Monthly Archives: January 2017

NORADRENALINE: PHARMACOLOGICAL HIGHLIGHTS & COMPARISON WITH ADRENALINE 

Posted on by

Noradrenaline (Norepinephrine) is a directly and indirectly acting sympathomimetic amine which stimulates alpha 1 and β1 adrenoceptors, but, in contrast to Adrenaline (epinephrine), has little effect on β2 adrenoceptors.

🖍These actions produce positive inotropic effects, intense vasoconstriction, increases in arterial pressure, and relative maintenance of cardiac output.

🖍Noradrenaline increases arterial pressure while simultaneously enhancing contractile state and venous return by reductions in venous capacitance, thereby augmenting stroke volume and ejection fraction. In contrast, pure alpha 1 adrenoceptor agonists such as phenylephrine and methoxamine further compromise cardiac output in failing myocardium and contribute to peripheral hypoperfusion despite an increase in arterial pressure.

🖍In contrast to adrenaline, noradrenaline does not substantially affect heart rate because activation of baroreceptor reflexes resulting from arterial vasoconstriction usually counteracts β1 mediated, direct, positive, chronotropic effects.

🖍Its arrhythmogenic potential is considerably less than that of adrenaline. Thus, substitution of noradrenaline for adrenaline may be appropriate in the therapeutic management of cardiogenic shock when atrial or ventricular arrhythmias are present.

🖍Intravenous infusions of noradrenaline (0.03–0.90 mg kg –1 per minute) have been shown to increase arterial pressure, LV stroke work index, cardiac index, and urine output in septic patients with hypotension that was unresponsive to volume administration, dopamine or dobutamine

🖍Causes relatively greater increases in systemic vascular resistance and diastolic arterial pressure than adrenaline.

🖍The drug has a duration of action of 30–40 minutes; tachyphylaxis occurs with prolonged administration.

🖍The drug produces coronary vasodilatation, leading to a marked increase in coronary blood flow. However, as myocardial work may increase, the balance of myocardial oxygen consumption and delivery may lead to ischaemia on noradrenaline.

🖍Reflex vagal stimulation leads to a compensatory bradycardia

🖍The cerebral blood flow and oxygen consumption are decreased by the administration of noradrenaline; mydriasis also occurs

🖍The glomerular filtration rate is usually well maintained with noradrenaline; but it decreases the renal blood flow and this represents a major limitation on the prolonged use of high doses of norepinephrine.

🖍Noradrenaline increases the contractility of the pregnant uterus; this may lead to fetal bradycardia and asphyxia

🖍Noradrenaline may decrease insulin secretion, leading to hyperglycaemia

🖍The drug is pharmaceutically incompatible with barbiturates and sodium bicarbonate

(Reference: Paul S. Pagel and David C. Warltier, Essential drugs in anesthesia practice Positive inotropic drugs, Anesthetic Pharmacology, 2nd edition)

Transurethral resection of the prostate (#TURP) syndrome : A summary 

Posted on by

🚩#TURPsyndrome is diagnosed based on clinical signs, symptoms and biochemical findings
🚩The manifestations are due to hypervolemia, hyponatremia and due to the direct toxicity of the irrigation fluids like 1.5% glycine
▪️FACTORS INCREASING THE ABSORPTION OF THE IRRIGATION FLUID ( AND THUS CONTRIBUTING TO THE HYPERVOLEMIA )
🚩Long duration of the surgery: the irrigation fluid is absorbed at the rate of 20-30 mL/ min and so the volume absorbed increases with the duration of the surgery
🚩High pressure delivery of the irrigation fluid especially from a considerable height; the minimum height required for adequate flow should be used (usually 70 cms)
🚩Low venous pressures
🚩Excessive bleeding (= there are more open veins)
🚩Large prostate (>50g)
▪️CLINICAL FEATURES:
🚩Headache, Restlessness, Agitation, Confusion, Convulsions, Coma; pulmonary oedema may also set in. If patient is under general anesthesia, these symptoms will get masked.
▪️MANAGEMENT FROM SURGICAL SIDE:
🚩Coagulating bleeding points and terminating surgery as soon as possible.
▪️ANESTHETIC MANAGEMENT:
🚩Reduce / stop fluid administration. Diuretics may be required in the presence of pulmonary oedema
🚩Intubation to protect the airway and mechanical ventilation to support respiration may be required
🚩Anti-convulsants, if needed, to treat seizures
🚩Hypertonic saline should be considered for severe hyponatremia (<120 mmol L−1) or in the presence of severe neurological symptoms.

