FP-C Guide
FP-C Guide
Paramedic
Certification‐
A Comprehensive
Study Guide
© 2011 L. Kyle Faudree APA‐C, NREMT‐P, FP‐C
1 December 2011
FP‐C Study Guide ©2011 by L. Kyle Faudree
Night Stalkers Don’t Quit!
Rangers Lead The Way!
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FP‐C Study Guide ©2011 by L. Kyle Faudree
This guide is dedicated to
SFC Marcus V. Muralles
160th Special Operations Aviation Regiment (Airborne)
He was born October 5, 1971 in New Orleans, Louisiana, and was raised in Shelbyville, Indiana.
Muralles joined the Army in Dec. 1988 as an infantryman. After completion of Basic Combat
Training and Advanced Individual Training he was assigned to 3rd Battalion, 75th Ranger
Regiment, Fort Benning, Ga. After completing his initial enlistment obligation, he was assigned
to the inactive ready reserve in 1993.
In August 1998 he returned to the active duty and graduated One Station Unit Training at Fort
Benning in the summer of 1998. His first duty station was Company B, 3rd Battalion, 75th
Ranger Regiment as a medical administrator, platoon medic, and company senior medic. In
August of 2003, Muralles was assigned to 3rd Battalion, 160th Special Operations Aviation
Regiment (Airborne) as an aerial flight medic.
His military schools include: Special Operations Medic Course (SOMED), the Basic Airborne
Course, the Ranger School, the Primary Leadership Development Course, The Jumpmaster
Course, National Registry EMT-Paramedic Course, The Basic Noncommissioned Officer
Course, and the Advanced Noncommissioned Officer Development Course.
Muralles’ military awards and decorations include the Meritorious Service Medal, the Army
Commendation Medal, the Army Achievement Medal, the Good Conduct Medal, the National
Defense Service Medal, the Armed Forces Expeditionary Medal, the Humanitarian Service
Medal, the Iraq Campaign Medal, the Afghanistan Campaign Medal, the Global War on
Terrorism Expeditionary Medal, and the Global War on Terrorism Service Medal. His badges
include the Expert Infantry Badge, the Combat Medical Badge, the Expert Field Medical Badge,
the Aviation Badge, and Master Parachutist Badge with two combat jumps and the Ranger Tab.
He was posthumously awarded the Bronze Star Medal, the Purple Heart, the Meritorious
Service Medal, the Air Medal for valor, and the Combat Action Badge.
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FP‐C Study Guide ©2011 by L. Kyle Faudree
Table of Contents
SECTION
PAGE
Acknowledgements 5
Disclaimer
6
Pass the test! 7‐9
Arterial Blood Gas Interpretation 10‐13
Burn Management
14‐15
Cardiac Critical Care 16‐39
Advanced Airway 40‐42
Respiratory Management
43‐48
Obstetrical Emergencies 49‐57
Neurological Emergencies 58‐62
General Medical Emergencies
63‐68
Pediatric Emergencies 69‐72
Neonatal Emergencies
73‐76
Environmental Injuries/Toxicology
77‐82
Flight Physiology 83‐86
Safety /CAMTS 87‐91
Trauma
92‐98
Recertification 99‐102
References 103‐105
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Acknowledgements
The author would like to thank following professionals for their
comments and suggestions:
Brock Benedict, D.O., FP‐C
Derek Carlson, D.O., FACEP, FP‐C
John Dobbins, NREMT‐P, FP‐C
Brandi Faudree, APA‐C, FP‐C
Scott Fisher, APA‐C, NREMT‐P, FP‐C
B.A. Graham, FP‐C, CCP‐C
Rick Hammersfahr, M.D., FP‐C
Mark Jacques, M.D., MPH, FP‐C, CCP‐C
Rob Kiely, NREMT‐P, FP‐C
Noah McPike, J.D.
Mandi Stowers, MBA
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FP‐C Study Guide ©2011 by L. Kyle Faudree
DISCLAIMER
This is document is not to be electronically altered, distributed, copied by any
means, or otherwise reproduced without the written permission of the author.
This document is protected under U.S. Copyright law. This document is for
reference use only and does not imply any level of medical competency. The
accuracy and completeness cannot be guaranteed. Any medical procedures
performed must be done so after individual accreditation and credentialing by
local medical authorities. The author accepts no liability of any medical
procedures performed. The Flight Paramedic Certification Guide ©2011 is an
independent publication and has not been authorized, sponsored, or otherwise
approved by BCCTPC Inc.
The opinions or assertions herein are the private views of the author and are
not to be construed as official or as reflecting the views of the U.S. Army Special
Operations Command, the Department of the Army, or the Department of
Defense.
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FP‐C Study Guide ©2011 by L. Kyle Faudree
Study Effectively!
When studying for this exam (or any other exam) remember that your brain can only absorb so
much material at a time. Adults learn best through repetition. Read a section, read it again, then move
on. Do not read several sections at once until you are doing a final review just before your test. When
studying, do so for no more than 50 minutes, and take a 10 minute break. Most knowledge is retained
during the first and last 15 minutes of each study session. This theory has been proven through many
studies of adult learning. Studying more does not mean studying effectively. Below are sample figures
for average test scores among a large group of selected test takers. It represents several preparatory
courses with varying lengths and test taking strategies. I recommend you go to the BCCTPC website
(www.bcctpc.org) for a list of review and renewal courses available. Pick one that best fits your needs
and schedule, prepare for it, then pass the FP‐C examination!
Respiratory
Ventilator Settings
Ventilator Settings
Vt (Tidal Volume) = 6‐10cc/k
Practice!
The minimum score required to pass the FP‐C exam varies based on the version taken, but is
normally around 75% (depending on the version of the exam). The FP‐C exam does not test the basic
Paramedic skill sets to include ACLS, PALS, etc. This exam is a test of critical care knowledge in the
rotary and fixed wing aviation environment. You should take an ACLS and PALS refresher within 6
months of taking an FP‐C prep course to refresh your memory. This certification guide covers materials
presented in FP‐C review courses and the material you will be tested on. Very little of the information in
this manual is “reference only,” nearly all of it must be memorized to pass the exam.
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FP‐C Study Guide ©2011 by L. Kyle Faudree
FP‐C Exam Question Breakdown
Trauma Management 9
Aircraft Fundamentals, safety and survival 12
Flight Physiology 10
Advanced Airway Management Techniques 5
Neurological Emergencies 10
Critical Cardiac Patient 20
Respiratory Patient 10
Toxic Exposures 6
Obstetrical Emergencies 4
Neonates 4
Pediatric 10
Burn Patients 5
General Medical Patient 16
Environmental 4
TOTAL 125
Take as many practice questions as possible. You only get faster by running faster, stronger by
lifting heavier weights, or better at taking tests by answering more sample test questions. When taking
my FP‐C course you will take two 135 question tests modeled after the BCCTPC exam. The first one is
taken before the class begins, and the last one is taken on the final day of the course. My course
typically has a higher pass average (around 80%) than the national pass average (62% in 2010). This is
because my students take a lot of practice questions!
If you find that you are unable to do the above mentioned strategies by yourself, find a study
partner. BE SELECTIVE! Again, no points for failing. A study group should be three people or less
(I recommend two people). If you have too many people in your study group it turns into a time to talk
about things other than the material. When asking questions to your partner ensure that he or she can
answer the question with understanding. This will be very useful when taking the exam and test stress
kicks in.
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FP‐C Study Guide ©2011 by L. Kyle Faudree
PASS THE TEST!
When taking this exam you must use a good test taking strategy. There are two ways to take
the test; paper or electronic based. If you are more familiar and comfortable with taking paper tests,
choose this method. It will require a little more work for you to find a testing site (can be found on the
BCCTPC website). You will also have to wait at least 3 weeks to get your results. If you are more
comfortable with computer based testing, I recommend the online version. This also needs to be
coordinated with the BCCTPC office, however it can be done at most major cities with approved testing
centers. This test method also allows you to receive your results within 24‐48 hours. In the event you
do not pass the exam, you must wait 30 days to retake it.
The strategy is simple. Remember that there are NO points for finishing first, and no one
impressed when you fail first. Take your time, you have 2 ½ hours to complete the exam. YOU ARE
ALLOWED TO USE A SIMPLE CALCULATOR ON THE TEST! Do not look at more than one question at a
time, and if taking the computer test only one question will be on the screen at a time. If you are taking
the paper test I recommend you take one of the pieces of note paper you are given and cover up the
rest of the questions. Cover the entire page, and only expose the question. Read it carefully! Pay
special attention to words like “always, never, is not, are, false, true, etc.” These words that are often
overlooked when stressed from test taking and will cause you to miss a question. Once you have read
and understand the question, uncover the answers. This is a multiple choice test with 4 to 6 possible
choices with only one correct answer.
You should use an elimination strategy when taking multiple choice tests. This is done by looking at the
possible answers and crossing off the ones you are sure don’t answer the question correctly. If there
are two similar answers, there is a good chance that one of them is the right one. If you have no idea
what the answer is, pick “C.” This is so you are consistent in your guessing, which will give you a better
statistical chance of guessing right.
If you are sure of your answer, go with it. DO NOT CHANGE YOUR ANSWER ONCE YOU CIRCLE
IT! The only reason to change answer would be that you are absolutely sure you answered something
wrong. You will almost always be wrong if you change your answer, study after study has proven this.
Move to the next question.
Take 5 minute breaks during the test! This can either be done during the test while sitting at
your desk or you can leave the room to clear your mind (I recommend you leave the room). I have
heard the story “I knew the material” more times than I can count, usually when that person is telling
me they failed some exam. It is often true that people who know given material fail tests because they
are “bad test takers.” This is why you need to use a good test taking strategy!
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FP‐C Study Guide ©2011 by L. Kyle Faudree
ABGs (Arterial Blood Gasses)
pH 7.35 – 7.45 (percentage of Hydrogen)
[technically pH is an inverse log of hydrogen ions]
CO2 35‐45 (Carbon Dioxide)
HCO3 22‐26 (Bicarbonate)
PaO2 80‐100 (Plasma concentration of Oxygen)
SaO2 >95% (Hemoglobin concentration of Oxygen)
BE ‐2 to 2 (Base excess)
CRITICAL ABGs (INTUBATE) pH <7.2, CO2 >55, or PO2 <60
Note‐ Blood gasses are worthless without K+
Interpreting ABGs
1. Is it Acidosis or Alkalosis?
<7.4 ACIDOSIS >7.4 ALKALOSIS
2. Is it Respiratory or Metabolic in nature?
Respiratory
CO2 (Carbon Dioxide) is an Acid, so more CO2 makes the ABG more acidotic (moves left)
Technically CO2 is not an acid. CO2 combines with H2O to form H2CO3 (Carbonic Acid)
which is an acid. This makes CO2 a reliable indicator of acidosis.
Metabolic
HCO3 (Bicarb) is Basic, so more HCO3 makes the ABG more Alkalotic (moves right)
3. Is it Compensated or Uncompensated?
Is the pH < 7.35 or > 7.45
If PaCO2 and HCO3 are moving in opposite directions, it is partially compensated.
If pH, PaCO2 and HCO3 are moving in the same direction, it is a mixed disturbance.
