arteriovenous malformation or aneurysm
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in cardiovascular arrhythmias, hypotension, and perfusion arrhythmias
Streptokinase (Kabikinase, Streptase)
Nonfibrin specific agent with a half-life of 23 min. Need for adjunctive therapy with heparin is controversial. Acts with plasminogen to convert plasminogen to plasmin. Plasmin degrades fibrin clots as well as fibrinogen and other plasma proteins. An increase in fibrinolytic activity that degrades fibrinogen levels for 24-36 h takes place with intravenous infusion of streptokinase.
Adult
1.5 million U in 50 mL D5W IV over 60 min
Pediatric
Not established
Antifibrinolytic agents may decrease effects of streptokinase; heparin, warfarin, and aspirin may increase risk of bleeding
Documented hypersensitivity; active internal bleeding; intracranial neoplasm; aneurysm; diathesis; severe uncontrolled arterial hypertension
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in severe hypertension, intramuscular administration of medications, and trauma or surgery in previous 10 d; measure hematocrit, platelet count, aPTT, TT, PT, or fibrinogen levels before therapy is implemented; either TT or aPTT should be less than twice the reference range control value following infusion of streptokinase and before (re)instituting heparin; PT, aPTT, TT or fibrinogen should be monitored 4 h after initiation of therapy
Reteplase (Retavase)
Recombinant plasminogen activator that forms plasmin after facilitating cleavage of endogenous plasminogen. In clinical trials, reteplase has been shown to be comparable to tPA in achieving TIMI 2 or 3 patency at 90 min.
Adult
10.8 U IV over 2 min; repeat in 30 min
Pediatric
Not recommended
Drugs that alter platelet function (aspirin, dipyridamole, abciximab) may increase risk of bleeding prior to, during, or after therapy; may give heparin with, and after, alteplase infusions to reduce risk of rethrombosis; either heparin or alteplase may cause bleeding complications
Documented hypersensitivity; stroke within last 2 mo; intracranial or intraspinal surgery or trauma; intracranial hemorrhage on pretreatment evaluation; active internal bleeding; intracranial neoplasm; arteriovenous malformation or aneurysm; bleeding diathesis; severe uncontrolled hypertension; suspicion of subarachnoid hemorrhage
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Monitor for bleeding, especially at arterial puncture sites, with coadministration of vitamin K antagonists; control and monitor blood pressure frequently during and following therapy (when managing acute ischemic stroke); caution in cardiovascular arrhythmias, hypotension, and perfusion arrhythmias
Do not use >0.9 mg/kg alteplase to manage acute ischemic stroke; doses >0.9 mg/kg may cause ICH
Platelet aggregation inhibitors
These agents inhibit platelet aggregation and reduce mortality.
Clopidogrel (Plavix)
Selectively inhibits adenosine diphosphate (ADP) binding to platelet receptor and subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation.
Adult
300 mg PO loading dose prior to PCI, then 75 mg PO qd
Pediatric
Not established
Coadministration with naproxen associated with increased occult GI blood loss; clopidogrel prolongs bleeding time; safety of coadministration with warfarin not established
Documented hypersensitivity; active pathological bleeding, such as peptic ulcer; intracranial hemorrhage
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in patients at increased risk of bleeding from trauma, surgery, or other pathological conditions; caution in patients with lesions with propensity to bleed (eg, ulcers)
Eptifibatide (Integrilin)
Antagonist of the platelet glycoprotein (GP) IIb/IIIa receptor, which reversibly prevents von Willebrand factor, fibrinogen, and other adhesion ligands from binding to the GP IIb/IIIa receptor. End effect is the inhibition of platelet aggregation. Effects persist over duration of maintenance infusion and are reversed when infusion ends.
Adult
180 mcg/kg IV load; followed by 2 mcg/kg/min IV for 72 h
PTCA: 135 mcg/kg IV bolus before procedure, followed by 0.5 mcg/kg/min IV for 20-24 h
Pediatric
Not established
Coadministration with heparin, warfarin, or aspirin may increase risk of bleeding; monitor closely when using other drugs that affect hemostasis
Documented hypersensitivity; severe hypertension (SBP >200 mm Hg), active internal bleeding, history of intracranial hemorrhage, intracranial neoplasm, arteriovenous malformation or aneurysm, acute pericarditis or bleeding diathesis; trauma or stroke within previous 30 d; platelet count <100,000/mm3; history of thrombocytopenia following prior exposure to this product; serum creatinine level >2 mg/dL (for the 180-mcg/kg bolus and 2-mcg/kg/min infusion) or >4 mg/dL (for the 135-mcg/kg bolus and 0.5-mcg/kg/min infusion)
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in platelet count <150,000/mm3 and hemorrhagic retinopathy; caution with concurrent use of drugs that affect hemostasis, such as thrombolytics, ticlopidine, NSAIDs, warfarin, dipyridamole, and clopidogrel; measure activated clotting time (ACT) and maintain aPTT between 50-70 s unless a PCI needs to be performed; maintain ACT between 300-350 s during a PCI; if platelets decrease to <100,000/mm3, perform additional platelet counts to exclude possibility of pseudothrombocytopenia; if thrombocytopenia is confirmed, discontinue GP IIb/IIIa inhibitors and heparin and appropriately monitor and treat the condition; monitor aPTT 6 h after start of heparin infusion and adjust to maintain aPTT higher than twice the baseline level
Tirofiban (Aggrastat)
Antagonist of the platelet glycoprotein (GP) IIb/IIIa receptor that reversibly prevents von Willebrand factor, fibrinogen, and other adhesion ligands from binding to the GP IIb/IIIa receptor, thereby inhibiting platelet aggregation. Effects persist over the duration of maintenance infusion and are reversed after stopping the infusion.
