Paramedic NREMT Maddy Kearns

CARDIOLOGY

BLOOD FLOW THROUGH HEART

pulmonary and systemic circulation

Deoxygenated blood enters the right atrium via the superior and inferior vena cava. The right
atrium contracts and blood flows via an open tricuspid valve into the right ventricle. From the
right ventricle, the pulmonary artery takes blood into the lungs/pulmonary circulation. At the
lungs , blood travels through capillary beds of the alveoli exchanging carbon dioxide for oxygen.
So, oxygenated blood returns via pulmonary veins into the left atrium. Blood flows via an open
mitral valve from the left atria to the left ventricle and out to the body via the aorta to systemic
circulation. The aorta branches into arteries, arterioles, and into capillaries where gas exchange
takes place- oxygen diffuses into the cells and metabolic waste and co2 diffuses into the blood
to return via venules, veins, and the vena cava to repeat the process.

Heart Layers: Inside to Outside

● Endocardium: Innermost layer. Made of endothelial cells that create a smooth,

non-adherent surface for blood to collect on.
● Myocardium: Middle Layer.Thick muscular layer that contracts and pushes blood out.
Drives cardiac cycle as it generates its own impulses (automaticity)
● Epicardium: (Visceral pericardium) Outermost layer. Forms the inner layer of the
pericardium
● Pericardium: Fibrous sac that encloses the heart and protects it. Fills with around 25ml
of pericardial fluid that aids in lubricating the heart. You know, so it doesn't hurt to have a
heartbeat.

Heart Valves and Heart Sounds

● Atrioventricular Valves (S1) : By breaking down the name, we can infer that these
valves are located in between the atria and ventricles, crazy how that works out. There
are two AV valves: on the right side is the Tricuspid that flows blood from the right atrium
to the right ventricle. Tri means 3 as it anatomically has 3 leaflets/flaps . On the left side
there is the Bicuspid (MITRAL) valve with two leaflets, blood flows from left atria to left
ventricle. HEART SOUND 1 = CLOSURE OF AV VALVES
● Semilunar Valves (S2): On the right is the pulmonic valve, blood flows from the right
ventricle to the pulmonary artery. On the left is the Aortic valve where blood flows from
the left ventricle to the aorta. HEART SOUND 2= CLOSURE OF SEMILUNAR
VALVES.
● S3 is a ventricular gallop indicates chf in adults
● S4 is an atrial gallop which indicates left ventricular failure or aortic stenosis
 Blood Pressure

Blood pressure is defined as SV x HR x SVR OR CO x SVR

Stroke Volume (blood ejected with each beat, approx. 70 ml)

X
Heart Rate (Number of times the heart beats per min approx 60-100bpm)
=
Cardiac Output ( Total blood volume pumped per min approx. 5L/min)
X
Systemic Vascular resistance (Resistance of blood being pushed through the
circulatory system. Think VESSEL DIAMETER)
=
Blood pressure

Factors of Stroke volume

PRELOAD: Pressure in ventricle at the end of diastole. An increased amount of venous

return will stretch myocardial cells and according to Frank Starling Law, the more these
cells stretch, the more force they'll use to “bounce back” much like a rubber band
(Contractility). The harder the contraction, the more volume can be pushed out with each
beat hence why it increases stroke volume.
INCREASE IN PRELOAD = INCREASE IN SV
DECREASE IN PRELOAD = DECREASE IN SV
AFTERLOAD: Resistance to which the ventricle must contract against during systole. If
there is an increase of blood, sv will decrease because the heart cannot push all of it
out. If there is decrease, the heart won't have to work very hard to push the blood out
and SV will increase. Inverse relationship.
INCREASE IN AFTERLOAD = DECREASE SV
DECREASE IN AFTERLOAD = INCREASE SV

MEAN ARTERIAL PRESSURE(MAP)

Measures level of tissue perfusion

MAP= Systolic BP + Diastolic BP (times 2) divided by 3
Ex.) Calculate the MAP of 120/80 BP

So, Map = 120 + 80(2) / 3 +93

 MAP Under 50 = HYPOPERFUSION/ORGAN FAILURE
MAP Over 150 = POSSIBLE BRAIN BLEED (think high bp like in cushing's triad)

Cardiac Conduction/Electrophysiology/EKG

Cardiac rhythm is established by specialized myocardial cells, capable of automaticity where

they spontaneously generate electrical impulses. These electrical impulses trigger a wave of
depolarization, where voltage gated ion channels allow an influx of Sodium Na+ ions that create
a positive charge in the cell's interior so it can contract. Normally, the Sinoatrial node Rate
60-100 located in the right atrium generates an excitation signal, or action potential, that begins
the depolarization wave (Na+ ions). The wave of depolarization spreads through the Atria
causing them to contract. Atrial Depolarization is represented in an ekg as a P wave.The brief
pause and plateau following the p wave occurs as the wave of depolarization carried slowly by
Calcium CA++ ions is conducted through the internodal pathways to the Atrioventricular node.
Rate 40-60 The Atrioventricular Node then conducts the depolarization wave rapidly with NA+
ions through the bundle of His then bifurcating into right and left bundle branches then into
terminal filaments of purkinje fibers Rate 15-40 to depolarize ventricular myocytes and cause
ventricular contraction. Ventricular depolarization is represented as the QRS complex on an
ecg. To recover and repeat the process, repolarization rapidly occurs where Potassium K+ ions
leave the myocytes and their internal charge is back to negative so the cell can rest.
Repolarization is represented by a horizontal line followed by a hump called the T wave.
Ventricular repolarization is represented by the T wave on an ekg.

Note: The QT interval until the end of the T wave represents the absolute refractory
period, meaning no stimulus will generate another wave of depolarization. At the end of
the T wave is the Relative Refractory Period where stimuli may generate abnormal
depolarization. For example, if a PVC hits during the relative refractory period, it could
potentially initiate VT.

Steps of EKG interpretation

1.look for P waves

2.look to see if the P waves are upright
3.look to see if there is one P wave for every QRS complex (If yes to all, normal sinus rhythm)
4.look to see if your rhythm is regular
5.Assess the rate
6.Assess your intervals (PR interval QT interval and ST segment)
Normal PR 0.12-0.20
Normal QRS 0.04-0.12
ST deviation from isoelectric line ? Concave ? convex?
● ST segment depression = Myocardial Ischemia
● ST segment elevation = Myocardial Infarction - figure out where!
Bonus: Look at wave morphology! Assessing this tells you so much!
 Premature Beats

Name indicates where ectpoi came from

● PAC (Premature Atrial Contraction) is a early beat that has a upright P wave
● PJC (Premature Junctional Contraction is a early beat that has either an inverted P
wave or no P wave at all (if there is no P wave, measure the QRS, it has to be less than
0.12sec to be considered a PJC)
● PVC (Premature Ventricular Contraction )is a early beat that has no P wave and is
greater than 0.12sec
Further Classifying Premature Beats

● Unifocal: morphology is the same (same site of ectopy)

● Multifocal: morphology is different (different sites of ectopy)
● Bigeminal Pattern: Every other beat is premature
● Trigeminal Pattern: Every third beat is premature
● Quadrigeminal pattern: Every fourth beat is premature
● 6 or more in a row is dangerous! Multiple pvcs in a row is a “run of V-Tach”

Late Beats

Ectopy presents the same but instead of being early you identified that it was late. The biggest
take away from late beats is that late beats are happening because the heart is trying to pick up
the rate.
 Treatment section: Cardiology

Treatment: Note stability refers to hemodynamic stability (blood pressure, signs of poor
perfusion such as AMS)
Identifying MI and Artery Involved

Pathophysiology of MI: The coronary arteries feed the heart during diastole. When any of these
arteries are blocked, the tissue in its respective area becomes ischemic resulting in ST segment
depression. Prolonged ischemia progresses into infarction as cells begin to die, reflected as ST
segment elevation. 1mm or more deviation from the isoelectric line indicates active MI.

>Check placement: Lead I will have a positive deflection and AVR will show negative deflection.

Leads Area Artery

II, III, AVF Inferior Right Coronary Artery

I, AVL High Lateral Left Circumflex Artery

V1, V2 Septal Left Anterior Descending Artery

V3, V4 Anterior Left Anterior Descending Artery

V5, V6 Lateral Left Circumflex Artery

> If you have ST depression in V1 V2 and V3 you have ST elevation in V7,V8,V9 which is the
posterior wall
>If you have ST elevation in II, III, AVF, move V4R. If positive, withhold nitrates

Myocardial Infarction (or angina) Treatment (v4r negative)

Mona or Fona based on protocol and presence of hypotension as Morphine may drop blood
pressure. Hypotensive MI = Fentanyl. Hyperpertensive MI = Morphine
● Morphine 2-4mg max 10 OR Fentanyl 50-100mcg
● Oxygen
● Nitroglycerin .4mg SL (verify no contraindications)
● Aspirin 324mg orally (give before morphine and ntg incase pt bottoms out)
Note: Order is Oxygen first, aspirin, nitro, morphine

Myocardial Infarction Treatment (v4r positive)

● Nothing to reduce preload/pressure!

● If hypotensive, check LS and give a fluid challenge
 ● Can give aspirin 324 mg
EKG findings that suggest prior MI: Pathological Q wave
● 0.04 wide
● 2mm deep
● 25% or ⅓ of R wave

Bundle branch blocks (RBBB AND LBBB)

Block in either right or left bundle branches that causes change in wave morphology and
creates a wide qrs complex
Distinguishing between RBBB and LBBB
RBBB: Look at V1: Wide QRS and upwards deflection its RBBB
If qrs looks like an M in V1 and a W in V6 its RBBB
LBBB: Look at V1: if it is wide and points down it is LBBB
If QRS looks like W in V1 and M in V6 its LBBB

New onset LBBB: TREAT LIKE AN MI!!!

