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Transcript
Medical I Refresher Lecture
Aaron J. Katz, AEMT-P, CIC
www.es26medic.net
Pharmacology

The study of drugs


Sources, characteristics and effects
Always refer to drugs as medications
EMTs can deliver some
medications and can assist the
patient in delivering some other
medications
Meds EMTs can deliver





Oxygen
Oral Glucose
Activated Charcoal
Epinephrine injectors (“EpiPen”)
Aspirin
Meds that EMTs can assist


Prescribed inhalers
Nitroglycerin
Drug Names


Chemical
Generic


E.g. Ibuprofin, Nitroglycerin
Trade

E.g. Advil, Nitrostat
Important terms

Action


Indications


Signs/Symptoms/Conditions for which a particular
medication should be used
Contraindications


The therapeutic effect that a drug is expected to have on
the body
Signs/Symptoms/Conditions or patient for which a
particular medication should NOT be used
Side effects

Any actions of a medication other than the desired ones
Drug Administration

Before administering any drug, know
the “four rights”




Right
Right
Right
Right
patient
medication
dose
“route”
Medication Routes









Intravenous (“IV”)
Oral (“PO”)
Sublingual (“SL”)
Intramuscular (“IM”)
Intraosseous (“IO”)
Subcutaneous (“SC”)
Transcutaneous
Inhalation
Rectal (“PR”)
References




PDR
USP
Merck Manual
The Pill Book


Not an “official” guide, but a very good
source
ePocrates
Survey of commonly used drugs
Anti-hypertensives
Accupril
Cozaar
Lotensin
Monopril
Lopressor
(Metoprolol)
Vasotec
Toprol XL
Prinivil
Zestril
Isoptin
(Verapamil)
Norvasc
Tenormin
(Atenalol)
Calan
(verapamil)
Diuretics





Lasix (Furosemide)
Bumex
Diazide
HCTZ
Hydrodiuril
Combination HTN, diuretics



Zestoretic
Prinzide
Vasaretic
Potassium supplements



K-Dur
K-Tab
Slo-K
Cholesterol Lowering






Lipitor
Mevacor
Lopid
Pravachol
Zocor
Crestor
Antianginals
Procardia XL
(Nifedipine)
Nitrostat (nitroglycerin)
Cardizem (Diltiazam)
Isordil (Isosorbide
Dinitrate)
Inderal (propranalol)
Imdur (Isosorbide
Mononitrate)
Capoten
Corgard
Oral Anti-hyperglycemics
Diabeta (Glyburide)
Diabenase
Glucotrol (Glipizide)
Glucophage
Glynase (Glyburide)
Micronase (Glyburide)
Avandia
Injected Anti-hyperglycemics





Humulin
Humalog
Lente
Lantus
And many others
Anti-epilepsy





Dilantin
Phenobarbitol
Depakote
Tegratol
Nerontin
Some cardiac meds

Lanoxin


Coumadin


Digoxin
Warfarin
Many of the anti-hypertensives and
anti-anginals are used for cardiac
conditions
Assorted respiratory inhalers


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Atrovent
Combivent/Duoneb
Alupent
Proventil, Ventolin (Albuterol)
Intal
Serevant
Beclovent
Advair
Azmacort
Aerobid
Respiratory Emergencies
Review of airway anatomy






Nose/Mouth
Oropharynx/Nasopharynx
Epiglottis
Trachea
Cricoid cartilage
Larynx/vocal cords
Review of airway anatomy-2





Bronchi
Bronchioles
Lungs
Alveoli
Diaphragm
Physiology


Inspiration
Expiration
Signs of normal breathing





Normal rate & depth
Regular pattern of inhaling/exhaling
“Good” breath sounds bilaterally
Regular rise and fall of the chest –
bilaterally
“Some” movement of the abdomen
Signs of abnormal breathing






RR<8 or RR>24
Excessive respiratory muscle usage
Pale or cyanotic skin
Cool, diaphoretic (“clammy”) skin
Shallow or irregular respiration
Pursed lips
Signs of abnormal breathing



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
Pursed lips
Nasal flaring
Tripod positioning
Tachycardia
Altered mental status (“AMS”)


Agitated  sleepy
Look for the yawn!
Some terms

Dyspnea



Apnea


Difficulty breathing
Shortness of breath (SOB)
No breathing
Hypoxia

Not enough oxygen
What causes us to breath

Normal individuals


COPD patients


Excessive CO2 levels in arterial blood
Low levels of O2 in arterial blood
COPD



Chronic Obstructive Pulmonary Disease
Emphysema
Chronic bronchitis
Causes of dyspnea

