ACLS Provider Textbook

Every resuscitation begins with a moment that no one planned for. A man collapses beside a checkout lane, a patient on a medical-surgical floor stops answering a nurse's greeting, a runner folds to the pavement at mile nine of a charity race. In each case the heart has stopped producing meaningful blood flow, the brain has perhaps ten to fifteen seconds before consciousness is lost, and the minutes that follow will decide whether a person returns to their family or does not. Advanced Cardiovascular Life Support (ACLS) is the body of knowledge, skills, and teamwork that trained health professionals bring to that moment.

1. 1.1 The Burden of Sudden Cardiac Arrest
2. 1.2 The Links in the Chain of Survival
3. 1.3 Out-of-Hospital and In-Hospital Systems of Care
4. 1.4 Cardiac Arrest Versus Myocardial Infarction
5. 1.5 The Scope and Responsibilities of the ACLS Provider
6. 1.6 How Resuscitation Guidelines Are Developed and Updated
7. 1.7 Factors That Shape Survival

Every rhythm you will ever interpret, every shock you will ever deliver, and every drug you will ever push during a resuscitation acts on a structure whose design you can understand. The heart is a muscular pump of four chambers and four valves, supplied by its own network of arteries, and coordinated by a specialized electrical wiring system that tells each region of muscle when to contract. When it fails, the failure almost always traces to a disturbance in one of three domains: the plumbing of the chambers and valves, the coronary blood supply that keeps the muscle alive, or the electrical activity that governs when and how the muscle contracts.

1. 2.1 Cardiac Structure and Blood Flow
2. 2.2 The Coronary Circulation
3. 2.3 The Cardiac Conduction System
4. 2.4 Action Potentials in Pacemaker and Working Myocardium
5. 2.5 Automaticity, Conduction, and Refractoriness
6. 2.6 Autonomic Control of Heart Rate and Contractility
7. 2.7 Electrolytes and Cardiac Excitability

Every algorithm you will learn in this book rests on a small number of physiological facts. A heart that has stopped pumping effectively cannot deliver oxygen, and tissues deprived of oxygen follow a predictable, time-dependent course from reversible dysfunction to irreversible death. The rhythms you will meet at the bedside, the doses you will push, and the sequence in which you will act all make sense only when you understand what is happening inside the cell, the capillary, and the circulation during each of those minutes. This chapter builds that understanding. It asks not only what happens when the heart stops, but why it stops, why it stops in one pattern rather than another, and why restoring a pulse is the beginning of a second, equally dangerous phase of injury rather than the end of the problem.

1. 3.1 Mechanisms That Precipitate Arrest
2. 3.2 Ventricular Fibrillation and Its Electrical Basis
3. 3.3 Pulseless Electrical Activity and Asystole
4. 3.4 Oxygen Delivery, Tissue Hypoxia, and the Phases of Arrest
5. 3.5 Coronary and Cerebral Perfusion During Compressions
6. 3.6 Ischemia-Reperfusion Injury
7. 3.7 Systemic Inflammatory Response After Return of Circulation

A cardiac arrest is one of the few events in medicine in which a patient's survival depends on the coordinated action of five, eight, or twelve people who may never have worked together before. The physiology in Chapter 3 told you what the patient needs: uninterrupted compressions, controlled ventilation, timely defibrillation, the right drug at the right moment, and a relentless search for the cause. None of those things happens by itself. Each of them is performed by a human being who is tired, frightened, distracted by an alarm, or unsure what the person beside them is doing. The best clinical knowledge in the room is wasted if it never becomes an action at the right time, and the commonest reason it does not is a failure of teamwork rather than a failure of knowledge.

