Hypertension Flashcards
What is the normal blood pressure?
Normal: SBP <120 mmHg and DBP <80 mmHg
What are the main risk factors for hypertension?
Family history
Black
High salt intake
Alcohol
Obesity
Inactivity
At what blood pressure is a patient prehypertensive?
Elevated (Prehypertensive): SBP 120–129 mmHg and DBP <80 mmHg
What is the workup for a patient who is prehypertensive?
lifestyle modification and routine follow up.
no meds.
At what blood pressure is a patient in Stage 1 Hypertension?
Stage 1 Hypertension:
SBP 130–139 mmHg or DBP 80–89 mmHg
What is the appropriate management strategy for patients in stage 1 hypertension?
lifestyle changes
What lifestyle modifications are effective in lowering blood pressure, and which has the greatest impact?
Weight loss: Greatest reduction in BP (5–20 mmHg per 10 kg lost).
DASH diet: High fruits/vegetables, low fat (8–14 mmHg reduction).
Reduced salt intake: ≤2.4 g sodium/day (2–8 mmHg reduction).
Exercise: Aerobic activity >30 min/day (4–9 mmHg reduction).
Alcohol reduction: ≤2 drinks/day for men, ≤1 for women (2–4 mmHg reduction).
At what blood pressure do patients get pharmacological intervention for their hypertension?
140/90 in an average risk patient.
130/80 in a high risk patient.
High risk patients: CAD, HF, Diabetes, CKD, Age >65, ASCVD 10 year risk >10%
When do patients with stage 1 HTN obtain medication?
when there is a comorbidity such as DM, CKD, or ASCVD or a 10-year risk of ASCVD of more than 10%
At what blood pressure is a patient in Stage 2 Hypertension?
Stage 2 Hypertension:
SBP ≥140 mmHg or DBP ≥90 mmHg
What is the appropriate management strategy for patients in stage 2 hypertension?
lifestyle changes with 1-2 anti-hypertensive medications.
At what blood pressure is a patient in hypertensive crisis?
Hypertensive Crisis:
SBP ≥180 mmHg and/or DBP >120 mmHg
Hypertensive crisis requires urgent management, with differentiation between urgency and emergency based on end-organ damage.
What is the appropriate workup for patients in stage 1 or 2 hypertension?
Patients in Stage 1 or 2 hypertension require individualized treatment strategies based on cardiovascular risk factors such as ASCVD, diabetes or chronic kidney disease (CKD). With these conditions, patients will require medication, even at stage 1. Otherwise, patients are managed conservatively. Medication with 1-2 agents is normally reserved for stage 2 HTN. Every patient will require lifestyle modifications.
What conditions may convolute the diagnosis of hypertension?
- White Coat Syndrome: Elevated BP in the doctor’s office.
- Masked hypertension: Falsely low in the doctor’s office.
Diagnose with a 24-hour BP monitoring system or at home monitoring.
What is considered to be diagnostic for hypertension?
- 2 readings over the span of a 4 week period.
- Ambulatory or home readings are preferred for confirmation.
- A BP over 130/80 mmHg.
What initial workup is recommended for newly diagnosed hypertension?
1) Rule out medication induced hypertension (steroids, NSAIDs, OCPs, or stimulants such as caffeine, nicotine,, or decongestants).
2) As part of initial workup, a fasting lipid profile should be ordered in all hypertensive patients to calculate the risk for cardiovascular events. The target blood pressure is determined, in part, by this risk, with lower targets recommended for those at increased risk. Labs include Renal function (BUN/Cr), urinalysis, CMP (electrolytes and glucose), lipid profile, TSH. An ECG is used to assess for left ventricular hypertrophy or ischemic changes.
Initial evaluation is oriented to the following objectives:
- Detecting end-organ damage that may require more aggressive management
- Assessing other cardiovascular risk factors
- Screening for common secondary causes of hypertension (eg, thyroid disorders, hyperaldosteronism)
- Identifying concurrent conditions and metabolic abnormalities that could influence the choice of antihypertensive therapy
What is the most common cause of hypertension in a female of reproductive age?
OCPs
What heart conditions are known to develop from chronic hypertension?
Left ventricular hypertrophy on ECG indicates chronic hypertension and an increased risk for cardiovascular complications like heart failure. Additionally, HFpEF can also develop from chronic HTN.
What are the first-line medications for hypertension, and how are they selected?
ACE inhibitors/ARBs: Preferred in diabetes, CKD, or heart failure.
Thiazide diuretics: Effective for Black patients or elderly with isolated systolic hypertension.
