칼륨은 세포 내 가장 많은 전해질이며 약 96%가 세포 내 존재하고 특히 위장관계에 풍부하다. 혈청 내 칼륨 농도: 3.5- 5.0 mEq/L (혈청 내 칼륨이 2.5 이하이거나 7.0 이상이면 심장마비를 초래할 수 있다) 정상인의 1일 칼륨 요구량: 40-60mEq/L이고 80-90%의 칼륨은 신장을 통해 배설되고 나머지는 대변으로 배설된다.

기능은

• 세포 내 삼투질 농도 조절
• 신경 자극의 전도와 골격근, 심장, 평활근의 수축을 도움
• 세포대사에서 효소활동과 간에 글리코겐의 저장을 도움
• 수소이온과 세포교환을 통해 산-염기 균형을 유지 (알칼리증→저칼륨혈증, 산증→고칼륨혈증 유발)
• 인슐린은 세포에서 칼륨흡수를 도모함 (따라서 인슐린이 부족한 환자는 종종 고칼륨혈증 발생함)
• 글루카곤은 혈청 칼륨농도를 상승시킴
• 코티졸, 알도스테론, 부신피질 호르몬은 신장에서 칼륨이 배설되고 나트륨이 정체되는 것을 도움

고칼륨혈증(hyperkalemia)은 혈청 내 칼륨이 5.0mEq/L이상 상승한 상태를 말한다. (고칼륨혈증은 신장기능이 정상인 사람에게는 드물게 나타나고 급성신부전이 있는 사람의 경우 50%이상 발생함)

1. 소변 배설량 감소로 체내에 K 정체: 신부전환자, 소변배설량이 감소된 수술환자, 부신피질부전환자
2. 조직손상, 화상, 세포용해, 산증으로 세포에서 K이 과다 유리된 경우 (신장기능이 감소되니까)
3. 칼륨을 포함한 IV용액의 과다투여: 많은 양의 칼륨을 구강 혹은 IV로 투여하고 신부전이 있으면 고칼륨혈증이 생길 수 있지만, 식이로 아무리 많은 양의 칼륨을 섭취하더라도 신장상태가 좋으면 고칼륨혈증이 잘 발생하지 않는다.

칼륨이 혈장 내에 많아지면 세포막의 흥분 역치를 상승시켜 세포의 흥분을 감소시킨다. 이로인해 신경과 근육의 과민성이 경감되고, 따라서 근육이 약화되고 마비가 발생.

급성 고칼륨혈증에서는 혈청 농도가 6.0mEq/L일 때 증상이 발생 고칼륨혈증이 서서히 발생한 경우에는 혈청농도가 7.0mEq/L이상이어도 증상이 나타나지 않을 수도 있다.

• 심혈관계: 초기에는 빈맥, 후기에는 서맥, 부정맥, 저혈압, 심근수축의 약화, 심장수축 약화, 심장마비
• 위장관계: 오심, 설사, 장경련, 장음의 항진(너무 빨리 평활근을 자극하므로)
• 신경근육계: 감각장애, 근육의 허약감, 후기에는 근육이 축 늘어지면서 마비가 옴, 안절부절 못함, 근육경련, 경련
• 신장계: 핍뇨 후기에는 무뇨

1. 혈청 내 칼륨 k> 5.0mEq/L
2. EKG의 변화: T파가 좁아지면서 뾰족해짐, QRS간격이 넓어짐, ST분절이 낮아짐, PR간격이 넓어짐, P파가 낮아짐

1. 고칼륨혈증이 경미할 경우엔 IV로 생리식염수를 투여하고 칼륨을 내보내는 이뇨제를 투여하여 소변량을 늘려서 치료할 수 있다.
2. 고칼륨혈증이 심할 경우엔 치명적인 심장장애가 발생하므로 즉각치료가 중요

