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Many conditions used as an adjunct to electroconvulsive therapy to prevent involving muscle weakness order 60mg dapoxetine fast delivery, such as paralysis caused by spinal injuries that might be caused by involuntary muscle contrac- cord injury order dapoxetine 30mg line, also present an increased risk of hyperkalemia tions buy dapoxetine 30 mg. Succi- (A) hallucinations nylcholine can also cause postoperative myalgia cheap dapoxetine 90 mg amex, particularly (B) bronchospasm in the muscles of the neck, back, and abdomen. This effect (C) hyperthermia probably results from the muscle fasciculations produced by (D) urinary retention the drug. Finally, succinylcholine has been associated with a (E) blurred vision rare complication known as malignant hyperthermia, 3. Topical ocular administration of tropicamide will cause which is also associated with inhalation anesthetics (see (A) contraction of the ciliary muscle Chapter 21). The therapeutic use of darifenacin is based on its • Muscarinic acetylcholine receptor antagonists relax ability to smooth muscle, increase heart rate and cardiac con- (A) relax bronchial smooth muscle duction, and inhibit exocrine gland secretion. They are also used to reduce Answers And explAnAtions salivary and respiratory secretions and to produce mydriasis and cycloplegia. Succinylcholine is the • Atropine toxicity can cause dryness of the mouth and only depolarizing neuromuscular blocking agent that skin, blurred vision, tachycardia, palpitations, urinary produces persistent depolarization of the motor end plate, retention, delirium, and hallucinations. Cholinesterase inhibitors, acting to increase depolarizing neuromuscular blocking agents known as acetylcholine levels, do not counteract the muscle curariform drugs, such as rocuronium and cisatracu- paralysis produced by succinylcholine and can actually rium. These drugs are used to produce muscle relax- increase the degree of paralysis by prolonging muscle ation during surgery. They do not cause muscle such as atropine and scopolamine cause relaxation of fasciculations, and their effects can be reversed by bronchial smooth muscle and bronchodilation. It produces Scopolamine causes blurred vision by relaxing the muscle fasciculations that are followed by muscle ciliary muscle, thereby producing cycloplegia (paralysis of paralysis. Tropicamide binds to muscarinic receptors and competi- tively blocks acetylcholine released by the parasympa- review Questions thetic oculomotor nerve. This action leads to relaxation of the iris sphincter muscle and dilation of the pupil 1. Which drug produces transient muscle fasciculations (mydriasis), thereby facilitating ophthalmoscopic exami- followed by muscle paralysis that is not reversed by nation of the peripheral retina. It is not (C) cisatracurium used to relax uterine, gastrointestinal, or bronchial smooth (D) succinylcholine muscle. The receptor subtypes have been cloned Catecholamines and their molecular structures determined. The α1-adrenoceptors are pri- • Norepinephrine marily located in smooth muscle at sympathetic neuroeffec- tor junctions, but these receptors are also found in exocrine Noncatecholamines a glands and in the central nervous system. Three main sub- • Albuterol (Proventil, Ventolin) b types of α1-adrenoceptors have been identifed (α1A, α1B, and • Apraclonidine (Iopidone) c α1D), but the functional roles of these receptors have not • Clonidine (Catapres) been clearly established. The α2-adrenoceptors are widely • Midodrine (Proamatine) distributed in presynaptic neurons, various tissues, and blood • Oxymetazoline (Afrin) platelets (see Fig. Indirect-Acting Adrenoceptor Agonists The α1-adrenoceptors mediate contraction of vascular • Amphetamine smooth muscle, the iris dilator muscle, and smooth muscle • Cocaine in the lower urinary tract (bladder, urethra, and prostate) and other tissues. The α2-adrenoceptors located on sympathetic Mixed-Acting Adrenoceptor Agonists postganglionic neurons serve as autoreceptors whose activa- • Ephedrine tion leads to feedback inhibition of norepinephrine release • Pseudoephedrine (Sudafed) from nerve terminals. The α -receptors are also found in 2 aAlso fenoterol (Berotec), formoterol (Foradil), arformoterol (Brovana), blood platelets and in ocular, adipose, intestinal, hepatic, levalbuterol (Xopenex), pirbuterol (Maxair), salmeterol (Serevent), and renal, and endocrine tissue. The adrenoceptor agonists are a large group of drugs whose Activation of β1-adrenoceptors produces cardiac stimula- diverse pharmacologic effects make them