2. INTRODUCTION
Definition= at 2 separate occasions(6
hours).
Systolic BP > or = 140
Diastolic BP > or = 90
Stages
Normal: SBP< 120, D BP< 80
Pre HTN: S BP- 120-139, D BP- 80-89
Stage-I : SBP- 140-159, D BP- 90-99
Stage II : SBP- > or= 160, D BP> or=100
Isolated SHTN: S BP>or=140, D BP<90
2
3. Isolated systolic hypertension
* is defined as systolic blood pressure
≥140 mm Hg with diastolic pressure <90 mm Hg.
*mainly affects people older than 55 years.
Secondary causes include
1.increased cardiac output (anemia,
thyrotoxicosis,arteriovenous fistula, Paget disease
of bone, and beriberi)
2. increased cardiac stroke volume (aortic
insufficiency and complete heart block).
3
4. • Exclude= recent physical exercise, use of tobacco
or caffeine, or a full urinary bladder.
•Office (white coat) hypertension: elevated BP in
the clinic environment.Diagnosis made by self-
measurement or average awake ambulatory level=
≥135/85 mm Hg.
• Pseudohypertension: inaccurately high cuff blood
pressure as a result of a stiff vascular tree in older
persons= an indication to IA BP measurment.
4
5. Risk factor for HTN
1.Nonreversible risk : older age, being African
American, and having a family history of
hypertension.
2. Reversible : prehypertension,
overweight,sedentary lifestyle, high-sodium–low-
potassium diet,excessive alcohol intake and
metabolic syndrome.
3.Genetic factor: Polygenic= two or greater
factors plus environmental factor, Monogenic- on
study
5
6. Metabolic syndrome
•is defined by the presence of at least three of the
following:
•.abdominal obesity (waist circumference >40
inches in men or >35 inches in women) vs BMI.
• impaired fasting blood glucose(fasting glucose
≥110 mg/dL),
•blood pressure ≥130/85 mmHg,
• plasma triglycerides ≥150 mg/dL, or
•HDL cholesterol <40 mg/dL in men or
• <50 mg/dL in women.
6
7. TOG
• Individual risk from hypertension is related to its
level, duration, and the presence of other risk
factors for cardiovascular disease or target organ
injury.
• At any given level of blood pressure, African
Americans and men are at the greatest risk.
*The MCOD is coronary artery disease(CHD).
• Target organ damage increases the risk of
cardiovascular disease events even if blood
pressure is subsequently controlled.
7
8. Risk factors for CHD
*HTN, tobacco use, hyperlipidemia, diabetes
mellitus, obesity, sedentary lifestyle,metabolic
syndrome, male gender, postmenopausal state,
older age, family history of premature cardiovascular
disease,PAD,Stroke and CKD.
8
9. Summary of basic facts on HTN
*Treatment of reversible risk factors can prevent or
delay the development of hypertension and lower
the risk of cardiovascular disease.
• Treatment of metabolic syndrome can prevent
cardiovascular disease and the development of
hypertension.
• Diastolic blood pressure is the best predictor of
cardiovascular disease in young people.
• Systolic blood pressure is the dominant predictor of
risk of cardiovascular disease in older people.
9
10. …
Mechanism of HTN
COP = SV =SHTN
TPR = D HTN = amount of blood return to the
heart due to arteriolar contraction at diastole=MCC
Intra vascular volume elevation.
Autonomic Nervous system over activity.
Renin Angiotensin Aldosterone System over
activity
Vascular factors:
*includes arterial stiffness, Increased vascular
smooth muscle tone and growth, Endothelial
damage( decreased NO & vasodilator peptide).
10
11. Hypertension during pregnancy:
*developing before the 20th week of gestation is
more likely to have a secondary form (caused by
renovascular disease, primary aldosteronism,
Cushing syndrome, or pheochromocytoma).
*Blood pressure ≥140 mm Hg systolic or ≥90 mm
Hg diastolic.
• Transient hypertension is a predictor of the future
development of essential hypertension.
• Consider secondary causes of hypertension in this
age group.
11
12. Mx of chronic HTN in pregnancy
*Lifestyle modifications can be used initially to
treat mild hypertension.
