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Approximately 6% of those who come to the emergency department with cocaine- associated chest pain have enzymatic evidence of myocardial necrosis discount lopressor 12.5 mg line arteria bologna 7 dicembre. The deleterious effects of cocaine on the myocardial oxygen supply and demand are substantially exacerbated by concomitant cigarette smoking buy generic lopressor prehypertension a literature-documented public health concern, which by itself induces coronary arterial vasoconstriction through an alpha-adrenergic mechanism order 25 mg lopressor visa pulse pressure over 70. Following concomitant cocaine use and smoking cheap lopressor 50mg with visa heart attack high bride in a brothel, the heart rate and systemic arterial pressure increase markedly, and coronary arterial vasoconstriction is more intense than with either alone. This low incidence of complications is caused, at least in part, by the young age and absence of extensive multivessel coronary artery disease in most patients with cocaine-related infarction. Following hospital discharge, continued cocaine use and recurrent chest pain are common. Cocaethylene In individuals who use cocaine in temporal proximity to the ingestion of ethanol, hepatic transesterification leads to the production of a unique metabolite, cocaethylene. Cocaethylene is often detected postmortem in subjects who are presumed to have died of cocaine and ethanol toxicity. Similar to cocaine, cocaethylene blocks the reuptake of dopamine at the synaptic cleft, thereby possibly potentiating the systemic toxic effects of cocaine. In humans, the combination of cocaine and ethanol causes a substantial increase in myocardial oxygen demand. The concomitant use of cocaine and ethanol is associated with a higher incidence of disability and death than use of either agent alone. Individuals presumably dying of a combined cocaine-ethanol overdose have much lower blood cocaine concentrations than do those presumably dying of a cocaine overdose alone, thus suggesting an additive or synergistic effect of ethanol on the catastrophic cardiovascular events that are induced by cocaine. Cocaine-Induced Myocardial Dysfunction Long-term cocaine abuse has been associated with left ventricular hypertrophy, as well as with left 26 ventricular diastolic and/or systolic dysfunction. In a recent study, cardiac magnetic resonance imaging detected cardiac abnormalities in 71% of asymptomatic consecutive cocaine abusers. The main findings were a decrease in systolic function of left and right ventricles, an increase of left ventricular mass, and the presence of focal fibrosis (late gadolinium enhancement). There was a significant association between years of cocaine use and probability of left ventricular systolic dysfunction. Aside from the effects of long-term cocaine use on myocardial performance, it may cause an acute deterioration in left ventricular systolic and/or diastolic function or transient apical ballooning (also called Takotsubo cardiomyopathy or “broken heart syndrome”) (see also Chapter 25). Cocaine may adversely affect left ventricular systolic function by several mechanisms. Second, the profound repetitive sympathetic stimulation induced by cocaine is similar to that observed in patients with pheochromocytoma; either may result in cardiomyopathy and characteristic microscopic changes of subendocardial contraction band necrosis. Third, the concomitant administration of adulterants or infectious agents may cause myocarditis, which has been seen on occasion in intravenous cocaine users studied after death. Fourth, studies in experimental animals have shown that cocaine increases the production of reactive oxygen species, alters cytokine production in the endothelium and in circulating leukocytes, stimulates the transcription of genes responsible for changes in the composition of myocardial collagen and myosin, and induces myocyte apoptosis. The development of lethal arrhythmias with cocaine use may require an underlying substrate of abnormal myocardium. Life- threatening arrhythmias and sudden death in association with cocaine use occur most often in individuals with myocardial ischemia or infarction or in those with nonischemic myocellular damage. Long-term cocaine use is associated with increased left ventricular mass and wall thickness, which are known risk factors for ventricular dysrhythmias. First, its sympathomimetic properties may increase ventricular irritability and lower the threshold for fibrillation. In so doing, it acts in a manner similar to that of a class I antiarrhythmic agent. Accordingly, Brugada-type electrocardiographic features and torsades de pointes have