SAINT LOUIS UNIVERSITY

HEART SOUNDS AND BLOOD PRESSURE DETERMINATION

GROUP 2 GROUP LEADER: SANTOS, Jever Lee Y. GROUP MEMBERS: TUVERA, Kerbick Carl BORJA, Marie Clare Ines DANGLOSI, JoaN LAZARO, Lorelie MACALINO, Janessa

I. Get the resting blood pressure Right arm of all the group mates. Record. NAME OF MEMBER SANTOS TUVERA BORJA DANGLOSI LAZARO MACALINO 120/90mmHg 100/70mmHg 100/80mmHg 110/80mmHg 100/80mmHg 100/80mmHg BP

II. Take resting Blood Pressure, Right Arm of a classmate, HR, PR RR. Let him/her drink 1 glass (250 ml) of coffee. Take BP, HR, and RR after 45 minutes. Record & note difference. RESTING 110/80 88 90 17 AFTER COFFEE INTAKE 120/100 85 80 19

BP HR PR RR

III. Take resting Blood Pressure, Right Arm of a classmate, HR, PR RR. Let him/her drink 1 glass (250 ml) of hot tea. Take BP, HR, and RR after 45 minutes. Record & note difference. RESTING 110/80 98 97 17 AFTER COFFEE INTAKE 120/100 94 88 27

BP HR PR RR

IV. Take resting BP, RA of group leader in: A.SEATED B. SUPINE C. STANDING POSITION 130/90 120/90 140/100

V. Palpate & grade PULSES of Group leader at resting state RADIAL BRACHIAL TEMPORAL CAROTID POPLITTEAL ANTERIOR TIBIAL DORSALIS PEDIS RIGHT RIGHT +2 +1 +2 +2 +1 +1 +2 LEFT +2 +1 +2 +2 +1 +1 +2

Let him do stationary jogging for 2 -3 minutes. Immediately, take A. BP, RA 160/90 B. HR 98 C. RR 42 D. RADIAL BRACHIAL TEMPORAL CAROTID POPLITTEAL ANTERIOR TIBIAL DORSALIS PEDIS RIGHT +3 +2 +3 +3 +1 +2 +2 LEFT +3 +2 +3 +3 +1 +2 +2

1. Draw the Anterior Chest Wall and Clinical vulvular areas and where S1, S2, S3 are best heard 2. What are determinants of Blood Pressure? 3. Enumerate DOs and DONTs o taking accurate BP? DOs It would be helpful if someone who knows how to take a blood pressure is present to supervise. Explain the procedure to the patient. Assess for factors that affect BP, such as medications, anxiety, and pain, or exercise, smoking, or caffeine consumption within the past 30 minutes. Select an appropriate arm. Avoid an arm that's injured or painful or that has a fistula or an I.V. or arterial line. If the patient has undergone breast or axilla surgery, avoid the arm on that same side. Select the appropriate cuff for his arm circumference. Extend the arm and support it at heart level. Also you avoid keeping the cuff inflated on someone's arm for too long. Check the tubing for holes of the Stethoscope Clean any wax from the ear tips. Point earpieces forward o the stethoscope Use the bell portion of the stethoscope to listen for Korotkoff's sounds. Be sure to place it lightly over the artery, with skin contact all around. Make sure the cuff size suits your patient. Check to see that the screw valve on the ball works properly. Pump up the bladder and watch for any air leaks. If the mercury column or aneroid needle doesn't rise steadily as you pump the ball, suspect a leak. Check that the needle is at the zero mark of the instrument at the start and the end of the measurement. If possible, have the patient sit or lie down for 5 minutes. Ask your patient not to talk during the measurement. Flex the arm and support it on a smooth surface at heart level. Place the center of the inflatable bladder over the brachial artery. With aneroid manometers, check before each use that the needle is on zero at baseline. If it isn't, recalibrate it to a mercury manometer using a Y connector attached to the tubing on both manometers. Compare pressures at several points along the scale. See to it that your patient is rested and relaxed while you're taking a reading, because it will give you a more reliable measurement. To ensure an accurate reading, position a mercury manometer with the meniscus at eye level and an aneroid manometer in your direct line of sight. To hear soft sounds that you might otherwise miss, deflate the cuff slowly. Taking a patient's blood pressure correctly requires keeping your eye not just on the manometer but on the rest of the equipment, the patient, and yourself as well. Avoid cold medicines with decongestants because they help your stuffy nose by tightening the tiny blood vessels in your nasal lining. Wear a comfortable short-sleeve shirt. Go to the bathroom before taking your reading. A full bladder can affect your BP reading. Take two or more readings 2 minutes apart and average them. Repeat on the other arm and use the higher reading. Head of stethoscope placed under edge of cuff (just above crease of patients elbow) held in place with thumb.

 Cuff should be placed on bare arm. Remove tight, bulky clothing from upper arm to prevent constriction. Position cuff with tubing over the brachial artery and aligned with small finger Have an accurate pressure measuring instrument, The correct size cuff as it relates to the circumference of the limb and Good measurement technique. DONTS Dont use too small cuff to measure an obese person's blood pressure because it can cause a falsely elevated reading. Dont use edematous limbs to take blood pressure on patients like obesity, peripheral edema because these diseases can diminish sound transmission. Dont fail to support the patient's arm, because it can cause isometric muscle contraction, can also lead to false measurements. Dont put the patients arm above heart level, because you'll get a low reading. Dont put the patients arm below heart level, because you'll get a high one. Dont quickly inflate the air of the cuff to accurately hear the sounds. 4. Tabulate advantage/disadvantage of ANEROID and MERCURIAL BAUMANOMETER?

DISADVANTAGE ANEROID BAUMANOMETER

> less accurate than mercurial

> Because the elasticity of the

metal bellows changes with time, the calibration must be checked frequently by a simultaneous measurement with a mercury sphygmomanometer device using a Y-tube adapter. > easily broken when dropped

ADVANTAGE > Much cheaper than the mercurial Baumanometer. > Have the advantage of
portability and easy of use. > Aneroid

equipment is often inexpensive, lightweight and more portable than > It's a fairly delicate and mercury. complicated mechanism. > The aneroid gauge will > The only way to tell if the function in any position if gauge is accurate is to check the reader is able to view it it against a mercury directly. sphygmomanometer at least > Some models have easyonce a year and when to-read, extra large gauge; dropped or bumped. D-ring cuff for one-handed > It can be easily damaged application and a selfwithout the user's bleeding deflation valve for knowledge and requires increased reading accuracy. factory repair and readjustment. > mercury-free > The gauge can be clumsy to position, and without a Dring cuff can be difficult to apply by oneself. > It may not work well for the hearing or visually impaired or for those unable to perform the hand movement needed to squeeze the bulb and inflate the cuff. MERCURIAL BAUMANOMETER > Not economical ( it has higher prize than aneroid) > Can yield inaccurate readings if the air vent at the top of the column is clogged or the mercury has oxidized. > Some can cause mercurial toxicity. > May be bulky to carry. > Must be kept upright on a flat surface during measurement; the gauge must be read at eye level for accuracy. > May not work well for the hearing or visually impaired or for those unable to perform the hand movement needed to squeeze the bulb and inflate the cuff. > Safe, accurate, and essential
in the accurate measurement of blood pressure.

