Question Answer
THE AARC WAS ORGANIZED IN 1946 AS INHALATION THERAPHY ASSOCIATION ( ITA)
WHAT ECONOMIC DEVELOPMENT IN THE 1960S CAUSED HEALTH CARE TO FLOURISH IN THE UNITED STATES INCEPTION OF MEDICARE AND MEDICAED
YOU ARE THE RESPIRATORY THERAPIST FOR A 20 BED MEDICAL INTENSIVE CARE UNIT, AND MUST CORRECT A MALFUNCTIONING MECHANICAL VENTILATOR. THIS REQUIRES THE USE OF WHICH OF THE FOLLOWING PROBLEM SOLVING SKILLS? TROUBLESHOOTING
A PIONEER IN PULMONARY MEDICINE, ORGANIZED AND EARLY INHALATION THERAPY PROGRAM IN 1943 AT CHICAGO’S MICHAEL REESE HOSPITAL EDWIN R. LEVINE
HEALTH CARE REFORM HAS CENTERED AROUND WHICH OF THE FOLLOWING ISSUES DECREASING COST IMPROVING QUALTIY EVALUTAING EFFECTIVENESS USING MEASURABLE OUTCOMES IMPROVING RESOURCE ALLOCATION
THE ART AND SCIENCE OF RESPIRATORY CARE ARE SUPPORTED BY THE JOUNALS OF THE AARC, WHICH INCLUDES RESPIRATORY CARE, AARC TIMES, EDUCATION ANNUAL SUBACUTE CARE TODAY
CRITICAL THINKING SKILLS HAVE BEEN RECONGNIZED AS AN ESSENTIAL PART OF THE RESPIRATORY CARE PROFESSION ACCORDING TO AMERICAN ASSOCIATION FOR RESPIRATORY CARE ( AARC), NATIONAL BORAD FOR RESPIRATORY CARE ( NBRC) COMMITTEE ON ACCREDITATION OF RESPIRATORY CARE( COARC)
THE AARC WAS ORGANIZED IN 1946 AS THE INHALATION THERAPY ASSOCIATION ( ITA)
WHAT ECONOMIC DEVELOPMENT IN THE 1960″S CAUSED HEALTH CARE TO FLOURISH IN THE UNITED STATES INCEPTION OF MEDICARE AND MEDICAID
THE INHALATION THERAPY ASSOCIATION ( ITA) WAS CHARTED BY APRIL 5, 1947 FOR WHAT PURPOSE PROMOTE HIGHER STANDARDS IN METHODS AND PROFESSIONAL ADVANCEMENT OF IT MEMBERS
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE NATIONAL BOARD FOR RESPIRATORY CARE ( NBRC) IT IS A VOLUNTARY HEALTH- CERTIFYING BOARD
WHICH OF THE FOLLOWING STATEMENTS BEST DESCRIBES THE FEE-FOR SERVICE AGREEMENTS AN INDIVIDUAL OR INSURANCE CARRIER PAYS THE HEALTH CARE PROVIDER WHEN SERVICES ARE RENDERED
THE AMERICAN ASSOCIATION FOR RESPIRATORY CARE (AARC) SUCCESSFULLY USED THE ______ AS A TEMPLATE FOR SCIENTIFIC EXAMINATION OF EVERY FORM OF CLINICAL RESPIRATORY THERAPY SINCE 1974 SURGERLOAF CONFERENCE
PROBLEM BASED LEARNING INCLUDES WHICH OF THE FOLLOWING ELEMENTS PROBLEM- SOLVING STRATEGIES
THE NBRC OFFERS SEVERAL HEALTH CARE EXAMINATION AND CREDITIALS, WHICH CREDENTIALS ARE GRANTED BY THE NBRC CRT- CERTIFIED RESPIRATORY THERAPIST
THE INHALATION THERAPY ASSOCATION ( ITA) WAS CHARTED BY APRIL 5, 1947 FOR WHAT PURPOSE CREATE MUTUAL UNDERSTANDING AND COOPERATION AMONG THE TECHINCIAN, PHYSICAN, AND ALL OTHERS WORKING IN THE INTEREST OF THE PUBLIC HEALTH
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE NATIONAL BOARD FOR RESPIRATORY CARE ( NBRC) IT WAS FIRST NAMED THE AMERICAN REGISTRY OF INHALATION THERAPISTS( ARIT)
THE NBRC OFFERS SEVERAL HEALTH CARE EXAMINATIONS AND CREDENTIALS, WHICH OF THE FOLLOWING CREDENTIALS ARE GRANTED BY THE NBRC? RRT- REGISTERED RESPIRATORY THERAPIST
WHICH OF THE FOLLOWING TRENDS DEVELOPED AS A RESULT OF HEALTH CARE REFORM A DECLINE IN THE ABILTY OF HEALTH CARE PROVIDERS TO DELIVER UNCOMPENSATED CARE
THE ARRC OFFERS SEVERAL EDUCATIONAL ADVANATAGES, INCLUDING THE SPONSORSHIP OF THE COMMITTE ON ACCREDITATION FOR RESPIRATORY CARE
MR. SUMMERS IS SCHEDULED FOR BYPASS SURGERY IN 3 DAYS. OBTAINING PRE-OPERATIVE INSPIRATORY CAPACITY MEASUREMENTS WOULD REQUIRE___ TO PLAN AHEAD AND ENVISION POTENTIAL PROBLEMS ANTICIPATION
PROFESSIONAL PUBLICATION PROVIDE IN DEPTH INFORMATION ON CURRENT MEDICAL STUDIES AND ADVANCES. THE ____ WAS THE FIRST REGULARLY APPEARING PUBLICATION OF THE RESPIRATORY PROFESSION INHALATION THERAPY ASSOCIATION BULLETIN
WHICH OF THE FOLLOWING TRENDS DEVELOPED AS A RESULT OF HEALTH CARE REFORM? A DECLINE IN THE POPULATON OF INDIVIDUALS WITH PRIVATE INSURANCE
THE NBRC OFFERS SEVERAL HEALTH CARE EXAMINATIONS AND CREDENTIALS. WHICH OF THE FOLLOWING CREDENTIALS ARE GRANTED BY THE NBRC CPFT- CERTIFIED PULMONARY FUNCTION TECHNOLOGIST
PROBLEM BASED LEARNING INCLUDES WHICH OF THE FOLLOWING ELEMENTS REFLECTION OF PAST EXPERIENCES
THE INHALATION THERAPY ASSOCATION ( ITA) WAS CHARTED BY APRIL 5, 1947 FOR WHAT PURPOSE ADVANCE KNOWLEDGE OF INHALATION THERAPY THROUGH INSTITUTES, LECTURES, AND OTHER MEANS OF SPONSORSHIP
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE NATIONAL BOARD FOR RESPIRATORY CARE ( NBRC) ITS PRIMARY PURPOSE IS TO PROVIDE HIGH QUALITY, VOLUNTARY CREDENTIALING EXAMINATIONS FOR RESPIRATORY CARE AND PULMONARY FUNCTION TECHNOLOGY
PROBLEM BASED LEARNING INCLUDES WHICH OF THE FOLLOWING ELEMENTS LOGICAL REASONING SKILLS
THE NBRC OFFERS SEVERAL HEALTH CARE EXAMATIONS AND CREDENTIALS. WHICH OF THE FOLLOWING CREDENTIALS ARE GRANTED BY THE NBRC? RPFT- REGISTERED PULMONARY FUNCTION TECHNOLOGIST
WHICH OF THE FOLLOWING TRENDS DEVELOPED AS A RESULT OF HEALTH CARE REFORM GROWTH IN THE TOTAL NUMBER OF UNINSURED INDIVIDUALS
THE AARC COMPRISES SEVERAL GOVERNANCE AND ADVISORY BODIES INCLUDING? BOARD OF DIRECTORS ( BOD), HOUSE OF DELEGATES ( HOD) BOARD OF MEDICAL ADVISORS ( BOMA), EXECUTIVE OFFICE
CANDIDATES WHO ATTEMPTING TO CHALLENGE THE NBRC EXAMINATION MUST FULFILL WHICH OF THE FOLLOWING REQUIREMENTS GRADUATE FROM A PROGRAM RECOGNIZED BY CoARC OR JRCRTE
THE STANDARDS BY WHICH CoARC MEASURES PROGRAMS INCLUDE WHICH OF THE FOLLOWING? SPONORING
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE NATIONAL ASSOCIATION FOR MEDICAL DIRECTION OF RESPIRATORY CARE ( NAMDRC)? PRIMARY GOAL IS TO FURTHER THE ROLE THAT RESPIRATORY CARE MEDICAL DIRECTION PLAYS IN THE ACHIEVEMENT OF HIGH-QUALITY RESPIRATORY CARE
THE AMEIRICAN COLLEGE OF CHEST PHYSICANS MEMBERSHIP INCLUDES MORE THAN 15,000 PHYSICIANS AND OTHER PROFESSIONALS DEDICATED TO THE ADVANCEMENT OF RESEARCH, TEACHING, AND CLINICAL PRACTICE
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE NATIONAL BOARD FOR RESPIRATORY CARE (NBRC) IT ESTABLISHES STANDARDS FOR THE CREDENTIALING OF PRACTITIONERS WHO WORK UNDER MEDICAL DIRECTION
THE NBRC OFFERS SEVERAL HEALTH CARE EXAMINATIONS AND CREDENTIALS. WHICH OF THE FOLLOWING CREDENTIALS ARE GRANTED BY THE NBRC P/PRCS- PERINATIAL/ PEDIATRIC RESPIRATORY CARE SPECIALIST
WHICH OF THE FOLLOWING TRENDS DEVELOPED AS A RESULT OF HEALTH CARE REFORM BUDGET REDUCTIONS IN MEDICARE AND MEDICAID
THE AARC OFFERS SEVERAL EDUCATIONAL ADVANTAGES INCLUDING A VENUE FOR EDUCATIONAL HIGHLIGHTS DURING THE ANNUAL CONVENTION
PROFESSIONAL PUBLICATIONS PROVIDE IN DEPTH INFORMATION ON CURRENT MEDICAL STUDIES AND ADVANCES. THE ____ WAS THE FIRST REGULARLY APPERAING PUBLICATION OF THE RESPIRATORY PROFESSION INHALATION THERAPY ASSOCIATION BULLETIN
WHICH STATEMENT BEST DESCRIBES THE COMMITTE ON ACCREDITATION FOR RESPIRATORY CARE ( CoARC) IT IS THE NATIONAL ACCREDITATION BODY FOR RESPIRATORY CARE EDUCATION PROGRAMS
TRADITIONAL SERVICES PROVIDED BY RESPIRATORY THERAPY INCLUDE OXYGEN THERAPY
MR. SIMPSON HAS NOT BEEN TAKING HIS ANTIBIOTICS AS PRESCIRBED. IN RELAYING THIS INFORMATION TO HIS PHYSICAN, YOU MUS HAVE A MASTERY OF WHICH OF THE FOLLOWING SKILLS? COMMUNICATION
RESPIRATORY THERAPIST FUNCTION AS PHYSICIAN EXTENDERS IN WHICH AREA? ACUTE CARE
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE NATIONAL ASSOCIATION FOR MEDICAL DIRECTION OF RESPIRATORY CARE ( NAMDRC) PRIMARY GOAL IS TO FURTHER THE ROLE THAT RESPIRATORY CARE MEDICAL DIRECTION PLAYS IN THE ACHIVEMENT OF HIGH-QUALITY RESPIRATORY CARE
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE NATIONAL ASSOCIATION FOR MEDICAL DIRECTION OF RESPIRATORY CARE (NBRC) SEEK TO PROVIDE SUPPORT ACCROS A FULL RANGE OF PULMONARY CARE RELATED SERVICES
EFFECTIVE NEGOTIATION SKILLS ARE PRIMARLY INFLUENCED BY ONE’S ABLILITY TO COMMUNICATE
____IS THE INITIATION OF DISCUSSION TO INFLUENCE OTHERS, ESPECIALLY THOSE WITH AN OPPOSING VIEW NEGOTIATION
IN THE CRITICAL THINK PROCESS NAME 1 OF THE 6 “R”S” RECOGNIZE
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE RELATIONSHIP BETWEEN THE AMERICAN SOCIETY OF ANESTHESIOLOGIST(ASA)AND RESPIRATORY CARE THE ASA IS A SPONSORING MEMBER OF THE AARC, NBRC, AND CoARC
WHICH OF THE FOLLOWING THE EXPECTED RESPIRATORY THERAPIST ROLE IN CLINICAL DECISION MAKING ASSESS TO OBTAIN DATA
WHAT IS A METHOD OF CLINICAL DECISION MAKING PROBLEM SOLVING
WHAT IS A NONTRADITIONAL ROLE OF A RESPIRATORY THERAPIST HOME HEALTH
TRADITIONAL SERVICES PROVIDED BY RESPIRATORY THERAPHY INCLUDE PHYSIOLOGIC MONITORING
RESPIRATORY THERAPIST FUNCTION AS PHYSICAIN EXTENDERS IN WHICH AREA? TRADITIONAL HOSPITAL SETTINGS
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE NATIONAL ASSOCIATION FOR MEDICAL DIRECTION OF RESPIRATORY CARE( NAMDRC) MAINTAINS A HIGHLY RESPECTED PROFILE WITH REGULATING AGENCIES AND LEGISLATORS
IN THE CRITICAL THINKING PROCESS WHAT IS 1 OF THE 6 “R’S” RATIONALE
WHICH OF THE FOLLOWING ARE CLASSIFIED AS NONTRADITIONAL ROLES OF RESPIRATORY THERAPIST DIAGNOSTICS
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE NATIONAL BOARD FOR RESPIRATORY CARE ( NBRC) IT IS A VOLUNTARY HEALTH CERTYING BOARD
CANDIDATES WHO ATTEMPT TO CHALLENGE THE NBRC EXAMINATION MUST FULFILL WHICH OF THE FOLOWING REQUIREMENTS BE 18 YEARS OF AGE OR OLDER
THE STANDARDS BY WHICH CoARC MEASURES PROGRAMS INCLUDE WHICH OF THE FOLLOWING OUTCOMES ORIENTATION
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE NATIONAL ASSOCIATION FOR MEDICAL DIRECTION OF RESPIRATORY CARE( NAMDRC) SEEK TO PROVIDE SUPPORT ACROSS A FULL RANGE OF PULMONARY CARE RELATED SERVICES
AMERICAN COLLEGE OF CHEST PHYSICIANS ( ACCP) DESIGNATION RCP INDICATES RECOGNITION AS A SPECIALIST IN THE FIELD
THE AARC OFFERS SEVERAL EDUCATIONAL ADVANTAGES INCLUDING A VECHILE FOR EXPOSURE OF RESEARCH BY RESPIRATORY THERAPIST AND OTHERS TO THE SCRUTINY OF THE MEDICAL COMMUNITY
TRADITIONAL SERVICES PROVIDED BY RESPIRATORY THERAPY INCLUDE VENTIALTION
RESPIRATORY THERAPISTS FUNCTION AS PHYSICIAN EXTENDERS IN WHICH AREA PHYSICIAN OFFICES
WHICH OF THE FOLLOWING ARE CLASSIFED AS NONTRADTIONAL ROLES OF RESPIRATORY THERAPIST SUBACUTE CARE
WHAT ARE 1 OF THE FOUR CLINICAL DECISION MAKING METHODS REASONING
WHICH OF THE FOLLOWING ARE EXPECTED RESPIRATORY THERAPIST ROLE CLINICAL DECISION MAKING ANALYZE DATA TO FORM AN INITIAL DIAGNOSIS
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE RELATIONSHIP BETWEEN THE AMERICAN SOCIETY OF ANESTHESIOLOGIS ( ASA) AND RESPIRATORY CARE THE ASA SUPPORTS AARC THROUGH ITS DEVELOPMENT OF POSITION STATEMENTS AND CLINCIAL PRACTICE GUIDELINES
IN THE CRITICAL THINKING PROCESS WHAT ARE 1 OF 6 “R’S” REFLECT
TRADITIONAL SERVICES PROVIDED BY RESPIRATORY THERAPY INCLUDE? RESPIRATORY THERAPEUTICS
PROBLEM BASED LEARNING INCLUDES WHICH OF THE FOLLOWING ELEMENTS RECALL OF FACTURAL INFORMATION
SOCIETY OF CRITICAL CARE MEDICING ( SCCM) IS DIRECTLY INVOLVED IN THE AARC THROUGH THE BOARD OF MEDICAL ADVISORS (BOMA)
THE AARC COMPRISES SEVERAL GOVERNANCE AND ADVISORY BODIES INCLUDING HOUSE OF DELEGATES (HOD)
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE NATIONAL BOARD FOR RESPIRATORY CARE ( NBRC) IT WAS FIRST NAMED THE AMERICAN REGISTRY OF INHALATION THERAPIST ( ARIT)
CANDIDATES WHO ATTEMPT TO CHALLENGE THE NBRC EXAMINATION MUST FULFILL WHICH OF THE FOLLOWING REQURIEMENTS GRADUATED FROM A PROGRAM ACCREDITED BY THE COMMISSION ON ACCREDITATION OF ALLIED HEALTH EDUCATION PROGRAMS ( CAAHEP)
THE AARC COMPRIES SEVERAL GOVERNANCE AND ADVISORY BODIES INCLUDING BORARD OF MEDICAL ADVISORS ( BOMA)
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE NATIONAL ASSOCIATION FOR MEDICAL DIRECTION OF RESPIRATORY CARE ( NAMDRC) MAINTAINS A HIGHLY RESPECTED PROFILE WITH REGULATING AGENCIES AND LEGISLATORS
THE STANDARDS BY WHICH CoARC MEASURES PROGRAMS INCLUDE WHICH OF THE FOLLOWING RESOURCES
IN THE CRITICAL THINKING PROCESS WHAT ARE 1 OF 6 “R’S” RAPID
WHICH OF THE FOLLOWING ARE EXPECTED RESPIRATORY THERAPIST ROLE IS CLININCAL DECISION MAKING DEVELOP A TREATMENT PLAN APPROPRIATE FOR EACH PATIENT
WHAT ARE 1 OF FOUR CLINICAL DECISION MAKING METHODS CRITICAL THINKING
WHICH OF THE FOLLOWING ARE CLASSIFIED AS NONTRADITIONAL ROLES OF A RESPIRATORY THERAPIST CASE MANAGEMENT
THE AARC OFFERS SEERAL EDUCATIONAL ADVANTAGES, INCLUDING PARTICIPATION IN PROGRAMS APPROVED FOR CONTINUING RESPIRATORY CARE EDUCATION UNITS ( CRCE)
