Saturday, March 31, 2007
Q; Which condition may mimic pseudo-atrial flutter on EKG and monitor?
A; Parkinsonian tremor
(first reported about 40 years ago 1 and later on many other reports confirmed it)
In this month of Mayo Clinic Proceedings, a case has been reported of pseudo atrial flutter with use of portable CD player by patient. 2
1. MUSCLE-TREMOR ARTIFACT DUE TO PARKINSON'S SYNDROME. IT STIMULATED ATRIAL FLUTTER AND DISAPPEARED DURING SLEEP - Postgrad Med. 1965 Jun;37:718-20.
2. Atrial flutter simulated by a portable CD player - mayo clinic proceedings - march 2006,82(3), Page 383 -pdf file
Friday, March 30, 2007
Serious medication errors are common in the ICU setting and are estimated to be around 15%. Per anecdotal reports, most of the errors are in late afternoons when most of the orders are carried or during the time nurses change shifts. There has been several ways to reduce these errors including
- trained intensivists running close units,
- dedicated ICU pharmacist,
- switching to electronic orders and barcode system,
- avoid (dangerous) abbreviations,
- use of smart pumps for infusions among others, and
- using TALLman letters,
What are TALLman letters:FDA's Office of Generic Drugs requested manufacturers of sixteen look-alike name pairs to voluntarily revise the appearance of their established names in order to minimize medication errors "by TALLing the confused letters". Examples are
DOBUTamine and DOPamine
GlipiZIDE and GlyBURIDE
Related link: Institute for safe medication practices
Thursday, March 29, 2007
Acetadote (IV mucomyst)
As we are seeing higher use of IV Mucomyst (Acedadote) for acetaminophen (Tylenol) overdose, it is not a bad idea to keep IV benadryl and steroid at bedside as flushing, urticaria and angioedema are frequent side effects. Also caution is advised in patients with asthma and bronchospasm.
Commercially available version (Acetadote) changes color from colorless to light pink / purplish once the stopper is punctured. This is a benign and expected effect and doesn't require any intervention. Acetadote can be prepared generically by hospital pharmacy, if commercial version is not available, and this color change may not be always apparent.
Related video/lecture: Acute Liver Failure: The Critical Team Approach (Dr. Lorenzo Rossaro, Head of the Liver Transplant Program at UC Davis Med Center (this video requires real player)
Related previous pearl: 4 Phases of Acetaminophen Toxicity And (r) Rumack-Matthew Nomogram.
Wednesday, March 28, 2007
Epogen and Iron
Erythropoetin (Epogen/Procrit) will not work if patient's Iron level is low. But important points to remember:
- Simply checking Fe level may not provide reliable answer to Fe storage 1.
- Erythropoetin, by stimulating erythropoiesis to greater than physiologic level, may itself induce iatrogenic functional iron deficiency.
- Oral iron may take longer and may not satisfy the requirement and extra dose of IV iron may be needed. IV loading dose followed by intermittent maintenance doses may be required.
The simple formula to see if a supplemental iron is required:
* some recommends 30%
References: click to get abstract/article if available
1. Diagnosis and management of iron-related anemias in critical illness. Critical Care Medicine. 34(7):1898-1905, July 2006
2. Optimization of Epoetin Therapy with Intravenous Iron Therapy in Hemodialysis Patients - Am Soc Nephrol 11:530-538, 2000
Tuesday, March 27, 2007
Q; Is equal breath sounds a reliable indicator of proper placement of ETT (endotracheal placement) ?
Atleast per one study, equal breath sounds can be heard in up to 60% of right main stem intubations and can't be count as a reliable indicator of proper placement of ETT. Only CXR and morely, a bronchoscopy is a reliable way to confirm ETT placement.
Related previous pearls: What's the right length of endotracheal tube (ETT) for oral intubation?
References: click to get abstract/article if available
1. Assessment of routine chest roentgenograms and the physical examination to confirm endotracheal tube position. Chest1989;96:1043-1045.
Monday, March 26, 2007
Etomidate for intubation - yes or no?
Dr. Annane says: ICU physicians should abandon the use of etomidate! 1 Even a single dose of Etomidate for intubation can induce longer than expected (24 -36 hours) adrenal insufficiency particularly in septic patients. But dilemma for ICU physicians never ends. Either they use other agents such as midazolam, fentanyl, propofol etc and manage post-intubation hypotension shrewdly to avoid essential organs damage or add irrespectively low dose steroid along with etomidate ?
