ACID-BASE IMBALANCE

ACID – BASE IMBALANCE

• DEFINITION:
Acids are substances that are capable of donating
protons and bases are those that accept protons.
e.g.: Acids : Hcl H + cl
Bases: Hco3 + H H2Co3
REGULATION OF ACID-BASE BALANCE
BUFFERS:
Buffers are solutions which can resist changes in pH when
acid or alkali is added
The body’s major buffer system is the Bicarbonate (HCO3)

and Carbonic acids (H2CO3) buffer system.
There are 20 parts of Bicarbonate to 1 part of Carbonic acid.

If this ratio is change, the pH also change.

REGULATION OF ACID-BASE
BALANCE
e.g: In a healthy individual :
HCO3,24 mEq/L [20 parts]
H2CO3,1.2 mq/L [1 part]
e.g: in Chronic obstructive lung disease:
HCO3,48 mEq/l [20 parts]
H2CO3,2.4 mEq/L [1 part]
 RENAL SYSTEM RESPIRATORY SYSTEM
 Kidneys reabsorb and conserve HC03 they  The lungs help maintain a normal pH by
filter and generate HC03 and eliminate excreting Co2 and H2O, which are by-
excess H+ as compensation for acidosis. products of cellular metabolism.
 When released into circulation,Co2 enters
The 3 mechanism of acids elimination are: RBCs and combines with H2O to form
• Secretion of small amounts of free hydrogen H2CO3.
into the renal tubule.
• Combination of H+ with ammonia (NH3) to  This H2CO3 dissociate into hydrogen ions
form ammonium. and Bicarbonate.
• Excretion of weak acids. CO2 + H20 H2CO3 H + HCO3
The free Hydrogen is buffered by Hemoglobin
 Kidneys excrete a portion of the acids molecules, and the bicarbonate diffuses into
produced by cellular metabolism, thus plasma.
kidneys excrete acidic urine (average pH
equal 6).  In the Pulmonary Arteries, this process is
reversed and CO2 is formed and excreted by
the lungs.
 RENAL SYSTEM
 As a compensatory mechanism, pH of the
urine can decrease to 4 or increase to 8.
 If the renal system is the cause of acid base
imbalance ,it loses its ability to correct pH
alteration.
RESPIRATORY SYSTEM
 With increased respiration, more CO2 is
expelled and less remains in the blood this
leads to less Carbonic acid and less pH.
 With decrease respirations, more Co2
remains in the blood. This leads to increased
Carbonic acid and more pH.
 As a compensatory mechanism, Respiratory
system acts on the CO2 + H2O side of
reaction by altering the rate and depth of
breathing to ‘blow off’ CO2.
ARTERIAL BLOOD GAS ANALYSIS

• Arterial blood gases are obtained to determine oxygenation status and

acid base status.
• The partial pressure of oxygen or the oxygen saturation(Sao2)and the
partial pressure of Co2(PaCo2) directly monitor the oxygen status.
• The parameters reported to monitor acid –base homeostasis are,
pH
PaCo2 and
Hco3- concentration.
ARTERIAL BLOOD GAS ANALYSIS CONT.,

• The PaCo2 is the measure of Co2 in the blood and is referred to as

the respiratory component of ABGs.
• The Hco3- concentration is referred to as the metabolic or renal
component of ABGs.
Term Normal Value Definition- Implication
pH 7.35-7.45 Reflects H ion concentration; acidity increases as H
ion concentration increases(pH value decreases as
acidity increases)
pH˂ 7.35 (Acidosis)
pH˃ 7.45 (Alkalosis)

PaCo2 35-45mmHg Partial pressure of Co2 in arterial blood.

When ˂ 35mmHg, Hypocapnia is said to be present.
( Respiratory Alkalosis)
When ˃ 45mmHg, Hypercapnia is said to be
present( respiratory Acidosis)

Pao2 80-100mmHg Partial pressure of Oxygen in arterial blood.

