205

Anästhesie (Subject) / Pharmakologie (Lesson)

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• Sympathikus: Rezeptoren Aktorius 182! Gefässe:  Vasokonstriktion: A 1 > A 2 Vasodilatation: B 2 > B1 Bronchien: Kontraktion: A 1 Dilatation: B2 > B1 Herz: Sinusknoten, AV-Knoten, Purkinje-Fasern, Arbeitsmyokard: B1>B2 NA-Axone: Transmitterfreisetzung:  Hemmung: A 2 Steigerung: B 2  
• Clonidin Alpha 2 > Alpha 1-Agonist. Alpha 2: Antihypertensiv, decreasing noradrenaline release from sympathetic nerve terminals  Alpha 1: transient increase in blood pressure and vasoconstriction central effects: dry mouth, mild sedation, decrease gastric and small bowel motility increases vagal tone: bradycardia  
• Forcierte Diurese: Zur schnelleren Ausscheidung basischer Gifte: Ansäuern des Harns: Ammoniumchlorid   Saurer Gifte: basisches Natriumlactat oder -citrat ZB bei Salicylat- und Barbituratvergiftung  Ca 500 ml/ h, abwechselnd: 500ml of 1.26% sodium bicarbonate 500ml of 5% dextrose and 500ml of 0.9% sodium chloride.
• AldosteronAGONIST Carbenoxolon-Natrium
• Tobramycin Aminoglykosid.  Breitspektrum. Pneumonie, HWI, Sepsis, Peritonitis, Endokarditis. NICHT: Anaerobier, Enterokokken, Streptokokken, Haemophilus NW: Nephro- und Vestibulo-, Ototoxizität KI: SS
• Adenosin Purin- Nucleosid Natürlicherweise: Reduktion O2- Verbrauch, Erhöhung coronarer Blutfluss, Vasodilatation (A2-Rezeptoren), Verlangsamung der AV Überleitung (V1-Rezeptoren) Transplatierte Herzen sind sensibler auf Adenosin NW: Cave Asthma! Antagonist der bronchodilatatoriachen Wirkung von Xanthinen Adenosine receptors are expressed on the surface of most cells, and four subtypes are known to exist (A1, A2A, A2B and A3) The A1 and A2 receptors are present both peripherally and centrally, with agonists at the A1 receptors being antinociceptive and agonists at the A2 receptors being algogenic (that is, activation results in pain).
• Puffersysteme Niere 1. Phosphat (HPO4): pKa 6,8 -> erst bei saurem Urin  2. Ammonium-/Ammoniakpuffer (NH4/NH3) 3. Bicarbonatpuffer (HCO3)
• Heparin, niedermolekular 2000-8000 Dalton Anti-FIIa (Thrombin): FXa = 1: 2-4 (Vgl. unfraktioniertes Heparin: 1:1) Geringe Inaktivierung auch: F IX, XI, XII    
• Aldosteron Mineralocorticoid zona glomerulosa der Nebennierenrinde Sekretion mit tageszyklischen Schwankungen: 75% zwischen 4 und 10 Uhr am morgen wirkt über intrazelluläre Steroidrezeptoren Mineralocorticoidrezeptor: Bindung von Aldosteron und Cortison mit gleicher Affinität! erhöht die Transkription der Na-K-ATPase Reabsorption Na2+, Sekretion H+ (distaler Tubulus und Sammelrohr) Aktivierung Natrium gegen Kalium Austausch (distaler Tubulus und Sammelrohr) erhöhte Natriumresorption aus Schweiß, Speichel Stress -> adrenocorticotrophic hormon -> Aldosteron Hyponatriämie/ Hyperkaliämie -> Nebennierenrinde: Aldosteron Blutverlust/ Hypovolämie -> Renin, Angiotensin, Aldosteron How then can aldosterone stimulate specific biological effects in this kind of system, particularly when blood concentrations of cortisol are something like 2000-fold higher than aldosterone? A large part of the answer is that in aldosterone-responsive cells, cortisol is effectively destroyed, allowing aldosterone to bind its receptor without competition. Target cells for aldosterone express the enzyme 11-beta-hydroxysteroid dehydrogenase, which has no effect on aldosterone, but converts cortisol to cortisone, which has only a very weak affinity for the mineralocorticoid receptor.  
