Anaesthetics - Lecture Note

ANAESTHETICS • • • • • • • • Pre-Operative Assessment Anaesthetic Principles The Recovery Room & Postoperative Problems Critical Care Analgesia Vascular Catheterisation Fluids And Electrolytes Shock 2 7 14 17 18 22 24 27 Pre-Operative Assessment • Describe the optimal preoperative evaluation of a patient Screening No need to attend pre-op assessment if: No co-existing medical problems Require no / only baseline obs, which are normal Have no potential for / history of anaesthetic complications Require peripheral surgery for which complications are minimal BUT these patients should be seen on admission To confirm the screening findings Check the results of any baseline obs Explain the type of anaesthetic to be used & the anaesthetist has the responsibility for deciding if it safe to proceed Pre-op assessment clinic To see nurse / surgeon - Have been picked up through screening: Have medical conditions that are well controlled / previously undiagnosed / less than optimally managed Have abnormal baseline investigations Have need for further tests – e.g. lung function / echocardiography Have had previous anaesthetic difficulties (e.g. difficult intubation) Suggest potential for anaesthetic difficulties (e.g. obese, prev / FH) Are undergoing major / complex surgery To see the anaesthetist in pre-op if: They have an actual / potential problem with the anaesthetic Or if they have been deferred pending further investigations This allows the anaesthetist to: Make a full assessment of the medical condition Review any previous anaesthetics Evaluate / order any further investigations Explain & consent the patient for the anaesthetic Discuss the plans for post-op care The anaesthetic assessment Medical history Cardiovascular – Ask specifically about IHD - Previous MI à increased risk of infarct during anaesthetic – aim to leave at least 6-8 weeks and have normal exercise ECG Heart failure – one of the most significant indicators of perioperative complications (increased mortality & morbidity). Descibe using NYHA scale New York Heart Association classification for heart failure Class I Class II Class III Class IV No limitation of physical activity No fatigue, palpitations, dyspnoea or angina Slight limitation of physical activity Asymptomatic at rest, exercise à fatigue/palpitations/dyspnoea/angina Marked limitation of activity Asymptomatic at rest, slight exercise à fatigue/palpitations/dyspnoea/angina Any physical activity limited by cardiac disease Symptoms of heart failure / angina at rest, increased with activity Hypertension – untreated/poorly controlled can à exaggerated cardiovascular responses during anaesthesia. Mild (sys 140-160, Dia 90-100) – no need to delay Mod (sys 160-170, Dia 100-110) – consider Rx review, if no change à close monitoring during surgery Sev (sys > 180, Dia > 110) – if elective postpone until controlled, if emergency will require invasive monitoring Conduction defects, Arrhythmias & Peripheral vascular disease also require monitoring & consideration Respiratory Check about – COPD, emphysema, asthma, infection & restrictive lung disease If infection – postpone until cleared if possible (esp if other lung disease) Exercise Tolerance A measure of cardiac & respiratory reserves. How far can you walking on the flat / up hill / up stairs? Could you run for a bus? Can you do the shopping? Can you do the housework? Can you care for yourself? Other conditions to check for Indigestion, heartburn, reflux, hiatus hernia – increase risk of regurgitation & aspiration Rheumatoid disease – limited movement makes positioning difficult. C-spine & TMJ can complicate airway management. Often also chronic anaemia Diabetes – increased risk of IHD, renal dysfunction & neuropathy. Increased complications – esp hypotension & infections Neuromuscular disorders – heart disease worsened by anaesthesia & restrictive lung disease à increased chest infection & possible need for post-op ventilation. Care needed with muscle relaxants Chronic renal failure – causes anaemia & electrolyte abnormalities, altered excretion affects choice of drugs, surgery & dialysis need to be considered Jaundice – altered drug metabolism, coagulopathy, care with opiods Epilepsy – avoid drugs which are epileptogenic (e.g. enflurane) Previous anaesthetics & operations Any nausea, vomiting, dreams, awareness, postoperative jaundice? Family history Inherited conditions – e.g. sickle cell, porphyria Any family members had problems with anaesthesia? Drug history and allergies ALL meds inc prescribed and OTC (inc herbal) Ask specifically about HRT & COCP Note allergies inc food, adhesives (plasters etc) Social history Smoking – Causes carboxyhaemoglobin (reduces O2 carrying capacity) & nicotine stimulates sympathetic NS à tachycardia, HT & coronary artery narrowing. Also increased risk of post-op chest infections. Even stopping 24 hrs before will improve O2 carrying capacity Alcohol - > 50 units / week à enzyme induction à increased tolerance to anaesthetic drugs. Also consider risk of alcohol withdrawal Drugs – ask about recreation drugs inc type, frequency & route. IV users may be difficult to establish IV access in. Withdrawal can occur Pregnancy – LMP in all child-bearing age in case X-ray required. Also risk of regurgitation & aspiration in late pregnancy Examination Cardvascular – arrhythmias, heart failure, HT, valve disease, peripheral vascular disease + check peripheral veins (re. IV access) Respiratory – resp failure, impaired ventilation, collapse, consolidation, effusion, addition / absent breath sounds NS – as relevant to history. NB MS may affect cardio & resp systems MSK – movement ranges, esp neck & jaw Airway Look for – Limitation of mouth opening, receeding jaw, position, no & heath of teeth inc caps & crowns, size of tongue, soft tissue swellings in front of neck, deviation of larynx / trachea, limitations in neck flexion & extension Mallampati criteria – graded I – IV based on visibility of pharynx. Grade III & IV suggest difficult intubation Thyromental distance – neck fully extended measure point of chin to thyroid cartilage. < 7cm suggests difficult intubation • Specify the indications for pre-operative investigations and how abnormalities of the following investigations may affect the choice of anaesthetic: Based on the health of the patient and the nature of the surgery Should only be done if the results would change the management of the patient U&Es – if on digoxin, diuretics, steroids, with DM, renal disease & D&V LFTs – Hx of > 50 units / week, metastatic disease or evidence of malnutrition Blood sugar – DM, severe peripheral arterial disease or long term steroids ECG – HT +/- signs of IHD, arrhythmias or DM > 40 yrs CXR – Sx of cardiac / respiratory disease, TB, malignancy, thoracic surgery Lung function tests – dyspnoea on mild exercise, COPD, asthma. If FEV1 < 60% should have ABG on room air Coag screen – anticoagulation, hx of diathesis, liver disease or jaundice Sickle cell screen – FH / ethnicity C-spine XR – Rheumatoid arthritis, Hx of trauma / surgery to neck / difficult intubation predicted Echo – in IHD / Valve disease Medical referral If unsuitable for anaesthetic due to co-existing illness • Outline specific problems associated with the following