ST elevation myocardial infarction nitrate therapy
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| Myocardial infarction Classification and external resources | |
 | |
|---|---|
| Diagram of a myocardial infarction (2) of the tip of the anterior wall of the heart (an apical infarct) after occlusion (1) of a branch of the left coronary artery (LCA, right coronary artery = RCA). | |
| ICD-10 | I21.-I22. |
| ICD-9 | 410 |
| DiseasesDB | 8664 |
| MedlinePlus | 000195 |
| eMedicine | med/1567 emerg/327 ped/2520 |
| Cardiology Network |
 Discuss ST elevation myocardial infarction nitrate therapy further in the WikiDoc Cardiology Network |
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Nitroglycerin
Mechanism(s) of Benefit
In determining whether nitrates should be administered and in determining the dose, the following mechanisms of benefit (as well as potential for harm) associated with nitrate administration should be kept in mind:
- 1. Reduction in preload via venodilation. While this may be of benefit in many STEMI patients, this may lead to hypotension and hypoperfusion in those patients with right ventricular infarction with ST segment elevation in lead V4R.
- 2. Reduction in afterload via arterial dilation. This may be of particular relevance in the patient with pulmonary edema or papillary muscle rupture or other mechanical complications.
- 3. Vasodilation of epicardial coronary arteries. While a modest component of vasoconstriction may be present in the majority of STEMI patients, relief of vasospasm may be particularly important in those rare patients with coronary spasm as the precipitating event.
- 4. Dilation of collateral vessels. This vasodilatory benefit must, however, be balanced against the load dependence of collateral filling and optimization of the subendocardial to epicardial flow ratio [1] [1] [1]
Clinical Trial Data
A large, definitive, randomized trial of nitrate administration (ISIS 4) demonstrated no significant mortality benefit of acute nitrate administration. Similarly, a pooled analysis involving more than 80.000 patients treated with nitrates either intravenously or orally in 22 trials demonstrated a mortality rate of 7.7% in the control group, which was reduced to 7.4% in the nitrate group. Taken together, randomized and pooled data are consistent with a possible modest treatment effect of nitrates such that 3 to 4 deaths might be prevented for every 1000 patients treated.
Dosing
The dose nitroglycerin is 0.4 mg administered sublingually. Intravenous nitroglycerin offers an advantage over sublingual administration in so far as it allows clinicians to titrate the therapy in response to the patient’s blood pressure. The usual intravenous nitroglycerin infusion rate is 5 to 10 mcg per minute with an increases of 5 to 20 mcg per minute until symptoms are relieved or mean arterial blood pressure (MAP) is reduced by 10% of its baseline level in normotensive patients and by up to 30% for hypertensive patients. In no case should the systolic blood pressure be lowered below 90 mm Hg or should the systolic blood pressure drop greater than 30 mm Hg below baseline. [1] [1]
Nitrates versus Beta-Blocker Administration
In so far as the mortality benefits of nitrates are limited, their dosing should be titrated to a blood pressure that does not limit the co-administration of beta-blockers, which have, in contrast, been associated with advantages in mortality and infarct size reduction.
Side Effects and Contraindications
The systolic blood pressure may drop rapidly following a sublingual nitroglycerine secondary to inability to control both the initial dose and rate of absorption. Nitrates in all forms should be avoided in patients with initial systolic blood pressures less than 90 mm Hg or greater than or equal to 30 mm Hg below baseline, marked bradycardia or tachycardia [1], or known or suspected right ventricular infarction. Patients with right ventricular infarction are especially dependent on adequate right ventricular preload to maintain cardiac output and may experience profound hypotension during administration of nitrates [1] Phosphodiesterase inhibitors potentiate the hypotensive effects of nitrates because of their mechanism of action in releasing nitric oxide and increasing cyclic guanosine monophosphate.[1] Therefore, it is useful clinical practice to ascertain whether such agents have been used, and nitrates should not be administered to patients who have received a phosphodiesterase inhibitor for erectile dysfunction in the prior 24 hours (48 hours for tadalafil).
Guidelines (DO NOT EDIT)
Class I
1. Patients with ongoing ischemic discomfort should receive sublingual nitroglycerin (0.4 mg) every 5 minutes for a total of 3 doses, after which an assessment should be made about the need for intravenous nitroglycerin. (Level of Evidence: C)
2. Intravenous nitroglycerin is indicated for relief of ongoing ischemic discomfort, control of hypertension, or management of pulmonary congestion. (Level of Evidence: C)
Class III
1. Nitrates should not be administered to patients with systolic blood pressure less than 90 mm Hg or greater than or equal to 30 mm Hg below baseline, severe bradycardia (less than 50 beats per minute [bpm]), tachycardia (more than 100 bpm), or suspected RV infarction. (Level of Evidence: C)
2. Nitrates should not be administered to patients who have received a phosphodiesterase inhibitor for erectile dysfunction within the last 24 hours (48 hours for tadalafil). (Level of Evidence: B)[1]
References
Acknowledgement and Attribution Regarding Sources of Content
Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .
