Hyperkalemia caused

Disequilibrium in the eleetrolyte balanee ean provide diagnostic clues. For example, hyperkalemia causes tail T-waves in leads II, III, V2 to V4, when the potassium balance exceeds 5.5 mmol/1. In conjunction, the amphtude of the P wave is reduced and QRS is widened. Hyperkalemia is usually present when the amphtude of the T-wave is higher than that of the R-wave. With increasing potassium concentration, P-waves widen and eventually disappear. Accentuated hyperkalemia results in asystole. 

Akbarpour F, Afrasiabi A, Vaziri ND. Severe hyperkalemia caused by indomethacin and potassium supplementation. South Med J 1985 78(6) 756-7. 

Acute hyperkalemia causes a hypopolarization of the cardiac muscle cell membrane, resulting in characteristic electrocardiographic changes followed by serious and often fatal arrhythmias in most cases there are no warning symptoms. Immediate treatment is needed and consists of giving sodium bicarbonate, glucose, and insulin intravenously to shift K+ into the cells calcium intravenously to minimize the cardiotoxicity of hyperkalemia and polysterene sodium (a Na/K exchange resin) rectally or orally to remove potassium from the body if all fails, the performance of dialysis may be required (S18). 

Palmer BF. Managing hyperkalemia caused by inhibitors of the renin-ai iotensin-aldoster-one system. NEnglJ Med (2004) 351,585-92. 

Hyperkalemia is an excess of potassium in the blood. Clinical symptoms are muscle weakness and cardiac arrhythmias. It is caused by, e.g., hyperaldosteronism and angiotensin-converting enzyme (ACE) inhibitors. 

The hypotensive effects of most antihypertensive dru are increased when administered with diuretics and other antihypertensives. Many dnigp can interact with the antihypertensive drugs and decrease their effectiveness (eg, antidepressants, monoamine oxidase inhibitors, antihistamines, and sympathomimetic bronchodilators). When the ACE inhibitors are administered with the NSAIDs, their antihypertensive effect may be decreased. Absorption of the ACE inhibitors may be decreased when administered with the antacids. Administration of potassium-sparing diuretics or potassium supplements concurrently with the ACE inhibitors may cause hyperkalemia. When the angiotensin II receptor agonists are administered with... 

Angiotensin receptor blockers show similar tolerability to ACE inhibitors with regard to hypotension and hyperkalemia, but they do not induce cough since ARBs do not cause an accumulation of bradykinin. Angiotensin receptor blockers can be considered in patients with ACE inhibitor-induced angioedema, but they should be initiated cautiously, as crossreactivity has been reported. Many of the other considerations for the use of ARBs are similar to those of ACE inhibitors,... 

Patients with acute hyperkalemia usually require other therapies to manage hyperkalemia until dialysis can be initiated. Patients who present with cardiac abnormalities caused by hyperkalemia should receive calcium gluconate or chloride (1 g intravenously) to reverse the cardiac effects. Temporary measures can be employed to shift extracellular potassium into the intracellular compartment to stabilize cellular membrane effects of excessive serum potassium levels. Such measures include the use of regular insulin (5 to 10 units intravenously) and dextrose (5% to 50% intravenously), or nebulized albuterol (10 to 20 mg). Sodium bicarbonate should not be used to shift extracellular potassium intracellularly in patients with CKD unless severe metabolic acidosis (pH less than 7.2) is present. These measures will decrease serum potassium levels within 30 to 60 minutes after treatment, but potassium must still be removed from the body. Shifting potassium to the intracellular compartment, however, decreases potassium removal by dialysis. Often, multiple dialysis sessions are required to remove potassium that is redistributed from the intracellular space back into the serum. 

Hyperkalemia is defined as a serum potassium concentration greater than 5 mEq/L (5 mmol/L). Manifestations of hyperkalemia include muscle weakness, paresthesias, hypotension, ECG changes (e.g., peaked T waves, shortened QT intervals, and wide QRS complexes), cardiac arrhythmias, and a decreased pH. Causes of hyperkalemia fall into three broad categories (1) increased potassium intake (2) decreased potassium excretion and (3) potassium release from the intracellular space. 

During phase I, each seizure causes a sharp increase in autonomic activity with increases in epinephrine, norepinephrine, and steroid plasma concentrations, resulting in hypertension, tachycardia, hyperglycemia, hyperthermia, sweating, and salivation. Cerebral blood flow is also increased to preserve the oxygen supply to the brain during this period of high metabolic demand. Increases in sympathetic and parasympathetic stimulation with muscle hypoxia can lead to ventricular arrhythmias, severe acidosis, and rhabdomyolysis. These, in turn, could lead to hypotension, shock, hyperkalemia, and acute tubular necrosis. 

