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Potassium excretion is increased by metabolic alkalosis chart of cholesterol lowering foods discount atorlip-5 uk, diuresis cholesterol ratio of 5.1 buy atorlip-5 5mg on line, increased aldosterone release and increased losses from the gastrointestinal tract-all of which occur commonly in the surgical patient cholesterol lowering foods omega 3 order generic atorlip-5 line. In hypokalaemia cholesterol medication natural cheap atorlip-5 5mg, for Other electrolyte disturbances Calcium Clinically significant abnormalities in calcium balance in the surgical patient are most frequently encountered in endocrine surgery (see Chapter 20). Magnesium Hypomagnesaemia is common in surgical patients who have restricted oral intake and who have been receiving intravenous fluids for several days. It is frequently associated with other electrolyte abnormalities, notably hypokalaemia, hypocalcaemia and hypophosphataemia. Consider oral or rectal calcium resonium (ion exchange resin) Antagonises the membrane actions of " K+ reducing the risk of ventricular arrhythmias Increases transcellular shift of K+ into cells Increases transcellular shift of K+ into cells Facilitates K+ clearance across gastrointestinal mucosa. Arterial blood gas analysis is a straightforward technique, with samples typically taken from the radial artery. Base deficit is a measure of the amount of bicarbonate required to correct acidosis. Metabolic acidosis can occur as a result of increased production of endogenous acid. Renal replacement therapy associated with a predisposition to tachyarrhythmias (most notably torsades de pointes [polymorphic ventricular tachycardia] and atrial fibrillation), but many of the clinical manifestations of magnesium depletion are nonspecific (muscle weakness, muscle cramps, altered mentation, tremors, hyperreflexia and generalised seizures). As magnesium is predominantly intracellular, serum magnesium levels poorly reflect total body stores. Despite this limitation, serum levels are frequently used to guide (oral or parenteral) magnesium supplementation. When hypokalaemia and hypomagnesaemia coexist it may be difficult to correct the former without correcting the latter. Most hypophosphataemia results from the shift of phosphate into cells and most commonly occurs in chronically malnourished and/or alcoholic patients commencing enteral or parenteral nutrition. The increased carbohydrate load leads to insulin secretion, which results in the rapid intracellular uptake of glucose and phosphate together with magnesium and potassium. To avoid this syndrome, feeding should be established gradually and accompanied by regular measurement and aggressive supplementation of serum electrolytes (phosphate, magnesium and potassium). The most common cause of metabolic acidosis encountered in surgical practice is shock and impaired tissue oxygen delivery (see section on shock). Treatment is directed towards restoring circulating blood volume and tissue perfusion. Adequate resuscitation typically corrects the metabolic acidosis seen in this context. Another common cause of acidosis is acute kidney injury, which will be evident from measurement of urea and creatinine, and clinical signs of oliguria. In the surgical patient, respiratory acidosis usually results from respiratory depression and hypoventilation. This is common on emergence from general anaesthesia and following excessive opiate administration. Occasionally, respiratory acidosis occurs in the context of pulmonary complications such as pneumonia. This is more usual in very sick patients or those with pre-existing respiratory disease. Patients with this cause of respiratory acidosis frequently require ventilatory support as the hypercapnia observed reflects inadequate respiratory muscle strength to cope with an increased work of breathing. Metabolic alkalosis Metabolic alkalosis is characterised by a decrease in plasma hydrogen ion concentration and an increase in bicarbonate concentration. The kidney has an enormous capacity to generate bicarbonate ions and this is stimulated by chloride loss. This is a major contributor to the metabolic alkalosis seen following significant (chloride-rich) losses from the gastrointestinal tract, especially when combined with loss of acid from conditions such as gastric outlet obstruction. Hypokalaemia is often associated with metabolic alkalosis because of the transcellular shift of hydrogen ions into cells and because distal renal tubular cells retain potassium in preference to hydrogen ions. Respiratory alkalosis is rarely chronic and usually does not need specific treatment. Patients may present with features of tetany due to a fall in the ionised levels of calcium due to alkalosis. These changes impair tissue oxygen delivery and are associated with significantly increased mortality (>40%). Sepsis usually arises from a localised infection, with gramnegative (38%) and increasingly gram-positive (52%) bacteria being the most frequently identified pathogens. Although shock is sometimes considered to be synonymous with hypotension, it is important to realise that tissue oxygen delivery may be inadequate even though the blood pressure and other vital signs remain normal. This results in cell dysfunction and ultimately cell death and multiple organ failure. Infection triggers a cytokine-mediated proinflammatory response that results in peripheral vasodilatation, redistribution of blood flow, endothelial cell activation, increased vascular permeability and the formation of microthrombi within the microcirculation. Cardiac output typically increases in septic shock to compensate for peripheral vasodilatation. However, despite a global increase in oxygen delivery, microcirculatory dysfunction impairs oxygen delivery to the cells. Compounding disturbances in oxygen delivery, mitochondrial dysfunction may block the normal bioenergetic pathways within the cell, impairing oxygen utilisation.
