Lower Respiratory Disorders PDF

PASSAGEWAY OF RESPIRATION MOUTH/NOSE > PHARYNX > LARYNX > TRACHEA> LUNGS> BRONCHUS> BRONCHIOLES > ALVEOLI > PROVIDES OXYGEN TO THE BLOOD> WHILE THE WASTES FROM THE BLOOD (CO2) GOES BACK TO THE ALVEOLI> EXHALED BACK THROUGH THE PASSAGEWAY AND GOES BACK OUT THROUGH THE MOUTH/ NOSE -ALVEOLI IS ACTUAL...

PASSAGEWAY OF RESPIRATION MOUTH/NOSE > PHARYNX > LARYNX > TRACHEA> LUNGS> BRONCHUS> BRONCHIOLES > ALVEOLI > PROVIDES OXYGEN TO THE BLOOD> WHILE THE WASTES FROM THE BLOOD (CO2) GOES BACK TO THE ALVEOLI> EXHALED BACK THROUGH THE PASSAGEWAY AND GOES BACK OUT THROUGH THE MOUTH/ NOSE -ALVEOLI IS ACTUALLY THE DEAD END OF THE AIR INHALED -ALVEOLI IS ALSO VERY CLOSE TO THE BLOOD  ATELECTASIS - IS THE COLLAPSE OF ONE OR MORE PARTS OF THE LUNG - SPECIFICALLY AFFECTS THE SMALL AIR SACS ALVEOLI HOW IT HAPPENED? WHEN YOU BREATHE IN, YOUR LUNGS FILLS UP AIR. THE AIR TRAVELS TO SACS OF YOUR LUNGS (ALVEOLI), WHERE OXYGEN MOVES INTO YOUR BLOOD. THE BLOOD DELIVERS THE OXYGEN TO THE ORGANS AND TISSUE THROUGHOUT YOUR BODY. INSUFFICIENT AIR COMING TO INFLATE THE ALVEOLI OR IF OUTSIDE PRESSURE IS PUSHING ON THEM, THEY CAN COLLAPSE (ATELECTASIS) TYPES OF ATELECTASIS 3 MAIN TYPES  COMPRESSIVE ATELECTASIS IS WHEN SOMETHING AROUND YOUR LUNG – LIKE FLUID, AIR, BLOOD OR TUMOR – PUSHES AGAINST IT, CAUSING COLLAPSE.  RESORPTIVE ATELECTASIS HAPPENS WHEN THE OXYGEN AND CARBON DIOXIDE IN YOUR ALVEOLI MOVE INTO YOUR BLOODSTREAM AN NO NEW AIR MOVES IN. THIS CAUSES YOUR ALVEOLI TO COLLAPSE. SURGERY THAT REQUIRES ANESTHESIA IS A COMMON CAUSE OF RESORPTIVE ATELECTASIS  RESORPTIVE ATELECTASIS SOMETHING BLOCKING THE INSIDE OF YOUR LUNG, KEEPING AIR FROM COMING INTO ALVEOLI, CAN ALSO CAUSE RESORPTIVE ATELECTASIS. ALSO CALLED OBSTRUCTIVE ATELECTASIS, THE BLOCKAGE CAN BE MUCUS, A TUMOR OR AN OBJECT THAT YOU ACCIDENTALLY INHALED CONTRACTION ATELECTASIS LUNG SCARRING (FIBROSIS) CAUSES CONTRACTION ATELECTASIS. SCARRING KEEPS THE ALVEOLI FROM OPENING PROPERLY CLINICAL MANIFESTATION DYSPNEA (SHORTNESS OF BREATH) COUGH SPUTUM PRODUCTION TACHYCARDIA TACHYPNEA PLEURAL PAIN CENTRAL CYANOSIS ORTHOPNEA –(DIFFICULTY BREATHING WHEN SUPINE)  CLINICAL MANIFESTATION IN ACUTE ATELECTASIS INVOLVING A LARGE AMOUNT OF LUNG TISSUE (LOBAR ATELECTASIS), MARKED RESPIRATORY DISTRESS MAY BE OBSERVED. SIGNS AND SYMPTOMS (PREVIOUS SLIDE)  CLINICAL MANIFESTATION IN CHRONIC ATELECTASIS, SIGNS AND SYMPTOMS ARE SIMILAR TO THOSE OF ACUTE ATELECTASIS. THE CHRONIC NATURE OF THE ALVEOLAR COLLAPSE PREDISPOSES PATIENTS TO INFECTION DISTAL TO THE OBSTRUCTION. THEREFORE, THE SIGNS AND SYMPTOMS OF A PULMONARY INFECTION ALSO MAY BE PRESENT NOTE: IF YOU HAVEN’T HAD A CHEST OR ABDOMINAL SURGERY RECENTLY, ATELECTASIS CAN INDICATE AN OBSTRUCTION OF YOUR AIRWAY THAT’S CAUSING A PARTIAL OR COMPLETE LUNG COLLAPSE.  ASSESSMENT AND DIAGNOSTIC FINDINGS THE USE OF ACCESSORY MUSCLES WHEN BREATHING –DELTOID, TRAPEZIUS, AND STERNOCLEIDOMASTOID HYPOXEMIA- DECREASED OXYGENATION IN THE BLOOD DECREASED BREATH SOUNDS AND CRACKLES ARE HEAR OVER THE AFFECTED AREA  A CHEST X-RAY MAY SUGGEST A DIAGNOSIS OF ATELECTASIS BEFORE CLINICAL SYMPTOMS APPEAR; THE X-RAY MAY REVEAL PATCHY INFILTRATES OR CONSOLIDATED AREAS DEPENDING ON THE DEGREE OF HYPOXEMIA, PULSE OXIMETRY MAY DEMONSTRATE A LOW SATURATION OF HEMOGLOBIN WITH OXYGEN (LESS THAN 90%) OR A LOWER-THAN-NORMAL PARTIAL PRESSURE OF ARTERIAL OXYGEN (PAO2) NURSING MANAGEMENT: PREVENTION FREQUENT TURNING EARLY MOBILIZATION STRATEGIES TO EXPAND THE LUNGS AND TO MANAGE SECRETIONS VOLUNTARY DEEP-BREATHING MANEUVERS (AT LEAST EVERY 2 HOURS) ASSIST IN PREVENTING AND TREATING ATELECTASIS NOTE: THE PERFORMANCE OF THESE MANEUVERS REQUIRES THE PATIENT TO BE ALERT AND COOPERATIVE. PATIENT EDUCATION AND REINFORCEMENT ARE KEY ELEMENTS TO SUCCESS OF THESE INTERVENTION  THE USE OF INCENTIVE SPIROMETRY OR VOLUNTARY DEEP BREATHING ENHANCES LUNG EXPANSION, DECREASES THE POTENTIAL FOR AIRWAY CLOSURE, AND MAY GENERATE A COUGH. INCENTIVE SPIROMETRY IS A HAND-HELD DEVICE THAT HELPS PEOPLE TO TAKE SLOW, DEEP BREATHS. IT’S LIKE EXERCISING EQUIPMENT FOR THE LUNGS TO KEEP THEM STRONG AND WORKING WELL MANAGEMENT IF THE CAUSE OF ATELECTASIS IS BRONCHIAL OBSTRUCTION FROM SECRETIONS, THE SECRETIONS MUST BE REMOVED BY COUGHING OR SUCTIONING TO ALLOW AIR TO REENTER THAT PORTION OF THE LUNG CHEST PHYSICAL THERAPY (CPT) AND POSTURAL DRAINAGE MAY ALSO BE USED TO MOBILIZED SECRETIONS SVN OR SMALL VOLUME NEBULIZERS TREATMENTS WITH A BRONCHODILATOR MAY BE USED TO ASSIST PATIENTS IN THE EXPECTORATION OF SECRETIONS  IF RESPIRATORY CARE MEASURES FAIL TO REMOVE THE OBSTRUCTION, BRONCHOSCOPY IS PERFORMED FOR SEVERE OR MASSIVE ATELECTASIS, IT MAY LEAD TO RESPIRATORY FAILURE, ESPECIALLY IN PATIENTS WITH UNDERLYING LUNG DISEASE. ENDOTRACHEAL INTUBATION AND MECHANICAL VENTILATION MAY BE NECESSARY IF THE CAUSE OF ATELECTASIS IS COMPRESSION OF LUNG TISSUE, THE GOAL IS TO DECREASE THE COMPRESSION. EXAMPLE- LARGE PLEURAL EFFUSION THAT COMPRESSES THE LUNG TISSUE AND CAUSING ALVEOLAR COLLAPSE, TREATMENT MAY INCLUDE THORACENTESIS KEY TO REMEMBER MANAGEMENT OF CHRONIC ATELECTASIS FOCUSES ON REMOVING THE CAUSE OF THE OBSTRUCTION OF THE AIRWAYS OR THE COMPRESSION OF THE LUNG TISSUE. FOR EXAMPLE, BRONCHOSCOPY MAY BE USED TO OPEN AN AIRWAY OBSTRUCTED BY LUNG CANCER OR A NONMALIGNANT LESION, AND THE PROCEDURE MAY INVOLVE CRYOTHERAPY OR LASER THERAPY.  