The correct answer is: 2. Hyperkalemia. Spironolactone, as a potassium-sparing diuretic, inhibits the action of aldosterone at the renal level, being responsible for a decrease in potassium excretion. Hyperkalemia produces repolarization disturbances that result in the installation of a large, symmetrical, narrow-based T, visible in the precordial leads. The QT space is shortened. These anomalies appear with a kalemia of around 5.5 to 6 mmol/l. Above 6.5 mmol/L, electrocardiographic changes are constant, and are dominated by conduction disturbances (making ventricular extrasystoles possible).

[HIDDEN] Hyperkalemia. Spironolactone, as a potassium-sparing diuretic, inhibits the action of aldosterone at the renal level, being responsible for a decrease in potassium excretion. Hyperkalemia produces repolarization disturbances that result in the installation of a large, symmetrical, narrow-based T, visible in the precordial leads. The QT space is shortened. These anomalies appear with a kalemia of around 5.5 to 6 mmol/l. Above 6.5 mmol/L, electrocardiographic changes are constant, and are dominated by conduction disturbances (making ventricular extrasystoles possible).

An 80-year-old patient with a history of hypertension and on treatment with enalapril and spironolactone comes to the hospital with asthenia and severe muscle weakness. Blood pressure is 110/70 mmHg. In the ECG, there are sharp and elevated T waves, ventricular extrasystoles and short QT. What is the most likely diagnosis?

Effects of presentation and electrocardiogram on time to treatment of hyperkalemia.

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.

Electrolyte disorders and arrhythmogenesis.

Electrolyte disorders can alter cardiac ionic currents kinetics and depending on the changes can promote proarrhythmic or antiarrhythmic effects. The present report reviews the mechanisms, electrophysiolgical (EP), electrocardiographic (ECG), and clinical consequences of electrolyte disorders. Potassium (K⁺) is the most abundent intracellular cation and hypokalemia is the most commont electrolyte abnormality encountered in clinical practice. The most significant ECG manifestation of hypokalemia is a prominent U wave. Several cardiac and non cardiac drugs are known to suppress the HERG K⁺ channel and hence the I(K), and especially in the presence of hypokalemia, can result in prolonged action potential duration and QT interval, QTU alternans, early afterdepolarizations, and torsade de pointes ventricular tachyarrythmia (TdP VT). Hyperkalemia affects up to 8% of hospitalized patients mainly in the setting of compromised renal function. The ECG manifestation of hyperkalemia depends on serum K⁺ level. At 5.5-7.0 mmol/L K⁺, tall peaked, narrow-based T waves are seen. At > 10.0 mmol/L K⁺, sinus arrest, marked intraventricular conduction delay, ventricular techycardia, and ventricular fibrillation can develop. Isolated abnormalities of extracellular calcium (Ca⁺⁺) produce clinically significant EP effects only when they are extreme in either direction. Hypocalcemia, frequently seen in the setting of chronic renal insufficiency, results in prolonged ST segment and QT interval while hypercalcemia, usually seen with hyperparathyroidism, results in shortening of both intervals. Although magnesium is the second most abudent intracellular cation, the significance of magnesium disorders are controversial partly because of the frequent association of other electrolyte abnormalities. However, IV magnesium by blocking the L-type Ca(⁺⁺) current can successfully terminate TdP VT without affecting the prolonged QT interval. Finally, despite the frequency of sodium abnormalities, particularly hyponatremia, its EP effects are rarely clinically significant.

Hyperkalemia

Hyperkalemia is an elevated level of potassium (K+) in the blood. Normal potassium levels are between 3.5 and 5.0mmol/L (3.5 and 5.0mEq/L) with levels above 5.5mmol/L defined as hyperkalemia. Typically hyperkalemia does not cause symptoms. Occasionally when severe it can cause palpitations, muscle pain, muscle weakness, or numbness. Hyperkalemia can cause an abnormal heart rhythm which can result in cardiac arrest and death. Common causes of hyperkalemia include kidney failure, hypoaldosteronism, and rhabdomyolysis. A number of medications can also cause high blood potassium including spironolactone, NSAIDs, and angiotensin converting enzyme inhibitors. The severity is divided into mild (5.5–5.9mmol/L), moderate (6.0–6.4mmol/L), and severe (>6.5mmol/L). High levels can be detected on an electrocardiogram (ECG). Pseudohyperkalemia, due to breakdown of cells during or after taking the blood sample, should be ruled out.

Licorice induced pseudohyperaldosteronism, severe hypertension, and long QT.

Excessive intake of licorice may cause pseudohyperaldosteronism which, in turn, may lead to hypertension and hypokalemia. Severe hypokalemia may lead to electrocardiogram (ECG) changes including long QT interval potentially progressing into malignant arrhythmias. Here we present a 43-year-old woman admitted to the hospital with chest pain and a stinging sensation in the upper extremities. Her peak blood pressure was 177/98 mmHg and the blood test revealed low plasma potassium of 1.9 mmol/L. The ECG revealed flattened T-waves and long QT interval. Prior to admission, the patient had increased licorice ingestion to a total of some 70 g daily. The licorice intake was stopped and potassium was administrated orally and intravenously. Plasma potassium normalized and the ECG changes remitted. To our knowledge a few other cases of licorice-induced pseudohyperaldosteronism and long QT interval have previously been reported. This underlines the importance of quantifying licorice intake in younger people with unexplained high blood pressure and low potassium. Even small amounts of licorice daily may increase the risk of developing hypertension; therefore, licorice should be asked for specifically. Even though licorice intake is very easy to cover in the patient's history, it is often missed. Excessive licorice intake may course severe hypokalemia causing long QT interval in the ECG recording, potentially progressing into arrhythmias and even cardiac arrest/sudden death. Hypokalemia <3 mmol/L and present ECG changes should be treated with potassium intravenously. Licorice-induced hypertension may be associated with syndrome of apparent mineralocorticoid excess (SAME). Plasma renin and aldosterone are both low at diagnosis and normalize when licorice is stopped.

