📋 Clinical Guideline · Assessment & Management of Hypertension

PART 1 Initial Assessment (The "Physiological Triage")

When a patient presents with elevated BP, our goal is to answer three questions:

• 1. Is this a crisis (immediate danger)?
• 2. Is this primary (essential) or secondary (fixable cause)?
• 3. What is the hemodynamic phenotype (High CO, High TPR, or High Volume)?

Step 1: Confirm the Diagnosis

• Do not treat based on one reading. Take 2–3 readings, 1–2 minutes apart, patient seated, back supported, feet flat.
• Confirm with Ambulatory Blood Pressure Monitoring (ABPM) or home readings if clinic BP is high (rule out "White Coat" hypertension).

Step 2: Rule out Hypertensive Emergency (The "Crisis" Triage)

• Check for target organ damage (TOD): chest pain, dyspnea, neurological changes, back pain (aortic dissection).
• Exam: fundi for hemorrhages/papilledema, lungs for crackles, check pulses.
• If TOD is present: Hypertensive Emergency. Lower BP by 20–25% within the first hour using IV agents (Labetalol, Nicardipine). Do NOT drop to normal immediately — risk of cerebral/renal ischemia.

PART 2 Identifying the Physiological Phenotype

Using our cheat sheet, we clinically predict the underlying hemodynamic driver:

Clinical Clue	Physiological Prediction	Likely Etiology
BP High + HR Fast (>85)	High Cardiac Output (Sympathetic drive)	Hyperthyroidism, Anemia, Pain/Anxiety, Pheochromocytoma
BP High + HR Normal/Slow	High TPR or High Volume	Essential HTN, Renal Artery Stenosis, Hyperaldosteronism
Wide Pulse Pressure (e.g., 180/70)	Stiff, non-compliant arteries (loss of elastin)	Isolated Systolic HTN (Aging / Arteriosclerosis)
Narrow Pulse Pressure (e.g., 130/110)	High diastolic resistance + low SV	Severe aortic stenosis or pericardial disease
Edema + Bounding Pulses	High Preload / Hypervolemia	Heart Failure, Kidney Failure, Primary Aldosteronism

Step 3: Basic Laboratory & Imaging Workup

• Blood: Basic Metabolic Panel (Creatinine/eGFR, Na, K), Fasting Glucose, Lipid Panel.
• Urine: Urinalysis (proteinuria suggests kidney damage).
• ECG: Check for LVH or ischemia.
• If secondary HTN suspected (young <30 or resistant):
  • High K⁺ + High BP → CKD or Renal Artery Stenosis.
  • Low K⁺ + High BP → Primary Aldosteronism (Conn's) → Aldosterone/Renin Ratio (ARR).
  • Episodic spikes + Sweating/Pallor → Pheochromocytoma → 24h urine Metanephrines.
  • Cushingoid features → 24h urine Cortisol.

PART 3 Non-Pharmacological Management (The "Physiological Reset")

Intervention	Physiological Target	Expected BP Reduction
Dietary Sodium Restriction (< 2g/day)	Reduces extracellular volume, unloads Na/K pump	~5–10 mmHg
DASH Diet (Fruits/Vegetables/Low Fat)	↑ K⁺, ↑ NO, reduces oxidative stress	~10–12 mmHg
Weight Loss (BMI < 25)	Reduces sympathetic tone, leptin-mediated outflow	~5–20 mmHg
Aerobic Exercise (150 min/week)	↑ shear stress → NO release, lowers resting HR	~5–8 mmHg
Alcohol Moderation	Reduces sympathetic activation and volume	~4 mmHg

PART 4 Pharmacological Management — Matching Drugs to Physiology

First-line agents (the "Big Four") and their physiological targets:

Drug Class	Physiological Target	Best For (Phenotype)	Mechanism
Thiazide Diuretic (Chlorthalidone)	Volume / Preload	Elderly, Edema, Heart Failure, High Salt	Reduces blood volume, lowers CO, restores Na/K pump
ACE Inhibitor (Lisinopril)	RAAS / TPR	Younger, Diabetics, CKD, High Angiotensinogen	Blocks Ang II → dilates arterioles, reduces aldosterone
ARB (Losartan)	RAAS / TPR	Same as ACEi (for cough intolerance)	Blocks AT1 receptor → prevents SR calcium release
Calcium Channel Blocker (Amlodipine)	Vascular Smooth Muscle / TPR	Isolated Systolic HTN, Black patients, Low-renin	Blocks VGCC → prevents calcium influx, relaxes arteriole
Beta-Blocker (Metoprolol)	Cardiac Output / HR	High HR, Angina, Heart Failure, Post-MI	Reduces HR and contractility → lowers CO

Stepwise Treatment Algorithm

PART 5 Special Circumstances

Condition	Physiological Quirk	Best Management
Chronic Kidney Disease (CKD)	Failing kidneys → volume overload	ACEi/ARB (renal protection) + Diuretic (Furosemide)
Diabetes Mellitus	Hyperglycemia damages endothelium, destroys NO; insulin resistance raises sympathetic tone	ACEi/ARB (first-line to reduce proteinuria) + CCB
Elderly (>65)	Aorta stiff (loss of elastin), wide pulse pressure	CCB (Amlodipine) or Diuretic (Chlorthalidone). Avoid Beta-blockers.
Pregnancy	Increased volume, but resistance drops; preeclampsia driven by placental factors	Methyldopa or Labetalol. AVOID ACEi/ARBs (fetal renal agenesis).
African-American Patients	Genetically low-renin, salt-sensitive	CCB or Diuretic are superior first-line compared to ACEi alone.

PART 6 Monitoring & Goal Targets

• General Goal: < 130/80 mmHg (ACC/AHA 2017) for most adults.
• Elderly (>65): Aim < 130/80 if tolerated, but avoid diastolic < 60 (compromises coronary filling).
• CKD/Diabetes: < 130/80 mmHg.

📋 The Final Physiological Cheat Sheet (Clinical Summary)

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