Glossary

A to-the-point reference of the terms the chapters lean on. Expand any entry.

136 terms

• Tachycardia

  An abnormally fast heart rate. The heart is a pump, and its rate is one of its two key levers (rate × stroke volume = how much blood it moves per minute). Tachycardia is often the first sign that the body is under stress and is accelerating the pump to keep blood pressure and flow up.

  Reference: Resting rate > 100 bpm in adults (normal ~60-100).

  How it works: The heart's natural pacemaker is the sinoatrial (SA) node, a cluster of cells in the right atrium. Between beats these cells slowly 'leak' positive ions inward through channels called funny channels (the If current), raising the resting voltage until it fires. Adrenaline acts on beta-1 receptors to make this leak faster, so the SA node fires sooner. When blood pressure falls, stretch sensors (baroreceptors) in the neck and aorta register the drop and send a signal that reflexively ramps the SA node up - this is how low volume leads to a fast, thready pulse.

  Common causes: Pain; Fever; Volume loss / dehydration; Blood loss; Hypoxia; Stimulants; Anxiety; Hyperthyroidism

  Red flags: Tachycardia with low blood pressure (shock); New irregular rhythm; Chest pain; Fainting

  Pearl: A normal blood pressure does not rule out shock - tachycardia often precedes the pressure fall because the heart accelerates to preserve output first.

  Analogy: The heart is like a pump; the SA node is its automatic timer. If pressure drops, the body turns the timer's dial up before the water pressure visibly falls.

• Bradycardia

  An abnormally slow heart rate. A slow rate is normal in athletes and during sleep, but if the pump is too slow to move enough blood, it can cause low pressure, lightheadedness, or fainting.

  Reference: Resting rate < 60 bpm (adults).

  How it works: The SA node sets the baseline tempo. Beta-blockers, certain calcium-channel drugs, high vagal tone, or damage to the conduction system can slow the pacemaker or block signals reaching the ventricles, so the heart cannot speed up when needed.

  Common causes: Athletic conditioning; Beta-blockers / calcium-channel blockers; Heart block; Hypothyroidism; High vagal tone; Sick sinus syndrome

  Red flags: Bradycardia with lightheadedness or fainting; Very slow rate with low blood pressure

  Pearl: Whether bradycardia is a problem depends on whether cardiac output is enough - a slow, strong pump may be fine; a slow pump that cannot meet demand is not.

  Analogy: The cardiac timer's dial is set low. Useful when you are resting, dangerous if your body needs the pump to speed up and it cannot.

• Hypotension

  Blood pressure that is too low to keep adequate blood flowing to organs. Because organs need pressure to push blood through their vessels, very low pressure starves the brain, kidneys, and heart of oxygen.

  Reference: Often cited as systolic < 90 mmHg, diastolic < 60 mmHg, or mean arterial pressure (MAP) < 65 mmHg; what matters most is whether organs are getting enough flow.

  How it works: Blood pressure is the product of how much blood the heart pumps (cardiac output) and how much the vessels resist that flow (systemic vascular resistance): MAP = CO × SVR. Pressure can fall because the pump fails (cardiogenic), volume is lost (hypovolemic), or vessels dilate too much (distributive/vasodilatory).

  Common causes: Volume/blood loss; Dehydration; Sepsis; Heart failure; Anaphylaxis; Severe bleeding; Obstruction (e.g., pulmonary embolism)

  Red flags: Faintness, confusion; Cold clammy skin; Rapid weak pulse; Low urine output; Lightheadedness on standing

  Pearl: The body's priority is defending blood flow to the brain and heart. When pressure drops, it constricts vessels, raises heart rate, and holds onto water to restore pressure.

  Analogy: Blood pressure is the water pressure in a hose. If the pump is weak, the tank is empty, or the hose is too wide, the pressure and the water reaching the end (your organs) both drop.

• Hypertension

  A chronic elevation of blood pressure that puts strain on the heart, arteries, brain, kidneys, and eyes. Because it is usually silent, it is called a 'silent killer' and is a major risk factor for heart attack, stroke, and kidney disease.

  Reference: Typically considered when systolic is ≥ 130 or diastolic ≥ 80 mmHg on repeat readings; exact cutoffs vary by guideline and age.

  How it works: Pressure is the product of cardiac output and vascular resistance. In hypertension, the small arteries become narrowed or stiff, so the heart must push harder against higher resistance, and over time the vessel walls thicken and the heart enlarges to cope.

  Common causes: Age; Family history; High salt intake; Obesity; Inactivity; Kidney disease; Chronic stress; Sleep apnea

  Red flags: Sudden very high pressure with headache; Chest pain; Vision changes; Neurologic symptoms

  Pearl: High pressure is often symptomless for years, which is why routine measurement matters - by the time it causes symptoms, organ damage may already be occurring.

  Analogy: It is like running a garden hose with the nozzle partly pinched: the pressure behind the pinch rises, but it stresses the whole system.

• Mean arterial pressure (MAP)

  The time-averaged arterial pressure that actually pushes blood into the brain, kidneys, and heart. It sits between systolic and diastolic pressure and is the number clinicians use to judge whether organs are being perfused.

  Reference: Normal roughly 70-100 mmHg; a common clinical target is ≥ 65 mmHg to keep organs perfused.

  How it works: MAP = Cardiac output × Systemic vascular resistance. Because the heart spends more time in diastole than systole, MAP is closer to diastolic pressure than systolic.

  Common causes: Low volume; Weak pump; Dilated vessels

  Red flags: Persistent MAP < 65 mmHg; With confusion or low urine output

  Pearl: Chasing the systolic number alone can mislead; MAP is the perfusion pressure that organs actually need.

  Analogy: Systolic is the peak of each wave; MAP is the water level that blood organs actually sit in.

• Cardiac output

  The amount of blood the heart ejects each minute, equal to heart rate × stroke volume. It is the 'flow' side of blood pressure and determines how much oxygen-rich blood reaches the tissues.

  Reference: Normal resting roughly 4-8 L/min, varying with body size and demand.

  How it works: CO = Heart rate × Stroke volume. The heart cannot increase output forever - stroke volume has limits - so raising heart rate is the quick lever, and both fall with severe volume loss or pump failure.

  Pearl: You cannot tell cardiac output from blood pressure alone: high resistance can keep pressure up even when flow is dangerously low.

  Analogy: Think of CO as gallons per minute from the pump; blood pressure is the pressure in the pipes. They are related but not the same.

• Stroke volume

  The volume of blood ejected by the left ventricle with each contraction. It depends on how much blood returns to the heart, how hard the muscle contracts, and how much resistance it must overcome.

  Reference: Normally roughly 60-100 mL per beat at rest.

  How it works: Influenced by preload (how full the ventricle is), contractility, and afterload (the pressure it must pump against). Low volume reduces preload, so stroke volume falls.

  Common causes: Blood/volume loss; Heart failure; Tight aortic valve; Large pulmonary embolism

  Pearl: When stroke volume falls and the body still needs output, the heart compensates with a faster rate - which is why volume loss shows up as tachycardia.

  Analogy: The amount of water each single pump stroke sends down the pipe.

• Systemic vascular resistance

  The sum of the resistance offered by all the small arteries and arterioles. Together with cardiac output it determines blood pressure (MAP = CO × SVR). Vessels can narrow (raise resistance) or relax (lower it).

  Reference: Reported in units of resistance; what matters is that MAP = CO × SVR.

  How it works: Small arteries have muscle in their walls. Noradrenaline and other signals constrict them to raise pressure; sepsis and anaphylaxis cause them to dilate, dropping resistance and pressure even if the heart is pumping hard.

  Common causes: Vasodilation in sepsis/anaphylaxis; Vasoconstriction in stress/hemorrhage

  Pearl: In distributive shock (like sepsis), vessels dilate and blood pressure falls despite a high cardiac output - a key diagnostic clue.

  Analogy: How wide the hose's nozzle is: a wide opening (low resistance) drops pressure even if the pump runs fast.

• Sinoatrial node

  A small cluster of cells in the right atrium that generates each heartbeat's electrical trigger. It sets the resting rhythm and speeds up or slows down in response to the autonomic nervous system.

  How it works: The SA node cells spontaneously depolarize: between beats, positive ions enter through funny channels (If current), slowly raising the cell's voltage (phase 4 depolarization) until it fires. Adrenaline speeds this leak; the vagus nerve slows it.

  Pearl: The SA node is why the heart beats on its own without instructions from the brain.

  Analogy: The metronome that sets the tempo; the brain and hormones turn the tempo knob.

• SA node

  Short for the sinoatrial node, the heart's natural pacemaker in the right atrium.

  Analogy: The heart's built-in metronome.

• Funny current

  A sodium/potassium ion current (called If, or 'funny') that flows in SA node cells between beats. It leaks positive charge in, pushing the cell toward its firing threshold - the engine of spontaneous heartbeat.

  How it works: Between beats, funny channels open and let a slow inward sodium current depolarize the cell during phase 4. Beta-1 stimulation by adrenaline makes this current larger and faster, raising heart rate.

