hypertension and vascular disease

1. HYPERTENSIVE VASCULAR
DISEASE
PRESENTER: DR AMINA
DR NAVEEN
MODERATOR: DR MADHUMATHI

2. NORMAL VESSELS
• Main components of vascular walls are
• Intima – endothelial cells
• Media – smooth muscle cells (SMC)
• Adventitia – extra cellular matrix (ECM) + vasavasorum
+ nerve fibres.

3. VASCULAR SYSTEM
Arterial system
Venous system
Lymphatic system

4. Large arteries
Medium arteries
Small arteries
Arterioles
Large veins
Medium veins
Small veins
Collecting venules
Post capillary venules
Capillaries

5. STRUCTURE OF BLOOD VESSELS

6. TYPES OF ARTERIES BASED ON THEIR
SIZE AND STRUCTURAL FEATURES
• Large / Elastic arteries
• Aorta and its large branches ( subclavian, common carotid, iliac)
• Medium / Muscular arteries
• Coronary arteries
• Renal arteries
• Small arteries (<2mm), arterioles (20-100 µm)
Note- Arterioles are the principal points of physiologic resistance to blood
flow.
• Capillaries(7-8m) have one cell thick wall and large cross
sectional area – useful in exchange of diffusible
substances

7. • Features of veins
• Large diameter - 2/3 of systemic blood is in venous system
• Large Lumina
• Thinner and less organized walls
• Valves to prevent reverse flow
• Veins are predisposed to
• Irregular dilation
• Compression
• Easy penetration by tumors

8. LYMPHATICS
• Thin walled endothelium lined channels
• Serve as a drainage system for retaining interstitial tissue
fluid to blood
• Important pathway for disease dissemination – bacteria,
tumour cells

9. FUNCTIONS OF ENDOTHELIAL CELLS
• Maintenance of permeability barrier
• Elaboration of anticoagulant and antithrombotic
molecules
• Elaboration of prethrombotic molecules
• Extra cellular matrix production
• Modulation of blood flow and vascular reactivity
• Regulation of inflammation and immunity
• Regulation of cell growth
• Oxidation of LDL

10. FUNCTIONS OF SMCs
• Vasoconstriction/dilation in response to
normal/pharmacologic stimuli
• Synthesize collagen, elastin and proteoglycans
• Elaborate growth factors and cytokines
• Migrate to the intima and proliferate after injury

11. VASCULAR DISORDERS
Vascular abnormalities cause clinical disease by two
mechanisms
• Narrowing or completely obstructing the Lumina
 Progressively- atherosclerosis
 Precipitously – thrombosis or embolism
• Weakening of the walls-leading to dilation or rupture

12. VASCULAR DISEASE
• Congenital anomalies
• Arteriovenous fistula – some times causes high-out put cardiac
failure
• Arteriosclerosis
• Atherosclerosis
• Monckeberg medial calcific sclerosis
• Arteriolosclerosis
• Hypertensive vascular disease
• Aneurysms and dissections
• Inflammatory vascular disease

13. oHypertension is one of the leading causes of global burden of
disease
oIt doubles the risk of cardiovascular diseases, ischemic and
hemorrhagic stroke , renal failure and peripheral arterial disease
oLarge segments of hypertensive population are either untreated or
inadequately treated

14. oClinically hypertension defined as that level of BP at which the
institution of therapy reduces BP related morbidity and mortality
oIt is the product of cardiac output and peripheral resistance
oIt is based on the average of two or more seated BP readings during
each of two or more out patient visits

15. oSBP is more important than dbp in the measurement of cardiovascular risk
except in young patients
opulse pressure(PP)=SBP-DBP
oMean arterial pressure=DBP+1/3PP
oIsolated systolic hypertension
oSBP>140 with DBP<90
oArteriosclerosis/AR/fever/thyrotoxicosis/AV fistula

16. AHA CLASSIFICATION
CATEGORY SYSTOLIC DIASTOLIC
NORMAL <120 <80
ELEVATED 120-129 <80
HYPERTENSION
STAGE 1 130-139 80-89
STAGE 2 >140 >90

