Respiratory Disorders PDF

Respiratory Disorders  Ventilation – movement of air Respiration between the atmosphere and Process of air exchange alveoli Perfusion – blood flow through the...

Respiratory Disorders  Ventilation – movement of air Respiration between the atmosphere and Process of air exchange alveoli Perfusion – blood flow through the Oxygen is obtained and lungs carbon dioxide is Pulmonary Diffusion – oxygen and eliminated carbon dioxide are transferred Gas exchange occurs in between alveoli and blood the alveoli Regulation – respiratory muscles and nervous system Airway resistance vs compliance- 1L/cm H2O  Respiratory Tract Nose, pharynx, larynx, trachea, bronchi Series of tubes that function as airway passages Filter, warm and humidify incoming air Respiratory System Nasal Cavity Throat Nose (pharynx) Mouth Windpipe (Trachea) Bronchus Left lungs Bronchiole Ribs Alveolus Diaphragm  Pharynx Contain the tonsils – normal function is to fight infection Larynx – voice box  Epiglottis Flexible cartilage – supported flap that covers the opening of the trachea or (glottis). It automatically closes the opening to the trachea during swallowing. If you eat food to fast it can get lodged in the trachea. Heimlich Maneuver  Trachea Trachea is lined with ciliated columnar epithelium and mucous cells. The chronic cough of smokers is caused by damage to cilia.  Have a very thin membrane Bronchi that allows rapid diffusion of oxygen and carbon dioxide The bronchi are small air between capillary blood and passages, composed of alveolar air spaces. hyaline cartilage, that Lined with surfactant to extend from the trachea prevent alveolar collapse. to the bronchioles. There are two bronchi in the human body that branch off from the trachea. The bronchi are lined with mucous membranes that secrete mucus and cilia that sweep the mucus and particles up and out of the airways. Surfactant Essential fluid that lines the alveoli and smallest bronchioles. Reduces surface tension of the lung allowing the oxygen and carbon dioxide across the membrane. Lack of Surfactant Premature infants can have Respiratory Distress Syndrome due to immaturity of lungs. Lungs Right side has 3 lobes Left side 2 lobes Contains the lower respiratory structures Pleural Cavity General symptoms of respiratory disease  Hypoxia : Decreased levels of oxygen in the tissues  Hypoxemia : Decreased levels of oxygen in arterial blood  Hypercapnia : Increased levels of CO2 in the blood  Hypocapnia : Decreased levels of CO2 in the blood  Dyspnea : Difficulty breathing  Tachypnea : Rapid rate of breathing  Cyanosis : Bluish discoloration of skin and mucous membranes due to poor oxygenation of the blood  Hemoptysis : Blood in the sputum  Abnormal Lung sounds= 5. Fine crackles/rales- high Normal (bronchial and pitched crackling sound, 1. High pitched wheeze/- like a high similar to fire crackling. vesicular) pitched musical instrument common Atelectasis, CHF during expiration. (asthma, COPD) 6. Pleural friction rub- low 2. Low pitched monophonic pitched harsh/grating wheeze/rhonchi- low pitched sound during inspiration whistling tune sound/snoring. and expiration. (asthma, COPD) (inflammation of tissues 3. Stridor- High pitched around the lungs) in pleural whistling/gasping sound with harsh effusion/pneumonia sound quality. (obstruction) 7. Ronchi- snoring sounds, 4. Coarse crackles/rales- low causes by large airway pitched bubbling sounds during obstruction. inspiration and expiration. (pneumonia, pulmonary edema) Guess? Location of abnormal lung sounds Nervous System Role Nervous system Listen to the different regulates the rate and lung sounds: depth of respirations. Medulla oblongata is https://youtu.be/ the respiratory control U8byn2NT_lo system of the brain Pons. Cough reflex is stimulated by nervous system. Percussion  Disorders of Respiratory Respiratory infections System Infections of the respiratory tract can occur in: 1. The upper respiratory tract or 2. The lower respiratory tract, or 3. Both. Organisms capable of infecting respiratory structures include: 4. bacteria. Streptococci, Staphylococci, Haemophilus Influenza, Pneumococci. 