第十三章 水和电解质代谢(1)
第十三章-电解质代谢紊乱
水和钠等比例丧失 而未予补充
细胞外液等渗，后 高渗，细胞内外液均有 丧失
脱水体征、休克、 口渴、尿少、脱水
脑细胞水肿
体征、休克
130以下
130～150
补充生理盐水或
补充偏低渗的氯化
3%氯化钠溶液
钠溶液
第二节 钾代谢紊乱
一、低钾血症 二、高钾血症
第二节 钾代谢紊乱
正常成年人含钾量为 31~57mmol/kg。 体钾的70%在肌肉，10% 在皮肤，其余在 红细胞、脑和内脏中。细胞外液钾占体钾 的2% ，血清 K+ 为 3.5~5.5 mmol/L；细胞 内液钾占98% ，浓度约为150mmol/L。
第十三章 电解质代谢紊乱
1. 理解水钠代谢紊乱：脱水概念、三种 脱水区别；
2. 认识钾代谢紊乱：概念、对心脏的影 响。
王某，男，15个月，因腹泻、呕吐4天入院。发病 以来，每天腹泻6～8次，水样便，呕吐4次，不能进 食，每日补5%葡萄糖溶液1000ml，尿量减少，腹胀。 体检：精神委靡，体温37.5℃（肛），脉搏速弱，150 次/min，呼吸浅快，55次/min，血压86/50mmHg，皮 肤弹性减退，两眼凹陷，前囟下陷，腹胀，肠鸣音减 弱，腹壁反射消失，膝反射迟钝，四肢凉。实验室检 查：血清Na+125mmol/L，血清K+3.2mmol/L。
图13-4 细胞外液减少机制图
二、低渗性脱水 （hypotonic dehydration）
2. 明显的失水体征。 3. 细胞内液的变化：细胞外液移向 细胞内（图13-4）；严重致细胞水肿特 别是脑水肿，可引起神经功能障碍。 4. 尿变化。
二、低渗性脱水 （hypotonic dehydration）
水和电解质的平衡及其调节PPT教学课件
毛细淋巴管壁 （各种物质单向渗透）
淋巴管 （回流）
水摄入与排出的途径及其平衡 请对应P44表2-2，分析下图： 1、回顾体液的组成和相互关系； 2、说出水的摄入、排出的途径、量和各个箭头的含义。 3、哪些是“不感觉失水”，其意义是什么？
①饮水+1200mL ②食物水+700mL
消化道
④排遗-100mL
管 内 渗 透 压 相 对 值 1 （血浆）
例：下图表示尿液形成过程中肾脏不同管道内的液体渗透压变化， 以血浆渗透压作为1。下列叙述错误的是（C ）
m n
a
b
c
d
21
尿液的形成过程 ▲尿液生成的主要过程： 血浆
肾小球的滤过 肾小管和集合管的重吸收
原尿
（含蛋白质）
（蛋白质很少； 糖、盐多）
肾小管的分泌
3
体液中的电解质及其主要功能
请阅读课本并分析P43表2-1，填写下表： 细胞外液中的 主要电解质
阳离子 阴离子
细胞内液中的 主要电解质
阳离子 阴离子
主要功能 （维持自稳态）
Na+
ClHCO3HCO3-
K+
HPO42H2PO4蛋白质
维持渗透压稳定 维持电中性
HPO42维持pH稳定 H2PO4蛋白质 说明：①Ca2+在细胞内液中含量极少； ②蛋白质含量：细胞内液﹥血浆﹥组织液； ③细胞内、外液总的渗透压相等（∵电解质离子总数相等）； 4 ④体液呈电中性（∵正负电荷总数相等）
2.2
水 和 电及 解其 质调 的节 平 衡
1
1、人体中水和电解质的含量
（1）细胞外液和细胞内液中的电解质 （2）体液中电解质的主要功能 （3）解析表2-1：细胞内液和细胞外液主要电解质的含量
水与电解质代谢紊乱概述与表现
脱水热 (dehydration fever)
因皮肤蒸发水减少引起的体温上升
水和电解质代谢紊乱概述和表现
高渗性脱水的主要发病环节 ECF高渗
ECF: Na+、Cl-、 HCO3ICF: K +、 HPO42- 、 Pr-
平均正常值
血[Na＋] 140 mmol/L 血[Cl－] 104 mmol/L 血[HCO3－] 24 mmol/L
三、体液的渗透压
(Osmotic pressure of body fluid)
渗透压的大小取决于溶质的微粒数 目，而与溶质微粒的大小无关
水和电解质代谢紊乱概述和表现
一、分类（ Classification ）
（一）根据细胞外液容量和渗透压
❖脱水(dehydration) ◆高渗性 ◆低渗性 ◆等渗性
❖水过多(water excess) ◆低渗性（水中毒） ◆高渗性（盐中毒） ◆等渗性（水 肿）
（二）根据血钠的浓度和体液容量 1.低钠血症 ❖低容量性低钠血症（低渗性脱水）
水和电解质代谢紊乱概述和表现
主要环节:细胞外液高渗
失水>失Na+ →皮肤蒸发↓ 脱水热
ECF量↓
早期不易休克
ECF渗透压↑→渴中枢 口渴
↓
ADH↑ 细胞内脱水
↓
肾重吸收水↑
↓
CNS功能障碍ຫໍສະໝຸດ 尿少比重高水和电解质代谢紊乱概述和表现
幻觉,躁动
3、高渗性脱水对机体的影响
1）口渴 2）细胞外液减少,但早期不易发生休克 3）尿量减少，比重增高 细胞外液高渗刺激ADH分泌 4）细胞内液向细胞外液转移，细胞皱缩 5）中枢神经系统功能障碍,蛛网膜下腔出血 6）脱水热
1 水、电解质代谢紊乱(1 disorders of water and electrolyte metabolism)
---------------------------------------------------------------最新资料推荐------------------------------------------------------1 水、电解质代谢紊乱（1 disorders of water andelectrolyte metabolism）1 水、电解质代谢紊乱（1 disorders of water and electrolyte metabolism） 1 水、电解质代谢紊乱（1 disorders of water and electrolyte metabolism） Dehydration (dehydration) \ hypotonic dehydration (Hypotonic dehydration) \ dehydration symptoms (Dehydrate, symptom) \ [hypertonic dehydration (Hypertonic, dehydration) / isotonic dehydration (Isotonic, dehydration) / water intoxication (Water, intoxication) \ hyponatremia (hyponatremia) \ hypernatremia (hypernatremia) A disorder of water and sodium metabolism Dehydration (dehydration): a decrease in body fluid volume (more than 2% of body weight) and a series of pathological disorders of function and metabolism. The water of the body is mainly the loss of extracellular fluid, while sodium ions are the most important cations in the extracellular fluid, so dehydration is often associated with the loss of sodium (I) hypotonic dehydration (Hypotonic, dehydration); Hypotonic dehydration: loss of sodium, more than water loss, serum sodium concentration 135mmol/L, plasma osmotic pressure 280mmol/L, and accompanied by decreased extracellular fluid volume, known as hypotonic dehydration.1 / 20Also called hyponatremia of low volume The etiology and pathogenesis of * * * * Mainly the loss of isotonic or hypotonic fluid. 1) extra renal causes A. digestive juices are lost in large amounts, B. fluids accumulate in large amounts in the body cavity, and C. accumulates large amounts of sweat or burns in large areas 2) renal causes A large number of long-term use of sodium intake or natriuretic drug limit A. (hydrochlorothiazide and furosemide and ethacrynic acid etc.)B. chronic renal interstitial disease, ascending limb of Henle and Na with renal dysfunction increased lostC. acute renal failure polyuria period, GFR increase, tubular function did not recover, sodium and water excretion increasedD. salt losing nephritis, tubular epithelial cell lesions of Ald (aldosterone) response to the decrease in sodium reabsorption in renal sodium excretion, reduce excessive The adrenal cortex and e., such as Addison disease, Ald secretion of Na, the decrease in tubular reabsorption and decrease renal sodium excretion and drainage increased