Hypertension | Clinical Medicine

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Hypertension is presented as a central concept in clinical medicine, underscoring its significance in understanding high blood pressure. The discussion pairs the clinical topic with a range of educational resources, including courses, comprehensive notes, and illustrative materials. Enhanced study aids and supplementary merchandise are available to support deeper learning and preparation.

Vessel Remodeling Fuels Elevated Resistance Essential hypertension predominantly arises from structural alterations in blood vessels that reduce their diameter. Aging, smoking, diabetes, and stress contribute to the thickening of arterial walls, which increases systemic vascular resistance. Enhanced sympathetic tone further narrows vessels through vasoconstriction, directly driving blood pressure upward.

Sodium Retention Boosts Cardiac Output and Pressure A high sodium intake challenges the kidneys, leading to excess sodium and water retention that increases blood volume. This rise in volume elevates preload and stroke volume, thereby boosting cardiac output. The combined effects of increased cardiac output and vascular resistance culminate in higher blood pressure, with obesity and genetic factors adding to the risk.

Refractory Hypertension in Young Adults Patients aged 25 to 55 can present with blood pressure that remains uncontrollably high despite treatment with three or more medications. An unyielding, refractory pattern is a clear signal of an underlying secondary process rather than essential hypertension. This clinical profile demands a thorough search for hidden causes driving the elevated pressure.

Renal and Endocrine Mechanisms Driving Elevated Pressure Renal disorders such as chronic kidney disease and renal artery stenosis disturb normal filtration, triggering an overactive renin-angiotensin-aldosterone system that promotes sodium retention and vasoconstriction. Thyroid imbalances affect cardiac output by causing either systolic spikes or diastolic increases in blood pressure. Adrenal hyperactivity—from hyperaldosteronism, Cushing syndrome, or pheochromocytoma—further intensifies the hypertension.

Neurological, Aortic, and Pregnancy-Associated Hypertension Neurological events that elevate intracranial pressure precipitate a triad marked by high blood pressure, slowed heart rate, and irregular respirations. Aortic coarctation creates a stark contrast, with markedly high pressures proximal to the narrowing and reduced flow distally. In pregnancy, placental ischemia leads to the release of vasoactive substances, resulting in proteinuria, edema, and the severe hypertension seen in preeclampsia.

Sympathomimetic and Sleep Apnea-Triggered Hypertension Certain drugs—such as cocaine, amphetamines, and PCP—drive a surge in sympathetic activity that sharply elevates blood pressure. Episodes of sleep apnea cause intermittent oxygen desaturation, which in turn induces a persistent sympathetic response and systemic vasoconstriction. Both drug-induced stimulation and disrupted breathing patterns contribute significantly to the development of refractory hypertension.

Normal blood pressure is defined as below 120 systolic and 80 diastolic, with levels rising into pre-hypertensive ranges between 120 and 130 systolic. Blood pressure readings between 130/80 and 140/90 indicate stage one hypertension, while values above 140/90 signify stage two, warranting closer medical intervention. Repeat elevated readings, especially when exceeding 180 systolic or 120 diastolic, raise immediate concerns, prompting the use of antihypertensive medications. A crucial distinction is made between hypertensive urgency, which lacks target organ damage, and hypertensive emergency, where organ damage is present, necessitating rapid action.

Hypertension Forces Cardiac Remodeling Sustained high blood pressure increases the workload on the left ventricle by raising afterload, which leads to ventricular thickening and reduced chamber filling. This remodeling process hampers effective blood entry into the heart and decreases cardiac output, eventually triggering diastolic heart failure with preserved ejection fraction. In acute scenarios, the severe pressure burden can suddenly impair blood ejection, resulting in flash pulmonary edema.

