The EDAIC Part 1 question bank

Why: The great radicular artery (artery of Adamkiewicz) is the major blood supply to the lower two-thirds of the spinal cord and originates between T9 and T12 in approximately 75% of cases.

Why: The anterior spinal artery supplies the anterior two-thirds of the spinal cord, including the motor tracts; the posterior spinal artery supplies the dorsal sensory columns.

Why: Spinal cord perfusion pressure is defined as distal mean aortic pressure minus CSF pressure or central venous pressure, whichever is greatest.

Why: During hypoxia or hypercapnia, autoregulation of spinal cord blood flow is lost, and flow becomes linearly related to perfusion pressure.

Why: CSF pressure often increases with aortic cross-clamping; draining CSF reduces this pressure and improves spinal cord perfusion pressure, lowering ischemic risk.

Why: Peripheral nerves are usually viewed in short axis rather than long axis during ultrasound-guided regional anesthesia.

Why: The honeycomb appearance on sonogram represents the fascicles of a polyfascicular peripheral nerve viewed in short axis.

Why: In the out-of-plane technique, the needle crosses the plane of imaging and appears as an echogenic dot on the sonogram.

Why: Most studies suggest that adequate visualization and correct identification of structures is more important than the specific needle approach for outcomes after regional blocks.

Why: Textured surfaces on echogenic needles are manufactured to improve needle tip detection by generating more recordable echoes compared with smooth conventional needles.

Why: Huang et al. (2014) conducted a Cochrane systematic review comparing cardiopulmonary resuscitation plus delayed defibrillation versus immediate defibrillation for out-of-hospital cardiac arrest, examining the optimal timing of defibrillation.

Why: Salen et al. (2005) investigated whether the presence or absence of sonographically identified cardiac activity predicts resuscitation outcomes, finding it to be a useful prognostic indicator during cardiac arrest.

Why: Chan et al. (2010) demonstrated that AED use was associated with improved survival after in-hospital cardiac arrest, supporting their deployment in hospital settings.

Why: FALSE — Trap: The Cochrane review by Huang et al. found that the benefit of CPR before defibrillation depends on the time to defibrillation. It is not recommended for all patients regardless of time to rhythm analysis; the benefit is primarily seen when there is a prolonged response time.

Why: Ruygrok et al. (2009) validated three termination of resuscitation criteria for predicting good neurologic survival after out-of-hospital cardiac arrest, providing evidence-based guidance for when resuscitation efforts may be ceased.

Why: Correct sizing of oropharyngeal airways involves measuring from the corner of the mouth to the angle of the jaw or the earlobe, as described in Miller's Anesthesia.

Why: Nasopharyngeal airways are less stimulating than oropharyngeal airways; oropharyngeal airways can precipitate coughing, retching, or laryngospasm because they contact the base of the tongue and epiglottis.

Why: The nasopharyngeal airway is designed to lift the soft palate off the pharyngeal wall, thereby eliminating this mode of airway obstruction.

Why: Oropharyngeal airways can precipitate coughing, retching, or laryngospasm and are not appropriate for use in conscious patients who have not had local anaesthetic applied to the airway.

Why: Inappropriately sized oropharyngeal airways can actually worsen airway obstruction, making correct size selection critically important.

Why: Sevoflurane is typically used for inhalational induction due to its low blood-gas partition coefficient and non-irritant properties, allowing smooth induction.

Why: The single-breath technique with high-concentration sevoflurane in a prefilled reservoir bag enables rapid induction in cooperative patients.

Why: FALSE — Trap: Ether has a very high blood-gas partition coefficient (12), making inhalational induction slow and technically challenging; it is not preferred for induction.

Why: FALSE — Trap: Maintenance concentrations of isoflurane are 1%–2%, not 3%–4%, once anaesthesia has been established.

Why: Complications during inhalational induction include problems during stage 2, when pharyngeal or laryngeal stimulation may trigger laryngeal spasm.

Why: Novel oral anticoagulants including these four agents are now commonly used for thromboprophylaxis in AF.

Why: FALSE — Trap: While warfarin was the mainstay in the past, novel oral anticoagulants are now commonly utilized and have largely supplemented warfarin.

Why: The benefit of stroke prevention is counterbalanced by the risk of both intracranial and extracranial bleeding with anticoagulation.

Why: Anticoagulation must be discontinued for AF patients with active bleeding in the ICU.

