NEPHROTIC AND NEPHRITIC

SYNDROME
PRESENTED BY

DR MARIA NILA B LOPEZ

SCOPE OF PRESENTATION

• OBJECTIVES
• REFERENCES
• DEFINITION OF TERMS
• BRIEF REVIEW OF
FILTERABILITY IN THE KIDNEYS
SCOPE OF PRESENTATION

• NEPHROTIC SYNDROME
• NEPHRITIC SYNDROME
• SUMMARY
 OBJECTIVES
• TO PRESENT AND DISCUSS WITH
THE PARTICIPANTS THE
CLINICAL CONDITIONS CALLED
NEPHROTIC SYNDROME AND
NEPHRITIC CONDITION

• TO DISCUSS WITH THE

PARTICIPANTS THE CONDITIONS
THAT GIVE RISE TO NEPHROTIC
AND NEPHRITIC SYNDROME
 OBJECTIVES

• AT THE END OF THE ACTIVITY THE

PARTICIPANTS SHALL HAVE AN
UNDERSTANDING OF THE
CLINICAL CONDITION CALLED
NEPHROTIC SYNDROME AND
NEPHRITIC CONDITION

• LIKEWISE THE PARTICIPANTS

SHALL LEARN OF THE
CONSEQUENCES OF NEPHROTIC
AND NEPHRITIC SYNDROME
 REFERENCES
• HARRISON’S PRINCIPLES OF
INTERNAL MEDICINE , 20TH
EDITION BY KASPER , FAUCI ,
HAUSER , ET. AL

• THE KIDNEY BY BRENNER AND

RECTOR , 9TH EDITION

• NEPHROLOGY : CLINICAL
CASES UNCOVERED BY
MENNA CLATWORTHY
 REFERENCES
• RENAL AND ELECTROLYTE
DISORDER BY ROBERT SCHRIER
8TH EDITION

• SMITH’S GENERAL UROLOGY 17TH

EDITION BY EMILY A . TANAGHO ,
JACK W. MCANICH

• CAMPBELL – WALSH UROLOGY 11TH

EDITION BY ALAN J. WEIN , LOUIS R.
KAVOUSSI , ALAN W. PARTIN ,
CRAIG A. PETERS
 REFERENCES
• CAUSES AND CONSEQUENCES OF
PROTEINURIA : THE KIDNEY
FILTRATION BARRIER AND
PROGRESSIVE RENAL FAILURE BY
K.TRYGGVASON & E. PETTERSSON ,
JOURNAL OF INTERNAL MEDICINE
2003 ; 254: 216-224

• ROBBINS AND COTRAN :

PATHOLOGIC BASIS OF DISEASES ,
8TH EDITION

• TEXTBOOK OF MEDICAL
PHYSIOLOGY , 11TH EDITION BY
GUYTON AND HALL
 REFERENCES
• CLINICAL ANATOMY BY REGIONS , BY
RICHARD S SNELL , 9TH EDITION

• PRINCIPLES OF ANATOMY AND

PHYSIOLOGY , 15TH EDITION BY
GERARD J TORTORA , BRYAN
DERRICKSON

• BATES’ GUIDE TO PHYSICAL

EXAMINATION AND HISTORY TAKING
12TH EDITION BY LYNN S BINCKLEY

• DE GOWIN’S DIAGNOSTIC
EXAMINATION : THE COMPLETE GUIDE
TO ASSESSMENT EXAMINATION
DIFFERENTIAL DIAGNOSIS 8TH EDITION
 DEFINITION OF A SYNDROME
SYNDROME *
A CONSTELLATION OF
SIGNS AND SYMPTOMS OR A
CONSTELLATION OF CONGENITAL
ANOMALIES BELIEVED TO BE
PATHOLOGICALLY RELATED , THAT
IS IN CONTRAST TO A SEQUENCE ,
CANNOT BE EXPLAINED ON THE
BASIS OF A SINGLE LOCALIZED ,
INITIATING DEFECT
IT IS CAUSED BY A SINGLE
ETIOLOGIC AGENT WHICH
SIMULTANEOUSLY AFFECTS
SEVERAL TISSUES

* PAGE 450 , ROBBINS AND COTRAN

PATHOLOGIC BASIS OF DISEASES , 8TH ED
CLINICAL SYNDROMES OF RENAL
DISEASES
CLINICAL SYNDROMES OF RENAL
DISEASES
• GLOMERULAR SYNDROMES
✓ NEPHROTIC SYNDROME
✓ ACUTE NEPHRITIC SYNDROME
✓ PULMONARY – RENAL SYNDROMES
✓ BASEMENT MEMBRANE SYNDROMES
✓ GOMERULAR VASCULAR SYNDROMES
✓ INFECTIOUS –DISEASE ASSOCIATED
SYNDROMES

• ACUTE KIDNEY FAILURE

• CHRONIC KIDNEY FAILURE
 CLINICAL MANIFESTATION OF
GLOMERULAR DISEASES
CLINICAL MANIFESTATION OF
GLOMERULAR DISEASES /
GN SYNDROME

• PROTEINURIA
• HEMATURIA ( CAN PRESENT
AS TEA – COLORED URINE)
• EDEMA
• HIGH BLOOD PRESSURE
 FILTERABILITY OF PROTEIN
• NEGATIVELY CHARGED LARGE
MOLECULES ARE FILTERED LESS EASILY
THAN POSITIVELY CHARGED
MOLECULES OF EQUAL SIZE

• MOLECULAR DIAMETER OF PLASMA

PROTEIN ALBUMIN IS ABOUT SIX (6)
NANOMETERS

• THE PORES OF THE GLOMERULAR

MEMBRANE ARE THOUGHT TO BE ABOUT
EIGHT (8) NANOMETERS ( 80
ANGSTROMS)

• ALBUMIN IS RESTRICTED FROM

FILTRATION DUE TO ITS NEGATIVE
CHARGE AND THE ELECTROSTATIC
REPULSION EXERTED BY NEGATIVE
CHARGES OF THE GLOMERULAR
CAPILLARY WALL PROTEOGLYCANS
 PROTEINURIA
PROTEINURIA
• PRESENCE OF PROTEIN IN
THE URINE