0 ACIDIC 7 Neutral 14 BASIC
CO2 Human pH 7.35‐7.45 HCO3
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Acid‐Base Disorder Primary Change Compensatory Response
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Respiratory Alkalosis/Acidosis
CO2 regulation is a function of MINUTE VOLUME (tidal volume (Vt) x respiratory rate (F))
Assess for excessive tidal volume
Peek inspiratory pressure (PiP)
Plateau pressure (<30) (PPLAT)
Absence of hypocapnea (low CO2 levels)
Remember that CO2 moves >20 times faster than O2
Respiratory Alkalosis
pH > 7.40 CO2 <35
This is a result of alveolar hyperventilation
Increased pH, decreased CO2 (<35)
Often caused by ASA poisoning (respiratory center stimulant), or Hyperthermia (heat injuries,
hypermetabolic states, fever)
If on a ventilator, check tidal volume first, then rate (Vt‐ volume, F‐ rate)
Respiratory Acidosis
pH < 7.40 CO2 >45
This is the result of a failure to remove CO2
Causes include: chest wall injury, CNS depression, lung injury
Decreased pH, Increased CO2 (>45)
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Anion Gap Acidosis
Sodium (+), Chloride (‐), and Bicarb (‐) are added together
If ≥16 the patient has an anion gap metabolic acidosis
The worse the gap (indicated by a larger number), the worse the acidosis
“Profound Anion Gap Acidosis” – Causes below
“MUDPILES”
Methanol (Alcohol poisoning)
Uremia (Kidney failure)
DKA (Diabetic Ketoacidosis)
Propylene Glycol (Liquid agent used in Diazepam/Lorazepam)
Isoniazid (INH)/Iron (Tuberculosis medication/Iron supplements)
Lactate (From anaerobic metabolism)
Ethylene Glycol (Antifreeze)
Salicylates (Aspirin)
Treatment
Ventilation must be secured before treatment (then treat the underlying cause)
Bicarb as a life sustaining rescue strategy if pH <7.0 (treat the underlying cause first)
If the patient has a high anion gap acidosis with an unknown cause, treat with Narcan and Flumazenil
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Burns (5)
Burn Formulas
Brooke 2cc x kg x BSA = fluids over 24hrs (1st half in 1st 8 hours from time of burn)
Universal 2‐4cc x kg x BSA = fluids over 24hrs (1st half in 1st 8 hours from time of burn)
Also called the “Consensus Formula”
Parkland 4cc x kg x BSA = fluids over 24hrs (1st half in 1st 8 hours from time of burn)
Parkland is the preferred formula
Lactated Ringers is the preferred fluid
The face is 4 ½ % BSA in the adult
Only count 2nd and 3rd degree burns
“Palmer Method” ‐ The palm represents 1% BSA in both adults and children
Average urine output for an adult is 30‐50ml/hr
Synthetic Material Fires
Fires involving the combustion of cellulose, nylon, wool, silk, asphalt, and polyurethane increase the
risk for hydrogen cyanide poisoning
Histotoxic hypoxia
Cyanide is released during the incomplete combustion of products such as plastics and acrylics
(carpet)
Cyanide poisoning is treated with Sodium Thiosulfate and Amyl Nitrate
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FP‐C Study Guide ©2011 by L. Kyle Faudree
Electrical Injuries
Predictors of severity = Voltage and Amperage (amperage is a better predictor)
Low voltage <1000 volts
High voltage >1000 volts
Resistance of internal body structure and tissue (dense parts of the body resist injury better)
Type of pathway and current
Duration and intensity of contact
Alternating current (A/C) will allow the victim pull away from the current
Direct Current (D/C) will cause continual muscle contractions
Victim will be UNABLE TO PULL THEMSELVES AWAY!
In the setting of hemochromogen or myoglobinuria, maintain a urine output of 100ml/h in
order to perfuse the kidneys and prevent renal failure
Most likely cause of death in electrical injuries is cardiac insult
Flexor crease burns are the hallmark of true conductive injury
Chemical Burns
Acids
Cause coagulative necrosis
Dilute with copious amounts of water
Neutralize hydrofluoric acid with calcium gluconate
Alkalis “Alkali = Liquefy”
Dehydrate cells causing saponification (liquefaction necrosis)
Dilute with copious amounts of water
WORSE THAN ACID BURNS
Inhalational Burns
CO intoxication causes asphyxiation
Hypemic hypoxia
Accounts for as much as 80% of fatalities from inhalation injury
CO causes false high SPO2 readings (get an ABG)
Supraglottic injury results from thermal insult
Treat with high flow 02, corticosteroids, supportive care
Infraglottic injury results from chemical insult
Treat with high flow 02, corticosteroids, supportive care
Hyperbaric chamber if available
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FP‐C Study Guide ©2011 by L. Kyle Faudree
Cardiac (20)
CO (Cardiac Output) = HR x SV (4‐8L/min)
By coincidence 4‐8L/min is also the normal minute volume
SV (Stroke Volume) is affected by preload/afterload/contractility
Preload ‐ the load that stretches cardiac tissue BEFORE contraction
Amount of blood returned to the right heart from the body
Amount of blood returned to the left heart from the lungs
Afterload ‐ the degree of vascular resistance to ventricular contraction
Right heart afterload is affected by the pulmonary arteries
Left heart afterload is affected by systemic vascular resistance (SVR)
Heart Sounds
Normal Heart Sounds
S1 “Lub” (bicuspid/tricuspid valve closure)
S2 “Dub” (aortic/pulmonic valve closure)
Abnormal Heart Sounds
S3 “Kentucky” Caused by the excess filling of the ventricles
Causes: CHF, chordae tendineae (heart string) dysfunction
S1 “Ken”
S2”Tuck”
S3 “Y”
S4 “Tennessee” Blood being forced into a stiff (non‐compliant) ventricle
Causes: Hypertropic cardiomyhopathy, HTN
S4 “Tenn”
S1”E”
S2 “Ssee”
Murmur Grading: Grade I – Barely Audible, Grade VI– Loud
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Auscultation Points
Aortic
Pulmonic
Erb’s (Aortic Insufficiency)
Tricuspid
Mitral
“APETM”
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Coronary Circulation
RCA (Right Coronary Artery)
Right Marginal (supplies inferior left ventricle)
Posterior Descending (supplies posterior Left ventricle in 55% of population)
LCA (Left Coronary Artery) “Widowmaker”
CX (Circumflex) supplies lateral Left ventricle/ posterior left vent in 45% of population
LAD (Left anterior descending)‐ supplies anterior left ventricle/ anterior septum
Acute Coronary Syndromes
STEMI
(ST Segment Elevation Myocardial Infarction)
“Cardiac death happening now”
ST Segment elevation in 2 contiguous leads >2mm
New onset LBBB – (downward deflection in V1)
(+) Positive cardiac markers
Partial artery occlusion causes depression (Ischemia/Angina), full occlusion causes elevation (STEMI)
Non‐STEMI
ST Depression or dynamic T wave changes in 2 contiguous leads
o ST Depression is caused by a lack of O2 to cardiac tissue (either occurring now or due to an old
infarct)
(+) Positive Cardiac enzymes
Unstable Angina
Angina that is not relieved by rest, nitro, or is different quality that the patients ”normal” chest pain
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Progression of EKG changes in AMI
Hyperacute T waves
ST Elevation (Injury)
Q waves (Necrosis)
ST Depression (Ischemia)
Cardiac Enzymes
Troponin I most sensitive and specific for MI
Creatinine Kinase (CK) not specific
Creatinine Kinase Myoglobin (CK‐MB) not specific
Myoglobin not specific
Cardiac Panel= Troponin, CK, CK‐MB
This panel is run at set intervals (based on local facility protocols)
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Inferior MI
(RCA)
Papillary muscle “heart strings” dysfunction
GET A RIGHT SIDED EKG! (RV4)
EKG changes in II, III, AVF
Can cause Bradycardia, 1°,2° AV Block
No nitro or β blockers!
Treatment ‐ 2L fluid challenge
Posterior MI
(LCX or RCA)
Reciprocal EKG changes in V1 – V4 (Reciprocal change = ST Depression)
ST depression predominantly in V1, V2
Anterior MI
(LCA)
EKG changes in V2, V3, V4
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Anteroseptal MI
(LAD)
Left ventricle and septum affected
Papillary muscle dysfunction‐ leads to cardiogenic shock
EKG changes in V1,V2,V3,V4
Lateral MI
(LCX)
Lateral/Posterior Wall, EKG changes in V1, V5, V6, AVL
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Summary of EKG Changes
I Lateral aVR V1 Septal V4 Anterior
II Inferior aVL Lateral V2 Septal V5 Lateral
III Inferior aVF Inferior V3 Anterior V6 Lateral
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Wolff‐Parkinson‐White Syndrome
Heart condition in which there is an extra electrical circuit in the heart. Causes tachycardia.
One of the most common causes of fast heart rate disorders in infants and children.
Treated by surgical ablation of the errant pathway
Causes a "delta wave" on EKG (see red arrow)
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Bundle Branch Blocks
Only V1 changes are present
Widened QRS (>0.12 sec)
Right BBB ‐ Amplitude up (Just like the turn signal on your car)
Left BBB ‐ Amplitude down
Associated with STEMI! (Just like the turn signal on your car)
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Angina
Stable‐ Discomfort /Pain lasts 1 to 5 minutes, relieved by rest, nitro, predictable course
Unstable‐ Stable angina that has changed, lasts >10 min, not relieved by rest or nitro
Variant (Prinzmetals).
Chest pain at rest, has a circadian rhythm, relieved with nitro
Most often seen in women, most commonly at night
Treated with Calcium channel blockers (CCBs)
Silent‐ no pain, but objective evidence of ischemia on EKG (ST depression)
Antidysrythmics
Class I Sodium Channel Blockers
Lidocaine, Phenytoin, Procainamide
Class II β Blockers
Carvedilol, Labetolol, Propanolol, Timolol, Esmolol, Metoprolol
Class III (Misc)
Amiodarone
Class IV Calcium Channel Blockers
Verapamil, Diltiazem
Class V
Adenosine, Digoxin
Cardiac Drugs
↑ SVR: Dopamine, Neo‐synephrine, Epi, Levophed
NorEpi (Levophed) ‐ used for patients in profound hypotension
↓ SVR : Nitroprusside, High Dose NTG, CCBs, ACEi, α Blockers, Dobutrex, Natrecor
Nitroprusside (Nipride) ‐ reduces preload and afterload by dilation (can cause cyanide
toxicity)
THIS IS NOT THE SAME AS NITROGLYCERIN!
↑ Preload: Vasoconstrictors, fluids
↓ Preload: Morphine, Lasix, Nitro
“Other” Cardiac Drugs
β Blockers‐ Reduces heart rate, reduces cardiac oxygen demand
Do not use if patient has a heart block
Nicardipine – reduces afterload (does not cause cyanide toxicity)
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Miscellaneous
Properly performed CPR is = 20% of normal Cardiac Output
Tricyclic anti‐depressant overdose (TCA) causes a prolonged QT interval
Cause of dysrhythmia in hypothermia ‐ increases in both lactate and K+ levels
AMI Treatment
Reduce Preload (“MONA”)
Reduce HR/O2 demand (β Blockers/CCBs)
Clot Prevention (ASA/G2B3A)
Reperfusion (Chemical or Surgical)
“MONA”
Morphine, Oxygen, Nitro, ASA (Aspirin)/GP2B3A (examples‐ Reopro, Integrilin, Aggrastat)
β Blockers
Not used in bi fasicular blocks or BBB
Heparin/Low Molecular Weight Heparin (Lovenox)
Prevents fibrinogen conversion to fibrin to decrease clot formation in the coronary arteries
ACEi and Plavix within 24hrs (+/‐ Statin therapy)
Fibrinolytics
(Chemical Reperfusion, breaks the clot)
Indications
Clinical presentation consistent with AMI within 12hrs of sx onset
EKG showing ST elevation (STEMI) in ≥2 leads or new onset LBBB
Absence of contraindications
Absence of cardiogenic shock
Absolute Contraindications
Prior intracranial hemorrhage (ICH)
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischemic stroke within 3 months
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding menses)
Significant closed‐head trauma or facial trauma within 3 months
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Relative Contraindications
History of chronic, severe, poorly controlled hypertension
Severe uncontrolled hypertension on presentation (SBP >180 mm Hg or DBP >110 mm Hg)
Traumatic or prolonged (>10 min) CPR or major surgery less than 3 weeks
Recent (within 2‐4 week) internal bleeding
Non‐compressible vascular punctures
For streptokinase/anistreplase ‐ Prior exposure (more than 5 days ago) or prior allergic
reaction to these agents
Pregnancy
Active peptic ulcer
Current use of anticoagulant (Warfarin, Heparin, Lovenox, etc.)
