Abg&acid base balance
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Transcript of Abg&acid base balance
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الرحمن الله الرحمن بسم الله بسم الرحيمالرحيم
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ABG analysis &Acid-base ABG analysis &Acid-base ImbalanceImbalance
By/Dr.Babiker Mohd. AhmedBy/Dr.Babiker Mohd. Ahmed
DR/ALA ELDIN HASSNDR/ALA ELDIN HASSN..
SHAAB T.HSHAAB T.H..
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What is an ABGWhat is an ABGArterial Blood Gas
Drawn from artery- radial, brachial, femoral
It is an invasive procedure.
Caution must be taken with patient on anticoagulants.
Arterial blood gas analysis is an essential part of diagnosing and managing the patient’s oxygenation status, ventilation failure and acid base balance.
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PrecautionsPrecautions Excessive Heparin Decreases bicarbonate
and PaCO2
Large Air bubbles not expelled from sample PaO2 rises, PaCO2 may fall slightly.
Fever or Hypothermia, Hyperventilation or breath holding (Due to anxiety) may lead to erroneous lab results
Care must be taken to prevent bleeding
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ABG analysisABG analysis
•Why do we care? –Critical care requires a good understanding –Helps in the differential and final diagnosis–Helps in determining treatment plan–Treating acid/base disorders helps medications work better
(i.e. antibiotics, vasopressors, etc.)–Helps in ventilator management–Severe acid/base disorders may need dialysis–Changes in electrolyte levels in acidosis (increased K+ and
Na+, and decreases in HCO3)
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Normal Arterial Blood Gas Normal Arterial Blood Gas ValuesValues**
PH 7.35-7.45PH 7.35-7.45 35-4535-45 mm Hg mm Hg PaCO PaCO22
70-10070-100 m Hgm Hg PaO PaO22
SaOSaO2 2 95-100%95-100% 22-2622-26 mEq/L mEq/L -- HCO3 HCO3--
% %MetHb <2.0%MetHb <2.0%< < 3.0%3.0% %%COHbCOHb
16-2216-22 ml Oml O22/dl/dl CaO CaO22
* * At sea level, breathing ambient air ** Age-At sea level, breathing ambient air ** Age-dependentdependent
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COMPONENTS OF THE COMPONENTS OF THE ABGABG
pH: Measurement of acidity or alkalinity, based on the hydrogen (H+)
7.35 – 7.45Pao2 The partial pressure oxygen that is dissolved in arterial blood.
80-100 mm Hg. PCO2: The amount of carbon dioxide dissolved in arterial blood.
35– 45 mmHgHCO3
: The calculated value of the amount of bicarbonate in the blood 22 – 26 mmol/L
B.E: The base excess indicates the amount of excess or insufficient level of bicarbonate. -2 to +2mEq/L(A negative base excess indicates a base deficit in blood)
SaO2:The arterial oxygen saturation. >95%
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Stepwise approach to ABGStepwise approach to ABG
•Step 1: Acidemic or Alkalemic? •Step 2: Is the primary disturbance
respiratory or metabolic? •Step 3. Asses to Pa O2. A value below 80mm
Hg indicates Hypoxemia. For a respiratory disturbance, determine whether it is acute
or chronic. •Step 4. For a metabolic acidosis, determine
whether an anion gap is present. •Step 5. Assess the normal compensation by
the respiratory system for a metabolic disturbance
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Interpretation: pHInterpretation: pH–Normal arterial pH = 7.36 to 7.44
•Determine Acidosis versus Alkalosis
–1 .pH <7.35: Acidosis
–2 .pH >7.45: Alkalosis
•Metabolic Conditions are suggested if
–pH changes in the same direction as pCO2/HCO3-
–pH is abnormal but pCO2 remains unchanged Respiratory Conditions are suggested if:
–pH changes in the opp direction as pCO2/HCO3-
–pH is abnormal but HCO3- remains unchanged
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10
EFFECTS OF pHEFFECTS OF pH•The most general effect of pH changes
are on enzyme function–Also affect excitability of nerve and muscle
cells
pHpH
ExcitabilityExcitability
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PH {Potential PH {Potential Hydrogen}Hydrogen}
The pH is a measurement of the acidity or alkalinity of the blood. It is inversely proportional to the no. of (H+) in the blood. The normal pH range is 7.35-7.45.Changes in body system functions that occur in an acidic state decreases the force of cardiac contractions, decreases the vascular response to catecholamines, and a diminished response to the effects and actions of certain medications.An alkalotic state interferes with tissue oxygenation and normal neurological and muscular functioning.Significant changes in the blood pH above 7.8 or below 6.8 will interfere with cellular functioning, and if uncorrected, will lead to death.
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pH is inversely related to [HpH is inversely related to [H++]; a pH change ]; a pH change of 1.00 represents a 10-fold change in [Hof 1.00 represents a 10-fold change in [H++]]
pH [H+] in nanomoles/L
7.00 1007.10807.30 50 7.40 40 7.52 30 7.70208.00 10
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Assess the PaCOAssess the PaCO22
•In an uncompensated state – when the pH and paCO2 moves in the same direction: the
primary problem is metabolic.
•The decreasing paco2 indicates that the lungs acting as a buffer response (blowing of the
excess CO2)
•If evidence of compensation is present but the pH has not been corrected to within the
normal range, this would be described as metabolic disorder with the partial respiratory
compensation.
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Assess the HCOAssess the HCO33
•The pH and the HCO3 moving in the opposite directions, we
would conclude that the primary disorder is respiratory and the
kidneys acting as a buffer response: are compensating by retaining HCO3 to return the pH
to normal range.
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HCO3- (bicarbonate):
SB (standard bicarbonate)
AB (actual bicarbonate)
SB: the contents of HCO3- of serum of arterial
blood in 38 , PaCO2 40mmHg, SaO℃ 2 100%.
Normal: 22-27mmol/L
mean: 24mmol/L
AB: The contents of HCO3- in actual
condition. In normal person: AB=SB
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AB and SB are parameters to reflect metabolism, regulated by kidney.
Difference of AB-SB can reflect the
respiratory affection on serum HCO3
-.