been observed following cocaine use. Third, cocaine increases the intracellular calcium concentration, which may result in afterdepolarizations and triggered ventricular arrhythmias. Fourth, it reduces vagal activity, thereby potentiating its sympathomimetic effects. Aortic Dissection Because aortic dissection or rupture has been temporally related to cocaine use, it should be considered a possible cause of chest pain in cocaine users (see also Chapter 63). Dissection probably results from a cocaine- induced increase in systemic arterial pressure. In addition to aortic rupture, cocaine-related rupture of mycotic and intracerebral aneurysms has been reported. Amphetamines Amphetamines were previously prescribed for the treatment of obesity, attention deficit disorder, and narcolepsy; at present, their use is strictly limited. Ice is a freebase form of methamphetamine that can be inhaled, smoked, or injected. Similar to cocaine, amphetamines may induce intense coronary arterial vasoconstriction with or without thrombus formation. Finally, dilated cardiomyopathy can develop following repetitive amphetamine use, with recovery of cardiovascular function occurring after drug discontinuation. Like cocaine and amphetamines, these substances produce stimulant effects and are therefore sometimes used as substitutes for the traditional illicit drugs. The leaves of khat (Catha edulis) are chewed for the central stimulant action of their cathinone content. Khat use is highly prevalent in East African and Middle Eastern countries, in particular, Somalia and Yemen, and it is an emerging problem in Australia and Europe. These compounds are marketed as “bath salts” or “plant food” and labeled “not for human consumption” to circumvent regulatory restrictions on drugs of abuse. They are used by the oral route, nasal insufflation (“snorting”), intramuscular or intravenous injection, and rectal insertion, with most ingestion occurring by nasal insufflation or oral ingestion (or both). Synthetic Cannabinoids These drugs consist of psychoactively inert dry plant material sprayed with synthetic cannabinoid receptor agonists. Ma Huang (Ephedra) The dietary supplement ephedra, also known as ma huang, contains ephedrine and its enantiomer pseudoephedrine. Ma huang increases catecholamines at synaptic areas in the brain and heart and directly stimulates alpha- and beta-adrenergic receptors. As a result, it typically induces an increase in heart rate, blood pressure, cardiac output, and peripheral resistance. Catecholamines and Beta-Adrenergic Receptor Agonists Catecholamines, administered exogenously or secreted by a neuroendocrine tumor (e. Similar abnormalities have been described with the excessive use of beta-adrenergic agonist inhalants and methylxanthines in patients with severe pulmonary disease. Several mechanisms may be responsible for the acute and chronic myocardial damage associated with catecholamines. They may exert a direct toxic effect on the myocardium through changes in autonomic tone, enhanced lipid mobility, calcium overload, free radical production, or increased sarcolemmal permeability. Alternatively, myocardial damage may be secondary to a sustained increase in myocardial oxygen demand and/or a decrease in myocardial oxygen supply (the latter caused by catecholamine-induced coronary arterial vasoconstriction or platelet aggregation). Energy Drinks Emergency department visits related to energy drinks have more than doubled to more than 20,000 visits annually. Cardiovascular complications reported after energy drink ingestion include arrhythmias (i. Adverse effects and toxicities associated with energy drinks have been attributed to (1) the high caffeine content and the fact that the drinks are often consumed in an excessive or rapid manner; (2) consumption by young individuals who may be caffeine naïve and prone to consume large quantities; (3) mixture with alcohol and other substances; and (4) other ingredients in the drinks that may increase the cardiovascular risks.
