美国重症医学FCCM的基础教程电解质代谢紊乱教材课程
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重症病人内环境紊乱诊治课件
测体重(有无失水)
减轻
未变
水丢失
水份转移到第三间隙
测尿量、尿渗透压
尿量明显减低渗透压明显增高 尿量尚可、渗透压未达高值
肾外丢失
渗透压明显降低 低
渗透压不
尿崩症
利尿剂 高血糖
18
人体钾含量及分布
钾在细胞内外间的转运，维持正常的血钾浓度
体内钾 (50mmol/Kg体重)
细胞外 2%
细胞内98% (140mmol/L)
所需碱= (正常BE－ 实测BE) ×0.25×kg 按HCO3-计算：
血清钾 (3.5-5.0mmol/L)
19
血钾调节
重吸收
远曲小管和集合管
食物来源， 90%的钾由小肠吸收， 90%由肾排泄 肾小球滤过钾，近曲小管和髓袢：约90%~95%吸收
影响：胰岛素、儿茶酚胺、 HCO3-、pH、渗透压等
分 泌 血Na+ 钾 血K+
H+
K+
主细胞
Na+ K+
H+ (－)
闰细胞 H+
临床表现：
取决于低钾血症发生的速度、持续时间、程度 和细胞内外钾浓度异常的轻重。
肌肉无力、抽搐、麻痹等，腱反射减退； 最大危险心脏骤停。 辅查:[k+]＜3.5mmol/L 、代碱、反常性酸性尿、 EKG
22
低钾血症
治疗 • 常规口服，不能口服或缺钾严重者静脉补钾 • 尿量＞30ml/h，危重患者尽可能中心静脉补钾 • 补钾浓度20~40mmol/L为宜，速度＜13.4 mmol/h
口渴强烈
晚/重：醛固酮t
细 血胞 浆外
液
脱水热
细
渗透压 体液量
美国重症医学(FCCM)的基础教程 休克的诊断与治疗
• Cardiogenic • Hypovolemic • Distributive • Obstructive
SHK 4
®
Cardiogenic Shock
• Decreased contractility • Increased filling pressures,
decreased LV stroke work, decreased cardiac output • Increased systemic vascular resistance – compensatory
SSHHKK 1111
®
Distributive Shock Therapy
• Restore intravascular volume • Hypotension despite volume therapy
– Inotropes and/or vasopressors • Vasopressors for MAP < 60 mm Hg • Adjunctive interventions dependent
SHK 13
®
Fluid Therapy
• Crystalloids – Lactated Ringer’s solution – Normal saline
• Colloids – Hetastarch – Albumin – Gelatins
• Packed red blood cells • Infuse to physiologic endpoints
®
Inotropic / Vasopressor Agents
• Norepinephrine – 0.05 g/kg/min and titrate to effect – Inotropic and vasopressor effects – Potent vasopressor at high doses
SHK 4
®
Cardiogenic Shock
• Decreased contractility • Increased filling pressures,
decreased LV stroke work, decreased cardiac output • Increased systemic vascular resistance – compensatory
SSHHKK 1111
®
Distributive Shock Therapy
• Restore intravascular volume • Hypotension despite volume therapy
– Inotropes and/or vasopressors • Vasopressors for MAP < 60 mm Hg • Adjunctive interventions dependent
SHK 13
®
Fluid Therapy
• Crystalloids – Lactated Ringer’s solution – Normal saline
• Colloids – Hetastarch – Albumin – Gelatins
• Packed red blood cells • Infuse to physiologic endpoints
®
Inotropic / Vasopressor Agents
• Norepinephrine – 0.05 g/kg/min and titrate to effect – Inotropic and vasopressor effects – Potent vasopressor at high doses
[医学]美国重症医学(FCCM)的基础教程 电解质代谢紊乱
![[医学]美国重症医学(FCCM)的基础教程 电解质代谢紊乱](https://img.taocdn.com/s3/m/823ec140a8114431b90dd888.png)
• Recognize acute adrenal insufficiency and appropriate treatment
• Describe management of severe hyperglycemic syndromes
MET 2 ®
Principles of Electrolyte Disturbances
Hypernatremia
• Etiology – H2O loss, H2O intake, Na intake
• Manifestations – neurologic, muscular • H2O deficit (L) =
• Deficit poorly estimated by serum levels