1. 4.1 Why Team Performance Determines Outcomes
2. 4.2 Roles of the Team Leader and Team Members
3. 4.3 Closed-Loop Communication
4. 4.4 Clear Messages and Constructive Intervention
5. 4.5 Mutual Respect and Knowing Your Limitations
6. 4.6 Cognitive Load and Error in High-Stress Events
7. 4.7 Debriefing and Learning From Every Event

Every advanced intervention described in the rest of this book rests on a foundation that is far simpler than any drug, airway device, or rhythm algorithm: a pair of hands pushing on the lower half of the sternum, hard enough and fast enough and without delay, while someone else brings a defibrillator to the bedside. Basic life support (BLS) is the set of skills that keeps blood moving through a heart that has stopped moving it by itself. It is called basic not because it is easy or unimportant but because it requires no equipment beyond a barrier device and an automated external defibrillator (AED), and because it must be performed in the first seconds and minutes of an arrest, before any advanced provider has arrived. An advanced cardiovascular life support (ACLS) provider who cannot deliver excellent BLS has little to offer the patient, because drugs and shocks depend on a circulation that only compressions can supply.

1. 5.1 Recognizing Arrest and Activating the Response
2. 5.2 Compression Depth, Rate, and Recoil
3. 5.3 Minimizing Interruptions and Compression Fraction
4. 5.4 Compression-to-Ventilation Coordination
5. 5.5 Feedback Devices and Real-Time Quality Monitoring
6. 5.6 Rescuer Fatigue and Rotation
7. 5.7 The Automated External Defibrillator in the Chain

High-quality compressions and early defibrillation keep a pulseless patient alive, but most of the patients an advanced cardiovascular life support (ACLS) provider meets are not yet pulseless. They are the breathless man on the medical ward whose oxygen saturation is drifting down, the woman in the emergency department with chest pressure and a heart rate of 38, the patient who has just been resuscitated and whose blood pressure is unstable. In each case the provider's first task is to understand what is happening quickly enough to act and accurately enough to act correctly. It converts a chaotic first impression into an ordered sequence of questions, each with an answer that guides an intervention, and it protects the provider from the single most common error in emergency care, which is to fix the problem that is most obvious while missing the one that is most dangerous.

1. 6.1 The Rationale for a Systematic Approach
2. 6.2 Primary Assessment: Airway, Breathing, Circulation, Disability, Exposure
3. 6.3 Rapid Recognition of the Deteriorating Patient
4. 6.4 Secondary Assessment: Symptoms, Allergies, Medications, Past History, Last Meal, Events
5. 6.5 Differential Diagnosis in the Unstable Patient
6. 6.6 Focused Physical Examination
7. 6.7 Diagnostic Testing at the Bedside

Every drug, shock, and compression delivered in a resuscitation depends on one assumption that is easy to forget until it fails: that oxygen can actually travel from the air in the room to the blood in the lungs. The airway is the doorway for that journey. When the doorway is blocked by a collapsed tongue, a bolus of food, a swollen larynx, or a misplaced tube, no amount of expert chest compression can compensate for long. Airway management is therefore not a side skill that belongs to anesthesiologists and respiratory therapists. It is a core competency of every advanced cardiovascular life support (ACLS) provider, and it is one of the few areas of resuscitation in which a single technical error can be fatal within minutes.

1. 7.1 Airway Anatomy and Causes of Obstruction
2. 7.2 Manual Maneuvers and Positioning
3. 7.3 Oropharyngeal and Nasopharyngeal Airways
4. 7.4 Bag-Mask Ventilation Technique
5. 7.5 Supraglottic Airways
6. 7.6 Endotracheal Intubation
7. 7.7 Confirming and Securing Advanced Airway Placement

Once an airway is open, a second set of questions begins, and these are the ones that quietly decide how well a resuscitation performs. How much oxygen should the patient receive? How many breaths per minute? How large should each breath be? What does the gas leaving the patient's lungs tell the team about whether the compressions are working? For decades these questions were answered by reflex: give as much oxygen as possible, breathe quickly, and squeeze the bag hard. The accumulated evidence has shown that two of those three reflexes are wrong. Maximal oxygen is reasonable during cardiopulmonary resuscitation (CPR), but fast, forceful breathing is harmful, and the harm comes through the circulation, not the lungs.

