Protamine

BURNS AND THE ANESTHESIOLOGIST

• First degree burns don't penetrate the epidermis and the areas of involvement should not be considered when calculating for fluid volume for resuscitation 
• Second degree burns penetrates the epidermis & extends into the dermis and will cause blisters
• Third degree burns involve epidermis, full thickness of dermis, deeper tissues, blood vessels and nerves
• The “rule of nines” is used to calculate the total body surface area (TBSA) .
• The Parkland formula recommends 4 mL/kg/% TBSA burned, to be given in the first 24 hours (half of this should be given in the first 8 hours and the rest over the following 16 hours).
•  The Modified Brooke protocol recommends 2 mL/kg/%TBSA.
•  Fluid leak may occur when patients are given volume beyond the intended calculations. This can lead to abdominal compartment syndrome, pulmonary edema, or pneumonia.
•  Carbon monoxide (CO) poisoning should be considered in all major burn injuries. 
• CO binds to hemoglobin (HbCO) with an affinity of 250 times that of oxygen and shifts the oxygen–hemoglobin dissociation curve to the left. 
• Pulse oximetry causes falsely elevated oxygen saturation because it is unable to distinguish HbO from HbCO, as CO-Hb has similar absorption spectra as that of oxy-Hb
• HbCO levels below 10% are not usually clinically significant, levels of 20% may require mechanical ventilation, and death from CO poisoning occurs at HbCO levels of 60%.
• In cases where CO poisoning is suspected, treatment should be with highflow 100% oxygen, which increases the speed of elimination of CO. Hyperbaric chambers are used to further increase the speed of CO removal.
• Burns patients have an inability to regulate body temperature and must be kept warm.
• Urgent airway management may be indicated by the presence of a hoarse voice, dyspnea, tachypnea, or altered level of consciousness.
• Succinylcholine can cause lethal elevations in potassium after the first 48 hours.
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THE AUTONOMIC NERVOUS SYSTEM (ANS) IN GENERAL: RANDOM POINTS RELEVANT FOR THE ANESTHESIOLOGIST

➿The autonomic nervous system is a division of the nervous system that controls the activity of internal organs.

➿The sympathetic division prepares the body for fight or flight reactions. The parasympathetic system promotes ‘rest and digest’ (restorative) functions.

➿Acetylcholine is the principal transmitter released by the preganglionic fibres of both the sympathetic and the parasympathetic nervous systems. The parasympathetic postganglionic fibres secrete acetylcholine onto their target organs, whereas norepinephrine is principally secreted by the postganglionic sympathetic fibres.

➿The central portions of the autonomic nervous system are located in the hypothalamus, brainstem and spinal cord. The limbic system and parts of the cerebral cortex send signals to the hypothalamus and lower brain centres, which can also influence the activity of the ANS

➿The posterior and lateral hypothalamic areas increase blood pressure and heart rate, whereas the preoptic area decreases blood pressure and heart rate. These effects are mediated by cardiovascular centres in the pontine and medullary reticular formation.

➿An autonomic nerve pathway involves two nerve cells. It is connected by nerve fibers to the other cell, which is located in a cluster of nerve cells (called an autonomic ganglion). Nerve fibers from these ganglia connect with internal organs.

➿In the ANS, the connection between the CNS and its effector consists of two neurons—the preganglionic neuron and the postganglionic neuron. The synapse between these two neurons lies outside the CNS, in an autonomic ganglion [The cell bodies of the post ganglionic neuron, located in chains alongside the vertebral column, in plexuses in the abdomen (Sympathetic) or within the innervated target organ (Parasympathetic)]. The axon of a preganglionic neuron enters the ganglion and forms a synapse with the dendrites of the postganglionic neuron. The axon of the postganglionic neuron emerges from the ganglion and travels to the target organ #TheLayMedicalMan

➿The sympathetic system has short preganglionic fibres and long
postganglionic fibres. As the parasympathetic ganglia are located near or within their effector organs, the parasympathetic postganglionic fibres are short.

➿The pre-ganglionic fibres are slow-conducting B or C fibres. The postganglionic fibres that originate from the ganglia and innervate target organs are largely slow-conducting, unmyelinated C fibres. #TheLayMedicalMan

➿There are more postganglionic fibres than preganglionic nerves and so the stimulation of a single preganglionic neuron can activate many postganglionic nerves, resulting in divergence. But in the superior cervical ganglion, numerous preganglionic fibres converge on a single postganglionic neuron, resulting in convergence.

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THE PARASYMPATHETIC NERVOUS SYSTEM: POINTS RELEVANT FOR THE ANESTHESIOLOGIST

🎳The anterior hypothalamus controls the parasympathetic nervous system

🎳The posterior and lateral hypothalamic areas increase blood pressure and heart rate, whereas the preoptic area decreases blood pressure and heart rate.

🎳The parasympathetic nervous system arises from neurons in the brainstem and spinal cord sacral segments (S2–S4). As the parasympathetic ganglia are located near or within their effector organs, the parasympathetic postganglionic fibres are short, and they all release acetylcholine. The distribution of parasympathetic outflow is restricted so that parasympathetic effects are more localized than sympathetic effects.

🎳Parasympathetic fibres follow the distribution of the third, seventh, ninth and tenth cranial nerves. Preganglionic fibres of the third cranial nerve arise from the oculomotor nucleus and pass through the orbit to the ciliary ganglion. Postganglionic f ibres from the ciliary ganglion supply the ciliary muscle  and  sphincter  of  the  iris  and  constrict  the pupils.

🎳Preganglionic fibres from the superior salivary nucleus of the seventh nerve form the chorda tympani and reach the submaxillary ganglion via the lingual nerve. Postganglionic fibres supply the submaxillary and sublingual salivary glands and cause salivary secretion. #TheLayMedicalMan

🎳Preganglionic fibres arising from the inferior salivary nucleus of the ninth nerve form the lesser superficial petrosal nerve and reach the otic ganglion. The postganglionic fibres are distributed to the parotid gland via the auriculotemporal nerve and also cause salivary secretion.