Respiratory acidosis: AB>SB
Respiratory alkalosis: AB<SB
Metabolic acidosis: AB = SB<Normal
Metabolic alkalosis: AB=SB>Normal
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Assessing OxygenationAssessing Oxygenation
•Normal value for arterial blood gas 80-100mmHg decreased progressively with
age•Normal value for venous blood gas
40mmHg•Normal SaO2
–Arterial: 97%–Venous: 75%–Hypoxemia is PaO2 < 80 mm Hg at RA
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Acceptable PaO2 Values on Acceptable PaO2 Values on Room AirRoom Air
Age GroupAccepable PaO2 (mm Hg)
Adults upto 60 yrs & Children
<80
Newborn40-70
70 yrs <70
80 yrs <60
90 yrs <50
60 yrs 80 mm Hg 1mm Hg/yr
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INDICATORS OF OXYGENATIONINDICATORS OF OXYGENATION
•Assessing the efficiency of oxygenation requires knowledge of
•Ventilation is the mechanical movement of air. Oxygenation is the process of transporting oxygen
from the alveolus across capillary membranes into pulmonary circulation.
A-a gradient (Alveolar to arterial gradient):
• Provides an assessment of alveolar-capillary gas exchange. To calculate you need the alveolar PO2
(PAO2) and arterial pO2 (paO2). The larger the gradient, the more serious the respiratory compromise
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P(A-a)OP(A-a)O22
P(A-a)O2 is the alveolar-arterial difference in partial pressure of oxygen. It is commonly called the “A-a gradient,” though it does not actually result from an
O2 pressure gradient in the lungs. Instead, it results from gravity-related blood flow changes within the lungs (normal ventilation-perfusion imbalance) .
PAO2 is always calculated based on FIO2, PaCO2, and barometric pressure .
PaO2 is always measured on an arterial blood sample in a “blood gas machine ”.
Normal P(A-a)O2 ranges from 5 to 25 mm Hg breathing room air (it
increases with age). A higher than normal P(A-a)O2 means the lungs are not transferring oxygen properly from alveoli into the pulmonary capillaries.
Except for right to left cardiac shunts, an elevated P(A-a)O2 signifies some sort of problem within the lungs.
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Compare Compare PPAAOO22 to P to PaaOO22
•Healthy people: PAO2 = PaO2
•Two Approaches to Comparison–)PAO2 - PaO2 (difference
–PaO2 / PAO2 ratio
.
A-a difference increases with pulmonary disease
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a/A ratioa/A ratio
•Normally averages just over 0.8 (Am. Rev. Resp.
Dis. 109: 142-145, 1974).•a/A ratio falls with pulmonary disease.•Lower limit normal:
–young (room air) : 0.74 –older (room air) : 0.78 –Both groups (100% O2): 0.82
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•A-a gradient = PAO2 - PaO2PaO2 (partial pressure of O2 in the artery)
--obtained from the arterial blood gases.PAO2 (partial pressure of O2 in the
alveoli)-- obtained from the Alveolar Gas equation.
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Alveolar Gas EquationAlveolar Gas Equation
PAO2 = PIO2 - 1.2 (PaCO2)where PIO2 = FIO2 (PB – 47 mm Hg)
Except in a temporary unsteady state, alveolar PO2 (PAO2) is always higher than arterial PO2 (PaO2). As a result,
whenever PAO2 decreases, PaO2 also decreases. Thus, from the AG equation:
If FIO2 and PB are constant, then as PaCO2 increases both PAO2 and PaO2 will decrease (hypercapnia causes hypoxemia).
If FIO2 decreases and PB and PaCO2 are constant, both PAO2 and PaO2 will decrease (suffocation causes hypoxemia).
If PB decreases (e.g., with altitude), and PaCO2 and FIO2 are constant, both PAO2 and PaO2 will decrease (mountain climbing leads to hypoxemia).
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Oxygen SaturationOxygen Saturation
•Oxygen Saturation ( SaO2 )
–This refers to the amount of oxygen being carried by the haemoglobin (Hb) molecules
•The Hb molecule is divided into two portionsGlobin - made of protein
•Haem - made of iron
•There are 4 groups of haem on each molecule of Hb
•Each haem group can bind 1 O2 molecule
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Important points for assessing Important points for assessing tissue oxygenationtissue oxygenation
•This is the O2 that’s really available at the tissue level.
•Is the THb normal?–Low THb means the ability of the blood to
carry the O2 to the tissues is decreased
•Is perfusion normal?–Low perfusion means the blood isn’t even
getting to the tissues
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PvO2: Oxygenic partial pressure of mixed venous blood.
Normal: 35-45mmHg
mean: 40mmHg
Significance: Pa-vO2 is to reflect the tissue absorbing oxygen.
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CaO2: The content of the oxygen of the arterial blood .
Normal: 19-21mmol/L
Significance: a comprehensive parameter to evaluate arterial oxygen.
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SaOSaO22 and Oxygen Content and Oxygen Content
Tissues need a requisite amount of oxygen molecules for metabolism. Neither the PaO2 nor the SaO2 tells how much
oxygen is in the blood. How much is provided by the oxygen content, CaO2 (units = ml O2/dl). CaO2 is calculated as:
CaO2 = quantity O2 bound + quantity O2 dissolved to hemoglobin in plasma
CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)
Hb = hemoglobin in gm%; 1.34 = ml O2 that can be bound to each gm of Hb; SaO2 is percent saturation of hemoglobin with
oxygen; .003 is solubility coefficient of oxygen in plasma: .003 ml dissolved O2/mm Hg PO2.
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SaOSaO22 – is it calculated or measured – is it calculated or measured??
SaO2 is measured in a ‘co-oximeter’. The traditional ‘blood gas machine’ measures only pH, PaCO2 and PaO2,, whereas the co-oximeter measures SaO2, carboxyhemoglobin, methemoglobin
and hemoglobin content. Newer ‘blood gas’ consoles incorporate a co-oximeter, and so offer the latter group of
measurements as well as pH, PaCO2 and PaO2.
Always make sure the SaO2 is measured, not calculated. If it is calculated from the PaO2 and the O2-dissociation curve, it provides no new information, and could be inaccurate --
especially in states of CO intoxication or excess methemoglobin. CO and metHb do not affect PaO2, but do lower
the SaO2.
