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1、Water and electrolytes disturbances Sodium balance Hypovolemia Water balance Hyponatremia Hypernatremia Potassium balance Hypokelemia hyperkelemiaICFECFISFIVF2/31/31/32/340% bw15% bw5% bw20% bw60% bwICF2/31/31/32/340% bw15% bw5% bw20% bw60% bwNa25150150.0126501404.51.22.4100251.2NaKMgCaClHCO3PhosWat
2、er and electrolytes disturbances Sodium balance Hypovolemia Water balance Hyponatremia Hypernatremia Potassium balance Hypokelemia hyperkelemiaSodium Balance In the steady state, urinary Na = dietary salt intake. This balance depends on: Afferent mechanisms that sense the volume of the ECF compartme
3、nt relative to its capacitance Effector mechanisms that modify the rate of renal sodium excretion收收縮縮血管血管心率心率腎臟腎臟重吸收重吸收收收縮縮血管血管腎臟腎臟重吸收重吸收口干口干收收縮縮血管血管腎臟腎臟水重吸收水重吸收Hypovolemia A reduction in the volume of the ECF compartment in relation to its capacitance. absolute hypovolemia, a deficit in sodium refl
4、ects negative sodium balance. Causes of hypovolemiaClinical features History: vomiting, diarrhea, trauma Symptoms: Thirst, postural dizziness, oliguria, cyanosis, Signs of intravascular volume contraction: decreased jugular venous pressure, postural hypotension, postural tachycardia Large and more a
5、cute fluid losses lead to hypovolemic shock: hypotension, tachycardia, peripheral vasoconstriction and hypoperfusion: (cyanosis, cold and clammy extremities, oliguria and altered mental status) 病史： 腎外：GI、皮膚、呼吸道； 腎臟丟失； 相對(duì)不足 臨床表現(xiàn)：組織灌流不足、機(jī)體代償反應(yīng) 輕度：心率加快、口干 中度：體位性低血壓、心動(dòng)過(guò)速、中心靜脈壓下降 大量、快速：休克Diagnosis Histor
6、y & physical examination Labs: BUN, SCr, BUN/SCr (20) UNa 20 mmol/L (exception: ATN, Vomiting, diuretics), UCl 20 mmol/L (GI)Treatment Goal: restore normovolumia Mild volume contraction: oral route Severe hypovolemia: IVWater and electrolytes disturbances Sodium balance Hypovolemia Hypervolemia Wate
7、r balance Hyponatremia Hypernatremia Potassium balance Hypokelemia hyperkelemiaPRIMARY AND SECONDARY RENAL SODIUM-RETAINING STATES Water and electrolytes disturbances Sodium balance Hypovolemia Water balance Hyponatremia Hypernatremia Potassium balance Hypokelemia hyperkelemia Filtration Active Na,
8、Cl reabsorption in TAL AVP尿比重尿比重尿滲透尿滲透壓壓改良莫改良莫- -森森試驗(yàn)試驗(yàn)自由水清除率自由水清除率NCC噻嗪類(lèi)噻嗪類(lèi)利尿利尿劑劑x Water balance is regulated mainly by thirst and urine concentration mechanism Maximal urine osmolality: 1200 mosmol/kg Minimal urine osmolality: 50 mosmo/kg Normally about 600 mosmols must be excreted per day The pri
9、ncipal determinant of renal water excretion is AVPAVP AVP secretion: systemic osmolality, threshold level of 285 mosmol/kg. blood volume and blood pressure. Nonosmotic stimuli: nausea, intracerebral angiotensin II, serotonin, and multiple drugs. Half-life in the circulation: 1020 minAVP AVP secretio
10、n: systemic osmolality, threshold level of 285 mosmol/kg. blood volume and blood pressure. Nonosmotic stimuli: nausea, intracerebral angiotensin II, serotonin, and multiple drugs. Half-life in the circulation: 1020 minAVP AVP secretion: systemic osmolality, threshold level of 285 mosmol/kg. blood vo
11、lume and blood pressure. Nonosmotic stimuli: nausea, intracerebral angiotensin II, serotonin, and multiple drugs. Half-life in the circulation: 1020 minHyponatremia Plasma sodium concentration less than 135 mmol/L, Hypo-osmolar Disorders Depletion: Primary Decreases in Total Body Solute + Secondary
