Repaso de anestesio (1).docx

ANESTHESIOLOGY TOPIC I. Preanesthetic preparation Anamnesis. It consists of preparing a patient's clinical history with special emphasis on detecting problems that may affect the anesthetic procedure. The anamnesis should pay special attention to: Drug and food allergies. Toxic consumption. Cardiov...

ANESTHESIOLOGY TOPIC I. Preanesthetic preparation Anamnesis. It consists of preparing a patient's clinical history with special emphasis on detecting problems that may affect the anesthetic procedure. The anamnesis should pay special attention to: Drug and food allergies. Toxic consumption. Cardiovascular pathology: hypertension, diabetes, ischemic heart disease, coronary stents, arrhythmias, etc. Respiratory pathology : asthma, COPD, sleep apnea-hypopnea syndrome. Kidney pathology: chronic kidney disease, glomerulonephritis. Hematological pathology : coagulopathies. Thyroid pathology : hyperthyroidism or hypothyroidism. Possible pregnancy. Previous surgical and anesthetic history. Family medical, surgical and anesthetic history. Updated complete treatment of the patient with special attention to antiplatelet medications. Physical exploration. Cardiovascular examination . Detection of arrhythmias, heart murmurs and edema in the lower extremities. Lung examination . Hypoventilation, respiratory sounds, prolonged expiration, clubbing. VA Exploration . Reports possible difficulty in ventilation and/intubation of the patient if necessary. Exploration of the body region where the anesthetic block is expected to be performed if it is regional. Quality of peripheral venous access . Anesthetic risk assessment. Supplementary tests. 5 recommendations not to do: Do not maintain deep levels of sedation in critically ill patients without a specific indication. Do not perform a chest x-ray in people under 40 years of age with low anesthetic risk. Do not systematically perform preoperative tests in cataract surgery, unless indicated based on clinical history or physical examination. Do not schedule elective surgery with risk of bleeding in patients with anemia. Do not perform laboratory tests in patients without systemic disease and prior to low-risk surgeries, with minimal estimated blood loss. For a correct preoperative assessment, it must be established based on different variables: Patient age. Pathological history and clinical health status of the patient. Type and/or magnitude of the surgical intervention. Type of anesthesia. Urgency of surgical intervention. Anesthetic premedication. The administration is benzodiazepines, short-term ones such as midazolam are more preferred (on the same day of surgery). Its objectives are: Reduce anxiety. Preoperative pain relief. Perioperative amnesia. Aspiration pneumonitis prophylaxis. Antihistamines and steroids. Topic II. Airway management Assessment of the airway. Prediction of a difficult airway. The evaluation of the VA should be carried out systematically before anesthesia, since it is essential to plan the techniques of choice for its management. VA assessment is carried out by: Clinic history: Personal and/or family history of difficulty managing VA. Diseases associated with the presence of VAD, such as: Thyroid pathology. It can cause compression, narrowing, and deviation of the VA. Previous cervical radiotherapy . Maxillofacial pathology : temporomandibular ankylosis, retrognathia, micrognathia, high-arched palate, etc. Pathology of the cervical spine. Obstructive sleep apnea syndrome . Symptoms suggestive of airway obstruction: dysphonia, dysphagia, stridor, etc. Physical examination : Here we see if intubation will be difficult or not. Mallampati Test : Degree of visualization of the pharyngeal structures, in a sitting position, with the head in a neutral position, maximum mouth opening, sticking out the tongue and without phonation. It estimates the relative size of the tongue with respect to the oral cavity, which is related to the ease with which the tongue could be displaced by direct laryngoscopy. It is valued in four grades: Grade I. View of the soft palate, uvula, tonsillar pillars and posterior wall of the pharynx. Grade II . View of the soft palate, uvula and only part of the posterior wall of the pharynx. Grade III . View of the soft palate and base of the uvula. Grade IV . Only vision of the soft palate. Grades I and II are associated with easy orotracheal intubation. Class II makes it a little more difficult while class IV raises it. Patil test or thyromental distance . Measures the anterior laryngeal space. With the head in maximum hyperextension and the mouth closed, the distance between the mandibular symphysis and the tip of the thyroid cartilage is measured. It is suitable if it is smaller than 6cm. Interdental distance . An interincisor distance of less than 3cm with the mouth completely open indicates difficulty for orotracheal intubation using direct laryngoscopy. Upper lip bite test . Assesses the ability to slide the mandible in front of the upper jaw. It has 3 grades: Grade I. Completely bite your upper lip. Grade II . Partially bites upper lip. Grade III . He can't bite his upper lip. Difficult ventilation prediction . The acronym OBESE : Or kiss B arba Age over 55 years. S AOS E dentulous (absence of teeth). Prediction of difficult intubation . The LEMON acronym : L ook externally. Search for external characteristics of the VA that are associated with VAD: facial abnormalities, retrognathia, obesity, macroglossia, goiter, etc. Evaluate . Evaluate the relationship between the pharynx, larynx and mouth axes. M allampati score. Or airway obstruction. N eck mobility. Cormack-Lehane classification Assess the difficulty in visualizing the glottis during laryngoscopy. Grade I. Complete visualization of the glottis. Grade II. Only the posterior third of the glottis and the posterior commissure are visible. Grade III. Glottis completely covered, only the epiglottis is visible. Grade IV . Only structures of the floor of the mouth are visualized, not even the epiglottis is visualized. Airway management devices Facial mask The goal is to maintain oxygenation, airway patency, and alveolar ventilation by delivering oxygen through a respiratory system and sealing the mask to the patient's face. Its usefulness is: Apnea phase prior to endotracheal intubation with the patient fasting. Anesthetic induction in children. Maintenance of general anesthesia, exclusively through the use of a mask. Oropharyngeal and nasopharyngeal cannulas They facilitate the maintenance of upper airway patency caused by loss of oropharyngeal muscle tone in anesthetized patients or patients with decreased level of consciousness. Supraglottic devices Placed above the vocal cords, they allow adequate ventilation and oxygenation of the patient. The most commonly used are laryngeal masks. They are indicated to control ventilation and oxygenation, administration of anesthetic gases in certain surgeries under general anesthesia, as well as a VAD rescue method. Laryngeal mask (ML). It consists of an oropharyngeal tube with a distal cuff that, once inflated, surrounds the entrance to the larynx, allowing ventilation. Used for the management of VA intermediate between the face mask and the endotracheal tube. Combitube or multifenestrated esophageal tube. VAD device that is only used for ventilation in emergency situations. laryngeal tube. Single-lumen supraglottic device with two sealing balloons, pharyngeal and esophageal. Indicated in short-term