Some of the high-fidelity micromanometer systems allow for over-the-wire insertion and angiography lopressor 12.5mg overnight delivery prehypertension is defined by what value. There are two basic elements in the interpretation of pressure waveforms in a two-dimensional scale: the individual absolute values (y dimension) and the contour of the aggregated values over time (x dimension) buy cheapest lopressor hypertension 28 years old. Accordingly discount 50mg lopressor overnight delivery normal pulse pressure 60 year old, the lack of this pattern indicates an abnormal relaxation pattern of the ventricle (also known as diastolic dysfunction) order generic lopressor line pulse pressure 27. The right atrial pressure waveform has three positive deflections or waves (a, c, and v) and two negative deflections or descents (x and y). It is followed by the x descent, which represents atrial relaxation and downward pulling of the tricuspid annulus as the right ventricle contracts. Atrial filling and compliance determine the height of the v wave, and under normal conditions, the v wave is smaller than the a wave. With subsequent opening of the tricuspid valve and emptying of the right atrium into the right ventricle, atrial pressure drops again: the y descent. Inhalation leads to a drop in intrathoracic and right atrial pressure, and exhalation has the opposite effect. While overall similar, the left atrial pressure is generally higher, with a higher v than a wave. This is not the case under circumstances of elevated pulmonary vascular resistance (hypoxemia, pulmonary embolism, chronic pulmonary hypertension). In general, “overwedging” of the balloon catheter leads to falsely low values, whereas “underwedging” leads to falsely high pressure readings. These two scenarios can be recognized by the pressure waveform lacking its desired atrial waveform configuration: noticeably flat with overwedging and appearing as a dampened pulmonary artery pressure tracing with underwedging (eFig. True wedge position of the catheter should always be confirmed by a blood sample documenting systemic oxygen saturation (normally near 100%). Duration of systole, isovolumic contraction, and relaxation are longer, and the ejection period is shorter in the left than in the right ventricle. In the early, rapid filling phase of diastole, ventricular pressure initially drops quickly and then increases again, reaching a plateau. This plateau is extended over the slow filling phase but ended by a slow rise due to atrial contraction. The three key elements of the pressure waveform in the great vessels are the systolic wave (the ejection of the stroke volume through the open semilunar valves), the incisura (the closure of the semilunar valves), and the diastolic phase of gradual decline in pressure. The difference between the systolic and diastolic pressure, also known as pulse pressure, is a reflection of the stroke volume and the compliance of the arterial system. As the pressure wave travels distally, an increase in systolic amplitude can be noted, whereas the diastolic amplitude decreases initially up to midthoracic level, then increases again. These differences can impact important measurements such as those of aortic gradients. Accordingly, in general, it is advisable to measure the central aortic pressure at the level of the coronary arteries. This also avoids interference with the effect of pressure recovery, which can become relevant in patients with mild to moderate aortic stenosis, particularly when the aorta is small. Elevated a wave (any increase in ventricular filling) Tricuspid stenosis Decreased ventricular compliance as a result of ventricular failure, pulmonic valve stenosis, or pulmonary hypertension D. Cannon a wave Atrial-ventricular asynchrony (atria contract against a closed tricuspid valve, as during complete heart block, following premature ventricular contraction, during ventricular tachycardia, with a ventricular pacemaker) E. Prominent y descent Constrictive pericarditis Restrictive myopathies Tricuspid regurgitation J. Cannon a wave Atrial-ventricular asynchrony (atria contract against a closed mitral valve, as during complete heart block, following premature ventricular contraction, during ventricular tachycardia, or with a ventricular pacemaker) E. Prominent x descent Tamponade Subacute constriction and possibly chronic constriction Right ventricular ischemia with preservation of atrial contractility I. Prominent y descent Constrictive pericarditis Restrictive myopathies Mitral regurgitation J. Elevated systolic pressure Primary pulmonary hypertension Mitral stenosis or regurgitation Congestive heart failure Restrictive myopathies Significant left-to-right shunt Pulmonary disease (pulmonary embolism, hypoxemia, chronic obstructive pulmonary disease) B. Reduced systolic pressure Hypovolemia Pulmonary artery stenosis Subvalvular or supravalvular stenosis Ebstein anomaly Tricuspid stenosis C. End-diastolic pressure elevated Hypervolemia Congestive heart failure Diminished compliance Hypertrophy Tamponade Regurgitant valvular disease Pericardial constriction D. Diminished or absent a wave Atrial fibrillation or flutter Tricuspid or mitral stenosis Tricuspid or mitral regurgitation when ventricular compliance is increased F. Dip and plateau in diastolic pressure wave Constrictive pericarditis Restrictive myopathies Right ventricular