respiratory system

The respiratory system has two major jobs:

1. Bring oxygen (O₂) into the body so cells can produce energy (ATP).

2. Remove carbon dioxide (CO₂) produced by cells.

The complete process:

1. Air enters the lungs.

2. O₂ passes from the alveoli into the blood.

3. The heart pumps oxygen-rich blood to body tissues.

4. Cells use O₂ to produce ATP and generate CO₂.

5. Blood carries CO₂ back to the lungs.

6. CO₂ leaves during exhalation.

Connection to Lesson 3:

• Respiratory system = gets O₂ into the blood.

• Cardiovascular system = delivers O₂ to tissues.

• Cells = use O₂ to make ATP.

Both systems must work properly to deliver enough oxygen to the body.

 

A. RESPIRATORY ANATOMY

1. Main Functions of the Respiratory System

Ventilation: Moving air in and out of the lungs.

Gas exchange: O₂ enters blood; CO₂ leaves blood.

pH regulation: Controls CO₂ removal, affecting blood acidity.

Air conditioning: Warms, filters, and humidifies inhaled air.

Protection: Mucus, cilia, coughing, and immune cells remove harmful material.

Speech: Air passing through the vocal folds produces sound.

Smell: Airborne chemicals stimulate olfactory receptors.

Four Important Processes

• Ventilation: Air moves into and out of lungs.

• External respiration: O₂ and CO₂ exchange between alveoli and pulmonary blood.

• Internal respiration: O₂ and CO₂ exchange between systemic blood and tissues.

• Cellular respiration: Cells use nutrients and O₂ to produce ATP, generating CO₂.

TEAS TRAP: Breathing and cellular respiration are NOT the same process.

2. Complete Air Pathway

Memorize this order:

Nose / mouth

↓

Pharynx

↓

Larynx

↓

Trachea

↓

Primary bronchi

↓

Secondary bronchi

↓

Tertiary bronchi

↓

Bronchioles

↓

Terminal bronchioles

↓

Respiratory bronchioles

↓

Alveolar ducts

↓

Alveolar sacs / alveoli

Easy way to understand:

Imagine an upside-down tree:

• Trachea = trunk.

• Bronchi = large branches.

• Bronchioles = small branches.

• Alveoli = tiny air sacs at the ends.

Remember: Air is transported through conducting airways before reaching the alveoli, where most gas exchange occurs.

3. Upper Respiratory Tract

Usually includes the nose, nasal cavity, sinuses, and pharynx. Classification of the larynx varies.

Nose and Nasal Cavity

Three main jobs:

• Filter: Nose hairs and mucus trap particles.

• Warm: Blood vessels transfer heat to incoming air.

• Humidify: Moistens air to protect lower airways.

Nasal conchae (turbinates):

• Curved bony structures inside the nose.

• Increase surface area.

• Create airflow turbulence.

• Improve filtering, warming, and humidification.

Paranasal sinuses:

• Air-filled spaces around the nasal cavity.

• Produce mucus.

• Reduce skull weight.

• Contribute to voice resonance.

Olfactory receptors: Detect odors.

Pharynx (Throat)

Shared by respiratory and digestive systems.

Three regions:

1. Nasopharynx: Behind the nose; carries air.

2. Oropharynx: Behind the mouth; carries air and food.

3. Laryngopharynx: Lower throat; carries air and food.

Order: Nasopharynx → Oropharynx → Laryngopharynx.

Food normally passes toward the esophagus, while air passes toward the larynx

2. Complete Air Pathway

Memorize this order:

Nose / mouth

↓

Pharynx

↓

Larynx

↓

Trachea

↓

Primary bronchi

↓

Secondary bronchi

↓

Tertiary bronchi

↓

Bronchioles

↓

Terminal bronchioles

↓

Respiratory bronchioles

↓

Alveolar ducts

↓

Alveolar sacs / alveoli

Easy way to understand:

Imagine an upside-down tree:

• Trachea = trunk.

• Bronchi = large branches.

• Bronchioles = small branches.

• Alveoli = tiny air sacs at the ends.

Remember: Air is transported through conducting airways before reaching the alveoli, where most gas exchange occurs.

3. Upper Respiratory Tract

Usually includes the nose, nasal cavity, sinuses, and pharynx. Classification of the larynx varies.

Nose and Nasal Cavity

Three main jobs:

• Filter: Nose hairs and mucus trap particles.

• Warm: Blood vessels transfer heat to incoming air.

• Humidify: Moistens air to protect lower airways.

Nasal conchae (turbinates):

• Curved bony structures inside the nose.

• Increase surface area.

• Create airflow turbulence.

• Improve filtering, warming, and humidification.

Paranasal sinuses:

• Air-filled spaces around the nasal cavity.

• Produce mucus.

• Reduce skull weight.

• Contribute to voice resonance.

Olfactory receptors: Detect odors.

Pharynx (Throat)

Shared by respiratory and digestive systems.

Three regions:

1. Nasopharynx: Behind the nose; carries air.

2. Oropharynx: Behind the mouth; carries air and food.

3. Laryngopharynx: Lower throat; carries air and food.

Order: Nasopharynx → Oropharynx → Laryngopharynx.

Food normally passes toward the esophagus, while air passes toward the larynx

4. Larynx — Voice Box

Location: Between the pharynx and trachea.

Functions:

• Keeps the airway open.

• Helps protect the airway during swallowing.

• Produces speech.

Important structures:

• Epiglottis: Helps prevent food/liquid from entering the airway.

• Vocal folds (cords): Vibrate to produce sound.

• Glottis: Opening between the vocal folds.

• Thyroid cartilage: Protects larynx; forms Adam's apple.

• Cricoid cartilage: Complete cartilage ring supporting the lower larynx.

How Swallowing Protects the Airway

Swallowing begins

→ Larynx elevates

→ Vocal folds close

→ Epiglottis helps protect the airway entrance

→ Food enters esophagus instead of trachea.

Aspiration: Food, liquid, or another substance enters the airway.

TEAS TRAP:

• Epiglottis = airway protection.

• Vocal folds = sound production.

5. Trachea — Windpipe

Function: Conducts air from larynx to bronchi.

Important structures:

• C-shaped hyaline cartilage rings.

• Trachealis smooth muscle.

• Mucus-producing cells.

• Ciliated epithelium.

Why C-shaped cartilage?

Cartilage holds the trachea open, while the open posterior portion allows the esophagus behind it to expand during swallowing.

Mucociliary Escalator

Particles/microbes enter airway

→ Mucus traps them

→ Cilia move mucus upward

→ Material reaches throat

→ Swallowed or coughed out.

Cilia: Tiny moving hairlike structures in respiratory epithelium.

Smoking: Can damage cilia → impaired mucus clearance → buildup of particles/mucus.

Carina: Ridge where the trachea divides into the primary bronchi. Sensitive to irritation and can trigger coughing.

6. Bronchi and Bronchioles

The trachea divides into the right and left primary bronchi.

Right Main Bronchus

• Wider.

• Shorter.

• More vertical.

Left Main Bronchus

• Narrower.

• Longer.

• More horizontal.

Why it matters: Aspirated objects tend to enter the right main bronchus more often in typical adult anatomy, although position affects this.

Airway Branching

• Primary bronchi: One to each lung.

• Secondary/lobar bronchi: Supply lung lobes.

• Tertiary/segmental bronchi: Supply bronchopulmonary segments.

• Bronchioles: Smaller airways with smooth muscle.

• Terminal bronchioles: End of conducting zone.

• Respiratory bronchioles: Beginning of respiratory zone.

Bronchi vs. Bronchioles

Bronchi:

• Have cartilage.

• Carry air into lung subdivisions.

Bronchioles:

• No cartilage.

• Contain smooth muscle.

• Diameter changes affect airway resistance.

Bronchoconstriction: Bronchioles narrow → resistance increases → airflow becomes harder.

Bronchodilation: Bronchioles widen → resistance decreases → airflow becomes easier.

7. Right Lung vs. Left Lung

Right Lung

• 3 lobes: superior, middle, inferior.

• Horizontal and oblique fissures.

• Generally shorter and wider.

Left Lung

• 2 lobes: superior and inferior.

• Oblique fissure.

• Has cardiac notch.

• Has lingula (tongue-shaped part of superior lobe).

Why two lobes on left? The heart occupies space on the left.

Cardiac notch: Indentation accommodating the heart.

Lingula: Region roughly corresponding to part of the right middle lobe.

MEMORIZE: Right = 3 lobes; Left = 2 lobes.

8. Conducting Zone vs. Respiratory Zone

Conducting Zone

Purpose: Move and prepare air.

Includes:

• Nose and nasal cavity.

• Pharynx.

• Larynx.

• Trachea.

• Bronchi.

• Bronchioles through terminal bronchioles.

Functions:

• Transport.

• Filtration.

• Warming.

• Humidification.

No major alveolar gas exchange occurs here.

Respiratory Zone

Purpose: Gas exchange.

Includes:

• Respiratory bronchioles.

• Alveolar ducts.

• Alveolar sacs.

• Alveoli.

Thin walls and nearby capillaries allow O₂ and CO₂ to diffuse.

TEAS TRAP: Terminal bronchioles = conducting zone. Respiratory bronchioles = respiratory zone.

9. Alveoli — Gas Exchange

Alveoli: Tiny air sacs where most pulmonary gas exchange occurs.

Why they're effective:

• Very thin walls → short diffusion distance.

• Large total surface area.

• Many surrounding capillaries.

• Moist surfaces allow gases to dissolve.

• Surfactant reduces surface tension.

Three Important Alveolar Cells

Type I alveolar cells:

• Very thin.

• Form most of the gas-exchange surface.

Type II alveolar cells:

• Produce surfactant.

Alveolar macrophages:

• Engulf microbes and debris.

