4 Water, Electrolyte, Acid-Base, and Hemodynamic

Disorders
Water and Electrolyte Disorders
Body fluid compartments
1. Total body water (TBW) is 60% of the body weight in g
a. !odium ("a
#
) is the ma$or e%tracellular fluid (&'() cation.
b. )otassium (*
#
) is the ma$or intracellular fluid (+'() cation.
c. &'( is subdi,ided into the interstitial and ,ascular compartments.
-. )lasma osmolality ().sm)
a. .smolality is the number of solutes in plasma (i.e./ tonicity of &'().
b. ).sm 0 - (serum "a
#
) # serum glucose112 # serum blood urea
nitrogen (B3")1-.2 0 -456-75m.sm1g
).sm roughly correlates with the serum "a
#
concentration.
c. 3rea diffuses freely between &'( and +'(.
8. "a
#
and glucose are limited to the &'(.
a. 'hanges in their concentration produce an osmotic gradient.
ii Water shifts between the &'( and +'( compartments by
osmosis.
iii Water mo,es from a low to high solute concentration.
iiii Water shifts do not occur with alterations in urea
concentration.
b. 9yponatremia (decreased ).sm) causes water to shift from &'( to
+'(
c. 9ypernatremia or hyperglycemia (increased ).sm) cause water to
shift from +'( to &'(
Water and Electrolyte Disorders
Body fluid compartments
1. Total body water (TBW) is 60% of the body weight in g (
a. !odium ("a
#
) is the ma$or e%tracellular fluid (&'() cation.
b. )otassium (*
#
) is the ma$or intracellular fluid (+'() cation.
c. &'( is subdi,ided into the interstitial and ,ascular compartments.
-. )lasma osmolality ().sm)
a. .smolality is the number of solutes in plasma (i.e./ tonicity of &'().
b. ).sm 0 - (serum "a
#
) # serum glucose112 # serum blood urea
nitrogen (B3")1-.2 0 -456-75m.sm1g
).sm roughly correlates with the serum "a
#
concentration.
c. 3rea diffuses freely between &'( and +'(.
8. "a
#
and glucose are limited to the &'(.
a. 'hanges in their concentration produce an osmotic gradient.
ii Water shifts between the &'( and +'( compartments by
osmosis.
iii Water mo,es from a low to high solute concentration.
iiii Water shifts do not occur with alterations in urea
concentration.
b. 9yponatremia (decreased ).sm) causes water to shift from &'( to
+'(
c. 9ypernatremia or hyperglycemia (increased ).sm) cause water to
shift from +'( to &'(
Body fluid compartments
1. Total body water (TBW) is 60% of the body weight in g (
a. !odium ("a
#
) is the ma$or e%tracellular fluid (&'() cation.
b. )otassium (*
#
) is the ma$or intracellular fluid (+'() cation.
c. &'( is subdi,ided into the interstitial and ,ascular compartments.
-. )lasma osmolality ().sm)
a. .smolality is the number of solutes in plasma (i.e./ tonicity of &'().
b. ).sm 0 - (serum "a
#
) # serum glucose112 # serum blood urea
nitrogen (B3")1-.2 0 -456-75m.sm1g
).sm roughly correlates with the serum "a
#
concentration.
c. 3rea diffuses freely between &'( and +'(.
8. "a
#
and glucose are limited to the &'(.
a. 'hanges in their concentration produce an osmotic gradient.
ii Water shifts between the &'( and +'( compartments by
osmosis.
iii Water mo,es from a low to high solute concentration.
iiii Water shifts do not occur with alterations in urea
concentration.
b. 9yponatremia (decreased ).sm) causes water to shift from &'( to
+'(
c. 9ypernatremia or hyperglycemia (increased ).sm) cause water to
shift from +'( to &'(
(luid mo,ement across a capillary1,enule wall into the interstitial
space is dri,en by !tarling pressures (not osmosis). The net
direction of fluid mo,ement depends on which !tarling pressure is
dominant. :n increase in plasma hydrostatic pressure or a decrease
in plasma oncotic pressure (i.e./ serum albumin) causes fluid to
diffuse out of capillaries and ,enules and into the interstitial space/
resulting in dependent pitting edema and1or body ca,ity effusions.
page 61
page 6-
Table 4-1. Isotonic and Hypotonic Disorders
Compartment
Alteration Psm!"a
#
EC$ %ol&me
IC$
%ol&me Conditions
"ormal "ormal "ormal "ormal hydration
"ormal
TB"a
#
1TBW
'ontracted "ormal :dult diarrhea
;oss of whole blood
"ormal
TB"a
#
1TBW
&%panded
!tarling pressure
alteration
"ormal &%cessi,e isotonic
(normal) saline
<ecreased
TB"a
#
1TBW
'ontracted &%panded ;oop diuretics
:ddison=s disease
-169ydro%ylase
deficiency
<ecreased
TB"a
#
1TBW
&%panded &%panded !+:<9
<ecreased
TB"a
#
1TBW
&%panded
!tarling pressure
alteration
&%panded >ight6sided heart failure
'irrhosis
"ephrotic syndrome
&'(/ e%tracellular fluid? +'(/ intracellular fluid? ).sm/ plasma osmolality? !+:<9/ syndrome of inappropriate
antidiuretic hormone? TB/ total body? W/ water.