F. excessive osmotic diuresis and renal excretion of Na and H2O increase 2. of the impact of the body The basic changes were obvious decrease of extracellular fluid and decrease of osmotic pressure Loss of sodium and water loss, the osmotic pressure of extracellular fluid, the decrease in---------------------------------------------------------------最新资料推荐------------------------------------------------------ extracellular to intracellular water transfer to intracellular water up to cell edema, extracellular fluid decreased more obviously Clinical manifestation 1) circulatory failure (Symptom of, circulatory, failure) The water from the cell to cell outward transfer of extracellular fluid and blood volume down down down down down down, blood pressure, shock 2) dehydration symptoms (Dehydrate, symptom) Lower skin elasticity, sunken socket, and three concave signs in infants.(3) other clinical manifestations (Other, manifestation); - thirsty: early without thirst; in late, there will be thirsty. CNS - symptoms: severe hypotonic dehydration with haziness, drowsiness, coma. - urinary sodium:: urinary sodium or no 10mmol/L. According to the clinical symptoms of the severity of clinical hypotonic dehydration of three degrees (two) hypertonic dehydration (Hypertonic, dehydration); Hypertonic dehydration: dehydration more than sodium loss, serum sodium concentration 145mmol/L, plasma osmotic pressure 310mmol/L, and accompanied by decreased extracellular fluid volume, Hypertonic dehydration. Also called low volume hypernatremia. 1. etiology and pathogenesis Dehydration or loss of low osmotic fluid is the main cause of3 / 20hypertonic dehydration 1) simple dehydration A. is C. through the lung, B. by the skin, and by the kidneys (2) loss of hypotonic fluid C. loss of hypotonic fluid through the gastrointestinal tract, B. profuse sweating, and repeated osmotic diuresis caused by repeated use of mannitol or hypertonic glucose in the a. 2., the impact on the body 1) compensatory response of organism - drink (except for thirst thirst disorder) Plasma osmotic pressure increases, osmoreceptor (+) - (+) - thirsty thirst Here, AGTII relax, thirsty central blood volume (+) - thirsty Hypertonic dehydration, saliva, throat dry down While the proportion of high - oliguria (excluding diabetes insipidus patients) In the water from the cell within the extracellular transfer to the osmotic pressure of extracellular fluid decreased somewhat These three aspects make the extracellular fluid osmotic pressure fall back, so that the early blood volume of dehydration is not easy to drop to the degree of shock 2) the clinical manifestation varies with the degree - urinary sodium Mild hypertonic dehydration (early stage) The osmotic pressure of extracellular fluid, increase blood volume decrease is not obvious, the reabsorption of water and sodium, high urine sodium. Medium and severe hypertonic dehydration---------------------------------------------------------------最新资料推荐------------------------------------------------------ (late) Blood volume and renal blood flow was significantly lower, Ald (aldosterone) secretion, increase urinary sodium down - CNS symptoms Severe hyperosmolar dehydration, intracellular fluid, brain cell dehydration and significantly decrease brain pressure decreases, the severity of the symptoms of CNS - thermal dehydration Here, the body temperature down to increase heat dissipation function, sweat gland secretory cells: liquid - shock, renal failure According to the severity of clinical symptoms, the hypertonic dehydration was three degrees (three) isotonic dehydration (Isotonic, dehydration); Isotonic dehydration: when water and sodium are lost in proportion or after losing fluid, the plasma osmotic pressure is still within normal range, the serum sodium concentration is 135~145mmol/L, and the plasma osmotic pressure is 280~ 310 mmol/L. 1. etiology and pathogenesis Vomiting and diarrhea, a large number of pleural and ascites formation, extensive burns and severe trauma, such as plasma loss. 2., the impact on the body Isotonic dehydration often has clinical manifestations of hypotonic and hypertonic dehydration. A massive loss of isotonic fluid, extracellular fluid, blood volume, blood pressure down, down to the decrease5 / 20in urine volume, body temperature, dehydration obvious appearance Isotonic dehydration can only be converted into hypotonic dehydration if only water is added to the treatment without attention to sodium supplementation. Water intoxication Water intoxication (Water intoxication): when the water intake, over regulating nerve endocrine system and kidney drainage ability, make a lot of water retention in the body, resulting in volume of intracellular fluid and extracellular fluid expansion, and the emergence of a series of diseases including hyponatremia, physical and physiological changes. 