Thread: hypertension

BY DEVANANTHAN ILENGHOVEN 041303024


HYPERTENSION > PATHOPHYSIOLOGY

Definition

• Normal - Systolic lower than 120, diastolic lower than 80
• Prehypertension - Systolic 120-139, diastolic 80-99
• Stage 1 - Systolic 140-159, diastolic 90-99
• Stage 2 - Systolic equal to or more than 160, diastolic equal to or more than 100

Based on the average of 2 or more readings taken at each of 2 or more visits after initial screening

prehypertension are patients at risk for progression to hypertension and that lifestyle modifications are important preventive strategies.

Hypertension may be either essential or secondary. Essential hypertension is diagnosed in the absence of an identifiable secondary cause.

Pathophysiology
Arterial blood pressure is a product of cardiac output and systemic vascular resistance.

Regulation of blood pressure
The factors affecting cardiac output include
sodium intake, renal function, and mineralocorticoids;
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the inotropic effects
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increase in heart rate and contractility.

Peripheral vascular resistance is dependent upon the sympathetic nervous system, humoral factors, and local autoregulation.

The humoral actions on peripheral resistance are also mediated by other mediators such as vasoconstrictors (angiotensin and catecholamines) or vasodilators (prostaglandins and kinins).

Autoregulation of blood pressure occurs by way of intravascular volume contraction and expansion, as well as by transfer of transcapillary fluid. Interactions between cardiac output and peripheral resistance are autoregulated to maintain a set blood pressure in an individual.

e.g. constriction of the arterioles
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elevates arterial pressure by increasing total peripheral resistance, venular constriction leads to redistribution of the peripheral intravascular volume to the central circulation
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increasing preload and cardiac output.

Pathogenesis of hypertension

The pathogenesis of essential hypertension is multifactorial.

Multiple factors modulate the blood pressure for adequate tissue perfusion and include humoral mediators, vascular reactivity, circulating blood volume, vascular caliber, blood viscosity, cardiac output, blood vessel elasticity, and neural stimulation. Also includes genetic predisposition, excess dietary salt intake, and adrenergic tone, may interact to produce hypertension.

The natural history of essential hypertension evolves from occasional to established hypotension. After a long invariable asymptomatic period, persistent hypertension develops into complicated hypertension causing target organ damage to the aorta and small arteries, heart, kidneys, retina, and central nervous system.

The progression begins with prehypertension in persons aged 10-30 years (by increased cardiac output)
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to early hypertension in persons aged 20-40 years (in which increased peripheral resistance is prominent)
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to established hypertension in persons aged 30-50 years,
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finally, to complicated hypertension in persons aged 40-60 years.

The early stage of hypertension has been described as high-output hypertension results from decreased peripheral vascular resistance and concomitant cardiac stimulation by adrenergic hyperactivity and altered calcium homeostasis.

In the chronic phase of essential hypertension characteristically has normal or reduced cardiac output and elevated systemic vascular resistance.

The vasoreactivity of the vascular bed is influenced by the activity of vasoactive factors, reactivity of the smooth muscle cells, and structural changes in the vessel wall and vessel caliber, (lumen-to-wall ratio).

Patients who develop hypertension are known to develop a systemic hypertensive response secondary to vasoconstrictive stimuli due to alterations in structural and physical properties of resistance arteries, as well as changes in endothelial function.

vascular remodeling occurs over the years as hypertension evolves, thereby maintaining increased vascular resistance irrespective of the initial hemodynamic pattern.


IN THE PERIPHERAL BLOOD VESSELS…

1. The arterial and arteriolar walls are thickened.
2. There is a high ratio of wall thickness to internal diameter.
3. Vascular contraction leads to an abnormally large increase in blood pressure
4. There is relative hypovolaemia
5. Vascular relaxation leads to a greater decrease in blood pressure.
6. Additionally, vascular relaxation unmasks the relative hypovolaemic state.
7. Rehydration following relaxation causes rebound hypertension

END ORGAN DYSFUNCTION PATHOPHYSIOLOGY…

1. THE HEART

BP = CO X PR

PERIPHERAL RESISTANCE (PR): circulating blood volume, vascular tone (smooth muscle and local vasoactive agents) sympathetic nervous system activity, renin-angiotensin – aldosterone axis, antidiuretic hormone, atrial natiuretic peptide.

CARDIAC OUTPUT (CO) = HR X SV

HEART RATE: depends on baroreceptor activity, sympathetic nervous system activity and vagal tone

STROKE VOLUME depends on Preload (LVEDV), Afterload (LV systolic wall tension and peripheral resistance), and contractility (Starling curve).

WALL TENSION:
Laplace’s Law:= transmural pressure X ventricular radius / 2 X wall thickness

In order to cope with the increased afterload, the heart hyerthropies
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leads to increased myocardial O2 requirement, and endomyocardial fibrosis.
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Cardiac dilatation eventually follows
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subsequent heart failure.


Hypertension causes:

1. Acceleration of atheromatous disease.
2. Myocardial ischaemia in the absence of coronary artery disease.
3. Decreased myocardial compliance and an increase in the atrial contribution to diastolic filling and cardiac output.
4. Congestive cardiac failure / pulmonary edema.

2. BRAIN

• Chronic Hypertension causes a shift to the right in cerebral and renal autoregulation
• Decreases in cerebral blood flow and cerebral ischaemia occur at higher blood pressures than in normotensive patients.
• Long term therapy: autoregulation curve shifts leftward normal.

Autoregulation of cerebral blood flow in hypertensive patients.
Lower limit of autoregulation was:
> 113mmHg in severe hypertension 73 mmHg in normotensive patients
> Lowest limit of blood pressure tolerated without symptoms was:65 mmHg in severe HTN, 53 mmHg in treated HTN, 43mmHg in normotensives
> This return to the right occurs after 8 – 12 months, maybe longer.

3. RENAL

• Chronic hypertension affects renal autoregulation in the same way as the brain.

• End organ damage to the kidneys from HTN
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• glomerular sclerosis, abnormal distribution of renal blood flow & decreased GFR.

"Prerenal" hypoperfusion due to a sudden and sustained decrease in BP (during anaesthesia for major surgery) leads to postoperative renal insufficiency.

Hypertension is high blood pressure. Blood pressure is the force of blood pushing against the walls of arteries as it flows through them. Arteries are the blood vessels that carry oxygenated blood from the heart to the body's tissues.As blood flows through arteries it pushes against the inside of the artery walls.

Heart and blood vessel diseases may occur when you have hypertension. The higher your BP, the more you are at risk of having a heart attack, stroke, heart failure, or kidney disease.Your caregiver may ask you to check your blood pressure between appointments. Tell your caregiver how high your BP readings are and how long you have been getting those readings. Ask your caregiver for more information about how to take a blood pressure