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Carbon monoxide – an important Carbon monoxide – an important cause of hypoxemiacause of hypoxemia
•Normal %COHb in the blood is 1-2%, from metabolism and small amount of ambient CO (higher in traffic-congested areas)
• All smokers have excess CO in their blood.•CO binds @ 200x more avidly to hemoglobin than O2, displacing
O2 from the heme binding sites .•CO : 1) decreases SaO2 by the amount of %COHb present, and 2)
shifts the O2-dissociation curve to the left, retarding unloading of oxygen to the tissues.
•CO does not affect PaO2, only SaO2. To detect CO poisoning, SaO2 and/or COHb must be measured (requires co-oximeter). In the presence of excess CO, SaO2 (when measured) will be lower
than expected from the PaO2.
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Physiologic causes of low PaOPhysiologic causes of low PaO22
Non-Respiratory P[A-a]O2Cardiac Right to Left Shunt IncreasedDecreased Pio2 NormalRespiratoryPulmonary Right to Left Shunt IncreasedV/Q Imbalance IncreasedDiffussion barrier IncreasedHypoventilatio [increased CO2] Normal
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Anion GAPAnion GAP
•Calculation of AG is useful approach to analyse metabolic acidosis
AG = (Na+ + K+) – (cl- + Hco3-)• *A change in the pH of 0.08 for each 10
mm Hg indicates an ACUTE condition.* A change in the pH of 0.03 for each 10 mm Hg indicates a CHRONIC condition.
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Anion gap (AG): the difference of undetermined anion
and undetermined cation in serum.AG={Na + K}-(Cl-+ HCO3
- )Normal: 8-16mmol/L Significance :
AG = acidosis: ketoacidosis, kidney failure AG normal acidosis: Cl , diarrhea, fixed
acid decrease to evaluate mix acid-basic disorder
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ANION GAPANION GAP
•The AG is estimated by substracting the sum of Cl and Hco3 concentration from the plasma Na: Na+unmeasured cations=Cl +Hco3 +unmeasured anions:
•AG={Na} – {Cl} +{Hco3}•The major unmeasured cations are
calcium,magnesium and potassium.•The major unmeasured anions are
albumin,sulphate, phosphate,lactate.
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ELEVATED AG ACIDOSISELEVATED AG ACIDOSIS
•Causes are best remembered by mnemonic KULT:
•K: Ketoacidosis (DKA,alcoholic ketoacidosis,starvation)
•U: Uraemia•L: Lactic acidosis
•T; Toxins (Ethylene glycol,methanol,salicylates,paraldehyde,INH{
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• K etoacidosis
•Uremia
• S epsis•Salicylate & other drugs
• M ethanol• A lcohol (Ethanol)
•Lactic acidosis• Ethylene glycol
REMEMBER
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BASE EXCESSBASE EXCESS
•Base Excess (BE)
•Rising levels of bicarbonate make the blood more alkaline and a depletion of
bicarbonate makes it more acidic
•Base excess refers to the amount of base (alkali) which needs to be added or taken
away from the blood to return the pH to 7.4
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BASE EXCESSBASE EXCESS
•Base Excess can be used in the following
•To interpretate change in Hco3 levels:
•1-If the base excess is between -2 and +2 then there is no metabolic acidosis or alkalosis based on observed Hco3 change.
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BASES EXCESSBASES EXCESS
•2- If the base excess is less than -2 {Base deficit} then there is metabolic acidosis which may be primary or compensatory process.
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BASE EXCESSBASE EXCESS
•3-If the base excess is greater than +2 then there is metabolic alkalosis which may be primary or compensatory process.
•=BASE EXCESS alone cannot differentiate between primary or compensatory process.
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FormulaFormula•With the base excess is -10 in a 50kg
person with metabolic acidosis mM of Hco3 needed for correction is:
= 0.3 X body weight X BE = 0.3 X 50 X10 = 150 mM
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Compensated or Uncompensated—Compensated or Uncompensated—what does this meanwhat does this mean??
.1Evaluate pH—is it normal? Yes
.2Next evaluate pCO2 & HCO3
•pH normal + increased pCO2 + increased HCO3 = compensated respiratory acidosis
•pH normal + decreased HCO3 + decreased pCO2 = compensated metabolic acidosis
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COMPENSATIONCOMPENSATION
•A patient can be uncompensated or partially compensated or fully compensated
•pH remains outside the normal range•pH has returned within normal range- fully
compensated though other values may be still abnormal
•Be aware that neither the system has the ability to overcompensate
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Partially compensatedPartially compensated
pHpaco2Hco3
Res.Acidosis
Res.Alkalosis
Met. Acidosis
Met.Alkalosis
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FULLY COMPENSATEDFULLY COMPENSATEDpHpaco2Hco3
Resp.AcidosisNormal
but<7.40
Resp.AlkalosisNormal
but>7.40
Met. AcidosisNormal
but<7.40
Met. AlkalosisNormal
but>7.40
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Clinical SignificanceClinical Significance
To evaluate respiratory failure
type 1 or type 2
To evaluate acid-basic disorder
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HypoxiaHypoxia
Mild: 80-60mmHgMediate: 60-40mmHgSevere: <40mmHg
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Respiratory FailureRespiratory Failure
PaO2<60mmHg respiratory failure
Notice: sea level, quiet, inspire air rule off other causes ( heart
disease)
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Classification of Respiratory FailureClassification of Respiratory Failure
Type 1 Type2 PaO2 (mmHg) <60 <60 PaCO2 (mmHg) ≤50 >50
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Other ParametersOther Parameters
SaO2: Saturation of arterial blood oxygen
Normal: 0.95-0.98
Significance: a parameter to evaluate hypoxia, but not sensitive
ODC ( Dissociation curve of oxygenated hemoglobin): “S” shape
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PH 2,3DPG temperature CO2
ODC to right deviation
Oxygenated hemoglobin release oxygen to tissue, prevent hypoxia of the tissue. But absorbed oxygen of hemoglobin is decreased from the alveoli.
Bohr effect: movement of ODC place is
induced by PH.
