低容量性低钠血症（Hyponatremia of low volume）

1、低容量性低钠血症（Hyponatremia of low volume）低容量性低钠血症（低血容量性低钠血症）特点是失Na+多于失水，血清Na+浓度130mmol/L，血浆渗透压280mmolL，伴有细胞外液量的减少也可称为低渗性脱水（低渗性脱水）。2、对机体的影响（1）细胞外液减少，易发生休克；（2）血浆渗透压降低，无口渴感，饮水减少，故机体虽缺水；（3）有明显的失水特征；（4）经肾失钠的低钠血症患者，尿钠含量增多。高钠血症（高钠血症）时血清钠浓度150mmolL。高钠血症患者血浆皆为高渗状态，但体Na+总量有减少、正常和增多之分；根据细胞外液量的变化可分为低容量性、高容量性和等容量性高钠血

2、症。低容量性高钠血症（低血容量性高钠血症）的特点是失水多于失钠，血清Na+浓度150mmol/L，血浆渗透压310mmolL。细胞外液量和细胞内液量均减少，又称高渗性脱水（高渗性脱水）。1、原因：（1）水摄入减少；（2）水丢失过多；1）经呼吸道失水；2）经皮肤失水；3）经肾失水；4）经胃肠道丢失。2、对机体的影响：（1）口渴；（2）细胞外液含量减少；（3）细胞内液向细胞外液转移；（4）血液浓缩。等渗性脱水（等渗性脱水）的特点是钠水呈比例丢失，血容量减少，但血清Na+浓度和血浆渗透压仍在正常范围。过多的液体在组织间隙或体腔内积聚称为水肿（水肿）。水肿不是独立的疾病，而是多种疾病的一种重要的病理过

3、程。如水肿发生于体腔内，则称之为积水（水肿），如心包积水、胸腔积水、腹腔积水、脑积水等。水肿的发病机制：1、血管内外液体交换平衡失调；（1）毛细胞流体静压增高；（2）血浆胶体渗透压降低：引起血浆白蛋白含量下降的原因主要有：蛋白质合成障碍，见于肝硬变和严重的营养不良。蛋白质丧失过多，见于肾病综合征时大量的蛋白质从尿中丧失；蛋白质分解代谢增强，见于慢性消耗性疾病，如慢性感染、恶性肿瘤等。（3）淋巴回流受阻：当淋巴干道被堵塞，淋巴回汉受阻或不能代偿性加强回流时，含蛋白的水肿液在组织间隙中积聚，形成淋巴性水肿。2、体内外液体交换平衡失调-钠、水潴留（1）肾小球滤过率下降；（2）近端小管重吸收钠水增多；

4、1）心房钠尿肽（ANP）分泌减少；（2）肾小球滤过分数滤过分数，FF）增加（3）远端小管和集合管重吸收钠水增加-远端小管和集合管重吸收钠、水受激素调节血清钾浓度低于3.5mmolL称为低钾血症：1、原因和机制：（1）钾摄入不足；（2）钾丢失过多；1）经消化道失钾；2）经肾失钾；3）经皮肤失钾。（3）细胞外钾转入细胞内1）碱中毒2）过量胰岛素使用；3）-肾上腺素能受体活性增强；4）某些毒物中毒；5）低钾性周期性麻痹。2、对机体的影响：（1）与膜电位异常相关的障碍；1）低钾血症对神经-肌肉的影响：主要有骨骼肌和胃肠道平滑肌，其中以下肢肌肉最为常见，严重时可累及躯干、上肢肌肉及呼吸肌。急性低钾血症：

5、轻症可无症状或仅觉倦怠和全身软弱无力；重症可发生驰缓性麻痹。慢性低钾血症：2) the effect of hypokalemia on myocardium:Changes in physiological characteristics of myocardium:A. increased excitability, increased B. automaticity, decreased C. conductivity, and altered D. contractilityThe changes of ECG and myocardial cells: in hypokalemia

