Advanced Skill Theory - Final Exam Review PDF

Advanced Skill Theory – Final Exam Review EtCO2 Respirations: The process by which oxygen and carbon dioxide diffuse in and out of the blood. Also referred to as gas exchange that occurs in two areas of the body – external and internal. External Respiration: refers to gas ex...

Advanced Skill Theory – Final Exam Review EtCO2 Respirations: The process by which oxygen and carbon dioxide diffuse in and out of the blood. Also referred to as gas exchange that occurs in two areas of the body – external and internal. External Respiration: refers to gas exchange across the respiratory membrane in the lungs. Internal Respiration: refers to gas exchange across the respiratory membrane in the metabolizing tissues (ie. Skeletal muscles). Ventilation: Pulmonary Ventilation: the process by which oxygen enters, and carbon dioxide exits the alveoli. Ventilation is the act or process of inhaling and exhaling – the movement of air. Oxygenation: Refers to the process of adding oxygen to the body system – how we get O2 to the tissues. SPO2: Saturation of peripheral capillary oxygenation. Pulse oximetry measures oxygen saturation levels. Noninvasive measurement – finger probe % of oxygen bound to red blood cells Issue: changes in ventilation can take minutes to be detected/artifact secondary to motion/circulatory status/nail polish. EtCO2: Measures ventilation status. Is the CO2 in the airway at the end of exhalation. Noninvasive measurement – “snapshot” of patients’ ventilatory status. Provides reading for every breath – so results are within seconds. Not affected by motion/circulatory status. 100% sensitive/100% specific. Ventilation + Circulation + Metabolism = Gas Exchange Dead Air Space: Ventilated areas that do not participate in gas exchange.  Total physiological dead air space = Anatomic Dead Space (airways leading to the alveoli) + Alveolar Dead Space (ventilated areas in the lungs without blood flow) + Mechanical Dead Space (artificial airways – including ventilator circuits) Capnography: Represents the amount of CO2 in exhaled air. Partial pressure of CO2 at the end of exhalation. Normal: 35-45mmHg Nasal prongs or attachment on BVM Respiratory Effort: Healthy lungs – brain responds to changes in CO2 levels in the blood, controlling ventilation, this is assessed by chest rise and fall, respiratory effort, breath sounds, and counting respiratory rate. As CO2 rises, respiratory rate should increase because the body wants to blow off some CO2. As CO2 falls, respiratory rate should decrease in order to retain CO2. Generally: ETCO2 less than 35mmHg (hyperventilation/hypocapnia) – you should hypoventilate the patient to increase their CO2 levels. ETCO2 greater than 45mmHg (hypoventilation/hypercapnia) – you should hyperventilate the patient to increase their CO2 levels. Why Use Capnography? To assess when patient is ventilated (SGA/ETT) – two primary and one secondary Primary Secondary Visualization ETCO2 Auscultation EDD Chest rise Other How is ETCO2 Measured? Quantitative – an actual numeric value usually associated with an electronic device (35- 45mmHg) Semi-Quantitative (Qualitative) – devices that give a range vs an actual number (low, medium, high) Wave Form Capnography Blood Gasses:  PaCO2 – partial pressure of carbon dioxide in arterial blood gasses. The PaCO2 is measured by drawing the ABGs, which also measures the arterial PH. If ventilation and perfusion are stable, PaCO2 should correlate with PetCO2. The Waveform: Capnogram waveform begins before exhalation and ends with inspiration. Phase 1 (A-B) – inspiratory baseline (low CO2 as it is inspired air) B – the start of alveolar exhalation Phase 2 (B-C) – exhalation upstroke (dead space gas mixes with lung gas) Phase 3 (C-D) – continuation of exhalation (gas is all alveolar now, rich in CO2) D – end tidal value, peak concentration Phase 4 (0) (D-E) – start of inspiration Abnormal Values and Wave Forms: Sudden Loss of Waveform: Tube disconnected, dislodged, kinked, or obstructed Loss of circulatory function Decreasing ETCO2: Tube cuff leak Tube in hypopharynx Partial obstruction CPR Assessment: Attempt to maintain a minimum value of 10mmHg Sudden Increase in ETCO2: Return of spontaneous circulation (ROSC) Bronchospasm (Shark Fin Appearance): Asthma COPD Why the slope – because movement