ACID-BASE DISORDERS

• Acidosis (Metabolic and Respiratory)

• Alkalosis (Metabolic and Respiratory)

Supplementary Information
• BUFFERING: The principle extracellular buffer is the H2CO3/HCO3 system
o Buffering - Ability of a weak acid and its corresponding anion (base) to resist change in the
pH of a solution on the addition of a strong acid or base
• Bicarbonate is independently regulated by kidney.
• Change in the ventilation that alter the PCO2 regulates the carbonic acid level in the blood.
o In the presence of carbonic anhydrase, carbonic acid is in equilibrium with carbon dioxide
• Alteration in blood pH serve as the basis for the diagnosis of acid-base disorders
o Blood hydrogen ion concentration may not be indicative of other compartment where pH of
cell in cerebrospinal fluid can be altered but will not cause any alteration in the blood pH
level.

Regulation of Acid-Base Homeostasis

• Metabolically produce CO2 = lost in respiration; blood CO2 is constant
o When respiratory function is normal, the amount of CO2 produced metabolically is equal to
the amount lost by respiration and blood concentration remains the same.
3 mechanism the maintains acid-base balance
• Extracellular Buffering – occurs rapidly and is the body’s first defense against sudden increase in
hydrogen ion concentration
o Bicarbonate/Carbonic acid
▪ Carbonic acid represents the respiratory components of buffer pair since its
concentration is directly proportional to the PCO2 which is determined by ventilation
▪ Bicarbonate represents the metabolic component because kidney can alter its
concentration by reabsorption, generation new bicarbonate or altering elimination
o Proteins
▪ Charged chain of amino acids provide buffering action
▪ Greater concentration intracellularly, more important as an intracellular buffer
o Phosphates
▪ Organic phosphate
• Intracellular buffer, phosphate is more useful because extracellular phosphate is
present only in low concentrations so its usefulness as buffer is limited
▪ Calcium phosphate
• Calcium phosphate in bone is relatively inaccessible as buffer. Prolonged
metabolic acidosis results in release of phosphate from bone

• Respiratory Regulation
o Increasing minute ventilation (total amount of air exhaled over a 1-minute period), by
increasing respiratory rate and/or tidal volume (amount of air exhaled in one breath), will
increase CO2 excretion and decrease blood PCO2
o Vice versa (decreasing minute ventilation decreases CO2 excretion and increases blood
PCOs
o Rapidly adjust within minutes to changes in acid-base balance
• Renal Regulation – kidney will excrete the excess hydrogen ion, with the result of returning acid-
base balance to normal

Definition
• Acid-base disorders are pathologic changes in carbon dioxide partial pressure (PCO2) or serum
bicarbonate (HCO 3 −) that typically produce abnormal arterial pH values.
o Acidosis – abnormal process of disease which reduces PH due to increase in acid or
decrease in alkali
o Alkalosis – abnormal process or disease which increases PH due to decrease in acid or
increase in alkali
o Acidemia – “acid blood” refers to a blood ph below normal (PH < 7.35) and increased H
ion concentration
o Alkalemia – “alkaline blood” refers to a blood above normal (PH > 7.35 and decrease in H
ion concentration

EPIDEMIOLOGY
• In the study entitled “Study of Acid-Base Disorders and Biochemical Findings of Patients in a
Tertiary Care Hospital: A Descriptive Cross-sectional Study”
o Out of arterial blood gas analysis of 1144 patients, the prevalence of acid base disorders
was 718 (62.76%)
o Respiratory alkalosis was most common among 134 (40.36%) cases in simple acid base
disorder
o Whereas metabolic acidosis and respiratory alkalosis was most common among 204
(52.85%) in mixed acid base disorder.

Shreewastav, R. K., Jaishi, K. P., Pandey, M. R., Singh, G. P., & Singh, A. G. (2019). Study of Acid-
Base Disorders and Biochemical Findings of Patients in a Tertiary Care Hospital: A Descriptive Cross-
sectional Study. JNMA; journal of the Nepal Medical Association, 57(220), 432–436.
https://doi.org/10.31729/jnma.4722

PATHOPHYSIOLOGY

Metabolic Acidosis
• This can result from the buffering (consumption of HCO 3 −) of an exogenous acid, an organic
acid accumulating because of a metabolic disturbance (e.g., lactic acid or ketoacids), or the
progressive accumulation of endogenous acids secondary to impaired renal function (e.g.,
phosphates and sulfates).
• loss of bicarbonate-rich body fluids (e.g., diarrhea, biliary drainage, or pancreatic fistula) or occur
secondary to the rapid administration of non-alkali–containing intravenous fluids (dilutional
acidosis).

Metabolic Alkalosis
• The generation of metabolic alkalosis can also result from excessive losses of hydrogen ion from
the kidneys or stomach or from a gain secondary to the ingestion or administration of
bicarbonate rich fluids.
• With vomiting and nasogastric suctioning, hydrogen ion is lost externally and metabolic alkalosis
results.
• Diarrhea results in excessive gastrointestinal losses of chloride-rich, bicarbonate-poor fluid and
thus leads to the generation of metabolic alkalosis.

