Hypertensive Crisis & Special Populations Study Guide

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Description and Tags

Comprehensive vocabulary flashcards covering the pathophysiology, clinical targets, pharmacology, resistant hypertension management, and special population considerations in hypertensive crisis.

55 Terms

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Hypertensive Crisis

An acute, severe elevation in blood pressure defined as a systolic blood pressure SBP≥180 mmHg\text{SBP} \ge 180\,\text{mmHg} and/or diastolic blood pressure DBP≥120 mmHg\text{DBP} \ge 120\,\text{mmHg}.

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Severe Hypertension

An acute, severe blood pressure elevation (BP>180/120 mmHg\text{BP} > 180/120\,\text{mmHg}) presenting without evidence of acute target organ damage, formerly termed hypertensive urgency.

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Hypertensive Emergency

An acute, severe blood pressure elevation (BP>180/120 mmHg\text{BP} > 180/120\,\text{mmHg}) presenting with evidence of acute, progressive target organ damage affecting the brain, heart, kidneys, or vascular system.

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Vascular Shear Stress

Physical mechanical stress exerted by extremely high intravascular pressure against arterial walls that strips endothelial cells, triggering increased vascular permeability, platelet and fibrin deposition, and fibrinoid necrosis.

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Spontaneous Natriuresis

Renal sodium and water excretion triggered by marked elevations in systemic vascular resistance, culminating in intravascular volume depletion.

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Normal Cerebral Autoregulation

The physiological mechanism in healthy individuals that maintains cerebral blood flow at approximately 700–750 mL/min700\text{--}750\,\text{mL/min} within a mean arterial pressure range of 60 to 120 mmHg60\text{ to }120\,\text{mmHg}.

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Right-Shift of Cerebral Autoregulation

Arteriolar remodeling occurring in chronic, uncontrolled hypertension that shifts the cerebral autoregulation curve to higher pressure ranges to protect brain tissue from excessive hydrostatic pressure.

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Iatrogenic Stroke Mechanism

Cerebral ischemia resulting from lowering blood pressure too rapidly into a conventional "normal" range in a patient with chronic hypertension, which drops cerebral blood flow below ≤300 mL/min\le 300\,\text{mL/min}.

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Cerebral Vascular Collapse Threshold

The critical hemodynamic threshold where cerebral blood vessels collapse completely, occurring when mean arterial pressure falls below 30 mmHg30\,\text{mmHg}.

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Fibrinoid Necrosis

Structural arterial damage caused by endothelial disruption and plasma protein leakage, leading to luminal narrowing, microvascular occlusion, and tissue ischemia.

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Maladaptive Neurohormonal Surge

A compensatory release of renin-angiotensin-aldosterone system hormones and catecholamines accompanied by a reduction in nitric oxide and prostacyclin in response to intravascular volume depletion, perpetuating a vicious cycle of blood pressure elevation.

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Hypertensive Encephalopathy

An acute central nervous system manifestation of target organ damage characterized by altered mental status and papilledema.

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Target Organ Damage: Cardiovascular Manifestations

Acute cardiovascular injuries precipitated by hypertensive crisis, including acute coronary syndrome (myocardial infarction, unstable angina), acute pulmonary edema with bilateral crackles, and acute aortic dissection.

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Target Organ Damage: Renal Manifestations

Acute kidney injury or acute renal failure evidenced by acute elevations in serum creatinine, blood urea nitrogen, and serum potassium.

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Hypertensive Emergency General BP Goal

In patients without a compelling condition, reduce systolic blood pressure by no more than 25%25\% within the first hour, achieve SBP<160/100 mmHg\text{SBP} < 160/100\,\text{mmHg} within 2–6 hours2\text{--}6\,\text{hours}, and reach 130–140 mmHg130\text{--}140\,\text{mmHg} over 24–48 hours24\text{--}48\,\text{hours}.

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Acute Aortic Dissection BP Target

Rapid reduction of systolic blood pressure to <120 mmHg< 120\,\text{mmHg} within 20 minutes20\,\text{minutes}, with maintenance of systolic blood pressure between 100–120 mmHg100\text{--}120\,\text{mmHg}.

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Acute Aortic Dissection Treatment Sequence

The mandatory administration of a parenteral beta-blocker (e.g., esmolol or labetalol) prior to initiating a vasodilator (e.g., nicardipine or nitroprusside) to prevent reflex tachycardia and shear stress.

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Acute Intracranial Hemorrhage BP Target

Rapid reduction of systolic blood pressure to 140 mmHg140\,\text{mmHg} within the first hour while maintaining stable intracranial pressure and mean arterial pressure.

