Levo vs. Neo: A Change of the Guards?

Vancomycin IV infiltration, yet we still give through PIV

From A&A May 2016: Should Norepinephrine, Rather than Phenylephrine, Be Considered the Primary Vasopressor in Anesthetic Practice?

http://www.ncbi.nlm.nih.gov/pubmed/27101504

GA = Sympathectomy, decreased NE and Epi concentrations

Phenylephrine (PE, trade name Neosynephrine aka Neo)
pure alpha 1 agonist
increase ABP, decrease HR
CO effect mixed +/- venous return, decreased HR

Norepinephrine (NE, trade name Levophed aka Levo)
alpha1 and beta1, some beta2
relaxation of venous resistance
NE enhances venous return +CO
+ionotropy, little chronotropy
+arterial vasoconstrict
+HR, +SV, +CO

Potency of NE:PE 20:1

NE levels increased in cardiac failure

PeriOp circulating Catecholamine levels

NE and Epi decreased by
-diazepam
-thiopental (even more in uremic)
-midazolam
-pancuronium
-spine surgery + prop or iso

NE and Epi increased by
-Ketamine
-1.5 mac Desflurane
-succinylcholine
-rapid increase in Isoflurane
-intubation
-abdominal surg + sevo/n2o
-emergence/extubation

little effect from roc/vec

Comparing NE to PE in specific studies and circumstances

Aortic stenosis
-PE resulted in higher MAP, no differencve in LV fx vs. Levo

CABG
-PE imparied LV function, unchanged with levo

Pulmonary HTN cardiac surgery pts
-CI maintained with NE, decreased with PE
-NE improved (reduvced) ratio of mean PA pressure to SBP

General Surgery, isoflurance
-NE increased LV performance
-PE decreased LV performance

General Surgery, prop+remi
-both PE/NE decreased CO and HR, increased MAP

C/S Spinal
-PE vs. NE infusion
-NE had same sbp, higher HR, higher CO c/w PE

If LV fx impaired, enhanced afterload from PE -> decreased CO and systemic perfusion

but what about infiltration? Largely overblown as, yes NE 7x more constrictive in radial ARTERY, yet only 76% more vasoconstrictive in veins and concentration of Levo is 20x less than PE

if infiltrate -> give phentolamine

 

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Fluorite

Calcium Fluoride

http://www.apsf.org/newsletters/html/2007/fall/03_sevoflurane.htm

Sevoflurane: The Challenges of Safe Formulation

Do you know the water content of your sevo?

From the anesthesia patient safety foundation newsletter:

An incident of Lewis acid mediated sevoflurane degradation occurred in 1996.5,6 Several bottles of sevoflurane had cloudy drug, a pungent odor, marked acidity (pH <1), and high fluoride (863 ppm), all indicating substantial anesthetic degradation and formation of HF, in quantities far exceeding the safe limits of 3 ppm over an 8 hr average. Abbott subsequently determined that increasing the water content in sevoflurane formulations decreased Lewis acid-dependent sevoflurane degradation.7 They changed the sevoflurane formulation to contain at least 300 ppm water, in order to prevent Lewis acid degradation and formation of toxic degradants. The new “water-enhanced” sevoflurane formulation was approved later that year by the U.S. Food and Drug Administration (FDA), and awarded patent protection.

Why is all this important? Generic sevoflurane formulations do not contain Lewis acid inhibitors, nor can they contain water in concentrations higher than 130 ppm. As Dr. Baker concludes, “a potential remains for sevoflurane instability, . . . therefore some vigilance regarding product integrity remains prudent.”

Ketamine for Total Hip Arthroplasty

Bad Times in the K Hole
Bad Times in the K Hole

From: http://www.ncbi.nlm.nih.gov/pubmed/19923527
Anesth Analg. 2009 Dec;109(6):1963-71. doi: 10.1213/ANE.0b013e3181bdc8a0.

The early and delayed analgesic effects of ketamine after total hip arthroplasty: a prospective, randomized, controlled, double-blind study.

The gist: Ketamine can reduce post-op pain scores and is opioid sparing when given to patients undergoing General Anesthesia hip replacement (note this is NOT generalizable to spinal anesthesia)

Methods: Pts received IV ketamine before incision (0.5 mg/kg), and a 24-h infusion (2 microg x kg(-1) x min(-1)) or a similar blinded saline bolus and infusion. Postoperative analgesia included IV acetaminophen, ketoprofen, plus morphine/droperidol patient-controlled analgesia for 48 h

Results: Ketamine decreased morphine consumption at 24 h from 19 +/- 12 mg to 14 +/- 13 mg (P = 0.004). At Day 30, ketamine decreased the proportion of patients needing 2 crutches or a walking frame from 56% to 31% (P = 0.0035). From Day 30 to Day 180, ketamine decreased the proportion of patients with persistent pain at rest in the operated hip (P = 0.008).

Other evidence [apparently – I’m looking at you DP who never bothers to comment] shows the one time bolus 0.5mg/kg vs. infusion makes little difference in post-op pain scores… so go for the bolus!

