Hypertension, or high blood pressure, is defined as a systolic blood pressure above 140 mmHg or a diastolic blood pressure above 90 mmHg. It can be classified based on severity from stage 1 to stage 2. Primary causes include sympathetic nervous system hyperactivity, renin-angiotensin system activity, and defects in natriuresis. Target organ damage may occur in the eyes, heart, brain, kidneys, and vasculature. Hypertensive emergencies require rapid blood pressure reduction to prevent end organ damage and include hypertensive encephalopathy and eclampsia. Intravenous drugs like sodium nitroprusside, labetalol, and hydralazine are used to slowly

1. Dr. Suman Chowdhury
CMCH
Examinee of FCPS

2. Hypertension:
 Hypertension is a condition in which arterial BP is
chronically elevated.

3. And, What is the upper
limit?

4. > 140/90 mmHg

5. For Diabetic Patients:
> 130/80mmHg

6. Is it a Sign or Disease?
 It is more than a sign
 It will not be an exaggeration if we consider it as a
disease!

7. Classification

8. Classification of Hypertension
Category
BHS JNC 7 SBP (mmHg) DBP (mmHg)
Optimal Normal < 120 < 80
Normal
Pre hypertension
< 130 < 85
High Normal 130-139 85-89
Hypertension Hypertension
Grade 1 (Mild) Stage 1 140-159 90-99
Grade 2 (Moderate)
Stage 2
160-179 100-109
Grade 3 (Severe) ≥ 180 ≥ 110
Isolated Systolic Hypertension
Grade 1 140-159 < 90
Grade 2 ≥ 160 < 90
BHS = British Hypertension Society
JNC 7= Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure

9. The Primary/Essential Hypertension
is said to be due to these following
mechanisms:

10.  Sympathetic nervous system hyperactivity
 This is most apparent in younger persons with hypertension,
who may exhibit tachycardia and an elevated cardiac output.
However, correlations between plasma catecholamines and blood
pressure are poor. Insensitivity of the baro-reflexes may play a
role in the genesis of adrenergic hyperactivity.
 Abnormal cardiovascular or renal development
 The normal cardiovascular system develops so that elasticity of
the great arteries is matched to the resistance in the periphery to
optimize large vessel pressure waves. In this way, myocardial
oxygen consumption is minimized and coronary flow maximized.
Elevated blood pressure later in life could arise from abnormal
development of aortic elasticity or reduced development of the
microvascular network. This has been postulated as the sequence
of events in low birth weight infants who have an increased risk
of hypertension developing in adulthood. Another hypothesis
proposes that the association between low birth weight and
hypertension arises from reduced nephron number.

11.  Renin–angiotensin system activity
 Renin, a proteolytic enzyme, is secreted by cells surrounding
glomerular afferent arterioles in response to a number of
stimuli, including reduced renal perfusion pressure,
diminished intravascular volume, circulating catecholamines,
increased sympathetic nervous system activity, increased
arteriolar stretch, and hypokalemia. Renin acts on
angiotensinogen to cleave off the ten-amino-acid peptide
angiotensin I. This peptide is then acted upon by angiotensin-
converting enzyme (ACE) to create the eight-amino-acid
peptide angiotensin II, a potent vasoconstrictor and stimulant
of aldosterone release from the adrenal glands. Despite the
role of renin in the regulation of blood pressure, it probably
does not play a central role in the pathogenesis of most
primary (essential) hypertension; only 10% of patients have
high renin activity, whereas 60% have normal levels, and 30%
have low levels. Black persons with hypertension and older
patients tend to have lower plasma renin activity, which may
be associated with expanded intravascular volume.

12.  Defect in natriuresis
 Normal individuals increase their renal sodium excretion in
response to elevations in arterial pressure. In hypertensive
patients, this pressure-natriuresis relationship is reset so that
maintenance of sodium homeostasis requires increased
extracellular fluid volume and higher arterial pressure.
 Intracellular sodium and calcium
 Intracellular Na+ is elevated in primary (essential)
hypertension. An increase in intracellular Na+ may lead to
increased intracellular Ca2+ concentration as a result of
facilitated exchange and might explain the increase in
vascular smooth muscle tone that is characteristic of
established hypertension.

