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8/14/2019 Acid Base Fall 2008
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Robin Connell MS RN
Fall 2008
Acid/Base Disorders
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Objectives
Define Acid/ Base influence in the body
Know the normal values of the components of BloodGas
Relate abnormal Blood Gases to ElectrolyteDisturbances
Discuss Treatment options for those with complexmetabolic disorders
Correlate patient diagnosis to potential acid/basedisturbances
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pH Scale
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Human pH Scale
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Acid / Base
Acid = a substance that can donate hydrogen ionsH2CO3 (carbonic acid) ( H+) + (HCO3-)
Base is a substance that can accept hydrogen ions
HCO3- + (H+) H2CO3
PaCO2- is controlled by the lungs and refers to thepressure exerted by dissolved CO2 gas in blood.
PaO2-refers to the pressure exerted by dissolved oxygen inthe blood
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pH in the Human Body
Normal Range pH 7.35 7.45
How does the body maintain this narrow normal
range?Chemical buffering mechanisms: Kidneys & Lungs
The more (H+) the more acidic the solution.
Compatibility with life pH 6.8 7.8. This range
equals a ten fold difference in (H+) concentration
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pH Laboratory Test
pH is most optimally determined by arterial blood gas
analysisBlood Gases can be done by one certified in this
procedure
RNs, RPT, Physicians
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Normal Arterial Blood Gas ValuesPH 7.35-7.45 pH< 7.35 acidosis
PaCO2 35-45 < 35 (respiratory alkalosis)
>45 (respiratory acidosis)
Pao2 80-100mmHg
HCO3 22-26 mEq/L
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Respiratory System
Lungs are the initial and primary organ in the control
of pH
Changes in the rate and the depth of respiration canhave significant and immediate affects on the pH of
the individual
Kidneys have a secondary affect and are called into
action if the respiratory system can not affect a changein the pH.
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Chemical Buffering Mechanisms
Buffering results in a change in the amount of H+ ions
through release or removal of H+ ions
Bodys Major Buffer is bicarbonate (HCO3-) andcarbonic acid (H2CO3)
Normally there are 20 to1 Ratio HCO3- to H2CO3 if
this ratio is upset the pH will change
Buffers prevent major changes in the pH of bodyfluids
by removing or replacing H+
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BuffersBodys major extracellular buffer is the bicarbonate-
carbonic acid buffer system
CO2 is a potential acid; when dissolved in H2O
(CO2+H2O)=H2CO3 so when CO2 carbonic acid is
also and vice versa
Kidneys regulate the bicarbonate level in the ECF
( In the presence of respiratory acidosis and most
metabolic acidosis kidneys excrete H+ and conservebicarbonate ions)
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Buffers
Lungs under influence of respiratory center (Medulla)
control CO2 (and thus carbonic acid)
It adjusts ventilation in response to the amount of
CO2, and to a lesser extent O2
CO2 has an immediate effect on respiratory efforts;
but declines over time for the next 1-2 days. So after 2
days elevation of blood CO2 has only a weak effect asa respiratory stimulant.
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LungsPartial pressure of O2 in arterial blood (PaO2)
influences respiration, but does not do so unless PaO2
falls below 60mmHg
Lungs compensate for metabolic disturbances by either
conserving or retaining CO2
Metabolic acidosis respirations is = elimination of
CO2 (lighten the acid load)
Metabolic alkalosis respiration is = retention ofCO2 (increasing the acid load)
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Effects of pH on Potassium
Generally acidic states cause potassium to shift from
the cells ECF plasma potassium concentration
The opposite happens in alkalemia; potassium shifts
the cells the plasma potassium concentration.
(metabolic and respiratory)
Hypokalemia is commonly present in patients in
patients with metabolic alkalosis15
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AcidemiaA shift in potassium out of the cells can occur in acidemia
(metabolic or respiratory) respiratory being a weaker stimulus
H+ ions shift the cells to correct the low plasma pH topreserve cellular electroneutrality cellular potassium shift from
the cells the ECF
Hyperkalemia is less marked when do to lactic acidosis orketoacidosis then when due to renal failure or diarrhea
Hyperkalemia does occur in untreated diabectic ketoacidosis,due more to insulin lack
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Metabolic Acidosis
Clinical disturbance characterized by pH and
bicarbonate concentration
Lungs hyperventilate to CO2 concentration
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Anion GapMetabolic Acidosis can be divided into two forms depending on
the values of the serum anion gap
Anion Gap (AG) = Na+ - (CL- + HCO3-)= 8-12mEq/L
or
Anion Gap (AG) = Na+ + K+ - (CL- + HCO3-) = 12-16mEq/L
Anion Gap reflects normally unmeasured anions (phosphates,sulfates, and protein in plasma)
An Anion Gap 16 suggests excessive accumulation of
unmeasured anions
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Clinical Manifestations
Headache, confusion, drowsiness, RR and depth ofrespirations, N/V, peripheral vasodilation, Cardiac
Output occurs when pH 7.0, BP, cold clammy skin,
dysrhythmias and shock
Lactic Acidosis-most commonly seen in patients with
significant cardiopulmonary problems and sepsis.