5. viruses: the majority of upper respiratory tract infections are caused by viruses as rhinovirus and parainfluenza virus. 6. fungi. Depending on the organism and extent of infection, the manifestations can range from mild to severe and even life threatening. Rhinitis-inflammation and irritation of the mucous The most common viral pathogens for the membrane of the nose. “common cold” are rhinovirus, parainfluenza virus, respiratory syncytial virus, adenovirus and coronavirus. Factors: odors, humidity, allergens. Most common nonallergic rhinitis is the common cold (Peters 2015) Presentation: headache, nasal congestion, with no fever.  Mode of transmission: airborne droplet sprays from infected people or direct hand contact with contaminated object. Treatment: 1. Antihistamine- most common 2. Corticosteroids(spray) 3. Decongestants/antihistamine- brompheniramine, 4. Vitamin C & Zinc this is not an indication for antimicrobial treatment unless it persists without signs of improvement 10-14 days suggesting possible sinusitis.  Sinusitis- inflammation of the sinusis Cause: streptococci or Haemophilus influenzae are the usual pathogens. Signs and symptoms: 1. headache 2. fever 3. purulent nasal discharges Treatment: 1. Antibiotics 2. Antihistamine 3. Paracetamol 4. Hot moist packs  Pharyngitis- Inflammation of the pharynx and throat Laryngitis- inflammation of the larynx Cause: virus, bacteria-( Grp B & G streptococci, Neisseria Gonorrhea, C. Pneumoniae)- (Chow & Doron 2018) Clinical manifestations Headache, Fever , Swallowing difficult, Anorexia, swelling For laryngitis, hoarseness is present 0r aphonia Diagnosis: PE & throat swab Therapeutic Management Antibiotics (penicillin, oral erythromycin) others Cephalosporins & Macrolides. Azithromycin OD x 3 days (Acerra 2018) Analgesic Nursing Considerations: Nursing diagnosis? The nurse often obtains a throat swab for culture. Instruct the parents about administering penicillin and analgesic as prescribed. Cold or warm compresses to the neck may provide relief. Warm saline gargles offer relief of throat discomfort. Soft to liquid diet- increase fluid intake For laryngitis- resting the voice and avoidance of irritants is needed.  Tonsillitis Tonsils are masses of lymphoid tissue located in the pharyngeal cavity. Etiology  Tonsillitisoften occurs with Pharyngitis.  Viral or bacterial  Streptococcus, staph Clinical manifestations Difficulty swallowing and breathing. The child breathes through the mouth. Fever(highgrade), body malaise Redness and swelling of the tonsils. Diagnosis: PE with throat swab to check for presence of Streptococcus (can cause RHD, glomerulonepritis)  Therapeutic management: Nursing diagnosis? Indication for surgery: 1. Warm saline gargle or antibacterial gargle, salt Surgery last resort if water gargle, liquid diet, more than 7 bouts of paracetamol, rest. tonsillitis in a year. 2. Antibiotics(penicillin Hyperthrophy of the grp.-1st line- tonsils cephalosporins) Other complications 3. Tonsillectomy- like otitis media. commonly performed (Shah 2018) Adenoidectomy Nursing considerations Postoperative nursing care  Discourage from coughing, Abdomen or side lying clearing their throat, position to facilitate blowing their nose that drainage of secretions. may aggravate the Prone or fowlers operation site. position leaning forward if bleeding occurs.  All secretions and vomitus Ice collar may be applied are inspected for evidence around the neck. of fresh bleeding. Risk of bleeding common that  Analgesics may be given compromises the airway rectally or intravenously to (Drake & Carr 2017) avoid the oral route.  Food and fluids are restricted until children are fully alert and there are no signs of bleeding.  Cool water, crushed ice, diluted fruit juice is given.  Soft foods, cooked fruits, mashed potatoes are started on the first or second postoperative day, avoid spicy and hot foods.  The nurse observe the throat directly for evidence of bleeding.(frequent swallowing, color of vomitus??)  