> Mercury is pushed down by

gravity and up by the blood pressure, and since gravity does not change, the gauge does not wear out. > If properly maintained, it can give accurate readings for decades. > The elemental mercury used in Baumanometers is safely contained in the Mylar Clad Calibrated Cartridge tube, which maintains its integrity even if the glass is broken, virtually eliminating the environmental risks associated with mercury.

It's the standard for blood pressure measurement. > It's durable, easy to read and doesn't require readjustment. > gravity to give consistent and accurate readings. It has a long, tubular gauge made of glass or plastic. > For safety, glass tubes should be wrapped in Mylar to prevent breakage. It's not often recommended for home use due to the hazards of mercury. > those made for home use are lightweight and relatively safe by design > It will easily last a lifetime with minimal maintenance.
>

5. What is pulse deficit? A pulse deficit designates a difference between the heart impact (Auskultation), as well as the peripheral measured pulse (A. Radialis at the wrist). The reason usually is because of a too weak heart muscle contraction, how it is e.g. with forecourt flares the case. It is often seen in atrial fibrillation. Pulse rhythm abnormality An abnormal pulse rhythm is an irregular expansion and contraction of the peripheral arterial walls. It may be persistent or sporadic and rhythmic or arrhythmic. Detected by palpating the radial or carotid pulse, an abnormal rhythm is typically reported first by the patient, who complains of palpitations. This important finding reflects an underlying cardiac arrhythmia, which may range from benign to lifethreatening. Arrhythmias are commonly associated with cardiovascular, renal, respiratory, metabolic, and neurologic disorders as well as the effects of drugs, diagnostic tests, and treatments. (See Abnormal pulse rhythm: A clue to cardiac arrhythmias, pages 506 to 509.) Application on Nursing Profession If an abnormal pulse rhythm is detected, quickly look for signs of reduced cardiac output, such as decreased level of consciousness (LOC), hypotension, or dizziness. Promptly obtain an electrocardiogram (ECG) and possibly a chest X-ray, and begin cardiac monitoring. Insert an I.V. catheter for administration of emergency cardiac drugs and fluids, and give oxygen by nasal cannula or mask. Closely monitor the patient's vital signs, pulse quality, and cardiac rhythm because accompanying bradycardia or tachycardia may result in deterioration of cardiac output. Keep emergency intubation, cardioversion, defibrillation, and suction equipment handy. History and physical examination If the patient's condition permits, ask if he's experiencing pain. If so, find out about its onset and location. Does the pain radiate? Ask about a history of heart disease and treatment for arrhythmias. Obtain a drug history and check the patient's compliance. Also, ask about caffeine or alcohol intake. Digoxin toxicity, cessation of an antiarrhythmic, and the use of quinidine, a sympathomimetic (such as epinephrine), caffeine, or alcohol may cause arrhythmias. Next, check the patient's apical and peripheral arterial pulses. An apical rate exceeding a peripheral arterial rate indicates a pulse deficit, which may also cause associated signs and symptoms of low cardiac output. Evaluate heart sounds: A long pause between S1 (lub) and S2 (dub) may indicate a conduction defect. A faint or absent S1 and an easily audible S2 may indicate atrial fibrillation or flutter. You may hear the two heart sounds close together on certain beatspossibly indicating premature atrial contractionsor other variations in heart rate or rhythm. Take the patient's apical and radial pulses while you listen for heart sounds. With some arrhythmias, such as premature ventricular contractions, you may hear the beat with your stethoscope but not feel it over the radial artery. This indicates an ineffective contraction that failed to produce a peripheral pulse. Next, count the apical pulse for 60 seconds, noting the frequency of skipped peripheral beats. Place the patient on a cardiac monitor and obtain an ECG to evaluate the cardiac rhythm. Report your findings to the practitioner. Medical causes Arrhythmias.An abnormal pulse rhythm may be the only sign of a cardiac arrhythmia. The patient may complain of palpitations, a fluttering heartbeat, or weak

and skipped beats. Pulses may be weak and rapid or slow. Depending on the specific arrhythmia, dull chest pain or discomfort and hypotension may occur. Associated findings, if any, reflect decreased cardiac output. Neurologic findings, for example, include confusion, dizziness, light-headedness, decreased LOC and, sometimes, seizures. Other findings include decreased urine output, dyspnea, tachypnea, pallor, and diaphoresis. Nursing considerations Monitor cardiac rhythm and obtain a 12-lead ECG. Prepare the patient for cardioversion, if indicated . Check vital signs frequently to detect hypertension or hypotension, tachypnea, and dyspnea. Also, monitor intake, output, daily weight, and pulse oximetry. Collect blood samples for serum electrolyte, cardiac markers, complete blood count, and drug level studies. Prepare the patient for a chest X-ray. Obtain a previous ECG with which to compare current findings. Patient teaching Explain the importance of keeping a diary of activities and any symptoms that develop to correlate with the incidence of arrhythmias. Instruct the patient to avoid tobacco and caffeine. Teach the patient how to take his pulse. Reinforce signs and symptoms that require prompt medical attention. Explain the underlying disorder and treatment plan. Teach the patient about prescribed medications, including dosage, administration, and possible adverse effects. Usefulness of pulse deficit to predict in-hospital complications and mortality in patients with acute type A aortic dissection. Vascular compromise seen with pulse deficits is common in patients with type A dissection. However, patient characteristics and in-hospital outcomes associated with pulse deficits have not been evaluated. Accordingly, we studied 513 patients (mean age 62 +/- 14 years, 65% men) with acute type A aortic dissection enrolled in the International Registry of Acute Aortic Dissection. Pulse deficits, defined as decreased or absent carotid or peripheral pulses as noted by clinicians and later confirmed by diagnostic imaging, at surgery or at autopsy were noted in 154 patients (30%). Age <70 years, male gender, neurologic deficit(s), altered mental status, and hypotension, shock, or tamponade on admission were all significantly higher in patients with than without pulse deficits. The etiology of aortic dissection, clinical symptoms, and imaging findings were similar in the 2 groups. In-hospital complications (hypotension, coma, renal failure, and limb ischemia) and mortality (41% vs 25%, p = 0.0002) were significantly higher in patients with pulse deficit. Cox proportional-hazards regression analysis identified pulse deficit as an independent predictor of 5-day in-hospital mortality (risk ratio 2.73, 95% confidence interval 1.7 to 4.4; p <0.0001). Further, overall mortality rates increased with an increasing number of pulse deficits (p for trend <0.0001). Pulse deficits are common findings in patients with type A aortic dissection and identify those at high risk of in-hospital adverse events. This simple clinical sign should direct physicians to consider a diagnosis of aortic dissection in patients with acute chest pain, and should help identify a subgroup of patients who would benefit from more aggressive strategies. A. How High Cholesterol Affect Pulse deficit: Comments about "good" and "bad" cholesterol refer to the type of carrier molecule that transports the cholesterol. These carrier molecules are made of protein and are called apoproteins. They are necessary because cholesterol and other fats (lipids) can't dissolve in water, which also means they can't dissolve in blood. When these apoproteins are joined with cholesterol, they form a compound called lipoproteins.

