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As a general rule purchase detrol with paypal medicine reviews, most conjugated brain purchase detrol discount treatment 5th metatarsal fracture, heart cheap detrol 4mg amex treatment 360, liver, and kidney, and this enables a rapid onset drug metabolites are inactive, but a few exceptions exist. Drugs are distrib- uted more slowly to less perfused tissues such as skeletal Formation of Active Metabolites muscle and even more slowly to those with the lowest blood Many pharmacologically active drugs, such as the sedative- fow, such as skin, bone, and adipose tissue. Some agents, known as prodrugs, are Plasma Protein Binding administered as inactive compounds and then biotrans- Almost all drugs are reversibly bound to plasma proteins, formed to active metabolites. This type of agent is usually primarily albumin, but also lipoproteins, glycoproteins, and developed because the prodrug is better absorbed than its β-globulins. Orally administered prodrugs, such as fuid and cells, drug molecules dissociate from plasma pro- the antihypertensive agent enalapril (Vasotec), are con- teins to maintain the equilibrium between free drug and verted to their active metabolite by hepatic enzymes during bound drug. Plasma protein binding is saturable, and a drug can be First-Pass Biotransformation displaced from binding sites by other drugs that have a high Drugs that are absorbed from the gut reach the liver via the affnity for such sites. However, most drugs are not used at hepatic portal vein before entering the systemic circulation high enough plasma concentrations to occupy the vast (Fig. Many drugs, such as the antihypertensive agent number of plasma protein binding sites. Drugs administered by the sublingual or rectal route Molecular size is a factor affecting the distribution of undergo less frst-pass metabolism and have a higher degree extremely large molecules, such as those of the anticoagulant of bioavailability than do drugs administered by the oral heparin. Lipid solubility is a major factor affect- Drug biotransformation can be divided into two phases, ing the extent of drug distribution, particularly to the each carried out by unique sets of metabolic enzymes. In brain, where the blood-brain barrier restricts the penetra- many cases, phase I enzymatic reactions create or unmask a tion of polar and ionized molecules. Drugs that are absorbed from the gut can be biotransformed by enzymes in the gut wall and liver before reaching the systemic circulation. Oxidative reactions are the most duplication, and each family is divided into subfamilies, common type of phase I biotransformation. The hydroxylated metabolite may be the example, ethanol is oxidized to aldehyde by alcohol dehy- end product of the reaction or serve as an intermediate that drogenase, and caffeine and the bronchodilator theophyl- leads to the formation of another metabolite. These include cholinesterase and and their role in metabolizing specifc drugs elucidated. Many drugs are biotransformed by oxidative, hydrolytic, or reductive reactions and then undergo conjugation with endogenous substances. Nitroglycerin, a vasodilator, under- flavoprotein flavoprotein reductase goes reductive hydrolysis catalyzed by glutathione-organic nitrate reductase. Conju- 1 gation enzymes, which are present in the liver and other Cytochrome tissues, join various drug molecules with one of these endog- P450 enous substances to form water-soluble metabolites that are Oxidized form more easily excreted. Except for microsomal glucuronosyl- of P450 transferases, these enzymes are located in the cytoplasm. Drug-reduced Most conjugated drug metabolites are pharmacologically P450–O2 inactive. Glucuronide formation, the 4 most common conjugation reaction, uses glucuronosyl- transferases to conjugate a glucuronate molecule with the Oxidized drug parent drug molecule. Third, the drug- the potassium-sparing diuretic triamterene, whose sulfate reduced form of P450 (i. Chapter 2 y Pharmacokinetics 15 Pharmacogenomics Other Variations in Drug Metabolism Enzymes Since the completion of the Human Genome Project, About 1 in 3000 individuals exhibits a familial atypical it is now fully