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MindMap Gallery Pathophysiology—Hypoxia

Pathophysiology—Hypoxia

The key points of the pathophysiology examination include commonly used blood oxygen indicators, classification of hypoxia, functional and metabolic changes of the body during hypoxia, hypoxia treatment, etc.

Edited at 2024-01-15 21:15:56

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Pathophysiology—Hypoxia

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Outline

hypoxia

Oxygen acquisition and utilization

hypoxia

Commonly used blood oxygen indicators

Blood oxygen partial pressure PO2

normal value

PaO2: 100mmHg

PvO2: 40mmHg

Influencing factors

PO2 of inhaled gas

respiratory function

Ventilation - trachea, bronchial foreign bodies, tumors

Ventilation - fluid leakage from alveoli, interstitial inflammation

venous blood flows into arteries

Blood oxygen capacity C-O2max

Normal value: 20ml/dl

C-O2max=1.34×15 (each gram of Hb combines 1.34mlO2)

Influencing factors

Quality and quantity of Hb

Blood oxygen content C-O2

Free oxygen is very small (0.3ml/dl), but it is important

normal value

Ca-O2 19ml/dl

Cv-O2 14ml/dl

→O2 utilization coefficient: 5ml/dl

Influencing factors

Hb quantity and quality

PO2

Blood oxygen saturation SO2

SO2=【C-O2】/C-O2max

normal value

SaO2 95～98%

SvO2 70～75%

Oxygen dissociation curve ODC

The difference in the middle segment reflects the metabolic level of tissue cells (the stronger the metabolism, the longer the middle segment)

PaO2-60mmHg or above-stable

PvO2-40mmHg (when quiet)

PvO2-15mmHg (during exercise) → indicates that the oxygen consumption of tissue cells increases, and the oxygen difference between the tissue cells and the oxygen in arterial blood is greater → tissue cells require more oxygen

P50

Normal 26~27mmHg

Reflects the binding ability of Hb and oxygen

P50 increases and the affinity of Hb to oxygen decreases

Influencing factors

PaO2 (mainly)

PaCO2

The more CO2, the less O2 content → the blood oxygen saturation becomes lower

The greater the H concentration, the lower the blood oxygen saturation

2,3-DPG

Inhibit the combination of Hb and O2 → blood oxygen saturation becomes lower

temperature

The higher the temperature, the lower the blood oxygen saturation

Arteriovenous oxygen difference Da-vO2

normal value

Ca-O2-Cv-O2=19-14=5ml/dl

Influencing factors

tissue metabolic rate

The faster the metabolism, the greater the arteriovenous oxygen difference.

Blood oxygen partial pressure PO2

The greater the PO2, the greater the arteriovenous oxygen difference.

blood flow velocity

The speed is slow and the arteriovenous oxygen difference increases.

ODC shifts to the right and arteriovenous oxygen difference increases

Classification of hypoxia

hypotonic hypoxia/hypoxic hypoxia

reason

Decreased PO2 of inspired air (atmospheric hypoxia)

External respiratory dysfunction (respiratory hypoxia)

Venous blood flows into arterial blood

Characteristics of blood oxygen changes and mechanism of hypoxia

Cyanosis

Normal person HHb2.6g/dl

In people with normal Hb, hypoxia and cyanosis are consistent

In people with abnormal Hb, hypoxia and cyanosis are often inconsistent

Patients with polycythemia → cyanosis (without hypoxia)

Anemic patients → Acyanosis (hypoxia)

Blood hypoxia/isotonic hypoxemia

The dissolved O2 in the blood remains unchanged→PaO2 is normal

reason

The amount of Hb decreases

anemic hypoxia

Changes in Hb quality

CO poisoning

mechanism

Higher affinity to hemoglobin, forming carboxyhemoglobin (HbCO) → reducing the amount of oxygen combined with hemoglobin

When CO combines with a heme in a hemoglobin molecule, it will increase the affinity of the other three hemes for oxygen → reduce the release of bound oxygen → shift the oxygen dissociation curve to the left

Inhibit glycolysis in red blood cells → reduce 2,3-DPG production → shift the oxygen dissociation curve to the left

Performance

The skin and mucous membranes are cherry red in color due to HbCO

Methemoglobinemia (HbFe3OH)—oxidant poisoning (nitrite)

Performance

enterogenic cyanosis

mechanism

After the hemoglobin molecule is poisoned, one of the four Fe2 is oxidized to Fe3 → the remaining Fe2 cannot release the bound oxygen → the oxygen dissociation curve shifts to the left

The affinity between Hb and O2 increases

Input a large amount of stock blood, alkalosis → oxygen dissociation curve shifts to the left

Characteristics of blood oxygen changes and mechanism of hypoxia

Cyclic hypoxia/hypodynamic hypoxia

reason

Tissue ischemia (decreased blood supply to tissue → decreased oxygen supply)

Systemic—shock, heart failure

Local - embolism (myocardial infarction)

tissue congestion

Increased difference in arteriovenous blood oxygen content

mechanism

When blood stays in capillaries for a long time, cells absorb more oxygen per unit volume of blood.

