BIOL220 - Spring2026 Exam Practice 1

What is the definition of flux in physiology?

Flux is the rate at which substances move from one place to another. It depends on two factors: driving force and conductance (or resistance). The equations are: flux = driving force × conductance, or flux = driving force / resistance.

What is bulk flow? Give an example in the respiratory system.

Bulk flow is the mass movement of molecules from an area of high total pressure to low total pressure. It is fast over big distances but non‑selective. Example: Air moving through the airways (trachea, bronchi) during ventilation – this is bulk flow.

What is the driving force for bulk flow?

The driving force for bulk flow is a difference in total pressure (a pressure gradient). For example, when the diaphragm contracts, thoracic volume increases, intra‑alveolar pressure drops below atmospheric pressure, and air moves down the total pressure gradient.

What factors create resistance to bulk flow in tubes (e.g., airways or blood vessels)?

Resistance to bulk flow depends on:

• Tube radius (to the 4th power! – small changes in radius have huge effects)
• Tube length (longer tubes = more resistance)
• Viscosity of the fluid (thicker fluid = more resistance)

What is molecular diffusion? Give an example in the respiratory system.

Molecular diffusion is the net movement of individual molecules from an area of high partial pressure (or high concentration) to low partial pressure. It is slow over big distances but selective. Example: O₂ moving from the alveoli across the alveolar‑capillary membrane into the blood.

What is the driving force for molecular diffusion of a gas like O₂?

The driving force for molecular diffusion of a gas is the difference in partial pressure (pO₂) across the membrane (the partial pressure gradient). For ions, the driving force is the electrochemical gradient (combination of concentration difference and charge difference).

What factors create resistance to molecular diffusion across a membrane?

Resistance to molecular diffusion depends on:

• Distance (thicker membrane or longer path = more resistance)
• Membrane permeability (how easily the substance crosses)
• Number of open membrane channels (more open channels = less resistance)

Why are capillaries critically important for O₂ diffusion into and out of the bloodstream?

Capillaries have extremely thin walls (only one cell layer thick), which minimizes the diffusion distance for O₂ and CO₂. This reduces resistance to molecular diffusion, allowing rapid gas exchange between blood and tissues or between alveoli and blood.

What is mass balance? How does it apply to alveolar pO₂?

Mass balance means the amount of a substance in a compartment changes based on influx (rate in) and outflux (rate out). For alveolar pO₂:

• Rate in = minute ventilation (bringing fresh O₂ into alveoli)
• Rate out = diffusion of O₂ from alveoli into the blood
  If rate in > rate out, alveolar pO₂ increases. If rate out > rate in, alveolar pO₂ decreases.

State Le Chatelier’s Principle. Give an example involving O₂ and hemoglobin.

Le Chatelier’s Principle says that a reversible reaction at equilibrium will shift to counteract any change. Example: O₂ + Hb ⇌ Hb(O₂)₄. If you increase O₂ concentration (add O₂), the reaction shifts right, loading more O₂ onto hemoglobin. If you decrease O₂ (remove O₂), the reaction shifts left, unloading O₂.

Write the reversible reaction for CO₂ in the body. Why is it important?

CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻ (bicarbonate). This reaction allows CO₂ to be transported in the blood as bicarbonate (HCO₃⁻). It is sped up by the enzyme carbonic anhydrase in red blood cells. The reaction also affects blood pH because H⁺ increases acidity.

Describe the chain of cause and effect for inhalation (breathing in) in mammals.

1. Diaphragm contracts (flattens) and external intercostal muscles contract (lift rib cage).
2. Thoracic cavity volume increases.
3. Intra‑alveolar pressure decreases (becomes more negative, below atmospheric pressure).
4. Air flows down the pressure gradient (bulk flow) into the lungs.

What is the difference between tidal volume, respiratory rate, and minute ventilation?

• Tidal volume (VT) = volume of air inhaled or exhaled in one breath (L/breath).
• Respiratory rate (RR) = number of breaths per minute (breaths/min).
• Minute ventilation (V̇E) = total air moved in/out of lungs per minute = VT × RR (L/min).

