Hyperkalemia is a common electrolyte imbalance characterized by elevated serum potassium. Hyperkalemia is defined as serum potassium concentrations greater than 5.5 mmol/L (normal range is 3.5 to 5.0 mmol/L). In the body, ninety-eight percent of potassium is intracellular, and the 2 % left is extracellular which is needed for nerve conduction and muscle contraction. For this reason, extracellular potassium concentration is tightly regulated through renal potassium excretion. Up to 90% of dietary intake of potassium is excreted by the kidney. As kidney function declines, the kidney compensates and aldosterone levels increase in order to boost potassium excretion. However, compensatory mechanisms may become overwhelmed, and result in hyperkalemia (Raymond & Wazny, 2010). Potassium plays an important role in nerve and muscle function. As a result of this role, abnormalities in serum potassium may trigger membrane excitability and considerable nerve, muscle and cardiac dysfunction leading to ventricular arrhythmias and subsequently sudden cardiac death. It is estimated that between 1% and 10% of patients admitted to a hospital experience hyperkalemia, with a mortality rate of 1 per 1,000 (Raymond & Wazny,2010).
Causes of Hyperkalemia Many causes of hyperkalemia are seen in clinical practice. The most typical causes are: renal disease, and also the consumption of medications that predispose the patient to hyperkalemia (Parham, W.; Mehdirad,
Potassium works with sodium to regulate the body’s water balance. The kidneys help to control the blood pressure by controlling the amount of fluid stored in the body. Therefore, the more fluid then the higher the blood pressure is. The kidneys do this by filtering out the blood and extracting any extra fluid, which then is stored in the bladder as urine. This is done very delicately as both sodium and potassium pull the water across the wall of the cells from the bloodstream into a collecting channel that leads to the bladder. When eating to much salt, the amount of sodium in the bloodstream will be imbalanced compared to the amount of potassium and thus reducing the ability of the kidneys remove the extra fluid. Eating more fruit and vegetables, the potassium levels increase and can help restore the chemical imbalance. However, there is a possibility of too much potassium, also known as hyperkalemia, which can lead to other issues like renal failure.
1. ECF potassium levels affect resting membrane potential. Hyperkalemia (excessive levels of potassium in the blood) and hypokalemia (abnormally low blood potassium levels) both affect the function of nerves and muscles.
I am concerned about potassium intake because it plays an important role in regulating heartbeat, lowering blood volume and blood pressure (Hammond, 2016d). The lack of potassium intake will lead to irregular heartbeat and life-threatened diseases such as hypokalemia (Hammond, 2016d). In order to increase my potassium consumption, animal foods and plant foods especial fresh vegetable and fruit are needed (Hammond, 2016d).
Metabolic alkalosis is a condition in which the body fluids have excess base. The kidneys and lungs maintain the proper balance of chemicals, called acids and bases, in the body. Decreased carbon dioxide or increased bicarbonate level makes the body too alkaline. There are different types of alkalosis such as: respiratory alkalosis, which is caused by a low carbon dioxide level in the blood. This can be due to: fever, lack of oxygen, lung disease, or liver disease; hypochloermic alkalosis is caused by an extreme lack or loss of chloride, from prolonged vomiting; hypokalemic alkalosis is caused by the kidneys’ response to an extreme lack of potassium, this can occur from taking certain water pills. Compensated alkalosis occurs when the body returns to the acid-base balance to normal in cases of alkalosis, but bicarbonate and carbon dioxide levels remain abnormal. Symptoms of alkalosis can include: confusion, hand tremor, light-headedness, muscle twitching, vomiting, and numbness or tingling in the face, hands, or feet. Treatment for alkalosis depends on
Hyperkalemic Periodic Paralysis Disease (HYPP) is a muscular disorder found prominently in horses that occurs due to an inherited genetic mutation [1]. Specifically, a point mutation in the sodium channel gene, found in the muscle of affected horses, is passed on to offspring [1]. Sodium channels found in the muscle cell membrane primarily control muscle fiber contraction [1]. According to research summarized by UC Davis, when this defective sodium channel gene is present, the channels “leak” due to fluctuation of blood potassium levels, causing the muscle to depolarize and to contract involuntarily [4]. These fluctuating potassium levels may result from a period of fasting, followed by intake of high potassium feed, such as alfalfa [1]. Ultimately, the depolarization causes the muscles to lose their effectiveness, and myopathy eventually develops [4]. All horses positive for the HYPP gene mutation are affected for their entire lives [2].
