This is a general process of oxygen entering into tissue ,and cells.
This process is complex ,troubles in any part will affect the oxygen supply to cell, and lead to hypoxia
Ventilation Transfer
O2 ——>HbO2 ——> Tissue utilization
diffusion Circulatory system
Hypoxia is an extremely important and common cause of cell injury and death.
Definition
Hypoxia is a pathological process, in which O2 supply to tissues or organs is inadequate to meet the demand of cells; or the tissue cells can not make use of O2, leading to changes in functions, metabolisms and structures of cells and tissues of the body.
Anoxia:
The absence of O2 in the tissues
Hypoxemia:
A deficiency of O2 in blood
Three key points of Concept :
1. Pathological process
2. Causes
I)Can’t obtain enough oxygen
II)Can’t fully utilize oxygen
3. Changes
Metabolism
Function
Structure
Oxgen supply = CaO2× Q
Oxygen consumption =(CaO2-CvO2)× Q
Parameters of blood O2
1. Partial pressure of O2 (PO2)
PO2 is the tension caused by O2 physically dissolved in the blood.
PaO2 : 100mmHg (13.3kPa )
PvO2 : 40mmHg (5.33kPa )
PO2(in the air) :159mmHg
PO2(in alveolar air):104mmHg
Determinants of PO2 :
O2 pressure in the inhaled air
respiratory function
abnormal right-to-left shunt in pathological conditions(e.g. ventricular septal defect)
Ventricular septal defect a common congenital heart defect; an abnormal opening in the septum dividing the ventricles allows blood to pass directly from the left to the right ventricle; large openings may cause congestive heart failure .
2. Oxygen capacity (CO2max)
The maximal amount of O2 combined by hemoglobin (Hb) in 100ml blood.
Fully saturated condition:PO2:150mmHg
PCO2:40mmHg
T:38℃
The level of Cp-O2max only depends on Hb :
① quantity of HB
② quality of HB
The normal value ：
Cp-O2max = 1.34 ml/g × 15 g/dl = 20 ml/dl
3. Oxygen content (C-O2)
The actual amount of O2 in blood.
>combined with Hb : 98.5%
>physically dissolved:1.5%（can be omitted）
The level of C-O2 depends on:
①PO2
②The level of Hb (quality and quantity)
The normal value of C-O2 ：
CaO2 ——19ml/dl
CvO2 ——14ml/dl
CaO2 - CvO2
(Arteriovenous Oxygen content difference)
normal value:
19ml/dl -14ml/dl = 5ml/dl
4. Oxygen saturation（SO2）
The percentage of hemoglobin present as oxyhemoglobin .
O2 content
SO2 can be calculated by : —–—–—–—–
O2 capacity
If 100ml blood contains 20ml O2 , the SO2 is 100%
when it contains 15ml O2 , how much is SO2 ?
The normal value ：
SaO2—95%
SvO2—75%
The level of SO2 only depends on PO2
Four parameters
1. Partial pressure of O2（PO2）
PaO2 : 100mmHg , PvO2: 40 mmHg
2. O2 content（C-O2）
CaO2 : 19ml/dl , CvO2: 14ml/dl
3. O2 capacity（Cp-O2max）= 1.34 ml/g × 15 g/dl
C-O2max : 20ml/dl
4. O2 saturation（SO2）
SaO2 : 95%, SvO2: 70%
Classification and pathogenesis
◆ Causes
(1) Decreased O2 pressure in the inspired air.
--- atmospheric hypoxia
①In enclosed room
② 3000 meters above sea level
(2) External respiratory dysfunctions
Peanuts, jelly or any other soft ,sweet food made from fruit juice and sugar boiled together ,used as a topping.
can cause
Paralysis of respiratory muscles, airway obstruction, asthma, emphysema, tuberculosis, pulmonary cancer, inflammation, and edema.
(3) Right-to-left shunt—Venous admixture
Some congenital heart diseases, such as ventricular septal defect, or if the foramen oval fails to close after birth.
◆ Characteristics of blood O2
PO2:↓
-O2 content :↓
-O2 capacity:
acute cases:N
chronic cases:↑
-O2 saturation:↓
NOTE: O2 content ↓(both in arterial and venous blood).
Oxygen capacity is normal in acute cases and is increased in chronic cases.
◆ Cyanosis
Cyanosis refers to a bluish color of the skin, nail beds and mucous membranes when deoxyhemoglobin concentration of blood in capillary is more than 5g per 100ml blood.
NOTE: Cyanosis is the most important clinical sign of hypotonic hypoxia.
The discolor of the skin, nail beds and mucous membrane.
Mechanism of Cyanosis
HbO2 (oxygenated Hb) ─bright red
Hb (unoxygenated Hb) ─bluish
CAUTION:
Not all the cyanosis means hypoxia
2. Hemic hypoxia (Isotonic hypoxia)
(1) Anemia
The concentration of Hb is less than 9g/100ml。
Patients with severe anemia will have no cyanosis, since their unoxygenated Hb can not reach 5g/100ml
(2) Carbon monoxide (CO) poisoning
Mechanism of CO poisoning
① Hb combine with CO instead of O2 & produce carboxy-hemoglobin (CO-Hb),the CO-Hb can’t carry O2 any more.
