1/30/2016
AEMCA
REVIEW
Alexander McLean
Anatomy of the Heart
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Endocardium, Myocardium, Epicardium, and Percardium
Each muscle cell is enclosed in a membrane called a sarcolemma. Within each
cell are mitochondria, the energy-producing parts of a cell, and hundreds of long,
tube-like structures called myofibrils. Myofibrils are made up of many
sarcomeres, the basic protein units responsible for contraction.
Atrial Kick Responsible for 30% of ventricle filling
Diameter of aorta is 2.5 cm
Acute Coronary Syndromes
Arteriosclerosis
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Chronic disease of arterial system characterized by abnormal thickening and
hardening of vessel walls
Atherosclerosis
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A form of arteriosclerosis
Thickening and hardening of vessel walls are caused by a buildup of fatty-like
deposits
Buildup results in ↓ blood flow (ischemia)
Angina
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Angina is a symptom of heart disease. Angina happens when there is not enough
blood flow to the heart muscle. This is often a result of narrowed blood vessels,
usually caused by hardening of the arteries (atherosclerosis).
Stable angina
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Stable angina has a typical pattern. You can likely predict when it will happen. It
happens when your heart is working harder and needs more oxygen than can be
delivered through the narrowed arteries. Examples include when you are:
Excercising, exposed to cold temperatures, sudden immense emotions, eating a
large mean, cocaine or amphetamine use
The pain goes away when you rest or take nitroglycerin. It may continue without
much change for years.
Unstable angina
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Unstable angina is unexpected. It is a change in your usual pattern of stable
angina. It happens when blood flow to the heart is suddenly slowed by narrowed
vessels or small blood clots that form in the coronary arteries. Unstable angina is
a warning sign that a heart attack may soon occur. It is an emergency. It may
happen at rest or with light activity. It does not go away with rest or nitroglycerin.
Myocardial Ischemia
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Imbalance between the metabolic needs of the myocardium (demand) and the
flow of oxygenated blood to it (supply)
Chronotropic Effect: Rate
Inotropic Effect: Contractility
Dromotropic Effect: Conduction
Baroreceptors
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Specialized nerve tissues that are found in internal carotid arteries/aortic arch
Detect changes in blood pressure
Chemoreceptors
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Chemoreceptors in the internal carotid arteries and aortic arch detect changes in
the concentration of hydrogen ions (pH), oxygen, and carbon dioxide in the
blood. The response to these changes by the autonomic nervous system can be
sympathetic or parasympathetic.
Parasympathetic (inhibitory) nerve fibers supply the SA node, atrial muscle, and the AV
junction of the heart by means of the vagus nerves.
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Norepinephrine acts on Alpha 1
Epinephrine acts on Beta 2
Cardiac Output = Stroke Volume × Heart Rate

Normal CO = 5-7 L/min
Blood Pressure = cardiac output (CO) × peripheral vascular resistance
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Stroke Volume is dependent on: Preload, Afterload, and Myocardial contractility
Frank-Starling Law of the Heart
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Up to a limit, the more a myocardial muscle is stretched, the greater the force of
contraction (and stroke volume). Influenced by preload and afterload
Preload
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Preload is the force exerted by the walls of the ventricles at the end of diastole
Afterload
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The pressure or resistance against which the ventricles must pump to eject blood
Automaticity
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Ability of pacemaker cells to initiate an electrical impulse without being stimulated
from another source
Excitability (irritability)
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Ability of cardiac muscle cells to respond to an outside stimulus
Conductivity
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Ability of a cardiac cell to receive an electrical stimulus and conduct that impulse
to an adjacent cardiac cell
Contractility
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Ability of cardiac cells to shorten, causing cardiac muscle contraction in response
to an electrical stimulus
Refractoriness
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The period of recovery that cells need after being discharged before they are
