lecture for undergraduate about systemic arterial hypertension. entailed a simplified approach from definition to management including hypertensive emergencies and urgencies

1. Arterial Hypertension
Motea Al-Awlaqi, MD
Assistant professor of cardiology, Aden University
Cardiologist Consultant, Al-Gamhoriah General Teaching Hospital

2. Introduction
 Hypertension is one of the common pathological entities in the world
 Hypertension is associated with the development and exacerbation of a variety of
cardiovascular disease, as well as the morbid and fatal outcome
 The systolic blood pressure increases in a linear fashion throughout life, whereas, the
diastolic blood pressure increases until 50 years of age and falls thereafter
 Hypertension remains the major preventable cause of cardiovascular disease(CVD) and
all-cause death globally
 The overall prevalence of hypertension in adults is around 30 - 45%, with a global age-
standardized prevalence of 24 and 20% in men and women, respectively, in 2015
 This high prevalence of hypertension is consistent across the world, irrespective of
income status, i.e. in lower, middle, and higher income countries
 Hypertension becomes progressively more common with advancing age, with a
prevalence of >60% in people aged >60 years
 Fewer than 30% of people with hypertension have the problem under control

3. Definition of hypertension
 Hypertension’ is defined as the level of BP at which the benefits of treatment (either with
lifestyle interventions or drugs) unequivocally outweigh the risks of treatment, as
documented by clinical trials
 Hypertension is defined as office SBP values > 140 mmHg and/or diastolic BP (DBP)
values > 90 mmHg
 Isolated systolic hypertension defined as elevated SBP (>140 mm Hg) and low DBP (< 90
mm Hg) is common in young and in elderly people. In young individuals, including
children, adolescents and young adults, isolated systolic hypertension is the most
common form of essential hypertension

4. Definitions of hypertension according to
office, ambulatory, and home blood pressure levels

5. Classification of hypertension

6. Etiology of Hypertension
ESSENTIAL HYPERTENSION SECONDARY HYPERTENSION
 Account for about 95% of cases
 No cause can be identified
(primary or essential HTN)
 The onset usually b/w the age 25-
55 years
 It is uncommon before the age of
20
 Account for 5% of cases
 A cause can be identified
 Most of the patients are young
 Most cases due renal, endocranial
causes and COA

7. Risk factors for primary hypertension
 Genetic factors
 Obesity
 Lack of exercise
 Heavy alcohol intake
 Excess salt intake
 Cigarette smoking
 Polycythemia
 NSAID
 Low potassium intake
 Sympathetic overactivity
 Insulin resistance

8. Secondary causes of hypertension
 Alcohol
 Obesity
 Pregnancy
 Renal disease
• Parenchymal renal disease, particularly GN
• Renal vascular disease
• Polycystic kidney disease
 Endocrine disease
• Phaeochromocytoma
• Cushing’s syndrome
• Primary hyperaldosteronism (Conn’s syndrome)
• Glucocorticoid-suppressible hyperaldosteronism
• Hyperparathyroidism
• Acromegaly
 Drugs
 COA
• Primary hypothyroidism
• Thyrotoxicosis
• Congenital adrenal hyperplasia due to 11ß-
hydroxylase or 17a-hydroxylase deficiency
• Liddle’s syndrome
• 11ß-hydroxysteroid dehydrogenase deficiency

9. Patient characteristics that should raise the suspicion of
secondary hypertension
 Younger patients (<40 years) with grade 2 hypertension or onset of any grade of hypertension in
childhood
 Acute worsening hypertension in patients with previously documented chronically stable normotension
 Resistant hypertension
 Severe (grade 3) hypertension or a hypertension emergency
 Presence of extensive HMOD
 Clinical or biochemical features suggestive of endocrine causes of hypertension or CKD
 Clinical features suggestive of obstructive sleep apnoea
 Symptoms suggestive of phaeochromocytoma or family history of phaeochromocytoma

