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BRUCE ROSEMAN, M.D.
TAKING YOUR BLOOD PRESSURE AT HOME by Mandie, Devincentis, R.N.
* The earpieces of the stethoscope should be pointing towards your noe.
* The blood pressure cuff has the word 'artery' written on it with a vertical line just below it. This is meant to help you position the cuff correctly and you should line it up so that it is just above your antecubital artery (located at the inner bend of your elbow).
* Wrap the cuff completely around your arm, between your shoulder & elbow, at the heart level. If you have another person at home this is the part where you will most likely need some assistance at first. The cuff should not be able to slip around or fall down your arm on it's own. Also, don't wrap the cuff around your arm too tightly. You should just be able to fit the head of your stethoscope underneath the cuff.
* It's easier to control the cuff inflation & deflation if you place the blood pressure cuff on your non-dominant limb. However, there is no reason why this is medically necessary. It's just easier this way.
* Before you begin inflating the cuff, make sure the air valve is closed (i.e. turn it to the right to close it). Also, make sure you can easily release the valve (by turning it to the left) with your thumb and index finger before pumping up the cuff.
* If you know (approximately) what your top number usually is, add 40 and pump up the cuff until the needle reaches around this number. Then slowly release the valve with your thumb & index finger by turning it to the left. The needle should fall steadily if done correctly.
* The FIRST beat you hear is the top number of your blood pressure. As the needle falls, the beats you hear will sound methodical & become softer. Listen closely because the LAST beat you hear is the bottom number of your blood pressure. This might take some practice.
* If you do not feel confident with your blood pressure reading after two attempts and want to try taking it again, you should either switch arms OR wait 10-15 minutes before trying again on the same arm. Taking it more than twice in a row on the same arm can increase the arterial pressure & give you an inaccurate reading.
* Never use the same side hand to inflate the cuff as the arm on which it is placed. In other words, if the cuff is placed around your left arm you don't want to pump it up with your left hand. This will give you an inaccurate reading because pumping your fist increases the arterial pressure in that arm.
* When documenting your BP reading note the time, date, & whether or not you have taken your medications. It's also a good idea to mention any changes recently made in your medications, how you are feeling (i.e. stressed, tired, relaxed, etc.) and anything else you may feel is important.
* Bring your documented blood pressure readings to your appointments. I will make a copy of them to keep in your chart.
* If you don't feel confident in your readings and would like me to show you again, just let me know and we will review it together at the office. We'll go over it as many times as you need, just ask.
Approximately 60 million Americans are affected by cardiovascular disease. Since the beginning of the 20th century, cardiovascular disease has consistently been the leading cause of death in the United States despite numerous advances in treatment. In 1998, approximately 1 million people died of cardiovascular disease. Hypertension and heart failure are the first and fifth most common causes of cardiovascular disease, affecting 50 million and 5 million Americans, respectively. The estimated economic burden resulting from hypertension and heart failure exceeds $60 billion/year. In addition, hypertension is the leading cause of heart failure and end-stage renal disease. Despite increased awareness and treatment of hypertension, only 27% of Americans with hypertension achieve modest control (blood pressure < 140/90 mm Hg), according to the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension is present in 75% of patients with heart failure, and from 1979-1998 heart failure deaths increased 135%.
The Clinical Problem
Hypertension (systolic pressure =" src="/math/ge.gif" border=0140 mm Hg or diastolic pressure =" src="/math/ge.gif" border=090 mm Hg) is present in one in four adults in the United States.1 The prevalence is higher among blacks and older persons, especially older women. Table 1 shows the classification of blood pressure according to the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.2 Hypertension is a risk factor for stroke, myocardial infarction, renal failure, congestive heart failure, progressive atherosclerosis, and dementia.3 Systolic pressure is a stronger predictor of cardiovascular events than is diastolic pressure,4 and isolated systolic hypertension, which is common among older persons, is particularly hazardous.5 There is a continuous, graded relation between blood pressure and the risk of cardiovascular disease; the level and duration of hypertension and the presence or absence of coexisting cardiovascular risk factors determine the outcome.6 Treatment of hypertension reduces the risk of stroke, coronary artery disease, and congestive heart failure, as well as overall cardiovascular morbidity and mortality from cardiovascular causes. However, only 54 percent of patients with hypertension receive treatment and only 28 percent have adequately controlled blood pressure.1
Many Methods to Reduce Blood Pressure
Source: American Diabetes Association
Publication date: 2002-07-02
The New York Times
July 2, 2002
By JANE E. BRODY
Three decades after the National High Blood Pressure Education Program started saying that controlling high blood pressure saves lives, rates of hypertension are rising.