Surgical Reperfusion
PTCA
Percutaneous Transluminal Coronary Angioplasty “Cardiac Cath”
Keep the leg straight during transport and for 30 minutes after cath removal
Administer G2B3A inhibitors
CABG
Coronary Artery Bypass Graft “Cardiac Bypass”
RCA (Right Coronary Artery)‐repaired using the Saphenous Vein
LAD (Left Anterior Descending)‐ repaired using the Inferior Mammary Artery (IMA)
Used for multiple vessel disease, Left main artery disease
Neurovascular System
α1‐ Vasoconstrict
β1‐ increase HR, contractility Reminder: 1 heart (β1)
β2‐ Dilate bronchioles/ Blood Vessels 2 lungs (β2)
Dopaminergic – gut kidney vessel dilation
Cholinergic – decrease HR
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Endocarditis
Sudden onset infection with NEW MURMUR
#1 cause is IV Drug abuse
Osler Nodes (painful red fingertips)
Janeway Lesions (red lesions on the palm and soles)
Often treated with IV antibiotics and sometimes heart valve replacement if damage is severe enough
Congestive Heart Failure (CHF)
Most common cause of right heart failure is left heart failure
Patient presents with progressive dyspnea, coughing up frothy sputum, etc
Butterfly pattern/ Kerley B Lines, Heart >50% width of the chest on CXR
ANP (Atrial Natriuretic Peptide) increase on bloodwork. BNP is released by the ventricles in response to
stretching and causes diuresis, reduced preload and reduced afterload
Treatment
Nitro is the most important drug therapy (high dose)
CPAP/BiPAP is often used to decrease work of breathing (WOB)
ACEi (Angiotensin Converting Enzyme inhibitor) to prevent ventricular remodeling (Enalipril, Captopril)
Lasix, β blockers (Carvidolol)
”Bilateral Diffuse Infiltrates” “Heart >50% width of chest”
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Pericarditis
Substernal chest pain when breathing or laying supine (pericardium rubs against the sternum)
Uremic Pericarditis: Can be seen in the patient that has just undergone dialysis because the
patient is in renal failure
Dressler’s Syndrome: pericarditis occurring in the post MI / post cardiac surgery patient
Global ST Elevation (see EKG below), rounded T waves
Also known as diffuse ST Segment elevation
Treated with NSAIDS (usually Indocin)
Aortic Dissection
Described as a “Ripping or Tearing” sensation between the shoulder blades (needs pain control)
Pain can also present in the chest or abdomen, still described as “ripping or tearing”
Common with Marfan’s syndrome
Ascending Aorta most common site of dissection
CXR shows widened mediastinum, loss of aortic knob, pleural effusion
Treat with β Blockers (Labetolol), Vasodilators (Nitroprusside)
DO NOT USE NITROPRUSSIDE FIRST BECAUSE IT CAUSES REFLEX TACHYCARDIA!
Pain meds
Morphine, Fentanyl
Restrict fluids unless hypotensive
Be aware that the treatment protocol for a Hypertensive Crisis is Labetolol and Nitroprusside
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Aortic Aneurysm
NOT THE SAME AS DISSECTION!
Aneurysm is an “outpouching” of either the cardiac aorta or the abdominal aorta
Typically found on routine CT scans for other medical problems or during physical exam (abdominal
aorta palpation >5cm).
Surgically repaired when >5cm, or symptomatic
Peripheral Vascular Disease (PVD)
Deep Venous Thrombosis (DVT)
Virchow’s Triad∆ Reminder: Virchow=Venous
Loss of vein integrity
Stasis (long seated ride, hospital bed)
Hypercoagulable state (cancer, pregnancy, etc)
Aching pain, WARM, red, and swollen
(+) Homan’s sign – dorsiflexion of the foot and constriction of the calf causing calf pain
Treated with Lovenox or Coumadin
Arterial Occlusion
Usually embolic (from DVT or clot in the heart)
COLD Limb
6 P’s
Pulselessness (late finding)
Paralysis (late finding)
Paresthesia
Pain (early finding)
Pallor
Poikilothermia (“cold blooded”)
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Hypertensive Urgency/Emergency
Hypertensive Urgency
Condition where a patient has extremely elevated blood pressure with NO signs or symptoms of end
organ damage
Blood pressure should be lowered slowly
Not an emergency (yet)
Hypertensive Crisis/Emergency‐
Condition where a patient has extremely elevated blood pressure WITH signs and symptoms of end
organ damage
Headache, Nausea/Vomiting, Visual Changes
Creatinine/RBCs in Urine
Treatment:
Lower B/P no more than 25% per hour, and no lower than patients “normal” pressure
Labetolol, Nitroprusside
Heart Transplant
If a heart transplant patient is decompensating, immediate cardioversion is indicated
Dopamine and Normal Saline fluid bolus should be used in the setting of bradycardia
Can also use Neosynephrine (sympathamometic)
DO NOT USE ATROPINE (It won’t work)
Pulmonary Artery Catheter
(Monitored with a Swann Ganz Catheter)
A Swan‐Ganz catheter is used to measure how much pressure blood is under when it goes into the
pulmonary artery. It also provides measurements of right heart afterload and left heart preload. A
pulmonary artery catheter and Swann‐Ganz Catheter utilize the same vascular access site.
Distal tip is used to measure pressures
Do not exceed 1.5cc air in distal cuff
Do not take wedge pressure readings for >15 seconds or 3 breaths
Take readings at the end of exhalation
PA port only for monitoring /lab sample blood draw (not fluid resuscitation)
When transporting a patient with a PA catheter, deflate the balloon to prevent an
inadvertent wedge pressure.
This is because the balloon size increase at altitude due to Boyle’s Law
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Hemodynamic Monitoring (Swan‐Ganz Catheter)
NORMAL VALUES
CVP (Central Venous Pressure)
2 to 6 mmHg
Measures right heart preload
RV (Right Ventricular pressure)
15‐25mmHg systolic
0‐5 mmHg diastolic
PA (Pulmonary Artery pressure)
15‐25mmHg systolic
8‐15 mmHg diastolic
PAWP (Pulmonary Artery Wedge Pressure)
8‐12 mmHg
Measures left heart preload
CO (Cardiac Output)
4‐6 L/min
Coronary Perfusion Pressure (CPP)
DBP‐PCWP
50‐60 mmHg
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PULMONARY ARTERY WAVEFORM
PA (Pulmonary artery pressure)
15‐25mmHg systolic
8‐15 mmHg diastolic
Dicrotic notch on the right side
”High Amplitude Waveform”
CORRECT
”High Amplitude Waveform”
RIGHT VENTRICULAR WAVEFORM
Right ventricular pressure
15‐25mmHg systolic
0‐5 mmHg diastolic
Inflate the cuff with 1.5 cc of air, have the patient cough, lay them on their side
This waveform may or may not have a Dicrotic notch
”High Amplitude Waveform”
INCORRECT
”High Amplitude Waveform”
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“Wedge Waveform”
“PAWP” (Pulmonary Artery Wedge Pressure)
Wedge pressure = 8‐12 mmHg (Left heart preload)
This waveform is caused by a blockage of the pulmonary artery by inflating the distal balloon. This is
what allows the machine to get a “PAWP” (Pulmonary Artery Wedge Pressure)
Low amplitude rolling waveform
“Low amplitude rolling waveform” of a correctly placed and inflated balloon to obtain a “PAWP” or
“PCWP”
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Cardiac Output
Pulmonary Vascular Resistance (PVR) ‐ measures afterload of Right Heart (50‐250 dynes)
↑PVR: Acidosis, Hypercapnia, Hypoxia, atelectasis
↓PVR: Alkalosis, Hypocapnea, vasodilating drugs
Systemic Vascular Resistance (SVR) ‐ measures afterload of Left Heart (800‐1200 dynes)
↑SVR: Hypothermia, Hypovolemia, decreased CO
↓SVR: Anaphylaxis , Neurogenic shock, vasodilating drugs
FYI ONLY ‐ Dyne: the force required to accelerate a mass of one gram at a rate of one centimeter per
second squared.
Cardiac Responses
In response to ↓ contractility, HR ↑
In response to hypoxia, pulmonary arteries constrict (pulmonary hypertension)
In response to a ↓ systemic perfusion, blood vessels constrict
Except in neurogenic and anaphylactic shock!
A systemic ↑ in vasoconstriction will ↓ CO
Cardiac Output Transducer
Utilizes a machine that is hooked up to the Swan‐Ganz Catheter (this is not a separately inserted line)
Placed at the phlebostatic axis (4th ICS, Mid Axillary Line)
Dicrotic notch is caused by aortic valve closure
Overdamping‐ system is not dynamic “Overdamping = Obstruction”
Kinked line
Obstruction in the tube
Underdamping‐ too dynamic
Pressure bag not full
air in the line
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Cardiogenic Shock
Objective signs of shock due to heart failure
PAWP >18‐20
↓UOP
SBP <80mmHg
Treat with Balloon Pump, Vasopressors (Dobutamine), Intubation
Diuretics make CO WORSE!
Intra‐Aortic Balloon Pump (IABP)
Indications‐ Acute MI with cardiogenic shock, post coronary artery bypass graft (CABG)
Contraindications‐ Aortic insufficiency/disease, severe peripheral vascular disease (PVD), or aortic
regurgitation
What the IABP does:
↑coronary perfusion
↓workload on heart
How the IABP functions
Timed off of EKG (can be manually adjusted)
Systole‐ Deflated
Diastole‐ Inflated
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IABP Placement
Sits in the descending aorta, distal to Left Subclavian Artery, above Renal Artery
The IABP is directed towards the heart from the Femoral Artery
Check placement by‐
Checking LEFT radial pulse (left subclavian artery blockage causing limb
ischemia)
Ensuring adequate UOP (Renal artery blockage)
CXR also confirms proper placement
Can cause thrombocytopenia due to hemolysis
IABP Tips
If there is a power failure, manually pump every 3‐5 minutes to prevent blood from clotting on the
balloon
There is no need to purge IABP when going to altitude (the machine will purge itself)
Ensure you carry extra helium tanks prior to transport (it is bad form to run out while in flight)
If you see brown or rust colored flakes in IABP tubing, the tubing has ruptured (the brown flakes are
clotted RBCs inside the tubing system).
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IABP Waveforms
This is what the IABP waveform should look like
NORMAL
This is LATE deflation of the balloon pump
MOST DANGEROUS
↑Afterload
This is EARLY inflation of the balloon pump
DANGEROUS
Causes aortic regurgitation
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Late Inflation
This is LATE inflation of the balloon pump
Sub‐optimal coronary perfusion
Early Deflation
This is EARLY deflation of the balloon pump
Retrograde coronary blood flow
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Advanced Airway (5)
Intubation Indications
Unable to swallow
Pt can’t ventilate/oxygenate
GCS <8
Expected clinical course (inhalational burns, anaphylaxis, etc.)