10. Pathophysiology of essential hypertension
The pathophysiology of essential hypertension is incompletely understood, but is
thought to be related to one or more of the following mechanisms:
1. Defects in RAAS
2. Disturbed autonomic function
3. ↑ COP may be the initial step and subsequently causes ↑ PVR
4. Salt sensitivity: some individuals are salt sensitive lead to ↑ BP. The cause
may be genetic defect in the ability of the kidney to excrete sodium load
5. Defective pressure naturesis: the normal Kidney respond to ↑ BP by ↑ sodium
excretion. If this mechanism is defective the renal role in regulating BP is
diminished
6. Insulin resistance and metabolic syndrome; this lead to compensatory
hyperinsulinemia which causes obesity, increased sympathetic activity,
increased sodium absorption in the renal tubules and dyslipidemia (↑ TG and
↓ HDL)

11. Pathophysiology of hypertension

12. Clinical features
Symptoms
 Hypertension is called a "silent killer". Most people with hypertension are asymptomatic
 When symptoms do occur, they can include
- headache (suboccipital pulsating headache characteristically occurring early in the
morning and subsiding during the day, is characteristic but any type of headache may
occur)
- Nosebleeds, irregular heart rhythms, vision changes, and buzzing in the ears
 Severe hypertension can cause fatigue, nausea, vomiting, confusion, anxiety, chest
pain, and muscle tremors
 Symptoms of secondary causes of hypertension if present. For example
pheochromocytoma may present with episodes of hypertension along with anxiety,
palpitation, profuse perspiration, pallor, tremor, nausea and vomiting
 Symptoms of complication such as heart failure, stroke and renal failure

13. Clinical features
signs
 High BP may be the only sign in the majority of patients
 Features of the cause of hypertension
- Abdominal bruit- renovascular hypertension
- Radiofemoral delay- COA
- Enlarged kidneys – PCKD
- Characteristic facies and habitus of Cushing's syndrome
 Evidence of risk factors for hypertension
- Central obesity
- Hyperlipidaemia
 Signs due to complication of hypertension
- Signs of LVH-↑ A2, S4
- AF (due to diastolic dysfunction or CAD)
- Signs of LVF (in absence of CAD or renal impairment)
- The optic fundi are often abnormal
- There may be evidence of generalised atheroma or specific complications, such as
aortic aneurysm, PAD or stroke

14. Arterial Hypertension as a risk factor
• Hypertension is a highly prevalent risk factor for cardiovascular disease
• Hypertension plays a major etiologic role in the development of cerebrovascular disease,
ischemic heart disease, cardiac and renal failure

15. Assessment of global cardiovascular risk in arterial
hypertension
• Grades of hypertension
• Total cardiovascular risk (coexistence different risk factors, organ damage, concomitant
diseases)

16. Assessment of global cardiovascular risk in arterial
hypertension

17. Hypertension Diagnosis
• Establishing BP values
• Identyfying secondary causes of AH
• Searching for :
- other risk factors
- subclinical organ damage
- concomitant diseases
- accompanying CV and renal complications
Diagnostic evaluation in arterial hypertension

18. Hypertension Diagnosis
 The measurement of BP in the office or clinic is most commonly the basis for hypertension
diagnosis and follow-up
 Auscultatory or oscillometric semiautomatic or automatic sphygmomanometers are the
preferred method for measuring BP in the doctor’s office
 Whenever possible, the diagnosis should not be made on a single office visit. Usually 2–3
office visits at 1–4-week intervals (depending on the BP level) are required to confirm the
diagnosis of hypertension
 The diagnosis might be made on a single visit, if BP is >180/110 mmHg and there is evidence
of cardiovascular disease (CVD)
 If possible and available, the diagnosis of hypertension should be confirmed by out-of-office BP
measurement
 Unattended office blood pressure: Multiple automated BP measurements taken while the
patient remains alone in the office provide a more standardized evaluation but also lower BP
levels than usual office measurements with uncertain threshold for hypertension diagnosis.
Confirmation with out-of-office BP is again needed for most treatment decisions
 Improper measurement of office BP can lead to inaccurate classification, overestimation of a
patient’s true BP, and unnecessary treatment
Office Blood Pressure Measurement

