week 12 htn crisis

Hypertension

• Autoregulatory failure, including baroreceptors and chemoreceptors, can lead to primary (essential) hypertension.
• Renal ischemia can trigger the RAAS system, increasing total peripheral resistance (TPR) and Na+ water retention.
• Hormonal hypertension can occur due to increased catecholamines, leading to increased heart rate, contractility, and sympathetic activity.

Primary vs. Secondary Hypertension

• Primary (essential) hypertension has no definitive cause, while secondary hypertension has an identified cause.
• Possible mechanisms of primary hypertension include renal hypertension, hormonal hypertension, and heredity.
• Secondary hypertension can be caused by pheochromocytoma, Cushing's syndrome, renal dysfunction/disease, pregnancy, and preeclampsia/eclampsia.

Risk Factors

• Risk factors for hypertension include diabetes, smoking, obesity, alcohol, caffeine, stress, and multiple antihypertensives.

Hypertensive Urgency vs. Hypertensive Emergency

• Hypertensive urgency is elevated blood pressure without signs of target organ damage.
• Hypertensive emergency is elevated blood pressure with signs of target organ damage, such as headache, blurred vision, shortness of breath, and chest pain.

Pathophysiology

• The pathophysiology of primary hypertension is not well understood, but likely involves dysregulation of the RAAS, inflammation, and genetic factors.

Hypertensive Crisis

• Hypertensive crisis is a medical emergency that can lead to acute organ damage if not reduced.
• Patients without a history of hypertension are at higher risk of worse outcomes.
• Causes of hypertensive crisis include renal disease/dysfunction, rebound hypertension, illicit drug use, and certain medications.

Clinical Presentation

• Symptoms of hypertensive crisis include headache, visual disturbances, dizziness, vomiting, papilledema, epistaxis, and dyspnea.
• Clinical presentation may also include proteinuria, hematuria, anemia, and elevated creatinine.

Nursing Assessment

• A thorough history, bilateral arm BP, presence of JVP, lung sounds, ECG, and lab results are necessary for nursing assessment.
• Neurological changes should also be monitored.

Target Organ Damage

• Cardiovascular damage can include aortic dissection, ACS, heart failure, pulmonary edema, and myocardial ischemia.
• Renal damage can include acute and chronic renal disease, hematuria, proteinuria, and acute tubular necrosis.
• Neurological damage can include cerebrovascular accident, intracerebral hemorrhage, and hypertensive encephalopathy.

Nursing Care

• Manage headache by reducing blood pressure gradually.
• Monitor glucose levels and check urine/urine saves.
• Darken room/photophobia to reduce symptoms.

General Principles

• Reduce BP gradually, not too quickly (no more than 25% in the first hour).
• Aim for 160/100 mmHg within 2-6 hours, then normal BP over 24-48 hours.
• Avoid excessive falls in BP to prevent organ ischemia.

Treatment

• Medications include vasodilators (e.g., GTN, sodium nitroprusside, hydralazine), central-acting adrenergic agents (e.g., clonidine), calcium channel blockers (e.g., verapamil, nicardipine, nifedipine), ACE inhibitors (e.g., captopril), and beta-adrenergic antagonists (e.g., atenolol).

Pre-eclampsia

• Hypertension during pregnancy with no identified cause can lead to pre-eclampsia.
• Relieved at the time of birth, but can worsen with HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome.
• Parenteral hydralazine, labetalol, and oral nifedipine are common treatments for pre-eclampsia.