This document provides information on interpreting arterial blood gas results to diagnose acid-base disorders. It discusses the four primary acid-base disorders: respiratory acidosis, metabolic acidosis, respiratory alkalosis, and metabolic alkalosis. Compensatory changes in response to these disorders are explained. The mechanisms by which the body controls acid-base balance through buffers, kidneys, and lungs are outlined. A stepwise approach to interpreting ABG results is provided to determine if there is acidemia/alkalemia, the primary disturbance, compensation, and high anion gap. Causes and characteristics of different acid-base disorders are described.
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
It is characterized by a yellow appearance of the (1) Skin (2) Mucous membranes and (3) Sclera caused by bilirubin deposition. It is the most specific clinical manifestation of Hepatic dysfunction.
Jaundice is usually present clinically when the plasma bilirubin concentration reaches 2 to 3 mg/dl.
When bilirubin clearance from the Liver to the Intestinal tract is impaired (as in acute hepatitis and bile duct obstruction) it may be accompanied by alcoholic (Gray coloured) stools.Solubility increases in water , soluble conjugated bilirubin leads to Tea coloured urine.
one can learn the step by step approach of ABG interpritation and its analysis from basics with the help of different case scenarios,Ref-NEJM article regarding physiological approach to acid base disbalance
Potassium is the principal cation of the intracellular fl uid
(ICF) where its concentration is between 120 and 150 mEq/L.
The extracellular fl uid (ECF) and plasma potassium concentration [K] is much lower––in the 3.5–5.0 mEq/L range.
The very large transcellular gradient is maintained by active
K transport via the Na-K-ATPase pumps present in all cell
membranes and the ionic permeability characteristics of
these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the
transcellular resting potential gradient, about 90 mV with
the cell interior negative . Normal cell function
requires maintenance of the ECF [K] within a relatively narrow
range. This is particularly important for excitable cells
such as myocytes and neurons. The pathophysiologic effects
of dyskalemia on these cells result in most of the clinical
manifestations.
It is characterized by a yellow appearance of the (1) Skin (2) Mucous membranes and (3) Sclera caused by bilirubin deposition. It is the most specific clinical manifestation of Hepatic dysfunction.
Jaundice is usually present clinically when the plasma bilirubin concentration reaches 2 to 3 mg/dl.
When bilirubin clearance from the Liver to the Intestinal tract is impaired (as in acute hepatitis and bile duct obstruction) it may be accompanied by alcoholic (Gray coloured) stools.Solubility increases in water , soluble conjugated bilirubin leads to Tea coloured urine.
one can learn the step by step approach of ABG interpritation and its analysis from basics with the help of different case scenarios,Ref-NEJM article regarding physiological approach to acid base disbalance
This presentation discuss about acid-base-gas normal ratio and its indication in relation to varying abnormal level and how to manage it. This includes clinical analysis practice.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
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The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
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Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journey
Arterial blood gas
1.
2. Learning outcomes:
Interpret arterial blood gas results in a stepwise and logical manner to
make a correct diagnosis
Know the causes of metabolic and respiratory acidosis and alkalosis
3. There are four primary acid base disorders:
Respiratory acidosis
Metabolic acidosis
Respiratory alkalosis
Metabolic alkalosis
They are usually accompanied by compensatory changes
These changes rarely compensate fully for the primary disorder
In a chronic disorder the magnitude of compensation is greater with
subsequent better protection of the pH
4. Always look at the clinical picture when
interpreting blood gas
5. There are 3 mechanisms by which the body controls the blood
acid-base balance within the narrow range (7.34 – 7.45 ):
Intracellular and extracellular buffers .
Regulation by the kidneys.(regulate the conc. Of HCO3 by adjusting renal excretion of
carbonic acid and the reabsorbtion of bicarbonate)
Regulation by the lungs.(Regulate Pco2 by adjusting rate of alveolar ventilation)
The most important buffer system involve :
Hemoglobin
Carbonic acid (weak acid formed from the dissolved CO2)
Bicarbonate (weak base )
6. Blood gas analysers directly measures pH and Pco2.
HCO3 is calculated from the Henderson-Hasselbalch equation.
