pH and [H+] : QUANTIFICATION & COMPARISON

✅For each one point increase in the pH scale, the concentration of hydrogen ions, and the acidity, changes by a factor of 10. 

✅Therefore, a solution with a pH of 4 is 10 times as acidic as a solution with a pH of 5, and 100 times more acidic than a solution with a pH of 6. 

✅The scale is relative in terms of [H +], so although a pH of 8 implies an alkaline solution, the number of H + ions still differs 100-fold from a solution with a pH of 10. 

✅HOW TO FIND pH WHEN WE KNOW THE STRENGTH OF THE SOLUTION 

🔹pH = –log10[ H +]

🔹If solution is 0.01 M solution ,[H+] = 10^2= –log (10^2) = pH 2 

🔹More simply put, the pH is the number of times you need to move the decimal point to get the first non zero value (here it's 1)

VASOACTIVE AGENTS; DO YOU KNOW ?

Evidence suggests that dopamine can produce mild cerebral vasodilatation.

Phenylephrine can be the drug of choice when the cardiac index (CI) is sufficient but MAP is below the goal

Dobutamine does not have any dopaminergic agonist action.

In case of Labetalol, a reduction in MAP usually occurs when the dose is sufficient to decrease HR

propanolol shifts the hemoglobin-oxygen dissociation curve to the right.

Milrinone can induce thrombocytopenia as well as hypotension.

SNP is associated with the activation of the renin-angiotensin system ; reflex tachycardia can interfere with blood pressure reduction.

Occasionally, patients demonstrate relative resistance to SNP and they are at particular risk for developing cyanide toxicity.

SNP causes more arteriolar than venular vasodilatation, while NTG causes more venular than arteriolar vasodilatation.

Vasopressin increases arterial tone ; it is administered as a constant infusion, and not titrated up to avoid severe complications of distal ischemia.

Reference: Newfield, Philippa; Cottrell, James E., Handbook of Neuroanesthesia, 4th Edition

THE SUCCESS OF KETAMINE IN REFRACTORY SEIZURES, WHERE BENZODIAZEPINES FAIL

🔴In status epilepticus is there is a reduction in expression of “benzodiazepine-sensitive” GABAA-R d2 subunits 

🔴Also there is a 20-fold loss of potency in benzodiazepine receptors after 30 minutes.

🔴But there is an increase in the expression of excitatory NMDA receptors occurs, leading to seizure propogation

🔴Continued seizures result in BBB dysfunction facilitating leakage of albumin into the CNS, with a resultant proconvulsant effect by stimulating astrocytes to release NMDA and causing cerebral vasoconstriction.

🔴With continuing seizures, inhibitory GABA receptors are internalized in clathrin-coated vesicles, and excitatory NMDA receptors are mobilized to the membrane. This receptor trafficking may result in decreased inhibitory control and increased excitation that may foster status epilepticus. 

🔴The strong NMDA antagonist effect of ketamine has anticonvulsant effects and has the potential to prevent glutamate-mediated neurotoxicity. 

🔴Williams et al used a dose of 5 mg/kg/h in patients to control the seizures. The literature shows that doses as high as 7.5 mg/kg/h used for up to 14 days were safe.

🔴"With ketamine use, a concern about increasing intracranial pressure has been raised in ventilated patients. However, ketamine may not significantly elevate intracranial pressure and may provide some degree of neuroprotection by inhibiting the NMDA-receptor activation and interfere with the inflammatory response to injury when used in typical sedative or anesthetic doses."

🔴Ketamine may be the ideal agent for the control of seizure in patients with refractory seizures and septic shock in the intraoperative setting.

REFERENCE:

Use of Ketamine for Control of Refractory Seizures During the Intraoperative Period ; Williams, George W. MD; Cheng, Yuen C. MD; Sharma, Aanchal MD, Journal of Neurosurgical Anesthesiology, October 2014, Volume 26, Number 4

THE SECOND COMING OF METHOXYFLURANE

Ⓜ️Initially developed as an inhalational anesthetic, but withdrawn due to concerns about nephrotoxicity and hepatotoxicity. 

Ⓜ️In view of its analgesic properties it is now used, mainly in Australia and New Zealand, to provide short-term analgesia for painful procedures and in the prehospital setting (Grindlay and Babl, 2009). 

Ⓜ️Administration is via a dedicated single-use inhaler dispensing 0.2–0.4% methoxyflurane. 

Ⓜ️The limited data on efficacy suggest that methoxyflurane administered as a single dose as described above provides effective analgesia resulting in high patient satisfaction with no evidence of toxicity (Grindlay and Babl, 2009). 

Ⓜ️There is no good evidence regarding the safety of repeated doses, for example, for analgesia during daily dressing changes.