realized that there is a great degree of cholinesterase that will not metabolize succinylcholine, a individual variation, called polymorphism, in the genes neuromuscular blocking agent, at a normal rate. Modern genetic individuals are subject to prolonged apnea after receiving studies were triggered by rare fatalities in children being the usual dose of the drug. Individuals exhibit slow or fast acetylation of some drugs because of genetically determined differences in N- acetyltransferase. In Renal Drug Excretion individuals with one wild-type enzyme and one faulty Most drugs are excreted in the urine, either as the parent variant, an intermediate phenotype is observed. Drugs are handled by bution of these phenotypes varies from population to the kidneys in the same manner as are endogenous sub- population. About 15% of Asians, 50% of Caucasians and stances, undergoing processes of glomerular fltration, active Africans, and more than 80% of Mideast populations have tubular secretion, and passive tubular reabsorption. The relationship rhythmic agent procainamide, and the antihypertensive among these processes, the rate of drug excretion, and renal agent hydralazine. If a drug well characterized, and human populations of “extensive has a large fraction bound to plasma proteins, as is the case metabolizers” and “poor metabolizers” have been identifed. This gives rise to an increase, active tubular secretion by transport systems located pri- reduction, or complete loss of enzyme activity and to differ- marily in proximal tubular cells. This process is compe- ent levels of enzyme expression that result in altered rates titively inhibited by other drugs of the same chemical class. Because 40% of penicillin G is free (unbound), the free drug plasma concentration is 0. The drug fltration rate is calculated by multiplying the glomerular fltration rate by the free 1 drug plasma concentration: 100 mL/min × 1. The drug secretion rate is calculated by sub- 2 tracting the drug fltration rate from the drug excretion rate: 1200 mg/min − 120 mg/min = 1080 mg/min. This amount indicates that 90% of the drug’s excretion occurs 3 by the process of tubular secretion. The ratio of the nonionized form to the ionized form of the drug in the urine is equal to the antilog of the pKa minus the pH: antilog of 2. Because most of the drug is ionized in the urine, the drug reabsorption rate is probably less than 1 mg/min. It was determined by measuring the 4 drug concentration in urine and multiplying it by the urine fow rate. Note that the drug excretion rate is equal to the Urine drug fltration rate (120 mg/min) plus the drug secretion rate (1080 mg/min) minus the drug reabsorption rate (<1 mg/min). Most nonelectrolytes, including ethanol, are passively molecules are excreted only in negligible amounts. Ionized weak acids and bases gation, particularly with glucuronate, increases biliary are not reabsorbed across renal tubular cells, and they are excretion. The proportion of ionized the glucuronate and sulfate metabolites of steroids, are and nonionized drugs is affected by renal tubular pH, excreted in the bile. After the bile empties into the intestines, which can be manipulated to increase the excretion of a drug a fraction of the drug may be reabsorbed into the circulation after a drug overdose (Box 2-3). Excreted conjugated drugs can be hydrolyzed back to the parent drug by intestinal Biliary Excretion and Enterohepatic Cycling bacteria, and this facilitates the drug’s reabsorption. Thus, Many drugs are excreted in the bile as the parent com- biliary excretion eliminates substances from the body only pound or a drug metabolite. Biliary excretion favors to the extent that enterohepatic cycling is incomplete, that compounds with molecular weights that are higher than is, when some of the excreted drug is not reabsorbed from 300 and with both polar and lipophilic groups; smaller the intestine. These meters, the frst step is to establish a mathematical model procedures have been used to enhance the excretion of that accurately relates the plasma drug concentration to the drugs and poisons, but they are not without risk to the rates of drug absorption, distribution, and elimination.
