Diagnostic-flowchart

Diagnostic Flowchart · Hypertension Phenotypes

🧩 The "Systemic Approach" Diagnostic Flowchart

Use the cheat sheet to predict which physiological “gear” has broken — and which drug will work.

Since hypertension is a disease of faulty regulation, you can work backward from the equation MAP = CO × TPR and the regulatory systems to predict the underlying cause.

Here is how a physician uses that cheat sheet as a diagnostic flowchart.

STEP 1

Is it High Cardiac Output (CO) or High Resistance (TPR)?

Check Pulse Pressure (Systolic – Diastolic) and Heart Rate.

▶ Prediction: If CO is high, pulse pressure will be wide (e.g., 180/70), and HR is often fast.

Possible cause Hyperdynamic circulation (anemia, hyperthyroidism, fever, severe anxiety / sympathetic overdrive). The heart pumps too much blood too fast.

▶ Prediction: If TPR is high, diastolic pressure is particularly elevated (e.g., 160/105), and HR is often normal or slow.

Possible cause Vascular resistance issues (essential hypertension, renal artery stenosis, endothelial dysfunction). The “faucets” are stuck closed.

STEP 2

Check the Kidneys (Volume / RAAS Axis)

Ask: Is the patient’s RAAS system inappropriately turned on, or are they volume-overloaded?

▶ Prediction: Bilateral leg edema, bounding pulse, hypertension hard to control → Volume-Expanded.

Possible cause Hyperaldosteronism (Primary Aldosteronism) – adrenal gland dumps aldosterone → kidneys hoard salt and water. OR Chronic Kidney Disease – kidneys can’t excrete daily salt load → raise BP to force diuresis (pressure-natriuresis).

▶ Prediction: Sudden, severe hypertension (through the roof) with normal volume, and you hear a bruit (whooshing) over the upper abdomen.

Possible cause Renal Artery Stenosis – blocked kidney artery. Kidney thinks the whole body has low pressure → floods system with Angiotensin II to raise systemic BP, sacrificing the rest of the body to save the single kidney.

STEP 3

Check the Sympathetic Nervous System (“Fight or Flight” Axis)

Ask: Is this patient’s autonomic nervous system stuck in “overdrive”?

▶ Prediction: Labile (wildly fluctuating) BP, tachycardia (resting HR > 90), sweaty palms, dilated pupils.

Possible cause Pheochromocytoma – rare tumor of adrenal medulla that dumps massive surges of epinephrine/norepinephrine.

▶ Prediction: Obese, thick neck, snores loudly, BP high primarily in the morning.

Possible cause Obstructive Sleep Apnea (OSA) – nocturnal hypoxia triggers massive sympathetic bursts to wake the brain, driving chronic sympathetic overactivity.

STEP 4

Check the Endothelium (The “Relaxer” Axis)

Ask: Is this patient missing their natural vasodilators?

▶ Prediction: Isolated systolic hypertension (high top number, normal bottom, e.g., 170/78), especially in elderly.

Possible cause Aortic Stiffness (Arteriosclerosis). Elastin breaks down, collagen takes over. Aorta loses “Windkessel” (shock-absorbing) effect. Endothelium can’t release enough NO to relax the stiff pipe. The heart pumps, and the stiff aorta blows up the pressure like a drum — mechanical cause, not hormonal.

STEP 5

The “Great Mimicker” – Secondary Causes

If the patient is young (< 30 years) and suddenly develops severe hypertension, your cheat sheet says it cannot be “essential” (idiopathic) — that takes decades of vascular remodeling.

▶ Prediction: Look for a single, fixable lesion.

Coarctation of the Aorta: congenital narrowing. Arms have sky-high BP, but legs have weak pulses & low BP (check femoral pulses!).
Cushing's Syndrome: excess cortisol mimics aldosterone → volume expansion & high BP. Look for “moon face” and purple stretch marks.

🔮 The Clinical “Crystal Ball” Prediction

Once you identify the physiological gear that is broken, you can predict exactly which drug will work without even trying others:

Broken Gear (Prediction)	Drug Class that Targets It
High Volume / RAAS overactivity	Diuretic (gets rid of salt) or ACEi/ARB (blocks Angiotensin II)
High Sympathetic Tone / High HR	Beta-Blocker (slows heart & reduces sympathetic output)
High TPR / Stiff Vessels	Calcium Channel Blocker (CCB) (dilates arterioles & overrides myogenic reflex)
High Aldosterone (Edema + low K⁺)	Spironolactone (blocks aldosterone receptor directly)

🧬 The ultimate physiological prediction:

• If you give a patient with high TPR (diastolic hypertension) a Beta-Blocker, you will slow their heart, but their BP won’t drop much because the resistance is in the vessels, not the rate.
• Conversely, if you give a patient with high CO (wide pulse pressure, anxiety-driven) a Calcium Channel Blocker, their BP will drop, but they will get severe swelling (edema) and headaches — because you dilated vessels that didn’t need dilating, causing fluid to leak out.

✅ Using the cheat sheet, you don’t just treat “high numbers.” You predict the hemodynamic phenotype.

physiology · hypertension · clinical reasoning