19. Office blood pressure measurement

20. How to measure blood pressure

21. Hypertension Diagnosis
 Out-of-office BP measurements (by patients at home or with 24-hour ambulatory blood
pressure monitoring [ABPM]) are more reproducible than office measurements, more
closely associated with hypertension-induced organ damage and the risk of
cardiovascular events and identify the white coat and masked hypertension phenomena
 Out-of-office BP measurement is often necessary for the accurate diagnosis of
hypertension and for treatment decisions. In untreated or treated subjects with office BP
classified as high-normal BP or grade 1 hypertension (systolic 130–159 mm Hg and/or
diastolic 85–99 mm Hg), the BP level needs to be confirmed using home or ambulatory
BP monitoring
Out-of-Office Blood Pressure Measurement

22. Investigations
A decision to embark on antihypertensive therapy effectively commits the patient to life-long
treatment, so readings must be as accurate as possible
The objectives are to:
• Confirm the diagnosis by obtaining accurate, representative BP measurements
• Identify contributory factors and any underlying causes
• Assess other risk factors and quantify cardiovascular risk
• Detect any complications that are already present
• Identify comorbidity that may influence the choice of antihypertensive therapy

23. Routine workup for evaluation of hypertensive patients

24. Screening and diagnosis of hypertension

25. Specialized investigation of hypertension
 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 the 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

26. Differential Diagnosis
It is important to identify white coat hypertension and masked hypertension correctly as over- or under-
treatment of hypertension can have significant morbidity and mortality.
White coat Hypertension
•Consistently elevated office blood pressure but normal out-of-office blood pressure
Masked Hypertension
•Consistently elevated out-of-office blood pressure but normal office blood pressure
Psuedohypertension
• a measurement of high BP value in the presence of normal intraluminal BP because of
noncompressible arteries
•This causes a false elevation of blood pressure reading
•Use of standing blood pressure measurement can help to differentiate pseudo-hypertension from true
hypertension
•The Osler maneuver (palpable radial or brachial artery when the cuff inflated above the SBP) may be
used although sensitivity and specificity are not very high
•Patients with poorly controlled blood pressure should be evaluated for pseudo-hypertension prior
to being labeled as resistant hypertension.

27. Complications of hypertension
The adverse effect of hypertension principally involves the CNS, retina, heart and kidneys
A) CNS
1. Diffuse cerebral atherosclerosis
2. Lacunar infarct
3. Stroke (ischemic or hemorrhagic)
4. Hypertensive encephalopathy: it is characterised by severe hypertension with neurological
symptoms e.g. transient disturbances of speech or vision, disorientation, fits and
unconsciousness
5. ICH
6. Subarachnoid hemorrhage
7. Muti-infarct dementia

28. Complications of hypertension
B) Retina
Hypertensive retinopathy are graded as the following

29. Complications of hypertension
C) Heart
- LVH
- LV diastolic dysfunction
- LV systolic failure
- IHD
D) Kidneys
- Nephrosclerosis (hypertensive nephropathy)
- Proteinuria
- Progressive renal failure
- Renal artery aneurysm
E) Vascular
- Accelerated atherosclerosis
- Hge from rupture of small vessels (e.g. epistaxis)
- Dissecting aneurysm of aorta
- PAD- ischemia of LL or intermittent claudication

30. Management of hypertension
 The management of hypertension typically involves both lifestyle modifications and
pharmacologic therapies
 Both are required to achieve target blood pressure
 Lifestyle modifications are initiated before pharmacologic interventions unless:
- The blood pressure is stage 2
- Target organ disease is present, or
- A comorbid condition exists which is favorably influenced by a specific antihypertensive drug

