HYPERTENSION

SAMIR EL ANSARY

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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 hypertension

is 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 crisisFour 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 hypertensionBoth 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 hypertension

Is 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 of

malignant 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

successful

treatment 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 nitroprussideis 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 hypertension

should be treated with extreme caution and

treatment regimens reviewed

with passage of time because the condition

undergoes

Spontaneous 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 to

Increased 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 reninEach 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 injury

The 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 encephalopathy

The 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, the

expert 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 setting

It 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

Include

Sodium 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 hypertension

because 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 increases

In 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

hypertensionIn 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.

Global Critical Carehttps://www.facebook.com/groups/1451610115129555/#!/groups/145161011512

9555/ Wellcome in our new group ..... Dr.SAMIR EL ANSARY

GOOD LUCK

SAMIR EL ANSARY

ICU PROFESSOR

AIN SHAMS

CAIRO

elansarysamir@yahoo.com