Calcium channel blockers (CCBs): Also effective in Black patients or in combination therapy for metabolic syndrome.
What pharmacologic measure would be appropriate for a young caucasian male with isolated hypertension?
In young Caucasian patients, ACE inhibitors or ARBs are preferred due to renin sensitivity.
Can ACE inhibitors and ARBs be combined?
No. ACE inhibitors should not be used with ARBs because of the risk for hyperkalemia and nephrotoxicity.
What advantage is there, if any, with combining CCB and ACE inhibitors?
The combination of an ACE inhibitor and a calcium channel blocker may be particularly effective with controlling hypertension and can minimize the edema associated with calcium channel.
What pharmacologic measure would be appropriate for a young black male with isolated hypertension?
Black patients without CKD should receive thiazides or CCBs first-line for hypertension. Combination therapy (CCB + thiazide) is often needed for optimal BP control if monotherapy is insufficient.
When is isosorbide dinitrate with hydralazine indicated as a first-line medication for hypertension?
The combination of a long-acting nitrate (eg, isosorbide dinitrate) with hydralazine is effective in controlling symptoms of heart failure in patients who cannot take ACE inhibitors or ARBs.
Are beta-blockers used as a first line antihypertensive?
Only when patients also have heart failure are Beta blockers given for hypertension. Beta blockers not normally recommended for the initial management of hypertension unless there are specific indications for their use (coronary heart disease or heart failure with depressed ejection fraction).
What is a major side effect of CCBs?
How can this be mitigated?
Lower extremity edema associated with the use of antihypertensive therapy, specifically due to Dihydropyridine calcium channel blockers (e.g., amlodipine, nifedipine), are known to cause dose-dependent peripheral edema. The mechanism involves precapillary arteriolar dilation without a corresponding dilation in postcapillary venules. This imbalance increases capillary hydrostatic pressure, causing extravasation of fluid into the interstitial space. Adding an ACE inhibitor or ARB, can reduce the pre-capillary dilation, while dilating the post-capillary venules, mitigating edema.
What is the “step-up” treatment approach for hypertension?
1) Start with one appropriate antihypertensive medication, (occasionally two medications for stage 2 HTN or high cardiovascular risk).
2) Then maximize the dose of the initial antihypertensive medication if the patient’s blood pressure has not been optimally reduced.
3) Add an additional antihypertensive if the maximum dose for the first antihypertensive has been reached and when the patient’s blood pressure is at or greater than 20/10 mmHg above the goal blood pressure.
4) Add a third antihypertensive if the maximum dose for the second antihypertensive has been reached.
5) If still hypertensive, evaluate for a secondary cause of hypertension.
What SHOULD occur prior to the initiation of a third antihypertensive medication?
1) Ensure lifestyle choices are optimal
2) Ensure medication adherence
How common is medication non-adherence a factor in uncontrolled HTN?
Medication nonadherence is the most common cause for uncontrolled hypertension and accounts for ~ 40% of cases. Medication nonadherence also is the most common cause for restenosis and thrombosis of heart stents following PCI.
Often times hypertension resolves. How is step down treatment managed for patients who were on chronic antihypertensives and desire to stop medication?
Gradually!
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Patients with well-controlled hypertension on a single-drug regimen, who have made significant lifestyle changes—such as achieving substantial weight loss—may often taper and discontinue their medication under close blood pressure monitoring. This approach is typically reserved for individuals whose blood pressure remains well-controlled after these lifestyle modifications, demonstrating that lifelong antihypertensive therapy may not always be necessary in such cases. If no lifestyle modifications have been made, discontinuation of antihypertensive medication will typically cause blood pressure to rise t pretreatment levels. To discontinue a long-acting medication, such as amlodipine, the medication can be taken either every other day or in a lower daily dose (eg, half tablet). Amlodipine carries little risk of rebound hypertension. For short-acting medications (eg, lisinopril), the medication should be taken daily but in a smaller dose (either a half tablet or a smaller prescribe tablet). discontinuation of short-acting beta blockers, which also are only occasionally used for hypertension, can cause rebound hypertension. The blood pressure should be monitored closely over 1-2 months, and if it remains well controlled, the medication can be discontinued and the blood pressure monitored for an additional 1-2 months. All of these medications can be tapered off within a few weeks (eg, 2-3 months), and a longer taper (eg, 6 months) is unnecessary. If the blood pressure rises above the target, the previous dose of medication should be reinstated. The same approach can be used to eliminate drugs from a multidrug antihypertensive regimen.
Why is medication usually used prior to chasing the secondary causes of hypertension?
