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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 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

Follow-up Further Inpatient Care
  1. All patients with known or suspected MI should be admitted to an ICU.
  2. Patients should continue to receive beta-blockers, nitrates, and heparin, as indicated.
  3. 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.
  4. 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
  1. 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:
    1. Patients with new or worsening hemodynamically significant mitral regurgitant murmurs
    2. Patients with known or suspected critical aortic stenosis and either ongoing ischemia or hemodynamic instability
    3. Patients who have received thrombolysis and fail to reperfuse
    4. Patients with significant LV dysfunction or cardiogenic shock
  2. 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
    1. 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.
    2. 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
  1. Patients should avoid risk factors when possible and act upon treatable risk factors.
  2. 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.
  3. 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
  1. 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.
  2. Tachyarrhythmia
    1. Sinus tachycardia is a poor prognostic sign that is indicative of ventricular dysfunction or failure.
    2. PVCs Simple (ie, <10/h), no need to treat
    3. PVCs Complex, NSVT/VT, lidocaine DOC
    4. Accelerated idioventricular rhythm (AIVR) is the most common reperfusion arrhythmia, but it usually is well tolerated and does not require treatment.
  3. Bradyarrhythmia
    1. 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.
    2. 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.
  4. Cardiogenic shock
    1. In the setting of an MI, cardiogenic shock is associated with an 80% in-hospital mortality rate.
    2. Patients should undergo thrombolysis or PCI, placement of an intra-aortic balloon pump, or CABG.
  5. Valvular insufficiency
    1. 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.
    2. Ischemia often responds to medical therapy and thrombolysis.
  6. 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.
  7. 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).
  8. 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.
  9. Other complications include pericarditis, ventricular aneurysm, and mural thrombus.
Prognosis
  1. 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.
  2. Better prognosis is associated with factors including the following:
    1. Successful early reperfusion
    2. Preserved LV function
    3. Short-term and long-term treatment with beta-blockers, aspirin, and ACE inhibitors
  3. Poorer prognosis is associated with the following:
    1. Delayed or unsuccessful reperfusion
    2. LV function is the strongest predictor of outcome in the post-MI patient.
  4. Ventricular dysrhythmias
    1. Recent experience with amiodarone suggests that it may improve long-term mortality in survivors of MI with ectopy and ventricular tachycardia.