Flight Medical Provider Study Guide: Current Concepts in Critical Care Transport (IA MED) 9781659090062, 1659090067

Table of contents :
Disclaimer
Dedication
Acknowledgements
Preface
Arterial Blood Gases
Advanced Airway Management
Ventilator Patient Management
Pulmonary Diseases
Laboratory Analysis And Diagnostic Studies
Endocrine Emergencies
Gastrointestinal And Genitourinary Emergencies
Flight Physiology & Stressors Of Transport
Aircraft Fundamentals, Ground Operations, Safety And Survival
Critical Care Cardiology
Hemodynamic Monitoring
Neurological Emergencies
Cerebrovascular Accidents
Trauma Patient Management
Burn Management
Environmental Injuries & Toxicology
Obstetrical Emergencies
Neonatal Emergencies
Pediatric Emergencies
References

Citation preview

   

FLIGHT MEDICAL PROVIDER STUDY GUIDE  

Current Concepts in Critical Care Transport  

 

 

Chris Smetana, AS, NRP, FP-C, CCP-C Lindsay Mauldin, RN, NRP, CFRN, FP-C, CCP-C

 

Lead Editor Sheila Moak  

Chapter Editors Andy Fidino, NRP, FP-C Zack Hatch, BS, NRP, CCP-C, CCEMT-P John Vonrosenberg, MA, NRP, FP-C, CCEMT-P Dillon Wenberg, NRP, FP-C, CCP-C

 

Reviewers Jared Corrigall, NRP, FP-C, CCEMT-P Jason Linn, RN, CEN, CCRN, CFRN, FAWM Anthony Riggs, NRP, FP-C, EMS-I Jordan White, BSN, RN, CFRN  

Medical Director Mike Hudson, MD, EM, EMS Air Medical Program Chief Medical Director Level I ED Trauma Physician  

Curriculum Designer Jonathan Reed, BA, NRP, ATP, TP-C, FP-C, 18D  

Cover Designer Michael Boone, BSN, RN, CFRN, CCRN  

DISCLAIMER All rights reserved. No part of the material protected by this copyright may be reproduced or utilized in any form, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without written permission from the authors & the copyright owner.  

The content, statements, views, and opinions herein are the sole expression of the respective authors and Immediate Action Medicine, INC. The procedures and protocols in this book are based on the most current recommendations of responsible medical sources at the time of publication. Immediate Action Medicine, INC makes no guarantee as to and assumes no responsibility for, the correctness, sufficiency, or completeness of such information or recommendations. Other or additional safety measures may be required under particular circumstances.  

This textbook is intended solely as a study guide to the appropriate procedures to be employed when rendering emergency care to the sick and injured. It is not intended as a standard of care required in an emergency, because circumstances and the patient’s physical condition can widely vary from one emergency to another. It is not intended that this study guide shall, in any way, advise emergency personnel concerning legal authority to perform the activities or procedures discussed. Such local determination should be made only with the aid of legal counsel, your medical director, and your agency's protocols.  

The Flight Medical Provider Study Guide is an independent publication. It has not been authorized, sponsored, or otherwise approved by the owners of the trademarks or service marks referenced in this product.  

Reference herein to any specific commercial product, process, or service by trade name, trademark, manufacturer, or otherwise does not constitute or imply its endorsement or recommendation by Immediate Action Medicine, INC, and such reference shall not be used for advertising or product endorsement purposes. All trademarks displayed are the trademarks of the parties noted herein.  

There may be images in this book that feature models; these models do not necessarily endorse, represent, or participate in the activities represented in the images. Any screenshots in this product are for educational and instructive purposes only. Any individuals and scenarios featured in the case studies or examples throughout this study guide may be real or fictitious but are used for instructional purposes only.  

 

Copyright © 2020 by Immediate Action Medicine, INC All rights reserved  

ISBN: 9781659090062  

 

Printed in the United States of America

DEDICATION We want to dedicate the Flight Medical Provider Study Guide to all of the students who have passed through our Flight Medical Provider course over the years. Students have provided us with continual feedback to improve our material and deliver both the knowledge and information they need to be successful as an advanced practicing medical clinician.  

We would also like to thank all of IA MED’s training partners throughout the United States and abroad for allowing us the opportunity to work with you in collaboration to help provide valuable education to your agencies and the communities you serve. We are truly honored and humbled to have been entrusted to do so.



ACKNOWLEDGEMENTS Chris  

 

I personally would like to thank the IA MED Team for their hard work and selfless dedication to help IA MED grow. Their contributions to the company and the impact they have left on both their students and the industry has been immeasurable. It truly takes a TEAM to make this happen and am thankful for our IA MED Family!  

To my friend and business partner Jon Reed, thank you for your support, mentorship, and all the heavy lifting and sacrifices you and Kate have had to endure to help make IA MED an industry leader. Thank you, brother. “Ride or Die”  

To my friends and family, I can never repay the debt for all the sacrifices you have had to endure to make this book and IA MED possible.  

To my daughter, Shay, thank you for always showing me the love and fun in life. You are a beautiful soul. To my son, Ben, thank you for being my sidekick watching Fireman Sam with me while working late.  

Lastly, to my wife Susie, I know how hard you have struggled with my long hours, no days off, and me continually being away while growing IA

MED. You have a given part of yourself to help me aspire to achieve my dreams. I can never repay that debt, but I always promise to be the loving husband by your side and give you all of me while trying every day. I am thankful to have been your partner and on this crazy adventure for the past 20 years. I truly thank you for your sacrifices and love your face!  

Lindsay  

 

This book would not have been possible without the support and encouragement of those in our industry and the desire for better education. Jon and Chris, thank you for the opportunity to be part of the IA Med family. It has truly been a fun ride, I’m lucky to have such great partners, and I look forward to where we go next.  

To my mentors in the industry, thank you for always pushing me, encouraging me, and motivating me to spread my wings. I am so lucky to have such an array of people to bounce ideas off of, all over the globe.  

To my mom, thank you for always believing in me, especially on the days I didn’t believe in myself. You have supported me in ways I can’t begin to count, even when my path has been the one less travelled.  

To my husband Chuck, you’re my bar. You have given endless support to help me achieve where I am today and continue to push me to be a better version of myself. You have been patient when I’m cranky from trying to fit 50 hours of work into a 24-hour day, or when I’m exhausted from travelling too much. Words cannot express how fortunate I feel to have both you and Pickles by my side through thick and thin. Thank you for your sacrifices .and everything you do.  

PREFACE Immediate Medicine Action, Inc. (“IA MED”) is a disabled veteranowned small business that provides cutting-edge specialty medical training, ranging from aeromedical critical care to austere tactical medicine. Our proprietary system has been continuously developed and refined since 2011, using a comprehensive data-driven approach. Critical care transport is a highly competitive industry, and to become a Flight Medical Provider™ you have to be the best.  

Since 2011, IA MED has helped thousands of students launch careers as advanced prehospital and critical care professionals by providing the most comprehensive, flexible, and accessible critical care education in the nation.  

By presenting complex medical concepts through straightforward instruction, we make learning critical care simple - regardless of your current medical ability or experience.  

Our unique approach to advanced medical education has made IA MED® the industry-standard and a fan-favorite among paramedics, nurses, and other industry providers.  

The Flight Medical Provider Study guide will review the fundamentals of advanced prehospital care and critical care transport while also helping students as they prepare and successfully challenge the industry's most challenging exams: the Flight Paramedic Certification (FP-C), Critical Care Paramedic Certification (CCP-C) and Certified Flight Registered Nurse (CFRN) exams!  

This is EMS. Re-imagined.  

The Flight Medical Provider course was designed for the practicing clinician by currently practicing clinicians.  

