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Heart and breath sounds

Glasgow coma scale

Cranial nerves Assessment and dysfunctions

Major deep tendon muscle stretch reflexes

Major superficial cutaneous reflexes

Inotropic and vasoactive medication infusions

Sample relaxation technique

Abbreviations used in this manual

Index

Ibc

Copyright

3251 Riverport Lane

St. Louis, Missouri 63043

MANUAL OF CRITICAL CARE NURSING: NURSING INTERVENTIONS AND COLLABORATIVE MANAGEMENT,

SEVENTH EDITION

ISBN: 978-0-323-18779-4

Copyright © 2016 by Elsevier, Inc. All rights reserved.

No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions.

This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher,

except that, until further notice, instructors requiring their students to purchase Book Title by Author, may reproduce the contents or parts thereof for instructional purposes, provided each copy contains a proper copyright notice as follows: Copyright © 2016 by Elsevier Inc. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions.

Notices

Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility.

With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of

any methods, products, instructions, or ideas contained in the material herein.

NANDA International, Inc. Nursing Diagnoses: Definitions & Classifications 2015-2017, Tenth Edition. Edited by T. Heather Herdman and Shigemi Kamitsuru. 2014 NANDA International, Inc. Published 2014 by John Wiley & Sons, Ltd. Companion website: www.wiley.com/go/nursingdiagnoses.

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Contributors

Patrice C. Al-Saden, BS, RN, CCRC, Senior Clinical Research Associate, Comprehensive Transplant Center, Feinberg School of Medicine, Chicago, Illinois

Sonia Astle, RN, MS, CCNS, CCRN, CNRN, Clinical Nurse Specialist, Critical Care, Inova Fairfax Medical Campus, Falls Church, Virginia

Carol Ann Batchelder, MSN, RN, CCRN, ACCNS-AG BC, Clinical Nurse Specialist, Intensive Care Units, Tri-campus, Northside Hospital System, Atlanta, Georgia

Risa Benoit, DNP, CNS-BC, Advanced Practice Nurse, Perioperative Services, Sarasota Memorial Healthcare System, Sarasota, Florida

Cheryl L. Bittel, MSN, APRN, CCNS, NP-C, CCRN, Clinical Nurse Specialist, Emory Saint Joseph’s Hospital, Atlanta, Georgia

Carolyn Blayney, BSN, RN, Clinical Operation Manager, Pediatrics, Harborview Medical Center, Seattle, Washington

Madalina Boitor, BScN, RN, PhD Student, Ingram School of Nursing, McGill University, Montreal, Canada

Jemma Brown, MSN-ED, RN, CCRN, CCM-BC, Stroke Program Coordinator, Emory University Hospital Midtown, Atlanta, Georgia

Susan B. Cali, MSN, RN, MHA, Infection Control Coordinator, Emory University Hospital Midtown, Atlanta, Georgia

Mimi Callanan, MSN, RN, Epilepsy Clinical Nurse Specialist, Stanford Comprehensive Epilepsy Center, Stanford Health Care, Stanford, California

Gretchen J. Carrougher, MN, RN, Research Nurse Supervisor, Department of Surgery, Harborview Medical, Center, Seattle, Washington

Cynthia Rebik Christensen, MSN, CVN, ARNP-BC, Nurse Practitioner, Family Practice, Certified Vascular Nurse, Mobile Medical Professionals, Ankeny, Iowa

Janice C. Colwell, MS, RN, CWOCN, FAAN, Advanced Practice Nurse, University of Chicago Medicine, Chicago, Illinois

Alice E. Davis, PhD, GNP-BC, ACNP-BC, FNP-BC, Associate Professor, School of Nursing, University of Hawaii at Hilo, Hilo, Hawaii

Joni L. Dirks, MS RN-BC, CCRN-K, Manager Clinical Educators & ICU Educator, Providence Health Care, Spokane, Washington

Beverly George Gay, MSN, RN, Assistant Professor, Department of Nurse Anesthesia, School of Allied Health Professions, Virginia Commonwealth University, Richmond, Virginia

Céline Gélinas, PhD, RN

Associate Professor, Ingram School of Nursing, McGill University Researcher, Center for Nursing Research and Lady Davis, Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canada

Patricia R. Gilman, APRN, MSN, ACNS-BC

Adult Health Clinical Nurse Specialist, Cardiac ICU, Emory University Hospital (2012–2014), Atlanta, Georgia

Robert Wood Johnson Nursing & Health, Policy Collaborative Fellow, University of New Mexico College of Nursing, Albuquerque, New Mexico