Structural changes in the left side of the heart and arterial vessels occur in response to systemic hypertension hdl cholesterol in shrimp order 5 mg atorlip-5 otc. Early alterations include hypertrophy of muscle cells and thickening of the walls of the ventricle and systemic resis tance vessels cholesterol medication new purchase atorlip-5 once a day. Late changes associated with deterioration of function include increases in connective tissue and loss of elasticity cholesterol ratio american heart association buy discount atorlip-5 5mg on line. The established phase of hypertension is associated with an increase in total peripheral resistance cholesterol chart by age generic 5mg atorlip-5 with visa. Cardiac output and/or blood volume may be elevated during the early developmental phase, but these variables are usually normal after the hypertension is established. The increased total peripheral resistance associated with established hyper tension may be due to (a) rarefaction (decrease in density) of microvessels, (b) pronounced structural adaptations that occur in the peripheral vascular bed, (c) continuously increased activity of the vascular smooth muscle cells,U 11 Continuous activation of vascular smooth muscle might be evoked by autoregulatory responses to increased blood pressure, as discussed in Chapter 6. A total body autoregulation could produce an increase in total peripheral resistance so that total systemic flow (ie, cardiac output) would remain nearly normal in the presence of increased mean arterial pressure. The chronic elevation in blood pressure does not appear to be due to a sustained elevation in sympathetic vasoconstrictor neural discharge nor is it due to a sus tained elevation of any blood-borne vasoconstrictive factor. Blood pressure-regulating reflexes (both the short-term arterial and cardiopul monary baroreceptor reflexes and the long-term, renal-dependent, pressure regulating reflexes) become adapted or "reset" to regulate blood pressure at a higher-than-normal level. Recall that the urinary output rate is influenced by arterial pressure, and, in the long term, arterial pressure can stabilize only at the level that makes urinary output rate equal to fluid intake rate. As shown by point N in Figure 11-6, this pressure is approximately 100 mm Hg in a normal individual. All forms of hypertension involve an alteration somewhere in the chain of events by which changes in arterial pressure produce changes in urinary output rate (see Figure 9-6) such that the renal function curve is shifted rightward, as indicated in Figure 11-6. The important feature to note is that higher-than-normal arterialpressure is required to produce a normal urinary output rate in a hypertensive individual. Although this condition is always present with hypertension, it is not clear whether it could be the common cause of hypertension or simply another one of the many adaptations to it. Recall from Figure 9-5 that whenever the fluid intake rate exceeds the urinary output rate, fluid volume must rise and consequently so will cardiac output and mean arterial pressure. With a normal fluid intake rate, this untreated hypertensive patient will ultimately stabilize at point A (mean arterial pressure 150 mm Hg). Recall from Chapter 9 that the baroreceptors adapt within days so that they have a normal discharge rate at the prevailing average arterial pressure. A most important fact to realize is that, although either high cardiac output or high total peripheral resistance must always ultimately sustain high blood pressure, neither needs be the primary cause of the hypertension. A shift in the relationship between arterial pressure and urinary output rate, as illustrated in Figure 11-6, however, will always produce hypertension. The possibility that the kidneys actually "set" the blood pressure is supported by evidence accumulating from kidney transplant studies. In these studies, the blood pressure is shown to "follow" the kidney (ie, putting a hypertensive kidney in a normotensive indi vidual produces a hypertensive individual, whereas putting a normotensive kidney in a hypertensive individual produces a normotensive individual). Further support for an essential role of the kidney comes from recent studies showing that catheter based, high-frequency radiowave ablation of renal sympathetic nerves effectively reduces hypertension in drug-resistant patients. Therapeutic Strategies for Treatment of Systemic Hypertension In certain hypertensive individuals, restricting salt intake produces a substantial reduction in blood pressure because of the reduced requirement for water reten tion to osmotically balance the salt load. In the example in Figure 11-6, this effect is illustrated by a shift from point A to point B. The efficacy of lowering salt intake to lower arterial pressure depends heavily on the slope of the renal function curve in the hypertensive individual. The arterial pressure of a healthy individual, for example, is affected only slightly by changes in salt intake because the normal renal function curve is so steep. Many diuretic drugs are available, but most have the effect of inhibiting renal tubular salt (and