Unstable angina non ST elevation myocardial infarction immediate management
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Overview of Immediate Management in UA / NSTEMI
Initial management of ACS begins with differentiating between the spectrum of ACS which includes unstable angina, NSTEMI and STEMI. Because the symptoms for all these can be similar, a medical evaluation is necessary as mentioned in earlier section. Information from the history, physical examination, 12-lead ECG, and initial cardiac biomarker tests can help in differentiating between the above three categories as well as categorize the patient into probable or definite ACS, chronic stable angina or non-cardiac cause of chest pain. Patients with STEMI must be evaluated for immediate reperfusion therapy. Patients with UA/NSTEMI, recurrent symptoms suggestive of ACS and/or ECG ST-segment deviations, or positive cardiac biomarkers who are stable hemodynamically should be admitted to an inpatient unit for bed rest with continuous rhythm monitoring and careful observation for recurrent ischemia and managed with either an invasive or conservative strategy(see Initial conservative versus initial invasive strategies). Once a patient with documented high-risk ACS is admitted, standard medical therapy is indicated which includes supplemental oxygen, ASA, beta blocker, anticoagulant therapy, a GP IIb/IIIa inhibitor, and a thienopyridine(for example clopidogrel), unless contraindicated.
Supplemental oxygen
In general oxygen is administered via nasal canula or face mask to patients with an uncomplicated course to maintain an oxygen saturation greater than 90%. However, endotracheal intubation may be required in those patients with a clinical course complicated by severe pulmonary edema, cardiogenic shock or mechanical complications (e.g. papillary muscle rupture, free wall rupture, or acquired ventricular septal defect). Finger pulse oximetry is useful for the continuous monitoring of SaO2 but is not mandatory in patients who do not appear to be at risk of hypoxemia. There is no evidence to support the administration of oxygen to all patients with ACS in the absence of signs of respiratory distress or arterial hypoxemia.
Antiischemic and analgesic therapy
Nitrates
Nitroglycerin, an endothelium-independent vasodilator, has both peripheral and coronary vascular effects. By venodilation, it decreases the myocardial preload, ultimately, decreasing the myocardial oxygen demand. It also dilates the coronary arteries, thus, decreasing the amount of stenosis and relieves pain. In addition, it promotes collateral flow and redistribution of coronary blood flow to ischemic regions. If three sublingual 0.4mg tablets of NTG fail to relieve the pain, intravenous NTG may be initiated along with oral or intravenous beta blocker. It will also be helpful in patients with heart failure and hypertension.
Morphine
Morphine sulfate is reasonable for patients whose symptoms are not relieved despite NTG (e.g., after3 serial sublingual NTG tablets) or whose symptoms recur despite adequate anti-ischemic therapy. Morphine sulfate has potent analgesic and anxiolytic effects, as well as hemodynamic effects, that are potentially beneficial in UA/NSTEMI. Morphine causes venodilation and can produce modest reductions in heart rate (through increased vagal tone) and systolic blood pressure to further reduce myocardial oxygen demand[1].
Beta blockers
In UA/NSTEMI, the primary benefits of beta blockers are due to inhibition of beta-1 adrenergic receptors, which results in a decrease in cardiac work and myocardial oxygen demand. Slowing of the heart rate also has a favorable effect, acting not only to reduce myocardial oxygen demand(MVO2) but also to increase the duration of diastole and diastolic pressure-time, a determinant of forward coronary flow and collateral flow[1]. In the absence of contraindication(especially hypotension, heart failure and hemodyanamic instability), beta blockers should be initiated either orally or intravenously within first 24 h. Patients with marked first-degree AV block (i.e., ECG PR interval greater than 0.24 s), any form of second- or third-degree AV block in the absence of a functioning implanted pacemaker, a history of asthma, severe LV dysfunction or HF (e.g., rales or S3 gallop) or at high risk for shock (see above) should not receive beta blockers on an acute basis. Two recent studies(GUSTO-I and COMMIT) have revealed that early aggressive beta blockade poses a substantial net hazard in hemodynamically unstable patients and should be avoided. In the COMMIT study[2], the utility of early intravenous followed by oral beta blockade (metoprolol) was tested in 45,852 patients with MI (93% had STEMI, 7% had NSTEMI) which showed that neither the composite of death, reinfarction, or cardiac arrest nor death alone was reduced for up to 28 d in the hospital. Overall, a modest reduction in reinfarction and ventricular fibrillation (which was seen after day 1) was counterbalanced by an increase in cardiogenic shock, which occurred early (first day) and primarily in those who were hemodynamically compromised or in HF or who were stable but at high risk of development of shock. Risk factors for shock were older age, female sex, time delay, higher Killip class, lower blood pressure, higher heart rate, ECG abnormality, and previous hypertension. In GUSTO-I retrospective analyses[3] , the administration of intravenous atenolol combined with late oral administration was associated with higher mortality than late oral administration alone. The authors concluded that late oral administration of atenolol might be sufficient and may offer just as good of outcomes as that coupled with early IV administration. Overall, the rationale for beta-blocker use in all forms of CAD, including UA, is generally favorable, with the exception of initial heart failure.
Calcium channel blockers
Calcium channel blockers(CCBs) consist of three subclasses:
- Dihydropyridines (e.g., nifedipine, amlodipine),
- Phenylalkylamines (e.g., verapamil), and
- Benzothiazepines (e.g., diltiazem).