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SaO2%
PO2
Oxygen dissociation curve
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Oxygen dissociation curve: SaOOxygen dissociation curve: SaO22 vs. PaO vs. PaO22
Also shown are CaOAlso shown are CaO2 2 vs. PaOvs. PaO22 for two different hemoglobin contents: 15 gm% for two different hemoglobin contents: 15 gm%
and 10 gm%. CaOand 10 gm%. CaO22 units are ml O units are ml O22/dl. P/dl. P5050 is the PaO is the PaO22 at which SaO at which SaO22 is 50% is 50% . .
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ODCODC
•Oxygen Dissociation Curve •The curve highlights the affinity of oxygen
to haemoglobin•When PO2 is high, oxygen is strongly
affiliated to haemoglobin, so oxygen saturation will be high
•When PO2 is low there is less affinity of oxygen to haemoglobin, so oxygen
saturation drops
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ODCODC
•Oxygen Dissociation Curve •It can be seen from the shape of the oxygen
dissociation curve that initially there is a slight drop in SaO2 when there is a reduced PO2
•However, at a certain point there is a sudden drop in saturation as indicated by the steep
decline in the curve–Therefore, SaO2 normally only drops sharply if the
PO2 is at a very low level8 kPa is the point at which the patient is hypoxaemic and is in respiratory failure
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Classification of Acid-basic DisorderClassification of Acid-basic Disorder
PH PaCO2 HCO3-
Rest. acidosis
Rest. alkalosis
Meta. Acidosis
Meta. Alkalosis
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Respiratory Acid Base DisordersRespiratory Acid Base Disorders
•Respiratory alkalosis most common of all the 4 acid base disorders (23-46%) -followed by met alkalosis - review of 8289 ABG analysis in ICU
pts Kaehny WD, MCNA 67(4), 1983 p 915-928
•Resp acidosis seen in 14-22% of pts•Attention to possibility of hypoxemia and its
correction always assumes priority in analysis of pts with a possible respiratory acid-base
disorder
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RESPIRATORY RESPIRATORY ACIDOSISACIDOSIS
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•is defined as a pH less than 7.35 with a paco2 greater than 45 mmHg.
•Acidosis –accumulation of co2, combines with water in the body to
produce carbonic acid, thus lowering the pH of the blood.
•Any condition that results in hypoventilation can cause
respiratory acidosis.
Res. Acidosis
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RESPIRATORY ACIDOSISRESPIRATORY ACIDOSIS•Caused by hyperkapnia due to
hypoventilation–Characterized by a pH decrease
and an increase in CO2
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RESPIRATORY ACIDOSISRESPIRATORY ACIDOSIS•The speed and depth of breathing control
the amount of CO2 in the blood
•Normally when CO2 builds up, the pH of the blood falls and the blood becomes acidic
•High levels of CO2 in the blood stimulate the parts of the brain that regulate breathing, which in turn stimulate faster and deeper
breathing
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RESPIRATORY ACIDOSISRESPIRATORY ACIDOSIS•Respiratory acidosis can also develop when
diseases of the nerves or muscles of the chest impair the mechanics of breathing
•In addition, a person can develop respiratory acidosis if overly sedated from narcotics and
strong sleeping medications that slow respiration
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RESPIRATORY ACIDOSISRESPIRATORY ACIDOSIS•The treatment of respiratory acidosis aims
to improve the function of the lungs•Drugs to improve breathing may help
people who have lung diseases such as asthma and emphysema
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RESPIRATORY ACIDOSISRESPIRATORY ACIDOSIS•Decreased CO2 removal
can be the result of:(1Obstruction of air
passages(2Decreased respiration
(depression of respiratory centers)
(3Decreased gas exchange between pulmonary
capillaries and air sacs of lungs
(4Collapse of lung
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Manifestations of Resp Manifestations of Resp AcidosisAcidosis
•NEUROMUSCULAR: Related to cerebral A vasodilatation & Cerebral BF
.1Anxiety
.2Asterixis
.3Lethargy, Stupor, Coma
.4Delirium
.5Seizures
.6Headache
.7Papilledema
.8Focal Paresis
.9Tremors, myoclonus
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•CARDIOVASCULAR: Related to coronary vasodilation
.1Tachycardia with N BP
.2Ventricular arrythmias (related to hypoxemia and not hypercapnia per se)
.3Senstivity to digitalis
•BIOCHEMICAL ABNORMALITIES: tCO2
Cl-
PO43-
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Homeostatic Response Homeostatic Response toto Respiratory AcidosisRespiratory Acidosis
•Imm response to rise in CO2 (& H2CO3) blood and tissue buffers take up H+ ions, H2CO3 dissociates and
HCO3- increases with rise in pH .•Steady state reached in 10 min & lasts for 8 hours.•PCO2 of CSF changes rapidly to match PaCO2.•Hypercapnia that persists > few hours induces an
increase in CSF HCO3- that reaches max by 24 hr and partly restores the CSF pH.
•After 8 hrs, kidneys generate HCO3 -•Steady state reached in 3-5 d
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•predicts rise in PaCO2 obligatory hypoxemia in pts breathing R.A .
•Resultant fall in PaO2 limits hypercapnia to 80 to 90 mm Hg
•Higher PaCO2 leads to PaO2 incompatible with life .
•Hypoxemia, not hypercapnia or acidemia, that poses the principal threat to life .