valuable in the tion, leading to a positive chronotropic effect (increased treatment of a wide spectrum of clinical conditions, ranging heart rate), a positive inotropic effect (increased contr- from cardiovascular emergencies to the common cold. The spec- ptors also increases renin secretion from renal juxtaglo- trum of effects produced by a particular adrenoceptor merular cells. For example, epi- epinephrine are equally potent at β1-receptors in cardiac nephrine and norepinephrine are more potent than tissue, epinephrine is more potent than norepinephrine at isoproterenol at adrenoceptors in smooth muscle, and these β2-receptors in smooth muscle. These recep- noceptors in cardiac tissue and these receptors were called tors appear to mediate lipolysis (breakdown of triglycerides β-adrenoceptors. Selective agonists have been β-adrenoceptors have been identifed on the basis of several identifed but not yet developed for clinical use. Whereas α1- and β2-adrenoceptors are primarily located in smooth muscle, β1-adrenoceptors are predominantly found in cardiac tissue. Some α2-adrenoceptors are located on sympathetic neurons, where they produce feedback inhibition of neurotransmitter release. Other α2- and β2-adrenoceptors are located in blood platelets and a variety of organ tissues. The Dopamine receptors are activated by dopamine but not by antihypertensive effect of clonidine appears to result from other adrenoceptor agonists. The subtypes of dopamine activation of both α2-adrenoceptors and imidazoline recep- receptors include D1 receptors, which mediate vascular tors in the central nervous system, leading to a reduced smooth muscle relaxation, and D2-receptors, which modu- sympathetic outfow to the heart and vascular smooth late neurotransmitter release. The pharmacologic properties of clonidine and agonist used in treating acute severe hypertension (see related drugs are discussed in Chapter 10. By this action, α1-adrenoceptor agonists cause vasoconstric- Tyrosine Sympathetic tion and increase blood pressure. This action reduces aqueous humor secretion in the eye and elicits the other effects of α2-adrenoceptor Cocaine agonists. The cellular response depends on the specifc proteins that are phosphorylated in each tissue. In cardiac Direct-acting tissue, calcium channels are phosphorylated, thereby aug- agonists menting calcium infux and cardiac contractility. Mechanisms of indirect-acting and direct-acting adrenocep- multiple targets; including potassium channels, calcium tor agonists. Cocaine blocks norepinephrine reuptake by the catecholamine channels, and myosin light chain kinase (see Fig. Amphetamine inhibits the storage of norepinephrine by neu- ronal vesicles, leading to reverse transport of norepinephrine into the synapse by the catecholamine transporter. The adrenoceptor agonists mimic the effect of sympathetic nervous system stimulation and are sometimes called sym- pathomimetic drugs. Each catecholamine Figure 8-2, the indirect-acting agonists increase the stimu- consists of the catechol moiety and an ethylamine side lation of adrenoceptors by increasing the concentration of chain (Fig. For this reason, these drugs have sympathetic neuron and thereby decreases the neuronal low oral bioavailabilities and short plasma half-lives, and reuptake of norepinephrine and increases its synaptic they must be administered parenterally when a systemic concentration. Amphetamine and related drugs are trans- action is required (such as in the treatment of anaphylactic ported into the sympathetic nerve terminal by the catechol- shock). As shown in Figure 8-3 and amphetamines inhibit the storage of norepinephrine by Table 8-2, the various catecholamines differ in their affni- neuronal vesicles. The size of the alkyl tion of norepinephrine, leading to reverse transport of substitution on the amine nitrogen (R2) determines the rela- norepinephrine into the synapse by the catecholamine trans- tive affnity for α- and β-adrenoceptors. Epinephrine is a potent agonist at all α- and Direct-Acting Adrenoceptor Agonists β-adrenoceptors. Norepinephrine differs from epinephrine The direct-acting agonists include several catecholamines only in that it has greater affnity for β1-adrenoceptors than and various noncatecholamine drugs. Because of this difference, norepi- nephrine constricts all blood vessels, whereas epinephrine Catecholamines constricts some blood vessels but dilates others. 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.
