The effect of hyperkalaemia on cardiac rhythm devices

To assess the time to treatment for emergency department (ED) patients with critical hyperkalemia and to determine whether the timing of treatment was associated with clinical characteristics or electrocardiographic abnormalities. The authors performed a retrospective chart review of ED patients with the laboratory diagnosis of hyperkalemia (potassium level > 6.0 mmol/L). Patients presenting in cardiac arrest or who were referred for hyperkalemia or dialysis were excluded. Patient charts were reviewed to find whether patients received specific treatment for hyperkalemia and, if so, what clinical attributes were associated with the time to initiation of treatment. Of 175 ED visits that occurred over a 1-year time period, 168 (96%) received specific treatment for hyperkalemia. The median time from triage to initiation of treatment was 117 minutes (interquartile range [IQR] = 59 to 196 minutes). The 7 cases in which hyperkalemia was not treated include 4 cases in which the patient was discharged home, with a missed diagnosis of hyperkalemia. Despite initiation of specific therapy for hyperkalemia in 168 cases, 2 patients died of cardiac arrhythmias. Among the patients who received treatment, 15% had a documented systolic blood pressure (sBP) < 90 mmHg, and 30% of treated patients were admitted to intensive care units. The median potassium value was 6.5 mmol/L (IQR = 6.3 to 7.1 mmol/L). The predominant complaints were dyspnea (20%) and weakness (19%). Thirty-six percent of patients were taking angiotensin-converting enzyme (ACE) inhibitors. Initial electrocardiograms (ECGs) were abnormal in 83% of patient visits, including 24% of ECGs with nonspecific ST abnormalities. Findings of peaked T-wave morphology (34%), first-degree atrioventricular block (17%), and interventricular conduction delay (12%) did not lead to early treatment. Vital sign abnormalities, including hypotension (sBP < 90 mmHg), were not associated with early treatment. The chief complaint of "unresponsive" was most likely to lead to early treatment; treatment delays occurred in patients not transported by ambulance, those with a chief complaint of syncope and those with a history of hypertension. Recognition of patients with severe hyperkalemia is challenging, and the initiation of appropriate therapy for this disorder is frequently delayed.

Hyperkalemia is a concern in heart failure (HF), especially in older patients with co-morbidities. Previous studies addressing this issue have focused mainly on younger patients. This study was aimed at determining the frequency and predictors of hyperkalemia in older patients with HF undergoing intense medical therapy. Frequency and predictors of hyperkalemia were defined in patients (n = 566) participating in the Trial of Intensified versus Standard Medical Therapy in Elderly Patients with Congestive Heart Failure, in which patients ≥60 years of age were randomized to a standard versus an intensified N-terminal brain natriuretic peptide-guided HF therapy. During an 18-month follow-up 76 patients (13.4%) had hyperkalemia (≥5.5 mmol/L) and 28 (4.9%) had severe hyperkalemia (≥6.0 mmol/L). Higher baseline serum potassium (odds ratio [OR] 2.92 per mmol/L), baseline creatinine (OR 1.11 per 10 μmol/L), gout (OR 2.56), New York Heart Association (NYHA) class (compared to NYHA class II, IV OR 3.08), higher dosage of spironolactone at baseline (OR 1.20 per 12.5 mg/day), and higher dose changes of spironolactone (compared to no dose change: 12.5 mg, OR 1.45; 25 mg, OR 2.52; >25 mg, OR 3.24) were independent predictors for development of hyperkalemia (p <0.05 for all comparisons). In conclusion, hyperkalemia is common in patients ≥60 years of age with HF undergoing intense medical therapy. Risk is increased in patients treated with spironolactone, in addition to patient-specific risk factors such as chronic kidney disease, higher serum potassium, advanced NYHA class, and gout. Careful surveillance of serum potassium and cautious use of spironolactone in patients at risk may help to decrease the incidence of potentially hazardous complications caused by hyperkalemia.

We studied the non-membrane potential-dependent effect of K+ on (dV/dt)max and threshold potential in guinea pig and cat ventricular myocardium. Membrane potential (MP) was changed uniformly in segments (length less than or equal to 1.0 mm) of papillary muscles by applying extracellular polarizing current pulses across a single sucrose gap. Control [K+]o was 5.4 mM and test [K+]o values were 2.0, 10.0, 11.5, 13.0, 16.2, 20, 22, and 24.0 mM. Each muscle was studied under four conditions: (1) control [K+]o and unaltered (control level) resting MP (Em); (2) one of the test [K+]o values and the unaltered (test level) Em; (3) the same test [K+]o and Em held at the control level; (4) control [K+]o and Em held at the test level. At all [K+]o greater than or equal to 11.5 mM, (dV/dt)max showed a decrease significantly (P less than 0.01) greater than the corresponding MP-dependent decrease in both guinea pig and cat myocardium. This non-MP-dependent decrease averaged 7.5% at 11.5 mM, 26.5% at 13.0 mM, 37.2% at 16.2 mM, and 22.7% at 20.0 mM. At [K+]o greater than or equal to 20.0 mM, (dV/dt)max was predominantly slow-channel-dependent; it was increased by hyperpolarization to -110 mV at [K+]o = 20 and 22 mM but not at [K+]o = 24mM. Threshold potential became progressively less negative with increasing [K+]o, but this effect was dependent only on MP. The membrane input resistance (rm) was determined by two opposing factors: at a given [K+]o, rm increased with depolarization; and at a given MP, rm decreased with increasing [K+]o. Our study shows that non-MP-dependent depression of (dV/dt)max in the ventricular myocardium occurs at [K+]o concentrations that may be encountered in vivo.