EMS Drug Handbook 2027

Every prehospital medication decision begins long before the drug is drawn up or the vial is cracked open. It begins with knowing what the thing in your hand actually is. A paramedic on a cardiac arrest reaches for epinephrine, an advanced emergency medical technician (AEMT) at a diabetic emergency reaches for dextrose, an emergency medical technician (EMT) at an overdose reaches for naloxone, and in each case the clinician is relying on a body of knowledge that connects a name on a label to a mechanism, an indication, a dose, a risk, and a legal framework. This book is built to teach that connected body of knowledge, and this first chapter lays the groundwork for everything that follows.

1. 1.1 Generic, Brand, and Chemical Names
2. 1.2 How Drugs Are Classified
3. 1.3 Drug Schedules and Regulatory Oversight
4. 1.4 The EMS Formulary and Scope of Practice
5. 1.5 Package Inserts, Protocols, and Medical Direction
6. 1.6 Reading a Drug Reference Critically
7. 1.7 Building a Personal Study System for Drug Knowledge

Chapter 1 gave you the vocabulary of drugs: their names, their classes, the rules that govern them, and the sources you can trust. This chapter begins the science. Pharmacokinetics is the study of what the body does to a drug over time, and it is conventionally divided into four processes: absorption, distribution, metabolism, and excretion. A drug must enter the body, travel to where it acts, be chemically changed, and eventually leave. Every one of those steps takes time, and every one of them can be altered by the patient in front of you. Pharmacokinetics is therefore the reason that the same dose can produce different results in two patients, and the reason that the same drug behaves differently by two routes.

1. 2.1 Absorption and Bioavailability
2. 2.2 Distribution and Protein Binding
3. 2.3 Metabolism and the First-Pass Effect
4. 2.4 Excretion and Renal and Hepatic Clearance
5. 2.5 Half-Life, Onset, Peak, and Duration
6. 2.6 How Shock, Hypothermia, and Poor Perfusion Alter Kinetics
7. 2.7 Clinical Correlation: Why Route and Timing Matter in the Field

Chapter 2 followed a drug through the body: how it is absorbed, distributed, metabolized, and eliminated. That field of study, pharmacokinetics, answers the question of how much drug is where, and when. This chapter turns to the companion question, which is what the drug actually does once it arrives. Pharmacodynamics is the study of the biochemical and physiologic effects of drugs and their mechanisms of action. It explains why epinephrine (adrenaline) raises a blood pressure, why naloxone (Narcan) reverses an opioid overdose without doing anything for a benzodiazepine overdose, and why the same dose of the same drug can be life-saving in one patient and dangerous in another.

1. 3.1 Receptors, Agonists, and Antagonists
2. 3.2 Dose-Response Relationships and Potency
3. 3.3 Therapeutic Index and Margin of Safety
4. 3.4 Tolerance, Tachyphylaxis, and Dependence
5. 3.5 Adverse Effects, Side Effects, and Toxicity
6. 3.6 Drug Interactions: Additive, Synergistic, and Antagonistic
7. 3.7 Special Considerations: Pregnancy, Age, and Comorbidity

Chapter 3 explained what drugs do once they reach their receptors. This chapter addresses the equally practical question of how they get there. A drug that works beautifully in theory is useless if you cannot deliver it, and a drug delivered by the wrong route may work too slowly, too unpredictably, or not at all. The route of administration determines how quickly the drug reaches the bloodstream, how much of the dose arrives intact, how easily the dose can be titrated, and how much risk the delivery itself carries. Those considerations, which are pharmacokinetic as much as practical, shape nearly every decision you make about a medication.

1. 4.1 Enteral Routes: Oral and Sublingual
2. 4.2 Intravenous Access and Administration
3. 4.3 Intraosseous Access and Administration
4. 4.4 Intramuscular and Subcutaneous Injection
5. 4.5 Intranasal and Inhaled Delivery
6. 4.6 Endotracheal, Rectal, and Topical Routes
7. 4.7 Infusion Pumps, Drip Sets, and Equipment Troubleshooting

Every chapter in this book that follows will teach you a drug, a class of drugs, or a way of thinking about a drug. None of that knowledge protects a patient unless the right medication, at the right dose, reaches the right person by the right route at the right time, and unless what happened is recorded so that the next clinician can build on it. This chapter closes Part One by turning the foundations of the preceding chapters into habits: the verification steps that precede every administration, the arithmetic that converts an order into a volume or a drip rate, and the documentation that turns a moment at the bedside into a lasting clinical and legal record.