This equation shows that the pH is determined by the ratio of HCO3
concentration to pCO2, not by the value of either one alone.
pH=(6.1) + log
𝐻𝐶𝑂3
(0.03)×𝑝𝐶𝑂2
The simplified version from the equation will help you to understand
the compensatory changes
pH∽
𝐻𝐶𝑂3
𝑝𝐶𝑂2
7. determine acid base balance
Determine oxygenation (arterial pO2 gives information about gas exchange)
Diagnose and establish the severity of respiratory failure (Pco2 gives
information about ventilation)
Guide therapy for example oxygen or non invasive ventilation in patients with
chronic obstructive pulmonary disease or therapy in patients with DKA,
8. Acidemia : this occurs when pH is < 7.35
Alkalemia : this occurs when pH is > 7.45
Acidosis :
• This is a process that cause acid to accumulate
• It does not necessarily result in abnormal pH
• from the Henderson-Hasselbalch equation you can see acidosis can be
induced by fall in HCO3 conc or rise in Pco2
• pH∽
𝐻𝐶𝑂3
𝑝𝐶𝑂2
• Occuring alone it tends to cause acidemia
• Occuring at the same time as an alkalosis the resulting pH may be normal
,high or low
9. Alkalosis
this is the process that cause alkali to accumulate
It does not necessarily result in abnormal pH
From th equation you can see the alkalosis can be induced by a rise in HCO3
conc. Or a fall in pCO2
pH∽
𝐻𝐶𝑂3
𝑝𝐶𝑂2
When it occurs alone it tends to cause alkalemia
When it occurs at the same time as an acidosis the resulting pH may normal
,high or low.
10. base excess
Is the quantity of base or acid needed to titrate one litre of blood to pH
7.4 with the pCO2 held constant at 5.3 kPa
11. Step 1 is there is an acidemia or an alkalemia ?
Step 2 is the primary disturbance respiratory or metabolic ?
Step 3 for metabolic acidosis is there a high anion gas ?
Step 4 is there compensation ? If there is ,is it appropriate ?
13. Look at the pH if it is:
< 7.35 the patient is acidaemic
> 7.45 the patient is alkalaemic
If the pH is normal look at the pCO2nn & the concentration of HCO3 IF either
one or both is abnormal the patient may have mixed disorder
14. Look at the pH , pCO2 and the concentration of HCO3:
If the pH is< 7.35 an acidosis is causing acidemia and:
* if pCO2 is increased there is a primary respiratory acidosis
* if the conc, of HCO3 is decreased there is primary metabolic
acidosis
If pH is> 7.45 an alkalosis is causing alkalemia and :
* if pCO2nn is decreased there is a primary respiratory alkalosis
* if the conc. Of HCO3 is increased there is a primary metabolic
alkalosis
15. you are called to see a 12 years old girl on the orthopedic unit who had a
right fracture femur 1 week ago . She become breathless . Her arterial blood
gas results are as follows:
pH : 7.48
pO2 : 62 mmHg
pCO2 : 25 mmHg
HCO3 : 25 mmol/L
What is her acid base disturbance ?
Step 1------- there is an alkalemia
Step 2-------her pCO2 is decreased so this is a primary respiratory
alkalosis . The DD would include pulmonary embolus and hospital acquired
pneumonia
16. You see 11 years boy in emergency departement . He has been vomiting for
the last 24 hours and feels unwell . His arterial blood gas results as follows :
Na : 138 mmol/L
K : 3 mmol/L
Urea : 7.8 mmol/L
Creatinine : 130 mmol/L
pH : 7.49
pO2 : 98 mmHg
pCO2 : 38.5 mmHg
HCO3 : 31 mmol/L
Step 1 : there is alkalemia
Step 2 : his conc. Of HCO3 is increased,so it is a primary metabolic alkalosis
( due to GIT loss of H ions from vomiting)(hypokalemia may also contributing
to the metabolic alkalosis)
17. for the metabolic acidosis is there a high anion gap
Identifying the type of acidosis will help you to narrow down the possible
underlying causes
What is the anion gap?