In addition, the proportion of patients being treated — or treated well enough to bring their blood pressure readings under control — is falling, creating waves of alarm among cardiovascular specialists.
As a result, stroke rates are going up and the decline in heart attacks has leveled off; both strokes and heart attacks are directly linked to uncontrolled hypertension.
In trying to account for these changes, experts point to a number of factors. One is the sharp increase in the percentage of Americans who are overweight or obese, creating for themselves the leading risk factor for hypertension.
Another is a basic quality of the condition: it is a silent disease, and a vast majority of people with it feel fine, even as it causes life-threatening or fatal damage. About 30 percent of people with hypertension don't know they have it.
A third factor is the unwillingness or inability of most people with high blood pressure to change their diets and try exercise and relaxation techniques that can bring their readings down to normal.
Fourth is the reluctance of many patients to take medications and the failure of many doctors to keep up with drug developments that would allow them to design individual treatments and prescribe the remedies likely to produce the most benefit with the fewest side effects.
Further complicating the picture are the insurance-dictated constraints on doctors. Many of them don't take the time to educate patients about the importance of continually monitoring their pressure readings.
Last but hardly least, the drug companies with the greatest financial interest in getting all people with hypertension into treatment may have had a detrimental effect on the acceptance of drug therapy.
At the expense of older, less expensive drugs, pharmaceutical companies have heavily promoted newer and more expensive medications that may not always be the best for a particular patient. These may also be too costly for many older patients, who, since Medicare does not pay for drugs, have been known to take half the prescribed dosages to stay within their budget.
There are six classes of medications and scores of different drugs and drug combinations that are tailored to control high blood pressure.
Which drug or drug combination is right is determined by factors like sex, age, systolic blood pressure (the higher number, representing the pressure on arteries when the heart beats), smoking habits, total cholesterol, level of protective H.D.L. cholesterol, and whether the patient has diabetes or an enlarged left ventricle, the heart's main pumping chamber.
The simplest remedy that achieves the desired goal is the best choice. For example, say most experts, among them Dr. Steven A. Dosh of Escanaba, Mich., patients who have no known underlying disease are best treated initially with diuretics, which bring blood pressure down by reducing the volume of fluid the heart has to pump to outlying tissues. Diuretics in low doses are well tolerated, safe, effective and cheap and need be taken only once a day.
But, as Dr. Dosh wrote recently in The Journal of Family Practice, for those who have already had a heart attack or are otherwise known to have coronary artery disease, beta-blockers, which slow the heart and reduce the force of its contractions, may be the initial drug of choice. When combined with a diuretic, beta-blockers were proved to be especially good at preventing strokes, though less effective than expected in preventing heart attacks, according to Dr. Michael Alderman, a hypertension specialist at Albert Einstein Medical Center in the Bronx.
But one newer, more expensive drug may be better for some patients. For example, for patients with diabetes or systolic hypertension after a heart attack, the best remedy may be ACE, or angiotensin-converting enzyme, inhibitors. They relax blood vessels by reducing production of angiotensin I, which is converted into angiotensin II, a hormone that constricts arteries.
If an ACE inhibitor's side effects — a cough and a rash — are troublesome, a patient could try an A.R.B, or angiotensin receptor blocker, which prevents the action of angiotensin II. Thus far, the A.R.B.'s appear to be more effective than beta-blockers in preventing strokes, though the drugs are equally effective in reducing blood pressure, Dr. Alderman said.
The other classes are vasodilators, which relax blood vessels, and calcium channel blockers, which also relax blood vessels but in a number of studies have been linked to an increased risk of cardiovascular disease, especially congestive heart failure. However, studies have also indicated that long-acting calcium channel blockers may be more effective at preventing strokes than the ACE inhibitors, Dr. Alderman said.
So far, neither the ACE inhibitors nor the calcium channel blockers have been shown to be better than diuretics in preventing heart attacks, he added.
What Should a Patient Do?