IF THE ATELECTASIS IS A RESULT OF OBSTRUCTION CAUSED BY LUNG CANCER, AN AIRWAY STENT OR RADIATION THERAPY TO SHRINK A TUMOR MAY BE USED TO OPEN THE AIRWAYS AND PROVIDE VENTILATION TO THE COLLAPSED AREA. HOWEVER, REOPENING THE AIRWAYS AND REAERATING THE AREA OF THE LUNG MAY NOT BE POSSIBLE IN PATIENTS WHO HAVE EXPERIENCED CHRONIC, LONG-TERM COLLAPSE. IN SOME CASES, SURGICAL MANAGEMENT MAY BE INDICATED ACUTE TRACHEOBRONCHITIS AN ACUTE INFLAMMATION OF THE MUCOUS MEMBRANES OF THE TRACHEA AND THE BRONCHIAL TREE OFTEN FOLLOWS INFECTION OF THE UPPER RESPIRATORY TRACT USUALLY AS A RESULT OF VIRAL INFECTION. PATIENTS WITH VIRAL INFECTIONS HAVE DECREASED RESISTANCE AND CAN READILY DEVELOP A SECONDARY BACTERIAL INFECTION ADEQUATE TREATMENT OF UPPER RESPIRATORY TRACT INFECTION IS ONE OF THE MAJOR FACTORS IN THE PREVENTION OF ACUTE TRACHEOBRONCHITIS PATHOPHYSIOLOGY INFECTION (STREPTOCOCCUS PNEUMONIAE, HEMOPHILUS INFLUENZAE, OR MYCOPLASMA PNEUMONIAE. A FUNGAL INFECTION (ASPERGILLUS) MAY ALSO CAUSE TRACHEOBRONCHITIS. A SPUTUM CULTURE IS ESSENTIAL TO IDENTIFY THE SPECIFIC CAUSATIVE ORGANISM. IN ADDITION TO INFECTION, INHALATION OF PHYSICAL AND CHEMICAL IRRITANTS, GASES, OR OTHER AIR CONTIMINANTS CAN ALSO CAUSE ACUTE BRONCHIAL IRRITATION CLINICAL MANIFESTATION INITIALLY, THE PATIENT WILL EXPERIENCE DRY, IRRITATING COUGH AND EXPECTORATES A SCANTY AMOUNT OF MUCOID SPUTUM. STERNAL SORENESS (CHEST PAIN) FROM COUGHING FEVER CHILLS NIGHT SWEATS HEADACHE GENERAL MALAISE CLINICAL MANIFESTATION AS THE INFECTION PROGRESSES, THE PATIENT MAY BE SHORT OF BREATH, HAVE NOISY INSPIRATION AND EXPIRATION INSPIRATORY STRIDER OR EXPIRATORY WHEEZE PRODUCE PURULENT (PUS-FILLED) SPUTUM IN SEVERE TRACHEOBRONCHITIS, BLOOD-STREAKED SECRETIONS MAY BE EXPECTORATED (HEMOPTYSIS) AS A RESULT OF THE IRRITATION OF THE MUCOSA OF THE AIRWAYS. MEDICAL MANAGEMENT ANTIBIOTIC TREATMENT (DEPENDING ON THE RESULT OF SPUTUM CULTURE) FLUID INTAKE IS INCREASED TO THIN VISCOUS AND TENACIOUS SECRETIONS PURULENT SECCRETION THAT CANNOT BE CLEARED BY COUGHING PLACE PATIENTS AT RISK FOR INCREASING AIRWAY OBSTRUCTION AND DEVELOPS MORE SEVVERE LOWER RESPIRATORY TRACT INFECTIONS SUCH AS PNEUMONIA. SUCTIONING AND BRONCHOSCOPY MAY BE NEEDED TO REMOVE SECRETIONS ET INTUBATION IS USED RARELY, UNLESS TRACHEOBRONCHITIS IS SEVERE AND LEADS TO RESPIRATORY FAILURE KEY TO REMEMBER ANTIHISTAMINES USUALLY ARE NOT PRESCRIBED, BECAUSE THEY CAN CAUSE EXCESSIVE DRYING AND MAKE SECRETIONS MORE DIFFICULT TO EXPECTORATE. MEDICAL MANAGEMENT STEAM INHALATIONS MAY HELP RELIEVE LARYNGEAL AND TRACHEAL IRRITATION, MOIST HEAT TO THE CHEST MAY RELIEVE THE SORENESS AND PAIN, MILD ANALGESICS MAY BE PRESCRIBED NURSING MANAGEMENT ACUTE TRACHEOBRONCHITIS IS USUALLY TREATED IN THE HOME SETTING. A PRIMARY NURSING FUNCTION IS TO ENCOURAGE BRONCHIAL HYGIENE SUCH AS: INCREASED FLUID INTAKE DIRECTED COUGHING TO REDUCE SECRETIONS ENCOURAGES AND ASSISTS THE PATIENT TO SIT UP FREQUENTLY TO COUGH EFFECTIVELY TO PREVENT RETENTION OF SPUTUM IF PATIENT IS IN ANTIBIOTIC TREATMENT, NURSE SHOULD REMIND THE PATIENT TO COMPLETE THE FULL COURSE AS PRESCRIBED TO PREVENT ANTIBIOTIC RESISTANCE FOR FATIGUE, MAKE A PLAN OF ACTIVITY AND CAUTIONS THE PATIENT AGAINST OVEREXERTION PNEUMONIA AN INFLAMMATION OF THE LUNCH PARENCHYMA CAUSED BY VARIOUS MICROORGANISMS INCLUDING BACTERIA, MYCOBACTERIA, FUNGI AND VIRUSES. PNEUMONITIS IS A MORE GENERAL TERM THAT DESCRIBES AN INFLAMMATORY PROCESS IN THE LUNG TISSUE THAT MAY PREDISPOSE OR PLACE THE PATIENT AT RISK FOR MICROBIAL INVASION  PNEUMONIA AND INFLUENZA ARE THE MOST COMMON CAUSES OF DEATH FROM INFECTIOUS DISEASE IN THE US. PNEUMONIA AND INFLUENZA ACCOUNTED FOR 55,567 DEATHS IN THE UNITED STATES IN 2017 CLASSIFICATION PNEUMONIA CAN BE CLASSIFIED INTO FOUR TYPES: 1.COMMUNITY ACQUIRED PNEUMONIA (CAP), 2.HEALTH CARE-ASSOCIATED PNEUMONIA (HCAP), 3.HOSPITAL- ACQUIRED PNEUMONIA (HAP), AND 4.VENTILATOR-ASSOCIATED PNEUMONIA (VAP)  COMMUNITTY-ACQUIRED PNEUMONIA CAP, A COMMON INFECTIOUS DISEASE, OCCURS EITHER IN THE COMMUNITY SETTING OR WITHIN THE FIRST 48 HOURS AFTER HOSPITALIZATION OR INSTITUTIONALIZATION. THE NEED FOR HOSPITALIZATION FOR CAP DEPENDS ON THE SEVERITY OF THE PNEUMONIA. T  CAUSATIVE PATHOGENS FOR CAP OUTPATIENTS: 1. STREPTOCOCCUS PNEUMONIAE (MOST