arterialbloodgasanalysisinterpretationegh nsg forumpalestine com 111226102625 phpapp02

116

Upload: yaqoobmd

Post on 08-Oct-2015

2 views

Category:

Documents


0 download

DESCRIPTION

ABGs

TRANSCRIPT

  • Arterial Blood Gas Analysis & interpretation

    Mohammed A. El-haj MPH07/12/2011

  • What is an ABG?The ComponentspH / PaCO2 / PaO2 / HCO3 / O2sat / BEDesired RangespH - 7.35 - 7.45PaCO2 - 35-45 mmHgPaO2 - 80-100 mmHgHCO3 - 21-27O2sat - 95-100%Base Excess - +/-2 mEq/L

  • Why Order an ABG?Aids in establishing a diagnosis Helps guide treatment planAids in ventilator managementImprovement in acid/base management allows for optimal function of medicationsAcid/base status may alter electrolyte levels critical to patient status/care

  • LogisticsWhen to order an arterial line --Need for continuous BP monitoringNeed for multiple ABGsWhere to place -- the optionsRadialFemoral BrachialDorsalis PedisAxillary

  • Acid Base BalanceThe body produces acids daily15,000 mmol CO250-100 mEq Nonvolatile acids

    The lungs and kidneys attempt to maintain balance

  • Acid Base BalanceAssessment of status via bicarbonate-carbon dioxide buffer system

    CO2 + H2O H2CO3 HCO3- + H+

    pH = 6.10 + log ([HCO3] / [0.03 x PCO2])

  • Normal values

  • Compensation 7.4

    7.35 7.45Partial compensated Partial

  • Respiratory AcidosispH, CO2, VentilationCausesCNS depressionPleural diseaseCOPD/ARDSMusculoskeletal disordersCompensation for metabolic alkalosis

  • Respiratory AcidosisAcute vs ChronicAcute - little kidney involvement. Buffering via titration via Hb for examplepH by 0.08 for 10mmHg in CO2Chronic - Renal compensation via synthesis and retention of HCO3 (Cl to balance charges hypochloremia)pH by 0.03 for 10mmHg in CO2

  • Respiratory AlkalosispH, CO2, Ventilation CO2 HCO3 (Cl to balance charges hyperchloremia)CausesIntracerebral hemorrhageSalicylate and Progesterone drug usageAnxiety lung complianceCirrhosis of the liverSepsis

  • Respiratory AlkalosisAcute vs. ChronicAcute - HCO3 by 2 mEq/L for every 10mmHg in PCO2Chronic - Ratio increases to 4 mEq/L of HCO3 for every 10mmHg in PCO2

    Decreased bicarb reabsorption and decreased ammonium excretion to normalize pH

  • Metabolic AcidosispH, HCO312-24 hours for complete activation of respiratory compensation PCO2 by 1.2mmHg for every 1 mEq/L HCO3 The degree of compensation is assessed via the Winters Formula PCO2 = 1.5(HCO3) +8 2

  • The CausesMetabolic Gap Acidosis

    M - MethanolU - UremiaD - DKAP - ParaldehydeI - INHL - Lactic AcidosisE - Ehylene GlycolS - Salicylate

    Non Gap Metabolic Acidosis

    HyperalimentationAcetazolamideRTA (Calculate urine anion gap)DiarrheaPancreatic Fistula

  • Metabolic AlkalosispH, HCO3 PCO2 by 0.7 for every 1mEq/L in HCO3CausesVomitingChronic diarrheaHypokalemiaRenal Failure

  • Mixed Acid-Base DisordersPatients may have two or more acid-base disorders at one time

    Delta GapDelta HCO3 = HCO3 + Change in anion gap >24 = metabolic alkalosis

  • The six steps to ABGs analysisLook at the pH if it is normal/acidotic/alkaloticLook at the PaCO2 if it is normal/acidotic/alkaloticLook at the HCO3 if it is normal/acidotic/alkaloticIf the pH match with the PCO2 or with the HCO3 If the value goes opposite direction of the pH (determine the compensation).Look at the Po2 and oxygen saturation

  • Sample problempH 7.49PCO2 40HCO3 28Uncompensated metabolic alkalosisVomiting/dearrheaIn this example the Bicarb is matching the pHNo compensation (Partial)