First, don't do what one woman in her 50's did. Having experienced swollen ankles and a rapid heart beat as a side effect of a calcium channel blocker prescribed for hypertension, she stopped taking the drug and never returned to the doctor.
All drugs have side effects, a fact especially troublesome for blood pressure treatment, since the disorder itself usually produces no symptoms. Diuretics in high doses force patients to the bathroom many extra times a day and several times a night.
Many diuretics also deplete the body of potassium and magnesium and may raise blood levels of cholesterol and glucose. Beta-blockers in full dose can make people groggy, slow the heart rate and cause bronchial spasms.
Vasodilators can cause headaches, fluid retention and rapid heart rate. ACE inhibitors commonly cause an annoying dry cough, whereas the A.R.B.'s, which are generally better tolerated, may cause high blood levels of potassium. And nearly all the antihypertensive medications can inhibit sexual function, particularly in men.
Dr. Alderman suggested that in many patients, the ideal treatment is a combination of low doses of two or more drugs. This has the advantage of limiting the likelihood of disturbing side effects while increasing the drugs' effectiveness.
Patients should be closely monitored in the first months of treatment and every six months afterward; if the treatment is or becomes ineffective, it must be changed, by increasing the dose or changing drugs. Home blood pressure monitoring can alert patients to the need to see a doctor.
And for any drug treatment to work optimally, otherwise healthy patients should also adopt protective habits, including eating diets rich in fruits, vegetables and low-fat dairy products and low in fat and salt and other sources of sodium.
Aerobic exercise for at least 45 minutes a day three times a week is highly recommended. And, if the patient is overweight, a loss of 10 percent of total body weight can be very beneficial. Relaxation exercises like meditation may also help.
This prospective, open-label, randomized study compared the outcomes in hypertensive subjects 65 to 84 years of age who received therapy with angiotensin-converting–enzyme (ACE) inhibitors or diuretic agents. The rate of cardiovascular events or death from any cause was lower among male subjects who received ACE inhibitors.
Treating hypertension in older persons with an ACE inhibitor may confer an advantage over a diuretic in terms of outcome, despite similar reductions of blood pressure. The difference may be particularly evident among men.
Not infrequently, on release of the results of major multicenter trials, the lay press promulgates an immediate response before physicians have had time to assess the peer-reviewed paper. By the next morning, physicians are greeted by a multitude of messages containing frantic questions from patients about how the reported results relate to their particular problems. When the report deals with a common disease (such as hypertension), the magnitude of the public's anxieties is intensified. Moreover, when results appear to conflict with those of a previous study, not infrequently described as "landmark," there is potential for mass confusion and loss of confidence in individual health care providers, exacerbated by media reports that pose this rhetorical question: "Just what are we to believe?"
In this issue of the Journal, Wing et al.1 report the results of a major trial comparing the effects of angiotensin-converting–enzyme (ACE) inhibitors with the effects of diuretics on the rate of cardiovascular events in elderly hypertensive patients. The investigation, the Second Australian National Blood Pressure Study (ANBP2), involved 6083 patients who were followed by 1594 family practitioners for a median of 4.1 years. Numbers of patients and the design and conduct of the study appear reliable, but some of the results contradict those of another major trial, the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT).2 ALLHAT was designed to compare the diuretic chlorthalidone with agents representing each of three other classes of antihypertensive drugs (ACE inhibitors, calcium antagonists, and alpha-adrenergic–receptor inhibitors) and involved more than 42,000 patients from the United States and Canada. The trials should therefore be comparable. But ANBP2 indicates that ACE inhibitors have an outcome advantage over diuretics (particularly among older men), whereas ALLHAT concluded that diuretics were more effective for blood-pressure control, as well as in terms of outcomes. So what are we to believe?
First, we should consider the sources. Both trials were sponsored and supervised by national health research institutions with academic participation and without commercial influence. A second issue might be whether the drugs studied in each class were equivalent. The honest answer is that we do not really know. ANBP2 used hydrochlorothiazide as the diuretic, whereas ALLHAT used chlorthalidone. Hydrochlorothiazide has an excellent track record and was used as the diuretic in most early trials of antihypertensive therapy; chlorthalidone is equally well accepted. However, there have been no head-to-head trials comparing the efficacy of and outcomes with these two diuretics. In addition, ANBP2 used enalapril as the ACE inhibitor, whereas ALLHAT used lisinopril. Again, questions may be raised, since it is possible that one agent may have a greater effect not only on blood pressure, but also on local renin–angiotensin systems that may affect disease outcomes.3 There have not been (nor are there likely to be) head-to-head comparisons of the long-term efficacy of and outcomes with the two ACE inhibitors. We may also ask whether these were the only drugs used to control blood pressure in these trials. The answer to this question is equivocal. In both trials, other antihypertensive medications were frequently required to achieve blood-pressure goals, and the use of these additional agents also compounds the complexities of any comparison between the trials.