TABLE OF CONTENTS Disclaimer Dedication Acknowledgements Preface Arterial Blood Gases Advanced Airway Management Ventilator Patient Management Pulmonary Diseases Laboratory Analysis And Diagnostic Studies Endocrine Emergencies Gastrointestinal And Genitourinary Emergencies Flight Physiology & Stressors Of Transport Aircraft Fundamentals, Ground Operations, Safety And Survival Critical Care Cardiology Hemodynamic Monitoring Neurological Emergencies Cerebrovascular Accidents Trauma Patient Management Burn Management Environmental Injuries & Toxicology Obstetrical Emergencies Neonatal Emergencies Pediatric Emergencies References  

ARTERIAL BLOOD GASES ABG pH CO2 HCO3 PaO2 SaO2 Base (Deficit/Excess)  

Normal Range 7.35 - 7.45 35 - 45 22 - 26 80-100 > 95% (-2) - (2+)

Regulation of pH Buffer Systems Bicarb (HCO3)/ Carbonic Acid (H2CO3)            react in seconds Lungs blow off/hold CO2                  react in minutes Kidneys resorb/excrete bicarb (HCO3)            react in hours to days  

ABG’s (Arterial Blood Gasses) pH 7.35 – 7.45 Percentage of hydrogen ions pH is an inverse log of hydrogen ions  

pCO2 35-45 mmHg Partial Pressure of carbon dioxide CO2 exists in the blood as a soluble gas CO2 is a normal byproduct of metabolism Measured in partial pressures (PCO2) CO2 is an indicator of acid CO2 regulation is a function of minute volume Minute volume = tidal volume [Vt] x respiratory rate [F]

 

HCO3 22-26 mEq/L Bicarbonate Metabolic Function Moves in the same direction as the pH HCO3 is alkalotic, or “basic” Low HCO3- = Low pH High HCO3- = High pH  

 

BE -2 to 2 mEq/L Base Deficit / Excess a base deficit of > -4 is an indicator for the potential need for blood transfusion a base deficit of >-19 correlates with a poor outcome (death likely) Replacement Formula: 0.1 x (-BE) x patient weight in kg = Bicarb needed  

Example: Patient weighs 100kg and has a BE of -5. .1 x (-5) x 100kg = 50 mEq Bicarb required  

pO2 80-100 mmHg Partial Pressure of Oxygen          

pO2 Levels SaO2 Levels 90 mmHg 100% 60 mmHg 90% 30 mmHg 60% 27 mmHg 50%  

A PaO2 of 60 mmHg is roughly equal to an SaO2 of 90%

PaO2 40 mmHg / 50 mmHg / 60 mmHg SaO2 70% / 80% / 90%  

SaO2 > 95% Hemoglobin saturation of oxygen This is the same measurement that a pulse oximeter gives Note the pulse ox is delayed – may not be a true representation of current oxygenation status  

Oxyhemoglobin Dissociation Curve  

 

Interpreting ABG’s Is the pH acidotic (7.45)? CO2 is an acid, so more CO2 makes the ABG more acidotic (moves left) HCO3 (bicarbonate) is basic, so more HCO3 makes the ABG more alkalotic (moves right)  

Is it Respiratory or Acidotic? If CO2 follows pH = Respiratory If HCO3 follows pH = Metabolic  

Is it compensated? The compensatory mechanism is the opposite of the primary problem Example: A respiratory acidosis is compensated by HCO3 (bicarb) Example: A metabolic alkalosis is compensated by CO2 (acid) If the pH is outside of normal values, and both respiratory and metabolic are outside normal values, it is partially compensated If the pH is inside normal values, but CO2 and HCO3 are both outside normal ranges, the ABG is said to be fully compensated

 

Critical ABG’s For Intubation pH < 7.2 pCO2 > 55 pO2 < 60  

 

 

Acid-Base Disorder

Primary Change

Compensatory Response

Respiratory Acidosis 45

HCO3 >26

Respiratory Alkalosis >7.45

CO2 26  

Too little H+ or too much HCO3 Usually the result of H+, K+, NA+, CL- Loss Caused by vomiting, nasogastric (NG) suctioning, diuretics, corticosteroids, antacid poisoning, Diamox Treat the underlying cause  

Metabolic Acidosis pH < 7.35      Bicarb < 22  

Too much H+ or too little HCO3 #1 cause is lactic acidosis (lactate >4) Caused by ketoacidosis, hyperthermia/fever, seizures, rhabdomyolysis Treat the underlying cause  

Respiratory Alkalosis pH > 7.45      CO2 < 35  

Result of alveolar hyperventilation (breathing too fast) Caused by ASA poisoning (a respiratory center stimulant), or hyperthermia/heat injuries, hypermetabolic states, fever, anxiety, pain, pregnancy, high altitude If on a ventilator, check tidal volume (Vt) first, then rate (F)  

Respiratory Acidosis

pH 45  

Failure to remove CO2 (breathing too slow) Caused by chest wall injury, CNS depression, lung injury, rib fractures, COPD, asthma Treat the underlying cause, increase respiratory rate  

CO2 Transport and Removal CO2 is a byproduct of metabolism Diffuses into circulation and transported to pulmonary capillaries Diffuses across capillary/alveolar membrane into the alveoli Cardiac output moves the blood to the tissues Minute volume can be increased to “blow-off” CO2 Body is limited by how much CO2 it can remove by hemoglobin Minute volume also increased in hyperthermic states (Malignant Hyperthermia)  

pH and ETCO2 Relationship For every change in 10 mmHg the ETCO2, you should expect the pH to change 0.08 the opposite direction Example: pH 7.20 (7.35 – 7.45) ETCO2 50 mmHg (35 – 45)       When ETCO2 is decreased by 20 mmHg, from 50 to 30 mmHg       pH will increase 0.16, from 7.20 to 7.36  

pH and Bicarbonate (HCO3) Relationship For each change of 0.15 in pH, you should expect HCO3 to change 10 mmol/L in the same direction  

Example: pH 7.20 (7.35 -7.45) HCO3 16 (3.5-5.0)       When pH is increased by 0.15, from 7.20 to 7.35 HCO3 will Increase from 16 to 26      

pH and Potassium (K+) Relationship For each change of 0.10 in pH, the K+ will inversely change 0.6 the opposite direction  

Example: pH 7.20 (7.35 -7.45) K+ 4.0 (3.5-5.0)       When pH is increased by 0.20, from 7.20 to 7.40       K+ will decrease by 1.2, from 4.0 to 2.8  

CO2 and Potassium (K+) Relationship For each change of 0.10 in pH, the K+ will inversely change 0.5 mEqs in the same direction  

Example: CO2 55 (35 - 45) K+ 4.0 (3.5-5.0)       When CO2 is decreased by 20, from 55 to 35 K+ will decrease by 1.0, from 4.0 to 3.0  

This is an important concept to remember. As pH lowers, potassium shifts outside of the cell giving a falsely elevated potassium level. When correcting the imbalance by raising the pH, either through bicarb or respiratory efforts, potassium will shift intracellularly, potentially leaving a life-threatening hypokalemic state.  

ADVANCED AIRWAY MANAGEMENT Why we Fail Lack of protocol Lack of planning or preparation Lack of plan “A, B, and C” Intubation failure Lack of equipment availability, use, or training Approach Communication failures  

“Failure to manage the airway is a major cause of preventable death in the prehospital setting. "  

Indications for Airway Management Unable to swallow Patient can’t ventilate/oxygenate Failed airway algorithm GCS 140 bpm Avoid ASA (Aspirin) ASA prevents binding of thyroglobulin, making the situation worse Treatment:

Give IV fluids first! Beta Blockers (Propranolol) Steroids (Dexamethasone) Tylenol for fever  

Hypothyroidism/ Myxedema Coma Caused by decreased levels of thyroid hormone, slowing down basic body functions and metabolism Patient presents with fatigue, cold intolerance, weight gain, puffy eyelids, sparse hair & goiter Primarily occurs in women > 90% cases in winter patient has cold intolerance and is now suffering from hypothermia High mortality rate from respiratory failure Becomes “Myxedema Coma” upon LOC change Altered mental status Failure of the thermoregulatory system Precipitating event (cold exposure, trauma, stroke, drugs)  

Treat with IV Levothyroxine (T4) or Triostat (T3) Levothyroxine is “Synthroid” Fluids for hypotension Glucocorticoid support Assists the hypothalamus in secreting more thyroid stimulating hormone (TSH) via the negative feedback system Passive external rewarming  

Adrenal Insufficiency /Adrenal Crisis       “Addison’s Disease”

Decreased hormonal output from the adrenal glands. Can be primary, secondary, or tertiary (rooting from dysfunction of the pituitary or hypothalamus, respectively) causing a decrease in cortisol Chronic hormonal disorder Patient will often present with depression, malaise, and salt craving Patient will often have bronze colored skin (JFK had Addisons) Acute Adrenal insufficiency Traumatic brain injury Abrupt changes in steroid use  

Presents with AMS Shock Severe pain in lower extremities Severe vomiting, diarrhea, dehydration Treated with oral steroids (Prednisone) Negative Adrenocorticotropic Hormone (ACTH) testing also referred to as corticotropin or cosyntropin test No Etomidate in RSI (due to adrenal suppression)  

