Basics of Acid-Base Balance

1
Basics of Acid-Base Balance

• Naveed Aslam, MD
• Consultant clinical tutor
• Department of Nephrology
• Prince Sultan Military Medical City

2
Key concepts

• Introduction
• Overview of pH
• Buffering systems
• Metabolic imbalances
• Respiratory imbalances
• Illustrative Cases

3
Acid Base balance

• Acid-base balance refers to the mechanisms the
  body uses to keep its fluids close to neutral pH
  (that is, neither basic nor acidic) so that the
  body can function normally.
• Arterial blood pH is normally closely regulated
  to between 7.35 and 7.45.

4

• acids?
• bases?

Any ionic or molecular substance that can act as
a proton donor. Strong acidHCl, H2SO4,
H3PO4. Weak acidH2CO3, CH3COOH.
Any ionic or molecular substance that can act as
a proton acceptor. Strong alkaliNaOH, KOH. Weak
alkaliNaHCO3, NH3, CH3COONa.
5
Origin of acids
Much more
Intracellular metabolism
Volatile acids
300400L CO2 (15mol H)
CO2H2OH2CO3

• Lactic acid
• Ketone bodies
• Sulfuric acid
• Phosphoric acid

50100 mmol H
Fixed acids
Origin of bases

• NH3 , sodium citrate, sodium lactate

less
6
pH Overview
7
pH overview

• pH is a measure of hydrogen (H) concentration in
  a solution
• H changes occur tenfold on the pH scale
• Body pH 7.35 7.45
• - pH is variable in certain areas (stomach,
  CSF, etc)

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pH

• - pH of ECF is between 7.35 and 7.45. Deviations,
  outside this range affect membrane function,
  alter protein function, etc.
• - You cannot survive with a pH lt6.8 or gt7.7
• Acidosis- below 7.35
• Alkalosis- above 7.45
• CNS function deteriorates, coma, cardiac
• irregularities, heart failure, peripheral
• vasodilation, drop in Bp.

9

• Given that normal body pH is slightly alkaline
  and that normal metabolism produces acidic waste
  products such as carbonic acid (carbon dioxide
  reacted with water) and lactic acid, body pH is
  constantly threatened with shifts toward acidity.
  
• In normal individuals, pH is controlled by two
  major and related processes
• - pH regulation is a function of the buffer
  systems of the body in combination with the
  respiratory and renal systems.
• - pH compensation requires further
  intervention of the respiratory and/or renal
  systems to restore normalcy.

10
ABB disorders
Alkalemia
Acidemia
7,40
Normal arterial blood pH 7.35 7.45
7.45
7.35
Normal range
acidosis
alkalosis
11
Definitions

• Normal pH is 7.35 - 7.45
• If this value is normal, but one of the below
  values is abnormal, the patient has compensated.
• Normal C02 is 35 -45 mmHg
• If this value is abnormal, the patient has
  respiratory acidosis or alkalosis.
• Normal HC03 is 22-26 mEq/L
• If this value is abnormal, the patient has
  metabolic acidosis or alkalosis
• Normal O2 Saturation is 80-100 ml/dl
• If this value is normal in a respiratory pH
  problem, patient is compensating.

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• Acid-base balance is maintained by
• normal pulmonary excretion of carbon dioxide,
• metabolic utilization of organic acids,
• and renal excretion of nonvolatile acids

13
Buffers

• Buffers are solutions which can resist changes
  in pH when acid or alkali is added.

14
Buffering Capacity in Body

• 52 of the buffering capacity is in cells
• 5 is in RBCs
• 43 of the buffering capacity is in the
  extracellular space
• of which 40 by bicarbonate buffer, 1 by
  proteins and 1 by phosphate buffer system

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15
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Buffering Systems

• The three different buffering systems are
• 1) Respiratory buffering system
• Uses bicarbonate
• 2) Blood buffering system
• Uses bicarbonate, phosphate, and protein
• 3) Renal buffering system
• Uses bicarbonate, phosphate, and ammonia

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Respiratory Buffering System

• Lungs (only if not a respiratory problem)
• If too much acid (low pH)respiratory system will
  ventilate more (remove CO2) and this will raise
  pH back toward set point
• If too little acid (high pH)respiratory will
  ventilate less (trap CO2 in body) and this will
  lower pH back toward set point
• Peripheral receptors detect CO2 concentration
  changes and send the appropriate signal to the
  respiratory system.

Low pH Hyperventilation
High pH Hypoventilation
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Blood Buffering System

• The blood buffering system uses three different
  chemical buffers phosphate, bicarbonate and
  proteins. The phosphate buffer is not abundant in
  blood. Blood contains a high concentration of
  proteins.

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Renal Buffering System

• The renal buffer system uses
• - bicarbonate,
• - phosphate
• - ammonium.
• In the kidneys, the bicarbonate buffer may
  increase plasma pH in three ways
• - secreton of H -- occurs mostly in proximal
  tubule
• - reabsorbtion of bicarbonate -- PCT
• - producing new bicarbonate -- intercalated
  cells

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How can the kidneys control acids and bases?

