Hyperkalemia and Hypokalemia

00:01 What happens when we have a lot of or an excess potassium, also known as hyperkalemia.

00:08 Hyperkalemia can reflect the removal of infusions, cellular breakdown such as tumor lysis or Rhabdo, trans-cellular shifting, which is actually very, very important and in this specific incidence in hyperkalemia, trans-cellular shifting is associated with acidemia.

00:30 There may be impaired renal excretion also contributing to hyperkalemia.

00:36 What are some clinical consequences? Classically, EKG changes.

00:41 Please commit this to memory.

00:43 EKG changes associated with hyperkalemia include shortened QT intervals, peaked T waves, widened QRS and potentially, can progress to ventricular fibrillation.

00:57 Please keep in mind, that the EKG changes depend on the concentration of potassium in your serum.

01:02 With a serum potassium of 5.5 to 6.5 you get tall peaked T-waves.

01:08 A serum potassium of 6.5 to 8 adds the loss of the P-wave.

01:13 And if your serum potassium rises above 8 you get a widened QRS-komplex with a tall T-wave.

01:19 There are priorities in the management of hyperkalemia.

01:23 Because of the extensive and severe consequences of hyperkalemia on the heart, the first step is to stabilize the myocardium.

01:33 Then redistribute the potassium.

01:36 And if necessary, excrete the excess.

01:39 Let's discuss the individual actions of how we can manage hyperkalemia.

01:45 First, calcium gluconate.

01:47 Calcium gluconate contributes to membrane stabilization of the myocardium, induced by hyperkalemia.

01:55 Next, use of bicarb.

01:57 Recall that acidemia causes trans-cellular shifting of intracellular potassium into the extracellular space.

02:05 Bicarb increases the pH and drives the trans-cellular shifting in the reverse process.

02:10 This also releases hydrogen from the cell in exchange for potassium.

02:16 Insulin.

02:17 Insulin is important.

02:19 It also - because it potentiates is a sodium potassium ATPase, allowing the maintenance of the normal trans-cellular gradient of mostly intracellular potassium and extracellular sodium.

02:34 Another option is the usage of ß2 Agonists.

02:37 They are stimulating the cellular uptake of potassium.

02:40 We can also use binders and exchangers.

02:42 An example of this is Kayexalate.

02:44 If all those mechanisms don't work, we can institute dialysis as a last solution.

02:51 Let's move on to a discussion of hypokalemia when the potassium is too low.

02:57 This can also be equally dangerous.

03:01 Hypokalemia may be a reflection of changes to the true inadequate intake or again trans-cellular shifting, except in this situation it’s due to alkalemia.

03:13 Lasix or loop diuretics often cause hypokalemia.

03:16 And overall weakness and overall muscle dysfunction can also cause hypokalemia.

03:23 What are the EKG changes? I also recommend you commit this to memory.

03:28 Prolonged QT intervals.

03:31 U waves.

03:32 ST depression.

03:34 Depressed T waves, which is different than hyperkalemia where we see peaked T waves.

03:40 And ultimately, it can cause torsades if coupled with hypomagnesium.

03:45 How do we fix hypokalemia? Well, it’s simple.

03:51 Give more.

03:52 Now, an important clinical pearl.

03:54 Sometimes, on the wards, you continue repleting the potassium and yet your plasma potassium levels never actually come up.

04:01 Part of the reason this is happening is because as you’re repleting the plasma potassium it is actually shifting intracellularly.

04:08 This suggests to you that there's been far more depletion of potassium than you first recognized.

04:15 This is an incredibly high yield slide.

04:19 Let’s spend a little time here.

04:21 Electrolyte disturbances, again, are not only important for physiologic daily function, but incredibly high yield test topics.

04:29 In hyponatremia, the manifestations is one that do not correct too quickly because if one corrects more than 12 meq/L in 24-hour period, it can lead to osmotic demyelination syndrome.

04:43 It was formerly known as CPM.

04:46 The first line treatment for the syndrome of inappropriate secretion of ADH is fluid restriction.

04:52 Severe symptomatic cases may include the use of ADH antagonist such as Tolvaptan or Conivaptan.

05:01 Next, hypermagnesium.

05:05 Hypermagnesium decreases your deep tendon reflexes.

05:08 Remember those OB patients.

05:10 OB patients oftentimes get infusions of magnesium.

05:14 Now, one of the signs that they have too much magnesium is decreased deep tendon reflexes.

05:19 Next, hypocalcemia.

05:21 Hypocalcemia causes prolonged QT intervals and numbness around the mouth, potentially Tetany if extreme.

05:31 Hypocalcemia is an important concept discussed in the parathyroid lectures.

05:37 And lastly, hypercalcemia.

05:39 Hypercalcemia associated with hyperparathyroidism is associated with bony pain, renal failure and neurological disturbances.

05:49 This slide should be committed to memory to help you answer standardized examination questions.

05:54 Thank you very much for joining me on this discussion of fluids and electrolytes.