Why: FALSE — Trap: The source states that aspirin alone can be considered for management based on patient preference and the clinical scenario.

Why: ICUAW includes CIP and CIM, both of which contribute to difficulty weaning from mechanical ventilation, prolonged ICU stay, and increased long-term morbidity and mortality. It is one of the most common neuromuscular complications in the ICU.

Why: FALSE — Trap: Early aggressive caloric supplementation has NOT been shown to reduce ICUAW; in fact, some evidence suggests that excessive early caloric loading may be harmful. Adequate protein delivery and early mobilization are more strongly associated with muscle preservation.

Why: The combination of neuromuscular blocking agents and corticosteroids is a well-established risk factor for critical illness myopathy, particularly the thick-filament myopathy variant. This combination should be minimized when possible.

Why: De Jonghe et al. demonstrated that respiratory weakness correlates with peripheral limb weakness and independently predicts prolonged weaning duration, highlighting the systemic nature of ICUAW.

Why: FALSE — Trap: Complete functional recovery within 3 months is NOT typical; many patients with ICUAW experience persistent functional limitations, reduced quality of life, and disability lasting months to years after ICU discharge.

Why: Clinicians should always consider the pathophysiology of pain and treat the underlying cause as possible, for example using high-dose single-fraction palliative radiation for a painful bone metastasis.

Why: FALSE — Trap: Scheduled dosing is recommended for continuous or chronic pain, based on the drug's half-life, whereas as-needed dosing is used for breakthrough pain and procedures.

Why: Studies show that opioids combined with adjuvants are more effective for neuropathic pain than opioids alone, and this approach reduces both the opioid dose and systemic side effects.

Why: The intravenous route of administration is recommended for pain crises in palliative care patients, as part of the pharmacologic principles guiding therapy.

Why: FALSE — Trap: Clinicians should screen for concerns about the use of controlled substances, including a history of addiction and fears of becoming addicted, as part of the comprehensive assessment of pain in advanced illness.

Why: The elimination half-time has limited clinical utility for predicting drug disposition of most anaesthetic agents because it does not account for intercompartmental distribution, which is a major determinant of plasma concentration changes in multicompartmental models.

Why: In a single-compartment model, elimination is the only process that can alter drug concentration, so the elimination half-time directly reflects the time for the concentration to decrease by 50%.

Why: The terminal elimination half-life (t1/2β) is determined by the volume to be cleared (distribution volume) and the efficiency of the metabolic clearance system.

Why: Context-sensitive half-time is a more clinically useful parameter than elimination half-time for lipophilic drugs because it accounts for the duration of infusion and the redistribution of drug from peripheral tissues.

Why: After stopping an infusion, the rate at which plasma concentration declines is largely governed by clearance, which is reflected in the terminal elimination half-life value.

Why: The major effect of class I agents is blockade of the fast inward sodium current responsible for the rapid upstroke and conduction of the action potential.

Why: Class IC agents have the most pronounced effect on phase 0 depolarization, causing a marked decrease and significantly slowed conduction velocity.

Why: Class IB agents shorten the action potential duration and are primarily effective in ventricular arrhythmias, not atrial arrhythmias.

Why: Class I drugs depress automaticity, with a particular effect on Purkinje fiber automaticity, in addition to their sodium channel blocking effects.

Why: There is substantial overlap in pharmacologic and electrophysiologic effects among the classes, and the linkage between observed effects and clinical antiarrhythmic effect is often tenuous.

Why: One newton is defined as the force required to accelerate a 1 kg mass at 1 m s⁻², which follows directly from Newton's second law (F = ma).

Why: Pressure is defined as force per unit area with the pascal as its SI unit; the conversion 1 kPa ≈ 7.5 mmHg is commonly used in medical practice.

Why: The SI unit of power is the watt, not the joule. The joule is the unit of energy or work; power is the rate of doing work (watts = joules/second).

Why: Weight is the force of gravitational attraction on a body and is measured in newtons, not kilograms. Mass is measured in kilograms; weight = mass × gravitational acceleration.

Why: Momentum is the product of mass and velocity, giving it the derived SI unit kg m s⁻¹. Force can also be expressed as the rate of change of momentum.

Why: Under normal resting conditions, DO₂ is approximately 1000 mL/min and VO₂ is about 250 mL/min, meaning the excess oxygen supply serves as a reserve that is not required to meet baseline metabolic demand.