Avoid too much talking and coughing  Assignment: STUDY OBSTRUCTIVE SLEEP APNEA Epistaxis- hemorrhage from the nose Cause: ruptured of tiny distended vessels in the mucous membrane Application of of the nose of varied origin. phenylephrine Risk factors: trauma, hypertension, spray to promote low platelet count, liver disease, vasoconstriction. tumor. Treatment: Applying direct pressure by pinching the soft outer portion of the nose or with a cotton, patient sits upright with the head tilted forward. Surgicel or Gelfoam patch (Papadakis et al 2018)  Lower respiratory tract Infections Defenses of the Respiratory System 1. Moist, mucus-covered surfaces : Trap particles and organisms 2. Cell surface IgA, lysosomes 3. Ciliated epithelium : Clears trapped particles and organisms from airway passages 4. Cough reflex and epiglottis : Prevents aspiration of particles and irritants into lower airways 5. Pulmonary macrophages : Phagocytize foreign particles and organisms in the alveolar spaces Pleural effusion- fluid in the pleural space Pneumothorax- air in the pleural space leads PLEURAL SPACE to collapse of the lungs. CONTAINS: 5-15 ml of clear liquid The 5 major types of pleural effusion are:  Transudate/spontaneous  Exudate (Empyema-pus- from pneumonia)  Hemorrhagic pleural effusion or hemothorax/trauma  Hydrothorax and pneumothorax CAUSES: pulmonary capillary pressure (CHF) Capillary permeability (Pneumonia) lymphatic obstruction (malignancy) TB, INJURY TO THE LUNGS MECHANICAL VENTILATION  TENSION PNEUMOTHORAX A MEDICAL EMERGENCY can lead to barotrauma.  Patients present with sudden onset of unilateral pleuritic pain and increasing breathlessness.  The main aim of treatment is to get the patient back to active life as soon as possible.  For open tension pneumothorax cover the area with a gauze only the??   Clinical manifestation “COLLAPSE” C- chest pain (sudden sharp) cyanosis. O- overt tachycardia & tachypnea L- low blood pressure L- low O2 saturation less than 90% A- absent breath sounds on affected side P- pushing trachea to unaffected side S- sucking sound(open), subcu emphysema (CO2 escaping to the skin) E- expansion of the chest unequal D- dyspnea Diagnosis Physical examination: breath sounds x ray The fluid itself can be seen at the bottom of the lung or lungs, hiding the normal lung structure. If heart failure is present, the x-ray shadow of the heart will be enlarged. ULTRASOUND  Management of Pleural effusion It can be therapeutic or diagnostic PURPOSE TO RE EXPAND THE LUNGS TO MAXIMIZE BREATHING Nursing intervention: nursing diagnosis? Assess for air leaks in the system? Monitor breath sounds Position of the bottle? Assess rise and fall of Trouble shooting if the chest breaks in the system? Assess vital signs, Intermittent subcu emphysema bubbling/constant? Administer O2 Excessive bubbling? Fowlers position Absence of bubbling? Maintaining chest Water seal tickles ^ & tube system decrease as the pt breaths.  Color of Fluid Color of Fluid Suggested Diagnosis Pale yellow (straw) Transudate, some exudates Red (bloody) Malignancy or embolism or TB Turbid Infected effusion Pus Empyema White (milky) Chylothorax or cholesterol effusion 44 Asthma Asthma- heterogeneous disease characterized by reversible bronchospasm and chronic inflammation of airway passages. (Global Initiative for Asthma-GINA 2019) Airway disorder characterized by  Hyper-reactivity to various stimuli - trigger  Broncho-constriction, mucosal edema, mucus production  Inflammation Pathophysiology Acute reaction to some trigger – reversible with treatment Mast cells release substances that cause inflammation and constriction(histamine) Broncho-constriction or bronchospasm Spasm aggravated by inflammation, mucosal edema and excessive mucus.(McCance 2019)  Precipitating Factors –intrinsic and extrinsic factors No cure Viral infections – especially with infants and young children Allergies Cigarette smoke Smoggy air – smoke from fires Windy weather – hot and dry Cold weather Allergens — Pollen, pet dander, fungi, dust Respiratory tract infections  Clinical Manifestations - Dyspnea – difficulty breathing, Asthma cyanosis (black people) Wheezing Chest tightness Cough – chronic cough may be the only symptom Sputum production Chest retraction Hypoxemia- (ABG & pulse ox) Air trapping leads to? Early symptoms? Peak flow- measure the highest airflow during a forced expiration- measure asthma severity  