1. 5.1 The Rights of Medication Administration
2. 5.2 Metric Conversions and Weight-Based Dosing
3. 5.3 Worked Examples: Concentration, Volume, and Dose
4. 5.4 Worked Examples: Drip Rates and Infusions
5. 5.5 Preventing and Recognizing Medication Errors
6. 5.6 Documentation and Reporting Standards
7. 5.7 Managing an Adverse Event or Error After It Happens

Part One of this book gave you the general principles of pharmacology and the habits of safe medication use. Part Two applies them to the drugs that act on the body's automatic control system, the autonomic nervous system (ANS). This is the network that adjusts heart rate, blood pressure, airway caliber, pupil size, gut activity, and sweating without any conscious effort. When a patient is in shock, wheezing, bradycardic, or poisoned, the problem is very often a disturbance of this system, and when you treat that patient with epinephrine, atropine, albuterol, or a vasopressor, you are borrowing the system's own language to correct it.

1. 6.1 Organization of the Autonomic Nervous System
2. 6.2 Sympathetic Division and Adrenergic Receptors
3. 6.3 Parasympathetic Division and Cholinergic Receptors
4. 6.4 Alpha, Beta-1, Beta-2, and Dopaminergic Effects
5. 6.5 Neurotransmitter Synthesis, Release, and Breakdown
6. 6.6 Predicting Drug Effects From Receptor Activity
7. 6.7 Clinical Correlation: Reading Patient Signs as Receptor Activity

Part One of this handbook built the foundation: how drugs move through the body, how they bind receptors, how routes and doses are chosen, and how you protect patients from medication error. Part Two now turns to the autonomic nervous system, the branch of the nervous system that controls heart rate, blood vessel tone, airway caliber, and the other involuntary functions that decide whether a critically ill patient lives through the next hour. Chapter 6 explained the receptors, the alpha, beta, dopaminergic, and muscarinic sites that autonomic drugs act upon. This chapter puts that vocabulary to work with the catecholamines, a family of naturally occurring and synthetic compounds that mimic the sympathetic nervous system's response to stress.

1. 7.1 Epinephrine: Mechanism and Indications
2. 7.2 Epinephrine: Concentrations, Routes, and Cautions
3. 7.3 Norepinephrine and Distributive Shock
4. 7.4 Dopamine and Dose-Dependent Receptor Effects
5. 7.5 Dobutamine and Inotropic Support
6. 7.6 Extravasation, Monitoring, and Titration
7. 7.7 Choosing a Vasoactive Agent for the Patient in Front of You

Chapter 7 showed how catecholamines drive the sympathetic nervous system, speeding the heart and tightening the vessels. This chapter covers drugs that do the opposite, either by blocking the parasympathetic brake on the heart, as atropine does, or by blocking sympathetic stimulation and calcium entry into cardiac and vascular cells, as beta blockers and calcium channel blockers do. Together these three families touch an enormous proportion of the patients you will treat. Millions of Americans take a beta blocker or a calcium channel blocker every day for hypertension, angina, heart failure, and arrhythmias, and the odds that your next older cardiac patient is taking one are high.

1. 8.1 Atropine and Symptomatic Bradycardia
2. 8.2 Atropine in Poisoning and Other Uses
3. 8.3 Beta Blocker Pharmacology and Prehospital Use
4. 8.4 Beta Blocker Overdose Recognition
5. 8.5 Calcium Channel Blockers: Diltiazem and Verapamil
6. 8.6 Calcium Channel Blocker Overdose Recognition
7. 8.7 Managing Patients Already Taking These Drugs

Part Three of this handbook turns to the cardiac emergency medications, and every one of them acts on a heart whose behavior is governed by electricity. Before you can understand why adenosine stops a reentrant tachycardia, why lidocaine works in ischemic ventricular tissue but not in healthy atria, or why a drug given to calm one rhythm can provoke a far worse one, you need a working model of how a cardiac cell generates and conducts an electrical signal. This chapter builds that model from the ground up, starting with the action potential of a single ventricular muscle cell and ending with the clinical question you face at the bedside: shock, drug, or both.

