[Thoughts on the rescue process of a patient with septic shock].

Q3 Medicine
Jing Dong, Yi Zheng
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Upon admission, the patient was in a coma and intubated by oral tube. The blood pressure was 128/82 mmHg (1 mmHg ≈ 0.133 kPa; intravenous pump of norepinephrine 0.2 μg×kg<sup>-1</sup>×min<sup>-1</sup>). Chest CT indicated lung infection, and infection markers were elevated. The main diagnoses were septic shock, pneumonia, acute cerebral infarction of left pontine arm and etc. At 12 hours after admission, according to arterial and central vein blood gas analyses, the oxygen uptake rate was 31% (> 30%), and the veno-arterial blood partial pressure of carbon dioxide (Pv-aCO<sub>2</sub>) was 7 mmHg (> 6 mmHg), blood lactic acid (Lac) increased, combined with the width of the inferior vena cava of 1.0-1.6 cm, also indicated a relative insufficiency of effective circulating blood volume, so appropriate fluid resuscitation was given. After fluid resuscitation, the urine volume of the patient increased from 40 mL/h to 100 mL/h, but the blood pressure did not increase significantly, indicating that there was no volume responsiveness, so dobutamine 3 μg×kg<sup>-1</sup>×min<sup>-1</sup> was added to enhance myocardial contractility. The heart rate did not increase significantly, and the blood pressure was relatively stable. At 21 hours after admission, the patient's systolic blood pressure (SBP) suddenly dropped from 110-120 mmHg to 60-70 mmHg, while heart rate dropped from 100-110 bpm to 80-90 bpm. Therefore, the dosage of norepinephrine was increased to 2 μg×kg<sup>-1</sup>×min<sup>-1</sup>, and the dosage of dobutamine was increased to 10 μg×kg<sup>-1</sup>×min<sup>-1</sup>, but the circulation could not be maintained. In addition, no tension pneumothorax was found in the chest radiography, and blood routine did not indicate the possibility of acute blood loss. 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引用次数: 0

Abstract

Septic shock is a common acute and critical illness in intensive care medicine. It can lead to multiple organ failure, of which the heart is one of the target organs. Fluid resuscitation plays an important role in the treatment of septic shock, but when a patient develops septic-induced cardiomyopathy, the circulation is often not improved by fluid resuscitation, and may even lead to deterioration of circulation. On October 2, 2023, a 52-year-old female patient with septic shock was admitted to the department of intensive care medicine of Civil Aviation General Hospital, whose circulation deteriorated during fluid resuscitation. The main complaint of the patient was left face numbness for more than 20 days, aggravated with unconsciousness for 5 days. Upon admission, the patient was in a coma and intubated by oral tube. The blood pressure was 128/82 mmHg (1 mmHg ≈ 0.133 kPa; intravenous pump of norepinephrine 0.2 μg×kg-1×min-1). Chest CT indicated lung infection, and infection markers were elevated. The main diagnoses were septic shock, pneumonia, acute cerebral infarction of left pontine arm and etc. At 12 hours after admission, according to arterial and central vein blood gas analyses, the oxygen uptake rate was 31% (> 30%), and the veno-arterial blood partial pressure of carbon dioxide (Pv-aCO2) was 7 mmHg (> 6 mmHg), blood lactic acid (Lac) increased, combined with the width of the inferior vena cava of 1.0-1.6 cm, also indicated a relative insufficiency of effective circulating blood volume, so appropriate fluid resuscitation was given. After fluid resuscitation, the urine volume of the patient increased from 40 mL/h to 100 mL/h, but the blood pressure did not increase significantly, indicating that there was no volume responsiveness, so dobutamine 3 μg×kg-1×min-1 was added to enhance myocardial contractility. The heart rate did not increase significantly, and the blood pressure was relatively stable. At 21 hours after admission, the patient's systolic blood pressure (SBP) suddenly dropped from 110-120 mmHg to 60-70 mmHg, while heart rate dropped from 100-110 bpm to 80-90 bpm. Therefore, the dosage of norepinephrine was increased to 2 μg×kg-1×min-1, and the dosage of dobutamine was increased to 10 μg×kg-1×min-1, but the circulation could not be maintained. In addition, no tension pneumothorax was found in the chest radiography, and blood routine did not indicate the possibility of acute blood loss. Troponin I (TnI) decreased from 3 778.8 ng/L to 2 025.9 ng/L, brain natriuretic peptide (BNP) increased from 15 ng/L to 1 638 ng/L. Myocardial enzymology changes were not consistent with acute myocardial infarction, and pulmonary hypertension was not found in cardiac color ultrasound. Therefore, it is considered that the decrease of blood pressure was caused by the decrease of cardiac function, which was combined with septic cardiomyopathy. After increasing the dobutamine pump dose to 20 μg×kg-1×min-1, lowering the infusion speed, reducing the cardiac preload, and continuing to use vasoactive drugs to boost blood pressure for about 1 hour, the patient's blood pressure increased, circulation became stable, and the rescue was successful. After 60 days of treatment, the pneumonia of the patient was effectively controlled, vasoactive drugs and dobutamine were successfully stopped, the patient was extubated, and was able to walk short distances with assistance when discharged. When the circulation of septic shock patients cannot be maintained, the three elements of maintaining blood pressure are effective circulating blood volume, cardiac function and peripheral vascular resistance. The three elements interact with each other and are affected by various factors. The difficulty of maintaining circulation in septic shock is to find out which is the main problem correctly. Individualized volume management, correct recognition and treatment of cardiac dysfunction, and rational use of vasoactive drugs are the keys to maintain circulation in septic shock patients.

