Critical Cardiac Notes

CRITICAL CARE 2016 Page 1 of 71
CRITICAL CARE NOTES

LESLIE HERNANDEZ
KEONI JAMES WONG
FM 18 [AUG-SEPT 2016]
EMPHASIS: Critical Cardiac, Medical, Flight Physiology (Safety & Survival)

CRITICAL CARDIAC
Sinus
Lead II inferior LV view (monitoring lead)
V1 septal view (diagnostic)- enlargements, hypertrophy, BB direction
P wave < 2.5 mm tall < .11 s/110 ms wide
atrial chamber enlargements would reflect in the p wave.

“p pulmonale” RAE. People at risk pulmonary HTN, pulmonary disease patterns, increased
intrapulmonary pressures…
Biphasic p wave in V1 is normal.
Wide notched p waves are LAE. Usually due to uncontrolled systemic HTN, mitral valve
prolapse. “p mitrale” LAE
Normal only means 60-100, w/ upright rounded p waves.

Bradycardia <60
Tachycardia >100
Dysrhythmia: breathing in & breathing out, changes in intrathoracic pressure. “Normal variation
associated with breathing. Inhalation would shorten R-R interval and expand with exhalation”.
PRI remains constant.
Arrest: Period of asystole. May resume as sinus or have escape pacemaker.
Atrial
P waves if seen will be “rip off’s” of the real thing.
Fibrillation: no p waves, >100 will make it RVR; irregularly irregular rhythm w no readily
discernible p waves. Identified as chronic or acute.
Flutter waves: flutter waves, >100 will make it RVR; can be regular or irregular (constant or
variable response). Identified as chronic or acute. Usually don’t sustain.
WAP: 3 or more different shaped p waves in one rhythm. Ventricular Response 60-100 (a.k.a.
Ectopic Atrial Response EAR). No tx unless rate is challenging.
MAT: 3 or more different shaped p waves in one rhythm. Ventricular Response >100 (a.k.a.
Ectopic Atrial Tachycardia EAT). No tx unless rate is challenging.
PSVT: abrupt starts and stops.
SVT: too fast
WPW: PRI < .12, QRS >.10, delta waves (best seen in anterior leads)
Sustained rhythm is >30s

New onset A-fib/A-Flutter w/ no precursor, acute onset, chest px, pt is having an MI until proven
otherwise. Not all pt’s require Cardizem.
Junctional
P waves if seen will be inverted before or after the QRS or can be buried; always regular, 40-60
junctional [escape] rhythm.
Accelerated junctional: 60-100
Tachycardia: >100
Bradycardia: <60 follows rules
WJP: 3 inverted different shaped p waves in one rhythm. No tx unless rate is challenging.
Ventricular
Rules:
No associated atrial activity
QRS must be greater than .12 (120 ms wide)
T wave opposite direction of QRS
Atrial: Depolarization & Repolarization same direction

Ventricular: Depolarization & Repolarization different direction
Idioventricular: very regular

Accelerated Idioventricular: very regular
Monomorphic Tachycardia: all the same
Polymorphic Tachycardia: multiple shapes (most common Torsades de Pointes caused by
hypomagnesemia); chronic alcoholics, malnourished individuals, and people w/ malabsorption
syndrome (Crohn’s disease) are the at risk patients.
Fibrillation: Coarse or fine, early should be coarse, every 1 minute 7-11% brain tissue necrosis.
Side Note: Chronic alcoholics at risk for liver failure. The liver breaks down by-products of
metabolism/digestion into BUN (Blood Uria Nitrogen). If unable to break down, it will remain as
ammonia leading to hepatic encephalopathy w/ tx of Lactulose.
Von-Williams classification of antiarrythmics

I: Sodium Channel Blockers, Lidocaine, Procainamide
II: Beta-Blockers, therapeutically depress pump function, Metoprolol, Lebatalol
III: Potassium Channel Blockers, Amiodarone
IV: Calcium Channel Blockers, Verapamil (Calan), Diltiazem (Cardizem)
V: Calcium enhancer, Adenosine
Amiodarone is a broad spectrum anti-arhythmic prolongs QTI (60-100 is 360-440ms or less than
half R-R), placing pt at risk for R on T, Max in 24 hr period is 2.2 G.
AV Blocks
1st Degree: prolonged PRI, only tx for rate/hemodynamics
2/3 degree rules:

1. More P waves than QRS
2. PRI constant or variable
1. constant 2nd Type II

2. variable need more information
3. R-R constant or variable
1. constant 3rd degree
2. variable 2nd Type I
3rd degree can be paced from junction or ventricles. A.k.a. Complete Heart Block.
Equations
Cardiac Output (CO): Heart Rate x Stroke Volume (HRxSV)
Cardiac Index (CI): Cardiac Output / Body Surface Area (CO/BSA)
Volume, Heart Failure, Blood Vessel dilation/constriction (SVR change)
Minute Volume (MV): Tidal Volume x Respiratory Rate (TVxRR)
Mean Arterial Pressure (MAP): Systolic + 2 x Diastolic / 3 (S+2(D))/3
Cerebral Perfusion Pressure (CPP): MAP-ICP (normal range 0-10)
Weight in kg: (Age in years x 2) + 8 = wt in kg
CPP can also mean Coronary Perfusion Pressure.

ICP monitors: Pressure transduced into waveform.
CPP: Bare bones minimum 60
1234’s of Heart (insert)

1. Heart, size of fist, retrosternal, in mediastinal space. pump effectively all life, chest x-ray
(AP) standing.
2. Sides
• R: low pressure pump, pulmonary circulation (CVP, RAP)
• L: High pressure pump, systemic circulation (PAOP, PACWP)
• preloads (associate preload w/ volume; L can only get what R gives it)
• afterloads (associate afterload w/ pressure & resistance)
• main arteries (pulmonary, aorta)
• blood pressure (systolic: SV, HR; diastolic: vascular resistance)
• coronary arteries (R: posterior descending, marginal, L: LAD, circumflex)
3. Layers
• Inner
• Endocardium; no pump, chambers & valves, chordae tendonae & papillary muscles
“velcro”, AV valves (b/t atria & ventricles) “velcro” more you open and close less
effective
• Middle
• Myocardium; contractile fibers (“filaments”), 4 major things: 1) actin, 2) myosin, 3)
Calcium, 4) Magnesium. “Calcium for contractility, magnesium to mitigate
contraction”. Actin & myosin enzymes, myosin not cardiac specific. Troponin is
cardiac specific
• Outer
• Epicardium; coronary arteries, comprised of two membranes: visceral pericardium
(adherent), parietal pericardium.
• Electrical Coops that generate electricity

• Sinoatrial (SA)
• Atria-ventricular junction (AV)
• Purkinje fibers
1. Chambers & Valves
• Chambers
• R atrium & ventricle
• L atrium & ventricle
• Valves
• Tricuspid
• pulmonic
• Mitral
• Aortic
Chest AP (Anterior Posterior): <50% of mediastinal space. Anchored by parietal pericardium

which is attached to the parietal pleura.
A slow leak of fluid can be an effusion and if not reabsorbed can lead to tamponade
Tamponade and tension cause distension a.k.a. mechanical/disruptive shock.

Hypoxic: Oxygen in and out
Hystotoxic: Chemical interference
Hypemic: Volume related (trauma patient)
Fetus & newborns R side is dominant and not a low pressure pump as in adults
CVP/RAP catheters above art
Nitroglycerin: preload reducer (works more on veins)
Nitroprusside: afterload reducer (works more on arteries), long-term use can cause cyanide
buildup as by-product (use sodium thiosulfate)
Pulmonary vascular resistance & systemic vascular resistance measured in dynes/sec^-5
BNP production by myocytes in heart failure to counteract aldosterone.
Ischemia: ST Depression and or T wave inversion; supply & demand imbalance of oxygen,
usually begin sub-endocardial
Injury: ST Elevation
Infarct: pathological Q waves
I: Inferior LV RCA PL dependent

SEE: Septal LV LAD afterload challenging
ALL: Anterior LV LAD afterload challenging
LEADS: Lateral LV Cx afterload challenging
Hypo/hyperkalemia are common w/ different presentation on a ECG

Hypokalemia: flat T, peaked p
Hyperkalemia (link): acidotic for any reason, 5 meq/L of potassium in blood and requires
calcium to stabilize cell walls. Consider alkalinizing urine, Glucagon, Kayexalate. Tall T flat P.
Beta-agonist (Albuterol/Xopanex), Bicarbonate. Very slow or very fast, w/ widened QRS.
Hypocalcemia more common than hypercalcemia.
Pericarditis: Global (Diffuse) ST Elevation
Pulmonary Embolus: S1Q3T3
• Lead I: Deep S wave
• Lead III: Deep Q wave inverted
D Dimer: developing bigger clots than usual.
Most of clots that kill form in thighs.
Basic Metabolic Panel

Sodium: Chief extracellular cation; 135-145 milliequivalents/L

Potassium: Chief intracellular cation; 3.5-5 milliequivalents/L
Chloride: Anion; 95-105 milliequivalents/L
Bicarbonate: Chief buffer Anion; 22-26 milliequivalents/L
Blood Uria Nitrogen: Hydration/kidneys; 10-15
Creatinine: Clearance; 1
Glucose: 70-110 mg/dL
Calculate Anion Gap:

Steps:
1. Add Sodium & Potassium values
2. Add Chloride & Bicarbonate values
3. Take both values and find the difference
4. Anion Gap would be difference +/- 4 due to whether considering K+
Arterial Blood Gases

pH: 7.35-7.45
PaCO2: 35-45
PaO2: 80-100
HCO3-: 22-26
SaO2: >/= 95%
BE: +/- 2
Note: A patient with a pH of 7.40, you should expect a PaCO2 of 40.
Complete Blood Count

White Blood Cells 5-10K
Red Blood Cells 5M
Hemoglobin 15M/Hematocrit 45M
Platelete 150-400K
Hypernatremia (link) (hypertonic)

Na+ > 145 mg/dl
Hypo-/hyper-/isovolemia (euvolemia)
Hypovolemic Hypernatremia Hypervolemic Hypernatremia Euvolemic Hypernatremia
Most common Rare Loss of free H2O

Lost more H2O than Na+ Na+ retention > H2O (IVF Loss of ADH
Overressucitation)
Renal: Mannitol (osmotic diuretic mineralcorticoid excess DI/nephrogenic DI

CI) Cushings syndrome/ADH
Tx: NS (isotonic fluids) to correct Tx: Diuretics (Na+ wasting) Tx: Free water replacement
volume prior to free water
Hyponatremia (link)
Na+ < 135 mg/dl
Osmolality: 2Na+ + Glu/18 + BUN/2.8 = 285 mg/dl (key number)
Tonicity: 2Na+ + Glu/18 = Tonicity (BUN can go freely between plasma membranes; causing no
effect between intercellular and extracellular)
ADH:
• secreted from the posterior pituitary after production in the hypothalamus
• works on the convoluted tubules for water reabsorption
Aldosterone: zona glomerulosa and works on the distal convoluted tubule (correlates to SIADH);
increase Na+ and H2O, decrease K+ and H+
Isotonic Hyponatremia Hypertonic Hyponatremia Hypotonic Hyponatremia
“lab error” a.k.a. Typically glucose; mannitol Most common

pseudohyponatremia
almost non-existent w/ modern decrease in Na+ due to oncotic

technology agents
[(Glu-100)/60] + Na+ = Na+

corrected
When adding normal saline (NS), which is an isotonic solution you would expect no changes in
Na+ concentration but change to volume in extracellular fluid (ECF). Whereas, adding D5W
(H2O), would decrease the Na+ concentration and using x—2x = y—2y, double the volume
affecting ECF would cross the permeable membrane into intercellular fluid (ICF).
Albumin: oncotic draw
Fibrinogen: clotting


ROME Pneumonic
Respiratory pH + PaCO2
Opposite direction
Metabolic pH + HCO3-
Equal
as pH goes down, hydrogen ion’s go up

as pH goes up, hydrogen ion’s go down
Buffer system: seconds

Respiration: 1-3 mins
Renal system: 8-48 hours
Diabetes Insipidus (DI) “dry” dehydration