difficult" conditions and specify appropriate precautions and strategies to minimize risks during anaesthesia: Diabetes mellitus Transfer the patient from metformin to glicazide If daycase / simple surgery omit morning dose of oral hypoglycaemic agent If complex / prolonged surgery put on GKI infusion until eating again after surgery Warfarin anti-coagulation Stop warfarin at least 4 days before – aim for target INR of 1.5-2 Transfer onto heparin – maintain APTTR at 1.5-2.5 Stop heparin 6 hours before surgery & restart 12 hours after surgery Rheumatoid arthritis Check joint ranges and provide appropriate support. Avoid / Adapt intubation if necessary • Specify the American Society of Anesthesiology (ASA) grading for risk Minor risks: (can occur even with uneventful surgery) Failed IV access ( = no surgery!) Cut lip, damage to teeth, caps & crowns Sore throat Headache Post operative nausea & vomiting Urine retention Major risks: Aspiration of gastric contents Hypoxic brain injury MI Cerebrovascular accident Nerve injury Chest infection Death – 1 in 100,000 ASA physical status scale: Class I II III IV V Physical status Healthy patient with no pathology except that being operated on (which is localised & causing no systemic upset Mild-moderate systemic disease, not limiting activities in any way (e.g. stable DM, treated HT and anyone > 80yrs) Severe systemic disease that imposes functional limitation on activity (e.g. IHD, COPD) A severe systemic disease which is a constant threat to life (e.g. unstable angina) A moribund patient unlikely to survive 24hrs with or without surgery Absolute mortality (%) 0.1 0.2 1.8 7.8 9.4 All surgery is considered based on a risk-benefit analysis, do the benefits of the procedure being successful outweigh the risks of the anaesthetic and surgery? Classification of the operation Elective operation at time to suit the patient & surgeon (e.g. hip replacement) Scheduled early, but not life saving, usually within 3 weeks (e.g. malignancy) Urgent ASAP after resuscitation & within 24hrs (e.g. intestinal obstruction) Emergency Life saving, done at same time as resus, within 1 hr of admission (e.g. major trauma with uncontrolled haemorrhage, extradural haematoma etc) • Specify appropriate pre-operative starvation times Standard starvation is: 6 hours for food 2 hours for clear fluids Increased risk of aspiration if: Delayed gastric emptying (trauma, ileus, pregnancy, alcohol, opiates, anticholinergics, DM) Gastro-oesophageal reflux Sx / known hiatus hernia Obesity Pregnancy / Children Surgical position (steep head down) • Specify the indications for premedication and list appropriate pre- medication drugs Premed = any drugs given in the period before anaesthesia Anxiolytics Temazepam 20-30 mg Diazepam 10-20 mg Lorazepam 2-4 mg à sedation & amnesia Well absorbed from the GI Tract Given orally 45-90 minutes before surgery Amnesia If a patient requests not to remember the events before theatre Use lorazepam = anteriorgrade amnesia Anti-emetic Used as prophylaxis in patients in high risk groups / undergoing high risk surgery See more on post op nausea & vomiting section Antacid If patient is unstarved (e.g. emergency surgery) or if gastic contents not emptied (e.g. high dose opioids, hiatus hernia à increased risk of regurgitation) Drugs used to increase the pH & decrease the volume § Oral sodium citrate – orally immediate preinduction à chemical neutralisation § Ranitidine (H2 antagonist) – 12 hr & 2 hr preop § Metoclopromide – increases gastric emptying & lower oesophageal sphincter tone. Often given with ranitidine § Omeprazole (PPI) – 3-4 hr preop § NG tube – can be used to aspirate gastric contents Anti-autonomic Anticholinergic (e.g. glycopyrrolate, atropine, hyoscine) § Reduce salivation – for fibre optic intubation or surgery on oral cavity § Reduce vagolytic effects on heart – before suxamethonium, surgery on eye muscles or zygoma surgery Antisympathomimetic § Avoids tachycardia & hypertension on intubation Analgesia Only usually if in pain preoperatively Use morphine, pethidine or fentanyl Others Steroids – if on long term / had within last 3 months Antibiotics – heart valve disease / undergoing joint surgery Anticoagulants – DVT prophylaxis Transdermal GTN – in IHD patients to reduce risk of coronary ischaemia EMLA (eutectic mixture of local anaesthetics) – to reduce pain of canula Anaesthetic Principles • Understand the concept of general anaesthesia, including the stages, and complications Ideal anaesthesia Hypnosis Paralysis Analgesia Drug induced coma Stages of anaesthesia First stage (analgesia) – Depression of CNS & higher cortical function until consciousness is lost. Pupils are normal & reactive. Muscle tone is normal & reflexes are present. Breathing uses intercostals muscles & diaphragm. End stage = loss of pain & smell Second stage (excitement) – Before / during loss of consciousness. Strong inhibition of central function. Increased muscle tone, breath holding, increased / irregular respiration, struggling & coughing. Vomiting & loss of temperature control, Pupils dilated & loss of eyelash response. Aim to move through this stage quickly Third stage (surgical anaesthesia) - Slow synchronised EEG. Reduced respiratory activity with progressive intercostals paralysis. Muscle tone reduced & laryngeal reflexes lost. Pupils start constricted and gradually dilate. Stage ends with diaphragmatic paralysis Fourth stage (medullary depression & overdose) – apnoea, loss of all reflex activity, fixed dilated pupils = catastrophe. EEG small / absent Induction IV – rapid loss of consciousness as concentration in brain rises quickly As redistribution occurs the brain concentration falls à recovery Not given to maintain (except propofol) as they accumulate (elimination is slow vie hepatic metabolism) Inhalation – anaesthetic in O2 / O2 + NO2 (Sevoflurane is most popular) Slower rise on concentration so slower induction Used if IV induction is not practical (e.g. no suitable veins, uncooperative child, needle phobia, airway compromise (IV drug may à apnoea)) Rapid sequence Induction Method of choice if risk of regurg & aspiration – should be used for all patients with full stomach *** unless difficult intubation expected *** Preoxygenate the patient for 3 minutes Then inject rapid acting induction agent Apply cricoid pressure to prevent aspiration Inject suxamethonium to facilitate intubation The cuff of the tube should be inflated before pressure is released Maintainence Maintain with 33% O2, N2O & inhalation agent + injection of muscle relaxant & analgesia Signs of inadequate depth = tachycardia, hypertension, sweating, lacrimation Total IV anaesthesia (TIVA = uses propofol) Use initial induction dose Then repeated injections at intervals based on response Potency compared by Min Alveolar Concentration (MAC) = concentration required to prevent movement in 50% of subjects following a surgical stimulus So 1 MAC = equivalent dose & can compare side effects (high MAC = low potency) Reversal Neuromuscular blockade is reversed (if it has been used) Secretions cleared from airway FB extubation Place patient in recovery position & monitor (with O2 +/- airway adjuncts) until patient is able to maintain their own airway Complications of general anaesthesia Cardiovascular – Hypo / hypertension, dysrhythmias, Myocardial ischaemia & MI Respiratory – Upper airway obstruction, hypoventilation, hypoxaemia Renal – failure due to altered BP Neurological – delayed wakening, focal neurological deficits Temperature – hypothermia is common, hyperthermia is rare • Demonstrate knowledge of the principles underlying safe anaesthesia, and describe common adverse effects, of the following types of anaesthesia: Local anaesthesia (infiltration anaesthesia) Can be used topically (mucous membrane e.g. eye / urethra), sub cutaneously, IV after application of the tourniquet, directly around nerves (regional block) Lignocaine (0.5%) for short procedures Bupuvicaine (0.5%) for pain relief from surgical incision Use with epinephrine if large dose or prolonged effect required BUT NOT around end arteries (fingers, toes, penis etc) Procedure Calculate volume that can be used Clean skin surrounding & allow to dry Insert needle, aspirate to check not in vein Inject as withdrawing Toxicity signs Mild - Perioral paresthesia, numbness of tongue, visual disturbances, light headedness. Slurred speech, twitching, restlessness, mild hypotension, bradycardia Severe – grand mal convulsions fb coma, respiratory depression, and eventual CVS collapse, profound hypotension & bradycardia & cardiac arrest Management – A, B, C & treat convulsions with 5-10mg diazepam IV Spinal (intrathecal) anaesthesia Drug injected into CSF - In sub arachnoid space = central neural blockade Can only be done between L2 & S1 (cauda equina) (The level between the Iliac spines is L4) Single injection used = limits duration of procedure Level is determined by Hyperbaric solution (heavier than CSF à sinks) – then use posture Position – Sitting = low lumbar & sacral, Supine = T5-6 (more if head down) Increasing dose (volume or concentration) High placement = higher block Side effects Hypotension (33%) – due to sympathetic block à reduced peripheral reistamce à venous pooling à low cardiac return. Drop of 25% requires Rx Bradycardia (13%) - if block extends above T5 the carioaccelerator nerves are blocked à unopposed vagal tone. Give atropine for bradycardia Nausea (18%) & Vomiting (7%) – can result from vagal stimulation during upper abdo surgery or due to low BP & hypoxia. Give metoclopromide Dysrhythmias (2%) à low cardiac output Post-dural puncture headache – due to persistent leak of CSF from a hole in the dura. Headache is worse on standing and straining Total spinal block – spread of the effect throughout all spinal nerves will remove the cough, cardioaccelerator and then the diaphragm innervation à apnoea. If this occurs the procedure must move to a GA Epidural anaesthesia/analgesia In extradural space = central neural blockade Deposition of LA in potential space outside the dura (C1 to sacrococcygeal memb) Thoracic region for abdominal surgery Lumbar for pelvic / lower limb Can be single injection / catheter infusion Indications For analgesia alone, e.g. childbirth As an adjunct to GA, reducing the opiates required As a sole technique for surgical anaesthesia e.g. C-section For post-operative analgesia, to ensure the patient is pain free and able to cough and mobilise early For the treatment of back pain. Injection of analgesics and steroids into the epidural space may improve some forms of back pain. For the treatment of chronic pain or palliation of symptoms in terminal care, usually in the short or medium term. Procedure Tuohy needle inserted until tip embedded in ligaments (blocks injection) Then advanced until ligament pierced (resistance rapidly drops) Bupivicaine 0.5-0.75 for muscle relaxant & 0.1-0.2% for post op analgesia Opioid can be added to increase quality and duration (e.g. fentanyl) Level is determined by Level of insertion (spread is faster in thoracic than lumbar) Volume injected Gravity – head up à spread down T12 = inguinal ligament, T10 = umbilicus, T4 = nipples • Demonstrate knowledge of the types of drugs commonly used in anaesthesia (including as examples): o Benzodiazepines: Relieve anxiety, cause sedation and amnesia BUT no analgesic properties so require separate analgesia Can cause respiratory depression in high dose Diazepam – long acting (slow metabolism) causing mild sedation & amnesia. Painful on injection Temazepam – shorter duration (approx 90 mins), more rapid onset than diazepam. Midazolam – 40-70s onset, 10-15min duration Dose dependent hypotension, some ventilatory depression, mild anticonvulsant, causes amnesia o Intra-venous anaesthetic agents: propofol, etomidate, thiopentone Propofol – rapid induction (30-45s), lasts 4-7 minutes Can cause hypotension, apnoea (upto 60s), decreases cerebral flow & ICP, painful on injection. Non cumulative so used for TIVA Etomidate – 30-40s onset, 3-6min duration Less CVS depression than propofol, some resp depression, decreases cerebral & ICP flow, anticonvulsant, can suppress steroid synthesis Thiopentone – (barbiturate) 20-30s onset, 9-10 min duration Dose dependent hypotension, similar other effects as above, may ‘taste’ garlic on injection. Cumulative with delayed onset after repeated doses o Muscle relaxants - Affect ACh at the motor end plate Depolarising blockers - Suxamethonium The only depolarising neuromuscular blocker (binds to receptors, activates them initially and then stays in position à paralysis) 1.5mg/kg in adults Short period of fasciculation fb paralysis in 40-60s Recovery within 4-6 minutes The rapid onset & recovery = used to facilitate intubation Problems: bradycardia in large doses, é serum K à dysrhythmias in some cases SE’s: malignant hyperpyrexia, é intraoccular pressure, muscular pain around limb girdles, histamine release, (can à anaphylaxis), prolonged apnoea if pseudocholinesterase deficiency Pseudocholinesterase deficiency – reduced enzyme levels à sux lasts longer. (moderate in 50/1000, severe in 1/1000) Non-depolarising blockers Compete with ACh for the receptors but don’t activate them Relatively slow onset (generally 1.5-3mins) Used to maintain relaxation after sux induction or for intubation in non emergencies Recovery is often slow, so anticholinesterase inhibitors are used Atracurium 90-120s induction 20-25 min duration itching, ê BP Rocuronium 90-100s 20-30 min Vercuronium 90-120s 15-20 min no H2 release Mivacurium 100-120s 10-15 min H2 if fast inject Pancuronium 120-150s 35-45 min é BP, é HR o Anticholinesterase: neostigmine Results in increase of ACh in cleft à reverses effect of muscle relaxants Speed of recovery depends on intensity of block when it is reduced Effects: bradycardia, spasm of bowel, bronchi & bladder (so give with atropine / glycopyrrolate to block unwanted muscarinic effects) Neostigmine – dose 2.5mg iv (+ 1.2mg atropine / glycopyrrolate 0.5mg) , 5min to max effect, lasts 20-30 mins o Anticholinergic: atropine, glycopyrrolate Used as premed to dry bronchial and salivary secretions Also used to reverse excessive bradycardia Can be used with neostigmine (to prevent its SE of bradycardia excessive salivation) during reversal of depolarising neuromuscular blockade o Volatile anaesthetic agents Absorbed through lungs in vapour phase Low blood solubility à rapid entry to brain Correlation between potency and solubility in oil Dose can be rapidly altered Blood : gas partition co-efficient