Bogale & Henok Acid Base Disorders Edited (1).pptx

የካቲት 12 ሆስፒታል ሜ/ኮ
YEKATIT 12 HOSPITAL M/C
Acid -Base Disturbances
Presenters : Dr. Bogale T. (IMR1) , Dr. Henok H. (IMR1)
Moderator: Dr. Getachew W. ( Consultant Internist,
Nephrologist)
July/2025

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Outline
• Introduction
• Basic concepts
• General principles of acid base disorders
• Diagnosis
• Metabolic Acidosis
• Metabolic Alkalosis
• Respiratory Acidosis
• Respiratory Alkalosis

3
NORMAL ACID-BASE HOMEOSTASIS
• Systemic arterial pH is maintained between 7.35 and 7.45 by
extracellular and intracellular chemical buffering together with
respiratory and renal regulatory mechanisms.
• The control of arterial CO2 tension (PaCO2) by the central nervous
system (CNS) and respiratory systems AND
• The control of the plasma bicarbonate by the kidneys stabilize the
arterial pH by excretion or retention of acid or alkali.

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HOMEOSTASIS...
• The concentration of H+ (pH) must be maintained within a strict range.
• This is because proteins in the body are very sensitive to pH.
• Abnormal pH can lead to denaturation of these proteins.
• Clinical consequences include:
• Poor vascular tone
• Myocardial pump failure
• Increased risk of arrythmia
• Impaired cellular respiration ,etc.

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HOMEOSTASIS ...
• The most important principle in acid-base balance is:
Net acid production = Net acid elimination
• Under physiologic state, the body produces 3 major classes of acids.
• CO2 which combines with water to form carbonic acid (H2CO3).
• Organics acids – lactic acid, citric acid etc.
• Non-volatile acids – sulfuric acid
• The body eliminates these acids by:
• Pulmonary excretion of CO2
• Metabolization of organic acids to neutral products and
• Renal excretion of non-volatile acids

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Example
A healthy person in acid-base homeostasis has a plasma [HCO3-
] of 24
mmol/L, an arterial PCO2 of 40 mm Hg, and calculating the plasma pH
So this normal plasma pH is :
pH = pKa + log(HCO3/s.PaCO2)
= 6.1 + log(24/0.03 × 40)
= 7.40

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Defense/Compensatory mechanisms to acid-base
disturbances
Mechanism Mechanism Onset
Chemical buffers By using 3 buffer systems
1. Bicarbonate
2. Phosphate
3. Protein
Seconds to minutes
Lungs By regulating the excretion of
CO2
Minutes to hours
Kidneys By regulating
1. The excretion of H+
2. The reabsorption of HCO3-
Hours to days

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Buffer solutions
• Aqueous solutions consisting of a weak acid and its conjugate base,
or vice versa.
• They resist changes in pH when strong acid or base are added to
them.
• This is because an equilibrium exists between the weak acid and its
conjugate base.
HA H
⇌ +
+ A−.
• When acid is added (more H+
) , the equation shifts to the left and when
base is added (less H+
), the equation shifts to the right.

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Buffer solutions Cont’d…
• The result is the change in the H+
will be less than expected from the
amount of acid or base added.
• The most important and predominant buffer in our body is the
bicarbonate buffering system.

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The Henderson-Hasselbalch equation
• According to the Henderson-Hasselbalch equation, the pH of any
buffer solution is calculated as:
• When this equation is applied to the bicarbonate buffering system,

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GENERAL TYPES OF ACID-BASE DISTURBANCES
Simple acid-base disorders (commonest)
Primary disturbances is the presence of only one of the acid- base
disorders with the appropriate respiratory or renal compensation for
that disorder.
• These compensatory responses are as follows:
Primary respiratory disturbances (primary changes in Paco2) invoke
compensatory metabolic responses (secondary changes in [HCO3
–
]), and
Primary metabolic disturbances elicit predictable compensatory
respiratory responses (secondary changes in Paco2).
The degree of respiratory compensation expected in a metabolic
acidosis can be predicted from the relationship: (Winter’s equation).
Paco2= (1.5 × [HCO3−]) + 8 ± 2

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[pH]

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: Algorithm used to describe acid-base disorders. PaCO2 defines the
presence of respiratory disorders; plasma [HCO3 − ] defi nes the presence
of metabolic disorders.

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Mixed acid-base disorder
Is an independently coexisting disorders, not merely
compensatory responses—are often seen in patients in critical
care units.
Diagnosis
1) identification of the primary disorder (Hx & P/E)
2) determination of whether the degree of compensation is
appropriate ,and
3) Analysis of the serum electrolytes and anion gap (AG).

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E.g if Metabolic Acidosis is the primary disorder,
• A PaCO2 substantially higher than expected means a coexisting
respiratory acidosis.
• A PaCO2 substantially lower than expected means a coexisting
respiratory alkalosis.
A. A patient with severe DKA (metabolic acidosis) precipitated by
pneumonia (respiratory acidosis).
B. An alcoholic patient with alcoholic ketoacidosis (metabolic acidosis)
and vomiting (metabolic alkalosis) hyperventilating due to severe
liver disease (respiratory alkalosis).
Mixed acid-base disorder…

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Mixed acid-base disorder Cont’d…
• bnbn

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Acid-base disorders Cont’d…
Acid-base nomogram Shown are the 90% confidence limits (range of values) of the normal respiratory and
metabolic compensations for primary acid base disturbances.

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Arterial blood gas (ABG)
• Is a test that measures the PaO2, PaCO2, pH, SaO2, and HCO3 in
arterial blood sample.
• Some blood gas analyzers also measure the levels of methemoglobin,
carboxyhemoglobin and hemoglobin.
• Blood sample can be obtained by percutaneous needle puncture or
from an indwelling arterial catheter.
• While pH, PaCO2 and PaO2 are directly measured, HCO3- is
calculated using the Henderson-Hasselbalch equation.