Obstructed lower airways






Due to fluid, infection, collapsed alveoli
Damaged alveoli
Damaged cilia in lower airways
Spasms, mucus plugs, floppy airways
Obstructed blood flow to lungs
Pleural space filled with air or fluid
Common respiratory disorders causing dyspnea



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
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Airway infections
Acute Pulmonary Edema (“APE”)
COPD
Spontaneous pneumothorax
Asthma, allergies, anaphylaxis
Pleural effusion
Prolonged seizures
FBAO
Pulmonary embolism
Hyperventilation syndrome
Severe pain
Infections






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Colds/flu
Bronchitis
Bronchiolitis
Pneumonia
Croup
Epiglottitis
 History will often “tell the story”
Acute pulmonary edema

Not really a respiratory problem





A cardiac problem
Congestive Heart Failure (“CHF”)
TBD with cardiac emergencies
Severe dyspnea
Pink frothy, blood-tinged sputum
COPD

Almost always caused by




Long-term smoking
Long term inhalation of “bad things”
Chronic bronchitis
Emphysema
Chronic bronchitis




Damaged respiratory pathway cilia
Excessive mucus production
Can’t “cough out” effectively
Very frequent bronchitis/pneumonia
Emphysema


Loss of alveolar elasticity and shape
Air pockets

Can not expel CO2
COPD



Most have elements of both diseases
Prolonged expiratory phase
Most common lung sound



Expiratory wheeze
Minor respiratory problemd exacerbates
COPD
Patient is usually old
COPD

Altered mental state over time


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Due to CO2 retention
Barrel shaped chest
Well developed respiratory muscles
Long term COPD may cause heart
failure
Spontaneous pneumothorax

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Collapsed portion of lung due to
weakness in lung tissue
No apparent cause
Sudden SOB
Pleuritic chest pain
Common in asthmatic/COPD
Common in tall thin men
Asthma/allergies

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
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Reversible spasm of bronchioles
Excessive mucus production
Normal inspiration
Difficult expiration
Expiratory wheezing – common
A quiet chest is an ominous sign


Be prepared for respiratory arrest
Be prepared to use BVM
Status astmaticus




An asthma attack that cannot be
“broken” after repeated doses of
bronchdilators
Needs aggressive airway
management
Needs rapid transport
Needs BVM
Pulmonary embolism



Embolus: something in the circulatory system that
travels from one place to a distant place – and
lodges there
Effective inspiration/expiration – BUT
Vessels leading to alveoli are blocked by:

Blood clots


Air bubbles


Often following open neck injuries
Bone marrow


Often following long bed rest
Often following a long-bone fracture
Amniotic fluid

Often following an “explosive delivery”
Pulmonary embolism

Very often a dangerous complication of
a “DVT”



Common in pt with varicose veins
“perfusion/ventilation mismatch”
Small emboli may cause no S/S
Pulmonary embolism

Common S/S



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
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
Dyspnea
Pleuritic chest pain
Hemoptysis
Cyanosis
Tachycardia
Tachypnia
A large embolus may cause sudden
cardiac arrest
Hyperventilation





Overbreathing – reduces CO2 level
excessively
May be emotional in nature
May be a sign of MANY serious
medical conditions
DO NOT WITHOLD Oxygen!
DO NOT HAVE THEM BREATH INTO
A BAG!
Hyperventilation

Patient may describe:




Numbness/tingling in hands/feet
Spasms in hands and feet
Called “carpal-pedal” syndrome
If all medical causes have been
ruled out IN THE HOSPITAL, the
condition is called
“Hyperventilation Syndrome”
Treating the dyspneic patient



Calm approach!
Call for ALS EARLY!
Position of comfort


Almost always sitting upright
NEVER lie them down


Especially an APE patient
High concentration oxygen



Even for COPD patients
NRB – if rate & depth are adequate
BVM – if not
Treating the dyspneic patient


Monitor V/S – especially resp rate
Look for signs of sleepiness



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
Yawning
Slowing RR – especially in COPD pt.
 pt is becoming too tired to breathe
Respiratory failure
Breathe for them  BVM
Treating the dyspneic patient



