alterations in acid & base balance

Normal arterial pH:

7.35–7.45

Acidosis:

pH < 7.35

Severe acidosis (life-threatening):

pH < 6.8

Alkalosis

pH > 7.45

Severe alkalosis (life-threatening):

pH > 7.8

small changes in pH have??

significant physiological impact.

PaO2 (arterial O2)

80–100 mmHg

PaO2 less than 80…

Hypoxemia

saO2 (O2 saturation):

>95%

◦ % of hemoglobin bound to O2

HCO3− (bicarbonate):

22–26 mEq/L

Acids

• Hydrogen ion (H+) donors; strength depends on how many H+ ions are released.

acids circulate in 2 forms:

1. volatile

2. nonvolatile

volatile acids

• (e.g., carbonic acid): Formed from CO2 and eliminated via the lungs

nonvolatile (fixed) acids

• (e.g., lactic acid, ketoacids): Formed from metabolism of proteins, fats, etc.; must be excreted by the kidneys.

• Accumulation of acids can lead to…

acidosis; type depends on whether the acid is volatile (respiratory) or nonvolatile (metabolic).

bases

• Hydrogen ion (H+) acceptors.

what is the main physiological base?

bicarbonate (HCO3−), which buffers excess H+ and helps maintain blood pH.

what is bicarbonate regulated by and play a key role in?

Bicarbonate is regulated by the kidneys and plays a key role in acid- base compensation.

know bicarbonate values

ph is maintained by?

Maintained by a 20:1 ratio of bicarbonate (HCO3−) to carbonic acid (H2CO3)

↓ Ratio (< 20:1):

Blood becomes acidic (pH < 7.35)

↑ Ratio (> 20:1):

Blood becomes alkalotic (pH > 7.45)

buffers

Weak acids/bases that neutralize strong acids/bases to minimize pH

changes.

buffers purpose

Keep pH in the normal range (7.35–7.45).

buffers limits

Buffers act quickly but can be overwhelmed with excess acid/base.

major buffer systems

▪ Intracellular

▪ Extracellular

▪Protein buffers

▪Bicarbonate buffer

When H+ increases in blood (acidosis) for intracellular buffer:

• H+ moves into cells, K+ moves out → ↑ serum potassium

When H+ decreases in blood (alkalosis) for intracellular buffer:

H+ moves out of cells, K+ moves in → ↓ serum potassium

proteins are?

amphoteric

• Can act as either base or acid

•Hemoglobin (most common), Albumin (most common), globulins are example proteins

Major plasma buffer:

H+ + HCO3− ⇌ H2CO3 ⇌ CO2 + H2O

▪Neutralizes excess H+ by binding it to bicarbonate

▪H2CO3 ≈ 20:1 to maintain pH ≈ 7.4

what the carbonic acid bicarbonate buffer does when H+ increases a little bit:

▪If H+ increases a little bit:

→ HCO3− binds H+ → forms H2CO3 → breaks down to CO2 → exhaled

what the carbonic acid bicarbonate buffer does when H+ decreases a little bit:

▪If H+ decreases:
→ H2CO3 dissociates to release H+ and stabilize pH

when carbonic acid bicarbonate buffer system overwhelmed:

▪Too much H+ or loss of HCO3− exceeds buffer capacity

▪Free H+ accumulates → pH drops further

what happens when CO2 diffuses into RBCs"?

CO2 diffuses into RBCs and reacts with H2O → H2CO3 (via carbonic anhydrase)

▪H2CO3 dissociates → H+ + HCO3−
▪H+ binds hemoglobin (prevents large pH change until overwhelmed)

▪HCO3− exits RBC, Cl− enters (chloride shift)

↑ CO2 leads to…

↑ H+ → ↓ pH

↓ CO2 leads to…

↓ H+ → ↑ pH

higher ratio of bicarbonate to carbonic acid:

higher pH (alkalosis)

lower ratio of bicarbonate to carbonic acid

lower pH (acidosis)

lung compensation of acidosis

• Respiratory rate/depth go up in an attempt to blow off acids

• Carbonic acid can be carried to the lungs where it is reduced to carbon dioxide (CO2) + water and exhaled

lung compensation in alkalosis

• respiratory rate and depth go down

• Carbon dioxide (CO2) is retained & carbonic acid builds to neutralize and decrease the strength of excess bicarbonate

lung compensation happens when?