Apnea
Airway obstruction
Respiratory failure pH <7.2, CO2 >55, PO2 <60
No more than 3 attempts of direct laryngoscopy (becomes a failed airway, need to Cric)
Keep Sp02 >90% by preoxygenating the patient for 3‐5 minutes
If SpO2 cannot be maintained >90% by any other means (can’t intubate, can’t ventilate), proceed to
Cric (6.0 ETT for adults)
7 P’s
Preparation
Preoxygenate (3‐5 minutes)
Pretreatement
Paralysis with induction
Protect (Sellick’s Maneuver)and position
Placement with proof
Post intubation management
LEMON
Look
Evaluate 3‐3‐2
3 fingers in mouth, 3 fingers btw jaw and hyoid, 2 fingers btw hyoid and thyroid
Mallampati (I‐IV)
Obstructions
Neck Mobility
LOAD
(RSI Pretreatment)
Lidocaine (Head / Lung Injury) (blunts the vagal response)
Opiates
Atropine for Pediatric patients
Defasiculating Dose
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Mallampati
(I‐IV)
I‐ Soft palate, uvula, anterior/posterior tonsillar pillars visible
II‐ Tonsillar Pillars hidden by tongue
III‐ Only the base of the uvula can be seen
IV‐ Uvula cannot be seen
Intubation Review
Equipment
Macintosh‐ Curved blade
Lifts the vallecula
Miller‐ Straight blade
Lifts the epiglottis
Sellick’s Maneuver: direct downward pressure on the thyroid cartilage, occludes the esophagous and
prevents aspiration during intubation
BURP: Backward, Upward, Rightward Pressure
Placement Confirmation
Gold standard of placement confirmation – Chest X Ray (distal tip of ETT should be 2‐3 cm above the
carina)
Next most reliable confirmation method‐ visualization of the tube passing through the vocal cords
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Rapid Sequence Induction/Intubation (RSI)
Succinylcholine
(Anectine)
Depolarizing Neuromuscular Blocking Agent (which causes fasiculations)
Dose: 1 ‐ 2 mg/kg
1‐2 minute onset, 4‐6 minute duration
Can cause hyperkalemia (tx under hyperkalemia protocols)
Contraindications – Crush injuries, Eye injuries, Narrow angle glaucoma, Hx of Malignant
Hyperthermia, Burns > 24 hrs, Hyperkalemia, any nervous system disorder (ex. Guillan barre,
Myasthenia gravis)
Can cause malignant hyperthermia, causing temps to rise above 105° (treat with Dantrolene
sodium)
Vecuronium/Rocuronium
(Norcuron/Zemeron)
Non‐Depolarizing Neuromuscular Blocking agents
Slower onset (4‐6 min), longer duration of action (30‐45 min)
Does not cause fasiculations
Defasiculating doses of a non‐depolarizing agent reduces increase in ICP during intubation
Used after succinylcholine to keep the patient paralyzed
Etomidate
(Amidate)
Induction agent,preferred for awake sedation (fast onset, short half life)
0.3 mg/kg
30‐60 second onset, 3‐5 minute duration
Causes almost no change in B/P, CO, and has NO ANALGESIC PROPERTIES
Can have vomiting when waking up
Contraindications‐ Some adrenal suppression (don’t use in septic shock)
Ketamine
(Ketalar)
Analgesic agent
Used to stop pain impulses (remember that NMBs and Etomidate DO NOT CONTROL PAIN)
Midazolam
(Versed)
Amnestic, some analgesic properties
“Helps you forget the event ever happened”
Use lowest dose possible, do not use with other benzodiapene medication
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Respiratory/Ventilators (10)
Chemoreceptors
Central‐ located in the medulla/pons; response is driven by CO2 and H+ levels
Peripheral‐ located in the aortic/carotid bodies; response is driven by O2, CO2, H+
V/Q
(Ventilation / Perfusion)
The Fick formula is used to tell you how much O2 a person is using (Cardiac output measurement
based on the principle that oxygen uptake by the lungs <VO2> equals oxygen delivery)
ATP
Adenosine Triphosphate (ATP) production requires glucose and O2, byproducts are CO2 and H2O
Lack of Glucose or O2 causes an alteration in ATP metabolism
Byproduct is Lactic acid from anaerobic metabolism
THE MOST DEFINTIVE ASSESSMENT OF SHOCK IS LACTIC ACIDOSIS (lactate)
In the presence of lactic acidosis, Hyperkalemia is often present
Ventilator Settings
Vt (Tidal Volume) = 6‐10cc/kg
F (Rate) = 8‐20/min
Ve (Minute Volume) = F x Vt (4‐8 L/min)
I:E (Inspiratory: Expiratory ratio) = 1:2 or 1:3
FiO2 (Fraction of Inspired Oxygen) = 0.21 to 1.0 (21% ‐ 100%)
Pplat (Plateau Pressure) = <30
PEEP (Peak End Expiratory Pressure) = 5
PEFR (Peak Expiratory Flow Rate) = 500 to 700 L/min for males, 380 to 500 L/min for females
Once a patient is on a ventilator, confirm settings with an ABG!
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Respiratory Failure
Hypercarbic respiratory failure
“Inability to remove CO2”
Evidenced by respiratory acidosis
Treatment‐ ↑ tidal volume, then the rate
Hypoxic respiratory failure
“Inability to diffuse O2”
Evidenced by low PaO2
Treatment ‐ ↑ minute volume and O2 concentration
Ventilation Control Modes
Controlled Mandatory Ventilation (CMV)
Delivers a pre‐set tidal volume at a pre‐set rate
Patient has NO ability to initiate their own breaths
Apneic or paralyzed patient
Example: SAVe Ventilator
Intermittent Mandatory Ventilation (IMV)
Patient determines tidal volume for SPONTANEUOUS BREATHs
Patient must overcome tubing resistance to take intermittent breaths
Breathing possible between mandatory ventilations
Synchronized Intermittent Mandatory Ventilation (SIMV)
Ventilator provides a pre‐set mechanical breath (pressure or volume limited) every specified
number of seconds
When the patient initiates a breath, the machine SYNCHRONIZES with inhalation to deliver a breath
to a preset tidal volume
Then patient must have an intact respiratory drive
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Assist‐Control Ventilation (AC)
Full tidal volume (Vt) regardless of respiratory effort or drive
Minute volume can be preset
Poor patient‐ventilator synchrony (asynchrony)
Leads to “breath stacking” or “auto‐PEEP”
Better tolerated than IMV
Pressure Support Ventilation (PSV)
Noninvasive ventilation
“Supports" ventilation during inspiration
Patient determines tidal volumes, rate (Minute Volume)
Requires consistent ventillatory effort by the patient
Monitor the patient to ensure adequate tidal volumes and minute ventilation
Capnography
If you see tick marks (cleft) on capnography, patient is choking, check ETT (curare cleft)
‐Patient needs to be resedated and paralyzed
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Pressure Alarms
Low Pressure
Patient disconnection from machine (most common cause)
Chest tube leaks
Circuit leaks
Airway leaks
Hypovolemia
High Pressure
Kinked line (most common cause)
Coughing
Secretions or mucus in the airway
Patient biting the tube
Reduced lung compliance (Pneumothorax, ARDS)
Increased airway resistance
Preoxygenation Required
(Give 10L/min via NRB for 15 Minutes prior to takeoff)
Obese pt’s (Bariobarotrauma)
Bariobarotrauma is caused by a sudden release of nitrogen stores in lipids when going
to altitude
Pregnant patients
Pediatrics
Asthma
Problem is breathing out (caused by air trapping)
Asthma attack
Increase the I:E ratio to 1:4
High flow O2 (high FiO2)
Bronchodilators (Albuterol, Duoneb, etc.)
IV Fluids
Use Ketamine for sedation in RSI during asthma attack!
Decreased or absent wheezing is ominous and precedes respiratory failure
Flattened diaphragm on CXR
Exhalation problems fatigue the quickest!
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COPD
Problem is breathing out (caused by air trapping)
Emphysema “blue bloaters”
Chronic Bronchitis “pink puffers”(pink color is due to polycythemia vera)
COPD Exacerbation‐ Keep FiO2 low (hypoxic drive)
High tidal volume (10cc/kg)
Increase PEEP (10)
Flattened diaphragm on CXR
Exhalation problems fatigue the quickest!
Pneumonia
Often viral, sometimes bacterial
CXR shows pleural effusions, lobar consolidation
Right Middle Lobe pneumonia is the most common
Tx with O2, IV Fluids, Bronchodilators, Antibiotics if indicated
ARDS
“Ground glass appearance” on CXR
↑PAWP
Focus on oxygenation with:
↑PEEP
High Tidal Volumes (>10cc/kg)
Pancreatitis and ARDS commonly occur together
Misc. Airway Facts
If on a ventilator, check tidal volume first, then the rate!
(Vt‐ volume, F‐ rate)
Gold Standard for oxygenation‐ pulse oximetry
Gold standard for ventilation‐ capnography
Ventilator acquired pneumonia (VAP) is the #1 cause of iatrogenic death in the U.S.
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2,3 DPG(Oxygen Dissociation)
LEFT SHIFT RIGHT SHIFT
Hypothermia Hyperthermia
Alkalosis Acidosis
Hypocapnia Hypercapnia
Decreased levels of 2,3 DPG Increased levels of 2,3 DPG
Left = Low = Love oxygen (fails to release oxygen)
Low Temperature
Low CO2
Low levels of 2,3 DPG
Alkalosis
Right = Raised = Readily Releases oxygen
Raised Temperature
Raised CO2
Raised 2,3, DPG
Acidosis
Remember: Transfusions of blood have high citrate levels and low 2,3 DPG levels. Thus, large
transfusions lower the 2,3, DPG level in the body.
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Obstetrics (4)
General Treatment Measures
Place pt in the right or left lateral recumbent position
LLR (Left Lateral Recumbent) is preferred because it does not cause compression of the
IVC (inferior vena cava)
Check temp (fever often indicates sepsis, give Ampicillin and Gentamycin (AMP+GENT)
FHR
IV LR
O2
Normal Maternal Changes
HR increases 15‐20 BPM
B/P decreases 5‐15 mmHG 2nd tri
B/P increases 10 mmHg 3rd tri
CO increases
Plasma increases 40% (increase in clotting factors)
Hormones Progesterone and Relaxin relaxes sphincters
Decreased functional / residual lung volume
Pregnancy Terms
Preterm‐ before 38 weeks
Full term 38‐42 weeks
PostTerm‐ after42 weeks
Assessment “DES”
Dilation (0‐10 cm)
Effacement (thickness of the cervix) NML is 2 CM
Station (fetal head in relation to the pubic bone (measured + or – in centimeters)
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Fetal Monitoring
External Fetal Monitoring using Doppler
Internal Fetal monitoring using scalp monitor
Gold Standard‐ internal fetal monitoring with uterine pressure monitor (tocometer)
Normal HR 120 to 160 BPM (baseline)
Variability ‐ single most important predictor of fetal well being
10‐15 bpm = normal variability
#1 cause of poor variability‐ fetal hypoxia
ACCELERATIONS ARE ALWAYS GOOD
Decelerations can be bad
Early Decelerations
Associated with head pressed against the cervix
Benign
MIRRORS CONTRACTIONS
FETAL HEART RATE
UTERINE CONTRACTION
(Tocometer)
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Late Decelerations
Always indicates ureteroplacental insufficiency causing the fetus to experience a hypoxic
bradycardia
Commonly associated with PIH / DM / Smokers / Late Deliveries
Always concerning!
FETAL HEART RATE
UTERINE CONTRACTION
(Tocometer)
Variable Decelerations
UTERINE CONTRACTION
Caused by cord compression
Nucchal: Cord is wrapped around the fetus’ neck (clamp and cut cord if needed)
Prolapsed: Cord is protruding from the mother’s vagina (raise cord to relieve
pressure, knees to chest, tocolytics, saline gauze over cord)
FETAL HEART RATE
“V”or”W” Shaped
UTERINE CONTRACTION(Tocometer)
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Sinusoidal Variations
Fetal Hypovolemia
Anemia
Caused by accidental tap of the umbilical cord during amniocentesis, fetomaternal transfusion,
placental abruption
Fetus is acidotic!
Ominous
EMERGENCY C‐SECTION INDICATED!
FETAL HEART RATE
“Looks like fine VFib”
UTERINE CONTRACTION
(Tocometer)
Emergency C‐ Section Indications
Multiple decelerations with poor rate / variability
Sustained Bradycardia (<120 BPM for >10 minutes)
Sinusoidal waveform
Stages of Delivery
1. Crowning (cervix is fully dilated)
2. Delivery of body
3. Delivery of placenta
Signs of Imminent Delivery
Vaginal bleeding (bloody show)
Contractions < q10 min and increasing intensity
Urge to push
Need to have a BM
Crowning
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Delivery Complications
Anaphylactoid Syndrome of Pregnancy
Caused by maternal exposure to fetal cells, not an amniotic fluid PE [pulmonary embolus] as
previously thought
DIC (disseminated intravascular coagulation) and anaphylaxis at the same time
Symptoms‐ sudden onset of pleuritic chest pain, tachypnea, tachycardia, fever
Treatment: Fluid resuscitation
Increase PEEP (patient is hypoxic)
FFP, Platelets, Cryoprecipitate
Meconium
Baby defecates while in the womb
Meconium inactivates surfactant
Deep suction only if baby is not vigorous (strong cry, pink, active)
Intubate and suction below the vocal cords before the first cry
Pre‐Term Labor
Any labor prior to 38 weeks gestation
True labor presents with regular uterine contractions WITH cervical change (effacement)
Most common cause of preterm labor is hypovolemia
Preterm Delivery
(<38 weeks)
Most common cause of preterm contractions is hypovolemia
Administer Tocolytics
Terbutaline 1st
Magnesium Sulfate 2nd
Stimulate fetal lung maturity
Steroids (Celestone, Dexamethasone)
Prevent infection
Avoid vaginal examinations, if exam is needed use sterile gloves
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Breech Delivery
Don’t touch until umbilicus is delivered
Don’t attempt a footling breech
Use Mauriceau’s maneuver
Shoulder Dystocia
Shoulders will not pass through the pelvis
Apply gentle traction to baby while applying suprapubic pressure
Umbilical Cord Prolapse
Elevate cord to relieve pressure (↑ fetal circulation)
Use saline soaked gauze to prevent the cord from drying (dessication)
Move to Trendelenburg position or knees to chest
Miscellaneous
Uterine inversion requires manual replacement
Gestational diabetic mothers are more likely to give birth to children with hypoglycemia
Treat neonatal bradycardia first (epinephrine), then treat hypoglycemia (glucose)
Oxytocin
Released in large amounts;
After distension of the cervix and uterus during labor
After stimulation of the nipples, facilitating birth
During breastfeedin
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Pitocin
(Synthetic Oxytocin)
Often used for uterine atony after placental delivery in the setting of continued maternal hemorrhage
What it does:
Letdown reflex (from nipple stimulation)
Uterine contraction – important for cervical dilation before birth and causes
contractions during the second and third stages of labor.