Syndrome of Inappropriate Anti-Diuretic Hormone (SIADH) “swollen” fluid-overload
Listen to the Aortic valve, 2nd ICS to the right of the sternum
Listen to the Pulmonic valve, 2nd ICS to the left of the sternum
Cardiac murmurs (turbulence) they go from 1 (barely audible)-6 (loud)
Post open-heart surgery: control K+ & Mg++; rate control beta/calcium channel blockers;
contractility inotropes (dobutamine, milrinone), temporary IABP; temperature control; closely
watch for emboli. Monitor for tamponade. Over-heparinized: administer protamine.
ABG PRACTICE (link)

Component Value Normal Label
pH 7.48 7.35-7.45 up
pCO2 42 35-45 ~
HCO3- 29 22-26 up
Interpretation UC MET ALK
pH 7.30 7.35-7.45 down
pCO2 42 35-45 down
HCO3- 29 22-26 down
Interpretation UC MET ACID
pH 7.49 7.35-7.45 up
pCO2 30 35-45 down
HCO3- 30 22-26 up
Interpretation UC MIXED ALK
pH 7.39 7.35-7.45 down~
pCO2 55 35-45 up
HCO3- 23 22-26 ~
Interpretation C RESP ACID
pH 7.49 7.35-7.45 up~
pCO2 48 35-45 up
HCO3- 35 22-26 up
Interpretation PC MET ALK


Chest X-ray (link, watch all 3)

1. Black: air
2. Dark grey: fat
3. Light grey: soft tissue
4. Off white: bone
5. Bright white: metal (pacemaker,
buckshot, etc.)
a. Trachea (deviation, ETT, etc.)

a. Atelectasis pulls
b. Effusion pushes
b. Bone
a. Clavicles
b. Horizontal is posterior ribs
c. Curved is anterior ribs
d. Spinal processes
e. Lytic lesions
c. Cardiac silhouette
a. Cardiomegaly (enlargement)
b. Hepatomegaly
c. Great vessels
d. Placement for Swan-Ganz, A-line etc.
e. Lingula (pneumonia, lobular)
d. Diaphragm
a. Right hemidiaphragm usually higher than left hemidiaphragm
b. Costophrenic angle
c. “C-3, 4 & 5 keep the diaphragm alive. C-4 breathe no more.”
d. Right or left loss of hemidiaphragm is that lobular pneumonia
e. Free air under diaphragm is a surgical emergency
f. Effusion
e. E and F Equal lung fields
f. E and F Equal lung fields
a. Need to zoom in
b. Westermark sign
c. Cephalization (vessels; think of CHF/pulmonary congestion)
d. Kurly B lines
e. Peribronchiole cuffing
Pressure Monitoring (link) (CVP/Art line)

Utilizing a bag of NS, a pressure bag is inflated to 300 mmHg because the pressure exerted on
the bag has to be higher than the pressure within the artery. Taking into consideration flight
physiology and Boyle’s law, adjustments must be made to compensate for ascent and descent.
A normal IV tubing set cannot be used, you must use a semi-rigid tubing, avoid making it
excessively long or else you could possibly change the waveform. You muse also ensure it does
not touch the floor or you may cause damping. Continuous infusion rate will be 3ml/hr to keep a
clot from forming (countering systolic pressure). Each monitoring system (VC/RA/PA) has it’s
own pressure filled bag to each port.
Ensure air-fluid interface is level at the pt’s phlebostatic axis.
Wedge pressure would be monitoring preload of the left. If you see wedge pressure spike, you
should be suspecting left ventricular heart failure (blood back up into the lungs causes pressure
spike). No more than 1.5 cc’s of air for the distal cuff when monitoring pulmonary artery wedge
pressure (PAWP) or else you can rupture the PA.
Allen Test (link)

Used to evaluate radial/ulnar artery patency by compressing both arteries and having the patient
clench his hand into a fist causing pallor. Simultaneously, you would have the pt open their hand
while you release the ulnar artery.
Square wave test

The square wave test (fast flush/dynamic response test) is essentially a bolus activated by the
air-fluid interface (a.k.a. stopcock)(will look like a square on waveform monitor) followed by
1-2 oscillations immediately after. Normal waveform should resume after the oscillations.
Overdamping troubleshoot
Identify waveform
Check your pt
Check positioning of stopcock
Check the insertion site
Check for air bubbles commonly in the pressure transducer & flushing system
Check tubing and connections for any leaks
300 mmHg with fluid on pressure bag
Check for any clots
Aspirate first
Underdamping troubleshoot
Identify waveform
Check your pt
Check positioning of stopcock
Check the insertion site
Check for air bubbles commonly in the pressure transducer & flushing system
Check tubing and connections for any leaks
300 mmHg with fluid on pressure bag
Check for any clots
Check tubing length
Aspirate first
A: Atrial contraction V: Atrial filling
C: Tricuspid valve closure Y: Atrial emptying
X: Atrial relaxation
A wave is atrial systole and should be highest wave on waveform.
Pulmonary hypoxia causes PA constriction

Hypercarbia causes PA dilation
Hypoxia & hypercarbia causes PA constriction due to sympathetic response.
INTRA AORTIC BALLOON PUMP
Helium fills the shuttle.

Every 1,000 feet of altitude change the helium will get swapped for a fresh sample
Usually won’t purge after 10,000 (fixed wing) because cabin pressurizes until descent.
Continuously check timing. You cannot check timing on a 1:1; have to able to check using 1:2
The balloon is placed in the descending thoracic aorta (below subclavian & above renal arteries)
& inflates/deflates in correlation to the cardiac cycle (inflates on diastole, deflates on systole).
Goal: reduce demand & improve supply of myocardium (coronary arteries). Constantly monitor
pt’s left radial pulse & urine output. If left radial pulse disappears, left subclavian artery has been
occluded. If urine output reduces the renal artery has been blocked (2nd & 3rd intercostal space)
IABP is only a temporary assist device (diastolic augmentation device) until a more permanent
assist device can be implanted i.e. LVAD or receive heart transplant.
Originally developed for medically refractory cardiogenic shock (pressure’s were already below
90; possibly in MODS). Used to be a surgical procedure.
Now, prophylactically used for support.
Atrial Systole-A wave

Isovolumetric Contraction-C wave (true beginning of systole)
Ventricular Ejection-occurs in three waves
1. Initial slow phase pressure in ventricle is higher than in the arterial system and ejects
20-25% is ejected (systole)
2. The rapid phase is the systolic peak in which 50% of blood is ejected. (peak systole)
3. The final slow phase ejects the last 30-35% of blood. (closure of aortic valve)
Isovolumetric Relaxation
Ventricular Filling
Ascending limb (base to peak; left) is the anacrotic limb ejecting 20% of blood w/ peak at 50%
Descending limb (peak to base; right) is the dicrotic limb and from peak to dicrotic notch,
remaining 30 % should eject.
Anacrotic notch is possible when in RV resembling atrial kick.
Dicrotic notch 1) represents true onset of diastole, 2) reflects closure of aortic valve (pressure
changes from higher pressure in arterial system than in the ventricles), 3) coronary arteries
supply blood to the heart during diastole, 4) is when you want IABP to inflate (in concert with
closure of aortic closure).
Contraindications: Aortic stenosis
Left Ventricular End Diastolic Pressure (LVEDP)
Left Ventricular Heart Failure (LVHF)

Stages of LVHF
Stage 1: Vasoconstriction
• Pumping efficiency decreases
• LV Volume & Pressure Baroreceptors activate
• Increase HR
• Increase release of catecholamines
• Increased SVR
• Increased oxygen demand
• Increase in preload
S/S
• Chest px
• Diaphoresis
• Pale, clammy skin
• Weakness
• Anxious, restless
• SOB
• Tachycardia
• Tachypnea
Tx’s
• Morphine decreases afterload in LVHF
• Oxygen to assist in supply and demand
• Nitroglycerine is a preload reducer
• Nitroprussid is a afterload reducer
• Beta blockers depress pumping function and lower HR
Stage 2: Hypervolemia
• Cardiac output decreases
• Glomerular Filtration Pressure decreases
• RAAS is activated (ADH)
• causing sodium and water reabsorption
• Increased LVEDP
• Afterload increases
• Cardiac output further depressed
• HR increases
• PAP increases
• Decrease in oxygen (crackles)
• IAB counterpulsation
S/S
• Changes in breath sounds
• Pulmonary edema (crackles)
• Increase in SOB
• Reduced urine output
• Increase in HR
Tx’s
• Vasopressors
• Vasodilators (reduce after/preload)
• Inotropes (Dobutamine cardiac contractility without chronotopic effect)
• Diuretics (increase urine output)
• Intubation (All PPV always reduces preload)
• Practice of good medicine: prior to extubation, administer lasix in or else influx of
preload causing further complications.
Stage 3:
• Pulmonary edema
• Decreased oxygenation
• Decreased inotropy
• Extreme decrease in CO
• Decrease in BP
• Anaerobic metabolism
• Lactic acid production
• Acidotic tissue
• Anoxia of tissue
Tx’s
• Vasopressors
• Vasodilators
• Inotropes
• Diuretics
• Intubation
• IAB counterpulsation
• Sodium bicarbonate
Counterpulsation has been found to be effective in the earlier stage (around stage 1) in
preparation for transplant/VAD.
Terms: Timing and Trigger

Timing refers to inflation and deflation of the balloon in correlation to dicrotic notch; utilizes
arterial waveform.
Trigger refers to the R wave in the QRS complex.
Four potential timing errors:

• Early inflation: extreme errors/effects
• Aortic valve closes prematurely
• increase in LVEDV/LVEDP
• increase in PCWP
• increase in afterload
• aortic regurgitation
• Late inflation: mediocre errors/effects
• Sub-optimal augmentation
• Sub-optimal coronary perfusion
• Early deflation: mediocre errors/effects
• Sub-optimal coronary perfusion
• retrograde coronary and carotid flow
• Sub-optimal afterload reduction
• Increase in myocardial oxygen demand
• Late deflation: extreme errors/effects and also being the most fatal error “late-departed”
• Afterload reduction is absent
• increase in myocardial oxygen
consumption
• prolonged isovolumetric contraction
• LV ejection impeded
Secondary effects of counterpulsation

• Improved CO
• Decreased HR (not requiring to be as tachycardic for compensation)
• Reduced PAD/PCW
• Reduced SVR (afterload)
• Decreased Systolic and end Diastolic Pressure
• Diastolic Augmentation in Early Diastole
• Increased MAP
Optimal Timing
Sharp “V” at dicrotic notch
Note diastolic augmentation supra-systolic
Reduced end diastolic pressure
Reduced systolic pressure
Increase MAP
1:1
Full assist
Cannot monitor timing
1:2
Every other cardiac cycle diastolic augmentation
Ability to monitor timing (and continuous for 1:2 on)
1:3
Every 3rd cardiac cycle diastolic augmentation
Example (1:2 assuming waveform continues)

Factors affecting diastolic augmentation

1. Patient
1. HR (time the balloon may be inflated)
2. Stroke volume
3. MAP
4. SVR
6. Catheter
1. IAB in sheath
2. IAB not unfolded
3. Kink in catheter
4. IAB size
5. IAB position
6. Low helium concentration
7. IAB leak
7. Pump
1. Timing of IAB
2. Position of IABP augmentation control

Important Receptor Sites Within the Body

Receptor Agonist effects
Alpha-1 Vasoconstriction
Alpha-2 Insulin restriction
Glucagon secretion
inhibition of norepinephrine release
Beta-1 Increased HR (chronotropic effect)
Increased myocardial contractility (inotropic effect)
Increased myocardial conduction (dromotropic effect)
Renin secretion for urinary retention
Beta-2 Bronchus & bronchiole relaxation
Insulin secretion
Uterine relaxation
Arterial dilation in certain key organs
Dopaminergic Vasodilation of renal and mesenteric arteries
(numerous receptor subtypes exist)
Nicotinic Present at neuromuscular junction, allowing acetylcholine (ACh) to
stimulate muscle contraction
Muscarinic-2 Present in the heart; activated by ACh to offset sympathetic
stimulation
Decreasing chronotropy, inotropy, and dromotropy
Rhythms to know (refresher from Cardiology Notes)