🎳The vagus nerve is the major part of the cranial parasympathetic outflow. The preganglionic fibres arise from the dorsal nucleus of the vagus in the medulla and terminate in the ganglia of plexuses or in the walls of visceral organs. Postganglionic fibres supply the heart and decrease cardiac excitability, contractility, conductivity and rate. Postganglionic fibres from the pulmonary plexus contract the circular muscles of the bronchi, producing bronchoconstriction. Vagal branches to the gastric plexus give rise to postganglionic fibres  to  the  stomach, liver, pancreas and spleen. Stimulation of the vagus causes increased gastric motility and secretions, with relaxation of the pyloric sphincter. The intestinal branches of the vagus  supply  the  small  and  large  intestines  down to the transverse colon and it's stimulation increases peristalsis and relaxes the ileocolic sphincter. #TheLayMedicalMan

🎳The sacral outflow of the parasympathetic system arises from the second, third and fourth sacral segments of the spinal cord, and fibres enter the hypogastric plexus to innervate the descending colon, rectum, bladder and uterus. It's stimulation contracts the muscular wall of the rectum, relaxes the internal sphincter of the anus and contracts the detrusor muscle of the bladder wall.

Ref: Principles of Physiology for the Anaesthetist , 3/e

#physiology , #anaesthesia

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THE SYMPATHETIC NERVOUS SYSTEM: POINTS RELEVANT FOR THE ANESTHESIOLOGIST

🔸Posterior hypothalamus is the principal site of sympathetic nervous outflow.

🔸The sympathetic system has short preganglionic fibres and long postganglionic fibres

🔸The sympathetic nerves originate from columns of preganglionic neurons in the grey matter of the lateral horn of the spinal cord from the first thoracic segment down to the second or third lumbar segment.

🔸The preganglionic fibres leave the spinal cord through the ventral roots with the spinal nerves and then leave the spinal nerves as white rami communicantes ( myelinated B fibres ) to synapse with the postganglionic neurons in the ganglia of the sympathetic chain.

🔸The ganglia form sympathetic chains. The post-ganglionic fibres leave the ganglia as grey rami communicantes (unmyelinated C fibres) and join the spinal nerves or visceral nerves to innervate the target organ.

🔸In general, the preganglionic fibres secrete acetyl choline as neurotransmitter, while the post ganglionic ones secrete norepinephrine. The postganglionic sympathetic nerves that innervate the blood vessels of muscles, sweat glands and the hair follicles in the skin release acetylcholine instead of norepinephrine (noradrenaline).

➡️The sympathetic chains extend down the length of the vertebral column and are divided into four parts:

🔸A cervical part consisting of superior, middle and inferior galglia, supplying the head, neck and thorax. The superior cervical ganglion sends postganglionic fibres to form the internal carotid plexus. The inferior cervical or stellate ganglion is fused with the first thoracic ganglion.

🔸Branches of the thoracic part, from T 1 –T 5 supply the aortic, cardiac and pulmonary plexuses. The greater and lesser splanchnic nerves are formed from the lower seven thoracic ganglia. The lowest splanchnic nerve arises from the last thoracic ganglion and supplies the renal plexus.

🔸The coeliac plexus is derived from the lumbar sympathetic ganglia

🔸The sacral ganglia contribute to the hypogastric and pelvic plexus #TheLayMedicalMan

SYMPATHETIC SYSTEM PRODUCE:

🔸Dilatation of the pupil and retraction of the eyelid (levator palpebrae)

🔸Thoracic visceral effects of positive inotropic and chronotropic cardiac effects, pulmonary blood vessel vasoconstriction and bronchial smooth muscle relaxation.

🔸Abdominal visceral effects of increased sphincteric tone and inhibition of peristalsis, leading to relaxation of the gut and reduced motility.

🔸Pelvic visceral effects of relaxation of the bladder wall and the rectum with sphincter closure. Contraction of the smooth muscle of the seminal vesicles and prostate produces ejaculation. #TheLayMedicalMan

🔸Cutaneous effects such as piloerection, vasoconstriction and sweating.

🔸In the limbs, the arterioles to the skin constrict, whereas the skeletal muscle arterioles vasodilate.

#physiology , #anaesthesia

THE SPECIFIC MECHANISMS OF ACTION OF #MANNITOL IN VARIOUS CLINICAL SITUATIONS

Mannitol is a monosaccharide available as 10% & 20% solutions

DURING NEUROSURGERY/ IN NEUROCRITICAL CARE:

✔️Mannitol is freely filtered in the glomerulus but won't get reabsorbed in the tubules; so it will drive water from the interstitium which gets eliminated as urine. Hence acts as an osmotic diuretic

✔️When blood brain barrier is intact, the osmotic gradient created by mannitol will move water from the cerebral extravascular compartment to the intravascular space, reducing ICP. If blood brain barrier is not intact, it will worsen cerebral edema. #TheLayMedicalMan

✔️The expansion of the plasma volume caused by mannitol will reduce the viscosity and improve cerebrovascular microcirculation and oxygenation. The increase in cardiac output can also cause an increase in regional blood flow which will cause a compensatory cerebrovascular vasoconstriction in areas where autoregulation is intact.

IN CRUSH INJURY / MYOGLOBINURIA

✔️Will release renal prostaglandins, which will cause renal vasodilation and increase tubular urine flow causing a solute washout and avoidance of tubular obstruction #TheLayMedicalMan

MECHANISMS BEHIND ADVERSE EFFECTS

✔️The initial increase in plasma volume as a result of drawing of water into the vascular component and the resultant increase in cardiac output can precipitate heart failure in cardiac patients

✔️The osmotic diuresis can cause hypernatremia [increases urinary losses of both sodium and electrolyte-free water] , metabolic acidosis and hyperosmolarity. It has been advised that therapy should be monitored and titrated so that osmolarity doesn't go up beyond 300 mOsm/L

✔️The rise in the plasma potassium concentration following hypertonic mannitol is due to the movement of potassium out of the cells into the extracellular fluid as the rise in cell potassium concentration induced by water loss favors passive potassium exit through potassium channels in the cell membrane #TheLayMedicalMan

✔️Though it has been used for renal protection, the reduction in renal perfusion resulting from hypovolemia caused by diuresis can adversely affect renal function; so should be avoided in patients with renal dysfunction

#Neuroanesthesia , #Anesthesia , #Neurology , #CriticalCare

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DESCRIPTION OF THE IMPORTANT EVENTS IN THE CARDIAC CYCLE SYNCHRONISED WITH THE EKG & VENOUS PRESSURE WAVE FORMS

1. ATRIAL CONTRACTION (Phase 1):  It is initiated by the P wave of the ECG which represents electrical depolarization of the atria. atrial contraction does produce a small increase in venous pressure that can be noted as the "a-wave". Just following the peak of the a-wave is the x-descent. Atrial contraction normally accounts ONLY for about 10% of left ventricular filling when a person is at rest. At high heart rates when there is less time for passive ventricular filling, the atrial contraction may account for up to 40% of ventricular filling. This is sometimes referred to as the "atrial kick." The atrial contribution to ventricular filling varies inversely with duration of ventricular diastole and directly with atrial contractility. The volume of blood at the end of the filling phase is the end diastolic volume and is around 120 mL in the adult. S4 sound is caused by vibration of the ventricular wall during atrial contraction.  Generally, it is noted when the ventricle compliance is reduced ("stiff" ventricle) as occurs in ventricular hypertrophy and in many older individuals.