"ormal (isotonic) saline (0.7%) appro%imates plasma tonicity
().sm). +t is infused in patients to maintain the blood pressure
when there is a significant loss of sodium6containing fluid (e.g./
blood loss/ diarrhea/ sweat).
page 6-
page 68
page 68
page 6@
page 6@
page 65
>apid intra,enous fluid correction of hyponatremia with saline in an
alcoholic may result in central pontine myelinolysis/ an irre,ersible
demyelinating disorder. :s a general rule/ all intra,enous
replacement of "a
#
6containing fluid should be gi,en slowly o,er the
first -@ hours.
+n these pitting edema states/ the cardiac output is decreased/
which causes the release of catecholamines/ acti,ation of the renin6
angiotensin6aldosterone system/ stimulation of :<9 release/ and
increased renal retention of "a
#
. The idney reabsorbs a slightly
hypotonic/ "a
#
6containing fluid (TB"a
#
1TBW). Because these
pitting edema states ha,e alterations in !tarling pressures/ the "a
#
6
containing fluid is redirected into the interstitial space/ causing
pitting edema and body ca,ity effusions.
Table 4-'. Hypertonic Disorders
Compartment
Alteration Psm!"a
#
EC$
%ol&me
IC$
%ol&me Conditions
+ncreased
TB"a
#
1TBW
'ontracted 'ontracted .smotic diuresisA
glucose
!weating
+nfant diarrhea
+ncreased
TB"a
#
1TBW
'ontracted
(mild)
'ontracted +nsensible water lossA
fe,er
<iabetes insipidus
+ncreased
TB"a
#
1TBW
&%panded 'ontracted +nfusion of a "a
#
6
containing antibiotic
+nfusion of "a9'.8
+ncreased
Blucose
"a
#
(dilutional
effect)
'ontracted 'ontracted <iabetic etoacidosis
9yperosmolar nonetotic
coma
&'(/ e%tracellular fluid? +'(/ intracellular fluid? ).sm/ plasma osmolality? TB/ total body? W/ water.
page 65
page 66
1. !erum "a
#
concentration (m&C1;) reflects the ratio of total body "a
#
(TB"a
#
)
to total body water (TBW).
a. !erum "a
#
TB"a
#
1TBW
TB"a
#
is the sum total of all the &'( "a
#
and is e%pressed in
mg1g of body weight.
b. &,aluation of TB"a
#
status
ii <ecreased TB"a
#
produces signs of ,olume depletion.
<ry mucous membranes
<ecreased sin turgor (i.e./ sin tenting when the
sin is pinched)
<rop in blood pressure and increase in pulse when
sitting up from a supine position (i.e./ positi,e tilt test)
iii +ncreased TB"a
#
may produce body ca,ity effusions (e.g./
ascites) and dependent pitting edema
<ependent pitting edema is due to an e%cess of "a
#
6
containing fluid in the interstitial space.
<ue to the low protein content in edema fluid/
fluid obeys the law of gra,ity and mo,es to
the most dependent portion of the body (e.g./
anles/ if the person is standing).
:n alteration in !tarling pressures must be present to
produce pitting edema and body effusions.
+n patients who ha,e no !tarling pressure alterations/
pitting edema and body effusions are not liely to
occur.
iiii "ormal TB"a
#
is associated with normal sin turgor and
hydration.
-. +sotonic fluid disorders
a. +sotonic loss of fluid
ii ).sm and serum "a
#
are normal (TB"a
#
1TBW).
The arrows represent the magnitude of change in
TB"a
#
and TBW.
iii There is no osmotic gradient or fluid shift between &'( and
+'(.
&'( ,olume contracts? howe,er/ the +'( ,olume
remains normal.
iiii !igns of ,olume depletion are present.
ivi &%amples include adult diarrhea/ loss of whole blood.
b. +sotonic gain of fluid
ii ).sm and serum "a
#
are normal (TB"a
#
1TBW).
iii There is no osmotic gradient or fluid shift between &'( and
+'(.
&'( ,olume e%pands? howe,er/ the +'( ,olume
remains normal.
iiii )itting edema and body ca,ity effusions may be present.
ivi &%ample is e%cessi,e infusion of isotonic saline.
8. 9ypotonic fluid disorders
a. 9yponatremia (decreased ).sm) is always present.
ii .smotic gradient is present.
iii Water shifts to the +'( compartment (e%pands).
b. 9ypertonic loss of "a
#
(TB"a
#
1TBW)
ii &'( ,olume contracts and +'( ,olume e%pands.
iii !igns of ,olume depletion appear.
iiii &%amples include increased renal loss of "a
#
(e.g./ loop
diuretic/ :ddison=s disease/ -16hydro%ylase deficiency).
