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Langlois and Gresham concluded that all one could say about a bruise with yellow coloration is that it is more than 18 hours old cheap viagra plus 400 mg on line erectile dysfunction pills canada. Color changes should be considered only as general guidelines in interpreting how old a bruise is purchase viagra plus canada erectile dysfunction treatment abu dhabi. The best thing to do is to just state that the bruise appears either recent or old viagra plus 400mg without a prescription erectile dysfunction urban dictionary. Postmortem Bruising One of the most commonly heard statements in regard to contusions is that they indicate that the injury was incurred prior to death, because one cannot form a contusion after death. Contusions can be produced postmortem if a severe blow is delivered to a body within a few hours of death. Postmortem contusions rarely occur and are most commonly seen in skin and soft tissue overlying bone or bony prominences such as in the head. Microscopic examination of a contusion to determine whether it is antemortem or postmortem is usually of no help, because, in most cases, the antemortem injuries are incurred immediately prior to death and there is insufficient time for tissue reaction. The Eyes and Eyelids Surgical removal of corneas or the globes of the eyes shortly after death can result in hemorrhage into the eyelids indistinguishable from antemortem traumas (Figure 4. Removal of vitreous shortly after death can result in scleral hemorrhage at the puncture site (Figure 4. Confluent hemorrhage in eyelids can occur after death in cases of head trauma with fracture of the orbital plates. One can prove this by taking the body of an individual with skull fractures, but without hemorrhage in the eyelids, and placing it face down for a number of hours. Blood will drain from the cranial cavity through the orbital plate fractures into the eyelids. Decomposed Bodies In decomposed bodies, especially in the scalp, hemolysis of erythrocytes produces a diffuse discoloration of the soft tissue, which makes attempts to 104 Forensic Pathology distinguish between an antemortem contusion and an area of livor mortis impossible. In areas of livor mortis, blood vessels break down with leakage of erythrocytes into the soft tissue. Erythrocytes still in the vessels and those that diffuse into soft tissue hemolyze. Erythrocytes in soft tissue from bruising will also hemolyze, giving identical appearances to these lesions. Lacerations A laceration is a tear in tissue caused by either a shearing or a crushing force (Figure 4. Just as with contusions, one can have lacerations of internal organs as well as the skin. The appearance of the laceration may not accurately reflect the instrument that produced it. Thus, a steel rod might produce not only a linear laceration of the scalp, but also a Y-shaped one. As a general rule, however, long, thin objects, such as pipes and pool cues, tend to produce linear lacerations, while objects with flat surfaces tend to produce irregular, ragged, or Y-shaped lacerations. Lacerations occur most commonly over bony prominences, such as in the head, where the skin is fixed and can more easily be stretched and torn. Since different components of soft tissue have different strengths, there is usually incomplete separation of the stronger elements, such as blood vessels and nerves, so that when one looks into the depth of the laceration, one sees “bridges” of tissue running from side to side (Figure 4. The presence of bridging proves decisively that one is not dealing with an incised wound. The depths of the laceration should be explored for the presence of foreign mate- rial that could have been deposited there by the weapon or surface that caused the laceration. If the blow or impact that causes a laceration is delivered at an angle, rather than perpendicular to the surface of the body, one will find under- mining of the tissue on one side, which indicates the direction that the blow was delivered (Figure 4. The other side of the laceration, the side from which the blow was coming, will be abraded and beveled. While most lacerations have irregular, abraded, even contused margins, if an individual is struck with a heavy object having a relatively sharp edge along the impacting surface, the wound produced may greatly resemble an incised wound (Figure 4. Careful examination of the wound, however, will usually reveal at least some abrasion of the margin, plus bridging in the depths of the wound. Occasionally, a very dull knife may produce an incised wound with abraded margins. Again, careful observation of the edges and base of the wound with a dissecting microscope usually makes differentiation Blunt Trauma Wounds 105 A B Figure 4. Differentiation of a laceration from an incised wound of the head in a decomposed body is often not possible. An avulsion or avulsive injury to the outside of a body is a form of laceration where the force impacting the body does so at