Standard Hco3 22-26meq/L Hco3˃ 26mmol/L( M.Alkalosis)
Hco3˂ 22mmol/L(M. Acidosis)
 ABG pH PaCo2 HCo3

Respiratory Normal
Acidosis

Respiratory Normal
Alkalosis

Metabolic Normal
Acidosis

Metabolic Normal
Alkalosis
BASE EXCESS- EXTRA CELLULAR FLUID

• In physiology, base excess and base deficit refer to an excess or

deficit, respectively, in the amount of base present in the blood.
• reported as a concentration in units of mEq/L
• positive numbers indicate an excess of base and negative a deficit
• A typical reference range for base excess is -2 to +2mEq/L
BASE EXCESS- EXTRA CELLULAR FLUID
Definition
• Base Excess is defined as the amount of strong acid that must be
added to each liter of fully oxygenated blood to return the pH to
7.40 at a temperature of 37˚C and a paCo2 of 40mmHg.
• A Base deficit can be correspondingly defined in terms of the
amount of strong base that must be added
BASE EXCESS- EXTRA CELLULAR FLUID CONT.,

Interpretation
Base excess beyond the reference range indicates
Metabolic alkalosis- more than +2mEq/L

Base Deficit beyond the reference range indicates

Metabolic acidosis- Less than -2mEq/L
 RESPIRATORY ACIDOSIS

• Definition
• Respiratory Acidosis is a state of relative excess of acid in body fluids
resulting from retention or excessive production of Co2.
• Acute Respiratory Acidosis develops and resolves within 3 days or less;
• Chronic Respiratory Acidosis persists over a longer period.
 ETIOLOGICAL FACTORS
Book Picture Patient picture
Acute Respiratory Acidosis
Acute Pulmonary Edema Mr. Viswas diagnosed to have PTE.
Pulmonary Thrombo Embolism

Aspiration of a foreign body X ray revealed Right basal small

consolidation

Atelectasis
Pneumothorox, Hemothorox
Cardiac arrest ECHO revealed RA/ RV dysfunction
ETIOLOGICAL FACTORS CONT.,
Severe Pneumonia Mrs. Renuka diagnosed to have
Fungal Pneumonia and Type 2
Respiratory failure
Mechanical ventilation improperly
regulated
Chronic Respiratory
Acidosis
Emphysema
Cystic Fibrosis
Advanced Multiple Sclerosis
Bronchiectasis
Bronchial Asthma
 ETIOLOGICAL FACTORS CONT.,

Factors favoring Hypoventilation

Obesity
Tight abdominal binder or dressing
Post operative pain
Abdominal Distention from Mr. Viswas abdominal
cirrhosis or bowel obstruction ultrasonography reveals abdominal
distention due to minimal ascitis.
 PATHOPHYSIOLOGY

• Hypoventilation

• Build up of Co2, resulting in an accumulation of carbonic acid in the blood

• Carbonic acid dissociates, liberating H ion

PATHOPHYSIOLOGY CONT.,

• Decrease in pH

• Renal compensation-Greater secretion of H ion and regeneration of bicarbonate

Chloride is excreted in greater amounts cause Hypochloremia

Renal retention of K+ and cellular cation shifts may lead to Hyperkalemia

 PATHOPHYSIOLOGY CONT.,

• Displacement of Calcium from albumin may result in Hypercalcemia

• Rapid rise in Paco2 results in Hypoxemia in clients who are breathing

room air because retained Co2 displaces oxygen in alveoli.
 CLINICAL MANIFESTATION

Book picture Patient Picture

Arterial Blood Gas
pH˂7.35 pH : 7.028
7.13
PaCo2˃45mm Hg PaCo2 : 60.8mmHg
36 mmHg
Hco3 normal or only slightly elevated Hco3 : 15.2mmol/L
21.2mmol/L
Manifestation of Hypoxemia
Confusion Both patients were sedated, and on
ventilator
Irritability
Lethargy
CLINICAL MANIFESTATION CONT.,
Manifestation of organ dysfunction
Hypotension
Cardiac dysrhythmias
Decreased myocardial contractility
Manifestation of Electrolyte
Imbalance
Mr.Viswas hypotensive at the time of
admission. BP : 90/60mm/Hg
Hyperkalemia : 6.71mEq/L
5.35mEq/L
Hyponatremia : 131mEq/L
129mEq/L
Hypochloremia: 93mEq/L
90mEq/L
CLINICAL MANIFESTATION CONT.,

