Fluid, Electrolyte Balance, and acid base imbalances

Fluid Compartments

Total body of water is divided into ICF and ECF. ECF (extracellular fluid) includes interstitial fluid, intravascular fluid, and transcellular fluid .

Interstitial fluid

Between cells/tissues

Intravascular fluid

Blood plasma

Transcellular fluid

Specialized fluids like CSF and peritoneal fluid

Osmosis

Movement of water across a semipermeable membrane toward higher solute concentration/osmolarity

Hydrostatic pressure

The pushing force exerted by fluid against capillary walls (driven by blood pressure), driving filtration out of capillaries into interstitial space.

Osmotic/ Oncotic (colloid osmotic) pressure

The pulling force exerted by solutes and plasma proteins(Albumin), which pulls fluid back into capilaries.

Diffusion

Passive movement of solutes from an area of higher concentration to lower concentration

Capillary permeability

How easily fluid and proteins leak through capillary walls, which increases during acute inflammation

Edema

Bujong—just means too much fluid accumulating in the interstitial space. WHY fluid builds up there? Picture your capillaries as flexible pipes with water pushing out and sponges pulling water back in.

Cause of edema

Simple idea: water pressure inside the blood vessels gets so high that it forces liquid out through the capillary walls into the tissues.

Why?

1. Increased capillary hydrostatic pressure (e.g., heart failure, fluid volume excess/hypervolemia). * heart failure: the failing heart can’t pump blood forward, so blood backs up into the veins, raising pressure and pushing fluid into the legs or abdomen( ascites) * kidney failure/fluid overload: the kidneys can’t excrete urine, expanding blood volume and raising blood pressure. * Gravitiy/standing long periods: gravitiy pools blood in the lower legs, raising capillary pressure in the feet

2. Decreased plasma oncotic pressure( low pull force/loss of sponges) - simple: Albumin( major plasma protein) acts like a chemical “sponge” inside your blood vessels, holding onto water so it doesn’t leak out. If you don’t have enough albuin, you loss that “pulling force” and water spills out into the tissue — why it happens: Liver cirrhosis: the damaged liver cannot manufacture albumin, protein malnutrition: not eating enough protein means the body can’t produce albumin , kidney disease (nephrotic syndrome) : damaged kidneys leak protein out of the urine.

3. Increased capillary permeability “ leaky pipes” (e.g., histamine release in acute inflammation or burns) Simple: the capillary walls normally keep large proteins and liquid inside. During inflammation or injury, chemical alarms (histamine, bradykinin) pokes holes in the vessel wall, making the capillaroes “leaky”. — why? Acute inflammation/ allergic reactions: histamine dilates vessels and opens gaps, letting water and protein flood the tissue. Severe burns: thermal damage destroys capillary walls, causing massive localized fluid leakage.

4. Lymphatic obstruction “blocked drain” : (e.g., lymphedema blocking drainage of interstitial fluid) — Simple: normally, a small amount of fluid always leaks into tissues, and the lymphatic system acts as a drainage system to collect it and dump it back into the blood. If the drain get blocked, fluid backs up. Why? Cancer surgery: removing lymph nodes (e.g. axillary nodes during breast cancer surgery) blocks lymph drainage. Tumor: a tumor physically compressing a lymph channel

This can lead to

• impaired oxygen diffusion

• Delayed wound healing

• Risk of skin breakdownn

Third-Spacing (fluid trapped in the wrong room)

Occurs when fluid shifts out of the intravascular space and becomes trapped in a non-functional body compartment or cavity (such as the peritoneum/ascites, pleural space, or an obstructed bowel loop). The patient exhibits signs of intravascualr fluid deficit/ hypovolemia (Hypotension, tachycardia) simultaneously with fluid excess trapped in body cavities. Ex. Peritoneal cavity in your abdomen (ascites, boksue), the pleural space around the lungs, or damaged/burned tissue. !! During the test, connect third spacing to intravascular hypovolemia (fluid volume deficit inside the blood vessels, heart racing (tachycardia, and blood is getting concentrated (elevated hematocrit and BUN) are signs of hypovolemia as well.

Hypovolemia, hypovolemic shock

This connects to dehydration and tonicity. Hypo=low vol=volume emia= in the blood. - low blood volume inside your blood vessels. Cause: you either lose fluid directly out of the body (ex.vomitting, diarrhea, sweating, diuretics-water pills) OR fluid shifts out of the blood vessels and gets trapped somewhere else inside the body. When the blood volume drops —>blood pressure drops. Skin turgor: skin elasticity “tenting” when pinched indicates fluid deficit. Heart speeds up ( Tachycardia) to try to keep blood moving, the kidney stop making urine to conserve water making urine dark and concentrated. LAB TREND (Hemoconcentration) : because there is less liquid water in the blood, red blood cells and protein become concentrated, causing elevated hematocrit and elevated BUN

Clinical presentation: when blood volume drops, blood pressure collapses and the heart speeds up to keep oxygen moving.

Lab signs: hemoconcentration: elevated hematocrit and elevated BUN.