of air at the alveoli is delayed, the rise to the plateau is more gradual and the plateau itself becomes sloped. Hypoventilation: Long/wide, stretched out Hyperventilation: Short and quick Decreased ETCO2: Apnea Sedation Hyperventilation - Low CO2 Levels: When a person hyperventilates, their CO2 levels go down. They are blowing off large amounts because of the increased rate of breathing. Can be caused by many factors - anxiety, bronchospasm, pulmonary embolus. Other reasons ETCO2 may be low – cardiac arrest, hypotension, decreased cardiac output, cold. Hypoventilation – High CO2 Levels: When a person hypoventilates, their CO2 levels go up. They are retaining CO2 due to the slow rate of breathing. Can be caused by – overdose, sedation, intoxication, postictal states, head trauma, stroke, tiring CHF. Other reasons ETCO2 may be high – fever, sepsis. ETCO2 and Cardiac Output: When cardiac output (blood flow) is normal – ETCO2 measures ventilation. When cardiac output (blood flow) is decreased – ETCO2 measures cardiac output. ETCO2 in Cardiac Arrest: Cardiac arrest is the ultimate shock state – there is no circulation, no metabolism, and no CO2 production unless effective CPR is being done. Capnography provides feedback on the quality of CPR. ETCO2 of 18 The longer the shaft, the slower the flow (friction loss) 16 Gauge – adolescents & adults only, critical trauma/burns, patients requiring large amounts of fluids 18 Gauge – adolescents & adults only, fluid resuscitation, colloid infusion 20 Gauge – children, adults, & adolescents, most infusions requiring medication, TKVO lines, smallest size for colloid infusion 22 Gauge – infants, toddlers, children, adolescents & adults (especially elderly patients), TKVO infusions, minor medication needs Flow Rate Complications: Venous pressure – position of patients’ extremity (arm bent) Vein spasm – irritating, or chilled fluids = reflex to occur Phlebitis & Thrombi – initial decrease in flow rate due to spasm = inflammation to vein or clot formation Viscosity – thickness of fluid (high concentrations of dextrose tend to flow at a slower rate) Amount of fluid in the bag – approx. 150cc if flow is affected Needle or gauge size – the smaller the needle, the slower the flow Height of fluid container – approx. 3’ above the site Needle/cannula position – cannula may be making contact at the valve/vein wall Tubing occlusions – kinking/pinched in the stretcher Infiltration – cannula actually slips out of vein = edema at interstitial site Local Complications: Infiltration – dislodgement of catheter or needle cannula, puncture of distal vein wall, leakage of solution/medication into surrounding tissue, poorly secured IV, poor vein site selection, irritating solution, improper cannula size, high delivery rate/pressure of solution/medication. Causes coolness of skin around IV site, swelling, sluggish or absent flow rate, infusion continues to infuse when pressure is applied to the vein, and no backflow of blood into IV tubing when clamp is fully opened. Hematoma – when amounts of blood collect outside of the vessel after catheter passes through the vein. Causes redness, tenderness, pain, and swelling.  Phlebitis – inflammation of the vein caused by injury to the vessel wall. Causes pain, swelling, redness, and tenderness. Local Infection – infection only present at or around the IV site, present after the IV initiation. Signs and symptoms occur usually 3-4 days after IV; redness, foul discharge or odor at site. Systemic Complications: Contamination and infection Hypersensitivity reactions Sepsis Emboli (blood clot, air, and catheter) Air Embolism – caused by air entering the bloodstream via the catheter tubing, risk is greatest when catheter is passed into central circulation (ie. Jugular vein). Signs and symptoms include hypotension, cyanosis, weak and rapid pulse, and loss of consciousness. Peripheral IV Procedure: Apply gloves Select puncture site Apply tourniquet Prepare puncture site – cleanse Remove protective cover from catheter Avoid puncture sites where there is injury or disease to an extremity Stabilize vein by applying distal pressure and tension to the point of entry With the bevel of the needle up, pass through the skin directly into the vein (from the side or directly on top) Advance the needle and catheter about 2mm beyond the