THE AARC COMPRIES SEVERAL GOVERNANCE AND ADVISORY BODIES INCLUDING EXECUTIVE OFFICE
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE NATIONAL BOARD FOR RESPIRATORY CARE ( NBRC) ITS PRIMARY PUPOSE IS TO PROVIDE HIGH QUALITY, VOLUNTRY CREDENTIALING EXAMINATIONS FOR RESPIRATORY CARE AND PULMONARY FUNCTION TECHNOLOGY
THE STANDARDS BY WHICH CoARC MEASURES PROGRAMS INCLUDE WHICH OF THE FOLLOWING STUDENT DISCLOSURE
IN THE CRITICAL THINKING PROCESS WHAT ARE 1 OF THE 6 “R’S” ROLE
WHAT 1 OF THE FOUR CLINICAL DECSION MAKING METHODS DECISION MAKING
HEALTH CARE REFORM HAS CENTERED AROUND WHICH OF THE FOLLOWING ISSUES DECREASING COSTS
WHAT ECONOMIC DEVELOPMENT INTHE 1960’S CAUSED HEALTH CARE TO FLOURISH INTHE UNITED STATES PROSPETIVE PAYMENT SYSTEM
WHAT OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE MANAGED CARE SYSTEM IT EVOLVED TO PALCE CONSTANT PRESSURE ON HEALTH CARE PROVIDERS TO RESTRAIN HEALTH CARE COSTS AND CONTROL USE
WHAT SIGNIFICANT CHANGES INDEOMGRAPHICS HAVE HAD A DIRECT INFLUENCE ON THE HEALTH CARE SYSTEM ETHNICITY
EPDEMIOLOGIC CHANGES HAVE BROUGHT ABOUT THE DEVELOPMENT AND EXPANSIONOF OUTPATIENT AND SUBACUTE CARE DUE TO THE PREVALENCE OF DISEASE SUCH AS ASTHMA
WHAT SOCIOLOGIC VARIABLES HAVE SHIFTED THE FOCUS OF HEALTH CARE DELIVERY RECOGNITION THAT HEALTH CARE REQUIRES INDIVIDUAL RESPONSIBLITY FOR ONE’S HEALTH
TECHNOLOGY HAS HAD AN INFLUENCE ON WHICH AREA OF HEALTHCARE DELIVERY DIAGNOSTICS
IN THE CRITICAL THINKING PROCESS WHAT IS 1 OF THE 6 “R’S” REASONING
WHAT CHANGES IN THE HEALTH CARE DELIVERY SYSTEM REDEFINED THE GOAL OF EDUCATION AND TRAINING OF HEALTHCARE PROFESSIONALS MANAGED CARE, PROSPECTIVE- PAYMENT SYSTEM, PATIENT FOCUS CARE
WHICH OF THE FOLLOWING TRENDS AS A RESULT OF HEALTH CARE REFORM A DECLINE IN THE ABILTY OF HEALTH CARE PROVIDERS TO DELIVER UNCOMPENSATED CARE
THE HISTORICAL EVOLUTION OF RESPIRATORY THERAPY INCLUDES CREATION OF THE INHALATION THERAPY ASSOCIATION ( ITA) IN 1946
THE ROLE OF THE RESPIRATORY THERAPIST HAS EXPANDED TO INCLUDE INDUSTRY RELATED JOBS SUCH AS TECHNOLOGIC DESIGN
HEALTH CARE REFORM HAS CENTERED AROUND WHICH OF THE FOLLOWING ISSUES IMPORVING QUALITY
YOU ARE ATTEMPTING THE HEIMLICH MANEVER ON MR. WILSON, SUDDENLY GOESUNCONSCIOUS. THIS SITUATION CALL FOR ___ SKILL IN ORDER TO PLAN AHEAD AND ENVISION POTENTIAL PROBLEMS PRIORTIZING” RAPID THINKING”
EFFECTIVE NEGOTIATION SKILLS ARE PRIMARLY INFLUENCED BY ONE’S ABLITY TO COMMUNICATE
DECISION MAKING SKILL REQUIRES ANALYSIS OF WHICH OF THE FOLLOWING INFORMATION FACTUAL INFOMATION, ASSURANCE OF TOTAL SUCCESS
WHICH OF THE FOLLOWING DESCRIBES THE CHARACTERISTICS OF A CRITICAL THINKER WELL INFORMED
IN TRADITIONAL CLASSROOM, WHICH OF THE FOLLOWING LEARNING TEACHING STRATEGIES ARE HIGHLY STRCTURED PRESENTATION OF FACTUAL INFORMATION
HEALTH CARE REFORM HAS CENTERED AROUND WHICH OF THE FOLLOWING ISSUES EVALUATING EFFECTIVENESS USING MEASURABLE OUTCOMES
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE MANAGED CARE SYSTEM MANAGED CARE BROUGHT ABOUT PROSPECTIVE PAYMENT SYSTEMS TO REPLACE FEE-FOR SERVICE AGREEMENTS
WHAT SIGNIFICANT CHANGES IN DEMOGRAPHICS HAVE HAD A DIRECT INFLUENCE ON THE HEALTH CARE SYSTEM GEOGRAPHIC DISTRIBUTION OF THE POPULATION
EPIDEMIOLOGIC CHANGES HAVE BROUGHT ABOUT DEVEOLPMENT AND EXPANSION OF OUTPATIENT AND SUBACUTE CARE DUE TO THE PREVALENCE OF DISEASE SUCH AS CHRONIC BRONCHITIS
WHAT SOCIOLOGIC VARIABLES HAVE SHIFTED THE FOCUS OF HEALTH CARE DELIVERY REALIZATION THAT FOUCUS OF HEALTH CARE CAN NO LONGER BE ON SPECIFIC ILLNESSES FOR INDIVIDUAL PATIENTS
TECHNOLOGY HAS BEEN AN INFLUENCE ON WHICH AREAS OF HEALTHCARE DELIVERY THERAPEUTICS AND DRUG DELIVERY
WHICH OF THE FOLLOWING TRENDS DEVELOPED AS A RESULT OF HEALTH CARE REFORM GROWTH IN THE TOTAL NUMBER OF UNINSURED INDIVIDUALS
THE HISTORCIAL EVOUTION OF RESPIRATORY THERAPY INCLUDE INTRODUCTION OF AIR/OXYGEN BLENDERS, PULSE OXIMETRY, OXYGEN CONCENTRATORS, PORTABLE LIQUID OXYGEN SYSTEMS AND INTERMITTENT MANDATORY VENTILATION ( IMV) IN THE 1970″S
THE ROLE OF THE RESPIRATORY THERAPIST HAS EXPANDED TO INCLUDE INDUSTRY RELATED JOBS SUCH AS CONSULTING
ENOUGH MONEY IS AVAILABLE FOR EITHER A HEART TRANSPLANT FOR ONE PATIENT OR VACCINES FOR HUNDREDS OF INFANTS. USING THE TELEOLOGICAL THEORY OF ETHICAL DECISION MAKING WHAT CHOICE WOULD BE MADE USE THE MONEY TO BY THE VACCINES
THE ROLE OF THE RESPIRATORY THERAPIST HAS EXPANDED TO INCLUDE INDUSTRY RELATED JOBS SUCH AS PRODUCT DEVELOPMENT, MARKETING AND SALES
THE HISTORICAL EVOLUTION OF RESPIRATORY THERAPY INCLUDES TECHNOLOGIC ADVANCES IN THE AREAS OF PRESSURE CONTROL VENTILATION AND EXTRACORPOREAL MEMBRANE OXYGENATION ( ECMO) IN THE 1980″S AND 1990″S
TECHNOLOGY HAS HAD AN INFLUENCE ON WHICH AREAS OF HEALTHCARE DELIVERY GENE THERAPIES AND ORGAN TRANSPLANTS, ORGAN TRANSPLANTS AND LASER SURGERIES
WHAT SOCIOLOGIC VARABLES HAVE SHIFTED THE FOCUS OF HEALTH CARE DELIVERY EMPHASIS ON THE PATIENT’S EXPERINCE INCLUDING THE PSYCHOLOGICAL, SOCIOLOGIC, AND SPIRTUAL VARIABLES
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE MANAGED CARE SYSTEMS HEALTH MAINTANCE ORGANIZATIONS( HMO)’S AND PREFERRED PROVIDER ORGANIZATIONS ( PPO)’S ARE CLASSIFED AS MANAGED CARE COMPANIES
EPIDEMIOLOGIC CHANGES HAVE BROUGHT ABOUT THE DEVELEOPMENT AND EXPANSION OF OUTPATIENT AND SUBACUTE CARE DUE TO THE PREVALENCE OF DISEASE SUCH AS CONGESTIVE HEART FAILURE
IN A TRADITIONAL CLASSROOM, WHICH OF THE FOLLOWING LEARNING AND TEACHING STRATEGIES ARE HIGHLY STRUCTURED TIME FOR QUESTIONS AND DISCUSSION
EHTICS IS BEST DESCRIBED AS THE DECISION MAKING PROCESS USED TO DETERMINE RIGHT FROM WRONG
WHAT SOCIOLOGIC VARIABLES HAVE SHIFTED THE FOCUS OF HEALTH CARE DELIVERY IDEOLOGY THAT PATIENTS SATISFACTION, WELLNESS, AND QUALITY OF LIFE ARE IMPORTANT DETERMINANTS OF HEALTH
HEALTH CARE REFORM HAS CENTERED AROUND WHICH OF THE FOLLOWING ISSUES IMPROVING RESOURCES ALLOCATION
AN ETHICLA THEORY THAT EMPASIZES DUTY IS DEONTOLOGICAL
THE WORLD WARS BROUGHT THREE FUNDMENTAL ADVANCES TO RESPIRATORY THERAPY DEMAND BREATHING VALVES, ANTIBIOTICS, NONREBREATHIN VALVES AND MASKS
WHAT OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE MANAGED CARE SYSTEM UNDER THE MANAGED CARE SYSTEM, THE HOSPITAL RECEIVES A SET FEE PER DIAGNOSIS ON EACH PATIENT COVERED
EPIDEMIOLOGIC CHANGES HAVE BROUGHT ABOUT DEVEOLPMENT AND EXPANSION OF OUTPATIENT AND SUBACUTE CARE DUE TO THE PREVALENCE OF DISEASE SUCH AS PNEUMONIA
WHICH OF THE FOLLOWING DESCRIBES THE CHARACTERISTICS OF A ” CRITICAL THINKER” FLEXIBLE
IN A TRADITIONAL CLASSROOM, WHCIH OF THE FOLLOWING LEARNING AND TEACHING STRATEGIES ARE HIGHLY STRUCTURED DELIVERY OF LECTURE CONTENT
AN EFFECTIVE TEACHING AND LEARNING MODEL DESIGNED TO ENHANCE SELF-LEARNING AND CRITICAL THINKING IS PROBLEM BASED LEARNING
SOME CULTURES MAY NOT REGARD THE TRUTH AS THE SAME AS AMERICAN CULTURE. AS A RESULT FAMILY MEMBERS MAY WANT TO WITHHOLD INFORMATION REGARDING A TERMINAL ILLNESS FROM THE PATIENT. IF THE INFORMATION IS NO FORTHRIGHTLY PRESENTED TO THE PATIENT IT IS CALLED? BENEVOLENT DECEPTION
DURING PROBLEM BASED LEARNING SESSION, GROUP DISCUSSION PROVIDE EACH INDIVIDUAL A CHANCE TO DEVELOP COMMUNICATION SKILLS
THE ETHICAL GUIDELINE FOR RESPIRATORY THERAPISTS IS THE AARC CODE ETHICS
EVALUATION OF STUDENTS IN PROBLEM BASED LEARNING MAY INCLUDE WHICH OF THE FOLLOWING ATTRIBUTES WRITTEN EXAMS
WHICH OF THE FOLLOWING DESCRIBES THE CHARTERISTICS OF A ” CRITICAL THINKER” INQUISTIVE
AN EXAMPLE OF A TYPICAL PROBLEM BASED COUSRE IN RESPIRATORY CARE IS ONE WHICH STUDENTS ARE GIVEN A ____THAT GRADUALLY UNFOLDS OVER SEVERAL GROUP SESSIONS TEXTBOOK AND REFERENCE SOURCES
A ____IS THE EXPERT PERSON USING PROBLEM BASED LEARNING IN A COURSE FACILITATOR
CRITICAL TO SUCCESSFUL PROBLEM BASED LEARNING IS THE ___ LEARNING PROCESS ACTIVE
BY 1947, OXYGEN DEMAND VALVES WERE USED IN IPPB DEVICES. THE IPPB DEVICES HAD NEBULIZERS USED TO DELIVER ANTIBOTIC, MUCOLYTIC AGENTS, BRONCHODIALTORS
WITH IPPB, THERAPIST COULD MODIFY THE PERCENT OF INSPIRED OXYGEN. THE ABBREVIATION FOR PERCENT OF INSPIRED OXYGEN IS FIO2
ATERIAL BLOOD GAS, ABG, ANALYSIS WAS A TECHNOLOGY THAT ADVANCED THE RESPIRATORY THERAPY PROFESSION. WHICH OF THE FOLLOWING ARE MEASURED ON AN ABG ANALYSIS PH, PCO2, PO2
DURING PROBLEM BASED LEARNING SESSION, GROUP DISCUSSION PROVIDE EACH INDIVIDUAL A CHANCE TO DEVELOP NEGOTIATION SKILLS
EVALUATON OF STUDENTS IN PROBLEM BASED LEARNING MAY INCLUDE WHICH OF THE FOLLOWING ATTRIBUTES PEER EVALUATION, ABILTIY TO DEELOP HYPOTHESES AND SOLUTIONS, TYPES OF QUALITY OF PRESENTATION AND DISCUSSION
DURING PROBLEM BASED LEARNING SESSIONS GROUP DISSCUSION PROVIDE EACH INDIVIDUAL A CHANCE TO DEVELOP REFELCTION ON IDEAS AND ACTIONS, DECISION MAKIING SKILLS
AS TECHNOLOGY ADVANCED THE EMPHASIS ON EXTERNAL RESPIRATION TRANSITIONED TO RESPIRATION. RESPIRATION HAS 3 COMPONENTS VENTILATION, DIFFUSION, PURFUSION
RESPIRATORY THERAPY CREDENTIALING AND BOARD EXAMS ARE THE FUNCTION OF THE NATIONAL BOARD OF RESPIRATORY CARE ( NBRC)
THE SURGARLOAF CONFERENCE OF 1974 REVIEWED THE EFFICACY OF OXYGEN THERAPY, AEROSOL THERAPY, PHYSICAL THERAPY, AND IPPB THERAPY. THIS CONFERENCE QUESTIONED THE USE AND MISUSE OF IPPB AS RESULT OTHER MODES OF THERAPY WITH BETTER EFFICACY REDUCED THE OVERUSE OF IPPB
THE ENTRY- LEVEL CREDENTIAL FOR RESPIRATORY THERAPY IS CERTIFIED RESPIRATORY THERAPIST ( CRT)
CANDIDATES FOR THE RRT CREDENTIAL MUST DEMOSTRATE SUFFICENT FACTUAL DATABASE INFORMATION ON A RRT EXAM
THE CREDENTIAL FOR THE NEONATAL AND PEDIATRIC SPECIALTY IN RESPIRATORY THERAPY IS NPS
THE AMERICAN ASSOCIATION FOR RESPIRATORY CARE, AARC PUBLISHES SEVERAL JOURNAL. THE AARC’S SCIENTIFIC JOURNAL RESPIRATORY CARE
THE LARGEST PAYER FOR HEALTH SERVICES IN THE USA IS MEDICARE
CANDIDATES FOR THE RRT CREDENTIAL MUST PROCESS AND ASSES PATIENT DATA INTO CLINCIAL PRACTICE ON A RRT EXAM, PROCESS THE CRT CREDENTIAL
DEMOGRAPHICALLY THE FASTEST GROWING SEGMENT IN THE US IS OVER AGE 85 POPULATION
CIGARETTE SMOKING CONTRIBUTES TO AN INCREASED INCIDENCE OF CHORNIC OBSTRUCTIVE PULMONARY DISEASE, HEART DISEASE, CANCER
THE PREVAILING METHOD OF REIMBURSING HEALTH CARE COST TO PROVIDERS IS PROSPECTIVE PAYMENT
THE NATIONAL CONSENUS CONFERENCE ON RESPIRATORY CARE EDUCATION RANKED 41 MOST IMPORTANT AREAS THAT WILL BE INCLUDED INTHE FUTURE RESPIRATORY THERAPY SCOPE OF PRACTICE INCLUDE A PERSON ETHIC OF SOCIAL RESPONSIBLITY AND SERVICE, PROVIDE EVIDENCE-BASED, CLINCIALL COMPETENT CARE, DEMONSTRATE CRITICAL THINKING AND PROBLEM SOLVING
THE EVOLVING SCOPE OF PRACTIVE FOR RESPIRATORY THERAPY INCLUDES ACLS/NRP/PALS, MECHANICLA CARDIC SUPPORT, STRESS/EXERCISE TESTING
THE NATIONAL INSTITUTES OF HEALTH, NIH DEFINES PULMONARY REHABILITION AS MULTIDIMENSIONAL, INTERDESCIPLINARY CARE, WITH THE GOAL TO MAXIMIZE AN INDIVIDUAL’S INDEPENDENCE AND FUCTIONING IN THE COMMUNITY
TO BE EFFECITVE PRACTITIONER DN A VITAL, FUNCTIONING MEMBER OF TODAY’S HEALTH CARE TEAM, RESPIRATORY THERAPISTS NEED MORE THAN JUST A KNOWLEDGE BASE. THEY CRITICAL THINKERS, SEL- DIRECTED LIFELONG LEANERS
RESPIRATORY CARE PROFESSION HAS PLACED CONSIDERALBLE EMPHASIS ON THE NEED TO TRAIN PRACTITIONERS WHO CAN GATHER INFORMATION AND MAKE APPROPRIATE CLINCIAL DECISON. THIS EMPHASIS IS PARTICULARLY EVIDENT IN THE NBRC RRT CREDENTIALING EXAMS
THE ROLE OF THE STUDENT IN PROBLEM BASED LEARNING IS TO AN ACTIIVE LEARNER
THE ETHICAL DECISION MAKING THEORY THAT COMBINES CHARACTERISTICES OF DUTY AND CONSEQUENCE, WHICH ENVOLVES CRITICAL THINKING AND PROBLEM SOLVING SKILLS AND IS MOST USED BY HEALTH PROFESSIONALS IS THE ANALYSIS METHOD
THE PROVEAILING METHOD OF REIMBURSING HEALTH CARE COSTS TO PROVIDERS IS PROSPECTIVE PAYMENT
MANY SCIENTISTS, PHYSIOLOGIST, AND CHEMISTS MADE DISCOVERIES IN THE 17TH, 18TH AND 19TH CENTURIES THAT ARE USED IN RESPIRATORY THERAPY TODAY. WHICH INDIVIDUAL IS ATTRIBUTED WITH THE ” DISCOVERY OF OXYGEN”? JOSEPH PRIESTLY
WHEN WAS MODERN RESPIRATORY CARE ESTABLISHED AS A DISCRETE DISCIPLINE SHORTLY AFTER WORLD WAR II
A PHYSICAIN, EDWARD R. LEVINE, STARTED THE FIRST INHALATION THERAPY PROGRAM BECAUSE PULMONARY PATIENTS REQUIRED SPECIALIZED TRAINING
