abg in ccu

Views:
 
Category: Entertainment
     
 

Presentation Description

No description available.

Comments

Presentation Transcript

ABG ANALYSIS IN CCU:

ABG ANALYSIS IN CCU dr.anil sathyadas january o9

pH:

pH The term pH was coined by the Danish chemist, Soren Peter Sorensen in 1909. He used it to refer to the negative log of hydrogen ion concentration. pH means ‘potenz’ (power) of Hydrogen . The power referred to is the power of 10 used as the base for the log and not to the acid strength of the solution.

PowerPoint Presentation:

‘pH’ which is defined as: pH = - log10[ H+] pH is the negative logarithm of H+ to the base 10 expressed in nmol/litres .

PowerPoint Presentation:

[H+] is 40 nmol/L or 0.000000040 moles/ L which is a very small number. Taking –ve log gives a number to speak of . But it disguises the magnitude of change in pH pH is just a number. No units

Site of collection:

Site of collection Radial artery Brachial artery Dorsalis pedis artery Femoral Neonate-ear lobe-aterialised

DRAWING Arterial blood for analysis :

DRAWING Arterial blood for analysis Through and through technique Single puncture technique USS Lignocaine can prevent arterial spasm

PowerPoint Presentation:

Keep area exposed Clear label-NO iv drugs Close iv administering port

PowerPoint Presentation:

Radial, brachial 20-30 o. Femoral : 70 o to skin Use 0.2-0.3 ml of lignocaine s/c Apply pressure for 5 minutes Do not forget Allen’s test 1-2 ml of blood is needed Keep sample in melting ice if transport time >5minutes Label any hazardous sample

PowerPoint Presentation:

pH 7.38-7.42 paO2 80-100 paCO2 36-44 HCO3 22-26 SaO2 95-100 7.36-7.39 38-42 44-48 20-24 75%

PROCEDURE::

PROCEDURE: * Wash hands prior to collection sample. * Assemble equipment; blood gas syringe, swabs, 5ml syringe, gauze to evacuate blood line onto. * Swab area on and around port. * Remove cap. * Attach syringe and open line to air. * Draw off line fluid and initial blood - approximately 5mls. * Discard 5ml syringe after closing 3 way stop cock _ way to both air and patient.

PROCEDURE::

PROCEDURE: Draw off sample. * Close stop cock to air. * Remove sample syringe. * Flush line. * Close stop cock to patient and flush blood line into gauze. * Discard. * Close stop cock to air. * Replace port cap.

Heparin syringe:

Heparin syringe 0.25 ml of Heparin (1000IU/ml) taken and used to rinse the syringe and then expelled Commercially available heparinised syringes with low resistance.

SPECIAL CONSIDERATIONS:

SPECIAL CONSIDERATIONS Agitate sample between palms of hands to mix blood and syringe content well prior to putting sample into machine. Samples that are being sent to the lab need to be transported on ice to prevent deterioration. Ensure correct labelling information is on blood sampling and form.

Wrong results:

Wrong results Air bubbles dilution with heparin improper transport

PowerPoint Presentation:

1. The PaCO2/[HCO3-] “rules” of the Boston school. 2. Strong ion difference (Stewart’s physical chemical approach). 3. Standard base excess (Copenhagen approach).

BOSTON:

BOSTON A/c respiratory acidosis. Expected [HCO3-]=24+(PaCO2-40)/10 Chronic respiratory acidosis. Expected [HCO3-]=24+4(PaCO2-40)/10 Acute respiratory alkalosis. Expected [HCO3-]=24-2(40-PaCO2)/10 Chronic respiratory alkalosis. Expected [HCO3-]=24- 5(40-PaCO2)/10 Metabolic acidosis. Expected PaCO2=1.5 [HCO3-]+8 Metabolic alkalosis. Expected PaCO2=0.9 [HCO3-]+9

Strong ion difference-Peter Stewart’s :

Strong ion difference- Peter Stewart’s pH and [HCO3-] are dependent variables determined by three independent variables, PaCO2, SID, total concentration of non-volatile weak acid buffer.[ATOT].

PowerPoint Presentation:

Na+, K+, Ca++, Mg++, Cl- and lactate. SID=strong cations–strong anions = 40 mEq/l.

PowerPoint Presentation:

To preserve electrical neutrality,the SID “space” is filled passively by the buffer base. The buffer base components of quantitative importance are HCO3- and “non-volatile buffer anions” (A-). Buffer base therefore=([A-]+[HCO3-]), and is numerically the same as [SID].

