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Deputy Director, University of Maryland School of Medicine
Ventricular fibrillation is the cause for most of the other instances of sudden cardiac arrest with a relatively small proportion of people developing asystole as the initial manifestation of sudden cardiac arrest menstruation 2 weeks long purchase discount ginette-35 on-line. The true incidence of the precipitating arrhythmia is not known because most sudden cardiac arrests occur out of hospital and typically menstrual period calendar generic 2 mg ginette-35 mastercard, several minutes pass before the rhythm can be assessed womens health questions answers buy 2 mg ginette-35 amex. The cardiac diseases that lead to the genesis of ventricular fibrillation resulting in cardiac collapse are varied women's health clinic yuma arizona buy ginette-35 2 mg low price, and the association with sudden death in some cases is not well understood. Similar to patients who have cardiovascular collapse from ventricular tachyarrhythmias, there are patients who develop ventricular fibrillation who do not have identifiable structural heart disease. Weisfeldt and Becker12 have proposed a t hree-phase model of resuscitation: the electrical phase, the circulatory phase, and the metabolic phase. The electrical phase begins with the cardiac collapse and lasts for approximately 4 m inutes; the circulatory phase represents an approximation of 6 minutes window from 4 to 10 minutes; and the metabolic window which commences at approximately 10 minutes. The best outcomes are achieved if the heart is defibrillated within the first 4 minutes after the cardiac arrest, during the electrical phase. This observation has been borne out by studies of patients who have an implantable cardioverter defibrillator. One meta-analysis of three large such studies that compared the administration of amiodarone to implantation of an implantable cardioverter defibrillator demonstrated decreased arrhythmias and improved survivability in patients who had an internal defibrillator. Another animal study showed that once the circulatory phase has begun, a threefold improvement in results is obtained if chest compressions are performed first, along with the administration of epinephrine and then defibrillation attempted compared to performing the defibrillation first and then performing chest compressions. Improvements in early hemorrhage control and resuscitation and the prevention and aggressive treatment of coagulopathy appear to have the greatest potential to improve outcomes in severely injured trauma patients. A cascade of life-threatening medical problems can begin with severe hemorrhage, and many of these occur simultaneously: (a) hemorrhage, (b) impaired resuscitation, (c) shock, (d) inflammation, and (e) coagulopathy. The severity of each problem is commonly associated with the extent of overall blood loss. Low blood pressure due to blood loss indicates immediate complications, including the incidence of multiple organ failure and life-threatening infections. Respiratory Arrest Respiratory and cardiac arrest are distinct, but if untreated, one inevitably leads to the other. There are a multitude of etiologies of respiratory arrest, and respiratory arrest per se implies any process that inhibits the delivery of sufficient oxygen to the mitochondria to maintain aerobic metabolism. The respiratory centers in the brainstem can be injured by penetrating injury and by increased intracranial pressure due to infection or intraventricular hemorrhage. There are a number of drugs that can depress the respiratory centers, most notably opioids, sedatives, and hypnotics. The hemoglobin in the circulating blood carries enough O2 for maintenance of aerobic metabolism for 1 to 3 m inutes. For a 70-kg p erson, breathing Hemorrhagic Shock In patients who sustain traumatic injury, hemorrhage accounts for 30% to 40% of the deaths. Among traumatized patients who arrive at the hospital, mortality in the first several hours correlates with inadequate resuscitation and the presence of coagulopathy. In both civilians and wounded warriors, it is impossible to quantify the amount of blood that is lost from the intravascular circulation, but an estimate can be made from the amount of blood transfused, the degree of lactic acidosis, and the alterations and vital signs. In an observational study of patients who refused blood transfusions because of religious beliefs, there was no 30-day mortality among patients whose hemoglobin was greater than 7. However, as the hemoglobin level decreased below 6 g/dL, mortality increased significantly. At 3 to 4 minutes of complete apnea, evidence of tissue ischemia would become apparent and at longer than 5 minutes, irreversible damage would occur, especially in the brain. Cardiac arrest would soon follow