Essential HypertensionRaheef Alatassi4th year medical studentInternal medicine

Objectives

Definition & classifications Prevention & detection & importance Causes HTN in pregnancy Management Goals of treatment Classes of drugs & side effects Specific management in e.g. IHD,DM HTN emergency & urgency with management

Definition &

classifications

Definition of essential hypertension

Essential, primary, or idiopathic hypertension is defined as high BP in which secondary causes such as Reno vascular disease, renal failure, aldosteronism, or other causes of secondary hypertension or mendelian forms (monogenic) are not present.

Essential hypertension accounts for 95% of all cases of hypertension.

Essential hypertension is a heterogeneous disorder, with different patients having different causal factors that lead to high BP.

Essential hypertension needs to be separated into various syndromes because the causes of high BP in most patients presently classified as having essential hypertension can be recognized.

Detection

Hypertension is diagnosed when systolic blood pressure is consistently equal to or

more than 140 mm Hg, or diastolic blood pressure is equal to or more

than 90 mm Hg;

a single elevated blood pressure reading is not sufficient to establish the diagnosis of hypertension.

Detection

Detection

Blood pressure should be measured with a well-calibrated sphygmomanometer.

The bladder length within the cuff should encircle at least 80% of the arm circumference.

Readings should be taken after the patient has been resting comfortably, back supported in the sitting or supine position, for at least 5 minutes and at least 30 minutes after smoking or coffee ingestion.

classification

Importance Sixty-six million Americans have

elevated blood pressure. The prevalence of hypertension

increases with age and is more common in blacks than in whites.

Cardiovascular morbidity and mortality increase as both systolic and diastolic blood pressures rise.

Importance

Prevention -1 Maintaining a healthy diet

a. Reduction of dietery sodium (salt) intake.

b. Minimizing saturated fat and cholestrol intake

c. Including fresh fruits and vegetables in every day meals.

Prevention-2 Maintaing a healthy weight.

Being overweight can raise BP and losing weight can lower BP.

Prevention -3 Physical activity.

An average of 2 hours and 30 minutes of moderate-intensity exercise weekly is ideal for preventing hypertension.

Prevention -4 Cessation of smoking

Smoking decreases the elasticity of the blood vessels and increase blood vessel resistance which causes hypertension.

Prevention -5 Limitation of alcohol intake .

Heavy drinkers who cut back to moderate drinking can lower their systolic blood pressure by 2 to 4 (mm Hg) and their diastolic blood pressure (by 1 to 2( mm Hg.

Causes of primary & secondary hypertension

PRIMARY (ESSENTIAL) HYPERTENSION

95% of the cases

The cause is unknown

Between the age of (25 – 50)

Precipitating Factors

Genetic factors

Obesity

Alcohol

Salt

Smoking

Low K intake

Sympathetic overactivity

Insulin resistance

NSAIDs

Polycythemia

SECONDARY ( IDENTIFIABLE ) HYPERTENSION

5% of the cases

The cause of hypertension can be discovered

Common in ages ( below 20 or after 50 )

Causes ofSECONDARY ( IDENTIFIABLE )

HYPERTENSION

SECONDARY

HTN

Endocrine

disease

Renal disease

Drugs

Hypertension and pregnancy

Its classified into 4 categories:1. Chronic hypertension.

2. Gestational hypertension.

3. Preeclampsia.

4. Preeclampsia superimposed on chronic hypertension.

1)Chronic hypertension Blood pressure is defined as BP exceeding 140/90 mm Hg before pregnancy or before 20 week’s gestation.

When hypertension is first identified during pregnancy and she is at less than 20 weeks gestation, blood pressure evaluation usually represent chronic hypertension.

2)Gestational hypertension:

Refers to hypertension onset in the latter part of pregnancy >20 weeks without any other features of preeclampsia and normalization of the BP postpartum .

Pathophysiology is still unknown.

Maternal and fetal outcome are usually normal.

Gestational hypertension can develop either of on of these four :

Preeclampsia (gestation hypertension + protein urea)

Acute fatty liver of pregnancy.

HELLP syndrome (hemolysis + elevated liver enzymes + low

platelets )

eclampsia (gestation hypertension + protein urea +

tonic-colonic seizure )

3) preeclampsia

Preeclampsia is a disorder of widespread vascular endothelial malfunction and vasospasm that occurs after 20 weeks' gestation and can present as late as 4-6 weeks’ postpartum. It is clinically defined by hypertension and proteinuria, with or without pathologic edema

Risk factors

Maternal RF

1. Women first pregnancy (primigravida)

2. Age younger than 18 or above 35

3. History of preeclampsia

4. Family history5. Obesity

Maternal medical RF

1. Chronic hypertension especially when its 2ndary (hyperaldostronisim , hypercortisolism)

2. Preexisting diabetes (I or II)

3. History of migraine 4. Use of SSRI beyond 1st

trimester.

Symptoms of preeclampsia 1. Visual disturbance.

