By.

SYED TABISH REHMAN

ABGs are indicated if the patient deterioration in an already critical condition such as: Decrease in oxygen saturations Confusion Fall in conscious level (Glasgow Coma Scale) Increased respiratory effort Cyanosis Assess the ventilatory status, oxygenation and acid base status Assess the response to an intervention

 Bleeding diathesis AV fistula Severe peripheral vascular disease, absence of an arterial pulse Infection over site

Arterial Blood Gas (ABG) Kit Prepackaged and contains all necessary equipment
3 5 cc syringe 22ga x 2 needle Alcohol swap Gauze pad Biohazard bag Misc. items
Pre-heparinized

 The radial artery is superficial, has collaterals and is easily compressed. It should almost always be the first choice. Other arteries (femoral, dorsalis pedis, brachial) can be used in emergencies

Step 1: tight fist x 20 sec Step 2: Occlude radial and ulnar arteries

 Step

3: open hand and look for blanching Step 4: release ulnar artery and look for capillary refill (5-7 sec)

Position wrist Prep skin Insert needle ~45 degrees, bevel up Apply pressure x 5min post procedure

 Sample should be analyzed as soon as possible

If iced sample can be stored
Glass syringe 1 hour Plastic syringe 15 minutes After specimen collected and air bubble removed, gently mix and invert syringe. Because the wbcs are metabolically active, they will consume oxygen. Plastic syringes are gas permeable. Key: Minimize time from sample acquisition to analysis.

Remember: Blood is living tissue that continues to consume O2 and produce CO2

Hematoma Arterial laceration Hemorrhage Vasovagal reaction

Sympathetic nervous system response to pain

Loss of limb

 a) b) a) b)

METABOLIC
Acidosis Alkalosis Acidosis Alkalosis

RESPIRATOY

DISORDER
Metabolic Acidosis

PRIMARY HCO3

COMPENSATORY pCO2

Metabolic Alkalosis Respiratory Acidosis

Respiratory Alkalosis

HCO3
pCO2 pCO2

pCO2
HCO3 HCO3

CO2 HYPER VENTILATION

compensation pH

LOW HCO3
LOW pH
HCO3 changes pH in same direction LOW pCO (compensated)
2

HCO3

Low Alkali

Primary lesion

METABOLIC ACIDOSIS

CO2

HYPO VENTILATION

compensation pH

HIGH HCO3 HIGH pH

BICARB CHANGES pH in same direction

HIGH pCO2
HCO3

(compensated)

High Alkali

Primary lesion

METABOLIC ALKALOSIS

BICARB

CO 2 CHANGES pH in opposite direction

compensation pH

HIGH pCO2 LOW pH

HIGH HCO3 (compensated)

CO 2

High CO2

Primary lesion

Respiratory acidosis ( Hypoventilation)

BICARB

CO 2 CHANGES pH in opposite direction

compensation pH

LOW pCO2 HIGH pH

LOW HCO3 (compensated)

CO 2

Low CO2

Primary lesion

Respiratory alkalosis ( Hyperventilation)

Bodys physiologic response to Primary disorder in order to bring pH towards NORMAL limit

Partial compensation No compensation. (uncompensated) BUT ph never overshoots, If a overshoot pH is there, it is a MIXED disorder

Phase of Respiratory Acidosis

Expected Changes For Each Incremental Increase Of pCO2 by 10 mmHg

ACUTE

pH decreases by 0.08 OR HCO3 increases by 1 mEq/L

pH decreases by 0.03 OR HCO3 increases by 4 mEq/L

CHRONIC

Phase Of Respiratory Alkalosis

Expected Change Foe Each Incremental Decreases Of pCO2 By 10 mmHg

ACUTE
CHRONIC

pH increases By 0.08 0r HCO3 decreases by 2 mEq/l

pH increeas by 0.03 OR HCO3 Decreases by 5 mEq/L

pCO2 will decrease 1.3 mmHg per 1 mEq/L decrease in HCO3 WINTERS FORMULA pCO2= (1.5 *HCO3)+ 8 2

pCO2 increases 0.7 mmHg per 1 mEq/L increase in HCO3 pCO2= 0.9[HCO3] +16

The difference between the commonly measured serum cations (positively charged particles) and the measured serum anions (negatively charged particles). Anion gap = [Sodium] - ([Chloride] + [Bicarbonate])

The normal anion gap depends on the laboratory set up (usually 12 2)

