Respiratory System Study Guide

Q: Where does gas exchange actually happen in the lungs?

Gas exchange happens in the alveoli — tiny air sacs at the end of the bronchial tree. Oxygen diffuses from the alveoli into the surrounding pulmonary capillaries, and carbon dioxide diffuses the other way to be exhaled. The alveolar-capillary membrane is extremely thin and surrounded by a dense capillary network to maximize surface area for diffusion.

Q: What does surfactant do?

Surfactant is a phospholipid substance produced by type II alveolar cells. It reduces surface tension inside the alveoli, preventing them from collapsing during exhalation (atelectasis). Premature infants often lack sufficient surfactant, causing respiratory distress syndrome (RDS). Fetal lung maturity is assessed with the L/S (lecithin/sphingomyelin) ratio — a ratio of 2:1 or higher indicates adequate surfactant.

Q: What are normal ABG values?

Normal arterial blood gas (ABG) values: pH 7.35–7.45, PaCO₂ 35–45 mmHg, HCO₃⁻ 22–26 mEq/L, and PaO₂ 80–100 mmHg. A pH below 7.35 is acidosis, above 7.45 is alkalosis. PaCO₂ is the respiratory component — high CO₂ causes acidosis. HCO₃⁻ is the metabolic component — high bicarb causes alkalosis. This is the foundation for ABG interpretation questions on the NCLEX-PN.

Q: How does the diaphragm cause breathing?

During inhalation, the diaphragm contracts and moves downward, increasing the thoracic cavity volume. This drops intrathoracic pressure below atmospheric pressure, and air rushes into the lungs. During exhalation, the diaphragm relaxes and moves upward, intrathoracic pressure rises, and air is pushed out. The diaphragm is innervated by the phrenic nerve, which originates from cervical nerves C3–C5.

Q: What is the difference between ventilation and respiration?

Ventilation is the mechanical movement of air in and out of the lungs (inhalation and exhalation). Respiration is the actual exchange of oxygen and carbon dioxide — this happens at the alveolar membrane (external respiration) and at the body's tissues (internal respiration). A patient on a ventilator may have adequate ventilation but still have poor respiration if alveoli are damaged.

Q: What controls the rate and depth of breathing?

The respiratory center in the medulla oblongata sets the baseline breathing rhythm. It responds primarily to rising CO₂ levels (and secondarily to falling pH) in the blood — high CO₂ stimulates faster, deeper breathing to blow off carbon dioxide. Oxygen levels are the secondary drive. Patients with chronic COPD may rely on a hypoxic drive (low O₂ triggers breathing) — which is why uncontrolled supplemental oxygen can sometimes suppress their respiratory effort.

Respiratory System Overview

The system that brings oxygen in, sends carbon dioxide out, and regulates blood pH.

The respiratory system is responsible for gas exchange — delivering oxygen to the body and removing carbon dioxide. It works closely with the cardiovascular system: the lungs oxygenate the blood, and the heart pumps that blood to every cell in the body. The respiratory system also plays a key role in regulating blood pH, vocalization, and the body's response to inhaled pathogens.

Two Functional Divisions

Conducting Zone: Structures: Nose, pharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles. Transports air, warms and humidifies it, filters debris. No gas exchange.
Respiratory Zone: Structures: Respiratory bronchioles, alveolar ducts, alveolar sacs, alveoli. Site of gas exchange between air and blood.

Key Functions of the Respiratory System

Pulmonary ventilation — movement of air into and out of the lungs (breathing)
External respiration — gas exchange between alveoli and pulmonary capillaries
Internal respiration — gas exchange between systemic capillaries and tissues
Acid-base balance — regulates blood pH by adjusting CO₂ levels
Defense — mucus, cilia, cough reflex, and alveolar macrophages trap and remove pathogens
Vocalization — air movement through the larynx creates sound
Olfaction — sense of smell originates in the nasal cavity

Why This Matters Clinically

Almost every nursing assessment includes a respiratory component — vital signs (RR, SpO₂), breath sounds, oxygen delivery, and ABG interpretation all build on this foundation. Understanding the anatomy and physiology makes it easier to predict how conditions like pneumonia, COPD, or pulmonary embolism affect oxygenation and ventilation.

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Upper Airway

The structures that warm, humidify, and filter air before it reaches the lungs.