Solubility in blood Lower figure = rapid induction & faster equilibrium Oil : Gas partition co-efficient Solubility in lipid Higher figure = higher potency Rate & depth of breathing & CO are important Increased cardiac output, increased alveolar concentration à decrease blood concentration Equilibrium takes longer à slows induction (cerebral blood flow is constant) NB: morphine à decreases resp rate à speeds induction Increased conc of anaesthetic à increased induction rate Increased ventilation à increased induction ? Increased blood solubility à decreased induction Increased CO à decreased induction Minimum alveolar concentration Measure of potency Eliminate movement in 50% patients challenged by skin incision Halothane (low MAC) > isofluorane > enfluorane > NO (high MAC) Halothane 3-4% for induction, 0.5-1% for maintainence Can cause hypotension, v/d, myocardial depression, arrhythmias, resp despression, increased CBF & ICP Assoc with halothane hepatitis (jaundice & é aminotransferases). High risk if repeated exposure within 3 months. Incidence 1:10-20,000 Isoflurane 5% for induction, 1-1.5% for maintainence Can cause hypotension, tachycardia, v/d, resp depression, slight increase CBF & ICP, very pungent so not good for induction Sevofluorane 6-7% for induction, 2-3% for maintainence Can cause hypotension, v/d, resp depression, little effect on CNS, popular for induction BUT very rapid changes in depth Desflurane 6-9% for maintainence, very pungent so not for induction Similat effects to sevoflurane o Local anaesthetics: Inhibit sodium ion channels in the neuronal membranes preventing conduction of the action potential (carrying the pain signal) EMLA (mixture of 50:50 lignocaine & prilocaine) Used as a cream for skin sites and has effect in approx 60 mins Ametop (4% amethocaine) Used like EMLA but acts in a shorter time Lignocaine 3mg/kg plain 200mg max, 6mg/kg (with epinephrine) 500mg max Rapid onset, 60-180 min duration Used for topical infiltration, nerve blocks, IVRA, epidural and intrathecally Bupivicaine 2mg/kg (+/- epinephrine), 150mg max in 4hrs Nerve block onset in 40 mins, duration upto 24hrs Epidural onset in 15-20 mins, duration 3-4 hrs Intrathecal in 30s, duration 2-3 hrs Mainly used for nerve blocks, epidural and intrathecal. *** Relatively CARDIOTOXIC *** o Opioids: Opioids = any drug acting on opioids receptors Opiate = any naturally occurring opioid (e.g. morphine) Produce euphoria, analgesia & sleep Stimulation of μ (mu) & κ (kappa) leads to analgesia & depression of ventilation(both), euphoria (μ), sedation (κ), and physical dependence (μ) ALL opioid receptors are inhibitory Inhibit adenylate cyclase & decreased cGMP NORMAL MORPHINE 1. AP ­K+ in ¯Ca2+ in Protein Kinase ¯cAMP 2. Ca2+ in AC ­Gi µ receptor 3. release 4. receptor 5. AP µ receptor ­K+ in, ¯Ca2+ in ¯ excitability ALL OPIOIDS ARE ANTAGONISED BY NALOXONE Side Effects Constipation (40% or oral users, no tolerance) Anti-tussive Dependence Tolerance (Receptors change à decreased effect à require é dose à resp ê) Morphine – strongest but most likely to cause nausea & vomiting Diamorphine – (heroin) causes less N&V than morphine Alifentanil – analgesia for short procedures (e.g. out pat / day case). Will suppress ventilation. Can cause hypertension & myoclonic movements Fentanyl – analgesic used in surgery Remifentanil – Rapidly metabolised & non-cumulative so used as an infusion during long surgery to allow a more rapid recovery than fentanyl Pethidine – prompt short acting analgesia, less potent than morphine. Used in labour. Also used to reduce / stop shaking due to spinal / GA. Codeine – for mild – moderate pain but too constipating for long term use Nalbuphine (nubaine) – synthetic agent. Antagonist at μ & partial agonist at κ. Good but cant be followed by morphine because is antagonist Tramadol – complex analgesia. Weak agonist at μ, inhibits NA uptake & 5HT release. 1/10 strength of morphine = approx equal to pethidine but less resp depression. Not a controlled drug. Naloxone (narcan) – pure antagonist. IV dose in adults 0.1-0.4mg, acts in < 60s, last 35-40mins. Limited effect on complex opioids. For severe OD may require infusion. o Vasoactive drugs Vasoconstrictor sympathomimetics raise BP by acting on alpha receptors to constrict peripheral vessels (e.g. used during spinal) BUT also cause some constriction in the renal vessels à compromises renal perfusion Ephidrine – alpha & beta agonist - (beta receptors à increased HR) Phenylephrine – alpha only. Longer duration of action o Nitrous Oxide (N2O) Colourless, sweet smelling, non irritant gas Good analgesic but poor anaesthetic (MAC 105%, but hypoxia occurs at 70%) Used with other inhaled anaesthetics to reduce the amount required Premixed as entonox (50:50) used by obstetrics and emergency services Systemic effects CVS depression (esp if preexisting CVS disease) é RR & ê tidal volume. Decreases resp response to CO2 & hypoxia Cerebral vasodilatation à é ICP Can cause air emboli, increased vol in gut & rise in pressure in middle ear Can cause bone marrow suppression (inhibits DNA synthesis) – can be from a few hours exposure, should recover within a week During recovery the N2O returns to the alveoli à hypoxia so give O2 • Describe the uses and drawbacks of the following forms of intra-operative monitoring: o o o o o Pulse oximetry Non invasive measurement of O2 saturation using spectrophotometry A probe with 2 LEDs, a photo detector & a microprocessor Gives info on tissue perfusion Performance is affected by hypoperfusion & severe vasoconstriction Sources of error – CO poisoning, nail varnish, methylene blue injection, drugs producing methaemoglobinaemia Accurate to +/- 2% Capnograph Monitors end-tidal CO2 (approx equal to arterial CO2 in healthy people) Works based on absorption of infrared light by CO2 Detects apnoea, hypoventilation, PE, malignant hyperpyrexia, malplacement / kinking / displacement of ET tube Continuous ECG monitoring Give HR & rhythm with beat-by-beat feedback Gives warning of ischaemia & electrolyte disturbances (K & Ca) Uses right shoulder (red), left shoulder (yellow), left lower chest (green) à gives lead II of 12 lead Doesn’t give info on cardiac output Non-invasive blood pressure Cuff width = 40% of arm circumference (if too small à overestimate) Gives systolic, diastolic & MAP Only gives intermittent readings Central venous pressure monitoring Catheter inserted via central vein (int jugular / subclavian) – tip lies at junction of SVC & R. atrium, connected to transducer to give waveform & pressure High CVP = fluid overload Low CVP = dehydration / fluid loss à fluid challenge to bring back up Used if potential for major fluid shift (bowel surgery) or blood loss (orthopaedics) The Recovery Room & Postoperative Problems • Specify the elements of immediate post-operative care (monitoring, airway protection) Patients should be nursed in an area that has facilities to deal with any potential problems. This requires: § Table can tilt head down (if low BP) § O2 supply § Suction § ECG monitoring § Pulse-oximeter § Non-invasive blood pressure monitoring And immediately available should be: § Airway equipment (OP & NP, ETTs & laryngoscopes, bronchoscope, & equipment for a cricothyroidotomy and tracheostomy) § Breathing & ventilation