able to respond to a stimulus
Absolute refractory period
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Cells cannot be stimulated to conduct an electrical impulse, no matter how strong
the stimulus
Onset of QRS complex to approximate peak of T wave
Relative refractory period
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Intrinsic Rates
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Cardiac cells can be stimulated to depolarize if the stimulus is strong
enough
Corresponds with downslope of T wave
SA node: 60–100 bpm
AV node & Bundle of His: 40–60 bpm
Bundle Branches and Purkinje Network: 20–40 bpm
Major Intracellular cation - K+ (Potassium) Major Extracellular cation - Na+ (Sodium)
Major Intracellular anion - PO4+ (Phosphate) Major Extracellular anion - Cl- (Chloride)
Cardiac Action Potential
Phase 0—Depolarization
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Sodium moves rapidly into cell
Potassium leaves cell
Calcium moves slowly into cell
Responsible for QRS Complex
Phase 1—Early Repolarization
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Na+ channels partially close
Brief outward movement of K+
Results in fewer positive electrical charges within the cell
Phase 2—Plateau Phase
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Slow inward movement of Ca++
Slow outward movement of K+
Responsible for ST segment on ECG
Phase 3—Final Rapid Repolarization
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K+ flows quickly out of the cell
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Entry of Ca++ and Na+ stops
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Cell becomes progressively more electrically negative and more sensitive to
external stimuli
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Corresponds with T wave on the ECG
Phase 4—Return to Resting State
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Heart is "polarized" during this phase
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Ready for discharge
AV nodal reentrant tachycardia (AVNRT)
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is the most common cause of supraventricular tachycardia (SVT). Patients
with AVNRT have at least two pathways of tissue in their AV node that allows for
an abnormal electrical circuit to perpetuate within their AV node. However, there
are many individuals who have dual pathways of AV nodal tissue, but never have
the electrical circuit perpetuate to develop sustained tachycardia. It is this
spinning circuit that goes "round-and-round" enclosed in the AV node that allows
for rapid stimulation of the ventricles through the normal His bundle, bundle
branches, and ultimately Purkinje fibers to the ventricular muscle.
Cardiogenic Pulmonary Edema
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The function of the right side of the heart is to receive blood from the body and
pump it to the lungs where carbon dioxide is removed, and oxygen is deposited.
This freshly oxygenated blood then returns to the left side of the heart which
pumps it to the tissues in the body, and the cycle starts again. When the heart
muscle is not able to pump effectively there is a back-up of blood returning from
the lungs to the heart; this backup causes an increase in pressure within the
blood vessels of the lung, resulting in excess fluid leaking from the blood vessels
into lung tissue.
Non-cardiogenic Pulmonary Edema
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Non-cardiogenic pulmonary edema is less common and occurs because of
damage to the lung tissue and subsequent inflammation of lung tissue. This can
cause the tissue that lines the structures of the lung to swell and leak fluid into
the alveoli and the surrounding lung tissue. Again, this increases the distance
necessary for oxygen to travel to reach the bloodstream.
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The following are some examples of causes of non-cardiogenic pulmonary
edema: Kidney failure, Inhaled toxins, High altitude pulmonary edema (HAPE),
Illicit drug use, Adult respiratory distress syndrome (ARDS), Pneumonia:
Pacemakers
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Fixed-Rate (Asynchronous) Pacemakers: Continuously discharge at a
preset rate (usually 70-80/min)
Demand (Synchronous, Noncompetitive) Pacemakers: Discharge only
when patient’s heart rate drops below pacemaker’s preset (base) rate
Electrocardiogram (ECG)
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Width of each small box = 0.04 second.
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Width of each large box (5 small boxes) = 0.20 second
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5 large boxes (each consisting of 5 small boxes) = 1 second.
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15 large boxes = 3 seconds.
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30 large boxes = 6 seconds.