This child probably has celiac disease order dapoxetine 90 mg otc, an immune-mediated inflammation of the small intestine in response to dietary gluten buy cheap dapoxetine 90mg. The symptoms in this patient began when additional items were added to the diet around 6 months of age cheap dapoxetine 90 mg mastercard. Commercial formulas are typically gluten free cheap dapoxetine 90mg line, so symptoms will typi- cally appear between 6 and 24 months of age once parents introduce gluten- containing foods. While presentation in childhood is “classic,” many children and adults will first present at an older age, some with constipation, with bulky and foul-smelling stools. Antibody screening has become quite reliable, but diagnosis requires a duodenal biopsy, and must be done while the child is on a gluten-containing diet. The most common causes of rectal bleeding in the infant period are a milk protein allergy and an anal fissure. The patient in the case presenta- tion has no physical examination finding, so milk protein allergy is more likely. However, with a normal physical examination and no emesis, this diagnosis is unlikely. The abdominal pain is periumbilical, started 12 hours prior, is 9 out of 10 on the pain scale, and is constant, dull, and achy in nature. The acetaminophen her mother gave her did not reduce the pain, but is diminished only by lying supine. She is not hungry and has had one episode of nonbilious emesis 2 hours after the onset of the pain and one small, loose bowel movement. She denies dysuria, urinary frequency, and her last menses a week ago was normal; she denies having any sexual contact. On examination, she appears uncomfortable, has a heart rate of 110 beats/min, and a temperature of 100°F (37°C). Her abdominal examination reveals hypoactive bowel sounds, right rectus abdominis muscle rigidity, and tenderness to palpation, particularly in the periumbilical region. Her pelvic examination shows neither vaginal discharge nor cervical motion tenderness, but she has some abdomi- nal tenderness with gentle bimanual palpation. She has pain at the right lower quadrant when she flexes the right thigh and extends the hip to place her leg into the stirrup for the bimanual examination. She has no dysuria or sexual activity, and the pain appears unrelated to her menses. Her physical examination shows a quiet, rigid, tender abdomen, and positive psoas sign. Despite this adolescent’s denial of sexual activity, a urine pregnancy test should always be obtained in postmenarchal females. Considerations The definitive diagnosis of appendicitis is made once the pathologist finds inflam- mation histologically on the appendix specimen obtained by surgical removal. For this patient, the initial periumbilical abdominal pain followed by anorexia and vomit- ing suggests appendicitis. The pain of appendicitis classically begins periumbilically and then migrates to the right lower quadrant with maximal discomfort at McBurney point. However, the pain can occur laterally if the appendix is retrocecal or it can become diffuse if perforation occurs. If a patient presents early in the disease process, is lacking the characteristic physical examination findings, has inconclusive imaging findings, and thus has a questionable diagnosis, the child may be observed and undergo serial abdominal examinations for a few hours. However, once appendicitis seems likely, surgical management should occur in a timely fashion; perforation rates exceed 65% if diag- nosis is delayed beyond 36 to 48 hours from symptom onset. The most common complications of appendicitis are wound infection and intra-abdominal abscess or phlegmon formation, all of which occur more frequently with appendiceal perfora- tion. Other serious complications are sepsis, shock, ileus, peritonitis, and adhesions causing small bowel obstruction. A person’s life- time risk of appendicitis has been estimated at 6% to 20%, with the peak incidence in adolescence and a slight predilection for males. Appendicitis can develop via several mechanisms but a frequent cause is when the appendiceal lumen becomes obstructed, leading to vascular congestion followed by ischemia, gangrene, and ultimately perforation with spillage of contaminated material into the peritoneum. Obstruction can be caused intrinsically by inspissated fecal material (a fecalith) or by external compression from enlarged lymph nodes associated with bacterial or viral infections. A thorough history of the illness with close attention to symp- toms in other organ systems can help identify these causes; for example, subacute weight loss, sore throat, dysphagia, cough, jaundice, rash, vaginal discharge, and arthralgias do not typically occur with appendicitis. However, diarrhea can