* Use drug therapy if
1.diastolic blood pressure is ≥100 mm Hg or
2.systolic blood pressure
* is ≥150 mm Hg in the second trimester or
• ≥160 mm Hg in the third trimester.
• Recommended initial drug therapy:
methyldopa.
12
13. … Types of TOD
Atherosclerosis is the cause
Heart
Diastolic dysfunction=stiff ventricle=SOB
-Early sign, caused by LVH and ischemia and
ejection fraction is ok.
-Diagnosis- Echocardiography and cardiac
catheterization
Left ventricular hypertrophy
- Genetic and hemodynamic risk factors - Wall
thickness – LVOO / CHD.
-CP=range No Symptom to syncope, chest pain,
palpitation, exercise intolerance, stroke,
sudden cardiac death
- Diagnosis – ECG, Echo
13
14. …
Management of LVH
Antihypertensive drugs: Lasix, Beta blockers,
ACEI
- decreases LV mass and prevent LVH and
progression
- Decreases CVD risks
- Due to decreased BP but mechanism of
action on the mass unknown
Treatment of HTN
- Decreases: CHF by 50%, CHD by 12-16%, SCD
by 21%, LVH by 35%.
14
15. Central Nervous System
•Stroke: Ischemic and Hemorrhagic.
•Treatment of HTN decreases stroke by 35-50%
•Decreased Cognition and dementia
•Hypertensive Encephalopathy=pupil edema.
15
16. …
Renal
• ARF =secondary to fibrinoid necrosis
• Chronic: Glomerulosclerosis and tubular ischemia
with atrophy
• HTN due to primary Vs CKD
- PU < 1 gm/d and no active Urine sediment in
cases of primary HTN
PAD
• Due to atherosclerosis: aneurysm, dissection,
rupture, stenosis
16
17. …
Primary HTN
Accounts for 85-95%, Familial, increases with age,
in twins concordance rate M=60%, W=35%.
Majority due to increased PVR but COP normal, in
the young due to increased COP and normal PVR
Peak age= 25-55
Low renin modulators accounts for 20% and are
diuretic responsive.
High renin non modulators accounts for 10-15%,
more in whites and ACEI /ARB responsive.
High aldosterone and low renin is common in
blacks and DM Pts, increased LVH, AS and PVR
with SCD and are spironolactone sensitive.
Associated with metabolic syndrome.
17
18. …
Secondary HTN
Accounts for 5-15% of HTN and major cause is
Renal paranchymal, next is renovascular HTN.
Indication of screening: age <25 and >55, poor
drug response; Hx, PE, Lab evidence of
underlying cause
Presentation
Majority asymptomatic found accidentally
Target organ damage
Hypertensive Emergency
Sn Sm of underlying cause
Basic Lab tests
CBC, RFT, UA, FBS, Lipid profile, Electrolyte,
TSH, T3 & T4, ECG, CXR
18
19. HYPERTENSIVE CRISIS
Emergency(TOD) Vs Urgency( no TOD)
Imminent / overt target organ damage in
association with acute onset or worsening of HTN
Needs urgent lowering BP with in two hrs for
emergency ( S BP < 160, D BP b/n 100 and 110)
or decreasing MAP by 1/4th
RAAS is activated
I- Encephalopathy
If focal sign R/O stoke by CT
Drug : Nitroprusside, Nicardipine, Labetolol
II-
19
20. Malignant HTN
Clinical syndrome associated with abrupt rise in
BP recognized by
Progressive retinopathy( arteriolar spasm,
hemorrhages, exudates, papilledema)
Deteriorating RF with PU
Microangiopathic hemolytic anemia
Encephalopathy
Rate of rise more important than the absolute
level of BP
Pathophysiology: Fibrinoid necrosis in the
arterioles of kidney, brain and retina, increased
plasma renin activity (pressure natiuresis, RV
injury), tissue renin activity
20
21. Management
If no Encephalopathy or other catastrophic
event lower BP over several minutes (over
hours) with PO short acting drugs with
frequent dosage
Captopril, Clonidine, Labetalol
21
22. HTN-Encephalopathy
oPresence of cerebral edema X-ized by non
localizing neurologic manifestations.