  Pearl: Blocking the funny current (e.g., with ivabradine) slows heart rate without the other effects of beta-blockade.

  Analogy: A slow drip filling a bucket until it overflows and triggers the next beat; adrenaline speeds up the drip.

• Phase 4 depolarization

  The gradual buildup of positive charge inside pacemaker (SA node) cells between beats that eventually triggers the next action potential. It is the electrical basis for automatic, rhythmic heartbeat.

  How it works: In phase 4, funny channels and other currents slowly depolarize the membrane. Firing occurs when the voltage reaches threshold. Faster phase 4 = faster heart rate.

  Pearl: This autorhythmic property is why the heart keeps beating even without nerve input.

  Analogy: The 'reload' phase of a repeating timer - speed it up and the timer fires more often.

• Baroreceptor

  Stretch-sensitive nerve endings in the carotid arteries and aortic arch that constantly measure blood pressure. When pressure falls, they send fewer signals, prompting a reflex that raises heart rate and constricts vessels.

  How it works: High pressure stretches baroreceptors, which signal the brain to slow the heart and dilate vessels. Low pressure unloads them, so the brain increases sympathetic output - faster heart rate and more vasoconstriction - to push pressure back up.

  Pearl: This baroreflex is why blood loss produces a fast, thready pulse: the sensors detect the pressure drop and reflexively speed the heart up.

  Analogy: A low-fuel gauge that automatically floors the accelerator when pressure (fuel) drops.

• Reflex tachycardia

  The heart speeding up in response to a sensed fall in blood pressure. It is a compensatory reflex, not the primary disease - it tells you the pump is working harder to defend pressure.

  How it works: Baroreceptors unload as pressure falls, reducing their inhibitory signal. The brain increases sympathetic (adrenergic) drive, accelerating the SA node via beta-1 receptors and vasoconstricting to raise resistance.

  Common causes: Volume loss; Bleeding; Dehydration; Vasodilation; Heart failure

  Red flags: Tachycardia with hypotension; Orthostatic symptoms

  Pearl: The reflex tries to keep blood pressure up by raising rate and resistance, which is why early hypotension can look 'compensated' with a fast pulse and normal-ish pressure.

  Analogy: If the tank begins to empty, the pump automatically speeds up to keep the pressure from dropping.

• Hypovolemic shock

  A state of inadequate organ perfusion caused by low circulating volume - from bleeding, severe dehydration, or fluid loss (vomiting, diarrhea, burns). The tank is too empty to fill the pump.

  How it works: Lost volume lowers preload, so stroke volume and cardiac output fall. Baroreceptors detect the pressure drop and trigger tachycardia and vasoconstriction to compensate; without volume replacement, this compensation fails and organs are underperfused.

  Common causes: Hemorrhage; Severe dehydration; Burns; Vomiting/diarrhea; Pancreatitis (fluid sequestration)

  Red flags: Confusion; Very low urine output; Cold clammy skin; Weak rapid pulse

  Pearl: The first treatment is replacing the lost volume - a dry tank cannot be fixed with a stronger pump.

  Analogy: A car running out of fuel: flooring the gas pedal briefly masks it, but there is no power until you add fuel.

• Distributive shock

  A form of shock in which blood pressure falls because the small vessels lose tone and dilate, even when the heart pumps hard. The blood is there, but it pools instead of being pushed to organs.

  How it works: In sepsis, anaphylaxis, or neurogenic injury, inflammatory mediators or nerve damage relax vascular smooth muscle, dropping systemic vascular resistance. MAP falls despite a high cardiac output, and blood pools in dilated vessels.

  Common causes: Sepsis; Anaphylaxis; Spinal cord injury; Adrenal crisis

  Red flags: Warm flushed skin (sometimes) with low pressure; Confusion; Fever; Exposure to allergen

  Pearl: Distributive shock often shows a fast heart, low blood pressure, but warm extremities - the opposite of the cold, clammy look of hypovolemia.

  Analogy: A hose whose nozzle has been opened too wide: the water never builds pressure even though the pump runs fast.

• Cardiogenic shock

  Inadequate organ perfusion because the heart cannot pump enough blood, most often after a major heart attack or in severe heart failure. The pump itself is the problem.

  How it works: When the left ventricle cannot eject enough blood, cardiac output and blood pressure fall while blood backs up into the lungs. The body tries to compensate, but the underlying pump failure limits improvement.

  Common causes: Large myocardial infarction; Severe heart failure; Severe valve disease; Myocarditis

  Red flags: Chest pain; Breathlessness; Low pressure; Pulmonary edema (fluid in lungs)

  Pearl: In cardiogenic shock, the problem is the pump, not the tank or the pipes - so the priority is supporting and treating the heart.

  Analogy: The pump itself is broken or seized, so no amount of water or open nozzles restores flow.

• Obstructive shock

  A form of shock where a physical blockage prevents the heart from filling or pumping - a tension pneumothorax compressing the chest, a massive pulmonary embolism, or cardiac tamponade squeezing the heart.

  How it works: Blood cannot circulate because something blocks the pathway. The body compensates with tachycardia, but relief requires removing or treating the obstruction.

  Common causes: Massive pulmonary embolism; Tension pneumothorax; Cardiac tamponade

  Red flags: Sudden severe breathlessness; Chest pain; Low pressure

  Pearl: Obstructive shock is an emergency where the obstruction (not volume or pump power) must be addressed.

  Analogy: A kink or blockage in the pipe itself - the pump runs, but nothing gets through.

• pH

  The concentration of hydrogen ions in the blood. Normal blood is kept in a very narrow range because enzymes and cells only work within it. Acid-base disorders push pH out of this range.

  Reference: Arterial blood pH ~7.35-7.45.

  How it works: pH is the negative log of hydrogen ion concentration: more hydrogen ions = lower pH = more acidic. The body has three lines of defense: blood buffers (like bicarbonate) act instantly, the lungs blow off CO2, and the kidneys excrete acid or retain bicarbonate over hours to days.

  Common causes: Lung disease (CO2 retained); Kidney failure; Diabetic ketoacidosis; Vomiting; Diarrhea

  Red flags: Extreme acidosis or alkalosis; Confusion; Breathing changes

  Pearl: CO2 is an acid in solution, so breathing faster lowers blood acid by exhaling CO2 - this is the body's rapid lever for pH.

  Analogy: pH is how 'sour' the blood is. Too sour or too bitter, and the body's machinery stops working.

• Acidosis

  A state in which blood pH falls below normal. It can result from too much acid added, too little acid removed, or too much bicarbonate lost.

  Reference: Arterial pH < 7.35.

  How it works: Metabolic acidosis comes from acid production or bicarbonate loss (e.g., ketoacidosis, diarrhea); respiratory acidosis comes from CO2 retention (e.g., hypoventilation, lung disease) because CO2 dissolves to form acid.

  Common causes: Diabetic ketoacidosis; Kidney failure; Diarrhea; COPD / hypoventilation; Lactic acidosis; Toxins

  Red flags: Deep rapid (Kussmaul) breathing; Confusion; Low blood pressure

  Pearl: The body may hyperventilate to blow off CO2 and 'blow off' acid - this is called respiratory compensation.

  Analogy: Too much sour ingredient in the recipe; the body either adds a base or vents the acid gas.

• Alkalosis

  A state in which blood pH rises above normal, from too much base, too much acid loss, or excessive CO2 blowing off.

  Reference: Arterial pH > 7.45.

  How it works: Metabolic alkalosis usually comes from losing acid (e.g., vomiting) or gaining bicarbonate; respiratory alkalosis comes from blowing off too much CO2 (e.g., hyperventilation from anxiety or pain).

  Common causes: Vomiting; Diuretics; Hyperventilation; Too much antacid/bicarbonate

  Red flags: Muscle twitching or cramping; Numbness/tingling; Confusion

  Pearl: Hyperventilation causes respiratory alkalosis by exhaling too much CO2 - which is why panic-driven fast breathing can cause tingling in the hands.

  Analogy: Too much bitter ingredient; the body adjusts by holding onto acid or slowing ventilation to retain CO2.

• Metabolic acidosis

  Acidosis originating in metabolism or kidney/bicarbonate handling rather than the lungs. The pH falls because too much acid is made, acids are not excreted, or bicarbonate is lost. The lungs compensate by blowing off CO2.

  Reference: Low pH with low bicarbonate (HCO3- < 22 mEq/L).

  How it works: Common causes produce an 'anion gap' (unmeasured acids, e.g., ketoacids, lactate) or a 'non-anion gap' pattern (bicarbonate loss, e.g., diarrhea or renal tubular acidosis). The body compensates fast by hyperventilating (Kussmaul breathing) and slower by the kidneys retaining bicarbonate.

  Common causes: Diabetic ketoacidosis; Lactic acidosis; Kidney failure; Diarrhea; Toxins (methanol, salicylate); Starvation

  Red flags: Deep rapid breathing; Confusion; Hypotension

  Pearl: Winters' formula predicts the expected respiratory compensation, so an unexpected blood pH helps spot a mixed disorder.