12、Water Retention Dilution: Primary Increases in Total Body Water Secondary Solute Depletion 低容量性低血鈉 經(jīng)腎丟失 利尿劑：噻嗪類(lèi) 低容量性低血鈉 經(jīng)腎丟失 利尿劑：噻嗪類(lèi) 小管間質(zhì)性疾病 腎外丟失：GI、皮膚、腦性失鹽綜合癥 等容量性 SIADH 進(jìn)入大量水和低鈉溶液 甲狀腺功能低下 腎上腺皮質(zhì)功能低下 高容量性低鈉血癥 水腫性疾?。盒乃?、肝硬化、腎病綜合癥 急、慢性腎衰 SIADH 低容量性低血鈉 經(jīng)腎丟失 利尿劑：噻嗪類(lèi) 小管間質(zhì)性疾病 腎外丟失：GI、皮膚、腦性失鹽綜合癥 等容量性 SIADH
13、進(jìn)入大量水和低鈉溶液 甲狀腺功能低下 腎上腺皮質(zhì)功能低下 高容量性低鈉血癥 水腫性疾病：心衰、肝硬化、腎病綜合癥 急、慢性腎衰 SIADHCauses of SIADHThe adaptation begins on the first and is complete within several daysClinical features The symptoms are primarily neurologic. Symptoms include headache, lethargy, seizures, and a progressively decreased level of con
14、sciousness that can progress to coma and death. Like drunk (chronic) The severity of these neurologic manifestations depends more on the rate of the hypotonic decline in plasma sodium concentration. 明確是否真性低鈉血癥 高血糖、高脂血癥、異常蛋白血癥 判斷血漿滲透壓下降速度和有效血容量 原發(fā)病的鑒別診斷Treatment Is the hyponatremia acute or chronic?
15、Does the patient have severe symptoms or intracranial pathology? What is the optimal rate of correction? Avoid overly rapid correction Overly rapid correction of severe hyponatremia can lead to osmotic demyelination syndrome Most cases of osmotic demyelination syndrome have occurred in patients with
16、 severe hyponatremia sodium concentration increased by more than 10 to 12 meq/L within 24 hours or more than 18 meq/L within 48 hoursThe Clinical Course in Seven Women Who Had Post-operative HyponatremiaArieff AI NEJM 1986;314:1529Hypernatremia Hypernatremia, defined as a plasma sodium concentration
17、 greater than 145 mmol/L, always reflects a state of hypertonicity.Causes of Hypernatremia Hypovolemia: associated with low total body sodium losses of both Na+ and water, but with a relatively greater loss of water: diarrheas, diuretics Euvolemia: associated with normal body sodium Most patients wi
18、th hypernatremia secondary to water loss appear euvolemic with normal total body Na+: febrile, mechanical ventilation, sweating Hypervolemia: associated with increased total body sodium administration of hypertonic solutions such as 3% NaCl, NaHCO3. Therapeutic hypernatremia: hypertonic saline solut
19、ions have emerged as a preferable alternative to mannitol for treatment of increased intracranial pressureDiabetes insipidus (DI) Characterized by polyuria and polydipsia Caused by defects in vasopressin action. central DI nephrogenic DI The differentiation between these entities: vasopressin levels
20、 and the response to a water deprivation test followed by vasopressin administration Clinical Manifestations Signs and symptoms mostly relate to the CNS and include altered mental status, lethargy, irritability, restlessness, seizures (usually in children), muscle twitching, hyperreflexia, and spast
21、icity. Fever, nausea or vomiting, labored breathing, and intense thirst can also occur. In adults, serum Na+ concentrations above 160 mmol/l are associated with a 75% mortality, although this may reflect associated comorbidities rather than hypernatremia per se Treatment of Hypernatremia Hypernatrem
