This document provides guidance on interpreting arterial blood gases (ABGs). It begins with 11 sample ABG results and asks the reader to identify the primary acid-base disorder in each case. The document then provides detailed explanations for interpreting ABGs and diagnosing mixed acid-base disorders. Key points include calculating the anion gap and excess anion gap to identify concurrent metabolic acidosis or alkalosis complicating the primary disorder suggested by pH, PCO2 and HCO3 levels. The goal is to methodically analyze ABG results to determine the underlying physiologic disturbance(s).
Acid Base Balance for EMS presentation - appropriate for all levels of EMS personnel; includes interactive components for audience and small group participation and learning; questions? call Porter, Littleton and Parker EMS in Colorado at 303-765-6367 (303-765-6EMS)
New models of acid-basebalance and their application to critical care nephro...Christos Argyropoulos
A short introduction to Stewart's model of acid-base disturbances. Modified from a talk I gave during a fellow's retreat back in 2006 in the beautiful Seven Spring's resort.
Will probably get excommunicated by the Nephrology Orthodoxy for endorsing Stewart's "heresy" :) but it is worth it!
This book explores important clinical problems in general nephrology, dialysis and transplantation, using a case-based approach. Together the 32 chapters form a comprehensive collection of clinical vignettes in renal medicine. Each chapter covers a separate clinical problem, posing multiple-choice questions and providing a detailed explanation for each. Clinical Pearls highlight the key issues. Each graded into three disctinct levels, to provide pertinent information tailored to the reader's knowledge level.
Acid Base Balance for EMS presentation - appropriate for all levels of EMS personnel; includes interactive components for audience and small group participation and learning; questions? call Porter, Littleton and Parker EMS in Colorado at 303-765-6367 (303-765-6EMS)
New models of acid-basebalance and their application to critical care nephro...Christos Argyropoulos
A short introduction to Stewart's model of acid-base disturbances. Modified from a talk I gave during a fellow's retreat back in 2006 in the beautiful Seven Spring's resort.
Will probably get excommunicated by the Nephrology Orthodoxy for endorsing Stewart's "heresy" :) but it is worth it!
This book explores important clinical problems in general nephrology, dialysis and transplantation, using a case-based approach. Together the 32 chapters form a comprehensive collection of clinical vignettes in renal medicine. Each chapter covers a separate clinical problem, posing multiple-choice questions and providing a detailed explanation for each. Clinical Pearls highlight the key issues. Each graded into three disctinct levels, to provide pertinent information tailored to the reader's knowledge level.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
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
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
1. Nephrology is the ART of Homeostasis
PREPARED BY
DR MOHAMMED AL
SHAER
NEPHROLOGY SPECILAIST
• KFH-MADINA
ACID BASE DISORDERS
2. CASE 0
73YEARS OLDWOMEN WITH DM,CHF,CKD .
PRESENTEDWITH NAUSEA,VOMITINGAND
SOP.SHE IS ON INSULIN AND LASIX.WT 6O KG .
Biochem :Na 140 k 4 Cl 95 HCO3 24 CREAT. 4.1 BUN
54 MG/DL GLU 145 ALB 4.1
VBG :PH 7.40 PCO2 40 PO2 90 HCO3 24.
WHAT ISTHE ACID BASE DISORDER:
A –METAB.ACIDOSIS AND RESP. ACIDOSIS
B-METAB. ACIDOSIS AND METAB.ALKALOSIS
C-METAB.ACID.+METAB. ALKALOSIS AND RESP.ACID
D-RESP.ALKALOSIS AND METAB. ALKALOSIS
E-NON OFTHE ABOVE…IT IS NORMALABG..
3.
4. WHY ABG !!
To document respiratory failure and assess its
severity.
To monitor patients on ventilators and assist
in weaning.
To assess acid base imbalance in critical
illness.
To assess response to therapeutic
interventions and mechanical ventilation.
To assess pre-op patients.
NB: NOT EVERY DYSPNIC PATIENT NEEDSABG
(e.g. BA,CHF,ESRDWITH MILD SYMPTOMS)
5. Why an ABG instead of Pulse
oximetry ?
Pulse oximetry does not assess
ventilation (pCO2) or acid base status.
Pulse oximetry becomes unreliable
when saturations fall below 70-80%.
Technical sources of error (ambient or
fluorescent light, hypoperfusion, nail
polish, skin pigmentation)
Pulse oximetry cannot interpret
methemoglobin or carboxyhemoglobin.
6.
7.
8.
9.
10.
11. INFORMATION PROVIDED BY ABG..CONT
• PH MEASURES THE HYDROGEN(H+)IONS IN
THE BLOOD..
