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By F. Campa. Lake Forest Graduate School of Management.

The decades from World War II through the implementation of Medicare are gen- erally considered American medicine’s “golden age cheap 40mg propranolol with mastercard. Dramatic increases in malprac- tice litigation toward the end of this period arguably sought to justify the public’s trust cheap 80 mg propranolol amex. Lawsuits imposed real emotional and reputational costs on defendants but seldom constituted a severe financial burden. As studies from the 1980s demonstrated, even substantial increases in liability insurance premiums were quickly passed through to patients and payers as higher fees (6,7). By contrast, the current malpractice crisis follows nearly two decades of sustained effort to rein in health care spending. Cost-based reimbursement and “usual and customary” fees are, in most cases, distant memories. Medicare pays administrative prices that are not responsive to unexpected jumps in short-term input costs for providers. Private health insurers are equally reluctant to renegotiate provider contracts. Lack of these safety valves potentially impairs access to care for patients in already underserved communities if hospitals or physi- cians find liability insurance unaffordable. Even in areas where the supply of physicians and hospitals remains high, the health care system is less financially resilient and a malpractice crisis can seriously disrupt medical careers and therapeutic relationships. Cost containment has also had important direct effects on malprac- tice exposure and on physicians’ reactions to it. Higher throughput to maintain revenue, greater delegation of tasks to nonprofessional staff, and complex administrative systems of managed care oversight all increase risk of error, and the undercurrent of financial motivation makes patients less trusting and more litigious. Against this backdrop of cost-containment, a widening malpractice crisis epitomizes physi- cians’ growing sense that they have lost control over their professional lives. This strikes physicians as particularly unfair because tort law still attributes to them a much higher degree of clinical autonomy and authority than their day-to-day experiences suggest. The litigation process is too slow, too costly, too uncertain, and too unpleasant. Premiums for primary liability coverage are too volatile and, for some physicians, too expensive. Excess coverage and reinsurance are becoming unaffordable for hospitals and other medical institutions. EXPOSED WEAKNESSES IN THE MALPRACTICE SYSTEM The pressures described in the preceding section have exposed major weaknesses in the way that allegations of medical malpractice are handled. Much like the American health care system itself, the mal- practice system is a patchwork of historically derived institutions and practices rather than a product of careful deliberation or rational social choice. The malpractice system has three basic goals: (a) reducing rates of iatrogenic injury (“deterrence”), (b) relieving the burden on those who have suffered such injury (“compensation”), and (c) distinguish- ing blameless from blameworthy conduct (“justice”). In pursuit of these goals, liability is filtered through three functional components of the malpractice system: patient care, legal process, and liability insurance (8,9). Available evidence indicates that all three com- ponents fall well short of ideal performance (see Table 1). Optimal levels of patient safety are achievable only if the health care system has clear, consistent incentives to gather information about errors, process that information into prevention strategies, coordinate the actions of individual and institutional providers, and communicate effectively with patients. The legal system should provide these incentives by exposing instances of iatrogenic injury, demanding persuasive evidence of avoidability, and awarding damages consistent with loss. The insur- ance markets should support the legal system by offering peace of mind to careful physicians and making compensation available to victims. Insurers should dispose of meritless claims, help providers improve their safety records, and weed out the worst offenders. Chapter 17 / New Directions in Liability Reform 255 Patient Care AVOIDABLE INJURIES The tort reform movement of the 1970s and 1980s was based on two related beliefs: (a) few incidents of actual negligence occur in health care, and (b) most litigation reflects social and financial influences apart from medical quality (10). Subsequent research, much of which is a direct outgrowth of public interest in malpractice reform, largely confirmed the second perception but refuted the first.

