data about hpn

7/29/2019 Data About HPN

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SAINT LOUIS UNIVERSITY

HEART SOUNDS AND BLOOD

PRESSURE DETERMINATION

GROUP 2

GROUP LEADER:SANTOS, Jever Lee Y.

GROUP MEMBERS:TUVERA, Kerbick CarlBORJA, Marie Clare InesDANGLOSI, JoaN

LAZARO, LorelieMACALINO, Janessa


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I. Get the resting blood pressure Right arm of all the group

mates. Record.

NAME OF MEMBER BP

SANTOS 120/90mmHg

TUVERA 100/70mmHgBORJA 100/80mmHg

DANGLOSI 110/80mmHg

LAZARO 100/80mmHg

MACALINO 100/80mmHg

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 AFTER COFFEE INTAKE

BP 110/80 120/100

HR 88 85

PR 90 80

RR 17 19

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 AFTER COFFEE INTAKE

BP 110/80 120/100

HR 98 94

PR 97 88

RR 17 27

IV. Take resting BP, RA of group leader in:

A.SEATED 130/90

B. SUPINE 120/90C. STANDING POSITION 140/100


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V. Palpate & grade PULSES of Group leader at resting state

Let him do stationary jogging for 2 -3 minutes. Immediately, take

A. BP, RA 160/90

B. HR 98

C. RR 42D.

RIGHT LEFT

RADIAL +2 +2

BRACHIAL +1 +1

TEMPORAL +2 +2CAROTID +2 +2

POPLITTEAL +1 +1

ANTERIOR TIBIAL +1 +1

DORSALIS PEDIS +2 +2

RIGHT LEFT

RADIAL +2 +2

BRACHIAL +1 +1

TEMPORAL +2 +2CAROTID +2 +2

POPLITTEAL +1 +1



RIGHT LEFT

RADIAL +3 +3

BRACHIAL +2 +2

TEMPORAL +3 +3

CAROTID +3 +3

POPLITTEAL +1 +1




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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 asmedications, 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 afistula 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.


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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?


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DISADVANTAGE ADVANTAGE

ANEROIDBAUMANOMETER

> less accurate than mercurial

> Because the elasticity of themetal bellows changes with time,

the calibration must be checkedfrequently by a simultaneousmeasurement with a mercurysphygmomanometer device usinga Y-tube adapter.> easily broken when dropped

> It's a fairly delicate and

complicated mechanism.

> The only way to tell if the

gauge is accurate is to checkit against a mercury

sphygmomanometer at leastonce a year and when

dropped or bumped.

> It can be easily damagedwithout the user's

knowledge and requires

factory repair and

readjustment.> The gauge can be clumsy

to position, and without a D-ring cuff can be difficult toapply by oneself.

> It may not work well for

the hearing or visuallyimpaired or for those unable

to perform the hand

movement needed tosqueeze the bulb and inflate

the cuff.

> Much cheaper than themercurial Baumanometer.

> Have the advantage ofportability and easy of use.

> Aneroid equipment is often

inexpensive, lightweightand more portable than

mercury.

> The aneroid gauge willfunction in any position if

the reader is able to view itdirectly.

> Some models have easy-to-read, extra large gauge;

D-ring cuff for one-handed

application and a self-bleeding deflation valve for

increased reading accuracy.

> mercury-free

MERCURIALBAUMANOMETER

> Not economical ( it hashigher prize than aneroid)

> Can yield inaccuratereadings 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 aflat surface during

measurement; the gaugemust be read at eye level foraccuracy.

> May not work well for the

hearing or visually impairedor for those unable to

perform the hand movement

needed to squeeze the bulband inflate the cuff.

> Safe, accurate, and essentialin the accurate measurement ofblood pressure.

> Mercury is pushed down bygravity and up by the bloodpressure, and since gravity does

not change, the gauge does notwear out.> If properly maintained, it cangive accurate readings fordecades.> The elemental mercury used

in Baumanometers is safelycontained in the Mylar CladCalibrated Cartridge tube, which

maintains its integrity even if theglass is broken, virtuallyeliminating the environmentalrisks associated with mercury.

> It's the standard for blood

pressure measurement.

> It's durable, easy to read

and doesn't requirereadjustment.

> gravity to give consistent

and accurate readings. Ithas a long, tubular gauge

made of glass or plastic.> For safety, glass tubesshould be wrapped in

Mylar to prevent breakage.

