The Respiratory System

RESPIRATORY DISORDERS

LOWER AIRWAY DISORDERS

ASTHMA  A disorder of the bronchial airways characterized by periods of reversible bronchospasm, hyperactive airways, increased mucus production

Etiology and Risk Fx.

   
Intrinsic Genetic Stress Emotion Exercise Extrinsic  Allergens (pollen, dust, dander)  Irritants (pollution, smoke)

PATHOPHYSIOLOGY
Allergen

Degranulation of mast cells Basophils

Release histamine, bradykinin, Prostaglandin, leukotrienes o Vascular permeability

bronchoconstriction

Airway edema

Non-specific irritants

Intrinsic Asthma Parasympathetic

Reflex bronchoconstriction

Sympathetic
o E receptor stimulation q F2 receptor stimulation

bronchoconstriction

bronchoconstriction

Assessment of severity of Asthma

Diagnostics: 1. CBC with WBC differential increased eosinophil 2. ABG - dec. O2, dec. pH, inc. CO2 3. Sputum exam increased eosinophils 4. Skin testing identify specific antigen 5. Pulmonary Function test- residual testvolume, expiratory volume 6. Curshmann spirals 7. Charcot Leyden crystals

Medical Mgt: 1. Reverse airway spasm  B2-Agonist, anticholinergics B2 Salbutamol, Ipratropium bromide,
Theophylline

 Supplemental oxygen (O2) 2. Control inflammation  Inhaled corticosteroids  Leukotriene inhibitors  Mast cell stabilizers

Nrsg Mgnt: 1. Monitor vital signs 2. Place client in High-Fowlers position High3. Administer O2 as ordered 4. Administer medications as ordered 5. Provide humidification/ hydration to loosen secretions. 6. Monitor for respiratory distress.
1. Status Asthmaticus - Subcutaneous epinephrine

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)  A disease state characterized by the presence of airflow obstruction that is generally progressive

CHRONIC OBSTRUCTIVE BRONCHITIS  inflammation of the bronchi resulting to increased mucus production and cough

Etiology and Risk Fx. 1. Cigarette smoking 2. Chronic respiratory infections 3. Irritants 4. Hereditary predisposition

What happens in chronic obstructive bronchitis?

 Increase in number and size of

Goblet cells  Excessive secretion of mucus  Edema and thickening of the airway walls

Chronic exposure to irritants/smoking

o Size & number of submucous glands

Thicker mucus

Impaired ciliary fxn

Impaired mucociliary defenses

Chronic infection

- oo mucus production - Thickening of bronchial walls & inflammation

Airway obstruction

Airway collapse

Air trapped in distal portion of the lung hypoxia acidosis

Reduced alveolar ventilation

Cyanosis, DOB, polycythemia Cor pulmonale CHF

Manifestations: 1. Productive cough  Lasting 3 months or more in 2 consecutive year  With copious amount of thick, tenacious sputum 2. Cyanosis 3. Distended neck vein 4. Edema 5. Wheezing and rhonchi upon auscultation

Laboratory and Dx Test: 1. CBC with WBC differential - RBC and hematocrit, WBC if infection is present. 2. ABG hypoxemia, hypercapnia, decreased pH 3. Pulmonary Function test- residual testvolume, expiratory volume

EMPHYSEMA  A disorder in which the alveolar walls are destroyed, leading to permanent over distention of air spaces

Emphysema - Cigarette smoking, Hereditary, Aging Process

Disequilibrium between Elastase and Antielastase

Loss of elastic recoil

Formation of blebs or bullae

Over distention of Alveoli Retention of CO2

o Ventilatory dead space DOB

Hypoxia

Etiology and Risk Fx. 1. Cigarette smoking 2. Aging 3. -1 anti-trypsin antideficiency 4. Chronic respiratory infections 5. Irritants 6. Hereditary predisposition

Types: 1. Centrilobular (Centriacinar)  Most common type of emphysema  Destruction in the respiratory bronchioles common in the upper lung regions 2. Paraseptal (Panacinar)  Destruction of entire acinus (respiratory bronchioles and alveolar walls)  Due to -1 antitrypsin deficiency

Manifestations: 1. Dyspnea 2. Cough 3. Thin 4. Tachypnea 5. Barrel chest 6. Use of accessory muscles 7. Diminished breath sounds 8. Hyperresonant sound on percussion

Manifestations: 9. Pursed lip breathing 10. Tends to assume an upright position 11. Alteration in LOC, skin color (pallor to cyanosis), skin temp (cold to touch) 12. Weakness , fatigue, anorexia, weight loss 13. Clubbing of fingers 14. Polycythemia

BARREL CHEST

Laboratory and Dx Test: 1. CBC with WBC differential - RBC and hematocrit, WBC if infection is present. 2. Serum -1 antitrypsin - deficient 3. ABG hypoxemia, hypercapnia, decreased pH 4. Pulmonary Function test- residual testvolume, expiratory volume 5. Chest X-ray flattened diaphragm due to Xhyperhyper-inflated lungs