Nasal cavity: Warms, humidifies, and filters air. Contains cilia and mucus that trap debris. Houses olfactory receptors.
Turbinates (conchae): Three bony projections that create turbulent air flow, maximizing contact with moist mucosa.
Paranasal sinuses: Air-filled cavities in the skull that lighten the head, produce mucus, and add resonance to voice.
Pharynx (throat): Passageway for air and food. Three regions: nasopharynx, oropharynx, laryngopharynx.
Larynx (voice box): Connects pharynx to trachea. Contains vocal cords. Houses the epiglottis.
Epiglottis: Flap of cartilage that covers the trachea during swallowing to prevent aspiration.

Clinical Significance

Nasal hair and mucus are the first line of defense against airborne particles
Sinus infections cause facial pain and pressure from inflammation of the paranasal sinuses
The pharynx is a shared pathway — aspiration is a major risk when the epiglottis does not close properly (dysphagia, stroke, sedation)
Laryngospasm can occur during anesthesia or in severe allergic reactions, completely blocking the airway

Why Bypassing the Upper Airway Matters

Endotracheal tubes and tracheostomies bypass the upper airway. The air going directly into the lungs is no longer warmed, humidified, or filtered — which is why heated humidification is essential for these clients to prevent thick secretions and airway damage.

Lower Airway & Lungs

From the trachea down to the alveoli, with all the branching in between.

The Tracheobronchial Tree

Trachea (windpipe): About 4-5 inches long. C-shaped cartilage rings keep it open. Lined with ciliated epithelium and goblet cells (mucus). Branches at the carina.
Right vs Left Main Bronchus: Right is shorter, wider, and more vertical — aspirated foreign objects most often end up here.
Lobar bronchi: 3 on the right (upper, middle, lower lobes), 2 on the left (upper and lower lobes).
Segmental and subsegmental bronchi: Continue branching, becoming progressively smaller.
Bronchioles: Less than 1 mm diameter. No cartilage — subject to bronchospasm. Smooth muscle responds to autonomic nervous system.
Terminal bronchioles: End of conducting zone; lead to respiratory bronchioles where gas exchange begins.

The Lungs

Right Lung: 3 lobes (upper, middle, lower) · slightly larger · cardiac notch absent.
Left Lung: 2 lobes (upper, lower) · smaller (cardiac notch accommodates heart) · has lingula (tongue-like projection).

The Pleura

The lungs are covered by a double-layered serous membrane called the pleura:

Visceral pleura — covers the lung surface
Parietal pleura — lines the thoracic cavity
Pleural cavity — the potential space between the two layers, containing a small amount of pleural fluid that acts as a lubricant and helps maintain negative pressure

Why Aspiration Goes Right

The right main bronchus is wider, shorter, and more vertical than the left. When clients aspirate food, vomit, or foreign objects, these most commonly lodge in the right lung — especially the right lower lobe. This is also why nasogastric and endotracheal tubes can accidentally enter the right main bronchus.

Pleural Disorders

Pleural effusion — excess fluid in the pleural space (CHF, infection, cancer)
Pneumothorax — air in the pleural space causing lung collapse
Hemothorax — blood in the pleural space (trauma)
Empyema — pus in the pleural space (infection)
Pleurisy — inflammation of the pleura, causing sharp pain with breathing

Alveoli & Surfactant

Where the actual work of gas exchange happens — and why surfactant is essential.

Alveolar Anatomy

Approximately 300-500 million alveoli in adult lungs, creating roughly 70-80 square meters of surface area for gas exchange
Single layer of squamous epithelium — thin walls allow rapid gas diffusion
Surrounded by pulmonary capillaries — creates the alveolar-capillary membrane (about 0.5 micrometers thick)
Gas exchange occurs by simple diffusion across this membrane

Three Types of Alveolar Cells

Type I pneumocytes: Make up 95% of the alveolar surface; thin, flat cells where gas exchange occurs.
Type II pneumocytes: Produce surfactant; also serve as stem cells to replace damaged type I cells.
Alveolar macrophages: Defense cells that engulf debris, bacteria, and dead cells (also called "dust cells").

Surfactant

Surfactant is a lipoprotein produced by type II pneumocytes. It is essential for normal lung function.

What Surfactant Does

Surfactant reduces surface tension within the alveoli. Without it, the small alveoli would collapse due to surface tension forces (like a soap bubble popping). It prevents alveolar collapse during exhalation, reduces the work of breathing, allows alveoli of different sizes to coexist, and begins production around 24-28 weeks gestation, with full maturity around 35-36 weeks.

