2. Qs.
What’s HTN ?!
Who at risk ?
How is’t occur ?
Pt. , How present ?
Emergency HTN !
How to approach ?
What about management ?
3. What’s HTN ?
Chronic medical condition in which blood pressure elevated.
Blood pressure is force which exerted by blood against the wall of the
blood vessels, which is adequate to maintain perfusion during activity
and rest.
Blood pressure;
A. Maximum systolic pressure in the artery when left ventricle
contract to force the blood into aorta & other arteries.
B. Minimum diastolic pressure in the artery when ventricle relaxed &
filling up, blood receiving from veins.
4. What’s HTN ?
Regulation of blood pressure;
A. Baroreceptor reflex in medulla “localization in Rt. & Lt. carotid sinus
and Aortic arch”
B. Renin angiotensin system “for long term”
• Kidney - composition
• Endogenous vasoconstriction - angiotensin I
C. Aldosterone release “adrenal cortex”
• Stimulate sodium retention & potassium execration by kidney
• Increases fluid retention
5. What’s HTN ?
Arterial blood pressure maintained by
cardiac output and systemic vascular
resistance, so the relation between
systemic arterial pressure and morbidity
appear to be quantitative rather than
qualitative
6. What’s HTN ?
Background;
A. Hypertension is one of the most common worldwide diseases afflicting humans
and is a major risk factor for stroke, myocardial infarction, vascular disease,
and chronic kidney disease.
B. Despite extensive research over the past several decades, the etiology of most
cases of adult hypertension is still unknown, and control of blood pressure is
suboptimal in the general population.
C. Hypertension is the most important modifiable risk factor for coronary heart
disease (the leading cause of death in North America), stroke (the third leading
cause), congestive heart failure, end-stage renal disease, and peripheral
vascular disease, Therefore, health care professionals must not only identify and
treat patients with hypertension but also promote a healthy lifestyle and
preventive strategies to decrease the prevalence of hypertension in the general
population.
7. What’s HTN ?
JNC-8 classification
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!
!
The classification is based on the average of 2 or
more readings taken at each of 2 or more visits
after initial screening.
Stage Systolic
pressure
Diastolic
pressureNormal < 120 mmHg < 80 mmHg
Pre -
hypertensive
120 - 139 mmHg 80 - 89 mmHg
Grade I
hypertension
140 - 159
mmHg
90 - 99 mmHg
Grade II
hypertension
> 160 mmHg > 100 mmHg
8. What’s HTN ?
Prehypertension, emphasizes that patients
with prehypertension are at risk for
progression to hypertension and that
lifestyle modifications are important
preventive strategies.
Hypertension may be categorized as either
essential “primary” or secondary.
9. Who at risk ?
Tobacco use, particularly cigarettes, including chewing tobacco
Elevated LDL cholesterol (or total cholesterol ≥240 mg/dL) or low HDL cholesterol:
component of metabolic syndrome
Diabetes mellitus: component of metabolic syndrome
Obesity (BMI ≥30 kg/m2): component of metabolic syndrome
Age greater than 55 years for men or greater than 65 years for women: increased risk
begins at the respective ages; the Adult Treatment Panel III used earlier age cut points to
suggest the need for earlier action
Estimated glomerular filtration rate less than 60 mL/min
Microalbuminuria
Family history of premature cardiovascular disease (men < 55 years; women < 65 years)
Lack of exercise
10. How is’t occur ?
Hypertension may be primary, which may develop as a
result of environmental or genetic causes, or secondary,
which has multiple etiologies, including renal, vascular,
and endocrine causes. Primary or essential hypertension
accounts for 90-95% of adult cases, and a small
percentage of patients (2-10%) have a secondary cause.
Hypertensive emergencies are most often precipitated by
inadequate medication or poor compliance.
11. How is’t occur ?
Primary (essential) hypertension is diagnosed in the
absence of an identifiable secondary cause. Risk
factor family Hx. of HTN or heart disease, a high
sodium diet, smoking, obesity, ethnicity
“black>white”, and advanced age.
