Room air contains about 21% oxygen, used as baseline for FiO₂ calculations.

Oxygen binds with hemoglobin forming oxyhemoglobin for efficient transport to tissues.

Marked bradypnea and decreased effort signal fatigue and impending failure.

Rising PaCO₂ and falling pH indicate fatigue and inadequate ventilation.

The bicarbonate-carbonic acid buffer maintains acid-base equilibrium in extracellular fluid.

Hypoxemia and hypercapnia occur due to airway obstruction and CO₂ retention.

Pulmonary embolism increases areas not perfused but ventilated.

Diabetic ketoacidosis and lactic acidosis increase unmeasured anions.

PaO₂ of 55 mmHg indicates moderate hypoxemia requiring oxygen therapy.

Hypoxemia not corrected even with high FiO₂ due to shunting.

Pancreatitis occurs due to premature enzyme activation causing pancreatic tissue autodigestion.

Low PaO₂ in arterial blood, e.g., in high altitude or airway obstruction.

The medulla oblongata automatically controls breathing rhythm and depth.

Carbon monoxide poisoning gives false high readings due to carboxyhemoglobin.

Blood passes unoxygenated through lungs, as in pneumonia or atelectasis.

The epiglottis closes the laryngeal opening during swallowing, preventing aspiration.

Potassium shifts into cells causing hypokalemia during respiratory alkalosis.

COPD patients depend on hypoxic drive (low O₂) to trigger respiration.

Increased CO₂ and H⁺ reduce hemoglobin’s oxygen affinity, aiding tissue oxygen release.

Increased alveolar-capillary permeability leading to non-cardiogenic pulmonary edema.

Diabetic ketoacidosis, lactic acidosis, or renal failure increase unmeasured acids.

Normal PaCO₂ is 35–45 mmHg; outside this range indicates respiratory acidosis or alkalosis.

Hypokalemia reduces muscle contractility, worsening ventilation.

The kidneys excrete bicarbonate (↓HCO₃⁻) to restore normal pH.

The terminal ileum specifically reabsorbs bile salts and vitamin B12 from intestinal contents.

Anion gap differentiates causes of metabolic acidosis like DKA or renal failure.

Low tidal volume (6 mL/kg) prevents overdistension and barotrauma.

pH <7.35, pCO₂ >45 mmHg, HCO₃⁻ slightly raised indicates partial renal compensation.

Cholecystokinin (CCK) from duodenum triggers bile ejection into the small intestine for fat digestion.

Use of accessory muscles, nasal flaring, and cyanosis indicate respiratory distress.

Pulse oximetry measures arterial oxygen saturation (SpO₂) non-invasively using light absorption.

pH >7.45 and HCO₃⁻ >26 with normal pCO₂ indicate uncompensated metabolic alkalosis.

Bicarbonate from pancreatic juice neutralizes gastric acid entering the duodenum.

pH normal, CO₂ and HCO₃⁻ both abnormal but balanced.

Hypoventilation increases CO₂ retention, causing respiratory acidosis (↑pCO₂, ↓pH).

The phrenic nerve, originating from C3–C5, controls the diaphragm and is vital for breathing.

In metabolic acidosis, bicarbonate (HCO₃⁻) decreases and pH falls below 7.35 due to excess acid or base loss.

Increased alveolar-capillary permeability leads to pulmonary edema and gas exchange failure.

Oxygenation of hemoglobin decreases its CO₂ carrying capacity, aiding CO₂ unloading.

Steatorrhea results from fat malabsorption due to pancreatic or bile deficiency.

Low pH with high pCO₂ confirms respiratory acidosis, typical of COPD or hypoventilation.

Allowing higher PaCO₂ prevents barotrauma and maintains low tidal volume ventilation.

Iron is mainly absorbed in the duodenum where it’s converted from ferric to ferrous form.

Residual volume is the air left in lungs after forced exhalation, preventing collapse.

55/0.5 = 110 → indicates severe ARDS.

Maintain FiO₂ <60% and titrate based on ABG results.

Acidosis shifts the curve rightward, releasing more oxygen to tissues (Bohr effect).

The alveoli are tiny sacs where oxygen diffuses into the blood and carbon dioxide diffuses out through thin membranes.

Occurs when respiratory failure is superimposed on metabolic acidosis, e.g., cardiac arrest.

Type II failure results from hypoventilation leading to CO₂ retention and respiratory acidosis.