Medical I Refresher Lecture

Preview:

DESCRIPTION

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. - PowerPoint PPT Presentation

Citation preview

Medical I Refresher Lecture

Aaron J. Katz, AEMT-P, CICwww.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

The therapeutic effect that a drug is expected to have on the body

Indications Signs/Symptoms/Conditions for which a particular

medication should be used Contraindications

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 patient Right medication Right dose Right “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 Isoptin (Verapamil)

Lotensin Monopril Norvasc

Lopressor (Metoprolol)

Toprol XL Tenormin (Atenalol)

Vasotec Zestril Calan (verapamil)

Prinivil

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)

AvandiaAvandia

Injected Anti-hyperglycemics

Humulin Humalog Lente Lantus And many others

Anti-epilepsy

Dilantin Phenobarbitol Depakote Tegratol Nerontin

Some cardiac meds

Lanoxin Digoxin

Coumadin Warfarin

Many of the anti-hypertensives and anti-anginals are used for cardiac conditions

Assorted respiratory inhalers 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

Pursed lips Nasal flaring Tripod positioning Tachycardia Altered mental status (“AMS”)

Agitated sleepy Look for the yawn!

Some terms

Dyspnea Difficulty breathing Shortness of breath (SOB)

Apnea No breathing

Hypoxia Not enough oxygen

What causes us to breath Normal individuals

Excessive CO2 levels in arterial blood COPD patients

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

Airway infections Acute Pulmonary Edema (“APE”) COPD Spontaneous pneumothorax Asthma, allergies, anaphylaxis Pleural effusion Prolonged seizures FBAO Pulmonary embolism Hyperventilation syndrome Severe pain

Infections

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 Due to CO2 retention

Barrel shaped chest Well developed respiratory

muscles Long term COPD may cause heart

failure

Spontaneous pneumothorax

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 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 Often following long bed rest

Air bubbles Often following open neck injuries

Bone marrow 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

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

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

Onset Provocation/Palliation Quality (of any pain) Radiation Severity Time

Interventions Also, help them with prescribed inhalers

Cardiac Emergencies

Mechanical structure 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

Cholesterol/calcium deposit buildup Arteriosclerosis

Hardening of the arteries Ischemia

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

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

40% never “make it” to the hospital Arrhythmias

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

Pedal edema, sacral edema Enlarged liver JVD Due to back-pressure from damaged right

ventricle Chronic condition

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

NRB or BVM PRN Aspirin 162mg PO Call for ALS EARLY!

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

Recommended