👉🏿N.B.- Central pontine myelinolysis or osmotic demyelinating syndrome (ODS) is more likely to occur with correction of serum Na greater than 8-12 mmol/day and in the setting of chronic hyponatremia (greater than 48 h)
👉🏿Faster rates of administration can potentially lead to central pontine myelinolysis. Treatment should stop once symptoms have resolved or the serum sodium is more than 125 mmol L−1. Such therapy is best delivered in a high-dependency environment.
🔻A template is given below for calculating the volume of hypertonic saline
#anesthesia , #urology ,#hyponatremia , #anaesthesiologist

2016-08-30-09-58-51

VIVA AID: BISPECTRAL INDEX

Posted on by

💆The EEG bispectrum is a high-order statistical computation derived from the analog EEG.

💆The BIS is a combination of three weighted parameters: (i) the burst suppression ratio (the proportion of isoelectric EEG signal in an epoch); (ii) the beta ratio (a measure of the proportion of signal power in the high vs medium frequency range); and (iii) the SynchFastSlow (relative synchrony of fast and slow waves)

💆Changes in frequency and power alone ( as done with conventional power spectral analysis) have been shown to be inconsistent when attempting to measure anesthetic depth.

💆Bispectral analysis incorporates information on power and frequency with the phase coupling information that is more indicative of anesthetic depth but not present in other clinical applications of EEG.

💆The BIS uses a combination of EEG subparameters that were selected after analysis of a large database of EEGs to demonstrate specific ranges for varying phases of anesthetic effect

💆These parameters were then combined to form the optimum configuration for monitoring of the hypnotic state.

💆The BIS is then displayed as a dimensionless number between 0 and 100 with the lower numbers corresponding to deeper levels of hypnosis.

💆There are normal, genetically determined low-voltage EEG variants among the population that can result in abnormally low BIS values in awake patients; therefore, it is important to obtain baseline values before the induction of anesthesia

💆BIS is not able to predict movement in response to surgical stimulation because the generation of reflexes is likely to be at spinal cord rather than cortical level

💆BIS does not fully reflect the synergistic effect of opioids with hypnotic agents

💆The presence of electromyographic artefacts, poor signal quality, and electrical artefacts such as those from electro-cautery and forced air warming units can cause spurious values to be displayed by the BIS monitor.

💆With the administration of ketamine, the BIS may remain high, possibly due to the excitatory actions of ketamine, and, therefore, the BIS monitor is not reliable when used to monitor hypnosis with ketamine.

💆There have been studies in which the BIS monitor has not been shown to reflect the hypnotic contribution to the anesthetic by nitrous oxide.

💆Potential benefits from the routine use of the BIS monitor include

➖decreased risk of awareness

➖improved titration of anesthetic agents and

➖decreased recovery room time

💆The BIS also gives the anesthetist additional information to consider when selecting drugs for interventions, for example, when making the decision whether to deepen anesthesia with a volatile agent, add more analgesia with an opioid, or use a vasoactive drug.

💆Also note:

➖The BIS may drop after giving a neuromuscular blocking agent if excessive EMG was present prior to giving it.

➖Ischemia attenuates the amplitude and frequency of the EEG signal, which may result in a decrease in BIS

➖Hypothermia decreases brain activity, and may decrease BIS

➖Muscle shivering, tightening, twitching etc may increase EMG and increase BIS

➖Artifacts in the higher frequency ranges [e.g. use of any mechanical device that could generate high frequency activity like patient warmer]can artificially increase the BIS value

➖Is the BIS decreasing when you think it should be increasing? Think of Paradoxical Delta pattern (characterized by a pronounced slowing of the EEG) which occurs over a short period of time (2-3 minutes).

➖If the sensor is placed over the temporal artery, pulse artifacts can cause the BIS value to be inappropriately low. Check EEG waveform for presence of pulse artifacts and move sensor if necessary.

➖Blinking or rolling his/her head by the patient, may cause artifacts that mimic slow frequency EEG patterns.