The density of these lipoproteins is determined by the amount of protein in the molecule. "Bad" cholesterol is the low-density lipoprotein (LDL), the major cholesterol carrier in the blood. High levels of these LDLs are associated with atherosclerosis. "Good" cholesterol is the high-density lipoprotein (HDL); a greater level of HDL--think of this as drain cleaner you pour in the sink--is thought to provide some protection against artery blockage. A high level of LDL in the blood may mean that cell membranes in the liver have reduced the number of LDL receptors due to increased amounts of cholesterol inside the cell. After a cell has used the cholesterol for its chemical needs and doesn't need any more, it reduces its number of LDL receptors. This enables LDL levels to accumulate in the blood. When this happens, the LDLs begin to deposit cholesterol on artery walls, forming thick plaques. In contrast, the HDLs--the "good" guys--act to remove this excess cholesterol and transport it to the liver for disposal. A third group of carrier molecules, the very low-density lipoproteins (VLDL) are converted to LDL after delivering triglycerides to the muscles and adipose (fat) tissue. The levels of HDL, LDL and total cholesterol are all indicators for atherosclerosis and heart attack risk. People who have a cholesterol level of 275 or greater (200 or less is desirable) are at significant risk for a heart attack, despite a favorable HDL level. In addition, people who have normal cholesterol levels but low HDL levels are also at increased risk for a heart attack.

The level of cholesterol in your blood is expressed in "milligrams per deciliter (mg/dL)," which indicates the weight of the cholesterol found in one deciliter of blood. Bloodcholesterol tests usually measure the total amount of cholesterol in your blood. Tests and calculations can also be performed to see how much of that cholesterol is contained in the form of LDLs and HDLs. If cholesterol is normally present in your blood, why should you worry about it? The reason is that the total amount of cholesterol in your blood reveals how efficiently your body is using and managing cholesterol. Excessive cholesterol in your blood may mean that something is going wrong with how your body is using cholesterol. When more of the cholesterol in your blood is being carried by HDLs, the "good" cholesterol, there is less danger of cholesterol accumulating in the body. If LDLs, the "bad" cholesterol, are carrying more of the cholesterol, the balance is tipped in favor of cholesterol remaining in the body. The consequences of high cholesterol can be serious. Most notably, high cholesterol raises the risk of heart disease. Risk for coronary heart disease increases as blood-cholesterol level rises, especially as it rises past 200 mg/dL. These high levels of blood cholesterol directly contribute to atherosclerosis and heart attack. Low HDL cholesterol and high levels of triglycerides are also factors of the metabolic syndrome, a condition that increases the risk of coronary heart disease

How To Lower Cholesterol Diet and lifestyle could be the most important way to lower high cholesterol and the risk of coronary heart disease. Emphasis on a healthy diet and lifestyle is crucial both for those who are at low risk but have many years ahead of them, and also for those who are older and at a higher risk. It's clear that high cholesterol levels not only can be controlled and even improved through changes in diet and lifestyle, but also can be prevented in those who have not yet developed them.

When diet isn't enough or more aggressive treatment is needed to lower cholesterol, medications are available. However, medication is not a substitute for a healthy diet. Even if you take medications to lower cholesterol, you should also adhere to a diet that's low in saturated fat, trans fat, and cholesterol. Exercise is also a key component to lowering cholesterol, either by losing weight or maintaining a healthy weight. Excess fat and calories are a significant cause of high cholesterol, and it's necessary to balance intake of calories with a corresponding output of physical activity. Other methods to lower cholesterol include reducing stress and invasive procedures.

B. How Diabetes Affect Pulse Deficit: Diabetes and heart disease can be a deadly combination, if not treated appropriately. This is because many of the problems caused by heart disease are also caused by diabetes. Added together, diabetes and heart disease mean double trouble. Heart disease causes damage to blood vessels as well as the heart. And unfortunately, diabetes damages blood vessels, too. This is problematic because every single cell in your body relies on blood vessels and the heart for life-sustaining energy and nourishment. Many diabetes complications -- from blindness to kidney disease -- begin with problems in the blood vessels. Unfortunately, vascular problems that affect blood flow to some pretty important organs -- the brain and the heart itself -- are among the most common of all diabetes-related complications. Statistics tell the story: About two-thirds of people with diabetes die of vascular diseases, especially heart attacks and strokes. Before you increase your activity level, you need to consider the possible presence of heart disease. Coronary heart disease is very common in people with diabetes, affecting perhaps as many as 50 percent of them. To assess risk, client and doctor need to take into account clients age, blood pressure, blood fats, whether client has protein in his/her urine, the length of time client have had diabetes, and clients family history. So before begin to increase level of activity, consult doctor and, if appropriate, have an exercise tolerance test. This test is done on a treadmill and reflects heart's ability to work under stress. Chances of having a positive result, indicating heart disease, increase with each risk factor one has. Even if one is at increased risk or have a positive test, he/she will likely still be able to increase physical activity; one will just need to work more closely with your diabetes care team to set safe guidelines for activity and, perhaps, to determine if medications to lower risk of heart trouble are in order. With some precaution, diabetes patients can use exercise to help control the disease and relieve some of its issues. However, for those with special conditions, such as loss of feeling in limbs or basic nerve damage, avoiding some types of exercise is advised. C. How does coarctation of aorta affect pulse?

The aorta is the major blood vessel that carries blood away from the heart to the body. When someone has coarctation of the aorta, that person's aorta is narrowed at some point. Here's how a healthy heart and aorta work: Blood that needs oxygen comes from all over the body and enters the right side of the heart, which pumps it to the lungs. The lungs fill the blood with oxygen, and this oxygen-rich blood returns from the lungs to the left side of the heart. The left side of the heart finishes up by pumping the blood out through the aorta. From the aorta, the blood travels through arteries that reach all of the body's organs and tissues, bringing them oxygen. Then the blood returns to the heart through veins and begins the cycle once again. When part of the aorta is narrowed, called a coarctation, that defect can affect the body's blood circulation because the left side of the heart has to work harder to pump blood through the narrowed aorta. Sometimes the narrowing is minor and may not even cause symptoms. In other cases the aorta may be more constricted, placing a strain on the heart's left ventricle (the chamber that pumps blood to the aorta and out to the body). A coarctation can occur anywhere in the aorta, but it is most often found after the point where the arteries that carry blood to the upper body and head branch off from the aorta. What Causes Coarctation of the Aorta? Coarctation of the aorta (or COA for short) is a congenital defect, meaning that someone is born with it. Doctors don't know for sure why certain people are born with this narrowing. COA accounts for up to 8% of all congenital heart defects. Almost twice as many boys as girls have COA. In many kids, the defect shows up with other birth defects or conditions, such as a ventricular septal defect (a hole in the wall between the heart's left and right ventricles). COA is also fairly common in girls born with Turner syndrome, a genetic disorder in which one of a girl's two X chromosomes is incomplete or missing. Most people with COA are diagnosed when they are babies or young children. But some may not be diagnosed until they are teens or even adults. Usually, in this case, the narrowing in the aorta is not severe enough to cause serious symptoms while the person is very young. But even those who do not have major symptoms usually need to be treated because the coarctation can eventually cause problems. The heart defect will not go away on its own. Signs and Symptoms Kids who have COA often do not have any symptoms or have only mild signs that are discovered by accident during a regular visit to the doctor. A child who does have symptoms may experience some or all of these:

cold legs and feet shortness of breath, especially when exercising

dizziness leg cramps after exercising strong, throbbing headaches fatigue nosebleeds fainting chest pain

