ABG series

ANAS SAHLE , MDDAMASCUSE

HOSPITAL

Acid-Base Disorders and the ABG 5

BREIF PREVIEW

Summary of the Approach to ABGs

1. Check the pH

2. Check the pCO2

3. Select the appropriate compensation formula

4. Determine if compensation is appropriate

5. Check the anion gap AG=NA – (HCO3 + CL):12±4

6. If the anion gap is elevated, check the delta-delta

G:G Ratio =Δ AG (12-AG) \ Δ HCO3 (24-HCO3)

7. If a metabolic acidosis is present, check urine pH

8. Generate a differential diagnosis

EXPECTED CHANGES IN ACID-BASE DISORDERS

From: THE ICU BOOK - 2nd Ed. (1998) [Corrected]

Expected Changes Primary Disorder

PCO2 = 1.5 × HCO3 + (8 ± 2) Metabolic acidosis

PCO2 = 0.7 × HCO3 + (21 ± 2) PCO2= 0.9 * HCO3 +16

Metabolic alkalosis

delta pH = 0.008 × (PCO2 - 40)ΔHCO3 = 0.1 × (PCO2-40)

Acute respiratory acidosis

delta pH = 0.003 × (PCO2 - 40)ΔHCO3 = 0.35 × (PCO2-40)

Chronic respiratory acidosis

delta pH = 0.008 × (40 - PCO2)ΔHCO3 = 0.2 × (40 – PCO2 )

Acute respiratory alkalosis

delta pH = 0.003 × (40 - PCO2)ΔHCO3 = 0.4 × (40 – PCO2)

Chronic respiratory alkalosis

PH

PH:7,37-7,43 MIXED VS NORMAL

PH>7,43 ALKALOSIS

PCO2>40

M.AL

PCO2<40

R.AL

PH<7,37 ACIDOSIS

PCO2<40

M.AC

PCO2>40

R.AC

Osmolal gap

Normal(10-15 )

High

Serum ethanol level

Intoxication(E G:methanol)

Correct osmolal gap

for ethanol

Normal

high

Osmolal gap = measured serum osmolality - (2 NA + gluco\18 + bun\2,8)Corrected osmolal gap = measured serum osmolality - (2 NA + gluco\18 + bun\2,8 + ETOH\4,6)

HIGH AG M.AC

Normal osmolal gap

Is ther CRF?

YES NO

Serum or urine ketones

Alcoholic

ketoacidosis

diabetic ketoacid

osis

Salicylate level

Aspirin toxicity

Lactic

acidosis

normal High

HIGH AG M.AC

Normal AG M.AC

cAG = AG+2,5(4 – alb)

High AG Normal AG

Expected PCO2 : Measured PCO2

Etiology of normal AG M.AC

Does the patient have GI loss of alkali ?

Stop

Medication inducsed ?Calcium chloride,

magnesium sulphate,cholestyramine,

cation exchange resinsStop

Recovery from ketoacidosis?

Stop

Rapid

saline

adminstration

(expansion

acidosis))

Stop

Calculate

urine

anion

gap ?

GI LOSS of ALKALI

Jejuna

l loop

Pancreatic ,biliary ,

enteric ) fistula

Diarrhea

YES NO

YES NO

YES NO

YES NO

Calculate urine AG

Consider : type (1; 2 ;4) RTA;

RTA of renal insufficiency

Plasma KLow

URINE PH

RTA 1 RTA 2

NormalRTA of renal insuffiency

(1;2) RTA

HighRTA 4

Consider causes of normal AG metabolic acidosis besides RTA

(i.e; GI loss )<5,5 >5,5Urine AG = (UNA +UK) - UCL

METABOLIC ALKALOSIS-2

CAUSES (in short phrase)

• Diuretics• Vomiting• Exogenous alkali• Hyper- aldosteronism• Post-hypercapneic state

Etiology of metabolic alkalosis

Administration of exogenous alkali ?Or massive blood transfusion?

Stop Ingestion of (MG\aluminum ) with exchange Resin?

Stop Avid milk drinker? Increased calcium supplements?

Hypercalcemia? CRF? Nephrocalcinosis?

Milk-alkali synSeveral weeks of starvation with Refeeding?

Refeeding alkalosisHyper-calcemia?