  Analogy: An acid spill, and the body has only two cleanup crews: the lungs (fast, venting CO2) and the kidneys (slow, excreting acid and saving base).

• Metabolic alkalosis

  Alkalosis from acid loss or bicarbonate gain. The body compensates by breathing more slowly to retain CO2 and, slowly, by the kidneys excreting bicarbonate.

  Reference: High pH with high bicarbonate (HCO3- > 28 mEq/L).

  How it works: Usually from losing hydrochloric acid through vomiting or gastric suction, or from diuretics. The kidneys try to excrete the excess bicarbonate.

  Common causes: Vomiting; Gastric suction; Diuretics; Hypokalemia; Mineralocorticoid excess

  Red flags: Muscle cramps; Weakness; Arrhythmia risk

  Pearl: Potassium abnormalities often accompany metabolic alkalosis, so electrolytes matter as much as the pH.

  Analogy: Losing acid (like bile) leaves the mixture too base; the body tries to hold breath and save acid.

• Respiratory acidosis

  When the lungs cannot blow off carbon dioxide (too slow or too shallow breathing, or lung disease), CO2 builds up and dissolves into acid, lowering pH.

  Reference: Low pH with high CO2 (pCO2 > 45 mmHg).

  How it works: CO2 + water → carbonic acid. If ventilation cannot clear CO2, acid accumulates. The kidneys compensate over hours to days by retaining bicarbonate and excreting acid.

  Common causes: COPD; Sedative/opioid overdose; Chest wall injury; Neuromuscular weakness; Severe asthma

  Red flags: Drowsiness; Confusion; Slow or shallow breathing; Headache

  Pearl: The dangerous clue is a rising CO2 with a falling level of consciousness - the patient may need ventilatory support.

  Analogy: A room where the air vent is blocked: CO2 (an acid gas) slowly builds up.

• Respiratory alkalosis

  When breathing is too fast or deep, CO2 is blown off faster than produced, so blood acid falls and pH rises.

  Reference: High pH with low CO2 (pCO2 < 35 mmHg).

  How it works: Hyperventilation removes CO2, reducing carbonic acid. Causes include pain, anxiety, fever, early sepsis, or high altitude.

  Common causes: Anxiety/hyperventilation; Pain; Fever; Early sepsis; High altitude; Liver disease

  Red flags: Hand/foot tingling; Muscle spasms; Lightheadedness

  Pearl: It is a common response to hypoxia or early sepsis, so it should be checked rather than dismissed as 'anxiety'.

  Analogy: Blowing too hard on a straw: you vent the acid gas faster than it forms, so the solution turns more basic.

• Compensation

  The body's corrective responses that mask or limit an underlying problem. The lungs and kidneys compensate for acid-base shifts on different timescales, and the heart and vessels compensate for pressure changes.

  How it works: For pH, three lines of defense act in order: chemical buffers (bicarbonate) work instantly; the lungs adjust CO2 within minutes by changing breathing; the kidneys adjust bicarbonate and acid excretion over 24-72 hours. For blood pressure, tachycardia and vasoconstriction compensate for low volume.

  Red flags: Compensation failing (decompensation) - e.g., pressure falling despite fast heart rate

  Pearl: Compensation masks early disease: a 'normal' number can hide a serious process until the body can no longer keep up, then the patient crashes.

  Analogy: A thermostat silently fighting to hold a set temperature - you cannot tell how hard it is working from the reading alone.

• Anion gap

  A value computed from the major measured ions that catches the presence of 'unmeasured' acids (lactate, ketoacids, toxins). A high anion gap means some acid is present that the standard panel does not directly measure.

  Reference: Roughly 8-12 mEq/L, but it varies by lab/assay - always compare to the local reference.

  How it works: The gap is (Na+) − (Cl− + HCO3−). When an extra acid (like lactic or keto acid) enters the blood, bicarbonate falls to buffer it, widening the gap. Causes are recalled by 'MUDPILES': methanol, uremia, diabetic ketoacidosis, propylene glycol, isoniazid, lactic acidosis, ethylene glycol, salicylates.

  Common causes: Lactic acidosis; Diabetic ketoacidosis; Renal failure; Methanol/ethylene glycol; Salicylate toxicity; Starvation

  Red flags: High anion gap acidosis (often emergency); Deep breathing; Confusion

  Pearl: A high anion gap metabolic acidosis is a launchpad for the differential - it means acid is being produced or added that the body cannot clear.

  Analogy: A shop's register that never balances: the gap is the unexplained 'missing' money (acid).

• Bicarbonate

  Bicarbonate is the chief buffer in the blood, soaking up hydrogen ions to keep pH stable. The kidneys control its level, so bicarbonate is a key number on the blood gas.

  Reference: ~22-28 mEq/L.

  How it works: Bicarbonate combines with hydrogen ions to form carbonic acid, which the lungs then exhale as CO2 and water. This is the instant chemical defense that the lungs and kidneys manage long-term.

  Pearl: Low bicarbonate = the body is buffering a metabolic acidosis; high bicarbonate = metabolic alkalosis or compensation.

  Analogy: A base (antacid) that neutralizes acid; the kidneys are the factory that restocks it, the lungs the exhaust pipe.

• Creatinine

  A byproduct of muscle metabolism that the kidneys filter out. Because it is produced at a fairly steady rate, a rising creatinine means the kidneys are filtering less well.

  Reference: Roughly 0.6-1.2 mg/dL in adults, but varies by muscle mass, age, sex, and lab.

  How it works: The kidneys filter creatinine from the blood into the urine. When kidney filtration drops, creatinine builds up in the blood, so it is a proxy for how well the kidneys are working.

  Common causes: Acute kidney injury; Dehydration; Chronic kidney disease; Some medications

  Red flags: Rapidly rising creatinine; Low urine output; Confusion

  Pearl: Creatinine rises only after substantial filtration is lost, so a 'normal' creatinine does not rule out early kidney disease.

  Analogy: Like a trash can filling when the pickup service (the kidneys) stops coming - the pile grows as service fails.

• BUN

  A waste product made as the body breaks down protein. It is filtered by the kidneys and rises when filtration drops or when the body is dehydrated and reabsorbing water.

  Reference: Roughly 7-20 mg/dL, varies with age, diet, and lab.

  How it works: The liver makes urea from ammonia (from protein breakdown); the kidneys excrete it and reabsorb some. Dehydration raises BUN disproportionately because water is reabsorbed, concentrating it. BUN is read with creatinine.

  Common causes: Dehydration; Kidney disease; High protein intake; Gastrointestinal bleeding

  Pearl: A high BUN-to-creatinine ratio often points to dehydration or bleeding rather than intrinsic kidney disease.

  Analogy: A byproduct pile that builds up when water waste isn't being flushed because there isn't enough water.

• Sodium

  The dominant electrolyte in the blood, which controls how water is distributed in the body and is essential for nerve and muscle signaling. Its level changes reflect body water, not just salt.

  Reference: ~135-145 mmol/L.

  How it works: Sodium concentration is really about the ratio of sodium to water. Low sodium (hyponatremia) is often too much water relative to salt, seen with SIADH, heart/liver/kidney failure, or excessive water intake.

  Common causes: Hyponatremia: excess water/SIADH; Hypernatremia: dehydration or salt overload

  Red flags: Confusion; Seizures (severe)

  Pearl: Sodium tells you about water balance - treating it too fast can be dangerous, so clinicians are cautious.

  Analogy: The salt concentration of soup: too much water and it is bland; too little water and it is overly salty.

• Potassium

  A charged particle concentrated inside cells that is critical for the electrical activity of nerves, muscles, and especially the heart. Both high and low potassium disturb heart rhythm.

  Reference: ~3.5-5.0 mmol/L.

  How it works: The body keeps most potassium inside cells, and the sodium-potassium pump maintains this. Kidney excretion takes time, so anything that shifts potassium in or out of cells, or kidney failure, can rapidly make it dangerous.

  Common causes: Hyperkalemia: kidney failure, cell breakdown, certain drugs; Hypokalemia: diuretics, vomiting, diarrhea

  Red flags: Hyperkalemia - arrhythmia risk; Muscle weakness; ECG changes

  Pearl: Potassium is the most dangerous electrolyte to be out of range because even moderate changes can trigger lethal heart rhythms.

  Analogy: The electrical charge that keeps the heart's wiring stable - too much or too little and the wiring 'arcs'.

• Electrolyte

  Dissolved salts (sodium, potassium, calcium, magnesium, chloride, bicarbonate) that carry electric charge. They are essential for nerve signaling, muscle contraction, hydration, and many chemical reactions.

  Reference: Each has its own reference range (e.g., sodium 135-145, potassium 3.5-5.0 mmol/L).

  How it works: Cells use the movement of charged electrolytes across their membranes to fire signals and contract. The kidneys fine-tune electrolyte levels continuously.

  Common causes: Dehydration; Vomiting/diarrhea; Kidney disease; Diuretics; Endocrine disorders

  Red flags: Severe derangement → arrhythmia, seizures, weakness

  Pearl: Labs like the BMP measure the key electrolytes and are interpreted together, not in isolation.

