Severe Hyperkalemia Research Articles

The safety and efficacy of low-dose mineralocorticoid receptor antagonists in dialysis patients: A meta-analysis.

Introduction:Our aim was to evaluate the safety and efficacy of low-dose mineralocorticoid receptor antagonists (MRAs) in dialysis patients.Methods:We systematically searched PubMed, EMBASE, and Cochrane libraries for clinical trials on the use of MRAs in dialysis patients. Review Manager 5.3 software was used to analyze relevant data and evaluate the quality of evidence.Results:We identified nine randomized controlled trials including 1128 chronic dialysis patients. In terms of safety, when hyperkalemia was defined as serum potassium level ≥5.5 mmol/L, low-dose MRAs were significantly associated with hyperkalemia (relative risk [RR] 1.76, 95% confidence intervals [CI] 1.07–2.89, P = .02); however, when hyperkalemia was defined as serum potassium level ≥6.0 mmol/L or serum potassium level ≥6.5 mmol/L, no significant association was observed between low-dose MRAs and hyperkalemia (RR 1.40, 95% CI 0.83–2.37, P = .20; RR 1.98, 95% CI 0.91–4.30, P = .09, respectively). Use of low-dose MRAs can reduce cardiovascular mortality by 54% compared with the control group (0.46, 95% CI 0.28–0.76, P = .003). Similarly, the RR of all-cause mortality for the low-dose MRAs group was 0.48 (95% CI 0.33–0.72, P = .0003).Conclusion:Low-dose MRAs may benefit dialysis patients without significantly increasing moderate to severe hyperkalemia.

Long-term mortality and trajectory of potassium measurements following an episode of acute severe hyperkalaemia.

BackgroundHyperkalaemia is a common condition in patients with comorbidities such as chronic kidney disease (CKD) or congestive heart failure (HF). Moreover, severe hyperkalaemia is a potentially life-threatening condition that is associated with a higher risk of adverse clinical events such as ventricular arrhythmias and sudden cardiac death. Currently, data regarding the prognostic implications of chronic hyperkalaemia are available; however, information about the long-term clinical consequences after an episode of severe hyperkalaemia remains scarce. The objective of this study was to evaluate the association between the trajectory of potassium measurements in patients with acute hyperkalaemia and long-term all-cause mortality.MethodsThis is a retrospective observational study that included patients with acute severe hyperkalaemia [potassium (K) >6 mEq/L] without haemolysis in the emergency room of Dr Peset University Hospital in Valencia, Spain searching the lab database from January 2016 to March 2017. The multivariable-adjusted association of serum potassium with mortality was assessed by using comprehensive state-of-the-art regression methods that can accommodate time-dependent exposure modelling.ResultsWe found 172 episodes of acute hyperkalaemia in 160 patients in the emergency room. The mean ± standard deviation age of the sample was 77 ± 12 years and 60.5% were males. The most frequent comorbidities were CKD (71.2%), HF (35%) and diabetes mellitus (56.9%). Only 11.9% of the patients were on chronic dialysis. A quarter of the patients did not have previous CKD, making hyperkalaemia an unpredictable life-threatening complication. During the acute episode, mean potassium and estimated glomerular filtration rate (eGFR) were 6.6 ± 0.6 (range 6.1–9.2) mEq/L and 23 ± 16 (range 2–84) mL/min/1.73 m2, respectively. After a median (interquartile range) follow-up of 17.3 (2.2–23.7) months, 68 patients died (42.5%). Recurrences of hyperkalaemia (K >5.5 mEq/L) were detected in 39.5% of the patients who were monitored during follow-up. We found that previous potassium levels during an acute severe hyperkalaemia episode were not predictors of mortality. Conversely, the post-discharge longitudinal trajectories of potassium were able to predict all-cause mortality (overall P = 0.0015). The effect of transitioning from hyperkalaemia to normokalaemia (K >5.5 mEq/L to K ≤5.5 mEq/L) after the acute episode was significant, and inversely associated with the risk of mortality.ConclusionsPotassium levels prior to a severe hyperkalaemic event do not predict mortality. Conversely, following an episode of acute severe hyperkalaemia, serial kinetics of potassium trajectories predict the risk of death. Further evidence is needed to confirm these findings and clarify the optimal long-term management of these patients.