BLUE BLOATER

PINK PUFFER

Complications: 1. Respiratory tract infection 2. Cor pulmonale

hypoxemia pulmonary vasoconstriction

Resp. failure

RVH

R- sided heart failure

3. Polycythemia 4. Spontaneous pneumothorax Collaborative Management: Management: 1. Medications - bronchodilators - antihistamines - antibiotics -expectorants /antitussives - mast cell stabilizers - flu vaccine, pneumovax - steroids - AAT replacement tx - O2 replacement tx
(caution in bronchitis)

2. Pulmonary hygiene - nebulized bronchodilators - postural drainage - chest physiotherapy 3. Exercises - does not improve lung function - enhance CV fitness & train skeletal muscles to function more effectively - walking - breathing (diaphragmatic)

4. Controlling complications * edema & cor pulmonale diuretics - digitalis * polycythemia phlebotomy - > 60% hct * continuous O2 inhalation 1-3 LPM (2 is 1safest) 5. Avoiding irritants - stop smoking - avoid high altitudes

6. Psychological support 7. Rest 8. Good oral care 9. Increase oral fluids if without edema 10. Dietary management - frequent small feedings - increase calorie for energy - increase protein maintain integrity of alveolar walls - low carbohydrate limits carbon dioxide production

BRONCHIECTASIS  an extreme form of bronchitis  it causes permanent abnormal dilation and distortion of bronchi and bronchioles

Incidence and Etiology: 1. Recurrent inflammation of the airway 2. Exposure to toxic gases 3. Abnormal lung or immunologic defenses 4. Localized airway obstruction

Manifestations: 1. Cough 2. Muco-purulent sputum Muco3. Fever 4. Hemoptysis 5. Nasal stuffiness Diagnostic: Chest X-ray and CT Scan - dilated Xbronchioles

DISEASE CHARACTER Etiology

EMPHYSEMA Smoking, genetic

CHRONIC BRONCHITIS Smoking, air pollution

ASTHMA-ACUTE Hypersensitivity type I, Hyperresponsive tissue Small bronchi, bronchioles Inflammation, bronchochonstriction, increased mucus produced, obstruction, repeat attacks lead to damage Cough and dyspnea, wheezing Thick, tenecious sputum If status asthmaticus Rare Some

Location Pathophysiology

Alveoli Destruction of alveolar walls,loss of elasticity, impaired expiration, barrel chest, hyperinflation

Bronchi Increased mucous glands and secretions, inflammation, and infection, obstruction Early, constant cough, some dyspnea Large amount, purulent Yes Common Frequent

Cough and Dyspnea Sputum Cyanosis Cor pulmonale Infection

Some coughing, marked dyspnea Little No Perhaps late Some

PARENCHYMAL AND PLEURAL DISORDERS

Atelectasis  Pertains to collapse of lung tissue or alveoli

Classifications: 1. Obstructive or resorption atelectasis  Total obstruction of the airway due to mucus or tumor

Etiology: 1. Airway obstruction by mucus, tumor, foreign body, airway edema 2. Chest wall disorders (e.g., scoliosis, flail chest) 3. Impaired diaphragmatic movement (e.g., obesity, ascites) 4. Central nervous system dysfunction (e.g., coma, neuromuscular disorders, over sedation) 5. Oxygen toxicity

2. Compression atelectasis
 Secondary to space occupying processes that cause crowding of the tissue and prevents normal expansion Etiology: 1. Pneumothorax 2. Pleural effusion 3. Pleural tumor

3. Contraction atelectasis
 Localized or generalized fibrotic changes in the lung or pleura that prevents the lung from expanding fully Etiology: 1. Interstitial fibrosis 2. Decreased surfactant (e.g., ARDS, inhalation anesthesia)

4. Postoperative atelectasis - Commonly occurs 24 to 72 hrs following surgery ( particularly abdominal surgery) - Factors implicated to PA: - restricted ventilation due to pain - slow shallow respirations due to anesthetics and analgesics - increased secretions due to supine position - decreased cough effort

Clinical Manifestations 1. Dyspnea 2. Tachypnea 3. Cyanosis 4. Tachycardia 5. Fever

Physical assessment: 1. Tracheal shift toward affected side 2. Decreased tactile fremitus over affected area 3. Dull percussion note 4. Decreased chest movement on involved side 5. Decreased breath sounds 6. Crackles upon auscultation

Diagnostic procedures: 1. Chest x-ray- patchy or consolidated area x-ray2. Pulse oximetry hypoxemia PaO2 < 90%

Medical Management: 1. Treatment of underlying cause 2. Keep airways open 3. Maintain adequate respiratory function 4. Prevent respiratory failure

Nursing Care: 1. Preventing atelectasis 2. Encourage frequent position changes 3. Encourage early ambulation 4. Perform deep breathing and coughing exercise 5. Use of incentive spirometry

Management: 1. Remove secretions by coughing, chest physiotherapy and suctioning 2. Assess respiratory status 3. Watch for signs of respiratory failure 4. Administer nebulization or bronchodilators as ordered 5. Provide supplemental O2 6. Assist in thoracentesis 7. Provide nursing care for patient on mechanical ventilators

INFECTIOUS DISORDERS
Pneumonia  inflammation of the lung parenchyma

Classifications: Affected area 1. Lobar- involvement of an entire lobe Lobar2. Lobular- involving part of a lobe Lobular3. Bronchopneumonia-involving distal airways Bronchopneumoniaand alveoli 4. Alveolar/ acinar pneumonia involving distal air spaces 5. Interstitial/ reticular pneumonia involving lung tissues surrounding air spaces & vascular structure rather than the air passages themselves

