ACUTE CARE NURSE PRACTITIONER TEXTBOOK

Few clinical roles ask as much of a single practitioner as that of the adult-gerontology acute care nurse practitioner (AG-ACNP). You are expected to stand at the bedside of a patient whose blood pressure is falling, whose oxygen saturation is drifting downward, or whose mental status has changed in the last hour, and to move from observation to a coherent diagnostic and therapeutic plan in minutes rather than days. That expectation rests on a deliberate foundation: advanced education in pathophysiology, pharmacology, and assessment; national certification in the acute care population; state licensure; and an institutional framework of credentialing and privileging that defines what you may do and where. This chapter describes that foundation so that the clinical content in the remainder of the book can be placed in its proper professional context.

1. 1.1 Scope of Practice and Population Focus
2. 1.2 Practice Settings: ICU, Step-Down, Emergency, and Inpatient Units
3. 1.3 Collaboration with Physicians, Nurses, and the Care Team
4. 1.4 Prescriptive Authority and Documentation
5. 1.5 Legal and Regulatory Frameworks for Advanced Practice
6. 1.6 Professional Boundaries and Escalation of Care
7. 1.7 Building Clinical Judgment in High-Acuity Practice

Every acutely ill patient presents a physiologic question before a diagnostic one: is the body holding its internal environment together, and if so, at what cost? A previously healthy young adult with a severe infection may show a normal blood pressure for hours while the heart rate climbs, the breathing quickens, and the skin turns cool, because powerful compensatory mechanisms are defending perfusion of the brain and heart. An older adult with the same infection may show almost none of these signs and then collapse abruptly, because the reserve that supports compensation is gone. This chapter develops the physiologic framework needed to interpret such differences: homeostasis, oxygen delivery and consumption, the neurohormonal stress response, the distinction between compensated and decompensated states, the inflammatory response to injury, and the way organ failures propagate.

1. 2.1 Homeostasis and Feedback Systems
2. 2.2 Cellular Oxygen Delivery and Consumption
3. 2.3 Neurohormonal Stress Response
4. 2.4 Compensated Versus Decompensated States
5. 2.5 Inflammation and the Systemic Response to Injury
6. 2.6 Organ Interdependence and Multiple Organ Dysfunction
7. 2.7 Recognizing the Failing Compensatory Mechanism

Assessment is the act that converts physiologic knowledge into clinical action. When you arrive at the bedside of a patient who is deteriorating, you do not have the luxury of an unhurried history and a leisurely examination, nor can you afford to be haphazard. The solution used by experienced acute care practitioners is a systematic approach that begins with the immediate threats to life, proceeds through a focused history and a complete examination, and continues as an ongoing process of reassessment. This chapter describes that approach step by step: the primary survey and initial stabilization, the history obtained under time pressure, the head-to-toe examination, the neurologic and mental status evaluation, the cardiopulmonary examination in unstable patients, the abdominal, skin, and extremity findings that so often reveal the cause of shock, and the early warning scores that help detect trajectory.

1. 3.1 The First Sixty Seconds: Primary Survey and Stabilization
2. 3.2 Focused History Under Time Pressure
3. 3.3 Head-to-Toe Physical Examination
4. 3.4 Neurologic and Mental Status Assessment
5. 3.5 Cardiopulmonary Examination in Unstable Patients
6. 3.6 Abdominal, Skin, and Extremity Findings
7. 3.7 Early Warning Scores and Trajectory Recognition

Every assessment you perform and every test you order ultimately serves a single cognitive task: deciding what is wrong with the patient in front of you and what to do about it before the window for effective treatment closes. In acute care this task is unusually hard. Data arrive incomplete, out of order, and contaminated by treatment already given. The patient may be unable to give a history, may carry five chronic diseases that each explain a portion of the picture, and may change character between one set of vital signs and the next. Clinical reasoning is the discipline that turns this disorder into a ranked list of explanations, a plan for discriminating among them, and a defensible decision about action.

