Finerenone's Impact on Major Adverse Cardiovascular Events in Chronic Kidney Disease and Type 2 Diabetes Mellitus: A Systematic Review.

Chronic kidney disease (CKD) impacts about 10% of adults globally and substantially elevates the risk of major adverse cardiovascular events (MACE), such as heart attacks, strokes, cardiovascular-related deaths, and hospital admissions due to heart failure. The interplay between CKD and cardiovascular disease (CVD) leads to poor health outcomes. Nevertheless, there is a scarcity of systematic reviews focusing on the effectiveness of finerenone, a new non-steroidal mineralocorticoid receptor antagonist (MRA), in lowering these risks. In this systematic review, we aim to evaluate the impact of finerenone on reducing MACE in individuals with CKD and type 2 diabetes mellitus (T2DM). CKD pathophysiology involves hyperglycemia, hypertension, and dyslipidemia, leading to glomerular hyperfiltration, inflammation, and fibrosis. Traditional treatments, including angiotensin-converting enzyme inhibitors (ACEi), angiotensin II receptor blockers (ARBs), and sodium-glucose cotransporter-2 inhibitors (SGLT2i), often fall short in preventing cardiovascular events. Steroidal MRAs like spironolactone and eplerenone, while effective in reducing proteinuria, are limited by hyperkalemia risks. Finerenone offers a more selective mechanism, reducing sodium retention, inflammation, and fibrosis, with a lower risk of hyperkalemia. We searched five electronic databases comprehensively, identifying studies consistently demonstrating that finerenone significantly reduces MACE and improves renal outcomes by reducing albuminuria and slowing the fall in estimated glomerular filtration rate (eGFR). However, limitations include study heterogeneity, short follow-up periods, and potential publication bias. In conclusion, finerenone shows promise as a therapeutic option for CKD and T2DM, reducing MACE and improving renal outcomes. Further research is needed to understand its long-term benefits and safety across diverse populations.

Cardiovascular events in crush syndrome: on-site therapeutic strategies and pharmacological investigations.

Crush syndrome often occurs after severe crush injury caused by disasters or accidents, and is associated with high mortality and poor prognosis. Cardiovascular complications, such as cardiac arrest, hypovolemic shock, and hyperkalemia-related cardiac dysfunction, are the primary causes of on-site death in crush syndrome. Prehospital evaluation, together with timely and correct treatment, is of great benefit to crush syndrome patients, which is difficult in most cases due to limited conditions. Based on current data and studies, early fluid resuscitation remains the most important on-site treatment for crush syndrome. Novel solutions and drugs used in fluid resuscitation have been investigated for their effectiveness and benefits. Several drugs have proven effective for the prevention or treatment of cardiovascular complications in crush syndrome, such as hypovolemic shock, hyperkalemia-induced cardiac complications, myocardial ischemia/reperfusion injury, ventricular dysfunction, and coagulation disorder experimentally. Moreover, these drugs are beneficial for other complications of crush syndrome, such as renal dysfunction. In this review, we will summarize the existing on-site treatments for crush syndrome and discuss the potential pharmacological interventions for cardiovascular complications to provide clues for clinical therapy of crush syndrome.

Management of hyperkalemia: Expert consensus from Kuwait - a Modified Delphi Approach.

Introduction: Hyperkalemia is common in heart failure (HF) patients on renin angiotensin aldosterone inhibitors (RAASi), in chronic kidney disease (CKD), and in hemodialysis, and it negatively impacts their management. New potassium binders, such as sodium zirconium cyclosilicate (SZC), are effective in management of acute and chronic hyperkalemia. However, guidelines inconsistencies and lack of standardized treatment protocols are hindering proper and wider use of such agents. Therefore, an expert panel from Kuwait developed a consensus statement to address hyperkalemia management in acute settings, in HF, in CKD, and in hemodialysis. Methods: A three-step modified Delphi method was adopted to develop the present consensus, which consisted of two rounds of voting and in-between a virtual meeting. Twelve experts from Kuwait participated in this consensus. Statements were developed and shared with experts for voting. A meeting was held to discuss statements that did not reach consensus at the first round and then the remaining statements were shared for final voting. Results: The consensus consists of 44 statements involving an introduction to and the management of hyperkalemia in acute settings, HF, CKD, and hemodialysis. Thirty-six statements approved unanimously in the first vote. In the second vote, four statements were removed and four were approved after editing. Conclusion: Hyperkalemia management lacks standardized definitions, treatment thresholds and consistent guidelines and laboratory practices. This consensus is in response to lack of standardized treatment in the Arabian Gulf, and it aims to establish guidance on hyperkalemia management for healthcare practitioners in Kuwait and highlight future needs.