Cause: 1. Noninfectious causes  Aspiration pneumonia aspiration of food or gastric acid  Hydrocarbons  Foreign bodies  Hypersensitivity reactions  Drug or radiation induced

2. Microbial causes
 Streptococcus pneumoniae most common cause of community acquired pneumonia  Kleibsella pneumoniae most common gram negative microorganism in the hospital  Staphylococcus aureus Most common causative agent of nosocomial pneumonia  Haemophilus influenzae common cause of pneumonia in children

Onset:  Community acquired pneumonia (CAP) - occurring in the community setting or 48 hours after hospitalization  Nosocomial pneumonia (hospital acquired) development of pneumonia 48 hours after admission to a health facility

Pathophysiology
Offending organism

Aspiration/inhalation q Immune response

Pneumonia

bloodstream

Lung capillaries

- Cough w/ : Tachypnea RR > 20 per minute Tachycardia CR >100 per minute Fever - Temp >37.8 rC Diminished breath sounds Rhonchi Crackles Wheeze

Pathophysiology: 4 stages: 1. Congestion  Local inflammation  Bacteria laden fluid fills alveoli  Edema in the alveoli  Edema may thicken alveolar walls

2. Red hepatization
 Occurs 2 -3 days after initial infection  Polymorphonuclear neutrophils (PMNs) rush to area  Lung tissues appear dry, granular and dark reddish-brown reddishresembling the liver

3. Gray hepatization
 Last 2 days or more after red hepatization  Macrophages replace PMNs and ingest debris  Alveoli is relatively bloodless due to the fibrin

4. Resolution
 Exudate is removed  Fibrin is removed or becomes a dense scar

Clinical Manifestations: 1. Dyspnea 2. High fever 3. Sudden onset of shaking chills 4. Productive cough with rusty brown or blood streaked purulent sputum 5. Stabbing pleuritic chest pain aggravated by respiration and coughing 6. Tachypnea

Elderly patients - may not present w/ dyspnea or fever - altered mental status - volume depletion

Physical Assessment: 1. Crackles upon auscultation 2. Increased bronchophony 3. Increased egophony 4. Increased whispered pectoriloquy 5. Increased tactile fremitus

Laboratory and Diagnostic Test: 1. Chest x-ray presence of infiltrates x2. WBC - increased 3. Sputum culture  Confirmatory test  Reveal inflammatory and bacterial cells 4. Bronchoscopy- allows collection of Bronchoscopyspecimen to identify specific infectious organism 5. ABG to assess need for supplemental oxygen

Nursing Management Assessment Ask: 1. Contact w/ other clients experiencing similar symptoms 2. Hx. of TB or exposure 3. Exposure to birds

Elderly Patients - high index of suspicion - assess for heart failure, CAL - usually bacteria from the GI tract

Pulmonary Tuberculosis Causative Agent: Mycobacterium Agent: tuberculosis Reservoir  Lungs of infected individual Portal of Exit:  Mouth and nose of infected individuals Mode of Transmission:  Droplet sneezes, cough, and talk  Indirect e.g contaminated objects, systemic infection Portal of Entry:  Mouth and nose  Wounds

Risk Factors: 1. Close contact with someone with active PTB 2. Immunocompromised status e.g. HIV infxn 3. Substance abuse (drug users and alcoholics) 4. Anyone without adequate health care (homeless, impoverished, minorities, children below 15 and young adults bet 15-44) 155. Preexisting medical condition and medical treatment (DM, CRF, malnourishment, selected malignancies, organ transplant, gastrectomy)

6.Immigrants from countries of high TB

prevalence. 7.Institutionalization (long term facilities, psych institution , prisons) 8.Living in overcrowded substandard housing 9.Being with health care provider performing high risk activities (medication administration, O2 administration, suctioning)

Incubation Period:  2 10 weeks Pathophysiology: Stages:  Primary Infection  Progressive primary tuberculosis  Secondary tuberculosis

Organs resistant to TB bacilli: bacilli: 1. Heart 2. Striated muscle 3. Thyroid 4. Pancreas

Clinical manifestations: 1. productive or nonproductive cough 2. low-grade fever in the afternoon low3. night chills and sweat 4. anorexia and weight loss 5. fatigue 6. dyspnea 7. hemoptysis 8. dull or pleuritic chest pain 9. chest tightness

Classification of TB
Class I (TB exposure) - exposed to an adult w/ active TB - (-) signs & symptoms of TB - (-) Mantoux test - (-) chest Xray - tx for adolescent/adult who infected the client - no chest xray, sputum culture

Class II (TB infection) - (+/-) exposure (+/- (+) Mantoux test - (-) signs & symptoms - (-) chest Xray - preclinical state of TB - risk of developing TB is 5 15% during 1st 10 yrs after 1r infection 1r

Class III (TB disease) At least 3 or more of the ff: 1. Exposure 2. (+)Mantoux test / (+) sputum AFB x3 3. (+) signs & symptoms 4. Abnormal CXR 5. Lab findings suggestive of TB sputum culture: gold standard