• Bicarbonate is filtered and enters nephron at
  Bowmans capsule
• Proximal convoluted tubule
• Can reabsorb all bicarbonate (say, when you need
  it to neutralize excessive acids in body)
• OR
• Can reabsorb some or NONE of the bicarbonate
  (maybe you have too much base in body and it
  needs to be eliminated)

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How can the kidneys control acids and bases?
Phosphate important renal tubular buffer HPO4-
H H2PO4

• Acidosis
• Intercalated cells
• Secrete excessive hydrogen
• Secreted hydrogen binds to buffers in the lumen
  (ammonia and phosphate bases)
• Secretion of hydrogen leads to formation of
  bicarbonate

HPO4- NH3
Ammonia important renal tubular buffer NH3
H NH4
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Acids must be buffered, transported away from
cells, and eliminated from the body.These are
the most important buffers.
Phosphate important renal tubular buffer HPO4-
H H2PO4 Ammonia important renal tubular
buffer NH3 H NH4 Proteins important
intracellular and plasma buffers H
Hb HHb Bicarbonate most important Extracellular
buffer and is also another important renal
tubular buffer.
H2O CO2 H2CO3 H HCO3 -
23
Buffering is good, but it is a temporary
solution. Excess acids and bases must be
eliminated from the body
gas
aqueous
H2O CO2 H2CO3 H HCO3 -
Kidneys can remove excess non-gas acids and bases
Lungs eliminate carbon dioxide
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Simple acid base disorder
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Definition of acid-base disorders

• An acid base disorder is a change in the normal
  value of extracellular pH that may result when
  renal or respiratory function is abnormal or when
  an acid or base load overwhelms excretory
  capacity.

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Excessive Acids and Bases can cause pH
changes---denature proteins

• Normal pH of body fluids is 7.40
• Alkalosis (alkalemia) arterial blood pH rises
  above 7.45
• Acidosis (acidemia) arterial pH drops below
  7.35

• Acidosis
• Too much acid
• Too little base
• Alkalosis
• Too much base
• Too little acid

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How can you detect if the acid-base imbalance is
from a kidney disorder or a lung disorder?
Acidosis pH lt 7.4
- Metabolic HCO3 -
- respiratory pCO2
Alkalosis pH gt 7.4
- Metabolic HCO3 -
- respiratory pCO2
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REASONS FOR METABOLIC ACIDOSIS AND ALKALOSIS
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What would happen if the respiratory system had a
problem with ventilation?Respiratory Acidosis
and Alkalosis

• Normal PCO2 fluctuates between 35 and 45 mmHg

• Respiratory Alkalosis (less than 35mmHg- lowered
  CO2)
• Hyperventilation syndrome/ psychological (fear,
  pain)
• Overventilation on mechanical respirator
• Ascent to high altitudes
• Fever

• Respiratory Acidosis (elevated CO2 greater than
  45mmHg)
• Depression of respiratory centers via narcotic,
  drugs, anesthetics
• CNS disease and depression, trauma (brain damage)
• Interference with respiratory muscles by disease,
  drugs, toxins
• Restrictive, obstructive lung disease (pneumonia,
  emphysema)

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What if your metabolism changed?

• Metabolic alkalosis
• bicarbonate ion levels higher (greater than
  26mEq/L)

• Metabolic acidosis
• Bicarbonate levels below normal (22 mEq/L)

• Excessive loss of acids due to loss of gastric
  juice during vomiting
• Excessive bases due to ingestion, infusion, or
  renal reabsorption of bases
• Intake of stomach antacids
• Diuretic abuse (loss of H ions)
• Severe potassium depletion
• Steroid therapy

• Ingestion, infusion or production of more acids
  (alcohol)
• Salicylate overdose (aspirin)
• Diarrhea (loss of intestinal bicarbonate)
• Accumulation of lactic acid in severe Diabetic
  ketoacidosis
• starvation

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Acid-Base Balance

• How would your ventilation change if you had
  excessive acid?
• You would hyperventilate
• How would your ventilation change if you had
  excessive alkalosis?
• Your breathing would become shallow

Low pH acidosis Hyperventilation
High pH alkalosis Hypoventilation
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Acidosis
Metabolic acidosis
Respiratory acidosis
Excessive amount of carbon dioxide in the blood
that results from poor lung function or slow
breathing
Excessive blood acidity caused by an
overabundance of acid in the blood or a loss of
bicarbonate from the blood
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• Metabolic acidosis
• Causes1) lose of bases (bicarbonate
  decreased)
• Gastrointestinal losses diarrhea
  Renal losses proximal renal tubular acidosis and
  distal renal tubular acidosis
• 2) Gaining acids (bicarbonate consumed in
  buffering) Lactic acidosis tissue hypoxia,
  impaired oxygen utilization, severe liver
  dysfunction, and shock Ketoacidosis
  diabetic,hepatic cirrhosis, alcoholic poisoning,
  or starvation Renal failure conservation
  of acids
• Exogenous acid intake ammonium chloride,
  salicylate, ethylene glycol (commonly used in
  antifreeze), or methanol intoxication