THE BETHANY MEDICAL CENTER RESPIRATORY THERAPY PROGRAM STARTED IN 1970 FORMED A PARTNERSHIP WITH KANSAS CITY COMMUNITY COLLEGE TO PROVIDE RESPIRATORY THERAPY EDUCATION IN WHAT YEAR 1984
WHICH OF THE FOLLOWING ARE RESPIRATORY THERAPY CREDENTIALS AWARDED BY THE NATIONAL BOARD FOR RESPIRATORY CARE CRT, RRT, CPFT, RPFT, NPS
RESPIRATORY CARE IS THE MODERN EXPRIESSIOIN TO DESCIBE THE RESPIRATORY THERAPY DISCIPLINE. IT IS USED BECAUSE? RESPIRATORY THERAPY IS MUCH MORE INVOLVE THAN THERAPY ALONE
THE EXPRESSION ” CODE BLUE” WAS FIRST COINED WHERE? KANSAS CITY’S BETHANY MEDICAL CENTER
THE PROTOTYPE POSITIVE PRESSURE MECHANICAL VENTIALOR, THE MA-1 OF THE 1970’S WAS MANUFACTURED BY A COMPANY BASED IN KANSAS CITY
A PHYSICAIN, EDWARD R. LEVINE, STARTED THE FIRST INHALATION THERAPY PROGRAM PULMONARY PATIENTS NEEDED MORE BEDSIDE CARE THAN PHYSICIANS COULD CONSISTENTLY GIVE
THE SUGARLOAF CONFERENCE HELD BY THE NHLI AND THE ATS IN 1974 RESULTED IN WHICH OF THE FOLLOWING? SCRUTINIZING IPPB
CoARC IS THE _______ THE ACCREDITATION AGENCY FOR RESPIRATORY THERAPY SCHOOLS
AARC IS THE _________ NATIONAL PROFESSIONAL ORGANIZATION FOR RESPIRATORY CARE PRACTITIONERS
RESPIRATORY CARE CLINICAL PRACTIVE GUIDELINES ARE__________ EVIDENCE- BASED BENCH MARKS FOR RESPIRATORY THERAPY
RESPIRATORY THERAPISTS MUST BE CRITICAL THINKERS. THERAPISTS SOLVE CLINICAL PROBLEMS FOR CLIENTS USING CRITICAL THINKING SKILLS. SUCH AS DECISION MAKING, TROUBLESHOOTING, ANTICIPATION
COMMUNICATION IS REFERRED TO AS PEOPLE THINK
WHAT ARE THE ABILITIES AND CHARACTERISTICS OF RESPIRATORY THERAPISTS WHO ARE CRITICAL THINKERS SELF-CONFIDENT, WELL INFORMED, INQUISTIVE
A PHYSICIAN, EDWARD R. LEVINE STARTED THE FIRST INHALATION THERAPY PROGRAM BECAUSE NURSES WERE TOO BUSY TO HANDLE ALL OF THE PULMONARY PATIENTS
PROBLEM BASED LEARNING IS A TERM TO DESCRIBE LEARNING THROUGH CRITICAL THINKING
A PHYSICIAN EDWARD R. LEVINE, STARTED THE FIRST INHALATION THERAPY PROGRAM BECAUSE TECHNOLOGY WAS DRIVING THE EVOLUTION OF RESPIRATORY CARE
IN PROBLEM BASED LEARNING ____? THE INSTRUCTOR IS A FACILITATOR
AN ETHICAL THEORY THAT EMPHASIZES DUTY IS DEONTOLOGICAL
THE ETHICAL GUIDELINE FOR RESPIRATORY THRAPISTS IS THE AARC CODE OF ETHICS
THE AARC STATEMENT OF ETHICS AND PROFESSIONAL CONDUCT INCLUDES A STATEMENT PATIENT CONFIDENTIALITY
THE INSTRUCTOR’S ROLE IN PROBLEM BASED LEARNING INCLUDES ALL OF THE FOLLOWING GUIDING STUDENTS, PROVIDING DIRECTION
THE STUDENTS PRIMARY ROLE IN PROBLEM BASED LEARNING IS _____? ACTIVE LEARNING
THE SUGARLOAF CONFERENCE HELD BY THE NHLI AND THE ATS IN 1974 RESULTED IN WHICH OF THE FOLLOWING AARC USING THE EXAMPLES AS A TEMPLATE FOR SCIENTIFIC BASED RESPIRATORY THERAPY
IN PROBLEM BASED LEARNING ALL OF THE FOLLOWING ELEMENTS STUDENTS ARE SELF- DIRCTED LEARNERS, PBL ALLOWS FOR INDIVIDULIZED INSTRUCTION
THE AARC STATEMENT OF ETHICS AND PROFESSIONAL CONDUCT INCLUDES A STATEMENT ON SCOPE OF PRACTICE, CONTINUING EDUCATION AND PROFESSIONAL COMPETENCE
THE POIOMYELITIS EPIDEMIC OF THE 1930’S LAUNCHED THE DEVELOPMENT OF THE ______FOR USE IN MECHANICAL VENTILATION NEGATIVE PRESSURE TANK VENTILATOR”IRON LUNG”
WHO DEVELOPED THE FIRST FULL-BODY IRON LUNG IN 1864 ALFRED F. JONES
_____WAS CREDITED WITH THE MANUFACTURING OF INEXPENSIVE OSYGEN BY USING FRACTIONAL DISTILLATION OF LIQUEFIED AIR IN THE PRODUCTION OF NITROGEN KARL VON LINDE
THE AARC STATEMENT OF EHTICS AND PROFESSIONAL CONDUCT INCLUDES A STATMENT ON ADVOCATING DISEASE PREVENTION AND WELLNESS
THE INSTRUCTOR’S ROLE IN PROBLEM BASED LEARNING INCLUDES GIVING FEEDBACK, PROMOTING DEBATE
A PATIENT HAS A “DO NOT RESUSCITATE” ORDER THAT HE DISCUSSED WITH HIS PHYSICIAN AND THEN ASKED HIS DOCTOR TO WRITE. THIS IS A FORM OF _____ AN ADVANCED DIRECTIVE
A “DO NOT RESUCITATE” ORDER MEANS_____ DO NOT PERFORM CARDIOPULMONARY RESUSCITATION AND ADVANCED CARDIOVASCUALR LIFE SUPPORT
A PATIENT WHO JUST FINISHED BREAKFAST REFUSES HIS AEROSOL BREATHING THERAPY HE MAY REFUSE THE TREATMENT, BUT THE THERAPIST SHOULD SEEK TO ASSURE THE PATIENT UNDERSTANDS WHAT THE THERAPY IS FOR
THE INSTRUCTOR’S ROLE IN PROBLEM BASED LEARNING INCLUDES HELPING RESOLVE CONFLICT
______A PIONEER IN PULMONARY MEDICINE, ORGANIZED AND EARLY INHALATION THERAPY PROGRAM IN 1943 AT CHICAGO’S MICHAEL REESE HOSPITAL EDWING R. LEVINE
WHICH OF THE FOLLOWING FUNDAMENTAL ADVANCES WAS A RESULT OF WWII INTRODUCTION OF ANTIBIOTICS
A PATIENT WHO JUST FINSHED BREAKFAST REFUSES HIS AEROSOL BREATHING THERAPY HE MAY REFUSE THE TREATMENT, BUT THE THERAPIST SHOULD SEEK TO UNDERSTAND WHY THE PATIENT IS REFUSING AD SEEK TO CLARIFY ANY MISUNDERSTANDING, AND ATTEMPT TO ACCOMMODATE THE PATIENT’S NEEDS
IN 1943, ALBERT H. ANDREWS WROTE THE ____WHICH PROPOSED THAT INHALATION THERAPY DEPARTMENTS OPERATE UNDER THE MEDICAL DIRECTION OF AN INFLUENTIAL STAFF PYSICIAN PROPOSAL OF INHALATION THERAPY PROCEDURES
THE INHALATION THERAPY ASSOCIATION ( ITA) WAS CHARED BY APRIL 5, 1947 FOR WHAT PURPOSE PROMOTE HIGER STANDARDS IN METHODS AND PROFESSIONAL ADVANCEMENT OF ITS MEMBERS
WHAT NOTABLE EVENT OF THE MID-1950’S HELED THE ITA OVERCOME ITS PERCEPTION AS A REGIONAL ASSOCIATION TRI-STATE HOSPITAL ASSEMBLY
THE AMERICAN ASSOCIATION FOR RESPIRATORY CARE ( AARC) SUCCESSFULLY USED THE _____AS A TEMPLATE FOR SCIENTIFIC EXAMINATIONOF EVERY FORM OF CLINICAL RESPIRATORY THERAPY SINCE 1974 SUGARLOAF CONFERENCE
WHICH OF THE FOLLOWING EVENTS ARE TRUE REGARDING THE HISTORY OF THE LICENSURE PROCESS U.S DEPARTMENT OF HEALTH EDUCATION AND WELFARE IMPOSED A VOLUNTARY 2 YEAR MORATORIUM ON ADDITIONAL STATE LICENSING
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE ESTABLISHMENT OF THE ACCREDITATION PROCESS THE AMERICAN MEDICAL ASSOCIATION ( AMA) HOUSE OF DELEGATES GRANTED FORMAL APPROVAL IN DECEMBER 1962
INCEPTION OF THE NATIOINAL STATE CREDENTIALING PROCESS WAS BASED ON WHICH OF THE FOLLOWING HISTORICAL PRINCIPLES AND EVENTS? CRITERION- REFERENCED VALIDATION STUDIES ARE CONDUCTED ON EACH EXAMINATION BEFORE IT IS GIVEN FOR THE FIRST TIME
___IS A MONTHLY SCIENCE JOURNAL ORGINALLY ESTABLISHED AS THE QUARTERLY PUBLICATION, INHALATION THERAPY, AND CURRENTLY PRUBLISHED FOR THE AARC BY DRAEDALUS ENTERPRIES, INC RESPIRATORY CARE
WHICH OF THE FOLLOWING FUNDAMENTAL ADVANCES WAS A RESULT OF WWII DEVELOPMENT OF THE DEMAND DEBREATHING VALVE
WHAT NOTABLE EVENTS OF THE MID-1950’S HELPED THE ITA COVERCOME ITS PERCEPTION AS A REGIONAL ASSOCIATION HIRING A CARRIER & JOBSON, INC. TO MANAGE BUSINESS AFFAIRS OF THE AAIT
WHICH OF THE FOLLOWING EVENTS ARE TRUE REGARDING THE HISTORY OF THE LICENSURE PROCESS THE MORATORIUM WAS SUPPORTED BY THE AARC
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING ESTABLISHMENT OF THE ACCREDITATION PROCESS JOINT REVIEW COMMITTE FOR INHALATION THERAPY EDUCATION ( JRCITE) WAS RENAMED JOINT REVIEW COMMITTE FOR RESPIRATORY THERAPY EDUCATION ( JRCRTE)
INCEPTION OF THE NATIONAL AND STATE CREDENTILAING PROCESS WAS BASED ON WHICH OF THE FOLLOWING HISTORICAL PRINCIPLES AND EVENTS ACCREDITED EDUCATIONAL PROGRAMS GENERALLY PREPARE THEIR GRADUATES TO PASS APPROPRIATE EXAMINATIONS AT THE LEVEL TO WHICH THEY WERE TRAINED
IN THE YEAR 2000___WAS ACCEPTED ININDEX MEDICUS, THE PRINCIPLE BIBLIOGRAPHIC DATABASE OF THE NATIONAL LIBRRARY OF MEDICINE AND ITS ONLINE COUNTERPART MEDLINE RESPIRATORY CARE
THE ____, A PRIVATE FOUNDATION FORMED BY THE PURITAN BENNETT CORPORATION OFFERED 50,000 GRANT TO THE ASSOCIATION FOR THE DEVELOPMENT OF NEW MULTILEVEL TRAINING MEDIA FOR HOSPITAL INSERVICE PROGRAMS AND FORMAL EDUCATIONAL PROGRAMS PARKER B. FRANCIS FOUNDATION ( PBFF)
THE ____WAS INCORPORATED IN JULY 1970 AS A CALIFORNIA NOT-FOR-PROFIT CORPORATION; IT CURRENTLY PROVIDES ANNUAL AWARDS, EDUCATION , ADN LITERARY RECOGNITION, FELLOWSHIPS AND GRANTS AMERICAN RESPIRATORY CARE FOUNDATION ( ARCF)
THE NATIONAL ASSOCIATON FOR MEDICAL DIRECTION OF RESPIRATORY CARE ( NAMDRC) OFFICAL SPONSOR OF THE AARC IN 1997, ASSISTS PHYSICIANS IN WHICH OF THE FOLLOWING PULMONARY SERVICES CRITICAL CARE, HYPERBARIC OXYGEN THERAPY, PULMONARY REHABILATION, PULMONAY MEDICINE, SLEEP DISORDERS
WHICH OF THE FOLLOWING FUNDAMENTAL ADBVANCES WAS A RESULT OF WWII DEVELOPMENT OF THE NON-REBREATHING VALVE AND MASK
WHICH OF THE FOLLOWING STATEMENTS ARE TRUE REGARDING THE ESTABLISHMENT OF THE ACCREDITATION PROCESS AARC SPONSORED A NEWLY FORMED RESPIRATORY CARE ACCREDITATION BOARD ( RCAB) IN 1994
INCEPTION OF THE NATIOINAL STATE CREDENTIALING PROCESS WAS BASED ON WHICH OF THE FOLLOWING HISTORICAL PRINCIPLES AND EVENTS THE REGISTRY BOARD ORGANIZED AND OFFERED A TWO-PART PILOT EXAMINATION IN NOVEMBER 1960 IN MINNEAPOLIS
INCEPTION OF THE NATIONAL AND STATE CREDENTIALING PROCESS WAS BASED ON WHICH OF THE FOLLOWING HISTORICAL PRINCIPLES AND EVENTS WRITTEN AND ORAL EXAMS WERE CONDUCTED UNTIL 1979; LATER, CLINICAL SIMULATION EXAMINATIONS ( CSEs) REPLACED THE ORAL FORMAT
WHICH OF THE FOLLOWING IS TRUE REGARDING THE SOCIETY OF CRITICAL CARE MEDICINE ( SCCM) THE SCCM PUBLISHES CRITICAL CARE MEDICINE A MONTHLY JOUNRNAL DEDICATED TO THE SCIENCE AND TREATMENT OF CRITICALLY ILL PATIENTS



Question Answer
When do you count a patient’s pulse or respiration for a full minute? When irregularities are present
What is one breath cycle? one inspiration, one expiration
How much mmHg above a patient’s usual readings do you pump? 30
If you let too much air out, what do you do? DO NOT attempt to pump it back up, let the air out and switch to other arm to repeat
What happens if you let air out too slowly? Your pressures may be false and/or your patient’s circulation may be cut off (fingers and arm will hurt)
What speed should you let air out? Maintain a slow but steady pace, which will enable you to hear the first beat
While performing blood pressure maneuver, what should you be doing? Listening for the sound AND watching the monometer
Four helpful items from medical record Recent diagnostic tests, past medical history, patient’s culture, education level, CHECK PREVIOUS VITAL SIGNS
Normal Heart Rate for adults 60 bpm to 100 bpm
Bradycardia A heart rate <60
Tachycardia A heart rate >100
If the HR of a patient changes by ___, we need to determine the underlying issue +/- 20 beats
Everyday situations that increase HR stress, anxiety, pain, exercise, caffeine
What is first clinical sign of hypoxemia in an adult > heart rate
What your patient develops tachycardia, assess for signs of… hypoxemia, postop pain, stress, hypoxemia
Pulse Rhythm Regular or Irregular
Pulse Quality weak, thready, bounding, strong (how it feels to the touch)
Two reasons why you may not be allowed toa ccess brachial or radial pulses on one side of the patient Mastectomy, Shunt for dialysis
Pulsus Paradoxus Pulse changes btw inspiration and experation
What kind of patients have pulsus paradoxus COPD
What is Pulsus Alternans strong then weak pulse
What kind of patients may experience Pulsus Alternans left ventricular heart failure
What is the normal RR for an adult btw 8 and 20
bradypnea RR <8
tachypnea RR > 20
What is the muscle of respiration called? diaphragm
Five Accessory Muscles Sternocleidomastoid, Scalene, Trapezius, Intercostals, Pectoralis Major
Orthopnea when laying down and can’t breathe
Orthopnea may be a symptom of what disease? Left ventricular heart failure
What is Platypnea sitting up and can’t breathe
Platynea may be a symptom of what disease COPD
What is Pleurodynia Pain in pleural cavity
Pleaurodynia may be a symptom of what disease pleuracy
Describe pursed lip breathing Short inspiration, long expiration thru pursed lips
What kind of patients develop pursed lip breathing involuntary and may be taught in pulmonary rehab COPD
How does pursed lip breathing help these patients pursing lips on expiration creates back pressure which may help open the obstructed lung
What are sternal retractions “sinking in” or “caving in” of the sternum
Describe what you see when a healthy patient takes a deep breath Chest (sternum) moves outward, abdomen moves inward
Abdominal paradox Chest/sternum retracts and abdomen protrudes when patient attempts a deep breath
Name one traumatic event that can cause this paradoxical breathing pattern Broken ribs with collapsed lung (pneumothorax”
What is a sign of respiratory distress in infants nasal flaring, grunting (babies breathe through nose at birth)