1. 8.1 Principles of Gas Exchange in Arrest
2. 8.2 Oxygen Delivery Devices
3. 8.3 Ventilation Rates and Volumes in Resuscitation
4. 8.4 Hyperventilation and Its Hemodynamic Cost
5. 8.5 Waveform Capnography
6. 8.6 Interpreting End-Tidal Carbon Dioxide During CPR
7. 8.7 Pulse Oximetry and Blood Gas Interpretation

A drug that never reaches the heart cannot help it. That plain statement sits underneath everything in this chapter. The preceding chapters taught you how to recognize arrest, deliver compressions, secure an airway, and ventilate and oxygenate a patient who cannot do either alone. Each of those skills works on the patient from the outside or through the airway. Medications are different: they must travel inside the body, through a vessel, to a receptor on a cell, and in a patient whose heart is not pumping, that journey is slow, unreliable, and easy to interrupt. Vascular access is therefore not a technical afterthought attached to the drug algorithm. It is the bridge between a decision made at the head of the bed and a pharmacologic effect at the myocardium.

1. 9.1 Principles of Drug Delivery in Low-Flow States
2. 9.2 Peripheral Intravenous Access
3. 9.3 Intraosseous Access
4. 9.4 Central Venous Access Considerations
5. 9.5 Endotracheal Drug Administration in Historical Context
6. 9.6 Medication Preparation and Safe Administration
7. 9.7 Flushes, Timing, and Documentation

Every decision in the cardiac arrest and peri-arrest algorithms begins with a question about rhythm. Is the heart fibrillating, and therefore shockable? Is it organized but slow, and therefore a candidate for atropine or pacing? Is it fast and narrow, wide and regular, or wide and chaotic? The answers come from the electrocardiogram (ECG), a graphic record of the electrical activity of the heart, and the ability to read it quickly and accurately is the dividing line between a provider who follows the algorithm and a provider who understands why the algorithm says what it says. The previous chapters taught you how to secure the airway, support ventilation, and obtain vascular access. This chapter teaches you how to look at the monitor and see what the heart is actually doing.

1. 10.1 Electrodes, Leads, and Monitoring Systems
2. 10.2 The Normal ECG Waveform
3. 10.3 Measuring Rate and Regularity
4. 10.4 Evaluating the P Wave, PR Interval, and QRS Complex
5. 10.5 The ST Segment, T Wave, and QT Interval
6. 10.6 A Stepwise Approach to Rhythm Strips
7. 10.7 Artifact and Monitoring Pitfalls

The previous chapter gave you the grammar of the electrocardiogram (ECG): how leads are placed, what each wave and interval represents, how to measure rate and regularity, and how to walk a rhythm strip through the same ordered questions every time. This chapter puts that grammar to work on the first family of rhythms you will meet, those that originate in the sinoatrial (SA) node or in the atrial muscle itself. Because these rhythms arise above the ventricles, they usually produce narrow QRS complexes, and most of them are compatible with a perfectly adequate cardiac output. That is the first lesson of the chapter: an abnormal rhythm is not the same thing as an unstable patient, and the provider's job is to read the rhythm and the patient together.

1. 11.1 Normal Sinus Rhythm and Sinus Variants
2. 11.2 Sinus Bradycardia and Sinus Tachycardia
3. 11.3 Premature Atrial Complexes
4. 11.4 Atrial Fibrillation
5. 11.5 Atrial Flutter
6. 11.6 Supraventricular Tachycardia
7. 11.7 Multifocal Atrial Tachycardia and Wandering Pacemaker

In the last chapter you studied rhythms that begin in the sinoatrial (SA) node or the atrial muscle. This chapter follows the electrical impulse down the conduction pathway and examines what happens when the atrioventricular (AV) junction, the ventricles, or the connection between atria and ventricles misbehaves. The three themes of the chapter are escape, irritability, and block. Escape is the safety net built into the heart: when the sinus node fails or its impulse cannot get through, lower pacemakers take over at their own slower rates. Irritability is the tendency of the ventricular myocardium to fire early or to sustain a rapid, dangerous rhythm of its own. Block is the interruption of conduction between the atria and ventricles or within the ventricular conduction system, which ranges from a harmless delay to a complete disconnection that can end in cardiac arrest.