Novel Use of Premixed Dialysate Bags during Water Supply Interruption in Acute Hospital Setting.

Patients on dialysis are exposed to large amounts of water during conventional intermittent hemodialysis; hence, there are strict regulations regarding the quality of water used to prepare dialysate. Occasionally, water systems fail due to natural disasters or structural supply issues, such as water-main breaks or unplanned changes in municipal or facility water quality. It is critical to regularly monitor and immediately recognize such a failure and take steps to avoid exposing the patients to contaminants. In addition to the recognition of the problem, the ability to pivot and continue to provide safe treatment to inpatients who are dependent on dialysis is essential, both from an ultrafiltration and a clearance standpoint. At our hospital, an unforeseen water disruption occurred and we were able to continue to provide KRT with premade, bagged dialysate to mitigate the effect on our patients on dialysis. This is a novel method using available machines and dialysate, which we normally stock for continuous KRT, for short dialysis sessions. The methodology is similar to that which has been widely used for short daily home hemodialysis with low dialysate flow rate. Because this situation occurred in the midst of the SARS-CoV-2 pandemic, we had to be mindful of dialysate volumes and staffing time. Here, we present our investigation into the cause of the water-system failure and how we quickly implemented the alternative dialysis method. Short dialysis with low-flow dialysate will not deliver the same Kt/V per session as standard dialysis; however, this method was successfully implemented and tailored with adjustments for patients requiring higher clearance for specific indications, such as severe hyperkalemia.

The timing of continuous renal replacement therapy initiation in sepsis-associated acute kidney injury in the intensive care unit: the CRTSAKI Study (Continuous RRT Timing in Sepsis-associated AKI in ICU): study protocol for a multicentre, randomised controlled trial

IntroductionAcute kidney injury (AKI) is one of the most common organ dysfunction in sepsis, and increases the risk of unfavourable outcomes. Renal replacement therapy (RRT) is the predominant treatment for...

Pediatric Extracorporeal Cardiopulmonary Resuscitation ELSO Guidelines.

Pediatric Extracorporeal Cardiopulmonary Resuscitation ELSO Guidelines.

Increased colonic K+ excretion through inhibition of the H,K-ATPase type 2 helps reduce plasma K+ level in a murine model of nephronic reduction

Hyperkalemia is frequently observed in patients at the end-stage of chronic kidney disease (CKD), and has possible harmful consequences on cardiac function. Many strategies are currently used to manage hyperkalemia, one consisting of increasing fecal K+ excretion through the administration of cation-exchange resins. In this study, we explored another more specific method of increasing intestinal K+ secretion by inhibiting the H,K-ATPase type 2 (HKA2), which is the main colonic K+ reabsorptive pathway. We hypothetised that the absence of this pump could impede the increase of plasma K+ levels following nephronic reduction (N5/6) by favoring fecal K+ secretion. In N5/6 WT and HKA2KO mice under normal K+ intake, the plasma K+ level remained within the normal range, however, a load of K+ induced strong hyperkalemia in N5/6 WT mice (9.1 ± 0.5 mM), which was significantly less pronounced in N5/6 HKA2KO mice (7.9 ± 0.4 mM, p < 0.01). This was correlated to a higher capacity of HKA2KO mice to excrete K+ in their feces. The absence of HKA2 also increased fecal Na+ excretion by inhibiting its colonic ENaC-dependent absorption. We also showed that angiotensin-converting-enzyme inhibitor like enalapril, used to treat hypertension during CKD, induced a less severe hyperkalemia in N5/6 HKA2KO than in N5/6 WT mice. This study therefore provides the proof of concept that the targeted inhibition of HKA2 could be a specific therapeutic maneuver to reduce plasma K+ levels in CKD patients.