✓ HUMANS WITH NORMAL NEPHRONS

EXCRETE ON AVERAGE 8–10 MGOF
ALBUMIN IN DAILY VOIDED URINE,
~20–60% OF TOTAL EXCRETED
PROTEIN
✓ THIS AMOUNT OF ALBUMIN, AND
OTHER PROTEINS, CAN RISE TO
GRAM QUANTITIES FOLLOWING
GLOMERULAR INJURY
 PROTEINURIA
MECHANISMS / CAUSES OF
PROTEINURIA
1. OVERPRODUCTION OF PLASMA
PROTEINS CAPABLE OF PASSING THE
NORMAL GLOMERULAR BASEMENT
MEMBRANE (GBM)
EXAMPLE : MULTIPLE MYELOMA

2. GLOMERULAR DYSFUNCTION
• A DEFECT IN THE GLOMERULAR
BARRIER THAT ALLOWS ABNORMAL
AMOUNTS OF PROTEINS OF
INTERMEDIATE MOLECULAR
WEIGHT TO ENTER BOWMAN’S
SPACE
• ALSO CALLED GLOMERULAR
PROTEINURIA
 PROTEINURIA
MECHANISMS / CAUSES
OF PROTEINURIA
3. TUBULAR DYSFUNCTION
• ALSO CALLED TUBULAR
PROTEINURIA
• DISEASES RESULTING IN THE
INABILITY OF THE KIDNEY TO
REABSORB NORMALLY
PROTEINS PRESENTED TO THE
RENAL TUBULES
 NEPHROTIC SYNDROME
NEPHROTIC SYNDROME
• A CONDITION CHARACTERIZED &
THAT RESULTS FROM
PROTEINURIA OF MORE THAN 3.5
GRAMS PROTEIN PER DAY AND IS
CHARACTERIZED BY EDEMA,
MINIMAL HEMATURIA,
HYPOALBUMINEMIA,
HYPERLIPIDEMIA AND
HYPERTENSION

• IT CAN BE CAUSED BY PRIMARY

(IDIOPATHIC) GLOMERULAR
DISEASES OR DUE TO OTHER
DISEASES / CLINICAL CONDITIONS
 NEPHROTIC SYNDROME (NS)
NEPHROTIC – RANGE
PROTEINURIA
• A CONDITION WHEREIN THE RANGE OF
PROTEIN IN THE URINE IS WITHIN 3 GM/
DAY OR MORE WITHOUT THE OTHER
CLINICAL MANIFESTATIONS SEEN IN
NEPHROTIC SYNDROME

• THE GLOMERULAR FILTRATION RATE

(GFR) IN THESE PATIENTS MAY
INITIALLY BE NORMAL OR, RARELY,
HIGHER THAN NORMAL, BUT WITH
PERSISTENT HYPERFILTRATION AND
CONTINUED NEPHRON LOSS, IT
TYPICALLY DECLINES OVER MONTHS
TO YEARS
 NEPHROTIC SYNDROME (NS)
KEY POINTS REGARDING
NEPHROTIC SYNDROME (NS)
• IF NS IS LEFT UNDIAGNOSED OR
UNTREATED, IT WILL
PROGRESSIVELY DAMAGE
ENOUGH GLOMERULI TO CAUSE
A FALL IN GFR, PRODUCING
RENAL FAILURE

• MULTIPLE STUDIES HAVE NOTED

THAT THE HIGHER THE 24-H
URINE PROTEIN EXCRETION,
THE MORE RAPID IS THE
DECLINE IN GFR.
 CLASSIFICATION OF DISEASES THAT
CAUSES OF NEPHROTIC SYNDROME
CLASSIFICATION OF CAUSES EXAMPLE OF CONDITION
OF NEPHROTIC SYNDROME
PRIMARY (IDIOPATHIC) • MINIMAL CHANGE DISEASE/GN
GLOMERULAR DISEASES • FOCAL SEGMENTAL
CONDITIONS THAT PRIMARILY GLOMERULOSCLEROSIS (FSGS)
INVOLVE THE KIDNEY AND NOT DUE • MEMBRANOUS GN
TO OTHER SYSTEMIC CAUSES • MEMBRANOPROLIFERATIVE GN
SECONDARY CAUSES
Nephrotic Syndrome Associated with
Specific Etiologic Events or in Which
Glomerular Disease Arises as a
Complication of Other Diseases
SYSTEMIC DISEASES • HYPERTENSION,DM ETC.
METABOLIC DISORDER • DIABETES MELLITUS, GRAVES
DISEASE,HYPOTHYROIDISM,
FABRY’S DISEASE
 CLASSIFICATION OF DISEASES THAT
CAUSES OF NEPHROTIC SYNDROME
CLASSIFICATION OF CAUSES EXAMPLE OF CONDITION
OF NEPHROTIC SYNDROME
SECONDARY CAUSES
Nephrotic Syndrome Associated with
Specific Etiologic Events or in Which
Glomerular Disease Arises as a
Complication of Other Diseases
INFECTIONS • BACTERIA : STREPTOCOCCUS,
INFECTIVE ENDOCARDITIS,
LEPROSY, MYCOPLASMA
INFECTION ETC.
• VIRUS : HEP B, HEP C, HIV,
• PROTOZOAL : MALARIA
,TOXOPLASMOSIS
• HELMINTHIC : SCHISTOSOMIASIS ,
FILARIASIS
 CLASSIFICATION OF DISEASES THAT
CAUSES OF NEPHROTIC SYNDROME
CLASSIFICATION OF CAUSES EXAMPLE OF CONDITION
OF NEPHROTIC SYNDROME
SECONDARY CAUSES
Nephrotic Syndrome Associated with
Specific Etiologic Events or in Which
Glomerular Disease Arises as a
Complication of Other Diseases
DRUGS / MEDICATIONS AND OTHER • WARFARIN, RIFAMPICIN, NSAIDS,
CHEMICALS ANTIBIOTICS, INSECT REPELLANT,
HEROIN
ALLERGENS, VENOMS, IMMUNIZING • VACCINES , Bee sting, POLLENS,
AGENTS SNAKE VENOM, ANTITOXIN (
SERUM SICKNESS), DIPTHERIA,
PERTUSSIS, TETANUS TOXOID,
ETC
 CLASSIFICATION OF DISEASES THAT
CAUSES OF NEPHROTIC SYNDROME
CLASSIFICATION OF CAUSES EXAMPLE OF CONDITION
OF NEPHROTIC SYNDROME
SECONDARY CAUSES
Nephrotic Syndrome Associated with
Specific Etiologic Events or in Which
Glomerular Disease Arises as a
Complication of Other Diseases
AUTOIMMUNE DISEASES • SLE , MIXED CONNECTIVE TISSUE
DISEASE, RHEUMATOID ARTHRITIS
NEOPLASMS SOLID TUMORS / CA
LEUKEMIA AND LYMPHOMA
 PRIMARY GLOMERULAR DISEASES THAT CAUSES
NEPHROTIC SYNDROME
PRIMARY GLOMERULAR DISEASES THAT CAUSES NEPHROTIC
SYNDROME
GLOMERULAR LESION NO. OF MALE/ WHITE/AFRICAN
SAMPLES FEMALE AMERICAN
RATIO RATIO