Normal Sinus Rhythm: upright rounded P waves in II, PRI .12-.20, QRS duration <.12 and </=
1/2 R-R, firing rate of 60-100, regular
Normal Sinus Bradycardia Rhythm: upright rounded P waves in II, PRI .12-.20, QRS duration
<.12 and </= 1/2 R-R, firing rate is slower than 60, regular
Normal Sinus Tachycardia Rhythm: upright rounded P waves in II, PRI .12-.20, QRS duration
<.12 and </= 1/2 R-R, firing rate is 101-150; you can be in Sinus Tachycardia up to 220-age. Px,
fever, fear, fluid, regular
Sinus Dysrhythmias : usually a physiologic phenomenon associated w/ breathing; The P-P

intervals & the R-R intervals change w/ respirations, producing an irregular rhythm, pay
attention to the PRI, should be no change in PRI.
Sinus Exit Block: a.k.a. “Sinus Pause”; Missing one full cycle of R-R & b/t the two is equivalent
to 2x the normal R-R, irregular
Sinus Arrest: More serious than Sinus Exit Block; Missing a full cycle w/ prolonged pause R-R
& b/t the two is greater than to 2x the normal R-R, irregular
PAC: Premature Atrial Complex, P waves (if seen) will usually be upright; different shape than
sinus P wave. Lack of P waves could be due to extremely fast rhythm, fibrillation/flutter waves;
best way to fix/treat PAC is fix the underlying rhythms
SVT: Narrow QRS complex tachycardia >150, regular
PSVT: Narrow QRS complex tachycardia >150 w/ abrupt starts/stops, irregular
Wandering Atrial Pacemaker (WAP): 3 or more different shaped P waves in a single rhythm.
Rhythm will be irregular. 60-100.
Multi-focal Atrial Tachycardia (MAT): 3 or more different shaped P waves in a single rhythm.
Rhythm will be irregular. >/=101.
A-Fib: always an irregularly irregular rhythm w/ no readily discernible P waves; considerations

are new onset/chronic, assess ventricular rate rapid ventricular response (RVR) (Cardizem for
A-fib/A-flutter RVR symptoms <48hrs)
A-Flutter: flutter waves are not p waves, no p waves=no PRI; “saw-tooth”/“picket fence”;
considerations are new onset/chronic, assess ventricular rate (RVR), regular/irregular (Cardizem
for A-fib/A-flutter RVR symptoms <48hrs)
WPW: occurs when an electrical impulse follows an abnormal electrical conduction pathway
“accessory pathway” (“bundle of Kent”) from atria-ventricle; requires an ablation. Origin from
birth that accessory pathway never closed. PRI <.12, QRS >.12, delta waves.
PJC: an early P wave if seen will be inverted before/after QRS, may be buried.
Junctional Rhythm: P waves if seen will be inverted before/after QRS, T waves going in the
same direction, P waves may be buried. Always regular.
Accelerated Junctional Rhythms: P waves if seen will be inverted before/after QRS, T waves
going in the same direction, P waves may be buried rhythm >60 but <100. Always regular.
Junctional Tachycardia: P waves if seen will be inverted before/after QRS, T waves going in the
same direction, P waves may be buried rhythm >100
Junctional Escape: Late P waves (post sinus arrest) if seen will be inverted before/after QRS, T
waves going in the same direction, P waves may be buried, (requires >2 junctional complexes)
PVC: Early, Unifocal/Uniform: all the same shape; Multifocal/Multiform: differently shaped
V-Tach: Pulse vs. Pulseless, >100; Monomorphic: no associated P waves, wide QRS >0.12, T
waves must go in opposite direction of QRS complex, Polymorphic: no associated P waves,
wide QRS >0.12, T waves must go in opposite direction of QRS complex, (i.e. Torsades de
Pointes: usually caused by hypomagnesia [alcoholics, renal failure/post or pre dialysis])
Idioventricular (IVR): no associated P waves, wide QRS >0.12, T waves must go in opposite
direction of QRS complex, rate of 20-40
Accelerated Idioventricular (AIVR): no associated P waves, wide QRS >0.12, T waves must go
in opposite direction of QRS complex, rate of 41-100
V-Fib: Pulseless, immediate CPR & early defib, coarse/fine
Ventricular Escape: Initial 2 ventricular complexes pre-ventricular rhythm. (requires >2

ventricular complexes)
Heart block rule: 1st Degree requires prolonged PR segment not abnormal P wave. (PRI=P+PR
segment). 2nd & 3rd Degree More P waves than QRS complexes, examine PRI of every full
cycle constant=2nd Degree Type II; varied=?, R-R interval constant=3rd Degree, varied= 2nd
Degree Type I. Usually 60 & below
1st Degree Heart Block: constant, prolonged PRI of >.20 per cardiac cycle
2nd Degree Type I Heart Block: R-R interval varied; always irregular, possibly worst of AVB’s.
Remember “going-going-gone”.
2nd Degree Type II Heart Block: PRI of every full cycle is constant
3rd Degree Heart Block: atria disassociated w/ ventricle, R-R interval constant P-P constant. “R
waves marching at their own beat, P waves marching at their own beat”
BBB (aberrant conduction)

1. Rhythm SV in origin (Sinus, Atrial, Junctional)
2. QRS >.12
3. Requires 12 L to diagnose
1. Look at V1 (diagnostic lead): HF indicators, BBB direction, etc. Ends in: R wave=
RBBB, S=LBBB, RSR (big fat M)=RBBB.
Ventricular rules
No associated P waves
QRS must be wider than 0.12; “wide & ugly”
T wave must go in opposite direction of QRS complex
Bigeminy: Occurs when every other QRS complex is a PVC. This rate of occurrence is more
serious than quadrigeminy or trigeminy because it usually indicates a higher degree of irritability
in the ventricular muscles.
Trigeminy: Occurs when every third QRS complex is a PVC
Quadrigeminy : Occurs when every fourth QRS complex is a PVC
Couplets: (paired) describes two PVCs in a row that are not separated by a complex of the
underlying rhythm.
Run of V-tach: occurs when three or more PVCs occur in a row, not separated by a QRS
complex of the underlying rhythm. A run of V-tach is of short duration, and the PVCs are
usually all unofficial, at a heart rate greater than 100. Both couplets and runs of V-tach indicate a
high degree of irritability in the ventricles & may lead to a lethal dysrhythmia. A run of V-Tach
may be called a salvo or burst of PVCs.
Noncompensatory pause: Measure from the R wave of the complex before the PAC to the R
wave of the complex after the PAC. This measurement will be less than x2 the R-R interval of
the underlying rhythm. A noncompensatory pause could indicate the development of increased
irritability in the SA node, causing it to generate an impulse sooner than expected in response to
the premature beat. This increase in irritability could lead to sinus-tach.
Compensatory pause: Measure from the R wave of the complex before the PAC to the R wave of
the complex after the PAC. This measurement will equal at least 2 times the R-R interval of the
underlying rhythm. In a compensatory pause, the SA node does not respond to the premature
beat. Therefore there is no change in the rate or regularity of the underlying rhythm.
Column 1: I, II, III

Column 2: AVR, AVL, AVF
Column 3: V1, V2, V3
Column 4: V4, V5, V6
P wave: <.12 seconds wide, <2.5 mm tall

PR Interval (PRI)= P wave + PR segment
QRS</=: .12 measure b/t Q-S
Q wave: </= 0.04 seconds wide, < 1/3 or 1/4 of the R wave
QTI: represents all phases of electricity w/in the ventricles; QRS+ST/T
60-100 bpm = .36-.44; QTI</= 1/2 R-R.
Depressed & elevated isoelectric segments
Wide & deep will be pathologic vs physiologic.
Wide QRS will always show conduction delay in the ventricles; >.12
Pathologic Q waves in anatomically contiguous leads indicate infarct, age undetermined.

PEDIATRICS
Bare Bones Minimum Systolic
0-1 mo: 60
1mo - 1y: 70
1y - 10y: (age in years x 2) + 70
Small children are very heart rate dependent for compensation in comparison to adults who can
compensate via SV.
Babies 2 mo’s and less are obligate nose breathers unless they are crying; an instinctual response.
Most of cardiac arrest in children are hypoxia induced—asystole commonly caused by hypoxia
induced bradycardia.
Cricoid ring is narrowest part of child’s airway; allowing uncuffed tube.
Considered appropriate to use straight blade under 1 year of age; because of a floppier epiglottis
prior to becoming cartilaginous in nature. After 1 year it’s professional courtesy.
Calculate Tube Size

• Cuffed
• (Age + 16) / 4
• (Age/4) +4
• Consider diameter of nares and/or consider diameter of pinky nail
Approximately until the age of 5/6 is when we utilize uncuffed tubes.
Trachea tube >30 days easier to re-tube
DOPE pneumonic
D - dislodgment/displacement
O - obstruction
P - pneumothorax
E - equipment failure (most common cause)
Neurology
Not as compartmentalized, allowing for continual use post-traumatic incidents.
The posterior fontanelle closes by approximately 2 mo’s of age, the anterior fontanelle closes
approximately 12-18 mo’s (posterior closes first because you lay the baby back down.
Bulging fontanelles can be ominous for cerebral hemorrhage and potential exsanguination.
80 ml/kg of blood is circulating volume.
Musculoskeletal
Green stick fractures (fx) which are incomplete fx’s.
Pediatrics rarely have rib fx’s; be suspicious for child abuse/negligence.
A child involved in an accident, recognize SCIWORA (Spinal Cord Injury With Out Radiologic
Abnormality). The damage is due to secondary swelling post-trauma leading to hypoperfusion
distal affected site.
Gastrointestinal
Pediatric patients have a propensity to vomit.
Consider PAT approach (Pediatric Assessment Triangle) done before gaining access to patient.
A-Awareness
B-Work of breathing (rate, rhythm, quality, dyspnea, etc.)
C-Circulation (mottling,
1-2 ml/kg/hr for urine output.

Children very susceptible to changes in temperature.
Very little glycogen stores in the liver.
Children lose 60% of body heat from their head.
Any stressor causes the release of ACTH that further allows the release of cortisol, required for
conversion of glycogen to glucose for metabolic utilization.
Pediatric medications always done in ml or mg or mcg/kg

• Epinephrine
• 0.01 mg/kg IV/IO
• 0.1 ml/kg
• Adenosine (#1 drug for SVT)
• 0.1 mg/kg
• 0.2 mg/kg (in 1-2 minutes)
• Cardioversion (refractory to Adenosine/Unstable)
• 0.5-1 joule/kg
• 1-2 joule/kg (if need to recardiovert)
• Defibrillation
• 2-4 joule/kg
• 4 joule/kg
• MAX 6-10 joule/kg
• Amiodarone
• 5 mg/kg
Pediatric in heart failure require inotropic & diuretic medications (as any heart failure patient)
Hypoglycemia side conversation.
Maintenance Rate & volume for hour D5 1/4 NS
Resuscitation 20 ml/kg of NS (can use 1ml/kg D10)
#G:100ml H2O whenever you see “%”
Croup Epiglottits
Viral Bacterial
Gradual Rapid
Low-grade fever High-fever
Seal-like bark Drooling
Respiratory syncytial virus (RSV) HBI
X-Ray: Steeple X-Ray: Thumbprint
Younger children (</= 3yo) Older children (3-7 y/o)
Croup & Epiglottis are both upper airway infections that you can hear stridor in w/ prolonged
inspiratory phase. Treatments would be humidified oxygen, position of comfort and avoid
manipulating airway to prevent laryngospasms
Upper Airway issues Lower Airway Issues
Snoring: Reposition airway Wheezes: Asthma
Stridor: Consider croup/epiglottitis Crackles: Secretions
Gurgling: Suction Rhonchi: Thicker secretions
Immediate intervention May require stethoscope
Prolonged inspiratory phase Prolonged expiratory phase
Bronchiolitis: usually younger kids, pulmonary disease problem. Tx as any bronchiole infection.
I:E ratio should be 1:2 (1 second inhalation, 2 seconds exhalation)

Prolonged I time would be upper airway.
Prolonged E time would be pulmonary problems; possibly requiring 1:3 I:E ratio.
Ensure rate with pulmonary problems is reduced with increased volume to allow for the
prolonged exhalation. Faster rates are not better due to possibility of air-stacking, barotrauma.
Spontaneous breathing would be negative pressure ventilation; anything else would be PPV.
Most common cause of airway obstruction is the tongue, food usually secondary.
Broncho Pulmonary Dysplasia: babies who were born without surfactant, leaves babies blue until
administration of artificial surfactant.
Hydration is a huge factor of pneumonia.