MET 5 ®
Hypokalemia
• Titrate administration of K+ against serum level and manifestations
• Correct hypomagnesemia • ECG monitoring with emergent administration • Allowable maximum iv dose per hour
• Frequent reassessment of electrolytes required
MET 4 ®
Hypokalemia
• Etiology – renal loss, extrarenal loss, transcellular shift, decreased intake
• Manifestations – cardiac, neuromuscular, gastrointestinal
• Describe management of severe hyperglycemic syndromes
MET 2 ®
Principles of Electrolyte Disturbances
Hypernatremia
• Etiology – H2O loss, H2O intake, Na intake
• Manifestations – neurologic, muscular • H2O deficit (L) =
• Deficit poorly estimated by serum levels
MET 5 ®
Hypokalemia
• Titrate administration of K+ against serum level and manifestations
• Correct hypomagnesemia • ECG monitoring with emergent administration • Allowable maximum iv dose per hour
• Frequent reassessment of electrolytes required
MET 4 ®
Hypokalemia
• Etiology – renal loss, extrarenal loss, transcellular shift, decreased intake
• Manifestations – cardiac, neuromuscular, gastrointestinal
美国重症医学(FCCM)的基础教程患者评估(英文)【27页】
Action
• Ensure physiological safety
– Oxygen –Intravenous access –Circulatory support
• Determine patient’s reserve • Assess likely diagnosis and
treatments
Key Points
• Identify patients at risk early • Recognize signs of critical illness • Stabilize first, then determine
diagnosis
• Obtain detailed history • Monitor response to treatment
microbiology, radiographs
• Arterial or venous blood gas • Lactate level
Metabolic acidosis is an important indicator of critical illness
Patient
Previous exam
abdomen
• Warm extremities
What information from the chart would be helpful?
Chart Review and Documentation
• Initial survey
–Vital signs –Fluid balance –Inspired oxygen concentration – Medications –Invasive parameters
病理生理学网络课件3章水电解质代谢紊乱课件精品教育文档
ECF容量↑ 渗透压↑
Effect
水份从细胞内 到细胞外
细胞脱水
严重时引起 中枢神经系 统功能障碍
Pathophysiologic basis of treatment
防治原发病。 肾功能正常者可用强效利尿剂，去除过
量的钠。 肾功能低下或对利尿剂反应差者，或血
清钠＞200mmol/L的患者，采用腹膜透 析。
第三章 水、电解质代谢紊乱
（Water and sodium disorders）
第一节 水、电解质正常代谢
(Normal Metabolism of Water and Electrolyte)
体液的含量 体液的分布 体液的组成 体液的平衡 体液的调节
Content of body fluid
plasma ISF
ICF
protein protein
protein
Na+ K+ Ca+ Mg+ K+ Na+ Ca+ Mg+
glucose aminoacid urea creatinine CO2 O2 Cl_ HCO3 _
water water
water
ECF
Electrolytes and their distribution in body fluid
– 抑制醛固酮分泌和肾素活 性。
– 减轻血容量降低后引起的 ADH升高的水平。
第二节 水钠代谢紊乱
（Disorders of Water and Sodium Metabolism）
分类（Classification）
Volume Status
容量减小
容量增大
ICU基础教材(美国,浙一翻译)