Due to its similarity to vasopressin, it can reduce the excretion of urine slightly
PIH
(Pregnancy Induced Hypertension)
New onset HTN with pregnancy
Can cause placental insufficiency
Treat with Labetolol (β Blocker) or Hydralazine (Alpresoline)
PreEclampsia
HTN
Proteinuria
Edema
NO SEIZURES
Risk factors‐ extremes of age, 1st pregnancy
Often causes LATE DECELERATIONS
Eclampsia
HTN/ Proteinuria/Edema
GENERALIZED SEIZURES
Seizures are treated with Magnesium Sulfate
Sign of Mag toxicity is ↓ DTRs (hyporeflexia)
Antidote for Mag Sulfate is Calcium Gluconate
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HELLP
(Hemolysis / Elevated Liver Enzymes / Low Platelets)
RUQ pain (liver), jaundice, malaise
Commonly seen with PreEclampsia and Eclampsia
Give MgSo4 (4‐6 G over 30 minutes)
Steroids (Celestone) (Stimulates fetal lung maturity)
HTN‐ use Labetalol or Hydralazine
Seizures refractory to Mag Sulfate‐ treat with valium
Note: Benzos are usually contraindicated in pregnancy; this is only indicated in the treatment of
seizures
Tocolytics
(Drugs that stop uterine contractions)
Magnesium Sulfate (MgSO4)
Mechanism of action‐ CNS depressant
“Mag Check”
DTRs(<2+)
Respirations (can cause pulmonary edema)
DO NOT rely on blood levels of Mag, they do not correlate with levels of toxicity
This is a long acting medication!
Terbutaline (Brethine)
Stops tetanic contractions of the uterus IMMEDIATELY
Subcutaneous 0.25mg q 15 min
This is a short acting medication!
Calcium Channel Blockers
Least preferred tocolytic
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Maternal Hemorrhage
Placenta Abruption
Any MVA/ blunt trauma is placental abruption until proven otherwise
Exsanguination/ placental insufficiency
Painful bleeding
Placenta Previa
Not an emergency
Painless bright red bleeding
DO NOT DISTURB THE VAGINA!
Postpartum Hemorrhage
>500 ml blood loss (anytime within 24 hours after delivery)
First line treatment for Post‐Partum Hemorrhage (PPH) is vigorous fundal massage!
Bimanual uterine compression
Oxytocin
Methergine
Uterine Rupture
“Stomach is as hard as a board”
Fetal parts presenting under the mother’s skin
#1 cause of maternal death is trauma
#1 cause of fetal death is maternal death
Rh Negative Mothers
Rhogam prevents mothers immune response to the baby’s Rh positive cells (prevents mom’s
immune system from attacking the baby).
If a mother is Rh negative, ALWAYS give Rhogam!
This means the mother has Rh antibodies
The majority of the population is Rh positive
When to give Rhogam‐
At 28weeks gestation
After delivery
After ANY trauma/bleeding/potential bleeding
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Neuro (10)
MAP (Mean Arterial Pressure) = SBP + (2 x DBP) Normal 80 to 100 mmHg (ideally 90mmHg)
3
CPP (Cerebral Perfusion Pressure) = MAP ‐ ICP Normal CPP 60‐80 mmHg
ICP normal value 0 – 10 mmHg
ICP Transducer is placed at the foramen of Monro (level of the ear)
Signs/Sx of Herniation
Change in LOC
Pupil reaction
Decorticate/Decerebrate posturing
Decerebrate
Decorticate “to the core”
Cushing’s Triad ‐ results from increased ICP
Hypertension
Bradycardia
Increased Pulse Pressure
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Respiratory Changes
Cheyne‐Stokes: breathing becoming shallower until it stops for a while and then breathing starts
again and rapidly crescendos to a peak before decreasing away
Hypoxia and Hypercapnia cause cerebral blood vessels to dilate, increasing blood flow and
volume, further escalating ICP
Tx of Herniation
Paralyze
Intubate
Hyperventilate (Goal PaCO2 30‐32mmHg)
Mannitol (Decrease fluid in the cranial vault)
Hypertonic Saline (Give slowly to prevent Central Pontine Myelinolysis)
Barbituate Coma (Lowers O2 demand)
Treat seizures with a Benzo or Phosphenytoin
DO NOT USE HYPOTONIC SOLUTIONS OR GLUCOSE!
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Head Trauma
Head injuries are the leading cause of death in the trauma victim!
Skull Fractures
DiastaticFx: along the sutures
Linear Fx: extends towards the base of the skull
Linear Stellate: multiple fractures that radiate form the compressed area (spider web appearance)
Basilar Skull Fx – Battle’s Sign, Raccoon Eyes, Otorrhea, clear rhinorrhea (CSF is leaking)
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Cerebral Bleeding
Subdural Hematoma – Venous bleed, often in the elderly, kids “Venous Lakes”
More common and more lethal than epidural hematomas
Epidural hematoma ‐ Arterial bleed, M/C vessel damaged is the middle meningeal artery “MMA”
LOC followed by a lucid interval and an second LOC
Pupil dilation after occulomotor nerve injury due to loss of parasympathetic tone
Subarachnoid Bleed ‐ Starfish Pattern on CT
“Worst HA of my life”
Avoid lumbar punctures
Keep systolic B/P below 140mmHg
Miscellaneous
Patients with persistent elevated B/P in the setting of intracranial hemorrhage‐ tx with Nipride
Interventricular hemorrhage has increased mortality
Sodium and Glucose are the primary concern when dealing with electrolyte abnormalities of the
brain
Important dermatomes: T4 nipples, T10 umbilicus
Concussions
Mild ‐ knocked out, no memory loss
Classic – Memory loss
Diffuse Axonal injury – Coma
Spinal Cord Injuries
Brown Sequard Lesion
Ipsilateral motor/vibratory sense loss
Contralateral Pain/ temp loss
Spinal Shock
Due to swelling of the spinal cord after trauma
Hypotensive‐ administer crystalloid IV fluids
Can treat with high dose steroids (controversial)
Central Cord injury
Motor weakness in upper extremities is greater than lower extremities
UE>LE
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Anterior Cord Syndrome
Loss of pain/temp everywhere
Sparing of proprioreception/vibration
Neurogenic Shock
(Distributive Shock)
Decreased Systemic Vascular Resistance (SVR) and normal heart rate
Hypotension
Warm red skin
No tachycardia
Treat with IV fluids/Vasopressors
Autonomic Dysreflexia
“Autonomic Hypereflexia”
Increased sympathetic discharge due to noxious stimuli (pinching, chemical irritants, hot/cold
temperatures)
Increases B/P, H/R, ICP
Insert/Drain the Foley catheter slowly
Herpes Simplex Encephalitis
Most common cause of encephalitis in the U.S.
Caused by Varicella / Herpes Simplex (HSV)
Treat HSV with IV Acyclovir
Cerebro Vascular Accident (CVA)
"Brain Attack"
IV (Intravenous) TPA if <3 hrs from incident
IA (Intrarterial) TPA <6hrs (medication pushed directly into the clot)
MERCI if 8 to 12 hrs old (roto‐rooter)
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General Medical (16)
DKA
(Diabetic Ketoacidosis)
Most common in Type I diabetic teens/children
Elevated glucose (>350mg/dl)
Elevated Ketones (ketosis) this is what causes fruity breath
ACIDOTIC (metabolic acidosis)
Kussmaul's respirations (rapid, deep, sighing respirations)
First line treatment is fluid administration, then insulin to reduce blood glucose levels (average fluid
deficit is 5‐10L)
May require IV infusion of short acting insulin
Do not lower glucose <100mg/dl per hour (do not lower less than 250mg/dL total)
HHNK
(Hyperglycemic Hyperosmolar Non‐Ketosis)
Common with Type II Diabetes
Extremely elevated glucose (>600mg/dl) sometimes >1000mg/dL
Normal ketones (non‐ketotic)
NON‐ACIDOTC
First line treatment is fluid administration, then insulin to reduce blood glucose levels (average fluid
deficit is 5‐10L)
May require IV infusion of short acting insulin
Do not lower glucose <100mg/dl per hour, do not lower less than 250mg/dL total
Treat hypokalemia if present (60mg oral or 10mg IV potassium, oral route is preferred)
SIADH
(Syndrome of Inappropriate Anti‐Diuretic Hormone)
Hyponatremia is the problem (Na <135meq/L)
<130meq/L = Symptoms typically begin
<120 meq/L = Coma
ADH = Desmopressin (there is too much of this hormone in the body)
Tx with Hypertonic saline if symptomatic (do not exceed 0.5 meq/l/hr)
Can lead to central pontine myleniolysis if Sodium is corrected too quickly (irreversible brain damage
evidenced by cerebral palsy, quadraplegia, death)
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DI
(Diabetes Insipidus)
Polydipsia (excessive thirst)
Polyuria (excessive urination)
Polyphagia (excessive hunger)
1st line treatment is fluid resuscitation (typically there is a 9L fluid deficit)
Tx with Vasopressin / Desmopressin (DDAVP)/ 3% Hypertonic Saline
Vasopressin/DDAVP causes fluid retention
ORAL FLUID RESTRICTION!
Usually a central neurogenic etiology. Also caused by of Dilantin overdose and head injuries.
Esophageal Varicies
Bleeding in the esophagous, most commonly due to chronic alcoholism
Patient will likely be vomiting bright red blood (hematemesis) and can also have bright
red diarrhea (hematochezia)
Patient often presents with syncope
Altered mental status due to hypovolemia
Life threatening!
Treat with Octreotide (Sandostatin)
Octreotide reduces splanchnic (spleen) and hepatic (liver) bloodflow, and reduces
variceal pressures
Balloon Tamponade‐ a Sengstaken Blakemore tube can be placed to provide direct pressure on the
bleeding (pt must be intubated first)
If there is excessive blood in the bowel, evacuate the bowel and stop the bleeding prior to transport
Mallory Weiss/Boerhaave’s Tears
Rupture of the esophagous
Commonly caused by chronic forceful vomiting (alcoholism, bulimia)
Presents with hematemesis
Often self‐resolving
If bleeding continues, treat like esophageal varicies
Can cause mediastinitis secondary to leak of gastric contents into the chest
Requires EGD (gold standard)
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Grave’s Dz / Thyrotoxicosis
("Thyroid Storm")
Pt often presents with weight loss, palpitations, nervousness, heat intolerance
Avoid ASA (Aspirin)
ASA prevents binding of thyroglobulin, making the situation worse
Treatment:
Give IV fluids first!
β Blockers
Dexamethasone (Steroids)
Tylenol for fever
Hypothyroidism/Myxedema Coma
Pt presents with fatigue, cold intolerance, weight gain, puffy eyelids, sparse hair, possibly goiter
Primarily occurs in women
> 90% cases in winter (because the patient has cold intolerance and is now suffering from
hypothermia)
Officially “Myxedema Coma” upon LOC change
Tx with IV Levothyroxine (T4) or Triostat (T3)
Cushing’s Syndrome
Buffalo hump, moon face, thin arms and legs, purple striae on abdomen
Caused by excessive use of corticosteroids (iatrogenic)
Usually resolves when corticosteroids are stopped
Addison’s Dz / Adrenal Insufficiency
Pt often presents with depression, malaise, salt craving
Negative ACTH test (cosyntropin test)
No Etomidate
Pancreatitis(evidenced by increased Lipase) + ARDS are common
Liver Failure
Liver breaks down ammonia
Increased ammonia leads to increased ICP
INR > 1.5
Treatment
Lactulose (removes ammonia)
Give K+ to increase Urinary Output
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Septic Shock
Someone who is in shock 2° to sepsis
Hypotensive with normal heart rate
Patient is hypotensive while being refractory to fluids
Pt needs IV fluid therapy and vasopressors
Levophed (Norepinephrine) is vasopressor of choice in profound hypotension
Do not use Etomidate!
