1. Cardiopulmonary Efficiency Test (Harvard Step Test)

• Q: Why 3 pulse readings in recovery, not one? A: To track the trend of recovery - more reliable than a single count.
• Q: Why does HR rise during exercise? A: Increased sympathetic drive + venous return to meet O2 demand.
• Q: What does a fast recovery indicate? A: Good cardiovascular fitness/efficiency.
• Q: Other cardiopulmonary efficiency tests? A: Master's 2-step test, treadmill (Bruce protocol), Astrand-Rhyming test, 12-min walk test.
• Q: Effect of training on PEI? A: Higher PEI - lower resting/exercise HR, faster recovery.
• Q: What is cardiac reserve? A: Heart's capacity to raise output above resting level under stress.

2. Cardiovascular Autonomic Function Tests

• Q: Aim? A: Test integrity of sympathetic/parasympathetic control of CVS reflexes (used to screen diabetic autonomic neuropathy).
• Q: Valsalva ratio - normal value? A: Longest R-R after strain / shortest R-R during strain; normal >1.21.
• Q: Which tests assess parasympathetic function? A: E:I ratio, 30:15 ratio, early Valsalva phase.
• Q: Which assess sympathetic function? A: BP response to standing, sustained handgrip BP rise.
• Q: Postural hypotension defined as? A: Fall in systolic BP >20 mmHg (or diastolic >10 mmHg) on standing.
• Q: Why does HR rise then fall on standing (30:15)? A: Initial vagal withdrawal/sympathetic reflex (tachycardia), then baroreceptor-mediated vagal rebound (~30th beat).
• Q: Valsalva phase 4 mechanism? A: BP overshoot with reflex bradycardia after release of strain (baroreceptor mediated).

3. Spirometry

• Q: Which volume can't be measured by simple spirometer? A: Residual volume (needs He dilution/N2 washout/body plethysmography) - so FRC & TLC also can't be measured directly.
• Q: Factors affecting VC? A: Age, sex, height, posture, body build, pregnancy, lung/chest wall disease.
• Q: VC vs FVC? A: VC = slow maximal expiration; FVC = forced/rapid version, may be slightly lower in obstructive disease.
• Q: Clinical use? A: Differentiate obstructive vs restrictive disease, monitor treatment, pre-op assessment.
• Q: Minute ventilation? A: TV × respiratory rate (~6-8 L/min at rest).
• Q: Anatomical dead space? A: ~150 mL - conducting airway air not taking part in gas exchange.

4. PEFR (Peak Expiratory Flow Rate)

• Q: Procedure? A: Max inspiration to TLC, tight lip seal, blast out as hard/fast as possible; best of 3 attempts taken.
• Q: Effort dependent or independent? A: Effort dependent.
• Q: Clinical use? A: Monitor asthma control/severity, bronchodilator response, diurnal variation.
• Q: Significant diurnal variation? A: >20% difference between morning and evening readings = poor asthma control.
• Q: PEFR in obstructive disease? A: Reduced (asthma, COPD).

5. FEV1

• Q: FEV1/FVC in obstructive disease (asthma/COPD)? A: Reduced (<70%) - FEV1 falls more than FVC.
• Q: FEV1/FVC in restrictive disease (fibrosis)? A: Normal or increased - both fall proportionately.
• Q: Bronchodilator reversibility criterion? A: >12% AND 200 mL rise in FEV1 post-bronchodilator = significant reversibility (suggests asthma).
• Q: FEV1 vs PEFR? A: FEV1 needs spirometer, reflects overall airway function over 1 sec; PEFR is instantaneous, more effort/large-airway dependent, simple meter.
• Q: Clinical significance? A: Grades severity of obstructive disease, monitors COPD/asthma, used in pre-op pulmonary risk assessment.
• Q: FEF 25-75%? A: Flow between 25-75% of FVC - reflects small airway function.

6. Stethography

• Q: What does the stethogram show? A: Rate, rhythm and depth of respiration.
• Q: Effect of breath holding on subsequent breathing? A: Hyperpnea - due to rising CO2 (main stimulus) and falling O2 acting on chemoreceptors.
• Q: Effect of hyperventilation? A: Transient apnea/reduced drive due to CO2 washout (hypocapnia) reducing chemoreceptor drive.
• Q: Normal breath-holding time? A: ~40-60 sec; prolonged after hyperventilation/O2, shortened after exercise.
• Q: Strongest respiratory stimulus? A: PaCO2 (central chemoreceptors); O2 and pH act mainly via peripheral chemoreceptors.
• Q: Hering-Breuer reflex? A: Lung stretch receptors inhibit further inspiration, preventing overdistension.
• Q: Effect of exercise? A: Increased rate and depth from CO2 production, proprioceptive and cortical inputs.
• Q: Effect of swallowing? A: Deglutition apnea - transient reflex pause to prevent aspiration.

7. Ergography

• Q: What is muscle fatigue? A: Progressive fall in force/work output with sustained repetitive activity.
• Q: Sites of fatigue? A: Central (CNS) and peripheral (NMJ, muscle metabolic - lactic acid, ATP/PCr depletion, Ca2+ handling changes).
• Q: What does the ergogram show? A: Progressively decreasing amplitude of successive contractions - fatigue curve.
• Q: Effect of occluding blood supply? A: Fatigue occurs faster (ischemia, metabolite accumulation).
• Q: Effect of rest? A: Recovery of work capacity via metabolite clearance and energy store restoration.
• Q: Fatigue index? A: Ratio comparing initial vs final work output - measures rate of decline.
• Q: Pathological fatigue example? A: Myasthenia gravis, myopathies (differs from normal physiological fatigue).

8. Perimetry

• Q: What is the blind spot? A: Corresponds to optic disc (no photoreceptors); ~15° temporal to fixation, size ~5-7°.
• Q: Why is nasal field smaller than temporal? A: Blocked by the nose.
• Q: Bitemporal hemianopia cause? A: Optic chiasma lesion (e.g., pituitary tumor) damaging crossing nasal fibers.
• Q: Homonymous hemianopia cause? A: Post-chiasmal lesion (optic tract/radiation/visual cortex).
• Q: What is a scotoma? A: Area of depressed/absent vision surrounded by relatively normal field.
• Q: Clinical use of perimetry? A: Early detection of glaucoma (peripheral field loss), localizing neurological visual pathway lesions.
• Q: Why is central vision sharper? A: Higher cone density and greater cortical representation at the fovea/macula.

9. Colour Vision

• Q: Theory of colour vision? A: Young-Helmholtz trichromatic theory (3 cone types - red/green/blue) + Hering's opponent-colour theory.
• Q: Most common colour blindness? A: Red-green (protan/deutan defects).
• Q: Inheritance? A: X-linked recessive - ~8% males, ~0.5% females affected.
• Q: Protanopia vs deuteranopia vs tritanopia? A: Absence of red cones / absence of green cones / absence of blue cones (tritanopia rare, autosomal).
• Q: Is it curable? A: No - congenital red-green colour blindness has no cure; special lenses/apps can help differentiate.
• Q: Occupational importance? A: Required screening for pilots, drivers, defense/railway jobs (traffic signal recognition).