17. ESC CLASSIFICATION
CATEGORY SYSTOLIC DIASTOLIC
OPTIMAL <120 <80
NORMAL 120-129 80-84
HIGH NORMAL 130-139 85-89
GRADE 1 140-159 90-99
GRADE 2 160-179 100-109
GRADE 3 >180 >110

18. SBP DBP
OFFICE/CLINIC >_140 90
SELF/HOME BP >_135 85
AMBULATORY(24HR
AVG)
>_135 85

19. oHome blood pressure measurement
-To identify white coat HTN
-Increases adherence to medication
-Detect masked HTN
oThe bladder length of bp cuff should be 80%
ideal width is 40%

20. • Ambulatory bp measurement
 Over a period of 24-48 hr
 Detect episodic HTN
 Hypotensive episodes
 Autonomic dysfunction
 Evaluation of sleep apnea
 Evaluate antihypertensives
 Resistant HTN

21. CATEGORY NORMAL HTN
24 HRS AVG 130/80 135/85
DAY /AWAKE 135/85 140/90
ASLEEP /NIGHTTIME 120/70 125/75

22. RISK FACTORS
MODIFIABLE
• Smoking
• High sodium intake
• Low Ca, K, Mg diet
• Physical activity
• Obesity
• Alcohol
• Stress
NON MODIFIABLE
• Age
• Family History of
hypertension
• Alpha adducin gene

23. PATHOPHYSIOLOGY
 Increased cardiac output
 Increased peripheral resistance
 Established HTN- increased peripheral resistance and normal cardiac
output

24. Increased CO
• Increased fluid volume-excess sodium intake increases
preload
• Renal sodium retention
• Renin angiotensin system
• Sympathetic nervous system overactivity-

25. • Increased peripheral vascular resistance
• Increased intracellular calcium
• Angiotensin 2, IGF,prostaglandins,endothelin
• Structural vascular remodelling and hypertrophy

28. AUTONOMIC NERVOUS SYSTEM
• Most rapidly responding regulator of blood pressure
• Control BP by changing blood distribution in the body and
by changing blood vessel diameter
• Sympathetic and parasympathetic activity will affect veins,
arteries and heart
• Receives continuous information from the baroreceptors
in carotid sinus and the aortic arch

29. • This information is relayed to the brainstem to the vasomotor centre
• Vasomotor centre is a cluster of sympathetic neurons found in medulla
found in medulla
• It sends efferent motor fibres that innervate smooth muscles of blood vessels
• A decrease in blood pressure causes activation of the sympathetic nervous
system resulting in increased contractility of the heart and vasoconstriction

31. HORMONAL MECHANISMS
• They act in various ways including
• Vasoconstriction
• Vasodilatation
• Alteration of blood volume

32. • Kidneys and adrenals are central players in blood pressure regulation
• They interact with each other to modify vessel tone and blood vessel through
various ways.

33. • The principal hormones raising blood pressure are
• adrenaline and noradrenaline secreted from the adrenal medulla in
adrenal medulla in response to sympathetic nervous system stimulation
They increase cardiac output and cause vasoconstriction
• Renin and angiotensin production is increased in the kidney when
stimulated by hypotension

34. CAPILLARY FLUID SHIFT MECHANISM
• Exchange of fluid that occurs across the capillary
membrane between the blood and the interstitial fluid
• Low blood pressure results in fluid moving from the
interstitial space into the circulation helping to restore
blood volume and blood pressure.

35. CLINICAL FEATURES
• Most of individuals with HTN-don’t feel any
symptoms
• High blood pressure (180/120 or higher)
experience symptoms
-Severe headache
-Breathing difficulty
-Chest pain
-Dizziness

36.  Nausea and vomiting
 Blurred vision or other vision changes
 Anxiety and confusion
 Epistaxis
 Abnormal heart rhythm

37. PRIMARY HYPERTENSION
o80-95% HTN patients are diagnosed as having primary or
essential hypertension inclusive of patients with obesity
and metabolic syndrome
oFamilial
oPrevalence increases with age
oObesity(bmi>30 kg/m2) have linear correlation with bp