Poor feeding terminology would be anorexia.
Bulimia
Binge & Purge
Acute Respiratory Distress Syndrome (ARDS)

• Leather lung
• CPAP
• PEEP
• Normal PEEP 3-5 cm/water
• A patient who requires PEEP normal starting point 5, add by 5
• Goal: Avoid derecruitment of alveoli (Domino affect).
• Atelectasis: complete collapse of alveoli.
Cardiac Abnormalities
Atrial Septal Defect (ASD)/Ventricular Septal Defect (VSD) most common cardiac
abnormalities.
ASD’s are less of a threat to life due to the low-pressure of the atria.
VSD’s are more life threatening. Two things could possibly happen:
• Right-to-left shunt deoxygenated blood shunts to LV causing cyanotic look; more
common due to the fact that right side of heart in newborns is more utilized
• Left-to-right shunt oxygenated blood shunts to RV causing reoxygenation; could be
seen in right hypoplasticity.
Direction of shunt will determent cyanotic/acyanotic heart defect.
Meningococcal infections
• Can be bacterial/viral
• Sudden onset
• Associated with nuchal rigidity (“stiff neck”)
• Photophobia: extreme sensitivity to light
• Splotchy rash
• Purpura: a rash of purple spots on the skin caused by internal bleeding from small blood
vessels.
• Petichiai: a small red or purple spot caused by bleeding into the skin.
• May or may not have high fever
• Positive Brudzinkski (Kernig-Brudzinski) sign.
• Movement of chin to chest causes knee’s come up.
• Can be indicative of subarachnoid bleed or meningitis
Tx would be supportive unless protocol to administer antibiotics
Head trauma
Linear skull fx
Linear stellate fx *
Depressed skull fx
Diastatic skull fx (when one part of the skull overrides the other side)
ICP same as others (0-10), ensure CPP
Herniations:
• Cingulate herniation (outside-in)
• Central herniation (top-bottom, bilateral pupil trauma, pressure on 3rd cranial nerve)
• Uncul herniation * (one pupil (ipsilateral change, outside in with top-bottom affect)
• Tonsillar herniation (swell through the foramen magnum; usually from nose down)
• Tx maintain MAP, possibly control rise of ICP (3% hypertonic
saline/Mannitol; both cause osmotic diuresis)
• Whenever possibly tube & place on ventilator; furthermore, reduce oxygen
demand by placing the patient in barbiturate coma
• Hyperventilation to 30-35 ETCO2
• titrate to eupneic rate
In a brainstem injury with medulla involvement, apneustic & ataxic respirations commonly
found from the pons.
Cushing’s Triad
Hypertension
Bradycardia
Abnormal respiratory patterns until hypoventilation
• Central Neurogenic Hyperventilation Syndrome
• attempt to expel CO2, attain O2, vasoconstric
• hyperpnea & tachypnea
• compensatory mechanism
• Biots
• Hyperpnea & tachypnea w/ periods of apnea
• Cheyne-Stokes
• Apneustic
• Agonal breathing
Cord syndromes
Anterior cord: everything above the injury site is good (“Clap can’t dance”)
Brown-Sequard: opposite effects (“bilateral effects” “Clap one arm, dance one leg”)
Central: weaker upper extremities than lower extremities (“Dance can’t clap”)
Posturing
Decorticate: arms adduction, toes pointed
Decerebrate: (worse than decorticate) arms abduction, toes pointed
Le Fort fx’s II & III usually seen with trismus.
Chest
Main difference b/t adults and pediatric chest trauma is that pediatrics are much less likely to
have open chest wounds/rib fx’s because the primary traumatic force is absorbed by the organs.
Late sign of tension pneumothorax would be tracheal shift away from injured site.
Pneumothorax
Hyperresonance
Hemothorax
Hyporesonance
Cardiac Tamponade
Early tx is fluid bolus and Gold standard is pericardiocentesis.
Start around 250ml bolus.

Tachycardic
Tachypneic
Muffled heart tones
Narrowing pulse pressures
Pulsus paradoxus- “also paradoxic pulse or paradoxical pulse, is an abnormally large decrease in
systolic blood pressure and pulse wave amplitude during inspiration. The normal fall in pressure
is less than 10 mm Hg.”
Pulsus alternans- “is a physical finding with arterial pulse waveform showing alternating strong
and weak beats. It is almost always indicative of left ventricular systolic impairment, and carries
a poor prognosis.”
Diaphragmatic rupture
Bowel sounds & fecal odor
Ensure NG/OG tube placement in a film that it is in the left anatomical position (stomach),
anywhere aside from that place is incorrect placement.
Abdominal
Rupture of a major organ (liver/spleen)
Intra-abdominal bleed
The Duodenum is first 10” of the small intestine, followed by the jejunum, followed by the
ileum. At the end of the small intestine, prior to the large intestine is the cecum.
Large intestine directions: ascending, transverse, descending, sigmoid, then rectum.
In an appendix issue, extreme pain is found and as soon as the appendix ruptures, the pain goes
away. The post-rupture and dependent of stool amount and content determines sepsis.
Pelvis
Pelvic fx’s very uncommon in pediatrics without presence of extreme high deceleration force.
Open-book fx separate at symphysis pubis.
Lower extremities
Bilateral femur fx’s can be fatal
Bilateral fx’s not fatal
Bivalve a cast less than 7 days for flight (Boyle’s law)
Burns
Parkland formula
Thermal burns are given a degree on depth not width.
Rule of 9’s or Palmar calculate width
• 1st degree “superficial”

• Epidermis
• No required tx
• Not included when calculating fluid resuscitation
• 2nd degree “partial-thickness”
• epidermis and dermis
• presents with blistering
• consider cooling for up to one minute
• never pop a blister
• cover burn with dry sterile dressing/tx for shock
• 3rd degree “full-thickness”
• epidermis, dermis, fatty tissue, nerve endings
• pain is associated with surrounding 2nd degree burns
4ml x kg x Body Surface Area (BSA) of 2nd & 3rd degree burns
Shock (link)
Heart failure patients have less than 40% ejection fraction.
Left heart failure patients buildup to lungs, right heart failure patients buildup to rest of the body.
SHOCK CHART
Hypovolemia Cardiogenic Septic
Cardiac Output (CO)

Heart Rate (HR)

Systemic Vascular Resistance

(SVR)
Ejection Fraction (EF)

Pulmonary Capillary Wedge

Pressure (PCWP)
Central Venous Pressure (CVP)

Blood Pressure (BP)

Skin Temperature

Think of PCWP as the left atrium and think of CVP as the right atrium.
Toxins in septic shock deregulates the blood vessels causing the SVR to decrease (vasodilation).
Shock & Sepsis tx’s (link)
Hypovolemia Cardiogenic Sepsis
RAAS system Digoxin ABX (within less than 1 hour)
ADH Dobutamine CVP of 8-12 with NS
NS Vasopressors (MAP >65)
Transfusion Dobutamine (CO)
DO2 “Delivery”
VO2 “What’s used” EX: 100 (DO2) - 25 (VO2) = 75 (SVO2)
SVO2 “What’s returning”
WET DRY
WARM IV diuretics (lasix, phenodilatory HF Curve

properties) Beta blockers
ACE inhibitors
PO Diuretics
COLD CCU End-stage HF (ESHF)

IV Diuretics Inotropes/pressors
Pump (inodilators [Dobutamine], VAD
Pressors [Levophed]) Heart transplant

OBSTETRICS
Pregnancy in general: every body system is effected.
Cardiovascular system
40% increase in blood volume.
30-50% increase in CO with half of that increase within 8 weeks.
Placenta takes 12 weeks to fully form, takes over production of progesterone while dealing with
nutrition of the baby and by products.
In twin pregnancy, its proven to be approximately 20% more than a single-fetus pregnancy.
HR of 10-15 bpm
Hemodynamic monitoring will remain the same for pregnancy (values).
Reduction in afterload due to decreased SVR (vasodilation).
Increase in clotting factors, nearly double fibrinogen.
BP decreases around 2nd trimester due to relaxation of blood vessels and return to normal
numbers by 3rd trimester.
Gastrointestinal
Increase in saliva production
Decrease in gastric motility allowing more time to absorb nutrients but places her at a higher risk
of aspiration.
Normal weight gain can be from 10-15 pounds depending on pre-pregnancy weight.
Decrease in bladder tone.
Respiratory
Decrease in functional residual capacity, expiratory reserve volume and residual volume.
(Decrease in expiratory phase)
The diaphragm is displaced 1-2”
Spreading of circumference of the chest.
Renal
25% CO filters through kidneys every minute
GFR increases
Hyperthyroidism can cause stillbirths, further complications for mother.

Increase in all hormones.
Posterior pituitary gland
• Oxytocin
• assist with uterine contractions
• ADH
• DI is dry (too little ADH)
• SIADH is swollen (too much ADH)
Loss of pregnancy prior to 20 weeks is termed “abortion”, after 20 weeks, termed “still-birth”.
G-Gravida: Number of times mom has been pregnant

A-Abortions: Includes still-births and miscarriage spontaneous or elected
P-Para: Live Births
T-Term: Full term is 37 weeks
L-Living children: children alive.
Fetus
Fetus has 1-2 minutes of reserve oxygen
Oxygenation happens through umbilical vein.
Possess fetal hemoglobin
Placenta Abruptio
Placenta abruptio presents suddenly with severe abdominal and back px and you’ll feel no fetal
movement. Tender abdomen and rigid uterus will be present due to internal bleeding and vaginal
bleeding may not be present.
Placenta Previa
Painless vaginal bleeding with fetal movement present, non tender abdomen and uterus will be
soft.
Uterine rupture
Most common time seen during labor.
Anyone with previous uterine rupture or previous uterine surgeries are at higher risk due to scar
tissue not being as tough as muscle tissue.
Vaginal Birth After Cesarean-section (VBAC) becoming more accepted with prior horizontal
incisions; however, not encouraged for linear and “T” incisions.
Preeclampsia
Classic S/S:
• BP 140/90 or greater
• Proteinuria
• Swelling
• Headache
• Visual changes (blurry/double)
• Oliguria
“The way you fix preeclampsia is delivery of the baby.”
Preeclampsia Complications
Maternal Fetal
CNS Preterm Delivery

• Seizures
• Cerebral Edema
• Cerebral Hemorrhage
• Strokes (thrombotic)
Hepatic Stillbirth (IUFD)
• Hepatic Failure Intrapartum Fetal Distress
• Hepatic Rupture
• Subcapsular Hemorrhage
Hematological Abruptio Placenta
• DIC
• Hemolysis Elevated Liver Function Tests Low
Platelet Count (HELLP)
Renal Uteroplacental Insufficiency

• Renal Failure • Hypoxic Neurological Injury
• Oliguria • IUGR
• Proteinuria leading to Hypoproteinemia • Oligohydraminos
causing glomerular injury
Lungs
• Pulmonary Edema
“It’s Not My Time!” Tocolytics

Indomethacin (NSAID)
Nifedipine (CA Channel Blocker)

Magnesium Sulfate
Terbutaline (Adrenergic Agonist)
Right shift:
Hyperthermia
Acidosis (decrease in pH)
Increase in 23DPG
Left Shift:
In utero, fetal hemoglobin has higher affinity for oxygen
NEONATAL
Heart rate is primary compensatory mechanism for volume