Bronchial asthma Staging of the Severity of an Acute Asthma Attack  Stage I (mild)  Mild Dyspnea  Diffuse wheezing  Adequate air exchange  Stage II (moderate)  Respiratory distress at rest  Marked wheezing  Stage III (severe)  Marked respiratory distress  Cyanosis  Marked wheezing or absence of breath sounds  Stage IV (respiratory failure)  Severe respiratory distress, lethargy, confusion Nursing Management: Nursing diagnosis? Assessment is key: Assess for cyanosis, chest retraction Assess peak flow meter reading Vital signs High fowlers Oxygen (95-99%) Bronchodilators Exercise- warm up, have brochodilators before exercise sessions. Diagnostics History Pulse Oximetry, Expiratory flow meter reading WBC: eosinophils will be elevated if allergy Arterial blood gas Chest x-ray- hyperinflation of airways & haziness.  Bronchial asthma Possible complications of asthma can include : Severe acute Asthma (status asthmatics), which is a life-threatening condition of prolonged bronchospasm that is often not responsive to drug therapy. Pneumothorax : is also a possible consequence as a result of lung pressure increases that can result from the extreme difficulty involved in expiration during a prolonged asthma attack. Respiratory failure: marked hypoxemia and alkalosis or acidosis might occur??. Other complications? Medical Management Primary focus is preventing impairment of lung function, minimizing symptoms and preventing exacerbations of symptoms (Papi et al 2018) (GINA 2019) First line of treatment: 1. Avoidance of triggers, and allergens. Improved ventilation of the living spaces, use of air conditioning, GIVE OXYGEN Treatment: 2. Bronchodilators (examples: albuterol, salbutamol, terbutaline): Short acting β2-Adrenergic receptor activators. May be administered as needed in the form of a nebulizer solution using a metered dispenser or may be given subcutaneously. These drugs block bronchoconstriction but do not prevent the inflammatory response. Watch out side effects? Treatment: 3. Long Acting Bronchodilators Salmeterol (Serevent) Formoterol (Foradil) Treatment Anticholinergic Bronchodilators (Phosphodiesterase Inhibitors) - The "anti-cholinergic" effect of ipratropium blocks the effect of cholinergic nerves, causing the muscles to relax and airways to dilate. ipratropium, tiotropium (short acting) watch out for dry mouth theophylline/aminophlline (long acting) high level toxicity avoid caffeine (10-20mcg/ml. Use with caution because of side effects (GOLD 2019) Anti inflammatories Corticosteroids- inhaled, IV,PO Long term- not in acute attacks Budesonide, Fluticasone Oral thrush a problem- rinse mouth use spacer. Use after bronchodilators Side effects of steroids?  Leukotrienes modifiers MAST CELL (example: Zafirlukast, STABILIZER Montelukast) : Cromolyn sodium New class of agents that (Crolom) : Anti-inflammatory blocks the synthesis of agent that blocks the key inflammatory both the early and mediators, leukotrienes. late phase of asthma. Stops mast Act as bronchodilators cells from secretion (decrease histamine release)  Immunomodulators Omalizumab- (subcu)- blocks the role of immunoglobulin E to decrease allergic response if other treatment is not working Status asthmaticus- exacerbation can range from mild to severe with potential respiratory arrest. (GINA 2019) Describe as rapid onset, severe and unresponsive to treatment. May precipitated by hypersensitivity to medications such as beta blockers, aspirin NSAIDs (American Academy of Allergy, Asthma & Immunology-AAAA II 2019) A ventilation-perfusion abnormality results in hypoxemia with decrease PCO2 -later leads to increase PCO2 Magnesium sulfate- a calcium antagonist ? Purpose? New treatment for severe uncontrolled asthma Bronchial thermoplasty- nondrug consist of controlled radiofrequency heating of the central airways through a bronchoscope  There are various types of inhalation devices:  1. Metered-dose inhalers (MDIs) Pressurized devices that deliver a measured dose of drug with each activation Hand-mouth coordination is required A. Spacers:  Use with MDIs  Increase delivery of drug to the lungs & decrease deposition of drug on the oropharyngeal mucosa  Especially important