Sgarbossa Criteria: Identifying MI when LBBB is present

Recall concordant patterns (QRS and ST in same direction) and discordant (QRS and ST in
opposite direction)
Criteria:
● Concordant ST elevation >1mm any lead
● Concordant ST depression V1-V3 >1 mm
● Discordant in excess of 5mm or more

Heart failure

Right sided heart failure presentation

As right ventricle fails as an effective forward pump and fluid accumulates, it creates backwards
pressure into systemic venous circulation resulting in the following symptoms:
● JVD
● Liver engorgement (hepatomegaly)
● spleen engorgement (splenomegaly)
● Pedal edema
● Fluid accumulation in abdomen (Ascites)
● Cor pulmonale (high pressure in pulmonary artery/pulmonary hypertension)

Treatment
If lung sounds are clear and it is indicated, give a fluid challenge. If lung sounds reveal rales
withhold fluids! Consider catecholamines such as dopamine 5-20 mcg/kg/min titrated to effect

Left sided heart failure presentation

As the left ventricle fails as an effective forward pump and fluid accumulates, it creates
backwards flow into pulmonary circulation resulting in RALES as fluid is in the lungs. Left
labored lungs lethal Rales due to pulmonary edema.

Note: some pts may experience paroxysmal nocturnal dyspnea which is when the pt will
randomly wake up in the middle of the night by shortness of breath. Usually indicates that HF is
getting worse. Treatment is based on two categories:

● Hypotensive HF with rales

NO FLUIDS.

catecholamines:

>Dopamine (Titrate to effect)

Make: 200 mg in 250ml NS yields 800mcg/ml
400 mg in 250ml NS yields 1600mcg/ml
800 mg in 500ml NS yields 16000mcg/ml

Starting dose: Dopamine 5-10mcg/kg/min IV drip to fix stroke volume by stimulating beta 1

…..If you fix stroke volume but BP is still bad then you must titrate to higher dose

Next Dose: Dopamine 10-20mcg/kg/min to directly raise blood pressure by pure alpha 1
stimulation (vasoconstrictor)

OR

>Epinephrine (Titrate to effect)

Make: Epi 1/10000 1mg into a 250ml NS will give you a concentration of 4mcg/ml dosing is
2-10mcg/min

OR

>Norepinephrine (Levophed) 2-12mcg/min

Make: 1mg into 250ml D5W will give you a concentration of 4mcg/ml
Run infusion at 4mcg/min (1ggts/sec) with microdrip set (60ggts/min)

No cpap if systolic 90 or lower!!

● Hypersensitive HF with rales

Rales can’t have fluids but because of hypertension AND they can’t have catecholamines
because they will make BP even higher

Go with acronym ONFM

O2- CPAP 7.5-10 cm H2O (reduces preload and afterload) if pt will tolerate it, preoxygenate with
15lmp NRB, consider sedating with 2mg versed to ease pt anxiety, explain procedure to patient!

Nitro- 0.4mg q every 3-5 mins max of 1.2mg (reduces preload and afterload)

Furosemide- 40mg to start if already taking lasix at home match home dose usually 80mg
(reduces preload) max 100mg

Morphine- start at 2-4 mg slow ivp max 10mg (reduces preload) Do not substitute morphine for
fentanyl here because it doesn’t reduce preload

Symptomatic Bradycardia(idioventricular/sinus bradycardia/ junctional)

Stable
Atropine 0.5mg-1mg, max of 3mg
Pacing 80ppm beginning at 40-60Ma until full electrical AND mechanical capture
Catecholamine Drip
Dopamine 5-10mcg/kg/min beta 1 stim frank starling
Dopamine 10-20mcg/kg/min alpha 1 stim vasoconstriction
Unstable
Pacing 80ppm till full electrical and mechanical capture
Dopamine 5-10 mcg/kg/min beta 1 stim frank starling
Dopamine 10-20mcg/kg/min alpha 1 stim vasoconstriction

Symptomatic Bradycardia (2nd type 2 and 3rd degree heart blocks)

Them bois need pacing if they’re symptomatic with these blocks

Supraventricular tachycardia (SVT)

Stable
Vagal maneuver
Adenosine 6mg rapid ivp 20cc flush
Adenosine 12mg rapid ivp 20cc flush
Unstable
Cardioversion 100J

V-Tach w/ pulse
Stable
Amiodarone 150mg in 50ml NS with a 10gtts over 10mins
Unstable
Cardioversion 100-200j

Atrial Fibrillation
Stable
Cardizem 0.25mg/kg
Unstable
Cardioversion 120j (if you have a lifepak its 125j)

Note: Pts with hx of a-fib are commonly prescribed digoxin which has a narrow therapeutic
index, beware of digitoxin toxicity. Pts with a hx of a-fib will also commonly be on blood thinners
such as eliquis and coumadin to prevent clotting.

Polymorphic V-tach (Torsades De Pointes)

Stable
Magnesium drip 2g into 50ml NS over 2 mins
Unstable
Overdrive pacing start 80ppm at 180Ma and work your way down till pt HR is normal (starting at
high energy makes the monitor the primary pacemaker allowing YOU to control rate) ask med
control doe

No pulse (defib V-TACH/V-FIB)

Always unstable
If witnessed arrest DEFIB IMMEDIATELY
If unknown downtime go to………
Compressions=circulation
Airway? Is it clear and patent
Breathing? Lube the tube? =intubation
EPI 1/10000 IVP 1mg
1 CPR cycle/DEFIB
Amio 300mg IVP/OR/lidocaine 1-1.5mg/kg
1 CPR Cycle/DEFIB
EPI 1/10000 IVP 1mg
1 CPR Cycle/DEFIB
Amio 150mg IVP/OR/lidocaine 1-1.5mg/kg
H’sand T’s

No pulse (PEA/Asystole)

Always unstable
Compressions=circulation
Airway? Is it clear and patent
Breathing? Lube the tube? =intubation
1 CPR Cycle
EPI 1/10000 IVP 1mg
1 CPR cycle
EPI 1/10000 IVP 1mg
1 CPR Cycle
H’s and T’s

Treat H’s and T’s

>Hypovolemia: Fluid challenge if lung sounds are clear (increases preload, EDV, activate frank
starling to increase contractility all to increase SV)

>Hypoxia: Ensure patent airway and adequate ventilation/oxygenation

>Hydrogen ion(acidosis): Sodium bicarbonate 1mEq/ml, increase the respiratory rate to help
blow off co2. Preexisting acidosis prior to death

>Hypokalemia: Flat T wave and presence of U wave on EKG. Magnesium 2g iv

>Hyperkalemia: moves from right to left Peaked T wave on EKG, in later stages the T wave will
merge with the QRS complex and p waves may be dropped as well as the presence of sine
waves. Recall normal potassium levels are 3.5-5.0 high 8.0-9.0 and 10 is incompatible with life
Albuterol 2.5mg 3ml neb/ calcium chloride 1g slow IVP and sodium bicarb slow IVP 1 Meq/ml
(in two separate IV’s to prevent making precipitate calcium carbonate which is chalk. If unable to
establish second IV, you can give in the same line IF it is followed by a 50-100cc flush)

>Hypothermia: Osborn wave on ecg “J wave”, warm pt gradually and evenly.

>Hypoglycemia: Dextrose

>Hypocalcemia: Prolonged repolarization. Calcium chloride 1g slow IVP

>Tension Pneumothorax: Decompress affected side 2nd-3rd intercostal midclavicular line using
large bore IV, stay on upper side of rib to avoid hitting neurovascular bundle.

>Tamponade(cardiac): Treated in hospital via pericardiocentesis, expedite transport

Pericardial Tamponade starts with Pleural Effusion where excess fluid collects in this space
slowly. When this fluid increases, it becomes a pericardial tamponade where the fluid is
accumulating drastically in this small space and cant leave so it ends up compressing the walls
of the heart and impairs ventricular filling. The heart can't fill = Lowered BP. Blood can't go
anywhere and excess pressure on vena cava= blood backing up causing JVD. In Pericardial
Tamponade you will see Beck's Triad: JVD, muffled heart sounds, hypotension with narrow
pulse pressure. So if you're trying to figure out why your patient has these symptoms, use that
stethoscope. Pericardial tamponade notoriously presents with pulsus paradoxus: drop in
systolic bp of over 10mmhg during inspiration

>Thrombosis/embolism: Signs of PE include acute respiratory distress, tachycardia, and

hypotension. Treated in hospital, provide adequate oxygenation and ventilation

>Toxins:
● Opioids =narcan 2mg max of 10mg (depends on your protocall) respiratory depression,
pupil constricted
● TCA OD (ex. AmitriptyLINE, NortriptyLINE) =sodium bicarb 1meq/ml IVP
● Beta Blocker (low hr low bp low bgl) and calcium blocker OD (low hr low bp high bgl)=
glucagon 1mg given with dextrose and calcium chloride 1G IVP if it does not work use
atropine or pacing AND IF THAT DOES NOT WORK LUNG SOUNDS =rales =dopamine
or epi=clear=fluids
 AV BLOCKS

Idioventricular blocks occur when there is a partial or complete interruption of transmission from
the atria to the ventricles. Often causes bradycardic rate.

First degree: characterized with a long pr interval greater than .20

Second degree Mobitz type 1 Wenckebach: PR interval progressively gets longer until QRS
drops
Second degree Mobitzz type 2: Constant PR interval but there will be P waves with no QRS
complex. If there are 2 P waves per QRS complex you would describe it as 2nd degree Mobitz
two with 2:1 AV conduction
Third Degree: Complete dissociation between P waves and QRS complexes, results in P waves
disappearing in the qrs or st segment.

Wolff-Parkinsons White Syndrome

Congenital condition, a type of Pre-excitation syndrome due to the presence of an accessory

pathway (bundle of kent). Its features include a short PR (<120ms) and a broad QRS that looks
slanted called a delta wave. Causes tachycardia. Usually treated with propranolol.