elective anesthesia. Transglottic devices They are semi-rigid guides that facilitate its passage through the glottis. Among them are: Sear or mandrel . Malleable device inserted inside the ETT allows it to maintain a specific shape that facilitates endotracheal intubation. Eschmann's Guide . Indicated in those cases where direct laryngoscopy demonstrates Cormack-Lehane grade II or III. Introducer of Fova . Similar to the previous one but oxygen can be insufflated and a certain degree of ventilation achieved during intubation if necessary. Laryngoscopes Instruments to allow direct visualization of the glottis and placement of the ETT through the vocal cords. They consist of a handle and a blade or shovel. Endotracheal tubes They are flexible plastic tubes, generally PVC, in the distal part of which there is a pneumatic tamponade balloon intended to isolate the trachea. To minimize the risk of bronchoaspiration, intubation should be performed using the rapid sequence induction technique. Topic III . Intravenous anesthetics Barbiturates Barbiturates depress the reticular activating system in the brain stem, which controls consciousness. Its main mechanism of action is believed to be through binding to the γ-aminobutyric acid type A (GABAA) receptor. Barbiturates potentiate the action of GABA by increasing the duration of openings of a specific chloride ion channel. Structures and responsibilities as ciated . Barbiturates are derived from barbituric acid. The substitution at the C5 carbon determines the hypnotic potency and anticonvulsant activity. The phenyl group of phenobarbital is anticonvulsant , while the methyl group of methohexital is not. Methohexital is therefore useful in providing anesthesia for electroconvulsive therapy when a seizure is desired . Replacing the oxygen at C2 (oxybarbiturates) with a sulfur atom (thiobarbiturates) increases lipid solubility. As a result, thiopental and thiamylal have greater potency, a more rapid onset of action, and a shorter duration of action (after a single “bedtime dose”) than pentobarbital. Pharmacokinetics. Distribution The duration of induction doses of thiopental, thiamylal, and methohexital is determined by redistribution, not by metabolism or elimination. The great lipid solubility of thiopental and the high non-ionized fraction (60%) explain the rapid cerebral absorption (in 30 s). If the central compartment is constricted (eg, hypovolemic shock), if serum albumin is low (eg, severe liver disease or malnutrition), or if the non-ionized fraction is increased (eg, acidosis), Higher concentrations will be reached in the brain and heart. for a given dose. Redistribution reduces plasma and brain concentrations to 10% of maximum levels within 20 to 30 minutes. Excretion Except for less protein-bound and less lipid-soluble agents, such as phenobarbital, renal excretion is limited to the water-soluble end products of hepatic biotransformation. Methohexital is excreted in the feces. Effects on organs. Cardiovascular . Intravenous bolus induction doses of barbiturates cause a decrease in blood pressure and an increase in heart rate. Depression of the medullary vasomotor center produces vasodilation of peripheral capacitance vessels, which increases peripheral blood pooling, mimicking reduced blood volume. Tachycardia after administration is probably due to a central vagolytic effect and reflex responses to lowering blood pressure. Respiratory. Barbiturates depress the medullary ventilatory center, decreasing the ventilatory response to hypercapnia and hypoxia. Apnea often follows an induction dose. During awakening, tidal volume and respiratory rate decrease. Barbiturates incompletely depress airway reflex responses to laryngoscopy and intubation, and airway instrumentation may cause bronchospasm (in asthmatic patients) or laryngospasm in lightly anesthetized patients. Cerebral. Barbiturates constrict the cerebral vasculature, causing a decrease in cerebral blood flow, cerebral blood volume, and intracranial pressure. Intracranial pressure decreases more than arterial pressure, so cerebral perfusion pressure (CPP) usually increases. (CPP is equal to cerebral artery pressure minus jugular venous pressure or intracranial pressure, whichever is greater.) Barbiturates may protect the brain from transient episodes of focal ischemia (eg, cerebral embolism) but probably do not protect from global ischemia (eg, cardiac arrest). Renal. Barbiturates reduce renal blood flow and glomerular filtration rate in proportion to the fall in blood pressure. Hepatic . Decreases hepatic blood flow. Chronic exposure to barbiturates leads to the induction of liver enzymes and an increased rate of metabolism. On the other hand, the binding of barbiturates to the cytochrome P-450 enzyme system interferes with the biotransformation of other drugs (eg, tricyclic antidepressants). Barbiturates promote aminolevulinic acid synthetase, which stimulates the formation of porphyrin (an intermediate in heme synthesis). This may precipitate acute intermittent porphyria or variegated porphyria in susceptible individuals. Immunological . Anaphylactic or anaphylactoid allergic reactions are rare. Sulfur-containing thiobarbiturates cause histamine release from mast cells in vitro, whereas oxybarbiturates do not. Benzodiazepines The binding of benzodiazepines to the GABAa receptor increases the frequency of openings of the associated chloride ion channel. Binding of the benzodiazepine receptor by an agonist facilitates the binding of GABA to its receptor. Flumazenil (an imidazobenzodiazepine) is a specific benzodiazepine receptor antagonist that effectively reverses most of the effects of benzodiazepines in the central nervous system . Structure-activity relationships . The chemical structure of benzodiazepines includes a benzene ring and a seven-membered diazepine ring. Substitutions at various positions on these rings affect potency and biotransformation. The imidazole ring of midazolam contributes to its water solubility at low pH. Diazepam and lorazepam are insoluble in water, so parenteral preparations contain propylene glycol, which can cause venous irritation. Pharmacokinetics Absorption Benzodiazepines are commonly administered orally and intravenously (or, less commonly, intramuscularly) to provide sedation (or, less commonly, to induce general anesthesia). Diazepam and lorazepam are well absorbed from the gastrointestinal tract, and peak plasma levels are usually achieved within 1 and 2 hours, respectively. Intravenous midazolam (0.05 to 0.1 mg/kg) administered for anxiolysis before general or regional anesthesia is almost ubiquitous. injections of diazepam are painful and are not reliably absorbed . In contrast, midazolam and lorazepam are well absorbed after intramuscular injection, with maximum levels reached in 30 and 90 min, respectively. Distribution Diazepam is relatively lipid-soluble and easily penetrates the blood-brain barrier. Although midazolam is soluble in water at reduced pH, its imidazole ring closes at physiological pH, increasing its lipid solubility. The moderate lipid solubility of lorazepam accounts for its slower cerebral absorption and onset of action. Effects on organ systems Cardiovascular . Benzodiazepines have minimal left ventricular depressant effects, even at doses of general anesthetics, except when administered concomitantly with opioids (these agents interact to produce myocardial depression and arterial hypotension). Benzodiazepines