point where blood returned in the hub Slide catheter over needle and into the vein Release tourniquet Secure hub with opsite Apply pressure on proximal end of catheter to stop escaping blood Withdraw needle while stabilizing catheter Attach IV tubing Open tubing clamp and allow fluid infusion to begin Anchor tubing Secure catheter Document procedure  Fluid Bolus Vs TKVO Bolus – Rapid infusion of fluid, rate is as fast as it can go. Macro drip sets. TKVO – to keep the vein open. Infusions that are set to a slow rate because the sole purpose is to keep the line patent. Cardiac Diseases Atherosclerosis: Thickening of the artery wall from accumulation of fatty material. Chronic disease Affects all the arteries, but primarily coronary, renal, aortic, femoral, carotid, and cerebral. Causes the majority of heart attacks. Creates issues as it leads to narrowing of the vessels and reduction of blood flow through them. 2 Mechanisms – chronic gradual narrowing and acute infarction (MI) Angina Pectoris: Also known as chest pain Occurs when there is a deficiency of O2 for the heart muscle Can occur when the heart is working harder than normal Stable Angina: Typically follows the same pattern for the patient – predictable pain, location, severity. Insufficient O2 supply – anerobic metabolism and accumulation of lactic acid and CO2 (typically lasts 1-5 minutes and is relieved by rest) Unstable Angina: Same etiology as stable, however, the pain is more severe, different feeling as it is not as easily relieved by rest or meds. Plaque build up is bigger or ruptured. Typically lasts longer than 15 minutes. Often indicative of pre-MI angina Does not follow the same pattern as their usual angina. Greater degree of obstruction of the coronary arteries High risk of imminent MI Signs and symptoms of Angina: Recurrent, intermittent episodes of substernal chest pain, usually triggered by physical or emotional stress Tightness or pressure in the chest that often radiates into the neck or left arm Pallor, diaphoresis, and nausea Acute Coronary Syndrome: Results from a prolonged cardiac disorder causing myocardial ischemia or infarction STEMI, Non-STEMI, and unstable angina Typically caused by a rupture of the plaque in the arteries and subsequent thrombosis or the coronary artery Acute Myocardial Infarction (AMI): Part of the coronary muscle is deprived of blood flow until that part subsequently dies (infarcts) Most common cause is plaque ruptured and thrombus formation (can also occur from spasm of coronary artery) Classified as either STEMI or Non-STEMI Location and size of the MI depends on which coronary artery is blocked Infarcted tissue area is inevitably surrounded by a ring of ischemic tissue, this is relatively deprived of O2 but still viable Ischemic tissue often is electrically unstable, this causes cardiac arrhythmias Most deaths from MI are from arrythmias Signs and Symptoms – CHEST PAIN, pain usually felt just beneath the sternum or the left side of the chest, described as heavy, squeezing, crushing or tight, patient unconsciously clenches fist when describing the pain (levine sign), may also describe as pressure or discomfort, may mistake the pain for indigestion. Signs and symptoms or silent MI – sudden dyspnea, pulmonary edema, hypotension, confusion, profound fatigue, or feeling weak. Sign and symptoms of MI in women – nausea, lightheadedness, epigastric burning, sudden onset of weakness or unexplained tiredness Other Signs of an MI – pain (sudden, substernal chest pain that can radiate into the jaw, neck, and left arm, usually described as severe, steady, and crushing – no relief with vasodilators), non pain (silent MI – gastric discomfort described as indigestion), pallor, diaphoresis, dizziness, weakness, anxiety and fear, hypotension, rapid and weak pulse, dyspnea. Dissecting Aortic Aneurysm: Aorta is subjected to massive hemodynamic forces, leads to degenerative changes in the middle layer of the aorta Over time, these changes in the middle layer lead to a tearing of the inner layer  Once this is torn, dissection begins Blood gets pumped into the unnatural layer between the inner and middle layer, this then chronically stretches and weakens the vessel Signs and symptoms – middle aged or older (chronic hypertension), main complaint is chest pain (often described as the worst pain