Cushing’s Syndrome Increased levels of stress hormone, or cortisol over a prolonged period of time Buffalo hump, moon face, thin arms and legs, purple striae on abdomen Causes: Excessive use of corticosteroids (iatrogenic- condition caused by treatment) Adrenal gland tumor (the adrenal cortex secretes cortisol/glucorticoids) Usually resolves when corticosteroids are stopped or tumor is removed

 

GASTROINTESTINAL AND GENITOURINARY EMERGENCIES Upper GI Bleeds GI bleeds are classified into one of two categories Upper GI Lower GI Bleed located in reference to the ligament of Treitz Upper GI bleeds occur up to six times more often    

Peptic Ulcers

 

Upper GI bleed Can be gastric or duodenal Most often caused by helicobacter pylori Other causes include: NSAID use Alcohol Tobacco

Stress Gastritis Presents as stomach pain  

Esophageal Varices       LIFE THREATENING

 

Bleeding in the esophagus, most commonly due to chronic alcoholism (cirrhosis) Vomiting bright red blood (hematemesis) Bright red diarrhea (hematochezia) Patient often presents with syncope Altered mental status due to hypovolemia  

Esophageal Varices Treatment Octreotide (Sandostatin) Octreotide reduces splenic (spleen) and hepatic (liver) blood flow, and reduces variceal pressures This medication is a synthetic form of Somatostatin Vasopressin may be used Reduces mesenteric blood flow, reducing portal hypertension  

 

Check Coagulation Values (PT/PTT/INR) to help anticipate the need for blood products Balloon Tamponade a Sengstaken Blakemore tube can be placed to provide direct pressure on the bleeding (patient must be intubated first) Do not insert an NG tube Can cause a lethal rupture of varices  

Mallory-Weiss Usually not life-threatening Rupture of the esophagus Commonly caused by chronic forceful vomiting (alcoholism, bulimia) Presents with hematemesis Often self-resolving If bleeding continues, treat like esophageal varices Can cause mediastinitis secondary to leak of gastric contents into the chest Requires EGD (Esophagogastroduodenoscopy)  

Boerhaave’s Tears

 

Complete transmural rupture of the lower thoracic esophagus Chest pain and shock Hamman’s Sign Crunching sound upon auscultation of the heart due to pneumomediastinum Subcutaneous Emphysema Requires EGD (Esophagogastroduodenoscopy) Gold standard  

Lower GI Bleeds Common lower GI bleeds include: Diverticulitis Hernias Adhesions Inflammatory bowel disease Foreign objects  

Most often do not require emergency intervention May be source for sepsis Increased risk of flying due to ileus Wet gas expansion (Boyle’s Law)  

Lab Findings for GI Bleeds Often appear normal during first 24-48 hours Hgb < 10 gm/dL Need for blood products Hematocrit will decrease as interstitial fluids shift Fluctuations over time indicate active bleeding Thrombocytopenia RBC < 4 million BUN may increase due to absorption of blood proteins BUN to Creatinine ratio greater than 30:1 Increase in WBC  

Liver Disease Caused by hepatitis, alcoholism, Tylenol overdose, etc. INR > 1.5 (due to decreased Albumin and coagulation factor production) Liver breaks down ammonia Increased ammonia leads to increased ICP Treatment is mainly supportive May need to treat with Lactulose (removes ammonia)  

Hepatitis Viral – 90% Hepatitis A, B, C, D, E Alcohol consumption Autoimmune disorders Toxins Drugs  

Laboratory Findings in Liver Disease Increased Liver enzymes ALT > 55 U/L AST > 48 U/L Decreased albumin > 5 g/dL Clotting concerns Increased bilirubin > 1.2 mg/dL Increased serum ammonia > ICP, LOC changes Decreased blood glucose Increased BUN > 30:1 Ratio  

Hepatic Encephalopathy Any disease process affecting normal liver functions can lead to hepatic encephalopathy Various neurologic symptoms including changes in consciousness, behavior changes, and personality changes Asterixis Coarse "flapping" muscle tremor may be observed during voluntary movement Treat with Lactulose Supportive care  

Pancreatitis

 

Digestive enzymes destroy the pancreas Most common causes are gallstones and alcohol abuse Unresolved cases may lead to SIRS Multisystem complications Atelectasis and pleural effusions common ARDS Increased Amylase and Lipase levels Can be up to 3 times normal values Amylase > 300 U/L Lipase > 150 U/L  

Pancreatitis Signs and Symptoms Pain often centered in the upper middle or upper left abdomen Radiates to back Begins or worsens after eating May worsen when lying flat Cullen’s Sign Periumbilical ecchymosis caused by hemorrhagic pancreatitis

Grey-Turner's Sign Flank ecchymosis caused by hemorrhagic pancreatitis May also be seen in retroperitoneal bleeds  

Cullen’s Sign (A) Grey-Turner’s Sign (B)

 

Pancreatitis Treatment Depends on severity May require surgery (cholecystectomy) Chronic pancreatitis often treated with enzyme pills to aid in digestion Pain management: Morphine can cause spasms of the Sphincter of Oddi, causing an obstruction in bile flow NSAIDS, Ketamine or Demerol used for pain No effect on Sphincter of Oddi  

Septic Shock Unresolved SIRS from pancreatitis may lead to septic shock HR > 90 beats/min RR > 20 breaths/min or ETCO2 < 30 mmHg Presence of fever WBC < 4K or > 12K Lactate > 4 mmol/L Hypotensive with normal heart rate refractory to fluid boluses IV Fluids and Pressors Levophed (Norepinephrine) Do not use Etomidate in RSI  

Initial Treatment (Hour One) INITIAL RESUSCITATION FOR SEPSIS AND SEPTIC SHOCK Measure lactate level >2 mmol/L indicates inadequate cellular perfusion. Remeasure lactate if initial lactate elevated (> 2mmol/L). Obtain blood cultures before administering antibiotics. Administer broad-spectrum antibiotics. Rapid administration of 30ml/kg crystalloid bolus for hypotension or lactate ≥4 mmol/L Apply vasopressors if hypotensive during or after fluid resuscitation to maintain a mean arterial pressure ≥ 65 mmHg Levophed preferred  

Abdominal Aortic Emergencies

 

Rate of mortality for ruptured AAA exceeds 80% Risk factors: Age Male gender Family history of AAA Smoking Immediate surgical intervention  

Peripheral Vascular Disease Deep Venous Thrombosis (DVT) Virchow’s Triad Virchow=Venous Vessel wall injury Surgery, chemical irritation, inflammation Stasis of blood Immobility, varicose veins, venous obstruction Hypercoagulability Cancer, thrombophilia, inflammatory disease, pregnancy Aching pain, WARM, red, and swollen Blood is getting into the limb, it just can’t get out Homan’s Sign dorsiflexion of the foot and constriction of the calf causing calf pain  

Arterial Occlusion

Usually embolic Presents with claudication (Latin for “limping”) Cramping pain felt in the extremities, usually referenced in how many blocks someone walks before the pain occurs (i.e.

pain after walking a single block would be “1 Block Claudication”) COLD Limb Blood is not getting into the limb Treatment Non-Surgical: Smoking cessation, lipid control, exercise Surgical: Only if life or limb-threatening condition exists 6 P’s of Arterial Occlusion

 

Poikilothermic: body temperature that varies with its surroundings

FLIGHT PHYSIOLOGY & STRESSORS OF TRANSPORT The Air Medical Role Advantages vs Disadvantages Relative contraindications Severe anemia Uncontrolled arrhythmia Pregnancy past 24 weeks gestation Weight or space confines

Basic Flight Terminology

 

Above Ground Level (AGL) Above Sea Level (ASL) Mean Sea Level (MSL)  

Atmospheric Composition Three gases constitute 99% of the atmosphere Nitrogen: 78% Oxygen: 21% Argon: 0.93% Same concentration at 1000’, 5000’, 25,000’ Daltons Law

Barometric Pressure Values Weight of air May be expressed in torr or mmHg Sea Level                   760 torr            (1 ATM) 10k ft. MSL      523 torr 18k ft. MSL             380 torr            (1/2 ATM) 63k ft. MSL             0 torr                  (0 ATM)  

Altitude Zones

 

Physiologic Zone       Sea Level to 10,000ft MSL Night Vision is decreased beginning at 5,000 ft. MSL  

Physiologically Deficient Zone       10k to 50kft MSL Oxygen or pressurization required to survive at these altitudes If in a pressurized cabin and a sudden decompression occurs Time of Useful Consciousness (TUC) is cut in half A sign of compression loss is cooler temperatures in the cabin and windows fogging Normally 90 seconds of useful consciousness at 30,000 ft. If a rapid decompression occurs, TUC is now around 45 sec  

Example- If you were in an altitude chamber at 30k ft. and took your oxygen mask off, you would normally have around 90 seconds of consciousness. If you took your mask off and the chamber was rapidly decompressed, you would only have 45 seconds consciousness.  