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Metabolic acidosis

• Compensation
• The body will compensate with hyperventilation
  and increased bicarbonate reabsorption in the
  kidney.
• Since the primary abnormality is a decrease in
  HCO3, the compensatory response includes
  extracellular buffering (by bicarbonate),
  intracellular buffering (by phosphate and
  proteins), respiratory compensation and renal
  hydrogen excretion.
• Metabolic acidosis stimulates an increase in
  ventilation (reducing pCO2).
• This hyperventilation is called Kussmaul's
  respiration.

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The Response to Metabolic Acidosis
36
Metabolic acidosis

• Symptoms
• Most symptoms are caused by the underlying
  disease or condition that is causing the
  metabolic acidosis.
• Metabolic acidosis itself usually causes rapid
  breathing.
• Confusion or lethargy may also occur.
• Severe metabolic acidosis can lead to shock or
  death.
• In some situations, metabolic acidosis can be a
  mild, chronic (ongoing) condition.

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Respiratory acidosis

• Respiratory acidosis is due to an accumulation of
  CO2 in the blood stream. This pushes the carbonic
  anhydrase reaction to the right, generating H
• carbonic anhydrase CO2          H2CO3    
     HCO3(-)     H

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Respiratory acidosis

• Cause
• The increase in CO2 in the blood is often caused
  by hypoventilation.
• This can be caused by asthma, COPD, and overuse
  of sedatives, barbiturates, or narcotics such as
  valium, heroin, or other drugs which make you
  sleepy.
• Any trauma where the breathing muscles are
  damaged (causing decreased ventilation), airway
  obstruction, or lung disease (pneumonia, cystic
  fibrosis, emphysema, etc.).

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Respiratory acidosis

• Compensation
• The kidneys will compensate by secreting H.
• If H excretion cannot restore the balance, the
  kidneys will also generate bicarbonate.
• Since the primary abnormality is an increase in
  pCO2, the compensatory response is intracellular
  buffering of hydrogen (by hemoglobin) and renal
  retention of bicarbonate, which takes several
  days to occur.

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Respiratory acidosis
Figure 27.12a
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Respiratory acidosis

• Symptoms
• May have no symptoms but usually experience
  headache, nausea, vomiting, and fatigue.
• Breathing becomes deeper and slightly faster (as
  the body tries to correct the acidosis by
  expelling more carbon dioxide).
• As the acidosis worsens, people begin to feel
  extremely weak and drowsy and may feel confused
  and increasingly nauseated.
• Eventually, blood pressure can fall, leading to
  shock, coma, and death.

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Respiratory acidosis

• Treatment
• Treatment is aimed at the underlying disease, and
  may include
• Bronchodilator drugs to reverse some types of
  airway obstruction
• Noninvasive positive-pressure ventilation
  (sometimes called CPAP or BiPAP) or a breathing
  machine, if needed
• Oxygen if the blood oxygen level is low

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Alkalosis
Metabolic alkalosis
Respiratory alkalosis
Excessive blood alkalinity caused by an
overabundance of bicarbonate in the blood or a
loss of acid from the blood
Loss of carbon dioxide in the blood that results
from rapid or deep breathing
44
Metabolic alkalosis

• Cause
• An increase in bicarbonate in the blood because
  of ingestion of excess bicarbonate in the form of
  an antacid (Tums), eating excess fruits
  (vegetarian diets and fad diets),
• Excessive loss of hydrogen ions, chloride or
  potassium ionsGastrointestinal H loss
  vomiting, gastric suctionRenal H loss
  Aldosteronism, cushings syndromethiazide
• Volume contraction DehydrationDiuretic therapy

45
Metabolic alkalosis 

• Compensation
• This is initially buffered by hydrogen buffers
  (such as plasma proteins and lactate).
• Chemoreceptors in the respiratory center sense
  the alkalosis and trigger hypoventilation,
  resulting in increased pCO2.
• The respiratory system will hypoventilate but
  this will not be effective because CO2 will
  accumulate and the CO2 receptors will override
  the pH receptors.
• In addition to respiratory compensation, the
  kidneys excrete the excess bicarbonate. However,
  this takes several days to occur.

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Metabolic Alkalosis
47
Metabolic alkalosis 

• Symptoms
• Confusion (can progress to stupor or coma)
• Hand tremor
• Light-headness
• Muscle twitching
• Nausea, vomiting
• Numbness or tingling in the face, hands, or feet
• Prolonged muscle spasms (tetany)

48
Respiratory alkalosis 

• Respiratory alkalosis is generally caused by
  hyperventilation, usually due to anxiety. The
  primary abnormality is a decreased pCO2.
• Cause
• Caused from a decrease in CO2 in the blood
  because the lungs are hyperventilating (anxiety,
  but not panting).
• Fever or aspirin toxicity may also cause
  respiratory alkalosis.