1. 12.1 Junctional Rhythms and Escape Mechanisms
2. 12.2 Premature Ventricular Complexes
3. 12.3 Ventricular Tachycardia
4. 12.4 Torsades de Pointes and Polymorphic Rhythms
5. 12.5 First-Degree and Second-Degree Type I Block
6. 12.6 Second-Degree Type II and Third-Degree Block
7. 12.7 Bundle Branch Blocks and Wide-Complex Rhythm Mimics

Every cardiac arrest, whatever its cause, ends up looking like one of four electrical pictures on the monitor: ventricular fibrillation (VF), pulseless ventricular tachycardia (pVT), asystole, or pulseless electrical activity (PEA). Those four rhythms are the vocabulary of the entire resuscitation algorithm that follows in the next chapter. Before you can use an algorithm, you have to be able to look at a moving line on a screen, or at a printed strip handed to you in the middle of a code, and decide in seconds which of the four you are facing, whether it is real, and whether the patient in the bed matches what the monitor claims. This chapter is about building that skill.

1. 13.1 Ventricular Fibrillation: Coarse and Fine
2. 13.2 Pulseless Ventricular Tachycardia
3. 13.3 Asystole and Confirming It
4. 13.4 Pulseless Electrical Activity
5. 13.5 Shockable Versus Nonshockable Rhythms
6. 13.6 Rhythm Checks and Reassessment
7. 13.7 Distinguishing True Arrest From Artifact and Pseudo-PEA

The Adult Cardiac Arrest Algorithm is the central organizing tool of advanced cardiovascular life support (ACLS). It is a single page, a flow of boxes and arrows, but it compresses decades of resuscitation science into a sequence that a team can carry out under extreme stress. Everything you have studied so far, from the physiology of arrest to high-quality basic life support, airway management, capnography, vascular access, and rhythm recognition, comes together here. The algorithm does not replace clinical judgment, but it gives the team a shared script, so that eight people who have never worked together can act as one unit within seconds of entering a room.

1. 14.1 Structure and Logic of the Algorithm
2. 14.2 The Shockable Pathway
3. 14.3 The Nonshockable Pathway
4. 14.4 Timing of Drugs, Shocks, and Rhythm Checks
5. 14.5 Advanced Airway Placement During the Algorithm
6. 14.6 Monitoring Resuscitation Quality
7. 14.7 Return of Spontaneous Circulation: Recognition and Transition

No intervention in resuscitation is as dramatic, as time dependent, or as often misunderstood as the electrical shock. A paddle or adhesive pad, a charging tone, a call of 'clear,' and a brief jolt of current across the chest: it is the image most people associate with advanced cardiovascular life support (ACLS). Yet the shock is not a restart button. It does not make a heart beat. What it does is far subtler and, once understood, far more instructive: it depolarizes enough myocardium at once to erase a chaotic electrical state, and then it relies on the heart's own pacemaker tissue, if that tissue is still adequately perfused and oxygenated, to take command again.

1. 15.1 How Defibrillation Terminates Fibrillation
2. 15.2 Waveforms and Energy Selection
3. 15.3 Pad Placement and Contact
4. 15.4 Safe Defibrillation Practice
5. 15.5 Synchronized Cardioversion
6. 15.6 Transcutaneous Pacing
7. 15.7 Implanted Devices and Special Considerations

Few areas of resuscitation have changed as much, or as quietly, as the pharmacology of cardiac arrest. Older generations of providers learned a crowded algorithm that called for atropine, calcium, bicarbonate, lidocaine, bretylium, procainamide, and vasopressin in various combinations, often given on a schedule rather than for a reason. Over several guideline cycles, as trials failed to show that most of these drugs improved survival with good neurologic function, the list shrank. Today the pharmacologic core of the adult cardiac arrest algorithm is short: epinephrine for every arrest, amiodarone or lidocaine for a shockable rhythm that persists, and a handful of drugs reserved for specific, identifiable causes. Knowing what to give is only half of the skill. Knowing what not to give, and why, protects the patient from distractions that take attention away from compressions and defibrillation.