equipment – BVM, mechanical ventilator & chest drain kits § Circulation equipment – defibrillator, drugs for CPR, IV fluids, pressure infusers & devices for IV access § Drugs – for resus & anaesthesia § Monitoring equipment – transducers & monitors capable of displaying arterial & CVP waveforms, end tidal CO2 & thermometer The patient is the responsibility of the anaesthetist until discharged from recovery and must meet the following criteria before discharge: § Fully consciousness (able to maintain own airway although may be sleepy) § Adequate breathing § Stable cardiovascular system (with minimal wound bleeding) § Adequate pain relief § Warm • Select the correct apparatus for post-operative oxygen therapy. Variable performance devices E.g. Hudson mask, nasal cannulae, non rebreather (trauma) mask The concentration of oxygen delivered is dependent on the rate and depth of the patients breathing as the delivery rate is slower than the peak inspiratory volume The inspired gas consists of: The oxygen flowing into the mask The oxygen accumulated in the mask during expiration The alveolar gas from the previous breath collected in the mask Air entrained during peak inspiratory flow from holes in and around the mask NB: the BVM / non rebreather supply the highest concentration of oxygen, but not a fixed concentration Fixed performance devices E.g. venturi masks Give a fixed concentration of oxygen Use the venturi effect (pull a fixed quality of air in with the oxygen) The output of gas is greater than the peak inspiratory rate – so it ensure the patient can breath that concentration by blowing away exhaled gases as well as filling the mask and surrounding area with oxygen at a fixed concentration During anesthetic recovery Initially the patient is bagged using 100% O2 from the anaesthetic machine via the ET tube Then once extubated the patient can be bagged using the same system Once a patient is breathing spontaneously an OP airway / jaw thrust can be used to support the airway with a Hudson mask to provide O2 • Describe in brief the types of respiratory failure and their relevance to oxygen therapy Type I failure = VQ mismatch Hypoxic with normal CO2 (or low Cos if hyperventilating) E.g. asthma, pulmonary oedema, pneumonia, PE, haemorrhage, Pneumothorax Type II failure = hypoventilation Hypoxic and raised CO2 E.g. severe COPD, drug overdose (opiates), chest wall trauma, neuromuscular pathology Hypoxic drive In some type II patients the drive to breath based on high CO2 levels is replaced by that of low oxygen levels. Giving high flow O2 provides sufficient O2 & causes the patient to reduce their RR (or even stop) • Specify the causes of nausea and vomiting and their drug and non-drug treatments Postoperative nausea & vomiting occur in 80% of patients following anaesthesia & surgery. Anatomy & Physiology CTZ is in the area postrema on the floor of the 4th ventricle (outside the BBB) This is affected by gut, anaesthetic drugs, opioids (via 5HT3 & DA2 receptors) Vomiting centre in the reticular formation of the medulla (within BBB) Afferents are: pain, vestibular (H2), cerebellar, cortical, chemoreceptors & baroreceptors (via ACh receptors & from CTZ) The vomiting process Nausea: Pallor, salivation, duodenal contents enter stomach Vomiting: Breath held mid inspiration Abdominal muscles contract Against a closed glottis Lower oesophageal sphincter relaxes Pyloric sphincter contracts Vomit expelled Factors involved are: § Gender – more common in women § Age – more common in the very young (childen & young women) & elderly § Site of surgery – abdominal, middle ear, posterior cranial fossa § The use of opioid analgesics – at any stage § Anaesthetic drugs – etomidate, N2O § Gastric dilation – poor technique whilst bagging the patient § Hypotension – due to hypovolaemia, or spinal / epidural § Patients prone to travel sickness Those who are high risk are given prophylactic antiemetic before the end of the surgery Drugs used include: § Antihistamines (H1) = IM cyclizine – also has anticholinergic effects & can cause tachycardia when given IV. Used for labyrinthine induced § 5HT3 antagonists = IV / PO ondansetron – blocks 5HT3 receptors in the gut’s mucosal vagal afferents. Used as 2nd line § Dopamine antagonists = IV / IM / PO Metoclopromide – minimally effective against PONV. Acts in the CTZ increasing gastric motility. Work for opioid § § § • Phenothiazine derivatives = IM / PO procholorperazine – can cause hypotension due to alpha blockade. Some antihistamine activity. May cause dystonic movements Anticholinergic = atropine, hyoscine – cause dry mouth, blurred vision etc. Work well for vagally induced nausea Steroids = dexamethasone may be useful in resistant cases Describe how drugs can act to reduce nausea and vomiting Emesis = inappropriate gastric emptying Stimulated by bacterial toxins, alcohol (15%), drugs, motion sickness, smells, migraine, pregnancy Motion sickness Menieres Labyrinth VIII Vestibular N H1 + Muscarinic receptors Anticholinergics Antihistamine Block with sedatives Drugs – morphine, L-dope, postanoids BBB window CTZ D2 & 5HT3 receptors Sensory afferents (sight, smell, pain) Nucleus tractus solitarus Vomiting Centre Muscarinic receptors D2 / 5HT3 antag No BBB @ CTZ so peripheral D2 antag will work anticholinergics VOMIT Anti emetics H1 receptor antagonists – e.g. promethazine Act on vestibular nuclei Effective in motion sickness Also has antimuscarinic actions Antimuscarinic Agents – e.g. hyoscine Effective in motion sickness and heartburn Has antimuscarinic SE (blurred vision, urinary retention etc) Dopamine antagonists – e.g. metoclopromide Acts in CTZ Has unwanted CNS side effects Effective against anti cancer induced emesis 5HT antagonists – e.g. ondansetron blocks 5HT at 5HT3 receptors Effective against anti-cancer induced emesis and post operative N&V Nabilone Canabinoid (synthetic cannabis based) Critical Care • Describe the concept of the Early Warning System / ACAT score and the use of this tool to trigger admission of the patient to the augmented care areas (HDU/ITU). MEWS (Modified Early Warning Score) Score 3 2 1 0 HR <40 40-50 51-100 BP ê45% ê30% ê15% Normal RR <8 9-14 Temp <35.0 35-38.4 CNS A Urine Nil <0.5 <1.0 UO = ml/kg/hr, BP = change from patient’s normal Score < 4 Score > 4 • 1 101-110 é15% 15-20 V >1.5 2 111-129 é30% 21-29 >38.5 P 3 >130 é45% >30 U = review in 1 hr = call Dr & review in 30 mins = if stays > 4 call registrar & consider HDU admission (single organ failure) or ICU (multi-organ failure) Describe the reasons for patient’s admission to ITU / HDU, specifically: a) pre-operative monitoring b) post-operative ventilation / stabilisation / monitoring c) critical illness or multi-system failure at any time Levels of patient care required Level 0 – needs can be met with normal ward care Level 1 – at risk of deterioration or recently relocated from higher level care but can be dealt with through outreach Level 2 (HDU) – more detailed monitoring required, single organ failure, some postop patients (major surgery in high risk patients), patients stepping down from ICU Level 3 (ICU) – requiring advanced respiratory support (intubated & ventilated) & patients with multi organ failure ICU has: Complex monitoring (ECG, ABP, CVP, Pulmonary artery