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ABG Cont’d…
Indications
• Assessment of acid-base
disturbances.
• Assessment of oxygenation and
ventilation.
• Identification of abnormal
hemoglobins.
• Obtaining blood samples when
the venous access is difficult.
Contraindications
• Local infection, thrombus, or
distorted anatomy at the puncture
site
• Severe peripheral vascular disease
of the selected artery
• Active Raynaud's syndrome
• Supratherapeutic coagulopathy,
thrombolytic infusion and severe
thrombocytopenia (relative)

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ABG Cont’d…
• Radial artery is commonly used, but brachial, axillary, femoral and
dorsalis pedis arteries can also be used.
• Ensure collateral flow
• Is to avoid ischemia distal to the puncture site
• Allen’s or Modified Allen’s test
• Approximately 2 to 3 mL of blood should be removed.
• The sample should be placed on ice during transport and then
analyzed as quickly as possible.

Reading ABG
• Step 1: pH
• Normal range 7.35-7.45. Use 7.40 as absolute normal
• Acid (7.39) or base (7.41)
• Step 2: pCO2
• Normal range 35-45. Use 40 as absolute normal.
• This step determines whether primary disorder is a respiratory or
metabolic process
• Step 3: expected compensation (hardest part, refer to table)
• This is calculated.
• Step 4: measured value match the expected?
• If NOT, there is an additional acid-base disturbance

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ABG Cont’d…
•Normal values:
• pH – 7.35 - 7.45
• PaCO2 – 35 - 45 mmHg
• HCO3 – 22 - 26 mEq/L
• PaO2 – 80 - 100mmHg
• SaO2 - >95%
• Carboxyhemoglobin – 3% in non-smokers and 10-15% in
smokers.
• Methemoglobin - 1%

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Steps in the diagnosis of Acid-Base Disorders
1. Obtain arterial blood gas (ABG) and electrolytes simultaneously.
2. Compare [HCO3
–
] on ABG and electrolytes to verify accuracy.
3. Calculate anion gap (AG).
4. Know four causes of high-AG acidosis (ketoacidosis, lactic acid
acidosis, renal failure, and toxins).
5. Know two causes of hyperchloremic or nongap acidosis
(bicarbonate loss from GI tract, renal tubular acidosis).
6. Estimate compensatory response
7. Compare AG and HCO3–.
8. Compare change in [Cl-
] with change in [Na+
].

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• Step 1 – establish the primary diagnosis
• Look at the pH to determine if acidemia or alkalemia is present. *
• Look at the pCO2 to determine if respiratory or metabolic disorder is present.
• If pH and pCO2 in the same direction – metabolic disorder.
• If pH and pCO2 in the opposite direction – respiratory disorder.
• Step 2 – check the degree of compensation
• Appropriate – simple acid-base disorder
• Inappropriate (too high or too low) – mixed acid base disorder*
• Step 3 – check the AG and correct it for albumin (if metabolic acidosis)
• Step 4 – check the delta ratio (if HAGMA)
• Step 5 – establish a differential diagnosis for the final acid-base disorder.
Steps in the diagnosis con’t…

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• Some exceptions to this approach
• A normal pH doesn’t rule out an acid-base disorder.
• Look at the CO2 and HCO3- and the AG
• An appropriate compensation doesn’t rule out a mixed acid-base disorder.
• Look at the AG
Steps in the diagnosis con’t…

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Steps in Diagnosis of simple acid-base disorders

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Example -1
• The arterial plasma from a patient yields the following ABG values:
• pH = 7.30,
• HCO2 =12.0 mEq/L, and
• PaCO2 = 25 mm Hg.
• With these values, what is the Acid –base disorder using the diagram?

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Example -2
A patient with the following ABG values:
• pH= 7.15,
• HCO2 = 7 mEq/L, and
• PCO2 =50 mm Hg.
• With these values, what is the Acid –base disorder using the diagram?

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The anion gap (AG)
• Is the difference between measured cation (Na+) and measured anions
(Cl- and HCO3-).
AG = Na+ – (Cl- + HCO3-).
• The normal value ranges from 6 to 12 mmol/L (average of 10).
• The plasma anion gap is mainly used to identify the cause of
metabolic acidosis.
• The presence of hypoalbuminemia underestimates the AG.
• Because HCO3 and Cl- increase to maintain electrical
neutrality.
• For every 1g/dL decrease in albumin from the normal (
4.5g/dL), 2.5mmol/L should be added to the reported AG.

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AG Cont’d…

Normal GAP (N-GAP)
Kidney could be the culprit
• Either GUT or KIDNEY

Na = 140
CL= 105
HCO3= 25
AG=
10-12
NOT REAL
Mathematically present
Electrically neutral
Albumin neutralizes the +(10
to 12)
Albumin is -(10 to 12)
Na = 140
CL= 115
HCO3= 15
AG=
10-12
N-AG
Mathematically present
Electrically neutral
The drop in Bicarbonate is
balanced by a rise in
Chloride
Hence the GAP stays the
same
How do you get a NORMAL/NON-gap ?

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AG Cont’d…
• High anion gap metabolic acidosis (HAGMA)
• Due to accumulation unmeasured anions which are acids that contain:
1. Inorganic anions (phosphate, sulfate),
2. Organic anions (ketoacids, lactate, uremic) or
3. Exogenous anions (salicylate).
• HCO3- neutralizes the H+ released from these acids, which widens the AG.

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AG Cont’d…
• Normal anion gap metabolic acidosis (NAGMA)
• Usually due to loss of HCO3-.
• The HCO−
3 lost is replaced by a Cl-, so there is a normal AG.
• It is therefore also known as hyperchloremic acidosis.