Pancreatitis
Signs: Grey‐Turner (flank ecchymosis), Cullen’s (periumbilical ecchymosis) caused by hemorrhagic
pancreatitis, increased lipase levels
Symptoms: Pain that is usually centered in the upper middle or upper left abdomen. Often radiates
from the front of the abdomen through to the back, begins or worsens after eating, lasts a few days,
and may feel worse when a person lies flat on his or her back.
Demerol for pain (because Morphine can cause spasms of the Sphincter of Oddi)
Hyperkalemia
(K+ >5.0)
First: Prevent V‐Tach with Calcium Gluconate
Second: Push K+ into the cells with Bicarb, Insulin, D50, Albuterol
Third: Excrete excess K+ with Lasix and Kayexalate through urine (lasix), and feces (kayexalate)
K+ will change about 0.6meq for every 0.1 change in pH
“Tented/Peaked T Waves”
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Hypokalemia
K+ <3.5
Pt often presents with malaise, weakness, history of poor dietary intake
Give oral potassium 60 mEq (preferred route)
If hypokalemia is severe, can give 10mEq IV potassium
Causes T wave DEPRESSION or inversion on EKG
“Flattened, Inverted T Waves”
Basic Metabolic Panel
(Chem 7)
Na 135‐145 (Sodium)
Cl 95‐105 (Chloride)
K 3.5 – 5.0 (Potassium)
CO2 22‐26 (Carbon Dioxide)
BUN 6‐24 (Blood Urea Nitrogen)
Cr .7 to 1.4 (Creatinine)
Glucose 80‐120 (Blood sugar)
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CBC
(Complete Blood Count)
HGB/HCT 15/45 (Hemoglobin/Hematocrit)
PLT 150k – 400k (Platelets)
WBC 5k – 10k (White Blood Cells)
CBC‐primary serum protein is albumin, produced by the liver
(maintains colloid osmotic pressure)
Coagulation
“Coag Panel”
PT 11 sec (prothrombin time) extrinsic pathway
PTT 21 ‐ 35 sec (partial thromboplastin time) intrinsic pathway
INR 1.0 (international normalized ratio)
Heparin overdose‐ treated with Protamine sulfate
Coumadin overdose‐ treated with Vitamin K
Urine Output
Infant 2cc/kg/hr
Child 1cc/kg/hr
Adult 0.5 cc/kg/hr
Average urine output for an adult is 30‐50ml/hr
Misc ‐ Normal serum osmolality 285‐295 mOSM/ml
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PEDS (10)
Age Ranges
Neonate‐ birth to 30 days
Infant‐ 30 days to 1 year old
Toddler‐ 1 year old to 2 years old
Child‐ >2 years old
Emergency Intervention Formulas
ETT Selection (16 + Age)/4
ETT insertion depth 3 x ETT size
Chest Tube 4 x ETT (i.e. 5mm ETT → 20fr chest tube)
Suction/NG/Foley 2 x ETT (i.e. 5mm ETT → 10fr Foley)
Normal B/P 90 + (2 x Age)
Hypotensive B/P 70 + (2 x Age)
Pediatric Maintenance Fluids “4/2/1”
Non‐Emergency Fluid Administration
1‐10 kg → 4cc/kg/hr
10‐20 kg → 2cc/kg/hr
>20 kg → 1cc/kg/hr
Example: A 25 kg child needs fluids. 1st 10kg= 40cc, 2nd 10kg = 20cc, last 5kg = 5cc
THESE RATES ARE cc PER HOUR!
CC and mL are the same thing!
Pediatric Fluid Resuscitation
Emergency
Neonate / Infant 10cc/kg (<1 year old)
Toddler/Child 20cc/kg (>1 year old)
*Do not give more than 2 bolus infusions
Average Circulating blood volume in a child = 75‐80 ml/kg
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Pediatric Glucose Management
D stick <60mg/dL
Neonate 2cc/kg D10
Infant/Toddler 2cc/kg D25
Child 2cc/kg D50
Pediatric Airway Problems
Stridor‐ Inhalation problem, involves the upper airway
Wheezing‐ Exhalation problem, involves the lower airway
Croup
(Swelling around the vocal cords) Usually not life threatening
Gradual onset with URI
“Seal Like” barking cough
Steeple sign on anterior neck x ray
Treatment: Racemic Epinephrine, steroids(Decadron)
Remember:
cRoup = Racemic epinephrine
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Bronchiolitis
(Swelling of the bronchiole walls) Usually not life threatening
>90% viral
Cough, shortness of breath, nasal flaring, wheezing/crackling on exam
Often caused by RSV (Respiratory syncytial virus)
WATCH FOR APNEA!
Treatment: Supportive care, O2, Fluids, Isolation
Epiglottitis
(Swelling of the epiglottis) LIFE THREATENING
Sudden onset
Pt presents in the “tripod position”
Thumb sign on lateral neck x ray
Drooling
Do not disturb the child due to possible rapid airway loss
Treatment: Antibiotics, humidified O2
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Pediatric Trauma
Waddel’s Triad (when hit by a car)
1) Car hits them
2) They hit the car
3) They hit the ground
When falling, children strike their heads first
Most common cause of traumatic death in peds is Motor Vehicle Accidents
Most commonly organ injured is the skin
Children do not show signs of hypotension until >25% blood loss (compensate with tachycardia)
Accidental Ingestion
Narcotics‐ Decreased respiratory drive and altered mental status
If unknown cause of ingestion, give Narcan
All other agents, give supportive care(Airway, IV, O2)
Misc. Peds bullets:
Peds are belly breathers
Infants are obligate nasal breathers
Bradycardia/Cardiac Arrest is most commonly secondary to hypoxia
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Neonates (4)
(Birth to 30 days old)
RDS
(Respiratory Distress Syndrome)
(also called Hyaline Membrane Disease)
Surfactant deficiency
Surfactant reduces surface tension in the alveoli
Newborn has increased work of breathing, tachypnea
#1 killer of premature infants (tx w/ surfactant via ETT)
Consider use of surfactant when transporting preterm infants
Neonatal Infectious Disease
Top 3 killers in 1st 24 hours – Sepsis, Respiratory complications, Cardiac problems
Infants and Peds lose heat quicker than adults because of their large body surface area to mass
index ratio
Neonatal Sepsis
Occurs in utero – often caused by Premature rupture of membranes (PROM)
Treat: Ampicillin + Gentamycin (Amp + Gent)
Most commonly caused by Group B Strep
Infant Seizures
Infant Seizures‐ S/Sx include lip smacking and tongue thrusting, eye fluttering, lowered O2 sats
Febrile Seizures
Rate of temperature increase is the most important factor (not overall temp)
Fever‐ Each 1° change >37° HR increases 10 BPM
Does not require further workup if the cause is known (ear infection, viral illness, etc.)
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Omphalocele
“O” Abdominal ring, protrusion of viscera (arrest of development of the abdominal wall)
Is attached to the umbilical cord
This condition is WORSE than Gastroschesis (high morbidity)
Treat like an abdominal evisceration!
Maintain body temperature
Cover with moist, sterile dressings
Keep NPO
Will require surgical repair
GASTROSCHESIS
Defect with completed development of internal organs. Abdominal contents are coming out of the body
on one side of the umbilical cord.
Treat like an abdominal evisceration!
Maintain body temperature
Cover with moist, sterile dressings
Keep NPO
Will require surgical repair
This is less severe than an Omphalocele!
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Choanal Atresia
Remember that Infants are obligate nasal breathers for the first 6 months
This condition results in a blocked nasal airway
Likely will require intubation
Cardiology
Neonatal/Infant Cardiac Abnormalities
Newborns with a HR ≤60 and a D‐Stick ≤60:
administer Epinephrine 1st , then glucose
Cardiomegaly + Hepatomegaly (enlarged heart and liver) means the child has CHF (congestive heart
failure)
Stop IV Fluids, administer Digitalis
Worsening cyanosis in a crying infant indicates a cardiac problem
Cyanotic lesions are often PDA dependent
Most common cardiac defect is VSD
Patent Ductus Arteriosis
(PDA)
PGE1 (prostaglandin E1)is what keeps the PDA open
PDA problems are often found on physical exam by checking for femoral pulses
If femoral pulses are absent, possible coarctation of the aorta, high likely hood of requiring
PDA to survive
Indocin (Indomethacin) is the drug of choice for closing a PDA (patent ductus arteriosis)
Oxygen also closes the PDA
Administer PGE1
Caution: PGE1 administration can cause apnea!
Tetralogy of Fallot
PDA
Aortic Coarctation
Transposition of Great Vessels
VSD
Left to Right Shunt
“Tet Spells”
Treat with knees to chest, Morphine
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Persistent Pulmonary Hypertension
Right to Left Shunt
Ventriculoperitoneal Shunt
“VP Shunt”
Treatment for increased CSF in congenital hydrocephalus
Cerebral spinal fluid can build up leading to an increase in intracranial pressure (ICP)
Intracranial hematoma
Cerebral edema
Herniation
Patient often presents with gastric distention and mental status changes, vomiting,↓LOC
Give Mannitol
Raise the head of the bead
Isolette (Incubator)
Device to put any preterm or term infant into to maintain heat, provide supplemental oxygen, and
to protect from the environment.
Commonly used for preterm infant
If a neonate is experience problems, and isolette should be used on those <5 kgs, less than 30 days
from date of birth
Shaken Baby Syndrome
Bulging fontanelles
Increased ICP
Retinal hemorrhages
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Environment (4) /Toxicology (6)
Patients with Thermoregulatory Problems
Pediatric
Paralyzed
Head Injuries (diffuse axonal injury)
Burn victims
Hypothermia
(Cold Injuries)
Treat with passive external and active external rewarming first!
If unsuccessful, treat with active internal rewarming
Heated IV fluids, warming packs, GI lavage with warmed fluids, etc.
Cause of dysrhythmia in hypothermia‐ increase in lactate and K+ levels
Osbourne wave on EKG
“Hypothermia hump”
Shivering is limited by glycogen stores (stops at 32° C)
No one is dead until they are warm and dead!
Hyperthermia
(Heat Injuries)
Respiratory alkalosis, heat cramps caused by Hyponatremia
Primary cation lost in heat injuries is Sodium (Na+)
NEVER USE COLLOIDS FOR FLUID REPLACEMENT!
Use crystalloids(LR,NS)
With heat exhaustion there is no neurologic impairment
Heat stroke is a heat injury with LOC change
Heat AND cold injuries can cause a change in EKG
Osborne or “J” waves
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Dehydration
Blood
↑HCT
↑BUN
Urine
↑ SG (Specific Gravity)
Ketones
Give a minimum of 2L crystalloids
Rhabdomyolysis
“Rhabdo”
Creatinine Kinase (CK) will be greatly elevated
Patient usually has dark cola or tea colored urine (myoglobinuria)
First line treatment is crystalloid IV fluid resuscitation
BiCarb (alkalinizes the urine)
Lasix(diuresis)
Mannitol (diuresis)
Malignant Hyperthermia
An adverse reaction adverse Succinylcholine administration
Can be caused by other anesthetic agents, but they are not used prehospital
Signs/Symptoms:
Masseter spasm / trismus (lockjaw)
Rapid increase in temperature (can become as high as 110⁰)
Increased ETCO2
Tachycardia / HTN
Mixed acidosis
Tx with Dantrolene
DO NOT GIVE CCBs
Drowning
Cold Water
Dry drowning (due to laryngospasms)
Warm Water
Wet drowning
Spinal immobilization
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ASA Poisoning
(Aspirin)
Nausea, vomiting, ringing in the ears (Tinnitus)
ASA poisoning can cause respiratory alkalosis (it is a respiratory center stimulant)
Respiratory alkalosis progresses to metabolic acidosis
Can lead to Reye’s syndrome in peds (potentially fatal liver and brain damage)
Liver fails causing ↑ammonia levels, which ↑ICP and leads to encephalopathy
Dialysis can be helpful
Tylenol Poisoning
(Each stage lasts 24hrs)
Stage I – Flu sx
Stage II – Flu sx stop, liver failure occurs, RUQ pn, increased liver enzymes
Stage III – Peak liver enzymes, RUQ pn, Flu sx (DEATH STAGE)
Stage IV – Resolution period
Tx with Mucomyst, Acetadote I.V.