an oblique or tangential angle to the skin, ripping skin and soft tissue off the underlying fascia or bone. In a case of extreme avulsion, an extremity or even the head can be torn off the body. Internally, organs can be avulsed or torn off in part or in toto from their attachments. A variation of an avulsive laceration is one produced by shearing forces, where the skin shows no signs of injury but the underlying soft tissue has been avulsed from the underlying fascia or connective tissue, creating a pocket that may be filled with a large quantity of blood. This injury is occasionally encountered on the backs of the thighs of pedestrians struck by motor vehicles. As the hood of the car impacts the back of the thigh and lifts up the pedestrian, it imparts a shearing force to this region, avulsing the skin and subcutaneous tissue off the fascia and creating pockets where blood can accumulate. There are generally abrasions and contusions on the back of the hands, wrists, forearms, and arms (Figure 4. Lacerations are less common and may contain embedded fragments of the weapon in the wounds. When these occur, they generally involve the forearm, and are incurred in attempts to ward off a blunt object. Determination of Whether a Wound is Ante- or Postmortem At present, determination of whether a wound is either ante- or post- mortem is made by gross or microscopic examination of the wound. The presence of bleeding into the tissue is presumed evidence that the deceased was alive, or, at least, the heart was beating at the time the injury was incurred. The problem with this principle is that, on occasion, trauma to a recently dead body can cause bleeding into soft tissue. This phenom- enon may cause confusion to a forensic pathologist who is unaware of it. Much rarer is the postmortem contusion of the scalp previously men- tioned in this chapter. Another method of determining if an injury is antemortem is micro- scopic examination of the injury in search of an inflammatory reaction. The problem with this technique is that some tissues do not show an Blunt Trauma Wounds 109 inflammatory reaction unless the victim has survived for at least several hours after the injury. Techniques to identify antemortem injuries involving use of histochem- istry, enzymology and biochemistry have been developed. Analysis of enzyme activity in antemortem wounds has demonstrated a zone of decreased enzyme activity at the center of the wound, with increased enzyme activity at the periphery. The increased enzyme activity occurs over a specific time interval, with the interval different for different enzymes. The enzyme activity can be used to demonstrate that a wound was antemortem as well as to date it.

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The interscalene approach to the brachial plexus is suitable for more proximal humerus procedures buy cheap viagra plus 400 mg on-line erectile dysfunction treatment home remedies. Procedures longer than 3 h usually require general anesthesia in addition to regional purchase online viagra plus erectile dysfunction doctor in los angeles. Regional anesthesia with sedation is usually well tolerated in shorter procedures generic viagra plus 400mg with amex erectile dysfunction hormones. General anesthesia: Regional anesthesia: Suggested Viewing Links are available online to the following videos: Shoulder Arthroscopy, Removal of Bone Spur (Subacromial Decompression): https://www. In most instances, little or no bone is removed, and therefore, this is not technically a laminectomy or laminotomy. These minimally invasive procedures typically are carried out in healthy young or middle-aged adults with sciatica and are not done for more involved pathology, such as deformity, tumor, or infection. Transpedicular fixation a n d short-segment fusions may be attempted using modifications of these techniques. The patient is placed in a prone or kneeling position, and the posterior landmarks are palpated to identify the approximate level (e. A spinal needle is placed to the level of the lamina, and an x-ray or fluoroscopic image is taken to confirm the level. A 1” incision is made over the proposed interspace, and using either traditional or specialized retractors, the soft tissue is displaced to expose the ligamentum flavum. With the use of an operating microscope, the ligamentum flavum is removed, the nerve retracted, and the extruded disc excised. For a single level, this should take between 30 and 90 min, depending on the size of the patient and whether there is any scarring or adhesions from previous surgery. Variant approach: Percutaneous discectomy through a posterolateral approach is usually reserved for “contained discs”—protrusions into, but not through, the outer annulus of the disc. The percutaneous instruments may be positioned using fluoroscopic guidance with or without a fiberoptic light source and camera/monitor setup. The surgeon usually avoids anesthetizing the area around the nerve root so that the patient can alert the