Minimal Change Glomerulopathy 522 1.1:1.0 1.9:1.0

Focal segmental glomerulosclerosis 1103 1.4:1.0 1.0:1.0

(FSGS) (typical)
Collapsing Variant of FSGS 135 1.2:1.0 1.0:7.8

Glomerular Tip Lesion Variant of 94 1.0:1.0 4.7:1.0

FSGS
Membranous glomerulopathy 1120 1.4:1.0 1.9:1.0

C1q Nephropathy 114 1.0:1.0 1.0:4.8

DATA ARE DERIVED FROM ANALYSIS OF 9605 NATIVE KIDNEY BIOPSY SPECIMENS EVALUATED AT
THE UNIVERSITY OF NORTH CAROLINA NEPHROPATHOLOGY LABORATORY.
 NEPHRITIC SYNDROME
NEPHRITIC SYNDROME
• PRODUCTION OF 1–2 G/24 H OF
PROTEINURIA, HEMATURIA WITH RED
BLOOD CELL CASTS, PYURIA,
HYPERTENSION, FLUID RETENTION

• PROTEINURIA IS LESS THAN 3 GRAMS

• MILD TO MODERATE PROTEINURIA

• HALLMARK IS HEMATURIA
 NEPHRITIC SYNDROME
NEPHRITIC SYNDROME
• IT CAN OCCUR AS AN
ISOLATED RENAL PROCESS OR
AS A FEATURE OF A SYSTEMIC
DISEASE OR HEREDITARY
DISORDER
• IF GLOMERULAR
INFLAMMATION DEVELOPS
SLOWLY, THE SERUM
CREATININE WILL RISE
GRADUALLY OVER MANY
WEEKS
NEPHROTIC VS NEPHRITIC
SYNDROME
 KEY POINTS ON THE CAUSES OF
NEPHROTIC SYNDROME & NEPHRITIC
SYNDROME
• DESPITE OF THE CAUSE OF
NEPHROTIC SYNDROME BE IT
PRIMARY GN OR SECONDARY
TO OTHER DISEASES , THE LOSS
OF SUBSTANTIAL AMOUNTS OF
PROTEIN IN THE URINE RESULTS
IN A SHARED SET OF
ABNORMALITIES THAT
COMPRISE NEPHROTIC
SYNDROME

• THE CAUSES FOR NEPHRITIC

SYNDROMES ARE THE SAME AS
THOSE OF NEPHROTIC
SYNDROME
 NEPHRITIC SYNDROME NEPHROTIC SYNDROME
• DUE TO GBM DISRUPTION , • PODOCYCTE DISRUPTION CHARGE
HYPERTENSION , INCREASED BUN& BARRIER.
CREATININE , OLIGURIA , HEMATURIA , • MASSIVE PROTEINURIA (> 3.5 G?DAY) WITH
RBC CAST IN URINE. HYPOALBUMINEMIA, HYPERLIPIDEMIA,
• PROTEINURIA OFTEN IN EDEMA. MAY BE PRIMARY (E.G. DIRECT
SUBNEPHROTIC RANGE (< 3.5 PODOCYTE DAMAGE ) OR SECONDARY (
GMS/DAY) BU TIN SECERE CASES PODOCYCTE DAMAGE FROM SYSTEMIC
MAY BE IN NEPHROTIC RANGE PROCESS I.E. DIABETES)
• ACUTE POST STREP GN • FOCAL SEGMENTAL GLOMERULOSCLEROSIS
• RPGN ( 1o OR 2o)
• IGA NEPHROPATHY • MININMAL CHANGE DISEASE ( 1o OR 2o)
• ALPORT’S SYNDROME • MEMBRANOUS NEPHROPATHY( 1o OR 2o)
• MEMBRANOPROLIFERATIVE GN • AMYLOIDOSIS( 2o)
• DIABETIC GLOMERULOPATHY ( 2o)

NEPHRITIC - NEPHROTIC SYNDROME

• SEVERE NEPHRITIC SYNDROME PROFOUND GBM DAMAGE THAT DAMAGES THE GLOMERULAR
FILTRATION CHARGE BARRIER NEPHROYIC – RANGE PROTEINURIA ( > 3.5 G/DAY) AND
CONCOMITTANT FEATURES OF NEPHROTIC SYNDROME. CAN OCCUR WITH ANY FORM OF NEOPHRITIC
SYNDROE, UT IS MOST COMMONLY SEEN WITH :
• DIFFUSE PROLIFERATIVE GLOMERULONEPHRITIS
• MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS

GLOMERULAR
DISEASES GRAMS OF PROTEIN EXCRETED PER DAY ( G/DAY OR G/24H )
0.25 > 3.5
SPECTRUM OF GLOMERULAR
DISEASE
 CLINICAL APPROACH TO PATIENTS WITH
NEPHROTIC AND NEPHRITIC SYNDROMES
CLINICAL APPROACH TO
NEPHROTIC AND NEPHRITIC
SYNDROME
1.THOROUGH MEDICAL HISTORY AND
PHYSICAL EXAMINATION
• WITH THE OBJECTIVE OF IDENTIFYING
THE POSSIBLE CAUSE
2. LABORATORY EXAMINATION
• CBC
• BLOOD CHEMISTRY
• IMMUNOLOGIC STUDY (ANTI-NUCLEAR
ANTIBODY (ANA); COMPLEMENT
LEVELS (C3 AND C4), ANTI-DOUBLE-
STRANDED DNA ANTIBODY (DSDNA);
• HEPATITIS PROFILE
CLINICAL APPROACH TO PATIENTS WITH
NEPHROTIC AND NEPHRITIC SYNDROMES
CLINICAL APPROACH TO
NEPHROTIC AND
NEPHRITIC SYNDROME
2. LABORATORY EXAMINATION
• ROUTINE URINALYSIS
✓ IT WILL SERVE AS AN INITIAL
SCREENING FOR PRESENCE
OF PROTEINURIA AND
APPROXIMATION OF ITS
AMOUNT
CLINICAL APPROACH TO PATIENTS WITH
NEPHROTIC AND NEPHRITIC SYNDROMES
PROTEINURIA ON ROUTINE
URINALYSIS
THE DIPSTICK RESULTS OF ROUTINE
URINALYSIS HAVE THE FOLLOWING
APPROXIMATE CORRELATIONS WITH
PROTEIN CONCENTRATION:
RESULT OF AMOUNT OF PROTEIN
TEST STRIP
NEGATIVE <15MG/DL