Anion gap should always be calculated b/c it helps differentiated b/w causes of metabolic acidosis A large anion gap (>20) always suggest primary metaolic acidosis regardless of pH and HCO3 level, b/c body can not generate large anion gap to compensate

Anion gap HCO3-

Anion gap HCO3-

Anion gap
HCO3-

Na+

Cl-

Na+

Cl-

Na+

Cl-

electroneutrality

Meta. acidosis: too little base More Cl- and anion gap same Diarrhea, renal acidosis

Meta. acidosis: too little base More Cl- and anion gap bigger Ketoacidosis, salicylate, lactate Chronic renal failure

 Acid-Base
pH

Information

PCO2

HCO3

[calculated vs measured]

Oxygenation

Information PO2 [oxygen tension] SO2 [oxygen saturation]

Assessing a patients acid base status requires arterial pH PCO2 and HCO3.
Blood gas analyzers measures PH and PCO2 where as HCO3 is calculated from Handerson Hasselbalch equation.

Acidemia PH <7.35 Alkalemia PH >7.45 Acidosis process which increases H+ ions. Alkalosis process that decreases H+ ions. Normal values PH (7.35-7.45) PCO2 (35-45) HCO3 (22-26)

Step 1: Acidemic, alkalemic, or normal? Step 2: Is the primary disturbance respiratory or metabolic? Step 3: For a primary respiratory disturbance, is it acute or chronic? Step 4: For a metabolic disturbance, is the respiratory system compensating OK? Step 5: For a metabolic acidosis, is there an increased anion gap?

Step 6: For an increased anion gap metabolic acidosis, are there other derangements?

 Rule

RULE

is on, the process that caused is the primary abnormality) Principle: The body doesn`t fully compensate for any disorders

1:-Look at the pH (whichever side of 7.40 the pH 2:-Calculate the Anion Gap (If the anion gap is

RULE

>20mmol/L the primary metabolic acidosis is present regardless of pH and HCO3 levels. Principle: The body doesn`t generate a large anion gap to compensate for primary disorder.

Calculate the Excess anion gap (The total Anion gap minus the normal anion gap) and add the value to measured bicarbonate concentration. If the sum is greater than a normal Serum HCO3 (>30 mmol/L) there is underlying metabolic alkalosis. If the sum is less than <23 mmol/L there is also underlying normal anion gap metabolic acidosis.

3:-

RESPIRATORY ACIDOSIS

pH decreases (< 7.4) pCO2 Increases Primary defect

HCO3 increases as a Compensatory Response

Results from Hypoventilation and subsequent hypercapnea

CENTRAL
1. Drugs (anaesthe tics, morphine ,sedatives 2. Stroke 3. infection

AIRWAY

PARENCHYMA NEUROMU SCULAR

MISCELL ANEOUS

1.obstruction 1. Emphysema

1.Poliomyelitis 1. Obesity

2. Asthma

2. Pneumoconiosis 2.Khyphoscoli ois 3. Bronchitis 4. ARDS 3.Myasthenia 4. Muscular dystrophosy

2.Hypoventil ation

Phase of Respiratory Acidosis

Expected Changes For Each Incremental Increase Of pCO2 by 10 mmHg

ACUTE

pH decreases by 0.08 OR HCO3 increases by 1 mEq/L

pH decreases by 0.03 OR HCO3 increases by 4 mEq/L

CHRONIC

Occurs when hyperventilation reduces the pCO2 pH increases pCO2 decreases primary defect HCO3 decreases as compensation Most common cause is Hyperventilation Other imp causes are bacterial septicemia

CNS STIMULATIO N
Pain Anxiety, psychosis Fever CVA

HYPOXEMIA

DRUGS/ HORMONES

CHEST RECEPTORS STIMULATIO N

Hemothorax Flail Chest

MISCELLANE OUS

High Altitude, pCO2 dec Pneumonia, pulmonary Edema Aspiration Severe Anemia

Pregnancy, progestrone Salicylates

Septicemia Hepatic Failure Heat exposure Recovery from metabolic acidosis Mechanical hyperventilati on