In references below, we are putting major articles in this regard from recent literature and here is a great review on said topic,
The uncertain risk of single dose Etomidate in the critically ill (reference: Hospial Pharmacy, Volume 40, number 8, 2005, page 658-661)
References: click to get abstract/article if available
1. ICU physicians should abandon the use of etomidate! -Intensive Care Med 2005, 31:325-326
2. Adrenocortical function in critically ill patients 24 h after a single dose of etomidate. - Anaesthesia 1999, 54:861-867
3. Should We Use Etomidate as an Induction Agent for Endotracheal Intubation in Patients With Septic Shock? - A Critical Appraisal -William L. Jackson, Jr, MD, FCCP - Chest. 2005;127:1031-1038
4. Etomidate for endotracheal intubation in sepsis: acknowledging the good while accepting the bad. - Chest 2005, 127:707-709
Saturday, March 24, 2007
Demerol and Zyvox
As Zyvox (linezolid) is getting more and more popularized in hospitals, it is important to remember an important drug interaction.
Demerol with Zyvox can be a deadly combination even if prescribed within last 2 weeks. It may induce 'symptom cluster' consisting of fever, agitation, seizure, coma or death.
Related previous pearl: Why PO Demerol is not a good idea !!
Friday, March 23, 2007
On reintubation rate
Here is a little twist if you are proud of your too low reintubation rate !!
"A reintubation rate of 5% to 15% is acceptable; lower rates indicate the patients are being kept on the ventilator too long, while higher rates suggest that they are being taken off too soon". - Dr. Neil R. Macintyre - at ACCP annual meeting, october 23, 2006
HOW TO ESTABLISH A VENTILATOR WEANING PROTOCOL , Gregory P. Marelich, MD - thoracic.org
When to wean from a ventilator: An evidence-based strategy, Ref: CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 70, NUMBER 5 MAY 2003 page 389
Related previous pearls:
Spontaneous Breathing Trial (SBT) - how long - 30 minutes or 120 minutes?,
IV steroid to reduces postextubation stridor
Thursday, March 22, 2007
Q: Why we call it cryoprecipitate?
A: The name explains everthing. cryoprecipitate means "cold precipitate". When FFP is thawed slowly at 4 degree C, a white precipitate forms at the bottom of the bag, which can then be separated from the supernatant plasma. This precipitate is rich in fibrinogen, factor VIII, von Willebrand factor, factor XIII, and fibronectin - and call crayoprecipitate. One unit of cryoprecipitate is derived from fresh frozen plasma (FFP) prepared from a unit of whole blood and as it is only a little precipitate at the bottom of the bag, 1 unit of cryoprecipitate comprised only a volume of 10-20 mL. Contents:
- 80-100 units of factor VIII, which consists of both the procoagulant activity and the von Willebrand factor,
- 150-250 mg of fibrinogen,
- 50-100 units of factor XIII, and
- 50-60 mg of fibronectin.
Wednesday, March 21, 2007
Citrate in CRRT
Q; Why we use citrate (when heparin is not used) to avoid filter clotting in CRRT / CVVHD (continuous renal replacement therapy) ?
A; Citrate combines with calcium and cause extracorporeal chelation of calcium and blocks calcium dependent steps of clotting cascade.
When extracorporeal blood mix with venous blood, the ionized calcium level get resotred and systemic anticoagulation get avoided. Also citrate get metabolized via liver and chelated calcium get release back in circulation which prevents hypocalcemia (though frequent checks required particularly in liver insuff.).
Related: Very nice review article: Acute Renal Failure in ICU (reference: nephrologyrounds.org, december 2006, volume 4, issue 10) - pdf file
Tuesday, March 20, 2007
Tuesday March 20, 2007
Ports of PICC
Do you know that, PICC lines have no distal or proximal port. They run side by side. This is because, PICC line needs to be trimmed from top depending on length per patient height. As PICC lines need to be trimmed, it is a good practice to document in chart the length of PICC at removal with length at insertion time. Obviously, they should be same. Length of PICC on removal ______ cm = Length of PICC on insertion ______ cm
Related previous posts:
Monday, March 19, 2007
Acute hyperglycemia may lower tPA effect in stroke patients
As benefits of blood sugar control is getting more and more attention, this new study published in stroke 1 from spain is noteworthy which found that "acute" (but not chronic) hyperglycemia may lower tPA effect in stroke patients. As known from before, hyperglycemia has a deleterious effect in stroke patients by accelerating ischemic brain damage. This study showed that antifibrinolytic effect of hyperglycemia may also influence reperfusion.