Often an abnormal blood pressure test is the first sign of COA detected by a doctor. During a physical exam, the doctor may find that a child with a coarctation has a higher blood pressure in the arms than in the legs. The doctor may also hear a heart murmur or notice that the pulse in the groin is weak or difficult to feel. CoA imposes significant afterload on the left ventricle (LV), which results in increased wall stress and compensatory ventricular hypertrophy. The afterload may be imposed acutely, as occurs following closure of the ductus arteriosus in neonates with severe coarctation. These infants may rapidly develop CHF and shock. Rapid constriction of the ductus arteriosus, producing sudden severe aortic obstruction, seems to be the most likely explanation. As the ductus (aortic end) constricts, the left ventricular afterload rapidly increases, with a resultant increase in left ventricular pressures (systolic and diastolic). This causes elevation of the left atrial pressure, which may open the foramen ovale, causing left-to-right shunt and dilatation of the right atrium and right ventricle. If the foramen ovale does not open, pulmonary venous pressures and pulmonary artery pressures increase, and right ventricular dilatation develops. Cardiomegaly revealed by chest roentgenography and right ventricular hypertrophy seen on ECG and echocardiography are related to the indirect effects of rapid development of severe aortic obstruction. LV afterload may also increase gradually, allowing children with less severe coarctation to develop arterial collateral vessels that partially bypass the aortic obstruction. These children may be asymptomatic until hypertension is detected or another complication develops. The mechanism for development of hypertension is not clearly understood; mechanical obstruction and renin-angiotensinmediated humoral mechanisms have been postulated. The mechanical obstruction theory explains the increased blood pressure by postulating that a higher blood pressure is required to maintain flow through the coarcted segment and collateral vessels. The stroke volume, ejected into the limited aortic receptacle, produces a higher pressure proximal to coarctation. However, this theory does not explain the following:

The lack of relationship between the degree of elevation of blood pressure and the magnitude of obstruction The increased peripheral vascular resistance distal to the site of obstruction The delayed or lack of reduction of blood pressure immediately following relief of obstruction

The humoral theory postulates activation of the renin-angiotensin system secondary to reduction of renal blood flow and appears to explain most of the clinical features. However, measurement of plasma renin activity in both animal models and human subjects did not show consistently elevated plasma renin levels in the early studies. The reasons for the inability to demonstrate elevation of renin levels may be related to inadequate measurement of salt intake, posture, extracellular fluid volume, and sympathetic influences on renin release. More recent studies demonstrated

abnormalities in renin-angiotensin-aldosterone systems. In addition, activation of central sympathetic nervous system may also be responsible for hypertension of aortic coarctation. Associated anomalies greatly influence pathophysiology. VSD often coexists, and coarctation exacerbates the associated left-to-right shunt. Other levels of left heart obstruction (aortic stenosis, subaortic stenosis) may be present and may add to LV afterload. A number of neurohumoral changes occur with CHF. Sympathetic nervous system activation occurs, resulting in increases in heart rate and blood pressure (BP). The reninangiotensin system is activated in patients with CHF, particularly in CoA in which lowerbody BP and renal perfusion may be reduced. Activation of the renin-angiotensin system results in vasoconstriction, cell hypertrophy, and the release of aldosterone. The role of the renin-angiotensin system in CHF and the use of drugs to modulate this system are an intense area of research. Unlike most cases of CHF, CoA is more complex because precoarctation and postcoarctation hemodynamics are quite different. Drugs typically used to treat patients with CHF, such as angiotensin-converting enzyme inhibitors and, more recently, angiotensin II antagonists, may have adverse effects in patients with CoA. Attempts to achieve a normal precoarctation BP with these drugs may result in inadequate lower-body perfusion and may precipitate renal failure. D. How does peripheral heart disease affect pulse?

The large arteries have two functions: to act as conduits and to act as cushions. Conduit function is to deliver blood with minimal loss of mean perfusion pressure to the tissues and organs of the body and according to need. Cushioning function smooths flow pulsations imposed by the intermittently contracting heart so that blood is directed through these organs and tissues in an almost steady stream. In experimental animals and healthy young humans, both functions are discharged with great efficiency. The mean pressure drop between the ascending aorta and a large peripheral artery in the forearm or leg is minute, perhaps only 2 to 3 mm Hg when the body is supine. The extra energy lost in the circulation on account of the intermittent action of the heart is normally only 10% or so greater than if the heart's output were continuous or nonpulsatile. Both functions, however, are disturbed by the arterial degeneration that occurs with aging and disease. Atherosclerosis is an example of disease that disturbs conduit function almost exclusively; this occurs through narrowing a major artery and causes ischemia or infarction of the organ or tissue downstream. Arteriosclerosis (stiffening and dilation of major arteries) in hypertension and with aging affects cushioning function and disturbs the heart upstream and the arteries in general by increasing pulse pressure and systolic pressure. This condition does not affect conduit function. These are two separate and distinct conditions, even though they are often seen together in older Western subjects. The first (atherosclerosis) is focal, primarily intimal, and principally occlusive. The second (arteriosclerosis) is diffuse, primarily medial, and dilatory (Fig 1). Aortic coarctation affects both conduit and cushioning function, the former by creating an impediment to blood flow into the lower body and the latter by restricting cushioning function to the proximal aorta and predominantly elastic arteries in the upper body. It is necessary to consider the details of cushioning function, since this is the major role of the large arteries and is most affected by arterial disease when it is generalized (as in arteriosclerosis) or when it involves the aorta itself (as in coarctation). The cushioning function of an individual artery can be described in terms of stiffness, distensibility, or compliance (Table). As described in the articles that follow, one has to be careful with these terms, since the properties are different in different arteries, in the

same artery at different distending pressures, and with activation of smooth muscle in the vessel wall. Both distensibility and stiffness are relative terms, with one the inverse of the other. Compliance is an absolute term, relating absolute diameter or volume change to change in pressure; hence, it is dependent on arterial caliber and is lowest in larger arteries and highest in smaller arteries. Yet none of these terms is sufficient to describe the whole arterial system, since the tubular, distributed nature of the arterial system leads to difference in absolute pressure along the arterial tree at the same point in time. The physical structure of the arterial system leads to generation of waves that travel along the arteries and that are reflected at regions of discontinuity (especially the peripheral arterioles). Wave travel and reflection are apparent in the secondary waves that are seen in diastole (in the young) or in systole (in older subjects) (Fig 3). The major changes of the arterial pulse as seen with hypertension or aging are attributable to arterial stiffening and more rapid travel of the pulse along the major arteries and to consequent early return of wave reflection from the periphery of the body (Fig 3). This is the reason for disappearance of the reflected wave from diastole and its movement into systole, with characteristic boost to pressure in late systole. This was recognized as the characteristic effect of hypertension and aging, as measured by the sphygmogram in 1872, 24 years before the sphygmomanometer cuff was first introduced.

