Acid Base Balance Flashcards
(175 cards)
1
Q
Any hydrogen-containing substance capable of donating a proton (hydrogen ion) to another substance
A
Acid
2
Q
Molecule or ion able to accept hydrogen ion from an acid
A
Base
3
Q
Example of a base that releases hydroxyl ions (OH⁻) in water.
A
Sodium hydroxide (NaOH)
4
Q
A strong acid in stomach juice (from parietal cells) that fully breaks down in water → more H⁺ → lower pH.
pH is inversely related to H⁺ concentration.
A
Hydrochloric Acid (HCl)
5
Q
Most abundant Volatile Acid
A
Carbonic acid (H₂CO₃)
5
Q
Two Types of Acids
A
- Volatile Acids
- Fixed, Nonvolatile Acids
6
Q
Acids removed by the lungs.
A
Volatile Acids
7
Q
How is carbonic acid removed?
A
H₂CO₃ → H₂O + CO₂
CO₂ is exhaled
8
Q
Why are they called “volatile”?
A
They evaporate easily (low boiling point)
8
Q
Example of a volatile acid in daily life?
A
Soda – fizzy from CO₂ 🥤
9
Q
Not removed by lungs — cleared by kidneys
A
Fixed, nonvolatile acids
10
Q
Two kinds of fixed, nonvolatile acids?
A
Inorganic Acids (No carbon)
Organic Acids (Contain carbon)
11
Q
Example of Inorganic Acids
A
H₂SO₄ (sulfuric)
H₃PO₄ (phosphoric)
12
Q
Where do inorganic acids come from?
A
- Sulfur AAs: Cysteine, Methionine
- Phosphorylated AAs: Serine, Threonine, Tyrosine
- Nucleotides → Phosphoric acid
13
Q
Example of Sulfur Amino Acids
A
Cysteine
Methionine
14
Q
Example of Phosphorylated Amino Acids
A
Serine
Threonine
Tyrosine
14
Q
What happens under nucleotides in inorganic acids?
A
Nucleotides → Phosphate → Phosphoric acid
15
Q
Example organic fixed acids
A
Acetoacetic acid
Lactic acid
16
Q
Where does acetoacetic acid come from?
A
From ketone bodies → turns into β-hydroxybutyric acid
17
Q
Example of Amino Acids that form Acetoacetic Acid (ketogenic & glucogenic)
A
Tyrosine
Isoleucine
Phenylalanine
Tryptophan
Leucine
18
Q
How is lactic acid formed?
A
From anaerobic glycolysis
Pyruvate → Lactic acid (via Lactate Dehydrogenase)
18
Q
Lactic acid vs. Lactate
A
Lactic acid = acid form
It breaks into H⁺ + Lactate⁻
Lactate = conjugate base
19
Q
Don’t fully dissociate in solution
Can give off H⁺, but not all at once
Partially lose protons
A
Weak Acids
20
Q
Completely dissociate in solution
High ability to give up H⁺ quickly
A
Strong Acids
21
Examples of Weak Acids
F – Formic acid (HCOOH)
B – Benzoic acid (C₆H₅COOH)
P – Phosphoric acid (H₃PO₄)
C – Carbonic acid (H₂CO₃)
A – Acetic acid (CH₃COOH)
H – Hydrofluoric acid (HF)
S – Sulfurous acid (H₂SO₃)
N – Nitrous acid (HNO₂)
21
Examples of Strong Acids
C – Chloric acid
H – Hydrobromic acid
H – Hydrochloric acid
H – Hydroiodic acid
N – Nitric acid
P – Perchloric acid
S – Sulfuric acid
22
3 Defense Mechanisms
1. Buffer system
2. Respiratory Mechanism
3. Renal Mechanism
23
Chemical ability to minimize changes in pH even when exposed to higher concentrations of acids/bases
Buffer System
24
Compounds resist excess changes in the pH/level of acidity; Rapid-acting
Buffers
25
What are buffers made of?
