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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 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 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 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 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 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 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 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