Quantification of the architectural of these numbers nearly double after a large meal generic 40mg propranolol. Unless the changes observed in intestinal arterioles from diabetic rats buy propranolol 40mg with mastercard. Blood flows of 70 to 100 mL/min high blood flow both at rest and during food absorption, per 100 g in this specialized tissue are probable and much the capillary blood pressure is usually 13 to 18 mm Hg higher than the average blood flow for the total intestinal and seldom higher than 20 mm Hg during food absorp- wall (see Table 17. Therefore, plasma colloid osmotic pressure is ing blood flow in the heart and brain. The interstitial space of the villi is mildly hy- sorption, the plasma protein reflection coefficient for the perosmotic ( 400 mOsm/kg H2O) at rest as a result of NaCl. It is assumed that to 600 to 800 mOsm/kg H2O near the villus tip, compared most of the decrease in reflection coefficient occurs in with 400 mOsm/kg H2O near the villus base. This lowers the ability of plasma cause of high osmolalities in the villi appears to be greater ab- proteins to counteract capillary filtration, with the net re- sorption than removal of NaCl and nutrient molecules. Eventu- is also a possible countercurrent exchange process in which ally, this fluid must be removed. Not surprisingly, the materials absorbed into the capillary blood diffuse from the highest rates of intestinal lymph formation normally oc- venules into the incoming blood in the arterioles. Food Absorption Requires a High Blood Flow Sympathetic Nerve Activity Can Greatly Decrease to Support the Metabolism of the Mucosal Intestinal Blood Flow and Venous Volume Epithelium The intestinal vasculature is richly innervated by sympa- Lipid absorption causes a greater increase in intestinal thetic nerve fibers. Major reductions in gastrointestinal blood flow, a condition known as absorptive hyperemia, blood flow and venous volume occur whenever sympa- and oxygen consumption than either carbohydrate or thetic nerve activity is increased, such as during strenuous amino acid absorption. During absorption of all three exercise or periods of pathologically low arterial blood classes of nutrients, the mucosa releases adenosine and pressure. Venoconstriction in the intestine during hemor- CO and oxygen is depleted. The hyperosmotic lymph and rhage helps to mobilize blood and compensates for the 2 venous blood that leave the villus to enter the submucosal blood loss. Gastrointestinal blood flow is about 25% of the tissues around the major resistance vessels are also major cardiac output at rest; a reduction in this blood flow, by contributors to absorptive hyperemia. By an unknown heightened sympathetic activity, allows more vital func- mechanism, hyperosmolality resulting from NaCl induces tions to be supported with the available cardiac output. Hyperosmolality result- decreased by a combination of low arterial blood pressure ing from large organic molecules that do not enter en- (hypotension) and sympathetically mediated vasoconstric- dothelial cells does not cause appreciable increases in NO tion that mucosal tissue damage can result. These observations suggest that NaCl entering the en- HEPATIC CIRCULATION dothelial cells is essential to induce NO formation. The hepatic circulation perfuses one of the largest organs in The active absorption of amino acids and carbohydrates the body, the liver. The liver is primarily an organ that and the metabolic processing of lipids into chylomicrons maintains the organic chemical composition of the blood by mucosal epithelial cells place a major burden on the mi- plasma. For example, all plasma proteins are produced by crovasculature of the small intestine. There is an extensive the liver, and the liver adds glucose from stored glycogen network of capillaries just below the villus epithelial cells to the blood. The villus capillaries are unusual in and bacteria and detoxifies many man-made or natural or- that portions of the cytoplasm are missing, so that the two ganic chemicals that have entered the body. These areas of fusion, or closed fenestrae, are thought to facilitate the uptake of absorbed materials by The Hepatic Circulation Is Perfused by capillaries. In addition, intestinal capillaries have a higher Venous Blood From Gastrointestinal Organs filtration coefficient than other major organ systems, which and a Separate Arterial Supply probably enhances the uptake of water absorbed by the villi (see Chapter 16). However, large molecules, such as plasma The human liver has a large blood flow, about 1. It is perfused by both the reflection coefficient for the intestinal vasculature is arterial blood through the hepatic artery and venous greater than 0. CHAPTER 17 Special Circulations 283 The venous blood arrives via the hepatic portal vein and accounts for about 67 to 80% of the total liver blood flow (see Table 17. The remaining 20 to 33% of the total flow is through the hepatic artery. The majority of blood flow to the liver is determined by the flow through the stomach and small intestine. About half of the oxygen used by the liver is derived from venous blood, even though the splanchnic organs have removed one third to one half of the available oxygen.

