Critical Care Services Updates

Never events

2011-02-16T04:32:00.000-08:00

http://www.nursingcenter.com/pdf.asp?AID=1100852\

What are they and how do we as front line nurses prevent them?

Interesting concept...needs more studies

2010-11-24T05:22:00.000-08:00

Nebulized Heparin in Mechanically Ventilated Patients
Gregory S. Martin, MD, MSc
Authors and Disclosures
Posted: 11/16/2010
$(document).ready(function() {adexGet('/ratetopcontent?contentId=732196','adexratethiscontainertop','autoloadwait1',undefined,handleFetchRatingTop);});
Nurse Rating:
( 0 Votes )

Rate This Article:

Print This
Email this
Share
Facebook Twitter

processing....

Nebulized Heparin Is Associated With Fewer Days of Mechanical Ventilation in Critically Ill Patients: A Randomized Controlled Trial
Dixon B, Schultz MJ, Smith R, Fink JB, Santamaria JD, Campbell DJCrit Care. 2010;14:R180
Study Summary
Ventilator-induced lung injury (VILI) is an important and relatively common condition among mechanically ventilated patients. Dixon and associates sought to determine if nebulized heparin might improve lung function by reducing pulmonary inflammation and fibrin deposition. This may be particularly important in patients most likely to develop VILI, such as those who require prolonged mechanical ventilation.
The investigators randomly assigned 50 patients who were expected to require mechanical ventilation for > 48 hours to receive either nebulized heparin (25,000 U) or placebo (normal saline) every 4 or 6 hours, depending on patient height, for a maximum of 14 days while mechanically ventilated. They found that nebulized heparin was not associated with any adverse events and did not improve oxygenation. There was no difference in survival, but patients treated with nebulized heparin had more days alive and free of mechanical ventilation (ventilator-free days at day 28: 22.6 vs 18.0, P = .02). On the basis of these results, the investigators concluded that nebulized heparin is associated with fewer days of mechanical ventilation in critically ill patients expected to require prolonged mechanical ventilation, and further trials are required to confirm these findings.
Viewpoint
This randomized clinical trial suggests that nebulized heparin may benefit critically ill mechanically ventilated patients. There are certainly other reports of potentially beneficial effects of anticoagulation in critically ill patients, including the US Food and Drug Administration-approved drug recombinant human activated protein C used to treat severe sepsis. Moreover, heparin use has specifically been associated with improved outcomes in critically ill patients with septic shock. However, little or no data have demonstrated the efficacy of nebulized heparin for mechanically ventilated patients. Although the novelty of this study makes the findings exciting, it also raises more questions about validity and clinical application. At present, there is no reason to be administering nebulized heparin to critically ill patients. As Dixon and associates conclude, these findings require replication to ensure their accuracy. While we wait for more data, how might we judge the veracity of the findings? Could nebulized heparin have truly reduced the duration of mechanical ventilation? One method is to apply specific criteria to strengthen the hopeful cause-and-effect association:
There is a clear temporal relationship, as always in a prospective treatment trial, between the intervention and the outcome;
The strength of the association is reasonably strong, with a 4.6-day (21%) reduction in the duration of mechanical ventilation;
There is biologic plausibility, with mechanistic considerations;
Pre-existing data suggest benefits in other populations;
In a randomized, controlled trial, few other (confounding) variables explain these findings;
No dose-response testing was done to strengthen the relationship; and
Findings have less coherence to existing paradigms on methods to shorten the duration of mechanical ventilation.
Kudos to the investigators for exploring this new world and opening the door to a potential new therapy!
Abstract

CEU review of Anticoagulants

2010-10-22T16:25:00.000-07:00

http://www.nursingcenter.com/library/JournalArticle.asp?Article_ID=1047254

You asked for it....

2010-06-26T17:34:00.000-07:00

For those of you who want to purchase your very own TAMC CCU logo gear I created a shop at cafe press with tee's, sweatshirt etc. You are part of an specially trained few in our organization so if you are as proud of the care we provide as I am, here's your opportunity to show it.

http://www.cafepress.com/TAMCCCU

2010-06-09T10:44:00.000-07:00

Mutual Respect is necessary to maintain dialogue. From the moment respect is at risk, the conversation is no longer about getting results and dialogue comes to a screeching halt.
Why? Because respect is like air: if you take it away, it's all people can think about. At that point, the conversation is all about defending dignity.
Use these telltale signs to recognize when respect is at risk during a conversation, and address that issue before trying to resolve the content of the conversation.

• Interruptions
• Pouting
•Name-calling
• Looks of pain, fear, or hurt feelings
• Anger
• Yelling
• Insults
• Threats

CAM ICU assessment

2010-05-09T15:10:00.000-07:00

http://docs.google.com/Doc?docid=0Aa1VeiReh57PZGZ4NjZ6cXFfMTU5ejdmc3g0Y2s&hl=en

2010-04-17T18:32:00.000-07:00

New Read...

2010-03-31T04:32:00.001-07:00

HTN urgency medicine article, peritnent given the volume of patients we have seen with this lately. A real shocker I found as I was reading through the article was this one....who knew?

i.v. nicardipine with i.v. sodium nitroprusside for the treatment of hypertensive emergency in a randomized trial of 40 patients. Significant reductions in SBP and DBP were observed in both groups, with no significant time-dependent differences between groups. Patients randomized to nicardipine had a greater drop in noradrenaline levels compared with patients treated with sodium nitroprusside.
Definetly safer given the thiocy-anate toxicity effects of Nipride.
http://www.medscape.com/viewarticle/715621_2

Newest of the new

2010-02-20T10:15:00.000-08:00

And along with the new heart monitors comes the ability to computerize our documentation! So iNet is coming in June. Some new assessment tools will need to be learned~ CAM and MAAS scores instead of Ramsey-check you email for more info on those tools-I'm having issues getting the images to show on here.

just a few images of installation day-we wouldn't have survived without a little therapeutic chocolate.

New Torsdes des Pointes AHA info

2010-02-20T09:55:00.000-08:00

http://circ.ahajournals.org/cgi/reprint/CIRCULATIONAHA.109.192704

There is a great table in there with drugs that induce torsades as well as QT and QTC measurements.

Are you thinking of Certification?

2010-01-18T06:22:00.000-08:00

http://www.aacn.org/DM/MainPages/CertificationHome.aspx

An optimist is a person who sees a green light everywhere, while a pessimist sees only the red stoplight... The truly wise person is color-blind.
Albert Schweitzer

Happy Holidays to each of you

2009-12-17T15:54:00.001-08:00

wishes for you......

that you come away from each shift feeling that you have made a difference in someone's care.
that you enjoy, truly enjoy, the people you work with-we may do the job differently but somehow, someway we all came into this to take care of people
that a patient makes your day in some small way
that you know you are valued in our unit, our organization but most of all by the community we serve
that your families know that we appreciate each and every time you come in extra, pick up the phone knowing that it's us asking to give more time to make the team work smoothly
that we encourage each other to be the best we can be, growth and change are part of the cycle of learning~is your wheel turning?
that during the holidays you spend time with your families and friends to restore your spirit
have a Merry Christmas and a Happy New Year!

Precedex for sedation

2009-12-15T16:56:00.000-08:00

http://precedex.hospira.com/default.aspx

Please review in light of Diprivan shortage you will probablybe seeing more of this used in the ventilator patients.

Open Chart Reviews

2009-12-03T07:29:00.000-08:00

Hey all-Chart reviews-you will find a book with the sheets in it to compete 2 per month along with a chart for you to check off once yours are complete for each RN. There is a reminder chart on the evolving new breakroom door. that resembles the one in the book.

Documentation resource

2009-11-13T08:06:00.000-08:00

You are all aware of issues concerning documentation. As we progress toward a totally integrated computer document (the first step is getting the new bedside monitors installed so that they communicate to Powerchart) I feel it is time to reemphasize the content of the infomantion we enter into the chart. This is an excellent site that discusses documentation and legalities. Please take some time to review it-I think you will find it helpful in your everyday practice.

http://www.corexcel.com/html/documentation.title.ceus.htm

H1N1 for professionals

2009-11-10T09:51:00.000-08:00

Nurses Air Flu FearsSome are skeptical about the new H1N1 vaccine, while infection control experts work to dispel 'myths'. By Joe Darrah
The debate concerning mandatory flu vaccinations for healthcare workers is likely to intensify as deadlines to receive them are enforced in New York and within various healthcare organizations across the country that are requiring vaccination.
Heated comments at the ADVANCE for Nurses Facebook page reveal a range of views on the topic among nurses, many strongly held. Some have no problem with the mandate and see it as the best way to increase the number of healthcare employees who are vaccinated. However, others express outrage at the idea they are being forced into vaccination, citing their concerns the vaccine can actually cause flu and their belief the mercury used in the shot can be linked to dementia and Alzheimer's. Additionally, many nurses have taken the opportunity to voice these same opinions through letters, phone calls, e-mails and comments at the ADVANCE for Nurses Web site.
"The myth that you can get sick from the flu vaccine is alive and well, and I don't know why," said Bill Schaffner, MD, chairman of the department of preventive medicine at Vanderbilt University and president-elect of the National Foundation for Infectious Diseases. "These are the same nurses who go through wonderful scientific training and use scientific principles in everything that they do. So, why would they have particular concern about this scientifically proven [vaccination] as opposed to other science-based treatments they tell their patients to take?"
But where do we draw the line separating myth and fact? How could certain segments of the nursing population believe their health is at risk by receiving the very vaccinations they offer and administer to their patients?
ADVANCE has attempted to get the answers to these questions.
H1N1 Fears
Particular concern recently expressed among nurses surrounds the soon-to-be-available vaccine for H1N1. Specific dates for the release of this vaccination have not been released by CDC officials, but a number of nurses have already contacted ADVANCE expressing fears of getting vaccinated specifically for H1N1 (the CDC has stated the H1N1 vaccine will be separate from the 2009 seasonal vaccination that's now available) because they believe it's being rushed. Many point to deaths reportedly associated with an H1N1 vaccine produced in 1976 - incidences that have been widely documented and refuted by some - as their evidence.
Among them is Melody Bowers Metz, RN, a critical-care nurse working in Ohio. A 2005 nursing graduate, Metz, 52, told ADVANCE she does receive the seasonal shot each year, but has real concerns regarding the H1N1 vaccine.
"In my honest opinion, the government and FDA rushed this through way too fast, and I am very leery about whether it is safe or not," she said. "It takes well over a year for a vaccine to be developed for the upcoming 'next' year and it is thoroughly tested. Those are the concerns that I personally have, and I will not be receiving the H1N1 vaccine."
Schaffner says she and anyone sharing the same sentiments are off base.
"They're just wrong," he said. "H1N1 is nothing new to us. To reach back to one unfortunate episode 33 years ago and say 'for that reason I'll never take flu vaccine' is like saying 'there was a plane crash in 1976; I'll never fly again.' We have 33 years of safety and lives saved, and we made this vaccine just the way we made other ones."
In fact, Schaffner said the regular trivalent seasonal influenza vaccine for 2009 contains killed H1N1 virus.
"I wonder if most know that?" he mused.
Metz told ADVANCE she didn't, but had already received her shot this year, so there's not much she can do.
"Knowing this in advance, no, I would not get the vaccine," she said.
Schaffner blames a lack of education for instances such as these.
"I think people have misunderstandings about flu," he said. "I think the major misunderstanding is this idea that you can know for sure you have it and you can segregate yourself until it's gone. All of our statistics show that doesn't work - that people have mild or asymptomatic illnesses, and that's probably when they're most at risk for spreading it. And that's the point we're trying to get across."
CDC Warnings
Though the CDC provides an abundance of information on the flu, it can come off as confusing, especially when addressing the issue of whether or not flu vaccine can cause illness. Officials clearly indicate the vaccine can cause side effects (beyond allergic reactions) that vary in degree depending on whether one receives the injected or nasal spray form.
While the injection form is made with inactivated virus, the nasal spray does include a live, albeit weakened, form, according to the CDC. Potential side effects to both vaccine varieties include low-grade fever.
So, who's not to say this getting a fever isn't a definition of being "sick?"
Janet Keen, MS, RN, CIC, director of infection prevention and control at Piedmont Hospital, Atlanta, offers clarification.
"A low fever is the body's normal response to making the antibodies that will protect it against flu," she said. "Typically, with influenza, you have a pronounced fever that lasts more than a day. There's a difference between being sick and not feeling well. The risk of acquiring the flu far outweighs the risks of experiencing serious side effects from the vaccination."
This is said to be true even of the nasal form.
Preference vs. Responsibility
"I encourage any nurse who feels uncomfortable with the vaccine to research it, to look at the CDC and other professional literature," Keen said.
At Piedmont Hospital, nursing staff is not currently required to receive either seasonal or H1N1 vaccination, but they're encouraged to, Keen said. She and hospital administrators have also established a mandatory educational program for all employees regarding flu.
"It dispels some of the myths and helps promote compliance with vaccination; and it's really helped," she said.
Concerning the use of mercury in the vaccine, Keen said she "hasn't read compelling literature that supports that."
Schaffner said nurses should weigh their preferences against their responsibilities.
"[Not getting the flu vaccine] is an example where the healthcare worker's interests are being put ahead of the interests of patients, and that's not the tradition of healthcare," he said. "The nurses I've worked with didn't run out of the hospital when we had patients with HIV or SARS or were exposed to anthrax - that's the kind of spirit I want to call forth from nurses and doctors now."
Joe Darrah is senior associate editor at ADVANCE.

Troponin

2009-10-18T08:24:00.001-07:00

Troponin-Based Risk Stratification of Patients With Acute Nonmassive Pulmonary Embolism
Systematic Review and Metaanalysis
David Jiménez, MD,
Fernando Uresandi, MD,
Remedios Otero, MD,
José Luis Lobo, MD,
Manuel Monreal, MD,
David Martí, MD,
Javier Zamora, MD,
Alfonso Muriel, MD,
Drahomir Aujesky, MD and
Roger D. Yusen, MD, FCCP
+ Author Affiliations

From the Respiratory Department (Dr. Jiménez), the Cardiology Department (Dr. Martí), and the Biostatistics Unit (Drs. Zamora and Muriel), Ramón y Cajal Hospital, Madrid, Spain; the Respiratory Department (Dr. Uresandi), Cruces Hospital, Bilbao, Spain; the Respiratory Department (Dr. Otero), Virgen del Rocío Hospital, Sevilla, Spain; the Respiratory Department (Dr. Lobo), Txagorritxu Hospital, Vitoria, Spain; the Medicine Department (Dr. Monreal), Germans Trias i Pujol Hospital, Barcelona, Spain; the Division of General Internal Medicine (Dr. Aujesky), University of Lausanne, Lausanne, Switzerland; and the Divisions of Pulmonary and Critical Care Medicine and General Medical Sciences (Dr. Yusen), Washington University School of Medicine, St. Louis, MO.
David Jiménez, MD, Respiratory Department, Ramón y Cajal Hospital, Colmenar Rd, Kilometer 9.100, 28034 Madrid, Spain; e-mail: djc_69_98@yahoo.com
Abstract
Background: Controversy exists regarding the usefulness of troponin testing for the risk stratification of patients with acute pulmonary embolism (PE). We conducted an updated systematic review and a metaanalysis of troponin-based risk stratification of normotensive patients with acute symptomatic PE. The sources of our data were publications listed in Medline and Embase from 1980 through April 2008 and a review of cited references in those publications.
Methods: We included all studies that estimated the relation between troponin levels and the incidence of all-cause mortality in normotensive patients with acute symptomatic PE. Two reviewers independently abstracted data and assessed study quality. From the literature search, 596 publications were screened. Nine studies that consisted of 1,366 normotensive patients with acute symptomatic PE were deemed eligible. Pooled results showed that elevated troponin levels were associated with a 4.26-fold increased odds of overall mortality (95% CI, 2.13 to 8.50; heterogeneity χ2 = 12.64; degrees of freedom = 8; p = 0.125). Summary receiver operating characteristic curve analysis showed a relationship between the sensitivity and specificity of troponin levels to predict overall mortality (Spearman rank correlation coefficient = 0.68; p = 0.046). Pooled likelihood ratios (LRs) were not extreme (negative LR, 0.59 [95% CI, 0.39 to 0.88]; positive LR, 2.26 [95% CI, 1.66 to 3.07]). The Begg rank correlation method did not detect evidence of publication bias.
Conclusions: The results of this metaanalysis indicate that elevated troponin levels do not adequately discern normotensive patients with acute symptomatic PE who are at high risk for death from those who are at low risk for death.
Footnotes
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).