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The Delta ratio (Δ ratio)
• Is used to compare the increase in AG to the decrease in the HCO3
concentration.
• Used only to identify acid-base disorders that coexist with HAGMA.
• The ratio can have one of four results:
• < 0.4 - pure NAGMA
• 0.4 – 0.8 – HAGMA + NAGMA
• 0.8 – 2.0 - pure HAGMA
• >2.0 - HAGMA + metabolic alkalosis
Δ ratio Disorders
<1 HAGMA + NAGMA
1-2 HAGMA only
>2 HAGMA + metabolic alkalosis

FOR METABOLIC ACIDOSIS
Metabolic acidosis is subdivided into increased AG and normal AG.
• Calculate a GAP (Na – (Cl+HCO3) = 12 (10-12)
• Use Winters (For both High-GAP and Normal-GAP)
• If GAP > 12 (High Anion GAP)
then
• Calculate DELTA DELTA (Only calculated for High Anion GAP)
• If GAP < 12 (Normal-GAP)
Then
• Calculate Urine Anion GAP (UNa + UK – UCl)
• If +ve = Renal Loss, If –ve = Negative- GUT

24 12 (10-12)
22
14
10 Acid
10 Base
The dreaded Delta-Delta
ONLY for GAP Metabolic Acidosis
Eg: Patients GAP is 20 and Bicarbonate is 14
DGAP + BICARB = 24 (No underlying disorder)
If > 24 = Added Alkalosis
If < 24 = Added Acidosis
GAP
HCO3 -
10
20

Albumin and its effect on GAP
BUT Only in the setting of Metabolic Acidosis
• Na – (Cl + HCO3) =
• 140 – (104 + 24) = +12
• To maintain electrical neutrality,
• 4 gm of Albumin = -12
• i.e: 1 gm on Albumin = Approx - 2.5 charge
• For every Gram of Albumin < 4, Add 2.5 to the GAP.

Cheat Sheet
• Met. Acidosis :
• Winters Formula: pCO2 = 1.5 x HCO3 + 8 + 2
• Met . Alkalosis :
• HCO3 up 10 meq = 6 meq rise in CO2 (5-7)
• Resp Acidosis :
• Acute
• PCO2 up 10 mmhg = 1 meq rise in HCO3
• Chronic
• PCO2 up 10 mmhg = 4 meq rise in HCO3
• Resp Alkalosis :
• Acute
• PCO2 down 10 mmhg = 2 meq drop in HCO3
• Chronic
• PCO2 down 10 mmhg = 5 meq drop in HCO3

41
APPROACH TO ACID-BASE
DISORDERS

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Stepwise Approach to Acid-Base Disorders
1. Assess the Clinical Context
2. Evaluate the Arterial Blood Gas(ABG) & pH
3. Determine the Primary Acid-Base Disorder
4. Check for Compensation
5. Calculate the Anion Gap(if metabolic acidosis present)
6. Evaluate for Mixed Acid-Base Disorders
7. Investigate and Treat the Underlying Cause

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 Evaluation of any acid-base disorder begins with
measurement of the serum bicarbonate
concentration, the arterial pH & PaCO2.

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Acid-Base Disorders
oDefinitions:
Acidemia – An arterial pH below the normal range (less than 7.35).
Alkalemia – An arterial pH above the normal range (greater than 7.45).
Acidosis – A process that tends to lower the extracellular fluid pH
• Respiratory acidosis – A disorder that elevates the arterial PaCO2 and reduces the pH.
• Metabolic acidosis – A disorder that reduces the serum HCO3 concentration and pH.
Alkalosis – A process that tends to raise the extracellular fluid pH
• Respiratory alkalosis – A disorder that reduces the arterial PaCO2 and elevates the pH.
• Metabolic alkalosis – A disorder that elevates the serum HCO3 concentration and pH.

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Acid-base disorders Cont.
In general compensatory responses return the pH toward, but not to,
the normal value.
• Chronic respiratory alkalosis when prolonged is an exception.
The expected degree of compensation for each acid-base disorder has
been determined empirically.
Compensatory responses that are not within the expected range
indicate the presence of mixed acid-base disorders.

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Case Scenario 1
A 33 yrs. old man with diabetes mellitus was found unconscious and unresponsive.
The results of arterial blood gas analysis showed the following abnormalities:
• PaO2 = 90 mm Hg
• PaCO2 = 36 mm Hg
• [HCO3-
] = 7 mEq/L (normal = 22–28 mEq/L)
• pH = 6.91 (normal = 7.35–7.45)
• Plasma [Na+] = 145 mEq/L and [Cl−] = 110 mEq/L.
Q. What is the acid-base disorder ?

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Diagnosis
The Acid base disorder is Metabolic Acidosis (low [HCO3- ]) with
no respiratory component , which is producing a severe acidemia (low
plasma pH).
Anion gap = [Na+] − ([CI −] + [HCO3−])
= [145] − ([110] + [7])
= 28 mEq /L (normal 8–16 mEq/L)
Therefore the patient has DKA, which produces an increased anion
gap. A metabolic acidosis is present with no respiratory compensation,
resulting in a severe life threatening acidemia.