Left ventricular hypertrophy

Indicates increased pressure on the left ventricle secondary to aortic stenosis

It is a classic presentation in long term hypertension

The sokolov lyon criteria is used to make the determination

Add the S wave in V1 plus the R wave in V5 or V6. If the sum is greater than 35
mm, LVH is present. You can also look at V4 and V5 or at V2 and V3 and if the
QRS complexes are touching than they have LVH
 RESPIRATORY

Ventilation: Mechanical process of breathing. The diaphragm contracts moving downward and
the intercostal muscles contract, both aiding expansion of the thoracic cavity. The increased
volume of the thoracic cavity means pressure is decreased (follows Boyle's law) creating a
negative pressure gradient compared to that of the atmosphere thus drawing air in like a
vacuum during inhalation. Inspiration is an active process. Exhalation however is a passive
process, muscles relax creating less volume in the thoracic cavity and more pressure thus
forcing air out during exhalation. However, it is important to note that the pathologies of
conditions such as asthma and copd impair exhalation causing it to become an active process
hence the use of accessory muscle use in these patient populations.
Regulation of Ventilation via Chemoreceptors: Increased Co2 and decreased pH = drive
to breathe.
● The carotid arteries and the aortic arch contain chemoreceptors that monitor the partial
pressure of carbon dioxide dissolved in blood (PaCO2).
Increased PaCO2 = breathing stimulation.
● Central chemoreceptors in the brain monitor the pH of cerebrospinal fluid. When pH
decreases and becomes acidotic (more CO2), respiratory centers of the brainstem
(medulla oblongata) signal lungs to increase rate and depth of breathing.
Hering-Breuer reflex: Stretch receptors send signals to the brain to prevent overexpansion of
the lungs during ventilation.
Respiration: Exchange of gasses (o2 and co2). There are TWO types.
● External Respiration: Exchange of gasses at the alveolar level in the LUNGS.
● Internal Respiration: Exchange of gasses within the TISSUES.
Oxygenation: Loading of o2 on hemoglobin. Oxygen saturation is measured by pulse oximetry.
False readings include:
● Acrylic nails
● Cold extremities/poor perfusion
● Low hemoglobin/anemia
● Carbon Monoxide Poisoning: CO binds with hemoglobin with a 250x greater affinity than
O2. Patient may be extremely hypoxic with a 100% 02 stat - Treat Patient not the
monitor, it is only a tool.
Acid Base Balance and respiratory regulation
The major byproduct of metabolism is carbon dioxide (co2). Co2 combines with water to create
carbonic acid (h2co3) which further breaks down into bicarbonate (hco3-) and hydrogen ions
(H+). H+ concentration is pH, pH literally translating into “power of hydrogen”. Hydrogen has an
inverse relationship with the pH scale meaning that the higher the hydrogen concentration the
lower the pH (more acidic) and the lower the hydrogen concentration the higher the pH (more

⬆️ ⬆️ ⬆️ ⬇️
alkaline/basic). So:

⬇️ ⬇️ ⬇️ ⬆️
● carbon dioxide bicarbonate hydrogen ions= pH(Acidosis)
● carbon dioxide bicarbonate hydrogen ions= pH(Alkalosis)
Normal pH value: 7.35-7.45
The respiratory system plays an important role in managing the amount of CO2 in the blood and
thus pH. The brain regulates the amount of co2 in the blood via central chemoreceptors that
adjust ventilations as explained earlier. When Co2 levels are high and pH low(acidic),
ventilations will increase in rate and depth as a compensatory way to blow off excess co2 and
raise pH to equilibrium. Similarly, when co2 is low and pH is high(Alkaline), ventilations may
briefly stop or slow to retain more co2 and lower pH back to equilibrium. When compensatory
methods fail and co2 accumulates the pt can go into metabolic alkalosis, if co2 is low the pt can
go into metabolic acidosis.

Respiratory Acidosis Respiratory Metabolic Acidosis Metabolic

Alkalosis Alkalosis

● Hypoventilation ● Excessive ● Lactic acidosis ● Excessive

● Co2 retention BVM use ● Compartment vomiting
via ● Hyperventil syndrome ● Anti Acid
asthma/copd ating ● DKA OD
● Aspirin OD

End tidal co2 (ETCO2) (Capnography)

Capnography measures etco2 (measures Co2 in expired air) and is a good indication of a
patient's respiratory status and pH. Capnography should be used on ALL respiratory calls and
cardiac arrest calls.

*Normal Etco2 value: 35-45

....Opposite to the ph scale:

Must know Capnography findings:

● Low etco2 reading indicates hyperventilation/alkalosis
● High etco2 indicates hypoventilation/co2 retention/acidosis
● “Shark-Fin” waveform indicates bronchospasm ex.) asthma
● Reverse Sharkfin = emphysema
● Sudden drop in Etco2 = CHECK PULSE
● Sudden rise of Etco2 during CPR = CHECK PULSE FOR ROSC
● Curare Cleft - dip in plateau , indicates that in RSI pt is taking spontaneous breaths so
you must readminister neuromuscular blockade
Capnography - Waveform phases
Phase 1 - Baseline, end of inhalation, no Co2
Phase 2 - beginning of exhalation
Phase 3 - Plateau phase ETCO2 IS MEASURED HERE
Phase 0 - inspiratory phase, Co2 drops to 0
Normal Bicarbonate: 22-26

Abnormal Lung Sounds “Adventitious”

Wheezing: High pitched whistling noise due to

bronchial constriction and swelling.
Common in anaphylaxis and asthma.

Rales (crackles): Crackling noise that indicates fluid in

lungs. Common in Left Heart Failure
(pulmonary edema), drowning, and
pneumonia.

Stridor: High pitched noise on inspiration.

Indicates severe upper airway swelling.
Ex.) Anaphylaxis, toxic inhalation,
epiglottitis

Rhonchi: Rumbling sound that indicates mucous in

larger airways (bronchi). Common in
bronchitis, pneumonia, copd

Normal Lung sounds

Bronchial: Loud high pitched hollow Heard over sternum

Bronchovesicular: Soft, low pitch Heard over scapula,2-3rd

intercostal space lateral to
sternum

Vesicular: Soft, very low pitched Heard in lung periphery

Abnormal Breathing Patterns

Biot’s (ataxic): Irregular periods of Increased Intracranial

breathing with gasping and Pressure
apnea

Cheyne Stokes: Increased rate and depth, Neurologic, brain stem

then decreased rate and injury
 depth, with periods of
apnea

Kussmaul: Rapid and deep DKA

Agonal: Not actually breathing, Cardiac arrest, stroke

gasp for air death is imminent

Apneustic: Long deep breaths that Neurologic such as cns

stop during inspiration and injury or stroke
are followed by apnea

Note: Bowel sounds as lung sounds = DIAPHRAGMATIC RUPTURE

Percussion sounds:

Resonant: Normal

Hyperresonant: AIR IN CHEST. Tension pneumothorax,

asthma, emphysema.

Dull BLOOD IN CHEST. Hemothorax. Thud =

Blood.

RESPIRATORY TREATMENT:

COPD - Chronic Obstructive Pulmonary Disorder

Group of diseases blocking airflow including: Emphysema and Bronchitis.

● Bronchitis = Bronchial tubes become inflamed + increased mucus production. “Blue

Bloaters” often have cyanotic skin, are overweight, have a productive cough, and lung
sounds of rhonchi and wheezing
● Emphysema = Small airways + alveoli collapse upon exhalation, alveoli lose elasticity.
“Pink Puffers” often have dry/pink skin, are underweight, pursed lips, barrel chest, have a
dry cough, and lung sounds include wheezing.
Treatment: Nebulized Albuterol 2.5mg and Atrovent .5mg @ 6-8lpm NRB. Consider giving
Solumedrol 125 mg. If these treatments fail and pt is able to maintain their airway and follow
commands, use CPAP starting at 5 PEEP titrated to effect at around 10 PEEP. Connect EtCo2
because COPD pts often retain CO2 causing “sharkfin” waveforms that indicate bronchospasm.
Return to a normal rectangular shape indicates pt improvement. Remember, these patients
have chronically low oxygen levels and chronically high co2 levels, these patients rely on the
hypoxic drive to breathe (oxygen chemoreceptors rather than co2 chemoreceptors). Never
withhold oxygen and carefully titrate oxygen levels and ask what the patient's baseline is.
 Asthma

Airways become inflamed, constricted, and have increased mucus production. Pts will often
have audible expiratory wheezing. Shark fin wave morphology on etco2 due to bronchospasm.
.
Treatment: Nebulized Albuterol 2.5mg and Atrovent .5mg @ 6-8lpm NRB. Consider giving
Solumedrol 125 mg. If these treatments fail, administer 2 g's of Magnesium Sulfate into a 50 cc
bag over 10 minutes (1gtts/sec).

Croup “laryngotracheobronchitis” Epiglottis

● Age: 6mo-3yo ● Any age, mostly children

● Gradual progression ● Acute onset
● Seal bark cough ● Drooling, dysphasia
● Viral ● Bacterial
● Mild fever ● High fever
● Rarely life threatening ● Life- threatening
● Treatment: blow by o2, humidified O2, ● Treatment: Do not agitate, blow by
racemic epi o2 if tolerated

Pulmonary embolism

Embolism in pulmonary artery

S&S: sudden onset SOB and tachycardia, pleuritic chest pain on inspiration/may be described
as sharp, cyanosis from the nipple line up

Risk Factors: DVT - Homans sign pain in calf with dorsiflexion of foot, post surgery, post birth,
bed ridden, recent fracture, immobility, pt on birth control and smokes

EKG CHANGES: SI QIII TIII

● S wave in in lead 1
● Pathological Q wave in lead 3
● T wave inversion in lead 3 (20% of cases)

Pneumonia
 Infection in lung(s). Commonly occurs due to aspiration or bacterial/viral/fungal infections

S&S fever, sob, rhonchi or crackles, productive cough with yellow sputum, typically
UNILATERAL. Elderly may present with AMS.

Assessment tool: Egophony:

Auscultate lungs and have Patient say the letter “A”, pneumonia changes vocal tone so it will
sound like an “E”, vice versa

Treatment: Ensure adequate ventilation and oxygenation

 NEUROLOGY

Functional units of the Nervous system are Neurons.