What is correct term for a blood pressure cuff? sphygmomanometer
Top number systole
bottom number diastole
What can’t you put aneroid manometer on the table to make it easier to see? must be level with heart
Question Answer
ABGs arterial blood gases
AFB acid fast bacillus
ARDS adult respiratory distress syndrome
BUN blood urea nitrogen
CBC complete blood count
CF cystic fibrosis
C&S culture and sensitivity
CO2 carbon dioxide
COLD chronic obstructive lung disease
COPD chronic obstructive pulmonary disease
CPR cardiopulmonary resuscitation
CXR chest x-ray
FEF forced expiratory flow
FEV forced expiratory volume
FRC functional residual capacity
FVC forced vital capacity
HCO3 bicarbonate
HMD hyaline membrane disease
IPPB intermitten positive-pressure breathing
IRDS infant respiratory distress syndrome
L liter, left, lumbar
mg milligram (1/1000 grams)
NMTs nebulized mist treatments
PCP pneumocystis carinii pneumonia
PE physical examination
PEFR peak expiratory flow rate
PFT pulmonary function test
pH symbol for degree of acidity or alkalinity
pO2 partial pressure oxygen
PND paroxysmal nocturnal dyspnea
PPD purified protein derivative
RAD reactive airway disease
RD respiratory disease
RDS respiratory distress syndrome
RSV respiratory syncytial virus
RV residual volume, right ventricle
SaO2 arterial oxygen saturation
SIDS sudden infant death syndrome
SOB shortness of breath
TB tuberculosis
TPR tempature, pulse, respiration
TV tidal volume
VC vital capacity
Question Answer
*Anticholinergic drugs block M receptors, <SLUD, atropine is prototype and is used to <secretions before anesthesia can also be called antimuscarinic, atropinic, antiparasypathetic and parasympatholytic
Anticholinergic action blocks M causing decrease SLUD
Calculating dose mg equals mL x % x 10 example how many mg’s are there in 2cc of a 20% solution? mg eq 2 x 20 x 10 or mg eq 400mg caution-do not move decimal.
Find the solution mg equals mL x % x 10 example if there are 30 mg in 2cc of a drug, what percent solution is this- 30
How many mg of Alupent are in .5ml of a 1:200 concentration 1:200 is g/mL*100 eq .5%, mg eq .5*.5%*10 answer is 2.5mg
How many mg per ml are in a 2.25% solution mg eq ml*%*10 so mg eq 1ml*2.25%*10 or 22.5
MDI technique shake, hold 1″ from mouth, exhale normally, squeeze MDI at beginning of slow deep inhalation, inhale fully and hold for 10 seconds, exhale-wait 15-30 sec (for SABA, none for other meds) and repeat.
*Sympathomimetic bronchodilator method of action aka adrenergic agonist, stimulate production of cAMP causing bronchodilation
*Adrenergic agonist method of action stimulates G protein in bronchial smooth muscle, G protein makes cAMP and cAMP equals bronchodilation (sympathomimetic)
*Sympathomimetic bronchodilator drugs terbuterline, albuterol, isoproterenol levelbuterol (adrenergic)
Atropine and method of action aka anticholinergic, aka antimuscarinic, blocks ACH receptor site (M), causes <SLUD by blocking ACH, competitive antagonist for M
*Parasympatholytic (<M) vs. parasympathetic (>M) patholytic is anti or against, parasympatholytic is anticholinergic (blocks M), parasympathetic is cholinergic (>M-causes bronchoconstriction)
*Cholinergic indirectly acts or mimics parasympathetic action (bronchoconstriction, SLUD), includes choline esters (>M recept), anticholinesterases(blocks ACHase)
Routes of administration PO aka oral (most common and safest), parenteral aka IM or IV, topical aka svn
Agonists drugs that combine with specific receptors to cause a drug action, drugs that stimulate action
Antagonists aka blocker, drugs that combine with a specific receptor and cause no action
Competitive antagonism antagonists and agonists compete for same receptor, example is antihistamine which competes for receptor with histamine, by reducing the binding of histamine, effects of histamine are reduced. Gum in keyhole
*ACH regulation 1. Metabolized by enzyme ACHase aka acetylcholinesterase 2. ACH blockers like atropine, Ipratropium or Tiotropium
*NE regulation at synapse 1 Reuptake via active transport, 2 MOA and COMT enzymes
*NE regulation at cells cells regulate NE by increasing cAMP or blocking phosphodiesterase (enzyme that breaks up cAMP)
*Alpha receptor a, adrenergic(sympathomimetic) receptor, located in most arteries and veins, NE is neurotransmitter, action is vasoconstriction. Epi (adrenal gland) action is vasoconstriction-<bleeding, <swelling, >BP
*B1 receptor adrenergic (sympathomimetic) receptor located in the heart, NE is neurotransmitter, action is moderate >HR and moderate > contractility, Epi action is greater > in HR and contractility
*B2 Receptor adrenergic(sympathomimetic) receptor located in bronchiolar smooth muscle, uterus and skeletal muscle blood vessels. NE is neurotransmitter but has no action, Epi action is bronchodilation, uterus relaxation and skeletal muscle vessel vasodilation.
Factors that alter drug effects pt compliance, placebo effect, pathological state, time of admin, sex, age, genetic variations, drug interactions
*Un-ionized un-ionized are very water and lipid soluble and absorb quickly, because they are able to pass easily through plasma membrane, non-charged, neutral
*Muscarinic receptor site of ACH, parasympathetic, class of drugs that stimulate ACH, action is decreased HR, bronchoconstriction and vasodilation
Potentiation special case of synergism where one has no effect but can increase the effectiveness of the other 1+0 eq 2
*NE norepinephrine, neurotransmitter of sympathetic nervous system, neuroeffector sites are smooth muscle and cardiac muscle, receptor are a, B1 and B2
*NE effects (fight or flight) vasoconstriction, >HR, >contractility of heart, <GI activity, pupil dilation, bronchodilation, bladder relaxation, urinary sphincter constriction
*ACH effects (rest & digest) <HR and contractility, >GI activity, pupil constriction, bronchoconstriction, bladder constriction, urinary sphincter relaxation. SLUD
*a action vasoconstriction, increased BP, stops bleeding, decreases swelling,
*B1 action increased HR, increased contractility, increased cardiac output
*B2 action smooth muscle relax, bronchodilation
Metabolism liver * alphabetically e and k come first in alphabet fallowed by l and m, so excretion- kidney and liver-metabolism
*Excretion kidneys * alphabetically e and k come first in alphabet fallowed by l and m, so excretion equal kidney and liver equals metabolism, excretions also takes place in lungs and GI tract
*ACHase acetylcholinesterase aka ACHE, enzyme that metabolizes excess ACH
*Drug absorption many membranes; stomach, capillaries and tissues-3 factors, transport mechanism, lipid solubility and drug ionization (un-ionized)
ACH aka acetylcholine, aka cholinergic, neurotransmitter of parasympathetic, receptor site M, action < HR, < BP, bronchoconstriction, neuroeffector site is smooth muscle, cardiac muscle and glands.
Potency more physiological effect with smaller dose, more potent-more toxic, lower the effective dose-more potent
Parenteral injectable aka IM, IV
Entral GI tract, pills caplets, suppository, elixir, suspension (most common)
Topical transdermal, cream patch ointment, inhaled, MDI, DPI, SVN, USN, atomized, vaporized
*Adrenergic aka sympathomimetic, term meaning a drug that mimics the action of the sympathetic nervous system. Stimulate receptor sites example
Pharmacokinetics quantifies the time required for drug absorption, distribution, metabolism and method of excretion
sympathomimetic aka adrenergic-drug that mimics action of sympathetic ns
*drug distribution plasma protein binding, tissue affinity and blood flow
*drug transport passive diffusion (most common) moves from high to low, filtration, and active transport
prototype “a drug that acts like” i.e. atropine is prototype anticholinergic and epinephrine is prototype adrenergic
Therapeutic dose recommended amount of a drug that should be used to obtain the desired clinical effect.
sympathetic nervous system fight or flight aka adrenergic, more dominant side of ANS, effector site neurotransmitter is Ne. >HR, >BP, vasoconstriction, bronchodilation, contractility
LD 50 median lethal dose
*TI Therapeutic Index, ratio of LD50 to ED50 indicates drugs safety, lower TI is the more toxic the drug, higher the TI, the safer the drug. TI eq LD50/ED50
Teratogens drugs that are known to cause birth defects
Carcinogens drugs that cause malignant neoplasms (cancer)
Antimuscarinic specifically blocks m receptor sites
*Competitive antagonist competes for receptor site, blocks but has no effect
*Functional antagonist effects of two drugs cancel each other out
ED50 effective dose, dose at which 50 percent of test animals show desired effects
Idiosyncrasy unexplained or unpredictable susceptibility to a drugs action
Tachyphylaxis rapidly developing tolerance to a drug
*Anticholinesterase blocks ACHase enzyme, allowing >ACH and increasing bronchoconstriction and SLUD
*COMP & MOA enzymes that metabolize excess Ne, can be injected or inhaled-never swallowed
Pharmacology study of drugs and their origin plants animals and minerals
Epinephrine not a neurotransmitter, released by adrenal gland in response to sympathetic activation
Ceiling effect response increases with dose until dosage increase does not increase effect-used to check relative potency of 2 or more drugs. Note; once ceiling effect is reached, increasing dose has no advantage and may be toxic.
*Phosphodiesterase enzyme that breaks up cAMP
Choline esters action stimulate m receptors and mimic effects of ACH, causes bronchoconstriction and SLUD
SLUD salivation, lacrimation, urination, defecation; to much ACH to much SLUD, to much SLUD → death
*Antagonist categories competitive (affinity but no effect), functional (effects of 2 cancel each other), chemical (physically chemically binds in blood stream)
Additive effect two drugs act on receptors to have a combined effect that is the sum of the two drugs effect 1+1 eq 2
Drug info USP, NF, PDR
*Synergistic response aka synergism when two drugs are combined and the effect is greater than the sum, 1+1 eq 3
*Parasympathetic aka cholinergic, rest and digest, neurotransmitter is ACH, receptor sites are Muscarinic and nicotinic, blocker is atropine, does not function as a unit
MDI on Mechanical Vent medial to pt on circuit, actuate at end expiration adjust dosage as needed, minimum 8 puffs may go to 20, 15 seconds between puffs
*High dosing Albuterol effective ceiling is 15 mg, heart neb for continuous, hazard is hypovolemia, decreased k+, increased glucose
Aerosol advantages immediate onset of action at site, reduced systemic side effects, smaller doses, pt can be taught to self admin, convenient and rapidly effective while minimizing side effects
Aerosol disadvantages exact dose is unknown, only 10-20% is deposited, breathing pattern effects airway deposit, 2/3 exhaled, much swallowed, wrong neb or flow effects delivery
*Nebulizer flow rates 6-7 L/min * however since neb can run at 10 L/min and not 4 L/min appropriate answer on test is 7-10 L/min
*SVN delivery factors inspiratory hold (3-5 seconds) is most important for distribution and retention of meds-slow deep breath, 6 L/min flow for 1-5 micron particles, 2.5-4 mL’s solution, inspiration only
MDI advantages convenient, inexpensive, no prep, new MDIs are patent actuated and assures proper aspiratory flow and pattern
MDI disadvantages requires pt coordination, pharyngeal deposits, abuse risks, cfc’s, 75% of pt’s and 50% of medical workers don’t know how to use them
Mech vent and SVN meds tend to stick to tube or baffle, 1.5 to 3% make it to airway, SVN should be distal to pt in circuit (close to flow source) often requires double dose
*SVN particle size 1-5 microns
Direct installation giving meds directly down ET tube or trach, 3-5 ml normal dose, no guarantee of dose, most often used for mucus plugging. Disadvantage, violent cough and systemic side effects
Direct installation drugs Epi-cardiac arrest, NS-sputum sample, B2, mucomyst, surfactant in preemies.