New Heparin Reference Standard

2009-10-15T15:10:00.000-07:00

Heparin: Change in Reference Standard
Audience: Pharmacists, physicians, hospital risk managers and consumers
[Posted - 10/01/2009] FDA notified healthcare professionals and patients of a change to heparin, effective October 1, 2009, which will include a new reference standard and test method used to determine the potency of the drug and able to detect impurities that may be present in heparin. The change, which will also harmonize the USP unit dose with the WHO International Standard unit dose, will result in approximately a 10% reduction in the potency of the heparin marketed in the United States.
This may have clinical significance in some situations, such as when heparin is administered as a bolus intravenous dose and an immediate anticoagulant effect is clinically important. Healthcare providers should be aware of the decrease in heparin potency as they monitor the anticoagulant effect of the drug; more heparin may be required to achieve and maintain the desired level of anticoagulation in some patients.
There will be simultaneous availability of heparin manufactured to meet the “old” and “new” USP monograph, with potential differences in potency. Products using the new “USP unit” potency definition are anticipated to be available on or after October 8. FDA is working with the manufacturers of heparin to ensure that an appropriate identifier is placed on heparin made under the new USP monograph. Most manufacturers will place an “N” next to the lot number. FDA is also working with the heparin manufacturers to study the impact of this variation in potency and will make the results available when the studies have concluded.
[10/01/2009 - Public Health Alert - FDA]
[10/01/2009 - Information for Consumers - FDA]

Chest Tubes

2009-10-01T15:17:00.000-07:00

American Heart for Healthcare Professionals

2009-08-24T11:45:00.000-07:00

http://www.americanheart.org/presenter.jhtml?identifier=3052043

All kinds of info on this site for all of us-there is also a section for patients and for home patient caregivers-very nicely done and organized as all AHA materials are.

http://pt.wkhealth.com/pt/re/aha/addcontent.11568289.htm;jsessionid=KSgMjhKL2nyJ0T0G5JpmbJ1TyLpn1k2FfsB26Ykp4KXX2vy5XKJQ!1642465697!181195628!8091!-1
Great article on Drug Eluding Stents on patients with Afib

2009-07-15T17:03:00.000-07:00

Biomarkers in Acute Cardiovascular Disease
Jill Howie-Esquivel PhD, RN, NP Megan White RN, MS, ACNP
Journal of Cardiovascular NursingMarch/April 2008 Volume 23 Number 2Pages 124 - 131

Jill Howie-Esquivel, PhD, RN, NP Associate Clinical Professor and Nurse Practitioner, Department of Physiological Nursing, University of California, San Francisco.
Megan White, RN, MS, ACNP Nurse Practitioner Cardiology, Bluhm Cardiovascular Institute, Northwestern Memorial Hospital, Chicago, Illinois.
Corresponding author Jill Howie-Esquivel, PhD, RN, NP, School of Nursing, University of California, #2 Koret Way, Box 0610, San Francisco, CA 94143 (jill.howie-esquivel@nursing.ucsf.edu).
Keywords: biomarkers, BNP, troponin
Abstract
Cardiovascular disease today remains a formidable foe affecting 1 in 3 Americans. The emergence of cardiac biochemical markers has provided clinicians unique insight into the state of the myocardium. In fact, cardiac biomarkers now represent an essential criterion in the definition of acute myocardial infarction. There has been impressive development of efficient and reliable assays to detect biomarkers in the serum. Together with patient history and electrocardiographic analysis, the invaluable information gained from serum cardiac biomarkers supports diagnosis, therapy selection, and determination of prognosis. Biomarkers such as troponin and creatine kinase MB have received well-deserved attention for their ability to detect myocardial ischemia. Clinicians today use cardiac markers to identify ischemia as well as alternate clinical states. B-type natriuretic peptide, for instance, reflects myocardial stretch as seen in heart failure exacerbations and may well have promising prognostic significance. The purpose of this review is to discuss current and emerging cardiac biomarkers in acutely ill patients. The advantages and disadvantages of biomarkers will also be presented in the context of their clinical uses. Present markers are highly sensitive and specific to myocardial injury; however they do not specifically identify the method of injury. An exciting potential exists for future biomarkers to demonstrate enhanced specificity and earlier detection of compromised myocardium.

Cardiovascular disease occurs in an estimated 79.4 million or in 1 of 3 American adults.1 Data from the Framingham Heart Study indicate the lifetime risk for cardiovascular disease is 2 in 3 for men and greater than 1 in 2 for women at age 40. Nearly 2,400 Americans die of cardiovascular disease each day with more lives claimed than from cancer, chronic respiratory diseases, accidents, and diabetes mellitus combined.1 Although this is the age of technological revolution, cardiovascular disease continues to account for more deaths than any other cause of death since 1900 (except 1918).
Each day millions of patients with dyspnea and chest pain present to emergency departments (EDs) with a substantial portion of them suffering from noncardiac conditions. The consequences for missing an evolving myocardial infarction (AMI) or acute exacerbation of heart failure (HF) may have severe adverse outcomes. Accordingly, there are unnecessary admissions to the hospital when discharge might be just as appropriate. Diagnostic challenges are experienced for patients with these cardiac conditions, but the emergence of biomarkers has improved the clinician's arsenal for detection.
For a biomarker to be clinically useful, it needs to assist in diagnosis, define prognosis, or guide therapy.2 Ideally, a biomarker in the acute care setting defines risk so appropriate disposition decisions can be made and subsequent events minimized.3 Although new biomarkers bring hope, an understanding of their function and limitations is important. The purpose of this review is to discuss current and emerging cardiac biomarkers in acutely ill patients. A description of current biomarkers, their strengths and limitations, and a summary of their clinical use will be provided followed by a discussion of future biomarkers that may provide promise.
Investigations of biomarkers have uncovered greater understanding related to the process of vascular inflammation (see Figure 1 ). For example, proinflammatory cytokines, such as interleukin-6, are present upstream from markers of ischemia and necrosis, that is, they are present before the ischemic event occurs and are not implicated in unstable angina (UA) at this time.3 In contrast, B-type natriuretic peptide (BNP) is present with myocardial stretch suggesting myocardial dysfunction, an event that can occur as a result of ischemia. Although new biomarkers such as cardiac troponins have greatly enhanced diagnostic accuracy, issues remain (Table 1 ). When evaluating a new analyte, there is bias in favor of positive reports. A negative evaluation of a biomarker is unlikely to be the first published report on that biomarker, and therefore, once a positive report is published, negative reports are less likely to be published because of comparisons with the positive reports.2,3 FIGURE 1. Biomarkers in vascular inflammation (adapted with permission from Apple et al 3 ). IL-6 indicates interleukin 6; TNF-[alpha], tumor necrosis factor alpha; MMP-9, metalloproteinase-9; MPO, myeloperoxidase; sSSCD40L, soluble SSCD40 ligand; PAPP-A, pregnancy-associated plasma protein A; CRP, C-reactive protein; IMA, ischemia-modified albumin; cTnT, cardiac troponin T; cTnI, cardiac troponin I; BNP, brain natriuretic peptide; NT-proBNP, N-terminal proBNP. *Biomarkers covered in this review.
TABLE 1 New Biomarker Questions

The acute coronary syndromes (ACS) broadly encompass the clinical states UA, ST elevation myocardial infarction, and non-ST elevation myocardial infarction. Each diagnosis is united by common pathophysiologic characteristics that include atherosclerotic plaque formation, rupture, thrombus formation, and ultimately discontinuous blood flow and compromised myocardium.4 The differentiation among the 3 states is made based on the degree of blood flow limitation and thus the extent of myocardial damage. Determining the latter is not always easy and requires information gathered from patient history, electrocardiogram (ECG), the measurement of cardiac biomarkers, and cardiac imaging. Chest pain characterized by varying duration and severity is commonly found in a patient experiencing ACS. However, chest pain may also not be cardiac in nature, making the differential diagnosis vast and complicated. Although the ECG is an invaluable diagnostic tool, in isolation it is neither sensitive nor specific enough to make a definitive diagnosis. A normal ECG, although reassuring, does not rule out an acute AMI.
Biomarkers may have the ability to detect ischemia earlier and with greater sensitivity than ECG changes, which may not happen until irreversible damage has occurred. In fact, the ECG is diagnostic only 40% of the time.5 Biochemical markers for ischemia include myoglobin, lactate dehydrogenase, cardiac troponin, and creatinine kinase (CK), and its subform creatinine kinase MB (CKMB). Cardiac troponin and CKMB are current biomarkers discussed here and may well enhance the clinician's ability to detect ischemic episodes earlier. Determining the diagnosis of AMI using cardiac troponin or CKMB provides higher sensitivity and specificity, when compared with past biomarkers, to detect myocardial-related ischemia or necrosis. The sensitivity of a biomarker provides an understanding of the proportion of people who truly have a disease, whereas specificity refers to the proportion of people who aretruly free of a disease.6 A test that provides a sensitivity and specificity of 100% will ensure with certainty that a person who has a disease will test positively (sensitivity) and a person without the disease will test negatively (specificity). An example where cardiac biomarkers have provided a diagnostic edge over the standard ECG is in a patient who presents with a non-ST elevation myocardial infarction and a clinical history suggestive of coronary disease. Additional information as provided by serum biomarkers has proven helpful in elucidating a final diagnosis, as well as risk-stratifying patients with ACS for future events.
Cardiac Troponin
Troponin T or I is superior to other markers for the diagnosis of AMI due to its cardiac specificity.7 Sensitivity is also improved because this assay will detect even minimal myocardial damage. Initial investigations into troponin considered the role it played in regulating cardiac muscle contraction. It is recommended that an elevation of troponin significant to detect necrosis exceed the 99th percentile of troponin values in a reference control group within 24 hours of the clinical event (ie, chest pain).7 Troponin is prognostic in addition to diagnostic as the higher the troponin level, the greater the infarct and poorer predicted outcome. Also, the longer the troponin is elevated, the more severe the infarct. Several reports have demonstrated in both ST elevation myocardial infarction and non-ST elevation myocardial infarction patients that troponin elevations are indicative of more extensive disease and ultimately higher mortality rates.8 Troponin is released 4 to 12 hours after myocardial necrosis, peaking at approximately 12 to 48 hours from initial symptom onset. Troponin is particularly efficient in diagnosing an AMI up to 2 weeks after symptom onset and may remain elevated 10 to 14 days after ischemia onset.9 Troponin may be elevated in a number of conditions not associated with coronary disease and myocardial injury.
However, there are limitations with the troponin biomarker. It does a poor job of detecting reinfarction and is not detectable until myocardial necrosis occurs.9 Troponin elevations may be present when oxygen demand exceeds supply as with sepsis and atrial fibrillation or other tachycardias.8,10 Heart failure may also cause increases in troponin levels, as well as pericarditis, myocarditis, and acute pulmonary embolism due to myocardial strain. Finally, direct cardiac trauma may cause elevated troponins, such as with structural heart disease, contusion, and implantable defibrillator shocks.8,10
Creatinine Kinase/Creatinine Kinase MB
Biomarkers are not a completely novel concept, as they were first reported in 1954 when elevated aspartate transaminase levels were found in patients with AMI.9 However, what has changed is the sensitivity and specificity with which these biochemical markers can detect ischemia. Lactate dehydrogenase and, subsequently, CK were linked to cardiac injury. creatinine kinase is found in skeletal and cardiac muscle, as well as the gastrointestinal tract. Total CK cannot be used alone to diagnose AMI, rather it can be used in combination with a more sensitive marker such as troponin or CKMB.7 Creatinine kinase MB, although useful, is far less specific to cardiac muscle than troponin. Overall, the assay has been found to be less dependable than cardiac troponin. For example, a CKMB elevation may occur in a patient with renal disease, a muscular injury, or myopathy. However, when the troponin assay is not available, CKMB is an appropriate alternative.7 The benefit of CKMB is that it can detect subsequent infarction (after the initial event); however, the assay loses specificity in setting of skeletal muscle injury or cardiac surgery.9 Creatinine kinase MB may rise within 3 to 4 hours of injury and decline to normal levels 24 to 36 hours later. The requirements for CKMB to detect myocardial necrosis are that values from 2 successive blood samples exceed the 99th percentile in a control group.7 For both troponin and CKMB, the recommendation is to draw blood tests serially upon admission, at 6 hours, and at 12 hours.7
The drawback of biomarkers is that they do not reflect the mechanism of injury. For example, after cardiac surgery, a patient may exhibit elevated cardiac enzymes, but the etiology is obscure as the elevation may be from the surgery itself (ie, direct trauma or surgical manipulation) or from an occluded vessel and acute infarction. In addition, in the absence of cardiac ischemia, the clinician must seek alternative differentials, such as myocarditis, HF, or pulmonary embolism. However, one can evaluate the value of marker increase; as the higher the value, the more damage sustained by the myocardium. As is the case of cardiac troponin; the higher the value, the more unfavorable the outcome.
Emerging Biomarkers
BNP and Pro-BNP
B-type natriuretic peptide is a 32-amino-acid peptide released from the ventricles in response to ventricular volume expansion and pressure overload.2 B-type natriuretic peptide is cosecreted with the inactive amino-terminal pro-BNP (NT-proBNP). Cleavage of proBNP produces 2 molecules: BNP, the active molecule, and NT-proBNP, the inactive molecule.11 Left ventricular end-diastolic wall stress and wall stiffness are thought to be the triggers of BNP release, and therefore, BNP is elevated in both systolic and diastolic HF. The severity of ventricular dysfunction determines individual BNP levels.12 Mitral regurgitation also contributes to increases in BNP levels.
The BNP and NT-proBNP values are useful for the detection of HF. B-type natriuretic peptide values <100 class="li-txtcontent" href="http://www.nursingcenter.com/library/static.asp?pageid=798256#68">13 B-type natriuretic peptide levels greater than 500 ng/L HF are very likely, with an associated positive predictive value of 90%. The values between 100 and 500 ng/L, where many patient values lie, have lower predictive value, and accuracy of the biomarker declines. For NT-proBNP values >450 ng/L in patients younger than 50 years, the biomarker is both sensitive and specific for HF.14 For NT-proBNP values >900 ng/L in patients older than 50 years, the biomarker is again both sensitive and specific for HF. Several studies have now demonstrated that, when used in combination with clinical judgment, BNP and NT-proBNP enhance diagnostic accuracy for patients with symptoms of HF.15,16
The potential prognostic value of BNP and NT-proBNP is promising.14,17 Patients with higher values upon hospital admission and at discharge generally have worse outcomes. Those who have substantial reductions in BNP values during treatment have better outcomes. However, the biological variability with BNP suggests that the natriuretic peptide system may take time to up-regulate and down-regulate.2 In other words, the time needed for the system to autoregulate is longer than expected despite the short half-life of both molecules (20 minutes for BNP and 2 hours for NT-proBNP).
The robust associations between natriuretic peptides and outcomes in patients with ACS imply that potential early risk stratification may be possible for patients with myocardial ischemia.14,18 A prospective study of ED patients with chest pain demonstrated that the use of BNP, CKMB, and troponin I used in combination upon admission increased sensitivity and negative predictive value when compared with CK-MB or troponin I alone.19 In addition, when patients had normal troponin I levels, elevated BNP levels were associated with a significantly greater risk of AMI. B-type natriuretic peptide and pro-BNP elevations are prognostic for death in ACS, but data are conflicting for recurrent MI.2 Higher BNP values do identify higher risk patients with ACS, but how this influences treatment is unclear. Only 1 trial has evaluated treatment options. The trial involved BNP or C-reactive protein (CRP) values in women with ACS. Women with elevated BNP or CRP benefited from early percutaneous coronary intervention even when cardiac troponin levels were normal.20 This could be an important adjunct when evaluating patients with ACS.
When BNP and then pro-BNP assays were first introduced, there had never been a blood test for HF; enthusiasm was abundant. Limitations of the biomarker are now evident. Women and older individuals have higher values.21 Those with renal failure have often substantially higher values,22 and obese individuals have lower values.23 This is more pronounced in NT-proBNP levels. Because there is substantial biologic variability, some suggest that if formal values are relied on, values need to half or double to suggest a definite change.2 It is now appreciated that patients with sepsis, volume overload, stroke, cor pulmonale, pulmonary edema, and acute mitral regurgitation have higher BNP and pro-BNP values. Finally, few studies have involved nonwhite or nonwhite ethnicity. Thus, questions arise regarding what are appropriate cutoff values in varied patient populations, genders, and conditions.
B-type natriuretic peptide and pro-BNP provide useful diagnostic information for patients who present to the ED with dyspnea. Patients with acute dyspnea present a challenging and time-consuming workup because the etiology of dyspnea is wide ranging. The prognostic value of BNP and pro-BNP at hospital discharge may also be relied upon to identify patients who will have poorer outcomes, although when these outcomes occur and in which patient populations are not clear. Until the limitations are further defined, BNP and pro-BNP use will be limited.
C-reactive Protein
C-reactive protein (CRP) is an acute-phase reactant (or one that elevates by 25% or more during inflammatory disorders) protein made in the liver.2 In 1997, it was reported that high-sensitivity CRP (hs-CRP) is an independent predictor of AMI and stroke in healthy men.24,25 C-reactive protein provided a new appreciation that atherothrombosis was, in part, an inflammatory disorder.26 Further investigation has shown elevated hs-CRP to predict type 2 diabetes and hypertension.27 In 2002, levels were established based on data from almost 28,000 healthy women followed for10 years such that an hs-CRP of 1, 1 to 3, and >3 mg/L represented lower, average, or higher vascular risk, respectively, when added to traditional risk factors.28 One group of investigators added hs-CRP to traditional risk factors to predict cardiovascular risk and found that 30% of individuals originally classified as 'intermediate risk“ were further reclassified into higher or lower risk categories enabling more specific risk prediction.29 The recently reported Reynolds Risk Score added the 2 biomarkers, hs-CRP and family history, to traditional risk factors and found that the accuracy of risk prediction was, again, markedly improved.27 Based on this evidence, many healthcare providers have come to use CRP in addition to other biomarkers to provide additional cardiovascular risk prediction.
Several reports address CRP in relation to the acute care setting and use of CRP levels after AMI. Initially, data suggested that the titration of statin therapy based on CRP levels would result in fewer events and enhance regression of atherosclerosis.21,30 Patients were given statins, and CRP values were obtained 30 days after AMI (not sooner so as to avoid the influence of myocardial necrosis on CRP). In patients who had low-density lipoprotein cholesterol levels <70 id="37" name="37">
There is controversy regarding CRP levels. Some argue that the levels of CRP vary greatly and fluctuate within individuals; if the patient is acutely ill or has an AMI, the test should be repeated 2 weeks later.31 C-reactive protein levels vary by gender and ethnicity,32 and values >10 mg/L are likely due to illness.33 Those values between 1 and 3 mg/L reflect an intermediate risk.29 Recent guidelines suggest the use of CRP in patients who are at intermediate risk for coronary disease to assist in determining treatment goals.34 For those clinicians following patients after AMI, CRP levels may be a helpful adjunct in gauging statin therapy.
Developing Biomarkers
Myeloperoxidase
Myeloperoxidase is a degranulation product from white blood cells 3 released into the systemic circulation during inflammatory conditions. This enzyme is found in higher concentrations in the culprit lesions of patients with UA or AMI than in stable coronary artery disease.3 Because current biomarkers measure only the onset of necrosis, myeloperoxidase offers an exciting alternative as it reflects inflammation or activation of hemostasis after plaque rupture that may give early information before irreversible injury.35
A few clinical studies have examined the role of myeloperoxidase as a marker of risk for ACS. In patients undergoing angiography, patients with coronary artery disease had higher activity levels of myeloperoxidase than in a comparison normal group, but no information was provided on subsequent rate of adverse events.36 Two groups of investigators studied myeloperoxidase in relation to risk stratification.37,38 In the CAPTURE trial myeloperoxidase concentration was measured in 1,090 ACS patients, with death and AMI rates determined 6 months after hospital discharge.37 Those with a cutoff of >350 µg/L had a more than 2 times greater hazard of death or AMI. Interestingly, the effects of myeloperoxidase were also noted in patients with negative cardiac troponin T levels; however, only the admission cardiac troponin T level was used. Another group examining 604 chest pain patients in the ED demonstrated an increased odds ratio for major adverse effects at 30 days and 6 months corresponding with increasing quartile myeloperoxidase concentrations.38 The results were similar to the CAPTURE study, but differences in study designs make it impossible to directly compare the results. One group used a higher cardiac troponin T cutoff of.10 µg/L, and neither used the same assay. Standardization of assays and comparisons with accepted cutoffs are needed. In summary, myeloperoxidase is a marker of plaque instability but is not unique to ACS. It is associated with neutrophil activation and can be found in association with any infectious, inflammatory, or infiltrative disease process.
Although this biomarker seems to provide additional important data in the evaluation of chest pain patients, considerable limitations require further investigation. Comparisons of myeloperoxidase with troponin levels have used high troponin cutoff levels or only admission troponin levels.2 In addition, myeloperoxidase lacks specificity and can be increased in other conditions.2 Not all institutions may offer the test or have timely results to assist in clinical decision making.
Pregnancy-Associated Plasma Protein
Pregnancy-associated plasma protein A (PAPP-A) is an insulin-like growth factor thought to be released when neovascularization occurs and therefore may be a marker of plaque rupture.3 The presence of PAPP-A was found in unstable plaques from patients who died sudden cardiac causes39 In a series of 136 patients presenting to the ED with suspected ACS, an increase in PAPP-A was an independent predictor of future ischemic events as well as percutaneous coronary intervention or cardiac bypass surgery.40 The correlation between PAPP-A and CKMB was poor, indicating that increases in PAPP-A cannot be associated with necrosis; that is, PAPP-A increases were associated with events before necrosis occurred. Elevated PAPP-A levels were also found in patients without increased concentrations of cardiac troponin I, potentially identifying high-risk patients who might not otherwise be identified.
Pregnancy-associated plasma protein A is thought to be different from PAPP-A collected during pregnancy versus the serum of ACS patients. The immunoassays that are designed to detect PAPP-A in pregnancy serum have not been developed for the measurement of PAPP-A as a cardiac marker.3 In addition, the concentration of PAPP-A is affected by some laboratory tube additives, so correct collection and measuring systems are needed.3 In summary, acceptance of PAPP-A as independent biomarker for cardiovascular risk in ACS requires more investigation.
Ischemia-Modified Albumin
Ischemia-modified albumin (IMA) is a novel marker of cardiac ischemia. It is measured in the serum by the albumin cobalt binding test, which is based on the premise that albumin in the blood of patients with myocardial ischemia demonstrated less ability to bind with cobalt than the albumin in serum of normal subjects.41 Therefore, the albumin cobalt binding test measures reduced albumin binding to cobalt.8 A positive IMA may reflect cardiac ischemia reflected as a reduced metal binding capacity of albumin.
One group of investigators examined the usefulness of IMA in patients presenting to the ED with chest pain, normal or indeterminate ECG, and negative troponin.42 One hundred thirty-one patients with suspected ACS were chosen based on arrival to the ED within 3 hours of last episode of chest pain, a normal or indeterminate ECG, and negative cardiac troponin upon admission.42 The results revealed higher IMA levels in those patients with ACS when compared with those found to have nonischemic chest pain. In addition, the authors found that using both IMA and troponin increases the sensitivity and specificity of identifying patients with ACS. The results also seemed to favor the idea that IMA levels increase before any change in troponin level, suggesting that IMA represents an earlier marker of myocardial ischemia.
Ischemia-modified albumin is not without its problems. It should be noted that elevated IMA levels have been found in patients with injury to other organs besides the myocardium.8 Ischemia-modified albumin levels also seem to be influenced by serum albumin levels.
Soluble CD40 Ligand
Another biochemical marker receiving attention due to its relationship with the inflammation process leading to coronary thrombosis is CD40 ligand. It is a protein within the tumor necrosis factor family and is expressed on cells such as platelets, vascular endothelial cells, smooth muscle cells, and monocytes.43 In the process of thrombus formation, CD40 expressed on the surface of platelets is cleaved into soluble CD40 ligand, which can then be detected in the blood. One study assessed the ability of CD40 to predict risk in patients with ACS when compared with a control group.43 Results showed that CD40 levels above the median in patients with ACS were associated with risk for recurrent AMI. The specificity of CD40, however, must be questioned given the fact that levels can be detected in other inflammatory conditions aside from coronary atherosclerosis. For example, elevated concentrations of CD40 have been seen in inflammatory disorders, such as inflammatory bowel disease, as well as multiple sclerosis, stroke, and diabetes.3
Conclusion
The development and standardization of new markers of cardiac damage is a rigorous process that ideally brings sensitive and specific information assisting clinical decision making. Questions are posed regarding the utility, reliability, cost, measurement, and handling of the assay.44 Perhaps the most crucial and appropriate question considered is what will this new biomarker assay add to patient care? And what is the purpose of a new assay: early detection, diagnosis, risk stratification, monitoring of disease progression, or to help to select appropriate therapies?3,44 Cardiac imaging provides additional valuable information about heart function and has become increasingly sophisticated. However, it is expensive and may not be accessible. Cardiac markers represent efficient, cost-effective measures of myocardial viability. Future markers may provide clinicians a magnified view of the impaired myocardium.
Although new cardiac markers are highly scrutinized, there are several on the horizon that have promising potential (Table 2 ). Emerging markers may help to further identify patients who require hospitalization versus those who can be safely discharged, thus reducing the number of unnecessary hospital admissions. The novel aspect of many of these markers is their ability to detect states of inflammation, injury, and stretch, or processes that occur before actual myocardial necrosis. Therefore, these markers could potentially identify damage earlier and further risk stratify patients when compared with present markers (ie, cardiac troponin and CKMB). TABLE 2 Strengths and Limitations of Developing Biomarkers 3,34,40,41