A rare electrocardiographic manifestation of a rare form of multiple electrolyte disturbances: hyperparathyroid crisis.

The surface electrocardiogram (ECG) has been used as a useful method for detection of metabolic disturbances for a long time. However, it may be difficult to distinguish the exact disturbance when more than one metabolic abnormality exists in a patient simultaneously. Although, "classic" ECG characterizations of common electrolyte disturbances are well described, multiple concurrent electrolyte disturbances may lead to ECG abnormalities that may not be easily detectable. This ECG concerns a 60-year-old male presented with general fatigue, weakness, epigastric pain, anorexia, nausea and extreme hypercalcemia (serum total and ionized calcium levels 20.5 mg/dL and 12.02 mg/dl, respectively), hypokalemia and hypomagnesemia associated with elevated parathyroid hormone (1160 pg/ml) and normal serum vitamin D level (97 ng/ml) . This rare manifestation of primary hyperparathyroidism has been named hyperparathyroid crisis in the literature. Hyperparathyroid crisis is an emergency form of multiple electrolyte abnormalities that manifest as a life-threatening hypercalcemia and simultaneous hypokalemia and hypomagnesemia; these two later are believed to be caused by diuretic effect of calcium on the renal tubules. The unique pattern of ECG in our patient first was misdiagnosed as prominent T waves with prolongation of the QT corrected (QTc) interval, which has been reported several times in patients with hyperparathyroidism crisis, compatible with our patient. But more investigation revealed that, the QTc interval not only is not prolonged, it is shortened as it is expected from the effect of hypercalcemia on electrocardiogram. The exact pattern of the patient`s ECG (figure 1) can be interpreted as it follows: (1) Flattening of the T wave, (2) a prominent U wave, (3) prolongation of the descending limb of the T wave such that it overlapped with the next U wave (4) virtual absence of ST segment and (5) shortening of the QT corrected interval. In conclusion, it should be emphasized when the T and U waves are separated by a very short segment they can mimic the appearance of a prolonged QT interval. However, more investigation can demonstrate the exact electrocardiographic pattern especially in multiple electrolyte disturbances, when "classic" ECG patterns are not expectable.

Child with acute weakness: don't forget the salts.

Case summaryA 10-year-old boy presented with severe progressive generalised weakness on a background of 3 days of diarrhoea and vomiting. Vital signs were normal. Peripheral neurological examination revealed grade 1-2 power in all limbs, hypotonia and hyporeflexia. Sensation was fully intact. Cranial nerve examination and speech were normal. The ECG (figure 1) and initial venous blood gas (figure 2) are shown.edpract;107/1/21/F1F1F1Figure 1ECG.edpract;107/1/21/F2F2F2Figure 2Venous blood gas. QUESTION 1: What abnormalities are present on the ECG?Peaked T waves, prolonged PR segment and loss of P waves?Shortening of the QT interval and Osborn waves (J waves)?T wave flattening/inversion, prominent U waves and long QU interval?Prolonged QT interval with multiple atrial and ventricular ectopics? QUESTION 2: How would you manage this patient's hypokalaemia? QUESTION 3: What is the likely diagnosis?Conversion disorder.Myasthenia gravis.Periodic paralysis.Guillain-Barré syndrome.Botulism. QUESTION 4: What interventions can be considered for long-term treatment of this condition? <iAnswers can be found on page 2</i.

Thyrotoxic periodic paralysis

Diagnosis Hypokalemia (low blood potassium levels) commonly occurs during attacks; levels below 3.0 mmol/l are typically encountered. Magnesium and phosphate levels are often found to be decreased. Creatine kinase levels are elevated in two thirds of cases, usually due to a degree of muscle injury; severe elevations suggestive of rhabdomyolysis (muscle tissue destruction) are rare. Electrocardiography (ECG/EKG) may show tachycardia (a fast heart rate) due to the thyroid disease, abnormalities due to cardiac arrhythmia (atrial fibrillation, ventricular tachycardia), and conduction changes associated with hypokalemia (U waves, QRS widening, QT prolongation, and T wave flattening). Electromyography shows changes similar to those encountered in myopathies (muscle diseases), with a reduced amplitude of the compound muscle action potentials (CMAPs); they resolve when treatment has commenced.

[Syncope caused by iatrogenic hypercalcemia].

A course of the disease of a 68-year-old female who had been taking medigoxin, furosemide, verapamil and an unknown amount of spironolactone and potassium salt due to congestive heart failure is presented. She was admitted to emergency department of the University Hospital Rebro after an episode of syncopal attack because of arrhythmia due to hyperkalemia (8.9 nmol/L). She has had a fast idioventricular rhythm, followed by atrial tachycardia after that and with fast ventricular rhythm, S-T segment depression and a tall and peaked T-wave. In the following electrocardiograms left anterior hemiblock appeared, a tall R-wave of the anterolateral location, supraventricular and ventricular premature beats and atrioventricular block of the first degree. The patient had signs of non-oliguric form of acute renal failure at the admission which was a partly explanation for the development of hyperkalemia, together with the use of spironolactone and potassium salt. After the treatment she had normal serum creatinine values. She suffered from combined mitral valve disease: stenosis with a predominant regurgitation of the II/III degree. She was discharged from the hospital in a compensated state with normal serum potassium values.