Vicki S. Good, RN, MSN, CENP, CPSS, System Director

Quality/Safety, CoxHealth, Springfield, Missouri

Phyllis Gordon, MSN, APRN, ACNS-BC

Clinical Nurse Specialist, Vascular Surgery, Division Clinical Assistant Professor, School of Nursing, University of Texas Health Science Center, San Antonio, San Antonio, Texas

Kimberly Graham, MSN, APRN, ACNS-BC, Clinical Nurse Specialist, General Medical, Emory University Hospital Midtown, Atlanta, Georgia

Vinay Paul Singh Grewal, B.Sc., Medical Student, Windsor University School of Medicine, St. Kitts

Kiersten Henry, MSN, ACNP-BC, CCNS, CCRN-CMC, Acute Care Nurse Practitioner, Chief Advanced Practice Provider, MedStar Montgomery Medical Center, Olney, Maryland

Adina Hirsch, PharmD, BCNSP

Clinical Specialist–Nutrition Support, Critical Care, Saint Joseph’s Hospital of Atlanta;

Assistant Professor of Pharmacy Practice, School of Pharmacy, Philadelphia College of Osteopathic Medicine, Atlanta, Georgia

Beth Hundt, MS, APRN, NP-C, ACNS-BC

Clinical Nurse Specialist, Marcus Stroke & Neuroscience Center, Grady, Health System, Atlanta, GA (2012–2014); Clinical Nurse Specialist, Neuroscience Center of Excellence, University, of Virginia Health System, Charlottesville, Virginia (current)

Susie Hutchins, DNP, RN, Associate Clinical Professor, Coordinator, Simulation and Standardized Patient Lab for, MEPN, University of San Diego, Hahn School of Nursing, San Diego, California

Anne E. Hysong, MSN, APRN, CCNS, Clinical Nurse Specialist, Critical Care, Gwinnett Medical Center–Duluth, Duluth, Georgia

Jonathan Wesley Kandiah, B.Sc., Medical Student, All Saints University, St. Vincents and the Grenadines

Roberta Kaplow, PhD, APRN-CCNS, AOCNS, CCRN, Oncology

Clinical Nurse Specialist, Emory University Hospital, Atlanta, Georgia

Alice S. Kerber, MN, APRN, ACNS-BC, AOCN, APNG, Clinical Nurse Specialist, Oncology, Advanced Practice Nurse in Genetics, Georgia Center for Oncology Research and, Education (Georgia CORE), Atlanta, Georgia

Kathleen Kerber, MSN, RN, ACNS-BC, CCRN, Clinical Nurse Specialist, Medical Intensive Care Unit/Critical Care, Step Down Unit, MetroHealth Medical Center, Cleveland, Ohio

Barbara McLean, MN, RN, CCNS-BC, NP-BC, CCRN, FCCM, Critical Care Clinical Specialist, Critical Care Division, Grady Health Systems, Atlanta, Georgia

James P. McMurtry, MSN, APRN, CNS-BC, CCRN, Clinical Nurse Specialist, MICU; Pulmonary Critical Care, Emory University Hospital Midtown, Atlanta, Georgia

Maria Paulsen, BSN, RN, Critical Care Nurse, Coordinator, Trauma Outreach Education, Program, Harborview Medical Center, Seattle, Washington

Lisa Reif, MSN, RN, APRN-CCNS, CCRN, Clinical Nurse Specialist, Neuroscience ICU, Emory University Hospital, Atlanta, Georgia

Alan Sanders, PhD, Director, Ethics, Trinity Health, Newtown Square Office, Pennsylvania

Paul E. Schmidt, RPh, BCPS, Clinical Pharmacist, Critical Care, Northside Forsyth Hospital, Cumming, Georgia

Elizabeth Scruth, PhD, RN, MPH, FCCM, CCNS, CCRN

Clinical Practice Consultant, Clinical Effectiveness Team, Kaiser Permanente Northern California, Regional Quality and Regulatory Services, Oakland, California

Critical Care Transport RN, Bayshore Ambulance, Foster City, California

Maureen A. Seckel, MSN, RN, APN, ACNS-BC, CCNS, CCRN, FCCM, Clinical Nurse Specialist, Medical Pulmonary Critical Care, Christiana Care Health System, Newark, Delaware

Kara A. Snyder, MS, RN, CCRN, CCNS, Director, Quality Improvement and Outcomes, Management, Banner University Medical Center, Tucson, and South Campuses, Tucson, Arizona