team if the root is struck by an instrument (quite painful). After the disc space is entered, fluoroscopic or camera images are used to guide the surgeon in the removal of the herniated disc. The disc material can be removed with specialized grabbers or automatic power-driven shavers. However, the morbidity of the approach, extensive blood loss, and length of postop recovery can offset the benefits of the intervention. One approach involves lateral approach via a small incision through retroperitoneal fat and the psoas major muscle for access to the lateral lumbar spine with the aid of neuromonitoring to avoid nerves of the lumbar plexus. The orientation of neural structures of the lumbar plexus has a relatively high level of variability, necessitating the use of neuromonitoring for this approach. Neuromuscular blockade should be avoided, and the use of intravenous anesthesia is encouraged. The patient is positioned in the lateral decubitus position and held in position with straps and tape. The arms should remain in a neutral position, and an axillary roll is placed just inferior to the axilla to support the area of the upper rib cage to relieve pressure on the axillary nerve and artery. The table is typically flexed to increase the distance between the iliac crest and the rib cage to gain access to the lateral lumbar spine. Fluoroscopic imaging is required to determine true anteroposterior and lateral axes of the desired spinal level. After the patient has been prepped and draped, an incision is made posteriorly at the border between the erector spinae muscles and the abdominal obliques to accommodate the surgeon’s index finger and help identify the retroperitoneal space. With care, perforation of the peritoneum is avoided, and the finger is used to sweep this anteriorly. After identifying the psoas muscle, the index finger is swept up to a previously marked direct lateral target over the center of the affected intervertebral segment. An incision is made on the patient’s side, through which dilators are placed, and the index finger is used to escort them safely to the psoas muscle, all while protecting the intraabdominal contents. Once the self-retaining retractor system is positioned, care is taken to determine the course of the lumbar plexus in relation to the blades of the retractor. Once the retractor is positioned over the disc space, under direct vision, a discectomy is performed. Care is taken not to disrupt the anterior longitudinal ligament and risk injury to the main vascular structures coursing anteriorly. Usual preop diagnosis: Chronic back pain; lumbar radiculopathy Suggested Reading 1. Adamus M, Hrabalek L, Wanek T, Gabrhelik T, Zapletalova J: Intraoperative reversal of neuromuscular block with sugammadex or neostigmine during extreme lateral interbody fusion, a novel technique for spine surgery. These patients must be awake to alert the surgeon to inadvertent nerve root contact. In some centers, regional anesthesia (spinal or epidural) is the anesthetic of choice. Schick U, Dohnert J: Technique of microendoscopy in medial lumbar disc herniation. These procedures initially were reserved for patients with significant deformities, especially kyphosis. More recently, the treatment of traumatic, neoplastic, and degenerative conditions have been included in Spinal Reconstruction and Fusion—Thoracic and Thoracolumbar Spinethe anterior approach. Regardless of the condition under treatment, the approach is similar for a given level. There are several more or less distinct types of surgical exposures, depending on the level. Cervicothoracic approach: Most cephalad and difficult is the approach to the upper thoracic spine (T1-T3). This generally includes a modified anterior cervical exposure with a caudal extension, including a resection of the clavicle, part of the manubrium, and sometimes the rib at the thoracic outlet. Dangers in this exposure are to the great vessels at the thoracic outlet, trachea (rare) and esophagus (more common), lung parenchyma, sympathetic ganglia, lymphatic duct (on the left), and brachial plexus. Once the spine is exposed and the discs and/or vertebrae are removed, the spinal cord is at risk. This procedure occasionally involves entering the thoracic cavity, in which case it is usually done intrapleurally—that is, through the parietal pleura. Transthoracic approach: Further down the spine, the levels from T5-T10 are more easily reached via a transthoracic approach (Fig. The level of the rib resection is usually 1–2 levels above the highest vertebral level being approached. The great vessels and lung parenchyma are at risk, as is the thoracic duct (on the left). The patient is in the lateral decubitus position, and the mediastinum and heart usually fall to the opposite side, out of harm’s way. Risk to the spinal cord depends on the difficulty and extent of the vertebral disease and the reconstruction. Because there is no (intended) violation of the lung parenchyma, air leaks and parenchymal repairs are not common.