REFERENCES
1. AHA. 2007 Heart and Stroke Statistical Update . Dallas, TX: American Heart Association; 2007. [Context Link]
2. Jaffe AS, Babuin L, Apple FS. Biomarkers in acute cardiac disease: the present and the future. J Am Coll Cardiol . 2006;48(1):1-11. [Context Link]
3. Apple FS, Wu AH, Mair J, et al. Future biomarkers for detection of ischemia and risk stratification in acute coronary syndrome. Clin Chem . 2005;51(5):810-824. [Context Link]
4. O'Rourke RA, Fuster V, Alexander RW et al, eds. Hurst's The Heart Manual of Cardiology. 11th ed. United States: McGraw-Hill Company; 2005. [Context Link]
5. Zimmerman J, Fromm R, Meyer D, et al. Diagnostic marker cooperative study for the diagnosis of myocardial infarction. Circulation . 1999;99:1671-1677. [Context Link]
6. Guyatt G, Rennie D. Users' Guides to the Medical Literature: Essentials of Evidence-Based Clinical Practice . Chicago, IL: AMA Press; 2002. [Context Link]
7. The Joint European Society of Cardiology/American College of Cardiology Committee. Myocardial infarction redefined. A consensus document of the Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction. J Am Coll Cardiol . 2000;36(3):959-969. [Context Link]
8. Babuin L, Jaffe AS. Troponin: the biomarker of choice for the detection of cardiac injury. CMAJ . 2005;173(10):1191-1202. [Context Link]
9. Rajappa M, Sharma A. Biomarkers of cardiac injury: an update. Angiology . 2005;56:677-691. [Context Link]
10. Jeremias A, Gibson CM. Narrative review: alternative causes for elevated cardiac troponin levels when acute coronary syndromes are excluded. Ann Intern Med . 2005;142:786-791. [Context Link]
11. Mueller C, Breidthardt T, Laule-Kilian K, Christ M, Perruchoud AP. The integration of BNP and NT-proBNP into clinical medicine. Swiss Med Wkly . 2007;137(1-2):4-12. [Context Link]
12. Troughton RW, Prior DL, Pereira JJ, et al. Plasma B-type natriuretic peptide levels in systolic heart failure: importance of left ventricular diastolic function and right ventricular systolic function. J Am Coll Cardiol . 2004;43(3):416-422. [Context Link]
13. Silver MA, Maisel A, Yancy CW, et al. BNP Consensus Panel 2004: a clinical approach for the diagnostic, prognostic, screening, treatment monitoring, and therapeutic roles of natriuretic peptides in cardiovascular diseases. Congest Heart Fail . 2004;10(5 suppl 3):1-30. [Context Link]
14. Januzzi JL Jr, Camargo CA, Anwaruddin S, et al. The N-terminal Pro-BNP investigation of dyspnea in the emergency department (PRIDE) study. Am J Cardiol . 2005;95(8):948-954. [Context Link]
15. Maisel AS, Krishnaswamy P, Nowak RM, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med . 2002;347(3):161-167. [Context Link]
16. Wright SP, Doughty RN, Pearl A, et al. Plasma amino-terminal pro-brain natriuretic peptide and accuracy of heart-failure diagnosis in primary care: a randomized, controlled trial. J Am Coll Cardiol . 2003;42(10):1793-1800. [Context Link]
17. Maisel A, Hollander JE, Guss D, et al. Primary results of the Rapid Emergency Department Heart Failure Outpatient Trial (REDHOT): a multicenter study of B-type natriuretic peptide levels, emergency department decision making, and outcomes in patients presenting with shortness of breath. J Am Coll Cardiol . 2004;44(6):1328-1333. [Context Link]
18. Kragelund C, Gronning B, Kober L, Hildebrandt P, Steffensen R. N-terminal pro-B-type natriuretic peptide and long-term mortality in stable coronary heart disease. N Engl J Med . 2005;352(7):666-675. [Context Link]
19. Bassan R, Potsch A, Maisel A, et al. B-type natriuretic peptide: a novel early blood marker of acute myocardial infarction in patients with chest pain and no ST-segment elevation. Eur Heart J . 2005;26(3):234-240. [Context Link]
20. Wiviott SD, Cannon CP, Morrow DA, et al. Differential expression of cardiac biomarkers by gender in patients with unstable angina/non-ST-elevation myocardial infarction: a TACTICS-TIMI 18 (Treat Angina with Aggrastat and determine Cost of Therapy with an Invasive or Conservative Strategy-Thrombolysis In Myocardial Infarction 18) substudy. Circulation . 2004;109(5):580-586. [Context Link]
21. Nissen SE, Tuzcu EM, Schoenhagen P, et al. Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: a randomized controlled trial. JAMA . 2004;291(9):1071-1080. [Context Link]
22. McCullough PA, Duc P, Omland T, et al. B-type natriuretic peptide and renal function in the diagnosis of heart failure: an analysis from the Breathing Not Properly Multinational Study. Am J Kidney Dis . 2003;41(3):571-579. [Context Link]
23. Krauser DG, Lloyd-Jones DM, Chae CU, et al. Effect of body mass index on natriuretic peptide levels in patients with acute congestive heart failure: a ProBNP Investigation of Dyspnea in the Emergency Department (PRIDE) substudy. Am Heart J . 2005;149(4):744-750. [Context Link]
24. Ridker PM, Glynn RJ, Hennekens CH. C-reactive protein adds to the predictive value of total and HDL cholesterol in determining risk of first myocardial infarction. Circulation . 1998;97(20):2007-2011. [Context Link]
25. Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med . 1997;336(14):973-979. [Context Link]
26. Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med . 2005;352(16):1685-1695. [Context Link]
27. Ridker PM. C-reactive protein and the prediction of cardiovascular events among those at intermediate risk: moving an inflammatory hypothesis toward consensus. J Am Coll Cardiol . 2007;49(21):2129-2138. [Context Link]
28. Ridker PM, Rifai N, Rose L, Buring JE, Cook NR. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N Engl J Med . 2002;347(20):1557-1565. [Context Link]
29. Cook NR, Buring JE, Ridker PM. The effect of including C-reactive protein in cardiovascular risk prediction models for women. Ann Intern Med . 2006;145(1):21-29. [Context Link]
30. Nissen SE, Tuzcu EM, Schoenhagen P, et al. Statin therapy, LDL cholesterol, C-reactive protein, and coronary artery disease. N Engl J Med . 2005;352(1):29-38. [Context Link]
31. Pearson TA, Mensah GA, Alexander RW, et al. Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation . 2003;107(3):499-511. [Context Link]
32. Khera A, McGuire DK, Murphy SA, et al. Race and gender differences in C-reactive protein levels. J Am Coll Cardiol . 2005;46(3):464-469. [Context Link]
33. Rifai N, Ridker PM. Proposed cardiovascular risk assessment algorithm using high-sensitivity C-reactive protein and lipid screening. Clin Chem . 2001;47(1):28-30. [Context Link]
34. Smith SC Jr, Anderson JL, Cannon RO 3rd, et al. CDC/AHA Workshop on Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: report from the clinical practice discussion group. Circulation . 2004;110(25):e550-e553. [Context Link]
35. Lippi G, Montagnana M, Salvagno GL, Guidi GC. Potential value for new diagnostic markers in the early recognition of acute coronary syndromes. CJEM . 2006;8(1):27-31. [Context Link]
36. Zhang R, Brennan ML, Fu X, et al. Association between myeloperoxidase levels and risk of coronary artery disease. JAMA . 2001;286(17):2136-2142. [Context Link]
37. Baldus S, Heeschen C, Meinertz T, et al. Myeloperoxidase serum levels predict risk in patients with acute coronary syndromes. Circulation . 2003;108(12):1440-1445. [Context Link]
38. Brennan ML, Penn MS, Van Lente F, et al. Prognostic value of myeloperoxidase in patients with chest pain. N Engl J Med . 2003;349(17):1595-1604. [Context Link]
39. Bayes-Genis A, Conover CA, Overgaard MT, et al. Pregnancy-associated plasma protein A as a marker of acute coronary syndromes. N Engl J Med . 2001;345(14):1022-1029. [Context Link]
40. Lund J, Qin QP, Ilva T, et al. Circulating pregnancy-associated plasma protein a predicts outcome in patients with acute coronary syndrome but no troponin I elevation. Circulation . 2003;108(16):1924-1926. [Context Link]
41. Panteghini M. Role and importance of biochemical markers in clinical cardiology. Eur Heart J . 2004;25:1187-1196. [Context Link]
42. Roy D, Quiles J, Aldama G, et al. Ischemia modified albumin for the assessment of patients presenting to the emergency department with acute chest pain but normal or non-diagnostic 12-lead electrocardiograms and negative cardiac troponin T. Int J Cardiol . 2004;97:297-301. [Context Link]
43. Freedman J. SSCD40 ligand: assessing risk instead of damage? N Engl J Med . 2003;348(12):1163-1165. [Context Link]
44. Morrow DA, DeLemos JA. Benchmarks for the assessment of novel cardiovascular biomarkers. Circulation . 2007;115:949-952. [Context Link]
KEY WORDS: biomarkers; BNP; troponin