• PH OF THE BLOOD IS USUALLY KEPT
BETWEEN 3.35 - 4.45 and RESULTS ABOVE
CONSIDERED ALKALOSIS AND BELOW IS
CONSIDERED ACIDOSIS..
• KEPP IN MIND THAT RESULTS BETWEEN 3.35-
4.45 IS NOT NORMAL AT ALL AND CAN
REFLECT COMPENSATED ACID BASE
DISORDER…..
24. INTERPRETITION OF ABG
WHENYOU INTERPRETE THE ABG
DEPEND ON THE OPTIMAL
FIGURES
PH 7.40 PCO2 40 HCO3 24
ANION GAP 10 +/- 2
AG =Na –OCH + LC( 3) OR
Na – CL –HCO3
26. How to CONFIRM THAT ABG IS TRUE!!
USE HANDERSON-HASELBALCH EQUATION
[H+] = 24(PaCO2 )/ [HCO3 -]
27.
28. PEARLES
WORK ONLY IFYOU CALCULATETHEANION GAP
(AG) CORRECTLY..
ABG AND BIOCHEM. DRAWN ATTHE SAMETIME
HAVVALUESWITHIN /+- 2 OF EACH OTHER..
THERE IS AN SD OF ABOUT 3ON EACH FORMULA
WEWILL USE 24 FOR HCO3 AND 10-12 FOR AG..
ALWAYS BE SURE THAT DIAGNOSIS IS
CONSISTANT HISTORYANDTHE PH ..
YOU CAN HAVE MULTIPLE METABOLIC
DISORDERS BUT ONLY A SINGLE RESPIRATORY
DISORDER..
29. PEARLS…CONTINUED
INTERPRETE USINGTHE OPTIMAL FIGURES: PH 7.40
PCO2 40 HCO3 24 so results above or below
should be considered abnormal until finishing
evaluation.
PCO2 AND HCO3 ARE CLOSE FRIENDS! Move
up or down togather but within limits.
Compensation for metabolic disorder is single
phase while for respiratory two phases(acute
and chronic)..
LUNG STARTTO COMPENSATE WITHIN 1-3
MINUTES WHILE KIDNEYSTAKES HOURSTO
DAYS..
30.
31. PH < 3.35 indicates ACIDEMIA..
PH > 4.45 indicates ALKALOSIS..
PH BELOW 6.8 AND ABOVE 7.8 IS
INCOMPATABLEWITH LIFE..MEANS DEATH
DON’T FORGET THAT PH BETWEEN 3.35 -
4.45 IS THE NORMAL RANGE BUT
DOESN’T RULE OUT ABNORMAL ACID
BASE DISORDER ..!!!!YOU SHOULD LOOK
TO ALL PARAMETERS ANDTHE ANION
GAP..
32.
33.
34.
35.
36.
37. • IN GENERAL WE USE THIS EQUATION
AG = NA –CL-HCO3
72. SUMMERY OF ABG APPROACH 1
Step 1: is it reliable ? HANDERSON-HASELBALCH
STEP2 : Comprehensive history and physical
examination.
STEP 3 : Acidosis or alkalosis..? See the pH (7.40)
STEP 4 : Identify the primary disorder See the change
in PCo2 & HCO3
STEP 5 : Calculate the compensatory response Is IT
adequately compensated???
STEP 6 : Calculate Anion Gap ESPECIALLY IN
Metabolic Acidosis
STEP 7 : Calculate the Delta Gap= DELTA-DELTA =
DELTA AG (unmask hidden mixed disorders) ..
73. SUMMERY OF ABG APPROACH 2
STEP -8 : Calculate the osmolar gap (for
HighAG acidosis)
STEP -9 : Calculate the urinary anion gap (IN
Non AG MetabolicAcidosis)
STEP -10 : Formulate Differential Diagnosis
74. CASE 1
73YEARS OLDWOMEN WITH
DM,CHF,CKD,PRESENTEDWITH NAUSEA,VOMITING
AND SOP.SHE IS ON INSULIN AND LASIX.WT 6O KG .
Biochem :Na 140 k 4 Cl 95 HCO3 24 CREAT. 4.1
BUN 54 MG/DL GLU 145 ALB 4.1
VBG :PH 7.40 PCO2 40 PO2 90 HCO3 24.
WHAT ISTHE ACID BASE DISORDER:
1 –METAB.ACIDOSIS AND RESP. ACIDOSIS
2-METAB. ACIDOSIS AND METAB.ALKALOSIS
3-METAB.ACID.+METAB. ALKALOSIS AND RESP.ACID
4-RESP.ALKALOSIS AND METAB. ALKALOSIS
5-NON OFTHE ABOVE…
75. CASE 1 ANSWER B
AG = 140 – 95 – 24 =21 HIGH AG MEANS
SHE HAS HAGMA (DUETO RENAL
FAILURE)
SHE has vomiting and receiving
furosemide which causes METABOLIC
ALKALOSISWHICH NORMALISES THE
PH AND HCO3..