2. Isovolumetric Contraction (Phase 2):   This phase of the cardiac cycle begins with the appearance of the QRS complex of the ECG, which represents ventricular depolarization. The AV valves close when intraventricular pressure exceeds atrial pressure. Closure of the AV valves results in the first heart sound (S1). During the time period between the closure of the AV valves and the opening of the aortic and pulmonic valves, ventricular pressure rises rapidly without a change in ventricular volume (i.e., no ejection occurs). Ventricular volume does not change because all valves are closed during this phase. Contraction, therefore, is said to be isovolumetric. The "c-wave" noted in the venous pressure may be due to bulging of A-V valve leaflets back into the atria. Just after the peak of the c wave is the x'-descent.

3. Rapid Ejection (Phase 3): Ejection begins when the intraventricular pressures exceed the pressures within the aorta and pulmonary artery, which causes the aortic and pulmonic valves to open. Left atrial pressure initially decreases as the atrial base is pulled downward, expanding the atrial chamber. Blood continues to flow into the atria from their respective venous inflow tracts and the atrial pressures begin to rise. This rise in pressure continues until the AV valves open at the end of phase 5.

4. Reduced Ejection (Phase 4): Approximately 200 msec after the QRS and the beginning of ventricular contraction, ventricular repolarization occurs as shown by the T-wave of the electrocardiogram. Repolarization leads to a decline in ventricular active tension and pressure generation; therefore, the rate of ejection (ventricular emptying) falls. Ventricular pressure falls slightly below outflow tract pressure; however, outward flow still occurs due to kinetic (or inertial) energy of the blood.  Left atrial and right atrial pressures gradually rise due to continued venous return from the lungs and from the systemic circulation, respectively.

5. Isovolumetric Relaxation (Phase 5): When the intraventricular pressures fall sufficiently at the end of phase 4, the aortic and pulmonic valves abruptly close (aortic precedes pulmonic) causing the second heart sound (S2) and the beginning of isovolumetric relaxation. Valve closure is associated with a small backflow of blood into the ventricles and a characteristic notch (incisura or dicrotic notch) in the aortic and pulmonary artery pressure tracings. Although ventricular pressures decrease during this phase, volumes do not change because all valves are closed. The volume of blood that remains in a ventricle is called the end-systolic volume and is ~50 ml in the left ventricle. The difference between the end-diastolic volume and the end-systolic volume is ~70 ml and represents the stroke volume. Left atrial pressure (LAP) continues to rise because of venous return from the lungs. DuThe Lay Medical Man:
ring isovolumetric ventricular relaxation, atrial pressure rises to 5 mmHg in the left atrium and 2 mmHg in the right atrium.

6. Rapid Filling (Phase 6): As the ventricles continue to relax at the end of phase 5, the intraventricular pressures will at some point fall below their respective atrial pressures. When this occurs, the AV valves rapidly open and passive ventricular filling begins. The opening of the mitral valve causes a rapid fall in LAP.  The peak of the LAP just before the valve opens is represented by the "v-wave."  This is followed by the y-descent of the LAP. A similar wave and descent are found in the right atrium and in the jugular vein. When a third heart sound (S3) is audible during rapid ventricular filling, and is often pathological in adults and is caused by ventricular dilatation.

7. Reduced Filling (Phase 7):  As the ventricles continue to fill with blood and expand, they become less compliant and the intraventricular pressures rise. The increase in intraventricular pressure reduces the pressure gradient across the AV valves so that the rate of filling falls late in diastole.  In normal, resting hearts, the ventricle is about 90% filled by the end of this phase. In other words, about 90% of ventricular filling occurs before atrial contraction (phase 1) and therefore is passive.

8. Right Vs Left: The major difference between the right and left side of the cardiac chambers, is that the peak systolic pressures of the right heart are substantially lower than those of the left heart, and this is because pulmonary vascular resistance is lower than systemic vascular resistance. Typical pulmonary systolic and diastolic pressures are 24 and 8 mm Hg, respectively. #TheLayMedicalMan

9. Jugular Venous Pressure Summary: Right atrial pressure pulsations are transmitted to jugular veins. Thus, atrial contractions produce the first pressure peak called the a wave. Shortly there- after, the second peak pressure called the c wave follows and this is caused by the bulging of the tricuspid valve into the right atrium. After the c wave, the right atrial pressure decreases (‘x’ descent) because the atrium relaxes and the tricuspid valve descends during ventricular emptying. As the central veins and the right atrium fill behind a closed tricuspid valve, the right atrial pressure rises towards a third peak, the v wave, as the right atrium fills with a closed tricuspid valve and blood returns to the heart from the peripheral vasculature. When the tricuspid valve opens at the end of ventricular systole, right atrial pressure decreases again as blood enters the relaxed right ventricle (‘y’ descent). The right atrial pressure begins to rise shortly as blood returns to the right atrium and the right ventricle together during diastole.

Ref: Principles of Physiology for the Anaesthetist, Peter Kam, Ian Power, www.cvphysiology. com

#CardiacCycle , #Physiology , #Anesthesia

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DELIRIUM TREMENS

DELIRIUM TREMENS

1. Is an alcohol withdrawal syndrome which is a neurological emergency and outcomes depend on successful early treatment; with treatment, mortality is 1-5% and without treatment, it's 20%.

