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学术前沿

威胁生命的电解质异常

发表者:张勇 2362人已读

整理:张勇  烟台经济技术开发区医院重症医学科(ICU)

Electrolyte abnormalities are commonly associated with cardiovascular emergencies. These abnormalities may cause or contribute to cardiac arrest and may hinder resuscitative efforts. In some cases therapy for life-threatening electrolyte disorders should be initiated before laboratory results become available.烟台业达医院ICU张勇

电解质异常通常伴随着心血管紧急事件,可引起或者加重心脏停搏,也可导致复苏不成功。某些情况下,不必等到可靠的实验室检查结果,就应开始治疗威胁生命的电解质异常。

一、Potassium (K)

The magnitude of the potassium gradient across cell membranes determines excitability of nerve and muscle cells, including the myocardium. Rapid or significant changes in the serum potassium concentration can have life-threatening consequences.

一、钾离子(K

细胞膜内外钾离子浓度梯度决定了神经细胞和肌肉细胞(包括心肌细胞)的兴奋性,血清钾浓度的快速或严重变化会带来生命危险。

Evaluation of serum potassium must consider the effects of changes in serum pH. When serum pH falls, serum potassium rises because potassium shifts from the cellular to the vascular space. When serum pH rises, serum potassium falls because potassium shifts from the vascular space into the cells. Effects of pH changes on serum potassium should be anticipated during therapy for hyperkalemia or hypokalemia and during any therapy that may cause changes in serum pH (eg, treatment of diabetic ketoacidosis).

对血清钾浓度的判断必须考虑到血清pH变化对血钾浓度的影响。当pH下降时,钾离子从细胞内转移到血管内,因此血清钾升高。当pH升高时,钾离子从血管内转移到细胞内,血清钾下降。在治疗高钾血症或低钾血症,以及任何可能引起血清pH变化的疾病时(如糖尿病酮症酸中毒的治疗),应想到pH改变对血清钾浓度的影响。

1、Hyperkalemia

Although hyperkalemia is defined as a serum potassium concentration >5 mEq/L, it is moderate (6 to 7 mEq/L) and severe (>7 mEq/L) hyperkalemia that are life-threatening and require immediate therapy. Hyperkalemia is most commonly seen in patients with end-stage renal disease. Other causes are listed in the Table. Many medications can contribute to the development of hyperkalemia. Identification of potential causes of hyperkalemia will contribute to rapid identification and treatment1–3.

1、高钾血症

高钾血症是指血清钾浓度>5 mEq/L,中度(6~7mEq/L)和重度(>7mEq/L)高钾血症常危及生命,需要立即给予治疗。高钾血症最常见于终末期肾脏病患者,其他原因见表。许多药物也可以导致高钾血症,识别引起高钾的潜在原因有利于快速识别和治疗高钾血症[1~3]

TABLE1. Common Causes of Hyperkalemia

Endogenous Causes

● Chronic renal failure

● Metabolic acidosis (eg, diabetic ketoacidosis)

● Pseudohypoaldosteronism type II (also known as Gordon’s syndrome; familial

hyperkalemia and hypertension)

● Chemotherapy causing tumor lysis

● Muscle breakdown (rhabdomyolysis)

● Renal tubular acidosis

● Hemolysis

● Hypoaldosteronism (Addison’s disease, hyporeninemia)

● Hyperkalemic periodic paralysis Exogenous Causes

● Medications: K_-sparing diuretics, ACE inhibitors, nonsteroidal anti-inflammatory

drugs, potassium supplements, penicillin derivatives, succinylcholine, heparin therapy (especially in patients with other risk factors), _-blockers

● Blood administration (particularly with large transfusions of older “bank” blood)

● Diet (rarely the sole cause), salt substitutes

● Pseudohyperkalemia (due to blood sampling or hemolysis, high white blood cell

count, high platelets, tumor lysis syndrome

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

内因:

慢性肾衰、代谢性酸中毒:如糖尿病酮症酸中毒、高钾性周期性麻痹、肾小管性酸中毒、溶血

II型假性醛固酮减少症:也称Gordon’s综合征;家族性高钾血症和高血压

化疗引起肿瘤溶解、肌肉破坏:横纹肌溶解症、醛固酮减少症(艾迪森氏病,肾素减少症)

外因:

药物:保钾利尿剂、ACEI、非甾体类抗炎药、钾补充剂、青霉素衍生物、琥珀胆碱、

肝素治疗(尤其是合并有其他危险因素者)、β受体阻滞剂

输血:(尤其是输大量库存血)、节食:(很少是单独原因),盐替代品

假性高钾血症:由于血样溶血,白细胞数增高,血小板增多,肿瘤溶解综合征)

ns and symptoms of hyperkalemia include weakness, ascending paralysis, and respiratory failure. A variety of electrocardiographic (ECG) changes suggest hyperkalemia. Early findings include peaked T waves (tenting). As the serum potassium rises further, flattened P waves, prolonged PR interval (first-degree heart block), widened QRS complex, deepened S waves, and merging of S and T waves can be seen. If hyperkalemia is left untreated, a sine-wave pattern, idioventricular rhythms, and asystolic cardiac arrest may develop.

