Anesthesia Emergencies – Flashcards

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Amount of time required to reduce the plasma drug concentration to one-half of the dose.
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Half Life
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what the body does to a drug, refers to the movement of drug into, through, and out of the body—the time course of its absorption, bioavailability, distribution, metabolism, and excretion.
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Pharmacokinetics
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what a drug does to the body, involves receptor binding (including receptor sensitivity), postreceptor effects, and chemical interactions. P
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Pharmacodynamics
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After a drug enters the systemic circulation, it is distributed to the body's tissues. Distribution is generally uneven because of differences in blood perfusion, tissue binding (eg, because of lipid content), regional pH, and permeability of cell membranes.
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Redistribution
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The kidneys, which excrete water-soluble substances, are the principal organs of excretion. The biliary system contributes to excretion to the degree that drug is not reabsorbed from the GI tract.
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Elimination
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Anxiolysis Akinesis Autonomic Control Amnesia Analgesia
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5 A's of Anesthesia
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TO EASE ANXIETY
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Anxiolysis
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TO RELAX THE MOVEMENTS OF THE MUSCLE
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AKINESIS
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CONTROL OVER BLOOD PRESSURE
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AUTONOMIC CONTROL
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TO FORGET (DRUGS)
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AMNESIA
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MEDICATIONS THAT RELAX
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ANALGESIA
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Agents you inhale. Utilized in their vapor state
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Inhalation Agents HOW ARE THEY UTILIZED
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Four elements of anesthesia produced by reversible inhibition of synaptic transmission
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Inhalation Agents MECHANISM OF ACTION
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Cause dose dependent depression of CNS, CV and respiratory system TV DROPS SO MUCH WHERE YOUR MV DROPS RRXTV = MINUTE VENTILATION
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INHALATION SIDE EFFECTS
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Agent to alveoli, absorbed into blood, and delivered to brain Reversing concentration gradient and allowing elimination of agent
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ANESTHESIA EFFECTS FOR INHALATION AGENTS
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ANE
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WHAT DO RAPID ACTING INHALATION AGENTS END IN
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Rapid acting Halothane (Fluothane) Enflurane (Ethrane) Isoflurane (Forane) - THEY USE THIS - MOST SOLUABLE - GOES ON THE SLOWEST AND COMES OFF THE SLOWEST. Desflurane (Suprane) - USE THIS LEAST SOULABLE - GOES THE QUICKEST AND COMES OFF THE QUICKEST Sevoflurane (Ultane) - USE THIS - INTERMEDIATE SOLUBILITY
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NAME SOME RAPID ACTING INHALATION AGENTS
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Reverse with Tincture of Time! / VENTILATION
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HOW CAN YOU REVERSE THE EFFECTS OF AN INHALATION AGENT
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NITROUS OXIDE- DELIVERED UP TO 70% CONCENTRATION
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WHAT IS A NON VOLATILE INHALANT AGENT
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Small, moves quickly, speeds wake-ups, can replace oxygen in the lungs! No side effects unless hypoxia present Need O2 by mask in PACU Nitrous oxide moves to alveoli and decreases stimulus to breathe until gone Encourage deep sigh to help remove ANXIOLYTIC AND ANALGESIC EFFECTS (EQUIVALENT TO 10MG OF MORPHINE) WHEN OFF ANAGESIC EFFECT GOES AWAY
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HOW DOES NITROUS OXIDE WORK
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Preoperative sedation Intraoperative sedation
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IV AnestheticsClinical Uses
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Primary Use-induction of Anesthesia
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IV Anesthetics Primary Use
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Rapid onset but long duration Produces CV and respiratory depression (dose dependent) No analgesia or muscle relaxation No antagonist - CANT REVERSE THEM Airway management and monitor CV status
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Barbiturates
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Used as sedatives pre and intra op Strong amnesic properties (Versed) Dose dependent CNS, CV & respiratory depression and analgesic effects No analgesia or muscle relaxation (no direct muscle relaxation but you have indirect muscle relaxation) Flumazenil (Romazicon) is reversal for benzodiazepines
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Benzodiazepines AND WHAT IS THE REVERSAL
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VALIUM VERSED
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NAME TWO Benzodiazepines
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Benzodiazepines Immediate onset Duration 20 min to 1 hr Elimination 20-40 hr "LAST TO LONG THIS TIME IS GENEROUS TAKES ALMOST TWO DAYS." AND IT HURTS WHEN INJECTED BECAUSE ITS IMMERSED IN ANTIFREEZE.
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Valium (IV)
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Benzodiazepines 3 times as potent Rapid onset Shorter duration Elimination 2-4 hr WATER SOLUBLE AND DOESNT HURT WHEN INJECTED.