Secondary hyper-calcemia

Uri

ne

chl

ori

de

Secondary hyper

-calce

mia :

Malignancy

Sarcoidosis

Vit-D intoxication

YES NO

YES NO

YES NO

YES NO

YES NO

Urine chloride

Chloride responsive metabolic alkalosis

Gastric losses? Diuretic therapy ?

Post-hyper-capnic ?Poorly re-absorbable anion

Chloride un-responsive metabolic alkalosis

Blood pressureGitelman-syn Bartter-syn

Hypo-magnesemia Hypo-kalemia

Plasma renin activity

< 20 mEq\L > 20 mEq\L

NORMAL HIGH

Plasma renin activity

Plasma aldosterone

Primary hyper-aldosteronisem

Consider Cushing syn?24-h urine

cortisolCushing syn

Exogenous

mineralcods?

Licorice ?Chewing tobacoo?

Stop

Bp >160\110,encephalopathy

papilledema? retinopathy?

Malignant HTN

Perform renal artery duplex scan?Renal

artery stenosi

s

Renin-secreting tumor

Nor \ decr

nor

yes No

Yes No

Case 1

A 43 year-old man with a history of a duodenal ulcer is admitted to the hospital after 3 days of anorexia and vomiting.

The physical examination shows mild orthostatic hypotension, flat neck veins, and decreased skin turgor.

LAB

chemistry138 NA

2,4 K

88 CL

40 HCO3

38 Urine SODIUM

60 Urine POTASSIUM

5 URINE CHLORIDE

ABG7,52 PH

50 PCO2

PH>7,37 •ALKALOSIS

PCO2>40 •METABOLIC

M.ALK COMP

•EXP p.co2=0,7(40)+(21)±2=49±2•50≈ 49

• PURE M.ALK •NOTE: There are wide variation in M.ALK equation

AG=10Normal AG (12±4)

•NORMAL AG

URINE CL <20

CASE 2

A 54 year old Mexican mestizo man was admitted to the Internal Medicine department

presenting with– altered mental status,– paresthesias,– hypokalemia, – and severe hypertension.

The patient worked as a teacher.

He was a 10 pack year smoker for 45 years and an occasional drinker.

He also has a history of using cocaine and smoking marijuana.

He lived a sedentary life, and was obese since childhood, being unable to lose weight with conventional diets.

He had no family history of cancer or surgical interventions.

CONT-The patient was in good health until three months before admission when he presented with:– fatigue, – intermittent paresthesias of all limbs,– cold intolerance, – polyuria, – weight gain, – and irritability.

He consulted a primary care physician that made a diagnosis of diabetes mellitus, hypertension, and dyslipidemia and began treatment with– Metformin 850 mg twice daily, – Glargine insulin 16 units in the morning, – Enalapril 10 mg twice daily, – and Atorvastatin 20 mg at night.

After one month, the patient discontinued the Enalapril on his own.

CONT-During the next few months the patient presented with generalized edema, abdominal striae, and depressive symptoms.

Also two days before admission he presented with confusion.

On arrival, the physical exam found him to be – obese, – with plethoric facies, – severe edema of the lower limbs, – bruising and red-purple abdominal striae.

He was confused without any sign of focalization or lateralization.

LAB

His vital signs showed

a blood pressure of 210/140 mmHg,

heart rate of 62 beats per minute,

respiratory rate of 14 per minute,

and temperature of 37.2 degree Celsius.

Blood biochemistry results were as follows:

CHEMISTRY

141 NA

1,8 K

99 CL

198 mg\dl GLUCO

0,74 mg\dl CREAT

702 LDH

26,7 ALT

91 CPK

3,2 ALBU

HEMATOLOGY

5,740 WBC

13,1 HB

161,000 PLAT

12 s PT

0,95 INR

URINE

45,9 NA

48,2 K

+++ GLUCO

+ PROTEIN

ABG

7,59 PH

50 PCO2

50,7 HCO3

90% SAO2

PH>7,37 •ALKALOSIS

PCO2>40 •METABOLIC

M.ALK COMP

•EXP p.co2=0,7(50,7)+(21)±2=56,49±2•50≠ 56,49

• concomitant R.ALK •NOTE: There are wide variation in M.ALK equation

AG= - 6Normal AG (12±4)