in the body the number of cations and anions are equal .blood tests measure
most cations but only a few anions ,therefore adding all the measured anions
and cations together leaves a gap that reflects unmeasured anions such as
plasma protein albumin
Because Na is the primary measured cation and CL&HCO3 are the primary
measured anions the anion gap is calculated using the following formula :
Na – ( HCO3 + CL )
The normal anion gap is ( 8- 16 ) mmol/l
Some hospital laboratories include K when caculating the anion gap , when K
is included the normal range is ( 12 -20) mmol /L
18. MAIN CAUSES OF HIGH ANION GAS ACIDOSIS
INABILITY TO EXCRETE ACIDSINCREASED EXOGENOUS ACID SINCREASED ENDOGENOUS ACID
PRODUCTION
Chronic renal failureMethanol
Ethylene glycol
Aspirin
KETOACIDOSIS
LACTIC ACIDOSIS
TYPE A: impaired tissue O2
TYPE B:tissue O2 not impaired
19. Impaired renal acid excretionLoss of bicarbonate
• Type 1( distal) RTA
• Type 4 RTA (hypoaldosteronism)
• GIT :
o diarrhoea
o ileostomy
o pancreatic ,biliary,intestinal
fistula
• Renal :
o type 2 proximal RTA
o carbonic anhydrase inhibitors
20. A patient with low albumin concentration may have a normal anion gap in the
presence of of a disorder that ususally produces a high anion gap
The anion gap is reduced by about 2.5 mmol/L for every 10 g/L fall in
albumin concentration
21. a 12 years old boy with chronic liver disease is admitted following an upper
GIT bleed. His blood pressure is 70/30 mm .. His arterial blood gas results as
follows:
Albumin : 20 g/L (n=40 g/L0
Na : 135 mmol/L
K : 3.5 mmol/L
CL : 100 mmol/L
pH : 7.3
pCO2 : 25.4 mmhg
HCO3 : 20 mmol/L
Lactate : 5 iu/L
What is the anion gap and what acid base disturbance does he have ?
22. Ist calculate the anion gap Na – (CL + HCO3)
135- (100+200) = 15 mmol/L
This is within the normal range of (8-16)
Next coreect the anion gap
Gap= 15
Albumin = 20 g/l
The anion gap is reduced by about 2.5 mmol/L for every 10 g/L fall in albumin
concentration.
Therefore the anion gap is reduced by 5 mmol/l
Anion gap = 15 +5 = 20
This patient therefore has a high anion gap metabolic acidosis
In view of high lactate and hypotension this is likely secondary to lactic acidosis
type 1
23. 9 years odgirl feels unwell .she is thirsty and drinking lots of fluids. Her
arterial blood gas results are as follows:
Glucose : 30 mmol/L
pH : 7.32
pO2 : 88.5 mmhg
pCO2 : 23.1 mmhg
HCO3 : 18 mmol/L
Na : 148 mmol/L
K : 3.5 mmol/L
CL : 100 mmol/L
What acid base disturbance does he have ?
24. Step 1 : there is acidemia
Step 2 : his concentration of HCO3 is decreased
so this is primary metabolic acidosis
Step 3 : the anion gap = Na – (CL + HCO3 ) = 148-118 = 30 mmol/L ⇡⇡⇡
This patient has a high anion gas acidosis most likely due to DKA.
25. 10 years old boy with ulcerative colitis has had severe diarrhoea for the past
2 days . His labs as follows:
Creatinine : 200 mmol/L
Urea : 17 mmol/L
pH : 7.31
pO2 : 96 mmhg
Pco2 : 30.7 mmhg
HCO3 : 14 mmol/L
Na : 135 mmol/L
K : 3.1 mmol/ L
CL : 113 mmol/L
What acid base disturbance does he have ?
26. Step 1 : acidemia
Step 2 : HCO3 ⇣⇣( primary metabolic acidosis )
Step 3 : the anion gap 135 – (113 + 14 ) = 8 mmol/L
This patient has normal anion gap metabolic acidosis most likely secondary
to loss o HCO3 from severe diarrhoea .
27. Compensation refer to the action taken by the body to restore the correct
acid base balance . The normal comensatory measures are:
Buffers : which include hemoglobin , plasma proteins ,bicarbonate and
phosphate . This response occurs in minutes.
Ventilatory response , which occurs in minutes to hours
Renal response which may take up to several days.
Recognising compensation will help you to separate primary disorders from
derangement that exist only because of 1ry disorder .
A useful aid is to be aware of the expected degree of compensation for the
primary disorder,
28. magnitude of compensationCompensatory
response
Initial chemical
change
Acid base disturbance
For every 10 mmhg increase in pCO2above
40 mmhg in acute respiratory acidosis :
The HCO3 increases by 1 mmol/L
The pH decreases by 0.07
For every 10 mmhg icrease in pCO2 above 40
mmhg in chronic respiratory acidosis
the HCO3 increases by 3.5 mmol/L
The pH decreases by 0.03
↑ HCO3↑ pCO2Respiratory
acidosis
for every 10 mmhg decrease in pCO2 below
40 mmhg in acute respiratory alkalosis
The HCO3 decreases by 2 mmol/L
The pHnn increses by 0.08
For every 10 mmhg decrease in pCO2nn below
40 mmhg in chronic respiratory alkalosis :
The HCO3 decreases by 5 mmol/L
The pHnn increases by 0.03
↓ HCO3↓ pCO2
Respiratory
alkalosis
29. Magnitude of compensationCompensatory
response
initial chemical
changes
Acid base disorder
Stimulation of the central and peripheral
chemoreceptors that control respiration results in
an increase in alveolar ventilation this in turn
causes a compensatory respiratory alkalosis
↓ pCO2↓ HCO3Metabolic acidosis
It is difficult to hypo ventilate to compensate
oxygenation also compromised by hypoventilation .