脓毒性休克患者抢救过程的思考
感染性休克是重症监护医学中一种常见的急危重症。它可以导致多器官衰竭,心脏是目标器官之一。液体复苏在脓毒性休克的治疗中具有重要作用,但当患者发生败血症性心肌病时,液体复苏往往不能改善循环,甚至可能导致循环恶化。2023年10月2日,民航总医院重症医学科收治一名感染性休克的52岁女性患者,液体复苏时循环恶化。患者主诉为左脸麻木20余天,加重至昏迷5天。入院时,患者处于昏迷状态,经口管插管。血压128/82 mmHg (1 mmHg≈0.133 kPa;去甲肾上腺素0.2静脉泵μg×kg-1×min-1)。胸部CT提示肺部感染,感染标志物升高。主要诊断为感染性休克、肺炎、左桥臂急性脑梗死等。入院后12 h,根据动脉和中心静脉血气分析,吸氧率31%(> 30%),静脉动脉血二氧化碳分压(Pv-aCO2) 7 mmHg (> 6 mmHg),血乳酸(Lac)升高,结合下腔静脉宽度1.0 ~ 1.6 cm,也提示有效循环血容量相对不足,给予适当的液体复苏。液体复苏后,患者尿量由40 mL/h增加至100 mL/h,但血压未明显升高,说明无容量反应性,故加入多巴酚丁胺3 μg×kg-1×min-1增强心肌收缩力。心率没有明显增加,血压也相对稳定。入院后21小时,患者收缩压(SBP)突然从110-120 mmHg下降到60-70 mmHg,心率从100-110 bpm下降到80-90 bpm。因此,将去甲肾上腺素的剂量增加到2 μg×kg-1×min-1,多巴酚丁胺的剂量增加到10 μg×kg-1×min-1,但仍不能维持循环。另外,胸片未见紧张性气胸,血常规未提示急性失血的可能。肌钙蛋白I (TnI)由3 778.8 ng/L下降至2 025.9 ng/L,脑钠肽(BNP)由15 ng/L上升至1 638 ng/L。心肌酶学变化与急性心肌梗死不一致,心脏彩超未见肺动脉高压。因此,认为血压下降是由心功能下降引起的,并合并脓毒性心肌病。将多巴酚丁胺泵剂量增加至20 μg×kg-1×min-1,降低输注速度,降低心脏预负荷,并继续使用血管活性药物升压约1小时后,患者血压升高,循环稳定,抢救成功。治疗60天后,患者肺炎得到有效控制,血管活性药物及多巴酚丁胺停用成功,拔管,出院时可在辅助下短距离行走。当脓毒性休克患者的循环不能维持时,维持血压的三个要素是有效循环血容量、心功能和周围血管阻力。这三个要素相互作用,并受到各种因素的影响。脓毒性休克维持循环的难点在于正确发现主要问题。个体化容积管理、正确认识和治疗心功能障碍、合理使用血管活性药物是维持感染性休克患者血液循环的关键。
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来源期刊
Zhonghua wei zhong bing ji jiu yi xue
Zhonghua wei zhong bing ji jiu yi xue Medicine-Critical Care and Intensive Care Medicine
CiteScore
1.00
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