Immunity

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Immunity: Innate vs. Adaptive

Fig. 5.1 - Principal components and kinetics of innate and adaptive immune responses (Robbins & Kumar Basic Pathology)

What Is Immunity?

The immune system exists to discriminate self from non-self and defend the body against microbial pathogens, toxins, and abnormal cells (e.g., tumors). It has two interconnected arms that operate on different timescales and use different strategies:

Feature	Innate Immunity	Adaptive Immunity
Onset	Immediate (minutes to hours)	Delayed (days)
Specificity	Broad patterns (PAMPs, DAMPs)	Highly specific (single antigen)
Memory	None	Yes (long-lived memory cells)
Receptors	Germline-encoded (~100 receptors)	Somatically rearranged (10^7-10^9 clones)
Key cells	Neutrophils, macrophages, NK cells, DCs, ILCs	T lymphocytes, B lymphocytes
Humoral arm	Complement, defensins, acute-phase proteins	Antibodies (immunoglobulins)

Innate Immunity

Innate immunity is always present and ready - it provides the first line of defense before adaptive responses can mobilize. - Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 168

Components

1. Epithelial Barriers The skin and mucosal surfaces of the GI and respiratory tracts act as mechanical barriers. Epithelial cells also produce antimicrobial molecules (e.g., defensins), and intraepithelial lymphocytes patrol these surfaces. - Robbins Pathologic Basis of Disease, p. 185

2. Phagocytic Cells

Neutrophils: First to arrive at infection sites (recruited from blood within minutes to hours)
Macrophages: Arise from blood monocytes (or tissue-resident precursors from yolk sac/fetal liver). Specialized resident macrophages include Kupffer cells (liver), microglia (brain), and alveolar macrophages (lung). They ingest and destroy pathogens.
Both cell types sense microbes, engulf them via phagocytosis, and destroy them with reactive oxygen species, lysosomal enzymes, and other mechanisms.

3. Dendritic Cells (DCs) Present in epithelia, lymphoid organs, and most tissues. DCs are sentinels: they capture protein antigens, sense microbes via pattern recognition receptors, produce cytokines (especially interferons), and present peptide antigens to T lymphocytes - bridging innate and adaptive immunity.

4. Natural Killer (NK) Cells NK cells kill cells that have downregulated MHC I expression (a common viral and tumor evasion strategy). They also produce IFN-γ to activate macrophages. They are part of the innate lymphoid cell (ILC) family.

5. Innate Lymphoid Cells (ILCs) Tissue-resident lymphocytes without T-cell receptors. Activated by cytokines rather than antigens. They are rapid sources of cytokines that help shape the subsequent adaptive response.

6. Plasma Proteins

Complement system: A cascade of plasma proteins that opsonize microbes, recruit phagocytes, and directly lyse pathogens (via the membrane attack complex)
Acute-phase proteins: C-reactive protein (CRP), mannose-binding lectin (MBL) - produced in the liver in response to inflammation

Pattern Recognition Receptors (PRRs)

The innate system does not recognize individual antigens. Instead, it uses ~100 receptors to detect a few thousand conserved molecular patterns: - Robbins & Kumar Basic Pathology, p. 132

PAMPs (Pathogen-Associated Molecular Patterns): Conserved structures essential to microbial survival - LPS from gram-negative bacteria, peptidoglycan, flagellin, viral RNA/DNA
DAMPs (Damage-Associated Molecular Patterns): Signals from injured/necrotic host cells (e.g., uric acid crystals, HMGB1, heat shock proteins)

Key PRR families:

Toll-like receptors (TLRs): Plasma membrane TLRs recognize extracellular bacterial products (e.g., LPS); endosomal TLRs detect viral/bacterial nucleic acids after phagocytosis. TLR activation drives NF-κB - stimulating cytokines, interferons, and costimulatory molecules
NOD-like receptors (NLRs): Cytosolic sensors; NLRP3 assembles the inflammasome, activating IL-1β and IL-18
RIG-like receptors (RLRs): Detect viral RNA in the cytoplasm; trigger type I interferon production
C-type lectin receptors: Recognize carbohydrates on fungal and bacterial surfaces

Reactions of Innate Immunity

Innate recognition produces: inflammation (via cytokines TNF, IL-1, IL-6, IL-12), antiviral defense (type I IFNs), and activation of DCs that initiate adaptive responses.