A child has tidal volume 0.25 L/breath and respiratory rate 20 breaths/min during quiet breathing. What is their minute ventilation? If they breathe hard at 1.0 L/breath and 40 breaths/min, what is their new minute ventilation?

Quiet breathing: 0.25 L/breath × 20 breaths/min = 5 L/min.
Hard breathing: 1.0 L/breath × 40 breaths/min = 40 L/min.
Minute ventilation increases 8‑fold.

What is the relationship between minute ventilation and alveolar pO₂?

Increasing minute ventilation (by breathing deeper or faster) generally increases alveolar pO₂ because you are bringing more fresh, O₂‑rich air into the alveoli. However, if the person already has fully saturated hemoglobin, the benefit may be minimal.

What is the normal total air pressure at sea level, and what is the approximate pO₂ of atmospheric air?

Total air pressure at sea level is ~760 mmHg (or 1 atmosphere). Air is ~20% O₂, so atmospheric pO₂ = 760 mmHg × 0.20 = ~152 mmHg (often rounded to 160 mmHg for simplicity).

Why is alveolar pO₂ (≈100 mmHg) lower than atmospheric pO₂ (≈160 mmHg)?

Alveolar pO₂ is lower because:

1. Inhaled air mixes with residual air in the lungs that already has lower O₂ and higher CO₂.
2. Inhaled air is humidified by water vapor, which dilutes the O₂ partial pressure.

What is the normal pO₂ of deoxygenated blood returning to the lungs (venous blood)?

~40 mmHg. This low pO₂ creates a steep partial pressure gradient with alveolar pO₂ (~100 mmHg), driving O₂ diffusion into the blood.

What is the shape of the oxygen‑hemoglobin dissociation curve, and why is that shape important?

The curve is sigmoidal (S‑shaped) because hemoglobin binds O₂ cooperatively – after one O₂ binds, the next binds more easily. The flat top (high pO₂) means that even if alveolar pO₂ drops from 100 to 80 mmHg, hemoglobin remains nearly saturated. The steep middle (around 40 mmHg) means that small drops in pO₂ at the tissues cause large O₂ unloading.

At sea level, alveolar pO₂ is ~100 mmHg. What is the approximate hemoglobin saturation at that pO₂? At 80 mmHg? At 40 mmHg?

• At 100 mmHg: ~98‑99% saturation (nearly full).
• At 80 mmHg: ~95% saturation (still very high).
• At 40 mmHg: ~75% saturation (steep part of curve – lots of O₂ unloaded).

Why does traveling from Seattle (0 ft) to Calgary (3000 ft) not cause altitude problems in healthy adults?

At 3000 ft, total air pressure is about 80% of sea level (~608 mmHg), so alveolar pO₂ drops to ~80 mmHg. But from the O₂‑Hb dissociation curve, hemoglobin is still nearly saturated (~95%) at 80 mmHg. The body still carries almost a full load of O₂.

If total air pressure at sea level is 760 mmHg, what is the total air pressure in Calgary at 3000 ft elevation? Use the relative air pressure graph (80% of sea level).

760 mmHg × 0.80 = ~608 mmHg. (You could also write as 760 mmHg × 0.8, or eyeball 0.82‑0.85 for partial credit.)

A scuba diver at 100 ft depth experiences 4 atm of pressure. If their tank contains 10% O₂ (instead of 20%), what is the pO₂ of the breathing gas at that depth? Will they suffer from lack of oxygen?

pO₂ = 4 atm × 0.10 = 0.4 atm. At sea level, air pO₂ is 0.2 atm. So 0.4 atm is double the normal pO₂. They will NOT suffer from lack of oxygen – in fact, they have more than enough.

What is oxygen toxicity, and how does it relate to scuba diving?