Monica Tennant, MSN, APRN, CCNS, Critical Care Clinical Nurse Specialist, Emory Saint Joseph’s Hospital, Atlanta, Georgia

Daryl Todd, MS, APRN-CNS, CCCC, ACNS-BC, Certified

Cardiovascular Care Coordinator, Clinical Nurse Specialist, Coordinator Bariatrics and Chest Pain, Centers of Excellence, Clinical Support for, Hospice and Observation Units, Emory University Hospital Midtown, Atlanta, Georgia

Sharon Vanairsdale, MS, APRN, ACNS-BC, NP-C, CEN, Clinical Nurse Specialist, Emergency Department and Serious Communicable Disease Unit, Emory University Hospital, Atlanta, Georgia

Colleen Walsh-Irwin, DNP, RN, ANP, CCRN Cardiology Nurse Practitioner, Northport VAMC, Northport, New York;

Cardiovascular Clinical Nurse Advisor, Department of Veterans Affairs, Washington, DC; Clinical Assistant Professor, Stony Brook University, Stony Brook, New York

Joyce Warner, MN, RN, CCRN, Nurse Clinician, Surgical Intensive Care Unit, Emory Healthcare, Atlanta, Georgia

Karen E. Zorn, MSN, RN, ONC, Enterprise Solution Architect, Acute Care Integration, Emory Healthcare, Atlanta, Georgia

Reviewers

Bimbola Fola Akintade, PhD, ACNP-BC, MBA, MHA, CoSpecialty Director and Assistant Professor, Adult Gerontological Acute Care Nurse, Practitioner/Clinical Nurse Specialist, Program, University of Maryland Baltimore, School of Nursing, Baltimore, Maryland

David Allen, MSN, RN, CCRN, CCNS-BC, Deputy Chief, Center for Nursing Science and, Clinical Inquiry, Brooke Army Medical Center, Fort Sam Houston, TX 78109

Penelope S. Benedik, PhD, CRNA, RRT, Associate Professor of Clinical Nursing, University of Texas Health Science Center at, Houston, Houston, TX

Marcia Bixby, RN, MS, CCRN, APRN-BC, Critical Care Clinical Nurse Specialist, Consultant, Randolph, Massachusetts

Marylee Bressie, DNP, RN, CCRN, CCNS, CEN, Assistant Professor, University of Arkansas Fort Smith and, Capella University, Ft Smith, Arkansas and Minneapolis, Minnesota

Diane Dressler, MSN, RN, CCRN, Clinical Assistant Professor, Marquette University College of Nursing, Milwaukee, WI

Jennifer L. Embree, DNP, RN, NE-BC, CCNS, Clinical Assistant

Professor and Consultant, Indiana University School of NursingIndiana, University Purdue University Indianapolis, Indianapolis, Indiana

Joyce Foresman-Capuzzi, MSN, RN, CCNS, CEN, CPN, CPEN, CCRN, CTRN, SANE-A, AFN-BC, EMT-P, FAEN, Clinical Nurse Educator, Lankenau Medical Center, Wynnewood, PA

David Goede, DNP, ACNP-BC, Assistant Professor of Nursing, Hospitalist, Nurse Practitioner, University of Rochester School of Nursing, Rochester New York

Vinay Paul Singh Grewal, B.Sc., Medical Student, Windsor University School of Medicine, Basseterre, Saint Kitts & Nevis

Elizabeth A. Henneman, PhD, RN, CCNS, FAAN, Associate Professor of Nursing, University of Massachusetts Amherst, Amherst, Massachusetts

Jennifer M. Joiner, MSN, RN, AGPCNP-BC, CCRN-CSC, Clinical Nurse Educator, CTICU, and CCU Robert Wood Johnson University Hospital, New Brunswick, NJ

Irena L. Kenneley, PhD, APHRN-BC, CIC, Assistant Professor/Faculty Development Coordinator, Case Western Reserve University, Cleveland, Ohio

Julene B. Kruithof, MSN, RN, CCRN, Nurse Educator, Spectrum Health, Grand Rapids, Michigan

Elaine Larson, PhD, RN, FAAN, Anna C. Maxwell Professor of Nursing, Research, School of Nursing and Professor, of Epidemiology,

Mailman School of Public, Health, Columbia University, Columbia University, NY, NY

Rosemary K. Lee, DNP, ARNP-BC, CCNS, CCRN, Clinical Nurse Specialist, Homestead Hospital, Homestead, FL