高钾血症的症状和体征包括虚弱无力、上行性麻痹和呼吸衰竭。高钾血症时出现多种心电图改变,早期T波高尖(幕状的),随着血钾浓度的进一步升高,出现P波低平,PR间期延长(一度房室传导阻滞),QRS波群变宽,S波加深以及S波和T波融合。如果高钾血症未及时处理,可能会出现正弦波,心室自主心律和心脏停搏。

Treatment of Hyperkalemia

The treatment of hyperkalemia is determined by its severity and the patient’s clinical condition. Stop sources of exogenous potassium administration (eg, consider supplements and maintenance IV fluids) and evaluate drugs that can increase serum potassium (eg, potassium-sparing diuretics, angiotensin- converting enzyme [ACE] inhibitors, nonsteroidal antiinflammatory agents). Additional treatment is based on the severity of the hyperkalemia and its clinical consequences. The following sequences list the treatments for hyperkalemia in order of priority.

高钾血症的治疗

高钾血症的治疗取决于高钾的严重程度和病人的临床情况。首先停止外源性钾摄入(比如,静脉液体的补充和维持),停服能引起血清钾升高的药物(如保钾利尿剂、ACEI和非甾体类抗炎药)。进一步治疗需要根据高钾的严重程度和病人的临床情况决定。可按以下顺序采取治疗措施。

For mild elevation (5 to 6 mEq/L), remove potassium from the body with

1. Diuretics: furosemide 40 to 80 mg IV

2. Resins: Kayexalate 15 to 30 g in 50 to 100 mL of 20% sorbitol either orally or by retention enema

轻度高钾(5~6 mEq/L):去除钾的来源后,可以采取下列治疗:

1、利尿剂:速尿40~80 mg静脉注射;

2、树脂:聚苯乙烯磺酸钠(阳离子交换树脂)15~30g加入20%山梨醇溶液50~100mL口服或保留灌肠。

For moderate elevation (6 to 7 mEq/L), shift potassium intracellularly with

1. Glucose plus insulin: mix 25 g (50 mL of D50) glucose and 10 Uregular insulin and give IV over 15 to 30 minutes.

2. Sodium bicarbonate: 50 mEq IV over 5 minutes (sodium bicarbonate alone is less effective than glucose plus insulin or nebulized albuterol, particularly for treatment of patients with renal failure; it is best used in conjunction with these medications 4,5).

3. Nebulized albuterol: 10 to 20 mg nebulized over 15 minutes

中度高钾((6~7 mEq/L):促进血清钾转移到细胞内:

1、葡萄糖+胰岛素:25g葡萄糖(50%GS50mL)加普通胰岛素10U静脉注射(15~30分钟);

2、碳酸氢钠:50 mEq静脉注射,5分钟推完(碳酸氢钠单独使用的效果不及葡萄糖加胰岛素或舒喘灵雾化吸入,尤其是在治疗肾衰患者时,最好能与其他药物联合使用[4~5]);

3、舒喘灵雾化吸入:10~20mg雾化吸入,15分钟吸完。

For severe elevation (>7 mEq/L with toxic ECG changes), you need to shift potassium into the cells and eliminate potassium from the body. Therapies that shift potassium will act rapidly but they are temporary; if the serum potassium rebounds you may need to repeat those therapies. In order of priority, treatment includes the following:

重度高钾(>7 mEq/L并有心电图上毒性表现),需要转移钾离子到细胞内,清除体内过多的钾。转移钾离子的治疗起效很快,但是作用短暂。如果钾离子重新返回血液,必须重复治疗措施。有序的治疗措施如下:

● Shift potassium into cells:

1. Calcium chloride (10%): 500 to 1000 mg (5 to 10 mL) IV over 2 to 5 minutes to reduce the effects of potassium at the myocardial cell membrane (lowers risk of ventricular fibrillation [VF])

2. Sodium bicarbonate: 50 mEq IV over 5 minutes (may be less effective for patients with end-stage renal disease)

3. Glucose plus insulin: mix 25 g (50 mL of D50) glucose and 10Uregular insulin and give IV over 15 to 30 minutes

4. Nebulized albuterol: 10 to 20 mg nebulized over 15minutes 5–7

● Promote potassium excretion:

5. Diuresis: furosemide 40 to 80 mg IV

6. Kayexalate enema: 15 to 50 g plus sorbitol PO or per rectum

7. Dialysis

● 转移钾离子到细胞内:

1、10%氯化钙:500~1000mg(5~10mL)静脉注射,2~5分钟推完,以减少钾对心肌细胞膜的影响(降低室颤[VF]危险);

2、碳酸氢钠:50 mEq在5分钟以上静脉推完(对终末期肾脏病患者效果欠佳);

3、葡萄糖+胰岛素:25g葡萄糖(50%GS50mL)加普通胰岛素10U静脉注射(15~30分钟);

4、舒喘灵雾化吸入:10~20mg在15分钟雾化吸入[5~7]

● 促进钾排泄:

5、利尿剂:速尿40~80 mg静脉注射;

6、聚苯乙烯磺酸钠灌肠剂:15~50g加入山梨醇溶液口服或保留灌肠;

7、透析。

 

2、Hypokalemia

Hypokalemia is defined as a serum potassium level <3.5 mEq/L. The most common causes of low serum potassium are gastrointestinal loss (diarrhea, laxatives), renal loss (hyperaldos- teronism, severe hyperglycemia, potassiumdepleting diuretics, carbenicillin, sodium penicillin, amphotericin B), intracellular shift (alkalosis or a rise in pH), and malnutrition.