• Suxamethonium depolarising neuromuscular blocking drug that causes inactivation of the voltage sensitive sodium channels in the muscle fibre membrane. Dosierung Kinder:1-2 mg/kg, Erwachsene: 0,6-1 mg/kg  Adipöse: entsprechend tatsächlichem KG!! Neostigmine and other anticholinesterase drugs potentiate the neuromuscular block induced by suxamethonium    UEW: Struktur: 2 verbundene ACh Moleküle > muskarinerge NW increased gastrointestinal motility and increased intraluminal pressure. Sinus - und Knotenbradykardien Hyperkaliämie Myalgia Raised intraocular pressure Anaphylaxis Malignant hyperthermia.   Hyperkalemic responses to suxamethonium have been associated with: Burns Certain neuromuscular diseases (including spinal cord injury, upper motor lesions, peripheral nerve injury, tetanus, and muscular dystrophy, myopathy) Closed-head injury Malignancy Abdominal sepsis Hypovolaemic shock Long term neuromuscular blockade, and Prolonged immobilisation.   Gefährlich bei Verbrennungen und Verletzungen des Rückenmarks nach 12-48 h! ( Proliferation extrajunctionaler Rezeptoren) Depolarisation -> Kaliumausstrom aus Zelle  Fasziculationen -> Kaliumanstieg um 0,5 mmol/l für 3-5 Min Anaphylaxie: Inzidenz: 1/1000  It is metabolised by plasma cholinesterase (pseudo-cholinesterase) and only 20% of the administered dose reaches the neuromuscular junction. A large total dose or repeated dosages of suxamethonium can cause a phase II block, characterised by: Fade Train-of-four ratio of < 0.7 Post-tetanic facilitation, and Reversal by anticholinesterases.                  
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• Atropin Muscarinrezeptor - Antagonist Alkaloid Indikation: Sinusbradykardie, Organophosphatvergiftung. Evtl. bei AV-Knoten-Block oder ventrikulärer Asystolie. Keine Wirksamkeit bei infranodalem Block (Typ II Mobitz).  Wirkdauer: 60-90 min (Glycopyrrolat:2-4h) The mydriasis and cycloplegia following topical application may last up to two weeks.  Bronchodilation -> Totraumerhöhung  
• clearance of drugs Clearance is the volume of plasma from which drug is completely removed per unit time. is calculated by dividing the dose of drug given by area under plasma concentration-time curve (-> Konzentration pro Zeit)  Clearance (CL)U = urinary creatinine concentration (mg/ml)V = volume of urine ml/minuteP = plasma creatinine concentration (mg/ml).Mathematically:CL= UxV/P
• Verteilungsvolumen (Volume of distribution Vd) Menge Medikament/ Plasmakonzentration Medikament Vd = dose/concentration at time 0 HWZ = 0,693 x Vd/Clearance Muskelrelaxantien: bei physiologischem pH überwiegend ionisiert -> gering fettlöslich -> niedriges Verteilungsvolumen  Hohe Proteinbindung -> Niedriges Vd If a drug is highly protein bound, only the small fraction that is free can cross the cell membrane and equilibrate with other compartments.   