Adaptive Immunity

Adaptive (acquired) immunity is antigen-specific, depends on prior exposure, and generates immunological memory. It becomes progressively dominant over the innate response with time. - Goodman & Gilman's Pharmacological Basis of Therapeutics, p. 494

Two Arms of Adaptive Immunity

Arm	Mediator	Targets	Mechanism
Humoral immunity	B lymphocytes → Antibodies	Extracellular microbes and toxins	Neutralization, opsonization, complement activation
Cell-mediated immunity	T lymphocytes	Intracellular microbes, cancer cells	Cytokine-driven macrophage activation (CD4+), direct cytotoxicity (CD8+)

Key Cells

B Lymphocytes

Mature in the bone marrow
Express surface immunoglobulin as the B-cell receptor (BCR)
When activated by antigen (+ T cell help), differentiate into plasma cells that secrete antibodies
Also form memory B cells for rapid secondary responses

T Lymphocytes

Mature in the thymus
Express the T-cell receptor (TCR), which only recognizes peptide fragments presented by MHC molecules (unlike BCR, which binds whole antigens)
Two main subsets:
- CD4+ helper T cells: Recognize antigen on MHC II (on APCs). Provide help to B cells and activate macrophages. Subsets include Th1 (activates macrophages via IFN-γ), Th2 (drives allergic responses via IL-4/5/13), Th17 (anti-fungal/bacterial defense via IL-17), and T-regulatory cells (suppress immune responses)
- CD8+ cytotoxic T lymphocytes (CTLs): Recognize antigen on MHC I (on all nucleated cells). Directly kill infected cells and tumor cells via perforin/granzyme mechanism

Antigen-Presenting Cells (APCs) Dendritic cells, macrophages, and B cells. Process and present peptide antigens on MHC molecules to T cells. DCs are the most potent APCs for initiating naive T-cell responses.

MHC (Major Histocompatibility Complex)

MHC I (HLA-A, B, C in humans): Expressed on all nucleated cells; presents endogenous (intracellular) peptides to CD8+ T cells
MHC II (HLA-DR, DP, DQ): Expressed only on APCs; presents exogenous (phagocytosed) peptides to CD4+ T cells

Clonal Selection

Before antigen exposure, lymphocytes specific for many different antigens already exist in small numbers (~1 in 100,000 lymphocytes per antigen). When an antigen enters, it selectively activates the cells bearing the matching receptor - those cells then proliferate into a large clone of effector cells (clonal expansion). This is the basis of immunological specificity. - Robbins Pathologic Basis of Disease, p. 186

Phases of an Adaptive Response

Antigen capture and presentation: DCs take up antigen, migrate to lymph nodes, present peptides to naive T cells
Lymphocyte activation: Naive T and B cells recognize antigen + receive costimulatory signals → proliferate and differentiate
Effector phase: Antibodies neutralize/opsonize microbes; effector T cells kill infected cells or activate macrophages
Contraction: ~90% of effector cells die by apoptosis after infection is cleared
Memory: Surviving memory T and B cells persist long-term, enabling faster and stronger responses to re-infection

How Innate and Adaptive Immunity Work Together

The two systems are deeply interdependent:

Innate initiates, adaptive refines: Innate responses are active within hours; adaptive immunity dominates from day 3 onward
DCs are the bridge: After sensing PAMPs/DAMPs, DCs upregulate MHC and costimulatory molecules (CD80/86) and migrate to lymph nodes to activate T cells - without this, adaptive responses fail
Adaptive boosts innate: Antibodies and cytokines produced in adaptive responses opsonize microbes for phagocytosis and activate NK cells and macrophages
Innate shapes the type of adaptive response: The cytokines produced during innate immunity (IL-12 drives Th1; IL-4 drives Th2; IL-6 + TGF-β drive Th17) determine the character of the adaptive response

Key Cytokines at a Glance

Cytokine	Source	Main Function
IL-1, TNF, IL-6	Macrophages, DCs	Pro-inflammatory; acute-phase response
IL-12	Macrophages, DCs	Drives Th1 differentiation; activates NK cells
IFN-α/β (Type I)	DCs, infected cells	Antiviral defense; activates NK cells
IFN-γ (Type II)	Th1 cells, NK cells	Activates macrophages (killing intracellular pathogens)
IL-4, IL-5, IL-13	Th2 cells	Drive B-cell class switching to IgE; allergic responses
IL-17	Th17 cells	Recruit neutrophils; anti-fungal/extracellular bacterial defense
TGF-β, IL-10	T-regulatory cells, macrophages	Suppress immune responses; prevent autoimmunity