Clinical Conditions Affecting Surfactant

Respiratory Distress Syndrome (RDS) in premature infants — surfactant deficiency causing alveolar collapse
Acute Respiratory Distress Syndrome (ARDS) in adults — surfactant becomes inactivated by inflammation
Atelectasis — collapsed alveoli, often from inadequate breathing or surfactant disruption
Betamethasone given to mothers in preterm labor (24-34 weeks) to accelerate fetal lung maturity and surfactant production

Mechanics of Breathing

How the body physically moves air in and out of the lungs.

Inspiration (Inhalation)

Active process requiring muscle contraction
Diaphragm contracts and moves downward, increasing the vertical dimension of the thoracic cavity
External intercostal muscles contract, lifting the ribs up and out, increasing the diameter
Thoracic volume increases — this decreases the intrathoracic pressure (now lower than atmospheric pressure)
Air flows in due to the pressure gradient, filling the lungs

Expiration (Exhalation)

Passive process at rest — relies on the elastic recoil of lungs and chest wall
Diaphragm and intercostal muscles relax
Thoracic volume decreases, increasing intrathoracic pressure
Air flows out down the pressure gradient
Active expiration uses internal intercostals and abdominal muscles, used during exercise, coughing, and respiratory distress

Accessory Muscles of Breathing

Muscles used in respiratory distress to assist breathing:

Sternocleidomastoid
Scalenes
Pectoralis minor
Abdominal muscles (during forced expiration)

Use of Accessory Muscles Is a Red Flag

If a client is using accessory muscles of respiration (visible neck and shoulder muscle contractions, retractions), they are in respiratory distress. This indicates the diaphragm and intercostals alone cannot meet the body's demand for oxygen. Common signs include nasal flaring, retractions (intercostal, subcostal, suprasternal), pursed-lip breathing, and tripod positioning. Notify the provider and prepare to support oxygenation.

Lung Volumes and Capacities

Tidal Volume (TV)~500 mL: Volume of air with each normal breath.
Inspiratory Reserve Volume (IRV)~3,000 mL: Maximum air that can be inhaled after a normal inspiration.
Expiratory Reserve Volume (ERV)~1,100 mL: Maximum air that can be exhaled after a normal expiration.
Residual Volume (RV)~1,200 mL: Air remaining in lungs after maximum exhalation (cannot be exhaled).
Vital Capacity (VC)~4,600 mL: Maximum air that can be expelled after maximum inhalation (TV + IRV + ERV).
Total Lung Capacity (TLC)~5,800 mL: Total volume the lungs can hold (VC + RV).

Compliance and Resistance

Compliance — how easily the lungs and chest wall expand. Decreased in fibrosis, pulmonary edema, ARDS. Increased in emphysema (loss of elastic recoil)
Airway resistance — opposition to air flow. Increased in asthma (bronchospasm), COPD, and obstructed airways

Gas Exchange & Oxygen Transport

How oxygen gets from the air to your cells — and how CO₂ gets out.

External Respiration (at the Alveoli)

Oxygen diffuses from alveoli (high O₂) into pulmonary capillaries (low O₂)
Carbon dioxide diffuses from pulmonary capillaries (high CO₂) into alveoli (low CO₂)
Driven by partial pressure gradients
Occurs across the thin alveolar-capillary membrane

Internal Respiration (at the Tissues)

Oxygen diffuses from systemic capillaries (high O₂) into tissue cells (low O₂)
Carbon dioxide diffuses from tissue cells (high CO₂) into capillaries (low CO₂)
Tissues use oxygen for cellular respiration and produce CO₂ as a waste product

Ventilation-Perfusion (V/Q) Matching

Effective gas exchange requires both air (ventilation) and blood (perfusion) to reach the alveoli together. When this matching is disrupted, oxygenation suffers.

Dead Spaceventilation without perfusion: Air reaches alveoli but no blood flow — gas cannot be exchanged. Causes: pulmonary embolism, severe hypotension.
Shuntperfusion without ventilation: Blood flows past alveoli with no air — blood returns to heart unoxygenated. Causes: pneumonia, atelectasis, ARDS, pulmonary edema.
Silent Unitneither: Neither ventilation nor perfusion — both blocked. Causes: severe ARDS, advanced lung disease.

Oxygen Transport in the Blood

Bound to hemoglobin97-98%: Forms oxyhemoglobin. Each Hgb can carry 4 oxygen molecules.
Dissolved in plasma2-3%: Small amount; reflected in PaO₂ on ABG.