c. Bain of water (TB"a
#
1TBW)
ii &%pansion of &'( and +'( ,olumes
iii "ormal sin turgor
iiii &%ample6syndrome of inappropriate secretion of antidiuretic
hormone (!+:<9/ e.g./ small cell carcinoma of the lung)
d. 9ypotonic gain of "a
#
(TB"a
#
1TBW)
ii &%pansion of the &'( and +'( ,olumes
iii 'aused by pitting edema states with !tarling pressure
alterations
>ight6sided heart failure with increase in ,enous
hydrostatic pressure
'irrhosis and nephrotic syndrome with decrease in
plasma oncotic pressure
@. 9ypertonic fluid disorders
a. +ncreased ).sm is most often due to hypernatremia or
hyperglycemia.
ii .smotic gradient is present.
iii Water shifts out of the +'( (contracts) to the &'(.
b. 9ypotonic loss of "a
#
(TB"a
#
1TBW)
ii 'ontraction of the &'( and +'( ,olumes
iii !igns of ,olume depletion
iiii &%amples6sweating/ osmotic diuresis (e.g./ glucosuria)/ infant
diarrhea
c. ;oss of water (TB"a
#
1TBW)
ii 'ontraction of the &'( (mild) and +'( ,olumes
iii "ormal sin turgor
iiii &%amples
<iabetes insipidus due to loss of :<9 or
refractoriness to :<9
+nsensible water loss (e.g./ fe,er)
d. 9ypertonic gain of "a
#
(TB"a
#
1TBW)
ii &'( ,olume e%pands and +'( ,olume contracts.
iii )itting edema and body ca,ity effusions may be present.
iiii &%amples include infusion of "a9'.8 or "a
#
6containing
antibiotics.
e. 9ypertonic state due to hyperglycemia
&%amples6diabetic etoacidosis (<*:)/ hyperosmolar
nonetotic coma
ii Water shifts from the +'( to the &'( compartment.
<ilutional effect on serum "a
#
causes hyponatremia.
+ncreased ).sm (due to hyperglycemia) and
hyponatremia (dilutional).
iii !igns of ,olume depletion
Blucosuria produces a hypotonic loss of water and
"a
#
(osmotic diuresis)/ causing signs of ,olume
depletion
)otassium (*
#
) disorders
Table 4-(. Ca&ses o) Hypo*alemia
Pat+o,enesis Ca&ses
<ecreased intae &lderly patients/ eating disorders
Transcellular shift :lalosis
<rugs enhancing "a
#
1*
#
6:T)ase pumpA insulin/ D-6agonists (e.g./ albuterol)
Bastrointestinal
loss
<iarrhea (80m&C1; in stool)
;a%ati,es
Eomiting (5m&C1; in gastric $uice)
>enal loss ;oop and thiaFide diuretics (most common cause)
.smotic diuresisA glucosuria
Gineralocorticoid e%cessA primary aldosteronism/ 116hydro%ylase deficiency/
'ushing syndrome
Table 4-4. Ca&ses o) Hyper*alemia
Pat+o,enesis Ca&ses
Tissue breadown +atrogenic (e.g./ ,enipuncture)
>habdomyolysis (rupture of muscle)
Transcellular shift :cidosis
<rugs inhibiting "a
#
1*
#
6:T)ase pumpA D6blocer (e.g./ propanolol)/ digitalis
to%icity/ succinylcholine
<ecreased renal
e%cretion
>enal failure (most common cause)
Gineralocorticoid deficiencyA :ddison=s disease/ -16hydro%ylase deficiency/
hyporeninemic hypoaldosteronism (destruction of $u%taglomerular
apparatus)
<rugsA spironolactone (inhibits aldosterone)? triamterene/ amiloride (inhibit
"a
#
channels)
1. (unctions of potassium
a. >egulation of neuromuscular e%citability and muscle contraction
b. >egulation of insulin secretion
9ypoalemia inhibits insulin secretion/ while hyperalemia
stimulates insulin secretion.
-. 'ontrol of potassium
a. :ldosterone
ii +ncreases the secretion of *
#
and 9
#
in the late distal and
collecting tubules
iii +ncreases reabsorption of *
#
by the 9
#
1*
#
6:T)ase pump in
the collecting tubules
b. :rterial p9
ii :lalosis causes 9
#
to mo,e out of cells and *
#
into cells
)otential for hypoalemia
iii :cidosis causes 9
#
to mo,e into cells (for buffering) and *
#

out of cells
)otential for hyperalemia
-. 9ypoalemia (serum *
#
H 8.5m&C1;)
a. 'auses of hypoalemia
b. 'linical findings
ii Guscle weaness
<ue to changes in the intracellular1e%tracellular *
#

membrane potential
iii 3 wa,es on an electrocardiogram (&'B/
iiii )olyuria
'ollecting tubules are refractory to :<9 (i.e./
nephrogenic diabetes inspidus).
Tubule cells are distended with fluid (called ,acuolar
nephropathy).
ivi >habdomyolysis
9ypoalemia inhibits insulin/ which decreases
muscle glycogenesis/ leading to rhabdomyolysis.
