Cardiovascular pathology hypertension

1. Hypertension

2. • Regulation of normal blood pressure:
The magnitude of the arterial blood pressure
depends on:
• Cardiac output
• Peripheral resistance
• Cardiac output: Is influenced by the blood
volume which depends itself on the (body
sodium, heart rate & cardiac contractility)
• Peripheral resistance: is determined by
(humoral factors, neural factors & local
factors).

3. • Humoral factors:
Constrictor humoral factors:
1. Angiotensin 2
2. Catecholamines
3. Thromboxane:
4. Leukotrienes
5. Endothelin
• Dilator humoral factors:
1. Prostaglandins
2. Kinins
3. Nitric oxide
4. Endothelium derived relaxing factor (EDRF)

4. • Role of the kidneys in hypertension:
The kidney influences sodium homeostasis & peripheral resistance.
• They secrete (renin) which converts plasma angiotensinogen to
angiotensin 1 which is converted to (angiotensin 2) by ACE.
– Angiotensin 2 alters blood pressure by causing vasoconstriction by direct action on
vascular smooth muscles.
– & also influences blood volume through stimulation of aldosterone Secretion which
increases the distal tubular re-absorption of Na/H2O.
• The kidneys also produce vascular relaxing substances:
– Prostaglandins
– Urinary Kallikrein-kinin system
– Nitric oxide
– PAF
• The kidneys increase reabsorption of sodium by the proximal
convoluted tubules when the GFR falls, attempting to expand blood
volume.
•
• (Atrial natriuretic factor inhibits sodium reabsorption by the distal
convoluted tubules, they also cause vasodilation when there is
volume expansion).

7. • Difinition:sustained diastolic pressures greater than 90 mm
Hg, &/or sustained systolic pressures in excess of 140 mm
Hg,
• major health problem especially in African race
• CAUSE: unknown (majority)
• Asymptomatic
• increasing the risk of:
1. stroke .
2. atherosclerotic coronary heart disease. (IHD)
3. cardiac hypertrophy.
4. heart failure (hypertensive heart disease).
5. aortic dissection.
6. multi-infarct dementia.
7. renal failure.

9. –Epidemiology of hypertension:
The Incidence of hypertension is increased
with age.
–Blacks are more affected & more vulnerable
to its complications.
–Reduction of blood pressure has marked
effects on the incidence & death rates of
(ischemic heart disease, heart failure &
stroke).
–30% are unaware of their hypertension.
–40% of patients are not receiving treatment.

11. • malignant hypertension:
• 5% of hypertensive patients
• rapidly rising pressure (systolic pressures > 200
mmHg or diastolic pressures > 120 mm Hg)
• associated with renal failure and retinal
hemorrhages& Exudates (± papilledema. )
• can arise de novo
• most commonly is superimposed on preexisting
benign hypertension
• if untreated, leads to death in within 1 to 2 years.

12. • Mechanisms of Essential Hypertension:
Reduced renal sodium excretion :
• Increased vascular resistance : due to either
vasoconstriction or structural changes in vessel
walls.
• Environmental factors, :stress, obesity, smoking,
physical inactivity, and high levels of salt
consumption,
• Genetic factors :important :shown by familial
clustering of hypertension .
• genes unknown

13. • Renal retention of excess sodium:
Genetic factors result in reduced renal sodium excretion
as the initiating event.
• This leads to:
• An increase in blood volume
• High cardiac output
• Peripheral vasoconstriction
• (Blood pressure is increased) → (Enough sodium
is excreted).
• The peripheral vasoconstriction occurs as a result
of (auto-regulation) to prevent (over-perfusion).

14. • Vasoconstriction & vascular hypertrophy:
• Vasoconstriction:
• Increased peripheral resistance is the primary cause, &
the increased peripheral resistance is caused by:
• Factors that induce functional vasoconstriction
• Behavioral or neurogenic factors
• Increased sensitivity of vascular smooth muscles to
constricting agents, & this is possibly caused by genetic
defects.
• (vasoconstriction causes structural changes in blood
vessels)
• Structural changes to the vessels wall:
• These are genetic or environmentally induced defects in
intracellular signaling in smooth muscle cells that modulate
growth & vascular tone.