Weak acids + Salt + conjugate base
26
Hemoglobin buffer system: Deoxygenated
Hb
27
Hemoglobin buffer system: Oxygenated
HbO₂
28
What is KHbO₂ made up of?
HbO₂ + potassium + salt
29
Hemoglobin buffer system: Conjugate base (reduced form)
HHbO₂
30
What predominates at pH 7.4?
Conjugate base is higher than the weak acid.
31
Does Phosphate buffer system follow the pH 7.4 rule?
Yes — conjugate base also outweighs weak acid at pH 7.4.
32
Main buffer for fixed, nonvolatile acids?
Bicarbonate buffer system
33
This system neutralizes acids like acetoacetic acid
Bicarbonate buffer system
34
What does acetoacetic do in the bicarbonate buffer system?
Releases H⁺ → becomes acetoacetate
Too much H⁺ = acidosis
35
How does the body respond to acidosis in bicarbonate buffer system?
NaHCO₃ binds H⁺ → forms H₂CO₃ →
Breaks down into CO₂ + H₂O → CO₂ is exhaled → Removes acid → helps balance pH
36
Henderson-Hasselbalch Equation
pH = pKₐ + log([A⁻]/[HA])
37
Equation Variables: What do they mean?
A⁻ (bicarbonate) ↑ = pH ↑
HA (H⁺) ↑ = pH ↓
pKₐ = acid strength
38
Alkali reserve (body’s base supply)
Sodium Bicarbonate
39
Low sodium bicarbonate?
Metabolic acidosis
Seen in DKA (diabetic ketoacidosis)
40
Too much sodium bicarbonate
Metabolic alkalosis
41
Important in buffering acids in the distal tubules of kidneys
Phosphate Buffer System
42
Reaction of Phosphate Buffer System
H₂PO₄⁻ ⇌ HPO₄²⁻ + H⁺
43
2 Components of the Phosphate Buffer System
1. Na or KH₂PO₄ (monopotassium dihydrogen phosphate)
2. Na₂ or K₂HPO₄ (dipotassium hydrogen phosphate)
44
Component of the Phosphate buffer system that is Weak acid (proton donor), Releases H⁺ when pH is too high (acidic)
Na or KH₂PO₄ (monopotassium dihydrogen phosphate)
45
Component of the Phosphate buffer system that is Weak base (proton acceptor), Absorbs H⁺ when pH is too low (alkaline)
Na₂ or K₂HPO₄ (dipotassium hydrogen phosphate)
46
Main extracellular buffer CO₂ from aerobic metabolism in the blood
Hemoglobin Buffer System
47
Reaction for Hemoglobin Buffer System
CO₂ + H₂O ⇌ H₂CO₃ ⇌ HCO₃⁻ + H⁺
(Reaction occurs via carbonic anhydrase)
48
HCO₃⁻ exits RBCs, Cl⁻ enters to balance charge
Chloride Shift
49
Percentage of blood buffering that comes from hemoglobin?
60% due to its high concentration in RBCs
50
Oxyhemoglobin vs. Deoxyhemoglobin: Acid Strength?
Oxyhemoglobin (HHbO₂): Stronger acid at pH 7.25 (acidosis)
Deoxyhemoglobin (HHb): Weaker acid
51
Oxyhemoglobin vs. Deoxyhemoglobin: Buffering Ability?
Oxyhemoglobin: Weaker buffer, releases more H⁺
Deoxyhemoglobin: Better buffer, holds onto H⁺
51
Oxyhemoglobin vs. Deoxyhemoglobin: H⁺ Release?
Oxyhemoglobin: Releases more H⁺ (1.88 mEq/mol)
Deoxyhemoglobin: Releases fewer H⁺ (1.28 mEq/mol)
52
Can Oxyhemoglobin buffer carbonic acid?
No, because it shares the same acid-base pair as bicarbonate
53
Can Deoxyhemoglobin buffer carbonic acid?