Infant and elderly vulnerability: they have lower fluid reserves and fail to compensate quickly can put them at high risk for rapid hypovolemic shock.

Isotonic dehydration

You lose equal amounts of water and salts. The blood concentration stays the same, so water doesn’t shift between cells and tissue

Hypotonic dehydration

You lose more salt than water (or drink pure water after heavy sweating). Blood becomes dilute(low osmolality), so water rushes into cells, causing them to swell.

Hypertonic dehydration

You lose more water than salt (like sweating in hot heat or diabetes insipidus), so water gets sucked out of cells, causing them to shrink.

Hemoconcentration

artificial increase in red blood cells and protein concentrations due to fluid loss

Sodium

The main positive ion outside cells (normal 135-145 mEq/L) — wherever sodium goes, WATER follows

3 regulating hormones for sodium: !!!!!!!!!!

Aldosterone: adrenal cortex hormone that tells the kidneys to save sodium and water, and kick out potassium.

Antidiuretic hormone (ADH) : posterior pituitary hormone that tells the kidneys to save free water

Atrial Natriuretic Peptide (ANP) : heart hormone released when heart chambers stretch from fluid overload; tells kidney to excrete sodium and water to lower blood pressure.

Hyponatremia ( < 135 mEq/L)

Hypo= lack natre= sodium (latin) emia = in the blood = low blood sodium = blood is too watery. Water shifts into brain cells (cellular swelling) —> headachem confusion, lethargy, seizures.

Hypernatremia (>145 mEq/L)

Hyper= over natre= sodium -emia-= in the blood ==high blood sodium. Blood is too salty, low in watrer. water is sucked out of braincells (cellular shrinkage) —> extreme thirst, dry/sticky mucous membrane, agitation, restlessness.

Sodium= brain function

Bc e=sodium governs water movement across cell membranes, sodium imbalances primary manifest with neurological symptoms. — connects to DI and SIADH

DI VS SIDAH connection— they’re the

Diabtetes inspiidus (DI) : Lack of ADH —> losing massive dilute urine —→ severe dehydration and hypernatremia

SIADH: Excess ADH —> holding free water —> dilutional hyponatremia and brain cells swelling

Aldosterone

Hormone promoting renal sodium/water reabsorption and potassium excretion

Antidiuretic Hormone (ADH)

Hormone promoting renal reabsorption of free water

Atrial Natriuretic Peptide (ANP)

Hormone promoting renal sodium and water excretion during fluid excess

Dilutional hyponatremia

Low serum sodium caused by excess water retention rather than actual sodium loss

Potassium (K+)

is a primary intracellular cation (normal 3.5- 5.0)

It sets the electrical “baseline” (resting membrane potential) for your nerve impulses, skeletal muscles, and especially your heart rhythm.

When your blood is acidosis (too many H+ ions in the blood), those extra hydrogen ions shift into your cells and get buffered.

to keep the electrical charges balanced, pottassium gets pushed out of the cells and into the blood, raising blood potassium levels. — hyperkalemia

Hypokalemia > 3.5 mEq/L

Cause: loop diuretics, vomitting, diarrhea, or not eating(NPO status)

Signs: decreased neuromuscular excitability (harder to stimulate the muscle membranes —> muscle weakness, leg cramps, fatigue, and sluggish bowels (abdominal ileus/bloating)

ECG/heart signs: flattened T waves, ST depression, and prominent U waves on a heart trace.

Hyperkalemia > 5.0 mEq/L

Hyper= excessive Kal= potassium emia = in the blood. Too much potassium in the blood

Cause: kidney failure (can’t excrete pottasium), severe acidosis, or tissue damages/burns (crushed/damaged cells rupture and spill their potassium into the blood) —metabolic acidosis

Signs: Increased resting membrane potential —> muscle twitching, paresthesias(muscle twitching) , weakness

ECG/heart signs: Tall peaked T waves, widened QRS complex — can cause cardiac arrest

Buffer ratio

The primary ECF chemical buffer is the bicarbonate-carbonic acid system, which maintains serum pH at a strict 20:1 ratio

Acidosis

Excess hydrogen ions enter cells to be buffered, forcing K+ out into the blood —> hyperkalemia

Acid= increased acidity Osis= abnormal condition

Alkalosis

Alkal = basic pH in the body osis= condition, disorder or abnormal state

Excessive alkalinity ( higher than normal pH)

Potassium moves into cells —> causing hypokalemia

Note: potassium = heart rhythm : even tiny shifts in k+ can trigger lethal cardiac dysthymias

Tissue injury link:

Crush injuries or severe burns destory cell membranes, releasing massive intracellular potassium into the bloodstream and causing acute hyperkalemia

Resting membrane potential

Electrical charge across a cell membranes at rest, governed by potassium

U wave

Abnormal ECG waves following the T wave, classic for hypokalemia

Peaked T waves

Tall narrow T waves on ECG, classic early sign of hyperkalemia

Calcium

Normal range 8.5-10.5 mg/dL.