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Respiratory alkalosis

• Compensation
• The body will reduce the breathing rate, and the
  kidney will excrete bicarbonate.

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Respiratory alkalosis

• Compensation
• The compensatory response to a respiratory
  alkalosis is initially a release of hydrogen from
  extracellular and intracellular buffers.
• This is followed by reduced hydrogen excretion by
  the kidneys.
• This results in decreased plasma bicarbonates.
• In chronic respiratory alkalosis, compensation
  can lead to pH returning to normal.

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Respiratory alkalosis
Figure 27.12b
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Summary
DISTURBANCE pH PRIMARY CHANGE RATIO SECONDARY CHANGE
Metabolic Acidosis Decreased Deficit of bi- carbonate lt20 Decrease in PaCO2
Metabolic Alkalosis Increased Excess of bicarbonate gt20 Increase in PaCO2
Respiratory acidosis Decreased Excess of carbonic acid lt20 Increase in bicarbonate
Respiratory alkalosis Increased Deficit of carbonic acid gt20 Decrease in bicarbonate
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Summary

• CO2 Acid
• ?CO2 ? pH (acidemia)
• ? CO2 ? pH (alkalemia)
• HCO3 Base
• ? HCO3 ? pH (alkalemia)
• ? HCO3 ? pH (acidemia)

Respiratory
Metabolic
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Reference ranges and points
Parameter Reference range Reference
point pH 7.35-7.45 7.40 PCO2 33-44 mm Hg 40 mm
Hg PO2 75-105 mm Hg 80mm Hg HCO3- 22-28
mEq/L 24mEq/L Anion gap 8-16 mEq/L 12 mEq/L
Osmolar gap lt10 mOsm/L
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Interpreting Arterial Blood Gases (ABG)

• This blood test is from arterial blood, usually
  from the radial artery.
• There are three critical questions to keep in
  mind when attempting to interpret arterial blood
  gases (ABGs). First Question Does the patient
  exhibit acidosis or alkalosis? Second Question
  What is the primary problem? Metabolic? or
  Respiratory? Third Question Is the patient
  exhibiting a compensatory state?

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Assessment Step 1

• Step One Determine the acid/base status of the
  arterial blood.
• If the blood's pH is less than 7.35 this is an
  acidosis, and if it is greater than 7.45 this is
  an alkalosis. You may hear nurses or doctors
  say "The patient is 'acidotic' or 'alkalotic'

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Assessment Step 1

• If the pH is low, it is acidosis.
• If it is high, it is alkalosis.

pH
58
Assessment Step 2

• Once you have determined the pH, you can move on
  to determine which system is the 'primary'
  problem respiratory or metabolic.

• To do this, examine the pCO2 and HCO3 levels.

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Assessment Step 2

• If the pCO2 is the only one that is abnormal, it
  is respiratory.
• If the HCO3 is the only one that is abnormal, it
  is metabolic.
• If they are both abnormal, we need to evaluate it
  further. Go to step 3.

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Assessment Step 3

• Determine if the body is attempting to compensate
  for the imbalance or not.
• If they are both high or both low, the patient is
  compensating.
• You will never have a case where one is high and
  one is low.

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• If both the pCO2 and HCO3 are high, what does it
  mean?
• If the pH is low, it is compensated respiratory
  acidosis.
• If the pH is high, it is compensated metabolic
  acidosis.

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Look at dirrection of arrows

• RESPIRATORY arrow dirrection oposite to PH
• pH HC03 PC02 RESPIRATORY
  ALKALOSIS
• pH HC03 PC02 RESPIRATORY
  ACIDOSIS

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Look at dirrection of arrows

• Metabolic all arrow same dirrection
• pH HC03 PC02 METABOLIC
  ACIDOSIS
• pH HC03 PC02 METABOLIC
  ALKALOSIS

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• If both the pCO2 and HCO3 are high, and the pH is
  low, how do you know it is compensated
  respiratory acidosis instead of compensated
  metabolic acidosis?
• In respiratory acidosis, the first thing to go
  wrong is the pCO2 will become high. To
  compensate, the HCO3 will become elevated.
• If it was metabolic acidosis, the first thing to
  go wrong would be the HCO3 levels would be too
  low. To compensate, the pCO2 levels would start
  dropping to raise the pH.

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Review the three essential steps of ABG analysis

• Number One
• Determine if the patient is demonstrating an
  acidotic (remember pH less than 7.35) or
  alkalotic (pH greater than 7.45) condition.
• Number Two
• What is the 'primary problem?
• If the patient is acidotic with a pC02 greater
  than 45 mmHg it is RESPIRATORY
• If the patient is alkalotic with a pC02 less than
  35 mmHg it is RESPIRATORY!
• If the patient is acidotic with a HC03 less than
  22 mEq/L it is METABOLIC!
• If the patient is alkalotic with a HC03 greater
  than 26 mEq/L it is METABOLIC!

