Bring the lecture to the bedside — open the complete Day 1 teaching collection →
Use these figures alongside Cases 1–3 and their linked lectures. Each image opens at full size and has a text companion and download. The case files supply the patient data; the mechanisms explain the decisions.
Moving potassium is not removing potassium
HD began six weeks ago and urine output remains about 1 L/day. Trimethoprim can therefore impair residual renal potassium secretion; missed dialysis and a potassium salt substitute add risk. Urine volume does not quantify potassium clearance. Potassium 7.3 with a wide QRS and pulmonary edema requires calcium, shifting therapy and urgent HD. Lokelma can be given during the wait; a possible loop response must not delay the run.
Protect the heart, redistribute potassium, then remove the body load
Read the serum, the urine, and the fluid
Normal saline contains 154 mEq/L sodium and has an osmolarity near 308 mOsm/L; 3% saline contains 513 mEq/L sodium and is about 1,026 mOsm/L. Do not compare sodium concentration directly with osmolality. Fluid osmolality above urine osmolality is a useful heuristic, not a universal requirement for sodium to rise. With persistent antidiuresis, sufficiently electrolyte-rich urine can excrete the infused salt in less water than was infused, leaving water behind (desalination). In volume depletion, saline may instead suppress ADH and release a water diuresis. Follow serial serum sodium, urine Na + K and urine volume.
Case 2: osmolality frames the problem; electrolytes explain the water balance
Why water stays when sodium is low
Case 2 pairs hypotonic blood with concentrated urine in a patient taking a thiazide who is volume depleted and eating poorly. This is a water-handling problem with several contributors. A concentrated urine, even with a high urine sodium, does not independently establish SIAD.
Read urine osmolality as the kidney's response to water
One thiazide, several connected abnormalities
A diuretic can keep urine sodium and chloride high despite volume depletion. Those results do not independently prove SIAD or chloride-resistant alkalosis. Stop the thiazide, assess symptoms and volume, replace deficits and follow the response. Restored water excretion and potassium replacement can accelerate sodium correction.
Impaired dilution, potassium loss, and the patient's intake interact
When recovery makes sodium rise too fast
Escalate urgently to a monitored setting and nephrology; stop sodium-raising infusions and reassess all inputs, including potassium replacement. Specialist-directed desmopressin halts aquaresis and titrated free water permits controlled relowering, guided by frequent sodium checks and hourly urine output. In the fictional course, sodium returns to 126 by hour 18 and stays there through hour 24; no ODS develops. Rescue does not establish that the preceding overshoot was safe.
A new water diuresis can outrun the original treatment plan
Why potassium may not stay corrected
Address magnesium alongside potassium; do not delay urgent potassium replacement while waiting for magnesium to finish. Route, dose and monitoring depend on severity, symptoms and kidney function. Recheck both electrolytes and remember that potassium replacement contributes to sodium correction in this hyponatremic patient.
Low magnesium can permit ongoing renal potassium loss
Ketoacidosis can hide behind a modest glucose
Insulin stops ketone production; dextrose supports continued insulin when glucose is already modest or falls. Follow blood ketones, pH or bicarbonate, electrolytes and clinical status. Anion gap alone can mislead during recovery, especially after chloride-rich fluids. Hold the SGLT2 inhibitor and use the case's separate specialist review before any restart.
SGLT2 therapy, poor intake, and illness can uncouple glucose from ketones
Acute hyperkalemia: potassium and the ECG
Recognize electrical toxicity; the ECG does not measure potassium.
Hyponatremia: follow the water
Follow the original lecture lanes: tonicity, urine dilution, then volume and urine sodium.
Treat hypotonic hyponatremia
Symptoms first, cause-directed treatment, and control of the correction.
Urine sediment: clues to the AKI mechanism
Read the cast, then test the clinical story and specimen quality.
Choose the fluid for the problem
Separate circulation, water balance and cerebral edema from routine maintenance.
Lactated Ringer’s versus normal saline
Different chloride and buffer profiles; possible kidney benefit with mixed clinical evidence.
Acute Kidney Injury: Recognize, Localize, Reassess
Prerenal, intrinsic and postrenal mechanisms can overlap. Reassess the response.
Acute hyperkalemia: buy time, then remove potassium
Calcium protection and intracellular shifts have different clocks; start removal planning immediately.
Hyperkalemia: remove potassium while the clock runs
Gut, dialysis and useful urinary clearance are removal routes; none should delay cardiac stabilization.
Treat urgent threats while you evaluate
Recognize danger, begin monitored care and keep investigating in parallel.