Ketamine Use for Intubation

2009-07-15T09:55:00.000-07:00

http://www.medscape.com/viewarticle/705503?src=mp&spon=24&uac=92170HG

Irony....but only one study folks, read on

2009-06-14T13:16:00.000-07:00

Full text
•
PDF

Acid-Suppressive Medication Use and the Risk for Hospital-Acquired Pneumonia
Shoshana J. Herzig, MD; Michael D. Howell, MD, MPH; Long H. Ngo, PhD; Edward R. Marcantonio, MD, SM
JAMA. 2009;301(20):2120-2128.
Context The use of acid-suppressive medication has been steadily increasing, particularly in the inpatient setting, despite lack of an accepted indication in the majority of these patients.
Objective To examine the association between acid-suppressive medication and hospital-acquired pneumonia.
Design, Setting, and Patients Prospective pharmacoepidemiologic cohort study. All patients who were admitted to a large, urban, academic medical center in Boston, Massachusetts, from January 2004 through December 2007; at least 18 years of age; and hospitalized for 3 or more days were eligible for inclusion. Admissions with time spent in the intensive care unit were excluded. Acid-suppressive medication use was defined as any order for a proton-pump inhibitor or histamine2 receptor antagonist. Traditional and propensity-matched multivariable logistic regression were used to control for confounders.
Main Outcome Measure Incidence of hospital-acquired pneumonia, defined via codes from the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM), in patients exposed and unexposed to acid-suppressive medication.
Results The final cohort comprised 63 878 admissions. Acid-suppressive medication was ordered in 52% of admissions and hospital-acquired pneumonia occurred in 2219 admissions (3.5%). The unadjusted incidence of hospital-acquired pneumonia was higher in the group exposed to acid-suppressive medication than in the unexposed group (4.9% vs 2.0%; odds ratio [OR], 2.6; 95% confidence interval [CI], 2.3-2.8). Using multivariable logistic regression, the adjusted OR of hospital-acquired pneumonia in the group exposed to acid-suppressive medication was 1.3 (95% CI, 1.1-1.4). The matched propensity-score analyses yielded identical results. The association was significant for proton-pump inhibitors (OR, 1.3; 95% CI, 1.1-1.4) but not for histamine2 receptor antagonists (OR, 1.2; 95% CI, 0.98-1.4).
Conclusions In this large, hospital-based pharmacoepidemiologic cohort, acid-suppressive medication use was associated with 30% increased odds of hospital-acquired pneumonia. In subset analyses, statistically significant risk was demonstrated only for proton-pump inhibitor use.
Author Affiliations: Divisions of General Medicine and Primary Care (Drs Herzig, Ngo, and Marcantonio), Pulmonary and Critical Care (Dr Howell), and Gerontology (Dr Marcantonio), Beth Israel Deaconess Medical Center, Boston, Massachusetts; and Harvard Medical School, Boston (Drs Herzig, Howell, Ngo, and Marcantonio).

AACN and NTI conference starts this week

2009-05-10T14:31:00.000-07:00

This website will have educational opportunites as the conference starts up-lots of good topics and they usually have some free CEU's available for download.

http://www.aacn.org/DM/NTI/NTIHome.aspx

Happy Nurses Day 2009

2009-05-06T12:24:00.000-07:00

A shift starts, call bells, phone calls, documentation, baths, medications, core measures, ordersets, report, consults, vitals, updating families...the list goes on.

It's not the kind of thing you do for glamour... you do it so that someone can just make it through the day. You do it by holding a hand or saying a few words to reassure or to calm. You do whatever you have to do because you care. And that makes all the difference.
Happy Nurses Day!

Staff Meeting-Tuesday April 14th 7:30 AM

2009-04-09T15:56:00.001-07:00

New Heparin Competency for RN's

Times they are achangin'....

2009-03-22T11:52:00.000-07:00

To exist is to change, to change is to mature, to mature is to go on creating oneself endlessly.

2009-03-19T14:31:00.000-07:00

All changes, even the most longed for, have their melancholy; for what we leave behind us is a part of ourselves; we must die to one life before we can enter another.
Anatole France

If we can recognize that change and uncertainty are basic principles, we can greet the future and the transformation we are undergoing with the understanding that we do not know enough to be pessimistic.
Hazel Henderson

If you want things to stay as they are, things will have to change.
Giuseppe Tomasi di Lampedusa

Everyone thinks of changing the world, but no one thinks of changing himself.
Leo Tolstoy

History may not repeat itself, but it does rhyme a lot.
Mark Twain

Breathe everyone, in and out- there, let's remember to get back to basics during this time of change. ~tracy

Elevated Troponins in non-Cardiac Patients= Increased Mortality

2009-03-08T09:45:00.000-07:00

http://www.medscape.com/viewarticle/587991?sssdmh=dm1.437729&src=confwrap

New Drugs-first one is new rx for HTN

2009-02-22T14:56:00.000-08:00

IN THIS ARTICLE, you'll learn about 10 new drugs, including:

* nebivolol HCl, the newest beta-adrenergic blocking agent for hypertension
* methylnaltrexone bromide, a subcutaneous injection for opioid-induced constipation
* alvimopan, a selective mu-opioid receptor antagonist to combat postoperative ileus.
Unless otherwise specified, the information in the following summaries applies to adults, not children. Consult the product insert for information about each drug's safety during pregnancy and breast-feeding. Also consult a pharmacist, the product insert, or a comprehensive drug reference for more details on precautions, drug interactions, and adverse reactions* for all these drugs.

SELECTED REFERENCES

Drug Facts and Comparisons. St. Louis, MO: Facts and Comparisons, Inc.; 2009.

Nursing2009 Drug Handbook. Ambler, PA: Lippincott Williams & Wilkins; 2009. [Context Link]

Physicians' Desk Reference. 63rd ed. Montvale, NJ: Medical Economics; 2009.

The author has disclosed that he has no significant relationship with or financial interest in any commercial companies that pertain to this educational activity.

*Common adverse reactions are italicized throughout this article.

ANTIHYPERTENSIVE AGENT
Nebivolol HCl
Third-generation beta-blocker
Nebivolol HCl (Bystolic, Forest) joins a large group of beta-adrenergic blocking agents that have been marketed to treat hypertension. Designated by some as a newer- generation or third-generation beta-blocker, the new drug has a combination of actions that distinguishes it from previous agents in this class.Nebivolol is a preferentially beta1-selective beta-blocker when used in doses of 10 mg or less in patients who are extensive metabolizers of the drug, as most people are. However, it inhibits both beta1 and beta2 receptors at higher doses and in patients who are poor metabolizers. It doesn't inhibit alpha1-adrenergic receptors. Because of its selective properties, the new drug may be safer to use than other beta-blockers in patients with bronchospastic diseases.

Although beta-blockers have been associated with increased vascular resistance, reduced exercise capacity, cold extremities, Raynaud's disease, and other adverse reactions, nebivolol and carvedilol appear to reduce vascular resistance, although by different mechanisms. Nebivolol increases nitric oxide–mediated vasodilation, which may reduce the risk of vascular symptoms. However, there isn't enough research to conclude that the new drug is safer to use in patients with peripheral vascular disease. Beta-blockers may mask signs of hyperthyroidism and place patients at risk for symptom exacerbation if treatment is abruptly discontinued.

Nebivolol may be used alone or in combination with other antihypertensive agents. Its effectiveness was established in placebo-controlled studies, and additional antihypertensive effects were demonstrated in patients who were also treated with up to two other antihypertensive agents but who had inadequate BP control. However, no data indicate that nebivolol is more effective than previously approved agents in reducing BP.

Nebivolol's only labeled indication is for hypertension, although some other beta-blockers also are indicated for heart failure, left ventricular dysfunction following myocardial infarction, angina, and migraine prophylaxis.

Precautions: (1) Contraindicated in patients with sick sinus syndrome or severe bradycardia and heart block greater than first degree (unless the patient has a pacemaker), cardiogenic shock, decompensated heart failure, or severe hepatic impairment. (2) The initial dosage should be reduced in patients with moderate hepatic impairment. (3) Concurrent use with digoxin may increase the possibility of bradycardia. Patients treated with both a beta-blocker and diltiazem or verapamil may experience negative inotropic and chronotropic effects, so closely monitor concomitant use. (4) Use cautiously if the patient also is taking antiarrhythmic agents (such as disopyramide) that decrease atrioventricular conduction. (5) Patients also taking catecholamine-depleting drugs such as reserpine or guanethidine may experience excessive reduction of sympathetic activity and become hypotensive. (6) Concurrent use with fluoxetine or other CYP2D6 inhibitors may increase the concentration of nebivolol and should be closely monitored. (7) Concurrent use with sildenafil has a synergistic effect on reducing BP, so warn the patient about the risk of hypotension. (8) If the patient has a history of severe anaphylactic reactions, taking nebivolol (or any beta-blocker) may make him more reactive to the allergen and less responsive to the usual doses of epinephrine used to treat allergic reactions. (9) The risks of general anesthesia and surgical procedures are increased in patients who are on beta-blockers during surgery or whose beta-blocker therapy is withdrawn before surgery.

Adverse reactions: headache, dizziness, nausea, diarrhea, fatigue

Supplied as: 2.5-, 5-, and 10-mg tablets

Dosage: 5 mg once a day, increased at 2-week intervals, as needed, up to 40 mg once a day. Patients with severe renal impairment or moderate hepatic impairment should start with a lower dosage (2.5 mg once a day).

Nursing considerations: (1) Tell the patient to assess how he responds to the medication before driving or engaging in other activities that require alertness. (2) Tell him he may take nebivolol without regard to meals. (3) If he misses a dose, tell him to take the next dose at the scheduled time, not to double the dose. (4) Warn him not to abruptly stop therapy. If the healthcare provider discontinues treatment, the drug should be tapered over 1 to 2 weeks if possible and the patient advised to minimize physical activity. (5) Warn your patient that beta-blockers may mask signs and symptoms of hypoglycemia (such as tachycardia) and may precipitate or aggravate symptoms in patients with peripheral vascular disease.

DRUG FOR OPIOID-INDUCED CONSTIPATION
Methylnaltrexone bromide
Subcutaneous solution for a discomforting problem
Each year, an estimated 1.5 million Americans take an opioid continuously to relieve pain associated with incurable cancer and other advanced illnesses. Opioids produce analgesia by acting on receptors in the central nervous system. But because they also act at opioid receptors in peripheral tissues such as the gastrointestinal (GI) tract, almost all patients who receive continuous opioid therapy experience constipation. Patients usually are told to follow a bowel regimen, typically a laxative and stool softener, but this may not prevent opioid-induced constipation.

Methylnaltrexone bromide (Relistor; Progenics, Wyeth) is an opioid antagonist related to naltrexone, which has been used for opioid and alcohol dependence. The new drug, which doesn't cross the blood-brain barrier, functions as a selective peripherally acting mu-opioid receptor antagonist in the GI tract and other tissues. As a result, it decreases the constipating action of opioids without reducing their analgesic effects.

Administered subcutaneously, methylnaltrexone is indicated for the treatment of opioid-induced constipation in palliative-care patients with advanced illness who haven't responded sufficiently to laxative therapy. Its effectiveness was demonstrated in placebo-controlled studies. In two studies testing the drug at several dosage intervals, about one-third of patients reported a laxative action within 30 minutes following administration of the drug. In a single-dose study, about 60% of patients treated with the new drug experienced a laxative action within 4 hours, compared with 16% of those taking placebo.

An orally administered formulation of methylnaltrexone is being evaluated, as is an I.V. formulation for treating postoperative ileus.

The use of methylnaltrexone for longer than 4 months hasn't been studied.

Precautions: Contraindicated in patients with known or suspected mechanical GI obstruction

Adverse reactions: abdominal pain, flatulence, nausea, dizziness, diarrhea

Supplied as: single-use vials containing 12 mg of the drug in 0.6 mL of solution

Dosage: 8 mg for patients weighing 84 to 135 pounds (38 to 61 kg), 12 mg for patients weighing 136 to 251 pounds (62 to 114 kg), administered subcutaneously in the upper arm, abdomen, or thigh once every other day, as needed. For patients weighing less than 84 pounds (38 kg) or more than 251 pounds (114 kg), administer 0.15 mg/kg.

Nursing considerations: (1) Don't give more than one dose in a 24-hour period. (2) Report severe or persistent diarrhea to the healthcare provider, who will probably discontinue the drug. (3) Expect to reduce the dosage by one-half in patients with severe renal impairment (creatinine clearance less than 30 mL/minute). Dosage adjustment isn't needed in patients with mild or moderate renal or hepatic impairment. The drug hasn't been evaluated in patients with severe hepatic impairment. (4) The drug may be stored at room temperature, protected from light. (5) If you don't give the drug immediately after drawing it into the syringe, store it at room temperature and administer within 24 hours. The syringe doesn't need to be kept away from light during this 24-hour period. (6) Discard the vial after one use, even if some drug remains; don't use the vial more than once. (7) Discontinue methylnaltrexone therapy as ordered if the patient stops taking an opioid.

DRUG FOR POSTOPERATIVE ILEUS
Alvimopan
Speeding GI recovery
Following major abdominal surgery and certain nonabdominal surgeries, some patients experience postoperative ileus as a result of impaired GI motility. Postoperative ileus is characterized by abdominal distension and bloating, nausea, vomiting, pain, accumulation of gas and fluids in the bowel, and constipation. Lasting 5 to 6 days or longer, the condition may delay recovery from surgery and hospital discharge.

Opioid analgesics are used to relieve postsurgical pain after most major abdominal surgeries, but these drugs inhibit GI motility and may prolong postoperative ileus.

Alvimopan (Entereg; Adolor, GlaxoSmithKline) is a selective antagonist of mu-opioid receptors in peripheral tissues. By binding to mu-opioid receptors in the GI tract, it antagonizes the peripheral effects of opioids on GI motility and secretion. Because it acts selectively at opioid receptors in peripheral tissues, it doesn't reverse the analgesic action of the opioids.

Alvimopan is similar in action to methylnaltrexone, which is indicated to prevent opioid-induced constipation, but its indications are different. Given orally, alvimopan is indicated for short-term use in hospitalized patients to accelerate the time to upper and lower GI recovery following partial large or small bowel resection with primary anastomosis. Many patients undergoing bowel resections have colorectal cancer and other serious conditions; alvimopan is the first drug to be approved to accelerate GI recovery following these procedures. Alvimopan isn't indicated to treat opioid-induced constipation because a long-term study raised questions about its cardiovascular safety.

In placebo-controlled studies, bowel recovery times ranged from 10 to 26 hours less for alvimopan- treated patients compared with placebo-treated patients. Patients who took the new drug (most of whom had taken opioid analgesics) were discharged home 13 to 21 hours sooner than patients receiving placebo.

Because of cardiovascular risks, the drug is supplied only to hospitals that have registered in and met requirements for the Entereg Access Support and Education program, which sets standards for distribution of the drug. Alvimopan may not be dispensed to patients after hospital discharge. For more information on the program, call 1-866-423-6567.

Although some patients in the clinical studies had total abdominal hysterectomies, alvimopan's effectiveness following this type of surgery hasn't been established. The drug is being studied in patients undergoing radical cystectomy.

Precautions: (1) Because of cardiovascular risks, the drug carries a black-box warning that establishes restrictions regarding its distribution and dosage. (2) Contraindicated in patients who've taken therapeutic doses of an opioid for more than 7 consecutive days immediately before taking alvimopan. (3) Not recommended for patients with end-stage renal disease or severe hepatic impairment. (4) Because of a greater possibility of GI adverse reactions (such as abdominal pain, nausea, and diarrhea), use with caution in patients receiving more than three doses of an opioid within the week before surgery.

Adverse reactions: hypokalemia, dyspepsia, anemia, constipation, flatulence, back pain, urinary retention

Supplied as: 12-mg capsules

Dosage: 12 mg administered 30 minutes to 5 hours before surgery, followed by 12 mg twice daily beginning the day after surgery for a maximum of 7 days or until discharge

Nursing considerations: (1) Dosage adjustments aren't needed in patients with renal impairment or mild to moderate hepatic impairment, but monitor these patients closely. (2) Administer no more than 15 doses of alvimopan to any hospitalized patient. (3) The drug may be taken without regard to meals. (4) Monitor the patient's response to the drug (specifically, return of bowel function). (5) Teach the patient to report adverse reactions.

ANTIVIRAL DRUG
Etravirine
Latest weapon against HIV
Etravirine (Intelence, Tibotec) is the 25th antiretroviral agent to be marketed to treat HIV infection and the 4th antiretroviral to be classified as a nonnucleoside reverse transcriptase inhibitor (NNRTI). However, etravirine is effective in some patients with HIV strains that are resistant to other NNRTIs.