•Consequently, oxygen administration represents a critical element in the management
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Causes of Chronic Respiratory Causes of Chronic Respiratory AcidosisAcidosis
•EXCRETORY COMPONENT PROBLEMS:
.1Ventilation:COPD
Advanced ILD•Restriction of thorax/chest wall:
Kyphoscoliosis, Arthritis
Fibrothorax
Hydrothorax
Muscular dystrophy
Polymyositis
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Treatment of Respiratory Treatment of Respiratory AcidosisAcidosis
•Ensure adequate oxygenation - care to avoid inadequate oxygenation while
preventing worsening of hypercapnia due to supression of hypoxemic resp drive
•Correct underlying disorder if possible•Avoid rapid decrease in ch elevated
PCO2 to avoid post hypercapnic met alkalosis (arrythmias, seizures
adequate intake of Cl-)
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•Alkali (HCO3) therapy rarely in ac and never in ch resp acidosis only if acidemia directly inhibiting
cardiac functions•Problems with alkali therapy:
.1Decreased alv ventilation by decrease in pH mediated ventilatory drive
.2Enhanced carbon dioxide production from bicarbonate decomposition
.3Volume expansion .•COPD pts on diuretics who develop met alkalosis
often benfefited by acetazolamide
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RESPIRATORY RESPIRATORY ALKALOSISALKALOSIS
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Manifestations of Resp Manifestations of Resp AlkalosisAlkalosis
•NEUROMUSCULAR: Related to cerebral A vasoconstriction & Cerebral BF
.1Lightheadedness
.2Confusion
.3Decreased intellectual function
.4Syncope
.5Seizures
.6Paraesthesias (circumoral, extremities)
.7Muscle twitching, cramps, tetany
.8Hyperreflexia
.9Strokes in pts with sickle cell disease
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•CARDIOVASCULAR: Related to coronary vasoconstriction
.1Tachycardia with N BP
.2Angina
.3ECG changes (ST depression)
.4Ventricular arrythmias
•GASTROINTESTINAL: Nausea & Vomitting (cerebral hypoxia)
•BIOCHEMICAL ABNORMALITIES:
tCO2PO43-
Cl- Ca2+
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RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Can be the result of:
–1 (Anxiety, emotional disturbances
–2 (Respiratory center lesions
–3 (Fever–4 (Salicylate poisoning
(overdose)–5 (Assisted respiration
•6 (High altitude (low PO2)
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RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Anxiety is an emotional
disturbance
•The most common cause of hyperventilation, and
thus respiratory alkalosis, is anxiety
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RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Usually the only treatment needed is to
slow down the rate of breathing
•Breathing into a paper bag or holding the breath as long as possible may help raise
the blood CO2 content as the person breathes carbon dioxide
back in after breathing it out
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RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Respiratory center
lesions–Damage to brain
centers responsible for monitoring
breathing rates•Tumors•Strokes
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RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Fever
–Rapid shallow breathing blows off
too much CO2
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RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Salicylate poisoning
(Aspirin overdose)–Ventilation is stimulated
without regard to the status of O2, CO2 or H+ in
the body fluids
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RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Assisted Respiration
–Administration of CO2 in the exhaled air of the care - giver
Your insurance won’t cover a ventilator any longer, so Bob here will be giving you mouth to mouth for the next several days
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RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•High Altitude
–Low concentrations of O2 in the arterial blood reflexly stimulates ventilation in an attempt to
obtain more O2
–Too much CO2 is “blown off” in the process
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RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Kidneys compensate by:
–Retaining hydrogen ions
–Increasing bicarbonate excretion
H+
HCO3-
HCO3-
HCO3-
HCO3-
HCO3-
HCO3-
HCO3-
HCO3-
HCO3-
HCO3-
H+
H+
H+
H+
H+
H+
H+
H+
H+
H+
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RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Decreased CO2 in the lungs will
eventually slow the rate of breathing–Will permit a normal amount of CO2 to
be retained in the lung
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Homeostatic Response to Resp Homeostatic Response to Resp AlkalosisAlkalosis
•In ac resp alkalosis, imm response to fall in CO2 (& H2CO3) release of H+ by blood and tissue buffers react with HCO3- fall in HCO3- (usually not less than
18) and fall in pH•Cellular uptake of HCO3- in exchange for Cl-•Steady state in 15 min - persists for 6 hrs•After 6 hrs kidneys increase excretion of HCO3- (usually
not less than 12-14) •Steady state reached in 11/2 to 3 days .•Timing of onset of hypocapnia usually not known except
for pts on MV. Hence progression to subac and ch resp alkalosis indistinct in clinical practice
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METABOLIC ACIDOSISMETABOLIC ACIDOSIS
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Metabolic AcidosisMetabolic Acidosis
•Bicarbonate less than 22mEq/L with a pH of less than 7.35.
•Renal failure•Diabetic ketoacidosis•Anaerobic metabolism•Starvation•Salicylate intoxication
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METABOLIC ACIDOSISMETABOLIC ACIDOSIS•The causes of metabolic acidosis can
be grouped into five major categories–1 (Ingesting an acid or a substance that is
metabolized to acid
–2 (Abnormal Metabolism
–3 (Kidney Insufficiencies
–4 (Strenuous Exercise
–5 (Severe Diarrhea
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METABOLIC ACIDOSISMETABOLIC ACIDOSIS•Unregulated
diabetes mellitus causes
ketoacidosis–Body metabolizes fat
rather than glucose–Accumulations of
metabolic acids (Keto Acids) cause
an increase in plasma H+
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METABOLIC ACIDOSISMETABOLIC ACIDOSIS•This leads to excessive production of
ketones:–Acetone–Acetoacetic acid–B-hydroxybutyric acid
•Contribute excessive numbers of hydrogen ions to body fluids
Acetone
Acetoacetic acid
Hydroxybutyric acid
H+
H+
H+
H+
H+H+H+
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METABOLIC ACIDOSISMETABOLIC ACIDOSIS•2 (Abnormal Metabolism
–The body also produces excess acid in the advanced stages of shock, when lactic
acid is formed through the metabolism of sugar
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METABOLIC ACIDOSISMETABOLIC ACIDOSIS
•3 (Kidney Insufficiencies
–Even the production of normal amounts of acid
may lead to acidosis when the kidneys aren't
functioning normally
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METABOLIC ACIDOSISMETABOLIC ACIDOSIS•3 (Kidney Insufficiencies
–Kidneys may be unable to rid the plasma of even the
normal amounts of H+ generated from metabolic
acids
–Kidneys may be also unable to conserve an
adequate amount of HCO3-
to buffer the normal acid load
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METABOLIC ACIDOSISMETABOLIC ACIDOSIS•3 (Kidney Insufficiencies
–This type of kidney malfunction is called renal tubular acidosis or uremic
acidosis and may occur in people with kidney failure or with abnormalities that
affect the kidneys' ability to excrete acid
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METABOLIC ACIDOSISMETABOLIC ACIDOSIS•Treating the underlying cause of metabolic
acidosis is the usual course of action–For example, they may control diabetes with
insulin or treat poisoning by removing the toxic substancefrom the blood
–Occasionallydialysis is needed
to treat severeoverdoses and
poisonings
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METABOLIC ACIDOSISMETABOLIC ACIDOSIS
•Metabolic acidosis may also be treated directly
–If the acidosis is mild, intravenous fluids and
treatment for the underlying disorder may be all that's
needed
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METABOLIC ALKALOSISMETABOLIC ALKALOSIS
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Metabolic alkalosisMetabolic alkalosis
•Bicarbonate more than 26m Eq /L with a pH more than 7.45
•Excess of base /loss of acid can cause•Ingestion of excess antacids, excess use of
bicarbonate, or use of lactate in dialysis.•Protracted vomiting, gastric
suction,hypchoremia,excess use of diuretics, or high levels of aldesterone.