*Headache, nausea, vomiting, restlessness,
confusion, seizure, coma could occur
*CT- R/O ischemia or infarction
oPathophysiology: disrupted cerebral auto regulation
leading to vasodilatation of cerebral microvasculature
*Level of BP: in chronic HTN at DBP >120, could
occur at DBP <100.
22
23. Treatment
*Rapidly lowering BP may precipitate ischemia(
brain, kidney, heart)
*Goal: to reduce BP to 160/100-110, with in minute
to 2hrs with initial fall of MAP not exceeding 25%
of the presenting value
*Drugs: IV Nitroprusside, Labetalol, Nicardipine
*After the target level of BP is achieved oral agents
should be started to bring DBP b/n 85-90 over two
to three months
*Prognosis: at continued risk for coronary, CV and
renal disease, survival improves with time (90% by
the 4th yr Vs 52 % in the 1st yr)
23
24. II.Stroke
1.Ischemic =Acute reatment is indicated= if S BP
>220 and DBP >130 ,provided no other indication
to RX, if fibrinolytic agent is indicated BP should
be < 185 and 110.
*ACEI+HCT after 7-10 days.
2.ICH= indication is when MAP > 130 or SBP
>220 and DBP >130.
3.SAH =when MAP > 130
24
25. …
III- Acute CHF
Treat with ACEI plus loop diuretic plus Digoxin
plus Nitrates
IV- ACS=Treat with Labetolol, Esmolo, Nitrates,
Nicardipine, ACEI.
V- ARF=Treat with CCB, Lasix, Dopamine, Dialysis
VI- Aortic dissection.Goal =SBP<125 with in 30-60
minute.
Treat with Esmolol, Labetolol, Nitroprusside
*CCB & Duretic are CI to avoid tachycardia.
VII- Pre ecclampsia and Ecclampsia
Hydralazine, Labetolol, Nicardipine, Aldomate
VIII-Hypertensive Urgency: Goal to put SBP< 160,
DBP<110 over 24hrs to few days
25
26. Hypertensive Retinopathy:
Defn
systolic BP >= 140
diastolic >= 90
The strong correlation linking arterial
hypertension with heart disease, stroke, and
renal failure makes it a leading cause of
morbidity and mortality among adults in the
United States.
26
27. Clinical findings of the retina in
hypertensive retinopathy are as follows:
Hemorrhages
Retinal and macular edema ¤
Edema residues (hard exudates) ¤
Inner retinal ischemic spots (cotton- wool
spots) ¤
¤ - indicate a more serious stage.
27
28. Modified Scheie classification of
Hypertensive Retinopathy:
Grade 0 - No changes
Grade 1 – barely detectable arterial
narrowing
Grade 2- Obvious arterial narrowing with
focal irregularities.
Grade 3 – Grade 2 plus retinal hemorrhage
and/or exudate.
Grade 4 - Grade 3 plus disc swelling.
28
29. Treatment of stable hypertensive patient
*Risk assessment and stratification: stage of
HTN, comorbid conditions, CVD risk factors,
beneficial effect on CV risks, age, availability
and cost of drugs
*Follow up: drug selection and acceptable
combination, base line clinical and Lab data
should be taken.
29
30. When to start and mode of treatment
Pre hypertension: those with risk factor for CVD
close follow up and risk reduction, treatment of
related disease conditions and life style
modification
Sage I : With out risk factors follow up for 3-6
months and if persistent HTN ,start drug therapy.
Stage I with risk and above: drug therapy from
the outset
Isolated systolic HTN with risk factor other than
age start drug treatment, if with out risk follow up
and treat accordingly oGoal of Rx : BP < 140/80
30
31. …
Single Vs Combination drug treatment
Depending on organ related risk (CVD related risk
reduction)
Patient related risk
Comorbid conditions
Stage of HTN>=II
BP=> 160|95, needs at least 2 drugs.
Degree of control of clinical conditions and BP
level.
31
32. • Combination therapy with two drugs should be
considered for stage 2 hypertension or if initial
blood pressure is >20/10 mm
Hg above the goal.
32
33. Life style changes
*Cessation of smoking.
*salt restriction.
*reduction of saturated and total fat intake.
*High fiber diet, fruits and vegetable.
* supplemental Ca, Mg and K .
*Alcohol: Men < 2 drink/d, women<1drink/d.