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Review the three essential steps of ABG analysis

• Number ThreeIs the patient compensating?
• Are both components (HCO3 and pCO2) shifting in
  the same direction?
• Both going up or both going down?
• If so, the patient is compensating. Their
  buffering systems are functioning and are trying
  to bring the acid-base balance back to normal.

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ACID BASE PARAMETERS(The problem chemical is in
yellow)
Respiratory Acidosis PH PCO2 HCO3 If compensating
Respiratory Alkalosis PH PCO2 HCO3 If compensating
Metabolic Acidosis PH PCO2 If compensating HCO3
Metabolic Alkalosis PH PCO2 If compensating HCO3
Or normal if not compensating
Or normal if not compensating
Or normal if not compensating
Or normal if not compensating
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Four Primary Disorders

• PCO2 lt 35 respiratory alkalosis
• PCO2 gt 45 respiratory acidosis
• HCO3 lt 22 metabolic acidosis
• HCO3 gt 26 metabolic alkalosis
• Can have mixed pictures with compensation
• Can have up to 3 abnormality simultaneously (1
  respiratory 2 metabolic)
• The direction of the pH will tell you which is
  primary!

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Compensation
Primary Disturbance pH HCO3- PCO2 Compensation
Respiratory acidosis lt7.35 Compensatory increase Primary increase Acute 1-2 mEq/L increase in HCO3- for every 10 mm Hg increase in PCO2 Chronic 3-4 mEq/L increase in HCO3- for every 10 mm Hg increase in PCO2
Respiratory alkalosis gt7.45 Compensatory decrease Primary decrease Acute 1-2 mEq/L decrease in HCO3- for every 10 mm Hg decrease in PCO2 Chronic 4-5 mEq/L decrease in HCO3- for every 10 mm Hg decrease in PCO2
Metabolic acidosis lt7.35 Primary decrease Compensatory decrease 1.2 mm Hg decrease in PCO2 for every 1 mEq/L decrease in HCO3-
Metabolic alkalosis gt7.45 Primary increase Compensatory increase 0.6-0.75 mm Hg increase in PCO2 for every 1 mEq/L increase in HCO3- , PCO2 should not rise above 55 mm Hg in compensation
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Find the patients CO2 and Bicarb pattern on this
table. Only look at the row with the patients
pHThat will tell you the patients condition and
compensation
Condition pH Resp CO2 Bicarb Compensating?
Resp acidosis Low Hypoventilating High High Yes
Resp acidosis Low Hypoventilating High Norm No
Resp alkalosis High Hyperventilating Low Low Yes
Resp alkalosis High Hyperventilating Low Norm No
Metab acidosis Low Normal Low Low Yes
Metab acidosis Low Normal High Norm No
Metab Alkalosis High Normal High High Yes
Metab Alkalosis High Normal Low Norm No
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Acute Respiratory Alkalosis
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Acute Respiratory Acidosis
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Chronic Respiratory Acidosis with Metabolic
Compensation
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Metabolic Alkalosis with Respiratory Compensation
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(No Transcript)
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ABG 7.40 / 40 / 80 / 24

• pH
• PaCO2
• PaO2
• HCO3

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Example 1Blood gas 7.50 / 29 / 23

• Alkalemic
• pH 7.50
• PaCO2 29
• HCO3 23

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Acute respirstory alkalosis

• Low PCO2 is the primary (respiratory alkalosis)
• No metabolic compensation acute process
• Acute Respiratory Alkalosis
• Acute 1-2 mEq/L decrease in HCO3- for every 10
  mm Hg decrease in PCO2

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Example 2
A 65-year-old man with a history of emphysema
comes to the physician with a 3-hour history of
shortness of breath.
pH 7.18 PCO2 58 mm Hg PO2 61 mm Hg HCO3- 25
mEq/L
Acute respiratory acidosis
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Acute Respiratory acidosis

• Racid acute-History suggests hypoventilation,
  supported by increased PCO2 and lower than
  anticipated PO2.
• Acute 1-2 mEq/L increase in HCO3- for every 10
  mm Hg increase in PCO2
• Chronic 3-4 mEq/L increase in HCO3- for every 10
  mm Hg increase in PCO2
• Respiratory acidosis (acute) incomplete/no renal
  compensation.