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METABOLIC ALKALOSISMETABOLIC ALKALOSIS•A reduction in H+ in the case of metabolic
alkalosis can be caused by a deficiency of non-carbonic acids
•This is associated with an increase in HCO3-
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METABOLIC ALKALOSISMETABOLIC ALKALOSIS
•Treatment of metabolic alkalosis is most often accomplished by replacing water and
electrolytes (sodium and potassium) while treating the underlying cause
•Occasionally when metabolic alkalosis is very severe, dilute acid in the form of
ammonium chloride is given by IV
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METABOLIC ALKALOSISMETABOLIC ALKALOSIS•Can be the result of:
–1 (Ingestion of Alkaline Substances
–2 (Vomiting ( loss of HCl )
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METABOLIC ALKALOSISMETABOLIC ALKALOSIS
•Baking soda (NaHCO3) often used as a remedy for gastric hyperacidity
–NaHCO3 dissociates to Na+ and HCO3-
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METABOLIC ALKALOSISMETABOLIC ALKALOSIS•Bicarbonate neutralizes high
acidity in stomach (heart burn)•The extra bicarbonate is
absorbed into the plasma increasing pH of plasma as
bicarbonate binds with free H+
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METABOLIC ALKALOSISMETABOLIC ALKALOSIS
•Commercially prepared alkaline products for gastric hyperacidity are not
absorbed from the digestive tract and do not alter the pH status of the plasma
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METABOLIC ALKALOSISMETABOLIC ALKALOSIS•2 (Vomiting (abnormal loss of HCl)
–Excessive loss of H+
Gastric juices contain large amounts of HClHCl
During HClHCl secretion, bicarbonate is added to the plasma
The bicarbonate is neutralized as HClHCl is reabsorbed by the plasma from the digestive tract
During vomiting H+H+ is lost as HClHCl and the bicarbonate is not
neutralized in the plasmaLoss of HClHCl increases the
plasma bicarbonate and thus results in an increase in pHpH
of the blood
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METABOLIC ALKALOSISMETABOLIC ALKALOSIS
•Reaction of the body to alkalosis is to lower pH by:
–Retain CO2 by decreasing breathing rate–Kidneys increase the retention of H+
CO2 CO2
H+
H+
H+
H+
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MIXED DISORDERSMIXED DISORDERS
.
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Mixed Acid-Base DisordersMixed Acid-Base Disorders
•Patients may have two or more acid-base disorders at one time
•Delta GapDelta HCO3 = HCO3 + Change in anion gap
< 24 = metabolic alkalosis
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Mixed Acid-base Disorders are Mixed Acid-base Disorders are CommonCommon
In chronically ill respiratory patients, mixed disorders are probably more common than single disorders, e.g., RAc
+ MAlk, RAc + Mac, Ralk + MAlk.
In renal failure (and other conditions) combined MAlk + MAc is also encountered.
Always be on the lookout for mixed acid-base disorders. They can be missed!
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Tips to Diagnosing Mixed Tips to Diagnosing Mixed Acid-base DisordersAcid-base Disorders
TIP 1. Do not interpret any blood gas data for acid-base diagnosis without closely examining
the serum electrolytes: Na+, K+, Cl-, and CO2 .•A serum CO2 out of the normal range always represents some
type of acid-base disorder (barring lab or transcription error).•High-serum CO2 indicates metabolic alkalosis &/or
bicarbonate retention as compensation for respiratory acidosis.
•Low-serum CO2 indicates metabolic acidosis &/or bicarbonate excretion as compensation for respiratory alkalosis.
•Note that serum CO2 may be normal in the presence of two or more acid-base disorders.
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Tips to Diagnosing Mixed Acid-base Tips to Diagnosing Mixed Acid-base Disorders Disorders (cont.)(cont.)
TIP 2. Single acid-base disorders do not lead to normal blood pH. Although pH can end up in the normal range
(7.35 - 7.45) with a single mild acid-base disorder, a truly normal pH with distinctly abnormal HCO3
- and PaCO2 invariably suggests two or more primary disorders .
Example: pH 7.40, PaCO2 20 mm Hg, HCO3- 12 mEq/L in a
patient with sepsis. Normal pH results from two co-existing and unstable acid-base disorders - acute respiratory alkalosis and
metabolic acidosis.
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Tips to Diagnosing Mixed Acid-base Tips to Diagnosing Mixed Acid-base Disorders Disorders (cont)(cont)
TIP 3. Simplified rules predict the pH and HCO3- for a given
change in PaCO2. If the pH or HCO3- is higher or lower
than expected for the change in PaCO2, the patient probably has a metabolic acid-base disorder as well .
The next slide shows expected changes in pH and HCO3- (in
mEq/L) for a 10-mm Hg change in PaCO2 resulting from either primary hypoventilation (respiratory acidosis) or
primary hyperventilation (respiratory alkalosis).