Yes, it can buffer carbonic acid (H₂CO₃)
54
Oxyhemoglobin vs. Deoxyhemoglobin: pH Stabilization?
Oxyhemoglobin: Weaker at stabilizing pH
Deoxyhemoglobin: Better at stabilizing blood pH by holding onto H⁺
55
This mechanism is quick acting, activated during pH imbalances (emergency), cannot fully restore acid-base balance alone (incomplete restoration), and primarily regulates CO₂ levels in the blood
Respiratory Mechanism
56
1st Chloride Shift: Process of CO₂ transport from Peripheral tissues
Transport from Peripheral Tissues:
1. Chloride Shift (1st): CO₂ forms carbonic acid (H₂CO₃), dissociates into HCO₃⁻ + H⁺ in RBC (slow hydration, uncatalyzed)
2. CO₂ in Plasma: CO₂ is physically dissolved in plasma
3. CO₂ in RBC: CO₂ forms carbaminohemoglobin
4. Carbonic Anhydrase Action: Inside RBCs, catalyzes CO₂ → HCO₃⁻ + H⁺
5. Bicarbonate Shift: HCO₃⁻ exits RBC for chloride (Cl⁻)
57
2nd Chloride Shift: Elimination in the Lungs
1. Chloride Shift (2nd): HCO₃⁻ enters RBC from plasma, Cl⁻ exits
2. Oxygen Binding: O₂ binds to HHb (protonated hemoglobin), releasing H⁺
3. H⁺ and Bicarbonate Reaction: H⁺ + HCO₃⁻ → H₂CO₃, then catalyzed to H₂O + CO₂
4. CO₂ Diffusion: CO₂ moves from RBC to plasma, then alveoli for exhalation
5. Bohr & Haldane Effects:
Bohr Effect: CO₂/H⁺ affect O₂ binding
Haldane Effect: O₂ release displaces CO₂
6. CO₂ Expulsion: CO₂ is exhaled
58
Slow acting, but completely restores pH balance
Regulates sodium bicarbonate (NaHCO₃) levels in the blood
Secretes H⁺ and absorbs HCO₃⁻ to maintain pH
Renal Mechanism
59
Two main roles of kidneys in mainraining acid-base balance
1. Reclaims HCO₃⁻: Prevents bicarbonate loss in the proximal convoluted tubule.
2. Regenerates HCO₃⁻: Synthesizes new bicarbonate to replace bicarbonate used as a buffer.
60
What happens to bicarbonate in the kidneys?
Filtration: Bicarbonate is filtered out in the glomerulus.
Reabsorption: Most of the filtered HCO₃⁻ is reabsorbed in the proximal convoluted tubule to avoid loss.
61
How much bicarbonate is filtered by kidneys daily?
4320 mmol/day of HCO₃⁻ is filtered (180 L/day × 24 mmol/L).
62
How much bicarbonate needs to be replenished daily in the kidneys?
1.0-1.5 mmol/kg/day of HCO₃⁻ must be replenished based on daily acid load.
63
How much bicarbonate is needed for a 60kg female with kidney disease?
60-90 mmol/day of bicarbonate replenishment is required when regeneration is impaired in chronic kidney disease (CKD).
64
Why bicarbonate replenishment important in CKD?
Maintaining acid-base balance when regeneration is impaired
65
Main site of bicarbonate reabsorption in the kidney
Proximal tubule: 75-90% of filtered bicarbonate (HCO₃⁻) is reabsorbed.
66
Ions involved in bicarbonate reabsorption in the proximal tubule
Na⁺ (Sodium) and HCO₃⁻ (Bicarbonate) are reabsorbed together.
H⁺ (Hydrogen ions) are secreted into the tubular fluid.
67
What happens inside the proximal tubule cells to facilitate bicarbonate reabsorption?
CO₂ from blood and water enter the proximal tubule cells.