*Combivent Ventolen(albuterol) + atrovent combination sympathomimetic and anticholinergic, best with copd’er
Bronchodilator categories sympathomimetic (increase cAMP), anticholinergic (block ACH), Xanthines (inhibit Phosphodiesterase increasing cAMP)
Xanthines aka theophylline, caffeine, thrombromine & theophylline, Phosphodiesterase inhibiter, used in treating neonate apnea and bradycardia, long term COPD, last resort in asthma, rare use, bad side effects.
Finding desired dose desired dose/dose on hand equals amount/X example morphine in 10 mg/5mL vial, need 4 mg…..10/5 eq 4/X so 10X/10 eq 20/10 so x eq 2 mg
*Anticholinergic bronchodilators blocks ACH-blocks SLUD, causes <secretions, >HR, bronchodilation, prototype is atropine (bad side effects) Ipratropium is safer alternative, good choice for bronchospasm in COPD with B2 agonist
*Swelling & edema treatment alpha (racemic epi) + steroids. Steroids also treats secretions, treat swelling and secretions will go down too.
what is Bronchoconstriction REDUCED AIRWAY LUMEN, caused by smooth muscle bronchospasm, swelling and edema, excess secretions
*the anticholinergic bronchodilators drugs are atropine (prototype), ipratropium (Atrovent) tiatropium (Spiriva) glycopyrrolate (Robinol-used for bronchorrhea in CHI)
*Albuterol dosage SD 2.5 mg/3mL or .5mL in 2.5cc NS q4-8, Exacerbation 2.5-5mg 20mins x 3 or 10-15mg/hr cont
*Xopenex/levalbuterol dosage SINGLE ISOMER SD .63mg/3mL, q4-6, exacerbation-adult 1.25-2.25mg 20 mins x3 then same q1-4 no cont neb (need to double ck max),
*Ipratropium dosage Atrovent, anticholinergic, parasympatholitic,(compet agonist) blocks cAMP, very safe, can mix with albuterol, for exacerbation .5mg 20mins x 3 then as need, STANDARD DOSE .2 qid
Prednisone dosage for asthma exacerbation child 1mg/kg 2 dose max/day(max 30mg) until PEF or FEV1 at 70%, adult 40-80 mg/day 1-2 doses until PEF or FEV1 at 70%, out pt burst 3-10 days
*Salmeterol dosage LABA, >5yrs DPI-50mcg/blister, 1 blister q12
Catecholamines bronchodilators naturally produced in the body in response to stress, epinephrine, receptor is a, B1, B2, metabolized by MAO & COMP (sympathetic, adrenergic, cholinergic)
Catecholamine drugs first synthetic adrenergic drug, strong a, B1, and B2 drugs, cannot be taken orally, (because of stomach MAO & COMT), very short duration 1- 3 hrs, epi, racemic epi (Vaponephrine), isoproterenal (Isuprel)
Finding desired dose desired dose/dose on hand equals amount/X example; bottle of Demerol has 50mg/5cc, how much do we need to deliver 25mg of Demerol? 50/5 eq 25/x so 125/50x reduce to 2.5/x or x equals 2.5cc
*resorcinol drugs are modified catecholamines, no a, B1, B2, some resistance to MAO and COMT, terbuterline (stops contractions) and metaproterenol (not used now because of B1 side effects, hard on heart) 4hrs
*Saligenin drugs modified catecholamines, SABA-short acting B2 agonist, last 6hrs, B2 preferential, very little B1, albuterol
*R-Isomer or single isomer drugs levelbuteral (Xopenex), also a saligenin but has no B1, and considered a LABA long acting beta agonist
*saligenin drugs are albuterol, levalbuterol, (Xopenex) and salmeterol (Serevent)
strong a, B1, B2 drugs epinephrine and racemic epinephrine (Vaponephrine)
Strong B2 agonist drugs levalbuterol (Xopenex) is the only single isomer B2 agonist drug, all others have some B1 effects
Strong B2, strong B1 agonist are isoproterenol (Isuprel)
Dose-response curve graphic representation of the relationship between dose in mg and the response to or effect of the drug.
Antitusuve anti cough
Expectorants increase fluid in resp tract and stimulate cough
SSKI potassium iodine-expectorant for asthma and bronchitis (no longer used)
*Bronchorrhea condition associated with excess thin watery pulmonary secretions, most often with head injury, drug of choice- glycopyrrolate (Robinal), hazard is mucus plugging
*Mucomyst n-acetylcysteine, mucolytic, breaks down disulfide bonds
Mucus molecule mucopolysaccaride chain, strands of amino acids and amino sugars connected by disulfide bonds
Mucolytics drugs dornase alfa (Pulmozyme), n-acetylcysteine (Mucomyst), sodium bicarb
*Dornase Alfa aka Pulmozyme, mucolytic, lyces bacteria and cellular debri DNA, most often used with CF & bronchiectisis, never mix with other drugs, need special jet neb (maint drug)
*Sodium Bicarb mucolytic, alters PH to disrupt amino acid chain, very rare alternative to mucomyst, asthma pt with thick secretions (done is 2% or 4.2%)
*The most effective method of mucolysis is aerosolized mucolytics
*Side effects of N-acetylcysteine (Mucomyst) bronchospasm, acute airway obstruction, oropharyngeal irritation
*Side effects of dornase alfa (Pulmozyme) pharygitis, laryngitis and voice alteration
*What are the contraindications for the use of Mucomyst administration without a bronchodilator, administration to semicomatose pt without suction equip and monitoring
*When should RT use sterile distilled water as dilute instead of NS with bronchodilator with pt is like Kay and has a salt restriction
mucolytic indicators thick inspissated secretions, aerosol – able to cooperate & deep breath, trach or endotrach by direct instillation
*Bland aerosol aerosols that do not have a direct effect on mucus molecule and usually no side effects. Normal saline (.9%NaCl), hypo (.45%NaCl) and hypertonic saline (5%NaCl), and sterile distilled water
Secretion patients CF, bronchiectisis and chronic bronchitis
increased secretion indicators tactile fremitise (you can feel it), rhonchi (low pitch rumble), caused by ineffective cough and muscle fatigue
Mucolytics agents that disrupt mucus molecule so that secretions can be removed (coughed or suction), cause mucolysis (breaking apart)
*Sterile distilled water most common solution in LVN for humidification of airway, also used as a dilute in SVN-TRACH PTS
Sputum induction used when pt has dry non-productive cough, hypertonic saline (5% to 10%) not to exceed 1500 mg/day
Hypotonic osmotic pressure is less than body fluid, most common is .45% NaCl (1/2 NS), used in LVN when pt cannot tolerate distilled water and as dilute in SVN for pt with severe salt restriction
*Hypertonic osmotic pressure is greater than body fluid, used for sputum production, most common 5-10% NaCl (hygroscopic droplets attract humidity and grow larger) NEVER TO ASTHMATIC
NS normal Saline, osmotic pressure is same as body fluid (0.9% NaCl), most common bronchodilator dilute, unlikely to cause bronchospasm, but can increase sodium
*Pulmozyme dose unit dose 2.5 mL, contain 1 mg dornase alfa/mL solution (1mg is 2.5 mL), use separate neb, q1 or q2, (refrig and protect from light)
Bland aerosol indicators pt who require humidity of resp tract, intubated or trach. As thinning agent prior to postural drainage and chest percussion, sputum induction. (continuous jet, Babington or USN)
*n-acetylcysteine aka Mucomyst, indicated for pt with excessive purulent thick or inspissated secretions, breaks disulfide bond, also used in acetaminophen (Tylenol) OD & renal protection, 10-20 % solution, bad smell, max 72 hrs
Mucomyst dose unit dose 10% or 20% solution, 20% solution can be mixed 1:1 with distilled water or NS if needed, refrig extra, date and discard after 4 days, 3-4mL/tx q4h with bronchodilator.
budesonide aka Pulmacort, aerosol corticosteroid (only SVN steroid) needs a specific jet neb
aerosol corticosteroid fluticasone-Flovent,flunisolide-Aerobid,triamcinolone-Azmacort
*Asthma attack anatomy mast cell exposed to allergen (antigen-antibody), mast cell degranulates releasing histamines (edema, mucus, constriction), cytokines (recruiters-cause late stage) and leukotrines (inflammatory mediator)
Bronchial asthma most common chronic lung disease, 4% of population and increasing, symptoms, dyspnea, diffuse wheezing, airway obstruction from bronchospasm, edema and mucus.
*S&S of serious asthma exacerbation marked breathless, short phrases only, use of accessory muscles, drowsiness, PEF 50-70% predicted use quick relief, PEF <50% ED
ED TX for mild-mod exacerbation >40%, O2 to achieve 90%SaO2, SABA up to 3x/hr, oral corticosteroid if not resp to SABA
ED TX for severe exacerbation <40% O2 to achieve 90% SaO2, high dose SABA + Ipratropium (20 mins or continuous), oral corticosteroids
TX for impending or actual resp arrest intubate and mech vent on 100%, SVN SABA and Ipratropium, IV Corticosteroids, consider adjunct therapies, admit to ICU, hourly SABA
Asthma mucus thickened & viscid (sticky) with eosinophils
What drug stabilizes the mast cell Intal aka cromolyn sodium
how often can we give Vaponephrine every hour
*advantages of steroids by aerosol rapid absorption at site of action with reduced systemic side effects
what is the only inhaled steroid available for svn budesonide
*the most effective method for mobilizing and improving mucokinetics is adequate hydration and fluid intake
Mucosal edema accumulation of fluid in the mucosal membrane, caused by infection, trauma, disease, or conditions like anaphylaxis or allergic reaction (most often treated with alpha racemic epi
*Asthma attack progression coughing, exp wheezes, I:E wheezes, insp wheeze (air trapping), vent failure (intubate)
Anti-asthmatic drug classes mast cell stabilizers & leukotriene blockers
Aerosol steroid advantage decreased systemic side effects, no addiction, no cushings
Aerosol steroid disadvantage increased expense, not for status asthmaticus, increased risk of superinfection, horseness, cough, requires pt effort and coordination
*CNS additive effects especially true with depressant drugs, alcohol and barbs will result in synergistic effect of both
*Antagonism of CNS drugs stimulants and depressants antagonism is variable, often unpredictable and extremely variable
Depressant drugs and excitation some may cause a brief period of excitation prior to depressant stage, example is general anesthetic
Acute or chronic excitation is often followed by what? depression,long term amphetamines or convulsive state, depression usually follows
Drug induced (chronic) depression is usually followed by what? period of excitation, usually following termination of chronic use of narcotics or barbs
*Sedative calming effect, decrease CNS activity and drowsiness
*Hypnotic drowsiness, facilitates onset of sleep
*Anti-anxiety agent (anxiolytic) reduces anxiousness, particularly incapacitating or inappropriate anxiety
*Barbiturates prototype of sedatives and hypnotics, very powerful, no analgesic properties, little cardio effect, redistribution, very addictive, can cause life threatening withdrawals, not normal REM
Sedation and hypnotic are related how? by dose, >sedation can cause sleep, <hypnotic can cause sedation
*Barb uses today induction agent in general anesthesia, anticonvulsants in treating epilepsy, backup sedative hypnotic agents
*Barbiturate drugs thiopental, pentobarbital and Phenobarbital (Luminal)-long acting anticonvulsant
*Benzodiazepines most widely used sedative hypnotic and anti-anxiety, replaced barbs, enhance GABA neurotransmitters in the brain, few side effects, rare OD
*Benzo drugs (>gaba) midazolam (Versed) short duration, amnesia
Alcohol ethyl alcohol, CNS depressant, side effects-cardio, GI, fetal development
*Tricyclic antidepressants TCA’s, most often used antidepressants, least side effects
*Monoamine oxidase inhibitors MAOI’s, antidepressant, greater toxicity and interact with some foods and drugs
*TCA’s & MAOI’s action increase levels of norepinephrine and/or serotonin in the brain tissue, CAUSE HYPERTENSION
Psychostimulant drugs amphetamines and methylphenidate, stimulants, paradoxical they are used in ADHD
*Anti-anxiety meds barbs, nonbarb sedative hypnotics, alcohol and benzos, benzos are the mainstay
*Epilepsy paroxysmal (sudden onset) increase in CNS activity that is recurrent, has stereotypic clinical characteristics and associated massive discharge of elec activity that is self limiting
*Partial seizures SIMPLE-local discharge without loss of Consciousness or COMPLEX-loss of consciousness with many ANS behavior (most difficult to diagnose)
*Primary generalized seizures PETIT MAL (absence)-rapid onset, loss of consciousness and mild rhythmic movement or GRAND MAL (tonic-clonic) 4-10% of seizures, asleep or awake, can be caused by lack of sleep, alcohol, fatigue
Anticonvulsant/anti-epileptic drugs break up a seizure, Phenobarbital (Luminal), valium and aderian????????
*Parkinsonism middle age and progressive, lack of dopamine-containing neurons in the substantia nigra area of one of the cerebral nuclei (in CNS), causes lack of balance in excitatory and inhibitory neurons
Symptoms of Parkinsonism develop slow at first, gradual become chronic, tremor, rigidity, akinesia(loss of movement), bradykinesia(slow move) and loss of balance, idiopathic (unknown) cause
*TX of Parkinsonism increase dopamine, Levodopa-passes blood brain barrier
*General anesthetics drug that induces the absence of all sensation
Anesthesia Stage I Analgesia aka twilight, midbrain and some spinal cord
Anesthesia Stage II Excitation via IV, amnesia
*Anesthesia Stage III Surgical Anesthesia via inhalation, intubation, for surgery, 4 planes (only seen when using ether)
Anesthesia Stage IV Medullary Supression effects respiratory and cardio, causes apnea, coma, and death
N*itrous Oxide low risk, gas, most widely used general anesthetic, especially as adjunct with general anesthetics to <need for more potent agents, rapid, good analgesic, metabolized in lung instead of liver, little cardio effect
Inhaled general anesthetics are gases-nitrous oxide and cyclopropane(no longer used), Volatile liquids-ether, halothane, methoxyflurane
*Fluothane halothane, volatile liquid delivered as vapor particularly in peds, also potent bronchodilator-last resort for status asthmaticus
*Thane or rane in drug name inhaled general anesthetics ie halothane methoxyflurane
*Anesthetic delivery generals are for body core, IV and IV nerve blocks are for peripheral
Fentanyl high dose narcotic, used with versed for conscious sedation, profound analgesia, also used as preanesthetic to create sedation
Propofol aka diprivan, high dose narcotic (will need intubated), used for anesthetic induction and maintenance
*Preanesthetic medications fentanyl, to create sedation and Atropine, to decrease salivary and bronchial secretions
*Narcotic analgesics drugs that decrease pain without loss of consciousness, aka opioid, used to treat visceral pain (severe pain)
B endorphins morphine-line substances
Dymorphines more recent group of narcotics
*Morphine prototype narcotic, oldest naturally occurring analgesic and best understood, standard for which others are compared, high addiction, high resp suppression, side effect constipation, dose-10mg
*Morphine effects on respiratory powerful depressant, <RR & <VT causing >CO2, can cause bronchospasm-caution with asthmatics
Classifications of narcotic analgesics agonist (stimulates opioid receptors), agonist-antagonist (stimulates some and blocks some opioid receptors) and antagonist (blocks receptors)
*Agonist narcotic drugs morphine (opium), hydromorphone (Dilaudid) and hydrocodone (Vicodin) (both are semisynthetic derivatives of morphine and codeine), meperidine (Demerol) synthetic derivative of morph and code
Agonist-antagonist drugs none we need to know
*Antagonist narcotic drugs naloxone (Narcan) treat opioid OD
Meperidine synthetic agonist narcotic, 1/10 to 1/5 as potent as morphine, dose 50-100 mg, mod-high addiction, high resp suppression, few side effects
Codeine 1/6 as potent as morphine, dose 60 mg, low addiction, low resp sup, few side effects
*Non-narcotic analgesics Salicylates,
*Salicylates acetylsalicylic acid (ASA; Aspirin), non-narcotic analgesia for mild to mod pain, antipyresis (<body temp), anti-inflammatory in joints and ligaments, anticoagulation
*Salicylate side effects GI(ulcers), Hypersensitivity (allergy) including bronchospasm, anticoagulant effect
*Acetaminophen Tylenol, nonsalicylate non-narcotic, analgesic, antipyresis, not an anti-inflammatory
*Non steroid anti-inflammatory Salicylates like aspirin and ibuprofen like Advil and Motrin (ibuprofen is also analgesic, antipyresis)
*CNS drugs can alter effects of neurotransmitters on CNS by antagonism, increased or decreased synthesis of neurotransmitter
*Can a sedative drug become hypnotic by increasing the dose? yes
*True Benzo statements have few side effects compared to barbs, main clinical use is TX of anxiety with some Tx of sedation, action is stimulate GABA neurotransmitters, can create additive effect w/alcohol or other depressants
*TCA’s and MAO inhibitors are antidepressants
*The major side effect of TCA’s and MAO inhibitors that is of greatest concern is hypertension
*Which antidepressants causes worse hypertension MAO’s
*The mainstay drug for Parkinsonism is Levodopa
*What is the caution with morphine with COPD reduced resp of morphine can cause death in copd’er with normal dose
*RACEMIC EPI NOT A BRONCHODILATOR, <K, >GLUCOSE, METABOLIC ADRENERGIC
*Sympathomymetics are fight or flight they do not <BP
Catecholamine duration short 1-3 hrs and cannot take orally
MUCOMYST DYSULFIDE BONDS
PULMOZYME LYCES DNA
SERUM THEOPHYLLINE LEVELS INCREASE WITH WHAT LIVER DISEASE AND ALCHOLISM
SIDE EFFECTS OF N-ACETYCYSTEINE BRONCHOSPASM


Question Answer
Quality control creating a measurement and documentation system to confirm accuracy and reliability
Accuracy aka precision, that measured value is true physiologically value
Reliability high degree of confidence that measured value is truly actual physiological value
Quality assurance broader term that means not only are values accurate and reliable but clinically useful, by written policy and procedure manual, record keeping, equip maint, staff train, error correcting
Calibration sets the accuracy of the instrument (usually 2 points)
quality control materials materials used to calibrate electrodes in blood gas analyzers
aqueous buffers water based for PH and CO2
Precision gases for PO2 0, 12, 20, 20.95 (from room air), 21 and 100%
Precision gases for CO2 0, 5, 10, and 12%
tonometered liquids exposed in lab to known O2 and CO2 levels, 3 types, human or animal serum, or whole blood
what tonometer is considered most accurate for for PO2 and CO2? whole blood
tonometered bovine blood since human blood cannot be used, bovine is best choice for O2, Co2 and Ph for tonometered liquids
Assayed liquids non water based liquids pretomonetered by manufacturer for PO2, CO2 and Ph, good for speed and accuracy
Oxygenated fluorocarbon based emulsions aka preflourinated compounds, accurate as whole blood, but less risk, good for PO2, CO2, Ph
Levy-Jennings charts quality control charts used to record calibrations
Westgard rules used to determine when analyzer is not working and applied to L-J chart.