Respiratory Acidosis
• Respiratory acidosis occurs when the lungs fail to excrete carbon dioxide resulting in a lower pH.
• This can be the result of conditions that centrally inhibit the respiratory center, diseases that
interfere with pulmonary perfusion or neuromuscular function, and intrinsic airway or
parenchymal pulmonary disease

Respiratory Alkalosis
• A decrease in Paco2 occurs when ventilatory excretion exceeds metabolic production.
• negative CO 2 balance is primarily caused by an increase in ventilatory excretion of CO 2
(hyperventilation).
• A decrease in Paco 2 can occur in patients with cardiogenic, hypovolemic, or septic shock
because oxygen delivery to the carotid and aortic chemoreceptors is reduced

ETIOLOGY

Types of Acid-Base Disorders

 DIAGNOSIS
Steps in Acid-Base Diagnosis
1. Obtain arterial blood gases (ABGs) and electrolytes simultaneously.
2. Compare [HCO 3− ] on ABG and electrolytes to verify accuracy.
3. Calculate anion gap (AG).
a. The anion gap is defined as serum sodium (Na) concentration minus the sum of serum
chloride (Cl−) and serum bicarbonate (HCO3−) concentrations.
4. Is acidemia (pH <7.35) or alkalemia (pH >7.45) present?
5. Is the primary abnormality respiratory (alteration in PaC O2) or metabolic (alteration in HCO 3
)?
6. Estimate compensatory response

7. Compare change in [Cl−] with change in [Na+].

 TREATMENT
Non-Pharmacological
• If patient’s blood oxygen level is too low, patient may require oxygen. Noninvasive positive
pressure ventilation or a breathing machine may be necessary.
• Diet rich with necessary electrolytes, essential elements and proteins (aid in the body in acid-
base homeostasis
Respiratory Alkalosis
• Rebreathing device such as paper bag to control hyperventilation
• Mechanical ventilation for life threatening alkalosis (capnograph and spirometer to have precise
adjustment of ventilator setting)

Acute Respiratory Acidosis

• Therapeutic goal: provide adequate oxygenation (intubation and use of mechanical ventilators is
usually required.)
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• g

Pharmacological
Metabolic Acidosis
• Mild to moderate acidemia managed with gradual correction of the acidemia, over a period of
days to weeks, using oral sodium bicarbonate or other alkali preparations
• If acidemia persists, alkali therapy should be instituted with the goal of normalization of blood
pH.
• In patients with chronic metabolic acidosis because of gastrointestinal bicarbonate losses,
maintenance therapy should provide sufficient alkali to replace ongoing bicarbonate losses.

Sodium Bicarbonate
• provides fluid and electrolyte replacement and increases arterial pH
• Alkalosis can also result if too much sodium bicarbonate is administered too quickly.
• The main therapeutic effect of sodium bicarbonate administration is increasing plasma
bicarbonate levels, which are known to buffer excess hydrogen ion concentration, thereby raising
solution pH

Tromethamine
• Act as proton acceptor to prevent or correct acidosis
• Combines with hydrogen ions from carbonic acid to form bicarbonate and a cationic buffer
• Osmotic diuretics – increase urine flow, urine PH, and excretion of fixed acids.

Carbicarb
• equimolar mixture of sodium carbonate (Na2CO3) and sodium bicarbonate (NaHCO3)
• carbonate ion is a stronger base than bicarbonate,
• buffers hydrogen ions resulting in the formation of bicarbonate rather than CO2.

Dichloroacetate
• an investigational agent
• facilitates aerobic lactate metabolism by stimulating the activity of lactate dehydrogenase, thus
reversing hyperlactatemia and elevating blood pH.
• DCA can cause mild drowsiness and peripheral neuropathy that can be ameliorated or prevented
with thiamine supplementation
Metabolic Alkalosis

Respiratory Alkalosis
• For chronic cases (pH not exceeding 7.5), treatment is usually not required
• For acute cases (pH exceeding 7.5), must consider first identifying and correcting the underlying
cause.

Respiratory Acidosis
Acute Respiratory Acidosis
• Underlying cause should be treated for example use of bronchodilators for treatment of severe
bronchospasm
• Bicarbonate is rarely necessary since it can eliminate patient’s respiratory drive or can precipitate
to metabolic acidosis
 • Cautious use of alkali (bicarbonate or THAM) can restore the responsiveness of bronchial muscles
to β -adrenergic agonists and thus can be beneficial for those patients with severe
bronchospasm.