Reference: The BIS monitor: A review and technology assessment, James W. Bard, AANA Journal/December 2001/Vol. 69, No. 6

A FEW PROSPECTIVE TECHNIQUES TO MEASURE ANALGESIA INTRA-OPERATIVELY 

Posted on by

🤖Current electroencephalogram (EEG)-derived measures like BIS, provide information on cortical activity and hypnosis but are less accurate regarding subcortical activity, which is expected to vary with the degree of antinociception. 
🤖Efforts to develop methods for monitoring these subcortical activities produced a few indices, which may provide some use intra-operatively 
🤖Recently, the neurophysiologically based EEG measures of cortical input (CI) and cortical state (CS) have been shown to be prospective indicators of analgesia/anti-nociception and hypnosis, respectively. Composite Cortical State (CCS) is an alternate measure of CS.
🤖Composite Variability Index (CVI) is another recently developed EEG-derived measure of antinociception based on a weighted combination of BIS and estimated electromyographic activity.
🤖CCS and BIS show strong correlations, suggesting that they behave similarly as indicators of hypnosis.
Reference: Comparisons of Electroencephalographically Derived Measures of Hypnosis and Antinociception in Response to Standardized Stimuli During Target-Controlled 

Propofol-Remifentanil Anesthesia, Mehrnaz Shoushtarian, Marko M. Sahinovic, Anthony R. Absalom, Alain F. Kalmar, Hugo E. M. Vereecke, David T. J. Liley and Michel M. R. F. Struys, anesthesia-analgesia, February 2016 • Volume 122 • Number 2

WHAT IS SURGICAL STRESS INDEX (SSI)❓

Posted on by

🔵 SSI is an index which measures the surgical stress response in patients under anesthesia

🔵 It assess the balance between the intensity of surgical stimulation and the level of antinociception (e.g. Opioid analgesia , neuraxial or nerve blockade)
🔵 SSI uses two continuous cardiovascular variables, both obtained from Photo Plethysmography (PPG) waveforms of SpO2
(1) The interval between successive hearts beats (HBI)
(2) PPG amplitude (PPGA)
🔵Photoplethysmography (PPG), i.e. pulse oximetry, is primarily used to produce an estimation of the relative concentration of oxyhemoglobin in blood.
🔵 PPG is related to volume changes and contains information about the peripheral blood circulation, including skin vasomotion. Skin vasomotion is controlled by the sympathetic nervous system, which is activated during surgical stress.
🔵 Changes in PPG amplitude (PPGA) reflect changes in the peripheral vascular bed, controlled by the sympathetic nervous system . Increased PPGA response has been associated with nociception during general anesthesia.
🔵SSI values near 100 correspond to a high stress level, and values near zero to a low stress level.
🔵 In trials, SSI correlated positively with the intensity of painful stimuli and negatively with the analgesic concentration
🔵 SSI has been shown to be capable of differentiating decreases in HR achieved with opioid from those accomplished with a beta blocker (Ahonen et al. 2007).
🔵 An optimal range for SSI during anesthesia has not yet been recommended.
Reference: Measurements of adequacy of anesthesia and level of consciousness during surgery and intensive care, Johanna Wennervirta, Department of Anesthesiology and Intensive Care Medicine, Helsinki University Hospital
#anaesthesia , #anaesthesiology , #anaesthesiologist

👁➖BE AWARE OF AWARENESS ➖👁

Posted on by

💣Premedication with amnestic reduces the chance of awareness. Also, if awareness occurs, psychological trauma is less likely without recall.
💣Light induction doses and liberal use of muscle relaxants ,without giving adequate concern to the depth of anaesthesia can increase the chance of awareness.
💣Better to give re-bolus with i.v. hypnotic during multiple intubation attempts. Consider using inhalation induction technique.
💣Beta-blockers, can reduce MAC-Awake and may also decrease the likelihood of PTSD.
💣We can consider ear plugs or headphones to reduce awareness of noises in the OR.
💣Nitrous oxide, Ketamine and Opioids suppress cortical arousal during painful stimulation, which may reduce the probability of awareness. But BIS (Bi Spectral Index) and other EEG monitors do not accurately predict the depth of anesthesia with these drugs. (Because, even though they produce hypnosis, they do not modulate GABA-A receptors and are associated with unchanged or increased high frequency EEG signals.)
💣Propofol, barbiturates, etomidate, and halogenated volatile anesthetic agents all modulate GABA-A receptor activity and shift the cortical EEG to lower frequencies. So, BIS and other EEG-based monitors provide strong correlation with hypnosis for this group of general anesthetics.
💣MAC for N2O & volatile anesthetics is additive (i.e. a mixture of 0.5 MAC N2O plus 0.5 MAC volatile suppresses movement in response to pain like 1 MAC volatile. The HYPNOTIC activities of nitrous oxide and volatile anesthetics are sub-additive. (i.e. a mixture of 0.5 MAC-awake N2O + 0.5 MAC-awake volatile anesthetic is not as hypnotic as 1 MAC-awake volatile. This suggests that N2O has an action which antagonizes the hypnosis induced by volatile anesthetics, perhaps via direct cortical arousal.
💣Many studies say, BIS is not useful in case of dexmedetomidine also; while some others say it will help.
#awareness , #anesthesia , #sedation , #AwarenessAnesthesia , #bis , #AwarenessSurgery

