Summary

This document discusses hypertensive crisis. It provides an overview of primary and secondary hypertension, risk factors, and potential causes. It also explains the difference between hypertensive urgency and emergency. The document also details target organ damage and treatment options.

Full Transcript

No definitive cause autoregulatory( Baroreceptors...

No definitive cause autoregulatory( Baroreceptors Chemoreceptors) failure Primary (Essential) Hypertension renal ischemia Triggers RAAS system, increases total renal hypertension peripheral resistance (TPR) and Na+ water retention Possible mechanisms Hormonal hypertension Increased catecholamines Increased HR Increased sympathetic Increased contractility Hypertension activity Increased SVR heredity Has an identified cause Secondary Hypertension pheochromocytoma, Cushing's syndrome, renal dysfunction/disease, pregnancy, preeclampsia/eclampsia Similar to cardiovascular disease risk factors: diabetes, smoking, obesity, alcohol, Risk Factors caffeine, stress, multiple antihypertensives Elevated blood pressure that can lead to acute organ damage if not reduced Definition Typically associated with diastolic BP >120- 130 mmHg and systolic >180 mmHg Urgency: Elevated BP without signs of target organ damage Hypertensive Urgency vs. Hypertensive Emergency Emergency: Elevated BP with signs of target organ damage (e.g., headache, blurred vision, shortness of breath, chest pain) Not well understood in primary hypertension Likely involves dysregulation of RAAS, Pathophysiology inflammation, and genetic factors Patients without a history of hypertension Hypertensive Crisis are at higher risk of worse outcomes Lack hypertrophied smooth muscle (which has protective effect) Exacerbation of any condition causing hypertension Causes Renal disease/dysfunction, rebound hypertension, illicit drug use, certain medications Headache, visual disturbances, dizziness, vomiting, papilledema, epistaxis, dyspnea, arrhythmias Hypertensive Emergency Department Crisis Proteinuria, haematuria, anemia, elevated creatinine Thorough history, bilateral arm BP, presence of JVP, lung sounds, ECG, lab Nursing Assessment results, neurological changes Clinical Presentation Cardiovascular: Aortic dissection, ACS, heart failure, pulmonary edema, myocardial ischemia Renal: Acute and chronic renal disease, hematuria, proteinuria, acute tubular Target Organ Damage necrosis Hypertensive encephalopathy involves a significant blood pressure rise disrupting Neurological: Cerebrovascular accident, cerebral autoregulation, leading to intracerebral hemorrhage, hypertensive cerebral edema and neurological encephalopathy symptoms. Titrate medications to effect Manage headache Nursing Care Darken room / photophobia Monitor glucose levels Check urine / urine saves Reduce BP gradually, not too quickly (no more than 25% in the first hour) Aim for 160/100 mmHg within 2-6 hours, General Principles then normal BP over 24-48 hours Avoid excessive falls in BP to prevent organ ischemia Use Poiseuille's Law to explain how vasoconstriction and vasodilation affect flow rate Treatment Vasodilators (e.g., GTN, sodium nitroprusside, hydralazine) Central-acting adrenergic agents (e.g., Medication Management clonidine) Calcium channel blockers (e.g., verapamil, nicardipine, nifedipine) ACE inhibitors (e.g., captopril) Beta-adrenergic antagonists (e.g., atenolol) Hypertension during pregnancy with no identified cause Relieved at the time of birth, but can worsen with HELLP (hemolysis, elevated Pre-eclampsia liver enzymes, low platelets)syndrome Catastophic Bleed Parenteral hydralazine, labetalol, and oral nifedipine are common treatments

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