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Acid-Base Balance Interactive Tutorial
Emily Phillips
MSN 621
Spring 2009E-mail:
All images imported from
Microsoft Clipart & Yahoo Image gallery
How to navigate this tutorial: To advance to the next slide click on the box To return to the previous slide click on
the box To return to the Main Menu: click the box Hover over underlined text for a
definition/explanation To return to the last slide viewed click on
the button Click the for additional information
Objectives: Define acid base balance/imbalance Explain the pathophysiology of organs
involved in acid base balance/imbalance Identify normal/abnormal and
compensated/uncompensated lab values
Explain symptoms related to acid base imbalances and compensated vs. uncompensated
Appropriate interventions and expected outcomes
Main Menu:
Acid-Base Pretest The Buffer Systems
ABG Interpretation& Case Studies
Acid-Base Review test
Diagnostic Lab Values
Metabolic Distubances
Respiratory Disturbances Acid-Base Compensation
Acid-Base Pretest: What is the normal
range for arterial blood pH?
7.38 – 7.46
7.40 – 7.52
7.35 – 7.45
Acid-Base Pretest:
What 2 extracellular substances work together to regulate pH?
Sodium bicarbonate& carbonic acid
Carbonic acid& bicarbonate
Acetic acid & carbonic acid
Acid-Base Pretest: Characterize an acid & a base based on the
choices below.
Acids release hydrogen (H+) ions& bases accept H+ ions.
Acids accept H+ ions & bases release H+ ions
Both acids & bases can release& accept H+ ions
Acid-Base Pretest: Buffering is a normal body mechanism
that occurs rapidly in response to acid-base disturbances in order to prevent changes in what?
HCO3-
H2CO3
H+
Acid-Base Pretest: What are the two systems in the body that
work to regulate pH in acid-base balance & which one works fastest?
The Respiratory & Renal systemsRenal
The Respiratory & Renal systemsRespiratory
The Renal & GI systemsRenal
Acid-Base Balance:
Homeostasis of bodily fluids at a normal arterial blood pH
pH is regulated by extracellular carbonic acid (H2CO3) and bicarbonate (HCO3
-)
Acids are molecules that release hydrogen ions (H+)
A base is a molecule that accepts or combines with H+ ions
Acids and Bases can be strong or weak:
A strong acid or base is one that dissociates completely in a solution
- HCl, NaOH, and H2SO4
A weak acid or base is one that dissociates partially in a solution
-H2CO3, C3H6O3, and CH2O
The Body and pH:
Homeostasis of pH is controlled through extracellular & intracellular buffering systems
Respiratory: eliminate CO2
Renal: conserve HCO3- and eliminate H+
ions Electrolytes: composition of extracellular
(ECF) & intracellular fluids (ICF)
- ECF is maintained at 7.40
Protein Buffer system
HCO3-
Buffersystem
K+ - H+
Exchange
Quick Review: Click the BoxesA donator of H+ ions An acceptor of H+
w/ pH <7.0 ions w/ pH >7.0
Regulated by EC Controlled by EC
H2CO3 & HCO3- & IC buffer systems
Eliminates CO2 Conserves HCO3-
Eliminates H+ ions
An Acid is: A Base is:
pH is:
Respiratory System:
pH is:
Renal System:
Respiratory Control Mechanisms:
Works within minutes to control pH; maximal in 12-24 hours
Only about 50-75% effective in returning pH to normal
Excess CO2 & H+ in the blood act directly on respiratory centers in the brain
CO2 readily crosses blood-brain barrier reacting w/ H2O to form H2CO3
H2CO3 splits into H+ & HCO3- & the H+
stimulates an increase or decrease in respirations
Renal Control Mechanisms: Don’t work as fast as the respiratory
system; function for days to restore pH to, or close to, normal
Regulate pH through excreting acidic or alkaline urine; excreting excess H+ & regenerating or reabsorbing HCO3
-
Excreting acidic urine decreases acid in the EC fluid & excreting alkaline urine removes baseH+ elimination
& HCO3-conservation
Mechanisms of Acid-Base Balance:
The ratio of HCO3- base to the volatile H2CO3
determines pH Concentrations of volatile H2CO3 are regulated
by changing the rate & depth of respiration Plasma concentration of HCO3
- is regulated by the kidneys via 2 processes: reabsorption of filtered HCO3
- & generation of new HCO3-, or
elimination of H+ buffered by tubular systems to maintain a luminal pH of at least 4.5
Phosphate Buffer system
AmmoniaBuffer system
Acid-Base Balance Review test:
The kidneys regulate pH by excreting HCO3
- and retaining or regenerating H+
TRUE
FALSE
Acid-Base Review test:
H2CO3 splits into HCO3- & H+ & it is the
H+ that stimulates either an increase or decrease in the rate & depth of respirations.