they have ever felt, ripping or tearing), pain usually comes on suddenly, located in the anterior chest or the back (between the shoulder blades) and can radiate into the back or abdomen, difference in BP between the two arms (disruption of blood flow through the brachiocephalic or left subclavian artery) Signs and symptoms depend on the site of the tear and the extent of the dissection Hypertensive Emergencies (Hypertension): Major cause of many cases of MI, heart failure, and stroke Most often a result of advanced atherosclerosis or arteriosclerosis Most common complications include renal damage, stroke, and heart failure Blood pressure at rest consistently greater than 130/80mmHg By the time symptoms start to occur, hypertension is already in a more advanced stage and has probably produced at least some damage to organs such as the heart, kidneys, and brain. Common signs and symptoms – headache, blurred vision, buzzing in the ears, chest pain, and altered LOC Respiratory Diseases Dyspnea: Subjective feeling of discomfort that occurs when a person is unable to inhale enough air Orthopnea: SOB that occurs when a person is lying down, results as blood pools in the lungs with gravity Cyanosis: Bluish discoloring of the skin resulting from large amounts of deoxygenated hemoglobin in the blood Upper Respiratory Tract Infection (URTI): Common cold caused by viral infection of the URT Spread through respiratory droplets either inhaled or touched  Signs and symptoms – red mucous membranes of the nose and pharynx, copious watery discharge, mouth breathing, changes in voice, and cough may develop from irritation of discharge Sinusitis: Bacterial infection secondary to a cold or allergy that has obstructed drainage of one or more sinuses Croup: Layrngotracheobronchitis Common viral infection in children Begins as an upper respiratory condition with nasal congestion and cough The larynx and subglottic area become inflamed with swelling and exudate which leads to characteristics such as barking cough, horse voice, and inspiratory stridor Often more severe at night Epiglottitis: Acute infection from a bacterial organism Most common in children aged 3-7 Infection causes swelling of the larynx, supraglottic area, and epiglottis Onset is rapid, fever and sore throat develop, and inability to swallow Excessive drooling is present Child will appear anxious, mouth open, struggling to breathe Pneumonia: May develop as a primary acute infection in the lungs or secondary to another respiratory or systemic condition Always risk following aspiration or inflammation in the lung, when fluids pool or cilia are reduced Most cases, the organism enters the lungs directly via inhalation or aspiration Can be classified as viral, bacterial, or fungal Tuberculosis: Infection that affects the lungs primarily, but may also invade the other organs Transmitted by oral droplets released from a person with active infection, and then inhaled into the lungs Primary infection – occurs when the microorganisms enter the lungs (fought off by your body’s immune system), creates a small area of necrotic tissues in the lungs, stays dormant for years. Secondary infection – active stage of infection  Signs and symptoms – malaise, fatigue, weight loss, low grade fevers, night sweats, cough that is prolonged and gets increasingly severe and often contains blood. Cystic Fibrosis: Genetic disorder that results in a thick, sticky mucous secretion in the lungs. Mucous obstructs airflow in the bronchioles causing air trapping and permanent damage to the alveoli Signs and symptoms – chronic cough, frequent respiratory infections, chest may appear overinflated, audible rhonchi, dyspnea, tachypnea, accessory muscle use, cyanosis, diminished breath sounds Aspiration: Passage of food or fluid, vomit or drugs, or any other foreign material into the trachea or lungs. Right lower lung is most commonly affected Signs and symptoms – coughing with dyspnea, stridor and hoarseness, wheezes, tachycardia, tachypnea, or with a complete obstruction – no sound COPD: Chronic obstructive pulmonary disease Group of chronic respiratory disorders that are characterized by progressive tissue degeneration and obstruction of the airways Causes irreversible damage to the lungs Debilitating conditions Emphysema, bronchitis, and asthma Asthma: Disease that