Pathology · Chapter 4
Water, Electrolytes, Acid–Base, and Hemodynamics
The chapter question
When the body gains or loses salt, water, protein or blood, where does the fluid go, and how do the bedside and the laboratory values show it?
Cell membrane
Osmosis
Water follows effective solutes (Na⁺ outside, K⁺ inside).
Sections 4.1–4.3
Capillary wall
Starling forces
Hydrostatic pressure pushes out; albumin holds in; lymph returns.
Sections 4.5
Circulation
Flow and pressure
Volume, pump, open vessels and tone keep tissues perfused.
Sections 4.6–4.7
Teaching schematic: each barrier has its own force.
Make a quick prediction
A man with SIADH retains 3 L of water and his serum sodium falls to 120 mEq/L. Where has most of that water gone?
Study path
Follow the order or jump to the concept you need. Every topic has a Deep Learning and a High-Yield view of the same facts, and ends with a short knowledge check.
- 4.118 minUp nextBody water compartments and tonicityWater crosses cell membranes freely, so it goes wherever effective solutes pull it. Sodium concentration tells you about water; the amount of sodium tells you about extracellular volume.Where body water livesOsmolality versus tonicitySodium concentration reports water; total sodium sets ECF volumeReading the compartments at the bedside
- 4.226 minFluid shifts: hyponatremia, hypernatremia and hyperglycemiaEvery gain or loss of salt and water can be read with two separate questions: which way does water move between cells and ECF, and does the ECF grow or shrink?Two questions for every disorderIsotonic loss and gainThree hyponatremiasThree hypernatremias+3
- 4.328 minADH, RAAS and potassiumADH decides how much water the kidney keeps; aldosterone decides how much sodium. Potassium lives inside cells, and anything that moves it across the membrane shows on the ECG.Two control systems: ADH for water, RAAS for sodiumDiabetes insipidus and the water deprivation testSIADH versus primary polydipsiaCorrecting sodium too fast: two opposite injuries+3
- 4.434 minAcid–base disordersRead a blood gas in the same order every time: pH, the variable that explains it, the expected compensation, the anion gap, and then whatever the numbers still do not explain.The workflow and the normal valuesFour primary disorders and their expected compensationAnion gap: high-gap and normal-gap acidosisToxic alcohols, salicylate and the osmolal gap+4
- 4.522 minEdema and effusionsFluid leaves capillaries when hydrostatic pressure pushes harder, oncotic pressure holds less, the wall leaks or lymphatics fail to bring it back. Sodium retention by the kidney keeps refilling the source.Starling forcesOne mechanism, six settingsIncreased hydrostatic pressureDecreased oncotic pressure+3
- 4.626 minThrombosis, embolism and DICA thrombus forms where the vessel wall, the flow or the blood itself is abnormal. Where it forms decides what it is made of, and where its fragments travel decides which organ infarcts.Virchow triadArterial versus venous thrombi; lines of ZahnWhat happens to a thrombusFrom deep vein thrombosis to pulmonary embolism+4
- 4.728 minShockShock is failure of tissue perfusion. Find where the circulation failed first (volume, pump, outflow or vessel tone) and the pressures upstream and downstream follow.What shock is, and how it looksHemodynamic profilesHypovolemic shock and the hemoglobin that does not fallCardiogenic shock and the markers of infarction+2
Practice
How the ideas connect
15 bridges carry one concept into the next, within this chapter and across chapters. Each is taught where you first need it.
- Osmosis → cell volume4.1 · Osmolality versus tonicity
- Salt and water → compartments4.2 · Fluid Compartment Predictor
- ADH for water, aldosterone for sodium4.3 · Two control systems
- Acid–base workflow4.4 · ABG Challenge
- Starling forces → edema → hyponatremia4.5 · Why edema keeps coming
- Shock profiles4.7 · Shock Profiles
- Pump-failure swelling vs osmotic swellingCh. 1 · Reversible injury
- Lactic acid from anaerobic glycolysisCh. 1 · ATP depletion
- Hypoxemia in pulmonary embolismCh. 1 · Causes of hypoxemia
- Thrombus → embolus → infarctCh. 1 · Three separate answers
- Exudate and vascular permeabilityCh. 2 · Acute inflammation
- Antiphospholipid syndromeCh. 3 · Autoimmunity
- Kwashiorkor edemaCh. 6 · Nutrition and eating disorders
- Methanol, ethylene glycol, salicylate: anion and osmolal gapsCh. 6 · Toxins
- SIADH and Trousseau syndromeCh. 7 · Paraneoplastic syndromes