  • Sample problempH 7.10PCO2 25HCO3 7Uncompensated metabolic acidosisDKA/Dearrhea/shock/bleeding/sepsisIn this example the Bicarb is matching the pHNo compensation (Partial)Severe metabolic acidosis

  • Sample problempH 7.42PCO2 18HCO3 11PO2 150O2 sat 99%compensated respiratory alkalosisThis pt is hyperventilated for too long (blowing off CO2)

  • Sample problempH 7.35PCO2 60HCO3 32PO2 92O2 sat 96%

    No need for correction or treatment because pH is normalCompensation is bringing the pH to the side of 7.4 but doesn't to the opposite side (stop in 7.4)

  • Sample problempH 7.37PCO2 33HCO3 18

    Metabolic acidosisFully compensated

  • Sample problempH 7.36PCO2 62HCO3 34PO2 70O2 sat. 90%

    Respiratory acidosisFully compensatedE.g. COPD

  • Respiratory AlkalosisMost common causes of respiratory alkalosis are:Hypoxemia ( PaO2< 60mmHg and O2 sat.
  • hypoxemiaConditions causing V/Q (Ventilation perfusion) miss matchShunt: loss of alveolar surface areaDead spaceDiffusion defect

  • Danger a headHypoxemia

    Respiratory alkalosisIncreased W.O.BMusclefatigueRespiratoryAcidosis

  • Danger a head( Hypoxemia causing fatigue and respiratory acidosis)

    In the path from respiratory alkalosis to respiratory acidosis, the acid/base will temporarily appear normal, however the Ve (minute ventilation) will be increased (and probably the W.O.B)

    RespiratoryAlkalosisNormal ABGRespiratoryAcidosis

  • Case 1A 26 year old man with unknown past medical history is brought in to the ER by ambulance, after friends found him unresponsive in his apartment. He had last been seen at a party four hours prior.ABG: pH 7.25Chem : Na+ 137 PCO2 60K+ 4.5 HCO3- 26Cl- 100 PO2 55 HCO3- 25

  • Case 2A 67 year old man with diabetes and early diabetic nephropathy (without overt renal failure) presents for a routine clinic visit. He is currently asymptomatic. Because of some abnormalities on his routine blood chemistries, you elect to send him for an ABG.

    ABG: pH 7.35Chem : Na+ 135 PCO2 34K+ 5.1 HCO3- 18Cl- 110 PO292 HCO3- 16 Cr 1.4

    Urine pH:5.0

  • Case 3A 68 year old woman with metastatic colon cancer presents to the ER with 1 hour of chest pain and shortness of breath. She has no known previous cardiac or pulmonary problems.

    ABG: pH 7.49Chem : Na+ 133 PCO2 28K+ 3.9 HCO3- 21Cl- 102 PO2 52HCO3- 22

  • DefinitionsAcidemia: Blood pH < 7.35Alkalemia: Blood pH > 7.45Acidosis:is a process that will result in acidemia if left unopposed. Alkalosis:is a process that will result in alkalemia if left unopposed Metabolic refers to a disorder that results from a primary alteration in [H+] or [HCO3-].Respiratory refers to a disorder that results from a primary alteration in PCO2 due to altered CO2 elimination. Normal HCO3- 24 meq/L; Normal PCO2 40 mm Hg ; Normal pH 7.35-7.45

  • Definitions (Continued)

    PH: - is a negative logarithm of Hydrogen ion concentration; and it is the initials of these two wards (puiessence Hydrogen) that mean the power of hydrogen

  • Definitions (Continued)An acid: - is a hydrogen ion or proton donor, and a substance which causes a rise in H+ concentration on being added to water. A base: - is a hydrogen ion or proton acceptor, and a substance which causes a rise in OH- concentration when added to water. Strength of acids or bases refers to their ability to donate and accept H+ ions respectively.

