A patient breathing in decompressed chamber where the barometric pressure 275mm斑27000 altitudes, 1/3 The oxygen saturation atmospheric). will be? 20 40 60 80 260 100
At a barometric pressure of 275 mmHg, the PO₂ of inspired air = 275 × 0.21 = ~57.75 mmHg. After subtracting water vapor pressure (~47 mmHg), the alveolar PO₂ is very low (~10-15 mmHg), giving an oxygen saturation of roughly 40%.
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The answer is 40%.
Here is the full step-by-step working:
Working Through the Problem
Given:
- Barometric pressure = 275 mmHg (approximately 27,000 ft altitude)
- Breathing atmospheric air (FiO₂ = 21%)
Step 1 - Calculate inspired PO₂ (PiO₂)
Using Dalton's Law:
PiO₂ = Barometric pressure × FiO₂ PiO₂ = 275 × 0.21 = 57.75 mmHg
Step 2 - Calculate alveolar PO₂ (PAO₂)
Using the alveolar gas equation (simplified):
PAO₂ = PiO₂ - Water vapor pressure - PACO₂/RQ
At altitude:
- Water vapor pressure = 47 mmHg (constant)
- Remaining pressure after water vapor = 275 - 47 = 228 mmHg
- Of this, ~21% is O₂ = 228 × 0.21 ≈ 47.9 mmHg
- After CO₂ correction (roughly 20-25 mmHg at altitude), PAO₂ ≈ ~20-25 mmHg
Step 3 - Determine O₂ saturation from PAO₂
Using the oxyhemoglobin dissociation curve:
- A PAO₂ of ~20-25 mmHg sits on the very steep part of the dissociation curve
- At PaO₂ ~27 mmHg = 50% saturation (P50)
- At PaO₂ ~20-23 mmHg = approximately 40% saturation
Textbook Confirmation (Rosen's Emergency Medicine, Table E13.2)
| Altitude (ft) | Barometric Pressure (mmHg) | O₂ Saturation (%) |
|---|---|---|
| 20,000 | 349 | ~70% |
| 25,000 | ~282 | ~56% |
| 27,000 | ~275 | ~40% |
| 30,000 | 226 | ~24% |
At ~27,000 ft with barometric pressure of 275 mmHg, the oxygen saturation falls to approximately 40%.
Answer: 40% ✓
The key concept: as barometric pressure falls, PO₂ falls proportionally (Dalton's Law). At 275 mmHg, the inspired PO₂ is only ~58 mmHg, alveolar PO₂ drops to ~20-25 mmHg, and at that point on the oxyhemoglobin dissociation curve, saturation is approximately 40% - (Guyton & Hall Medical Physiology, Table 44.1; Rosen's Emergency Medicine, Table E13.2).
Lactogenesis is by ? A-Oxytocin and prolactin B-oxytocin prolactin and cortisol
Lactogenesis requires prolactin as the primary driver, but cortisol (and other glucocorticoids) are also essential co-factors for milk synthesis, while oxytocin drives milk ejection (let-down), not milk production. So the answer leans toward B, but the framing needs careful examination.
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Answer: B - Oxytocin, Prolactin, and Cortisol
The textbooks confirm this clearly. Here is the breakdown:
Hormones of Lactogenesis
| Hormone | Role |
|---|---|
| Prolactin | Primary driver - stimulates milk synthesis in alveolar cells |
| Cortisol (corticoids) | Essential co-factor for milk synthesis alongside prolactin |
| Insulin | Also required for milk synthesis |
| Oxytocin | Milk ejection (let-down reflex) - contracts myoepithelial cells |
Key Textbook Quotes
"In addition to prolactin, insulin and corticoids are essential to milk synthesis."
- Creasy & Resnik's Maternal-Fetal Medicine
"Breast development and function are initiated by a variety of hormonal stimuli, including estrogen, progesterone, prolactin, oxytocin, thyroid hormone, cortisol, and growth hormone."
- Schwartz's Principles of Surgery
"Prolactin is the primary hormonal stimulus for lactogenesis in late pregnancy and the postpartum period."
- Schwartz's Principles of Surgery
Why NOT option A alone?
Oxytocin alone with prolactin is incomplete - cortisol/corticoids are essential for actual milk synthesis. Option A misses the permissive role of cortisol.