38. oMetabolic syndrome-insulin resistance ,abdominal obesity, HTN, dyslipidemia
oHeritable as a polygenic condition
oExpression is modified by environmental factors
oHyperinsulinemia- marker of insulin resistance-predict the development of htn
and cardiovascular disease
oInsulin- antinatriuretic effect

39. •SECONDARY CAUSES OF HTN

40. RENAL PARENCHYMAL DISEASES, RENAL CYSTS( POLYCYSTIC KIDNEY
RENAL TUMOURS(RENIN SECRETING TUMOURS),
UROPATHY
RENOVASCUL
AR
ARTERIOSCLEROTIC, FIBROMUSCULAR DYSPLASIA
ADRENAL PRIMARY ALDESTERONISM, CUSHINGS SYNDROME,
PHEOCHROMOCYTOMA, 17 ALPHA HYDROXYLASE
BETA HYDROXYLASE DEF
AORTIC
COARCTATIO
N
OBSTRUCTIVE
SLEEP APNEA
PREECLAMPSI
A/ECLAMPSIA
NEUROGENIC DIENCEPHALIC SYNDROME, FAMILIAL
POLYNEURITIS(A/C PORPHYRIA, LEAD

41. ENDOCRINE HYPOTHYROIDISM, HYPERTHYROIDISM,
HYPERCALCEMIA, ACROMEGALY
MEDICATIONS HIGH DOSE ESTROGENS, ADRENAL STERIODS,
DECONGESTANTS, AMPHETAMINES,
TCA, ATYPICAL ANTIPSYCHOTICS, MAO-
NSAIDS, ALCOHOL, COCAINE
MENDELIAN FORMS
OF HTN
LIDDLES SYNDROME, PCKD,
GORDONS SYNDROME, 11BETA
17ALPHA HYDROXYLASE DEF

42. RENAL PARENCHYMAL DISEASES
M/C/C of secondary hypertension
HTN is more severe in glomerular diseases than in
interstitial
HTN causes nephrosclerosis

43. RENOVASCULAR HYPERTENSION
HTN due to an occlusive lesion of renal artery
Curable
Plaque obstructing renal artery, fibromuscular dysplasia
Considered in patients with other evidence of
atherosclerotic vascular disease

44. oSevere or refractory HTN /recent loss of HTN control/carotid or femoral artery
bruit/flash pulmonary edema/unexplained deterioration of RFT/deterioration
associated with ace inhibitor
oDoppler ultrasound / gadolinium contrast MR angiography
oFunctionally significant if stenosis is >70%/ presence of collaterals/renal vein
renin ratio>1.5 of affected side/contralateral side

45. Interventions-PTRA, placement of stent, surgical renal revascularization
BP adequately controlled + RFT stable- no intervention needed
Fibromuscular d/s - young age, favourable outcome

46. PRIMARY ALDOSTERONISM
 Independent of renin angiotensin system
 sodium retention, HTN, hypokalemia, low PRA,kidney
damage and CVS diseases
 diagnosed at 3rd or 4th decade
 asymptomatic
 polyuria, polydypsia, paresthesia ,muscle weakness due
to hypokalemic alkalosis

47.  Refractory HTN/ HTN with unprovoked hypokalemia
 Patients on diuretics- S potassium<3.1
 Screening test
 PA/PRA >30:1 PA>550 pmol(20ng/dl)
 ARB & ACEI affect this ratio- should be stopped 4-6 wks before testing
 Aldosterone biosynthesis is K+ dependent- hypokalemia corrected with oral
supplements

48. • Patients with elevated PA/PRA ratio –diagnosis confirmed with failure
to supress PA by
Oral sodium loading/Saline infusion
Fludrocortisone/Captopril

49. • Sporadic / familial
• Sporadic- adenoma/ bilateral adrenal hyperplasia/adrenal
carcinoma/ectopic malignancy
• Imaging- high resolution CT/adrenal scintigraphy
• B/L adrenal venous sampling- high sensitivity and specificity
• To differentiates U/L & B/L