It's not often recommended

for home use due to thehazards of mercury.

> those made for home use

are lightweight andrelatively safe by design

> It will easily last a

lifetime with minimalmaintenance.


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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 isbecause of a too weak heart muscle contraction, how it is e.g. with forecourt flares thecase. It is often seen in atrial fibrillation.

An abnormal pulse rhythm is an irregular expansion and contraction of theperipheral arterial walls. It may be persistent or sporadic and rhythmic or arrhythmic.Detected by palpating the radial or carotid pulse, an abnormal rhythm is typicallyreported first by the patient, who complains of palpitations. This important findingreflects an underlying cardiac arrhythmia, which may range from benign to life-

threatening. 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 cardiacarrhythmias, pages 506 to 509.)

If an abnormal pulse rhythm is detected, quickly look for signs of reducedcardiac output, such as decreased level of consciousness (LOC), hypotension, ordizziness. Promptly obtain an electrocardiogram (ECG) and possibly a chest X-ray, andbegin 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 thepatient's vital signs, pulse quality, and cardiac rhythm because accompanyingbradycardia or tachycardia may result in deterioration of cardiac output. Keepemergency intubation, cardioversion, defibrillation, and suction equipment handy.

If the patient's condition permits, ask if he's experiencing pain. If so, find outabout its onset and location. Does the pain radiate? Ask about a history of heart diseaseand treatment for arrhythmias. Obtain a drug history and check the patient'scompliance. Also, ask about caffeine or alcohol intake. Digoxin toxicity, cessation of anantiarrhythmic, 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 causeassociated signs and symptoms of low cardiac output. Evaluate heart sounds: A longpause between S1 (lub) and S2 (dub) may indicate a conduction defect. A faint or absentS1 and an easily audible S2 may indicate atrial fibrillation or flutter. You may hear thetwo heart sounds close together on certain beatspossibly indicating premature atrialcontractionsor other variations in heart rate or rhythm. Take the patient's apical andradial pulses while you listen for heart sounds. With some arrhythmias, such aspremature ventricular contractions, you may hear the beat with your stethoscope butnot 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 thefrequency 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.

Arrhythmias.An abnormal pulse rhythm may be the only sign of a cardiacarrhythmia. The patient may complain of palpitations, a fluttering heartbeat, or weak


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and skipped beats. Pulses may be weak and rapid or slow. Depending on the specificarrhythmia, dull chest pain or discomfort and hypotension may occur. Associatedfindings, 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, anddiaphoresis.

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, anddyspnea. 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.

Explain the importance of keeping a diary of activities and any symptoms that developto 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, andpossible adverse effects.

Usefulness of pulse deficit to predict in-hospital complications and mortality inpatients with acute type A aortic dissection.

Vascular compromise seen with pulse deficits is common in patients with type Adissection. However, patient characteristics and in-hospital outcomes associated withpulse deficits have not been evaluated. Accordingly, we studied 513 patients (mean age62 +/- 14 years, 65% men) with acute type A aortic dissection enrolled in theInternational Registry of Acute Aortic Dissection. Pulse deficits, defined as decreased orabsent carotid or peripheral pulses as noted by clinicians and later confirmed bydiagnostic imaging, at surgery or at autopsy were noted in 154 patients (30%). Age


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The density of these lipoproteins is determined by the amount of protein in themolecule. "Bad" cholesterol is the low-density lipoprotein (LDL), the major cholesterolcarrier 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 ofthis as drain cleaner you pour in the sink--is thought to provide some protection againstartery blockage.

A high level of LDL in the blood may mean that cell membranes in the liver havereduced the number of LDL receptors due to increased amounts of cholesterol inside thecell. After a cell has used the cholesterol for its chemical needs and doesn't need anymore, it reduces its number of LDL receptors. This enables LDL levels to accumulate inthe 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 thisexcess cholesterol and transport it to the liver for disposal.

A third group of carrier molecules, the very low-density lipoproteins (VLDL) areconverted to LDL after delivering triglycerides to the muscles and adipose (fat) tissue.