• calcium gluconate IV(심근에 미치는 칼륨과다의 길항효과를 감소시키기위함 즉 심장의 흥분을 가라앉혀주기 위함) calcium gluconate는 5분 이내로 작용.
• insulin, 포도당, bivon투여(세포에서 칼륨이 흡수되는 것을 도움)
• albuterol 0.5mg IV (30분이내에 혈청 칼륨농도가 감소시킴, 효과는 6시간동안 지속됨)
• kalimate enema(장에서 K과 Na이 교환되고 교환된 K은 대변으로 배설됨) kalimate enema시 kayexalate가 변비를 초래할 수 있으므로 sorbitol을 함께투여.
• 신부전이 심한 경우 혈액투석 또는 복막투석
• 식이요법 - 혈청칼륨농도가 5.0-5.5mEq/L정도이면 칼륨이 적게 포함된 고탄수화물식이를 제공하여 교정함.

1. EKG 지속적 사정.
2. 고칼륨혈증이 경미하면 V/S, 장기능, urine output, 폐음, 말초부종을 4-8시간마다 사정.
3. K, BUN, Cr 확인
4. 신부전 환자는 hourly urine check
5. 만약 환자가 수혈을 받아야 할 경우 2주이상 된 혈액은 고칼륨혈액의 위험이 있으므로 사용금지.

1. 곡류: 귀리, 기장, 메밀, 수수, 엿기름, 오트밀, 팥, 옥수수, 조, 팝콘, 호밀 감자튀김
2. 과실류: 곶감, 대추, 무화과, 바나나, 참외, 건포도, 살구 자두, 딸기, 오렌지
3. 아채류: 고사리, 마른미역, 말린 통고추, 파래 톳, 고춧잎, 근대, 연근, 냉이, 단무지, 호박, 양배추, 상치, 생강,쑥갓, 부추, 마른버섯, 당근, 시금치, 오이, 토마토
4. 육류: 소고기, 돼지고기, 새우
5. 음료수: 원두커피, 토마토주스, 야채주스

1. 곡류: 국수, 도넛, 밀가루, 식빵, 백미, 쌀밥, 현미밥, 찹쌀, 카스테라, 콘프레이크
2. 과실류: 귤, 레몬, 배, 사과, 수박, 파인애플, 포도
3. 야채류: 옥수수, 무, 숙주, 콩나물, 감자, 고구마
4. 육류: 닭 넓적다리, 소꼬리, 두부, 조개, 해삼
5. 음료수: 인스턴트커피, 콜라, 레몬주스

용혈된 혈액 검체로 인함.

• 혈액 채취시 지혈대를 너무 꽉 조였을 때
• 혈액을 채취하기 위해 같은부위에 여러번 찔렀을 때
• 혈액검체를 주사기로 흡인할 때
• 시험관으로 옮길 때 너무 과한 힘을 가할 때

What is hyperkalemia?

Hyperkalemia is common; it is diagnosed in up to 8% of hospitalized patients in the U.S. Fortunately, most patients have mild hyperkalemia (which is usually well tolerated). However, any condition causing even mild hyperkalemia should be treated to prevent progression into more severe hyperkalemia. Extremely high levels of potassium in the blood (severe hyperkalemia) can lead to cardiac arrest and death. When not recognized and treated properly, severe hyperkalemia results in a mortality rate of about 67%.

Technically, hyperkalemia means an abnormally elevated level of potassium in the blood. The normal potassium level in the blood is 3.5-5.0 milliequivalents per liter (mEq/L). Potassium levels between 5.1 mEq/L to 6.0 mEq/L reflect mild hyperkalemia. Potassium levels of 6.1 mEq/L to 7.0 mEq/L are moderate hyperkalemia, and levels above 7 mEq/L are severe hyperkalemia.

How does hyperkalemia affect the body?

Potassium is critical for the normal functioning of the muscles, heart, and nerves. It plays an important role in controlling activity of smooth muscle (such as the muscle found in the digestive tract) and skeletal muscle (muscles of the extremities and torso), as well as the muscles of the heart. It is also important for normal transmission of electrical signals throughout the nervous system within the body.