ICU 基础教材（美国）第 1 章 危重病人的识别和评估........................................................................ 2 第 2 章 气道管理 .............................................................................................. 6 第 3 章 心肺脑复苏 .......................................................................................... 12 第 4 章 急性呼吸衰竭的诊断和处理................................................................ 16 第 5 章 机械通气 .............................................................................................. 22 第 6 章 血流动力学、氧合和酸碱平衡监测.................................................. 34 第 7 章 休克的诊断和治疗 .......................................................................... 42 第 8 章 神经支持 ................................................................................................ 49 第 9 章 基础创伤与烧伤支持治疗.................................................................. 56 第 10 章 急性冠脉综合征.................................................................................. 65 第 11 章 危胁生命的感染：诊断和抗生素治疗选择 ................................ 76 第 12 章 危及生命的电解质和代谢紊乱的处理............................................ 84 第 13 章 特殊治疗 ............................................................................................ 951第 1 章 危重病人的识别和评估目的● 阐明对可能发生危重疾病或损伤风险的患者的早期识别和早期干预的重要性。
钾代谢紊乱专题知识讲座培训课件
肾脏浓缩功能↓ 多尿、夜尿
钾代谢紊乱专题知识讲座
22
高钾血症
（一）原因和发生机制（Causes and mechanism） 1．摄钾过多（Increased intake of potassium）
静脉输入钾过快或浓度过高可立即引起严重的高钾血症，
并导致患者猝死。
钾代谢紊乱专题知识讲座
24
高钾血症
钾代谢紊乱专题知识讲座
16
2．对心脏的影响（Effects on heart） 心律失常，严重时出现心室纤维颤动和心力衰竭。 （1）低钾对心脏生理特性的影响 ■ 自律性（Automaticity） 增加
[K+]e↓ 自律细胞膜对钾电导↓ 钾外流↓
Na+(窦房结)或Ca2+(浦肯野)内向电流↑ 自律细胞自动除极化速度↑ 自律性↑
0期除极化幅度、速度↓
■ 收缩性（Contraction） 增强
急性低钾血症 慢性低钾血症
2期Ca2+内流加速
心肌收缩性↑
细胞内缺钾
心肌收缩性↓
钾代谢紊乱专题知识讲座
18
低钾血症
（2）心电图（ Electrocardiogram, ECG）特征 ■ QRS波增宽
[K+]e↓ 传导性↓ P-R间期延长 QRS波（轻度）增宽
21
低钾血症
5．其他方面影响（Other Effects）
（1）对洋地黄类强心药物毒性的敏感性增高 低钾血症 洋地黄与Na+-K+-ATP酶的亲和力↑
洋地黄导致心律失常毒性作用↑ （2）肾损害（Kidney damage） 【Structure】 ■ 缺钾初期：髓质集合管出现小管上皮细胞肿胀、增生等。 ■ 长期、严重缺钾：损害可波及各段肾小管，甚至肾小球。 【Function】 损伤集合管对ADH反应性↓、升支粗段对NaCl重吸收↓
钾代谢紊乱专题知识讲座
22
高钾血症
（一）原因和发生机制（Causes and mechanism） 1．摄钾过多（Increased intake of potassium）
静脉输入钾过快或浓度过高可立即引起严重的高钾血症，
并导致患者猝死。
钾代谢紊乱专题知识讲座
24
高钾血症
钾代谢紊乱专题知识讲座
16
2．对心脏的影响（Effects on heart） 心律失常，严重时出现心室纤维颤动和心力衰竭。 （1）低钾对心脏生理特性的影响 ■ 自律性（Automaticity） 增加
[K+]e↓ 自律细胞膜对钾电导↓ 钾外流↓
Na+(窦房结)或Ca2+(浦肯野)内向电流↑ 自律细胞自动除极化速度↑ 自律性↑
0期除极化幅度、速度↓
■ 收缩性（Contraction） 增强
急性低钾血症 慢性低钾血症
2期Ca2+内流加速
心肌收缩性↑
细胞内缺钾
心肌收缩性↓
钾代谢紊乱专题知识讲座
18
低钾血症
（2）心电图（ Electrocardiogram, ECG）特征 ■ QRS波增宽
[K+]e↓ 传导性↓ P-R间期延长 QRS波（轻度）增宽
21
低钾血症
5．其他方面影响（Other Effects）
（1）对洋地黄类强心药物毒性的敏感性增高 低钾血症 洋地黄与Na+-K+-ATP酶的亲和力↑
洋地黄导致心律失常毒性作用↑ （2）肾损害（Kidney damage） 【Structure】 ■ 缺钾初期：髓质集合管出现小管上皮细胞肿胀、增生等。 ■ 长期、严重缺钾：损害可波及各段肾小管，甚至肾小球。 【Function】 损伤集合管对ADH反应性↓、升支粗段对NaCl重吸收↓
水电解质代谢紊乱本PPT培训课件
HPO42- Pr-
细胞内、外液的主要电解质成份
(三)体液的渗透压
(Osmotic pressure of body fluid)
血浆渗透压 280~310 mmol/L (四) 水的生理功能和水平衡
(Physiologic function of water and Water balance )