Glucose level at admission was recorded in 139 consecutive stroke patients who were treated with intravenous tissue-type plasminogen activator (tPA). The existence of previous chronic hypergycemia was determined by glycosylated hemoglobin (HbA1c) and fructosamine.
- Transcranial Doppler monitoring assessed complete recanalization 2 hours after tPA bolus.
- National Institutes of Health Stroke Scale (NIHSS) scores were obtained at baseline and 48 hours.
Results — Patients who recanalized showed lower admission glucose levels but no differences in HbA1c or fructosamine.
Patients with an admission glucose level more than 158 mg/dL had lower recanalization rates (16% vs 36.1%) and a higher NIHSS score at 48 hours (7 vs 14.5). After adjustment for stroke etiology, age, and risk factors, the only independent predictors on admission of no recanalization were
Study concluded that in tPA-treated patients, the acute but not chronic hyperglycemia state may hamper the fibrinolytic process, delaying reperfusion of the ischemic penumbra. Early measures to reduce blood glucose may favor early recanalization.
Reference: Click to get abstract
1. Acute Hyperglycemia State Is Associated With Lower tPA-Induced Recanalization Rates in Stroke Patients -Stroke. 2005;36:1705
Saturday, March 17, 2007
Lets have an easy sunday !
Why mobile computer at bedsides is called "cow"?
COW = Computer On Wheels
Friday, March 16, 2007
Anchor sutures at chest tube !
Falling off of chest tube is a major problem. Though never been tested in a clinical trial but applying 2 side by side anchor sutures along with mattress suture have been anecdotally said to void this problem. See step by step application of anchor and mattress sutures here (ref. Eur. Respir. journal 1998; 12: 958-959) - pdf link
Related: BTS guidelines for the insertion of a chest drain
While removing IABP
While removing IABP (IntraAortic Balloon pump), it is important to keep manual pressure at site for atleast 45 minutes to avoid bleeding
DO NOT get tempted to peek during compression at site as it may wash away the building/immature clot with flush of arterial wave. It is also recommended to apply clamp for 60 minutes after manual compression as extra precaution against bleeding.
Note: Same apply for big bore catheters at femoral site
Thursday, March 15, 2007
What's the right length of endotracheal tube (ETT) for oral intubation?
As a gold standard the only way to make sure that tip of ETT is atleast 2 cm away from carina (or at appropriate place) is via chest X-ray. But there are many bedside quick tricks/formulae described in literature. One such formula 1 which also found to have good clinical correlation, is
ETT length (incisors to midpoint of trachea, cm) = patient's height (cm)/10+5
Like, if patient's height is 170 cm, ETT should be taped at
170/10 + 5 = 22 cm
Another trick is to have ETT's cuff palpable at sternal notch, a technique described about 40 years ago ! 2 .
Related previous pearl:
Movement of endotracheal tube (ETT) with neck
1. Anaesthesia Intensive Care 1992; 20:156;
2. Anesthesiology 1964; 25:169
Wednesday, March 14, 2007
Heparin Induced HyperKalemia
Hyperkalemia from Heparin is a well know phenomenon and has been detected particularly on geriatric, renal insufficient and diabetic patients. Hyperkalemia can be anywhere from .3 to 1.7 mEq/Litre. It usually occurs around on day 3 with SQ heparin (as for DVT prophylaxis) but can occur early with IV heparin 1,2,3,4. Hyperkalemia has been reported with low- molecular weight heparins too but risk is low 5, 6, 7.
Mechanism of action: Heparin induce hypoaldosteronism and can subsequently lead to hyperkalemia 6.
Treatment: Best thing is to discontinue the culprit but if heparin is absolutely required, fludrocortisone (.1 mg/day) has been reported to be effective in heparin-induced hyperkalemia 8.
References: Click to get abstracts/articles
1. Case report - Heparin-induced hyperkalemia after cardiac surgery - Ann Thorac Surg 2002;74:1698-1700
2. Heparin-induced hyperkalemia -The Annals of Pharmacotherapy: Vol. 24, No. 3, pp. 244-246.
3. Heparin Induced HyperKalemia - Endocrine Abstracts (2002) 4 P26
4. Heparin-Induced Hyperkalemia Confirmed by Drug Rechallenge. American Journal of Physical Medicine & Rehabilitation. 79(1):93-96, January/February 2000.