TRUE
FALSE
Acid-Base Review test: Plasma concentration of HCO3
- is controlled by the kidneys through reabsorption/regeneration of HCO3
-, or elimination of buffered H+ via the tubular systems.
TRUE
FALSE
Acid-Base Review test:
The ratio of H+ to HCO3- determines
pH.
TRUE
FALSE
Acid-Base Review test:
Secreted H+ couples with filtered HCO3-
& CO2 & H2O result.
TRUE
FALSE
Metabolic Disturbances: Alkalosis: elevated HCO3
- (>26 mEq/L) Causes include: Cl- depletion (vomiting,
prolonged nasogastric suctioning), Cushing’s syndrome, K+ deficiency, massive blood transfusions, ingestion of antacids, etc.
Acidosis: decreased HCO3- (<22 mEq/L)
Causes include: DKA, shock, sepsis, renal failure, diarrhea, salicylates (aspirin), etc.
Compensation is respiratory-related
Metabolic Alkalosis: Caused by an increase in pH (>7.45)
related to an excess in plasma HCO3-
Caused by a loss of H+ ions, net gain in HCO3
- , or loss of Cl- ions in excess of HCO3-
Most HCO3- comes from CO2 produced
during metabolic processes, reabsorption of filtered HCO3
-, or generation of new HCO3
- by the kidneys Proximal tubule reabsorbs 99.9% of
filtered HCO3-; excess is excreted in urine
Metabolic Alkalosis Manifestations: Signs & symptoms (s/sx) of volume
depletion or hypokalemia Compensatory hypoventilation,
hypoxemia & respiratory acidosis Neurological s/sx may include mental
confusion, hyperactive reflexes, tetany and carpopedal spasm
Severe alkalosis (>7.55) causes respiratory failure, dysrhthmias, seizures & coma
Treatment of Metabolic Alkalosis:
Correct the cause of the imbalance May include KCl supplementation for K+/Cl-
deficits Fluid replacement with 0.9 normal saline
or 0.45 normal saline for s/sx of volume depletion
Intubation & mechanical ventilation may be required in the presence of respiratory failure
Metabolic Acidosis: Primary deficit in base HCO3
- (<22 mEq/L) and pH (<7.35)
Caused by 1 of 4 mechanisms Increase in nonvolatile metabolic acids,
decreased acid secretion by kidneys, excessive loss of HCO3
-, or an increase in Cl-
Metabolic acids increase w/ an accumulation of lactic acid, overproduction of ketoacids, or drug/chemical anion ingestion
Metabolic Acidosis Manifestations:
Hyperventialtion (to reduce CO2 levels), & dyspnea
Complaints of weakness, fatigue, general malaise, or a dull headache
Pt’s may also have anorexia, N/V, & abdominal pain
If the acidosis progresses, stupor, coma & LOC may decline
Skin is often warm & flush related to sympathetic stimulation
Treatment of Metabolic Acidosis:
Treat the condition that first caused the imbalance
NaHCO3 infusion for HCO3- <22mEq/L
Restoration of fluids and treatment of electrolyte imbalances
Administration of supplemental O2 or mechanical ventilation should the respiratory system begin to fail
Quick Metabolic Review:
Metabolic disturbances indicate an excess/deficit in HCO3
- (<22mEq/L or >26mEq/L
Reabsorption of filtered HCO3- &
generation of new HCO3- occurs in the
kidneys Respiratory system is the compensatory
mechanism ALWAYS treat the primary disturbance
Respiratory Disturbances: Alkalosis: low PaCO2 (<35 mmHg)
Caused by HYPERventilation of any etiology (hypoxemia, anxiety, PE, pulmonary edema, pregnancy, excessive ventilation w/ mechanical ventilator, etc.)