Happens within seconds

•when the cause is metabolic and buffer systems in blood are overwhelmed

• Meaning when the cause of the pH imbalance is not due to the respiratory system

kidney compensation of pH imbalance

This response is the main way the body compensates for pH imbalances caused by the respiratory system when buffer systems are no longer effective.

what happens when the kidneys themselves are the source of the problem?

The kidneys can also correct metabolic imbalances, but if the kidneys themselves are the source of the problem, their ability to compensate is limited.

kidney compensation in acidosis:

▪Kidneys secrete more H+ into the tubules

▪Reabsorb more bicarbonate (HCO3−)

kidney compensation in alkalosis

▪Kidneys secrete less H+

▪Excrete more bicarbonate

kidneys vs lungs compensation

kidneys are slower than the lungs to compensate

renal compensation takes hours to start and up to 2–3 days to fully correct pH.

all acid base imbalances are classified as:

1. respiratory

2. metabolic

based on the underlying cause

Respiratory Acidosis / Alkalosis

▪Caused by abnormal CO2 levels due to changes in ventilation

▪Key indicator: PaCO2

respiratory acidosis is:

high co2

respiratory alkalosis is:

low CO2

metabolic acidosis/alkalosis

▪Caused by all other non-respiratory factors

▪Key indicator: HCO3−

metabolic acidosis is:

↓ HCO3−

metabolic alkalosis is:

↑ HCO3−

compensation

The body attempts to correct pH by using the opposite system:

▪ If the cause is respiratory, the kidneys respond
▪ If the cause is metabolic, the lungs primarily respond

metabolic acidosis

• Total bicarbonate (HCO3−) concentration is low

• There is a relative excess of hydrogen ions (H+)

• Caused by accumulation of non-volatile acids that exceed available HCO3−

low HCO3− level indicates…

metabolic acidosis

metabolic acidosis compensation:

The body responds by increasing respiratory rate and depth to eliminate CO2 and raise pH.

metabolic acidosis causes

1. diabetic ketoacidosis

2. renal failure

3. hypoxia

4. aspirin overdose

5. severe diarrhea

6. excessive fat catabolism

7. high fat diet

how does diabetic ketoacidosis cause metabolic acidosis

↑ Fat metabolism → buildup of ketones and acids

how does renal failure cause metabolic acidosis

↓ H+ excretion and ↓ HCO3− reabsorption

↓ Ammonium (NH4+) excretion

how does hypoxia cause metabolic acidosis

Anaerobic metabolism → ↑ lactic acid

how does aspirin overdose cause metabolic acidosis

↑ H+ concentration from excess acetylsalicylic acid

how does severe diarrhea cause metabolic acidosis?

Loss of alkaline intestinal/pancreatic secretions → ↓ base

how does excessive fat catabolism cause metabolic acidosis?

↑ ketones and acid buildup

how does high fat diet cause metabolic acidosis?

↑ Fat metabolism → ↑ ketone production

anion gap

Measures the balance between positive and negative ions in the blood

which is the main positive ion for anion gap?

Na+

what are the main measured negative ions for anion gap?

Cl− and HCO3−

anion gap formula

Formula: AG = [Na+] – ([Cl−] + [HCO3−])

▪Normal range: 8–16 mEq/L

what are other unmeasured negative ions for anion gap?

lactate, phosphate, and sulfate

why does the anion gap matter?

Used to help find the cause of metabolic acidosis

▪High anion gap acidosis:

Extra acids (like lactic acid); HCO3− decreases, Cl− stays the same

Normal anion gap acidosis:

HCO3− is lost; Cl− increases to keep balance (electroneutrality)

High Anion Gap Common Causes:

▪Lactic acidosis (e.g., shock, heart failure)

▪Diabetic ketoacidosis

▪Aspirin (salicylate) poisoning

▪Renal failure (↓ acid excretion)

▪Normal Anion Gap Common Causes:

▪Bicarbonate loss:

▪ Diarrhea
▪ Intestinal suction
▪ Carbonic anhydrase inhibitors

▪Hormonal cause:
▪ Hypoaldosteronism (↓ bicarbonate retention)

▪Chloride gain:
▪ Excess Cl− reabsorption by kidneys

▪ Large volumes of NaCl infusion

neural metabolic acidosis manifestations

▪ Weakness
▪ Lethargy
▪ General malaise ▪ Twitching
▪ Confusion
▪ Stupor
▪ Coma

cardio metabolic acidosis manifestations

▪ Peripheral vasodilation → warm, flushed skin
▪ ↓ Heart rate (bradycardia)
▪ Risk of cardiac dysrhythmias due to electrolyte shifts

