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Fluids & Electrolytes
GJ, a 55-year-old male, presents to the ED with substernal chest discomfort (8/0-10) unrelieved by rest. Emergency medical services (EMS) personnel administered nonenteric-coated aspirin and sublingual nitroglycerin (NTG) without relief. GJ reports experiencing three episodes of chest discomfort or pain in the last 24 hours.
Initial assessment findings in the ED include temperature, 37[degrees]C (98.6[degrees]F); heart rate 88, normal sinus rhythm; respirations, 18; SpO2, 95% on room air; BP, 130/70, chest discomfort rated 5/0-10. ECG findings included ST-segment depression in leads V3-4. Initial serum troponin T (TnT), creatine kinase (CK), and CK-myocardial band (CK-MB) levels are all within normal limits.
The patient has a history of type 2 diabetes and hypertension and a family history of heart disease: His father died at age 45 following a myocardial infarction (MI). His current medications include metformin, aspirin, and metoprolol.
GJ is admitted to the chest pain unit to rule out a non-ST-segment elevation myocardial infarction (NSTEMI). Are you prepared to care for this patient according to the latest guidelines?
In 2011, the American College of Cardiology Foundation (ACCF) and the American Heart Association (AHA) Task Force on Practice Guidelines updated the 2007 guidelines for management of patients with unstable angina (UA) and NSTEMI. These clinical practice guidelines provide recommendations that are supported by the best-available evidence and expert opinion. This article reviews the current guidelines and discusses how to apply them to patient care.
As defined in the current guidelines, UA/NSTEMI is a clinical syndrome that's considered a subset of acute coronary syndromes (ACS). Usually caused by atherosclerotic coronary artery disease, it's associated with increased risk of MI.1
Although UA and NSTEMI are closely related with similar treatments, they have slightly different characteristics. Both are characterized by chest pain or anginal equivalent (an anginal symptom other than chest pain, such as dyspnea or extreme fatigue), and ST-segment depression or prominent T-wave inversion on ECG; in UA, however, changes are usually transient if present at all. NSTEMI is differentiated by the presence of positive biomarkers of necrosis, such as troponin in the absence of ST-segment elevation.
UA reflects an imbalance between oxygen supply and demand. The guidelines describe three principal presentations of UA:
* angina occurring at rest
* new onset (less than 2 months) of severe angina pain
* angina increasing in frequency, duration, or intensity.
A 12-lead ECG shows minimal or transient changes indicating ischemia, or no changes. (See ECG waveform review.) Serum cardiac biomarkers (troponins and CK-MB) remain within normal limits, indicating no myocardial injury.
In contrast, pain associated with NSTEMI is usually prolonged and more intense than rest angina or anginal equivalent. It's also caused by an imbalance between oxygen supply and demand; however, in NSTEMI the ischemia is severe enough to cause myocardial damage that is detectable via elevated serum cardiac biomarker levels. The patient may have non-specific ST-segment and T-wave changes on 12-lead ECG. If unrecognized, NSTEMI may lead to ST-segment elevation myocardial infarction (STEMI). In STEMI, the imbalance between oxygen supply and demand is severe enough to cause tissue necrosis, and the patient requires emergency revascularization.
The ACCF/AHA grades each new recommendation in the guidelines according to the strength of the evidence supporting it. This is expressed as certainty of treatment effect (Level A through C) and the size of treatment effect (Class I, Class IIa, Class IIb, and Class III).1
Thienopyridines, a class of drugs that prevent platelet aggregation, are an important component of treatment for UA/NSTEMI. The previous guidelines recommended clopidogrel for antiplatelet therapy. At the time, clopidogrel was the only FDA-approved thienopyridine available. Since then, another thienopyridine, prasugrel, has been approved.