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Versed
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Induction agent - USED FOR SEDATION ALL THE TIME BUT PRIMARY USE IS ANESTHESIA Rapid onset, short duration, quick elimination Synergistic with Versed CNS depression with LOC Drop in SVR - if too much is given No muscle relaxation or analgesia - again you have indirect muscle relaxation
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Propofol (Diprivan)
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Dissociative agent- eyes may be open! Rapid onset, moderate duration & quick elimination Intense analgesia with unconsciousness "People try to tell you its not." Excellent for peds, poor risk pts and burns that require surgical treatment Excellent for patients on long term opioids, covers different pain receptors- Burn Pts
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Ketamine
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ONLY INDUCTION AGENT WITH AN ANALGESIC EFFECT Causes a chemical thalmectomy - Used to reverse drug tolerance, can reset pain tolerance receptors. 1.5-5KG.
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Ketamine
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BURN PATIENT AND PAIN RECEPTORS due to blocking mmda receptors.
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WHO USES KETAMINE IN THE ARMY
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Emergence hallucinations "NIGHT TERRORS" More common in adults Keep stimuli to a minimum-not so much Give with benzos to alleviate problems Contraindicated in those at risk for INCREASED ICP - DUE TO KETAMINE RELEASE OF CATECHOLMINES WHICH WILL INCREASE ICP UNLESS HEAD IS OPEN. Increases cerebral blood flow leading to increased ICP
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KETAMINE KNOCKS
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Rapid onset of unconsciousness CV stability - GOOD HEMODYNAMIC STABILITY CAUSES LEAST DROP IN BLOOD PRESSURE Used on patients with poor cardiac reserve No analgesia Involuntary muscle movement common Give with fentanyl, versed, etc to control sympathetic response in a healthy pt. WHEN GIVEN WITH STEROID SO THAT CORTISAL ADRENOCORTIOD IS NOT SUPPRESSED.
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Etomidate / Amidate "EVOMIDATE"
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Effects last into PACU phase Bind to opioid receptors Morphine is the standard post-op Cardiac contractility unaffected Used for analgesia Autonomic stability and amnesia at high doses NO PAIN BUT STILL AWARE. NARCAN IS REVERSAL FOR OPIODS WHICH BLOCKS RECEPTION AT MU RECEPTOR. DO NOT GIVE WHOLE DOSE BECAUSE YOU WILL BLOCK PAIN RECEPTOR GIVE 1 CC AT A TIME WHEN 0.4MG IS MIXED IN 10CC OF NS.
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Opioids
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High doses may cause thoracic rigidity, "Mahogany Chest" - TEMPORARY MAY LEAD TO tx w/ succinylcholine! - BECAUSE MAHOGANY CHEST IS SKELETAL MUSCLE ALSO WORKS WITH LARYNGOSPASM. WILL NOT WORK WITH BRONCHOSPASM DUE TO IT BEING SMOOTH MUSCLE. GIVE ANESTIC WITH MUSCLE RELAXANT. Respiratory depression Dose dependent, rapid (minutes) Medullary ventilatory centers affected Ventilatory response to rising CO2 diminished Be aware of OD Treatment is mech vent and slow titration of Narcan (half life is short, beware!) No muscle relaxation 1+1 = 3 DUE TO SYNERGISTIC EFFECT WITH INHALANT AGENTS.
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Opioids SIDE EFFECTS
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Skeletal muscle paralysis Uses Onsets and durations vary No amnesia or analgesia
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Neuromuscular Blocking Agents
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Depolarizing - Succinylcholine Onset 1-2 min- used for intubation Duration @8 min- don't have to reverse Nondepolarizing Onset 2-3 min Duration ranges from 20 min to 2 hr depending on med and dosage - reverse, provider dependent.-used for paralysis during the case
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Neuromuscular Blocking Agents WHAT ARE TWO TYPES
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Remember-Half life of reversal agent may be shorter than the drug trying to reverse Narcan- opioids Flumazenil (Romazicon)- benzodiazepines Anticholinesterases (Neostigmine, physostigmine)-Non-Depolarizing neuromuscular blocking agents (atracurium, cisatracurium)
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Reversal Agents
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Vasopressors Short term response-ephedrine Continuous infusion-dopa, neo, vaso, epi. Anticholinergics -atropine and glycopyrolate - THEY DRY YOU UP AND INC HR For bradycardia secretion control Antihypertensives NTG, Nitroprusside - DONT LAST LONG Beta blockers One time dose or continuous infusion
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Adjuncts
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"ARM OR LEG" Local anesthetic (LA) injected close to a nerve to interrupt membrane depolarization and impulse conduction Sedation for comfort Duration of anesthesia depends on LA used DONT HAVE TO ANESTHETIZE THE ENTIRE BODY AGAIN GIVE WITH SEDATION( PROPAFOL, MEDAZAPAM) TYPICALLY GIVEN FOR SHOULDER BLOCK
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Regional Anesthesia "REGIONAL AREA"
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"EPIDURAL OR SPINAL SPACE" GIVE A ANESTHISIA IN EPIDURAL OR SPINAL SPACE. CANNOT RESPOND BELOW BLOCK AND WILL GET HYPOTENSIVE BELOW BLOCK IF HIT TO HIGH T1-T4 -->HYPOTENSION Primary objective is blockade of pain impulses from region of surgery Epidural or subarachnoid techniques Autonomic and motor function may be blocked, esp with spinal Generally procedures below the thorax High blocks cause severe hypotension and resp depression- IF IS SPINAL SPACE FROM EPIDURAL -. GOES TO BRAIN-->CAN LEAD TO COMOTOSE.