Clinical and electrocardiogram presentations of patients with high serum potassium concentrations within emergency settings: a prospective study.

Elevated potassium level is a common and reversible peri-arrest condition. Diagnosis and management of hyperkalemia in a short time is critical, where electrocardiogram (ECG) alterations might be helpful. We aimed to investigate the role of clinical features and ECGs in early diagnosing and treating hyperkalemia. Prospectively, adult patients who presented to the emergency department (ED) from July 2019 to March 2020 with hyperkalemia (serum potassium ≥5.5mmol/L) were included. History was obtained, and laboratory investigations and ECGs were performed at the presentation and before initiating hyperkalemia therapy. Hyperkalemia severity was divided into mild (5.5-5.9mmol/L), moderate (6.0-6.4mmol/L), and severe (≥6.5mmol/L). A cardiologist and emergency physician blinded to laboratory values, study design, and patients' diagnoses interpreted ECGs and presenting symptoms independently to predict hyperkalemia. Sixty-seven hyperkalemic patients with a mean (±SD) serum potassium level of 6.5±0.7mmol/L were included in this study. The mean age was 63.9±15.1, and 58.2% were females. Hyperkalemia was mild in 10.4%, moderate in 40.3%, and severe in 49.3%. Almost two thirds of patients (71.6%) had hypertension, 67.2% diabetes, and 64.2% chronic kidney disease. About one-quarter of patients (22.4%) were asymptomatic, while fatigue (46.3%), dyspnea (28.4%), and nausea/vomiting (20.9%) were the most common presenting symptoms. Normal ECGs were observed in 25.4% of patients, while alterations in 74.6%. Atrial fibrillation (13.4%), peaked T wave (11.9%), widened QRS (11.9%), prolonged PR interval (10.5%), and flattening P wave (10.5%) were the most common. Peaked T wave was significantly more common in severe hyperkalemia (87.5%) than in mild and moderate hyperkalemia (12.5%, 0.0%, respectively) (p=0.041). The physicians' sensitivities for predicting hyperkalemia were 35.8% and 28.4%, improved to 51.5% and 42.4%, respectively, when limiting the analyses to severe hyperkalemia. The mean (±SD) time to initial hyperkalemia treatment was 63.8±31.5 min. Potassium levels were positively correlated with PR interval (r=0.283, p=0.038), QRS duration (r=0.361, p=0.003), peaked T wave (r=0.242, p=0.041), and serum levels of creatinine (r=0.347, p=0.004), BUN (r=0.312, p=0.008), and CK (r=0.373, p=0.039). The physicians' abilities to predict hyperkalemia based on ECG and symptoms were poor. ECG could not be solely relied on, and serum potassium tests should be conducted for accurate diagnosis.

A case of massive pericardial effusion associated with hypocalcemic cardiomyopathy.

A 60-year-old woman with a 6-year history of numbness in her hands was admitted to hospital with dyspnea. Laboratory findings showed the elevation of creatine kinase (creatine kinase MB isoenzyme was less than 4 IU/l). Chest X-ray revealed cardiomegaly and pulmonary edema. Electrocardiogram showed a T wave inversion in V<sub2-5</sub and a prolonged QT interval. Echocardiography demonstrated reduced left ventricular ejection fraction (LVEF) and massive pericardial effusion. The patient was diagnosed with heart failure. Further testing found hypocalcemia and idiopathic hypoparathyroidism. In addition to diuretics, calcium replacement therapy for hypocalcemia improved the LVEF and reduced pericardial effusion. Hypocalcemia rarely leads to heart failure and pericardial effusion. In our case, heart failure and the massive pericardial effusion were secondary to hypocalcemia due to idiopathic hypoparathyroidism. <<bLearning objective:</b Hypocalcemia should be considered in patients with heart failure, reduced ejection fraction, and massive pericardial effusion. Supportive findings for diagnosis of heart failure caused by hypocalcemia are numbness, elevation of creatine kinase, T wave inversion, and prolonged QT interval.>.

InternalMed_Harrison

FIguRE 269e-24 Prominent U waves (II, III, and V4–V6) with ventricular repolarization prolongation in a patient with severe hypokalemia. CHAPTER 269e Atlas of Electrocardiography FIguRE 269e-25 Abbreviated ST segment such that the T wave looks like it takes off directly from QRS in some leads (I, V4, aVL, and V5) in a patient with severe hypercalcemia. Note also high takeoff of ST segment in V2/V3 simulating acute ischemia. PART 10 Disorders of the Cardiovascular System FIguRE 269e-26 SR with LVH, left atrial abnormality, and tall peaked T waves in the precordial leads with inferolateral ST depressions (II, III, aVF, and V6); left anterior fascicular block and borderline prolonged QT interval in a patient with renal failure, hypertension, and hyperkalemia; prolonged QT is secondary to associated hypocalcemia.

Global T-wave inversions with isolated hypomagnesemia.