1. 4.1 Hypothesis Generation and Differential Diagnosis
2. 4.2 Pretest Probability and Diagnostic Testing Logic
3. 4.3 Cognitive Biases and Diagnostic Error
4. 4.4 Prioritizing Problems in Multisystem Illness
5. 4.5 Risk Stratification Tools
6. 4.6 Communicating Diagnostic Uncertainty
7. 4.7 Reassessment and Revising the Working Diagnosis

Laboratory testing is the most frequently used diagnostic modality in acute care, and in many patients the laboratory results supply the first objective evidence that something is seriously wrong. A hemoglobin that has fallen by three grams per deciliter in twelve hours, a troponin that rises across two draws, a potassium of 6.9 mEq/L, a lactate of 6 mmol/L, or a gram-positive cocci reported from a blood culture bottle can each redirect an entire resuscitation. Yet laboratory data are not self-interpreting. Each value reflects a physiologic process, a sampling process, and an analytic process, and a competent practitioner must understand all three to know whether a number deserves belief and what action it demands.

1. 5.1 Complete Blood Count and Coagulation Studies
2. 5.2 Chemistry Panels and Renal Function
3. 5.3 Cardiac Biomarkers
4. 5.4 Arterial and Venous Blood Gas Interpretation
5. 5.5 Lactate and Markers of Perfusion
6. 5.6 Microbiology Cultures and Rapid Diagnostics
7. 5.7 Pitfalls: Hemolysis, Timing, and Spurious Results

Imaging answers the question that the history, examination, and laboratory studies can only pose: what is the anatomy, and what is it doing? In acute care, the right image at the right moment confirms a pneumothorax before it becomes a tension physiology, identifies an aortic dissection before the intima fails, or shows a hemorrhage that changes the entire management of a patient who was thought to have a simple infarct. The wrong image, or an unnecessary one, exposes the patient to radiation, contrast, transport risk, and incidental findings that generate more testing without benefit. Selecting, ordering, and interpreting imaging is therefore a core clinical skill, not a task delegated entirely to radiology.

1. 6.1 Chest Radiography in the Acute Setting
2. 6.2 Computed Tomography: Indications and Contrast Considerations
3. 6.3 Magnetic Resonance Imaging in Acute Illness
4. 6.4 Principles of Point-of-Care Ultrasound
5. 6.5 Cardiac and Lung Ultrasound
6. 6.6 Abdominal, Vascular, and Volume Assessment by Ultrasound
7. 6.7 Radiation Safety and Imaging Stewardship

The electrocardiogram and the hemodynamic monitor are the two instruments through which the acute care nurse practitioner watches the heart work in real time. Laboratory values and imaging, which occupied the previous two chapters, describe the patient at a moment that has already passed. The tracing on the monitor describes the patient right now, beat by beat, and it is often the first place that deterioration announces itself. A rhythm change, a falling mean arterial pressure, or a pulse pressure that swings with each breath can precede overt collapse by minutes or hours, and the practitioner who can read these signals fluently has time to act while the problem is still small.

1. 7.1 Systematic 12-Lead ECG Interpretation
2. 7.2 Continuous Cardiac Monitoring
3. 7.3 Arterial Line Monitoring and Waveform Analysis
4. 7.4 Central Venous Pressure and Central Access
5. 7.5 Pulmonary Artery Catheter Principles
6. 7.6 Cardiac Output and Dynamic Fluid Responsiveness
7. 7.7 Noninvasive and Minimally Invasive Monitoring

Few areas of acute care medicine reward a systematic mind as consistently as acid-base, fluid, and electrolyte disorders. The numbers are plentiful, the physiology is quantitative, and the errors of interpretation are costly: a missed anion gap, a sodium corrected too quickly, or a potassium treated without regard to its cause can each convert a manageable problem into a catastrophe. In the intensive care unit, nearly every patient has at least one of these disorders, and many have several that interact. The practitioner's task is to find the pattern that explains the numbers, identify the process that is driving it, and correct the process rather than only the value.