1. 9.1 The Cardiac Action Potential
2. 9.2 Ion Channels and Where Drugs Act
3. 9.3 The Vaughan Williams Classification
4. 9.4 Mechanisms of Arrhythmia
5. 9.5 Proarrhythmia and the QT Interval
6. 9.6 Choosing Between Cardioversion and Medication
7. 9.7 Clinical Correlation: Matching Rhythm, Stability, and Drug

Chapter 9 gave you the electrical logic of the heart: how an action potential is built, where drugs bind, how rhythms arise, and how to decide between a shock and a medication. This chapter applies that logic to the drugs themselves. Adenosine, amiodarone, lidocaine, and procainamide are the antiarrhythmics most commonly found on paramedic drug lists, and each has a distinct mechanism, a distinct niche, and a distinct set of hazards. Learning them as a set, and learning why one is preferred over another in a given rhythm, is what turns a list of drugs into a decision framework.

1. 10.1 Adenosine and Supraventricular Tachycardia
2. 10.2 Amiodarone: Mechanism, Uses, and Hazards
3. 10.3 Lidocaine and Ventricular Arrhythmias
4. 10.4 Procainamide and Other Alternatives
5. 10.5 Wide-Complex Tachycardia: A Drug Selection Framework
6. 10.6 Stable Versus Unstable Presentations
7. 10.7 Adverse Effects and Post-Conversion Monitoring

Acute coronary syndrome (ACS) is the family of emergencies that begins when blood flow through a coronary artery is suddenly and critically reduced. It includes unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). Few conditions in emergency medicine reward fast, organized prehospital care as consistently as this one, because the heart muscle that is starved of oxygen when you arrive is still alive and can often be saved if the right medications are given and the patient is delivered to the right destination. This chapter belongs to Part Three of the handbook, which concerns the drugs that act on the heart and circulation themselves.

1. 11.1 Pathophysiology of Acute Coronary Syndrome
2. 11.2 Aspirin and Antiplatelet Therapy
3. 11.3 Nitroglycerin: Mechanism, Contraindications, and Cautions
4. 11.4 Anticoagulants and Heparin
5. 11.5 Opioid and Non-Opioid Analgesia in Chest Pain
6. 11.6 Fibrinolytics and Reperfusion Strategy
7. 11.7 Right Ventricular Infarction and Medication Hazards

Few calls produce as much fear in a patient as acute pulmonary edema. A person who went to bed breathing normally wakes at night sitting bolt upright, gasping, drenched in sweat, coughing up pink froth, and convinced they are drowning. In a very real sense they are, because fluid that belongs inside the blood vessels has been forced into the air spaces of the lungs. This chapter addresses acute decompensated heart failure (ADHF), the pulmonary edema that so often accompanies it, the hypertensive emergencies that can provoke it, and the cardiogenic shock that represents its most dangerous form. All of these conditions share a common theme: the heart's ability to move blood forward has fallen out of balance with the pressures that push fluid backward.

1. 12.1 Pathophysiology of Acute Decompensated Heart Failure
2. 12.2 Nitroglycerin in Pulmonary Edema
3. 12.3 Furosemide and Diuretic Action
4. 12.4 Pharmacologic Adjuncts to Noninvasive Ventilation
5. 12.5 Hypertensive Emergency Versus Urgency
6. 12.6 Cardiogenic Shock and Medication Choices
7. 12.7 Monitoring Response and Recognizing Deterioration

Cardiac arrest is the one emergency in which every drug you carry is secondary to something that contains no pharmacology at all: high-quality chest compressions, early defibrillation for shockable rhythms, and effective ventilation or oxygenation. This chapter opens Part Three's work on resuscitation by placing medications in their proper, and often humbling, position. You will learn what epinephrine actually does inside a pulseless chest, why antiarrhythmic drugs are reserved for a narrow group of patients, how the reversible causes of arrest point you toward specific drug therapy, and what changes the instant a pulse returns. The goal is not to memorize an algorithm as a recipe but to understand why each step exists, so you can adapt when a real patient does not follow the textbook.