2. Symptoms include delirium, hyperpyrexia, hallucinations, sympathetic overactivity, tremulousness etc

3. CBC, urine/serum toxicology screen, septic screen, heavy metal screen, ABG, LP to rule out CNS infections, CT brain to rule out bleed, ECG and EEG, Serum Thiamine/ Folate levels are important investigations

4. Fixed dose benzodiazepine regimens are the main stay of treatment e.g. Lorazepam 2 mg iv/im Q6H for 4 doses followed by 1 mg iv/im Q6H for 8 doses; taper by 50% every day, after 48 hours). Beta blockers to control adrenergic over activity (e.g. Atenelol 25-100 mg OD to BD titrated to heart rate. Thiamine 1 mg iv OD for 3 days ( especially prior to glucose administration. to prevent Wernicke's encephalopathy) , Folic acid 1 mg po daily 

5. Watch for arrhythmias, electrolyte abnormalities, aspiration pneumonia, sepsis, dehydration 

6. Care in high dependency unit, in a well lit room

CO2 ABSORBENTS

1. CO2 combines with water to form carbonic acid. CO2 absorbents are hydroxide salts which neutralise the carbonic acid.

2. Colour conversion of a pH indicator dye (e.g., ethyl violet from white to purple) by increasing hydrogen ion concentration signals absorbent exhaustion. Absorbent should be replaced when 50% to 70% has changed colour

3. CO2 absorbants absorb (this may contribute towards delayed induction and emergence) and degrade volatile agents

4. Soda Lime and Amsorb are the commonly used CO2 absorbents

5. Soda lime  consists of Ca(OH)2 [80%], NaOH, water and KOH. It is capable of absorbing up to 23 L of CO2 per 100 g of absorbent. Addition of silica decreases the danger of inhalation of NaOH dust and reduces the resistance to gas flow. The drier the soda lime, the more likely it will absorb and degrade volatile anesthetics.

6. Amsorb consists of Ca(OH)2, CaCl2, CaSO4 and polyvinylpyrrolidone to increase hardness. It is more inert towards volatile agents, so their degradation is less with Amsorb

7. The dry absorbents may break down the volatile anesthetics to carbon monoxide (CO) (e.g., sodium or potassium hydroxide). The formation of CO is highest with desflurane. Compound A is a byproduct of degradation of sevoflurane by absorbent.

Ⓜ️NEMO> CO-Des 'CODES' CoA-Sevo 'CAuSE'

Negative pressure pulmonary oedema (NPPO)

NPPO is associated with upper airway obstruction in a spontaneously breathing patient. 

It occurs in 0.05–0.1% of all general anaesthetic cases and laryngospasm has been reported as being the cause in 50% of cases.

The clinical course is most frequently observed on emergence from anaesthesia where incomplete recovery from general anaesthesia increases the likelihood of the development of laryngospasm, but it has also been reported after airway obstruction with a foreign body and blockage and biting of tracheal tubes, hanging, and strangulation. 

Pulmonary oedema is typically described as developing within 2 min of the obstruction.

Once the airway is occluded, the spontaneously breathing patient will continue to generate negative intrathoracic pressure which will increase substantially as respiratory distress develops.

There is an associated increase in sympathetic tone due to the stress of hypoxia and airway obstruction which increases SVR and elevates pulmonary artery pressure. 

This is further exacerbated by hypoxic pulmonary vasoconstriction. 

The combination of these processes creates a pressure gradient across the capillary–alveolar membrane which favours the movement of fluid into the lung parenchyma.

It is most common in younger patients, presumably because they are able to generate higher negative inspiratory pressures and, arguably, have a higher sympathetic tone and better cardiac function. 

The condition may resolve rapidly after definitive management of the airway obstruction, but in some cases, copious pulmonary oedema may form and it can be associated with pulmonary haemorrhage suggesting capillary membrane damage.

After recognition of the cause of obstruction, the treatment required ranges from relatively modest support such as brief periods of CPAP for 2 h to positive pressure ventilation over a period of 24 h.

Ref: Neurogenic pulmonary edema

Ronan O'Leary, 

Justin McKinlay 

Contin Educ Anaesth Crit Care Pain (2011) 11 (3): 87-92.

WHAT IS POYNTING EFFECT

This is an effect described with regards to the anesthetic gas ENTONOX

ENTONOX is a 50:50 mixture of gaseous oxygen and nitrous oxide

If the cylinder is stored below -6 degree (the pseudocritical temperature of ENTONOX) Celsius, the nitrous oxide component can separate as a liquid (lamination)

This can lead the delivery of uneven mixtures, too much oxygen at the beginning and too much N2O at the end of the cylinder life

Danger of lamination can be avoided by immersing the cylinder in water at 52 degree Celsius and inverting it 3 times, or by keeping it above a temperature of 10 degree Celsius for 2 hours before use.

Other methods are keeping the cylinder horizontal, at a temperature of 5 degrees or more for more than 24 hours OR by connecting a tube from the valve housing at the top to a point near the bottom which prevents the withdrawal of pure nitrous oxide

N.B. The critical temperature of a gas is the maximum temperature at which compression can cause liquefaction. Mixing gases may change their critical temperature. The Poynting effect produces a 50:50 mixture which reduces the crtical temperature of N20 (Critical temperature is 36.5 degree Celsius); so Entonox has a pseudocritical temperature of -6 degree Celsius

A FEW POINTS ABOUT A SHARED LUNG

🔸In the pregnant patient, the respiratory function deviates from the normal

🔸There is increased CO2 production by the mother and the foetus; but mostly you see a respiratory alkalosis. Why?

🔸This is because the stimuli from the raised pCO2 levels and that by the respiratory stimulant, progesterone,  sets the minute ventilation approximately 30% higher than the normal levels and this is more than what is needed to compensate for the increased CO2 production

🔸It is mainly the reduction in FRC (a reduction by 10-25% ; appears by 12th week ; is due to the reduced chest wall compliance ; lung compliance is normal ) which makes the patient more vulnerable to hypoxia.

🔸The alveolar diffusing capacity is reported to be normal during pregnancy

#SCAVENGING IN #ANESTHESIA

Scavenging refers to the method of extracting waste gases from the breathing system and venting them to an area where they will not be directly inhaled by staff or other patients.

Scavenging systems can be classified as open or closed.

Open refers to the basic system of extracting the gas from its point of entry into the theatre

Closed systems are more common and can be further subdivided into active and passive

No conservation of volatile agent is possible with either the active or the passive systems; conservation must occur within the anaesthetic breathing system itself, by the use of a circle system and low-flow anaesthesia.

The active and the passive both pass any waste gas to the atmosphere, polluting it to the same extent.

In the passive scavenging system an exhaust port collects the waste gases from the expiratory valve of the breathing system or from the ventilator and the gases pass through the transfer system (which consists of 30 mm low-resistance tubing) to the outside of the building, preferably above roof level.

If the theatre air is not recirculated, the waste gases can be piped to the exit port of the theatre ventilation system.