administered alone slightly decrease blood pressure, cardiac output, and peripheral vascular resistance and sometimes increase heart rate. Respiratory. Benzodiazepines depress the ventilatory response to CO2. This depression is usually insignificant unless the drugs are administered intravenously or together with other respiratory depressants. Although apnea may be relatively uncommon after induction with benzodiazepines, even small intravenous doses of these agents have caused respiratory arrest. Cerebral. Benzodiazepines reduce cerebral oxygen consumption, cerebral blood flow, and intracranial pressure, but not to the extent that barbiturates do. They are effective in controlling grand mal seizures. Sedative doses often produce anterograde amnesia. The mild muscle relaxation property of these drugs is mediated at the level of the spinal cord. Benzodiazepines are associated with a slower rate of unconsciousness and a longer recovery. Ketamine Ketamine has multiple effects throughout the central nervous system and is well known to inhibit N-methyl-D-aspartate (NMDA) channels and neuronal hyperpolarization-activated cation channels (HCN1). However, the exact way in which ketamine produces anesthesia or analgesia remains controversial . Ketamine functionally "dissociates" sensory inputs from the limbic cortex (which is involved with awareness of sensation). Ketamine has mood effects , and infusions of this agent are now widely used to treat severe treatment-resistant depression, particularly when patients have suicidal ideation . Small doses of ketamine infusion are also used to supplement general anesthesia and reduce the need for opioids during and after the surgical procedure . Low-dose ketamine infusions have been used for analgesia in postoperative patients and others who are refractory to conventional analgesic approaches. Ketamine is used for intravenous induction of anesthesia , particularly in settings where its tendency to produce sympathetic stimulation is useful (hypovolemia, trauma). When intravenous access is lacking, ketamine is useful for intramuscular induction of general anesthesia in uncooperative children and adults . Ketamine can be combined with other agents (eg, propofol or midazolam) in small bolus doses or infusions for conscious sedation during procedures such as nerve blocks and endoscopy. Effect on organ systems. Cardiovascular. These indirect cardiovascular effects are due to central stimulation of the sympathetic nervous system and inhibition of norepinephrine reuptake after its release from nerve terminals. These changes accompany increases in pulmonary artery pressure and myocardial work. For these reasons, ketamine should be administered with caution to patients with coronary artery disease, uncontrolled hypertension, congestive heart failure, or arterial aneurysms. The direct myocardial depressant effects of large doses of ketamine, probably due to inhibition of calcium transients, are unmasked by sympathetic blockade (e.g., spinal cord transection) or depletion of catecholamine stores (e.g. (e.g., severe shock in the terminal stage). Respiratory . Ventilatory drive is minimally affected by induction doses of ketamine, although combinations of ketamine with opioids can produce apnea. Racemic ketamine is a potent bronchodilator, making it a good induction agent for asthmatic patients; however, S(+) ketamine produces minimal bronchodilation . Upper airway reflexes remain largely intact, but partial airway obstruction may occur, and patients at increased risk for aspiration pneumonia ("full stomach") should be intubated during general anesthesia with ketamine. Cerebral . The received dogma about ketamine is that it increases cerebral oxygen consumption, cerebral blood flow, and intracranial pressure. These effects would seem to preclude its use in patients with space-occupying intracranial lesions, such as those that occur with head trauma; However, recent publications offer convincing evidence that when combined with a benzodiazepine (or another agent that acts on the same GABA receptor system) and controlled ventilation (in techniques that exclude nitrous oxide), ketamine is not associated with an increase of intracranial pressure. Etomidate Etomidate depresses the reticular activation system and mimics the inhibitory effects of GABA. Specifically, etomidate, particularly the R(+) isomer, appears to bind to a subunit of the GABAA receptor, increasing the receptor's affinity for GABA. Etomidate may have disinhibitory effects on parts of the nervous system that control extrapyramidal motor activity. Etomidate is dissolved in propylene glycol for injection. This solution often causes pain on injection that can be relieved by a prior intravenous injection of lidocaine. Pharmacokinetics Absorption. Etomidate is available only for intravenous administration and is primarily used for the induction of general anesthesia. It is sometimes used for the brief production of deep (unconscious) sedation, such as before placement of retrobulbar blocks. Distribution . Although highly protein-bound, etomidate is characterized by a very rapid onset of action due to its high lipid solubility and large non-ionized fraction at physiological pH. Effects on organ systems Cardiovascular . Etomidate has minimal effects on the cardiovascular system when administered alone. A slight reduction in peripheral vascular resistance is responsible for a decrease in blood pressure. Myocardial contractility and cardiac output are generally unchanged. Etomidate does not release histamine. However, etomidate alone, even in large doses, produces relatively light anesthesia for laryngoscopy , and marked increases in heart rate and blood pressure may be recorded when etomidate provides the only anesthetic depth for intubation. Respiratory . Ventilation is less affected with etomidate than with barbiturates or benzodiazepines. Even induction doses do not usually produce apnea unless opioids have also been administered. Cerebral . Etomidate decreases cerebral metabolic rate, cerebral blood flow, and intracranial pressure. Due to minimal cardiovascular effects, cerebral perfusion pressure is well maintained. Although the EEG changes resemble those associated with barbiturates, etomidate (like ketamine) increases the amplitude of somatosensory evoked potentials. Postoperative nausea and vomiting are more common after etomidate than after propofol or barbiturate induction. Etomidate lacks analgesic properties. Endocrine . Induction doses of etomidate transiently inhibit enzymes involved in the synthesis of cortisol and aldosterone. When infused for sedation in the intensive care unit (ICU), etomidate has been reported to produce sustained adrenocortical suppression with an increased mortality rate in critically ill (particularly septic) patients. Propofol It is used for induction and maintenance of anesthesia. Biotransformation . The use of propofol infusion for long-term sedation of critically ill children or young adult neurosurgical patients has been associated with sporadic cases of lipemia, metabolic acidosis, and death, the so-called propofol infusion syndrome. Effects on organ systems Cardiovascular. The main cardiovascular effect of propofol is a decrease in blood pressure due to a decrease in systemic vascular resistance (inhibition of sympathetic vasoconstrictor activity), preload and cardiac contractility. Hypotension following induction is usually reversed by stimulation accompanying laryngoscopy