Sources: Robbins & Kumar Basic Pathology, p. 131-140 | Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 168-193 | Goodman & Gilman's Pharmacological Basis of Therapeutics, p. 494 | Cellular and Molecular Immunology (Abbas et al.) | Janeway's Immunobiology 10e

Ventilation perfusion ration

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Ventilation-Perfusion Ratio (V/Q)

Definition

The ventilation-perfusion ratio (V/Q or V̇/Q̇) is the ratio of alveolar ventilation (V̇A, in L/min) to pulmonary blood flow (Q̇, in L/min). It quantifies how well the air supply to the alveoli matches the blood supply to the pulmonary capillaries. Perfect gas exchange requires close matching of the two. - Costanzo Physiology 7th Edition, p. 236

Normal V/Q = 0.8

This means alveolar ventilation is about 80% of cardiac output:

Normal total alveolar ventilation ≈ 4 L/min
Normal pulmonary blood flow (cardiac output) ≈ 5 L/min
V/Q = 4/5 = 0.8

When V/Q is 0.8, PaO₂ = 100 mm Hg and PaCO₂ = 40 mm Hg (normal values). Any deviation causes impaired gas exchange. - Costanzo Physiology, p. 233

The Two Extremes: Dead Space and Shunt

The key to understanding V/Q is grasping the two physiological extremes:

Condition	V/Q	Ventilation	Perfusion	Alveolar Gas	Effect
Dead space	= ∞	Present	Absent	Equals inspired air (PO₂ 150, PCO₂ 0)	Wasted ventilation
Normal	= 0.8	Present	Present	PO₂ 100, PCO₂ 40	Ideal exchange
Shunt	= 0	Absent	Present	Equals venous blood (PO₂ 40, PCO₂ 46)	Wasted perfusion

Dead space (V/Q = ∞): Ventilation with no blood flow. No gas exchange occurs. The alveolar air stays similar to inspired air. Classic example: pulmonary embolism. - Guyton & Hall Medical Physiology
Shunt (V/Q = 0): Perfusion with no ventilation. Blood passes through without being oxygenated and mixes into systemic circulation as deoxygenated blood. Classic example: airway obstruction, right-to-left cardiac shunts. - Costanzo Physiology, p. 237

V/Q Defects diagram showing dead space, high V/Q, low V/Q, and right-to-left shunt

Fig. 5.30 - V/Q defects: from dead space (V/Q = ∞) to right-to-left shunt (V/Q = 0). (Costanzo Physiology 7th Ed.)

Regional Variation in the Upright Lung

V/Q is not uniform throughout the lung. In the upright position, gravity creates regional differences in both ventilation and perfusion - but the effect on perfusion is greater than on ventilation. This results in a gradient of V/Q from apex to base:

V/Q distribution across the three zones of the lung

Fig. 5.28 - V/Q distribution in the three zones of the upright lung. (Costanzo Physiology 7th Ed.)

Zone	Location	Blood Flow (Q̇)	Ventilation (V̇)	V/Q	PaO₂	PaCO₂
Zone 1	Apex	Lowest	Lower	Highest (~3.0)	130 mm Hg	28 mm Hg
Zone 2	Middle	Intermediate	Intermediate	~0.8 (average)	~100 mm Hg	~40 mm Hg
Zone 3	Base	Highest	Higher	Lowest (~0.6)	89 mm Hg	42 mm Hg

Why? Blood flow is governed by gravity - the base of the lung has higher hydrostatic pressure so more blood pools there. Ventilation also increases toward the base (alveoli at the apex are already stretched at resting FRC and have less room to expand), but this increase is less steep than the change in perfusion. Therefore:

Apex: relatively over-ventilated for its blood flow → high V/Q (behaves like dead space)
Base: relatively over-perfused for its ventilation → low V/Q (behaves like shunt)

The average V/Q of 0.8 is a mixed value from all zones. - Costanzo Physiology, p. 234-235

Effect of V/Q on Gas Tensions

The alveolar PO₂ and PCO₂ in any lung unit are determined primarily by its V/Q ratio:

↑ V/Q → more ventilation relative to blood flow → alveolar air blown off → PO₂ rises, PCO₂ falls
↓ V/Q → less ventilation relative to blood flow → gas accumulates from metabolism → PO₂ falls, PCO₂ rises

Regional PO₂ differences across zones are much larger than PCO₂ differences, because:

O₂ and CO₂ have very different dissociation curve shapes
Hemoglobin is nearly fully saturated at normal PO₂, so even high-V/Q zones cannot over-compensate for low-V/Q zones on the O₂ side
CO₂ dissociation is more linear, allowing high-ventilation areas to blow off extra CO₂ and partially compensate

This is why V/Q mismatch causes hypoxemia more readily than hypercapnia - the normal compensatory response (increased ventilation) can correct CO₂ but cannot fully restore O₂. - Murray & Nadel's Textbook of Respiratory Medicine, p. 603

Physiological Dead Space and Physiological Shunt

In a healthy upright lung, the apex (high V/Q) contributes physiological dead space and the base (low V/Q) contributes physiological shunt. These are normal:

Physiological dead space ≈ anatomical dead space (airways, ~150 mL) + alveolar dead space (over-ventilated alveoli)
Physiological shunt < 10% of cardiac output in health

During exercise, cardiac output increases, blood flow to the apex rises, and the V/Q gradient flattens - making gas exchange more efficient. - Guyton & Hall Medical Physiology

V/Q Mismatch in Disease

Disease	Mechanism	Dominant Defect
Pulmonary embolism	Clot obstructs blood flow to ventilated alveoli	↑ Dead space (high V/Q)
Pneumonia / pulmonary edema	Alveoli filled with fluid, no ventilation	↓ Shunt (low V/Q or V/Q = 0)
COPD / emphysema	Bronchial obstruction (↓ ventilation) + alveolar wall destruction (↓ perfusion)	Both dead space AND shunt
Asthma	Bronchoconstriction → uneven ventilation	Low V/Q areas (shunt-like)
ARDS	Widespread alveolar flooding/collapse	True shunt (V/Q = 0)

In COPD, some regions have severe physiological shunt and others have severe physiological dead space, sometimes reducing lung gas exchange effectiveness to as little as one-tenth of normal - the most prevalent cause of pulmonary disability today. - Guyton & Hall Medical Physiology, p. 520

Key Clinical Point: Response to Supplemental O₂

This distinguishes dead space/V/Q mismatch from true shunt:

V/Q mismatch (low V/Q, not zero): hypoxemia responds to supplemental O₂, because some ventilation is present to deliver O₂ to the alveolus
True shunt (V/Q = 0): hypoxemia does not respond to 100% O₂, because blood bypasses ventilated alveoli entirely and is never exposed to the inspired O₂

Sources: Guyton & Hall Textbook of Medical Physiology, p. 515-520 | Costanzo Physiology 7th Edition, p. 233-237 | Murray & Nadel's Textbook of Respiratory Medicine | Sabiston Textbook of Surgery

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Ventilation-Perfusion Ratio (V/Q)

Definition: The ratio of alveolar ventilation (V̇A) to pulmonary blood flow (Q̇).

Normal value = 0.8 (ventilation ~4 L/min ÷ cardiac output ~5 L/min)

The Two Extremes

Condition	V/Q	Cause	Example
Dead space	= ∞	Ventilation, no perfusion	Pulmonary embolism
Shunt	= 0	Perfusion, no ventilation	Pneumonia, airway obstruction

Regional Distribution (Upright Lung)

Apex (Zone 1): V/Q ~3.0 → high PO₂ (130 mmHg), low PCO₂ (28 mmHg) - behaves like dead space
Base (Zone 3): V/Q ~0.6 → low PO₂ (89 mmHg), high PCO₂ (42 mmHg) - behaves like shunt

Reason: Gravity reduces perfusion more than ventilation at the apex.

Effect of Changing V/Q

↑ V/Q → PO₂ rises, PCO₂ falls
↓ V/Q → PO₂ falls, PCO₂ rises

Key Clinical Point

V/Q mismatch causes hypoxemia more than hypercapnia because:

High-V/Q zones cannot compensate for O₂ loss (Hb already near-saturated)
CO₂ is more readily blown off by hyperventilation

O₂ response test:

Low V/Q mismatch → responds to supplemental O₂
True shunt (V/Q = 0) → does NOT respond to 100% O₂

Clinical

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V/Q Ratio - Clinical Correlations

V/Q Mismatch is the Most Common Cause of Hypoxemia

Low V/Q (perfusion exceeding ventilation) is the single most common cause of hypoxemia in clinical practice. Almost every lung disease worsens V/Q matching. - Murray & Nadel's Textbook of Respiratory Medicine