An Evidence-Based Narrative Review of the Emergency Department Management of Acute Hyperkalemia

The normal range for potassium is within narrow limits. Hyperkalemia is an electrolyte disorder that frequently affects patients in the emergency department (ED), and can result in significant morbidity and mortality if not identified and treated rapidly. This article provides an evidence-based narrative review of the management of hyperkalemia, with focused updates for the emergency clinician. We searched in MEDLINE, EMBASE, Web of Science, and Scopus databases for articles in English published in peer-reviewed journals and indexed up until May 2020. We used multiple search terms, including hyperkalemia, potassium, acute hyperkalemia, emergency department, dyskalemia, potassium disorders, kidney disease, epidemiology, electrolyte disturbance, severe hyperkalemia, and emergency management. In the ED, interventions aimed to protect patients from the immediate dangers of elevated serum potassium are divided into the following: stabilizing cardiac membrane potentials, reducing serum potassium levels through shift from the extracellular fluid to intracellular fluid, and elimination of potassium through excretion via urinary or fecal excretion. Calcium is widely recommended to stabilize the myocardial cell membrane, but additional research is necessary to establish criteria for use, dosages, and preferred solutions. Redistribution of potassium ions from the bloodstream into the cells is based on intravenous insulin or nebulized β2-agonists. Hyperkalemia is a frequent electrolyte disorder in the ED. Because of the risk of fatal dysrhythmia due to cardiac membrane instability, hyperkalemia is a medical emergency. There is a lack of scientific evidence on the optimal management of hyperkalemia and more research is needed to establish optimal strategies to manage acute hyperkalemia in the emergency department.

Timing of renal replacement therapy initiation for acute kidney injury in critically ill patients: a systematic review of randomized clinical trials with meta-analysis and trial sequential analysis

BackgroundAcute kidney injury (AKI) is a common serious complication in critically ill patients. AKI occurs in up to 50% patients in intensive care unit (ICU), with poor clinical prognosis. Renal replacement therapy (RRT) has been widely used in critically ill patients with AKI. However, in patients without urgent indications such as acute pulmonary edema, severe acidosis, and severe hyperkalemia, the optimal timing of RRT initiation is still under debate. We conducted this systematic review of randomized clinical trials (RCTs) with meta-analysis and trial sequential analysis (TSA) to compare the effects of early RRT initiation versus delayed RRT initiation.MethodsWe searched databases (PubMed, EMBASE and Cochrane Library) from inception through to July 20, 2020, to identify eligible RCTs. The primary outcome was 28-day mortality. Two authors extracted the data independently. When the I2 values < 25%, we used fixed-effect mode. Otherwise, the random effects model was used as appropriate. TSA was performed to control the risk of random errors and assess whether the results in our meta-analysis were conclusive.ResultsEleven studies involving 5086 patients were identified. Two studies included patients with sepsis, one study included patients with shock after cardiac surgery, and eight others included mixed populations. The criteria for the initiation of RRT, the definition of AKI, and RRT modalities existed great variations among the studies. The median time of RRT initiation across studies ranged from 2 to 7.6 h in the early RRT group and 21 to 57 h in the delayed RRT group. The pooled results showed that early initiation of RRT could not decrease 28-day all-cause mortality compared with delayed RRT (RR 1.01; 95% CI 0.94–1.09; P = 0.77; I2 = 0%). TSA result showed that the required information size was 2949. The cumulative Z curve crossed the futility boundary and reached the required information size. In addition, early initiation of RRT could lead to unnecessary RRT exposure in some patients and was associated with a higher incidence of hypotension (RR 1.42; 95% CI 1.23–1.63; P < 0.00001; I2 = 8%) and RRT-associated infection events (RR 1.34; 95% CI 1.01–1.78; P = 0.04; I2 = 0%).ConclusionsThis meta-analysis suggested that early initiation of RRT was not associated with survival benefit in critically ill patients with AKI. In addition, early initiation of RRT could lead to unnecessary RRT exposure in some patients, resulting in a waste of health resources and a higher incidence of RRT-associated adverse events. Maybe, only critically ill patients with a clear and hard indication, such as severe acidosis, pulmonary edema, and hyperkalemia, could benefit from early initiation of RRT.