The physiological actions of magnesium within the cardiac conduction system and myocytes have yet to be fully elucidated. Because concurrent hypocalcemia or hypokalemia were also present in previous human reports, specific electrocardiographic effects of isolated hypomagnesemia have not been clearly delineated. We report a case in which dynamic electrocardiogram (ECG) changes were demonstrated in isolated hypomagnesemia. A 37-year-old man with history of heavy alcohol use was admitted for syncope. The ECG showed global T-wave inversions with prolonged corrected QT (QTc) duration on ECG. Extensive work-up including cardiac catheterization was unremarkable. His serum magnesium was noted to be low at 1.1 mg/dL, and his serum calcium and potassium were within normal limits. The patient received magnesium infusion with subsequent ECGs showing resolution of his global T-wave inversions and prolonged QTc. This case is unique because it reports dynamic ECG changes in a patient with isolated hypomagnesemia. Although isolated hypomagnesemia is commonly believed to result in dysrhythmia, we were unaware of any previous cases of ECG abnormalities in humans. Clinically, we advise checking serum magnesium and correcting hypomagnesemia when prolonged QTc duration and global T-wave inversions are seen on ECG.

Electrocardiography

Electrolytes disturbances and intoxication: Digitalis intoxication Calcium: hypocalcemia and hypercalcemia Potassium: hypokalemia and hyperkalemia Serotonin Toxicity Ischemia and infarction: Wellens' syndrome (LAD occlusion) de Winter T waves (LAD occlusion) ST elevation and ST depression High Frequency QRS changes Myocardial infarction (heart attack) Non-Q wave myocardial infarction NSTEMI STEMI Sgarbossa's criteria for ischemia with a LBBB Structural: Acute pericarditis Right and left ventricular hypertrophy Right ventricular strain or S1Q3T3 (can be seen in pulmonary embolism) History

Sodium Polystyrene Sulfonate -- Monitoring

Since SPS is not selective for potassium ions, other electrolyte imbalances may occur while using SPS in hyperkalemic patients. Patients should be monitored carefully for the signs and symptoms of other electrolyte abnormalities such as hypokalemia,  hypomagnesemia, and hypocalcemia. Hypokalemia may be associated with cardiac arrhythmias and severe muscle weakness. Hypokalemia may be evident as prolongation of the QT interval, T-wave inversions, prominent U waves (an extra upward wave after the T-wave) in Electrocardiogram (ECG). Some patients may present with significant symptoms of rebound hyperkalemia, which may be evident in ECG as a tall peaked T wave. Hypomagnesemia can present with muscle weakness and potentiate hypokalemia. Hypocalcemia presents with tremors, muscle weakness, tetany, and rarely, seizures.

Thyrotoxic periodic paralysis with ventricular tachycardia.

A 47-year-old man presented to our emergency department (ED) with limbs weakness for 2 h. His heart rate was 127 beats per minute and blood pressure was 95/49 mm Hg. He found weakness of limbs after 4-h sleep. Physical examinations revealed that the muscle strength of upper limbs is 3/5, and lower limbs are 2/5. Electrocardiogram (ECG) revealed wide QRS complex, monomorphic ventricular tachycardia (VT) with ST-segment depression and long QT interval. Serum potassium level was extremely low as 1.0 mEq/L. This led to periodic hypokalemic paralysis. Due to severe hypokalemia with possible atrioventricular block, the patient was admitted to the intensive care unit. During hospitalization, his potassium level returned to 5.1 mEq/L on the first day. He had a low level of thyroid stimulating hormone (TSH) of <0.03 micro-IU/mL (normal range: 0.25-4.00) and a high free thyroxine (T4) level of 2.43 ng/dL (normal range: 0.89-1.79 ng/dL). Therefore, hyperthyroidism was diagnosed, and 5 mg of methimazole was administered twice a day. The patient was discharged on the seventh day after admission. The final diagnosis is thyrotoxic periodic paralysis (TPP), also as known as nocturnal paralysis or night palsy.

Diagnosis and clinical approach in Gitelman's syndrome.

Hypokalemia, defined as a plasma potassium concentration <3.5 mmol/l, is the most common electrolyte abnormality encountered in our clinical practice. Unfortunately, in many cases, the etiologies were unclear and resulted in a wrong treatment. Indeed, the true etiology could be such a 'rare' one and could be found by doing a comprehensive work up. One of this is Gitelman's syndrome, a rare genetic disorder characterized by hypokalemic alkalosis, hypomagnesemia, hypocalciuria, and secondary aldosteronism without hypertension. Since this disorder is found in 1% Caucasian populations, this is one of the most frequently inherited renal tubular disorders. A 27 year old man came to emergency room with weakness and generalised muscle cramps. He was investigated three months before for a similar electrolyte disturbance which was found to be inconclusive. The routine laboratory data in emergency room revealed a potassium concentration of 2.3 mmol/l. He had never used diuretics or hormonal therapy nor had history of vomiting or diarrhea. He had normal blood pressure and the blood gas analysis revealed metabolic alkalosis. On his ECG (electrocardiography), we found the prominent U wave. Despite his low concentration of serum potassium and cloride, the concentration of these electrolytes in urine were extremely high. We also found hipomagnesemia. The calcium concentration in serum was normal with slightly hypocalciuria. Even with aggressive oral and intravenous potassium suplementation, the patient remained hypokalemic. In cases when the etiology of hypokalemia is unclear, we should perform some investigations to confirm the diagnosis and give the proper treatment. In Gitelman's syndrome, where the defect in the distal tubule cannot be corrected, the treatment must be a life-long. Most patients require oral potassium and magnesium supplementation, since drug therapy is usually incompletely effective.