The point at which the QRS complex and the ST segment meet = “J point” or junction
PRI
Normally measures 0.12–0.20 sec
Heart Rates
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A “tachycardia” exists if rate is more than 100 bpm
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A “bradycardia” exists if rate is less than 60 bpm
Limb Leads
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Right arm electrode is always negative
Left leg electrode is always positive
Lead 2 Interpretation
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Rate, Rhythm, P-Waves, PR Interval, QRS, Underlying Rhythm
Types of Rhythms
Sinus Rhythms
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Sinus
Sinus Arrhythmia
Sinus Bradycardia
Sinus Tachycardia
Sinus Pause
Sinus Arrest
Atrial Rhythms
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Premature Atrial Contractions
Atrial Tachycardia (150-250 Beats, P wave almost hidden in T wave)
Atrial Flutter (200 to 350 Beats)
Atrial Fibrillation (Irregularly Irregular)
Wandering Pacemaker (P-waves constantly changing, PR always less than 0.20,
irregular rhythm, usually 60-100 BPM)
Junctional Rhythms
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P-Waves are inverted and less than 0.12
Wolff-Parkinson-White Syndrome (PR less than 0.10, QRS looks slurred)
Premature Junctional Contraction (Irregular Rhythm, P-Wave inverted & less
than 0.12)
Junctional Escape Rhythm (Regular at a rate of 40 to 60 BPM, P-Wave Inverted,
PRI less than 0.12)
Acclerated Junctional Rhythm (Rate 60 to 100 BPM)
Junctional Tachycardia (3 or more PJC’s occur in a row, Rate 100 to 200 BPM)
Ventricular Arrhythmias
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Premature Ventricular Contraction (QRS is wide and bizarre, Rhythm is Irregular
 2 PVC’s in a row are called a couplet or pair
 Multiform PVC’s
 Bigeminy PVC’s that occur every other beat
 Trigeminy PVC’s that occur every third beat
Idioventricular Rhythms (Rate less than 40 BPM, QRS wide and bizarre)
Accelerated Idioventricular Rhythms (Rate 40 to 100 BPM, QRS wide and
bizarre)
Ventricular Tachycardia (Rate 100 to 250 BPM, QRS wide and bizarre)
Torsades de Pointes
Ventricular Fibrillation
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Asystole
Atrioventricular Blocks
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1st degree (PR Longer than 0.20)
2nd degree type 1 (PRI gets progressively longer until a QRS is dropped)
2nd degree type 2 (Atrial rhythm is regular, ventricular rhythm is irregular, PRI is
constant, QRS dropped)
3rd degree (P-wave occurs without QRS Complex
Bundle Branch Blocks
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Prolonged (very high or very low) QRS High is Left Low is Right
Pace Makers
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Atrial Pacing: Produces pacemaker spike followed by a P wave
Ventricular Pacing: Produces pacemaker spike followed by a wide QRS,
resembling a ventricular ectopic beat
Electrical Capture: Usually indicated by wide QRS and broad T wave
Failure to Capture: Recognized on the ECG by visible pacemaker spikes not
followed by P waves
Failure to Sense: Recognized on the ECG by pacemaker spikes that follow too
closely behind the patient’s QRS complexes
Number
of Large
Boxes
Heart
Rate
Number
of Large
Boxes
Heart
Rate
1
300
6
50
2
150
7
43
3
100
8
38
4
75
9
33
5
60
10
30
Shock
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Inadequete circulation to the cells of the body
Aerobic Metabolism (Kreps Cycle) uses oxygen for energy production
Anaerobic Metabolism does not use oxygen and causes lactic acid build up
Stages: Compensatory  Decompensatory > Irreversible
Hypovolaemic
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Meaning not enough blood volume. Causes include bleeding, which could be
internal (such as a ruptured artery or organ) or external (such as a deep wound)
or dehydration. Chronic vomiting, diarrhoea, dehydration or severe burns can
also reduce blood volume and cause a dangerous drop in blood pressure
Cardiogenic
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Caused when the heart cannot effectively pump blood around the body. Various
conditions including heart attack, heart disease (such as cardiomyopathy) or
valve disorders may prevent a person’s heart from functioning properly
Neurogenic
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Injury to a person’s spine may damage the nerves that control the diameter
(width) of blood vessels. The blood vessels below the spinal injury relax and
expand (dilate) and cause a drop in blood pressure
Septic
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An infection makes the blood vessels dilate, which drops blood pressure. For
example, an E. coli infection may trigger septic shock
Anaphylactic
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A severe allergic reaction causes blood vessels to dilate, which results in low
blood pressure
Obstructive
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Blood flow is stopped. Obstructive shock can be caused by cardiac (pericardial)
tamponade, which is an abnormal build-up of fluid in the pericardium (the sac
around the heart) that compresses the heart and stops it from beating properly,
or pulmonary embolism (a blood clot in the pulmonary artery, blocking the flow of
blood to the lungs)
Endocrine
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In a critically ill person, a severe hormonal disorder such as hypothyroidism may
stop the heart from functioning properly and lead to a life-threatening drop in
blood pressure.