② Hb may combine with both CO and O2 more tightly,so Hb can’t release O2 to tissues.
CO combines with Hb form carboxyhemoglobin (COHb), the color is cherry-red. The cherry-red/pink color will be visible in the skin, nail beds and mucous membrane during CO poisoning. It will have no cyanosis.
(3) Methemoglobinemia
Normal： ferrous state (Fe2+)
oxidized ：ferric state (Fe3+)
Hb containing Fe3+ : methemoglobin
Appearance: Methemoglobin is brown, the patients will appear brown color.
NOTE: Many chemicals and drugs can oxidize the iron in Hb.(such as: amyl nitrite, aniline, nitrobenzene, acetanilid, phenacetin, and salicylates)
Enterogenous cyanosis
◆ Characteristics of blood O2
PO2 ：N (isotonic hypoxia)
O2 content : N or ↓
O2 capacity : N or ↓
O2 saturation: N
3. Circulatory hypoxia
◆ Causes
circulatory deficiency
e.g;
embolism
shock, heart failure embolism.
atherosclerosis
thrombosis
tourniquet
Ischemic hypoxia
Stagnant hypoxia
◆ Characteristics of blood O2
PaO2 ：N
C-O2 ：N
Cp-O2max ：N
SO2 : N
Note: Oxygen supplied for cell in unit time is inadequate.
PO2 in A and O2 content in A are normal; because when blood flow passes through tissues slowly, the PO2 and O2 content in venous blood are decreased. C(a-v) is increased.
C(a-v): ↑ blood flow passes through tissues slowly, the PO2 and O2 content in venous blood are decreased. C(a-v) is increased.
4. Histogenous hypoxia
Histotoxic hypoxia
◆ Causes
(1) Tissue poisoning
(2) cell injured by biological or physical factor
(3) vitamin deficiency ---vit B1
NOTE:The toxic agent substances include cyanide, arsenic, barbiturates.
◆ Characteristics of blood O2
PaO2 ：N
CO2 ：N
CO2max ：N
SO2 : N
Note: In Histogenous hypoxia;
Cell can’t fully utilize oxygen
The color of skin in hypoxia
1.Anemia —————— pale
2.CO poisoning ———— cherry red
3.Methemoglobinemia—— brown
4.Histotoxic hypoxia—— rose red
Effects on body
Take “Hypotonic hypoxia” for an example
> Functional
> Metabolic
mild or chronic hypoxia: compensatory response
severe or acute hypoxia: organic dysfunction
1. Respiratory system
PaO2 ＞ 60mmHg:no obvious changes
PaO2 ＜ 60mmHg：compensation
decompensation
lower segment, Middle, upper segment
remain at a high level
With the changes in the horizontal axis, vertical axis did not change significantly
The slope is very steep.
2. Circulatory system
(1) In response to hypoxia
I) The heart rate increases (tachycardia),cardiac output increases,due to:
1. Myocardial contractility↑
2. heart rate↑
3. venous return↑
II) Peripheral vasodilation occurs.
(2) Pulmonary vasoconstriction
Due to: Sympathetic nerve(+)
Humoral factors :
Vasoconstrictive substance ↑↑
Vasodilative substance↑
significance? --- to maintain the VA/Q
(3) Redistribution of blood flow
sympathetic nerve(+)---- vasoconstriction
Local metabolites ----- vasodilation
(4) Capillary proliferation
hypoxia
|
VEGF ↑
|
Capillary hyperplasia
Severe hypoxia ---- decompensation
• Myocardiac systolic and diastolic dysfunction
• Pulmonary hypertension
• Cardiac arrhythmia:
• Venous return↓
Hypoxia acidosis hyperkalemia Arrhythmia
3. Hemic system
Hypoxia can stimulate the function of red bone marrow to produce more red blood cells.
4.Central nervous system
• Acute hypoxia : headache、impaired attention
• Chronic hypoxia : sleepiness, depression
• Severe hypoxia : confusion, coma, convulsion
Mechanism:
1. energy deficiency
2. acidosis
5. Cellular alterations
Adaptation
• Ability to use O2↑:
number of mitochondia increase
• Anaerobic glycolysis↑:
phosphofructokinase activity increase
• Low metabolic state:
caused by acidosis
• Myoglobin↑
Cellular damage (seen in severe hypoxia)
（1）Cell membrane
（2）Mitochondria
（3) Lysosome
Consequences at the cellular level
Lack of ATP may let the sodium pump have no activity, the result is cellular swelling. Hypoxia can increase the cell-membrane permeability, intracellular enzymes enter the ECF.
Myocardial cells contain the enzymes GOT (glutamic-oxaloacetic transaminase), LDH (lactic dehydrogenase), and CPK (creatine phosphokinase), following myocardial infarction the serum levels of these enzymes rise.
GOT and LDH are also abundant in the lungs, liver, pancreas, and kidneys.
Only the heart, brain, and skeletal muscles contain CPK.
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