therefore fluid) reabsorption. The net effect of diuretic therapy, as shown in Figure 11-6, is that the urinary output rate for a given arterial pressure is increased; that is, diuretic therapy raises the renal function curve. The combined result of restricted fluid intake and diuretic therapy for the hypertensive indi vidual in Figure 11-6 is illustrated by point C. A third therapeutic intervention is treatment with -adrenergic blockers that inhibit sympathetic influences on the heart and renal renin release. This approach is most successful in hypertensive patients who have high circulating renin levels. Alterations in life style, including reduction of stress, decreases in caloric intake, limitation of the amount of saturated fats in the diet, and establishment of a regular exercise program, may help reduce blood pressure in certain individuals. The possibility of catheter-based renal sympathetic denervation for treatment of refractory hypertension is quite intriguing and may become another approach to handling this condition in the future. Treatment may be based upon a dictated "standard of care" and, although concern for the patient is present, the thought process is limited. Understanding the basic principles of normal cardiovascular operation should provide a firm foundation for identify ing the underlying abnormalities, distinguishing the primary disturbances from the compensatory responses, understanding the mechanisms responsible for the symptoms, and appropriately treating the condition. The primary disturbances that can lead to shock can be categorized as those that directly interfere with pump function, those that interfere with ventricular filling, or those that cause sustained vascular dilation. Shock is usually accompanied by a compensatory increase in sympathetic activity aimed at maintaining arterial pressure via augmented cardiac output and vascu lar resistance. Decompensatory processes precipitated by the shock state are generally caused by inadequate tissue blood flow, loss of local homeostasis, and tissue damage leading to a progressive and irreversible fall in arterial pressure. Acute heart failure due to an abrupt blockage of a major coronary artery is a form of cardiogenic shock. Systolic heart failure is defined as a reduction of cardiac muscle contractility and results in a depressed cardiac output at all preloads with reduced ejection fraction. Compensatory fluid retention mechanisms are evoked in heart failure to improve cardiac filling, but when fluid retention is excessive, congestive complications arise (eg, pulmonary edema and abdominal ascites). Diastolic dysfunction resulting from reduced cardiac compliance and impaired diastolic filling may precipitate heart failure even though ejection fraction is preserved.
The critical step in blood clotting is the formation of thrombin from prothrom bin cholesterol vitamins cost of atorlip-5, which then catalyzes the conversion of fibrinogen to fibrin cholesterol test drug store atorlip-5 5 mg without a prescription. Vessel injury or tissue damage with blood exposure to subendothelial cells that release thromboplastin ("tissue factor") cholesterol ratio chart canada cheap atorlip-5 5 mg without a prescription. Activates platelets (makes them sticky cholesterol in shrimp and lobster buy atorlip-5 in united states online, induces degranulation, and pro motes attachment of various factors that participate in clotting). Recruits the "intrinsic pathway," which amplifies further formation of fac tor Xa and facilitates the conversion of prothrombin to thrombin by pro moting the following reactions: a. Conversion of factor V to its activated form, Va, which attaches to activated platelets and accelerates conversion of prothrombin to thrombin. Aspirin and other cyclooxygenase inhibitors are anticoagu lants because they prevent the formation of thromboxane. These agents promote the formation of plasmin from plasminogen, which enzymatically attacks the clot, turning it into soluble peptides. However, in certain situations-especially when there are multiple disturbances on the cardiovascular system-a more detailed understanding is helpful. Consequently, the operation of the arterial baroreflex is presented in this appendix with a more formal control system approach. The complete arterial baroreceptor reflex pathway is a control system made up of two distinct portions, as shown in Figure E-1: (1) an effector portion, includ ing the heart and peripheral blood vessels; and (2) a neural portion, including the arterial baroreceptors, their afferent nerve fibers, the medullary cardiovascular centers, and the efferent sympathetic and parasympathetic fibers. Mean arterial pressure is the output of the effector portion and simultaneously the input to the neural portion. Similarly, the activity of the sympathetic (and parasympathetic) cardiovascular nerves is the output of the neural portion of the arterial barorecep tor control system and, at the same time, the input to the effector portion. For convenience, we omit continual reference to parasympathetic nerve activity in the following discussion. Throughout, however, an indicated change in sympathetic