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Case Scenario 2
A 45 yrs. old woman presents with 03 weeks of profuse, watery diarrhea(6-8
episodes/day). The diarrhea started after she took Ciprofloxacin for suspected bacterial
gastroenteritis & it persisted despite stopping ciprofloxacin. There is no blood in stool, but
she noticed significant weight loss(4 kgs) due to anorexia. For this she occasionally uses
loperamide. She complains of fatigue, muscle cramps, & lightheadedness. She is a known
hypertensive on lisinopril, hypothyroidism pt on levothyroxine. No hx of DM, cardiac
illness or kidney disease.
V/S. BP=110/70 PR=88 RR=18 Temp=36.7 SPO2=96%
Mild dehydration signs
Cardiopulmonary. Normal
Abdomen. Hyperactive bowel sounds
CNS. Mild proximal muscle weakness(due to hypokalemia)

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Workups
pH=7.30
HCO3=16
Na=138
K=2.9
Cl=112
BUN=18mg/dl
Creatinine=0.8mg/dl
RBS=92mg/dl
Anion Gap=10
Lactate=1.2mmol/L
Albumin=3.8gm/dl

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Diagnosis
Non-Anion Gap Metabolic Acidosis(NAGMA) due to Chronic Diarrhea
Loss of bicarbonate-rich intestinal fluid leading to Metabolic acidosis, Cl
retention(kidneys reabsorb Cl to maintain electroneutrality),
Hypokalemia(K loss in stool + secondary hyperaldosteronism from
volume depletion)
No ketones/lactate/toxins
Hyperchloremia compensates for lost HCO3.
oDDX. Renal Tubular Acidosis(RTA), Acetazolamide use, Post-
hypocapnia(if recent respiratory alkalosis)

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Management
oTreat underlying cause
S/E for infective Vs Antibiotic-associated diarrhea
Consider Clostridium difficile PCR(given that there is antibiotic exposure)
If persistent, evaluate for secretory Vs osmotic diarrhea.
oCorrect Acidosis & Electrolytes
Oral Potassium(KCl) supplementation
IV fluids(NS)
Oral bicarbonate replacement(if severe acidosis, e.g. NaHCO3 tablets).
oMonitor Response
Repeat electrolytes & acid-base status in 24-48 hrs.

Metabolic Acidosis
Metabolic acidosis can be defined as a low arterial pH (normal 7.40, with
a range of 7.35-7.45) & a low serum bicarbonate concentration (normal
24 mEq/L, with a range of 22-28 mEq/L).
Refers to all other types of acidosis besides those caused by
excess CO2 in the body fluids.
GI loss of HCO3 (Severe diarrhea/ severe Vomiting )
 Increased acid generation (lactic acidosis or ketoacidosis)
Increased ingestion/ acetylsalicylic (aspirin)
 Decreased renal excretion (CKD, type I/IV renal tubular
acidosis)

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Increased acid generation
Lactic acidosis
Ketoacidosis due to uncontrolled diabetes mellitus,
excess alcohol intake, or fasting
Ingestions
Methanol or ethylene glycol
Aspirin
Toluene

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Loss of bicarbonate
Diarrhea or ureteral diversion as the ureters are
implanted into the sigmoid colon or a short loop of
ileum
Proximal (type 2) renal tubular acidosis, in which
proximal bicarbonate reabsorption is impaired

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Diminished renal acid excretion
Renal failure &
Distal (type 1) renal tubular acidosis.

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Dilution acidosis
refers to a fall in serum bicarbonate concentration that is
solely due to expansion of the extracellular fluid volume as
could occur with the administration of large volumes of
intravenous fluid that does not contain bicarbonate or an
anion that can be metabolized to bicarbonate such as lactate.
The fall in serum bicarbonate is substantially less than
predicted from the degree of volume expansion, presumably
due to the contribution of intracellular and bone buffers.
Dilution acidosis is not likely to produce a marked metabolic
acidosis unless an extraordinarily large volume of isotonic
fluid containing neither acids nor alkali is infused.

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Normal anion gap acidosis
Diarrhea and proximal (type 2) renal tubular acidosis
Some patients with renal failure
Impaired renal acid excretion due to distal (type 1)
renal tubular acidosis or hypoaldosteronism
After the successful treatment of ketoacidosis.

High Anion-Gap Metabolic Acidosis
 A CAT MUDPILES
• Analgesics (massive NSAID,
acetaminophen)
• Cyanide, Carbon monoxide
(Lactate)
• Arsenic, Alcoholic ketoacidosis
• Toluene
• Methanol, Metformin
• Uremia
• Diabetic ketoacidosis
• Paraldehyde, Phenformin
• Iron, Isoniazid
• Lactic acidosis
• Ethylene glycol
• Salicylates

Non-AG Metabolic Acidosis
•GI vs Renal causes
ABCD
•Addison disease
•Bicarbonate loss (GI or renal, including
RTA)
•Chloride (hyperchloremia)
•Drugs
• NSAIDs
• K sparing diuretics

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Overlap
oWith severe diarrhea, as can occur in cholera, there may be
an increase in the AG due to the triad of hypoperfusion-
induced lactic acidosis, volume contraction-induced
hyperalbuminemia, and hyperphosphatemia that
results from acidemia-induced movement of phosphate out
of the cells.
oIn DKA, if renal function and volume status are well
maintained, some or many of the excess ketone anions will
be excreted in the urine as the sodium and potassium salts.
The net effect is that the rise in the AG may be much less
than expected from the severity of the metabolic acidosis.

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COMPENSATORY RESPIRATORY
RESPONSE
The body responds to any acid-base disorder by making
compensatory respiratory or renal responses in an
attempt to normalize the pH.
These responses are probably mediated at least in part
by parallel alterations in pH in renal tubular or
respiratory center cells.
In metabolic acidosis, ventilation is increased, resulting
in a fall in PCO2, which tends to raise the pH toward
normal.

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Cont.
The respiratory compensation results in a 1.2 mmHg
fall in the PCO2 for every 1 mEq/L reduction in the
serum bicarbonate concentration.
This response begins within the first 30 minutes and is
complete by 12 to 24 hours.
 An inability to generate this hyperventilatory response
is generally indicative of significant underlying
respiratory disease.