ischemia Acute dilation associated with tricuspid or mitral regurgitation G. Systolic pressure elevated Systemic hypertension Arteriosclerosis Aortic insufficiency B. Widened pulse pressure Systemic hypertension Aortic insufficiency Significant patent ductus arteriosus Significant rupture of sinus of Valsalva aneurysm D. Reduced pulse pressure Tamponade Congestive heart failure Cardiogenic shock Aortic stenosis E. Pulsus paradoxus Constrictive pericarditis Tamponade Obstructive airway disease Pulmonary embolism G. Spike-and-dome configuration Obstructive hypertrophic cardiomyopathy Cardiac Output Measurements Although extremely important, often requested and tested, cardiac output measurements represent only estimates of the true cardiac output on the basis of several assumptions. Three methods are used in the catheterization laboratory: thermodilution, Fick, and ventriculography. Thermodilution Method Thermodilution is based on the principle of washout of a temperature change induced by injection of a defined fluid volume cooler than the body temperature. In practice a bolus of liquid (usually 10 mL of normal saline kept at room temperature) is injected into the proximal port of the catheter, and the change in temperature from baseline is measured by a thermistor at the distal end of the catheter and displayed as a function over time. Cardiac output correlates inversely with the area under the curve and can be calculated when the temperature and specific gravity of the injectate and the blood as well as the volume of the injectate are known (eFig. Configurations of thermodilution curves in high and low cardiac output states (middle) and with improper injection technique (bottom). However, thermodilution is less accurate in patients with significant tricuspid or pulmonic regurgitation, intracardiac shunts, low cardiac output, or irregular rhythms. Fick Method The Fick method relies on the principle that blood flow is proportional to the difference in the concentration of oxygen between arterial and venous blood and the rate of oxygen uptake in the lungs (Fig. Fluid containing a known concentration of an indicator (Cin) enters a system at a given flow rate, adding to the concentration of the indicator already present and thereby raising the concentration of the indicator in the outflow (Cout). In a steady state, the rate of indicator leaving the system must equal the rate at which it enters plus the rate at which it is added. When oxygen is used as the indicator, cardiac output can be determined by measuring oxygen consumption (V̇), arterial oxygen content (CaO ), and mixed venous oxygen content (2 ).
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What is the probability of an acute coronary syndrome buy lopressor 12.5mg without a prescription blood pressure dehydration, given an abnormal troponin test? The post-test probability depends on a prior estimate of the probability for that particular patient discount lopressor 25mg fast delivery arrhythmia omega 3 fatty acids, combined with the strength of the test result purchase lopressor 100 mg otc blood pressure medication gain weight. Bayesian reasoning requires both a prior estimate of probability and an estimate of the strength of a test result purchase lopressor 50 mg with mastercard heart attack what to do. Prior estimates can come from experience or published data on the prevalence of a disease. A 17 classic paper by Diamond and Forrester, for example, provides estimates of the prevalence of coronary artery disease in patients depending on age, gender, and symptom features. This type of observational research can be used to provide us with the prior probabilities needed for bayesian reasoning. A laboratory test might be measured in a population of presumably normal individuals to determine a distribution and to define a normal range, as shown in the probability density curve in the left panel of Fig. A normal range is usually defined as the inner 95% cumulative probability, and the abnormal range is defined as values falling outside the normal range. Right panel shows how a normal and abnormal test result is defined by the line of demarcation between distributions of normal and abnormal test subjects, as defined by another, independent “gold standard” test. Another way of defining a test result is by measuring the test result in a group of individuals who are defined as “normal” and “abnormal” by another, independent “gold standard” test, as shown in the right panel of Fig. Typically, patients with and without disease will have test results that are distributed as bell-shaped curves. We can draw a line of demarcation to define how a new test would separate patients with positive