InternalMed_Harrison

Hyperkalemia is defined as a serum potassium level >5.5 mmol/L (>5.5 meq/L) and can neurologically present as muscle weakness with or without paresthesias. Hyperkalemia becomes life threatening when it produces electrocardiographic abnormalities such as peaked T waves or a widened QRS complex. In these cases, prompt treatment is essential and consists of strategies that protect the heart against arrhythmias (calcium gluconate administration); promote potassium redistribution into cells (with glucose, insulin, and β2-agonist medications); and increase potassium removal (through sodium polystyrene sulfonate, loop diuretics, or hemodialysis). Hypercalcemia usually occurs in the setting of either hyperparathyroidism or systemic malignancy. Neurologic manifestations include encephalopathy as well as muscle weakness due to reduced neuromuscular excitability. Seizures can occur but are more common in states of low calcium.

Electrocardiography

Diagnosis Numerous diagnoses and findings can be made based upon electrocardiography, and many are discussed above. Overall, the diagnoses are made based on the patterns. For example, an "irregularly irregular" QRS complex without P waves is the hallmark of atrial fibrillation; however, other findings can be present as well, such as a bundle branch block that alters the shape of the QRS complexes. ECGs can be interpreted in isolation but should be applied – like all diagnostic tests – in the context of the patient. For example, an observation of peaked T waves is not sufficient to diagnose hyperkalemia; such a diagnosis should be verified by measuring the blood potassium level. Conversely, a discovery of hyperkalemia should be followed by an ECG for manifestations such as peaked T waves, widened QRS complexes, and loss of P waves. The following is an organized list of possible ECG-based diagnoses.

Hypokalemia -- History and Physical

Hypokalemia can result in a variety of cardiac dysrhythmias. Although cardiac dysrhythmias or ECG changes are more likely to be associated with moderate to severe hypokalemia, there is a high degree of individual variability and can occur with even mild decreases in serum levels. This variability is dependent on concomitant factors such as magnesium depletion, digitalis therapy, among others. Moreover, characteristic ECG changes do not manifest in all patients. The ECG changes that occur are T-wave flattening initially, followed by ST depression and the appearance of a U wave that can be difficult to distinguish from the T wave. The U wave is often seen in the lateral precordial leads of V4 to V6. Prolongation of the PR and QT interval can also occur. Risk of arrhythmias is highest in older patients, those with heart disease and those receiving digoxin or antiarrhythmic drugs. Administration of anesthesia in the setting of hypokalemia is also a risk for dysrhythmias and impaired cardiac contractility but more so with acute rather than chronic hypokalemia.

Hyperkalemia -- Evaluation

The first test that should be ordered in a patient with suspected hyperkalemia is an ECG since the most lethal complication of hyperkalemia is cardiac condition abnormalities which can lead to dysrhythmias and death. Elevated potassium causes ECG changes in a dose-dependent manner: K = 5.5 to 6.5 mEq/L ECG will show tall, peaked t-waves K = 6.5 to 7.5 mEq/L ECG will show loss of p-waves K = 7 to 8 ECG mEq/L will show widening of the QRS complex K = 8 to 10 mEq/L will produce cardiac arrhythmias, sine wave pattern, and asystole

Periodic paralysis: rare presenting symptom of thyrotoxicosis.

Paralysis due to hypokalemia results from an acute shift of potassium into cells or excessive potassium deficit. In the absence of potassium deficit, it is observed in Familial Hypokalemic Periodic Paralysis and in Thyrotoxic Hypokalemic Periodic Paralysis (TPP). This report describes the initial presentation of hyperthyroidism as sudden quadriplegia associated with hypokalemia. A healthy 25-year-old Puerto Rican policeman came to the emergency room with sudden paralysis in the four extremities of five hours evolution. He woke up in the morning and could not get up. The day before admission his legs felt weak, and it was hard to get out of bed. He arrived home at 7:00 PM, ate pasta and vegetables, and went to sleep at 10:00 PM. He had no diarrhea or weight loss, no history of medications or illicit drugs. He has a cousin and an aunt with the diagnosis of hypo-thyroidism. The admission temperature was 36.0 degrees C, pulse 96 per minute, respiratory rate 18 per minute, blood pressure 160/70 mmHg. He was alert and oriented as to time, place and person. He could talk properly and was in no respiratory distress. He had no exophtalmos or lid lag. The thyroid was not enlarged or tender. No pseudoclubbing or pretibial edema was found. There was flaccid paralysis of all extremities, 0/5 legs and 1/5 arms. Deep tendon reflexes could not be elicited. The cranial nerves and sensory examination were normal. The hemogram was within normal limits as were the renal and liver functions. Serum sodium was 140 mEq/L, potassium 1.48 mEq/L, phosphorus 1.4 mEq/L. A random glucose was 155 mg/dl and the arterial Ph was 7.41. The urine potassium was 7.04 mEq/L, sodium 60.8 mg/dl. TSH levelwas < 0.03 ug/d], TUP 50.69% (24-40%), T4 17.6 ug/dl (4.7-11.4 ug/dl) Free T4 Index 28.23. He was managed with intravenous potassium chloride, 80 mEq in a period of seven hours with cardiac monitor. The serum potassium level, after the infusion was completed, was 6.70 mEq/L. No cardiac arrhythmia was documented. Muscle strength recovery was gradual and it was complete 4 hours after the infusion was initiated. The next day the potassium level was within normal limits but a wide pulse pressure and tachycardia still persisted.