1. 8.1 Stepwise Acid-Base Interpretation
2. 8.2 Metabolic Acidosis and the Anion Gap
3. 8.3 Metabolic Alkalosis and Respiratory Disorders
4. 8.4 Sodium Disorders
5. 8.5 Potassium Disorders
6. 8.6 Calcium, Magnesium, and Phosphate
7. 8.7 Choosing and Dosing Resuscitation Fluids

Acute coronary syndromes (ACS) are the clinical expression of a sudden mismatch between myocardial oxygen supply and demand, almost always caused by the disruption of an atherosclerotic plaque and the formation of thrombus within a coronary artery. The spectrum runs from unstable angina, in which myocardial injury is absent, through non-ST-elevation myocardial infarction (NSTEMI), in which a troponin leak reveals injury without persistent ST-segment elevation, to ST-elevation myocardial infarction (STEMI), in which a coronary artery is usually occluded and myocardium is dying minute by minute. For the acute care nurse practitioner these are among the highest-stakes diagnoses in medicine, because both the cost of delay and the cost of overtreatment are measured in lives.

1. 9.1 Coronary Anatomy and Plaque Pathophysiology
2. 9.2 Presentation and Early Recognition
3. 9.3 ST-Elevation Myocardial Infarction
4. 9.4 Non-ST-Elevation ACS and Unstable Angina
5. 9.5 Antiplatelet, Anticoagulant, and Reperfusion Therapy
6. 9.6 Complications of Myocardial Infarction
7. 9.7 Post-ACS Care and Secondary Prevention

Acute heart failure is the most common reason for hospital admission among adults over sixty-five in the United States, and it is a syndrome that spans an enormous clinical range. At one end is the hypertensive patient who arrives gasping with flash pulmonary edema and improves dramatically within hours of vasodilator therapy. At the other end is the patient in cardiogenic shock, whose failing pump cannot sustain perfusion of the brain, kidneys, and gut, and whose mortality remains high even in expert hands. The acute care nurse practitioner (NP) must be able to place any patient with a failing heart somewhere along that range within minutes, because the correct therapy for one end of the range can be harmful at the other.

1. 10.1 Pathophysiology of Acute Decompensated Heart Failure
2. 10.2 Clinical Profiles: Congestion and Hypoperfusion
3. 10.3 Diuretic and Vasodilator Strategies
4. 10.4 Inotropes and Vasopressors in Low-Output States
5. 10.5 Cardiogenic Shock Recognition and Management
6. 10.6 Mechanical Circulatory Support
7. 10.7 Transition to Guideline-Directed Therapy

Disturbances of cardiac rhythm account for a large share of the emergencies that acute care nurse practitioners (NPs) manage, from the stable patient with newly detected atrial fibrillation to the pulseless patient in ventricular fibrillation. The electrocardiogram (ECG) rhythm strip is deceptively simple to obtain and notoriously easy to misread under pressure, and the consequences of error are asymmetric: treating a stable rhythm aggressively can cause harm, while hesitating in an unstable one can be fatal. This chapter equips you with a framework that begins with the patient rather than the tracing, asking first whether the rhythm is the cause of instability or a consequence of something else, and then proceeds to rhythm identification and targeted therapy.

1. 11.1 Mechanisms of Arrhythmia
2. 11.2 Atrial Fibrillation and Flutter
3. 11.3 Supraventricular Tachycardias
4. 11.4 Ventricular Tachycardia and Fibrillation
5. 11.5 Bradyarrhythmias and Heart Block
6. 11.6 Cardioversion, Defibrillation, and Pacing
7. 11.7 Antiarrhythmic Drugs and Proarrhythmia Risk

Some of the most time-sensitive conditions in cardiovascular medicine arise not from the heart muscle or its rhythm but from the vessels and the sac that surrounds the heart. A blood pressure that has climbed high enough to injure the brain, heart, kidneys, or retina; a tear in the wall of the aorta that propagates in minutes; a pericardial effusion that accumulates quickly enough to compress the heart; and an infected valve that fails abruptly are conditions that demand rapid recognition and a precise, often counterintuitive, choice of therapy. In each of them, the physical examination and a few bedside tests suggest the diagnosis, and imaging confirms it, but the decisions that save the patient are frequently made before imaging is complete.