MEMORIZE:

• Type I = gas exchange.

• Type II = surfactant.

• Macrophages = defense.

Surfactant

Definition: Substance produced by Type II cells that reduces alveolar surface tension.

Why it's necessary:

The liquid lining alveoli creates surface tension that tends to make them shrink.

Surfactant decreases surface tension

→ Alveoli inflate more easily

→ Less effort needed to breathe

→ Less risk of collapse.

Low surfactant:

↓ Surfactant → ↑ Surface tension → ↓ Lung compliance → harder inflation → risk of atelectasis.

Atelectasis: Collapse of alveoli or part of a lung.

Premature newborns: May lack sufficient surfactant → neonatal respiratory distress syndrome.

TEAS TRAP:

• Mucus traps particles.

• Surfactant reduces surface tension.

They are NOT interchangeable.

B. HOW BREATHING WORKS

10. Diaphragm

Diaphragm: Dome-shaped skeletal muscle underneath the lungs.

Primary muscle of quiet inspiration.

Controlled by the phrenic nerve (C3–C5).

During Inhalation

Diaphragm contracts

→ Flattens/moves DOWN

→ Chest volume increases

→ Air enters.

During Exhalation

Diaphragm relaxes

→ Returns UP to dome shape

→ Chest volume decreases

→ Air exits.

IMPORTANT: The diaphragm doesn't pull air inside directly. Its movement changes chest/lung volume, producing a pressure difference.

11. Boyle's Law

Boyle's Law: Gas pressure and volume move in opposite directions when temperature and gas amount stay constant.

Formula: P₁V₁ = P₂V₂

Main rule:

• ↑ Volume → ↓ Pressure.

• ↓ Volume → ↑ Pressure.

Air flows from HIGH pressure to LOW pressure.

Breathing Connection

Inhalation:

↑ Lung volume → ↓ Alveolar pressure → Air IN.

Exhalation:

↓ Lung volume → ↑ Alveolar pressure → Air OUT.

Example: Pulling back a syringe plunger increases internal volume and lowers pressure, drawing air inward.

TEAS TRAP: Increased chest volume makes alveolar pressure decrease, not increase.

12. Inspiration (Inhalation)

Quiet inspiration is an ACTIVE process because muscles contract.

Exact Sequence

1. Diaphragm contracts and moves downward.

2. External intercostal muscles elevate the ribs.

3. Thoracic cavity expands.

4. Lungs expand.

5. Alveolar pressure decreases below atmospheric pressure.

6. Air moves INTO lungs.

7. Near the end of inspiration, pressures equalize and airflow stops briefly.

External intercostals: Muscles between ribs that help elevate the rib cage during inspiration.

Remember: Muscle contraction causes volume change, which causes pressure change, which causes airflow.

13. Expiration (Exhalation)

Quiet expiration is normally PASSIVE.

Exact Sequence

1. Diaphragm and inspiratory muscles relax.

2. Diaphragm moves upward.

3. Rib cage returns toward resting position.

4. Lungs recoil inward.

5. Lung volume decreases.

6. Alveolar pressure rises above atmospheric pressure.

7. Air moves OUT.

8. Pressures equalize at the end of expiration.

Elastic recoil: Lung tissue naturally returns toward a smaller size after being stretched.

TEAS TRAP: Quiet exhalation is usually passive. Forced exhalation is active.

14. Quiet vs. Forced Breathing

Quiet Inspiration

• Active.

• Diaphragm + external intercostals contract.

Quiet Expiration

• Mostly passive.

• Inspiratory muscles relax.

• Elastic recoil expels air.

Forced Inspiration

• Active.

• Diaphragm + external intercostals + accessory muscles.

Accessory muscles: Include sternocleidomastoid and scalenes.

Forced Expiration

• Active.

• Abdominal muscles contract.

• Internal intercostals (especially interosseous portions) help lower ribs.

Why: Abdominal muscles increase abdominal pressure, pushing the diaphragm upward and reducing chest volume more forcefully.

Applications: Exercise, coughing, respiratory distress.

15. The Three Breathing Pressures

Atmospheric Pressure (Patm)

Pressure of air outside the body.

At sea level, absolute atmospheric pressure is approximately 760 mmHg.

When comparing breathing pressures, Patm is often assigned a relative value of 0.

Intra-Alveolar Pressure (Palv)

Air pressure inside alveoli.

• Palv below Patm → air IN.

• Palv above Patm → air OUT.

• Palv equal to Patm → no net airflow.

Intrapleural Pressure (Ppl)

Pressure between visceral and parietal pleural membranes.

Normally negative relative to atmospheric pressure during spontaneous quiet breathing.

Breathing Pressure Sequence:

Before inspiration: Palv = Patm → no airflow.

During inspiration: Palv < Patm → air enters.

End inspiration: Palv = Patm → no airflow.

During expiration: Palv > Patm → air exits.

End expiration: Palv = Patm → no airflow.

Important: Relative pressure of 0 does NOT mean atmospheric pressure is absent.

16. Pleura & Why Lungs Stay Expanded

Pleura: Double-layered membrane surrounding each lung.

Visceral Pleura

Directly covers lung surface.

Parietal Pleura

Lines inside of chest wall, diaphragm, and associated mediastinal surfaces.

Pleural Cavity

Thin fluid-filled space between pleural layers.

Pleural fluid:

• Reduces friction.

• Helps couple lungs to chest-wall movement.

Why Is Intrapleural Pressure Negative?

Two opposite elastic forces:

• Lung tissue naturally recoils INWARD.

• Chest wall tends to spring OUTWARD.

Together → intrapleural pressure stays below atmospheric pressure under normal conditions.

Transpulmonary Pressure

Formula:

Transpulmonary pressure = Alveolar pressure − Intrapleural pressure.

Ptp = Palv − Ppl

This pressure difference helps keep lungs expanded.

Pneumothorax

Definition: Air enters pleural cavity.

Air enters pleural space

→ Normal pressure relationship is disrupted

→ Lung loses expanding pressure

→ Lung may recoil inward/collapse

→ Ventilation and oxygenation may decrease.

Pleural Effusion

Definition: Excess fluid in pleural space.

Can restrict lung expansion.

TEAS TRAP:

• Air inside alveoli = normal.

• Air inside pleural cavity = pneumothorax.

• Excess fluid inside pleural cavity = pleural effusion.

17. Lung Compliance vs. Elastic Recoil

Compliance

Definition: How easily lungs stretch/expand.

Formula: Compliance = Change in volume ÷ Change in pressure.

High compliance = easy expansion.

Low compliance = difficult expansion.

Elastic Recoil

Definition: Tendency of stretched lungs to return inward.

Important Conditions

Pulmonary fibrosis:

• Scar tissue makes lungs stiff.

• ↓ Compliance.

• Harder to inflate.

• Often reduced lung volumes.

Emphysema:

• Destruction of alveolar walls and elastic tissue.

• Often ↑ Compliance.

• ↓ Elastic recoil.

• Harder to empty lungs.

• Air trapping.

Surfactant deficiency:

• ↑ Surface tension.

• ↓ Compliance.

• Increased work of breathing.

• More collapse risk.

Pulmonary edema:

• Fluid in lung tissue/alveoli.

• Often ↓ Compliance.

• More difficult expansion.

TEAS TRAP: High compliance is not always good. Emphysema causes unusually easy expansion but poor recoil.

18. Airway Resistance

Airway resistance: Opposition to air moving through airways.

Main adjustable factor = airway radius.

Bronchoconstriction

Smooth muscle contracts

→ Airway narrows

→ Resistance increases

→ Less airflow for the same pressure difference.

Bronchodilation

Smooth muscle relaxes

→ Airway widens

→ Resistance decreases

→ More airflow for the same pressure difference.

Autonomic Control

Parasympathetic stimulation:

• Acetylcholine acting at M₃ receptors.

• Bronchoconstriction.

• Increased mucus secretion.

β₂-adrenergic stimulation:

• Relaxes bronchial smooth muscle.

• Causes bronchodilation.

Asthma Connection

Airway inflammation + bronchoconstriction + mucus

→ Narrowed airways

→ Increased resistance

→ Difficult airflow, often especially during expiration.

Bronchodilators relax smooth muscle and widen the airways.

TEAS TRAP: The problem with narrowed airways is difficulty moving air—not necessarily a lack of oxygen in the surrounding atmosphere.

C. LUNG VOLUMES & MEASUREMENTS

19. Respiratory Rate (RR)

RR: Number of complete breaths per minute.

Normal resting adult RR: Approximately 12–20 breaths/min.

One breath = one inspiration + one expiration.

Important Terms

• Eupnea: Normal, quiet breathing.

• Tachypnea: Abnormally rapid breathing.

• Bradypnea: Abnormally slow breathing.

• Apnea: Temporary absence of breathing.

• Dyspnea: Feeling short of breath or difficulty breathing.

• Hyperpnea: Increased depth, often with increased rate.

• Orthopnea: Difficulty breathing when lying flat.

TEAS TRAP: Tachypnea = increased breathing rate. Hyperventilation = excessive ventilation relative to CO₂ production; they are not automatically the same.

20. Four Main Lung Volumes

Tidal Volume (TV)

Air moved during ONE normal, quiet breath.

Typical adult example: approximately 500 mL.

Inspiratory Reserve Volume (IRV)

Extra air you can forcefully inhale AFTER a normal inhalation.

Expiratory Reserve Volume (ERV)

Extra air you can forcefully exhale AFTER a normal exhalation.

Residual Volume (RV)

Air remaining inside lungs AFTER maximal exhalation.

Memory:

• TV = normal breath.

• IRV = extra IN.

• ERV = extra OUT.

• RV = air LEFT.

Why Residual Volume Exists

Lungs do not empty completely because of their mechanical properties and closure of small airways at low volumes.