Important distinction:
- Lactogenesis (milk production/synthesis) = Prolactin + Cortisol (+ insulin)
- Milk ejection/let-down = Oxytocin
So while oxytocin is involved in the overall lactation process, the answer B is more complete and correct because cortisol is an essential co-factor for lactogenesis itself.
Answer: B
Main determinant of CO is ? HR SV Venous pressure Venous return
Cardiac output (CO) = HR × SV. Both are determinants, but the main/primary determinant is Venous Return, because the heart can only pump what it receives (Frank-Starling law). Venous return sets the upper limit of CO.
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Answer: Venous Return
This is a conceptually important question that tests understanding of the Frank-Starling mechanism.
Why Venous Return is the MAIN determinant:
The fundamental equation is:
CO = HR × SV
Both HR and SV are factors in the equation, but neither is the primary controller in the physiological sense. The main determinant is venous return because:
- The heart can only pump what it receives - the Frank-Starling law ensures that CO always equals venous return in steady state
- As venous return increases → end-diastolic volume (EDV) increases → fiber length increases → stroke volume increases → CO increases
- Conversely, when venous return falls (e.g., hemorrhage/hypovolemic shock), CO falls proportionally
"Stroke volume and cardiac output correlate directly with end-diastolic volume, which correlates with venous return. The Frank-Starling relationship governs normal ventricular function and ensures that the volume the heart ejects in systole equals the volume it receives in venous return. In the steady state, cardiac output equals venous return."
- Costanzo Physiology, 7th Edition
Understanding the other options:
| Option | Relationship to CO | Why not the "main" determinant |
|---|---|---|
| HR | CO = HR × SV; HR is a factor | Changes in HR can be compensated by changes in SV |
| SV | CO = HR × SV; SV is a factor | SV itself is determined by venous return (preload) |
| Venous pressure | Related but indirect | Venous return depends on pressure gradient, not pressure alone |
| Venous return ✓ | Direct controller via Frank-Starling | Sets the EDV, which drives SV and thus CO |
The key physiological concept:
The cardiac function curve and vascular function curve intersect at the steady-state operating point where CO = Venous Return. Any change in venous return shifts this equilibrium and is the primary driver of CO changes.
Answer: Venous Return ✓
(Costanzo Physiology, 7th Ed.; Robbins Pathologic Basis of Disease)
In AV nodal delay PR interval should increase or PR segment?
In AV nodal delay, the PR interval increases. The PR segment reflects conduction after the AV node (His-Purkinje), while the PR interval (from start of P wave to start of QRS) encompasses the entire AV nodal conduction time.
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Answer: PR Interval increases in AV nodal delay
This is a key ECG concept. Here is the precise anatomical breakdown:
PR Interval vs PR Segment - What they represent:
ECG: |--P wave--|----PR segment----|--QRS--|
|<---------PR interval-------->|
| ECG Component | What it represents | Electrical event |
|---|---|---|
| P wave | Atrial depolarization | SA node → atrial muscle |
| PR segment | Isoelectric line after P wave | His-Purkinje conduction (infranodal) |
| PR interval | P wave START → QRS START | AV nodal delay + His-Purkinje |
Key distinction:
- PR interval = Atrial-His (A-H) interval + His-Ventricular (H-V) interval
- A-H interval = intra-atrial conduction + AV node delay (up to 140 ms)
- H-V interval = His bundle → bundle branches → Purkinje (40-60 ms) → represented by the PR segment
"The SA-His interval corresponds to intra-atrial conduction and delay in the atrioventricular node. A small portion of the isoelectric segment of the PR interval (i.e., the PR segment) represents infranodal conduction through the His-Purkinje system."
- Goldman-Cecil Medicine
Therefore:
- AV nodal delay prolongs the A-H interval
- This lengthens the PR interval (normal: 120-200 ms)
- The PR segment is NOT affected by AV nodal delay - it reflects His-Purkinje (infranodal) conduction
Clinical correlate:
| Condition | ECG finding |
|---|---|
| AV nodal delay (1st degree AV block) | PR interval > 200 ms |
| His-Purkinje delay | PR segment prolonged (rare, bundle branch disease) |
| Vagal stimulation | PR interval increases (slows AV node) |
Answer: PR Interval increases in AV nodal delay ✓
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