Space Equivalent Zone       >50kft MSL If you are here, congratulations on becoming an astronaut!  

GAS LAWS Boyle’s Law

Image: AAOS: Critical Care Transport

 

“Boyle’s = Balloon = Barotrauma” The pressure of a gas is inversely proportional to the volume of a gas at a constant temperature Affects ETT cuffs, MAST trousers, Air splints, IV drip rates (increases rate) If the patient has a Pneumocephalus intracranial pressure will increase Open or depressed skull fractures  

P1 V1 = P2 V2  

Charles’ Law

Image: AAOS: Critical Care Transport

 

“Charles Centigrade” At a constant pressure, the volume of gas is directly proportional to the absolute temperature of the gas Example- When you charge an oxygen tank, the tank gets hot This law has very little effect on the human body Does relate to how well an aircraft performs at various temperatures Ideal flying conditions are a cold, dry day  

V1 / T1 = V2 / T2  

Dalton’s Law      

 

“Dalton’s Gang” Law of Partial Pressures This is an additive gas law The total pressure of a gas mixture is the sum of the partial pressures of all the gases in the mixture Responsible for soft tissue swelling at altitude (uptake of inert gasses into tissue)  

Fick’s Law

Image: AAOS: Critical Care Transport

 

Diffusion of gas is: Proportional to the difference in partial pressure Proportional to the area of the membrane Inversely proportional to the thickness of the membrane Gas diffusion across the alveoli  

Henry’s Law

Image: AAOS: Critical Care Transport

 

“Henry = Heineken” Solubility of gas in liquid The quantity of gas dissolved in 1 cm3 (1 mL) of a liquid is proportional to the partial pressure of the gas in contact with the liquid Affects divers, can lead to decompression sickness “the bends”

Every 33ft = (1 ATM) Compresses nitrogen molecule allowing it to disassociate from adipose tissue  

The bends are the most common form of decompression sickness  

Gay-Lussac’s Law Directly proportional relationship between temperature and pressure Example- an oxygen cylinder left outside overnight will have a lower pressure reading in the morning due to temperature drop  

P1 / T1 = P2 / T2  

This is the gas law that explains the reason you need to add air to your tires in the winter colder temps lead to lower pressures  

Universal Gas Law (Ideal Gas Law) Relates the thermodynamics of temperature and barometric pressure in relation to altitude changes Boyle’s Law Charles’ Law Gay-Lussac’s Law The ratio between the pressure volume product and the temperature system remains constant  

P1V1 / T1 = P2V2 / T2  

Graham’s Law “Graham’s = Grape Jelly”

Law of Gaseous Diffusion “Gas exchange at the cellular level” The rate of diffusion of a gas through a liquid medium is directly related to the solubility of the gas and inversely proportional to the square root of its density Limits gas ability to move through liquid Example- O2 molecule traveling through surfactant versus CHF (plasma) or Pneumonia (mucus)   Gas Law

Action

Practical Application

Boyle's Law

⬆ Altitude = ⬇ Pressure = ⬆ Volume

With higher altitudes, gasses expand

Charles' Law

⬆ Temperature = ⬆ Volume

Air expands when hot. Best aircraft life in cold, dry air

Dalton's Law

Total Pressure = P1 + P2 + P3...

As altitude increases, partial pressure decreases. Supplemental O2 is needed

Fick's Law

⬆ Partial Pressure = ⬆ Oxygenation

Add FIO2 and PEEP, partial pressure and surface area increase, thickness of capillary membrane will decrease

Gay-Lussac's Law

⬇ Pressure = ⬇ Temperature

O2 tank pressure changes, colder at flight level

Graham's Law

⬆ Diffusion = ⬇ Molecular weight

Lower molecular weight can diffuse better (CO2)

Henry's Law

⬆ Pressure = ⬆ Gas Solubility

Diving adds pressure, when surfacing nitrogen comes out of solution

 

Oxygen Adjustment Calculation (FiO2 x P1) / P2 = FiO2 required for ascent FiO2= Fraction of inspired oxygen P1=       the pressure you are at (on the ground) P2= the pressure you are flying to (cruising altitude)  

Example: You have a patient on a mechanical ventilator at 0.5 FiO2 and you are at sea level. You will be flying to an altitude with a torr of 500. What will be the oxygen requirement at this pressure? 0.5 (760) / 500 = 0.76  

Altitude Effects A cold, dry, high altitude environment has the greatest negative outcome to your patient Every 1,000-foot increase in elevation causes temperatures to drop 2° C Temperature is inversely proportional to altitude Greatest amount of pressure changes occur closest to sea-level  

Barodontalgia (Teeth)

 

Occurs on Ascent Air trapped in fillings expands due to Boyles law Also referred to as “Aerodontaigia”  

Barotitis (Ears)

 

Occurs on Descent

Air trapped in the middle ear can't vent through the blocked Eustachian Tube Eustachian Tube Dysfunction This is why you MUST be able to Valsalva before flying (clearing your ears to equalize pressure) “Ear Block”  

Barosinusitis (Sinuses)

 

Can occur on BOTH Ascent and Descent Epistaxis common after rupture of sinus membranes “Sinus Block” Can also cause referred maxillary pain This is not the same as barodontalgia (occurs only on ascent)  

 

Decompression Sickness "The Bends" Related to Henry’s Law Normally excess nitrogen diffuses into the capillaries in a solution Rapid decrease in pressure causes nitrogen to leave as a gas There are actually 6 different types of DCS Only 2 types on exams  

Type I (Joint & Skin) Nitrogen related, painful joints (knees/shoulders), mottled skin, pruritic (itching) Patient may also feel like “ants are crawling on their skin” Cutis marmorata- mottled skin, can often look like a sunburn  

Type II (Neuro) Neurologic signs & symptoms (rapid ascending paralysis), hypovolemic shock Pulmonary “Chokes” symptoms include cough, hemoptysis (coughing up blood), dyspnea Ground transport is preferred for all diving injuries Can use pressurized fixed wing aircraft or fly 15) Waveform has 3 parts: P1: Percussion wave – Arterial pulsation P2: Tidal wave – intracranial compliance P3: Dicrotic wave – venous P2 - P3 Aortic valve Closing  

ICP Transducer placed at the Foramen of Monro  

Traumatic Brain Injuries Primary Brain Injury Contact phenomena injuries Acceleration-deceleration injuries

Secondary brain injuries Classified as insults of either systemic or intracranial origin Systemic: Hypoxia, hypercarbia, hypotension, fever, hyponatremia, anemia Intracranial: Hematoma, vasospasms, ICP, hydrocephalus, infection  

Skull Fractures Linear Fracture

 

Single fracture line Hematomas, soft tissue swelling, point tenderness. Linear Stellate Multiple fractures radiating from point of impact Open fracture at higher risk for infection  

Diastatic Fracture

 

Occurs along the suture line, causing a widening or separation Most often seen in infants or pediatrics  

Depressed Skull Fracture Direct trauma to the skull Classified as open or closed depending on if the dura mater has been breached Can lead to a Pneumocephalus if any of the sinus cavities are fractured Caution transporting Pneumocephalus patient by air  

Basilar Skull Fracture Often results from a blow to temporal, parietal, or occipital regions Blood migrating to mastoid region cause Battle sign, while migration to periorbital area referred to as raccoon eyes. May have CSF leaking  

Orbital Fracture

 

Potentially serious complication of the inferior rectus eye muscle becoming trapped Have the patient look up – if the injured eye does not move consensually and the patient is experiencing double vision, it is a surgical emergency  

Le Forte Fractures WATCH FOR AIRWAY COMPROMISE! Le Forte I Horizontal across the maxilla, maxilla and maxillary teeth are moveable Le Forte II Bridge of nose and around the mouth, usually from a downward blow to the nose Le Forte III Transverse Fracture, aka “Craniofacial Disassociation”  

 

 

Brain Injuries

   

Subdural Hematoma

 