8. 9yperalemia (serum *
#
I 5.0m&C1;)
a. 'auses
b. 'linical findings
ii Eentricular arrhythmias
!e,ere hyperalemia (e.g./ 462 m&C1;) causes the
heart to stop in diastole.
iii )eaed T wa,es on an &'B
<ue to accelerated repolariFation of cardiac muscle
iiii Guscle weaness
9yperalemia partially depolariFes the cell
membrane which interferes with membrane
e%citability
Acid-Base Disorders
)rimary alterations in arterial )co
-
()aco
-
/ 886@5 mm 9g)
Table 4--. Ca&ses o) .espiratory Acidosis and Al*alosis
Anatomic
/ite .espiratory Acidosis .espiratory Al*alosis
'"!
respiratory
center
<epression of centerA trauma/
barbiturates
.,erstimulationA an%iety/ high altitude/ normal
pregnancy (estrogen1progesterone effect)/
salicylate poisoning/ endoto%ic (septic) shoc/
cirrhosis
3pper airway .bstructionA acute epiglottitis
(Hemophilus influenzae)/ croup
(parainfluenFa ,irus)

Guscles
respiration
)aralysisA :;!/ phrenic ner,e
in$ury/ Buillain6BarrJ syndrome/
hypoalemia/ hypophosphatemia
(:T))
>ib fractureA hyper,entilation from pain
;ungs .bstructi,e diseaseA chronic
bronchitis/ cystic fibrosis
.therA pulmonary edema/ :><!/
><!/ se,ere bronchial asthma
>estricti,e diseaseA sarcoidosis/ asbestosis
.thersA pulmonary embolus/ mild bronchial
asthma
:;!/ amyotrophic lateral sclerosis? :><!/ acute respiratory distress syndrome? :T)/ adenosine triphosphate?
><!/ respiratory distress syndrome.
page 62
page 67
page 67
page 40
'ompensation refers to respiratory and renal mechanisms that bring
the arterial p9 close to but not into the normal p9 range (4.8564.@5).
+n primary respiratory acidosis and alalosis/ compensation is
metabolic alalosis and metabolic acidosis/ respecti,ely. +n primary
metabolic acidosis and alalosis/ compensation is respiratory
alalosis and respiratory acidosis/ respecti,ely. When the e%pected
compensation remains in the normal range/ an uncompensated
disorder is present. +f compensation mo,es outside the normal
range but does not bring p9 into the normal range/ a partially
compensated disorder is present. When compensation brings the
p9 into the normal range/ full compensation is present/ which rarely
occurs.
page 40
page 41
1. >espiratory acidosis
a. 'auses of respiratory acidosis
b. )athogenesis
i. :l,eolar hypo,entilation with retention of '.-
ii. )aco- I @5 mm 9g
p9 9'.81)co-
c. Getabolic alalosis is compensation
i. !erum 9'.8 80 m&C1; in acute respiratory acidosis
ii. !erum 9'.8
6
I 80 m&C1; (indicates renal compensation) in
chronic respiratory acidosis
d. 'linical findings
i. !omnolence
ii. 'erebral edema (,asodilation of cerebral ,essels)
-. >espiratory alalosis
a. 'auses of respiratory alalosis (see
b. )athogenesis
i. :l,eolar hyper,entilation with elimination of '.-
ii. )aco- H88 mm 9g
p9 9'.8
6
1 )'.-
c. Getabolic acidosis is compensation.
i. !erum 9'.8 12 m&C1; in acute respiratory alalosis
ii. !erum 9'.8
6
H 12 m&C1; but I 1- m&C1; (indicates renal
compensation) in chronic respiratory alalosis
d. 'linical findings
i. ;ight6headedness and confusion
ii. !igns of tetany
Thumb adduction into the palm (carpopedal spasm)
)erioral twitching when the facial ner,e is tapped
('h,oste sign)
)erioral numbness and tingling
:lalosis increases the number of negati,e charges on albumin
(more '..
6
groups on acidic amino acids). Therefore/ calcium is
displaced from the ioniFed calcium fraction and is bound to albumin/
causing a decrease in ioniFed calcium le,els and signs of tetany.
Table 4--. Ca&ses o) .espiratory Acidosis and Al*alosis
Anatomic
/ite .espiratory Acidosis .espiratory Al*alosis
'"!
respiratory
center
<epression of centerA trauma/
barbiturates
.,erstimulationA an%iety/ high altitude/ normal
pregnancy (estrogen1progesterone effect)/
salicylate poisoning/ endoto%ic (septic) shoc/
cirrhosis
3pper airway .bstructionA acute epiglottitis
(Hemophilus influenzae)/ croup
(parainfluenFa ,irus)

Guscles
respiration
)aralysisA :;!/ phrenic ner,e
in$ury/ Buillain6BarrJ syndrome/
hypoalemia/ hypophosphatemia
(:T))
>ib fractureA hyper,entilation from pain
;ungs .bstructi,e diseaseA chronic
bronchitis/ cystic fibrosis
.therA pulmonary edema/ :><!/
><!/ se,ere bronchial asthma
>estricti,e diseaseA sarcoidosis/ asbestosis
.thersA pulmonary embolus/ mild bronchial
asthma
:;!/ amyotrophic lateral sclerosis? :><!/ acute respiratory distress syndrome? :T)/ adenosine triphosphate?
><!/ respiratory distress syndrome.
page 62
page 67
page 67
page 40
'ompensation refers to respiratory and renal mechanisms that bring
the arterial p9 close to but not into the normal p9 range (4.8564.@5).
