Changes In Plasma Potassium Levels Research Articles

Association Between Average Plasma Potassium Levels and 30-day Mortality During Hospitalization in Patients with COVID-19 in Wuhan, China.

Background: Coronavirus disease 2019 (COVID-19) has resulted in more than 610,000 deaths worldwide since December 2019. Given the rapid deterioration of patients' condition before death, markers with efficient prognostic values are urgently required. During the treatment process, notable changes in plasma potassium levels have been observed among severely ill patients. We aimed to evaluate the association between average plasma potassium (Ka+) levels during hospitalization and 30-day mortality in patients with COVID-19.Methods: Consecutive patients with COVID-19 hospitalized in the Zhongfaxincheng branch of Tongji Hospital in Wuhan, China from February 8 to 28, 2020 were enrolled in this study. We followed patients up to 30 days after admission.Results: A total of 136 patients were included in the study. The average age was 62.1±14.6 years and 51.5% of patients were male. The median baseline potassium level was 4.3 (3.9-4.6) mmol/L and Ka+ level during hospitalization was 4.4 (4.2-4.7) mmol/L; the median number of times that we measured potassium was 4 (3-5). The 30-day mortality was 19.1%. A J-shaped association was observed between Ka+ and 30-day mortality. Multivariate Cox regression showed that compared with the reference group (Ka+ 4.0 to <4.5 mmol/L), 30-day mortality was 1.99 (95% confidence interval [CI]=0.54-7.35, P=0.300), 1.14 (95% CI=0.39-3.32, P=0.810), and 4.14 (95% CI=1.29-13.29, P=0.017) times higher in patients with COVID-19 who had Ka+ <4.0, 4.5 to <5.0, and ≥5.0 mmol/L, respectively.Conclusion: Patients with COVID-19 who had a Ka+ level ≥5.0 mmol/L had a significantly increased 30-day mortality compared with those who had a Ka+ level 4.0 to <4.5 mmol/L. Plasma potassium levels should be monitored routinely and maintained within appropriate ranges in patients with COVID-19.

Pre0induction hypokalaemic phenomenon in Nigerian adult population

Anaesthesia in the perioperative period is characterized by acute changes in plasma potassium (K+) which may be caused by anxiety. Anxiety leads to an intracellular shift of potassium which may lead to hypokalaemia. These fluctuations in plasma potassium may sometimes induce arrhythmias. This study was designed to determine the acute changes in plasma potassium levels in the immediate pre-induction period in a sample of Nigerian patients and to determine the incidence of arrhythmias correlating with these changes. Sixty ASA I and II adults aged 14 to 70 years, both genders, undergoing elective surgery under general anaesthesia at the Lagos University Teaching Hospital were prospectively and consecutively recruited. Preoperative plasma potassium level was determined 1-3 days before surgery. Premedication was with oral diazepam 10-20 mg given nocte and on the morning of surgery. Pre-induction plasma potassium level was determined within 5 minutes before induction of anaesthesia. Mean preoperative K+ was 3.98 +/- 0.38 mEq.L(-1) (range of 3.5 - 4.9 mEqL(-1)). The mean pre-induction plasma K+ level was 3.01 +/- 0.35 mEq.L(-1) (range of 2.1 - 3.6). This represented a fall of 24% (0.97 +/- 0.39 mEq.L(-1)) which was significantly different (p < 0.001). More than 80% of the patients exhibited some fall in plasma K+. No arrhythmias were recorded during the study period. Pre-induction hypokalaemia occurred frequently despite the administration of anxiolysis with diazepam. There is a need to consider this phenomenon and measure K+ levels immediately pre-induction especially in patients with existing borderline normal K+ levels.

Acute aldosterone antagonism improves cardiac vagal control in humans

ObjectivesWe have examined the acute effects (<45 min) of aldosterone antagonism on heart rate variability and baroreflex sensitivity, markers of cardiac vagal control, in 13 healthy subjects. BackgroundEvidence for the beneficial effects of aldosterone antagonists comes from studies showing increased survival rates following their addition to standard heart failure therapy. Many mechanisms have been suggested for this action, including effects upon the autonomic nervous system. MethodsHeart rate variability and baroreflex sensitivity were examined 30 min following the administration of potassium canrenoate (intravenous) (aldosterone antagonist) or saline (control). ResultsActive treatment reduced resting heart rate (−6 ± 1 beats/min [mean ± standard error mean]) compared to control (0 ± 1 beat/min) (p < 0.001) and increased measures of high frequency (HF) heart rate variability. Root mean square of successive RR interval differences increased by 21 ± 5 ms versus −6 ± 5 ms control (p < 0.001); HF power increased by 1,369 ± 674 ms2with aldosterone antagonism compared to −255 ± 431 ms2following saline infusion (p < 0.01). Baroreflex sensitivity (alpha-HF) was increased after active treatment (+4 ± 2 ms/mm Hg vs. 0 ± 1 ms/mm Hg control [p < 0.05]). No changes in plasma potassium levels were observed. ConclusionsThese results provide evidence that aldosterone antagonists acutely improve cardiac vagal control, irrespective of any diuretic effects, and may in part explain their beneficial effects in treatment of heart failure.