Ref: 

Acute Pain Management; A Practical Guide, Pamela E. Macintyre , Stephan A. Schug, 4/e

Predictors of mortality after subarachnoid hemorrhage

<Ⓜ️nemo : "POOR PreDICTOR"

P͞͞O͞͞O͞͞R͞͞  neurologic condition at hospital admission, a function of rate and volume of bleed

P͞͞R͞͞E͞͞existing illness

D͞͞epressed level of consciousness after initial bleed

I͞͞ncreased blood pressure

C͞͞irculation affected: if Basilar 

T͞͞hick clot in the brain substance or ventricles on initial computed tomographic scan

O͞͞lder age

R͞͞epeat hemorrhage

ADVERSE EFFECTS OF UNDER TREATED SEVERE ACUTE PAIN

(Reference: Pamela E. Macintyre,Stephan A. Schug. ACUTE PAIN MANAGEMENT; A PRACTICAL GUIDE)

👹Tachycardia, hypertension

👹increased myocardial oxygen consumption, myocardial ischemia

👹 Decreased lung volumes, atelectasis, decreased cough, sputum retention, infection, hypoxemia

👹Decreased gastric and bowel motility 

👹Urinary retention 

👹Increased catabolic hormones: glucagon, growth hormone, vasopressin, aldosterone, renin, and angiotensin 

👹Reduced anabolic hormones: insulin, testosterone 

👹Catabolism leads to hyperglycemia, increased protein breakdown and negative nitrogen balance; ➡️impaired wound healing and muscle wasting 

👹 Muscle spasm, immobility (increasing risk of deep-vein thrombosis-->pulmonary embolism) and muscle wasting 

👹 Chronic (persistent) pain due to central sensitization 

👹 Anxiety, fear, helplessness, sleep deprivation—leading to increased pain and potential long-term psychological effects

Trouble Shooting the Arterial Blood Pressure Tracing: OVER DAMPENING & UNDER DAMPENING ▪️▪️▪️▪️▪️

Over dampened tracing 

➖➖➖➖➖➖➖➖➖

⏺May result in an under-reading of pressures 

⏺This may cause an underestimation of the systolic pressure and overestimation of diastolic pressure. 

▶️Check the transducer position as it may be too high above RA. 

▶️Kinking of the catheter at the insertion site may also cause the waveform to become dampened. 

Under dampened tracing 

➖➖➖➖➖➖➖➖➖

⏺noted by a high initial spike in the waveform 

⏺because of inadequate damping of the transducer, which causes an excessive resonance in the system. 

⏺ May result in an overestimate of systolic pressure and an underestimate of diastolic pressure. 

▶️check the transducer position. It may be too low below the RA. 

Better to re-zero the transducer to atmospheric pressures, in both of the above situations

ANESTHESIA INFO FROM THE LAY MEDICAL MAN- Facebook Page

🔴T̠H̠E̠ B̠A̠S̠I̠C̠S̠ O̠F̠ R̠E̠S̠P̠I̠R̠A̠T̠O̠R̠Y̠ P̠H̠Y̠S̠I̠O̠L̠O̠G̠Y̠ & A̠B̠G̠🔴 A FEW POINTS

⚡️CO2  is the most important stimulus for respiration

😇Receptors for CO2  are found in the medulla of the brain (central chemoreceptors)

❤️Receptors for O2  are found mainly in carotid and aortic bodies 

👑CO2  is the more important gas as the body has more capacity to store CO2  than O2 or hydrogen ions 

1️⃣0️⃣In normal people at sea level, only 10% of the respiratory drive is due to hypoxic stimulation. 

▶️◀️Unlike the central stimulation of hypercapnia, hypoxia causes central depression of the respiratory drive. 

▶️◀️Acidosis (high H + /low blood pH) stimulates respiration; conversely alkalosis depresses it.

😳For gas exchange, the lungs provide an interface of total surface area about 55 m2 via 700 million alveoli

🎯Alveolar ventilation’ is that part of the total ventilation (i.e. all gas entering the lungs) that participates in gas exchange with pulmonary capillary blood; it is equal to total ventilation minus the ventilation of the conducting airways (i.e. dead-space ventilation).The average alveolar ventilation is about 4 L/min.

📥The alveolar–arterial oxygen gradient ( P(A-a)O2 ) is a measure of the oxygen that has reached the arterial blood supply as a ratio of the total oxygen in the alveoli. It is a useful index of pulmonary gas exchange function. 

➡️This requires that three elements are working correctly: 

⏺Circulatory anatomy is normal. Anomalies such as ASD & PDA can cause anatomical shunting,  i.e. venous blood passes through routes that are not exposed to alveolar air 

⏺Ventilation and perfusion are matched 

⏺The respiratory membrane allows sufficient free diffusion of gases between air and blood.  A diffusion defect impairs the alveolar–capillary membrane, e.g. in interstitial lung fibrosis

🔢In a healthy individual breathing room air (at FiO2 21) the PO2  in alveolar air is 104 mmHg and in arterial blood 95 mmHg . PAO2 exceeds PaO2 by 15 mmHg .Thus, at an FiO2 of 21, the P(A–a)O2 is 15 mmHg 

🎭In blood, CO2  is present as: 

✔️Dissolved in blood plasma (5.3% in arterial blood)

✔️Bound to haemoglobin as carbaminohaemoglobin within erythrocytes (4.5%) 

✔️In the form of bicarbonate attached to a base (90%) As CO2 diffuses from peri

Reference:"Understanding ABGs & Lung Function Tests"  Muhunthan Thillai, Keith Hattotuwa