Important: Ordinary spirometry cannot directly measure RV because it remains in the lungs.

21. Lung Capacities

Lung capacity = combination of two or more volumes.

Inspiratory Capacity (IC)

IC = TV + IRV.

Maximum amount inhaled after a normal exhalation.

Vital Capacity (VC)

VC = IRV + TV + ERV.

Maximum movable air between full inhalation and full exhalation.

Functional Residual Capacity (FRC)

FRC = ERV + RV.

Air remaining AFTER normal exhalation.

Total Lung Capacity (TLC)

TLC = IRV + TV + ERV + RV.

Total air inside lungs after maximal inhalation.

Worked Example

Given:

• TV = 500 mL.

• IRV = 3,000 mL.

• ERV = 1,100 mL.

• RV = 1,200 mL.

Calculations:

• IC = 500 + 3,000 = 3,500 mL.

• VC = 3,000 + 500 + 1,100 = 4,600 mL.

• FRC = 1,100 + 1,200 = 2,300 mL.

• TLC = 3,000 + 500 + 1,100 + 1,200 = 5,800 mL.

These are example values, not normal values for everyone.

TEAS TRAP:

• VC does NOT include RV.

• TLC DOES include RV.

• FRC = air left after normal expiration.

22. Spirometry & Pulmonary Function

Spirometry: Measures inhaled/exhaled air volumes and airflow.

Important Measurements

FVC (Forced Vital Capacity):

Total amount forcefully exhaled after maximal inhalation.

FEV₁:

Amount forcefully exhaled in the FIRST second.

FEV₁/FVC:

Fraction of FVC exhaled during the first second.

PEF (Peak Expiratory Flow):

Highest flow rate during forced expiration.

Obstructive Lung Disorders

Main problem: Difficulty moving air OUT.

Examples:

• Asthma.

• COPD.

Characteristics:

• Increased airway resistance and/or decreased recoil.

• FEV₁ often decreases significantly.

• FEV₁/FVC generally decreases.

• Air trapping may occur.

Example: Trying to exhale through a narrow straw.

Restrictive Lung Disorders

Main problem: Difficulty expanding lungs.

Examples:

• Pulmonary fibrosis.

• Restrictive chest-wall conditions.

Characteristics:

• Decreased lung expansion.

• TLC decreased.

• FEV₁/FVC often normal or increased.

Example: Trying to inflate a very stiff balloon.

Important: Spirometry may suggest restriction, but reduced TLC confirms a restrictive ventilatory defect.

Ordinary spirometry does NOT directly measure RV, FRC, or TLC.

23. Minute Ventilation

Minute ventilation (VE): Total volume of air moved per minute.

Formula:

VE = Respiratory rate × Tidal volume.

VE = RR × TV

Example

RR = 12 breaths/min.

TV = 500 mL/breath.

VE = 12 × 500 = 6,000 mL/min = 6 L/min.

Important: Total ventilation is not the same as effective alveolar ventilation.

Some inhaled air remains inside conducting airways.

24. Dead Space

Dead space: Air that does not participate in effective gas exchange.

Anatomical Dead Space

Air inside conducting airways, including:

• Trachea.

• Bronchi.

• Conducting bronchioles.

Typical adult example: approximately 150 mL, varying by body size.

Example:

TV = 500 mL.

Anatomical dead space = 150 mL.

Fresh air reaching respiratory regions ≈ 500 − 150 = 350 mL/breath.

Alveolar Dead Space

Air reaches alveoli, but blood flow is inadequate for effective gas exchange.

Physiological Dead Space

Physiological dead space = Anatomical dead space + Alveolar dead space.

TEAS TRAP: Air reaching alveoli is not always effectively used; alveoli also need blood flow for gas exchange.

25. Alveolar Ventilation

Alveolar ventilation (VA): Fresh air reaching functioning alveoli per minute.

Formula:

VA = (TV − VD) × RR

Where:

• TV = tidal volume.

• VD = physiological dead space.

• RR = respiratory rate.

Example

TV = 500 mL.

VD = 150 mL.

RR = 12/min.

VA = (500 − 150) × 12

VA = 4,200 mL/min = 4.2 L/min.

Why Fast, Shallow Breathing Can Be Inefficient

Patient A:

• RR = 12.

• TV = 500 mL.

• VE = 6 L/min.

• VA = (500 − 150) × 12 = 4.2 L/min.

Patient B:

• RR = 20.

• TV = 300 mL.

• VE = 6 L/min.

• VA = (300 − 150) × 20 = 3.0 L/min.

Both move 6 L of air per minute, but Patient A delivers MORE fresh air to functioning alveoli.

Why? A larger fraction of each shallow breath is wasted in dead space.

TEAS TRAP: Faster breathing doesn't automatically equal more effective ventilation.

 

D. CONTROL OF BREATHING

26. Brainstem Respiratory Centers

You normally breathe automatically because the brainstem controls respiratory muscle activity.

Medulla Oblongata

Generates and regulates the basic breathing rhythm.

Important regions:

Ventral Respiratory Group (VRG):

• Involved in rhythm generation.

• Helps activate breathing muscles, including during active breathing.

Dorsal Respiratory Group (DRG):

• Integrates sensory information from receptors.

• Helps regulate respiratory responses.

Pre-Bötzinger Complex:

• Neural network important for inspiratory rhythm generation.

Pons

• Adjusts breathing pattern.

• Helps regulate depth and timing.

• Smooths transitions between inspiration and expiration.

Memory:

• Medulla = breathing rhythm.

• Pons = modifies pattern.

Signal to Diaphragm

Brainstem

→ Spinal respiratory pathways

→ Phrenic nerve (C3–C5)

→ Diaphragm contraction

→ Inspiration.

Intercostal nerves activate intercostal muscles.

Advanced: Damage to phrenic nerve pathways may impair diaphragm function and ventilation.

27. Central vs. Peripheral Chemoreceptors

Chemoreceptors: Sensors that detect chemical conditions affecting breathing.

Central Chemoreceptors

Location: Associated with medulla/brainstem.

Respond mainly to CO₂-related changes in CSF pH.

How:

CO₂ enters brain extracellular fluid/CSF

→ Forms carbonic acid

→ Releases H⁺

→ Central chemoreceptors stimulated

→ Ventilation increases.

Peripheral Chemoreceptors

Locations:

• Carotid bodies.

• Aortic bodies.

Respond to:

• ↓ Arterial O₂.

• ↑ Arterial CO₂.

• ↑ H⁺ / ↓ pH.

Low O₂ becomes a particularly strong stimulus when arterial PaO₂ falls to approximately 60 mmHg or below.

Very Important Difference

Carotid bodies: Detect chemical changes.

Carotid sinus baroreceptors: Detect arterial pressure/stretch.

TEAS TRAP: Carotid bodies and carotid sinus are NOT the same receptors.

28. Why CO₂ Controls Breathing

A major normal stimulus for breathing is increased CO₂, not just decreased oxygen.

CO₂ and Acid-Base Chemistry

CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻

Definitions:

• H₂CO₃ = carbonic acid.

• H⁺ = hydrogen ion.

• HCO₃⁻ = bicarbonate.

When CO₂ Rises

↑ CO₂

→ ↑ H⁺ in CSF

→ Central chemoreceptors stimulated

→ Respiratory centers increase ventilation

→ More CO₂ exhaled

→ CO₂ falls toward normal.

This is NEGATIVE FEEDBACK because the response opposes the original CO₂ increase.

29. Hypoventilation vs. Hyperventilation

Hypoventilation

Definition: Too little effective alveolar ventilation for metabolic CO₂ production.

↓ Ventilation

→ CO₂ accumulates

→ ↑ PaCO₂

→ ↑ H⁺

→ ↓ pH

→ Respiratory acidosis tendency.

Hyperventilation

Definition: More effective ventilation than needed to remove metabolic CO₂.

↑ Ventilation

→ More CO₂ removed

→ ↓ PaCO₂

→ ↓ H⁺

→ ↑ pH

→ Respiratory alkalosis tendency.

Quick Comparison

Hypoventilation:

• CO₂ ↑.

• H⁺ ↑.

• pH ↓.

• Respiratory acidosis.

Hyperventilation:

• CO₂ ↓.

• H⁺ ↓.

• pH ↑.

• Respiratory alkalosis.

TEAS TRAP: Respiratory rate alone does not determine hyperventilation; depth and CO₂ production also matter.

30. Other Factors Affecting Breathing

Cerebral cortex:

• Voluntary breathing control.

• Example: Holding your breath.

Hypothalamus:

• Emotions and temperature affect breathing.

Exercise/proprioceptors:

• Help adjust breathing to physical activity.

Lung stretch receptors:

• Detect inflation.

• Can help limit excessive inspiration.

Irritant receptors:

• Detect airway irritants.

• Trigger coughing and other protective responses.

Chemoreceptors:

• ↑ CO₂/H⁺ → generally ↑ breathing drive.

• Markedly ↓ arterial O₂ → ↑ peripheral chemoreceptor stimulation.

Hering–Breuer Inflation Reflex

Lung stretch receptors signal brainstem centers when lungs inflate substantially.

Purpose: Limit excessive inflation.

More important during large breaths; less prominent during ordinary quiet breathing in most healthy adults.

31. Protective Respiratory Reflexes

Cough:

• Forcefully clears irritants/material from lower airways.

Sneeze:

• Removes irritants from nasal passages.

Mucociliary clearance:

• Moves trapped particles toward throat.

Alveolar macrophages:

• Engulf pathogens/debris in alveoli.

Swallowing reflex + epiglottis:

• Help prevent aspiration.

Important: Impaired airway defenses can increase the risk of respiratory infections or aspiration.

 

E. PUTTING EVERYTHING TOGETHER

32. Asthma Attack — Follow the Process

Main problem: Airway inflammation + bronchoconstriction + mucus.