5. Early onset of hyperkalemia in patients treated with low molecular weight heparin: a prospective study - Pharmacoepidemiol Drug Saf.2004 May;13(5):299-302.
6. Effect of Low-Molecular-Weight Heparin on Potassium Homeostasis - Pathophysiology of Haemostasis and Thrombosis 2002;32:107-110
7. Low Molecular Weight Heparins Can Lead To Hyperkalaemia The Internet Journal of Geriatrics and Gerontology . 2005. Volume 2 Number 2.
8. Fludrocortisone for the treatment of heparin-induced hyperkalemia - The Annals of Pharmacotherapy: Vol. 34, No. 5, pp. 606-610
Tuesday, March 13, 2007
While doing bedside 'line' procedure under ultrasound make sure you use sterile gel packet (instead of gel bottle hanging at the side of machine), otherwise it will defeat the whole purpose of sterile field and will invite for sure line infection !!
Monday, March 12, 2007
ARDS as a complication of Acute Pancreatitis (AP)
Today's Pearl contributed by
Surindra J. Singh, M.D.
VAMC, Salem, VA 24153
Acute Pancreatitis is rather common condition in ICU population, with mortality rate of approaching 15%, most patients dying form SIRS and MODS. Pulmonary complication is the most critical development and include hypoxia, atelectasis, pleural effusion and ARDS.
Early recognition of AP as well as any pulmonary sign should be dealth with aggressive intervention to improve the outcome of patients with AP.
See article: Pathophysiology of pulmonary complications of acute pancreatitis , (World J Gastroenterol 2006 November 28; 12(44): 7087-7096)
Refrence: click to get article
Predicting development of infected necrosis in acute necrotizing pancreatitis , Medicina (Kaunas) 2006; 42(6), Institute for Biomedical Research, Kaunas University of Medicine, Lithuania
Sunday, March 11, 2007
Sunday March 11, 2007
Pulmonary Artery Catheter (PAC) supplement
ccforum.com is a valuable read on this debate.
In recent years, use of PAC and it benefits has been questioned in many studies. Recent supplement on PAC (available free on net) at
As Professor Jean-Louis Vincent wrote in its editorial:..."So, amidst all of these gloomy reports, does the PAC have a future or is it doomed to gather dust at the back of ICU equipment cupboards before reaching its final resting place as a curiosity in museums of medical history? I believe that the PAC still has a place in today's ICU, and that the information it provides can be integrated with that derived from newer equipment to optimize patient care. The PAC is a monitoring tool; if it is used to direct therapy and there is no improvement in outcome, then the therapy does not help. We know that PAC-derived data can prompt therapy to improve patient outcomes but such improvements are not always achieved (e.g. sometimes physicians do not make the necessary changes to their therapy as suggested by the measurements) or indeed there may be overzealous application of therapies (e.g. fluid challenge for low cardiac filling pressure when there is no need for it). Thus, there is a need for better strategies based on the measurements obtained."
Articles include topics like
- Hemodynamic optimization of sepsis-induced tissue hypoperfusion
- Clinical relevance of data from the pulmonary artery catheter
- Oxygen uptake-to-delivery relationship: a way to assess adequate flow
- What role does the right side of the heart play in circulation?
- Which cardiac surgical patients can benefit from placement of a pulmonary artery catheter?
- Which general intensive care unit patients can benefit from placement of the pulmonary artery catheter?
- Evidence-based review of the use of the pulmonary artery catheter: impact data and complications
Access full supplement
Saturday, March 10, 2007
What is cell saver
"Cell saver" is a machine which suctions, washes, and filters blood so it can be given back to the patient's body instead of being thrown away (see figure below). In other words, patient receives his own blood. Newer machines have now flexibility of even salvaging less amount of blood loss down to 70 cc.
The cell saver is a viable choice for patients with Jehovah's Witness belief. Literature is full of controversy about its cost effectiveness and efficacy but in surgery with higher "EBL" (estimated blood loss) definitely it is a valuable technology.
See article: Intraoperative blood salvage in vascular surgery – worth the effort? (Critical Care 2004, 8(Suppl 2):S53-S56)
click on picture to see bigger image
Friday, March 9, 2007
Anti-diabetic pills overdose remained one of the leading cause of drug overdose worldwide. Among anti-diabetic pills sulfonylureas are the most dangerous and hard to correct. Overdose of metformin rarely causes clinically evident hypoglycemia (It has its own danger of cardiovascular collapse and renal failure, due to severe lactic acidosis).
