LAST MIN FUCKING STUDYING

Comprehensive Respiratory Exam Study Guide

I. Arterial Blood Gas (ABG) Interpretation

Normal ABG Values

Parameter	Normal Range	Function
pH	7.35 – 7.45	Acid–base balance
PaCO₂	35 – 45 mmHg	Reflects respiratory function
HCO₃⁻	22 – 26 mEq/L	Reflects metabolic/renal function
PaO₂	75 – 100 mmHg	Oxygenation
O₂ Sat	94 – 100%	Oxygen saturation
Base Excess (BE)	–2 to +2 mmol/L	Degree of metabolic compensation

ROME Mnemonic

Respiratory = Opposite

Metabolic = Equal

Disorder	pH	PaCO₂	HCO₃⁻	Mechanism
Respiratory Acidosis	↓	↑	Normal	Hypoventilation → CO₂ retention
Respiratory Alkalosis	↑	↓	Normal	Hyperventilation → CO₂ loss
Metabolic Acidosis	↓	Normal/↓	↓	Loss of base or acid retention
Metabolic Alkalosis	↑	Normal/↑	↑	Loss of acid or excess base

Compensation Rules:

If pH is normalizing but PaCO₂ or HCO₃⁻ are abnormal → compensated.
If pH is still abnormal → uncompensated.

Stepwise Interpretation

Check pH → acidotic (<7.35) or alkalotic (>7.45).
Check PaCO₂ → if opposite of pH → respiratory origin.
Check HCO₃⁻ → if same direction as pH → metabolic origin.
Check PaO₂ → for oxygenation.
Assess compensation → see if body trying to correct imbalance.

Pathophysiologic Example

Case	ABG Findings	Interpretation	Underlying Pathophysiology
Panic Attack (Hyperventilation)	pH 7.49 ↑, PaCO₂ 27 ↓, HCO₃⁻ normal	Respiratory Alkalosis (acute)	↓CO₂ from hyperventilation → ↓carbonic acid → ↑pH
Vomiting & Diarrhea	pH 7.33 ↓, PaCO₂ 22 ↓, HCO₃⁻ 17 ↓	Metabolic Acidosis with Respiratory Compensation	HCO₃⁻ loss from GI tract → ↓pH → lungs blow off CO₂ to compensate

Mnemonic for Causes

ROME – “ACID–BASE HARM”

Acidosis	Alkalosis
Respiratory – hypoventilation (COPD, drug overdose)	Respiratory – hyperventilation (panic, pain, fever)
Metabolic – diarrhea, DKA, renal failure	Metabolic – vomiting, NG suction, antacids

II. Respiratory Failure

Types

Type	Definition	ABG Pattern	Primary Problem
Type I (Hypoxemic)	Inability to meet oxygen demands	↓PaO₂, normal/↓PaCO₂	Gas exchange problem (alveolar-capillary damage, V/Q mismatch)
Type II (Hypercapnic)	Inability to remove CO₂	↑PaCO₂, ↓pH	Pump failure — “won’t breathe” or “can’t breathe” (CNS, chest wall, diaphragm, lung disease)

Pathophysiology Simplified

Type I: Alveoli perfused but not ventilated → V/Q mismatch.
- Causes: ARDS, pneumonia, pulmonary edema, PE.
- ↓O₂ diffusion → hypoxemia → tissue hypoxia.
Type II: ↓ventilation → CO₂ retention → respiratory acidosis.
- Causes: COPD, neuromuscular disease, CNS depression, chest trauma.

V/Q Mismatch in ARDS

Normal: Low O₂ → pulmonary vasoconstriction → match perfusion with ventilation.

ARDS: Inflammation damages alveolar membrane → leaky capillaries → edema + collapse → no ventilation but perfusion continues → shunt → hypoxemia.

🧠 Mnemonic: “Shunt = perfusion without ventilation”

ABG Findings for Respiratory Failure

Disorder	pH	PaCO₂	HCO₃⁻	Interpretation
Respiratory Acidosis	↓	↑	Normal/↑	Hypoventilation
Respiratory Alkalosis	↑	↓	Normal/↓	Hyperventilation
Metabolic Acidosis	↓	↓	↓	Acid/base loss
Metabolic Alkalosis	↑	↑	↑	Base retention

ARDS (Acute Respiratory Distress Syndrome)

Definition: Life-threatening inflammatory injury → leaky alveolar-capillary membrane → noncardiogenic pulmonary edema.
Patho Sequence:
1. Insult (sepsis, aspiration, trauma) → cytokine release
2. ↑Permeability → fluid in alveoli
3. ↓Surfactant → alveolar collapse
4. ↓Compliance → stiff lungs → ↓O₂ diffusion
5. V/Q mismatch → refractory hypoxemia

