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HYPERTENSIONSAMIR EL ANSARY
Hemodynamic determinants of blood pressure (BP)
Arterial BP is the product of cardiac output (CO) and systemic vascular resistance (SVR).
BP = CO x SVR (analogous to Ohm law)
Malignant hypertensionis caused by
Increased SVR.
Hypertensive crisisHypertensive crisis is the turning point in the course of hypertension in which immediate
management of the elevated BP has a decisive role in the eventual outcome.
It is a condition of severe and uncontrolled increase in the BP.
An acute increase in BP can occur in the absence or presence of acute
or chronic target organ dysfunction.
Target organs affected by hypertensive crisis
Four organs are the usual target of severely elevated BP:
Kidneys: acute kidney injury caused by proliferative endarteritis and fibrinoid necrosis of afferent artery
Brain: hypertensive encephalopathy, cerebrovascular accidents (CVA)
Eye or retina: retinal hemorrhage or exudates or papilledema .
Heart: acute coronary syndrome, decompensated heart failure, aortic dissection, and acute
intravascular hemolysis .
Malignant hypertension and accelerated hypertension
Both are syndromes in which a markedly elevated BP is associated with hypertensive
neuro retinopathy. In accelerated hypertension, there may be
Flame hemorrhages or cotton wool exudates.
Malignant hypertensionIs diagnosed when papilledema occurs
as well.
Hypertensive urgency (HU) OR Non-emergent hypertension (NEH)
When severe hypertension occurs in the absence of any acute end-organ damage, it is
classified as HU-NEH. Because the complications from HU are not
immediate, this condition can be treated safely outside the intensive care unit and hospital with
gentle reduction in BP achieved over hours to days.
Hypertensive encephalopathy
Hypertensive encephalopathy occurs in the setting of sudden and sustained elevation in
BP. It occurs in both benign and malignant
hypertension. The clinical presentation is that of altered mental status and/or seizures, but focal neurologic findings are uncommon.
This condition can be difficult to distingui-sh from a primary neurologic event.
Causes ofmalignant and accelerated
hypertensionIn contrast to ambulatory hypertension (over 90% essential) as many as 50% of patients with malignant or accelerated hypertension
have secondary causes.
The most important of secondary causes are medications, chronic kidney disease, and
renal artery stenosis (RAS).
The short-term treatment of hypertension and hypertensive
emergency
The short-term treatment of choice is intravenous (IV) sodium nitroprusside.
The initial dose is 0.5 mcg/kg/min, and this should be increased by 0.5 mcg/kg/min every 2 to 3 minutes until a diastolic BP < I10 mm Hg has been attained. Further acute decreases in BP should be avoided to
prevent hypoperfusion to vital organ(s) because Blood flow autoregulation may have been altered
to accommodate chronically elevated BP.
Acceptable alternative parenteral drugs for the short-term treatment of malignant hypertension
include
Labetalol, Nicardipine,Enalaprilat, or Fenoldopam.
Extreme caution should be taken while using agents known to cause
or further worsen intravascular volume status because patients with hypertensive emergency
often present with
Intravascular volume depletion.
Outline the typical long-term antihypertensive regimen after
successfultreatment of malignant
hypertension or hypertensive crisis.
Because malignant hypertension is mediated by increased SVR, it is recommended that longterm
therapy include a vasodilator such as
Hydralazine or minoxidil.
Vasodilators cause reflex tachycardia and sodium retention
Therefore it is usually also necessary to
Include a- p-blocker (labetalol) and a diuretic
agent.
In some cases, long-term BP reduction may be achieved with less potent vasodilators, such as
Angiotensin-converting enzyme (ACE) inhibitors or calcium channel blockers.
The appropriate short-term treatment for hypertension in a patient with
pheochromocytoma
Hypertension from pheochromocytomas is caused by
Vascular smooth muscle a-receptor activation, which results in
vasoconstriction.