Life–Threatening Hyperkalemia Presenting with Cardiac Arrest during Combined Therapy with Angiotensin – Converting Enzyme Inhibitor and Spironolactone: a Case Report

A 56-year-old man with history of previous coronary artery bypass graft (CABG) surgery and prior history of mild renal impairment was brought to the emergency department at mid night in gasping state. On presentation his pulse and blood pressure (BP) were non recordable. Cardiopulmonary resuscitation (CPR) was started immediately and he was intubated in the emergency room. Within few minutes his pulse became perceptible but BP still remained non recordable. His bed side 12 leads electrocardiogram (ECG) revealed sine wave configuration,suggestive of severe hyperkalemia with heart rate 30-35 beats per minute (bpm).Urgently he was transferred to cardiac catheterization laboratory for temporary pacemaker insertion (TPI). After putting TPI he regained consciousness and BP raised to normal. His blood gas analysis showed severe hyperkalemia (Serum potassium level-9.4 mmol/L). In coronary care unit (CCU) he was commenced on standard treatment of hyperkalemia and his electrolyte imbalance normalized within 24 hours. His cardiac rhythm reverted back to sinus within 24 hours of admission and he was extubated next day and discharged from the hospital after 5 days in a relatively stable state.&#x0D; J Dhaka Medical College, Vol. 28, No.2, October, 2019, Page 212-215

Electrocardiogram (ECG) changes of a patient with severe hyperkalemia

A 55-year-old gentleman with underlying type 2 diabetes mellitus, dyslipidemia, hypertension, and end stage renal disease presented with shortness of breath, vomiting and worsening fatigue for one day after missing his scheduled hemodialysis. Physical examination in revealed tachypnoea with a respiratory rate of 30 breaths per minute, and fine mid inspiratory crepitations at the lung bases. Initial blood investigations in the emergency department revealed severe metabolic acidosis and hyperkalemia with a potassium of 7.6 mmol/L. A 12 lead electrocardiogram was done and several features that suggest hyperkalemia were detected such as a narrow based and symmetrical tall, tented T wave. In V1 the QRS complex is reminiscent of Brugada type 1 which is probably Brugada phenocopy and are often seen in hyperkalemia. There is ST elevation in V2, a single precordial lead. There is no reciprocal ST depression, and a lone ST elevation does not indicate ischemia. This may be caused by hyperkalemia as well. There is a broad QRS of 136ms, widened QRS is characteristic of hyperkalemia. There is a broad P wave and the PR interval is approximately 200ms. Left ventricular hypertrophy is also present. Due to impending respiratory collapse, he was subsequently intubated. His hyperkalemia was treated with intravenous short acting human insulin, dextrose 50%, calcium gluconate, sodium bicarbonate and calcium polystyrene sulfonate. He was subsequently admitted to the intensive care unit (ICU) and had undergone emergency hemodialysis.

Accidental systemic administration of 1 litre of cardioplegia solution during paediatric cardiac surgery

SummaryCardioplegia is used to induce cardiac arrest in order to facilitate cardiac surgery in patients supported by cardiopulmonary bypass. It is administered directly into the coronary vessels after the heart has been isolated from the systemic circulation. We describe the case of a 9‐year‐old boy who mistakenly received 1 l of high strength St Thomas’ Harefield cardioplegia solution delivered into the systemic circulation during cardiac surgery. Although the patient’s heart did not stop, the subsequent physiological derangements were severe. The presenting features were refractory hypotension and dilutional anaemia along with severe hyperkalaemia, hypermagnesaemia and hyperchloraemic metabolic acidosis. Local anaesthetic systemic toxicity from the procaine contained within the cardioplegia solution was also a concern. Treatment required vasopressor administration and an extended period of cardiopulmonary bypass while serum electrolyte concentrations were corrected by haemodiafiltration. The systemic administration of cardioplegia solution is a rare but important iatrogenic clinical emergency that anaesthetists working in cardiac centres should be aware of. This case demonstrates that full recovery is possible.