1. 16.1 Epinephrine: Mechanism and Role
2. 16.2 Vasopressin and Other Vasopressors
3. 16.3 Amiodarone
4. 16.4 Lidocaine
5. 16.5 Magnesium Sulfate
6. 16.6 Sodium Bicarbonate, Calcium, and Other Adjuncts
7. 16.7 Drugs That No Longer Have a Routine Role

Every cardiac arrest has a reason. Sometimes the reason is a diseased coronary artery that has finally closed, and the rhythm that follows is ventricular fibrillation (VF) that responds to a shock. But in a large share of arrests, particularly those that begin as pulseless electrical activity (PEA) or asystole, the heart is the victim rather than the culprit. Blood has been lost, oxygen has run out, a lung has collapsed under pressure, a poison has been swallowed, or a clot has lodged in the pulmonary artery. In these patients, the best compressions and the best drugs in the world will fail unless someone identifies and removes the underlying problem. The reversible causes of cardiac arrest, taught for decades as the Hs and Ts, are the clinician's organized way of asking one persistent question during every resuscitation: why did this patient's heart stop, and can I fix it?

1. 17.1 Hypovolemia and Hypoxia
2. 17.2 Hydrogen Ion Excess and Hypo- and Hyperkalemia
3. 17.3 Hypothermia and Hypoglycemia
4. 17.4 Tension Pneumothorax and Cardiac Tamponade
5. 17.5 Toxins
6. 17.6 Thrombosis: Pulmonary and Coronary
7. 17.7 Using Bedside Ultrasound to Find a Cause

The adult cardiac arrest algorithm is built for the average patient: an adult whose heart has stopped for an unknown or cardiac reason, in a setting where nothing unusual is happening. Real patients are less obliging. Some arrest because a breathing drive was erased by a synthetic opioid, because a bee sting triggered a catastrophic allergic reaction, because they went under the surface of a lake, because they were buried in a snowdrift, because they touched a downed power line, because a car hit them, or because they swallowed something that poisons the heart. In each, the cause is so dominant that the algorithm has to bend around it: the sequence of actions changes, certain drugs move up or down in priority, and the meaning of recovery differs from the typical cardiac patient.

1. 18.1 Opioid-Associated Arrest
2. 18.2 Anaphylaxis
3. 18.3 Drowning and Submersion
4. 18.4 Accidental Hypothermia
5. 18.5 Electrical Injury and Lightning
6. 18.6 Trauma and Hemorrhage
7. 18.7 Toxicologic and Electrolyte Emergencies

For most of the history of resuscitation, the moment a pulse returned was treated as the finish line. Teams cheered, a monitor showed a rhythm, and the patient was wheeled toward the intensive care unit as though the hard work were done. The modern understanding is almost the opposite. Return of spontaneous circulation (ROSC) is the moment at which a second, equally demanding phase of care begins, and the quality of that phase largely determines whether the patient who was saved from death ever wakes up, walks out of the hospital, and returns to a recognizable life. A great many patients who regain a pulse subsequently die in the hours and days that follow, and most of those deaths come from the brain injury, the stunned heart, and the body-wide inflammatory response that the arrest itself created, not from a repeat of the original rhythm.

1. 19.1 The Post-Cardiac Arrest Syndrome
2. 19.2 Immediate Priorities After Return of Circulation
3. 19.3 Oxygenation, Ventilation, and Blood Pressure Targets
4. 19.4 Identifying and Treating the Cause
5. 19.5 Coronary Angiography and Reperfusion
6. 19.6 Targeted Temperature Management
7. 19.7 Seizures, Glucose, and Organ Support

Every resuscitation eventually arrives at a question that no algorithm can answer by itself: what is going to happen to this patient, and what do we owe them and their family given what we know? The preceding chapters taught you how to restore circulation and how to protect the brain and heart afterward. This chapter addresses the decisions that surround those technical skills. They include estimating the likely outcome of an arrest, doing so for the comatose survivor in a way that is honest about uncertainty, deciding when continued efforts no longer serve the patient, honoring the wishes the patient expressed before the crisis, welcoming or excluding family at the bedside, telling people that someone they love has died, and offering the possibility of donation. These are clinical tasks that call for as much skill and preparation as any defibrillation.