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Example 3Blood gas 7.34 / 60 / 31

• Acidemic
• Elevated CO2 is primary (respiratory acidosis)
• Metabolic compensation has occurred chronic
  process
• Chronic Respiratory Acidosis with Metabolic
  Compensation
• true metabolic compensation takes 3 days (72hrs)

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Example 4Blood gas 7.50 / 48 / 36

• Alkalemic
• Elevated HCO3 is primary (metabolic alkalosis)
• Respiratory compensation has occurred acute
  /chronic ?
• Metabolic Alkalosis with Respiratory
  Compensation-incomplete
• Respiratory compensation takes only minutes

83
Example 5Blood gas 7.20 / 21 / 8

• Acidemic
• Low HCO3 Is primary (metabolic acidosis)
• Respiratory compensation is present
• Metabolic Acidosis with Respiratory Compensation

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Case Study 1

• A patient recovering from surgery in the
  post-anesthesia care unit is
• difficult to arouse two hours following surgery.
  The nurse in the PACU
• has been administering Morphine Sulfate
  intravenously to the patient for
• complaints of post-surgical pain. The patients
  respiratory rate is 7 per
• minute and demonstrates shallow breathing. The
  patient does not
• respond to any stimuli! The nurse assesses the
  ABCs (remember Airway,
• Breathing, Circulation!) and obtains ABGs STAT!
  The STAT results
• come back from the laboratory and show
• pH 7.15 (low)C02 68 mmHg (high) HC03 22
  mEq/L (normal)
• Compensated Respiratory Acidosis
• Uncompensated Metabolic Acidosis
• Compensated Metabolic Alkalosis
• 4. Uncompensated Respiratory Acidosis

85
Answer

• The answer is 4
• Uncompensated respiratory acidosis

86
Case Study 2

• An infant, three weeks old, is admitted to the
  Emergency Room. The mother reports that the
  infant has been irritable, difficult to
  breastfeed and has had diarrhea for the past 4
  days. The infants respiratory rate is elevated
  and the fontanels are sunken. The Emergency Room
  physician orders ABGs after assessing the ABCs.
• The results from the ABGs come back from the
  laboratory and show pH 7.37 (normal)C02
  29 mmHg (low)HC03 17 mEq/L (low)
• 1. Compensated Respiratory Alkalosis
• Uncompensated Metabolic Acidosis
• Compensated Metabolic Acidosis
• 4 Uncompensated Respiratory Acidosis

87
Answer

• Answer is 3
• Compensated Metabolic Acidosis

88
Case Study 3

• A patient, 5 days post-abdominal surgery, has a
  nasogastric tube. The nurse notes that the
  nasogastric tube (NGT) is draining a large amount
  (900 cc in 2 hours) of coffee ground secretions.
  The patient is not oriented to person, place, or
  time. The nurse contacts the attending physician
  and STAT ABGs are ordered. The results from the
  ABGs come back from the laboratory and show
• pH 7.52 (high)C02 35 mmHg (normal) HC03
  29 mEq/L (high)
• Compensated Respiratory Alkalosis
• Uncompensated Metabolic Acidosis
• Compensated Metabolic Acidosis
• Uncompensated Metabolic Alkalosis

89
Answer

• Answer is 4
• Uncompensated Metabolic Alkalosis

90
Case Study 4

• A patient is admitted to the hospital and is
  being prepared for a craniotomy (brain surgery).
  The patient is very anxious and scared of the
  impending surgery. He begins to hyperventilate
  and becomes very dizzy. The patient looses
  consciousness and the STAT ABGs reveal
• The results from the ABGs come back from the
  laboratory and show
• pH 7.57 (high)
• C02 26 mmHg (low)
• HC03 24 mEq/L (normal)
• Compensated Metabolic Acidosis
• Uncompensated Metabolic Acidosis
• Uncompensated Respiratory Alkalosis
• Uncompensated Respiratory Acidosis

91
Answer

• The answer is 3
• Uncompensated Respiratory Alkalosis

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Case Study 5

• A two-year-old is admitted to the hospital with a
  diagnosis of asthma and respiratory distress
  syndrome. The father of the infant reports to the
  nurse that he has observed slight tremors and
  behavioral changes in his child over the past
  three days. The attending physician orders
  routine ABGs following an assessment of the ABCs.
  The ABG results are
• pH 7.36 (normal)
• C02 69 mmHg (high)
• HC03 36 mEq/L (high)
• Compensated Respiratory Alkalosis
• Uncompensated Metabolic Acidosis
• Compensated Respiratory Acidosis
• Uncompensated Respiratory Alkalosis

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Answer

• Answer is 3
• Compensated Respiratory Acidosis

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Anion Gap (AG)

• The calculated difference between the positively
  charged (cations) and negatively charged (anions)
  electrolytes in the body
• AG Na - (Cl- HCO3 -)
• Normal AG 12 2 (10 14)

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Rule

• Calculate the anion gap. If the anion gap is ?
  20, there is a primary metabolic acidosis
  regardless of pH or serum bicarbonate
  concentration
• Principle The body does not generate a large
  anion gap to compensate for a primary disorder
  (anion gap must be primary)

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High anion metabolic acidosis

• Renal failure
• DKA
• ETHANOL OR METHANOL POISONING

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Rule

• Calculate the excess anion gap (total anion gap
  normal anion gap) and add this value to the
  measured bicarbonate concentration
• if the sum is gt than normal bicarbonate (gt 30)
  there is an underlying metabolic alkalosis
• if the sum is less than normal bicarbonate (lt
  23) there is an underlying non anion gap
  metabolic acidosis
• Excess AG Total AG Normal AG (12)
• Excess AG measured HCO3 gt 30 or lt 23?

