Hypertension

• Symptoms of hypertensive crisis include headache, dizziness, nausea, vomiting, visual disturbances, chest pain, shortness of breath, seizures, confusion, and stroke-like symptoms.
• Hypertensive crisis is defined as BP >180/120 mmHg with symptoms or target organ damage
• The goal of treatment for hypertensive emergencies is to lower blood pressure by 25% within the first hour and then gradually over several hours.
• Malignant hypertension is characterized by severe elevation of blood pressure (BP) associated with end-organ dysfunction such as retinopathy, encephalopathy, cardiac failure, renal insufficiency, and pulmonary edema.
• The pathophysiology of malignant hypertension involves the activation of the renin-angiotensin system leading to vasoconstriction, increased sodium and water retention, and decreased glomerular filtration rate.
• Treatment options for malignant hypertension include intravenous antihypertensive medications, diuretics, and supportive care measures.
• Treatment options for malignant hypertension include intravenous antihypertensives like sodium nitroprusside, labetalol, nicardipine, hydralazine, and phentolamine.
• In malignant hypertension, there are no specific diagnostic criteria but it can be diagnosed based on clinical features.
• Oral medications used for treating hypertension include diuretics, ACE inhibitors, ARBs, calcium channel blockers, beta-blockers, alpha-blockers, and vasodilators.
• Diuretics are also commonly used in the management of malignant hypertension to reduce preload and decrease peripheral resistance.
• Supportive care measures may be necessary in patients with malignant hypertension, including oxygen therapy, monitoring of vital signs, electrolyte balance, and close observation for complications.
• Diuretics are used to reduce preload and decrease peripheral resistance.
• ACE inhibitors work by blocking angiotensin converting enzyme, reducing peripheral resistance, and increasing urinary excretion of salt and water.
• ARBs prevent binding of angiotensin II to AT1 receptors, resulting in reduced aldosterone secretion and improved endothelial function.
• Calcium channel blockers reduce vascular smooth muscle contraction and decrease peripheral resistance.