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Alternative extracorporeal methods include continuous hemofiltration discount viagra plus express erectile dysfunction 43, hemodialysis buy viagra plus on line amex erectile dysfunction drugs and melanoma, or hemodiafiltration discount viagra plus 400 mg with amex erectile dysfunction 37 years old. The primary endpoint was total weight loss during the first 48 hours of randomization and the change in dyspnea score during the first 48 hours of randomization. In addition to extracorporeal methods for relieving volume overload, peritoneal dialysis can be used as a viable alternative therapy for the short-term management of refractory congestive symptoms for patients in whom vascular access cannot be obtained, or for whom appropriate extracorporeal therapies are not available. Participants treated with enalapril had significantly lower mortality than those treated with the vasodilatory combination of hydralazine plus isosorbide dinitrate (which does not directly inhibit neurohormonal systems). Nonetheless, it should be emphasized that patients with a low blood pressure (<90 mm Hg systolic), or impaired renal function (serum creatinine >2. Thus the efficacy of these agents for this latter patient population is less well established. Potassium retention may also become problematic if the patient is receiving potassium supplements or a potassium-sparing diuretic. The combination of hydralazine and an oral nitrate should be considered for these latter patients (see Table 25. Therefore the problems of symptomatic hypotension, azotemia, and hyperkalemia will be similar for both these agents. However, compliance with this combination has generally been poor because of the large number of tablets required and the high incidence of adverse reactions. A, Death from cardiovascular causes or hospitalization for heart failure (the primary endpoint). There are additional concerns about effects of sacubitril/valsartan on the degradation of beta- amyloid peptide in the brain, which could theoretically accelerate amyloid deposition. Beta blockers interfere with the harmful effects of sustained activation of the central nervous system by competitively antagonizing one or more alpha- and beta-adrenergic receptors (α , β ,1 1 and β ). Although there are a number of potential benefits to blocking all three receptors, most of the2 deleterious effects of sympathetic activation are mediated by the β -adrenergic receptor. The dose of beta blocker should be increased until the doses used are similar to those reported to be effective in clinical trials (see Table 25. Therefore, it is important to optimize the dose of diuretic before starting therapy with beta blockers. The increased fluid retention can usually be managed by increasing the diuretic dose. Nonetheless, a subset of patients (10% to 15%) remain intolerant to beta blockers because of worsening fluid retention or symptomatic hypotension. Metoprolol tartrate at an average dose of 108 mg/day reduced the prevalence of the primary endpoint of death or need for cardiac transplantation by 34%, which did not quite reach statistical significance (P = 0. The benefit resulted entirely from a reduction by metoprolol in the morbidity component of the primary endpoint, with no favorable trends in the mortality component. Lancet 1999;353:2001-7; and Packer M et al, for The Carvedilol Prospective Randomized Cumulative Survival Study Group. The two strategies were compared in a blinded manner with regard to the combined primary endpoint of all-cause mortality or hospitalization, as well as with regard to each of the components of the primary endpoint individually. Trials Program, composed of four individual trials managed by single Steering and Data and Safety Monitoring Committee, was stopped prematurely because of a highly significant (P < 0. Rates of hospitalization were also significantly lower for patients treated with carvedilol (48%) compared to placebo (58%). Carvedilol was associated with a significant 33% reduction in all-cause mortality compared with metoprolol tartrate 8,12 (33. Not all studies with beta blockers have been universally successful, suggesting that their effects should not necessarily be viewed broadly as a class effect. Indeed, early studies with the first-generation of nonspecific β and β receptors without ancillary vasodilating properties (e. The differential response of bucindolol in white patients has been suggested to be secondary to a polymorphism (Arginine 389) in the β -adrenergic receptor that is more prevalent in white patients (see online supplement,1 Pharmacogenomics in Heart Failure). Side Effects of Beta Blockers The adverse effects of beta blockers are generally related to the predictable complications that arise from interfering with the adrenergic nervous system. These reactions generally occur within several days of initiating therapy and are generally responsive to adjusting concomitant medications, as previously described. Treatment with a beta blocker can be accompanied by feelings of general fatigue or weakness. In most patients, the increased fatigue spontaneously resolves within several weeks or months; in some, however, it may be severe enough to limit the dose of beta blocker or require the withdrawal or reduction of treatment. Therapy with beta blockers can lead to bradycardia and can exacerbate heart block. Moreover, beta blockers (particularly those that block the α receptor) can lead to vasodilatory side effects. Thus the dose of beta blockers1 should be decreased if the heart rate decreases to less than 50 beats/min and/or second- or third-degree heart block develops, or symptomatic hypotension develops. Continuation of beta blocker treatment 33 during an episode of acute decompensation is safe, although dose reduction may be necessary. Beta blockers are not recommended for patients with asthma who have active bronchospasm. The dose of aldosterone antagonist should be increased until the doses used are similar to those shown to be effective in clinical trials (see Table 25. As previously noted, potassium supplementation is generally stopped after the initiation of aldosterone antagonists, and patients should be counseled to avoid high–potassium-containing foods. Potassium levels and renal function should be rechecked within 3 days and again at 1 week after initiation of an aldosterone antagonist. Subsequent monitoring should be dictated by the general clinical stability of renal function and fluid status but should occur at least monthly for the first 6 months. Although the mechanism for the beneficial effect of spironolactone has not been fully elucidated, prevention of extracellular matrix remodeling (see Chapter 23) and prevention of hypokalemia levels are plausible mechanisms. Importantly, the effect of eplerenone was consistent across all prespecified subgroups. Aldosterone antagonists are not recommended when the serum creatinine is greater than 2. The development of worsening renal function should lead to consideration of stopping aldosterone antagonists because of the potential risk of hyperkalemia. Painful gynecomastia may develop in 10% to 15% of patients who use spironolactone, for whom eplerenone may be substituted. I Channel Inhibitor f Ivabradine is a heart rate–lowering agent that acts by selectively blocking the cardiac pacemaker If (“funny”) channel current that controls the spontaneous diastolic depolarization of the sinoatrial node. Ivabradine blocks I channels in a concentration-dependent manner by entering the channel pore from thef intracellular side, and thus it can only block the channel when it is open.