Carbonic anhydrase converts CO₂ and H₂O into carbonic acid (H₂CO₃).
Carbonic acid dissociates into H⁺ and HCO₃⁻.
68
How is bicarbonate (HCO₃⁻) reabsorbed in the proximal tubule?
HCO₃⁻ formed in the proximal tubule is reabsorbed into the blood.
H⁺ is secreted into the tubular fluid and buffered by NaHCO₃, forming carbonic acid, which dissociates into CO₂ and H₂O.
CO₂ and H₂O are reabsorbed into the tubule and converted back into NaHCO₃.
69
What happens to NaHCO₃ in the proximal tubule?
Most of the NaHCO₃ is reabsorbed back into the blood.
A small amount is excreted in the urine.
70
Percentage of bicarbonate is reabsorbed in the distal tubule?
10-25% of remaining bicarbonate is reabsorbed.
71
How much new bicarbonate (HCO₃⁻) is generated in the distal tubule per day?
1.0–1.5 mmol/kg/day
72
Main buffers in distal tubule?
Phosphate (PO₄²⁻) and Ammonia (NH₃)
73
When does NH₃ production increase?
1–2 days after acidosis
74
Ammonia role in acidosis?
Neutralizes H⁺ → forms NH₄⁺ → excreted as NH₄Cl
75
How does aldosterone affect the distal tubule in terms of acid-base balance?
Regulates Na⁺ and helps acidify urine → regulates pH
76
Phosphate buffer result?
Forms monosodium phosphate → lowers urine pH
77
End goal of distal tubule?
Reabsorb HCO₃⁻, excrete H⁺
78
HCO₃⁻ in ECF
350–400 mEq in ECF
79
H⁺ & pH regulation depends on?
CO₂ partial pressure, regulated by kidneys
80
Metabolic disorders are due to?
Nonvolatile acids or alkali
81
HCO₃⁻ role in ECF?
Buffers nonvolatile acids, gets consumed in process
82
Kidney's acid-base role?
Excretes acid anions, replenishes HCO₃⁻
83
New HCO₃⁻ generation via?
Titratable acid & NH₄⁺ excretion
83
Why reabsorb HCO₃⁻?
To prevent urinary loss
84
Free H⁺ excretion amount?
Only 0.1 mEq/L (even if pH = 4.0)
85
Titratable acid = ?
H⁺ excreted with phosphate buffer
86
Urine pH < 6.5 → HCO₃⁻ excretion?
Minimal; acid excretion = titratable acid + NH₄⁺
87
NH₄⁺ excretion importance?
Returns 1 HCO₃⁻ to body per NH₄⁺
88
H⁺ secretion functions?
Reabsorb HCO₃⁻, lower urine pH, excrete NH₄⁺
89
% of HCO₃⁻ reabsorbed in proximal tubule?
80%
90
% of HCO₃⁻ reabsorbed in thick ascending limb?
15%
91
Carbonic anhydrase role?
Facilitates H⁺ secretion in Proximal Tubule & Thick Ascending Limb
92
Main H⁺ transporters (Proximal Tubule & Thick Ascending Limb)?
Na⁺/H⁺ antiporter & H⁺-ATPase
92
Main H⁺ transporters (Distal Tubules & Collecting Ducts)?
H⁺-ATPase & H⁺-K⁺ ATPase
93
Main pathway of Proximal Tubule & Thick Ascending Limb:
Na+/H+ antiporter
94
Acidosis vs. Acidemia
Acidosis = excess H⁺
Acidemia = pH < 7.35
95
Alkalosis vs. Alkalemia
Alkalosis = excess HCO₃⁻
Alkalemia = pH > 7.45
96
ABG: What to analyze?