Case Report: A patient with extreme hyperkalemia beats all the odds

Hyperkalemia is a common finding in patients in hemodialysis and is typically classified as mild, moderate or severe. Severe hyperkalemia is a complex and life-threatening clinical entity, closely associated with increased mortality rates. It generally presents with ascending muscle weakness and paralysis, cardiac arrhythmias and specific ECG changes. Herein, we present the case of a 30-year-old patient with end-stage renal disease, on hemodialysis. He presents to his hemodialysis session with complaints of progressive weakness and paralysis of his lower extremities, palpitations and dyspnea. His last session was 5 days prior to his ER presentation, after having missed 2 sessions. Laboratory studies revealed a serum potassium level of 10.9 mg/ dL. Intravenous calcium infusion was administered urgently and subsequently underwent urgent hemodialysis. The next day he underwent another session due to the post-hemodialysis rebound effect, but on physical examination the lower limb paralysis had improved and normal, sinus rhythm was present. Considering its silent development and ambiguous clinical presentation, hyperkalemia should invariably be considered in patients with CKD presenting with cardiac and neurological symptoms. Reported cases of severe hyperkalemia with potassium concentrations higher than 10 mg/dL, as in the case of our patient, are sparse and represent rapidly deteriorating, life-threatening conditions, requiring emergent medical interventions to prevent fatal cardiac arrhythmias.

Successful resolution of urothorax secondary to non-traumatic uroabdomen in a cat managed with peritoneal dialysis as a bridge to surgery

Case summaryA 9-year-old neutered male domestic shorthair cat was presented for evaluation of severe hemodynamic collapse and suspected lower urinary tract disease. On admission, severe metabolic acidosis, hyperkalemia and azotemia, and electrocardiographic findings consistent with cardiotoxicity were identified. The diagnosis of uroabdomen was made based on abdominal fluid to plasma concentration ratios of creatinine and potassium. A central line catheter was placed percutaneously into the abdomen for peritoneal drainage and used for peritoneal dialysis as a bridge to surgery. Retrograde contrast cystography confirmed rupture of the urinary bladder. Point-of-care ultrasound of the chest postoperatively revealed the presence of mild pleural effusion. Echocardiography was then performed showing no evidence of cardiac disease. Pleural fluid analysis revealed a transudate with a creatinine ratio of 2.38 ([Creatinine]pleural fluid/[Creatinine]plasma), consistent with the diagnosis of urothorax. The cat recovered uneventfully from surgery and was monitored for signs of respiratory distress during the rest of its stay in hospital. The cat was discharged 4 days later and the pleural effusion resolved without further medical intervention.Relevance and novel informationThere is limited information on the causes of urothorax and uroabdomen management of feline patients. Pleural effusion is a complication observed in critically ill cats secondary to fluid overload, underlying cardiomyopathy, primary thoracic pathology or a combination of these. To our knowledge, this is the first report of urothorax in a cat secondary to non-traumatic uroabdomen. Careful monitoring of respiratory signs consistent with pleural space disease is recommended in cases of uroabdomen.

Hyponatremia and other electrolyte abnormalities in patients receiving immune checkpoint inhibitors.

Hyponatremia due to endocrinopathies such as adrenal insufficiency and hypothyroidism has been reported in patients receiving immune checkpoint inhibitors (ICIs). We determined the risk and predictors of hyponatremia and other electrolyte abnormalities in a 'real-world' sample of patients receiving ICIs to treat advanced malignancies. This was a retrospective observational study of all patients who received ICIs from a single cancer center between 2011 and 2018. Patients were followed for 12 months after initiation of ICIs or until death. Common Terminology for Cancer Adverse Events version 5.0 criteria were used to grade the severity of hyponatremia and other electrolyte abnormalities. The predictors of severe (Grade 3 or 4) hyponatremia were determined using a multivariable logistic regression model. The etiology of Grade 3 or 4 hyponatremia was determined by chart review. A total of 2458 patients were included. Their average age was 64 years [standard deviation (SD) 13], 58% were male and 90% were white. In the first year after starting ICIs, 62% experienced hyponatremia (sodium <134 mEq/L) and 136 (6%) experienced severe hyponatremia (<124 mEq/L). Severe hyponatremia occurred on average 164 days (SD 100) after drug initiation. Only nine cases of severe hyponatremia were due to endocrinopathies (0.3% overall incidence). Risk factors for severe hyponatremia included ipilimumab (a cytotoxic T lymphocyte antigen-4 inhibitor) use, diuretic use and non-White race. Other severe electrolyte abnormalities were also commonly observed: severe hypokalemia (potassium <3.0 mEq/L) occurred in 6%, severe hyperkalemia (potassium ≥6.1 mEq/L) occurred in 0.6%, severe hypophosphatemia (phosphorus <2 mg/dL) occurred in 17% and severe hypocalcemia (corrected calcium <7.0 mg/dL) occurred in 0.2%. Hyponatremia is common in cancer patients receiving ICIs. However, endocrinopathies are an uncommon cause of severe hyponatremia.