In the passive system, the gases are pushed to the atmosphere solely by the expiratory power of the patient

If the pathway to the atmosphere involves a vertical passage of gas, then the patient must overcome the atmospheric pressure required to push the gas over this distance; may be several floors of hospital! Means significant forces has to be overcome.

The use of gases with higher density, like nitrous oxide, adverse atmospheric conditions like high winds etc, will further increase the forces required to expel waste gases; this can even affect the cardiopulmonary status of the patient.

#anaesthesia , #TheLayMedicalMan , #EnviornmentalPollution , #MedicalProfessionalHealthHazard

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OSTEOGENESIS IMPERFECTA (OI) : POINTS OF ANESTHETIC RELEVANCE

🎲Bones and teeth are easy to break.The mandible is prone to fracture,but the facial bones are less so. Rib fractures have been reported. In the severest form, forced extension of the head during intubation carries a risk of vertebral fracture. Violent suxamethonium fasciculations can cause fractures.

🎲n the severe types of the disease,concern has been expressed that a blood pressure cuff may damage the humerus. Direct arterial monitoring has been suggested as an alternative

🎲Macrocephaly can be there. Airway problems may occur if the head is large, if there is macroglossia, or if the skeletal deformities are severe. If the head is large,a pillow placed under the chest may assist tracheal intubation.

🎲There is some evidence of hypermetabolism in this disease. Half of the patients have increased serum thyroxine levels. Hypermetabolic states, with hyperthermia, acidosis, sweating and cardiovascular instability, have been reported, but these are unrelated to Malignant Hyperthermia (MH).

🎲Surgery should be avoided in the pyrexial patient. Core temperature, oxygen saturation and ETCO2 should be monitored throughout surgery. Hyperthermia is reported to have responded to cooling alone.

🎲Platelet dysfunction may occur and produce a mild bleeding tendency, although the platelet count may be normal. But coagulopathies have been reported.

🎲Aortic and mitral valve insufficiency results from the defective connective tissue formation, but may be clinically inapparent. Sometimes cardiac surgery may be required

🎲Cranial developmental defects may cause brainstem compression, hydrocephalus, or vascular disruption. Softening of the basal portion of the occipital bone and upward movement of the cervical spine can combine to cause secondary basilar impression. Warning signs include cough, headache,vertigo, and trigeminal neuralgia.

🎲Those patients with kyphoscoliosis may have restrictive pulmonary defects. Sixty per cent have significant chest wall deformities. A thoracic scoliosis of more than 60 degrees will have severe effects on lung function, with a reduction in vital capacity to below 50%

🎲Although skeletal deformities and deranged coagulation may make regional anaesthesia technically difficult, successful and safe epidural anaesthesia has been reported in patients with OI.

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#anaesthesia , #TheLayMedicalMan , #Orthopedics , #OsteogenesisImperfecta , #fracture

INTRACRANIAL PRESSURE ( #ICP ) MEASUREMENT & HOW IT CAN GUIDE THERAPY❓

🔸ICP data can be used to

✔️predict outcome and evolution of intracranial pathology

✔️calculate and manage cerebral perfusion pressure (CPP) [without an ICP monitor, CPP is not known].

✔️direct management strategies, and

✔️limit the use of potentially deleterious therapies.

🔸Cerebral herniation is a pressure issue and an ICP monitor may allow early detection; it is preferable to avoid herniation than to treat it

🔸Information from an ICP monitor may provide useful information to guide patient care. For example, a patient with a worrisome-appearing CT scan who does not have intracranial hypertension may not require the same degree of treatment as a patient with a similar scan but elevated ICP.  Similarly, a patient with elevated ICP that is refractory to escalating management becomes an early candidate for “second tier” treatments or if very high, even withdrawal of care.

🔸ICP values have prognostic value and so it can guide management and discussions with the family about outcomes

🔸Even transient episodes of severely raised ICP and ischemia can be devastating to the traumatized brain, making it critical to accurately and continuously monitor ICP & CPP. Because insertion of intraparenchymal ICP monitors is safe, the ability to monitor CPP per se is a supportable argument for widespread ICP monitoring.

🔸Perhaps more important than a single ICP threshold may be a trend over time, ICP waveform analysis, or whether the ICP value is associated with other detrimental effects.

🔸When both ICP and brain oxygen are treated, the outcome may be better than if just ICP is treated after TBI

🔸The ICP waveform is a modified arterial pressure tracing

🔸 It has 3 peaks: P1, P2 & P3

🔸 P1 is a result of transmitted pressure from choroid plexus

🔸 The amplitude of P2 changes with brain compliance. If compliance is poor, amplitude will be high ( can even exceed that of P1) and vice versa

🔸P3 represents the dicrotic notch

🔸 Lundberg (A) or Plateau waves are steep rise of ICP to over 50 mm of Hg and lasting for 5-20 minutes; then it falls abruptly. Are always pathological and indicates significantly reduced compliance

🔸 Lundberg (B) waves are oscillations occurring every 1-2 minutes where ICP rises to over 20-30 mm of Hg from baseline in a crescendo manner. They are supposed to be result of altered cerebral (B)lood volume and altered tone of cerebral (B)lood vessels

🔸 Lundberg (C) waves are oscillations whose amplitude is less than that of B waves and are supposed to result because of interactions between cardiac and respiratory (C)ycles. They occur also in healthy individuals

METHODS OF MEASUREMENT OF ICP

➿ Intraventricular catheter - ventriculostomy represents the "gold standard" for pressure measurement

✔️Normally placed in the frontal horn of lateral ventricle

✔️Allows therapeutic CSF drainage

✔️Creates a pathway for infection

✔️In case of the Integra Neuroscience external drainage catheter, ICP readings are based on a fluid-filled transduction system that transmits changes in ICP through a saline-filled tube to a diaphragm on a strain gauge transducer. This monitor must be leveled with the foramen of Monro (approximately the level of the external auditory canal) after insertion and should be zero-balanced daily. The level of the drain can be adjusted to allow more or less CSF drainage.