Oxygen delivery
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Respiration: Mechanism to ensure a constant oxygen supply
and the removal of excess carbon dioxide
External respiration (pulmonary respiration)
Internal respiration (cellular respiration)
Normal anatomical dead space in an adult is 150 cc’s
Normal Tidal Volume = 400 – 500 cc’s
Gas exchange surface area is 70 M^2
Minute volume = Respitory Rate x Tidal Colume
Normal PAO2: 80 -100 mmHg
Normal PCO2: 35 - 45 mmHg
98% of O2 is in hemoglobin 2% is dissolved in plasma
CO2 diffuses 20 times more readily than O2 (20:1 Ratio)
CO2 Is a potent vasodilator
Trachea 10 cm long in an adult
Lyrnx contains the vocal cords
Bohr Effect: O2 affinity in Hemoglobin is stronger in alkali states and weaker in
acidic ones
Intrapulmonary Pressure = 760 mmHg
Atmosphereic air contains 21% Oxygen (body uses 5%) and 79% Nitrogen, 1%
other
Oxygen Toxicity (40% O2 >24 Hours)
Fresh Water Drowning
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Hypotonic Solution forces fluid into circulating volume
Washes out surfactant
Hemolysis
Salt Water Drowning
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Hypertonic Solution forces fluid into the alveoli
Pulmonary Edema
Nasal Cannula
Litres Per Minute
Oxygen Percentage
1
24%
2
28%
3
32%
4
36%
5
40%
6
44%
Non-rebreather
Liters Per Minute
Oxygen Percentage
10 - 15
90-100%
Simple Face Mask
Liters Per Minute Oxygen Percentage
6-8
40-60%
Bag Valve Mask
Liters Per Minute Oxygen Percentage
15
100%
Epinephrine Pharmacology
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Classification: Sympathomimetic Onset: 5-15 Min Duration: 1-4 Hours
Pharmacodynamics: Alpha1 effects: vasoconstriction
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Beta 1effects: Increased H.R., Increased force of cardiac contraction
Beta 2 effects (moderate): bronchodilation
Inhibits histamine release
+ve chronotropic, +ve dromotropic and +ve inotropic effects
Characteristics
Onset
Temperature
Cause
Signs and Symptoms
Epiglottis
Sudden
High Fever
Bacterial
Horse voice, difficulty
swallowing, large
amounts of drooling,
sore throat
Croup
Slow
Low grade fever
Viral
Barking cough, strider,
difficulty breathing
CPAP – Continuous Positive Pressure Ventilation
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A treatment modality for patients in acute respiratory distress from COPD
exacerbation or acute pulmonary edema.
CPAP reduces the preload, thereby reducing the workload on the heart, while
also allowing for a reduction in the pulmonary capillary pressure.