unless oxygenation and ventilation were immediately rapidly restored. A spinal cord transection above C4 would result in apnea because the phrenic nerves arise from C1 through C4. Likewise, patients with amyotrophic lateral sclerosis in which upper and lower motor neurons in the motor cortex, in the brainstem, and in the spinal cord die over time are unable to maintain respiratory effort. Any process that decreases the alveolar to arterial O2 gradient can likewise interfere with the delivery of O2 to tissues, for example, drowning or acute respiratory distress syndrome. Cyanide poisoning is the most well-known cause of inhibition of O2 use within mitochondria by inhibiting cytochrome C o xidase. The best example for anesthesiologists would be a helium quench from a magnetic resonance imaging scanner. If the required safety valves in the room were not working correctly, the helium could displace all the O2 in the room. Dopamine is its precursor, and in turn, epinephrine is the precursor for norepinephrine. Chromaffin cells in the adrenal medulla and the terminal boutons of certain nerves produce and release epinephrine, which gains its biologic activity by binding to a- and b-adrenergic receptors. Among its many effects, epinephrine activation of a receptors produces vasoconstriction in the peripheral vasculature, whereas activation of b receptors within the heart increases chronotropy, inotropy, dromotropy, and lusitropy. The majority of epinephrine produced is metabolized within the same cells; it was synthesized simply because there is so much leakage of the catecholamine from the vesicles where it is stored into the cytoplasm. There is a very dynamic equilibrium between vesicular and cytoplasmic epinephrine. On the arterial side, the vasoconstriction caused by a receptor activation constricts the peripheral arterial system further centralizing the circulation to perfuse vital organs with the highest oxygen requirement. The increase in cardiac output with an increased systemic vascular resistance is hypothesized to improve coronary artery and carotid artery blood flow. If the effects of epinephrine are attributed to its effect on a-adrenergic receptors, then drugs with even more a receptor specificity might be indicated.
Likewise womens health zeeland purchase ginette-35 from india, dopamine and acetylcholine may provide emetic signals to the chemoreceptor trigger zone women's health clinic des moines iowa order ginette-35 amex. Following stimulation of the vomiting center (directly or indirectly via neural pathways) menstrual headache symptoms proven 2 mg ginette-35, vomiting is mediated by efferent pathways including the vagus and phrenic nerves menstruation rectal pain order 2mg ginette-35 free shipping, and innervation of the abdominal musculature. The initial manifestation of vomiting often involves nausea in which gastric peristalsis is reduced or absent and the tone of the upper small intestine is increased and gastric reflux occurs. Ultimately, the upper portion of the stomach relaxes while the pylorus constricts and the coordinated contraction of the diaphragm and abdominal muscles leads to expulsion of gastric contents. Risk factors for postoperative nausea and vomiting include female sex, young age (children), history of motion sickness, abstinence from tobacco, and obesity (perhaps reflecting emetic anesthetic drugs stored in adipose tissue). When more than 50% of the small intestine is resected, the absorption of nutrients and vitamins is so compromised that development of malnutrition is likely. Secretions of the Small Intestine Mucus glands (Brunner glands) present in the first few centimeters of the duodenum secrete mucus to protect the duodenal wall from damage by acidic gastric fluid. Stimulation of the sympathetic nervous system inhibits the protective mucus-producing function of these glands, which may be one of the factors that causes this area of the gastrointestinal tract to be the most frequent site of peptic ulcer disease. This fluid provides a watery vehicle for absorption of substances from chyme as it passes through the small intestine. The most important mechanism for regulation of small intestine secretions is local neural reflexes, especially those initiated by distension produced by the presence of chyme. This rapid growth of new cells allows prompt repair of any excoriation that occurs in the mucosa. This rapid turnover of cells also explains the vulnerability of the gastrointestinal epithelium to chemotherapeutic drugs (see Chapter 42). The epithelial cells in the mucosa of the small intestine contain digestive enzymes that most likely are responsible for digestion of food substances because they are absorbed across the gastrointestinal epithelium. These enzymes include peptidases for splitting peptides into amino acids, enzymes for splitting