State Establishment “Dnipropetrovsk Medical Academy of Health Ministry of
Ukraine”
Department of Internal Medicine 1
SECONDARY HYPERTENSION
HYPERTENSIVE CRISIS
Associate Professor,
Olha Cherkasova, M.D., Ph.D.
Dnipro, 2020
• Hypertension is sustained elevation of
resting systolic BP (≥ 140 mm Hg)
and/or diastolic BP (≥ 90 mm Hg), based
on the average of two or more seated
BP readings during each of two or more
outpatient visits.
Definition
• Secondary hypertension is defined as increased systemic
blood pressure (BP) due to an identifiable cause. Only 5–
10% of patients suffering from arterial hypertension have
a secondary form
When to suspect secondary hypertension
clinically (1)
Absence of family history of hypertension
Severe hypertension ˃180/110 mm Hg with onset at age
<20 years or ˃ 50 years
Difficult-to-treat or resistant hypertension with significant
end-organ damage feature
Presents with combination of pain (headache), palpation,
pallor and perspiration – 4 P’sof phaeochromocytoma
When to suspect secondary hypertension
clinically (2)
Polyuria, nocturia, proteinuria or hematuria – indicative of
renal disease
Persons with short or thick neck – Obstructive Sleep
Apnoea
Hypertension in children
Significant elevation of plasma creatinine with use of ACE
inhibitors
Causes of secondary hypertension with clinical indications
Common causes
Renal parenchymal disease
Renovascular disease
Primary aldosteronism
Obstructive sleep apnea
Drug or alcohol induced
Uncommon causes
Pheochromocytoma/paraganglioma
Cushing’s syndrome
Hypothyroidism
Hyperthyroidism
Aortic coarctation (undiagnosed or repaired)
Primary hyperparathyroidism
Congenital adrenal hyperplasia
Mineralocorticoid excess syndromes other than primary aldosteronism
Acromegaly
Renal Parenchymal Diseases
CAUSES
• glomerulonephritis,
• diabetic nephropathy (diabetic kidney disease),
• kidney damage in the course of systemic connective tissue diseases
(systemic lupus erythematosus, systemic sclerosis, systemic vasculitis),
• tubulointerstitial nephritis,
• obstructive nephropathy,
• polycystic kidney disease, large solitary kidney cysts (rare),
postirradiation nephropathy, hypoplastic kidney, renal tuberculosis
(rare).
Renovascular Hypertension
Patients groups
• older arteriosclerotic patients who have a plaque obstructing the
renal artery, frequently at its origin,
• patients with fibromuscular dysplasia
Patient with suspected atherosclerotic renal artery
stenosis
Primary Aldosteronism
PA is defined as a group of disorders in which aldosterone
production is inappropriately high for sodium status, relatively
autonomous of the major regulators of secretion (angiotensin II,
plasma potassium concentration), and nonsuppressible by sodium
loading. Excess aldosterone, inappropriately high for the salt intake
status, causes hypertension, cardiovascular and renal damage,
sodium retention, suppression of plasma renin, and increased
potassium excretion that (if prolonged and severe) may lead to
hypokalemia. PA is commonly caused by an adrenal adenoma,
unilateral or bilateral adrenal hyperplasia, or in rare cases adrenal
carcinoma or inherited conditions of familial hyperaldosteronism .
Patients with suspected primary aldosteronism
Cushing's Syndrome
Clinical Features
• Symptoms associated with hypercortisolemia include
weight gain, lethargy, weakness, menstrual irregularities,
loss of libido, depression, hirsutism, acne, purplish skin
striae, and hyperpigmentation.
• The signs associated with Cushing's syndrome are
extremely varied and differ in severity. Signs that
differentiate Cushing's syndrome from pseudo-Cushingoid
states most reliably include the presence of proximal
myopathy, easy bruising, and thinness and fragility of the
skin.
Pheochromocytoma
• Pheochromocytomas and paragangliomas are tumors derived from
chromaffin cells in the adrenal medulla or extra-adrenal paraganglia.