Clinical Signs	Nursing Findings	Treatment Goals
Crackles, dyspnea, low PaO₂ despite O₂, bilateral infiltrates on CXR	ABG shows ↓PaO₂/FiO₂ <300	Maintain oxygenation, prevent barotrauma, use low tidal volume, high PEEP, permissive hypercapnia

Mnemonic:

🫁 Alveolar damage

💦 Refractory hypoxemia

💣 Decreased compliance

🔥 Systemic inflammation

III. Mechanical Ventilatory Support

Ventilator Settings Overview

Setting	Definition	Normal Range / Starting Point	Clinical Focus
FiO₂	% of oxygen delivered	0.21–1.0	↑ to correct hypoxemia
VT (Tidal Volume)	Volume of each breath	8–10 mL/kg IBW	Too high = barotrauma
PEEP	Pressure at end expiration	5–10 cm H₂O	Prevents alveolar collapse
Rate (RR)	Breaths per minute	12–20	Controls CO₂ elimination
PS (Pressure Support)	Assists spontaneous breaths	~5–10 cm H₂O	↓work of breathing

Ventilator Modes

Mode	Description	Key Points
VAC (Volume Assist-Control)	Delivers preset volume with each breath	Full control; risk of hyperventilation
PAC (Pressure Assist-Control)	Delivers breath until pressure limit reached	Prevents barotrauma
SIMV (Synchronized Intermittent Mandatory Ventilation)	Delivers set # of breaths but allows spontaneous breaths	Used for weaning; needs pressure support

Complications & Nursing Priorities

Complication	Pathophysiology	Nursing Care
Barotrauma	Overdistention of alveoli from high pressure → rupture → pneumothorax/subQ emphysema	Monitor for ↑peak pressure, ↓breath sounds, ↑HR; use lower VT
Unplanned Extubation	Tube dislodged → hypoxia	Maintain sedation, secure tube, monitor agitation
Right Mainstem Intubation	Tube inserted too deep → ventilates right lung only	Assess bilateral breath sounds, confirm with CXR
Decreased CO	↑Intrathoracic pressure → ↓venous return	Monitor BP, UO; fluids as ordered
Stress Ulcers & VTE	Immobility, stress response	PPI + heparin prophylaxis

Non-Invasive Ventilation

Device	Mechanism	Key Considerations
CPAP	Continuous positive pressure throughout cycle	Keeps alveoli open
BiPAP	Provides different pressures during inspiration (iPAP) and expiration (ePAP)	Reduces work of breathing, prevents intubation
Mask Ventilation	Must protect airway	Risk: skin breakdown, gastric insufflation

Endotracheal Intubation

Indications:

Airway protection (decreased LOC)
Acute respiratory failure
Hypoxemia unresponsive to O₂
Anticipated deterioration

Nursing Roles:

Gather equipment (ETT, laryngoscope, BVM, monitors)
Assist provider with sniffing position
Verify placement via ETCO₂ + bilateral breath sounds
Document cm marking at lip
Post-intubation ABG within 20–30 min

🧠 Mnemonic: “P.A.I.R.”

Preoxygenate
Assist during procedure
Insert verification (listen, confirm)
Reassess vitals and sedation

IV. Quick-Reference Mnemonics

Topic	Mnemonic	Meaning
ABG interpretation	ROME	Respiratory Opposite, Metabolic Equal
Causes of Respiratory Acidosis	DEPRESS	Drugs (opioids), Edema, Pneumonia, Respiratory center damage, Embolism, Spasms, Secretions
Causes of Respiratory Alkalosis	TACHYPNEA	Temperature ↑, Aspirin toxicity, Controlled ventilation, Hyperventilation, Pain, Neurological, Embolism, Anxiety
Causes of Metabolic Acidosis	MUDPILES	Methanol, Uremia, DKA, Propylene glycol, Isoniazid, Lactic acid, Ethylene glycol, Salicylates
Causes of Metabolic Alkalosis	ALkALI	Aldosterone ↑, Loop diuretics, alKali ingestion, Anticoagulants (citrate), Loss of fluids (vomit), Increased NaHCO₃

V. Key Exam Takeaways

Identify whether the problem is respiratory or metabolic using ROME.
Type I vs Type II respiratory failure: oxygen vs ventilation issue.
ARDS hallmark: refractory hypoxemia, bilateral infiltrates, decreased compliance.
PEEP prevents alveolar collapse but can ↓CO.
Barotrauma = too high pressure or volume.
Always assess bilateral breath sounds post-intubation.
Permissive hypercapnia = accepting high CO₂ to prevent lung injury.