Acidosis: elevated PaCO2 (>45 mmHg) Caused by HYPOventilation of any etiology
(sleep apnea, oversedation, head trauma, drug overdose, pneumothorax, etc.)
Compensation is metabolic-related
Respiratory Alkalosis:
Characterized by an initial decrease in plasma PaCO2 (<35 mmHg) or hypocapnia
Produces elevation of pH (>7.45) w/ a subsequent decrease in HCO3
- (<22 mEq/L)
Caused by hyperventilation or RR in excess of what is necessary to maintain normal PaCO2 levels
Respiratory Alkalosis Manifestations:
S/sx are associated w/ hyperexcitiability of the nervous system & decreases in cerebral blood flow
Increases protein binding of EC Ca+, reducing ionized Ca+ levels causing neuromuscular excitability
Lightheadedness, dizziness, tingling, numbness of fingers & toes, dyspnea, air hunger, palpitations & panic may result
Treatment of Respiratory Alkalosis:
Always treat the underlying/initial cause Supplemental O2 or mechanical
ventilation may be required Pt’s may require reassurance,
rebreathing into a paper bag (for hyperventilation) during symptomatic attacks, & attention/treatment of psychological stresses.
Respiratory Acidosis:
Occurs w/ impairment in alveolar ventilation causing increased PaCO2 (>45 mmHg), or hypercapnia, along w/ decreased pH (<7.35)
Associated w/ rapid rise in arterial PaCO2 w/ minimal increase in HCO3
- & large decreases in pH
Causes include decreased respiratory drive, lung disease, or disorders of CW/respiratory muscles
Respiratory Acidosis Manifestations: Elevated CO2 levels cause cerebral
vasodilation resulting in HA, blurred vision, irritability, muscle twitching & psychological disturbances
If acidosis is prolonged & severe, increased CSF pressure & papilledema may result
Impaired LOC, lethargy/coma, paralysis of extremities, warm/flushed skin, weakness & tachycardia may also result
Treatment of Respiratory Acidosis:
Treatment is directed toward improving ventilation; mechanical ventilation may be necessary
Treat the underlying cause Drug OD, lung disease, chest
trauma/injury, weakness of respiratory muscles, airway obstruction, etc.
Eliminate excess CO2
Quick Respiratory Review: Caused by either low or elevated PaCO2
levels (<35 or >45mmHg) Watch for HYPOventilation or
HYPERventilation; mechanical ventilation may be required
Kidneys will compensate by conserving HCO3
- & H+
REMEMBER to treat the primary disturbance/underlying cause of the imbalance
Compensatory Mechanisms:
Adjust the pH toward a more normal level w/ out correcting the underlying cause
Respiratory compensation by increasing/decreasing ventilation is rapid, but the stimulus is lost as pH returns toward normal
Kidney compensation by conservation of HCO3
- & H+ is more efficient, but takes longer to recruit
Metabolic Compensation: Results in pulmonary compensation
beginning rapidly but taking time to become maximal
Compensation for Metabolic Alkalosis: HYPOventilation (limited by degree of rise
in PaCO2)
Compensation for Metabolic Acidosis: HYPERventilation to decrease PaCO2
Begins in 1-2hrs, maximal in 12-24 hrs
Respiratory Compensation:
Results in renal compensation which takes days to become maximal
Compensation for Respiratory Alkalosis: Kidneys excrete HCO3
-
Compensation for Respiratory Acidosis: Kidneys excrete more acid Kidneys increase HCO3
- reabsorption
DIAGNOSTIC LAB VALUES & INTERPRETATION
Normal Arterial Blood Gas (ABG)Lab Values:
Arterial pH: 7.35 – 7.45 HCO3
-: 22 – 26 mEq/L
PaCO2: 35 – 45 mmHg
TCO2: 23 – 27 mmol/L
PaO2: 80 – 100 mmHg
SaO2: 95% or greater (pulse ox)
Base Excess: -2 to +2 Anion Gap: 7 – 14
Acid-Base pH and HCO3-
Arterial pH of ECF is 7.40 Acidemia: blood pH < 7.35 (increase in H+) Alkalemia: blood pH >7.45 (decrease in H+)
If HCO3- levels are the primary disturbance,