and intubation. Factors associated with propofol-induced hypotension include large doses, rapid injection, and old age. Propofol markedly alters the normal arterial baroreflex response to hypotension. Respiratory . Propofol is a profound respiratory depressant that usually causes apnea after an induction dose. Even when used for conscious sedation at subanesthetic doses, propofol inhibits the hypoxic ventilatory drive and depresses the normal response to hypercapnia. As a result, only appropriately trained and qualified personnel should administer propofol for sedation. Propofol-induced depression of upper airway reflexes exceeds that of thiopental, allowing intubation, endoscopy, or laryngeal mask placement in the absence of neuromuscular blockade. Cerebral . Propofol decreases cerebral blood flow, cerebral blood volume, and intracranial pressure. In patients with elevated intracranial pressure, propofol may cause a critical reduction in CPP (<50 mm Hg) unless measures are taken to maintain mean arterial pressure. Propofol and thiopental provide a comparable degree of brain protection during experimental focal ischemia. Unique to propofol are its antipruritic properties . Its antiemetic effects provide further reason for it to be a preferred drug for outpatient anesthesia. Induction is occasionally accompanied by excitatory phenomena such as muscle spasms, spontaneous movements, opisthotonus or hiccups. Propofol has anticonvulsant properties, has been used successfully to terminate status epilepticus, and can be safely administered to epileptic patients. Propofol decreases intraocular pressure. Fospropofol Fospropofol is a water-soluble prodrug that is metabolized in vivo to propofol, phosphate, and formaldehyde. It produces more complete amnesia and better conscious sedation for endoscopy than midazolam plus fentanyl . It has a slower onset and slower recovery than propofol, offering little reason for anesthesiologists to prefer it over propofol. The place (if any) of fospropofol relative to other competing agents has not yet been established in clinical practice. Dexmedetomidine Dexmedetomidine is an α2 adrenergic agonist that can be used for anxiolysis, sedation, and analgesia. Strictly speaking, it is not an anesthetic in humans; however, anesthesiologists have used it in combination with other agents to produce anesthesia. It has also been used in combination with local anesthetics to prolong regional blocks. This drug can be used for nasal (1 to 2 mcg/kg) or oral (2.5 to 4 mcg/kg) premedication in children in which it compares very favorably with oral midazolam. Most commonly, dexmedetomidine is used for procedural sedation (e.g., During awake craniotomy procedures or fiberoptic intubation), ICU sedation (e.g., ventilated patients recovering from cardiac surgery), or as an adjunct to general anesthesia to reduce the need for intraoperative opioids or to reduce the likelihood onset of delirium (most commonly in children) after an inhalation anesthetic. It has also been used to treat alcohol withdrawal and the side effects of cocaine intoxication. Dexmedetomidine has a very rapid redistribution and a relatively short elimination half-life. It is metabolized in the liver by the CYP450 system and by glucuronidation. Almost all metabolites are excreted in the urine. Opioids All opioid receptors are coupled to G proteins ; The binding of an agonist to an opioid receptor produces membrane hyperpolarization. The acute effects of opioids are mediated by inhibition of adenylyl cyclase (reductions in intracellular cyclic adenosine monophosphate concentrations) and activation of phospholipase C. Opioids inhibit voltage -gated calcium channels and activate potassium channels . inward rectifiers. The effects of opioids vary depending on the duration of exposure, and opioid tolerance leads to changes in opioid responses. Receiver Clinical effects Agonists μ Supraspinal analgesia (μ1) Respiratory depression (μ2) physical dependency Muscular stiffness Morphine Met-enkephalin Β- endorphin Fentanyl κ Sedation Spinal analgesia Morphine Nalbuphine Butorphanol Dinorfin Oxycodone δ Analgesia Behavior Epilepsy Leu-encephalic Β-endorphin σ Dysphoria Hallucinations Respiratory stimulation Pentazocine Nalorphine Ketamine Opioid receptor activation inhibits presynaptic release and postsynaptic response to excitatory neurotransmitters (e.g., acetylcholine, substance P) released by nociceptive neurons. Effects on organ systems Cardiovascular. In general, opioids have minimal direct effects on the heart. Meperidine tends to increase heart rate (it is structurally similar to atropine and was originally synthesized as a replacement for atropine), while higher doses of morphine, fentanyl, sufentanil, remifentanil, and alfentanil are associated with nerve-mediated bradycardia . lazy. With the exception of meperidine (and only then in very large doses), opioids do not depress cardiac contractility as long as they are administered alone (which is almost never the case in surgical anesthetic settings). However, blood pressure often decreases as a result of opioid-induced bradycardia, venodilation , and decreased sympathetic reflexes. The inherent cardiac stability provided by opioids is greatly diminished in practice when other anesthetic drugs, such as benzodiazepines, propofol, or volatile agents, are added. Respiratory . Opioids depress ventilation, particularly respiratory rate. Therefore, respiratory rate and end-tidal CO2 tension (in contrast to arterial oxygen saturation) provide simple metrics for early detection of respiratory depression in patients receiving opioid analgesia. Opioids increase the partial pressure of carbon dioxide (PaCO2) and blunt the response to a CO2 challenge, resulting in a shift of the CO2 response curve downward and to the right. These effects are the result of opioids binding to neurons in the respiratory centers of the brainstem. The apneic threshold (the highest Paco2 at which the patient remains apneic ) increases and the hypoxic drive decreases. Morphine and meperidine can cause histamine-induced bronchospasm in susceptible patients. Rapid administration of larger doses of opioids (particularly fentanyl, sufentanil, remifentanil, and alfentanil ) may induce chest wall stiffness severe enough to make bag-mask ventilation nearly impossible. Cerebral. The effects of opioids on cerebral perfusion and intracranial pressure must be separated from any effects of opioids on PaCO2. In general, opioids reduce cerebral oxygen consumption, cerebral blood flow, cerebral blood volume, and intracranial pressure, but to a much lesser extent than propofol, benzodiazepines, or barbiturates, as long as normocarbia is maintained by artificial ventilation. . Gastrointestinal. Opioids slow gastrointestinal motility by binding to opioid receptors in the intestine and reducing peristalsis. Biliary colic may result from opioid-induced contraction of the sphincter of Oddi. Biliary spasm, which can mimic a common bile duct stone on cholangiography, is reversed with the opioid antagonist naloxone or glucagon. Endocrine . The neuroendocrine stress response to surgery is measured in terms of the secretion of specific hormones, including catecholamines, antidiuretic hormone, and cortisol. Large doses of fentanyl or sufentanil inhibit the release of these hormones in response to surgery more completely than volatile anesthetics. Benzodiazepines They are psychotropic drugs that act on the CNS. They manifest