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ABG FROM THEORY TO THERAPY PRESENTED BY: DR HUSSAM AFIFY

acid base ABG from theory to therapy

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Page 1: acid base ABG from theory to therapy

ABG FROM THEORY TO THERAPY PRESENTED BY:

DR HUSSAM AFIFY

Page 2: acid base ABG from theory to therapy

WHAT IS PH ? pH=-log[H+] concentration,

which is read: the pH is equal to minus the log of the H+

concentration. For example is the H+ concentration is very low, lets say about

0.0000001M, then the pH is pH= -log[.0000001] whis is the same as -log[1 X 10-7]

the term log[1 X 10-7] = -7 - (-7) = 7

Page 3: acid base ABG from theory to therapy

WHAT IS P STAND FOR ?The exact meaning of the "p" in "pH" is disputed Power :-o according to the Carlsberg Foundation, pH stands for "power of hydrogen".o It has also been suggested that the "p" stands for the German Potenz (meaning "power"), o others refer to French puissance (also meaning "power", based on the fact that the Carlsberg Laboratory was French-speaking)

Pondus :- Another suggestion is that the "p" stands for the Latin terms pondus hydrogenii (engl. quantity of hydrogen)

Page 4: acid base ABG from theory to therapy

WHAT IS OPTIMUM PH FOR OUR BODY?

Page 5: acid base ABG from theory to therapy

WHAT IS HOMEO-STASIS ?

is the property of a system in which a variable (e.g. the concentration of

a substance in solution, or its temperature etc.) is actively

regulated to remain very nearly constant.

Page 6: acid base ABG from theory to therapy
Page 7: acid base ABG from theory to therapy

HOMEO-STASIS …..DISEASE

imbalance Balance

hypothermia

hyperthermia

loss Production Temperature

cachexia obesity loss Production Energy

alkalosis acidosis Loss Production H ion

Hypo Hyper Loss ( shift)

Gain ( retention)

Electolytes ( CA ,K ,

Na…… Bleeding thrombosis fibrinolysi

sCoagulation Blood

Hemostasis

Page 8: acid base ABG from theory to therapy

FROM WHERE WE CAN GET H IONS ? Most hydrogen ions originate from cellular metabolismBreakdown of phosphorus containing proteins releases phosphoric acid into the ECF

Anaerobic respiration of glucose produces lactic acid

Fat metabolism yields organic acids and ketone bodies

Transporting carbon dioxide as bicarbonate releases hydrogen ions

Page 9: acid base ABG from theory to therapy

Life is a long acid trip

Page 10: acid base ABG from theory to therapy

WHAT IS ACID AND WHAT IS THE BASE ?

volatile Organic Carbonic 1 -hydrochloric

acid 2 -lactic acid

3 -DNA RNA4 -amino acids

5 -fatty acids

Page 11: acid base ABG from theory to therapy

WHAT IS DIFFERENCE BETWEEN ION AND ANION ?

Ion :- Carry charge in its outer

surface

Page 12: acid base ABG from theory to therapy

WHY FIXED PH IS IMPORTANT ?Electrical Neutrality

Page 13: acid base ABG from theory to therapy

ELECTRICAL NEUTRALITY

Nerve conduc

tion

Muscle contraction

Platelets

function

Electrolytes

homeostasis

Dissociation of oxygen

Page 14: acid base ABG from theory to therapy

WHAT IS DIFFERENCE BETWEEN ACIDEMIA AND ACIDOSIS ?

Acidosis AcidemiaPrimary physiologic process that may lead to acidemia

hypoperfusion lactic acidosis

hypoventilation respiratory acidosisPh may be normal

or

or

Blood PH less than 7.35

Page 15: acid base ABG from theory to therapy

WHAT IS DIFFERENCE BETWEEN ALKALEMIA AND ALKALOSIS ?