1. 13.1 The Role of Drugs in Resuscitation
2. 13.2 Epinephrine in Cardiac Arrest
3. 13.3 Antiarrhythmics in Shockable Rhythms
4. 13.4 Reversible Causes and Targeted Drug Therapy
5. 13.5 Vasopressors and Sedation After ROSC
6. 13.6 Temperature, Oxygenation, and Ventilation Targets
7. 13.7 Termination of Resuscitation and Medical Direction

Electrolytes are the quiet currency of the heart. Every heartbeat is a coordinated movement of sodium, potassium, and calcium ions across cell membranes, and a small shift in their concentrations can turn a stable rhythm into a lethal one. The drugs in this chapter, calcium, magnesium, and sodium bicarbonate, are among the oldest in the EMS drug box, yet they are also among the most misunderstood. They are not general-purpose cardiac drugs, and giving them without a reason can do harm. Used with a clear indication, however, they can reverse a dying rhythm within minutes, which makes them some of the most dramatic medications you will ever administer.

1. 14.1 Potassium Disorders and Their ECG Signs
2. 14.2 Calcium Chloride and Calcium Gluconate
3. 14.3 Magnesium Sulfate: Cardiac and Non-Cardiac Uses
4. 14.4 Sodium Bicarbonate and Acid-Base Principles
5. 14.5 Hyperkalemia Emergencies and Dialysis Patients
6. 14.6 Tricyclic and Sodium Channel Blocker Toxicity
7. 14.7 Compatibility and Administration Cautions

This chapter opens Part Four of the handbook, which turns to the respiratory, allergic, and metabolic emergencies that fill so much of an ambulance's workload. Few calls are as frightening to a patient, or as immediately rewarding to treat well, as the patient who cannot get air out of the chest. Asthma, chronic obstructive pulmonary disease (COPD), and the wheezing that accompanies reactive airway disease, anaphylaxis, and even heart failure all share a final common pathway: narrowed lower airways, trapped air, and a body working harder and harder to move gas through a pipe that has become too small. The medications in this chapter are the tools that reopen that pipe, and understanding how each one works lets you choose among them, combine them, and recognize the moment when they are no longer enough.

1. 15.1 Airway Physiology and Bronchospasm
2. 15.2 Albuterol and Beta-2 Agonists
3. 15.3 Ipratropium and Anticholinergic Bronchodilation
4. 15.4 Corticosteroids in Asthma and COPD
5. 15.5 Magnesium and Epinephrine in Severe Asthma
6. 15.6 Nebulizer Delivery, CPAP, and Combination Therapy
7. 15.7 Recognizing Treatment Failure and Impending Arrest

Anaphylaxis is the allergic emergency that can kill within minutes, and it is one of the few conditions in prehospital medicine where a single drug, given promptly by the correct route, changes the outcome more than everything else you do combined. A patient may go from a mild itch after a bee sting or a restaurant meal to airway swelling, wheezing, and shock in a quarter of an hour. Your job is to recognize the pattern early, to give epinephrine without hesitation, and to avoid the common trap of reaching first for the drugs that are comfortable and familiar but do not reverse the life-threatening features of the reaction.

1. 16.1 Pathophysiology of Hypersensitivity Reactions
2. 16.2 Epinephrine as First-Line Therapy
3. 16.3 Antihistamines: Diphenhydramine and Others
4. 16.4 Corticosteroids and Adjunctive Therapy
5. 16.5 Refractory Anaphylaxis and Vasopressor Support
6. 16.6 Angioedema and Non-Allergic Mechanisms
7. 16.7 Observation, Biphasic Reactions, and Transport Decisions

Few emergencies in the prehospital setting are as common, as reversible, and as easy to miss as a disturbance of blood sugar. A patient whose brain is starved of glucose can look intoxicated, postictal, psychotic, or stroke-stricken, and a patient whose glucose is dangerously high can look dehydrated, septic, or simply tired. In both cases the diagnosis is made in seconds by a fingerstick, and in the hypoglycemic patient the treatment can restore a person to full consciousness before you have finished documenting the call. That combination of high frequency and dramatic reversibility makes glucose management one of the most valuable skills in your scope, and one of the most unforgiving when it is neglected.