By placing the patient’s airways under a constant level of pressure throughout
the respiratory cycle, the alveoli are not only kept open, BUT any fluid
(pulmonary edema) will also be "pushed" back into the vascular space, allowing
for the exchange of gases
Right and Left sided Ischemic CVA’s
Left Hemisphere
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Right visual deficits
Tight sided weakness
Expressive Aphasia
Receptive Aphasia
Intellectual Impairment
Slow and Cautious Behaviour
Right Hemisphere
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Left visual deficits
Left sided weakness
Spatial-perceptual deficits
Neglect of the affected side
Distractible
Impulsive behaviour
Loss of flow of speech
Hemorrhagic CVA
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Severe Headache
Nausea/Vomiting
Altered Level of Awareness
Unconsciousness
Seizure
Coma
Cushing's triad
 Hypertension
 Bradycardia
 Abnormal respirations
Amyotropic Lateral Sclerosis (Lou Gehrigs Disease)
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Degeneration of nerve cells in brain and spinal cord
18 month survivle
Occurs mostly between 40 to 70 year olds
Does not affect senses
Meningitis
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Viral and bacterial (bacterial is the most common cause)
Causes hydrocephalus
Bradykinin: stimulates pain at nerve endings and causes release of histamine
Hypothalamus: Center for activities of smooth muscle and endocrine glands
C3, C4, C5 contain the phrenic nerve which controls the diaphragm
Endocrine
Endocrine glands release into blood stream
Exocrine glands release substances outside of the blood stream
Adrenal medulla releases Epinephrine and Norepinephrine (both are classified as catecholamines)
Thymus is responsible for the production of T lymphocytes
Diabetes
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The Pancreas secretes the hormones insulin (beta) and a small protein,
glucagon (alpha) into the bloodstream. The release of insulin into the blood
lowers the level of blood glucose (sugar) by allowing glucose to enter the body
cells, where it is metabolized. If blood glucose levels get too low, the pancreas
secretes glucagon to stimulate the release of glucose from the liver.
There are 500,000 to 1 million pancreatic islets dispersed among the ducts and
the Acini of the Pancreas.
Each islet is composed of:
 beta cells that secrete insulin at a daily average of 0.6 units/kg of body
weight
 alpha cells that secrete glucagon
 delta cells that secrete the hormone somatostatin, inhibiting the secretion
of the growth hormone.
Type 1 Diabetes or IDDM
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characterized by inadequate production of biologically effective insulin by the
pancreas. It appears to be an autoimmune phenomenon resulting from a genetic
abnormality that causes the body to destroy it’s own insulin-producing cells.
The symptoms of IDDM usually present suddenly and include polyuria,
polydipsia, dizziness; blurred vision; and rapid, unexplained weight loss.
Type 2 Diabetes or NIDDM
Characterized by a decrease production of insulin by the beta cells of the pancreas
and diminished tissue sensitivity to insulin. Resulting in variable insulin levels that
are insufficient to maintain glucose homeostasis.The disease occurs most often in
adult over 40 years of age and in those who are overweight.
Glucagon
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To increase blood glucose levels by stimulating the liver to release glucose
stores from glycogen and other glucose storage sites (glycogenolysis).
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To stimulate gluconeogenesis (glucose formation) through the breakdown of fats
and fatty acids, thereby maintaining a normal blood glucose level.
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Pharmacodynamics: Onset: 8-10 Min Duration 19-32 Min
accelerates the breakdown of glycogen (glycogenolysis) to glucose in the liver
glucagon: secreted by the alpha cells of the pancreas. It elevates blood glucose
levels by increasing the breakdown of glycogen to glucose and inhibiting
glycogen synthesis
 Parenteral administration of glucagon produces relaxation of the smooth muscle
of the stomach, duodenum, small bowel and colon
 exerts a positive inotropic action on the heart by increasing intracellular cAMP
concentration via the secondary messenger system (treatment of beta blocker or
Ca++ channel blocker OD).
 only effective in treating hypoglycemia if liver glycogen is available
Special Notes:
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In patients with pheochromocytoma, glucagon may cause the tumor to release
catecholamines which may lead to marked hypertension, tachycardia and
intracerebral hemorrhage.