Alkalosis AlkalemiaPrimary physiologic process that may lead to alkalemia

diarhia metabolic alkalosis hyperventilation respiratory

alkalosis

Ph may be normal or

or

Blood PH more than 7.45

Page 16: acid base ABG from theory to therapy

NORMAL PH BUT ABNORMAL ABG , WHY ?Compensation Concomitant

disorders 1- over or under compensation ( secondary disorders ) 2- tertiary disorders

Page 17: acid base ABG from theory to therapy

HYDROGEN ION REGULATION = COMPENSATION Concentration of hydrogen ions is regulated sequentially by:1. Chemical buffer systems act within seconds2. The respiratory center in the brain stem acts within

1-3 minutes3. Renal mechanisms require hours to days to affect

pH changes

Page 18: acid base ABG from theory to therapy

1- BUFFERS …SECONDS 1. A buffer is a solution whose

function is to minimize the change in pH when a base or an acid is added to the solution 

2. Most buffers consist of a weak acid (which releases H+ ions) and a weak base (which binds H+ ions)

3. If an acidic solution is added to a buffer solution, the buffer will combine with the extra H+ ions and help to maintain the pH

4. If a basic solution is added to a buffer solution, the buffer will release H+ ions to help maintain the pH 

Page 19: acid base ABG from theory to therapy

2- RESPIRATORY …MINUTES 1. physiological buffering system2. There is a reversible equilibrium

between: Dissolved carbon dioxide and water Carbonic acid and the hydrogen and

bicarbonate ions CO2 + H2O « H2CO3 « H+ + HCO3¯

3. When hypercapnia or rising plasma H+ occurs:

Deeper and more rapid breathing expels more carbon dioxide

Hydrogen ion concentration is reduced4. Alkalosis causes slower, more shallow

breathing, causing H+ to increase

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3- RENAL …DAYS

Page 21: acid base ABG from theory to therapy

CAN ABG DISORDERS AFFECT OXYGENATION

Page 22: acid base ABG from theory to therapy

INDICATIONS OF ABG TEST Muakkassa and coworkers studied the relationship between the presence of an arterial line and ABG sampling . These authors demonstrated that patients’ with an arterial line had more ABGs drawn than those who did not regardless of the value of the PaO2, PaCO2, APACHE II score or the use of a ventilator. In this study, multivariate analysis demonstrated that presence of an

arterial line was the most powerful predictor of the number of ABGs

drawn per patient independent of all other measures of the patient’s clinical status

Page 23: acid base ABG from theory to therapy
Page 24: acid base ABG from theory to therapy

WHAT IS YOUR METHOD ?

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OUR METHOD WILL BE ……!!!!!!!

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P & P ……. !!!!!!!!!!!Patient Paper

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WHY THE PATIENT IS IMPORTANT ?History S & S Diabetic CKD Intoxication Shock

Respiratory HyperventilationShift of Oxy-Hb curve to right

Cardiovascular Myocardial depressionTissue catecholamine resistance

Pulmonary vasoconstrictionHyperkalaemia

Metabolic acidosis

Page 28: acid base ABG from theory to therapy

WHY THE PATIENT IS IMPORTANT ?History S & S COPD Opoid After general anethesia

Vasodilation, sweaty, tachycardic, mydriasis, asterixis Confusion Drowsy and ALOC

Respiratory acidosis

Page 29: acid base ABG from theory to therapy

WHY THE PATIENT IS IMPORTANT ?History S & S Vomiting Diarrhia Diuretics Hypovolemic hypokalemic

Shift O2 dissociation curve to left (increased affinity for Hb-O2) Right shift with increase TEMP, 2-3 DPG, H+

Hypokalemia, hypocalcaemia, hypochloraemia

Symptoms related to HYPOcalcaemia and HYPOkalaemia Dizzy, light-headedChest tightnessAnxiety, dysphasia…..laryngospasm

Metabolic alkalosis

Page 30: acid base ABG from theory to therapy

WHY THE PATIENT IS IMPORTANT ?History S & S Pain Fever stress Agitated Early in athma PE !!!

Associated changes HYPOcalcaemia, HYPOkalaemia, HYPOphosphatemia

Decreased Co2 reduces H+ binding, increases negative charge of proteins and increases binding of calcium to proteins Thus reducing ionised calcium

Hypocalcaemia with tetany and carpopedal spasm

Shift 02 dissociation curve to the left (Alkalosis) (Increased affinity of Hb for O2)Respiratory

alkalosis

Page 31: acid base ABG from theory to therapy

Prediction – actual analysis

Mixed disorder

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Page 33: acid base ABG from theory to therapy

ANATOMY OF ABG PAPER A ………. Acid B ………. Base C ……... Contents of oxygen and Co2 D ……... Delivery of O2 ….. E …….... Electrolytes ( ?) F ……… Fetal HB and other forms of abnormal HB G ……... glucose H ……... Hemoglobin I ……… Inhaled CO L ……... Lactate