6、when changes of electrophysiological characteristics are closely related, the typical manifestations are: represents the repolarization phase of 2 ST segment depression; equivalent to the repolarization phase of 3 T wave and U wave were increased (supernormality extension caused by the equivalent);

7、ventricular action potential duration Q-T (or Q-U) prolongation; severe hypokalemia also showed P wave increased and P-Q prolongation and wide QRS complex.(2) potassium supplementation: potassium supplementation should be done in time for severe hypokalemia or obvious complications, such as arrhythm

8、ia or muscle paralysis. It is better to take oral potassium, but not to take orally or when the condition is serious, to consider intravenous drip of potassium supplement. Note: the urinary potassium intravenous potassium supplement is small, daily urine volume more than 500ml to intravenous potassi

9、um; the input liquid potassium concentration should be 2040mmol/L; the hourly input quantity is 1020mmol; close observation of heart rate, heart rhythm, timing determination of serum potassium concentration.Serum potassium concentration is higher than 5.5mmol/L, which is called hyperkalemia.1, reaso

10、n(1) excessive intake of potassium;(2) decrease of potassium excretion;(3) intracellular potassium shifts to the extracellular region:1) acidosis; 2) hyperglycemia combined with insulin deficiency; 3) use of some drugs; 4) tissue breakdown; 5) hypoxia; 6) hypokalemic periodic paralysis;(4) pseudo hy

11、perkalemia.2, the impact on the body(1) the effect of hyperkalemia on neuromuscular function:1) acute hyperkalemia: acute mild hyperkalemia; acute severe hyperkalemia.Regulation of acid base balance:(1) the buffering effect of bloodThe characteristics of the bicarbonate buffer system: 1 all fixed ac

12、id buffer, the buffer can not be volatile acids; the strong buffering capacity, is a buffer system of extracellular fluid was the highest, accounting for more than the total amount of blood content of 1/2 buffer (see Table 4-2); the system can open carbonate dissolution and regulation, can regulate

13、body fluids the CO2 balance and breathing; the buffering potential, through the lung and kidney in the regulation of H2CO3 and HCO3- that the buffer material is easy to supplement and discharge.Regulating function of lung in acid-base balance:The central regulation of respiration: the central respir

14、atory chemoreceptors are very sensitive to PaCO2 changes, so breathing can regulate PaCO2, regulation of PaCO2 increased while not directly stimulate the central chemoreceptors, but by the change of cerebrospinal fluid and brain interstitial fluid pH, increase H+, stimulation in the ventrolateral su

15、perficial parts of H+ central chemosensitive receptors, thereby exciting respiratory center, increased pulmonary ventilation.The peripheral regulation of respiratory movement by peripheral chemoreceptor stimulation and excitement, especially the aortic body of carotid body chemoreceptor, hypoxia, pH

16、 and CO2 can feel the stimulation, when PaCO2 decreased, pH decreased or increased PaCO2, the peripheral chemoreceptor reflex is caused by respiratory stimulant,. Dyspnea, increased CO2 excretion.Regulation of tissue cells in acid-base balance in the body of the buffer pool within the tissue cells i

17、s fluid acid-base balance, buffer cells mainly through ion exchange, red blood cells, muscle cells and bone tissues can play this role.Regulating function of kidney in acid-base balance:1, proximal tubule H+ and reabsorption of NaHCO3;2. The excretion of H+ and reabsorption of NaHCO3 in the distal r

18、enal tubule and collecting duct;3, NH4+ dischargeIn normal subjects, the arterial blood pH was 7.357.45, with an average value of 7.40, where pH was below 7.35, and decompensated pH was higher than 7.45.Arterial blood CO2 partial pressure: the normal value is 3345mmHg (4.396.25kPa), the average valu

19、e is 40mmHg (5.32kPa). PaCO2 33mmHg (4.39kPa), said the excessive pulmonary ventilation, CO2 discharge excessive, in metabolic acidosis poisoning or compensated respiratory alkalosis; PaCO2 46mmHg (6.25kPa), said the lung hypoventilation, CO2 retention,Respiratory acidosis or compensatory alkalosis.