•NEGATIVE AG

Typical causes of a low anion gap

hypo-albuminemia , hyper-calcemia ,hyper-kalemia ,

hyper-magnesemia, lithium toxicity ,

multiple myeloma

Other causes of a low anion gap

• Increased chloride– Hypertriglyceridemia– Bromide– Iodide

• Decreased “Unmeasured anions”– Albumin– Phosphorous– IgA

• Increased “Unmeasured cations”– Hyperkalemia– Hypercalcemia– Hypermagnesemia– Lithium– Increased cationic

paraproteins• IgG

AlbuminPhosIgA

Chloride

Bicarb

Sodium

PotassiumCalcium

Magnesium

IgG

Normal Anion gap

Low serum anion gaplaboratory error Most frequent cause of low anion gap

underestimation of serum sodium

Most frequent with severe hyper-natremia or hyper-triglyceridemia

overestimation of serum chloride Rare with ion selective electrodes

overestimation of serum bicarbonate Spurious elevation in serum HCO3− if cells not

separated from sera

hypoalbuminemia Second most common cause of low serum anion gap

monoclonal IgG gammopathy Level of anion gap correlates with serum concentration of paraprotein

polyclonal gammopathy Might be more common cause of low anion gap than monoclonal gammopathy

bromide intoxication Anion gap depends on serum bromide concentration

lithium intoxication Low anion gap with lithium >4 mEq/L

Hyper-calcemia Inconsistent finding more likely with hypercalcemia associated with primary hyper-parathyroidism

Hyper-magnesemia Theoretical cause but not documented in literature

polymyxin B Anion gap depends on serum level; occurs with preparation with chloride

iodide intoxication Rare cause

Negative serum anion gap

laboratory error May be most common cause

bromide intoxication Second most common cause; values as low as −60 mEq/L reported

multiple myeloma Rare cause, more likely to have low anion gap

iodide intoxication Rare cause of negative anion gap

INVESTIGATION:

The electrocardiogram showed a first degree AV block.

The lungs where clear under auscultation.

The chest X-ray showed an undefined nodular opacity in the hilar region of the right lung (Figure 2).

We started: intravenous administration of large amount of potassium chloride (20 mEq per hour),

intravenous insulin,

and an intravenous antihypertensive (sodium nitroprusside).

Following the treatment he experienced complete remission of mental confusion, and improvement,

however his blood pressure did not normalize (150/100 mmHg).

INVESTIGATION:. Forty-eight hours later basal plasma renin activity and aldosterone were measured and determined as normal.

The respective values were 0.53 ng/ml/h (normal values between 0.2-2.8 ng/ml/h) and 52.5 pg/mL (normal values between 10-160 pg/mL).

The abdominal CT scan showed diffuse enlargement of the adrenal glands without focal lesions, without any abnormalities of the liver or spleen (Figure 3).

Plasma renin activity

Plasma aldosterone

Primary hyper-aldosteronisem

Consider Cushing syn?24-h urine

cortisolCushing syn

Exogenous

mineralcods?

Licorice ?Chewing tobacoo?

Stop

Bp >160\110,encephalopathy

papilledema? retinopathy?

Malignant HTN

Perform renal artery duplex scan?Renal

artery stenosi

s

Renin-secreting tumor

Nor \ decr

nor

yes No

Yes No

INVESTIGATION:The 24 hour free cortisol urinary levels were 6600 μg (normal values 4-100 μg) using the immunoenzymatic method.

The ACTH levels were 107 pg/mL (normal values are less than 46 pg/mL), by the quimioluminiscence method.

High dose dexamethasone suppression test (8 mg) showed suppression of approximately 8% of the cortisol serum levels.

A brain CT scan, including the sellar region was normal.

Final Diagnosis

On day 24 a CT guided fine-needle lung biopsy was performed,

showing histopathological results of a small cell neoplasm.

CONTIN:we started ketoconazole 400 mg twice daily with a rapid normalization of blood pressure and potassium plasma levels.

Seventy two hours later the patient presented with sepsis due to a right leg cellulitis that was treated with meropenem.

Despite a partial response to the medical treatment the patient worsened and developed bilateral pleural effusions, and respiratory failure that required assisted mechanical ventilation dying a few days later.