Babies can’t shiver until 1 y/o; therefore, nonshiviering thermogenesis is primary source of heat
production.
Metabolic acidosis can happen if temperature is not regulated.
Brown-fat, only found in infants (after 30 weeks gestation) is what’s used for thermogenesis.
Brown-fat reacts with nor-epinephrine creates triglycerides which is used for heat production.
Premies are really poor at thermoregulation to include low glycogen stores; meaning high-risk
for hypothermia and hypoglycemia.
Hypoglycemia in neonates is found in 45 and in pediatrics at 60.
Acrocyanosis and pallor are normal signs for babies who are cold.
Tidal volume for neonates is 5-7 ml/kg; look for chest-rise
Infants are obligate nose-breathers; clear their nose. They only breathe through their mouth when
they cry.
Fetal hemoglobin stays in the system until 6 months of age (approximately); causes left shift of
oxyhemoglobin dissociation curve.
Wharton's jelly (substantia gelatinea funiculi umbilicalis) is a gelatinous substance within the
umbilical cord also present in vitreous humor of the eyeball, largely made up of
mucopolysaccharides (hyaluronic acid and chondroitin sulfate). It also contains some fibroblasts
and macrophages.
Ductus arteriosus closes within 24-48 hours.
Indomethacin used to close a PDA (normal in utero).
PGE1 is given to all neonates with PDA required CHD to keep it open.
Foramen ovale takes up to 6 weeks to close.
Manage any types of pain.
If APGAR score 3 or less after 20 minutes they are at high-risk for neurologic deficits.
Apnea is a pause in respirations of more than 20 seconds.
Primary apnea: present at birth, responds well to stimulation and oxygenation.
Secondary apnea: bradycardia and drop in BP, only responds to assisted ventilation and
oxygenation.
Fixed anatomic obstructions: bilateral choanal atresia, Pierre Robin sequence, laying baby flat
without padding.
Intubation is last-resort even with meconium present. Each suctioning requires a separate
intubation.
Respiratory distress in a neonate can be caused by meconium-stained amniotic fluid, pneumonia,
respiratory distress syndrome (withholding of amniotic fluid), or pneumothorax due to PPV.
Pulmonary hypertension can be caused by NSAIDS, meconium aspiration, etc. The right
chambers of the heart enlarge as they struggle to function.
Omphalocele the intestines, liver, and other organs remain outside of the abdomen in a sac
Gastroschisis the intestines are outside of the abdomen through a hole in the abdominal wall
Imperforated anus: “no butt hole”

cephalhematoma
subgaleal hemorrhage
extradural hemorrhage
Seldom see tonic-clonic seizures in infants
Hypoxic Ischemic Encephalopathy
hypocalcemia low birth weight, 2-3 days after birth.
congenital adrenal hyperplagia: electrolytes, hydrocortisone, fluids
ASD’s/VSD’s
In trunkus arteriosus, one trunk, right to left shunt due to deoxygenated blood pumping through
systemically.
Diuretics, digitalis, ACE inhibitors are the treatments
Prostaglandin infusion is not beneficial if it’s just trunkus arteriosus
Transposition of the great arteries requires a patent foramen ovale (PFA)/ASD so that the
oxygenated blood can reach the blood flow.
MEDICAL
Endocrine system:
• Pineal gland
• Melatonin
• Pituitary gland
• Posterior pituitary
• Oxytocin
• Contractions/post-partum hemorrhage
• ADH
• SIADH
• DI
• Anterior pituitary
• Follicle Stimulating Hormone (FSH)
• Gonads
• Progesterone
• Thyroid Stimulating Hormone (TSH)
• Luteinizing Hormone (LH)
• Androgen production (males)
• Estrogen production (females)
• Human Growth Hormone
• Adrenocorticotropic Hormone
• Releases cortisol
• Melanin Stimulating Hormone
• Skin color
• Prolactin
• Mammary tissue
• Thyroid
• T3
• T4 Thyroxine
• Myxedema coma: hypothyroidism
• Grave’s disease: hyperthyroidism
• Thyrotoxicosis: extreme hyperthyroidism (a.k.a. Thyroid Storm)
• Calcitonin
• Serum Ca++ levels
• move Ca++ back to bones, urinate it, don’t absorb
• checks and balances between calcitonin
• Parathyroid
• Parathyroid hormone
• Expel Ca++, retain, absorb
• checks and balances between calcitonin
• Thymus
• Pancreas
• ARDS secondary to pancreatitis
• Insulin
• Glucagon
• Adrenal Glands
• Epinephrine
• Norepinephrine
• Cortisol
• Cushing’s high level of cortisol
• Aldosterone
• Life threatening adrenal crisis
HHNC/HHNK/HONK: Type II diabetics (sugar problem not insulin problem)
Hemolytic reactions
epi and benadryl for anaphylaxis, shut off and fluids
Hematocrit/HGB values:
• The patients blood is considered balanced if the HGL level is 1/3 of the hematocrit value & the
RBC count is 1/3 of the HGL level
• Hematocrit: gives the overall proportion of RBC’s in the blood
• HGL: HGL count, oxygen carrying molecule

Counts of formed elements:
• Account for 45%
• 99% of 45% are RBC’s
• WBC’s & platalets
• High WBC’s is indicative of infection, High/Low RBC’s indicative of hematologic disorder
i.e. Anemia (low hematocrit)

Normal RBC/WBC: Produced by the stem cells within red marrow of the bone

Liver clotting factors:
• Liver produces clotting factors
• VIII disorder is type A/1
• IX disorder type B/2

Basic Blood Type
A, B, O
AB+: Universal recipient
O-: Universal donor
Don’t mix them up unless O- or AB+ i.e. A+ gets A+; B- gets B- etc.

Types of Immunity:
Cellular Immunity: “cell-mediated immunity, body produces special white blood cells called
T-Lymphocytes that attack & destroy invaders
Humoral Immunity: B-Lymphocytes produces antibodies that dissolve in the plasma and lymph
to wage war on invading organisms
Acquired immunity: administration of vaccine allows the body to produce antibodies w/o having
to experience the disease
Natural immunity: the body encounters the antigen & experiences a full immune response w/ all
the pathology of the disease

Primary response of foreign object:
Phagocytosis by macrophages

Different WBC’s & Jobs:
Granulocytes:
• Neutrophils: destroy bacteria, antigen-antibody complexes, foreign matter
• Eosinophils: function in allergic response
• Basophils: least common allergic/inflammatory reactions & contain large amounts of
histamine (increases tissue inflammation) & heparin (inhibit blood clotting), produce chemical
mediators “granules eject & explode”
Agranulocytes
• Lymphocytes: smallest agranulocyte, production of antibodies, cell-mediated immune response
• Monocytes/Macrophages: first lines of defense engulfing microbes (phagocytosis)

Role of Histamine:
Mediates allergic reaction
• Physiologic effects:
• Systemic vasodilation
• Increased permeability of blood vessels
• Decreased inotropy
• Decreased coronary blood flow
• Dysrhythmias
• Bronchoconstriction
• Pulmonary vasoconstriction

Allergic reactions S/S:
• Utilize environment of scene & patient history
• Urticaria
• Erethema
• Pruritus
• Nasal congestion
• Watery, red eyes
• Abdominal pain
• Abnormal (high-pitched) breathing sounds
• Anxiety
• Chest discomfort or tightness
• Cough
• Diarrhea
• Difficulty breathing
• Difficulty swallowing
• Dizziness or light-headedness
• Flushing or redness of the face
• Nausea or vomiting
• Palpitations
• Swelling of the face, eyes, or tongue
• Unconsciousness
• Wheezing

Different shock:
• Septic shock results from bacteria multiplying in the blood and releasing toxins. Common
causes of this are pneumonia, urinary tract infections, skin infections (cellulitis),
intra-abdominal infections (such as a ruptured appendix), and meningitis.
• Anaphylactic shock is a type of severe hypersensitivity or allergic reaction. Causes include
allergy to insect stings, medicines, or foods (nuts, berries, seafood), etc.
• Cardiogenic shock happens when the heart is damaged and unable to supply sufficient blood to
the body. This can be the end result of a heart attack or congestive heart failure.
• Hypovolemic shock is caused by severe blood and fluid loss, such as from traumatic bodily
injury, which makes the heart unable to pump enough blood to the body, or severe anemia
where there is not enough blood to carry oxygen through the body.
• Neurogenic shock is caused by spinal cord injury, usually as a result of a traumatic accident or
injury.
• Isotonic crystalloid fluids, IV, O2, Monitor, ETCO2, blood products if available/protocol
dependent.
• Pressor choices:
• Norepinephrine (Cardiogenic): .1-.5 mcg/kg/min titrate to effect (average for 70 kg pt 7-35
mcg/min) Pedi: .1-.2 mcg/kg/min titrate to effect. Onset: 1-3 mins, duration 5-10 mins/1 min
after infusion DC
• Dopamine (Cardiogenic, Septic, Distributive): 2-20 mcg/kg/min titrate to effect (start off 10
mcg/min). Onset: 1-4 mins, ends quickly after DC
• Vasopressor: 40 Units, .02-.04 U/min Pedi: .4-1 U/kg to max 40 U. Onset: Immediate,
duration variable.
• Epinephrine: Mild allergic: .3-.5 mg of 1:1000 SQ; Anaphylaxis .1 mg of 1:10,000 IV/IO
over 5 mins Pedi: .01 mg/kg of 1:10,000 IV/IO over 5 mins

Epidemiology
Endemic: localized to geographic area w/ stable numbers
Epidemic: localized to geographic area w/ increasing numbers
Pandemic: world-wide spread w/ large numbers of infection

Bioavailability: is a subcategory of absorption and is the fraction of an administered dose of
unchanged drug that reaches the systemic circulation, one of the principal pharmacokinetic
properties of drugs.
• Injection: 100%; Most rapid onset
• IM: 75 to less than/equal to 100; Large volumes often feasible, may be painful
• SQ: 75 to less than/equal to 100; Smaller volumes than IM, may be painful
• PO: 5 to < 100; most convenient; first pass effects may be significant
• PR: 30 to < 100; less first pass effect than PO
• Inhalation: 5 to < 100; Often rapid onset
• ID: 80 to less than/equal to 100; usually very slow absorption; used for lack of first pass
effects, prolonged duration of action

Routes of toxic exposure:
• Inhalation
• As long as the patient remains in the toxic environment he/she will still be inhaling the
poison as well as the paramedic w/o proper PPE. UNSAFE SCENE.
• Home medications & household chemicals most commonly responsible
• Mixed chemicals are usually colorless and odorless
• “From the anatomic & physiologic perspective, inhaled toxins reach the alveoli quickly,
providing almost instant access to the circulation.”
• CO has higher affinity for HGL than O2
• Scene safety
• Industrial site/enclosed spaces
• IV, O2, Monitor, SpO2, ETCO2
• Ingestion
• May be immediate or delayed for several hours
• Medications/household chemicals most common sources of ingested poisoning
• S/S: N/V
• Management of poisoning by ingestion aims to remove or neutralize the poison before it
gains access to the intestines
• Injection
• Usually gain access by stings/bites; drug abusers (Heroin, Cocaine, Amphetamines, Speed)
• Environment/geographic area plays huge roll
• Frequently the patient may be able to identify the culprit
• Solution to Pollution is Dilution: IV, fluid boluses, O2, Monitor; Drug abusers: consider
naloxone 2mg slow IVP for respiratory compromise
• Absorption
• Pesticides such as organophosphates are often the most serious
• Consider Atropine 2-3 mg (20-30 mL of .1mg/mL solution) 20-30 mins, 2 PAM 1-2G IV
over 15-30 mins infusion, IV, O2, Monitor

Psych questions (not OBS but cause):
• Organic Brain Syndrome (OBS) patients are those who present w/ psychiatric symptoms and
are actually being affected by biologic or organic influences that interfere w/ normal cerebral
function
• Common causes: chronic hypoxia, seizure, TBI, chronic alcohol/drug abuse, brain tumors.
• Most common offenders are alcoholic/drug abusers [dementia/delirium should be considered]
• Alcohol: IV, O2, BGL, Monitor, possible benzodiazepines, fluid boluses
• Drug: Solution to Pollution is Dilution; IV, O2, Monitor [hypoxia induced dysrhythmias],
2mg naloxone slow IVP for respiratory depression, fluid boluses

Thought in Assessment:
• Flight of Ideas: patients mind plunging from one thought to another
• Loosening of Associations: logical connection b/t one idea & the next becomes obscure (to the
listener)
• Delusions: persecution
• Thought of broadcasting: belief that thoughts are broadcasted aloud & can be heard by others
• Thought of insertion: belief that thoughts are being thrust into his/her mind by another person
• Thought withdrawal: belief that thats are being removed
Most EMS systems rarely respond to hematologic emergencies.