The levels of HDL, LDL and total cholesterol are all indicators for atherosclerosisand heart attack risk. People who have a cholesterol level of 275 or greater (200 or lessis desirable) are at significant risk for a heart attack, despite a favorable HDL level. Inaddition, people who have normal cholesterol levels but low HDL levels are also atincreased 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. Blood-cholesterol tests usually measure the total amount of cholesterol in your blood. Testsand calculations can also be performed to see how much of that cholesterol is containedin 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 efficientlyyour body is using and managing cholesterol. Excessive cholesterol in your blood maymean 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 ofcholesterol remaining in the body.

The consequences of high cholesterol can be serious. Most notably, highcholesterol raises the risk of heart disease. Risk for coronary heart disease increases asblood-cholesterol level rises, especially as it rises past 200 mg/dL.

These high levels of blood cholesterol directly contribute to atherosclerosis andheart attack. Low HDL cholesterol and high levels of triglycerides are also factors of themetabolic syndrome, a condition that increases the risk of coronary heart disease

Diet and lifestyle could be the most important way to lower high cholesterol andthe risk of coronary heart disease. Emphasis on a healthy diet and lifestyle is crucialboth for those who are at low risk but have many years ahead of them, and also forthose who are older and at a higher risk.

It's clear that high cholesterol levels not only can be controlled and even improvedthrough changes in diet and lifestyle, but also can be prevented in those who have notyet developed them.


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When diet isn't enough or more aggressive treatment is needed to lowercholesterol, medications are available. However, medication is not a substitute for ahealthy diet. Even if you take medications to lower cholesterol, you should also adhereto a diet that's low in saturated fat, trans fat, and cholesterol.

Exercise is also a key component to lowering cholesterol, either by losing weightor maintaining a healthy weight. Excess fat and calories are a significant cause of highcholesterol, and it's necessary to balance intake of calories with a corresponding outputof physical activity.

Other methods to lower cholesterol include reducing stress and invasiveprocedures.

Diabetes and heart disease can be a deadly combination, if not treatedappropriately. This is because many of the problems caused by heart disease are alsocaused by diabetes. Added together, diabetes and heart disease mean double trouble.

Heart disease causes damage to blood vessels as well as the heart. Andunfortunately, diabetes damages blood vessels, too. This is problematic because everysingle cell in your body relies on blood vessels and the heart for life-sustaining energyand nourishment.

Many diabetes complications -- from blindness to kidney disease -- begin withproblems in the blood vessels. Unfortunately, vascular problems that affect blood flow tosome pretty important organs -- the brain and the heart itself -- are among the mostcommon of all diabetes-related complications. Statistics tell the story: About two-thirdsof people with diabetes die of vascular diseases, especially heart attacks and strokes.

Before you increase your activity level, you need to consider the possiblepresence of heart disease. Coronary heart disease is very common in people withdiabetes, affecting perhaps as many as 50 percent of them. To assess risk, client anddoctor need to take into account clients age, blood pressure, blood fats, whether clienthas protein in his/her urine, the length of time client have had diabetes, and clientsfamily 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'sability to work under stress. Chances of having a positive result, indicating heartdisease, increase with each risk factor one has. Even if one is at increased risk or have apositive test, he/she will likely still be able to increase physical activity; one will justneed to work more closely with your diabetes care team to set safe guidelines foractivity and, perhaps, to determine if medications to lower risk of heart trouble are inorder.

With some precaution, diabetes patients can use exercise to help control thedisease and relieve some of its issues. However, for those with special conditions, suchas loss of feeling in limbs or basic nerve damage, avoiding some types of exercise isadvised.

C. How does coarctation of aorta affect pulse?


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The 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 allover 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 , 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 (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 defect, meaning thatsomeone 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 arediscovered 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
http://www.kidshealth.org/parent/medical/sexual/turner.htmlhttp://www.kidshealth.org/parent/medical/sexual/turner.html


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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 ductusarteriosus in neonates with severe coarctation. These infants may rapidly develop CHFand shock. Rapid constriction of the ductus arteriosus, producing sudden severe aorticobstruction, seems to be the most likely explanation. As the ductus (aortic end)constricts, the left ventricular afterload rapidly increases, with a resultant increase in leftventricular pressures (systolic and diastolic). This causes elevation of the left atrialpressure, which may open the foramen ovale, causing left-to-right shunt and dilatationof the right atrium and right ventricle. If the foramen ovale does not open, pulmonaryvenous pressures and pulmonary artery pressures increase, and right ventriculardilatation develops. Cardiomegaly revealed by chest roentgenography and right

ventricular hypertrophy seen on ECG and echocardiography are related to the indirecteffects of rapid development of severe aortic obstruction.

