Acid-Base Balance and Arterial Blood Gases

Sasha Rarang, MSN, CCM, RN
 Maintain a balance between acids and bases to achieve
 Homeostasis or State of equilibrium
State of equilibrium in body
Naturally maintained by adaptive responses
Body fluids and electrolytes are maintained within narrow
 Health problems lead to imbalance
 Diabetes mellitus
 Vomiting and diarrhea
 Respiratory conditions
 Chemotherapy- N/V
Water Content of the Body
 60% of body weight in adult
 45% to 55% in older adults
 70% to 80% in infants
 Varies with gender, body mass, and age
Changes in Water Content with Age
 Intracellular fluid (ICF)
 Extracellular fluid (ECF)
 Intravascular (plasma)
 Interstitial
 Transcellular
Fluid Compartments of the Body
Intracellular Fluid (ICF)
 Located within cells
 42% of body weight
Extracellular Fluid (ECF)
 One third of body weight
 Between cells (interstitial fluid), lymph,
plasma, and transcellular fluid
Transcellular Fluid
 Part of ECF
 Small but important
 Approximately 1 L
Includes fluid in:
 Cerebrospinal fluid
 Gastrointestinal tract
 Pleural spaces
 Synovial spaces
 Peritoneal fluid spaces
 Measure of H+ ion concentration
 Blood is slightly alkaline at pH 7.35 to 7.45.
 <7.35 is acidosis.
 >7.45 is alkalosis.
Range of pH
Fig. 17-16. The normal range of plasma pH is 7.35 to 7.45. A normal pH is maintained by a ratio of 1 part
carbonic acid to 20 parts bicarbonate.
Regulators of Acid/Base
 Metabolic processes produce acids that must be
neutralized and excreted.
 Regulatory mechanisms
 Buffers
 Respiratory system
 Renal system
Regulators of Acid/Base
 Buffers: Act chemically to neutralize acids or change
strong acids to weak acids
 Primary regulators
 React immediately
 Cannot maintain pH without adequate respiratory and
renal function
 The buffers in the body include
carbonic acid–bicarbonate
monohydrogen- dihydrogen phosphate
intracellular and plasma protein
 Substances whose molecules dissociate into ions
(charged particles) when placed into water
 Cat ions: positively charged
 An ions: negatively charged
International standard is millimoles per liter (mmol/L)
U.S. uses milliequivalent (mEq)
Electrolyte Composition
 Prevalent cation is K+ (Potasium)
 Prevalent anion is PO4- (Phosphate)
 Prevalent cation is Na+ (Sodium)
 Prevalent anion is Cl- ( Chloride)
Mechanisms Controlling Fluid and Electrolyte
 Diffusion - Movement of molecules from high to low concentration .
Occurs in liquids, solids, and gases
Membrane separating two areas must be permeable to
diffusing substance. Requires no energy
Mechanisms Controlling Fluid and
Electrolyte Movement
 Facilitated diffusion
Movement of molecules from high to low concentration
without energy
Uses specific carrier molecules to accelerate diffusion
 Active Transport
Process in which molecules move against concentration
Example: sodium–potassium pump
External energy required
Sodium–Potassium Pump
Mechanisms Controlling Fluid and Electrolyte
 Osmosis
Movement of water between two compartments by a membrane
permeable to water but not to solute
Moves from low solute to high solute concentration
Requires no energy
Mechanisms Controlling Fluid and Electrolyte
 Osmotic Pressure
Amount of pressure required to stop osmotic flow of
water. Determined by concentration of solutes in
 Hydrostatic Pressure
Force within a fluid compartment
Major force that pushes water out of vascular system
at capillary level
 Oncotic Pressure
Osmotic pressure exerted by colloids in solution (colloidal
osmotic pressure)
Protein is major colloid
Fluid Movement in Capillaries
Amount and direction of fluid movement is determined
 Capillary hydrostatic pressure
 Plasma oncotic pressure
 Interstitial hydrostatic pressure
 Interstitial oncotic pressure
Fluid Exchange Between Capillary
and Tissue
Fluid Shifts
Plasma to interstitial fluid shift results in :
 Edema
 Elevation of hydrostatic pressure
 Decrease in plasma oncotic pressure
 Elevation of interstitial oncotic pressure
Interstitial fluid to plasma results in:
 Fluid drawn into plasma space with increase in plasma
osmotic or oncotic pressure
 Compression stockings decrease peripheral edema
Fluid Movement between
 Water deficit (increased ECF)
Associated with symptoms that result from cell
shrinkage as water is pulled into vascular system.
Water excess (decreased ECF)
Develops from gain or retention of excess water.
Fluid Spacing
First spacing - Normal distribution of fluid in ICF and ECF
Second spacing - Abnormal accumulation of interstitial
fluid (edema)
Third spacing
Fluid accumulation in part of body where it is not easily
exchanged with ECF.