COMMON BACTERIAL CAUSE OF CAP IN PEOPLE YOUNGER THAN 60 YEARS WITHOUT COMORBIDITY AND IN THOSE 60 YEARS AND OLDER WITH COMORBIDITY) 2. MYCOPLASMA PNEUMONIAE 3. HAEMOPHILUS INFLUENZAE 4. C PNEUMONIAE (CHLAMYDIA) 5. RESPIRATORY VIRUS HOSPITALIZED PATIENTS: NON-ICU 1. S. PNEUMONIAE 2. M. PNEUMONIAE 3. C. PNEUMONIAE 4. H. INFLUENZAE 5. LEGIONELLA HEALTH CARE- ASSOCIATED PNEUMONIA AN IMPORTANT DISTINCTION OF HCAP IS THAT THE CAUSATIVE PATHOGENS ARE OFTEN MULTIDRUG – RESISTANT ORGANISMS BECAUSE OF PRIOR CONTACT WITH A HEALTH CARE ENVIRONMENT. CONSEQUENTLY, THIS TYPE OF PNEUMONIA IN AREAS SUCH AS THE EMERGENCY DEPARTMENT IS CRUCIAL. BECAUSE HCAP IS OFTEN DIFFICULT TO TREAT, INITIAL ANTIBIOTIC TREATMENT MUST NOT BE DELAYED. INTIAL ANTIBIOTIC TREATMENT OF HCAP IS OFTEN DIFFERENT FROM THAT FOR CAP DUE TO POSSIBILITY OF MDRO’S HOSPITAL-ACQUIRED PNEUMONIA HAP DEVELOPS 48 HOURS OR MORE AFTER HOSPITALIZATION AND DOES NOT APPEAR TO BE INCUBATING AT THE TIME OF ADMISSION. A NOSOCOMIAL TYPE CERTAIN FACTORS MAY PREDISPOSE PATIENTS TO HAP BECAUSE OF IMPAIRED HOST DEFENSES (SEVERE ACUTE OR CHRONIC ILLNESS) A VARIETY OF COMORBID CONDITIONS, SUPINE POSITIONING AND ASPIRATION, COMA, MALNUTRITION, PROLONGED HOSPITALIZATION, HYPOTENSION, METABOLIC DISORDERS. HOSPITALIZED PATIENTS ARE ALSO EXPOSED TO POTENTIAL BACTERIA FROM OTHER SOURCES – RESPIRATORY DEVICES AND EQUIPMENT, TRANSMISSION OF PATHOGENS BY THE HANDS OF HEALTH CARE PERSONNEL. COMMON ORGANISMS RESPONSIBLE FOR HAP 1. ENTEROBACTER SPECIES 2. ESCHERICHIA COLI (E. COLI) 3. H. INFLUENZAE 4. KLEBSIELLA PNEUMONIAE 5. PSEUDOMONAS AERUGINOSA 6. ACINETOBACTER SPECIES 7. METHICILLIN-SENSITIVE OR METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS (MRSA) 8. AND S PNEUMONIAE VENTILATOR-ASSOCIATED PNEUMONIA VAP CAN BE THOUGHT OF AS A SUBTYPE OF HAP; HOWEVER, IN SUCH CASES, THE PATIENT HAS BEEN ENDOTRACHEALLY INTUBATED AND HAS RECEIVED MECHANICAL VENTILATORY SUPPORT FOR AT LEAST 48 HOURS. VAP IS A COMPLICATION IN AS MANY AS 27% OF PATIENT WHO REQUIRE MECHANICAL VENTILATION.  THE ETIOLOGIC BACTERIOLOGIC AGENTS ASSOCIATED WITH VAP TYPICALLY DIFFER BASED ON THE TIMING OF THE OCCURRENCE OF THE INFECTION RELATIVE TO THE START OF MECHANICAL VENTILATION. VAP OCCURRING WITHIN 96 HOURS OF THE ONSET OF MECHANICAL VENTILATION IS USUALLY DUE TO ANTIBIOTIC-SENSITIVE BACTERIA THAT COLONIZE THE PATIENT PRIOR TO HOSPITAL ADMISSION, WHEREAS VAP DEVELOPING AFTER 96 HOURS OF VENTILATORY SUPPORT IS MORE OFTEN ASSOCIATED WITH MDRO’S  PNEUMONIA IN THE IMMUNOCOMPROMOMISED HOST PNEUMONIA IN THE IMMUNOCOMPROMISED HOST CAN OCCUR WITH THE USE OF CORTICOSTEROIDS OR OTHER IMMUNOSUPPRESSIVE AGENTS, CHEMOTHERAPY, NUTRITIONAL DEPLETION, THE USE OF BROAD- SPECTRUM ANTIMICROBIAL AGENTS, ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS), GENETIC IMMUNE DISORDERS AND LONG-TERM ADVANCED LIFE SUPPORT TECHNOLOGY. *NURSING MANAGEMENT FOR PATIENTS TAKING CORTICOSTEROIDS- AVOID CROWDED PLACES  ASPIRATION PNEUMONIA REFERS TO THE PULMONARY CONSEQUENCES RESULTING FROM ENTRY OF ENDOGENOUS OR EXOGENOUS SUBSTANCES INTO THE LOWER AIRWAY THE MOST COMMON FORM OF ASPIRATION PNEUMONIA IS BACTERIAL INFECTION FROM ASPIRATION OF BACTERIA THAT NORMALLY RESIDE IN THE UPPER AIRWAYS ASPIRATION PNEUMONIA MAY OCCUR IN THE COMMUNITY OR HOSPITAL SETTING. COMMON PATHOGENS ARE: 1. ANAEROBES 2. S. AUREUS 3. STREPTOCOCCUS SPECIES 4. GRAM-NEGATIVE BACILLI.  ASPIRATION PNEUMONIA SUBSTANCES OTHER THAN BACTERIA MAY BE ASPIRATED INTO THE LUNG, SUCH AS: GASTRIC CONTENTS, EXOGENOUS CHEMICAL CONTENTS, OR IRRITATING GASES. THIS TYPE OF ASPIRATION OR INGESTION MAY IMPAIR THE LUNG DEFENSES, CAUSE INFLAMMATORY CHANGES, AND LEAD TO BACTERIAL GROWTH AND A RESULTING PNEUMONIA. RISK FACTORS HEART FAILURE DIABETES ALCHOLISM COPD AIDS CAUSATIVE PATHOGENS FOR CAP ICU PATIENTS 1. S. PNEUMONIAE 2. STAPHYLOCOCCUS AUREUS 3. LEGIONELLA 4. GRAM- NEGATIVE BACILLI 5. H. INFLUENZAE CLINICAL MANIFESTATIONS CHILLS FEVER 38.5 TO 40.5 DEGREE CELSIUS PLEURITIC CHEST PAIN THAT IS AGGRAVATED BY DEEP BREATHING AND COUGHING TACHYPNEA USE OF ACCESSORY MUSCLES IN RESPIRATION ASSESSMENT AND DIAGNOSTIC FINDINGS PHYSICAL EXAMINATION CHEST X-RAY BLOOD CULTURE SPUTUM EXAMINATION MEDICAL MANAGEMENT PRESCRIBING APPROPRIATE ANTIBIOTICS FOR BACTERIAL PNEUMONIA ASSISTING THE PATIENT TO GET ADEQUATE REST AND HYDRATION MANAGING COMPLICATIONS IF THEY OCCUR SUPPLEMENTAL OXYGENATION MAY BE PRESCRIBED NURSING PROCESS ASSESSMENT: RESPIRATORY ASSESSMENT NURSING DIAGNOSIS IMPAIRED AIRWAY CLEARANCE ASSOCIATED WITH COPIOUS TRACHEOBRONCHIAL SECRETIONS FATIGUE AND ACTIVITY INTOLERANCE ASSOCIATED WITH IMPAIRED RESPIRATORY FUNCTION RISK FOR HYPOVOLEMIA ASSOCIATED WITH FEVER AND A RAPID RESPIRATORY RATE IMPAIRED NUTRITIONAL STATUS LACK OF KNOWLEDGE ABOUT THE TREATMENT REGIMEN AND PREVENTIVE MEASURES OR REFER ABC’S