LV afterload may also increase gradually, allowing children with less severe coarctationto develop arterial collateral vessels that partially bypass the aortic obstruction. Thesechildren may be asymptomatic until hypertension is detected or another complicationdevelops.

The mechanism for development of hypertension is not clearly understood; mechanicalobstruction and renin-angiotensinmediated humoral mechanisms have been postulated.

The mechanical obstruction theory explains the increased blood pressure by postulatingthat a higher blood pressure is required to maintain flow through the coarcted segmentand collateral vessels. The stroke volume, ejected into the limited aortic receptacle,produces a higher pressure proximal to coarctation. However, this theory does notexplain the following:

The lack of relationship between the degree of elevation of blood pressure andthe 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 ofobstruction

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


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abnormalities in renin-angiotensin-aldosterone systems. In addition, activation of centralsympathetic nervous system may also be responsible for hypertension of aorticcoarctation.

Associated anomalies greatly influence pathophysiology. VSD often coexists, andcoarctation exacerbates the associated left-to-right shunt. Other levels of left heartobstruction (aortic stenosis, subaortic stenosis) may be present and may add to LVafterload.

A number of neurohumoral changes occur with CHF. Sympathetic nervous systemactivation occurs, resulting in increases in heart rate and blood pressure (BP). The renin-angiotensin system is activated in patients with CHF, particularly in CoA in which lower-body BP and renal perfusion may be reduced. Activation of the renin-angiotensin systemresults in vasoconstriction, cell hypertrophy, and the release of aldosterone. The role ofthe renin-angiotensin system in CHF and the use of drugs to modulate this system arean intense area of research. Unlike most cases of CHF, CoA is more complex becauseprecoarctation and postcoarctation hemodynamics are quite different.

Drugs typically used to treat patients with CHF, such as angiotensin-converting enzymeinhibitors and, more recently, angiotensin II antagonists, may have adverse effects inpatients with CoA. Attempts to achieve a normal precoarctation BP with these drugsmay 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 andto act as cushions. Conduit

function is to deliver blood withminimal loss of mean perfusion pressure to the tissues

and organs of

the body and according to need. Cushioning function smooths

flowpulsations imposed by the intermittently contracting heartso that blood is directed

through these organs and tissues inan almost steady stream. In experimental animals and

healthyyoung humans, both functions are discharged with great efficiency.The meanpressure drop between the ascending aorta and a largeperipheral artery in the forearm or

leg is minute, perhaps only2 to 3 mm Hg when the body is supine. The extra energy lost

in the circulation on account of the intermittent action ofthe 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 occurswith 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 orinfarction of the organ or tissuedownstream. Arteriosclerosis (stiffening and dilation of

majorarteries) in hypertension and with aging affects cushioningfunction and disturbs

the heart upstream and the arteries in general by increasing pulse pressure and systolic

pressure. Thiscondition does not affect conduit function. These aretwo separate anddistinct conditions, even though they are oftenseen 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). Aorticcoarctation affects both conduit andcushioning function, the former by creating an

impediment toblood flow into the lower body and the latter by restricting cushioning

function to the proximal aorta and predominantly elastic arteriesin the upper body.

It is necessary to consider the details of cushioning function,since this is the major role ofthe large arteries and is mostaffected 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 describedin terms of stiffness,

distensibility, or compliance (Table).As described in the articles that follow, one has tobe carefulwith these terms, since the properties are different in differentarteries, in the


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same artery at different distending pressures,and with activation of smooth muscle in the

vessel wall. Bothdistensibility and stiffness are relative terms, with one the inverseof the

other. Compliance is an absolute term, relating absolute diameteror volume change tochange in pressure; hence, it is dependent onarterial caliber and is lowest in larger

arteries and highestin smaller arteries. Yet none of these terms is sufficient to describe

the whole arterial system, since the tubular, distributed nature

of the arterial system leadsto difference in absolute pressurealong the arterial tree at the same point in time. The

physical structure of the arterial system leads to generationof waves that travel along the

arteries and that are reflectedat regions of discontinuity (especially the peripheralarterioles). Wave travel and reflection are apparent in the secondarywaves that are seen

in diastole (in the young) or in systole (in older subjects) (Fig 3). The major changes of

the arterialpulse as seen with hypertension or aging are attributable toarterial stiffening

and more rapid travel of the pulse alongthe major arteries and to consequent early returnof wave reflectionfrom the periphery of the body (Fig 3). This is the reason for

disappearance of the reflected wave from diastole and its movementinto systole, with

characteristic boost to pressure in latesystole. This was recognized as the characteristic

effect of hypertension and aging, as measured by the sphygmogram

in 1872, 24 yearsbefore the sphygmomanometer cuff was firstintroduced.

