Causes and treatment of Hypertension

1. Hypertension
Professor Mohammed Bamashmoos

2. Introduction
• Blood pressure is the force on the walls of the
arteries as the blood circulates.
• Blood pressure allows blood to flow and deliver
nutrients to the body.
• We measure blood pressure with two numbers.
• The top number is the blood pressure when your
heart beats.
• The bottom number is your blood pressure when
your heart relaxes and refills with blood.
• The higher your numbers and the longer they are
high, the more damage is caused to your blood
vessels.

3. • Blood pressure increases with age .
• High blood pressure is the leading risk for
death.
• High blood pressure can cause strokes, heart
attacks, and heart and kidney failure.
• It is also related to dementia and sexual
problems.
• These problems can be prevented if high
blood pressure is controlled.

4. Definition
• Hypertension is defined as the presence of a
blood pressure(BP) elevation to a level that
places patients at increased risk for target
organ damage in several vascular beds
including the retina, brain, heart, kidneys and
large conduit arteries.

5. • Hypertension : BP≥140/90 mmHg
• Isolated systolic hypertension
- sBP ≥ 140 and dBP <90
- associated with progressive reduction in vascular compliance
- usually begins in 5th decade; up to 11 % of 75 yr olds
• Accelerated hypertension
- significant recent increase in BP over previous hypertensive levels
associated with evidence of vascular damage on fundoscopy but without
papilledema
• Malignant hypertension
- sufficient elevation in BP to cause papilledema and other manifestations of
vascular damage
(retinal hemorrhages, bulging discs, mental status changes, increasing
creatinine)
- not defined by absolute level of BP, but often requires BP of >200/140
- develops in about 1 % of hypertensive patients
• Hypertensive urgency :
- sBP >210 or dBP > 120 with minimal or no target-organ damage
• Hypertensive emergency
- high BP + acute target-organ damage

6. Hypertensive Emergencies
1. Malignant HTN with papilledema
2. Cerebrovascular:
- Hypertensive encephalopathy
- CVA with severe hypertension
- Intracerebral hemorrhage
- SAH
3. Cardiac:
- Acute aortic dissection
- Acute refractory LV failure
- Acute MI with persistent ischemic
- pain after CABG

7. 4. Renal:
- Acute glomerulonephritis
- Renal crises from collagen vascular diseases
- Severe hypertension following renal transplantation
5. Excessive circulating catecholamines:
- Pheochromocytoma
- Tyramine containing foods or drug
- Sympathomimetic drug use (e.g. cocaine)
- Rebound HTN after cessation of antihypertensive drugs (e.g.
clonidine)
6. Eclampsia
7. Surgical:
- Severe HTN prior to emergent surgery
- Severe post-op HTN
- Post-op bleeding from vascular suture lines
8. HTN following severe burns
9. Severe epistaxsis

8. Classification of hypertension
Category Systolic BP mm Hg Diastolic BP mmHg
Normal <120 <80
Prehyprtension 120-139 80-89
Stage I hypertension 140-159 90-99
Stage II hypertension 160-199 100-109

9. World Health Organization 2002

10. Epidemiology
• 20-25% of adults have HTN (up to 50%
undiagnosed)
• 16% have adequate BP control
• Approximately 50% of adult are hypertensive
by age 60
• 3rd leading risk factor associated with death
• Risk factor for CAD, CHF, cerebrovascular
disease, renal failure, peripheral vascular
disease

11. Risk Factors
• Age
• Alcohol
• Cigarette Smoking
• Diabetes mellitus
• Elevated serum lipids
• Excess dietary sodium
• Gender
• Family history
• Obesity
• Ethnicity – IS AN IMP. FACTOR IN OVERALL CARDIAC
DISEASE
• Sedentary lifestyle
• Socioeconomic status
• stress

12. • Etiology :
– Of all 90% have Essential hypertension
– The remainder have secondary hypertension

13. Causes of secondary hypertension
•Alcohol
•Pregnancy
•Renal disease:
– Renal artery stenosis,
– Glomerulonephritis,
– Polycystic kidney disease
•Endocrine disease:
– Pheochromocytoma, cushing’s disease, conn’s syndrome,
hyperparathyroidism,
– acromegaly, primary hyperthyroidism, thyrotoxicosis,
– congenital adrenal hyperplasia
•Drugs:
– OCPs, anabolic steroids, corticosteroids,
– NSAIDs, sympathomimetics.
•Co-arctation of aorta.

14. Pathophysiology
• For HTN, there must be an increase in either CO or SVR. The hallmark of
classic HTN is increased SVR.
• Heredity
• Water/Sodium retention
• Altered renin-angiotensin mechanism
• Stress and increased sympathetic NS activity
• Insulin resistance and hyperinsulinemia
– High insulin concentration stimulates SNS activity and impairs nitric
oxide-mediated vasodilation
– Pressor effects of insulin include vascular hypertrophy and increased
renal sodium reabsorption
• Endothelial Cell Dysfunction
– Enodthelin produces pronounced and prolonged vasoconstriction.