RECOMMENDATION/MONITORING
• It is important to monitor dietary intake since some food can sometimes induce alkalosis (food
that contains baking soda) and acidosis (high-fat diet that’s low in carbohydrates)
• Stay dehydrated
• Arterial blood gases should be monitored closely to ensure that the respiratory acidosis is
resolving without creating a metabolic alkalosis as the result of compensatory elevation in HCO3–
and decrease in Paco2.
• To prevent alkalosis, it is recommended to take foods high in nutrients and potassium can help
combat electrolyte deficiencies such as carrots, banana and other more
• Avoid smoking and alcohol.

METABOLIC ACIDOSIS: CASE STUDY & FARM

Case Study: “I just feel so weak all the time.”

Sue Rider is a 67-year-old woman with progressively declining renal function, due to hypertension, who is
being seen in the nephrology clinic for management of fatigue, dyspnea, somnolence, and lethargy. She
further reports that over the last few months she has experienced a decrease in appetite and occasionally
feels nauseated without vomiting. She reports frequent nonadherence to her antihypertensive regimen
“when I feel good.” She also reports no history of diarrhea. According to her Post Medical History she had
a HTN (Hypertension), Declining renal function due to HTN (Hypertension) and Seasonal allergic rhinitis.
She is a retired school teacher who lives with her husband of 38 years and has three grown children. She
denies alcohol use. There is no history of tobacco habituation or recreational drug use. However, history
of CAD (Coronary artery disease) in her mother’s family. She has been taking Amlodipine 5 mg po (by
mouth) daily, Lisinopril 20 mg po daily, Metolazone 2.5 mg po daily, taken intermittently for lower
extremity edema (reports that she has not taken any for the last few months) and she had no known drug
allergy.

FARM:

Findings:

Name: Sue Rider

Age: 67-year-old

Gender: Female

Vital Signs:
Blood Pressure: 145/85 (hypertension)

Pulse: 78/min

Respiratory Rate: 22/min

Temperature: 37.2°C

Weight: 75 kg

Height: 5'4''

She experienced:

• decrease in appetite
• feels nauseated without vomiting
• No history of diarrhea
• Somnolence (A state of drowsiness; sleepiness)
• Lethargy (lack of energy and enthusiasm)

Laboratory tests results:

(Na) Sodium blood test: 132 mEq/L (low which means hyponatremia) – because the normal range for
blood sodium levels is 135 to 145 milliequivalents per liter (mEq/L). Hyponatremia is more likely in
people living with certain diseases, like kidney failure, congestive heart failure, and diseases affecting
the lungs, liver or brain. In general, too much water in your body is usually the main problem and this
dilutes the sodium levels. Much less frequently, hyponatremia is due to significant sodium loss from
your body. Example is people who run in long races or run on hot days. They lose both salt and water in
their sweat and often replace these losses with mostly water.
(CO2) Carbon Dioxide test: 16 mEq/L (too low) – because normal CO2 ranges between 23 to 29 meq/L.
A low CO2 level can be a sign of several conditions, including: Kidney disease, Diabetic ketoacidosis,
which happens when your body's blood acid level goes up because it doesn't have enough insulin to
digest sugars. Metabolic acidosis, which means your body makes too much acid.
(BUN) Blood Urea Nitrogen / Creatinine test result: 37 mg/dL (too high) – because the normal
creatinine ratio for adults over 60 years of age range between 8-23 mg/dL (mg/deciliter) High level of
BUN is a sign of kidney dysfunction, while low BUN levels can indicate liver problems
(SCr) Serum Creatinine: 2.9 mg/dL (High) – the typical range for adult women is between 0.59 to 1.04
mg/dL. Her result indicates kidneys are not working well
(Ca) Calcium blood test: 7.4 mg/dL (low which means hypocalcemia) a normal reference range for the
blood total calcium test in adults is between 8.6 and 10.2 milligrams per deciliter (mg/dL). Her result
indicates Hypocalcemia shows low blood calcium level
Systemic pH: 7.28
Reduced serum bicarbonate which is only 15.5 mEq/L
Urine pH: 5.0 (under 5.0 is acidic)

Assessment:

1. Metabolic acidosis
2. Hypertension
3. Electrolyte abnormalities (hyponatremia, hypocalcemia)
4. Stage 4 CKD (Chronic Kidney Disease)

Resolution:

▪ Pharmacologic
- Amlodipine 5 mg po (by mouth) daily
- Lisinopril 20 mg po daily
- Metolazone 2.5 mg po daily
- vitamin D
▪ Non-therapeutic

Monitoring:

- Electrolytes (Na, Ca, bicarbonate) after 2 weeks

- Blood pressure after 2 weeks
- Monitor metabolic acidosis status every 4 months
- Spot urine/creatine ratio if we want to change her antihypertensive drugs
- Monitor vital signs, laboratory results and level of consciousness frequently
- Record intake and output accurately to monitor renal function.

For hypertension:

- Increasing the dose of amlodipine up to 10 mg daily

- continue on lisinopril 20mg daily
- add loop Diuretic like furosemide 20mg

For hyponatremia:

- make an assessment for the patient’s:

✓ volume status
✓ electrolytes in the urine
✓ serum osmolality