MAKE YOUR SELF CLEAR

1)

CO poison -

Carbon Monoxide (inhibits

cytochrome oxidase)
2)
CN poison - Cyanide (inhibits
cytochrome oxidase)
3)
Methemoglobinemia Hb Fe
(Normal Hb Fe)
4)
Nitrates-Produce NO by cystein->
smooth muscle relaxation
5)
Nitroprusside-> CN + NO
NOTE= Solubility CO > CO >> O
CO

FEATUR
ES
Causes

CO
POISON
Automobile
exhaust,
smoke,
Wood stoves,
Indoor
gasoline
powered
generatore,
Methane gas

Affinity to Hb - CO > O >

CN
POISON
Combustion of
synthetic
products in
house fire,
(also
automobile
exhaust),
Prolonged
exposure to
nitroprusside,
Amygdalin in
almond,
Suicidal
attempt-CN
consumption

METH.H
b
Oxidant
stress e.g.
nitrite/sulfure
containig
drugs,
Nitrates(fertil
izing agents),
Sepsis,
Congenital
deficiency of
cytochrome
b5 reductase
[ MethHb
reduction in
RBC : NADH
electrone ->
cyt b5 -> cyt
b5 reductase

-> Fe]

Pathogen
esis

Clinical
findings

1) High
affinity ->
competes
with O
for
binding
on Hb->
Sao,
impaires
O
unloading
-> left
shift OBC
2) Inhibits
cytochro
me
oxidase
-> shuts
down ETC
-> O
consumpt
ion
intracell
ular
NADH/NA
D and
FADH/FA
D ratio,
ATP

CHERRY RED
discoloration
of skin &
blood,
Headache 1st

1) Inhibits
cytochrom
e oxidase
-> shuts
down ETC
-> O
consumpti
on
intracellu
lar
NADH/NAD
and
FADH/FAD
ratio, ATP

BITTER ALMOND
smell of breath,
Seizure,
Coma,
Arrythmia,

1) Fe
cant
bind O
->
Sao
2) Fe
imapires
unloadin
g of O
-> left
shift
OBC

CHOCOLATEBROWN color
of blood,
Cyanosis at
<20%,

symptom at
level of 10%20%,
Dyspnea,
dizziness at
20%-30%,
Seizure, coma
at 50%-60%,
Atraumatic
rhabdomyolysi
s,
Delayed
neurologic
deficits
CO in blood,
Lactic acidosis> increased
anion gap
metabolic
acidosis
Normal

Cardiovascular
collapse

Headache,
anxiety,
dyspnea,
tachycardia
at >20%,
Confusion,
lethargy,
lactic
acidosiss at
>40%

Lactic acidosis> increased

anion gap
metabolic
acidosis

Lactic
acidosis->
increased
anion gap
metabolic
acidosis
Normal

O
content

SaO

OBC (O
binding
curve)
Cytochro
me
oxidase
Treatment

Left shifted

Mixed venouse
O content
similar to the
arterial O
content
Normal (O not
removed from
blood)
Normal

Left shifted

Inhibited

Inhibited

Normal

Lab
findings

PaO

100% O
therapy,

Normal

1) Infusion of
sodium

Intravenous
methylene

Hyperbaric
oxygen
therapy

nitrite
followed
by
thiosulfate
2) Infusion of
hydroxyco
balamine

Nitroprusside

blue->
accelerates
NADPH
methemoglob
in reductase> reduction
of MetHb

sodium nitrite/ amyl

nitrite
MetHb <Hb

NO + Cyanide (+ MetHb )

MatHb binds to the CN in blood

before CN inhibits Cytochrome
oxidase in motochindria

Cyanomethemoglobin

Liver
Methelyne blue->OxHb

Cyanide + MetHb

Thiosulfate
infusion
SULFER TO
RHODANASE

thicyante-> excretes
by
kidney