Atherogenesis: Development of the Atherosclerotic

Plaque

Theories on atherogenesis must consider mechanical factors. In an older Western man

who smokes and whose cholesterollevel is high, atherosclerosis develops in theepicardial coronaryarteries 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 arterywhere this arterypasses through the petrous temporal bone. Clearly, tensilestress in thearterial wall is an important factor in atherogenesis.This is confirmed by the higher

prevalence of atherosclerosisin hypertension. But tensile stress cannot explain all, since

lesions show a predilection for certain sites, such as aroundorifices or just beyondbifurcations. At these sites, thereare 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 atherosclerosiswithin affected arteries. It is also possible thatfurther disturbancescreated 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 atteststo the difficulty in

gaining data on shear stress at the vascularinterface. In the past, atherogenesis wasrelated tolow shear and to high shear by respected authorities. It now appears that

variable shear related to secondary nonlaminarflow, and especially to pulsatile flow, is

the major etiologicfactor. Shearing stress may be accentuated by the presence ofthe

plaque itself, so that the process becomes self-perpetuating.The mechanism wherebyaltered shear causes the development ofplaque has not yet been determined, with some

schools subscribingto easier entry of lipoproteins and others to deposition of platelets

onto the vessel wall. The common factor is disturbance of the endothelial cells by theviscous drag (shearing stress)on their interface with blood.

Atherosclerosis appears to occur preferentially at sites wherearteries 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 narrowartery is subject to rapid and variable flow (theinfrarenal aorta). All these points must

give clues as to the mechanicalfactors that are important in atherogenesis. Factors include

expansion of the wall and drag on the vascular interface, bendingand flexing (coronaryand femoral), presence of secondary flow(carotid), and high variable shear (abdominal

aorta). The infrarenalsegment of the aorta is far more susceptible to atherosclerosisthan


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is the aorta above the renal arteries. Here the aorta isrelatively 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 variablethan in the suprarenal aorta.

This subject has a high priority in medical research, althoughit was not addressed in

depth at this conference.

Atherosclerosis: Plaque Rupture and Thrombotic

Occlusion

It is now generally accepted that coronary occlusion is usuallydue to growth of an

occlusive thrombus from an area where an atherosclerotic plaque has ruptured, exposingblood elements to intimal elementsbelow the endothelium. Plaque rupture is the initial

event.This may be silent if just a tiny thrombus is formed, may precipitatethe syndrome

of unstable angina or subendocardial infarction

if coronary thrombus causes subocclusivenarrowing, or may leadto 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 infarctionand other acute coronarysyndromes. There are some clues, bothepidemiological and pathological. Coronary

occlusion with onsetof myocardial infarction can come on at any time in a susceptible

person but is most common soon after waking, during the arousalresponse, when heartrate and blood pressure are high. Coronaryocclusion 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 ananatomic viewpoint,plaques fracture at their edge, below the fibrous cap, wherethe wallof the plaque is thin and poorly supported by the softatheromatous material below the

intimal layer. This region is most susceptible to disruptive mechanical forces. Modeling

experiments have shown that mechanical shearingforces are greatest in this region ofplaque.

Mechanical forces are definitely involved in plaque rupture,but we still cannot be certain

how they are involved. Suddenrises in pressure, flow, or heart rate may increase the risk

of plaque rupture 100-fold but only increase the risk of coronaryocclusion from perhapsone chance per million hours to one chanceper 10 000 hours, ie, to one chance per 36

million pulsatilecycles of stretch on the weakened endothelium. The wonderis not how

mechanical forces cause damage but how resilientatherosclerotic plaques are at resistingdamage.

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 bloodpressure, heart disease or heart attack. One very well-known study examined more than 85,000 womenover 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 specificallystated 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, theresults are complicated and only consider short-term effects.