TRACE 15 – 30 MG/DL
1+ 30 – 100 MG/DL
2+ 100 – 300 MG /DL
3+ 300 – 1000 MG /DL
4+ > 1000 MG /DL
CLINICAL APPROACH TO PATIENTS WITH
NEPHROTIC AND NEPHRITIC SYNDROMES
CLINICAL APPROACH TO
NEPHROTIC AND
NEPHRITIC SYNDROME
2. LABORATORY EXAMINATION
• ROUTINE URINALYSIS
✓ IT WILL SERVE AS AN INITIAL
SCREENING FOR PRESENCE
OF PROTEINURIA AND
APPROXIMATION OF ITS
AMOUNT
CLINICAL APPROACH TO PATIENTS WITH
NEPHROTIC AND NEPHRITIC SYNDROMES
CLINICAL APPROACH TO
NEPHROTIC AND
NEPHRITIC SYNDROME
2. LABORATORY EXAMINATION
• 24 HOUR TOTAL URINE
PROTEIN AND CREA
CLEARANCE
✓ IT WILL PROVIDE
QUANTITATIVE INFORMATION
AS TO THE AMOUNT OF
PROTEIN PRESENT IN THE
URINE FOR 24 HOURS
CLINICAL APPROACH TO PATIENTS WITH
NEPHROTIC AND NEPHRITIC SYNDROMES
CLINICAL APPROACH TO
NEPHROTIC AND
NEPHRITIC SYNDROME
2. LABORATORY EXAMINATION
• 24 HOUR TOTAL URINE
PROTEIN AND CREA
CLEARANCE
✓ IT WILL PROVIDE
QUANTITATIVE INFORMATION
AS TO THE AMOUNT OF
PROTEIN PRESENT IN THE
URINE FOR 24 HOURS
CLINICAL APPROACH TO PATIENTS WITH
NEPHROTIC AND NEPHRITIC SYNDROMES
CLINICAL APPROACH TO
NEPHROTIC AND
NEPHRITIC SYNDROME
2. LABORATORY EXAMINATION
CHEST XRAY
ULTRASOUND OF KUB

3. KIDNEY BIOPSY
• TO INVESTIGATE AND
DIAGNOSE KIDNEY DISEASE AS
WELL AS FOR
PROGNOSTICATION
 RESULT OF KIDNEY BIOPSY AMONG
PATIENTS WITH NEPHROTIC SYNDROME
GRAPH DEPICTING THE
FREQUENCIES OF
DIFFERENT FORMS OF
GLOMERULAR DISEASE
IDENTIFIED IN RENAL
BIOPSY SPECIMENS
FROM PATIENTS WITH
PROTEINURIA OF MORE
THAN 3 G OF PROTEIN
PER DAY EVALUATED AT
THE UNIVERSITY OF
NORTH CAROLINA
NEPHROPATHOLOGY
LABORATORY
 COMPLICATIONS OF NEPHROTIC
SYNDROMES
COMPLICATIONS OF
NEPHROTIC SYNDROMES
• THROMBOEMBOLISM
✓ DVT +/- PULMONARY EMBOLISM
✓ THROMBOSIS OF RENAL VEIN

• INFECTION
• HYPERLIPIDEMIA
• MALNUTRITION
• ACUTE RENAL FAILURE
 THERAPEUTIC APPROACH
• ONE OF THE MAIN GOALS OF
TREATMENT IS THE REDUCTION
OR ELIMINATION OF
PROTEINURIA
• TREAT THE UNDERLYING CAUSE
• LIMIT DIETARY SODIUM
• TREAT THE DYSLIPIDEMIA
• INSTITUTION OF
CORTICOSTEROID WITH
REGULAR MONITORING FOR
RESPONSE AND TAPERING OF
DOSE
• DIURETICS AND OTHER MEDS
SUMMARY
• NEPHROTIC SYNDROME IS A CONDITION
CHARACTERIZED & THAT RESULTS
FROM PROTEINURIA OF MORE THAN
3.5 GRAMS PROTEIN PER DAY AND IS
CHARACTERIZED BY EDEMA, MINIMAL
HEMATURIA, HYPOALBUMINEMIA,
HYPERLIPIDEMIA AND HYPERTENSION

• NEPHRITIC SYNDROME IS A
CONDUCTION CHARACTERIZED BY
PRODUCTION OF 1–2 G/24 H OF
PROTEINURIA, HEMATURIA WITH RED
BLOOD CELL CASTS, PYURIA,
HYPERTENSION, FLUID RETENTION
SUMMARY
• BOTH NEPHROTIC AND NEPHRITIC
SYNDROMES ARE CAUSED BY
EITHER PRIMARY RENAL DISORDER
OR SECONDARY CONDITIONS
WHEREIN THERE ARE CONDITIONS
THAT EVENTUALLY INVOLVED THE
KIDNEYS

• THE AIM OF THE MANAGEMENT IS TO

ADDRESS THE CAUSE AND RESOLVE
THE PROTEINURIA

• PROTEINURIA IS KNOWN TO CAUSE

DTERIORATION OF THE KIDNEYS
 FLUIDS AND ELECTROLYTE
IMBALANCE AND ACID –BASE
DISORDER
PRESENTED BY

DR MARIA NILA B LOPEZ

SCOPE OF PRESENTATION

• OBJECTIVES
• REFERENCES
• BRIEF REVIEW OF THE RENAL
ANATOMY AND FUNCTION
SCOPE OF PRESENTATION

• FLUIDS AND ELECTROLYTE

IMBALANCE
• ACID – BASE DISORDER
• SUMMARY
 OBJECTIVES
• TO PRESENT AND DISCUSS WITH
THE PARTICIPANTS THE COMMON
ELECTROLYTE IMBALANCE
ENCOUNTERED CLINICALLY