Bronchioles narrow

→ Airway resistance ↑

→ Airflow becomes harder

→ Expiration may be prolonged

→ Air trapping may occur

→ Severe attacks can impair gas exchange.

Why Wheezing Happens

Air moving through narrowed airways may produce a musical sound.

Why β₂-Agonists Help

β₂ receptor stimulation

→ Airway smooth muscle relaxes

→ Bronchioles widen

→ Resistance decreases

→ Airflow improves.

Advanced trap: Severe asthma may produce little audible wheezing if airflow becomes extremely limited.

33. Pulmonary Fibrosis vs. Emphysema

Pulmonary Fibrosis

Scar tissue develops

→ Lungs stiffen

→ Compliance decreases

→ Harder to inflate

→ Often reduced lung volumes.

Pattern: Restrictive.

Emphysema

Alveolar walls/elastic tissue damaged

→ Elastic recoil decreases

→ Lungs empty less effectively

→ Air trapping increases.

Compliance often increases.

Pattern: Obstructive.

Main Difference

• Fibrosis = hard to expand.

• Emphysema = hard to empty.

34. Pneumothorax

Problem: Air in pleural cavity.

Air enters pleural space

→ Normal negative pressure relationship disrupted

→ Transpulmonary distending pressure decreases

→ Lung recoils inward

→ Lung may collapse

→ Ventilation decreases.

Compare with Asthma

Asthma: Airway narrowing.

Pneumothorax: Loss of the normal pleural pressure system supporting lung expansion.

35. Why Rapid, Shallow Breathing Can Be Ineffective

Smaller TV

→ Larger proportion of breath remains in dead space

→ Less fresh air reaches alveoli

→ Alveolar ventilation may decrease.

Remember:

• RR = number of breaths.

• TV = amount of air per breath.

• VA = fresh air reaching functioning alveoli per minute.

All matter.

36. Why Oxygen Delivery Needs Both Lungs and Heart

Lungs: Bring O₂ into alveoli and blood.

Heart: Pumps oxygen-rich blood to tissues.

Effective tissue O₂ delivery requires:

• Adequate ventilation.

• Effective alveolar gas exchange.

• Enough blood hemoglobin/O₂ content.

• Adequate cardiac output.

• Adequate tissue perfusion.

Example 1: Healthy lungs + failing heart = potentially inadequate tissue O₂ delivery.

Example 2: Strong heart + severe lung disease = potentially inadequate blood oxygenation.

Main concept: Good breathing alone does not guarantee good tissue oxygen delivery.

 

F. HIGH-YIELD TEAS REVIEW

37. Essential Cause-and-Effect Relationships

Diaphragm contracts → moves DOWN → inspiration.

Diaphragm relaxes → moves UP → passive expiration.

Chest volume increases → alveolar pressure decreases.

Chest volume decreases → alveolar pressure increases.

Alveolar pressure below atmospheric → air enters.

Alveolar pressure above atmospheric → air exits.

Bronchoconstriction → resistance increases.

Bronchodilation → resistance decreases.

Surfactant decreases → surface tension increases → collapse risk.

Compliance decreases → lung becomes harder to expand.

Elastic recoil decreases → air trapping increases.

Normal negative pleural pressure disrupted → lung may collapse.

CO₂ increases → ventilation usually increases.

Hypoventilation → CO₂ increases → pH decreases.

Hyperventilation → CO₂ decreases → pH increases.

Ventilation without enough pulmonary perfusion → inefficient gas exchange.

Very shallow breaths → more dead-space ventilation relative to tidal volume.

38. Common TEAS Mistakes

Incorrect: Diaphragm moves up during inhalation.

Correct: It contracts and moves down.

Incorrect: Quiet expiration always requires muscle contraction.

Correct: Normally passive due to elastic recoil.

Incorrect: Increased lung volume increases alveolar pressure.

Correct: Increased volume decreases pressure.

Incorrect: Air enters because alveolar pressure rises.

Correct: Air enters when alveolar pressure falls below atmospheric pressure.

Incorrect: All airways exchange gases.

Correct: Conducting airways transport air; respiratory zone exchanges gases.

Incorrect: Terminal bronchioles are the main exchange sites.

Correct: Respiratory bronchioles begin the respiratory zone; alveoli are the main exchange sites.

Incorrect: Type I alveolar cells produce surfactant.

Correct: Type II cells produce surfactant.

Incorrect: Surfactant increases surface tension.

Correct: It decreases surface tension.

Incorrect: Both lungs have 3 lobes.

Correct: Right has 3, left has 2.

Incorrect: Left main bronchus is more vertical.

Correct: Right main bronchus is generally more vertical.

Incorrect: Pneumothorax means pleural fluid.

Correct: Pneumothorax = air; effusion = fluid.

Incorrect: High compliance always means healthy lungs.

Correct: Emphysema can cause high compliance with poor recoil.

Incorrect: Ordinary spirometry measures RV directly.

Correct: RV remains in lungs and cannot be measured directly with ordinary spirometry.

Incorrect: Faster breathing always gives more alveolar ventilation.

Correct: Small breaths may waste more air in dead space.

Incorrect: Only low O₂ triggers breathing.

Correct: CO₂-related pH changes are major normal breathing stimuli.

Incorrect: Carotid sinus and carotid bodies do the same thing.

Correct: Sinus = pressure; bodies = chemical changes.

Incorrect: Low tissue O₂ always means inadequate inhalation.

Correct: Gas exchange, perfusion, and hemoglobin also affect oxygen delivery.

39. Important Formulas

Boyle's law:

P₁V₁ = P₂V₂

Minute ventilation:

VE = RR × TV

Alveolar ventilation:

VA = (TV − VD) × RR

Inspiratory capacity:

IC = TV + IRV

Vital capacity:

VC = IRV + TV + ERV

Functional residual capacity:

FRC = ERV + RV

Total lung capacity:

TLC = IRV + TV + ERV + RV

Transpulmonary pressure:

Ptp = Palv − Ppl

Formula Memory Guide

• TV: Normal breath.

• IRV: Extra inhaled air.

• ERV: Extra exhaled air.

• RV: Air remaining after maximum exhalation.

• VC: Everything you can move in/out.

• TLC: All air, including RV.

• FRC: Air left after normal exhalation.

• VE: Total air moved per minute.

• VA: Fresh air reaching functioning alveoli per minute.

 

G. UNDERSTANDING CHECK

Before the practice exam, explain these without looking at your notes.

1. Why does moving the diaphragm downward cause inhalation?

Because diaphragm contraction increases thoracic and lung volume, lowering alveolar pressure below atmospheric pressure so air enters.

2. Why does surfactant make breathing easier?

It decreases alveolar surface tension, making alveoli easier to inflate and less likely to collapse.

3. Why can a pneumothorax collapse a lung?

Air in the pleural cavity disrupts the normal pressure difference that holds the lung expanded.

4. Why does emphysema cause air trapping?

Damage to elastic tissue reduces lung recoil, making expiration less effective.

5. Why can identical minute ventilation produce different alveolar ventilation?

A greater proportion of shallow breaths remains in dead space, so less fresh air reaches alveoli.

6. Why can CO₂ stimulate breathing even when O₂ is normal?

CO₂ changes CSF pH, stimulating central chemoreceptors and increasing ventilation.

RESPIRATORY SYSTEM II: GAS EXCHANGE, OXYGEN TRANSPORT & ACID–BASE BALANCE

START HERE: HOW EVERYTHING CONNECTS

The respiratory system doesn't just move air. Its main purpose is to exchange gases so cells can make energy and eliminate waste.

The entire process:

1. Ventilation: Air containing O₂ reaches the alveoli.

2. External respiration: O₂ enters pulmonary blood; CO₂ enters alveoli.

3. Transport: Hemoglobin carries O₂ through the bloodstream.

4. Internal respiration: O₂ leaves blood and enters body tissues.

5. Cellular respiration: Cells use O₂ to produce ATP and release CO₂.

6. CO₂ transport: Blood carries CO₂ back to the lungs.

7. Exhalation: CO₂ leaves the body.

Remember:

• Lungs = exchange gases.

• Heart = transports blood.

• Hemoglobin = carries most O₂.

• Cells = use O₂ to produce ATP.

• Kidneys + lungs = help regulate blood pH.

The main idea behind nearly every question in this lesson is:

Gases move according to partial-pressure gradients, and the body adjusts ventilation and blood flow to make that exchange effective.

 

A. GAS EXCHANGE — HOW OXYGEN ENTERS BLOOD

1. Ventilation vs. Respiration

These terms describe different steps.

Term	Meaning
Pulmonary ventilation	Air moves in/out of lungs
External respiration	Gas exchange between alveoli and pulmonary blood
Internal respiration	Gas exchange between systemic blood and tissues
Cellular respiration	Cells produce ATP, often using O₂

Example:

You inhale → O₂ reaches alveoli → enters blood → reaches muscle → muscle cells use it.

TEAS TRAP: Moving air into the lungs does not automatically mean oxygen reaches body tissues. Gas exchange and blood circulation must also work.

2. External Respiration

External respiration = O₂ and CO₂ exchange between alveoli and pulmonary capillaries.

Oxygen:

Alveolar air → pulmonary capillary blood.

Carbon dioxide:

Pulmonary capillary blood → alveolar air.

Why does this happen?

Each gas diffuses from an area of higher partial pressure to lower partial pressure.

No ATP is required for this simple diffusion.

Blood Flow Connection

Right ventricle

→ Pulmonary arteries

→ Pulmonary capillaries

→ Gas exchange

→ Pulmonary veins

→ Left atrium.

Important:

• Pulmonary arteries bring relatively O₂-poor blood to lungs.

• Pulmonary veins return O₂-rich blood to heart.