2、低钾血症

血清钾浓度<3.5 Eq/L称为低钾血症。低钾最常见的原因是胃肠丢失(腹泻或者服用泻药)、肾脏丢失(醛固酮增多症、严重高血糖、排钾利尿剂、羧苄青霉素、青霉素钠和两性霉素B)、细胞内转移(碱中毒或pH值升高)和营养不良。

The major consequences of severe hypokalemia result from its effects on nerves and muscles (including the heart). The myocardium is extremely sensitive to the effects of hypokalemia, particularly if the patient has coronary artery disease or is taking a digitalis derivative. Symptoms of mild hypokalemia are weakness, fatigue, paralysis, respiratory difficulty, constipation, paralytic ileus, and leg cramps; more severe ypokalemia will alter cardiac tissue excitability and conduction. Hypokalemia can produce ECG changes such as U waves, T-wave flattening, and arrhythmias (especially if the patient is taking digoxin), particularly ventricular arrhythmias. Pulseless electrical activity or asystole may develop.

严重低钾的后果主要在于对神经肌肉的影响(包括心脏)。心肌对低钾尤其敏感,特别是当病人患有冠心病或正在服用洋地黄类药物时。轻度低钾表现为软弱无力、瘫痪、呼吸困难、便秘、麻痹性肠梗阻和腿部肌肉痛性痉挛;更严重的低钾会改变心肌组织的兴奋性和传导性。低钾血症的心电图改变有出现U波、T波低平、心律失常(特别是当病人正在服用地高辛时),室性心律失常尤为多见,无脉性电活动和心脏停搏也可发生。

Treatment of Hypokalemia

The treatment of hypokalemia consists of minimizing further potassium loss and providing potassium replacement. IV administration of potassium is indicated when arrhythmias are present or hypokalemia is severe (potassium level of<2.5 mEq/L). Gradual correction of hypokalemia is preferable to rapid correction unless the patient is clinically unstable

低钾血症的治疗

低钾血症的治疗包括尽量减少钾丢失和补钾。有心律失常或严重低钾(血钾<2.5 mEq/L=是静脉补钾的适应症。除了病人的临床状况十分不稳定外,缓慢纠正低钾血症比快速纠正低钾效果更好。

Administration of potassium may be empirical in emergent conditions. When indicated, the maximum mount of IV potassium replacement should be 10 to 20mEq/h with continuous ECG monitoring during infusion. A more concentrated solution of potassium may be infused if a central line is used, but the tip of the catheter used for the infusion should not extend into the right atrium.

在紧急情况下补钾是经验性的,有补钾指征时,静脉补钾的最大剂量可以达到10~20 mEq/h,输入过程中要有心电图连续监测。如果中心静脉开放,补钾溶液的浓度可以更大,但要避免导管的顶端伸入右心房。

If cardiac arrest from hypokalemia is imminent (ie, malignant ventricular arrhythmias are present), rapid replacement of potassium is required. Give an initial infusion of 10 mEq IV over 5 minutes; repeat once if needed. Document in the patient’s chart that rapid infusion is intentional in response to life-threatening hypokalemia.

低钾血症造成的心脏停搏情况十分危急(尤其是出现恶性室性心律失常时),常需要快速补钾。起始剂量10 mEq静脉注射,5分钟推完;如有必要可重复一次。对威胁生命的低钾血症,快速补钾应在病历中记录。

二、Sodium (Na+)

Sodium is the major intravascular ion that influences serum osmolality. An acute increase in serum sodium will produce an acute increase in serum osmolality; an acute decrease in serum sodium will produce an acute fall in serum osmolality.

二、钠(Na+

钠是血管内影响血浆渗透压的主要离子。血清钠急剧升高将使血浆渗透压急剧升高,血清钠迅速下降也将使血浆渗透压迅速下降。

Sodium concentration and osmolality in the intravascular and interstitial spaces equilibrate across the vascular membrane. Acute changes in serum sodium will produce free water shifts into and out of the vascular space until osmolality equilibrates in these compartments. An acute fall in serum sodium will produce an acute shift of free water from the vascular into the interstitial space and may cause cerebral edema.8,9 An acute rise in serum sodium will produce an acute shift of free water from the interstitial to the vascular space. Rapid correction of hyponatremia has been associated with development of pontine myelinolysis and cerebral bleeding 10.12. For these reasons, monitor neurologic function closely in the patient with hypernatremia or hyponatremia, particularly during correction of these conditions. Whenever possible, correct serum sodium slowly, carefully controlling the total change in serum sodium over 48 hours and avoiding overcorrection.13,14

钠离子浓度和血管内渗透压以及组织间隙渗透压通过血管膜保持平衡。血清钠急剧变化将引起自由水进出血管,直到各部分渗透压达到平衡。血清钠急剧下降会引起自由水快速转移到组织间隙,可能导致脑水肿[8,9]。同样,血清钠急剧升高会使自由水从组织间隙快速转移到血管腔内。快速纠正低钠常伴随着脑桥脱髓鞘病变和大脑出血 [10~12]。基于上述原因,对高钠或低钠病人,特别是在治疗时,应该密切观察神经系统功能变化。无论什么时候,都要在48小时以上缓慢纠正血清钠异常,注意机体的整体变化,避免矫枉过正 [13,14]

1、Hypernatremia

Hypernatremia is defined as a serum sodium concentration>145 to 150mEq/L. It may be caused by a primary gain in Na_ or excess loss of water. Gains in sodium can result from hyperaldosteronism (excess mineralocorticoid), Cushing’s syndrome (excess glucocorticoid), or excessive hypertonic saline or sodium bicarbonate administration. Loss of free water can result from gastrointestinal losses or renal excretion(eg, osmotic diuresis or diabetes insipidus). Hypernatremia may cause neurologic symptoms such as altered mental status, weakness, irritability, focal neurologic deficits, and even coma or seizures. The severity of symptoms is determined by the speed and magnitude of the change in serum sodium concentration.