Low dialysis potassium bath is associated with lower mortality in end-stage renal disease patients admitted to hospital with severe hyperkalemia.

BackgroundHyperkalemia is a modifiable risk factor for sudden cardiac death, a leading cause of mortality in hemodialysis (HD) patients. The optimal treatment of hyperkalemia in hospitalized end-stage renal disease (ESRD) patients is nonexistent in literature, which has prompted studies from outpatient dialysis to be extrapolated to inpatient care. The goal of this study was to determine if low-potassium dialysate 1 mEq/L is associated with higher mortality in hospitalized ESRD patients with severe hyperkalemia (serum potassium >6.5 mmol/L).MethodsWe conducted a retrospective study of all adult ESRD patients admitted with severe hyperkalemia between January 2011 and August 2016.ResultsThere were 209 ESRD patients on HD admitted with severe hyperkalemia during the study period. Mean serum potassium was 7.1 mmol/L. In-hospital mortality or cardiac arrest in ESRD patients with severe hyperkalemia was 12.4%. Median time to dialysis after serum potassium result was 2.0 h (25, 75 interquartile range 0.9, 4.2 h). Totally, 47.4% of patients received dialysis with 1 mEq/L concentration potassium bath. The use of 1 mEq/L potassium bath was associated with significantly lower mortality or cardiac arrest in ESRD patients admitted with severe hyperkalemia (odds ratio 0.27, 95% confidence interval 0.09–0.80, P = 0.01).ConclusionWe conclude that use of 1 mEq/L potassium bath for treatment of severe hyperkalemia (>6.5 mmol/L) in hospitalized ESRD patients is associated with decreased in-hospital mortality or cardiac arrest.

Abstract 16378: Increased Extracellular Sodium and Calcium Modify the Extracellular Potassium and Cardiac Conduction Velocity Relationship in a Langendorff-perfused Guinea Pig Heart

Background: Previous studies have demonstrated a biphasic relationship between extracellular potassium (K o ) and cardiac conduction velocity (CV). With moderate hyperkalemia, CV increases in what is referred to as supernormal conduction, but further increases in K o lead to severe conduction slowing and asystole. We recently demonstrated that altering extracellular sodium (Na o ) and extracellular calcium (Ca o ) modulates CV dependence on gap junctions (GJs). We have also shown that increasing Na o and Ca o can attenuate conduction loss caused by global ischemia ischemia. The purpose of this study was to determine if increasing Na o and Ca o would alter the K o -CV relationship and preserve CV at high K o . Hypothesis: Increasing Na o and Ca o will mitigate conduction slowing and the incidence of asystole associated with severe hyperkalemia in conditions of both normal and uncoupled GJs. Methods: Langendorff-perfused guinea pig hearts were optically mapped to measure CV. Na o was set to 145 or155mM and Ca o to 1.25 or 2.0mM. K o was varied from 4.6, 6.4, 8, to 10 mM in each experiment. Perfusion order was blinded and randomized. GJs were inhibited using carbenoxolone. Results: A biphasic K o -CV relationship was observed under all conditions. Maximum CV was achieved at either 6.4 or 8.0mM K o followed by a decrease in CV with increased K o . Importantly, the degree of CV slowing in the presence of 10mM K o was significantly reduced with the 155mM Na o / 2.0mM Ca o perfusate compared to all other Na o /Ca o combinations. Carbenoxolone reduced CV across all K o , but did not alter the K o -CV relationship. With 145mM Na o / 1.25mM Ca o , all hearts became asystolic at K o =10.0mM. Increasing Na o and Ca o significantly reduced the incidence of asystole at K o =10.0mM. Conclusions: Elevating Na o and Ca o preserves CV during severe hyperkalemia with or without strong GJ coupling. Increasing Na o and Ca o significantly reduces the incidence of asystole during severe hyperkalemia. These data suggest that non-linear and combinatorial effects of sodium, calcium, and GJ uncoupling can differentially modulate cardiac conduction during hyperkalemic perfusion. These results have important implications for cardioplegic arrest and ischemic heart disease when potassium and calcium homeostasis are disrupted.