1. 12.1 Hypertensive Urgency Versus Emergency
2. 12.2 Target-Organ Injury and Controlled Blood Pressure Reduction
3. 12.3 Acute Aortic Dissection
4. 12.4 Aortic Aneurysm and Peripheral Arterial Emergencies
5. 12.5 Pericarditis and Pericardial Effusion
6. 12.6 Cardiac Tamponade
7. 12.7 Endocarditis and Acute Valvular Emergencies

Few clinical problems move as quickly from subtle to lethal as acute respiratory failure. A patient who is talking in full sentences at the start of a shift can, within an hour, be using every accessory muscle, unable to finish a phrase, and approaching the point at which exhaustion converts a compensated state into respiratory arrest. The acute care nurse practitioner (NP) is frequently the first provider with prescriptive authority at the bedside when this transition begins, and the decisions made in the first several minutes, which device to apply, whether to escalate, whether to intubate, and what underlying process to chase, shape everything that follows. This chapter builds the physiologic and practical framework for those decisions.

1. 13.1 Gas Exchange and Mechanisms of Hypoxemia
2. 13.2 Hypoxemic Versus Hypercapnic Respiratory Failure
3. 13.3 Assessment of Work of Breathing
4. 13.4 Oxygen Delivery Devices and High-Flow Nasal Cannula
5. 13.5 Noninvasive Ventilation
6. 13.6 Pulmonary Embolism and Pulmonary Hypertension
7. 13.7 Pleural Disease, Pneumothorax, and Effusion

Securing an airway and placing a patient on a mechanical ventilator are among the most consequential procedures in acute care. Done well, they restore oxygenation, relieve the work of breathing, and buy time for the underlying disease to be treated. Done poorly, they can precipitate hypoxemic cardiac arrest, hemodynamic collapse, aspiration, and ventilator-induced lung injury. For the acute care nurse practitioner (NP), competence here means more than technical skill with a laryngoscope. It means anticipating difficulty, selecting medications that fit the physiology of the particular patient, choosing initial ventilator settings that protect the lung, and recognizing when and how to liberate the patient from the machine.

1. 14.1 Airway Anatomy and Difficult Airway Prediction
2. 14.2 Indications for Intubation
3. 14.3 Rapid Sequence Intubation and Medication Selection
4. 14.4 Ventilator Modes and Initial Settings
5. 14.5 Lung-Protective Ventilation
6. 14.6 Ventilator Alarms, Troubleshooting, and Patient-Ventilator Dyssynchrony
7. 14.7 Liberation from Mechanical Ventilation

The diseases in this chapter account for a large share of intensive care unit admissions and a still larger share of the ventilator days that the acute care nurse practitioner (NP) manages. Acute respiratory distress syndrome (ARDS) is the archetype of severe hypoxemic respiratory failure, a diffuse inflammatory injury to the lung that demands precise ventilator management and a willingness to use rescue therapies. Pneumonia is both the commonest cause of ARDS and the commonest infectious cause of death in hospitalized patients. Chronic obstructive pulmonary disease (COPD) and asthma, at the opposite physiologic pole, produce failure through airflow obstruction, air trapping, and respiratory muscle exhaustion, and they require nearly the opposite ventilator strategy.

