Hypertension - B. Pharma 2nd Semester Pathophysiology notes pdf

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