Structures/Functions of neurons include:
● Dendrite: sends impulses it receives to the cell body(soma)
● Axon: Sends impulse away to an adjacent neuron
● These impulses are action potentials that cause the release of
neurotransmitters shared between the synapse (junction/gap) between
the axon of a depolarized Neuron (pre-synaptic) to the dendrite of the
adjacent neuron (post-synaptic)

The Nervous System is Protected by Meninges:

● Pia Mater: Directly attached to surface
● Arachnoid: Middle layer, Spiderweb like structure
● Dura: Outermost layer, thick and durable

The Nervous System is Bathed in:

● Cerebrospinal Fluid: Produced by the choroid plexus and covers the brain and spinal
cord to aid in protecting it. Aids in maintaining pH. Flows in the subarachnoid space.

The Nervous system is divided into two sections:

● Central nervous system (CNS): Made up of the brain and spinal cord.
● Peripheral nervous system (PNS): made up of nerves branching directly off the brain
(cranial nerves) and spinal cord (spinal nerves) and into a vast network of nerves that
spread throughout the periphery.

The nerves of the PNS are divided into:

● Somatic (Afferent) : Sensory information from the PNS and sent to the CNS
● Autonomic (Efferent) : CNS sends motor information to the PNS
ex.) You touch a hot stove, the Afferent nerves send nociceptive (pain) signals to the
brain. The brain then sends a signal to the muscles of the hand and arm via different
nerves to move away from the stove.

The Autonomic Nervous system divides into:

● Sympathetic: fight or flight - Neurotransmitter is norepinephrine
● Parasympathetic: rest and digest - Neurotransmitter is Acetylcholine
 The brain itself is divided into 3 sections:
● Cerebellum: Balance, posture, coordination
● Brainstem:
➔ Midbrain
➔ Pons: Connection between Connection between brain and spinal cord
➔ Medulla oblongata: regulates Cardiovascular and Respiratory functions.
WE LIVE AND DIE IN THE BRAINSTEM
● Cerebrum (makes up majority of brain) and is divided into
Four lobes: “FPOT”
➔ Frontal Lobe: Perception, Intelligence, Impulses, Memory
➔ Parietal Lobe: Somatosensory information of touch, pressure, temperature,
and pain
➔ Occipital Lobe: vision, spatial processing
➔ Temporal: Auditory Processing
Other Important areas of the brain:
● Reticular Activating system: Maintains consciousness, wakefulness
● Cerebral Cortex: Outer surface of the brain
● Corpus Callosum: connects right and left hemispheres of the brain
Must know spinal nerves:
Total of 31 pairs of spinal nerves!
C-4 directly supplies diaphragm, injury here can result in respiratory paralysis

C-5-C-7 also have to do with diaphragm, injury here will make it difficult to breathe

Spinal Vertebrae
7 Cervical > C1 is the “atlas” and C2 is “axis”
12 Thoracic
5 Lumbar
Sacral 5 fused
Coccyx 4 fused
 Cranial Nerves

Cranial Nerve Sensory vs. Motor Function/significance

Olfactory Sensory Innervates olfactory mucosa to send sensory info

about smell to brain

Optic Sensory Innervates retina to send visual sensory info to brain

Oculomotor Motor Innervates pupillary sphincter to constrict pupils,

innervates most extraocular muscles except two

Trochlear Motor Innervates superior oblique eye muscle

Trigeminal Both Motor movement for mastication (chewing). Sensory

info from 3 regions of the face
(Ophthalmic,maxillary,mandibular). Trigeminal
Neuralgia: “tic douloureux” Chronic condition due to
dysfunction of this nerve that causes extreme
unilateral facial pain.

Abducens Motor Innervates lateral rectus eye muscle

Facial Both Sensory info from the anterior ⅔ of tongue.

Sublingual salivation, lacrimal (crying), facial
expressions. Facial Palsy: Sudden unilateral
weakness/paralysis of facial muscles due to
dysfunction of this cranial nerve.

Vestibulocochlear Sensory Vestibule: Balance

Cochlear: Hearing

Glossopharyngeal Both Motor is a gag reflex. Sensory info from posterior ⅓ of

the tongue.

Vagus Both Parasympathetic stimulation of abdominal and

thoracic viscera

Spinal Accessory Motor Motor movement of neck innervates trapezius and

sternocleidomastoid muscles to move neck

Hypoglossal Motor Swallowing and speech

 Stroke:

● Occlusive 80%
➔ Ischemic: Occlusion in cerebral artery due to an embolus. Characterized by severe
headache.
➔ Thrombotic: Most common cause is atherosclerosis. Thrombus Gradually develops as
plaque builds up and occluded cerebral artery
● Hemmorhagic 20%
Bleeding in the brain. Sudden onset severe headache, commonly caused by uncontrolled HBP.
● Transient Ischemic Attack (TIA) Brief stroke-like attack that subsides in 24hrs. Not an
actual stroke but may be a precursor to an actual stroke.

Stroke Risk Factors:

● Uncontrolled hypertension
● Aneurysm - weak arterial walls can break due to hypertension
● Atherosclerosis - narrows and occludes vessel, pieces can break off
● Atrial fibrillation - when blood pools it coagulates and can create clots
● Deep Vein Thrombosis - can send emboli to cerebral artery

Stroke Assessment: Rapid Arterial oCclusion Evaluation

Symptom Score

Facial Palsy None=0 Moderate=1 Severe=2

Arm Motor None=0 Moderate=1 Severe=2

Impairment

Leg Motor None=0 Moderate=1 Severe=2

Impairment

Head Gaze/Eye None=0 Presence=1

Deviation

Hemiparesis Left Right

Time? When was the last time the patient was seen normal?

Aphasia:
 ● Brocas: “expressive aphasia”. Can understand speech but cannot express speech.
ex.) Patient responds to question with incomprehensible sounds like “awooga”
● Wernikies: “receptive aphasia”. Has trouble understanding speech but can express
words normally
ex.) You ask the patient their birthday and they reply with, “salad”
● Global Aphasia: involves both weirnikes and broca's area. Involves both
expressive aphasia and receptive aphasia.

Brain Bleeds:
Epidural Hematoma:
➔ Between skull and dura mater
➔ Fast arterial bleed (usually middle meningeal artery), rapid onset of symptoms
➔ Transient LOC followed by a brief lucid period then decreased LOC
Subdural Hematoma:
➔ Between dura and arachnoid Mater
➔ Slower venous bleed (usually bridging veins), slower onset of symptoms
that are often missed and can occur hours to days after injury
➔ N/V, Decreased LOC, abnormal posturing, severe headache
Subarachnoid:
➔ Sudden severe headache, “worst headache of my life”
➔ Bleeding is within the brain

All can have: Decreased level of consciousness, Cushing’s Triad, Low Glasgow Coma Scale,
unequal pupils/non-reactive pupils

Increased Intracranial Pressure: Cushing's Triad

● Bradycardia
● Hypertension with widening pulse pressure
● Irregular Respirations

Glasgow Coma Scale

Eyes Verbal Motor

4.) Open Spontaneously 5.) Oriented conversation 6.) Obeys commands

3.) Open to verbal stimuli 4.) Confused conversation 5.) Localizes Pain
2.) Open to painful stimuli 3.) Inappropriate words 4.) Withdraws from pain
1.) Do not open 2.) Incomprehensible sounds 3.) Decorticate posturing
1.) None (abnormal flexion)
2.) Deceberate posturing
(abnormal extension)
1.) None

Highest score: 15
 Lowest score: 3

Amnesia:
● Retrograde: Can't recall events before injury
● Antegrade: Can't form new memories after injury

Seizures
Erratic misfiring of neurons, categorized by two types: Generalized and Partial with their
respective subtypes.

● Generalized seizures: “Grand Mal”

Involves entire brain and has a specific progression of events:
1. Aura - sensations that precede a seizure
2. Loss of consciousness
3. Tonic - Tensing of muscles
4. Hypertonic - Extreme muscle rigidity with hyperextension of the back
5. Clonic - Forceful contractions. Pt is not moving air in and out at this time. Pt may
suffer incontinence and trauma. ex.) biting tongue or hitting objects.
6. Postictal - period following a seizure where pt slowly regains consciousness and
may be very confused and disoriented
➔ Absence seizure: “Petit Mal”
Type of generalized seizure that involves the entire brain but instead of forceful movements,
there is a cessation of movement. Pt may be speaking mid sentence, experience an absence
seizure and stop talking, moving, and stare into space, then go right back to where they left off.

● Partial Seizures
Involves only part of the brain. May spread and become a generalized seizure.
➔ Simple Partial: Chaotic movement of one part of the body
➔ Complex Partial: Distinct auras, may include hallucinations

Status epilepticus
Serious medical emergency. Characterized by a prolonged seizure that:

● Lasts longer than 5 minutes

● Is Recurrent
● Has no return of consciousness

Treatment: Benzodiazepines
Benzodiazepines work by enhancing the neurotransmitter Gamma-Aminobutyric Acid (GABA),
which slows down the Central Nervous system. Examples include:
● Valium (diazepam) 5-10mg IV/IM, max 30mg
● Ativan (lorazepam) 1-4mg IV/IM, 8mg max
● Versed (Midazolam) 2-5mg IV/IM/IN, max 10mg

Considerations:
● Most common cause for adults: Non-compliance with medications
● New onset seizures in adults most commonly caused by neoplasms(tumors)
● Most common cause of seizures in children: Fever (febrile seizure) and
Hypoglycemia
Things to do on EVERY neurological call:
● AAOx? AVPU? GCS?
● Pupils : dilated (mydriasis), constricted (miosis), unequal (anisocoria)
● BGL
● Stroke Assessment
● IV access
● Trauma?