Obstetrics
Gravida: number of Pregnancies
Para: Number of deliveries
Due date: LNMP – 3 months + 7 days
Pre-eclampsia BP > 140/90 (severe pre-eclampsia Diastolic >110)
Clamp umbilical cord 15 cm away from baby and then 5-7 cm away from 1st clamp
Asses neonate every 30 seconds for a period of 6 seconds
Stages of Labour
Stage 1: Dilation Stage
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From 1st contraction to when cervix is fully dilated
Contractions are 5-15 min apart lasting 10-30 sec*
Stage lasts 8-12 hours in primaparas
Lasts 6-8 hours in multiparas
Amniotic sac ruptures toward the end of the stage
Stage 2: Expulsion Stage
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Lasts from full dilation to delivery
Contractions are 2-3 mins apart lasting 1 minute
Urge to bear down present
Lasts 1-2 hours in primapara
Lasts 30 mins in multipara
Crowning*
Stage 3: Placental Stage
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Delivery of the placenta
Uterine contractions compress blood vessels causing the placenta to detach
Occurs in 5-60 mins
Each trimester lasts 13 weeks
1st trimester: egg is fertilized and travels to uterus forming fetus and placenta
Most spontaneous abortions happen between week 12 & 14
Ectopic pregnancies are diagnosed between 4 – 10 weeks
2nd trimester
2 most common causes of bleeding are placental abruption and placenta previa
Placenta accerta: Placenta grows into uterine wall and surrounding tissues
4 M’s multiple births, meconium, maternal drug use, maturity of fetus
Pediatrics
Neonate: birth to 28 days
BSA vs total weight is greater than in adults
O2 consumption is 2x than that of an adult
Children land head first
Newborns to 4 months are obligate nose breathers
Fontenals: posterior forms from birth – 3 months, anterior fuses 9 – 18 months
Abdominal breathers until age 8
Assessment triangle (appearance, work of breathing, circulation)
Head bobbing may indicate respiratory failure
Blood pressure is hard to obtain for those under 3 years old
Respiratory arrest is the primary cause of cardiac arrest
Bruises
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Less than 24 hours old: reddish, with blue or purple shadding
1-3 days old: blue to blue/brown
5-7 days old: greenish
10-14 days old: yellowish
Renin-Angiotensin System
 Decreased blood flow to Kidneys-> Hypoprofusion sensed by Juxtaglomerular
Cells, causes kidneys secrete renin->Renin acts on Angiotensinogen (protein
from liver)->Angiotensine 1->at lungs converted to Angiotensine 2 by ACE->
Angiotensine 2 powerful vasoconstrictor and stimulates Adrenal Cortex to
secrete Aldosterone
 Aldosterone stimulates kidneys to retain sodium with that water overall increasing fluid
volume
Fluids & Electrolytes
Normal Circulating Blood Volumes
Adult: 70 mL/Kg
Ped’s 80 mL/Kg
Infant 90 mL/Kg
PH: negative log of hydrogen ion concentration
Normal PH: 7.35 to 7.45
Death occurs at a PH <6.8 and >7.9
More acidity means more hydrogen ions
PH Regulation done by:
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Buffering system
Respitory System
Renal System
Normal hemoglobin: 14 – 16 grams in 100 mL of blood
Aldosterone is released from the adrenal glands which causes kidneys to retain sodium
and therefore retain water
Water distribution:57% Adult Female - 60% Adult male - 70% 1 year old - 80% Newborn
(33% extracellular, 66% Intracellular)
Body water volume: approximately 42 Liters
Fluid Balance: Daily Intake = Daily Loss
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Intake (Drinking & Eating) Loss (Urine, Skin, Lungs, GI)
Basic functional unit of the kidney is the nephrone (> 2 million)
Kidneys Process 180 L per day and produce 1 – 2 L of urine
Parkland Burn Formula: Fluid Requirements = TBSA burned(%) x Wt (kg) x 4mL
Give 1/2 of total requirements in 1st 8 hours, then give 2nd half over next 16 hours.