1. 20.1 Predicting Outcomes After Arrest
2. 20.2 Neurologic Prognostication
3. 20.3 When to Stop: Termination of Resuscitation
4. 20.4 Advance Directives and Do-Not-Attempt-Resuscitation Orders
5. 20.5 Family Presence During Resuscitation
6. 20.6 Communicating Death and Supporting Families
7. 20.7 Organ and Tissue Donation

Up to this point in the book, the central drama has been the heart that has already stopped: the fibrillating ventricle, the electrical activity without a pulse, the flat line. Part Five turns to the patient who has not yet arrived there. Peri-arrest rhythms occupy the narrow, dangerous territory between a stable circulation and cardiac arrest, and the provider's task in that territory is fundamentally different. In arrest you replace the circulation. In a peri-arrest state you still have a circulation to protect, a brain that is still perfusing, and a window of minutes in which the right decision keeps the patient from ever needing compressions. Bradycardia, the subject of this chapter, is the first and in many ways the most deceptive of these states. The word comes from the Greek bradys, meaning slow, and kardia, meaning heart, and the slowness it names is only the visible surface of a problem that is really about perfusion.

1. 21.1 Defining Symptomatic Bradycardia
2. 21.2 Causes of Bradycardia
3. 21.3 Signs of Instability
4. 21.4 The Adult Bradycardia Algorithm
5. 21.5 Atropine and Its Limits
6. 21.6 Dopamine, Epinephrine, and Pacing
7. 21.7 Bradycardia in High-Risk Settings

Chapter 21 examined a heart that beats too slowly to meet the body's demand. This chapter examines the mirror image: a heart that beats so quickly that it defeats its own purpose. The paradox of a dangerous tachycardia is that the very feature that seems to promise more blood flow, a faster rate, can reduce it. The ventricle fills during diastole, and diastole is the portion of the cardiac cycle that shortens most as the rate climbs. The coronary arteries also fill chiefly in diastole. A heart racing at 190 beats per minute therefore spends less time filling, ejects a smaller stroke volume, and receives less coronary blood flow, all while its oxygen demand rises. In a young patient with a normal ventricle the system tolerates this for a surprisingly long time. In an older patient with a stiff, ischemic, or failing ventricle it can collapse in minutes.

1. 22.1 Defining Stable and Unstable Tachycardia
2. 22.2 Causes and Compensatory Tachycardia
3. 22.3 The Adult Tachycardia Algorithm
4. 22.4 Narrow-Complex Tachycardia: Vagal Maneuvers and Adenosine
5. 22.5 Rate Control in Atrial Fibrillation and Flutter
6. 22.6 Wide-Complex Tachycardia
7. 22.7 Synchronized Cardioversion in Practice

The two preceding chapters taught you how to decide what to do when a patient with a pulse has a rhythm that is too slow or too fast. The algorithms in those chapters name drugs: adenosine, a beta-blocker, a calcium channel blocker, procainamide, amiodarone, atropine, dopamine, epinephrine. An algorithm is only a map, and it does not tell you why a road leads where it does. This chapter supplies the pharmacology that sits behind those boxes, so that you can choose a drug because you understand what it does to the electrical and mechanical behavior of the heart, not merely because a flowchart pointed to it.