Atherogenesis: Development of the Atherosclerotic Plaque

Theories on atherogenesis must consider mechanical factors. In an older Western man who smokes and whose cholesterol level is high, atherosclerosis develops in the epicardial coronary arteries but not in systemic veins or in pulmonary arteries or veins of similar caliber, and not at all in the intramural coronary arteries or in the carotid artery where this artery passes through the petrous temporal bone. Clearly, tensile stress in the arterial wall is an important factor in atherogenesis. This is confirmed by the higher prevalence of atherosclerosis in hypertension. But tensile stress cannot explain all, since lesions show a predilection for certain sites, such as around orifices or just beyond bifurcations. At these sites, there are disturbances of flow patterns and alterations in shear stress (Fig 4) at the vascular interface. It is possible that such alterations in shear stress can explain localization of atherosclerosis within affected arteries. It is also possible that further disturbances created by a plaque may cause further growth of the plaque. However, the details have so far eluded us. The multiplicity of theories relating shear stress to atherogenesis attests to the difficulty in gaining data on shear stress at the vascular interface. In the past, atherogenesis was related to low shear and to high shear by respected authorities. It now appears that variable shear related to secondary nonlaminar flow, and especially to pulsatile flow, is the major etiologic factor. Shearing stress may be accentuated by the presence of the plaque itself, so that the process becomes self-perpetuating. The mechanism whereby altered shear causes the development of plaque has not yet been determined, with some schools subscribing to easier entry of lipoproteins and others to deposition of platelets onto the vessel wall. The common factor is disturbance of the endothelial cells by the viscous drag (shearing stress) on their interface with blood. Atherosclerosis appears to occur preferentially at sites where arteries are poorly supported or where they are subject to repetitive bending (ie, the coronaries, the femoral vessels at the groin), where an artery is dilated (the carotid bifurcation), or where a relatively narrow artery is subject to rapid and variable flow (the infrarenal aorta). All these points must give clues as to the mechanical factors that are important in atherogenesis. Factors include expansion of the wall and drag on the vascular interface, bending and flexing (coronary and femoral), presence of secondary flow (carotid), and high variable shear (abdominal aorta). The infrarenal segment of the aorta is far more susceptible to atherosclerosis than

is the aorta above the renal arteries. Here the aorta is relatively narrow, so that flow velocity is relatively high, while backflow is appreciable during diastole into the renal arteries, so that shear stress is both higher and more variable than in the suprarenal aorta. This subject has a high priority in medical research, although it was not addressed in depth at this conference.

Atherosclerosis: Plaque Rupture and Thrombotic Occlusion

It is now generally accepted that coronary occlusion is usually due to growth of an occlusive thrombus from an area where an atherosclerotic plaque has ruptured, exposing blood elements to intimal elements below the endothelium. Plaque rupture is the initial event. This may be silent if just a tiny thrombus is formed, may precipitate the syndrome of unstable angina or subendocardial infarction if coronary thrombus causes subocclusive narrowing, or may lead to full Q-wave transmural infarction when complete occlusion results. The question arises as to what causes plaque rupture. If this were known, we would understand what triggers the onset of myocardial infarction and other acute coronary syndromes. There are some clues, both epidemiological and pathological. Coronary occlusion with onset of myocardial infarction can come on at any time in a susceptible person but is most common soon after waking, during the arousal response, when heart rate and blood pressure are high. Coronary occlusion is also more common during exercise than at rest, especially if exercise is vigorous and unaccustomed. Again, these peaks correspond to increase in heart rate and blood pressure and cardiac output. From an anatomic viewpoint, plaques fracture at their edge, below the fibrous cap, where the wall of the plaque is thin and poorly supported by the soft atheromatous material below the intimal layer. This region is most susceptible to disruptive mechanical forces. Modeling experiments have shown that mechanical shearing forces are greatest in this region of plaque. Mechanical forces are definitely involved in plaque rupture, but we still cannot be certain how they are involved. Sudden rises in pressure, flow, or heart rate may increase the risk of plaque rupture 100-fold but only increase the risk of coronary occlusion from perhaps one chance per million hours to one chance per 10 000 hours, ie, to one chance per 36 million pulsatile cycles of stretch on the weakened endothelium. The wonder is not how mechanical forces cause damage but how resilient atherosclerotic plaques are at resisting damage. 6. Discuss the effect on heart and BP of the following
A. discuss the effect of caffeine on heart and BP Caffeine, Blood Pressure, and the Heart
Evidence has repeatedly shown that consumption of caffeine does not increase the risk of high blood pressure, heart disease or heart attack. One very well-known study examined more than 85,000 women over a ten-year period and found that there was no increased risk of these diseases, even in women who drank more than six cups of coffee per day. The Joint National Committee on Hypertension has specifically stated that there is no evidence linking coffee/tea and high blood pressure. While some recent studies have shown a weak link between caffeine and elevations in blood pressure, the results are complicated and only consider short-term effects. For example, one widely quoted study found that blood pressure rose slightly in subjects almost immediately after consuming a caffeinated beverage, and that this blood pressure rise was more pronounced in people with pre-existing high blood pressure. However, these elevations were not very large and only lasted a short

time. The study also showed that in about 15 percent of people with existing high blood pressure, drinking a caffeinated beverage actually caused a decrease in blood pressure. Two important studies published in 2007 further supported the existing body of evidence by again demonstrating that:

caffeine-induced blood pressure changes were small and short-lived caffeine does not contribute to disorders of the blood vessels associated with high blood pressure and cardiovascular disease

One interesting study showed that the caffeine-blood pressure relationship may be more complicated than expected. The study examined how the amount of coffee consumed affected the risk of developing high blood pressure. While the results showed that the risk of high blood pressure was the lowest for those who drink no coffee, it also showed that those who drink a lot of coffee have almost the same risk. In an unexpected twist, people who drank only small amounts of coffee (1-3 cups per day) seemed to have the highest risk. It is believed that over time, the body becomes tolerant to the stimulant effects of caffeine.