低渗性脱水 (Hypotonic dehydration)
2.原因 (causes)
钠平衡调节：
多吃多排，少吃少排，不吃不排
丢失过多(lost from ECF)
❖肾性失钠(renal losses) ❖胃肠道丢失(gastrointestinal losses) ❖ 皮肤丢失(skin losses) ❖ 液体积聚在第三间隙
1.概念(concept)
❖ 低渗性液体在体内潴留的病理过程 ❖ serum[Na+] < 130 mmol/L ❖ plasma osmotic pressure
< 280 mmol/L
水中毒 (water intoxication)
2.原因 (causes)
(1) 水排出减少 (decrease of water excretion) ❖ 急、慢性肾功能障碍
第一节 水、钠代谢障碍
(Disturbances of water and sodium)
一、正常水、钠代谢
(Normal metabolism of water and sodium)
(一)、体液的容量和分布
(Volume and distribution of body fluid)
体液(body fluid)
（1）投标人之间协商投标报价等投标文件的实质性内容； 另外，电梯每到达相应的楼层，服务小姐都会向顾客介绍该楼层主要销售的商品信息，如：二楼是日用百货，三楼是儿童产品，四楼 是贵妇人产品、五楼是绅士产品。一旦百货公司建立这样的制度，很多顾客都非常喜欢享受这种服务，这些行销手段都值得我们的百 货企业学习和模仿。
细胞内、外液的主要电解质成份
(三)体液的渗透压
(Osmotic pressure of body fluid)
血浆渗透压 280~310 mmol/L (四) 水的生理功能和水平衡
(Physiologic function of water and Water balance )
低渗性脱水 (Hypotonic dehydration)
2.原因 (causes)
钠平衡调节：
多吃多排，少吃少排，不吃不排
丢失过多(lost from ECF)
❖肾性失钠(renal losses) ❖胃肠道丢失(gastrointestinal losses) ❖ 皮肤丢失(skin losses) ❖ 液体积聚在第三间隙
1.概念(concept)
❖ 低渗性液体在体内潴留的病理过程 ❖ serum[Na+] < 130 mmol/L ❖ plasma osmotic pressure
< 280 mmol/L
水中毒 (water intoxication)
2.原因 (causes)
(1) 水排出减少 (decrease of water excretion) ❖ 急、慢性肾功能障碍
第一节 水、钠代谢障碍
(Disturbances of water and sodium)
一、正常水、钠代谢
(Normal metabolism of water and sodium)
(一)、体液的容量和分布
(Volume and distribution of body fluid)
体液(body fluid)
（1）投标人之间协商投标报价等投标文件的实质性内容； 另外，电梯每到达相应的楼层，服务小姐都会向顾客介绍该楼层主要销售的商品信息，如：二楼是日用百货，三楼是儿童产品，四楼 是贵妇人产品、五楼是绅士产品。一旦百货公司建立这样的制度，很多顾客都非常喜欢享受这种服务，这些行销手段都值得我们的百 货企业学习和模仿。
钾代谢紊乱ZCM知识课件知识讲稿
第三节 钾代谢紊乱
(Disorders of potassium metabolism)
第四节 镁代谢紊乱
(Disorders of magnesium metabolism)
Hale Waihona Puke 第三节 钾代谢紊乱(Disorders of potassium metabolism)
一、正常钾代谢(Normal potassium metabolism)
K+
+30
动作电位
0
-30
-60
Et
-90
Em
-120
低
高
高
低
[K+]e [K+]e [Ca++]e [Ca++]e
细胞外液[K+]e 、 [Ca++]e和正常骨骼肌Em与Et的关系
2)对心脏的影响 ①对心肌生理特性的影响
1)兴奋性↑：K+↓→心肌细胞膜对钾通透性↓ → K+外流↓ → 静息电位负值↓ （图） 2)传导性↓：静息电位负值↓ → 0相去极化时Na+内流 速 度↓ →去极化波扩布慢 3)自律性↑：K+↓→钾通透性↓→ 4期K+外流↓而Na+内流 相对↑→4期自动去极化↑ 4)收缩性↑：急性低钾血症：复极2期Ca2+内流↑
②对肾脏的影响 以尿浓缩功能障碍为主
3. 对酸碱平衡的影响
•碱中毒
•反常性酸性尿
小管上皮细胞
K+ -- Na+↓ H+
K+
H+
Na+↑
K+↓
（三）防治原则
补钾：
❖ 先口服后静脉 ❖ 见尿补钾 ❖ 控制量和速度
(Disorders of potassium metabolism)
第四节 镁代谢紊乱
(Disorders of magnesium metabolism)
Hale Waihona Puke 第三节 钾代谢紊乱(Disorders of potassium metabolism)
一、正常钾代谢(Normal potassium metabolism)
K+
+30
动作电位
0
-30
-60
Et
-90
Em
-120
低
高
高
低
[K+]e [K+]e [Ca++]e [Ca++]e
细胞外液[K+]e 、 [Ca++]e和正常骨骼肌Em与Et的关系
2)对心脏的影响 ①对心肌生理特性的影响
1)兴奋性↑：K+↓→心肌细胞膜对钾通透性↓ → K+外流↓ → 静息电位负值↓ （图） 2)传导性↓：静息电位负值↓ → 0相去极化时Na+内流 速 度↓ →去极化波扩布慢 3)自律性↑：K+↓→钾通透性↓→ 4期K+外流↓而Na+内流 相对↑→4期自动去极化↑ 4)收缩性↑：急性低钾血症：复极2期Ca2+内流↑
②对肾脏的影响 以尿浓缩功能障碍为主
3. 对酸碱平衡的影响
•碱中毒
•反常性酸性尿
小管上皮细胞
K+ -- Na+↓ H+
K+
H+
Na+↑
K+↓
（三）防治原则
补钾：
❖ 先口服后静脉 ❖ 见尿补钾 ❖ 控制量和速度
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MET 10 ®