Normal blood levels of potassium are critical for maintaining normal heart electrical rhythm. Both low blood potassium levels (hypokalemia) and high blood potassium levels (hyperkalemia) can lead to abnormal heart rhythms.

The most important clinical effect of hyperkalemia is related to electrical rhythm of the heart. While mild hyperkalemia probably has a limited effect on the heart, moderate hyperkalemia can produce EKG changes (EKG is an electrical reading of the heart muscles), and severe hyperkalemia can cause suppression of electrical activity of the heart and can cause the heart to stop beating.

Another important effect of hyperkalemia is interference with functioning of the skeletal muscles. Hyperkalemic periodic paralysis is a rare inherited disorder in which patients can develop sudden onset of hyperkalemia which in turn causes muscle paralysis. The reason for the muscle paralysis is not clearly understood, but it is probably due to hyperkalemia suppressing the electrical activity of the muscle.

Hyperkalemia can be asymptomatic, meaning that it causes no symptoms. Sometimes, patients with hyperkalemia report vague symptoms including:

nausea,

fatigue,

muscle weakness, or

tingling sensations.

More serious symptoms of hyperkalemia include slow heartbeat and weak pulse. Severe hyperkalemia can result in fatal cardiac standstill (heart stoppage). Generally, a slowly rising potassium level (such as with chronic kidney failure) is better tolerated than an abrupt rise in potassium levels. Unless the rise in potassium has been very rapid, symptoms of hyperkalemia are usually not apparent until potassium levels are very high (typically 7.0 mEq/l or higher).

Symptoms may also be present that reflect the underlying medical conditions that are causing the hyperkalemia.

What causes hyperkalemia?

The major causes of hyperkalemia are kidney dysfunction, diseases of the adrenal gland, potassium sifting out of cells into the blood circulation, and medications.

Kidney dysfunction

Potassium is normally excreted by the kidneys, so disorders that decrease the function of the kidneys can result in hyperkalemia. These include:

acute and chronic renal failure,

glomerulonephritis,

lupus nephritis,

transplant rejection, and

obstructive diseases of the urinary tract, such as urolithiasis (stones in the urinary tract).

Furthermore, patients with kidney dysfunctions are especially sensitive to medications that can increase blood potassium levels. For example, patients with kidney dysfunctions can develop worsening hyperkalemia when given salt substitutes that contain potassium, when given potassium supplements (either orally or intravenously), or medications that can increase blood potassium levels. Examples of medications that can increase blood potassium levels include:

ACE inhibitors,

nonsteroidal anti-inflammatory drugs (NSAIDs),

Angiotensin II Receptor Blockers (ARBs), and

potassium-sparing diuretics (see below).

Diseases of the adrenal gland

Adrenal glands are small glands located adjacent to the kidneys, and are important in secreting hormones such as cortisol and aldosterone. Aldosterone causes the kidneys to retain sodium and fluid while excreting potassium in the urine. Therefore diseases of the adrenal gland, such as Addison's disease, that lead to decreased aldosterone secretion can decrease kidney excretion of potassium, resulting in body retention of potassium, and hence hyperkalemia.

Potassium shifts

Potassium can move out of and into cells. Our total body potassium stores are approximately 50 mEq/kg of body weight. At any given time, about 98% of the total potassium in the body is located inside of cells (intracellular), with only 2% located outside of cells (in the blood circulation and in the "extracellular" tissue). The blood tests for measurement of potassium levels measure only the potassium that is outside of the cells. Therefore, conditions that can cause potassium to move out of the cells into the blood circulation can increase the blood potassium levels even though the total amount of potassium in the body has not changed.

