Hypertension

Hypertension can be classified into various stages based on blood pressure readings: normal (<120/<80), elevated (120-129/<80), stage 1 (130-139/80-89), and stage 2 (≥140/≥90). Primary hypertension, formerly known as essential hypertension, accounts for over 90% of cases. The mean arterial pressure (MAP) is calculated by the formula SV x HR x SVR, where SV stands for stroke volume, HR for heart rate, and SVR for systemic vascular resistance. Short-term blood pressure control involves peripheral baroreceptors in the carotid and aortic arch which modulate sympathetics to regulate HR, SVR, and SV. Renin plays a crucial role in short-term BP control, converting to ATII that regulates SVR, leading to aldosterone production which, in turn, manages body volume and stroke volume. Long-term control is managed by pressure natriuresis.

The pathogenesis of primary hypertension involves mechanisms such as impaired natriuresis due to kidney dysfunction, which leads to increased sodium reabsorption. This impaired function causes the blood pressure to rise until salt and water excretion returns to normal levels. Another contributing factor is chronic sympathetic activity that also promotes sodium retention at the nephron, leading to similar effects. Risk factors for primary hypertension include age, high sodium intake, excessive alcohol consumption, obesity, sedentary lifestyle, and family history. Black patients have a heightened risk, with hypertension presenting earlier and more severely. In the elderly, hypertension frequently manifests as isolated systolic hypertension due to decreased arterial compliance. This reduction in compliance is attributed to the accumulation of collagen and calcium in the arterial walls, as well as degraded elastin. This condition in the elderly is often associated with an increased pulse pressure, marked by a rise in systolic and a drop in diastolic pressures.

Secondary hypertension is considerably less common than primary hypertension and arises from specific causes. It can result from conditions such as renovascular hypertension, fibromuscular dysplasia, obstructive sleep apnea, and hyperaldosteronism, as well as acute or chronic kidney disease. Several drugs, including OCPs, NSAIDs, corticosteroids, and stimulants like cocaine/meth, can also induce secondary hypertension.

Renovascular hypertension is a form of secondary hypertension initiated by stenosis of the renal artery, which reduces renal perfusion. This triggers increased renin secretion from the juxtaglomerular apparatus (JGA), leading to elevated levels of angiotensin II (ATII) that promote vasoconstriction, and aldosterone which causes volume retention. A prevalent cause of this condition is atherosclerosis of the renal artery.

Fibromuscular dysplasia, predominantly seen in women, involves collagen deposition and smooth muscle hyperplasia in the renal artery. This leads to reduced renal perfusion and elevated RAAS activity. A hallmark of this condition is the 'string of beads' appearance of the renal artery, resulting from fibromuscular hyperplasia interspersed with regions of aneurysm. Many patients with fibromuscular dysplasia also manifest carotid involvement, which can present as headache, tinnitus, and an increased risk of TIA and strokes. Clinically, bruits may be heard on auscultation, indicative of turbulent flow, in both renal arteries and carotids, a tell-tale sign of renovascular hypertension or fibromuscular dysplasia. Additionally, a poorly perfused kidney may atrophy, leading to asymmetric kidney sizes. Regarding treatment, patients with renovascular hypertension and fibromuscular dysplasia might experience an adverse reaction to ACE therapy. They rely on ATII to constrict the efferent arterioles to preserve glomerular filtration rate (GFR).

Hyperaldosteronism, due to excessive mineralocorticoid activity, can lead to salt and water retention, causing secondary hypertension accompanied by hypokalemia. Obstructive sleep apnea is also associated with secondary hypertension.

Chronic hypertension can lead to multiple complications. In the heart, it results in concentric hypertrophy due to increased afterload, progressing to heart failure. Furthermore, it is associated with aortic dissection, and the damage it inflicts on the endothelium can hasten the development of atherosclerosis. The vessel walls also weaken, becoming susceptible to aortic aneurysms. In the brain, chronic hypertension escalates the risk of cerebrovascular accidents, including both ischemic and hemorrhagic strokes. In the eyes,retinopathy characterized by retinal hemorrhages and exudates, and papilledema can manifest. The kidneys are also targeted, leading to nephrosclerosis & glomerulosclerosis, which in turn aggravates chronic kidney disease (CKD) and worsens the hypertension in a vicious cycle.

Chronic hypertension can result in two key histological changes in vessels. The first is hyaline arteriolosclerosis, characterized by hyaline deposition in the vessel wall. This arises from endothelial damage and the subsequent leak of plasma proteins into the media, thickening the vessel walls and causing luminal narrowing. A related complication in the kidneys is glomerulosclerosis, where hyaline damages the glomerular capillaries. The second change, typically seen in chronic severe hypertension or hypertensive emergencies, is hyperplastic arteriolosclerosis. Here, smooth muscle hypertrophy, basement membrane replication, and concentric thickening provide the vessel walls with an ‘onion skin’ appearance. Acute hypertensive emergencies can also trigger fibrinoid necrosis of the vessel wall. Histologically, this translates to an accumulation of necrotic debris and fibrin (visible as pink) in the vessel wall, accompanied by an inflammatory infiltrate, and often culminating in luminal narrowing or obliterating.

Emergency conditions are pivotal in hypertension management. Hypertensive urgency is marked by a BP >180/120 but without end-organ damage. In contrast, hypertensive emergency also presents with a BP >180/120 but is compounded by end-organ damage, manifesting as symptoms such as encephalopathy, AKI, intracranial hemorrhage (ICH), papilledema, pulmonary edema, and heart failure.