 ➿Subdural bolt / Catheters

✔️ less invasive

✔️ Bolts commonly use fiberoptic technology that allows continuous ICP monitoring without CSF drainage. The fiberoptic type of catheter can be placed in the subdural space or in the brain parenchyma

✔️ Usually subdural space over frontal lobe of non-dominant hemisphere is selected

✔️ Prone to signal damping and calibration drift

✔️ Potential risk of infection

✔️ Doesn't require penetration of brain tissue

✔️Camino Post Craniotomy Subdural Pressure Monitor utilizes the craniotomy bur holes and flap as a point of entry. The monitor is zero-balanced and then tunneled under the scalp toward the craniotomy bur hole of choice and positioned in the subdural space. This monitor contains a microtransducer at the tip, which is similar to the OLM ICP monitor ( see below)

✔️Gaeltec ICT/B pressure sensor is intended to monitor ICP subdurally. It contains a balloon-covered pressure sensor that is activated when filled with air. This monitor is self–zero-balanced in vivo and is reusable.

➿Intracerebral transducer

✔️Parenchymal devices are easier to place, particularly when altered ventricular anatomy may limit ventricular catheter placement.

✔️However, intraparenchymal fiber-optic and electronic strain gauge systems are more expensive and cannot be recalibrated once in situ

✔️Inability to check zero calibration & drain CSF

✔️ Risk of infection

✔️Less reliable

✔️The Camino OLM ICP monitor measures ICP in the intraparenchymal tissue or subarachnoid space. It contains a transducer at the distal tip, thus measuring pressure without a fluid-filled system. The catheter is secured to the skull through an adjustable bolt, allowing placement at variable depths (up to 5 cm).

✔️The Codman Microsensor catheter can be used as an intraparenchymal or intraventricular monitor, depending on the depth of the catheter

✔️ Spiegelberg ICP monitors measure ICP through an air-pouch system attached to a pressure transducer connected to an electronic device. The probes differ, depending on where they rest (Epidural or Intraparenchymal)

🔸The incidence of infection ~ 2-7% with monitoring ≥ 5 days

🔸The risks are slightly greater with dural penetration

🔸The zero reference point of the transducer is usually taken as the external auditory meatus

🔸 Rather than the waveform type, the important factors appear to be the degree and duration of ICP elevation

🔸Two emerging non-invasive ICP monitoring methods include measuring the optic nerve sheath diameter  (ONSD) as seen on an ultrasound probe placed on the superolateral aspect of the orbit and the pulsatility index (PI) which is cal- culated from transcranial Doppler studies (TCD).

#NeuroAnesthesia , #anaesthesia , #TheLayMedicalMan , #NeuroCriticalCare , #CriticalCare , #NeuroICU

NORMAL SWALLOWING & DISORDERS OF SWALLOWING: For the #NeuroCriticalCare #Physician & #Anesthesiologist

👅Cranial nerves V,VII,IX,X,XI,XII contributes to swallowing

👅2 brain stem nuclei control swallowing: (1) Nucleus Tractus Solitarius(NTS) which is a pure sensory nucleus in the medulla (2) Nucleus Ambiguous (NA) which is a motor nucleus situated deep in the reticular formation in medulla
 
👅Sensory info sent via cranial nerves to NTS. Interneurons relay info to NA & surrounding reticular formation which sends efferent messages to cranial nerve pathways.

👅Muscles innervated by Trigeminal nerve helps in Mastication, jaw closure, upward movement of larynx, backward movement of tongue to soft palate, tensing and elevation of soft palate and posterior pharyngeal wall constriction

👅Muscles innervated by Facial nerve helps in mandibular depression and contributes to hyoid elevation

👅Glossopharyngeal nerve supplies Stylopharyngeus , contributes to palatoglossus - portion of middle pharyngeal constrictor Ⓜ️NEMO> “Glossy nerve helps Stylish Middle Class”

👅Vagus supplies muscles of soft palate (except Tensor Veli Palatini) - Superior, middle and inferior pharyngeal constrictors - Intrinsic muscles of larynx and muscles of esophagus Ⓜ️NEMO> “Vague nerve helps all classes”
 
👅Recurrent Laryngeal Nerve innervates Cricopharyngeus muscle.
 
👅Hypoglossal nerve innervates all intrinsic and some extrinsic muscles of tongue and geniohyoid ; hence responsible for all movements of the tongue
 
👅Aetiology of swallowing disorders: Stroke, Traumatic Brain Injury, Brain Tumor , Cerebral Palsy, Neuroleptic drug- induced Tardive dyskinesia , Surgery ( Generally damage to the pharyngeal plexus may occur with anterior cervical fusion. Injury of the seventh, tenth, and twelfth cranial nerves may occur with carotid endarterectomy, as these nerves are close to the carotid bifurcation), various forms of dementia, Movement disorders including Parkinsons disease, Multiple Sclerosis , Amyotrophic Lateral Sclerosis (ALS)
 
👅It has been suggested that recovery of swallowing in acute stroke patients may be rapid, warranting reassessment within 3 weeks of the initial swallowing evaluation
 
👅Abnormal volitional cough, abnormal gag,dysarthria,dysphonia, cough after swallow, voice change after swallow are indicators of risk of aspiration after acute stroke
 
👅But many of the neurologic disorders that affect swallowing are progressive; thus swallowing can be expected to decline as the disease worsens.
 
👅Dysarthria may correlate with dysphagia with bulbar Amyotrophic Lateral Sclerosis (ALS). Dysphagia increases as respiratory capacity decreases regardless of the form of ALS. Vital capacity should be consistently measured, as accurate and timely assessment of a clinically relevant decline in respiratory status is crucial for determining the timing of feeding tube placement
 
👅Pneumonia can be a frequent complication in patients with dysphagia owing to CNS disease
 
👅Although an abnormal gag reflex may be apparent in patients with dysphagia resulting from various neurologic disorders, it may be absent in healthy control subjects or it may be normal in patients with neurogenic dysphagia
 
👅The two imaging tools used to evaluate oropharyngeal dysphagia are Video Fluoroscopic Swallow Study (VSS- Gold Standard) and videoendoscopy. The Penetration-Aspiration Scale (PAS) provides an objective way during the VSS to measure the depth, response, and clearance of material entering the larynx and trachea.
 
👅They are also valuable in identifying and teaching maneuvers that may facilitate swallowing and prevent aspiration in a patient.
 
👅When significant aspiration cannot be prevented, alternatives to oral feeding such as percutaneous endoscopic gastrostomy (PEG) tube placement should be considered.
 
👅Patients with oropharyngeal dysphagia owing to CNS lesions are best managed by a team approach including a speech pathologist, neurologist, and gastroenterologist.
 