sedative, anxiolytic, amnesic, hypnotic, anticonvulsant and muscle-relaxing effects. midazolam is approved for intravenous anesthetic induction ; the rest of the benzodiazepines are used for sedation, amnesia or as adjuvants to other drugs. They are located in the olfactory bulb, cerebral cortex, cerebellum, hippocampus, substantia nigra, inferior colliculus, spinal cord and striatum. GABA alpha-1 : Sedative, amnesic and anticonvulsant. GABA-A-alpha 2 : Anxiolytics and muscle relaxant. They inhibit gabamodulin, which decreases its binding sites and its affinity to binding sites. Short duration : Midazolam (IM) Intermediate duration : Lorazepam. Long duration : Diazepam (EV). Side effects : Reduces oxygen consumption, blood flow, anticonvulsant, amnestic, potentiates GABA, central respiratory depression, decreased tidal volume, depression of the diaphragm, decreased peripheral vascular resistance, maintains HR, phlebitis, thrombophlebitis, etc. Antidote : Flumazenil. Topic IV. Neuromuscular blocking agents. Depolarizing Succinylcholine. It is made up of two joined acetylcholine molecules. Creates intubation conditions 30 seconds after administration at 1 mg/kg IV. Effects : tachycardia, increased cardiac contractility and blood pressure with high doses. If the dose is repeated, it produces bradycardia, so all patients must be atropinized before a second dose of early succinylcholine. After its administration it produces very characteristic fasciculations and hyperkalemia. Fasciculations can produce brain stimulation, increased cerebral blood flow and, consequently, an increase in ICP. Succinylcholine can also cause myalgia, possibly related to the contractions it produces. It is one of the drugs that trigger malignant hyperthermia. Use . Currently, the use of succinylcholine is practically reserved for emergency intubation or for those cases in which VAD and difficulty with intubation are anticipated, because its effect lasts only 10 minutes. Contraindications (they are derived from its previously mentioned effects): personal or family history of malignant hyperthermia, intracranial hypertension or history of recent stroke, myopathies, neurological diseases that cause muscle denervation, rhabdomyolysis, hyperkalemia, polytraumatized patients, prolonged immobilization (ICU patients) , exotoxin-producing infection (botulism, tetanus), sepsis. Antagonists of muscle relaxants In clinical anesthetic practice, several drugs are available that antagonize the effect of certain neuromuscular relaxants: Cholinesterase inhibitors . They cause the blockage of ACh metabolism, increasing its concentration in the motor plate and, therefore, ACh competes with the neuromuscular relaxant molecule for the synaptic receptor. The most used is neostigmine . Reverses the blockade of non-depolarizing relaxants (all except mivacurium). Neostigmine also acts at the level of nicotinic receptors in the autonomic ganglia and cardiac muscarinic receptors, producing bradycardia, increased bronchial secretions, and miosis (parasympathomimetic effects). It is used at 0.04 mg/kg, together with atropine. It should be administered when part of the recovery has begun. of muscle blockage, not being useful in deep blockage. Depolarizing muscle blockade cannot be reversed by neostigmine. Sugammadex . Specific antagonist of rocuronium and, to a lesser extent, vecuronium. Its mechanism of action consists of the formation of sugammadex-rocuronium complexes, inactivating its action. It has no activity on ACh. The necessary dose depends on the depth of the neuromuscular blockade, varying between 2-16 mg/kg and achieving a total reversal of the neuromuscular blockade. Its action lasts 24 hours, so in case of need for reintubation and use of neuromuscular relaxant, something other than rocuronium and vecuronium should be used. The availability of sugammadex and the complete reversal of the blockade through its use mean that rocuronium has recently become a first-line neuromuscular relaxant in the case of VAD. Non-depolarizing Atracurium Metabolism and excretion Atracurium is metabolized so extensively that its pharmacokinetics are independent of renal and hepatic function, and less than 10% is excreted unchanged via the renal and biliary tract. Two separate processes are responsible for metabolism. A. Ester hydrolysis This action is catalyzed by nonspecific esterases, not by acetylcholinesterase or pseudocholinesterase. B. Hoffmann elimination Spontaneous non-enzymatic chemical degradation occurs at physiological pH and temperature. Side effects and clinical considerations Atracurium triggers a dose-dependent histamine release that becomes significant at doses above 0.5 mg/kg. A. Hypotension and tachycardia Cardiovascular side effects are unusual unless doses greater than 0.5 mg/kg are administered. Atracurium may also cause a transient drop in systemic vascular resistance and an increase in cardiac index independent of any histamine release. A slow injection rate minimizes these effects. B. Bronchospasm Atracurium should be avoided in asthmatic patients. Severe bronchospasm is occasionally seen in patients without a history of asthma. C. Laudanosine toxicity Laudanosine, a tertiary amine, is a degradation product of the Hofmann elimination of atracurium and has been associated with excitation of the central nervous system, resulting in elevation of the alveolar trough concentration and even precipitation of seizures. Concerns about laudanosine are probably irrelevant unless the patient has received an extremely high total dose or has liver failure. Laudanosine is metabolized in the liver and excreted in urine and bile. D. Sensitivity to temperature and pH Due to its unique metabolism, the duration of action of atracurium can be markedly prolonged by hypothermia and, to a lesser extent, by acidosis. E. Chemical incompatibility Atracurium will precipitate as free acid if introduced into an intravenous line containing an alkaline solution such as thiopental. F. Allergic reactions Rare anaphylactoid reactions to atracurium have been described. Proposed mechanisms include direct immunogenicity and acrylate-mediated immune activation. Immunoglobulin E-mediated antibody reactions directed against substituted ammonium compounds, including muscle relaxants, have been described. Reactions to acrylate, a metabolite of atracurium and a structural component of some dialysis membranes, have also been reported in patients undergoing hemodialysis. Cisatracurium Metabolism and excretion Like atracurium, cisatracurium is degraded in plasma at physiological pH and temperature by organ-independent Hofmann elimination. The resulting metabolites (a monoquaternary acrylate and laudanosine) have no neuromuscular blocking effects. Due to the greater potency of cisatracurium, the amount of laudanosine produced with the same degree and duration of neuromuscular blockade is much less than with atracurium. Side effects and clinical considerations Unlike atracurium, cisatracurium does not produce a consistent, dose-dependent increase in plasma histamine levels after administration. Cisatracurium does not alter heart rate or blood pressure, nor does it produce autonomic effects, even at doses up to eight times the ED95. Cisatracurium shares with atracurium laudanosine production, pH and temperature sensitivity, and chemical incompatibility. Mivacurio Mivacurium is a short-acting, nondepolarizing benzylisoquinoline neuromuscular blocker. Metabolism and excretion