Содержание

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Parameters Classification, etiology and mechanism of hypoxia Alterations of metabolism and

Parameters
Classification, etiology and mechanism of hypoxia
Alterations of metabolism and function in

the body
Pathophysiological basis of prevention and treatment
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parameters PO2 CO2max CO2 SO2 P50

parameters

PO2
CO2max
CO2
SO2
P50

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PO2 partial pressure of oxygen PO2 is the tension produced by

PO2 partial pressure of oxygen

PO2 is the tension produced by the

oxygen molecules physically dissolved in plasma.

Normal PaO2: 100mmHg
PvO2: 40mmHg

Determined by PiO2 and pulmonary function

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CO2max oxygen binding capacity of hemoglobin CO2max refers to the maximal

CO2max oxygen binding capacity of hemoglobin

CO2max refers to the maximal amount

of oxygen that could be bound by the hemoglobin, which reflects the ability of hemoglobin carrying oxygen.

Normal value: 20ml/dl

Determined by quantity and quality of Hb

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CO2 oxygen content CO2 includes oxygen that is bound to hemoglobin

CO2 oxygen content

CO2 includes oxygen that is bound to hemoglobin and

physically dissolved in the blood (0.3ml/dl).

Normal value: CaO2:19ml/dl
CvO2:14ml/dl

The arteriovenous oxygen content difference (CaO2-CvO2) reflects the oxygen volume of tissue uptake.

Determined by PO2 and CO2max

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SO2 oxygen saturation SO2 is the percentage of hemoglobin present as

SO2 oxygen saturation

SO2 is the percentage of hemoglobin present as oxyhemoglobin

.

Normal value: SaO2: 95%
SvO2: 75%

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The relation between oxygen partial pressure and oxygen saturation is shown

The relation between oxygen partial pressure and oxygen saturation is shown

as oxygen dissociation curve (ODC).

An increase in 2,3-diphosphoglyceric acid (2,3-DPG), H+, PCO2 and temperature will shift the curve to the right, in turn to the left.

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P50 means the oxygen partial pressure required to saturate 50% of

P50 means the oxygen partial pressure required to saturate 50% of

the hemoglobin, which reflects the affinity of hemoglobin for oxygen.

Normal value P50:26-27mmHg

P50

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Classification, etiology, mechanism of hypoxia Hypotonic hypoxia Hemic hypoxia Circulatory hypoxia Histogenous hypoxia

Classification, etiology, mechanism of hypoxia

Hypotonic hypoxia
Hemic hypoxia
Circulatory hypoxia
Histogenous hypoxia

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Hypotonic hypoxia hypoxic hypoxia Hypotonic hypoxia is characterized by the decrease of PaO2(less than 60mmHg).

Hypotonic hypoxia
hypoxic hypoxia

Hypotonic hypoxia is characterized by the decrease

of PaO2(less than 60mmHg).
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Etiology and mechanism Decreased PO2 of inspired air high altitude External

Etiology and mechanism

Decreased PO2 of inspired air
high altitude
External respiratory dysfunction

hypoventilation
impaired diffusion
partial ventilation-perfusion imbalcance
Venous-to-arterial shunt
congenital heart disease, Tetralogy of Fallot
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Characteristics of blood oxygen PaO2↓, SaO2↓, CaO2 ↓, CO2max N, CaO2-CvO2

Characteristics of blood oxygen

PaO2↓, SaO2↓, CaO2 ↓, CO2max N, CaO2-CvO2 ↓/N

Cyanosis

refers to the bluish color of skin, nails, lips and mucous membranes when the deoxyhemoglobin concentration of the blood in the capillaries is more than 5g/dl.
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Hemic hypoxia isotonic hypoxia Hemic hypoxia refers to the altered affinity

Hemic hypoxia
isotonic hypoxia

Hemic hypoxia refers to the altered affinity of

Hb for oxygen or decrease in amount of Hb in the blood.
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Etiology and mechanism Anemia Carbon monoxide poisoning CO can react with

Etiology and mechanism

Anemia
Carbon monoxide poisoning
CO can react with

Hb to form carboxyhemoglobin which can not take up oxygen. So there is a deficiency of Hb that can carry oxygen.
CO can inhibit glycolysis in RBC, which reduces the production of 2,3-DPG and shifts the ODC to the left, decreasing the amount of oxygen released.
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Methemoglobinemia The ferrous state (Fe2+) in Hb may be oxidized to

Methemoglobinemia
The ferrous state (Fe2+) in Hb may be oxidized

to the ferric state (Fe3+) under the action of oxidizers, e.g. nitrite and nitrobenzene, to form methemoglobin (HbFe3+OH), which loses the ability to carry oxygen.
Methemoglobin can also make the ODC of normal HbO2 shift to the left.
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when a lot of pickled vegetables containing nitrate are taken, the

when a lot of pickled vegetables containing nitrate are taken, the

reabsorbed nitrite reacts with HbFe2+ to form HbFe3+. The skin appears to coffee color. This phenomenon is called enterogenous cyanosis.

Enterogenous cyanosis

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High affinity of Hb for O2 Alkaline solution Depot blood

High affinity of Hb for O2

Alkaline solution
Depot blood

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Characteristics of blood oxygen PaO2 N, SaO2N, CaO2 ↓/N, CO2max ↓/N,

Characteristics of blood oxygen

PaO2 N, SaO2N, CaO2 ↓/N, CO2max ↓/N, CaO2-CvO2


CaO2-CvO2 is below normal because PO2 in the capillary is declined rapidly due to reduced CaO2.