Regulated by parathyroid hormone (raises blood calcium) and calcitonin

Acts as a stabilizer for nerve and skeletal muscle membranes

Hypocalcemia <8.5 mg/dL

Causes: hypoparathyroidism, malabsorption, pancreatitis, renal failure, or alkalosis

Loss of membrane stability increases neuromuscular excitability —>

Signs: tingling( paresthesias) around mouth/fingers, muscle cramps, tetany, largyngospasm,

Chvoestek’s sign (facial twitch), positive Trousseau’s sign (carpopedal spasm with BP cuff)

heart effect: weaker cardiac contractions and prolonged QT interval

Hypercalcemia >10.5 mg/dL

Causes: HYPERparathyroidism, bone cancer/maliganancies(destroying bone), prolonged immobility or excess vitamin D/calcium supplements

Stabilizes membranes too much, decreasing neuromuscular excitability —>

Signs: “bones,stones,groans and moans” muscle weakness, lethargy, constipation, kidney stgones (renal calculi), shorten QT interval

Magnesium (mg2+)

Low magnesium (hypomagnesemia) casues neuromuscular hyperirritability, tremors, and cardiac arrhythmias

Phosphate

Inversely related to calcium; high phosphate presents with the same signs as hypocalcemia

Chloride

Major negative ion in ECF, exchanged with bicarbonate (chloride shift). Vomiting stomach acid leads to metabolic alkalosis

Hypomagnesemia

Causes neuromuscular hyperirritability, tremors, and cardiac arrhythmias

Skeletal vs cardiac muscle paradox

Low calcium makes skeletal muscle twitchy (tetany) because nerve membranes become unstable. However, cardiac muscle relies on extracellular calcium entering through channels to contract— so low calcium causes weaker heart contractions.

Tetany

Continuous, painful muscle spasms from severe hypocalcemia

Chvostek’s sign

Facial muscle twitching when tapping in front of the ear (hypocalcemia)

Trousseau’s sign

Carpopedal spasm in the hand when inflating a blood pressure cuff (Hypocalcemia)

Parathyroid hormone (PTH)

Hormone that increases blood calcium via bone respiration and renal reabsorption

Chloride shift

Exchange of chloride and bicarbonate ions across red blood cells to maintain electrical neutrality

Normal pH range

7.35-7.45

Buffer ratio

main buffer, bicarbonate

Bicarbonate to carbonic acid must stay at a 20:1 ratio to maintain a normal pH

Speed of regulation

Chemical buffers: act instantly in the blood

Respiratory system: acts in minutes by altering breathing rate to blow off or hold CO2 acid

Renal system: Takes 24-72 hours to excrete acid and conserve HCO-3 base

Respiratory Acidosis

Low pH, High PaCO2

Caused by hypoventilation retaining off too much CO2, Chronic obstructive pulmonary disease, or opioid respiratory depression

Renal compensation: kidneys retain bicarbonate, and excrete H+

Respiratory Alkalosis

H pH, L PaCO2

Hyperventilation blowing off too much CO2, anxiety, or fever

compensation: kidneys excrete bicarb

Metabolic acidosis

L pH , L HCO-3

Caused by DKA, severe diarrhea,(loss of bicarb), renal failure, or lactic acidosis

Compensation: lungs perform deep, rapid kussmual respiration to blow off CO2

Metabolic Alkalosis

H PH, H HCO3

Caused by vomitting or NG suction (losing stomach acid)

Compensation: Lungs hypoventilate to retain Co2

Compensation vs Decompensation

Compensated: The unaffected organ system (lungs or kidneys) alters its function to restore the 20:1 ratio and bring pH back toward normal

Decompensated: compensatory mechanism fail, leaving serum pH outside 7.34-7.45.

Acidosis decompensation

CNS depression, (headache, confusion, lethargy, coma)

Acidosis simply means your blood has become too acidic. — serum pH drops below 7.35, meaning too much H+

• this slows down cellular enzymes and nervous system activity, causing central nervous system depression (CNS depression) therefore resulting extreme fatigue, weak, coma.

Alkalosis decompensation

Neuromuscular irritability ( paresthesias, muscle twitching, tetany, seizures)

Kussmaul respiration

Deep, rapid breathing pattern used by the lungs to compensate for metabolic acidosis

Skeletal vs cardiac muscle in hypocalcemia

Low calcium increases skeletal muscle excitability (causing tetany and spasms) because it destabilizes nerve membranes.

however, cardiac muscles lacks internal calcium stores and relies on extracellular calcium entering through channels, so low serum calcium causes

Weaker cardiac contractions

Potassium shift in acidosis!!!

In metabolic acidosis, excess extracellular H+ moves into cells to be buffered. to maintain electrical neutrality, intracellular k+ is pushed out into the blood, causing hyperkalemia

Diarrhea vs vomiting

Diarrhea loses bicarnobante-rich intestinal fluid —→ metabolic acidosis Compensation

Vomiting loses hydrocholoric acid —> metabolic alkalosis