Spinal Injuries

Type Cause S&S

Anterior Cord Syndrome Flexion-Extension Injury, Loss motor, loss of sensation

damages vertebral artery (pain,touch,temp) BELOW
injury site

Brown Sequard Syndrome Penetrating injury to one side Weakness/paralysis on side

of the spinal cord side of the body, loss of
sensation on the other side

Cauda Equina Syndrome Herniated disk, fracture of Legs and bladder do not work
lower spine

Central Cord Syndrome Hyper-extension of c-spine. Motor weakness of upper

Typically from a forward fall extremities

Neurogenic Shock
 Type of distributive shock resulting from a spinal injury that causes impairment of sympathetic
nerve conduction with unopposed vagal tone. This results in widespread vasodilation and
hypotension. Heart rate may be normal due to lack of compensatory sympathetic stimulation.
Skin may appear dry OR skin above injury is pale and clammy while skin below injury may be
dry and cold. Dopamine is a great drug choice here.

Other Neurological Disorders

Guillain Barre Syndrome: Rare autoimmune condition where a bacterial or viral infection
triggers the immune system to mistakenly attack nerves destroying the myelin sheath. S&S
include tingling, progressive muscle weakness, eventually paralysis, and fever.
Myasthenia Gravis: Autoimmune disease causing breakdown of nerves and muscles. S&S
include neuromuscular weakness, eyelid drooping (ptosis), double vision (diplopia), trouble
swallowing (dysphagia), eventually can cause difficulty breathing as muscles to breathe atrophy
Multiple Sclerosis: progressive condition, Inflammation of nerve cells diplopia, nystagmus,
speech difficulty, poor coordination, weakness
Parkinsons: Loss of dopamine causes impaired coordination, tremors. Progressive and chronic
condition.
Creutzfeldt Jakob Disease: Infection from contaminated beef, always fatal. Ataxia (poor
coordination of muscle movement), jerky movements, visual impairment, mental deterioration
Pick's Disease: Genetic. Obsessive/inappropriate behavior, mental highs and lows, tremors,
incontinence.

Meningitis
Inflammation of the meninges. Most common is viral but there is also bacteria which is typically
more severe and highly contagious.
S&S: Fever, neck stiffness, nuchal rigidity, bulging fontanelles in infants, may cause ams
Petechial rash - pin prick red dot rash
Purpuric rash - blotchy rash, looks like bruises
Brudzinski sign: hips and knees flex when neck is flexed
Kernig's sign: unable to straighten leg when hip is flexed

Suspected meningitis cases call for a patient to wear a surgical mask and you the responder to
wear proper PPE like an N95
 Endocrinology
Endocrine system is made up of a network of organs/glands (ductless) that secrete chemical
messengers called hormones into the bloodstream.

Hypothalamus

Junction between CNS and endocrine system. Regulates the four F’s: Fahrenheit (body temp),
Food (hunger and thirst), feelings, fornication (sexual activity). Also regulates Pituitary functions
which then regulates other endocrine glands. The pituitary gland is divided into Anterior and
Posterior Pituitary.

Anterior Pituitary

● ACTH: Adrenocorticotropic hormone. Stimulates the production of cortisol, a “stress

hormone” that maintains blood pressure and blood sugar levels.
● FSH: Follicle-stimulating hormone. Promotes sperm production and stimulates the
ovaries to produce estrogen.
● LH: Luteinizing hormone. Stimulates ovulation in women and testosterone production in
men.
● GH: Growth hormone. Helps maintain healthy muscles and bones and manage fat
distribution.
● PRL: Prolactin. Causes breast milk to be produced after childbirth. It also affects
hormones that control the ovaries and testes, which can affect menstrual periods, sexual
functions and fertility.
● TSH: Thyroid-stimulating hormone. Stimulates the thyroid gland, which regulates
metabolism, energy and the nervous system.

Posterior Pituitary

● ADH: Antidiuretic Hormone or “vasopressin”. Antidiueretic effect, causes water retention

and decreases urinary output to maintain adequate fluid volume.
> In compensated shock, ADH is produced to increase circulating volume.
>Diabetes Insipidus: NOTHING to do with BGL. Occurs when the body does not produce
enough ADH resulting in increased thirst and increased urine production that is highly dilute.
● Oxytocin: Stimulates uterine contraction and lactation in women.
>Immediate breastfeeding following childbirth stimulates oxytocin to help mother produce milk
for baby and it can also lessen risk of postpartum hemorrhage by causing uterine contractions
> Slowing onset of preterm labor via fluid bolus: In theory, a fluid bolus can temporarily stop
preterm labor by increasing circulating volume which then suppresses adh and oxytocin
secretion. Less oxytocin=less contractions=less force to push out baby early

Thyroid

● Produces Thyronines (T3 and T4) to increase metabolism

● Produces Calcitonin to decrease calcium levels
● Thyroid needs Iodine to to create thyroid hormones, Iodine is not naturally produced and
must be absorbed through foods containing it

Hyperthyroidism - Too much Thyroid Hypothyroidism - Too little Thyroid

Hormones Hormones

Associated with Graves disease, a chronic Can be associated with Hashimoto's disease,
form of hyperthyroidism most common in the inflammation of the thyroid. Metabolism is
young females. Metabolism is heightened. slowed.

S&S: Goiter (enlarged thyroid), exophthalmos S&S: Slow onset, extreme fatigue, increased
(protruding eyes), Increased appetite, weight gain, dry skin, cold intolerance, may
Increased weight loss, diaphoresis, heat also have goiter. These patients are often
intolerance prescribed levothyroxine (synthroid)

These thyroid imbalances may become exacerbated leading to lethal conditions...

Thyrotoxic crisis/thyroid storm - way Myxedema Coma - way too little Thyroid
too much Thyroid Hormones! hormones!

Thyroid hormones rise to unmanageable Thyroid hormones extremely underproduced,

level driving body into hypermetabolic state often precipitated by exposure to cold

S&S: High fever, Tachycardia, N/V/D, S&S: Decreased LOC/Unresponsive, Severe

Diaphoresis, seizures, decreased BGL, hypothermia, potential cardiac arrest
Dehydration

Treatment: 1L NS to combat dehydration, Treatment: Passive rewarming- apply heat to

passive cooling, Benzos if indicated (may groin, axillae, neck. Blankets.
need up to 3x normal dose due to Monitor EKG and apply precautionary pads in
hypermetabolic state), Dextrose (may need the event of cardiac arrest
to readminister due to hypermetabolic state),
Beta Blockers to lower HR (preferred choice
Propranolol 0.5-1mg slow ivp)
 Parathyroid Gland

● PTH: Parathyroid hormone raises calcium. Limits excretion of calcium from

kidneys and increases reabsorption of calcium from bone. PTH is the antagonist
to Calcitonin, levels of each determine calcium level.

>Hyperparathyroidism: Excess PTH. Can present as kidney stones, osteoporosis,

pathological fractures due to continuous reabsorption of bone calcium

Adrenal Glands are Divided into two sections: the outside (Adrenal Cortex) and the inside
(Adrenal Medulla). The Adrenal glands sit atop each kidney.

Adrenal Medulla

●
Produces Catecholamines epinephrine and norepinephrine
Pheochromocytoma - Tumor of the adrenal medulla that secretes excess
catecholamines

Adrenal Cortex

● Mineralocorticoids like salt

● Aldosterone to regulate blood pressure
● Glucocorticoids Stress hormone Cortisol. Needs ACTH from pituitary to
stimulate cortisol production

Addison's Disease - Adrenal insufficiency, Cushing’s Syndrome - Adrenal

too little cortisol! overproduction, too much cortisol!

S&S: weight loss, fatigue, GI problems, salt S&S: Increased BGL, rhabdomyolysis, weight
cravings gain only in face (moon face), between
shoulders (buffalo hump), and in trunk

Addisonian Crisis: Physical or emotional Caution: do not give steroids like

stress without normal compensation of methylprednisolone (solumedrol). Cushings is
stress hormone cortisol sends pt into often caused by adrenal or pituitary adenomas
catastrophic shock! S&S: Hypotension, (benign tumors)
Hyponatremia due to sodium retention and
 Hyperkalemia due to Potassium Excretion.

Pancreas

Located in the LUQ. Contains islets of langerhans to produce:

● Alpha cells (Glucagon) to raise BGL

● Beta Cells (insulin) to lower BGL
● Delta cells (somatostatin) inhibits production of glucagon and insulin

>Pathophysiology of using glucose:

Glycogenolysis: Glucagon stimulates breakdown of Glycogen (storage unit of glucose) into its
individual glucose molecules into the bloodstream.
Glucogenesis: Synthesis of glucose via non-sugar sources.
Role of Insulin: Needed for glucose to permeate cell membrane and be used by cells.

Diabetic Mellitus Conditions

Insulin Dependent Diabetes “type one” Insulin Resistant Diabetes “Type two”

Genetic and non-preventable. Onset is in Attributed to lifestyle, preventable. Onset is

childhood and teens. typically mid adulthood. Accounts for most
cases of diabetes.

Occurs when pancreas is unable to produce Occurs when pancreas can produce insulin but
insulin the body does not respond well to it/unable to
fully utilize it

3 P’s of undiagnosed type one: Polyphagia Can present similarly

(increased appetite), Polydipsia (increased
thirst), Polyuria (increased urination)

Treatment: These patients need constant Treatment: Controlled through diet and lifestyle
supply of daily insulin, typically through changes. Some patients also take pills such as
injections. Many have a port on the abdomen. Metformin to help control BGL.

Untreated diabetes or diabetes that is being poorly managed may result in severe diabetic
emergencies such as….

Diabetic Ketoacidosis (DKA)

 Pathophysiology: Typically Too much glucose, no insulin to use glucose results in
hyperglycemia in type 1 diabetics - often occurs when pt misses an insulin dose. Since the body
cannot use glucose for energy, it then uses energy from sources like fat. The liver then breaks
this down into highly acidic byproducts called ketones. Ketones accumulate in the bloodstream
leading to metabolic acidosis(low Ph).