Manifestation of central
Nervous System
Tremors Both the patients are in coma
Stage
Seizures Mrs. Renuka had one episode
of focal seizure
Lethargy
Stupor and Ultimately Coma
 TREATMENT

BOOK PICTURE PATIENT PICTURE

Bronchodilators-Bronchial Spasm
Antibiotics- Respiratory Infections Patient No: 1
Inj. Netilmycin 200mg BD
Inj. Colistin 30000Iu BD
Patient No : 2
Inj. Tigecycline50mg BD
Inj. Sulbactum500mgBD
Pulmonary Hygiene measures Intermittent suctioning done. Head end
elevated.
Adequate Hydration RT feed 2000ml/ day
Supplemental Oxygen
A mechanical respirator used cautiously, Both patients are in Mechanical
may improve pulmonary ventilation Ventilation
 METABOLIC ACIDOSIS

• Definition
Metabolic acidosis is a clinical disturbance Characterized by a low
pH(increased Hydrogen ion concentration) and a low plasma bicarbonate
concentration. It can be produced by a gain of hydrogen ion or a loss of
bicarbonate.
In compensation the lungs hyperventilate to decrease the PaCo2
concentration.
 ANION GAP

• The Anion gap is the difference between primary measured cations (sodium) and the primary measured anions
( chloride cl- and bicarbonate-) in serum.
• Anion Gap(AG) = Na+ -(Cl+Hco3-)
12±2mEq/L
Patient No: 1 AG=130-(93+15.2)
=130-108.2
AG =21.8
Patient No: 2 AG=125-(90+20.3)
AG= 14.7mEq/L
 ANION GAP CONT.,

• In some situations, these anions are markedly increased and the AG is greater
than expected. These situations are referred to as High Anion Gap
Metabolic acidosis.
• On the other hand, if the primary problem is direct loss of bicarbonate, gain
of chloride, or decreased renal ammonia production, the AG will be within
normal limits. This is called as Normal Anion Gap Metabolic acidosis.
 CAUSES OF METABOLIC ACIDOSIS
CLASSIFIED AS HIGH AG OR NORMAL AG
High Anion Gap Normal Anion Gap
Diabetic Ketoacidosis Diarrhea
Starvational Ketoacidosis Biliary or Pancreatic Fistulas
Alcoholic Ketoacidosis Excessive administration of
Lactic acidosis isotonic saline or ammonium
Renal Failure chloride
Poisonings Ureteroenterostomies
 Salicylate Renal tubular acidosis
 Ethylene glycol Acetazolamide(Diamox)
 Methyl alcohol Both patients diagnosed to
have Renal failure
 PATHOPHYSIOLOGY

• Acid accumulation (ketoacid,Lactic acid)

• Loss of Bicarbonate (Diarrhea)

• Kidney loss their ability to reabsorb Hco3- and secrete H ion

• The compensatory response to metabolic acidosis is to increase Co2 excretion by
the lungs
• Results in Kussmaul breathing.
 CLINICAL MANIFESTATION

Book Picture Patient Picture

Defining Signs
Hyperventilation (Kussmaul’s
respiration or air hunger)
Arterial Blood Gases
Fall in pH˂7.35 pH: 7.028
7.13
Hco3˂22mmol/L Hco3: 15.2mmol/L
20.1mmol/L
PaCo2˂35mmHg PaCo2: 60.8mmHg
36mmHg
CLINICAL MANIFESTATION CONT.,

Commonly Seen
Hyperkalemia Patient No: K+ 6.71mEq/L
Patient No: K+ 5.35

Increasing serum chloride Chloride level was normal

level and anion gap both the patients. Anion gap
increased in both patients.
Stress response following by
lethargy
Dyspnea Both patient had dyspnea
CLINICAL MANIFESTATION CONT.,
Signs of severe imbalance
Bradicardia or other Both patients were on
Dysrhythmia Mechanical Ventilation
Decreased Cardiac Output
Gastrointestinal distention
Hypotension
Nausea
Vomiting
 TREATMENT