1. etiology and pathogenesis 1) take in or enter too much electrolyte free liquid 2) acute or chronic renal insufficiency 3) excessive secretion of ADH Excessive secretion of ADH is defined as abnormal secretion of ADH under certain pathological conditions. (a) ADH abnormal growth syndrome (SIADH): Hypothalamic diseases (encephalitis, brain tumors) and ectopic ADH secretion (lung, oat cell carcinoma) B) other reasons In pain, nausea and emotional stress: relax, ADH secretion of water intoxication In the case of adrenocortical function: GC (glucocorticoid), inhibition of hypothalamic ADH secretion function down down - exogenous ADH input (vasopressin and oxytocin) 4) certain special---------------------------------------------------------------最新资料推荐------------------------------------------------------ pathological states A) heart failure, hepatic ascites, effective circulating blood volume down, down to the water load increase renal drainage and water poisoning (b) hypotonic dehydration - a large amount of electrolyte free water intoxication 2., the impact on the body Prominent manifestation: increased intracellular fluid volume or cell edema When water poisoning occurs, the extracellular fluid increases obviously, and the low permeability of extracellular fluid causes a large amount of water to enter the cell Mild water intoxication, the increase of intracellular and external fluid is not obvious, the symptoms are not obvious, may be weak, dizziness and so on Acute poisoning with water intoxication can cause brain cell edema and increased intracranial pressure, which can be life-threatening test questions 1. the balance of osmotic pressure inside and outside cells mainly depends on the movement of the following substances A., Na+, B., K+, C., Cl-, D., H2O, Ca++, E. 2., a large amount of water is added to the patients with severe hypotonic dehydration, while no sodium salt is added A. hypertonic dehydration, B. isotonic dehydration, C. poisoning, D. hypokalemia, E. edema 3. what are the major characteristics of hypotonic dehydration? 4.7 / 20why is hypertonic dehydration less prone to circulatory failure in the early stage? 5., we compared the similarities and differences between hypotonic dehydration and hypertonic dehydration. Case analysis Male patients, 2 years old, diarrhea 2 days, 6-7 times a day, watery stools; vomiting 3 times, vomiting is the milk consumed, can not eat. Accompanied by thirst, oliguria and bloating. Physical examination: the spirit of malaise, T37oC, BP11.5/6.67KPa (86/50mmHg), skin elasticity, eyes sag, bregmatic subsidence, fast heartbeat and weak, no abnormal lung, abdominal distension, abdominal reflex, decreased bowel sounds, knee reflex, cold extremities. Laboratory tests: serum K+3.3mmol/L, Na+140mmol/L. What kind of water and electrolyte disorder occur in the child? On the basis of what? Comparison of three kinds of dehydration Disturbance of sodium metabolism 1. hyponatremia Hyponatremia (hyponatremia) refers to serum sodium concentrations below 135mol/l. Plasma osmolality mainly depends on the concentration of serum sodium ions, so hyponatremia is usually associated with low osmolarity. (I) hypotonic hyponatremia (hypotonic, hyponatremia): The vast majority of hyponatremia is associated with a decrease in plasma osmolality 1) low capacity hyponatremia (hypovolemic,---------------------------------------------------------------最新资料推荐------------------------------------------------------ hyponatremia) The loss of sodium is more than the loss of water, and the volume of extracellular fluid is decreased, that is, hypotonic dehydration 2) hyponatremia (isovolemic) It is seen in ADH secreting abnormal growth syndrome and osmotic reset 3) high capacity hyponatremia (hypervolemic, hyponatremia) The main causes are congestive heart failure, liver cirrhosis, ascites, nephrotic syndrome and so on, which lead to the pathological changes of the effective circulation and blood loss. Water intoxication (two) isotonic hyponatremia (chronic hyponatremia) (isotonic, hyponatremia); Hyperlipidemia or hyperlipoproteinemia patients, due to the increase of