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Mixed Acid-Base Disorders
99
Macid high AG
A 20-year-old man with a history of diabetes is
brought to the emergency department with a 3-day
history of feeling ill. He is non-adherent with
his insulin. Urine ketones are 2 and glucose is
4. pH 7.26 Na 136
mEq/L PO2 110 mm Hg K 4.8 mEq/L PCO2 19 mm
Hg Cl- 101 mEq/L HCO3- 8 mEq/L CO2, total 10
mEq/L Glucose 343 mg/dL Urea 49 mg/dL
Creatinine 1 mg/dL .
100
Example 1
pH 7.26 Na 136 mEq/L PO2 110 mm Hg K 4.8
mEq/L PCO2 19 mm Hg Cl- 101 mEq/L HCO3- 8
mEq/L Glucose 343 mg/dL Urea 49
mg/dL Creatinine 1 mg/dL 1.2 mm Hg decrease in
PCO2 for every 1 mEq/L decrease in HCO3-. HCO3-
decrease 24-8 16 mEq/L PCO2 decrease
predicted 1.2 x 16 19 mm Hg. subtract from 40
mm Hg (reference point) 21 mm Hg
101

• History suggests diabetic ketoacidosis.
• AG 136-101-827 mEq/L
• Metabolic acidosis with appropriate respiratory
  compensation

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A 43-year-old man comes to the physician with a
3-day history of diarrhea. He has decreased skin
turgor. pH 7.31 Na 134
mEq/L PO2 -- mm Hg K 2.9 mEq/L PCO2 31 mm
Hg Cl- 113 mEq/L HCO3- 16 mEq/L Urea 74
mgl/dL Creatinine 3.4 mmol/L History is
limited. Metabolic acidosis with respiratory
compensation.
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Description
pH 7.31 Na 134 mEq/L PO2 -- mm Hg K 2.9
mEq/L PCO2 31 mm Hg Cl- 113 mEq/L HCO3- 16
mEq/L Urea 74 mg/dL Creatinine 3.4 mg/dL AG
134-113-165 mEq/L 1.2 mm Hg decrease in PCO2 for
every 1 mEq/L decrease in HCO3-. HCO3- decrease
24-16 8 mEq/L PCO2 decrease predicted 1.2 x
8 10 mm Hg. subtract from 40 mm Hg (reference
point) 30 mm Hg
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Remember the Rules

• Look at the Ph
• Calculate the anion gap if AG ? 20 there is a
  primary metabolic acidosis (regardless of pH or
  HCO3)
• Calculate the excess anion gap, add it to HCO3
• Excess AG Total AG Normal AG (12)
• Excess AG HCO3 ?
• If sum gt 30 there is an underlying metabolic
  alkalosis
• If sum lt 23 there is an underlying nonanion gap
  metabolic acidosis

105
Example 1Blood gas 7.50 / 20 / 15 Na 140,
Cl 103

• Alkalemic
• Low CO2 is primary (respiratory alkalosis)
• Partial metabolic compensation for chronic
  condition?
• AG 22 (primary metabolic acidosis)
• Excess AG (AG 12) HCO3 25 (no other primary
  abnormalities)
• Respiratory Alkalosis and Metabolic Acidosis
• The patient ingested a large quantity of ASA and
  had both centrally mediated resp. alkalosis and
  anion gap met. Acidosis associated with
  salicylate overdose

106
Example 2Blood gas 7.40 / 40 / 24Na 145,
Cl 100

• pH normal
• AG 21 (primary metabolic acidosis)
• Excess AG (AG 12) HCO3 33 ( underlying
  metabolic alkalosis)
• Metabolic Acidosis and Metabolic Alkalosis
• This patient had chronic renal failure (met.
  acidosis) and began vomiting (met. alkalosis) as
  his uremia worsened. The acute alkalosis of
  vomiting offset the chronic acidosis of renal
  failure normal pH

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Example 3Blood gas 7.50 / 20 / 15Na 145, Cl
100

• Alkalemic
• Low CO2 is primary (respiratory alkalosis)
• AG 30 (primary metabolic acidosis)
• Excess AG (AG 12) HCO3 33 (underlying
  metabolic alkalosis)
• Respiratory alkalosis, Metabolic Acidosis and
  Metabolic Alkalosis
• This patient had a history of vomiting (met.
  alkalosis), poor oral intake (met. acidosis) and
  tachypnea secondary to bacterial pneumonia (resp.
  alkalosis)

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How Many Primary Abnormalities Can Exist in One
Patient?