[Life threatening hyperkalemia: the value of the electrocardiogram].

In two men, aged 19 and 64, with chronic renal insufficiency and subacute symptoms of malaise and weakness of the leg muscles, broad QRS complexes were seen in the ECG. The younger patient developed an asystole and resuscitation was unsuccessful. His blood potassium level was found to be 8.3 mmol/l. The older patient recovered after administration of calcium gluconate. His blood potassium level was found to be 8.5 mmol/l. An 80-year-old woman who was taking various drugs because of heart failure also complained of muscle weakness. Her blood potassium level was 7.2 mmol/l and her ECG showed narrow complexes. She recovered without calcium gluconate after a change in medication. Hyperkalemia is a potentially life-threatening electrolyte disorder that may require immediate treatment. The changes in the ECG, especially widening of the QRS complexes, are the most important clues to the severity of the hyperkalemia. A treatment protocol based on ECG changes may reduce the mortality in these patients.

Electrolyte imbalance

Treatment Primary treatment of hypercalcemia consists of administering IV fluids. If the hypercalcemia is severe and/or associated with cancer, it may be treated with bisphosphonates. For very severe cases, hemodialysis may be considered for rapid removal of calcium from the blood. Hypocalcemia Hypocalcemia describes when calcium levels are too low in the blood, usually less than 8.5 mg/dL. Causes Hypoparathyroidism and vitamin D deficiency are common causes of hypocalcemia. It can also be caused by malnutrition, blood transfusion, ethylene glycol intoxication, and pancreatitis. Symptoms Neurological and cardiovascular symptoms are the most common manifestations of hypocalcemia. Patients may experience muscle cramping or twitching, and numbness around the mouth and fingers. They may also have shortness of breath, low blood pressure, and cardiac arrhythmias.

Torsades de pointes

The ECG tracing in torsades demonstrates a polymorphic ventricular tachycardia with a characteristic illusion of a twisting of the QRS complex around the isoelectric baseline (peaks, which are at first pointing up, appear to be pointing down for subsequent "beats" when looking at ECG traces of the "heartbeat"). It is hemodynamically unstable and causes a sudden drop in arterial blood pressure, leading to dizziness and fainting. Depending on their cause, most individual episodes of torsades de pointes revert to normal sinus rhythm within a few seconds; however, episodes may also persist and possibly degenerate into ventricular fibrillation, leading to sudden death in the absence of prompt medical intervention. Torsades de pointes is associated with long QT syndrome, a condition whereby prolonged QT intervals are visible on an ECG. Long QT intervals predispose the patient to an , wherein the R-wave, representing ventricular depolarization, occurs during the relative refractory period at

Electrocardiographic manifestations in patients with thyrotoxic periodic paralysis.

Thyrotoxic periodic paralysis (TPP) commonly precedes the overt symptoms and signs of hyperthyroidism and may be misdiagnosed as other causes of paralysis (non-TPP). Because the cardiovascular system is very sensitive to elevation of thyroid hormone, we hypothesize that electrocardiographic manifestations may aid in early diagnosis of TPP. We retrospectively identified 54 patients who presented to the emergency department (ED) with hypokalemic paralysis during a 3.5-year period. Thirty-one patients had TPP and 23 patients had non-TPP, including sporadic periodic paralysis, distal renal tubular acidosis, diuretic use, licorice intoxication, primary hyperaldosteronism, and Bartter-like syndrome. Electrocardiograms during attacks were analyzed for rate, rhythm, conduction, PR interval, QRS voltage, ST segment, QT interval, U waves, and T waves. There were no significant differences in age, sex distribution, and plasma K+ concentration between the TPP and non-TPP groups. Plasma phosphate was significantly lower in TPP than non-TPP. Heart rate, PR interval, and QRS voltage were significantly higher in TPP than non-TPP. Forty-five percent of TPP patients had first-degree atrioventricular block compared with 13% in the non-TPP group. There were no significant differences in QT shortening, ST depression, U wave appearance, or T wave flattening between the 2 groups. Relatively rapid heart rate, high QRS voltage, and first-degree AV block are important clues suggesting TPP in patients who present with hypokalemia and paralysis.

Not your regular high: cardiac dysrhythmias caused by loperamide.