and negative test results. Because there is overlap in individuals with and without disease, there will be false-positive and false-negative test results, as shown. The utility of a test result depends in part on the operating characteristics of a test: the sensitivity and specificity. These are rates, meaning the sensitivity and specificity are proportions with different units for the numerator and denominator. The denominators of sensitivity and specificity are patients with disease and patients with no disease, respectively. In clinical practice, when test results are reported as positive or negative, however, the results are reported using terms with different denominators. The difficulty of keeping track of denominators can be alleviated by using likelihood ratios rather than sensitivity and specificity. It should be noted that sensitivity and specificity can change if the spectrum of test subjects 2 that defined them is different from the spectrum of patients for whom the test is used. If the operating characteristics of the test are defined in a narrowly defined population (Fig. This frequently occurs with tests such as troponin testing, where the clinical sensitivity and specificity of the test are defined in a research setting, but the test is used indiscriminately in practice. True negative test results for troponin levels are shown in red, and true positive results are shown in green. Left panel shows the results when the test is ordered on a narrowly defined population of test subjects, and right panel shows the results when the test is ordered on a broadly defined population of test subjects, resulting in spectrum bias and a marked decrease in specificity of the test (80% to 53% in this example). Clinicians, as with decision 3,9 makers in general, use a heuristic that psychologists call “anchoring and adjusting. For a patient with chest pain, for example, the anchor would be an estimate of the pretest probability of coronary artery disease, which would be intuitively adjusted on the basis of new information, such as a stress test result, to estimate a post-test probability. One fallacy, called “anchoring,” is when the decision maker becomes too anchored on the pretest probability estimate and does not adequately adjust in estimating the post-test probability. The second fallacy is called “base-rate neglect,” when the decision maker overly responds to the new information to estimate a post-test probability, without regard for the pretest probability. For example, troponin tests may be positive because of renal failure or sepsis in patients with a low pretest probability of acute thrombotic myocardial infarction. Awareness of this heuristic and its pitfalls can help clinicians avoid this common reasoning error. Their advantage is that, unlike sensitivity and specificity, likelihood ratios are dimensionless numbers, so the need to keep track of the numerator and denominator is alleviated. Likelihood ratios give a measure of the persuasiveness of a positive and negative test result and can be used intuitively or used to calculate post-test odds. A likelihood ratio is defined as the percentage of diseased patients with a given test result divided by the percentage of nondiseased patients with that same test result. It is easy to calculate the positive and negative likelihood ratios from sensitivity and specificity. Once calculated, these numbers can be used to multiply the pretest odds to calculate the post-test odds of a diagnosis. They are multipliers, so a higher positive likelihood ratio and a lower negative likelihood ratio (which is a fraction) have stronger multiplying effects. A likelihood ratio that is close to 1 is weak because it would have very weak multiplying effect, meaning it has minimal effect on the pretest assessment. Some tests are asymmetric, meaning that their positive or negative likelihood ratio is stronger. For example, congestion on a chest x-ray film has a very strong positive likelihood ratio of 13. This reflects that the chest radiograph is highly specific but not very sensitive for heart failure. In other words, congestive findings on a chest radiograph are highly suggestive of heart failure, whereas their absence would not be reassuring about lack of heart failure. Tests that are highly specific are better for ruling in a diagnosis, and this can be remembered using the mnemonic “SpPin” (highly specific tests, if positive, are good for ruling in). On the other hand, a D- dimer for a pulmonary embolus has a very strong negative likelihood ratio of 0. This reflects that a D-dimer is highly sensitive but not very specific for pulmonary embolus. Tests that are highly sensitive are better for ruling out a