  • Importance of acid-base balanceThe hydrogen ion (H+)concentration must be precisely maintained within a narrow physiological range

    Small changes from normal can produce marked changes in enzyme activity & chemical reactions within the body

  • Acidosis - CNS depression, coma (pH ~ 6.9) Alkalosis - CNS excitability, tetany, siezures Hydrogen ion concentration is most commonly expressed as pH (= negative logarithm of the H+ concentration)

  • ACID-BASE CALCULATIONSThe Henderson equation is easier to use, but only applies when pH is between 7.2 and 7.6. For this equation, one must calculate [H+] from pH. [H+] = 40 nEq/L when pH is 7.4. The [H+] increases 10 nEq/L for a 0.1 unit drop in pH.Henderson Eq. [H+] = 24 PCO2 / [HCO3-]

  • phH+ (nmol/l) 71007.1807.2637.3507.36447.4407.44367.5327.6257.720

  • Normal pH:

    Arterial blood: 7.35 - 7.45 Venous blood, interstitial fluid: 7.35 Intracellular: 6.0-7.4 (average 7.0)

  • Regulation of pH*Buffer systems - very rapid (seconds), incomplete *Respiratory responses - rapid (minutes), incomplete *Renal responses - slow (hours to days), complete

  • Background H+ + H+CO3- H2CO3 H2O + CO2

    -Metabolic Disorders: Affect HCO3-: (Normal 22-26 meq/L) -Metabolic Acidosis Acid neutralizes HCO3- H+CO3-, pH -Metabolic Alkalosis H+CO3- Production Drives Rxn to Right H+ pH

  • Primary Abnormality in Acid Base DisordersH+ + H+CO3- H2CO3 H2O + CO2

    AcidosisAlkalosisRespiratory pCO2Metabolic

  • Primary Abnormality in Acid Base DisordersH+ + H+CO3- H2CO3 H2O + CO2

    AcidosisAlkalosisRespiratory pCO2 pCO2Metabolic

  • Primary Abnormality in Acid Base DisordersH+ + H+CO3- H2CO3 H2O + CO2

    AcidosisAlkalosisRespiratory pCO2 pCO2Metabolic H+CO3-

  • Primary Abnormality in Acid Base DisordersH+ + H+CO3- H2CO3 H2O + CO2

    AcidosisAlkalosisRespiratory pCO2 pCO2Metabolic H+CO3- H+CO3-

  • Simple Acid-Base Disorders:

    Type of Disorder

    pH

    PaCO2

    [HCO3]

    Metabolic Acidosis

    (

    (

    (

    Metabolic Alkalosis

    Acute Respiratory Acidosis

    Chronic Respiratory Acidosis

    Acute Respiratory Alkalosis

    Chronic Respiratory Alkalosis

  • Simple Acid-Base Disorders:

    Type of Disorder

    pH

    PaCO2

    [HCO3]

    Metabolic Acidosis

    Metabolic Alkalosis

    (

    (

    Acute Respiratory Acidosis

    Chronic Respiratory Acidosis

    Acute Respiratory Alkalosis

    Chronic Respiratory Alkalosis

  • Simple Acid-Base Disorders:

    Type of Disorder

    pH

    PaCO2

    [HCO3]

    Metabolic Acidosis

    Metabolic Alkalosis

    (

    (

    (

    Acute Respiratory Acidosis

    Chronic Respiratory Acidosis

    Acute Respiratory Alkalosis

    Chronic Respiratory Alkalosis

  • Simple Acid-Base Disorders:

    Type of Disorder

    pH

    PaCO2

    [HCO3]

    Metabolic Acidosis

    Metabolic Alkalosis

    Acute Respiratory Acidosis

    (

    (

    Chronic Respiratory Acidosis

    (

    (

    Acute Respiratory Alkalosis

    Chronic Respiratory Alkalosis

  • Simple Acid-Base Disorders:

    Type of Disorder

    pH

    PaCO2

    [HCO3]

    Metabolic Acidosis

    Metabolic Alkalosis

    Acute Respiratory Acidosis

    (

    (

    (

    Chronic Respiratory Acidosis

    (

    (

    ((

    Acute Respiratory Alkalosis

    Chronic Respiratory Alkalosis

  • Simple Acid-Base Disorders:

    Type of Disorder

    pH

    PaCO2

    [HCO3]

    Metabolic Acidosis

    Metabolic Alkalosis

    Acute Respiratory Acidosis

    Chronic Respiratory Acidosis

    Acute Respiratory Alkalosis

    (

    (

    Chronic Respiratory Alkalosis

    (

    (

  • Simple Acid-Base Disorders:

    Type of Disorder

    pH

    PaCO2

    [HCO3]

    Metabolic Acidosis

    Metabolic Alkalosis

    Acute Respiratory Acidosis

    Chronic Respiratory Acidosis

    Acute Respiratory Alkalosis

    (

    (

    (

    Chronic Respiratory Alkalosis

    (

    (

    ((

  • Simple Acid-Base Disorders:

    Type of Disorder

    pH

    PaCO2

    [HCO3]

    Metabolic Acidosis

    (

    (

    (

    Metabolic Alkalosis

    (

    (

    (

    Acute Respiratory Acidosis

    (

    (

    (

    Chronic Respiratory Acidosis

    (

    (

    ((

    Acute Respiratory Alkalosis

    (

    (

    (

    Chronic Respiratory Alkalosis

    (

    (

    ((

  • CompensationFor each acid-base disorder , there is a compensatory response mediated by the kidneys or the lungs that tends to bring the pH back towards normal. Compensation is never complete (i.e. pH never returns to 7.4). Therefore if the pH < 7.4, the primary process is an acidosis. If the pH > 7.4 the primary process is an alkalosis

  • Compensated Abnormality in Acid Base Disorders H+CO3- H+CO3- pCO2 pCO2H+ + H+CO3- H2CO3 H2O + CO2

    AcidosisAlkalosis1 Respiratory

    Compensation pCO2 pCO2 1 Metabolic

    Compensation H+CO3- H+CO3-

  • Compensation (Continued)Formulas predict normal compensation in both acute and chronic conditions.Inadequate compensation tells you that something else is wrong!Metabolic compensation takes time and is more complete in chronic conditions than acutely

  • Buffer SystemsA substance that can prevent major changes in the pH of body fluids by removed or releasing hydrogen ions ,they can act quickly to prevent excessive changes in hydrogen ion concentration Bicarbonate, phosphate and protein buffering systems are the three major buffering systems

  • Bicarbonate buffer system

    *Primary extracellular buffer system (>50% of extracellular buffering) *Accurate assessment - readily calculated from PCO2 and pH using available blood gas machines *Consists of carbonic acid (weak acid) and bicarbonate

  • *CO2 regulated by the lungs - rapidly*HCO3- is regulated by the kidneys slowly *Not powerful *pKa = 6.1)the pK of a buffer system identifies the pH at which the concentration of acid and base in that system is equal)

  • Protein buffer system*Most powerful *75 % of all intracellular buffering *Hemoglobin -important extracellular buffer due to large concentration of hemoglobin in blood -buffering capacity varies with oxygenation -reduced hemoglobin is a weaker acid than oxyhemoglobin -dissociation of oxyhemoglobin results in more base available to combine w/ H+

  • Plasma protein

    *acid buffer *important intracellular buffer system

  • Phosphate buffer system

    *H2PO4- and HPO42- *important renal buffering system*extracellular concentration, 1/12 that of bicarbonate *pKa = 6.8 *phosphate is concentrated in the renal tubules

  • Respiratory Responsesoccurs within minutes of alteration in pH due to stimulation/depression of respiratory centers in the CNS H+ acts directly on respiratory center in Medulla Oblongata alveolar ventilation increases/decreases in response to changes in CO2 alveolar ventilation is inversely proportional to PaCO2 *2 x ventilation pH 7.4 to 7.63 * ventilation pH 7.4 to 7.0 incomplete response because as the change in alveolar ventilation brings pH back towards normal, the stimulus responsible for the change in ventilation decreases .

  • Renal Responsesthe kidneys regulate pH by either acidification or alkalinization of the urine complex response that occurs primarily in the proximal renal tubules with acidosis, rate of H+ secretion exceeds HCO3- filtration with alkalosis, rate of HCO3- filtration exceeds H+ secretion occurs over hours/days, and is capable of nearly complete restoration of acid/base balance

  • Renal & Respiratory Compensation

    Primary DisorderPrimary changePredicted Compensatory ResponseMetabolic acidosis HCO31.2 PaCO2 per 1 meg HCO3Metabolic Alkalosis HCO3.7 PaCO2 per 1meq HCO3Respiratory acidosis: AcutePaCO21 meq HCO3 per 10 mm PaCO2Respiratory acidosis: ChronicPaCO23.5 meq HCO3 per 10 mm PaCO2Respiratory alkalosis: AcutePaCO22 meq HCO3 per 10mm PaCO2Respiratory alkalosis: ChronicPaCO24 meq HCO3 per 10mm PaCO2

