Pathophysiology of Systemic Hypertension
Pathophysiology of Systemic Hypertension
Week # 4
INTRODUCTION:
Hypertension- is a chronic elevation of arterial Blood Pressure.
-with aging the arteries become stiffer, if you have a stiffer artery it will create a higher pressure than it you would see more compliant arteries (which are able to give a little and relieve the pressure of blood flow). This is why for older people the upper limits of BP are a little bit higher. Remember that all arteries are exposed to the same pressure
-140/90mmHg- is now considered to be borderline hypertension. High systolic pressure will create the same problems as high diastolic so pay attention to both pressures.
-For 20% of the adult population in the United States, hypertension will lead to. MI, stroke, permanent damage to the kidney and retina (blindness)
-Patients are normally asymptomatic until disaster strikes; this is why screening is important
-Blood pressure increases with age, the risk of complications will also increase with the increase in blood pressure.
Criteria for DX of Hypertension (on repeated examinations)
|Blood Pressure mmHg |Category |
|DIASTOLIC | |
|Less than 90 |Normal |
|90-104 |Mild hypertension |
|105-114 |Moderate hypertension |
|Greater than 114 |Severe hypertension |
|Greater than 140 |Malignant |
|SYSTOLIC | |
|Less than 140 |Normal |
|140-159 |Borderline Systolic hypertension |
|Greater than 160 |Isolated Systolic Hypertension |
|STAGES of Hypertension |SYSTOLIC |Diastolic |
|1 |140-159 |90-99 |
|2 |160-179 |100-109 |
|3 |Greater than 180 |Greater than 110 |
The numbers in the above chart are constantly being revised.
Now the new normal is less than 85 diastolic and less than 135 systolic
Prevention: Intervention might reduce the occurrence of hypertension
-keep weight as close to optimal as possible
-limit sodium intake to less than 2300 mg/day.
-Maintain adequate intake of potassium, calcium, and magnesium (a high diet in fruits, vegetables, and low fat dairy products. If you give certain drugs you will be loosing these minerals so they must be given. Dairy products are a big culprit
-exercise regularly (dynamic exercise counts more). Standing and lift weights isn’t as effective as aerobic exercise like running and climbing stairs.
-relaxation techniques are important. Don’t go to the sauna, this is dry heat. Sitting in steam like in the shower is more relaxing in Dr. Patel’
*these things are most important in individuals with a family history of hypertension
REGULATION OF BP:
-vascular resistance- Mean BP / flow (or cardiac output).
-BP = C.O x Vascular Resistance
-C.O. = stroke volume x Herat rate
Resistance = 8nL/πR4. You can change the radius by dilatation or constriction with giving certain drugs
-BP can only be lowered by reducing Cardiac output or resistance. Dialating arterioles will reduce resistance. Most drugs will act on both of these aspects. Even non pharmacological things are working on both of these aspects of BP. Resistance is changed more so than cardiac output is changed.
-There are three systems involved in BP regulation
-Heart
-BV’s
-Kidney- it is always involved with hypertension. Kidney disease will cause hypertension and vice versa. The kidney regulates volume and this will effect cardiac output. Maintenance of chronic hypertension will require renal participation.
-Remember, Radius is the most dominant factor, TPR is proportional to 1/R^4
-TPR: N.O. is starting to play a bigger role as a vasodilator.
-S.V.- effected by cardiac contractility. When the muscle contracts very strongly the is more blood output.
Venous return- what goes in must come out, depends on venous tone and on blood volume.
-No matter how high the C.O. and how restricted the BV’s, renal excretion has the capacity to return BP all the way to normal by reducing intravascular volume.