Combined with other antiretroviral agents, etravirine is indicated for the treatment of HIV infection in antiretroviral-treatment-experienced adults who have evidence of viral replication and HIV strains resistant to an NNRTI and other antiretroviral agents. The drug isn't indicated for initial treatment in treatment-naive patients. The use of etravirine should be guided by the treatment history and, when possible, resistance testing. In patients who've experienced virologic failure on an NNRTI- containing regimen, etravirine shouldn't be used in combination with only nucleoside/nucleotide reverse transcriptase inhibitors.

As part of a combination regimen, the new drug has been effective in placebo-controlled trials, reducing viral load in 60% of patients, compared with 40% of those who received a placebo in addition to the background regimen.

Precautions: (1) Etravirine may interact with other antiretroviral agents. Concurrent use with another NNRTI isn't recommended because the concentration and activity of etravirine may be altered. (2) Etravirine shouldn't be given with tipranavir/ ritonavir, fosamprenavir/ritonavir, atazanavir/ritonavir, ritonavir (600 mg twice a day), or other protease inhibitors without the coadministration of low-dose ritonavir. (3) Use cautiously in patients also taking lopinavir/ritonavir, as the activity of etravirine may be significantly increased. (4) Etravirine is an inducer of CYP3A4 and an inhibitor of CYP2C9 and CYP2C19 metabolic pathways. The new drug's action may be reduced by the concurrent use of carbamazepine, phenobarbital, phenytoin, rifampin, rifabutin, dexamethasone, and St. John's wort. The drug's activity may be increased by the concurrent use of azole antifungal agents or clarithromycin. (5) Etravirine may decrease the activity of certain statins, immunosuppressants, antiarrhythmic agents, and sildenafil. (6) Warfarin concentrations may be increased when the drug is used concurrently with etravirine. See the product insert for more details about potential drug interactions.

Adverse reactions: rash, nausea

Supplied as: 100-mg tablets

Dosage: 200 mg twice a day following a meal

Nursing considerations: (1) Teach the patient to take etravirine after a meal, as directed. (2) If he can't swallow tablets, he can crush the tablet and disperse its contents in a glass of water, stir well, and drink immediately. (The contents won't dissolve completely.) Tell him to then fill the glass with water several times and swallow the water to make sure he got the full dose. (3) If he misses a dose, teach him to take a tablet after a meal if it's within 6 hours of the scheduled time, then take the next dose at the regularly scheduled time. If the dose is more than 6 hours overdue, he should skip that dose and take his next dose at the regularly scheduled time. Warn him not to take double doses to make up for a missed dose. (4) Advise him that a rash may occur, most often in the second week of therapy, but it usually resolves within 1 to 2 weeks. Tell him to report a severe rash to his healthcare provider, who may discontinue treatment. (5) As the immune system responds to the treatment, patients may develop an inflammatory response to indolent or residual opportunistic infections, which may require further evaluation and treatment. Tell the patient to contact his healthcare provider if he develops signs or symptoms of inflammation. Antiretroviral regimens are also associated with redistribution or accumulation of body fat, including central obesity, buffalo hump, peripheral wasting, breast enlargement, and “cushingoid appearance.” (6) Closely monitor a patient on methadone maintenance therapy for withdrawal symptoms. The healthcare provider may need to adjust the methadone dosage. (7) Etravirine is classified in Pregnancy Category B and should be used during pregnancy only if the anticipated benefit justifies the risk to the fetus. If the drug is used during pregnancy, prescribers are encouraged to register patients in the Antiretroviral Pregnancy Registry by calling 1-800-258-4263.

ANTIDEPRESSANT
Desvenlafaxine succinate
New once-daily dosing for major depressive disorder
Desvenlafaxine succinate (Pristiq, Wyeth) is the major active metabolite of venlafaxine (Effexor). Like venlafaxine, desvenlafaxine is a serotonin-norepinephrine reuptake inhibitor (SNRI). It hasn't been directly compared with venlafaxine, and there's no reason to consider it more effective.

Unlike venlafaxine and other SNRIs, which have been approved for various other indications including panic disorder and social anxiety, desvenlafaxine is approved only for major depressive disorder. It's being studied for the treatment of vasomotor symptoms of menopause, neuropathic pain, and fibromyalgia, and its labeled indications will probably expand as research continues.

Precautions: (1) The labeling for all SNRIs includes a black-box warning about the increased risk of suicidal thinking and behavior (suicidality) in children, adolescents, and young adults (ages 18 to 24). Closely monitor all patients being treated with one of these drugs for worsening depression, suicidality, and behavior changes, particularly during the first several months of therapy and after dosage adjustments. (2) Contraindicated in patients with a history of hypersensitivity to desvenlafaxine or venlafaxine, in patients treated with a monoamine oxidase inhibitor (MAOI), and in those who discontinued an MAOI within the past 14 days. (3) Don't administer desvenlafaxine concurrently with venlafaxine. (4) Use with caution in patients with cardiovascular or cerebrovascular disease. (6) Concurrent use of anticoagulants, aspirin, and nonsteroidal anti-inflammatory drugs raises the risk of bleeding events such as ecchymosis, epistaxis, and hematoma. (7) Monitor patients with elevated intraocular pressure and those at risk for acute narrow-angle glaucoma for mydriasis. (8) Use caution when administering desvenlafaxine concurrently with other CNS-active drugs or other drugs that may affect serotonergic neurotransmitter systems (such as SSRIs and triptans). (9) Concurrent use of desvenlafaxine with serotonin precursors (such as tryptophan supplements) isn't recommended. (10) Concurrent use of a potent CYP3A4 inhibitor such as ketoconazole or clarithromycin may increase the bioavailability of desvenlafaxine.

Adverse reactions: nausea, dizziness, dry mouth, hyperhidrosis, constipation, insomnia, fatigue, decreased appetite, somnolence, hypertension, and sexual function disorders such as decreased libido

Supplied as: 50- and 100-mg extended- release tablets

Dosage: 50 mg once a day. The dosage may be increased in some patients. (See the product insert for details.)

Nursing considerations: (1) Because desvenlafaxine may increase BP, monitor the patient's BP regularly during treatment. Make sure preexisting hypertension is under control before the patient starts treatment with desvenlafaxine. (2) Tell the patient to swallow the tablet whole with fluid. Warn him not to divide, crush, chew, or dissolve the tablet. (3) Tell him he can take desvenlafaxine without regard to food. (4) Advise him not to be concerned if he sees the inert matrix tablet in the stool. (5) Closely monitor him for signs and symptoms of serotonin syndrome, activation of mania/hypomania, seizures, hyponatremia, and interstitial lung disease and eosinophilic pneumonia. Tell him to watch for and report these signs and symptoms. (6) Tell him to avoid alcoholic beverages while being treated with desvenlafaxine. (7) Warn him not to stop therapy abruptly. To reduce the risk of new symptoms (such as irritability, anxiety, and abnormal dreams), his healthcare provider will taper the dosage if the drug is to be discontinued.

DRUG FOR CROHN'S DISEASE
Certolizumab pegol
Less-frequent dosing for this TNF blocker
Crohn's disease is a chronic, progressive inflammatory bowel disease typically characterized by inflammation at the end of the small intestine (ileum) and the beginning of the large intestine (colon). About half a million Americans have Crohn's disease and experience an ongoing cycle of flare-ups and remissions throughout their lives. Signs and symptoms include diarrhea, fever, abdominal pain and cramping, rectal bleeding, narrowing of the GI tract, GI obstruction, and fistulas. Corticosteroids, immunosuppressants, and other drugs, including tumor necrosis factor (TNF) inhibitors, are used to treat the disease.

Certolizumab pegol (Cimzia, UCB) is the third TNF blocker to be approved to treat Crohn's disease, joining infliximab and adalimumab. All of the TNF blockers are administered parenterally. Certolizumab is administered less frequently (every 4 weeks for maintenance doses) than adalimumab, but each dose is administered as two injections; adalimumab is administered as a single injection. Also, certolizumab and infliximab should be prepared and administered by a healthcare professional; adalimumab may be self-administered by patients.

Administered subcutaneously, certolizumab is indicated to reduce signs and symptoms of Crohn's disease and maintain clinical response in adults with moderately to severely active disease who've had an inadequate response to conventional therapy. Infliximab and adalimumab also are indicated for other conditions, such as rheumatoid arthritis, psoriatic arthritis, plaque psoriasis, and ankylosing spondylitis, but these aren't labeled indications for certolizumab.

Precautions: (1) Potentially fatal infections (such as tuberculosis [TB] and invasive fungal infections) are the subject of a black-box warning in the new drug's labeling. (2) Certolizumab and anakinra (an interleukin-1 antagonist) shouldn't be used concurrently because this increases the risk of serious infections. (3) Certolizumab shouldn't be used in patients with active infections including chronic or localized infections. (4) Assess patients for TB risk factors and test for latent TB infection before therapy begins. (5) Certolizumab may reactivate hepatitis B virus in patients who are chronic carriers of this virus. (6) The TNF blockers are associated with a risk of malignancies such as lymphomas in children and young adults. (7) Certolizumab may cause hypersensitivity reactions, exacerbation or new onset of central nervous system demyelinating disorders such as multiple sclerosis, exacerbation or new onset of heart failure, hematologic reactions such as pancytopenia, and lupuslike syndrome.

Adverse reactions: upper respiratory tract infection, urinary tract infection, arthralgia, opportunistic or fungal infections

Supplied as: a lyophilized powder in single-use vials containing 200 mg of the drug

Dosage: 400 mg given as two subcutaneous injections of 200 mg initially and at weeks 2 and 4. If the patient responds well, follow with 400 mg subcutaneously every 4 weeks.

Nursing considerations: (1) Prepare two 200-mg vials for each dose. Reconstitute each vial with sterile water as directed in the product insert. Gently swirl the contents of the vial without shaking to thoroughly mix the lyophilized powder with the sterile water. (2) After reconstituting both vials, leave them undisturbed to permit complete reconstitution, which may take as long as 30 minutes. The doses should warm to room temperature before you administer them. (3) Following guidelines in the product insert, administer the doses subcutaneously at two separate sites in the abdomen or thigh. Monitor the sites for injection-site reactions. (4) Store drug vials in the refrigerator. If you can't administer reconstituted solution within 2 hours after preparation, you can refrigerate it for up to 24 hours before administering it. Let the drug rewarm to room temperature before administering it. (5) Teach the patient to notify his healthcare provider immediately if he experiences any signs and symptoms of infection. Give him a copy of the medication guide for certolizumab prepared by the manufacturer. (6) Don't administer live or attenuated vaccines to a patient being treated with certolizumab. (7) Certolizumab may cause erroneously elevated activated partial thromboplastin times in patients who don't have coagulation abnormalities.

ANTINEOPLASTIC DRUG
Bendamustine HCl
New weapon against chronic lymphocytic leukemia
The most common form of leukemia in adults, chronic lymphocytic leukemia (CLL), is a slowly progressing blood and bone marrow disease. In the United States, about 15,000 new cases are diagnosed each year. For many years, alkylating agents such as chlorambucil and cyclophosphamide were the primary treatment, but these seldom provided a complete response. The purine nucleoside analogue fludarabine has been demonstrated to be more effective than the alkylating agents, but concurrent use of the two types of agents hasn't been shown to improve response rate or overall survival.

Bendamustine HCl (Treanda, Cephalon), described as a bifunctional mechlorethamine derivative, has a unique structure that includes a component that acts as an alkylating agent as well as a purinelike benzimidazole component. Although its exact mechanism of action isn't known, the new drug appears to damage DNA in cancer cells to cause apoptosis (programmed cell death) and also acts through a nonapoptotic pathway. A designated orphan drug, bendamustine is administered I.V.

When bendamustine was compared with oral chlorambucil in clinical trials, the overall and complete response rates with the new drug were 59% and 8%, respectively, compared with 26% and less than 1% with chlorambucil. The median progression-free survival was 18 months with bendamustine and 6 months with chlorambucil. Bendamustine hasn't been directly compared with other agents used to treat CLL.

Bendamustine is being studied for the treatment of other types of cancer, and recently was also approved for treating indolent non-Hodgkin's lymphoma.

Precautions: (1) Not recommended for patients with moderate or severe hepatic impairment or severe renal impairment (creatinine clearance less than 40 mL/minute). (2) Use with caution in patients with mild hepatic impairment or mild or moderate renal impairment. (3) Closely monitor patients who are concurrently using the new drug with a CYP1A2 inhibitor such as ciprofloxacin or a CYP1A2 inducer such as omeprazole or smoking. (4) Consult the product insert for additional precautions and interactions.

Adverse reactions: neutropenia, pyrexia, thrombocytopenia, nausea, anemia, leukopenia, vomiting, asthenia, fatigue, malaise, weakness, dry mouth, somnolence, cough, constipation, headache, mucosal inflammation, stomatitis, skin rash

Supplied as: single-use vials containing 100 mg of the drug as lyophilized powder

Dosage: 100 mg/m 2 given as an I.V. infusion over 30 minutes on days 1 and 2 of a 28-day cycle, for up to six cycles

Nursing considerations: (1) Most patients treated with bendamustine experience myelosuppression and may need a dosage reduction or a delay in continuing treatment. See the product insert for details. (2) Because patients with myelosuppression are more susceptible to infection, administer antimicrobial drugs as ordered if the patient has signs and symptoms of infection. (3) Monitor the patient for an anaphylactic or anaphylactoid reaction, a rare but serious complication that's most likely to occur in the second and subsequent cycles of therapy. Treatment may be discontinued in patients with a grade 3 or 4 infusion reaction. Pretreat patients who've experienced a grade 1 or 2 infusion reaction with an antihistamine, antipyretic, or corticosteroid before subsequent treatment cycles, as ordered. (4) To reduce the risk of tumor lysis syndrome, maintain adequate volume status, closely monitor the patient's blood chemistry, and administer allopurinol during the first 1 to 2 weeks of therapy in high-risk patients. (5) Discontinue or suspend therapy if the patient develops severe or progressive skin reactions, such as rash or toxic skin reactions. (6) Tell women to avoid becoming pregnant throughout treatment and for 3 months after treatment is discontinued. Men treated with bendamustine should use reliable contraception for the same period. (7) Consult the product insert for recommendations about delaying treatment and adjusting dosages in patients who experience hematologic or nonhematologic toxicity. (8) Reconstitute the drug with 20 mL of sterile water for injection, providing a drug concentration of 5 mg/mL. See the product insert for details. Administer the drug as soon as possible following preparation. (9) The final admixture is stable for 24 hours when refrigerated or for 3 hours at room temperature. Complete administration of the drug within 24 hours (if it was refrigerated) or 3 hours (if it was kept at room temperature).

DRUG FOR ALLERGIC RHINITIS
Ciclesonide
Seventh intranasal spray for sneezes and sniffles
Ciclesonide (Omnaris; Nycomed, Sepracor) is the seventh corticosteroid to be marketed as an intranasal spray for treating allergic rhinitis. Its effectiveness has been demonstrated in placebo-controlled studies, but it hasn't been directly compared with other intranasal corticosteroids. Although it was approved by the FDA in October 2006, it wasn't marketed until 2008.

Ciclesonide is indicated to treat nasal symptoms of seasonal rhinitis in adults and children age 6 and older and nasal symptoms of perennial allergic rhinitis in adults and adolescents age 12 and older. These labeled indications are more limited than those for other corticosteroid nasal sprays.

In clinical trials, ciclesonide's onset of effect occurred within 24 to 48 hours, with further symptomatic improvement over 1 to 2 weeks in patients with seasonal allergic rhinitis and over 5 weeks in patients with perennial allergic rhinitis.

In early 2008, a formulation of ciclesonide for oral inhalation (Alvesco) was approved as an asthma maintenance medication; the drug was marketed in late 2008.

Precautions: (1) Concurrent use with a potent CYP3A4 inhibitor, such as clarithromycin, may increase levels of des-ciclesonide, raising the possibility of nasal irritation and headache. (2) Use of ciclesonide or another intranasal corticosteroid may delay wound healing in patients who've had recent nasal surgery or nasal septal ulcers. Treatment shouldn't be initiated until healing has occurred. (3) Immune system suppression from corticosteroid use increases the patient's susceptibility to infection. (4) Intranasal corticosteroids may delay or impair growth in children.

Adverse reactions: headache, epistaxis, nasopharyngitis, ear pain

Supplied as: a metered-dose pump spray that contains 120 metered doses of 50 mcg each

Dosage: 200 mcg/day administered as two sprays (50 mcg/spray) in each nostril once a day

Nursing considerations: (1) Warn the patient not to exceed the recommended dosage and to contact his healthcare provider if symptoms persist or worsen. (2) Teach him to recognize and report signs and symptoms of localized fungal infection of the nose and pharynx. If he's using ciclesonide over several months or longer, tell him to see his healthcare provider periodically to be checked for evidence of Candida infection. (2) Closely monitor the patient for adrenal insufficiency if he was switched from prolonged systemic corticosteroid therapy to ciclesonide therapy. (3) Tell him to gently shake the bottle and prime the pump before the first use by pressing on the applicator eight times. If, after priming, he doesn't use the product for 4 or more consecutive days, he should gently shake the bottle and reprime the pump with one spray or until a fine mist appears. (4) Tell him to discard the bottle after 120 sprays following initial priming or after 4 months, whichever occurs first.

