Chapter 21 Marini Acute Coronary Syndromes

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SECTION II • Medical and Surgical Crises

pericardial effusion, free wall or septal perforations, acute mitral insufficiency, or aortic dissection). Apart from its value in risk stratification, echo is also instrumental in diagnosing complications of infarc- tion (e.g., chordal disruption, papillary muscle dys- function, septal perforation, pericardial effusion, free wall rupture, ventricular aneurysm, mural thrombus). The addition of transesophageal echocardiography to the diagnostic armamentarium has substantially increased the ability to detect subtle MR, small ven- triculoseptal defects (VSDs), papillary muscle dam- age, and posterior wall infarction (see Chapter 2). Treatment During the last four decades, advances in coronary care—aggressive treatment of coronary ischemia and arrhythmias—have reduced the mortality of AMI from 30% to less than 10%. In part, this relates to timeliness of intervention and rapid triage to facilities in which definitive care can be provided (Fig. 21-4).

Recently, the major therapeutic goal has been to limit infarct size, primarily by achieving early reper- fusion. Reperfusion is achieved by pharmacologic or mechanical means and is performed in conjunc- tion with measures to minimize myocardial oxygen demand. The early therapy of AMI has now evolved to a five-armed attack: (1) relieve pain and anxiety; (2) achieve reperfusion using thrombolytic therapy or PTCA in appropriate candidates; (3) improve the balance between myocardial oxygen supply and demand by using supplemental oxygen, nitrates, and β -blockers; (4) initiate antithrombotic therapy (aspi- rin and heparin) to prevent reformation of a second occlusive thrombus; and (5) limit infarct expansion, prevent adverse ventricular remodeling, and improve ventricular function. These initial steps are followed by critically important secondary prevention efforts, which include early use of aspirin, high-dose statins and clopidogrel; appropriate and cautious use of beta-blockers and ACE inhibitors; and subsequent modification of cardiac risk factors (Fig. 21-5).

STEMI patient who is a candidate for reperfusion*

Initially seen at a PCI-capable hospital

Initially seen at a non-PCI-capable hospital**

Target time <30 min

Transfer for primary PCI FMC-device time as soon as possible and < 120 min

Administer fibrinolytic agent within 30 min of arrival when

Send to cath lab for primary PCI FMC-device time < 90 min

anticipated FMC- device >120 min

Diagnostic angiogram

Transfer for angiography and revascularization within 2-24 h for other patients as part of an invasive strategy**

Urgent transfer for PCI for patients with evidence of failed reperfusion or reocclusion

Medical therapy only

PCI

CABG

* ECG by EMS ** Reperfusion therapy is reasonable for STEMI and symptom onset prior 12 to 24 hours (PCI preferred) **Patients with cardiogenic shock or severe heart failure should be transferred for cardiac catheterization as soon as possible.

FIGURE 21-4. Triage and reperfusion sequence for acute myocardial infarction with ST segment elevation (STEMI).