The addition of prasugrel is a major change in the new guidelines. In clinical trials comparing the new drug with clopidogrel, prasugrel was superior in reducing clinical events but increased the risk of bleeding.1,2
Prasugrel is a prodrug that must pass through the liver first to convert to its active metabolite. It binds to the platelet P2Y12 receptor and inhibits adenosine diphosphate, disrupting platelet production and aggregation.1,3
Prasugrel is packaged with a boxed warning about the risk of "significant, sometimes fatal, bleeding," including specific contraindications for use. For example, prasugrel shouldn't be used in patients with active pathologic bleeding or in those likely to need urgent coronary artery bypass graft (CABG) surgery. If possible, prasugrel should be discontinued at least 7 days before any surgery. Prasugrel isn't recommended in patients age 75 or older, patients with a history of stroke, or patients who weigh less than 60 kg.2
At this time, the consensus group doesn't recommend administering prasugrel routinely prior to coronary angiography or if a decision to proceed to percutaneous coronary intervention (PCI) hasn't been made.1 If the patient is referred for CABG surgery, prasugrel should be held for at least 7 days unless the risk of holding the medication outweighs the benefit.1-3
Clopidogrel is also a prodrug but requires several passes through the liver to convert to its active metabolite. It should be administered prior to PCI because onset of action occurs in about 6 hours.
A few patients don't respond to clopidogrel because their ability to convert it to its active metabolite is impaired for genetic reasons. If this is suspected due to thrombotic events, the patient should undergo platelet function or genetic testing.1 Genetic testing, however, isn't readily available and is expensive.
After publication of the guidelines, a third option, ticagrelor, was approved for dual antiplatelet therapy. Although not currently part of the guidelines, this medication is being used in practice. (See Ticagrelor: A new treatment option.)
If the patient receives a bare metal stent, dual therapy with aspirin and a thienopyridine should continue for at least a year. It should continue for 15 months or longer if patient received a drug-eluding stent (DES).1
The patient must continue dual therapy with aspirin and the prescribed thienopyridine upon discharge for the recommended period. If the patient abruptly discontinues the medication, he or she is at high risk for restenosis and STEMI.
Unfortunately, many patients stop the thienopyridine due to its high cost, so assess the patient's ability to pay for the medication. If the patient can't afford it, a social worker or case manager should be contacted for assistance.
Because of the bleeding risk associated with antiplatelet/anticoagulant therapies, educate patients about signs and symptoms to watch for and report. (See Teach patients about bleeding risks.)
GJ receives I.V. NTG, which relieves his chest discomfort; his pain intensity rating is now 0/0-10. Home medications of aspirin and metoprolol are continued and a HMG-CoA reductase inhibitor (statin) is added. Metformin is held in anticipation of the possible need for cardiac catheterization. His blood glucose levels are to be checked before meals and at bedtime with correction insulin.
Serum cardiac biomarkers are checked every 6 hours. The second set reveals an elevated TnT of 0.6 ng/mL (normal, less than 0.2 ng/mL); CK, 400 ng/mL (normal, 0 to 120 ng/mL); and CK-MB, 10 ng/mL (normal, 0 to 3 ng/mL). Due to the patient's ECG abnormalities and longstanding history of diabetes and hypertension, the cardiologist suspects that GJ has significant coronary artery disease and defers prescribing a thienopyridine in case the patient needs CABG surgery. (See Coronary arteries: A closer look.)
Patients who are already on dual antiplatelet therapy with aspirin and clopidogrel and are either at low risk for ischemic events or high risk for bleeding shouldn't have glycoprotein (GP) IIb/IIIa inhibitors initiated.1 GP IIb/IIIa inhibitors should be considered in addition to clopidogrel to prevent further platelet aggregation in patients for whom an initial conservative strategy is chosen, and in high-risk patients who are on aspirin and a thienopyridine and are at low risk for bleeding.