Loperamide, a non-prescription anti-diarrheal agent, is a peripheral mu-opioid receptor agonist that is excluded from the blood-brain barrier by p-glycoprotein at therapeutic doses. Overdoses of loperamide penetrate the central nervous system (CNS), leading to abuse. We report cardiac conduction abnormalities and dysrhythmias after ingestion of a recreational supra-therapeutic dose of loperamide confirmed with an elevated blood loperamide concentration. A 48-year-old woman with a history of alcohol and benzodiazepine abuse presented to the emergency department (ED) with somnolence, weakness and slurred speech. She was taking 20 to 40 tablets of 2 mg loperamide 1-2 times/day for weeks along with clonazepam and whiskey. Vital signs were: blood pressure (BP), 124/90 mmHg; heart rate (HR), 88/min; respiratory rate(RR), 20/min; T, 36.9 °C; O2 saturation 100% on room air (RA). Glucose was 6.4 mmol/L. Electrocardiogram (ECG) had a ventricular rate of 58/min, QRS 164 ms, QT 582 ms with no discernable p-waves. Lactate was 3.5 mmol/L and potassium was 6.2 mEq/L. Labs were notable for an anion gap of 20 mEq/L, ethanol of 3.9 mmol/L, creatinine of 2.3 mg/dL and loperamide concentration of 210 ng/mL (average therapeutic plasma concentration 1.2 ng/mL). She became hypotensive, but responded to fluids. Following treatment for hyperkalemia with calcium, insulin, dextrose, and hypertonic sodium bicarbonate a repeat ECG had a ventricular rate of 66/min, QRS 156 ms, and QT 576 ms. Magnesium was given and pacer pads were placed. During the infusion of magnesium, her BP fell to 92/58 mmHg with a HR of 54/min, RR 14/min, O2 saturation of 97% on RA so the infusion was stopped. The ECG after the magnesium infusion had a ventricular rate of 51/min, QRS of 134 ms, and QT 614 ms. In the ICU she had multiple runs of non-sustained ventricular tachycardia that did not require therapy. Over the next 48 h she improved and was transferred to a floor bed. On day four of hospitalization the patient left against medical advice. At that time, her ECG showed sinus tachycardia with a heart rate 114/min, QRS 82 ms, QT 334 ms. Loperamide produces both QRS and QT prolongation at supra-therapeutic dosing. A blood loperamide concentration of 210 ng/mL is among the highest concentrations reported. Supra-therapeutic dosing of loperamide is promoted on multiple drug-use websites and online forums as a treatment for opioid withdrawal, as well as for euphoric effects. With the current epidemic of prescription opioid abuse, toxicity related to loperamide, an opioid agonist that is readily available without a prescription is occurring more frequently. It is important for clinicians to be aware of the potentially life-threatening toxicity related to loperamide abuse in order to provide proper diagnosis, management and patient education.

Hypovolemic shock

Again, the above is outlined for a healthy 70 kg individual. Clinical factors must be taken into account when assessing patients. For example, elderly patients taking beta blockers can alter the patient's physiologic response to decreased blood volume by inhibiting mechanism to increase heart rate. As another, patients with baseline hypertension may be functionally hypotensive with a systolic blood pressure of 110 mmHg. Non-bleeding Various laboratory values can be abnormal in hypovolemic shock. Patients can have increased BUN and serum creatinine as a result of pre-renal kidney failure. Hypernatremia or hyponatremia can result, as can hyperkalemia or hypokalemia. Lactic acidosis can result from increased anaerobic metabolism. However, the effect of acid–base balance can be variable as patients with large GI losses can become alkalotic.

Ventricular fibrillation as the first manifestation of primary hyperaldosteronism.

50 years old female patient, with history of diabetes mellitus and hypertension, receiving metformin (500 mg BID) and atenolol (50 mg BID), presented to the Emergency Room with asthenia and dizziness. The patient was also receiving alternative medication (Dragon Blanco) which contains no licorice. During the emergency workup she developed syncope and three episodes of ventricular fibrillation. She was electrically defibrillated and treated with amiodarone and potassium replacement. The patient was admitted to the Intensive Care Unit. Physical exam: BP: 160/90 mm Hg, RR: 15, Pulse: 83: Cardiovascular: grade II systolic murmur which irradiated to the neck. The rest of the examination was unremarkable. Labs: Na: 138 meg/dl, K: 1.6 meg/dl, Cl: 84 meg/dl, BUN: 17 mg/dl, Creat.: 1.1 mg/dl, Gluc.: 148 mg/dl, Renin: < 0.15 mcgr/ml, Aldosterone: 20.1 mcg%. Aldosterone-Renin ratio: 133. Chest X-Ray: cardiomegaly. EKG: RBBB, long QT segment and prominent broad "u" waves compatible with severe hypokalemia. A CT SCAN of the Abdomen/Pelvis showed a 3.2 cm right adrenal mass, most likely adenomatous. The patient was discharged with the diagnosis of primary aldosteronism. Due to the diagnosis of diabetes mellitus, hypertension and the three episodes of ventricular fibrillation, surgical treatment was postponed until stress tests and eventual coronary angiographic studies were performed. We found in our review of the medical literature 9 reports of fibrillation associated with hyperaldosteronism. Of those, only two were associated with primary aldosteronism, one of them with a fatal outcome. This case is highly unusual and emphasizes the importance of an adequate diagnosis of secondary hypertension.

Severe Hyperkalemia: Can the Electrocardiogram Risk Stratify for Short-term Adverse Events?

The electrocardiogram (ECG) is often used to identify which hyperkalemic patients are at risk for adverse events. However, there is a paucity of evidence to support this practice. This study analyzes the association between specific hyperkalemic ECG abnormalities and the development of short-term adverse events in patients with severe hyperkalemia. We collected records of all adult patients with potassium (K+) ≥6.5 mEq/L in the hospital laboratory database from August 15, 2010, through January 30, 2015. A chart review identified patient demographics, concurrent laboratory values, ECG within one hour of K+ measurement, treatments and occurrence of adverse events within six hours of ECG. We defined adverse events as symptomatic bradycardia, ventricular tachycardia, ventricular fibrillation, cardiopulmonary resuscitation (CPR) and/or death. Two emergency physicians blinded to study objective independently examined each ECG for rate, rhythm, peaked T wave, PR interval duration and QRS complex duration. Relative risk was calculated to determine the association between specific hyperkalemic ECG abnormalities and short-term adverse events. We included a total of 188 patients with severe hyperkalemia in the final study group. Adverse events occurred within six hours in 28 patients (15%): symptomatic bradycardia (n=22), death (n=4), ventricular tachycardia (n=2) and CPR (n=2). All adverse events occurred prior to treatment with calcium and all but one occurred prior to K<sup+</sup-lowering intervention. All patients who had a short-term adverse event had a preceding ECG that demonstrated at least one hyperkalemic abnormality (100%, 95% confidence interval [CI] [85.7-100%]). An increased likelihood of short-term adverse event was found for hyperkalemic patients whose ECG demonstrated QRS prolongation (relative risk [RR] 4.74, 95% CI [2.01-11.15]), bradycardia (HR<50) (RR 12.29, 95%CI [6.69-22.57]), and/or junctional rhythm (RR 7.46, 95%CI 5.28-11.13). There was no statistically significant correlation between peaked T waves and short-term adverse events (RR 0.77, 95% CI [0.35-1.70]). Our findings support the use of the ECG to risk stratify patients with severe hyperkalemia for short-term adverse events.