for inhaled corticosteroids 63  2. Dry-powder inhalers (DPIs) Include Turbuhalers & Accuhalers Drugs are in the form of dry, micronized powder No propellant is employed Breath activated, much easier to use 64  Directions for use of inhaler Shake well Exhale (breathe out) through your nose while keeping mouth shut Close lips around mouth piece Take slow, deep breath through the mouthpiece as you press down on container to release the medication Hold breath for 5-10 seconds Exhale slowly May give up to 3 treatments at 20 minute intervals If no relief need to call PMD or go to ED  Remove the cap and hold the inhaler upright Tilt the head back slightly and breathe out all the way. Keep the chin up and the inhaler upright (not aimed at the roof of the mouth or the tongue). Repeat puffs as directed by the doctor. Wait 1 minute before taking the second puff. A delay of 10–20 minutes between successive doses of the bronchodilator drug has been suggested in order to let the first act to improve the penetration Nursing management- nursing diagnosis? Priority nursing diagnosis? Monitoring & assessment Fluids?  Acute bronchitis- is acute infection of the bronchial mucosa, without obstruction. ETIOLOGY: Respiratory viruses – parainfluenza, adenoviruses, Rarely pneumococci, H.influenzae, staphylococi and streptococi Clinical manifestation  Dry, hacking, nonproductive cough  within 4-5 days the cough becomes productive  often preceded by an upper respiratory tract infection  afebrile patient or low grade fever  auscultation – rough high pitched rhonchi  Ng diagnosis Treatment  Infants pulmonary drainage is facilitated by frequent shifts in position  Keep well hydrated, humidified air if possible  Treat fever: Paracetamol in t°> 38  antibiotics, antihistamines  Expectorants in irritating and paroxysmal coughing: Bromhexin (suspension, tabl.) , Ambroxol, Carbocisteine (drops)  Refer to hospital  Presence of general danger signs  Fever > 39°C resistant to antipyretic treatment  Acute respiratory distress and cardiac failure  Chronic cough > 30 days duration  Hemoptysis What is COPD?  Preventable and treatable slowly progressive respiratory disease of airflow obstruction involving the airways, pulmonary parenchyma or both (Global Initiative for Chronic Obstructive Lung Disease- GOLD 2019)  COPD patients report they are “hungry” for air  Associated with inflammation of the lungs as they respond to noxious particles or gases. Two Major Causes of COPD Chronic Bronchitis is characterized by  Chronic inflammation and excess mucus production  Presence of chronic productive cough  “Blue Bloaters” they are often cyanotic. Two Major Causes of COPD Emphysema is characterized by  Damage to the small, sac- like units of the lung that deliver oxygen into the lung and remove the carbon dioxide Loss of elasticity of the lung tissue Distention of airspaces & destruction of alveolar walls Han, Martinez 2018) “Pink Puffers” hyperventilate to maintain adequate oxygen levels – this prevents hypoxia   Pathophysiology In COPD, less air flows in and out of the airways because of one or more of the following: The airways and air sacs lose their elastic quality. The walls between many of the air sacs are destroyed. The walls of the airways become thick and inflamed- tissue scarring leads to narrowing of the airway lumen (GOLD 2019). The airways make more mucus than usual, which tends to clog them. Cont. Impaired oxygen Complications: right diffusion leads to sided heart failure(Cor hypoxemia, carbon pulmonale. dioxide elimination is Atelectasis, impaired Pneumonia Pneumothorax Polycythemia??  