Dilantin Overdose
Can cause SVT/Ventricular dysrhythmias
Coma, confusion, tremors
Can cause Diabetes Insipidus (DI) like symptoms
treat under Diabetes Insipidus protocols
Supportive care (airway, IV, O2)
Gastric Lavage (charcoal use is controversial)
Organophosphates
Think CBRNE (chemical agent poisoning)
SLUDGE
Salivation, Lacrimation, Urination, Defecation, Gastroenteritis, Emesis
Tx with Atropine, 2 Pam Chloride
Iron Overdose
Typically from elemental iron supplements
Common in children
Antidote is Defroxamine
Pink urine indicates a therapeutic level of defroxamine
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Hypocalcemia
Ca<8.5mg/dL
Chovstek’s(cheek muscle spasms when tapped) sign
Trousseue’s(forearm tetany when B/P cuff is applied) sign
Treat with Calcium Gluconate
β Blocker Overdose
Examples‐ Labetolol, Carvidolol, Esmolol
Symptoms‐ hypotension, bradycardia, conduction delays
Glucagon is the antidote (glucagon can also be used to treat a Clonidine overdose)
Consider cardiac pacing
Fluids for hypotension
Calcium Channel Blocker Overdose
Examples‐ Amlodipine, Verapamil, Cardizem, Diltiazem
Symptoms‐ hypotension, bradycardia, conduction delays
Tx overdose with Calcium Gluconate
Fluids for hypotension
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Tricyclic Antidepressant (TCA) overdose
Examples: Amitriptyline (Elavil) Nortriptyline (Pamelor)
Tachycardia and widened QRS common, prolonged QT intervals
Torsades de Pointes occurs after prolonged QT interval
Treatment is Bicarb
Dialysis is not helpful
Digitalis Toxicity
Flu like sx, visual disturbances
Yellow / Green halos (life looks like Van Gogh paintings)
Slurred upslope on QRS
Treat with Digibind
Avoid electricity (cardioversion, pacing, etc.)
Ethylene Glycol / Methanol Poisoning
Ethylene Glycol‐drinking antifreeze
Methanol‐ Alcohol poisoning
Profound anion‐gap acidosis (≥16)
Treat with IV ethanol
Competes with methanol to avoid conversion to toxic metabolites
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Hydrocarbons
(Drinking volatile fuels)
Decreased viscosity causes aspiration
Causes chemical pneumonitis
Intubate!
DO NOT induce vomiting!
Cocaine
Antidote is benzos‐ Valium/Ativan
Do not give β blockers (leads to unopposed α adrenergic activity)
DO NOT use drugs like Esmolol, Propanolol, etc.
Benzodiazepine Overdose
Use Romazicon (Flumazenil)
Remember the ½ life of the benzo is usually longer than the ½ life of the Romazicon
FLUMAZENIL ½ LIFE approximately 40 to 80 minutes
Opioid Overdose
Use Naloxone (Narcan)
Any altered mental status, consider use of Narcan
Remember the ½ life of the opioid is usually longer than the ½ life of Narcan
NARCAN ½ LIFE approximately 45 minutes
When pushing Narcan , use the lowest dose possible to avoid complete blockade of the opioid
receptors (leads to a complete inability to control pain in the patient)
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Flight Physiology (10)
GAS LAWS
Boyle’s Law
“Boyle’s = Balloon”
The pressure of a gas is inversely proportional to the volume of a gas at a constant temperature
P1V1 = P2V2
Affects ETT cuffs, MAST trousers, Pneumocephalous, IV drip rates (increases rate)
Dalton’s Law
“Dalton’s Gang”
Law of Partial Pressures
The total pressure of a gas mixture is the sum of the partial pressures of all the gases in the mixture
P = P + P + P + … + P
T 1 2 3 n
Charles’s Law
“Charles = Centigrade”
At a constant pressure, the volume of gas is directly proportional to the absolute temperature of the
gas
V1 / T1 = V2 / T2
Example‐ Putting a can of shaving cream into a fire, can explodes because volume increases when
heated
This law has very little effect on the human body (we are at a relatively constant temperature)
Gay‐Lussac’s Law
Directly proportional relationship between temperature and pressure
P / T = P / T
1 1 2 2
Example‐ an oxygen cylinder left outside overnight will have a lower pressure reading in the morning
due to temperature drop
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Henry’s Law
“Henry = Heineken”
Solubility of gas in liquid
3
The quantity of gas dissolved in 1 cm (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”
This is an arterial gas embolism
The bends are the most common form of decompression sickness
Decompression Sickness
(Ground transport is preferred for BOTH)
Type I – Nitrogen related, painful, mottled skin, pruritic (itching)
Type II– Neurologic signs/sx, hypovolemic shock
There are actually 6 different types, too in depth for this subject
Arterial Gas Embolism requires immediate hyperbaric chamber treatment
Graham’s Law
“Graham’s= Grey Matter”
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‐ gas bubbles coming out of exposed grey matter when at altitude
Atmosphere Calculations
Every 33 feet below water 33ft = 1 ATM (atmosphere)
Sea Level= 1 ATM
33 ft under water = 2 ATM
66ft under water = 3 ATM
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Oxygen Adjustment Calculation
FiO2xP1 = FiO2 required for ascent
P2
Torr (P) Values
Sea Level = 760 torr (1 ATM)
18k Ft MSL = 380 torr (1/2 ATM)
63k ft MSL = 0 torr (0 ATM)
Example: You have a patient on an NRB 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 x 760/500= 0.76 FiO2 required for ascent
Types of Hypoxia
Hypemic = anemic
Anemia, hemorrhage, sulfonamides, carbon monoxide
Reduction in the O2 carrying capacity of blood
Histotoxic = poisoning
Cyanide, ethyl alcohol
A result of poisoning or metabolic disorders
Hypoxic= not enough Oxygen in the air
↓partial pressure of oxygen at altitude
Deficiency in alveolar O2 exchange
Stagnant = blood isn’t moving
High G forces, cardiogenic shock
Reduced cardiac output or pooling of blood
Stages of Hypoxia “ICDC”
Indifferent
Compensated
Disturbance
Critical
…….Indifferent stage is most important (because you can still think)
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Pilot Stressors
“DEATH”
Drugs
Exhaustion (fatigue)
Alcohol
Tobacco
Hypoglycemia (diet)
Altitude Effects
Barondontalgia (teeth)
Ascent
“Aerodontaligia”
Barotitis (ears)
Descent
“Ear Block”
Barosinusitis (sinuses)
Ascent/Descent
“Sinus Block”
Night Vision is decreased beginning at 5,000 ft MSL (Mean Sea Level)
Physiologically deficient zone‐ 10k to 50k MSL (Mean Sea Level)
If in a pressurized cabin and a sudden decompression occurs Time of Useful Consciousness (TUC) is
cut in half (90 seconds of useful consciousness at 30,000 ft)
G Forces
The human body is most susceptible to injury during LATERAL forces (gY)
G forces cause B/P to drop
People most affected by high G forces
On B/P meds (especially Beta Blockers)
Dehydrated
A cold, dry, high altitude environment has the greatest negative outcome to your patient
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Safety/CAMTS (12)
General
Safe operation of the aircraft comes before patient care!
The PIC is in charge and has the final say!
The only time you don’t need to wear a seat belt is during straight and level flight
Or when the PIC directs you to
Standard of Care
(Negligence)
Presence of duty
Breach of duty
Foreseeability
Causation
Injury
Damages
Duty to Report
Child abuse
Elder abuse
Violent crime
FAA Rules
FAR Part 91 ‐ Applies to everyone (general FAA rules)
No duty day
No weather minimums (PIC assumes risk)
FAR Part 135 ‐ Flying passengers for $ (taxi services)
Max 14 hour duty day
8 hours total flying time
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HLZs
Hasty/unsecured HLZ at night
Must have communication with the ground
100’ x 100’ HLZ
1 approach and departure heading
Permanent helipad
Must have 2 approach and departure headings
Lighting on the helipad
Weather Minimums
(FAR Part 135)
Local
Day 500’ ceiling and 1 mile visibility
Night 800’ ceiling and 2 miles visibility
Cross Country
Day 1000’ ceiling and 1 mile visibility
Night 1000’ ceiling and 3 miles visibility
Marginal Weather: weather that is very close to minimums (can fly, but accepting risk)
Below minimums: weather that is UNDER weather minimums (can’t fly)
If bad weather is encountered while enroute, divert to the nearest facility!
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Flight Rules
Visual Flight Rules (VFR): This means that you can fly only in weather conditions that you can see
where you are flying
Visual Meteorological Conditions [VMC]
There is NO intended instrument flying under these rules.
Instrument Flight Rules (IFR): This means that the weather condition do not allow safe flight by sight
alone, and the pilot must be able to use his instruments to fly
Instrument Meteorological Conditions [IMC]
If the weather conditions allow VFR/VMC, a pilot may still fly under these
conditions.
Inadvertent Instrument Meterological Conditions (IIMC): This means that the pilot began flying in
VFR weather and unexpectedly encountered weather that required flying by instruments.