50.  Adenoma- surgical Mx-U/LAdrenelectomy
 Hyperplasia –medical Mx- aldosterone blockers
Spironolactone, eplerenone

51.  GLUCOCORTICOID REMEDIABLE HYPERALDOSTERONISM-
• Ad/ Mod to severe HTN at young age
• over production of both aldosterone and steroid
• Rx- supression of ACTH by low dose glucocorticoids

52. CUSHING’S SYNDROME
M/C/C- iatrogenic steroids
ACTH dependent-pitutary adenoma/ ectopic acth
ACTH independent- adrenal tumours
Overnight dexamethasone supression test or 24 hour
urinary cortisol or late night salivary cortisol
Rx – surgical and medical

53. PHEOCHROMOCYTOMA
oCatecholamine secreting tumours in adrenals
oIn extra adrenal paraganglion tissue –paraganglioma
oHeadache/palpitaion/sweating/episodic HTN/Orthostatic
hypotension
oInv-24hr fractionated metanephrins/plasma free
metanephrins
oCT/MRI
oRx-alpha blockers- beta blockers-surgery

54. OBSTRUCTIVE SLEEP APNEA
oHTN due to sympathetic activation caused by intermittent hypoxia
and fragmented sleep
oBP remain elevated during night time- reversE dippers
oCPAP ventilation is the treatment
oIt abolishes apnea,prevents intermittent BP surges,restores normal
dipping pattern

55. VASCULAR PATHOLOGY IN
HYPERTENSION
• Accelerates atherogenesis
• Degenerative changes in large and medium arteries leads
to
• Aortic dissection
• Cerebrovascular haemorrhages
• Myocardial infarction
• Small vessel changes
• Hyaline arteriolosclerosis
• Hyperplastic artriolosclerosis

56. ACCELERTAED ATHEROGENSIS

58. HYPERTENSION CHANGES
• Heart
• Brain
• Kidney
• Eye
• Peripheral arteries

59. EFFECT ON HEART
• Heart disease- most common cause of death in hypertensive
patients
• Acute changes: acute pulmonary edema
• Hypertensive heart disease- lead to
 Left ventricular hypertrophy
 CHF

60.  Atherosclerotic coronary artery disease
 Microvascular disease
 Cardiac arrythmias

61. • Individuals with LVH-increased risk for CHD, stroke, CHF
and sudden death
• Control of hypertension-regress or reverse LVF and reduce
risk of cardiovascular diseases

62. HYPERTENSIVE HEART DISEASE
LVF sustained pressure
load on myocardium
Metabolic recruitment
of hypertrophic
myocardium increased
Hypertrophic
myocardium becomes
stiff
No increase in number
of capillaries
Simultaneous decrease
in diastolic filling and
stroke volume
Increased wall tension
Unable to meet
metabolic demand
Chronic HTN also
predisposes to AS
Hypertrophic
myocardium undergoes
ischemic injury

63. GROSS
• Weight of the heart usually increased
• Hypertrophy typically involved the ventricular wall in a
symmetric ,circumferential pattern
• Concentric hypertrophy
• Some times involve the septal area- mimicking
hypertrophic cardiomyopathy

64. SIZE OF THE CHAMBER
• Normal in the early stage
• Dilation is common in long – standing
• As LV failure progresses-
• RV hypertrophy and dilation

65. AORTIC DISSECTION
• DEFINITION - Disruption of the media layer of the aorta
with bleeding within and along the wall of the aorta ,
presenting with severe chest pain and acute
hemodynamic compromise.
• Male:female - 2:1
• Circumferential tears > Transverse tears

66. PATHOPHYSIOLOGY
• Primary rupture of intima with secondary rupture of media
• Hemorrhage within the media with subsequent rupture of
the overlying intima .
• PRIMARY EVENT - Intimal tear
• PRE REQUISITE- Degeneration of the media or cystic medial
necrosis

67. • Blood flows into the media creating a false lumen .
• This propogates proximal or dismally leading to various complications leading to
end organ ischemia , valvular incompetence and tamponade .

