Anästhesie (Subject) / Notfälle (Lesson)

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• CO 200-300 x stärkere Bindung an Hämoglobin als O2 it binds to and inhibits other haemoproteins (myoglobin, cytochrome c and reduced cytochrome P450) 35xstärkere Bindung im Myoglobin Linksverschiebung der O2-Bindungskurve entsteht u.a. wenn Volatile über trockenen Absorberkalk strömen Elemination unter Atmosphärendruck 1-2h, unter HBO-Therapie 20-30 Minuten. Sofortige Oxygenierung. Sauerstofftransport durch physikalische Lösung Komplikation: Cortikale Erblindung bei CO> 40% Keine Reaktion der Carotid bodys. SpO2-Messung nahe 100%, da CO-Hb als oxygeniertes Hb gelesen wird. .  
• Spinaler Schock autonome Hyperreflexie: RückenmarksVerletzung oberhalb TH 6  --> sympathische Hyperaktivität Bradykardie: oberhalb TH1  
• Methämoglobinämie Hb mit Fe3+ > schlechtere O2-Bindung + Linksverschiebung O2-Dissoziationskurve angeboren oder erworben mögliche Ursache: Prilocain + Cyanid > Cyanmethämoglobin Therapie: Methylenblau  
• Sectio: 4-Punkte -Klassifikation Grade 1/Emergency:Immediate threat to maternal or foetal life Grade 2/Urgent: Maternal or foetal compromise that is not immediately life threatening Grade 3/Scheduled: Needing early delivery, no maternal or foetal compromise Grade 4/Elective: At a time chosen to suit the operative team and the mother.
• LAMA   Laryngeal masks airways (LMAs) are available in sizes 1 to 6. Grössen: 1: bis 5 kg, 1,5: 5-10 kg 2: 10-20 kg 2,5: 20-30 kg 3: 25-50 kg 4: 50-70 kg 5: 70-100 kg 6: > 100 kg The volume of air required to inflate the cuff is as follows: Size 1 is 4 mls Size 2 is 10 mls Size 2 ½ is 14 mls Size 3 is 20 mls Size 4 is 30 mls Size 5 is 40 mls Size 6 is 50 mls. The internal diameters are as follows: Size 2 is 7 mm Size 3 and Size 4 is 10 mm Size 5 is 11.5 mm. verstärkt: länger, kleinerer Innendurchmesser > höherer Widerstand UEW: 10%: Airway-Obstruktion wegen nach unten drücken der Epiglottis  
• Blutverlust- Klassifikation (ATLS)   Class I haemorrhage (blood loss up to 15%): <750 ml of blood loss Minimal tachycardia No changes in blood pressure, RR or pulse pressure Normally not require fluid replacement as will be restored in 24 hours, but in trauma correct. Class II haemorrhage (15-30% blood volume loss): Uncomplicated haemorrhage requiring crystalloid  resuscitation Represents about 750 - 1500 ml of blood loss Tachycardia, tachypnoea and a decrease in pulse pressure (due to a rise in diastolic component due action of catecholamines) Minimal systolic pressure changes Anxiety, fright or hostility Can usually be stabilised by crystalloid, but may later require a blood transfusion. Class III haemorrhage (30-40% blood volume loss): Complicated haemorrhagic state in which at least crystalloid and probably blood replacement are required Classical signs of inadequate perfusion, marked tachycardia, tachypnoea, significant changes in mental state and measurable fall in systolic pressure Almost always require blood transfusion, but decision based on patient initial response to fluid resuscitation. Class IV haemorrhage (> 40% blood volume loss): Preterminal event, patient will die in minutes Marked tachycardia, significant depression in systolic pressure and very narrow pulse pressure (or unobtainable diastolic pressure) Mental state is markedly depressed Skin cold and pale Need rapid transfusion and immediate surgical intervention. Loss of >50% results in loss of consciousness, pulse and blood pressure.  
• Anaphylaxie First line: Adrenalin i.v. 50 mcg Second line pharmacological treatments include: Chlorphenirame 10 mg IV (H1-Blocker) Hydrocortisone 200 mg. Persistant bronchospasm can be treated using: Salbutamol (IV or inhaled) Aminophylline Magnesium sulphate.
