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The patient, female, 40 years old, was admitted to the emergency department due to abdominal pain during ectopic pregnancy.
Sudden coma, respiratory and cardiac arrest occurred during the examination, and he was admitted to the operating room after emergency CPR for about 30 minutes.
Machine controlled ventilation with pure oxygen after induction of anesthesia, the operation starts quickly, blood pressure 70/40mmHg, heart rate 75 beats/min, finger pulse oxygen 100%, tidal volume 520ml, respiratory rate 14 beats/min, emergency infusion to expand and correct acidosis .
Due to the poor peripheral blood flow, the central venous catheter was inserted through the internal jugular vein puncture; after the right radial artery puncture failed, the blood gas was drawn through the central vein for blood gas analysis, the blood color was bright red, PH 6.
87, PCO2=60mmhg, PO2= 232mmhg, Lac >15mmol/L, HCT <15%, but the blood group can't be supplied with the red during the operation.
400ml of plasma and 250ml of 20% mannitol should be transfused during the operation.
After the operation, the patient should enter the intensive care unit to infuse a proper amount of red and other blood products.
(Remember this condition) I saw a significant increase in oxygen partial pressure to 232mmHg.
At first I thought that the central venous puncture mistakenly penetrated the artery.
Check that the central venous infusion is unobstructed.
The central venous pressure is about 15cmH2O and the blood pressure is 90/40mmHg.
Wrong arteries, postoperative ultrasound examination also proved this.
Analysis of the increased partial pressure of venous carbon dioxide in patients is partly due to supplementation of alkaline liquid sodium bicarbonate, but what is the reason for such high partial pressure of venous oxygen (PvO2)? We know that the central venous blood passes through the right heart circulation to the pulmonary artery.
Clinically, PvO2 is obtained by blood collection through the pulmonary artery catheter.
Normally, the value of blood taken from the central venous is not much different, while the PvO2 of normal adults is about 40mmHg when inhaling air.
We know that there are two forms of oxygen transport in the blood, namely physical dissolution and chemical combination of hemoglobin.
The amount of physical dissolved oxygen increases in proportion to the partial pressure of blood oxygen.
When a normal person breathes air under normal temperature and pressure, the physical dissolved amount of arterial blood is 0.
3ml/100ml, PaO2 is about 100mmHg, arterial oxygen and hemoglobin SaO2 are close to 100%; PvO2 is about 40mmHg, SvO2 is about 75%.
Source "Miller Anesthesiology" 8th edition P1396 For normal people with Hb of 15g/dl, the arterial oxygen content (oxygen supply) and oxygen release (oxygen consumption) in a calm state can be calculated: (1) Arterial oxygen content CaO2=0.
0031ml /(dl·mmHg)×100mmHg+100%×15g/dl×1.
34ml/g=20.
4ml/dl⑵Venous oxygen content CvO2=0.
0031ml/(dl·mmHg)×40mmHg+75%×15g/dl×1.
34ml /g=15.
2ml/dl (3) The difference in arterial and venous oxygen content Ca-vO2=CaO2-CvO2=5.
2ml/dl Normal adult cardiac output is about 5000ml/min (ie 50dl/min) when calm, so the arterial oxygen content (oxygen supply) =20.
41ml/dl×50dl/min=1020.
5ml/min, total oxygen release (oxygen consumption)=5.
2ml/dl×50dl/min=260ml/min, of which oxygen dissolved release is about 0.
0031×(100-40 )×50=9ml/min, the hemoglobin release is 251ml/min, of which the dissolved oxygen release only accounts for about 3.
5%, and the dissolved oxygen of normal adults participates in the oxygen release very little.
"Kaplan Cardiac Anesthesiology" Generally speaking, when a patient is ventilated with pure oxygen under general anesthesia, the air source oxygen concentration is 100%, and the PO2 is atmospheric pressure 760mmHg, but the arterial blood oxygen partial pressure eliminates the airway saturated water vapor pressure and alveolar carbon dioxide.
After partial pressure, alveolar air artery blood oxygen partial pressure difference and other factors, clinically, it can be estimated by PaO2=FiO2×600, that is, PaO2 is about 600mmHg in pure oxygen. "Morgan Anesthesiology" returns to this patient, assuming that the patient’s cardiac output is 5000ml/min (50dl/min) with the support of infusion and vasoactive drugs, and the patient’s arterial PaO2 under pure oxygen is taken as 600mmHg.
SaO2=100%; blood gas prompts PvO2 to be 232mmHg, SvO2=99%, Hb<5g/dl, so: ⑴Arterial oxygen content (oxygen supply)<(0.
0031×600+100%×1.
34×5)×50=428ml/ min⑵Physical dissolved oxygen release=(600-232)×0.
0031×50=55.
2ml/min; ⑶Hemoglobin oxygen release<(1-0.
99)×5×1.
34×50=3.