Five Physiological Causes of Hypoxemia

Cause	V/Q Pattern	A-a Gradient	Responds to O₂?
V/Q mismatch	Low V/Q	↑	Yes
Shunt	V/Q = 0	↑	No (minimal)
Hypoventilation	Normal V/Q	Normal	Yes
Diffusion limitation	Variable	↑	Yes
Low inspired O₂	Normal	Normal	Yes

The first three explain the vast majority of hypoxemia in clinical/perioperative settings. Diffusion limitation is rarely clinically significant at sea level. - Miller's Anesthesia 10e

The Critical Clinical Test: Response to Supplemental O₂

Algorithm for distinguishing clinical causes of hypoxemia based on response to supplemental oxygen

Fig. 44.3 - Algorithm for distinguishing major clinical causes of hypoxemia (Murray & Nadel's Respiratory Medicine)

Responds well to O₂ → Low V/Q or hypoventilation

Check ABG: elevated A-a gradient = low V/Q (asthma, COPD); normal A-a gradient = hypoventilation

Does NOT respond to O₂ → Shunt

Chest X-ray: focal opacities = pneumonia/atelectasis; diffuse opacities = pulmonary edema/ARDS; clear = pulmonary embolism, intracardiac shunt, AVMs

Disease-by-Disease Breakdown

1. COPD / Emphysema

Bronchial obstruction → alveoli beyond obstruction unventilated → low V/Q approaching 0 (shunt)
Alveolar wall destruction → ventilation with no blood flow → high V/Q (dead space)
Both defects coexist - gas exchange can fall to 1/10 of normal
Classic ABG: hypoxemia with hypercapnia (PaCO₂ ↑)

2. Asthma

Bronchoconstriction creates regional low V/Q areas
Hypoxemia responds to O₂ (some ventilation still present)
With severe attack: PaCO₂ initially ↓ (hyperventilation), then ↑ (fatigue/obstruction) - a rising PaCO₂ in asthma = danger sign

3. Pulmonary Embolism (PE)

Clot blocks perfusion → high V/Q / dead space in affected region
Adjacent areas receive redirected blood flow → low V/Q in other regions
Net effect: V/Q mismatch + increased dead space
ABG: hypoxemia, hypocapnia (compensatory hyperventilation), elevated A-a gradient
Does NOT cause shunt (unless massive PE raises right heart pressure and opens a patent foramen ovale)

4. Pneumonia / Lobar Consolidation

Alveoli filled with fluid/pus → no ventilation but perfusion continues → true shunt (V/Q = 0)
Hypoxemia poorly responsive to supplemental O₂
Chest X-ray: focal consolidation

5. ARDS (Acute Respiratory Distress Syndrome)

Widespread alveolar flooding + collapse → large true shunt
Refractory hypoxemia despite high FiO₂ - hallmark of ARDS
Managed with PEEP (recruits collapsed alveoli, converts shunt to low V/Q)

6. Obesity / Atelectasis

Low lung volumes → compression of basal alveoli → low V/Q at bases
Worsens supine (gravity-dependent collapse)
Common cause of post-operative hypoxemia

7. General Anesthesia

V/Q mismatch worsens due to: reduced FRC, diaphragm shift, atelectasis formation
Increases physiological shunt from <5% to ~10-15% of cardiac output

The A-a Gradient: Key Bedside Tool

A-a PO₂ gradient = PAO₂ - PaO₂

Normal ≈ 5-15 mm Hg (increases with age: ~2.5 × age/4)

Finding	Interpretation
Hypoxemia + normal A-a gradient	Hypoventilation (alveoli are fine, not enough air moved)
Hypoxemia + elevated A-a gradient	V/Q mismatch, shunt, or diffusion limitation

PEEP and V/Q in Mechanical Ventilation

Positive End-Expiratory Pressure (PEEP) is the primary tool to treat shunt physiology:

Recruits collapsed/flooded alveoli → restores ventilation to perfused units
Converts V/Q = 0 (shunt) to low V/Q → now responds to supplemental O₂
Over-distension with high PEEP can create high V/Q dead space in other regions

Sources: Murray & Nadel's Textbook of Respiratory Medicine | Miller's Anesthesia 10e | Goldman-Cecil Medicine | Guyton & Hall Medical Physiology

What is abg

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Arterial Blood Gas (ABG)

What Is an ABG?