Hyperkalemia and maintenance of renin-angiotensin system inhibitor therapy after initiating SGLT-2 or DPP-4 inhibitors.

BACKGROUND: Post-hoc analyses of clinical trials suggest that sodium-glucose cotransporter-2 inhibitors (SGLT-2i) lower the risk of hyperkalemia and facilitate the use of renin-angiotensin system inhibitors (RASi) in people with type 2 diabetes. Whether this is also observed in routine care is unclear. We investigated whether SGLT-2i lowered the risk of hyperkalemia and RASi discontinuation as compared to dipeptidyl peptidase 4 inhibitors (DPP-4i). METHODS: Using the target trial emulation framework, we studied adults with type 2 diabetes (T2D) who started SGLT-2i or DPP-4i in Stockholm, Sweden (2014-2021). The outcomes were incident hyperkalaemia (potassium > 5.0 mmol/L), mild hyperkalemia (potassium > 5-≤5.5 mmol/L) and moderate to severe hyperkalemia (potassium > 5.5 mmol/L). Among RASi users, we studied time to RASi discontinuation through evaluation of pharmacy fills. Cox regression with inverse probability of treatment weighting was used to estimate per-protocol hazard ratios (HRs). RESULTS: 29 849 individuals (15 326 SGLT-2i and 14 523 DPP-4i initiators) were included (mean age 66 years, 37% women). About one third of participants in each arm discontinued treatment within a year. Compared with DPP-4i, SGLT-2i use was associated with a lower rate of hyperkalemia (HR 0.77; 95% CI: 0.64-0.93), including both mild (0.76; 0.62-0.93) and moderate/severe (0.53; 0.40-0.69) hyperkalemia events. Of 19.116 participants that used RASi at baseline, 7% discontinued therapy. Initiation of SGLT-2i vs. DPP-4i was not associated with the rate of RASi discontinuation (0.97; 0.83-1.14). Results were consistent in intention-to-treat analyses and across strata of age, sex, cardiovascular comorbidity, and baseline kidney function. CONCLUSIONS: In patients with diabetes managed in routine clinical care, the use of SGLT-2i was associated with lower rates of hyperkalemia compared with DPP-4i. Possibly because of a relatively high rate of treatment discontinuations, this was not accompanied by higher persistence on RASi therapy.

Mortality Risk Stratification Utilizing Artificial Intelligence Electrocardiogram for Hyperkalemia in Cardiac Intensive Care Unit Patients.

Background: Hyperkalemia has been associated with increased mortality in cardiac intensive care unit (CICU) patients. An artificial intelligence (AI) enhanced electrocardiogram (ECG) can predict hyperkalemia, and other AI-ECG algorithms have demonstrated mortality risk-stratification in CICU patients. Objectives: The authors hypothesized that the AI-ECG hyperkalemia algorithm could stratify mortality risk beyond laboratory serum potassium measurement alone. Methods: We included 11,234 unique Mayo Clinic CICU patients admitted from 2007 to 2018 with a 12-lead ECG and blood potassium (K) level obtained at admission with K ≥5 mEq/L defining hyperkalemia. ECGs underwent AI evaluation for the probability of hyperkalemia (probability >0.5 defined as positive). Hospital mortality was analyzed using logistic regression, and survival to 1 year was estimated using Kaplan-Meier and Cox analysis. Results: In the final cohort (n = 11,234), the mean age was 69.6 ± 10.5 years, 37.8% were females, and 92.4% were White. Chronic kidney disease was present in 20.2%. The mean laboratory potassium value for the cohort was 4.2 ± 0.3 mEq/L. The AI-ECG predicted hyperkalemia in 33.9% (n = 3,810) of CICU patients and 12.9% (n = 1,451) of patients had laboratory-confirmed hyperkalemia (K ≥5 mEq/L). In-hospital mortality increased in false-positive, false-negative, and true-positive patients, respectively (P < 0.001), and each of these patient groups had successively lower survival out to 1 year. Conclusions: AI-ECG-based prediction of hyperkalemia, even with a normal laboratory potassium value, was associated with higher in-hospital mortality and lower 1-year survival in CICU patients. This study demonstrated that AI-ECG probability of hyperkalemia may enable rapid individualized risk stratification in critically ill patients beyond laboratory value alone.