the problem is metabolic Acidosis: loss of nonvolatile acid & gain of
HCO3-
Alkalosis: excess H+ (kidneys unable to excrete) & HCO3
- loss exceeds capacity of kidneys to regenerate
Acid-Base PCO2, TCO2 & PO2
If PCO2 is the primary disturbance, the problem is respiratory; it’s a reflection of alveolar ventilation (lungs) PCO2 increase: hypoventilation present PCO2 decrease: hyperventilation present
TCO2 refers to total CO2 content in the blood, including CO2 present in HCO3
-
>70% of CO2 in the blood is in the form of HCO3
- PO2 also important in assessing respiratory
function
Base Excess or Deficit:
Measures the level of all buffering systems in the body – hemoglobin, protein, phosphate & HCO3
-
The amount of fixed acid or base that must be added to a blood sample to reach a pH of 7.40
It’s a measurement of HCO3- excess or
deficit
Anion Gap: The difference between plasma
concentration of Na+ & the sum of measured anions (Cl- & HCO3
-)
Representative of the concentration of unmeasured anions (phosphates, sulfates, organic acids & proteins)
Anion gap of urine can also be measured via the cations Na+ & K+, & the anion Cl- to give an estimate of NH4
+
excretion
Anion Gap The anion gap is increased in conditions
such as lactic acidosis, and DKA that result from elevated levels of metabolic acids (metabolic acidosis) A low anion gap occurs in conditions that
cause a fall in unmeasured anions (primarily albumin) OR a rise in unmeasured cations
A rise in unmeasured cations is seen in hyperkalemia, hypercalcemia, hyper-magnesemia, lithium intoxication or multiple myeloma
Sodium Chloride-Bicarbonate Exchange System and pH: The reabsorption of Na+ by the kidneys
requires an accompanying anion
- 2 major anions in ECF are Cl- and HCO3
-
One way the kidneys regulate pH of ECF is by conserving or eliminating HCO3
- ions in which a shuffle of anions is often necessary
Cl- is the most abundant in the ECF & can substitute for HCO3
- when such a shift is needed.
Acid-Base Interpretation Practice: Please use the following key to interpret
the following ABG readings. Click on the blue boxes to reveal the
answers Use the button to return to the key at
any time Or use the “Back to Key” button at the
bottom left of the screen
Acid-Base w/o Compensation:
Parameters: pH PaCO2 HCO3-
Metabolic
Alkalosis
Normal
Metabolic
Acidosis
Normal
Respiratory
Alkalosis
Normal
Respiratory
Acidosis
Normal
Interpretation Practice:
pH: 7.31 Right! PaCO2: 48 Try Again
HCO3-: 24 Try Again
pH: 7.47 Try Again PaCO2 : 45 Right!
HCO3- : 33 Try Again
Back to Key
Resp. Acidosis
Resp. Alkalosis
Metabolic Acidosis
Resp. Alkalosis
Metabolic Alkalosis
Metabolic Acidosis
Interpretation Practice:
pH: 7.20 Try Again PaCO2: 36 Try Again
HCO3-: 14 Right!
pH: 7.50 Try Again PaCO2 : 29 Right!
HCO3- -: 22 Try Again
Metabolic Alkalosis
Resp. Acidosis
Metabolic Acidosis
Metabolic Alkalosis
Resp. Alkalosis
Resp. Acidosis
Back to Key
Acid-Base Fully Compensated:
Parameters: pH PaCO2 HCO3-
Metabolic
Alkalosis
Normal
>7.40
Metabolic
Acidosis
Normal
<7.40
Respiratory
Alkalosis
Normal
>7.40
Respiratory
Acidosis
Normal
<7.40
Interpretation Practice:
pH: 7.36 Try Again PaCO2: 56 Try Again
HCO3-: 31.4 Right!
pH: 7.43 Right! PaCO2 : 32 Try Again
HCO3: 21 Try Again
Compensated Resp. Alkalosis
Compensated Metabolic Acidosis
Compensated Resp. Acidosis
Compensated Resp. Alkalosis
Compensated Metabolic Alkalosis
Compensated Metabolic Acidosis
Back to Key
Acid-Base Partially Compensated:
Parameters: pH PaCO2 HCO3-
Metabolic
Alkalosis
Metabolic
Acidosis
Respiratory
Alkalosis
Respiratory
Acidosis
Interpretation Practice:
pH: 7.47 Right! PaCO2: 49 Try Again
HCO3-: 33.1 Try Again
pH: 7.33 Try Again PaCO2 : 31 Try Again
HCO3- : 16 Right!
