The two articles below are from American College of Sports Medicine and are position stands. Both of these articles are helpful for the heart patient to understand in the care and prevention of heart conditions. A couple of things to point out to the rehabilitating heart patient would be, the expected drop in blood pressure from exercise is 5-7 mmHg, but can remain lower for quite some time afterwards. This is why you must be alert for dizziness, lightheadedness, fainting, especially after getting up from lying or seated positions.
The article mentions controlled hypertension.Understand you blood pressure as there are levels of hypertension mild moderate and severe. Exercise is not recommended when blood pressure is elevated in the severe ranges. Most should focus their effort in keeping the intensity mild to moderate. This is harder than you think keeping exercise light to moderate, be patient.
The second article, yes there are risks involved with exercise and they can be life threatening. What can you do to lower the risk? The intensity of exercise is important to understand. Learn about MET levels and exercise intensity here after you finish reading the article.
Hypertension (HTN), one of the most common medical disorders, is associated with an increased incidence of all-cause and cardiovascular disease (CVD) mortality. Lifestyle modifications are advocated for the prevention, treatment, and control of HTN, with exercise being an integral component. Exercise programs that primarily involve endurance activity prevent the development of HTN and lower blood pressure (BP) in adults with normal BP and those with HTN. The BP lowering effects of exercise are most pronounced in people with HTN who engage in endurance exercise with BP decreasing approximately 5-7 mm Hg after an isolated exercise session (acute) or following exercise training (chronic). Moreover, BP is reduced for up to 22 h after an endurance exercise bout (e.g., postexercise hypotension), with the greatest decreases among those with the highest baseline BP.
The proposed mechanisms for the BP lowering effects of exercise include neurohumoral, vascular, and structural adaptations. Decreases in catecholamines and total peripheral resistance, improved insulin sensitivity, and alterations in vasodilators and vasoconstrictors are some of the postulated explanations for the antihypertensive effects of exercise. Emerging data suggest genetic links to the BP reductions associated with acute and chronic endurance exercise. Nonetheless, definitive conclusions regarding the mechanisms for the BP reductions following endurance exercise cannot be made at this time.
Individuals with controlled HTN and no CVD or renal complications may participate in an exercise program or competitive athletics, but should be evaluated, treated, and monitored closely. Preliminary peak or symptom-limited exercise testing may be warranted, especially for men over 45 and women over 55 yr planning a vigorous exercise program (i.e., ≥ 60% V̇O2R, oxygen uptake reserve). In the interim, while formal evaluation and management are taking place, it is reasonable for the majority of patients to begin moderate intensity exercise training (40-<60% V̇O2R) such as walking. When pharmacologic therapy is indicated in physically active people it should, ideally: a) lower BP at rest and during exertion; b) decrease total peripheral resistance; and, c) not adversely affect exercise capacity. For these reasons, angiotensin converting enzyme (ACE) inhibitors (or angiotensin II receptor blockers in case of ACE inhibitor intolerance) and calcium channel blockers are currently the drugs of choice for recreational exercisers and athletes who have HTN.
Exercise remains a cornerstone therapy for the primary prevention, treatment, and control of HTN. The optimal training frequency, intensity, time, and type (FITT) need to be better defined to optimize the BP lowering capacities of exercise, particularly in children, women, older adults, and certain ethnic groups. Based upon the current evidence, the following exercise prescription is recommended for those with high BP:
Frequency: on most, preferably all, days of the week
Intensity: moderate-intensity (40-<60% of V̇O2R)
Time: ≥ 30 min of continuous or accumulated physical activity per day
Type: primarily endurance physical activity supplemented by resistance exercise
Habitual physical activity reduces coronary heart disease events, but vigorous activity can also acutely and transiently increase the risk of sudden cardiac death and acute myocardial infarction in susceptible persons. This scientific statement discusses the potential cardiovascular complications of exercise, their pathological substrate, and their incidence and suggests strategies to reduce these complications. Exercise-associated acute cardiac events generally occur in individuals with structural cardiac disease. Hereditary or congenital cardiovascular abnormalities are predominantly responsible for cardiac events among young individuals, whereas atherosclerotic disease is primarily responsible for these events in adults. The absolute rate of exercise-related sudden cardiac death varies with the prevalence of disease in the study population. The incidence of both acute myocardial infarction and sudden death is greatest in the habitually least physically active individuals. No strategies have been adequately studied to evaluate their ability to reduce exercise-related acute cardiovascular events. Maintaining physical fitness through regular physical activity may help to reduce events because a disproportionate number of events occur in least physically active subjects performing unaccustomed physical activity. Other strategies, such as screening patients before participation in exercise, excluding high-risk patients from certain activities, promptly evaluating possible prodromal symptoms, training fitness personnel for emergencies, and encouraging patients to avoid high-risk activities, appear prudent but have not been systematically evaluated.
Regular physical activity is widely advocated by the medical community in part because substantial epidemiological, clinical, and basic science evidence suggests that physical activity and exercise training delay the development of atherosclerosis and reduce the incidence of coronary heart disease (CHD) events (1-4). Nevertheless, vigorous physical activity can also acutely and transiently increase the risk of acute myocardial infarction (AMI) and sudden cardiac death (SCD) in susceptible individuals (5-7). This scientific statement presents the cardiovascular complications of vigorous exercise, their pathophysiological substrate, and their incidence in specific patient groups and evaluates strategies directed at reducing these complications. The goal is to provide healthcare professionals with the information they need to advise patients more accurately about the benefits and risks of physical activity.