NURSING MANAGEMENT IMPROVES AIRWAY PATENCY PROMOTING REST AND CONSERVING ENERGY PROMOTING FLUID INTAKE MAINTAINING NUTRITION PROMOTING PATIENT’S KNOWLEDGE MONITORING AND MANAGING POTENTIAL COMPLICATIONS REFER ALSO TO ACUTE TRACHEOBRONCHITIS MANAGEMENT ASPIRATION IS INHALATION OF FOREIGN MATERIAL (OROPHARYNGEAL OR STOMACH CONTENTS) INTO THE LUNGS. A SERIOUS COMPLICATION THAT CAN CAUSE PNEUMONIA AND RESULT IN THE FOLLOWING CLINICAL PICTURE: TACHYCARDIA, DYSPNEA, CENTRAL CYANOSIS, HYPERTENSION, HYPOTENSION, AND POTENTIALLY DEATH. PATHOPHYSIOLOGY THE PRIMARY FACTORS RESPONSIBLE FOR DEATH AND COMPLICATIONS AFTER ASPIRATION ARE THE VOLUME AND CHARACTER OF THE ASPIRATED CONTENTS. ASPIRATION PNEUMONIA DEVELOPS AFTER INHALATION OF COLONIZED ORAL OR PHARYNGEAL MATERIAL. THE PATHOLOGIC PROCESS INVOLVES ACUTE INFLAMMATORY RESPONSE TO BACTERIAL PRODUCTS. MOST COMMONLY, THE CAUSATIVE AGENTS RISK FACTORS SEIZURE ACTIVITY BRAIN INJURY DECREASED LEVEL OF CONSCIOUSNESS FROM TRAUMA, DRUG OR ALCOHOL INTOXICATION, EXCESSIVE SEDATION, OR GENERAL ANESTHESIA FLAT BODY POSITIONING STROKE SWALLOWING DISORDERS CARDIAC ARREST  PREVENTION MAINTAIN HEAD OF BED ELEVATED AT AN ANGLE OF 30 TO 45 DEGREES, UNLESS CONTRAINDICATED USED SEDATIVES AS SPARINGLY AS POSSIBLE BEFORE INITIATING ENTERAL TUBE FEEDING, CONFIRM THE TIP LOCATION FOR PATIENTS RECEIVING TUBE FEEDINGS, ASSESS PLACEMENT OF THE FEEDING TUBE AT 4- HOUR INTERVALS, ASSESS FOR GASTROINTESTINAL RESIDUAL FOR PATIENTS RECEIVING TUBE FEEDINGS, AVOID BOLUS FEEDINGS IN THOSE AT RISK FOR ASPIRATION CONSULT WITH PRIMARY PROVIDER ABOUT OBTAINING A SWALLOWING EVALUATION BEFORE ORAL FEEDINGS ARE STARTED FOR PATIENTS WHO WERE REFENTLY EXTUBATED BUT WERE PREVIOUSLY INTUBATED FOR >2 DAYS COMPENSATING FOR ABSENT REFLEXES SOFT DIET ENCOURAGE TO TAKE SMALL BITES INSTRUCT PATIENT TO KEEP THE CHIN TUCKED AND THE HEAD TURNED WITH REPEATED SWALLOWING STRAWS SHOULD NOT BE USED * (CAN INCREASE THE RISK OF ASPIRATION) PULMONARY TUBERCULOSIS (TB) IS AN INFECTIOUS DISEASE THAT PRIMARILY AFFECTS THE LUNGS PARENCHYMA. IT MAY ALSO BE TRANSMITTED TO OTHER PARTS OF THE BODY: MENINGES, KIDNEYS, BONES, AND LYMPH NODES.  INFECTIOUS AGENTS M. TUBERCULOSIS- AN ACID-FAST AEROBIC ROD THAT GROWS SLOWLY AND IS SENSITIVE TO HEAT AND ULTRAVIOLET LIGHT. MYCOBACTERIUM BOVIS AND MYCOBACTERIUM AVIUM HAVE RARELY BEEN ASSOCIATED WITH THE DEVELOPMENT OF A TB INFECTION.  TB IS A WORLDWIDE PUBLIC HEALTH PROBLEM THAT IS CLOSELY ASSOCIATED WITH POVERTY, MALNUTRITION, OVERCROWDING, SUBSTANDARD HOUSING, AND INADEQUATE HEALTH CARE. MORTALITY AND MORBIDITY RATES CONTINUE TO RISE; M.TUBERCULOSIS INFECTS AN ESTIMATED ONE THIRD OF THE WORLD’S POPULATION AND REMAINS THE LEADING CAUSE OF DEATH FROM INFECTIOUS DISEASE IN THE WORLD. TRANSMISSION AND RISK FACTORS TB SPREADS FROM PERSON TO PERSON BY AIRBORNE TRANSMISSION AN INFECTED PERSON RELEASES DROPLET NUCLEI THROUGH: -TALKING -COUGHING -SNEEZING -LAUGHING -SINGING  TRANSMISSION LARGER DROPLETS SETTLE SMALLER DROPLETS REMAIN SUSPENDED IN THE AIR AND ARE INHALED BY A SUSCEPTIBLE PERSON. RISK FACTORS CLOSE CONTACT WITH SOMEONE WHO HAS ACTIVE TB IMMUNOCOMPROMISED STATUS (EG., HIV INFECTION, CANCER, TRANSPLANTED ORGANS, AND PROLONGED HIGH-DOSE OF CORTICOSTEROID THERAPY). SUBSTANCE USE DISORDER (INDIVIDUALS WHO USE IV/INJECTION DRUG OR ABUSE ALCOHOL) LIVING IN OVERCROWDED, SUBSTANDARD HOUSING BEING A HEALTH CARE WORKER PERFORMING HIGH-RISK ACTIVITIES PATHOPHYSIOLOGY SUSCEPTIBLE PERSON INHALES MYCOBACTERIA AND BECOMES INFECTED> BACTERIA ARE TRANSMITTED THROUGH THE AIRWAYS> TO THE ALVEOLI (WHERE THEY ARE DEPOSITED AND BEGIN TO MULTIPLY) THE BACILLI ALSO ARE TRANSPORTED VIA THE LYMPH SYSTEM AND BLOOD STREAM> TO OTHER PARTS OF THE BODY (KIDNEYS, BONES, CEREBRAL CORTEX) AND OTHER AREAS OF THE LUNGS (UPPER LOBES) THE BODY’S IMMUNE SYSTEM RESPONDS BY INITIATING AN INFLAMMATORY REACTION > PHAGOCYTES (NEUTROPHILS AND MACROPHAGES)> ENGULF MANY OF THE BACTERIA, AND TB-SPECIFIC LYMPHOCYTE DESTROY THE BACILLI AND NORMAL TISSUE  TISSUE REACTION> ACCUMULATION OF EXUDATE IN THE ALVEOLI> CAUSING BRONCHOPNEUMONIA THE INITIAL INFECTION USUALLY OCCURS 2 TO 10 WEEKS AFTER EXPOSURE GRANULOMAS, NEW TISSUE MASSES OF LIVE AND DEAD BACILLI> SURROUNDED BY MACROPHAGES> FORMS A PROTECTIVE WALL> THEY ARE THEN TRANSFORMED TO A FIBROUS TISSUE MASS, THE CENTRAL PORTION OF WHICH IS CALLED A GHON TUBERCLE. > THE BACTERIA AND MACROPHAGES BECOMES NECROTIC> FORMING A CHEESY MASS> THIS MASS MAY BECOME CALCIFIED AND FORM A COLLAGENOUS SCAR > PULMONARY FIBROSIS CLINICAL MANIFESTATION LOW GRADE FEVER COUGH NIGHT SWEATS FATIGUE WEIGHT LOSS MUCO-PURULENT SPUTUM MAY BE EXPECTORATED HEMOPTYSIS MEDICAL MANAGEMENT RIPE= FIRST LINE ANTI-TUBERCULOUS DRUG NAMES RIFAMPYCIN (RIFAMPIN) ISONIAZID PYRAZINAMIDE ETHAMBUTOL NURSING MANAGEMENT PROMOTING AIRWAY CLEARANCE ADVOCATING ADHERENCE TO THE TREATMENT REGIMEN PROMOTING ACTIVITY AND NUTRITION PREVENTING TRANSMISSION  LUNG ABSCESS IS A MICROBIAL INFECTION OF THE LUNG THAT RESULTS IN NECROSIS OF THE PULMONARY PARENCHYMA PATHOPHYSIOLOGY COMPLICATION OF BACTERIAL PNEUMONIA OR ARE CAUSED BY ASPIRATION OF ORAL ANAEROBES INTO THE LUNG ABSCESSES ALSO MAY OCCUR SECONDARY TO MECHANICAL OR FUNCTIONAL OBSTRUCTION OF THE BRONCHI BY A TUMOR, FOREIGN BODY, OR BRONCHIAL STENOSIS, OR FROM NECROTIZING PNEUMONIAS, TB, PULMONARY EMBOLISM, OR CHEST TRAUMA.  