• TO PRESENT AND EXPLAIN ACID –

BASE DISORDER

• AT THE END OF THE PRESENTATION

AND DISCUSSION THE
PARTICIPANTS WILL HAVE AN
UNDERSTANDING OF THE COMMON
ELECTROLYTE IMBALANCE
ENCOUNTERED IN THE CLINICAL
AREA
 OBJECTIVES
• AT THE END OF THE
ACTIVITY THE
PARTICIPANTS SHALL
APPRECIATE AND
UNDERSTAND THE
ACID – BASE
DISORDER
 REFERENCES
• HARRISON’S PRINCIPLES OF
INTERNAL MEDICINE , 20TH
EDITION BY KASPER , FAUCI ,
HAUSER , ET. AL

• THE KIDNEY BY BRENNER AND

RECTOR , 9TH EDITION

• RENAL AND ELECTROLYTE

DISORDER BY ROBERT
SCHRIER 8TH EDITION
 REFERENCES
• NEPHROLOGY : CLINICAL
CASES UNCOVERED BY MENNA
CLATWORTHY

• ROBBINS AND COTRAN :

PATHOLOGIC BASIS OF
DISEASES , 8TH EDITION

• TEXTBOOK OF MEDICAL
PHYSIOLOGY , 11TH EDITION
BY GUYTON AND HALL
 REFERENCES
• BATES’ GUIDE TO PHYSICAL
EXAMINATION AND HISTORY TAKING
12TH EDITION BY LYNN S BINCKLEY

• DE GOWIN’S DIAGNOSTIC EXAMINATION

: THE COMPLETE GUIDE TO
ASSESSMENT EXAMINATION
DIFFERENTIAL DIAGNOSIS 8TH EDITION

• CLINICAL ANATOMY BY REGIONS , BY

RICHARD S SNELL , 9TH EDITION

• PRINCIPLES OF ANATOMY AND

PHYSIOLOGY , 15TH EDITION BY
GERARD J TORTORA , BRYAN
DERRICKSON
 BODY FLUID COMPARTMENTS
TWO COMPARTMENTS
WHERE BODY FLUID IS
DISTRIBUTED
1. INTRACELLULAR FLUID (ICF)
• FLUID THAT IS INSIDE THE
CELL
• IT COMPRISES 40 PER CENT
OF THE TOTAL BODY WEIGHT
IN AN “AVERAGE” PERSON
• IT COMPRISES 2/3 OF TOTAL
BODY WATER IN AN AVERAGE
PERSON
 BODY FLUID COMPARTMENTS
TWO COMPARTMENTS
WHERE BODY FLUID IS
DISTRIBUTED
2. EXTRACELLULAR FLUID
(ECF)
• FLUID THAT IS OUTSIDE
THE CELL
• TOGETHER THESE FLUIDS
ACCOUNT FOR ABOUT 20
PER CENT OF THE BODY
WEIGHT, OR ABOUT 14
LITERS IN A NORMAL 70-
KILOGRAM ADULT
 BODY FLUID COMPARTMENTS
TWO COMPARTMENTS
WHERE BODY FLUID IS
DISTRIBUTED
2. EXTRACELLULAR FLUID
(ECF)
• IT COMPRISES 1/3 OF
BODY FLUID
• IT IS COMPOSED OF :
A. INTERSTITIAL FLUID - THE
FLUID IN BETWEEN CELLS. IT
MAKES UP ¾ (80%) OF THE
ECF
B. BLOOD PLASMA - THE FLUID
INSIDE THE BLOOD VESSELS.
IT MAKES UP ¼ (20%) OF THE
ECF VOLUME
 BODY FLUID COMPARTMENTS
• THE PLASMA IS THE NONCELLULAR
PART OF THE BLOOD; IT EXCHANGES
SUBSTANCES CONTINUOUSLY WITH
THE INTERSTITIAL FLUID THROUGH
THE PORES OF THE CAPILLARY
MEMBRANES. THESE PORES ARE
HIGHLY PERMEABLE TO ALMOST ALL
SOLUTES IN THE EXTRACELLULAR
FLUID EXCEPT THE PROTEINS.

• THE EXTRACELLULAR FLUIDS ARE

CONSTANTLY MIXING, SO THAT THE
PLASMA AND INTERSTITIAL FLUIDS
HAVE ABOUT THE SAME
COMPOSITION EXCEPT FOR
PROTEINS, WHICH HAVE A HIGHER
CONCENTRATION IN THE PLASMA
 BODY FLUID COMPARTMENTS
BLOOD VOLUME
• BLOOD PLASMA AND THE
INTERSTITIAL FLUID IS IN
CONSTANT EXCHANGE WITH
EACH OTHER

• BLOOD CONTAINS BOTH

EXTRACELLULAR FLUID (THE
FLUID IN PLASMA) AND
INTRACELLULAR FLUID (THE
FLUID IN THE RED BLOOD CELLS)

• BLOOD IS CONSIDERED TO BE A
SEPARATE FLUID COMPARTMENT
BECAUSE IT IS CONTAINED IN A
CHAMBER OF ITS OWN, THE
CIRCULATORY SYSTEM
 BODY FLUID COMPARTMENTS
BLOOD VOLUME
• THE BLOOD VOLUME IS ESPECIALLY
IMPORTANT IN THE CONTROL OF
CARDIOVASCULAR DYNAMICS

• THE AVERAGE BLOOD VOLUME OF

ADULTS IS ABOUT FIVE (5) LITERS

• ABOUT 60 PER CENT OF THE BLOOD

IS PLASMA AND 40 PER CENT IS
RED BLOOD CELLS, BUT THESE
PERCENTAGES CAN VARY
CONSIDERABLY IN DIFFERENT
PEOPLE, DEPENDING ON GENDER,
WEIGHT, AND OTHER FACTORS
ELECTROLYTES IN THE BODY FLUID

NONELECTROLYTES IN THE
PLASMA
SUBSTANCES IN THE ECF AND ICF
 TYPES OF INTRAVENOUS FLUIDS
BROAD CATEGORIES OF
INTRAVENOUS (IV) FLUIDS
A. CRYSTALLOID IV FLUID B. COLLOID IV FLUID
 TYPES OF INTRAVENOUS FLUIDS
BROAD CATEGORIES OF IV
FLUIDS
CRYSTALLOIDS
• BASICALLY CONTAINS WATER
WITH ELECTROLYTES AND SOME
WATER SOLUBLE MOLECULES

