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

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

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

Potassium shifts into cells causing hypokalemia during respiratory alkalosis.

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

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

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

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

55/0.5 = 110 → indicates severe ARDS.

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

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

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

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

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

Carbon monoxide poisoning gives false high readings due to carboxyhemoglobin.

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

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

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

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

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

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

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

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

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

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

Hypokalemia reduces muscle contractility, worsening ventilation.

Marked bradypnea and decreased effort signal fatigue and impending failure.

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

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

PaO₂ of 55 mmHg indicates moderate hypoxemia requiring oxygen therapy.

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

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

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

Bicarbonate from pancreatic juice neutralizes gastric acid entering the duodenum.

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

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

The medulla oblongata automatically controls breathing rhythm and depth.

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

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

Rising PaCO₂ and falling pH indicate fatigue and inadequate ventilation.

Hypoxemia not corrected even with high FiO₂ due to shunting.

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

Diabetic ketoacidosis and lactic acidosis increase unmeasured anions.

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

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

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

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

Pulmonary embolism increases areas not perfused but ventilated.

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

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