Patients with renal failure, tissue destruction, adrenal gland disease and certain medication can increase potassium levels in the body. High levels of potassium can lead to cardiac arrest. Potassium rich food should be avoided until potassium levels return to normal. Medication such as a water pill can be administered to remove excess potassium via the urinary track. High amounts of potassium can lead to life threatening heart changes and intake of potassium should be stopped until potassium is within normal range.
of aldosterone falls too low, the kidneys cannot regulate salt and water balance, resulting in the
Importantly, an administration of 0.9% NaCl or hypertonic NaCl (3 – 7.5% NaCl) also causes corrected hyperchloremia since it contains significantly higher proportion of chloride concentrations compared to sodium concentration ([Na+] = [Cl-] in 0.9% NaCl) than physiologically normal serum concentrations ([Na+] > [Cl-]). Development of corrected hyperchloremia and subsequent metabolic acidosis is also exacerbated by KCl supplementation. For example, 0.9% sodium chloride supplemented with 20 mEq/L KCl has a final chloride concentration of 174 mEq/L ([Na+] < [Cl-]). Experimentally, chronic respiratory alkalosis causes renal chloride retention in dogs, and patients with chronic hypocapnia may be expected to develop corrected hyperchloremia leading to compensatory metabolic
In addition to the disorders in the metabolism, patients with DKA experience a condition known as Hyperglycemia-Induced Osmotic Diuresis characterized by the intracellular and extracellular shift of increased glucose levels in the blood, and leads to electrolyte imbalance, increased serum osmolality, and dehydration. Affected electrolytes include sodium, potassium, magnesium, calcium, and phosphorus. Hypokalemia occurs as a result of absorption of potassium from cell to skeletal muscle (Gosmanov, Gosmanova, & Dillard-Cannon 2014). These changes may cause a false elevation of serum potassium levels (Sole et al. 2013).
Hyponatremia is a common electrolyte imbalance seen by medical professionals. The cause is a disruption of sodium water homeostasis usually maintained by “complex multi-system physiological mechanism” explained Soiza et al (2014).
Chronic kidney disease is linked with the following fluids and electrolyte imbalance; fluid retention, hyperkalemia, hypernatremia, and hypomagnesemia (Kohan & Barton, 2014). Hyperkalemia is the accumulation of potassium ions in the blood which leads to muscle weakness, tiredness, and cramping of the abdomen (Nyhan, 2017). On the other hand,
In multi-cellular organisms, cells are characterized by energetically favorable gradient moving potassium from the intracellular to the extracellular environment. Inwardly rectifying potassium-selective (Kir), channels encoded by the KCNJ gene family are constitutively active and favor the influx of potassium more readily than its efflux from the cells, thereby maintaining potassium homeostasis. Kir channels are also known as IRK or KCNJ channels. Fifteen mammalian KCNJ gene products have been described which result in seven distinct Kir channels (Hibino et al., 2010; Sharman et al., 2011). These channels are located within the plasma membrane of most cell types, where they regulate membrane potential and potassium homeostasis (Table 1)
When someone is diagnosed with hypertension or elevated blood pressure they are advised to lower their sodium intake and increase their potassium intake. This is based on the idea when there is an increase in the levels of sodium in our system this causes retention of higher levels of fluid. This in turn increases our blood pressure by increasing total peripheral resistance. Potassium has a complimentary role in blood pressure regulation not only does it compliment the excretion of sodium to maintain homeostasis it is vasoactive, meaning it is able to increase blood flow by means of vasodilatation.
In particular, too much potassium can be harmful to people with kidney disorders and older people whose kidneys are less able to remove potassium from their blood.