Older adults can present with stroke, syncope, a change in mental status, and/or generalized weakness.
Table 22-1 ▪ ACC/AHA STEMI/NSTEMI PERFORMANCE MEASUREMENT SET: DIMENSIONS OF CARE INPATIENT MEASURES MATRIX | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Patients with symptoms suggestive of ACS should be instructed to call 911 and should be transported to the emergency department by ambulance rather than by private transport. (Class I, level of evidence: B)
The prehospital emergency medical providers should administer at this time aspirin 162 to 325 mg to the patient suspected of ACS unless contraindicated or if already taken by the patient. More rapid buccal absorption occurs with non-enteric-coated formulations and is recommended. (Class I, level of evidence: C)
Health care providers performing initial assessment of a patient suspected of ACS that has had NTG prescribed should instruct the patient not to take more than one dose of NTG sublingually in response to chest discomfort. If chest discomfort is unimproved or is worsening 5 minutes after dosing, it is recommended that the patient or family member call 911 immediately to access emergency medical services (EMS). In patients with chronic stable angina whose symptoms have improved after one NTG, it is appropriate to instruct the patient to repeat NTG every 5 minutes for a maximum of three doses. If symptoms do not resolve completely after three doses, 911 should be called for evaluation and treatment of symptoms. (Class I, level of evidence: C)
Patients with suspected ACS who have chest discomfort or other ischemic symptoms at rest for greater than 20 minutes, hemodynamic instability, or recent presyncope/syncope should be referred immediately to an emergency department for further evaluation. Patients experiencing less severe symptoms and who have none of the high-risk features described in the next section can be seen initially in an outpatient facility able to provide an acute evaluation. This recommendation would include patients who responded to an NTG dose. (Class I, level of evidence: C)
If the EMS providers have the capability, a 12-lead ECG should be performed in the field and transmitted to an emergency physician. The ECG assists in triage decisions, allowing transport to the most appropriate emergency department. ECGs with validated computer-generated interpretation are recommended in this setting. (Class IIa, level of evidence: B)
Table 22-2 ▪ APPLYING CLASSIFICATION OF RECOMMENDATIONS AND LEVEL OF EVIDENCE | ||||||||||||||||||||||||||||||||||||||||||||||||||||||
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A rapid clinical determination of risk for obstructive CAD that focuses on history, physical findings, ECG findings, and cardiac biomarker integration should be made in all patients experiencing chest discomfort suggestive of ACS. (Class I, level of evidence: C)
A 12-lead ECG should be performed and evaluated by an emergency department physician of any patient with chest discomfort or anginal equivalent within 10 minutes of arrival to the facility. (Class I, level of evidence: C)
If the initial ECG demonstrates no evidence of ischemia but the patient remains symptomatic, serial ECGs at 15- to 30-minute intervals should be performed to detect the development of ST-segment elevation or depression. (Class I, level of evidence: B)
Cardiac biomarkers should be measured in all patients who present with chest discomfort indicative of ACS. Cardiac-specific troponin is the preferred biomarker and should be measured in all patients presenting with chest discomfort suggestive of ACS. Patients with negative cardiac biomarkers within 6 hours from the onset of symptoms should have biomarkers remeasured in 8 to 12 hours after the onset of symptoms. (Class I, level of evidence: B)
For patients with suspected ACS, troponin-I is the laboratory marker of choice as it is found exclusively in the myocardium. Because of its specificity and sensitivity for detecting myocardial ischemia, troponin-I has become the preferred method of measurement. Other markers of pathophysiologic mechanisms implicated in ACS are under investigation, including markers of coagulation, platelet activation, inflammation, and heart failure. B-type natriuretic peptide, used to indicate the presence of heart failure, has been shown to provide incremental prognostic value in patient cohorts with STEMI and UA/NSTEMI.8, 9, 10
Various forms of imaging are often used to evaluate patients with symptoms that are suggestive of ACS. Bedside echocardiography is useful for diagnosis and risk stratification of patients with ACS in the emergency department.2 A portable chest radiograph is a Class I recommendation by the ACC guidelines in STEMI. It should not however delay reperfusion strategies.