Regulation of Water Balance
 Hypothalamic Regulation - Osmoreceptors in
hypothalamus sense fluid deficit or increase.
Stimulates thirst and antidiuretic hormone (ADH)
release. Result in increased free water and decreased
plasma osmolarity.
 Pituitary Regulation - Under control of hypothalamus,
posterior pituitary releases ADH. Stress, nausea,
nicotine, and morphine also stimulate ADH release.
 Adrenal Cortical Regulation - Releases hormones to
regulate water and electrolytes –
Glucocorticoids - Cortisol
Mineralocorticoids - Aldosterone
Factors Affecting
Aldosterone Secretion
Fluid Regulations
 Primary organs for regulating fluid and electrolyte
 Adjusting urine volume
 Selective reabsorption of water and electrolytes
 Renal tubules are sites of action of ADH and aldosterone
Cardiac Regulation
 Natriuretic peptides are antagonists to the RAAS
 Produced by cardiomyocytes in response to increased atrial
 Suppress secretion of aldosterone, renin, and ADH to
decrease blood volume and pressure
Fluid Regulations
Gastrointestinal Regulation
 Oral intake accounts for most water
 Small amounts of water are eliminated by
gastrointestinal tract in feces. Diarrhea and vomiting
can lead to significant fluid and electrolyte loss
Insensible Water Loss
 Invisible vaporization from lungs and skin to regulate
body temperature
 Approximately 600 to 900 ml/day
is lost
 No electrolytes are lost
Gerontologic Considerations
 Structural changes in kidneys decrease ability to
conserve water
Hormonal changes lead to decrease in ADH and ANP
Loss of subcutaneous tissue leads to increased loss of
Reduced thirst mechanism results in decreased fluid
Nurse must assess for these changes and implement
treatment accordingly
Fluid and Electrolyte Imbalances
 Common in most patients with illness
 Directly caused by illness or disease (burns or heart
 Result of therapeutic measures
(IV fluid replacement or diuretics)
Regulators of Acid/Base
 Respiratory system: Eliminates CO2
 Respiratory center in medulla
controls breathing.
 Responds within minutes/hours to changes in acid/base.
 Increased respirations lead to
increased CO2 elimination
decreased CO2 in blood.
Regulators of Acid/Base
• When released into circulation, CO2 enters RBCs and combines
with H2O to form H2CO3.
• This carbonic acid dissociates into hydrogen ions and
• The free hydrogen is buffered by hemoglobin molecules, and the
bicarbonate diffuses into the plasma.
• In the pulmonary capillaries, this process is reversed, and CO2 is
formed and excreted by the lungs.
• As a compensatory mechanism, the respiratory system acts on the
CO2 + H2O side of the reaction by altering the rate and depth of
breathing to “blow off” (through hyperventilation) or “retain”
(through hypoventilation) CO2.
• If a respiratory problem is the cause of an acid-base imbalance
(e.g., respiratory failure), the respiratory system loses its ability to
correct a pH alteration.
Regulators of Acid/Base
 Renal system: Eliminates H+ and reabsorbs HCO3 Reabsorption and secretion of electrolytes
(e.g., Na+, Cl-)
 Responds within hours to days.
 Hyperkalemia results from decreased renal excretion.
 Na+ may also be retained resulting to water retention,
edema, hypertension, and heart failure.
Regulators of Acid/Base
• The three mechanisms of acid elimination are
• secretion of small amounts of free hydrogen into the renal
• combination of H+ with ammonia (NH3) to form ammonium
(NH4+), and
• excretion of weak acids.
• The body depends on the kidneys to excrete a portion of the
acid produced by cellular metabolism.
• Thus the kidneys normally excrete acidic urine (average pH
equals 6).
• As a compensatory mechanism, the pH of the urine can
decrease to 4 and increase to 8.
Alterations in Acid-Base Balance
 Imbalances occur when compensatory mechanisms
 Classification of imbalances
 Respiratory: Affect carbonic acid concentration
 Metabolic: Affect bicarbonate
Respiratory Acidosis
 Carbonic acid excess caused by
 Hypoventilation
 Respiratory failure
 Compensation
 Kidneys conserve HCO3- and secrete H+ into urine.
Respiratory Acidosis
• Hypoventilation results in a buildup of CO2
• carbonic acid accumulates in the blood
• Carbonic acid dissociates, liberating H+, and a decrease
in pH occurs.
• If CO2 is not eliminated from the blood, acidosis results
from the accumulation of carbonic acid.
• In acute respiratory acidosis, the renal compensatory
mechanisms begin to operate within 24 hours.