Standard base excess- standard bicarbonate :

Standard base excess- standard bicarbonate converted small volumes of blood to fully oxygenated specimens with a PCO2 of 40 mmHg at 38°C, and then measured the plasma pH. “Standard bicarbonate” determined by substituting the PCO2 (40 mmHg) and the measured pH value in the Henderson-Hasselbalch equation.

PowerPoint Presentation:

CO2-invariance was thus ensured by physically returning the PCO2 to 40 mmHg. Any offset of the standard bicarbonate from 24.4 mmol/l signified a metabolic acid-base process.

PowerPoint Presentation:

BE is the mmol/l of strong acid which brings the pH to 7.4 (while PCO2 continues to be maintained at 40 mmHg). BE then has a positive sign. If pH<7.4, BE is quantified by the strong base required (BE then has a negative sign). A negative BE is sometimes referred to as a “base deficit”.

:

The body’s response to a change in acid-base status has three components: First defence : Buffering Second defence : Respiratory : alteration in arterial pCO2 Third defence : Renal : alteration in HCO3- excretion Response to an Acid-Base change

PowerPoint Presentation:

Buffer refer to a solution containing substances that have the ability to minimize changes in the pH when an acid or base is added to it . The major buffers are – bicarbonate, plasma protein, haemoglobin phosphates. Buffer base and the base excess are the indicators of reserve of buffers.

PowerPoint Presentation:

The Major Body Buffer Systems Site Buffer System Comment ISF Bicarbonate For metabolic acids Phosphate Not important because concentration too low Protein Not important because concentration too low Blood Bicarbonate Important for metabolic acids Haemoglobin Important for carbon dioxide Plasma protein Minor buffer Phosphate Concentration too low ICF Proteins Important buffer Phosphates Important buffer Urine Phosphate Responsible for most of 'Titratable Acidity' Ammonia Important - formation of NH 4 + Bone Ca carbonate In prolonged metabolic acidosis

The Bicarbonate Buffer System :

The Bicarbonate Buffer System The major buffer system in the ECF Responsible for about 80% of extracellular buffering It is the most important ECF buffer for metabolic acids But it cannot buffer respiratory acid-base disorders. The components are easily measured and are related to each other by the Henderson-Hasselbalch equation.

Buffers:

Buffers H+ + HCO3  H2CO3  H2O + CO2 weak buffer corner stone

Base excess :

Base excess BE is an index of the magnitude of the metabolic contribution to an acid- base disturbance. It is a measure of the quantity of acid or base in milliequivalent needed to titrate 1 litre of blood to a pH of 7.4 at a temperature of 37  C and a PaCO 2 of 40 mm Hg.

PowerPoint Presentation:

The normal BE is in the range of  2 mEq /l . A BE less than –2 signifies the presence of metabolic acidosis A BE more than +2 signifies the presence of metabolic alkalosis. The larger the base excess value, the more severe is the metabolic alkalosis.

Henderson-Hasselbach Equation:

Henderson-Hasselbach Equation pH=pKa+ log HCO 3 PCO 2 6.1+log metabolic/respiratory Henderson equation H+ = 24x pCO2 HCO3

Basic Terminology :

Basic Terminology Acidemia is present when blood pH <7.35 Alkalemia is present when blood pH >7.45 Acidosis is a process that will result in acidemia if left unopposed. Alkalosis is a process that will result in alkalemia if left unopposed.

PowerPoint Presentation:

Metabolic refers to a disorder that results from a primary alteration in [HCO3]. Respiratory refers to a disorder that results from a primary alteration in PCO2 due to altered CO2 elimination.

Basic Principles:

Basic Principles pH=negative log H+ concentration pH of 7.4 equivalent to H+ of 40nmol/L Tolerable range = 6.8 to 7.8 Importance: Electrical charges of chemical substances Disturb vital enzymes Degree of ionisation

PowerPoint Presentation:

Arterial pH- 7.36- 7.44 venous pH- 7.32- 7.42 at 7.4 pH H+conc is 40 nmol/ l 1.25 / 0.8 method (Fagen) each 0.1 decrement 40X1.25 each increment of 0.1 40X 0.8

Analysis………………..:

Analysis……………….. Don’t forget pO2 See the pH- WNL/ acidemia/ alkalemia PCO2-WNL/ resp acidosis/ alkalosis PCO2 coincides with the pH value ? HCO3- WNL/ low/ high HCO3 coincides with pH ? pH - compensated or not ? PCO2 coincides with HCO3 ? Anion gap, electrolytes, BE, osmolar gap