disaccharides into monosaccharides, and intestinal lipases. Small Intestine the small intestine consists of the duodenum (from the pylorus to the ligament of Treitz), the jejunum, and the ileum (ending at the ileocecal valve). There is no distinct anatomic boundary between the jejunum and ileum, but the first 40% of small intestine after the ligament of Treitz is often considered the jejunum. The small intestine is presented with approximately 9 L of fluid daily (2 L from the diet and the rest representing gastrointestinal secretions), but only 1 to 2 L of chyme enters the colon. The small intestine is the site of most of the digestion and absorption of proteins, fats, and carbohydrates (Table 32-3). Chyme moves through the 5 m of small intestine at an average rate of 1 cm p er minute. As a result, it takes 3 to 5 hours for chyme to pass from the pylorus to the ileocecal valve. On reaching the ileocecal valve, chyme may remain in place for several hours until the person eats another meal. An inflamed appendix can increase the tone of the ileocecal valve to the extent that emptying of the ileum Table 32-3 Site of Absorption Duodenum Glucose Amino acids Fatty acids Bile salts Water-soluble vitamins Vitamin B12 Sodium Potassium Hydrogen Chloride Calcium 11 11 111 0 111 0 111 0 0 111 111 Jejunum 111 111 11 1 11 1 11 0 1 11 11 Ileum 11 11 1 111 0 111 111 1 11 1 1 Colon 0 0 0 0 0 0 111 11 11 0 Daily absorption of sodium is 25 to 35 g, emphasizing the rapidity with which total body sodium depletion can occur if excessive intestinal secretions are lost as occurs with extreme diarrhea. Active transport of sodium ions in the small intestine is important for the absorption of glucose, which is the physiologic basis for treating diarrhea by oral administration of saline solutions containing glucose. Bacterial toxins as from cholera and staphylococci can stimulate the chloride-bicarbonate ion exchange mechanism, resulting in life-threatening diarrhea consisting of loss of sodium, bicarbonate, and an isosmotic equivalent of water. Secretions of the Colon Epithelial cells lining the colon secrete almost exclusively mucus, which protects the intestinal mucosa against trauma. The alkalinity of the mucus due to the presence of large amounts of bicarbonate ions provides a barrier to keep acids that are formed in the feces from attacking the intestinal wall. Irritation of a segment of colon as occurs with bacterial infection causes the mucosa to secrete large quantities of water and electrolytes in addition to mucus, diluting the irritating factors and causing rapid movement of feces toward the anus. Pancreas the pancreas lies parallel to and beneath the stomach, serving as both an endocrine (insulin or glucagon) and exocrine gland. Regulation of Pancreatic Secretions Pancreatic secretions are regulated more by hormonal than neural mechanisms. For example, secretin is released by duodenal mucosa in response to hydrochloric acid. Th s hormone enters the circulation and causes the pancreas to produce large amounts of alkaline fluid necessary to neutralize the acidic pH of gastric fluid. In addition to the release of secretions, the presence of food in the duodenum causes the release of a second polypeptide hormone, cholecystokinin. Cholecystokinin also enters the circulation and causes the pancreas to secrete digestive enzymes (trypsins, amylase, lipases). Trypsins are activated in the gastrointestinal tract by the enzyme enterokinase, which is secreted by the gastrointestinal mucosa when chyme is exposed to the mucosa. Damage to the pancreas or blockade of a pancreatic duct may cause pooling of proteolytic enzymes, resulting in acute pancreatitis due to autodigestion by these enzymes. In general, pancreatic secretions are stimulated by the parasympathetic nervous system and inhibited by the sympathetic nervous system. Colon the functions of the colon are absorption of water and electrolytes from the chyme and storage of feces.
Protein Buffering System Like hemoglobin menopause water retention cheap ginette-35 2mg amex, other histidine-containing proteins are important intracellular buffers menstrual cramps 9 days before period order cheap ginette-35. Proteins are localized in high concentrations within the cell where it is estimated that approximately 75% of all the buffering of body fluids occurs breast cancer 9mm tumor generic ginette-35 2 mg amex, mostly by proteins breast cancer necklace purchase ginette-35 without a prescription. Of particular importance is the local buffering of hydrogen ions by proteins in the mitochondria. Although the relatively low concentration of plasma proteins limits their role as extracellular buffers, hypoproteinemia will further reduce buffering capacity, especially in the critically ill patient. Phosphate Buffering System the phosphate buffering system is important in