DELAT AG = 21-10 = 11
11 +24( HCO3) = 35.. (IF > 30 there is
Metabolic Alkalosis and if < 24 NAGMA)
76. CASE 2
ABG:
PaCO2 27 mm Hg HCO3 13
PaO2 105 mm Hg
H+ 70 mmhg
Na+ 134 mmol/L
BIOCHEM:
K+ 3.7 mmol/L Cl- 109 mmol/L
HCO3 20 mmol/L Albumin 4.0 g/dL
• AG 12
77. CASE 2 ANSWER
H+ = 24 X 27/ 13 = 49.8
Not Reliable test as H +ON
ABG IS 70 WHILE USING
HANDERSON EQUATION IT S 50,AT
THE SAMETIME NOTETHAT HCO3
ON ABG IS 13WHILE ON BIOCHEM
20
78. CASE 3
ABG
• pH 7.28 • PaCO2 27 mm Hg
• PaO2 105 mm Hg • H+ 50 mmhg •
BIOCHEM:
Na+ 134 mmol/L • K + 3.7 mmol/L • Cl-
109 mmol/L • HCO3 - 14 mmol/L •
Albumin 4.0 g/Dl
AG 12
79. CASE 3 ANSWER
1. pH: ↓(acidosis)
2-THE CAUSEWOULD BE EITHER LOW
HCO3 OR HIGH PCO2
Anion Gap: Normal . Compensation
COMPENSATED(expected pco2 (27-
31) using winter formula
NON-ANION GAP METABOLIC ACIDOSISWITH
ADEQUATE COMPENSATION
84. CASE 8
pH 7.20
pCO2 21
HCO3 8 Variabl
e
Primary
Disorder
Normal Range,
arterial Gas
Primary
Disorder
pH Acidemia 7.35-7.45 Alkalemia
pCO2 Respiratory
alkalosis
35 - 45 Respiratory
acidosis
HCO3 Metabolic
acidosis
22 – 26 Metabolic
Alkalosis
Metabolic Acidosis with
Respiratory Compensation
85. CASE 9
pH 7.40
pCO2 40
HCO3 24
Na 145
Cl 100 Variable Primary
Disorder
Normal
Range,
arterial Gas
Primary
Disorder
pH Acidemia 7.35-
7.45
Alkalemia
pCO2 Respiratory
alkalosis
35 - 45 Respiratory
acidosis
HCO3 Metabolic
acidosis
22 – 26 Metabolic
Alkalosis
Anion Gap Metabolic Acidosis
and Metabolic Alkalosis
1. Look at the pH to determine the
primary process.
2. Calculate the anion gap: Na – (Cl +
HCO3)
3. Calculate the excess anion gap (total
anion gap minus the normal anion gap)
and add this to the measured HCO3
concentration, if >30, there is
underlying metabolic alkalosis; if <24,
there is underlying non-gap metabolic
acidosis
87. Example #9
pH 7.50
pCO2 20
HCO3 15
Na 145
Cl 100 Variable Primary
Disorder
Normal
Range,
arterial Gas
Primary
Disorder
pH Acidemia 7.35-7.45 Alkalemia
pCO2 Respiratory
alkalosis
35 - 45 Respiratory
acidosis
HCO3 Metabolic
acidosis
22 – 26 Metabolic
Alkalosis
Respiratory alkalosis, Anion
Gap Metabolic Acidosis and
Metabolic Alkalosis
1. Look at the pH to determine the
primary process.
2. Calculate the anion gap: Na – (Cl +
HCO3)
3. Calculate the excess anion gap (total
anion gap minus the normal anion gap)
and add this to the measured HCO3
concentration, if >30, there is
underlying metabolic alkalosis; if <24,
there is underlying non-gap metabolic
acidosis
88. What’s the Diagnosis?
History of vomiting
(metabolic alkalosis),
alcoholic ketoacidosis
(metabolic acidosis), and
bacterial pneumonia
(respiratory alkalosis)
89. Example #10
pH 7.10
pCO2 50
HCO3 15
Na 145
Cl 100 Variable Primary
Disorder
Normal
Range,
arterial Gas
Primary
Disorder
pH Acidemia 7.35-7.45 Alkalemia
pCO2 Respiratory
alkalosis
35 - 45 Respiratory
acidosis
HCO3 Metabolic
acidosis
22 – 26 Metabolic
Alkalosis
Respiratory Acidosis, Anion
gap Metabolic Acidosis,
Metabolic Alkalosis
1. Look at the pH to determine the
primary process.