PowerPoint Presentation:

For 12 mmHg a/c PCO2 change pH changes by 0.1 For 6 mmol change HCO3 pH changes by 0.1

PowerPoint Presentation:

Diabetic patient with irregular treatment presents to ED with altered level of consciousness. ABG showed pH of 7.1 pO2 90mmHg pCO2=38 mmHgHCO3=6 BE=-15 pH=7.1 HCO3= 6 (Low) Suggests metabolic ?pH corresponds to the HCO3.Delta HCO3=24-6=18. For every 6 pH changes by 0.1 so for 18 pH should change by 0.3 change from normal=7.4-0.3=7.1.So pH corresponds to HCO3

Compensation:

Compensation Compensation occurs in the other compartment Compensation usually does not return the pH to normal

PowerPoint Presentation:

pH= 7.36 pco2= 60 HCO3=26 BE=5 Here the pH does not match with pCO2. Delta CO2=20 expected pH=7.233. But pt’s pH has been compensated to near normal. How to calculate compensation?

Compensation for respiratory acidosis:

Compensation for respiratory acidosis 10 mmHg a/c rise in PCO2 - HCO3 rises by 1mEq 10 mmHg c/c rise in PCO2 - HCO3 rises by 4 mEq LIMITS: acute-till HCO3 of 30 chronic – till a HCO3 of 45

PowerPoint Presentation:

Acute on chronic respiratory failure.pH7.36 pco2= 60 HCO3=26 BE=5 Here the pH matches with pCO2. Delta co2=20 expected pH=7.23. But pts pH has been compensated to near normal. For 10 mmHg acute increase in PCO2: HCO3 increases for compensation by 1. As HCO3 is 2 near full compensation has occurred.

PowerPoint Presentation:

If there is a primary respiratory disturbance, is it acute ? .08 change in pH ( Acute ) .03 change in pH ( Chronic ) 10 mm Change PaCO 2 =

Compensation for respiratory alkalosis:

Compensation for respiratory alkalosis 10 mmHg a/c fall in PCO2 - HCO3 falls by 2 mEq 10 mmHg c/c fall in PCO2 - HCO3 falls by 4 mEq LIMITS: acute-till HCO3 of 20 chronic – till a HCO3 of 12-14

Compensation for metabolic acidosis and alkalosis:

Compensation for metabolic acidosis and alkalosis 1meq fall in HCO3 PCO2 falls by 1.25 Limit: till a PaCO2 of 10mmHg 1 meq rise in HCO3 PCO2 rise by 0.7 Limit: till a PaCO2 of 55mmHg

Compensation for Metabolic acidosis:

Compensation for Metabolic acidosis pCO2= Value after the 7 in the pH Winters formula= 1.5xHCO3 +8 +/- 2 paCO2=HCO3+15

PowerPoint Presentation:

70 yr old after laparotomy in recovery room FiO2=0.6 pH=7.3 pCO2=58 pO2=90 HCO3=25 pH-acidemia pCO2=respiratory acidosis HCO3= can be taken as normal/increased Delta pCO2=18 pH for this CO2=18x0.1/12=0.15 So expected pH=7.4-0.15=7.25 Compensation (a/c increase in PaCO2) 10----1 So for 18 HCO3 should be 18x1/10=1.8+24=25.8 So diagnosis of partially compensated respiratory acidosis

65 female DM,COPD for AKA.pH7.1 pCO2=38 pO2=88 FiO2=0.4HCO3=6 BE=-12 Na145 Cl 105 K5:

65 female DM,COPD for AKA.pH7.1 pCO2=38 pO2=88 FiO2=0.4HCO3=6 BE=-12 Na145 Cl 105 K5 pH-Acidemia CO2-Alkalosis side/normal HCO3- Metabolic acidosis Delta HCO3=24-6=18 pH should be 18x0.1/6=0.3. pH=7.4-0.3=7.1 Compensation: PaCO2 = 1.5x6 +8 +/- 2=15to19 but co2=38 So COPD may have prevented compensation Diagnosis = metabolic acidosis

34 female post GJ+RTA in PACU day2 pH 7.55pCO2= 46 pO2 110 FiO20.5 Hco3 34 K=3 Na= 143:

34 female post GJ+RTA in PACU day2 pH 7.55pCO2= 46 pO2 110 FiO 2 0.5 Hco 3 34 K=3 Na= 143 pH-Alkaemia CO 2 -acidosis/n HCO 3 =alkalosis delta=10 exp pH=10x0.1/6=0.16+7.4=7.56 Compensation 1  0.7 so for 10 CO2 must increase by 7 or 40+7=47 Diagnosis of Metabolic Alkalosis partially compensated

24 male #femur in shock, resuscitated with blood,pH7.38,pCO2=30 pO2 90 FiO2 0.6 HCO3=16:

24 male #femur in shock, resuscitated with blood,pH7.38,pCO2=30 pO2 90 FiO2 0.6 HCO3=16 pH Acidaemia/N CO2 = Alkalosis HCO3=Acidosis 24-16=8 pH=8x0.1/6=0.133 7.4-0.133=7.26 Compensation 1 1.25 so for 8 co2 should decrease by 8x1.25/1=10 co2=40-10=30 So diagnosis of compensated met acidosis

Metabolic acidosis:

Metabolic acidosis Increased anion gap: Acid gain LA/DKA/RF/Methanol/salicylates/ethylene glycol Normal anion gap- HCO3 loss usually hyperchloremic hypokalemic acidosis normal/ hyperkalemic acidosis

Anion gap:

Anion gap Anions other than chloride and bicarbonate that counterbalance the positive charge of sodium Na+ - (Cl - + HCO3 - ) 12+/- 2 mEq/L

Anion gap:

Anion gap increased when…..rise in organic acids (lactate, ketoacids) inorganic acids (sulfate, phosphate) Toxins (salicylate, glycolate, formate)

High Anion gap Metabolic acidosis:

High Anion gap Metabolic acidosis Lactic acidosis Ketoacidosis Uremia Methanol These are Normochloremic acidosis

Normal Anion gap Met Acidosis:

Normal Anion gap Met Acidosis GUT: Diarrhoea Fistula Ileal loop Renal: RTA Carbonic anhydrase inhibitor Post hypercapnia These are Hyperchloremic acidosis

PowerPoint Presentation:

Albumin is the major unmeasured anion and so Hypoalbuminaemia causes a low anion gap Every one gram decrease in albumin will decrease anion gap by 2.5 to 3 mmoles . A lactic acidosis in a hypoalbuminaemic patient will commonly be associated with a normal anion gap.

NaHCO3 Indications:

pH < 7.1 BE > 10 Dose =BE x 0.3 x Wt (kg) Half correction & repeat ABG analysis Mol wt=23+1+14+(16x3)=86 So 8.4% solution 1ml=0.97meq 7.5% solution 1ml=0.87meq NaHCO3 Indications

Goals of bicarbonate therapy :

Goals of bicarbonate therapy The main goal of alkali therapy is to counteract the extracellular acidaemia with the aim of reversing or avoiding the adverse clinical effects of the acidosis ( esp on the CVS) Emergency management of hyperkalaemia To promote alkaline diuresis ( eg to hasten salicylate excretion)

PowerPoint Presentation:

Hypernatraemia Hyperosmolality Volume overload Rebound or ‘overshoot’ alkalosis Hypokalaemia Impaired oxygen unloading due to left shift of the oxyhaemoglobin dissociation curve

Reasons to limit bicarbonate dose :

Reasons to limit bicarbonate dose Injected into plasma volume: The initial dose would hugely “over-treat” the small plasma space. Causes respiratory acidosis The bicarbonate given can increase the pH only if the CO2 produced can be removed by adequate ventilation. For each 100 mEq of bicarbonate, which is converted, about 2.24 litres of carbon dioxide has to be exhaled , which would be equivalent to ten minutes normal production .

PowerPoint Presentation:

Raises intracellular Pco2 Bicarbonate may cause clinical deterioration if tissue hypoxia is present increased lactate production (removal of acidotic inhibition of glycolysis ) and the impairment of tissue oxygen unloading (left shift of ODC). Bicarbonate is probably not useful in most cases of high anion gap acidosis

Mixed disorders:

Mixed disorders

MAC+RAC:

MAC+RAC Cardiac arrest COPD + metabolic acidosis Combined pulmonary and renal failure methanol, SNP low HCO3 normal / high PCO2

Respiratory acidosis & Metabolic alkalosis:

Respiratory acidosis & Metabolic alkalosis COPD in failure treated with diuretics

Metabolic & Respiratory alkalosis:

Metabolic & Respiratory alkalosis Post surgical patients pregnancy massive blood transfusions

Respiratory alkalosis & metabolic acidosis:

Respiratory alkalosis & metabolic acidosis Liver disease with vomiting/NGA End stage renal d/s+ Primary hypocapnia Salicylate poisoning Lactic acidosis

Metabolic acidosis + Met.Alkalosis:

Metabolic acidosis + Met.Alkalosis Diarrhoea and vomiting Lactic acidosis and vomiting Clue: increase in anion gap exceeds fall in HCO3

Mixed metabolic acidosis:

Mixed metabolic acidosis A) Mixed normal AG & high AG acidosis HCO3 loss and lactic acidosis Early CRF + interstitial nephritis RTA with high AG acidosis Resolving DKA

Mixed metabolic acidosis:

Mixed metabolic acidosis B) Mixed high AG acidosis Ketoacidosis and LA Uraemia + other high AG acidosis

Mixed metabolic acidosis:

Mixed metabolic acidosis C) Mixed hyperkalemia acidosis Diarrhoea in a pt with RTA Hyperalimenation and diarrhoea

How to recognise mixed disorder?:

How to recognise mixed disorder? MAC+RAK If expected paCO2 is much lower RAK is present

How to recognise mixed disorder?:

How to recognise mixed disorder? In met Acidosis with increase in AG : increase in AG is generally equal to fall in HCO 3 If delta AG > delta HCO3 co-existing MAK+ If delta AG < delta HCO3: MAC Normal AG+ MAC High AG

PowerPoint Presentation:

The Delta Ratio The Delta Ratio is defined as: Delta ratio = (Increase in anion gap / Decrease in bicarbonate ) The importance of this lies in its usefulness in assessing metabolic acidosis.

Delta Ratio Assessment Guideline :

Delta Ratio Assessment Guideline < 0.4 Hyperchloraemic normal anion gap acidosis 0.4 - 0.8 Consider combined high AG & normal AG acidosis 1 to 2 Uncomplicated high-AG acidosis > 2 Suggests a pre-existing elevated HCO 3 level: consider a concurrent metabolic alkalosis or a pre-existing compensated respiratory acidosis.

How to recognise mixed disorder?:

How to recognise mixed disorder? Clinical picture Other Lab tests

With respiratory disorders:

With respiratory disorders if HCO3 is unexpectedly high there is met alkalosis also If HCO3 is lower than expected met acidosis is also present

With respiratory disorders:

With respiratory disorders AG if increased more than 5 from the expected value the pt has probably a metabolic acidosis.

How to detect Lab errors :

How to detect Lab errors AG: very low or negative Insert H+,HCO3,pCO2 in Hendersons equation. >10% abnormal

Urinary Anion Gap :

Urinary Anion Gap Cations:Na+, K+, NH4+, Ca++ and Mg++. Anions:Cl-, HCO3-,SO4,PO4, organic anions. Only Na+, K+ and Cl- are commonly measured in urine. So the other charged species are the unmeasured anions (UA) and cations (UC). Cl- + UA = Na+ + K+ + UC UAG = ( UA - UC ) = [Na+]+ [K+] - [Cl-] The urinary anion gap can help to differentiate between GIT and renal causes of a hyperchloraemic metabolic acidosis.

Effects of pH disturbance in various systems:

Effects of pH disturbance in various systems CVS - depressed myocardial contractility, coronary vasoconstriction,vasoconstriction & dialatation, ODC shift Enzyme activity altered Cerebral blood flow Tetany Pharmcodynamics-opioids, muscle relaxants

Delta anion gap:

Delta anion gap Delta AG=Observed AG-Upper normal AG Delta HCO3=Lower Normal-observed AG>delta HCO3 =Mixed High AGMAC+MAK Delta HCO3>Delta AG =High AG+NAGMAC =Mixed high AGMAC+ c/c RAK with compensatory hyper Cl met acidosis

Methods to interconvert pH and [H+] :

Methods to interconvert pH and [H+] 1. Rule of Thumb Drop the 7 and Decimal Point Next take the difference of the number from 40. Add that value to 40 if the pH is less than 7.40 and subtract it if the pH is greater than 7.40; the result is the  H + .

PowerPoint Presentation:

2. The 0.1 pH Change Rule For every 0.1 unit increase in pH from 7.00, multiply the  H + by 0.8. For values less than 7.00, divide by 0.8 (or multiply by 1.25).

PowerPoint Presentation:

3. Log Table 4. A Simple Way to Convert between pH & [H+] Changes in the [H+] by a factor of 2 cause a pH change of 0.3

mm:

mm

authorStream Live Help