“Venous Lakes” Tearing of the bridging veins to the subdural space Six times more common than epidural with a higher mortality Elderly and children highly susceptible Intraventricular hemorrhage has increased mortality  

Types:

Acute Signs/symptoms appear within 24 hours of injury Often seen with acceleration-deceleration injuries Subacute Signs/symptoms appear between 2 days and 2 weeks Chronic Signs/symptoms appear after 2 weeks  

Epidural Hematoma

 

Described as lenticular in shape Most are arterial in nature, as a result of a blow to the temporal region and concomitant disruption of the middle meningeal artery Loss of consciousness followed by a lucid interval May last minutes to hours Secondary rapid deterioration of consciousness Tentorial herniation may cause pupillary changes Increased pressure against CN III (Oculomotor) Increasing ICP may lead to other clinical manifestations Headache, vomiting, seizures, respiratory distress, Cheynestokes Respirations degrading to brainstem patterns, posturing  

 

Sub Arachnoid Hemorrhage

 

“Worst headache of my life” Starfish Pattern on CT Avoid lumbar punctures until CT scan complete Keep systolic B/P below 140mmHg  

Treatment: Treat with Nimodipine (Nimotop) Helps prevent cerebral vasospasm Persistent elevated blood pressure Nitroprusside (Nipride) or Nicardipine (Cardene)  

Diffuse Injuries Concussions Mild (grade 1)

No loss of consciousness May be accompanied by nausea, headache, confusion, and brief memory loss Symptoms typically last less than an hour Moderate (grade 2) No loss or very brief loss of consciousness Similar to grade 1 symptoms, but last between 30 minutes to a day Severe (grade 3) Unconsciousness followed by concussion symptoms Diffuse axonal injuries (DAI) (Coma) Often due to rapid acceleration-deceleration forces  

Increased ICP Clinical Features of Rising ICP

 

Decreased level of consciousness Pupil reaction Posturing Decorticate vs Decerebrate Changes in vital signs Cushing Triad  

Cushing’s Triad Arterial Hypertension Widened pulse pressures Bradycardia Respiratory Changes Depend on the level of brainstem involved Midbrain: Cheyne-Stokes respirations

 

Treatment of Increased ICP Positioning of patient Intubation and mechanical ventilation RSI and increase minute volume to maintain CO2 level of 3034 Signs of Herniation Consider Osmotherapy Mannitol or Hypertonic saline Barbiturates Consider corticosteroids, monitor for seizures, monitor glucose levels, and lab values  

Spinal Cord Injuries Causes Flexion-Extension Injuries Typically involve the cervical region C3-4-5 keep the diaphragm alive C5-C6 most susceptible Vertical Compression Rotation with Flexion  

Anterior Cord Syndrome

 

Incomplete SCI resulting from displacement of bony fragments into the anterior portion of the spinal cord Anterior cord carries pain and temp sensations as well as motor function Posterior cord carried vibration and touch and positioning (able to locate) Motor paralysis below the level of the insult with loss of pain and temperature sensation with preservation of proprioception.

 

Central Cord Injury

 

Often due to hyperextension injuries to cervical area Rarely associated with fractures or bone disruption Presents with greater loss of function in the upper extremities than in the lower extremities, with variable loss of sensation to pain and temperature  

Brown Sequard Lesion

 

Penetrating trauma accompanied by complete damage to all spinal tracts on the involved side.

Presents with motor loss, loss of sensation to touch, proprioception, and vibration on same side, and loss of sensation of pain and temperature on the opposite side.  

Spinal Shock Temporary local neurologic condition after spinal trauma Causes paralysis and absent reflexes Typically subsides within 24-72 hours  

Neurogenic Shock Temporary loss of sympathetic nervous system outflow Classic presentation: Hypotension Bradycardia Warm, Flushed, Dry below lesion Decreased Systemic Vascular Resistance (SVR) and lownormal heart rate SVR 220/120mmHg) Labetalol, Nitroprusside, Nicardipine Treat seizures with Lorazepam/ Fosphenytoin ELEVATE THE HEAD OF THE BED 30%

Neurologic Disorders Seizures Seizure Management Management dependent on the type of seizure: Petite mal seizures should be monitored Grand Mal and Focal seizures may require immediate action Etomidate for RSI will relax muscles if intubation is necessary Administer anticonvulsants if patient is actively seizing Ativan, Valium, Versed, Keppra Assess blood glucose levels  

Status Epilepticus One continuous, unremitting seizure lasting longer than 5 minutes Recurrent seizures without regaining consciousness between seizures for greater than 30 minutes  

Encephalitis Inflammation of the brain Often causes flu-like symptoms May progress to confusion, increased ICP, or seizures Most common cause of encephalitis in the U.S. is Herpes Simplex HSV-1 – treat with acyclovir (Valtrex)  

Myopathies

Progressive hereditary disorders such as Duchenne muscular dystrophy and myotonic dystrophy Complications include direct effect of muscle weakness to the respiratory system Abnormal respiratory drive, sleep-related breathing disorders, ineffective cough May quickly deteriorate to respiratory failure  

Myasthenia Gravis Chronic disorder of the neuromuscular junction that interferes with the chemical transmission of acetylcholine in voluntary muscles Commonly presents with weakness that improves with rest Patient may take Tensilon, corticosteroids or have a thymectomy. Acute respiratory failure common Increased risk of prolonged paralysis with NMBAs  

Guillain-Barré Peripheral nerve syndrome Presents with hyporeflexia, pain, and numbness Cause is unknown; often follows respiratory, GI infection, and lymphomas Increased risk of respiratory failure  

TRAUMA PATIENT MANAGEMENT Newton’s Laws of Motion

 

Newton’s First Law: Law of Inertia A body in motion remains in motion in a straight line unless acted upon by an outside force  

Newton’s Second Law Acceleration is dependent on mass of the object and the force upon the object  

Newton’s Third Law For every action, there is an equal and opposite reaction  

Types of Trauma Blunt Deceleration Shearing, rupture of body organs Penetrating Stab wounds Gunshot wounds High velocity weapons fire projectiles >2000 fps  

 

Triage

 

System of prioritizing patients based on injury severity START triage, JumpSTART, SALT Immediate Delayed Minimal Expectant  

 

SALT Triage (Sort, Assess, Lifesaving Interventions, Transport)

 

 

Trauma Scoring Systems

 

Glasgow Coma Score Revised Trauma Score Respiratory rate Systolic blood pressure GCS Survival probability Abbreviated Injury Scale (AIS) Sensitive to blunt injuries  

 

Trauma Triad of Death

 

Hypovolemic Shock Too little circulating blood within the vascular system HR increases SVR increases CO drops Cold extremities and worsening mental status Early fluid resuscitation and blood products  

 

Hypovolemic Shock – Classes of shock

 

Trauma Imaging

 

X Rays CT Scans Ultrasounds FAST/EFAST RUSH exam  

Injury Patterns - Kinematics of Trauma

Side Impact Rib fractures Splenic rupture secondary to rib fracture (+) Kehr’s Sign (referred pain) Hypovolemia Clavicular fractures Femur fractures  

Front Impact

Rib fractures Possible hemo/pneumothorax Possible Liver / Splenic Laceration Concussion, skull fracture

Dislocated hips Acetabular fractures  

Rear Impact

 

T12-L1 is the most common back injury T12 Fracture is also called a “Chance fracture” Increased chance of splenic injury C2 (Hangman’s) fracture also common  

   

Rollover Unpredictable injury pattern Possible C1 (Jefferson’s Fx) from axial loading Burst Fracture  

 

 

 

Lap Belt Injuries Lap belt injuries are evidenced by ecchymosis over the abdomen and chest High index of suspicion for internal injuries May present with Cullen’s sign due to peritoneal bleeding  

 

 

Motorcycle Crash

 

Energy is directly absorbed by the rider Head-on collisions Lower extremities Abdominal injuries Side Impact Leg/foot Open lower extremities fracture  

Off-road Vehicles

 

All-Terrain Vehicles (ATVs) Risk of ejection or rollover Clavicular fracture Sternal fracture  

Snowmobiles Most accidents involve striking an object Extremity fracture C-spine injury C2 (Hangman’s)  

Falls

 

Falls from 15-20 feet (or 3 x standing height) are associated with severe injury Children tend to fall head first Deceleration and compression injuries Calcaneus fractures (compression) Axial loading to the spine T12-L1 Bilateral wrist fractures FOOSH Colle’s Fracture (distal radius)  