• Vancomycin ANaerob + Aerob gram positiv  inklusive MRSA Cave: Dosisanpassung bei NI
• Aztreonam aerob Gram negativ Pseudomonas
• Metronidazol anaerob bes. gyn + GIT
• Imipenem Breit anaerob + aerob grampositiv, gramnegativ
• Trimethoprim aerob gram negativ Hemmt Tatrahydrofolsäurereduktase E. coli, Klebsiellae, Enterobacter, Morganella morganii, Proteus vulgaris, Proteus mirabilis
• Flumazenil zentraler Benzodiazepinrezeptor-Antagonist schwache, lipophile Base 50% gebunden an Plasmaproteine (davon 65% an Albumin) starke Umverteilung nach extravasal. Verteilungvolumen im steady state: 1 l/kg. Wirkdauer < 1h (hoher first pass Metabolismus in Leber) HWZ: 7-15 min (initial), 20-30 min (brain), 40-80 min (terminal).  UEW: Übelkeit, Erbrechen, senkt Krampfschwelle, Hypertension, Schwindel, Flushing, Ks, Angstzustände, Arrhythmien 0,2 mg iv, max 2 mg
• Epoprostenol Prostazyclin Ind: Pulmonale Hypertonie. Wirkung: Gefäss erweiternd, Tc-Aggregationshemmung (cAMP -> Hemmung Tc-Phospholipase, Cyclooxygenase)
• Dipyridamol Ind: Sekundärprävention ischämischer Insulte und TIAs Stimuliert Adenylatzyclase > cAMP > hemmt Phospholipase, Cyklooxygenase > Plättchenhemmung NW:  Myalgia  hypotension tachycardia Rel. KI: myasthenia gravis Migräne Asthma Drug interactions: Adenosin: verlängerte und verstärkte Blockade des AV-Knotens  verstärkte antikoagulatorische Wirkung von Heparin
• N2O   It is 1.5 times denser than air  The molecular weight is 44 It has a boiling point of -88°C The critical temperature is 36.5°C The solubility coefficients are 0.47 (blood gas) and 1.4 (oil/gas). critical pressure 72 bar MAC 105%   Vorratsflasche: enthält flüssiges N20 mit Dampf im oberen Bereich. Druck 4400 kPa bei Raumtemperatur (44 bis 54 bar; 40 bar at 15°C). Nur zu 0,67 bis 0,75 gefüllt (je nach Klimazone). French blue cylinder. Herstellung: erhitzen von Ammoniumnitrat auf 240°C. Nebenprodukte, die entfernt werden: Ammoniak, Salpetersäure, höhere Oxide von Nitrogen u.a.   The higher oxides of nitrogen which are formed include: Nitric oxide (NO) Nitrogen dioxide (NO2) Nitrogen trioxide (N2O3) which decomposes to NO and NO2. They are all irritant to the respiratory tract if inhaled and may cause pulmonary oedema hours after exposure. A severe fibrotic reaction may occur after several weeks, which destroys the lung tissue. N2O cylinders can be tested for contamination with higher oxides of nitrogen, by exposing moistened starch-iodide paper to the gaseous contents of a cylinder, which turns blue if contaminants are present.   Antagonist an NMDA Rezeptoren 25- 34 x löslicher als Stickstoff (N2) -> Zunahme luftgefülllter Räume (auch im Innenohr. UEW postop Hörverlust)   inaktiviert Methioninsynthetase nach längerer Zufuhr > Knochenmarksdepression, megaloblastäre Anämie, periphere Neuropathie, weniger Methionin, Thymidin, Tetrahydrofolsäure, DNA beeinträchtigt Synthese weisser Blutzellen KI: SS, erhöhter Hirndruck, Immunsuppression, häufige AA    Cerebral autoregulation is impaired, but when used with propofol it is maintained. It is a non-flammable gas which supports combustion, breaking down at high temperatures into oxygen and nitrogen.   Treibhausgas (absorbiert und emmitiert infrarote Strahlung) NW: verringertes Tidalvolumen, erhöhte Respirationsrate    The molecular weight of nitrous oxide is 44 g. One mole of an ideal gas will occupy a volume of 22.4 litres at STP (standard temperature and pressure, 0°C and one atmosphere pressure). Tare weight of a cylinder is that when empty. Weight of cylinder - tare weight = weight of remaining N2O (g). In this example 0.44 kg of nitrous oxide remains in the cylinder or 440 grammes. Therefore amount left in cylinder is number of gN2O/44x22.4 litres of N2O. 440/44x22.4  = 224 litres.    