3. Internal Respiration

Internal respiration = gas exchange between systemic capillaries and body tissues.

Oxygen:

Blood → tissue fluid → cells.

Carbon dioxide:

Cells → tissue fluid → blood.

Why?

Cells continuously use O₂ and produce CO₂.

Therefore:

• Cells usually have lower O₂ partial pressure than arterial blood.

• Cells usually have higher CO₂ partial pressure than incoming arterial blood.

TEAS TRAP:

• External respiration happens at lungs.

• Internal respiration happens at tissues.

4. Respiratory Membrane

Respiratory membrane = thin barrier separating alveolar air from pulmonary blood.

O₂ must cross this barrier to enter blood.

Layers, in simplified order:

Alveolar air

→ Alveolar fluid/surfactant layer

→ Type I alveolar epithelium

→ Fused or closely apposed basement membranes

→ Capillary endothelium

→ Blood plasma

→ Red blood cells.

Designed for fast diffusion because it has:

• Extremely thin walls.

• Large surface area.

• Many nearby capillaries.

• Moist surfaces.

Type I alveolar cells: Main thin gas-exchange lining.

Type II alveolar cells: Produce surfactant.

Alveolar macrophages: Remove debris and pathogens.

Why Thickness Matters

Normal membrane → short diffusion distance → efficient gas exchange.

Thickened membrane → longer diffusion distance → slower gas movement.

Example: Pulmonary fibrosis can thicken the exchange barrier.

5. Diffusion

Diffusion = movement from higher to lower concentration or partial pressure.

Respiratory gases diffuse based on partial-pressure differences.

O₂:

• Higher PO₂ in alveoli.

• Lower PO₂ in incoming pulmonary blood.

• O₂ moves into blood.

CO₂:

• Higher PCO₂ in incoming pulmonary blood.

• Lower PCO₂ in alveoli.

• CO₂ moves into alveoli.

Diffusion is passive: It does not directly require cellular ATP.

6. Partial Pressure

Partial pressure = pressure exerted by one gas in a mixture.

Abbreviations:

• PO₂ = partial pressure of oxygen.

• PCO₂ = partial pressure of carbon dioxide.

• PaO₂ = arterial oxygen partial pressure.

• PaCO₂ = arterial carbon dioxide partial pressure.

Key rule:

Higher partial pressure → lower partial pressure.

Typical Values at Rest, Near Sea Level

Location	PO₂	PCO₂
Alveolar air	~104 mmHg	~40 mmHg
Blood entering pulmonary capillaries	~40 mmHg	~45 mmHg
Systemic arterial blood	~95–100 mmHg	~40 mmHg
Systemic venous blood	~40 mmHg	~45 mmHg

These are approximate teaching values and vary with physiology and environment.

Understand the Numbers

Oxygen:

Alveoli = 104 mmHg.

Incoming blood = 40 mmHg.

104 > 40 → O₂ diffuses into blood.

Carbon dioxide:

Incoming blood = 45 mmHg.

Alveoli = 40 mmHg.

45 > 40 → CO₂ diffuses into alveoli.

Important: CO₂ has a much smaller pressure gradient than O₂ but is far more soluble, allowing effective exchange.

7. Dalton's Law

Dalton's law: Total gas pressure equals the sum of individual gas partial pressures.

Formula:

Ptotal = P₁ + P₂ + P₃ + ...

Dry atmospheric air at sea level is approximately:

• 78% nitrogen.

• 21% oxygen.

• 0.04% carbon dioxide.

• Small amounts of other gases.

Total atmospheric pressure ≈ 760 mmHg.

Example

O₂ makes up about 21% of dry atmospheric air.

PO₂ ≈ 0.21 × 760 = 160 mmHg.

Why is alveolar PO₂ lower (~104 mmHg)?

Because:

1. Inhaled air becomes humidified.

2. O₂ continuously enters blood.

3. CO₂ enters the alveoli.

4. Fresh air mixes with existing alveolar gas.

TEAS TRAP: Atmospheric PO₂ and alveolar PO₂ are not identical.

8. Henry's Law

Henry's law: The amount of gas dissolved in a liquid depends on its partial pressure and solubility.

Simple relationship:

↑ Gas partial pressure → more gas dissolves, if other factors stay constant.

Example:

• Higher O₂ partial pressure can increase dissolved blood O₂.

• CO₂ is much more soluble than O₂.

Advanced connection: Deep-sea divers breathing compressed gas dissolve more nitrogen into tissues. If pressure decreases too quickly, nitrogen bubbles may form, causing decompression sickness.

TEAS TRAP: Dalton's law explains partial pressures in gas mixtures; Henry's law explains gas dissolution in liquids.

9. Fick's Law — What Controls Diffusion Speed?

Gas exchange is influenced by:

• Surface area.

• Membrane thickness.

• Partial-pressure gradient.

• Gas diffusion properties.

Main relationships:

↑ Surface area → ↑ Diffusion.

↑ Pressure gradient → ↑ Diffusion.

↑ Membrane thickness → ↓ Diffusion.

Examples

Emphysema: Alveolar walls are destroyed → ↓ surface area → less efficient exchange.

Pulmonary fibrosis: Membranes thicken → ↑ diffusion distance → slower exchange.

Pulmonary edema: Fluid increases the diffusion barrier and may impair ventilation.

Exercise: More pulmonary capillaries are recruited and exchange capacity can increase.

TEAS TRAP: Problems with lung gas exchange can occur even when air enters the lungs normally.

10. Why CO₂ Diffuses Efficiently

CO₂ is roughly 20 times more soluble than O₂ in biological fluids.

Therefore, CO₂ can diffuse effectively despite a smaller partial-pressure gradient.

O₂ gradient across lungs: Approximately 104 − 40 = 64 mmHg.

CO₂ gradient: Approximately 45 − 40 = 5 mmHg.

Important: Efficient CO₂ exchange depends on solubility as well as partial pressure.

11. Diffusion vs. Perfusion Limitations

Gas exchange can be limited by different problems.

Diffusion limitation:

• Gas has difficulty crossing the membrane.

• Examples: Fibrosis; severe interstitial disease.

Perfusion limitation:

• Blood flow is insufficient to carry additional gas away.

• Example: Inadequate pulmonary blood flow.

Ventilation limitation:

• Insufficient fresh air reaches alveoli.

• Examples: Severe airway obstruction or hypoventilation.

Main idea: Normal oxygenation requires ventilation, diffusion, and blood flow.

B. VENTILATION–PERFUSION MATCHING (V/Q)

12. What Are Ventilation and Perfusion?

Ventilation (V): Air reaching alveoli.

Perfusion (Q): Blood flowing through pulmonary capillaries.

For effective gas exchange, the lungs need BOTH.

Easy comparison:

• Ventilation delivers O₂ to alveoli.

• Perfusion brings blood to collect O₂.

Example

An alveolus contains oxygen, but no blood reaches it.

Result: O₂ cannot be carried away effectively.

Another alveolus receives blood, but no fresh air enters.

Result: Blood cannot receive enough O₂.

TEAS TRAP: Adequate ventilation alone does not guarantee efficient gas exchange.

13. V/Q Ratio

V/Q ratio = alveolar ventilation ÷ pulmonary blood flow.

Typical whole-lung resting values:

• Alveolar ventilation ≈ 4 L/min.

• Pulmonary perfusion ≈ 5 L/min.

V/Q ≈ 4 ÷ 5 = 0.8.

This is an approximate whole-lung average; individual regions differ.

Understand the Ratio

Normal matching: Air and blood flow are reasonably balanced.

Low V/Q: Too little ventilation relative to blood flow.

High V/Q: Too little blood flow relative to ventilation.

Important: V/Q does not have to equal exactly 1.0 for normal function.

14. Low V/Q — Not Enough Air

Low V/Q = ventilation is low compared with perfusion.

Blood continues entering pulmonary capillaries, but too little fresh air reaches the alveoli.

Examples:

• Asthma with airway narrowing.

• Pneumonia filling alveoli with inflammatory material.

• Some regions affected by COPD.

• Mucus obstruction.

Sequence:

↓ Air reaching alveoli

→ O₂ in alveoli falls

→ Blood receives less O₂

→ Hypoxemia may develop.

Extreme Low V/Q = Shunt-Like Physiology

If blood flows past alveoli receiving NO effective ventilation:

V = 0, Q > 0.

V/Q = 0.

This acts as a pulmonary shunt.

Shunt: Blood passes through pulmonary circulation without becoming adequately oxygenated.

TEAS TRAP: Low V/Q is primarily a ventilation problem relative to blood flow.

15. High V/Q — Not Enough Blood Flow

High V/Q = ventilation is high relative to perfusion.

Air reaches alveoli, but little blood is available for exchange.

Example: Pulmonary embolism obstructing pulmonary blood flow.

Sequence:

Pulmonary vessel blocked

→ ↓ Blood reaching alveoli

→ Alveoli may still receive air

→ Ventilation is wasted.

Extreme High V/Q = Dead Space

If an alveolus receives air but NO blood:

V > 0, Q = 0.

V/Q approaches infinity.

This is alveolar dead space.

TEAS TRAP: A pulmonary embolism primarily affects perfusion, not necessarily air entry into alveoli.

16. Shunt vs. Dead Space

Shunt	Dead Space
Blood without effective ventilation	Ventilation without effective blood flow
V/Q = 0 at extreme	V/Q approaches infinity at extreme
Example: fully obstructed/filled alveoli with preserved blood flow	Example: completely unperfused alveoli
Blood doesn't receive enough O₂	Air is not effectively used for gas exchange

Memory:

Shunt = blood goes past without enough AIR.

Dead space = AIR goes in without enough BLOOD.

Advanced: Significant true shunts respond less effectively to supplemental O₂ than ordinary low-V/Q regions because some blood bypasses ventilated alveoli.

