In acute coronary syndrome, medications may be used to treat a patient's pain, increase coronary perfusion, and increase cardiac contractility. In an ACLS situation, it’s important for practitioners to know how each medication (in the proper dosage) can help a patient’s condition. This means understanding the pharmacology, side effects, and potential drug interactions of each medication to make the proper decision according to the ACLS algorithm.
Nitroglycerin is a potent venous and arterial vasodilator. It is used to treat chest pain in acute coronary syndrome by increasing coronary perfusion. In addition, nitroglycerin infusions may be used to treat acute cardiogenic pulmonary edema.
Let’s take a closer look at Nitroglycerin in an ACLS context to help prepare for real clinical scenarios.
Nitroglycerin was first compounded in 1847 and used for the treatment of angina (chest pain) in 1867. It was later used for the treatment of hypertension, two indications for which nitroglycerin is still used today.
Nitroglycerin comes in sublingual tablet, spray, and intravenous formulations. Once in the body, nitroglycerin is converted to nitric oxide. Through a series of reactions, nitric oxide causes smooth muscle relaxation causing both arterial dilatation and venous dilatation. Nitroglycerin is mainly used in the treatment of acute coronary syndrome. It can also be used for the treatment of acute cardiogenic pulmonary edema. The main side of the nitroglycerin effect is hypotension caused by vasodilation.
Nitroglycerin is used in the treatment of chest pain caused by acute coronary syndrome (ACS). Acute coronary syndromes are any conditions that cause ischemia or infarction of the heart muscles. Types of ACS include acute myocardial infarction and angina.
The drug works by dilating coronary vasculature, thus increasing blood flow and oxygen to the heart. By increasing blood flow to an oxygen delivery to the heart, it decreases ischemia thereby reducing chest pain. In patients with acute cardiogenic pulmonary edema, nitroglycerin dilates both the arterial and venous systems.
By dilating the venous system, preload is reduced, decreasing the amount of fluid the heart needs to pump. By dilating the arterial vasculature, afterload is reduced, thereby allowing more blood to be pumped with each cardiac contraction.
Once in the body, nitroglycerin is rapidly metabolized to nitric oxide. Inside of smooth muscle cells, a series of molecular reactions occur which causes dephosphorylation of myosin light chains, an important protein in the regulation of muscle contraction.
Once dephosphorylation occurs, the smooth muscle relaxes, leading to the arterial and venous dilatation. Nitroglycerin is rapidly absorbed through the sublingual route. It starts working within one minute and has its peak effect at approximately five minutes.
When given through the intravenous route, a nitroglycerin drip begins working immediately. The effects of nitroglycerin tablets will last approximately 25 minutes while the effects of intravenous nitroglycerin disappear almost immediately once the infusion is discontinued.
Once cardiac monitoring is initiated and intravenous access is obtained, ACLS providers should consider administering nitroglycerin. Nitroglycerin is indicated for the treatment of chest pain from suspected or known myocardial infarction. Initially, it is administered sublingually either in tablet or spray form. After three doses, if the nitroglycerin is having a positive effect, the clinician may choose to initiate a nitroglycerin infusion (also known as nitroglycerin drip). In acute decompensated cardiogenic heart failure, nitroglycerin should be administered through the intravenous route.
For the most accurate information about using Nitroglycerin in a life support scenario, also consult the current ACLS algorithm and guidelines.
Nitroglycerin is a potent vasodilator and can easily cause hypotension. When administering nitroglycerin, patients should have continuous cardiac monitoring and frequent blood pressure monitoring. There should also be intravenous access prior to administration of nitroglycerin in case of hypotension.
NOTE: Nitroglycerin should not be administered to any patient with a systolic blood pressure less than 110 mmHg. In addition, nitroglycerin is contraindicated in patients who have taken sildenafil citrate (Viagra) or tadalafil (Cialis) within the last 48 hours.
If any side effects occur, a nitroglycerin infusion should be stopped immediately. Primary side effects include:
Nitroglycerin has a severe interaction with sildenafil citrate (Viagra) or tadalafil (Cialis) as both medications work by causing nitric oxide release. Nitroglycerin may also interact with other medications that lower blood pressure such as beta blockers, calcium channel blockers, or morphine.
There is no specific antidote for nitroglycerin toxicity. However, side effects can be managed once administration of the drug is stopped.
Hypotension should be managed with crystalloid fluids and vasopressors medications (such as norepinephrine) as needed. Hypotension is generally short-lived and will resolve with minimal intervention. Headaches can be managed with acetaminophen and usually resolve once the nitroglycerin is metabolized.
Q: Why is nitroglycerin given to patients with chest pain?
A: Nitroglycerin is a vasodilator that increases blood flow through the coronary arteries to ischemic areas of the heart thus relieving pain.
Q: What is the protocol for nitroglycerin?
A: Nitroglycerin dosage depends on the patient’s specific condition:
Q: How fast can I give nitroglycerin?
A: Once again, this depends on the condition:
Nitroglycerin is a critical medication to administer to patients with ischemic chest pain. Sublingual dosing is one tablet or spray (0.3mg) every five minutes to a maximum of three doses followed by a nitroglycerin drip of 10 mcg/minute-200 mcg/minute intravenously. The main side effect is hypotension, which is generally short-lived.
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SOURCES
Marsh N, Marsh A. A short history of nitroglycerine and nitric oxide in pharmacology and physiology. Clin Exp Pharmacol Physiol. 2000 Apr;27(4):313-9. doi: 10.1046/j.1440-1681.2000.03240.x. PMID: 10779131.
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