Treatment of Underlying Disorder

Treatment involves restoration of normal tissue oxygenation and perfusion.
 Dialysis for the patient with extremely acidotic renal failure
Insulin administration and fluid replacement to correct very low pH values in patient with
Ketoacidosis.
Electrolyte imbalance is treated only if it is life-threatening because it normally resolves with
correction of the underlying disorder.
Both patient underwent Hemodialysis
 TREATMENT CONT.,

Respiratory Support
Assisted mechanical ventilation may be indicated for clients whose ability to hyperventilate in compensation
is limited.
Both the patients were on mechanical ventilation
Administration of Exogenous Alkali
There are three types of alkali that can be used
Bicarbonate
Salt of organic acids( Lactate, Acetate and Citrate)that are metabolized to bicarbonate
Tromethamine(THAM)
 SENARIO-1

• A 32 year old man is admitted in a very ill state. He had been drinking with friends.
On admission he is barely conscious and breathing heavily. His ABG report shows
• pH : 7.01
• PaCo2: 38mmHg
• Pao2: 85%
• Hco3: 15.1mEq/L
• What is your Diagnosis?
 SENARIO-2

• A 44 year old lady with a long history of indigestion begins to vomit at home.
She becomes unwell after 4 days and is admitted to hospital because of marked
muscle weakness.ABG report shows
• pH: 7.65
• PaCo2: 35mmHg
• Hco3: 28mEq/L
• What is your diagnosis?
 SENARIO-3

• A 56 year old man , who has smoked heavily for many years developing a
worsening cough with purulent sputum and is admitted to hospital because of
difficulty in breathing. He is drowsy and cyanosed. ABG report shows
• pH: 7.02
• PaCo2: 68mmHg
• Hco3: 40mEq/L
• What is your diagnosis?
 SENARIO-4

• A 13 year old school boy is brought to the emergency department having become actually
unwell in the head masters office. He is alert and agitated, the respiratory rate is 35/ minute
and he complains of tingling in hands
• ABG report shows the following findings
• pH: 7.82
• PaCo2: 30mmHg
• Hco3: 22mEq/L
• What is your diagnosis?
 RESPIRATORY ALKALOSIS
DEFINITION:
• Respiratory alkalosis is a state of excess of base in the
body fluids resulting from increased respiratory
elimination of CO2.
• Acute respiratory alkalosis lasts for 24hours or less.
• Chronic respiratory alkalosis persist longer.
 BOOK PICTURE PATIENT PICTURE
ETIOLOGICAL FACTORS:
Pneumonia
Mr. Nanda Gopal came with
Pulmonary embolism
complaint of breathing difficulty,
Asthma
left sided chest pain which was
Adult respiratory distress
diagnosed with Lower
syndrome
Respiratory Tract Infection.
Pulmonary edema
Cystic fibrosis
Acute anxiety or pain or response
to respiratory stimulant drugs
such as Epinephrine and
Salicylates
Neural disorders like Stroke,
Intracranial Lesions
 BOOK PICTURE PATIENT PICTURE

 Other common causes:

• Progressive high fever  Mr. Nanda Gopal have fever with
• Hypoxemia 101* F.
• Gram negative bacteria  Hypoxemia.
• Thyrotoxicosis
• Excessive ventilation by
mechanical ventilation
 PATHOPHYSIOLOGY
Hyperventilation (due to hypoxemia from pulmonary disorders ,
anxiety, CNS disorders, mechanical over ventilation)

Decrease in the partial pressure of arterial Co2

Decrease Carbonic acid concentration

Respiratory alkalosis
 BOOK PICTURE PATIENT PICTURE
CLINICAL MANIFESTATIONS:
 CNS Manifestations:  Mr. Nanda Gopal complaint of
• Paresthesia Lightheadedness.
• Lightheadedness
• Confusion
• Seizure
 Musculoskeletal and Cardiac :
• Hypocalcemia
• Hypokalemia  Mr. Nanda Gopal was having left
• Dysrhythmias sided chest pain, breathing difficulty
• Muscle weakness and lower limb weakness.
• Chest pain
 BOOK PICTURE PATIENT PICTURE
20
CLINICAL MANIFESTATIONS:
 Mr. Nanda Gopal was suffering from
 Gastrointestinal Manifestations:
• Nausea loose stool and vomiting since 2days.
• Vomiting
• Diarrhea