For example, one widely quoted study found that blood pressure rose slightly in subjects almost immediatelyafter consuming a caffeinated beverage, and that this blood pressure rise was more pronounced in peoplewith pre-existing high blood pressure. However, these elevations were not very large and only lasted a short


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time. The study also showed that in about 15 percent of people with existing high blood pressure, drinking acaffeinated beverage actually caused a decrease in blood pressure.

Two important studies published in 2007 further supported the existing body of evidence by againdemonstrating 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 thanexpected. The study examined how the amount of coffee consumed affected the risk of developing highblood pressure. While the results showed that the risk of high blood pressure was the lowest for those whodrink no coffee, it also showed that those who drink a lot of coffee have almost the same risk. In anunexpected twist, people who drank only small amounts of coffee (1-3 cups per day) seemed to have thehighest 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 ofCirculation: 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 amountof 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 over-

activation 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 anddiastolic 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.


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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 predispositionto 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


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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 cholesterolintake. 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 aresult, 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 increasetheir 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.


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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 BloodPressure

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 drankfewer than 12 grams of alcohol a day; those who drank 12grams to 22 grams per day; those who drank 23 grams to 45grams per day; and those who drank more than 46 grams perday. One glass of wine would contain about 20 grams ofalcohol.

Researchers observed that as the alcohol consumption rate

went up, so did blood pressure. In the 12 grams to 22 gramsper day group, systolic blood pressure went up 1.4 points inthose between the ages of 25 and 35, but increased 5.4

points for men between the ages of 48 and 59, indicating thatdrinking 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


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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 haveborderline 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 ofHypertension: 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 heart-

protective 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


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7.

hypertension

Hypertension, commonly referred to as "high blood pressure" orHTN, is a medical

condition in which theblood pressure is chronically elevated.[1] While it is formally called

arterial hypertension, the word "hypertension" without a qualifier usually refers toarterial hypertension. Hypertension can be classified as eitheressential (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 bloodpressure is a result of (i.e. secondary to) another condition, such as kidney diseaseor

certain tumors (especially of the adrenal gland). Persistent hypertension is one of the risk

factors forstrokes, heart attacks, heart failureand arterialaneurysm, and is a leadingcause ofchronic 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 unlessappropriately treated.[2]

Hypertension is considered to be present when a person's systolic blood pressure is

consistently 140 mmHg or greater, and/or theirdiastolicblood 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 BloodPressure[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 Clinicwebsite 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 diabetesmellitus orkidney disease studies have shown that blood pressure over 130/80 mmHgshould 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 averageof 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; inaddition, 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 ofdeveloping hypertension and reduces blood pressure in those who have moderate

hypertension, but seems to have little effect on those with severe hypertension. TheAmerican 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 dogsand cats. Temporary episodes of hypertension occur in all animals suffering severe pain,

and in horses with acute laminitis.

Renal hypertensionHypertension produced by diseases of the kidney. This includes diseases such as