Blood performs respiratory, nutritional, excretory, regulatory, and defensive functions.
Blood is made up of plasma and formed elements, or cells, including red blood cells, white blood
cells, and platelets.
Laboratory tests commonly performed on blood are red blood cell count, hemoglobin level, and
hematocrit measurement.
Blood tests that measure subtypes of white blood cells can provide valuable information about
the status of the immune system.
During the primary assessment of a patient with a hematologic disorder, note any signs and
symptoms that may be immediately life threatening.
While taking a history and during the secondary assessment, look for changes in the level of
consciousness such as vertigo, feelings of fatigue, or syncopal episodes.
General management for any patient with problems related to a blood disorder should include the
following elements: oxygen, fluids, ECG, transport, medications, and psychological support.
Hematologic disorders include sickle cell crisis, anemia, leukopenia, thrombocytopenia,

leukemia, lymphomas, polycythemia, DIC, hemophilia, multiple myeloma, and complications of
blood transfusions.
A patient experiencing a sickle cell crisis will experience significant pain due to congested
vessels and may have a serious infection that can lead to sepsis and death.
A patient with anemia has a hemoglobin or red blood cell level that is lower than normal.
Anemia may be caused by an underlying hematologic or hemolytic disorder.
Leukopenia is a reduction in the number of white blood cells and thrombocytopenia, a reduction
in the number of platelets; both are conditions often seen in patients with anemia or leukemia.
Leukemia is a type of cancer that affects the production of white blood cells. Patients often
experience bleeding, bruising, infections, and fever.
Lymphomas are a group of malignant disorders that arise within the lymphoid system. The two
types are non-Hodgkin (making up the majority of cases) and Hodgkin lymphoma.
Polycythemia is characterized by an overabundance or overproduction of red blood cells, causing
hyperviscosity of the circulatory system.
Disseminated intravascular coagulation (DIC) may result from a massive injury, sepsis, or
obstetric complications. In the first stage, too much blood clotting results from an overactivated
coagulation system. In the second stage, the body’s natural reaction to breaking up these clots
causes uncontrolled hemorrhage.
Hemophilia is a bleeding disorder found primarily in the male population in which clotting does
not occur or occurs insufficiently. Type A is due to a low level of factor VIII, and type B is due
to a deficiency in factor IX.
Multiple myeloma is a cancer of the bone marrow caused by malignant plasma cells.
Complications of blood transfusions are similar to anaphylactic reactions and are caused by a
mismatch of the patient’s blood type to that received or an allergic reaction to preservatives or
agents in the transfused product.

• Gestational diabetes is a form of glucose intolerance that usually manifests itself late in
pregnancy.
• Adrenal insufficiency is characterized by underproduction of cortisol and aldosterone, which
leads to weakness, dehydration, and the body’s inability to maintain adequate blood pressure
or to properly respond to stress. Primary adrenal insufficiency (also known as Addison
disease) is caused by atrophy or destruction of both adrenal glands, leading to deficiency of
all the steroid hormones produced by these glands.
• Secondary adrenal insufficiency is defined as a lack of adrenocorticotropic hormone (ACTH)
secretion from the pituitary gland.
• Acute adrenal insufficiency is referred to as an addisonian crisis, which may result from an
acute exacerbation of chronic insufficiency, usually brought on by a period of stress, trauma,
surgery, or severe infection.
• Cushing syndrome is caused by an excess of cortisol production by the adrenal glands or by
excessive use of cortisol or other similar corticosteroid (glucocorticoid) hormones.
• Pheochromocytoma is generally a nonmalignant tumor of the adrenal gland, usually in the
medulla, that causes excessive release of the hormones epinephrine and norepinephrine.
• Congenital adrenal hyperplasia (CAH) is a condition of the adrenal gland in which there is
not enough production of cortisol and aldosterone.
• Thyroid hormones are critical for cell metabolism and organ function. If their supply
becomes inadequate, organ tissues do not grow or mature (due to the decreased metabolic
rate), energy production declines (a cause of the decreased metabolic rate), and the actions of
other hormones are affected.
• Graves disease is the most severe and common cause of hyperthyroidism. The disease can
produce goiter, exophthalmos, and pretibial myxedema.
• Hashimoto disease, another cause of hyperthyroidism, is an autoimmune disease in which the
thyroid gland is enlarged as a result of the infiltration of T lymphocytes and plasma cells.
• Symptoms of hypothyroidism include feeling fatigued, feeling cold, gaining weight, having
dry skin, and being sleepy. Continued decrease of thyroid hormone levels may lead to
myxedema coma.
• Myxedema coma is a condition in which a general slowing of the body’s metabolic processes
occurs in the setting of reduced or absent thyroid hormone.
• Thyrotoxicosis is a toxic condition caused by excessive levels of circulating thyroid
hormone. A thyroid storm is a rare, life-threatening condition that may occur in patients with
thyrotoxicosis.
• In hyperparathyroidism, blood calcium levels increase, resulting in hypercalcemia and
decreased phosphate blood levels.
NEUROLOGY
The cranium is also called the calvarium.

PO vessels
CSF allows for floating and protection of the brain inside the calvarium
Medulla primary respiratory center
Pons secondary respiratory center (apneustic respirations)
Uncus (location of uncle herniation)
Corpus callosum: broad band of nerve fibers joining the two hemispheres of the brain.
The spinal cord is small and soft tissue.

Cauda equina “horsetail” begins at L2 and down; sensory and motor nerves.
Damage to the caudal equina allows for regeneration and rarely results in permanent paralysis.
Circle of Willis (circulus arteriosus cerebri)
Epidural
The thinnest piece of skull piece is the
temporal bones. Nestled behind the temporal
bones are the middle meningeal arteries. If
MOI is traumatic to temporal bone, you have
to be suspicious of a middle meningeal artery
rupture indicative of epidural (above the dura
below the skull) bleed.
Immediate loss of consciousness, followed by
a lucid interval, followed by deterioration in
mental status and possible death.
Lenticular bleed (looks like the lens of an eye
or contact lens)
Subdural
Below the dura
Venous (insidious) bleed
Confused, no report of unconsciousness, altered mentation.
Subarachnoid
Most commonly caused by a burst of the circulus arteriosus cerebri due to an aneurysm and
associated vessels.
Most CSF (80%) is produced in the choroid plexus which is located in one of the ventricles of
the brain. It is circulated in the subarachnoid space.
The arachnoid and dura are adherent to each other, the pia is the actually covering the brain/cord.
Peripheral nervous system

Parasympathetic nervous system a.k.a. cholinergic nervous system/rest-and-digest

Acetylcholine parasympathetic nervous system and is inhibited by acytlecholinesterase
Causes slowing of the heart
SLUDGE pneumonic
S-salivation
L-lacrimation
U-urination
D-defecation
G- gastrointestinal
E-emesis
Sympathetic nervous system a.k.a. adrenergic nervous system/fight-or-flight

epinephrine and norepinephrine excreted from the adrenal medulla
High C-spine injuries

Above T-6 you will have sympathetic (not parasympathetic) stimulation
Comes into play with quadriplegics who have “battle” between sympathetic and parasympathetic
stimulation
• Autonomic dysreflexia
• above injury increased sympathetic stimulus
• below injury increased parasympathetic stimulus
• Most common stimulus is full urinary bladder
• At risk for aspiration due to inability to move
• Foley the pt.
Hypertensive encephalopathy
Sustained MAP of greater than 150
Eclampsia can fall under this category due to it’s hypertensive crisis.
Reflex testing
Grasp reflex should only be used on
newborns/neonates/infants; not as effective test on
adults. Most basic test.
Babinski testing: (stroke lateral sole of foot) if

plantar response occurs, negative babinski test
meaning normal. Extension of toes is the positive
test indicative of positive spinal cord injury.
Reverse in newborns.
Meningeal irritation
“chin-to-chest knee’s will flex”
Traumatic Brain Injury (TBI)

Becoming more common on point of injury
Can be mild, moderate, or severe.

Thought to be caused by coup-contra-coup which is evidence of Newton’s (link) third law (states
that for every action (force) in nature there is an equal and opposite reaction.)
Newton’s (link) first law: states that every object will remain at rest or in uniform motion in a
straight line unless compelled to change its state by the action of an external force.
Review skull fx’s
Diffuse Axonal Injury (DAI)

TBI deep in the brain spreading out
Mild
• patient has a coma lasting from 6-24 hours
• usually not associated with long-term morbidity/death
Moderate
• longer than 24 hours
• continuous to show brainstem signs absent
• don't have intact brain stem
• if survived, patient always have impairments
Severe
• protracted coma
• patient usually dies
ICP
0-10; nothing greater than 20
Uncul herniations with ipsilateral pupil change
Transducer should line up with the canthus of the eye (foramen of monro)
Tx’s
Eliminate as much stimulus as possible (phenobarbital comas)
Cold and dry is biggest stressor for weather
Attain cerebral vasoconstriction
• possible ventilation to ETCO2 between 30-35
Strokes
Thrombotic/embolic
Hemorrhagic tend to be more debilitating. “Worst headache of my life”.
Seizures
Benzodiazepines (Lorazepam “Ativan”)
Generic Name: Lorazepam
Trade name: Ativan
Pharm. Class: Benzodiazepine
Therapeutic class: Sedative Agent/Anticonvulsant
MOA: CNS depressant, GABA (selective to hypothalamus, cortex, limbic)
Reason given: Epileptic seizures, seizures, sedation, anxiety, pacing, cardioversion
Dosage: Adult: 2-4 mg slow IV/IM at 2 mg/min; for sedation up to 4 mg IM. Peds: 0.05-0.2
mg/kg
Pre Admin (interactions/contraindications): narrow-angle glaucoma (increase ocular
pressure), decreased respiratory (CNS depressed), hypersensitivity
Post Admin (adverse reactions): headache, hypotension, respiratory depression/arrest, reflex
tachycardia.
Paramedic Considerations (special considerations): Reduce dose by 50% for elderly patients;
used mainly for epileptic seizures, have advanced airway ready

RESPIRATORY
Mechanical Ventilator (link)

AC (assist control)
CMV is different from AC
AC
Ideal would be 8 ml/kg IBW range 6-10 ml/kg
Patient triggers vent
Rate = 12 - 5 sec
Synchronized Intermittent Mandatory Ventilation SIMV
High levels of PEEP in a lobular injury causes VQ mismatch. PEEP will take path of least
resistance affecting the unaffected lobes. This causes no/limited blood flow with high oxygen in
the unaffected lobes; continuous blood flow in the affected lobe but no oxygenation
ARDS
High PEEP (10-20) LOW tidal volume (6 ml/kg goal; as low as 4)
pH
PCO2: problem here, change RR/TV
PO2: problem here, change FiO2/PEEP
Winter’s formula/rule
10 mmHg that CO2 rises, HCO3- will increase by 1

TOXICOLOGY/ENVIRONMENTAL
Safety is always priority; remember basics.

Immediate life threats: ABC’s
• Airway
• If the patient is A&Ox4 and able to speak, patent airway. Vaporous substances can’t
react inside a person’s airway making the situation worse.
• Be cautious when burns/toxins that can possibly cause laryngospasms, airway won’t
be patent after that
• Presence of an ETT does not guarantee a patent airway (monitor constantly)
• Patency of an airway can become compromised during transport
• Be cautious for possibility of aspiration in a patient who’s been administered
activated charcoal/syrup of ipecac
• Stridor, snoring respirations, gurgling noises are all indications of a compromised
airway
• Breathing
• Ensure oxygenation is adequate to meet patients metabolic needs
• Physiologic stress, acidosis, hypermetabolic state, toxic substances require greater
oxygenation
• Asphyxiants, organophosphates, neuromuscular blockers are all possibly toxic to gas
exchange, airway diameter (bronchoconstriction), lung tissue and ventilation
• Opiates, benzodiazepines, tricyclic anti-depressants, and ethanol are all indirect
toxins that can impair respiratory drive
• Hypoxic, hypemic, histotoxic and stagnant hypoxia can occur
• Compromise can occur from trauma, burns, or aspiration
• Circulation
• Ensuring adequate perfusion to major organs is key.
• Otherwise healthy patients may experience alterations in hemodynamic parameters
without losing end-organ tissue perfusion
• Persons with preexisting health conditions may not compensate as well as healthy
patients to circulatory compromise
• Numerous mechanisms may impair the functionality of cardiovascular system.
• Possible factors that lead to decline in patient condition can be direct exposure to
toxic substances, fluid volume loss or redistribution, electrolyte disturbances,
airway/respiratory compromise, preexisting conditions, and altered oxygen-carrying
capacity.
• Other life threatening hemorrhage (falls under circulation, however, H-ABC’s as in TC3)
Additional assessments
• What was the substance involved?
• Time, quantity, and/or duration of the exposure
• Route(s) of the exposure (inhalation, injection, absorption etc.)
• Clinical status of the patient
• Initial decontamination (what were the treatments provided prior to arrival of any EMS crew)
• Other information (any information can be good information)
• Maintain a patent airway and ensure oxygenation

• Attempt to prevent absorption of the toxins involved
Vital signs
• Marry the effects to the chemical baseline
• Stable or unstable?
• Basic interventions
Toxic Event possibilities

