Intravenous Potassium Administration Research Articles

Hypokalemic Cardiac Arrest: Narrative Review of Case Reports and Current State of Science

PurposeHypokalemic cardiac arrest is an uncommon occurrence in the emergency department. Electrocardiogram findings related to hypokalemic cardiac arrest include prolonged QT, U waves, and preventricular contractions leading to Torsades de Pointes and then arrest. Literature evaluating the prevalence of hypokalemic cardiac arrest is scarce, and its management is lacking. This review provides a summary of current literature, recommendations from current guidelines, and proposed management strategies of hypokalemic cardiac arrest. SummaryIntravenous potassium administration is the treatment for hypokalemic cardiac arrest. Although the treatment for hypokalemic cardiac arrest is known, there is limited evidence on the proper procedure for administering intravenous potassium appropriately and safely. Owing to the time-sensitive nature of treating hypokalemic cardiac arrest, rapid administration of intravenous potassium (10 mEq/100 mL of potassium chloride over 5 minutes) is warranted. Concerns regarding rapid potassium administration are not without merit; however, a risk-benefit analysis and potential mitigation strategies for unwanted side effects need to be considered if hypokalemic cardiac arrest is to remain a reversible cause. It is imperative to identify hypokalemia as the cause for arrest as soon as possible and administer potassium before systemic acidosis, ischemia, and irreversible cell death. ConclusionsMore evidence is necessary to support treatment recommendations for hypokalemic cardiac arrest; however, it is the authors' opinion that, if identified early during cardiac arrest, intravenous potassium should be administered to treat a reversible cause for cardiac arrest.

Comparison of interference in 4 Jaffe creatinine assays using acute diabetic ketoacidosis samples

Background and aim Creatinine assays are now standardised, however the effect of elevated glucose and ketoacids during acute diabetic ketoacidosis (DKA) on different Jaffe creatinine assays is unknown. We aim to assess this interference on different platforms using the Vitros enzymatic creatinine method as the gold standard. Methods Samples were collected from patients presenting to Emergency Department with DKA and analysed using 4 Jaffe assays (Architect, Roche, Beckman Coulter and Siemens) and 1 enzymatic assay (Vitros). Results Of the eighteen patients (12 M, 6F, age 32.1 ± 12.4 years), admission pH was 7.12 ± 0.16, HCO3 was 8.2 ± 4 mmol/L, glucose was 36.2 ± 13.8 mmol/L and capillary ketone was 5.7 ± 1.2 mmol/L. The average enzymatic creatinine value was 115.3 ± 64.2 μmol/L. All Jaffe creatinine results were significantly higher (p Discussion Falsely elevated plasma creatinine results might delay the administration of intravenous potassium in DKA patients and clinicians need to be aware of this potential interference which appeared most marked on the Abbott platform.

Knowledge and practices of nurses concerning intravenous potassium administration in a Turkish hospital

Objective: Based on this literature review, it is clear that intravenous potassium is a potentially toxic electrolyte, which has been responsible for a large number of deaths in hospitals. In Turkey, research on intravenous potassium administration is limited in the available literature. In addition, clinical observations made by the researchers suggests there is knowledge and practice deficiencies among nurses related to potassium administration. Thus, this study aimed to determine how wide the knowledge and practice deficiencies among nurses was concerning intravenous potassium administration in a Turkish Hospital. Design: This was a descriptive study. Setting: This study was conducted in a university hospital in Turkey. Subjects and Method: The sample of this study consisted of a total 105 nurses working in surgery clinics or surgical intensive care units of a university hospital, who volunteered to participate in the study.The questionnaire used in this study was developedby the researchers with the help of material obtained from the literature review. Questionnaires were distributed and collected to participants by researcher. In the calculation of knowledge and practice scores, every correct answer was assigned 1 point, while incorrect answers were assigned 0. Mean, percentage, ANOVA, the kruskal-wallis h test, the mann-whitney u test and pearson correlation were used for data analysis. Results: The mean knowledge score of nurses on intravenous potassium administration was found to be 9.48±3.21, while the mean practice score was 10.85±2.04. These results suggest that the nurses’ knowledge and practice scores were found to be relatively lower compared to 17 which is the highest scores of both knowledge and practice about intravenous potassium administration. It is also important to state that statistically significant and positive relationship was found (r: 0.595; p< 0.05). The majority of the nurses (61.9%) did not know all the elements of a correct potassium order. The differences in nurses’ knowledge scores according to the type of hospital unit and training status on liquid electrolyte balance were found to be statistically significant (p<0.05). Nurses with duration of employment of over 10 years were found to have higher knowledge scores than nurses with employment duration of below four years. This difference was found to be statistically significant (p<0.05). Conclusion: In light of the findings of this study it is recommended that nursing curriculum and in-service training programs in Turkey should address intravenous potassium administration more extensively and that protocols related to intravenous potassium administration be developed and implemented.