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The most important function of the (B) Contracting and forcing lymph underlying the vascular myogenic re- microcirculation is into larger lymphatics sponse discount 80 mg propranolol mastercard. Baltimore: wastes between blood and tissue valves in the lymph vessels Williams & Wilkins order propranolol 40 mg with visa, 1982;11–96. Modelling the capillaries pressure inside the lymph vessel structural pathways for transcapillary (C) The regulation of vascular (E) Closing the opening between exchange. Symp Soc Exp Biol resistance adjacent lymphatic endothelial cells 1995;49:323–345. The ability of the heart to pump blood depends almost ex- because of its limited oxygen requirements, but flow and clusively on oxygen supplied by the coronary microcircula- oxygen use can increase up to or beyond 20-fold during in- tion. The skin has a low oxygen requirement, but the high blood and require additional oxygen. The regulation of intestinal blood flow during nutrient ab- large amount of heat for dissipation to the external envi- sorption depends on the elevated sodium chloride concen- ronment. The liver receives the portal venous blood from the gas- blood supply, using the combined maternal and fetal pla- trointestinal organs as its main blood supply, supple- cental circulations. Skeletal muscle tissue receives minimal blood flow at rest ing blood in the fetus and adult. The features of each vasculature, which ment in blood flow constitutes the coronary blood flow re- are related to the specific functions and specialized needs serve. The ability to increase the blood flow to provide addi- of each organ or tissue, are described. Heart tissue extracts almost the anatomy and physiology of the fetus and placenta and the maximum amount of oxygen from blood during resting con- circulatory changes that occur at birth are also presented. Because the heart’s ability to use anaerobic glycolysis The pulmonary and renal circulations are discussed in to provide energy is limited, the only practical way to increase Chapters 20 and 23. The production of lactic acid by the heart is an omi- nous sign of grossly inadequate oxygenation. CORONARY CIRCULATION The Work Done by the Heart Determines Its Cardiac Blood Flow Decreases During Systole and Oxygen Use and Blood Flow Requirements Increases During Diastole The coronary circulation provides blood flow to the heart. Blood flow through the left ventricle decreases to a minimum During resting conditions, the heart muscle consumes about when the muscle contracts because the small blood vessels 276 CHAPTER 17 Special Circulations 277 TABLE 17. Blood flow in the left coronary artery during derived from the breakdown of adenosine triphosphate cardiac systole is only 10 to 30% of that during diastole, (ATP) in cardiac cells, is a potent vasodilator, and its release when the heart musculature is relaxed and most of the blood increases whenever cardiac metabolism is increased or flow occurs. The compression effect of systole on blood flow blood flow to the heart is experimentally or pathologically is minimal in the right ventricle, probably as a result of the decreased. Blockade of the vasodilator actions of adenosine lower pressures developed by a smaller muscle mass with theophylline, however, does not prevent coronary va- (Fig. Changes in blood flow during the cardiac cycle sodilation when cardiac work is increased, blood flow is in healthy people have no obvious deleterious effects even suppressed, or the arterial blood is depleted of oxygen. Vasodilatory prostaglandins, H , The heart musculature is perfused from the epicardial CO2, NO, and decreased availability of oxygen, as well as (outside) surface to the endocardial (inside) surface. Mi- myogenic mechanisms, are capable of contributing to coro- crovascular pressures are dissipated by blood flow friction nary vascular regulation. No single mechanism adequately as the vessels pass through the heart tissue. Therefore, the explains the dilation of coronary arterioles and small arter- mechanical compression of systole has more effect on the ies when the metabolic rate of the heart is increased, or blood flow through the endocardial layers where compres- when pathological or experimental means are used to re- sive forces are higher and microvascular pressures are strict blood flow. This problem occurs particularly in heart diseases of dothelial cells—in response to blood flow-mediated dila- all types, and most kinds of tissue impairment affect the tion (see Chapter 16) and in response to ATP, adenosine subendocardial layers. Coronary Vascular Resistance Is Primarily Coronary arteries and arterioles are innervated by the Regulated by Responses to Heart Metabolism sympathetic nervous system and can be constricted by nor- Animal studies indicate that about 75% of total coronary epinephrine, whether released from nerves or carried in the vascular resistance occurs in vessels with inner diameters of arterial blood. This observation is supported by more important in equalizing blood flow through the lay- clinical measurements in humans that show little arterial ers of the heart than in reducing blood flow to the heart pressure dissipation in normal coronary arteries prior to muscle in general. The coronary arteries and larger arteri- their smaller branches entering the heart muscle tissue. The oles predominately have 1 receptors, which induce vascu- majority of the coronary resistance vessels—the small ar- lar constriction when activated by norepinephrine.