Compression Fracture

 

Abdominal Trauma Splenic Rupture Most commonly injured solid organ in blunt trauma Often associated with MVC’s Potentially asymptomatic Abdominal tenderness or referred pain Positive Kehr’s sign Positive Ballance’s sign May exhibit signs of hemorrhagic shock  

Liver

Most commonly injured solid organ in penetrating trauma Extremely vascular        Risk of sheering in sudden deceleration  

Colon / Small intestine Most commonly injured hollow organ from penetrating trauma Significant risk for sepsis due to bacteria  

REBOA Resuscitative Endovascular Balloon Occlusion of the Aorta  

 

 

Pelvic Trauma

 

Pelvic Fracture Pelvic fractures result from significant force Possibility for other injuries Lateral pelvic fracture Rarely has life threatening bleeding Open-book fractures Anterior/Posterior force involved Vertical shear Highest potential for catastrophic hemorrhage  

 

Fat Embolism Increased risk associated with long bone and lower extremity factors Does not have to be a complicated fracture Patient may present with: Respiratory distress Petechial rash Diffuse infiltrates Hypoxemia Confusion Fever Tachycardia Genitourinary Trauma  

Genitourinary Trauma Involves the kidneys bladder, urethra and genitals Usually from blunt force trauma Common signs: Blood at the urethral meatus Blood in the labia/ scrotum (Coopernail’s sign) Pelvic fracture High riding or non-palpable prostate Urinary catheter is contraindicated  

Hematuria is the hallmark sign  

Coopernail’s Sign Scrotal or labial ecchymosis most often associated with pelvic fractures May also be related to abdominal bleeding  

Thoracic Trauma Pneumothorax Accumulation of air in the thoracic cavity, Blunt or penetrating trauma Spontaneous pneumo is from rupture of blebs Open pneumothorax Sucking chest wound Defect must be >2/3 of the diameter of trachea  

Tension Pneumothorax

Life-threatening injury Shift in mediastinum Clinical signs include dyspnea, anxiety, JVD, tachypnea, and tracheal deviation JVD and deviation are late signs Sudden increase in PIP/PPLAT indicates probable tension pneumo  

Initial treatment

Occlusive dressing if sucking chest wound Needle decompression Between 2nd and 3rd ICS Mid-Clavicular Line (MCL) 5th ICS Mid-Axillary Line (MAL) Always guide the needle over the top of rib Avoids neurovascular bundle  

Definitive Treatment Tube Thoracotomy 5th or 6th ICS Mid Axillary Line (MAL) Can use the Anterior-Axillary Line (AAL)  

Hemothorax

Accumulation of blood in the thoracic cavity Inferior Mammary Artery (IMA) Massive Hemothorax is defined as >1500mL of blood or 1/3 of patient’s blood volume Treat the same as a tension pneumothorax Document blood return  

Rib Fracture Can be diagnosed clinically based on history and presentation Ribs 1-3 Associated with head, neck, spinal cord injuries Ribs 10-12 Associated with liver and spleen injuries Treat with analgesics Ensure the patient takes deep breaths Prevents atelectasis Decreases risk for pneumonia Consider NPPV Provides a form of splinting from the inside

 

Flail Chest

Defined as 2 or more ribs broken in 2 or more places Paradoxical movement of flail segment Associated with pulmonary contusion Attempt to stabilize flail segment Transport injured side down Consider NPPV  

Traumatic Diaphragmatic Hernia

 

Associated with blunt force trauma from MVC Most commonly occurs on the left side

Right side protected by liver Bowels sounds auscultated during chest exam Scaphoid Abdomen Looks like an empty bowl  

 

Cardiac Tamponade Accumulated fluid around the heart either due to blunt or penetrating trauma >150mL of blood accumulation can be fatal Kussmaul’s Sign- Rise in venous pressure on inspiration spontaneous breathing patients  

Early Signs Pulsus Paradoxus Tachycardia Treat with IV Fluids to improve preload  

 

Late Signs Beck’s Triad ∆ Muffled heart tones Narrowed pulse pressure JVD Treat with pericardiocentesis  

Electrical Alternans Associated with cardiac tamponade Remember, the EKG is a “camera” In electrical alternans the heart is getting closer to and further away from the camera as it moves around inside the sac of fluid (pericardium)  

 

Tracheobronchial Disruption

Rare but life-threatening Most occur within 1.5” of carina Subcutaneous emphysema Hamman's Crunch

Crunching, rasping sound, synchronous with the heartbeat  

Traumatic Asphyxia

Severe, sudden crushing injury to the chest and abdomen Patient appears blue/purple in color Deoxygenated blood accumulates Not often fatal, as name implies Concurrent injuries are far more serious May cause a crush injury and associated rhabdomyolysis  

Rhabdomyolysis and Crush Syndrome Can be caused by Crush injuries Hyperthermia Excessive exercise Drugs The breakdown of muscle fibers that leads to the release of muscle fiber contents (myoglobin) into the bloodstream  

Rhabdomyolysis Damage causes: Influx of calcium and sodium into the cells Release of myoglobin into circulation Also releases lactate, uric acid, potassium, and phosphorus Extracellular hypocalcemia and hyperkalemia Peaked T waves on EKG, prolonged QT CK levels increase Treat with fluids, Bicarbonate, and Calcium if needed Follow hyperkalemia protocol if signs are present  

Facial Trauma Avulsed teeth Put in gauze soaked in NS, milk, or between the cheek and gum  

Tripod fracture

involves the zygoma Commonly at the zygomatic arch  

Hyphema blood in the anterior chamber of the eye Risk of increased intraocular pressure  

Damage Control Resuscitation (DCR) Fluid Resuscitation Fluids (either crystalloid or colloid) are used to bring up B/P in trauma (not vasopressors) Hypotension starts at 30% blood loss Fluid replacement ratio is 1:3 (blood loss to crystalloid fluid) 2 Large Bore IVs ATLS standards, remember that this test is not based on TCCC standards) Landmarks for femoral line insertion in the Femoral Triangle Lateral to Medial: Nerve, Artery, Vein, Lymph node (NAVEL)  

Tranexamic Acid

 

Synthetic antifibrinolytic agent Inhibits clots from breaking down to promote clotting Plasminogen Inhibiting plasminogen also reduces inflammation Loading dose of 1g during 10 minutes followed by an infusion of 1g during 8 hours  

 

Blood Products Packed RBCs (PRBCs)

Retains nearly all characteristics of whole blood 250mL of platelet-rich plasma removed Citric acid added as an anticoagulant Low 2,3-DPG Reduced risk of febrile reactions 70% of leukocytes removed ABO and Rh factor matching required (outside of initial O- transfusion)  

Platelets

Isolated from whole blood Indications Low platelet counts Bleeding due to thrombocytopenia Disseminated Intravascular Coagulation Massive transfusions Used in conjunction with PRBC transfusions Does not require ABO and Rh matching, but it is preferred  

Fresh Frozen Plasma (FFP)

Plasma that has had RBCs separated Primarily water, proteins, salts, and clotting factors Most useful for the clotting factors it contains Coagulation deficiencies Warfarin reversal FFP requires ABO compatibility Does not require Rh matching  

Citric acid may bind with calcium and cause hypocalcemia  

Cryoprecipitate (Cryo)

Created from FFP Contains Factor VIII, Factor XIII, von Willebrand Factor (vWF), Fibrinogen In trauma it is most often used to treat DIC Can also be used to treat Hemophilia and von Willebrand’s disease. Does not require ABO or Rh matching Preferred, along with same donor matching  

 

Transfusion Reactions Drop in blood pressure Fever Tachycardia Pallor        

Stop the transfusion if there is any adverse reaction  

Hemolytic Reaction Palpitations, abdominal/back pain, syncope, “sense of doom” Caused by ABO incompatibility Slow onset (45-90 minutes) Stop the infusion Keep urine output high (100ml/hr) Monitor  

Febrile Reaction Fever, flushing, palpitations Caused by bacterial lipopolysaccharides and anti-leukocyte antibodies Administer IV Acetaminophen (Ofirmev™) Infusion can continue if no other symptoms present  

Urticarial/Allergic Reaction Local erythema, hives, itching Administer IV Benadryl

Administration can continue unless other adverse reactions occur  

Anaphylactic Reaction Urticaria, pruritus, hypotension, tachycardia Caused by Anti-IgA antibodies Rapid onset (within 30 minutes of infusion) Stop the transfusion Epinephrine       Steroids Benadryl  