Unfortunately very few clinicians use the real antidote for sulfonylurea which is Octreotide (Sandostatin) in resistant hypoglycemia. Infusion of glucose to achieve euglycemia in the early phase is an appropriate treatment but there is some literature available which argues that prolong infusion of dextrose in sulfonylurea overdose may make hypoglycemia longer and worse by stimulating insulin release. The dose for Octreotide is 50 mcg SC every 8 hours with adjustment of dose according to blood glucose level. Octreotide is a somatostatin analogue, which activates G-protein K channel and hyperpolarization of the beta cell results in inhibition of Ca influx and insulin release.
Another antidote for sulfonylurea overdose beside octreotide is Diazoxide. Exact mechanism is unknow but probably it increases blood glucose by inhibiting pancreatic insulin release. It is found to be effective within 60 minutes of administration. The usual dose is 5 mg/kg/day intravenously and should be divided every 8 hours. Dose can be increased if needed but still its experience in comparison to octreotide is limited.
References: click to get abstracts/articles
1. Octreotide for sulfonylurea-induced hypoglycemia following overdose - The Annals of Pharmacotherapy: Vol. 36, No. 11, pp. 1727-1732
2. Clinical spectrum of sulfonylurea overdose and experience with diazoxide therapy - Archives of Internal Medicine Vol. 151 No. 9, September 1, 1991
Thursday, March 8, 2007
Q: What is the basic difference between 2 major modes of 'Bilevel' ventilation - BiPhasic and APRV (Airway pressure Release Ventilation) ?
A: "BiLevel" is relatively a newer mode of ventilation which allows patient to breath normally at any level of PEEP. It is a PC (pressure control) mode of ventilation that allows both spontaneous and mandatory breaths. It has 2 levels of PEEP;
- High PEEP (PEEPH) and
- Low PEEP (PEEPL)
BiPhasic: allows patient to breath at any level of PEEP.
APRV: allows patient to breath only at high PEEP. APRV has established Time High (TH) to breath on higher PEEP and smaller Time Low (TL) to relieve pressure.
Read good description here from puritanbennett site.
Wednesday, March 7, 2007
Ever get shocked while putting central line?
We found this interesting case in Academic Emergency Medicine 1.
While putting central line, patient developed arrthymia as guidewire entered the cardiac structure. Pt. had automatic implantable cardioverter defibrillator (AICD) which get activated with arrhythmia and shock was transmitted and felt by the operating physician !! No harm happened to physician or patient.
Lesson learned: To avoid extensive insertion of wire more than needed.
Related previous pearl: Appropriate length of guide wire to advance
Reference: click to get abstract/article
An Unexpected Complication of Central Line Placement - Acad Emerg Med.2001; 8: 854.
Tuesday, March 6, 2007
What if plasma exchange is not available as treatment for TTP
Q: You just diagnosed a patient with thrombotic thrombocytopenic purpura (TTP) but you were informed by the nursing supervisor that plasma exchange with fresh frozen plasma is not available in hospital due to technical reason and it will take time before patient can be transferred to a facility where the said services are available. What would be your alternate plan to bridge that time?
A; High-dose plasma infusion with rate of 25-30 mL/kg per day. When immediate plasma exchange with fresh frozen plasma is not available, simple plasma infusion can be performed until transfer to a higher care facility is available. There is always a substanial risk of fluid overload with such high plasma infusion and you have to weigh risks and benefits of the clinical decision or to watch patient closely while plasma is infusing.
Reference: click to get abstract/article
High-dose plasma infusion versus plasma exchange as early treatment of thrombotic thrombocytopenic purpura/hemolytic-uremic syndrome - Medicine. 82(1):27-38, January 2003.
Monday, March 5, 2007
ScVO2 and SVO2 - debate going on !!
There is an intensified debate about correlation between mixed venous (SVO2) and central venous oxygen saturation (ScVO2) since inclusion of ScVO2 as a marker in "River's early goal directed therapy" for sepsis. And publication of article: Lack of Equivalence Between Central and Mixed Venous Oxygen Saturation by Chawla and coll. in chest (2004)
We had previously posted pearl with references regarding this debate and recommended approach of its use. See our previous pearl ScvO2 or SvO2 ?
Another attempt to look into this issue has been published recently in Indian Journal of Critical Care Medicine. 298 comparative sets of samples from 60 adult patients were obtained, after a Pulmonary Artery Catheter and triple lumen catheter was inserted through right IJV. Mixed venous oxygen saturations and central venous oxygen saturations were compared.