35ml/min; note that pure inhalation PaO2 increased rapidly after oxygen, and at the same time, the patient's oxygen consumption decreased significantly under special conditions, which eventually caused a significant increase in venous oxygen partial pressure.
In this case of extreme hemorrhagic shock, both oxygen supply and oxygen consumption (oxygen release) are greatly reduced.
Oxygen supply is only 428/1020.
5=42%, and oxygen release accounts for 58.
5/260=22.
5% of normal people in a quiet state.
To 1/4! Clinically, it is difficult to reach 600mmHg for the oxygen partial pressure of inhaling pure oxygen.
In fact, the oxygen supply and oxygen consumption should be less; at this time, it can be seen that physical dissolved oxygen is almost the only source of oxygen consumption in the body! (55.
2ml/min VS 3.
35ml/min) So, if the oxygen consumption is less than 1/4 of the normal state, can it satisfy the patient's current state? The patient was in severe shock.
Under severe acidosis, hypothermia, and general anesthesia for tracheal intubation and muscle relaxation, the body was in a state of low oxygen consumption.
The regulation mechanism prioritized the limited oxygen supply to important organs such as the brain and heart; intraoperative blood pressure Maintained at 90-110/50-60mmHg, operation time 50min, no obvious hypoxia occurred, blood transfusion after entering the intensive care unit, fortunately, awake about 10 hours later, extubation after 7 days, clear thinking, fluent speech, the following is the operation On the sixth day after the middle concentration oxygen therapy (FiO2=40%), the results of the central venous blood gas analysis! This shows that intraoperative oxygen demand should be met most fundamentally, and it also reminds us that when anemia cannot be quickly corrected, maintain stable hemodynamics and high concentration oxygen (especially pure oxygen ventilation) to increase the physical dissolution zone.
The oxygen supply that comes can sometimes bring hope to patients. Clinically, the ability of hemoglobin to carry oxygen is far greater than physical dissolution, but when the arterial partial pressure of oxygen reaches 1700mmHg, the physical dissolution of oxygen reaches 5ml/dl, and physical dissolution can completely rely on physical dissolution to meet the basic physiological oxygen consumption.
At the same time, we know 1 standard Atmospheric pressure (ATA) when inhaling pure oxygen, PaO2 can reach up to 600mmHg, and 2-3 ATA can meet the above requirements.
This is the simple working principle of the clinical hyperbaric oxygen chamber.
A little thought, inadequate, please correct me .
.
.
(original documents have amendments and supplements) Author: Jinxiang County, Shandong Province, People's Hospital, Department of Anesthesiology TONG Yu Shun modify the layout: Jiang Jianfeng
Sudden coma, respiratory and cardiac arrest occurred during the examination, and he was admitted to the operating room after emergency CPR for about 30 minutes.
Machine controlled ventilation with pure oxygen after induction of anesthesia, the operation starts quickly, blood pressure 70/40mmHg, heart rate 75 beats/min, finger pulse oxygen 100%, tidal volume 520ml, respiratory rate 14 beats/min, emergency infusion to expand and correct acidosis .
Due to the poor peripheral blood flow, the central venous catheter was inserted through the internal jugular vein puncture; after the right radial artery puncture failed, the blood gas was drawn through the central vein for blood gas analysis, the blood color was bright red, PH 6.
87, PCO2=60mmhg, PO2= 232mmhg, Lac >15mmol/L, HCT <15%, but the blood group can't be supplied with the red during the operation.
400ml of plasma and 250ml of 20% mannitol should be transfused during the operation.
After the operation, the patient should enter the intensive care unit to infuse a proper amount of red and other blood products.
(Remember this condition) I saw a significant increase in oxygen partial pressure to 232mmHg.
At first I thought that the central venous puncture mistakenly penetrated the artery.
Check that the central venous infusion is unobstructed.
The central venous pressure is about 15cmH2O and the blood pressure is 90/40mmHg.
Wrong arteries, postoperative ultrasound examination also proved this.
Analysis of the increased partial pressure of venous carbon dioxide in patients is partly due to supplementation of alkaline liquid sodium bicarbonate, but what is the reason for such high partial pressure of venous oxygen (PvO2)? We know that the central venous blood passes through the right heart circulation to the pulmonary artery.
Clinically, PvO2 is obtained by blood collection through the pulmonary artery catheter.
Normally, the value of blood taken from the central venous is not much different, while the PvO2 of normal adults is about 40mmHg when inhaling air.
We know that there are two forms of oxygen transport in the blood, namely physical dissolution and chemical combination of hemoglobin.
The amount of physical dissolved oxygen increases in proportion to the partial pressure of blood oxygen.
When a normal person breathes air under normal temperature and pressure, the physical dissolved amount of arterial blood is 0.
3ml/100ml, PaO2 is about 100mmHg, arterial oxygen and hemoglobin SaO2 are close to 100%; PvO2 is about 40mmHg, SvO2 is about 75%.