1、高钠血症

血清钠浓度>145~ 150 mEq/L 称为高钠血症 。引起高钠的原因可以是钠摄入过多,也可以是水分丢失过多。钠过多的原因包括醛固酮增多症(盐皮质激素过多)、库欣氏综合征(糖皮质激素过多)、过多输入高张生理盐水或碳酸氢钠。水分丢失常因胃肠丢失或肾脏排泄(如渗透性利尿或尿崩症)。高钠血症可以引起神经系统症状,如意识状态改变,虚弱无力,易激惹,局灶性神经功能缺失,甚至昏迷或癫痫发作。临床症状的严重程度取决于血清钠浓度改变的速度和程度。

Treatment of hypernatremia includes reduction of ongoing water losses (by treating the underlying cause) and correction of the water deficit. For stable, asymptomatic patients, replacement of fluid by mouth or through a nasogastric tube is effective and safe.

高钠血症的治疗主要是防止继续失水(治疗基础疾病)和纠正缺水。对于病情稳定的无症状患者,口服或通过鼻胃管补充液体是安全有效的。

In hypovolemic patients the extracellular fluid (ECF) volume is typically restored with normal saline or a 5% dextrose in half-normal saline solution to prevent a rapid fall in the serum sodium concentration. Avoid D5W because it will reduce the serum sodium too rapidly. During rehydration, monitor serum sodium closely to ensure a gradual fall (and prevent rapid fall) in serum sodium.

血容量不足的病人,最好用生理盐水或者5%葡萄糖加同等量生理盐水来恢复细胞外液(ECF)容量,以防血钠浓度快速下降。应避免单独输入5%葡萄糖溶液,因为这样会导致血钠快速下降。补液过程中要密切监测血钠水平,保证血钠逐渐缓慢下降(避免快速下降)。

The quantity of water needed to correct hypernatremia can be calculated by using the following equation:

纠正高钠血症的需水量可以通过下面公式计算:

Water deficit (in liters)=plasma Na+ concentration-140/140× total body water

需水量(升)=(血浆钠浓度-140)/140×体液总量

Total body water is approximately 50% of lean body weight in men and 40% of lean body weight in women. For example, if a 70-kg man had a serum Na_ level of 160mEq/L, the estimated free water deficit would be 160-140×(0.5×70)=5 L      140

体液量约占男性体重的50%,女性体重的40%。例如,如果一个70公斤的男性患者血清钠浓度为160mEq/L,估计的缺水量为160-140×(0.5×70)=5L                    140

Once the free water deficit is calculated, administer fluid to lower serum sodium at a rate of 0.5 to 1 mEq/h with a decrease of no more than approximately 12mEq/L in the first 24 hours and the remainder over the next 48 to 72 hours.

计算出需水量后,第一个24小时以0.5 ~ 1 mEq/h的速度输入液体以降低血钠,使血钠下降不超过12 mEq/L,余下的液体量在以后的48~72小时输入。

2、Hyponatremia

Hyponatremia is defined as a serum sodium concentration<130 to 135 mEq/L. It is caused by an excess of water relative to sodium. Most cases of hyponatremia are caused by reduced renal excretion of water with continued water intake or by loss of sodium in the urine. Impairment of renal water excretion may be caused by

2、低钠血症

血清钠浓度<130~135mEq/L称为低钠血症,主要指水相对多于钠。大多数低钠血症的病人见于肾脏排水减少但仍继续摄水,或者尿中失钠过多。肾排水异常可由以下原因引起:

● Use of thiazide diuretics

● Renal failure

● ECF depletion (eg, vomiting with continued water intake)

● Syndrome of inappropriate antidiuretic hormone (SIADH) secretion

● Edematous states (eg, congestive heart failure, cirrhosis with ascites)

● Hypothyroidism

● Adrenal insuffici

使用噻嗪利尿剂

肾功能衰竭

细胞外液丢失(例如,呕吐后只补充水分)

抗利尿素分泌失调综合征(SIADH)

水肿(如充血性心力衰竭、肝硬化腹水)

甲状腺功能低下

肾上腺功能不全

Most cases of hyponatremia are associated with low serum osmolality (so-called hypo-osmolar hyponatremia). The one common exception to this is in uncontrolled diabetes, in which hyperglycemia leads to a hyperosmolar state despite aserum sodium that is below normal (hyperosmolar hyponatremia).

大多数低钠血症的病人血清渗透压降低(所谓的低渗性低钠血症)。但一个常见的例外是控制不佳的糖尿病,虽血清钠低于正常,但高血糖仍会导致高渗状态(高渗性低钠血症)。

Hyponatremia is usually asymptomatic unless it is acute or severe (<120 mEq/L). An abrupt fall in serum sodium produces a free water shift from the vascular to the interstitial space that can cause cerebral edema. In this case the patient may present with nausea, vomiting, headache, irritability, lethargy, seizures, coma, or even death.

