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

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

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

PaO₂ of 55 mmHg indicates moderate hypoxemia requiring oxygen therapy.

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

Pulmonary embolism increases areas not perfused but ventilated.

Potassium shifts into cells causing hypokalemia during respiratory alkalosis.

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

Diabetic ketoacidosis and lactic acidosis increase unmeasured anions.

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

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

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

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

The medulla oblongata automatically controls breathing rhythm and depth.

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

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

Hypokalemia reduces muscle contractility, worsening ventilation.

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

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

Marked bradypnea and decreased effort signal fatigue and impending failure.

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

Carbon monoxide poisoning gives false high readings due to carboxyhemoglobin.

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

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

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

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

Hypoxemia not corrected even with high FiO₂ due to shunting.

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

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

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

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

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

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

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

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

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

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

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

55/0.5 = 110 → indicates severe ARDS.

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

Rising PaCO₂ and falling pH indicate fatigue and inadequate ventilation.

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

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

Bicarbonate from pancreatic juice neutralizes gastric acid entering the duodenum.

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

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

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

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

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

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