Pt. asymptomatic until complication develop, so pt.
should evaluated for end organ damage to the
brain”stroke, dementia”, eye “cotton wall exudate,
hemorrhage” , heart “LVH” and kidney “chronic kidney
disease, proteinuria & artery stenosis”
12. How is’t occur ?
Secondary forms of hypertension, for identifiable causes, such as primary
hyperaldosteronism, account for 20% of resistant hypertension (hypertension in which
BP is >140/90 mm Hg despite the use of medications from 3 or more drug classes, 1 of
which is a thiazide diuretic).
other causes;
A. Renal causes 2.5-6% “Chronic renal disease, polycystic kidney disease, urinary
tract obstruction, renin producing tumor, liddl syndrome”
B. Renovascular hypertension “RVHT” causes .2-4% of cases.
C. Vascular causes “Coarctation of aorta, vasculitis, collagen vascular disease”
D. Endocrine causes account for 1-2% include, exogenous causes include
administration of steroids. Another endocrine causes oral contraceptive use oral
contraceptive use in association with mild renal disease, family Hx., female older
than 35 year
13. How is’t occur ?
E. Exogenous administration of the other steroids used for therapeutic
purposes also increases blood pressure (BP), especially in susceptible
individuals, mainly by volume expansion, they blocks both “COX-1” and
“COX-2” which can inhibit natriuretic effect, which in turn increase
sodium retention, also inhibit vasodilation of prostaglandins and produce
vasoconstriction enzyme endothelin-1
F. Endogenous hormonal causes;
1. Primary hyperaldosteronism
2. Cushing syndrome
3. Pheochromocytoma
4. Congenital adrenal hyperplasia
14. How is’t occur ?
G. Drugs and toxin;
1. Alcohol
2. cocaine
3. NSAIDs
H. Other causes;
1. Hyperthyroidism & hypothyroidism
2. Hypercalcemia
3. Hyperparathyroidism
4. Obstructive sleep apnea
5. Pregnancy induced hypertension
15. How is’t occur ?
I. Neurogenic causes, include;
1. Brain tumor
2. Bulbar poliomyelitis
3. Intrcranial hypertension
16. How is’t occur ?
Environmental and genetic/epigenetic causes;
A. Hypertension develops secondary to environmental factors, as
well as multiple genes, whose inheritance appears to be complex.
Furthermore, obesity, diabetes, and heart disease also have
genetic components and contribute to hypertension.
B. In an attempt to elucidate the genetic components of
hypertension, multiple genome wide association studies (GWAS)
have been conducted, revealing multiple gene loci in known
pathways of hypertension as well as some novel genes with no
known link to hypertension as of yet
17. How is’t occur ?
C. Epigenetic phenomena, such as DNA methylation and histone
modification, have also been implicated in the pathogenesis of
hypertension. For example, a high salt diet appears to unmask
nephron development caused by methylation.
D. Despite these genetic findings, targeted genetic therapy seems to
have little impact on hypertension. In the general population, not
only does it appear that individual and joint genetic mutations
have very small effects on BP levels, but it has not been shown
that any of these genetic abnormalities are responsible for any
applicable percentage of cases of hypertension in the general
population
18. Pt. how present ?
Asymptomatic, pt. unaware they have HTN until complicate
Non-specific symptom, mild symptom
Headache
Confusion
Morning headache
Fatigue
SOB
Nausea
19. Pt. how present ?
Anxiety
Nose bleeding
Heart palpitation
Chest pain
Pale skin
Change of vision
21. Emergency HTN
The most common hypertensive emergency is a rapid unexplained
rise in BP in a patient with chronic essential hypertension, which
lead to end organ damage
Most patients who develop hypertensive emergencies have a
history of inadequate hypertensive treatment or an abrupt
discontinuation of their medications
Other causes of hypertensive emergencies include the use of
recreational drugs, abrupt clonidine withdrawal, post
pheochromocytoma removal, and systemic sclerosis, as well as
causes of secondary HTN that listed before.