• Lokalanästhetika, Toxizität Lidocain ab 5 mcg/ml Biphasische ZNS Toxizität:  1. Blockade inhibitorischer Leitungen > Kribbeln, Taubheit, Krämpfe 2. Blockade erregender Leitungen > Bewusstlosigkeit, Atemdepression Später: Kardiovaskulär: Vasodilatation, Re-entry-Arrhythmien, Blockade Sinusknoten, AV-Knoten, Sinustachykardie   Verstärkung der Toxizität durch:    Hypoxie Azidose Hypoproteinämie Leberversagen Protein binding of levobupivacaine is more than 97%, mainly to acid alpha1-glycoprotein, rather than to albumin. This union to proteins is somewhat higher than the union of racemic bupivacaine to proteins (95%). This means that less than 3% is free in plasma. It is the free levobupivacaine, a small fraction of the total concentration that can have an action on other tissues, causing side effects, and toxicity. In hypo-proteinaemic, undernourished patients, patients with the nephrotic syndrome and in the newborn there is less protein for binding, causing higher levels of free drug, resulting in toxic effects being seen at lower doses.  
• Nitrate Glyceryl Trinitrat + Thiol > NO > Aktivierung Guanylatzyclase > intrazelluläres cGMP > weniger cytoplasmatishes Calcium > Vasodilatation; Hemmung der Plättchenaggregation UEW: Methämoglobin, Toleranzentwicklung Nipruss: Dilatation von Arterien und Venen Gabe nur i.v. Bei Rkt mit Licht Entstehung von Cyanidionen! Glyceryl Trinitrat: Vasodilatation venös > arteriell Gabe i.v., buccal, sublingual
• Ephedrin Alpha-,Beta-Agonist, Freisetzung von NA aus sympathischen Nervenendigungen Tachyphylaxie (Abnahme des Effekts) mit längerer Anwendung durch Verbauch des NA-Vorrats in sympath. Nervenendigungen Blut-Hirnschrankengängig, Steigerung des cerebralen Blutflusses erhält Blutfluss in Plazenta und Uterus  NW Bronchodilatation Harnretention (erhöhter Blasenmm. tonus) supraventr. Tc.  Überquert Plazentaschranke> Tc und  Azidose beim Fötus.  Keine Erhöhung des Muskeltonus des Uters 272 Pharmacology for anaesthesists  
• Betablocker, 3.Generation Beta1-Blocker, Beta2-Agonist Celiprolol, Dilevalol > Reninfreisetzung vermindert (Beta1-Blockade) > Bronchodilatation > im Ggs zu traditionellen Betablockern kein Anstieg des BZ (Wechselwirkung mit Insulin), Senken HDL, Erhöhung LDL
• Kolloidale Artificial colloids are suspensions of large molecules in 0.9% saline and so contain 154 mmol per litre of sodium zB Haemacell Molekulargewicht 35 000 Dalton modifikation von tierischer Gelatine HWZ 4 h isotonisch UEW: Allergische Rkt
• Dopamin Dopamine does not cross the blood-brain barrier but its precursor         L-dopa does Rezeptoren G-Protein gekoppelte Rezeptoren: 1-5 D1: Erweiterung renale und mesenteriale Blutgefässe > GFR steigt, Tubuluszellen > Natriurese, Reninfreisetzung Fenoldopam: D1-Rez. Agonist: Vasodilatation, Verbesserung des renalen Blutflusses, Natriumausscheidung und Diurese D2: Nigrostriatal   L-dopa does cross the blood brain barrier and is therefore used in the treatment of Parkinson's disease Hypothalamus: Inhibition Prolactinfreisetzung Chemorezeptortriggerzone: Übelkeit, Erbrechen Dopamine acts predominately at dopamine receptors at low dose (1-5 mcg/kg/min) Beta adrenoceptors at intermediate doses (5-10 mcg/kg/min) and Alpha receptors at high doses (10-15 mcg/kg/min). HWZ: 2 min. Abbau durch die dopamine ß-hydroylase, Catechol-O-Methyltransferase und Monoaminoxidase in Leber, Niere und Plasma Cave: is inactivated by alkaline solution such as sodium bicarbonate. Antagonisten: Antidepressiva, trizyklische Neuroleptika, Antiemetika            
• Morphin Struktur: Phenanthren terminale HWZ: 3 h p.o. > 5-50% systemisch (hoher first pass Effekt) Metabolismus in Leber > 75 - 85% Morphin-3-Glucuronid: nicht analgetisch. (NW in hoher Dosis: Hyperalgesie, Myoklonus. Nicht über Opiatrez. vermittelt) > 5 - 10% Morphin-6-Glucuronid: potenter als Morphin Prodrug: Diamorphin: fast keine Affinität zum Opioidrezeptor NW: ADH-Ausschüttung, Bradykardie, Hisaminausschüttung > bronchospastik, vasodilatation.     