Abstract 15474: New Onset Left Bundle Branch Block Secondary to Severe Hyperkalemia

Case presentation: A 79-year-old female with history of renal failure on hemodialysis (HD) presented with generalized weakness. Her last HD was 3 days ago. On examination, she was vitally stable. Blood tests demonstrated a potassium (K+) of 8.3 mmol/L, confirmed on repeat testing. ECG revealed wide QRS, tall T waves and a new left bundle branch block (Figure 1). She was immediately treated with calcium chloride, insulin, dextrose and polystyrene sulfonate. The patient was admitted to the ICU and underwent emergent HD. Repeat K+ post HD reversed to 4.0 mmol/L and ECG reflected normal sinus rhythm with resolution of ST-T wave changes (Figure 2). Discussion: Hyperkalemia can lead to cardiac arrhythmias and sudden death. The ECG changes are dependent on severity of hyperkalemia. It can vary from narrow based, peaked T waves to ventricular fibrillation. Hyperkalemia can also lead to interventricular conduction delays, which, with severity, can take the form of right or left bundle branch block (LLLB). The conduction delay from hyperkalemia usually lasts only in initial or terminal portions as opposed to throughout the QRS complex as seen in bundle branch block disease. Association of LLLB with hyperkalemia is an uncommon but important occurrence and has only scarcely been reported in literature. Its prevalence remains unknown. With the growing use of renin-angiotensin aldosterone system inhibitors, more patients are prone to experience life threatening electrolyte disturbances. A thorough knowledge of the ECG manifestations related to hyperkalemia is crucial to ensure emergent treatment. This may result in improved outcomes in such patients with cardiovascular and renal diseases.

Cardiovascular and Renal Outcomes of Mineralocorticoid Receptor Antagonist Use in PARAGON-HF