involves periodic episodes of severe but reversible bronchial obstruction in persons with hypersensitive/hyper responsive airways May be acute or chronic Can be triggered by inhaled antigen or respiratory infections, exposure to cold, exercise, drugs, or stress Bronchi and bronchioles respond to stimuli in 3 ways – inflammation of the mucosa with edema, constriction of the smooth muscles (bronchoconstriction), or increased secretions of thick mucous in the passages. Partial obstruction of the bronchioles results in air trapping and hyperinflation of the lungs Air passes into the areas distal to the obstruction and is only partially expired Air builds up and the patient tries to force expiration which leads to collapse of the bronchial walls Residual volume increases – becomes more difficult to breathe fresh air and cough to remove the mucous (hyperinflation analogy)  Total obstruction of the bronchioles results when mucus plugs completely block flow or the already narrowed passages This leads to non aeration of the tissue distal Air in the distal area diffuse out and is not replaced, resulting in collapse of that section of the lung O2 demands increase as the body senses stress response to hypoxia as the patient fights for air Signs and symptoms – cough, dyspnea, tightness in chest, agitation as obstruction increases, wheezes as air passes through narrowed bronchioles, rapid, laboured breathing with accessory muscle use, thick tenacious mucus coughed up, tachycardia, decreased LOC, and respiratory failure. Status Asthmaticus – persistent severe asthma attack that does not respond to therapy, fatal secondary to hypoxia and cardia arrythmias Asthma Exacerbation – severe narrowing of the airways in an asthma attack to the point that no air is able to pass through, results in no respiratory rate and no breath sounds (silent chest) Emphysema: Destruction of the alveolar walls which leads to large, permanently inflated alveolar air spaces “pink puffers” Breakdown of alveolar walls results in loss of surface area for gas exchange, loss of elastic fibers affecting lung recoil, altered V/Q ratios, decreased support for bronchial structures leading to obstruction of airflow in expiration, thickening of bronchial walls leads to narrowed airways, difficult expiration leads to air trapping and increased residual volumes and over inflation, fixation of ribs in inspiratory position (barrel chest), hypercapnia, and hypoxic drive as the patient’s respiratory center adapts to high CO2 levels and fails to be the respiratory centers regulatory mechanism, the large air spaces (bleb) can create the tissues and pleural membranes around the bleb to rupture (causing pneumothorax), frequent infections as secretions are difficult to remove, pulmonary hypertension and cor pulmonale develop as pulmonary blood vessels are destroyed, causing increases in pressure in the pulmonary circulation. Signs and symptoms – dyspnea (initially on exertion, eventually on rest), hyperventilation with prolonged expiratory phases and accessory muscle use, barrel chest from hyperinflation, tripod positioning to facilitate breathing, fatigue (contributes to weight loss), clubbed fingers, polycythemia Chronic Bronchitis: Significant changes to the bronchi resulting from constant irritation from smoking or exposure to pollutants Effects are irreversible and progressive  Results in inflammation and obstruction to the bronchi, repeated infections, and chronic coughing Patho – mucosa are inflamed and swollen, hypertrophy of mucous glands and increased secretions are produced, chronic irritation and inflammation lead to thickening of bronchial walls and further obstruction, secretions pool and are difficult to remove, low O2 levels (cyanosis will be evident), “blue bloaters” (edema, cyanosis, and low O2 levels), severe dyspnea and fatigue interfere with nutrition, pulmonary hypertension results. Signs and symptoms – constant productive cough, tachypnea, shortness of breath, frequent secretions that are thick, rhonchi (usually more prevalent when secretions have pooled), cyanosis and hypoxia. Pulmonary Embolus: Blood clot or mass of other material that obstructs the pulmonary artery or branch of it, blocking blood flow through the lung tissue Signs and symptoms – transient chest pain that often increases with coughing or deep