Page 34: acid base ABG from theory to therapy

5 STEPS 1.Confirm2.Classify 3.Calculate 4.Causes 5.Correct

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1- CONFIRM Patient Errors 1.Same patient2.Same date 3.Same time

Lab Errors 1. Calculate the H ion

concentration from the equation

2. This calculated H ion should be cross ponded to H ion in the ABG report

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VALIDITY 1-

2- subtract the last two digits of the pH (e.g., 20 in pH 7.20) from 80; this value is approximately equal to the H+ concentration

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2- CLASSIFY ….. WHAT IS PRIMARY ? 7.4

alkalosis Norrmal Acidosis

More than 7.45 7.35 – 7.45 LESS than 7.35 Ph

Less than 35 35 -- 45 More than 45 PaCO2(Respiratory)

More than 26 22 – 26 LESS than 22 HCO3(Metabolic)ROM

E

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3- CALCULATE ….. 1- compensation

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ANION GAP

Na + ( 1.6 × g – 100/100 )

Na – ( Cl + Hco3 ) 12 ± 4

AG + 2.5 ( 4 – Albumin )

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NOT ONLY IN METABOLIC ACIDOSIS

Critical care secret page 311

Page 41: acid base ABG from theory to therapy

LOW ANION GAP 1- Decrease in unmeasured anions (albumin, dilution) 2- Increase in unmeasured cations (multimyeloma (cationic IgG paraprotein), hypercalcaemia, hypermagnesaemia, lithium OD, polymixin B)

bromide OD (causes falsely elevated chloride measurements) Atrovent (Ipratropium) bromideAvelox (moxifloxacin)Celebrex (celecoxib)Cipro (ciprofloxacin)Crestor (rosuvastatin)Diflucan (fluconazole)Lescol (fluvastatin)Levaquin (levofloxacin)Lexapro (escitalopram)Lipitor (atorvastatin)Pulmicort (budesonide)Risperdal (risperidone)Tobra Dex (from dexamethasone)

Page 42: acid base ABG from theory to therapy

URINE AG For non-gap metabolic acidosis, calculate the urine anion gap

UAG = UNA + UK – UCL If UAG>0: renal problem If UAG<0: nonrenal problem (most commonly GI) ……. neGUTive !

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3- CALCULATE 2- tertiary disorders

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4- CAUSES

Page 45: acid base ABG from theory to therapy

CAUSES OF METABOLIC ACIDOSIS Metaboli

c acidosis

HAGMA NAGMA

Page 46: acid base ABG from theory to therapy

HAGMA …… OSMOLAR gap Measured – calculated

15

Page 47: acid base ABG from theory to therapy
Page 48: acid base ABG from theory to therapy

isopropan

ol

Ethylene

glycol

methanol

Acetone Glycolate ( false ↑ lactate )Oxylate ( crystals )

FormaldehydeFormic acid

metabolites

Elevated Early :- elevatedLate :- normal

OG

Normal Early :- normalLate :- elevated

AG

AKI Blindness Clues

Page 49: acid base ABG from theory to therapy
Page 50: acid base ABG from theory to therapy

HAGMA

HOSG

1- methanol2- ethanol3- diuritics (mannitol)4- isopropyl alcohol5- ethylene glycole

NOSG

1-lactic acidosis2- renal failure3- DKA

Page 51: acid base ABG from theory to therapy
Page 52: acid base ABG from theory to therapy

NAGMA

POSITIVE UAG

RENAL

NEGUTIVE UAG

GIT

Page 53: acid base ABG from theory to therapy

1- dirrhia2- colostomy3- fistula4- uretric diversion5- hyperalimentaion

Page 54: acid base ABG from theory to therapy

CAUSES OF METABOLIC ALKALOSIS

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Page 56: acid base ABG from theory to therapy

CAUSES OF RESPIRATORY ACIDOSIS

Page 57: acid base ABG from theory to therapy

CAUSES OF HYPERCAPNIA

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CAUSES OF RESPIRATORY ALKALOSIS TACHYPNIA

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5- CORRECT THE CAUSES 1- sodium bicarb 2- acetazolamide

Please see evidence based book pp 340

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HOW TO DECREASE THE ABUSESEE PAUL MRIK PP 330

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Thank you