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This classification may prove useful in predicting both the efficacy and the toxicity of a specific agent (Brown and Wendel purchase 12.5 mg lopressor with visa heart attack history, 1989) discount lopressor 50 mg with mastercard blood pressure ranges too low. Antiarrhythmics have been classified into six classes according to their major mode of action or effect (Vaughan Williams purchase generic lopressor online arteria y vena histologia, 1984), as shown in Tables 3. Lidocaine Commonly used as an amide local anesthetic, lidocaine is also effective in the treatment of ventricular and supraventricular tachycardias. Lidocaine rapidly crosses the placenta and fetal levels reach about 50 percent of maternal levels within less than an hour 54 Cardiovascular drugs during pregnancy (Rotmensch et al. Lidocaine’s half-life is twice as long in the fetus/neonate (3 h) than in the mother (1. Importantly, most information available regarding pharmacokinetics of lidocaine in pregnant and postpartum women and newborns is from studies of regional or local anesthesia (Rotmensch et al. No published data are available on lidocaine from women who received the drug for cardiac arrhythmias. However, local anesthetics given in toxic doses may result in central nervous system and cardiac side effects in both the mother and the fetus. Lidocaine is not known to be ter- atogenic at acute therapeutic levels in humans or in chronic doses in animals (Fujinaga and Mazze, 1986; Heinonen et al. Toxicity risk is mini- mal when maternal lidocaine levels are maintained at less than 4 mg/mL (Bhagwat and Engel, 1995). Amide-type local anesthetics given for paracervical block are associated with spasm of the uterine arteries, causing decreased uterine blood flow. Procainamide Another amide compound, procainamide, is used to treat ventricular tachycardia. There is little information regarding the pharmacokinetics of this drug during pregnancy. However, it has been estimated that fetal levels are approximately one-fourth the mater- nal levels (Garite and Briggs, 1987). Scientific evidence of the safety of procainamide for use during pregnancy does not address possible human teratogenicity. However, given the safety profile of a closely related drug (lidocaine), procainamide seems to not pose a great risk when used during pregnancy (Little and Gilstrap, 1989). Chronic use of this drug should be avoided, unless necessary for life-threatening conditions, because a lupus-like syndrome may occur (Rotmensch et al. Breastfeeding is not contra- indicated in mothers on procainamide (American Academy of Pediatrics, 1994). Encainide and flecainide Two other lidocaine-related antiarrhythmic medications are encainide and flecainide. Encainide was not teratogenic in rats and rabbits when given at doses up to 9 and 13 times the human dose (data from the manufacturer’s insert). Flecainide has been reported to cause teratogenic and embryotoxic effects in some species of rabbits when given in doses four times the usual adult dose. It was not, however, teratogenic in rats, mice, and other species of rabbits when given in the usual adult dose, according to its manufacturer. Flecainide has been used to treat fetal arrhythmias, but fetal deaths have occurred with this treatment. Given the alternative related medications available, fle- cainide should be avoided, or at least the drug of last resort when others have failed. Tocainide Tocainide is another amide antiarrhythmic agent, closely related to lidocaine. It was not teratogenic in animals at doses several times the usual adult dose, but it may be embry- otoxic. There are no human studies during pregnancy, but it is closely related to lido- caine and its data may be extrapolated to tocainide. Antiarrhythmics 55 Disopyramide Similar in action to quinidine, disopyramide is used to treat supraventricular and ven- tricular arrhythmias. Dysopyramide crosses the placenta readily, with fetal levels approximately half those of the mother (Rotmensch et al. The drug was embryo- toxic in laboratory animals when given at several times the human dose, but no pattern or specific malformations were noted (data from the manufacturer’s insert). Disopyramide use during the third trimester has been associated with premature onset of labor (Leonard et al. Bretylium This drug is primarily indicated for life-threatening ventricular arrhythmias, such as ven- tricular tachycardia and ventricular fibrillation. Bretylium was reported to be ‘without effect’ in one rat study published by West (1962). Amiodarone This drug is used primarily to treat life-threatening ventricular arrhythmias (e. Amiodarone has limited ability to cross the placenta, with newborn concentrations reaching only 10–25 percent of maternal serum levels (Rotmensch et al. Of six pregnancies exposed to amiodarone after 10 weeks ges- tation, hypothyroidism (n = 2) and small size for gestational age (n = 4) was observed (Magee et al. Learning disabilities were unusually frequent in two small series of children exposed to amiodarone during gestation (Bartalena et al. When administered chronically during pregnancy, fetal goiter is a major risk after 10 weeks gestation. Fetal death is consistently reported in animal studies of the drug dur- ing pregnancy. A possible association between fetal cretinism has also been suggested, especially from direct fetal injection (Pinsky et al. Otherwise, the frequency of congenital anomalies was not increased among 30 infants exposed to amiodarone dur- ing the first trimester (Bartalena et al. Mexiletine Similar in action to lidocaine, mexiletine is a local anesthetic type of antiarrhythmic agent (Zipes and Troup, 1978). Mexiletine is used primarily to treat ventricular arrhyth- mias (ventricular tachycardia, premature ventricular contractions). No studies of con- genital anomalies in infants exposed to mexiltene have been published. A few anecdotal case reports suggest no adverse effects on the fetus or on labor, but the importance of such observations is not clear. Mexiletine was not teratogenic in various laboratory ani- mals (data from the manufacturer’s insert). Cord blood concentrations of this drug were similar to maternal levels, and therapeutic levels may be found in breast milk (Timmis et al. However, breastfeeding is not contraindicated when the mother is using mexiletine (American Academy of Pediatrics, 1994). Verapamil is used to transplacentally treat fetal supraventricular tachycardia (Klein and Repke, 1984; Rey et al. Verapamil should be used with caution in pregnant patients because it might reduce uterine blood flow by 25 percent or more (Murad et al. Importantly, 10–20 percent of neonates who received this drug intraveneously for supraventricular tachycardia and congestive heart failure devel- oped cardiac depression and cardiac arrest (Kleinman and Copel, 1991). Therefore, ver- apamil is not recommended for use in infants of less than 1 year (Garson, 1987).