Oxygen toxicity occurs when breathing too high a pO₂ (usually >1.6 atm), causing lung damage, seizures, and other problems. Deep scuba divers must use low‑O₂ gas mixtures (e.g., 6% O₂ at 365 ft) to keep pO₂ safe. Breathing normal air (20% O₂) at great depth would produce lethal pO₂.

In the 1992 athlete study, which breathing gas created greater driving force for O₂ into the blood: air or pure O₂?

Pure O₂. Breathing pure O₂ greatly increases alveolar pO₂ (to ~760 mmHg at sea level), which increases the partial pressure gradient between alveoli and blood. That is the driving force for diffusion.

In the 1992 athlete study, which breathing gas created greater resistance to O₂ entering the bloodstream: air, pure O₂, or equal?

Equal. Resistance to O₂ diffusion depends on the distance the O₂ must travel (thickness of alveolar‑capillary membrane) and membrane permeability. The gas being breathed does not change the resistance.

What were the results of the 1992 athlete study (exercise at sea level breathing air vs. pure O₂)?

There was no measurable difference in the rate of O₂ flux into the bloodstream between breathing air and breathing pure O₂. The graph showed essentially identical O₂ uptake.

Explain why breathing pure O₂ during exercise at sea level does not increase O₂ flux into the blood.

When breathing air, alveolar pO₂ is ~100 mmHg, and hemoglobin is already nearly saturated (~98‑99%) with O₂. The vast majority of O₂ in blood is bound to hemoglobin, not dissolved in plasma. Even with pure O₂, hemoglobin cannot carry more – it's already full. The tiny additional dissolved O₂ is negligible.

What is the only way to meaningfully increase O₂ delivery to tissues in a healthy person at sea level?

Increase cardiac output (heart rate × stroke volume) to move more blood (and thus more O₂‑loaded hemoglobin) to tissues per minute. Increasing alveolar pO₂ does not help because hemoglobin is already saturated.

Suppose a magician snaps their fingers and turns all O₂ in your lungs into N₂ (total pressure unchanged). You inhale, snap, wait 30 seconds, then exhale. Will the pO₂ of your exhalation be zero? Why or why not?

No. The pO₂ in the alveoli becomes zero, but the blood returning to the lungs still has a pO₂ of ~40 mmHg. This creates a driving force for O₂ to diffuse from the blood back into the alveoli. Over 30 seconds, O₂ will flux into the lung, raising exhaled pO₂ above zero.

At high body temperature (fever), the O₂‑Hb dissociation curve shifts down‑right (lower saturation at any given pO₂). Is it worthwhile for someone with a fever to breathe high‑pO₂ oxygen from a tank?

No, not worthwhile. At fever, hemoglobin is slightly less saturated at the lungs (e.g., 90‑95% instead of 99%), but it unloads O₂ more easily at the tissues (because the curve is also lower at 40 mmHg). The net O₂ delivered to tissues is about the same or even higher without supplemental O₂.

Which of the following patients would substantially benefit from breathing high‑pO₂ oxygen? (Check all that apply)

• someone with thickened alveoli walls
• someone with few red blood cells (anemia)
• someone breathing too quickly (hyperventilation)
• someone who just ran fast and used lots of O₂

Thickened alveoli walls (increased diffusion resistance – higher driving force helps). Possibly anemia (debated; some credit). Not hyperventilation (they already have high alveolar pO₂). Not post‑exercise (hemoglobin already saturated).

Why does breathing high‑pO₂ oxygen help someone with thickened alveoli walls?

Thickened walls increase resistance to diffusion (Fick's Law: rate ∝ 1/thickness). To maintain adequate O₂ flux, you can increase the driving force (partial pressure gradient) by breathing high‑pO₂ O₂. This compensates for the higher resistance.

Why does breathing high‑pO₂ oxygen NOT substantially help someone who just ran fast and used lots of O₂?

During exercise, the problem is not lack of alveolar pO₂ – it's that the body is already extracting almost all O₂ from hemoglobin. Hemoglobin is fully saturated at the lungs. Increasing alveolar pO₂ only increases the tiny amount of O₂ dissolved in plasma, which is negligible compared to what hemoglobin carries.