Δ HCO₃⁻ and Δ CO₂ — larger change = primary disorder
96
Metabolic vs. Respiratory Disorder
Metabolic = HCO₃⁻ change
Respiratory = pCO₂ change
97
Respiratory Acidosis: Cause & Compensation
↑ pCO₂ → Kidneys ↑ HCO₃⁻ (acid excretion)
98
Respiratory Alkalosis: Cause & Compensation
↓ pCO₂ → Kidneys ↓ HCO₃⁻ (less acid excretion)
99
Metabolic Acidosis: Cause & Compensation
↓ HCO₃⁻ → Hyperventilation (↓ CO₂)
100
Metabolic Alkalosis: Cause & Compensation
↑ HCO₃⁻ → Hypoventilation (↑ CO₂)
101
Step 1 in ABG Analysis
Check pH:
< 7.35 = acidosis
> 7.45 = alkalosis
102
Step 2: Identify the Cause
Check HCO₃⁻ (metabolic) and pCO₂ (respiratory)
103
Step 3: Determine Compensation
Respiratory problem → renal compensation
Metabolic problem → respiratory compensation
104
Respiratory Acidosis
↑ pCO₂ (hypoventilation) → renal ↑ HCO₃⁻
105
Respiratory Alkalosis
↓ pCO₂ (hyperventilation) → renal ↓ HCO₃⁻
106
Metabolic Acidosis
↓ HCO₃⁻ → respiratory ↓ CO₂
107
Metabolic Alkalosis
↑ HCO₃⁻ → respiratory ↑ CO₂
108
Key Principle: Compensation
One system always compensates for the other.
109
Key Principle: Balance
↑ Acid → ↑ Base to neutralize (and vice versa)
110
How to Determine Acid-Base Balance
Step 1: Check pH
Normal: 7.35–7.45
pH < 7.35 → Acidosis
pH > 7.45 → Alkalosis
Step 2: Check pCO₂ (Respiratory)
Normal: 35–45 mmHg
↑ = Respiratory Acidosis
↓ = Respiratory Alkalosis
Step 3: Check HCO₃⁻ (Metabolic)
Normal: 22–26 mEq/L
↓ = Metabolic Acidosis
↑ = Metabolic Alkalosis
111
ABG Quick Case: 7.55 | pCO₂ 32 ↓
Respiratory Alkalosis
112
ABG: 7.34 | pCO₂ 28 ↓ | HCO₃⁻ ↓
Metabolic Acidosis with Respiratory Compensation
113
ABG: 7.34 | pCO₂ 53 ↑
Respiratory Acidosis
114
Expected pCO₂ = 1.5 × [HCO₃⁻] + 8 ± 2
Compare actual vs expected pCO₂ for compensation check
Winter’s Formula (for Metabolic Acidosis)
115
Winter's Example: HCO₃⁻ = 10
Expected pCO₂ = 1.5(10) + 8 ± 2 = 23 ± 2 (21–25)
→ If actual:
< 21 → Respiratory Alkalosis
25 → Respiratory Acidosis
21–25 → Proper compensation
116
What is the compensation when renal ↑ HCO₃⁻ to neutralize excess CO₂
Respiratory Acidosis
117
What is the compensation when renal ↓ HCO₃⁻ to balance low CO₂
Respiratory Alkalosis
118
What is the compensation when lungs ↓ CO₂ via hyperventilation
Metabolic Acidosis
119
What is the compensation when lungs ↑ CO₂ via hypoventilation
Metabolic Alkalosis
120
Normal pH, altered pCO₂ and/or HCO₃⁻
Fully Compensated
121
Abnormal pH, compensation in progress
Partially Compensated
122
Abnormal pH, no compensation seen
Uncompensated
123
pH: ↓ (e.g., 7.20)
pCO₂: ↑ > 25
Compensation: Partial (↑ HCO₃⁻)
Respiratory Acidosis
124
pH: ↓ (e.g., 7.20)
pCO₂: ↓ < 21
Compensation: Partial (↓ HCO₃⁻)
Respiratory Alkalosis
125
pH: Normal
pCO₂: 21–25
Compensation: Full (↓ pCO₂ via lungs)
Metabolic Acidosis (Compensated)
126
pH: ↓ (e.g., 7.20)
pCO₂: < 21
Compensation: Excessive (mixed disorder)
Metabolic Acidosis + Concomittant Resp. Alkalosis
127
Purpose of ABG
Measures:
pH
pCO₂
pO₂
HCO₃⁻
base excess
O₂ saturation
128
No prep needed
Blood drawn from an artery, not a vein
Done by a respiratory therapist
ABG Procedure
129
Why Artery?