pressures, pulse ox, transoesophageal echo) Facilities for organ support (dialysis, ventilators) Nurse : Patient ratio of 1:1 A doctor on the unit 24:7 • Describe situations when it is inappropriate to refer a patient to ITU / HDU. Where ITU will not improve the patient’s standard & duration of life (similar to DNAR) § Advanced terminal cancer (death within weeks) § Sepsis § Pneumonia on admission § Renal failure § Hypotension § Severe disability § Deteriorating consequences (e.g. stroke) § Arrest due to GI haemorrhage NB – patient’s primary pathology is reversible à ITU Analgesia • Specify a definition of pain “An unpleasant sensory & emotional experience associated with actual or potential tissue damage or described in terms of such damage” o o o o Pain is a subjective experience, influences by cultural & social factors Involves situational, attention & cognitive features Single most compelling reason to consult 50-80% of people experience inadequate pain relief Types of pain Organic – linked to tissue damage Psychogenic – no observable physical cause, discomfort from psychological factors, commonl chronic pain Acute - < 6 months, axiety subsides when pain is over Chronic - >6 months, anxiety persists, hopeless & helpless à depression à immune system problems, affects daily activities Chronic recurrent – repeated intense episodes, separated by pain free intervals (e.g. migraine) Chronic progressive – increasing intensity (e.g. cancer) Cancer pain – depends on stage, type, effects, Rx & individual pain threshold Referred pain – due to convergence of pathways Pain without detectable damage – persists after healing, may spread or increase in intensity, may become stronger than initial pain Neuralgia – shooting / stabbing along a nerve, innoculus stimulus, affects cognition, attention etc, Rx = difficult Causalgia – recurrent severe burning pain, from region with earlier injury, affects sleep, concentration etc Phantom limb pain – due to cortical remapping & unmasking Sensory threshold Usually similar in all people Lowered by inflammation Raised by analgesia, lesions & anaesthetics Emotion & psychological factors affect pain AD appears to increase threshold • Outline the ‘specificity’ and ‘gate-control’ theories of pain perception Specificity Theory Pain is a specific entity (as sight / olfaction etc) Pain has its own nervous system Pain, touch, cold, warmth = 4 modalities Oversimplification but 2 pricinples persist Specialised peripheral receptors Eventual destination indicates type of stimulus Pattern theory Specific receptors & fibres for pain do not exist Free nerve endings respond to non-selective stimuli Responses = different patterns of impulses Increase frequency of impulses à pain Summation theory Pathological pain syndromes due to reverberating circuits in the dorsal horn Gate control theory Gates open (by small diameter fibres) – pain messages can reach brain Gates closed (by large diameter fibres) – signals blocked Gating mechanism in the substantia gelatinosa Through pre & post synaptic inhibition SG neurones block activation of 2nd order neurones Descending nerve fibres also influence gating (it is possible to block pain) • Describe the various types of primary afferent fibres, in particular nociceptive afferents. Sensory receptor Sensory Axon Muscle Axon • Proprio Mechano Pain/Temp Aa Ab Ad I II III Myelinated Myelinated Finely Myelinated Pain/Temp C IV Unmyelinated Describe the adverse physiological effects of pain Increased HR & RR (with shallow respiration) à decreased O2 saturation Increased BP Nausea, vomiting, flushing & sweating Increased catecholamines, glucagons, cortisol, aldosterone & corticosteroids à hyperglycaemia à utilisation of far stores poor wound healing à protein breakdown Pain on deep inspiration à suppression of cough à chest infections And psychological effects include slow mobilisation (à increased DVT risk) & poor motivation. • Describe the WHO pain ladder o o o o • Paracetamol + NSAID + weak opiate + strong opiate +/- adjuvant (e.g. TCA, tens etc) at any stage Specify the 4 common groups of drugs used in acute pain o Paracetamol - simple analgesic (1g QDS oral or IV) Analgesic & antipyretic properties Indirectly blocks COX enzyme à analgesic without NSAID effects Metabolised by the liver & then the metabolites are excreted by the kidneys Cyt P450 converts paracetamol to an active metabolite Then conjugated to harmless metabolite & excreted renally Toxicity due to active metabolite (builds up due to saturation of pathway) – more information in the overdose notes o Non-steroidal anti-inflammatory drugs (NSAIDs) Analgesic, antipyretic & antiinflammatory Blocks COX1 & 2 à blocks prostaglandin synthesis Anti-inflammatory à v/d & decreases oedema Analgesic à decreases pain Eicosanoids (PG, TX, LT) Phosholipids à arachiodonic acid à eicosanoid Contribute to inflammatory response Rate limiting step = PLA2 (liberation of AA) Synthesis is driven by different stimuli in cell damage AA metabolised by COX enzymes (Cox 1 & 2) PGI2 & PGE2 are hyperalgesics o o • Antipyretic à affect PG COX1 production in Constituative hypothalamus (resets most tissues blood platelets thermostat) by v/d & tissue homeostasis increasing sweatting COX2 Can be used with opioids = induced in inflammatory cells by IL1 & TFNa reduce amount responsible for producing PG mediators of required = “opioid inflammation sparing” Interactions Should not be used if on warfarin Can decrease effectiveness of ACEi’s Can oppose diuretics à fluid retention Contraindications Previous allergy Peptic ulcers - as PG is protective for the stomach Renal impairment – as can affect renal afferent arterial flow Asthma – reduction of PG production à increased leukotriene production (alternative pathway) à bronchospasm Coagulopathy – haemophilia, warfarin, heparin etc (due to reduced platelet aggregation) Aspirin 300-900mg every 4-6 hours (max 4g daily) Irreversible inactivation of COX1 & COX2 1st order elimination 75% metabolism in liver Rapid absorption T1/2 = 4 hrs Myocardial infarction therapy (75mg od) Side effects due to the COX1 effects Diclofenac (volterol) Max daily dose 150mg (in 2-3 divided doses) Used for MSK pain (esp rheumatoid arthritis) Can be given PO, IM, IV, PR Opioids (see notes on anaesthetic principles) Local anaesthetics (see notes on anaesthetic principles) Describe the mechanism and uses of Patient controlled analgesia (PCA) Can be used IV or epidurally On pressing a button a bolus dose of analgesia is delivered The machine then times out (usually 5 minutes) during which time another dose cannot be delivered The dose & timeout are calculated to ensure the patient cannot overdose even if they are given the maximum number of doses Advantages Pain relief is rapid (don’t have to wait for the nurses) Reduces nursing work load Keeps medication to minimum Can be monitored to indicate current pain level (no of doses & no of tries) Allows the patient to feel in control Disadvantages It is not active when the patient is asleep (should be given a background infusion) Patients may be unwilling to use it if they experience nausea with the opioid Patients may be unable to use it Relatives can potentially interfere with it • Describe the use of Tens as non-phamacological pain relief TENS (Transcutaneous