Published Oct 27, 2006
S.T.A.C.E.Y, LPN
562 Posts
Pt in clinical today developed sudden respiratory distress. He was admitted to a medical floor with MULTIPLE issues, none of which had been respiratory. As soon as he had shortness of breath, one of the students & the nurse immediately responded raising the head of the bed, providing Oxygen, and taking vitals.
Then the nurse gave nitro. The student specifically asked the patient if he had chest pain, and he responded no. The nurse was aware of this, but gave the nitro anyways. Twice.
We discussed this afterwards, but none of us could figure out why the nitro would have been given. What benefit would it have had, if the patient said there was no chest pain, just difficulty breathing. I've been trying to look this up, but haven't found anything yet. Possible explanations??
robfall
37 Posts
NTG is also used to treat CHF/pulmonary edema. It's a quick way to reduce cardiac preload.
VickyRN, MSN, DNP, RN
49 Articles; 5,349 Posts
I agree. Pulmonary edema can cause respiratory symptoms of dyspnea and anxiety, and classic signs of crackles, wheezing, coughing up frothy pinkish or blood-tinged sputum, tachypnea, falling saO2, S3 heart sound, and diaphoresis. Sudden onset of pulmonary edema is called 'flash pulmonary edema.' If a client is experiencing flash pulmonary edema, this is a medical emergency, and the usual treatment is STAT furosemide IV, nitroglycerin (sublingual, spray, or an IV drip), and a foley catheter (besides giving oxygen and placing in high Fowler's, as you did). Furosemide and nitroglycerin are great preload-reducing agents. And you intervened appropriately, by raising the head of the bed to high fowler's, providing oxygen, taking vitals, and urgently notifying your primary nurse and instructor. Furosemide and nitroglycerin should not be given if blood pressure is low (generally, systolic less than 100).
Nitroglycerin (Nitro-Bid, Nitrol, Nitrostat) -- SL nitroglycerin and nitrospray are particularly useful in the patient who presents with acute pulmonary edema with a systolic blood pressure of at least 100 mm Hg.Similar to SL, nitrospray's onset is 1-3 min with a half-life of 5 min. Applicability of nitrospray may be easier, and storage is up to 4 y. One study demonstrated significant and rapid hemodynamic improvement in 20 patients given nitrospray with pulmonary edema in an ICU setting.
Similar to SL, nitrospray's onset is 1-3 min with a half-life of 5 min. Applicability of nitrospray may be easier, and storage is up to 4 y. One study demonstrated significant and rapid hemodynamic improvement in 20 patients given nitrospray with pulmonary edema in an ICU setting.
http://www.emedicine.com/emerg/topic108.htm
Nrs_angie, BSN, RN
163 Posts
Hello there,
Let me say first that I do not have any websites or journals to guide you to the correct answer as many of the postings to threads on these forums like to do. I prefer to give my own simple explanation of what I think is the answer you are looking for. So please take it for what it's worth.
Ok that being said... as you probably know Nitro is for chest pain right? Why do people get chest pain? Think of it this way... if there is some kind of blockage in the coronary arteries, perhaps a clot, or perhaps atherosclerotic plaque, the blood can't get to all areas of the heart that it needs to go. The heart is a muscle right? Well muscles need oxygen to function. Without it, you get an ischemic area in the heart. Ischemia leads to myocardial infarction, or simply known as heart attach. Infarction simply means death of cells.
Ok, so have you ever worked out so much, that your muscles ached? Or ever ran too fast and you got this burning sensation in your calves? Well that's lactic acid. When muscles dont get the oxygen they need, lactic acid builds up. Same as with the heart. If the heart doesnt get the oxygen, lactic acid causes chest pain. There is a much more technical way to explain the pathophysiology, but remember I am just giving my simple version.
Well, why do we give nitro for chest pain? Because it is a vasodilator... If we open up the arteries that bring oxygen to the heart, the lactic acid is carried away, or metabolized. Then the pain decreases. By decreasing the pain, the workload of the heart is decreased. Because as you know, the harder the heart has to work, the more oxygen it requires.
So by now you are saying, but the patient denied having any chest pain. So then why am i rambling on and on about ischemia, and lactic acid, and MI. Well as you know, when the body is not getting the oxygen it needs, homeostasis kicks in and compensates for that. So what do we get? Increased respiratory rate and the pattern might become more shallow. Hyperventilation can cause someone to feel "shortness of breath".
So by doing this, you decrease the Oxygen demand of the heart, thus decreasing shortness of breath.
I am guessing that your patient probably had some kind of cardiac history, hence the standing order to give nitro.
Hope this helps!!
Angie
Pt in clinical today developed sudden respiratory distress. He was admitted to a medical floor with MULTIPLE issues, none of which had been respiratory. As soon as he had shortness of breath, one of the students & the nurse immediately responded raising the head of the bed, providing Oxygen, and taking vitals. Then the nurse gave nitro. The student specifically asked the patient if he had chest pain, and he responded no. The nurse was aware of this, but gave the nitro anyways. Twice. We discussed this afterwards, but none of us could figure out why the nitro would have been given. What benefit would it have had, if the patient said there was no chest pain, just difficulty breathing. I've been trying to look this up, but haven't found anything yet. Possible explanations??