17. Pulmonary Blood Flow Regulation

The lungs can redirect blood away from poorly ventilated areas.

Hypoxic pulmonary vasoconstriction:

Low alveolar O₂

→ Nearby pulmonary arterioles constrict

→ Blood is redirected toward better-ventilated alveoli

→ V/Q matching can improve.

Why This Is Important

In the lungs, localized low O₂ often causes pulmonary vasoconstriction.

In many systemic tissues, low O₂ promotes vasodilation to deliver more blood.

TEAS TRAP: Low oxygen has different effects on pulmonary versus many systemic vessels.

Advanced: If widespread lung regions become hypoxic, pulmonary vasoconstriction can raise pulmonary arterial pressure and increase right ventricular workload.

18. Effects of Gravity on Lung Perfusion

When standing upright:

• Both ventilation and perfusion generally increase toward lung bases.

• Perfusion increases more strongly than ventilation.

• V/Q is usually higher at lung apices and lower at bases.

Important: This is a normal regional difference, not automatically a disease.

 

C. OXYGEN TRANSPORT

19. How Oxygen Travels Through the Body

Complete oxygen pathway:

Alveoli

→ Pulmonary capillaries

→ RBC hemoglobin

→ Pulmonary veins

→ Left atrium

→ Left ventricle

→ Aorta

→ Systemic arteries

→ Tissue capillaries

→ Body cells

→ Mitochondria use O₂ for aerobic ATP production.

Most O₂ travels attached to hemoglobin, not freely dissolved in plasma.

20. Hemoglobin (Hb)

Hemoglobin = iron-containing protein inside RBCs that carries oxygen.

Each hemoglobin molecule contains:

• 4 globin chains.

• 4 heme groups.

• 1 Fe²⁺ ion per heme.

Each heme binds 1 O₂ molecule.

Therefore, one Hb can bind up to 4 O₂ molecules.

Two Important Forms

Oxyhemoglobin: Hb with O₂ bound.

Deoxyhemoglobin: Hb with less or no O₂ bound.

Oxygen binding is reversible.

In lungs: Hb binds O₂.

In tissues: Hb releases O₂.

21. Hemoglobin Saturation

Oxygen saturation (SaO₂): Percentage of hemoglobin O₂-binding sites occupied.

Example:

98% saturation means about 98% of available Hb O₂-binding sites are occupied.

Important: Saturation does NOT tell you how much total hemoglobin is present.

Example

Patient A has normal Hb and 98% saturation.

Patient B has severe anemia and 98% saturation.

Both have similar saturation, but Patient B carries much less TOTAL oxygen because there is less hemoglobin.

TEAS TRAP: Normal oxygen saturation does not always mean adequate tissue oxygen delivery.

22. PaO₂ vs. SaO₂ vs. Oxygen Content

Measurement	What it tells you
PaO₂	Pressure of O₂ dissolved in arterial blood
SaO₂	% of Hb O₂-binding sites occupied
SpO₂	Estimated saturation from pulse oximeter
Oxygen content (CaO₂)	Total amount of O₂ in arterial blood

Key Difference

PaO₂: Dissolved oxygen pressure.

SaO₂: Hemoglobin saturation.

CaO₂: Actual total oxygen carried per volume of blood.

Most CaO₂ comes from hemoglobin-bound O₂.

Example: Severe anemia may cause low CaO₂ with a normal PaO₂ and SaO₂.

23. Hemoglobin–Oxygen Dissociation Curve

The curve shows how Hb saturation changes with PO₂.

Shape: S-shaped (sigmoidal).

Why? Cooperative binding.

When one O₂ binds to hemoglobin, it becomes easier for additional O₂ molecules to bind.

Two Important Regions

High PO₂ in lungs:

• Hb becomes highly saturated.

• Curve approaches a plateau.

• Provides a margin of protection against moderate PO₂ decreases.

Lower PO₂ in tissues:

• Hb releases O₂ more readily.

• The steeper region supports unloading when tissues consume O₂.

TEAS TRAP: Hemoglobin does not release all its O₂ at once.

24. Right Shift — More Oxygen Release

Right shift = lower Hb affinity for oxygen.

Hemoglobin releases O₂ more easily at a given PO₂.

Causes:

• ↑ CO₂.

• ↑ H⁺ / ↓ pH.

• ↑ Temperature.

• ↑ 2,3-BPG.

Example: Exercising Muscle

Muscle works harder

→ Uses more O₂

→ Produces more CO₂ and heat

→ H⁺ increases

→ Hb affinity decreases

→ More O₂ released to muscle.

Memory: Right shift = RELEASE oxygen.

25. Left Shift — Oxygen Held More Tightly

Left shift = higher Hb affinity for oxygen.

Hb binds O₂ more tightly and releases less at a given PO₂.

Causes:

• ↓ CO₂.

• ↓ H⁺ / ↑ pH.

• ↓ Temperature.

• ↓ 2,3-BPG.

• Fetal hemoglobin (HbF) compared with adult Hb.

Fetal Hemoglobin

HbF has higher O₂ affinity than adult hemoglobin.

Why? Helps fetal blood obtain O₂ from maternal circulation across the placenta.

TEAS TRAP: Higher Hb affinity is not always better for tissues. Hb must also be able to release its oxygen.

26. Bohr Effect

Bohr effect = increased CO₂ and H⁺ reduce Hb's affinity for O₂.

In active tissues:

↑ CO₂ + ↑ H⁺

→ Hb affinity decreases

→ O₂ unloading increases.

This helps deliver extra O₂ where metabolism is high.

Short memory: Bohr effect = CO₂/H⁺ help Hb release O₂.

27. Oxygen Delivery

Oxygen delivery depends on TWO major components:

1. Cardiac output (blood flow).

2. Blood oxygen content.

Relationship:

O₂ delivery = Cardiac output × arterial O₂ content.

If cardiac output is in L/min and arterial O₂ content is in mL/dL, multiply by 10 for matching units.

Why This Matters

Even if lungs oxygenate blood normally, cells may receive inadequate O₂ if:

• Cardiac output is too low.

• Hemoglobin is too low.

• Blood cannot reach the tissues.

Advanced equation:

CaO₂ ≈ (1.34 × Hb × SaO₂) + (0.003 × PaO₂)

Hb in g/dL; SaO₂ expressed as a decimal.

The first term represents Hb-bound O₂. The second represents dissolved O₂.

Priority for TEAS: Understand how hemoglobin, saturation, and cardiac output affect delivery. Memorizing every constant is lower priority.

28. Hypoxemia vs. Hypoxia

These terms are not identical.

Hypoxemia: Abnormally low oxygen level in arterial blood, typically judged by PaO₂.

Hypoxia: Inadequate oxygen availability/use at the tissue level.

Examples

Severe lung disease:

Poor gas exchange → ↓ PaO₂ → hypoxemia → possible tissue hypoxia.

Severe anemia:

Low Hb → low O₂ content → possible tissue hypoxia even if PaO₂ is normal.

Low cardiac output:

Less oxygenated blood delivered → possible tissue hypoxia even if lungs function normally.

Carbon monoxide exposure:

CO binds Hb strongly → decreases effective O₂ carrying capacity and impairs unloading → tissue hypoxia.

TEAS TRAP: Normal PaO₂ does NOT rule out tissue hypoxia.

29. Pulse Oximetry vs. Arterial Blood Gas

Pulse oximeter:

• Noninvasive.

• Estimates SpO₂.

• Does NOT directly measure PaCO₂, pH, or hemoglobin concentration.

• Does not determine tissue oxygen delivery.

Arterial blood gas (ABG):

• Measures arterial pH.

• Measures PaCO₂.

• Measures PaO₂.

• Often reports calculated HCO₃⁻ and saturation.

Limitations of Pulse Oximetry

Readings may be affected by:

• Poor peripheral perfusion.

• Motion.

• Nail products.

• Device factors.

• Certain abnormal hemoglobins.

• Skin pigmentation can affect accuracy, particularly at lower saturations.

Important: Standard pulse oximetry can be misleading during carbon monoxide poisoning because it may mistake carboxyhemoglobin for oxyhemoglobin.

TEAS TRAP: A normal SpO₂ does not guarantee that hemoglobin concentration or cardiac output is normal.

30. Cyanosis

Cyanosis = bluish discoloration caused by increased deoxygenated hemoglobin in tissues/blood.

Possible sites:

• Lips.

• Tongue.

• Nail beds.

• Skin.

Important: Cyanosis is not a reliable measure of oxygenation by itself.

Severe anemia may make cyanosis difficult to detect even during significant hypoxemia.

 

D. CARBON DIOXIDE TRANSPORT

31. Where Does CO₂ Come From?

Cells produce CO₂ during aerobic metabolism.

Pathway:

Cells produce CO₂

→ CO₂ diffuses into systemic capillaries

→ Blood carries CO₂ to lungs

→ CO₂ enters alveoli

→ Exhalation removes it.

CO₂ is important because it affects blood pH.

32. Three Forms of CO₂ Transport

Transport form	Approximate proportion
Bicarbonate (HCO₃⁻)	~70%
Bound to hemoglobin/proteins	~20–25%
Dissolved in plasma	~5–10%

Percentages vary with physiology.

Most CO₂ is transported as bicarbonate.

33. Bicarbonate Formation in RBCs

CO₂ enters RBC

→ Combines with water

→ Forms carbonic acid

→ Carbonic acid separates into H⁺ and HCO₃⁻.

Equation:

CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻

Carbonic anhydrase: Enzyme inside RBCs that rapidly catalyzes the reaction.

In systemic tissues: CO₂ is converted largely into bicarbonate for transport.

34. Chloride Shift

As HCO₃⁻ leaves an RBC, Cl⁻ enters.

Why? Helps maintain electrical charge balance.