If the decision is made to implement an invasive strategy, dual antiplatelet therapy should be started upon presentation in medium- to high-risk patients. Dual platelet therapy should include aspirin plus one of the following: clopidogrel or an I.V. GP IIb/IIIa inhibitor (either eptifibatide or tirofiban). Prasugrel may be used in place of clopidogrel if clopidogrel hasn't been administered prior to PCI. If bivalirudin is chosen as the anticoagulant used intraprocedure and the patient has already received an oral loading dose of clopidogrel 6 hours prior to PCI, administration of IIb/IIIa inhibitors can be eliminated.1
In addition to aspirin, a continuous infusion of eptifibatide is prescribed for GJ. His platelet count will be checked in 4 hours. The nurse places GJ on bleeding precautions and teaches him signs and symptoms of bleeding. The nurse encourages GJ's wife to bring in an electric razor because shaving with a straight razor may cause bleeding.
Over the past several years, multiple studies have looked at the interaction between clopidogrel and proton pump inhibitors (PPIs) such as omeprazole, lansoprazole, pantoprazole, rabeprazole, and esomeprazole. Providers prescribe PPIs to help reduce the gastrointestinal adverse reactions of dual antiplatelet therapy, such as ulceration and related bleeding, and to allow therapy to continue for the recommended 12-month period.
The studies have had mixed results. Some indicate that PPIs, omeprazole in particular, interfere with clopidogrel's antiplatelet function.4,5 Other studies refute this.6,7 Although the updated guidelines don't prohibit the use of PPIs in patients taking clopidogrel, they advise providers to weigh the risks versus the benefit.8 Other medications, such as H2 blockers, may be an alternative. Instruct the patient not to take any over-the-counter medications, in particular omeprazole, without the healthcare provider's approval.
When patients with chronic kidney disease (CKD) undergo PCI, intravascular contrast media can worsen kidney function. In the 2007 guidelines, isosmolar contrast agents were recommended as the preferred agent for patients with CKD. Since that time, many studies that looked at the development of contrast-induced nephropathy (CIN) have shown that the choice between isosmolar and low-osmolar contrast agents doesn't affect the rate of development of CIN or the worsening of renal function.9 For patients with CKD, the focus should be on adequate hydration and the total contrast volume administered. Several hydration protocols are available, and the ACCF/AHA doesn't recommend a particular regimen.1
When caring for a patient who will undergo PCI, notify the healthcare provider if creatinine is more than 1.5 mg/dL (normal, 0.6 to 1.2 mg/dL for males; 0.4 to 1.0 mg/dL for females) or estimated glomerular filtration rate (GFR) is less than 60 mL/minute to discuss an appropriate hydration protocol for the patient preprocedure. Intraprocedure, the cath lab nurse needs to be aware of the amount of contrast used and communicate that volume to the cardiologist. The goal is to limit the total dose.
Acetylcysteine is commonly used off-label to help prevent CIN. However, the mechanism of action isn't well understood and studies on its use as a nephroprotective agent are mixed. The guidelines make no recommendations for or against the use of acetylcysteine for CIN.
The basic metabolic profile shows that GJ's creatinine is 1.7 mg/dL. In anticipation of coronary angiography and PCI in the next 6 to 12 hours, the nurse administers oral acetylcysteine and initiates an I.V. infusion of 0.9% sodium chloride at 150 mL/hour, as prescribed. The nurse provides preprocedure patient education, including the rationale for the medication.
The 2004 and 2007 guidelines recommended strict glycemic control to achieve a preprandial blood glucose of less than 100 mg/dL and a daily goal of less than 180 mg/dL. After release of the 2007 guidelines, the Normoglycemia in Intensive Care Evaluation-Survival Using Glucose Algorithm Regulation (NICE-SUGAR) trial demonstrated that strict glycemic control increases the risk of death at 90 days, most likely related to episodes of hypoglycemia.10 In addition, the American Association of Clinical Endocrinologists and the American Diabetes Association (ADA) have released consensus statements suggesting that the reduction in blood glucose and not the intensive use of insulin is what improves outcomes following MI. The ACCF/AHA consensus writers have concluded more research is needed.
Until further studies are available, the recommendation from the 2004 and 2007 guidelines have been deleted and healthcare providers are referred to the ADA guidelines. In addition, a recommendation to maintain blood glucose levels at less than 180 mg/dL with the goal of avoiding hypoglycemia has been added.