Severe anemia : pallor
CO poisoning : cherry red
Methemoglobinemia: coffee color

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Circulatory hypoxia hypokinetic hypoxia Circulatory hypoxia refers to inadequate blood flow

Circulatory hypoxia
hypokinetic hypoxia

Circulatory hypoxia refers to inadequate blood flow leading

to inadequate oxygenation of the tissues, which is also called hypokinetic hypoxia.
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Etiology and mechanism Tissue ischemia shock, left heart failure, thrombosis, arterial

Etiology and mechanism

Tissue ischemia
shock, left heart failure, thrombosis, arterial stenosis


Tissue congestion
shock, right heart failure
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PaO2N, SaO2N, CaO2 N, CO2max N, CaO2-CvO2 ↑ Characteristics of blood

PaO2N, SaO2N, CaO2 N, CO2max N, CaO2-CvO2 ↑

Characteristics of blood oxygen

Because

the blood flows slowly in the capillary due to ischemia or congestion, the tissues will take more oxygen from unit volume blood.

Patient with circulatory hypoxia may appear cyanosis.

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Histogenous hypoxia Histogenous hypoxia refers to the tissue cells can not

Histogenous hypoxia

Histogenous hypoxia refers to the tissue cells can not make

use of the oxygen supplied to them, though the amount of oxygen delivered to them is adequate.
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Etiology and mechanism Inhibition of oxidative phosphorylation - tissue intoxicity cyanides,

Etiology and mechanism

Inhibition of oxidative phosphorylation
- tissue intoxicity

cyanides, sulphuret, rotenone,
( cytochrome oxidase)
Mitochondria injury
bacteriotoxin, radiation, free radical
Absence of Vitamin
Vit B1, Vit B2, Vit PP co-enzyme
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Characteristics of blood oxygen PaO2 N, SaO2N, CaO2 N, CO2max N,

Characteristics of blood oxygen

PaO2 N, SaO2N, CaO2 N, CO2max N, CaO2-CvO2


Oxygen content in vein increased because cells utilize less oxygen. The color of skin and mucous membrane are pink red flush.

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Alterations of metabolism and function Respiratory system Circulatory system Hematologic system

Alterations of metabolism and function

Respiratory system
Circulatory system
Hematologic system
Central nervous system
Tissues

and cells
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Respiratory system Compensatory response Low PaO2 stimulates the chemoreceptor in carotid

Respiratory system

Compensatory response

Low PaO2 stimulates the chemoreceptor in carotid and aortic

body, which reflexly causes ventilation to increase.
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High altitude pulmonary edema Central respiratory failure respiratory inhibition, irregular respiratory

High altitude pulmonary edema
Central respiratory failure
respiratory inhibition, irregular respiratory rhythm

and frequency, hypoventilation, e.g. periodic breathing, Cheyne-Stoke respiration, Biot’s breathing

Injury manifestation

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Circulatory system Compensatory response Increased cardiac output hyperventilation and pulmonary expansion

Circulatory system

Compensatory response

Increased cardiac output
hyperventilation and pulmonary expansion stimulate

lung stretch receptors, which reflexly excite sympathetic nerve.
Pulmonary vasoconstriction
Ca2+ influx↑, the action of vasoconstrictive substances and SN
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Redistribution of blood vasodilatation : heart and brain hypoxia metabolites, lactic

Redistribution of blood
vasodilatation : heart and brain
hypoxia metabolites,

lactic acid,
adenosine
Ca2+ influx↓
vasoconstriction : skin, kidney,
gastrointestinal tract
Capillary hyperplasia
HIF→VEGF
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Injury manifestation Pulmonary hypertension Decreased diastolic and systolic myocardial function Arrhythmia

Injury manifestation

Pulmonary hypertension
Decreased diastolic and systolic myocardial function
Arrhythmia Vagus Nerve
Decreased venous

return to heart
severe hypoxia
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Hematologic system Compensatory response Increase in the amount of RBCs and

Hematologic system

Compensatory response

Increase in the amount of RBCs and Hb
More

EPO produced and released by kidney
Improved RBC oxygen release capability
More 2,3-DPG produced from glycolysis process
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Plasma viscosity↑, blood flow resistance ↑, afterload of heart ↑ When

Plasma viscosity↑, blood flow resistance ↑, afterload of heart ↑
When PO2

is low markedly, 2,3-DPG will cause CaO2 to decrease.

Injury manifestation

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Central nervous system Acute hypoxia: headache, agitation, poor faculty of memory,

Central nervous system

Acute hypoxia: headache, agitation, poor faculty of memory, inability

to make judgment, depress or loss of coordination
Chronic hypoxia: impaired concentration, fatigue, drowsiness
cerebral edema and neuron injury
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Tissues and cells Compensatory response Enhanced cell capacity for use of

Tissues and cells

Compensatory response

Enhanced cell capacity for use of oxygen
number

and membrane surface of mitochondria↑
activity of succinic dehydrogenase and cyt-oxidase ↑
Enhanced anaerobic glycolysis
ATP↓ and ATP/ADP ↓→phosphofructokinase ↑
Enhanced myoglobin
Low metabolic state
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Injury manifestation Cell membrane injury Na+ influx cell swelling K+ efflux

Injury manifestation

Cell membrane injury
Na+ influx cell swelling
K+ efflux

synthetic disorder
Ca2+ influx
phospholipase
Ca2+-dependent protein kinase
Mitochondria injury severe hypoxia
Lysosome injury