  Analogy: The ions are like the battery charge of the body - each cell is a tiny battery powered by moving charged particles.

• Hemoglobin

  The molecule inside red blood cells that binds oxygen in the lungs and releases it in the tissues. Hemoglobin levels reflect how much oxygen the blood can carry.

  Reference: Roughly 13.5-17.5 g/dL in men, 12-15.5 g/dL in women; varies by age and altitude.

  How it works: Each hemoglobin molecule has iron that grabs oxygen. Low hemoglobin (anemia) means less oxygen delivered; the body may compensate with a faster heart rate and deeper breathing.

  Common causes: Anemia: blood loss, iron deficiency, marrow disorders, hemolysis

  Red flags: Pale, tired, breathless, fast heart rate

  Pearl: Hemoglobin is a measure of carrying capacity, not of how well oxygen is loading - that depends on the lungs and saturation.

  Analogy: The cargo trucks that carry oxygen; if you have half the trucks, you deliver half the oxygen.

• Hematocrit

  The percentage of blood volume that is red blood cells. It tracks hemoglobin and rises or falls with red-cell mass and hydration.

  Reference: Roughly 40-50% in men, 36-45% in women.

  How it works: Centrifuging blood separates the red cells (bottom) from plasma. The proportion is the hematocrit. Acute bleeding lowers it; dehydration can transiently raise it by concentrating the red cells.

  Common causes: Bleeding, anemia (low); Dehydration, polycythemia (high)

  Pearl: Hematocrit is about 3× the hemoglobin in g/dL as a rough cross-check.

  Analogy: The density of cargo trucks in traffic: it says how concentrated the red cells are.

• Platelet

  Small fragments that plug leaks in blood vessels and build clots. Too few platelets (thrombocytopenia) raises bleeding risk; too many raises clotting risk.

  Reference: ~150-400 × 10^9/L.

  How it works: When a vessel is injured, platelets stick to the site, change shape, and clump, forming the first plug and releasing signals that build a fibrin clot.

  Common causes: Low: bone marrow problems, drugs, immune destruction; High: reactive or clonal

  Red flags: Sudden bruising/bleeding with low platelets

  Pearl: A platelet count that trends down fast is an emergency even if a single reading looks 'low-normal'.

  Analogy: Scabs-in-waiting: the fragments that rush to any hole in the vessel wall.

• White blood cell

  A family of blood cells (neutrophils, lymphocytes, monocytes, eosinophils, basophils) that defend the body. The total and the breakdown (differential) help point to infection versus inflammation.

  Reference: ~4.5-11 × 10^9/L.

  How it works: White cells are made in the marrow and travel in the blood to sites of infection or injury. Different types respond to different threats: neutrophils to bacteria, lymphocytes to viruses, eosinophils to allergy/parasites.

  Common causes: High: infection, inflammation, stress; Low: marrow suppression, overwhelming infection

  Pearl: The pattern of white-cell subtypes (the differential) is often more informative than the total count alone.

  Analogy: The various branches of a police force, each specialized to a different kind of invader.

• Oxygen saturation (SpO2)

  A noninvasive measure (by pulse oximeter) of how much of the blood's oxygen-carrying capacity is currently loaded. Low saturation means little oxygen is being delivered to tissues.

  Reference: Normally 94-100% at sea level; lower at altitude or with lung disease.

  How it works: The oximeter shines light through tissue and infers how much hemoglobin is bound to oxygen. It is a snapshot of the lungs loading oxygen, not of how much the tissues receive.

  Common causes: Low: lung disease, low oxygen in air, shunt, anemia (sometimes)

  Red flags: Sustained low SpO2; Breathlessness; Confusion

  Pearl: A normal SpO2 does not guarantee normal oxygen delivery - a low hemoglobin or poor circulation can still starve tissues.

  Analogy: The fuel-gauge for oxygen: it shows how full the tank (hemoglobin) is, not the flow to the engine.

• Kidney

  One of two organs that filter the blood, remove wastes, regulate water and electrolytes, and control acid-base balance. Each contains about a million filtering units (nephrons).

  How it works: Blood flows into each nephron's filter (glomerulus), where water and small molecules pass into the tubule while blood cells and protein stay in. The tubule then reabsorbs what the body needs and excretes the rest as urine, and secretes hydrogen ions to manage acid.

  Red flags: Sudden fall in urine output; Rising creatinine; Swelling

  Pearl: The kidney is the slow but powerful acid-base regulator - it takes hours to days but can excrete a huge acid load.

  Analogy: A sophisticated recycling plant: filters the blood, keeps what is useful, and flushes the waste while managing the water level and acidity.

• Nephron

  The functional unit of the kidney, made of a filter (glomerulus) and a tubule that adjusts what is reabsorbed and excreted. About a million nephrons work in each kidney.

  How it works: The glomerulus filters blood; the tubule reabsorbs water, salt, and nutrients and secretes waste and acid. In acidosis, tubular cells generate new bicarbonate and excrete hydrogen ions (via H+/K+ ATPase and ammoniagenesis).

  Pearl: Kidney injury is quantified by how much filtration is lost across the million nephrons.

  Analogy: One tiny workbench on a large factory floor, each doing the same filtering job.

• Glomerulus

  A ball of tiny blood vessels where blood is filtered. It holds back blood cells and large proteins while letting water, salt, and small wastes through to become urine.

  How it works: Blood pressure pushes fluid out of the glomerular capillaries into the tubule. Protein and cells are too large to cross the filter; when the filter is damaged (glomerulonephritis), protein and blood leak into the urine.

  Common causes: High pressure; Diabetes; Autoimmune disease; Infection

  Red flags: Blood or foamy urine; Swelling

  Pearl: Protein in the urine (proteinuria) often means the glomerular filter is leaking.

  Analogy: A sieve at the top of a drain: fine enough to hold back coffee grounds (cells/protein) while letting water pass.

• Sepsis

  A serious condition in which an infection triggers a widespread, dysregulated inflammatory response that can damage organs and drop blood pressure. When blood pressure falls despite fluids, it becomes septic shock.

  Reference: Sepsis is a clinical diagnosis, not a single lab value; markers often include raised lactate, high white count, and low pressure.

  How it works: Infection triggers immune cells to release inflammatory signals, which dilate blood vessels (low systemic vascular resistance) and make vessels leaky. Blood pools, pressure falls, and organs receive too little oxygen - a distributive shock.

  Common causes: Pneumonia; Urinary infection; Skin/wound infection; Abdominal infection; Intravascular catheters

  Red flags: Confusion; Fast heart rate; Fast breathing; Fever or low temperature; Low blood pressure

  Pearl: Sepsis is time-critical - 'hour-1' recognition and treatment (antibiotics + fluids) improve survival dramatically.

  Analogy: An alarm that the whole town overreacts to: everyone runs, roads jam, and essential deliveries (oxygen to organs) are delayed.

• Septic shock

  The most severe form of sepsis, in which infection causes such widespread vessel dilation and leakiness that blood pressure cannot be maintained, starving organs of oxygen despite fluid replacement.

  How it works: Inflammatory mediators massively dilate and leaky vessels drop systemic vascular resistance. Blood pressure falls (MAP < 65 mmHg is a common target), requiring vasopressors to keep organs perfused.

  Common causes: Severe bacterial, fungal, or viral infection

  Red flags: Need for vasopressors; High lactate; Confusion; Low urine output

  Pearl: In septic shock the vessels are 'wide open', so treatment adds vasoconstrictors, not just more fluid.

  Analogy: A fire alarm that opens every water main at once, flooding and emptying pressure everywhere.

• Hypoxia

  A state where body tissues do not get enough oxygen, which can starve organs. It can arise from low oxygen in the blood, poor circulation, too few red cells, or cells unable to use oxygen.

  How it works: Oxygen must move: lungs load it, blood carries it (hemoglobin), circulation delivers it, and cells use it. Failure at any step causes tissue hypoxia, prompting faster breathing and heart rate as compensation.

  Common causes: Lung disease; Low oxygen in air; Anemia; Heart failure; Hypoperfusion/shock

  Red flags: Confusion; Blue lips or nails; Breathlessness; Chest pain

  Pearl: SpO2 measures blood oxygen, but tissue oxygen also depends on flow and hemoglobin - so circulation matters too.

  Analogy: Starvation at the cellular level: even full food trucks (oxygen in the lungs) help nothing if the roads (circulation) are blocked.

• Ischemia

  Insufficient blood supply to a tissue, depriving it of oxygen and nutrients. If severe or prolonged, it causes cell death (infarction) - as in heart attack or stroke.

  How it works: A blocked or narrowed artery reduces flow. The tissue consumes the oxygen it has and begins to fail. Pain (like angina with the heart, or claudication with legs) is often the tissue's signal of oxygen shortage.

  Common causes: Atherosclerosis (plaque); Blood clot; Vasospasm; Low blood pressure

  Red flags: Chest pain; Sudden weakness/numbness; Cold painful limb

  Pearl: Ischemia is reversible if blood flow is restored quickly; infarction is the point of no return.