New buzz on coffee: It's not the caffeine that raises blood pressure
DALLAS, Nov. 19 People who enjoy the occasional decaf latte may be getting more of a lift than they know, scientists report in todays rapid access issue of Circulation: Journal of the American Heart Association. Swiss scientists studying caffeines effects in a small group of people report markedly elevated blood pressure and increased nervous system activity when occasional coffee drinkers drank a triple espresso, regardless of whether or not it contained caffeine. Surprisingly, people who drank coffee on a regular basis showed increased stimulation of sympathetic nerve pathways but no increase in blood pressure. This is the first time such disparities in reactions to coffee have been reported, says lead researcher Roberto Corti, M.D., a cardiologist at University Hospital in Zurich. The results suggest that some unknown ingredient or ingredients in coffee not caffeine is responsible for cardiovascular activation, he explains. Coffee contains several hundred different substances. Until now we have attributed the cardiovascular effects of coffee to caffeine, but we found non-coffee drinkers given decaffeinated coffee also display these effects, Corti says. This demonstrates how little we know about the effects of one of our most popular beverages and the most abundantly consumed stimulant worldwide. Coffees cardiovascular safety remains controversial, he says. The possible health hazards have been related to its main ingredient caffeine. The researchers measured blood pressure, heart rate and muscle sympathetic nervous system activity (MSA) in 15 healthy volunteers (ages 27 to 38) six habitual coffee drinkers and nine who either abstained or drank coffee only occasionally. Measurements were recorded before, during and after participants consumed a triple espresso, a decaf triple espresso or intravenous administration of the equivalent amount of caffeine, or a placebo. None of the subjects knew whether they were receiving caffeine. Sympathetic nervous system activity plays an important role in the regulation of blood pressure and overactivation has been linked with high blood pressure. The non-habitual or occasional coffee drinkers had systolic blood pressure (the top number in a blood pressure reading) increases of 12 millimeters of mercury (mm Hg) after 60 minutes. No significant change was observed in habitual drinkers blood pressure. MSA increased in both caffeine and decaffeinated coffee groups by 29 percent after 30 minutes and 53 percent after 60 minutes, with almost identical activation times. In non-habitual coffee drinkers given decaffeinated espresso, systolic blood pressure increased despite no increase in blood concentrations of caffeine. MSA activity was only marginally increased, and heart rate and diastolic blood pressure remained unchanged. Recent epidemiological studies have revealed a possible beneficial effect on cardiovascular disease and deaths in habitual coffee drinkers, he says. But our study strongly supports the hypothesis that ingredients other than caffeine are responsible for the stimulating effects of coffee on the cardiovascular system.

The lack of blood pressure elevation in coffee drinkers suggests the effects may be mediated through increased tolerance, the researcher notes. However, sympathetic nerve activation occurred in both groups when caffeine was administered intravenously, and habitual drinkers MSA increased after drinking caffeinated espresso, both of which suggest tolerance to coffee does not appear to be related to caffeine. He concludes that the potential adverse effects attributed to coffee could be less hazardous in regular consumers with normal blood pressure. In such people, especially those without a hereditary predisposition to hypertension, coffee drinking cant be considered a risk factor for hypertension. What remains to be seen is whether people with hypertension should be advised to avoid decaffeinated coffee as well, Corti says. The American Heart Association says studies investigating a direct link between caffeine, coffee drinking and coronary heart disease have produced conflicting results. However, moderate coffee drinking (one two cups per day) doesnt seem harmful.

Caffeine was first discovered in tea in 1827, and was named theine. It was later found in mate and various other plants. Eventually it was shown that the theine of tea was identical with the caffeine of coffee, and the term theine was then dropped. Caffeine is the most widely used drug in the world today. Found in beverages like coffee, tea and soft drinks, it is consumed by 8 out of 10 adults in the Western world today. Its toxic effect is without doubt. In the study, a group of 10 healthy volunteers were given either inactive placebo capsules or capsules containing 100 milligrams of caffeine--a quantity equivalent to one cup of coffee or 2-3 cups of tea. The volunteers were then given the opposite capsule from the previous dosage on another day. The results showed that caffeine consumption caused an increase in wave reflection -- a measure of arterial stiffness -- for at least 2 hours. Just one cup of coffee or two cups of tea is enough to harden a person's arteries for several hours afterwards. This puts extra pressure on the heart, thus increasing the risk of heart attack or stroke. The same amount of caffeine can raise the blood pressure by 5 to 10 millimeters of mercury. If this increase is on a regular basis, it could have negative repercussions on a person's long-term prognosis. It is evident today that many of our cancers are related to a dominance of estrogen. In a world flooded with estrogen and estrogen-like compounds, it is important for our body to have as low an estrogen load as possible. Studies have shown that drinking more than two cups of coffee (400 mg of caffeine) a day may increase estrogen levels in women. It could also lead to problems such as endometriosis and breast pain. Having high levels of estrogen for women in such cases can be detrimental as it can lead to breast cancer in women and prostate cancer in men. Those who have a family history of cancer also have a higher risk. In a clinical trial conducted, about 500 women between the ages of 36 to 45 were studied. These women were not pregnant, not breast-feeding or having hormonal treatment. They were interviewed regarding their diets, smoking habits, height and weight. Their hormone levels during the first five days of their menstrual cycle was also measured. The results showed that women who consumed more than one cup of coffee ( or two cups of tea) a day had significantly higher levels of estrogen during the early follicular phase of their menstrual

cycle. Those who consumed at least 500 mg of caffeine daily, the equivalent of four or five cups of coffee (or 10 cups of tea in caffeine equivalent) had nearly 70% more estrogen than women who consumed less than 100 mg of caffeine daily. Caffeine intake from all sources was associated with higher estrogen levels regardless of the women's age, body mass index (BMI), caloric intake, smoking habits, alcohol and cholesterol intake. Caffeine consumption increases estradiol levels. There are three different forms of estrogen in the body - estrone, estradiol, and estriol. Estradiol is the form that is pro-cancerous. Women should limit their intake of coffee to not more than one to two cups daily to decrease their risk of having more serious health problems. Chronic high caffeine intake can also lead to adrenal gland exhaustion and the reduction of production of progesterone.

C> Smoking And Your Heart

Understanding the effects of smoking on your heart and blood vessels is important. When you smoke, you inhale several chemicals into your lungs that can hurt your heart and blood vessels. As blood travels through your lungs to pick up oxygen, it also picks up these chemicals. Nicotine is one of the major chemicals you inhale while smoking. Once it gets into your bloodstream, it makes your heart beat faster and your blood pressure rise. This increases the work of the heart. Eventually, your heart can become damaged from the extra work. Nicotine also speeds up coronary artery disease and increases the risk of clot formation in the bloodstream. The arteries become narrowed, resulting in less blood and oxygen traveling through them to the heart. This increases your chances of having a heart attack or myocardial infarction. Remember that a heart attack can occur when a clot totally blocks an artery on the outside of your heart. Carbon monoxide is another chemical inhaled while smoking. Nicotine and carbon monoxide together decrease the amount of oxygen supplied to your tissues. Nicotine causes your blood vessels to narrow (constrict). This allows less blood to travel through them. Carbon monoxide replaces the oxygen normally carried by your blood. As a result, the amount of oxygen supplied to the various parts of your body can drop below the amount needed. Permanent damage can result. If you are wondering whether low-tar or low-nicotine cigarettes are better for your heart, the answer is NO. Studies have shown that changing over to this type of cigarette results in smoking more cigarettes per day. It also results in a tendency to inhale more deeply when smoking. As a result, harmful amounts of nicotine and carbon monoxide are still inhaled. If you need further assistance to quit smoking, there are various methods available. Ask your doctor to go over the various quit smoking methods, so that you can determine the one that is best for you.

Smoking and Heart Attack

Cigarette smoke, high blood pressure, high levels of cholesterol in the blood and physical inactivity are the four major risk factors for heart attack that can be changed. People who already have high blood pressure, high blood cholesterol (or both) and who smoke cigarettes increase their risk of heart attack even more. The more cigarettes a person smokes, the greater their risk of heart attack. People who smoke a pack of cigarettes a day have more than twice the risk of heart attack of people who've never smoked. And people who smoke two or more packs have an even higher risk.