Hyponatremia – Treatment
• Hypovolemic Na – give normal saline, rule out adrenal insufficiency
• Hypervolemic Na – increase free H2O loss • Euvolemic hyponatremia
• Hypocalcemia – Calcium chloride or gluconate – Bolus + continuous infusion
• Hypercalcemia – Rehydration with normal saline – Loop diuretics
MET 16 ®
Other Electrolyte Disorders
<250-300 mg/dL (13.9-16.7 mmol/L) • Treat electrolyte changes (K, PO4) • NaHCO3 rarely needed
MET 22 ®
Pediatric Considerations – DKA
• Insulin – bolus not used, titrate iv infusion
Electrolyte and Metabolic Disturbances
MET 1 ®
Objectives
• Review causes and clinical manifestations of severe electrolyte disturbances
• Outline emergent management of electrolyte disturbances
MET 18 ®
Acute Adrenal Insufficiency
• Baseline blood samples • Volume and glucose infusion • Dexamethasone or hydrocortisone • ACTH stimulation test if needed • Treat precipitating conditions
• Deficit poorly estimated by serum levels
MET 5 ®
Hypokalemia
• Titrate administration of K+ against serum level and manifestations
• Correct hypomagnesemia • ECG monitoring with emergent administration • Allowable maximum iv dose per hour
• Implies an underlying disease process • Treat the electrolyte change, but seek the
cause • Clinical manifestations usually not specific to
a particular electrolyte change, e.g., seizures, arrhythmias
Myxedema Coma
• Manifestations of severe hypothyroidism
• Supportive measures – airway, fluids, glucose, warming
MET 20 ®
Hyperglycemic Syndromes – Laboratory
• Hyperglycemia/hyperosmolality • Ketonemia/ketonuria (DKA) • Increased anion gap metabolic acidosis
(DKA) • Electrolyte changes (K, PO4, Na)
– Restrict free water intake – Increase free water loss – Normal or hypertonic saline • Correct slowly due to possibility of demyelinating syndromes
MET 11 ®
• All are primarily intracellular ions, so deficits difficult to estimate
• Titrate replacement against clinical findings
MET 15 ®
Other Electrolyte Disorders
MET 3 ®
MET 4 ®
Hypokalemia
• Etiology – renal loss, extrarenal loss, transcellular shift, decreased intake
• Manifestations – cardiac, neuromuscular, gastrointestinal
• Supportive measures • Specific measures
– Propylthiouracil or methimazole – Propranolol – Potassium or sodium iodide – Dexamethasone, sodium ipodate
MET 24 ®
MET 19 ®
Hyperglycemic Syndromes
• Diabetic ketoacidosis (DKA) • Hyperglycemic hyperosmolar state
(HHS) • Manifestations – dehydration, polyuria/
polydipsia, altered mental status, BP, nausea, emesis, abdominal pain
Hypernatremia
• Etiology – H2O loss, H2O intake, Na intake
• Manifestations – neurologic, muscular • H2O deficit (L) =
[ 0.6 wt (kg) ] [ obs Na - 1 ] 140
inhaled -agonist • Remove from body – diuretics, sodium