13. Though secondary causes are only
5%, the list is not too short!!!!

14. Identifiable causes of Hypertension
 Sleep apnea
 Drug-induced or drug-related
 Chronic kidney disease
 Primary aldosteronism
 Renovascular disease
 Long-term corticosteroid therapy and Cushing syndrome
 Pheochromocytoma
 Coarctation of the aorta
 Thyroid or parathyroid disease

15. Hypertensive Crisis

16. Hypertensive
Emergency
Hypertensive Crisis
 These include patients with
asymptomatic severe
hypertension, very high blood
pressure diastolic > 120 to 130 mm
Hg
There is no target organ damage
 BP at these levels often worries
the physician; however, acute
complications are unlikely, so
immediate BP reduction is not
required.
 Patients should be started on a
2-drug oral combination, and
close evaluation (with evaluation
of treatment efficacy) should be
continued on an outpatient basis.
Hypertensive
Urgency
 May be defined as acute and rapidly developing end
organ damage with significant hypertension. Here
blood Pressure is usually > 220 mm of Hg.
Hypertensive emergencies require substantial
reduction of blood pressure within 1 hour to avoid
the risk of serious morbidity or death
There is target organ damage.
Hypertensive emergencies are treated in an ICU
 BP is progressively (although not abruptly) reduced
using a short-acting, titratable IV drug.
 Choice of drug and speed and degree of reduction
vary somewhat with the target organ involved, but
generally a 20 to 25% reduction in MAP over an hour
or so is appropriate, with further titration based on
symptoms. Then if stable, to 160/100–110 mmHg
within the next 2–6 hours.

17. Target Organ damage
Signs and
Symptoms
Hypertensive
Retinopathy
Grade 4
Renal Retinal
Transient disturbances of
speech or vision,
paraesthesiae, fits,
disorientation, and loss
of consciousness,
Papilloedema is common
A CT scan of the brain
often shows haemorrhage
in and around the basal
ganglia.
Cardiac
CNS
Organs
'Cotton wool'
exudates are
associated with
retinal
ischaemia or
infarction,
central retinal
vein
thrombosis
Hypertensive
nephropathy
Hematuria,
proteinuria
,and
progressive
kidney
Acute MI, acute
left ventricular
failure with
pulmonary
edema, unstable
angina pectoris,
dissecting aortic
aneurysm
Hypertensive
Encephalopathy
Disorders
Chest pain,
Dyspnoes,
sudden
severe pain
in back with
shock

18.  And also,
Preeclampsia
+
Convulsion
Signs and
Symptoms
Eclampsia
Preeclampsia
Disorders
In Pregnancy
Proteinuria,
Edema

19. Attention!!!
 Interesting to note that, in case of Hypertensive
encephalopathy, we have to very cautious to exclude
stroke of any kind. For which, even an early MRI (T2
weighted) should be done if we are not confident
enough after history, and physical (neurological)
examination!!
 Because, the target and the management plan will be
totally changed in case of stroke.

20. Regarding anti
Hypertensive in stroke
SAH
In Haemorrhagic
stroke*
In ischaemic
stroke
Intracerebral Who are not
candidates for
thrombolytic
therapy
If thrombolytic
therapy is to be
used
Target is
MAP >
130mmHg
Target is SBP>
180mmHg
and DBP >
130mmHg
Target is
SBP>
185mm Hg
and DBP >
110mm Hg
Target is
SBP>
220mmHg
and DBP>
130mmHg

21. Suggested Recommended Guidelines for Treating
Elevated Blood Pressure in Spontaneous ICH
 If SBP is 200 mm Hg or MAP is 150 mm Hg, then consider
aggressive reduction of blood pressure with continuous
intravenous infusion, with frequent blood pressure
monitoring every 5 minutes
 If SBP is 180 mm Hg or MAP is 130 mm Hg and there is
evidence of or suspicion of elevated ICP, then consider
monitoring ICP and reducing blood pressure using
intermittent or continuous intravenous medications to
keep cerebral perfusion pressure 60 to 80 mm Hg

22. Accelerated Hypertension Malignant Hypertension
1. Complication with high blood pressure,
target organ damage
1. Malignant hypertension is by historical
definition characterized by encephalopathy or
nephropathy with accompanying
papilledema
2. Complication of high blood pressure
characterized by very elevated high blood
pressure
2. There is no fibrinoid necrosis of
arterioles and small arteries
2. There is fibrinoid necrosis of arterioles and
small arteries.
3. Target organ(eyes, heart, lungs, kidney)
damage is present
3. Target organ(eyes, heart, lungs, kidney)
damage is present
4. Fundoscopy shows flame shaped
hemorrhages, or soft exudates, but no
papilledema.
4. Fundoscopy shows papilledema
5. There is no microangiopathic hemolytic
anemia.
5. There is microangiopathic hemolytic anemia
6. There is no such demarcation 6. Systolic and diastolic blood pressures are
usually greater than 240 and 120, respectively.