In tissues:

CO₂ enters RBC

→ HCO₃⁻ forms

→ HCO₃⁻ moves into plasma

→ Cl⁻ enters RBC.

In lungs: The exchange reverses so bicarbonate can be converted back into CO₂.

TEAS TRAP: The chloride shift helps CO₂ transport; it is not the same as oxygen binding to hemoglobin.

35. What Happens to CO₂ in Lungs?

In pulmonary capillaries:

HCO₃⁻ enters RBC

→ Combines with H⁺

→ Forms H₂CO₃

→ Carbonic anhydrase helps convert it into CO₂ + H₂O

→ CO₂ diffuses into alveoli

→ CO₂ is exhaled.

Key idea: The bicarbonate reaction is reversible.

36. Haldane Effect

Haldane effect: The oxygenation state of hemoglobin affects CO₂ and H⁺ transport.

In tissues:

Hb releases O₂

→ Deoxygenated Hb can carry more CO₂ and buffer more H⁺

→ Helps collect CO₂ from tissues.

In lungs:

Hb binds O₂

→ Hb releases CO₂ and H⁺ more readily

→ CO₂ is exhaled.

Bohr vs. Haldane

Bohr effect: CO₂/H⁺ affect Hb's O₂ binding.

Haldane effect: O₂ binding affects Hb's CO₂/H⁺ carrying ability.

Memory:

Bohr = CO₂ changes O₂ unloading.

Haldane = O₂ changes CO₂ transport.

E. RESPIRATORY CONTROL OF BLOOD pH

37. Normal Blood pH

Normal arterial pH is approximately:

7.35–7.45

• Below 7.35 = acidemia.

• Above 7.45 = alkalemia.

pH is inversely related to H⁺ concentration.

↑ H⁺ → ↓ pH (more acidic).

↓ H⁺ → ↑ pH (more alkaline).

Important: pH is logarithmic, so relatively small changes represent meaningful changes in hydrogen-ion concentration.

38. Why CO₂ Affects pH

Recall the bicarbonate reaction:

CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻

When CO₂ Increases

↑ CO₂

→ ↑ Carbonic acid formation

→ ↑ H⁺

→ ↓ pH.

When CO₂ Decreases

↓ CO₂

→ ↓ Carbonic acid/H⁺

→ ↑ pH.

Memory: CO₂ acts like an acid in blood chemistry.

39. Buffers

Buffer = substance that resists large changes in pH.

Main buffer systems:

• Bicarbonate/carbonic acid.

• Proteins, including hemoglobin.

• Phosphate.

Bicarbonate Buffer System

HCO₃⁻ helps accept excess H⁺.

The bicarbonate system links blood chemistry to:

• Lungs, which regulate CO₂.

• Kidneys, which regulate HCO₃⁻ and H⁺.

Why this matters: Blood pH can be affected by both breathing problems and metabolic problems.

40. Lungs vs. Kidneys in pH Regulation

Lungs	Kidneys
Control CO₂ removal	Control H⁺ excretion and HCO₃⁻ balance
Can respond within minutes	Major adjustments take hours to days
Respiratory component	Metabolic/renal component

Lungs:

↑ Ventilation → ↓ CO₂ → ↑ pH.

↓ Ventilation → ↑ CO₂ → ↓ pH.

Kidneys:

• Excrete H⁺.

• Reabsorb filtered bicarbonate.

• Generate new bicarbonate when needed.

Important: Chemical buffers act quickly, but cannot eliminate the underlying excess acid or base from the body.

41. Respiratory Acidosis

Definition: Primary increase in PaCO₂ causes decreased blood pH.

Main cause: Inadequate effective alveolar ventilation.

Sequence:

Hypoventilation

→ CO₂ retention

→ ↑ PaCO₂

→ ↑ H⁺

→ ↓ pH

→ Respiratory acidosis.

Possible Causes

• Severe COPD with CO₂ retention.

• Medication-induced respiratory depression.

• Severe neuromuscular weakness.

• Inadequate ventilation from respiratory failure.

Expected ABG

• pH ↓.

• PaCO₂ ↑.

• HCO₃⁻ may increase if kidneys compensate.

Compensation: Kidneys increase bicarbonate retention/generation and H⁺ excretion over time.

42. Respiratory Alkalosis

Definition: Primary decrease in PaCO₂ causes increased blood pH.

Main cause: Excessive alveolar ventilation relative to CO₂ production.

Sequence:

Hyperventilation

→ Too much CO₂ removed

→ ↓ PaCO₂

→ ↓ H⁺

→ ↑ pH

→ Respiratory alkalosis.

Possible Causes

• Anxiety-related hyperventilation.

• High altitude.

• Fever.

• Some pulmonary embolisms.

• Certain early stages of respiratory illness.

Expected ABG

• pH ↑.

• PaCO₂ ↓.

• HCO₃⁻ may decrease if kidneys compensate.

Compensation: Kidneys excrete more bicarbonate over time.

Important: Hyperventilation can also be a response to a metabolic problem; the breathing pattern alone does not identify the primary disorder.

43. Metabolic Acidosis

Definition: Primary decrease in bicarbonate or increase in nonvolatile acid causes decreased pH.

Common Causes

• Diabetic ketoacidosis (DKA).

• Lactic acidosis.

• Severe kidney dysfunction.

• Bicarbonate loss from diarrhea.

Expected ABG

• pH ↓.

• HCO₃⁻ ↓.

• PaCO₂ often ↓ if respiratory compensation occurs.

Compensation

↓ HCO₃⁻ / ↑ Acids

→ pH falls

→ Breathing becomes deeper/faster

→ More CO₂ removed

→ pH moves toward normal.

Kussmaul breathing: Deep, often rapid breathing associated with marked metabolic acidosis, classically DKA.

TEAS TRAP: Fast/deep breathing in DKA is usually a compensatory response, not primary respiratory alkalosis.

44. Metabolic Alkalosis

Definition: Primary increase in bicarbonate or loss of acid causes increased pH.

Common Causes

• Prolonged vomiting with loss of gastric acid.

• Some diuretic effects.

• Certain states of excess mineralocorticoid activity.

Expected ABG

• pH ↑.

• HCO₃⁻ ↑.

• PaCO₂ may ↑ due to respiratory compensation.

Compensation

↑ pH

→ Ventilation may decrease

→ CO₂ retained

→ H⁺ tends to increase

→ pH moves toward normal.

Limitation: The body cannot safely decrease ventilation indefinitely because it must still maintain adequate oxygenation.

45. All Four Acid–Base Disorders

Disorder	Primary change	pH	Compensation
Respiratory acidosis	↑ PaCO₂	↓	Kidneys retain/generate HCO₃⁻
Respiratory alkalosis	↓ PaCO₂	↑	Kidneys excrete HCO₃⁻
Metabolic acidosis	↓ HCO₃⁻	↓	Lungs exhale more CO₂
Metabolic alkalosis	↑ HCO₃⁻	↑	Lungs retain more CO₂

Core rule:

Respiratory problems = primary CO₂ changes.

Metabolic problems = primary bicarbonate/acid changes.

46. Compensation vs. Correction

Compensation: Another system responds to the original disorder.

Examples:

• Respiratory acidosis → kidneys conserve more bicarbonate.

• Metabolic acidosis → lungs remove more CO₂.

Important distinctions:

• Compensation reduces the pH disturbance.

• Compensation does not necessarily remove the original cause.

• Compensation can be partial or substantial.

• Mixed acid–base disorders can occur.

• Respiratory compensation is relatively fast.

• Renal compensation is slower.

Advanced TEAS trap: A normal pH does not prove that PaCO₂ and bicarbonate are normal.

F. ARTERIAL BLOOD GASES (ABGs)

47. Normal ABG Values

Measurement	Approximate reference
pH	7.35–7.45
PaCO₂	35–45 mmHg
HCO₃⁻	22–26 mEq/L
PaO₂	~80–100 mmHg near sea level, varies with age
SaO₂	Often ~95–100% in healthy individuals near sea level

PaO₂ and saturation references depend on age, altitude, and clinical circumstances.

Prioritize these three for acid–base questions:

pH = 7.35–7.45.

PaCO₂ = 35–45.

HCO₃⁻ = 22–26.

48. How to Interpret an ABG

Use three steps.

STEP 1: Check pH

pH below 7.35 → acidemia.

pH above 7.45 → alkalemia.

STEP 2: Check PaCO₂

PaCO₂ ↑ → pushes pH DOWN.

PaCO₂ ↓ → pushes pH UP.

STEP 3: Check HCO₃⁻

HCO₃⁻ ↓ → pushes pH DOWN.

HCO₃⁻ ↑ → pushes pH UP.

Determine which change explains the pH disturbance.

Remember:

CO₂ moves opposite to pH.

HCO₃⁻ usually moves in the same direction as pH.

Then check whether the other variable is compensating.

49. ABG Example — Respiratory Acidosis

Values:

• pH = 7.28.

• PaCO₂ = 55.

• HCO₃⁻ = 25.

Step 1: pH low → acidemia.

Step 2: CO₂ high → acidifying.

Step 3: Bicarbonate roughly normal.

Answer: Primary respiratory acidosis, with little/no evident metabolic compensation.

50. ABG Example — Respiratory Alkalosis

Values:

• pH = 7.49.

• PaCO₂ = 30.

• HCO₃⁻ = 23.

Step 1: pH high → alkalemia.

Step 2: CO₂ low → alkalinizing.

Step 3: Bicarbonate roughly normal.

Answer: Primary respiratory alkalosis, with little/no evident metabolic compensation.

51. ABG Example — Metabolic Acidosis

Values:

• pH = 7.25.

• PaCO₂ = 30.

• HCO₃⁻ = 13.

Step 1: pH low → acidemia.

Step 2: CO₂ low → would raise pH.