ObjectivesThis study sought to evaluate the efficacy and safety of sacubitril/valsartan in patients with heart failure with preserved ejection fraction (HFpEF) according to background mineralocorticoid receptor antagonist (MRA) therapy. BackgroundCurrent guidelines recommend consideration of MRAs in selected patients with HFpEF. This study assessed cardiovascular outcomes, renal outcomes, and safety of sacubitril/valsartan compared with valsartan in patients with HFpEF according to background MRA treatment. MethodsPARAGON-HF (Prospective Comparison of ARNI [angiotensin receptor-neprilysin inhibitor] with ARB [angiotensin-receptor blockers] Global Outcomes in HF with Preserved Ejection Fraction) randomized 4,796 patients with HFpEF to sacubitril/valsartan or valsartan. In a pre-specified subgroup analysis, the effect of sacubitril/valsartan versus valsartan was evaluated according to baseline MRA use on the primary study composite of total heart failure hospitalizations and cardiovascular death using semiparametric proportional rates methods, as well as the renal composite of ≥50% decrease in estimated glomerular filtration rate, development of end-stage renal disease, or death from renal causes using Cox proportional hazards regression models. Annual decline in estimated glomerular filtration rate was analyzed with repeated-measures mixed-effect models. Key safety outcomes included incidence of hypotension, hyperkalemia, and elevations in serum creatinine above predefined thresholds. ResultsPatients treated with MRAs at baseline (n = 1,239, 26%), compared with MRA nonusers (n = 3,557, 74%), were younger (72 vs. 73 years), more often male (52% vs. 47%), had lower left ventricular ejection fraction (57% vs. 58%), and a higher proportion of prior HF hospitalization (59% vs. 44%) (all p < 0.001). Efficacy of sacubitril/valsartan compared with valsartan with regard to the primary cardiovascular (for MRA users: rate ratio: 0.73; 95% confidence interval [CI]: 0.56 to 0.95; vs. for MRA nonusers: rate ratio: 0.94; 95% CI: 0.79 to 1.11; pinteraction = 0.11) and renal endpoints (for MRA users: hazard ratio: 0.31; 95% CI: 0.13 to 0.76; vs. for MRA non-users: HR: 0.59; 95% CI: 0.36 to 0.95; pinteraction = 0.21) did not significantly vary by baseline MRA use. The incidence of key safety outcomes including hypotension and severe hyperkalemia (K > 6.0 mmol/l) did not vary by baseline MRA use. However, annual decline in estimated glomerular filtration rate was less with the combination of MRA and sacubitril/valsartan (for MRA users: absolute difference favoring sacubitril/valsartan: +1.2 ml/min/1.73 m2 per year; 95% CI: 0.6 to 1.7; vs. for MRA nonusers: +0.4; 95% CI: 0.1 to 0.7; pinteraction = 0.01). ConclusionsClinical efficacy of sacubitril/valsartan compared with valsartan with regard to predefined cardiorenal composite outcomes in PARAGON-HF was consistent in patients treated and not treated with MRA at baseline. Addition of sacubitril/valsartan rather than valsartan alone to MRA appears to be associated with a lesser decline in renal function and no increase in severe hyperkalemia. These data support possible added value of combination treatment with sacubitril/valsartan and MRA in patients with HFpEF. (Prospective Comparison of ARNI [angiotensin receptor -neprilysin inhibitor] with ARB [angiotensin-receptor blockers] Global Outcomes in HF with Preserved Ejection Fraction [PARAGON-HF]; NCT01920711)

An unusual precipitant of acute heart failure-ANCA-associated vasculitis in a patient with ischaemic cardiomyopathy: a case report.

BackgroundAntineutrophil cytoplasmic antibody (ANCA)-associated pulmonary renal vasculitis is an uncommon disease entity. Its presentation as acute heart failure for the first time in a patient with established coronary artery disease (CAD) is even rarer. We present here a case of such an association and an approach to managing this clinical situation.Case summaryA 60-year-old male patient presented to the emergency room with recent-onset dyspnoea New York Heart Association Class IV. He was having hypertension, uncontrolled diabetes mellitus, chronic kidney disease (CKD), and CAD. He also underwent a percutaneous coronary intervention to left anterior descending in the past for acute coronary syndrome and had moderate left ventricular dysfunction. He was being managed as a case of acute decompensated heart failure (ADHF) and was mechanically ventilated. Suddenly his ventilator requirement increased and endotracheal aspirate contained blood. The chest radiograph showed bilateral hilar infiltrates. Simultaneously he also had recurrent episodes of ventricular tachycardia (VT) requiring direct current (DC) cardioversion. Blood investigations showed deranged renal function and severe hyperkalaemia, but no evidence of coagulopathy. High-resolution computed tomography chest showed features of diffuse alveolar haemorrhage. Further investigations revealed high titres of c-ANCA and raised inflammatory biomarkers. A diagnosis of ANCA-associated vasculitis presenting as acute on CKD with dyselectrolytaemia (hyperkalaemia) leading to VT was made. Apart from standard management for associated illness, he was treated with plasma exchange, steroids, and cyclophosphamide to which he responded and was later on discharged.DiscussionAntineutrophil cytoplasmic antibody-related pulmonary renal vasculitis can lead to rapidly progressing renal failure and may present as ADHF in a patient with existent CAD. The associated VT storm in our patient can be attributed to hyperkalaemia secondary to acute renal failure. A multidisciplinary approach is required for the successful management of such a complex clinical scenario.

Acute kidney injury with severe hyperkalaemia requiring haemodialysis in a patient with Pituitary Apoplexy - a Case Report

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