be present with appendicitis due to bowel inflammation or because enteric infection may have led to the initial appendiceal inflammation. Appendicitis usually begins with nonspecific symptoms of malaise and anorexia and then abdominal pain following in a few hours. Localization to the right lower quadrant may take 12 to 24 hours to appear, and pain will then be made worse with movement. Observation of the child getting on and off the examination table can be revealing; children with appendicitis avoid sudden movements. They may walk in a manner to decrease movement of the right side of the abdomen, such as a shuffle, refuse to hop off the table, or brace the abdomen against coughing. The abdomen is inspected, auscultated for bowel sounds, followed by gentle palpation for the area of maximal tenderness and rigidity. Gentle finger percussion is the best method to assess for peritoneal irritation (“rebound tenderness”). The utility of a rectal examination for children with suspected appendicitis is debatable so it is not routinely performed; it can, however, be helpful for localizing the pain source in a female adolescent. Thereafter, it would be expected to be greater than 10,000/mm3 and in cases of perforation, it may be greater than 20,000/mm3. Urinalysis is important to evaluate for glucose and large ketones or pyuria with nitrites and bacteria because these findings sug- gest diabetic ketoacidosis or urinary tract infection respectively. Mild hematuria or pyuria can occur with acute appendicitis because of irritation of the bladder or ure- teral wall. Psoas shadow obliteration, right lower quadrant intestinal dilation, scoliosis toward the affected region, and an appendicolith (seen in 10% of cases) support appendicitis. In a facil- ity experienced in using ultrasonography in children, ultrasound is the preferred imag- ing modality for a child suspected of having appendicitis. Its main limitation is that the appendix cannot always be visualized, which can occur if the appendix has already perforated, the patient is obese, or if there is a lot of bowel distention. If pelvic views are included, it can evaluate for ovarian pathology as the cause of the abdominal pain. Its disad- vantages are the amount of radiation exposure generated, increased cost, and it may give limited information without the use of contrast. Electrolyte abnormalities and volume depletion should be corrected preopera- tively as surgery within 48 hours from diagnosis does not influence perforation rate but reduces the risk of surgical complications. Analgesia should be given because it has been shown that it does not interfere with identifying the correct diagnosis. For perforated appendicitis, initial management consists of intravenous antibiotics and fluid replacement. Percutaneous catheters can be used to drain any abscess and then appendectomy is performed at a later time. Sickle cell disease (Case 13) may present as an abdominal pain crisis or with gall bladder disease. Pneumonia (Case 14) of the lower lobes is classically described as possibly causing abdominal pain similar to appendicitis. In the smaller child with significant lead poisoning (Case 25), abdominal pain along with achy joints, change in behavior, and encephalopathy can be seen. Bacterial enteritis (Case 28), especially when caused by Campylobacter or Yersinia sp. While malrotation (Case 34) typically occurs in smaller children, the presentation with abdominal pain may be similar; as part of the surgical procedure to correct a malrotation, an appendectomy typically is performed. Diabetic ketoacidosis (Case 42) presents in a vari- ety of ways, among which is abdominal pain; measurement of a serum sugar typically is performed as part of the evaluation of a patient with possible appendicitis. The patient with severe sore throat, abdominal pain, and fever may have streptococcal pharyngitis; the later complication of this condition is poststreptococcal glomerulonephritis (Case 52). Her mother says that she has also had poor appetite and two loose stools the day prior. Because of the pain, she is unable to sit up for lung auscultation or percussion of the costovertebral angles. For which of the following condi- tions would exclude appendicitis from the differential diagnosis?