• Muskelrelaxantien, nicht depolarisierend Bis-Bezylisochinolinium (Atracurium) oder Aminosteroide (Vecuronium) Antagonismus an postsynaptischen nicotinergen ACh Rezeptoren Fade durch Blockade der präsynaptischen ACh Rezeptoren und somit des pos. Feedback  Dauer Wirkeintritt: Applikation bis fehlendes Ansprechen auf single Twitch  
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• Propofol 2, 6 di-isopropylphenol, 178 dalton, pKa of 11   grüner Urin und Haare nach langer Applikation (Phenole)   HWZ:   Verteilung: 1-2 Min Elimination: 1-5 h terminal: 3- 12 h Kurze Wirkdauer. Bei langer Anwendung allerdings Rückverteilung! Verteilungvolumen 4 l/kg. Fettlöslich > Öl-Wasser-Emulsion; 98% proteingebunden  isoton   Wirkung:   Agonist an GABA A Rezeptoren (increases the duration of chloride channel opening) Agonist an Cannabisrezeptoren Agonist an Glycinrezeptoren Antagonist an Natriumkanälen (verringert die Öffnungsdauer)   Kreislaufwirkungen: reduction in the systemic vascular resistance (SVR) by up to 80% myocardial depression decreasing the cardiac output by up to 20%. Normo- bis Bradykardie (evtl. wegen Reset Barorezeptor Reflex). erhöht Latenz und verringert Amplitude von somatosensorisch evoziierten Potentialen (SSEPs). A major disadvantage of intravenous propofol administration is the pain on injection. Pre-treatment with Lidocaine Opioids Ephedrine Metoclopramide Ketorolac Neostigmine Metoprolol and Magnesium sulphate have all been reported to reduce the incidence and severity of pain.
• Oxytocin/ Syntocinon Dosis nach Sectio: 5 E als KI Uteruskontraktion, Milchejektion UEW: Hypertonie, Allergie, Vasodilatation, Reflextachykardie, Wasserretention, Hyponatriämie, Übelkeit Oxytocin is synthesised in the paraventricular nucleus of the hypothalamus and is then transported in secretory granules along axons to the posterior pituitary gland, from which it is released. The primary role of oxytocin is to eject milk from the lactating mammary gland in response to suckling. It achieves this by causing contraction of the myoepithelial cells that surround the alveoli of the mammary gland. The principal clinical uses of synthetic oxytocin are to induce labour at term and to induce sustained uterine contraction which is required for post-partum or post-termination haemostasis. By lowering the threshold for depolarisation of uterine smooth muscle, oxytocin exerts a contracting effect on the gravid uterus. The sensitivity of the uterus to oxytocin increases as the pregnancy progresses. Oxytocin has only 0.5 - 1% of the antidiuretic activity of ADH (antidiuretic hormone) when administered in high doses, introducing the possibility of water intoxication.