+n primary respiratory acidosis and alalosis/ compensation is
metabolic alalosis and metabolic acidosis/ respecti,ely. +n primary
metabolic acidosis and alalosis/ compensation is respiratory
alalosis and respiratory acidosis/ respecti,ely. When the e%pected
compensation remains in the normal range/ an uncompensated
disorder is present. +f compensation mo,es outside the normal
range but does not bring p9 into the normal range/ a partially
compensated disorder is present. When compensation brings the
p9 into the normal range/ full compensation is present/ which rarely
occurs.
page 40
page 41
1. >espiratory acidosis
a. 'auses of respiratory acidosis
b. )athogenesis
i. :l,eolar hypo,entilation with retention of '.-
ii. )aco- I @5 mm 9g
p9 9'.81)co-
c. Getabolic alalosis is compensation
i. !erum 9'.8 80 m&C1; in acute respiratory acidosis
ii. !erum 9'.8
6
I 80 m&C1; (indicates renal compensation) in
chronic respiratory acidosis
d. 'linical findings
i. !omnolence
ii. 'erebral edema (,asodilation of cerebral ,essels)
-. >espiratory alalosis
a. 'auses of respiratory alalosis (see
b. )athogenesis
i. :l,eolar hyper,entilation with elimination of '.-
ii. )aco- H88 mm 9g
p9 9'.8
6
1 )'.-
c. Getabolic acidosis is compensation.
i. !erum 9'.8 12 m&C1; in acute respiratory alalosis
ii. !erum 9'.8
6
H 12 m&C1; but I 1- m&C1; (indicates renal
compensation) in chronic respiratory alalosis
d. 'linical findings
i. ;ight6headedness and confusion
ii. !igns of tetany
Thumb adduction into the palm (carpopedal spasm)
)erioral twitching when the facial ner,e is tapped
('h,oste sign)
)erioral numbness and tingling
:lalosis increases the number of negati,e charges on albumin
(more '..
6
groups on acidic amino acids). Therefore/ calcium is
displaced from the ioniFed calcium fraction and is bound to albumin/
causing a decrease in ioniFed calcium le,els and signs of tetany.
Gi%ed acid6base disorders
page 4@
page 45
1. Blend of two or more primary acid6base disorders occurring at the same time
-. 'lues that suggest a mi%ed disorder
a. )resence of a normal p9 due to a combination of a primary acidosis
and a primary alalosisA
i. !alicylate into%ication/ particularly in adults
!alicylic acid produces a primary metabolic acidosis.
!alicylates o,erstimulate the respiratory center
causing primary respiratory alalosis.
ii. )atient with chronic bronchitis who is taing a loop diuretic
'hronic bronchitis produces a primary respiratory
acidosis.
;oop diuretics produce a primary metabolic alalosis.
b. &%treme acidemia due to a primary metabolic acidosis plus a primary
respiratory acidosis
&%ample6cardiorespiratory arrest with primary respiratory
acidosis (no ,entilation) and primary metabolic acidosis
(lactic acidosis from hypo%ia)
!elected electrolyte profiles
Table 4-0. /elected Electrolyte Pro)iles
/er&m
"a
#

1mE2!34
/er&m
5
#

1mE2!34
/er&m
Cl
-

1mE2!34
/er&m
HC(
-

1mE2!34 Disc&ssion
18561@4 8.565.0 756105 --6-2 "ormal ranges
112 8.0 2@ -- !+:<9A dilutional effect of e%cess water on
all electrolytes
1-2 5.7 76 -0 :ddison=s diseaseA lac of aldosterone
causes loss of "a
#
(hyponatremia)/ retention
of *
#
(hyperalemia)/ and decreased
synthesis of 9'.8
6
(metabolic acidosis? see
180 -.7 20 86 EomitingA loss of "a
#
and *
#
in ,omitus
(hyponatremia/ hypoalemia)? ,olume
depletion causes increased reclamation of
9'.8
6
in pro%imal tubule (metabolic
alalosis)
;oop and thiaFide diureticsA hypertonic loss
"a
#
in urine (hypernatremia)? augmented
e%change of "a
#
for *
#
(hypoalemia) and
increased regeneration of 9'.8
6
in late distal
"a
#
1*
#
#9
#
channels (metabolic alalosis/ see
15- -.2 110 88 Gineralocorticoid e%cessA primary
aldosteronism? augmented e%change of "a
#

for *
#
(hypernatremia/ hypoalemia)/ and
increased synthesis of 9'.8
6
in late distal
"a
#
1*
#
#9
#
channels (metabolic alalosis/ see
!+:<9/ syndrome of inappropriate antidiuretic hormone.