CLINICAL MANIFESTATIONS MILD PRODUCTIVE COUGH FEVER PRODUCTIVE COUGH WITH MODERATE TO COPIOUS AMOUNTS OF FOUL-SMELLING, BLOODY, SPUTUM. DYSPNEA PLEURISY OR DULL CHEST PAIN WEAKNESS ANOREXIA AND WEIGHT LOSS ASSESSMENT AND DIAGNOSTIC FINDINGS PE OF THE CHEST MAY REVEAL DULLNESS ON PERCUSSION DECREASED OR ABSENT BREATH SOUNDS WITH AN INTERMITTENT PLEURAL FRICTION RUB GRATING OR CREAKING SOUND ON AUSCULTATION CRACKLES MAY BE PRESENT ASSESSMENT AND DIAGNOSTIC FINDINGS CONFIRMATION OF OF THE DIAGNOSIS IS MADE BY CHEST X-RAY, SPUTUM CULTURE, AND, IN SOME CASES, FIBEROPTIC BRONCHOSCOPY. PREVENTION THE FOLLOWING MEASURES REDUCE THE RISK OF LUNG ABSCESS: APPROPRIATE ANTIBIOTIC THERAPY BEFORE ANY DENTAL PROCEDURES IN PATIENTS WHO MUST HAVE TEETH EXTRACTED WHILE THEIR GUMS AND TEETH ARE INFECTED ADEQUATE DENTAL AND ORAL HYGIENE, BECAUSE ANAEROBIC BACTERIA PLAY A ROLE IN THE PATHOGENESIS OF LUNG ABSCESS APPROPRIATE ANTIMICROBIAL THERAPY FOR PATIENTS WITH PNEUMONIA MEDICAL MANAGEMENT ADEQUATE DRAINAGE OF THE LUNG ABSCESS MAY BE ACHIEVED THROUGH POSTURAL DRAINAGE AND CHEST PHYSIOTHERAPY. ASSESS PATIENT FOR AN ADEQUATE COUGH DIET HIGH IN PROTEIN AND CALORIES LOBECTOMY IS PERFORMED IF MASSIVE HEMOPTYSIS OCCURS OR IF THERE IS LITTLE OR NO RESPONSE TO MEDICAL MANAGEMENT IV ANTIMICROBIAL THERAPY DEPENDS ON THE RESULTS OF THE SPUTUM CULTURE AND SENSITIVITY AND IS GIVEN FOR AN EXTENDED PERIOD NURSING MANAGEMENT THE NURSE ADMINISTERS ANTIBIOTICS AND IV TREATMENT AS PRESCRIBED MONITOR FOR ADVERSE EFFECTS CPT IS INITIATED AS PRESCRIBED TO FACILITATE DRAINAGE OF THE ABSCESS EDUCATE PATIENT ON HOW TO PERFORM DEEP BREATHING AND COUGHING EXERCISES TO HELP EXPAND THE LUNGS TO ENSURE PROPER NUTRITIONAL INTAKE (HIGH PROTEIN AND HIGH CALORIES) OFFER EMOTIONAL SUPPORT, BECAUSE THE ABSCESS MAY TAKE A LONG TIME TO RESOLVE PLEURAL DISORDERS PLEURAL DISORDERS INVOLVE THE MEMBRANES COVERING THE LUNGS PLEURA- COVER OF THE LUNGS PARTS: 1. VISCERAL- INNER 2. PARIETAL- OUTER BETWEEN: PLEURAL SPACE – PREVENTS FRICTION OF PLEURAL LAYER PRESSURE: NEGATIVE – TO ALLOW LUNG EXPANSION ENVIRONMENTAL PRESSURE- POSITIVE  POSITIVE PRESSURE IN PLEURAL SPACE> DECREASES LUNG EXPANSION> CAUSES LUNG COLLAPSE (ATELECTASIS)  PLEURISY PLEURITIS REFERS TO INFLAMMATION OF BOTH LAYERS OF THE PLEURAE (PARIETAL AND VISCERAL) PLEURISY MAY DEVELOP IN CONJUNCTION WITH PNEUMONIA OR AN UPPER RESPIRATORY TRACT INFECTION, TB, OR COLLAGEN DISEASE; AFTER TRAUMA TO THE CHEST; PULMONARY INFARCTION, OR PE; IN PATIENTS WITH PRIMARY OR METASTATIC CANCER; AND AFTER THORACOTOMY. CLINICAL MANIFESTATION THE CHARACTERISTIC OF PLEURITIC PAIN IS ITS RELATIONSHIP TO RESPIRATORY MOVEMENT. TAKING A DEEP BREATH, COUGHING, OR SNEEZING WORSENS THE PAIN. PLEURITIC PAIN IS LIMITED IN DISTRIBUTION RATHER THAN DIFFUSE IT USUALLY OCCURS ON ONE SIDE THE PAIN MAY BECOME MINIMAL OR ABSENT WHEN THE BREATH IS HELD IT MAY BE LOCALIZED OR RADIATE TO THE SHOULDER OR ABDOMEN LATER, AS PLEURAL FLUID DEVELOPS, THE PAIN DECREASES  ASSESSMENT AND DIAGNOSTIC FINDINGS IN THE EARLY PERIOD, WHEN LITTLE FLUID HAS A ACCUMULATED, A PLEURAL FRICTION RUB CAN BE HEARD WITH THE STETHOSCOPE DISAPPEAR LATER AS MORE FLUID ACCUMULATES AND SEPARATES THE INFLAMED PLEURAL SURFACES. DIAGNOSTIC TEST INCLUDE CHEST X RAYS SPUTUM ANALYSIS THORACENTESIS- TO OBTAIN A SPECIMEN OF PLEURAL FLUID FOR EXAMINATION, AND, LESS COMMONLY, A PLEURAL BIOPSY MEDICAL MANAGEMENT THE OBJECTIVES OF TREATMENT ARE TO DISCOVER THE UNDERLYING CONDITION CAUSING THE PLEURISY AND TO RELIEVE THE PAIN. AS THE UNDERLYING DISEASE (PNEUMONIA, INFECTION) IS TREATED, THE PLEURITIC INFLAMMATION USUALLY RESOLVES MONITOR PATIENT FOR SIGNS AND SYMPTOMS OF PLEURAL EFFUSION SUCH AS: -SOB -PAIN - ASSUMPTION OF A POSITION THAT DECREASES PAIN  PRESCRIBED ANALGESIC AGENTS AND TOPICAL APPLICATIONS OF HEAT OR COLD PROVIDE SYMPTOMATIC RELIEF NONSTEROIDAL INFLAMMATORY DRUG- PAIN RELIEF AND ALLOWS PATIENT TO TAKE DEEP BREATHS AND COUGH MORE EFFECTIVELY NURSING MANAGEMENT ENHANCE COMFORT, SUCH AS TURNING FREQUENTLY ONTO THE AFFECTED SIDE TO SPLINT THE CHEST WALL AND REDUCE THE STRETCHING OF THE PLEURAE EDUCATE THE PATIENT TO USE THE HANDS OR A PILLOW TO SPLINT THE RIB CAGE WHILE COUGHING PLEURAL EFFUSION A COLLECTION OF FLUID IN THE PLEURAL SPACE RARELY A PRIMARY DISEASE PROCESS; IT USUALLY SECONDARY TO OTHER DISEASES. NORMALLY, THE PLEURAL SPACE CONTAINS A SMALL AMOUNT OF FLUID (5 – 15ML), ACTS AS A LUBRICANT THAT ALLOWS THE PLEURAL SURFACES TO MOVE WITHOUT FRICTION.  