1. 15.1 Pathophysiology and Diagnosis of ARDS
2. 15.2 Management of ARDS: Proning, Paralysis, and Rescue Therapies
3. 15.3 Community-Acquired and Hospital-Acquired Pneumonia
4. 15.4 Aspiration and Ventilator-Associated Events
5. 15.5 Acute Exacerbation of COPD
6. 15.6 Status Asthmaticus
7. 15.7 Extracorporeal Support Concepts

Few clinical situations compress the interval between recognition and irreversible harm as sharply as an acute cerebrovascular event. A large vessel occlusion can destroy roughly two million neurons every minute that blood flow remains absent, and an expanding hematoma can convert a talkative patient into a comatose one within an hour. For the acute care nurse practitioner (NP), stroke and related intracranial emergencies are not rare consultative problems; they are daily encounters in the emergency department, on the stroke unit, in the neurologic intensive care unit, and on general medical and surgical floors where a hospitalized patient suddenly develops a new deficit. This chapter builds the knowledge you need to recognize these syndromes quickly, to sort ischemic from hemorrhagic injury, and to deliver time-sensitive treatment safely.

1. 16.1 Cerebral Blood Flow and Autoregulation
2. 16.2 Acute Ischemic Stroke Recognition and Scoring
3. 16.3 Thrombolysis and Thrombectomy Candidacy
4. 16.4 Intracerebral Hemorrhage
5. 16.5 Subarachnoid Hemorrhage
6. 16.6 Intracranial Pressure and Herniation
7. 16.7 Post-Stroke Complications and Early Rehabilitation

Altered mental status is the most common neurologic complaint in acute care and one of the least specific. A confused patient may have a primary brain disorder such as seizure, stroke, infection, or trauma, but just as often the brain is the victim of a problem elsewhere: hypoglycemia, hyponatremia, hypoxemia, sepsis, uremia, hepatic failure, or a drug effect. The acute care nurse practitioner (NP) must sort these possibilities quickly because some of them, such as hypoglycemia, are reversible in minutes while others, such as herpes simplex encephalitis or status epilepticus, cause permanent damage within hours if treatment is delayed. This chapter teaches a structured approach to the patient with impaired consciousness and then applies it to the major disorders that produce it.

1. 17.1 Approach to the Patient with Altered Consciousness
2. 17.2 Status Epilepticus
3. 17.3 Delirium: Detection, Prevention, and Management
4. 17.4 Traumatic Brain Injury
5. 17.5 Encephalitis and Meningitis
6. 17.6 Neuromuscular Emergencies
7. 17.7 Brain Death Evaluation and Organ Donation Considerations

Acute kidney injury (AKI) is among the most common and consequential complications of hospitalization. It develops in a large fraction of critically ill patients, it independently increases mortality, and even mild episodes leave survivors at higher risk of chronic kidney disease, cardiovascular events, and rehospitalization. The kidney is also unusually exposed in acute illness: it receives a quarter of cardiac output, it concentrates drugs and toxins in its tubules, and it sits at the downstream end of every shock state. For the acute care nurse practitioner (NP), AKI is rarely the presenting problem. It is the problem you must prevent, recognize early, and manage in partnership with every other organ system.

1. 18.1 Renal Physiology and Perfusion
2. 18.2 Definitions and Staging of Acute Kidney Injury
3. 18.3 Prerenal, Intrinsic, and Postrenal Causes
4. 18.4 Contrast and Drug-Induced Nephropathy
5. 18.5 Management of Volume, Electrolytes, and Uremia
6. 18.6 Indications and Modalities of Renal Replacement Therapy
7. 18.7 Dosing Medications in Renal Impairment

Endocrine emergencies occupy an unusual place in acute care practice. The hormones involved, insulin, cortisol, thyroid hormone, parathyroid hormone, and vasopressin, do not act on a single organ. They set the operating conditions for every organ at once, which means that when one of them fails or surges, the patient may arrive with a confusing mixture of cardiovascular collapse, altered mental status, acid-base disturbance, and electrolyte derangement. The presentation often points away from the true cause. A patient in refractory shock may have adrenal crisis, a patient with agitated delirium and fever may have thyroid storm, and a patient with unexplained coma may have myxedema or severe hypercalcemia. This chapter teaches you to see the endocrine signature beneath the multisystem picture and to treat it with the right drug at the right time.