• Three primary abnormalities is the max because a
  person cannot simultaneously hyper and
  hypoventilate
• One patient can have both a metabolic acidosis
  and a metabolic alkalosis usually one chronic
  and one acute

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Example 5Blood gas 7.15 / 15 / 5Na 140, Cl
110

• Acidemic
• Low HCO3- primary (metabolic acidosis)
• AG 25 (metabolic acidosis is anion gap type)
• Excess AG HCO3 18 (underlying nonanion gap
  metabolic acidosis)
• Anion Gap and Nonanion gap Metabolic Acidosis
• Diabetic ketoacidosis was present (anion gap
  met. acidosis). Patient also had a hyperchloremic
  nonanion gap met. acidosis secondary to failure
  to regenerate bicarbonate from ketoacids lost in
  the urine.

110

• 40 year male admitted to surgical unit due to
  infected diabetic foot, other co-morbidities
  hypertension and dyslipidemia were reasonabally
  controlled. He was febrile with temperature 38.5c
  and blood pressure 130/80. His laboratory
  investigations showed.
• WBC 12, Hb 9.6, Platelets 822 while renal
  profile showed. Serum Urea 8mmol/L ,Serum
  creatinine 76 umol/L, Serum Na 142 mmol/L serum K
  6.5 mmol/L. ABGs PH.7.4, Hco3 24, K 4.9 mmol/L.
• What is most likely diagnosis.
• A.Type IV Renal tubular acidosis
• B.Pseudohperkalemia
• C.Type II renal tubular acidosis
• D.Type I renal tubular acidosis
• E.Addisons disease.

111

• AnswerB
• Type IV renal tubular acidosis is common in
  diabetic patients with acidosis and hyperkalemia,
• While others two types I II have hypokalemia
  and acidosis.Patient did not have acidosis or
  features of Addisons disease.Postassium in ABGs
  was within normal limits which suggested patient
  had pseudohyperkalemia secondary to
  thrombocytosis.

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• A 20 years female known to have type 1 diabetes
  mellitus,she missed her insulin dose presented to
  emergency room complaining of recurrent
  vomiting,on examination she is tachypnic with
  repiratory rate of 22, blood pressure 100/60mmHg.
  Pulse 95/min and afebrile. Other systemic review
  unremarkable.
• Laboratory investigations showed Urine ketone
  3, Glucose 2. ABGs.PH 7.2, HCO3 26, PCO2 30.
  Renal profile urea 5mmol/L, creatinin 65 umol/L
  Na140mmol/L, K 3.5mmol/L Cl.95, Random blood
  sugar 20 mmol/L.
• What is acid base abnormality in this patient.
• A. Metabolic acidosis
• B. Respirtaory acidosis
• C. Mixed metabolic and respiratory acidosis
• D. High anion gap metabolic acidosis,metablolic
  and respiratory alkalosis
• E. Normal anion gap metabolic acidosis, metabolic
  and respiratory alkalosis.

113

• Answer D. This young female developed High anion
  gap metabolic acidosis secondary to ketones in
  the blood, Repiratory alkalosis due to tachypnia
  secondary to anxiety and metabolic alkalosis due
  to recurrent vomiting. Her Calculated Anion gap
  is 140-(9526)19

114

• A 16 years female was referred for further
  investigations for short stature and stone
  disease. She was behind her milestones.Laboratory
  investigations showed.MSU, PH 7 otherwise bland
  sediment.Renal profile.Na 135mmol/L K 2.9 mmol/L
  Chloride 115 mmolL, Serum urea and Creatinine
  normal.Serum HCO3 10.what is the diagnosis.
• A.Type 1 renal tubular acidosis
• B.Type 2 renal tubular acidosis
• C.Type 4 renal tubulare acidosis
• D.High anion gap metabolic acidosis
• E.Metabolic alkalosis.

115

• Answer A. Anion gap for this patient is 10 while
  the patient having low bicarbonate suggesting
  metabolic acidosis.It is normal anion gap
  metabolic acidosis.As there is history of
  nephrolithiasis and patient is hypokalemia which
  favours the diagnosis of type 1 renal tubular
  acidosis.Urinary PH is 7 which is high and these
  patient can not acidify urine and maintain
  urinary PH always above 5.5 due to defect in the
  secretion of H ion in the distal convoluted
  tubules.

116

• 60 years old male was treated ifosfamide based
  chemotherapy for soft tissue sarcoma.He was found
  persistant hypokalemia with low serum bicarbonate
  level on laboratory investigations.His current
  laboratory investigations are as following.Renal
  profile.Serum Urea 7 mmol/L, Serum creatinine 95
  umol/L, Serum Na 140mmol/L and Serum K 3 mmol/L,
  Serum chloride 113mmol/L.ABGs.PH.7.4,HCO3,18 and
  PCO2.47.What kind of acid base disorder happened.
• A..Metabolic alkalosis
• B..Type 1 renal tubular acidosis
• C..Type 2 renal tubular acidosis
• D..Type 4 renal tubular acidosis
• E..Respiratory acidosis.

117

• Answer C. Ifosfamide chemotherapy is effective
  in treating soft tissue cancer and it causes
  proximal renal tubular defect leading to proximal
  renal tubular acidosis with hyperchloremic,hypokal
  emic,normal anion gap metabolic acidosis.Here
  anion gap is 9.

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