👅Swallowing therapy may include compensatory or rehabilitative strategies. Compensatory therapy does not change the physiology of the swallow; rather, bolus flow is redirected
 
👅Compensatory strategies consist of manipulation of posture, consistency of the liquid, and sensory input. Facilitatory postures that have been studied in the neurogenic population include chin tuck and head rotation to the weak side
 
👅Rehabilitative therapy includes muscular strengthening and range of motion exercises, thermal-tactile application, and swallowing maneuvers
 
👅Vocal fold medialization is the procedure generally performed to treat aspiration owing to an incompetent larynx
 
👅A tracheotomy may be performed for neurologic patients with chronic aspiration. Although it does not improve swallowing, it facilitates pulmonary toileting
 
👅Laryngotracheal separation is a more radical attempt to prevent chronic aspiration while allowing for oral intake. Although patients may return to oral diets, the ability to phonate is eliminated. If physiologic aspects of swallowing improve sufficiently, this procedure can be reversed, as the glottis is not affected.

#Swallowing , #Anesthesia , #TheLayMedicalMan , #CriticalCare , #Anatomy , #Physiology , #GastroEnterology

ICTAL BRADYCARDIA &ASYSTOLE: AN ENTITY ALL ANESTHESIOLOGISTS SHOULD KEEP IN MIND WHEN SEEING BRADYCARDIA IN A PATIENT WITH EPILEPSY

📌Ictal bradycardia/asystole is a poorly recognised cause of collapse late in the course of a typical complex partial seizure

📌It is important to identify ictal bradycardia as a potential harbinger of lethal rhythms, such as asystole, as this may be one important mechanism leading to sudden unexpected death in epilepsy (SUDEP)

📌Tachycardia is the most common rhythm abnormality occurring in 64–100% of temporal lobe seizures. Ictal bradycardia has been reported in less than 6% of patients with complex partial seizures

📌The ictal bradycardia syndrome occurs in mostly in patients with temporal lobe seizures.

📌It is believed that abnormal neuronal activity during a seizure can affect central autonomic regulatory centres in the brain leading to cardiac rhythm changes.

📌Ictal bradycardia/asystole may be unrecognised until documented during video-electroencephalograph (video EEG)–electrocardiogram (ECG) monitoring in those with refractory epilepsy, often in the context of pre-surgical evaluation

📌Other rhythm abnormalities which can occur are change in heart rate variability, ictal tachycardias and atrioventricular (AV) block

📌If sufficiently severe, the ictal-induced bradyarrhythmia temporarily impairs both cerebral perfusion and cortical function; the result has the dual effect of terminating the seizure, while at the same time triggering syncope with consequent loss of consciousness and postural tone. In essence, a complex partial seizure patient may manifest both seizure and syncope features during the same episode.

📌There are currently no guidelines on who should undergo further cardiovascular investigations ; dual chamber pacemaker implantation has been suggested as a treatment in the long term, for epilepsy patients who manifest this syndrome and suffer repeated falls; but there is not much mention in literature  both about diagnosis and about pharmacological and non pharmacological interventions to counter such episodes when presenting as an emergency situation in the perioperative scenario , especially when the patient is under anesthesia.

#Neurology , #NeuroCriticalCare , #Anesthesia , #LayMedicalMan , #CriticalCare , #Epilepsy , #Cardiology , #CardiacAnesthesia

Reference: Ictal bradycardia and atrioventricular block: a cardiac manifestation of epilepsy; Salman S. Allana  Hanna N. Ahmed  Keval Shah  Annie F. Kelly, Oxford Medical Case Reports, British Journal of Cardiology : Ictal Bradycardia and Asystole Associated with Intractable Epilepsy: A Case Series Elijah Chaila, Jaspreet Bhangu, Sandya Tirupathi, Norman Delanty; Ictal Asystole-Life-Threatening Vagal Storm or a Benign Seizure Self-Termination Mechanism? David G. Benditt, Gert van Dijk, Roland D. Thijs (Editorial:Circulation )

JNC 8 GUIDELINES FOR TREATMENT OF SYSTEMIC HYPERTENSION: A SUMMARY

(1)📌In the general population aged 60 years or more , initiate pharmacologic treatment to lower blood pressure (BP) at systolic blood pressure (SBP) ≥150 mm Hg or diastolic blood pressure (DBP) ≥ 90 mm Hg and treat to a goal SBP <150 mm Hg and goal DBP <90 mm Hg

(2)📌In the general population aged ≥60 years, if pharmacologic treatment for high BP results in lower achieved SBP (eg, <140 mm Hg) and treatment is well tolerated and without adverse effects on health or quality of life, treatment does not need to be adjusted.

(3)📌In the general population <60 years, initiate pharmacologic treatment

(a) to lower BP at DBP ≥90mmHg and treat to a goal DBP <90mmHg.

(b) to lower BP at SBP ≥140 mm Hg and treat to a goal SBP <140 mm Hg.

(4)📌In the population aged ≥18 years with (i) diabetes & (ii) chronic kidney disease (CKD), initiate pharmacologic treatment to lower BP at SBP ≥140 mmHg or DBP ≥90 mmHg and treat to goal SBP <140mmHg and goal DBP <90mmHg.

(5)📌In the general nonblack population, including those with diabetes, initial antihypertensive treatment should include a thiazide-type diuretic, calcium channel blocker (CCB), angiotensin-converting enzyme inhibitor
(ACEI), or angiotensin receptor blocker (ARB).

(6)📌In the general black population, including those with diabetes, initial antihypertensive treatment should include a thiazide-type diuretic or CCB.

(7)📌In the population aged 18 years with CKD, initial (or add-on) antihypertensive treatment should include an ACEI or ARB to improve kidney outcomes. This applies to all CKD patients with hypertension regardless of race
or diabetes status.

(8)📌If goal BP is not reached within a month of treatment, increase the dose of the initial drug or add a second drug from one of the classes : thiazide-type diuretic, CCB,ACEI, or ARB. The clinician should continue to assess BP and adjust the treatment regimen until goal BP is reached.

(9)📌If goal BP cannot be reached with 2 drugs, add and titrate a third drug from the list mentioned above (). Do not use an ACEI and an ARB together in the same patient.

(10)📌If goal BP cannot be reached using only the drugs mentioned above, because of a contraindication or the need to use more than 3 drugs to reach goal BP, antihypertensive drugs from other classes can be used.