1. 19.1 Diabetic Ketoacidosis
2. 19.2 Hyperosmolar Hyperglycemic State
3. 19.3 Inpatient Glycemic Management and Hypoglycemia
4. 19.4 Adrenal Crisis and Critical Illness-Related Corticosteroid Insufficiency
5. 19.5 Thyroid Storm and Myxedema Coma
6. 19.6 Calcium and Parathyroid Emergencies
7. 19.7 Diabetes Insipidus and SIADH

The gastrointestinal tract and liver are easy to overlook in a critically ill patient until they fail dramatically. A patient bleeding from a duodenal ulcer can lose a third of the circulating volume before the blood pressure falls. A patient with mesenteric ischemia can have an abdomen that looks deceptively soft while the bowel dies. A patient with acute liver failure may arrive with nothing more than fatigue and mild jaundice, then develop cerebral edema within days. This chapter equips you to recognize these emergencies early, to resuscitate before you diagnose, and to know when the definitive answer is an endoscope, a scalpel, an antidote, or a transplant center.

1. 20.1 Upper Gastrointestinal Bleeding
2. 20.2 Lower Gastrointestinal Bleeding
3. 20.3 Acute Pancreatitis
4. 20.4 Bowel Obstruction, Ischemia, and Perforation
5. 20.5 Acute Liver Failure
6. 20.6 Complications of Cirrhosis
7. 20.7 Stress Ulcer Prophylaxis and Gastrointestinal Protection

Nutrition in critical illness is often treated as a housekeeping task, delegated to a standard order set and revisited only when a dietitian raises a concern. This habit understates its importance. Critically ill patients lose muscle at a startling pace, as much as a pound of lean tissue a day in the sickest, and that loss shapes how long they stay on the ventilator, how well they fight infection, and whether they walk out of the hospital or are transferred to a facility. At the same time, feeding is not a harmless act. Overfeeding produces hyperglycemia, fatty liver, and excess carbon dioxide, underfeeding accumulates an energy deficit, and feeding too aggressively in a malnourished patient can trigger refeeding syndrome and cardiac arrest.

1. 21.1 Metabolic Response to Critical Illness
2. 21.2 Nutritional Assessment
3. 21.3 Enteral Nutrition: Timing and Delivery
4. 21.4 Parenteral Nutrition
5. 21.5 Refeeding Syndrome
6. 21.6 Nutrition in Specific Conditions
7. 21.7 Monitoring Tolerance and Adequacy

Few conditions in acute care medicine demand as much speed, judgment, and coordination as sepsis. It is the final common pathway of severe infection from nearly every source, including the lungs, abdomen, urinary tract, skin, and bloodstream, and it remains one of the leading causes of death among hospitalized adults in the United States. Sepsis is not a single disease with a single treatment. It is a syndrome in which a dysregulated host response to infection injures the patient's own organs, and the acute care nurse practitioner (NP) must recognize it early, resuscitate it deliberately, find and control its source, and then guide the patient through the long recovery that often follows survival.

1. 22.1 Definitions and Epidemiology
2. 22.2 Pathophysiology of Dysregulated Host Response
3. 22.3 Early Recognition and Screening
4. 22.4 Initial Resuscitation and Source Control
5. 22.5 Vasopressors and Adjunctive Therapy
6. 22.6 Antimicrobial Selection and De-escalation
7. 22.7 Long-Term Outcomes and Post-Sepsis Care

Hospitals exist to heal, yet the very devices and treatments that sustain critically ill patients also create new routes for microbial invasion. A central venous catheter bypasses the skin, a urinary catheter bypasses the urethral defenses, a mechanical ventilator bypasses the glottis, and broad-spectrum antibiotics bypass the protective gut microbiome. Healthcare-associated infections (HAIs) are therefore not rare accidents but predictable consequences of invasive care, and a substantial proportion of them are preventable through consistent, evidence-based practice. In the United States, HAIs contribute to thousands of deaths each year, prolong hospital stays, and increase costs, and they are tracked as quality measures that influence institutional reporting and reimbursement.