The respiratory system therefor rarely retain
pCO2nn to > 58 mmhg. A value greater than this
suggests a mixed disorder .that is metabolic
alkalosis and respiratory acidosis rather than a
compensated metabolic alkalosis
↑ pCO2↑ HCO3Metabolic alkalosis
30. You should suspect a mixed acid-base disorder when:-
The compensatory response occurs but the level of compensation is in
adequate or too extreme.
As a rule of thumb
When the pCO2 is ↑and the HCO3 CONC is↓respiratory acidosis and
metabolic acidosis coexist.
When the pCO2 is ↓HCO3 IS ↑respiratory alkalosis and metabolic alkalosis
coexist.
31. 3 years old boy presented to ER after accidental ingestion of benzodiazepine
his mother had depression on medication.
His ABG as follows:
pH : 7.3
pO2 : 85 mmhg
pCO2 : 60 mmhg
HCO3 : 25 mmol/L
Step1: acidemia
Step 2: pCO2nn is raied so this is primary respiratory acidosis
Step 4: his concentration of bicarbonate is normal,so there is no compensation.
The history is acute . Metabolic compensation takes days
He has acute respiratory acidosis 2ry to CNS depression of his respiratory drive
by the benzodiazepine overdose
32. ABG
pH : 7.34 ↓
pO2: 69 mmhg ↓
pCO2 : 60 mmhg ↑
HCO3 : 32 mmol/L ↑
What is the acid base disturbance
33. 17 years old with Duchene muscular dystrophy is admitted with UTI . He has
a temp of 39 c .he feels warm and peripherally vasodilated with a blood
pressure of 90/60 mmhg . Since being catheterized one hour ago he passed
5 ml urine. His ABG
pH : 7.28 ↓
pO2 :83mmhg ℕ
pCO2 : 45 mmhg ↑ℕ
HCO3 : 18 ↓
Na : 146
K : 4.5
CL : 101
34. pH : 7.28 ↓
pO2 :83mmhg ℕ
pCO2 : 46 mmhg ↑ℕ
HCO3 : 18 ↓
Na : 146
K : 4.5
CL : 101
Step 1 : acidemia
Step 2 : pCO2nn upper normal and his HCO3 concentration is decreased
Step 3 ; the anion gap 146 – ( 18 + 101 ) = 27 mmol/L ↑↑
Step 4 : for metabolic acidosis you would expect the pCO2 to be reduced .
For respiratory acidosis you would expect the HCO3 to be increased .
Therefore he had mixed acid-base disorder . He has high anion gap
metabolic acidosis most likely from septic shock and a respiratory acidosis
rom DMD.
35. 12 years girl is admitted following a mixed overdose of ibuprofen and
paracetamol. She currently appears well sitting up in bed and conversing
normally. (HR 79 bpm, RR 16 pm ,blood pressure 112/71 ,saturation 98 %,
temp 36.5 c) her blood gas shows
pH : 7.37
pO2 : 51.6 mmhg
pCO2 : 47 mmhg
HCO3 : 28 mmol/L
Saturation 76%
What does it show ?
A. A fully compensated respiratory acidosis
B. Acute hypoxia type 1 respiratory failure
C. A venous blood gas
D. A fully compensated metabolic alkalosis
36. pH : 7.40
pO2 : 65 mmhg
pCO2 : 60 mmhg
HCO3 : 44 mmol/L
What is the acid base balance ?
A. Mixed respiratory acidosis and metabolic alkalosis
B. Metabolic alkalosis with appropriate respiratory compensation
C. Respiratory acidosis with appropriate metabolic compensation
37. o pH : 7.33
o pO2 : 90 mmhg
o pCO2 : 34.6 mmhg
o HCO3 : 18 mmol/L
o Na : 135
o K : 3.5 mmol/L
o CL : 110 mmol/L
o Urea : 6.8 mmol/L
o Creatinine : 125 umol/L
o Albumin : 30 g /L
What is the acid base disturbance ?
A. High anion gap metabolic acidosis
B. Normal anion gap metabolic acidosis