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The positions of the mitral and tricuspid valves before they start to close also change the intensity of S1. With a short PR interval, the wide-open valves close suddenly, causing a loud S1. With a long PR interval, the open valves take a longer time to float closed, resulting in a soft S1. The rhythm is usually regular, but it may become irregular at the slower heart rate.
The electrical impulse originates at the sinus node, so a P wave appears before each QRS complex. See Comparing ECGs.
Common among the elderly, sinus bradycardia may occur during sleep and with severe pain, inferior-wall myocardial infarction, and drugs such as digitalis and beta blockers. Elderly patients with healthy hearts tolerate slow heart rates well. Those with severe heart disease, however, may not be able to compensate for a slow rate, leading to low cardiac output.
Unless the patient has signs and symptoms of poor perfusion, observation is the only intervention. Before the patient receives effective pacing, 0. This dose may be repeated to a total dose of 3 mg. Identifying complete heart block When you listen to the heart of an elderly patient with complete heart block third-degree atrioventricular block , you hear an S1 whose volume changes with each beat.
It may be soft, intermediate, or loud. Thus, the PR interval varies, causing the loudness of S1 to vary. Under the control of separate pacemakers, the atria and the ventricles function independently of each other.
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In the elderly, complete heart block usually results from heart disease or drug toxicity. It also may result from an injury to the electrical conduction system during heart surgery. Complete heart block may be a medical emergency, with severe signs and symptoms of poor perfusion, shock, and a serious risk of cardiac arrest. A patient with poor perfusion will require a pacemaker. Selected references Cheitlin MD.
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Cardiovascular physiology—Changes with aging. Am J Geriatr Cardiol. Barbara A. I ma 64 years old woman. It most stores records of common user and of ambulatory Blood Pressure data. A reduction in LDL cholesterol of about 0. Epidemiological studies show regular fish consumers to be at lower risk of fatal CHD, including sudden death. Trans fatty acids are usually derived from industrial hydrogenation of monounsaturated or polyunsaturated fats and in some epidemiological studies dietary intake is positively related to the risk of CVD. Fruit and vegetable consumption in a meta-analysis of epidemiological studies is inversely related to risk of CHD 35 but, apart from one trial in hypertension, 36 there is no other randomised controlled trial evidence.
In the DASH dietary approaches to stop hypertension trial a diet rich in fruit, vegetables, and low fat diary products with reduced content of both total and saturated fat, reduced blood pressure.
A reduction of sodium intake, especially in the form of sodium chloride, will also reduce blood pressure 37 and is additive to the more comprehensive dietary intervention used in DASH. Randomised controlled trials of vitamin supplementation alpha-tocopherol or vitamin E , vitamin C, and beta-carotene retinol in coronary, stroke, and others at high cardiovascular risk have shown no benefit on CVD mortality or total mortality. A professional dietary intervention should be offered to all high risk people. The key elements of a cardiovascular protective diet are shown in table 5.
Alcohol consumption ranging between 1—3 alcohol units per day a unit equates to about 80 ml of wine, ml of normal strength beer, and 30—50 ml of spirits is associated with the lowest all cause mortality. Optimum consumption is lower for women than men. There is no evidence of any difference in cardiovascular benefit of any one source of alcohol compared with another.
A sedentary lifestyle is associated with an increased risk of CVD. In asymptomatic people aerobic physical activity and cardiorespiratory fitness are associated, in a dose response fashion, with a significant reduction in cardiovascular and all cause mortality. Physical activity, either at work or in leisure time, is associated with a lower risk of CHD in men and women.
The largest reduction in risk is between sedentary and moderately active individuals, with a more modest reduction between moderate and vigorous activity. This cardiovascular benefit is lost when physical activity is discontinued. Physical activity has a beneficial effect on other cardiovascular risk factors. Physical activity can prevent or delay the development of high blood pressure, 67— 69 increases HDL cholesterol concentration, and lowers the risk of developing diabetes.
So an organised programme of cardiovascular prevention and rehabilitation for people with CHD which addresses smoking, diet and physical activity, together with the management of other risk factors, and use of cardioprotective drug therapies, will reduce cardiac mortality and all cause mortality. Weight reduction interventions include dietary modification, increased physical activity, and some drug treatments, all of which are effective over the short term, especially when used together.
Caloric intake can be most efficiently reduced by reducing the consumption of high energy dense foods, especially saturated fats, refined carbohydrates, and some alcoholic drinks, and for the obese it will be necessary to restrict calories as well. Foods with a high fat content should be replaced with vegetables, fruit, and cereal products.