Mivacurium, like succinylcholine, is metabolized by pseudocholinesterase . Consequently, patients with low pseudocholinesterase concentration or activity may experience prolonged neuromuscular blockade after mivacurium administration. However, like other nondepolarizing agents, cholinesterase inhibitors will antagonize mivacurium-induced neuromuscular blockade. Edrophonium more effectively reverses mivacurium blockade than neostigmine because neostigmine inhibits plasma cholinesterase activity. Side effects and clinical considerations Mivacurium releases histamine to approximately the same degree as atracurium. The onset time of mivacurium is approximately 2 to 3 min. The main advantage of mivacurium compared to atracurium is its relatively short duration of action (20 to 30 min). Pancuronium It is a non-depolarizing neuromuscular blocking agent. Belonging to the pharmacological group of antimuscarinics, it produces muscle relaxation and is used in surgical interventions carried out with endotracheal intubation and assisted respiration. Side effects and clinical considerations A. Hypertension and tachycardia These cardiovascular effects are caused by the combination of vagal blockade and sympathetic stimulation. The latter is due to a combination of ganglionic stimulation, release of catecholamines from adrenergic nerve endings, and decreased reuptake of catecholamines. Large bolus doses of pancuronium should be administered with caution to patients in whom an increase in heart rate would be particularly harmful (eg, coronary artery disease, hypertrophic cardiomyopathy, aortic stenosis). B. Arrhythmias Increased atrioventricular conduction and catecholamine release increase the likelihood of ventricular arrhythmias in predisposed individuals. The combination of pancuronium, tricyclic antidepressants and halothane has been reported to be particularly arrhythmogenic. C. Allergic reactions Patients hypersensitive to bromides may have allergic reactions to pancuronium (pancuronium bromide). Vecuronium It is a satisfactory drug for patients with renal failure , its duration of action will be moderately prolonged. Following prolonged administration of vecuronium to patients in intensive care units, prolonged neuromuscular blockade (up to several days) may occur after discontinuation of the drug, possibly due to accumulation of its active 3-hydroxy metabolite, changes in clearance of the drug and, in some patients, to the development of polyneuropathy. Risk factors appear to include female sex, renal failure, long-term or high-dose corticosteroid treatment, and sepsis. Therefore, these patients should be monitored closely and the dose of vecuronium should be carefully adjusted. Long-term administration of relaxants and subsequent prolonged lack of ACh binding at postsynaptic nicotinic ACh receptors can mimic a state of chronic denervation and cause long-lasting receptor dysfunction and paralysis. Tolerance to nondepolarizing muscle relaxants can also develop after prolonged use. The best approach is to avoid unnecessary paralysis of patients in intensive care units. Side effects and clinical considerations Cardiovascular. Even at doses of 0.28 mg/kg, vecuronium lacks significant cardiovascular effects. Potentiation of opioid-induced bradycardia may be seen in some patients. Liver failure. Although dependent on biliary excretion, the duration of action of vecuronium is not usually significantly prolonged in patients with cirrhosis unless doses greater than 0.15 mg/kg are administered. Vecuronium requirements are reduced during the anhepatic phase of liver transplantation. Rocuronium In adults and pediatric patients (from full-term newborns to adolescents 0-18 years old) as an adjuvant to general anesthesia to facilitate tracheal intubation during routine induction, and to achieve relaxation of skeletal muscles in surgery. Side effects and clinical considerations Rocuronium (at a dose of 0.9 to 1.2 mg/kg) has an onset of action approaching that of succinylcholine (60 to 90 s), making it a suitable alternative for rapid sequence inductions, but at the cost of a much longer duration of action. This intermediate duration of action is comparable to that of vecuronium or atracurium. Sugammadex allows rapid reversal of rocuronium-induced dense neuromuscular blockade. Rocuronium (0.1 mg/kg) has been shown to be a rapid (90 s) and effective (decreased fasciculations and postoperative myalgias) agent for pre-curerization before administration of succinylcholine. He has slight vagolitic tendencies. Topic V. Inhaled anesthetics. Nitrous oxide It is colorless and essentially odorless. Although neither explosive nor flammable, nitrous oxide is just as capable of supporting combustion as oxygen. Unlike powerful volatile agents, nitrous oxide is a gas at room temperature and ambient pressure. Effects on organ systems Cardiovascular . Nitrous oxide has a tendency to stimulate the sympathetic nervous system. Therefore, although nitrous oxide directly depresses myocardial contractility in vitro, blood pressure, cardiac output, and heart rate remain essentially unchanged or slightly elevated in vivo due to its stimulation of catecholamines. Myocardial depression may be unmasked in patients with coronary artery disease or severe hypovolemia. Constriction of pulmonary vascular smooth muscle increases pulmonary vascular resistance, resulting in a generally modest elevation of right ventricular end-diastolic pressure. Despite vasoconstriction of cutaneous vessels, peripheral vascular resistance is not significantly altered. Respiratory . Nitrous oxide increases respiratory rate (tachypnoea) and decreases tidal volume as a result of stimulation of the CNS and, perhaps, activation of pulmonary stretch receptors. The net effect is a minimal change in minute ventilation and resting arterial CO2 levels. The hypoxic drive, the ventilatory response to arterial hypoxia mediated by peripheral chemoreceptors in the carotid bodies, is markedly depressed by even small amounts of nitrous oxide. Cerebral . By increasing CBF and cerebral blood volume, nitrous oxide produces a mild elevation of intracranial pressure. Nitrous oxide also increases cerebral oxygen consumption (CMRO2). Nitrous oxide concentrations below MAC may provide analgesia in dental surgery, labor, traumatic injuries, and minor surgical procedures. Neuromuscular . Unlike other inhalation agents, nitrous oxide does not provide significant muscle relaxation. In fact, at high concentrations in hyperbaric chambers, nitrous oxide causes skeletal muscle stiffness. Nitrous oxide is not a triggering agent for malignant hyperthermia. Kidney . Nitrous oxide appears to decrease renal blood flow by increasing renal vascular resistance. This leads to a drop in glomerular filtration rate and urine production. Hepatic . Hepatic blood flow probably decreases during anesthesia with nitrous oxide, but to a lesser extent than with volatile agents. Gastrointestinal . The use of nitrous oxide in adults increases the risk of postoperative nausea and vomiting, presumably as a result of activation of the chemoreceptor trigger zone and vomiting center in the medulla. Contraindications. Examples of conditions in which nitrous oxide may be dangerous include venous or arterial air embolism, pneumothorax, acute intestinal obstruction with intestinal distention, intracranial air (pneumocephaly after dural closure or pneumoencephalography), pulmonary air cysts, intraocular air bubbles, and