  Analogy: Watering a plant with a kinked hose: it wilts right away (ischemia) but dies only if the kink stays (infarction).

• Coronary

  The coronary arteries supply oxygenated blood to the heart muscle. Coronary artery disease is narrowing or blockage of these vessels, a leading cause of heart attack.

• Antibiotic resistance

  The ability of bacteria to survive drugs that once killed them. Overuse and broad-spectrum use drive resistance, making infections harder to treat.

• Corticosteroids

  Cortisol and its synthetic relatives (e.g., prednisone, dexamethasone) that broadly dampen inflammation and immune activity by altering gene expression.

• Beta-adrenergic receptors

  Cell-surface receptors that respond to adrenaline and noradrenaline. Beta-blockers attach to them, blocking the stimulatory effects on the heart.

• Plasmin

  An enzyme that breaks down the fibrin mesh of a clot. Thrombolytic drugs convert plasminogen into plasmin to dissolve dangerous clots.

• Lumbar puncture

  A procedure that samples cerebrospinal fluid (CSF) from the space around the spinal cord. It is the definitive test for meningitis and a key tool for other nervous-system conditions.

  How it works: Neuroimaging before LP is not routine - it is reserved for specific high-risk features (new focal deficit, new seizure, papilledema, immunocompromise, or altered consciousness) because LP can be dangerous with raised pressure. In suspected acute bacterial meningitis, empiric antimicrobials must never be delayed for the LP.

  Red flags: Delay antibiotics for imaging - never in suspected acute bacterial meningitis

  Pearl: Meningitis is a time-critical emergency: start empiric antibiotics without delay; the LP follows.

• Granuloma

  A collection of immune cells that forms in response to chronic inflammation, seen in sarcoidosis, tuberculosis, and some infections.

• Granulomas

  Clusters of immune cells (macrophages and lymphocytes) that wall off persistent inflammation or infection; characteristic of sarcoidosis, tuberculosis, and fungal infections.

• Systemic lupus erythematosus

  An autoimmune disease where the immune system attacks skin, joints, kidneys, blood cells, and brain. It is a 'great imitator' diagnosed with clinical criteria and specific antibodies.

• Paraneoplastic syndrome

  A set of symptoms caused not by the tumor itself but by the body's immune response to it, or by substances the tumor releases. Symptoms can appear before the cancer is found.

• Differential diagnosis

  The structured list of possible diagnoses that could account for a patient's symptoms and findings, ranked by likelihood and danger, revised as new data arrives.

• Cognitive biases

  Systematic errors in thinking that distort how evidence is weighed, such as anchoring, confirmation bias, and premature closure. They are a major cause of diagnostic error.

• Occam's razor

  The principle that the simplest explanation - one disease explaining all findings - is usually correct. It is a useful starting bias, not proof.

• Hickam's dictum

  The counter-principle to Occam's razor: patients can have as many diseases as they please, so sometimes findings are several separate problems rather than one unifying disease.

• Anaphylaxis

  A severe, potentially life-threatening allergic reaction causing swelling, breathing trouble, and low blood pressure. It is an emergency treated with epinephrine.

• Empiric therapy

  Treatment begun based on the most likely diagnosis before test results confirm it, often broad-spectrum, then narrowed once the organism or cause is identified.

• Allosteric site

  A site on a receptor separate from the main binding site. Binding there (as benzodiazepines do on GABA-A) changes how the receptor responds to its main signal.

• Chelation

  A treatment that uses drugs to bind heavy metals in the body so they can be excreted. It is used for lead, mercury, and other heavy-metal poisoning under specialist guidance.

• Prion

  An abnormal misfolded protein that can recruit normal proteins to misfold, spreading through the brain and causing rare, fatal neurodegenerative disease.

• Anticoagulation

  Medication that reduces the blood's ability to clot, used to treat or prevent dangerous clots such as deep vein thrombosis, pulmonary embolism, and some strokes.

• Thrombolytic

  A medication that dissolves blood clots by activating the body's clot-dissolving system. It is used for the most dangerous clots in stroke, heart attack, and pulmonary embolism.

  Pearl: For STEMI, fibrinolysis is chosen only when primary PCI cannot be delivered within the acceptable time window and there are no contraindications - PCI is the preferred reperfusion when timely.

• Ventilator

  A machine that supports or replaces a patient's breathing when they cannot do so themselves, delivering oxygen and removing carbon dioxide through an airway tube.

• Pneumothorax

  A condition where air collects in the space around the lung, causing it to collapse. It can occur spontaneously or from trauma or procedures and may require drainage.

• Hemoptysis

  Coughing up blood from the respiratory tract. It is a concerning symptom that requires investigation for infection, tumor, or bleeding disorders.

• Autoimmune disease

  A condition in which the immune system mistakenly attacks the body's own cells and organs, such as lupus, rheumatoid arthritis, and vasculitis.

• Aphasia

  Impaired ability to understand or produce language, caused by damage to the language areas of the brain, such as from stroke, tumor, or inflammation.

• Encephalitis

  Inflammation of the brain, usually from infection or an autoimmune cause, causing fever, confusion, seizures, and neurologic symptoms.

• Meningitis

  Inflammation of the meninges, the membranes covering the brain and spinal cord, usually from infection. It is a medical emergency diagnosed by lumbar puncture.

• Granulomatous

  Describing a pattern of inflammation that forms granulomas, seen in sarcoidosis, tuberculosis, and certain fungal infections.

• Vasculitis

  Inflammation of blood vessel walls that can affect any organ, causing a wide range of symptoms depending on which vessels are involved.

• Amyloid

  Insoluble clumps of misfolded protein that deposit in organs such as the heart, kidneys, and nerves, disrupting their function in amyloidosis.

• Anchoring

  A cognitive bias in which the clinician fixates on an initial diagnosis and fails to adjust it as new, conflicting evidence arrives.

• Confirmation bias

  The tendency to notice and value evidence that supports a favored hypothesis while ignoring evidence against it, a major cause of diagnostic error.

• Premature closure

  The cognitive error of accepting a diagnosis once a plausible explanation is found, without fully considering alternatives.

• GABA

  Gamma-aminobutyric acid, the primary inhibitory neurotransmitter in the brain. It dampens neuronal activity and is the target of many sedative and anticonvulsant drugs.

• GABA-A

  An ion-channel receptor for GABA that, when activated, allows chloride ions in and inhibits the neuron. Benzodiazepines bind an allosteric site on it to enhance GABA's effect.

• GABA-A receptor

  An ion-channel receptor for GABA that, when activated, allows chloride ions in and inhibits the neuron. Benzodiazepines bind an allosteric site on it to enhance GABA's effect.

• Lorazepam

  A benzodiazepine (brand name Ativan) used for anxiety, seizures, and sedation. It enhances GABA-A receptor function, producing calming and anticonvulsant effects.

• Neutrophils

  The most abundant type of white blood cell, a first-line defender against bacterial infection. High counts suggest bacterial infection or inflammation; low counts raise infection risk.

• Lymphocytes

  White blood cells that include T cells and B cells. They drive viral immunity and antibody production; high counts suggest viral infection or certain blood disorders.

• Eosinophils

  A white blood cell type that rises with allergic reactions, asthma, and parasitic infections. High eosinophils are a useful diagnostic clue.

• Basophils

  The least common white blood cell, involved in allergic and inflammatory responses. Abnormal levels can point to certain blood or allergic conditions.

• Monocytes

  White blood cells that migrate into tissues and become macrophages, engulfing debris and pathogens. They rise in chronic infection and inflammation.

• Ketoacidosis

  A metabolic state in which the body breaks down fat for fuel, producing acidic ketones. It occurs in diabetic ketoacidosis and starvation and causes a high-anion-gap acidosis.

• Gadolinium

  A contrast agent used in MRI that brightens areas of abnormal blood-brain barrier, inflammation, or tumor. It is generally avoided in severe kidney disease.

• Infarction

  Death of tissue caused by interruption of its blood supply. Common examples include heart attack (myocardial infarction) and stroke (cerebral infarction).

• Anion gap (high)

  See 'Anion gap'. A high anion gap metabolic acidosis means extra acid is present that routine panels do not directly measure.

• Kussmaul breathing

  A pattern of very deep, sometimes rapid breathing seen when the body tries to compensate for metabolic acidosis by exhaling carbon dioxide, which is acidic in solution.

  How it works: Acid builds up (e.g., in diabetic ketoacidosis), so the brain drives deeper, faster breathing to blow off CO2. CO2 + water forms carbonic acid, so removing CO2 raises pH. It is a visible emergency sign of metabolic acidosis.

  Common causes: Diabetic ketoacidosis; Lactic acidosis; Uremia

  Red flags: Deep, heavy breathing in a sick patient - emergency

  Pearl: The body is literally breathing out acid as CO2 gas.

  Analogy: The body's emergency fume hood: it ventilates the acid gas until it can get to the cause.

• Renal compensation

  Over 24-72 hours, the kidneys adjust acid-base balance by retaining or generating bicarbonate and excreting hydrogen ions. It is slower than lung compensation but can handle a large acid load.