Pathophysiology of S&S:
Kussmaul respirations: Increased rate and depth of respirations as a compensatory way to
blow off excess co2 and raise Ph.
Increased Urination: The Kidneys can only reabsorb glucose at a concentration of approx. 180
mg/dl, any higher concentrations of glucose will be lost in urine (glycosuria). Increased urination
occurs via osmotic diuresis where glucose is so highly concentrated it cannot be reabsorbed by
the kidneys, raising osmotic pressure and subsequently drawing large amounts of water into
the kidneys. Excessive urination lowers circulating volume and causes severe dehydration as
well as the loss of electrolytes which can lead to cardiac dysrhythmias.
Acetone/sweet breath: Fatty acids are metabolized into ketones, one of which is acetone.
Traces can be smelled in the breath of DKA pts.

Prehospital treatment: Monitor BGL. Dilute excess glucose with 1L normal saline, will also help
combat dehydration and hyponatremia. 12 lead ekg, monitor for electrolyte related ekg changes.
Rapid transport, pt needs definitive treatment in the hospital via controlled insulin.

Hypoglycemia

Pathophysiology: High insulin levels, low glucose. Can potentially happen to anyone but mostly
occurs when a diabetic: takes too much insulin, eats too little, or overexerts themselfs. In
prolonged hypoglycemic states, cerebral hypoglycemia occurs where the brain is not getting
enough glucose to function which can eventually lead to brain damage.

Pathophysiology of S&S: Most symptoms can be attributed to cerebral hypoglycemia which

decreases brain function leading to: confusion, disorientation, combativeness, and
unresponsiveness. Physical symptoms may include: Tachycardia, diaphoresis, and even
seizures.

Prehospital Treatment: Verify hypoglycemia via glucometer. Recheck BGL after every
intervention.
>If patient is able to follow commands/swallow/fully responsive: Oral glucose
>If the patient is alertered/having severe symptoms: Establish IV access and give dextrose. If
doing push instead of drip, push very slowly and aspirate every 10 mls to prevent tissue
necrosis.
>If unable to establish IV: Use IM glucagon 1mg
 Obstetrics

Menstrual cycle

1.) Proliferative phase (follicar) Increased estrogen, approx 2 weeks. Endometrial cells
proliferate and the endometrium (lining of uterus) thickens with blood
2.) Secretory phase relates to ovulation (release of the egg)
3.) Ischemic Phase If fertilization does not occur there is a drop of estrogen and
progesterone leading to the next phase
4.) Menstrual phase endometrial tissue sheds, a “period”
NOTE: Fertilization of the egg means endometrial tissue does not shed hence loss of
period in pregnancy.
Development of pregnancy

Fertilization of egg typically occurs in the fallopian tube and is then implanted into the wall of the
uterus. Around 3 weeks later, the placenta develops to provide the fetus with nutrients and is
connected to the baby via the umbilical cord. The umbilical cord has two arteries with
deoxygenated blood and one vein with oxygenated blood. The fetus develops and is
encased in the amniotic sac to protect it and facilitate movement. The size of the uterus grows
as the baby does:
● 3 months in : uterus is at the level of the top of the pelvis
● 4-6 months in: uterus is at level of the umbilicus
● 9 months in: uterus is at the level of the diaphragm
Fundal Height: The fundus is the part of the uterus that forms a rounded dome. Fundal height
estimates the age of the fetus and is measured from the top of the uterus to the pubic
symphysis. After 24 weeks of pregnancy, the fundal height often matches number of weeks
pregnant
Stages of Labor
1.) Cervical effacement and dilation around 10cm
2.) Begins with full dilation of the cervix and ends with the delivery of the baby
3.) Begins with delivery of the baby and ends with the delivery of the placenta

Signs of imminent delivery

● Crowning (DEFINITIVE SIGN)
● Rupture of the amniotic sac “water break”
● Bloody show - expulsion of a plug of blood and mucous
● Urge to push and defecate
● Contractions less than 2 mins apart lasting 30-60secs
 ● Lightening - fetus moving down into birth canal
Note: Contraction length is measured from the start of one to the start of the next

Pregnancy Complications

Spontaneous Abortion (miscarriage)

● Natural loss of pregnancy

● S&S include bilateral lower abdominal pain, bleeding and clots (bag clots in biohazard
bag and deliver to hospital)
● Typically occurs in early weeks of pregnancy

Ectopic Pregnancy

● Fetus develops outside the uterus, typically in the fallopian tube.

● Pts with pelvic inflammatory disease or tubal ligation are predisposed
● Typically occurs in early weeks of pregnancy
● S&S: UNILATERAL abdominal pain, Kehr's sign (referred pain to shoulder), shock if
ruptured
● Differential diagnosis: ovarian cyst, can also present as unilateral abdominal pain

Abruptio Placenta

● Placenta tears away from abdominal wall, typically caused by trauma especially in
deceleration injuries as seen with MVA’s
● Typically occurs in late pregnancy, 3rd trimester
● S&S: Dark red bleeding, tearing pain, shock

Placenta Previa

● Placenta is implanted over cervical opening

● Typically occurs in late pregnancy, 3rd trimester
● S&S: Bright red vaginal bleeding, painless

Supine Hypotensive Syndrome

● When placed supine, the excess weight from pregnancy causes pressure on vena cava,
decreasing venous return to the heart. This leads to hypotension and often syncope
 ● Last trimester pts should ALWAYS be transported on their left side, even if backboarded
● In the event of cpr on a pregnant women, displace uterus to the left

Preeclampsia & Eclampsia (Hypertensive Syndrome of Pregnancy/Toxemia)

● S&S: Hypertension, edema, headache, vision changes, SOB

● Preeclampsia becomes Eclampsia in the presence of seizures
● Treatment: Left lateral position, Magnesium Sulfate 2-4g in 50cc bag over 10 mins,
benzodiazepines refractory to magnesium treatment

Gestational diabetes:
Pregnancy induced diabetes in 2nd half of pregnancy

Hyperemesis Gravidarum: 1st or 2nd trimester excessive vomiting

Terms:
● Gravida - Number of times pregnant
● Para - Number of live births
● Amenorrhea - Loss of period
● Cephalic Delivery - Head first (normal)
● Braxton Hicks Contractions - False labor contractions

Notes:
● Normal pregnancy lasts 40 weeks, or nine months
● Blood volume increases by up to 45%
● Increased blood volume means a pregnant woman can lose a significant amount
of blood 15-35% before showing signs of shock

Fetal Circulation

2 arteries with deoxygenated blood and one vein with oxygenated blood. Contains shunts made
to bypass the lungs and the liver because they do not work fully until after birth.

Ductus Venosus: Bypasses the liver

Foramen Ovale: Bypasses the lungs. Moves blood from right to left atrium

Ductus Arteriosus: Bypasses the lungs. Moves blood from pulmonary artery to aorta
 Delivery Complications: The Fetus

Condition Description Management notes

Amniotic sac intact Baby is still enclosed in Pinch and remove from face, suction
amniotic sac mouth then nose if there are secretions
with a bulb syringe, squeezing it before
insertion

Nuchal Cord Cord wrapped around baby's Check for nuchal cord as soon as the
neck head drivers, use fingers to slip cord over
neck, may need to prematurely cut cord

Prolapsed Cord Cord delivers before baby Place mother in knee-chest position (or
and protrudes from the trendelenburg), use your sterile gloved
vaginal opening. This puts hand and raise the presenting part of the
pressure on the cord and cuts cord to relieve compression. Never push
off fetal circulation. the cord back in and dress it in moist
sterile dressing. (towel soaked in saline
will work)

Limb Presentation Arm or leg presenting before DO NOT deliver. Rapid transport with the
head patient in the knee chest position with
their pelvis elevated.

Breech Delivery Buttocks presenting before Place mother supine with the pelvis
head elevated, place your sterile gloved hand
into the vagina and create a V with your
hand to allow baby to breathe

Shoulder Dystocia Shoulder gets caught in the Mcroberts Maneuver - place mothers
pelvic opening during buttocks off the edge of the bed and flex
delivery. Turtle sign - Head the legs into the abdomen while applying
delivers then retracts back suprapubic pressure(this creates more
into the vagina space to open the birth canal/aligns
shoulder past pelvis). Fetus may deliver
with a broken clavicle.

Multiple Births Still in labor after delivery Prepare for second delivery, 1st baby will
often be premature and prone to hypoxia,
hypothermia, and arrest
Premature Birth Delivered before 37 weeks, Prone to hypoxia, hypothermia, and
less than 5 lbs arrest

Delivery Complications: The Mother

Condition Description Management Notes

Postpartum Hemorrhage Excessive blood loss Fundal massage, administer

following delivery. Normal Oxytocin (Pitocin) in 1000ml
blood loss up to 500ml is NS, If baby does not need
expected, more is a medical resuscitation encourage
emergency. mother to breastfeed to
stimulate natural release of
oxytocin

Pulmonary Embolism During or after delivery, can Shock treatment, adequate

even occur about two weeks ventilation /oxygenation
postpartum

Uterine Rupture Pt will have an extremely Treat for shock

painful contraction and then
be pain free and labor will
stop

Uterine Inversion Uterus turned inside out after Transport supine, one
delivery and extends through attempt to push fundus but do
the cervix not try to detach placenta,
treat for shock

Placenta not delivered Placenta does not deliver Treat for shock, if left
within 30 mins of the birth of untreated pt may develop
the baby sepsis

Erythroblastosis Fetalis (hemolytic disease in newborns)

THE RH FACTOR. Incompatibility between RH negative mother and a second RH positive
fetus(or previous blood transfusion). Basically, the mother creates antibodies that attack the
fetus’ red blood cells.

Delivery Notes:
● Suction mouth then nose only if there are obvious secretions, always squeeze bulb
syringe before inserting it
● When head delivers look for presence of nuchal cord
● Clamp and cut the umbilical cord AFTER it stops pulsating
● Always warm, dry, and stimulate baby, suction mouth then nose if needed
 ● Calculate apgar score at 1 and 5 minutes

Neonates

Birth to 1 month

Neonate routine care after delivery

Always dry baby, maintain adequate body temperature, stimulate baby, Ensure patent airway -
suction mouth then nose with bulb syringe squeezing before insertion if necessary. If the baby is
stable, place the baby with the mother and encourage breastfeeding as it stimulates oxytocin to
reduce the risk of postpartum hemorrhage and stimulates lactation. Remember - a crying baby
is a good baby. Document time of delivery. Conduct your apgar scores.

