NOTE THROUGHOUT THESE NOTES, POTASSIUM MAY BE REFERRED TO AS "K", WHICH IS ITS ELEMENTAL SYMBOL... CHECK OUT THE PERIODIC TABLE BRO
MORE RESOURCES ON HYPERKALEMIA
https://www.hcplive.com/view/electrophysiologic_basis
https://www.uptodate.com/contents/potassium-balance-in-acid-base-disorders
https://www.tandfonline.com/doi/full/10.3402/jchimp.v1i4.7372
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3061004/
https://www.ncbi.nlm.nih.gov/books/NBK470284/
https://academic.oup.com/ndt/article/34/Supplement_3/iii2/5652181
HYPERKALEMIA
What is Hyperkalemia?
When serum potassium levels are above the upper limit of normal (> 5-5.5 mEq/L)
This can be life threatening, leading to cardiac arrhythmia and/or paralysis
Brief Facts on Physiology and Potassium Maintenance
Potassium is the most abundant intracellular cation (K+)
90% of potassium excreted leaves the body from the kidneys, 10% via GI
The Na/K+-ATPase regulates potassium cellular concentration by pumping Na out and K into the cell to maintain cellular membrane potential
Kidney is also a major controller of potassium regulation; it is reabsorbed by proximal tubule diffusion and NKCC2 receptors in the Thick ascending Loop of henle. It is secreted into tubular fluid via ROMK channels in the thick ascending loop of henle and by aldosterone mediated Na/K ATPase channels in the cortical collecting duct
Catecholamines acting on muscular beta-2 receptors stimulate Na/K ATPase channes to cause intracellular K+ shifts
Insulin acts to stimulate Na/K+-ATPase receptors, mostly in the liver and muscle cells; can cause increased potassium intracellular shifts
Etiology (can be split into three categories)
increased potassium intake
- this is uncommon; only a big deal in pts with ESRD who cannot get rid of potassium in a normal physiologic fashion
- some foods high in K= fried fruit, seaweed, nuts, molasses, avocado, spinach, potatoes, red meats
intracellular potassium shifts
- rhabdomyolysis or tumor lysis syndrome cells get destroyed and release intracellular potassium
- metabolic acidosis too much H+… some of this is buffered in the cells, so the cells kick out K+ to maintain electroneutral environment
- insulin deficiency/diabetic ketoacidosis.... normally insulin acts on cells and causes an Na/K-ATPase to activate, causing flush of sodium out and potassium into cells
- medications- succinylcholine
impaired potassium excretion
- KIDNEY DISEASE…. AKI or CKD
- impaired renin-aldosterone axis
- Addison’s Disease, hypoaldosteronism, angiotensin insensitivity
- Congenital Adrenal Hyperplasia
- prostaglandin inhibitors, beta blockers, ACE-inhibitors or Angiotensin receptor blockers, tacrolimus, heparin
- Type 4 renal tubular acidosis
- Dehydration
Presentation of Hyperkalemia
Symptomatic hyperK may not be seen until close to 6.5 mEq/L, and the more acute the change, the more dramatic the symptoms (chronic change allows body to adapt somewhat)
Muscle Weakness or Paralysis (Why? because too much K lowers the resting membrane potential of cells and prevents repolarization….)
Paresthesias (why? because too much K lowers the resting membrane potential and prevents repolarization….)
Cardiac Conduction abnormalities; there may be 2nd/2rd degree heart blocks, wide complex tachycardia, ventricular fibrillation, leading to asystole (see below for further details on physiology)
Bradycardia may be seen on physical exam; Patients may be complaining of palpitations and/or syncope
on EKG, YOU WILL SEE THESE COMMONLY TESTED STEPWISE FEATURES
K 5.5-6.5meq/L= tall peaked T waves
K 6.5-7.5meq/L= absent p waves
K 7-8meq/l= wide QRS
K 8-10= cardiac arrhythmia, asystole, death!!!!
