Thursday, May 25, 2017


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


✔️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.


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


✔️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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Wednesday, May 24, 2017


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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Monday, May 22, 2017



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

Friday, May 19, 2017


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.


Thursday, May 18, 2017

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

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

Monday, May 15, 2017


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

Tuesday, May 2, 2017


🔸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

Monday, April 3, 2017


😤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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Saturday, March 4, 2017


🎲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

Tuesday, February 21, 2017


🔸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


➿ 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