Adrenal tumors and tumors located in the sympathetic paraganglia will
be referred to as pheochromocytomas. Pheochromocytomas are found
in 0.2-0.6% of subjects with hypertension. The cost-effectiveness of
diagnostic workup of pheochromocytoma is markedly restricted by low
specificity of clinical symptoms together with symptoms overlapping
within a wide variety of other conditions, including idiopathic
hypertension, hyperthyroidism, heart failure, migraines, and anxiety.
• Hypertension occurs in about 80-90% of patients with
pheochromocytoma. About half of these patients develop sustained
hypertension, another 45% present with paroxysmal hypertension,
while 5-15% are normotensive.
• Several additional endocrine disorders, including thyroid
diseases and acromegaly, cause hypertension.
• Mild diastolic hypertension may be a consequence of
hypothyroidism, whereas hyperthyroidism may result in
systolic hypertension.
• Hypercalcemia of any etiology, the most common being
primary hyperparathyroidism, may result in
hypertension.
Obstructive sleep apnea
• Obstructive sleep apnea (OSA) is a disease caused by
recurrent episodes of upper airway collapse (causing
apnea) or upper airway narrowing (causing hypopnea – a
marked decrease in airflow) at the level of the pharynx
with normal function of the respiratory muscles. Apnea,
hypopnea, or both cause episodes of nocturnal
hypoxemia and arousals from sleep that lead to sleep
fragmentation (patients are unaware of most of these
episodes).
Patients with suspected obstructive sleep apnoea
Coarctation of the aorta
• Coarctation of the aorta refers to a narrowing of the aorta, most frequently at
the level of the aortic isthmus, ie, distal to the origin of the left subclavian
artery, opposite to the ligamentum arteriosum.
CLINICAL FEATURES
1. Symptoms usually develop in the second or third decade of life and are
associated with prestenotic hypertension in the aorta. They include headaches,
epistaxis, and disturbances of vision.
2. Signs involve hypertension (blood pressures measured on the upper
extremities are >10 mm Hg higher than those measured on the popliteal artery);
different blood pressures on both brachial arteries in patients with stenosis
including the origin of the left subclavian artery; weak or absent pulse on the
femoral arteries; and rarely, intermittent claudication (usually collateral
circulation is well developed).
Drug-related hypertension
• NSAIDs
• glucocorticoids
• diet pills (i.e. phenylpropanolamine and sibutramine),
stimulants (i.e. amphetamines and cocaine),
• decongestants (i.e. phenylephrine hydrochloride and
naphazoline hydrochloride);
• cocaine
• licorice
• Oral contraceptives (oestrogen + progestin)
Drug-related hypertension (2)
• Antidepressant agents (i.e. venlaflaxine and monoamine oxidase
inhibitors)
• Immunosuppressive agents, particularly cyclosporine A,
• Inhibitors of vascular endothelial growth factor (VEGFi) (i.e.
bevacizumab, Avastin®) or tyrosine kinase inhibitors (i.e.
sunitinib, Sutent®, sorafenib, Nexavar®)
Hypertensive crisis
• Hypertensive crisis (acute severe hypertension): an acute
severe increase in systolic blood pressure ≥ 180 mm Hg
and/or diastolic blood pressure ≥ 120 mm Hg with a high
risk of complications.
• The two categories of hypertensive crises are: urgent and
emergency.
Hypertensive Urgency
• Hypertensive crisis that is either asymptomatic or with
isolated nonspecific symptoms (e.g., headache, dizziness,
or epistaxis) without signs of organ damage
• Blood pressure can be brought down safely within a few
hours with blood pressure medication
Hypertensive emergency
• hypertensive crisis with signs of end-organ damage,
mainly in the cardiovascular, central nervous, and renal
systems
• Blood pressure must be reduced immediately to prevent
imminent organ damage. This is done in an intensive care
unit of a hospital.