COPD Causes Smoking (GOLD 2019) Air pollution genetic (hereditary) risk  Primary Symptoms Chronic Bronchitis  Chronic cough  Shortness of breath  Increased mucus  Frequent clearing of throat Emphysema  Chronic cough  Shortness of breath  Limited activity level  Difficulty of breathing  Coarse crackles  Physical examination Distended neck vein on expiration The presence of barrel chest, flatted diaphragm Observe for abdominal breathing The use of pursed lips breathing and chest movement Auscultate the chest& listen for musical wheezes characteristics of chronic bronchitis (crackles) Pink to reddish color related to polycythemia. Prolonged expiration- take note  COPD Diagnostic tests Symptoms Physical examination Sample of sputum Chest x-ray- hyperinflation High-resolution CT scan Pulmonary function test (spirometry) – evaluate airflow obstruction Arterial blood gases test- reveals acidosis, increase Pco2 Pulse oximeter- decrease O2 saturation Nursing diagnosis  Ineffective breathing pattern related to increase need of O2  Ineffective airway clearance related to excessive accumulation of secretions  Impaired gas exchange related to impaired expiration &co2 retention  Preventive measures To prevent irritation and infection of the airways, instruct the patient to: Avoid exposure to cigarette, pipe, and cigar smoke as well as to dusts and powders. Stay indoors when the pollen count is high. Stay indoors when temperature and humidity are both high Practice purse lip breathing to eliminate CO2. Preventive measures diaphragmatic breathing- to strengthen the abdominal muscles, slowing down the breathing rate, make breathing easier. Diaphragm is used followed by a purse lip breathing  Preventive measures Use air conditioning to help decrease pollutants and control temperature Diet high calories, high protein small frequent meals Avoid exposure to persons known to have colds or other respiratory tract infection Avoid enclosed, crowded areas during cold and flu season. Proper hydration helps to cough up secretions or tracheal suctioning when the patient is unable to cough. Obtain immunization against influenza(yearly) and Pneumococcal vaccination reduces the incidence of community acquired pneumonia (GOLD 2019).  Medical management Stop smoking Oxygenation with low concentration during the acute episodes(O2 at 1-2L/min) 88-93% hypoxic drive is low O2. FIRST LINE OF TREATMENT (GOLD 2019) Oxygen toxicity may occur when too high concentration is given for an extended period of time (Kacmarek, Stoller & Heuer 2017) The high O2 levels can then suppress CO2 chemoreceptors which in turn depress the respiratory drive disrupting ventilation-perfusion balance (Kacmarek et al 2017) Increase fluids intake to correct loss of diaphoresis and inaccessible loss of hyperventilation. Intubations and mechanical ventilation if there is respiratory failure.  antibiotics to treat infection Medical management 2. bronchodilators to relieve bronchospasm, reduce airway obstruction, mucosal edema and liquefy secretions. Inhaled Anticholinergic drugs such as Aminophylline. 2.1 Short acting bronchodilators (Albuterol, Salbutamol) Chest physiotherapy and postural drainage to improve pulmonary ventilation. 3. Steroid therapy if the patient fails to respond to more conservative treatment. Decrease inflammation.(oral,IV, inhalation) Phosphodiestrace 4 inhibitors (Roflumilast)- reduce the risk of COPD exacerbation by reducing the inflammation. side effects include: suicidal tendencies and weight loss. SURGICAL OPTIONS BULLECTOMY Complications of COPD 1. Cor pulmonale- enlargement of the right side of the heart due to pulmonary hypertension caused by constriction of the pulmonary vessels in response to hypoxia + polycythemia leads to RIGHT SIDED HEART FAILURE. 2. Pneumonia- cause by prolonged sputum production. 3. Possible pneumothorax- ruptured of air sacs 4. Atelectasis Pneumonia Classification: Is an inflammatory According to causes process of the lung Bacterial (the most parenchyma that is common cause of commonly caused by pneumonia) infectious agents. Viral pneumonia Fungal pneumonia Chemical pneumonia (ingestion of kerosene or inhalation of irritating substance) Inhalation pneumonia (aspiration pneumonia) Hypostatic pneumonia  Classification according to source 1. Community acquired pneumonia (CAP) 2. Health care associated pneumonia (HCAP) ex. Dialysis unit, chemotherapy unit 3. Hospital acquired pneumonia (HAP)- 48 hours or more after admission 4. Ventilator associated pneumonia (VAP) (American Thoracic Society & Infectious Disease Society of America 2005) (Klompas 2019) Identified Pathogens in Community-acquired Pneumonia/Hosp acquired Others include: Ventilator associated pneumonia New pathogens: The SARS coronavirus  Streptococcus COVID19 