20、Standard bicarbonate and actual bicarbonate: PaCO2 = 40mmHg (5.32kPa), temperature 38 C, hemoglobin oxygen saturation 100%, the amount of HCO3- measured in plasma.Buffer base: the normal value is 4552mmol/L (average value is 48mmol/L).Base residual: the normal range of whole blood BE is -3.0+3.0mmol

21、/L, BE is not affected by respiratory factors, it is an indicator of metabolic factors, BE negative value increases when metabolic acidosis occurs; BE positive value increases during metabolic alkalosis.Anion gap: fluctuation range is 12mmol/L + 2mmol/LMetabolic acidosisOne, reason1. Renal dysfuncti

22、on due to retention of acids and alkalis;2, HCO3- directly lost too much;3. Metabolic dysfunction;4, other reasons: (1) excessive intake of exogenous fixed acid, HCO3- buffer consumption; (2) high K+ blood; (3) blood dilution, so that the concentration of HCO3- decreased.Compensatory regulation of o

23、rganism:1. Buffering and compensatory regulation of blood and intracellular and extracellular ion exchange;2, the compensatory regulation of lung: its compensatory significance is to make the blood H2CO3 concentration (or PaCO2) secondary decrease, maintain the ratio of HCO3-/H2CO3 close to normal,

24、make the blood pH tend to normal.3, the compensatory regulation of kidney: metabolic acidosis caused by other reasons is through the strengthening of the ability of renal excretion of acid and alkali to play a compensatory role.Influence on organism:1. Changes of cardiovascular system;(1) ventricula

25、r arrhythmias;(2) decrease of myocardial contractility;(3) the response of the vascular system to catecholamine is decreased, which makes the blood vessels dilate, the blood pressure drops, the blood volume decreases, and the blood pressure drops.2, the central nervous system changes: mainly for con

26、sciousness disorders, fatigue, perception, and even lethargy or coma, and finally can be respiratory center and vasomotor center paralysis and death.3. Changes in skeletal system.Respiratory acidosisRespiratory acidosis (respiratory acidosis) is a type of acid-base disturbance characterized by incre

27、ased plasma H2CO3 concentration and decreased tendency of pH, which is caused by CO2 discharge disorder or excessive inhalation.One, reason1. Inhibition of respiratory center;2. Airway obstruction;3. Respiratory muscle paralysis;4. Thoracic lesions;5. Pulmonary diseases;6, CO2 inhalation too much.Co

28、mpensatory regulation of organism:1, acute respiratory acidosis, due to renal compensatory action is very slow, it mainly depends on the intracellular ion exchange and intracellular buffer, this regulation and compensation is very limited, often expressed as a compensatory deficiency or decompensate

29、d.2, chronic respiratory acidosis may be compensatory due to the compensatory effect of the kidney.Metabolic alkalosisMetabolic alkalosis (metabolic alkalosis) is a type of acid-base imbalance in extracellular liquid increase or loss of H+ caused by the increase of plasma HCO3- and pH were character

30、ized by sleep or trend.Reason and mechanism:All factors that cause H+ loss or HCO3- increase in extracellular fluid can cause elevated plasma HCO3- levels. Under normal circumstances, when the plasma concentration of HCO3- exceeds 26mmol/L, the kidney can reduce the reabsorption of HCO3-, so that th

31、e concentration of plasma HCO3- returned to normal, and it has the ability to correct metabolic alkalosis. But some factors, such as the effective circulation of blood deficiency, lack of chlorine, can cause renal dysfunction of regulation of HCO3-, so that plasma HCO3- maintained at a high level, t

