Description
Approaching hypertensive emergencies requires swift action to prevent life-threatening complications. The first step involves assessing the severity of hypertension, including signs of end-organ damage such as headache, blurred vision, chest pain, or altered mental status. In severe cases, immediate reduction of blood pressure is necessary to prevent complications such as stroke, heart attack, or organ failure. Intravenous medications such as nitroprusside, labetalol, or nicardipine are commonly used for rapid blood pressure control in a controlled setting. Continuous monitoring of blood pressure, cardiac function, and organ perfusion is essential during treatment. Additionally, identifying and addressing underlying causes such as renal artery stenosis or preeclampsia is crucial for long-term management. Collaborative care involving emergency medicine, cardiology, and nephrology specialists ensures comprehensive management and follow-up care for patients with hypertensive emergencies. Regular monitoring and adjustment of antihypertensive medications are necessary to prevent recurrence and optimize long-term blood pressure control.
Résumé
- Hypertensive emergencies are defined by significantly elevated blood pressure (systolic ≥ 180 and/or diastolic ≥ 120) accompanied by signs and symptoms of acute target organ damage. Initial assessment involves checking for traumatic brain injuries, neurological symptoms, chest discomfort, back pain, dyspnea, or pregnancy, along with potential drug use. Common workups include ECG, chest x-ray, urine analysis, serum electrolytes, cardiac biomarkers, and brain imaging.
- Blood pressure lowering should be gradual, aiming for a 10-20% reduction in mean arterial pressure in the first hour, followed by a further 5-15% reduction over the next 23 hours. Exceptions to this rule include acute ischemic stroke, aortic dissection, and intracerebral hemorrhage. For patients undergoing thrombolysis for acute ischemic stroke, blood pressure should be maintained below 180/105 mmHg, and monitoring is crucial.
- In acute aortic dissection, the target is to maintain a heart rate less than 60 bpm and systolic BP around 100-120 mmHg. Esmolol or labetalol are commonly used, followed by sodium nitroprusside if systolic BP remains elevated after heart rate control. Vasodilator therapy shouldn't be used without first controlling heart rate.
- For intracerebral hemorrhage patients with systolic BP between 150-220 mmHg, gradual lowering to a target of 140 mmHg is suggested within the first hour. Those with systolic BP > 220 mmHg require rapid lowering to a target range of 140-160 mmHg. Nitrous oxide and nitrates are typically avoided as they can increase intracranial pressure.
- In acute cardiogenic pulmonary edema or acute coronary syndrome, diuretics and vasodilators like nitroglycerin are favored. Drugs that increase cardiac work, such as hydralazine, or those that acutely decrease contractility, like labetalol, should be avoided. If hydralazine is used, the goal is volume reduction and improved pulmonary edema.
- Several drug options for hypertensive emergencies were discussed, including nitroprusside, nitroglycerin, clevidipine, nicardipine, fenoldopam, esmolol, labetalol, and hydralazine. Nitropusside carries a risk of cyanide toxicity, while nitroglycerin has less anti-hypertensive efficacy but can be useful in patients with CAD. Clevidipine and nicardipine (though not always available) reduce blood pressure without affecting cardiac filling pressures, with specific cautions regarding arotic stenosis and lipid metabolism disorders. Beta-blockers are avoided in asthma, COPD, and heart failure and should be administered only after adequate Alpha blockade in hyperadrenergic states.
- Aortic dissection classification includes DeBakey and Stanford systems, which have slight differences in categories but determine approach and management.
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