Hy Hy poxia poxia
Jan 03, 2016
ConceptConcept
Oxgen supply = CaO2× Q
Oxygen consumption = ( CaO2 - CvO2 ) × Q
Tissue cells can’t obtain enough oxygen
or can’t fully utilize oxygen
metabolic, functional and structural changes
CO2 - dissolved O2
CO2maxO2 saturation ( SO2 ) = ×100%
SaO2 95%, SvO2 70%
Parameters of blood gasParameters of blood gasPartial pressure of O2 ( PO2 ) PaO2 100mmHg , PvO2 40 mmHg O2 content ( CO2 ) = CO2max×SO2 + dissolved O2
CaO2 19ml/dl , CvO2 14ml/dl
O2 capacity ( CO2max ) = 1.34 ml/g × Hb g/dl
Classification, etiology and pathogenesisClassification, etiology and pathogenesis 1. 1. Hypotonic hypoxiaHypotonic hypoxia — — PaOPaO22↓ ↓
Causes : 1) PiO2↓
2) pulmonary dysfunction
3) shunt
Results : PaO2↓→ SaO2↓→ CaO2↓ hypotonic hypoxemia, cyanosis ( PaO2 - PMO2 )↓ →( CaO2 - CvO
2 )↓
PaO2 < 60mmHg → VO2↓ ?
Results : CO2max↓↓ CaO2 ↓↓
( CaO2 - CvO2 ) ↓ P50 ↓ ( CaO2 - CvO2 ) ↓
2.2. Hemic hypoxia — COHemic hypoxia — CO22maxmax ↓
Causes : 1) anemia
2) carboxyhemoglobinemia
3) methemoglobinemia
enterogenous cyanosis
4) P50↓ : transfusion of depot blood
Result : Q↓↓→ CvO2↓
→ ( CaO2 - CvO2 )↑
Causes : general circulatory failure
local circulatory disorder
3. 3. Circulatory H — Q↓Circulatory H — Q↓
··
4. Histogenous hypoxia
Causes: 1) histotoxic H
cyanide poisoning
2) cell injured by biological or p
hysical factor
3) vitamin deficiency --- B1
Result : CvO2↑ → ( CaO2 - CvO2 )↓
Hypotonic hypoxia
PaO2 < 60mmHg → compensation < 30mmHg → severe disturbances
Functional and metabolic alterationsFunctional and metabolic alterations
1. 1. Respiratory systemRespiratory system
• Respiratory rate and depth ↑
arrive at 4000m high →ventilation ↑ 65%
few days later → ventilation ↑ 5 – 7 times
long residents → 15 % more than at sea level
•
• Hyperventilation→PaO2↑→CaO2 ↑
↘O2 consumption ↑
occur in any type of hypoxia?
Severe hypoxia→pulmonary edma
↘Inhibition of respiratory center
2. 2. Circularory systemCircularory system
• Cardiac output↑ due to: 1. cardiac contractility↑ 2. heart rate↑ 3. venous return↑
• Redistribution of blood flow α-Adrenoceptor vasoconstriction Local metabolites vasodilation
Pulmonary vasoconstriction (HPV)→PaO2 ↑
Sympathetic nerve
Humoral factors — AT 、 ET 、 LTs 、 TxA2
PGI2 、 NO 、 histamine
Direct effect of O2 on SMC — Kv
How to prove?
Capillary proliferation --- VEGF
Severe hypoxia
• Myocardiac systolic and diastolic dysfunction
• Cardiac arrhythmia ---
Hypoxia acidosis hyperkalemia
Arrhythmia
• Venous return↓
• Pulmonary hypertention right ventricle
4.4.Central nervous systemCentral nervous system
• Acute H → headache 、 impaired attention • Chronic H → sleepiness, depression
• Severe H → confusion, coma, convulsion
due to : energy deficiency and acidosis
decreased RMP
abnormal neurotransmitter synthesis
cell damage
vasodilation and cerebral edema
5. 5. Cellular alterationsCellular alterations
AdaptationAdaptation
• Ability to use O2↑---
number of mitochondia , it’s enzymes
• Anaerobic glycolysis↑
ATP/ADP↓ → phosphofructokinase
activity
• Low metabolic state --- caused by acidosis
• Myoglobin↑
• Cell membrane
decreased permeability + ion pump dysfunction
[ Na+ ]i → Cellular swelling
[ K+ ]i ↓ → Synthetic metabolism↓
[ Ca2+ ]i → Mitochondria damage
ROS
Lysosome damage
Severe H → Cellular damage
• Mitochondria Respiratory function ↑ (PmO2< 1mmHg)
PmO2< 1mmHg dehydrogenase activity
• Lysosome Acidosis phospholipase activity
hydrolases release
Factors influencing the tolerance to hypoxiaFactors influencing the tolerance to hypoxia
• Oxygen consumption rate
• Compensatory ability to hypoxia