Source "Miller Anesthesiology" 8th edition P1396 For normal people with Hb of 15g/dl, the arterial oxygen content (oxygen supply) and oxygen release (oxygen consumption) in a calm state can be calculated: (1) Arterial oxygen content CaO2=0.
0031ml /(dl·mmHg)×100mmHg+100%×15g/dl×1.
34ml/g=20.
4ml/dl⑵Venous oxygen content CvO2=0.
0031ml/(dl·mmHg)×40mmHg+75%×15g/dl×1.
34ml /g=15.
2ml/dl (3) The difference in arterial and venous oxygen content Ca-vO2=CaO2-CvO2=5.
2ml/dl Normal adult cardiac output is about 5000ml/min (ie 50dl/min) when calm, so the arterial oxygen content (oxygen supply) =20.
41ml/dl×50dl/min=1020.
5ml/min, total oxygen release (oxygen consumption)=5.
2ml/dl×50dl/min=260ml/min, of which oxygen dissolved release is about 0.
0031×(100-40 )×50=9ml/min, the hemoglobin release is 251ml/min, of which the dissolved oxygen release only accounts for about 3.
5%, and the dissolved oxygen of normal adults participates in the oxygen release very little.
"Kaplan Cardiac Anesthesiology" Generally speaking, when a patient is ventilated with pure oxygen under general anesthesia, the air source oxygen concentration is 100%, and the PO2 is atmospheric pressure 760mmHg, but the arterial blood oxygen partial pressure eliminates the airway saturated water vapor pressure and alveolar carbon dioxide.
After partial pressure, alveolar air artery blood oxygen partial pressure difference and other factors, clinically, it can be estimated by PaO2=FiO2×600, that is, PaO2 is about 600mmHg in pure oxygen. "Morgan Anesthesiology" returns to this patient, assuming that the patient’s cardiac output is 5000ml/min (50dl/min) with the support of infusion and vasoactive drugs, and the patient’s arterial PaO2 under pure oxygen is taken as 600mmHg.
SaO2=100%; blood gas prompts PvO2 to be 232mmHg, SvO2=99%, Hb<5g/dl, so: ⑴Arterial oxygen content (oxygen supply)<(0.
0031×600+100%×1.
34×5)×50=428ml/ min⑵Physical dissolved oxygen release=(600-232)×0.
0031×50=55.
2ml/min; ⑶Hemoglobin oxygen release<(1-0.
99)×5×1.
34×50=3.
35ml/min; note that pure inhalation PaO2 increased rapidly after oxygen, and at the same time, the patient's oxygen consumption decreased significantly under special conditions, which eventually caused a significant increase in venous oxygen partial pressure.
In this case of extreme hemorrhagic shock, both oxygen supply and oxygen consumption (oxygen release) are greatly reduced.
Oxygen supply is only 428/1020.
5=42%, and oxygen release accounts for 58.
5/260=22.
5% of normal people in a quiet state.
To 1/4! Clinically, it is difficult to reach 600mmHg for the oxygen partial pressure of inhaling pure oxygen.
In fact, the oxygen supply and oxygen consumption should be less; at this time, it can be seen that physical dissolved oxygen is almost the only source of oxygen consumption in the body! (55.
2ml/min VS 3.
35ml/min) So, if the oxygen consumption is less than 1/4 of the normal state, can it satisfy the patient's current state? The patient was in severe shock.
Under severe acidosis, hypothermia, and general anesthesia for tracheal intubation and muscle relaxation, the body was in a state of low oxygen consumption.
The regulation mechanism prioritized the limited oxygen supply to important organs such as the brain and heart; intraoperative blood pressure Maintained at 90-110/50-60mmHg, operation time 50min, no obvious hypoxia occurred, blood transfusion after entering the intensive care unit, fortunately, awake about 10 hours later, extubation after 7 days, clear thinking, fluent speech, the following is the operation On the sixth day after the middle concentration oxygen therapy (FiO2=40%), the results of the central venous blood gas analysis! This shows that intraoperative oxygen demand should be met most fundamentally, and it also reminds us that when anemia cannot be quickly corrected, maintain stable hemodynamics and high concentration oxygen (especially pure oxygen ventilation) to increase the physical dissolution zone.
The oxygen supply that comes can sometimes bring hope to patients. Clinically, the ability of hemoglobin to carry oxygen is far greater than physical dissolution, but when the arterial partial pressure of oxygen reaches 1700mmHg, the physical dissolution of oxygen reaches 5ml/dl, and physical dissolution can completely rely on physical dissolution to meet the basic physiological oxygen consumption.
At the same time, we know 1 standard Atmospheric pressure (ATA) when inhaling pure oxygen, PaO2 can reach up to 600mmHg, and 2-3 ATA can meet the above requirements.
This is the simple working principle of the clinical hyperbaric oxygen chamber.
A little thought, inadequate, please correct me .
.
.
(original documents have amendments and supplements) Author: Jinxiang County, Shandong Province, People's Hospital, Department of Anesthesiology TONG Yu Shun modify the layout: Jiang Jianfeng