Hypertension Drives Atherosclerotic and Aortic Catastrophes Chronic hypertension initiates and accelerates atherosclerosis by fostering plaque formation in coronary and peripheral arteries, thereby diminishing oxygen delivery to tissues. Reduced perfusion can precipitate myocardial ischemia, coronary artery disease, and even myocardial infarction when a plaque rupture nearly occludes a vessel. Additionally, excessive shear forces from elevated blood pressure compromise the integrity of the aortic wall, leading to potentially fatal dissections or aneurysms, especially in the abdominal region.

Plaque buildup in the vessels supplying the brain narrows the vessel lumen, reducing blood flow and provoking transient ischemic events. Narrowing at critical junctions like the carotid bifurcation or blockages in major arteries can lead to reduced oxygen delivery, resulting in tissue ischemia and cerebrovascular accidents. Excessive blood pressure may cause the compromised vessels to rupture, forming aneurysms that burst in life-threatening intracerebral or subarachnoid hemorrhages.

Excessive blood pressure forces a high volume of blood through the renal circuit, elevating the glomerular filtration rate and stressing the kidney’s filtering system. The afferent arteriole thickens and undergoes sclerosis, which reduces blood flow to multiple regions of the glomerulus and triggers ischemia. This ischemic process damages kidney cells, potentially leading to an abrupt acute kidney injury or a progressive chronic kidney disease, with high pressure sometimes rupturing vessels to cause blood in the urine. Hypertension, along with diabetes, stands out as a primary risk factor for these renal complications.

Chronic high blood pressure initiates a process in retinal vessels where initial sclerosis reduces oxygen supply, manifesting as subtle AV nicking. Continued elevation in pressure leads to small hemorrhages and the development of microaneurysms alongside cotton wool spots. In acute settings, severe vessel damage results in extensive edema and blurred optic discs, known as papilledema, signaling a hypertensive emergency and target organ damage.

The approach starts by measuring blood pressure in both arms to avoid missing conditions like aortic dissection or subclavian stenosis. Consistently high readings over multiple office visits confirm hypertension, while rechecking within one to four weeks helps differentiate stage severity. Ambulatory blood pressure monitoring distinguishes true hypertension from white coat effects, and blood pressures over 180/120 prompt evaluation for urgency or emergency based on the presence of target organ damage.

Managing chronic hypertension starts with rigorous lifestyle adjustments—weight loss, following the DASH diet, regular exercise, and reduced sodium and alcohol intake. For those with blood pressures in the pre-hypertensive or stage one range, continuing these modifications is essential, with antihypertensive medications introduced when cardiovascular risk is elevated. When blood pressure consistently exceeds 140/90, immediate pharmacologic treatment becomes critical alongside lifestyle measures. First-line drugs include ACE inhibitors, ARBs, thiazides, or calcium channel blockers, with the latter offering additional benefits for African-Americans due to low renin hypertension.

Antihypertensive selection is optimized by carefully matching drug profiles with patient comorbidities. Beta blockers, ACE inhibitors, and ARBs play a central role in managing myocardial infarction and heart failure, while beta blockers, calcium channel blockers, and nitrates are used to address coronary artery disease and associated angina. In cases of atrial fibrillation, beta blockers and calcium channel blockers are preferred, and diabetic patients with CKD benefit from ACE inhibitors or ARBs due to their renal protective effects. Pregnancy-related hypertension is managed safely with options like nifedipine, hydralazine, labetalol, and methyldopa, with thiazides and alpha blockers offering additional support in osteoporosis and BPH, respectively.

Managing blood pressure above 180/120 requires an immediate evaluation for target organ damage such as neurological deficits, chest pain, pulmonary edema, aortic complications, or kidney injury. If no complications are found, a gradual reduction to below 160/100 with oral medications over one to two days is essential to prevent ischemia from abrupt drops. In cases with organ damage, mean arterial pressure is carefully reduced by approximately 25% in the first one to two hours using IV agents like nicardipine, hydralazine, or labetalol, followed by further controlled adjustments. It is crucial to avoid rapid reductions and certain treatments in patients with gout due to the risk of hyperuricemia.

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