Because the vast majority of causes of hypertension is essential, which means idiopathic, meaning not caused by the known secondary causes for hypertension. However, if there is no or limited response to antihypertensive medications, then the secondary causes should be investigated.
A young patient (<35 years) with severe or refractory hypertension (on three anti-hypertensives) should be screened for …?
Secondary causes for hypertension
particularly renal artery stenosis secondary to fibromuscular dysplasia or pheochromocytoma.
When does TRUE resistant HTN occur, how is it defined?
True resistant hypertension exists in patients whose BP remains uncontrolled despite adherence to a regimen of 3 or more antihypertensive medications (1 being a diuretic) and reasonable optimization of lifestyle changes (eg, weight loss, low-sodium diet) and lack abnormal findings (young age [< 30 years old], abrupt onset, or abnormal findings.
What clinical findings raise suspicion for secondary hypertension and warrant further evaluation for underlying risk factors?
Evaluation for secondary causes of hypertension is advised for patients with ANY of these four conditions:
1) Have resistant hypertension (persistent hypertension despite an appropriate 3-drug regimen).
2) Have an abrupt onset of hypertension.
3) Have developed hypertension at an unusual age (eg, age <30).
4) Have specific abnormal findings on initial evaluation (eg, hypokalemia, hematuria, abdominal bruit, or evidence of end-organ damage [retinal hemorrhage or heart failure]).
What are common causes of secondary hypertension, and how do you screen for them?
Renal artery stenosis:
Renal Doppler ultrasound (renal artery stenosis).
Aortic coarctation:
Compare BP in the upper and lower extremities or weakened or delayed femoral pulses
CKD:
Creatinine
Primary hyperaldosteronism:
Plasma aldosterone/renin ratio (primary hyperaldosteronism).
Pheochromocytoma:
24-hour urine metanephrines (pheochromocytoma).
Cushing syndrome:
Cortisol levels
Obstructive sleep apnea (OSA):
Polysomnography (OSA).
OCPs:
Look at history.
What is used to screen for kidney damage secondary to hypertension?
- Frequent UTIs, increased abdominal girth, elevated creatinine, proteinuria, or hematuria, may indicate an underlying genetic cause for renal induced hypertension, requiring work-up for polycystic kidney disease starting with a renal ultrasound.
- Renal artery stenosis could be implicated with elevated creatinine, but the first screening tool is with a renal ultrasound.
- Diabetes may cause microalbuminuria on urinalysis indicates end-organ kidney damage and may require early ACE inhibitor or ARB therapy.Microalbuminuria is when the urine albumin/creatinine is greater than 29 mg/g.
When should ACEi be avoided?
Avoid ACE inhibitors in pregnancy (teratogenic) or patients with bilateral renal artery stenosis.
A 77-year-old man with a history of coronary artery disease presents to the emergency department for evaluation of two days of worsening shortness of breath. He has noticed decreased urine output. He has not had fevers, chest pain, or recent travel. Additional past medical history is significant for hypertension for which the patient takes amlodipine.
He was also started on lisinopril two weeks ago. The patient has a 40 pack-year smoking history. Temperature is 36.8°C (98.2°F), blood pressure is 190/100 mmHg, pulse is 102/min, respiratory rate is 22/min, and oxygen saturation is 90% on room air. Physical examination reveals rales at the bilateral lung bases and an S4 heart sound. There is bilateral lower extremity pitting edema to the mid calves without overlying erythema. Laboratory findings are significant for an increase in serum creatinine level from 1.2 to 2.2 mg/dL over the past two weeks. Urinalysis reveals mild proteinuria. Chest X-ray is significant for bilateral pulmonary edema. What is the most likely diagnosis?
Renal artery stenosis (RAS) can cause secondary hypertension, and patients can present with symptoms of fluid overload and decreased renal function following ACE inhibitor initiation. It is caused by the narrowing of one or both renal arteries, which triggers the renin-angiotensin-aldosterone system, leading to hypertension. This patient with a history of coronary artery disease, smoking, and hypertension presents with symptoms of pulmonary edema and decreased renal function following the initiation of an angiotensin-converting enzyme (ACE) inhibitor. These findings strongly suggest renal artery stenosis (RAS). Renal artery stenosis (RAS) is narrowing of one or both renal arteries and can result in secondary hypertension due to activation of the renin-angiotensin-aldosterone system (RAAS). This process increases blood pressure and can lead to systemic hypertension. ACE inhibitors, which are often used for managing hypertension, can worsen renal insufficiency in these patients. They reduce angiotensin Il-mediated efferent arteriole vasoconstriction, which can reduce glomerular filtration, thereby raising serum creatinine levels. In addition, RAS may be associated with episodes of “flash” pulmonary edema, leading to acute respiratory distress. A significant physical exam finding that may be present is an abdominal bruit, typically heard in the upper abdomen or flanks, which suggests turbulent blood flow due to the narrowed renal artery. Patients with RAS often have other manifestations of atherosclerotic disease, such as coronary artery disease, peripheral artery disease, and cerebrovascular disease.