• Status epilepticus   In all cases the first priority is to establish a patent airway, give high-flow oxygen and ensure blood glucose levels are checked and corrected if needed. Step 1 (Five minutes after start of seizures): Many children may have already undergone step 1 before arrival at hospital and it is important to remember this. If intravascular access is available then initial treatment is lorazepam 0.1 mg/kg IV If no intravascular access then give buccal midazolam 0.5 mg/kg or rectal diazepam 0.5 mg/kg. Step 2 (Ten minutes after start of seizure): If the convulsions continue give a second dose of benzodiazepine, call for senior help and start to prepare phenytoin No more than two doses or benzodiazepines should be given (including any doses given before arrival at hospital) If still no IV access then obtain intraosseous access (IO). Step 3 (Ten minutes after step 2) Senior help along with anaesthetic/ICU help should be sought Phenytoin 20 mg/kg IV over 20 minutes If the seizure stops before the full dose of phenytoin is given then the infusion should be completed as this provides up to 24 hours of anticonvulsant effect In children already receiving phenytoin as treatment for epilepsy then an alternative is phenobarbitone 20 mg/kg IV over five minutes Once the phenytoin is started, senior staff may wish to give rectal paraldehyde 0.4 mg/kg although this is no longer incuded in the routine algorithm recommended by APLS. Step 4 (20 minutes after step 3) If 20 minutes after starting phenytoin the child remains in status epilepticus then rapid sequence induction of anaestheisa with thiopentone and a short acting paralysing agent is needed and the child transferred to paediatric intensive care.  
• Ketoazidose The most important initial therapeutic intervention in diabetic ketoacidosis (DKA) is appropriate fluid replacement followed by insulin administration. The main aims for fluid replacement are: Restoration of circulatory volume Clearance of ketones, and Correction of electrolyte imbalance. Typically, the average fluid deficit is 100 ml/kg. A priming dose of insulin in the treatment of DKA is not necessary provided that the insulin infusion is started promptly. A fixed rate intravenous infusion calculated on 0.1 units per kilogram infusion is recommended. Insulin has the following effects: Suppression of ketogenesis Reduction of blood glucose Correction of electrolyte imbalance. Adequate fluid and insulin therapy will resolve the acidosis in DKA and the use of bicarbonate is not indicated. The acidosis may be an adaptive response as it improves oxygen delivery to the tissues by causing a right shift of the oxygen dissociation curve. Excessive bicarbonate may cause a rise in the CO2 partial pressure in the cerebrospinal fluid (CSF) and may lead to a paradoxical increase in CSF acidosis.
• Organophosphatvergiftung   Vergiftungen mit Insektiziden aus der Gruppe der Organophosphate (Alkylphosphate, Alkylthiophosphate, Phosphorsäureester, Thiophosphorsäureester), z. B. Parathion = E 605® forte Hemmung der Acetylcholinesterasen (AChe + Plasma Cholinesterase) parasympathischer Erregungserscheinungen wie Miosis, Bronchospasmus, Brechdurchfall, Bradykardie, Koliken und Kollaps; dazu gehören ferner Krämpfe bzw. fibrilläre Muskelzuckungen, Atemdepression, Lungenödem, Koma.   Treatment consists of atropine to antagonise the cholinergic effects, and oxime (pralidoxime) to limit the inhibition of cholinesterase and diazepam to prevent seizures. Atropine can be used to reverse the muscarinic effects but will not prevent the central effects, seizures or nicotinic effects.      
• Streptokinase Thrombolyse KI:  Pregnancy Bleeding (gut, menstrual) Recent stroke or surgery Uncontrolled severe hypertension GI malignancy Prolonged CPR.
• Asthma     In a patient presenting with acute asthma any one of the following suggests acute severe asthma: PEFR 33-50% best/predicted Respiratory rate ≥25/min Heart rate ≥110/min or Inability to complete a sentence in one breath. Saturations of less than 92% in this context suggest life threatening asthma. Patients with oxygen saturations of less that 92% on or off oxygen warrant arterial blood gas analysis looking for normo- or hypercarbia. A chest x ray is indicated in the following circumstances: Suspected pneumomediastinum or pneumothorax Life threatening asthma Suspected consolidation Failure to respond to treatment Requirement for ventilation. One criterion to suggest life threatening asthma is arrhythmia. In case of tachycardia an ECG would be indicted.   