Step 3: HCO₃⁻ low → lowers pH.

Answer: Primary metabolic acidosis with respiratory compensation.

Why? The lungs are lowering CO₂ to oppose the acidic pH.

52. ABG Example — Metabolic Alkalosis

Values:

• pH = 7.50.

• PaCO₂ = 48.

• HCO₃⁻ = 36.

Step 1: pH high → alkalemia.

Step 2: CO₂ high → would lower pH.

Step 3: HCO₃⁻ high → raises pH.

Answer: Primary metabolic alkalosis with respiratory compensation.

Advanced note: The complete assessment of compensation may require predicted compensation calculations, clinical history, and evaluation for mixed disorders.

G. RESPIRATORY DISORDERS — APPLY THE SCIENCE

53. Pneumonia

Pneumonia = infection/inflammation of lung tissue, often involving alveoli.

Possible effects:

• Alveoli fill with inflammatory fluid/material.

• Less air reaches affected exchange surfaces.

• O₂ diffusion and V/Q matching worsen.

• Hypoxemia may develop.

Sequence:

Alveoli become fluid-filled

→ ↓ Ventilation to affected regions

→ Continued perfusion

→ Low V/Q or shunt-like physiology

→ ↓ Blood oxygenation.

TEAS TRAP: Pneumonia affects alveolar gas exchange, not just the upper airway.

54. Asthma

Asthma = variable airway inflammation and narrowing, often reversible.

Major mechanisms:

• Bronchoconstriction.

• Airway inflammation.

• Increased mucus.

Effects:

• ↑ Airway resistance.

• Airflow limitation, especially expiration.

• Possible air trapping.

• Uneven ventilation → V/Q mismatch.

Medication concept: β₂-agonists relax bronchial smooth muscle.

Important: Severe asthma can impair both oxygenation and CO₂ removal, particularly when ventilation becomes inadequate.

55. COPD and Emphysema

COPD = chronic airflow limitation, commonly involving chronic bronchitis and/or emphysema.

Chronic Bronchitis

Typical features:

• Chronic airway inflammation.

• Excess mucus.

• Productive cough.

• Airflow limitation.

Emphysema

Typical features:

• Destruction of alveolar walls.

• ↓ Surface area for diffusion.

• Loss of elastic recoil.

• Air trapping.

• Often increased lung compliance.

Why gas exchange worsens:

Less alveolar surface area + airflow limitation + V/Q mismatch → impaired oxygenation.

Some patients develop chronic CO₂ retention.

TEAS TRAP: Asthma and COPD are both obstructive, but their mechanisms and reversibility differ.

56. Pulmonary Fibrosis

Fibrosis = lung scarring.

Scar tissue

→ Thickened/stiff lung tissue

→ ↓ Compliance

→ Reduced expansion

→ Impaired diffusion

→ Possible hypoxemia.

Pattern: Restrictive.

Compare:

• Emphysema: loss of alveolar surface area + recoil.

• Fibrosis: thickened membrane + low compliance.

57. Pulmonary Edema

Pulmonary edema = excess fluid in lung interstitial tissue and/or alveoli.

Possible causes include elevated pulmonary capillary pressure from left-sided heart failure.

Sequence:

Poor LV pumping

→ Blood pressure builds upstream in lungs

→ Fluid enters lung tissue

→ Diffusion becomes harder; alveolar ventilation may decrease

→ Oxygenation worsens.

Important: Pulmonary edema is fluid accumulation; it is not synonymous with pneumonia.

58. Pulmonary Embolism (PE)

Pulmonary embolism = blockage in pulmonary circulation, commonly from a clot originating in deep veins.

Sequence:

Clot blocks pulmonary artery branch

→ ↓ Blood flow to affected alveoli

→ Ventilation may continue

→ High V/Q / increased dead space

→ Inefficient gas exchange.

TEAS TRAP: PE primarily blocks blood flow, not the trachea or bronchi.

A large PE can also strain the right ventricle and decrease cardiac output.

59. Acute Respiratory Distress Syndrome (ARDS)

ARDS = severe inflammatory lung injury causing impaired oxygenation.

Features may include:

• Increased alveolar-capillary permeability.

• Protein-rich fluid entering alveoli.

• Reduced compliance.

• Alveolar collapse.

• Severe V/Q mismatch and shunt.

Main result: Oxygen has difficulty reaching arterial blood.

Important: ARDS can cause severe hypoxemia even when oxygen is being supplied.

60. High Altitude

At high altitude:

• The percentage of atmospheric oxygen remains approximately 21%.

• Atmospheric pressure decreases.

• Inspired PO₂ decreases.

• Alveolar PO₂ decreases.

• Less O₂ may enter blood.

Immediate response:

↓ Arterial O₂

→ Peripheral chemoreceptors stimulate ventilation

→ More CO₂ exhaled

→ PaCO₂ decreases

→ Respiratory alkalosis may occur.

Longer-term acclimatization:

• Kidney excretion of bicarbonate helps compensate.

• EPO production can rise, increasing RBC production over time.

• RBC 2,3-BPG may increase, promoting O₂ unloading.

TEAS TRAP: High altitude does not significantly reduce the percentage of oxygen in air; it reduces oxygen partial pressure.

61. Exercise and Gas Exchange

Exercise increases ATP demand.

Active muscles:

• Use more O₂.

• Produce more CO₂.

• Generate more heat.

• May increase H⁺.

Responses:

• Ventilation increases.

• Cardiac output increases.

• More blood flows to active muscles.

• Hemoglobin releases more O₂ to tissues.

• Pulmonary gas-exchange capacity can increase.

Important: Increased breathing during ordinary exercise is often hyperpnea—ventilation rises appropriately to meet metabolic demand.

Hyperventilation means ventilation exceeds what is needed for CO₂ production, causing PaCO₂ to fall.

 

H. DIFFICULT TEAS CONCEPTS

62. Important Cause-and-Effect Relationships

↑ Membrane thickness → ↓ gas diffusion.

↓ Alveolar surface area → ↓ gas exchange.

↑ Alveolar PO₂ → promotes O₂ movement into blood.

↑ Tissue CO₂ → promotes O₂ unloading from Hb.

↑ Temperature/H⁺/CO₂ → right shift → easier O₂ release.

↓ Temperature/H⁺/CO₂ → left shift → tighter O₂ binding.

↓ Alveolar ventilation relative to perfusion → low V/Q.

↓ Pulmonary perfusion relative to ventilation → high V/Q.

No effective alveolar ventilation + continued perfusion → shunt.

No alveolar perfusion + continued ventilation → dead space.

Hypoventilation → ↑ CO₂ → ↓ pH.

Hyperventilation → ↓ CO₂ → ↑ pH.

↓ Bicarbonate → metabolic acidosis tendency.

↑ Bicarbonate → metabolic alkalosis tendency.

↓ Hemoglobin → ↓ total O₂-carrying capacity.

↓ Cardiac output → ↓ tissue O₂ delivery, if other factors remain constant.

63. Common TEAS Traps

Incorrect idea	Correct explanation
Gas exchange requires ATP	O₂ and CO₂ cross by passive diffusion
Gases move down total-pressure gradients only	Each gas follows its own partial-pressure gradient
Atmospheric and alveolar PO₂ are identical	Alveolar PO₂ is lower
CO₂ needs a larger gradient than O₂	CO₂ is much more soluble
Pulmonary embolism mainly blocks airways	It blocks pulmonary blood flow
Low V/Q means too little blood	Low V/Q means too little ventilation relative to blood
High V/Q means too little air	High V/Q means too little perfusion relative to air
Pneumonia always increases V/Q	Pneumonia often creates low-V/Q regions
Oxygen saturation equals oxygen content	Content also depends strongly on Hb
Normal SpO₂ guarantees adequate O₂ delivery	Low Hb or CO can still impair delivery
Right shift means tighter binding	Right shift means easier O₂ unloading
Bohr and Haldane effects mean the same thing	Bohr concerns O₂ affinity; Haldane concerns CO₂/H⁺ carriage
Most CO₂ is carried attached to Hb	Most is carried as bicarbonate
Increased CO₂ makes blood alkaline	Increased CO₂ tends to lower pH
Faster breathing always causes alkalosis	Only excessive ventilation relative to CO₂ production does
Metabolic acidosis is caused by primary CO₂ retention	Metabolic acidosis primarily involves low HCO₃⁻ or excess nonvolatile acid
DKA deep breathing is primary respiratory alkalosis	It is usually compensation for metabolic acidosis
Kidney compensation works immediately	Major renal compensation takes hours to days
High altitude means lower O₂ percentage	O₂ fraction stays about the same; partial pressure falls
Low oxygen always produces low oxygen saturation	Tissue hypoxia can occur with normal saturation if Hb/flow are inadequate

64. Formulas and Values to Know

Dalton's law:

Ptotal = Sum of gas partial pressures.

Approximate dry inspired O₂ partial pressure at sea level:

PO₂ ≈ 0.21 × 760 ≈ 160 mmHg.

Ventilation/perfusion ratio:

V/Q = Alveolar ventilation ÷ Pulmonary perfusion.

Typical average ≈ 0.8.

Oxygen delivery:

DO₂ = Cardiac output × Arterial oxygen content (with matching units).

Bicarbonate reaction:

CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻.

ABG reference values:

• pH: 7.35–7.45.

• PaCO₂: 35–45 mmHg.

• HCO₃⁻: 22–26 mEq/L.

• PaO₂: Approximately 80–100 mmHg near sea level.

High-yield values:

• Alveolar PO₂ ≈ 104 mmHg.

• Incoming pulmonary blood PO₂ ≈ 40 mmHg.

• Alveolar PCO₂ ≈ 40 mmHg.

• Incoming pulmonary blood PCO₂ ≈ 45 mmHg.

These are approximate reference values.