1. 23.1 Classification of Antiarrhythmic Drugs
2. 23.2 Adenosine
3. 23.3 Beta-Blockers and Calcium Channel Blockers
4. 23.4 Procainamide, Sotalol, and Other Wide-Complex Agents
5. 23.5 Vasoactive Infusions: Norepinephrine, Dopamine, Epinephrine
6. 23.6 Dobutamine and Inotropic Support
7. 23.7 Adverse Effects, Interactions, and Monitoring

Of all the conditions that bring a patient to the edge of cardiac arrest, none is more common in adults than acute myocardial ischemia. This chapter goes upstream of the arrhythmias described in the preceding chapters, to the event in the coronary artery that so often starts the sequence. Acute coronary syndromes (ACS) is the umbrella term for the presentations that result from an abrupt reduction of blood flow to a region of heart muscle: unstable angina, non-ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). They share a common pathology, the disruption of an atherosclerotic plaque with thrombus formation, but they differ in how completely the artery is occluded and therefore in how urgently the patient must be reperfused.

1. 24.1 Coronary Atherosclerosis and Plaque Rupture
2. 24.2 Recognizing Acute Coronary Syndromes
3. 24.3 The 12-Lead ECG in Acute Coronary Syndromes
4. 24.4 ST-Elevation Myocardial Infarction and Reperfusion
5. 24.5 Non-ST-Elevation Acute Coronary Syndromes
6. 24.6 Initial Pharmacologic Management
7. 24.7 Complications: Arrhythmia, Heart Failure, and Cardiogenic Shock

Few emergencies in the ACLS curriculum punish delay as severely, or as silently, as acute stroke. A patient in ventricular fibrillation announces the problem on the monitor within seconds. A patient with a blocked cerebral artery may look only slightly unwell: a drooping corner of the mouth, a hand that will not hold a cup, a sentence that comes out as nonsense. Behind that quiet presentation, brain tissue is dying at a rate that is difficult to picture. A large vessel occlusion can destroy millions of neurons every minute that it persists, and the tissue that is lost does not regenerate. The central message of stroke care therefore sounds like the message of cardiac arrest care: speed matters, and the time to act is measured from the first moment of symptoms, not from the moment the patient is noticed by a professional.

1. 25.1 Ischemic and Hemorrhagic Stroke
2. 25.2 Cerebral Vascular Anatomy
3. 25.3 Prehospital Recognition and Stroke Scales
4. 25.4 Emergency Department Evaluation and Imaging
5. 25.5 Fibrinolytic Therapy: Eligibility and Risks
6. 25.6 Endovascular Thrombectomy
7. 25.7 Blood Pressure, Airway, and Supportive Care

Most cardiac arrests in hospitalized patients are not sudden in the way that a ventricular fibrillation arrest in a healthy marathon runner is sudden. They are the end of a trajectory. Hours before the arrest, the patient's respiratory rate was climbing, the blood pressure was drifting down, the heart rate was creeping up, or the mental status was dimming, and each of those signs was a message that oxygen delivery was failing. When the failure runs its full course, the heart that was once beating in a normal rhythm slows, loses its electrical organization, and stops, usually as pulseless electrical activity or asystole rather than as a shockable rhythm. For this reason, the survival rates of in-hospital arrest from respiratory failure and shock are lower than those of primary arrhythmic arrest, and for this reason the most effective resuscitation is the one that happens before the arrest.

1. 26.1 Recognizing Shock Before Arrest
2. 26.2 Hypovolemic and Distributive Shock
3. 26.3 Cardiogenic and Obstructive Shock
4. 26.4 Acute Heart Failure and Pulmonary Edema
5. 26.5 Acute Respiratory Failure and Impending Arrest
6. 26.6 Pulmonary Embolism
7. 26.7 Stabilizing the Patient Who Is Failing

Everything you have learned so far has been built around a patient who is, in a sense, an abstraction: an adult of average size with a heart that was healthy until it suddenly was not. The algorithms in this book were written for that patient, and for the great majority of the people you will treat they work exactly as written. But the people who actually arrest in front of you are not abstractions. They are twenty-eight weeks pregnant, or ninety-one years old and frail, or four hundred pounds and wedged into a narrow bed. They have a pacemaker, a defibrillator, or a left ventricular assist device humming in their chests. They are on dialysis, or they are a nineteen-year-old who collapsed in the third quarter of a basketball game. Each of them brings anatomy, physiology, equipment, or circumstance that quietly changes what high-quality resuscitation looks like, and the provider who knows only the generic algorithm will sometimes do the right thing for the wrong reasons and, occasionally, the wrong thing for the right reasons.