Justin Milici, MSN, RN, CEN, CPEN, CFRN, CCRN, TNS, RN III Emergency Department, Parkland Health and Hospital System, Dallas, Texas

Fadi B. Nahab, MD

Associate Professor, Department of Necrology and Pediatrics, Emory University

Medical Director, Stroke Program, Emory University Hospitals, Atlanta, Georgia

Michaelynn Paul, MS, RN, CCRN, Assistant Professor, Walla Walla University, College Place, Washington

Julia Retelski, MSN, RN, CNRN, CCRN, CCNS, Clinical Nurse Specialist Neurosurgical Intensive Care Unit, Carolinas Health Care System, Charlotte, NC

Johnnie Robbins, MSN, RN, CCRN, CCNS, Critical Care Clinical Nurse Specialist, US Army Institute of Surgical Research, Fort Sam Houston, Texas

Tara L. Sacco, MS, RN, CCRN, ACNS-BC, ACCNS-AG, Visiting Assistant Professor, St. John Fisher College Wegmans School of, Nursing, Rochester, New York

Diane Vail Skojec, MS, DNP, CRNP, Nurse Practitioner,

Department of Surgery, The Johns Hopkins Hospital, Baltimore, Maryland

Scott C. Thigpen, DNP, RN, CCRN, CEN, Dean and Professor of Nursing, South Georgia State College, Douglas, Georgia

Judith A. Young, DNP, RN, CCRN, Clinical Assistant Professor, Indiana University School of Nursing, Indianapolis, Indiana

Preface

Manual of Critical Care Nursing is a clinical reference for both practicing nurses and students in critical care, progressive care, and complex medical-surgical units. It is the most comprehensive of the critical care handbooks available, yet is a concise and easy reference with an abbreviated outline format and a portable, trim size. This handbook provides quick information for more than 75 clinical phenomena seen in critical care and other high acuity care environments, which promotes evidence-based practice in planning goal-driven care.

Who will benefit from this book?

Nurses from novice to expert will have access to key information used to perform appropriate assessments, plan and implement care, and evaluate the outcomes of interventions provided to critically ill and acutely ill patients. The textual information and numerous tables will serve as a focused review for the practicing nurse and advanced practice providers. Academicians may find the book helpful in teaching students to apply didactic classroom information to clinical practice. Students will have an excellent tool for assessing the patient systematically, and setting priorities for nursing interventions.

Why is this book important?

The book provides information concisely, with emphasis on evidencebased practice and outcomes achievement. Goal-directed care is vital to patient safety, and promoting interdisciplinary collaboration. Both a collaborative plan of care, and specific nursing care plans are

presented. Given the increasing acuity of hospitalized patients, problems previously managed in critical care such as using arterial blood gas interpretation to correct acid-base imbalances, medically managing dysrhythmias with medication infusions, or controlling blood pressure with vasoactive drugs can be part of daily care of patients in progressive care units, telemetry, stepdown units, and high-acuity medical-surgical units. Accordingly, the care plans presented are applicable across the spectrum of high-acuity care, from complex medical-surgical to critical care. The book addresses the highly technical life-support equipment as part of the care options for each condition, and in detail for those who are actively using the technology in separate, detailed sections.

Benefits of using this book

The primary goal of this reference is to present the information necessary to provide patient- and family-centered care in a technologically advanced environment in a concise, easy-to-use format. The whole patient is addressed with care recommendations for physical, emotional, mental, and spiritual distress involved in illness. The prevention of potentially life-threatening complications is crucial to patient safety and addressed through collaborative, evidence-based care planning. The intent is to offer a thorough selection of prioritized actions that can be chosen as needed in planning individualized care.

How to use this book

Manual of Critical Care Nursing is organized for easy access and logical presentation. Information regarding general concepts of patient care, including those unique to the critical care environment, is presented in the first two chapters, General Concepts in Caring for the Critically Ill and Managing the Critical Care Environment. Following is a chapter on Trauma and related disorders. Chapters 4 through 10 cover disorders classified by body systems, and Chapter 11 addresses Complex Special Situations, such as high-risk obstetrics and organ

transplantation.