If the occlusion is incomplete or if the thrombus undergoes spont aneous lysis order 30mg dapoxetine with amex, unst able angina occurs order 60 mg dapoxetine free shipping. If t he occlusion is complet e and remains for more t h an 30 minut es buy 90mg dapoxetine otc, in farct ion occurs generic 60 mg dapoxetine fast delivery. In cont rast, the mech an ism of ch ron ic st able angina usually is a flow-limit ing st enosis caused by at herosclerot ic plaque that causes ischemia during exercise without acute thrombosis (Table 3– 1). It is of t he same charact er as angina pect oris— described as heavy, squeezing, or crushing— and is localized to the retrosternal area or epigastrium, sometimes wit h radiat ion to t he arm, lower jaw, or neck. In contrast to stable angina, however, it persists for more than 30 minutes and is not relieved by rest. T h e pain oft en is accompanied by sweat ing, nausea, vomit ing, and/ or t he sense of impending doom. Cardiac auscult at ion may reveal an S gallop, r eflect in g 4 myocardial noncompliance because of ischemia; an S gallop, representing severe 3 systolic dysfunct ion; or a new apical systolic murmur of mit ral regurgit at ion caused by ischemic papillary muscle dysfunction. The earliest changes are tall, positive, hyperacute T waves in the ischemic vas- cu lar t er r it or y. Cardiac-specific t roponin I (cTnI) and cardiac-specific t roponin T (cTnT ) are more specific t o heart muscle and are t he preferred markers of myocardial injury. Cardiac-specific troponin I levels may remain elevated for 7 to 10 days and cTnT levels for 10 t o 14 days. Aortic dissection often presents with unequal pulses or blood pres- sures in the arms, a new murmur of aortic insufficiency, or a widened mediastinum on ch est x-r ay film. Because the process is caused by acut e t h rom- bosis, antiplatelet agents such as aspirin an d ant icoagu lat ion wit h heparin are u sed. To limit infarct size, beta-blockers are u sed t o d ecr ease myocar dial oxygen d eman d, and nitrates are given t o in crease coron ar y blood flow. In addition, morphine may be given to reduce pain and the consequent tachycardia, and patients are placed on supple- mental oxygen (Figure 3– 3). Becau se myocar d iu m can be salvaged on ly befor e it is ir r ever sibly in ju r ed (“t ime is muscle”), pat ient s benefit maximally when the drug is given early, for example, within 1 to 3 hours after the onset of chest pain, an d the r elat ive ben efit s declin e wit h time. Because systemic coagulopathy may develop, the major risk of thrombolytics is bleeding, wh ich can be pot ent ially disast rou s, for example, int r acran ial h emor- rhage. The risk of hemorrhage is relatively constant, so the risk begins to outweigh the benefit by 12 hours, at which time most infarctions are completed, that is, the at -risk myocardium is dead. Alg o r it h m fo r a s s e s s m e n t a n d t r e a t m e n t o f c h e s t p a in. Sometimes intraluminal expandable stents are deployed, which may improve vessel patency. Life-t h reat ening vent ricular arrhythmias, such as vent ricular t achycardia ( V T ) and vent ricular fibrillat ion ( V F), are common, especially in the fir st 24 h ours. This has diminished in recent years wit h earlier and more aggressive t reat ment of ischemia and arrhyt hmias. T h ey are t r eat ed wit h defibrillation, followed by in fu sion of intravenous antiarrhythmics such as amiodarone. Elect rolyt e deficien cy, such as hypokalemia or hypomagnesemia, which can potentiate ventricular arrhythmias, should be correct ed. O ne benign vent ricular arrhyt hmia t hat is generally not sup- pressed by antiarrhythmics is the accelerated idioventricular rhythm. This is a wid e- complex escap e r h yt h m bet ween 60 an d 110 bpm that fr equ ent ly accompan ies reperfusion of the myocardium but causes no hemodynamic compromise. If the heart rate is slow enough to cause cardiac output and blood pressure to fall, int ravenous atropine usually is administ ered. Patients in persistent complete heart block will require placement of a permanent pacemaker. Ischemic reduction in vent ricular diastolic compliance may lead to t ransient pulmonary congest ion, associated with elevated left-sided filling pressures. Extensive myocardial necrosis and less contracting heart muscle may cause systolic failure and reduced cardiac output. Patients with hypotension frequently are evaluated by pulmonary artery (Swan-Ganz) catheterization to assess hemodynamic parameters. Cardiogenic shock is diagnosed when the patient has hypotension with systolic arterial pres- 2 sure less t han 80 mm H g, markedly reduced cardiac index less than 1. Clinically, such pat ient s appear hypot ensive, wit h cold extrem it ies becau se of p er iph er al vasocon st r ict ion, pu lmon ar y ed ema, an d elevated jugular venous pressure, reflect ing high left - and right -sided filling pres- sures. Support ive t reat ment includes hemodynamic monit