Partially Compensated Metabolic Alkalosis
Partially Compensated Resp. Alkalosis
Partially Compensated Metabolic Acidosis
Partially Compensated Metabolic Alkalosis
Partially Compensated Resp. Acidosis
Partially Compensated Metabolic Acidosis
Back to Key
Case Study 1:
Mrs. D is admitted to the ICU. She has missed her last 3 dialysis treatments. Her ABG reveals the following: pH: 7.32 Low, WNL = 7.35-7.45 PaCO2: 32 Low, WNL = 35-45mmHg
HCO3-: 18 Low, WNL = 22-26mEq/L
Assess the pH, PaCO2 & HCO3-. Are the
values high, low or WNL?
The pH is:
The PaCO2 is:
The HCO3- is:
Case Study 1 Continued:
What is Mrs. D’s acid-base imbalance?
Right!
Try Again
Remember the difference between full & partial compensation. Go back & use the appropriate key if necessary.
Partially Compensated Metabolic Acidosis
Fully Compensated Resp. Acidosis
Case Study 2:
Mr. M is a pt w/ chronic COPD. He is admitted to your unit pre-operatively. His admission lab work is as follows: pH: 7.35 WNL = 7.35-7.45 PaCO2: 52 High, WNL = 35-45mmHg
HCO3-: 50 High, WNL = 22-26mEq/L
Assess the above labs. Are they abnormal or WNL?
The pH is:
The PaCO2 is:
The HCO3- is:
Case Study 2 Continued:
What is Mr. M’s acid-base disturbance?
Try Again
Right!
Think about appropriate interventions- if the problem is metabolic, the respiratory system compensates & vice versa
Fully Compensated Metabolic Acidosis
Fully Compensated Resp. Acidosis
Case Study 3: Miss L is a 32 year old female admitted
w/ decreased LOC after c/o the “worst HA of her life.” She is lethargic, but arouseable; diagnosed w/ a SAH.
Her ABG reads: pH: 7.48 High; WNL = 7.35-7.45 PaCO2: 32 Low; WNL = 35-45mmHg
HCO3-: 25 High; WNL = 22-26mEq/L
What is the significance of her ABG values?
The pH is:
The PaCO2 is:
The HCO3- is:
Case Study 3 Continued:
What is Miss L’s imbalance?
Right!
Try Again
Great Job! You’ve reached the end of the tutorial & I hope you found it helpful. Thank you!
Resp. Alkalosis
Metabolic Alkalosis
REFERENCES:http://www.healthline.com/galecontent/acid-base-balance?utm_medium=ask&utm_source=smart&utm_campaign=article&utm_term=Acid+Base+Equilibrium&ask_return=Acid-Base+Balance
. Retrieved 3/5/09.
Porth, C.M. (2005). Pathophysiology Concepts of Altered Health States (7th ed.). Philadelphia: Lippincott Williams & Wilkins.
http://en.wikipedia.org/wiki/Dissociation_(chemistry). Retrieved 3/6/09.
http://www.clt.astate.edu/mgilmore/pathophysiology/Acid and Base.ppt#1. Retrieved 3/6/09.
http://www.uhmc.sunysb.edu/internalmed/nephro/webpages/Part_E.htm.
Retrieved 3/6/09.
http://medical-dictionary.thefreedictionary.com/Volatile+acid. Retrieved 3/6/09.
REFERENCEShttp://wiki.answers.com/Q/How_does_the_phosphate_buffer_system_help_in_maintaining_the_ph_of_our_body
. Retrieved 3/10/09.
Alspach, J.G. (1998). American Association of Critical-Care Nurses Core Curriculum for Critical Care Nursing (5th ed.). Philadelphia: Saunders.
http://medical-dictionary.thefreedictionary.com. Retrieved 4/14/09.
Acid-Base Balance & Oxygenation Power Point. (2007). Milwaukee: Froedtert Lutheran Memorial Hospital Critical Care Class.