Cardiac Failure

Cardiac Failure Pulmonary Embolism

Tumor

Phase Of Respiratory Alkalosis

Expected Change Foe Each Incremental Decreases Of pCO2 By 10 mmHg

ACUTE
CHRONIC

pH increases By 0.08 0r HCO3 decreases by 2 mEq/l

pH increeas by 0.03 OR HCO3 Decreases by 5 mEq/L

a) b) c)

pH decreases HCO3 decrease- Primary defect pCO2 also decreases as a Compensatory response Classified On the basis of anion gap Base deficit caused by Increase in Endogenous acid production eg: (Lactic acid, ketoacid) Loss of bIcarb from body (Diarrhea) Accumulation of endogenous acid

Lactic Acidosis

a) b) c) a) b) c) d)

Ketoacidosis Diabetic Alcoholic Starvation

Toxins Ethylene Glycol Methanol Salicylates Propylene glycol Renal Failure

Gastrointestinal HCO3 loss Renal Tubular Acidosis Post Hypocapnea Hyperalimentation (Arginine and lysine in pareneral nutrition) Other Acid Loads( Ammonium chloride, Hyperalimentation) Expansion acidosis (rapid saline administration)

a) b)

Increase Renal NH4Cl excretion to Enhance H+ removal is a normal physiological response to metabolic acidosis Normal daily Urinary excretion of NH4CL is about 30 mEq/L which can be inc upto 200 mEq/l UAG Reflect the ability of kidney to excrete NH4Cl UAG = [Na +K] [CL]

UAG helps in distinction b/w GI and Renal Causes of Hyperchloremic acidosis In GI loss (diarrhea) renal acidification ability remains normal and NH4Cl excretion increases in response to acid and UAG becomes Negative ( [Cl] > [Na+K]

When UAG is Positive ( [Na+K] > [Cl]) urinary ammonium is low because of inability kidney to excrete NH4Cl.

Alkalemia, pH increases
Primary defect is a increase in serum Bicarb Compensatory mechanism leads to hypoventilation

MAK involves a generative phase in which loss of acid usually causes Alkalosis and then a maintenance phase in which kidney fail to compensate by excreting HCO3

It is useful to classify Mak in two Groups based on Saline responsiveness or urinary chloride.

Saline Responsive (U cl <25 mE/l)

Renal Alkalosis

a) Diuretic Therapy b) Post Hypercapnea c) Poorly reabsorbable anion therapy: carbenicillin, penicillin

GASTROIINTESTINAL ALKALOSIS
a) b) c) d)

Loss of HCL from Vomiting , NG suction Chloride Diarrhea Transfusion Antacids

CONTRACTION ALKALOSIS

SALINE UNRESPONSIVE ( U cl >40 mEq/L)

RENAL ALKALOSIS
NORMOTENSIVE
Bartter Syndrome Gitelman syndrome

HYPERTENSIVE
Endogenous mineralocorticoid a) Primary aldosteronism b) Hyperreninism c) Liddle Syndrome d) Adrenal enzyme deficiency :11 and 17 hydroxylase

Severe Potassium depletion

Exogenous Alkali

Hypercalcemia

Exogenous Mineralocorticoids Licorice

MIXED METABOLIC AND RESPIRATORY

METABOLIC ACIDOSIS + RESPIRATORY ALKALOSIS METABOLIC ACIDOSIS + RESPIRATORY ACIDOSIS
High or normal AG Mac, prevailing pCO2 below predicted values

High or normal AG MAc , prevailing pCO2 above predicted value

METABOLIC ALKALOSIS + RESPIRATORY ALKALOSIS

METABOLIC ALKALOSIS + RESPIRATORY AIDOSIS
pCO2 Higher than predicted ,ph normal

pCO2 does not increase as predicted and pH higher than expected

MIXED METABOLIC DISORDERS-METABOLIC ACIDOSIS + METABOLIC ALKALOSIS

( eg: uremia with vomiting)

METABOLIC ACIDOSIS + METABOLIC ACIDOSIS

Mixed high AG Normal AG Acidosis ( Eg: diarrhea and Lactic acidosis , Treatment of DKA)

-- pH normal, abnormal PCO2 n HCO3 -- Degree of compensation for primary disorder is inappropriate -- Combination of respiratory acidosis and Alkalosis can not coexist -- Find Delta Delta Gap/ Excess Anion gap

Equivalent rise of AG and Fall of HCO3

.Pure Anion Gap Metabolic Acidosis

Discrepancy.. in rise & fall

+ Non AG M acidosis, + M Alkalosis

 Delta
Delta

Delta gap = = AG/HCO3

(+ AG M Acidosis)
(+ AG M

Delta Gap = 1-2.Pure AG acidosis

< 1 = non AG acidosis

Acidosis)

