 Welcome to the video on hyperkalemia. In this section, we will talk about the causes, investigations, and treatment in the emergency department. Hyperkalemia is defined as a serum potassium that's more than 5 millimoles per liters. Why is hyperkalemia a problem? Hyperkalemia causes poor conduction in the heart. It leads to prolonged QRS and eventually ventricular fibrillation. And a systole. Therefore, hyperkalemia is a must-not-miss diagnosis. What are the causes for hyperkalemia? We will look at shift and renal clearance. First, shift. Potassium is a mostly intracellular ion. The serum potassium level will go up if there is leakage of potassium from the cells. It can be caused by tissue injury. Such as burns and reptomyelysis. Potassium can also get out of the cells in exchange for another ion getting into the cells. Specifically in acidosis, hydrogen ion will enter the cell where potassium will get out of the cells. Second, renal clearance. Potassium is excreted by the kidneys. If there is renal failure, potassium builds up in the body. The kidney also excrete potassium based on aldosterone. Inhibiting aldosterone production or decreased aldosterone production will decrease the renal clearance for potassium. They can include congenital syndrome or medications. Such as ACE inhibitor, angiotensin 2 blockers and spurnolactone. There is one common reason for a fictitiously hyperclinia that is a falsely elevated reading. Remember that potassium is mostly an intracellular ion. When the blood is being drawn, if there is a lot of hemolysis, because it was a difficult poke or the turnkey was put on for a long time, potassium will leak into the serum portion and therefore will get a falsely high reading. Therefore, we often want to know if the sample was hemolyzed when there is a high potassium reading. If the patient truly has hyperclinia, these are the items you want to hit on history. Whether they had any history of tissue injury, whether they had any trauma, burns, and intense physical activity. For acidosis, we want to ask patients about whether they have any symptoms or causes for metabolic acidosis. For example, DKA or sepsis. For renal causes, we need to know whether the patient has a history of renal failure. And for chronic renal failure patients who are on dialysis, whether they have missed any sessions. For medication, we need to ask about new medications. Specifically, ACE inhibitor, angiotensin 2 receptor blockers and sperm electro. These are the main history items we want to ask. What are the clinical symptoms of patients with hyperclinia? They're pretty nonspecific and includes muscle weakness and lethargy. The investigation of patients with hyperclinia is simply a serum potassium level and also an ECG. We want to do an ECG in patients with hyperclinia. Since in patients with hyperclinia, there are ECG changes the higher the potassium level is. The sequence of ECG changes isn't the same in all patients, but they may hit the next broad categories. These ECG changes are important for us to know. We will talk about these ECG changes in sequence. We will start with the T waves, the P waves, and the cure of complexes. Let's begin. In hyperclinia, it is a common for us to see peaked T waves. Let's say this is a normal cure as complex with the T wave. A peaked T wave will look like that. On an ECG strip, it will look like this. It is easy to see the tall peaked T waves here. On a 12-leaf ECG, we might be able to see the tall peaked T waves only in certain leads. Can you spot them out? You can see them very clearly in the inferior leads and the pre-cordial leads. As the potassium level goes higher, the atrium begins to fail. That leads to changes in the P waves. First, the PR interval lengthens, and then the P wave disappears. Think of it as almost like there is a string pulling on the left side, making the PR interval longer and eventually pulling the P wave flat, like that. Let's first look at the PR lengthening on a hyperclinia ECG. If you look at the PR interval in this ECG, you will notice it's more than five small squares. In this ECG, you can still see P waves. As the potassium level goes higher, the QRS now lengthens. Think of a string pulling on the right side now. Once it starts pulling, the QRS now lengthens. The next ECG will illustrate the lack of P waves and a prolonged QRS complex. Note the lack of P waves and the prolonged QRS complex. You will also see the peaked T waves. As the potassium level goes higher, the QRS gets longer and longer, eventually looking like a sine wave. On an ECG strip, it will look like this. On a 12-lead ECG, it will look like this. If the potassium goes higher, the patient will go into V-Fib or a systole. How do we manage patients with hyperclinia? It consists of monitoring the patient, stabilizing the myocardium, shifting the potassium into the cells, and eliminating potassium from the body. We'll discuss each one of them. First, monitor. The patient needs to be put on a cardiac monitor. If we haven't done so already, a 12-lead ECG needs to be done. In patients with hyperclinia, we are much more worried about the patients who have prolonged QRS complexes. We stabilize the myocardium by giving calcium. We give calcium to patients with prolonged QRS complexes. It can be given as calcium chloride or calcium gluconate. Remember that potassium is an interest cellular ion. We can treat serum hyperclinia by driving potassium into the cell. We can do this by multiple methods. The first one is insulin. Insulin kicks potassium back into the cell. The dose is 10 units regular IV. We will also give dextrose-containing solutions such as D50 to prevent hypoglycemia. The second is beta-2 agonists such as cell butamol. It also pushes potassium into the cell. The dose is 10 to 20 mg by an ambulizer. Remember, acidosis is also a cause for hyperclinia. Giving bicarbonate will neutralize the acidosis. Lastly, we may wish to eliminate extra potassium from the body. It can be given by giving loop diuretics such as ferrosamide. We sometimes use a binding agent in the GI tract. In these resins, potassium is being extracted from the serum in exchange for sodium or calcium. Since it usually takes hours for it to work, it is mostly used in the inpatient setting. Lastly, the most efficient method of eliminating extra potassium from the body is dialysis. In summary, we discussed the causes for hyperclinia, whether there is muscle injury, a shift from the cells, or if the kidney is not working. We talked about the ECG changes in patients, starting from a peaked T-wave to a prolonged PR interval and the disappearing of the people. A prolonged QRS, a sine wave, and to a systolic or VF arrest. We discussed the management, including stabilizing the membrane, shifting potassium into the cells, and eliminating it from the body. Hyperclinia is one of the most often seen electrolyte abnormality in the emergency department. Because the patient can get really low blood pressure, because the patient can get really sick quickly, we need to know our management very well. We hope you find that useful. Thank you for watching.