22、ia occurs in predictable clinical settings, allowing opportunities for prevention recovery from acute kidney injury, catabolic states, therapy with hypertonic solutions, uncontrolled diabetes burns Water deficit should be corrected slowly over 48 72h. The plasma Na concentration be lowered by 0.5 mm
23、ol/l/h and by no more than 12 mmol/L over the 1st 24h Route: mouth or via a nasogastric tube or 5% dextrose or half-isotonic saline iv CDI Desmopressin Low salt diet + low-dose thiazide diuretics Drugs that stimulate AVP section or enhance its actionPotassium balance K intake: 1 mmol/kg/d Immediatel
24、y following a meal, most K enter cells (plasma K, insulin, catecholamine) Steady state, K ingestion matches with excretion 細(xì)胞內(nèi)外K平衡 影響ATPase： 胰島素、b2腎上腺素受體激動(dòng)劑、醛固酮促進(jìn)K進(jìn)入細(xì)胞； a腎上腺素受體激動(dòng)劑促進(jìn)K出細(xì)胞 酸堿 高滲 K攝入和排泄 每日飲食攝入 1mmol/kg, 90%從腎臟排出 腎臟維持K平衡中的作用 細(xì)胞內(nèi)外K平衡 影響ATPase： 胰島素、b2腎上腺素受體激動(dòng)劑、醛固酮促進(jìn)K進(jìn)入細(xì)胞； a腎上腺素受體激動(dòng)劑促進(jìn)K出細(xì)胞
25、酸堿 高滲 K攝入和排泄 每日飲食攝入 1mmol/kg, 90%從腎臟排出 腎臟維持K平衡中的作用 The filtered K is 10 -20 fold of ECF K content 90% of filtered K is reabsorbed in proximal tubule and loop of Henle All regulation of renal K excretion and total body K balance occurs in the distal nephron K secretion is regulated by aldosterone and
26、 hyperkalemia K secretion is facilitated by increased distal Na deliveryHigh sodium delivery and high levels of aldo Hypokalemia refers to a low plasma K+. Etiology Redistribution Increased net loss: extrarenal potassium loss renal potassium loss Decreased net intake Pseudohypokalemia Metabolic alka
27、losis Insulin (diabetic ketoacidosis) Stress-induced catecholamine/Beta2 agonist Hypokalemic periodic paralysis genetic defect in a dihydropyridine-sensitive calcium channel hyperthyroidism Excessive sweating Diarrhea Vomiting or gastric suction metabolic alkalosis the intravascular volume depletion
28、 result in secondary hyperaldosteronism NaHCO31. Increased collecting duct Na reabsorption2. Volume expansion3. Increased K section低血鉀低血鉀+ +堿中毒堿中毒+ +高血壓高血壓低血鉀低血鉀+ +堿中毒堿中毒+ +正常血壓正常血壓低血鉀低血鉀+ +酸中毒酸中毒+ +正常血壓正常血壓 Hypokalemia may produce electrocardiographic (ECG) abnormalities: including a flattened T wa
29、ve and a U wave Severe hypokalemia is associated with variable degrees of skeletal muscle weakness, even to the point of paralysis On rare occasions, diaphragmatic paralysis from hypokalemia can lead to respiratory arrest There may also be decreased motility of smooth muscle, manifesting with ileus
30、or urinary retention Rarely, severe hypokalemia can result in rhabdomyolysisTreatment The primary short-term risks are cardiovascular arrhythmias and neuromuscular symptoms. Conditions requiring urgent therapy are rare. The clearest indications are hypokalemic periodic paralysis, severe hypokalemia
31、in a patient requiring urgent surgery acute myocardial infarction in the patient with significant ventricular ectopy Severe hypokalemia or those unable to take anything by mouth require IV replacement Maximum concentration: 40 mmol/L via peripheral vein or 60 mmol/L via a central vein The rate of in
32、fusion should not exceed 20 mmol/h unless paralysis or malignant ventricular arrhythmias are present 病因治療 糾正低鎂血癥 鉀細(xì)胞內(nèi)外平衡需15小時(shí) 使用洋地黃和抗心律失常藥物患者，低鉀易發(fā)嚴(yán)重心律失常；肝性腦病患者，低鉀增加氨的產(chǎn)生Etiology Metabolic acidosis (hyperchloremic acidosis) Insulin deficiency and hyperglycemia Beta-blockers Hyperkalemic periodic paral