tympanic membrane graft. Nitrous oxide will even diffuse into the cuffs of the tracheal tube, increasing the pressure against the tracheal mucosa. Halothane It is a powerful anesthetic whose properties allow a gentle and fairly rapid loss of consciousness, which passes into anesthesia with abolition of responses to painful stimuli. Its vapors are neither unpleasant nor irritating to mucous membranes. Effects on organ systems Cardiovascular. A dose-dependent reduction in blood pressure is due to direct myocardial depression; 2.0 MAC of halothane in patients not undergoing surgery results in a 50% decrease in blood pressure and cardiac output. Cardiac depression due to interference with sodium-calcium exchange and intracellular calcium utilization causes an increase in right atrial pressure. Although halothane is a vasodilator of the coronary arteries, coronary blood flow is decreased due to the drop in systemic blood pressure. Adequate myocardial perfusion is usually maintained, as oxygen demand also decreases. Normally, hypotension inhibits baroreceptors in the aortic arch and carotid bifurcation, causing a decrease in vagal stimulation and a compensatory increase in heart rate. Halothane mitigates this reflection. Decreased conduction of the sinoatrial node can cause a junctional rhythm or bradycardia. In infants, halothane decreases cardiac output through a combination of decreased heart rate and decreased myocardial contractility. Respiratory . Halothane usually causes rapid, shallow breathing. The increase in respiratory rate is not sufficient to counteract the decrease in tidal volume, so alveolar ventilation decreases and PaCO2 at rest increases. The apneic threshold , the highest PaCO2 at which a patient remains apneic , also increases because the difference between it and resting PaCO2 is not altered by general anesthesia. Halothane is considered a potent bronchodilator, often reversing asthma-induced bronchospasm. Cerebral. By dilating cerebral vessels, halothane reduces cerebral vascular resistance and increases cerebral blood volume and CBF. Autoregulation, maintaining constant CBF during changes in blood pressure, is reduced. Neuromuscular . Halothane relaxes skeletal muscle and potentiates nondepolarizing neuromuscular blocking agents (NMBA). Like other potent volatile anesthetics, it is a trigger of malignant hyperthermia. Renal. Halothane reduces renal blood flow, glomerular filtration rate, and urine output. Part of this decrease may be explained by a drop in blood pressure and cardiac output. Hepatic. Halothane causes hepatic blood flow to decrease in proportion to the depression of cardiac output. Vasospasm of the hepatic artery has been reported during halothane anesthesia. Contraindications. Halothane, like all inhalation anesthetics, should be used with caution (and only in combination with moderate hyperventilation) in patients with intracranial mass lesions due to the possibility of intracranial hypertension secondary to increased cerebral blood volume and blood flow. Hypovolemic patients and some patients with severe reductions in left ventricular function may not tolerate the negative inotropic effects of halothane. Sensitization of the heart to catecholamines limits the usefulness of halothane when exogenous epinephrine is administered (eg, in local anesthetic solutions) or in patients with pheochromocytoma. Isoflurane Isoflurane is a nonflammable volatile anesthetic with a pungent ethereal odor. Effects on organ systems Cardiovascular . Isoflurane causes minimal left ventricular depression in vivo. Cardiac output is maintained by an increase in heart rate due to partial preservation of baroreflexes carotids . Mild β-adrenergic stimulation increases skeletal muscle blood flow, decreases systemic vascular resistance, and lowers blood pressure. Rapid increases in isoflurane concentration result in transient increases in heart rate, blood pressure, and plasma norepinephrine levels. Isoflurane dilates the coronary arteries. Respiratory . Respiratory depression during isoflurane anesthesia resembles that of other volatile anesthetics, except that tachypnea is less pronounced. The net effect is a steeper drop in minute ventilation. Cerebral . At concentrations greater than 1 MAC, isoflurane increases CBF and intracranial pressure. These effects are believed to be less pronounced than with halothane and are reversed by hyperventilation. Neuromuscular . Isoflurane relaxes skeletal muscle. Kidney . Isoflurane decreases renal blood flow, glomerular filtration rate, and urine output. Hepatic . Total hepatic blood flow (hepatic artery and portal vein flow) may be reduced during isoflurane anesthesia. Contraindications Isoflurane has no unique contraindications. Patients with severe hypovolemia may not tolerate its vasodilatory effects. It can trigger malignant hyperthermia. Desflurane It is a highly volatile general anesthetic at room temperature, which must be stored in closed bottles. It is frequently used in outpatient surgeries due to its rapid onset of action and quick recovery. Effects on organ systems Cardiovascular . The cardiovascular effects of desflurane appear to be similar to those of isoflurane. An increase in concentration is associated with a decrease in systemic vascular resistance leading to a decrease in blood pressure. Respiratory. Desflurane causes a decrease in tidal volume and an increase in respiratory rate. There is a general decrease in alveolar ventilation that causes an increase in PaCO2 at rest. Like other modern volatile anesthetic agents, desflurane depresses the ventilatory response to increased PaCO2. Cerebral. Like the other volatile anesthetics, desflurane directly vasodilates the cerebral vasculature, increasing CBF, cerebral blood volume, and intracranial pressure in normotension and normocapnia . Counteracting the decrease in cerebral vascular resistance is a marked decrease in cerebral oxygen metabolic rate (CMRO2) that tends to cause cerebral vasoconstriction and moderates any increase in CBF. Neuromuscular . Desflurane is associated with a dose-dependent decrease in the response to train of four and peripheral tetanic nerve stimulation. Renal. There is no evidence of significant nephrotoxic effects caused by exposure to desflurane. Contraindications Desflurane shares many of the contraindications of other modern volatile anesthetics: severe hypovolemia, malignant hyperthermia, and intracranial hypertension. Sevoflurane It is a general anesthetic that is used in surgery in both adults and children. It is an inhalation anesthetic (given as a vapor for inhalation). Inhaling this vapor produces deep, painless sleep. It also maintains deep, painless sleep (general anesthesia) during which surgery can be performed. Effects on organ systems Cardiovascular . Sevoflurane slightly depresses myocardial contractility. Systemic vascular resistance and blood pressure decrease slightly less than with isoflurane or desflurane. Because sevoflurane causes little or no increase in heart rate, cardiac output is not maintained as well as with isoflurane or desflurane. Sevoflurane may prolong the QT interval, the clinical significance of which is unknown. QT prolongation may occur 60 minutes after emergence from anesthesia in infants. Respiratory . Sevoflurane depresses respiration and reverses bronchospasm to a similar degree as isoflurane. Cerebral . Like isoflurane and desflurane, sevoflurane causes slight increases in CBF and intracranial pressure in