Why is L-J and Westgard rules used for ABG’s? guarantees 95% accuracy, includes random errors and systematic errors
random errors 1-2S, 1-3S and R4S, imprecision, unpredictable aboration of QC material, need to rerun control
systematic errors 2-2S, 4-1S, 10X, accuracy problem, must be investigated, corrected and documented, contaminated buffers, incorrect gas concentration or incorrect procedures, mach problem
S standard deviation, amount of difference from the mean that is used to measure in Westgard rules, can be plus or minus from the mean
Mean average of total quality control tests on a specific machine, mean and deviation are set when testing is done on ABG’s
12S rule Westgard random error rule, where if 1 control measurement is more than 2 standard deviations from the mean, it will be rejected or warned, depending on preset rules
13S rule Westgard random error rule, where if 1 control measurement is more than 3 standard deviations from the mean, it is considered “out of control” and will be rejected
R4S rule random error rule, if 2 consecutive measurements are 4 standard deviations or more apart, they will be rejected (control 1 is up or down 2 and control 2 is up or down in opposite direction)
22S rule systematic error, 2 consecutive are above or below 2 standard deviations and will be rejected
41S rule systematic error
10X rule aka 10 mean, rejects when 10 consecutive are on one side of the mean
“out of control” single or series is outside of the established limit (two standard deviations)
Ph high/low calibration 6.84-7.38
PCO2 high/low calibration 5-12%
PaO2 high/low calibration 0-10%
what is the accuracy of the 12S rule 95%
ABG samples provide what precise measurement of Acid-Base balance and lungs ability to oxygenate the blood and remove CO2
Accurate interpretation of ABG require what knowledge of pt total clinical picture including any TX receiving
where are mixed venous blood samples drawn rt atrium or pulm artery
what is mixed venous blood sample used for evaluate overall tissue oxygenation
why not venous samples only give metabolic rates so little value, exposed to peripheral vascular beds
normal ABG values for arterial blood is Ph 7.35-7.45, PaO2 80-100 mmHg, PaCO2 35-45 mmHg, HCO3 22-26, BE +-2
Normal ABG for mixed venous blood is Ph 7.34-7.37, PaO2 38-42 mmHg, PaCO2 44-46, HCO3 24-30
Prior to ABG draw, what should RT review for in Pt chart low platelet count or increased bleeding time (meds etc)
Preferred site of ABG arteriotomy (needle into artery) radial artery
Sites for ABG arteriotomy in adult are radial artery, brachial artery, dorsalis pedis, or femoral artery.
What must be evaluated prior to a radial stick collateral circulation of the hand, via modified Allens test
how is modified Allens test performed have pt make tight fist, RT compress both radial and ulnar artery, instruct pt to open hand and relax, RT release ulnar
what is a positive Allens test hand pinks w/in 10-15 seconds after release of ulnar artery, means circulation is adequate for puncture site
what should RT do if Allen test is negative try other arm then try brachial
what should RT do for pt who needs frequent ABG’s insert indwelling arterial catheter (only in ICU)
what do bubbles in sample do may equilibriate w/blood and cause bad sample-need to remove bubbles immediately after draw
How should RT handle sample after draw remove bubbles, store in ice water to stop metabolism, analyze with in 1 hr
room temp samples must be analyzed how soon 10-15 mins
how long should pressure be applied to stick wound 3-5 mins or longer if clotting problem
ABG and VGB samples are used to evaluate what acid-base balance (Ph, PaO2 PaCO2, HCO3 BE), oxygenation status (PaO2, SaO2, CaO2, PvO2), and adequate ventilation (PaCO2)
What does PaO2 reflect O2 in plasma of arterial blood, reflects ability of lungs to transfer O2 into blood
Predicted PaO2 is dependent on what pt age, FIO2, PIO2 (Pb and altitude)
effects of age on PaO2 103.5-(.42xage)+- 4, so if old fart like Jeff and age is 60 then 103-(.42×60) is 78.3 so normal range of PaO2 for Jeff is 74-82
hypoxemia PaO2 less than normal predicted range, at any age, for pt breathing room air or PaO2 <65mmhg, severe <40mmHg (any age) in pt with increased FIO2
Does hypoxemia exist if pt is on >FIO2 and his PaO2 is normal? NO, hypoxemia is only a <PaO2 lower than predicted regardless of FIO2
Hypoxia inadequate tissue oxygenation
how are hypoxemia and hypoxia related hypoxemia may result in hypoxia in pts with <CO, but they are not synonymous
most common cause of hypoxemia is >V/Q mismatch, in pts with lung disease
increased V/Q mismatch decrease in V/Q matching, perfusion is god, but ventilation is not, mucus plugging, secretions, bronchospasm, in specific portions of the lung
decreased V/Q matching is what (has been on last two Vent tests), an increase in V/Q mismatch
causes of hypoxemia >V/Q mismatch, diffusion defects, >CO2 from hypoventilation, Drug OD (>CO2), <PIO2 (altitude), equip failure
SaO2 norm >95%, O2 saturation, actual amount of O2 bound to Hb expressed as a %
how is SaO2 determined can be calculated, but true SaO2 must be can only be gotten from co-oximeter
Oxyhemoglobin disassociation curve shows the effects of O2 loading and unloading in relationship to Hb
Left shift in HbO2 disassociation curve >Ph, >SaO2, >Hb affinity, <temp, <CO2, <fetal Hb, <2,3 DPG, (increased affinity makes unloading at tissue more difficult)
Right shift in HbO2 disassociation curve <Ph, <SaO2, <Hb affinity, >temp, >CO2, >fetal Hb, >2,3 DPG, (decreased affinity makes unloading at tissue easier)
Ph and Hb affinity for O2 as Ph changes Hb affinity for O2 is directly affected (Bohr effect), Ph up, Hb affinity also up, Ph down Hb affinity also down
2,3 DPG organic phosphate in RBC, stabilizes deoxygenated Hb, reducing its affinity for O2, without it Hb would never unload O2 at the tissue
what >2,3DPG Alkalosis, chronic hypoxemia, anemia
what <2,3DPG acidosis
Shunt V/Q is equal to 0, perfusion with no ventilation, alveoli blocked, refractory to O2
decreased V/Q mismatch shunt effect, perfusion in excess of ventilation, non-refractory to O2, partial obstruction, hypoventilation, COPD, interstitial disease
Normal V/Q matching .8
increased V/Q matching ventilation in excess of perfusion, deadspace effect, regional hyperventilation, often seen in PPV and <CO
Deadspace ventilation no perfusion, increased PaO2 with a decreased CO2 (usually less than 40) emboli
CaO2 (Hb x 1.34)xSaO2+(PaO2x.003), norm 16-20 vol%, O2 bound to Hb and O2 in plasma, very important because of influence to tissue oxygenation
how is CaO2 measured can only truly accurate w/co-oximeter
decreased CaO2 anemia (normal PaO2 & SaO2 with <Hb), polycythemia (<PaCO2 & SaO2 w/normal CaO2), Hb bound by another gas (co-monoxide, metho)
P(A-a)O2 norm 10-15 mmHg on room air, or 25-65on 100%, predicted dependent on age and FIO2, increase is resp defect, every increase of 50 is 2% shunt above normal of 2-3%
Can A-aDo2 be calculated on nasal canulla? no, FIO2 must be known, never calc on low flow devices
A-aDO2 for old pt (age x 0.4), old fart like Jeff at age 70 x .4 equals 28 mmHg on room air
When might you see hypoxemia w/normal A-a diff hypoventilation or <PIO2
A-a DO2> 350 on 100% is what indication for mech ventilation w/refractory hypoxemia
PvO2 norm 38-42, mixed venous, must be drawn from pulmonary artery
Oxygen delivery is a function of what? CO and CO2
PaO2, SaO2 and CaO2 evaluate what respiratory component
how is tissue oxygenation assessed PvO2
decreased PvO2 <35 most often from impaired circulation, hypovelemia, PPV, LHF
normal or increase PVO2 in a very sick pt is usually caused by tissue hypoxia still exists, PVO2 is unreliable-mechanism is unknown
C(a-v)O2 norm 3.5-5 vol%, increased w/stable VO2 indicates perfusion to organs is decreasing
a-v diff >6vol% cardiovascular decompensation and tissue oxygenation is inadequate
a-v diff <3.5 vol% perfusion exceeds normal (if steady VO2), if VO2 is down then hypothermia
HbCO norm .5%, carboxyHb, carbon monoxide poisoning, must use co-oximeter, 200-250 x greater affinity than O2 for Hb
increased HbCO causes what tissue hypoxia, inhibits unloading of O2 at tissue, >of 5-10% w/smokers, >40-60% causes visual disturbances, myocardial toxicity, LOC, eventual death
S&S of increased HbCO headache, dyspnea, nausea, tachycardia, tachypnea
what effect does HbCO have o PaO2 and SaO2 if co-oximeter is not used, both will be normal
significance of PAO2 + PaO2 (on room air) 110-130 is hypoxemia due to hypoventilation, <110 is hypoxemia due to lung defect, >130 is pt on >FIO2 or error
First sign of hypoxemia is short of breath especially on exertion
clinical manifestations of hypoxemia are tachycardia, tachypnea, hypertension, cyanosis, confusion
severe hypoxemia may result in tissue hypoxia, met acidosis, bradycardia, hypotension, coma
In ICU pt, how do we identify tissue hypoxia PvO2 <35 and a-v diff >5 vol%
lungs remove CO2 by ventilation
kidneys role in acid-base balance is what remove small quantities of acid, restore buffer capacity of fluids by replenishing HCO3
Ph hydrogen ion concentration in blood, reflects acid-base balance
acid solutions capable of donating H+
bases solutions capable of accepting H+
PaCo2 respiratory component of acid-base balance, identifies degree of ventilation in relation to metabolic rate
hypercarbia mot often results from hypoventilation, CO2 >45
hypocarbia is usually caused by hyperventilation, CO2 <35
How is uncompensated resp acidosis identified Ph,CO2, with normal HCO3 and normal BE
what is fully/completly compensated resp acidosis? CO2, with normal HCO3 aHCO3 enough to bring Ph within normal range
What is the most reliable measurement of pt ventilation CO2, and should be interpreted in light of a normal VE w/CO2 or >VE w/normal CO2
HCO3 bicarb, norm is 22-26 mEq/L, primary metabolic component of acid-base balance, regulated by renal system, usually requires 12-24 hrs for compensatory response
A decrease in CO2 (to the left in O2 curve) reduces HCO3 how much CO2 <5mmHg will <HCO3 by 1
An increase in CO2 (to the right) will increase HCO3 how much CO2 >10-15 will >HCO3 by 1
BE+- base excess base deficit, standard deviation of HCO3 that takes buffering of RBC’s into account. Calculated with Ph, CO2 and Hematocrit and is a more complete analysis of metabolic buffering capability
Base excess positive value indicates either base has been added or buffer removed, larger the number the more sever the metabolic component
what is the importance of BE allows analysis of pure metabolic components of acid-base balance, changes in met components alter acid-base, respiratory components do not
do changes in CO2 effect BE? NO, only metabolic changes alter BE
Simple respiratory acidosis is inadequate ventilation, elevated CO2
common causes of resp acidosis acute upper airway obstruction, severe diffuse airway obstruction (acute or chronic), massive pulm edema
Common non-respiratory problems that cause resp acidosis drug OD, spinal cord injury, neuromuscular diseases, head trauma, trauma to thoracic cage
How is acute resp acidosis compensated none, renal changes are to slow
How is chronic resp acidosis compensated kidneys increase absorption of HCO3
How is uncompensated resp acidosis identified Ph,CO2, with normal HCO3 and normal BE
What is partially compensated resp acidosis HCO3, but Ph is not yet w/in normal limits
what is fully/completely compensated resp acidosis? HCO3 enough to bring Ph within normal range
How is degree of compensating determined in resp acidosis acute-HCO31 for every 10-15 in CO2, chronic- HCO34 for every 10 CO2
If expected level of HCO3 compensation is not occurring for acute or chronic acidosis what should RT suspect? complicating metabolic disorder is also present
neuromuscular disease or obstructive disorder w/resp acidosis, pt will RR will be what short of breath and RR
Drug OD or impaired resp center pt w/ resp acidosis pt RR will be what reduced
what effect does acute elevation of CO2 and acidosis have on CNS anesthetic, confused, semi-conscious and eventually coma
in acute resp acidosis how high does CO2 get for Pt to reach coma around 70 mmHg
because CO2 causes systemic vasodilation, what cardiac manifestations should be expected? warm flush skin, bounding pulse, arrhythmias
because CO2 causes cerebral vasodilation, what might be expected ICP, retinal venous distension, papilledema, headache
when HCO3 levels are up, what happens to chloride levels if result of renal compensation, then chloride will be
resp Alkalosis abnormal condition in which there is an increase in ventilation relative to the rate of CO2
How does RT identify resp alkalosis in ABG PaCO2 below expected level indicating ventilation is exceeding the normal level, hyperventilation
what are the common causes of resp alkalosis hyperventilation caused by pain, hypoxemia (PaO2 55-60), acidosis, anxiety
how do the kidneys compensate for resp alkalosis excrete HCO3
What is the expected compensation for acute resp Alkalosis none, Ph, PaCO2, normal HCO3
What is the expected compensation for partially compensated resp Alkalosis Ph, HCO3
What is the expected compensation for fully compensated resp Alkalosis normal Ph, HCO3
Expected compensation is not present for HCO3 in resp alkalosis, what should RT suspect complicating metabolic disorder is also present
In resp alk what is the advantage of a PaCO2 an PAO2 and therefor less chance of hypoxemia being present, or if present it will be better than if CO2 is up.