A classmate says: "Plaques in arteries are bad because they increase the distance O₂ must diffuse from the bloodstream to the working tissue, increasing resistance to O₂ flux." Correct their error.

The error: O₂ does not diffuse directly from arteries to working tissue. Arteries have thick walls that resist diffusion. Instead, O₂ is delivered by bulk flow of blood. Plaques reduce the radius of the artery, which increases resistance to bulk flow (radius⁴ effect), decreasing blood flow and O₂ delivery. Also, plaques can break off and block vessels entirely (stroke).

What is the key difference between bulk flow and molecular diffusion in terms of speed and selectivity?

Bulk flow is fast over long distances but non‑selective (everything moves together). Molecular diffusion is slow over long distances but selective (only specific molecules move down their partial pressure/concentration gradient).

Why are gills and alveoli structured with huge surface area and very thin walls?

To maximize molecular diffusion of O₂ and CO₂. Large surface area increases flux (directly proportional), and thin walls decrease diffusion distance (decreasing resistance, increasing flux). This follows Fick's Law: flux ∝ (area × ΔP) / thickness.

What is Fick's Law of Diffusion for a gas across a membrane?

Rate of diffusion = (Surface area × Partial pressure gradient) / Membrane thickness. Or: rate ∝ (A × ΔP) / T.

When anchovies are born, they have no functional gills or blood flow. Are they more vulnerable to low O₂ at 1 week old or 3 weeks old? Explain.

3 weeks old (just before gills develop). At 1 week, the fish is tiny – all cells are close to the surface, so molecular diffusion alone can supply O₂. At 3 weeks, the fish is larger, so inner cells are far from the water – diffusion distance is too large, but bulk flow (gills + blood) hasn't started yet. They are most vulnerable when large but still relying on diffusion.

What is the driving force for molecular diffusion of O₂ into the blood of adult anchovies (or any fish with gills)?

The difference in pO₂ between the water passing over the gills and the pO₂ of the blood in the gill capillaries. Higher pO₂ in water drives O₂ into the blood.

Are capillaries important for CO₂ flux from working tissue into the bloodstream? Why?

Yes. Capillaries are thin‑walled vessels that run very close to working tissue, minimizing the diffusion distance for CO₂. Short distance = low resistance = high flux.

As CO₂ enters the blood from working tissue, what happens to the concentration of H⁺ in the blood? Explain using Le Chatelier's principle.

H⁺ concentration increases (blood becomes more acidic). The reaction is CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻. Adding CO₂ shifts the equilibrium to the right, producing more H⁺ and HCO₃⁻.

Which of the following require membrane transport proteins to cross cell membranes: H⁺, HCO₃⁻, both, or neither?

Both H⁺ and HCO₃⁻ are charged molecules. Phospholipid bilayers strongly resist the flux of charged molecules (ions). They require channels or carriers to cross.

Suppose a person's heart stops (no blood circulation), but they can still breathe. What happens to the pO₂ in the lung alveoli? Explain using mass balance.

Alveolar pO₂ increases. Reason:

• Rate in (minute ventilation) does not change – they are still breathing.
• Rate out (O₂ diffusing into blood) decreases because blood in lung capillaries quickly becomes saturated with O₂ and stops taking up more (no fresh deoxygenated blood is arriving).
• With rate in unchanged and rate out decreased, alveolar pO₂ rises.

Same scenario (heart stops, breathing continues). What happens to the pO₂ in the capillaries near working tissue?

pO₂ decreases. No blood flow means no O₂ is delivered to the tissues, and existing O₂ is used up.

Describe the cause‑and‑effect chain for buccal pumping in nurse sharks (as if water behaved like a gas).

1. Shark fills mouth with water.
2. Shark closes mouth and squeezes cheeks (muscles contract).
3. Volume of mouth cavity decreases.
4. Pressure in mouth cavity increases.
5. Pressure in mouth becomes higher than pressure outside gill slits.
6. This pressure difference drives bulk flow of water from mouth over the gills.