May present w/ : Cough > 2 weeks Fever > 2 weeks Painless cervical or other lymphadenopathy Weight loss/ loss of appetite Failure to respond to appropriate therapy Failure to make a quick return to normal health after an infection

Class IV (TB inactive) - (+/-) hx of previous TB (+/- (+/-) previous chemotherapy (+/- (+) radiologic evidence of healed/ calcified TB - (+) Mantoux test - (-) s/sx - (-) smear

Identifying TB Symptomatics One smear (+) case will infect 10-20 10persons/year, persons/year, if left undiagnosed half of them will die within two years One smear (-) case may infect 1-2 (persons/year

Lab and Dx Test: 1. Tuberculin Skin Testing a 5 units or 0.1 ml of PPD is injected intradermally and will be checked for induration after 48 72 hours. 2. Acid Fast Bacillus Smear - sputum is obtained for 3 consecutive days and analyzed under the microscope to determine nature of microorganism. 3. Chest X-ray presence of cavities X4. Sputum Culture  usually takes 7 days before microorganism grows  Confirmatory test

Nursing Responsibilities 1. Administer medications as ordered 2. Prevent transmission.  Strict isolation not required if client/significant others adhere to special respiratory precautions for tuberculosis.  Client should be in a well-ventilated wellprivate room, with the door kept closed at all times.

 All visitors and staff should wear masks when in contact with the client and should discard the used masks before leaving the room; client should wear a mask when leaving the room for tests.  Hand washing is required after direct contact with the client or contaminated articles.

3. Promote adequate nutrition.

 Make ongoing assessments of clients appetite and do kcal counts for 3 days  Offer small, frequent feedings and nutritional supplements  Weigh client at least twice a week.  Encourage activity as tolerated to increase appetite.

4. Provide client teaching and discharge

planning concerning  Medication regimen: prepare a sheet with each drug name, dosage, time due, and major side effects; stress importance of following medication schedule for prescribed period of time (usually 6 months); include significant others

 Transmission prevention: client should cover mouth when coughing, expectorate into a tissue and place it in a paper bag; client should also wash hands after coughing or sneezing; stress importance of plenty of fresh air; include significant others  Importance of notifying physician at the first sign of persistent cough, fever, or hemoptysis (may indicate recurrence)  Need for follow-up care including physical followexam, sputum cultures, and chest x-rays x-

Medical Management: 1ST LINE MEDS R-ifampicin E-thambutol S-treptomycin P-yrazinamide I- soniazid (INH)
All anti Kochs Meds are hepatotoxic!

MINOR SIDE EFFECTS Side Effects GastroGastro-Intestinal Intolerance Mild Skin Reactions Orange/Red colored urine Pain at injection site Peripheral Neuropathy Drug Rifampicin/INH Any kind Rifampicin Streptomycin Isoniazid What to do? Give medication at bedtime Or give small meals Give Anti-histamines AntiReassure patient Apply warm compress Rotate sites of Injection Vitamin B6 100-200mg daily 100for TX 10mg daily for prevention ASA or NSAID or Allopurinol (do uric acid determination and manage accordingly) Give Antipyretics

Arthralgia due to Hyperuricemia

Pyrazinamide

FluFlu-like symptoms

Rifampicin

MAJOR SIDE EFFECTS Side Effects Severe skin rash due to hypersensitivity Jaundice due to Hepatitis Oliguria or Albuminuria Due to renal disorder Impairment of visual acuity and color vision due to Optic Neuritis Psychosis and convulsion Hearing impairment, tinnitus, dizziness due to damage CN VIII Thrombocytopenia, Anemia, shock Drug All (especially Streptomycin) INH/RIF/PZA Streptomycin Rifampicin Ethambutol Discontinue Anti-TB AntiDrugs and Refer to DOTS Physician What to do

Isoniazid Streptomycin

Rifampicin

Class I - HR x 4 months or HE x 6 months

- repeat PPD in 2 months
if (+) treat as class II if (-) stop tx (-

Class II - HR x 4 months
- HE x 6 months

Class III - HRZE x 2months : initial phase

- HR x 4 months : continuation phase

Things to remember: remember: 1. If patient cannot complete tx, better not start tx. 2. Instill in patients mind the need to complete 6 months tx.
- DOTS - give meds 1 hr before meals or R 1 hr before breakfast E - 1 hr before lunch Z 1 hr before supper

3. Allowance for non-compliance is 2 wks. non4. Follow up monthly 5. If symptomatic after 6 months continue meds but rpt AFB. - assess if patient has MDRTB 6. If asymptomatic x 2 yrs long term cure 7. Not infective after 2 wks of meds

Guidelines for sputum collection a. First interview with the patient (Day 1) Collect spot specimen, then the patient is specimen, given a cup and instruct to collect early morning specimen. b. Second interview with the patient (day 2) Patient returns with early sputum specimen. Collect 2nd spot specimen. specimen.

Instructions to produce good sputum specimen Breathe deeply two times, hold breathe for few seconds after each inhalation then exhale slowly. Repeat entire sequence twice. After inhaling deeply for the third time, at the height of deep inspiration, instruct the patient to cough forcefully and spit the sputum in the proper container.