Clinical S&S associated w/ resp alkalosis tachypnea, dizziness, sweaty, tingling in fingers and toes, muscle weakness and spasms
when does RT need to be cautious not to induce resp alkalosis? during IPPB and mech vent
simple met acidosis HCO3 or BE falls below normal, caused when buffers are not produce in enough quantity (high Gap), or when buffers are lost (normal Gap)
Anion Gap normal 11 (8-16 mEq/L), when fixed acids accumulate in the body, H+ reacts to HCO3 causing it to,leading to a anion gap
Causes of met acidosis with high anion gap can be divided into two categories what are they metibolicy produced acid gains or ingestion of acids
High anion gap met acidosis from metabolicy acid gains lactic acidosis (hypoxia, sepsis), ketoacidosis (diabetes, starvation, lack of glucose), renal failure (retained sulfuric acid)
High anion gap metabolic acidosis from ingestion of acids salcylate poisoning (aspirin), methanol, ethylene glycol
normal anion gap metabolic acidosis (hyperchloremic acidosis) from loss of HCO3 is caused by diarrhea or pancreatic fistula
normal anion gap met acidosis from failure to reabsorb HCO3 is most often caused by renal failure
normal anion gab met acidosis from ingestion may be caused by ammonium chloride or IV nutrition
what signs may be present w/renal disease blood urea, nitrogen and creatinine, urine output
How does the body compensate for met acidosis CO2(hyperventilation)
If normal or PaCO2 is present w/met acidosis what should RT suspect resp defect is also present (combination resp/met acidosis)
What is the predicted compensation of PaCO2 for met acidosis PaCO2 eqs (1.5xHCO3)+8+-2, if PaCO2 is not at predicted level based on calc, resp abnormality is present
what is the most common and obvious sign of met acidosis Kussmaul’s breathing
what is Kussmaul’s respiration very rapid, very deep ventilation
S&S and Pt complaints w/severe met acidosis dyspnea, headache, nausea, vomiting followed by confusion and stupor. Vasoconstriction, pulm edema, arrhythmias (if severe enough)
simple met alkalosis above normal HCO3
most common causes of met alk hyperkelemia, hypochloremia, ng suction (acid), vomiting (acid), post hypercapnic disorder, diuretics, steroids or to much bicarb therapy
how does body compensate for met alkalosis hypoventilation to PaCO2
fully compensated met alk is identified by in PaCO2 enough to return Ph to normal (hypercarbia may be present and may appear as resp acidosis)
when should RT suspect a mixed acid base disorder normal or near normal Ph w/severe abnormal HCO3 or PaCO2
where should RT look for clues of mixed acid base disorders pt hx, physical exam, lab tests, knowing primary disorders, expected compensations
expected compensation for acute resp acidosis PaCO215-HCO31
expected compensation for chronic resp acidosis PaCO210-HCO34
expected compensation for acute resp alkalosis PaCO25-HCO31
expected compensation for chronic resp alkalosis PaCO210-HCO3 5
expected compensation for met acidosis PaCO2 eqs (1.5xHCO3)+8+-2 (shortcut is last two digits of Ph is equal to PaCO2) or HCO31-PaCO2.6
mixed/combined resp met acidosis PaCO2 HCO3
why is combined resp/met acidosis so easy to identify hypercapnia and low HCO3 work synergistically to significantly reduce Ph, often resulting in profound acidosis
common causes of resp/met acidosis are cardio pulm resuscitation, COPD and hypoxia, poisoning and drug OD
cardio pulm resuscitation and resp/met acidosis heart stops-blood circulation stops, apnea causes resp acidosis, and hypoxia causes lactic acidosis (metabolic)
COPD and hypoxia w/resp met acidosis chronic COPD w/compensated resp acidosis suddenly gets met disturbance like hypotension or renal failure, causing hypoxia and lactic acidosis
mixed/combined met resp alkalosis HCO3 w/below normal PaCO2-additive effects may result in severe alkalosis
When met alk is super imposed on resp alk, why does it become so severe when superimposed there is no compensation
what clinical situation will RT most likely see met/resp alkalosis hypoxemia, hypotension, neuro damage, to much mech vent, anxiety, pain, or any of above in combo
What pts most often get combined met resp alkalosis chronic COPD w/elevated HCO3, suddenly reduction in PaCo2 from mech vent will cause resp alk onto the met alk pt already has
Mixed met acidosis with resp alkalosis are difficult to recognize because either abnormality usually compensates for the other
met acidosis with Paco2 lower than predicted for degree of acidosis resp alk is also occurring simultaneously, Ph will be just above 7.4 (appearing to compensate for for resp alk)
what is the prognosis for met acidosis on resp alkalosis poor, most likely seen in critically ill
sleep related breathing problems occur in what % of adults 5% (more often in men)
incidence of sleep-related problem  to what after age 60 37%
two basic types of sleep are non-rem and rem
NREM and REM cycle every 60-90(book) minutes (Karel says 70-90)
NREM non-rapid eye movement, the beginning of sleep, 4 stages
Stage 1 NREM, beginning of sleep, large eye rolls/low amp waves, drowsiness, lasts only minutes
Stage 2 NREM, sleep spindles (12-14 Hz), w/large K complexes (77uV), deeper sleep, lasts 20-30 mins, PREDOMINANT STAGE OF SLEEP IN ADULTS
Stage 3 & 4 NREM, slow wave sleep, difficult to rouse, high amp waves (75 UV), increase (time) with age and pathological state
Stage 4 aka Delta
NREM & ventilation RR slows and becomes irregular (becomes more regular as in Delta), PaCO2(in early stages), BP 5-10% in stages 1-2% and 8-14% in Delta
REM begins 60-90 mins after sleep begins
Dreams NREM-dreamlike, REM-dreaming
REM per night 4-5, getting progressively longer and more intense during the night
1st REM episode of the night lasts how long 5 mins
REM toward morning is how long 30-60 mins
% of REM sleep in a lifetime 20-25%
% of REM sleep in an infant 55-80, tapers till meeting adult % at 6 months
Physical changes of REM partially paralyzed, resp effort is chaotic, diminished response to hypercapnia & hypoxemia, upper airway tone
sleep continuity theory as sleep interruption goes up, daytime alertness goes down
does the amount of time spent in any sleep stage 1234 or REM predict performance or degree of sleepiness? no, only interruption of sleep
sleep apnea cessation of airflow for at least 10 seconds during sleep, 3 types obstructive, central and mixed
OSA obstructive sleep apnea, airflow reduction >70%, in the presence of resp effort
CSA central sleep apnea, 10 seconds or more of apnea w/no effort to breath, intermittently normal
Mixed sleep apnea periods of OSA & CSA during the same night of sleep
hypopnea OSA w/30% reduction of airflow and >4% in SaO2 during sleep, results in hypoxemia-causes temp arousal from sleep
what can cause temp arousal from sleep during sleep? hypopnea and OSA
UARS upper airway resistance syndrome, neg intrathoracic press from WOB (but no O2 desaturation)
what can disturb ventilation during sleep apnea, hypopnea and UARS
why don’t UARS pts remember be awaken from apnea episodes in the night? usually just arouse to lighter stage not fully awake
best way to determine exact type and severity of of sleep disorder PSG-polysomnogram
RDI resp disturbance index, positive if >5 (incidences in a night)
RDI measures obstructive apnea’s, hypopnea’s, central apnea’s per hour
RDI for infants >1 per hr, SaO2 <95%, end VT CO2 >53 during apnic episode
REM behavior disorder people who act out in dreams
% of people w/sleep disorders 15%
SDC sleep disorder criterion, RDI 5-20 mild, 20-40 moderate, >40 severe
what is the difference between UARS and OSA UARS do not become hypoxic during sleep, (they have excessive sleepiness from poor continuity of sleep)
Best TX for UARS CPAP (nasal)
What are the most common forms of SDB in adult OSA and hypopnea
cause of OSA upper airway occlusion during sleep
causes of hypopnea partial closure of the airway
anatomical abnormalities that may lead to OSA/hypopnea micrognathia (sm lower jaw), large tongue, large tonsils/adenoids, retrognathia (under developed mandible), deviated septum
most common site of obstruction in OSA/hypopnea pharynx (soft pallet to glottic inlet)
pathophysiology of an upper airway obstruction during sleep airway relaxes, narrows or occludes, causing WOB causing intrathoracic press to overcome obstruction, causing narrowing airway
what does upper airway obstruction cause hypoxemia and sleep arousal
what % of pts w/sleep apnea are obese? 60-90%
what is the most dangerous symptom of OSA? excessive daytime sleepiness
EDS excessive daytime sleepiness, impairs cognitive and psycho-motor function
typical Hx of OSA pt obese middle age male, loud snoring, excessively sleepy, stops breathing at night
hallmark of OSA loud snoring
cardinal symptoms of OSA 3S rule-Snore (loud, habitual), Spousal (reports apnic episodes), Sleepiness (daytime, excessively)
clinical features of OSA snores, EDS, morning headaches, fragmented sleep, memory loss, confused awakenings, personality changes, impotence, night sweats, dysrrhthmias, BP, CHF, enuresis (bed wetting)
airway features of OSA may include nasal obstruction, low soft palate, large uvula, enlarged tonsils/adenoids, macroglosia, large neck (>17.5)
%of OSA w/hypertension 50%
what is the biggest risk factor of OSA in children obesity
cardiac changes w/OSA bradycardia during apnic episodes, then tachycardia follow, PVC’s and CHF
what % of OSA have PVC’s 20, asystole 10%
TX for OSA CPAP
what is the Hallmark symptom of OSA in children snoring
% of sleep apnea that is CNA 10%
CSA cessation of airflow resulting from lack of movement of the diaphragm-loss of vent drive
when afferent input of vent drive is absent during sleep CSA
what factors may play a role in /csa in children cardiac, hematologic, metabolic, neurologic, gastro, or nuero abnormalities
most significant difference between OSA and CSA pts body size, smaller in CSA and fewer daytime daytime side effects
SIDS leading cause of death in children under age 1, unknown cause, peaks at 2-4 months
ALTE apparent life threatening event, child appears to be dying because of apnea (pallor and cyanosis)
best way to prevent SIDS supines sleeping position, decreases by 50%, parental non smoking and removal of soft bedding
RT should observe sleeping pt for what if they notice a pause in pts breathing time episodes, sleeping position, presence/absence cyanosis, note breathing effort
primary tool to evaluate sleeping disorders PSG
what is used to determine sleep stage EEG, electroencephalogram
EOG electrooculogram
Chin EMG chin muscle activity, also used to detect REM
Tools of PSG EEG(stage), EOG, Chin EMG and leg EMG (REM), 1 lead ECG (arrhythmias), electrodes for respiration, snoring microphones and pulse ox
can pulse ox be used for diagnosis of UARS not reliable, need cooximeter
what is the gold standard for diagnosing sleep apnea PSG (polysomnogram)
MSLT multiple sleep latency test, recommended for pts who’s reported sleepiness is more than his/her level of SDB indicates
sleep latency amount of time required to fall asleep
what is the most reliable and valid test of daytime sleepiness MSLT, 4-5 daytime naps
what is the normal time for a person to fall asleep for a nap if they have severe sleepiness 5-8 mins (norm 15)-no specific disorder, can be any
what % of men have sleep related problems 5%
what is the predominant stage of NREM 2
T/F breathing tends to be irregular during early stages of NREM? T
T/F BP tends to during initial stages of sleep? T
T/F During REM sleep, sleeper is partially paralyzed? T
T/F breathing is chaotic/irregular during REM in most sleepers T
what is the key concept in central sleep apnea intermittent absence of respiratory effort
hypopneas are most closely related to what? OSA
all of the following are believed responsible for the onset of OSA relaxation of the upper airway, big in resistance, more forceful contraction of insp muscles, significant static compliance
all of the following clinical feature are typical for adult pts w/OSA excessive daytime sleepiness, loud snoring, impaired cognitive function
most common arrhythmia seen in OSA PVC’s (20%)
all of the following are seen in children w/OSA daytime sleepiness, hyperactivity, aggressive behavior
peak onset for SIDS 2-3 months
all of the following are monitored during polysomnogram EEG, ECG, leg emg
what test is for measuring daytime sleepiness MSLT
how long are naps during MSLT min 20 minutes, max 35 mins
actigraphy wristwatch like device worn for several days
tx mild osa lose weight, oral devicem avoid alcohol and caffeine
moderate sleep apnea tx CPAP
tx of severe sleep apnea bilevel, surgical procudures UPPP, LAUP
caution of CPAP with OSA can cause central sleep apnea is some cases
tritrating CPAP 30 day trial, set up at 4epap, up 1 for 20 breaths until stable
TX of mild OSA lose weight, sleep on one side, oral mouth guard, avoid alcahol and caffeine
TX of moderate OSA CPAP, set at 4 and adjust up in incriments of 1 until obstruction relieved
why do we repeat polysomnogram in 30 days after start of CPAP in OSA? to make sure CSA is not underlying issue
TX for severe OSA Bilevel, or surgury (UPPP, LAUP or tracheostomy)
TX for CSA Auto-SV (bipap w/auto backup) or CPAP (infants only)
what is Auto-SV records and targets pt peak flow and RR over a 4 minute period, adjusts press down as pt peak press rises (similar to CPAP+press support), automatically increases press if breathing stops and lowers it again if breathing is normal
Initial settings for Auto-SV Epap-4, Ipap-same as E or max of 10, RR set to pt with minimum 10, re-evaluate in 20 mins
Hypopnea TX CPAP or BIpap, set at 2 ipap, increase at 1 until relief found, set back up at 1.2 second IT
primary hypoventilation syndrom CSA
what SA is frequently associated with heart disease CSA
types of CSA primary and cheynes-stokes
primary CSA mostly in premies, cause unkown
Cheyne stokes CSA caused by heart failure, stroke, or kindney failure, drug OD
length of breath absence in cheyne-stokes id’s disease 50-70 sec heart failure, 20-40 sec altitude, neuro disease, renal failure
ASV adaptive servo-ventilaltion, new tx for CSA, records pt breathing pattern and then uses data to normalize breathing as necessary
CCHS congenital central hypoventilation, very rare CSA children get, have no hypoxic drive while sleeping, have to trached and mech vented at night
what neurvous system regulates HR and BP autonomic
Question Answer
INSPECTION LEVEL ONE GENERAL APPEARANCE, APPEARANCE OF CHEST, RESPIRATORY PATTERN, SENSORIUM,POSTURE,PATIENT COLOR,
PALPATION LEVEL ONE HEART BEAT, PULSE ALWAYS PICK
HISTORY LEVEL ONE HISTORY OF PRESENT ILLNESS, MEDICAL, FAMILY,DNR
WHAT IS LEVEL ONE WHAT YOU CAN SEE.
WHAT IS LEVEL TWO ASSESSMENT YOU NEED TO DO TO GATHER MORE INFORMATION.
VITAL LEVEL TWO RESPIRATORY RATE,BLOOD PRESSURE,TEMPERATURE
LEVEL TWO – TAPING ON THE CHEST PERCUSSION.
LEVEL TWO AUSCULTATION BREATHER SOUND,HEART SOUND, BOWEL SOUND(FOR BABY ONLY).
LEVEL THREE LAB STUDIES CBC, ELECTROLYTES,
LEVEL THREE RADIOLOGICAL STUDIES CHEST XRAY
LEVEL THREE BLOOD SAMPLES ARTERIAL BLOOD GAS
LEVEL THREE CARDIOPULMONARY TESTING. ELECTROCARDIOGRAM
LEVEL FOUR LAB STUDIES SPUTUM CULTURE, URINALYSIS.
LEVEL FOUR PFT VOLUME, FLOWS, PRE-POST BRONCHODILATOR.
LEVEL FOUR RADIOLOGICAL STUDIES BRONCHOGRAMS,LATERALNECK, ANGIOGRAMS,MRI,CT SCANS, PET CANS
LEVEL FOUR CARDIOPULMONARY TESTING. BRONCHOSCOPY,STRESS TESTING, ECHOCARDIOGRAM,ANGIOGRAPHY.
LEVEL FOUR HEMODYNAMIC MONITORING ARTERIAL LINE, PULMONARY ARTERIAL LINE ICP
LEVEL FIVE OTHER TEST
SWEAT CHLORIDE TEST DIAGNOSTIC TEST FOR CYSTIC FIBROSIS
V/Q SCAN USING RADIOACTIVE GAS TO DETECT A PULMONARY EMBOLISM
ELISA TEST/ HIV USE TO DETERMINE THE PRESENCE OF HIV VIRUS,POSITIVE TEST IS DIAGNOSIS OF AIDS.A SPECIFIC TEST TO BE ORDER FOR ANY DRUG ABUSER.
TENSILON TEST DIAGNOSTIC TEST FOR MYASTHENIA GRAVIS
APGAR SYSTEM OF SCORING INFANT PHYSICAL CONDITION AT ONE AND FIVE MINUTE
CARDIAC ENZYMES CHEST PAIN
POLYSOMNOGRAPHY SLEEP STUIDES
OXYGEN THERAPY EQUIPMENT, FiO2
HYPERINFLATION THERAPY INCENTIVE SPIROMETRY, IPPB
MECHANICAL VENTILATION VT/PRESSURE,RATE,FiO2, SIMV,ASSIST/CONTROL,CONTROL,PEEP/CPAP PCV,PSV,APRV,IRV,HFJV,NIPPV
AIRWAY MANAGEMENT INTUBATION,SUCTION, CHEST PHYSICAL THERAPY
AEROSOL THERAPY ULTRA NEBUILZER,HEATED AEROSOL,OXYGEN TENTS,MEDICATION NEBULIZER,MDI,DPI
REHABILITATION/HOME CARE EQUIPMENT,PROCEDURES
PHARMACOLOGY BRONCHODILATORS,CARDIOVASCULAR,STEROIDS/DECONGESTANTS, ANTIBIOTICS/ANTIVIRALS, MUCOLYTICS/WETTING ANGENTS,SEDATION/PAIN MEDS,CHOLINERGICS,SURFACTANT,PARALYZING AGENTS,DIURETICS,NICOTINE PATCH,NITRIC OXIDE,RESPIRATORY STIMULANTS
Question Answer
Signs of acute respiratory failure (6) Dyspnea, Cyanosis, Skin, HR, RR, BP
Define Acute respiratory failure (ARF) Absent of insufficient respiratory activity resulting in inadequate oxygen uptake and CO2 clearance
ARF clinically observed as: PaO2 below the predicted normal range; PaCO2 greater than 50 and rising; pH falling below 7.25
Types of ARF (2) Lung Failure and Ventilatory pump failure
What is lung failure vent/perf mismatch, diffusion defects, R-L shunting, alveolar hypoventilation, inadequate FIO2
What is Ventilatory pump failure Inability of the body to maintain a normal PaCO2.