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Adenosine has a differential effect on coronary resistance 4 arteries generic 400mg viagra plus erectile dysfunction doctors in ct, primarily dilating vessels smaller than 100 µm discount 400mg viagra plus amex erectile dysfunction rates. Although adenosine has no direct effect on larger resistance arteries and conduit arteries order viagra plus 400mg with amex erectile dysfunction kegel exercises, these dilate through endothelium-dependent vasodilation 3 from the concomitant increases in local shear stress as arteriolar resistance falls. Despite the attractiveness of adenosine as a local metabolic control mechanism, substantial in vivo experimental data now demonstrate convincingly that it is not required for adjusting coronary flow to increases in 6 metabolism or autoregulation. However, adenosine may contribute to vasodilation during hypoxia as 2 well as during acute exercise-induced myocardial ischemia distal to a stenosis. It is a potentially attractive mechanism, because many of the other candidates for metabolic flow regulation (e. Studies demonstrating a direct effect of oxygen on metabolic or autoregulatory adjustments are lacking, however, and the vasodilator response to reduced arterial oxygen delivery may simply reflect the close relation between myocardial metabolism and flow. Arterial hypercapnia and acidosis are potent stimuli shown to produce coronary vasodilation independent of hypoxia. Because there is considerable oxygen extraction reserve, coronary flow decreases as pressure is reduced and oxygen delivery is maintained by increased extraction. Epicardial artery stenoses arising from atherosclerosis increase coronary resistance and reduce maximal myocardial perfusion. Abnormalities in coronary microcirculatory control also can contribute to causing myocardial ischemia in many patients. Separating the role of a stenosis from coronary resistance vessels can be accomplished by simultaneously assessing coronary flow and distal coronary pressure using intracoronary transducers currently available 11,12 for clinical care (see Chapter 62). Stenosis Pressure-Flow Relation The angiographically visible epicardial coronary arteries are normally able to accommodate large increases in coronary flow without producing any significant pressure drop and thus serve a conduit function to the coronary resistance vasculature. This fixed component of resistance increases with stenosis severity and limits maximal myocardial perfusion. As a starting point, it is helpful to consider the idealized relation among stenosis severity, pressure drop, and flow, as validated in animals as well as in humans studied under circumstances where diffuse atherosclerosis and risk factors that can impair microcirculatory resistance vessel control are minimized. The relation between pressure drop across a stenosis and coronary flow for stenoses between 30% and 90% diameter reduction can be described using the Bernoulli principle. The total pressure drop across a stenosis is governed by three hydrodynamic factors—viscous losses, separation losses, and turbulence—although the last usually is a relatively minor component of pressure loss. The most important determinant of stenosis resistance for any given level of flow is the minimum lesional cross-sectional area within the stenosis (see Classic References, Klocke, 1983). Because resistance is inversely proportional to the square of the cross- sectional area, small dynamic changes in luminal area caused by thrombi or vasomotion in asymmetric lesions (where vascular smooth muscle can relax or constrict in a portion of the stenosis) lead to major changes in the stenosis pressure-flow relation and reduce maximal perfusion during vasodilation. Separation losses determine the curvilinearity or “steepness” of the stenosis pressure-flow relation and become increasingly important as stenosis severity or flow rate increases. Stenosis length and changes in cross-sectional area distal to the stenosis are relatively minor determinants of resistance for most coronary lesions. It is inversely related to the minimum stenosis cross-sectional area and varies with the square of the flow rate as stenosis severity increases. A , Area of the normal segment; A , area of then s stenosis; f , viscous coefficient; f , separation coefficient; L, stenosis length; µ, viscosity of blood; ρ,1 2 density of blood; ΔP, pressure drop; Q̇, flow. Diffuse abluminal outward remodeling with thickening of the