Closely monitor any patient with UA/NSTEMI for both hypo- and hyperglycemia. The patient should be able to demonstrate competency with blood glucose testing and insulin administration (if indicated), preferably by return demonstration. Review signs and symptoms of hypo- and hyperglycemia and treatment with the patient and make sure the patient can verbalize understanding.
Metformin is held in anticipation of coronary angiography. Patients receiving contrast media are at risk for CIN. If a patient receiving metformin develops CIN, the patient is at increased risk for development of lactic acidosis, so the recommendation is to hold metformin before the procedure and for 48 hours postprocedure. It may be safely resumed when normal renal function is confirmed.
GJ's blood glucose is 300 mg/dL and the nurse administers insulin as prescribed. The patient and his wife are concerned that he may need to go home on insulin. The nurse explains the rationale for holding the metformin and reviews signs and symptoms of hypo- and hyperglycemia and treatment with GJ and his wife.
GJ proceeds to the cardiac catheterization suite, where access is gained via the right femoral artery. Findings include nonobstructive stenoses of the right coronary and circumflex artery, and 95% stenosis of the left anterior descending (LAD). A DES is placed in the LAD. Because GJ's serum creatinine was elevated preprocedure, the cath lab nurse communicates with the cardiologist regarding the amount of contrast administered throughout the procedure and ensures that I.V. hydration continues. Prasugrel is administered at the end of the procedure.
When the patient returns to the progressive care unit, the nurse provides postprocedure care, including assessment of vital signs, pain intensity rating, neurovascular function, and access site every 15 minutes for 1 hour, every 30 minutes x2, then hourly x4. The nurse also documents accurate intake and output. A repeat ECG shows resolution of ischemic changes and no pathologic Q waves, which would indicate an MI.
Besides the recommended changes discussed, be aware that many of the previous guidelines are unchanged. For example, NTG should be taken for episodes of chest discomfort. On discharge, instruct patients on the use of sublingual NTG. Teach patients with known or suspected ACS to call EMS immediately if chest discomfort continues or worsens 5 minutes after one dose, then take another sublingual dose (rather than waiting to call EMS after taking three doses without relief). Teach patients with chronic stable angina that if one NTG dose eases the pain, they should take another dose every 5 minutes to a maximum of three doses, and call EMS if pain doesn't resolve completely after three doses.1
Beta-blockers remain a mainstay of medical therapy. They should be started within the first 24 hours unless the patient has signs of heart failure, is hemodynamically unstable, or has a relative contraindication (such as active asthma). Beta-blockers help to slow the heart rate, which decreases myocardial workload and myocardial oxygen demand. They also lower mortality in patients undergoing PCI and are a secondary prevention strategy.1,11
Patients should undergo left ventricular function evaluation before discharge, via 2-D echocardiogram, radionuclide angiogram, or left ventriculogram. If the ejection fraction is less than 40%, the patient exhibits signs of heart failure, or the patient is hypertensive, an angiotensin-converting enzyme inhibitor or angiotensin receptor blocker should be added to the medication regimen, unless contraindicated. (Expressed as a percentage, the ejection fraction is the proportion of left ventricular end-diastolic volume ejected from the left ventricle during systole.12)
The next day, GJ's access site and serum creatinine are stable. He walks around the cardiac unit and doesn't experience any cardiac dysrhythmias. His 2-D echo reveals an ejection fraction of 50% (normal, 60% to 75%). At discharge, GJ is continued on aspirin, clopidogrel, a beta-blocker, and a statin, and is instructed to restart metformin on day 3 post-PCI.
The nurse educates GJ and his wife about the importance of continuing dual platelet therapy as prescribed. GJ can verbalize the signs and symptoms of bleeding. Fortunately, the patient has a prescription plan and prasugrel is on formulary.
As the landscape of cardiovascular disease management changes, nurses must be able to quickly review new standards and guidelines and adapt them to practice. Educating patients with UA/NSTEMI about their condition and prescribed treatment will help them manage their condition after discharge and recognize signs and symptoms requiring immediate intervention in the future.