Electrical Nerve Stimulator) Produces electrical signals used to stimulate nerves through unbroken skin Stimulation of the A beta sensory fibres reduces the transmission of the noxious stimulus from the ‘c’ fibres, through the spinal cord and hence on to the higher centres. (Gate control theory) Stimulation of the A delta fibres activates the opioid mechanisms, and provide pain relief by causing the release of an endogenous opiate (encephalin) in the spinal cord which will reduce the activation of the noxious sensory pathways. Vascular Catheterisation • List the indications for, necessary evaluation of a patient's circulatory status prior to (eg Allens test), care and complications of Arterial catheters A cannula (20-22G parallel sided teflon) inserted into an artery Connected to a transducer (at the level of the left ventricle) by a tube with a continuous column of saline Usually radial artery (as the partial occlusion of the artery is compensated for by the ulnar artery) To prevent the cannula blocking the line feeds in a continual slow flow of heparinised saline Advantages over NIBP Accuracy of pressure measurement Beat-by-beat observation of changes (esp when vasoactive drugs used) Accuracy at low pressures Ability to obtain blood samples through the line (inc ABG) Complications Requires skill to insert correctly Bleeding Pain on insertion (done under GA if for post op monitoring) Arterial damage & thrombosis Embolisation of thrombus or air Ischamic damage to tissues distal to puncture site Late development of fistula or aneurysm • List the indications for, care and complications of Central venous catheters A measure of the blood within the venous system A simple manometer measures the pressure on the end of the line (the fluid filled tube transmits the pressure wave Low pressure = hypovolaemia If a fluid challenge has little effect on the CVP the patient is hypovolaemic High pressure = volume overload A marked increase in pressure indicates fluid overload 4 Common routes of catheterisation Long line – into antecubital fossa. Using basilic and cephalic veins but difficult to advance past shoulder and require X-ray to confirm position. Thrombosis is common if left for more than 24hrs Femoral catheters – inserted below inguinal ligament. Large gauge so allow rapid transfusion of fluids. Skin sepsis more likely due to skin crease Internal jugular – most common. But point of insertion is very close to vital structures (Carotid artery, lung, brachial plexus and C-spine). Now placed under US guidance Subclavian – same problems as IJV but easier to anchor to the skin. If arterial puncture occurs direct pressure is almost impossible. Only used if IJV contraindicated Indications Monitoring of the (CVP) in acutely ill patients to quantify fluid balance Parenteral nutrition Drugs that are prone to cause phlebitis (Calcium chloride, Chemotherapy, Potassium chloride, Amiodarone) Need for intravenous therapy (Blood, meds or fluids) when peripheral venous access is impossible Care Regular flushing with heparinised solution keeps the line from embolising Care of entry site reduces infection in the line Complications Acute: Arrhythmias - caused during the insertion process when the wire comes in contact with the endocardium. It typically resolved when the wire is pulled back Bleeding - apply pressure to the wound site Air embolus - rarely a problem, air reaches the pulmonary vessels & diffuses back out. Can cause pulmonary vessel spasm à increase in RV pressure. If patent foramen ovale à arterial circulation à ischaemic damage to tissues Pneumothorax - CXR ordered after insertion to check location & lung fields Damage to stuctures (thoracic duct, oesophagus, carotid artery, stellate ganglion) – insert under US guidance. Never attempt if not trained! Catheter embolisation - avoid by flushing the line with heparin after insertion Delayed: Sepsis usally S.aureus/epidermidis – lines coated in Abx / silver & good wound hygiene should prevent sepsis. If central line & fever with no obvious cause consider IV Abx & removing line Thrombosis – of veins local to insertion. Consider clot busters and arrange anticoagulation if appropriate. Cardiac rupture – Rx supportively unless tamponade. May require surgical repair • List the indications for, care and complications of Swan-Ganz (pulmonary artery floatation catheter) catheters Central venous pressure measures filling of the RA BUT cardiac output depends on LA filling pressures Swan-Ganz have the ability to determine CO and Left atrial pressure Long catheter, several lumen, thermistor near tip & balloon at the tip As the catheter is advanced the pressures in the RA, RV & Pulmonary artery The balloon wedges in the pulmonary artery à occludes the artery à ‘wedge’ pressure in pulmonary artery capillaries (reflects LA pressure) Indications Management of complicated myocardial infarction(Ventricular septal rupture (VSR) vs acute mitral regurgitation, Severe left ventricular failure, Right ventricular infarction, Unstable angina, Refractory ventricular tachycardia) Assessment of respiratory distress (Cardiogenic vs non-cardiogenic pulmonary oedema, Primary vs secondary pulmonary hypertension ) Assessment of type of shock (Hypovolemia vs cardiogenic) Assessment of therapy (Afterload reduction, Vasopressors, Beta blockers, Intraaortic balloon counterpulsation ) Assessment of fluid requirement in critically ill patients (Hemorrhage, Sepsis, Acute renal failure, Burns) Management of postoperative open heart surgical patients Assessment of valvular heart disease Assessment of cardiac tamponade/constriction Complications Arrhythmias with catheter manipulation Damage to tricuspid & pulmonary valves Knotting of catheter Pulmonary infarct if balloon left inflated Pulmonary artery rupture with balloon inflated Cardiac rupture Fluids And Electrolytes Assumptions The student understands the importance of the 'aqueous environment' in body composition, the distribution of fluids and electrolytes in the body compartments, and the role of the kidney in regulating fluid and electrolyte balance. • List the physiological limits of normal blood gases. pH: PaCO2: PaO2: HCO3- : Base excess: 7.35-7.45 4.7 – 6.0 kPa >10.6 kPa 22-30 +/- 2 mmol/l Respiratory acidosis (e.g. hypoventilation / COPD) Rise in CO2 è rise in H+ = acidosis Compensation is metabolic (by HCO3-) As normally filtered bicarb is all reabsorbed kidney must excrete more H+ Metabolic acidosis (e.g. DKA / Exercise) Decrease in HCO3- è less buffering è acidosis Compensation is respiratory by hyperventilation & by H+ secretion from kidney Hyperventilation cannot be maintained long term è Rx required Mixed acidosis e.g. heart stops, no O2 in, no CO2 out Respiratory alkalosis (e.g. hyperventilation) Decrease in CO2 è decrease in H+ = alkalosis Compensation is metabolic Increase excretion of HCO3- (requires loss of Na+ & therefore H2O) Metabolic alkalosis (e.g. vomiting) Increase in HCO3- (relative to H+ lost in vomit) = alkalosis Compensation is respiratory by hypoventilation Mixed alkalosis e.g. vomiting and hyperventiation PCO2 (mmHg) Resp Acidosis PH 7.4 Increase = acidosis Decrease = alkalosis Compensation 40 Metabolic Acidosis Mixed Cause Mixed Cause HCO3- changes are metabolic Metabolic Alkalosis Increase = alkalosis