Oxygen-Hemoglobin Dissociation Curve

The relationship between oxygen saturation (SaO₂) and the partial pressure of oxygen (PaO₂) is described by the oxygen-hemoglobin dissociation curve. Several factors shift this curve:

Shift LEFT (binds O₂ tighter): Decreased CO₂ · Increased pH (alkalosis) · Decreased temperature · Decreased 2,3-DPG
Shift RIGHT (releases O₂ more easily): Increased CO₂ · Decreased pH (acidosis) · Increased temperature (fever) · Increased 2,3-DPG

Clinical Significance of the Curve

A right shift helps deliver more oxygen to tissues — which is what your body needs during exercise (high CO₂, low pH, high temperature). A left shift means hemoglobin holds onto oxygen more tightly, making it harder to release at the tissues — problematic in conditions like alkalosis or hypothermia.

Carbon Dioxide Transport

CO₂ is transported in three forms:

As bicarbonate (HCO₃^-) — about 70%, most common form
Bound to hemoglobin (carbaminohemoglobin) — about 23%
Dissolved in plasma — about 7%

Respiratory Regulation

How the brain controls breathing automatically and adjusts to changing demands.

Respiratory Centers in the Brain

Medullary Respiratory CenterMedulla oblongata: Primary center; sets basic rate and rhythm of breathing.
Pontine Respiratory CenterPons: Modifies medullary output; smooths transitions between inspiration and expiration.

Chemoreceptors

Specialized cells that sense changes in blood chemistry and signal the respiratory centers to adjust breathing.

Central ChemoreceptorsMedulla: Detect increased CO₂ (and decreased pH) in cerebrospinal fluid — the PRIMARY drive to breathe.
Peripheral ChemoreceptorsAortic arch and carotid bodies: Detect decreased O₂ (hypoxia), changes in pH and CO₂.

Other Factors That Affect Breathing

Stretch receptors in lung tissue — prevent overinflation (Hering-Breuer reflex)
Voluntary control — breath holding, deep breathing, speaking (cerebral cortex)
Emotional factors — anxiety, fear, pain can all increase respiratory rate
Temperature — fever increases respiratory rate
Sleep — respiratory rate naturally decreases

Oxygen Administration in COPD

Normally, breathing is driven by rising CO₂ levels detected by central chemoreceptors. In clients with chronic CO₂ retention (advanced COPD), the body adapts to high CO₂, and breathing becomes driven by low oxygen levels (hypoxic drive) detected by peripheral chemoreceptors. If too much oxygen is given to these clients, it can suppress their drive to breathe and cause CO₂ retention, respiratory acidosis, and respiratory failure. Typically, oxygen is titrated to keep SpO₂ at 88-92% in chronic CO₂ retainers, not the usual 95% or higher. Always check provider orders and assess respiratory status closely.

Normal Respiratory Rates by Age

Newborn: 30-60 breaths/min
Infant (1-12 mo): 30-50 breaths/min
Toddler (1-3 yr): 24-40 breaths/min
Preschool (3-5 yr): 22-34 breaths/min
School age (6-12 yr): 18-30 breaths/min
Adolescent (13-18 yr): 12-20 breaths/min
Adult: 12-20 breaths/min
Older adult: 12-20 (may be slightly slower)

ABGs & Clinical Application

Putting it all together — what arterial blood gases tell you about respiratory function.

Normal ABG Values

pH7.35 – 7.45: Acid-base balance of the blood.
PaCO₂35 – 45 mmHg: Respiratory component — how much CO₂ is in arterial blood.
HCO₃^-22 – 26 mEq/L: Metabolic component — bicarbonate level (controlled by kidneys).
PaO₂80 – 100 mmHg: Partial pressure of oxygen in arterial blood.
SaO₂95% – 100%: Percentage of hemoglobin saturated with oxygen.

Quick Memory Trick: "ROME"

Respiratory Opposite, Metabolic Equal. For respiratory imbalances, pH and PaCO₂ move in opposite directions: Respiratory acidosis = low pH, high CO₂; Respiratory alkalosis = high pH, low CO₂. For metabolic imbalances, pH and HCO₃^- move in the same direction: Metabolic acidosis = low pH, low HCO₃; Metabolic alkalosis = high pH, high HCO₃.

? A patient with COPD has a pH of 7.30, PaCO₂ of 55, and HCO₃ of 28. What type of imbalance is this?

Respiratory acidosis with metabolic compensation. Low pH + high PaCO₂ = respiratory acidosis (ROME: opposite). The elevated HCO₃ shows the kidneys have tried to compensate by retaining bicarbonate.