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Treatment- treat the underlying cause.
DKA: Insulin is key. Bicarbonate only if pH < 6.9
Alcoholic ketoacidosis: Saline + 5% dextrose, correct electrolyte
disturbances
Lactic acidosis: Treat cause, improve perfusion; NaHCO if pH <
₃
7.00 (goal: pH 7.2 or HCO ~12)
₃
CKD: Maintain HCO in range 23–29 mEq/L per KDIGO 2013
₃
Alkali therapy indicated for: pH < 7.10, Normal AG acidosis, High
AG acidosis without 'potential bicarbonate' in plasma

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Alkali Therapy – Target , Benefits & Risks
Target: Increase [HCO3] to 10–12 mmol/L and pH to 7.20;
Preferred alkali: NaHCO3 (50 mEq in 300 mL NS IV over
30–45 min)
Benefits: Decreased hyperventilation, slowed CKD
progression, prevent nephrocalcinosis, improved skeletal
growth
 Risks: Paradoxical cerebral acidosis, post-treatment
alkalosis, slowed recovery from ketosis

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Case Scenario 3
45 yrs. old female patient presenting with progressive weakness, muscle
cramps & lightheadedness of 03 days duration. No fever, chest pain or
shortness of breath. She has been having repeated non projectile, non
bilious vomiting due to viral gastroenteritis. She has anorexia. She is
hypertensive on HCT. No hx of DM, Kidney or cardiac disease.
On P/E: BP=90/60 PR=110 RR=20 Temp=36.9 SPO2=95%
RBS=145mg/dl
Dry buccal mucosa, decreased skin turgor
Na=136mmol/L, K=2.8mmol/L, Cl=88mmol/L, HCO3=34mmol/L,
pH=7.48, PaCO2=47mmHg, BUN/Creatinine=Elevated

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Diagnosis
Metabolic alkalosis secondary to:
1. Gastrointestinal loss of Hydrogen ion….due to the vomiting.
2. Volume depletion activates RAAS promoting Hydrogen & Potassium
Ion loss.
3. Use of thiazide diuretic causes renal loss of Hydrogen & Potassium
Ion.
N.B. Elevated PaCO2 indicates respiratory compensation.

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Case Scenario 4
58 yrs. old male who is a known hypertensive & GERD pt on HCT 25 mg PO daily &
Omeprazole 20 mg PO BID respectively. He is a known Stage 2 CKD pt & he uses
NSAIDs occasionally for chronic back pain. Currently presented to OPD & said “ I’ve
been feeling weak & dizzy & my muscles keep twitching.” For the past 03 days, the
patient has experienced increasing fatigue, muscle cramps, & lightheadedness. He
reports frequent vomiting due to dyspepsia over the past 48 hrs. Has been taking extra
doses of baking soda(sodium bicarbonate) to relieve heartburn. He denies diarrhea,
fever, or chest pain.
V/S. BP=142/88 PR=92 RR=18 SPO2=98%
Mild dehydration
Chest, CVS & Abdomen. Non-remarkable findings.
CNS. Hyperreflexia, positive Chvostek’s sign

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ABG, Serum Electrolytes & RFT
pH=7.50
PaCO2=48mmHg
HCO3=36mEq/L
Na=140mEq/L
K=2.8mEq/L
Cl=88mEq/L
CO2=34mEq/L
BUN=22mg/dL
Creatinine=1.4mg/Dl
Urine Chloride<10mEq/L

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Diagnosis
Metabolic Alkalosis(Chloride Responsive) due to:
Loss of gastric acid(from vomiting)
Excessive alkali intake(baking soda use)
Hypokalemia(worsened by HCT)

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Management
NS(0.9% NaCl) to restore volume & chloride
KCl Supplementation(oral or IV)
Discontinue baking soda & adjust GERD management
Monitor electrolytes & ABG for resolution
Consider switching HCT to potassium-sparing diuretic if alkalosis
persists

08/19/2025 71
Metabolic Alkalosis
 Established by an elevated arterial pH, an increase in the
serum [HCO3−], a loss of Hydrogen ions and an increase in
PaCo2 as a result of compensatory alveolar hypoventilation .
Volume contraction (vomiting, NG suction, loop or thiazide
diuretics).
Excess glucocorticoids or mineralocorticoids (eg, Cushing’s
syndrome).
Alkali ingestion/ infusion (eg, baking soda).

08/19/2025 72
Causes:
Loss of gastric acid(HCl)..vomiting, NG suction
Excess bicarbonate intake ..Antacids(especially sodium bicarbonate),
IV bicarbonate administration.
Diuretic use: Loop diuretics, Thiazides(cause loss of Cl, Na, K, H)
Mineralocorticoid excess: Cushing Syndrome, Primary
hyperaldosteronism(Conn Syndrome) promotes H & K loss in urine
Post-hypercapnia: after rapid correction of respiratory acidosis,
kidneys may retain bicarbonate for a while.

08/19/2025 73
Causes of Metabolic Alkalosis

08/19/2025 74
.

08/19/2025 75
Lab Findings
opH> 7.54, Increased bicarbonate, Compensatory hypoventilation,
hypokalemia, hypochloremia
oThe lungs compensate by hypoventilation to retain CO2, which is
acidic, but this is limited due to the risk of hypoxia.
 To determine the cause, we can check urine chloride:
Urine Cl < 10 mEq/L…volume responsive e.g. vomiting, diuretics
withdrawal.
Urine Cl > 20 mEq/L…Chloride resistant e.g. hyperaldosteronism

08/19/2025 76
.

08/19/2025 77
ETIOLOGY & PATHOGENESIS
Metabolic alkalosis occurs as a result of net gain of [HCO3−] or loss
of nonvolatile acid (usually HCl by vomiting) from the extracellular
fluid.
When vomiting causes loss of HCl from the stomach, HCO3 −
secretion cannot be initiated in the small bowel, and thus, HCO3− is
retained in the extracellular fluid.
Upon cessation of vomiting, the maintenance stage ensues because
secondary factors prevent the kidneys from excreting HCO3 −
appropriately.