Because of this difference generic detrol 1mg on-line treatments yeast infections pregnant, norepi- nephrine constricts all blood vessels discount detrol online visa symptoms magnesium deficiency, whereas epinephrine Catecholamines constricts some blood vessels but dilates others cheap detrol online amex symptoms joint pain fatigue. Isoproter- The naturally occurring catecholamines include norepi- enol is a selective β1- and β2-adrenoceptor agonist because nephrine, an endogenous sympathetic neurotransmitter; it has little affnity for α-receptors. Dobutamine primarily epinephrine, the principal hormone of the adrenal medulla; stimulates β1-receptors, with smaller effects on β2- and and dopamine, a neurotransmitter and the precursor to α-receptors. Lower doses of epinephrine produce greater stimula- tion of β2-receptors than α1-receptors, especially in the vascular beds of skeletal muscle, thereby causing vasodilation Catechol Ethylamine and decreasing diastolic blood pressure. It usually lowers the diastolic and mean arterial pressure, but it can R1 R2 increase the systolic pressure by increasing the heart rate and contractility. In patients with heart failure, this effect contributes to an increased Isoproterenol stroke volume and cardiac output (see Chapter 12). At slightly 3 higher doses, dopamine activates β1-adrenoceptors in the heart, thereby stimulating cardiac contractility and increas- Dopamine H H ing cardiac output and tissue perfusion. At even higher (D1 > β1 > α) doses, dopamine activates α1-adrenoceptors and causes vasoconstriction. Catecholamines can cause excessive vaso- constriction, leading to tissue ischemia and necrosis. The amine intravenous drug infusion or from the accidental injection nitrogen substitution (R2) determines the relative affnity for α- and of epinephrine into a fnger, such as when a patient is β-adrenoceptors, with larger substitutions (e. Note that dopamine has an even higher affnity for dopamine D receptors than for adrenoceptors. For this reason, dopamine is both a can cause hyperglycemia secondary to glycogenolysis, and direct-acting and an indirect-acting receptor agonist. Figure 8-4 compares the cardiovas- cular effects when norepinephrine, epinephrine, isoprotere- Specifc Drugs nol, and dopamine are given by intravenous infusion. The cardiovascular effects of norepinephrine primarily Shock is a condition in which the circulation to vital organs result from activation of α1-adrenoceptors. Activation is profoundly reduced as a result of inadequate blood produces vasoconstriction and increases peripheral resis- volume (hypovolemic shock), inadequate cardiac function tance, which in turn increases the systolic and diastolic blood (cardiogenic shock), or inadequate vasomotor tone (neu- pressure. Septic shock is associated blood pressure increases suffciently to activate the barore- with massive vasodilation secondary to the production of ceptor refex. It is sometimes called Epinephrine increases the systolic blood pressure but can “warm shock” to distinguish it from hypovolemic and increase or decrease the diastolic blood pressure. The increased cardiogenic shock, in which the patient’s extremities are systolic pressure results partly from an increased heart rate usually cold because of inadequate blood fow. The effect on diastolic pressure depends of septic shock, however, may also cause hypoperfusion on the relative stimulation of α1- and β2-adrenoceptors, and cold extremities. Norepinephrine, which is a potent vasoconstrictor, is Catecholamine drugs that increase blood pressure are used to treat septic shock and is often given to persons with called vasopressors. These drugs are used in treating shock cardiogenic shock when the response to dopamine is inad- when organ function is impaired because mean arterial equate or is accompanied by marked tachycardia. Hypovolemia should nephrine is also used to treat hypotension caused by decreased always be corrected by intravenous fuid administration peripheral resistance such as can occur in persons who have before the use of vasopressors, because vasopressors will not received excessive doses of a vasodilator drug. In cases of cardiogenic rine is also used for this purpose, as described later in this shock, mechanical devices (e. By producing bronchodilation and increas- performance while reducing myocardial ischemia and cardiac ing blood pressure, epinephrine counteracts the effects of work. Such devices are often used in conjunction with vaso- histamine and other mediators that are released from mast pressor drugs in the treatment of this condition. Epinephrine is used as a vasoconstrictor to reduce when patients remain hypotensive despite adequate fuid bleeding during surgery and to prolong the action of local administration. Dopamine is usually started at a dose of anesthetics by retarding their absorption into the general 2 mg/kg body weight per minute, and then the dose is circulation. Epinephrine is also used as a cardiac stimulant titrated to achieve the desired blood pressure. Although low in the treatment of cardiac arrest and ventricular fbrilla- doses of dopamine can increase urine output by augmenting tion. Isoproterenol is used to treat refractory bradycardia renal blood fow in normal subjects, ample evidence indi- and atrioventricular block when other measures have not cates that low doses of dopamine are