32、o maintain the existence of metabolic alkalosis.1, excessive loss of acidic substances:(1) loss of stomach;(2) loss of kidney:1) use diuretics;2) excessive adrenal cortical hormone;2, HCO3- overload3, H+ move to the cellCompensatory regulation of organism:1. Buffering and compensatory regulation of

33、blood and intracellular and extracellular ion exchange;In 2, pulmonary compensatory adjustment: because the H+ concentration decreased, respiratory inhibition, slow breathing becomes shallow, alveolar ventilation volume decreased, PaHC2 or plasma H2CO3 secondary to maintain the ratio of HCO3-/ incre

34、ased, H2CO3 decreased to pH close to normal.3. Compensatory regulation of kidney: due to the decrease of secretion of H+ and secretion of NH4+, the increase of HCO3- excretion, the maximum compensatory time for HCO3- excretion in metabolic alkalosis is usually 35 days.Influence on organism:1, the ce

35、ntral nervous system function changes: because GABA inhibits the central nervous system weakened, so patients have irritability, delirium, delirium, consciousness disorders and other central nervous system symptoms.In metabolic alkalosis, pH increased, CSF H+ decreased and respiratory center suppres

36、sed. The patients respiration became shallow and slowed down.2. The hemoglobin oxygen dissociation curve shifts left3, the neuromuscular impact: the plasma free calcium decreased; but as long as the plasma Ca2+ concentration decreased, manifested as tendon reflex hyperfunction, facial and limb muscl

37、e twitching, hand foot twitch.4. Hypokalemia.Respiratory alkalosis:Respiratory alkalosis (respiratory alkalosis) is the type of acid-base disturbance characterized by the decrease of plasma H2CO3 concentration and the elevation of pH.Compensatory regulation of organism:1. Intracellular and extracell

38、ular ion exchange and intracellular buffering in acute respiratory alkalosis2, kidney compensatory regulation of chronic respiratory alkalosis will occur when the kidney compensatory regulationCommonly used indicators of blood oxygenFirst, partial pressure of oxygenNormal arterial oxygen pressure (a

39、rterial partial pressure of oxygen, PaO2) is about 100mmHg, mainly depends on the suction gas partial pressure of oxygen and respiratory function; venous blood oxygen partial pressure (venous partial pressure of oxygen, 400mmHg, PvO2) mainly depends on oxygen uptake and oxygen ability.Two. Blood oxy

40、gen capacity: the normal value is about 20ml/dl. The capacity of blood oxygen reflects the ability of blood to carry oxygen.Three, blood oxygen content: arterial blood oxygen content (CaO2) is about 19ml/dl; venous oxygen content (CvO2) is about 14ml/dl. The difference between the blood oxygen conte

41、nt of the vein and the vein reflects the oxygen uptake capacity of the tissue, which is about 5ml/dl at normal.Four. Hemoglobin oxygen saturation: oxygen saturation of Hb (SO2)The normal arterial oxygen saturation (SaO2) was 95%97%, and the venous oxygen saturation (SvO2) was 75. P50 is an index ref

42、lecting the affinity between Hb and oxygen, which refers to the partial pressure of oxygen when Hb oxygen saturation is 50%, and the party is 2627mmHg.Hypotonic hypoxia, isotonic hypoxia, low dynamic hypoxia, and obstructive anoxia.Hypoxia hypoxiaHypoxia characterized by decreased arterial oxygen pr

43、essure is called hypoxic hypotonic (hypoxic hypoxia), that is, hypotonic hypoxemia (hypotonic hypoxia), also known as hypotonic hypoxemia.(1) reasons:1, the external environment is too low PO2;2. External respiratory dysfunction;3. Venous blood pressure into the arterial blood.Two. Blood hypoxiaBeca

44、use of the decrease or change of the number of hemoglobin, the ability of the blood to carry oxygen is reduced or the oxygen released by the hemoglobin is not easy to release. The hypoxia is called hemic hypoxia.(1) reasons1, anemia;2. Carbon monoxide poisoning;3, methemoglobin, when hemoglobin mole