All of these are straightforward questions whose answers could explain the differences between the conclusions. There are also some more complex questions. Which agent controlled blood pressure better? The ANBP2 report indicates that there were similar reductions in blood pressure in the two treatment groups, whereas in ALLHAT, the diuretic-based regimen was more efficacious (as indicated both by the blood pressures and by the percentage of patients in whom the blood-pressure goal was achieved). We may well ask why there was a difference in blood pressure if the participating physicians were allowed to achieve the goal with the addition of the other classes of antihypertensive drugs.
What about clinical outcomes? Again, we must equivocate, because the trials used vastly different definitions of primary and secondary outcomes. The primary outcome in ANBP2 was the total number of fatal and nonfatal cardiovascular events, which favored enalapril. In ALLHAT, the treatment groups were similar in terms of the primary outcome of death from coronary causes or nonfatal myocardial infarction, but when combined with the secondary cardiovascular events, outcomes favored chlorthalidone. Perhaps comparison of the demographic and clinical characteristics of the subjects in the two trials can help. Age, sex, and body-mass index were similar. Ninety-five percent of the subjects in ANBP2 were white, whereas 35 percent of the subjects in ALLHAT were black. In ANBP2, the pretreatment blood pressures were higher. Could the differential in achieved blood pressure between the chlorthalidone group and the lisinopril group in ALLHAT have affected its results? The percentages of patients with diabetes, smokers, and patients with coronary heart disease or cerebrovascular disease in ANBP2 were lower. These characteristics could also have an effect on outcomes.4,5
In order to obtain firm answers to these questions for ourselves and our patients, medical leaders and responsible health care providers should assume more direct oversight of the interpretation of such studies. Whereas epidemiologists focus on responses at the population level in order to develop therapeutic guidelines, health care providers must deal with the specific relationship between the physician and the patient. This relationship is where the therapeutic tire meets the road, and there is no place for absolute or categorical answers. Population-based studies of therapies help to point the way but are not analogous to the care of individual patients.
Elsewhere in this issue of the Journal, there is an informative article by August6 that describes an exceedingly common clinical problem faced by all primary care physicians: the initial treatment of patients with less severe essential hypertension. Although such hypertension was formerly considered to be "mild," we must recognize that all hypertension is severe in that it is associated with an increased risk of premature illness and death. August outlines the importance of a comprehensive evaluation and the necessity for prompt recognition and treatment of hypertension.
Now we can develop specific resolutions to the apparent dilemma presented by the results of ANBP2 and ALLHAT. For patients with essential hypertension but without complications, it makes sense for the prescribing physician to choose a diuretic in a dose that does not cause potassium wasting, precipitate gout, or have other unwanted effects. In ANBP2 and ALLHAT, it was frequently necessary to prescribe a second or third medication in order to control blood pressure. In such a circumstance, the addition of an ACE inhibitor makes sense. Furthermore, a diuretic alone is not sufficient for the achievement of blood-pressure goals in some patients with hypertension, and both ACE inhibitors and diuretics are valuable and currently available as generic compounds. One should not lose sight of the fact that both diuretics and ACE inhibitors are extremely effective in improving clinical outcomes.7,8,9 However, patients with hypertension — particularly elderly patients — frequently have associated coexisting conditions. If a patient has diabetes, it would certainly be wise to initiate therapy with an ACE inhibitor, as long-term studies have clearly demonstrated.10,11,12 If a patient has cardiac failure, one might use both a diuretic and an ACE inhibitor. If there is a history of myocardial infarction, an ACE inhibitor diminishes the risks of future cardiac failure, a second infarction, and subsequent death13,14,15; a beta-blocker is also indicated for such a patient.7 If the patient has angina pectoris, whether from atherosclerotic epicardial coronary artery disease or from hypertensive arteriolar disease, it may also be wise to use a calcium antagonist. Dihydropyridine calcium antagonists not only relieve chest pain, but also help to prevent strokes.7,16
The answer to our question about what we are to believe has now become apparent. First, measure blood pressure in all patients. Second, if blood pressure remains elevated, control it with medication so as to achieve the blood-pressure goal (systolic blood pressure of less than 140 mm Hg and diastolic blood pressure of less than 90 mm Hg). In selecting appropriate therapy, choose a drug or a combination of drugs for which there is strong evidence of effectiveness in persons with the type of problem found in the patient.