Each body system–specific chapter includes a general physical assessment, and several chapters include generic plans of care applicable to patients with all disease processes affecting that body system. Each disorder includes a brief review of pathophysiology, physical assessment, diagnostic testing, collaborative management, NANDA-approved nursing diagnoses and nursing interventions, patient/significant other teaching, desired outcomes, and diseasespecific discharge planning considerations. Gerontologic icons highlight material relevant to the care of older adults, bariatric icons have been added for care specific to people of size, and safety alerts highlight key information needed to prevent complications. Desired nursing care outcomes and interventions are based on the University of Iowa’s Nursing Intervention Classification (NIC) and Nursing Outcomes Classification (NOC) systems and are highlighted throughout the text. Nursing interventions are linked to nursing diagnoses, and suggested outcomes include specific measurement criteria for physical parameters and time frames for attainment of expected outcomes. The suggested time frames for outcomes achievement are guidelines. Each patient’s response to the illness and interventions is unique.

For clarity and consistency throughout the book, normal values are given for hemodynamic monitoring and other measurements. All values should be individualized to each patient’s baseline health status.

New to this edition

The seventh edition has been revised to further emphasize evidencebased practices and patient safety and mirrors a practicing nurse’s approach to patient care. Changes include:

• Enhanced patient safety information, including new patient safety alerts.

• Updated evidence-based guidelines, including evolving strategies for management of heart and respiratory failure, and advances in

technology associated with mechanical ventilation, cardiac mechanical assist devices, and hemodynamic monitoring.

• Information to help assess and plan care for bariatric patients.

• Enhanced medical and nursing management information for correction of acid-base imbalances, management acute asthma, brain injury, burns, sepsis, organ transplantation, obstetric emergencies, cardiogenic shock, heart and respiratory failure, and the management of altered mental status including delirium.

• Appropriate resuscitation interventions within the section on Dysrhythmias and Conduction Disturbances.

I hope that critical care and high-acuity acute care providers, students, and academicians will find that the new edition of Manual of Critical Care Nursing provides a wealth of updated, concisely comprehensive, easy-to-access knowledge applicable to clinical practice as well as the classroom.

Acknowledgments

I want to thank many individuals who supported the development of this manuscript. In particular, I am grateful for the time and efforts of the Elsevier Science staff, including Melissa Rawe, Content Development Specialist, and Marquita Parker, Senior Project Manager, Book Production. I appreciate the guidance of Lee Henderson, Executive Content Strategist. I thank all the contributors for their work, as well as all the reviewers whose comments helped guide our revisions. All are recognized as shining stars in their own right. Both perseverance and patience are the fundamental characteristics inherent in all participants.

Marianne Saunorus Baird

I acknowledge the support of my daughter Rachel, my best cheerleader, and my husband Thom for his patience. I also cannot thank the authors enough for your attention to detail; particularly all the new authors who “filled the gaps” from Emory Healthcare, Atlanta, Georgia. I would also like to acknowledge Savannah Davis, who helped the team begin our process with Elsevier Science.

CHAPTER 1

General concepts in caring for the critically ill

Acid-base imbalances

Cells must transport ions, metabolites, and gases to function appropriately in their respective roles in the body. For this to occur, the chemical environment of the bloodstream must be electrically stable. The stability of the environment is measured by the arterial pH and must be chemically neutral (pH 7.40) for all systems to function properly. The arterial blood gas (ABG) is the most commonly used analysis to measure acid-base balance and to assess the efficacy of oxygenation. Respiratory (CO2) and metabolic acids (H+) are generated as cells work and must be buffered or eliminated to maintain a neutral chemical environment. When the chemical environment is no longer neutral, the patient has an acid-base imbalance. Ineffective metabolism (tissue level), renal dysfunction, and/or problems with ventilation (breathing gasses effectively) are often the cause of acid-base imbalance.

There are two main types of acid-base imbalance: acidosis and alkalosis. The kidneys and lungs work in tandem to maintain chemical neutrality, but it is actually cellular function that produces acid. When either the kidneys or lungs are overfunctioning or underfunctioning, the other system is designed to have the opposite response to compensate and bring the pH back to a normal range. When the kidneys fail to regulate metabolic acids (H+), the lungs must compensate. When the lungs fail to regulate respiratory acid (CO2), the kidneys must compensate. Additional buffering mechanisms are also available to help regulate the accumulation of acids. Control of

alkaline states, resulting from accumulation of bases or loss of acids, is maintained in a similar manner between the lungs and kidneys.