Released in 2011, ticagrelor is a P2Y12 platelet inhibitor used in UA/NSTEMI patients to prevent thrombosis. It's used in combination with low-dose aspirin-use of full-strength aspirin with ticagrelor has been shown to decrease ticagrelor's efficacy. Major adverse reactions include bleeding and dyspnea, which is usually self-limited. If a patient is expected to undergo CABG surgery, hold ticagrelor for at least 5 days preprocedure.
Before a patient is discharged on antiplatelet/anticoagulant therapy, review signs and symptoms of bleeding; for example, nosebleeds, black tarry stools, easy bruising or purple spots on the skin, blood in the urine, coughing up or vomiting blood or material resembling coffee grounds, and feeling weak or dizzy. The patient should immediately contact the healthcare provider or call 911 if bleeding develops. The healthcare provider will weigh the risk of bleeding versus the benefit of the medication to determine if the dosage should be adjusted or the medication discontinued.
1. Wright RS, Anderson JL, Adams CD, et al. 2011 ACCF/AHA focused update of the Guidelines for the Management of Patients with Unstable angina/non-ST-elevation Myocardial Infarction (updating the 2007 guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2011;123(18):2022-2060. [Context Link]
2. Effient (prasugrel) tablets. Highlights of prescribing information. http://pi.lilly.com/us/effient.pdf. [Context Link]
3. Wiviott SD, Braunwald E, McCabe CH, et al. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007;357(20):2001-2015. [Context Link]
4. Juurlink DN, Gomes T, Ko DT, et al. A population-based study of the drug interaction between proton pump inhibitors and clopidogrel. CMAJ. 2009;180(7):713-718. [Context Link]
5. Ho PM, Maddox TM, Wang L, et al. Risk of adverse outcomes associated with concomitantuse of clopidogrel and proton pump inhibitors following acute coronary syndrome. JAMA. 2009;301(9):937-944. [Context Link]
6. Ramirez JF, Selzer F, Chakaprani R, et al. Proton pump inhibitor and clopidogrel combination is not associated with adverse clinical outcomes after PCI: the NHLBI dynamic registry. J Am Coll Cardiol. 2009;53(suppl A):A27-A28. [Context Link]
7. Simon T, Verstuyft C, Mary-Krause M, et al. Genetic determinants of response to clopidogrel and cardiovascular events. N Engl J Med. 2009;360(4):363-375. [Context Link]
8. Abraham NS, Hlatky MA, Antman EM, et al. ACCF/ACG/AHA 2010 expert consensus document on the concomitant use of proton pump inhibitors and thienopyridines: a focused update of the ACCF/ACG/AHA 2008 expert consensus document on reducing the gastrointestinal risks of antiplatelet therapy and NSAID use. J Am Coll Cardiol. 2010;56(24):2051-2066. [Context Link]
9. Rudnick MR, Davidson C, Laskey W, Stafford JL, Sherwin PF; VALOR investigators. Nephrotoxicity of iodixanol versus ioversol in patients with chronic kidney disease: the Visipaque angiography/interventions with laboratory outcomes in renal insufficiency (VALOR) trial. Am Heart J. 156(4):776-782. [Context Link]
10. Finfer S, Chittock DR, Su SY, et al. Intensive versus conventional glucose control in critically ill patients. N Engl J Med. 2009;360(13):1283-1297. [Context Link]
11. Ellis K, Tcheng JE, Sapp S, Topol EJ, Lincoff AM. Mortality benefit of beta blockade in patients with acute coronary syndromes undergoing coronary intervention: pooled results from the Epic, Epilog, Epistent, Capture and Rapport trials. J Interv Cardiol. 2003;16(4):299-305. [Context Link]
12. Porth CM. Essentials of Pathophysiology. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2011. [Context Link]
13. Brilinta (ticagrelor). Highlights of prescribing information. http://www1.astrazeneca-us.com/pi/brilinta.pdf. [Context Link]
14. Wallentin L, Becker RC, Budaj A, et al. Ticagrelor versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2009;361(11):1045-1057. [Context Link]
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