如果不是急性的或严重的低钠(<120 mEq/L),患者通常无症状。血清钠急剧下降使水分由血管内转移到组织间隙,引起脑水肿。病人表现为恶心,呕吐,头痛,易激惹,嗜睡,癫痫发作,昏迷,甚至死亡。

Treatment of Hyponatremia

Treatment of hyponatremia involves administration of sodium and elimination of intravascular free water. If SIADH is present, the treatment is restriction of fluid intake to 50% to 66% of estimated maintenance fluid requirement. Correction of asymptomatic hyponatremia should be gradual: typically increase the Na_ by 0.5mEq/L per hour to a maximum change of about 12mEq/L in the first 24 hours. Rapid correction of hyponatremia can cause coma, which may be associated with osmotic demyelination syndrome or central pontine myelinolysis, lethal disorders thought to be caused by rapid fluid shifts into and out of brain tissue10–12.

低钠血症的治疗

低钠血症的治疗包括补钠和排除血管内游离水。如果是SIADH,治疗应该严格限制液体摄入,控制到维持需要量的50%~66%。无症状低钠血症的纠正应该使Na逐渐恢复,从0.5 mEq/L/h开始,在第一个24h最多增加12 mEq/L。快速纠正低钠血症会引起昏迷,与渗透性脱髓鞘或脑桥中央髓鞘溶解综合征有关,液体快速进出脑组织会引起致死性疾病[10~12]

If the patient develops neurologic compromise, administer 3% saline IV immediately to correct (raise) the serum sodium at a rate of 1 mEq/L per hour until neurologic symptoms are controlled. Some experts recommend a faster rate of correction (ie, increase concentration 2 to 4 mEq/L per hour) when seizures are present. After neurologic symptoms are controlled, provide 3% saline IV to correct (raise) the serum sodium at a rate of 0.5 mEq/L per hour.

如果病人出现神经系统损害症状,需立即予3%生理盐水静脉注射,以1 mEq/L/h的速度纠正(升高)血清钠,直到神经系统症状得到改善。一些专家认为,当出现癫痫发作时应以更快的速度纠正低钠(如每小时可增加Na浓度为2~4mEq/L),当神经系统症状改善后,继用3%生理盐水以每小时0. 5mEq /L纠正(提高)低钠。

To determine the amount of sodium (eg, 3% saline) required to correct the deficit, calculate the total body sodium deficit. The following formula may be used:

Na deficit = (desired [Na+] - current [Na+])×0.6*×body wt (kg)

 (*use 0.6 for men and 0.5 for women).

纠正低钠所需的钠量(例如3%盐水),可以先用下列公式计算体内总的缺钠量:

缺钠量=(正常血Na+值-实测血Na+值)×0.6*×体重(kg)

(*男性×0.6,女性×0.5)

Once the deficit is estimated, determine the volume of 3% saline (513 mEq/L Na) necessary to correct the deficit (divide the deficit by 513mEq/L). Plan to increase the sodium by 1 mEq/L per hour over 4 hours (or until neurologic symptoms improve); then increase the sodium by 0.5 mEq/L per hour. To calculate this amount, use the amount you wish to correct the sodium in an hour (eg, 0.5mEq/L) and multiply by 0.6 (or 0.5 in women) and then multiply by the body weight; that will calculate the amount of sodium to administer that hour. Check serum sodium frequently and monitor neurologic status.

估算出体内缺钠量后,就可以算出纠正低钠所需的3%盐水(513 mEq/L Na)量。预计前4小时每小时补钠1 mEq/L(或直到神经系统症状有改善),然后以每小时0.5 mEq/L的速度增加补钠量。算出每小时要增加的钠量(例如 0.5 mEq/L) 乘以0.6(女性乘以0.5),再乘以体重,就可以得到该小时补钠量。注意经常复查血清钠,监测神经系统功能状态。

三、Magnesium (Mg++)

Magnesium is the fourth most common mineral and the second most abundant intracellular cation (after potassium) in the human body. Because extracellular magnesium is bound to serum albumin, magnesium levels do not reliably reflect total body magnesium stores. Magnesium is necessary for the movement of sodium, potassium, and calcium into and out of cells, and magnesium plays an important role in stabilizing excitable membranes. Low potassium in combination with low magnesium is a risk factor for severe arrhythmias. Thus, magnesium balance is closely tied to sodium, calcium, and potassium balance

三、镁(Mg++

镁是人体第四重要的矿物质,也是细胞内含量第二的阳离子(居于钾之后)。由于细胞外的镁主要结合于血清白蛋白,所以血清镁水平不能准确反映体内总镁量。镁是钠、钾和钙进出细胞所必须的物质,在稳定细胞膜的兴奋性方面也有着重要作用。低钾常常伴随着低镁,这也是造成严重心律失常的一个重要危险因素。因此,镁平衡与钠、钙和钾的平衡紧密相关。

1、Hypermagnesemia

Hypermagnesemia is defined as a serum magnesium concentration>2.2 mEq/L (normal: 1.3 to 2.2 mEq/L). The most common cause of hypermagnesemia is renal failure. Note that pre-eclampsia in pregnant women is treated with magnesium administration, often titrated to maintain the serum magnesium near the maximum normal concentration,without complications of hypermagnesemia.

1、高镁血症

血清镁浓度>2.2 mEq/L (正常:1.3~2.2 mEq/L)称为高镁血症。高镁血症最常见的原因是肾功能衰竭。注:治疗先兆子痫使用镁剂时,常常使镁浓度保持接近于正常最高浓度,不会并发高镁血症。

Neurologic symptoms of hypermagnesemia are muscular weakness, paralysis, ataxia, drowsiness, and confusion. Moderate hypermagnesemia can produce vasodilation; severe hypermagnesemia can produce hypotension. Extremely high serum magnesium levels may produce a depressed level of consciousness, bradycardia, cardiac arrhythmias, hypoventilation, and cardiorespiratory arrest15.