Transfusion Associated Circulatory Overload (TACO) Hypertension, distended neck veins Can occur at any time Stop the transfusion Administer Lasix More likely in those with kidney or cardiac disease  

Transfusion Related Acute Lung Injury (TRALI) Patient presents with dyspnea, tachycardia, fever, cyanosis Caused by a reaction to leukocyte antibodies in plasma portion of blood products Symptoms begin 1 to 6 hours after transfusion Leading cause of transfusion related death STOP THE TRANSFUSION Causes acute pulmonary edema

 

BURN MANAGEMENT Thermal Burns

 

Anatomy of a Burn Zone of coagulation Zone of stasis Zone of hyperemia  

Systemic Inflammatory Response of Burns

 

Burn Definitions 1st Degree or Superficial Sunburns 2nd Degree or Partial thickness Blisters 3rd Degree or Full thickness Completely destroyed tissue  

Estimation of Burn Size

 

Referral Criteria Partial thickness burns greater than 10% TBSA Burns that involve areas of function 3rd degree burns in any age group Electrical, Chemical, or Inhalation burns Concomitant trauma Preexisting medical disorders that delay healing Burned pediatrics without qualified pediatric personnel  

Burn Formulas Brooke 2ml x kg x BSA = fluids over 24hrs 1st half in 1st 8 hours from time of burn  

Universal/Consensus 2-4ml x kg x BSA = fluids over 24hrs 2ml x kg x BSA for adults, 3-4 ml x kg x BSA for pediatrics 1st half in 1st 8 hours from time of burn  

Parkland 4ml x kg x BSA = fluids over 24hrs 1st half in 1st 8 hours from time of burn  

General Burn Considerations Patients with burns >20% BSA can also have an adynamic ileus NG or OG tubes before flying Wet gas expansion due to third spacing Patients are in extreme pain Hypothermia Risk of renal failure and rhabdomyolysis, as well as electrolyte abnormalities (K and Na)  

Circumferential Burns Risk of compartment syndrome Edema in extremities may cause vascular compromise Chest burns Escharotomy Field use to preserve life or limb  

 

 

Electrical Injuries Voltage Low voltage 1000 volts  

Resistance Tissues with nerves, blood vessels and muscles Tendons, fat  

Type of pathway and current Duration and intensity of contact  

Type of Current Alternating Current (AC) Tetanic contraction that “freezes” victim to source Higher potential for Ventricular Fibrillation Tetanic chest muscle contractions Explosive exit wound  

Direct Current (DC) Able to pull away from current Asystole often results from depolarizing the entire myocardium Discreet exit wound  

Electrical Injuries

 

Flow path of electricity CNS injuries Tissue Necrosis Flexor crease burns Oral commissure burns 40° C (104° F) Patient often has respiratory alkalosis due to hyperventilation (blowing off CO2) With heat exhaustion there is no neurologic impairment Heat stroke is any heat injury with LOC change Patient doesn’t have to stop sweating to have a heat stroke Administer crystalloid fluids (NS/LR) for volume replacement (minimum 2 liters)  

Cold Emergencies Always begin treatment by removing patient from the environment Frostbite Hypothermia Core temperature below 95°F (35°C) Mild: 90-95°F (32.2-35°C) Severe: Below 90°F (32.2°C) Shivering is limited by glycogen stores Ceases at core temp below 32° C (89.6° F)  

Hypothermia Defined as a core temp below 35° C (95° F) Paradoxical undressing is a hallmark sign of hypothermia (due to delirium) Shivering is limited by glycogen stores (stops at core temp of 32° C / 89.6° F) Treat with passive external and active external rewarming first! Heated blankets, Hypothermia Prevention and Management Kit (HPMK), etc. If unsuccessful, treat with active internal rewarming Heated IV fluids, warming packs, GI lavage with warmed fluids, etc. IV fluids should be warmed to 39° C (102.2° F)  

After Drop

 

Return of cold blood to the core induced by external rewarming and peripheral vasodilation Dysrhythmia in hypothermia- caused by an increase in lactate and K+ levels Cardiac irritability begins at 33° C (91.4° F) “Osborn Wave”, “J Wave”, or “Hypothermia Hump” on EKG  

 

 

Drowning Hypothermia is always a concern Consider spinal immobilization Initiate ventilation Widespread atelectasis and pulmonary shunt possible Consider increased PEEP Treat bronchospasm with beta2 agonist Mammalian diving reflex Apnea Bradycardia Vasoconstriction to maintain cerebral perfusion  

Diving injuries and Decompression Sickness Diving Injuries All divers are subject to pressure effects Nitrogen dissolves into fatty tissues Displaces O2 in the brain Nitrogen Narcosis Expands during ascent Bends Boyle’s Law Divers should avoid flying for 12 hours after dive completion  

Decompression Sickness Type I painful, mottled skin, pruritic (itching) Type II Neurologic signs and symptoms, hypovolemic shock Pressurized cabins are preferred Rotor Wing: fly under 1,000 ft MSL  

Ground transport may subject patients to increased physiological stressors and worsen conditions  

Dive-Associated Barotrauma Ascent or descent Pulmonary Overpressurization Syndrome (POPS) ” Breath Holding”

Pneumothorax Subcutaneous or mediastinal emphysema Greatest pressure changes occur 4 feet below the surface  

Arterial Gas Embolism Patient presents with stroke-like symptoms May also have a cough and epistaxis nosebleed AGE requires immediate hyperbaric treatment Fly in a pressurized aircraft (fixed wing) or rotary wing 8200 feet (>2500 m) Headache Symptomatic

GI symptoms, dizziness fatigue or weakness, difficulty sleeping  

High Altitude Pulmonary Edema (HAPE) Onset occurs 2-4 days after rapid ascent              10,000 ft. Symptoms: Rales Tachycardia       Tachypnea Dyspnea at rest Fever Non-productive cough May have pink frothy sputum  

Image: www.mayoclinic.org

 

HAPE Treatment Descend Supplemental O2 Nifedipine Promotes pulmonary vasculature dilation Consider CPAP Portable hyperbaric therapy  

High Altitude Cerebral Edema (HACE) Considered a life-threatening emergency Mental status changes and/or ataxia after rapid ascent Often >12,000 ft. MSL Typically after 5 days at sustained high altitudes Occurs the latest of all altitude injuries Visual changes Paresthesia Mental status changes Coma  

Image: www.mayoclinic.org

 

HAPE Treatment Descend O2 if possible Dexamethasone Diuretics are not indicated Harmful alterations in fluid volume Hyperbaric therapy  

Toxicological Emergencies Ensure all safety concerns are properly addressed Utilize proper PPE Ensure patient is properly decontaminated to avoid additional exposures Consider laboratory assessments as diagnostic  

Acetaminophen (Tylenol) Most commonly ingested drug resulting in overdose Toxic signs and symptoms delayed Documentation of time/duration and amount ingested Rumack-Matthew Nomogram Useful for acute exposures, not those lasting hours of days Determines need for N-Acetylcysteine (NAC) Also known as Mucomyst or Acetadote  

 

Acetaminophen (Tylenol) Poisoning Stage 1 Flu Symptoms Stage 2 Liver injury develops Stage 3 Peak Liver enzymes Stage 4 Recovery if survivable  

 

Acetylsalicylic Acid Poisoning Aspirin overdose Nausea Vomiting Ringing in the ears (Tinnitus) Respiratory alkalosis Progresses to metabolic acidosis Can lead to Reye’s syndrome in pediatrics

Potentially fatal liver and brain damage Liver fails causing ↑ ammonia levels ↑ICP and possible encephalopathy Hepatic Encephalopathy Treat with Sodium Bicarbonate and dialysis (if needed)  

Benzodiazepine Overdose Valium, Ativan, Versed, etc Risk of profound CNS and respiratory depression Increases with ethanol, narcotic, or other sedative use Activated charcoal can adsorb orally ingested benzos Reversal Agent: Romazicon (Flumazenil) Pushing Romazicon too fast can lead to seizures Also works for Ambien  

Opioid Overdose Oxycodone, Norco, Fentanyl, Morphine, Demerol, Percocet, etc. Risk of profound CNS and respiratory depression Reversal Agent: Naloxone (Narcan) May precipitate severe, violent withdrawal symptoms Opiate’s half-life may exceed the half-life of Narcan May need to re-administer Remember the ½ life of the opioid is usually longer than the ½ life of Narcan Narcan ½ life approximately 45 minutes Use the lowest dose possible to avoid complete blockade of the opioid receptors (leads to a complete inability to control pain in the patient)  

Beta Blocker Overdose Labetalol, Carvedilol, Esmolol, Metoprolol Symptoms: Hypotension Bradycardia Conduction delays Hypoglycemia Bronchospasms Pulmonary edema Treatment Glucagon is the antidote 5-10mg IV bolus, followed by infusion at 1-5mg/hr in adults Increases Calcium concentration Consider atropine and/or cardiac pacing Treat hypotension with fluids May require vasopressor support  

Calcium Channel Blocker Overdose Amlodipine, Verapamil, Cardizem, Nifedipine Symptoms Hypotension Bradycardia Conduction delays Metabolic acidosis Hyperglycemia Calcium Chloride/ Gluconate is the antidote Activated charcoal for recent ingestions Consider atropine and/or cardiac pacing Treat hypotension with fluids

May require vasopressor support  

Cardiac Glycosides Digoxin Derived from Foxglove plant Flu like symptoms, visual disturbances Yellow / Green halos Risk of hyperkalemia Slurred upslope on QRS Normal finding on EKG Treat with Digibind (Digoxin Immune Fab) Avoid electricity (cardioversion, pacing, etc.)  