nerve activity should usually be taken to imply a reciprocal change in the activity of the cardiac parasympathetic nerves. A host of reasons why mean arterial pressure increases when the heart and peripheral vessels receive increased sympathetic nerve activity are discussed in Chapters 2 through 8. All this information is summarized by the curve shown in the lower graph in Figure E-1, which describes the operation of the effector por tion of the arterial baroreceptor system alone. In Chapter 9, how increased mean arterial pressure acts through the arterial baroreceptors and medullary cardiovas cular centers to decrease the sympathetic activity has also been discussed. This information is summarized by the curve shown in the upper graph in Figure E-1, which describes the operation of the neural portion of the arterial baroreceptor system alone. When the arterial baroreceptor system is intact and operating as a closed loop, the effector portion and neural portion retain their individual rules of opera tion, as described by their individual function curves in Figure E-1. The analysis of the complete system begins by plotting the operating curves for the neural and effector portions of the systems together on the same graph as in Figure E-2A. To accomplish this superimposition, the graph for the neural portion (the upper graph in Figure E-1) was flipped to interchange its vertical and horiwntal axes. Consequently, the neural curve but not the effector curve) in Figure E-2A must be read in the unusual sense that its independent variable, arterial pressure, is on the vertical axis and its dependent variable, sympathetic nerve activity, is on the horizontal axis. Whenever there is any outside disturbance on the cardiovascular system, the operating point of the arterial baroreceptor system shifts. This happens because all cardiovascular disturbances cause a shift in one or the other of the two curves in Figure E-2A. Operation of the arterial baroreceptor control system: (A) normal balance and (B) operating point shift with disturbance on the effector portion. The disturbance in this case could be anything that reduces the arterial pressure produced by the heart and vessels at each given level ofsympathetic activity. As shown by point 2 in Figure E-2B, any pressure-lowering disturbance on the heart or vessels causes a new balance to be reached within the baroreceptor system at a slightly lower than normal mean arterial pressure and a higher than normal sympathetic activity level. As indicated previously in this chapter, many disturbances act on the neural portion of the arterial baroreceptor system rather than directly on the heart or vessels. These disturbances shift the operating point of the cardiovascular system because they alter the operating curve of the neural portion of the system. For example, the influences listed in Figure 9-4 that raise the set point for arterial pressure do so by shifting the operating curve for the neural portion of the arterial baroreceptor system to the right, as shown in Figure E-3A, because they increase the level of sympathetic output from the medullary cardiovascular centers at each and every level of arterial pressure (ie, at each and every level of input from the arterial baroreceptors). For example, a sense of danger will cause the components of the arterial baroreceptor system to come into balance at a higher than normal arterial pressure and a higher than normal sympathetic activity, as shown by point 2 in Figure E-3A. Conversely, but not shown in Figure E-3, any of the set-point lowering influences listed in Figure 9-4 acting on the medullary cardiovascular centers will shift the operating curve for the neural portion of the arterial barore ceptor system to the left, and a new balance will be reached at lower than normal arterial pressure and sympathetic activity. Many physiological and pathological situations involve simultaneous distur bances on both the neural and effector portions of the arterial baroreceptor system. The set-point-increasing disturbance on the neural portion of the system alone causes the equilibrium to shift from point 1 to point 2. Superimposing a pressure-lowering disturbance on the heart or vessels further shifts the equilibrium from point 2 to point 3. Note that, although the response to the pressure-lowering disturbance in Figure E-3B (point 2 to point 3) starts from a higher than normal arterial pressure, it is essen tially identical to that which occurs in the absence of a set-point-increasing influence on the cardiovascular center (see Figure E-2B). Thus, the response is an attempt to prevent the arterial pressure from falling below that at point 2. The overall implication is that any of the set-point-increasing influences on the med ullary cardiovascular centers listed in Figure 9-4 cause the arterial baroreceptor system to regulate arterial pressure to a higher than normal value. Conversely, the set-point-lowering influences on the medullary cardiovascular centers listed in Figure 9-4 would cause the arterial baroreceptor system to regulate arterial pres sure to a lower than normal value.
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