45、cules of the 4 Fe2+ and hydroxyl (-OH) firmly combined, and lose the ability to carry oxygen. The release of oxygen from the hemoglobin to the tissue cells leads to the shift of the oxygen dissociation curve to the left. Perchlorate and other oxidants can also cause methemoglobin.(two) the character

46、istics of blood oxygen change and the mechanism of hypoxiaThe characteristics of blood oxygenation changes is mainly: the ability of blood oxygen deep solution is no exception, so PaO2 is normal; because the oxygen saturation mainly depends on the PaO2, the PaO2 of normal oxygen saturation during hy

47、poxia is also normal; the change of hemoglobin (CO poisoning and methemoglobin formation) and volume change (severe anemia) and make the blood oxygen capacity decreased, so that reduce the oxygen content of arterial blood oxygen content; the normal or decreased HbCO CO poisoning patients in the bloo

48、d increased, oxygen content decreased, but did not reduce the total amount of hemoglobin;When the blood is fully saturated with oxygen in vitro, the hemoglobin binding CO can be replaced by oxygen, and the blood oxygen capacity measured can be normal.The color of the skin and mucous membrane varies

49、with the cause of the disease in the patients with hematological hypoxia. Severe anemia patients, because hemoglobin decreased significantly and pale; CO poisoning patients with skin and mucosa showed a cherry red, with bright red blood HbCO; but severe hypoxia due to skin vasoconstriction, skin, mu

50、cosa is pale. Methemoglobin is brown, the nitrite poisoning patients skin and mucosa was brown; methemoglobinemia due to eating leads to a large number of hemoglobin oxidation caused also known as enterogenous cyanosis (enterogenous cyanosis).Three. Circulatory hypoxiaCirculatory hypoxia refers to t

51、he lack of oxygen caused by the decrease of tissue blood flow, also known as low dynamic hypoxia (hypokinetic hypoxia).(1) reasons1, systemic circulation disorders;2. Local circulatory disturbance.Four. Tissue hypoxia(1) reasons1. Tissue poisoning2, vitamin deficiency3. Mitochondrial damageFirst, ch

52、anges in the respiratory system(a) compensatory response is: respiratory motion enhanced compensation: increase in alveolar ventilation and alveolar gas PO2, which increased PaO2; the thoracic movement strengthens the pleural pressure increase, promote venous return and increase blood volume, increa

53、se cardiac output and pulmonary blood flow, beneficial blood uptake and movement more oxygen. Thus, the increase of pulmonary ventilation is the most important compensatory response to acute hypotonic hypoxia.(two) damage changes1. High altitude pulmonary edema;2. Central respiratory failure.Two, ch

54、anges in the circulatory system(I) compensatory responseThe compensatory responses of the circulatory system caused by hypotonic hypoxia are mainly increased cardiac output, pulmonary vasoconstriction, blood redistribution and capillary hyperplasia.1. Cardiac output increased;2. Pulmonary vasoconstr

55、iction;3. Redistribution of blood flow;4, the capillary density increased.Etiology of shock:(1) blood loss and loss of fluid1, blood loss;2. Lost fluid(two) burn(three) trauma(four) infection(five) allergy(six) nerve stimulation(seven) cardiac and macrovascular diseasesAccording to the initial onset

56、 of shock of link classification:1. Hypovolemic shock;2. Cardiogenic shock;3, distribution of abnormal shockCompensatory stage of shock:Compensatory stage of (shock) is the early stage of shock development, also known as early shock.1. Redistribution of blood2, blood transfusion vein system is the c

57、apacity of blood vessels, which can accommodate the total blood volume 60%70%, muscular venules and small vein contraction, and blood storage austerity can rapidly and transiently reduce vascular bed volume, increased blood volume, the compensation to the self blood transfusion, is the first line of Defense shock increased return to the heart .3, self infusion due to the micro artery, after arteriole