22. Emergency HTN
Pt. with end organ damage revealed by renal disease,
chest pain “MI or ischemia”, back pain “aortic
dissection”, or change in mental status “hypertensive
encephalopathy”
23. How to approach ?
Obtain a history of the patient’s use of over-the-counter medications;
herbal medicines such as herbal tea containing licorice, ephedrine/
ephedra, current and previous unsuccessful antihypertensive medication
trials; oral contraceptives; ethanol; and illicit drugs such as cocaine
The patient’s lifestyle factors should also be included, such as changes
in weight, dietary intake of sodium and cholesterol, exercise level, and
psychosocial stressors
The historical and physical findings that suggest the possibility of
secondary hypertension are a history of known renal disease, abdominal
masses, anemia, and urochrome pigmentation
24. How to approach ?
A history of sweating, labile hypertension, and palpitations
suggests the diagnosis of pheochromocytoma
A history of cold or heat tolerance, sweating, lack of energy,
and bradycardia or tachycardia may indicate hypothyroidism
or hyperthyroidism
A history of obstructive sleep apnea may be noted A history
of weakness suggests hyperaldosteronism.
Kidney stones raise the possibility of hyperparathyroidism
25. How to approach ?
Physical examination revealed elevated blood pressure
Routine investigation of the HTN pt include;
A. ECG
B. Urine dipstick test for protein and blood
C. Fasting blood for lipids “total and HDL cholesterol” and glucose
D. Serum urea, creatine and electrolyte
26. How to approach ?
If the urea or creatinine is elevated, more specific are
renal investigation are indicated
A low serum potassium may indicate an endocrine
disorder (primary hyperaldosteronism or glucocorticoid
excesses)
27. What about management ?
Drugs
1. ACEIs; arterial & venous vasodilation, has advantage in HTN pt. with CHF & diabetic nephropathy.
2. beta-blocker; which decrease heart rate, cardiac out put, ideal in HTN pt. with angina.
3. CCBs; which cause arterial vasodilation.
4. alpha-blocker; cause relaxation of smooth muscle, which has advantage in pt. w/ BPH
5. ARBs; Has benefit of ACEs apart form side its effect “cough”.
6. Diuretics; decrease plasma volume, useful in CHF, smoker & chronic urinary disease.
Surgical intervention
Life style modification
28. What about management ?
Stage
Systolic
pressure
Diastolic
pressure
Life style
modification
Drug therapy
Normal < 120 mmHg < 80 mmHg Encourage -
Pre -
hypertensive
120 - 139 mmHg 80 - 89 mmHg Yes No indication
Grade I
hypertension
140 - 159 mmHg 90 - 99 mmHg Yes
Thiazide
Diuretic, ACEIs,
beta blocker,
CCBs
Grade II
hypertension
> 160 mmHg > 100 mmHg Yes
2 drugs
combination,
Diuretic +
ACEIs, ARB,
29. What about management ?
Treatment of primary HTN
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!
!
Population Agent
Uncomplicated
Diuretics, beta-blocker,
ACEIs
CHF
Diuretics, beta-blocker,
ACEIs, ARBs, Aldosteron
antagonist
Diabetic
Diuretics, beta-blocker,
ACEIs, ARBs, CCBs
Post- MI
beta-blocker, ACEIs, ARBs,
aldosteron antagonist
Chronic kidney dosease ACEIs, ARBs
30. What about management ?
Etiology Management
1ْ Renal disease ACEIs
Renal artery stenosi May treated with angioplasty or
stinting
OCP user Discontinue “may delayed”
Pheochromocytoma alpha agonist & beta blocker, then
removal of tumor
Conn’s syndrome “hyper
aldosteronism”
Removal of tumor
Cushing’s syndrome Removal of tumor & exogenous
steroids
Aortic Coarctation Surgical repair
31. What about management ?
Treatment of Emergency HTN
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!
!
Status Management
Hypertensive urgency
oral hypertensive “beta blocker,
clonidine, ACEIs”, with goal
lowering BP within 24h
Hypertensive emergency
IV medication “labetalol,
nitroprusside, nicardipine”, with
goal lowering BP 25% over first 2
hour to prevent cerebral hypo