2. Headache (women describe it as throbbing)

3. Epigastric pain or RUQ (due to hepatic swelling ).

4. Retinal vasospasm (if severe)

5. Hyperactive reflexes (severe stage)

6. On auscultation the presence of S4 suggests LV Hypertrophy or diastolic dysfunction.

New seizures in pregnancy suggest preeclampsia-eclampsia .

Management

Management

Current control rates (SBP <140 mmHg and DBP <90 mmHg).

In the majority of patients, reducing SBP has been considerably more difficult than lowering DBP.

the majority will require two or more antihypertensive drugs

Goals of treatment reduce cardiovascular and renal

morbidity and mortality. Treating SBP and DBP to targets that are

<140/90 mmHg is associated with a decrease in CVD complications.

In patients with hypertension and diabetes or renal disease, the BP goal is <130/80 mmHg

Management of HTN Adoption of healthy lifestyles by all

persons is critical for the prevention of high BP.

Two types of management:1) Lifestyle modification. 2) Pharmacologic Treatment.

Lifestyle modification

NO Modification Approximate SBP Reduction(Range)

1 Weight reduction 5–20 mmHg

2 Adopt DASH eating plan 8–14 mmHg

3 Dietary sodium reduction

2–8 mmHg

4 Physical activity 4–9 mmHg

Classes of drugs & side effects

Classes of drugs & side effects

More than 2/3 of hypertensive individuals cannot be controlled on one drug and will require two or more antihypertensive agents selected from different drug classes.

Mild Hypertension can be often controlled with a single drug.

Classes of drugs & side effects

Cardiac output & peripheral resistance controlled by two mechanism:1) Baroreflexes.2) Renin-angiotensin-aldosterone system.

Anti HTN

Diuretics

ACE I

ARBS

Ca Channel Blockers

Beta blockers

Alpha blockers

Diuretics

tx: mild to moderate HTN First drug of treatment Also tx. heart failure or kidney disease Used with other antihypertensives to

enhance effectiveness Reduce edema assos. with CHF

Diuretics Actions

DiureticsAction

Reduce blood volume through urinary excretion of water and electrolytes

Electrolyte imbalances can occur (mainly hypokalemia)

Also, Hyperglycemia, Hyperuricemia,HyperCa

Side effects

Orthostatic hypotension Dry mouth,irritation Disorientation Dehydration

HyperK: with K sparingGynecomastia

Angiotensin-Converting Enzyme Inhibitors

“ACE” inhibitors Mainstay of oral vasodilator therapy More effective when used with diuretics First line of therapy if the Diuretics or

betaB are contraindicated.

ACE INHIBITORS

ACE INHIBITORS

Angiotensin Converting Enzyme (ends in PRIL)

captopril enalapril benzapril(Capoten) (Vasotec) (Lotensin)

ACE INHIBITORSACTION

peripheral vascular resistanse without

Ø cardiac output

Ø cardiac rate

Ø cardiac contractility

Side effects

Headache Orthostatic hypotension-infrequent dry Cough Hyperkalemia AKF Skin rash

Are fetotoxic & should not be used in pregnancy.

Drug interactions Diuretics specially K sparing Alcohol Beta-blockers

All the above enhance the effects

It’s standerd in the care of patient following a myocardial infarction

Angiotensin 2 Receptor antagonists

Alternative of ACE I . Same effect to ACE I . Produce arteriole and venous dilatation . Inhibit aldosterone secretion.

ARBS

Don’t increase Bradykinin levels.Decrease Nephrotoxixty of

Diabetes.Decrease Dry cough

Don’t use it in pregnancy

Calcium Channel Blockers

Emerged as major drug to tx. HTN when the preferred first line are contraindicated.

Used for arrythmias also Alternative to B-blocker (hx. Asthma) Avoid High dose of SA. CCB because of inc.

risk of Myocardial infarction.

Calcium Channel Blockers Examples

Verapamil Very

Procardia (nifedipine)-HTN Nice

Cardizem (diltiazem)-arrythmias Drugs

Calcium Channel Blockers

Calcium Channel Blockers Action

blocks ca+ access to muscle cells contractility + conductivity of the ______________________ demand for oxygen PVR (relaxing arterioles)

Calcium Channel Blockers

SIDE EFFECTS BP Bradycardia vertigo Headache constipation Peripheral edema A-V block (due to –ve Inotopic&

dromotropic)

Adrenergic ReceptorsReview of ANS

Sympathetic Nervous System

Alpha 1 = vasoconstriction Alpha 2 = vasodilation Beta 1 = increases heart rate Beta 2 = bronchodilation

Beta Adrenergic Blocking Agents

Known as Beta-blockers Axn: Inhibit cardiac response to

sympathetic nerve stimulation by blocking Beta receptors

Decreases heart rate and C.O. Decreases blood pressure First line of therapy in HF

Beta Adrenergic Blocking Agents

Examples – “olol” names Beta 1: Atenolol & Metoprolol Beta 1 and 2: Propranolol

Implications

Can not be abruptly discontinued Check baseline b.p. Check hx. of resp. condition-aggravates

bronchoconstriction

Side effects

Bradycardia Bronchospasm, wheezing Diabetic: hypoglycemia Insomnia Sexual Dysfunction

Alpha-1 adrenergic blockers

Alternative if B-blockers and diuretics do not work

Also used to tx. mild to mod. urinary obstructive dx.