arterial wall is common in coronary atherosclerosis but does not alter the pressure-flow characteristics of the stenosis for a given intraluminal geometry. By contrast, diffuse inward remodeling effectively reduces minimal lesion area along the length of the vessel and can lead to underestimation of stenosis severity using relative diameter or area measurements (see Chapter 20) and at the same time can contribute to a significant longitudinal pressure 10 drop that also reduces maximum perfusion. Stenosis pressure drop and resistance increase exponentially as minimum lesional cross-sectional area decreases (Fig. This reflects that the pressure drop becomes flow dependent and varies with the square of the flow or flow velocity. As a result, the instantaneous stenosis resistance progressively increases during vasodilation. This becomes particularly important in determining the stenosis pressure- flow behavior for severely narrowed arteries, leading to a situation in which small reductions in luminal area result in large reductions in poststenotic coronary pressure that limit maximum coronary perfusion of the distal microcirculation. Red circles and lines depict resting flow, and blue circles and lines show maximal vasodilation for stenoses of 50%, 70%, and 90% diameter reduction. As shown in A, the stenosis pressure-flow relation becomes extremely nonlinear as stenosis severity increases. Thus the instantaneous resistance of the stenosis increases during vasodilation (B). As a result of the nonlinear stenosis pressure-flow behavior, very little pressure drop across a 50% stenosis is seen, and distal coronary pressure and vasodilated flow remain near normal. By contrast, a 90% stenosis critically impairs flow and, because of the steepness of the stenosis pressure-flow relation, causes a marked reduction in distal coronary pressure. Interrelation of Distal Coronary Pressure, Flow, and Stenosis Severity Because maximum myocardial perfusion is ultimately determined by the coronary pressure distal to a stenosis, it is helpful to place the epicardial stenosis pressure-flow relation into the context of the coronary autoregulatory and vasodilated coronary pressure-flow relations. Because of coronary autoregulation, flow remains constant as stenosis severity increases. Thus imaging resting perfusion cannot identify hemodynamically significant stenoses (see Chapter 16). By contrast, the maximally vasodilated pressure-flow relation is much more sensitive to detect increases in stenosis severity. There is normally substantial coronary flow reserve, and flow can increase approximately five times the resting flow values. As stenosis severity exceeds 50%, the curvilinear coronary stenosis pressure-flow relation steepens, and increases in stenosis resistance are accompanied by concomitant increases in ΔP across the stenosis (Fig. This reduces distal coronary pressure, the major determinant of perfusion to the microcirculation, and maximum vasodilated flow (and coronary flow reserve) decreases. A critical stenosis, one in which subendocardial flow reserve is completely exhausted at rest, usually develops when stenosis severity exceeds 90%. Under these circumstances, pharmacologic vasodilation of subepicardial resistance vessels results in a reduction in distal coronary pressure that actually redistributes flow away from the 6 subendocardium, leading to a “transmural steal” phenomenon. Concept of Maximal Perfusion and Coronary Reserve 10 Gould originally proposed the concept of coronary reserve. With technological advances, it has become possible to characterize this in humans using invasive catheter-based measurements of intracoronary pressure and flow (Fig. Because of these complexities, multiple complementary approaches frequently are required to define limitations in myocardial perfusion that arise from stenosis severity versus abnormalities of the coronary microcirculation. The three major indices currently used to quantify coronary flow reserve are absolute, relative, and fractional flow reserve (Fig. After intracoronary adenosine administration, flow velocity transiently increases and mean distal coronary pressure (Pd) falls. A, Absolute flow reserve is the ratio of coronary flow during vasodilation to the resting value. B, Relative flow reserve compares maximal vasodilated flow in a stenotic region with an assumed normal region in the same heart and is most commonly measured with perfusion imaging during stress.

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