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Central Neuraxis Blockade
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LA to subarachnoid space LA disperses in CSF based on specific gravity compared to CSF Isobaric- same specific gravity as CSF Hyperbaric- higher Spec. grav (heavier, so it sinks from the point of entry) Hypobaric- lower Spec grav (lighter, so it rises from the point of entry)
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Subarachnoid Block
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same specific gravity as CSF
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Isobaric-
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higher Spec. grav THAN CSF (heavier, so it sinks from the point of entry)
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Hyperbaric
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lower Spec grav THAN CSF (lighter, so it rises from the point of entry)
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Hypobaric
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LA in CSF depends on drug selection, dose, and position
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Subarachnoid Block Level of blockade is affected by spread of
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unintentional migration of anesthetic. ex- saddle block for rectal surgery requires having the pt. in the sitting position for 10 minutes, using hyperbaric anesthesia
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WHEN USING A SUBARACHNOID BLOCK Proper position to prevent
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LA to epidural space Larger volumes of more dilute LA Level of block unaffected by gravity but by amount of LA injected Catheters for repeated dosing/postop infusion of narcotics for pain management- can be positional
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Epidural
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Brachial Plexus Block FOR SHOULDER OR ANYTHING GOING DOWN TO ARM LA into sheath surrounding brachial plexus LOCAL ANESTHIA TOXICITY POSIBBLE IF NOT PLACE AROUND THE NERVE.
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Peripheral Nerve Block IS LOCATED WHERE
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Axillary Interscalene Infraclavicular Supraclavicular
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Peripheral Nerve Block TECHNIQUES ARE
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Nerve stimulator, excellent anatomy knowledge
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Peripheral Nerve Block IS WHAT KIND OF STIMULATOR
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HAND SURGERY - DEVASCULAR ARM Large amount LA into veins of an extremity distal to an occlusive tourniquet Useful for emergency procedures on forearm and hand Tourniquet time limits procedures Sensation returns in a short time with no residual analgesia(?).
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Bier Block
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ALWAYS MAKE SURE BLOCK IN BEFORE YOU TAKE OFF TORNIQUET = LA TOXICITY
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Bier Block AND TORNIQUETS YOU SHOULD
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IN THE OR
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WHEN DOES POST ANESTH. CARE BEGIN
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Depends on Time last agents given Reversal agents given, if any How much given The patient
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WHAT ANESTHETIC FACTOR AFFECT RECOVERY
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when patient SHOWS signs of emergence from anesthesia
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WHEN SHOULD YOU TRANSFER A PATIENT TO THE PACU
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Spontaneous ventilation Protective airway reflexes Consciousness
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WHAT ARE SOME signs of emergence from anesthesia
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ABC'S
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WHAT ARE YOUR PRIORITIES IN THE PACU
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TPR, Sat, BP Level of blockade Quick assessment of dressings and drains for gross bleeding
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WHAT WILL YOU DO ON YOUR INTIAL ASSESSMENT
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Name of pt and surgery performed Pertinent medical hx Pre-op vital signs Agents used, reversals and response Complications or unexpected events I/O- IVF, EBL, UOP Special considerations
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WHAT SHOULD YOU RECIEVE IN REPORT FROM ANESTHETIST
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Vital signs PARS score - IS PATIENT CONCIOUS BP W/IN NORMAL LIMITS Any problems or concerns
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WHAT SHOULD THE NURSE REPORT TO THE ANESTHETIST
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Do the ABCs and contact anesthesia Usually have standing orders - eg. a standing O2 order,
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IF YOU EXPERIENCE PROBLEM WITH SEDATED OR INTUBATED PATIENT YOU SHOULD
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Tongue most common cause e.g. Snoring which you can fix with a chin lift or a nasal airway
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WHAT IS A MAJOR CAUSE OF AIRWAY OBSTRUCTION
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Prevent by keeping artificial airways in until protective reflexes return Tongue most common cause Simple maneuvers Secretions - Suction immediately available - for secretions
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HOW DOES THE NURSE PREVENT AIRWAY OBSTRUCTION IN ANESTHESIA
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Due to vocal cord spasm and stimulation, EXTUBATION OR INTUBATION TO EARLY. Early emergence from GETA Positive pressure O2 Small dose succinylcholine, reintubation or trach
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HOW CAN A LARYNGOSPASM OCCUR
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HYPOXEMIA
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WHAT IS A RESPIRATORY COMPLICATION POST ANESTHESIA.