The history, physical examination, 12-lead ECG, and initial cardiac biomarkers should be utilized to categorize the chest discomfort into one of four groups: noncardiac diagnosis, chronic stable angina, possible ACS, and definite ACS. (Class I, level of evidence: C)
Patients with possible ACS but whose initial 12-lead ECG and cardiac biomarker levels are normal should be observed with ongoing cardiac monitoring, serial ECGs, and repeat biomarker measurement. (Class I, level of evidence: B)
In patients with symptoms suggestive of ACS in whom ischemic heart disease is present or suspected, but the follow-up 12-lead ECG and cardiac biomarkers measurements are normal, a stress test (exercise or pharmacologic) to provoke ischemia should be performed in the emergency department within 72 hours of discharge. (Class I, level of evidence: C)
In the patient population recommended for outpatient stress testing, precautionary appropriate pharmacotherapy should be prescribed including aspirin, β-blockers, and/or sublingual NTG. If the patient is discharged from the emergency
department for outpatient stress testing he/she should receive instruction on activity, medication, and follow-up care with an appropriate health care provider. Patients with definite ACS and ongoing ischemia, positive cardiac biomarkers, new ST-segment deviations, new deep T-wave inversions, hemodynamic abnormalities, or a positive stress test in the emergency department should be admitted to the hospital for further treatment and possible invasive management. Admission to the critical care unit is advised for those patients with active, ongoing ischemia and hemodynamic or electrical instability. (Class I, level of evidence: C)
Any patient presenting with STEMI, new or presumed new left bundle-branch block (LBBB) should be evaluated for immediate reperfusion therapy (Class I, level of evidence: A)
At this point, bed rest should be maintained to decrease activity and myocardial oxygen consumption. Supplemental oxygen should be administered to patients with ACS particularly if any degree of respiratory insufficiency or hypoxia is present. Oral or intravenous (IV) β-blocker therapy should be administered to those patients with STEMI without a contraindication, irrespective of concomitant fibrinolytic therapy or performance of primary PCI (Class I, level of evidence: A)
In the absence of contraindications, morphine sulfate is the analgesic of choice for the management of pain associated with STEMI (Class I, level of evidence: C). Analysis of retrospective data has raised a question as to the potentially adverse effects of morphine in patients with UA/NSTEMI.1 As a result morphine use in that patient population has been reduced to a Class IIa recommendation.
IV NTG is recommended for ongoing chest discomfort unrelieved by sublingual NTG dosing, control of hypertension, or management of pulmonary congestion (Class I, level of evidence: C)
▪ Figure 22-4 ACSs algorithm for chest discomfort suggestive of ischemia. (Reproduced with permission of the American Heart Association, 2006.) |
Table 22-3 ▪ AMERICAN COLLEGE OF CARDIOLOGY/AMERICAN HEART ASSOCIATION GUIDELINES FOR SELECTING A REPERFUSION STRATEGY | |||||||||||||||||||||||||
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Table 22-4 ▪ COMPARISON OF FIBRINOLYTIC AGENTS | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
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thrombus. Streptokinase is a single chain polypeptide protein derived from β-hemolytic streptococcus. It binds to plasminogen to form the streptokinase-plasminogen activator complex and then converts plasminogen to plasmin, which initiates fibrinolysis. As described by Bates,40 early studies of IV streptokinase showed inconsistent improvement in LV function and mortality, likely because doses were inconsistent and administered too late. With improvements in both time-to-administration and consistent dosing protocol (1.5 million units of streptokinase infused over 60 minutes), patency rates at 60 to 90 minutes and at 2 to 3 hours of approximately 50% and 70%, respectively, were attained.
Table 22-5 ▪ CONTRAINDICATIONS AND CAUTIONS FOR FIBRINOLYSIS USE IN STEMI | ||||||
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Patients undergoing percutaneous or surgical revascularization should receive UFH. (Class I, level of evidence: C)
UFH should be given intravenously to patients undergoing reperfusion therapy with alteplase, retaplase, or tenecteplase. (Class I, level of evidence: C)Stay updated, free articles. Join our Telegram channel
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