高镁血症的神经系统症状表现为肌肉无力、瘫痪、共济失调、嗜睡和意识模糊。轻度的高镁血症可使血管扩张;严重的高镁血症可以造成低血压。极度高镁可以导致意识抑制、缓慢性心律失常、肺通气不足和心跳呼吸停止[15]

Treatment of Hypermagnesemia

Hypermagnesemia is treated with administration of calcium, which removes magnesium from serum. It is important eliminate sources of ongoing magnesium intake. Cardiorespiratory support may be needed until magnesium levels are reduced. Administration of 10% solution of calcium chloride (5 to 10 mL [500 to 1000 mg] IV) will often correct lethal arrhythmias. This dose may be repeated if needed.

高镁血症的治疗

钙剂可以降低血镁,故高镁血症常用钙剂治疗。此外,还应注意停止镁的继续摄入,在血镁水平下降之前,心肺支持也是必要的。10%氯化钙溶液(5~10mL[500~1000mg]静脉注射)常可以纠正致死性心律失常。必要时可重复使用。

Dialysis is the treatment of choice for severe hypermagnesemia. If renal function is normal and cardiovascular function adequate, IV saline diuresis (administration of IV normal saline and furosemide [1 mg/kg]) can be used to increase renal excretion of magnesium until dialysis can be performed. Diuresis can also increase calcium excretion; the development of hypocalcemia will make signs and symptoms of hypermagnesemia worse.

重度高镁血症可以选择透析治疗。如果肾功能和心血管功能尚可,在透析治疗之前可以静脉注射盐水利尿(静脉注射生理盐水和速尿[1 mg/kg])增加肾脏排镁。但是利尿也能使钙排出增加,低钙血症反会使高镁血症的病情恶化。

2、Hypomagnesemia

Hypomagnesemia, defined as a serum magnesium concentration<1.3 mEq/L, is far more common than hypermagnesemia. Hypomagnesemia usually results from decreased absorption or increased loss of magnesium from either the kidneys or intestines (diarrhea). Alterations in thyroid hormone function and certain medications (eg, pentamidine, diuretics, alcohol) can also induce hypomagnesemia.

2、低镁血症

血清镁浓度<1.3 mEq/L称为低镁血症,远比高镁血症常见。低镁血症通常是由于镁的吸收减少、肾脏或肠道(腹泻)镁的丢失增加。甲状腺功能改变和某些药物(例如,戊烷脒、利尿剂、酒精)也可引起低镁血症。

Hypomagnesemia interferes with the effects of parathyroid hormone, resulting in hypocalcemia. It may also cause hypokalemia. Symptoms of low serum magnesium are muscular tremors and fasciculations, ocular nystagmus, tetany, altered mental state, and cardiac arrhythmias such as torsades de pointes (multifocal ventricular tachycardia). Other possible symptoms are ataxia, vertigo, seizures, and dysphagia.

低镁会影响甲状旁腺激素的作用,导致低钙,也可低钾。低镁血症主要表现为肌肉震颤和肌束自发性收缩,眼震,手足搐搦,神志改变和心律失常,例如尖端扭转性室速。其他可能的症状还有共济失调、眩晕、癫痫发作和吞咽困难。

Treatment of Hypomagnesemia

The treatment of hypomagnesemia is determined by its severity and the patient’s clinical status. For severe or symptomatic hypomagnesemia, give 1 to 2 g of IV MgSO4 over 5 to 60 minutes. For torsades de pointes with cardiac arrest, give 1 to 2 g of MgSO4 IV push over 5 to 20 minutes. If torsades de pointes is intermittent and not associated with arrest, administer the magnesium over 5 to 60 minutes IV. If seizures are present, give 2 g IV MgSO4 over 10 minutes. Administration of calcium is usually appropriate because most patients with hypomagnesemia are also hypocalcemic16.

低镁血症的治疗

低镁的治疗取决于低镁的严重程度以及病人的临床情况。严重的或有症状的低镁血症静脉注射1~2g硫酸镁(5~60分钟)。如果尖端扭转性室速是间歇性的,且没有出现心跳停止,可以在5~60分钟内静脉注射镁剂。如有癫痫发作,立即给予2g硫酸镁,10分钟静脉推入。因为大多数低镁患者都伴有低钙,所以可常规补钙[16]

四、Calcium (Ca++)

Calcium is the most abundant mineral in the body. Many processes depend on intracellular calcium, such as enzymatic reactions, receptor activation, muscle contraction, cardiac contractility, and platelet aggregation. Calcium is essential for bone strength and neuromuscular function. Half of all calcium in the ECF is bound to albumin; the other half is in the biologically active, ionized form. Calcium concentration is normally regulated by parathyroid hormone and vitamin D.

四、钙(Ca++

钙是人体内含量最多的矿物质。体内的酶促反应、受体激活、肌肉收缩、心脏收缩性和血小板聚集等许多生理过程都需要细胞内钙离子的参与。钙在维持骨骼强度和神经肌肉功能方面尤为重要。细胞外液中1/2的钙结合于白蛋白,另外1/2是具有生物活性的离子钙。钙浓度通常受甲状旁腺激素和维生素D调节。

Total serum calcium is directly related to the serum albumin concentration. The total serum calcium will increase 0.8 mg/dL for every 1 g/dL rise in serum albumin and will fall 0.8 mg/dL for every 1 g/dL fall in serum albumin.

