Hypertensive Emergencies and Target Organ Damage!
Hypertensive emergencies are defined as a major sudden elevation in blood pressure (BP) associated with progressive and acute target-organ dysfunction. They are true medical emergencies requiring prompt treatment to reduce BP. The pathophysiology of hypertensive emergencies is not well understood. Failure of normal autoregulation and an abrupt rise in systemic vascular resistance (SVR) are typically the initial steps in the disease process. Increases in SVR are thought to occur from the release of humoral vasoconstrictors from the wall of a stressed vessel. The increased pressure within the vessel then starts a cycle of endothelial damage, local intravascular activation of the clotting cascade, fibrinoid necrosis of small blood vessels, and the release of more vasoconstrictors. If the process is not stopped, a cycle of further vascular injury, tissue ischemia, and autoregulatory dysfunction ensues.
@sampurno The clinical presentation is easily classified according to the target organ involved. Single-organ involvement is found in approximately 83% of patients presenting with hypertensive emergencies. Two-organ involvement is found in 14% of patients, and multiorgan involvement (>3 organ systems) is found in approximately 3% of patients presenting with a hypertensive emergency. During hypertensive emergencies, the left ventricle is unable to compensate for an acute rise in SVR. This leads to left ventricular failure and pulmonary edema or myocardial ischemia. Chronic hypertension increases arterial stiffness, increases systolic BP, and widens pulse pressures. These factors decrease coronary perfusion pressures, increase myocardial oxygen consumption, and lead to the development of left ventricular hypertrophy (LVH). In LVH, the myocardium undergoes structural changes in response to increased afterload. Cardiac myocytes respond with hypertrophy, allowing the heart to pump more strongly against the elevated pressure. However, the contractile function of the left ventricle remains normal until later stages. Eventually, LVH reduces the chamber lumen, limiting diastolic filling and stroke volume. The left ventricular diastolic function is markedly compromised in long-standing hypertension.