Serum Potassium Monitoring Using AI-Enabled Smartwatch Electrocardiograms.

BACKGROUND: Hyperkalemia, characterized by elevated serum potassium levels, heightens the risk of sudden cardiac death, particularly increasing risk for individuals with chronic kidney disease and end-stage renal disease (ESRD). Traditional laboratory test monitoring is resource-heavy, invasive, and unable to provide continuous tracking. Wearable technologies like smartwatches with electrocardiogram (ECG) capabilities are emerging as valuable tools for remote monitoring, potentially allowing for personalized monitoring with artificial intelligence (AI)-ECG interpretation. OBJECTIVES: The purpose of this study was to develop an AI-ECG algorithm to predict serum potassium level in ESRD patients with smartwatch-generated ECG waveforms. METHODS: A cohort of 152,508 patients with 293,557 ECGs paired serum potassium levels obtained within 1 hour at Cedars Sinai Medical Center was used to train an AI-ECG model ("Kardio-Net") to predict serum potassium level. The model was further fine-tuned on 4,337 ECGs from 1,463 patients with ESRD using inputs from 12- and single-lead ECGs. Kardio-Net was evaluated in held-out test cohorts from Cedars Sinai Medical Center and Stanford Healthcare (SHC) as well as a prospective international cohort of 40 ESRD patients with smartwatch ECGs at Chang Gung Memorial Hospital. RESULTS: The Kardio-Net, when applied to 12-lead ECGs, identified severe hyperkalemia (>6.5 mEq/L) with an AUC of 0.852 (95% CI: 0.745-0.956) and a mean absolute error (MAE) of 0.527 mEq/L. In external validation at SHC, the model achieved an AUC of 0.849 (95% CI: 0.823-0.875) and an MAE of 0.599 mEq/L. For single-lead ECGs, Kardio-Net detected severe hyperkalemia with an AUC of 0.876 (95% CI: 0.765-0.987) in the primary cohort and had an MAE of 0.575 mEq/L. In the external SHC validation, the AUC was 0.807 (95% CI: 0.778-0.835) with an MAE of 0.740 mEq/L. Using prospectively obtained smartwatch data, the AUC was 0.831 (95% CI: 0.693-0.975), with an MAE of 0.580 mEq/L. CONCLUSIONS: We validate a deep learning model to predict serum potassium levels from both 12-lead ECGs and single-lead smartwatch data, demonstrating its utility for remote monitoring of hyperkalemia.

BRASH (Bradycardia, Renal Failure, Atrioventricular Nodal Blockade, Shock, and Hyperkalemia) Syndrome: A Frequently Underrecognized Condition Often Confused With Simple Hyperkalemia.

BRASH syndrome, defined by bradycardia, renal failure, atrioventricular nodal blockade, shock, and hyperkalemia, is a relatively new and often underrecognized condition. In this article, we present a case of an elderly female who developed an episode of syncope. She was found to have refractory shock and bradycardia in the emergency department. Laboratory results and other findings led to the diagnosis of a BRASH syndrome, which was refractory to medical therapy alone, requiring transvenous pacing, hemodialysis, and vasopressor support.

Octreotide Causing Hyperkalemia: A Case Report and Review of the Literature.