➖➖➖➖➖➖➖➖➖➖➖➖➖➖➖➖➖➖
Reference:

CampagnaJA,MillerKW,FormanSA:Mechanismsofactionsof inhaled anesthetics. N Engl J Med 348:2110-2124, 2003
SleighJW,BarnardJP:Entropyisblindtonitrousoxide.Canwesee why? Br J Anaesth 92:159-161, 2004 39.
ChortkoffBS,BennettHL,EgerEI2nd:Doesnitrousoxideantagonize isoflurane-induced suppression of learning? Anesthesiology 79: 724-732, 1993 40.
KatohT,IkedaK,BitoH:Doesnitrousoxideantagonizesevofluraneinduced hypnosis? Br J Anaesth 79:465-468, 1997
Update on Bispectral Index monitoring Jay W. Johansen,Best Practice & Research Clinical Anaesthesiology Volume 20, Issue 1, March 2006, Pages 81–99

EXPLICIT AND IMPLICIT AWARENESS DURING ANESTHESIA

Posted on by

😐(Explicit = Fully and clearly expressed)

😐(Implicit =Implied or understood though not directly expressed)

😐The incidence of awareness is around 0.1–0.2%

😐Explicit Awareness is intentional or conscious recollection of prior experiences as assessed by tests or recall or recognition, which are also called direct memory test.

😐Implicit Awareness is perception without conscious recall. The patient denies recall, but may remember “something” under hypnosis.

😐Awareness (deliberate)

Surgery conducted under local or regional anaesthesia. During some neurosurgical procedures, the patient is woken up to assess whether surgery has affected, or will affect, important areas.

😐STAGES OF AWARENESS ( Griffith and Jones )

1. Conscious perception with explicit memory;

2. Conscious perception without explicit memory;

3. Dreaming;

4. Subconscious perception with implicit memory;

5. No perception and no implicit memory.

😐CAUSES

🔻may result from a failure of the apparatus to deliver adequate concentrations of anesthetic agent. Such failures include leaks, faulty or empty vaporizers, a misconnected or disconnected breathing system, inaccurate pumps, misplaced venous cannula and occluded infusion tubing

🔻failure of the clinician to monitor the concentrations of inspired and expired volatile agents may result in inadequate anesthetic agent being delivered. TIVA is more difficult to monitor in this respect.

🔻may result from an inadequate dosing of the anesthetic agent as represented by the alveolar concentration (it is important to remember that the MAC value that is quoted is only the MAC 50 ) or the computed blood concentration in target-controlled infusion (TCI).

🔻may result from an altered physiology or pharmacodynamics in the patient e.g. Anxiety may increase dose requirements

🔻may result from the wearing off of the induction agent during a difficult intubation sequence or with the anesthetic techniques for rigid bronchoscopy

😐CLINICAL SIGNS

🔻In the spontaneously breathing patient who is not paralyzed, awareness may be manifest by purposeful movement.

🔻Sympathetic stimulation: the main clinical signs are tachycardia, hypertension, diaphoresis and lacrimation; but their absence does not exclude awareness. Attempts have been made to quantify these objectively by using the PRST scoring system (blood Pressure, heart Rate, Sweating, Tear formation)..

😐SEQUELAE:

Commonest is the occurrence of a post-traumatic stress syndrome, whose typical features may include nightmares, insomnia, panic attacks and agoraphobia.

😐CHECKLIST FOLLOWING A COMPLAINT OF AWARENESS DURING GENERAL ANAESTHESIA

1. Visit the patient as soon as possible, along with a witness (Preferably a consultant)

2. Take a full history and document the patient’s exact memory of events

3. Attempt to confirm the validity of the account

4. Keep your own copy of the account

5. Give a full explanation to the patient

6. Offer the patient follow-up, including psychological support, and document that this has been offered

7. Reassure the patient that they can safely have further general anaesthetics, with minimal risk of a further episode of awareness

8. If the cause is not known, try to determine it

9. Notify your medical defence organisation

10. Notify your hospital administration

11. Notify the patient’s GP
#awareness , #ptsd , #AnesthesiaComplications , #TheLayMedicalMan , From http://www.facebook.com/drunnikrishnanz , partial reference from frca.uk , #anaesthesia