DRUG FOR GENITAL WARTS
Sinecatechins ointment
Green tea treatment for a common infection
Most genital warts are caused by human papillomavirus (HPV) types 6 and 11. Highly contagious, this virus is one of the most common sexually transmitted diseases, accounting for an estimated 6.2 million new infections every year in the United States. Typically, genital warts have been treated with cryotherapy, topical application of tissue-destructive agents such as podophyllin or trichloroacetic acid, or intralesional use of interferon alfa-2b and interferon alfa-n3. Although these treatments usually destroy wart tissue, they don't eradicate the virus, which recurs in about 25% of patients who initially respond to treatment.

Sinecatechins (Veregen, Bradley) is a botanical product that has been approved for the topical treatment of external genital and perianal warts in immunocompetent patients age 18 years and older. It's a partially purified fraction of an extract of green tea leaves. How sinecatechins treats genital and perianal warts isn't clear, although antioxidant activity is one possibility. In two studies, the sinecatechins ointment completely cleared warts in 54% of patients, compared with 35% of those treated with a placebo. Both groups had similar rates of wart recurrence at 12 weeks following completion of treatment. The new product hasn't been directly compared in clinical studies with other treatments for genital warts, nor has it been evaluated for the treatment of urethral, intravaginal, cervical, rectal, or intra-anal HPV disease or in immunosuppressed patients.

Precautions: Use during pregnancy only if the anticipated benefit outweighs the risk to the fetus.

Adverse reactions: erythema, pruritus, burning, pain/discomfort, erosion/ ulceration, edema, induration, vesicular rash

Supplied as: a water-free ointment including the drug in a 15% concentration

Dosage: a strand of ointment (about 0.5 cm) applied three times a day to all external genital and perianal warts

Nursing considerations: (1) The product should be stored in a refrigerator until it's dispensed; after that, it may be stored refrigerated or at room temperature up to 77° F (25° C). (2) Tell the patient to wash her hands before and after ointment application. (3) Tell her she needn't wash the ointment off the treated area before the next application. The treated areas shouldn't be covered or wrapped with an occlusive dressing. (4) Tell her to continue treatment until the warts are gone, but for no longer than 16 weeks. (5) Warn her that the ointment may weaken condoms and vaginal diaphragms, so unless she's trying to become pregnant, she should avoid relying on these birth control devices and engaging in sexual contact while the ointment is on the skin. (6) Tell her that the ointment may stain clothing and bedding.

DRUG FOR CRYOPYRIN-ASSOCIATED PERIODIC SYNDROMES
Rilonacept
First drug for these chronic inflammatory diseases
Cryopyrin-associated periodic syndromes (CAPS) are a group of rare, inherited chronic inflammatory diseases characterized by recurrent rash, fever and chills, joint pain, fatigue, and eye pain or redness. About 1 in 1 million Americans are affected with one of the three autoinflammatory diseases categorized as CAPS:

Familial cold autoinflammatory syndrome (FCAS), which begins during early childhood or adolescence. Symptoms are triggered by exposure to cooling temperatures.

Muckle-Wells syndrome (MWS), which often is associated with hearing loss or amyloidosis (an accumulation of amyloid protein in organs such as the kidney). Symptoms are triggered by random, unknown factors and possibly exercise, stress, or cold.

Neonatal-onset multisystem inflammatory disease (NOMID), which is the most severe form of CAPS. Characterized by significant central nervous system complications, it usually causes signs and symptoms shortly after birth.

In most but not all cases, CAPS are caused by mutations in the gene that encodes cryopyrin, a protein that regulates inflammation. The mutation causes increased activity of cryopyrin and overproduction of interleukin-1 beta, resulting in an inflammatory response and the symptoms of CAPS.

Rilonacept (Arcalyst, Regeneron), the first drug to be approved to treat CAPS, is an interleukin-1 blocker that's administered subcutaneously to treat FCAS and MWS in adults and children age 12 and older. It hasn't been evaluated in patients with NOMID.

In a study of patients with FCAS or MWS, the new drug improved symptoms within several days after the start of therapy.

Precautions: (1) Don't use in patients with active or chronic infections because rilonacept may interfere with the immune response to infections. (2) Concurrent use with a TNF inhibitor or the interleukin-1 blocker anakinra isn't recommended because of the increased risk of infection. (3) Because rilonacept causes immunosuppression, it may also increase the risk of malignancies.

Adverse reactions: injection-site reactions, upper respiratory tract infections

Supplied as: single-use vials containing 220 mg of the drug as a lyophilized powder

Dosage: Adults—a loading dose of 320 mg given as two 2-mL subcutaneous injections of 160 mg each on the same day at two different sites, followed by single injections of 160 mg once a week.

Children and adolescents ages 12 to 17—a loading dose of 4.4 mg/kg (up to a maximum of 320 mg), given as one or two subcutaneous injections with a maximum single-injection volume of 2 mL, followed by single injections of 2.2 mg/kg (up to a maximum of 160 mg) once a week.

Nursing considerations: (1) Don't administer live vaccines to a patient being treated with rilonacept. He should receive all recommended vaccinations before starting therapy. (2) Reconstitute the vial with 2.3 mL of preservative-free sterile water for injection. Shake the vial for about 1 minute and then let it sit for 1 minute. The resulting solution is viscous and contains the drug in a concentration of 80 mg/mL. (3) Withdraw the volume of solution needed to provide the recommended dose from the vial using a new 27-gauge, half-inch needle attached to a new 3-mL syringe for subcutaneous injection. (4) Protect the reconstituted solution from light and use it within 3 hours of reconstitution. Reconstituted solution may be kept at room temperature. (5) Administer the drug as directed, no more often than once a week. (6) Store vials in a refrigerator and in their original carton to protect them from light. (7) Monitor the patient's lipid profiles; increases in blood lipid concentrations have been reported during rilonacept treatment. Teach him about lipid-lowering therapy if indicated. (8) Teach the patient to rotate injection sites in the left and right sides of the abdomen or left and right thighs. If someone other than the patient is administering the drug, she may also use sites on the upper arms. (9) Teach the patient to immediately report signs and symptoms of infection to his healthcare provider, who will discontinue therapy if the infection is serious.

Copyright (c) 2000-2008 Ovid Technologies, Inc.
By accessing or using OvidSP, you agree to Ovid's terms of use, conditions and all applicable laws. If you do not agree to these terms you may not use this Site.
Version: OvidSP_UI02.00.06.101, SourceID 38781

Care of Patients with Temporary Pacers

2009-02-22T14:52:00.001-08:00

http://www.nursingcenter.com/library/JournalArticle.asp?Article_ID=841496
Good article

Nursing Documentation

2009-02-19T12:40:00.000-08:00

http://www.brainshark.com/brainshark/vu/view.asp?pi=871020673

Good information-Webcast format

February...it's "our" Month

2009-02-19T10:07:00.000-08:00

Have a cuppa and read on...

February for our units means time:

To get TB tests from Infection control
Head down there on Monday, Tuesdays or Wednesdays to get yours planted and most importantly get it read 48-72 hours later and send back to Infection Control.

To get your glucose competency done.
So catch up with me to get your glucometer competency completed before you expire at the end of the month. You have all been seeing the countdown to when you are about to expire if you are using it, if you have done it with me then I have sent your papers down to Emily Cyr (the new coordinator for point of care tests) and she has to process them before we are all renewed.

For Change:
We are all still in a holding pattern for the move to Med/Surg. I have heard that the maintenance has commenced to get wiring set up and we are still on a day by day basis but bear with us, I know it's challenging but we will get there when the time is right, we need to do this safely for our patients no matter how frustrating it gets for us in the throes of the change.

still sipping on your cuppa good-have a good day/night!

Competency For RN's only

2009-01-21T10:27:00.001-08:00

After you complete the questions return to Vilma-some of you may have the packets in your mailbox or received them at this week's staff meetings, some are missing questions 5 & 6 so here is the complete Power Point that you can review anytime.

Thank you!

More on Silver Coated ET tubes

2009-01-21T09:22:00.000-08:00

Protection Against Ventilator-Associated Pneumonia by Silver-Coated Endotracheal Tubes: An Unresolved Issue
Tamar F. Barlam, M.D.; Dennis L. Kasper, M.D.
AccessMedicine from McGraw-Hill. 2008; ©2008 The McGraw-Hill CompaniesAll rights reserved. From Tintinalli's Emergency Medicine
Posted 01/12/2009
Ventilator-associated pneumonia (VAP) is a major nosocomial infection that results in significant morbidity, mortality, and health care costs. Most strategies to reduce VAP attempt to decrease rates of colonization of the aerodigestive tract and aspiration of infected secretions. Silver has antimicrobial properties in vitro and may reduce biofilm formation on and bacterial adherence to the endotracheal tube. Kollef and colleagues (2008) conducted a prospective, randomized, multicenter, single-blind, controlled study in patients requiring >24 h of intubation to determine whether silver-coated endotracheal tubes can reduce the incidence of microbiologically confirmed VAP.
Patients recruited from December 2002 to March 2006 at 54 centers in North America were assigned to treatment groups in a 1:1 ratio, using block randomization by site. Each patient was intubated with either the experimental silver-coated tube or a control tube (Hi-Lo endotracheal tube; Mallinckrodt, St. Louis). Apart from the silver coating, the two types of tubes were similar. Bronchoalveolar lavage (BAL) fluid was subjected to quantitative culture if VAP was suspected. The primary outcome was VAP incidence, which was defined as a quantitative BAL fluid culture with ≥104 colony-forming units (CFU)/mL after intubation for ≥24 h. Secondary outcomes were time to occurrence of VAP; duration of endotracheal intubation, intensive care unit (ICU) stay, and hospital stay; and mortality rate.
Of 2003 patients randomized, 968 received the experimental tube and 964 received the control tube; 423 patients were intubated for <24 p =" .007)." p =" .03).">90% of these patients were taking antibiotics at the time of BAL. Staphylococcus aureus, Pseudomonas aeruginosa, and Enterobacteriaceae were the most common pathogens. In patients with silver-coated tubes, the relative risk of VAP incidence within 10 days of intubation was reduced and the occurrence of VAP was delayed (p = .005) in comparison with the control group; however, other secondary outcomes—mortality rate and duration of intubation, ICU stay, or hospital stay—did not differ between the two groups. The frequency and severity of adverse events were similar for the two types of endotracheal tubes.
The authors conclude that, compared with the uncoated tube, the silver-coated endotracheal tube is associated with a significant reduction in the incidence of VAP and a delay in VAP occurrence. They note that the silver-coated tube offers a unique approach to VAP prevention because it is user-independent after intubation and requires no further action on the part of the clinician. In an accompanying editorial, Chastre (2008) discusses the limitations of the study and the lack of robustness of the results. Only three more cases of VAP in the coated-tube group would have rendered the study statistically inconclusive. In addition, BAL culture results were probably affected by antibiotic use, which was not further described in the study, and the greater proportion of patients with COPD in the control group could have biased the results. Thus, although the silver-coated endotracheal tube may be appropriate for patients at very high risk of developing early-onset VAP (e.g., trauma patients), its use should not be viewed as definitively beneficial for VAP prevention until further data confirm its efficacy and cost benefit.
References
Chastre J: Preventing ventilator-associated pneumonia: Could silver-coated endotracheal tubes be the answer? (editorial) JAMA 300:842, 2008
Kollef MH et al: Silver-coated endotracheal tubes and incidence of ventilator-associated pneumonia: The NASCENT randomized trial. JAMA 300:805, 2008
Tamar F. Barlam, M.D., Associate Professor of Medicine, Boston University School of Medicine, Boston.Dennis L. Kasper, M.D., William Ellery Channing Professor of Medicine, Professor of Microbiology and Molecular Genetics, Harvard Medical School; Director, Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston.

Stay tuned for a Competency

2009-01-08T14:38:00.000-08:00

2009-01-03T15:46:00.001-08:00

2008-12-27T18:16:00.001-08:00

Med/Surg Education Day Decemebr 30th feel free to stop by for any topics of interest.

Merry Christmas Every One!

2008-12-21T12:41:00.000-08:00

As the year ends I want to take the time to thank each of you for all that you do every shift.

The little things that make the job so much more than a job-we develop friends but we all strive to make the patients and their families lives better by what you choose to do.This nursing thing is a vocation and you each bring a little (and sometimes, alot) of yourselves to it each time you interact with a patient~Thank you for choosing our units to do that-I appreciate how tough this can be and that sometimes you leave that little bit of your self with a patient too-I hope that you come away from this year knowing that you make a difference, to me, your coworkers, but mostly to the community we serve. So no matter what happens in the year to come, please remember that our team has had it's challenges (what's life without them?) but that you each contribute to what makes our team great.

Have a Merry Christmas! ~tracy

Nikki-welcome and we love seeing that smile!

Deana~you are important so I couldn't not post a pix of you-Thank you!

Sandi spreading the hugs to Nicole-we all need that sometimes.

Shannon-go to girl-study hard-May will be here before you know it!

Sandi-I'll make you charge material yet!

And even though I have not captured each of you in photos here please know that I appreciate that something that you bring to work each day-we couldn't do the jobs we do without each of you.

New Fall Prevention Policy and Procedure-SEE EDUCATION BOARD IN PCU BREAKROOM TO SIGN OFF ON

2008-11-29T14:16:00.000-08:00

You may have already seen the new yellow wrist bands on patients and signs outside patient rooms. On the Bulletin Board in the PCU break room there is a review of the new Policy and Procedure as well as a sign off/attendance sheet that you all need to sign. The Board is generally changed monthly by educational services so time is of the essence. This is all part of best practice for our patients, new to the policy is the HOMESAFEHOME Tips to Improve Home Safety that will will provide at discharge to patients so this is a slight change to our current practice but the items on the sheet are things that all of us review but there is no written education provided for discharge...problem solved. Thanks for all each of you do to give good care.

Critical Care Online Expo

2008-11-09T09:42:00.000-08:00

I wanted to post this awhile ago but couldn't get the links to work before the event was webcasted on November 5th but I finally got on and here is a link to a webcast/powerpoint from a national speaker AnneMarie Palatnick-her name is well known as an educator for nursing in critical care. There are many available offerings in this expo so take advantage of some great FREE education here.

http://vts.inxpo.com/scripts/InXpo.nxp?LASCmd=AI:1;F:SF!42000&EventKey=7556

Enjoy!
Tracy

From Medscape for Nurses-Evidence Based Best Practice for ETT suctioning-Is Saline Instillation Beneficial?