Adult
0.4 mcg/kg/min IV for 30 min; followed by 0.1 mcg/kg/min
Pediatric
Not established
Coadministration with heparin, warfarin, and aspirin may increase risk of bleeding
Documented hypersensitivity; history of intracranial hemorrhage; severe hypertension (SBP >200 mm Hg), active internal bleeding, intracranial neoplasm, arteriovenous malformation or aneurysm, acute pericarditis and bleeding diathesis; trauma or stroke within previous 30 d; platelet count <100,000/mm3, history of thrombocytopenia following prior exposure to this product; serum creatinine level >2 mg/dL (for the 180-mcg/kg bolus and 2-mcg/kg/min infusion) or >4 mg/dL for the 135-mcg/kg bolus and the 0.5-mcg/kg/min infusion
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in platelet count <150,000/mm3 and hemorrhagic retinopathy; caution with concurrent use of drugs that affect hemostasis, such as thrombolytics, ticlopidine, NSAIDs, warfarin, dipyridamole, and clopidogrel; measure activated clotting time (ACT) and maintain aPTT between 50-70 s unless a PCI needs to be performed; maintain ACT between 300-350 s during a PCI; if platelets decrease to <100,000/mm3, perform additional platelet counts to exclude possibility of pseudothrombocytopenia; if thrombocytopenia is confirmed, discontinue GP IIb/IIIa inhibitors and heparin, and appropriately monitor and treat condition; monitor aPTT 6 h after start of heparin infusion and adjust to maintain aPTT higher than twice baseline level
Abciximab (ReoPro)
Chimeric human-murine monoclonal antibody approved for use in elective/urgent/emergent PCI. Binds to receptor with high affinity and reduces platelet aggregation by 80% for as long as 48 h following infusion. Prevents acute cardiac ischemic complications in unstable angina unresponsive to conventional therapy.
Adult
0.25 mg/kg IV bolus, followed by 10 mcg/min IV for 12 h
Pediatric
Not established
Toxicity increases with coadministration of anticoagulants, antiplatelets, and thrombolytics
Documented hypersensitivity; bleeding diathesis; thrombocytopenia (<100,000 cells/mcL); recent trauma; intracranial tumor; severe uncontrolled hypertension; history of vasculitis; stroke within 2 y
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Bleeding complications may occur in patients <75 kg body weight, >65 years, with history of GI disease, or who recently received thrombolytic therapy; severe thrombocytopenia may occur within first 24 h of use
Analgesics
These agents reduce pain, which decreases sympathetic stress. They may provide some preload reduction. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who experience chest discomfort resulting from a myocardial infarction.
Morphine sulfate (Duramorph, Astramorph, MS Contin)
DOC for analgesia because of reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Various IV doses are used; commonly titrated until desired effect obtained.
Adult
1-3 mg IV; repeat and titrate to pain relief
Pediatric
Not established
Phenothiazines may antagonize analgesic effects of opiate agonists; tricyclic antidepressants, MAOIs, and other CNS depressants may potentiate adverse effects of morphine
Documented hypersensitivity; hypotension; potentially compromised airway where establishing rapid airway control would be difficult
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Caution in severe hypotension, respiratory depression, nausea, emesis, constipation, urinary retention, atrial flutter, and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate
Angiotensin-converting enzyme (ACE) inhibitors
These agents prevent conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, causing lowered aldosterone secretion.
Captopril (Capoten)
Has short half-life, which makes it important drug for initiation of ACE inhibitor therapy. Can be started at low dose and titrated upward as needed and as patient tolerates.
Adult
6.25 mg PO tid initially; may titrate to total 450 mg/d
Pediatric
Not established
Patients receiving diuretic therapy, other vasodilator agents, agents causing renin release, agents increasing potassium, or agents affecting sympathetic activity should be monitored carefully
Documented hypersensitivity
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Administer with caution in patients with renal insufficiency and in those with borderline low blood pressure; may worsen renal function, especially in patients with bilateral renal artery stenosis; administer cautiously in patients with aortic stenosis because afterload reduction may worsen coronary perfusion
More on Myocardial Infarction |
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Further Reading
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