Decrease = acidosis Compensation Takes the point back towards the line Compensation Resp Alkalosis 24 CO2 changes are respiratory [HCO3-] mmol / l In general acidotic shifts are more life threatening than alkalotic ones • List the electrolyte values in serum Na+ K+ Ca2+ Creatinine Urea Albumin Proteins 135 –145 mmol / L 3.5 – 5.0 mmol / L 2.12 – 2.65 mmol / L 70 – 150 μmol / L 2.5 – 6.7 mmol / L 35 – 50 g / L 60 – 80 g / L Daily ion requirements Na+ K+ Ca++ ClH20 • • Per kg mass (mmol) 1-1.5 1 0.1 1 35ml Total (average male) 70-100 70 7 70 2500ml Given a patient's weight, calculate the extracellular, intra-cellular and intravascular volume. Total body water = 50% b.wt male = approx 40l = 60% b.wt female Intracellular fluid Extracellular fluid Intravascular fluid = 2/3 of total body water = 2/9 of total body water = 1/9 of total body water Calculate sensible and insensible fluid and electrolyte losses in routine post-operative care & in a febrile patient Normal fluid balance Output (ml) Urine Faeces Lungs* Skin* Total 1500 100 400 600 2600 Intake (ml) Drink Food Metabolic 1500 750 350 Total 2600 Losses that must be considered are: Any deficit accrued (pre-op fasting, vomiting, haemorrhage, pyrexia) (standard maintainence = 1.5 ml/kg/hr) Maintenance during the procedure (only if recovery delayed / procedure is long) Losses due to surgery Evaporation – due to body cavity / large area exposure Trauma – tissue oedema is similar to extracellular fluid (3rd space loss) Blood loss – depends on type of surgery – most patients can compensate for 20% loss but Hb should be maintained above 8g/dl and INR below 1.7 (also check platelets and fibrinogen) Any vasodilatation due to anaesthetic process (esp regional anaesthesia) Increased temperature – increase maintenance by 10% for each oC above normal • Write post-operative fluid orders for an unstressed, uncomplicated 70kg patient who has had a gastric procedure. Basic fluids: 3l / day with approx 100 mmol of Na & 70mmol of K Regime 1 1l 1l 1l 5% dextrose 5% dextrose Saline Regime 2 3 x 1l Dextrose/Saline • + 20mmol KCl + 20mmol KCl + 20mmol KCl 8o + 20mmol KCl (each bag) List the symptoms and physical findings of dehydration. Clinical signs Dry mouth and lips Thirst Loss of appetite Oliguria Tachycardia Hypotension Tachycardia Low urine output • 8o 8o 8o Severity % Body wt loss Litres deficit Mild 4% 3 Moderate 5-8% 4-6 Severe 8-10% 7 List the electrolyte composition of the following solutions: Na+ K+ Ca++ Normal Saline (0.9%) 154 0 0 Ringers Lactate = Hartmanns 131 5 4 5% dextrose 0 0 0 Dextrose(4%) saline(0.18%) 31 0 0 Albumin 130-160 0 0 * - the lactate is converted by the liver to the bicarb • Cl154 112 0 31 154 HCO30 29 * 0 0 0 pH 5.5 6.5 4.1 4.5 6.7-7.3 Osmolality 300 281 278 284 270-300 Describe the common fluid and electrolyte and acid base abnormalities in patients with the following problems: o excessive gastric losses Normal gastric secretions = 1.5l / day Gastric aspirate contains H+,K+, Cl- (hypochloraemic and hypokalaemic) Replace with Nacl 0.9% with KCl Metabolic alkalosis o high volume pancreatic fistula Normal pancreatic secretions = 500 ml / day Pancreatic fluid is very high in HCO3- o ileal fistula Normal ileal secretions is 3l / day Ileal fluid is high in Na & Cl o bile fistula Normal bile flow is 800 ml / day Mostly isotonic Shock • Define shock. A condition of profound haemodynamic and metabolic disturbance characterised by failure of the circulatory system to maintain adequate perfusion of vital organs, it may result from inadequate blood volume (hypovolaemic shock), inadequate cardiac function (cardiogenic shock) or inadequate vasomotor tone (neurogenic shock, septic shock) • List the types & causes of each type of shock. Hypovolaemic Bleeding, burns, heat exhaustion, D&V, sequestration, sepsis (--> peritonitis --> 3rd space losses), excess urine loss Low perfusion = cold, pale, oliguria & drowsy Increased sympathetic tone = increased HR & sweaty Metabolic acidosis common Cardiogenic MI, arrhythmias, valve prolapse, aortic dissection, myocarditis Poor coronary flow Signs of cardiac failure (increased JVP, gallop rhythm) Obstructive shock Large PE, tension Pneumothorax, Tamponade Increased JVP, pulsus paradoxus, signs of PE / Pneumothorax Distributive shock Sepsis, anaphylaxis, A-V shunt, mass vasodilataion, sequestration Signs of sepsis / anaphylaxis etc • List the physical findings that characterise each kind of shock. Hypovolaemic shock Anxiety, restlessness, altered mental state due to decreased cerebral perfusion and subsequent hypoxia. Hypotension due to decrease in circulatory volume. A rapid, weak, thready pulse due to decreased blood flow combined with tachycardia. Cool, clammy skin due to vasoconstriction and stimulation of vasoconstriction. Rapid and shallow respirations due to sympathetic nervous system stimulation and acidosis. Hypothermia due to decreased perfusion and evaporation of sweat. Thirst and dry mouth, due to fluid depletion. Fatigue due to inadequate oxygenation. Cold and mottled skin (cutis marmorata), especially extremities, due to insufficient perfusion of the skin. Cardiogenic shock, similar to hypovolaemic shock but in addition: Distended jugular veins due to increased jugular venous pressure. Absent pulse due to tachyarrhythmia. Obstructive shock, similar to hypovolaemic shock but in addition: Distended jugular veins due to increased jugular venous pressure. Pulsus paradoxus in case of tamponade Septic shock, similar to hypovolaemic shock except in the first stages: Pyrexia and fever, or hyperthermia, due to overwhelming bacterial infection. Vasodilation and increased cardiac output due to sepsis. Neurogenic shock, similar to hypovolaemic shock except in the skin's characteristics. In neurogenic shock, the skin is warm and dry. Anaphylactic shock Skin eruptions and large welts. Localised oedema, especially around the face. Weak and rapid pulse. Breathlessness and cough due to narrowing of airways and swelling of the throat. • For each type of shock outline the general principles of fluid, pharmacological and surgical management as appropriate. Monitor pulse, RR, BP, temp & LOC Support the patient whilst assessing for & treating the cause Hypovolaemic Maintain / increase intravascular volume Decrease any future loss Give O2 Cardiogenic O2 therapy Administer cardiac drugs (increase pumping ability through meds) Septic Restore intravascular volume via IV fluids Give O2 Identify & treat any source of infection Remove risk factors for infection Anaphylactic Identify and remove causative organism Give Adrenalin (0.5 ml of 1 in 1000 IM) O2 therapy & IV fluids • Understand the classes of hypovolaemic shock and their features Patients requiring urgent resuscitation Blood loss Pulse BP Pulse Pressure Resp Rate UO Mental State Fluid to give Class I <750ml <15% <100 bpm Normal Normal / up 14-20 >30ml/hr Slightly anxious Crystalloid Few symptoms Class II 750-1500ml 15-30% > 100bpm Normal Down 20-30 20-30ml/hr Marked anxious Crystalloid Thirst & some weakness NB: Based on 70kg man with blood volume for 5l Class III Class IV 1500-2000ml >2000ml 30-40% >40% >120bpm >140bpm Dropped Dropped Down Down 30-40 > 35 5-15ml/hr Negligible Confused Lethargic Crystalloid + Blood Class IV: BP may be unrecordable!