The blood stays in the capillaries for a long time, the carbon dioxide content increases, the oxygen dissociation curve shifts to the right, and the release of oxygen increases

But the tissue is still hypoxic because the blood flow into the capillaries per unit time is reduced.

Organizational hypoxia/oxygen utilization disorder hypoxia

reason

Inhibition of mitochondrial oxidative phosphorylation by drugs or poisons

Cyanide, arsenide, H2S

Respiratory enzyme synthesis disorder

lack of vitamins

mitochondrial damage

Performance

Red or rose color of skin and mucous membranes

Functional and metabolic changes of the body during hypoxia

Influencing factors

Cause, speed, location, and duration of hypoxia

body's compensatory capacity

respiratory system

Compensatory response (hypoxic ventilatory response)—increased pulmonary ventilation

Features

The degree of changes in pulmonary ventilation is related to the time of hypoxia

Early stage: PaO2 decreases, stimulating peripheral chemoreceptors → respiratory center becomes excited → breathing deepens and accelerates

Later stage: peripheral chemoreceptor sensitivity decreases → hypoxia ventilatory response decreases

Changes in pulmonary ventilation are the main compensatory response to hypotonic hypoxia

significance

Increase PaO2 and increase blood return to the heart

damaging changes

high altitude pulmonary edema

Appears 1 to 4 days after entering a plateau above 3000 meters.

clinical manifestations

Difficulty breathing, wet rales in the lungs, pink frothy sputum, severe cyanosis

Pathogenesis

Pulmonary vasoconstriction → increase in pulmonary capillary internal pressure and effective hydrostatic pressure

Increased permeability of pulmonary vascular endothelial cells

Intra-alveolar fluid clearance disorder

central respiratory failure

PaO2＜30mmHg→Inhibit respiratory center→Respiratory depression, irregular respiratory rhythm and frequency

circulatory system

heart

compensation

increased cardiac output

increased heart rate

Increased pulmonary ventilation→stimulation of pulmonary stretch receptors→sympathetic nerve excitement→accelerated heart rate

Severe hypoxia inhibits the cardiovascular motor center and slows the heart rate

Increased myocardial contractility

Sympathetic nerve excitement→cardiac B receptor→enhanced contractility

Myocardial contractility decreases during severe hypoxia

Increased venous return

In severe hypoxia, the heart rate slows down, myocardial contractility weakens → venous return disorder, and the amount of blood returned to the heart decreases

Structural changes in the heart—right ventricular hypertrophy

damage

Decreased myocardial contractility

Arrhythmia

Decreased blood return to the heart

blood flow

blood redistribution

Increased blood supply to the heart and brain, reduced blood flow to the skin, internal organs, skeletal muscles and kidneys

Hypoxia → Sympathetic nerve excitement → Increased release of catecholamines → High density of a receptors in blood vessels of the skin, internal organs, and kidneys → Obvious vasoconstriction and reduced blood flow

Cardio-cerebral hypoxia produces a large amount of lactic acid and adenosine metabolites → causes local blood vessel dilation → increases cardio-cerebral blood flow

hypoxic pulmonary vasoconstriction

Hypoxia inhibits pulmonary vascular smooth muscle potassium channels → increases calcium influx → pulmonary vasoconstriction

Sympathetic nervous excitement

Increased intracranial pressure caused by excessive blood supply to the brain

lung

Hypoxic pulmonary vasoconstriction (=compensation)

significance

Reduce the blood flow around the hypoxic alveoli and divert this part of the blood flow to the well-ventilated alveoli → maintain the ventilation and blood flow ratio to be compatible

Hypoxic excessive pulmonary vasoconstriction leads to high altitude pulmonary edema

damage

Pulmonary hypertension—the central link in the development of cor pulmonale and high altitude heart disease

tissue capillary proliferation

blood system

compensatory changes

Increased red blood cells and hemoglobin, increasing tissue oxygen supply

Erythropoietin EPO

Increased 2,3-DPG → Increased ability of red blood cells to release oxygen to tissues

damaging changes

Excessive red blood cells and increased blood viscosity → microcirculation disorder → aggravated tissue hypoxia

Increase in 2,3-DPG → hinder the combination of Hb and oxygen in lung tissue → decrease in oxygen content

central nervous system

Performance

Acute hypoxia - headache, irritability, memory loss, incoordination of movements

Chronic hypoxia—fatigue, lethargy, difficulty concentrating, depression

Severe hypoxia - brain cell damage, cerebral edema, coma and death

mechanism

Cerebral blood vessels dilate and hydrostatic pressure increases → fluid leakage

Acidosis, cell damage → increased vascular permeability → fluid leakage

Brain tissue energy metabolism disorder → sodium and water retention → brain cell swelling

Reduced nerve cell membrane potential

tissue cells

compensatory response

Increased ability to utilize oxygen

Increased anaerobic glycolysis

Increased expression of oxygen-carrying proteins

hypometabolic state

damaging changes

Cell membrane, mitochondrial damage, lysosome rupture

hypoxia treatment

Treat primary disease

Oxygen therapy—most effective for hypotonic hypoxia