Hyponatremia, hypernatremia, hyperkalemia, hypocalcemia, hypomagnesemia, and hypoglycemia can cause SE... 

NSAIDs can cause renal insufficiency when administered to patients whose renal function depends on prostaglandins. Patients with chronic renal insufficiency or left ventricular dysfunction, the elderly, and those receiving diuretics or drugs that interfere with the renin-angiotensin system are particularly susceptible. Decreased glomerular filtration also may cause hyperkalemia. NSAIDs rarely cause tubulointerstitial nephropathy and renal papillary necrosis. 

Electrolyte disturbances that develop in patients with tumor lysis syndrome should be managed aggressively to avoid renal failure from hyperphosphatemia and hypocalcemia and cardiac signs from hyperkalemia. One exception pertains to the use of intravenous calcium for hypocalcemia. Adding calcium may cause further calcium phosphate precipitation in the presence of hyperphosphatemia and should be used cautiously. 

Na K+,ATPase. It also promotes the conservation of K and can cause the adverse reaction of hyperkalemia. 

SuccessM treatment of PEA and asystole depends almost entirely on diagnosis of the underlying cause. Potentially reversible causes include (1) hypovolemia, (2) hypoxia, (3) preexisting acidosis, (4) hyperkalemia, (5) hypothermia, (6) hypoglycemia, (7) drug overdose, (8) cardiac tamponade, (9) tension pneumothorax, (10) coronary thrombosis, (11) pulmonary thrombosis, and (12) trauma. 

Cough and angioedema are the most common causes of ACE inhibitor intolerance. Caution should be exercised when ARBs are used in patients with angioedema from ACE inhibitors because cross-reactivity has been reported. ARBs are not alternatives in patients with hypotension, hyperkalemia, or renal insufficiency due to ACE inhibitors because they are just as likely to cause these adverse effects. 

Potassium-sparing diuretics may cause hyperkalemia, especially in patients with chronic kidney disease or diabetes, and in patients receiving concurrent treatment with an ACE inhibitor, ARB, NSAID, or potassium supplement. Eplerenone has an increased risk for hyperkalemia and is contraindicated in patients with impaired renal function or type 2 diabetes with proteinuria. Spironolactone may cause gynecomastia in up to 10% of patients, but this effect occurs rarely with eplerenone. 

ARBs appear to have the lowest incidence of side effects compared with other antihypertensive agents. Because they do not affect bradykinin, they do not cause a dry cough like ACE inhibitors. Like ACE inhibitors, they may cause renal insufficiency, hyperkalemia, and orthostatic hypotension. Angioedema is less likely to occur than with ACE inhibitors, but crossreactivity has been reported. ARBs should not be used in pregnancy. 

Bruising, local irritation, mild pain, erythema, histamine-like reactions, and hematoma can occur at the site of injection. Hypersensitivity reactions involving chills, fever, urticaria, and rarely bronchospasm, nausea, vomiting, and shock have been reported in patients with HIT. Long-term UFH has been reported to cause alopecia, priapism, hyperkalemia, and osteoporosis. 

There is evidence that y-aminobutyric acid A receptors may be modified during SE and become less responsive to endogenous agonists and antagonists. Two phases of GCSE have been identified. During phase I, each seizure produces marked increases in plasma epinephrine, norepinephrine, and steroid concentrations that may cause hypertension, tachycardia, and cardiac arrhythmias. Muscle contractions and hypoxia can cause acidosis, and hypotension, shock, rhabdomyolysis, secondary hyperkalemia, and acute tubular necrosis may ensue. 

Primary causes of true hyperkalemia are increased potassium intake, decreased potassium excretion, tubular unresponsiveness to aldosterone, and redistribution of potassium to the extracellular space. 

Calcium gluconate - To decrease capillary permeability in allergic conditions, nonthrombocytopenic purpura and exudative dermatoses such as dermatitis herpetiformis for pruritus of eruptions caused by certain drugs in hyperkalemia, calcium gluconate may aid in antagonizing the cardiac toxicity, provided the patient is not receiving digitalis therapy. 

Oral Severe renal impairment with oliguria or azotemia untreated Addison disease hyperkalemia from any cause adynamia episodica hereditaria acute dehydration heat cramps patients receiving potassium-sparing diuretics or aldosterone-inhibiting agents. 

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