1. 17.1 Glucose Metabolism and Hormonal Control
2. 17.2 Hypoglycemia and Dextrose
3. 17.3 Glucagon and Alternative Rescue Options
4. 17.4 Hyperglycemia, DKA, and Fluid Resuscitation
5. 17.5 Oral Glucose and Non-IV Approaches
6. 17.6 Insulin Types and Patient-Administered Medications
7. 17.7 Special Cases: Alcohol, Starvation, and Sulfonylurea Overdose

Circulating volume is the foundation of perfusion. Every drug in this handbook that acts on the heart, the vessels, or the lungs assumes that there is enough blood in the system to carry it, and every patient in shock needs that volume restored or preserved in some form. Intravenous (IV) fluid is among the oldest and most frequently used prehospital treatments, and it has also been among the most debated. Over the past two decades, the understanding of how to resuscitate a bleeding or septic patient has changed substantially, moving away from large volumes of crystalloid toward earlier hemorrhage control, balanced products, and a more restrained use of fluid in specific conditions.

1. 18.1 Body Fluid Compartments and Osmosis
2. 18.2 Crystalloids: Normal Saline and Lactated Ringer's
3. 18.3 Colloids and Hypertonic Solutions
4. 18.4 Tranexamic Acid and Antifibrinolytic Therapy
5. 18.5 Prehospital Blood Products and Permissive Hypotension
6. 18.6 Fluid Choices in Sepsis, Burns, and Head Injury
7. 18.7 Complications of Fluid Therapy

Few emergencies look as dramatic to bystanders, or feel as helpless to new providers, as a seizure. A person who was talking a moment ago is rigid, then jerking, cyanotic, and unresponsive, while family members shout that you must do something. Most seizures stop on their own within a minute or two and need nothing from you except protection of the airway and the patient's body. But a seizure that does not stop is a true time-dependent neurologic emergency, and the drugs you carry are the only thing that can end it before the brain and the rest of the body pay a lasting price. This chapter, the first of Part Five on neurologic, analgesic, and sedative pharmacology, teaches you how those drugs work and how to choose among them.

1. 19.1 Pathophysiology of Seizure Activity
2. 19.2 Benzodiazepines: Midazolam, Lorazepam, and Diazepam
3. 19.3 Route Selection: IV, IM, and Intranasal
4. 19.4 Second-Line Agents and Levetiracetam
5. 19.5 Eclampsia, Hypoglycemia, and Toxic Seizures
6. 19.6 Pediatric Seizures and Febrile Convulsions
7. 19.7 Respiratory Depression and Post-Seizure Monitoring

Pain is the most common reason people call for help, and relieving it is one of the oldest obligations in medicine. For years, prehospital pain treatment lagged behind the emergency department, and patients with fractures, burns, kidney stones, and chest pain frequently arrived in agony after a long transport. That has changed. Current practice treats pain as a clinical priority that deserves systematic assessment, a plan, and reassessment, and the pharmacologic options available to EMS clinicians have broadened well beyond morphine. This chapter, the second in Part Five, teaches how pain is generated and carried to the brain, and how each drug class interrupts that process at a different point.

1. 20.1 Pain Physiology and Assessment
2. 20.2 Opioid Receptors and Fentanyl
3. 20.3 Morphine and Hydromorphone
4. 20.4 Ketamine for Analgesia
5. 20.5 Acetaminophen, NSAIDs, and Multimodal Analgesia
6. 20.6 Nitrous Oxide and Regional Techniques
7. 20.7 Opioid Adverse Effects, Reversal, and Stewardship

Sedation is one of the few areas of prehospital medicine where you deliberately take a patient who is awake, breathing on their own, and protecting their own airway, and move them toward a state in which those protections may weaken. You do it because the benefits are real: a dislocated shoulder reduced without agony, a cardioversion that the patient will not remember, a combative or terrified patient who can finally be examined, packaged, and transported safely. This chapter covers the drugs and the judgment that make those benefits achievable without turning a painful problem into an airway emergency.

1. 21.1 The Sedation Continuum
2. 21.2 Midazolam and Benzodiazepine Sedation
3. 21.3 Ketamine for Procedural Sedation
4. 21.4 Etomidate and Propofol
5. 21.5 Monitoring: Capnography, Oximetry, and Airway Readiness
6. 21.6 Sedating the Hemodynamically Unstable Patient
7. 21.7 Preparing for Complications

Rapid sequence intubation (RSI) is the most consequential medication-driven procedure in prehospital airway management. In a single, tightly choreographed sequence, you give a potent sedative-hypnotic and a neuromuscular blocking drug, together producing unconsciousness and complete paralysis within about a minute, so that an endotracheal tube can be passed through the vocal cords under the best possible conditions. Done well, RSI secures an airway that could not otherwise be controlled and protects a patient from aspiration, hypoxia, and the secondary brain injury that follows them. Done badly, it converts a patient who was still breathing into one who is not breathing at all, with an airway you may be unable to secure. The drugs are the easy part to memorize. The difficult part is knowing when to use them, in what order, and what to do if the plan fails.