• CRYSTALLOID FLUIDS FUNCTION

TO EXPAND INTRAVASCULAR
VOLUME WITHOUT DISTURBING
ION CONCENTRATION OR
CAUSING SIGNIFICANT FLUID
SHIFTS BETWEEN
INTRACELLULAR, INTRAVASCULAR,
AND INTERSTITIAL SPACES.
 TYPES OF INTRAVENOUS FLUIDS
ADVANTAGES OF
CRYSTALLOIDS

1. COST EFFECTIVINESS
2. SIMPLICITY
3. AVAILABLE IN
DIFFERENT
COMBINATIONS
4. NO IMMUNE
RESPONSE
 TYPES OF INTRAVENOUS FLUIDS
CRYSTALLOIDS
THREE TYPES OF
CRYSTALLOIDS BASED
ON OSMOLALITY

1. ISOTONIC
2. HYPOTONIC
3. HYPERTONIC
 TYPES OF CRYSTALLOIDS
THREE TYPES OF
CRYSTALLOIDS BASED ON
OSMOLALITY
1. ISOTONIC
• THESE ARE SOLUTIONS WITH THE
SAME OSMOTIC CONCENTRATION
OF PARTICLES AS THAT OF THE
ECF OR PLASMA. HENCE IT WILL
NOT CAUSE ANY SHIFT IN FLUID
OR CHANGE IN IONS BETWEEN
ICF AND ECF
• THEY CAN HAVE AN OSMOLALITY
OF 250 – 375 MOSM
 TYPES OF CRYSTALLOIDS
THREE TYPES OF
CRYSTALLOIDS BASED ON
OSMOLALITY
2. HYPERTONIC
• THESE ARE SOLUTIONS HAVE
GREATER OSMOTIC
CONCENTRATION (> 375
MOSM)
• THIS WILL RESULT TO FLUID
BEING PULLED OUT FROM
THE CELL . FLUID MOVING OUT
OF ICF INTO ECF
 TYPES OF CRYSTALLOIDS
THREE TYPES OF
CRYSTALLOIDS BASED ON
OSMOLALITY
3. HYPOTONIC
• THESE ARE SOLUTIONS WITH
LESS CONCENTRATION OF
PARTICLES , HENCE LESS
OSMOTIC CONCENTRATION
(< 250 )

• THIS WILL RESULT TO FLUID

MOVING FROM THE ECF INTO
THE ICF . HENCE CELL SWELL
TYPES OF CRYSTALLOIDS
 COMMONLY USE IVF (CRYSTALLOIDS)

FLUID OSMO NA+ CL- K+ Ca+ Mg2+ HCO3 - LACTATE

PLASMA 280-290 135 - 96 - 3.5 - 4.4 - 1.8 - 22-26 1
145 106 5.2 5.2 2.4
NORMAL 308 154 154 - - - - -
SALINE (0.9
NSS)
LACTATED 273 130 109 4 3 - - 28
RINGER
(LR)
PLASMALYTE 295 140 98 5 - 4 - ACETATE
27
GLUCONATE
23

ISOTONIC SOLUTIONS
 COMMONLY USE IVF (CRYSTALLOIDS)

FLUID OSMO NA+ CL- K+ Ca+ Mg2+ HCO3 - LACTATE

PLASMA 280-290 135 - 96 - 3.5 - 4.4 - 1.8 - 22-26 1
145 106 5.2 5.2 2.4
3% NSS 1030 154 154 - - - - -
0.45 NSS 154 77 77 - - - - -

HYPOTONIC SOLUTIONS

HYPERTONIC SOLUTIONS
 COMMONLY USE IVF (CRYSTALLOIDS)

DEXTROSE CONTAINING IVF

• AS DEXTROSE IS METABOLIZED IT RESULT IN
DECREASE IN OSMOLALITY

• DEXTROSE ADDS CALORIES

➢ 5% DEXTROSE = 50 G/ L =170 CALORIES / LITER
➢ 10% DEXTROSE =100 G/ L= 340 CALORIES
/LITER
 DEXTROSE CONTAINING IVF
ISOTONIC IVF
D5W (5% DEXTROSE –WATER)
• OSMO : 253
• D5W FREE WATER ( HYPOTONIC)
HYPERTONIC
D5 .45NSS
• OSMO : 406 .45 NSS (HYPOTONIC)
D5 0.9 NSS
• OSMO: 560 0.9NS (ISOTONIC)
D5LR – OSMO : 527 LR (ISOTONIC)
D10WATER – OSM : 505 FREE WATER (ISOTONIC)
 TYPES OF INTRAVENOUS FLUIDS
COLLOIDS
• REFERRED TO AS VOLUME OR
PLASMA EXPANDERS

• CONTAINS LARGE INSOLUBLE

MOLECULES (PROTEINS?)

• GELATINOUS SOLUTIONS THAT

MAINTAIN A HIGH OSMOTIC
PRESSURE IN THE BLOOD

• HIGHER OSMOTIC PRESSURE –

THE PROTEINS DO NOT PASS
FROM VASCULATURE INTO THE
INTERSTITIAL SPACE HENCE
PULLING FLUIDS INSIDE THE
VASCULAR AND KEEP IT THERE
FOR LONGER PERIOD OF TIME
 TYPES OF INTRAVENOUS FLUIDS
COLLOIDS
• MORE EXPENSIVE THAN
CRYSTALLOIDS

• POTENTIATE IMMUNE
RESPONSE

• EXAMPLE OF COLLOID
FLUIDS
✓ ALBUMIN – AVAILABILITY 5% ,
25%
✓ DEXTRAN
 POTASSIUM
POTASSIUM
• POTASSIUM PLAYS A KEY ROLE IN
MAINTAINING CELL FUNCTION
• THE MAJORITY (98%) OF THIS K+ IS
WITHIN CELLS WITH ONLY 2% IN THE
EXTRACELLULAR FLUID
• THE NORMAL CONCENTRATION OF
K+ IN THE EXTRACELLULAR FLUID IS
3.5 TO 5.3 MEQ/L
• APPROXIMATELY 90% OF THE DAILY
K+ INTAKE IS EXCRETED IN THE
URINE, WHILE 10% IS EXCRETED BY
THE GASTROINTESTINAL TRACT
 POTASSIUM
FACTORS THAT CAN ALTER POTASSIUM DISTRIBUTION BETWEEN THE
INTRA- AND EXTRACELLULAR FLUID
FACTORS THAT SHIFT K+ INTO FACTORS THAT SHIFT K+ OUT OF
CELLS THE CELLS
(DECREASE EXTRACELLULAR K) (INCREASE EXTRACELLULAR K)