plasma lipid or protein content, serum water proportion decreased, so the serum sodium concentration under normal water, plasma sodium concentration in the clinically measured reduced, then called isotonic hyponatremia. (three) hypertonic hyponatremia (hypertonic, hyponatremia); Hyperosmolar hyponatremia: Sodium by outside impermeable solute permeability caused by increased extracellular fluid pressure increased, the water inside the cells to transfer, extracellular fluid sodium concentration decreases, which leads to the occurrence of hyponatremia in. 2. hypernatremia9 / 20Hypernatremia (hypernatremia): serum sodium concentration is higher than 145mmol/l. With the increase of plasma osmotic pressure, the basic changes of hypernatremia are common when the cells are dehydrated. (I) hyponatremia of low volume Mainly because of the large loss of water or hypotonic fluid, the loss of water exceeds the loss of sodium, which leads to the decrease of extracellular fluid and the increase of serum sodium concentration, which is called hypertonic dehydration (two) hypernatremia with equal capacity It is found in primary hypernatremia, impaired central nervous system and so on (three) hypernatremia with high volume The main reason is the excessive input of sodium solution. In patients who have been rescued from cardiac arrest and respiratory arrest, a large amount of NaHCO3 is added to fight lactic acidosis, resulting in an increase in extracellular fluid volume and sodium concentration. Two 、potassium metabolism disorder Disturbance of potassium metabolism: abnormal changes in K+ concentration in extracellular fluid (especially serum), and the patient’s clinical symptoms and signs depend mainly on the speed and extent of abnormal changes in blood potassium concentration (I) hypokalemia (hypokalemia); When serum potassium concentration is below 3.5mmol/L, it is called---------------------------------------------------------------最新资料推荐------------------------------------------------------ hypokalemia. Potassium depletion: intracellular potassium and loss of total potassium in the body. 1. causes and mechanisms 1) lack of potassium intake 2) excessive potassium loss The loss of potassium through the stomach and intestines (hypokalemia) Loss of kidney by potassium (a) loss of kidney due to increased renal flow at the distal end of the renal tubule A large number of diuretics use: increasing the distal flow velocity of the renal tubule and increasing the exchange of Na with K Renal insufficiency, renal failure (b) aldosterone: aldosterone is the major mineralocorticoid that promotes reabsorption of sodium and the secretion of potassium and hydrogen, causing potassium loss (c) renal tubule transmembrane potential increases negatively, resulting in potassium loss D) loss of potassium caused by low Mg blood Magnesium deficiency in the body, caused by the thick ascending limb of Henle epithelial cell Na, inactivation of the K-ATP enzyme, caused by potassium reabsorption and potassium loss.E) other Type I renal tubular acidosis: obstruction of the distal convoluted tubule to H+ Type II renal tubular acidosis: reabsorption of proximal convoluted tubules in HCO3- Type IV renal tubular acidosis: simultaneous presence of malabsorption11 / 20of Na+ and obstruction of the distal convoluted tubule with H+ Loss of skin by potassium 3) potassium to intracellular transfer (a) alkalosis (b) the use of insulin (c) hypokalemic familial familial periodic paralysis (d) barium poisoning, crude cottonseed oil poisoning 2. effects of hypokalemia on the body Related to the speed, amplitude and duration of blood potassium lowering, the faster the rate of blood potassium lowering, the lower the serum potassium concentration, the greater the impact on the body. 1) the effect on neuromuscular excitability The excitability and conductivity of nerve and muscle tissue are significantly affected Acute hypokalemia, extracellular fluid with constant liquid concentration decreased, intracellular potassium concentration, the results make the intracellular potassium concentration, the ratio of increase of intracellular potassium efflux increased, the absolute value of the resting membrane potential increases, and increase the threshold potential gap, the stimulation threshold excited should also be increased, it caused the excitability of nerve muscle cells decreased. When chronic hypokalemia occurs, the extracellular potassium can be replenished by intracellular potassium, because the