Octreotide, a synthetic analog of somatostatin, is widely utilized for its inhibitory effects on various hormones, including growth hormone, insulin, and glucagon. Its applications span conditions such as acromegaly, carcinoid tumors, and gastrointestinal bleeding due to its ability to reduce portal venous pressure. Additionally, it serves a crucial role in nuclear medicine imaging and the management of hepatorenal syndrome. We report a case of a 44-year-old man with type 2 diabetes mellitus (T2DM) and stage 5 chronic kidney disease (CKD), not yet on hemodialysis, who presented with persistent severe hypoglycemia. Despite multiple oral glucose administrations, his blood glucose levels remained critically low. The patient was treated with octreotide for sulfonylurea-induced hypoglycemia. However, he developed hyperkalemia as a side effect of octreotide treatment. Traditional therapies for sulfonylurea-induced hypoglycemia often involve intravenous and oral dextrose and glucagon, which may lead to recurrent hypoglycemia due to their stimulatory effects on insulin release. Octreotide directly inhibits insulin release from the pancreas, thus preventing rebound hypoglycemia. However, its administration in patients with renal impairment poses a risk of hyperkalemia due to its suppression of insulin-mediated cellular potassium uptake, and it should be used with caution. This case highlights the potential for life-threatening hyperkalemia induced by octreotide in non-dialysis CKD patients. Physicians must be vigilant about this side effect, particularly in patients with underlying renal impairment. Close monitoring of potassium levels and appropriate management strategies are essential to ensure the safe use of octreotide. This case aims to raise awareness and contribute to a better understanding of octreotide-induced hyperkalemia in CKD patients.

Patiromer Facilitates Angiotensin Inhibitor and Mineralocorticoid Antagonist Therapies in Patients With Heart Failure and Hyperkalemia.

BACKGROUND: Hyperkalemia (HK) is associated with suboptimal renin-angiotensin system (RAS) inhibitor and mineralocorticoid receptor antagonist (MRA) use in heart failure with reduced ejection fraction (HFrEF). OBJECTIVES: This study sought to assess characteristics and RAS inhibitor/MRA use in patients receiving patiromer during the DIAMOND (Patiromer for the Management of Hyperkalemia in Subjects Receiving RAASi Medications for the Treatment of Heart Failure) run-in phase. METHODS: Patients with HFrEF and HK or past HK entered a run-in phase of ≤12 weeks with patiromer-facilitated RAS inhibitor/MRA optimization to achieve ≥50% recommended RAS inhibitor dose, 50 mg/d MRA, and normokalemia. Patients achieving these criteria (randomized group) were compared with the run-in failure group (patients not meeting the randomization criteria). RESULTS: Of 1,038 patients completing the run-in, 878 (84.6%) were randomized and 160 (15.4%) were run-in failures. Overall, 422 (40.7%) had HK entering run-in with a similar frequency in the randomized and run-in failure groups (40.3% vs 42.5%; P = 0.605). From start to the end of run-in, in the randomized group, an increase was observed in target RAS inhibitor and MRA use in patients with HK (RAS inhibitor: 76.8% to 98.6%; MRA: 35.9% to 98.6%) and past HK (RAS inhibitor: 60.5% to 98.1%; MRA: 15.6% to 98.7%). Despite not meeting the randomization criteria, an increase after run-in was observed in the run-in failure group in target RAS inhibitor (52.5% to 70.6%) and MRA use (15.0% to 48.1%). This increase was observed in patients with HK (RAS inhibitor: 51.5% to 64.7%; MRA: 19.1% to 39.7%) and past HK (RAS inhibitor: 53.3% to 75.0%; MRA: 12.0% to 54.3%). CONCLUSIONS: In patients with HFrEF and HK or past HK receiving suboptimal RAS inhibitor/MRA therapy, RAS inhibitor/MRA optimization increased during patiromer-facilitated run-in.

Cardiovascular and Renal Treatment in Heart Failure Patients With Hyperkalemia or High Risk of Hyperkalemia: Rationale and Design of the CARE-HK in HF Registry.

BACKGROUND: Despite guideline recommendations, many patients with heart failure (HF) do not receive target dosages of renin-angiotensin-aldosterone system inhibitors (RAASis) in clinical practice due, in part, to concerns about hyperkalemia (HK). METHODS AND RESULTS: This noninterventional, multinational, multicenter registry (NCT04864795; 111 sites in Europe and the USA) enrolled 2558 eligible adults with chronic HF (mostly with reduced ejection fraction [HFrEF]). Eligibility criteria included use of angiotensin-converting-enzyme inhibitor/angiotensin-II receptor blocker/angiotensin-receptor-neprilysin inhibitor, being a candidate for or treatment with a mineralocorticoid receptor antagonist, and increased risk of HK (eg, current serum potassium > 5.0 mmol/L), history of HK in the previous 24 months, or estimated glomerular filtration rate < 45 mL/min/1.73 m2). Information on RAASi and other guideline-recommended therapies was collected retrospectively and prospectively (≥ 6 months). Patients were followed according to local clinical practice, without study-specific visits or interventions. The main objectives were to characterize RAASi treatment patterns compared with guideline recommendations, describe RAASi modifications following episodes of HK, and describe RAASi treatment in patients treated with patiromer. Baseline characteristics for the first 1000 patients are presented. CONCLUSIONS: CARE-HK is a multinational prospective HF registry designed to report on the management and outcomes of patients with HF at high risk for HK in routine clinical practice.