polystyrene sulfonate, dialysis
MET 8 ®
Pediatric Considerations – Potassium
• Replace at maximum iv rate <–1.0 mmol/kg/hr; monitor ECG
• Decrease serum Na no faster than 0.5 mmol/L/hr
MET 14 ®
Other Electrolyte Deficits Ca, PO4, Mg
• May produce serious but nonspecific cardiac, neuromuscular, respiratory, and other effects
• Hypophosphatemia – Replacement iv for level < 1 mg/dL (0.32 mmol/L)
• Hypomagnesemia – Emergent administration over 5–10 mins – Less urgent administration over 10–60 mins
• Recognize acute adrenal insufficiency and appropriate treatment
• Describe management of severe hyperglycemic syndromes
MET 2 ®
Principles of Electrolyte Disturbances
MET 21 ®
Hyperglycemic Syndromes – Treatment
• Identify and treat precipitating factors • Restore fluid/electrolyte balance • Insulin – iv bolus and infusion • Add glucose to infusion when glucose
• Hyperkalemia – ECG abnormality: calcium gluconate or chloride – Shift: NaHCO3, glucose + insulin, inhaled -agonists – Removal: diuretic, sodium polystyrene sulfonate, dialysis
• Manifestations – cardiac, neuromuscular
MET 7 ®
Hyperkalemia – Treatment
• Stop intake • Give calcium for cardiac toxicity • Shift K+ into cell – glucose + insulin, NaHCO3,
rapid correction
MET 13 ®
Pediatric Considerations – Sodium
• Hyponatremia – seizures: titrate 3% NaCl; usual dose 1.5-2.5 mmol/kg
Hyponatremia – Treatment
• Hypovolemic Na – give normal saline, rule out adrenal insufficiency
• Hypervolemic Na – increase free H2O loss • Euvolemic hyponatremia
• Hypocalcemia – Calcium chloride or gluconate – Bolus + continuous infusion
• Hypercalcemia – Rehydration with normal saline – Loop diuretics
MET 16 ®
Other Electrolyte Disorders
<250-300 mg/dL (13.9-16.7 mmol/L) • Treat electrolyte changes (K, PO4) • NaHCO3 rarely needed
MET 22 ®
Pediatric Considerations – DKA
• Insulin – bolus not used, titrate iv infusion
Electrolyte and Metabolic Disturbances
MET 1 ®
Objectives
• Review causes and clinical manifestations of severe electrolyte disturbances
• Outline emergent management of electrolyte disturbances
MET 18 ®
Acute Adrenal Insufficiency
• Baseline blood samples • Volume and glucose infusion • Dexamethasone or hydrocortisone • ACTH stimulation test if needed • Treat precipitating conditions
• Deficit poorly estimated by serum levels
MET 5 ®
Hypokalemia
• Titrate administration of K+ against serum level and manifestations
• Correct hypomagnesemia • ECG monitoring with emergent administration • Allowable maximum iv dose per hour
• Implies an underlying disease process • Treat the electrolyte change, but seek the
cause • Clinical manifestations usually not specific to
a particular electrolyte change, e.g., seizures, arrhythmias