usually not effective in been successful. Although it has been used to treat asthma, preventing and treating acute renal failure. The most effec- a selective β2-adrenoceptor agonist is usually preferred for tive means of protecting the kidneys in patients with shock this indication because it does not increase the heart rate as appears to be the maintenance of mean arterial pressure of much as isoproterenol. Comparison of the cardiovascular effects of four catecholamines when a low dose of each drug is given by intravenous infusion. The blood pressure recordings show systolic, diastolic, and mean arterial pressure. Peripheral resistance is expressed on an arbitrary scale, ranging from 0 to 4 units. The refex mechanism, adrenoceptors (α1, β1, and β2), or dopamine (D1) receptors responsible for changes in the heart rate and peripheral resistance are illustrated. Norepinephrine increases peripheral resistance and blood pressure, and this leads to refex bradycardia. Epinephrine increases heart rate while reducing peripheral resistance, and the mean arterial blood pressure increases slightly. Isoproterenol increases heart rate but signifcantly lowers peripheral resistance, and the mean arterial pressure declines. Dopamine increases heart rate (and increases cardiac output) while lowering vascular resistance, and the mean arterial pressure increases. Stings in the oropharyn- developed edema of the face, lips, eyelids, tongue, and geal area have a greater potential to cause airway obstruc- throat and experienced breathing diffculties. Paramedics tion and may require intubation and more aggressive administered subcutaneous epinephrine and transported the treatment than stings in other areas of the body. Hypersen- patient to the hospital, where he received intravenous dexa- sitivity reactions are mediated by immunoglobulin E, which methasone (a corticosteroid). The child previously had an cross-links antigens on mast cells and basophils, leading to allergic reaction to a bee sting that did not require hospital- the release of histamine and other chemical mediators that ization. Because of his respiratory distress, he was intubated cause edema and laryngospasm. The edema sub- hypersensitivity reactions (anaphylaxis) typically includes sided, and the boy was extubated and discharged in good epinephrine, antihistamine drugs, and corticosteroids. It is used as a cardiac stimulant to situations in which hypotension is caused by bradycardia. Albuterol and terbutaline can also be noncatecholamines are effective after oral administration given orally, and terbutaline is available for injection. They Phenylephrine are partly metabolized to inactive compounds before under- Pharmacokinetics. About 50% of albuterol is converted after oral or topical administration and can also be admini- to an inactive sulfate conjugate.
This is the time when the basic shape of internal organs and other structures is being established order detrol with american express treatment resistant depression. Because the fetus is especially vulnerable during the embryonic period purchase generic detrol medicine buddha, pregnant patients must take special care to avoid teratogen exposure during this time buy detrol 1mg low price symptoms diabetes type 2. Of the developmental processes that occur in the fetal period, growth and development of the brain are especially important. Disruption of brain development can result in learning deficits and behavioral abnormalities. Identification of Teratogens For the following reasons, human teratogens are extremely difficult to identify: • The incidence of congenital anomalies is generally low. Drugs whose teratogenicity has been documented (or at least is highly suspected) are listed in Table 7. It is important to note, however, that lack of proof of teratogenicity does not mean that a drug is safe—it only means that the available data are insufficient to make a definitive judgment. Conversely, proof of teratogenicity does not mean that every exposure will result in a birth defect. In fact, with most teratogens, the risk for malformation after exposure is only about 10%. To prove that a drug is a teratogen, three criteria must be met: • The drug must cause a characteristic set of malformations. Obviously, we cannot do experiments on humans to determine whether a drug meets these criteria. The best we can do is systematically collect and analyze data on drugs taken during pregnancy in the hope that useful information on teratogenicity will be revealed. Studies in animals may be of limited value, in part because teratogenicity may be species specific. Conversely, and more important, drugs that fail to cause anomalies in animals may later prove teratogenic in humans. In studies with pregnant animals, thalidomide was harmless; however, when thalidomide was taken by pregnant patients, about 30% had babies with severe malformations. The take-home message is this: lack of teratogenicity in animals is not proof of safety in humans. Thalidomide represents a fast-acting teratogen: a single dose can cause malformation. In contrast, alcohol (ethanol) must be taken repeatedly in high doses if gross malformation is to result. The best example is diethylstilbestrol, an estrogenic substance that causes vaginal cancer in female offspring 18 years or so after they were born. Behavioral changes are often delayed and therefore may