08/19/2025 78
Cont.
 Maintenance of metabolic alkalosis, therefore, represents a failure of the
kidneys to eliminate excess HCO− from the extracellular compartment.
 The kidneys will retain, rather than excrete, the excess alkali and maintain
the alkalosis if
(1) volume deficiency, chloride deficiency, and K+ deficiency exist in
combination with a reduced GFR (associated with a low urine [Cl–])
(2) hypokalemia exists because of autonomous hyperaldosteronism (normal
urine (Cl–)

08/19/2025 79
Genesis phase: Cause of HCO excess?
₃
•
 Maintenance phase: Why isn't HCO being excreted?
₃
•
 Contributors: H+ shift, GI loss, renal loss, exogenous alkali

08/19/2025 80
DIFFERENTIAL DIAGNOSIS
In Metabolic alkalosis , it is necessary to assess the status of the
ECFV, the recumbent and upright blood pressure (to determine if
orthostasis is present), the serum [K+], the urine [Cl–], and in some
circumstances, the renin-aldosterone system.

08/19/2025 81
Cont.
Example, the presence of chronic hypertension and chronic
hypokalemia in an alkalotic patient suggests either
 Mineralocorticoid excess or
 That the hypertensive patient is receiving diuretics.
Low plasma renin activity and values for urine [Cl−] >20 meq/L in a
patient who is not taking diuretics suggest
 Primary mineralocorticoid excess.

08/19/2025 82
Cont.
The combination of hypokalemia and alkalosis in a normotensive, non
edematous patient can be due to:
 Bartter’s or Mitelman's syndrome,
 Magnesium deficiency,
 Vomiting,
 Exogenous alkali, or diuretic ingestion.

08/19/2025 83
Cont.
 If the urine is alkaline, with an elevated [Na+] and [K+] but low [Cl−] ,
the diagnosis is usually, either
 Vomiting or
 Alkali ingestion.
 If the urine is relatively acid with low concentrations of Na+, K+, and
Cl−, the most likely possibilities are
 Prior vomiting,
 Post hypercapnic state, or
 Prior diuretic ingestion.

08/19/2025 84
Metabolic Alkalosis Associated With ECFV Contraction, K+
Depletion, And Secondary Hyperreninemic Hyperaldosteronism
Gastrointestinal loss of H+ from
 Vomiting or
 Gastric aspiration causes simultaneous addition of HCO3− into
the extracellular fluid.
During active vomiting
The filtered load of bicarbonate reaching the kidneys is acutely
increased.
Will exceed the reabsorptive capacity of the proximal tubule for
HCO3− absorption.

08/19/2025 85
Renal Origin
Diuretics such as thiazides and loop diuretics increase excretion of salt
and acutely diminish the ECFV without altering the total body
bicarbonate content.
The serum [HCO3−] increases because the reduced ECFV “contracts”
around the [HCO3−] in plasma (contraction alkalosis).

08/19/2025 86
NON-REABSORBABLE ANIONS AND MAGNESIUM
DEFICIENCY
Administration of large quantities of the penicillin derivatives
Carbenicillin
 Ticarcillin
cause their non-reabsorbable anions to appear in the distal tubule.
This increases the transepithelial potential difference in the collecting
tubule and thereby enhances H+ and K+ secretion.

08/19/2025 87
Cont.
Mg2+ deficiency may occur with chronic administration of
Thiazide diuretics,
Alcoholism,
 Malnutrition.

08/19/2025 88
Metabolic Alkalosis Associated With ECFV Expansion, Hypertension,
And Mineralocorticoid Excess
Increased aldosterone levels may be the result of autonomous primary
adrenal overproduction or of secondary aldosterone release due to
renal overproduction of renin.
Mineralocorticoid excess increases net acid excretion and may result
in metabolic alkalosis, which is typically exacerbated by associated
K+ deficiency.

08/19/2025 89
POTASSIUM DEPLETION
Chronic K+ depletion may be due to :
• extreme dietary potassium insufficiency,
• diuretics, or
• alcohol abuse
 Potassium depletion often occurs concurrent with magnesium
deficiency in alcoholics with malnutrition.

08/19/2025 90
Cont.
Patients typically present with:
Hypertension,
Hypokalemia,
 Metabolic alkalosis.

08/19/2025 91
Treatment- Metabolic Alkalosis
Volume depletion: Isotonic saline, correct hypokalemia
Stop vomiting or NG suction
Discontinue diuretics & treat endocrine disorders.
Chloride depletion: Chloride salts
Potassium depletion: KCl (20–80 mEq/day); avoid K citrate/acetate
Renal failure: Hemodialysis with low HCO , high Cl dialysate
₃ ⁻
Acetazolamide for edematous states (CHF, cirrhosis, nephrotic syndrome)
Severe metabolic alkalosis: HCO > 50 mEq/L or pH > 7.55 in dialysis-ineligible
₃
patients
In severe cases… acetazolamide or dialysis(if renal failure)

08/19/2025 92
Case Scenario 5
68 yrs. old male patient presented with increasing shortness of breath,
drowsiness, & confusion over the past 02 days. He has hx of COPD &
recently developed a productive cough with greenish sputum & a low
grade fever. He reports worsening dyspnea, especially at rest & difficulty
clearing secretions. He has 50 pack-year smoking hx. He is hypertensive
but no hx of DM or cardiac illness. He is taking Albuterol/Ipratropium
inhaler, Tiotropium. Occasionally uses prednisolone. No home oxygen.
On P/E: BP=135/85 PR=102 RR=10 SPO2=84% 0n room air
Lethargic, slow to respond, use of accessory muscles, diminished breath
sounds with coarse crackles & wheezing.

