Hypertension

Clinical Orientation

A 52-year-old man comes for a routine physical. BP: 162/98. He feels fine. "I'm not worried, doc — I feel great." He doesn't understand why the nurse insists on rechecking, why they're talking about salt, and why they want him to come back in two weeks. "If it doesn't hurt, how can it be dangerous?" This chapter answers: What mechanism links hypertension to bedside findings, tests, red flags, and nursing priorities?

What Is Normal?

Blood pressure regulation: BP is the product of cardiac output and systemic vascular resistance. Short-term regulation: baroreceptors (carotid sinus, aortic arch) → medullary cardiovascular center → adjust SNS/PNS tone to vessels and heart. Long-term regulation: kidneys through pressure natriuresis (higher BP → more sodium/water excretion) and the RAAS.

Endothelial function: The endothelium is not just a passive lining — it actively regulates vascular tone by releasing nitric oxide (vasodilator), endothelin (vasoconstrictor), and other mediators. Healthy endothelium keeps vessels appropriately dilated and prevents platelet adhesion and inflammation.

BP classification (adults):

• Normal: <120/<80
• Elevated: 120-129/<80
• Stage 1 HTN: 130-139/80-89
• Stage 2 HTN: ≥140/≥90
• Hypertensive crisis: >180/>120 (urgency if no organ damage; emergency if organ damage present)

Verify current guidelines; these classifications evolve.

What Goes Wrong?

Primary (essential) hypertension: ~90-95% of cases. No single identifiable cause. Multifactorial: genetic predisposition + environmental factors (high sodium intake, obesity, physical inactivity, alcohol, stress). Mechanisms: increased SNS activity, RAAS overactivity, endothelial dysfunction with decreased nitric oxide, renal sodium retention resetting pressure natriuresis to a higher BP.

Secondary hypertension: Identifiable cause — renal artery stenosis, pheochromocytoma, primary hyperaldosteronism, Cushing syndrome, coarctation of the aorta, thyroid/parathyroid disease, sleep apnea, medications (NSAIDs, oral contraceptives, decongestants, steroids).

Why asymptomatic hypertension still matters: Chronic pressure elevation causes:

• Brain: Accelerated atherosclerosis → stroke, TIA. Weakened vessel walls → lacunar infarcts, microhemorrhages, aneurysm formation.
• Heart: Increased afterload → LV hypertrophy → increased oxygen demand + decreased subendocardial perfusion → ischemia, diastolic dysfunction, eventually systolic failure. Accelerated coronary atherosclerosis.
• Kidneys: Glomerular hypertension → hyperfiltration injury → proteinuria → progressive nephrosclerosis → CKD.
• Eyes: Hypertensive retinopathy → arteriolar narrowing, hemorrhages, exudates, papilledema.
• Vessels: Endothelial injury → accelerated atherosclerosis everywhere. Aortic aneurysm, dissection risk.

Causes and Risk Factors

• Nonmodifiable: Age, family history, African ancestry (higher prevalence, earlier onset, more severe), genetic factors.
• Modifiable: High sodium intake, low potassium intake, obesity, physical inactivity, excessive alcohol, stress, smoking.

What the Nurse May See

• Primary hypertension: Usually asymptomatic for years. This is why it's called the "silent killer."
• Target organ damage signs: LVH on ECG (tall R waves in left precordial leads, strain pattern), S4 gallop, retinopathy on fundoscopic exam, elevated creatinine/proteinuria.
• Hypertensive urgency: BP >180/>120 without acute organ damage. Headache, epistaxis, anxiety possible.
• Hypertensive emergency: BP >180/>120 WITH acute organ damage: encephalopathy (confusion, seizure, visual changes), acute heart failure/pulmonary edema, acute coronary syndrome, aortic dissection, acute kidney injury, papilledema.

Tests, Labs, and Monitoring

• Proper BP measurement: Patient seated, back supported, feet flat, arm at heart level, no talking, empty bladder, no caffeine/exercise/smoking for 30 min. Cuff size appropriate. Confirm with manual reading if automated reading is abnormal.
• Home BP monitoring: Avoids white-coat effect. Multiple readings over time are more reliable than clinic readings.
• Basic labs: BMP (renal function, potassium), lipid panel, glucose/HbA1c, urinalysis (proteinuria).
• ECG and echocardiogram: Assess for LVH and diastolic dysfunction.
• Retinal exam: Assess for hypertensive retinopathy.

Nursing Priorities

1. Accurate BP measurement: Proper technique — incorrect technique causes misdiagnosis and inappropriate treatment.
2. Assess for target organ damage: Fundoscopic exam findings, renal function, LVH on ECG, neurologic changes.
3. Patient education for lifestyle modification: DASH diet (rich in fruits, vegetables, low-fat dairy; low in saturated fat and sodium), sodium restriction (<2300 mg/day, ideally <1500 mg), weight loss, regular physical activity, alcohol moderation, smoking cessation.
4. Medication adherence: HTN medications cause few perceptible benefits (patient feels fine without them) but have perceptible side effects. Teach the long-term risk picture. Monitor adherence.
5. Recognize hypertensive emergency: BP >180/>120 with confusion, chest pain, dyspnea, or acute renal failure → immediate provider notification.

Red Flags

Common Student Mistakes

1. Assuming asymptomatic = not dangerous: HTN causes damage silently over years. Lack of symptoms does NOT equal lack of harm.
2. Treating the number instead of the patient: An asymptomatic patient with chronic BP 170/95 should have medication adjusted gradually, not dropped to 120/80 in hours (risk of cerebral hypoperfusion). A patient with acute stroke and BP 190/110 may need permissive hypertension (to perfuse the penumbra) rather than aggressive lowering.