It’s just that normally they don’t HAVE to! And they are QUITE capable of initiating an action potential in regular myocardial cells (His-Purkinje and regular working myocytes). They are also the ones that prolong Phase 2 to allow Ca++ entry to help trigger myocardial contraction. Those L-type Ca++ channels are the same ones that initiate the sinus impulse (up to 150+ beats/minute!) and carry the impulse through the AV node. While the Na+ channels are referred to as the “fast” channels and the Ca++ channels as the “slow” channels (the same ones used by the SA and AV nodes) – the Ca++ channels really aren’t all THAT slow – at least from our perspective. Now, let me put something in perspective. This is not meant to initiate an action potential – the heart is preparing for excitation-contraction coupling! It has almost no effect on depolarization as far as we are able to see on the ECG tracing. The table below contains the medications listed above and their most common dosages.During Phase 0 depolarization, the L-type Ca++ channels begin to open around -60 mV and Ca++ starts to enter the cell – even while all the Na+ is rushing in. When hyperkalemia is severe, administration of calcium chloride lowers the risk of ventricular fibrillation. Along with this, Calcium Chloride should be given over 2 to 5 minutes to reduce the effects of high potassium levels on the heart. The measures listed above in each category should be utilized.

Sodium Bicarbonate: 50 mEq IV over 5 minutes.įor severe elevation, both removal of potassium from the body and shifting potassium to the intracellular space is critical.

Nebulized albuterol: 10 to 15 mg nebulized over 15 minutes.

The administration of glucose + insulin (50ml D50 + 10 units regular insulin) can be given over 5 minutes.

Kayexalate can be administered orally or by retention enema.įor moderate elevation, potassium can be shifted from the vascular space (serum) to intracellular space using the 3 methods listed below: Resins like Kayexalate can also be used to remove potassium from the body. One example of a diuretic which does not spare potassium is furosemide. The treatment of hyperkalemia depends on the severity and the patient’s clinical presentation.įor mild hyperkalemia removal of potassium from the body is achieved with diuretics which cause the release of potassium in the urine. Severe hyperkalemia can lead to asystolic cardiac arrest. If hyperkalemia is left untreated idioventricular rhythms may occur and a sine-wave pattern. Mild hyperkalemia can cause peaked T waves.Īs potassium levels continue to rise, there may be flattened p-waves, a prolonged PR-interval, and other anomalies. There are some ECG signs that may suggest hyperkalemia. Signs and symptoms of hyperkalemia include weakness, ascending paralysis, and respiratory failure. When the kidneys fail, excess potassium cannot be removed, and it accumulates in the blood. When serum pH drops (metabolic acidosis) serum potassium rises, and potassium shifts from intracellular to extracellular (into the blood).Īnother condition that is a common cause of hyperkalemia is end-stage renal disease. Metabolic acidosis causes a decrease in serum pH which has a direct effect on serum potassium levels. When potassium levels in the blood rise, this reduces the electrical potential and can lead to potentially fatal abnormal heart rhythms.

The amount of potassium (K+) in the blood determines the excitability of nerve and muscle cells, including the heart muscle or myocardium. There are several conditions which can significantly affect serum potassium levels and cause them to rise. High serum potassium levels (hyperkalemia) can be life-threatening and requires immediate therapy.

Antidote for high potassium level