Other than intermittent palpitations, diaphoresis, headache, and tachycardia, what other symptom tends to be associated with pheochromocytoma?
Orthostatic hypotension
Pheochromocytomas typically present with episodic hypertension, headaches, palpitations, and diaphoresis.
Other than Pheochromocytoma, what is the other endocrine cause for secondary hypertension that also involves diaphoresis and heart palpitations?
Hyperthyroidism.
Other than Pheochromocytoma, what is the other endocrine cause for secondary hypertension that also involves low potassium levels and high bicarbonate levels?
Primary aldosteronism.
Other than Pheochromocytoma, what is the other endocrine cause for secondary hypertension that also involves low mood and weight gain?
Cushing syndrome.
What congenital heart condition, also associated with a bicuspid aortic valve, can lead to secondary hypertension?
Coarctation of the aorta.
What assessment tool is used to determine if obstructive sleep apnea is the underlying cause for secondary hypertension?
POLYSOMNOGRAM
What are the symptoms of hypertensive urgency versus emergency?
Both: Severely elevated BP (≥180/≥120 mmHg).
Hypertensive Urgency: No evidence of end-organ damage. Symptoms (if present) may include mild headache, dizziness, or anxiety.
Hypertensive Emergency: Evidence of end-organ damage.
CNS: Stroke, encephalopathy, seizures, confusion.
Renal: Acute kidney injury, hematuria, proteinuria, MAHA.
Cardiovascular: Myocardial ischemia, heart failure, aortic dissection.
Pulmonary: Pulmonary edema (shortness of breath, hypoxia, rales, crackles, tachypnea).
Ophthalmic: Hypertensive retinopathy with papilledema.
What are the first line antihypertensives for hypertensive urgency or emergency when are they used?
oral antihypertensive agents (e.g., clonidine, captopril) are used in hypertensive urgency
IV agents like nitroglycerin, labetalol, hydralazine, nicardipine, esmolol, or nitroprusside.
A 68-year-old man with a history of hypertension is brought to the emergency department for evaluation of altered mental status and shortness of breath. He stopped taking his antihypertensive medications due to side effects and has not seen his primary physician since then. Temperature is 37.0°C (98.6°F), pulse is 110/min, blood pressure is 220/120 mmg, respiratory rate is 20/min, and oxygen saturation is 96% on 5L nasal cannula. The patient has labored breathing. He is oriented to person only. Pulmonary examination reveals bilateral rales. Fundoscopic examination is significant for papilledema. The electrocardiogram shows evidence of left ventricular hypertrophy without ST elevations or depressions or T-wave abnormalities. Lab results show serum creatinine of 2.5 mg/dL (1.7 mg/dL baseline) and hematuria on urinalysis. Which of the following is the best next step in management?
This patient presents with a hypertensive emergency as evidenced by a severely elevated blood pressure (220/120 mmHg) and evidence of end-organ damage, including neurological (altered mental status, papilledema), cardiovascular (respiratory distress, bilateral rales), and renal impairment (serum creatinine of 2.5 mg/dL). Treatment with intravenous labetalol should be initiated immediately. A hypertensive emergency is characterized by severe hypertension (BP > 180/120 mmHg) with evidence of end-organ damage. In the case of a hypertensive emergency, it is crucial to lower blood pressure promptly to prevent further damage; however, it must be done in a controlled manner to avoid ischemic events. In general, the goal is to reduce the mean arterial pressure (MAP) by no more than 25% within the first hour, followed by a gradual reduction toward 160/100-110 mmHg over the next 2-6 hours. Intravenous antihypertensives (labetalol, esmolol, nicardipine, and hydralazine) should be administered based on the presence of specific comorbid conditions and the side effect profiles of the medications. Intravenous antihypertensive agents, like labetalol, are used for blood pressure control in patients with hypertensive emergencies. Blood pressure should be reduced by no more than 25% within the first hour to avoid potential complications related to rapid correction, such as cerebral hypoperfusion and cardiac ischemia.
What short-acting alpha-2 agonist that is occasionally used for severe hypertensive episodes?