Why do nurse sharks (and many fish) need to ensure water flows over their gills?

As O₂ diffuses from water into the gill blood, the water becomes O₂‑depleted (and CO₂‑loaded). Stale water must be replaced with fresh, O₂‑rich water to maintain a high partial pressure gradient for O₂ diffusion. Water flow prevents the gradient from collapsing.

What is ram ventilation? Which sharks rely on it?

Ram ventilation is a method where a fish swims with its mouth open, allowing water to flow over the gills without buccal pumping. Sharks that cannot buccal pump (e.g., great whites, makos) must keep swimming to breathe – they die if they stop.

Icefish blood has no hemoglobin, so their blood is clear instead of red. Why does no hemoglobin present a challenge for O₂ delivery?

Hemoglobin binds O₂ reversibly and allows blood to carry 50‑100 times more O₂ than plasma alone. Without hemoglobin, icefish blood can only hold the tiny amount of O₂ dissolved in plasma. That is insufficient for most fish, so icefish need adaptations.

Name one adaptation icefish might have to boost O₂ delivery despite no hemoglobin.

Very large blood volume. Icefish have about 4× more blood than similar fish with hemoglobin. More blood means more total O₂ molecules can be carried in plasma, even though the O₂ concentration per volume is low.

Name one aspect of the icefish's environment that helps O₂ delivery.

Very cold water (Antarctic). Cold water holds twice as much dissolved O₂ as warm tropical water. Higher water pO₂ creates a larger driving force for O₂ diffusion into the blood.

What is the difference between external respiration and internal respiration?

• External respiration: gas exchange between alveoli and pulmonary capillary blood (O₂ loading, CO₂ unloading).
• Internal respiration: gas exchange between systemic capillary blood and body tissues (O₂ unloading, CO₂ loading).

What is the role of carbonic anhydrase in CO₂ transport?

Carbonic anhydrase is an enzyme in red blood cells that speeds up the reaction CO₂ + H₂O ⇌ H₂CO₃. This allows rapid conversion of CO₂ to bicarbonate (HCO₃⁻), which is the main form of CO₂ transport in blood (~70% as bicarbonate).

What is the chloride shift?

In red blood cells, bicarbonate (HCO₃⁻) is exchanged for chloride (Cl⁻) across the cell membrane to maintain electrical neutrality. HCO₃⁻ leaves the RBC and enters plasma; Cl⁻ enters the RBC. This happens when CO₂ is being converted to bicarbonate.

What is the Haldane effect?

Deoxygenation of hemoglobin (as it unloads O₂ in tissues) increases its ability to carry CO₂. Conversely, oxygenation of hemoglobin in the lungs promotes CO₂ unloading. It is the reciprocal of the Bohr effect.

What is the Bohr effect?

An increase in pCO₂ and/or a decrease in pH (increase in H⁺) decreases hemoglobin's affinity for O₂, shifting the dissociation curve to the right. This promotes O₂ unloading in metabolically active tissues (where CO₂ is high and pH is low).

During exercise, what four mechanisms increase O₂ delivery to tissues?

1. Increased cardiac output (heart rate and stroke volume)
2. Increased minute ventilation (rate and depth of breathing)
3. Vasodilation of blood vessels in active muscles
4. Rightward shift of O₂‑Hb curve (due to increased temperature, CO₂, and H⁺) to unload more O₂.

What is hypoventilation? How does it affect alveolar pO₂ and pCO₂?

Hypoventilation is breathing at an abnormally slow or shallow rate, leading to decreased minute ventilation. Alveolar pO₂ decreases (not enough fresh O₂), and alveolar pCO₂ increases (not enough CO₂ blown off).

What is hyperventilation? How does it affect alveolar pO₂ and pCO₂?