INSULIN INSULIN DEFICIENCY ( DIABETES

MELLITUS)
ALDOSTERONE ALDOSTERONE DEFICIENCY (
ADDISON’S DISEASE)
B-ADRENERGIC STIMULATION B-ADRENERGIC BLOCKADE
ALKALOSIS ACIDOSIS
CELL LYSIS
STRENUOUS EXERCISE
INCREASED ECF OSMOLALITY
 POTASSIUM
POTASSIUM
• HYPERKALEMIA DEFINED AS
POTASSIUM LEVEL OF 5.5
MMOL/L OR HIGHER .
ALTHOUGH IN SOME STUDIES
5.0-5.4 MMOL/L QUALIFY FOR
THE DIAGNOSIS

• HYPOKALEMIA DEFINED AS A
PLASMA POTASSIUM (K)
CONCENTRATION OF LESS
THAN 3.6 MMOL/L
 HYPERKALEMIA AND
HYPOKALEMIA
CONSEQUENCES OF
HYPERKALEMIA
• HIGH LEVELS OF POTASSIUM CAUSE
ABNORMAL HEART AND SKELETAL
MUSCLE FUNCTION BY LOWERING
CELL-RESTING ACTION POTENTIAL
AND PREVENTING REPOLARIZATION,
LEADING TO MUSCLE PARALYSIS

• CLASSIC ECG FINDINGS BEGIN WITH

TENTING OF THE T WAVE (PEAKED T
WAVE), FOLLOWED BY LENGTHENING
AND EVENTUAL DISAPPEARANCE OF
THE P WAVE AND WIDENING OF THE
QRS COMPLEX (PVC)
 APPROXIMATE RELATIONSHIP BETWEEN HYPERKALEMIC
ELECTROCARDIOGRAPHIC (ECG) CHANGES AND SERUM
POTASSIUM CONCENTRATION**
SERUM POTASSIUM ECG ABNORMALITY
CONCENTRATION
5.5-6.5 mmol/L • Tall peaked T waves with narrow base, best
seen in precordial leads
6.5-8.0 mmol/L • Peaked T waves
• Prolonged PR interval
• Decreased amplitude of P waves
• Widening of QRS complex
>8.0 mmol/L • Absence of P waves
• Intraventricular blocks, fascicular blocks,
bundle branch blocks,
• QRS axis shift
• Progressive widening of the QRS complex
• “Sine-wave” pattern (sinoventricular rhythm),
ventricular fibrillation, asystole
** PAGE 651 CHAPTER 17 DISORDERS OF POTASSIUM BALANCE , BRENNER & RECTOR’S THE KIDNEY ,
9TH EDITION
ECG CHANGES ASSOCIATED WITH
HYPERKALEMIA
ECG CHANGES ASSOCIATED WITH
HYPERKALEMIA
 HYPOKALEMIA
HYPOKALEMIA
• DEFINED AS A PLASMA POTASSIUM
(K) CONCENTRATION OF LESS THAN
3.6 MMOL/L

• RELATIVELY COMMON FINDING IN

BOTH OUTPATIENTS AND
INPATIENTS, PERHAPS THE MOST
COMMON ELECTROLYTE
ABNORMALITY ENCOUNTERED IN
CLINICAL PRACTICE
 HYPOKALEMIA
HYPOKALEMIA
• THE MOST COMMON CAUSATIVE
FACTORS IN HOSPITALIZED
PATIENTS WITH HYPOKALEMIA
ARE GASTROINTESTINAL LOSSES
OF POTASSIUM, DIURETIC
THERAPY, AND
HYPOMAGNESEMIA

• KNOWN TO BE MILD, WITH K+

LEVELS IN THE 3.0 TO 3.5 MMOL/L
RANGE, BUT IN UP TO 25% IT CAN
BE MODERATE TO SEVERE (<3.0
MMOL/L)
 HYPOKALEMIA
CONSEQUENCES OF
HYPOKALEMIA
• CAUSES EXCITABLE MUSCLE AND
HEART TISSUE
CARDIAC CONSEQUENCES
✓ CAUSES VENTRICULAR AND ATRIAL
ARRYTHMIAS
✓ MOST COMMON ECG FINDING
ASSOCIATED WITH HYPOKALEMIA ARE:
1. BROAD OR FLAT “T” WAVES
2. ST DEPRESSION
3. QT PROLONGATION
THESE ECG CHANGES ARE MORE
MARKED AT SERUM K CONCENTRATION
OF LESS THAN 2.7 MMOL/L
 HYPOKALEMIA
CONSEQUENCES OF
HYPOKALEMIA
• IT WORSENS HEART
FAILURE

• HYPOKALEMIA WORSENS
HYPERTENSION

• IT CAUSES MUSCLE
WEAKNESS AND
PARALYSIS
 ARTERIAL BLOOD GASES (ABG)

ARTERIAL BLOOD GAS

IT ASSESSES THE
EFFECTIVENESS OF GAS
EXCHANGE OF THE HUMAN
BODY BY MEASURING THE
PARTIAL PRESSURES OF
OXYGEN AND CARBON
DIOXIDE IN A SAMPLE OF
BLOOD OBTAINED BY
ARTERIAL PUNCTURE
 ARTERIAL BLOOD GASES (ABG)
IMPORTANCE OF ABG
1. HELP DETERMINE SEVERITY OF
DISEASES
2. INFORMATION ON OXYGENATION
3. ADEQUACY OF VENTILATION AND
PERFUSION
4. DETERMINE METABOLIC STATUS
5. HELP PLAN TREATMENT

INDICATIONS FOR DOING ABG

1. RESPIRATORY FAILURE – ACUTE
AND CHRONIC STATES
2. ILLNESS THAT WILL LEAD TO
METABOLIC ACIDOSIS
3. VENTILATED PATIENTS
4. FOR PROGNOSIS OF CLINICAL
CONDITION
 ARTERIAL BLOOD GASES (ABG)
MECHANISM THAT
COMPENSATES FOR CHANGES
IN ABG
1. BUFFER SYSTEM
- WITHIN A FRACTION OF A SECOND
- DOES NOT ELIMINATE H+ BUT TIED IT
UP UNTIL BALANCE IS ACHIEVED