not become apparent until the child goes to school. By this time, it may be difficult to establish a correlation between drug use during pregnancy and the behavioral deficit. Although we have been discussing the effect of teratogens, it is important to note that drug-related effects are not limited to the distortions of gross anatomy caused by teratogens. For example, benzodiazepines taken late in pregnancy may cause hypoglycemia and respiratory complications along with a hypotonic state that is commonly called floppy infant syndrome. Although the teratogen risk of aminoglycosides is low, children born to women taking streptomycin have been born with congenital deafness. According to this system, drugs can be put into one of five risk categories: A, B, C, D, and X (Table 7. Drugs in Risk Category A are the least dangerous; controlled studies have been done in pregnant patients and have failed to demonstrate a risk for fetal harm. In contrast, drugs in Category X are the most dangerous; these drugs are known to cause human fetal harm, and their risk to the fetus outweighs any possible therapeutic benefit. Drugs in Categories B, C, and D are progressively more dangerous than drugs in Category A and less dangerous than drugs in Category X. The law does not require classification of drugs that were in use before 1983, so many drugs are not classified. B Slightly more risk than A: Animal studies show no fetal risk, but controlled studies have not been done in women. C Greater risk than B: Animal studies show a risk for fetal harm, but no controlled studies have been done in women. D Proven risk for fetal harm: Studies in women show proof of fetal damage, but the potential benefits of use during pregnancy may be acceptable despite the risks (e. X Proven risk for fetal harm: Studies in women or animals show definite risk for fetal abnormality. Manufacturers of previously used drugs are allowed a transition period during which they may continue to use Pregnancy Risk Categories. Drugs approved before June 30, 2001 must remove the Pregnancy Risk Category letter while keeping other pregnancy labeling information. Human data Animal data Pharmacology Clinical Considerations Information is provided for the following five headings. Appendix A: Organization and Format for Pregnancy, Lactation, and Females and Males of Reproductive Potential Subsections. Pregnancy, Lactation, and Reproductive Potential: Labeling for Human Prescription Drug and Biological Products—Content and Format. It is crucial to include not only prescription drugs but also over-the-counter and nutritional supplements, as well as recreational drug use, at every visit. Vitamin A, which is designated Pregnancy Risk Factor X, can cause craniofacial defects and central nervous system, cardiac, and thymus abnormalities. If pregnancy status is unknown and a high-risk drug is recommended for management of a condition, a pregnancy test should be performed before prescribing. However, even with these disorders, in which drug therapy reduces the risk for disease-induced fetal harm, we must still take steps to minimize harm from drugs. Accordingly, drugs that pose a high risk for danger to the developing embryo or fetus should be discontinued and safer alternatives substituted. Some anticancer drugs, for example, are highly toxic to the developing fetus, yet cannot be ethically withheld from the pregnant patient. If a patient elects to use such drugs, termination of pregnancy should be considered. Reducing the risk for dangerous drug effects also applies to female patients who are not pregnant because about 50% of pregnancies are unintended. Accordingly, if a patient of reproductive age is taking a teratogenic medication, she should be educated about the teratogenic risk as well as the necessity of using at least one reliable form of birth control. Responding to Teratogen Exposure When a pregnant patient has been exposed to a known teratogen, the first step is to determine exactly when the drug was taken and exactly when the pregnancy began. Next, at least two ultrasound scans should be done to assess the extent of injury.
Syndromes
The drug undergoes extensive hepatic metabolism followed by excretion in the bile discount detrol online medicine zocor. Adverse Effects Blockade of alpha receptors can cause 1 orthostatic hypotension cheap detrol american express treatment 02 academy, reflex tachycardia discount detrol 4mg online treatment for depression, and nasal congestion. Patients should be educated about the symptoms of orthostatic hypotension and be advised to sit or lie down if they occur. Also, patients should be informed that orthostatic hypotension can be minimized by moving slowly when changing from a supine or sitting position to an upright position. About 1% of patients lose consciousness 30 to 60 minutes after receiving their initial prazosin dose. To minimize the first-dose effect, the initial dose should be small (no more than 1 mg). Patients who are starting treatment should be forewarned about the first-dose effect and advised to avoid driving and other hazardous activities for 12 to 24 hours. Administering the initial dose immediately before going to bed eliminates the risk for a first-dose effect. Terazosin Actions and Uses Like prazosin, terazosin is a selective, competitive antagonist at alpha -1 adrenergic receptors. Terazosin undergoes hepatic