Myxedema Coma
• Manifestations of severe hypothyroidism
• Supportive measures – airway, fluids, glucose, warming
MET 20 ®
Hyperglycemic Syndromes – Laboratory
• Hyperglycemia/hyperosmolality • Ketonemia/ketonuria (DKA) • Increased anion gap metabolic acidosis
(DKA) • Electrolyte changes (K, PO4, Na)
– Restrict free water intake – Increase free water loss – Normal or hypertonic saline • Correct slowly due to possibility of demyelinating syndromes
MET 11 ®
• All are primarily intracellular ions, so deficits difficult to estimate
• Titrate replacement against clinical findings
MET 15 ®
Other Electrolyte Disorders
MET 3 ®
MET 4 ®
Hypokalemia
• Etiology – renal loss, extrarenal loss, transcellular shift, decreased intake
• Manifestations – cardiac, neuromuscular, gastrointestinal
• Supportive measures • Specific measures
– Propylthiouracil or methimazole – Propranolol – Potassium or sodium iodide – Dexamethasone, sodium ipodate
MET 24 ®
MET 19 ®
Hyperglycemic Syndromes
• Diabetic ketoacidosis (DKA) • Hyperglycemic hyperosmolar state
(HHS) • Manifestations – dehydration, polyuria/
polydipsia, altered mental status, BP, nausea, emesis, abdominal pain
Hypernatremia
• Etiology – H2O loss, H2O intake, Na intake
• Manifestations – neurologic, muscular • H2O deficit (L) =
[ 0.6 wt (kg) ] [ obs Na - 1 ] 140
inhaled -agonist • Remove from body – diuretics, sodium
polystyrene sulfonate, dialysis
MET 8 ®
Pediatric Considerations – Potassium
• Replace at maximum iv rate <–1.0 mmol/kg/hr; monitor ECG
• Decrease serum Na no faster than 0.5 mmol/L/hr
MET 14 ®
Other Electrolyte Deficits Ca, PO4, Mg
• May produce serious but nonspecific cardiac, neuromuscular, respiratory, and other effects
• Hypophosphatemia – Replacement iv for level < 1 mg/dL (0.32 mmol/L)
• Hypomagnesemia – Emergent administration over 5–10 mins – Less urgent administration over 10–60 mins
• Recognize acute adrenal insufficiency and appropriate treatment
• Describe management of severe hyperglycemic syndromes
MET 2 ®
Principles of Electrolyte Disturbances
MET 21 ®
Hyperglycemic Syndromes – Treatment
• Identify and treat precipitating factors • Restore fluid/electrolyte balance • Insulin – iv bolus and infusion • Add glucose to infusion when glucose
• Hyperkalemia – ECG abnormality: calcium gluconate or chloride – Shift: NaHCO3, glucose + insulin, inhaled -agonists – Removal: diuretic, sodium polystyrene sulfonate, dialysis
• Manifestations – cardiac, neuromuscular
MET 7 ®
Hyperkalemia – Treatment
• Stop intake • Give calcium for cardiac toxicity • Shift K+ into cell – glucose + insulin, NaHCO3,
rapid correction
MET 13 ®
Pediatric Considerations – Sodium
• Hyponatremia – seizures: titrate 3% NaCl; usual dose 1.5-2.5 mmol/kg