Thus the best short-term treatment is IV administration of the
a1-blocker phentolamine. Sodium nitroprusside is also a reasonable choice.
B-Blockers should initially be avoided because they cause both
unopposed peripheral a-receptor stimulation and
decreased CO.
Describe the short-term treatment of cocaine-induced hypertensive crisis.Cocaine-induced hypertensive crisis
falls under “Catecholamine-associated
hypertension."Cocaine causes hypertension by inhibiting catecholamine reuptake at nerve terminals.
Therefore drugs that can block a-receptors such as labetalol or phentolamine are effective.
Selective p-blockers without a1 blockade such as propranolol are not recommended because of the risk of
unopposed a1 action.
If hypertension is severe, sodium nitroprusside is the drug of choice.
In the setting of cocaine-related myocardial ischemia, nitroglycerin and benzodiazepines are effective against both cocaine-induced hypertension
and vasoconstriction of the coronary arteries.
Coca-ethylene : Is a compound formed in vivo
when cocaine and ethyl alcohol(EtOH) have been ingested
simultaneously. It produces greater increases in heart rate, rate-
pressure product, and euphoria compared with the effects of cocaine
alone.
Coca-ethylene :Therefore the treatment of hypertension tends
to pose greater therapeutic challenge in patients consuming EtOH as well as cocaine.
Cocaine-induced hypertensionshould be treated with extreme caution and
treatment regimens reviewedwith passage of time because the condition
undergoesSpontaneous resolution when cocaine
is metabolized.
How is hypertension treated in the short term in patients with aortic
dissection?Aortic dissection begins with a tear in the intima of
the aorta; this is propagated by the aortic pulse wave (dp/dt).
Myocardial contractility, heart rate, and BP contribute to
the aortic pulse wave. The goal of treatment is to decrease
myocardial contractility and heart rate.
This goal has traditionally been best achieved with
Sodium nitroprusside and esmolol.
Labetalol alone is also effective in this
setting.
Why is BP elevated in patients with CVA?
Patients with CVA often have a severe increase in BP potentially resulting from a
central mechanism and/or compensatory increase
in response toIncreased intracranial pressure.
Stress responses to hospitalization, headache, urinary retention, or
concomitant infection may lead to abnormal autonomic activity and
raised levels of circulating catecholamines.
Greater than 60% .of patients with CVA will have
An acute hypertensive response.
Central mechanismThe primary cause is damage or compression of
specific regions in the brain that mediate autonomic control.
Increased sympatho-adrenal tone and subsequent release of renin
Each in isolation or together, can also contribute to high BPS.
Failure of autoregulation of cerebral blood flow and response to increased intracranial pressure (ICP)
With acute brain injuryThe ability of the brain to autoregulate and maintain cerebral blood flow is impaired.
AutoregulationIs a mechanism by which the brain can maintain
a constant cerebral blood flow despite a wide fluctuation in cerebral perfusion pressure (CPP)
(from the range of 60-180 mm Hg).
Cerebral blood flow = CPP/Cerebral vascular resistance
CPP is the difference between mean arterial pressure (MAP) and ICP.
Under physiologic circumstances cerebral venous pressure
(backflow in the cerebral venous system)is the primary determinant of ICP.
In absence of any pathologic condition,
Cerebral venous pressure is zero; thus the arterial pressure
determines CPP.When the ICP goes up because of increase
in cerebral venous pressure (as in CVA), MAP goes up in an attempt to maintain
adequate CPP.
How should hypertension be treated in patients with CVA?
Hypertensive encephalopathyThe goal is gradual and careful reversal of
vasogenic subcortical edema.
MAP should be cautiously reduced by no more than 15% over a 2- to 3-hour period.
Severe neurologic complications have occurred
with MAP reductions at 40% or more.