metabolism followed by excretion in the bile and urine. Adverse Effects Like other alpha-blocking agents, terazosin can cause orthostatic hypotension, reflex tachycardia, and nasal congestion. To minimize this first-dose effect, the initial dose should be administered at bedtime. Pharmacokinetics Doxazosin is administered orally, and peak effects develop in 2 to 3 hours. Adverse Effects Like prazosin and terazosin, doxazosin can cause orthostatic hypotension, reflex tachycardia, and nasal congestion. As with prazosin and terazosin, the first dose can cause profound hypotension, which can be minimized by giving the initial dose at bedtime. Tamsulosin Actions and Uses Tamsulosin [Flomax] is an alpha -adrenergic antagonist that causes “selective”1 blockade of alpha receptors on smooth muscle of the bladder neck (trigone and1 sphincter), prostatic capsule, and prostatic urethra; blockade of vascular alpha1 receptors is weak. Between 8% and 18% of patients experience abnormal ejaculation (ejaculation failure, ejaculation decrease, retrograde ejaculation). Drug Interactions Combined use with cimetidine increases tamsulosin serum levels, which may cause toxicity. Alfuzosin Actions and Uses Like tamsulosin, alfuzosin [Uroxatral, Xatral ] is an alpha blocker with1 selectivity for alpha receptors in the prostate and urinary tract. Pharmacokinetics Alfuzosin is formulated in extended-release tablets, and hence absorption is slow. In patients with moderate to severe hepatic impairment, alfuzosin levels increase threefold to fourfold. Although alfuzosin does not lower blood pressure much, combining it with other hypotensive agents could produce a more dramatic reduction. Silodosin Actions and Uses Silodosin [Rapaflo] is an alpha-adrenergic antagonist that selectively blocks alpha receptors in the prostate, bladder, and urethra. However, like tamsulosin, silodosin can greatly reduce or eliminate release of semen during orgasm. Although blockade of vascular alpha receptors is usually minimal, silodosin can produce dizziness, lightheadedness, and nasal congestion. Phentolamine Actions and Uses Like prazosin, phentolamine [OraVerse, Rogitine ] is a competitive adrenergic antagonist. However, in contrast to prazosin, phentolamine blocks alpha2 receptors as well as alpha receptors. Phentolamine has three approved1 applications: (1) diagnosis and treatment of pheochromocytoma; (2) prevention of tissue necrosis after extravasation of drugs that produce alpha -mediated1 vasoconstriction (e. Phentolamine1 blocks epinephrine-mediated vasoconstriction and thereby increases local blood flow, which increases the rate of anesthetic removal. Because it blocks alpha2 receptors, phentolamine produces greater reflex tachycardia than prazosin. If reflex tachycardia is especially severe, heart rate can be reduced with a beta blocker. Epinephrine should not be used because the drug can cause blood pressure to drop even further. In the presence of alpha1 blockade, the ability of epinephrine to promote vasodilation (through activation of vascular beta receptors) may outweigh the ability of epinephrine to cause2 vasoconstriction (through activation of vascular alpha receptors). Further1 lowering of blood pressure is not a significant problem with norepinephrine because norepinephrine does not activate beta receptors. However, unlike all of the other alpha-adrenergic1 2 antagonists, phenoxybenzamine is a noncompetitive receptor antagonist. Adverse Effects Like the other alpha-adrenergic antagonists, phenoxybenzamine can produce orthostatic hypotension, reflex tachycardia, nasal congestion, and inhibition of ejaculation. Reflex tachycardia is greater than that caused by prazosin and about equal to that caused by phentolamine. If dosage is excessive, phenoxybenzamine, like phentolamine, will cause profound hypotension. Furthermore, because hypotension is the result of irreversible alpha blockade, it cannot be corrected with an alpha agonist. To1 1 restore blood pressure, patients must be given intravenous fluids, which elevate blood pressure by increasing blood volume. P a t i e n t E d u c a t i o n Alpha -Adrenergic Antagonists1 Forewarn patients about first-dose hypotension. Advise them to sit or lie down if dizziness or lightheadedness occurs on standing. Teach patients to move slowly when changing from a supine or sitting position to an upright posture. Urge them to avoid driving and other hazardous activities for 12 to 24 hours after the initial dose. Reinforce the importance of taking the initial dose at bedtime to minimize the first-dose effect. Instruct them to hold the drug and notify the provider if sustained bradycardia or hypotension develop. Beta-Adrenergic Antagonists Therapeutic and Adverse Responses to Beta Blockade In this section we consider the beneficial and adverse responses that can result from blockade of beta-adrenergic receptors. Therapeutic Applications of Beta Blockade Practically all of the therapeutic effects of the beta-adrenergic antagonists result from blockade of beta receptors in the heart. Because of these effects, beta blockers are useful in a variety of cardiovascular disorders. Angina Pectoris Angina pectoris (cardiac pain due to ischemia) occurs when oxygen supplied to the heart through coronary circulation is insufficient to meet cardiac oxygen demand.
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