oring, adequat e ven- tilation and oxygenation, and blood pressure support with vasopressors such as dobut amine and dopamine. T hese patients also may require mechanical assist ance to augment blood pressure while providing afterload reduction, using intra-aortic balloon counterpulsation. Diuretics or nitrates that might lower the preload can be disastrous in these patients by causing hypotension and cardiovascular collapse, and thus should be avoided. T his is in contrast with papillary muscle rupture, wh ich pr odu ces a flail m it r al leaflet and acute mitral regurgitation with development of heart failure and car- diogenic shock. Development of acute heart failure and shock in association with a new holosystolic murmur also may signify ventricular septal rupture. In all of them, stabilization of cardiogenic shock is accomplished using afterload reduction with intravenous nitroglycerin or nitroprusside and sometimes with intra-aortic balloon counterpulsation until definitive, urgent, surgical repair can be accomplished. The most catastrophic mechanical complication is rupture of the ventricular free wall. As blood fills the per icardium, cardiac t ampon ade develops r apidly, wit h sudden pulselessness, hypot ension, and loss of consciousness. Submaximal exercise stress testing is generally performed in stable patients before hospital discharge to detect residual ischemia and ventricular ectopy and to provide a guideline for exercise in t he early recovery period. Per- cut an eou s coron ar y int er vent ion can be per for med t o redu ce angin al sympt oms, and coronary artery bypass surgery sh ou ld be con sid er ed for patient s wit h multives- sel atherosclerotic stenosis and impaired systolic function because the surgery may reduce symptoms and prolong survival. Q uit t in g t obacco u se can r edu ce the r isk of fat al or n on fat al car diac event s by mor e t h an 50%, m or e t h an an y ot h er m edical or su r gical t h er apy available. A number of ot h er t herapies reduce the risk of recurrent cardiovascu- lar events and prolong survival in patients with coronary artery disease. Antiplate- let agent s such as aspirin and clopidogrel reduce the risk of thrombus formation, beta-blockers r ed u ce m yocar d ial oxygen d em an d an d m ay h elp su p p r ess ven t r icu lar arrhyt hmias, and cholesterol-lowering agent s such as statins reduce t he number of cor on ar y event s an d pr olon g su r vival. The pain occurs particularly after meals, especially when she lies down, and is not precipitated by exertion. Initiation of an antidepressant such as a selective serotonin reuptake inhibitor E. Five days later, she get s into an argument wit h her husband and complains of chest pain. It is ap p r op r iat e t o evalu at e ch est p ain t o fir st r u le ou t car d iac isch em ia. O n e of the most common causes of “chest pain” particularly in a younger patient is gast r oesoph ageal r eflu x or esop h ageal sp asm. This patient h as classic sym p - toms of reflux esophagitis and is best treated with a proton pump inhibitor. If the chest pain has the characteristics of angina pectoris (substernal location, precipitated by exertion, relieved by rest or nitroglycerin), it should be investi- gat ed wit h a st r ess t est or cor on ar y an giogr ap h y. A 56 year old woman is admitted to the hospital with a 2 hour history of ch est pain. Sinu s br adycar dia is oft en seen wit h in fer ior wall M I, becau se the right coronary artery supplies the inferior wall of the left ventricle and the sinoat rial node. Underst anding which leads reflect which port ion of the heart allows for an understanding of the aspect of the heart that is affected. Also understanding the area of the heart perfused by the various coronary arteries allows for correlat ion of associated symptoms or therapy. Diabetic patients can have myocardial ischemia or infarction with atypical or absent symptoms. Troponin levels often remain elevated for 7 to 10 days and should not be used to diagnose reinfarction, especially if the levels are trending down- ward. Asp ir in is the fir st agen t that sh ou ld b e u sed aft er oxygen an d n it r oglycer in. Clinical assessment t o exclude ot h er cau ses of ch est pain sh ou ld be u n d er t aken. T h e ot h er an swer ch oices are aimed toward diagnostic tests and may be important, but the first and foremost priority should be to “save myocardium. Bypass surgery may be indicated for patients with multivessel stenosis and impaired systolic function to reduce symptoms and prolong survival.
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