• Unusual odors, smoke, or vapors
• Placards, signs, or markings (transport trucks/industrial complexes, attempt to acquire
MSDS)
• Known vehicles/complexes that possess toxins
• Bystanders who unexpectedly become ill or unconscious
• Multiple patients with unexpected but similar symptoms
Laboratory assessments
• Utilize current labs for transfers
• Future considerations for labs in the field could potentially appear (possibly more accurate
for fixed wing CCT)
Toxic Syndromes
• Anticholinergic syndrome (parasympathetic system is effected e.g. atropine OD)
• Cholinergic syndrome (essentially SLUDGEM)
• Opioid syndrome (CNS depressants)
• Sympathomimetic syndrome (increased sympathetic response)
Medication reaction syndromes

• Malignant hyperthermia or malignant hyperpyrexia is a rare life-threatening condition that is
usually triggered by exposure to certain drugs used for general anesthesia — specifically the
volatile anesthetic agents and succinylcholine, a neuromuscular blocking agent.
• Neuroleptic malignant syndrome is a life-threatening, neurological disorder most often
caused by an adverse reaction to neuroleptic or antipsychotic drugs. Symptoms include high
fever, sweating, unstable blood pressure, stupor, muscular rigidity, and autonomic
dysfunction.
• Serotonin syndrome is any of a group of symptoms that may be an indication of any number
of potentially life-threatening drug interactions that may occur following therapeutic drug
use, combination, overdose of particular drugs, or the recreational use of certain drugs.
• Rhabdomyolysis is a breakdown of muscle tissue that releases a damaging protein into the
blood. Possibly caused by excessive alpha-1 stimulation (extreme vasoconstriction)
General Management
• Primary decontamination
• Removal of external clothing
• Skin decontamination
• Ocular damage
• Secondary Decontamination
• Orogastric/nasogastric lavage
• Activated charcoal (sorbitol)
• Whole-bowel irrigation
Enhanced elimination
• Multiple-dose charcoal
• Urinary manipulation (diuretics)
• Dialysis, hemoperfusion, and continous renal replacement therapy.
Pharmaceutical/Abuse agents
• Acetaminophen can cause liver damage (cirrhosis) kidney failure, severe constipation,
urinary retention etc.
• Amphetamines
• Benzodiazepines
• Beta-adrenergic blocking agents
• Calcium antagonists
• Cardiac glycosides
• Cocaine
• Opioids and opiates
• Salicylates
• SSRI’s Selective serotonin re-uptake inhibitors or serotonin-specific re-uptake inhibitors are
a class of drugs that are typically used as antidepressants in the treatment of major depressive
disorder and anxiety disorders.
• Toxic alcoholics (not regular alcohol)
• Tricyclic antidepressants
Chemical agents
• Acetylcholinesterase inhibitor
• Carbon monoxide
• Caustics and corrosives
• Chlorine, ammonia, and asphyxiate gases
• Cyanide poisoning
• Hydrocarbons
• Hydrofluoric acid (calcium)/hydrogen fluoride
• Highly toxic substances
HAZMAT
Personal safety, stay safe, stage.
Risk Factors of Environmental

Age of patients (young/elderly)
Medications
Preexisting medical conditions

• Diabetes
• Cardiovascular
• Lung disease
• Thyroid diseases
• Psychiatric
Thermoregulation
Hypothalamic-Hypophyseal portal system
Interrelationship between hypothalamus and pituitary gland is called the hypothalamic-pituitary
axis
First “job” the brain dumps is the process and ability of thermoregulation
Heat response: vasodilation, perspiration is increase to 10 times normal, increases in muscle
activity, including shivering are inhibited.
Cold response
Stimulation of posterior hypothalamus causes a constriction of blood vessels
Basal Metabolic Rate

Can determine how much body heat is being exerted
Expect the Unexpected

A person can have a temperature emergency in any environment
CCTP must be aware of patients inability to regulate temperature and take steps to maintain
warmth and prevent overheating
If thermoregulation mechanisms fail, the core body temperature can rise to 106 degrees
fahrenheit in 15 minutes.
Heat Cramps
Involuntary muscle pains usually in abdomen and or lower extremities as a result of profuse
sweating and loss of sodium
A person may attempt to quench thirst by drinking excessive amounts of water causing water
toxicity.
Cool the patient down and replace lost fluids.
Patient may need emergency care in case of hyponatremia
important for CCTP to avoid rapid correction of sodium level. Devastating neurologic injuries
can occur.
Heat Exhaustion
Water-depleted exhaustion occurs in elderly persons, younger workers and athletes who do not
replenish fluids properly
Even in rain, mud or anything involve “wet” can have hyperthermia and heat exhaustion
Heat Stroke
Least common but most deadly

Severe disturbance of body’s core regulation
10% of people die
Body temperature of more than 104 degrees fahrenheit
Critical thermal maximum is reached when core body temperature exceeds 109.4 degrees
fahrenheit
Classic
Occurs during heat waves
affects extremes of age, and bedridden
Also affects chronically ill, alcoholics, and people on certain medications
Exertional
Affects young, healthy people who over-exert themselves in a hot environment
S/S
AMS
Confusion
Tachycardia
tachypnea
dry, red skin
normal or hypotensive

FLIGHT PHYSIOLOGY
Gas laws to know:

• Boyle’s law
• Easy way to remember “Boyle’s Balloon”
• The pressure of gas is inversely proportional to the volume of a gas at a constant
temperature
• The higher the pressure the more volume that is present and vice versa
• Very important to remember with splints involving air and trauma due to ICP
increase
• Dalton’s law
• Easy way to remember (book) “Dalton’s Gang” (me) “Dalton’s Dumb Ass”
• The total pressure of a gas mixture is the sum of the partial pressures of all the gases
in the mixture (think of the composition of the air we breathe)
• The uptake of inner gasses into tissue will affect swelling in soft tissue with altitude
• Charles’ law
• Easy way to remember “Charles Centigrade”
• At a constant pressure, the volume of gas is directly proportional to the absolute
temperature of the gas
• E.g. When you charge an oxygen tank, the tank gets hot.
• Very little effect on the human body, more relative to equipment
• Gay-Lussac’s law
• Easy way to remember “Lussac was gay and had a relationship between temperature
and pressure”
• Directly proportional relationship between temperature and pressure
• E.g. an oxygen cylinder left outside overnight will have a lower pressure reading in
the morning due to temperature drop
• Why you have to add air in you tires during the winter.
• Graham’s law
• Easy way to remember “Graham’s = Grey Matter”
• This is the 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
• E.g. gas bubbles coming out of exposed grey matter when at altitude
• Henry’s law
• Easy way to remember “Henry’s Heineken”
• This law involves the solubility of gas in liquid
• The quantity of gas dissolved in 1cm^3 (1ml) 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”; which is the most
common form of decompression sickness.
• Type 1 is nitrogen related with painful joints, mottled skin (cutis marmorata)
often in the appearance of sunburn, and will be pruritic, feeling like “ants are
crawling on their skin”.
• Type II is neurologic signs and symptoms will be present with hypovolemic
shock and ground transport is preferred for all types of dive injuries/DCS.
Three to focus on: Henry’s law due to DCS, Boyle’s law due to splints/tubes, and Dalton’s law
due to swelling at altitude.
Arterial Gas Embolism (AGE)

This is related to Boyle’s law also in a sense that it is another diving related injury associated
with breath holding and ascent. The air pushes through the alveoli, entering the skin in the
neck/chest possibly causing a pneumothorax.
Air is also pushed into the blood vessels causing what we know as an emboli causing ischemia.
Be aware for stroke-like symptoms such as AMS, syncope, or dizziness and potentially a cough
or epistaxis.
This requires immediate hyperbaric chamber tx and if flight is requested, attempt to fly
pressurized in fixed wing transport, or <1000 ft mean sea level (MSL)
Pulmonary Over-pressurization (POP)

Also related to Boyle’s law and commonly associated with inexperienced divers.
This condition is also an ascent complication with the diver holding their breath causing lung
over expansion and rupture of the alveoli.
Further leads to pneumothorax or mediastinal emphysema.
Atmosphere (ATM) calculations

Every 33 feet below water is equivalent to 1 ATM
Sea level is considered 1 ATM.
E.g. a diver who is diving at 66 feet underwater is also under 3 ATM.
Divers Alert Network (DAN)

Is a 24 hour hotline for any type of diving related injuries/questions.
www.diversalertnetwork.org (919)-648-9111
Atmosphere Zones
Physiologic zones (sea level to 10,000 ft. MSL)
Night vision is decreased beginning at 5,000 ft. MSL
Physiologically Deficient Zone (10,000 to 50,000 ft. MSL)

Oxygen or pressurization required to survive at these altitudes
Time of useful consciousness (TUC) is cut in half during sudden decompression
Windows fogging with cooler temperatures are a sign of compression loss
Normally 90 seconds TUC at 30,000 ft.
Rapid decompression, TUC cut in half to 45 seconds.
Space Equivalent Zone (>50,000 ft. MSL)

No healthcare provided in this zone
Hypoxemia-Hypoxia
High-altitude
• Higher you go up in altitude, decrease in O2 volume (Boyle’s law)
• Total barometric pressure (TBP) 760 mmHg at sea level
• (760 mmHg - 47 mmHg) x .21 = 150 mmHg PaO2 at SL
• 47 mmHg is a constant to account for moisture
• Calculating torr .21 x torr at level going to. (i.e. 162 x .21 = 34 torr)
• With decent lungs you should be able to have a PaO2 5 times your FiO2.
• Decrease in TBP (760 mmHg)
• Place a patient on 100% O2; PaO2 increase
• Normal (Aa [A: Alveolus; a: artery gradient) difference in alveolus vs. capillary (something’s
that interferes with Aa gradient are for example CHF, decrease in surfactant, etc.)
Diffusion
• Pulmonary cystic fibrosis (example)
• Saturation problem during exertion due to blood flowing faster
• Increase in Aa gradient
• (Age/4) + 4 (simplified Aa gradient)
• High Aa gradient is indicative of diffusion problem in the capillaries
• Responds to 100 % oxygen (supplemental)
• Anything that increases a barrier in the interstitium of the alveolus (A) and the capillary
membrane
Hypoventilation
• Narcotics for example
• Normal Aa gradient
• Increase in PCO2
• Respiratory acidosis
• Responds to increase in O2 (supplemental)
Shunting
• ASD’s, VSD’s, PDA’s, ARDS
• 50% (just an example; can be more or less) of blood goes to the lungs; the other 50% goes to
shunts where it cannot become oxygenated.
• DO2 is directly proportional to the SaO2
• Want to achieve a 95% SaO2 in order to have between 80-100 PaO2
• Shifts to the left means oxygen will “linger” (“Left Lingers”)
• Tissue hypoxia
• Fetal Hemoglobin
• Shifts to the right means oxygen will “readily releases” (“Right Releases”)
• Not better/worse than left
• Attempt to stay on the curve
• Generically you can get shifts by changes in pH, CO2, temperature, 23DPG
• Does not readily respond to 100% O2 (supplemental)
VQ mismatch
• The most common cause of hypoxemia (i.e. pneumonia, PE [S1Q3T3 configuration; positive
D dimer], COPD)
• V: Ventilation
• Q: Perfusion
• More perfusion done in the lower lobes
• High VQ ratio in the upper lobes due to the lower perfusion
• High O2
• Low VQ ratio in the lower lobes due to the higher perfusion
• Low O2
• Unlike shunt, VQ mismatch does respond to 100% O2
Shifts to Oxygen-Hemoglobin Dissociation Curve; refer to MEDCRAM (link) video.