One example of potassium shift causing hyperkalemia is diabetic ketoacidosis. Insulin is vital to patients with type 1 diabetes. Without insulin, patients with type 1 diabetes can develop severely elevated blood glucose levels. Lack of insulin also causes the breakdown of fat cells, with the release of ketones into the blood, turning the blood acidic (hence the term ketoacidosis). The acidosis and high glucose levels in the blood work together to cause fluid and potassium to move out of the cells into the blood circulation. Patients with diabetes often also have diminished kidney capacity to excrete potassium into urine. The combination of potassium shift out of cells and diminished urine potassium excretion causes hyperkalemia.

Another cause of hyperkalemia is tissue destruction, dying cells release potassium into the blood circulation. Examples of tissue destruction causing hyperkalemia include:

trauma,

burns,

surgery,

hemolysis (disintegration of red blood cells),

massive lysis of tumor cells, and

rhabdomyolysis (a condition involving destruction of muscle cells that is sometimes associated with muscle injury, alcoholism, or drug abuse).

Medications

Potassium supplements, salt substitutes that contain potassium and other medications can cause hyperkalemia.

In normal individuals, healthy kidneys can adapt to excessive oral intake of potassium by increasing urine excretion of potassium, thus preventing the development of hyperkalemia. However, taking in too much potassium (either through foods, supplements, or salt substitutes containing potassium) can cause hyperkalemia if there is kidney dysfunction or if the patient is taking medications that decrease urine potassium excretion such as ACE inhibitors and potassium-sparing diuretics.

Examples of medications that decrease urine potassium excretion include:

ACE inhibitors,

ARBs,

NSAIDs,

potassium-sparing diuretics such as:

spironolactone (Aldactone),

triamterene (Dyrenium), and

trimethoprim-sulfamethoxazole (Bactrim). Even though mild hyperkalemia is common with these medications, severe hyperkalemia usually do not occur unless these medications are given to patients with kidney dysfunction.

How is hyperkalemia diagnosed?

Blood is withdrawn from a vein (like other blood tests). The potassium concentration of the blood is determined in the laboratory. If hyperkalemia is suspected, an electrocardiogram (ECG or EKG) is often performed, since the ECG may show changes typical for hyperkalemia in moderate to severe cases. The ECG will also be able to identify cardiac arrhythmias that result from hyperkalemia.

Treatment of hyperkalemia must be individualized based upon the underlying cause of the hyperkalemia, the severity of symptoms or appearance of ECG changes, and the overall health status of the patient. Mild hyperkalemia is usually treated without hospitalization especially if the patient is otherwise healthy, the ECG is normal, and there are no other associated conditions such as acidosis and worsening kidney function. Emergency treatment is necessary if hyperkalemia is severe and has caused changes in the ECG. Severe hyperkalemia is best treated in the hospital, oftentimes in the intensive care unit, under continuous heart rhythm monitoring.

Treatment of hyperkalemia may include any of the following measures, either singly or in combination:

A diet low in potassium (for mild cases).

Discontinue medications that increase blood potassium levels.

Intravenous administration of glucose and insulin, which promotes movement of potassium from the extracellular space back into the cells.

Intravenous calcium to temporarily protect the heart and muscles from the effects of hyperkalemia.

Sodium bicarbonate administration to counteract acidosis and to promote movement of potassium from the extracellular space back into the cells.

Diuretic administration to decrease the total potassium stores through increasing potassium excretion in the urine. It is important to note that most diuretics increase kidney excretion of potassium. Only the potassium-sparing diuretics mentioned above decrease kidney excretion of potassium.

Medications that stimulate beta-2 adrenergic receptors, such as albuterol and epinephrine, have also been used to drive potassium back into cells.

Medications known as cation-exchange resins, which bind potassium and lead to its excretion via the gastrointestinal tract.

Dialysis, particularly if other measures have failed or if renal failure is present.

Treatment of hyperkalemia naturally also includes treatment of any underlying causes (for example, kidney disease, adrenal disease, tissue destruction) of hyperkalemia.

• 출처: http://www.medicinenet.com/hyperkalemia/index.htm