Apparent mineralocorticoid excess syndrome

Apparent mineralocorticoid excess is an autosomal recessive disorder causing hypertension (high blood pressure), hypernatremia (increased blood sodium concentration) and hypokalemia (decreased blood potassium concentration). It results from mutations in the HSD11B2 gene, which encodes the kidney isozyme of 11β-hydroxysteroid dehydrogenase type 2. In an unaffected individual, this isozyme inactivates circulating cortisol to the less active metabolite cortisone. The inactivating mutation leads to elevated local concentrations of cortisol in the aldosterone sensitive tissues like the kidney. Cortisol at high concentrations can cross-react and activate the mineralocorticoid receptor due to the non-selectivity of the receptor, leading to aldosterone-like effects in the kidney. This is what causes the hypokalemia, hypertension, and hypernatremia associated with the syndrome. Patients often present with severe hypertension and end-organ changes associated with it like left ventricular

Severe hypokalemic paralysis as a manifestation of a mitochondrial disorder.

Mitochondrial disorder (MtD) is usually a multisystem disease due to impaired mitochondrial energy production. Severe hypokalemia resulting in muscle weakness and rhabdomyolysis has not been reported as a phenotypic feature of MtD. Here we describe a 60-year-old male patient who developed myalgias followed by generalized muscle weakness a few days before admission. Symptoms were attributed to severe hypokalemia that occurred after the patient had discontinued spironolactone, a competitive antagonist of the aldosterone receptor, four months earlier on his own judgment. Spironolactone was given for 10 years to treat suspected primary hyperaldosteronism (Conn's syndrome). He presented with myopathic face, bilateral ptosis, hypertelorism, brachydactylia, weakness of the axial and limb muscles, and bilateral leg edema. Hypertelorism and brachydactylia are known as physical traits of MtD. Laboratory investigations revealed hypokalemia of 1.7 mmol/l and elevated serum levels of creatine kinase (2,772 U/l). Electrocardiogram showed sinus rhythm, left bundle-branch-block, repolarization abnormalities, and prolonged QTc (571 ms), which is associated with a propensity to ventricular arrhythmias. Diagnostic work-up revealed bilateral adenomas of the suprarenal glands. Conn's syndrome was regarded as a manifestation of MtD, since MtDs are frequently associated with endocrine abnormalities. The patient also presented with occasional double vision, ptosis, renal insufficiency, bilateral renal cysts, hypertriglyceridemia, arterial hypertension, and hypertrophic cardiomyopathy. Taken together, we have made the diagnosis of MtD. In conclusion, MtD may be associated with adrenal adenomas, which may cause severe symptomatic hypokalemia, manifesting as generalized weakness and myalgias due to rhabdomyolysis. Endocrine involvement may be a phenotypic feature of MtD.

A somnolent woman in her fifties with acute circulatory failure.

A woman in her fifties was admitted to hospital with decreased awareness and circulatory failure. She had been treated with left atrial cryoablation a few weeks before admission and had been cardioverted a few days after the procedure because of relapse of atrial fibrillation. On admission, the patient had systolic blood pressure of 80 mm Hg and an ECG with broad QRS-complexes at 380 ms. We suspected intoxication and she was intubated to administer activated charcoal after gastric lavage. She was cardiovascularly unstable and in need of intravenous infusion of noradrenaline and adrenaline. Further investigations at her home suggested that she had poisoned herself with 4-5 g flecainide, 0.3 g oxazepam and 0.5 g meclizine. After administration of 500 mmol sodium bicarbonate and 5 mmol calcium chloride, the QRS complexes narrowed temporarily. On day 2, due to sustained bradycardia and hypotension despite receiving adrenergic medications, a temporary pacemaker was implanted, leading to improved heart rate and blood pressure. She experienced several complications including hypertensive pulmonary oedema, atrial fibrillation, extensively prolonged QT interval because of polypharmacy and Takotsubo cardiomyopathy. She was discharged from the hospital in good health on day 17. At a follow-up visit at the outpatient clinic 12 weeks later, cardiac function had normalised. The QT interval was now normal; however, there were persistent T-wave inversions in leads I, aVL and V4-6. Flecainide blocks sodium channels in cardiomyocytes. Intoxication with flecainide is rare, with mortality rates of about 10 %. Sodium bicarbonate in larger doses has been reported to stabilise patients with flecainide intoxication due to modification of the binding of flecainide to sodium receptors in cardiomyocytes, and due to alkalisation which makes flecainide detach from sodium receptors. Our patient had a temporary effect with narrowing of QRS complexes after receiving sodium bicarbonate. She also showed a beneficial effect from implantation of a temporary pacemaker, although earlier case reports have described problems with high thresholds and capture failure.