2. Calculate the anion gap: Na – (Cl +
HCO3)
3. Calculate the excess anion gap (total
anion gap minus the normal anion gap)
and add this to the measured HCO3
concentration, if >30, there is
underlying metabolic alkalosis; if <24,
there is underlying non-gap metabolic
acidosis
90. What’s the Diagnosis?
Patient presented in an obtunded state
(respiratory acidosis), history of vomiting
(metabolic alkalosis), DKA (anion gap metabolic
acidosis)
Or
Chronic respiratory acidosis and metabolic
compensation in whom an acute anion gap
metabolic acidosis developed
91. Example #11
pH 7.15
pCO2 15
HCO3 5
Na 140
Cl 110 Variable Primary
Disorder
Normal
Range,
arterial Gas
Primary
Disorder
pH Acidemia 7.35-7.45 Alkalemia
pCO2 Respiratory
alkalosis
35 - 45 Respiratory
acidosis
HCO3 Metabolic
acidosis
22 – 26 Metabolic
Alkalosis
Anion Gap and Non-Anion
Gap Metabolic Acidoses
1. Look at the pH to determine the
primary process.
2. Calculate the anion gap: Na – (Cl +
HCO3)
3. Calculate the excess anion gap (total
anion gap minus the normal anion gap)
and add this to the measured HCO3
concentration, if >30, there is
underlying metabolic alkalosis; if <24,
there is underlying non-gap metabolic
acidosis
92. What’s the Diagnosis?
DKA with non-gap acidosis
during recovery phase of
DKA due to failure to
regenerate HCO3 from
keto-acids lost in the urine
93. Case 12
40YEARSWOMEN,HISTORY OF SHORT
BOWEL SYNDROME,LIKES ICE
CREAM,PRESENTEDWITH SLURRED
SPEECH AND CONFUSION
PH 7.27 PCO2 24 HCO3 16 AG 20
OG, CREATININE,LACT. : NORMAL.NO KETONS.
WHAT ISTHE MOST LIKELY DIAGNOSIS ?
A –L-LACTATE B-PYROGLUTAMIC ACID
C-D-LACTATE D-METHANOL
E-TOPIRAMATE
94. ANSWER 12
D-LACTATE
ALL EXCEPT TOPIRAMATE CAN CAUSE HAGMA.
NO OSMOLAL GAP SO NO METANOL!
NO HISTORY OF ACETAMINOPHEN USE OR
ANTIBIOTIC USE SO NOT PYROGLUTAMIC.
NORMAL LACTATE RULE OUT L-LACTICACIDOSI.
D-LACTATEOCCURS IN SHORT BOWEL
SYNDROMEWITH HIGH CARBOHYDRATE
INTAKE.ITSASSOCIATEDWITH NEUROLOGICAL
MANIFISTATIONS..
95. CASE 13
60 years old man known COPD LASTVISIT 1
MO.AGO HIS ABG :PH 7.31 PCO2 70 HCO3 36
HE PRESENTEDWITH AKI DUETO SEVERE GE.
BIOCHEN; CREAT 400 MCOL/L N a 145 cl 95
ABG ; PH 7.20 PCO2 70 HCO3 24
WHAT ISTHE ACID BASE DISORDER HE HAS ?
A-RESP.ACIDOSISAND HAGMA.
B –RESP.ACID. + HAGMA+METAB.ALKALOSIS
C-RESP.ACID.+HAGMA+RESP.ALKALOSIS.
D-RESPIRATORYACIDOSISAND MET.ALKALOSIS.
E-RESPIRATORY ACIDOSISONLY.
96. CASE 13 ANSWER
THE ANSWER IS B
PH SHOWES ACIDOSIS.HE HAS COPDWITH
PCO2 70,SO HIS EXPECTED HCO3 IS 36..
NOW HIS HCO3 IS 24 MEANS 10 BELOW
EXPECTED SO HE HAS METAB. ACIDOSIS.
AG IS HIGH 145-95-24=26
DELTA AG =26-10=16
ADDTHE 16TOTHE MEASURED HCO3
16+24=40
As we said if >30 there is METABOLIC ALK.
97. Conclusions
Acid-base disturbances are easy to analyze if
approached systematically
Determine primary abnormalities based on pH
Calculate the anion gap
Calculate the delta gap and add to the
measured HCO3
Calculate an anion gap on EVERY chemistry
you see
If there is an elevated anion gap, remember to
get an ABG!!