• Addison Krise Akute Nebennierenrindeninsuffizienz > Mangel an Mineralo- und Glucocorticoiden
• acidosis in cardiac arrest   The use of bicarbonate causes generation of carbon dioxide which diffuses rapidly into cells causing: Worsening intracellular acidosis Negative inotropy to ischaemic myocardium Large osmotic load high in sodium to a failing circulation and brain Leftward shift of the oxygen dissociation curve to the left. Reference: Resuscitation Council Guidelines, 2010. The administration of bicarbonate is recommended only if the cardiac arrest is associated with tricyclic antidepressant overdose or hyperkalaemia.  
• Präeklampsie Diagnostic criteria for severe pre-eclampsia is severe hypertension with significant proteinuria, or moderate hypertension diastolic >100 mmHg and proteinuria and two other clinical features or HELLP. Severe hypertension: systolic BP >160-170 mm Hg or diastolic >110 mm Hg on two occasions. Significant proteinuria: >1 g/l or 5 g/24 hr or > 3+ on dipstick. HELLP: haemolysis, elevated liver enzymes, low platelets. Other features: Renal: oliguria - <400-500 ml/24 hours (or less than 100 ml over a 4 hour period) or raised creatinine Pulmonary oedema or respiratory compromise CNS: headache, visual disturbance, clonus or convulsions Epigastric pain (or right upper quadrant), liver rupture Low platelet count: <100 ×109/L Elevated liver enzymes: ALT or AST > 70 IU.
• fall in the intravascular blood volume- physiological response The veins of the body contain 70% of the circulating blood volume, in contrast to the 15% in the arterial system. Veins act as a reservoir, and venous tone is important in maintaining the return of blood to the heart, for example in severe haemorrhage, when sympathetic stimulation causes venoconstriction. The liver receives approximately 30% of resting cardiac output and is therefore a very vascular organ. The hepatic vascular system is dynamic, meaning that it has considerable ability both to store and release blood - it functions as a reservoir within the general circulation. In the normal situation, 10-15% of the total blood volume is in the liver, with roughly 60% of that in the sinusoids . When blood is lost, the liver dynamically adjusts its blood volume and can eject enough blood to compensate for a moderate amount of haemorrhage. The sympathetic nerves constrict the presinusoidal resistance vessels in the portal venous and hepatic arterial systems. More importantly, sympathetic stimulation causes a marked reduction in the capacitance of the portal system and helps to divert blood towards the heart. During haemorrhage net transcapillary absorption of interstitial fluid from skeletal muscle into the intravascular space compensates effectively for the blood loss. This absorption of fluid is mainly linked to decrease of the capillary hydrostatic pressure (Pc), as caused by reflex adrenergic readjustment of the ratio of pre- to postcapillary resistance. These fluid shifts become significant within a few hours after blood loss further diluting haemoglobin and plasma proteins. Increased albumin synthesis begins at approximately 48 hours. Renin is released by the juxtamedullary complex in response to decreased mean arterial pressure, leading to increased aldosterone levels and eventually to sodium and water resorption. Increased levels of antidiuretic hormone (ADH) further contribute to the retention of water.
• Traumatic head injury Intracranial pressure (ICP) is important as it affects cerebral perfusion pressure and cerebral blood flow. Normal ICP is between 5 and 13 mmHg. Constituents within the skull include the Brain (80%/1400 ml) Blood (10%/150 ml) and Cerebrospinal fluid (CSF 10%/150 ml). The skull is a rigid box so if one of the three components increases in volume, then there must be compensation by a decrease in the volume of one or more of the remaining components otherwise the ICP will increase (Monro-Kellie hypothesis). Primary brain injury occurs at the time of the head injury and is unavoidable except through preventative measures to reduce the incidence of head injury. Secondary brain injury is caused by a reduction in oxygen delivery due to hypoxaemia (low arterial PaO2) or anaemia, a reduction in cerebral blood flow due to hypotension or reduced cardiac output, and factors which cause a raised ICP and reduced CPP. Secondary brain injury is preventable through appropriate management. The most important initial management needs to ensure: Airway and cervical spine protection Ventilation and adequate oxygenation Adequate blood pressure and cerebral perfusion pressure (CPP). Once these management principles are achieved further strategies to reduce ICP and preserve cerebral perfusion are required. Techniques that can be employed to reduce ICP are aimed at reducing the volume of one or more of the contents of the skull. Reduce brain tissue volume Reduce blood volume Reduce CSF volume. Techniques to reduce brain tissue volume include: Tumour resection or abcess removal Steroids (especially dexamethasone) to reduce cerebral oedema Mannitol/furosemide or hypertonic saline to reduce intracellular volume Decompressive craniectomy to increase intracranial volume. Techniques to reduce blood volume include: Evacuation of haematomas Barbiturate coma to reduce cerebral metabolic rate and oxygen consumption and therefore cerebral blood volume Arterial: avoiding hypoxaemia, hypercarbia, hyperthermia, vasodilatory drugs, hypotension Venous: patient positioning with 30° head up, avoiding neck compression with ties/excessive rotation, avoiding PEEP/airway obstruction/CVP lines in neck. Techniques to reduce CSF volume include: Insertion of external ventricular drain or ventriculoperitoneal shunt to reduce CSF volume (although more a long term measure).