diagnosis, and this can be 19 remembered using the mnemonic “SnNout” (highly sensitive tests, if negative, are good for ruling out). The likelihood ratios, however, are only as useful and precise as the sensitivity and specificity that are used to calculate them. They give an approximate quantitative estimate of the strength of new information that provides a mechanism for calibrating intuitive probability estimates. When used with odds, likelihood ratios provide a way to calculate the conditional probabilities that are used for bayesian reasoning. Proceeding through this calculation demonstrates the conceptual framework for reasoning through iterative hypothesis testing. Test-Ordering Strategies Clinical reasoning should guide not only test interpretation, but also test ordering. Tests that are ordered for good reasons are more conclusive, and tests that are ordered indiscriminately can cause clinicians to arrive at the wrong conclusions. This effort is driven by both the need to avoid excessive false-positive test results and the need to contain the costs of medical care.
Patients should be asked Patients with a history of previous cervical spine surgery about over-the-counter medication including herbal prod- may have scarring or altered anatomy purchase 50mg lopressor amex heart attack 64. Patients of reproductive age should be such as catheter placement from a thoracic level or trans- questioned about pregnancy cheap 25 mg lopressor overnight delivery blood pressure chart british heart foundation, tested if necessary discount lopressor 25mg otc blood pressure 00, and foraminal blunt needle approach as an alternative to a shielded from ﬂuoroscopy order lopressor 12.5 mg fast delivery blood pressure medication can you stop. Uncontrolled diabetes, hypertension, and heart failure If small-caliber (20–22 gauge) needles are used, it is may become exacerbated by corticosteroid administration. Unusual contrast cephlo- dominant psychological factors, or other psychiatric prob- caudal spread may represent intracord injection. Lateral lems should be stabilized or referred for more appropriate views will conﬁrm the location of the needle tip and injec- care prior to interventional pain procedures. Even small amounts of intracord injection may allergy to contrast is not uncommon, and while not an lead to syrinx formation and/or permanent cord injury. Contrast should be visualized in the epidural try) and the procedure is an important consideration. The space, which is distinguishable from subarachnoid collec- procedure must be performed under ﬂuoroscopy guidance tion. Subdural contrast injection is of concern and some- with appropriate radiation protection equipment including times requires multiple views to conﬁrm. A ﬂuoros- injection may be detected by visualized contrast ﬂow in a copy unit with a freeze-frame screen and hard-copy printer vein or artery but also may only be recognized by a lack of is preferred. Loculation of Special attention to technique is necessary so that the contrast may indicate additional risk of cord compression. Contrast Patients with rapidly worsening pain, numbness, weak- should be water-soluble or nonionized such as Omnipaque ness, hyperreﬂexia, changes in bladder function, and other 240 or other myelogram-quality contrast. A suspected cord le- patient is not allergic to iodine-containing solutions such sion from a hematoma or other compression requires as betadine. Potential problems time, partial thromboplastin time, platelet count, and func- have been recognized for years. Patients need upper cervical area if the needle tip ends up off midline, to discuss their periprocedure anticoagulation with the laceration of segmental arteries can be followed by a rap- prescribing physician. Patients with mechanical valves, idly expanding arterial hematoma with pain, numbness, recent deep venous thrombosis, or other conditions pro- and evidence of cord compression. Midline interlaminar hibiting discontinuing anticoagulation may convert from needle placement, especially without lateral ﬂuoroscopic coumadin to lovenox 5 days prior to the procedure, and visualization, may result in intracord needle placement and lovenox can be held for 12 hours immediately prior to the injection. Plavix should be held for 1 week, and other for local anesthetic inﬁltration, an 18-gauge, B-bevel nee- prescription anticoagulants should be held for the appro- dle for opening up a hole through the skin, an 18-gauge, priate time. Aspirin is stopped 1 week prior to a procedure 3-1/2-inch R-X Coudé needle, and in some instances, the 130 Head and Neck 18-gauge reverse R-X Coudé needle. The patient may be positioned in the contrast while the physician’s