Hypoxemia vs Hypoxia

Hypoxemia — low oxygen level in the blood (PaO₂ < 80 mmHg)
Hypoxia — inadequate oxygen at the tissue level
You can have hypoxemia without significant hypoxia (compensation), or hypoxia without hypoxemia (severe anemia, poor circulation)

Signs of Inadequate Oxygenation

Early signs: restlessness, anxiety, irritability, mild confusion, tachypnea, tachycardia, mild hypertension
Late signs: cyanosis, severe confusion or stupor, bradycardia, hypotension, bradypnea (ominous)
Cyanosis is a LATE finding — do not wait for it to act

Restlessness Is the First Sign of Hypoxia

Restlessness, anxiety, and subtle confusion are often the earliest indicators of inadequate oxygenation — appearing BEFORE changes in oxygen saturation or vital signs. A client who suddenly becomes restless, agitated, or seems "off" should be assessed for respiratory status before assuming pain or anxiety. Always check oxygenation first.

Oxygen Delivery Devices — Quick Reference

Nasal cannula1-6 L/min: Approximate FiO₂: 24-44%
Simple face mask5-10 L/min: Approximate FiO₂: 40-60%
Venturi mask4-12 L/min: Approximate FiO₂: 24-50% (precise)
Partial rebreather mask6-15 L/min: Approximate FiO₂: 60-75%
Non-rebreather mask10-15 L/min: Approximate FiO₂: 80-95%
High-flow nasal cannulaup to 60 L/min: Approximate FiO₂: 21-100%

Common Conditions That Tie Back to Anatomy

Asthma — bronchospasm in the smooth muscle of bronchioles
Emphysema — destruction of alveolar walls reduces surface area for gas exchange
Chronic bronchitis — excess mucus and chronic inflammation in the airways
Pneumonia — inflammation and fluid in the alveoli (shunt physiology)
Pulmonary embolism — clot blocks pulmonary artery (dead space physiology)
Pneumothorax — air in pleural space disrupts negative pressure, lung collapses
ARDS — severe alveolar damage, surfactant inactivation, and decreased compliance

Frequently Asked Questions

Common student questions on this topic.

Where does gas exchange actually happen in the lungs?

Gas exchange happens in the alveoli — tiny air sacs at the end of the bronchial tree. Oxygen diffuses from the alveoli into the surrounding pulmonary capillaries, and carbon dioxide diffuses the other way to be exhaled. The alveolar-capillary membrane is extremely thin and surrounded by a dense capillary network to maximize surface area for diffusion.

What does surfactant do?

Surfactant is a phospholipid substance produced by type II alveolar cells. It reduces surface tension inside the alveoli, preventing them from collapsing during exhalation (atelectasis). Premature infants often lack sufficient surfactant, causing respiratory distress syndrome (RDS). Fetal lung maturity is assessed with the L/S (lecithin/sphingomyelin) ratio — a ratio of 2:1 or higher indicates adequate surfactant.

What are normal ABG values?

Normal arterial blood gas (ABG) values: pH 7.35–7.45, PaCO₂ 35–45 mmHg, HCO₃⁻ 22–26 mEq/L, and PaO₂ 80–100 mmHg. A pH below 7.35 is acidosis, above 7.45 is alkalosis. PaCO₂ is the respiratory component — high CO₂ causes acidosis. HCO₃⁻ is the metabolic component — high bicarb causes alkalosis. This is the foundation for ABG interpretation questions on the NCLEX-PN.

How does the diaphragm cause breathing?

During inhalation, the diaphragm contracts and moves downward, increasing the thoracic cavity volume. This drops intrathoracic pressure below atmospheric pressure, and air rushes into the lungs. During exhalation, the diaphragm relaxes and moves upward, intrathoracic pressure rises, and air is pushed out. The diaphragm is innervated by the phrenic nerve, which originates from cervical nerves C3–C5.

What is the difference between ventilation and respiration?

Ventilation is the mechanical movement of air in and out of the lungs (inhalation and exhalation). Respiration is the actual exchange of oxygen and carbon dioxide — this happens at the alveolar membrane (external respiration) and at the body's tissues (internal respiration). A patient on a ventilator may have adequate ventilation but still have poor respiration if alveoli are damaged.

What controls the rate and depth of breathing?

The respiratory center in the medulla oblongata sets the baseline breathing rhythm. It responds primarily to rising CO₂ levels (and secondarily to falling pH) in the blood — high CO₂ stimulates faster, deeper breathing to blow off carbon dioxide. Oxygen levels are the secondary drive. Patients with chronic COPD may rely on a hypoxic drive (low O₂ triggers breathing) — which is why uncontrolled supplemental oxygen can sometimes suppress their respiratory effort.

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