  • SUMMARY OF SIMPLE ACID-BASE DISORDERS AND COMPENSATION

    Primary Acid-Base Disorder Primary Defect Effect onpH Compensatory Response Expected Range of Compensation Limits of Compensation Respiratory Acidosis Hypoventilation (PCO2) HCO3- Generation [HCO3-] =1-4 mEq/L for each 10 mm Hg PCO2 [HCO3-] =45 mEq/L Respiratory AlkalosisHyperventilation (PCO2) HCO3- Consumption [HCO3-] =2-5 mEq/L for each 10 mm Hg PCO2 [HCO3-] =12-15 mEq/L Metabolic Acidosis Loss of HCO3- or gain of H+( HCO3-) Increase in Ventilation(PCO2) PCO2 =1.5[HCO3-] + 8 PCO2 =12-14 mm Hg Metabolic Alkalosis Gain of HCO3- or loss of H+( HCO3-) Decrease in Ventilation (PCO2 ( PCO2 =0.6 mm Hg for each 1 mEq/L [HCO3-] PCO2 =55 mm Hg

  • GENERAL ASPECTS OF ACID-BASE DISORDERS A primary alteration in [H+], [HCO3-] or PCO2 results in abnormal pH. The body has several mechanisms to correct pH towards the normal range. -In the acute phase (minutes to hours), the extra- and intra-cellular buffer systems (most importantly the bicarbonate system) minimize the pH changes. - In the chronic phase (hours to days), renal or respiratory compensation partially or completely restore pH towards normal. There are limits to both types of compensation. Compensation does not result in over correction of pH.

  • DATA REQUIRED TO DIAGNOSE ACID-BASE DISORDERSAn arterial blood gas shows the blood pH, PCO2 and [HCO3-]. A chemistry panel shows the [total CO2], [Cl-], [K+] and [Na+], [glucose], [BUN] and [creatinine]. The [total CO2] is the sum of the measured [CO2] + [HCO3-]. Thus the [HCO3-] from the blood gas and the [total CO2] from the electrolyte panel usually are within 2 mEq/L. Otherwise the measurements are in error or were taken at different times.

  • NORMAL LABORATORY VALUES Arterial Blood Gas: pH7.35-7.45[H+]35-45 nmol/L or neq/LPCO235-45 mm Hg[HCO3-]22-26 mmol/L or mEq/LPlasma Electrolytes [Na+] 135-145 mEq/L [K+ ]3.5-5.0 mEq/L [Cl-]96-109 mEq/L [total CO2]24-30 mEq/L

  • SIMPLE ACID-BASE DISORDERSSimple acid-base disorders have one primary abnormality. The four primary disorders are respiratory acidosis, respiratory alkalosis, metabolic acidosis and metabolic alkalosis.Mixed acid-base disorders have more than one abnormality. Two to three primary disorders can be combined together to result in a mixed disorder.

  • Metabolic AcidosisSecondary to Acid production or H+CO3- lossCharacterized by low serum H+CO3-( by hyperventilation PCO2 HCO3- )Divided into two categories:Anion gap metabolic acidosis (High anion gap)NonAnion gap metabolic acidosis (Normal anion gap)

  • Anion GapThe anion gap (AG) represents the difference between the major plasma cations and anions ,and reflects usually unmeasured anions such as sulfate. Anion Gap = [Na+] - ( [H+CO3-] + [Cl-] )Normal 14 +/- 2

  • Why does this help us in patients with metabolic acidosis?Secondary to Acid production or H+CO3- lossIn disorders associated with acid production there anions accumulate anion gap whereasIn disorders associated with H+CO3- loss, there is no accumulation of unmeasured anions and the anion gap is normal

  • Unmeasured anions which accumulate Anion Gap AcidosisLactateKetonesSulfates and phosphatesOther organic acids