31. Lifestyle modification
 Weight reduction. Target body mass index of 18.5 to 24.9 kg/m2. Average systolic blood
pressure (SBP) reduction of 5 to 20 mm Hg per 10 kg weight loss.
 Moderate alcohol intake. Men: limit to =2 drinks (15 mL of ethanol). Women and lighter weight
persons: limit to =1 drink per day. Average SBP reduction of 2 to 4 mm Hg.
 Regular aerobic physical activity. Brisk walking at least 30 minutes per day, most days of the
week. Average SBP reduction of 4 to 9 mm Hg.
 Reduce dietary sodium intake. Decrease to =100 mmol/ day (2.4 g of Na or 6 gm of NaCl).
Average SBP reduction of 2 to 8 mm Hg.
 Dietary Approaches to Stop Hypertension (DASH) diet. Adopt a diet rich in fruits, vegetables,
and low fat dairy products with reduced content of saturated and total fat. Average SBP
reduction of 2 to 8 mm Hg.

32. Pharmacological therapy
 A variety of drugs are available to manage the patient with hypertension. These agents can be
classified into seven categories (prototypes)
 Diuretics (hydrochlorothiazide).
 Adrenergic inhibitors
- α-blocker: prazosin
- ß-blocker: Bisoprolol
- Mixed: labetalol
- centrally acting: clonidine
 Direct vasodilators (hydralazine).
 Calcium channel blockers (CCBs), such as nifedipine.
 Converting-enzyme inhibitors (CEI) such as captopril
 Angiotensin I (AT1)-receptor blockers (losartan).
 Direct inhibitors of renin (aliskiren)

33. Diseases affecting the choice of drugs for hypertension
(compelling indications)

34. Compelling and possible contraindications to the use
of specific antihypertensive drugs

35. Benefits of Lowering BP
Average reduction
Stroke incidence 35–40%
Myocardial infarction 20–25%
Heart failure 50%

36. Aim of antihypertensive therapy
• The primary goal of treatment is to achieve maximum reduction in the long-term total risk
of CV disease
• For this reason lowering BP therapy (at least < 140/90 mm Hg) and treatment of all
reversible risk factors are indicated
• In diabetes and in high and very high risk patients BP target should be at least < 130/80
mmHg

37. When to initiate antihypertensive treatment?

38. Summary of office blood pressure thresholds for treatment

39. Core drug treatment strategy for uncomplicated hypertension

40. Ideal Characteristics of Drug Treatment

41. Office blood pressure treatment target range

42. Resistant hypertension
 Hypertension is defined as resistant to treatment when the recommended treatment
strategy fails to lower office SBP and DBP values to <140 mmHg and/or <90 mmHg,
respectively, and the inadequate control of BP is confirmed by ABPM or HBPM in
patients whose adherence to therapy has been confirmed
 The recommended treatment strategy should include
- Appropriate lifestyle measures and
- Treatment with optimal or best-tolerated doses of three or more drugs, which should
include a diuretic, typically an ACE inhibitor or an ARB, and a CCB.
- Pseudo-resistant hypertension and secondary causes of hypertension should also have
been excluded

43. Characteristics of patients with resistant hypertension
Resistant hypertension is associated with
- older age (especially >75 years)
- male sex
- black African origin
- higher initial BP at diagnosis of hypertension, highest BP ever reached during the
patient’s lifetime
- frequent outpatient visits
- Obesity
- Diabetes
- atherosclerotic disease and HMOD, CKD, and
- a Framingham 10 year coronary risk score >20%

44. Causes of resistant hypertension
1. Pseudo-resistant hypertension
- Poor adherence to prescribed medicines
- White-coat phenomenon
- Poor office BP measurement technique
- Marked brachial artery calcification
- Clinician inertia, resulting in inadequate doses or irrational combinations of BP-lowering
drug therapies
2. Other causes of resistant hypertension
- Lifestyle factors, such as obesity or large gains in weight, excessive alcohol
consumption, and high sodium intake
- Intake of vasopressor or sodium-retaining substances, drugs prescribed for conditions
other than hypertension, some herbal remedies, or recreational drug use (cocaine,
anabolic steroids, etc.)
- Obstructive sleep apnoea (usually, but not invariably, associated with obesity)
- Undetected secondary forms of hypertension
- Advanced HMOD, particularly CKD or large-artery stiffening