most fluid compartments but is especially important in renal tubules, where phosphate is concentrated. Renal tubular fluid is more acidic than extracellular fluid, bringing the pH of renal tubular fluid closer to the pKa (6. Phosphate is a very important intracellular buffer because it is the most abundant intracellular anion. Furthermore, the relatively acidic pH of intracellular fluid is closer to the pKa of the phosphate buffering system than is the pH of extracellular fluid. Furthermore, the optimal function of several organelles, including lysosomes and mitochondria, require that their local pH is significantly different from the general pHi. Thus there are highly regulated mechanisms to maintain local pHi including intracellular buffer systems and membrane-bound proton transporters. As in the extracellular compartment, intracellular protons are rapidly bound to weak acids and bases resulting in a low free proton concentration. Ventilatory Responses Ventilation is quantitatively the most important mechanism of acid removal, given the enormous daily production of volatile acid compared to nonvolatile acid. This reflects the fact that the intensity of the stimulus responsible for increases or decreases in alveolar ventilation will begin to diminish as pH returns toward 7. As a "buffer," ventilatory responses are able to buffer up to twice the amount of acids or bases as all the chemical buffers combined. However, compensation for extreme metabolic acidosis imposes a significant respiratory burden. Further, it is likely that the insult causing severe metabolic acidosis will also adversely affect respiratory muscle function, thus compromising the respiratory response. Intracellular pH Regulation Although blood pH is commonly measured clinically, it is the intracellular pH (pHi) that is of functional importance. The routine measurement and manipulation of pHi is not possible in current practice. Indeed, during hypothermic cardiopulmonary bypass and hibernation, the pHi in heart and brain tissue appears to be highly regulated despite significant deviations in systemic pH. Active sodium ion extrusion from the renal tubular cell into the peritubular circulation favors sodium diffusion from the tubular lumen into the tubular cell in exchange for hydrogen ions. Hydrogen in the renal tubular fluid then combines with filtered bicarbonate to form carbonic acid. Carbonic anhydrase facilitates the dissociation of carbonic acid into water and carbon dioxide that both enter the renal tubular cell. Carbon dioxide and water generate bicarbonate, which enters the peritubular circulation accompanied by sodium. The remaining hydrogen ions are secreted into the lumen in exchange for sodium. Inhibition of carbonic anhydrase by acetazolamide interferes with the reabsorption of bicarbonate ions from renal tubular fluid. As a result, excess bicarbonate ions are lost in the urine and the plasma bicarbonate concentration is decreased. Hydrogen ions are secreted into renal tubules by epithelial cells lining proximal renal tubules, distal renal tubules, and collecting ducts. At the same time, sodium ions are reabsorbed in exchange for the secreted hydrogen ions and combine with bicarbonate ions in the peritubular capillaries. As a result, the amount of sodium bicarbonate in the plasma is increased during the secretion of hydrogen ions into renal tubules. In renal insufficiency, the capacity to generate urinary ammonia is impaired, thus reducing hydrogen ion excretion. Renal responses that regulate hydrogen ion concentrations do so by acidification or alkalinization of the urine. In the presence of acidosis, the rate of hydrogen ion secretion exceeds the net loss of bicarbonate ion into the renal tubules. In the presence of alkalosis, the effect of the titration process in the renal tubules is to increase the number of bicarbonate ions filtered into the renal tubules relative to the secretion of hydrogen ions. Excess bicarbonate ions are excreted into the urine accompanied by cations, most often sodium. Extracellular fluid is electroneutral such that the sum of the positive charges of all cations must equal the sum of negative charges of all anions. In the process of altering the plasma concentration of bicarbonate ions, it is mandatory to remove some other anion each time the concentration of bicarbonate ions is increased or to increase some other anion when the bicarbonate concentration is decreased. Typically, the anion that follows changes in the concentration of bicarbonate ions is chloride. As the most abundant extracellular anion, physiologic manipulation of chloride appears to be an important element of pH control. Conceptually, when bicarbonate ions are replaced by chloride ions, the pH will generally tend to decrease as a weak acid (carbonic acid) is replaced by a strong acid (hydrochloric acid).