  • NameTitle

    NameTitle

    NameTitle

    NameTitle

    NameTitle

    NameTitle

    Team Title

    Name

    Company Name

    Company NameDepartment Name

    Metabolic Acidosis

    Anion Gap Acidosis

    NonAnion Gap Acidosis

    Ketoacidosis

    Uremic Acidosis

    Lactic Acidosis

    Organic Acidosis

  • Lactic AcidosisFundamentally what causes a lactic acidosis?Answer: Anaerobic metabolism

  • The differential diagnosis of Lactic AcidosisLactic acidosis occurs whenever the cells are unable to utilize aerobic respiration: i.e. whenever the cells are unable to obtain or utilize oxygenConsider Murphys law: Whatever can go wrong will go wrong! (i.e. take each step in oxygen absorption and distributionany one of them can go away and cause lactic acidosis.)

  • The differential diagnosis of Lactic Acidosis (2)Low environmental O2Inability to absorb O2O2 unable to bind HgUnable to pump O2Tissues unable to utilize O2High altitudeLung DiseaseCO poisoningShock (cardiogenic)Septic shockFocal vascular obstructionCyanide poisoning

  • NameTitle

    NameTitle

    NameTitle

    NameTitle

    NameTitle

    NameTitle

    Team Title

    Name

    Company Name

    Company NameDepartment Name

    Metabolic Acidosis

    Anion Gap Acidosis

    NonAnion Gap Acidosis

    Ketoacidosis

    Uremic Acidosis

    Lactic Acidosis

    Organic Acidosis

    Lung DiseaseCO poiseningCardiogenic shockSeptic shockHypovolemic shockFocal vascular obstructionCyanide poisening

  • KetoAcidosisOccurs whenever the cells are unable to utilize glucose

  • KetoAcidosisThree etiologiesDiabetic KetoacidosisPrimarily in type 1 diabetes mellitusSevere, life threateningOften associated with precipitating illnessStarvation ketoacidosisMild acidosisAlcoholic ketoacidosisMild acidosis

  • NameTitle

    NameTitle

    Metabolic Acidosis

    Anion Gap Acidosis

    NonAnion Gap Acidosis

    Ketoacidosis

    Uremic Acidosis

    Lactic Acidosis

    Organic Acidosis

    Lung DiseaseCO poiseningShock (cardiogenic)Septic shockFocal vascular obstructionCyanide poisening

    DKA (Type 1)StarvationAlcoholic

  • Other anion gap acidosisUremiaFailure to excrete daily metabolic acid loadAccumulation of phosphates and sulfatesOrganic acidosisMethanolEthylene GlycolSalicylates

  • NameTitle

    NameTitle

    Metabolic Acidosis

    Anion Gap Acidosis

    NonAnion Gap Acidosis

    Ketoacidosis

    Uremic Acidosis

    Lactic Acidosis

    Organic Acidosis

    Lung DiseaseCO poiseningShock (cardiogenic)Septic shockFocal vascular obstructionCyanide poisening

    DKA (Type 1)StarvationAlcoholic

    MethanolEthylene GlycolSalicylate intoxication

  • Non-anion gap metabolic acidosis Bicarbonate lossDiarrheaSevere BurnsUrinary loss (renal tubular acidosis)

  • NameTitle

    NameTitle

    Metabolic Acidosis

    Anion Gap Acidosis

    NonAnion Gap Acidosis

    Ketoacidosis

    Uremic Acidosis

    Lactic Acidosis

    Organic Acidosis

    Lung DiseaseCO poiseningShock (cardiogenic)Septic shockFocal vascular obstructionCyanide poisening

    DKA (Type 1)StarvationAlcoholic

    MethanolEthylene GlycolSalicylate intoxication

    DiarrheaBurns (severe)RTA

  • Clinical ManifestationHeadacheConfusionDrowsiness RR and depthNausea and vomitingPeripheral vasodilation and decreased Cardiac output (pH 7 )BPHyperkalemias

  • Metabolic Acidosis: TreatmentTreat underlying causeAlkali replacementAcute metabolic acidosisindicated when is pH less than ~7.15goal is to raise serum [HCO3] to ~15mmol/Lbicarbonate dose = 0.5 x BW (kg) x{[HCO3]desired - [HCO3]actual}Chronic metabolic acidosisgoal of treatment is to prevent long term sequelaeserum [HCO3] should be normalized