Hyperkalemia Incidence in Patients With Non-Dialysis Chronic Kidney Disease: A Large Retrospective Cohort Study From United States Clinical Care.

Rationale & Objective: Estimates of the incidence of hyperkalemia in patients with chronic kidney disease (CKD) vary widely. Our objective was to estimate hyperkalemia incidence in patients with CKD from routine clinical care, including by level of kidney damage or function and among important patient subgroups. Study Design: Retrospective cohort study. Setting & Participants: 1,771,900 patients with stage 1-4 CKD identified from the US Optum De-Identified electronic health records database. Exposures or Predictors: Impaired kidney damage or function level at baseline based on urinary albumin-creatinine ratio (UACR) and estimated glomerular filtration rate (eGFR), respectively, and selected patient subgroups. Outcomes: Hyperkalemia: 2 elevated serum potassium values (≥5.5 mmol/L) from the inpatient setting (2-24 hours apart) or outpatient setting (maximum 7 days apart), or 1 elevated serum potassium value plus pharmacotherapy initiation or hyperkalemia diagnosis (maximum 3 days apart). Analytical Approach: Incidence rates of hyperkalemia were calculated. Estimates were stratified by UACR and eGFR level at baseline and patient subgroups. Results: Over a mean follow-up of 3.9 years, the incidence of hyperkalemia was 3.37 events/100 person-years (95% confidence intervals, 3.36-3.38). Higher incidence rates were observed with increased UACR and lower eGFR. Highest rates were observed with UACR ≥3,500 (up to 19.1/100 person-years) irrespective of decreased eGFR level. High rates also occurred in patients with type 2 diabetes mellitus (T2DM, 5.43/100 person-years), heart failure (8.7/100 person-years), and those prescribed steroidal mineralocorticoid receptor antagonists (sMRAs, 7.7/100 person-years). Limitations: Potential misclassification of variables from possible medical coding errors; potential data incompleteness issues if patients received care at institutions not included in Optum. Conclusions: Hyperkalemia is a frequent occurrence in CKD, particularly in patients with T2DM, heart failure, or prescribed sMRAs, indicating the need for regular serum potassium and UACR monitoring in this patient population to help mitigate risk.

People with chronic kidney disease (CKD) have a higher risk of illness, hospitalization, and death than those without CKD. Medicines that are commonly used to slow down CKD progression can sometimes lead to hyperkalemia, where levels of potassium in the blood are higher than normal and which can be potentially dangerous. Concerns about hyperkalemia have led some people with CKD to stop taking their medication. Our study of 1.7 million patients from the United States found that patients with severe kidney damage, as well as those with type 2 diabetes mellitus or heart failure, have a higher risk of hyperkalemia than other patients, indicating they are priority groups for having their potassium levels and level of kidney damage checked regularly.

Rare electrocardiographic findings in a young woman with acute barium poisoning: A case report.

Background: Barium, as a heavy divalent alkaline earth metal, can be found in various products such as rodenticides, insecticides, depilatories, and fireworks. Barium can be highly toxic upon both acute and chronic exposure. The toxicity of barium compounds is dependent on their solubility. Both suicidal and accidental exposures to soluble barium can cause toxicity. Case summary: We report a case characterized by two different wide QRS complex tachycardia in a patient with acute barium poisoning, one due to barium-induced ventricular tachycardia (VT) under hypokalemia and, subsequently, sino-ventricular conduction with intraventricular conduction delay due to hyperkalemia after aggressive potassium supplementation. The latter may be misdiagnosed as VT for the history of acute barium poisoning and the absence of peaked T wave in hyperkalemia. Of note, another hemodynamically unstable VT and profound hypokalemia occurred during the potassium-lowering therapy, which, in addition to barium poisoning, may also be due to the iatrogenic hypokalemia. We also observed the prominent T-U waves at serum potassium of 4.6 mM 12 hours after admission, which may indicate that barium had not been completely cleared from the plasma at that moment. There are some parallels to the Andersen-Tawil syndrome with prominent T-U waves and risk of ventricular tachycardias. To our knowledge, this is the first case report of conversion from hypokalemia to hyperkalemia, and in a short moment, from hyperkalemia to hypokalemia, in acute barium poisoning. Conclusion: In addition to profound hypokalemia secondary to acute barium poisoning, hyperkalemia may also occur after aggressive potassium supplementation. A more careful rather than too aggressive potassium supplementation may be suitable in these cases of hypokalemia due to an intracellular shift of potassium. And a iatrogenic hypokalemia risk in the treatment of rebound hyperkalemia in barium poisoning must be considered.

