Cardiovascular disease heart rate

Many drugs and surgical techniques now in use are able to decrease the death rate and improve the quality of life for persons suffering from heart disease. However, heart disease remains the number-one killer of Americans. Known medically as cardiovascular disease, heart disease results from any condition that decreases the flow of blood, and consequently oxygen, to the heart or diminishes the ability of the heart to beat regularly and function in a normal... 

Contraindications are the same as for immunotherapy for inhalant allergy, but are relative in nature because of the life-saving potential of venom immunotherapy. Elderly patients, especially with preexisting cardiovascular disease, are at a high risk to develop severe or even fatal anaphylaxis [26]. Therefore, venom immunotherapy is often recommended in patients over 50-60 years of age. Since (3-blocker treatment is associated with a significantly increased survival rate in patients with coronary heart... 

Disulfiram works by irreversibly blocking the enzyme aldehyde dehydrogenase, a step in the metabolism of alcohol, resulting in increased blood levels of the toxic metabolite acetaldehyde. As levels of acetaldehyde increase, the patient experiences decreased blood pressure, increased heart rate, chest pain, palpitations, dizziness, flushing, sweating, weakness, nausea and vomiting, headache, shortness of breath, blurred vision, and syncope. These effects are commonly referred to as the disulfiram-ethanol reaction. Their severity increases with the amount of alcohol that is consumed, and they may warrant emergency treatment. Disulfiram is contraindicated in patients who have cardiovascular or cerebrovascular disease, because the hypotensive effects of the disulfiram-alcohol reaction could be fatal in such patients or in combination with antihypertensive medications. Disulfiram is relatively contraindicated in patients with diabetes, hypothyroidism, epilepsy, liver disease, and kidney disease as well as impulsively suicidal patients. 

Traditional CNS stimulants have the potential to increase blood pressure and heart rate when used long term. In addition, excessive CNS stimulation can cause tremors and tics and can carry over into evening hours, where initiation of normal nighttime sleep can be disrupted. Caution should be used in patients with underlying cardiovascular or cerebrovascular disease and in patients with a history of seizures because stimulants may lower the seizure threshold. 

Cardiac effects Use atomoxetine with caution in patients with hypertension, tachycardia, or cardiovascular or cerebrovascular disease because it can increase blood pressure and heart rate. Measure pulse and blood pressure at baseline, following dose increases, and periodically while on therapy. 

Cardiovascular disease Acute administration of 2 drops of apraclonidine has had minimal effect on heart rate or blood pressure however, observe caution in treating patients with severe cardiovascular disease, including hypertension. 

Anesthesia induction with propofol causes a significant reduction in blood pressure that is proportional to the severity of cardiovascular disease or the volume status of the patient, or both. However, even in healthy patients a significant reduction in systolic and mean arterial blood pressure occurs. The reduction in pressure appears to be associated with vasodilation and myocardial depression. Although propofol decreases systemic vascular resistance, reflex tachycardia is not observed. This is in contrast to the actions of thiopental. The heart rate stabilization produced by propofol relative to other agents is likely the result of either resetting or inhibiting the baroreflex, thus reducing the tachy-cardic response to hypotension. 

Monitor patients with a cardiovascular disease for an increase in the frequency duration, or severity of angina or changes in blood pressure or heart rate... 

Atomoxetine also may increase heart rate and blood pressure and should be used with caution in patients with hypertension, tachycardia, cardiovascular disease, or cerebrovascular disease. Orthostatic hypotension also has been reported with atomoxetine therapy. 

Nitrous oxide has both a direct depressant and sympthomimetic effect on the myocardium. In healthy patients these tend to counterbalance each other, the resultant effect being minimal cardiovascular depression. In patients with car-diovascular disease or who are taking conconcurrent medication with, e.g. 3 blockers, its depressant effect may be more obvious. Nitrous oxide supplementation of high-dose opioid-based anaesthesia may result in a reduction in cardiac output and heart rate although the mechanism of this is unclear. Nitrous oxide may have a venoconstrictor effect resulting in increased pulmonary vascular resistance, particularly in the presence of pulmonary hypertension. 

Etomidate, when administered as the sole agent, produces little effect on cardiovascular function. It produces a slight reduction in systemic pressure and an increase in heart rate. Myocardial oxygen consumption is not significantly affected by etomidate. The drug does not release histamine and can be safely used in the presence of cardiorespiratory disease. 

Although ketamine produces direct myocardial depression, it has significant indirect cardiovascular effects through sympathomimetic effects and stimulation of the vasomotor centre. The heart rate and systolic blood pressure increase by 30% and occasionally up to 100%. Owing to the increased cardiac work and myocardial consumption, ketamine adversely affects the balance between myocardial oxygen supply and demand. Consequently, it is not recommended for use as the sole agent in adults with severe cardiovascular disease. However, the same haemodynamic effects, particularly the raised systemic vascular resistance, make the agent particularly suitable for children with cyanotic heart disease. 

A modest but not significant inverse correlation between the intake of flavonols and flavones and subsequent mortality rates was found in a prospective cohort study of US Health Professionals by Rimm et al [206]. The authors do not exclude that flavonoids have a protective effect in men with established coronary heart disease although strong evidence was missing. Also other studies failed to demonstrate a significant statistical association between the intake of polyphenols and CHD. In Great Britain for instance coronary and total mortality even rose with the intake of the major flavonol source, tea [207], The most likely explanation for the latter observation is that in this study tea consumption merely acted as a marker for a lifestyle that favours the development of cardiovascular disease. Indeed, men with the highest intake of tea and flavonols tended to be manual workers, and they smoked more and ate more fat [208],... 

Brief History. M.R. is a 48-year-old man with a history of coronary artery disease and cardiac rhythm disturbances. Specifically, he has experienced episodes of paroxysmal supraventricular tachycardia, with his heart rate often exceeding 180 beats per minute. He has been treated for several years with the nonspecific beta blocker propranolol (Inderal). Oral propranolol (60 mg/d) has successfully diminished his episodes of tachycardia. In an effort to improve his myocardial function and overall cardiovascular fitness, M.R. recently enrolled as an outpatient in a cardiac rehabilitation program. Under the supervision of a physical therapist, he attended cardiac training sessions three times each week. A typical session consisted of warm-up calisthenics, bicycle ergometry, and cool-down stretching activities. Each session lasted approximately 45 minutes. 

Hypertension is the most common cardiovascular disease. Thus, the third National Health and Nutrition Examination Survey (NHANES III), conducted from 1992 to 1994, found that 27% of the USA adult population had hypertension. The prevalence varies with age, race, education, and many other variables. Sustained arterial hypertension damages blood vessels in kidney, heart, and brain and leads to an increased incidence of renal failure, coronary disease, cardiac failure, and stroke. Effective pharmacologic lowering of blood pressure has been shown to prevent damage to blood vessels and to substantially reduce morbidity and mortality rates. Many effective drugs are available. Knowledge of their antihypertensive mechanisms and sites of action allows accurate prediction of efficacy and toxicity. As a result, rational use of these agents, alone or in combination, can lower blood pressure with minimal risk of serious toxicity in most patients. 

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