Smokers who have a heart attack have less chance of surviving than nonsmokers. And people who keep smoking after a heart attack increase the chances that they'll have a second attack.

D.

Drinking Alcohol and Blood Pressure

Even Small Amounts Can Increase Hypertension

Even modest alcohol consumption can cause blood pressure to increase, according to two recent studies conducted in Japan. Dr. Noriyuki Nakanishi, from the department of social and environmental medicine at Osaka University Graduate School of Medicine in Japan, lead author of the first study, concluded that "Alcohol use represents an important modifiable risk factor for hypertension." Previous research has demonstrated some health benefits for those who drink small amounts of alcohol, but the two new studies indicate that even very low alcohol consumption can be a health risk for many -- almost one in every four Americans.

Alcohol Effects Olders Persons More

The first study involved more than 5,000 Japanese male office workers, between the ages of 23 and 59, for more than four years.

The subjects were grouped into four categories: those who drank fewer than 12 grams of alcohol a day; those who drank 12 grams to 22 grams per day; those who drank 23 grams to 45 grams per day; and those who drank more than 46 grams per day. One glass of wine would contain about 20 grams of alcohol. Researchers observed that as the alcohol consumption rate went up, so did blood pressure. In the 12 grams to 22 grams per day group, systolic blood pressure went up 1.4 points in those between the ages of 25 and 35, but increased 5.4 points for men between the ages of 48 and 59, indicating that drinking affects older persons more. Risk of Hypertension
In the second of the two studies, researchers from Kyushu University followed more than 1,100 people over age 40 for 10 years. During that study, 101 men and 106 women developed hypertension with the risk of developing hypertension higher for both men and women who drank, even those who drank less than 23 grams daily. More than 17,000 people die each year from high blood pressure complications in the U.S. and almost one in four Americans has high blood pressure, according to the Centers for Disease Control and Prevention. Hypertension can cause stroke, heart disease and kidney failure. Alcohol still heart healthy in the right amount

April 18, 2005 -- Beer and red wine can raise your blood pressure, but researchers say alcohol is still heart healthy in the right amount. It's well known that alcohol can raise blood pressure, but it's been unclear if different types of alcohol have the same effect, says Renate R. Zilkens, PhD, research fellow in the School of Medicine and Pharmacology at the University of Western Australia. Red Wine vs. Beer Zilkens and colleagues wanted to see if the antioxidant chemicals in red wine could offset some of the blood pressure effects of alcohol. So they compared it with beer. The researchers divided 24 healthy men into four different groups for four weeks: Some men drank no wine or beer and served as a comparison group Some men drank 13 ounces of red wine daily Some men drank 13 ounces of red wine with the alcohol removed to see if the alcohol accounted for any blood pressure effect Some men drank 38 ounces of beer daily (just over three beers)

The men made no other changes in their lifestyle other than limiting tea to less than 2 cups a day (since tea can also raise blood pressure) and avoiding antioxidants (to avoid any potential effect on blood vessels). The men wore blood pressure and heart rate monitors 24 hours a day. Blood Pressure, Heart Rate Climb Compared with the men who did not drink any alcohol, the red wine drinkers had a nearly a 2.5 point jump in their systolic blood pressure. Beer drinkers' blood pressure rose nearly two points. Systolic blood pressure is the top number of a blood pressure reading. It measures the pressure in blood vessels when the heart pumps. While this doesn't sound like much, even a few points can make a difference in people who have borderline or high blood pressure. Ideally, blood pressure should be less than 120/80. Blood pressure between 120/80 and 140/90 is called prehypertension. Heart rate also rose. The researchers tested heart rate during sleep to rule out any effect of activity. Red wine drinkers' heart rate climbed five points for eight to 10 hours after drinking. Beer drinkers' heart rate rose four points. Removing alcohol from the red wine did not lower the blood pressure. The researchers say that the blood pressure effects of red wine and beer appear to be similar. Since the men in the study did not have high blood pressure, it's unclear how these findings apply to people who do. The study appears in the new issue of Hypertension: Journal of the American Heart Association. So how is alcohol good for your heart if it raises blood pressure? It's a delicate balance, say researchers. Men should drink less than two drinks per day, Zilkens says in a news release. Women should have no more than one drink a day because they are more sensitive to the potential damaging effects of alcohol due to body size and metabolism. Zilkens says at recommended alcohol levels men and women will still benefit from heartprotective effects of alcohol. Men in the current study drank more than the amount recommended by the American Heart Association (AHA). One drink equals a 5 ounce glass of wine, a 12 ounce beer, or 1 ounce of liquor. Alcohol's Heart-Healthy Benefits Heart-healthy benefits of alcohol include: Raises HDL "good" cholesterol that helps reduce the risk of heart disease Helps decrease risk of blood clots (heart attacks and strokes are caused by blood clots)

The AHA says people who do not already drink alcohol should not start since there is no way to know who may become dependent on alcohol

7.

hypertension Hypertension, commonly referred to as "high blood pressure" or HTN, is a medical condition in which the blood pressure is chronically elevated.[1] While it is formally called arterial hypertension, the word "hypertension" without a qualifier usually refers to arterial hypertension. Hypertension can be classified as either essential (primary) or secondary. Essential hypertension indicates that no specific medical cause can be found to explain a patient's condition. Secondary hypertension indicates that the high blood pressure is a result of (i.e. secondary to) another condition, such as kidney disease or certain tumors (especially of the adrenal gland). Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm, and is a leading cause of chronic renal failure. Even moderate elevation of arterial blood pressure leads to shortened life expectancy. At severely high pressures, mean arterial pressures 50% or more above average, a person can expect to live no more than a few years unless appropriately treated.[2] Hypertension is considered to be present when a person's systolic blood pressure is consistently 140 mmHg or greater, and/or their diastolic blood pressure is consistently 90 mmHg or greater.[3] Recently, as of 2003, the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure[4] has defined blood pressure 120/80 mmHg to 139/89 mmHg as "prehypertension." Prehypertension is not a disease category; rather, it is a designation chosen to identify individuals at high risk of developing hypertension. The Mayo Clinic website specifies blood pressure is "normal if it's below 120/80" but that "some data indicate that 115/75 mm Hg should be the gold standard." In patients with diabetes mellitus or kidney disease studies have shown that blood pressure over 130/80 mmHg should be considered high and warrants further treatment. Even lower numbers are considered diagnostic using home blood pressure monitoring devices. In adults, blood pressure is abnormally high when the average of several supine measurements of systolic pressure is equal to or more than 140 mmHg, and the average of several measurements of diastolic pressure is equal to or more than 90 mmHg. Hypertension increases the risk of cardiovascular diseases and kidney failure because it adds to the workload of the heart, causing it to enlarge and, over time, weaken; in addition, it may damage the walls of arteries. Arterial hypertension occurs in about 20% of adults in western countries. Mild, regular aerobic exercise reduces the chances of developing hypertension and reduces blood pressure in those who have moderate hypertension, but seems to have little effect on those with severe hypertension. The American Academy of Pediatrics, Committee on Sports Medicine advise those with severe hypertension to avoid weight and power lifting, body building exercises, and strength training. Persistently high blood pressure. Hypertension may also be detected sporadically in animals partly due to the technical difficulties in diagnosis and the lack of recognizable signs. Greyhounds normally have a higher blood pressure than is found in crossbred dogs with features resembling essential hypertension in humans. Secondary hypertension due to advanced renal disease, hyperthyroidism and hyperadrenocorticism does occur in dogs and cats. Temporary episodes of hypertension occur in all animals suffering severe pain, and in horses with acute laminitis. Renal hypertension Hypertension produced by diseases of the kidney. This includes diseases such as polycystic kidney disease or chronic glomerulonephritis. Hypertension can also be