15. • MORPHOLOGY:
• Hyaline arteriolosclerosis : benign hypertension.
• homogeneous, pink hyaline thickening of the arteriolar walls, and luminal
narrowing
• In the kidneys, leads to nephrosclerosis (glomerular scarring).
• hyaline : leakage of plasma components across injured endothelial cells,
into vessel walls and increased ECM production by smooth muscle cells
• Hyperplastic arteriolosclerosis : severe hypertension.
• “onionskin,” concentric, laminated thickening of arteriolar walls and
luminal narrowing
• The laminations consist of smooth muscle cells and thickened,
reduplicated basement membrane.
• necrotizing arteriolitis : malignant hypertension
• fibrinoid necrosis in vessel wall
• particularly prominent in the kidney

16. • Complications:
1. stroke .
2. atherosclerotic coronary heart disease. (IHD)
3. cardiac hypertrophy.
4. heart failure (hypertensive heart disease).
5. aortic dissection.
6. multi-infarct dementia.
7. renal failure.

17. HYPERTENSIVE HEART DISEASE
• Hypertensive heart disease includes:
• Left ventricular hypertrophy.
• Coronary artery disease.
• Conducting system diseases.
• Systolic/diastolic dysfunction.
• Hypertensive heart disease can present as:
• Angina
• Myocardial infarction
• Cardiac arrhythmias
• Congestive heart failure
• Acute elevation of blood pressure, which can lead to accentuation of
underlying disease.

18. • Left ventricular hypertrophy:
• Mechanism:
• Myocyte hypertrophy occur as a compensatory
response to the increased afterload.
• Mechanical & neurohormonal stimuli lead to
activation of myocardial cell growth.
• Action of angiotensin 2 leads to growth of
interstitium & cell matrix
components.(interstitial fibrosis)
• Left atrial hypertrophy

19. • Others:
• Valvular disease: chronic & severe
hypertension can cause aortic root dilatation
leading to significant aortic insufficiency.
• Myocardial ischemia:.
• angina can occur in the absence of coronary
artery disease.

20. • Types of hypertensive heart disease:
• Pulmonary Hypertensive Heart Disease—Cor
Pulmonale( Right side ).
• Systemic (left sided)hypertensive heart
disease

21. • Systemic (left sided)hypertensive heart disease:
Morphology
• Circumferential hypertrophy without dilation of
the left ventricle.
• Left ventricular wall thickness may exceed 2 cm,
& the weight may exceed 500 grams
• thickness cause stiffness that impairs diastolic
filling, then the left atrium may become enlarged.
• Hypertrophy can lead to (myocardial dysfunction,
cardiac dilatation, congestive heart failure &
sudden death).
• left atrial dilation.
• Very late : ventricular dilation

22. concentric thickening of the left
ventricular wall causing reduction
in lumen size

23. • C/F
• Asymptomatic
• elevated blood pressure
• CHF because of:
1. hypertrophic myocytes fail to contract
efficiently
2. vascular supply is inadequate for
hypertrophied muscle

24. • Pulmonary Hypertensive Heart Disease—Cor
Pulmonale:
• Right sided hypertrophy, dilation & potentially
failure secondary to pulmonary hypertension
• Types:
• Acute cor pulmonale: can follow massive
pulmonary embolism.
• Chronic cor pulmonale: which is secondary to
prolonged pressure overload owing to
(obstruction of pulmonary arteries or arteriols or
compression or obliteration of septal capillaries).

25. • Cor pulmonale : right ventricular hypertrophy
+ dilation +right heart failure
• caused by pulmonary hypertension
• MORPHOLOGY
Hypertrophy & dilation of both the right
ventricle and the right atrium
• tricuspid regurgitation

26. • Disorders predisposing to cor pulmonale:
1. Diseases of the pulmonary parenchyma:
a. COPD
b. Diffuse interstitial pulmonary fibrosis
c. Pneumoconiosis
d. Cystic fibrosis
e. Bronchiectasis
1. Diseases of the pulmonary vessels:
a. Recurrent pulmonary thromboembolisms
b. Pulmonary hypertension
c. Pulmonary arteritis
d. Drugs & toxins
e. Pulmonary tumor micro-embolism
1. Disorders affecting chest movement:
a. Kyphosis
b. Marked obesity
c. Neuromuscular disorders

27. The right ventricle is markedly dilated
and hypertrophied