Sputum should be collected in open air or designated sputum collection area. Ideal appearance of good quality sputum specimen: purulent, yellowish, cheesy-like cheesymaterial, 3-5 ml (1/2 to 1 teaspoon). 3-

2nd line Drugs: Drugs: Ciprofloxacin Ofloxacin Amikacin Cycloserine Terizidone

AntiAnti-TB Drug Therapy: New Solutions

1. DOTS (Directly Observed Treatment ShortShort-course) 2. FDC (Fixed-Dose Combination) (Fixedformulation

Pleural Effusion  Pleural effusion is an accumulation of fluid in the pleural space

Etiology 4 major categories: 1. Increased hydrostatic pressure in the capillaries

  Caused by disorders that increase blood volume in the pulmonary circulation e.g., congestive heart failure, congenital heart defects that cause left to right shunting Disorders that causing protein loss e.g., liver and renal failure

2. Reduced capillary oncotic pressure

 

3. Increased capillary permeability

 Caused by chemical mediators of inflammation  E.g. infection, trauma 4. Impaired lymphatic function  Disorders that interferes with drainage of pleural fluid by the lymphatic  E.g. lymphatic obstruction due to tumor

Types of fluid:  Transudate  Fluids that have pass through a membrane or tissue surface  Usually clear serous fluid  Exudate  Fluids that have escaped the blood vessel

Types of exudative pleural effusion: 1. Hemothorax  Accumulation of blood in the pleural space  If <300 ml of blood no intervention is required 2. Empyema  Accumulation of pus in the pleural space  Undrained pus may become thick and almost solidified or contain cavities

3. Chylothorax
 Chyle accumulation in the pleural space  Chyle is a cloudy liquid product of digestion consisting mainly of emulsified fats 4. Pleural effusion with cloudy serous fluid

Clinical Manifestations: 1. signs and symptoms of underlying cause e.g. if caused by pneumonia expect increased temperature and chest pain 2. dyspnea 3. tachypnea 4. pleural pain 5. dry or productive cough

Assessment Findings: 1. Diminished breath sounds over affected lung 2. Asymmetric chest expansion 3. Decreased tactile fremitus 4. Dull percussion note 5. Tracheal deviation if mediastinal shift is present

Diagnostic Findings: 1. Thoracentesis identify fluid type 2. Pleural fluid analysis identify fluid composition 3. Chest X-ray positive if more than 250 ml X4. CT scan 5. Pulmonary Function Test assess degree of respiratory impairment 6. ABG reveal decrease O2 and increased carbon dioxide levels

Medical Management: 1. Treat underlying cause 2. Thoracentesis:  Remove excess fluid to allow lung expansion 3. Drug therapy  Antibiotics: either systemic or directly into pleural space  Fibrinolytic enzymes: trypsin, streptokinase to decrease thickness of pus and dissolves fibrin clots 4. Closed chest drainage

Thoracentesis  Thoracentesis, also known as pleural fluid aspiration, aspiration of pleural fluid for diagnostic and therapeutic purpose Indications:  obtain a sample of pleural fluid for analysis  relieve lung compression  obtain a lung tissue biopsy specimen.

Thoracentesis Significance  Pleural fluid may contain blood, chyle, or pus and necrotic tissue. A high percentage of neutrophils suggest septic inflammation. Pleural fluid glucose levels that are 30 to 40 mg/dl (SI, 1.5 to 2 mmol/L) lower than blood glucose levels may indicate cancer, bacterial infection, nonseptic inflammation, or metastasis.

Nursing considerations

 Obtain an informed consent  Explain procedure to the client  Ensure that chest x-ray examination is done xbefore and after the procedure  Assist in and support the client in a sitting position  Set up a sterile field for the physician  Assess pulse and respirations before, during, and after the procedure

Nursing considerations

 Inform the client not to cough during the    

procedure to prevent trauma to the lungs After the procedure, label and send specimens for laboratory tests Note and record the amount, color, and clarity of the fluid withdrawn Place the client on the unaffected side with the head of the bed elevated 45 degrees Monitor for respiratory distress, pneumothorax

Pleurisy  Pleurisy refers to inflammation of both layers of pleura Etiology  Pleurisy develops in combination with disease states in the lungs characterized by infection and inflammation  e.g. pneumonia, TB, chest trauma, pulmonary emboli, lung cancer, thoracotomy

Clinical Manifestations 1. Sharp, knife-like chest pain aggravated by knifebreathing, coughing and sneezing. May be minimally absent when holding breath. May be localized or radiating to shoulder or abdomen 2. Slow shallow breathing 3. Dyspnea 4. Symptoms of underlying cause

Physical assessment and Diagnostic findings: 1. Pericardial friction rub low pitched grating sound made by the 2 pleural lining rubbing against each other 2. Chest X-ray X3. Sputum examination 4. Thoracentesis

Management: 1. Treatment of underlying cause 2. Non steroidal anti-inflammatory drugs anti3. Intercostal nerve block

Nursing Responsibilities: 1. Monitor extent of dyspnea 2. Assessed characteristic of pain 3. Administer analgesics as prescribed 4. Teach splinting of chest wall during coughing 5. Assist client in assuming comfortable position 6. Provide topical applications of heat and cold over affected area

CHEST TRAUMA Pneumothorax  life threatening situation wherein air enters the pleural cavity causing a lung to collapse partially or completely on the affected side, resulting in a reduction in tidal volume and gas

Types: 1. Spontaneous  Most common type of closed pneumothorax  Air accumulates within the pleural space without an obvious cause.  Rupture of a small bleb on the visceral pleura most frequently produces this type of pneumothorax

2. Traumatic
 Open Pneumothorax: Laceration in the parietal pleura that allows atmospheric air to enter inside.  Closed Pneumothorax- Laceration in Pneumothoraxthe visceral pleura that allows air in the lung to enter the pleural space.