An Arterial Blood Gas (ABG) is a blood test taken from an artery (usually the radial artery at the wrist) that directly measures the partial pressures of oxygen and carbon dioxide in the blood, along with pH. It is the gold standard for assessing oxygenation, ventilation, and acid-base status. - Murray & Nadel's Textbook of Respiratory Medicine

Parameters Measured

Parameter	What It Measures	Normal Value
pH	Acidity/alkalinity of blood	7.35 - 7.45
PaO₂	Partial pressure of oxygen in arterial blood	80 - 100 mm Hg
PaCO₂	Partial pressure of carbon dioxide	35 - 45 mm Hg
HCO₃⁻	Bicarbonate (calculated)	22 - 26 mEq/L
SaO₂	Oxygen saturation of hemoglobin (calculated)	95 - 100%
Base excess (BE)	Metabolic component; how much acid/base deviation	-2 to +2 mEq/L

Other values often included: lactate, hemoglobin, electrolytes (Na⁺, K⁺, Cl⁻). - Tintinalli's Emergency Medicine

Why Arterial (Not Venous)?

Arterial blood reflects the gas content after it has passed through the lungs - before any tissue gas exchange occurs. This gives a true picture of how well the lungs are functioning. Venous blood has already given up O₂ and taken on CO₂ from tissues, so it cannot assess pulmonary oxygenation. - Tintinalli's Emergency Medicine

How to Interpret an ABG - Step-by-Step

Step 1: Look at pH

< 7.35 = Acidosis
> 7.45 = Alkalosis

Step 2: Identify the Primary Disorder

pH	PaCO₂	HCO₃⁻	Disorder
↓	↑	Normal	Respiratory Acidosis
↑	↓	Normal	Respiratory Alkalosis
↓	Normal	↓	Metabolic Acidosis
↑	Normal	↑	Metabolic Alkalosis

Rule: PaCO₂ moves same direction as pH change in metabolic disorders; opposite in respiratory disorders.

Step 3: Check for Compensation

The body always tries to bring pH back to normal:

Primary Disorder	Compensation	Timing
Respiratory acidosis	Kidneys retain HCO₃⁻	2-5 days (chronic)
Respiratory alkalosis	Kidneys excrete HCO₃⁻	2-5 days (chronic)
Metabolic acidosis	Lungs hyperventilate → ↓ PaCO₂	Minutes to hours
Metabolic alkalosis	Lungs hypoventilate → ↑ PaCO₂	Hours (max PaCO₂ ~55 mm Hg)

Key rule: Compensation brings pH toward normal but never fully corrects it (pH does not overshoot 7.40).

Step 4: Assess Oxygenation

PaO₂ < 80 mm Hg = Hypoxemia
Calculate A-a gradient = PAO₂ - PaO₂ (normal ~5-15 mm Hg)
- Normal A-a gradient with hypoxemia → hypoventilation
- Elevated A-a gradient → V/Q mismatch, shunt, or diffusion limitation

Common Clinical ABG Patterns

Clinical Situation	pH	PaCO₂	HCO₃⁻	PaO₂
COPD exacerbation	↓	↑↑	↑ (compensated)	↓
Asthma (severe)	↓	↑ (late/dangerous sign)	Normal/↑	↓
Pulmonary embolism	↑	↓	↓	↓
Pneumonia/ARDS	↓	↓ (early)	Normal	↓↓
DKA	↓	↓ (Kussmaul breathing)	↓↓	Normal
Anxiety/hyperventilation	↑	↓	↓	Normal/↑

Technique

Sample drawn from radial artery (preferred), brachial, or femoral
Collected anaerobically in heparin-coated syringe (air bubbles falsely ↑ PO₂, ↓ PCO₂)
Analyzed immediately or placed on ice (delay causes ↑ PCO₂, ↓ PO₂, ↓ pH due to ongoing cellular metabolism) - Fishman's Pulmonary Diseases, p. 1200

ABG vs. Pulse Oximetry

	ABG	Pulse Oximetry
Measures	PaO₂, PaCO₂, pH, HCO₃⁻	SpO₂ only
Detects hypoventilation	Yes (via PaCO₂)	No (especially on supplemental O₂)
Detects CO poisoning	Yes (carboxyhemoglobin)	No (falsely normal)
Invasive	Yes	No

Critical point: Pulse oximetry cannot detect hypoventilation in a patient on supplemental O₂ - SpO₂ stays normal even as PaCO₂ rises dangerously. ABG is essential in this scenario. - Murray & Nadel's Respiratory Medicine

Sources: Fishman's Pulmonary Diseases & Disorders | Tintinalli's Emergency Medicine | Murray & Nadel's Textbook of Respiratory Medicine | Rosen's Emergency Medicine

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