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Permissive Hypertension

The strategy in acute ischemic stroke of allowing elevated blood pressure to maintain cerebral perfusion, intervening to lower blood pressure by 15%15\% only if BP≥220/120 mmHg\text{BP} \ge 220/120\,\text{mmHg}, or keeping SBP<180/105 mmHg\text{SBP} < 180/105\,\text{mmHg} for 24 hours24\,\text{hours} if tPA is administered.

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Acute Coronary Syndrome BP Target

Immediate reduction of systolic blood pressure to <140 mmHg< 140\,\text{mmHg} with an ultimate goal of normotension.

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Acute Pulmonary Edema BP Management

Immediate reduction of blood pressure targeting normotension using intravenous vasodilators (nitroglycerin, clevidipine, or nitroprusside), while strictly avoiding beta-blockers.

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Eclampsia / Preeclampsia BP Target

Reduction of blood pressure to <160/110 mmHg< 160/110\,\text{mmHg} within 30–60 minutes30\text{--}60\,\text{minutes}, maintained below 160/110 mmHg160/110\,\text{mmHg} until delivery.

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Catecholamine Excess BP Management

Rapid reduction of blood pressure and symptom control using phentolamine as first-line therapy, clevidipine, or nicardipine; unopposed beta-blockers are contraindicated.

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Severe Hypertension (Urgency) Strategy

Adjustment or reinstitution of oral outpatient antihypertensive regimens over 24–48 hours24\text{--}48\,\text{hours} while withholding acute intravenous or oral loading doses to prevent post-discharge hypotension and stroke.

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Nicardipine

An intravenous dihydropyridine calcium channel blocker with an onset of 5–15 minutes5\text{--}15\,\text{minutes} and duration of 30–40 minutes30\text{--}40\,\text{minutes}, contraindicated in advanced aortic stenosis.

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Clevidipine

A lipid-emulsion dihydropyridine calcium channel blocker with an onset of 2–4 minutes2\text{--}4\,\text{minutes} and duration of 5–15 minutes5\text{--}15\,\text{minutes}, contraindicated in soy allergy, egg allergy, hyperlipidemia, and pancreatitis.

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Sodium Nitroprusside

A parenteral nitric oxide vasodilator with immediate onset and 1–2 minute1\text{--}2\,\text{minute} duration that increases intracranial pressure and carries a risk of cyanide and thiocyanate toxicities.

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Cyanide and Thiocyanate Toxicity Risk Factors

Complications associated with sodium nitroprusside infusions occurring in patients with chronic kidney disease, infusion rates >3 mcg/kg/min> 3\,\text{mcg/kg/min}, or administration durations >3 days> 3\,\text{days}.

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Nitroglycerin (IV)

A parenteral nitrate vasodilator with an onset of 2–5 minutes2\text{--}5\,\text{minutes} and duration of 3–5 minutes3\text{--}5\,\text{minutes}, contraindicated with PDE-5 inhibitors or volume depletion, and prone to tachyphylaxis.

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Labetalol (IV)

A combined α1\alpha_1 and non-selective β1,2\beta_{1,2} blocker with an onset of 2–5 minutes2\text{--}5\,\text{minutes} and duration of 2–4 hours2\text{--}4\,\text{hours}, contraindicated in severe asthma, COPD, second- or third-degree heart block, and decompensated heart failure.

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Esmolol

A cardioselective β1\beta_1 blocker with an onset of 1–2 minutes1\text{--}2\,\text{minutes} and duration of 10–20 minutes10\text{--}20\,\text{minutes}, preferred in aortic dissection, acute coronary syndrome, and perioperative hypertension.

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Phentolamine

A parenteral non-selective alpha-adrenergic antagonist with an onset of 1–2 minutes1\text{--}2\,\text{minutes} and duration of 10–30 minutes10\text{--}30\,\text{minutes}, indicated as first-line therapy for catecholamine crises (cocaine toxicity, pheochromocytoma, clonidine withdrawal).

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Fenoldopam

A dopamine DA-1 agonist with an onset of 5–10 minutes5\text{--}10\,\text{minutes} and duration of 30–60 minutes30\text{--}60\,\text{minutes}, indicated for acute kidney injury but contraindicated in glaucoma, elevated intraocular pressure, and sulfite allergy.

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Hydralazine (IV)

A direct parenteral vasodilator with an onset of 10–30 minutes10\text{--}30\,\text{minutes} and duration of 2–4 hours2\text{--}4\,\text{hours} that produces an unpredictable blood pressure reduction, making it undesirable as a general first-line emergency agent.

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Resistant Hypertension

Blood pressure remaining uncontrolled (≥130/80 mmHg\ge 130/80\,\text{mmHg}) despite concurrent adherence to ≥3\ge 3 full-dose antihypertensive agents of different classes (including a diuretic), or controlled blood pressure requiring ≥4\ge 4 medications.