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Arterial Blood Gas(ABG)
• pH=7.28
• PaCO2=65mmHg
• HCO3=29mmol/L
• PaO2=58mmHg
• SPO2=84%

08/19/2025 94
Diagnosis
Primary Respiratory Acidosis due to Acute-on-Chronic CO2 retention
from a COPD exacerbation likely triggered by infection.
Compensatory Mechanism: Mildly elevated HCO3 due to renal
compensation, which is partially compensating consistent with chronic
component.

08/19/2025 95
Case Scenario 6
A 65 yrs. old male with a history of COPD presents to the emergency
department with increased shortness of breath, confusion, & drowsiness
over the past 24 hrs. His family reports that he has had a productive cough
with greenish sputum & a low grade fever for the past few days. He is a
long term smoker & has been on home oxygen therapy.
V/S. BP=150/90 PR=110 RR=8 breaths/min(shallow & slow) SPO2=85%
on room air(92% with supplemental O2) Temp=38.1
Chest. Diffuse wheezing, prolonged expiratory phase, decreased breath
sounds at basal area. Cyanosis of lips & nail beds, use of accessory muscles
CNS. Lethargic, confused(disoriented to time, place & person)

08/19/2025 96
ABG
pH=7.28
PaCO2=68mmHg
HCO3=32mEq/L
PaO2=55mmHg

08/19/2025 97
Diagnosis
Acute-on-Chronic Respiratory Acidosis caused by hypoventilation
due to COPD exacerbation likely 2ry to Pneumonia
Chronic CO2 retention
Acute worsening due to infection & increased airway inflammation &
mucus plugging & hypoventilation & further CO2 retention
Renal compensation(elevated HCO3) is insufficient to correct pH…
Compensatory metabolic alkalosis

08/19/2025 98
Management
Oxygen therapy
Bronchodilators(nebulized albuterol + ipratropium)
Steroids(IV methylprednisolone or oral prednisone) to reduce
inflammation.
Antibiotics(if pneumonia is suspected)
Non-invasive ventilation(BiPAP) if hypercapnia worsens
Monitor ABG & electrolytes(watch for worsening acidosis)

08/19/2025 99
RESPIRATORY ACIDOSIS
Respiratory acidosis occurs as a result of
Severe pulmonary disease,
Respiratory muscle fatigue,
Abnormalities in ventilatory control
is recognized by an increase in PaCO2 and decrease in pH .
In acute respiratory acidosis, there is a compensatory elevation in
HCO3− (due to cellular buffering mechanisms) that increases
1 mmol/L for every 10-mmHg increase in PaCO2.

08/19/2025 100
Acute Respiratory Acidosis…sudden onset
Respiratory Depression e.g. opioid overdose, sedatives, CNS trauma
Airway obstruction e.g. chocking, severe asthma
Neuromuscular disorders e.g. GBS, myasthenia gravis
Acute pulmonary disease e.g. pneumonia, pulmonary edema
Minimal renal compensation, bicarbonate increases slightly.

08/19/2025 101
Chronic Respiratory Acidosis…slow onset
with renal compensation
• COPD
• Obesity hypoventilation Syndrome
• Neuromuscular disorders with slow progression
• Chest wall deformities e.g. kyphoscoliosis
Kidneys retain more bicarbonate over days to compensate.

08/19/2025 102
Symptoms
• Headache
• Confusion, drowsiness
• Flushed skin
• Shallow, slow breathing
• If severe: coma, cardiac arrhythmia

08/19/2025 103
Causes of hypoventilation
CNS depression (sedatives, CNS disease, sleep apnea)
Pleural disease (large pneumothorax or pleural effusion)
Lung disease (ARDS, COPD, pulmonary edema, severe
pneumonia)
Acute airway obstruction (laryngospasm, sleep apnea,
asthma exacerbation)
Neuromuscular disorders (GBS, myasthenia gravis,
botulism)
Thoracic cage injury (flail chest)

08/19/2025 104
Cont.
oA rapid increase in PaCO2 (acute hypercapnia) may cause
Anxiety,
Dyspnea,
Confusion,
Psychosis,
 Hallucinations,
May progress to coma.

08/19/2025 105
Cont.
oChronic hypercapnia may cause
Sleep disorders;
Loss of memory;
Daytime somnolence;
Personality changes;
Impairment of coordination;
Motor disturbances such as tremor, myoclonic jerks, and asterixis.

08/19/2025 106
Diagnosis
oA detailed history and physical examination often indicate
the cause.
oThe diagnosis of respiratory acidosis requires the
measurement of
PaCO2
 Arterial pH.

08/19/2025 107
Cont.
oPulmonary function studies, including
Spirometry,
 Diffusion capacity for carbon monoxide
Lung volumes,
And arterial PaCO2 and O2 saturation,
usually make it possible to determine if respiratory
acidosis is secondary to lung disease.

08/19/2025 108
.

08/19/2025 109
Treatment
Treat the underlying cause: reverse opioid overdose(naloxone),
Bronchodilators for asthma/COPD
Oxygen therapy especially in COPD
Improve ventilation: Non-invasive ventilation(CPAP/BiPAP)
& Intubation & mechanical ventilation if necessary
Avoid excessive Oxygen in chronic cases because it can worsen CO2
retention in COPD.