APGAR SCORE

● Conducted at minute 1 following birth and minute 5

● Highest score is a 10 indicating a very healthy baby
● Lowest score is 0

APGAR 0 (worst) 1 2(best)

Appearance Completely cyanotic Extremities cyanotic Completely pink

(acrocyanosis)

Pulse None Below 100 bpm Above 100 bpm

Grimace (irritability) No cry Grimace or weak cry Strong, vigorous cry

Activity (muscle Limp, not moving Some flexion, limited Active movement
tone) movement

Respirations Absent Slow and/or irregular Strong, fast, regular

Neonatal resuscitation post delivery

1.) Tactile stimulation, warm/dry to ensure adequate body temperature, reposition and
suction airway
2.) Supplemental Oxygen
3.) Positive Pressure Ventilation
4.) Intubation
5.) Begin Chest Compressions
 6.) Medications
>What is causing this? Hypoxia, airway not patent, premature, cold ? Hypoglycemic?

Gastrointestinal

3 types of pain:
● Visceral: Generalized/hard to locate, diffuse, dull pain due to organs being innervated
by different levels of the spinal cord
● Somatic: Pinpoint, sharp pain due to being innervated by a specific nerve route
● Referred: Pain away from site of injury
Note: If pt can pinpoint pain, palpate that area last!

Abdominal Quadrants:

Right Upper Quadrant: Left Upper quadrant

● Liver ● Spleen
● Gallbladder (sits under liver) ● Pancreas
● Stomach ● Stomach

Right Lower Quadrant Left Lower Quadrant

● Appendix ● Left Ovary/Fallopian tube
● Right ovary/fallopian tube ● Bladder if distended
● Bladder if distended

Note: Small and Large intestine are part of all quadrants

Kidneys and adrenal glands are located in the retroperitoneal space

Peritonitis

Pathophysiology: Inflammation of the abdominal lining due to infection. Typically occurs if one of
the abdominal organs like the colon spills its contents into the abdominal cavity causing
bacterial infection and irritation.

S&S: Fever, vomiting, pain in entire abdomen, distention and rigidity of the abdomen,
guarding(tensing of muscles to protect from pain),
Rebound Tenderness (Blumberg sign): Pain upon removal of palpation rather than the
application of it. Indicates peritonitis.

Mallory Weiss Tear

Pathophysiology: Esophageal tear typically triggered by vomiting

S&S: No pain, hematemesis (transport in reverse trendelenburg)

GI HEMORRHAGE UPPER VS LOWER:

● Upper GI tract: Typically occurs from ulcers. May have:

>Melena: black tarry stools
>Coffee ground emesis (indicates partially digested blood)
>Hematemesis (blood in vomitus)

● Lower GI tract: Typically occurs from anal fissures or hemmoriods. May have:
>Hematochezia (bright red or wine colored stool)
>blood after wiping

Appendicitis

Pathophysiology: Inflammation of the appendix which may burst

S&S: starts with periumbilical pain and being sick for several days then pain in
the RLQ (at McBurney's Point ⅔ away from navel to the RLQ) May present with
a low grade fever, high if it ruptured.
Ruptured = Rovsing's sign: Pain in right side of abdomen with palpation of the
left side

Cholecystitis

Pathophysiology: Inflammation of the gallbladder. Typically occurs after eating a high fat meal

S&S: Green/yellow emesis, recent ingestion of a high fat meal, RUQ pain, Murphy's sign pain
when taking a deep breath upon palpation of the RUQ

Gallbladder terms:
> Cholestasis: flow of bile from liver stops
>Cholelithiasis: Fancy word for gallstones. Pain with gallstones is associated with the
contraction of muscles trying to push stones out.

Pancreatitis

Pathophysiology: inflammation of the pancreaswhich is located in the LUQ and produces

digestive enzymes and metabolic hormones (glucose and insulin)

S&S: Pain in LUQ that may radiate to the back, tachycardia, sepsis, acutely ill
 Abdominal Aortic Aneurysm (AAA)

Pathophysiology: Tear in the large aortic vessel that branches off to the abdomen. Significant
blood loss can lead to shock quickly.

S&S: Pulsating mass around the navel, extreme tearing/shearing pain in abdomen that may
radiate to the back, signs of shock, impending doom, urge to defecate due to blood in the
retroperitoneal space, hypertensive history, unequal pulses in lower extremities

RAPID TRANSPORT BUT BE CAREFUL WITH BUMPS

Thoracic Aortic Aneurysm

Pathophysiology: Tear in the large Aortic Vessel that branches off into the chest. Significant
blood loss can quickly lead to shock.

S&S: Tearing pain in upper chest and between shoulder blades, impending doom, signs of
shock, unequal pulses in upper extremities

RAPID TRANSPORT BUT BE CAREFUL WITH BUMPS

What are the stages of an allergic reaction, what are the characteristics of each? How
should we treat each ?
All: Oxygen therapy - 15lmp via NRB. Ensure adequate ventilation and oxygenation - ventilate if
necessary.
Mild: Characterized by urticaria. No wheezing nor hypotension. Treat with O2 and Benadryl
50mg IM
Moderate: Characterized by urticaria and wheezing, no hypotension. Treat with O2, Benadryl
50mg IM, nebulizer 2.5mg Albuterol , Epi 1:1000 .3mg
Severe/True anaphylaxis: Reaction is systemic and characterized with wheezing and
hypotension! Urticaria may or may not be present due to hypoperfusion. Treat with O2, Benadryl
25mg Ivp, Epi 1:10,000 .3mg (note difference in volume to concentration), Solumedrol 125mg
IVP, and Nebulizer 2.5 mg Albuterol
 Pharmacology
Therapeutic index - Safety of drug based on two factors:
● Effective dose ED50: Dose provides therapeutic effects in 50% of a given population
● Lethal dose LD50: Dose kills 50% of a given population
> the larger the therapeutic index, the safer the drug ex.) Narcan
> the lower the therapeutic index, the more dangerous the drug ex.) Digoxin
Therapeutic Threshold - Window of doses that achieve greatest therapeutic benefit while also
avoiding toxicity.

Half life - time that drug is metabolized into half of its total amount
ex.) If a 50mg drug has a half life of 2 hours, after 2 hours it will become 25mg
Note: Adenosine has an extremely low half life of only a few seconds so we must push it fast!

Pharmacokinetics: Movement of drugs throughout the body

1. Absorption: process of a drug reaching its target tissue(systemic circulation). Directly

related to surface area available and route of administration. The parenteral route has
the fastest absorption. Bioavailability: amount of drug still active after reaching its target
tissue
2. Distribution: Process of drug being distributed throughout the body via systemic
circulation
3. Biotransformation (metabolism): Transformation of drug into a more or less active
metabolize for the body to use. Drugs given the enteral route ex.) orally are subject to
hepatic alteration (first pass effect) as the GI tract sends drugs to be processed by the
liver where it can sometimes completely deactivate the drug. To bypass the first pass
effect, drugs are given via the parenteral route Ex.) IV which skips processing by the
liver as it goes directly into the bloodstream. Biotransformation also can make a drug
more water soluble to facilitate elimination.
4. Elimination: Eliminating drug out of the body

Pharmacodynamics: How drugs affect the body. Think mechanism of action, drug binds to
receptors to either stimulate or inhibit effects

Affinity: drugs desire to attach to a receptor

Efficacy: drugs ability to create an effect once attached to a receptor
Agonist: Attaches to receptor and causes an action to occur
Antagonist: drug that inhibits other drugs from attaching to a receptor
Competitive agonist: Two drugs competing for the same site, whatever drug has a higher
concentration wins (reversible)
Non Competitive agonist: Another drug cannot interact with the site regardless of its
concentration
Synergism: two drugs together that produce a greater effect than either drug produces alone
Potentiation: two drugs in combination induce effects greater than the sum of their individual
effects

Medications that act on the parasympathetic nervous system

Parasympathomimetic “cholinergic”: Stimulates “mimics” parasympathetic ns effects
Parasympatholytic “anticholinergic”: Inhibits “limits” effects of the parasympathetic Ns
> Primary neurotransmitter of parasympathetic ns = Acetylcholine (ACH)
> Deactivating enzyme: Actetylcholinerase

Medications that act on the sympathetic nervous system

Sympathomimetic “Adrenergic”: Stimulates “mimics” sympathetic ns effects
Sympatholytic “Anti-Adrenergic”: Inhibits “limits” effects of sympathetic ns
>Primary neurotransmitter: Norepinephrine
>Deactivating enzyme: Monoamine oxidase (MAO) and Cathecholomethytransterase (comt)

Adrenergic receptors:
● Alpha 1: Vasoconstriction
● Beta 1: Chrontrophic (HR) Inotropic (contractility) Dromotropic (conduction)
● Beta 2: Bronchodilation

CARDIAC DRUGS

Ace Inhibitors
The angiotensin converting enzyme ACE converts angiotensin I into angiotensin II which is a
powerful vasoconstrictor. So, Ace inhibitors prevent ace from creating angiotensin II therefore
reducing high blood pressure as vessels will remain dilated. All end in “pril” ex.) Lisinopril

Antidysrhythmic drug classification

“so-be-po-ca” “stupid blood pressure cuff”

● Class I - Sodium-channel blockers:

A sodium channel blocker, as the name implies, helps limit the sodium entering the cell.
This will slow conduction of the depolarization wave (does not act on firing rate of SA or
AV nodes, just slows the firing rate. It's like starting a car, it doesn't stop the car from
starting, rather slows how fast that car can travel from point A to point B). Also plays a
role in slowing repolarization. Ex) procainamide (1A) and Lidocaine (1B)
 ● Class II - Beta-blockers:

Beta-blockers are drugs that bind to beta-adrenoceptors in nodal tissue of the heart and
block the binding of norepinephrine and epinephrine to these receptors. This inhibits
normal sympathetic effects that act through these receptors. Has a negative chronotropic
effect (decrease HR) . Anything that ends in LOL is pretty much a beta blocker - Ex.)
labetalol propranolol acebutolol. Good for treating tachycardias that are secondary to
excessive sympathetic stimulation.