Arterial blood has more O₂ → more accurate for gas exchange
130
Common Sites (in order of use)
1. Radial artery (wrist) – most common
2. Femoral artery (groin)
3. Brachial artery (arm)
4. Dorsalis pedis (foot) – least common
131
Arterial Line (for monitoring)
Order: Radial > Femoral > Brachial > Dorsalis pedis
132
Why ABG is Done?
Assess severity of respiratory disorders:
→ Asthma, COPD, Cystic Fibrosis
Evaluate effectiveness of lung disease treatment
133
Hypoventilation leads to CO₂ trapping, increasing pCO₂.
Respiratory Acidosis
134
Examples of Respiratory Acidosis
Asthma – CO₂ trapped from excess bronchoconstriction
Morphine poisoning – ↓ respiratory drive; respiratory depression
Pulmonary edema – fluid accumulation in alveoli impairs gas exchange
Atelectasis – collapsed lung segment
Acute laryngospasm – sudden airway closure
135
Body's compensation for respiratory acidosis
Rapid, shallow breathing.
136
Common symptom of respiratory acidosis due to CO₂ buildup
Headache (cerebral vasodilation from ↑ CO₂).
137
Non-respiratory causes like cerebral disease, neuromuscular disorders, drug overdose, severe pneumonia, pulmonary edema, or status asthmaticus.
Acute respiratory acidosis
138
How does CO₂ buildup occur in acute respiratory acidosis?
Impaired ventilation leads to CO₂ accumulation, regardless of lung condition.
139
Examples of chronic respiratory acidosis
Chronic emphysema, chronic bronchitis, Pickwickian syndrome (obesity hypoventilation syndrome), obstructive sleep apnea
140
Body compensate in chronic respiratory acidosis
Kidney retention of HCO₃⁻ over time.
141
Hyperventilation causes CO₂ to decrease, leading to increased pH.
Respiratory Alkalosis
142
Examples and causes of respiratory alkalosis
CNS stimulation (hysteria, anxiety, encephalitis)
Early salicylate poisoning
Fever
Excessive mechanical ventilation
Acute hypoxia (e.g., pneumonia, status asthmaticus, pulmonary edema)
Chronic hypoxia (e.g., pulmonary fibrosis)
143
Common signs and symptoms of respiratory alkalosis
Light-headedness, confusion, circumoral/peripheral paresthesias, cramps, syncope
144
Mechanism behind the symptoms in respiratory alkalosis
Altered cerebral blood flow and pH due to low CO₂.
145
Decreased HCO₃⁻ → Decreased pH (acidic)
Metabolic Acidosis
146
Common causes of Metabolic Acidosis
Diabetic ketoacidosis (DKA) – ketone buildup
Renal failure – decreased acid excretion
Diarrhea – loss of HCO₃⁻
Lactic acidosis – increased lactate (e.g., cancer, CO poisoning)
Toxins – CO poisoning, methanol
147
Role of HCO₃⁻ in metabolic acidosis
HCO₃⁻ neutralizes acids like ketones or lactate. In metabolic acidosis, HCO₃⁻ is depleted due to the excess acids.
148
The difference between measured cations (Na⁺, K⁺) and anions (Cl⁻, HCO₃⁻) in the blood.
