Rising PaCO₂ and falling pH indicate fatigue and inadequate ventilation.

Hypokalemia reduces muscle contractility, worsening ventilation.

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

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

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

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

Diabetic ketoacidosis and lactic acidosis increase unmeasured anions.

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.

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

Carbon monoxide poisoning gives false high readings due to carboxyhemoglobin.

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

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

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

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

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

Bicarbonate from pancreatic juice neutralizes gastric acid entering the duodenum.

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

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

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

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

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

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

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

Pulmonary embolism increases areas not perfused but ventilated.

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

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

Potassium shifts into cells causing hypokalemia during respiratory alkalosis.

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

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

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

PaO₂ of 55 mmHg indicates moderate hypoxemia requiring oxygen therapy.

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

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

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

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

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

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

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

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

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

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

Marked bradypnea and decreased effort signal fatigue and impending failure.

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

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

The medulla oblongata automatically controls breathing rhythm and depth.

Hypoxemia not corrected even with high FiO₂ due to shunting.

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

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

55/0.5 = 110 → indicates severe ARDS.