In Flight Emergencies
Land immediately – engine failure/fire
Land as soon as possible – low transmission pressure/chip light
Land as soon as practical – go to closest convenient place
EMTALA
(Emergency Medical Treatment and Active Labor Act)
You must act if someone requires emergency care to sustain life or is actively giving birth
“150 Yard rule” – if someone is injured within 150 yards of a hospital, they must be treated
Sending physician is responsible for the patient until they arrive at next facility
CAMTS
(Commission for the Accreditation of Medical Transport Systems)
Sterile cockpit – only essential communication during all phases of flight except straight and level
flight
Critical phases of flight: Takeoff, Landing, and Taxi (ground or air)
Flight following
15 min flying, 45 min sitting on the ground
Emergency action plan activated 15 minutes after failure to report in
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Flame retardant clothing (flight suit) – must be able to pull ¼” away from body
AMRM – Air Medical Resource Management (distributes workload)
“The operational practice of involving ALL members of the flight team (pilot and clinical crew
members) in the mission planning, decision making, and mission safety
Referred to as CRM (Crew Resource Management) in the military
FAA Rules‐ Aircrew may resume flying duties as long as they have not had a drink in the last 8 hours
“8 hours bottle to throttle”
Ground ambulances must have a 175 mile range
Required to do 5 live intubations before beginning missions
Quarterly intubations thereafter
Air Transport Team Members
Flight Nurse
Flight Paramedic
Respiratory Therapist
Flight Physician
Rotary Wing Pilot in Command Qualifications
(Helicopters)
Min 2000 hours total flight time
1000 hours as PIC
100 hours as PIC at night
Airline Transport Pilot (ATP) certificate is strongly encouraged (not required)
Area Orientation – 5 hours total w/ 2 at night (completed before solo mission acceptance)
Fixed Wing Pilot in Command Qualifications
(Airplanes)
2000 hours total flight time
1000 hours as PIC
100 hours at night as PIC
Must possess an ATP certificate
Must be instrument rated
Fixed wing MUST file IFR and VFR Flight Plans
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Crash Procedures
Pre‐Crash Sequence:
Lay the patient flat
Turn off any oxygen
Assume the crash position
Seat belt secured
Sit up straight (seats are designed to absorb impact)
Helmet strap tight/visor down
Knees together, Feet 6” apart, flat on the floor
Not underneath the seat (they will get broken)
Arms crossed on chest
Chin to chest
Post‐Crash sequence
Turn Power Control Levers (PCLs) OFF, turn off the battery
Exit the aircraft (assist anyone who needs assistance)
Assemble at the 12 o’clock position
Begin building a shelter, build a fire, gathering water, create a signal
(In that order)
Emergency Locator Transmitter (ELT) self‐activates at 4Gs (can be manually activated)
Emergency transmit frequency is 121.5 MHz
#1 cause of crashes is weather (#2 is night flight)
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Trauma (9)
st
Newton’s 1 Law of Motion: Unless it is acted on by a force, a body at rest will remain at rest and a
body in motion will move at constant speed in a straight line
Law of Inertia
nd
Newton’s 2 Law of Motion: When a force is applied to a body, the body accelerates, and the
acceleration is directly proportional to the force applied and inversely proportional to the mass of the
body
Force = (mass)(acceleration)
rd
Newton’s 3 Law of Motion: For every action there is an equal and opposite reaction
Injury Patterns
Motor Vehicle Crash (MVC)
Side Impact
Rib fractures, clavicular fractures, femur fractures, splenic rupture secondary to rib fracture
Front Impact
Rib fractures (with possible hemo/pneumothorax), concussion, skull fracture, dislocated
hips, acetabular fractures
Rear Impact
T12‐L1 m/c back injury, C2 (Hangman’s) Fx also common
T12 Fx is also called a “Chance fracture,”has increased chance of splenic injury
Rollover
Unpredicitable injury pattern
Possible C1 (Jefferson’s) Fx from axial loading
Motorcycle Crash
Front Impact
All lower extremities from impact with handlebars while moving forward, abdominal injuries
Side Impact
Open lower extremities fracture
Misc.Crashes
ATVs: Clavicular and sternal Fx
Snowmobiles: C2 (Hangman’s) Fx
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Abdominal Trauma
Spleen Fracture/Rupture
M/C injured solid organ in blunt trauma
Massive hemorrhage due to vascular supply of spleen
Kehr’s Sign: left shoulder irritation secondary to diaphragmatic irritation from blood
Colon / Small intestine‐ Most commonly injured hollow organs from penetrating trauma
Liver ‐ Most commonly injured solid organ in penetrating trauma
Diaphragmatic Hernia
MCC is blunt force trauma during MVC
Most commonly occurs on the left side (right side is protected partially by the liver)
Abdominal contents are forced into the chest
Bowels sounds auscultated during chest exam
Scaphoid Abdomen
Coopernails Sign: scrotal or labial ecchymosis from abdominal trauma or pelvic fracture
Femoral Artery Catheterization Landmarks
Nerve, Artery, Vein, Lymphatics
LATERAL MEDIAL
Nerve Lymph
Artery Vein
“NAVEL"
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Cardiac Tamponade
Accumulated fluid around the heart either due to blunt or penetrating trauma
Pulsus Paradoxis‐ ↓SBP >15 mmHg during inspiration
Beck’s Triad
Muffled heart tones
Narrowed pulse pressure
JVD
“Electrical Alternans” on EKG
Treat with pericardiocentesis to the left of the
xiphoid process, directed towards the right shoulder
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Hemothorax
Accumulation of blood in the thoracic cavity, most commonly form the inferior mammary artery
Treatment: Tube Thoracostomy
5thor 6thICS ANTERIOR axillary line
Pneumothorax
Accumulation of air in the thoracic cavity, can be from blunt or penetrating trauma, as well as
spontaneous rupture of blebs(tall, thin males)
Initial Treatment: Occlusive dressing over the wound (Three sided)
Sudden increase in PPLAT indicates probable tension pneumo
Needle decompression if symptomatic
Guide needle over the top of rib (avoids neurovascular bundle)
2nd/3rd ICS Mid‐Clavicular Line (MCL)
5th IC Mid‐Axillary Line (MAL)
Definitive Treatment: Tube Thoracostomy
5thor 6th ICS MIDAXILLARY Line (MAL)
Placement in the 4th ICS MAL can lead to lung damage (too high)
Placement in the 7th ICS MAL can lead to splenic damage (too low)
In order to be a “Sucking Chest Wound” the chest wall defect must be >1/3 of the diameter of
the trachea
Rib Fracture
Can be diagnosed clinically based on history and presentation
Difficulty taking deep breaths is common
Treat with analgesics and ensure the patient takes deep breaths (despite pain) to prevent
atelectasis (lung tissue collapse)
Provide pain control
Flail Chest
Defined as 2 or more ribs broken in 2 or more places
Flail segment should be stabilized with tape and bulky dressings
High flow O2
Transport injured side down
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Killers In Flight
Tension Pneumothorax
Pericardial Tamponade
Hypovolemia
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Fluid Resuscitation
Hypotension starts at 30% blood loss
Fluid replacement ratio is 1:3 (blood loss to crystalloid fluid)
2 Large Bore IVs (ATLS standards)
Transfusion Reactions
Stop the transfusion if there is any adverse reaction
Drop in blood pressure
Fever
Tachycardia
Pallor
Cyanosis
Anaphylactic reaction (urticaria, pruritis, hypotension, tachycardia)
Caused by Anti‐IgA antibodies
Rapid onset (within 30 minutes of infusion)
Stop the transfusion
Epinephrine
Steroids
Benadryl
No method to anticipate anaphylaxis
Overload reaction (hypertension, distended neck veins)
Can occur at any time
Stop the transfusion, administer Lasix
More likely in those with kidney or cardiac disease
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
Urticarial reaction (local erythema, hives, itching)
Further evaluation unnecessary unless fever, chills, other adverse reactions are present
ONLY transfusion reaction that the infusion can continue
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Misc. Trauma Bullets
Avulsed teeth?‐ put in gauze soaked in NS, milk, or between the cheek and gum
Unstable pelvic fx is always life threatening (vertical shear is the worst)
Lap belt injuries – “Clasp knife effect”
High velocity weapons fire projectiles >2000 fps (rifle rounds)
Velocity is the most important factor in GSW damage
The most commonly damaged organ is the skin
THE MOST DEFINTIVE ASSESSMENT OF SHOCK IS LACTIC ACIDOSIS (lactate >4)
Tracheobronchial injury‐ "Hamman's Crunch"
‐ Crunching, rasping sound, synchronous with the heartbeat
Leforte Fractures
Le Forte I: Horizontal fracture, affects lower maxilla, maxilla and maxillary teeth are moveable
Le Forte II: Pyramidal fracture, usually from a downward blow to the nose
LeForte III: Transverse Fracture, aka “Craniofacial Disassociation”
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FP‐C Recert Requirements
You must have 100 Continuing Education hours in critical care medicine (flight physiology, trauma
medicine, toxicology, etc.) and have attended a certified recertification course (16 hours minimum).
Although your certification is good for 4 years, you need to start your recertification process 6 months
prior to certification expiration. Remember that CME logs are 100% audited, so don’t fake your records.
Things that are not acceptable for CEUs are BLS, ACLS, PALS, PHTLS, PEPP, etc. Keep good track of CEUs
you do. Your Training/Medical Officers can give you classes related to CEUs,and you can also get credit
for conference attendance. It is your responsibility to remain educated and relevant to your mission.
Recertification Guide http://bcctpc.org/Recert/Guideline_for_Renewal_by_CE.pdf
BCCTPC
4835 Riveredge Cove
Snellville,GA
30039
(770)978‐4400
[email protected]
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Continuing Education (CE) Verification Log
Full Name: ________________________________________________________ FP‐C Number:
Mailing Address: _____________________________________________________________
Email Address: ________________________________________________ Phone:
Employer:
I affirm that the following information is true. (sign) _________________________________ Date:
CE Renewal
FP‐C 's seeking certification renewal must accumulate 100 Contact Hours (continuing education credits) within the
four‐year period prior to certification expiration. At least 75 of the contact hours must be in the CLINICAL category,
and up to 25 may be in the OTHER category.
Directions
Print or type all information legibly. Please refer to the CE guidelines for more information. This form may be
photocopied. Submit your verification log, copies of CE documents and required fees to: BCCTPC, Attn: CE Renewal,
4835 Riveredge Cove, Snellville, GA 30039
.
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.
.
.
14.
TOTAL
Category: Publications
TOTAL
Category: Item Writing
Month/Year when Number of Clinical Other
Questions were Written Questions Written CE's CE's
Name of Professional Exam Awarded Awar
TOTAL
Category: Presentations/Lectures
Clinical Other
Date of
CE's CE's
Lecture
Conference Name Lecture Title Awarded Award
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Category: Preceptorship
(Contact hours are earned only when you provide training to a student for a quarter, semester or
trimester)
Name of Academic Course Semester, Number of Course Clinical Other
(provided practical Quarter or Credit Hours (the CE's CE's
training) Month/Year Trimester student earned) Awarded
TOTAL
Category: Academia
Semester, Total Clinical Other
Quarter or Course CE's CE’s
Name of Academic Course Month/Year Trimester Credit Hrs Grade Awarded
1.
2.
3.
TOTAL
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References
Advanced Trauma Life Support Program for Doctors: ATLS. Chicago: ACS, 2004. Print.
Bledsoe, Bryan E., and Randall W. Benner.Critical Care Paramedic. Upper Saddle River, NJ: Pearson
Dubin, Dale. Rapid Interpretation of EKG's: a New, Simplified Approach for Systematically Reading
Holleran, Reneé Semonin. ASTNA Patient Transport: Principles and Practice. St. Louis, MO: Mosby,
2010. Print.
Marx, John A., Robert S. Hockberger, Ron M. Walls, James Adams, and Peter Rosen.Rosen's
Print.
Pierce, Graham. "Flight Paramedic Certification Testing and Renewal."BCCTPC. BCCTPC, 15 Jan.
Rayman, Russell B. Clinical Aviation Medicine. New York, NY: Professional Pubishing Group, 2006.
Print.
Reinhart, Richard O. Basic Flight Physiology. New York: McGraw-Hill, 2008. Print.
Walls, Ron M., and Michael F. Murphy.Manual of Emergency Airway Management. Philadelphia:
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FP‐C Study Guide ©2011 by L. Kyle Faudree
Images
12 Lead EKG. Photograph. Nursing Community for Nurses - Allnurses.com.Web. 05 Aug. 2011.
<http://www.allnurses.com>.
Axillary Lines. Photograph. Wikipedia, the Free Encyclopedia. Web. 04 July 2011.
<http://en.wikipedia.org>.
Cardiac Auscultation Points. Photograph. Main Page - Physiopedia- the Free Resource for the
Cardiac Output Transducer. Photograph. ISPUB - Internet Scientific Publications. Web. 02 July 2011.
<http://www.ispub.com>.
Cardiac Tamponade Chest Xray. Photograph. BMJ Case Reports - BMJ Journals.Web. 02 July 2011.
<http://casereports.bmj.com>.
Coronary Artery Diagram. Photograph. Texas Heart Institute. Web. 02 July 2011.
<http://texasheartinstitute.org>.
Fetal Heart Rate Monitoring. Photograph. Continuing Education for Nurses.Web. 02 July 2011.
<http://nurse411.com>.
<http://bestpractice.bmj.com>.
Intraortic Balloon Pump. Photograph. U S Food and Drug Administration Home Page.Web. 02 July
2011. <http://www.fda.gov>.
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FP‐C Study Guide ©2011 by L. Kyle Faudree
<http://tirthankaronline.blogspot.com>.
Pediatric Neck Xrays. Photograph. Wikipedia, the Free Encyclopedia. Web. 02 July 2011.
<http://en.wikipedia.org>.
Phlebostatic Axis. Photograph. Continuing Education for Nurses.Web. 02 July 2011.
<http://nurse411.com>.
Prehospital 12 Lead ECG: Contiguous and Reciprocal Lead Charts. Photograph. Paramedic Class
contiguous-and-reciprocal-lead-charts/>.
Rule of Nines Burn Chart. Photograph. Medical Lecture Notes Online.Web. 02 July 2011.
<http://medicalpptonline.blogspot.com>.
www.weillcornell.org
www.nurse411.com
If you have any questions, comments, or suggestions to make this program
better, let me know! Send an email to me at [email protected].
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FP‐C Study Guide ©2011 by L. Kyle Faudree
Flight Paramedic Certification‐
A Comprehensive Study Guide©
This book is a thorough exam preparation guide that prepares the candidate
for FP‐C certification. It was written for both civilian and military medics at all
levels of experience and expertise, explaining critical care aeromedical concepts in
an easy to understand format. The material is to the point, while providing
insight and clarity to complex critical care medicine concepts and procedures.
The course material utilizes a detailed curriculum and is a approved for continuing
education by the Board of Critical Care Transport Paramedic Certification
(BCCTPC), the organization that grants FP‐C Certification. Congratulations in
advance for purchasing this book and working towards becoming a certified flight
paramedic!
A portion of the proceeds from this book
is donated to the Special Operations
Warrior Foundation (SOWF), an 106
organization that provides support to
wounded Special Operators and their
families.
FP‐C Study Guide ©2011 by L. Kyle Faudree
BAR CODE BOTTOM RIGHT
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