Human Urinary System: Acid-Base Regulation

Learning Objectives: Students should be able to define pH, acidosis, alkalosis, volatile and fixed acids; discuss how the body defends against pH changes (blood buffers, respiratory system, kidneys); and provide examples of acid-base balance pathophysiology.

Hydrogen Ions (H+): Source of acidity in blood.
pH: Potential of H+ ion concentration in body fluids. Arterial blood pH is 7.35-7.45.
Buffer: Agent that prevents or minimizes pH change when acid or base is added. Buffers consist of a weak acid and its salt, or a weak base and its salt. They reversibly bind or release H+ ions.

Normal Arterial Blood pH: 7.35-7.45
Acidosis: pH below 7.35
Alkalosis: pH above 7.45
Incompatibility with Life: pH below 6.8 or above 7.8
Fixed Acids: Sulphuric acid, phosphoric acid, and ammonia. Needing the kidneys for excretion.
Volatile Acid: Carbon dioxide (CO2). Excreted by the lungs.

Filtrate Acidification: Kidneys acidify glomerular filtrate from a pH of 7.4 to approximately 6.
Urine pH Range: Depending on acid-base balance, urine pH can range from 4.5 to 8.0 (normal average is about 6.0).

CO2 Importance: Important source of acid and bicarbonate (alkali).
CO2 Tension (Partial Pressure): Normal arterial CO2 tension (PaCO2) is 38-42 mmHg.
HCO3- Concentration: Normal arterial HCO3- concentration is 22-28 mEq/L(average 24 meq/L).
CO2 as Acid & HCO3- as Alkali: Practical purposes, CO2 is considered acid because dissolved CO2 creates carbonic acid(H2CO3). HCO3- is an alkali.
Respiratory Factor: CO2
Metabolic Factor: HCO3-

Mechanism: Control pH via CO2 removal or retention.
Time Frame: Acts within seconds or fraction of a second; relatively short-term response.
Increase in PaCO2: Respiratory acidosis (e.g., hypoventilation).
Decrease in PaCO2: Respiratory alkalosis (e.g., hyperventilation).
[H+] affects Alveolar Ventilation: Lower pH increases ventilation rate 4-5 times, while higher pH decreases it.
Negative Feedback: Respiratory system acts as a negative feedback to control [H+].

Mechanism: Slow, but powerful (days or more) buffering mechanism. Kidneys can secrete acidic or alkaline urine to regulate blood pH.
HCO3- Filtration: Continuously filtering HCO3- into tubules.
Buffering Systems: Employing bicarbonate, phosphate, and ammonia buffering mechanisms.
Renal Bicarbonate Buffering: Three mechanisms include H+ secretion, HCO3- reabsorption, and new bicarbonate ion production, all situated in distal tubules and collecting ducts.
Renal Phosphate Buffering: Intracellular and renal tubular fluid buffer. Components are H2PO4- and HPO42-.HCI (strong acid) is replaced by the weaker NaH2PO4, minimizing pH decrease.
Ammonia (NH3) Buffering: Ammonia ionizes, forming ammonium ion (NH4+), which is a useful buffer. Decreased ECF pH stimulates glutamine metabolism, leading to more NH4+ and HCO3- production. For every glutamine molecule that's metabolized, 2 new HCO3- ions are created.

Respiratory Acidosis: Kidneys increase plasma HCO3- levels (compensatory mechanism).
Metabolic Acidosis: Increase in ventilation and kidneys make new HCO3- (compensatory mechanism).
Respiratory Alkalosis: Increased renal excretion of HCO3- (compensatory mechanism).
Metabolic Alkalosis: Decreased Ventilation, increased CO2, and increased renal excretion of HCO3− (compensatory mechanism).

Condition: Decreased ventilation (hypoventilation) increases CO2 and causes acidosis (PaCO2 over 45mmHg, pH under 7.35).
Common Causes: Acute pulmonary edema (excess fluid in lungs), other conditions like pneumonia
Symptoms: Dyspnea ("shortness of breath"), suffocating or drowning feelings, wheezing, gasping, cyanosis ("bluish skin"), cough with frothy sputum, and possibly blood tinged. Central bat-wing pattern observed on chest X-rays can be a sign of respiratory acidosis.
Significance: Medical emergency, requiring prompt attention to restore proper ventilation and respiratory function.

Condition: Excessive anxiety or hyperventilation reduces CO2, causing alkalosis (PaCO2 under 35 mmHg, pH over 7.45).
Symptoms: Extreme worry, anxiety, agitation, panic, confusion, weakness, or dizziness.
Physiology: Reduced CO2 in blood reduced blood flow to the brain, resulting in nervous system/emotional symptoms.

Condition: Often caused by renal failure or other metabolic disturbances; imbalance in acid-base homeostasis leads to a decrease in blood pH (below 7.35).
Symptoms: Increased heart rate, rapid breathing, fatigue, muscle pain, mental confusion, edema (e.g. facial puffiness or swelling in lower limbs), headache, sleepiness, loss of appetite, further complications
Physiology: Respiratory compensation leads to a decrease in PaCO2 (below 35 mmHg) to counteract the metabolic acidosis. HCO3- levels in the blood are also decreased.

Condition: Increases in blood bicarbonate (HCO3−) often occur with prolonged vomiting, excessive ingestion of antacids, or other conditions. Blood pH becomes elevated.
Symptoms: Hand tremors, nausea, vomiting, and numbness or tingling in face, hands, and/or feet, further complications
Physiology: The cause is an increase in blood HCO3− concentration (typically above 28mEq/L), often coupled with a lower than normal level of blood CO2 as the body tries to compensate resulting changes toward metabolic alkalosis.