08/19/2025 110
Case Scenario 7
A 28 yrs. old female arrives at the emergency department with rapid breathing,
dizziness, & tingling in her fingers & lips. She reports experiencing sudden
chest tightness & difficulty catching her breath after an intense argument with
her partner. She has a hx of anxiety disorder but no significant medical history.
V/S. BP=118/76 PR=98 RR=28breaths/min(rapid & deep) SPO2=99% on
room air Temp=37
Chest. Clear chest, good air entry.
CVS. S1 & S2 are well heard. No murmur or gallop.
MSS. Mild carpopedal spasm
CNS. Alert but anxious, positive Chvostek’s sign

08/19/2025 111
ABG
pH=7.52
PaCO2=24mmHg
HCO3=22mEq/L
PaO2=102mmHg

08/19/2025 112
Diagnosis
Acute Respiratory Alkalosis due to hyperventilation & excessive
CO2 exhalation from anxiety attack(panic disorder)
Low PaCO2
Rising pH & ionized calcium decreases & neuromuscular
irritability(tingling, spasms)
No renal compensation yet(HCO3 is normal)

08/19/2025 113
Management
Reassurance & relaxation(breathing into a paper bag to rebreathe CO2
if severe)
Address underlying anxiety(short-term benzodiazepine if needed, e.g.
lorazepam)
Monitor for electrolyte disturbances(hypocalcemia, hypokalemia)
Rule out other causes(pulmonary embolism, sepsis, CNS disorders if
symptoms persist)

08/19/2025 114
Case Scenario 8
26 yrs. old female patient presents with acute onset of
lightheadedness, shortness of breath, & tingling sensation in her
fingers & lips. These symptoms started about 30 minutes ago while
she was at work. She reports feeling extremely anxious due to an
upcoming public presentation & believes she had a panic attack.
She denies chest pain, palpitations, or any previous episodes like this.
No hx of DM, hypertension or cardiac illness. She has Generalized
anxiety disorder, has follow-up for this. She occasionally uses
lorazepam, but no recent medication changes.

08/19/2025 115
Cont.
On P/E: BP=120/75 PR=98 RR=28 SPO2=99% on room air
RBS=36.7 Temp=37.8
Chest is clear with good air entry.
She appears anxious, alert & oriented.
No focal neurological deficits.
oABG: pH(arterial)=7.49 PaCO2=29 mmHg HCO3=22 mmol/L
PaO2=100 mmHg

08/19/2025 116
Diagnosis
Primary Respiratory Alkalosis caused by hyperventilation due to
Acute Anxiety/panic attack
Rapid breathing & excessive CO2 exhalation, low CO2 & increased
pH(alkalosis), causes vasoconstriction(dizziness) & calcium
shift(paresthesias)

08/19/2025 117
RESPIRATORY ALKALOSIS
Results from Increased Ventilation and Decreased PCO2
ocauses with hyperventilation
• CNS disease (CVA)
• Toxins (Salicylates)
• High altitude
• Severe anemia
• Pregnancy
• Lung disease/hypoxia (asthma, pneumonia, PE, pulmonary edema,
pulmonary fibrosis)
• Cirrhosis of the liver
• Fever (Sepsis)

08/19/2025 118
Central causes(increased respiratory drive)
• Anxiety/panic attacks
• Pain
• Fever
• Stroke, head trauma, tumor
• Salicylate poisoning(early phase)

08/19/2025 119
Hypoxemia-induced hyperventilation
• High altitude
• Pulmonary embolism
• Pneumonia
• Heart failure

08/19/2025 120
Mechanical ventilation
• Over-ventilation in intubated patients

08/19/2025 121
,

08/19/2025 122
Cont.
oAcute.. kidneys haven’t had time to respond.. normal bicarbonate
oChronic.. Kidneys excrete HCO3 to compensate
In chronic cases, kidneys retain Hydrogen ion and excrete HCO3 to
restore acid-base balance, but this takes 2-3 days.

08/19/2025 123
Symptoms
• Dizziness or lightheadedness
• Numbness/tingling(especially around the mouth and in fingers)
• Chest tightness
• Confusion
• Seizures(in severe cases)
• Syncope(fainting)
Reason: Because alkalosis causes calcium to bind more to albumin,
reducing free(ionized) calcium…hypocalcemia-like effects.

08/19/2025 124
Cont.
Alveolar hyperventilation
Decreases Paco2
 Increases the HCO3−/Paco2 ratio,
Thus increasing pH.
Hypocapnia develops when a sufficiently strong ventilatory stimulus
causes CO2 output in the lungs to exceed its metabolic production by
tissues.
 Full renal adaptation to respiratory alkalosis may take several days
and requires normal volume status and renal function.

08/19/2025 125
Cont.
Reduced cerebral blood flow as a consequence of a rapid decline in Paco2 may
cause
 Dizziness,
 Mental confusion,
 Seizures, even in the absence of hypoxemia.
Respiratory alkalosis is often an early finding in gram-negative septicemia, before
 Fever,
 Hypoxemia,
 Hypotension develops.

08/19/2025 126
Diagnosis
•Measure arterial pH and PaCO2.
•The plasma [K+] is often reduced and the [Cl−]
increased.
In general, the HCO3− concentration falls by 2.0
mmol/L for each 10-mmHg decrease in Paco2.
The decline in PaCO2 reduces the serum [HCO3−] by
4.0–5 mmol/L for each 10-mmHg decrease in Paco2.

08/19/2025 127
Cont.
• When the diagnosis of respiratory alkalosis is made, its cause should
be investigated.
• In difficult cases, it may be important to rule out other conditions such
as
pulmonary embolism,
coronary artery disease,
 hyperthyroidism.

08/19/2025 128
Treatment
Identify and treat the underlying causes & reduce hyperventilation.
Reassurance + breathing coaching e.g. breath into a paper bag if
anxiety-induced.
Pain control
Adjust mechanical ventilation settings if needed.
Oxygen if hypoxemia is the cause.

08/19/2025 129
REFERENCES
• Comprehensive Clinical Nephrology, 7th Edition
• Guyton textbook of medical physiology,12th edition
• Harrison Internal Medicine , 21st edition
• UpToDate 2023 online

130
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