Basic Sciences Flashcards

According to the Stewart physicochemical model of acid-base balance, which of the following is correctly classified as a DEPENDENT variable — one that cannot be independently altered by physiological mechanisms?

Answer: Bicarbonate concentration [HCO₃⁻]

In Stewart's model, only three variables independently determine [H⁺]: the Strong Ion Difference (SID), total weak acid concentration (Atot), and PCO₂. Bicarbonate is a DEPENDENT variable — it is mathematically derived from these three independent variables and cannot be altered in isolation. This fundamentally differs from the traditional Henderson-Hasselbalch approach, which treats HCO₃⁻ as an independent buffer. Clinically, this means a rising bicarbonate in metabolic alkalosis is a consequence of a rising SID (e.g., chloride depletion), not the cause of alkalosis.

During one-lung ventilation for a right upper lobectomy, the non-ventilated lung receives continued perfusion, creating an obligate shunt. Which anesthetic technique BEST preserves hypoxic pulmonary vasoconstriction (HPV) in the non-ventilated lung, minimizing this shunt fraction?

Answer: Total intravenous anesthesia (TIVA) with propofol and remifentanil

All volatile halogenated agents (sevoflurane, desflurane, isoflurane) dose-dependently inhibit HPV by directly relaxing pulmonary vascular smooth muscle, increasing shunt fraction and worsening hypoxemia during one-lung ventilation. Intravenous agents — particularly propofol — do not inhibit HPV and may even preserve or modestly augment it. Remifentanil likewise has no effect on HPV. TIVA with propofol and remifentanil is therefore the technique that best preserves this critical compensatory vasoconstriction. Ketamine causes systemic sympathomimetic effects but does not reliably preserve HPV over volatile agents.

The Tec 6 vaporizer heats desflurane to 39°C and delivers it at a fixed internal pressure of approximately 1.5 atm, unlike all other modern volatile agents that use variable bypass vaporizers. What is the PRIMARY physical reason this specialized design is necessary for desflurane?

Answer: Desflurane's boiling point (~22.8°C) and very high saturated vapour pressure (~669 mmHg at 20°C) make output from a standard vaporizer dangerously unpredictable near room temperature

Desflurane has a boiling point of approximately 22.8°C — dangerously close to ambient theatre temperature. Its saturated vapour pressure (~669 mmHg at 20°C) means that minor temperature increases could cause it to boil within a standard vaporizer, producing unpredictably high and potentially lethal concentrations. The Tec 6 resolves this by heating desflurane to 39°C (fully vaporized into a gas reservoir) and metering precise volumes into the fresh gas flow at a fixed pressure. Importantly, desflurane actually has the LOWEST oil:gas partition coefficient (0.45) of modern agents — accounting for its fastest offset, not a high one. Compound A production is a concern for sevoflurane with low-flow soda lime, not desflurane.

After a 6-hour continuous infusion of equi-analgesic doses of fentanyl and remifentanil are simultaneously discontinued, which of the following MOST accurately predicts the subsequent pharmacokinetic behaviour?

Answer: Fentanyl's 50% decrement time will be markedly prolonged (>200 minutes), whereas remifentanil's will remain approximately 3–4 minutes regardless of infusion duration

Context-sensitive half-time (CSHT) is the time for a 50% plasma concentration decrease after ceasing an infusion of a given duration. After a 6-hour fentanyl infusion, CSHT exceeds 200 minutes because fentanyl is highly lipophilic and accumulates in deep peripheral compartments (muscle, fat); redistribution back into plasma sustains high concentrations long after stopping. Remifentanil is fundamentally different: it is hydrolysed by ubiquitous nonspecific plasma and tissue esterases, not hepatic CYP enzymes. It does not accumulate in peripheral compartments and its CSHT remains ~3–4 minutes whether infused for 1 hour or 12 hours — making it uniquely titratable for procedures of any duration.

Sugammadex reverses rocuronium-induced neuromuscular blockade through which primary mechanism, and which unique pharmacological consequence does this confer over neostigmine?

Answer: Encapsulation of rocuronium within a toroidal lipophilic cavity, creating a plasma sink that draws rocuronium away from the NMJ — allowing reversal even of deep block (PTC 1–2)

Sugammadex is a modified γ-cyclodextrin whose toroidal (donut-shaped) structure forms a tight 1:1 inclusion complex with rocuronium (and vecuronium) via hydrophobic interactions within its lipophilic core. By encapsulating free plasma rocuronium, it creates a steep concentration gradient that drives rocuronium off nicotinic receptors at the neuromuscular junction into the plasma, where it remains irreversibly bound. The complex is then renally excreted. Crucially, sugammadex does NOT interact with the NMJ itself — it acts purely in the plasma and interstitial space. This mechanism is effective at any depth of block including profound (PTC 0–2), unlike neostigmine which requires at least 2 visible twitches (TOF ≥ 2) and carries a ceiling effect due to anticholinesterase saturation.

A 58-year-old patient with longstanding poorly controlled hypertension (habitual MAP ~125 mmHg) undergoes elective surgery under general anaesthesia. Their MAP falls to 72 mmHg intraoperatively. Regarding cerebral blood flow (CBF), which statement is MOST accurate?

Answer: The cerebral autoregulatory curve is shifted rightward in chronic hypertension; a MAP of 72 mmHg may fall below this patient's lower autoregulatory limit, risking cerebral hypoperfusion

In normotensive individuals, cerebral autoregulation maintains constant CBF across a MAP range of approximately 50–150 mmHg. Chronic hypertension causes structural remodelling of cerebral resistance arterioles (medial hypertrophy, reduced luminal compliance), shifting the entire autoregulatory curve to the right. The lower autoregulatory limit in a chronically hypertensive patient may be approximately 70–80 mmHg rather than 50 mmHg. Consequently, a MAP of 72 mmHg that would be entirely safe for a normotensive patient may place this patient below their individual lower limit, causing pressure-passive CBF reduction and cerebral ischaemia. Autoregulation is not abolished — it is shifted. CO₂ reactivity remains intact throughout this range.