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The inferior cerebellar peduncle (restiform (A4) cheap propranolol 80mg fast delivery, the central lobule (A5) 40mg propranolol visa, the nodulus body) (AC22), which ascends from the (A6), the uvula (A7), and also the flocculus lower medulla oblongata; it contains the (A8). The vallecula of the cerebellum (A9) is spinocerebellar tracts and the connec- surrounded on both sides by the tonsillae tions to the vestibular nuclei (A10). The medial cerebellar peduncle (brachium pontis) (AC23) with the fiber masses The following parts are also visible: biven- from the pons, which originate from the tral lobule (A11), superior semilunar lobule pontine nuclei and represent the con- (A12), inferior semilunar lobule (A13), tinuation of the corticopontine tracts simple lobule (A14), quadrangular lobule! The superior cerebellar peduncle (brachium (A15), and wing of the central lobule (A16). It receives fibers from the cortex of the vermis, the vestibular nuclei, and the olive. It sends fibers to the vestibular nuclei and other nuclei of the medulla oblongata. The globose nucleus (B19), too, is thought to receive fibers from the cortex of the vermis and to send fibers to the nuclei of the medulla oblongata. Fibers of the cerebellar cortex from the region between vermis and hemisphere (intermediate part) are thought to terminate at the hilum of the dentate nu- cleus in the emboliform nucleus (B20). The fibers of the latter nucleus run through the Kahle, Color Atlas of Human Anatomy, Vol. Cerebellar Peduncles and Nuclei 155 4 15 2 16 5 14 1 6 7 24 23 3 22 8 12 11 10 9 13 A Anterior view 18 19 21 20 25 B Cerebellar nuclei 26 27 33 17 28 24 22 23 29 30 31 32 C Cerebellar peduncles (according to Büttner) Kahle, Color Atlas of Human Anatomy, Vol. Projection of the convoluted relief of (primary and secondary dendrites) have a the human cerebellum onto a plane results smooth surface (C7) and are covered with in an expanse of 1m in length in the oro- synapses. The fine terminal branches are caudal dimension (from the lingula to the dotted with short spines (C8). The cortex is regularly structured cell carries approximately 60000 spinous throughout all regions of the cerebellum. Different fiber systems terminate consists of three layers: at the smooth and spiny sections of the cell:! The molecular layer (A1) lies beneath the The axon (B9) departs from the base of the surface; it contains few cells and consists Purkinje cell and extends through the mainly of unmyelinated fibers. The neurons we can distinguish the outer stel- axons of Purkinje cells terminate at neurons late cells (lying close to the surface) and the of the cerebellar nuclei (p. Purkinje cells use layer (ganglionic layer) (A2) is formed by GABA as neurotransmitter. It is very rich in cells, consisting of densely packed, small neurons, the granule cells. Purkinje Cells (B–D) The Purkinje cell represents the largest and most characteristic cell of the cerebellum. The Nissl stain shows the pear-shaped cell body (B4) filled with coarse Nissl bodies. Also visible are the basal portions of two or three dendrites (B5) at the upper pole of the cell. However, the cell’s entire expanse with all its processes can only be visualized by Golgi impregnation or intracellular staining. The primary stems of the dendrites ramify into further branches, and these again into finearborizationsthatformthedendritictree (B6). The dendrites spread in a two-dimen- sional plane like the branches of an espalier tree. The Purkinje cells are arranged in a strictly geometric fashion; spaced at rela- tively regular intervals, they form a row be- tween granular and molecular layers and sendtheirdendritictreesintothemolecular layer toward the surface of the folium. Cerebellar Cortex 157 1 2 3 A Cerebellar folium, Nissl stain 5 6 4 B Purkinje cell, silver im- pregnation (according to Fox) and Nissl stain 9 7 8 D Arrangement of the Purkinje cells C Detail of B within a folium Kahle, Color Atlas of Human Anatomy, Vol. Their dendritic trees, neurons run in all directions and reach ap- which ramify predominantly in the molecu- proximately 12 Purkinje dendritic trees. The cells have short axons, which In the lower third of the molecular layer lie either terminate in a glomerulus or ramify the slightly larger basket cells (A1). The Golgi long axons run horizontally above the cells belong to the inhibitory interneurons. Purkinje cell bodies and give off collaterals, the terminal branches of which form net- Glia (D) works (baskets) around the Purkinje cell Apart from the regular glial cell types, such bodies. The electron-microscopic image as the oligodendrocytes (D5) and proto- shows that the basket cell fibers form plasmic astrocytes (D6) commonly found in numerous synaptic contacts (B2) with the the granular layer, there are also glial cells Purkinje cell, namely, at the base of the cell that are characteristic for the cerebellum: body (axon hillock) and at the initial seg- Bergmann’s glia and the penniform glia of ment of the axon up to where the myelin Fañanás.

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