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Expected changes in pH and HCOExpected changes in pH and HCO33-- for for a 10-mm Hg a 10-mm Hg
changechange in PaCOin PaCO22 resulting from either primary resulting from either primary hypoventilation (respiratory acidosis) or primary hypoventilation (respiratory acidosis) or primary
hyperventilation (respiratory alkalosis)hyperventilation (respiratory alkalosis):: ACUTE CHRONIC
Resp Acidosis
pH ↓ by 0.07pH ↓ by 0.03HCO3
- ↑ by 1*HCO3- ↑ by 3 - 4
Resp AlkalosispH ↑ by 0.08pH ↑ by 0.03HCO3
- ↓ by 2HCO3- ↓ by 5
Units for HCO3- are mEq/L
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Predicted changes in HCOPredicted changes in HCO33-- for a directional for a directional
change in PaCOchange in PaCO22 can help uncover mixed can help uncover mixed
acid-base disordersacid-base disorders . .(aA normal or slightly low HCO3
- in the presence of hypercapnia suggests a concomitant metabolic acidosis, e.g., pH 7.27,
PaCO2 50 mm Hg, HCO3- 22 mEq/L. Based on the rule for
increase in HCO3- with hypercapnia, it should be at least 25
mEq/L in this example; that it is only 22 mEq/L suggests a concomitant metabolic acidosis.
b)A normal or slightly elevated HCO3- in the presence of hypocapnia
suggests a concomitant metabolic alkalosis, e.g., pH 7.56, PaCO2 30 mm Hg, HCO3
- 26 mEq/L. Based on the rule for decrease in HCO3
- with hypocapnia, it should be at least 23 mEq/L in this example; that it is 26 mEq/L suggests a
concomitant metabolic alkalosis.
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TIP 4. In maximally-compensated metabolic acidosis, the numerical value of PaCO2 should be the same
(or close to) as the last two digits of arterial pH. This observation reflects the formula for expected
respiratory compensation in metabolic acidosis:Expected PaCO2 = [1.5 x serum CO2] + (8 ± 2)
In contrast, compensation for metabolic alkalosis (by increase in PaCO2) is highly variable, and in some cases there may be no or
minimal compensation.
Tips to Diagnosing Mixed Acid-base Tips to Diagnosing Mixed Acid-base Disorders Disorders (cont.)(cont.)
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RESPONSES TO:RESPONSES TO:ACIDOSIS AND ALKALOSISACIDOSIS AND ALKALOSIS
•Mechanisms protect the body against life-threatening changes in hydrogen
ion concentration–11 ( (Buffering Systems in Body FluidsBuffering Systems in Body Fluids
–22 ( (Respiratory ResponsesRespiratory Responses
–33 ( (Renal ResponsesRenal Responses
•44 ( (Intracellular Shifts of IonsIntracellular Shifts of Ions
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(1(1Buffer SystemsBuffer Systems 2) Respiratory Responses2) Respiratory Responses3) Renal Responses3) Renal Responses4) Intracellular Shifts of Ions4) Intracellular Shifts of Ions
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BUFFERSBUFFERS•A buffer is a combination of chemicals
in solution that resists any significant change in pHpH
•Able to bind or release free HH++ ions
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BUFFERSBUFFERS•Buffering systems provide an
immediate response to fluctuations in pH: pH: 1) Phosphate1) Phosphate
–22 ( (ProteinProtein
–33 ( (Bicarbonate Buffer SystemBicarbonate Buffer System
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121
BUFFERSBUFFERS•Chemical buffers are able to react immediately
(within milliseconds)
•Chemical buffers are the first line of defense for the body for fluctuations in pHpH
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122
•Regulates pHpH within the cells and the urine
–Phosphate concentrations are higher intracellularly and within the kidney tubules
–Too low of aconcentration in
extracellular fluidto have much
importance as anECFECF buffer system
PHOSPHATE BUFFER PHOSPHATE BUFFER SYSTEMSYSTEM
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•11 ( (Phosphate buffer systemPhosphate buffer system
Na2HPO4 + H+ NaH2PO4 +
Na+ –Most important in the intracellular system
PHOSPHATE BUFFER PHOSPHATE BUFFER SYSTEMSYSTEM
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PROTEIN BUFFER SYSTEMPROTEIN BUFFER SYSTEM
•22 ( (Protein Buffer SystemProtein Buffer System–Behaves as a buffer in both plasma and
cells
–Hemoglobin is by far the most important protein buffer
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PROTEIN BUFFER SYSTEMPROTEIN BUFFER SYSTEM
•Proteins are excellent buffers because they contain both acid and base groups
that can give up or take up HH++
•Proteins are extremely abundant in the cell
•The more limited number of proteins in the plasma reinforce the bicarbonate
system in the ECFECF
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PROTEIN BUFFER SYSTEMPROTEIN BUFFER SYSTEM•Hemoglobin buffers HH++ from metabolically
produced COCO22 in the plasma only
•As hemoglobin releases OO22 it gains a great affinity for HH++
HHbb
O2
O2 O2
O2
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BICARBONATE BUFFER BICARBONATE BUFFER SYSTEMSYSTEM
•33 ( (Bicarbonate Buffer SystemBicarbonate Buffer System–Predominates in extracellular fluid (ECFECF)
HCOHCO33- - + added H+ added H++ H H22COCO33
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BICARBONATE BUFFER BICARBONATE BUFFER SYSTEMSYSTEM
•This system is most important because the concentration of both components can
be regulated:–Carbonic acidCarbonic acid by the respiratory system
•BicarbonateBicarbonate by the renal system
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BICARBONATE BUFFER SYSTEMBICARBONATE BUFFER SYSTEM
•HH22COCO33 <=> HH++ + HCO + HCO33--
–Hydrogen ions generated by metabolism or by ingestion react with bicarbonate base
to form more carbonic acid
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BICARBONATE BUFFER SYSTEMBICARBONATE BUFFER SYSTEM
•Equilibrium shifts toward the formation of acid
–Hydrogen ions that are lost (vomiting) causes carbonic acid to dissociate yielding
replacement HH++ and bicarbonate
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Loss of HCl
Addition of lactic acid
BICARBONATE BUFFER BICARBONATE BUFFER SYSTEMSYSTEM
HH++ HCOHCO33--
HH22COCO33HH22
OOCOCO22+ ++
Exercise
Vomiting
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RESPIRATORY RESPONSERESPIRATORY RESPONSE•Neurons in the medulla oblongata and
pons constitute the Respiratory CenterRespiratory Center•Stimulation and limitation of respiratory
rates are controlled by the respiratory center