Renin-Angiotensin System
-decrease in BP, Sympathetic stimulation, increase in sodium and decrease in sodium NaCl will all activate this system. Renin acts on angiotensin to make angiotensin I (which by itself has no effect, it must be converted to angiotensin 2). This conversion occurs by cleavage of amino acids. Angiotensin I will go to the lungs and be converted in the lung capillaries to Angiotensin II by the ACE enzyme. The lung capillaries produce this enzyme. AII will act on blood vessels to cause vasoconstrictor, and blood pressure will then rise to correct this. ACE inhibitors they will work very well in preventing the formation of Angiotensin II. ATII will increase aldosterone production which will work on the kidney in the distal tubules to increase sodium and water reabsorption. ATII will work on the pituitary to activate ADH. This will increase water reabosrption, and will increase thirst. So giving a give diruretic will make you want to urinate more and this can help to contribute to the control of BP.
TYPES OF HYPERTENSION (two types)
Essential Hypertension: Seen in 90% of hypertension cases, we don’t know what the cause of the hypertension is. Back in the day they thought that some hypertension would be good for supplying the brain (only borderline hypertension though). So this is why it was called essential hypertension, this was later proven to be wrong.
-clinical clues( age of onset which is usually be 20-50 years. Family history of hypertension, Serum K+, and urinanalyisis (look for proteinuria).
-severity- the higher it is the more trouble there is
-family history- it is 4 times more common in African American males, especially in the 20 to 40 age group. They are the ones who tend not to worry about therapy, because there are usually no symptoms. There are also many side effects of the drugs and impotence In males is one of these.
-arterial smooth muscles are more susceptible to the sympathetic stimulation in susceptible individuals. If you stimulate the system a little bit the pressure will rise higher.
-Natural History: Cardiac output has a tendency to decrease with age and vascular resistance has a tendency to increase with age. This is because the vasoconstriction will keep occurring more frequently, sooner or later there will be structural changes occurring in the vessel that will be irreversible (like hypertrophy of arteries, fibrosis of arteries). It is therefore important to treat and not let this process go on. As evident in the graph (sorry its kinda bootleg) there will be a point where they will both cross (and we are around that age frame)
[pic]
-Psychological stress is important
-LV hypertrophy will occur if the heart is constantly pumping against a high pressure. The heart will compensate but eventually the coronary blood supply will not be able to keep up with enlarging heart.
-If vasoconstriction keeps occurring, the smooth muscle will begin to react more to even slight changes in BP.
-With rareification some arterioles are absent or gone, loss of vessels due to hypertension and decrease in perfusion
-baroreceptor will get used to hypertension, the only deal with temporary flucuations in pressure. Hypertension means that the BP will continually stay set at a high value. The Barocreptors will also get fatigued and used to the high levels of BP.
-in older persons they are more prone to orthostatic hypotension, so they must be warned to get up slowly when they get out of the bed in the morning or at night, so that they don’t faint.
-Theories for development of EH
-Neurogenic- Initially vessels will respond as the heart muscle does, but as this process goes on (with continued vasoconstriction), than even a little bit of stimulation will have a bigger effect.
-Guyton: initial defect is in the kidney, and Na and water excretion is diminished by the kidney, this will therefore give an increase in volume that will raise venous return and cardiac output. Ultimately TPR will increase
-Page: There are many factors that regulate blood pressure. If two or more factors are working against you than your chances of building up hypertension are high.
Secondary Hypertension: seen in 5-10% of the hypertension cases, in which you actually know the cause. Most of the money spent in investigation of hypertension goes into secondary hypertensive treatment. In some of these cases the hypertension can be treated and cured if caught early enough. If allowed to continue the body will adjust to the high pressure. Age of onset is less than 20 years, or greater than 50 years.
-Renal Causes: there is an interrelationship between hypertension and kidney complication
-renal artery stenosis( when you constrict the renal artery you will get hypertension. This can be corrected surgically. This can be congenital, or there can be atherosclerotic plaques that can build up in the renal arteries as well.