The mean difference between Svo2 and Scvo2 was - 5.14
Study concluded that Scvo2 and Svo2 are closely related and are interchangeable.
Editor's note: One limitation of this study we noticed, is single type patient population with first 30 hours of post-operative period. Caution is advise before applying to all section of critically ill patients.
References: Click to get abstract/article
1. Lack of Equivalence Between Central and Mixed Venous Oxygen Saturation Chest. 2004;126:1891-18962. Correlation of mixed venous and central venous oxygen saturation and its relation to cardiac index, Indian Journal of Critical Care Medicine, Year 2006, Volume : 10, Issue : 4, Page : 230-234
Sunday, March 4, 2007
Vancomycin dosing in CRRT
Vancomycin dosing is different in CRRT (Continuous Renal Replacement Therapy) from IHD (Intermittent HemoDialysis) as vancomycin is effectively removed during CRRT. Vancomycin is 14K daltons and CRRT filter removes upto 20K daltons size molecules. Frequent monitoring of Vancomycin level is required. Different intervals has been described from 24 to 48 hours. Most agree on 10 mg/kg every 24 hours. Ultimate goal is to keep vancomycin trough atleast between 10 - 15 mcg/ml.
Related: ppt slides on CRRT from Gregory M. Susla Pharm.D here .
References: Click to get abstract/article
1. Vancomycin dosing and monitoring - Division of Infectious Diseases, Department of Medicine, Columbia University Medical Center (CUMC), columbia.edu
2. CVVH Initial Drug Dosing Guidelines - from thedrugmonitor.com
Saturday, March 3, 2007
Antidote for vasoconstrictor extravasation in skin and tissues (dopamine, epinephrine, or norepinephrine) is PHENTOLAMINE.
Infiltrate 5-15 mg of PHENTOLAMINE in 10 ml of normal saline into the area of extravasation as soon as possible. Treatment may be applied and effective up to 12 hours post extravasation of vasoconstrictor. Phentolamine may drop blood pressure so keep yourself ready for intravenous fluid bolus post treatment.
Mechanism of action: Phentolamine is a nonspecific alpha-adrenergic blocking agent which inhibits vasoconstriction and allow improved blood circulation through the affected area.
References: Click to get abstract or article
1. Drug Monographs - Phentolamine - lhsc.on.ca
2. Treating Extravasation Injuries - extravasation.org
3. The use of phentolamine in the prevention of dopamine-induced tissue extravasation - J Crit Care 1998 Mar;13(1):13-20
Friday, March 2, 2007
Vancomycin induced thrombocytopenia
So far Vancomycin was not blamed for thromboctopenia but this week in The New England Journal of Medicine, case series of 34 patients with vancomycin induced thrombocytopenia has been reported. The mean nadir platelet count was 13.6, with severe bleeding reported in 10 patients. Drug-dependent, platelet-reactive antibodies of the IgG class, the IgM class, or both were identified.
Platelet levels returned to baseline after vancomycin was stopped.
Related previous pearl: Vancomycin-induced Stevens-Johnson syndrome
Reference: click to get abstract
Vancomycin-Induced Immune Thrombocytopenia - Volume 356:904-910, The New England Journal of Medicine, March 1, 2007, number 9
Wednesday, February 28, 2007
Regarding Dexmedetomidine (Precedex)
One sedative which has been successfully used in cardiothoracic ICUs but didn't made real penetration in medical ICUs is Dexmedetomidine (Precedex).
The unique property of precedex of no respiratory depression helps in extubating agitated patients and can be continued beyond extubation (which is in contrast to other sedatives) . Another advantage of Precedex is its analgesic property. It minimize the simultaneous use of other analgesics. It possesses anxiolytic, anesthetic, hypnotic, and analgesic properties.
The dose is IV bolus of 1 mcg/kg over a 10-minute period, followed by a continuous IV infusion of 0.2 mcg/kg per hour which can be titarted upto 0.7 mcg/kg. Due to lack of data on this drug some hospitals restrict its use for 24 to 48 hours.
This drug should be avoided with bradycadia and heart blocks. Interestingly, continuous infusion cause hypotension as like propofol but hypertension can occur with loading dose !!
See nice review article: The Role of Dexmedetomidine (Precedex) in the Sedation of Critically Ill Patients (ref: P&T, Vol. 30 No. 3 • March 2005 , 158-161)