2. RESPIRATORY SYSTEM
3. KIDNEYS
 PRIMARY ACID-BASE DISTURBANCES
PRIMARY ACID-BASE
DISTURBANCES
• RESPIRATORY ACIDOSIS: LOW PH,
HIGH PaCO2, NORMAL OR HIGH
NORMAL BICARBONATE.
CAUSES: NEUROMUSCULAR
WEAKNESS, INTRINSIC LUNG
DISEASE - EG, COPD

• RESPIRATORY ALKALOSIS: HIGH

PH, LOW PaCO2, NORMAL OR HIGH
NORMAL BICARBONATE.
CAUSES: ANY CAUSE OF
HYPERVENTILATION - EG, ANXIETY,
PAIN
 PRIMARY ACID-BASE DISTURBANCES
PRIMARY ACID-BASE
DISTURBANCES
• METABOLIC ACIDOSIS: LOW PH,
NORMAL OR LOW NORMAL
PACO2, LOW BICARBONATE.
CAUSES: SEE ANION GAP TABLE,
ABOVE

• METABOLIC ALKALOSIS: HIGH

PH, NORMAL PACO2, HIGH
BICARBONATE.
CAUSES: VOMITING, BURNS,
INGESTION OF BASE.
 THE ABG REQUEST
THE FOLLOWING
INFORMATION MUST BE
WRITTEN IN THE REQUEST
FROM FOR ABG
• NAME OF PATIENT
• AGE / GENDER OF PATIENT
• ROOM / WARD ASSIGNMENT
• PATIENT’S TEMPERATURE
• LATEST HGB
• LEVEL OF OXYGEN BEING
CONSUMED
 INTERPRETATION OF ABG
STEPS IN INTERPRETING
AN ABG
1. KNOW THE PH
2. DETERMINE THE PRIMARY
CHANGE
3. NOTE FOR ANY
SECONDARY CHANGE

NORMAL VALUES
PH - 7.35 - 7.45
PO2 - 85 – 100
PCO2 - 35 - 45
HCO3 - 22 - 26 MEQ
 ARTERIAL BLOOD GASES (ABG)
PH - 7.35 – 7.45 / 7.38 - 7.42
DEGREE ACIDOSIS ALKALOSIS
MILD 7.33 – 7.37 7.43 – 7.47
MODERATE 7.30 – 7.32 7.48 - 7.52
SEVERE < 7.29 > 7.53

DEGREE OF HYPOXEMIA ( PO2 - 85 -100)

DEGREE RANGE OF VALUE
MILD HYPOXEMIA 75-84
MODERATE 65-74
HYPOXEMIA
SEVERE 50-64
VERY SEVERE < 50
 ARTERIAL BLOOD GASES (ABG)
RULES IN INTERPRETING ABG
1. IF PCO2 IS BELOW NORMAL IT IS
RESPIRATORY ALKALOSIS

2. IF PCO2 IS ABOVE NORMAL IT IS

RESPIRATORY ACIDOSIS

3. IF HCO3 IS ABOVE NORMAL IT IS

METABOLIC ALKALOSIS

4. IF HCO3 IS BELOW NORMAL IT IS

METABOLIC ACIDOSIS
 FORMULAS FOR ABG
INTERPRETATION
FORMULAS TO DETERMINE WHETHER
THERE IS SECONDARY CHANGES OR
PURE
1. RESPIRATORY ACIDOSIS
(40-PCO2) X 0.4 + 24 + 2

2. RESPIRATORY ALKALOSIS
( 40 –PCO2) X 0.5 – 24 + 2

3. METABOLIC ACIDOSIS
1.5 X HCO3 + 8.4 + 2

4. METABOLIC ALKALOSIS
24 – (HCO3) X (.5 & I ) + 40 + 2
 SAMPLE PROBLEM
PH 7.10 ACIDOTIC
A 30 YEAR OLD PATIENT WAS
PCO2 22 ALKALOSIS
RUSHED TO ER DUE TO
TACHYPNEA & DYSPNEA. ABG HCO3 12 ACIDOTIC
DONE SHOWED THE FOLLWING
RESULTS: O2 75 LOW

PH 7.10
PCO2 22
HCO3 12 1. KNOW THE PH

O2 75 2. KNOW THE PRIMARY

CHANGE
O2 Sat 96 %
3. NOTE FOR ANY SECONDARY
CHANGE
CALCULATIONS
1. PRIMARY CHANGE – METABOLIC
ACIDOSIS
FORMULA:
1.5 X HCO3 + 8.4 +2

=1.5 + 12 + 8.4 +2
= 21.9 +2
= 23.9 – 19.9

2. TAKE NOTE FOR ANY SECONDARY

CHANGE
PCO2 = 22 COMPUTED PCO2 = 23.9 – 19. 9
CALCULATIONS
INTERPRETATION :
SEVERE METABOLIC ACIDOSIS WITH SEVERE
HYPOXEMIA

FORMULA FOR CORRECTION OF

ACIDOSIS
(DESIRED HCO3 – ACTUAL HCO3) X KG BODY WT X .4
2

(22- 12) X 50 KG X .4 / 2 = 200/2 = 100 MEQ TO BE

GIVEN AS SLOW IV PUSH
SUMMARY
• THE BODY FLUIDS IS DISTRIBUTED
INTO TWO MAIN COMPARTMENT :
THE INTRACELLULAR FLUID AND
THE EXTRACELLULAR FLUID

• THE EXTRACELLULAR FLUID IS

FURTHER COMPOSED OF
INTERSTITIAL FLUID AND PLASMA

• THE TOTAL BODY FLUID OF A

PERSON IS AFFECTED BY AGE,
GENDER, DEGREE OF OBESITY AND
OTHER MEDICAL CONDITIONS
SUMMARY
• A CLEAR UNDERSTANDING OF
FLUIDS AND ELECTROLYTES IS
IMPRORTANT TO UNDERSTAND
THE PRINCIPLE OF FLUID
RESUSCITATION

• IVF FLUIDS ARE BROADLY

CATEGORIZED AS
CRYSTALLOIDS AND COLLOID

• VARIOUS MEDICAL CONDITIONS

ARE ACCOMPANIED BY
CHANGES IN ARTERIAL BLOOD
GASES