23. Management

24. A person with
Increased BP
If not available,
manage in Ward
Look for compelling
indications
Select drugs after excluding
compelling Contraindications
IV GTN, Hydralazine, Labeteolol
IV drugs with
titratable doses
Call for ICU/HDU
Yes No
Look for Hypertensive
Crisis
e.g. Captopril
Start Oral
drugs
Emergency
Urgency Establish HTN*
Look for co-morbid conditions
When the blood pressure has been brought under
control, combinations of oral antihypertensive agents
can be added as parenteral drugs are tapered off
over a period of 2–3 days. Most subsequent regimens
should include a diuretic.
If not
controlled
Add other
drugs later
if necessary
Life style
Modification
Drug Rx §
Consider special

25. • * Persistent Raised BP:
• Measured at past two visits and
• Systolic BP or DBP or Both are > 140/90mmHg
• § Threshold for offering Drug treatment:
• BP > 160/100mmHg, or
• Isolated Systolic HTN (Systolic BP> 160 mmHg), or
• BP > 140/90mmHg, and
• 10 yr CVD risk at list 20 % or
• Existing CVD or
• Target organ damage

26. Management of Hypertensive urgency

27. General strategies:
All patients should be provided a quiet room to rest; this can lead to a fall in BP
of 10 to 20 mmHg or more. The approach varies depending on whether the
patient has already been treated for hypertension or is untreated.
Previously treated
hypertension
Previously
Untreated
hypertension
1. Increase the dose of existing
antihypertensive medications, or add
another agent.
2. Reinstitution of medications in non-
adherent patients.
3. Addition of a diuretic, and
reinforcement of dietary sodium
restriction, in patients who have
worsening hypertension due to high
sodium intake.
In the previously untreated patient, several
options are available. The approach should take
into consideration:
1. The individual patient's risk with persistence
of severe hypertension
2. The likely duration of severe hypertension,
3. Of cerebrovascular or myocardial ischemia
with rapid reduction in blood pressure
4. Relatively rapid initial blood pressure
reduction (over several hours). We use Oral
captopril

28.  Following administration of drugs, the patient is observed for a
few hours, to ascertain a reduction in blood pressure of 20 to 30
mmHg. Thereafter, a longer acting agent is prescribed and the
patient is sent home to follow up within a few days. The drop in
blood pressure may take relatively longer with captopril, and may
be too large among patients with hemodynamically significant
unilateral renal artery stenosis.
 Blood pressure reduction over one to two days. There are no data
supporting the use of a particular agent in this setting although
we generally do not begin therapy with extended release
preparations or with a diuretic alone. Depending on the patient, a
calcium channel blocker (but not sublingual nifedipine), beta
blocker or angiotensin converting enzyme (ACE) inhibitor or
receptor blocker can be started, like ramipril 10 mg once daily.

29.  The choice of agent should take into consideration the type of
antihypertensive agent that is most appropriate in the long term
(eg, calcium channel blockers and thiazide-like diuretics are
preferred over ACE inhibitors and beta blockers as monotherapy
in blacks), and underlying conditions that may be favorably or
adversely affected by the antihypertensive agent .
 Some experts initiate therapy with two agents or a combination
agent, one of which is a thiazide diuretic. The rationale is that
most patients with blood pressure ≥20/10 mmHg above goal will
require two or more antihypertensive agents in order to achieve
the goal blood pressure .
 It is unlikely that a diuretic in combination with a modest dose of
another agent will cause a dangerous reduction in the blood
pressure; however, initiation of two agents simultaneously must
be done with close blood pressure follow-up, since the full effects
of both agents may not occur for a few days, and adverse
consequences may ensue if the blood pressure is lowered too
quickly. This is particularly true among patients with
cerebrovascular disease in whom more cautious blood pressure
reduction is warranted.

30. Monitoring and
follow-up

31.  The patient with severe asymptomatic hypertension is usually
managed in the emergency room, since exclusion of acute end-
organ damage requires laboratory testing, and the patient may
require administration of medications and several hours of
observation. However, the patient can often be safely managed in
the physician's office if the evaluation and management can be
carried out.
 The management of a patient who does not have established
HTN, follow-up is difficult. Rarely, such patients may require
admission.
 In addition, patients at high risk for cardiovascular events (e.g,
long-standing diabetes, known coronary artery disease or prior
stroke), should probably be admitted.