• Modus (engl. mode) häufigster Wert
• Thrombozytopenie, medikamenteninduziert Thiazide diuretics Aspirin Alcohol toxicity Quinine Gold Heparin Alpha-methyldopa
• Hartmann's solution (Sodium Lactat) Sodium 131 mmol/l Chloride 111 mmol/l Potassium 5 mmol/l Calcium 2 mmol/l Lactate 29 mmol/l.  lactate is metabolised to bicarbonate 278 mosmol/kg
• N-acetyl cysteine (NAC) N-acetyl cysteine (NAC) is most effective within 24 hrs of a documented paracetamol overdose and is also clinically beneficial in non-paracetamol acute liver failure. It should be administered at the earliest opportunity, regardless of blood results and paracetamol concentrations, as early treatment has a great impact on outcome. NAC maintenance should be continued until the INR improves to less than 2.0. The microcirculation has been shown to improve. Non-toxic sulphation of paracetamol is increased by NAC and it has additional antioxidant properties. Anaphylactoid reactions can occur in as many as 15% of patients
• drugs with high hepatic extraction ratio The hepatic clearance of drugs is dependent on the hepatic blood flow and the intrinsic hepatic metabolism of the drug. For many drugs the hepatic clearance is equivalent to the intrinsic hepatic metabolism and these drugs have a low extraction ratio. So hepatic clearance is independent of hepatic blood flow, but an increase in hepatic blood flow may lead to a decrease in the extraction ratio. The clearance of these drugs may be increased by enzyme induction. Lidocaine, etomidate, propofol and the opioids have a high intrinsic clearance and their clearance is dependent on hepatic blood flow. As they already have a high extraction ratio they are unaffected by enzyme induction. When given orally they have a low bioavailability due to high first pass metabolism.
• Lidocain   Pka 7.8-7.9 Lidocaine is an amide-type local anaesthetic, and is also classified as a Vaughan Williams class I antiarrhythmic drug (not class IV). It has no intrinsic vasoconstrictor activity and can cross the blood brain barrier. Lidocaine has a stabilising effect on central neurones (sodium channel blockade) and has previously been used therapeutically to control seizure activity. However, in overdosage convulsions and coma can occur. Ester type local anaesthetics are metabolised by pseudocholinesterase (not lidocaine).  
• The principal mechanisms of antibacterial action include interference with   Cell wall (peptidoglycan) synthesis Penicillins Cephalosporins Vancomycin Cell membrane integrity Polymyxin B Nucleic acid synthesis Fluoroquinolones Metabolic pathway (folate biosynthesis) Sulphonamides Trimethoprim Protein synthesis Aminoglycosides Tetracyclines Erythromycin/clindamycin Chloramphenicol. DNA-Synthese Nitroimidazol (Metronidazol)
• Thiazide, zB Metolazon Wirkungen: Wirkung ab GFR von 50 ml/min hemmen Wideraufnahme von 3-5% des filtrierten Natriums und von Chlorid im distalen Tubulus. Exkretion von Kalium und Wasserstoff nach hohen Dosen zusätzlich Carboanhydrase-Hemmwirkung im proximalen Tubulus > Alkalisierung des Harns  mit 1-2 Wochen Latenz Senkung des peripheren Widerstandes. Reduktion der renalen Calcium-Ausscheidung  UEW: Hyperglykämie (weniger Insulinsekretion, weniger Glukoneogenese, mehr Glukoneogenese) Hypo: -kaliämie, -natriämie, -magnesiämie Hyperkalzämie Hypochlorämische Alkalose  (due to renal loss of acid) moderater Anstieg von Cholesterol und Triglyceriden im Plasma zu Therapiebeginn (reversibel) Harnsäureanstieg (Steigerung der Reabsorption von Harnsäure) sehr selten: Thrombozytopenie, Purpura, Agranulozytose Hy-perparathyreoidismus Bendroflumethiazid: reduzierte Lithiumexkretion  Pankreatitis Photosensitivität Herzstillstand wegen Hypokaliämie The inhibition of sodium reabsorption and stimulation of chloride excretion, together with excretion of sodium and potassium, and reduced excretion of bicarbonate, results in an increase in water excretion. The reduction in extracellular fluid volume (blood volume and cardiac output) leads to the activation of the renin-angiotensin-aldosterone and adrenergic systems in an attempt to re-establish central blood volume. Eventually blood volume and cardiac output return to normal but the peripheral resistance is reduced. The activation of these counter-regulatory systems may take up to nine days and explains their variable interpersonal antihypertensive efficacy.  