polycystic kidney disease or chronicglomerulonephritis. Hypertension can also be
http://en.wikipedia.org/wiki/Blood_pressurehttp://en.wikipedia.org/wiki/Hypertension#_note-0%23_note-0http://en.wikipedia.org/wiki/Arteryhttp://en.wikipedia.org/wiki/Secondary_hypertensionhttp://en.wikipedia.org/wiki/Kidney_diseasehttp://en.wikipedia.org/wiki/Kidney_diseasehttp://en.wikipedia.org/wiki/Tumorhttp://en.wikipedia.org/wiki/Adrenal_glandhttp://en.wikipedia.org/wiki/Strokehttp://en.wikipedia.org/wiki/Myocardial_infarctionhttp://en.wikipedia.org/wiki/Heart_failurehttp://en.wikipedia.org/wiki/Heart_failurehttp://en.wikipedia.org/wiki/Aneurysmhttp://en.wikipedia.org/wiki/Aneurysmhttp://en.wikipedia.org/wiki/Aneurysmhttp://en.wikipedia.org/wiki/Chronic_renal_failurehttp://en.wikipedia.org/wiki/Hypertension#_note-1%23_note-1http://en.wikipedia.org/wiki/Hypertension#_note-1%23_note-1http://en.wikipedia.org/wiki/Systole_(medicine)http://en.wikipedia.org/wiki/Torrhttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Hypertension#_note-2%23_note-2http://en.wikipedia.org/wiki/Hypertension#_note-jnc7%23_note-jnc7http://www.mayoclinic.com/health/high-blood-pressure/DS00100/DSECTION=6http://www.mayoclinic.com/health/high-blood-pressure/DS00100/DSECTION=6http://en.wikipedia.org/wiki/Diabetes_mellitushttp://en.wikipedia.org/wiki/Diabetes_mellitushttp://en.wikipedia.org/wiki/Nephropathyhttp://en.wikipedia.org/wiki/Kidneyhttp://en.wikipedia.org/wiki/Polycystic_kidney_diseasehttp://en.wikipedia.org/wiki/Glomerulonephritishttp://en.wikipedia.org/wiki/Glomerulonephritishttp://en.wikipedia.org/wiki/Blood_pressurehttp://en.wikipedia.org/wiki/Hypertension#_note-0%23_note-0http://en.wikipedia.org/wiki/Arteryhttp://en.wikipedia.org/wiki/Secondary_hypertensionhttp://en.wikipedia.org/wiki/Kidney_diseasehttp://en.wikipedia.org/wiki/Tumorhttp://en.wikipedia.org/wiki/Adrenal_glandhttp://en.wikipedia.org/wiki/Strokehttp://en.wikipedia.org/wiki/Myocardial_infarctionhttp://en.wikipedia.org/wiki/Heart_failurehttp://en.wikipedia.org/wiki/Aneurysmhttp://en.wikipedia.org/wiki/Chronic_renal_failurehttp://en.wikipedia.org/wiki/Hypertension#_note-1%23_note-1http://en.wikipedia.org/wiki/Systole_(medicine)http://en.wikipedia.org/wiki/Torrhttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Hypertension#_note-2%23_note-2http://en.wikipedia.org/wiki/Hypertension#_note-jnc7%23_note-jnc7http://www.mayoclinic.com/health/high-blood-pressure/DS00100/DSECTION=6http://www.mayoclinic.com/health/high-blood-pressure/DS00100/DSECTION=6http://en.wikipedia.org/wiki/Diabetes_mellitushttp://en.wikipedia.org/wiki/Diabetes_mellitushttp://en.wikipedia.org/wiki/Nephropathyhttp://en.wikipedia.org/wiki/Kidneyhttp://en.wikipedia.org/wiki/Polycystic_kidney_diseasehttp://en.wikipedia.org/wiki/Glomerulonephritis


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produced by diseases of therenal 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-angiotensinsystem.

Adrenal hypertension

Hypertension is a feature of a variety of adrenal cortical abnormalities. In primaryaldosteronismthere is a clear relationship between the aldosterone-induced

sodium retention and the hypertension.

In patients withpheochromocytoma increased secretion ofcatecholamines such asepinephrine 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 norepinephrineand/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 todraw more water, increasing the pressure on the bloodvessel 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. Certainmedications, especially NSAIDS (Motrin/ibuprofen) and steroids can cause

hypertension. Imported licorice (Glycyrrhiza glabra) inhibits the 11-hydroxysteroid 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 bloodpressure with salt

restriction are clinically significant and approach thatachieved with medication. In

others, little or no change in blood pressureoccurs, whereas in still others, blood pressuremay actually increase withsalt restriction. The heterogeneous responses are partly

acquired andinvolve the influences of age, the intake of other electrolytes, and the

influence of certain medications. Genetic predisposition may also play a substantial rolebecause salt sensitivity is increased in black individualsand in persons with non- insulin-

dependent diabetes mellitus. Some uncommonbut readily diagnosed salt-sensitive genetic

syndromes, such asglucocorticoid- remediable aldosteronism and Liddle syndrome, havebeenidentified. Short-term volume expansion and contraction and longer-termdietary

interventions appear to be reproducible and may be used to identifysalt-sensitive and

salt-resistant individuals; however, these maneuvers arecumbersome and cannot be usedon a large scale. Molecular genetictechniques for identifying individuals with salt-

sensitive and salt-resistant essential hypertension are not yet available, but if the putative

gene polymorphisms are identified, such techniques may replace the currenttrial-and-