32.  Ideally, the patient should be observed for a few hours to
ascertain that the blood pressure is stable or improving, and that
indeed they are asymptomatic. If so, the patient can be sent
home with close follow-up over the subsequent days directed
towards evaluation for symptoms related to hypertension or
hypotension, and adjustment of medications to achieve the
initial blood pressure goal of ≤160/100 mmHg.
 In reliable patients who can monitor their blood pressure at
home, close phone follow-up may substitute for direct physician
visits. If the patient does not have a physician, follow-up may
need to be in the emergency room or other acute care setting.
 Over the subsequent weeks and months, the dose and selection
of medications should be adjusted as needed to achieve the
desired blood pressure goals. These issues are discussed
elsewhere.

33. Drugs for the Hypertensive Crisis

34. I.V. Drugs for Hypertensive Emergency:
Drugs Dosage
Sodium Nitropruside Initially 0.3 µg/kg/min, then 0.25–10 μg/kg/min
IV infusion (maximum dose for 10 min only)
Labetelol 20-80 mg IV bolus over 2 min, followed q 10 min by 40 mg,
then up to 3 doses of 80 mg; or 0.5–2 mg/min IV infusion
Nicardipine Initial 5mg/hr , Max. 15 mg/hr
Nitroglycerine Initial 5 μg/min , then titrate 5 μg/min at 3-5 mins interval
Range is: 5–100 μg/min IV infusion
Hydralazine 10-50mg at 30 mins interval , (10–40 mg IV, 10–20 mg IM)
Esmolol 250–500 μg/kg/min for 1 min, then 50–100 μg/kg/min for 4
min; may repeat sequence
Enalapril 0.625-1.25 mg over 5mins. Every 6-8 hrs, max. 5mg/hr

35. Preferred I.V drugs in Selected conditions:
Situations Drugs
Hypertensive encephalopathy Nitropruside, Nicardipine, Labetelol
Acute LVF Nitroglycerine, Enalapril, Loop diuretics
MI, Unstable angina Nitroglycerine, Nicardipine, Labetelol, Esmolol
Eclampsia Labetelol, Hydralazine
Aortic dissection Nitropruside, Esmolol, Labetelol

36. Management:
 Non pharmacologic therapy:
 Lifestyle modification may have an impact on morbidity
and mortality. A diet rich in fruits, vegetables, and low-fat
dairy foods and low in saturated and total fats (DASH diet)
has been shown to lower blood pressure.

37. Lifestyle modifications to manage hypertension
Modification Recommendation Approximate
Systolic BP
Reduction,
Range
Weight reduction Maintain Norma l Body weight (BMI 18.5-24.9) 5-20mmHg, 10
kg weight loss
Adopt DASH
eating plan
Consume a diet rich in fruits, vegetables, and low-
fat dairy products with a reduced content of
saturated fat and total fat
8–14 mm Hg
Dietary Sodium
restriction
Reduce dietary sodium intake to no more than 100
mEq/d (2.4 g sodium or 6 g sodium chloride)
2–8 mm Hg
Physical activity Engage in regular aerobic physical activity such as
brisk walking (at least 30 minutes per day, most
days of the week)
4–9 mm Hg
Moderation of
alcohol
consumption
Limit consumption to no more than two drinks
per day (1 oz or 30 mL ethanol [eg, 24 oz beer, 10 oz
wine, or 3 oz 80-proof whiskey]) in most men and
no more than one drink per day in women and
2–4 mm Hg

38. Pharmacological approach:
 Depends mainly on:
 Compelling indications
 Contraindications
 Presence of co-morbid conditions
 Some special situations

39. Compelling Indications:
 CVD risk+ IHD+ (Previous H/O CVD= ACEi, ARB
 Cardiac:
 Post MI=ACEi, Aldosterone antagonists
 LVF = ARB, Aldosterone antagonists
 DM Type 1= ACEi
 DM Type = ARB
 Older patients+ Isolated Systolic HTN= Thiazide or Thiazide
like diuretics
 CKD= ARB, ACEi

40. Old Concept New Concept

41. That means, Beta blocker is less
favored as an Antihypertensive
drug!!

42. Contraindications:
 Pregnancy: No ACEi, ARB
 Asthma+ COPD= No β Blocker
 Young male patient = No β Blocker (Relative)
 Significant Renal artery stenosis = ARB, ACEi
 Hyperkalaemia = ARB, ACEi

43. Investigations:
 For all patients:
 Urinalysis for blood, protein and glucose
 Blood urea, electrolytes and creatinine
 N.B. Hypokalaemic alkalosis may indicate primary
hyperaldosteronism but is usually due to diuretic therapy
 Blood glucose
 Serum total and HDL cholesterol
 12-lead ECG (left ventricular hypertrophy, coronary
artery disease)