3. Tension Pneumothorax  Air enters the pleural space with each inspiration but cannot escape Causes increased intrathoracic pressure and shifting of the mediastinal contents to the unaffected side (mediastinal shift)

Etiology/ Classification: 1. Penetrating common cause of open pneumothorax 2. Blunt chest trauma- common cause of traumaclose pneumothorax 3. Rupture of alveoli 4. Medical procedure

Manifestatons: 1. tachypnea 2. dyspnea 3. sudden sharp pain 4. asymetrical chest expansion 5. diminished breath sound on affected side 6. hyperresonance 7. acute respiratory distress 8. anxiety 9. increased use of accessory muscles

Lab. And Dx. Test:  Chest x-ray xMed. Mgt.  Closed Chest Drainage

Disorders of the Pulmonary Vasculature

Pulmonary Embolism  an occlusion of a portion of the pulmonary blood vessels by an embolus

Virchows triad: triad: 1. Venous stasis 2. Hypercoagulable state 3. Vessel injury Etiology: Etiology: Sites of thrombus formation: 1. Iliofemoral venous system most common 2. Prostatic veins 3. Pelvic veins

D/O of the Pulmonary Vasculature Pulmonary Embolism

Precipitating factors: factors: 1. Exercise 2. Straining on defecation Other sources of emboli: emboli: 1. Tumors 5. Amniotic fluid 2. Air 6. Septic thrombi 3. Fat 7. Vegetations on heart 4. Bone marrow valves

D/O of the Pulmonary Vasculature Pulmonary Embolism

Risk factors: factors: 1. Previous surgery on the pelvis / legs. 2. Trauma of long bones. 3. Immobility 4. Obesity early ambulation leg exercises weight loss

5. DVT Homans sign dont massage calf area - avoid restrictive clothing on legs - prolonged standing / sitting

D/O of the Pulmonary Vasculature Pulmonary Embolism

Pathophysiology
DVT
Emboli single or multiple IVC obstruction o Resistance to blood flow Pulmonary HPN RV strain Pulmonary infarction
lungs, bronchial circulation, pulmonary circulation

RV

Pulmonary arteries

Release of humoral substances

V/Q Mismatch

Vasoconstriction throughout lungs

RV failure
Lungs have 3 sources of O2:

D/O of the Pulmonary Vasculature Pulmonary Embolism

Clinical manifestations: 1. Dyspnea at rest 2. Chest pain similar to MI 3. Pleuritic chest pain when pulmonary infarction occurs 4. Syncope w/ q CO 5. Tachypnea, tachycardia, low grade fever 6. q breath sounds, dullness, cyanosis

D/O of the Pulmonary Vasculature Pulmonary Embolism

Diagnosis: 1. Chest X Ray - usually normal - wedge-shaped density wedge2. ECG - diff. Between MI & PE - sinus tachycardia: most common - peaked P waves 3. ABGs - q PO2 : hypoxia - q PCO2: hyperventilation - q PCO2 opH : mild acute respiratory alkalosis.

D/O of the Pulmonary Vasculature Pulmonary Embolism

Perfusion scanning

- most specific for PE

- blood is labeled w/ radioactive tracer Xenon ventilation scan patient inhales tracer Pulmonary angiography gold standard

D/O of the Pulmonary Vasculature Pulmonary Embolism

Medical Management: Management: 1. Anticoagulants - heparin: DOC - PTT at 2 2.5x the normal value - coumadin: begin 3 days before heparin is stopped to provide a transition - warfarin x 3 6 months 2. O2 inhalation 3. Bed rest

D/O of the Pulmonary Vasculature Pulmonary Embolism

4. Thrombolytic agents - used when occlusion has produced RHF 5. Surgery - inferior vena caval ligation - clipping, plication - umbrella/Greenfield filter - embolectomy

Nursing Management 1. Monitor for hypoxemia and respiratory compromise. 2. Monitor for manifestations of right sided heart failure. 3. Facilitate breathing by elevation of head and administration of supplemental O2 as ordered 4. Elevate leg slowly and avoid severe flexure of hips 5. Administer analgesics for pain (Morphine) 6. Watch out for adverse reaction of anticoagulant

Obstruction of Upper Airway Acute Airway Obstruction 1. Acute laryngeal edema - associated w/ inflammation, injury or anaphylaxis - hoarseness or DOB - ET tube - epinephrine : anaphylaxis - steroids

2. Laryngospasm - anesthetics - repeated intubation - foreign substances - hypocalcemia - Give 100% O2 - Neuromuscular blocker: succinylcholine - emergency cricothyroidotomy or tracheotomy

Epistaxis - irritation, trauma, infection, tumors - systemic diseases (HPN, blood dyscrasias - most common cause: nose picking - most common site: Kiesselbachs plexus - pinch nose for 5 10 mins - lean forward - apply ice - nasal packing w/ antimicrobial ointment x 48 72 hrs

- Avoid petrolatum gauze - posterior plugs for post. Epistaxis (for 5 days) - arterial ligation: internal maxillary or ethmoid artery ligation. - avoid strenuous activity, blowing nose, sneezing, stooping, lifting.