coronavirus pneumoniae 20- Community-acquired 60% methicillin-resistant Staphylococcus aureus  Haemophilus Opportunistic influenzae 3- RISK FACTORS: 10% Elderly, smoker  Staphylococcus Children aureus 3-5% Immunocompromised Post surgery client Pre existing disease  Gram-negative bacilli 3- 10%  According to areas involved Lobar pneumonia; if one or more lobe is involved Broncho-pneumonia; the pneumonic process has originated in one or more bronchi and extends to the surrounding lung tissue. Mode of transmission Ways you can get pneumonia include: Bacteria and viruses living in your nose, sinuses, or mouth may spread to your lungs. You may breathe some of these germs directly into your lungs (droplets infection). You breathe in (inhale) food, liquids, vomit, or fluids from the mouth into your lungs (aspiration pneumonia). Pneumonia occurs in person with certain underlying disorders such as heart failure, diabetes, alcoholism, COPD, AIDS (Klompas 2019) Pathophysiology The streptococci reach the alveoli and lead to inflammation and pouring of an exudates into the air spaces. WBCs migrates to alveoli, the alveoli become more thick due to its filling consolidation, involved areas by inflammation are not adequately ventilated, due to secretion and edema. This will lead to partial occlusion of alveoli and bronchi causing a decrease in alveolar oxygen content. Pneumonia-Pathophysiology Venous blood that goes to affected areas without being oxygenated and returns to the heart. This will lead to arterial hypoxemia and even death due to interference with ventilation. Respiratory acidosis ABG Clinical manifestations- older patient has vague symptoms Shaking chills Rapidly rising fever ( 39.5 to 40.5 degree) Stabbing chest pain aggravated by respiration and coughing Tachypnea, nasal flaring Patient is very ill and lies on the affected side to decrease pain Use of accessory muscles of respiration e.g. abdomen and intercostals muscles Cough with purulent, blood tinged, rusty sputum Shortness of breath (high PCO2>45, O2 sat. 15mm+ (positive to everyone) >10mm+ (immigrants, IV drug user, tight living condition, immunocompromised) >5mm+ (HIV, contact with TB client, organ transplant) Diagnostic test Sputum culture and sensitivity test AFB smear Client will cough for sputum collection Must be 3 consecutive collection in the morning upon arising before breakfast Diagnostic test Chest x ray Latent TB granulomas can be seen on a chest xray Diagnostic test: blood test Interferon-gamma release assays (IGRAs) A. QuantiFERON-TB Gold T SPOT Use for people received the BCG vaccine Tuberculosis Treatment Directly Observed Treatment, Short- course. DOTS is a strategy used to reduce the number of tuberculosis (TB) cases. In DOTS, healthcare workers observe patients as they take their medicine. ACTIVE-- isoniazid (INH) rifampin (RIF) ethambutol (EMB) pyrazinamide (PZA) o LATENT--  isoniazid (INH)  Person is not infectious after 2-3 weeks of therapy  Initial phase- 4 months  Continuation- 4 months Medical management- 6-12 3. Rifampin- stops RNA months 1. Pyrazinamide- kills the bacteria polymerase- it kills the bacteria side effects: body fluids turning side effects: uric acid build into orange, birth control less up effective, sunburn easily No alcohol GI upset- adm with food S/S of liver issues; jaundice. Monitor liver/kidney 4. Isoniazid (INH)- kills the function test bacteria and stops its growth. 2. Ethambutol- stop RNA side effects: peripehral synthesis neuropathy thus it decrease Vit. B6 level side effects: peripheral Monitor liver function test and neuropathy, affects the neurotoxicity optic nerve- have regular 5. STREPTOMYCIN- can cause eye checks 8 cranial nerve damage.  