 

Dilantin Overdose Dilantin (Phenytoin) is used to treat and prevent seizures Symptoms Supraventricular tachycardia (SVT) Ventricular dysrhythmias Coma Confusion Tremors Dilantin overdose can cause Diabetes Insipidus (DI) like symptoms Supportive care Fluid resuscitation and O2 administration as needed

Severe overdoses consider gastric lavag  

Cocaine Overdose Shares similar toxic properties with most amphetamines Chest pain Hypertension Seizures Rhabdomyolysis Treatment is supportive Fluids Benzodiazepines Caution with β-Blockers  

Other illicit Drugs MDMA Risk of overheating, hyponatremia, serotonin syndrome, side effects if cut with other drugs Molly Ecstasy Jimson weed LSD PCP Treat with sedatives. Ketamine (for excited delirium) can worsen the situatio  

Tricyclic Antidepressant (TCA) Overdose Amitriptyline (Elavil), Nortriptyline (Pamelor) Patients with a TCA overdose often present with an anticholinergic-like toxidrome

Widened QRS on ECG along with prolonged QT intervals > 0.45 Sec  

 

Treatment If QRS is widened or patient is in a ventricular arrhythmia Treat with sodium bicarbonate Fluid boluses Maintain serum pH at 7.50-7.55 Add vasopressors for refractory hypotension Dialysis is not helpful DO NOT USE PHYSOSTIGMINE Cardiac arrest due to complete heart block  

Iron Overdose Typically from elemental iron supplements, common in children Antidote is Deferoxamine Vin rose urine Iron is cleared once urine returns to normal  

 

Alcohol Poisoning Drinking too much alcohol Hypoglycemia is common in alcoholics Pancreatitis Watch for Delirium Tremens Treat with Benzos Can still occur in intubated patients  

Toxic Alcohols Cause profound, lethal anion-gap acidosis (≥16) Ataxia Slurred speech Characteristics of ETOH Ethylene Glycol Antifreeze       Methanol Methyl alcohol, windshield wiper fluid, sterno Treatment Treat with IV/oral ethanol OR Fomepizole (Antizol) Metabolites cause central nervous system poisoning Consider hemodialysis to rapidly remove toxic alcohols Re-administer antidotes after dialysis  

 

 

Hydrocarbons Lamp oils, kerosene, lighter fluid, paint thinner, “huffing” Chemical pneumonitis Decreased viscosity causes aspiration DO NOT induce vomiting Consider intubation if CNS depression occurs  

Organophosphate Toxicity Cholinergic poisoning Presents with cholinergic toxidrome SLUDGE / DUMBBELLS Common in those who work with pesticides Treatment Atropine 0.5-2mg IV

Decreases airway secretions Pralidoxime 1-2 grams IV, or 600mg IM "2-Pam Crowbar" Pulls the organophosphate off the ACh If seizures are present, use benzodiazepines  

Anticholinergic Poisoning Drugs like Atropine Scopolamine (motion sickness) Dimenhydrinate (Dramamine) Diphenhydramine (Benadryl) Meclizine (Antivert) Promethazine (Phenergan) Cyclic antidepressants (TCAs) Treatment Patient presents with anticholinergic toxidrome Physostigmine (0.5-2 mg slow IVP) Do not to exceed 1 mg/min Atropine may be needed to reverse increased secretions  

 

 

Management of Poisonings and Overdoses Critical Care Transport Providers must ensure transport team safety Consult specialty resources Toxicologist Poison Control Center Reliable toxicology references Revert back to ABC’s  

 

 

 

Toxic Agent Alkalis Anticholinergics Aspirin (ASA) Benzodiazepines Beta Blockers Calcium Channel

Blockers Carbon Monoxide (CO) Cocaine Coumadin (Warfarin) Crotalinae (Pit Viper) Cyanide Digitalis Dilantin Ethylene Glycol Heparin/LMWH

(Lovenox) Hydrocarbons Hydrofluoric Acid Isoniazid (INH) Iron Methanol Opioids Organophosphates Tricyclic Antidepressants (TCAs) Tylenol  

 

Treatment/Antidote Copious Water Physostigmine Bicarb Flumazenil (Romazicon) Glucagon Calcium Gluconate Oxygen & Hyperbaric Chamber Benzodiazepines Vitamin K CroFab, FabAV Sodium Thiosulfate/Sodium Nitrite/ Amyl Nitrate Digibind/ Digoxin Immune Fab Supportive Care IV Ethanol or Fomepizole Protamine Sulfate Intubate Calcium Gluconate Pyridoxine (Vitamin B6) Deferoxamine (Desferal) IV Ethanol or Fomepizole Naloxone (Narcan) Atropine & 2-Pam Chloride Bicarb Mucomyst/Acetadote

OBSTETRICAL EMERGENCIES Physiologic Changes During Pregnancy Cardiovascular Cardiac output increases 20-40% Increased plasma and decreased vascular resistance Increase in pulse by 10-15bpm Blood pressure decreases 10-15 Systolic ECG Changes Axis deviation Inverted T waves  

Blood volume and composition changes Plasma and erythrocytes increase Dilutional Anemia Hematocrit value decreases Leukocytes Serum Albumin Clotting factors  

Respiratory changes Increased rate and minute volume Lower PCO2 – 30mmHg due to fundal height pH ranging from 7.40-7.47  

GI System

Delayed GI emptying increases risk for aspiration  

Endocrine Increased risk of insulin resistance  

Pregnancy Terms Preterm- before 38 weeks Full term 38-42 weeks Post Term- after 42 weeks Consider GTPAL assessment  

General Assessments Place patient in the left lateral recumbent position Check temperature Potential for sepsis Group B strep common Early treatment with Ampicillin and Gentamycin Blood pressure PIH, pre-eclampsia, eclampsia Oxygen saturation  

“DELS” Assessment Dilation Cervix dilates to allow passage of fetus through the birth canal 0 – 10 cm Considered fully dilated at 10cm (4 inches) Premature gestations may fit through a cervix that is not fully dilated  

 

Effacement Cervix will gradually soften, become shorter and thinner (cervical ripening) Normal is 2cm (0%) 1cm (50%)  

True Labor is when the patient has uterine contractions with cervical changes  

Lie Transverse Vertex Breech  

 

Station Fetal head in relation to the pubis symphysis Measured + or – in centimeters  

   

FETAL MONITORING Oxygen content of the fetus is lower than the pregnant woman Small reserves of oxygen Fetal heart rate sensitive to changes in oxygen Fetal heart rate is an indicator of fetal well being        FHR is between 120—160 BPM       Fetal movement after 28 weeks Continuous electronic monitoring should be used during high-risk transports Internal monitoring with scalp monitor External monitoring with Doppler Alterations in fetal heart rate correlates with fetal oxygenation Movement is a reliable indicator that the fetus is not acidotic  

 

 

Fetal Monitoring – Interpretation

 

Variability The single most important predictor of fetal well being Fetus neurologically intact Baseline Rate Accelerations Decelerations Changes and trends over time 10-15 bpm = normal variability  

#1 cause of poor variability- Fetal hypoxia  

 

 

 

   

Variability – VEALS CHOPE

 

Variable Decelerations Caused by cord compression during uterine contraction  

Onset to Nadir