血清总钙浓度与血清白蛋白浓度直接相关。血清白蛋白每增加1 g/dL,血清总钙就升高 0.8 mg/dL,血清白蛋白每减少1 g/dL,血清总钙就下降0.8 mg/dL。

Although total serum albumin is directly related to total serum calcium, the ionized calcium is inversely related to serum albumin. The lower the serum albumin, the higher the portion of the total calcium that is present in ionized form. In the presence of hypoalbuminemia, although total calcium level may be low, the ionized calcium level may be normal

尽管血清白蛋白量与血清总钙浓度直接相关,但离子钙与血清白蛋白的关系却相反。血清白蛋白越低,血清钙中离子钙的比例就越高。在低白蛋白血症的时候,血清总钙水平已经低于正常,但离子钙水平仍可在正常范围内。

Calcium antagonizes the effects of both potassium and magnesium at the cell membrane. For this reason it is extremely useful for treating the effects of hyperkalemia and hypermagnesemia.

钙对细胞膜的作用与钾和镁相反。因此,钙用于对抗高钾和高镁的毒性作用。

1、Hypercalcemia

Hypercalcemia is defined as a total serum calcium concentration >10.5 mEq/L (or an elevation in ionized calcium>4.8 mg/dL). Primary hyperparathyroidism and malignancy account for >90% of reported cases17. In these and most forms of hypercalcemia, release of calcium from the bones and intestines is increased, and renal clearance may be compromised.

1、高钙血症

高钙血症是指血清总钙>10.5 mEq/L(或离子钙>4.8 mg/dL),90%以上的高钙血症由原发性甲状旁腺功能亢进和恶性肿瘤引起[17]。高钙患者骨钙动员和肠道排钙是增加的,肾脏排钙能力相对较弱。

Symptoms of hypercalcemia usually develop when the total serum calcium concentration is ≥12 to 15 mg/dL. Neurologic symptoms are depression, weakness, fatigue, and confusion at lower levels. At higher levels patients may experience hallucinations, disorientation, hypotonicity, seizures, and coma. Hypercalcemia interferes with renal concentration of urine; the diuresis can cause dehydration.

当血清总钙浓度≥12~15 mg/dL时出现高钙症状,神经系统症状为抑郁,虚弱,疲劳和意识水平低下。血钙更高时可有幻觉,定向力障碍,肌张力减退,癫痫发作和昏迷。高钙还影响肾脏对尿液的浓缩功能,排尿增多又可以引起脱水。

Cardiovascular symptoms of hypercalcemia are variable. Myocardial contractility may initially increase until the calcium level reaches >15 mg/dL. Above this level myocardial depression occurs. Automaticity is decreased and ventricular systole is shortened. Arrhythmias occur because the refractory period is shortened. Hypercalcemia can worsen digitalis toxicity and may cause hypertension. In addition, many patients with hypercalcemia develop hypokalemia. Both of these conditions contribute to cardiac arrhythmias18. The QT interval typically shortens when the serum calcium is>13 mg/dL, and the PR and QRS intervals are prolonged. Atrioventricular block may develop and progress to complete heart block and even cardiac arrest when the total serum calcium is >15 to 20 mg/dL.

高钙的心血管系统表现多样,血钙>15 mg/dL之前心肌收缩力增强,当血钙高于这个水平时,心肌反而受到抑制,自律性下降,心室收缩期缩短。由于不应期缩短,易于发生心律失常。高钙血症可以加重洋地黄的毒性作用,还可引起高血压。此外,许多高钙病人都伴有低钾血症,二者都可以促成心律失常的发生[18]。血清钙>13 mg/dL时,QT间期缩短,PR间期和QRS间期延长。血清钙继续升高>15 ~20 mg/dL时,可以出现房室传导阻滞,进一步发展则为完全性房室传导阻滞,甚至心脏停搏。

Gastrointestinal symptoms of hypercalcemia include dysphagia, constipation, peptic ulcers, and pancreatitis. Effects on the kidney include diminished ability to concentrate urine; diuresis, leading to loss of sodium, potassium, magnesium, and phosphate; and a vicious cycle of calcium absorption in the intestines and calcium release from the bones that worsens hypercalcemia.

高钙血症的消化系统症状包括吞咽困难,便秘,消化性溃疡和胰腺炎。对肾脏的影响主要是降低肾浓缩尿的能力;利尿可以导致钠、钾、镁和磷酸盐的丢失;肠道吸收钙和骨钙释放增加,这样一个恶性循环更加重了高钙血症。

Treatment of Hypercalcemia

Treatment for hypercalcemia is required if the patient is symptomatic (typically a total serum concentration of approximately>12 mg/dL) or if the calcium level is>15 mg/dL. Immediate therapy is directed at restoring intravascular volume and promoting calcium excretion in the urine. In patients with adequate cardiovascular and renal function this is accomplished with infusion of 0.9% saline at 300 to 500 mL/h (saline diuresis) until any fluid deficit is replaced and diuresis occurs (urine output ≥200 to 300 mL/h). Once adequate rehydration has occurred, the saline infusion rate is reduced to 100 to 200 mL/h. During this therapy, monitor and maintain potassium and magnesium concentrations closely because the diuresis can reduce potassium and magnesium concentrations.