Thromboembolic cerebrovascular disease
The goal is salvation of ischemic penumbra
For patients thought to be candidates for reperfusion therapy
{ Thrombolytic therapy }, systolic BP (SBP) >I85 mm Hg and diastolic BP (DBP) >I10 mm
Hg warrant treatment.
For the subset of patients who are not candidates for reperfusion
therapy, theexpert opinion is to treat SBP >220
mm Hg and DBP >I20 mm Hg with a goal of 15% to 25% reduction
in MAP over the first 24 hours.
Subarachnoid hemorrhagePoorly controlled BP increases the risk of
rebleeding. The presence of blood in the subarachnoid
space induces intense vasospasm and increases the risk of severe ischemia 4 to 12
days after the first bleeding.
The goal is 20% to 25% reduction in BP over a 6- to 12-hour period but not less than 160 to
180/100 mm Hg.
Intracerebral hemorrhage
The consensus guidelines on treatment of intracerebral bleeding:
IV medications should be used to treat SBP > 200 mm Hg or MAP >I50 mm Hg with BP monitoring
done every 5 minutes.
In suspected intracranial hypertension, BP should be lowered with a parenteral agent if SBP is >I80 mm Hg or MAP >I30 mm Hg while maintaining
CPP above 60 to 80 mm Hg.
In the absence of elevated ICP, treat SBP >I80 mm Hg and MAP > 130 mm Hg with a
target BP of 160/90 mm Hg or a MAP of 110 mm Hg.
The rate of BP reduction should be slowed if the patient's neurologic status deteriorates.
Oral therapy should be instituted before parenteral treatment is discontinued.
Clonidine or a-methyldopaShould be avoided because of the risk of
impaired cerebral function.
Describe the short-term treatment of hypertension in patients with ischemic
heart disease and ongoing angina.
Hypertension can precipitate ischemic chest pain in patients with severe coronary artery disease.
Alternatively, hypertension can result from chest pain, which results in marked increases in catecholamines and secondary reactive
hypertension. In either setting, hypertension is associated with an increase in SVR and increases in myocardial
oxygen demand.
Describe the short-term treatment of hypertension in patients with ischemic heart disease and ongoing angina.
Hypertension can precipitate ischemic chest pain in patients with severe
coronary artery disease.
Alternatively, hypertension can result from chest pain, which results in marked
increases in catecholamines and secondary reactive hypertension.
In either setting, hypertension is associated with an increase in SVR and increases in myocardial oxygen
demand.
Nitroglycerin and p-blockers
Are the initial agents of choice. Because nitroprusside
increases heart rate and myocardial oxygen demand in
this settingIt is considered a secondary
agent.
How should hypertension
associated with preeclampsia be
treated?
How should hypertension associated with preeclampsia be
treated?The traditional treatments of choice are
Hydralazine or a-methyldopa. If these drugs are ineffective or poorly tolerated,
labetalolIs a reasonably safe and effective alternative.
Medications to be avoided because of potential teratogenesis
IncludeSodium nitroprusside,
trimethaphan, diazoxide, ACE inhibitors, p-blockers, and calcium
channel blockers.
Unfortunately, the safety profile of many antihypertensive drugs during pregnancy is
unknown.
Because
Preeclampsia and eclampsiamay be life threatening, sometimes it may
be necessary to prescribe potent antihypertensive agents
(Sodium nitroprusside or Minoxidil) with unclear fetal toxicity potential.
Causes of RAS{ Renal artery stenosis }
And how should it be evaluated?
The major causes are fibromuscular dysplasia (especially in young women) and atherosclerosis (in those aged >55 years in association with polycystic
kidney disease). Although Doppler ultrasonography of the renal
vasculature is an excellent noninvasive test to confirm RAS, it has not been standardized, and magnetic
resonance angiography is recommended.
Reactive hypertensionPatients with stage 1 or 2 hypertension that is poorly
controlled with medications can have marked elevation in BP to stressors such as pain or shortness
of breath.