 Arterial blood gas:

• pH > 7.45 • pH – 7.57
• PaCo2 < 35 mm Hg • PaCo2 – 32.7 mm Hg
• HCo3 < 22mEq/L • HCo3 – 20 mEq
• Po2 < 80 mm Hg • Po2 – 77 mm Hg
 BOOK PICTURE PATIENT PICTURE
TREATMENT:
 Treatment of the underlying causes:
• Treatment of mild, chronic Mr. Nanda Gopal was being treated with
respiratory alkalosis is usually not :
warranted because it produces • IVF NS:RL @ 75ml/hr.
little risk and few symptoms. • Inj. Ceftriaxone 2gm IV
• Aggressive treatment of the • Inj. Optineuron
underlying causes of hypoxemia • Tab Dolo 650 mg
is essential and electrolyte • Inj. Metronidazole
imbalance usually resolve with • Inj. Emeset
treatment of underlying cause.
 BOOK PICTURE PATIENT PICTURE

 Respiratory support:
• Oxygen therapy to correct  He was put on Oxygen therapy
underlying hypoxemia through nasal cannula with 4lit 02.
• Rebreathing of Co2 (as from
breathing into paper bag or other
closed system) provides prompt
but short-term relief in anxiety-
related respiratory alkalosis.
 METABOLIC ALKALOSIS
DEFINITION:
Metabolic alkalosis is characterized by a high pH
and a high plasma bicarbonate concentration. It can be
produced by a gain of bicarbonate or loss of hydrogen ion.
 BOOK PICTURE PATIENT PICTURE
ETIOLOGY:
 Vomiting or Gastric suction  Mr. Gopal Nath came with complaints of
 Hypokalemia shortness of breath on minimal exertion,
 Hyperaldosteronism Cough with expectorations, fever,
 Cushing’s syndrome tachypnea and tachycardia which he was
 Potassium losing diuretics (e.g. diagnosed with Congestive cardiac
Thiazides, Furosemides, Ethacrynic failure with NSTEMI , Sepsis related to
acids) LRTI and Type II Diabetes Mellitus.
 Alkali ingestion (bicarbonate containing
antacids)  Potassium – 2.2 mEq/L

 Parenteral NaHCO3 administration for  He was on Inj. Lasix 40mg Od.

Cardiopulmonary resuscitation
 Abrupt relief of chronic respiratory
acidosis
 PATHOPHYSIOLOGY

Loss of acid or gain of bicarbonate

Buffering occurs in the Extracellular fluid where buffer are

much less effective for base load than acid load

Severe alkalemia

Organ dysfunction (neurologic and cardiovascular system are

primarily affected)

Decreased respiratory rate to increase plasma Co2

Plasma Co2 stimulates Chemoreceptors results in Ventilation.

 BOOK PICTURE PATIENT PICTURE
CLINICAL MANIFESTATIONS:
 ABG analysis:  ABG:
• pH > 7.45 • pH – 7.517
• HCO3 > 26mEq/L • HCO3 – 35.3 mEq/L
• PaCo2 >45 mmHg • PaCo2 – 46.1 mm Hg
 Neurologic  Mr. Gopal Nath complaints of
• Dizziness dizziness and headache.
• Lightheadedness
• Confusion headache
• Decrease level of consciousness
 Cardiovascular:
• Tachycardia  Pulse rate – 112 b/min
• Dysthymias  BP – 90/60 mm Hg
• Hypotension
 BOOK PICTURE PATIENT PICTURE
CLINICAL MANIFESTATIONS:
 Gastrointestinal:  Mr. Gopal Nath food intake was
• Nausea, vomiting and anorexia decrease due to anorexia.
 Respiratory:  Mr. Gopal Nath have difficulty in
• Hypoventilation breathing in lying down position.
 Others:
• Hypocalcemia  Magnesium – 1.5 mEq/L
• Hypochloremia
• Hypomagnesemia
 BOOK PICTURE
TREATMENT:
 Treatment of underlying disorders:
• Replacement of lost fluids and
electrolytes
and support of renal function are
often main
steps of therapy.
 Administrations of Acetazolamide
• Is a diuretic that inhibits CA and
promote loss of Bicarbonate in
the urine.
 Administration of Oxygen.
PATIENT PICTURE
 Mr. Nanda Gopal is treated with:
 Inj. KCL 40 mEq in 500ml NS over
4hrs
 Syp. Potklor 15ml tds
 Inj. MgSo4 1gm in 100ml
 Inj. Piptaz 4.5gm
 Inj. Amikacin 750mg
 Tab Dolo 650mg
 BOOK PICTURE PATIENT PICTURE
TREATMENT:
• In severe alkalemia,the  Oxygen therapy through oxygen
intravenous administration of acid mask with 6Lit O2
(HCL) or HCL precursors
(ammonia chloride or organic  Nebulization with Ipravent and
monohydro-chloride) maybe Budecort nebulization.
required to enhance physiologic
compensations
 MIXED ACID BASE DISORDER
 A mixed acid base disorder occurs when two or more disorders
are present at the same time.