RHINITIS inflammation of nasal cavities Types:  Acute Rhinitis- inflammation of the nasal Rhinitiscavities as a result of a viral infection, most frequently in conjunction with coryza (common cold)  Chronic Rhinitis chronic inflammation of the mucous membrane caused by repeated acute infections, by an allergy, or vasomotor rhinitis

 Allergic Rhinitis nasal inflammation

that results from an antigen-antibody antigenreaction - symptoms appear or worsens at a specific time of year or after exposure to certain substance

Clinical Assessment and Findings

 Acute Rhinitis
1. 2. 3. 4. 5. 6. 7. Mucoid nasal discharge Sneezing Sore throat Headache Malaise Cough Decreased sense of smell and taste

Acute Rhinitis Diagnostics: 1. Patient history and physical findings 2. WBC 3. Throat, nose/nasopharynx culture

 Allergic
1. 2. 3. 4. 5. 6. Nasal congestion Watery thin discharge Sneezing Allergic shiners Swollen eyelids Reddened conjunctiva

Diagnostics:  Patient history  Nasal smear  Radioallergosorbent test (RAST)  Skin test

 Medical Management:  No specific treatment exists for the

common cold. The goals of treatment are to:  relieve symptoms  inhibit spread of infection  reduce the risk of bacterial complication

Chronic Rhinitis 1. Careful medical follow-up is indicated. follow2. When nasal obstruction persists, surgery may be necessary to remove the polyps (polypectomy) or to remove tissue obstruction (septoplasty). 3. If nasal passages are dry, a nasal spray of normal saline can be purchased in a drug store or it can be made by mixing 1 tsp of salt in 1 quart of water. Homemade solution should be made fresh daily. The solution is best administered from a spray bottle with both nostrils open

Allergic Rhinitis

1. Relieve nasal congestion and enhance

Eustachian tube function decongestants (sympathomimetic amines) e.g., Afrin 0.05% (oxymetazolin) and Otrivin 0.1% (xylometazoline).

2. Room humidifiers are helpful in liquefying

nasal secretions. 3. Oral antihistamines can also be helpful. 4. Maintain an allergen-free environment. allergen5. Hyposesnsitization or desensitization (administering the allergen in gradually increasing doses to establish an immunity).

Nursing Management: 1. Obtain additional rest. 2. Drink at least 2 3 L of fluid daily. 3. Medications: Use nasal spray or nose drops 2 to 3 times/day as ordered 4. Prevent further infection:  Blow nose with both nostrils open to prevent infected matter from being forced into Eustachian tube,

 Cover mouth with disposable tissues when coughing and sneezing to prevent droplet nuclei from contaminating the air,  Avoid exposure when possible (e.g., avoid crowds, people with colds, specific allergens).  Disposed used tissues properly.  Wash hands frequently and especially after coughing, sneezing, and so on.  Seek medical attention if the following is present:

a. High fever, severe chest pain, earache b. Symptoms lasting longer than 2 weeks c. Recurrent colds

SINUSITISSINUSITIS- inflammation of the mucous membranes of one or more of the sinuses. A. Acute Sinusitis condition that block the nasal ostia and impede sinus drainage which contribute to stasis of secretions and subsequent infection - complication of the common cold B. Chronic Sinusitis- develops Sinusitiswhen mucosal disease in sinuses produces irreversible epithelial changes.

Plugging of ostia or impaired ciliary action Accumulation of mucus Infection

Predisposing Conditions: 1. Anatomic obstruction of the nasal passages e.g nasal septal deviation 2. Foreign bodies e.g. nasal packing, nasogastric intubation 3. Inflammation of the nasal mucosa e.g. rhinitis 4. Impairment of ciliary function e.g. exposure to tobacco smoke/ air pollution

Clinical Assessment and findings A. Acute 1. Nasal congestion 2. Pressure sensation over paranasal sinus area 3. Throbbing head and face pain 4. Headache exacerbated by bending, stooping or straining 5. Thick yellow/ green nasal discharge 6. Fever and chills 7. Body malaise

B. Chronic 1. Persistent nasal discharge 2. Nasal obstruction 3. Diminished sense of smell 4. Purulent secretions with unpleasant order 5. Halitosis 6. Red, swollen mucosa

Diagnostic Tests: 1. Trans-illumination Trans2. Radiologic Test 3. Increased WBC 4. Drainage Culture

Medical Mgnt 1. Pharmacology  Broad-spectrum antibiotics Broad Oral/topical decongestant  Antihistamines  Saline nose drops/ spray  Mucolytics

Surgery: 1. Antral Irrigation-Also Irrigationknown as sinus lavage. A trocar is inserted through an opening (ostium) in the inner wall of the nose to the affected. Saline solution is then injected to rinse the sinus

2. Functional Endoscopic Sinus Surgery (FESS) an endoscope is inserted through the nasal cavity to the sinus, allowing visualization, removal of diseased tissues, and widening of the sinus opening