Hyperventilation is breathing at an abnormally fast or deep rate, leading to increased minute ventilation. Alveolar pO₂ increases (more fresh O₂), and alveolar pCO₂ decreases (excess CO₂ blown off). This can cause dizziness due to reduced cerebral blood flow.

At high altitude, total air pressure decreases. How does this affect the partial pressure gradient for O₂ from alveoli to blood?

Atmospheric pO₂ is lower, so alveolar pO₂ is lower. The gradient between alveolar pO₂ and venous blood pO₂ (still ~40 mmHg) is reduced, making it harder for O₂ to diffuse into the blood.

Name two physiological adaptations to high altitude that help maintain O₂ delivery.

1. Increased ventilation rate (hypoxic ventilatory response) – raises alveolar pO₂.
2. Increased red blood cell production (erythropoiesis) over days to weeks – increases blood's O₂‑carrying capacity.

What is the difference between a uniporter, symporter, and antiporter?

• Uniporter: moves a single type of substance down its gradient (passive).
• Symporter: moves two substances in the same direction; one downhill provides energy for the other uphill (secondary active transport).
• Antiporter: moves two substances in opposite directions; one downhill provides energy for the other uphill.

Give an example of a uniporter.

GLUT (glucose transporter) – moves glucose down its concentration gradient into cells. Also urea transporters (UT).

Give an example of a symporter.

Na⁺/glucose cotransporter (SGLT) in the kidney proximal tubule – Na⁺ moves downhill into the cell, and glucose moves uphill into the cell (same direction).

Give an example of an antiporter.

Na⁺/Ca²⁺ exchanger (NCX) – Na⁺ moves downhill into the cell, and Ca²⁺ moves uphill out of the cell (opposite directions).

What is primary active transport? Give an example.

Primary active transport uses energy directly from ATP to move a substance against its electrochemical gradient. Example: Na⁺‑K⁺ ATPase pump – pumps 3 Na⁺ out and 2 K⁺ in, both against their gradients.

What is secondary active transport? Give an example.

Secondary active transport uses the energy stored in an electrochemical gradient (created by primary active transport) to move another substance uphill. Example: Na⁺/glucose symporter – the Na⁺ gradient (low inside, high outside) drives glucose uptake.

Why does a pore (leak channel) allow faster transport than a carrier?

A pore is always open, and multiple ions can flow through simultaneously (like a tunnel). A carrier must bind one molecule, change shape, release it, and reset – a slower cycle.

What is a ligand‑gated channel? Give an example.

A channel that opens or closes when a specific ligand (signaling molecule) binds. Example: Na⁺ channels at the muscle endplate open when acetylcholine binds.

What is a voltage‑gated channel? Give an example.

A channel that opens or closes in response to changes in membrane potential. Example: Voltage‑gated Ca²⁺ channels in the heart open when the membrane depolarizes.

What is the difference between a pore and a gated channel?

A pore is always open (e.g., aquaporin, nuclear pore). A gated channel has a gate that can be opened or closed by a signal (ligand or voltage).

Why do charged ions like Na⁺ and K⁺ need channels or carriers to cross the membrane?

The phospholipid bilayer is hydrophobic in its interior. Charged ions (and polar molecules) cannot dissolve in the hydrophobic tail region. They require transmembrane proteins to provide a hydrophilic passage.

What is the difference between passive transport and active transport?

Passive transport moves substances down their electrochemical gradient (no energy required). Active transport moves substances against their gradient (energy required – ATP or secondary coupling).

What is the primary function of the diaphragm in ventilation?

The diaphragm is a muscle that contracts and flattens to increase thoracic cavity volume, lowering intra‑alveolar pressure and drawing air into the lungs (inhalation). It is the main driver of bulk flow for inspiration.

What happens to the lung if a hole (pneumothorax) opens the pleural space to the atmosphere?

The negative pressure in the thoracic cavity is lost. When the diaphragm contracts, air is drawn into the pleural space through the hole rather than into the lung via the trachea. The lung collapses (atelectasis).

What is anatomical dead space? How does it affect alveolar ventilation?