1. 27.1 Cardiac Arrest in Pregnancy
2. 27.2 The Older Adult
3. 27.3 Patients With Obesity
4. 27.4 Patients With Implanted Devices and Mechanical Support
5. 27.5 Cardiac Arrest in Patients With Chronic Kidney Disease
6. 27.6 Cardiac Arrest in Athletes and Young Adults
7. 27.7 Pediatric Considerations for the Adult ACLS Provider

A cardiac arrest does not begin when the monitor alarms or when the team leader says 'start compressions.' It begins in a kitchen, a grocery store, a hospital ward at three in the morning, or a field beside a road, and its outcome is shaped by what happened in the minutes before any ACLS provider touched the patient: whether anyone recognized that the person was in trouble, whether a telephone call was made, whether a stranger pushed on the chest, whether a defibrillator was within reach, and whether the next team to arrive had been prepared, equipped, and organized to do the right thing in the right order. The previous chapters taught you the technical content of advanced cardiovascular life support (ACLS). This chapter steps back and asks what must surround that content for it to save lives. The answer is a system of care, a deliberately designed arrangement of people, technology, training, and measurement that turns individual skill into reliable population-level outcomes.

1. 28.1 Out-of-Hospital Cardiac Arrest and Emergency Medical Services
2. 28.2 Dispatcher-Assisted CPR and Public Access Defibrillation
3. 28.3 In-Hospital Cardiac Arrest and Rapid Response Teams
4. 28.4 Early Warning Scores and Recognizing Deterioration
5. 28.5 Extracorporeal CPR and Advanced Rescue Therapies
6. 28.6 Registries, Quality Measures, and Performance Improvement
7. 28.7 Handoff and Transitions of Care

Twenty-eight chapters have given you the pieces of resuscitation one at a time: the anatomy and electrophysiology that explain why hearts fail, the mechanics of compressions and airways, the grammar of rhythm strips, the algorithms, the drugs, the electrical therapies, and the systems that surround all of it. A real patient does not arrive in pieces. A real patient arrives as a gray, diaphoretic man on a telemetry bed whose monitor has just turned into a chaotic scribble, or as a woman found on a bathroom floor with a bystander counting compressions aloud, and everything you know must be recalled, sequenced, and delegated in a few seconds while other people look to you for direction. This chapter is where the pieces are assembled.

1. 29.1 Approaching a Megacode Scenario
2. 29.2 Ventricular Fibrillation Case Studies
3. 29.3 Pulseless Electrical Activity and Asystole Case Studies
4. 29.4 Bradycardia and Tachycardia Case Studies
5. 29.5 Acute Coronary Syndrome and Stroke Case Studies
6. 29.6 Post-Arrest and Special Circumstance Case Studies
7. 29.7 Common Errors and How to Avoid Them

Completing a course, passing a skills station, and leading a well-run simulated code all demonstrate that you can do something on a given day. They do not guarantee that you will be able to do it eighteen months later, at three in the morning, when a patient you have known for four hours stops breathing. Resuscitation is an unusual clinical domain because the skills are high stakes and rarely used. A nurse on a general medical unit may lead or participate in only a handful of true cardiac arrests across an entire year, and a paramedic in a low-volume rural system may go many months between them. Most other clinical skills are reinforced by daily repetition. Resuscitation skills must be reinforced on purpose.

1. 30.1 Skill Decay and the Case for Frequent Practice
2. 30.2 Simulation and Deliberate Practice
3. 30.3 Debriefing Frameworks
4. 30.4 Cognitive Aids and Checklists
5. 30.5 Provider Well-Being After Critical Events
6. 30.6 Professional Standards and Scope of Practice
7. 30.7 A Roadmap for Lifelong Learning in Resuscitation