Respiratory Alkalosis
 Carbonic acid deficit caused by
 Hyperventilation
 Hypoxemia from acute pulmonary disorders
Metabolic Acidosis
 Base bicarbonate deficit caused by
 Ketoacidosis
 Lactic acid accumulation (shock)
 Severe diarrhea
 Kidney disease
 Metabolic acidosis (base bicarbonate deficit) occurs when
an acid other than carbonic acid accumulates in the body,
or when bicarbonate is lost from body fluids.
 Compensatory mechanisms
 Increased CO2 excretion by lungs
 Kussmaul respirations (deep and rapid)
 Kidneys excrete acid
Metabolic Alkalosis
 Base bicarbonate excess caused by
 Prolonged vomiting or gastric suction
 Gain of HCO3-
 Compensatory mechanisms
 Decreased respiratory rate to increase plasma CO2
 Renal excretion of HCO3-
Blood Gas Values
 Arterial blood gas (ABG) values provide information
 Acid-base status
 Underlying cause of imbalance
 Body’s ability to regulate pH
 Overall oxygen status
Interpretation of ABGs
 Diagnosis in six steps:
 Evaluate pH.
 Analyze PaCO2.
 Analyze HCO3-.
 Determine if CO2 or HCO3- matches the alteration.
 Decide if the body is attempting to compensate.
Normal Blood Gas Values
Table 17-15. Normal Arterial Blood Gas Values *.
Sample ABG Interpretation
Table 17-16. Arterial Blood Gas (ABG) Analysis.
Acid-Base Mnemonic—ROME
 Respiratory
 Opposite
 Alkalosis↑ pH ↓ PaCO2
 Acidosis ↓ pH ↑ PaCO2
 Metabolic
 Equal
 Acidosis ↓ pH ↓ HCO3
 Alkalosis↑ pH ↑ HCO3
Interpretation of ABGs
pH 7.18
PaCO2 38 mm Hg
PaO2 70 mm Hg
HCO3- 15 mEq/L
What is this?
 Metabolic acidosis
Interpretation of ABGs
 pH 7.58
 PaCO2 35 mm Hg
 PaO2 75 mm Hg
 HCO3- 50 mEq/L
 What is this?
 Metabolic alkalosis
A patient with an acid-base imbalance has an altered
potassium level. The nurse recognizes that the potassium
level is altered because:
1. Potassium is returned to extracellular fluid when
metabolic acidosis is corrected.
2. Hyperkalemia causes an alkalosis that results in
potassium being shifted into the cells.
3. Acidosis causes hydrogen ions in the blood to be
exchanged for potassium from the cells.
4. In alkalosis, potassium is shifted into extracellular fluid
to bind excessive bicarbonate.
 Answer: 3
 Rationale: Changes in pH (hydrogen ion concentration)
will affect potassium balance.
 In acidosis,
 hydrogen ions accumulate in the intracellular fluid (ICF),
 and potassium shifts out of the cell to the extracellular fluid to
maintain a balance of cations across the cell membrane.
 In alkalosis,
 ICF levels of hydrogen diminish,
 and potassium shifts into the cell.
If a deficit of H+ occurs in the extracellular fluid, potassium will shift
into the cell.
Acidosis is associated with hyperkalemia
Alkalosis is associated with hypokalemia.
Case Study 1: Jeri
 Jeri’s been on a 3-day party binge.
 Friends are unable to awaken her.
 Assessment reveals level of consciousness difficult to
 Respiratory rate 8
 Shallow breathing pattern
 Diminished breath sounds
What ABGs do you expect?
What is your treatment?
Case Study 1: Jeri
 What ABGs do you expect?
 Respiratory acidosis reflected by pH <7.35 and PCO2 >45 mm
Hg. The HCO3 will be normal (20-30 mEq/L) if her respiratory
depression has lasted less than 24 hours; if longer than 24 hours,
the HCO3 may be elevated as the result of compensation. The
PaO2 may be <80 mm Hg because of respiratory depression
leading to hypoxemia.
 2. What is your treatment?
 Determine the cause of the respiratory depression. If induced by
opioids or benzodiazepines, treat with appropriate antagonists.
If induced by alcohol or other CNS depressants, breathing must
be stimulated until the effects of drugs have worn off.
Mechanical ventilation may be necessary to increase respiratory
rate and depth, increasing oxygenation and promoting excretion
of carbon dioxide.
Case Study 2: Mayna
 Presented to the ED after a sexual assault
 Examination reveals hysteria and emotional distress.
 Respiratory rate 38
 Lungs clear
O2 sat 96%What ABGs do you expect?
What is your treatment?
Copyright © 2011, 2007 by Mosby, Inc., an affiliate
of Elsevier Inc.
Case Study 2: Mayna
 1. What ABGs do you expect?
 Respiratory alkalosis indicated by pH >7.45 and PCO2
<35 mm Hg. The HCO3 will be normal (20-30 mEq/L)
because compensation will not occur in this acute
 2. What is your treatment?
 Relieve her anxiety and coax her to take slow breaths.
