Blood Biochemical Analysis Case Study Example
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Electrolytes are present inside the body in various compartments and their concentrations are kept under strict control owing to their major role in electric potential. Movements and exchange of the ions causes alteration in the polarity of the cell and its membrane. This dynamism in polarity ultimately compels the electrical potential to reach the threshold to elicit and sustain action potentials. In a normal milieu, this process is done several times whenever signals are received from higher centers to generate an action potential. In this process, necessary amount of these electrolytes are consumed but they are essentially replaced rapidly. Therefore, any condition or process that may lead to either decreased intake or increased turnover of these electrolytes produces various symptoms which are manifested in all the systems of the body.
Before explaining the pathologic state, it is very essential to understand the normal distribution of these electrolytes along the various physiological compartments of the body. According to Barrett, Boitano, Barman and Brooks (2010), the unequal distribution of these electrolytes is crucial to the body. Sodium is more abundant in the extracellular fluid compared to small amounts of potassium. On the contrary, potassium is abundantly residing in the intracellular fluid while sodium is present in minute quantities.
According to Guyton and Hall (2006), potassium is maintained predominantly by the kidneys and only 5-10% of the total intake is excreted through fecal matter. Like other electrolytes, kidney is therefore the key organ in adjusting rapidly and accurately according to the intake and demand of potassium in the body. According to Papadakis and McPhee (2015), described decreased potassium as the most common cause of hypokalemia and it tops the list of causes of hypokalemia. According to El-Sherif and Turitto (2011), it is the most common electrolyte imbalance condition that occurs clinically and the authors also described the underlying mechanism that leads to the deleterious events caused by hypokalemia. Hypokalemia causes deficit of positive charge which ultimately increases the negativity making the resting membrane potential (RMP) higher during the cardiac diastole. The raised resting membrane potential makes the membrane refractory to excitation due to difference in threshold potential (TP) and widened resting membrane potential. The decreased extracellular potassium upholds the action potential duration and procrastinates repolarization. Hypokalemia also alters the action potential by increasing the phase two initially and then decreasing it. The slant of phase 3 decelerates. The relative refractory period (RRP) is increased with a decrease in difference between threshold potential and resting membrane potential at the end of the action potential. The cardiac tissue becomes frequently excitable and conduction is slowed due to incomplete repolarization of fibers. According to Lee (2010), hypokalemia may cause a highly unwanted complicated related to the cardiovascular system that may prove fatal and is associated with adverse outcomes and bad prognosis, which is development of cardiac arrhythmias. According to Barrett, Boitano, Barman and Brooks (2010), hypokalemia may be manifested as various peculiar electrocardiographic recordings. They are depression of ST-segment, PR-interval becomes 0.2 seconds, QRS interval becomes 0.06 seconds, appearance of a prominent U wave that follows T wave instantly. The authors also mentioned that at a dangerously low potassium levels, PR interval may be prolonged as much as 0.32 seconds with ST depression and inversion of T waves followed by prominent U wave. Lee (2010) also suggests that hypokalemia may cause flattening of T-wave that can become evident on the electrocardiogram. It is very pivotal to understand that Mr. Fluentsa developed electrolyte imbalance mainly because of inadequate intake but also because he was started on gentamycin, an aminoglycoside. According to Katzung, Masters and Trevor (2012), aminoglycosides are nonreabsorbable anions which have the tendency to cause hypokalemia owing to their property to cause obligatory potassium loss through urine. Therefore, the development of arrhythmia secondary to hypokalemis in Mr. Fluentsa is justified when he complained of feeling of jumping heart.