#hypertension , #medicine , #TheLayMedicalMan , #jnc8 , #HTN , #anesthesia , #pharmacology , #BloodPressure ,#BP

#EPINEPHRINE ( #Adrenaline) : Pharmacological Highlights

🔻Epinephrine is an agonist of alpha 1, β1 , and β2 adrenoceptors. An intravenous infusion of epinephrine produces an increase in mean arterial pressure (MAP) characterized by selectively enhanced systolic pressure with no change in diastolic pressure. 

🔻Epinephrine exerts positive chronotropic and inotropic actions by stimulation of β1 adrenoceptors

🔻Epinephrine also increases the rate of myocardial relaxation and enhances early LV filling, thereby improving diastolic function. These combined effects result in a dramatic increase in cardiac output.

🔻Epinephrine (0.01–0.03 ug kg –1 min –1 ) has been shown to produce similar hemodynamic effects with less pronounced tachycardia than dobutamine (2.5–5.0 ug kg–1 min–1 ) in patients after coronary artery bypass graft (CABG) surgery

🔻Predictable increase in cardiac output, favours the use of epinephrine as the primary inotropic drug for the management of LV dysfunction after cardiopulmonary bypass

🔻Epinephrine causes direct positive dromotropic effects ( leading to increase in conduction velocity and reduction of the refractory period of the AV node, His bundle, Purkinje fibers, and ventricular muscle)

🔻This may contribute to detrimental increases in ventricular rate in patients with atrial flutter or fibrillation and the occurrence of ventricular arrhythmias

🔻The overall effect of epinephrine on blood flow to a specific organ depends on the relative balance of alpha 1 and β2 adrenoceptors located in the vasculature.

🔻β2 -Adrenoceptors are sensitive to lower doses of epinephrine and, as a result, peripheral vasodilation and modest reductions in arterial pressure are observed with such doses

🔻In contrast, the effects of epinephrine on alpha 1 -adrenoceptors predominate at greater doses with marked increases in systemic vascular resistance and arterial pressure.

🔻The intense vasoconstriction produced by high doses of epinephrine may adversely impede LV ejection by increasing after load after cardiopulmonary bypass. Thus, greater doses of epinephrine may be used in combination with arterial vasodilators such as sodium nitroprusside to optimize contractile performance in such situations .

🔻Adrenaline via alpha 1 receptors also mediates (1) venoconstriction & enhanced venous return (2) Pulmonary vasoconstriction and increases in pulmonary arterial pressures.

🔻 Pre-existing β-blockade by nonselective β-blocker propranolol abolishes the decrease in systemic vascular resistance from epinephrine-induced stimulation of β2 adrenoceptors and potentiates peripheral vasoconstriction mediated by unopposed alpha 1 adrenoceptors.

🔻The positive inotropic and chronotropic effects of epinephrine are also attenuated in the presence of pre-existing β-blockade and greater doses of epinephrine are required to overcome this competitive blockade

🔻Complete pharmacologic blockade of β1 and β2 adrenoceptors may theoretically make the hemodynamic effects of epinephrine indistinguishable from those of the pure alpha 1 adrenoceptor agonist phenylephrine.

#NorAdrenaline , #CriticalCare , #vasopressors , #TheLayMedicalMan , #IntensiveCare , #Pharmacology, #anesthesia , #anaesthesia, #drugs

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

#NORADRENALINE : PHARMACOLOGICAL HIGHLIGHTS & COMPARISON WITH #ADRENALINE

🖍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.

🖍Noradrenaline 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

#ClinicalPharmacology , #IntensiveCare , #CriticalCare , #EmergencyMedicine , #pharmacology , #anaesthesiology , #anaesthesia , #anesthesiology ,


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

TURP SYNDROME AND THE ANESTHESIOLOGIST

🚩#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.

BISPECTRAL INDEX

💆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

EXPLICIT AND IMPLICIT AWARENESS DURING ANESTHESIA

EXPLICIT AND IMPLICIT AWARENESS DURING ANESTHESIA

😐(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

🔻may result from a 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 www.facebook.com/drunnikrishnanz , partial reference from frca.uk , #anaesthesia

Tapentadol

🚩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❓

😤 Olfactory receptors1️⃣ 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 cribiform 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 cells2️⃣ 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

☢️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

The science behind the pulse oximetry

☝️️Pulseoximeter measures the percentage of arterial hemoglobin in the blood that is saturated with oxygen
☝️️It consists of 2 LEDs & a photodiode arranged on either side of an adhesive strip and an electronic processor 
☝️️Light from LEDs travel through the patient's body part and is detected by the photodiode
☝️️One LED emits light at 660 nm (red light) and the other at 940 nm (infrared light). 
☝️️Oxyhaemoglobin and deoxyhaemoglobin absorb these wavelengths differently
☝️️Oxyhaemoglobin absorbs more infrared light (940 nm) and allows more red light (660 nm) to pass through. 
☝️️Deoxyhaemoglobin absorbs more red light (660 nm) and allows more infrared light (940 nm) to pass through.

☝️️Isobestic point is at 806 nm

☝️️The LEDs flash in sequence: one on, then the other, then both off (to allow correction for ambient light). This triplet sequence happens 30 times per second

☝️️The amount of light transmitted through the patient at each frequency is detected by the photodiode. 
☝️️The microprocessor corrects for ambient light, and also for the difference between arterial and venous saturations by deducting the minimum transmitted light, during diastole, from the maximum during systole.
☝️️After this, the ratio of oxy to deoxyhaemoglobin is determined and from this the percentage oxygen saturations is determined, using an empirical table derived from healthy volunteers who were exposed to varying degrees of hypoxia.
💅🏽Apart from the common causes like movement, nail varnish, diathermy,  others like 
🔻severe anaemia 

🔻cardiac arrhythmias 

🔻Methaemoglobinaemia (characteristically cause saturations to be measured at around 85%) 

🔻Increased venous pulsation, e.g. severe tricuspid regurgitation 

🔻i.v. methylene blue dye (because it absorbs light in the 660–670 nm range 
also may cause erroneously low readings)
💅🏻Carboxy hemoglobin (CO-Hb has similar absorption spectra as that of oxy-Hb) is detected by normal pulse oximeters as oxy hemoglobin--> erroneous high readings 
💅🏻Cyanide prevents oxygen being utilised in respiration and so its extraction from the blood falls; so in cyanide poisoning, though the value is not inaccurate, it should be interpreted as inappropriately high.
☝️️Fetal haemoglobin and Hb S (sickle) do not affect readings
☝️️The human volunteers used to construct empirical saturation tables did not have their oxygen saturations dropped below approximately 85%; hence readings below this number are extrapolated, not validated.