1. 23.1 Central Line-Associated Bloodstream Infection
2. 23.2 Catheter-Associated Urinary Tract Infection
3. 23.3 Clostridioides difficile Infection
4. 23.4 Multidrug-Resistant Organisms
5. 23.5 Invasive Fungal Infections
6. 23.6 Principles of Antimicrobial Stewardship
7. 23.7 Infection Prevention Bundles and Isolation Practice

Blood is both the medium of oxygen delivery and the guardian of vascular integrity, and when its cells or clotting proteins fail, the consequences are immediate. A patient may bleed from a trivial wound because of an acquired factor deficiency, or clot an entire limb or lung because of an unregulated procoagulant stimulus. Anemia reduces oxygen-carrying capacity, thrombocytopenia removes the first line of hemostatic defense, and malignancy, with its treatments, introduces a distinct set of emergencies in which cell turnover, immune suppression, and metabolic derangement collide. The acute care nurse practitioner (NP) meets these problems in every intensive care unit, emergency department, and inpatient service, and often has to decide quickly between opposing hazards such as thrombosis and hemorrhage.

1. 24.1 Coagulation Physiology and the Coagulation Cascade
2. 24.2 Anemia and Transfusion Strategy
3. 24.3 Thrombocytopenia, Heparin-Induced Thrombocytopenia, and Thrombotic Microangiopathy
4. 24.4 Disseminated Intravascular Coagulation
5. 24.5 Venous Thromboembolism Prophylaxis and Treatment
6. 24.6 Reversal of Anticoagulants
7. 24.7 Tumor Lysis Syndrome, Neutropenic Fever, and Other Oncologic Emergencies

Few presentations in acute care medicine are as time-sensitive, as varied, or as frequently underestimated as the poisoned patient. Toxic exposures reach the emergency department and the intensive care unit through intentional self-harm, accidental ingestion, therapeutic misadventure, recreational use, occupational exposure, and the environment itself. A single patient may arrive with an unreliable history, an unknown substance, a mixed ingestion, and a physiology that is changing by the minute. The acute care nurse practitioner (NP) must be able to stabilize the airway, breathing, and circulation first, recognize a toxidrome from the bedside examination, choose a small number of high-yield diagnostic tests, and give the right antidote early, often before any confirmatory result returns.

1. 25.1 General Approach to the Poisoned Patient
2. 25.2 Acetaminophen, Salicylate, and Common Analgesic Overdoses
3. 25.3 Opioid, Sedative, and Stimulant Toxicity
4. 25.4 Toxic Alcohols and Other Metabolic Poisons
5. 25.5 Withdrawal Syndromes
6. 25.6 Heat Illness and Hypothermia
7. 25.7 Drowning, Electrical Injury, and Carbon Monoxide Poisoning

Shock is the final common pathway of circulatory failure: a state in which oxygen delivery to the tissues is inadequate to meet metabolic demand. It is not a blood pressure, although hypotension is its most familiar sign, and it is not a diagnosis in itself. It is a physiologic syndrome that demands two simultaneous tasks from the acute care nurse practitioner (NP): restoring perfusion immediately, and discovering and treating the cause. A patient in shock may look deceptively well for a time, with a normal blood pressure maintained by intense vasoconstriction and tachycardia, while the microcirculation is already failing. By the time the pressure falls, compensation has often been exhausted and mortality has risen sharply.

1. 26.1 Classification of Shock
2. 26.2 Hypovolemic and Hemorrhagic Shock
3. 26.3 Distributive Shock Beyond Sepsis
4. 26.4 Obstructive Shock
5. 26.5 Vasoactive Medication Selection
6. 26.6 Resuscitation Endpoints and Perfusion Targets
7. 26.7 Cardiac Arrest and Post-Arrest Care

Trauma remains a leading cause of death among Americans under the age of 45, and the acute care nurse practitioner (NP) meets injured patients in many settings: the emergency department, the trauma intensive care unit, the step-down unit, and the surgical ward, where complications of injury declare themselves days after the initial insult. Injury is also unusual among acute illnesses in that its physiology is predictable, its treatment is highly protocolized, and its outcomes are strongly determined by the speed with which life-threatening problems are identified and corrected. A systematic approach, practiced until it is automatic, is the most important clinical tool you bring to an injured patient.