  • Metabolic AlkalosisGeneration

    Maintenance

  • Metabolic Alkalosis: GenerationAcid lossrenal acid lossesdiuretic therapymineralocorticoid excessCushings syndromesevere potassium depletionBartters syndromeLiddles syndrome

    gastrointestinal lossesgastric acid losschloride diarrhea

  • Metabolic Alkalosis: GenerationAlkali gainbicarbonate administrationmilk alkali syndromeinfusion of organic anionscitrateacetatelactaterapid correction of chronic hypercapnia

  • Metabolic Alkalosis: MaintenanceDecreased GFRrenal failureIncreased proximal HCO3- reabsorptionchloride depletionIncreased distal tubular H+ secretion hypokalemia

  • Metabolic Alkalosis: TreatmentSaline responsiveintravascular volume expansion with normal salinepotassium repletionSaline resistantpotassium repletionmineralocorticoid antagonistsacetazolamide

  • Respiratory AcidosisThink Murphys Law againFrom Brain to alveolus, many problems can cause hypoventilation PaCO2 pH (Respiratory acidosis)

  • Respiratory AcidosisBrain

    Spinal Cord

    Peripheral NerveNeuroMuscular JunctionLung and Pleural diseaseStrokeDrug IntoxicationC spine injury,

    Guillan BarreMyasthenia GravisAsthma, COPD, ARDS, etc

  • Clinical Manifestation HypercapniaPulse RRBPMental cloudinessFeeling of fullness in the headICP HeadacheHyperkalemia

  • Respiratory AlkalosisHyperventilation PaCO2 pHEtiologiesFeverPainAnxietyPulmonary diseaseSepsisSalicylate intoxicationNeurologic disorders

  • MIXED ACID-BASE DISORDERSMixed acid-base disorders include all combinations of 2-3 simple acid base disorders. One must be able to recognize mixed acid-base disorders. This can be accomplished by examining the degree of compensation and calculating an anion gap. If the pH, PCO2 and [HCO3-] do not fit the rules of compensation for a simple disorder, one must hypothesize that there is a mixed acid-base disorder (or hypothesize that there is an error in the data).

  • If there is extreme acidemia or alkalemia, one could hypothesize multiple acid-base disorders that that are additive. If there is a mild acidemia or alkalemia, or pH is normal, particularly with an anion gap one could hypothesize multiple acid-base disorders that cancel each other out.

  • Summary of the Approach to ABGsCheck the pHCheck the pCO2Select the appropriate compensation formulaDetermine if compensation is appropriateCheck the anion gapIf the anion gap is elevated, check the delta-deltaIf a metabolic acidosis is present, check urine pHGenerate a differential diagnosis

  • Putting it Together

  • What is the clinical picture?Generate hypothesis!

    What is the pH?

    Acidemia

    Alkalemia

    Check HCO3- & PaCO2Is it respiratory or metabolic?

    Check: Is compensation appropriate?

    Check Anion Gap

    Reach Final Diagnosis

  • Case 1A 26 year old man with unknown past medical history is brought in to the ER by ambulance, after friends found him unresponsive in his apartment. He had last been seen at a party four hours prior.ABG: pH 7.25Chem 7:Na+ 137 PCO2 60K+ 4.5 HCO3- 26Cl- 100 PO255 HCO3- 25

  • Case 2A 67 year old man with diabetes and early diabetic nephropathy (without overt renal failure) presents for a routine clinic visit. He is currently asymptomatic. Because of some abnormalities on his routine blood chemistries, you elect to send him for an ABG.

    ABG: pH 7.35Chem 7:Na+ 135 PCO2 34K+ 5.1 HCO3- 18Cl- 110 PO292 HCO3- 16 Cr 1.4Urine pH:5.0

  • Case 3A 68 year old woman with metastatic colon cancer presents to the ER with 1 hour of chest pain and shortness of breath. She has no known previous cardiac or pulmonary problems.