Patiromer for Heart Failure Medication Optimization in Patients With Current or Past Hyperkalemia: DIAMOND Subanalysis.

BACKGROUND: For heart failure with reduced ejection fraction (HFrEF), suboptimal use of renin-angiotensin-aldosterone system inhibitors (RAASis), including mineralocorticoid receptor antagonists (MRAs), due to hyperkalemia, may be improved by potassium binders. OBJECTIVES: This prespecified analysis of the phase 3 DIAMOND (Patiromer for the Management of Hyperkalemia in Subjects Receiving RAASi Medications for the Treatment of Heart Failure) trial assessed the effect of patiromer in patients with HFrEF and either current or past hyperkalemia. METHODS: Patients with HFrEF and current or past (within 1 year before enrollment) hyperkalemia (serum potassium [sK+] >5.0 mmol/L) entered a single-blind, run-in phase to optimize RAASis while receiving patiromer. They were subsequently randomized, double-blind, to continue patiromer or change to placebo. RESULTS: Of the 1,038 patients who completed run-in, 354 (83.9%) of 422 with current hyperkalemia and 524 (85.1%) of 616 with past hyperkalemia achieved RAASi optimization and were randomized to treatment. During the double-blind phase, patiromer lowered sK+ levels compared with placebo in both the current and past hyperkalemia subgroups: difference in adjusted mean change from baseline: -0.12 (95% CI: -0.17 to -0.07) and -0.08 (95% CI: -0.12 to -0.05), respectively; Pinteraction = 0.166. Patiromer was more effective than placebo in maintaining MRA at target dose in patients with current vs past hyperkalemia (HR: 0.45 [95% CI: 0.26-0.76] vs HR: 0.85 [95% CI: 0.54-1.32]; Pinteraction = 0.031). Adverse events were similar between subgroups. CONCLUSIONS: The use of patiromer facilitates achieving target doses of RAASis in patients with HFrEF with either current or past hyperkalemia. For those with current hyperkalemia before RAASi optimization, use of patiromer may be more beneficial in helping to maintain sK+ control and achieve MRA target dose. (Patiromer for the Management of Hyperkalemia in Subjects Receiving RAASi Medications for the Treatment of Heart Failure [DIAMOND]; NCT03888066).

Efficacy of anti-hyperkalemic agents during cardiopulmonary resuscitation in out-of-hospital cardiac arrest.

Aim: We assessed the efficacy of anti-hyperkalemic agents for alleviating hyperkalemia and improving clinical outcomes in patients with out-of-hospital cardiac arrest (OHCA). Methods: This was a single-center, retrospective observational study of OHCA patients treated at tertiary hospitals between 2010 and 2020. Adult patients aged 18 or older who were in cardiac arrest at the time of arrival and had records of potassium levels measured during cardiac arrest were included. A linear regression model was used to evaluate the relationship between changes in potassium levels and use of anti-hyperkalemic medications. Cox proportional hazards regression analysis was performed to analyze the relationship between the use of anti-hyperkalemic agents and the achievement of return of spontaneous circulation (ROSC). Results: Among 839 episodes, 465 patients received anti-hyperkalemic medication before ROSC. The rate of ROSC was higher in the no anti-hyperkalemic group than in the anti-hyperkalemic group (55.9 % vs 47.7 %, P = 0.019). The decrease in potassium level in the anti-hyperkalemic group from pre-ROSC to post-ROSC was significantly greater than that in the no anti-hyperkalemic group (coefficient 0.38, 95 % confidence interval [CI], 0.13-0.64, P = 0.003). In Cox proportional hazards regression analysis, the use of anti-hyperkalemic medication was related to a decreased ROSC rate in the overall group (adjusted hazard ratio [aHR] 0.66, 95 % CI, 0.54-0.81, P < 0.001), but there were no differences among subgroups classified according to initial potassium levels. Conclusions: Anti-hyperkalemic agents were associated with substantial decreases in potassium levels in OHCA patients. However, administration of anti-hyperkalemic agents did not affect the achievement of ROSC.