15. Symptoms and signs of Hypertension
• Mostly asymptomatic
• Symptoms as a result of arterial pressure:
– headache(occipital, early morning for several hours),
– dizziness,
– palpitation,
– easY fatigability,
– impotance.
• Symptoms of hypertensive vascular disease:
– epistaxis,
– hematuria,
– blurring of vision,
– episodic weakness(TIA),
– angina,
– dyspnoea (HF),
– chest pain(dissection of aorta)
• Symptoms of underlying disease (secondary HTN)
High blood pressure has no warning signs or symptoms – which is why it is often
called a “silent killer”.

16. • Physical examination :
– Cardiac murmurs
– neurologic deficits
– elevated jugular pressure
– rales
– retinopathy
– unequal pulses
– abdominal bruits

17. • History :
– Note the presence of medication ( decongestants,
OCP, NSAIDs, exogenous thyroid hormone, recent
alcohol consumption, cocaine)
– Secondary HTN should be considered :
• Age <30 or >60
• Not controlled by therapy
• Occurrence of HTN crisis
• Sign & symptoms of scondary causes – HYPERKALEMIA ,
METABOLIC ACIDOSIS
• FAMILY HISTORY

18. Complications
Target Organ Diseases
• Heart (hypertensive heart disease)
– Coronary artery disease (leading to MI and angina)
– Left ventricular hypertrophy (from high cardiac workload
leading to heart failure)
– Heart failure (shortness of breath on exertion, nocturnal
dyspnea, fatigue, enlarged heart)
• Brain (cerebrovascular disease)
– Stroke/transischemic attacks
– Hypertensive encephalopathy (cerebral edema)

19. • Peripheral vasculature (peripheral vascular disease)
– Atherosclerosis in peripheral blood vessels
• Aortic aneurysm, aortic dissection, peripheral vascular
disease
• Intermittent claudication (pain with activity or lack of
oxygen to tissues)

20. • Kidneys (nephrosclerosis)
– End stage renal disease (ischemia from
narrowed intrarenal vessels)
• Urinalysis
– Microalbuminuria
– Proteinuria
– Elevated blood urea nitrogen/elevated Serum creatinine
» Usually ratio of 10:1 or 15:1.
» BUN: 5-25 mg/dl
» Creatinine: 0.5 – 1.5 mg/dl
» Microscopic hematuria
• Earliest sign of renal damage is nocturia

21. • Eyes (retinal damage)
– Eyes are only place vessels can be directly
observed.
– Retinal damage can indicate damage in other
target organs.
– Signs/Symptoms
• Blurry vision
• Retinal hemorrhage
• Loss of vision

22. Investigations
• For all patients with hypertension (D)
- CBC, electrolytes, Cr, fasting glucose and lipid profile, 12-
lead ECG, urinalysis.
• For specific patient subgroups (D)
- DM OR renal disease: urinary protein excretion
- Increasing Cr OR history of renal disease OR proteinuria
OR HTN resistant to 3 meds OR presence of abdominal
bruit: renal ultrasound, captopril renal scan, MRA/CTA (B)
- If suspected endocrine cause: plasma aldosterone, plasma
renin (D)
-If suspected pheochromocytoma: 24 h urine for
metanephrines and catecholamines (C)
- Echo cardiogram for left ventricular dysfunction
assessment if indicated (C)

23. Keys to Grade of Recommendations
for Hypertension Diagnosis and
Treatment
Grade
• A = High levels of internal validity and statistical
precision
• B/C = Lower levels of internal validity and
statistical precision
• D = Expert opinion

24. • Monitoring
– BP monitoring should be done under nonstressful
circumstance ( rest, sitting,comfortable)
– Should not be diagnosed on the basis of one
measurement alone (unless > 210/120 mmofHg or
with target organ damage. Two or more than two
abnormal reading over a period of several weeks
should be obtained before considering)
– Pseudohypertention in elderly excluded due to
stiff vessels

25. Approach to Hypertension

27. Treatment
• Behavioral
– Nonpharmacological therapy
– Lifestyle modification ( exercise , cessation of
smoking, reduction of body weight, judicious
consumption of alcohol and adequate nutritional
intake)

28. Diuretics
• First line of defense
• Thiazides (Hydrodiuril )
– Inhibit sodium reabsorption in the distal convoluted tubule; increase excretion of
sodium; decreases ECF; sustains a decrease in SVR
– Lowers BP moderately in 2-4 weeks
– hydrochlorothiazide 12.5 -25 mg/ day
– S/E: fluid/electrolyte imbalances; CNS effects; GI effects; sexual impotence;
dermatologic effects(photosensitivity); decreased glucose tolerance
– Monitor for orthostatic hypotension, hypokalemia and alkalosis.
– Watch for digoxin toxicity.
– Avoid NSAIDS.
– Eat K+-rich foods

29. • Loop Diuretics (furosemide/Lasix)
– Inhibits NaCl reabsorption in ascending limb of loop of Henle;
increases excretion of sodium and chloride.
– More potent than thiazides, but of shorter duration; less
effective for HTN
– S/E: fluid/electrolyte imbalances(hypokalemia);ototoxicity;
metabolic effects (hyperglycemia); increasedLDL and
triglycerides with decreased HDL
– Monitor for orthostatic hypotension and electrolyte
abnormalities. Loop diuretics remain effective despiterenal
nsufficiency. Diuretic effect increases at higher doses

