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In patients with suspected acute cardiac ischemia, prompt evaluation and triage is mandatory to permit assignment to syndrome-specific critical care pathways (Figure 24–4). For detailed, up-to-date discussion of management considerations particular to UA/NSTEMI and STEMI, readers are encouraged to refer directly to current American College of Cardiology/American Heart Association guidelines.9,10

Figure 24–4

Diagnostic algorithm for patients with suspected acute cardiac ischemia.

ACS, acute coronary syndrome; ECG, electrocardiogram; NSTEMI, non-ST elevation myocardial infarction; STEMI, ST elevation myocardial infarction; UA, unstable angina. (Adapted with permission from Anderson JL, Adams CD, Antman EM, et al. 2012 ACCF/AHA focused update incorporated into the ACCF/AHA 2007 guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, J Am Coll Cardiol 2013;61(23):e179-347.)

Acute Cardiac Ischemia in the Setting of Stable Coronary Artery Disease

Myocardial infarction “type 2” may result from anatomically stable coronary artery disease when physiologic derangements result in an acute imbalance between myocardial oxygen supply and demand and elevation in serum biomarkers of myocardial injury. The key to management of this syndrome is identification and correction of the underlying cause of increased myocardial oxygen demand. Potential etiologies of myocardial infarction type 2 are listed in Table 24–6. In conjunction with this disease-directed approach, supportive measures to mitigate cardiac ischemia include use of anti-ischemic therapies, as discussed earlier.

Table 24–6Common sources of myocardial infarction type 2 and management.

Of note, demand-mediated acute ischemia in the intensive care unit may not present with classical angina. Symptoms may be atypical or absent (“silent ischemia”). Among patients with known coronary artery disease or coronary risk factors, such silent ischemia is common in the intensive care unit, often unrecognized, and linked with increased morbidity and mortality.11 Reported incidence has varied in series studying different settings and using test modalities with different sensitivities, with ischemic ST changes observed in 11% to 21% and troponin elevations noted in 15% to 38% of patients in published series.11,12,13 Continuous electrocardiographic monitoring using 5 electrodes and 2 leads (typically II and V5) has a low sensitivity in comparison with a standard 12-lead electrocardiogram and may miss clinically important ischemia.13 It is important to recognize, however, that elevation in serum biomarkers of myocardial infarction may occur in the absence of epicardial coronary artery disease, deriving instead from direct effects of catecholamines or other circulating toxins on myocardial cells.


UA and NSTEMI account for the majority of ACS. When a diagnosis of UA/NSTEMI is suspected, the early priority of management is risk stratification. High-risk cases of UA/NSTEMI benefit from an early invasive management strategy, whereas lower-risk cases may be managed with an initial conservative strategy and provisional invasive angiography. Clinical features indicating high risk include refractory angina, hemodynamic or electrical instability, left ventricular systolic dysfunction, elevated serum biomarkers of cardiac injury, and ST-segment deviation. Global risk scores are also useful for risk stratification; commonly used scores include the TIMI, GRACE, and PURSUIT risk scores.

Regardless of risk profile, all patients diagnosed with UA/NSTEMI should be managed with dual antiplatelet therapy, anticoagulation, a high-potency statin, and optimal anti-ischemic therapy, as discussed earlier. Useful markers of therapeutic efficacy include resolution of chest pain and ST-segment deviations and a downward trend in serum CK-MB. Patients judged to be at high-risk and assigned to an early invasive strategy should undergo invasive angiography to define coronary anatomy and facilitate triage to an appropriate revascularization strategy. Patients deemed to be at low risk may be evaluated first using noninvasive stress testing, with subsequent triage to invasive angiography as warranted.


STEMI is a medical emergency. Most commonly resulting from acute thrombotic occlusion of a coronary artery in the setting of coronary atherosclerosis, STEMI reflects severe, acute often transmural cardiac ischemia. “Time is muscle”: reperfusion therapy is time-sensitive to save jeopardized myocardium. As such, management algorithms for STEMI, including interhospital systems of care, are designed to minimize time to reperfusion therapy, for which primary percutaneous coronary intervention is preferred. Reperfusion therapy is indicated in all eligible patients within 12 hours of symptom onset; between 12 and 24 hours after symptom onset, reperfusion therapy may still be indicated for patients with clinical or electrocardiographic evidence of ongoing ischemia. Current time to reperfusion therapy systems goals include a door-to-needle time of 30 minutes (for fibrinolytic therapy) and a door-to-device time of 90 minutes (for primary percutaneous coronary intervention). In conjunction with expeditious reperfusion therapy, patients diagnosed with STEMI should receive dual antiplatelet therapy, anticoagulation, a high-potency statin, and optimal anti-ischemic therapy, as discussed above. In a limited proportion of cases, patients ineligible for reperfusion therapy will be managed with these medical therapies alone.

Complications of STEMI are of particular concern, and become the focus of critical care following reperfusion therapy. These may be grouped in terms of ischemic, electrical, and mechanical complications.

Ischemic complications include reinfarction and, following percutaneous coronary intervention with stent implantation, acute or subacute stent thrombosis. Symptoms and signs may include recurrent ischemic chest discomfort, ST-segment deviations, and a new rise in serum biomarkers of cardiac injury. Management may require intensification of antithrombotic and anti-ischemic therapy and may include repeat invasive angiography.

Electrical complications may include new onset bradyarrhythmias (including conduction blocks) and tachyarrhythmias, and in particular within the first 24 to 48 hours, ventricular tachycardia. Continuous electrocardiographic monitoring is mandatory to permit prompt identification and acute management of dysrhythmia; indeed, facilitation of prompt defibrillation was a primary motivating factor in the creation of coronary care units.

Mechanical complications include pump failure and cardiogenic shock; acute mitral regurgitation; ventricular septal defect formation; and free wall rupture with pericardial tamponade. Clinicians must maintain a high index of suspicion for these mechanical complications, which may manifest as fulminant clinical deterioration and which, importantly, may present late, 3 to 7 days following myocardial infarction.

In addition to these complications of STEMI itself, attention must be paid to the complications of our therapy. In particular, patients with both STEMI and UA/NSTEMI are exposed to risk of bleeding as a consequence of the acute provision of antiplatelet, anticoagulant, and invasive vascular therapies. Bleeding complications of ACS are important, with adverse prognostic implications. Patients who bleed are at risk for morbidity and mortality related to bleeding itself as well as heightened risk of recurrent ischemic events, which may relate to withholding of antithrombotic therapies or adverse effects of transfusion.

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