> 2 = metabolic alkalosis

CALCULATE EXCESS ANION GAP (EAG) EAG = Anion Gap - 12 meq/L +bicarbonate

EAG > 30 mEq/L: Metabolic Alkalosispresent EAG < 23 mEq/L: Non-Anion Gap Metabolic Acidosis

Tripple acid base disorders are not common

Patient develop tripple disorder only if a mixed disorder coexist with respiratory acidosis or alkalosis
Are usually seen in patient with severe metabolic disorder AKAAG gap acidosis+ Metabolid alkalosis (dehydration)+ respiratory acidosis (respiratory depression) DKA AG gap Acidosis + Metabolic Alkalosis ( dehydration)+ Respiratory Alkalosis (hyperventilation from pneumonia or sepsis)

a) b) c) a) b) c)

CO2 HYPER VENTILATION

compensation pH

LOW HCO3
LOW pH changes HCO
pH in same direction LOW pCO2 (compensated)
3

HCO3

Low Alkali

Primary lesion

METABOLIC ACIDOSIS

CO2

HYPO VENTILATION

compensation pH

HIGH HCO3
HIGH pH CHANGES BICARB
pH in same direction

HIGH pCO2
HCO3

(compensated)

High Alkali

Primary lesion

METABOLIC ALKALOSIS

BICARB

CO 2 CHANGES pH in opposite direction

compensation pH

HIGH pCO2 LOW pH

HIGH HCO3 (compensated)

CO 2

High CO2

Primary lesion

Respiratory acidosis

BICARB

CO 2 CHANGES pH in opposite direction

compensation pH

LOW pCO2
HIGH pH

LOW HCO3 (compensated)

CO 2

Low CO2

Primary lesion

Respiratory alkalosis

ABG Gases

pH 7.24 pCO2 24 mmHg [HCO3] 10 mEq/L

SERUM CHEMISTRY
130 4 94

Na K Cl

STEP 1: Evaluate the ph and narrow down to two possibilty pH < 7.36= Acidosis (met or resp) STEP 2:Evaluate the pCO2 and narrow down to one definite process pCO2 < 40 mmHg Atleast metabolic acidosis is present STEP 3: Apply Compensation formula and compare predict pCO2 with actual pCO2 Expected pCO2= 1.5[HCO3]+82 = 2125 Actual pCO2 = 24 (compensated)

STEP 4: Determine if any other process exist The expected pCO2 = Acual pCo2 A pure Metabolic acidosis With no other process STEP 5: Evaluate Anion Gap AG= 130- (94+10) 26

CONCLUSION:

AN ELEVATED ANION GAP METABLOIC ACIDOSIS

ABG GASES pH 7.52 pCO2 20mmHg [HCO3] 19 mEq/l SERUM CHEMISTRY

Na 136 Cl 103

STEP 1: Evaluate the ph and narrow down to two possibilities pH > 7.44 = Alkalosis ( metab or Resp) STEP 2: Evaluate the pCO2 and narrow down to definite process pCO2 < 40 (atleast resp alkalosis is present)

STEP 3: Apply compensation formula for resp alkalosis ( based on history apply for acute) For every decrease of 10mmhg pCO2 [HCO3] decrease 2 meq (from 24) bec pco2 dec by 20 [HCO3] should dec by 4 Expected [HCO3]= 20 meq, Actual [HCO3] = 19 meq

STEP 4: Determine if any other process is there the actual and expected [HCO3] closely matches. No other disorder STEP 5: Evaluate Anion Gap AG = 136- (103+19) = 14 (normal)

CONCLUSION:

SIMPLE ACUTE RESPIRATORY ALKALOSIS

ABG
pH 7.47 pCO2 21 [HCO3] 15 mEq/l

SERUM CHEMISTRY
Na 136 Cl 110

STEP 1: pH > 7.44 = Alkalosis( meta or resp) STEP 2: pCO2 < 40 = atleast Resp Alkalosis STEP 3: Apply compensation formula For chronic Resp Alkalosis (as u know the history) For every decrease of 10mmhg pCO2 [HCO3] expect to dec 5 mEq/l Bec pCO2 dec by 20 HCO3 should dec 10 mEq (24-10 =14) Expected HCO3 = 14 Actual = 15

STEP 4: Determine if any other processare present Both the actual and [HCO3] match the expected changes closely No other Acid base disorder STEP 5: Evaluate the Anion Gap AG= 136-(110+15) = 11 (normal)

CONCLUSION: SIMPLE CHRONIC RESPIRATORY

ALKALOSIS (COMPENSATED)

ABG
pH pCO2 [HCO3] 7.47 21 mmHg 15 mEq/l

SERUM CHEMISTRY
Na 136 Cl 109

STEP 1: pH> 7.44 = Alkalosos (metab or Resp) STEP 2: pCO2 < 40 = Atleast metab. Alkalosis STEP 3: Apply formula for compensation, now u dont know acute or chronic, Therefore apply Both formulas.