!elected arterial blood gas profiles
Table 4-16. /elected Arterial Blood 7as Pro)iles
pH
PaC'
1mm H,4
HC(
-

1mE2!34 Disc&ssion
4.856
4.@5
886@5 --6-2 "ormal ranges
4.00 5- 18 Gi%ed disorder (e%treme acidemia)A primary metabolic
acidosis (9'.8
6
H -- m&C1;) #primary respiratory acidosis
()a'.- I @5 mm 9g)
&%ampleA cardiorespiratory arrest
4.-0 4@ -2 :cute respiratory acidosis/ uncompensated ()a'.- I @5 mm
9g/ 9'.8
6
H 80 m&C1;)
&%amplesA '"! respiratory center depression (e.g./
barbiturate poisoning)
4.88 60 81 'hronic respiratory acidosis with partially compensated
metabolic alalosis ()a'.- I @5 mm 9g/ 9'.8
6
I 80 m&C1;)
&%amplesA chronic bronchitis/ cystic fibrosis
4.-2 -2 1- Getabolic acidosis with partially compensated respiratory
alalosis (9'.8
6
H -- m&C1;/ )a'.- H 88 mm 9g)
&%amplesA disorders associated with increased and normal
anion gap metabolic acidosis
4.@- -- 1@ Gi%ed disorder (normal p9)A primary metabolic acidosis
(9'.8
6
H -- m&C1;) # primary respiratory alalosis ()a'.- H
88 mm 9g)
&%ampleA salicylate poisoning
4.50 @4 85 Getabolic alalosis with partially compensated respiratory
acidosis (9'.8
6
I -2 m&C1;/ )a'.- I @5 mm 9g)
'ausesA loop1thiaFide diuretics/ ,omiting/ mineralocorticoid
e%cess
4.56 -@ -1 :cute respiratory alalosis with partially compensated
metabolic acidosis ()a'.- H 88 mm 9g/ 9'.8
6
H -- m&C1;)
'ausesA an%iety/ pulmonary embolus/ normal pregnancy
'"!/ central ner,ous system.
Edema
)resence of increased fluid in the interstitial space of the &'( compartment
Types of edema fluid
1. Transudate
a. )rotein6poor (H8 g1d;) and cell6poor fluid
b. )roduces dependent pitting edema and body ca,ity effusions
-. &%udate
a. )rotein6rich (I8 g1d;) and cell6rich (e.g./ neutrophils) fluid
b. )roduces swelling of tissue but no pitting edema
8. ;ymphedema
a. )rotein6rich fluid
b. "onpitting edema
@. Blycosaminoglycans
a. +ncrease in hyaluronic acid and chondroitin sulfate
b. "onpitting edema called my%edema
)athophysiology of edema
page 45
page 46
page 46
page 44
page 44
page 42
1. :lteration in !tarling pressure
a. )roduces a transudate
b. +ncreased ,ascular hydrostatic pressureA
i. )ulmonary edema in left6sided heart failure
ii. )eripheral pitting edema in right6sided heart failure
iii. )ortal hypertension in cirrhosis producing ascites
c. <ecreased ,ascular plasma oncotic pressure (hypoalbuminemia)A
i. Galnutrition with decreased protein intae
ii. 'irrhosis with decreased synthesis of albumin
iii. "ephrotic syndrome with increased loss of protein in urine (I
8.5 g1-@ hours)
i,. Galabsorption with decreased reabsorption of protein
d. >enal retention of sodium and water
i. +ncreases hydrostatic pressure (increased plasma ,olume)
ii. <ecreases oncotic pressure (dilutional effect on albumin)
iii. &%amples6acute renal failure/ glomerulonephritis
-. +ncreased ,ascular permeability
a. )roduces an e%udate
b. &%ample6acute inflammation (e.g./ tissue swelling following a bee
sting)
8. ;ymphatic obstruction
a. )roduces lymphedema
b. &%amples
i. ;ymphedema following modified radical mastectomy and
radiation
ii. (ilariasis due to Wuchereria bancrofti
iii. !crotal and ,ul,ar lymphedema due to lymphogranuloma
,enereum
i,. Breast lymphedema due to blocage of subcutaneous
lymphatics by malignant cells
@. +ncreased synthesis of e%tracellular matri% components (e.g./
glycosaminoglycans)
a. T6cell cytoines stimulate fibroblasts to synthesiFe
glycosaminoglycans.
b. &%ample6pretibial my%edema and e%ophthalmos in Bra,es= disease
T+rombosis
: thrombus is an intra,ascular mass attached to the ,essel wall and is
composed of ,arying proportions of coagulation factors/ >B's/ and platelets.
)athogenesis of thrombi
1. &ndothelial cell in$ury
o <ue to turbulent blood flow at arterial bifurcations or o,erlying
atherosclerotic plaCues? cigarette smoe
-. !tasis of blood flow
o !luggish blood flow due to prolonged bed rest or sitting
8. 9ypercoagulability
a. :cti,ation of coagulation system
b. 'auses of hypercoagulability
i. 9ereditary or acCuired factor deficiencies
&%ample6hereditary antithrombin +++ deficiency or
acCuired deficiency due to oral contracepti,es
ii. :ntiphospholipid syndrome
<ue to lupus anticoagulant or anticardiolipin
antibodies
Types of thrombi
1. Eenous thrombi
a. )athogenesis
i. !tasis
)rocoagulants (e.g./ tissue thromboplastin) released
from damaged endothelium cause localiFed
acti,ation of the coagulation system.
ii. 9ypercoagulable state
b. !ites
i. <eep ,ein in the lower e%tremity below the nee
ii. .ther sites
!uperficial saphenous/ hepatic/ and renal ,eins?
dural sinuses
c. 'omposition
i. :dherent/ occlusi,e/ dar red fibrin clot
'ontains entrapped >B's/ white blood cells/ and
platelets
ii. +n the lower e%tremities/ they propagate (e%tend) toward the
heart.