2008-11-02T12:54:00.000-08:00

Instilling Normal Saline With Suctioning: Beneficial Technique or Potentially Harmful Sacred Cow?
Margo A. Halm, RN, PhD, CNS-BC; Kathryn Krisko-Hagel, RN, MS
Am J Crit Care. 2008;17(5):469-472. ©2008 American Association of Critical-Care Nurses
Posted 10/28/2008
Introduction
Normal saline has been widely used in acute care settings during endotracheal and tracheostomy suctioning. Clinicians have held fast to this long-standing tradition because many were taught that normal saline breaks up secretions and aids in their removal (especially tenacious secretions). In this clinical review, we summarize current evidence related to the following questions: Does instilling normal saline during suctioning increase sputum yield? Alternatively, is this practice associated with adverse physiological and psychological effects?
Methods
The strategy included searching MEDLINE, CINAHL, Cochrane Library, Joanna Briggs Institute, and TRIP databases. Key words included endotracheal tubes, tracheostomies, normal saline, and suctioning. All types of evidence (nonexperimental, experimental, qualitative studies, systematic reviews) were included.
Results
In the past 2 decades, investigators have studied the physiological and psychological effects of instillation of normal saline. The impact of the instillation of normal saline on sputum recovery, oxygenation, subjective symptoms, hemodynamic alterations, and infection was measured in 14 studies[1-14] ( Table 1 ). The effects of 2, 5, or 8 mL of normal saline on physiological parameters were evaluated at intervals of 5, 10, or 20 minutes (5 minutes most common). In one study,[1] researchers investigated saline deposition by radioactively labeling normal saline with technetium (Tc 99m). Samples included anesthetized dogs and ventilator-dependent patients in general, coronary artery bypass, and neurological intensive care units (ICUs). In addition to these studies, a guideline on tracheal suctioning from the Joanna Briggs Institute[15] was retrieved.
Sputum Recovery
Sputum volume or weight was measured in 5 of the 14 studies (36%).[1-5] In 3 of those 5 studies (60%), instillation of normal saline was associated with significantly increased retrieval of sputum. The difference in sputum volume ranged from 1 to 2 g, which may not be of clinical importance. In another study,[1] radioactively labeled normal saline was noted near the bottom of the endotracheal tube within 1 minute of instillation (rather than mixing with secretions) and was then rapidly absorbed by the cardiopulmonary system, providing evidence that normal saline and secretions do not mix. Furthermore, suctioning recovered a mean of only 18.7% of normal saline instilled in humans.
Oxygenation
Arterial blood gas analysis and measurement of the nadir and recovery time of oxygen saturation (most common) or mixed venous oxygen saturation were done in 9 studies.[2-6,9,10,12,13] Results of 56% of those studies indicated that use of normal saline was significantly associated with decreased oxygenation and desaturation that worsened over time after suctioning. Oxygen saturation was a mean of 1% to 2% lower when normal saline was used, which may, in itself, not be clinically significant. However, instillation of normal saline may impair gas exchange as evidenced by continued desaturation. More clinically impressive was the 6-point decrease in mixed venous oxygen saturation that Kinloch[10] observed in patients suctioned 5 minutes after instillation of normal saline (compared with controls), as well as the doubled recovery time. These findings demonstrate the detrimental effect of normal saline on global tissue oxygenation.
Subjective Symptoms: Pain, Anxiety, Dyspnea
Subjective symptoms associated with instillation of normal saline were explored in 2 studies[8,11] (14%). Exploring the experience of being suctioned with normal saline, Jablonski[8] found that patients reported anxiety and dread, as well as increased pain. In another study, O'Neal et al[11] found increased perceived dyspnea in patients over age 60 that persisted for up to 10 minutes after suctioning, a finding that may be related to decreased pulmonary compliance with aging.
Hemodynamic Alterations
Hemodynamic effects were investigated in 3 studies[4,9,12] (21%). Results of 1 of these studies[12] demonstrated that instillation of normal saline was associated with increased heart rate 4 to 5 minutes after suctioning; however, no effect on blood pressure or respiratory rate was uncovered. The increased stimulation of the cough reflex associated with instillation of normal saline may have other detrimental effects such as increased mean arterial pressure and intracranial pressure.[15,16]
Infection
Risk of infection was investigated in 2 studies[7,14] (14%). Hagler and Traver[7] found sputum cultures that showed growth due to the dislodgment of bacterial colonies. Up to 5 times as many colonies were dislodged when normal saline was instilled, and therefore this practice may contribute significantly to lower airway contamination. Newer evidence from a randomized controlled trial[14] suggests that instillation of normal saline was associated with a lower incidence of ventilator-associated pneumonia. It is unclear from this abstract whether the researchers controlled for other standard interventions to avoid ventilator-associated pneumonia[17,18] such as oral care, aspiration of subglottic secretions, maintenance of cuff pressure on the endotracheal tube, and prophylaxis of peptic ulcer and deep vein thrombosis.
Recommendation Based on Current Evidence
Collectively, these studies provide class III evidence of the adverse physiological and psychological effects of instillation of normal saline, and therefore, support against the routine use of normal saline with suctioning ( Table 2 ). Normal saline and mucus do not mix. Therefore, normal saline does not thin or mobilize secretions. Rather, ensuring adequate hydration is one way that nurses can facilitate removal of secretions.[15] The best-known interventions for managing thick tenacious secretions and preventing mucus plugs in ventilator-dependent patients are hydration, adequate humidification, use of mucolytic agents, and effective mobilization.[16,18,20]
In addition to an unappreciable increase in sputum recovery, use of normal saline adversely affects arterial and global tissue oxygenation and dislodges bacterial colonies, thus contributing to lower airway contamination. Because no solid scientifically based benefits for routine use of normal saline have been shown, it is highly recommended that this potentially harmful "sacred cow" be abandoned. Instead, treatment considerations should center on ways to prevent the development of thick, tenacious secretions.[20]
Normal saline may be indicated in situations where it is necessary to elicit a cough,[4,18] and normal saline may be useful for clearing the catheter after suctioning to avoid reintroducing pathogens into the airway.[21] Good handwashing is essential to reduce infection when opening vials of normal saline because increased contamination has been documented when clinicians use the nongloved thumb to twist off the tops of the vials.[22]
Despite these recommendations, organizational change toward best suctioning practices has not been without challenges. In a recent multisite study,[23] three large institutions had policies that recommended instilling normal saline for thick secretions. Suctioning surveys[23,24] also indicate that 2 to 3 times as many respiratory therapists as nurses report continued use of normal saline—a finding that is not so surprising given that the American Association of Respiratory Care's guideline[25] has not been updated since 1993 (and still advocates that normal saline dilutes and mobilizes secretions).
Promisingly, among nursing circles, researchers in the United Kingdom reported that although observed suctioning practices were contrary to many research recommendations,[26] educational interventions proved effective in advancing the knowledge and translation of research-based suctioning practices of critical care nurses at the bedside.[27]
Others have also reported high compliance rates of nurses with evidence-based guidelines recommending avoidance of normal saline.[28] More studies are needed to document clinical adherence to evidence-based guidelines so that we can better connect processes of care to outcomes for patients.
I think that this evidence says it all-No Saline!
And here is the link to the same article-
http://www.medscape.com/viewarticle/581620_print

Put down the Penlights...Neuro assessment

2008-10-23T15:04:00.000-07:00

Changes in behavior are an early sign of neurologic compromise. They are not specific to neurologic problems, but they are the earliest sign. Keep a close eye on the patient for problems with speech and disorientation. Many nurses start assessing neurologic function by pulling out their penlight and checking the patient's pupils. This is very stimulating to your neuro patient and is not the first thing that is going to change.
If your patient is alert and oriented and you are just trying to follow him to see if his condition is getting worse, the first thing that is going to change is his behavior. Behavior is the highest level of function. Next the patient will have changes in his speech. Speech patterns and the ability to perform speech tell you a lot about the patient's neurologic function. The third level down is content of arousability, and this is what is referred to as orientation. The forth level is arousability; whether or not the patient wakes up when you walk into the room or you have to touch him or use painful stimuli.
If your patient is already unconscious, assess systolic blood pressure as an indicator of intracranial pressure. As intracranial pressure increases, systolic pressure has to increase to continue to perfuse the brain. The very lowest level is the pupil reflex. Changes in pupils do not tell you much about the patient. Pupil changes indicate a very small lesion that is right around the optic nerve or a huge lesion that is causing the patient to herniate.
Check speech first. Put down the penlights and watch the patient's behavior changes.
Best wishes,David W. Woodruff, MSN, RN-BC, MSN, CENPresident, Ed4Nurses, Inc.www.Ed4Nurses.com www.dwoodruff.com

Amiodarone Competency~for RN's

2008-10-10T14:33:00.000-07:00

You will find in your mailboxes a competency for Amiodarone. Each RN needs to complete the quiz and return it to Vilma's mailbox outside the office and while you are there sign the Attendance sheet posted there also.

AHRQ and You-Evidences Based Best Practice Handbook

2008-10-08T11:39:00.000-07:00

You just never know what you find when you are surfing the net these days but looky here a handbook developed from the Agency for Healthcare Research and Quality (AHRQ) for nurses. Sponsored by the Robert Wood Johnson Foundation this is a virtual (literally) treasure trove of best practices from the nurses point of view and get this...researched as best practice, not just "we do it that way because that's how we've always done it" reasons.
The whole book can be accessed.....online-for nothing...and you can order your own 3 volume printed copy or a researchable CD if you so desire but why when this will be updated periodically long before the printed stuff will be available.
http://www.ahrq.gov/qual/nurseshdbk/

What a treat! Take a gander around and see what we can improve on to keep our patients safe and well cared for.
We all have a hand in this so read on McDuff !! :)
Tracy

And they're on their own..

2008-10-01T10:21:00.000-07:00

The new grads are off orientation and are all doing great! We also had a great weekend at ACLS and I am happy to say that Susan Plissey passed without a speck of nerves showing, Dorothy, Jen and I all recerted successfully! The next ACLS is December 6 & 7th. The new grads will be scheduled in the spring class(es) once the dates are annouced I'll post them here.

Just a couple pix of the preceptors with their new grads...

Thank you to all who attended the Wound Update on Monday...if you missed it there will be more at the skills fair in November also. Remember the new regs go into effect today so let the providers know if there are any pressure ulcers on your patients so they can assess and document them in their admission work. Thanks for all you do!

Wound Ulcer Staging and New Standards for Documentation

2008-09-20T13:34:00.001-07:00

Inservice: September 29th every hour on the hour in McCain B with Rhonda Bossie starting at 0700 with the last session starting at 1600.

Starting October 1st there are new CMS regulations going into effect that will effect repayment on pressure ulcers. The long and short of it is that if a pressure ulcer isn't documented at the time of admission(POA or present on admission) by the provider then payment is not guarenteed for the care of this ulcer. i.e. patient A admitted for CHF and hyperglycemia and has a stage II on his heel if the provider doesn't dictate or document the ulcers presence and the ulcer either gets worse or we have treatments to administer (lets say we order an air mattress) it's won't be reimbursed. Since the doctors rely heavily on our documentation of these items we need to be certain that the admitting provider is aware of these as soon as possible to ensure that money is captured by the coding folks.

Here are the staging guidelines for review.
http://www.medicaledu.com/staging.htm
and let's be measuring these-I have found that the white boards are helpful for communication of this info to any provider (wound/ostomy nurses and MD's) in addition to our coworkers who may be changing the dressing after you.

Rhonda will be reviewing some of this info also but I figured having it here too will be a resource for you also. And some of you have already attended the webcast Sept. 9th. This is not a repeat presentation of that information.

So attend 1 session with Rhonda on September 29th for one hour-it starts at 0700 until 1600-if you aren't working that day you have some latitude on what time to attend and if you are working we will do our best to get everyone there.

Questions and answers from the presentation on Sept. 9th; some of you had some questions and I poised them to Rhonda after the session I attended.

Q: Are the physicians being trained?
A: Yes at their monthly meeting this month.

Q: Can we take pcitures of wounds to document them?
A: Not at this time-there is alot of training necessary for this plus obtaining cameras for each unit and only specific formats are allowed by Medical records.

Q: Are we going to purchase/use the "Solutions Algorithms" mentioned in the webinar?
A: Not at this time but the Wound/Ostomy Affiliate group is working on standardized treatments based on the products we use in the system.

One more time: September 29th for an hour in McCain B-Wound updates with Rhonda Bossie.

Thanks for reading!
Tracy

Back to School time SCIP= Core Measures=Best Practice

2008-09-05T15:59:00.000-07:00

Surgical Care Improvement Project

What does this mean to us-well similar to Core Measures it provices a framework of researched best practices only instead of it being about CHF, MI & Pneumonia that Cores target these are specific to pre and post op measures. You may have already seen them as part of ordersets-for instance stopping antibiotics after a set number of doses or VTE prophylaxis/screening. Other measures that we already know work were researched by other studies and are integrated into these measures-like all the respiratory measures SCU staff will recognize as IHI's 100,000 Lives Campaign; having the HOB greater than 30 degrees in a ventilated patient and Ulcer prophylaxis.

Here is a link to all the SCIP measures-and yes this is monitored and reported since repayment is contingent on our completing each step in the process and like Cores if we miss one measure of the whole surgical experience then we fail the whole"bundle" and payment.

http://www.premierinc.com/quality-safety/tools-services/safety/topics/scip/downloads/sci p-final-10-14-05.pdf

One to note especially for SCU staff who commonly recover the big bowel cases is #7 :

Colorectal surgery patients with immediate postoperative normothermia.

Translation: We have 15 minutes to get the postop colorectal patients temp above 96.8.

Everyone is working hard to meet this measure, but even I was unaware that this was the standard until we had already missed one-unfortunate since it decreases the patients risk negative post op issues but now that I know I want you all to be in to make our patients safer also.

Please take the time to read through the measures on the link so that you ar aware also and we can all help each other to facilitate giving our patients the best care research says works.

Thanks for all you are doing for Cores-I went to the meeting on Friday and we were 100% for all measures in June-YEAH US!!!

So if we can do it for Cores-SCIP should be a breeze with a little attention to detail.

Silver Coated ET tubes decrease VAP rates

2008-08-30T17:19:00.000-07:00

Who is getting ready for some changes soon??? ;)

***AND***

Latest JAMA article to decrease VAP in ICU
http://www.medscape.com/viewarticle/579239

Dr. Jimenez is back from a recent mission trip.

More KUDOS!!!

2008-07-10T10:46:00.000-07:00

Woo-Who! Look at this guys. Great Job!
Also for the month of June, SCU did 100% of their chart reviews.
Vilma
_____________________________________________
PYXIS Inventory 2nd Quarter
Due Date SCU Days Delinquent
4/2/2008- 4/9/2008 0
4/16/2008 - 4/23/2008 0
4/30/2008 - 5/7/2008 0
5/14/2008 - 5/21/2008 0
5/21/2008 - 5/28/2008 0
6/4/2008 - 6/11/2008 0
6/18/2008 - 6/25/2008 0

Due Date PCU Days Delinquent
4/2/2008 - 4/9/2008 0
4/16/2008 -4/18/2008 2 LATE
4/23/2008 - 4/30/2008 0
5/7/2008 - 5/14/2008 0
5/21/2008 - 5/28/2008 0
6/4/2008 - 6/11/2008 0
6/18/2008 - 6/18/2008 0
6/25/2008 0

Congrats!!!

2008-07-09T06:21:00.000-07:00

Celebrate the peers amoung us! So far Nic, Nicole (Nikki) Ouellette, Louise, and Becki have all passed their RN boards!!! Latricia (Trish) passed her boards on July 8th! Great job all of you!!
Another Kudos goes out to Wendy Samaroo for passing her Basic Rhythms-as a self study I might add-so far as I know she is the first one to successfully complete this without taking the complete class! Great Job! Wendy will be transitioning to the MT role over the next few weeks so congratulate her when you see her.

What am I?-a Rhythm Quiz

2008-06-21T13:12:00.000-07:00

Scenario: An 83 year old woman with ischemic cardiomyopathy goes into her PCP for a routine checkup. She is receiving appropriate medical management with pharmacological agents and has no acute symptoms.

So evaluate her rhythm:

Rate- normal,brady or tachy?

Rhythm-regular,irregular, irregularly regular?

P waves-one for each QRS, less than one for each QRS, more than one for each QRS, unable to determine ?

PR interval-normal, short, prolonged, can't determine?

QRS duration-normal or wide?

ST segment-negative and less than 0.12, negative and greater than 0.12, positive and greater than 0.12?

T wave-normal or inverted?

QTc-normal or lengthened(greater than 0.47)?

Please print and return to me for competency credit for June. I will post answers after I receive everyone's answers.

Also please copy your certificate from attending Bob Pages EKG interpretation workshop and place it with your items in the competency 3 ring binders on each unit. Thanks!

No More Lead II in Critical Care Services

2008-06-20T15:12:00.000-07:00

http://homepage.mac.com/edutainment/Menu3.html

Here is the link to Bob Page's presentation and practice 12 Leads.

Hope you all enjoyed the information and yes you can expect some competencies on EKG interpretation towards fall. I know several of you purchased Bob's book that was available at the conference and Vilma purchased a book for each unit's resource library also, please make use of them, they are tools in your practice young Padawans. Before long we'll all be Jedi masters of the EKG. 15 leads are in your reach and join me in monitoring in MCL1 my friends, the difference is amazing!

EKG class at P I Inn and Convention Center Tomorrow!!!

2008-06-18T12:54:00.000-07:00

Just a reminder...registration at 7:30...See you there!

Also got this cool article in my email today and thought it was sooo useful...Cardiac meds demystified.

http://www.nursingcenter.com/library/JournalArticle.asp?Article_ID=770337

From Nursing 2008

Have you met a new grad yet?

Big Week

2008-06-14T17:03:00.001-07:00

First off-the new grads will be in the floor starting this week. Please Welcome Nick, Latricia, Nicole, Becki, and Louise as they start the venture to "Registered Nursehood".

"Don't let your past dictate who you are now
but let it be a part of of who you will become "

Next off-the Rep will be here this week for the new Kangaroo Feeding pump-I sent out an email with a link to the companies website with a video tutorial. If you missed it here it is-please try and make it down to the McCain rooms for a hands on also.

http://www.kangarooepump.com/Epump/pageBuilder.aspx?webPageID=131032&topicID=131032

And the EKG class is happening Thursday and Friday at the Presque Inn and Convention Center (yes the Old Keddys) from 8-4 each day-registration starts at 7:30. This will be a great break from the busy floors and get some great info for our brains to enhance our bedside practice.

Thanks for all the extra people have been doing to cover each other with the recent bugs floating around. Really appreciate all you do!

Until next update..
~Tracy

Room supplies

2008-05-22T12:06:00.000-07:00

Bag 1 supplies: Nasal cannula, oxygen extension, tubing connector, Venti mask, and 100% NRB
Bag 2 Supplies: Yankeur Suction, Suction Catheter kit, suction tubing, 80 mm oral airway,
90 mm oral airway, & 100 cm oral airway

Above you see pictures of 2 bags that will be at hand at each patient's bedside.
If you open the supplies for a patient they are only to be used for that patient for the duration of their stay.
Housekeeping will be wiping off the bags if they are not opened but if the seal is opened then the bag "belongs" to that patient.
New supplies in a new bag will be replaced if the bag is opened for a prior patient.
I expect that the suction cannister if used will be replaced in the room other wise housekeeping is only wiping down the exterior surfaces of everything.
This is in an effort to decrease patient exposure especially given the volume of isolation patients we see on a daily basis.

Thanks for your help in keeping our patients safe.