normocarbia, although some studies show a decrease in CBF. Neuromuscular . Sevoflurane produces muscle relaxation adequate for intubation after inhalation induction, although most physicians will deepen anesthesia with various combinations of propofol, lidocaine, or opioids; administer a neuromuscular blocker before intubation; or a combination of these two approaches. Kidney . Sevoflurane slightly reduces renal blood flow. Its metabolism to substances associated with impaired renal tubular function (e.g., decreased ability to concentrate) is discussed below. Hepatic. Sevoflurane decreases portal vein blood flow but increases hepatic artery blood flow, thereby maintaining total hepatic blood flow and oxygen delivery. Contraindications Contraindications include severe hypovolemia, susceptibility to malignant hyperthermia, and intracranial hypertension. Topic VI. Lidocaine It is a drug belonging to the family of local anesthetics, specifically of the amino amide type, which also includes dibucaine, mepivacaine, etidocaine, prilocaine and bupivacaine. Currently, it is widely used by dentists. It also has an antiarrhythmic effect, and is indicated intravenously or transtracheally in patients with malignant ventricular arrhythmias, such as ventricular tachycardia or ventricular fibrillation. 90 percent of lidocaine is metabolized in the liver, through hydroxylation of the aromatic nucleus, and there are other metabolic pathways not yet identified. It is excreted by the kidneys. It works more quickly and lasts longer than local anesthetics derived from esters such as cocaine and procaine . The half-life of lidocaine administered intravenously is approximately 109 minutes. Very useful in case of superficial surgeries , in dentistry, it is a drug of choice for epidural anesthesia in veterinary and human (spinal) medicine. For racehorses, it is used as a perineural anesthesia technique in the diagnosis of joint diseases and is used in cases when an episiotomy (cut in the vulva) is performed in a normal birth so as not to feel the suture or the cut. Contraindications Its use should be avoided in cases of regional ischemia or hypersensitivity to Lidocaine. It is contraindicated in all patients with known hypersensitivity to local anesthetics of the amide type, as well as in a state of shock or heart block. It should not be applied when there is inflammation in the area where it is going to be infiltrated to obtain local anesthesia. The intravenous administration of Lidocaine is contraindicated in patients with Adams-Stokes Syndrome or with severe degrees of intraventricular, atrioventricular or sinoatrial heart block . Secondary and Adverse Reactions As a local anesthetic : Side reactions may occur resulting from high plasma levels of lidocaine due to rapid absorption, inadvertent intravascular injection or an excess in the dose used. Other causes of these reactions are hypersensitivity to the medication, idiosyncrasy or decreased tolerance. Reactions due to overdose (high plasma levels) are systematic and involve the central nervous system and the cardiovascular system. The former are characterized by excitement and/or depression, nervousness, vertigo, blurred vision, tremor, convulsion, loss of consciousness and can lead to respiratory arrest. The latter include myocardial depression, hypotension, bradycardia and even cardiac arrest. Allergic reactions are characterized by late-onset skin lesions, urticaria, and other manifestations of hypersensitivity. Topic VII. Anticholinergic agents Atropine Clinical considerations Atropine has particularly potent effects on the heart and bronchial smooth muscle and is the most effective anticholinergic for treating bradyarrhythmias . Patients with coronary artery disease may not tolerate the increased myocardial oxygen demand and decreased oxygen delivery associated with tachycardia caused by atropine. A derivative of atropine, ipratropium bromide , is available in a metered-dose inhaler for the treatment of bronchospasm. The effects of atropine on the central nervous system are minimal after usual doses, although this tertiary amine can rapidly cross the blood-brain barrier. Atropine has been associated with mild postoperative memory deficits, and toxic doses are often accompanied by excitatory reactions. An intramuscular dose of 0.01 to 0.02 mg/kg reliably provides an antisialagogue effect. Atropine should be used with caution in patients with narrow-angle glaucoma, prostatic hypertrophy, or bladder neck obstruction. atropine is used in the treatment of organophosphate pesticide and nerve gas poisoning . Organophosphates inhibit acetylcholinesterase, producing overwhelming stimulation of nicotinic and muscarinic receptors leading to bronchorrhea, respiratory collapse, and bradycardia. Atropine can reverse the effects of muscarinic stimulation, but not muscle weakness resulting from nicotinic receptor activation. Adverse effects and overdose. Its side effects include dry mouth, hypohidrosis, mydriasis, urinary retention, tachycardia, and constipation. Reduced sweat production can result in hyperthermia. In severe cases the drug can cause neurological symptoms, coma, or death. Physostigmine is used as an antidote in cases of iatrogenic overdose or poisoning by plants such as Datura stramonium and Atropa belladonna that They contain atropine. Scopolamine Scopolamine is a more potent antisialagogue than atropine and causes greater effects on the central nervous system. Clinical doses usually cause drowsiness and amnesia, although restlessness, dizziness, and delirium are possible. Sedative effects may be desirable for premedication, but may interfere with awakening after short procedures. Scopolamine has the additional virtue of preventing motion sickness . Lipid solubility allows transdermal absorption, and transdermal scopolamine (1 mg patch) has been used to prevent postoperative nausea and vomiting. Because of its pronounced mydriatic effects, scopolamine is best avoided in patients with angle-closure glaucoma. Adverse effects. The effects of scopolamine administration are manifested as a decrease in glandular secretion, suspension of saliva production, which causes dry mouth and thirst; difficulty swallowing and speaking; dilation of the pupils, which react slowly to light; blurred vision for close objects and, sometimes, temporary blindness. Tachycardia is recorded, which may be accompanied by hypertension. Redness of the skin due to vasodilation and decreased sweating is characteristic along with scarlet-like outbreaks on the face and trunk, as well as increased body temperature or fever that can reach up to 42° C. It causes bladder dilation with spasm of the sphincter and urinary retention. In some cases it may be accompanied by temporary amnesia or drowsiness. Glycopyrrolate Glycopyrrolate cannot cross the blood-brain barrier and has almost no ophthalmic and central nervous system activity. Potent inhibition of secretions from the salivary glands and respiratory tract is the main reason to use glycopyrrolate as premedication. Heart rate generally increases after intravenous, but not intramuscular, administration. Adverse effects. Cardiovascular: The use of glycopyrrolate may cause palpitations, tachycardia, paradoxical bradycardia, and orthostatic hypotension. Gastrointestinal: Constipation, dry mouth, vomiting, epigastric discomfort, dysphagia, abdominal distension and loss of taste. Genitourinary: Urinary retention and difficulty in beginning the act