END-ORGAN DAMAGE OF HYPERTENSION Flashcards
Hypertensive Urgencies and Emergencies
Management:
General recommendations:
Gradual BP reduction is generally recommended:
MAP reduction by ~10% to 20% in first hour, then by
An additional 5% to 15% over the next 23 hours, with
Total 24 hour BP reduction < 25%
Hypertensive Urgencies and Emergencies
Exceptions to gradual BP reduction over the first day:
Acute phase of ischemic stroke: BP not lowered unless >185/110 mm Hg in candidates for reperfusion therapy or >220/120 mm Hg for non-candidates.
Acute aortic dissection: SBP should be lowered to target of 100 to 120 mm Hg within 20 minutes and heart rate reduced to <60 beats per minute.
Hypertensive Urgencies and Emergencies
Keep patient euvolemic to reduce further activation of the renin–angiotensin–aldosterone system, with caution not to worsen HTN with excess sodium load.
Head trauma
Treat if cerebral perfusion pressure (mean arterial pressure minus intracranial pressure [ICP]) is >120 mm Hg and ICP is >20 mm Hg.
Acute heart failure
Consider use of intravenous vasodilator such as sodium nitroprusside, nitroglycerin to reduce afterload.
Acute heart failure
Avoid hydralazine (can increase cardiac work) or β-blockers, for example, labetalol (can decrease cardiac contractility).
Acute coronary syndrome
Consider use of IV nitroglycerin, clevidipine, nicardipine, or esmolol to reduce myocardial oxygen consumption/ischemia.
Acute hypertensive nephrosclerosis, renal emergencies
Clinical manifestations: new-onset microscopic hematuria, elevated creatinine
Acute hypertensive nephrosclerosis, renal emergencies
Renal histopathology: Fibrinoid necrosis of small arterioles (pink, amorphous fibrinoid materials within vessel wall due to necrosis) and “onion skinning” of small renal arteries.
Acute hypertensive nephrosclerosis, renal emergencies
“Onion skinning” is used to describe hyperplastic arteriosclerosis with thickened concentric smooth muscle cell layer with thickened, duplicated basement membrane and narrowed lumen. In malignant HTN, these hyperplastic changes may be accompanied by fibrinoid necrosis of the arterial intima and media.
Acute hypertensive nephrosclerosis, renal emergencies
Renal ischemia activates the renin–angiotensin -aldosterone system (RAAS), thus excerbates the underlying HTN.
Acute hypertensive nephrosclerosis, renal emergencies
BP lowering may lead to worsening kidney function, particularly CCB due to the potential vasodilating effect on afferent arterioles leading to transmission of systemic HTN into glomeruli.
Acute hypertensive nephrosclerosis, renal emergencies
Fenoldopam is associated with a temporary improvement in renal function and may be useful in renal hypertensive emergencies.
Ingestion of sympathomimetic agents (e.g., ingestion of tyramine-containing foods in patients on chronic monoamine oxidase inhibitors, cocaine, amphetamine) or severe autonomic dysfunction (e.g., Guillain–Barré, Shy–Drager syndromes), acute spinal cord injury.
Treat with IV phentolamine or nitroprusside.
Use of β-blockers is contraindicated due to unopposed α-adrenergic vasoconstriction. NOTE: nonselective β-blockers such as labetalol and carvedilol still have predominant β-blocking activity with β-to-α blocking ratio of 7:1 or greater.
Antihypertensive Medications Used in Hypertensive Emergencies
Nitrates: nitroglycerin, nitroprusside:
NO induces arteriolar and venous vasodilatation by activation of calcium sensitive potassium channels (via cGMP) in cell membranes.