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Objectives:
Define acid base balance/imbalance
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
Metabolic Distubances
Respiratory Disturbances
Acid-Base Compensation
Acid-Base Pretest:
What is the normal
7.40 7.52
7.35 7.45
Acid-Base Pretest:
What 2 extracellular substances work together
to regulate pH?
Sodium bicarbonate & carbonic acid
Acid-Base Pretest:
Characterize an acid & a base based on the
choices below.
Acids release hydrogen (H+) ions & bases accept H+ ions.
Acid-Base Pretest:
Buffering is a normal body mechanism
that occurs rapidly in response to acidbase disturbances in order to prevent changes in what?
HCO3-
H2CO3
H+
Acid-Base Pretest:
What are the two systems in the body that
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
HCO3Buffer system
K+ - H+ Exchange
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
An acceptor of H+ A Base is: ions w/ pH >7.0 Controlled by EC pH is: & IC buffer systems Conserves HCO3Renal System: Eliminates H+ ions
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
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 base H+ elimination
& HCO3conservation
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
TRUE
FALSE
H+ that stimulates either an increase or decrease in the rate & depth of respirations.
TRUE
FALSE
controlled by the kidneys through reabsorption/regeneration of HCO3-, or elimination of buffered H+ via the tubular systems.
TRUE
FALSE
pH.
TRUE
FALSE
TRUE
FALSE
Metabolic Disturbances:
Alkalosis: elevated HCO3- (>26 mEq/L)
Causes include: Cl- depletion (vomiting, prolonged nasogastric suctioning), Cushings syndrome, K+ deficiency, massive blood transfusions, ingestion of antacids, etc. 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)
Caused by a loss of H+ ions, net gain in HCO3- , or loss of Cl- ions in excess of HCO3-
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
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
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
Increase in nonvolatile metabolic acids, decreased acid secretion by kidneys, excessive loss of HCO3-, or an increase in Cl-
& dyspnea Complaints of weakness, fatigue, general malaise, or a dull headache Pts 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
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
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.)
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
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
ventilation may be required Pts 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
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
Drug OD, lung disease, chest trauma/injury, weakness of respiratory muscles, airway obstruction, etc.
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) HYPERventilation to decrease PaCO2 Begins in 1-2hrs, maximal in 12-24 hrs
Respiratory Compensation:
Results in renal compensation which
Kidneys excrete HCO3Kidneys excrete more acid Kidneys increase HCO3- reabsorption
TCO2: 23 27 mmol/L
PaO2: 80 100 mmHg SaO2: 95% or greater (pulse ox)
Base Excess: -2 to +2
Anion Gap: 7 14
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 HCO3Alkalosis: excess H+ (kidneys unable to excrete) & HCO3- loss exceeds capacity of kidneys to regenerate
>70% of CO2 in the blood is in the form of HCO3PO2 also important in assessing respiratory function
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 Its 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, hypermagnesemia, lithium intoxication or multiple myeloma
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.
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
Normal
Normal
Normal
Interpretation Practice:
pH: 7.31 PaCO2: 48 HCO3-: 24 pH: 7.47 PaCO2 : 45 HCO3- : 33
Resp. Acidosis Right! Resp. Try Alkalosis Again
Back to Key
Interpretation Practice:
pH: 7.20
PaCO2: 36 HCO3-: 14 pH: 7.50 PaCO2 : 29
Try Again Metabolic Alkalosis Try Again Resp. Acidosis Metabolic Right! Acidosis
Try Again Metabolic Alkalosis Right! Resp. Alkalosis Resp. Acidosis Try Again
HCO3- -: 22
Back to Key
Interpretation Practice:
pH: 7.36 PaCO2: 56 HCO3-: 31.4 pH: 7.43 PaCO2 : 32
Compensated Resp. Alkalosis Try Again Compensated Metabolic Acidosis Try Again
HCO3: 21
Back to Key
Interpretation Practice:
pH: 7.47
PaCO2: 49 HCO3-: 33.1 pH: 7.33 PaCO2 : 31
Partially Compensated Metabolic Alkalosis
Right! Partially Compensated Try Again Resp. Alkalosis Partially Compensated Metabolic Acidosis Try Again
Partially Compensated Metabolic Alkalosis Try Again Partially Compensated Try Again Resp. Acidosis
HCO3- : 16
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:
The pH is: Low, WNL = 7.35-7.45 The PaCO Low, WNL = 35-45mmHg 2 is: The HCO Low, WNL = 22-26mEq/L 3 is:
Case Study 2:
Mr. M is a pt w/ chronic COPD. He is
The pH is: WNL = 7.35-7.45 The PaCO High, WNL = 35-45mmHg 2 is: The HCO High, WNL = 22-26mEq/L 3 is:
abnormal or WNL?
the problem is metabolic, the respiratory system compensates & vice versa
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:
The is: High; WNL =pH 7.35-7.45 The PaCO Low; WNL = 35-45mmHg 2 is: The HCO High; WNL = 22-26mEq/L 3 is:
values?
REFERENCES:
http://www.healthline.com/galecontent/acid-basebalance?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.
REFERENCES
http://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.