1. 22.1 Indications and the Pharmacology of Intubation
2. 22.2 Pretreatment Agents
3. 22.3 Induction Agents Compared
4. 22.4 Depolarizing Paralytics: Succinylcholine
5. 22.5 Nondepolarizing Paralytics: Rocuronium and Vecuronium
6. 22.6 Post-Intubation Analgesia and Sedation
7. 22.7 Failed Airway and Rescue Considerations

Few calls test a prehospital clinician the way an acutely agitated patient does. The scene is loud, the patient may be frightened, intoxicated, injured, or psychotic, bystanders and law enforcement are watching, and the pressure to do something fast is intense. This chapter is about doing the right thing in the right order. Agitation is a symptom, not a diagnosis, and the same outward behavior can come from low blood sugar, a brain injury, methamphetamine toxicity, alcohol withdrawal, sepsis, or a primary psychiatric illness. Each cause demands a different response, and a sedative given before the cause is considered can hide a dying patient behind a quiet face.

1. 23.1 Recognizing Medical Causes of Agitation
2. 23.2 De-escalation Before Medication
3. 23.3 Ketamine in Severe Agitation
4. 23.4 Antipsychotics: Haloperidol, Droperidol, and Olanzapine
5. 23.5 Benzodiazepines in Agitation
6. 23.6 Excited Delirium Terminology and Safety Concerns
7. 23.7 Post-Sedation Monitoring and Restraint Safety

Nausea and vomiting are among the most common complaints you will treat, and they are also among the most misunderstood. A patient who is vomiting is not simply uncomfortable; vomiting can threaten the airway, drain fluid and electrolytes, signal a surgical abdomen or a myocardial infarction, and make every other treatment harder, from oral glucose to a trauma airway. The medications in this chapter are among the safest and most frequently given in EMS, yet the careless use of even a familiar antiemetic can mask a serious diagnosis, prolong the QT interval, or injure a vein.

1. 24.1 Physiology of Nausea and Vomiting
2. 24.2 Ondansetron and Serotonin Antagonists
3. 24.3 Promethazine, Metoclopramide, and Others
4. 24.4 Antacids, Proton Pump Inhibitors, and Upper GI Bleeding
5. 24.5 QT Prolongation and Drug Interaction Cautions
6. 24.6 Pediatric and Pregnancy Considerations
7. 24.7 Choosing an Antiemetic in the Field

Part Six turns from the drugs you give to patients on purpose to the drugs, chemicals, and poisons that patients take, breathe, or absorb by accident, by self-harm, or by misadventure. Poisoning and overdose are among the most common reasons the 911 system is activated in the United States, and they are also among the most diagnostically demanding. A patient with a depressed level of consciousness and a slow respiratory rate may have taken an opioid, a sedative, an alcohol, a combination of all three, or may be suffering from hypoglycemia or a stroke. Your assessment, your airway management, and in a small number of cases a carefully chosen antidote determine whether that patient reaches the emergency department alive and with a functioning brain.

1. 25.1 Principles of Toxicologic Management
2. 25.2 The Major Toxidromes
3. 25.3 Naloxone and Opioid Overdose
4. 25.4 Flumazenil and Benzodiazepine Reversal
5. 25.5 Activated Charcoal and Decontamination
6. 25.6 Acetaminophen, Salicylate, and Other Common Ingestions
7. 25.7 Stimulants, Synthetic Drugs, and Novel Agents

The previous chapter taught a framework for the patient who has swallowed, injected, or inhaled a drug of abuse or a common medication. This chapter addresses a different and in some ways more frightening group of exposures: the poisons that come from agriculture, industry, fire, war, and the natural world, and the prescription drugs whose overdose behaves like a poison because there is so little margin for error. Pesticide workers, house fire victims, patients exposed to nerve agents in a terrorist attack, hikers bitten by rattlesnakes, and patients who have swallowed a handful of their grandmother's heart pills all require recognition and treatment in the first minutes, usually before any laboratory can confirm the diagnosis.