Pathophysiology of acid-base regulation

Arterial pH is an indirect measurement of CO2 and H+ concentration, which reflects the overall level of acid and effectiveness of maintaining the balance. The normal acid-base ratio is 1:20 1 part acid (the H+ and CO2 component of H2CO3) to 20 parts base (HCO3 ). If the ratio is altered through an increase or a decrease in either acid H+ , or CO2, or the base, HCO3 , the pH changes. Chemically, the CO2 does not contain H+ , but when dissolved in water (plasma), CO2 + H2O yields H2CO3 (carbonic acid). CO2, when combined with H2O, becomes the largest contributor of H+ (acids), which must be eliminated or buffered to maintain normal pH. Too many H+ ions in the plasma create acidemia (pH less than 7.35), whereas too few H+ ions create alkalemia (pH greater than 7.45).

Maintaining the 1:20 ratio (“the balance”) depends on the ability of the lungs and kidneys to help normalize concentrations of carbonic acid (H2CO3), a product of hydrogen ion (H+) plus bicarbonate buffer (HCO3 ). Both the kidneys and lungs are designed to eliminate carbonic acid effectively, and therefore without the presence of lung or kidney disease, the pH should always be in the normal range. A pH change is a symptom that there is a significant problem with one or both of the systems.

• Acidosis: Extra acids are present or base is lost, with a pH less than 7.35.

1. Cellular acidosis: When cells are hypoxic or processing proteins to yield glucose, there is an increase in lactic acid or ketoacid.

2. Respiratory acidosis: If lung function is inadequate, such as in chronic obstructive pulmonary disease (COPD), the failure to effectively ventilate results in the inability to excrete CO2, and that failure causes carbonic acid to increase (more acid) and pH to decrease.

3. Renal acidosis: When the kidney function is inadequate, the ability to break down carbonic acid into H+ and HCO3 is impaired. When this failure occurs, carbonic acid increases (more acid) and pH decreases.

• Buffering of acid or compensation for acidosis occurs in three primary ways:

1. Plasma and cellular buffering: Using bicarbonate, proteins, intracellular electrolytes, and chloride to buffer H+ , the most common is the marriage of H+ and HCO3 , which yields carbonic acid (H2CO3).

2. Hyperventilation (lungs): The presence of increased carbonic acid stimulates a hyperventilation response. This allows for exhaling (“blow off”) more of the CO2 component of carbonic acid. This compensatory response for metabolic acidosis occurs within minutes and should bring the pH to a normal range.

3. Acid excretion (kidneys): A functional kidney will use increased carbonic acid by breaking H2CO3 into bicarbonate and H+ , excreting H+ and retaining bicarbonate. This should compensate for the increased respiratory acidosis but is very slow, taking 4 to 48 hours for compensation to occur.

• Alkalosis: Extra base is present or there is loss of acid, with a pH greater than 7.45.

1. Respiratory alkalosis: When hyperventilation is the primary problem, there is a very rapid removal of CO2, causing carbonic acid to decrease (less acid) and pH to increase.

2. Renal alkalosis: If kidney function is overstimulated (e.g., with aggressive diuresis), there may be excessive loss of hydrogen ions (H+), causing carbonic acid to decrease (less acid) and pH to increase.

3. Other contributors: Gastric and intestinal removal of acids may occur when patients have diarrhea, vomiting, or when excessive gastric drainage influences the acid-base balance.

• Compensation for alkalosis occurs in two ways:

1. Hypoventilation: The respiratory system responds by

slowing ventilation and retaining CO2 (acid) to help compensate for metabolic alkalosis from any cause. This response occurs within minutes.

2. Renal response: The kidneys respond by retaining more acid (H+) and excreting more bicarbonate to help correct respiratory alkalosis. This response occurs within 4 to 48 hours.

Example of compensation (pH regulation)

When metabolic acids accumulate, they are drawn to bicarbonate. The binding of H+ and HCO3 buffers the acid. This yields an increase in carbonic acid (H2CO3) and causes the pH to decrease. Chemoreceptors are stimulated by the presence of this acid and the hypothalamus, if not damaged, triggers a hyperventilation response. Because H+ is not measured directly, the indirect calculation of bicarbonate or the base is used to evaluate the presence or absence of metabolic acid. As H+ increases, the bicarbonate or base decreases. When evaluating the acid-base balance, it is simplest to look at bicarbonate but to think of it in terms of how bicarbonate level also reflects the acid level. These values travel in completely opposite directions (when bicarbonate decreases, H+ increases and vice versa).

The lungs increase buffering to compensate for a failure of the kidneys or a cellular excess acid production to keep the pH balanced. The lungs do this by effectively exhaling more CO2 than usual, breaking down carbonic acid and therefore bringing the pH back toward normal.