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Normal Anion Gap Acidosis
Diarrhea-direct loss of Bicarbonate in the stool, ECF
volume depletion, and concentration of the remaining
chloride, also referred to as hyperchloremic acidosis
Excessive chloride due to IV infusion
Use of diuretics
A reduced or negative anion gap is primarily causedby hypoproteinemia usually a rare occurance.
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Metabolic Acidosis
ABGs look like: Bicarbonate 22 mEq/L pH 7.35
serum Bicarb level
Hyperkalemia may accompany shift K+ out of the cell
into the ECF
Hyperventilation to decrease CO2 as compensatory
mechanism
Management: correct metabolic defectif Cl- eliminate source
Give Bicarb for pH 7.1 or HCO3 10
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Metabolic Acidosis
Example: Patient with diabetic ketoacidosis
pH = 7.05
HCO3 = 5 mEq/L( primary disturbance)PaCO2 = 12mmHg (compensatory
hyperventilation)
Base excess (BE) = -30
Acidosis depresses myocardial contractility, lowers thefibrillation threshold.
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Metabolic AlkalosisExcess HCO3High pH (decreased H+ concentration)
High plasma bicarbonate concentration
Causes= by a gain in bicarbonate or loss of hydrogen
Compensation=lungs hypoventilate to increase PaCO2
Common causes = vomiting or gastric suction ( loss of H+
and CL- ionsOveruse of diuretics, Excessive alkali ingestion
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Hypokalemia & Alkalosis
Kidneys conserve K+ H+ excretion increases
Cellular K+ moves out of the cell ECF to helpmaintain serum level. (as K+ leaves the cell H+ enters
to maintain electroneutrality.
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Respiratory Acidosis
H2 CO3 Excess can be acute or chronicAcute is more dangerous
Renal compensation is very slow
High PaCO2 can quickly produce a sharp decrease inplasma pH
Causes: always due to inadequate excretion of CO2
(inadequate ventilation)
Pulmonary Edema, pneumothorax, atelectasis, overdoseof sedatives etc
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Signs and Symptoms
PaCo2 pulse and Respiratory rate,BP, mentalcloudiness, and a feeling of fullness in the head
cerebrovascular vasodilation
Example: Acute Respiratory Acidosis
pH 7.26
PaCO2 56
HCO3 2428
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Chronic Respiratory Acidosis
Patient may complain of weakness, dull headachepH may be low normal like 7.35 (if complete
compensation has occurred)
PaCO3 45 mmHg
Example: Chronic Respiratory Acidosis
pH 7.38
PaCO2 76
HCO3 42BE +14
Remember when PaCO2 is chronically elevated??????? 29
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Respiratory Alkalosis
H2CO3 deficit due to hyperventilation causing excess
blowing off of CO2 decrease in Plasma H2CO3
Signs and Symptoms:
Fever, extreme anxiety, hypoxemia, gram negative
Bacteremia, Pulmonary Emboli, Excessive ventilation
by ventilators
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RespiratoryAlkalosis
Acute: pH 7.52
PaCO2 30mmHg
HCO3 24
BE +2.5mEq/L
Chronic: pH 7.40
PaCO2 30
HCO3 18mEq/L
BE -5 31
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Mixed Acid Base Imbalances
Respiratory Alkalosis Plus Metabolic AcidosisExample:
pH 7.4
PaCO2 18mmHg
HCO3 16mEq/L
BE -10
Examples of Disorders that cause mixed acid/baseimbalances: Cardiopulmonary Arrest, Salicylate
Intoxication, Renal failure and vomiting etc
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Systemic Assessment of Blood Gas
First look at the pH:
Determine the primary cause of the disturbance this is
done by evaluating the PaCo2 and HCO3 in relation to
the pH
Determine if compensation has occurred
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Questions??????
Practice on Blood Gas Problems
Look on-line