*Aerobic exercise: 30min daily or every other day
*Tea and coffee: limited amount.
33
34. …
Specific clinical conditions and drug choices
DM: ACEI, beta blocker, Loop diuretic, ASA,
statin, CCB, Diltiazem (Verapamil ), glycemic
control. If no proteinuria =goal of BP < 130/80
-If PU BP < 125/75
CKD: ACEI, BB, Loop diuretics, CCB, statin,
Warfarin (if needed)
CHF and CHD: ACEI, BB, diuretic
Stroke: ACEI, BB, CCB, HCT, ASA, Statin.
Pregnancy: Aldomate, CCB, Labetolol
Post MI: BB, ACEI, statin, ASA
Blacks: diuretic plus BB/ACEI or CCB plus
BB/ACEI
PAD: ASA plus CCB plus surgery if needed(70%
had IHD=BB+CCB).
Elderly: thiazide, CCB, Labetolol
34
35. …
Refractory HTN
Persistent BP of > 140/90 using three
drugs and above with appropriate
combination, indication and good
adherence
Common in old age
DDx: Pseudo hypertension, poor
adherence, salt intake, obesity, excess
alcohol intake, 2ry HTN,
hyperaldosteronism
35
36. …
Screening and prevention of HTN
For non risk groups once every three
to five years and at any clinic visit.
For risk groups every six to twelve
months Bp measurement
In general when to start screening
and it’s benefit is not well established,
but at age>=3 years.
36
38. History
*Most pts are asymptomatic.
*Severe hypertension may lead to headache,
epistaxis,or blurred vision.
Clues to Specific Forms of Secondary
Hypertension
*Use of OCP& glucocorticoids.
*paroxysms of headache, sweating, or tachycardia
(pheochromocytoma);
*history of renal disease or abdominal bruie (renal
hypertension).
38
39. Physical Examination
*Measure bp in both arms as well as a leg (to
evaluate for coarctation).
•Clues to secondary forms of hypertension
include cushingoid appearance, thyromegaly,
abdominal bruit (renal artery stenosis), delayed
femoral pulses (coarctation of aorta).
39
40. 1.RAS: MR angiography, captopril renogram, renal
duplex ultrasound and measurement of renal vein
renin;
(2) Cushing’s syndrome: dexamethasone
suppression test.
(3) pheochromocytoma: 24-h urine collection for
catecholamines, metanephrines, and
vanillylmandelic acid or measurement of plasma
metanephrine;
40
41. (4) primary hyperaldosteronism: depressed plasma
renin activity and hypersecretion of aldosterone,
both of which fail to change with volume expansion.
(5) renal parenchymal disease= RFT and CAST, PU
and kideny US=small or increased echopaterrn.
6.CBC=Myelo proliferative disorders.
41
42. Renal parenchymal disease:
•the most common secondary cause of
hypertension.
•CKD=elevated RFT&PU>+1.
•*AGN=RBC casts+elevated RFT
•*Chronic pyelonephritis=pus cell+elevated RFT
and WBC casts.
• Treatment include sodium restriction, diuretics
appropriate to level of renal function,and ACEIs.
• ACEIs slow the progression of proteinuric renal
disease.
42
43. • Renovascular disease
*MC=potentially curable secondary hypertension.
•cp=
•*sudden onset of hypertension,refractory to usual
antihypertensive therapy.
•*Abdominal bruit often audible; mild hypokalemia
due to activation of the RAAS.
*• Unilateral disease is associated with renin-
dependent hypertension.
*whereas bilateral disease is associated with
volume-dependent hypertension.
*Drop of BP, decreased UO, elevated k+ and
creatinine after ACEI medication in BRAS.
43
44. • Fibromuscular disease(FMD)=10% of RAS
** especially women of child bearing age.
• Medial fibromuscular dysplasia is the most
common subtype and has a string-of-beads
appearance on angiography.
• Dissection and thrombosis of a renal artery are
complications most commonly seen with rare
subtypes.•
*Renal artery occlusion is rare.
44
45. Atheromatous disease=90% of RAS.
• is the most common cause of renovascular
hypertension in middle-aged>55 years or older
persons.
• The disease is bilateral in 30% of cases and
progressive in 35%.
• It can cause renal artery occlusion unlike FMD.