44. Cont……
 For Selected Patients:
 Chest X-ray: to detect cardiomegaly, heart failure, coarctation of
the aorta
 Ambulatory BP recording: to assess borderline or 'white coat'
hypertension
 Echocardiogram: to detect or quantify left ventricular hypertrophy
 Renal ultrasound: to detect possible renal disease
 Renal angiography: to detect or confirm presence of renal artery
stenosis
 Urinary catecholamines: to detect possible phaeochromocytoma
 Urinary cortisol and dexamethasone suppression test: to
detect possible Cushing's syndrome
 Plasma renin activity and aldosterone: to detect possible
primary aldosteronism

45. RESISTANT HYPERTENSION
 Resistant hypertension is defined in JNC 7 as the failure to
reach blood pressure control in patients who are adherent
to full doses of an appropriate three drug regimen
(including a diuretic). In this situation, the clinician
should first exclude identifiable causes of hypertension, and
then carefully explore reasons why the patient might not be
at goal blood pressure.
 The clinician should pay particular attention to the type of
diuretic being used in relation to the patient's kidney
function. Aldosterone may play an important role in
resistant hypertension and aldosterone receptor blockers
can be very useful. If goal blood pressure cannot be
achieved following completion of these steps, consultation
with a hypertension specialist should be considered.

46. Causes of resistant hypertension
 Improper blood pressure measurement
 Volume overload and pseudotolerance
 Excess sodium intake
 Volume retention from kidney disease
 Inadequate diuretic therapy
 Drug-induced or other causes:
 Nonadherence
 Inadequate doses
 Inappropriate combinations
 Nonsteroidal anti-inflammatory drugs; cyclooxygenase-2
inhibitors
 Cocaine, amphetamines, other illicit drugs
 Sympathomimetics (decongestants, anorectics)

47.  Oral contraceptives
 Adrenal steroids
 Cyclosporine and tacrolimus
 Erythropoietin
 Licorice (including some chewing tobacco)
 Selected over-the-counter dietary supplements and
medicines (eg, ephedra, ma huang, bitter orange)
 Associated conditions
 Obesity
 Excess alcohol intake

48.  Once antihypertensive drug therapy is initiated, most patients
should return for follow up and adjustment of medications at
monthly intervals or until the BP goal is reached and laboratory
testing limited to tests appropriate for the patient and the
medications used.
 More frequent visits will be necessary for patients with stage 2
hypertension or with complicating co morbid conditions. Serum
potassium and creatinine should be monitored at least one to
two times per year. Yearly monitoring of blood lipids is
recommended, and an electrocardiogram should be repeated at 2-
to 4-year intervals depending on whether initial abnormalities are
present, the presence of coronary risk factors, and age.
Follow-Up of Patients Receiving Hypertension Therapy

49.  Optimal target blood pressures during
antihypertensive treatment:
No diabetes Diabetes
Clinic measurements < 140/85 mmHg < 130/80 mmHg
Mean day-time ambulatory or
home measurement
< 130/80 mmHg < 130/75 mmHg

50.  After BP is at goal and stable, follow up visits can usually be at 3-
to 6-month intervals. Co morbidities such as HF, associated
diseases such as diabetes, and the need for laboratory tests
influence the frequency of visits. Other cardiovascular risk
factors should be monitored and treated to their respective goals,
and tobacco avoidance must be promoted vigorously.
 Low-dose aspirin therapy should be considered only when BP is
controlled because of the increased risk of hemorrhagic stroke
when the hypertension is not controlled. Pharmacy care
programs have been shown to improve compliance with
medications. Patients who have had excellent blood pressure
control for several years, especially if they have lost weight and
initiated favorable lifestyle modifications, should be considered
for "step-down" of therapy to determine whether lower doses or
discontinuation of medications are feasible.

51. Interesting to note:
 Target BP is similar to that for younger patients.
 Antihypertensives are tolerated in elder patients as well
as in younger patients.
 Not only the SBP, but DBP is also equally important
regarding treatment
 Sometimes, antihypertensives are used not only to reach
the target BP, but also for some other beneficial effects.
 We should be cautious about the combination
antihypertensive drugs, as they causes Electrolytes
Imbalance, Bradycardia, Exacerbation of Br. Asthma etc.

52. Cont……..
 It is helpful if we consider the contraindications rather
than the indications
 Effectiveness of some antihypertensive drugs may only
be seen after a long period, so we should not hurry