FP-C REVIEW
FLIGHT PHYSIOLOGY/SAFETY
• Weather and when to abort, regardless of patient condition: personal safety is priority
• If diminished visibility (CAMTS 10E…) turn down flight
• Crash situation in blizzard—lone survivor, 1 hour daylight, set up shelter
• Upon crash grab your survival kit
• If pilot announces an air emergency (think as a team—answer refers to you) turn off oxygen,
sit patient upright, manual trigger ELT if g-force <4
• Henry’s Law (Henry’s Heineken) “amount of gas dissolved in a solution is directly
proportional to the pressure of the gas over the solution
• Air embolism requires immediate re(de)compression chamber (Text Book 729/B-2-B 425)
• Discuss HEMS (human error or weather; pg. 49) Human error is the number 1 cause of
accidents (68%), Weather #2 cause (30%), but number one contributing factor decreased
visibility.
• Ascent—barodontalgia—tooth pain after dental work, air trapped in tooth
• Descent—Barotitis Media—head cold, unable to equalize pressure
• Barobariotrauma—high flow O2 via NRB for 15 minutes prior liftoff
• Sterile cockpit—scenario with reporter and tower (note appropriate and innappropriate): crew
member broke appropriately
• Which type of hypoxia responds best to O2—hypoxic hypoxia
• Communication tower and crew then activate plan 15 30 45 (CAMS 9; research 10)
• Where are patients more susceptible to physiologic changes in altitude? Humidity and
temperature (lower altitudes less stressful and high altitudes more stressful)
• Patient with history of seizure will be affected by—Flicker Vertigo
• Ileus—Boyle’s Law, will expand and may rupture—increase
• 1/4” space for Nome Flight Suits
• How the changes in partial pressure O2 at altitud effects a patient—need to increase O2
• Oxygen adjustment calculation Initial FiO2 x Initial Barometric Presssure / Barometric
pressure at altitude
• Explosive decompression—Time of Useful Consciousness (TUC) 1-5 mins, but cut in half
for rapid decompression. PICK THE SHORTEST TIME.
• When more susceptible to—temperature and humidity
• In response to HAZMAT—where to land aircraft—uphill, upwind, ask direction
• What increases survivability—preplanning and education with community
• Rule of 3’—3 min without O2, 3 hours with shelter, 3 days without water, 3 weeks without
food
• It is more stressful on a patient to go from low altitude to high altitude
• For patient family to fly, must be manifested and PC must approve.
Review:
Pharmacology
Alpha, beta, dopaminergic etc. responses
Electrolyte imbalance (K+, Ca++, Mg++)
Pericarditis
BMP/ABG/CBC
OB complications
Subdural, epidural, subarachnoid hematomas
Look up:
Anti-platelet aggregator vs. Fibrinolytic (links)
Hepatic Encephalopathy
Systolic vs. Diastolic heart failure.
Tonsilar herniation
Cingulet herniation
Central herniation
Uncul herniation
Neseritide
Leather lung
Bronchoscopy Surfactant (dose)
Bivalve cast
Junctional tourniquets
Digitalis Toxicity: pathway of J-Tach

Junctional rhythms can be a sign of digitalis toxicity and can be normal rate,
accelerated/tachycardic by having a direct effect/adrenergic influence or bradycardic because of
enhanced vagal tone, dysfunctional pacemakers found in organic heart disease or hyperkalemia.
Wernicke-Korsakoff Syndrome (link)

Summary: Thiamine (vitamin B-1) deficiency leading to a neurologic deficit triad conformed of
acute mental confusion, ataxia, and ophthalmoplegia. Furthermore, with related memory loss
brings the clinical condition commonly referred as Wernicke-Korsakoff Syndrome. Commonly
associated with chronic alcoholism but can be associated without the use of alcohol in conditions
such as prolonged starvation, hyperemesis gravidarum, HIV/AIDS, and infants without proper
intake of thiamine in their formula.
Hypoplasticity of heart
Hypoplastic left heart syndrome (HLHS) is a congenital complex & rare heart defect in which
the left side of the heart is critically underdeveloped. The condition causes the right side of the
heart to pump to systemic circulation also. Medications and surgical procedures are required to
prevent the ductus arteriosus from closing (required to allow oxygenated blood to flow to
systemic circulation).
BACK TO BASICS
CRITICAL CARE TRANSPORT CERTIFICATION REVIEW
ORCHID LEE LOPEZ RN, CFRN, NREMT-P, FP-C
MODULE 1
1. ST-elevation in leads II, III, AVF with reciprocal change in lateral leads I, V6. Inferior MI
8. RCA provides majority of circulation for the inferior portion of the heart.
9. V1-V6 are unipolar (“precordial”) leads.
10. The J point (“Junction point”) is where the S wave changes it’s direction and location used to
determine ST-elevation
11. Abnormal R wave progression in right precordial leads indicative of posterior MI.
12. ST-elevation is a sign of myocardial injury. Depression is ischemia and pathological Q
waves are signs of infarct (“age undetermined”)
13. Hyperkalemia presents on an ECG finding as peaked T waves.
14. Precordial leads V3 & V4 present with ST-elevation indicative to a anterior wall MI with
reciprocal change in inferior leads.
15. Patients with a history of Wolff-Parkinson White (WPW) possess and extrinsic pathway
which “bypasses” the AV node causing periods of R-SVT with the key identifier of a delta
wave.
16. With the presence of R-R intervals that are equal, P-P intervals that are equal (some buried in
T waves and QRS complexes; you can pick out the abnormalities) with a widened QRS
complex is indicative of a 3rd Degree AVB a.k.a. Complete AV Block.
17. ST-depression can be indicative of digitalis toxicity, myocardial ischemia, and infarct (“age
undetermined”); however, ST-elevation is indicative of acute myocardial injury.
18. Pathological Q waves present with ST-elevation is an ominous sign of possible acute
myocardial injury.
19. Pacer spikes are present prior to a wide QRS complex indicative of a ventricular paced
rhythm.
20. ST-elevation is present in II, III, AVF with reciprocal change in V6 & I indicative of
possible inferior MI.
21. With the irregularity being somewhat regular (able to pick out irregularities and find pattern
present) this rhythm (assuming it continues) is known as Torsades de Pointes which is a form
of polymorphic ventricular tachycardia.
22. ST-elevation in leads II, III, AVF is indicative of inferior wall infarct with right side
involvement. Nitroglycerin is contraindicated in inferior and right sided infarct due to the
fact that they are preload dependent.
23. ST-elevation in precordial leads V1-4 is indicative of an anteroseptal injury with T-wave
inversion present in lateral leads
24. The order of the valves of the heart is tricuspid, pulmonary, mitral, aortic (“toilet paper my
ass”)
25. Peaked T-waves in precordial leads V1-6 indicative of hyperkalemia.
26. The rhythm presented is irregularly-irregular with no discernible P-waves, and ST-elevation
indicative of atrial fibrillation with ST-elevation.
27. Flattened T-waves in the presence of peaked P-waves and U-waves seen is indicative of
hypokalemia
28. QUESTION. No discernible P-waves with irregularly-irregular appearing R-R intervals with
(utilizing “turn-signal” method) a left bundle-branch block
29. In a inferior wall MI, the RCA is occluded
30. ST-elevation in all precordial leads V1-6 to include leads I & AVL, with reciprocal changes
in inferior leads II, III & AVF indicative of anteroseptal-lateral wall injury
31. PRI remains constant with extra P-waves and regular R-R intervals indicative of 2nd degree
Type II AVB.
32. ST-depression with abnormal R-wave progression is indicative of a posterior wall MI;
confirm with 18-Lead.
33. ST-elevation in inferior leads II, III, AVF, and lateral leads V5, V6, with reciprocal change
in leads I, AVF, is indicative of inferior-lateral wall MI.
34. In the rhythm presented, there is failure to capture of the pacer.
35. ST-elevation is present in lateral leads I and AVL, with reciprocal change in inferior leads II,
III, AVF, which are signs of lateral MI.
36. Leads I, AVL, V5, and V6 are lateral leads and ST-elevation to these leads are indicative of
lateral wall injury.
37. TCA overdose is seen on the ECG with prolonged QTI/wide QRS >.12
38.
MODULE 4
1. metabolic and respiratory acidosis
2. Increase I:E ratio
3. 4th and 5th ICS anterior axillary
4. Respiratory acidosis
5. Respiratory alkalosis
6. Hyperventilation (increase RR)
7. Anteroseptal MI
8.
RESOURCES
Hyperkalemia: https://www.youtube.com/watch?v=tyl4Ob522Bw
Hypernatremia: https://www.youtube.com/watch?v=xHA_GTWSDQk
Hyponatremia:
https://www.youtube.com/watch?v=0a3gt6UQgeM&list=PLO4IRjU1gxO38DKbndu1wCQ_4R
PPqrLgA
ABG Practice: https://abg.ninja
Chest X-ray: https://www.youtube.com/watch?v=8snjqtrnV1I
CVP/A line: https://www.youtube.com/watch?v=8xpKr1t7YQE
Swan Ganz Physiology: https://www.youtube.com/watch?v=7putxZN7ij4
Maquet Intra-Aortic Balloon Pump Counterpulsation Theory:
https://getinge.training/static/d/16.05.16/scorm/player/index.htm?uc=855942&randomNumber=6
ec8f6c2-5991-11e6-b82f-1a9c5f63554a
RH Catheterization-Pressures: https://www.youtube.com/watch?v=_ieon7HyYMI
Wernicke-Korsakoff Syndrome link: http://emedicine.medscape.com/article/794583-overview
Shock link: https://www.youtube.com/watch?v=CbM4UihE1TQ
Hypoplasticity:
http://www.mayoclinic.org/diseases-conditions/hypoplastic-left-heart-syndrome/home/ovc-2016
4178
Oxygen-Hemoglobin Dissociation Curve: https://www.youtube.com/watch?v=HYbvwMSzqdY
The Unfixed Brain https://www.youtube.com/watch?v=jHxyP-nUhUY
The Unfixed Spinal Cord https://www.youtube.com/watch?v=RiGgNarlvK4
Hypoxemia:
https://www.youtube.com/watch?v=hKACkc5aUTE&list=PLQ_IRFkDInv9INje6o21PxV1pIpH
V_QrT
Mechanical Ventilator:
https://www.youtube.com/watch?v=gk_Qf-JAL84&list=PLQ_IRFkDInv9YPT5fNaZ8sbZJFSi6
8UoF

Critical Cardiac Notes

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CRITICAL CARE 2016 Page 1 of 71

CRITICAL CARE NOTES

EMPHASIS: Critical Cardiac, Medical, Flight Physiology (Safety & Survival)

P wave < 2.5 mm tall < .11 s/110 ms wide

atrial chamber enlargements would reflect in the p wave.

Biphasic p wave in V1 is normal.

Normal only means 60-100, w/ upright rounded p waves.

Sustained rhythm is >30s

Atrial: Depolarization & Repolarization same direction

Idioventricular: very regular

Von-Williams classification of antiarrythmics

1st Degree: prolonged PRI, only tx for rate/hemodynamics

2/3 degree rules:

1. constant 2nd Type II

CPP can also mean Coronary Perfusion Pressure.

1234’s of Heart​ (insert)

• Electrical Coops that generate electricity

Chest AP (Anterior Posterior): <50% of mediastinal space. Anchored by parietal pericardium

Tamponade and tension cause distension a.k.a. mechanical/disruptive shock.

I: Inferior LV RCA PL dependent

Hypo/hyperkalemia are common w/ different presentation on a ECG

Basic Metabolic Panel

Sodium: Chief extracellular cation; 135-145 milliequivalents/L

Calculate Anion Gap:

Arterial Blood Gases

Complete Blood Count

Hypernatremia​ (link) (hypertonic)

Most common Rare Loss of free H2O

Renal: Mannitol (osmotic diuretic mineralcorticoid excess DI/nephrogenic DI

Isotonic Hyponatremia Hypertonic Hyponatremia Hypotonic Hyponatremia

“lab error” a.k.a. Typically glucose; mannitol Most common

almost non-existent w/ modern decrease in Na+ due to oncotic

[(Glu-100)/60] + Na+ = Na+

as pH goes down, hydrogen ion’s go up

Buffer system: seconds

Diabetes Insipidus (DI) “dry” dehydration

ABG PRACTICE​ (link)

pH 7.48 7.35-7.45 up

pCO2 42 35-45 ~

HCO3- 29 22-26 up

Interpretation UC MET ALK

Component Value Normal Label

pH 7.30 7.35-7.45 down

pCO2 42 35-45 down

HCO3- 29 22-26 down

Interpretation UC MET ACID

Component Value Normal Label

pH 7.49 7.35-7.45 up

pCO2 30 35-45 down

HCO3- 30 22-26 up

Interpretation UC MIXED ALK

Component Value Normal Label

pH 7.39 7.35-7.45 down~

pCO2 55 35-45 up

HCO3- 23 22-26 ~

Interpretation C RESP ACID

Component Value Normal Label

pH 7.49 7.35-7.45 up~

pCO2 48 35-45 up

HCO3- 35 22-26 up

Interpretation PC MET ALK

Chest X-ray​ (link, watch all 3)

1234’s of Heart (insert)

Hypernatremia (link) (hypertonic)

ABG PRACTICE (link)

Chest X-ray (link, watch all 3)

Pressure Monitoring (link) (CVP/Art line)

Allen Test (link)

Shock & Sepsis tx’s (link)