Discussion: The case reported here was presented as a hypertensive crisis associated with hypokalemia, severe metabolic alkalosis and neuropsychiatric symptoms.

The rapid deterioration of his health, and some cushingoid characteristics, strongly suggested that the clinical symptoms were secondary to some cause of Cushing's syndrome .

Once the blood pressure of the patient decreased, and large amounts of potassium were administrated, a rapid improvement in his neurological status was observed.

However, the patient continued to demonstrate minor depressive symptoms (mainly apathy, hypersomnia, irritability, and hopeless thoughts).

Discussion: In patients with EAS, psychiatric symptoms are frequently reported in about 50% of cases.

The most frequent are depression and psychosis .

The elevated levels of ACTH, free urinary cortisol excretion, a positive high dexamethasone suppression test and the hilar opacity observed in chest X-ray strongly suggested that the clinical symptoms were due to a malignant ACTH secreting neoplasm.

Discussion

The gold standard for the differential diagnosis of pituitary and ectopic ACTH-dependent Cushing's syndrome is the bilateral inferior petrosal sinus sampling after administration of CRH (1 μg/kg).

A ratio greater than 3.0 after the administration of CRH is consistent with Cushing's disease.

Patients with EAS will have a ratio less than 2 before and after CRH administration because the endogenous hypercortisolism suppresses pituitary ACTH release through negative feedback mechanisms (sensitivity 97%, specificity 100%).

High-dose dexamethasone suppression tests have lower sensitivity (81%) and specificity (67%).

QUIZE

The SCLC is a well recognized origin of EAS.

The incidence of SCLC is about 13% of all newly diagnosed lung cancers in Mexico.

Ketoconazole has been used to treat Cushing's syndrome by inhibiting adrenal glucocorticoid synthesis.

Treatment with ketoconazole promotes a palliative hormonal response in more than 50% of patients.

In this patient, ketoconazole (400 mg twice daily) promoted a rapid resolution of hypokalemia and hypertension.

Due to a rapid clinical deterioration, the patient was not able to receive standard chemotherapy with carboplatin and etoposide for SCLC.

Conclusion

EAS requires a well established diagnostic work up, and must be considered strongly in patients with:

– hypertension .– severe hypokalemic metabolic alkalosis. – especially when a lung mass is discovered.

Case 3

A 56 y.o. male with a history of hypertension and gout is seen for routine follow up by his primary care physician.

Medications include metoprolol, colchicine, aspirin and meloxicam.

On PE the BP is 130/80, HR 86, RR 16, T 36.1. The heart exam shows an S4 gallop.

The remainder of the exam is benign.

Case 3 :LabsSerum

Sodium 140

Potassium 5.9

Chloride 110

Bicarbonate 18

BUN 18

Creatinine 1.1

Glucose 76

ABG

pH 7.35

pCO2 35

pO2 106

Urine

Sodium 26

Potassium 22

Chloride 28

Urinalysis shows pH 5.2, (-) glucose, (-) blood, no casts. Urine P/C = 0.052.

Which of the following is the most likely cause for the laboratory abnormalities?

A. Increase potassium intake

B. Rhabdomyolysis

C. Distal RTA(4)

D. Adverse effect of meloxicam

E. Adverse effect of colchicine

PH<7,37 •ACIDOSIS

PCO2<40 •METABOLIC

M.AC COMP

•EXP p.co2=1,5(18)+(8)=35±2•35=35• pure M.AC

AG=12Normal AG (12±4)

•NORMAL AG M.AC

Calculate urine AG

Consider : type (1; 2 ;4) RTA;

RTA of renal insufficiency

Plasma KLow

URINE PH

RTA 1 RTA 2

NormalRTA of renal insuffiency

(1;2) RTA

HighRTA 4

Consider causes of normal AG metabolic acidosis besides RTA

(i.e; GI loss )<5,5 >5,5Urine AG = (UNA +UK) - UCL

)+( 20 URINE AG=

K=5,9

Which of the following is the most likely cause for the laboratory abnormalities?