Nursing management: nursing diagnosis? For active TB: Isolated Airborne precaution+ standard precaution- use N95 mask/negative pressure room When the client leave the room wear a surgical mask After 3 weeks of drug treatment client is no longer contagious Multidrug resistance  ACUTE RESPIRATORY DISTRESS SYNDROME Clinical syndrome characterized by severe inflammatory process causing diffuse alveolar damage that results in sudden pulmonary edema, increasing bilateral infiltrates on chest x ray, hypoxemia unresponsive to oxygen supplementation and absence of an elevated left atrial pressure, and reduce lung compliance (Siegel 2019) ACUTE RESPIRATORY DISTRESS SYNDROME  Interstitial and intra- alveolar edema and hemorrhage  Alveolar consolidation  Pulmonary surfactant deficiency or abnormality  Atelectasis  Etiology: Direct/indirect cause  Aspiration/drowning Multitude of Factors  Congestive heart failure  Disseminated intravascular coagulation  Infections (pneumonia)  Inhalation of toxins and irritants  Sepsis (burns) Pathophysiology-damage surfactants Clinical manifestation A-atelectasis Increased heart rate, respiratory rate (alkalosis then acidosis), R- refractory hypoxemia blood pressure D- decrease lung compliance Substernal/intercostal retractions/cyanosis S- surfactant less Cyanosis leads to refractory hypoxemia(even with high O2) (Siegel 2019) Difficulty of breathing Chest assessment findings  Dull percussion note  Crackles(pulmonary edema)  Diagnosis ARDS was defined as a syndrome of : 1- Acute onset (developed respiratory distress within 48 to 72 hours ) 2- Bilateral infiltrates on CXR consistent with pulmonary edema 3-Arterial blood gas reveals decrease PO2(less than 60mmhg) despite administration of high O2..  Treatment: Mechanical  standard therapy for ARDS Ventilation (it open alveoli sacs that are collapse)  Positive End Expiratory Pressure (PEEP)- 10-20cm H2O, PaO2>60mmhg, O2 sat>90%, Prone position- Better ventilation-perfusion matching, ^ O2 without ^O2 content. heart and diaphragm are not pressing against the lungs, which means that pleural pressure is reduced. Decrease atelectasis (Siegel 2019)  Complications:  ^ thoracic pressure- pneumothorax> decrease cardiac output  General Management of ARDS Nursing diagnosis? Prophylaxis against Medications and procedures gastrointestinal stress commonly prescribed by the physician ulceration and deep venous thrombosis.  Antibiotics Option: Sedation- to  Diuretics decrease oxygen  Corticosteroids consumption  SpO2 goal for these (Midazolam) clients tends to be Neuromuscular blocking approximately 92-94%. agents (pancuronium,  FiO2- 95-100%- prolonged atracurium)- to allow oxygen leads to toxicity ventilation more easily Corona virus- COVID19 Covid 19 caused by a new type of corona virus.-Wuhan Dec 2019 SARS- Severe Acute Respiratory Sydrome- China 2003 MERScov- Middle East Respiratory Syndrome- Saudi Arabia 2012  How deadly is COVID19 According to WHO 80%- have mild symptoms and will recover. 14%- have severe disease including pneumonia. 5%- have critical disease (respiratory failure,septic shock, multi organ failure) 2%- fatal effects cause death. Prone to infection are the childen, elderly and with existing medical condition.  Mode of Transmission Direct contact- droplet infection Airborne transmission Ways COVID19 can spread: Imported case- direct contact Local transmission- direct contact Community- transmission? Incubation period? Signs and Symptoms: Flu like symptoms Asymptomatic clients are contageous PREVENTION: 1. Hand hygiene, cover mouth when sneeze 2. Avoid touching your T areas 3. Use of mask 4. Stay at home avoid travel 5. Social distancing 6. Disinfect surfaces COVID HAS NO CURE! Only symptomatic treatment HOW TO COMBAT COVID19? SPEED OF INFECTION experts use the basic reproduction number, called the R0 (pronounced “R naught”). That refers to how many other people one sick person will infect on average in a group that doesn’t already have immunity. The higher the R0, the higher the likelihood that many people will get sick. Covid 19 Pneumonia (viral type) 1. Anticoagulants as prophylaxis low molecular weight heparin (enoxaparin) given twice daily (Kim & Gandhi 2020)- for higher incidence of venous thromboembolism. 2. Prone positioning with high flow oxygen therapy can prevent eventual ET intubation in some patient with severe COVID 19 pneumonia (Caputo et al 2020) 3. Antiviral Remdesivir- improving recovery times and overall outcomes (Beigel, Tomashek, Dodd 2020) 4. Convalescent plasma- transfuses antibodies from patients recovered from Covid 19 into patient with severe disease (Kim & Gandhi 2020) 5. Antibiotic- as needed , Ventilator as needed