45
46. Primary aldosteronism:
•Main subtypes:
1.unilateral aldosterone-producing adenoma and
2.bilateral adrenal hyperplasia.
Suspect primary aldosteronism in persons with
*spontaneous hypokalemia & TOD.
* Peripheral edema is rare.
*marked hypokalemia precipitated by usual doses of
diuretics.
*resistant hypertension.
* hypertension and an adrenal mass.
* hypokalemia despite use of ACEIs or ARBs.
46
47. Pheochromocytoma:
*remember “rule of 10.”
• 90% are in one or both adrenal glands.
• Tumors may occur anywhere along the sympathetic
chain (paragangliomas).
• It is malignant in up to 10% of cases.
• An extra-adrenal tumor produces only
norepinephrine.
• An adrenal tumor can produce an excess of
epinephrine or norepinephrine (or both).
47
48. • Classic triad of symptoms= paroxysms of
headache, diaphoresis, and palpitations.
• Paroxysms can be induced by exercise, bending,
urination, defecation,induction of anesthesia,
smoking, or infusion of contrast media.
48
49. Coarctation of the aorta
•is usually just beyond the takeoff of the left
subclavian artery.
• It usually is detected in childhood but may not be
identified until adulthood.
•*mechanism =renal artery constriction causing fluid
retention and inappropriate renin secretion.
• Classic feature: increased blood pressure in the
upper extremities and low or unobtainable blood
pressure in the lower extremities.
49
50. • Symptoms: headache, cold feet, and exercise-
induced leg pain.
• Signs: murmurs in the front or back of the
chest, visible pulsations in the neck or chest wall
and weak-delayed femoral pulses.
• Transesophageal echocardiography or MRI is
used to make the diagnosis.
• Treatment is with balloon angioplasty or
surgery.
50
51. Hypothyroidism =sv low.
*can cause diastolic hypertension due to high CAM
to have tissue perfussion
*CP= narrow PP, puffy face, dylipidemia and low
temp.Low tT&T4 with high TSH.
Hyperthyroidism
*can cause systolic hypertension,wide PP
*Dermopathy and exophthalmus.
Hyperparathyroidism=
*nephrolithiasis and increses tissue sensitivity to
CAM &vasospasm.
*Rx of hypercalcemia decreases BP.
51
52. Acromegaly
*may be associated with 35% hypertension.
*CHD due to AS.
*DM,LVH.
*Fluid overload and|or PVR.
Cushings syndrome
*B-hydroxy steroid hydrogenase excess.
*lead to cortxol excess+_mineralocorticoid.
*lead to activation of RAAS.
*DM and low potassium.
*not due to fluid overload.
52
53. Obstructive sleep apnea
*upper body obesity.
*refractory to medication.
*headache+snorring history+day time sleepness.
*hypoxia lead to increased release of SANS
activity=Metanephrine releases.
Brain tumors in the posterior fossa and panic
syndrome
*can cause labile hypertension, suggesting
pheochromocytoma.
Acute stress can increase blood pressure.
53
54. Drug induced HTN
• Oral contraceptives =age>35 years,by inducing
sodium retention, increasing renin substrate, and
facilitating the action of catecholamines.
*D|C of OCP recovery from HTN after 6 months.
*
• NSAIDS=by inducing sodium retention by blocking
the formation of renal vasodilating, natriuretic PG
and also interfere with the effectiveness of diuretics,
β-blockers, and ACEIs.
• TCA= inhibit the action of centrally acting agents
(methyldopa and clonidine).
54
56. Drug Therapy of Essential Hypertension.
*Goal is to control hypertension with minimal side
effects using a single drug if possible.
*First-line agents include diuretics, beta blockers,
ACE inhibitors, angiotensin receptor antagonists,
and calcium antagonists.
56
57. Diuretics
. 1.Thiazides =preferred over loop diuretics because of
longer duration of action; however, the latter are more
potent when GFR 25 mL/min.
Major side effects include
hypokalemia, hyperglycemia&ca+2, and hyperuricemia,
which can be minimized by using low dosage (e.g.,
hydrochlorothiazide 12.5–25 mg qd).
Diuretics are particularly effective in elderly and black
pts. Prevention of hypokalemia is especially important in
pts on digitalis glycosides.
