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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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)

Vasopressors part 1

Part 1 of ___ … on some general notes on vasopressors.

Metabolism

Catecholamine class (epi, levo, dopa, dobutamine, isoproterenol) all metabolized by Catechol-O-methyltransferase (COMT) and MAO. Phenylephrine also metabolized by MAO.

*indirect acting sympathomimetics (phenylephrine) greater risk of hypertensive crisis due to reliance on MAO metabolism, direct acting also metabolized by COMT so less risk, also patients taking TCAs.

Milrinone and ephedrine both excreted unchanged in urine, while Vaso is metabolized by vasopressinases in liver and kidney.

Levosimendan metabolized into active compounds and effects linger for up to 1 week after discontinuing.

Alpha Beta – A Review

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