30. • Potassium-Sparing (spironolactone/Aldactone)
– Reduce K+ and Na+ exchange in the distal tubules;
Reduces excretion of K+, H+, Ca++ and Mg++;
Inhibitthe Na+ retaining and K+ excreting effects
of aldosterone.
– S/E: hyperkalemia, N/V, diarrhea, headache,leg
cramps, dizziness, maybe gynecomastia,
impotence,decreased libido, menstrual irregularis

31. Angiotensin Inhibitors
Angiotensin-Converting Enzyme Inhibitors (ACE-Inhibitors) (“-pril”)
• First line of defense for diabetics
• Inhibit angiotensin-converting enzyme; reduce conversion of angiotensin I
to angiotensin II; prevent angiotensin II mediated vasoconstriction.
• Inhibits angiotensin-converting enzyme when oral agents are not
appropriate.
• Enalapril 20 mg , ramipril 5-10 mg
• S/E: Hypotension, loss of taste, cough, hyperkalemia, acute renal failure,
skin rash angioneurotic edema.
• ASA/NSAIDS may reduce drug effectiveness.
• Diuretic enhances drug effect.
• Do not use with K+-sparing diuretics. Fetal morbidity or mortality

32. Antiotensin II Receptor Blockers (ARBs) (“-sartan”)
• Prevents action of angiotensin II and produces
vasodilation and increased salt and water
excretion.
• S/E: Hyperkalemia, decreased renal function.
• Full effect on BP takes 3 to 6 weeks.

33. Calcium Channel Blockers(“-dipine”)
• Blocks movement of extracellular calcium into cells, causing vasodilation
and decreased SVR.
• Effective and well tolerated particularly in the elderly
- Verapamil 240mg , Diltazem, amlodipine 2.5-10mg
• S/E: Nausea, headache, dizziness, peripheral edema. Reflex tachycardia
(with dihydropyridines). Reflex decreased heart rate; constipation.
• Use with caution in patients with heart failure.
• Contraindicated in patients with second- or third-degree heart block. IV
use available for HTN crisis.

34. Beta Blockers (“-olol”)
• Reduces BP by antagonizing beta adrenergic effects.
• Decreases CO and reduces sympathetic vasoconstrictor tone.
• Decreases renin secretion by kidneys.
• Also used as first line therapy
• Metoprolol 100-200mg, atenolol 50-100 mg
• S/E:Bronchospasm, a/v conduction block; impaired peripheral circulation;
nightmares; depression; weakness; reduced exercise capacity; may
exacerbate heart failure; Sudden withdrawal may cause rebound
hypertension and cause ischemic heart disease.
• Monitor pulse regularly; use with caution in diabetics because drug may
mask signs of hypoglycemia

35. Combined Alpha/Beta Blockers (labetalol/Normodyne)
• Produces peripheral vasodilatation and decreased
heart rate.
• S/E: dizziness, fatigue, N/V, dyspepsia, paresthesia,
nasal stuffiness, impotence, edema. HEPATIC TOXICITY
• Keep patient supine during IV administration.
• Assess pt tolerance of upright position (severe
postural hypotension) before allowing upright
activities

36. Alpha-1 Adrenergic Blocker (“-azosin”)
• Blocks alpha-1 effects producing peripheral vasodilation (decreases
SVR and BP)
• Prazosin 0.5 – 20mg ; doxazosin 1-16mg
• S/E: Hypotension dependent on volume. May produce syncope
within 90 minutes of initial dose; retention of sodium and water;
cardiac arrhythmias, tachycardia, weakness, flushing; abdominal
pain; N/V and exacerbation of peptic ulcer.
• Reduced resistance to the outflow of urine in benign prostatic
hyperplasia. Take drugs at bedtime(orthostatic hypotension);
beneficial effects on lipid profile.

37. How to Combine Antihypertensive
Medications

38. Common side effects
• Orthostatic hypotension
• Sexual dysfunction (ask provider about changing med/dose
or getting Viagra)
• Dry mouth (chew sugarless gum or hard candy)
• Frequent voiding (take diuretics earlier in the day to avoid
nocturia)
• Sedation (take med in the evening)
• BP is lowest during the night and highest after
awakening…take med with 24-hour duration as early in the
morning aspossible.

39. Follow-Up
• Assess and encourage adherence to pharmacological and
non-pharmacological therapy at every visit .
• lifestyle modification - 3-6months
• Pharmacological
- 1 -2months until BP under target for 2 consecutive visits
- more often for symptomatic HTN, severe
HTN,antihypertensive drug intolerance, target organ
damage
- 3-6months once at target BP
• Referral is indicated for cases of refractory hypertension,
suspected secondary cause or worsening renal failure
• Hospitalization is indicated for malignant hypertension

40. Pharmacologic Treatment of Hypertension in
Patients with Unique Conditions

42. Pharmacologic Treatment of
Hypertension in Patients with Unique
Conditions (continued)