Mixed venous oxygen content (CvO2) is the oxygen concentration in 100mL of mixed venous blood taken from the pulmonary artery. It is usually 12-17 mL/dL (70-75%). It is represented mathematically as:

CvO2 = (1.34 x Hgb x SvO2 x 0.01) + (0.003 x PvO2)

Where,

1.34 = Huffner’s constant
Hgb = Haemoglobin level (g/dL)
SvO2 = % oxyhaemoglobin saturation of mixed venous blood
PvO2 = 0.0225 = mL of O2 dissolved per 100mL plasma per kPa, or 0.003 mL per mmHg

Therefore,

CvO2 = (1.34 x 10 x 70 x 0.01) + (0.003 x 50)

CvO2 = 9.38 + 0.15 = 9.53 mL/100mL

Drugs cross the placenta by Simple, Ion channel and Facilitated diffusion; Exocytosis and Endocytosis, Osmosis, and Active transport (primary and secondary)

The following factors influence rate of diffusion across the placenta:

Protein binding
Degree of ionisation
Placental blood flow
Maternal and foetal blood pH
Materno-foetal concentration gradient.
Thickness of placental membrane
Molecular weight of drug <600 Daltons cross by diffusion
Lipid solubility (lipid soluble molecules readily diffuse across the placenta)

Rocuronium has a F/M ratios of 0.16, a 30% plasma protein binding, low lipid solubility, a low volume of distribution (0.25L/kg), and a high molecular weight (530Da).

Breathing system is an assembly of components which connects patient’s airway to anaesthesia machine through which controlled composition of gas mixture is dispensed. It delivers gas to the patient, removes expired gas and controls the temperature and humidity of the inspired mixture. It allows spontaneous, controlled, or assisted respiration. It may also provide ports for gas sampling, airway pressure, flow and volume monitoring.

Breathing systems have been classified by Conway and Mapleson.
Conway suggested a functional classification:
– Circuits requiring a CO2 absorber
– Circuits not requiring a CO2 absorber

William Mapleson designated varying arrangements of breathing system components (masks, breathing tubes, fresh gas flow inlets, adjustable pressure-limiting valves, and reservoir bags) as Mapleson A-E circuits.
Mapleson A: Arranged as FGF inlet, reservoir bag, APL valve, mask.
In this circuit, because the reservoir bag is between the FGF inlet valve and the APL valve, expired gas from the patient may re-enter the system and fill the reservoir bag during controlled ventilation. This is the most efficient system for spontaneous breathing as the FGF must only be equal to a patient’s minute ventilation to prevent rebreathing.

Mapleson B: Arranged as reservoir bag, FGF inlet, APL valve, mask.
In this circuit, the FGF inlet is closer to the APL valve, which helps prevent the rebreathing concern in the Mapleson A circuit as above during controlled ventilation.

Mapleson C: Arranged as reservoir bag, FGF inlet, APL valve, mask.
In this circuit, the arrangement is the same as the Mapleson B circuit. However, this circuit is shorter as it does not contain elongated corrugated tubing. This circuit also has the FGF inlet close to the APL valve to aid in preventing rebreathing.

Mapleson D: Arranged as reservoir bag, APL valve, FGF inlet, and mask.
In this circuit, the arrangement interchanges the FGF inlet and APL valve of the Mapleson A circuit. This system prevents rebreathing by directing FGF towards the APL valve rather than towards the patient during exhalation.

Mapleson E: Arranged as corrugated tubing, FGF inlet, and mask.
In this circuit, there is no reservoir bag and no APL valve. Given the inability to alter the pressure of the circuit, this is ideal for spontaneously ventilating neonates or paediatric patients where low-pressure ventilation is desired. The system prevents rebreathing, similar to the Mapleson D circuit.

Jackson Rees later modified the Mapleson E by adding an open ended bag, which has since become known as the Mapleson F.
Mapleson F: Arranged as APL valve directly connected to reservoir bag, corrugated tubing, FGF inlet, and mask.
The system prevents rebreathing similarly to Mapleson D by directing FGF towards the APL valve.

Because enflurane is much less soluble in blood and has a blood: gas partition coefficient of 1.8, both wash-in and wash-out should be faster.

Sevoflurane’s sweet-smelling, non-irritant nature, combined with a low blood: gas partition coefficient, would result in similar offset and onset characteristics.

Isoflurane and enflurane have a molecular weight of 184.

The oil: gas partition coefficient on a volatile agent is a measure of lipid solubility, potency, and thus MAC. Halothane has an oil: gas partition coefficient of 220 and a MAC of 0.74. One would expect the MAC to be higher with an oil gas partition coefficient of 180 (less lipid soluble).

The conversion of halothane (20%) to trifluoroacetic acid via oxidative metabolism has been linked to the development of hepatitis.

P450 2E1 converts sevoflurane to hexafluoroisopropanol, which results in the release of inorganic fluoride ions. It’s the only fluorinated volatile anaesthetic that doesn’t break down into trifluoracetic acid.