• MAOI   Two monoamine oxidase isoenzymes, A and B exist: MAO-A acts mainly on serotonin, noradrenaline and adrenaline. It is the main form of MAO found in the human brain. MAO-B metabolises non-polar aromatic amines such as phenylethylamine and methylhistamine, and is responsible for 75% of MAO activity, mainly in the gastrointestinal tract, platelets and most other non-neural cells. Non-selective irreversible MAOIs These drugs are of two types Hydrazines such as phenelzine and isocarboxazid, and Non-hydrazines such as tranylcypromine.   MAO takes three weeks to resynthesise! > stop taking MAOIs at least three weeks preoperatively   Reversible inhibitors of MAO-A (RIMAs) Moclobemide selectively inhibits MAO-A, so that the response to tyramine (metabolised mainly by MAO-B) is much less and patients do not need the same level of dietary restriction. Because it is reversible, and short-acting with an elimination half life of two to four hours, the risk of drug interactions is reduced, and MAO activity returns to normal within 24 hours of stopping the drug.     Anaesthesia for a patient on MAOI Although continuation of MAOI carries risks, these can be minimised by careful anaesthetic technique. For elective surgery, the decision as to whether to stop MAOI therapy preoperatively should be made in advance, on an individual basis with the involvement of the patient and psychiatric team. If the MAOI is to be stopped, this should be for the minimum period, with gradual reduction of dose and regular psychiatric review. Late cancellations of surgery should be avoided, and treatment restarted as soon as possible post operatively. If continuing the MAOI, or in the emergency situation, the following steps can minimise the risks: Avoid sympathetic stimulation. Ensure patient is adequately hydrated. Treat hypotension initially with intravenous fluids, then with cautious doses of direct acting sympathomimetics, for example, phenylephrine 10 - 20 mcg initially titrated to effect as patients may have an enhanced effect due to receptor hypersensitivity Pethidine and indirectly acting sympathomimetics are absolutely contraindicated Regional anaesthesia avoids the risks of general anaesthesia, but care must be taken in treating hypotension as described above.   Drugs that should be avoided include: Adrenaline Noradrenaline Ephedrine Pseudoephedrine Phenylephrine Dopamine Dopexamine Dexamfetamine Doxapram Pethidine Metaraminol Ketamin Pancuronium Cocain The metabolism of sympathomimetics is inhibited which may potentiate their pressor action, and the pressor effect of tyramine (found in mature cheese, meat and yeast extracts) may also be potentiated. Alcoholic and low alcohol drinks should also be avoided.   Morphine may be the opioid of choice, although fentanyl has been safely used despite its being related to pethidine. Naloxone is safe to be used but doxapram is considered unsafe. Further interactions: Enhance the hypotensive effects of angoitensin-II receptor antagonists, clonidine and verapamil Enhance the hypoglycaemic effect of metformin, insulin and sulphonylureas and Antagonise the anticonvulsant effect of carbamazepine and barbiturates.  
• Etomidat Imidazol UEW: PONV venöse Thrombosen Nebennierenrindensupression: Decreased cortisol and aldosterone levels due to this adrenal suppression (reversible and concentration-dependent blockade of 11β-hydroxylase) have been documented to occur approximately 30 minutes after a single induction dose of etomidate with the duration of the effect being as long as 24 hours to 48 hours.
• Tokolytisch Ritrodin (Beta2-Agonist mit Beta 1-NW-Profil), Progesteron Drugs used as tocolytics include: Ritodrine Atosiban Terbutaline Salbutamol Nifedipine Magnesium GTN, and Indomethacin. They work: By acting on beta 2 adrenergic receptors As calcium channels blockers As oxytocin receptor antagonists As myosin light chain inhibitors Through nitric oxide production, or Through their non-steroidal effects.
