7.2 Hypertension

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All right, the next section deals with hypertension,

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and hypertension basically is an increase in blood pressure.

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Now,

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it's important to recall that when we have hypertension,

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that can involve either the pulmonary circuit or the systemic circuit,

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so we have two independent circuits in the body,

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and either one can develop high blood pressure.

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We will talk about pulmonary hypertension,

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however, we'll do that in Chapter 9.

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So at this particular point,

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we're focused on the systemic circuit,

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and we're talking about systemic hypertension or systemic high blood pressure.

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Now, systemic hypertension is defined as blood pressure greater than 140

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over 90.

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This definition changes on occasion,

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but it's a pretty good baseline number to be familiar with.

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When we think about this definition of hypertension,

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with this number we can define about 25 % of the U .S.

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population as hypertensive.

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Recall that the normal blood pressure is less than 120 over 80,

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and so if anyone's greater than 140 over 90,

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we would then classify them as hypertension.

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Usually when patients have hypertension,

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both the systolic and the diastolic pressures are increased.

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You can have isolated increases in systolic or diastolic

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pressure and that would also qualify as hypertension.

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Remember that when we have systemic hypertension,

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we can divide it based on the etiology into primary

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and secondary hypertension.

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In primary hypertension,

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we don't know the etiology.

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It basically represents about 95 % of cases.

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And because we don't understand the etiology,

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the only thing we can really talk about are the risk factors.

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And so there are some specific risk factors that are related to primary

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hypertension.

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For example,

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age is an important risk factor.

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We know that as patients age or as people age,

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hypertension becomes much more prevalent within the society.

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Race is also an important risk factor.

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There's a much higher risk in African Americans,

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and there's a relatively lower risk in Asians.

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Obesity,

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obviously, is a risk factor.

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We're all well aware of that.

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Stress is thought to be a risk factor,

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lack of physical activity,

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and a high salt diet.

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Now,

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when you think about high salt,

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remember that your systemic blood pressure is a function of your stroke volume,

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and the diastolic blood pressure is actually a function of the total

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peripheral resistance.

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And sodium,

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interestingly, actually increases both the blood volume and the total peripheral

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resistance.

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And so sodium has an effect on both the systolic and the diastolic blood

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pressures.

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Secondary hypertension,

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on the other hand,

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is due to an identifiable cause.

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It only makes up for about 5 % of cases of hypertension.

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One classic cause among many is renal artery stenosis.

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And the idea here...

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is that if this is the aorta and this is the renal artery,

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if you have stenosis of the renal artery so that there's

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less blood flow going through the renal artery,

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then that low blood flow would decrease blood flow to the glomerulus.

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Recall that the juxtaglomerular apparatus of the glomerulus will respond by

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secreting renin,

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and renin converts angiotensinogen to angiotensin 1.

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Of course,

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angiotensin 1 then goes to the vasculature of the lung

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and gets converted to angiotensin 2 by angiotensin converting enzyme.

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Angiotensin 2 does two things to raise the blood pressure,

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so it's kind of conveniently named.

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Again,

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angiotensin 2...

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There's two things to raise the blood pressure.

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Number one,

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it directly contracts arterial or smooth muscle.

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So that increases the peripheral resistance.

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And so that's the first way by which it raises blood pressure.

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And the second thing that angiotensin II does is that it promotes adrenal release

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of aldosterone.

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Of course,

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aldosterone then goes to the distal convoluted

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tubule, and it increases resorption of sodium.

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Basically, it grabs sodium and dumps potassium.

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And when it grabs sodium,

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eventually water will follow,

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expanding the plasma volume.

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So angiotensin II raises the blood pressure by directly contracting arteriolar

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smooth muscle and by promoting release of aldosterone from the adrenal,

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which will then grab sodium from the distal convoluted tubule and eventually

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expand the plasma volume.

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So this is a very important physiologic relationship to be aware of.

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It's very high yield for examinations.

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Now,

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of course, if you've got renal artery stenosis,

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then you're activating the juxtaglomerular apparatus,

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so you're going to be releasing a ton of renin.

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And so in patients with secondary hypertension,

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you often see an increase in the plasma renin.

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And if you look at both kidneys,

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usually the stenosis is going to involve one kidney.

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And when it involves one kidney,

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there's going to be a decrease in blood flow across that kidney.

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And so this particular kidney will become smaller.

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And so you'll have unilateral atrophy of the affected kidney in

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renal artery stenosis.

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What can cause renal artery stenosis?

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There's two very high yield causes to be familiar with.

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The first would be atherosclerosis,

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and this is what we would classically see in an elderly male.

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So atherosclerosis can cause stenosis of the renal artery and decrease the

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blood supply that's going to the kidney.

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The other way by which we can get renal artery stenosis,

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at least classically,

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is something called fibromuscular dysplasia.

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This is a developmental defect of the blood vessel wall.

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It results in irregular thickening of large and medium -sized arteries,

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especially the renal artery,

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and it's classically seen in young females.

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So renal artery stenosis in an elderly male,

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you think about atherosclerosis,

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and renal artery stenosis in a young female,

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you think about fibromuscular dysplasia.

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Now, we can separately classify hypertension as benign or

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malignant as well,

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so this would be another way to look at hypertension.

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In benign hypertension,

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we have a mild or moderate elevation in blood pressure,

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and most cases of hypertension are actually benign.

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This is clinically silent,

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and it damages vessels and organs over time,

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and we'll discuss some of that damage as we move forward in this particular chapter.

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Malignant hypertension,

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on the other hand,

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is a severe increase in blood pressure,

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characteristically greater than 200 over 120,

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and this can arise in one of two ways.

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It can either arise in a patient who has pre -existing benign hypertension,

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for example,

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the patient's got some long -standing hypertension and all of a sudden develops malignant

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hypertension, but it can also arise de novo in that the patient doesn't even have

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to have a history of hypertension.

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They can simply present with malignant hypertension.

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Patients with malignant hypertension are gonna present with acute end organ damage,

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classically with acute renal failure,

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headache and papilledema,

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and of course this is a medical emergency.

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Now remember that patients who have severe hypertension,

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they can develop fibrinoid necrosis of the blood vessel wall,

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and we talked about that in chapter one.

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So that concludes our discussion on hypertension.

7.2 Hypertension

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