Source: https://www.grepmed.com/images/10025/electrocardiogram-changes-ecg-progression-potassium
PATHOGENESIS OF CARDIAC ABNORMALITIES IN THE SETTING OF HYPERKALEMIA
Source: https://www.google.com/url?sa=i&url=http%3A%2F%2Fhyperphysics.phy-astr.gsu.edu%2Fhbase%2FBiology%2Fecg.html&psig=AOvVaw03UW6jQxnYrVL35k4XsRNB&ust=1649965615553000&source=images&cd=vfe&ved=0CAwQjRxqFwoTCJiIrofnkfcCFQAAAAAdAAAAABAb
REVIEW YOUR CARDIAC CONDUCTION PHYSIOLOGY HERE: http://www.pathophys.org/physiology-of-cardiac-conduction-and-contractility/
Normally, intracellular potassium is abundant and helps to maintain resting membrane potential
When there is too much potassium extracellularly, the ratio of extracellular:intracellular potassium is decreased and causes increased cell depolarization
Initial effect= increased excitability and conduction velocity because the resting membrane potential becomes less negative (closer to the threshold potential) and fast sodium channels are readily activated
As potassium continues to rise, the action potential duration continues to shorten, and PEAKED T WAVES. are seen on EKG (representing premature repolarization of masses of ventricular myocytes as )
However, the higher the potassium increases, the conduction velocity is further reduced to the point here action potential is no longer initiated. Why? because the membrane potential is so depolarized, that there is steady inactivation of Na leak channels (remember that the channels on the myocytes are voltage gated, they open and then they need to “recharge”)
Myocardial cells in the atrium are more sensitive than ventricular myocytes to electrolyte changes; so as K increases to around 7.5meq/L, you may see loss of P waves or increased PR interval before you see changes in QRS.
Why are PR intervals increased? because remember, conduction velocity is decreasing…. see above as a reminder
Refractory period will also increase as potassium increases and rushes through potassium leak channels… this is the origin point of heart block
Repolarization will now last so long that it starts to merge with depolarization, leading to Q-T shortening
Treatment
If the patient is symptomatic, has ECG changes, or confirmed hyperkalemia of greater than or equal to 6.5 meq/L, TREAT TREAT TREAT or face the risk of asystole
1st step: Calcium therapy (calcium gluconate IV) to stabilize the cardiac tissue and prevent further cardiotoxicity by restoring appropriate electrical gradients
CALCIUM DOES NOT LOWER POTASSIUM LEVELS
2nd step: Shift potassium back into the cells;
Insulin is the first line!! (but be careful not to lower blood sugar, so D50 may be indicated)
What else can be used to lower potassium? Beta agonists promote intracellular shift; diuretics (loop, thiazides) can increase excretion
If the patient is acidotic, sodium bicarb is indicated
If the patient has renal insufficiency, you can give them a cation exchanger that will bind potassium in GI tract and prevent its absorption to prevent potassium from rising (sodium polystyrene sulfonate)
Hemodialysis if there is ESRD, or severe refractory hyperkalemia
SOURCES:
Lehnhardt A, Kemper MJ. Pathogenesis, diagnosis and management of hyperkalemia. Pediatr Nephrol. 2011;26(3):377-384. doi:10.1007/s00467-010-1699-3https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3061004/
Robert W Hunter, Matthew A Bailey, Hyperkalemia: pathophysiology, risk factors and consequences, Nephrology Dialysis Transplantation, Volume 34, Issue Supplement_3, December 2019, Pages iii2–iii11, https://doi.org/10.1093/ndt/gfz206https://academic.oup.com/ndt/article/34/Supplement_3/iii2/5652181 Bottom of Form
Simon LV, Hashmi MF, Farrell MW. Hyperkalemia. [Updated 2022 Feb 16]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470284/
Yelena Mushiyakh, Harsh Dangaria, Shahbaz Qavi, Noorjahan Ali, John Pannone & David Tompkins (2012) Treatment and pathogenesis of acute hyperkalemia, Journal of Community Hospital Internal Medicine Perspectives, 1:4, DOI: 10.3402/jchimp.v1i4.7372https://www.tandfonline.com/action/showCitFormats?doi=10.3402%2Fjchimp.v1i4.7372
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