 

 

Magnesium: a versatile drug for anesthesiologists

From: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3726845/

MOA: multiple including blockade of nmda and Calcium channels 

Magnesium has multiple advantages including:

  • Reduced opioid reqs post op
  • Reduced Mac with tiva
  • Tiva reduced remi use -> reduced hyperanalgesia post op
  • Intrathecal MG prolongs labor analgesia, especially motor block and iv Mg prolongs muscle blockade when spinal wearing out 
  • Potentiates Nondepolarizing blockade,  can improve incubating conditions while reducing hemodynamic response to intubation 
  • Reduced post op shivering >70%

However caution:

  • Reduced inh Mac questionable 
  • Blunts release of NE / epi watch out in critically ill patients 
  • Cardiovascular depression possible when given as bolus 

Dosing: 

loading dose of 30-50 mcg/kg followed by a maintenance dose of 6-20 mcg/kg/h (continuous infusion) until the end of surgery; alternatively 4mg bolus

Who is Brugada?

 

There is not just one Brugada, but a family of them!

It all began in 1987 when Professor Brugada was running the electrophysiology laboratory at the University of Maastricht in the Netherlands and a Polish man brought his son to see him. The boy was 3 years old and had a history of repeated episodes of fainting and cardiac arrest; his father had resuscitated him several times. His sister had suffered similar symptoms and had died at the age of 3 in spite of treatment with a pacemaker and amiodarone.
“The electrocardiogram of that boy was never seen before and something you could not find in any publication,” Professor Brugada remembers. “I was very fortunate that the father was able to return to Poland and bring the electrocardiograms of the sister, which turned out to be exactly the same as those of the brother. Remember, it was 1987; the Berlin Wall was still there, so everything that this guy was doing was illegal.”
It took 4 years for the Brugadas to find 2 more patients with similar ECGs – one from the Netherlands and the other from Belgium. They presented the 4 cases as an abstract to an American Heart Association conference, and several doctors who had come across similar cases contacted them. A year later, they published details of 8 patients [in JACC: http://www.sciencedirect.com/science/article/pii/073510979290253J%5D.

AICD Indications

Secondary Prevention of death due to VF/VT in settings of:

1. prior VT/VF req’ing resuscitation, or unstable VT with unknown cause
-includes idiopathic vf/vt and congenital long qt
-excludes vt/vf w/in 48hrs of MI

2. spontaneous sustained VT in presence of heart disease (valvular, ischemic, hypertrophic, dilated, infiltrative cardiomyopathy or channelopathies)

Primary Prevention

For the primary prevention of VT/VF in patients at risk of sudden cardiac death due to vf/vt, who are optimized under medical management, such as:

1. Prior MI (40+ days ago) and LVEF <= 30%

2. Cardiomyopathy, NYHA class 2-3 + LVEF <=35% ( if nonischemic this means 3 months of med tx)

The others:

Syncope + documented VT/VF

Underlying disorders:
-congenital long qt
-hypertrophic cardiomyopathy
-Brugada Syndrome
-arrhythmogenic RV cardiomyopathy

Who is Brugada?

Two terms: syndrome and pattern
One EKG: pseudo-right bbb and persistent ST elevations V1-V2

Pattern = ECG findings + ASYMPTOMATIC

Syndrome = ECG findings + at least one episode of sudden cardiac death or sustained VT

Anesthetic implications (See http://bja.oxfordjournals.org/content/89/5/788.full)

-likely has AICD, so disable it
-avoid alpha agonists
-avoid neostigmine
-Contraindicated / MUST avoid class 1 antiarythmics ( see: https://en.wikipedia.org/wiki/Antiarrhythmic_agent#Class_I_agents)
so NO LIDOCAINE OR PHENYTOIN!
-caution with iso? (http://www.jcvaonline.com/article/S1053-0770%2801%2907405-5/abstract)

Midazolam for PONV

From Wick, Elizabeth, and Christopher L. Wu. “The Effect of Intravenous Midazolam on Postoperative Nausea and Vomiting: A Meta-Analysis.” (2015).

The gist: Midaz at any point reduces PONV by up to 40%!

BACKGROUND: Research has shown that high-risk surgical patients benefit from a multimodal therapeutic approach to prevent postoperative nausea and vomiting (PONV). Our group sought to investigate the effect of administering IV midazolam on PONV.
METHODS: This meta-analysis included 12 randomized controlled trials (n = 841) of adults undergoing a variety of surgical procedures that investigated the effect of both preoperative and intraoperative IV midazolam on PONV in patients undergoing general anesthesia.
RESULTS: Administration of IV midazolam was associated with significantly reduced PONV (risk ratio [RR] = 0.55; 95% confidence interval [CI], 0.43–0.70), nausea (RR = 0.62; 95% CI, 0.40–0.94), vomiting (RR = 0.61; 95% CI, 0.45–0.82), and rescue antiemetic administration (RR = 0.49; 95% CI, 0.37–0.65) within 24 hours. Individual subgroup analyses of trials excluding the use of thiopental for induction, trials of either female sex or high-risk surgery, trials involving nitrous oxide maintenance, and trials using midazolam in combination with known antiemetics all yielded similar reductions in PONV end points within 24 hours of surgery.
CONCLUSIONS: Administration of preoperative or intraoperative IV midazolam is associated with a significant decrease in overall PONV, nausea, vomiting, and rescue antiemetic use. Providers may consider the administration of IV midazolam as part of a multimodal approach in preventing PONV.