A. Increase potassium intake

B. Rhabdomyolysis

C. Distal RTA(4)

D. Adverse effect of meloxicam

E. Adverse effect of colchicine

Causes of Type IV Distal RTA

• Diabetic nephropathy• Tubulointerstial

disease• Cyclosporine and

tacrolimus• Transplant rejection• Adrenocorticoid

insufficiency

Drugs– NSAIDS, Cox 2 inhibitors– ACE inhibitors– Heparin– Beta-blockers– Ketoconazole– Spironolactone, eplerenone– Triamterene, amiloride,trimethoprim, pentamidine

Obstructive uropathy*

Sickle cell nephropathy**Probably due to “voltage

dependent” type I RTA which

has a similar clinical picture

(hyperkalemia, non-gap acidosis)

Inhibitors of the Renin-Angiotensin-Aldosterone System

Case 4 A 26 y.o. male with severe asthma presents with nausea, vomiting,

increased anxiety and dyspnea. Medications include albuterol, Advair, prednisone and theophylline. He was recently prescribed ciprofloxacin for symptomatic diarrhea

after returning home from vacation in Mexico. On exam he is tremulous. BP 110/80. He is in moderate respiratory distress using accessory respiratory

muscles. HR is 120 with frequent extra systoles. Lungs show poor air movement and wheezes. There is no edema.

ABG

pH 7.27

pCO2 70

pO2 60

SerumSodium 138

Potassium 3.2

Chloride 95

Bicarbonate 31

BUN 26

Creatinine 1.4

Glucose 68

PH<7,37 •ACIDOSIS

PCO2>40 •RESPIRATORY

ACUTE.R.AC COMP

•∆HCO3=0,1(70- 40)=3 (+24)•27≠ 31

• concomitant M.ALK •NOTE: There are wide variation in M.ALK equation

AG=12Normal AG (12±4)

•NORMAL AG

Which best describes the acid-base status of this patient?

A. Mixed acute respiratory acidosis with superimposed metabolic alkalosis

B. Mixed metabolic acidosis and chronic respiratory acidosis

C. Acute and chronic respiratory acidosis

D. Mixed respiratory alkalosis and metabolic acidosis

QUIZE

Theopyliine toxicity:Narrow therapitic range.

symptoms

Drugs intraction

CASE 5

A 55 year old insulin dependent diabetic woman was brought to Casualty by ambulance.

She was semi-comatose and had been ill for several days.

Past history of left ventricular failure.

Current medication was:– digoxin.– thiazide diuretic.

LAB

• Glucose = 1206 mg\dl

CHEMISTRY 2,7 K

67mmol\l GLUCO

34 AG

ABG7,41 PH

32 PCO2

82 PO2

19 HCO3

PH:7,37-7,43 •NORMAL ∕ MIXED

PCO2<36 •RES.ALK

HCO3<21•METABOLIC .AC•EXP p.co2=1,5(19)+(8)±2=36,5 ±2•36≠ 32•CONCOMITANT RES.ALK•

AG=34Normal AG (12±4)

•HIGH AG M.AC

GAP:gap>2=(22\5) •Concomitant M.ALK

What etiology for each disorders ?•High AG M.AC•M.ALK•R.ALK

Discussion This lady is a known diabetic and she presents with mental obtundation and severe hyperglycaemia.

The clinical diagnosis suggested by the history is – diabetic ketoacidosis (DKA) or – hyperosmolar non-ketotic coma (NKHC).

There are several other points to always be aware of in diabetic patients:

They may have a non-diabetic cause of coma (eg stroke, head injury, sub-arachnoid haemorrhage, hyponatraemia) so don't immediately assume a diabetic cause

Coma is uncommon in patients presenting with DKA

There may be other acid-base disorders complicating the picture – metabolic alkalosis from vomiting or from diuretic use; – respiratory acidosis from pneumonia and respiratory failure; – respiratory alkalosis from anxiety; – lactic acidosis from peripheral circulatory failure)

A patient with an "obvious diabetic ketoacidosis" should always be approached with these considerations in mind

Which diagnosis is true?

DKA

NK-HC

LACTIC ACIDOSIS

VOMITING IN DKA

DIURETIC EFFECT IN DKA

Which diagnosis is true?

DKA (urine.serum ketones?,coma?)

NK-HC ( high AG M.AC ?)

LACTIC ACIDOSIS (blood pressure?)

VOMITING IN DKA (urine CL?)

DIURETIC EFFECT IN DKA (urine CL?)

NEXT LECTURE

1. Respiratory disorders2. Cases