  How it works: In acidosis, kidney tubular cells generate new bicarbonate and excrete hydrogen ions, partly via the H+/K+ ATPase and by ammoniagenesis (producing ammonia to carry out acid as ammonium). This restores bicarbonate over days.

  Pearl: Renal compensation takes time - a sudden acid load is handled first by buffers and the lungs, then by the kidneys.

  Analogy: The slow, thorough cleanup crew that finally restocks the base after the fast venting is done.

• Ammoniagenesis

  The kidney's process of producing ammonia from amino acids, used to shuttle hydrogen ions out in the urine as ammonium. It is a key way the kidneys excrete acid during metabolic acidosis.

  How it works: During acidosis, kidney cells generate ammonia (from glutamine) which combines with hydrogen ions to form ammonium ions excreted in urine, allowing large amounts of acid to be removed while generating new bicarbonate. This ramps up over 24-72 hours.

  Pearl: This is why the kidneys can excrete acid far beyond what free hydrogen ions alone would allow.

  Analogy: Adding a chemical 'sponge' (ammonia) that safely packs acid into the trash (urine) so more can be removed.

• Winters' formula

  A formula that predicts the degree of respiratory compensation expected for a metabolic acidosis, so a mismatched result flags a mixed acid-base disorder.

  How it works: Expected PaCO2 ≈ 1.5 × HCO3− + 8 (± 2). If the measured CO2 is close, the lungs are compensating as expected; if it is off, there is an additional respiratory problem.

  Pearl: Ranges rely on measured units and are a teaching tool - interpret with clinical context, never as a standalone diagnostic rule.

  Analogy: A rough 'expected answer' to check your work: if the breathing response is way off, you likely missed a second problem.

• Auscultation

  Listening to internal body sounds - heart, lungs, and vessels - with a stethoscope. It turns the examiner into a sensor, spotting murmurs, crackles, wheezes, and added heart sounds.

  How it works: Organ movements and blood flow create sounds. The stethoscope transmits them to the ear; the clinician interprets their timing, pitch, and location against the cardiac/respiratory cycle.

  Pearl: A changed new murmur or a rub can be the first clue to valve disease, infection, or inflammation.

  Analogy: A mechanic putting an ear to a running engine - listening for the sound that does not belong.

• Heart sounds S1 and S2

  S1 ('lub') is the sound of the atrioventricular valves closing as the ventricles begin to contract; S2 ('dub') is the semilunar valves closing as the ventricles relax. They mark the two phases of the mechanical cycle.

  How it works: S1 occurs at the start of ventricular systole when the mitral and tricuspid valves snap shut. S2 occurs at the end of systole when the aortic and pulmonary valves close. Blood flow through a diseased valve adds a murmur.

  Red flags: A new or loud murmur; Extra sounds; Chest pain

  Pearl: These two sounds let you time a murmur, which is how you tell which valve and phase it comes from.

  Analogy: The door-slams of a pump: the two valves snapping at different moments in each cycle.

• Murmur

  A blowing or whooshing sound caused by turbulent flow through a valve or vessel. Murmurs are timed (systolic vs diastolic) and graded, and help identify valve disease.

  How it works: Smooth laminar flow is silent; turbulence makes noise. A narrowed valve (stenosis) or a leaking valve (regurgitation) disrupts flow, creating a murmur timed to the valve's phase.

  Common causes: Valve stenosis; Valve regurgitation; High cardiac output; Some congenital defects

  Red flags: New murmur with syncope/chest pain; Diastolic murmur; Murmur with fever (endocarditis)

  Pearl: Timing is everything: a systolic murmur happens between S1 and S2; a diastolic murmur between S2 and S1.

  Analogy: A river making noise only where it narrows or meets an obstacle - the turbulence is the clue.

• Electrocardiogram (ECG)

  A recording of the heart's electrical signals from electrodes on the skin. It reveals rate, rhythm, ischemia, and damage by showing the sequence of electrical activation.

  How it works: Each heartbeat generates a small electrical wave that depolarizes the atria (P wave), ventricles (QRS), and repolarizes (T wave). The ECG plots this voltage over time.

  Pearl: The ECG shows electricity, not pumping - a normal ECG does not guarantee a healthy pump.

  Analogy: A seismograph of the heart's electrical impulses over time.

• P wave

  The first small wave on the ECG, representing the atria depolarizing (electrically firing) to squeeze blood into the ventricles.

  How it works: The SA node fires, and the wave spreads across the atria - this electrical activation appears as the P wave. Following it, the impulse reaches the AV node and then the ventricles.

  Red flags: Absent/abnormal P waves (often atrial fibrillation)

  Pearl: Missing P waves with an irregular rhythm is the classic clue for atrial fibrillation.

  Analogy: The ignition step of the heartbeat on the electrical chart.

• QRS complex

  The tall deflection on the ECG representing the ventricles depolarizing and contracting - the main pumping event. A wide QRS means the impulse is spreading slowly.

  Reference: Normal QRS width about 0.08-0.12 s (2-3 small squares).

  How it works: The impulse travels through specialized fibers to the ventricles, producing the QRS. A wide QRS suggests a conduction delay (bundle branch block) or a ventricular origin of the rhythm.

  Common causes: Bundle branch block; Ventricular rhythms; Electrolyte abnormalities

  Red flags: Very wide QRS; Fast wide QRS (may be ventricular tachycardia)

  Pearl: The QRS separates normal (narrow) from ventricular (often wide) rhythms.

  Analogy: The big 'firing' spike when the main pump chambers switch on.

• ST segment

  The flat portion between the QRS and the T wave, representing the ventricle between depolarization and repolarization. Elevation or depression here flags heart ischemia or injury.

  How it works: When part of the heart is starved of oxygen (ischemia or acute infarction), its electrical recovery is abnormal, shifting the ST segment up (elevation) or down (depression) relative to baseline.

  Common causes: Myocardial ischemia/infarction; Pericarditis; Left ventricular hypertrophy

  Red flags: ST elevation (emergency - think STEMI)

  Pearl: ST elevation on the ECG is one of the fastest ways to identify a blocked-coronary heart attack needing emergency action.

  Analogy: A flat section of road that tilts uphill - a warning the engine (heart muscle) is straining.

• T wave

  The upright wave after the QRS representing the ventricles repolarizing (recharging) after a beat. Abnormal T waves can signal ischemia or electrolyte imbalance, especially potassium.

  How it works: After pumping, the ventricular muscle restores its electrical state for the next beat; this repolarization produces the T wave. Potassium problems and ischemia distort it.

  Common causes: Ischemia; Hyper/hypokalemia; Digoxin

  Red flags: Tall peaked or inverted T waves with chest pain

  Pearl: Very tall, 'peaked' T waves are a classic early sign of high potassium (hyperkalemia).

  Analogy: The recharging curve of the heart's battery after each squeeze.

• Alveolus

  One of millions of tiny air sacs in the lungs where oxygen enters the blood and carbon dioxide leaves it, across a thin membrane.

  How it works: Oxygen diffuses from the air in the alveolus across the thin membrane into the blood, while CO2 diffuses the other way to be exhaled. The membrane must be thin and wet for efficient exchange.

  Common causes: Pneumonia (fluid in alveoli); Pulmonary edema; Emphysema (destroyed alveoli)

  Red flags: Low oxygen, breathlessness

  Pearl: Gas exchange is all about surface area and a thin membrane - damage to either drops oxygenation.

  Analogy: Millions of tiny balloons where air touches blood; the surface area across them is huge.

• Diffusion

  The passive movement of molecules from an area of higher concentration to lower concentration, across a membrane. It is how oxygen and CO2 move in the lungs and how many drugs act.

  How it works: Oxygen is more concentrated in the alveolus than the blood, so it diffuses in; CO2 is more concentrated in the blood, so it diffuses out. No energy is needed.

  Pearl: A thickened or fluid-filled membrane (e.g., pulmonary edema) slows diffusion and lowers oxygenation.

  Analogy: Perfume scent spreading across a room: it moves from where it is strong to where it is weak.

• Surfactant

  A soap-like substance lining the alveoli that reduces surface tension, keeping the tiny air sacs open on exhalation. It is key to normal breathing.

  How it works: Without surfactant, the liquid lining of each alveolus would pull the sac shut (like a wet balloon). Surfactant lowers this tension so small alveoli stay open.

  Common causes: Prematurity (deficient surfactant); ARDS

  Red flags: Neonatal breathing trouble

  Pearl: Preterm infants get surfactant replacement for respiratory distress syndrome - an underdeveloped lung cannot make enough.

  Analogy: Dish soap added to water - it stops the bubbles from collapsing on themselves.

• Loop of Henle

  The hairpin-shaped middle segment of the nephron that creates a concentration gradient in the kidney, allowing water reabsorption and concentrated urine.

  How it works: The descending limb lets water out; the ascending limb pumps salt out (and is impermeable to water). This 'countercurrent' arrangement builds a salt gradient in the kidney tissue that the collecting duct uses to pull water out.