Finally, we must not join the clamor of media and industry, allowing newscasts to declare immediately which class of drugs is best. Treatment of the individual patient with hypertension is complicated, requiring time and judgment. In choosing between a diuretic and an ACE inhibitor, the physician can make a reasonable selection by reviewing the patient's history and course. We must remember that trials describe population averages for the purposes of developing guidelines, whereas physicians must focus on the individual patient's clinical responses.
Ibuprofen Could Be Bad for Heart Patients
Fri Feb 14, 7:31 AM ET By EMMA ROSS, AP Medical Writer
LONDON - Fresh evidence adds to suspicions that ibuprofen could be dangerous for most heart patients because it can block the blood-thinning benefits of aspirin.
New research published this week in The Lancet medical journal found that those taking both aspirin and ibuprofen were twice as likely to die during the study period as those who were taking aspirin alone or with other types of common pain relievers.
Scientists believe ibuprofen clogs a channel inside a clotting protein that aspirin acts on. Aspirin gets stuck behind the ibuprofen and cannot get to where it is supposed to go to thin the blood.
Aspirin is considered the most important medicine for heart disease. Nearly all heart patients take it every day because it prevents the clots that cause heart attacks and strokes. Ibuprofen, which is in Motrin and Advil among other brands, is widely used for arthritis and other aches and pains.
Scientists at the Medicines Monitoring Unit of Britain's Medical Research Council checked the medical records of 7,107 heart patients who had been discharged from hospitals between 1989 and 1997 with aspirin prescriptions and had survived at least one month after leaving the hospital.
They were divided into four groups according to their prescriptions.
The first group included those on aspirin alone.
The second were given aspirin and ibuprofen and the third group had aspirin with another pain killer, diclofenac. Ibuprofen and diclofenac both belong to a widely used class of pain relievers known as nonsteroidal anti-inflammatory drugs, or NSAIDs.
The last group included those taking aspirin with any other NSAID, such as acetaminophen, which is in Tylenol.
The researchers found that those taking ibuprofen were almost twice as likely as those taking aspirin alone to die by 1997. That meant that for every 1,000 patients treated, there were 12 extra deaths a year when ibuprofen was taken with aspirin.
For heart-related deaths, ibuprofen was linked to three extra deaths per 1,000 patients treated per year.
Experts say it is important to track both heart-related deaths and deaths in general because deaths are sometimes attributed to the wrong cause and heart-related cases may be missed. For instance, a death certificate may say the person died in a car crash when, in fact, a heart attack or stroke at the wheel caused the crash.
No extra deaths were seen in the groups taking the other types of NSAIDs.
"The message here is beginning to be 'go for something other than ibuprofen,'" said Garret FitzGerald, who was not connected with the latest study, but whose research sparked concerns about the combination just over a year ago.
"Mechanistically, you have a very clear rationale for why it should happen," said FitzGerald, professor of cardiovascular medicine and chair of pharmacology at the University of Pennsylvania. "Now we have four studies each coming out with the same message. It's several pieces of ancillary evidence that when assembled are more persuasive than when taken in isolation."
"Lots of people take these two kinds of drugs chronically and probably a large number take both together chronically," FitzGerald said. "Talk to your doctor before you embark on this combination thinking that it's totally innocuous because both are available over the counter."
Dr. Tom MacDonald, who led the Lancet study, said taking the odd ibuprofen for a few days would not be a problem. It's regular use that seems to be at issue.
But the findings are not rock solid, experts said.
"This definitely raises a red flag ... but I don't think this can be viewed as the definitive answer on the question," said Dr. Veronique Roger, head of cardiovascular research at the Mayo Clinic in Rochester, Minn., who was not connected to the study.
It could be that heart patients who take ibuprofen have additional conditions that in turn make them more prone to premature death and were not accounted for in the study, she noted.