68. INTIMAL TEAR
AHA 2010 classification-
• Class 1-classical dissection with intimal tear and double
lumen
• Class 2- Aortic intramural hematoma
• Class 3-limited dissection [intimal tear without
hematoma]
• Class 4-penetrating atherosclerotic ulcer
• Class 5-iatrogenic / traumatic dissection

69. CLASSIFICATIONS OF AORTIC
DISSECTION-
DeBakey classification-
• Class 1-dissection involving both ascending and descending aorta
• Class 2-dissection involving only ascending aorta
• Class 3-dissection involves only descending aorta

70. Stanford classification-
• Class A-any dissection involving ascending aorta .
• Class B-ay dissection involving descending aorta .
• Stanford class A =DeBakeys class 1 & 2
• Stanford class B=DeBakeys class 3

72. TYPE A DISSECTION -
• Sharp tearing chest pain
• Syncope [stroke/tamponade]
• More common
• Most common site-right lateral wall of ascending aorta
[because sheer stress is maximum here] .
• Complications- Acute AR , Acute MI [RCA],Tamponade
,Hemothorax ,Stroke , Horners , Recurrent laryngeal nerve
palsy .

73. TYPE B DISSECTION-
• Back & Abdominal pain
• Presents with hypertension and unequal pulses .
• Less common
• Most common site - Distal to Ligamentum Arteriosum
• Complications - Hypertension , shock ,End organ
Ischemia [AKI , Mesenteric Ischemia , Spinal Ischemia ,
limb Ischemia

74. DIAGNOSIS-
SYMPTOMS-
• Abrupt thoracic or Abdominal pain [ sharp , tearing and/or
ripping character ]
• SIGNS-
• Pulse deficit or variation in BP>20mmHg

75. • CHEST X RAY - Widened Mediastium
• 2 of these 3 findings indicate Aortic dissection.

76. PRINCIPLES OF ACUTE MEDICAL
MANAGEMENT -
• HYPERTENSION PATIENT- Beta blockers are drug of choice
• Initially IV
• Target Heart Rate- <60 BPM , Target BP-100-120mmHg
• we can switch to oral beta blockers after Heart Rate control .
• Alternatives to Beta blockers is ACE inhibitors
• AVOID HYDRALAZINE AND IONOTROPES .

77. HYPOTENSIVE PATIENT -
• LOOK FOR-Blood loss , hemopericardium with tamponade ,
Valvular Dysfunction , Left Ventricular Systolic Dysfunction .
• IV fluids
• Avoid IONOTROPES-because it increases the sheer stress —
—>further propagating the tear
• Bedside TEE

78. EFFECT ON BRAIN
• Elevated BP- Strongest risk factor for stroke
• 85% stroke- Infarction
• 15% stroke- Intracerebral /sub –arachnoid
hemorrhage
• Incidence of stroke- increases with increase
in SBP, in individuals>65yrs

79. • Impairment of cognition and dementia in elderly
• Single infarct causing occlusion of a strategic larger vessel or multiple
lacunar infarct- subcortical white matter ischemia
• Hypertension-beta amyloid deposition, major pathological factor in
dementia

80. HYPERTENSIVE ENCEPHALOPATHY
• Failure of autoregulation of cerebral blood flow at
upper pressure limit
• Vasodilation and hyperperfusion
• Clinical features
 Severe headache, vomiting
 Alteration in mental status
 Focal neurological signs

81. TRANSIENT ISCHEMIC ATTACK-
● Complete improvement occurs < 24hrs
● no evidence of infarction in Imaging
● Risk of recurrence is 10-15% in next 3 months.
● Ischemia of brain , spinal cord or retinal cells
● cochlear involvement
● Non marching Focal Neurological Deficit

82. STROKE-
● Focal neurological deficit which is hyper acute in onset
secondary to decrease or absence of blood flow to the brain
.

83. INTRACRANIAL HAEMORRHAGE

84. SUBARCHANOID HEMORRHAGE
• Saccular aneurysms occur at the bifurcations of the large-
to medium-sized intracranial arteries.
• rupture is into the subarachnoid space in the basal
cisterns and sometimes into the parenchyma of the
adjacent brain.