Most studies of exercise-related cardiovascular events have examined events associated with sports participation in young subjects and with vigorous exercise in adults. Vigorous exercise is usually defined as an absolute exercise work rate of at least 6 metabolic equivalents (METs), which is historically assumed to equal an oxygen uptake (V˙O2) of 21 mL·kg-1·min-1. Six METs approximates the energy requirements of activities such as jogging. Six METs is an arbitrary threshold and does not account for the fact that the myocardial oxygen demands of any physical activity are more closely related to the V˙O2requirements relative to maximal exercise capacity than to the absolute work rate per se. Consequently, exercise work rates < 6 METs may still place considerable stress on the cardiovascular systems of unfit and older individuals.
Can anger cause a heart attack to take place? You bet it can! For people who have underlying heart disease, the physical response to anger and rage can be lethal.
In a classic study at Harvard, researchers reported that the probability of suffering a heart attack in the two hours after an episode of anger increased two- to threefold.
One thing that always surprised me in cardiac rehabilitation was the understanding of using Nitroglycerin (nitro). I think over the years I saw and heard every way imaginable to ensure nitro tablet wouldn’t work if needed. Or the other one is when patients would carry it for years and then not use it when it is most appropriate to use. The take home message is if you are having discomfort that you suspect is heart related use a nitro ASAP.
Nitroglycerin dilates blood vessels that supply the areas of the heart where there is not enough oxygen thereby delivering oxygen to the heart tissue that needs it most. The dilation of veins and arteries reduces the amount of blood returning to the heart so that the heart does less work and requires less blood and oxygen. Dilation of the arteries lowers the pressure in the arteries against which the heart must pump. As a consequence, the heart works less and requires less blood and oxygen.
Here is the thing Nitro is a very volatile compound. It breaks down rapidly with light, heat, oxygen, time and exposure to plastic. It is packed in a glass vial because plastic will leach the active ingredient out of it and all you have left is the inert ingredients that hold the tablet together. Therefore don’t transfer it to a container that is plastic, don’t put a couple in a baggy and put them in your wallet. Yes it is a pain in the butt to carry the bottle everyday, but find a way, or use a metal nitro vial which you can wear around your neck.
Heat will break down the nitro tablets. If you carry your Nitro in your pants pocket every day the heat from your body will gradually make the nitro less potent. What I teach patients is to take a good marker and write on the bottle the date three months from when they started to carry the bottle. That is when it should be considered to replace. Sometimes it can go six months, but if you look at the bottle…hold it up to the light, don’t open it…and the tablets are looking powdery or crumbled….then replace the bottle. If you leave them in your pocket and they go through the dryer…time to replace. If you leave them in your car and your car is 100* or more…replace the bottle. That was a common one…”I leave them in the glove box in my car.” NO NO NO!
If you have opened the bottle you have exposed the tablets to oxygen. Oxygen breaks down the nitro. Once the bottle has been opened, label the bottle for six months from the time you opened it. Replace the bottle at six months. A story I would frequently hear that would make me cringe would be when a patients loved one or child would say ” I poured a couple in a paper cup and have them in my cupboard in case they need one while at my house”…UHG!!!! Won’t work sorry!
The bottle is brown to prevent sunlight from destroying the tablets as well. Don’t transfer them to any other bottle, there is a reason they come this way.
The most common mistake in using nitro is when patients would tell me the pain wasn’t bad enough to use it. The instructions for nitro don’t say wait until the discomfort is 9 out of 10, the instructions are to use the nitro if you have heart symptoms that do not go away with rest. This means any heart discomfort, no matter how minor if is present for 5 minutes, would indicate using the nitro. If you wait until you are really in pain, you probably will have damage done to the heart. The point of this drug is to prevent the damage to the heart by improving the blood flow preventing damage from occurring.
One discussion I frequently have with patients goes as follows: You may carry your nitro faithfully for years and never need it, but if and when you do need it, you want it to be fresh so it can work. On the other hand some will need to use occasional nitro. This isn’t a bad thing. Your physician prescribed it for a reason. Use it!!!! There are common times when people need one…Exposure to cold air, Exertion that is strenuous, Emotional Stress, and after Eating a large heavy meal. Where the medical community get concerned is if you are requiring 2-3 nitro to clear your symptoms, if you are having more frequent symptoms, or if your symptoms are coming on at rest or waking your from your sleep. The escalation in symptoms should be reported to your physician ASAP.
Keep a log of your nitro use. Put on your log, the date, what you were doing when the symptoms occurred, and how many nitro it took to clear the symptoms. When you have a followup appointment with either your cardiologist or your primary care physician present them with the log. Sometimes we are able to find a pattern, do your symptoms come on at a certain time of day? Thus we can probably adjust medication timing to prevent this. Do they come on with a certain level of exertion? We call this your angina threshold and we watch to see is the threshold improving or worsening. Often through exercise we can improve the angina threshold.
There are long acting nitroglycerin medications that slowly release nitro into your system throughout the day. These are usually taken during the hours you are up and active. Rarely are they used twice a day, as your body needs a period of time in which it is free of nitro, or else it gets to where the nitro doesn’t work as effectively. It is still ok to use the fast acting nitro if you are on this medication.
Take a Tylenol. The headache won’t kill you but the heart attack might.