Hypertension

Contents

Hypertension

•       Definition

•       Classification

•       Pathogenesis

•       Complications

Objective

At the end of this PDF, student will be able to

•         Define hypertension

•         Classify 
various types of hypertension

•         Explain the pathogenesis involved in the
development of hypertension

•        Describe the complications associated with the
development of hypertension

Hypertension

Persistently elevated
arterial blood pressure [BP]

Associated with both
functional and morphologic alteration of blood vessels

•      
Arterial
BP – generated by the interplay between blood flow and the resistance to blood
flow

•      
Measured
in mmHg

2 types of arterial
blood pressure

•       Systolic BP (SBP)- achieved during cardiac
contraction

•       Diastolic BP (DBP)- achieved after contraction
when the cardiac chambers are filling

SBP – DBP = pulse pressure (measure of arterial wall
tension)

―     Cardiac output – major determinant of SBP

―     Total peripheral resistance determines DBP

•       Mean arterial pressure [MAP] – Average pressure
throughout the cardiac cycle of contraction

•       During cardiac cycle 2/3rd time spent in
diastole and 1/3rd time in systole

MAP= [SBP (1/3)] +[DBP (2/3)]

BP= Cardiac output × Total peripheral
resistance

Clinical classification of hypertension

Category	Systolic (mm Hg)	Diastolic (mm Hg)
Normal	< 130	<85
High normal	130-139	85-89
Hypertension
•       Mild (Stage 1)	140-159	90-99
•       Moderate (Stage 2)	160-179	100-109
•       Severe (Stage 3)	180-209	110-119
•       Very severe (Stage 4)	≥ 210	≥ 120
Malignant hypertension	> 200	≥ 140

Etiological classification of hypertension

A. Primary essential hypertension

•      
Genetic
factors

•      
Racial and
environmental factors

•      
Risk
factors modifying the course  of HT

B. Secondary hypertension

•      
Renal –
Renovascular

                              Renal
parenchymal disease

•       Endocrine – 
Adrenocortical hyperfunction

                                      Hyperparathyroidism

                                      Oral contraceptives

•       Coarctation of aorta

•       Neurogenic

Clinical classification of primary and secondary
hypertension

Benign hypertension

•       Observed in 95% of patients

•       Slow rise in BP taking years to develop

Malignant/ accelerated
hypertension

•       Observed in 5-10% of patients

•       Rapid rise in BP to 200/140 mm Hg or more

•       If left untreated, patient’s life expectancy
decreases

Symptoms of 

Hypertension

When BP is severe,
following symptoms are observed

•       Nose bleeding

•       Irregular heart beat

•       Head ache

•       Dizziness

•          Fatigue

•          Flushed face

•          Breathing difficulties

•          Strong
tendency to uinate

•          Vertigo, tinnitus, etc.,

Malignant hypertension
is characterized by

•       Pulsating headache beneath the eye

•       Visual disturbance

•       Nausea and vomiting

•       Disturbed sleep

Pathogenesis of 

Hypertension

BP is the product of

•       Cardiac output

•       Total peripheral vascular resistance

• Cardiac output

 – Volume of blood that circulates through systemic blood vessels each
minute

–         
Dependent
on stroke volume (SV) 

–         
SV –
Volume of blood ejected by the left ventricle during each contraction

• Peripheral resistance depends on

̶           
Viscosity
of blood

̶           
Diameter
of the blood vessel

̶           
Compliance

•       High viscosity 
– high pressure to pass through vascular bed

•       High pressure 
to pass through constricted and non-complaint blood vessels

BP is controlled by

• Neural component

• Peripheral auto regulatory mechanism

• Humoral mechanism

• Vascular endothelial mechanism

Neural component

•       Both CNS & ANS controls BP

Centers in CNS are

̶           
Vasomotor
center in Medulla

̶           
Vagal nucleus

̶           
Area
postrema

̶           
Nuclues
tractus solitarii

̶           
Maintenance
of BP by sympathetic nervous system through α and
β adrenergic receptors

++ post synaptic α₁ receptors ―
vasoconstriction ― ↑ BP

++ pre synaptic α₂  receptors ― negative feedback on NA release

++ β₁ in heart ― ↑ HR and
contractility

++ β₂ in arterioles and
venules ― vasodilation

Change in BP senses by
barro receptors in carotid artery and aortic arch

•       Respond to change in arterial pressure

•       Transmitted to brain through IX cranial nerve
and vagus nerve

•       ↑ discharge from barroreceptors − depression of
vasomotor center − excitation of nucleus ambiguus − reverts change in BP

Peripheral auto
regulatory mechanism

•       Normal case – volume and pressure adaptive
mechanism of kidney maintains BP

↓ BP – adaptation of
kidney  ̶ 
more Na⁺ and H₂O retention

↑BP  – adaptation of kidney  ̶  Na⁺
and H₂O excretion –  ↓ blood
volume & cardiac output

Humoral mechanism

• Renin Angiotensin Aldosterone system

• Natriuretic hormone

• Insulin resistance and hyperinsulinemia

Renin-Angiotensin-aldosterone system

Natriuretic hormone

•       Inhibits Na⁺ /K⁺ ATP ase

•       Interferes with Na⁺ transport across
cell membrane

•       ↑ Na⁺ in body fluids – ↑ Natriuretic
hormone  – ↑ urinary excretion of Na⁺
and H₂O

•       Blocks active transport of Na⁺ out
of the walls of arterioles –  ↑ vascular
tone and BP 

Insulin resistance
and hyper insulinemia

•       Causes Na⁺ retention

•       Increases sympathetic activity

•       Increases vascular resistance

•       Increases BP

Vascular
endothelial mechanism

•       Regulates blood vessel tone

•       Vasodilating substances – Nitric oxide,
Prostacyclin (PI₂) and bradykinin – Hypotension

•       Vasoconstrictors – Angiotensin II and
Endothelin I – ↑BP

Effect of dietary
Na⁺ Ca²⁺ K⁺ on BP

•       ↑ intra cellular Ca²⁺ – alters
smooth muscle function on blood vessels – ↑ Peripheral vascular resistance

•       K⁺ depletion – ↑ Peripheral vascular
resistance

•       ↑ Na⁺ in body fluids & in
arterial wall – ↑ BP

Complications of 

Hypertension

•       Blood vessels 
–  Large arterioles dialatess

                        – Smaller arterioles
get damaged

•       Eye – Arterial narrowing, haemmorhage

•       Heart – 
Hypertropy of left ventricles, heart failure

•       Kidney – Nephrosclerosis, renal damage, death
in uremia

•       Brain – Rupture of damaged blood vessels,
encephalopathy, cerebral edema

Summary

•       Persistently elevated arterial blood pressure
is called hypertension

•       Hypertension can be classified as benign or
malignant or accelerated hypertension

•       HT can also be classifies as primary and
secondary HT based on etiology

•       BP is controlled by neuronal component, humoral
mechanism, peripheral autoregultory mechanism and vascular endothelial
mechanism

•       Any defects in the functioning of these
mechanisms leads to the development of HT

•       HT is affects kidneys, blood vessels, brain and
predisposed to many cardiovascular diseases