3. Caldwell-Luc Procedure Caldwellused to removed diseased tissue from the Maxillary sinus

4. External Sphenoethmoidectomy procedure performed to removed diseased tissues, from the ethmoid or sphenoid sinuses.

Nursing Management: Health Teachings for Non-Surgical Patients Nonwith Sinusitis: 1. Avoid factors that contribute to sinusitis.  Avoid chilling and cold, damp atmospheres  Avoid air conditioning when outside air is warm and moist, if this precipitates sinus irritation.  Avoid smoking and being around smokers  Avoid fatigue

2. Maximize treatment of sinusitis

       Use acetaminophen for pain Apply moist heat over sinus During an acute sinus infection, get additional rest and drink 2 3 L of fluids per day, Take antibiotic for prescribed time period even if symptoms abate. Keep room temperature constant (changes in room temperature aggravate sinusitis) Increase humidity with bedside humidifier and nasal sprays If allergens are a contributing factor, prepare an environmentally controlled bedroom

Postoperative Care for Patients with Sinus Surgery: 1. After general anesthesia, position patient well onto the side to prevent swallowing or aspiration of bloody drainage. 2. Administer cool mist via face tent or collar, or provide humidifier 3. When the patient is awake, remind him or her to expectorate secretions and not swallow them. 4. Encourage Fowlers position when fully awake to promote drainage and decrease edema. 5. Apply ice compresses over nose (or ice bag over maxillary or frontal sinuses) in the early postoperative period.

6. Monitor patient for:

Excessive bleeding from nose (may be evidenced by repeated swallowing).  Decreased visual acuity, especially diplopia, indicating damage to optic nerve or muscles of globe of eye.  Complaints of pain over the involved sinus, which may indicate infection or inadequate drainage.  Fever 7. Give frequent mouth care using a soft toothbrush. If there is an oral incision, mouth care is given before meals to improve appetite and after meals to decrease danger of infection. 

8. Change nasal pad when it is soiled. 9. Encourage liberal fluid itake 10.Teach patient to:
       Avoid blowing nose for at least 48 hours after packing is removed to prevent bleeding. Avoid sneezing; if patient must sneeze, he or she should keep mouth open. Avoid lifting heavy objects. Report signs of infection to surgeon Expect tarry stools from swallowed blood for a few days. Avoid constipating because straining can increase on postoperative site. Take prophylactic antibiotics as prescribed

PHARYNGITISPHARYNGITIS general term for any inflammation of the pharynx  sore throat Etiology: 1. Infection with viruses, bacteria, fungi  most common is Beta hemolytic streptococcus 2. Irritation 3. Neoplasms

Manifestations: 1. Scratchy or mild sore throat 2. Malaise 3. Headache 4. Odynophagia 5. Fever 6. Local tenderness

Diagnostics: 1. Throat culture 2. WBC differential

Medical management: 1. Oral antibiotics. 2. Intramuscular penicillin 3. IV fluids 4. Lozenges containing a mild anesthetic may help relieve the local soreness. 5. For adults, aspirin administered orally as a gargle

Nursing Management: 1. Warm saline gargle. 2. Ice collar may make the person feel more comfortable. 3. Moist inhalations may help relieve the dryness of the throat. 4. Liquids (Fluids of at least 2 3 L/ day; soft bland diet)

5. Oral hygiene to prevent cracking and

drying of the lips, refreshes the mouth 6. Encourage bed rest when febrile. 7. Symptoms of recurrence requiring medical attention: fever, excessive pain, pus, dysphagia. 8. Explain the importance of adherence to the antibiotic regimen

TONSILITIS ETIOLOGY:  Usually streptococcus microorganisms Types 1. Acute Tonsilitis inflammation of any tonsils Manifestations: 1. Throat pain 2. Dysphagia 3. Odynophagia 4. Otalgia 5. Malaise

2. Chronic tonsillitis - recurrent

inflammation of the tonsils Manifestations: 1. Halitosis 2. Pus on tonsils 3. Unpleasant mouth taste Diagnostics: Throat Culture, CBC

Medical and Nursing Management: 1. Encourage rest. 2. Increase oral fluid intake 3. May have warm saline throat irrigation. 4. Antibiotics for streptococcal tonsillitis 5. Acetaminophen (Tylenol) may be given for pain 6. Ice collar may relive discomfort

Laryngitis Inflammation of the larynx Etiology:  Viral/ bacterial infection  Vocal abuse

A. Acute Laryngitis
Manifestations: 1. Hoarseness 2. Throat pain 3. Fever 4. Malaise 5. Dysphagia 6. Laryngeal edema Diagnostics: Laryngoscopy

Treatment: 1. Voice rest 2. Rest in humidified room 3. Warm saline gargle 4. Throat lozenges

B. Chronic Laryngitis-presence of hoarseness Laryngitisover 2 weeks Other causes: 1. Smoking 2. Chronic sinusitis 3. Chronic bronchitis Manifestations: 1. Mild throat pain 2. Tickling sensation 3. Need to clear voice before speaking

Nursing Management: 1. Provide other means of non-verbal noncommunication. 2. Follow prescribed antibiotic regimen 3. Advise patient to quit smoking 4. Referral to support group wanting to quit smoking 5. Increase fluid intake

Thank you very much ..

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