#Tapentadol

Posted on by

🚩Is a new centrally acting analgesic that relies on a dual mechanism of action. These are mu opioid receptor agonism and norepinephrine (noradrenaline) reuptake inhibition
🚩It is therefore not a classical opioid, but represents a unique class of analgesic drug (MOR-NRI).
🚩It is now registered for use in the treatment of moderate to severe chronic pain that proves unresponsive to conventional non-narcotic medications in many countries.
🚩Tapentadol has a much lower affinity (20 times less) to the mu receptor than morphine, but its analgesic effect is only around three times less than morphine.
🚩This discrepancy is explained by its inhibitory effect on norepinephrine reuptake, strengthening descending inhibitory pathways of pain control
🚩Tapentadol is seen by some as similar to tramadol, but differs in a number of important points:
▶️It is not a racemic mixture of two enantiomers with different pharmacological effects
▶️Has no active metabolites (which are relevant for tramadol’s mu opioid receptor agonism)
▶️Has only minimal serotonin effects
🚩This means that interactions with other serotonergic drugs (such as anti-depressants) are unlikely, reliance on metabolism by the cytochrome P450 system for increased efficacy is not required and retention of active metabolites causing potential adverse effects is not a concern.

NB

🔻Tramadol is a 4 phenyl piperidine analogue of codeine
🔻It has a weak central action at opioid receptors
🔻And also on descending monaminergic pathways (also responsible for the side effects)
🔻Hence known as an atypical centrally acting opioid
🔻It’s M1 metabolite has more affinity to opioid receptors than parent compound
🔻So metabolites are important in maintaining efficacy
#Opioids , #Pharmacology , #analgesia , #PalliativeCare , #Pain , #SideEffects , #NewDrugs , #medicine , #anaesthesia
Reference: Recent advances in the pharmacological management of acute and chronic pain Stephan A. Schug, Catherine Goddard, Annals of Palliative Medicine, Vol 3, No 4 October 2014

NEURO #ANATOMY OF THE OLFACTORY SYSTEM : How some smells induce tears and sniffing in you❓

Posted on by

😤 Olfactory receptors 1️⃣ are the most important cells of the olfactory epithelium and they are the first order neurons of the cranial nerve I
😤There are approximately 100 million such receptors in the olfactory epithelium found along the roof of the nasal cavity including the superior and upper middle conchae
😤Olfactory receptors project through the cribriform plate in the ethmoid bone
😤They have multiple cilia immersed in a surrounding matrix of mucus and a long dendrite
😤Odiferous chemicals get dissolved in this mucus and then trigger the olfactory receptors
😤The impulses pass through the neuron to the olfactory bulb (lies in base of frontal cortex in anterior fossa), which has projections to cortical areas
😤The primary olfactory area in the temporal lobe process such informations through it’s connections with the hypothalamus, thalamus and frontal cortex
😤The other major cell type is basal cells 2️⃣ found deep to the olfactory neurons (olfactory neurons have a half-life of one month) and replace them, as they mature
😤3️⃣Sustentacular or supporting cells constitute the columnar mucus epithelium found between the receptors
😤There are 4️⃣Olfactory (Bowman’s) glands found in the connective tissue beneath the olfactory epithelium which produce the mucus in which the odiferous chemicals dissolve
❓➡️ 🅰️ Finally answer to the question
😤The innervation of the olfactory epithelial cells from cranial nerve VII (facial nerve) explains the tears and sniffing evoked by some smells.
Reference: Tortora GJ, Grabowski SR. Principles of Anatomy and Physiology, 8th edn. New York, NY: HarperCollins, 1996; pp. 454–5
#smell , #Olfaction , #PhysiologyForExams , #NeuroAnatomy , #anesthesiology

♈️#PhysicsForAnesthesiologist : Beer-Lambert Law

Posted on by

☢️The #pulseoximeter works based on Beer-Lambert law, which relates the attenuation of light to the properties of the material through which the light is travelling.
☢️It helps us in the calculation of the absorbance of a solution.
☢️According to the law, the absorbance of a solution depends on:
🖍The concentration of that solution, i.e. the more molecules of a light-absorbing compound there are in the sample, the more light will be absorbed.
🖍The path-length of light travelling through the solution, i.e. the longer the length of the sample container, the more light will be absorbed because the light will come into contact with more molecules.
🖍A = εlc where
🔻A is absorbance of light
🔻ε is the molar extinction coefficient(l mol–1 cm–1). It compensates for variance in concentration and the path-length, to allow comparison between solutions.
🔻l is the length of solution that the light passes through.
🔻c is the concentration of the compound in solution, expressed in mol L–1
☢️In the pulse oximeter, the concentration and molar extinction coefficient are constant. The only variable becomes the path length, which alters as arterial blood expands the vessels in a pulsatile fashion.
#Anesthesia, #PhysicsAndMedicine , #MedicalExams