Anion Gap
149
Formula of Anion gap (without K+)
Na⁺ - (Cl⁻ + HCO₃⁻)
150
Formula of Anion gap (with K+)
Na⁺ + K⁺ - (Cl⁻ + HCO₃⁻)
151
Normal range of the anion gap (without K+)
~17 mmol/L
152
Normal range of the anion gap (with K+)
12-14 mmol/L
153
Why is an increased anion gap important?
It indicates metabolic acidosis (e.g., DKA, lactic acidosis, renal failure).
154
Two Calculation methods of Anion Gap
1. First anion gap formula
Anion Gap = Na+ - (Cl- + HCO3-)
2. Second anion gap formula
Anion Gap = (Na+ + K+) - (Cl- + HCO3-)
155
Two Primary Mechanisms
High Anion Gap
Normal Anion Gap
156
Increased non-volatile organic acids lead to a decrease in HCO₃⁻ to balance the excess
High Anion Gap Metabolic Acidosis
157
Causes of high anion gap metabolic acidosis (CAT MUDPILES)
C: Carbon monoxide, Cyanide
A: Aminoglycoside toxicity (antibiotics with -ycin)
T: Theophylline (coffee or rugby)
M: Methanol
U: Uremia
D: Diabetic ketoacidosis (ketoacidosis → starvation or alcohol ketoacidosis)
P: Paraldehyde poisoning, Paracetamol toxicity
I: Isoniazid toxicity (tb treatment), Iron toxicity
L: Lactic acidosis
E: Ethanol, Ethylene glycol
S: Salicylates (Aspirin)
157
Examples of High Anion Gap Metabolic Acidosis
Lactic acidosis – increased lactate
Ketoacidosis – increased ketones (e.g., DKA)
Toxins – methanol, salicylates
158
Causes increased production of acids in high anion gap metabolic acidosis
1. Ketoacidosis (Diabetes, Starvation, Alcoholism)
↑ acetoacetic acid and beta-hydroxybutyric acid
2. Lactic Acidosis (Circulatory/Respiratory failure, Drugs like Metformin)
↑ lactate
3. Poisoning (Salicylates, Methanol)
Accumulation of toxic acids
159
Renal failure contribute to metabolic acidosis
↓ renal acid excretion
↓ ammonia excretion
↑ bicarbonate excretion
160
It occurs due to the loss of HCO₃⁻ (bicarbonate), without an excess of organic acids to counterbalance the loss.
Normal Anion Gap Metabolic Acidosis
161
Causes of Normal Anion Gap Metabolic Acidosis: HARD UP
H: Hyperalimentation
A: Acetazolamide (carbonic anhydrase inhibitor)
R: Renal Tubular Acidosis (↑ clearance of HCO₃⁻)
D: Diarrhea (↑ HCO₃⁻ secretion)
U: Ureterosigmoid Fistula (HCO₃⁻ is lost)
P: Pancreatic Fistula (HCO₃⁻ is released)
162
Other Causes of Normal Anion Gap Metabolic Acidosis
Renal Tubular Dysfunction (defective renal tubular acidification)
Hypoaldosteronism (↓ hydrogen ion excretion)
Hyperkalemia (↓ ammonia production)
Drugs: Carbonic anhydrase inhibitors (e.g., Acetazolamide)
163
Common signs and symptoms of Metabolic Acidosis
Accelerated heartbeat (tachycardia)
Confusion or dizziness
Fatigue (feeling very tired)
Loss of appetite
Headache
Rapid breathing or long, deep breathing
Nausea and vomiting
Weakness
164
Ingestion of sodium bicarbonate
Treatment of peptic ulcers with alkali (sodium bicarbonate tablets)
Hypochloremic alkalosis (prolonged vomiting, high intestinal obstruction)
Metabolic Alkalosis
165
Common signs and symptoms of Metabolic Alkalosis
Confusion (can progress to stupor or coma)
Hand tremor
Lightheadedness
Muscle twitching
Nausea and vomiting
Numbness or tingling in the face, hands, or feet
Prolonged muscle spasms (tetany)