PLEURAL EFFUSION MAY BE A COMPLICATION OF HEART FAILURE, TB, PNEUMONIA, PULMONARY INFECTIONS (PARTICULARLY VIRAL INFECTIONS), NEPHROTIC SYNDROME, CONNECTIVE TISSUE DISEASE, PE, AND NEOPLASTIC TUMORS. MOST COMMON MALIGNANCY WITH A PLEURAL EFFUSION IS BRONCHOGENIC CARCINOMA PLEURAL EFFUSION TYPES 1. HEMOTHORAX- BLOOD IN THE PLEURAL SPACE 2. HYDROTHORAX- H20 IN PLEURAL SPACE 3. PYOTHORAX- PUS IN THE PLEURAL SPACE PNEUMOTHORAX- PRESENCE OF AIR IN THE PLEURAL SPACE (NOT A TYPE OF PLEURAL EFFUSION, BUT PART OF PLEURAL DISORDERS THAT CAUSES POSITIVE PRESSURE IN THE PLEURAL SPACE WHICH MIGHT CAUSE COMPRESSIVE ATELECTASIS IN THE LONG RUN IF UNTREATED) CLINICAL MANIFESTATION USUALLY, THE CLINICAL MANIFESTATIONS ARE CAUSED BY THE UNDERLYING DISEASE PNEUMONIA CAUSES FEVER, CHILLS, PLEURITIC CHEST PAIN MALIGNANT EFFUSION MAY RESULT IN DYSPNEA, ORTHOPNEA, COUGHING THE SEVERITY OF SYMPTOMS IS DETERMINED BY THE SIZE OF THE EFFUSION ASSESSMENT AND DIAGNOSTIC FINDINGS ASSESSMENT OF THE AREA OF THE PLEURAL EFFUSION REVEALS DECREASED OR ABSENT BREATH SOUNDS DECREASED FREMITUS DULL, FLAT SOUND O PERCUSSION IN EXTREME LARGE PLEURAL EFFUSION, ACUTE RESPIRATORY DISTRESS IS NOTED TRACHEAL DEVIATION FROM THE AFFECTED SIDE MAY ALSO BE APPARENT  PHYSICAL EXAMINATION CHEST X-RAY CHEST CT THORACENTESIS CONFIRM THE PRESENCE OF FLUID PLEURAL FLUID IS ANALYZED BY BACTERIAL CULTURE, GRAM STAIN, AFB STAIN (FOR TB) RBC AND WBC COUNT MEDICAL MANAGEMENT THE OBJECTIVES OF TREATMENT ARE TO DISCOVER THE UNDERLYING CAUSE OF THE PLEURAL EFFUSION SPECIFIC TREATMENT IS DIRECTED AT THE UNDERLYING CAUSE (HEART FAILURE, PNEUMONIA, CIRRHOSIS). THORACENTESIS AND CTT IS PERFORMED TO REMOVE FLUID NURSING MANAGEMENT SUPPORT MEDICAL REGIMEN PREPARES AND POSITION PATIENT FOR THORACENTESIS OFFERS SUPPORT THROUGHOUT THE PROCEDURE EDUCATE PATIENT AND FAMILY FOR THE MANAGEMENT FOR PLEURAL CATHETER ASSESS PATIENT’S PAIN LEVEL ADMINISTER ANALGESICS AS PRESCRIBED FOR PAIN ACUTE RESPIRATORY FAILURE RESPIRATORY FAILURE IS A SUDDEN AND LIFE-THREATENING DETERIORATION OF GAS EXCHANGE FUNCTION OF THE LUNGS AND INDICATES FAILURE TO PROVIDE ADEQUATE OXYGENATION OF VENTILATION FOR THE BLOOD. TERMINOLOGIES ACUTE RESPIRATORY FAILURE IS DEFINED AS: HYPOXEMIA- A DECREASE IN ARTERIAL OXYGEN TENSION (PAO2) TO LESS THAN 60MM HG) HYPERCAPNIA- AN INCREASE IN ARTERIAL CARBON DIOXIDE TENSION (PACO2) ACUTE VERSUS CHRONIC RESPIRATORY FAILURE CHRONIC RESPIRATORY FAILURE IS DEFINED AS DETERIORATION IN THE GAS EXCHANGE FUNCTION OF THE LUNGS THAT HAS DEVELOPED INSIDIOUSLY OR HAS PERSISTED FOR A LONG PERIOD AFTER AN EPISODE OF ACUTE RESPIRATORY FAILURE. TWO CAUSES OF COPD WILL BE DISCUSSED LATER PATHOPHYSIOLOGY-ARF IN ACUTE RESPIRATORY FAILURE, THE VENTILATION OR PERFUSION MECHANISMS IN THE LUNGS ARE IMPAIRED. VENTILATORY FAILURE MECHANISMS THAT LEADS TO ARF: IMPAIRED FUNCTION OF THE CENTRAL NERVOUS SYSTEM(DRUG OVERDOSE, HEAD TRAUMA, INFECTION, HEMORRHAGE, SLEEP APNEA), NEUROMUSCULAR DYSFUNCTION(MYASTHENIA GRAVIS, GUILLAIN-BARRE SYNDROME, AMYOTROPHIC LATERAL SCLEROSIS, SPINAL CORD TRAUMA), MUSCULOSKELETAL DYSFUNCTION, AND PULMONARY FUNCTION. -WE WILL DISCUSS FURTHER ABOUT THESE DISORDERS NEXT SEMESTER OXYGENATION OR PERFUSION FAILURE MECHANISMS LEADING TO ACUTE RESPIRATORY FAILURE INCLUDE: PNEUMONIA, ARDS (ACUTE RESPIRATORY DISTRESS SYNDROME), HEART FAILURE, COPD, PULMONARY EDEMA, AND RESTRIVE LUNG DISEASE CLINICAL MANIFESTATIONS EARLY SIGNS: RESTLESSNESS FATIGUE HEADACHE DYSPNEA AIR HUNGER TACHYCARDIA INCREASED BLOOD PRESSURE AS THE HYPOXEMIA PROGRESSES: CONFUSION LETHARGY TACHYCARDIA TACHYPNEA CENTRAL CYANOSIS DIAPHORESIS RESPIRATORY ARREST MEDICAL MANAGEMENT THE OBJECTIVE OF TREATMENT ARE TO CORRECT THE UNDERLYING CAUSE AND TO RESTORE ADEQUATE GAS EXCHANGE IN THE LUNGS. ET INTUBATION AND MECHANICAL VENTILATION MAY BE REQUIRED TO MAINTAIN ADEQUATE VENTILATION AND OXYGENATION WHILE UNDERLYING CAUSE IS CORRECTED  NURSING MANAGEMENT ASSISTING WITH INTUBATION AND MAINTAINING MECHANICAL VENTILATION (ICU NURSE) ASSESS RESPIRATORY STATUS BY MONITORING THE LEVEL OF RESPONSIVENESS ARTERIAL BLOOD GAS PULSE OXIMETRY AND VITAL SIGNS TURNING SCHEDULE, MOUTH CARE, SKIN CARE, AND RANGE OF MOTION OF EXTREMITIES TO PREVENT COMPLICATIONS ASSESS UNDERSTANDING OF THE MANAGEMENT STRATEGIES HEALTH TEACHING ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) OCCURS WHEN FLUID BUILDS UP IN THE TINY, ELASTIC AIR SACS (ALVEOLI) IN YOUR LUNGS. RISK FACTORS SEPSIS INHALATION OF HARMFUL SUBSTANCES SEVERE PNEUMONIA HEAD, CHEST OR OTHER MAJOR INJURY CORONAVIRUS DISEASE (2019) ASPIRATION DRUG INGESTION AND OVERDOSE METABOLIC DISORDERS (PANCREATITIS, UREMIA) SHORT PATHOPHYSIOLOGY ASPIRATION, TRAUMA, SHOCK (SEPTIC, CARDIOGENIC, HYPOVOLEMIC) > DAMAGE: ALVEOLAR CAPILLARY MEMBRANES/ WALL> LEAKAGE OF FLUID: ALVEOLI> FLUID ACCUMULATION: ALVEOLI> COMPLICATION= PULMONARY EDEMA > HYPOXEMIA >DAMAGE: TYPE 2 PNEUMOCYTE > DECREASED SURFACTANT PRODUCTION > LUNG COLLAPSE: ATELECTASIS NURSING DIAGNOSIS: IMPAIRED GAS EXCHANGE *ARDS = LIFE THREATENING MEDICAL MANAGEMENT IDENTIFICATION AND TREATMENT OF THE UNDERLYING CONDITION ET INTUBATION AND MECHANICAL VENTILATION CIRCULATORY SUPPORT ADEQUATE FLUID VOLUME NUTRITIONAL SUPPORT- 35 TO 45 KCAL/KG/DAY TO MEET CALORIC REQUIREMENTS ENTERAL FEEDING IS THE FIRST CONSIDERATION; HOWEVER, PARENTERAL NUTRITION ALSO MAY BE REQUIRED SIGNS AND SYMPTOMS PINK FROTHY SPUTUM LABORED BREATHING / AIR HUNGER CRACKLES/ RALES SEVERE ANXIETY HYPOXIA AND NOT RESPONSIVE TO 02 CHEST RETRACTION- DELINEATION COUGH CYANOSIS NURSING MANAGEMENT 1. RESPIRATION: ASSESS V/S- RR, BREATH SOUNDS POSITION: FOWLERS >HF/ SF DEEP BREATHING AND COUGHING EXERCISE – EQUIPMENT: INCENTIVE SPIROMETRY BE PREPARED FOR POSSIBLE ET TUBING AND MECHANICAL VENTILATION 2. ASSIST IN NUTRITIONAL THERAPY 3. ADMINISTER MEDICATIONS AS ORDERED PULMONARY EDEMA (NON-CARDIOGENIC) DEFINED AS ABNORMAL ACCUMULATION OF FLUID IN THE LUNG TISSUE, THE ALVEOLAR SPACE, OR BOTH. IT IS A SEVERE, LIFE-THREATENING CONDITION. OCCURS DUE TO DAMAGE OF THE PULMONARY CAPILLARY LINING CAUSES DIRECT INJURY TO THE LUNG- CHEST TRAUMA, ASPIRATION, AND SMOKE INHALATION) HEMATOGENOUS INJURY TO THE LUNG- SEPSIS, PANCREATITIS, MULTIPLE TRANSFUSION, CARDIOPULMONARY BYPASS) SIGNS AND SYMPTOMS LABORED BREATHING / AIR HUNGER CRACKLES/ RALES HYPOXIA AND NOT RESPONSIVE TO 02 COUGH CYANOSIS PULMONARY EMBOLISM PE REFERS TO THE OBSTRUCTION OF THE PULMONARY ARTERY OR ONE OF ITS BRANCHES BY A THROMBUS (OR THROMBI) THAT ORIGINATES SOMEWHERE IN THE VENOUS SYSTEM OR IN THE RIGHT SIDE OF THE HEART. DEEP VEIN THROMBOSIS (DVT), A RELATED CONDITION, REFERS TO THROMBUS FORMATION IN THE DEEP VEINS, USUALLY IN THE CALF OR THIGH. – AS DISCUSSED IN PERIPHERAL VASCULAR DISEASE THROMBUS/ THROMBI WHEN DETACHED BECOMES AND EMBOLUS/EMBOLI SIGNS AND SYMPTOMS AIR HUNGER- INCREASED RR BLOOD TINGED SPUTUM CHEST PAIN DOB ELEVATED TEMPERATURE OR FEVER (MILD)  BLUNT TRAUMA OVERALL, BLUNT THORACIC INJURIES ARE DIRECTLY RESPONSIBLE FOR 20% TO 25% OF ALL TRAUMA DEATHS. CAUSES MOTOR VEHICLE CRASH (TRAUMA FROM STEERING WHEEL, SEAT BELT) FALLS BICYCLE CRASHES (TRAUMA FROM HANDLEBARS TYPES CJEST WALL FRACTURES DISLOCATIONS BAROTRAUMAS (INCLUDING DIAPHRAGMATIC INJURIES; INJURIES OF THE PLEURA, LUNGS, AND AERODIGESTIVE TRACTS; AND BLUNT INJURIES OF THE HEART, GREAT ARTERIES, VEINS, AND LYMPHATICS INJURIES TO THE CHEST ARE OFTEN LIFE-THREATENING AND RESULT IN ONE OR MORE OF THE FOLLOWING PATHOLOGIC STATES: HYPOXEMIA FROM DISRUPTION OF THE AIRWAY; INJURY T THE LUNG PARENCHYMA, RIB CAGE, AND RESPIRATORY MUSCULATURE HYPOVOLEMIA FROM MASSIVE FLUID LOSS FROM THE GREAT VESSELS, CARDIAC RUPTURE, OR HEMOTHORAX CARDIAC FAILURE FROM CARDIAC TAMPONADE, CARDIAC CONTUSION, OR INCREASED INTRATHORACIC PRESSURE ASSESSMENT PATIENT MUST BE ASSESSED IMMEDIATELY TO DETERMINE THE FOLLOWING: 1. TIME ELAPSED SINCE INJURY OCCURRED 2. MECHANISM OF INJURY 3. LEVEL OF RESPONSIVENESS 4. SPECIFIC INJURIES 5. ESTIMATED BLOOD LOSS 6. RECENT DRUG OR ALCOHOL USE 7. PREHOSPITAL TREATMENT ASSESSMENT INITIAL ASSESSMENT OF THORACIC INJURIES INCLUDES: 1. ASSESSMENT OF THORACIC INJURIES INCLUDES ASSESSMENT OF AIRWAY OBSTRUCTION 2. TENSION PNEUMOTHORAX 3. OPEN PNEUMOTHORAX 4. MASSIVE HEMOTHORAX 5. FLAIL CHEST 6. CARDIAC TAMPONADE SIGNS AND SYMPTOMS DOB STRICOR CYANOSIS NASAL FLARING USE OF ACCESSORY MUSCLES DROOLING MEDICAL MANAGEMENT THE GOALS OF TREATMENT ARE TO EVALUATE THE PATIENT’S CONDITION AND TO INITIATE AGGRESSIVE RESUSCITATION AN AIRWAY IS IMMEDIATELY ESTABLISHED WITH OXYGEN SUPPORT AND, IN SOME CASES, ET INTUBATION AND VENTILATORY SUPPORT REESTABLISHING FLUID VOLUME AND NEGATIVE INTRAPLEURAL PRESSURE AND DRAINING INTRAPLEURAL FLUID AND BLOOD ARE ESSENTIAL NURSING MANAGEMENT THE CHEST IS ASSESSED FOR: SYMMETRY OF MOVEMENT SYMMETRY OF BREATH SOUNDS OPEN CHEST WOUNDS ENTRANCE OR EXIT WOUNDS IMPALED OBJECTS TRACHEAL SHIFT DISTENDED NECK VEINS PENETRATING TRAUMA ANY ORGAN OR STRUCTURE WITHING CHEST IS POTENTIALLY SUSCEPTIBLE TO TRAUMATIC PENETRATION THESE ORGANS INCLUDE THE CHEST WALLM LUNG AND PLEURA, TRACHEOBRONCHIAL SYSTEM, ESOPHAGUS, DIAPHRAGM, AND MAJOR THORACIC BLOOD VESSELS, AS WELL AS HEART AND OTHER MEDIASTINAL STRUCTURE. MEDICAL MANAGEMENT THE OBJECTIVE OF IMMEDIATE MANAGEMENT IS TO RESTORE AND MAINTAIN CARDIOPULMONARY FUNCTION. EXAMINATION FOR SHOCK AND INTRATHORACIC AND INTRA-ABDOMINAL INJURIES IS NECESSARY PATIENT IS UNDRESSED COMPLETELY SO THAT ADDITIONAL INURIES ARE NOT