A high renin level is consistent with renal artery stenosis cheap 50 mg lopressor mastercard heart attack labs, but not diagnostic of it order 100 mg lopressor amex blood pressure medication ok for pregnancy. Hypervolumic or hyperviscosity states are extremely rare and order generic lopressor 2013, when present, are usually associated with other chemical and laboratory findings. Unfortunately, 95% or more cases of hypertension in the general population remain without a definitive cause (primary or essential hypertension). Since most cases fall in the "mild" category and can be controlled with readily available drugs, a search for underlying causes is now usually reserved for those patients who are young, whose hypertension is very resistant to usual medication or to patients with clinical clues suggesting one of the above -mentioned conditions 1. The consequences of prolonged hypertension can be identified at 3 sites: 1) Cardiac 2) Large Arteries and 3) Small Arteries. The increased cardiac work determined by the higher pressure at time of onset of ejection (arterial diastolic pressure) rising to peak systolic pressure requires increased myocardial O2 delivery. With the development of myocardial hypertrophy in response to increased pressure, the need for O2 is augmented. Over a prolonged course of severe hypertension the myocardial effort fails, ejection fraction falls, ventricular diastolic filling pressures rise and myocardial dilatation occurs. This sequence of events defines the hemodynamics of left-sided congestive heart failure, an important complication of hypertension. The ventricular combination of pressure load, hypertrophy and dilatation (through the Laplace relationship) all augment left ventricular O2 demand and make the myocardium more vulnerable to ischemic lesions (angina pectoris, myocardial infarction). The elevated mean pressure within the larger arteries is traumatic to the endothelial cells and plays an important role in accelerating atherosclerosis. At any given pressure, any increase in radius of the aorta increases wall tension so that a positive feedback loop occurs, whereby the wall tension -and the aortic distention -- increase at a faster rate as the aneurysm (dilated segment) enlarges. In the brain, arteries are thinner-walled than elsewhere, and defects in continuity of the arterial muscular media Hypertension - Stanley Rockson, M. These loci may burst in hypertensives, leading to hemorrhagic stroke and loss of function or death. When hypertension is severe, it may enter a phase of severe elevation of pressure (e. In the kidney it leads to acute renal failure and multiple ischemic areas which in turn cause increased renin release, further raising blood pressure and peripheral resistance. In the brain, the weaker blood vessel walls, although also showing vasospasm (actually visible in the ocular fundus where smaller retinal artery branches --visible with the ophthalmoscope -- are of arteriolar size and show focal spasm) are less able to resist the higher pressures and edema formation occurs. Combinations of edema and focal hemorrhages are seen in the optic fundus (remember, that the retina, through the optic nerve, is an extension of the brain) and in sections of the brain at post-mortem when individuals die secondary to malignant hypertension. The treatment of hypertension is rationally based upon attempts to reduce venous return, to reduce myocardial contractility and to cause arterial vasodilatation. The use of diuretic agents causes enhanced urinary loss of Na+ and H2O and thus reduces venous return and cardiac output. The -receptor blockers, by their competition at 1 receptors in the heart, cause reductions in cardiac output and have been used with great success to treat hypertension. However, their blockade of 2 receptors in the periphery might be expected to leave  receptors unopposed, thus tending to raise arterial pressure. Ca++-antagonists, nitrates, sodium nitroprusside) cause a direct lowering of peripheral resistance and of blood pressure. Other substances counteract the sympathetic nervous system at the central or peripheral level to lower peripheral resistance. Newer agents are now available which