Increases in catecholamines of stress lead to severe elevations in BP that should be distinguished
from primary hypertensionbecause the approaches to therapy differ.
In reactive hypertension it is necessary to treat the cause of BP, for example, chest pain or pancreatitis, rather than the elevated BP.
Why does lowering of BP potentially result in a decline in glomerular filtration rate
(GFR) in severe hypertension?Normally, GFR is maintained despite decreases in
BP by compensatory increasesIn efferent arteriolar tone
Two major causes exist of loss of GFR after reduction of BP in the setting of severe
hypertension:
RAS{ Renal artery stenosis } Long-standing essential hypertension
RAS{ Renal artery stenosis } In a patient with a fixed
atherosclerotic lesion of the main renal artery, a drop in BP can cause a fall in GFR because the fixed lesion limits afferent arteriolar flow to such
an extent that even maximal elevation in efferent arteriolar tone cannot compensate and maintain
GFR.
Long-standing essential hypertension
In this setting, no macrovascular abnormalities are present; the problem is
Marked sclerosis of the microvasculature of the kidney, including the afferent artery.
Because of afferent arteriolar sclerosis, the afferent artery is unable
to vasodilate in response to a drop in BP.
Hence, GFR falls when BP is lowered even with increases in efferent arteriolar tone that normally would offset, at least partially, decreases in BP.
When should an evaluation for secondary
hypertension be considered?
At initial presentation of malignant hypertension
(especially if the patient is white, younger than 30 years, or older
than 50 years of age)
When rapid onset of severe hypertension occurs within less
than 5 years
When an increase in serum creatinine level occurs after the
initiation of ACE inhibitor treatment
In compliant patients whose BP is difficult to control after an adequate
trial with a combinationof Diuretic, p-blocker, and potent
vasodilator
Important causes of secondary hypertension
Secondary hypertension accounts for 5% of cases of hypertension.
Renal:Renovascular disease, renal
parenchymal disease, polycystic kidney disease, Liddle syndrome, syndrome of
apparent mineralocorticoid excess, hypercalcemia
EndocrineHyperthyroidism, hypothyroidism, primary hyperaldosteronism, Cushing syndrome, pheochromocytoma, congenital adrenal
hyperplasia
DrugsPrescription (e.g., estrogen, cyclosporine, steroids); over-the-counter (e.g.,pseudo-phedrine, nonsteroidal anti-inflammatory
drugs); illicit (e.g., tobacco smoking, ethanol, cocaine) .
NeurogenicIncreased intracranial pressure,
spinal cord section
MiscellaneousCoarctation of aorta, obstructive sleep apnea, polycythemia Vera
Causes of primary aldosteronism, and how should they be
distinguished?
The major causes are unilateral aldosterone-producing adenoma (APA)
And bilateral idiopathic adrenal hyperplasia (IAH).
Primary aldosteronism should be suspected in a patient with hypokalemia and hypertension with metabolic alkalosis.
Primary aldosteronism should be suspected in a patient with hypokalemia
and hypertension with metabolic alkalosis.
It is necessary to first demonstrate renal potassium wasting (high urine K+ in
association with low serum K+) followed by a decrease in renin and an elevated
aldosterone level. The plasma aldosterone/renin ratio (>40)
is often used.
The plasma aldosterone/renin ratio (>40) is often used.
If the ratio is elevated, the aldosterone response to either NaCl infusion or
fludrocortisone is used and considered positive if the plasma aldosterone level
remains elevated (> 10 pg/mL).
Treatment of APA { aldosterone-producing adenoma } is surgical adrenalectomy, whereas mainstays of treatment of IAH
{ idiopathic adrenal hyperplasia } are mainly medical.
Adrenal imaging can sometimes distinguish between APA and IAH, but it is often
necessary to pursue a more definitive study to verify the diagnosis of APA.
By far, selective adrenal vein sampling is the most validated technique used to differentiate
APA from IAH.