33、ysis (autosomal dominant)Etiology Pseudohyperkalemia Redistribution severe hyperglycemia (due to effects of osmolarity) Insulin deficiency severe nonorganic acidosis -blockers. Hyperkalemic peroidic paralysis Rhabdomyolysis Excess Intake if renal potassium excretion is impaired, for example, by drug
34、s or renal impairment Etiology cont Impaired Renal Potassium Secretion chronic hyperkalemia is difficult to produce unless renal potassium secretion is impaired. Factors that affect renal potassium excretion are classified into those due to reduced nephron number and those due to intrinsic impairmen
35、t of renal potassium handling. Etiology cont Specific Medicines The renin-angiotensin-aldosterone Intrinsic Renal Defect pseudohypoaldosteronism type 2, ( Gordons syndrome) hypertension, hyperkalemia, metabolic acidosis, and normal GFR Mutations in WNK1 or WNK4, increase sodium absorption and inhibi
36、t potassium secretion in the distal convoluted tubule and collecting ductClinical manifestation Hyperkalemia may be asymptomatic but still life-threatening The most prominent effect of hyperkalemia is alteration of cardiac conduction. This is demonstrable on the ECG. Hyperkalemia also affects muscle
37、 contraction. weakness severe hyperkalemia, respiratory failure may occur from paralysis of the diaphragm. Metabolic acidosis: hyperkalemia inhibits renal ammoniagenesisTreatment Approach to therapy depends on the degree of hyperkalemia as determined by Plasma K concentration Muscular weakness ECG S
38、evere hyperkalemia requires emergent treatment Minimizing membrane depolarization Shifting K into cells Promoting K lossClinical features History: vomiting, diarrhea, trauma Symptoms: Thirst, postural dizziness, oliguria, cyanosis, Signs of intravascular volume contraction: decreased jugular venous
39、pressure, postural hypotension, postural tachycardia Large and more acute fluid losses lead to hypovolemic shock: hypotension, tachycardia, peripheral vasoconstriction and hypoperfusion: (cyanosis, cold and clammy extremities, oliguria and altered mental status)Diagnosis If the etiology is not readi
40、ly apparent and the patient is asymptomatic, pseudohyperkalemia should be excluded Medications that impair K handling and sources of K intake The severity of hyperkalemia is determined by Symptoms Plasma K concentration ECGBlood Urea Nitrogen (BUN)Urea is the main waste product of nitrogen-containin
41、g chemicals in the body.Urea is freely filtered, Approximately 40 to 50 percent of the filtered urea is passively reabsorbed, mostly in the proximal tubule. Urea1.Dietary Protein2.Endogenous protein 低容量性低血鈉 經(jīng)腎丟失 利尿劑：噻嗪類(lèi) 小管間質(zhì)性疾病 腎外丟失：GI、皮膚、腦性失鹽綜合癥 等容量性 SIADH 進(jìn)入大量水和低鈉溶液 甲狀腺功能低下 腎上腺皮質(zhì)功能低下 高容量性低鈉血癥 水腫性疾
42、?。盒乃?、肝硬化、腎病綜合癥 急、慢性腎衰 SIADH提升血清提升血清鈉鈉的方法的方法 Treat the underlying disease, if possible. Fluid restriction. Sodium Oral or intravenous sodium chloride in patients with true volume depletion. In patients the with SIADH using either oral salt tablets or hypertonic saline. In contrast, isotonic saline is often not effective and may worsen the hyponatremia in SIADH. Salt administration is generally contraindicated for chronic therapy in edematous patients (eg, heart failure, cirrhosis, renal failure) Administration of a vasopressin receptor antagonist.
內(nèi)科學(xué)課件：33 electrolytes acid base