1. 26.1 Organophosphate Poisoning: Atropine and Pralidoxime
2. 26.2 Cyanide Toxicity and Hydroxocobalamin
3. 26.3 Carbon Monoxide and Oxygen Therapy
4. 26.4 Nerve Agent Autoinjectors
5. 26.5 Envenomation and Antivenom Principles
6. 26.6 Tricyclic, Beta Blocker, and Calcium Channel Blocker Antidotes
7. 26.7 Poison Control and Medical Direction

Pregnancy and birth change the rules of prehospital pharmacology in a way no other patient population does. When you treat a pregnant woman, you are caring for two patients whose physiology is intertwined, and whose responses to a drug may be very different from one another. The mother's blood volume, cardiac output, kidney clearance, and breathing pattern have all shifted from the nonpregnant baseline, and the drugs you give may cross the placenta to reach a fetus that cannot metabolize them well. At the moment of delivery, a third challenge appears: a newborn who has just moved from a fluid-filled world to an air-filled one and who sometimes needs your help to make that transition. This chapter gathers the medications and reasoning that serve these patients.

1. 27.1 Physiologic Changes of Pregnancy That Affect Drug Use
2. 27.2 Magnesium Sulfate in Eclampsia
3. 27.3 Oxytocin and Postpartum Hemorrhage
4. 27.4 Medications to Avoid or Use Cautiously in Pregnancy
5. 27.5 Neonatal Resuscitation Medications
6. 27.6 Epinephrine and Fluids in the Newborn
7. 27.7 Placental Transfer and Fetal Effects

Children are not small adults, and nowhere is that statement more literally true than in pharmacology. A child's body composition, organ maturity, airway, metabolism, and tolerance for error all differ from an adult's, and they change continuously from the first day of life through adolescence. A drug that is safe at one dose in a ten-year-old can be dangerous in a ten-month-old, and a calculation that is trivial for an adult becomes a multistep problem when the weight is unknown, the child is frightened, and the parents are watching your hands. Pediatric medication errors are among the most feared events in EMS, and the best protection against them is a combination of knowledge, tools, and systems.

1. 28.1 How Children Differ From Adults Pharmacologically
2. 28.2 Weight Estimation and Length-Based Tools
3. 28.3 Worked Examples: Pediatric Dose Calculations
4. 28.4 Pediatric Resuscitation Medications
5. 28.5 Pediatric Analgesia, Sedation, and Seizure Management
6. 28.6 Avoiding Tenfold Errors
7. 28.7 Communicating With Caregivers About Medications

Every drug in this book was studied, taught, and dosed with a reference patient somewhere in the back of the author's mind, and that reference patient was rarely eighty-three years old, taking eleven medications, living alone, and managing a kidney that works at half its youthful capacity. Yet this is the patient you will meet more and more often. Older adults make up a large and growing share of the people who call 911 in the United States, and they are the group in whom a medication is most likely to be the cause of the emergency, the complication of the treatment you deliver, or the hidden reason a standard protocol needs to be bent. This chapter turns the pharmacology of the previous twenty-eight chapters toward that patient.

1. 29.1 Age-Related Changes in Drug Handling
2. 29.2 Polypharmacy and the Medication List
3. 29.3 Anticoagulants and Bleeding Risk
4. 29.4 High-Risk Home Medications for EMS Providers
5. 29.5 Common Dangerous Interactions
6. 29.6 Adjusting Treatment Decisions for the Older Patient
7. 29.7 Gathering an Accurate Medication History

Knowing what a drug does is only one part of being allowed to give it. Every medication you administer in the field is administered inside a web of authority: a state that licenses you, a medical director who delegates to you, a protocol that defines when and how much, a patient who consents or refuses, a regulator that tracks controlled substances, and a record that will be read months or years later by people who were not there. A paramedic who understands pharmacology but not this framework is only half prepared, because an error in authority, consent, documentation, or storage can harm a patient as surely as an error in dose.

1. 30.1 Scope of Practice, Standing Orders, and Online Medical Control
2. 30.2 Controlled Substance Handling and Accountability
3. 30.3 Consent, Refusal, and Medication Administration
4. 30.4 Documentation and Liability
5. 30.5 Quality Assurance and Medication Event Review
6. 30.6 Stocking, Storage, and Expiration Management
7. 30.7 Staying Current: Protocol Updates and Continuing Education