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Common after GETA or sedation Causes Atelectasis Hypoventilation Shivering Aspiration PE/edema Closely assess adequacy of ventilation Administer supplemental O2
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WHAT CAUSES HYPOXEMIA WITH ANESTHESIA AND WHAT CAN YOU DO TO FIX IT
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HYPOTENSION
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WHAT IS THE MOST COMMON CV COMPLICATION WITH ANESTHESIA
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Treatment directed at cause Compare pre-op to post-op for significance
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HOW TO TREAT HYPOTENSION R/T ANESTHESIA
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Treatment directed at cause Transient hypertension may occur Pain is most common cause WITH AGITATED PT Fluid overload, hypoxemia and pre-existing HTN also related to post-op HTN E.G. KIDNEY SURGERY
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Hypertension R/T ANESTHESIA
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Tachycardia Arterial hypoxemia, hypovolemia, pain Bradycardia Hypoxemia, hypothermia, anticholinesterase PVCs Hypoxemia, myocardial ischemia, electrolyte imbalances, respiratory acidosis HTN often increases cardiac irritability ONLY TREAT IF IT IS SYMPTOMATIC -IF VITALS ARE OK
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Cardiac Dysrhythmias WHAT TO LOOK FOR
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A KIT TO REINTUBATE PATIENT.
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what do you need in the PACU AT ALL TIMES WHEN RECIEVING PATIENT
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May delay discharge from PACU Complications associated with Wound disruption/dehiscence Aspiration Electrolyte disturbances Increased pain Give antiemetics carefully May potentiate narcotics
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Nausea and Vomiting CAN CAUSE WHAT COMPLICATIONS IN PACU HOW DO WE FIX IT
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THE NURSE. Increased risk when emerging from GETA or regaining sensation, motor control and proprioception Emergence delirium More common in healthy patients and among children
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WHEN THE PATIENT FIRST GETS UP IN PACU WHO SHOULD BE THERE
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Contributing Factors Vasodilation Cold OR environment Decreased basal metabolic activity Restore baseline temp ASAP Warm blankets Heating lamps Warm IV fluids Active warming blankets (BAIR hugger
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Hypothermia
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KEEP IN PACU FOR 24 CAUSE IT CAN REOCCUR
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PATIENT HAS MALIGNANT HYPERTHERMIA WHAT DO YOU DO
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Hypermetabolic syndrome May be triggered by depolarizing neuromuscular blockers, halogenated inhalation agents and post-op pain Rare, inherited, more prone in those with muscular abnormalities
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MALIGNANT HYPERTHERMIA WHAT KIND OF SYNDROME HOW IS IT TRIGGERED WHO IS MORE PRONE TO GET IT
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Rapid increase in temperature since induction of anesthesia Unexplained tachycardia Muscle rigidity Unstable BP Very hot skin Masseter muscle rigidity after admin of succinylcholine is earliest warning
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Malignant Hyperthermia Clinical manifestations
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Dantrolene 100% O2 Correction of acid base imbalances Cooling measures Icing down patient, cold fluids
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Malignant HyperthermiaTreatment
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After acute phase In ICU at least 24 hrs Dantrolene 1 mg/kg q6 for 24-48 hr Oral dantrolene may then be used Monitor ABGs, CK, K, Ca, serum myoglobin, clotting studies q6 Complications Renal failure due to myoglobinuria or hypotension DIC, acute HF and pulmonary edema
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Malignant Hyperthermia AFTER ACUTE PHASE
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After GETA PARS 9-10 Arousable, oriented, protective reflexes intact Stable VS Reasonably comfortable No narcotics 30 min before Able to summon help if needed Adequate ventilation and oxygenation
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PACU Discharge CRITERIA
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Awake from sedation, stable VS Upper extremity blocks don't need complete resolution Lower extremity blocks such as those from SAB, MUST be resolved.
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PACU Discharge After regional
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YES.
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CAN YOU REGURGITATE WITHOUT ASPIRATION
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