potassium concentration in the---------------------------------------------------------------最新资料推荐------------------------------------------------------ extracellular fluid is slowed down, so the symptoms are not obvious. Clinical manifestations: symmetrical limbs, flaccid paralysis, even soft paralysis, paralytic ileus, abdominal distension and so on. Physical examination: reduction of muscle tone in the limbs and decrease or disappearance of tendon reflex. Reason: the excitability of skeletal muscle cells decreases, and the gastrointestinal smooth muscle can also be involved 2) the effect on the heart Mainly cause arrhythmia, severe ventricular fibrillation, leading to heart failure A) physiological changes of myocardium [K +]e decreased, membrane permeability decreased, phase 4 K + efflux decreased, Na + or Ca2 + increased, and autonomic cells automatically increased rapidly and increased automaticity; The reduced membrane permeability decreased [K]e?? Em cell move, Em-Et spacing increased excitability?; The Em shift and Em-Et spacing decrease, the slope of the 0 phase curve increases, the front potential decreases, and the conductivity decreases; The [K +]e decreased 2? Ca2 + influx of [Ca2 +]i increased rapidly accelerated?? myocardial contractility increased (severe and chronic hypokalemia due to intracellular potassium deficiency, affecting cell metabolism, myocardial damage,13 / 20decrease of myocardial contractility). (b) electrocardiographic changes The obvious U wave after S-T segment depression and T wave is characteristic of hypokalemia Conduction prolongation, P-R interval prolongation, ORS wave presentation and broadening The calcium influx in the 2 stage accelerates the potassium efflux, the 2 stage repolarization accelerates and the S-T depression decreases The 3 phase of potassium efflux slowed down to repolarization, and the 3 phase extended to U wave obviously C) arrhythmia In hypokalemia, the myocardial excitability increased, the supernormal period prolonged and the ectopic pacemaker increased automaticity. At the same time, the conductivity decreased, the conduction slow and the effective refractory period shortened, and it was easy to cause excited reentry. Therefore, hypokalemia is prone to premature beats, atrioventricular block, ventricular fibrillation, and other arrhythmias. 3) the influence on acid-base equilibrium Hypokalemia may cause alkalosis (paradoxical uric acid) 4) the effect on the kidney The accumulation of renal dysfunction occurs in the so-called depletion of postassiun (nephropathy) 5) the effect on blood vessels Reducing peripheral vascular resistance to hypokalemia is associated with vertigo, hypotension and other---------------------------------------------------------------最新资料推荐------------------------------------------------------ symptoms 3. prevention and treatment principle of hypokalemia 1) prevention and treatment of primary diseases 2) proper potassium supplementation during treatment. The principle of potassium supplementation: feeding can be taken orally as possible potassium supplement; intravenous potassium supplementation should pay attention to low concentration (20~40 mmol/L) and low flow rate (10 mmol/h); daily potassium supplementation can be controlled at 40~120 mmol. Special attention should be paid to intravenous potassium supplementation only when the renal function is good. When the amount of urine is greater than 500 ml, the potassium supplementation is safe. Potassium deficiency is caused by magnesium deficiency, Magnesium should be supplied before potassium can be effectively supplied. Attention should be paid to the acid-base balance of the patient. (two) hyperkalemia (hyperkalemia); Serum K + concentration greater than 5.5 mmol/L is called hyperkalemia. 1. causes and mechanisms 1) excessive penetration 2) renal excretion of potassium decreased Acute renal failure, oliguria stage, end-stage renal failure. High potassium type distal tubular acidosis Decreased aldosterone secretion or decreased renal15 / 20tubular aldosterone response to aldosterone Long term use of diuretics that can cause potassium retention 3) extracellular release of stromal cells Acidosis A great deal of hemolysis or tissue damage and necrosis When diabetic ketoacidosis occurs Membrane dysfunction of sodium pump Familial familial periodic paralysis of hyperkalemia 2. effects of hyperkalemia on the body 1) the effect on neuromuscular excitability Mild hyperkalemia (5.5 ~ 7.0mmol/L) often results in increased excitability. There are hand foot and foot abnormalities, tremors, myalgia, or colic, and diarrhea; Severe hyperkalemia (7 ~ 9.0mmol/L) often makes the muscle cells appear to be depolarized and blocked, causing muscle paralysis, and clinical weakness of muscle, flaccid paralysis and other symptoms. 