When CO2 is retained or increased because of respiratory failure, the kidneys should, in turn, respond by processing the increased H2CO3. The kidneys separate the carbonic acid into H+ and HCO3 and excrete the H+ while retaining HCO3 bicarbonate. If either the kidneys or lungs do not respond to a pH change (no compensation) or they provide an ineffective response (partial compensation), the patient will remain in acid-base imbalance. If the pH is outside the normal

range, then there is a primary problem and compensation is inadequate or has failed. Patients may have a pure acidosis or alkalosis and the overall problem may be masked by compensation or two problems presenting at the same time.

Unless the patient has ingested acid (aspirin, ethanol, etc.), all acid in the bloodstream has been produced at the cellular level (Table 1-1). When evaluating patients, care providers must have a basic understanding of the acid-base balancing system. The main formula for maintenance of acid-base balance is:

Table 1-1

PRODUCERS AND REGULATORS OF ACID

Acid Pathways

Cells produce acid (acid production increases).

Cause

Hypermetabolic states, such as pain, hyperthermia, or inflammation. The respiratory and heart rates increase, and bicarbonate is initially consumed by buffering.

Tissues are hypoxic; anaerobic metabolism ensues resulting in lactic acidosis

Absolute insulin deficiency results in failure of glucose to be transported into cells.

Cells regulate acids When acid production (H+) increases, pH decreases, bicarbonate is initially consumed by buffering, and CO2 is exhaled in larger amounts, and H+ exchanges for K+ as cells buffer acid

Lungs regulate acid

When acid increases as a result of hypermetabolic states such as pain, hyperthermia, or inflammation, carbonic acid (H2CO3) increases and rapidly converts to CO2 and H2O The respiratory rate increases to blow off CO2

Measure

HCO3

Lactate level ↑

Blood glucose level ↑ Ketoacids ↑

pH ↓ HCO3↓ K+↑

Total serum CO2↓

Paco2↓

Kidneys regulate

When acid increases, tubules are affected by low blood pH, and work to neutralize increased carbonic acid

HCO3↑ Kidney function is

acid. (H2CO3) by separating it into H+ and bicarbonate HCO3. Kidneys excrete what is necessary to sustain normal pH if renal function is normal. If abnormal, kidneys may not perform this task.

assessed by serum blood urea nitrogen and creatinine; elevated blood urea nitrogen and creatinine indicate abnormal kidney function

The most important component identified is H2CO3 or carbonic acid. As carbonic acid increases (“goes up”), the pH decreases (“goes down”), reflecting the presence of acid. If carbonic acid decreases (“goes down”), the pH increases (“goes up”), reflecting the absence of acid. The equation is constantly shifting from left to right and right to left to maintain a normal H2CO3 and therefore a normal pH. Whatever causes the change of carbonic acid concentration (may be related to a regulation failure by either the lungs or kidneys or a metabolic acid production state) is the “primary culprit.” Identifying the origin or cause of the change in pH direction identifies the problem. Therefore, if the problem is too much acid (either increased CO2 or H+), carbonic acid increases and pH decreases. The primary problem is acidosis. Further evaluation is needed to determine whether failure to regulate the acid was ineffective regulation by the lungs, the kidneys, or an increase in cellular acid production (ketoacidosis or lactic acidosis).

Changes in pH are associated with changes in the potassium level. As the plasma level of nonvolatile or metabolic acid (H+) increases, H+ moves into the cells to reduce the acidemia. In this case, H+ “exchanges places” with the intracellular potassium (K+), resulting in a measured serum hyperkalemia but is actually an intracellular hypokalemia. The positively charged intracellular potassium ions are replaced by positively charged hydrogen ions. During an alkalotic state, K+ may shift into cells as H+ is released into the serum, creating a transient hypokalemia. As pH changes, it is imperative for the care providers to observe the corresponding

changes in the K+ level, and manage K+ carefully. When the pH normalizes, the K+ will shift back to its original location. If a transient K+ change is managed too aggressively, the patient may experience dangerous hypokalemia or hyperkalemia when pH normalizes.

Understanding the arterial blood gas (ABG)

The ABG is the most commonly used measurement to help assess the origin of problems with acid-base imbalance and to guide treatment designed to restore pH balance and effective oxygenation. “Perfect” values reflect chemical neutrality. There are normal variations or a range for each value.

Arterial blood gas values

Blood gas analysis is usually based on sampling of arterial blood. Mixed venous blood sampling from a pulmonary artery (PA) catheter (SVO2) and central venous sampling from a central intravenous (IV) line (ScVO2) may also be performed for patients who are very critically ill. Venous values are given for reference only.