block peripheral angiotensin by competition (Saralasin) or by inhibition of angiotensin converting enzyme (Captopril), blocking the conversion Hypertension - Stanley Rockson, M. Such agents can be used as physiologic probes to determine the relative role of the renin- angiotensin system in the genesis of hypertension in a single patient. Ultimately the test of any therapeutic program is its antihypertensive effect balanced against its economic and biologic cost. As may be imagined, fatigue (due to low cardiac output, excessive diuresis and potassium loss), postural hypotension (syncope) and interference in other autonomically regulated functions (leading to impotence) may compromise the desirability of any therapeutic program. On a stroke-by- stroke basis, stroke volume, cardiac contractility, aortic compliance, heart rate and peripheral resistance all play parts in the shape and magnitude of the cyclic arterial pressure curve. These determinants change with age, activity and super imposed pathologic events affecting the heart, its valves and the circulatory system. Mean blood pressure over longer periods is affected by mean cardiac output and total peripheral resistance. Any change is sensed by short and longer-acting feedback regulatory systems -- which normally act to maintain arterial pressure at a level compatible with optimal cardiac output to all organs, but particularly the brain -- in an upright posture. The carotid sinus responds on a beat-to-beat basis and offers protection from abrupt postural variations. It "resets" after several days at higher pressure and is therefore not a useful defense against chronic hypertension. Longer-acting regulation depends upon the kidney, which through the renin-angiotensin system, can provide significant rise in peripheral resistance in response to hypotension of the renal circulation. Conversely, long-term systemic hypertension can ensue if a kidney is ischemic secondary to pathologic stenosis of the renal artery. Autoregulation may be involved if the hypertensive state is brought about by increased cardiac output. A rise in peripheral resistance (afterload) would then return output and perfusion to normal at the price of persistent hypertension. The consequences of sustained hypertension are the development of myocardial hypertrophy and eventual congestive heart failure, the increased rate of a atherosclerosis of large and medium- sized arteries, as well as the tendency for distention and rupture of those vessels, and finally, malignant hypertension with severe arteriolar vasospasm, loss of vision and cerebral edema. Drug treatment of hypertension is addressed to the physiologic determinants when no primary cause can be found and removed. Diuretics, 1-blockers and vasodilators compose the majority of effective agents and respectively lower venous return, myocardial contractility (output) and peripheral arterial resistance. It is important to have covered this area but a great deal of emphasis is not necessary compared with other cardiac diseases such as valvular and coronary artery disease. You should know the physiologic effect of pericardial effusions and also that of chronic, healed pericarditis. It is thought, however, that clinically the incidence is much higher and that in many cases the disease is subclinical and can regress and the patient recover fully. There is some circumstantial evidence only that myocarditis may lead to cardiomyopathy. Myocarditis can be caused by bacterial, rickettsial, viral, protozoal and parasitic, fungal and spirochetal agents. In myocardial lesions associated with infectious diseases, the inflammation may be due to an actual invasion of the myocardium by the organisms or to the action of their toxins, although it is possible that an allergic mechanism is responsible in some cases. Gross: The gross appearance of the heart in acute myocarditis is not distinctive, but usually the myocardium is pale and flabby and the chambers are dilated. Abscesses may appear as small yellow or streaky foci occasionally become confluent. In some cases small abscesses may form in the myocardium such as in staphylococcal bacterial endocarditis while interstitial inflammation is minimal.