高钙血症的治疗

当高钙血症患者出现临床症状(通常血清总钙大约>12 mg/dL)或者血钙浓度>15 mg/dL时应给予治疗。首先是恢复血管内容量和增加尿钙排泄。如果病人的心血管功能和肾功能良好,输入0.9%生理盐水300~500mL/h(盐水利尿),直至液体缺乏纠正并出现利尿作用(尿量≥200 to 300 mL/h)。恢复血管内容量后,盐水输注速度减为100~200 mL/h。因为利尿会降低血钾和血镁,所以治疗过程中需密切监测钾镁浓度。

Hemodialysis is the treatment of choice to rapidly decrease serum calcium in patients with heart failure or renal insufficiency19. Chelating agents (eg, 50 mmol PO4 over 8 to 12 hours or EDTA 10 to 50 mg/kg over 4 hours) may be used for extreme conditions.

对心衰和肾功能不全的患者,为了尽快降低血清钙可以行血透治疗[19]。紧急情况下还可以使用螯合剂(例如,50mmol磷酸盐8~12小时输入 或者依地酸 10~50mg/kg 4小时输入)。

Use of furosemide (1 mg/kg IV) for treatment of hypercalcemia is controversial. In the presence of heart failure, administration of furosemide is required, but it can actually foster release of calcium from bone, thus worsening hypercalcemia.

高钙血症使用速尿(1 mg/kg IV)治疗尚存争议。如有心衰,可以使用速尿,但是速尿促进骨钙释放,会加重高钙血症。

2、Hypocalcemia

Hypocalcemia is defined as a serum calcium concentration <8.5 mg/dL (or ionized calcium<4.2 mg/dL). Hypocalcemia may develop with toxic shock syndrome, with abnormalities in serum magnesium, after thyroid surgery, with fluoride poisoning, and with tumor lysis syndrome (rapid cell turnover with resultant hyperkalemia, hyperphosphatemia, and hypocalcemia).

2、低钙血症

血清钙浓度<8.5 mg/dL(或离子钙<4.2 mg/dL)称为低钙血症。低钙血症可见于中毒性休克综合征、血镁异常、甲状腺手术后、氟化物中毒、以及肿瘤溶解综合征(快速细胞破坏导致高钾血症,高磷血症和低钙血症)。

Symptoms of hypocalcemia usually occur when ionized levels fall to<2.5 mg/dL. Symptoms include paresthesias of the extremities and face, followed by muscle cramps, carpopedal spasm, stridor, tetany, and seizures. Hypocalcemic patients show hyperreflexia and positive . Cardiac effects include decreased  myocardial contractility and heart failure. Hypocalcemia can exacerbate digitalis toxicity.

通常离子钙<2.5 mg/dL时出现低钙症状,包括四肢和面部感觉异常,接着是肌肉痛性痉挛,腕足痉挛,喘鸣,手足搐搦和癫痫发作。低钙患者常伴反射亢进,Chvostek 和Trousseau 征阳性。

Treatment of Hypocalcemia

Treatment of hypocalcemia requires administration of calcium. Treat acute, symptomatic hypocalcemia with 10% calcium gluconate, 93 to 186 mg of elemental calcium (10 to 20 mL) IV over 10 minutes. Follow this with an IV infusion of 540 to 720 mg of elemental calcium (58 to 77 mL of 10% calcium gluconate) in 500 to 1000 mL D5W at 0.5 to 2 mg/kg per hour (10 to 15 mg/kg). Alternatively, administer 10% calcium chloride, giving 5 mL (136.5 mg of elemental calcium) over 10 minutes, followed by 36.6 mL (1 g) over the next 6 to 12 hours IV. Measure serum calcium every 4 to 6hours. Aim to maintain the total serum calcium concentration at 7 to 9 mg/dL. Correct abnormalities in magnesium, potassium, and pH simultaneously. Note that untreated hypomagnesemia will often make hypocalcemia refractory to therapy. Therefore, evaluate serum magnesium when hypocalcemia is present and particularly if hypocalcemia is refractory to initial calcium therapy.

低钙血症的治疗

低钙血症的治疗需补充钙剂。对急性有症状的低钙用10%葡萄糖酸钙(含元素钙93~86mg)10~20mL静脉注射>10分钟。接着静脉注入540~720mg元素钙(10%葡萄糖酸钙58~77mL)加入5%葡萄糖液500~1000mL以每小时0.5~2mg/kg(10~15 mg/kg)的速度输入。也可用10%氯化钙5mL/h(136.5mg元素钙)10分钟输入,接下来6~12小时静脉注射36.6mL(1g)。每4~6小时复查一次血清钙,治疗目标是保持血清总钙浓度7~9 mg/dL,同时纠正血镁、血钾和pH异常。需注意,未经治疗的低镁血症常常使低钙难以纠正。因此,低钙时应估计血清镁浓度,尤其是低钙对治疗反应不佳时。

六、Summary

Electrolyte abnormalities are among the most common causes of cardiac arrhythmias, and they can cause or complicate attempted resuscitation and postresuscitation care. A high degree of clinical suspicion and aggressive treatment of underlying electrolyte abnormalities can prevent these abnormalities from progressing to cardiac arrest.

六、小结

电解质异常是心律失常最常见的原因之一,常影响复苏和复苏后治疗的效果。临床上对潜在的电解质异常应给予高度重视和积极治疗,从而预防心脏停搏的发生。

七、参考文献 References

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