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Pseudoresistance

Apparent treatment resistance attributable to inaccurate cuff size, white-coat effect, or medication non-adherence.

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SYMPATHY Trial

A clinical trial documenting a 50–80%50\text{--}80\% prevalence of medication non-adherence among patients evaluated for apparent resistant hypertension.

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NSAID-Induced Hypertension

The leading drug-induced cause of resistant hypertension, mediated by renal cyclooxygenase inhibition that reduces prostaglandins, induces sodium and water retention, and blunts antihypertensive efficacy.

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Chlorthalidone Optimization

The substitution of hydrochlorothiazide with chlorthalidone (12.5–25 mg12.5\text{--}25\,\text{mg} daily) to achieve superior 24-hour and overnight blood pressure control, which requires close monitoring of serum potassium.

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Spironolactone (in Resistant HTN)

A mineralocorticoid receptor antagonist added at 25–50 mg25\text{--}50\,\text{mg} daily as the preferred fourth-line agent for resistant hypertension, requiring serum creatinine and potassium monitoring within 3 to 7 days3\text{ to }7\,\text{days}.

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Chronotherapy

The clinical practice of shifting 11 or 22 antihypertensive medications to bedtime to improve nocturnal blood pressure dipping and decrease cardiovascular events.

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MEPAC Trial

The clinical trial demonstrating that bedtime dosing of antihypertensive medications improves nocturnal blood pressure dipping and reduces cardiovascular events.

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"He Loves My Neonate"

A clinical mnemonic identifying the first-line antihypertensive medications considered acceptable during pregnancy: Hydralazine, Labetalol, Methyldopa, and Nifedipine.

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Gestational Blood Pressure Nadir

The expected physiological low point in maternal blood pressure occurring between 16–18 weeks16\text{--}18\,\text{weeks} of gestation.

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Fetotoxic Antihypertensive Classes

Antihypertensive agents contraindicated in pregnancy: ACE inhibitors, ARBs, direct renin inhibitors, mineralocorticoid receptor antagonists (spironolactone/eplerenone), atenolol, and nitroprusside.

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Atenolol in Lactation

A beta-blocker to avoid during breastfeeding due to extensive milk excretion that causes infant bradycardia and lethargy.

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Candesartan (in Migraine Prophylaxis)

An angiotensin receptor blocker demonstrating superior efficacy for comorbid hypertension and migraine prophylaxis, characterized by a number needed to treat (NNT) of 3–43\text{--}4.

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Unopposed Alpha-Stimulation

Severe paradoxical vasoconstriction and blood pressure elevation caused by administering a pure beta-blocker (such as propranolol) in the setting of cocaine toxicity or pheochromocytoma, leaving alpha-1 receptors unchecked.

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Beta-Blocker Withdrawal Syndrome

Rebound tachycardia, elevated myocardial oxygen demand, angina, or infarction resulting from abrupt cessation of chronic beta-blocker therapy due to beta-receptor upregulation.

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Beta-Blocker Tapering Protocol

The protocol used to prevent withdrawal rebound by reducing the beta-blocker dose by 50%50\% every 3–7 days3\text{--}7\,\text{days} while restricting physical exertion.

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Clonidine Withdrawal Rebound

Severe rebound hypertension (BP>190/110 mmHg\text{BP} > 190/110\,\text{mmHg}) caused by the sudden cessation of central alpha-2 agonists, which removes negative feedback and triggers excessive norepinephrine release onto upregulated alpha-1 receptors.

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Reflex Tachycardia (from Vasodilators)

A compensatory sympathetic reflex response to rapid arterial vasodilation (from short-acting/crushed nifedipine, hydralazine, or minoxidil) that increases heart rate, myocardial oxygen demand, and ischemic risk.

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Fatal Triple AV Block ("Triple Whammy")

Complete heart block, profound bradycardia, and cardiogenic shock produced by the combined, synergistic AV-nodal suppression of digoxin, a beta-blocker, and a non-dihydropyridine calcium channel blocker (verapamil or diltiazem).

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Preload-Mediated Iatrogenic Heart Failure

Volume overload and heart failure exacerbation caused by renal sodium and water retention from medications such as NSAIDs, COX-2 inhibitors, corticosteroids, thiazolidinediones, and high-sodium OTC products.

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Negative Inotropic Iatrogenic Heart Failure

Direct suppression of myocardial contractility precipitating heart failure decompensation, caused by non-DHP CCBs (verapamil, diltiazem), nifedipine, non-approved beta-blockers (propranolol), or antiarrhythmics (disopyramide, flecainide).