1. 27.1 Trauma Systems and the Primary Survey
2. 27.2 Thoracic and Abdominal Trauma
3. 27.3 Orthopedic Injury, Compartment Syndrome, and Rhabdomyolysis
4. 27.4 Spinal Cord Injury
5. 27.5 Damage Control Resuscitation and Massive Transfusion
6. 27.6 Burn Assessment and Resuscitation
7. 27.7 Inhalation Injury and Wound Care

Surgery is a controlled physiologic insult. Anesthesia suppresses protective reflexes and vascular tone, incision and tissue handling trigger an inflammatory and neurohormonal stress response, blood and fluid shift between compartments, and the patient emerges into a recovery environment where pain, immobility, and organ dysfunction compete for attention. For most patients the insult is well tolerated. For the acutely ill adult, whose reserve has already been spent on sepsis, heart failure, respiratory insufficiency, or renal injury, the same insult can convert a stable trajectory into a cascade of complications. The acute care nurse practitioner (NP) is frequently the clinician who stands at both ends of that cascade: asked to assess whether a patient is fit for the operating room, and asked again within hours to explain why that patient is hypotensive, hypoxemic, bleeding, or confused on the first postoperative night.

1. 28.1 Preoperative Risk Assessment
2. 28.2 Medication Management Around Surgery
3. 28.3 Postoperative Hemodynamic and Respiratory Complications
4. 28.4 Postoperative Bleeding, Ileus, and Wound Complications
5. 28.5 Cardiac Surgery and Transplant Recipients in the ICU
6. 28.6 Enhanced Recovery Principles
7. 28.7 Postoperative Delirium and Cognitive Dysfunction

Few aspects of critical care affect both the patient's experience and the patient's outcome as directly as the management of pain, agitation, and distress. For decades, deep sedation was treated as a kindness and a safety measure: a quiet, motionless patient on a ventilator was assumed to be a comfortable one. Experience and observation have overturned that assumption. Excess sedation prolongs mechanical ventilation, promotes delirium, obscures the neurologic examination, and leaves survivors with memories of fear and persistent psychological harm, whereas untreated pain drives tachycardia, hypertension, catecholamine release, immobility, and chronic pain syndromes. The modern approach asks the clinician to treat pain first, use the lightest sedation that allows safe care, and keep the patient awake, oriented, and participating whenever possible.

1. 29.1 Pain Assessment in Nonverbal and Ventilated Patients
2. 29.2 Multimodal Analgesia and Opioid Stewardship
3. 29.3 Sedation Strategies and Daily Interruption
4. 29.4 Neuromuscular Blockade
5. 29.5 Goals-of-Care Conversations
6. 29.6 Symptom Management at End of Life
7. 29.7 Ethics, Capacity, and Surrogate Decision-Making

Every preceding chapter has described what to do for a patient in a particular state of illness. This final chapter addresses a different question: how to ensure that what we know actually reaches the patient, reliably, at three in the morning, across handoffs, and through the transition from the intensive care unit (ICU) to the ward and from the hospital to home. Acute care is performed under conditions that predispose to error: high acuity, time pressure, incomplete information, complex technology, interruptions, fatigue, and a continuous stream of medications and procedures. Studies of hospital harm have consistently shown that a substantial fraction of patients experience an adverse event during admission, and a large proportion of those events are preventable. Safety is therefore not an add-on to clinical expertise but a property of the systems in which expertise is exercised.

1. 30.1 Safety Culture and Error Reduction
2. 30.2 ICU Liberation and Care Bundles
3. 30.3 Rapid Response and Early Mobilization
4. 30.4 Family Engagement and Communication
5. 30.5 Medication Reconciliation and Handoffs
6. 30.6 Discharge Planning and Post-Intensive Care Syndrome
7. 30.7 Evidence-Based Practice and Quality Improvement