MISSED STOP BLEEDING PATIENT’S BLOOD IS TYPED AND CROSS-MATCHED IN CASE BLOOD TRANSFUSION IS REQUIRED DIAGNOSTIC TESTS CHEST X-RAY CHEMISTRY PROFILE ABG ANALYSIS PULSE OXIMETRY ECG PNEUMOTHORAX OCCURS WHEN THE PARIETAL OR VISCERAL PLEURA IS BREACHED AND THE PLEURAL SPACE IS EXPOSED TO POSITIVE ATMOSPHERIC PRESSURE NORMALLY, THE PRESSURE IN THE PLEURAL SPACE IS NEGATIVE; THIS NEGATIVE PRESSURE IS REQUIRED TO MAINTAIN LUNG INFLATION. WHEN EITHER PLEURA IS BREACHED, AIR ENTERS THE PLEURAL SPACE, AND THE LUNG OR A PORTION OF IT COLLAPSES TYPES OF PNEUMOTHORAX INCLUDES SIMPLE, TRAUMATIC, AND TENSION PNEUMOTHORAX SIMPLE PNEUMOTHORAX A SIMPLE, OR SPONTANEOUS, PNEUMOTHORAX OCCURS WHEN AIR ENTERS THE PLEURAL SPACE THROUGH A BREACH OF EITHER THE PARIETAL OR VISCERAL PLEURA CLOSE OR SPONTANEOUS OCCURS AS AIR ENTERS THE PLURAL SPACE THROUGH THE RUPTURE OF A BRONCHOPLEURAL FISTULA MAY OCCUR IN AN APPARENTLY HEALTHY PERSON IN THE ABSENCE OF TRAUMA DUE TO RUPTURE OF AN AIR-FILLED BLEB, OR BLISTER, ON THE SURFACE OF THE LUNG, ALLOWING AIR FROM THE AIRWAYS TO ENTER THE PLEURAL CAVITY TRAUMATIC PNEUMOTHORAX OCCURS WHEN AIR ESCAPES FROM A LACERATION IN THE LUNG ITSELF AND ENTERS THE PLEURAL SPACE OF FROM A WOUND IN THE CHEST WALL. IT MAY RESULT FROM A BLUNT TRAUMA, PENETRATING CHEST OR ABDOMINAL TRAUMA (STAB, GUNSHOT WOUNDS). ALSO MAY OCCUR DURING INVASIVE THORACIC PROCEDURES (THORACENTESIS, LUNG BIOPSY, ETC.) A TRAUMATIC PNEUMOTHORAX RESULTING FROM MAJOR INJURY TO THE CHEST IS OFTEN ACCOMPANIED BY HEMOTHORAX  TRAUMATIC OR OPEN OCCURS WHEN A WOUND IN THE CHEST WALL IS LARGE ENOUGH TO ALLOW AIR TO PASS FREELY IN AND OUT OF THE THORACIC CAVITY WITH EACH ATTEMPTED RESPIRATION. TENSION PNEUMOTHORAX AIR ENTERS INTO THE PLEURAL SPACE BU CANNOT ESCAPE OR TRAPPED IT CANNOT BE EXPELLED DURING EXPIRATION THROUGH THE AIR PASSAGES OR THE OPENING IN THE CHEST WALL WITH EACH BREATH, TENSION(POSITIVE PRESSURE( IS INCREASED WITHING THE AFFECTED PLEURAL SPACE> CAUSES THE LUNG TO COLLAPSE AND THE HEART, THE GREAT VESSELS, AND THE TRACHEA TO SHIFT TOWARDS THE UNAFFECTED SIDE OF THE CHEST (MEDIASTINAL SHIFT) CLINICAL MANIFESTATIONS THE SIGNS AND SYMPTOMS ASSOCIATED WITH PNEUMOTHORAXS DEPEND ON ITS SIZE AND CAUSE ANXIETY DYSPNEA AIR HUNGER INCREASED USE OF ACCESORY MUSCLES CENTRAL CYANOSIS SEVERE HYPOXEMIA MEDICAL MANAGEMENT THE GOAL OF THE TREATMENT IS TO EVACUATE THE AIR OR BLOOD FROM THE PLEURAL SPACE COPD CHRONIC OBSTRUCTIVE PULMONARY DISEASE OR CHRONIC AIRFLOW LIMITATION (OTHER TERM) RISK FACTORS C-IGARETTE SMOKING O-VER EXPOSURE TO INFECTION P-OLLUTION D-EFICIENCY IN ALPHA ANTRYPSIN- HEREDITARY LUNG DISEASE BRONCHITIS A CONDITION THAT DEVELOPS WHEN THE AIRWAYS IN THE LUNGS, CALLED BRONCHIAL TUBES, BECOME INFLAMED AND CAUSE COUGHING, OFTEN WITH MUCUS PRODUCTION. SIGNS AND SYMPTOMS INCREASED MUCUS > HYPERSECRETION> CRACKLES COUGH – PRODUCTIVE (+) FOR SPUTUM =THICK, TENACIOUS WHITE/GRAY NURSING DIAGNOSIS: INFECTIVE AIRWAY CLEARANCE >DECREASED O2 IN BLOOD (HYPOXEMIA) > DECREASED O2 IN CELLS AND TISSUE (HYPOXIA) > BLUISH DISCOLORATION: CYANOSIS = BLUE BLOATER EMPHYSEMA EMPHYSEMA DEVELOPS OVER TIME AND INVOLVES THE GRADUAL DAMAGE OF LUNG TISSUE, SPECIFICALLY THE DESTRUCTION OF THE ALVEOLI (TINY AIR SACS). NURSING DIAGNOSIS: IMPAIRED GAS EXCHANGE >CO2 TRAPPING > CAUSING RESPIRATORY ACIDOSIS > COMPENSATORY: PUFFING OR PROLONGED EXPIRATION > AKA: PINK PUFFERS SIGNS AND SYMPTOMS HYPOXIA – FIRST SIGN: RESTLESSNESS DYSPNEA (INCREASED RR, USE OF ACCESSORY MUSCLES, NASAL FLARING, ORTHOPNEA) BARREL CHEST- INCREASED ANTERIOR/POSTERIOR DIAMETER LONG EFFECT > DIMINISHED BREATH SOUNDS FATIGUE COUGH- NON PRODUCTIVE HYPERRESONANCE UPON PERCUSSION CLUBBING OF FINGERS- LATE SIGN  BARREL CHEST IS A VISIBLE SYMPTOM OF COPD, EMPHYSEMA, OSTEOARTHRITIS, AND CF. THE LUNGS FILL WITH AIR AND ARE UNABLE TO FULLY BREATHE OUT. THIS GIVES THE CHEST A PRONOUNCED BARREL SHAPE. THE TREATMENT OF BARREL CHEST FOCUSES ON MANAGING SYMPTOMS OF THE UNDERLYING CONDITION AND LIMITING THE EXTENT OF LUNG DAMAGE DIAGNOSTIC TEST ABG X-RAY O2 SATURATION MEDICAL MANAGEMENT BRONCHODILATORS- BETA AGONIST (ALBUTEROL, SALBUTAMOL, ISOPROTENOL NURSING MANAGEMENT 1. PROMOTE AIRWAY- REMOVE SECRETION INCREASE FLUID TO LOOSEN SECRETIONS COUGHING TO EXPEL SECRETION 3SUCTION AS NEEDED CPT- BEFORE MEAL OR 2 HOURS AFTER MEAL POSTURAL DRAINAGE 2. PROMOTE BREATHING POSITIONING: ORTHOPNEIC POSITION BREATHING: PURSED LIP> TO EXPEL CO2 INHALE (NOSE) – EXHALE (MOUTH) 2X LONGER AND PUCKER MOUTH VENTILATOR- MECHANICAL VENTILATOR= NON INVASIVE IPPB (INTERMITTENT POSITIVE PRESSURE BREATHING) 3. HEALTH TEACHING REST AVOID SMOKING INFECTION PREVENTION- HANDWASHING, AVOID CROWDED PLACES DIET: INCREASE CALORIE (ENERGY), INCREASE PROTEIN; DECREASE CARBOHYDRATES > LOWERS PRODUCTION OF CARBON DIOXIDE THE END THANK YOU FOR LISTENING!