Tracy

Question for you

2008-05-14T12:46:00.000-07:00

Your diabetic patient is to receive Tenormin (Atenolol) this morning.
As her nurse you should assess which lab value:
a. Glucose
b. Potassium
c. Calcium
d. Magnesium

{courtesy of David Woodruff Med/Surg Certification Review}
Answers can be posted here or email.

2008-05-11T15:18:00.000-07:00

We appreciate all you do!

2008-05-08T16:22:00.000-07:00

The Lady With the Lamp National Nurses Week is always May 6-12, ending on Florence Nightingale's birthday. National Nurses Week is always May 6-12, ending on Florence Nightingale's birthday. By ADVANCE staff
Test your knowledge about the founder of modern day nursing with some of these lesser known facts:
Nightingale's father was a pioneer in epidemiology and tutored Florence in mathematics/statistics, an area she excelled in later in her career.
A gifted statistician in her own right, Nightingale was fond of using pie charts when presenting her statistics.
Among many studies, Nightingale did a statistical analysis of sanitation in India.
Nightingale was the first female to be elected to Royal Statistical Society.
Florence Nightingale defied her extremely wealthy family and upper class conventions in choosing to become a nurse in 1845.
Nightingale not only fought for better medical care, but also championed social issues such as reform of the British Poor Laws.
Nightingale's first published work was on a German Lutheran religious community in 1851.
Most famous for her care of soldiers during the Crimean War, Nightingale entered Turkey in 1854 with 38 nurses she personally trained.
In Nightingale's first winter at Scutari in the Crimea, the death toll rose with more than 4,077 soldiers dying.
Nightingale's first evidence-based practice research involved collecting evidence that poor living conditions were the cause of most soldier deaths during the Crimean War.
The Times of London is widely considered responsible for labeling Nightingale "the lady with the lamp."
The U.S. government consulted Nightingale on setting up military hospitals during the Civil War.
As a woman, Nightingale could not serve on the British Royal Commission on the Health of the Army even though she played a critical role in its formation.
What is now the Florence Nightingale School of Nursing and Midwifery, part of King's College London, was established by her to train nurses in 1860.
Notes on Nursing also sold well as a popular book in the 1860s.
In 1867, poet Henry Longfellow's poem "Santa Filomena" further ensured Nightingale's image with the lines, "Lo! In that hour of misery A lady with a lamp I see Pass through the glimmering gloom."
In the 1870s, Nightingale trained Linda Richards, the first formally trained American nurse.
Nightingale died in 1910, but her family declined to have her buried in Westminster Abbey with kings, queens and other English nobility. She is buried in the churchyard at St. Margaret's Church, East Wellow, Hampshire, England.
Nightingale's maternal grandfather was the British abolitionist Will Smith.
Nightingale is named after her birthplace, Florence, Grand Duchy of Tuscany (Italy).
To read more about Florence Nightingale and her continuing influence on nurses, see this selection of editor's picks from the ADVANCE for Nurses archives:
Led by the LampThe Nightingale Initiative for Global Health has created the Nightingale Declaration, designed to bring health to the forefront of world consciousness.For Florence Dee Jones composes and performs a song about nursing's heroine.
Merion Publications

Multi-Lead Medics 12 Lead ECG Interpetation Workshop

2008-05-06T11:44:00.000-07:00

You will notice that on June 19th or 20th you are each scheduled for an 8 hour EKG class. This an interpretation class that will be from 7:30 until 4pm at Presque Isle Inn and Convention Center. Bob Page is the presenter and he is nationally known author on this topic. This should be an excellent presentation and I hope you all bring alot of information back to your practices.

I have placed one copy of the Seminar Workbook on each unit for you to peruse prior to the presentation if you wish but they will be passed out at each session, so don't feel like you have to copy it unless you really want to have a copy ahead of time.

Vilma and I sincerely hope that this is a beneficial conference for all of you.

Tracy

Chart Review/Performance Improvement

2008-04-22T14:59:00.001-07:00

In the FYI section-please welcome Mark Morrow back to PCU, he will be providing his compassionate care on PCU days in the near future.

Congrats go to Susan Plissey for passing her RN boards-she is finishing up orientation with Nicole on PCU nights and will be on her own around the first of May.

Bunny Estabrook is the proud grandmother of the Little Miss PI runner up.

Welcome to Robert Garrett a new CNA on PCU-he joins us from AHC and has already proven to be "johnny on the spot" with a lift so far.

We are missing Blossom Cyr's can do attitude on PCU and we wish her the best with getting her new business venture off the ground and will still she her as a casual staff on weekends.

New travelers for both areas on nights are Amanda Dobson, Robert Pina and Bill Bourke have joined the force in time to cover vacations-welcome them and help them with things as they arise.

Heather Michaud will be returning to SCU in the next few weeks-be sure to give her an understanding smile as she rejoins the fold as a mother of 3!

Thank you to Louanne Langley for all the organizing she has done with what remains in paper-we all appreciate having the needed paper in the files when we reach for it.

Carrie Haas has been working hard at the SCU orientation materials and checkoff lists. I know I appreciate the time she has taken with this project as well as Judy Morrill for serving as our tireless typist:) We love you Judy!

And drumroll please...as promised here are the actual numbers for our Performance Improvement Measures for Chart Reviews the First Quarter.

SCU - overall 86%

PCU- overall 91%

SCU started the year with a bang-Each nurse completed 2 reviews each for 100% compliance, February we dropped to 83% and March was down again to 75%. I can't stress enough how we all impact these items.

PCU for January and February was 86% and improved to 100% for March-these numbers demonstrate that we are capable of achieving greatness; please strive to be the best by doing your part.

Of all of the measures we monitor the most telling is the Critical Lab Reporting. SCU was 89% for the 1st quarter (100-100-67%) And PCU was 84% (75-25-34%) This is a no argument area our expectation is 100%. We have to document each critical result that we obtain. The process is clear. Whichever department that has the result {be that radiology with a positive CT finding to the lab with a high BUN or nuclear with a positive stress test} is to call the unit with this result, the registered nurse will read back the results[RBV] to whomever is calling. Document the result in Ad Hoc in Powerchart in the Provider Notification form clicking the critical result reporting button, sign the form. Page the provider, who understands that criticals have a 1 hour time limit to be reported-this includes the lab running time so often we have 30 minutes to relay the information. When the provider returns the page open the Provider Notification form from the FORMS tab and by right clicking on it to modify it and document actions taken/MD response.

Please know that I fully appreciate the time it takes to get the job done and all your efforts are not ignored. However we still have a way to go to get where we have to be, so your attention to these items shows on reviews.

Next week employee surveys will commence and you will be asked to go to the designated area to complete one starting April 28th.

O.K. how is this working as a mode of communication? I need some feedback....
Until next time.....
Tracy

Chart Reviews and Coumadin dosing

2008-04-17T13:33:00.000-07:00

A few of you have raised a question on the timing of coumadin dosing. I have checked and doubled checked to be certain and according to Dr. Tewksbury and Cheri Fitzpatrick in the lab we will NOT affect lab results if we administer Coumadin at 1600 instead of 2000. 1600 is the default time set in order sentences so it will eliminate the retiming issues that we have had since we went live with Powerchart. So although this will be a change for us to adminster coumadin on day shift instead of nights rest assured we will not disrupt the lab results and most patients usually dose at this time at home so it will be more continuitity of care for them.

Chart reviews~yes, RN's are still expected to complete 2 charts per month. Our most recent quarter results are still lacking. With our decrease in the number of RN's it really shows if only one of us is not completing their share.

I will post the actual numbers but it was staggering the effect that just one person not completing them has on our statisitics. Thank you to those of you that are completing them-keep up the good work!

Tracy

Did you know?

2008-04-02T08:07:00.000-07:00

For bystanders-AHA reccomends that calling 911 and doing chest compressions enhances survival rates - no mouth to mouth necessary-very interesting!

Hands-Only (Compression Only) Cardiopulmonary Resuscitation: A Call to Action for Bystander Response to Adults Who Experience Out of Hospital Sudden Cardiac Arrest

When you see an adult suddenly collapse, use Hands-Only CPR: that's CPR without mouth-to-mouth breaths. And it can help save lives.
Hands-Only CPR is CPR without mouth-to-mouth breaths. It is recommended for use by bystanders who see an adult suddenly collapse in the "out-of-hospital" setting. It consists of two steps:
Call 911 (or send someone to do that).
Begin providing high-quality chest compressions by pushing hard and fast in the center of the chest with minimal interruptions
The American Heart Association recommends conventional CPR (that is, CPR with a combination of breaths and compressions) for all infants and children, for adult victims who are found already unconscious and not breathing normally, and for any victims of drowning or collapse due to breathing problems.
Read the full Hands-Only CPR Advisory statement.
To learn more about Hands-Only CPR visit: americanheart.org/handsonlycpr

General Updates

2008-03-13T09:59:00.000-07:00

Vilma and I are still working through API stuff as you are so please keep doing a paper timecard until we tell you to stop.
While reviewing charts with our chart reviewer this week it was brought up that we should be adding a comment to every IV medication or fluid we are infusing to state that it is infusing on a pump to justify the charge.
We should make sure that the time we are receiving the patient is not the same time as the prior caregivers time-we would be charging services at the same time(i.e. day surgery or ER)
Please obtain a written order for patients on bariatric beds.

Reminder-staff meetings for PCU are Monday and Wed.-see times to the right.

Topics of meeting to include:

API
Blog
Vacations
Future staff meetings

Please let us know if there is anything else you need.

Our condolances to Barb Caron and her family on her recent loss of her father.

Don't forget-Medication Reconcillation Class

2008-03-09T13:05:00.000-07:00

Schedules are posted on each unit-about an hour long class at City Drug with Karla-yes there is a badge reader inside the entrance before you go down the stairs. Please badge in and out as usual to get credit for attending. These are the last classes that are being offered-see me if you have any questions. Thanks!

Tracy

Powerchart Updates for March 18

2008-03-06T04:57:00.000-08:00

Here are the quarterlyupdates for Powerchart there are several upcoming changes and just general updates to forms-please go through these 2 pages and let me know if you find any issues-these are meant to make things easier and to clarify issues that have been raised to our attention. Thank you for taking the time.

https://webmail.emh.org/exchange/TWhitten@tamc.org/Sent%20Items/March%2018%20Powerchart%20Updates.EML/PC%20-%20Update%20for%20Quarterly%20Update%20March%2018%202008TAMC.doc/C58EA28C-18C0-4a97-9AF2-036E93DDAFB3/PC%20-%20Update%20for%20Quarterly%20Update%20March%2018%202008TAMC.doc?attach=1
Tracy

Part One of New Drugs 2008- API

2008-03-02T08:48:00.000-08:00

Sorry for the link but I tried to add just the PDF to the blog but it wouldn't cooperate...but thought this was important since we often don't research these new drugs until we get a patient that is taking them.

http://www.nursingcenter.com/library/journalarticleprint.asp?Article_ID=770334

Things are progressing with API-how are you finding things? Vilma is working on getting everyone PC access, please remember that it takes some time for the info to "cross" from the badge reader to the computer system so if you badge is don't badge in on the PC-from what I have seen it's taken at least 20 minutes to see your badge on the PC account. Please make sure when you are badging out of "charge" in the middle of a shift that you badge yourself back in for the rest of the shift. Everyone is really doing well overall-I know it's frustrating to not "see" what you just badged show up on the reader itself but we can help you until you get PC access.

A fond and sad goodbye to Crystal Laster was given on Wednesday in the form of a pot luck that I heard was delicious. We interviewed a couple of potential candidates this past week and are hoping things pan out in that area. I did type a couple we are being proactive since we anticipate some of our staff(Becki) to graduate in the spring and we want to be prepared to have folks step into spots as that and vacations start in earnest for the summer.

If you have any ideas of what you want to see here please let me know and I will do what I can to get it here.

Have a great week!
Tracy

Pain, Potty and Position~Hourly Rounding improves patient satisfaction and decreases falls

2008-02-24T09:06:00.000-08:00

Pain, Potty and Position-the new motto...

Bob Murphy raised this as a way to raise our patient satisfaction at Spring Fever the past couple days. So along that vein, Here is an article to support this expectation.

I know we are all about making the patient's stay a better one while making our jobs a pleasant experience at the same time. This article with research discusses the stress "bellringers" place and how hourly rounding can decrease patient and caregiver stress.

http://www.medscape.com/viewarticle/570242

This is a focus for our areas this year-increasing patient satisfaction through hourly rounding will affect our Avatar patient satisfaction scores if we remember to round on our patients and remind them that they may receive a survey in the mail after discharge that we use to make us better and that we rely on their responses to do just that, judge what we are doing well and improve on our weak areas.

Tracy

API starts today :)

2008-02-24T04:57:00.000-08:00

Of course those of you at work are aware of this. Try to remember to clock/badge in and out using special codes for incentive/reward shifts as well as charge if they apply. I'm sure there will be lots of questions as things come up-please don't hesitate to ask questions. Please continue to do your paper timecard until we tell you to stop; this will just help us to double check your badged time against what you really worked in case the codes weren't entered at the time you badged.

Take a deep breath and remember It usually takes a long time to find a shorter way.

Be patient we will get there together.
Tracy

Heart Failure Reading-Core Measures

2008-02-23T06:26:00.000-08:00

We are deep in Heart Failure season so thought it was appropriate to review some things to meet the Core measures that affect our repayment on Heart Failure admissions.

Here are some reading links for you....
http://www.nursingcenter.com/library/JournalArticle.asp?Article_ID=741530

http://www.jointcommission.org/PerformanceMeasurement/PerformanceMeasurement/Heart+Failure+Core+Measure+Set.htm

You all have been doing well with reminding caregivers and education of patients but a little review never hurts to keep us all current!

Kudos to Otie for someone out of our department noticing what we all see each day you work-Norman Roy mentioned that even though she was busy one day she took the time to review a patients needs with him. Again something we do each day but feels good to know that we are valued for our knowledge of our patients.

Dr. Hanf also recognized Wanda's efforts with a difficult end of life situation and managed her up to the family as well as to Rosalie Dwyer which went a long way to making the death experience for the family as much of a positive experience as could be expected.

Nice job Ladies!

Have a nice weekend!

Tracy

EKG Quiz for RN's

2008-02-21T01:49:00.000-08:00

Alrighty so here is the first competency for this year. Print off and complete for this years competency. It's not as hard as it looks. Drumroll please...

EKG Quiz
1. You’re caring for a patient with a history of mitral valve prolapse(MVP). Based on your knowledge of the heart’s anatomy, you know the mitral valve is located between the :
a. the left atrium and left ventricle
b. the left ventricle and the right ventricle
c. the right atrium and the right ventricle
d. the right ventricule and the pulmonary artery

2. A 45 year old patient is admitted to your floor for observation after undergoing cardiac catherization. His test results reveal a blockage in the circumflex artery, which supplies oxygenated blood to which area of the heart?
a. anterior wall
b. lateral wall
c. inferior wall
d. septal wall
3. Which of the following choices is responsible for slowing heart rate?
a. norepinephrine
b. vagus nerve
c. epinephrine
d. isoproterenol
4. A 65 year old patient diagnosed with angina is admitted to your telemetry unit. You begin cardiac monitoring and record a rhythm strip. Using the 8-step method of rhythm strip interpretation what should you do first?
a. Calculate the heart rate
b. Evaluate the P wave
c. Check the rhythm
d. Measure the PR interval
5. A 76 year old patient with heart failure is receiving furosemide(lasix) 40mg IV twice daily. When you look at her rhythm strip, you note prominent U waves. Which condition may have caused the U waves to appear on your patient’s rhythm?
a. hypokalemia
b. hypocalcemia
c. worsening heart failure
d. pericarditis
6. A patient with a history of paroxysmal atrial tachycardia {PAT} develops digoxin toxicity, which may cause prolongation of the PR interval, so you must monitor his cardiac rhythm closely. What’s the duration of a normal PR interval?
a. 0.06 to 0.10 second
b. 0.12 to 0.20 second
c. 0.24 to 0.30 second
d. 0.36 to 0.44 second
7. A patient is admitted to your telemetry unit with a diagnosis of sick sinus syndrome. Which medication should you keep readily available to treat symptomatic bradycardia?
a. isoproterenol( Isuprel)
b. verapamil (Calan)
c. lidocaine
d. atropine

source:ECG Interpretation made Incredibly Easy! Lippincott Williams & Wilkins, 2005there are many quick quizzes like this available @ http://www.nursing2007.com/ (click the educators button)

By popular demand the answers are as follows:
1-A 2-B 3-B 4-C 5-A 6-B 7-D {added on 3mar08}

Welcome All !!!

2008-02-21T01:15:00.000-08:00

Here you go-a blog just for us....I'll try to keep this as THE source for updates.

The first post is dedicated to API-hey we all like to get paid right? Vilma and I will be learning the system as you are. If you think you have forgotten to badge/clock in or out for a shift we will be able to help the process. Sunday February 24th is our first day to badge. We have some of your badges and are distributing them as we see you-you have to turn in our old badge with the cover to receive the new one.

Please let me know what kinds of things you want to see here and I will oblige as much as I can :)

Until the next time,
Tracy