breathing, cough, SOB, tachypnea, hypoxia, anxiety, restlessness, tachycardia, Massive emboli can cause – crushing chest pain, low BP Atelectasis: Non aeration or collapse of a lung or part of a lung, leading to decreased gas exchange or hypoxia When alveoli become airless, they shrivel up This interferes with blood flow through the lungs and alters both ventilation and perfusion Signs and symptoms (of large areas) – dyspnea, tachycardia, tachypnea, chest expansion may appear abnormal or asymmetrical Pleural Effusion: Presence of excessive fluid in the pleural cavity Pleurisy may follow – inflammation/swelling of the pleural membranes The fluid creates higher pressure which prevents normal lung expansion, leading to atelectasis Signs and symptoms – dyspnea, chest pain, tachycardia, tachypnea, absence of breath sounds over affected area, tracheal deviation, hypotension Adult Respiratory Distress Syndrome (ARDS): Restrictive disorder Secondary to an injury Usually occurs 1-2 days after an injury Often associated with multiple organ dysfunction  Changes in the lungs results from injury to the alveolar wall and capillary membranes, this leads to increased alveolar permeability, increased fluid in the alveolar and interstitial areas of the lungs. This results in decreased diffusion of O2, reduced blood flow to the lungs, difficulty in expanding the lungs, reductions in tidal volumes. Signs and symptoms – dyspnea, restlessness, rapid shallow respirations, tachycardia, accessory muscle use as lung congestion increases, crackles, productive cough with frothy sputum Acute Respiratory Failure: End result of many pulmonary disorders Happens when there are inadequate O2 and CO2 levels for the body’s needs at rest CNS including the respiratory control center is affected Ends in respiratory arrest SGA – When to Place and Procedure Supraglottic Airways: King LT and Igel are most common Inserted to pharynx to allow oxygenation and ventilation Blind/quick insertion Patient must be GCS 3 Max number of attempts = 2 When to Insert: BLS airways are ineffective, or definitive need for advanced airway Prolonged extrication Ineffective management with other devices Ensure insertion does not compromise the quality of other interventions Confirmation of Placement: ETCO2 waveform Chest auscultation Chest rise and fall Non waveform ETCO2 Tube misting King LT Airway:  How does it work – has a distal and proximal balloon to occlude the esophagus and oropharynx, which prevents gastric inflation and aspiration. Creates a direct route for oxygen/ventilation to the trachea and lungs. Contraindications – does not eliminate the risk of vomiting/aspiration, high airway pressures can cause air to leak into stomach or out of mouth, do not use in patients with intact gag reflexes, esophageal disease or who has ingested caustic substances, or airway obstructions. Complications – laryngospasm, vomiting, hypoventilation, trauma (from insertion), ventilation may be difficult if pharyngeal balloon pushes the epiglottis over the glottic opening. Sizing – Yellow (3) = adults 4-5ft, cuff volume 50mL, Red (4) = 5-6ft, cuff volume 70mL, Purple (5) = adults >6ft, cuff volume 80ml Igel Airway: Does not require inflation 3 adult and 4 pediatric sizes (2-90+kg) High seal pressures, resulting in reduced trauma to airway upon insertion Tip is designed to fit into the proximal esophagus Sizing – 1 Pink (2-5kg Neonate), 1.5 Blue (5-12kg Infant), 2 Black (10-25kg Small pediatric), 2.5 White (25-35kg Large pediatric), 3 Yellow (30-60kg Small adult), 4 Green (50-90kg Medium adult), 5 Orange (90+kg Large adult) Complications – trauma to the pharyngo-laryngeal framework, downfolding epiglottis, gastric insufflation, regurgitation, and inhalation of gastric contents, nerve injuries, vocal cord paralysis, lingual or hypoglossal nerve injuries, if placed too high in pharynx may result in poor seal and cause excessive leakage, laryngospasm SGA Medical Directive: Indications – need for ventilatory assistance or airway control AND other airway management is ineffective Conditions – absent gag reflex Contraindications – airway obstructed by foreign object, known esophageal disease, trauma to the oropharynx, and caustic ingestion Treatment – consider supraglottic airway insertion, the maximum number of SGA insertion attempts is 2 Confirmation