45. Hypertensive crisis
 Hypertensive crisis is a generic term refer to the sudden or rapid development of severe
hypertension (SBP > 180 mmHg and/or DBP > 120 mmHg) that have the potential to
cause target organ damage (heart, vascular, kidneys, eyes and brain)
 Hypertensive crises represents 3% of all medical urgencies, with a prevalence of 24%
and 76%, for hypertensive emergencies and urgencies, respectively
 Prompt recognition, evaluation and appropriate treatment of these crises are critical to
prevent high morbidity and mortality
 Risk factors include:
- Female sex
- Obesity
- High BMI
- Hypertensive or coronary heart disease
- Higher number of antihypertensive drugs and,
- Most importantly, nonadherence to medication

46. Hypertensive emergency
 Hypertension emergencies are situations in which substantially elevated BP is
associated with acute HMOD, which is often life-threatening and requires immediate but
careful intervention to lower BP, usually with intravenous (i.v.) therapy
 Typical presentations of a hypertension emergency are:
- Patients with malignant hypertension
- Patients with severe hypertension associated with other clinical conditions who are likely
to require an urgent reduction of BP, e.g.
• acute aortic dissection
• acute myocardial ischaemia, or
• acute heart failure
• ICH
 Patients with sudden severe hypertension due to phaeochromocytoma, associated with
organ damage
 Pregnant women with severe hypertension or preeclampsia
 The definition intentionally are devoid of any absolute BP numbers because the level at
which the individual develop TOD can vary depending on the clinical substrate and the
rapidity of which BP rise

47. Hypertensive emergency
Malignant hypertension
 A specific form of hypertensive emergency Characterized by Severe BP elevation
(commonly >200/120 mm Hg) associated with advanced bilateral retinopathy (flame
haemorrhages and/or papilloedema), microangiopathy, and disseminated intravascular
coagulation, and can be associated with encephalopathy (in about 15% of cases), acute
heart failure, and acute deterioration in renal function
 The hallmark of this condition is small artery fibrinoid necrosis in the kidney, retina, and
brain.
 The term ‘malignant’ reflects the very poor prognosis for this condition if untreated
 Hypertensive encephalopathy: Severe BP elevation associated with lethargy, seizures,
cortical blindness and coma in the absence of other explanations

48. Hypertensive emergency vs hypertensive urgency

49. Diagnostic workup for patients with a suspected hypertension
emergency

50. Management of hypertensive emergency
 Prompt BP control within minutes or a few hours by intravenous administration of
antihypertensive drugs
 Lower MAP initially up to 25%
 Prompt intravenous administration of short-acting and titratable drugs is preferred in the
first few minutes of treatment
- Aim for DBP of 100-105 mmHg within 6-8 hrs
- Avoid lowering of SBP below 160 mmHg in the acute setting (given changes in cerebral
autoregulation)
- Exception: aortic dissection where goals of SBP 120 mmHg, MAP 80 mmHg, achieved
over 5-10 minutes
- Reduce BP to goal on oral medications, gradually over 2-3 months

51. Hypertensive urgency
 It is an acute increase in BP in the absence of, or with minimal, target end-organ damage
 The decrease in BP may be obtained in hours or few days by oral anti-hypertensives.
 Most cases do not need hospitalization and are managed effectively on outpatient follow-
up
(a) Immediate goal—lower blood pressure within 24–72 h
(b) Treatment setting—clinical discretion is required
(c) Medications—oral medications with rapid onset of action; occasionally intravenously
Goals of decreasing BP

52. Hypertensive emergencies requiring immediate blood pressure
lowering with intravenous drug therapy

53. Drug types, doses, and characteristics for treatment of
hypertension emergencies

54. Drugs for hypertensive urgencies