• Acetazolamid   Carbonic anhydrase inhibitors Hemmen Na-H+ -Austausch im prox.Tubulus UEW:   Metabolic acidosis Hypokalaemia Hyponatraemia Renal calculi but not hypercalcaemia Fatigue and paraesthesia of limbs Stevens-Johnson's syndrome.  
• Tautomerie Wenn Moleküle zwar die gleiche Summenformel besitzen, aber die einzelnen Atome unterschiedlich verknüpft sind, spricht man von Isomeren. Als Tautomere bezeichnet man Isomere, die durch die Wanderung einzelner Atome oder Atomgruppen schnell ineinander übergehen, d. h. die beiden Isomere in einem schnellen chemischen Gleichgewichtmiteinander stehen. Tautomerism refers to the dynamic interchange between two forms of a molecule, which may be precipitated by a change in the physical environment. Midazolam is ionised (water soluble) in solution at pH 4, changes to an unionised (lipid soluble) ring structure at physiological pH. The solubility of thiopental depends on transformation from the keto to the enol form, which occurs in an alkaline solution. Morphine also displays the keto-enol transformation. Nitrous oxide exists in two forms, with dynamic interchange between N+=N-=O and N-≡N+-O.  
• intravenous fluids pH values  Sodium chloride 0.9% is 5.0 Hartmann's is 6.0 Glucose 5% is 4.15 Gelofusine is 7.4 Dextran 70 in 5% glucose is 4.5 Dextran 40 in 0.9% saline is 6.0. Osmolarität Sodium bicarbonate 8.4%: hyperosmolar (2000 mOsmol/l) Dextrose saline 0.18% saline in 4% dextrose  30 mmol/L of Natrium, 30 mmol/L Cl.   160 calories per litre  (4 g dextrose per 100 ml) Hyperglykämie durch Infusionslösungen Blood: in large volumes will cause hyperglycaemia Gelofusine and Hartmann's solution do not contain glucose but the lactate in Hartmann's solution may be metabolised to glucose and hyperglycaemia has been demonstrated in diabetic patients. 0.45% saline in 5% dextrose ( nicht so: 0.45% saline in 2.5% dextrose)    
• Gabapentin   Gabapentin binds to alpha-2-delta calcium channels subunits, acts on voltage dependent calcium channels and NMDA receptors and also increases the level of glutamate decarboxylase to facilitate conversion of glutamate to GABA. It is well tolerated. It is used in the management of add-on therapy in partial or generalised seizures and in chronic pain conditions such as diabetic neuropathy and post herpetic neuralgia.   
• EMLA   EMLA is theeutectic mixture of local anaesthetics. Eutectic mixture is formed by two compounds mixing to produce a substance of a single set of physical characteristics. EMLA contains 2.5% lidocaine and 2.5% prilocaine in oil:water emulsion. The melting point is lowered to produce an oil at room temperature. Unlike amethocaine (22-25 minutes), it has a slower speed of onset of 60 minutes. EMLA may cause the formation of methaemoglobin due to the o-toluidine produced when prilocaine is metabolised.  Therefore, it should be avoided in patients with methaemoglobinaemia. It should not be used on mucous membrane due to excessive systemic absorption.  
• Stickoxydul (Lachgas, N2O) Entonox is a gaseous mixture of oxygen and nitrous oxide (not nitric) in equal proportions (50:50) Hohe analgetische Potenz: 20 Vol.-% entsprechen ca. 15 mg Morphin  narkotische Kraft des Stickoxydul ist gering, da selbst ein Anteil von 80 Vol.-% in der Atemluft noch keine tiefe Narkose auslöst narkotische Effekt durch Hemmung eines Glutamat-Rezeptors vom NMDA-Typ UEW: supraventrikuläre Rhythmusstörungen, Halluzinationen
• Cocain   inhibitor of the reuptake of noradrenaline, dopamine and serotonin (pre-synaptic) It should never be given intravenously due to its toxicity and the risk of ventricular fibrillation and death. The administration of doses greater than 3 mg/kg topically can lead to symptoms of overdose, which should be treated with alpha and beta adrenoreceptor antagonists.  

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