Carbon dioxide may be administered by mask, or she
may be asked to breathe into a paper bag placed over
her nose and mouth.
Case Study 3: Allen
 17 years old
 History of
 Feeling bad
 Fatigue
 Constant thirst
 Frequent urination
 Blood sugar is 484 mg/dL.
 Respirations are 28 and deep.
 Breath has a fruity odor.
 Lungs are clear.
What ABGs do you expect?
What is your treatment?
Case Study 3: Allen
 What ABGs do you expect?
 A diabetic ketoacidosis is a metabolic acidosis indicated by
a pH <7.35 and a HCO3 <20 mEq/L. The PCO2 will be
within the normal range if the acidosis is uncompensated,
but will be <35 mm Hg if compensation has occurred. The
PaO2 will not be affected.
 2. What is your treatment?
 Administration of insulin to promote normal glucose
metabolism and administration of fluids and electrolytes
to replace those lost because of the hyperglycemia.
Fluid volume deficit
 Can occur with
 Abnormal loss of body fluids
Diarrhea, hemorrhage, polyuria
 Inadequate fluid intake
 Shift of fluid from plasma into interstitial space
• Treatment
 Correct the underlining cause
 Replace the fluid and electrolyte (LR or NS isotonic solutions)
Fluid volume excess
 May result from
 excessive intake of fluid
 Abnormal retention of fluids(heart failure, renal failure)
 Shift of fluid from interstitial fluid into plasma fluid
o Collaborative care
ID primary cause
Diuretics and fluid restriction
Restriction of Na intake
Fluid excess may result to ascites or pleural effusion, and
paracentesisi or thoracentsis may be necessary.
Commonly prescribed crystalloid solutions
 Dextrose in water
 5% isotonic
 10% hypertonic
 Saline
 0.45% hypotonic
 0.9% isotonic
 3.0% hypertonic
 Dextrose in Saline
 5% in 0.225% isotonic
 5% in 0.45% hypertonic
 5% in 0.9% hypertonic
 Multiple Electrolyte Solutions
 Ringer’s solution- isotonic, includes CL, Na, K, Ca
 Lactated Ringer’s solution- isotonic-Na, K, Cl, Ca, and
lactate(the precursor of bicarbonate)
 Catheters placed in large blood vessels of people who
require frequent access to the vascular system
 Subclavian vein, jugular vein
 Three different methods
 Centrally inserted catheter(by MD)
 Peripherally inserted central catheter
 Implanted ports( by MD)
 Permit frequent, continuous, rapid, or intermittent
administration or monitoring
 Indicated for patients with limited peripheral vascular
access or need for long-term vascular access
Centrally Inserted Catheter
 Inserted into a vein in the neck, chest, or groin with tip
resting in the distal end of the superior vena cava
 Single, double, triple, or quad lumen
 Nontunneled or tunneled
Central .Venous Catheter
 Central venous catheters inserted into a vein in the
 Single or multilumen, nontunneled
 For patients who need vascular access for 1 week to 6
 Complications include catheter occlusion and
Copyright © 2011, 2007, 2004, 2000, 1996, 1992,
1987, 1983 by Mosby, Inc., an affiliate of Elsevier
Implanted Infusion Ports
 Central venous catheter connected to an
implanted, single or double subcutaneous injection
 Port is metal sheath with self-sealing silicone
Implanted Infusion Port
Implanted Infusion Port
 Port accessed with special Huber-point needle
 Advantages
 Good for long-term therapy
 Low risk of infection
 Cosmetic discretion
 Care requires regular flushing.
 Complication: (table 17-21 page 330)
 Cath occlusion(kinked, precipitate build up)
 Embolism( dislodgment of thrombus, air entry, cath
 Cath related infection
 Cath Migration
Nursing Management
Inspect catheter and insertion site.
Assess pain.
Change dressing and clean according to institution policies.
Change injection caps.
Flushing is important.
• Catheter and insertion site assessments include inspection of the
site for redness, edema, warmth, drainage, and tenderness or pain.
Observation of the catheter for misplacement or slippage is
• Transparent dressing or gauze may be used.
• Discuss cleaning techniques with chlorhexidine-based
preparations, povidone-iodine, and isopropyl alcohol
• Teach the patient to turn the head to the opposite side of the
CVAD insertion site during cap change.
• Flushing: Use a normal saline solution in a syringe that has a
barrel capacity of 10 mL or more to avoid excess pressure on the
catheter. If resistance is felt, force should not be applied.
Removing CVADs
 Should be done according to policy and procedures.
 Gently withdraw.
 Apply pressure.
 Ensure that catheter tip is intact.

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