Desflurane is likely to cause airway irritation, which can lead to coughing, apnoea, and laryngospasm, despite its low blood:gas partition coefficient (0.42).

Alfentanil is less lipid-soluble than fentanyl and thus is less permeable to the membrane making it less potent.

Alfentanil is a phenylpiperidine opioid analgesic with rapid onset and shorter duration of action.

Alfentanil has less volume of distribution due to its high plasma protein binding (92%)

It can cause respiratory depression and can cause sedation

Elimination of phenytoin from the body follows first-order kinetics. This means that the rate of elimination is proportional to plasma concentration.

The rate of elimination can be described by the equation:

C = C0·e-kt

Where:

C = drug concentration
C0 = drug concentration at time zero (extrapolated)
k = Rate constant
t = Time

Enzyme systems become saturated when phenytoin concentrations exceed the normal range and elimination of the drug becomes zero-order. At this point, the drug is metabolised at a fixed rate and metabolism is independent of plasma concentration.

Aspirin and ethyl alcohol are other drugs that behave this way.

A beta-1 adrenoreceptor agonist is most likely the ligand that causes increased automaticity, increased chronotropy, increased excitability, and increased inotropy on the sino-atrial node. However, alpha-1 adrenoreceptor effects may cause an increase in systemic vascular resistance. Noradrenaline, adrenaline, dopamine, and ephedrine are examples of drugs with mixed alpha and beta effects.

Adrenaline, noradrenaline, dopamine, dopexamine, dobutamine, ephedrine, and isoprenaline are examples of drugs that have some beta-1 activity. The beta-1 receptor is a G protein-coupled metabotropic receptor. When the beta-1 agonist binds to the cell surface membrane, it causes a conformational change in the Gs unit, which triggers a cAMP-dependent pathway and a calcium influx into the cell.

Catecholamines also help to relax the heart muscle (positive lusitropy). Dromotropy is the ability to increase the atrioventricular (AV) node’s conduction velocity.

Inodilators cause an increase in intracellular calcium as a result of phosphodiesterase III (PDIII) inhibition. Milrinone, enoximone, and amrinone are some examples. Positive inotropy is caused by increased calcium entry into the myocytes. Lusitropy is also increased by phosphodiesterase inhibitors. Increased cAMP inhibits myosin light chain kinase, resulting in reduced phosphorylation of vascular smooth muscle myosin, lowering systemic and pulmonary vascular resistance.

The mechanism of action of alpha-1 adrenoreceptor agonists is an increase in intracellular calcium caused by an increase in inositol triphosphate (IP3). IP3 is a second messenger that causes an increase in systemic vascular resistance by stimulating the influx of Ca2+ into smooth muscle cells. Reflex bradycardia can occur as a result of the subsequent increase in blood pressure. Phenylephrine and metaraminol are examples of pure alpha-1 agonists.

Levosimendin is a novel inotrope that makes myocytes more sensitive to intracellular Ca2+. It causes a positive inotropy without changing heart rate or oxygen consumption significantly.

The Na-K-ATPase membrane pump in the myocardium is inhibited by digoxin. This inhibition promotes sodium-calcium exchange, resulting in an increase in intracellular Ca2+ and increased contraction force. The parasympathetic effects of digoxin on the AV node result in bradycardia. Systemic vascular resistance will not be affected by it.

The relationship between bacterial growth and time is a tear-away exponential. The mathematical relationship between y and x in this case is:

y = ex

Where: the power is x, and the base is e.

Euler’s number (e) is a mathematical constant that is the base for all logarithms occurring naturally. Its value is 2.718.

The statement X increasing with an increase in Y is proportional to Y refers to the change in y in terms of x when considering any exponential relationship.

This is not a build-up exponential, and that is mathematically stated as y = 1-e-kt.

The negative x axis being a horizontal asymptote and the y intercept being 0, 1 are examples of tearaway exponentials , but do not describe an exponential process.

The ureter runs anterior to the vertebrae at the level of L2 to L5, and stones are usually seen at these points on x-ray.

They can also be seen at the level of the sacro-iliac joints.

Tramadol is weak agonist at the mu receptor. It inhibits the neuronal reuptake of serotonin and norepinephrine, and inhibits pain neurotransmission. It is given for moderate pain, chronic pain syndromes, and neuropathic pain.

Fluoxetine is a selective serotonin reuptake inhibitor (SSRI). It inhibits the neuronal reuptake of serotonin by inhibiting the serotonin transporter (SERT). It is the drug of choice for major depressive disorder, and is given for other psychiatric disorders such as anxiety, obsessive-compulsive, post-traumatic stress, and phobias.

When tramadol is given with SSRIs, serotonin syndrome may occur. Serotonin syndrome is characterized by fever, agitation, tremors, clonus, hyperreflexia and diaphoresis. The onset of symptoms may occur within a few hours, and the first-line treatment is sedation, paralysis, intubation and ventilation.