  Common causes: Loop diuretics (like furosemide) act here

  Pearl: Loop diuretics block salt reabsorption in the ascending limb - which is why they are so powerful.

  Analogy: A hairpin tube where salt is pumped out along one side to create a strong gradient the rest of the system taps into.

• Distal convoluted tubule

  A nephron segment after the loop of Henle that adjusts salt reabsorption and calcium balance, and is a site for certain diuretics (thiazides).

  How it works: The DCT reabsorbs sodium and is a site where parathyroid hormone acts on calcium. Thiazide diuretics block sodium reabsorption here, increasing urine output.

  Pearl: Because thiazides work here (not in the loop), they cause a different electrolyte pattern than loop diuretics.

  Analogy: A fine-tuning station where salt and calcium levels get their last precise adjustment.

• Collecting duct

  The final nephron segment where antidiuretic hormone (ADH) controls water reabsorption and where acid is finally adjusted, deciding how concentrated and acidic the urine is.

  How it works: ADH makes the duct permeable to water, so water is pulled out by the surrounding gradient (concentrated urine). Meanwhile, cells here secrete hydrogen ions (via H+/K+ ATPase and ammonia) to excrete acid and regenerate bicarbonate.

  Common causes: ADH problems (diabetes insipidus, SIADH); Renal tubular acidosis

  Pearl: Without ADH, the duct stays impermeable to water and the patient produces large volumes of dilute urine.

  Analogy: The final gate: it decides how much water and acid to release in the urine.

• Antidiuretic hormone (ADH)

  A hormone released when the body is dehydrated that acts on the kidney's collecting duct to reabsorb water and concentrate urine, preserving body water.

  How it works: ADH makes the collecting duct permeable to water, so water leaves the urine and returns to the blood. Low ADH (diabetes insipidus) causes huge volumes of dilute urine; too much (SIADH) causes water retention and low sodium.

  Common causes: Dehydration (high ADH); Diabetes insipidus (low ADH); SIADH (too much)

  Pearl: ADH and thirst together are the body's main defense of water balance.

  Analogy: A dam operator who, when water runs low, decides how much to release downstream (to urine) versus hold back.

• Aldosterone

  A hormone that acts on the kidney to reabsorb sodium and excrete potassium, which pulls water with the sodium and raises blood pressure.

  How it works: Aldosterone makes kidney cells reabsorb sodium and secrete potassium, driven by the sodium-potassium pump and channels. Sodium retention pulls water in, expanding volume and raising pressure.

  Common causes: High: aldosteronism (hypertension, low potassium); Low: Addison's disease

  Red flags: Hypertension with low potassium

  Pearl: Aldosterone is a key target of blood-pressure drugs that block its action to reduce salt retention.

  Analogy: A supervisor ordering the kidney to hold onto salt; salt drags water with it, filling the tank.

• Preload

  The degree of stretch of the ventricular muscle at the end of filling, determined by how much blood returns to the heart. More stretch usually means a stronger squeeze (Frank-Starling).

  How it works: Up to a point, the more the muscle is stretched (higher preload), the more forcefully it contracts - like a stretched rubber band. Low volume reduces preload, so the pump does not fill and output falls.

  Common causes: Low: blood loss, dehydration; High: fluid overload, heart failure

  Pearl: This is why giving fluid to a volume-depleted patient helps - it restores preload so the pump can fill.

  Analogy: How full the balloon is before you squeeze it: a fuller balloon gives a stronger pop, up to a limit.

• Afterload

  The pressure the ventricle must overcome to push blood out. High afterload (like hypertension or a narrowed valve) makes the heart work harder to eject.

  How it works: The ventricle must generate enough pressure to open the valve and push blood into the aorta against systemic resistance. Raising afterload forces the heart to work harder for the same output.

  Common causes: Hypertension; Aortic stenosis; Vasoconstriction

  Pearl: Lowering afterload (vasodilators) eases the heart's workload - a key principle in heart-failure treatment.

  Analogy: Pedaling a bike uphill: the steepness of the hill is the afterload, and a flatter road eases the effort.

• Frank-Starling law

  The principle that the heart contracts more forcefully when its chambers are more filled before a beat, up to a physiological limit. It matches cardiac output to venous return.

  How it works: Greater preload stretches the muscle fibers, optimizing the overlap of the contracting proteins (actin and myosin) so the contraction is stronger and more blood is ejected.

  Pearl: This is why a healthy heart automatically balances the blood returning to it with what it pumps out.

  Analogy: A rubber band shot further the more you stretch it - but only up to its limit.

• Tension pneumothorax

  A life-threatening condition where air enters the chest and gets trapped, building pressure that collapses the lung and pushes the heart and major vessels, cutting off blood return.

  How it works: Air enters the pleural space on inspiration but cannot leave, so pressure keeps rising. This compresses the lung and, more dangerously, the vena cava and heart, dramatically dropping cardiac output and blood pressure.

  Common causes: Lung puncture (trauma); Ventilator pressure; Some procedures

  Red flags: Sudden breathlessness, chest pain; Low blood pressure; Absent breath sounds on one side; Shifted windpipe (very late)

  Pearl: This is a clinical (not imaging) emergency - a one-sided loss of breath sounds with hypotension after trauma warrants immediate decompression.

  Analogy: A one-way valve letting air in but not out: the tire (chest) inflates until it crushes everything around it.

• Acute coronary syndrome

  A group of conditions caused by sudden reduced blood flow to the heart muscle - unstable angina, and myocardial infarction (heart attack) with or without ST elevation.

  How it works: A plaque in a coronary artery ruptures and a clot forms, reducing or blocking flow. Muscle beyond the blockage becomes ischemic (chest pain) and can die (infarction). The ECG and troponin help classify it.

  Common causes: Atherosclerotic plaque rupture; Coronary spasm; Thrombosis

  Red flags: Crushing chest pain; Pain to arm/jaw; Sweating, breathlessness; ST changes on ECG

  Pearl: Time is muscle: the fastest, guideline-preferred reperfusion is primary percutaneous coronary intervention (PCI) when it can be delivered in time (door-to-device under about 90-120 minutes depending on the pathway). Fibrinolysis is reserved for settings where PCI would be delayed beyond the acceptable window and there is no contraindication.

  Analogy: A traffic accident blocking the main supply road to a factory - goods (oxygen) stop arriving and the factory starts failing.

• Diabetic ketoacidosis

  A serious complication of diabetes (most often type 1) in which, without enough insulin, the body breaks down fat for fuel, producing acidic ketones and causing a high-anion-gap metabolic acidosis.

  How it works: Lack of insulin → cells cannot use sugar → body burns fat → ketones (acids) accumulate → blood becomes acidic → the body hyperventilates (Kussmaul breathing) to blow off CO2. Water and potassium are also lost in the osmotic diuresis from high sugar.

  Common causes: Missed/inadequate insulin; Infection; Stress; New-onset diabetes

  Red flags: High blood sugar; Kussmaul breathing; Dehydration; Confusion

  Pearl: The treatment is insulin (to stop ketone production), fluids, and electrolyte (potassium) replacement - careful because potassium can drop as insulin works.

  Analogy: The body, unable to use its preferred fuel (sugar), burns fat and dumps harmful acidic byproducts into the blood.

• Sensitivity

  The proportion of truly diseased patients the test correctly identifies as positive (true positives / all with disease). A very sensitive test rarely misses disease, so a negative result helps rule it OUT.

  How it works: Sensitivity = TP / (TP + FN). A sensitive test rarely gives a false negative. Mnemonic: SnNOUT - a sensitive negative rules out.

  Pearl: Used to 'rule out' - a negative result on a highly sensitive test makes disease unlikely.

  Analogy: A metal detector that beeps on almost every real nail: it rarely lets a nail through (misses disease).

• Specificity

  The proportion of truly healthy people the test correctly identifies as negative (true negatives / all without disease). A very specific test rarely mislabels healthy people as diseased, so a positive result helps rule disease IN.

  How it works: Specificity = TN / (TN + FP). A specific test rarely gives a false positive. Mnemonic: SpPIN - a specific positive rules in.

  Pearl: Used to 'rule in' - a positive result on a highly specific test makes disease likely.

  Analogy: A key that only opens the intended lock, rarely opening the wrong door (few false positives).

• Pretest probability

  The estimated likelihood of the disease in a patient before a test result is known, based on the population, risk factors, and presentation. It determines how much the test actually changes your decision.

  How it works: The same sensitivity and specificity perform very differently at high vs low pretest probability. This is why screening an entire healthy population is different from testing a high-risk patient.

  Pearl: The value of a test depends on pretest probability - a perfect test applied where the disease is nearly absent still yields many false positives.

  Analogy: The base strength of a signal before you add noise: the same test 'signal' matters more or less depending on how strong the background is.

• Positive predictive value

  The proportion of positive test results that are true positives (how likely a positive result is correct). It rises with specificity and with pretest probability.

  How it works: PPV = TP / (TP + FP). Even a good test gives many false positives when the disease is rare.

  Pearl: PPV depends heavily on how common the disease is in the tested population.

  Analogy: Of all the alarms that ring, how many are real fires rather than false alarms.