2) the effect on the heart The effect on the heart, like hypokalemia, can also cause arrhythmias or ventricular fibrillation, but unlike hyperkalemia, severe hyperkalemia can cause cardiac arrest. (a) characteristics of myocardial physiological changes [K +]e increased, and the permeability of the membrane to K + increased after the repolarization of the self regulatory cells. The 4 phase of K + flow increased, the automatic depolarization slowed down, and the automaticity decreased. Increase of [K +]e, decrease of---------------------------------------------------------------最新资料推荐------------------------------------------------------ Em negative value in cardiac working cells, decrease of Em-Et distance, increase of excitability in mild disease and decrease in severe condition. The Em-Et interval is reduced. In the 0 stage, the depolarization is decreased and the potential is decreased, and the conductivity is decreased. Increase of [K +]e, decrease of calcium influx in 2 stage and decrease in contractility. B) changes in the electrocardiogram The action potential of cardiac myocytes decreased and P wave decreased, widened or disappeared The conductivity decreased, prolonged P-R interval, QRS composite is wide The T wave is high, the Q-T interval shortens and the S-T elevation (c) the manifestation of arrhythmia Acute hyperkalemia is reduced and slow conduction conductivity caused by unidirectional conduction block, and effective refractory period shortened, and also easy to cause the reentry arrhythmia, including ventricular fibrillation. Severe hyperkalemia can result in cardiac arrest due to reduced automaticity, block of conduction, and loss of excitability 3) the influence on acid-base equilibrium Hyperkalemia results in the metastasis of H + to the extracellular region and the decrease of H + in kidney, so metabolic acidosis can occur. (paradoxical alkaline urine) 3.17 / 20prevention and treatment principle of hyperkalemia 1) prevention and treatment of primary diseases 2) reduce blood potassium: myocardial toxicity against high potassium; promote K+ into cells; accelerate K+ excretion Hypokalemia * reasons Insufficient intake of potassium: can not eat or fasting, stomach, parenteral K solution too much: often iatrogenic, such as kidney dysfunction, more rapid, potassium supplementation Potassium loss or discharge excessive vomiting, diarrhea, intestinal fistula; using Paul sodium and osmotic diuresis; renal dysfunction and interstitial renal disease; aldosterone; magnesium deficiency; sweat reduction; renal failure and some kidney diseases; Adrenal cortical insufficiency; potassium sparing diuretic use * k the abnormal distribution of extracellular potassium into the cell: alkalosis; insulin; periodic paralysis; intracellular potassium escape cell barium poisoning: acid poisoning; severe hypoxia; periodic paralysis; hemolysis or serious tissue damage excessive muscle movement; the use of digitalis or propranolol. Effects on the organism * nerve muscle excitability is chronic; varies little Acute: lower chronic: little change Acute: mild increase, severe decrease * cardiac automaticity increases and decreases Excitability increased, slightly increased, decreased when---------------------------------------------------------------最新资料推荐------------------------------------------------------ severe Decreased conductivity Decreased contractility Extend the ECG characteristics of the P-R interval, QRS wave width; S-T segment depression, T wave flat, U wave, Q-T wave, P wave interval prolonged low width, prolonged P-R interval, QRS wave width; S-T elevation, T wave tip The Q-T interval is shortened or normal * clinical presentation, tachycardia, arrhythmia, or ventricular fibrillation, arrhythmia, or cardiac arrest * acid base balance secondary metabolic alkalosis secondary metabolic acidosis * gastrointestinal peristalsis, abdominal distension, paralytic ileus, colic, diarrhea Three, acid-base balance and acid-base balance disorders Under physiological conditions, the pH of the extracellular fluid is between pH37.35-7.45 and the average value is 7.40. Extracellular fluid pH is in this relatively stable state, that is called acid-based (balance), that is, the relative concentration of hydrogen ion concentration ([H+]) in the blood. The maintenance of acid-base balance depends on the humoral buffer system and the mediation of the lungs and kidneys. The acid-base equilibrium disorder refers to various causes accumulation or lack of body acidic or alkaline substances, leading to environmental damage in body fluid acid-base19 / 20homeostasis, which is caused by various reasons of arterial blood [H+] exceeded the normal range (increase or decrease) of the pathological changes.。