Also used for treat of benign prostate hyperplasia

Alpha-1 Adrenergic Blocking Agents

Action Block postsynaptic alpha-1 adrenergic

receptors to produce arteriolar and venous vasodilation

Reduces peripheral-vascular resistance

Examples of Apha-1 blockers

Cardura (doxizosin) Minipress (prazosin) Hytrin (terazosin)

Examples – “ZOSIN” names

Side effects Drowsiness Headache Weakness,lethargy

Centrally Acting Alpha-2 Agonists

Stimulate Alpha-2 receptors in brainstem

Decreases HR, SBP and DBP More frequent side effects – drowsiness,

dry mouth, dizziness Never suddenly DC = rebound HTN Clonidine – Catapres Methyldopa – (used in Pregnancy)

Direct Acting Vasodilators

Action: direct arteriolar smooth muscle relaxation, decreasing PVR

Uses: HTN, renal dx., Ex: Hydralazine, Minoxidel SE: tachycardia, orthostatic

hypotension,dizziness, palpitations, nausea, nasal congestion

Hypertension and ischemic heart disease

Case study 55 year old man known case of IHD and he now diagnosed with HT what is the drug of choose to treat him?

1-BB 2-ACEI 3-CCB

Hypertensive patients are at increased risk for MI or other major coronary events Why?

1-increase in heart o2 demand 2- increase heart work (life ventricle hypertrophy)

If the patient have HT and IHD that even increase the risk more

Stable angina and silent ischemia BBs (propranolol) will lower BP; reduce

symptoms of angina; improve mortality; and reduce cardiac output heart rate, and AV conduction

Treatment should also include smoking cessation, management of diabetes, lipid lowering, antiplatelet agents, exercise training and weight reduction in obese patients.

If angina and BP are not controlled by BB therapy alone, or if BBs are contraindicated, as in the presence of severe reactive airways disease, severe peripheral arterial disease, high-degree AV block,or the sick sinus syndrome

Use dihydropyridine or nondihydropyridine type CCBs (amlodipine Verapamil)

If angina or BP is still not controlled on this two-drug regimen, nitrates can be added, but these should be used with caution in patients taking phosphodiesterase-5 inhibitors such as sildenafil. Short-acting dihydropyridine CCBs should not be used because of their potential to increase mortality,particularly in the setting of acute MI.

Diabetes and HT The combined unadjusted prevalence of total

diabetes and impaired fasting glucose in those over age 20 is 14.4 percent and is the leading cause of blindness, ESRD, and nontraumatic amputations

The United Kingdom Prospective Diabetes Study (UKPDS)174 demonstrated that each 10 mmHg decrease in SBP was associated with average reductions in rates of diabetes-related mortality (15 percent), myocardial infarction (11 percent)

American Diabetes Association recommended that BP in diabetics be controlled to levels of 130/80 mmHg or lower

ACEIs(captopril), BBs(propranolol), ARBs(valsartan), and calcium antagonists(Verapamil) have a demonstrated benefit in the treatment of hypertension in both type 1 and type 2 diabetics

The question of which class of agent is superior for lowering BP is somewhat moot because the majority of diabetic patients will require two or more drugs to achieve BP control

The ADA has recommended ACEIs for diabetic patients older than 55 years of age at high risk for CVD, and BBs for those with known CAD

showed a reduction in combined MI, stroke, and CVD death of about 25 percent and a reduction in stroke by about 33

the ADA has recommended both ACEIs and ARBs for use in type 2 diabetic patients with CKD

BB is indicated in a diabetic with IHD but may be less effective in preventing stroke than an ARB as was found in the LIFE study

CCBs may be useful to diabetics, particularly as part of combination therapy to control BP

The Appropriate Blood Pressure Control in Diabetes (ABCD) Trial in diabetics was stopped prematurely when it was found that the dihydropyridine nitrendipine was inferior to lisinopril in reducing the incidence of ischemic cardiac events.

Hypertensive emergencies

Hypertensive emergencies are characterized by severe elevations in BP (>180/120 mmHg) complicated by evidence of impending or progressive target organ dysfunction

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of BP and parenteral administration of an appropriate agent

The initial goal of therapy reduce mean arterial BP by no more than 25 percent (within minutes to 1 hour)

then if stable, to 160/100–110 mmHg within the next 2–6 hours

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided. For this reason, short-acting nifedipine is no longer considered acceptable

further gradual reductions toward a normal BP can be implemented in the next 24–48 hours

References