57
58. Beta Blockers
*decreases SCD, AMI& CKD.
*Particularly effective in young pts with
“hyperkinetic” circulation.
*Begin with low dosage (e.g., atenolol 25 mg qd).
*Relative contraindications: bronchospasm, CHF,
AV block, bradycardia, and “brittle” insulin-
dependent diabetes.
58
59. ACE Inhibitors
**decreases SCD, AMI,STROKE& CKD.
*Side effects are uncommon and include rash,
angioedema, proteinuria, or leukopenia, particularly
in pts with elevated serum creatinine.
*A nonproductive cough in up to 10% of
patients,1.2-3% angioedema requiring an
alternative regimen.
•renal function may deteriorate as a result of ACE
inhibitors in pts with bilateral renal artery stenosis.
59
60. CCB.
1.Dihydropyridines
=amlodipine, felodipine, isradipine, nicardipine,
nifedipine, nisoldipine,and nitrendipine.
2. Dihydropyridines
*diltiazem and verapamin.
*Only long-acting forms are approved for
use in hypertension.
*The short-acting forms should not be used.
60
61. furosemide:
*Indication= hypertension associated with chronic
kidney disease and estimated GFR <30 mL/min.
• Metabolic effects: hypokalemia, hyperuricemia,
fasting hyperglycemia,hypochloremic alkalosis, and
increased urinary calcium excretion (hypocalcemia).
• Adverse effects: reversible deafness and postural
hypotension.
61
62. spironolactone
Important indications for : primary aldosteronism
and states of secondary aldosteronism, especially
severe heart failure.
• The diuretic effect is antagonized by the
concomitant use of salicylates.
• Adverse effects: hyperkalemia, gynecomastia,
mastodynia, menorrhagia,and skin rash.
Eplerenone
Eplerenone is a mineralocorticoid receptor
antagonist similar to spironolactone, and its
indications for use are generally the same as
for spironolactone. may be better tolerated than
spironolactone, primarily because of less risk of
gynecomastia in men.
62
63. Triamterene
* inhibits renal potassium wasting by blocking the
epithelial sodium channel in the distal tubule of the
nephron.
• Do not use in combination with indomethacin or
during pregnancy.
Amiloride
Amiloride limits renal potassium wasting by the
same mechanism as triamterene and is used most
often in combination with thiazide diuretics. Its side
effects are hyperkalemia, gastrointestinal distress,
and skin rash.
Summary Of the potassium-sparing diuretics,
only spironolactone and eplerenone can cause
gynecomastia
63
65. oNitroprusside
Dilates arterioles and veins
Dosage- 0.3micg/Kg/min, max 10micg/Kg/min
for 10min
Onset of action- 2-5min
S/E- cyanide poisoning
oNitroglycerine
Relatively greater venodilation
Dosage 5micg/min titrated by 5micg/min Q 3-
5min
S/E- reflex tachycardia
65
66. oNicardipine
Dihydropiridine CCB given as IV form
Dosage- 5mg/hr, titrate by 2.5mg/hr Q 5-15 min,
max 15mg/hr
oLabetalol
Combined alpha-1 & beta-1 blocker
Onset of action in seconds
Dosage- 2mg/min(infusion) or 20mg over 2min
then 40-80mg Q10min, max 300mg
66
67. oEsmolol
Ultra short acting beta adrenergic blocker
Onset of action 1-5min, duration of action
15-30min
Dosage 500micgm/Kg bolus which may be
repeated after 5min or 50-100micgm/Kg/min
and increased to 300micgm/Kg/min
oFenoldopam
A selective peripheral dopamine-1 receptor
agonist that induce systemic vasodilatation
Dosage- initial 0.1micgm/Kg/min, titrated at
15 min interval
67
68. oEnalaprilat
Is an Iv preparation of active form of ACEI.
Dosage- 0.625-1.25mg over 5min q 6-8hr,
max of 5mg/dose
Onset of action with in 15min, duration 12-
24hr
C/I in pregnancy, hypovolemia with high RA
oPhentolamine
Non selective alpha adrenergic blocker,
specially used for Pheochromocytoma
Dosage 5-15mg bolus
oHydralazine
10-50mg at 30min interval, used in
pregnancy
68