Organ damage associated with hypertensive emergency
may include
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Changes in mental status, such as confusion
Bleeding into the brain (stroke)
Heart failure
Chest pain (unstable angina)
Fluid in the lungs (pulmonary edema)
Heart attack
Aneurysm (aortic dissection)
Eclampsia (occurs during pregnancy)
Signs and symptoms of end-organ dysfunction (1)
Cardiac
• Heart failure exacerbation, pulmonary edema: dyspnea,
crackles on examination
• Myocardial infarction: chest pain, diaphoresis
• Aortic dissection: chest pain, asymmetric pulses
Neurologic
• Hypertensive encephalopathy: headache, vomiting,
confusion, seizure, blurry vision, papilledema
• Ischemic or hemorrhagic stroke: focal neurological
deficits, altered mental status
Signs and symptoms of end-organ
dysfunction (2)
Renal
• Acute renal failure: azotemia and/or oliguria, edema
Ophthalmic
• Acute hypertensive retinopathy: blurry vision, decrease in
visual acuity, retinal flame hemorrhages, papilledema
Other
• Microangiopathic hemolytic anemia: fatigue, pallor
Additional clinical features that may be present
• Signs of sympathomimetic drug toxicity
• In pregnant patients (in the second or third trimester ):
signs of pre-eclampsia or eclampsia
• Signs of catecholamine-secreting tumors
Approach to management (1)
1. Confirm blood pressure manually and on bilateral upper
extremities.
2. Determine if there are signs of end-organ damage.
• Focused history/physical
• Select screening tests
3. For hypertensive emergencies
• ABCDE approach
• Admit patients (ideally to ICU).
• Lower the blood pressure acutely using IV agents and aim for
targets based on the affected end-organs
• Evaluate and treat underlying disorders.
Approach to management (2)
For hypertensive urgency
• Select, reinstitute, or modify oral antihypertensive therapy.
• In patients with a new diagnosis, evaluate for secondary
causes of hypertension.
• Arrange follow-up, monitoring, and counseling.
Red flags for hypertensive crisis
• Dyspnea
• Chest pain
• Altered mental status
• Focal neurologic symptoms
Treatment
Hypertensive urgency (1)
• Outpatient treatment is recommended.
• Move patient to a quiet room for 30 minutes.
• Reinstitute or increase the dosage of existing oral antihypertensive
therapy.
• For patients with nonspecific symptoms that do not constitute endorgan damage (e.g., isolated headache, nonspecific dizziness, and
epistaxis), consider a rapid-acting oral antihypertensive agent prior to
discharge.
• Clonidine
• Captopril
• Labetalol
• Prazosin
Treatment
Hypertensive urgency (2)
• Monitor the patient for a few hours to ensure BP is improving.
• For patients with a first diagnosis of hypertension, consider
evaluation for secondary hypertension.
• Discharge and follow-up
• Ensure close follow-up with an outpatient provider.
• Long-term treatment goals: See “Treatment” of hypertension.
• Sodium restriction diet
• Hypertensive urgency is usually caused by nonadherence to
antihypertensive therapy. Aggressive intravenous
antihypertensive therapy is not reiqured.
Hypertensive emergency
General principles
• ICU admission and immediate initiation of intravenous
antihypertensive therapy (see table below)
• Continuous cardiac monitoring
• Consider intra-arterial blood pressure monitoring.
• Identify and treat any contributing comorbidities (e.g., chronic
renal failure).
• IV fluids if signs of volume depletion
• Monitor BMP every 6 hours.
Hypertensive emergency
Rate and target of blood pressure reduction
General goal
• Reduce BP by max. 25% within the first hour to prevent coronary
insufficiency and to ensure adequate cerebral perfusion pressure.
• Reduce BP to ∼ 160/100–110 mm Hg over the next 2–6 hours.
• Reduce BP to patients baseline over 24–48 hours.
Intravenous antihypertensives
Calcium channel blockers
• Nicardipine
Nitric-oxide dependent vasodilators
• Sodium nitroprusside
• Nitroglycerin
Direct arterial vasodilators: hydralazine
Antiadrenergic drugs
Selective beta-1 antagonist: esmolol
Nonselective beta blocker with alpha-1 antagonism: labetalol
Nonselective alpha antagonist: phentolamine
ACE inhibitor: enalaprilat