•accomplished byresponding to CO2
and H+
concentrations inthe blood
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CHEMOSENSITIVE AREASCHEMOSENSITIVE AREAS•Chemosensitive areas of the respiratory
center are able to detect blood concentration levels of CO2 and H+
•Increases in CO2 and H+ stimulate the respiratory center
–The effect is to raiserespiration rates
•But the effectdiminishes in1 - 2 minutes
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CHEMOSENSITIVE AREASCHEMOSENSITIVE AREAS•The effect of
stimulating the respiratory centers by increased CO2 and H+
is weakened in environmentally
increased CO2 levels
•Symptoms may persist for several days
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CHEMORECEPTORSCHEMORECEPTORS•Chemoreceptors are also present in the
carotidcarotid and aorticaortic arteries which respond to changes in partial pressures of O2 and CO2
or pH•Increased levels of
CO2 (low pHpH) ordecreased levels of
O2 stimulaterespiration rates
to increase
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CHEMORECEPTORSCHEMORECEPTORS•Overall compensatory response is:
–HyperventilationHyperventilation in response to increased CO2 or H+ (low pHpH)
–HypoventilationHypoventilation in response to decreased CO2 or H+ (high pHpH)
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RENAL RESPONSERENAL RESPONSE•The kidney compensates for Acid - Acid -
BaseBase imbalance within 24 hours and is responsible for long term control
•The kidney in response:–To AcidosisTo Acidosis
•Retains bicarbonate ions and eliminates hydrogen ions
–To AlkalosisTo Alkalosis•Eliminates bicarbonate ions and retains
hydrogen ions
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Intracellular Shifts of IonsIntracellular Shifts of Ions
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HYPERKALEMIAHYPERKALEMIA•HyperkalemiaHyperkalemia is generally associated
with acidosis–Accompanied by a shift of H+ ions into
cells and K+ ions out of the cell to maintain electrical neutrality
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HYPOKALEMIAHYPOKALEMIA•HypokalemiaHypokalemia is generally associated with
reciprocal exchanges of H+ and K+ in the opposite direction
–Associated with alkalosis
•Hypokalemia is a depressed serum K+
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ELECTROLYTE SHIFTSELECTROLYTE SHIFTS
cell
HH++
KK++
AcidosisAcidosisCompensatory Response Result
- HH++ buffered intracellularly
- Hyperkalemia
HH++
KK++
cell
AlkalosisAlkalosisCompensatory Response Result
- Tendency to correct alkalosis
- Hypokalemia
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Arterial Blood Gases: Arterial Blood Gases: Test Your Overall UnderstandingTest Your Overall Understanding
Case 1. A 55-year-old man is evaluated in the pulmonary lab for shortness of breath. His regular medications include a diuretic for hypertension and one aspirin a day. He smokes a pack of cigarettes a day.
FIO2 .21 HCO3- 30 mEq/L
pH 7.53 %COHb 7.8%
PaCO2 37 mm Hg Hb 14 gm%
PaO2 62 mm Hg CaO2 16.5 ml O2/dl SaO2 87%
How would you characterize his state of oxygenation, ventilation, and acid-base balance?
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Arterial Blood Gases: Arterial Blood Gases: Test Your Overall UnderstandingTest Your Overall Understanding
Case 1 - Discussion
OXYGENATION: The PaO2 and SaO2 are both reduced on room air. Since P(A-a)O2 is elevated (approximately 43 mm Hg), the low PaO2 can be attributed to V-Q imbalance, i.e., a pulmonary problem. SaO2 is reduced, in part from the low PaO2 but mainly from elevated carboxyhemoglobin, which in turn can be attributed to cigarettes. The arterial oxygen content is adequate.
VENTILATION: Adequate for the patient's level of CO2 production; the patient is neither hyper- nor hypo-ventilating.
ACID-BASE: Elevated pH and HCO3- suggest a state of metabolic alkalosis,
most likely related to the patient's diuretic; his serum K+ should be checked
for hypokalemia.
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Arterial Blood Gases: Arterial Blood Gases: Test Your Overall UnderstandingTest Your Overall Understanding
Case 2. A 46-year-old man has been in the hospital two days with pneumonia. He was recovering but has just become diaphoretic, dyspneic, and hypotensive. He is breathing oxygen through a nasal cannula at 3 l/min.
pH 7.40
PaCO2 20 mm Hg
%COHb 1.0%
PaO2 80 mm Hg
SaO2 95%
Hb 13.3 gm%
HCO3- 12 mEq/L
CaO2 17.2 ml O2/dl
How would you characterize his state of oxygenation, ventilation, and acid-base balance?
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Arterial Blood Gases: Arterial Blood Gases: Test Your Overall UnderstandingTest Your Overall Understanding
Case 2 - Discussion
OXYGENATION: The PaO2 is lower than expected for someone hyperventilating to this degree and receiving supplemental oxygen, and points to significant V-Q imbalance. The oxygen content is adequate.
VENTILATION: PaCO2 is half normal and indicates marked hyperventilation.
ACID-BASE: Normal pH with very low bicarbonate and PaCO2 indicates combined respiratory alkalosis and metabolic acidosis. If these changes are of sudden onset, the diagnosis of sepsis should be strongly considered, especially in someone with a documented infection.
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Arterial Blood Gases: Arterial Blood Gases: Test Your Overall UnderstandingTest Your Overall Understanding
Case 3. A 58-year-old woman is being evaluated in the emergency department for acute dyspnea.
FIO2 .21
pH 7.19
PaCO2 65 mm Hg
%COHb 1.1%
PaO2 45 mm Hg
SaO2 90%
Hb 15.1 gm%
HCO3- 24 mEq/L
CaO2 18.3 ml O2/dl
How would you characterize her state of oxygenation, ventilation, and acid-base balance?
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Arterial Blood Gases: Arterial Blood Gases: Test Your Overall UnderstandingTest Your Overall Understanding
Case 3 - Discussion
OXYGENATION: The patient's PaO2 is reduced for two reasons - hypercapnia and V-Q imbalance - the latter apparent from an elevated P(A-
a)O2 (approximately 27 mm Hg).
VENTILATION: The patient is hypoventilating.
ACID-BASE: pH and PaCO2 are suggestive of acute respiratory acidosis plus metabolic acidosis; the calculated HCO3
- is lower than expected from acute respiratory acidosis alone.
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ENDEND ACID - BASE ACID - BASE
BALANCEBALANCE
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[
ENDEND