Another important mineral that is decreased in Mr. Fluentsa’s body fluids is calcium. Besides performing a crucial role in nerve signal transmission, calcium is responsible to carry out various other functions in the body which are very essential for the human body and its systems. This lowering of calcium may have contributed to the cardiac symptoms developed by Mr. Fluentsa later on 3rd post-hospitalization day. According to Fulop (1998), hypocalcemia may develop in intensive care unit (ICU) based critically ill patients like Mr. Fluentsa. The author mentioned that hypomagnesemia may lead to hypocalcemia as proved and published by Suh, Tashjian, Matsuo, Parkinson and Fraser (1973). The authors suggested that this synergism is not very extensively explained but it is thought that it results when end organs becomes refractory or resistant to circulating parathyroid hormone (PTH). But this theory is controversial and evidence has been collected to negate this hypothesis. Hinkle (2011) describes the central role of calcium in the cardiac contractility and integrity. The author suggested that calcium maintains the integrity of the cardiac cell wall and regulate its permeability. It is the main mineral that is required for the formation of actin-myosin cross bridges whenever myocardium is to contract. It is also stated that calcium generates cardiac action potentials and function of the pacemaker. Lee (2010) further states that ICU based patients have bad prognosis and higher mortality rate if they have developed hypocalcemia. The author also mentioned few symptoms of hypocalcemia that are tetany, papilledema, and seizures. In a long standing hypocalcemia, neurological and psychiatric symptoms may develop like emotional lability, calcification of basal ganglia, and extrapyramidal dysfunction. The most important cardiovascular manifestation is prolonged QT syndrome, arrhythmias and cardiac failure. El-Sharif and Turitto (2011) explained the electropathophysiologyof cardiac manifestations of hypocalcemia. During the plateau phase of action potential, low concentrations of calcium causes decreased intracellular calcium concentration and causes slowing of the inward current. Decreased intracellular calcium leads to prolongation of action potential and the duration of refractory period which ultimately leads to decreased cardiac contractility. Hinkle (2011) also described the electrocardiographic findings of hypocalcemia and stated that patient may present with prolongation of ST segment, prolongation of QT interval and may also cause flattening or inversion of T wave which can be recorded on electrocardiogram.Papadakis and McPhee (2015) mentions prolonged QT interval as the sole culprit behind the development of ventricular arrhythmias in a hypocalcemic state.Based on the existing evidence, it is quite easily comprehensible that calcium also has a very important role in the overall integrity of the cardiac contractility and its functioning. Therefore, in Mr.Fluentsa’s case, there is a possibility that hypocalcemia co existent with hypokalemia may have potentiated the effects that leads to the development of arrhythmias. In such a case, meticulous monitoring and necessary intervention is warranted to decrease the mortality.
According to Limaye, Londhey, Nadkar and Borges (2011), magnesium is the second most common cation present intracellularly. It has many functions like homeostasis, as an ATP co-factor for the hydrolysis and hair integrity. The authors also mentioned that magnesium can be decreased if a patient is taking aminoglycosides. In Mr. Fluentsa’s case, he was recently started on gentamycin which is an aminoglycoside. Lee (2010) suggests that hypomagnesemia is more common in patients who are hospitalized in an intensive care unit. The author also mentioned that severe hypomagnesemia may lead to cardiogenic symptoms like arrhythmia, torsades de pointes, seizure, coma and death. It is also postulated that it is always coexistent with other electrolyte imbalance like hypocalcemia or hypokalemia. El-Sherif and Turitto (2011) explained the electrophysiology and stated that magnesium exerts an alternating force that affects the currents modulating duration of ventricular action potential. The study also concluded that hypomagnesemia is arrythmogenic only if it is coexistent with hypokalemia
In a nut shell, it is very apparent based on the facts and evidence mentioned in the previous text that electrolytes are to be maintained vigilantly and should remain confined to their respective compartments. In Mr. Fluentsa’s case, it is possible that electrolyte imbalance is a result of combination of decreased intake or it could also be drug induced. Nevertheless, all three electrolytes that are deranged in this case are linked to each other on etiopathogenetic basis. It is also very clear that they are associated with bad prognosis and higher mortality. Therefore, intensive care with aggressive interventions should be done to minimize the risk associated with it.
Barrett, K., Brooks, H., Boitano, S., & Barman, S. (2010). Cardiovascular Physiology. In Ganong's Review of Medical Physiology (23rd ed.). New York: McGraw-Hill Medical.
El-Sharif, N., &Turitto, G. (2011).Electrolyte disorders and arrhythmogenesis. Cardiology Journal, 18(3), 233-245.
Fulop, M. (1998).Algorithms for diagnosing some electrolyte disorders. The American Journal of Emergency Medicine, 16(1), 76-84.
Guyton, A., & Hall, J. (2006). Textbook of Medical Physiology (11th ed.). Philadelphia: Elsevier Saunders.
Hinkle, C. (2011). Electrolyte Disorders In The Cardiac Patient. Critical Care Nursing Clinics of North America, 23, 635-643.
Katzung, B., Masters, S., & Trevor, A. (2012). Chapter 45; Aminiglycosides and Spectinomycin. In Basic and Clinical Pharmacology (12th ed.). New York: McGraw-Hill Medical Publishing Division.
Lee, J. (2010). Fluid and Electrolyte Disturbances in Critically Ill Patients. Electrolytes & Blood Pressure, 8, 72-81.
Limaye, C., Londhey, V., Nadkar, M., & Borges, N. (2011).Hypomagnesemia in Critically Ill Medical Patients. Journal of the Association of Physicians of India, 59, 19-22.
Papadakis, M., & McPhee, S. (2015).Electrolyte & Acid-Base Disorders. In Current Medical Diagnosis & Treatment 2015 (54th ed.). New York: McGraw-Hill Education/Medical.
Suh, S. M., Tashjian, A. H., Matsuo, N., Parkinson, D. K., & Fraser, D. (1973). Pathogenesis of Hypocalcemia in Primary Hypomagnesemia: Normal End-Organ Responsiveness to Parathyroid Hormone, Impaired Parathyroid Gland Function. Journal of Clinical Investigation, 52(1), 153–160.
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