Reducing the risk of harm from intravenous potassium: A multi-factorial approach in the haematology setting

To describe the implementation of safety systems for the use of intravenous potassium chloride in haematology patients. We assessed the use of intravenous potassium in a haematology ward at a tertiary hospital. Initially, we prospectively analysed the prescribing and administration of intravenous potassium to all patients over a two-week period. To complement this data, we retrospectively analysed all clinical incidents involving intravenous potassium and the dispensing patterns of potassium ampoules for the past 12 months. Drawing on evidence and recommendations from international safety literature, gaps in the safe use of potassium were identified, and a multi-factorial approach to system change was implemented. A total of 18 patients were analysed with 90 intravenous bags of potassium prepared on the ward using 624 ampoules. We identified multiple opportunities for error and a lack of standardisation of therapy. The following safety systems were introduced: (i) a new prescribing and monitoring form that included dose calculation, prescriber support and pre-printed orders; (ii) removal of potassium ampoules and introduction of premixed bags; (iii) independent double checking by nursing staff at point of administration; (iv) dedicated labelling of intravenous lines; (v) extensive clinician training supported by guidelines; and (vi) introduction of 'smart pump' infusion software. The number of incidents significantly reduced from 23 to 9 (p < 0.001), and the number of ampoules dispensed reduced from 10,100 to 0. A multi-factorial approach to the safe prescribing, dispensing and administration of intravenous potassium has reduced the potential for patient harm in the haematology setting.

Thyrotoxic hypokalemic periodic paralysis: a rare complication of a common disease

Thyrotoxic periodic paralysis (TPP) is an uncommon but potentially lethal manifestation of hyperthyroidism characterized by muscle paralysis and hypokalemia. We have reported 3 cases of TPP in male patients, which manifested with morning muscle weakness evolved into paralysis. In all patients were found severe hypokalemia, abnormalities on electrocardiogram, and Graves' hyperthyroidism. Intravenous potassium administration led to normalization of potassium levels, and resolution of neurological symptoms. In addition, beta blockers and methimazole were started. Two patients required total thyroidectomy for poor control of hyperthyroidism with antithyroid drug. In patients presenting with periodic paralysis or diffuse muscle weakness thyroid function should be investigated in order to find out the cases secondary to unknown hyperthyroidism and to start an early appropriate combined therapy. The correct management of TPP can prevent serious cardiopulmonary complications.

Enteral potassium supplementation in a pediatric cardiac intensive care unit: Evaluation of a practice change

Potassium supplementation is a common practice in critically ill children, especially those with heart disease. Intravenous potassium supplementation is the standard route of administration in most intensive care units. Although the enteral route is safer and thus may be a reasonable alternative, data on the efficacy of enteral potassium administration are lacking. A change of practice to encourage use of enteral potassium was instituted in the cardiac intensive care unit at Texas Children's Hospital, and a review of this practice change was undertaken. The primary outcome of interest was the comparable efficacy of enteral and intravenous potassium administration. Patient demographic data, including urine output, diuretic use, route of potassium administration, and adverse events were documented and analyzed. Seventy-six patients met inclusion criteria and received 399 bolus doses of potassium (166 intravenous and 233 enteral). No patients became hyperkalemic after either route of administration. The increase in serum potassium was similar in both groups of patients. Side effects of the two routes of administration were not different. The efficacy of enteral potassium is comparable to intravenous potassium for potassium replacement in pediatric patients after congenital heart surgery.

À propos de deux cas de paralysie périodique hypokaliémique

We report on two cases of hypokaliemic periodic paralysis due to a potassium shift from the extracellular to the intracellular compartment of skeletal muscle cells. The first case occurred in a 15-year-old boy who experienced rapid onset flaccid tetraplegia without neurological abnormalities. Physical exam revealed facial dysmorphy, and EKG a long QT. Biology evidenced shift hypokalemia that was quickly reversible after administration of intravenous potassium. After exclusion of Andersen-Tawil syndrom, hypokalemic familial paralysis (Westphall disease) was diagnosed by molecular genetic testing (disease-causing mutation in CACNA1S) in the proband and in three other family members. The second case occurred in a 24-year-old male who experienced rapid onset flaccid tetraplegia due to intracellular potassium shift that was quickly reversible after administration of intravenous potassium. Biology revealed thyrotoxicosis due to Grave's disease. To the best of our knowledge, this is the first case described in a people from pacific origin. The clinical, biological, and electromyographic findings of the most frequent causes of periodic paralysis are underlined as well as the molecular genetic diagnosis in familial forms.