Respiratory acidosis combined with Metabolic alkalosis.

e.g. a patient with COPD also treated with a Thiazide diuretic
may result in a new normal pH.

Respiratory acidosis combined with Metabolic Acidosis will

cause a greater decrease in pH.

e.g. patient in cardiac arrest

 COMPENSATION OF ACID-BASE IMBALANCE
RESPIRATORY ALKALOSIS:
1.CELL BUFFER:
•In the acute stage there is 0.1mM decrease in [HCo3] for each mmHg decrease in PaCo2.
This decrease is due to enhance dissociation of H+ from cell buffers when the [H+]
decrease due to the low PaCo2.
•Cell H+ exchange for ECF Na+ and K+ and react with ECF HCO3 reducing its
concentration.
•Some extracellular HCO3 enters cells in exchange for Cl and is titrated by H+ dissociating
from the cell buffers.
•In the chronic stage, there is 0.5mM decrease in [HCO3] for each mm Hg decrease in
PaCO2.
 COMPENSATION OF ACID BASE IMBALANCE

2. RENAL COMPENSATION:
• Due to increase HCO3 excretion associated with low PaCo2,which
decreases HCO3 reabsorption.
• Urinary excretion of NH4 and titratable acids are transiently reduced,
leading to accumulation of metabolic and dietary acids which help produce
ECF [HCO3 < 22mM].
• Eventually HCO3 excretion ceases and excretion of NH4 and titratable acid
resumes.
3. METABOLIC COMPENSATION:
• By increase production of Lactic and Citric acids that react with the reduce
[HCO3]ecf.
 COMPENSATION OF ACID BASE
IMBALANCE
METABOLIC ALKALOSIS:
1. RENAL COMPENSATION:
• Increase in blood pH depress respiratory centers.
• Hypoxemia as a result of progressive hypoventilation activates oxygen sensitive
chemoreceptors which stimulates ventilation and limits compensatory pulmonary
response.
• PaCo2 does not rise >55mmHg in response to Metabolic Alkalosis
• PaCo2 increase 0.25-1mmHg for each 1mEq/L increase in [HCO3]
 COMPENSATION OF ACID BASE
IMBALANCE
2. RENAL:
• Renal excretion of HCO3 rises when its concentration in plasma increase.
• Lowering of HCO3 is limited by high renal absorption rate stimulated by high PaCo2,
by ECF volume contraction, Hyperaldosteronism, K+ depletion and hypochloremia
which perpetuate the high HC03.
• Beta-intercalated cells in CCD secrete HC03,increasing its urinary excretion.
 COMPENSATION OF ACID BASE
IMBALANCE
3. CELL IONIC EXCHANGE:
• 25% of HC03 load is neutralize by H+ from intracellular buffers that exchange the
H+ for extracellular Na+.
• 2% of extracellular HC03 enters red cell in exchange for Cl.
4. METABOLIC:
• Increases in endogenous organic acid production neutralized by H+ derived from
-5% of an acute HC03 load.
• High pH increases production of Lactic and Citric acid which decrease HC03.
• High pH stimulates Glycolysis and inhibits Citric acid cycle.