Anatomical dead space is the volume of air that remains in the conducting airways (trachea, bronchi) and never reaches the alveoli. Alveolar ventilation (V̇A) = (VT – VD) × RR. Dead space reduces the amount of fresh air that participates in gas exchange.

A patient has a tidal volume of 0.5 L, dead space of 0.15 L, and respiratory rate of 12 breaths/min. What is their alveolar ventilation?

V̇A = (0.5 L – 0.15 L) × 12 = 0.35 L × 12 = 4.2 L/min. Minute ventilation would be 0.5 × 12 = 6 L/min, but 1.8 L/min is wasted on dead space.

Why is water a more challenging medium than air for gas exchange?

Water holds less O₂ than air (even at the same pO₂), and it is denser and more viscous than air, requiring more energy to move over gills. This is why aquatic animals often have lower metabolic rates.

What is the approximate pO₂ in the alveoli at sea level? At 3000 ft elevation (80% air pressure)?

Sea level: ~100 mmHg. At 3000 ft: alveolar pO₂ ≈ 80 mmHg (since 100 × 0.80 = 80 mmHg). Still sufficient for near‑full hemoglobin saturation.

In the O₂‑Hb dissociation curve, what is the P50 value?

P50 is the partial pressure of O₂ at which hemoglobin is 50% saturated. For normal human hemoglobin, P50 is about 26 mmHg. A lower P50 means higher affinity; a higher P50 means lower affinity.

How would a rightward shift of the O₂‑Hb curve (decreased affinity) affect O₂ delivery to tissues?

A rightward shift increases O₂ unloading at the tissues (because at a given tissue pO₂ of ~40 mmHg, saturation is lower). However, it also slightly decreases O₂ loading at the lungs (saturation at 100 mmHg is slightly lower). Net effect is usually beneficial during exercise or at high altitude.

How would a leftward shift of the O₂‑Hb curve (increased affinity) affect O₂ delivery?

A leftward shift decreases O₂ unloading at the tissues (hemoglobin holds O₂ more tightly). This can impair O₂ delivery. It may occur in conditions like alkalosis or carbon monoxide poisoning.

What is the primary reason that breathing pure O₂ at sea level does not increase O₂ flux into blood during exercise?

Hemoglobin is already ~98‑99% saturated when breathing air. There is no capacity to bind more O₂. The tiny additional O₂ dissolved in plasma is negligible compared to the O₂ carried by hemoglobin.

A patient with pneumonia has fluid in their alveoli, increasing the diffusion distance for O₂. Would breathing high‑pO₂ oxygen help? Why?

Yes. The increased diffusion distance (resistance) can be compensated by increasing the driving force (alveolar pO₂) with supplemental O₂. Fick's Law: flux = (A × ΔP) / T. Increasing ΔP can offset increased T.

What is the difference between conductance and resistance?

They are inverses. If resistance doubles, conductance is halved. Conductance = 1 / resistance. Flux = driving force × conductance = driving force / resistance.

In the context of bulk flow through a tube, why is radius such an important factor?

Resistance to bulk flow is proportional to 1 / (radius⁴). Halving the radius increases resistance 16‑fold (2⁴ = 16). That's why small changes in blood vessel diameter (vasoconstriction/vasodilation) have huge effects on blood flow.

What is the difference between an artery and a vein? Which has higher O₂ content in systemic circulation?

Arteries carry blood away from the heart; veins carry blood toward the heart. In systemic circulation, arteries carry oxygenated blood (high pO₂) and veins carry deoxygenated blood (low pO₂). In pulmonary circulation, it's reversed.

What is the difference between blood plasma and red blood cells in terms of O₂ transport?

Blood plasma carries only a small amount of dissolved O₂ (about 1‑2% of total). Red blood cells contain hemoglobin, which binds ~98‑99% of O₂ in the blood. RBCs are essential for high O₂ capacity.

Why do icefish have clear blood? How does that affect their appearance?