GI function metabolic acidosis manifestations

▪ Anorexia
▪ Nausea & vomiting

▪ Abdominal pain

skeletal metabolic acidosis manifestations

• Bone disease (acid can accumulate in bone tissue)

endocrine metabolic acidosis manifestation

▪Fruity breath (in diabetic ketoacidosis)

metabolic acidosis respiratory manifestations

▪Kussmaul respirations

▪↑ RR & depth

metabolic acidosis electrolyte shifts manifestations

▪ Hyperkalemia
▪Hypercalcemia (increased ionized calcium)

▪ Cells take up H+ and release K+ into blood

metabolic acidosis renal compensation manifestations

▪↑ Ammonium in urine

metabolic acidosis interventions

▪Identify and treat the underlying cause
▪Monitor vital signs and respiratory status
▪Ensure a patent airway
▪Assess LOC for signs of CNS depression
▪Monitor electrolytes, especially potassium
▪Maintain strict I&O; assist with fluid/electrolyte replacement ▪Implement seizure/precaution protocols if risk of coma ▪Administer prescribed IV fluids

▪Monitor potassium closely—levels may drop as acidosis is corrected

Lactic Acidosis interventions

Administer oxygen to improve tissue perfusion and reduce anaerobic metabolism

Diabetic Ketoacidosis (DKA) compensation

Give insulin to move glucose into cells, reducing fat metabolism and ketone

production

•Renal Failure (RF) compensation

• Dialysis to remove waste products contributing to acidosis
• Low-protein, high-calorie diet to reduce protein catabolism and acid load

primary compensation in metabolic acidosis

Respiratory (Primary, Fast)
▪ Hyperventilation increases CO2 loss
▪ ↓ CO2 (< 35 mmHg) → respiratory alkalosis

▪ Example: Kussmaul respirations
▪ Starts within minutes to hours

secondary compensation in metabolic acidosis

▪Renal (Secondary, Slow – if needed)

▪ ↑ H+ excretion (as NH4+)
▪ ↑ HCO3− reabsorption and generation

▪ Takes hours to days

if cause is renal failure compensation:

▪ Kidneys can’t excrete H+ or regenerate HCO3−
▪ Respiratory compensation is the only effective mechanism

▪ Acidosis may persist unless treated with:

– Dialysis

– Bicarbonate (sometimes)
– Low-protein, high-calorie diet

metabolic alkalosis

• Deficit of carbonic acid (H2CO3) and ↓ hydrogen ion concentration
• Caused by accumulation of base or loss of non-volatile acid without equivalent base loss

metabolic alkalosis compensation

Hypoventilation → ↑ CO2 retention → ↑ carbonic acid to help restore pH

common causes of metabolic alkalosis

• Excessive intake of sodium bicarbonate (e.g., Alka-Seltzer)
• GI acid loss: vomiting, nasogastric suction
• Diuretics (especially loop and thiazide)
• Hyperaldosteronism:

how does hyperaldosteronism lead to metabolic alkalosis?

aldosterone leads to ↑ H+ secretion, leads to hypokalemia

◦ → Triggers K+/H+ shift (H+ enters cells, worsening alkalosis)

◦ Aldosterone also causes ↑ K+ secretion further making the hypokalemia worse

• Massive blood transfusion: citrate metabolized to bicarbonate

metabolic alkalosis neural manifestations

Confusion
• Hyperactive DTRs
• Tetany
• Convulsions
• Paresthesias (fingers, toes) • Circumoral paresthesias
• Carpopedal spasm
• Restlessness

cardiac metabolic alkalosis

Hypotension
• Dysrhythmias (e.g., sinus tachycardia)

gi function metabolic alkalosis

Nausea and vomiting

metabolic alkalosis manifestations compensation

• ↓ Respiratory rate and depth

• ↑ Urine pH

metabolic alkalosis manifestations electrolyte imbalances

• Hypokalemia
• Hypocalcemia (less ionized calcium)

metabolic alkalosis treatment

· Correct the underlying cause of the imbalance

· Administer IV fluids (normal saline) and electrolyte replacements (K+, Cl−)

· Provide adequate chloride to promote NaCl reabsorption and HCO3− excretion

· Monitor cardiac rhythm for signs of hypokalemia

· Patient education:
◦ Risks of excessive sodium bicarbonate use
◦ Importance of KCl supplementation with loop/thiazide diuretics