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Depending on how much of the drug has been used for how long order lopressor toronto blood pressure zones, withdrawal symptoms can be mild or strong lopressor 50 mg for sale blood pressure levels exercise. Mild cases may simply involve trembling buy cheapest lopressor blood pressure 200 over 120, reduced appetite, and trouble falling asleep. In bad cases a person can experience per- spiration, muscle cramps and tremors, vomiting, and convulsions. Sudden stoppage of long-term diazepam dosage can provoke seizures, so doses need to be tapered off instead. Effect of a diazepam dose can be lengthened by propoxyphene and by the ulcer drugs omeprazole and cimetidine. The 120 Diazepam more tobacco cigarettes people smoke, the less drowsy diazepam makes them. Body weight also affects diazepam actions, with drug build-up and elimina- tion taking longer in bodies of fatter people. Experimenters have even found that drug effects can vary by time of day; at night diazepam prolongs the presence of an ibuprofen dose. Experimentation shows diazepam to have potential for causing cancer in mice, results causing researchers to suspect the same possibility in humans. Ex- amination of medical records from almost 13,000 diazepam users found no link to a higher cancer rate. Several other investigations found no connection between the drug and assorted human cancers, but results have been mixed on association with ovarian cancer. Hamsters receiving the drug during pregnancy can produce off- spring with cleft palate and other skull abnormalities. Diazepam experiments with rats have re- sulted in fewer pregnancies and higher death rates for pups. Some rat exper- iments produce birth defects and some do not; size of dose may be important. If pregnant mice receive the drug, their male offspring may have difficulty with sexual functioning as adults. They also may act more nervous than pups who lack fetal exposure, although rats that have no fetal exposure, but instead receive multiple doses soon after birth, act less uneasy in later life after dosage has stopped. A number of rodent studies find that prenatal ex- posure to diazepam may produce assorted behavioral effects that do not ap- pear until adolescence or adulthood. Those effects are measured by various tests (running mazes and the like) that are difficult to extrapolate to human experience, but the point is that diazepam’s effects may be unapparent in newborns and take years to emerge. A study of 689 pregnant women taking assorted antidepressants was unable to attribute any birth defects to diazepam, and the same results came from a smaller study; but nonetheless the drug is suspected of causing malformations. Measurements from pregnant women indicate that diazepam passes to the fetus and builds up there; blood levels of the drug in newborns can be higher than the mother’s. A case report notes severe multiple malformations in an infant whose mother used diazepam during pregnancy but does not establish cause and effect. Researchers tracked medical histories of several thousand women whose babies had major malformations and found an association between diazepam and cleft lip, the association becoming even stronger if women had smoked while taking diazepam during pregnancy. Additional research has associated diazepam with birth defects involving the heart, stomach obstruc- tion, and hernia. In- deed, other research has found no association between diazepam and cleft lip or any other congenital malformation. One study found that newborns with fetal exposure to diazepam tend to weigh less than normal, but they soon gain weight and reach a normal level. Infants have exhibited withdrawal symptoms Diazepam 121 if their mothers used diazepam during pregnancy; those symptoms may not appear immediately after birth. Nursing mothers are advised to avoid the drug, which can continue to pass into breast milk long after drug use is halted. The drug can build up in babies, enough that they can be sedated by milk from mothers using diazepam, and the infants may lose weight while nursing. Methaqualone and diazepam each have the nick- name “Ludes,” but the drugs are different substances. Humans find the drug’s effects similar to those of dextroamphetamine but at a weaker level. One experiment found dextroamphetamine 6 to 11 times stronger than diethylpropion when given orally, 10 to 20 times stronger when given by subcutaneous injection. Although diethylpropion was created in the 1920s, this amphetamine derivative was not marketed for weight loss until around 1960. The compound breaks up sleep and interferes with dreaming but has fewer stimulant effects than some other anorectics. Users feel less fatigue than with fenfluramine, and undesirable effects of diethylpropion disappear faster than those of fenfluramine when the drug is stopped. Studies of weight loss patients using diethylpropion found only trivial impact on heart rate or blood pressure, and the compound is considered a good choice for patients with high blood pressure. Diethylpropion has been used experimentally to reduce craving for cocaine, with some success. Some researchers question that finding, however, pointing out that craving for cocaine diminishes in a hospital setting regardless of Diethylpropion 123 whether patients receive diethylpropion or a placebo. In a two-week study, former crack cocaine users receiving diethylpropion showed no change in tests of thinking abilities. That result is interpreted as meaning that short-term use of diethylpropion may cause no measurable harm to brain function. Patients experienced increase of comfort but no increase in ability to use af- fected joints. In a study of 132 patients taking the drug, about 3% had experiences such as euphoria, muscle tremors, or trouble with sleeping. As- sorted scientific reports indicate the drug rarely has untoward physical effects; the medical literature mentions an addict who ingested 30 to 100 times the recommended amount each day without major impact. Diethylpropion is suspected of being involved in a case where someone suffered minor strokes (transient ischemic attacks), is suspected of contributing to a case of heart trouble, and is known to cause heart trouble if an overdose is taken. A rare affliction ascribed to the drug is overdevelopment of the vestigial male mammary glands. One user felt under assault from persons using mental telepathy; another heard voices; another thought a television set was observing her; an- other began worrying about someone using the “evil eye” to kill a child. In some cases those problems ceased after the diet drug stopped; in others the affliction reappeared. A therapist reporting on the latter type of cases sus- pected that the persons would have developed psychosis regardless of whether they used diethylpropion. The typical sufferer is a female 25 to 40 years old, leading a troubled life with a history of mental instability and drug abuse. Drugs abused by these women often include amphetamines, an im- portant factor because a former amphetamine abuser who later takes another stimulant can quickly shift back into the old abuse mode. Often such persons begin taking diethylpropion to help them lose weight but afterward continue taking it for pleasurable psychic effect. That special group’s experience, how- ever, is not commonplace among users in general. The drug’s amphetamine-type effects are strong enough to have produced an illicit market for diethylpropion in the 1960s, but large surveys determining levels of abuse for various drugs yielded no mention of diethylpropion during the drug’s peak of popularity in the mid-1970s.

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