<anger of pulmonary artery emboliFation
d. :nticoagulants heparin and warfarin pre,ent formation of ,enous
thrombi.
-. :rterial thrombi
a. )athogenesis
i. &ndothelial cell in$ury due to turbulent blood flow
)latelets adhere to areas of in$ury.
ii. 9ypercoagulable state
b. !ites
i. &lastic and muscular arteries
ii. Ga$ority of thrombi o,erlie atherosclerotic plaCues
&%ample6coronary artery thrombosis
c. 'omposition of thrombi in muscular arteries and aortic branches
i. :dherent/ usually occlusi,e/ gray6white fibrin clot composed
of platelets
ii. :spirin and other inhibitors of platelet aggregation pre,ent
formation of these thrombi.
d. 'omposition of thrombi in the heart and aorta
i. ;aminated thrombi with alternating pale and red areas (lines
of Kahn)
)ale areas are composed of platelets held together
by fibrin.
>ed areas are composed predominantly of >B's.
Gi%ed type of thrombus
ii. &%amples of thrombi in the heart
Thrombus in left ,entricle due to a transmural
myocardial infarction (mural thrombus)
Thrombus in left atrium in patients with mitral
stenosis complicated by atrial fibrillation
iii. Thrombi in the aorta usually de,elop in aneurysms.
&%ample6abdominal aortic aneurysm
i,. :spirin along with anticoagulant therapy helps to pre,ent
these types of thrombi.
e. 'linical findings in arterial thrombosis
i. +nfarction (e.g./ acute myocardial infarction/ stroe)
ii. &mboliFation
8. )ostmortem clot
a. (ibrin clot of plasma (resembles chicen fat) without entrapped cells
b. +t is not attached to the ,essel wall.
Embolism
<etached mass (e.g./ clot/ fat/ gas) that is carried through the blood to a
distant site
)ulmonary thromboembolism
1. !ite of origin
a. Ga$ority originate from the femoral ,ein (e%tension of deep ,ein
thrombus).
b. .thers originate from the pel,ic ,eins or ,ena ca,a.
-. 'linical findings
a. !udden death
<ue to a saddle embolus occluding the ma$or pulmonary
artery branches
b. )ulmonary infarction
ii !mall thromboemboli occlude medium6siFed or small
pulmonary arteries.
iii ;ess than 10% of thromboemboli produce infarction.
b. )arado%ic embolism
Eenous thromboembolus passes through an atrial septal
defect into the systemic circulation.
!ystemic embolism
page 20
page 21
&mboli tra,eling in the arterial system
1. 'auses of systemic embolism
a. Thrombi from the left side of the heart (20% of cases)
i. Gural thrombus in left ,entricle following acute myocardial
infarction
ii. Thrombus in the left atrium in mitral stenosis
:trial fibrillation predisposes to atrial clot formation
and emboliFation.
b. :trial my%oma/ ,egetations from aortic or mitral ,al,e
-. !ites of embolism
a. ;ower e%tremities (most common)
b. Brain (,ia the middle cerebral artery)
c. !mall bowel (,ia the superior mesenteric artery)
d. !pleen and idneys
8. 'linical findings
a. )ale infarctions in the digits/ spleen/ and idneys
b. 9emorrhagic infarctions in the brain and small bowel
(at embolism
1. 'auses
a. Gost often due to traumatic fracture of the long bones (e.g./ femur)
b. .ther causes include trauma to fat6laden tissues/ fatty li,er.
-. )athogenesis
a. Gicroglobules of fat from the bone marrow obstruct micro,asculature
)roduces ischemia and hemorrhage
b. (atty acids damage ,essel endothelium.
(ormation of platelet thrombi in areas of in$ury
8. 'linical findings
a. !ymptoms begin -@ to 4- hours after trauma.
b. >estlessness/ delirium/ coma
c. <yspnea/ tachypnea
(at microglobules in pulmonary capillaries cause hypo%emia.
d. )etechiae de,elop o,er the chest and upper e%tremities.
<ue to thrombocytopenia from platelet adhesion to
microglobules of fat
e. <eath results in less than 10% of cases.
:mniotic fluid embolism
1. .ccurs during labor or immediately postpartum.
-. )athogenesis
a. Tears in placental membranes or uterine ,eins
b. +nfusion of amniotic fluid with procoagulants into the maternal
circulation
8. 'linical findings
a. :brupt onset of dyspnea/ cyanosis/ hypotension/ and bleeding
i. <yspnea is due to pulmonary edema or acute respiratory
distress syndrome.
ii. Bleeding is due to disseminated intra,ascular coagulation
(<+').
iii. <iagnosis is most often confirmed at autopsy.
(etal sCuamous cells are present in the pulmonary
,essels.
b. Gaternal mortality rate ,aries from -0% to 60%.
<ecompression sicness
(orm of gas embolism
1. !cuba and deep sea di,ing is the most common cause.