• Aspirinüberdosierung Aspirin increases O2 consumption and CO2 production and may, paradoxically, cause initial a respiratory alkalosis in adults due to the direct effect of high concentrations of salicylates on the respiratory centre. The excretion of bicarbonate, potassium and water is increased which results in hypokalaemia, dehydration and a metabolic acidosis. The metabolic acidosis occurs later and is due to uncoupling of oxidative phosphorylation, increased fat metabolism and inhibition of the tricarboxylic acid cycle. The metabolic acidosis tends to occur more rapidly and more commonly in children under the age of 12. The urinary pH in aspirin overdosage is initially alkaline and then becomes acidic. It may present with Tinnitus Deafness Pyrexia Hypoglycaemia (Hemmung Glucogenese der Leber) oder Hyperglykämie Haematemesis Hyperventilation  Hypokalaemia. Aspirin-auch in normaler Dosierung: Warfarin and sulphonamides are highly bound to plasma proteins and aspirin displaces them which increases their unbound proportion and potentiates their effect.  
• Serotonin Syndrom Selegiline, the anti-parkinsonism drug is an MAO-B inhibitor and the same precautions regarding anaesthetic drugs apply as for other types of MAO inhibitors. It is not necessary to stop selegiline if taken in doses of <10 mg/day. At this dose there is no reaction with sympathomimetics. Pethidine however, should still be avoided. There are two distinct types of reaction that can occur between MAOIs and opioids. Type I (excitatory) reaction occurs only in patients given pethidine and dextromethorphan, both of which inhibit serotonin re-uptake. The features are those of serotonin syndrome - sudden agitation, headache, hyper- or hypotension, muscle rigidity, hyperthermia, seizures and coma. The reaction is not seen with other opioids and morphine, fentanyl, alfentanil and remifentanil can all be used safely. Type II (depressive) reaction, which is very rare, is thought to be due to MAOI inhibition of hepatic enzymes, resulting in enhanced effects of all opioids. It is reversed by naloxone.
• Blood transfusion: management of massive haemorrhage. GUIDELINES from the Association of Anaesthetists of Great Britain and Ireland Hospitals must have a major haemorrhage protocol in place and this should include clinical, laboratory and logistic responses. Immediate control of obvious bleeding is of paramount importance (pressure, tourniquet, haemostatic dressings). The major haemorrhage protocol must be mobilised immediately when a massive haemorrhage situation is declared. A fibrinogen < 1 g.l)1 or a prothrombin time (PT) and activated partial thromboplastin time (aPTT) of > 1.5 times normal represents established haemostatic failure and is predictive of microvascular bleeding. Early infusion of fresh frozen plasma (FFP; 15 ml.kg)1) should be used to prevent this occurring if a senior clinician anticipates a massive haemorrhage. Established coagulopathy will require more than 15 ml.kg)1 of FFP to correct. The most effective way to achieve fibrinogen replacement rapidly is by giving fibrinogen concentrate or cryoprecipitate if fibrinogen is unavailable. 1:1:1 red cell:FFP:platelet regimens, as used by the military, are reserved for the most severely traumatised patients. A minimum target platelet count of 75 · 109.l)1 is appropriate in this clinical situation. Group-specific blood can be issued without performing an antibody screen because patients will have minimal circulating antibodies. O negative blood should only be used if blood is needed immediately. In hospitals where the need to treat massive haemorrhage is frequent, the use of locally developed shock packs may be helpful. Standard venous thromboprophylaxis should be commenced as soon as possible after haemostasis has been secured as patients develop a prothrombotic state following massive haemorrhage.   