of SGA Placement: Primary – ETCO2 waveform capnography Secondary – ETCO2 (non waveform device), auscultation, and chest rise Cardiac Arrest Causes of Cardiac Arrest: Atherosclerosis (#1 cause) Genetic disorders Cardiomyopathies Electrocution, drowning, trauma, overdose Management of Cardiac Arrest: Scene safety Additional crew, fire, police Ensure patient is on flat, hard surface C-A-B to ensure patient is in cardiac arrest Check carotid and radial pulses in 24 hours old to < 8yeares old = initial: 2j/kg, subsequent: 4j/kg, interval: 2 mins > 8 years old, Zoll = 120, 150, 200, Lifepack = 200, 300, 360 Shockable – Vtach and Vfib Non Shockable – asystole and PEA Medical TOR: Age greater than or equal to 16 years of age Altered LOA Arrest not witnessed by EMS and no ROSC after 20 mins of resuscitation, and no defib delivered When to Transport Early After 1 analysis (and shock if needed) – pregnancy presumed to be greater than 20 weeks, hypothermia, airway obstruction, non-opioid drug overdose/toxicology, and other known reversible cause of arrest not addressed For patients in refractory Vtach or Vfibb, transport of the patient should begin after the third consecutive shock Trauma Cardiac Arrest: Cardiac arrest secondary to severe blunt or penetrating trauma Manual defib – 1 shock/analysis maximum prior to transport (and total) Trauma TOR: Greater than or equal to 16 years of age No palpable pulses AND No defib delivered AND Rhythm asystole AND No signs of life at anytime since fully extricated OR Signs of life when fully extricated with the closest ED greater than or equal to 30 mins transport time away OR Rhythm PEA with the closest ED greater than or equal to 30 mins transport time away Trama TOR Contraindications: Age less than 16 years Defib delivered Signs of life at anytime since fully extricated medical contact Rhythm PEA and closest ED is less than 30 minutes away Patients with penetrating trauma to the torso/neck and lead trauma hospital is less than 30 minutes away Manual Defib – don’t need to pull over ambulance to shock SAED – must pull over ambulance to defibrillate Hypothermia: Must be cardiac arrest secondary to hypothermia 1 analysis. Then transport Cold waxy skin/core Blanching Rigid extremities Passive/gentle rewarming Limit movement – can cause lethal arrythmias ROSC: Fluid bolus: 10mL/kg, reassess every 100mL (2-12) and 250mL (12+), BP, auscultation, vitals Target ETCO2 30-40mmHg Titrate SPO2 94-98% 12 lead Supine or head elevated slightly Oxygen Medical Math and Drug Conversion Syringe Formula – how much you are drawing up in a syringe (Desired dose/dose on hand) x volume on hand = volume to deliver Iv Infusion Formula – how much fluid to give your patient over an amount of time (amount to be infused(mL)/time(mins)) x drop factor (gtts/mL) = drops/min Drug Conversion: Concentration Ratio – amount of drug (x) in 1 mL, xmg:1mL Serial Dilution – the constant is 1gram in various amounts of fluid, 1g/xmL % Dilution or % Concentration – the constant is amount of grams of drug in 100mLs, %xdrug: 100mL STEMI Bypass Indications under the STEMI Hospital Bypass Protocol Transport to a PCI center will be considered for all patients who meet ALL of the following: Greater than or equal to 18 years of age Chest pain or equivalent consistent with cardiac ischemia/myocardial infarction Time from onset of current episode of pain is less than 12 hours 12-Lead ECG indicates and acute AMI/STEMI: atleast 2mm of ST elevation in leads V1- V3 in at least two contiguous leads AND/OR at least 1mm of ST elevation in at least 2 other anatomically contiguous leads OR 12 lead ECG computer interpretation of STEMI and paramedic agrees Once activated, continue to follow the STEMI hospital bypass protocol, even if ECG normalizes Contraindications under the STEMI hospital bypass protocol: ANY of the following exclude the patient from being transported under the STEMI hospital bypass protocol: CTAS 1 and the paramedic is unable to secure patient’s airway or ventilate 12 Lead ECG is consistent with LBBB, ventricular paced rhythm, or any other STEMI imitator Transport to a PCI is greater than or equal to 60 minutes from patient contact Patient is experiencing complication requiring PCP diversion – moderate to severe respiratory distress or use of CPAP, hemodynamic instability or symptomatic SBP