produced by diseases of the renal arteries supplying the kidney. This is known as renovascular hypertension; it is thought that decreased perfusion of renal tissue due to stenosis of a main or branch renal artery activates the renin-angiotensin system. Adrenal hypertension Hypertension is a feature of a variety of adrenal cortical abnormalities. In primary aldosteronism there is a clear relationship between the aldosterone-induced sodium retention and the hypertension. In patients with pheochromocytoma increased secretion of catecholamines such as epinephrine and norepinephrine by a tumor (most often located in the adrenal medulla) causes excessive stimulation of [adrenergic receptors], which results in peripheral vasoconstriction and cardiac stimulation. This diagnosis is confirmed by demonstrating increased urinary excretion of epinephrine and norepinephrine and/or their metabolites (vanillylmandelic acid). Coarctation of the aorta

Sodium is the environmental factor that has received the greatest attention. Approximately 60% of the essential hypertension population is responsive to sodium intake[citation needed]. This is due to the fact that increasing amounts of salt in a person's bloodstream causes the body to draw more water, increasing the pressure on the blood vessel walls. Diet The North American diet that is high in fat and salt has been proven to exacerbate hypertension. A study in the U.S. found that patients placed on a strict vegetarian diet showed a significant benefit to their condition over the one year. Certain medications, especially NSAIDS (Motrin/ibuprofen) and steroids can cause hypertension. Imported licorice (Glycyrrhiza glabra) inhibits the 11hydroxysteroid hydrogenase enzyme (catalyzes the reaction of cortisol to cortison) which allows cortisol to stimulate the Mineralocorticoid Receptor (MR) which will lead to effects similar to hyperaldosteronism, which itself is a cause of hypertension Blood pressure responses to increases and decreases in dietary salt intake are heterogeneous. In some hypertensive individuals, decreases in blood pressure with salt restriction are clinically significant and approach that achieved with medication. In others, little or no change in blood pressure occurs, whereas in still others, blood pressure may actually increase with salt restriction. The heterogeneous responses are partly acquired and involve the influences of age, the intake of other electrolytes, and the influence of certain medications. Genetic predisposition may also play a substantial role because salt sensitivity is increased in black individuals and in persons with non- insulindependent diabetes mellitus. Some uncommon but readily diagnosed salt-sensitive genetic syndromes, such as glucocorticoid- remediable aldosteronism and Liddle syndrome, have been identified. Short-term volume expansion and contraction and longer-term dietary interventions appear to be reproducible and may be used to identify salt-sensitive and salt-resistant individuals; however, these maneuvers are cumbersome and cannot be used on a large scale. Molecular genetic techniques for identifying individuals with saltsensitive and salt- resistant essential hypertension are not yet available, but if the putative gene polymorphisms are identified, such techniques may replace the current trial-anderror methods. One of salt's major functions is to regulate blood volume and pressure including the flexibility of the blood vessels. The human heart is a big pump. When it contracts, it forces blood through the arteries of the circulatory system; that pressure is "systolic," the

"top" number. Between heartbeats, the heart relaxes. Pressure measured between heartbeats is "diastolic," the "bottom" number. When blood volume increases or the blood vessel walls don't expand enough, blood pressure increases. Normal blood pressure is less than 130/85 according to the National Heart, Lung and Blood Institute. In a population, blood pressures are a good indicator of the incidence of cardiovascular events like heart attacks and strokes. As long ago as 2,000 B.C. when the famous Chinese "Yellow Emperor" Huang Ti recorded salt's association with a "hardened pulse," we have known of a relationship between salt and blood pressure. Thats not news. Nor is the fact that manipulating sodium intake can change blood pressure in sensitive individuals, those termed "salt sensitive" (a condition with roots in both genetics and lifestyle ( 1 2). For a century, medical researchers have been able to measure sodium and have documented that by increasing or decreasing sodium in the body, many peoples blood pressure moves up or down in small but often-detectable amounts. What is more newsworthy is that over the past quarter-century, weve learned that the body often makes physiologic adjustments to correct for such changes and preserve blood pressure at the proper level (e.g. changes in renin system response). And all this leads to the final point about salt and blood pressure: the only rationale offered for reducing salt to reduce blood pressure (in some people) is that it will lessen their risk of a heart attack or stroke. The news today is that not a single study has shown improved health outcomes for populations on reduced sodium diets.

8. Discuss practical DOs and DONTs to have a healthy heart. DOs Eat healthy foods and cutting back on calories are good for our hearts. A hearthealthy diet includes low-saturated fat protein sources, lots of fresh fruits and vegetables, and adequate healthful fats, including omega-3 essential fatty acids. High protein diets have a slight edge, but really any diet that includes hearthealthy foods and calorie control will benefit your heart. To somehow mange stress we must understand and be self-aware because when we must separate from a loved one we have reactions that are physiological and emotional that are beyond our control. However, our emotional intelligence skills can help us manage and tame them. Share your thoughts, vent your anger, or ask for help because keeping them inside may cause heart diseases because of stress If you have adequate opportunities to share feelings and receive feedback, you'll have fewer symptoms related to stress. Replace some of the carbohydrates with healthful proteins or healthful oils reduced the risk for heart disease even more than the traditional heart-healthy higher carbohydrate diet. Realize that if you change from a poor diet to a healthy diet, you will have a much better chance of having a healthy heart. Have a Check-up for even at least once a month Eat foods with high Omega-3 because Omega-3 lowers triglycerides. Exercise to burn fats After your exercise session, always stretch your body and do some light exercise. So that, the body comes back to the normal condition and the blood circulation becomes normal again.

 Before you really take some huge decisions in your life regarding rigorous workouts and exercise, consult a doctor. He really has more brains and can definitely guide you better. Have a balance and enough sleep to give the body enough energy. Do some yoga or meditation to relieve stress Eat foods that contain vitamins, minerals and fibers. live a healthy life style avoid things that are detrimental to your health Avoid having an acquired Hypertension DONTS Dont smoke or stop smoking because it can cause diseases such as heart diseases Dont drink liquor if you drink only little amounts for cleansing Dont eat foods with high cholesterol Dont eat food with Trans fat such as baked foods. Never ever go on DIETING. Here is the reason, when you go on dieting, you limit the food intake. The body is a wonderful piece of machine. It is cleverer than you think. In your dieting phase, it starts extracting more nutrients than usual. So when you are dieting, the extraction process is on a full scale. Dont eat junk foods or foods that contain msg. Dont think too much of the pressure and problems. Although it's tempting to take higher doses of supplements, in some cases too much can harm your health.