error 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
http://en.wikipedia.org/wiki/Renal_arteryhttp://en.wikipedia.org/wiki/Renal_arteryhttp://en.wikipedia.org/wiki/Renovascular_hypertensionhttp://en.wikipedia.org/wiki/Stenosishttp://en.wikipedia.org/wiki/Aldosteronismhttp://en.wikipedia.org/wiki/Aldosteronismhttp://en.wikipedia.org/wiki/Pheochromocytomahttp://en.wikipedia.org/wiki/Catecholamineshttp://en.wikipedia.org/wiki/Catecholamineshttp://en.wikipedia.org/wiki/Epinephrinehttp://en.wikipedia.org/wiki/Norepinephrinehttp://en.wikipedia.org/wiki/Vanillylmandelic_acidhttp://en.wikipedia.org/wiki/Coarctation_of_the_aortahttp://en.wikipedia.org/wiki/Salt#Health_effectshttp://en.wikipedia.org/wiki/Wikipedia:Citing_sourceshttp://en.wikipedia.org/wiki/Wikipedia:Citing_sourceshttp://en.wikipedia.org/wiki/Wikipedia:Citing_sourceshttp://en.wikipedia.org/wiki/Osmosishttp://en.wikipedia.org/wiki/Osmosishttp://en.wikipedia.org/wiki/Vegetarianhttp://www.merck.com/pubs/mmanual_home/sec3/25.htmhttp://en.wikipedia.org/wiki/Renal_arteryhttp://en.wikipedia.org/wiki/Renovascular_hypertensionhttp://en.wikipedia.org/wiki/Stenosishttp://en.wikipedia.org/wiki/Aldosteronismhttp://en.wikipedia.org/wiki/Pheochromocytomahttp://en.wikipedia.org/wiki/Catecholamineshttp://en.wikipedia.org/wiki/Epinephrinehttp://en.wikipedia.org/wiki/Norepinephrinehttp://en.wikipedia.org/wiki/Vanillylmandelic_acidhttp://en.wikipedia.org/wiki/Coarctation_of_the_aortahttp://en.wikipedia.org/wiki/Salt#Health_effectshttp://en.wikipedia.org/wiki/Wikipedia:Citing_sourceshttp://en.wikipedia.org/wiki/Osmosishttp://en.wikipedia.org/wiki/Vegetarianhttp://www.merck.com/pubs/mmanual_home/sec3/25.htm


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"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 pressureis 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 manipulatingsodium 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, manypeoples blood pressure moves up ordown 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 bloodpressure: 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 thatnot 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 heart-

healthy 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 heart-healthy foods and calorie control will benefit your heart.

To somehow mange stress we must understand and be self-aware because whenwe must separate from a loved one we have reactions that are physiological and

emotional that are beyond our control. However, our emotional intelligence skillscan help us manage and tame them.

Share your thoughts, vent your anger, or ask for help because keeping them insidemay 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.
http://hyper.ahajournals.org/cgi/reprint/42/6/1206http://hyper.ahajournals.org/cgi/reprint/42/6/1206http://www.ajcn.org/cgi/content/abstract/65/2/612Shttp://www.ajcn.org/cgi/content/abstract/65/2/612Shttp://www.ajcn.org/cgi/content/abstract/65/2/587Shttp://www.ajcn.org/cgi/content/abstract/65/2/708Shttp://www.ajcn.org/cgi/content/abstract/65/2/708Shttp://www.ajcn.org/cgi/content/abstract/65/2/712Shttp://bmj.com/cgi/content/full/312/7041/1283http://bmj.com/cgi/content/full/312/7041/1283http://bmj.com/cgi/content/full/312/7041/1283http://www.ajcn.org/cgi/content/abstract/65/2/594Shttp://hyper.ahajournals.org/cgi/reprint/42/6/1206http://hyper.ahajournals.org/cgi/reprint/42/6/1206http://www.ajcn.org/cgi/content/abstract/65/2/612Shttp://www.ajcn.org/cgi/content/abstract/65/2/612Shttp://www.ajcn.org/cgi/content/abstract/65/2/587Shttp://www.ajcn.org/cgi/content/abstract/65/2/708Shttp://www.ajcn.org/cgi/content/abstract/65/2/712Shttp://bmj.com/cgi/content/full/312/7041/1283http://bmj.com/cgi/content/full/312/7041/1283http://www.ajcn.org/cgi/content/abstract/65/2/594S


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Before you really take some huge decisions in your life regarding rigorous

workouts and exercise, consult a doctor. He really has more brains and candefinitely 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 youthink. 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.

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