Most often breast cancer walks 2014 order ginette-35 with paypal, this a2 agonist is used in the intensive care and operating room settings as a sedative and analgesic due to its central sympatholytic effects women's health clinic in el paso tx generic 2mg ginette-35 visa. Dexmedetomidine undergoes extensive biotransformation in the liver and is excreted mostly in the urine; liver impairment can dramatically increase plasma levels and duration of action due to signifi antly decreased metabolism during infusion women's health center memphis tn order ginette-35 2 mg on line. Most a2 receptors are found in the central nervous system especially in the brainstem and the locus ceruleus pregnancy kit cost purchase generic ginette-35 line. Peripherial inhibition of a2 receptors can result in inhibition of insulin release and induction of glucagon from the pancreas. Clinical pharmacologic effects include hypotension, bradycardia, and central sedation with some mild effects of analgesia all related to the sympatholytic effects. Drug-induced b-adrenergic blockade prevents the effects of catecholamines and sympathomimetics on the heart and smooth muscles of the airways and blood vessels. Mechanism of Action b-Adrenergic receptor antagonists exhibit selective affinity for b-adrenergic receptors, where they act by competitive inhibition. Binding of antagonist drugs to b-adrenergic receptors is reversible such that the drug can be displaced from the occupied receptors if sufficiently large amounts of agonist become available. Competitive antagonism causes a r ightward displacement of the dose-response curve for the agonist, but the slope of the curve remains unchanged, emphasizing that sufficiently large doses of the agonist may still exert a full pharmacologic effect. Chronic administration of b-adrenergic antagonists is associated with an increase in the number of b-adrenergic receptors. The net effect of badrenergic stimulation in the heart is to produce positive chronotropic, inotropic, and dromotropic effects and these are the responses that are blunted by b-adrenergic receptor antagonists. It is estimated that about 75% of b receptors in the myocardium are b1, whereas b2 receptors account for about 20% of b receptors. Substitutions on the benzene ring determine whether the drug acts on b-adrenergic receptors as an antagonist or agonist. The levorotatory forms of b antagonists and agonists are more potent than the dextrorotatory forms. For example, the dextrorotatory isomer of propranolol has less than 1% o f the potency of the levorotatory isomer for blocking b-adrenergic receptors. Classification b-Adrenergic receptor antagonists are classified as nonselective for b1 and b2 receptors (propranolol, nadolol, timolol, pindolol) and cardioselective (metoprolol, atenolol, acebutolol, betaxolol, esmolol, bisoprolol) for b1 receptors (Tables 19-1 and 19-2). It is important to recognize that b receptor selectivity is dose dependent and is lost when large doses of the antagonist are administered. This emphasizes that selectivity should not be interpreted as specificity for a specific type of b-adrenergic receptor. Drugs that exhibit cardiac selectivity for b1 receptors (cardioselective) are better suited for administration to patients with asthma and reactive airway disease. Theoretically, cardioselective drugs are better suited for treatment of patients with essential hypertension as these drugs lack inhibition of peripheral b2 receptors that produce vasodilation. The result is a d ecrease in myocardial oxygen demand, with a s ubsequent decrease in the occurrence of myocardial ischemia during exercise. The decrease in heart rate also increases diastolic perfusion time, which may enhance myocardial perfusion. Th s membrane stabilization effect, however, is detectable only at plasma concentrations that are far higher than needed to produce clinically adequate b-adrenergic blockade. Pharmacokinetics the principal difference in pharmacokinetics between all the b-adrenergic receptor antagonists is the elimination half-time ranging from brief for esmolol (about 10 minutes) to hours for the other drugs (see Table 19-1). Elimination half-time is considered in the perioperative period when redosing intervals are being developed or when conversion to another b-adrenergic receptor drug is planned. Among the b-adrenergic receptor antagonists, only propranolol is highly protein bound. The therapeutic plasma concentration varies greatly among these drugs and between patients (interpatient variability). Explanations for interpatient variability include differences in basal sympathetic nervous system tone, flat dose-response curves for the drug so changes in plasma concentrations evoke minimal changes in pharmacologic effects, impact of active metabolites, and genetic differences in b-adrenergic receptors that influence how an individual patient responds to a given drug and plasma concentration. Propranolol Propranolol is a n onselective b-adrenergic receptor antagonist that lacks intrinsic sympathomimetic activity and thus is a pure antagonist (see Table 19-1). As the first b-adrenergic antagonist introduced clinically, propranolol is the standard drug to which all b-adrenergic antagonists are compared. Typically, propranolol is administered in stepwise increments until physiologic plasma concentrations have been attained, as indicated by a resting heart rate of 55 to 60 beats per minute. Cardiac Effects the most important pharmacologic effects of propranolol are on the heart. Because of b1-receptor blockade, propranolol decreases heart rate and myocardial contractil- ity, resulting in decreased cardiac output. These effects on heart rate and cardiac output are especially prominent during exercise or in the presence of increased sympathetic nervous system activity. Heart rate slowing induced by propranolol lasts longer than the negative inotropic effects, suggesting a possible subdivision of b1 receptors. Concomitant blockade of b2 receptors by propranolol increases peripheral vascular resistance, including coronary vascular resistance. As a r esult, propranolol may relieve myocardial ischemia, even though drug-induced increases in coronary vascular resistance oppose coronary blood flow.
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