Why: When DO₂ decreases, VO₂ initially remains unchanged due to increased oxygen extraction, demonstrating supply independence. VO₂ only falls when DO₂ drops below a critical threshold, at which point supply dependency occurs.

Why: The relationship CO = HR × SV is fundamental, and stroke volume is modulated by three key determinants: preload, afterload, and contractility. Alterations in any of these contribute to different types of circulatory shock.

Why: Despite the many clinical contexts in which the term shock is used, the common pathophysiological hallmark is acute circulatory failure leading to inadequate oxygen utilisation at the cellular level.

Why: While Rivers et al. (2001) demonstrated benefit of early goal-directed therapy in severe sepsis and septic shock, subsequent large trials have not consistently shown that targeting supranormal DO₂ values reduces mortality across all populations.

Why: Procedure type including head-and-neck, thoracic, upper abdominal, and aortic surgery are identified as procedure-related risk factors for pulmonary complications.

Why: Emergency procedures and long-duration procedures are both listed among the procedure-related risk factors for pulmonary complications.

Why: FALSE — Trap: Residual neuromuscular blockade IS listed as a procedure-related risk factor for postoperative pulmonary complications, alongside general anesthesia and emergency procedures.

Why: FALSE — Trap: Neurosurgical procedures ARE listed among the procedure types associated with increased pulmonary complication risk, along with head-and-neck, thoracic, upper abdominal, and aortic procedures.

Why: General anesthesia is explicitly listed as a procedure-related risk factor for postoperative pulmonary complications.

Why: The source explicitly states that popliteal blockade is the technique of choice in the presence of infection or swelling at the ankle, as it allows nerve blockade proximal to the affected area while avoiding needle passage through infected or edematous tissue. (Clinical Anesthesia p.2323)

Why: The source confirms that peripheral blockade avoids the cardiovascular and respiratory side effects, as well as urinary retention, associated with neuraxial and general anaesthesia. (Clinical Anesthesia p.2323)

Why: The source notes that additional onset time is required with bupivacaine and ropivacaine, making mepivacaine and lidocaine more appropriate in the ambulatory setting. (Clinical Anesthesia p.2323)

Why: FALSE — Trap: The source explicitly states that sural nerve block is not necessary for hallux valgus surgery. Including it as mandatory misrepresents the block requirements for forefoot procedures. (Clinical Anesthesia p.2323)

Why: FALSE — Trap: The source lists suggested needle lengths for sciatic nerve blocks as 80–150 mm depending on the approach. Recommending 25–50 mm, which is the range for interscalene blocks, could result in insufficient depth for sciatic nerve access. (Essentials of Equipment in Anaesthesia, Critical Care and Peri-operative Medicine p.224)

Why: Sevoflurane is typically used for inhalational induction in paediatric anaesthesia due to its favourable airway properties and rapid onset.

Why: The single-breath technique with a prefilled reservoir bag containing sevoflurane 8% in oxygen results in smooth induction within 20–30 seconds.

Why: FALSE — Trap: Maintenance concentrations of sevoflurane are 2%–3%, not 4%–6%. The higher range would risk excessive depth and delayed recovery.

Why: Upper airway obstruction, including epiglottitis, is a recognised indication for inhalational induction to preserve spontaneous ventilation.

Why: FALSE — Trap: The single-breath technique uses sevoflurane 8% in oxygen or nitrous oxide 50% in oxygen as alternative carrier gases, but nitrous oxide 50% is not the initial mixture before sevoflurane—it is an alternative to oxygen alone.

Why: Power is the probability of detecting a true effect of a given size and is mathematically defined as 1 − β, where β is the type II error rate (the probability of failing to reject a false null hypothesis). Adequate power (typically 80% or 90%) is essential in trial design.

Why: Increasing the sample size increases statistical power and decreases the probability of a type II (false-negative) error; the statement reverses this relationship and is false.

Why: An underpowered trial has a high type II error rate, meaning it is likely to miss a real treatment effect. This can lead to the erroneous conclusion that an effective intervention has no benefit, potentially depriving patients of useful therapies.

Why: Performing multiple subgroup analyses inflates the overall type I error rate, so an apparently significant result can arise by chance even when no true effect exists in any subgroup.

Why: The NNT is a measure of clinical effect size (the number of patients who need to be treated to prevent one additional adverse outcome), not a measure of statistical power. Sample size calculations depend on the expected effect size, the chosen alpha level, the desired power, and the variability of the outcome measure.