水和电解质代谢
第十三章水和电解质代谢一、选择题【单选题】1.体液的组成成分是A. 水、无机盐、核酸B. 水、无机盐、糖C. 水、无机盐、脂类D. 水、无机盐、低分子有机物和蛋白质E. 以上都不是2.体液量最多的是A. 细胞内液B. 细胞外液C. 血浆D. 淋巴液E. 组织间液3.新生儿含水量约为A. 60%B. 50%C. 75%D. 80%E. 65%4.关于水的含量在个体间的差异，下列哪项是错误的A. 成人多，老年人少B. 胖者多，瘦者少C. 婴儿多，成人少D. 男性多，女性少E. 瘦者多，胖者少5.细胞内液的主要阳离子是A. 钠离子B. 镁离子C. 钾离子D. 钙离子E. 锰离子6.细胞外液的主要阳离子是A. 钠离子B. 钾离子C. 钙离子D. 镁离子E. 锰离子7.细胞内外渗透压的平衡主要是靠哪种物质的移动A. 钠离子B. 钾离子C. 葡萄糖D. 蛋白质E. 水8.细胞外液的主要阴离子是A. HCO3-B. Cl-C. HPO42-D. Pr-E. SO42-9.按摩尔电荷浓度计算，细胞内液电解质总量高于细胞外液，因此渗透压A. 细胞内液大于细胞外液B. 细胞外液大于细胞内液C. 细胞内液与细胞外液基本相等D. 细胞内液大于组织间液E. 以上都不是10.血浆与组织间液的重要差别是A. 渗透压不同B. 钾离子不同C. 钠离子不同D. 蛋白质含量不同E. 以上都不对11.有关水的功能错误的是A. 调解体温B. 运输物质C. 防御作用D. 润滑作用E. 促进、参与化学反应12.各种消化液体丢失后，共同缺乏的电解质是A. 钠离子B. 钾离子C. 氯离子D. 碳酸氢根离子E. 钙离子13.成人每日最低需水量为A. 1000mlB. 1500mlC. 2000mlD. 2500mlE. 500ml14.正常成年人每日尿量约为A. 500mlB. 1000mlC. 1500mlD. 2000mlE. 2500ml15.人体每日最少尿量为A. 2500mlB. 500mlC. 1500mlD. 350mlE. 150ml16.不能进食的人每日最低补液量为A. 2500mlB. 500mlC. 1500mlD. 350mlE. 100ml17.既能增强神经肌肉的兴奋性又能降低心肌兴奋性的离子是A. Ca2+B. Mg2+C. Cl-D. OH-E. K+18.对ADH的描述，下列哪项是正确的A. 促进肾远曲小管分泌H+，重吸收Na+B. 促进肾远曲小管排K+,重吸收Na+C. 促进肾远曲小管和集合管对水的重吸收D. 促进远曲小管对K+的吸收E. 以上都不对19.对于醛固酮的描述正确的是A. 促进肾远曲小管对K+的重吸收B. 它是由肾上腺髓质分泌的C. 属于含氮类激素D. 促进肾远曲小管分泌H+, 排K+, 重吸收Na+E. 以上都不对20.一次摄入大量水分后，尿量增加是由于A. ADH分泌减少B. ADH分泌增加C. ADH分泌不变D. 与ADH分泌无关E. 以上都不对21.大量出汗可出现A. 低渗性脱水B. 高渗性脱水C. 等渗性脱水D. 水中毒E. 以上都不对22.影响ADH分泌的因素有A. 血浆渗透压B. 血容量C. 血压D. 精神因素E. 以上都是23.下列哪一种情况不引起ADH分泌增加A. 缺水B. 大量饮水C. 血容量减少D. 血浆渗透压升高E. 血压下降24.直接刺激肾上腺皮质球状带细胞分泌醛固酮的是A. 肾素B. 血管紧张素ⅠC. 血管紧张素ⅡD. 血管紧张素原E. 血容量减少25.下列关于肾脏对钾排泄的叙述哪一项是错误的A. 多吃多排B. 少吃少排C. 不吃不排D. 不吃也排E. 吃得少，排的少26.下列能引起血钾浓度降低的是A. 创伤B. 高烧C. 饥饿D. 呕吐E. 缺氧27.醛固酮分泌减少导致A. 血K+浓度降低B. 血Na+浓度增高C. 血HCO3-浓度升高D. 尿PH升高E. 血容量升高28.有关钙的叙述错误的是A. 降低神经肌肉的兴奋性B. 降低心肌的兴奋性C. 降低毛细血管的通透性D. 参与血液凝固E. 构成骨与齿29.血钙增高可引起A. 心率减慢B. 心肌兴奋性增强C. 骨骼肌兴奋性增强D. 抽搐E. 以上都不对30.当给病人注射胰岛素和葡萄糖以后，体内钾代谢的变化是A. 无变化B. 细胞外钾进入细胞C. 细胞内钾出细胞D. 尿钾增多E. 血钾增多31.一慢性肾功能衰竭患者有酸中毒表现，在补充碳酸氢钠液体时，患者出现手足搐搦，此时应补充的电解质是A. Na+B. K+C. Ca2+D. Mg2+E. H+32. 一两岁幼儿有睡眠不安、好哭、易出汗等现象，且有方颅、囟门闭合晚、站立时两腿呈“X”型，该患儿最可能的病因是缺乏A. 钙B. 钾C. 锌D. 维生素DE. 铁33.细胞内液约占体重A.5%B.15%C.20%D.40%E.60%34.体液总量约占体重A.5%B.15%C.20%D.40%E.60%35.细胞外液约占体重A.5%B.15%C.20%D.40%E.60%36.血浆约占体重A.5%B.15%C.20%D.40%E.60%37.细胞间液约占体重A.5%B.15%C.20%D.40%E.60%38.血清浓度为3.5—5.5mmol/L的离子是A.Na+B.Cl-C.K+D.HPO42-E.Ca2+39.细胞内液的主要阴离子A.Na+B.Cl-C.K+D.HPO42-E.Ca2+40.降低神经肌肉兴奋性的是A.Na+B.Cl-C.K+D.HPO42-E.Ca2+【多选题】41.体液中电解质分布和含量的特点是A.各体液中正负离子总量相等（以mEq/l计）B.细胞内外液电解质组成有很大差异C.细胞内液电解质总量高于细胞外液D.细胞内外液渗透压相等E.细胞内液渗透压高于细胞外液42.水的功能是A. 促进化学反应B. 运输物质C. 调节体温D. 润滑作用E. 维持体液的酸碱平衡43.使醛固酮分泌增加的是A. 血钾升高B. 血钾降低C. 血钠下降D. 血钠升高E. 血钙升高44.引起ADH分泌增加的是A. 血浆渗透压升高B. 血容量降低C. 血压降低D. 精神紧张E. 血钾升高45.在高血钾时，心脏可发生A. 心动过速B. 心动过慢C. 心脏停止于收缩期D. 心脏停止于舒张期E. 心肌收缩加强二、名词解释1. 体液2. 每天必然丢失水量3. 高渗性脱水4. 血浆有效胶体渗透压5. 成骨作用三、填空题1. 正常成人体液总含量约占体重的 , 其中细胞内液占体重的，细胞外液占体重的，血浆占体重的，细胞间液占体重的。
生化习题集第十三章 水和电解质代谢
第十三章水和电解质代谢一、名词解释1．体液 2．细胞内液3．细胞外液 4．代谢水5．结合水 6．非显性出汗7．可扩散钙 8．非扩散钙9．钙磷乘积 10．溶骨作用11．活性维生素D3 12．微量元素二、填空题1.正常成人的体液总量约占自身体重的_________％，其中细胞内液为_________，血浆为_________，细胞间液为_________。
2.以细胞膜为界体液可分为_________和_________。
3.人体体液的含量因_________，_________和胖瘦程度有关。
4.细胞内液的电解质总量较细胞外液_________，但细胞内液与细胞外液的_________仍相等。
5.人体与外界物质交换包括两大过程一是_________,二是_________这两个过程的完成是依靠体液在_________,_________,及________三者之间的交换来实现的。
6.有效滤过压等于_________与细胞间液的_________之和减去_________与_________之和。
7.细胞间液与细胞内液的交换是通过_________来实现的。
8.决定细胞内液渗透压的主要是_________, 决定细胞外液渗透压的主要是_________。
9.体内的水按照其自由状态的不同可分为自由水和结合水，后者主要是指体内大部分水与_________,_________,和_________等物质结合而存在心肌主要含________故能维持一定的形态，而血液中主要含 _________,故呈流体。
10.正常成人每日水的进出量大致相等,约为________毫升, 每日尿量约为_________ 毫升，最低尿量不能低于_________毫升, 否则视为少尿,造成尿毒症。
11.每克糖完全氧化时产生水_________ml, 每克脂肪完全氧化时产生水_________ml, 每克蛋白质彻底氧化产生水_________ml,混合膳食情况下,成人每日“代谢水”的产量约为_________ml。
本节重点抗利尿激素的调节作用
5
本节重点
抗利尿激素的调节作用。
6
6
一、神经调节
7
7
二、激素调节
1.抗利尿激素的调节
细胞外液 渗透压增高 + 渗透压感受器 + 视上核 血管紧张素II 疼痛、情绪紧张 + 视交叉 容量感受器 颈动脉窦 压力感受器 神经垂体 动 脉 血 压 升 高 血 容 量 增 加 -
抗利尿激素
8
水重吸收
细 胞 外 液 压 降 低
8
二、激素调节
2. 醛固酮的调节
9
9
二、激素调节
3. 心钠素的调节 血容量↑血Na+ ↑ 心房牵张 感受器 ANP↑ 钠、水重 吸收↓ 肾素-醛固酮 ↓ 10 利尿、利钠
10
限制ADH↑
全国高职高专护理类专业“十三五”规划教材
（供护理、助产专业用）
生物化学
主编 张向 常陆林
第十三章 水与电解质代谢
目录
第一节 水代谢
第二节 电解质代谢