Normal Arterial Values Normal Venous Values

pH: 7.35–7.45 pH: 7.32–7.38

Paco2: 35–45 mm Hg Pvco2: 42–50 mm Hg

Pao2: 80–100 mm Hg Pvo2: 40 mm Hg

Sao2: 95%–100% Svo2: 60%–80%

Base excess (BE): –2 to +2 BE: –2 to +2 (only calculated on ABG analyzer)

HCO3 : 22–26 mEq/L Total serum CO2 : 23–27 mEq/L

pH (perfect 7.40, normal range 7.35 to 7.45): This reflects the level of respiratory and metabolic acids found in the blood during the continuous “balancing act” that regulates the acid environment. If this

balance is altered, derangements in pH occur. Any alteration in pH should be evaluated. If the pH has changed from perfect, it can only be one of two reasons: normal variation or abnormality with compensation. When pH is less than 7.35 or greater than 7.45, it is considered an acute change that is uncompensated. When full compensation is attained for an acid-base imbalance, the pH normalizes. Failure to bring the pH into normal range means there is failure to compensate, despite the body attempting to mount a response. Traditionally, if the body made an attempt to compensate, this was known as partial compensation. This term is no longer advocated.

PaCO2 (perfect 40, normal range 35 to 45 mm Hg): This is a measure of pressure (partial pressure designated by the P) that the dissolved CO2 exerts in the arterial blood. The dissolved gas exerts the pressure of CO2, enabling it to diffuse across the capillary and alveolar cell wall.

CO2 is released during aerobic metabolism and is the main contributor to serum acid. CO2 is controlled through ventilation. In the normal lung, CO2 is regulated by changes in the rate and depth of alveolar ventilation. CO2 is carried both bound to hemoglobin and dissolved in the blood. The measured CO2 is termed PaCO2. PaCO2 is directly measured (not calculated) and is a reliable indicator of respiratory acid-base regulation. The correlation between PaCO2 and respiratory-based pH changes is direct, consistent, and linear. In other words, if PaCO2 is up and pH is down, the cause is respiratory deregulation. If the issue is metabolic, and respiratory compensation has occurred, the PaCO2 will decrease to bring pH back to normal levels. Respiratory compensation typically occurs rapidly in metabolic acid-base disturbances as long as respiratory function is not impaired. When a patient hyperventilates, PaCO2 decreases as it is “blown off” by rapid exhalations. During hypoventilation (slow and/or shallow breathing), PaCO2 increases. Although the only way to evaluate true lung function is by the gas exchange, the capacity of the lungs (CO2 regulation response) is measured via the minute ventilation (VE or

MV). This measures the amount of volume exhaled per minute (VE) calculated as respiratory rate (RR) multiplied by tidal volume (VT).

Normal MV is approximately 8 to 10 L/min.

PaO2 (perfect 95 to 100 mm Hg, normal range 80 to 100 mm Hg): The partial pressure of oxygen (O2), or PaO2, is a measure of the dissolved (usable) gas in the arteries. The dissolved gas exerts the pressure of O2, enabling it to diffuse across the capillary and cell wall to oxygenate cells. PaO2 normally declines in the older adult.

• Hypoxemia (PaO2 less than 80 mm Hg): Low partial pressure of O2 affects the cellular levels of oxygen available and may result in cellular metabolic dysfunction reflected by lactic acid production and metabolic acidosis.

• FIO2: Fraction of inspired O2 or the percentage of the atmospheric pressure that is oxygenated. Room air is 21% or 0.21 O2. O2 delivery devices can increase the FIO2 to 100% or 1.00.

P/F ratio (greater than 300): PaO2 is evaluated in relationship to FIO2, that is, the higher the percent O2 pressure that is delivered to the lungs, the higher the O2 in the blood should be.

SaO2 (perfect 100% or 1.0, normal range 95% to 100% or 0.95 to 1.0): O2 saturation (SaO2) reflects the loading of O2 onto hemoglobin (Hgb) in the lungs. When Hgb is loaded with O2, it is termed oxyhemoglobin. Hgb is the primary transporter of O2 and supplies a reservoir (reserve) of O2 for cellular use. Each Hgb molecule carries 1.34 to 1.36 mL of O2. O2 must be released from the Hgb, dissolve in blood (PaO2), and exert pressure to diffuse across the cell wall. The uptake/use of O2 by the tissues is measured by SVO2 and/or ScVO2

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