● Class III - Potassium-channel blockers:

Binds and blocks the potassium channels that are responsible for repolarization (resting
state). Therefore, blocking these channels slows (delays) repolarization, which leads to
an increase in action potential duration to slow HR. Useful in the treatment of SVTs.
Classic one is Amiodarone.

● Class IV - Calcium-channel blockers:

These channels are responsible for regulating the influx of calcium into muscle cells,
which in turn stimulates smooth muscle contraction and cardiac myocyte contraction.
Calcium channel blockers actually act on the rate of firing of the SA and AV nodes
making them useful for A-fib where the actual firing needs to slow down. EX. Cardizem

● Class V - Miscellaneous -

Adenosine, mag sulfate, electrolyte supplement (magnesium and potassium salts),

digitalis compounds (cardiac glycosides)

Adenosine
Classification: antidysrhythmic misc
MOA: reduce electrical conduction through AV node
Indications: hemodynamically stable supraventricular tachycardia
Dose: 6mg rapid ivp followed by 20cc flush, second dose 12mg rapid ivp followed by 20cc flush
Pediatric Dose: 0.1mg/kg rapid ivp with flush, second dose 0.2mg/kg rapid ivp with flush
Contraindications: Bradycardia, 2nd or 3rd degree HB
Note: has extremely short half life, methylxanthine stimulants like caffeine and theophylline can
antagonize adenosine

Amiodarone (coradone)
Classification: antidysrhythmic type III potassium channel blocker
MOA: prolongs repolarization and duration of next action potential
Indications: V-fib, V-tach
Dose:
>V-tach with a pulse: 150 mg in 50cc bag over 10 mins
>Pulseless V tach/vfib: 300 mg IVP 1st dose, 150 mg IVP 2nd dose
Pediatric dose: 5mg/kg
Contraindications bradycardia, cardiogenic shock, 2nd or 3rd degree HB

Atropine
Classification: Parasympatholytic, anticholinergic
MOA: inhibits action of ACH of the parasympathetic ns
Indications: symptomatic bradycardia, organophosphate poisoning
Dose:
>Symptomatic bradycardia: 1mg, max 3mg
>Organophosphate poisoning: 2-5mg, given with pralidoxime
Pediatric dose: 0.02mg/kg
Contraindications: glaucoma, tachycardia

Cardizem (dilatizem)
Classification: Antidysrhythmic type IV Calcium channel blocker
MOA: inhibits calcium influx to slow conduction
Indications: A-fib, A-flutter, SVT refractory to adenosine administration
Dose: 0.25mg/kg
Pediatric Dose: Not recommended
Contraindications: hypotension, extreme caution when pt is on beta blockers, WPW, 2nd or 3rd
degree HB

Epinephrine 1:10000 concentration

Classification: Catecholamine, sympathomimetic
MOA: Acts on adrenergic receptors A1,B1,B2
Indications: Cardiac Arrest
Dose: 1mg IVP/IO q 3-5 mins
Pediatric Dose: 0.01mg/kg

Lidocaine (xylocaine)
Classification: Antidysrhythmic class I sodium channel blocker
Indications: Cardiac arrest
Dose: 1-1.5mg/kg 1st dose. 0.75mg/kg 2nd dose
Pediatric Dose:
Contraindications: Av blocks, wpw

Procainamide (pronestyl)
Classification: Antidysrhythmic class I sodium channel blocker
Indications: SVT refractory to adenosine, afib in WPW
Dose: 20 mg/min max 17 mg/kg
Contraindications: 2nd or 3rd degree HB

Magnesium Sulfate
Classification: Electrolyte
MOA: Reduces striated muscle contraction by reducing release of acetylcholine
Indications: Eclamptic seizures, torsades de pointes (polymorphic v tach), hypomagnesemia,
status asthmaticus
Dose: 2-4mg in 50cc bag over 10 mins
Contraindications: Hypotension

Calcium Chloride
Classification: Electrolyte
MOA: Increase serum calcium
Indications: Hyperkalemia, calcium channel blocker/beta blocker od
Dose: 1g
Contraindications: Hypercalcemia

Metoprolol (lopressor)
Classification: II Antidysrhythmic Beta Blocker
MOA: Blocks Beta Adrenergic receptors causing negative chronotropy, negative inotropy,
negative dromotropy
Indications: MI, SVT, Afib
Dose: 5mg slow IVP
Contraindications: Pt on calcium channel blockers

Furosemide (Lasix)
Classification: Loop Diuretic
MOA: Inhibits reabsorption of sodium in proximal loop of henle thus reducing edema
Indications: Edema in congestive heart failure
Dose: Match home dose or 40mg IVP slow
Contraindications: Hypotension
 Catecholamine Infusions

Dopamine (inotropin)
Classification: Sympathomimetic
MOA: Dose dependent
Indications: hypotension with absence of hypovolemia, cardiogenic, septic, neurogenic shock,
hypotensive chf
Dose: 2-20mcg/kg/min
>Low dose: 2-5mcg/kg/min stimulates dopaminergic receptors causing mesenteric and renal
dilation
>Medium Dose: 5-10mcg/kg/min stimulates beta 1 receptors to increase hr and co
>High Dose:10-20mcg/kg/min stimulates alpha 1 receptors to cause vasoconstriction to raise bp
Make:
>200 mg in 250ml NS yields 800mcg/ml
>400 mg in 250ml NS yields 1600mcg/ml
>800 mg in 500ml NS yields 16000mcg/ml
Contraindications: Hypovolemia/Trauma

Norepinephrine (levophed)
Classification: Sympathomimetic
MOA: Alpha 1 and beta 1 agonist. Pure vasoconstriction
Indications: Hypotension with absence of hypovolemia, cardiogenic, septic, neurogenic shock
Dose: infusion of 2-4mcg/min
Make: Add 1mg Levophed into 250ml D5W for concentration of 4mcg/ml
>Initial: Run infusion at 4mcg/min(1ggts/sec) using a microdrip set (60gtts/ml)
>Increased BP: Titrate lower to 2mcg/min by running 2ggts/sec
Contraindications: Hypovolemia/Trauma

Epinephrine 1:10000 (Adrenalin)

Classification: Sympathomimetic
MOA: Alpha and beta adrenergic receptors
Indications: Hypotension with absence of hypovolemia, cardiogenic, septic, neurogenic shock
Dose: infusion of 2-10mcg/min
Make: Epi 1/10000 1mg into a 250ml NS will give you a concentration of 4mcg/ml
Contraindications: Hypovolemia/Trauma
 Respiratory & Anaphylaxis Drugs

Albuterol (proventil)
Classification: Sympathomimetic, b2 agonist
MOA: Stimulates beta 2 receptors to cause bronchial dilation
Indications: Asthma, anaphlaxis, bronchospasm
Dose: 2.5mg/3ml
Pediatric Dose: Same
Contraindications: Tachycardia, Hypersensitivity

Atrovent (Ipratropium Bromide)

Classification: Parasympatholytic, anticholinergic
MOA: Blocks ACH in bronchial smooth muscle causing bronchial dilation, reduces mucus
production
Indications: Asthma, anaphlaxis, bronchospasm
Dose: .5mg/3ml
Pediatric Dose: Under 8yo reduce to .25mg
Contraindications: Tachycardia, Hypersensitivity

Epinephrine 1:1000
Classification: Sympathomimetic
MOA: Acts on adrenergic receptors A1,B1,B2
Indications: Anaphylaxis, asthma unresolved with bronchodilators
Dose: 0.3-0.5mg SQ/IM
Pediatric Dose: 0.01mg/kg SQ/IM

Racemic Epinephrine
Classification: Sympathomimetic
MOA: When epi is used via inhalation, it produces local effects like bronchial dilation,and anti
inflammatory
Indications: Stridor, croup
Dose: 0.5ml of a 2.25% solution OR 3ml epi 0.1% in 3ml ns yields 0.25, both nebulized
Contraindications: Tachycardia

Diphenhydramine (Benadryl)
Classification: Antihistamine
MOA: Blocks H1 receptors to inhibit release of Histamine
Indications: Anaphylaxis, dystonic reactions
Dose: 25mg IV 50 mg IM
Pediatric Dose: 1mg/kg
Contraindications: MAO inhibitors

Methylprednisolone (Solumedrol)
Classification: Corticosteroid
MOA: Suppression of inflammation
Indications: Anaphylaxis, Asthma
Dose: 125mg IVP
Pediatric Dose: 1-2mg/kg
Contraindications: Cushings

Classification: Sympathomimetic
MOA:
Indications:
Dose:
Pediatric Dose:
Contraindications:
Naloxone (Narcan)

Classification: Opioid Antagonist

MOA: Competitive opioid Antagonist, competes with opioid receptors to inhibit their effects
Indications: Respiratory depression secondary to opioid OD
Dose: 2mg IV/IM, Max 10mg
Pediatric Dose: 0.1mg/kg

Seizure & Sedation

Diazepam (Valium)

Class: Benzodiazepine
MOA: Increase inhibitory effects of the neurotransmitter GABA thereby producing a sedative
effect
Indications: Seizure, anxiety, sedation, alcohol withdrawal seizures, premedication
Dose:
Seizure: 5-10mg over 2 mins IV/IN
Premedication: 5-15mg over 2 mins IV/IN
Pediatric Dose: 0.1mg-0.2mg over two mins IV/IN
Contraindications: CNS depression

Midazolam (Versed)

Class: Benzodiazepine
MOA:Increase inhibitory effects of the neurotransmitter GABA thereby producing a sedative
effect
Indications:Seizure, anxiety, sedation, alcohol withdrawal seizures, premedication
Dose: 2-5mg max 10mg
Pediatric Dose: 0.1-0.2mg/kg
Contraindications: CNS depre