第三节 水和电解质的调节 第四节 钙、磷代谢
第三节 水和电解质的调节
本节知识点
1.神经调节
2.抗利尿激素的调节作用
3.醛固酮的调节作用 4.心钠素的调节作用
简述水、电解质的代谢PPT课件
水和钠的代谢紊乱
▪ 在细胞外液中，水和钠的关系非常密切，故一旦 发生代谢紊乱，缺水和失钠常同时存在。在不同 原因引起的水和钠的代谢紊乱，在缺水和失钠上 的程度上也会有所不同。
▪
不同类型缺水的特征
缺水类型
等渗性 低渗性 高渗性
丢失成分
等比钠、水 钠＞水 水＞钠
典型病症
肠瘘 慢性肠梗阻 食道癌梗阻
临床表现
简述水、电解质的代谢
1
▪ 体液的主要成分是水和电解质。 ▪ 体液可分为细胞内液和细胞外液。 ▪ 电解质包括钠、钾、钙、镁、磷。
Na+ K+
2
钠的作用特点
▪ （1）调节体液渗透压、电解质平衡和酸碱平衡。 ▪ A、通过钠-钾泵，将钾离子、葡萄糖和氨基酸输入细胞内。 ▪ B、调节体内水恒定—钠多则水增加，钠少则水减少（摄
▪ （2）、水转入细胞内—见于剧烈运动、抽搐— 乳酸性酸中毒；糖原分解为小分子乳酸，使细胞 内渗透压过高，水移到细胞内。
▪ （3）原发性醛固酮症或皮质醇增多症—钠潴留。
7
低钠血症—血钠＜135mmol/L。病因：
（1）、胃肠道消化液持续性丢失，如反复呕 吐、长期胃肠减压引流或慢性肠梗阻，以 致大量钠随消化液而排出。
10
钾
▪ 体内98%的钾存在于细胞内。心肌和神经 肌肉都需要钾离子维持应激性。正常血钾： 3、5—5、5mmol/L，平均4、2mmol/L。
▪ 血清钾过高—抑制心肌—使心脏在舒张期停搏； ▪ 血清钾过低—兴奋心肌—使心脏在收缩期停搏。
▪ 对神经肌肉的作用与心肌相反。
11
高钾血症—血钾＞5、5mmol/L,高于7、 0mmol/L则为严重高钾血症。常见于：
（2）、大创面的慢性渗液。 （3）、应用排钠利尿剂（如氯噻酮、依他尼
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2）促进并参与物质代谢：因水为良好的溶剂，同时直接参加反应。
3）运输作用：因为水是良好的溶剂、粘度小、易流动。
4）润滑作用
5）维持组织、器官的形态、硬度和弹性：主要为结合水的作用。
二、水平衡——水的摄入与排出
一）摄入：饮水：约1200mL/d
食物：约1000mL/d
一、体液的分布与含量
1.分布：据分布位置不同可分为2大部分：细胞内液与细胞外液。其中细胞外液又分为血浆与组织间液（细胞间液）
2.含量：
体液总量:成人约占体重60%
细胞内液(40%)
体液:血浆(5%)
细胞外液(20%)
组织间液(15%)
3.各种体液的生理作用
细胞内液提供大部分生化反应场所
体液:血浆沟通了各组织、器官之间的联系
3．各处等渗各种体液渗透压基本相等
4．血浆与组织间液的最大差别:血浆蛋白质含量远远大于组织间液，作用：利于血浆与组织间液间水的交换
三、体液的交换
(一)血浆与组织间液之间的交换
交换部位：毛细血管
交换力量：有效滤过压
心功能不全静脉回流受阻毛细血管压水肿
低蛋白血症血浆胶体渗透压组织液回流
(二)细胞内液与组织间液之间的交换
钠是细胞外液的主要阳离子。钠主要来自食物中的盐，每天需要的氯化钠约5~9g。约有45%的钠存在于骨组织，45%的钠分布在细胞外液，只有10%的钠在细胞内液。正常人血钠浓度为136~145 mmol / L。
肾对血钠浓度的调节能力很强，血钠过高则很容易由肾排走；若过低，则刺激肾小管对钠的重吸收能力；若无钠摄入，则肾排钠量可以降至零。
水和电解质平衡的调节，钙磷代谢
主要经验
课堂讲述内容和医学实践相结合，可提高学生学习的积极性。
存在问题改进措施
入细胞极为缓慢。
静脉注射同位素钾，15h才能与细胞内钾达到平衡，心脏病患者则要45h才能达到平衡。因此，临床上在补钾时一定要慎重，首先在肾功能基本正常的前提下，应尽可能选择口服补钾。若静脉注射，则浓度不宜过高，且要缓慢、均匀地输入，以免因过多、过快而造成暂时性的高血钾。
血钾还受代谢的影响。当糖原、蛋白质合成时，钾将进入细胞内，参与反应过程。实验证明，当合成1g糖原时，有0.15mmol的钾进入细胞；而合成1g蛋白质时，将有0.45mmol的钾进入细胞。反之，当它们分解时，则有同量的钾释出细胞。因此，在创伤愈合期、组织生长旺盛期或静脉注射胰岛素加葡萄糖时，由于合成糖原和蛋白质增多，可能造成血钾下降。反之，当严重创伤（包括烧伤、大手术）、感染和缺氧的情况下，应注意有引起高血钾的可能。
使用教材
全国医药类高职高专“十二五”规划教材《生物化学》邱烈王文玉主编，第四军医大学卫生出版社，2010年1月第1版。实验指导为本校自编《生物化学实验指导》。
教案续页
基本内容
辅助手段和时间分配
第十三章水和电解质代谢
第一节体液
概念：体液是指体内由水及溶解于其中的无机盐和有机物构成的、广泛分布于细胞内外的液体。
钠作为重要的无机盐，对于人体的功能是重要的，但钠过量所造成的危害性更加令人关注。据流行病学调查，钠过量是造成高血压、肥胖及动脉硬化的重要诱发因素之一。钠在肿瘤形成过程中也起促进作用。另外，过高的钠将造成肾的损伤等。不幸的是，在我国，尤其在沿海与北方地区，钠的摄入量远超过正常需求量，应引起高度警惕。
钠主要由肾排出，少量由粪便与汗液排走。
2．最低生理需要量：1500ml/d
3．每日进出水量：2500ml/d
第三节电解质平衡
一、电解质的生理功能
1．维持体液渗透压和酸碱平衡
2．维持神经、肌肉兴奋性
各种无机离子的浓度决定神经肌肉的应激性。
无机离子对心肌细胞的应激性也大有影响。
3．构成组织细胞成分
4．参与物质代谢
二、钠、氯、钾的代谢
（一）钠的代谢
商洛职业技术学院教案教案首页
课程名称
生物化学
序次
23
专业班级
2009级护理
授课教师
王文玉
职称
副教授
类型
理论
学时
2
授课题目
(章,节)
第十三章水和电解质代谢
第一节体液
第二节水平衡
第三节电解质平衡
教学目的
与要求
1．掌握体液含量与分布特点，水、无机盐的生理功能，水的摄入与排出。
2．熟悉体液交换部位、促进力量及意义，钠、氯、钾的含量、分布、吸收与排泄特点
3．临床补钾原则：不过早，不过快，不过浓，不过量
5分钟
10分钟
此处主要讲清体液丢失量与机体的功能的关系，教育学生在健康状况良好的情况下应积极的义务献血。
10分钟
挂图或幻灯片：体液中电解质分布与含量表。结合该表引导学生自己总结特点。
10分钟
挂图或幻灯片：体液交换图
提问：体液交换的部位及生理意义是什么？
交换部位：细胞膜
交换力量：主要为细胞内、外液的Na+、K+产生的晶体渗透压
类型
交换特点
部位
力量
意义
血浆与组织间液
毛细
血管
有效
滤过压
营养物质入组织间液，代谢废物入血浆
组织间液与细胞内液
细胞膜
晶体
渗透压
营养物质入细胞，代谢废物入组织间液
第二节水平衡
一、水的功能
1．水在体内的存在状态：结合水与自由水
2．水的生理功能：
通过列表比较钠、氯、钾的来源、分布、血清中的含量、吸收、排泄特点等方面讲解钠氯钾的代谢；讲清物质代谢、氢离子的代谢对钾分布的影响，以便学生们在今后临床工作中更好的应用
教案末页
小结
5分钟
总结本次课重点内容：体液的分类与分布特点、体液中电解质分布与含量特点、水与无机盐的主要生理功能、水的来源与去路、肾脏排钠与排钾的特点
（二）钾的代谢
钾是细胞内的主要阳离子。钾主要来自植物性食物及肉类。正常成人每天需钾约2.5g。体内钾主要储存于肌细胞中，约占70%。血清中钾含量较少，约3.5~5.3mmol /L，但相当稳定。
钾主要由肾排出，肾有很强的排钾能力，但与排钠不同的是，肾对钾的控制能力远不如对钠那么严格而有效。肾每天至少排钾10mmol，即使在人体总体缺钾时，肾仍然以一定的速度排出钾。所以对长期不能进食的患者要监测其血钾含量，以确定是否需要补钾。
K+的平衡还受血浆pH的影响。当H+升高时，组织细胞膜处的H+与K+交换加强，使K+释出细胞；同时肾小管细胞泌H+作用加强，减弱了正常的K+排出。这些都可能导致高血钾。所以在临床上酸中毒易并发高血钾。反之，碱中毒将诱发低血钾。
钠、氯、钾代谢比较如下：
钠、氯、钾的代谢比较表
钠
氯
钾
体内含量约(mmol/kg)
教学重点
1.体液含量与分布特点
2.水、无机盐的生理功能
3.水的摄入与排出
4.钠、钾排泄特点
教学难点
电解质的维持神经肌肉兴奋性的作用及影响钾分布的因素
教学方法和手段
课堂讲述和多媒体教学相结合
复习内容
1.信息分子、受体的概念，受体的种类，受体作用特点
2.细胞信号转导的基本过程,环核苷酸信号转导途径
3.G蛋白结构特点,PKA、PKC、CaM-PK、TPK的激活及作用（5分钟）
复习思考题
及作业题
1．何谓体液？体液中电解质分布与含量有何特点？
2．体液交换的部位及生理意义是什么？
3．体内水有何作用？水的正常出入量为多少？水有哪些来源与去路？
4．电解质有何生理功能？
5．钾对心肌的作用是什么？低血钾与高血钾对机体有何危害？
6．肾排泄钠钾有何特点？哪些因素影响钾的分布？
下次教学
预习要点
按含量不同可分为：
1.主要电解质：主要有K+、Na+、Ca2+、Mg2+、Cl-、HCO3-、HPO42-、有机酸根和Pr-等
2.微量电解质：主要有铁、铜、锌、硒、碘、钴、锰、钼、氟、硅等
(二)体液电解质分布的特点
1．各处等电，即电中性
2．细胞内液主要阳、阴离子为K+、HPO42-和蛋白质阴离子；细胞外液主要阳、阴离子为Na+、Cl-、HCO3-
40~50
47
31~57
血清浓度约（mmol/L）
142
103
3.5~5.5
主要分布
细胞外液与骨
细胞外液
细胞内液
来源
食盐
食盐
各动植物食物
吸收
小肠
小肠
小肠
排泄
肾
肾
肾
排泄特点
多吃多排
少吃少排
不吃不排
伴钠而排
多吃多排
少吃少排
不吃也排
注意：
1．肾对钠、钾排泄特点的不同
2．物质代谢、氢离子的代谢对钾分布有影响
列表比较各种体液交换特点
10分钟
提问：体内水有何作用？
10分钟
提问：水的正常出入量为多少？水有哪些来源与去路？
注意讲清这组数字的来源及临床意义
10分钟
提问：电解质有何生理功能？
提问：钾对心肌的作用是什么？低血钾与高血钾对机体有何危害？
15分钟
提问：肾排泄钠钾有何特点？
提问：哪些因素影响钾的分布？
幻灯片：钠、氯、钾的来源、分布、血清中的含量、吸收、排泄特点比较表
代谢水：约300mL/d
共计：约2500ml/d
二）排出：呼吸蒸发：约350mL/d
皮肤蒸发：约500mL/d（按非显性出汗计）
粪便排出：约150mL/d
肾脏排尿：约1500mL/d
共计：约2500 mL/d