-nephrons are damaged, and you would be unable to excrete Na. Na is retained and water will be retained along with it to set up a case fro hypertension
-Mechanical- Born with coarctation of the aorta, this can be surgically corrected. This can’t been done when the patient is too young or too hold. Collateral circulation will develop around the coartaction
-Coarcation in most cases occurs distal to the subclavian artery. There will normally be collateral circulation. You want to correct this at a proper age b4 the collaterals start to develop. It is important to take the blood pressure in both the arms and the legs. If the pressure is very high in the arms and low in the legs this will be evident of coarctation of the aorta. So when you see a patient for the first time it is important to do this. You also want to take the pressure in the supine and standing positions as well. Let the patient lay for a few minutes then take the pressure. You will see that this is a sign of the baroreceptor reflex. When the patient stands up in certain cases the pressure will drop to the point where the patient will pass out (orthostatic hypotension). So you must be aware of this. If you put your stethoscope between the two scapula you can hear evidence of coarctation. When looking at an xrays the ribs will be notched because lots of collaterals are trying to build up.
-Endocrine Causes
-Primary aldosteronism- there can be hyperplasia off the adrenal cortex, or an adenoma (which can be removed).
-cushings syndrome- ACTH secreting tumor in the pituitary that will react with other hormones
-phechromocytoma- catecholamine secreting tumor of the medulla, this can be removed. Patients will have night sweats, weakness, hirutism, paroxysm (tumor secretes more and less to give palpitation from time to time), sweating, and anxiety. When patients go to surgery there will be lots of ups and downs.
CONSEQUENCES OF HYPERTENSION
Organ Damage
-more load will be placed on the ventricles and the heart will eventually become ischemic due to an increased in oxygen demand.
-LV Hypertrophy- Initially impulse comes down around the septum on both sides and will initially go from left to right. V1 and V2 sample the RV, Looking at V5 and V6 they sample the Left ventricle. You will have a very tall R wave in V6
-Aortic Dissection- With high BP, especially malignant, this accelerates the degenerative changes in the media of the aorta. When weakened the wall is exposed to further high pressure, the intima may then tear.
-Myocardial infract- the coronaries are getting atherosclerosis. There is high systolic work load and increased LV muscle mass. Not only is the MI more common among hypertensive patient than normo-tensives, the former also have a higher incidence of post-MI complications such as rupture of the ventricle wall, left ventricular aneurisms formation, and congestive heart failure.
-Retina- This is one of the few places where you can see small vessels, with the ophthalmoscope. This is particularly important with malignant hypertension. As the pressure advances and as the vessels becomes thicker you will see AV nicking. When Arteries and Veins cross, if the artery is damaged or stiffer, this will cause a knick in the vein. This is also referred to as Copper of Silver Wiring. When you see this, you are at an advanced stage.
-when at a malignant stage, the disk will become raised (papillademia), and the disk will loose its round shape. There will be a lot of av nicking. There will be exudates called cotton wool spots. You will see some hemorrhage, in which some BV’s will break.
[pic][pic]
In picture on the left- note papilledema with blurred disc margin and dialated tortuous vessels. In picture on the right you can see AV nicking.
-Kidney- You will end up with renal failure due to dam age to the renal vasculature.
Malignant Hypertension( very serious condition in which the diastolic BP is above 140mmhg. Patient must be hospitalized immediately
TREATMENT OF HYPERTENSION
Nonpharmacologic treatment
-obesity- the link between this and hypertension is not directly known. Plasma insulin levels will be high. Try to get your patient to a normal weight via a change in diet. You will find that taking several small meals will be better than taking one large meal.
-increase K+ intake, since K+ will exchange for sodium in the kidney.
-decreasing smoking is very key
-cutting down saturated fats
-relaxation but don’t not use the sauna because this is dry heat and that can raise pressure, steam is better.
-pharmacologic
-Diuretics- mostly use thiazides to get rid of sodium and water.
-sympatholyitics- to reduce sympathetic tones giving alpha and beta blockers that work at the center to decrease tone. Beta blockers are among the most common. Beta blockers will block dilating fibers. This will help the renal response.
-calcium channel blockers can be used for vasodilation.
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C.O. contribution to BP
TPR contribution to BP
Increasing Age (((
CO
TPR
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