Icefish lack hemoglobin, so their blood is colorless (clear). Their gills appear white/clear instead of red, and their blood vessels are visible as clear tubes.

What is one trade‑off of having no hemoglobin? (Icefish)

Without hemoglobin, icefish have very low O₂‑carrying capacity per volume of blood. To compensate, they have evolved very large blood volume (4× normal) and live in cold, O₂‑rich water. But they are still limited to low‑activity lifestyles.

In the nurse shark buccal pumping question, why did the answer key say "as if liquids behaved like gasses"?

Because in reality, water is incompressible – when you squeeze a water‑filled cavity, water flows immediately, not because of pressure build‑up but because of bulk flow from displacement. The pressure‑volume relationship for liquids is different from gases, but the conceptual chain (squeeze → volume decrease → pressure increase → flow) is a useful analogy.

What is the normal partial pressure of O₂ in the blood plasma of a healthy person at sea level?

~100 mmHg (in arterial blood). This is in equilibrium with alveolar pO₂. However, the amount of O₂ dissolved in plasma is only about 0.3 mL O₂ per 100 mL blood (vs. 20 mL O₂ per 100 mL blood bound to hemoglobin).

A person has a fever. Their O₂‑Hb curve shifts right. How does this affect the saturation at the lungs (pO₂=100 mmHg) and at the tissues (pO₂=40 mmHg)?

At lungs (100 mmHg): saturation drops from ~98% to ~90‑95%. At tissues (40 mmHg): saturation drops from ~75% to ~60‑65%. The difference in saturation (lungs‑tissues) is about the same or slightly larger, so O₂ delivery is maintained or even increased.

What is the most important takeaway from the athlete breathing study (air vs. pure O₂)?

For healthy people at sea level, increasing alveolar pO₂ beyond normal does not increase O₂ uptake because hemoglobin is already saturated. The body's O₂ delivery is limited by blood flow (cardiac output) and hemoglobin concentration, not by alveolar pO₂.

A patient has thickened alveolar walls due to fibrosis. Would you expect their arterial pO₂ to be low, normal, or high? Why?

Low. Thickened walls increase resistance to O₂ diffusion. Even if alveolar pO₂ is normal, less O₂ can diffuse into the blood per unit time. The blood may not reach full saturation by the time it leaves the lung capillary.

How would you treat a patient with thickened alveolar walls to raise their arterial pO₂?

Give supplemental O₂ (high‑pO₂ gas). This increases the driving force (ΔP) across the thickened membrane, compensating for the increased resistance. Fick's Law: flux = (A × ΔP) / thickness. Increasing ΔP can offset increased thickness.

What is the effect of carbon monoxide (CO) on O₂ transport?

CO binds to hemoglobin with ~200‑250× higher affinity than O₂. It occupies heme sites, preventing O₂ binding (reduces O₂ capacity). It also shifts the O₂‑Hb curve left (increases affinity for remaining O₂), impairing O₂ unloading. CO poisoning is lethal.

Why does hyperventilation cause dizziness?

Hyperventilation lowers arterial pCO₂, which increases blood pH (respiratory alkalosis). The high pH causes cerebral vasoconstriction (blood vessels in the brain constrict), reducing blood flow to the brain. This can cause lightheadedness, tingling, and fainting.

What is the normal pCO₂ in arterial blood? What happens if it rises too high?

Normal arterial pCO₂ is ~40 mmHg. If it rises (hypercapnia), it causes respiratory acidosis (low pH) and can lead to confusion, drowsiness, and eventually coma. The body responds by increasing ventilation.

In the heart stop scenario (still breathing), why does alveolar pO₂ increase even though the person is not moving blood?

Mass balance: O₂ enters the alveoli via ventilation (rate in unchanged). O₂ leaves the alveoli by diffusing into blood (rate out). With no blood flow, the blood in lung capillaries quickly becomes saturated and stops taking up O₂ – rate out drops to nearly zero. So alveolar pO₂ rises toward the pO₂ of inspired air.