Stone heart syndrome: A curious case of digoxin toxicity and calcium infusion.

Stone heart syndrome has a complex interaction with digoxin toxicity, where, theoretically, the administration of intravenous calcium can worsen a patient's condition. Research on this subject is conflicting, so it is imperative to approach it cautiously.

Comparison of Metabolic, Ionic, and Electrolyte Responses to Exhaustive Low-Load Strength Training With and Without Blood Flow Restriction and High-Load Resistance Training.

Low-load blood-flow-restriction resistance training (LL-BFR-RT) is gaining popularity, but its physiological effects remain unclear. This study aimed to compare LL-BFR-RT with low-load resistance exercise (LL-RT) and high-load resistance exercise (HL-RT) on metabolism, electrolytes, and ions in the lower extremities by invasive catheter measurements, which are crucial for risk assessment. Ten healthy men (27.6 ± 6.4 years) completed three trials of knee-extensor exercises with LL-RT (30% 1RM), LL-BFR-RT (30% 1RM, 50% limb occlusion pressure), and HL-RT (75% 1RM). The exercise protocol consisted of four sets to voluntary muscle failure with 1 min of rest between sets. Blood gas analysis was collected before, during, and after each trial through intravenous catheters at the exercising leg. LL-BFR-RT had lower total workload (1274 ± 237 kg, mean ± SD) compared to LL-RT (1745 ± 604 kg), and HL-RT (1847 ± 367 kg, p < 0.01), with no difference between LL-RT and HL-RT. Pain perception did not differ significantly. Exercise-induced drop in oxygen partial pressure, lactate accumulation and electrolyte shifts (with increased [K+]) occurred during under all conditions (p < 0.001). Creatine kinase and lactate dehydrogenase increased significantly 24- and 48-h postexercise under all three conditions (p < 0.001). This study, using invasive catheter measurements, found no significant differences in metabolic, ionic, and electrolyte responses among LL-BFR-RT, LL-RT, and HL-RT when exercised to voluntary muscular failure. LL-BFR-RT reduced time to failure without specific physiological responses.

Prevalence of Hyperkalemia and Familial Hyperkalemic Hypertension in 5100 Patients Referred to a Tertiary Hypertension Unit.

BACKGROUND: Hyperkalemia is a frequent electrolyte alteration whose prevalence varies widely, depending on the adopted cutoff, the setting (inpatients versus outpatients), and the characteristics of the study population. Familial hyperkalemic hypertension (FHH) is a rare cause of hypertension, hyperkalemia, and hyperchloremic metabolic acidosis. METHODS: In this retrospective observational study, we investigated the prevalence of hyperkalemia (serum K+ >5.2 mmol/L on 2 repeated measurements) in 5100 referred patients affected by arterial hypertension, the potential causes, and the associated cardiovascular risk profile. RESULTS: Overall, 374 (7.3%) patients had hyperkalemia. This was associated with drugs known to increase K+ levels (74.6%), chronic kidney disease (33.7%), or both (24.3%). Among the 60 patients with unexplained hyperkalemia, 3 displayed a clinical and biochemical phenotype suggestive of FHH that was genetically confirmed in 2 of them (0.04% in the entire cohort). FHH prevalence rose to 3.3% in patients with unexplained hyperkalemia and up to 29% (2/7) if they had serum K+>5.8 mmol/L. The genetic cause of FHH was a missense variant affecting the acidic motif of WNK1 in 1 family and a rare CUL3 splicing variant, whose functional significance was confirmed by a minigene assay in another. Finally, we observed a significant association between hyperkalemia and the occurrence of cardiovascular events, metabolic syndrome, and organ damage, independent of potential confounding factors. CONCLUSIONS: The identification of hyperkalemia in patients with hypertensive has prognostic implications. A timely diagnosis of FHH is important for effective management of hypertension, electrolyte imbalance correction with tailored treatment, and genetic counseling.