Reversible hypophosphatemia during moderate hypothermia therapy for brain-injured patients.

Because plasma potassium, which may similarly change as plasma phosphate (P), decreases during moderate hypothermia, plasma P, a requisite electrolyte for the cell function, may alter during therapeutic moderate hypothermia for brain-injured patients. In 22 such patients who underwent moderate hypothermia or were treated with normothermia, plasma concentrations of P and other chemicals were examined. A prospective study. The intensive care unit of a medical university hospital. In 15 consecutive patients with brain injury who underwent moderate hypothermia and 7 serial patients treated with normothermia, plasma concentrations of P, potassium, glucose, blood gas tension and pH, daily urine volume, and water balance were examined. Inequality in the numbers of patients of the two groups was the result of patient exclusion because of multiple trauma, aluminum hydroxide administrations, hyperventilation, preexisting diabetes mellitus, or administration of insulin. Daily blood sampling was done around 8 am. Inclusion criteria included a Glasgow Coma Scale score assessment < or = 8 at admission to the emergency room and evidence of injury on computerized tomography scanning of the brain. Hypothermia decreased plasma P levels as compared with those of normothermia within 4 days after the injury (this period was similar to the duration of the hypothermic phase in the hypothermia group). Such reduction related to changes in blood glucose levels, but not to any in the urine volume, or water balance. The P decrease occurred during the hypothermic phase, but subsequently there was a recovery of P after the rewarming phase. The changes in plasma potassium levels were similar to those in plasma P concentrations during the course. Such changes were accompanied by a recovery of decreased heart rate that occurred during the hypothermic phase. The results suggest that moderate hypothermia of 32-33 degrees C decreases plasma P levels. Further studies are required to examine whether P repletion may overcome certain hemodynamic derangements during moderate hypothermia in brain-injured patients.

Induced Hypocalcaemia in Cows and Sheep II. Changes in Plasma Potassium Levels

Mean plasma potassium levels were significantly lowered by 0·39 mmol/l ( P < 0·01) and 0·48 mmol/l ( P < 0·05) respectively for a decrease of 1 mmol/l in EDTA titratable plasma calcium level in two groups of cows in which hypocalcaemia was induced to the ‘recumbent comatose’ stage by the infusion of Na 2 EDTA over approximately three hours. In these cows plasma potassium levels did not return to normal in parallel with plasma calcium and did not start to rise until at least two hours after the nadir of hypocalcaemia. Plasma potassium levels remained relatively constant in a control experiment in which saline infusions over a similar period of time were carried out in the larger group of cows. Analysis of variance of the results in this group of cows showed a significant ( P < 0·01) cow × infusion interaction. No difference in response of plasma potassium levels was observed in two groups of six wethers, one of which was infused with 0·9% saline and acted as a control group while the other was infused with Na 2 EDTA and hypocalcaemia induced. The possible roles of parathormone and stress in producing the observed changes in plasma potassium levels are discussed.

Potassim-aldosterone-renin interrelationships.

The present study was performed to assess the sensitivity of the renin-angiotensin-aldosterone axis to small changes in plasma potassium concentration within the physiologic range. Small increments in potassium levels were accomplished by graded constant infusions of potassium chloride over 2 h (0.17 meq/min; 0.33 meq/min; 0.5 meq/min) in 8 normal subjects on a 10 meq sodium-100 mgq potassium intake. Plasma levels of aldosterone, renin activity, angiotensin II, cortisol, potassium and sodium were measured at frequent intervals. There were no significant changes observed in plasma sodium, renin activity or angiotensin II levels while cortisol levels declined in the expected diurnal pattern. During the 0.17 meq/min (10 meq/h) infusion potassium levels did not increase significantly until 120 min while plasma aldosterone levels rose significantly at 30-60 min. The mean increment above control during the lowest infusion rate was 0.2 meq/liter (5%) for plasma potassium and 13 ng/100 ml (46%) for plasma aldostreone. Although there was a stepwise increase in the increments above control of both potassium and aldosterone levels as the rate of the infusion was increased, the most sensitive area of the dose response curve appears to be 0.1-0.5 meq/liter. in six normal subjects the potassium-lowering effect of glucose ingestion (0.25 g/kg/15 min over a 2-h period) was assessed. The mean maximal potassium decrement below control 0.3 meq/liter (8%) at 90 min was coincident with the mean plasma aldosterone decrement below control of 11 ng/100 ml (46%). Plasma aldosterone then rose to peak levels at 180 min (mean increment 22 ng/100 ml above nadir) while potassium levels remained below control. The rise in plasma aldosterone was associated with a parallel but more rapid rise in plasma renin activity, peaking at a level 108% above control. Ninety minutes after the termination of the glucose ingestion, plasma aldosterone returned to control levels but now in the setting of reduced levels of plasma potassium and elevated levels of plasma renin activity. The data support an important role for physiologic changes in extracellular potassium concentration in the control of aldosterone secretion and indicate that interpretation of studies assessing acute changes in plasma aldosterone must carefully consider minor simultaneous changes in plasma potassium levels. The data also document that acute changes in extracellular potassium concentration play a role in the regulation of renin secretion.