-. )athogenesis
a. :tmospheric pressure increases by 1 for e,ery 88 ft of descent into
water.
b. "itrogen gas is forced out of the al,eoli and dissol,es in blood and
tissues.
c. >apid ascent causes nitrogen to e%pand and form gas bubbles in
tissue and ,essel lumens.
8. 'linical findings
a. )ain de,elops in $oints/ muscles/ and bones.
'alled Lthe bendsL
b. )neumothora%
ii 'omplication of a sudden rise to the surface
iii <ue to rupture of a pree%isting subpleural bleb
iiii 'auses dyspnea and pleuritic chest pain
b. )ulmonary embolus
ii )ressure on the ,eins in the lower e%tremities produces
stasis and thrombus formation.
iii )ulmonary thromboembolism occurs
iiii 'auses dyspnea and pleuritic chest pain
c. 'hronic changes
:septic necrosis in bones (femur/ tibia/ humerus) from bone
infarctions
ii Treatment
o >ecompression (nitrogen forced into solution) followed by slow
decompression
/+oc*
!hoc is reduced perfusion of tissue/ which results in impaired o%ygenation of
tissue.
Types of
shoc
page 2-
page 28
page 28
page 2@
1. 9ypo,olemic shoc
a. <ue to e%cessi,e fluid loss (e.g./ blood/ sweat)
b. 9emorrhage
i. ;oss of greater than -0% of blood ,olume (1000 m;)
results in shoc.
ii. No initial effect on hemoglobin and hematocrit concentration
:bsolute neutrophilic leuocytosis is the first
hematologic sign.
+nfusion of 0.7% saline immediately unco,ers the
>B' deficit.
iii. )lasma is replaced first with fluid from the interstitial space.
3nco,ers the >B' deficit within hours to days
i,. >B' response in the bone marrow begins in 5 to 4 days.
c. )athophysiology of hypo,olemic shoc
i. <ecreased cardiac output ('.)
<ue to decreased ,olume of blood
ii. <ecreased left ,entricular end6diastolic pressure (;E&<))
iii. +ncreased peripheral ,ascular resistance ()E>)
<ue to ,asoconstriction of arterioles from
catecholamines and angiotensin ++/ which are
released in response to the decreased '.
d. 'linical findings in hypo,olemic shoc
i. 'old/ clammy sin due to ,asoconstriction of sin ,essels
ii. 9ypotension? rapid/ wea pulse (compensatory response to
decreased '.)
-. 'ardiogenic shoc
a. Gost commonly caused by an acute myocardial infarction
b. )athophysiology of cardiogenic shoc
i. <ecreased '.
<ue to decreased force of contraction in the left
,entricle
ii. +ncreased ;E&<)
Blood accumulates in the left ,entricle.
iii. +ncreased )E>
!ame mechanism as in hypo,olemic shoc
c. 'linical findings in cardiogenic shoc
'hest pain followed by signs similar to hypo,olemic shoc
ii !eptic shoc
a. !epticemia is most commonly due to gram6negati,e pathogens (e.g./
Escherichia coli).
b. )athogenesis
i. &ndoto%ins damage endothelial cells.
'auses the release of ,asodilators such as nitric
o%ide and prostaglandin +-
ii. &ndoto%ins acti,ate the alternati,e complement pathway.
:naphylato%ins ('8a and '5a) are produced/ which
stimulate mast cell release of histamine (,asodilator)
iii. +nterleuin 1 and tumor necrosis factor are released from
macrophages.
:cti,ate neutrophil adhesion molecules/ causing
neutrophil adherence to pulmonary capillaries
b. )athophysiology of septic shoc
i. +nitial increase in '.
<ue to rapid blood flow through dilated arterioles/
causing increased return of blood to the heart
Tissues are unable to e%tract o%ygen/ because of the
increased blood flow.
ii. <ecreased ;E&<)
<ue to neutrophil transmigration through the
pulmonary capillaries into al,eoli producing
noncardiogenic pulmonary edema
iii. <ecreased )E>
<ue to ,asodilation of peripheral resistance arterioles
c. 'linical findings in septic shoc
i. Warm sin/ due to ,asodilation of sin ,essels
ii. Bounding pulse/ due to increased '.
iii. :cute respiratory distress syndrome
<ue to neutrophil transmigration into al,eoli
i,. <isseminated intra,ascular coagulation
<ue to acti,ation of the intrinsic and e%trinsic
coagulation system
8. !ummary of pathophysiologic findings in shoc
Table 4-11. /&mmary o) Pat+op+ysiolo,ic $indin,s in Hypo8olemic,
Cardio,enic, and /eptic /+oc*
Type C P%. 3%EDP
9ypo,olemic
'ardiogenic
&ndoto%ic (septic)
'./ cardiac output? ;E&<)/ left ,entricular end6diastolic pressure? )E>/ peripheral ,ascular resistance.
'omplications associated with shoc
1. +schemic acute tubular necrosis
o 'oagulation necrosis of pro%imal tubule cells and cells in the thic
ascending limb
-. Gultiorgan dysfunction
o Gost common cause of death
8. ;actic acidosis due to tissue hypo%ia