CCBs inhibit both myocardial and vascular smooth muscle contraction. They also cause AV block and sinus node slowing. The degree of these effects varies amongst the three classes with nifedipine and amlodipine having the most peripheral arterial dilatory effects but few or no AV or sinus node effects, whereas verapamil and diltiazem having prominent AV and sinus node effects and but only some peripheral arterial dilatory effects. Although different CCBs are structurally and, potentially, therapeutically diverse, superiority of 1 agent over another in UA/NSTEMI has not been demonstrated, except for the increased risks posed by rapid-release, short-acting dihydropyridines such as nifedipine. Calcium channel blockers may be used to control ongoing or recurring ischemia-related symptoms in patients who already are receiving adequate doses of nitrates and beta blockers, in patients who are unable to tolerate adequate doses of 1 or both of these agents, and in patients with variant angina. Definitive evidence for a benefit of CCBs in UA/NSTEMI is predominantly limited to symptom control. When beta blockers cannot be used, and in the absence of clinically significant LV dysfunction, heart rate–slowing CCBs are preferred.[1].
Inhibitors of Renin-Angiotensin-Aldosterone axis
This class of medication includes Angiotensin converting enzyme(ACE) inhibitors, angiotensin receptor blockers and aldosterone receptor blockers. Angiotensin converting enzyme inhibitors is amongst the class of medications which have been shown to reduce mortality in patients with MI, recent MI and left ventricular dysfunction, and high risk chronic CAD with normal left ventricular function. HOPE trial[4] was a landmark study in evaluating the role of ramipril(an ACE inhibitor) in a broad category of high risk patients. In this randomized, placebo controlled trial involving 9297 high risk patients, Ramipril was shown to significantly reduce the rates of death, myocardial infarction, and stroke in a broad range of high-risk patients who are not known to have a low ejection fraction or heart failure.
ACC / AHA Guidelines (DO NOT EDIT) [1]
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Class I1. The history, physical examination, 12 lead ECG, and initial cardiac biomarker tests should be integrated to assign patients with chest pain into 1 of 4 categories: a non cardiac diagnosis, chronic stable angina, possible ACS, and definite ACS. (Level of Evidence: C) 2. Patients with probable or possible ACS but whose initial 12 lead ECG and cardiac biomarker levels are normal should be observed in a facility with cardiac monitoring (e.g., chest pain unit or hospital telemetry ward), and repeat ECG (or continuous 12-lead ECG monitoring) and repeat cardiac biomarker measurement(s) should be obtained at predetermined, specified time intervals. (Level of Evidence: B) 3. In patients with suspected ACS in whom ischemic heart disease is present or suspected, if the follow-up 12 lead ECG and cardiac biomarkers measurements are normal, a stress test (exercise or pharmacological) to provoke ischemia should be performed in the ED, in a chest pain unit, or on an outpatient basis in a timely fashion (within 72 h) as an alternative to inpatient admission. Low-risk patients with a negative diagnostic test can be managed as outpatients. (Level of Evidence: C) 4. In low-risk patients who are referred for outpatient stress testing, precautionary appropriate pharmacotherapy (e.g., ASA, sublingual NTG, and/or beta blockers) should be given while awaiting results of the stress test. (Level of Evidence: C) 5. Patients with definite ACS and ongoing ischemic symptoms, positive cardiac biomarkers, new ST-segment deviations, new deep T-wave inversions, hemodynamic abnormalities, or a positive stress test should be admitted to the hospital for further management. Admission to the critical care unit is recommended for those with active, ongoing ischemia/injury or hemodynamic or electrical instability. Otherwise, a telemetry step-down unit is reasonable. (Level of Evidence: C) 6. Patients with possible ACS and negative cardiac biomarkers who are unable to exercise or who have an abnormal resting ECG should undergo a pharmacological stress test. (Level of Evidence: B) 7. Patients with definite ACS and ST-segment elevation in leads V7 to V9 due to left circumflex artery occlusion should be evaluated for immediate reperfusion therapy. (Level of Evidence: A) 8. Patients discharged from the ED or chest pain unit should be given specific instructions for activity, medications, additional testing, and follow-up with a personal physician. (Level of Evidence: C) Class IIa1. In patients with suspected ACS with a low or intermediate probability of CAD, in whom the follow up 12 lead ECG and cardiac biomarkers measurements are normal, performance of a non invasive coronary imaging test (i.e., Cardiac / Coronary CT Angiography) is reasonable as an alternative to stress testing. (Level of Evidence: B) |
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See Also
Sources
- The ACC/AHA 2007 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction [1]
References
- ↑ 1.0 1.1 1.2 1.3 1.4 Anderson JL, Adams CD, Antman EM; et al. (2007). "ACC/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-Elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients With Unstable Angina/Non-ST-Elevation Myocardial Infarction) developed in collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine". JACC. 50 (7): e1–e157. PMID 17692738. Text "doi:10.1016/j.jacc.2007.02.013 " ignored (help); Unknown parameter
|month=ignored (help) - ↑ Early intravenous then oral metoprolol in 45,852 patients with acute myocardial infarction: randomised placebo-controlled trial. Chen ZM, Pan HC, Chen YP, Peto R, Collins R, Jiang LX, Xie JX, Liu LS; COMMIT (ClOpidogrel and Metoprolol in Myocardial Infarction Trial) collaborative group. Lancet. 2005 Nov 5;366(9497):1622-32. PMID: 16271643
- ↑ Pfisterer M, Cox JL, Granger CB; et al. (1998). "Atenolol use and clinical outcomes after thrombolysis for acute myocardial infarction: the GUSTO-I experience. Global Utilization of Streptokinase and TPA (alteplase) for Occluded Coronary Arteries". J. Am. Coll. Cardiol. 32 (3): 634–40. PMID 9741504. Unknown parameter
|month=ignored (help) - ↑ Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. N Engl J Med. 2000 Jan 20;342(3):145-53. Erratum in: 2000 May 4;342(18):1376. N Engl J Med 2000 Mar 9;342(10):748. PMID: 10639539