• Raised urine pH helps excretion of: salicylates tricyclic poisoning thiopental Barbiturate
• Defibrillation 5-40 Joule am offenen Herz  Paddels 13cm im Durchmesser (Erwachsene)  
• trizyklische Antidepressiva-Vergiftung Patients with a GCS of less than 8 should undergo a rapid sequence induction at the earliest opportunity. It may be considered earlier if the airway is obtunded or if the patient is having seizures. Activated charcoal may be considered for use within one hour of tricyclic antidepressant (TCA) ingestion but only in patients with an intact and secure airway. The risk of aspiration should be considered before use. Serial ECGs should be examined for QRS prolongation and a QTc prolongation (>430 ms). These changes identify patients that are at high risk of developing complications following TCA overdose. Prolongation of the QRS duration >100 ms predicts a higher risk of arrhythmia and is an indication for systemic sodium bicarbonate administration. Serum alkalinisation favours dissociation of the tricyclic away from myocardial sodium channels, and the extracellular sodium load improves sodium channel function. Vasopressors are indicated for the treatment of hypotension following TCA overdose when patients fail to respond to fluids and bicarbonate. Magnesium sulphate is used for the management of arrhythmias if the patient fails to respond to bicarbonate therapy.
• Verbrennungen -hyperkatabol. Bei schweren Verbrennungen: 2 fach erhöhte metabolische Rate! - Energiereduktion durch warmes Umfeld (mindestens 30°C) - Schutz vor Wasserverlusten durch Abdecken der Wunden -intestinale Barriere ist unmittelbar zerstört. Wichtig: früher enteraler Kostaufbau - Proteinreiche Ernährung: carbohydrate, 30% as lipids or fat and up to 20% as protein or amino acids. Ggf. zusätzliche parenterale Ernährung.
• Paracetamolintoxikation Paracetamol hepatotoxicity is due to toxic oxidative metabolites combining with sulphydryl groups of hepatocyte proteins, causing centrilobular necrosis. The metabolites are usually scavenged by glutathione, but in a severe overdose this scavenging mechanism is rapidly overwhelmed. Treatment is based upon N-acetylcysteine, which provides additional sulphydryl groups to scavenge the toxic metabolites. The initial clinical features of the overdose do not provide a reliable guide to the severity of poisoning, with more serious complications developing after 36 hours. These include: Acute haemolytic anaemia Hypothermia Hypoglycaemia Metabolic acidosis Delerium  Acute hepatic failure (AHF). The prothrombin time is the most sensitive indicator of impending AHF.   Therapie Activated charcoal should be given to adult patients if ALL of the following criteria are met:   Presentation with an hour Cooperative patient, and Ingestion of greater than 10 g or 200 mg/kg of paracetamol Paracetamol levels should be taken at four or more hours following ingestion and the level plotted against a nomogram. If the level is above the nomogram line then N acetyl cysteine should be given. If the level is below the nomogram line then the paracetamol levels should be measured and compared again four hours later. Evidence of hepatocellular damage in the form of a raised aspartate transaminase is likely to emerge more than eight hours post ingestion. Advice from a regional liver unit would be helpful once there is clinical and/or biochemical evidence of hepatocellular dysfunction.  
• Dehydratation. Flüssigkeitsersatz beim Kind. Body weight: 1-10 kg 4 ml/kg/hour 10-20 kg 40 ml + 2 ml/kg/hour above 10 kg 20 kg 60 ml + 1 ml/kg/hour above 20 kg.
• Antidot In the management of overdosage and poisoning, specific antidotes exist for particular drugs: N-acetylcysteine may be indicated in a paracetamol overdose Glucagon is given for an overdose of beta blockers Ethanol is given for methanol poisoning The antidote for iron poisoning is deferoxamine which chelates iron Flumazenil is the antidote for benzodiazepine toxicity Naloxone is the antidote for opiate toxicity.

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