Download CAUSES OF HYPERTENSION Increase of systemic arterial

CAUSES OF HYPERTENSION
Increase of systemic arterial pressure greater than the normal values of 120 mm Hg systolic
and 80 mm Hg diastolic leads to a constellation of changes known ashypertensive
cardiovascular disease. The pathophysiologic basis of HTN is excessive
arteriolar constriction leading to increased peripheral vascular resistance.This may be
exacerbated by factors promoting increased cardiac output. The fundamental etiology of
HTN is unknown in most patients, although genetic predisposition and certain
environmental
influences, particularly high sodium intake, are known to be important factors. This
condition is known as essential, idiopathic, or primary HTN. In approximately 10% of
patients, HTN is secondary to a recognizable lesion or disease. Parenchymal renal disease
and renovascular disease are the most common of these entities thatare amenable to
surgical treatment. Endocrine disorders and coarc-tation of the aorta are less common
THE KIDNEYS IN HYPERTENSION: BENIGN AND MALIGNANT
The natural history of HTN follows 2 general patterns. Benign HTN is characterized by mild to
moderate increase of blood pressure and an asymptomatic period of several years before the
inevitable onset of symptoms and end-organ damage (hence, the condition is not truly
benign). Malignant HTN is characterized by marked increase of blood pressure and rapid
progression over a few weeks to end-organ failure. Most patients with essential HTN follow
the benign pattern, although it may accelerate to malignant HTN. The characteristic vascular
lesion of benign essential HTN is widespread hyaline arteriolosclerosis manifest by thickening of
the walls of the small arteries and arterioles composed of degenerated smooth cells and deposited
plasma proteins. Hyaline arteriolosclerosis with associated small cortical
scars (hyaline arteriolonephrosclerosis) is commonly seen in the
kidneys. Hyperplastic arteriolosclerosis, marked luminal narrowing by cellular intimal proliferation in a lamellar, "onionskin" pattern, is the characteristic lesion of
malignant HTN. In severe malignant HTN, fibrinoid necrosis of the glomerular arterioles occurs.
An associated ischemic injury develops rapidly, leading to petechial hemorrhages in multiple
organs, including the kidneys (hyperplastic arteriolonephrosclerosis).
by amorphous eosinophilic material
THE HEART IN
HYPERTENSION:
CONCENTRIC
HYPERTROPHY,
Hypertension, even of moderate degree, leads rapidly to cardiac hypertrophy, a
compensatory increase of mass of the LV. The typical pattern of concentric hypertrophy of
the LV, characterized by a thick wall and a relatively small chamber volume, is produced by
a pressure load (afterload) on the ventricle. The heart ssilhouette is relatively normal, but the
ECG shows increased voltage. When the limits of compensation are reached, the patient may
have progressive cardiacdecompensation accompanied by cardiac dilation. Cardiac hypertrophy
is an independent risk factor for ventricular arrhythmias and sudden cardiac death.
ize on cardiac
PATHOPHYSIOLOGY OF HEART FAILURE
Heart failure is a state in which the heart fails as a pump to provide sufficient volume of
circulating blood to meet the metabolic demands of the body. Because the dominant symptoms
usually result from pulmonary or systemic venous congestion, the condition is termed congestive
heart failure (CHF). Most commonly, heart failure is of the low cardiac output variety, but some
conditions, including thiamine deficiency (beriberi), thyrotoxicosis, and severe anemia, produce
cardiac failure with an increased circulating blood volume (high output cardiac failure), as shown
here. The failure may be left-sided, right-sided, or combined left- and right-sided heart failure.
This illustration shows the major manifestations of failure of the left and right ventricles. Cardiac
transplantation or an artificial heart is the last therapeutic option. The most common conditions
necessitating cardiac transplantation are end-stage ischemic heart disease
(ischemic cardiomyopathy) and dilated (congestive)cardiomyopathy.
LEFT-SIDED HEART FAILURE: ECCENTRIC HYPERTROPHY,
Most cases of CHF result from diseases that affect the LV initially or primarily, most
commonly HTN and CAD. In response to chronic stress, the affected part of the heart
undergoes compensatory hypertrophy. When the heart reaches a critical weight of 550 g, reserve is lost and progressive cardiac decompensation ensues. Heart failure results in
progressive ventricular dilatation superim- posed on the hypertrophy, which produces a
pattern of so-called eccentric hypertrophy, as shown here. A severe acute load on the heart
can produce failure and cardiac dilatation without previous hypertrophy. Stress of the atria
can result in atrial fibrillation and formation of mural thrombi. The frequent coexistence of
HTN and CAD can result in myocardial infarction of the hypertrophied LV.
ISSECTING ANEURYSM OF THE AORTA
The effects of HTN with excessive hemodynamic trauma on a weakened aortic wall can
lead to the formation of a hematoma in the media. The hematoma dissects longitudinally to
split the media, which creates a dissecting hematoma or a dissecting aneurysm, a doublebarreled aorta with true and false lumens. In most cases, aproximal intimal tear allows
blood to enter the false lumen under systemic pressure. In type A dissections, the
proximal intimal tear is in the ascending thoracic aorta, whereas in type В dissections, the
proximal intimal tear is in the aortic arch or the descending thoracic aorta. Type A
dissections, which are prone to external rupture into the mediastinum or pericardial
cavity, necessitate surgical intervention. Some dissections develop distal tears and
become chronic with the potential for late rupture. Blood pressure control is key in the
treatment of any aortic dissection.