Nervous System
Cerebrum: Largest part of brain, interprets sensory impulses, controls voluntary muscles,
memory, thought and reasoning
Cerebellum: responsible for posture and fine muscle control
Meningies: Dura, Arachnoid, Pia
Pons: part of respiratory center
Medulla oblongata: cardiac center, vasomotor, respiratory center, vomiting, coughing,
hiccupping
Spinal cord is approximately 45 cm long and ends at the conus medullaris (L1)
31 spinal nerves
Afferent are sensory nerves and impulses travel towards the brain
Efferent are motor impulses and travel away from the brain
Brain has 4 ventricles
Reticular activating system: responsible for wakefulness/consciousness
Dendrite: receives information
Axon: sends information away from the cell body
Autonomic Neurotransmitters
The brain receives 16% of the total cardiac output and uses 20% of the bodies O2 consumption
 Acetylcholine & epinephrine
 Neurons that release Acetylcholine are cholinergic
 Neurons that release epinephrine are called adrenergic
 Parasympathetic pre and post ganglionic neurons are cholinergic
Sympathetic post ganglionic neurons are adrenergic
Bell’s Palsy effects cranial nerve #7
Parkinson’s causes dopamine producing cells to die
Alchol withdrawl happens 6 – 24 hours after reducing or ceasing intake
Anaphylaxis
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Over production of IgE
Mast cells and basophiles release histamine (increases vascular permeability),
serotonin, prostaglandin, leukotrines, kinins, prostglycans
Routes of Expose
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Inhalation
Ingestion
Injection
Absorption
Miscellaneous
Geriatrics
4 M’s: multiple disease process, multiple prescription drugs, multiple
complications/adverse effects, multiple problems
Common medical causes for combativeness:
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Hypoglycemia
Hypoxia
Head injury
Hypo/hyper thermia
Drug/alcohol ingestion
Equipment
Bag Valve Mask Spec’s
Adult Bag: 1600 mL + 2700 mL reservoir
Pediatric Bag: 450 mL + 1200 mL
Weight Limit of Scoop, Stair Chair, #9 Stretcher, KED: 350 lb (159 Kg)
*(The Stair Chair that Peel Uses goes up to 500lb)
Pedimate
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15 – 45 degree angle on stretcher
10 lb – 40 lb
35A Max weight: 500 lb
Sagar
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10% of body weight up to 15 lb of pressure per femur (30 lb for bilateral femur
fractures)
4 year old – Adult
Abdomen
Viceral Pain
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Stimulated by distension, inflammation, ischemia
Dull, Achy, Cramping Pain
Somatic/Parietal Pain
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Chemical/bacterial irritation of nerves
Constant, Localized, Sharp Pain
Refered Pain
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Pain located else where
Kehr's sign:
The occurrence of acute pain in the tip of the shoulder due to the presence of blood or
other irritants in the peritoneal cavity when a person is lying down and the legs are
elevated. Kehr's sign in the left shoulder is considered a classical symptom of
a ruptured spleen. May result from diaphragmatic or peridiaphragmatic lesions, renal
calculi, splenic injury or ruptured ectopic pregnancy.
Burns
Epidermis
Dermis
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Nerve endings, blood vessles, hair follicles, sebaceous glands, sweat glands
Subcutaneous tissue

Adipose tissue, Muscles
1st Degree (superficial)
Epidermis
2nd degree (partial thicknes)
Epidermis and dermis
Red, Hot Dry
Red, hot, blisters
3rd (full thickness)
Epidermis, dermis,
subcutaneous tissue
White, brown, black
Parkland Burn Formula: Fluid Requirements = TBSA burned(%) x Wt (kg) x 4mL
Give 1/2 of total requirements in 1st 8 hours, then give 2nd half over next 16 hours.
** Taken from CEPCP Paramedic Pocket Reference Guide 2011 Version. 1.1