Ventilaroty pump failure causes CNS disorders, neuromuscular disorders, disorders that increase WOB
Early signs of Hypoxia or Hypercapnia Tachycardia, Dyspnea, Tachypnea, Hypertension
Later signs of Hypoxia or Hypercapnia PaO2< normal range, PaCO2 > 50, pH < 7.25, Confusion, Lethargy, Convulsions, Hallucinations, Coma
Indications of ARF & need for MV (ventilation) pH <7.25; PaCO2 55 and rising; Deadspace to VT ratio > 0.6
Indications of ARF & need for MV (Oxygenation) PaO2 <70 on FIO2 >.60; P(A-a)O2 >450 on O2; Pa02/PAO2 <0.15; PaO2/FIO2 <200
Standard criteria for instituting MV Apnea or absence of breathing, ARF, Impending RF, Refractory Hypoxemia
What % of patients do not require slow weaning? 80%
What is weaning gradual reduction of ventilatory support from a patient who is clinically improving
What are weaning protocols A set plan of action to enable the clinician to wean the patient according to established criteria resulting in extubation
Modes of weaning from MV CPAP; SIMV; T-piece trials; PSV; Closed Loop Modes; MMV; ASV; Bi Level
Weaning and extubating parameters VC >10; Ve <15; VT >4-6; F <30; MIP -20 or less; WOB <0.8; Dynamic CL >25; VD/VT <0.6
What is the most frequently used study and very reliable predictor of successful extubation Rapid Shallow Breathing Indes (RSBI)=f/Vt; Normal range 60-105
Post extubation complications Horseness, sore throat, cough, subglottic edema, increased WOB, Airway obstruction, Laryngospasm, Risk of aspiration
what are scalers Graphs measured over time
What are the 3 main types Flow VS. Time; Volume VS. Time; Pressure VS Time
How many views for Flow VS Time 5: Rectangular, Sinusoidal, Ascending, Descending, Exponential
How many views for Volume VS time 2: Ascending Ramp or sinusoidal
How many views for Pressure VS time 2: Rectangular or Exponential
What is auto PEEP or intrinsic PEEP When patient does not fully exhale inspired volume
Actions to eliminate auto PEEP Suction, bronchodilator, increase expiration time, increase PEEP
What does pressure volume loop show? Compliance of the lung, looks like a football, the narrower, the more compliant

 

Question Answer
Na+ Sodium 135-145 meq/L
what causes clinical increases in Na+ Cushing syndrome, hyperadrenocorticism, excessive intake, decrease H20 ( dehydration) hyperpnea, diabetes, diuretics, cardiac failure.
What are signs and symptoms of increased Na+ thirst, viscous mucous, dry rough tongue
What causes clinical decrease in Na+ adrenal insufficiency, alkli, burns, diuretics, dehydration, trauma, If you have increase in Body H20 Na+ decreases from decreased renal output, artificial hyperglycemia, CHF, cirhoisis, innapropriate ADH, renal insufficiency.
What are signs and symptoms of decrease in Na+ Increased heart rate, Increased blood pressure, cold clammy skin, apprehension, convulsions.
What is Na+ Major extracellular cation comprises majority of osmotically active solute, greatly affects distribution of body water.
K+ 3.5+5.0 mEq/L
What is K+ Major intracellular cation, maintains, intracellular osmolality, affects muscle contraction, plays role in nerve impulses, enzyme action, and cell membrane function.
What causes increases in K+ Excessive administration, Shift from the cells- Acidosis(metabolic), infection, sucinylcholine, trauma, decreased urine output.
What are signs and symptoms of increased K+ Arrythmias, muscle weakness
What causes decrease in K+ Shift INTO cells- Alkalosis, GI loss- anorexia, diarrhea,ng suctioning, vomiting. Increased urine output- cushings syndrome, diabetic ketoacidosis causes the shift as a compensatory mechanism.
What are signs and symptoms of Decreased K+ arrythmias, muscle weakness
Cl- 95-105 mEq/L
What is Cl- Principle extracellular anion, important in acid base balance.
What causes increase in Cl- Cardiac decompensation, renal insufficiency, salt intake.
What causes decreases in Cl- COPD, Cushings syndrome, dehydration, diabetic ketoacidosis, diuretics, fever, meatabolic acidosis, pneumonia.
Po4 1.4–2.7 MEq/L
What is the P04 major intracellular anion
What causes increase in the Po4 Renal insufficiency
What causes decrease in the Po4 Diabetic ketoacidosis.
Ca++ 4.5-5.8
What is Ca++ Essential anion for bones, teeth, mucoproteins. Role in cell membrane, muscle contraction and coagulation.
What causes increases in Ca++ Acidosis, adrenal insufficiency, diuretics, ( Thiazide) imobilization, sarcoidosis, tumors.
Symptoms of increased Ca++ Increased HR.
What causes decreased Ca++ Alkalosis, diarrhea, hypoproteinemia, osteomalacia, renal insufficiency, steroid therapy, vitamin D deficiency.
Mg++ 1.3-2.5 mEq/L
What is Mg++ Intracellular cation, important in ATP function, acetylcholine release at the N-M junction.
What causes an increase in Mg++ Antacid ingestion, parathyroidectomy, renal insufficiency.
What causes a decrease in Mg++ Chornic alcoholism, diabetic acidosis, diarrhea, NG Sx, severe renal disease.
RBCs Males= 4.6- 6.2 million/UL Females= 4.2- 5.4 million/UL
What is the clinical significance of RBC’s Number of cells available to carry O2/Co2
What causes an increase in RBC’s 1: Polythycemia 2: polythycemia from chronic hypoxemia, severe diarrhea and dehydration.
What causes a decrease in RBC’s Anemia, Leukemia, hemorrhage followed by restored blood volume.
What is Hgb grams of hemoglobin in 100 ml of whole blood.
what causes increase in Hgb Polycythemia, CHF, COPD, deyhdration, high altitudes.
What causes a decrease in Hgb Acute blood loss, anemias, increased fluid intake, pregnancy.
Hematocrit ( Hct) Males= 39-55% Females= 36-48%
What is Hematocrit ( Hct) % of blood volume occupied by RBC’s
What causes an increase in Hematocrit (Hct) COPD, dehydration, erythrocytosis, shock.
What causes a decrease in Hematocrit (Hct) Acute blood loss, anemia’s, increase fluid intake, pregnancy.
WBCs 5,000- 10,000/UL SI= 5-10x10to the 9th/L
What is the significance of WBC’s Blood cells which fight infection.
What causes increase in WBC’s Leukocytosis: acute infection, post surgery, trauma. Bacterial infection, neoplasm, epinephrine, steroids, chronic infection, viral infection ( hepatitis, mono) TB.
What causes a decrease in WBC’s Leukopenia: Cancer therapy, overwhelmed or suppressed immune system, CHF, HIV< renal failure.
Neutrophils 40-75%
Neutrophil Segs Immature
Neutrophil Bands mature cells.
Lymphocytes T-B cells 20-45%
Monocytes 2-10%
Eosinophils 1-6%
Eosinophils and basophils are elevated in? Allergy/Collagen. Asthma
Basophils 0-1%
Platelets 150,000-400,000/UL
What is the significance of Platelets? Blood constituent for clotting.
What causes an increase in Platelets COPD, high altitude, inflammation, malignancy, PE, TB, trauma, many drugs.
What causes a decrease in Platelets Acute leukemia, anemias, bleeding, lupus.
Anion Gap 7-16 mEq/L
Anion Gap Na+ – (Cl- + HCo3)
What causes increase in the Anion Gap Keto or lactic acidosis,, salicylate, or ethylene glycol poison, dehydration.
Creatine Kinase ( CPK) Male 38-174 U/L Female 26-140 U/L
What is the significance of Creatine Kinase (CPK) Enzyme in the heart, skeletal muscle.
What causes increases in Creatine Kinase (CPK) MI, muscle disease, severe exercise, polymyositis.
What causes decreases in Creatine Kinase (CPK) Relative cardiac enzyme levels in blood following myocardial infarction, so a couple days after infarct they drop!
Creatine phoso-kinase MB band (CPK- MB) (CK-MB) SPecific CK isoenzyme for the heart muscle. Normal is 0-6%
What causes an increase in Creatine Phoso-kinase Acute MI, severe angina, cardica surgery, cardiac ischemia, mycarditis, hypokalemia, cardiac defib.
Creatinine 0.6-1.5 mg/dl
What is the significance of Creatinine By product of muscle metabolism.
What causes Creatinine to increase Nephritis, renal insufficiency, urinary tract obstruction, (indicator of kidney function)
What causes Creatinine to decrease Debilitation
glucose 60-110 mg/dl Blood sugar
What causes an increase in Glucose Diabetes mellitus, infections, stress, steroids, trauma, uremia.
What causes a decrease in Glucose Adrenal insufficiency. Insulin
Protein 6-8 gm/dl
What is the clinical significance of Protein Blood proteins affecting colloidal pressure,
What causes an increase in Proteins Dehydration, shock
What causes a decrease in protein. Hemorrhage, liver disease, leukemia, malnutrition, nephrosis, neoplastic disease.
Lactic Acid 5-20 mg/dl
What is the clinical significance of Lactic Acid By product of aerobic metabolism.
What causes increase in Lactic Acid. Hypoxia, CHF, Increased muscle activity, hemorrhage, shock.
Theophylline 10-20 mg/dl
What is the clinical significance of Theophylline. Relaxes smooth muscle of bronchi and pulmonary blood vessels.
What causes increases in Theophylline. Abdominal discomfort, anorexia, dysrhythmias, nausea, vomiting, nervousness, irritability, tachycardia.
what causes a decrease in Theophylline. Smoking and phenytoin (Dilantin) shortens half-life.
Urea Nitrogen (BUN) 8-25 mg/dl
What is the significance of the Urea Nitrogen (BUN) End product of protein metabolism.
What causes an increase in Urea Nitrogen (BUN) Adrenal or renal insufficiency, CHF, dehydration, decreased renal flow, N2 metabolism, GI bleed, shock, urine obstruction.
What causes a decrease in Urea Nitrogen (BUN) Hepatic failure, low protein diet, nephroiss, pregnancy.
Urine output! Males= 900-1800 ml/day Femals= 600-1600 ml/day
What is normal urine output an hour about 66 ml an hour.
What is the clinical significance of Urine out put. Urine output may change the acid base balance.
What causes an increase in Urine output. Diuretics, diabetes, insipidus, excessive intake.
What causes a decrease in Urine output Dehydration, hypovolemia, injury, kidney dysfunction, shock.
Urine pH 4-5-8.0
What causes an increase in Urine pH >7= bacterial infection in tract, metabolic alkalosis, a decrease in K+, vegetarian diet.
what causes a decrease in Urine pH <6= metabolic acidosis, protein diet.
Mucoid Sputum Clear, thin, frothy
What Clinical presentation exhibits Mucoid Sputum Asthma, Chronic bronchitis, emphysema, lung cancer, Mycoplasma pneumonia, pulmonary edema, TB, Viral pneumonia.
Purulent Sputum Yellow or green, thick, viscid, offensive odor, (pus)
What Clinical presentation exhibits Purulent sputum Brochiectisis, Lung abscess, Pneumococcal pneumonia, pseudomonas pneumonia, staphlococcal pneumonia, TB
Mucopurlent SPutum. Both mucoid and purulent.
What Clinical presentation exhibits Mucupurlent sputum Asthma, chronic bronchitis, Cystic fibrosis, emphysema, Lung Abscess, Lung cancer, Pseudomonas pneumonia, TB
Hemoptysis Sputum Bright red, Frothy blood
What clinical presentation exhibits Hemoptysis sputum Bronchietasis, Lung cancer, Neoplasm, Pulmonary Infarct, TB
Currant Jelly Sputum Blood clots
what clinical presentation exhibits Currant Jelly sputum. Lung cancer, neoplasm.
Rusty Sputum. Mucopurulent with red tinge.
What clinical presentation exhibits Rusty sputum. Bronchiectasis, Neoplasm, pneumococcal pneumonia.
Prune Juice Sputum Dark brown, mucopurulent with red tinge.
What clinical presentation Exhibits Prune Juice sputum. Klebsiella pneumonia, pneumococcal pneumonia
What clinical presentation exhibits Blood streaked sputum. pneumococcal and pseudomonas pneumonias.
What clinical presentation exhibits Pink Frothy sputum Pulmonary edema.
Question Answer
ODC shift left More alkalosis, less DPG, hemoglobin has more affinity for O2, P50 decreases, Hgb is more saturated at a given PO2.
ODC shift right More acidic, more DPG, hemoglobin has less affinity for O2, P50 increases, Hgb is less saturated at a given PO2.
Normal P50 27mmHg
CO2 diffusion rate 20 times faster than O2
Dead space anatomic 1ml per pound, alveolar dead space can not be calculated, physiological dead space the sum of alveolar and anatomical deadspace.
Anatomic Shunt (true shunt) The portion of cardiac output that enters the left side of the heart without comming in contact with an alveolus for gas exchange.
Causes of Anatomic Shunts Congenital heart disease, Intrapulmonary fistula, Vascular tumors.
Capillary Shunt (true shunt) No gas exchange at alveoli.
Absolute shunt When more O2 doesn’t help/ refractory to oxygen therapy.
Shunt-like effect When pulmonary capillary perfusion is in excess of alveolar ventilation.
Causes of Capillary Shunts Atelectasis, alveolar fluid accumulation, or consolidation.
% of total CO2 transported to the lungs in RBC’s by bicarbonate (HCO3) 63%
The Haldane Effect Deoxygenated blood enhances loading of CO2 and oxyegnated blood enhaces the offload of CO2.
The Bohr Effect The effect of PCO2 and PH on the oxyhemoglobin curve.
Anatomic Shunt normals 2 to 5%
Things that move ODC right Temp increase, PCO2 increase, PH decrease (more H+), DPG increase.
Question Answer
What is the difference between respiratory distress and respiratory arrest? Respiratory Arrest-When someone is NOT getting ANY air. Respiratory distress-When someone is struggling to get air.
Universal sign for choking? Hands grabbing at the neck.
What do you do when you see that someone is choking? 1. Ask if they are choking 2. Tell them to keep coughing 3. Get someone to call 9-1-1 4. (if they stop coughing) Tell them your name and that you are trained, then ask if you can help them 5. Complete procedure
why do you tell them to keep coughing? They may be able to cough the object up on their own. When they are coughing they are still getting air at that point.
Why call 9-1-1? Even if they are coughing and getting air they might stop getting air at some point. They may have also damaged their airway from what they were choking on.
What do you do if they stop coughing? If they stop coughing, you are now in a resperiatory arrest situation. You will need to begin the life saving techniques used when someones airway is completely blocked.
What does express onsent mean? 1- Say your name 2- Say you are trained 3- Ask if you can help
What do you do when you begin helping someone who is having a respiratory arrest? (step 1) Stand beside them, with one foot up next to theirs and your back leg behind them. This will help you catch them if they become unconcious. Place your arm across their chest reaching for the other shoulder. Bend them over until parallel with the floor.
Step 2? Place the heel of one hand between their shoulder blades. Give 5 back blows, you should hear a hollow sound when you are hitting the right spot. Stant them back up and place yourself behind them.
Step 3? Find their naval and place two fingers above it. Place your fist where your fingers are with your thumb against their stomach. Reach around them with your other hand and hold your fist. Give five quick upper thrusts into the diaphragm.
What are you doing when you give abdominal thrusts? You are pushing up on the diaphragm and forcing air out of the lungs to push them out.
What do you do if they become unconcious? Lock your arms under their shoulders and pull them towards your body. Support their body and head as you lower them to the ground. Always be aware of their head and lay gently on the ground.
When caring for a conscious choking person you give ___________ followed by ____________. Five back blows, five abdominal thrusts.
What muscle do you push up on when caring for a conscious choking person and why? Diaphragm,because when pushing up on the diaphragm you are forcing air out of the lungs to push the object out.