• Negative predictive value

  The proportion of negative test results that are true negatives (how likely a negative result is correct). It rises with sensitivity and with how unlikely the disease already is.

  How it works: NPV = TN / (TN + FN). A negative result is more reassuring when disease was already unlikely.

  Pearl: A negative result on a sensitive test in a low-pretest patient is very reassuring.

  Analogy: Of all the 'all clear' signals, how many truly mean no fire.

• Likelihood ratio

  The factor by which a test result shifts pretest to posttest probability. A positive likelihood ratio (LR+) raises the odds of disease; a negative one (LR-) lowers it. Values far from 1 are more informative.

  How it works: LR+ = sensitivity / (1 - specificity); LR- = (1 - sensitivity) / specificity. Large LRs (>10) strongly raise the chance of disease; tiny ones (<0.1) strongly lower it.

  Pearl: Likelihood ratios let you update probability without needing disease prevalence, making them the most clinically portable summary of test performance.

  Analogy: A multiplier on a bet: a big multiplier (LR+ > 10) dramatically shifts the odds in favor of disease.

• CT scan

  An imaging method using rotating X-rays to build cross-sectional slices of the body. Fast and detailed, it is excellent for trauma, chest, abdomen, bleeding, and guiding procedures.

  How it works: A rotating X-ray tube scans the body and a computer reconstructs cross-sections. It uses ionizing radiation, so it is chosen for speed and detail when clinically needed.

  Red flags: Contrast (iodinated) is avoided where renal function is poor

  Pearl: Fast and anatomically detailed, at the cost of radiation.

  Analogy: Slicing a loaf digitally and reassembling the slices to see inside.

• MRI

  An imaging method using strong magnetic fields and radio waves to image soft tissue in fine detail, ideal for the brain, spinal cord, joints, and soft tissue.

  How it works: Uses a strong magnet to align protons, then radio pulses to create signals reconstructed as images. There is no ionizing radiation.

  Red flags: Screening for unsafe implants/ferromagnetic material before scanning; MR-conditional devices are allowed only under strict conditions (field strength/Tesla, SAR limits, specific device settings)

  Pearl: It is not simply 'no metal' - most modern implants are MR-conditional under defined conditions, but every patient is screened for safety.

  Analogy: Using magnetic alignment to photograph soft tissue in remarkable detail, like a high-res map of water-containing tissues.

• PET scan

  An imaging method that detects where cells are metabolically active, lighting up cancers, infections, and inflammation rather than just anatomy.

  How it works: A radioactive tracer (like glucose with a label) accumulates where metabolism is high, and the camera detects its emissions. High uptake = intense activity.

  Pearl: Shows function/activity, not just structure - invaluable for staging cancer and finding occult inflammation.

  Analogy: A heat map of the body showing where energy is being burned.

• CSF

  Cerebrospinal fluid bathes the brain and spinal cord, cushioning and nourishing them. It is sampled by lumbar puncture to diagnose meningitis, hemorrhage, inflammation, and CNS malignancy.

  How it works: Produced in the brain's ventricles, CSF circulates and is reabsorbed. Its cell count, protein, glucose, and pressure are diagnostic.

  Pearl: The lumbar puncture is the definitive test for meningitis - but never delay empiric antibiotics for it.

  Analogy: The cushioning 'bath' fluid around the brain that carries clues about what is happening inside.

• ANA

  An antibody that attacks the cell nucleus, found in most patients with systemic lupus (SLE) and some other autoimmune diseases. It is sensitive but not very specific.

  Reference: Reported as positive/negative, sometimes with a titer.

  How it works: The immune system in SLE produces antibodies against its own nuclear material. A positive ANA is sensitive for SLE but also occurs in healthy people, so it is a screen, not a diagnosis.

  Pearl: A positive ANA supports SLE but is not diagnostic on its own; specific antibodies (like anti-dsDNA) add certainty.

  Analogy: A broad screening beacon: it catches many autoimmune signals, but you still need a more specific detector to confirm.

• ANCA

  An antibody against white blood cells associated with ANCA-associated vasculitides, which inflame small blood vessels and often cause pulmonary-renal syndrome.

  How it works: These antibodies target proteins in neutrophils and are linked to small-vessel inflammation affecting the lungs and kidneys.

  Pearl: Positive ANCA supports an ANCA-associated vasculitis, which can present with hemoptysis plus kidney injury (pulmonary-renal syndrome).

  Analogy: A blood marker that fingerprints a specific family of vessel-inflaming diseases.

• DIC

  A dangerous condition in which widespread clotting consumes the clotting factors and platelets, then triggers bleeding. It complicates sepsis, trauma, obstetric emergencies, and malignancy.

  How it works: A massive trigger activates clotting throughout the small vessels, consuming platelets and coagulation factors while causing microclots that harm organs - then the depleted system bleeds.

  Common causes: Sepsis; Major trauma; Obstetric emergencies; Malignancy

  Red flags: Abnormal bleeding; Low platelets + prolonged clotting tests; Organ dysfunction

  Pearl: DIC causes simultaneous clotting (microthrombi) and bleeding - both problems at once.

  Analogy: A fire alarm that triggers every sprinkler until the water runs out, leaving you soaked but still burning.

• HELLP syndrome

  A serious hypertensive disorder of pregnancy characterized by hemolysis (red-cell breakdown), elevated liver enzymes, and a low platelet count, often related to preeclampsia.

  How it works: Related to preeclampsia, HELLP involves red-cell destruction, liver injury, and platelet consumption. It is an emergency and often warrants delivery.

  Common causes: Preeclampsia/eclampsia spectrum

  Red flags: Right upper abdominal pain; Headache; Hypertension; Nausea/vomiting in pregnancy

  Pearl: HELLP is a medical emergency in pregnancy - recognition and urgent (often delivery-based) management are critical.

  Analogy: The letters describe the three failing systems at once: blood, liver, and platelets.

• Wilson disease

  An autosomal-recessive disorder (caused by mutations in ATP7B) in which copper is not properly transported and accumulates in the liver and brain, causing hepatic and neuropsychiatric disease.

  How it works: A defective copper transporter prevents copper excretion into bile, so copper builds up. It can cause liver disease, movement disorders, psychiatric changes, and Kayser-Fleischer rings.

  Common causes: Inherited ATP7B mutations

  Red flags: Jaundice; Tremor/ataxia; Personality change; Psychiatric symptoms

  Pearl: Because psychiatric and subtle neurologic changes can be the first sign, copper metabolism should be considered in unexplained behavioral or liver disease in younger patients.

  Analogy: A recycling plant that cannot ship out copper, so the metal accumulates until it poisons the liver and brain.

• Hereditary angioedema

  A genetic disorder, often from C1-inhibitor deficiency, causing recurrent episodes of non-hive swelling (skin, abdomen, airway) that does not respond to allergy treatment.

  How it works: Lack of functional C1 inhibitor lets the immune system overproduce bradykinin, which leaks fluid into tissues and causes swelling. It can be life-threatening when it involves the airway.

  Common causes: C1-inhibitor gene mutations

  Red flags: Airway swelling; Abdominal pain with skin swelling; Non-responsive to antihistamines

  Pearl: HAE is often misdiagnosed as allergy; it does not respond to antihistamines or epinephrine and needs specific treatment.

  Analogy: A broken brake on the swelling pathway, so fluid keeps leaking into tissues in episodic waves.

• Carbon monoxide

  A toxic gas, from combustion (fires, heaters, exhaust), that binds hemoglobin far more tightly than oxygen, reducing oxygen delivery to tissues and causing hypoxia without a low SpO2 necessarily obvious.

  How it works: CO binds hemoglobin with much higher affinity than oxygen, displacing oxygen and shifting the oxygen-dissociation curve, starving tissues. Symptoms can improve rapidly when removed from the source.

  Common causes: Incomplete combustion; Household heaters; Fires; Vehicle exhaust

  Red flags: Headache, dizziness, confusion; Symptoms in multiple people in the same space; Rapid improvement away from the source

  Pearl: Symptoms that rapidly improve when leaving an enclosed space strongly suggest an acute inhalational exposure such as carbon monoxide, not a chronic toxin.

  Analogy: A thief who locks up your oxygen cargo so tightly that it cannot be delivered to the tissues.

• Shock

  A state in which organs do not receive enough oxygen because of low blood flow, low volume, vessel dilation, pump failure, or obstruction. The four broad types are hypovolemic, distributive, cardiogenic, and obstructive.

  How it works: Whatever the cause, shock ends in underperfusion of the brain, kidneys, and heart. Early signs include a fast heart rate and low pressure (MAP); advanced shock shows confusion and low urine output.

  Common causes: Volume loss; Sepsis/anaphylaxis; Heart failure; Obstruction

  Red flags: Confusion; Very low blood pressure; Low urine output; Cold or mottled skin

  Pearl: Recognize and treat shock early - compensated shock (fast pulse, normal-ish pressure) can become irreversible if missed.

  Analogy: A water-supply failure: whether the tank is empty, the pump is broken, or a pipe is blocked, the end result is dry fields (organs).

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