Clonidine
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Abrupt discontinuation can lead to severe rebound hypertension.
what is the MAX that a patient’s BP should be decreased by when experiencing hypertensive emergency or urgency?
The MAP should be reduced by a maximum of 20% in the first hour but no more than 25% within the first 24 hours.
Overaggressive reduction in the BP can lead to ischemic end organ damage due to the inability to auto-regulate appropriately.
When the patient is in hypertensive emergency and their BP is being reduced, aside from reducing the BP by 25% from baseline, what marker of reduction can be used instead?
less than 160/100 mmHg
What complications are associated with untreated hypertension?
Cerebrovascular: Stroke (80% thromboembolic). Hypertension is the most important risk factor for cerebral infarctions. BP control reduces the risk of stroke and heart failure more effectively than any other intervention.
Cardiac: Left ventricular hypertrophy, heart failure, coronary artery disease.
Renal: Chronic kidney disease, nephrosclerosis.
Vascular: Aortic dissection, aneurysm.
Ophthalmic: Hypertensive retinopathy.
What retinal changes occur secondary to hypertensive states?
Hypertensive retinopathy presents with papilledema, flame hemorrhages, or cotton-wool spots on fundoscopic examination.
What is the management strategy for hypertensive urgency versus hypertensive emergency?
Hypertensive Urgency: No evidence of end-organ damage; managed by gradually lowering BP over 24 hours with oral antihypertensive agents (e.g., clonidine, captopril).
Hypertensive Emergency: Evidence of end-organ damage (e.g., stroke, encephalopathy, AKI, aortic dissection). BP should be lowered by 25% in the first hour, then gradually over 24–48 hours using IV agents like nicardipine, esmolol, or nitroprusside.
A 55-year-old man with a history of untreated hypertension presents to the emergency department with severe headache, nausea, and confusion that began 6 hours ago. On examination, his blood pressure is 220/125 mmHg, heart rate is 90/min, and respiratory rate is 18/min. Neurological examination reveals mild disorientation and difficulty with attention but no focal deficits. Fundoscopic examination shows bilateral papilledema. Serum creatinine is 2.4 mg/dL (baseline 1.1 mg/dL), and urinalysis reveals proteinuria and hematuria. Head CT shows no evidence of intracranial hemorrhage.
What is the most appropriate next step in management?
a) Oral clonidine
b) Intravenous nicardipine
c) Intravenous furosemide
d) Observation and repeat blood pressure in 2 hours
e) Intravenous labetalol
This patient has hypertensive emergency characterized by severely elevated blood pressure and evidence of end-organ damage, including hypertensive encephalopathy (headache, confusion, papilledema) and acute kidney injury (elevated creatinine). The goal is to reduce mean arterial pressure (MAP) by no more than 20% in the first hour to avoid ischemia, then gradually normalize BP over 24–48 hours, ensuring that there is no more than a 25% reduction of BP in the first 24-hours. IV nicardipine, a calcium channel blocker, is ideal for controlled BP reduction in this scenario.
Labetalol (e) is an alternative but not preferred in renal impairment due to its combined beta- and alpha-blocking effects.
Clonidine (a) is used for hypertensive urgency but is too slow for hypertensive emergencies.
Furosemide (c) is not first-line unless there is pulmonary edema.
Observation (d) is inappropriate given the end-organ damage.
A 48-year-old woman with a history of essential hypertension presents to her primary care clinic complaining of mild headache and lightheadedness for 2 days. Her home blood pressure readings have been consistently high over the last week, averaging 180–190/110–115 mmHg. She denies chest pain, shortness of breath, vision changes, or neurologic symptoms. On examination, her blood pressure is 185/115 mmHg, pulse is 88/min, and the remainder of her physical exam is unremarkable. Basic metabolic panel, urinalysis, and fundoscopic examination show no evidence of end-organ damage.
What is the most appropriate next step in management?
a) Initiate IV labetalol
b) Administer oral clonidine in the office
c) Schedule outpatient follow-up within 1 week
d) Start oral captopril and reassess in 30 minutes
e) Admit for observation and continuous BP monitoring
This patient has hypertensive urgency, defined as severely elevated blood pressure (≥180/≥110 mmHg) without end-organ damage. The goal is to lower BP gradually over 24–48 hours to prevent ischemia from overly aggressive BP reduction. Oral captopril, a short-acting ACE inhibitor, is an appropriate option for BP control and allows reassessment in the clinic before discharge.
IV labetalol (a) and hospital admission (e) are unnecessary in the absence of end-organ damage.
Clonidine (b) is another option but may cause rebound hypertension if not continued.
Follow-up alone (c) is inadequate without an initial intervention.