EVALUATING USING FORMULA FOR CHRONIC for every dec. Of 10mmHg in pCO2 [HCO3] decby 5 mEq/l Expected [HCO3] = 14 Actual [HCO3] = 15 SIMPLE CHRONIC RESPIRATORY ALKALOSIS

EVALUATE USING FORMULA FOR ACUTE PROCESS For every dec of pCO2, expect [HCO3] to dec By 2mEq/l Expected [HCO3] = 20 Actual [HCO3] = 15

STEP 4: Determine if any other process exist Actual HCO3 is lower than expected Now which process can lower HCO3 from expected, answer is Metabolic Acidosis, as two Respiratory cant coexist

STEP 5 : Evaluate the Anion Gap AG= 136- (109+15) = 12 (normal)

CONCLUSION: Without the clinical history we can conclude Either a) SIMPLE CHRONIC RESP.

ALKALOSIS b) MIXED RESP. ALKALOSIS + MET. ALKALOSIS

ABG
pH: 7.01 pCO2: 70 mmHg [HCO3]: 19 mEq/L
Na 140 CL 99

SERUM CHEMISTRY

STEP 1: Evaluate the pH pH < 7.35 Acidosis (resp or Metabolic) STEP 2: Evaluate the pCO2 pCO2 > 40 Atleast Respiratory Acidosis STEP 3: Apply compensatory formula For acute resp acidosis For every increase of 10 mmHg in pCO2,[HCO3] expected to increase 1 mEq/l Bec pCO2 inc. By 30, [HCO3] should inc by 3 to 27 mEq/l (from 24) EXPECTED [HCO3] = 27 mEq/L ACTUAL [HCO3] = 19 mEq/L

STEP 4: Determine if any other process exist Actual [HCO3] is lower than predicted, this suggest other than resp acidosis there is metabolic acidosis which is lowering [HCO3]

STEP 5: Evaluate the Anion Gap AG = 140 (99+19)= 22 An Elevated gap Metabolic acidosis STEP 6: Calculate delta delta change = AG- Normal AG/ HCO3- calculated HCO3 = 22-12 = 10 / 24- 19= 5 =2

CONCLUSION: MIXED RESPIRATORY

ACIDOSIS+ AN ELEVATED GAP METABOLIC ACIDOSIS

ABG
pH: 7.27 pCO2: 62 [HCO3]:28
Na 134 Cl 85

SERUM CHEMISTRY

STEP 1: Evaluate the pH pH < 7.35 = Acidosis (metab or resp) STEP 2: Evaluate the pCO2 pCO2 > 40 Atleast Respiratory acidosis is present STEP 3: Apply formula of compensation for acute resp. Acidosis for every increas of 10 mm in pCO2, [HCO3] expected to inc 1 mEq/l Bec pCO2 inc by 20 HCO3 should inc by 2 Exected HCO3 = 26 Actual HCO3 = 28

STEP 4: Determine if any other process Since Actual HCO3 slightly higher than expected, a small metabolic alkalosis may be present STEP 5: Evaluate the Anion Gap AG= 134- (85+28) = 23 Elevated AG Metabolic acidosis also present

STEP 6: Calculate Delta Delta Gap = (23-12)/ (28-24) = 11/4 =>2 Metabolic Alkalosis is present

CONCLUSION: A TRIPPLE ACID BASE DISORDER

a) Respiratory Acidosis b) Elevated AG Metabolic Acidosis c) Metabolic Alkalosis

The resp acidosis is due to respiratory depression from Alcohol Intoxication and BZ overdose The mild met. Alkalosis is due to emesis and resultant volume Depletion The Elevated AG met. Acidosis is likely caused by Alcoholic ketoacidosis

THANKYOU FOR YOUR TIME

HARRISONS MEDICINE 17 EDITION CMDT 2010 E-MEDICINE RED BOOK FRED FERRI