85. INTRACEREBRAL HAEMORRHAGE
• Hypertensive ICH usually results from spontaneous
rupture of a small penetrating artery deep in the brain.
• The most common sites are the Putamen, globus pallidus,
thalamus, cerebellar hemisphere, pons
• Chronic hypertension produces hemorrhage from small
(~30–100 μm) vessels in these regions

87. • chronic;- atrophy
• small vessel ischemic changes
• Gliotic changes
• Vascular dementia

88. EFFECT ON KIDNEYS
• Hypertension- risk factor for renal injury and
ESRD
• Hypertension related vascular lesions
- Primarily affect preglomerular arterioles
- Lead to ischemic changes in glomerulus

89. • Progressive renal injury
-Lead to loss of autoregulation of renal blood flow
-Lower blood pressure threshold for renal damage

90. • Vicious cycle of renal damage and nephron loss
-Severe HTN, glomerular hyperfiltration and further renal damage
• Clinically- Macroalbuminuria and microalbuminuria are early
markers of renal injury

92. • Arterial stiffness- measured as carotid pulse pressure/carotid -femoral pulse
wave velocity associated with
 Stroke
 Heart disease
 Renal failure

93. HYPERTENSIVE RETINOPATHY
• Fundus changes that occur in patients with severe hypertension
• Clinical presentation include changes of
• Retinopathy
• Choroidopathy
• Optic neuropathy

94. PATHOGENESIS
• 3 factors play role in pathogenesis
• Vasoconstriction
• Arteriosclerotic changes
• Increased vascular permeability

95. PATHOPHYSIOLOGY
Systemic
chronic
hypertension
Arteriosclerosis
Narrowing of
retinal
arterioles
Retinal Ischemia Hypoxia
Increased
capillary
permeability
Focal Retinal Oedema, retinal
haemorrhage, cotton wool spots, hard
exudates

96. EYE-KEITH AND WAGNER’S GRADING
OF HYPERTENSIVE RETINOPATHY
GRADE 1 THICKENINGAND TORTUOSITY OF
ARTERIES SHOWING SILVER WIRE
APPEARANCE
GRADE 2 GRADE 1 CHANGES +
ARTERIOVENOUS NIPPING
GRADE 3 GRADE 2 CHANGES +
FLAME SHAPED HEMORRHAGES
AND COTTON WOOL EXUDATES
GRADE 4 GRADE 3 CHANGES+PAPILLEDEMA

97. BASIC LABORATORY TEST FOR
INITIAL EVALUATION
SYSTEM TEST
RENAL MICROSCOPIC URINALYSIS,ALBUMIN
EXCRETION ,SERUN BUN,AND
CREATININE(eGFR)
ENDOCRINE SERUM
SODIUM,POTASSIUM,CALCIUM,
TSH
METABOLIC FBS,LIPID PROFILE
OTHERS CBC,ECG

98. HYALINE ARTERIOLOSCLEROSIS
High BP
• leakage of plasma components across vascular
endothelium
• excessive ECM production by SMCs secondary to
• chronic hemodynamic stress of HT
• Metabolic stress in DM
• Accentuates EC injury

99. MORPHOLOGY
• Homogenous, pink, hyaline thickening of the walls of
arteriole with
• loss of underlying structural detail
• narrowing of the lumen.
• Major morphologic characteristic of benign
nephrosclerosis.

100. HYPERPLASTIC ARTERIOLOSCLEROSIS
• Related to more acute or sever elevations of blood
pressure
• Characteristic of but not limited to malignant
hypertension.

102. MORPHOLOGY
• Light Microscopy
• Onion skin, concentric, laminated thickening of the walls of
arterioles with progressive narrowing of the lumina.
• In electron microscope
• laminations are seen to consist of SMCs and thickened and
reduplicate basement membrane

103. FIBRINOID NECROSIS
• In malignant HT hyperplastic changes are accompanied by
• fibrinoid deposits
• Acute necrosis of the vessel wall
Known as Necrotizing arteriolitis particularly in the kidney.

105. THANK YOU

106. TAKE HOME MESSAGE
• Pulse wave velocity is gold standard for diagnosis of hypertension.
• Dash diet to be followed