    ABG: pH 7.49Chem 7:Na+ 133 PCO228K+ 3.9 HCO3- 21Cl- 102 PO252HCO3- 22

  • pH7.34, PaCO2 60 , HCO3- 31

    Primary DisorderPrimary changePredicted Compensatory ResponseMetabolic acidosis HCO31.2 PaCO2 per 1 meg HCO3Metabolic Alkalosis HCO3.7 PaCO2 per 1meq HCO3Respiratory acidosis: AcutePaCO21 meq HCO3 per 10 mm PaCO2Respiratory acidosis: ChronicPaCO23.5 meq HCO3 per 10 mm PaCO2Respiratory alkalosis: AcutePaCO22 meq HCO3 per 10mm PaCO2Respiratory alkalosis: ChronicPaCO24 meq HCO3 per 10mm PaCO2

  • Case 1A 52 y.o. man with COPD is admitted to the hospital with a lower extremity cellulitis.HypothesisLabs: Na+ 139, K+ 4.9, Cl- 98, HCO3- 31ABG: pH 7.34, PaCO2 60, PaO2 69Is he acidemic or alkalemic?Is this metabolic (from sepsis) or respiratory (from COPD)?Is this acute or chronic? Why does that matter?

  • Case 1: AnswerA 52 y.o. man with COPD is admitted to the hospital with a lower extremity cellulitis.Labs: Na+ 139, K+ 4.9, Cl- 98, HCO3- 31ABG: pH 7.34, PaCO2 60, PaO2 69Why is he acidemic?Is this metabolic (from sepsis) or respiratory (from COPD)?Is this acute or chronic? Why does that matter?Dx: Chronic Respiratory AcidosisNot from sepsisNo need for intubation or ICU careNote AG 10

  • Case 2A 45 y.o. man reports 6 days of persistent nausea and vomiting. PE supine BP 100/60 pulse 105; Standing BP 85/55 pulse 125. Neck veins are flatHypotheses?Labs: Na+ 140, K+ 2.2, Cl- 86, HCO3 42 BUN 80, Cr 1.9ABG: pH 7.53, PaCO2 53, PaO2 82Urine Na+ 2 meg/LAcidemic or Alkalemic?Metabolic or Respiratory?What is his acid base disorder?Why is he alkalemic? How would you fix it? Whats with the urine sodium?Answer: Metabolic alkalosis. Correct with NaCL

  • Case 379 y.o. woman with CC of abdominal painPatient c/o abdominal pain for 2 days. Pain is moderately severe & diffuse, associated with vomiting. She reports passing no bowel movements or flatus for 2 days.PE: Elderly appearing woman in moderate distress; Vital signs T 38.5, RR 20, BP 115/60, HR 95. Abdominal exam: absent bowel sounds, diffusely distended, mild tenderness, without rebound or guarding. Rectal FOBT negative

  • Case 3 (continued)Labs:WBC 18K, 82% neutrophils, 10% bandsHCT 37Na 138, K 4.2 HCO3- 6 CL 106 BUN 45 Cr. 1.0 Glucose 110ABG: pH 7.10, PaCO2 20mm Hg, PaO2 90What is her acid base disorder? What does it tell you?

  • NameTitle

    NameTitle

    Metabolic Acidosis

    Anion Gap Acidosis

    NonAnion Gap Acidosis

    Ketoacidosis

    Uremic Acidosis

    Lactic Acidosis

    Organic Acidosis

    Lung DiseaseCO poiseningShock (cardiogenic)Septic shockFocal vascular obstructionCyanide poisening

    DKA (Type 1)StarvationAlcoholic

    MethanolEthylene GlycolSalicylate intoxication

    DiarrheaBurns (severe)RTA

  • Who gets your last ICU bed? 75 y.o. WF with COPD with CC cough & SOB R.A. ABG 7.35, PaC02 60, Pa02 48.

    70 y.o. WM with COPD with CC purulent sputum, SOB. ABG on 4L 7.2, PaC02 60, Pa02 of 70

  • What is the clinical picture?Generate hypothesis!

    What is the pH?

    Acidemia

    Alkalemia

    Check HCO3- & PaCO2Is it respiratory or metabolic?

    Check: Is compensation appropriate?

    Check Anion Gap

    Reach Final Diagnosis

  • Arterial puncture

  • Problems of taking arterial blood samples Bleeding Vessel obstruction Infection

  • Allen's test. The radial and ulnar arteries are occluded by firm pressure while the fist is clenched. The hand is opened and the arteries released one at a time to check their ability to return blood flow to the hand

  • **