hand is out of the ﬁeld of sitting position, but the prone or lateral positions facilitate radiation is useful. Hand scrub and bactericidal foam are important practices for the physician prior to any procedure. Sterile prepara- Imaging Studies tion of the skin with Hibiclens followed by alcohol prepara- tion and sterile drapes and strict technique are essential. Plain ﬁlms comprise a minimum in order to rule out bone destruction from tumor, spondylolisthesis, or other process. The image intensiﬁer of the C-arm is Written informed consent, which includes risks of paraly- placed in the cephalad position, and the x-ray tube of the sis, pain, numbness, bowel, bladder or sexual dysfunction, bleeding, and infection, needs to be obtained. Preoperative Medication Patients should be advised to avoid ingestion of food and drink, except for their usual medications, prior to proce- dures requiring sedation or local anesthetic with the po- tential for spinal block. Patients with diabetes should be placed early on the schedule to prevent losing blood sugar control. However, a responsive patient is a source of a wealth of information during a procedure. Patient history is the cornerstone of diagnosis, even during interven- tional pain procedures, and it should be surrendered cau- tiously. Preprocedure education, high-quality bedside manner, and meticulous local anesthetic placement can signiﬁcantly reduce sedation requirements for many patients. For preoperative medication, use the standard rec- ommendations for conscious sedation by the American Society of Anesthesiologists. If it is difﬁcult to keep the patient in a “true” lateral decubitus position, the ﬂuoroscopic avoid general anesthesia as it masks warning symptoms C-arm or the ﬂuoroscopic table may be rotated obliquely to create an during procedures. C-arm is rotated in the caudad direction to visually open up the interspace for improved target selection, usually at C7, T1, or T1-T2 interspaces. When the tip of the needle reaches on top of the T1 an 18-gauge R-X Coudé needle, which has a wide-open lamina, near the midline, the C-arm is rotated into the tip (rather than the leading curved cutting end of the lateral view. The 18-gauge R-X Coudé is advanced the way, but this problem is solved by obtaining a swim- with a curved tip pointing medially crossing over the mer’s view, which is rotating the image intensiﬁer of the lamina (Figures 8-4 and 8-5). The angulated lateral needle travels can be inﬂuenced by rotation of the curved view shows a clear path to the base of the spinous process. The base of the spinous process appears as a “straight line,” which is actually hockey stick J-shaped. This ap- pearance comes from the four layers of bony cortex on the lamina on the outside, inside, inside, and outside again overlapping. Using this radio- graphic anatomy, one can precisely determine the location of the ligamentum ﬂavum whether there is any loss of Dotted needle track- resistance or not from the presence or absence of the gap beneath skin but outside spinal canal in the ligamentum ﬂavum. The needle at this point is Skin entry point advanced by rotating the tip of the needle anteriorly and advanced on the lateral ﬂuoroscopic view to the level of the straight line (Figures 8-6 and 8-7). The tip of the R-X Coudé needle is parallel to the ligamentum ﬂavum and slowly advanced until the loss of resistance is obtained (Figure 8-8). If a Tuohy needle was used, the tip of the needle has a sharp cutting end, but the working part of the lumen is farther posterior. The sharp tip penetrates rather easily through structures without necessarily giving the physician a chance to experience the various tissue planes. The needle is advanced until a loss of resistance or loss of bounce when the needle tip enters the epidural space. Aspiration is performed to test for blood or spinal ﬂuid; however, contrast injection is useful to conﬁrm epidural placement. Contrast injection with Omnipaque or other myelogram-grade contrast is performed to rule out super- ﬁcial, subdural, subarachnoid, or intravascular injection. The direc- tion of the injection can be inﬂuenced by rotating the tip of the R-X Coudé needle 180 degrees and/or to the left or right, and/or by injecting a small amount of contrast (Figures 8-9 and 8-10). Lateral ﬂuoroscopic visualization with swimmer’s view is used to verify the location of in- jected contrast and the needle tip. Then a test dose injec- tion of the mixture of local anesthetic and steroids can be carried out. Every injection should be proceeded by aspira- tion as the injected material may be into a vascular struc- ture, whether it is a vein or artery, subarachnoid space, or even the spinal cord.