Increasing physical activity can make an important contribution to weight loss, in preserving a stable weight and in preventing weight gain. A sustained weight loss of around 0. Approved anti-obesity medications include: i inhibitors of intestinal fat absorption; and ii those acting on the central nervous system to suppress appetite, to reduce food intake, to increase satiety, or increase thermogenesis. In a meta-analysis, orlistat, an inhibitor of fat absorption, reduced weight by 2.
Gastrointestinal side effects were the most common side effect.
Volume XIII; Heart Block
In another meta-analysis sibutramine, a centrally acting drug, reduced weight by 4. All high risk people—people with established atherosclerotic disease, people with diabetes, and asymptomatic people at high total risk of developing CVD—should be given professional support to make lifestyle changes to prevent first or recurrent atherosclerotic events. In asymptomatic people without a history of CVD priority should be given to lifestyle table 5.
Indeed, for many people whose total CVD risk is not sufficiently high to justify pharmacotherapy at their present age, lifestyle intervention can be the only approach offered for CVD prevention. However, where the total risk of CVD is sufficiently high to justify more intensive intervention, or when the level of any one risk factor is already associated with target organ damage, lifestyle measures alone are usually not sufficient and drugs will be required to achieve targets table 6. As blood pressure increases so does the risk of stroke, CHD, and heart failure.
Lower intervention thresholds and lower optimal treatment targets are set for people at higher total CVD risk. The CVD risk associated with elevated blood pressure is determined by both the level of blood pressure and the presence of other risk factors for atherosclerotic disease. In the elderly up to 80 years the benefits of drug treatment for hypertension, including isolated systolic hypertension, have been clearly demonstrated. Meta-analyses and systematic reviews have consistently demonstrated that no one class of blood pressure lowering drug is any more effective than another at preventing CHD in people with treated hypertension—the benefit of treatment in preventing CHD being driven by the quality of blood pressure control.
In studies in which blood pressure control has been less effective than the comparator with ARB based therapy, 27 the rates of CHD have been higher with ARB based therapy. These observations confirm the importance of blood pressure control in the prevention of CHD and do not suggest any specific advantage or disadvantage of ARBs in preventing CHD relative to other classes of drug therapy, at equivalent levels of blood pressure control. Grades of hypertension are defined in table 7.
Measurements should be made under standardised conditions using accurate, validated, and well maintained monitors with an appropriate cuff size. All adults from 40 years onwards should have their blood pressure measured as part of an opportunistic CVD risk assessment in primary care. For people already on antihypertensive drug therapy at the time CVD risk is first estimated, the blood pressure level before drug treatment was started should always be used to estimate risk, not the blood pressure level on treatment.
If this measurement is not available assume the pre-treatment systolic blood pressure was at least mm Hg for the purposes of estimating total CVD risk. Those who are not found at this cardiovascular risk assessment to be at high total CVD risk, and are not started for other reasons on drug therapy to lower blood pressure, lipids or glucose, should have their blood pressure and risk assessment repeated, ideally within five years. For people with established atherosclerotic disease or diabetes the blood pressure level should be viewed in relation to the target blood pressure for this group.
The British Hypertension Society recommendations www. The average of two readings at each of several visits should be used to guide the decision to treat. Box 1: Blood pressure measurement by standard mercury sphygmomanometer or semiautomated device. Measure sitting blood pressure routinely: standing blood pressure should be recorded in elderly and diabetic people.
Remove tight clothing, support arm at heart level, ensure hand relaxed, and avoid talking during the measurement procedure. Take the mean of at least two readings; more recordings are needed if notable differences between initial measurements are found. For full details of methods, download references from www.
Heart Failure Therapies During Hospitalization
The period of observation is dependent on severity. In mild stage 1 uncomplicated hypertension, at least four pairs of measurements should be repeated over a period of 3—6 months. However, in people with CVD, target organ damage, or more severe hypertension, antihypertensive drugs should be initiated after weeks rather than months of observation.
The evaluation of blood pressure levels in older people can be more difficult. Older people show greater blood pressure variability and it is important that multiple measurements are taken on several occasions. Sitting and standing values should be taken to assess postural blood pressure changes in view of the high prevalence of orthostatic hypotension in this age group. Blood pressure thresholds for intervention with drug therapy are outlined in fig 3.
Risk thresholds and targets for blood pressure in asymptomatic people without CVD. Box 2: Target organ damage.