A Case Report of Hypokalemic Periodic Paralysis with Arrhythmia

The hypokalemic periodic paralysis is characterized by intermittent flaccid paralysis of extremities with spontaneous recovery. It is rarely accompanied by cardiac arrhythmia, especially fatal ventricular tachycardia or torsades de pointes. We observed a 29 year old man, who had suffered from intermittent periodic paralysis and fatal ventricular tachyarrhythmia. He had the first episode of muscle weakness in his low grade of elementary school, which lasted for 20-30 hours. Similar episodes of muscle weakness occurred 1–7 times per year, especially after carbohydrate rich food. On admission to emergency room, his chief complaints were generalized weakness and chest tightness, serum potassium level was 1.6mEq/L, and four extremities showed Grade 0 motor weakness. His electrocardiography(ECG) showed Atrioventricular dissociation due to sinus tachycardia and accelerated junctional rhythm, intraventricular conduction disturbance. During intravenous potassium administration, ECG showed sustained ventricular tachycardia and cardiovascular collapse occurred. So we carried out resuscitation and cardioversion. After resuscitation, he recovered from cardiovascular collapse and ECG showed sinus tachycardia. But during continuous monitoring ECG showed torsades de pointes with cardiovascular collapse. We carried out resuscitation and defibrillation repeatedly. Serum potassium level was 1.7-1.8mEq/L at that time. After successful resuscitation, ECG showed sinus rhythm, and his mental status was fully recovered. After he admitted to intensive care unit, paralytic attack and cardiac arrhythmia did not occurred any more. Serum potassium level was maintained between 3.9-6.1mEq/L during his hospital days. He was fully recovered but could not take any medications(e.g. acetazolamide, potassium supplying agent and antiarrhythmic drugs) due to severe gastrointestinal disturbances. During the 30 months of postdischarge period, he experienced three mild paralysis attacks, but they were not accompanied by chest tightness, palpitation or syncope.

A Case of Familial Hypokalemic Periodic Paralysis Associated with Cardiac Arrest

A 27-year-old men was admitted to our hospital because of hypokalemic periodic paralysis. He had been receiving potassium supplements since his first attack at the age of 17 years. Complete quadriplegia had set in at the time of admission, but his consciousness was clear and blood pressure was normal. He was treated with acute intravenous potassium administration but serum potassium level did not normalize quickly and cardiac arrest occurred. Repeated DC shock and a large amount of potassium infusion (1,000 mEq/4 hours) saved his life. His father and some members of his kindred had experienced similar attacks. There were no signs and symptoms known to trigger of periodic paralysis i. e., potassium loss from gastrointestinal tract or kidney and excess of hormones such as thyroxine, aldosterone or insulin. This is a rare case in which unusual cardiac arrest was followed by hypokalemic periodic paralysis.

Influence of acute potassium loading on renal phosphate transport in the rat kidney.

This study examined 1) whether potassium-induced depression of phosphate excretion is a parathyroid hormone-dependent phenomenon, and 2) whether such stimulation of tubular phosphate reabsorption capacity involves increased phosphate reabsorption in the distal tubule. Potassium was infused into intact rats (25 mumol X min-1 X kg-1) during stepwise addition of phosphate to the infusion and led to a significant drop in phosphate excretion; this effect was abolished in thyroparathyroidectomized (TPTX) animals. In intact rats the maximal tubular Pi reabsorption per milliliter of glomerular filtrate (max TRPi/ml GF) was significantly higher in the potassium group (2.54 +/- 0.06 mumol/ml GF) compared with the control group (2.31 +/- 0.06 mumol/ml GF) (means +/- SE). In TPTX rats no difference in max TRPi/ml GF was observed: 3.44 +/- 0.07 and 3.49 +/- 0.07 mumol/ml GF during potassium and sodium infusion, respectively. Free-flow micropuncture was carried out on superficial distal tubules of intact rats and fluid samples were analyzed for [3H]inulin and phosphorus (electron microprobe). Phosphorus delivery into the distal tubule was similar in control and potassium-loaded rats. Whereas net phosphorus reabsorption along the distal tubule was absent in the control group, intravenous potassium administration stimulated distal phosphorus reabsorption. potassium stimulates renal phosphate reabsorption capacity, an effect that is abolished after TPTX. The potassium effect on phosphate occurs along the distal tubule.

The occurrence of a rapid ventricular rate during atrial fibrillation as a paradoxical manifestation of digitalis intoxication

1. 1. Three patients with long-standing atrial fibrillation were observed to have an increase in ventricular response to atrial fibrillation while taking large doses of digitalis. 2. 2. The increase in rate in each instance followed recent administration of a mercurial diuretic and was thought to be associated with loss of potassium during diuresis. 3. 3. Administration of intravenous potassium resulted in prompt and progressive slowing of the ventricular rate over a 2-hour period. 4. 4. In one case, digoxin given intravenously, after the rate had been slowed with potassium, caused the rate to increase. Additional potassium again effected slowing. 5. 5. The evidence suggests that during atrial fibrillation, digitalis toxicity may be paradoxically manifest by an increase in ventricular response without alteration of the pacemaker mechanism. 6. 6. Since this paradoxical response simulates a classical indication for digitalis, it represents a dangerous paradox if unrecognized as a toxic potential of the cardiac glycosides. 7. 7. This manifestation of toxicity seems prone to occur in patients with refractory congestive failure treated with rigid salt restriction, frequent mercurial diuretics, and large doses of digitalis.