The “counting test”
SAMPLE HISTORY
OPQRST – medical assessment Q’s


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


Onset
Provocation/Palliation
Quality (of any pain)
Radiation
Severity
Time
Interventions

Also, help them with prescribed inhalers
Cardiac Emergencies
Mechanical structure




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
Atria
Ventricles
One way valves
Pulmonary arteries
Pulmonary veins
Aorta
Coronary arteries


Provide O2 and nutrients to the heart muscle
Myocardium – the heart muscle
Electrical structure

SA Node






The “dominant pacemaker”
Internodal pathways
AV Node
Bundle of HIS
Bundle branches
Purkinje Fibers/Network
Cardiovascular abnormalities

Atherosclerosis


Arteriosclerosis


Hardening of the arteries
Ischemia


Cholesterol/calcium deposit buildup
Temporary interruption of O2 to tissues
Infarction

Death of tissue after “a period of uncorrected
ischemia”
Risk factors


Controllable
Uncontrollable
Angina pectoris




Chest pain
Supply of O2 does not meet hearts
requirement
Partial blockage
Spasm? (“Prinzmetal’s Angina”)
Angina -- triggers


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Exercise
Emotion
Fear
Cold
Large meal
elimination
Angina -- presentation






Crushing/squeezing pain in midchest,
under sternum (“substernal”)
Radiation to jaw, arms, midback
Nausea
Dyspnea
Diaphoresis
Rarely lasts more than 15 minutes
Angina-promptly relieved by



Rest
Oxygen
Nitroglycerine


Dilates blood vessels
Increases blood flow to heart muscle
Acute myocardial infarction






“AMI”, “MI”, “Heart attack”
May have same S/S as angina, but
Longer in duration
Often not relieved with rest, O2, nitro
May be onset at rest with no
“triggers”
 Treat angina as AMI
Complications of AMI

Sudden death


Arrhythmias



40% never “make it” to the hospital
Most frequent cause of death in early
hours following AMI
Congestive Heart Failure (“CHF”)
Cardiogenic shock

At least 40% of the heart is infarcted
Sad facts



Unfortunately, the left ventricle is the
portion of the heart most often
infarcted
The left ventricle is the highest powered
portion of the heart
Pumping power of the heart may be
severely reduced
Classical S/S of AMI







All, some or none of the following:
Sudden onset of weakness, nausea, sweating
Crushing chest pain – does not change with
breathing
Pain radiating to jaw, arms, neck
Sudden arrhythmias causing syncopy
Acute Pulmonary Edema
Cardiac Arrest
Classical S/S of AMI -- 2

Vital signs -- commonly:







Pulse: increased, irregular
BP: Usually normal; dropping in cardiogenic shock
RR: Usually normal, elevated in APE
Feeling of doom
Looks frightened
Denial
 Diabetics and the elderly 
Congestive Heart Failure



Pathophysiology
Right sided CHF
Left sided CHF
Right sided CHF

Dependent edema





Enlarged liver
JVD
Due to back-pressure from damaged right ventricle
Chronic condition


Pedal edema, sacral edema
People often live with it for years
Controlled by:


Medication (Lasix, Digitalis)
Salt free diet
Left sided CHF







“APE”
Fluid in the lungs due to back pressure from
damaged left ventricle
Patient feels like they are drowning
Acute condition
Frequent recurrences
Often results in death
Controlled by:



Medication (Lasix, Bumex, Digitalis)
Salt free diet
Often a result of long-standing HTN
APE Calls


Most of them are due to either:
Poor diet control


They eat too much sodium filled foods
Poor compliance with medications

Lasix is a diuretic

Annoying side effects
Cardiogenic Shock


Heart muscle is so damaged that it can
no longer pump enough to meet bodily
demands
Very high mortality rates


Even with the best treatment
S/S of shock immediately after or within
hours or days of AMI
Treating the patient with “CP”



Calm reassuring approach
Cardiac arrest – CPR/AED
High-con Oxygen



Aspirin 162mg PO
Call for ALS EARLY!


NRB or BVM PRN
For any cardiac/respiratory problem
Position of comfort


Usually sitting upright (dyspniac patient)
NEVER let an APE pt lie down!
Treating the patient with “CP”

Focused history

OPQRST – and in addition





Previous MI history
Previous “heart problems”
Family history / risk factors
Monitor vital signs
Other interventions

Assist pt with prescribed nitro – SL

If systolic BP > 120