ACC/AHA 2007 guideline update for the

e186 Circulation August 14, 2007
can be mobilized to a chair and use a bedside commode
when symptom free. Subsequent activity should not be
inappropriately restrictive; instead, it should be focused on
the prevention of recurrent symptoms and liberalized as
judged appropriate when response to treatment occurs.
Patients with cyanosis, respiratory distress, or other highrisk
features should receive supplemental oxygen. Adequate
arterial oxygen saturation should be confirmed with direct
measurement (especially with respiratory distress or cyanosis)
or pulse oximetry. No evidence is available to support
the administration of oxygen to all patients with ACS in the
absence of signs of respiratory distress or arterial hypoxemia.
Its use based on the evidence base can be limited to those
with questionable respiratory status and documented hypoxemia.
Nevertheless, it is the opinion of the Writing Committee
that a short period of initial routine oxygen supplementation
is reasonable during initial stabilization of the
patient, given its safety and the potential for underrecognition
of hypoxemia. Inhaled oxygen should be administered
if the arterial oxygen saturation (SaO2) declines to less than
90%. 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. Patients should
undergo continuous ECG monitoring during their ED
evaluation and early hospital phase, because sudden, unexpected
ventricular fibrillation is the major preventable cause
of death in this early period. Furthermore, monitoring for
the recurrence of ST-segment shifts provides useful diagnostic
and prognostic information, although the system of
monitoring for ST-segment shifts must include specific
methods intended to provide stable and accurate recordings.
3.1.2. Use of Anti-Ischemic Therapies
3.1.2.1. NITRATES
Nitroglycerin reduces myocardial oxygen demand while
enhancing myocardial oxygen delivery. Nitroglycerin, an
endothelium-independent vasodilator, has both peripheral
and coronary vascular effects. By dilating the capacitance
vessels (i.e., the venous bed), it increases venous pooling to
decrease myocardial preload, thereby reducing ventricular
Table 14. NTG and Nitrates in Angina
wall tension, a determinant of myocardial oxygen demand
(MVO 2). More modest effects on the arterial circulation
decrease systolic wall stress (afterload), which contributes to
further reductions in MVO 2. This decrease in myocardial
oxygen demand is in part offset by reflex increases in heart
rate and contractility, which counteract the reductions in
MVO 2 unless a beta blocker is concurrently administered.
Nitroglycerin dilates normal and atherosclerotic epicardial
coronary arteries and smaller arteries that constrict with
certain stressors (e.g., cold, mental or physical exercise).
With severe atherosclerotic coronary obstruction and with
less severely obstructed vessels with endothelial dysfunction,
physiological responses to changes in myocardial blood flow
are often impaired (i.e., loss of flow-mediated dilation), so
maximal dilation does not occur unless a direct-acting
vasodilator like NTG is administered. Thus, NTG promotes
the dilation of large coronary arteries, as well as
collateral flow and redistribution of coronary blood flow to
ischemic regions. Inhibition of platelet aggregation also
occurs with NTG (300), but the clinical significance of this
action is not well defined.
Intravenous NTG can benefit patients whose symptoms
are not relieved in the hospital with three 0.4-mg sublingual
NTG tablets taken 5 min apart (Tables 12 and 14) and with
the initiation of an oral or intravenous beta blocker (when
there are no contraindications), as well as those with HF or
hypertension. Note that NTG is contraindicated after the
use of sildenafil within the previous 24 h or tadalafil within
48 h or with hypotension (301–303). The suitable delay
before nitrate administration after the use of vardenafil has
not been determined, although blood pressure had generally
returned to baseline by 24 h (304). These drugs inhibit the
phosphodiesterase that degrades cyclic guanosine monophosphate,
and cyclic guanosine monophosphate mediates
vascular smooth muscle relaxation by nitric oxide. Thus,
NTG-mediated vasodilatation is markedly exaggerated and
prolonged in the presence of phosphodiesterase inhibitors.
Nitrate use within 24 h after sildenafil or the administration
of sildenafil in a patient who has received a nitrate within
24 h has been associated with profound hypotension, MI,
Compound Route Dose/Dosage Duration of Effect
NTG Sublingual tablets 0.3 to 0.6 mg up to 1.5 mg 1 to 7 min
Spray 0.4 mg as needed Similar to sublingual tablets
Transdermal 0.2 to 0.8 mg per h every 12 h 8 to 12 h during intermittent therapy
Intravenous 5 to 200 mcg per min Tolerance in 7 to 8 h
Isosorbide dinitrate Oral 5 to 80 mg, 2 or 3 times daily Up to 8 h
Oral, slow release 40 mg 1 or 2 times daily Up to 8 h
Isosorbide mononitrate Oral 20 mg twice daily 12 to 24 h
Oral, slow release 60 to 240 mg once daily
Pentaerythritol tetranitrate Sublingual 10 mg as needed Not known
Erythritol tetranitrate Sublingual 5 to 10 mg as needed Not known
Oral 10 to 30 mg 3 times daily Not known
Adapted from Gibbons RJ, Abrams J, Chatterjee K, et al. ACC/AHA 2002 guideline update for the management of patients with chronic stable angina. Available at: http://www.acc.org/qualityandscience (4).
NTG nitroglycerin.
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