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Patient’s with problems of gas exchange Part two. By Linda Self. Pulmonary tuberculosis. Infectious disease affecting lung parenchyma Can be extrapulmonary as well Primary causative pathogen is Mycobacterium tuberculosis Sensitive to heat and ultraviolet light

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Patient s with problems of gas exchange part two l.jpg

Patient’s with problems of gas exchangePart two

By Linda Self


Pulmonary tuberculosis l.jpg

Pulmonary tuberculosis

  • Infectious disease affecting lung parenchyma

  • Can be extrapulmonary as well

  • Primary causative pathogen is Mycobacterium tuberculosis

  • Sensitive to heat and ultraviolet light

  • Estimated to affect one third of the world’s population

  • Cause of death in 11% of those with AIDS

  • Anti-TB drugs developed in 1952

  • Occurrence gradually decreased until 1985


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Pulmonary tuberculosis

  • Spreads by airborne transmission including talking, coughing, sneezing, laughing or singing

  • Pathophysiology—bacteria >>airways>>alveoli>>

    Immune response>>tissue reaction results in exudate>>bronchopneumonia 2-10 weeks after exposure

  • Granulomas contain live and dead bacilli, are surrounded by macrophages>>protective wall, central portion is called Ghon tubercle

  • Ghon tubercle contains cheesy mass, may scar, bacteria dormant until appropriate conditions


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Pulmonary tuberculosis

  • Reactivation allows release of cheesy material into bronchi

  • Bacteria then become airborne resulting in spread of the disease


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Risk factors for tuberculosis

  • Close contact w/someone with TB—duration, proximity, degree of ventilation

  • Immunocompromise

  • Substance abuse

  • Indigent

  • Immigration from countries with high prevalence—SE Asia, Africa, Latin American, Caribbean

  • Institutionalization

  • Living in overcrowded, substandard housing

  • Health care workers performing high risk activities


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Signs and symptoms of tuberculosis

  • Fever

  • Cough

  • Night sweats

  • Fatigue

  • Weight loss

  • Extrapulmonary much more common in those with AIDS


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Assessment and diagnosis

  • Mantoux test with PPD—read 48-72 h, assess erythema and induration

  • 5mm significant in those at risk (known exposure and or positive chest xray) or are HIV positive

  • 10mm significant in those with normal immunity

  • BCG effective in 76% who receive it


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QuantiFERON-TB gold test

  • 2005 FDA approved Gold test

  • Is enzyme linked immunosorbent assay (ELISA) that detect release of interferon-gamma by WBCs when infected blood is incubated with specific peptides

  • Available in 24h

  • Not affected by prior BCG

  • Still not widely used


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classification

  • Class 0—no exposure

  • Class 1—exposure, no infection

  • Class 2—latent infection; no disease (positive PPD but no evidence of active TB

  • Class 3—disease; clinically active

  • Class 4—disease; not clinically active

  • Class 5—suspected disease; diagnosis pending


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TB and gerontologic considerations

  • May be atypical in elderly

  • May exhibit unusual behavior and altered mental status

  • May have fever, anorexia and weight loss

  • May have delayed or no reaction to tuberculin skin test


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Medical management

  • Treated with chemotherapeutic agents for 6-12 months

  • Resistance increasing. May be primary, secondary, or multidrug resistant.

  • Primary—resistance to one of first line drugs in those who have not had prior treatment

  • Secondary—resistance to one or more anti-TB drugs in patients undergoing tx

  • Multidrug resistance—resistance to two agents, INH and rifampin.


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First-Line antituberculosis medications

  • INH—B6, check AST and ALT

  • Rifadin (rifampin)—check AST and ALT, orange secretions

  • Mycobutin (rifabutin)—avoid protease inhibitors, check liver enzymes, plts

  • Pyrazinamide—monitor uric acid, AST, ALT

  • Myambutol (ethambutol)—optic neuritis, caution w/renal disease.

  • Rifamate (combination INH and rifampin)


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Treatment guidelines

  • Two parts—initial tx phase then a continuation tx phase

  • Initial phase consists of INH, rifampin, pyrazinamide, and ethambutol, usually for 8 weeks

  • Then INH and either rifampin or rifapentine for four months

  • Seven month period of tx for those with cavitary disease, those with +sputum after two months of tx, see test

  • Considered non-infectious after 2-3 weeks of tx

  • Total number of doses of chemotherapy more accurate than actual duration of treatment


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Treatment Guidelines

  • INH should be considered for those at risk for significant disease

  • Household members of patients with active disease

  • Pt’s with HIV infection who have PPD with 5 mm induration or >

  • Patients with fibrotic lesions indicative of old TB and a PPD reaction w/5mm induration or more

  • Skin test converters

  • Users of IV drugs w/ PPD 10mm or >, foreign born from high risk country, institutionalized, high-risk, medically underserved


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Side effects of medication therapy

  • Take medication on empty stomach or 1h before meals

  • On INH, avoid foods with tyramine and histamine (tuna, aged cheese, red wine, soy sauce, yeast extracts)—SE include: HA, hypotension, palpitations, diaphoresis, lightheadedness

  • Significant drug interations with rifampin


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Spread of tuberculosis

  • Dissemination to non-pulmonary sites is called miliary TB

  • Usually result of reactivation of dormant infection in the lung or elsewhere

  • Can affect kidneys, liver, meninges, spleen, other

  • Can occur rapidly or slowly progressive

  • Nurse monitors fever, cognition, renal and liver function, cough and dyspnea

  • Tx same as for pulmonary TB


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Pleural effusion

  • Is a collection of fluid in the pleural space

  • Usually develops secondary to other diseases

  • May be complication of heart failure, TB, pneumonia, pulmonary infections, CT disease, nephrotic syndrome, neoplastic tumors

  • May be r/t bronchogenic cancer


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Pleural effusion

  • Fluid accumulates in pleural space. Normal amount is 5-15 ml.

  • Can be a transudate—filtrate of plasma that moves across capillary walls. R/T factors affecting formation and reabsorption of pleural fluid. Indicates no pleural disease. Often heart failure.

  • Exudate—extravasation of fluid. Usually results from inflammation by bacterial products or tumors.


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Clincal manifestations

  • s/s r/t underlying disease

  • Severity r/t size of effusion, speed of formation and underlying lung disease


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Assessment and diagnostic findings

  • Decreased breath sounds and fremitus

  • Dull with percussion

  • Chest xray, CT and thoracentesis reveal fluid

  • Patient lies on affected side, can see air-fluid levels on chest xray

  • Pleural fluid –culture, gram stain, acid-fast, RBCs and WBCs, chemistry, cytologic analysis and pH.


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Medical management

  • Find cause

  • Prevent reaccumulation

  • Relieve s/s

  • Thoracentesis—may be with ultrasound guidance

  • May have chemical pleurodesis to prevent reaccumulation. Instill talc into chest tube, clamp for 60-90 minutes.

  • Malignant pleural effusions-small catheter, surgical pleurectomy, insertion of pleuroperitoneal shunt


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Nursing management

  • Implement medical regimen

  • Prepare patient for thoracentesis

  • Label specimens

  • Prepare chest tube and water seal system

  • Monitor drainage

  • Pain management

  • Education


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Pulmonary edema

  • Abnormal accumulation of fluid in lung tissue, alveolar space or both

  • Pathophysiology—2ndary increased microvascular pressure from abnormal cardiac function

  • Backup of blood into pulmonary vasculature from inadequate left ventricular function; increased microvasc. Pressure and fluid leaks into interstitium and alveoli

  • Other causes—hypervolemia, post-pneumonectomy, or following re-expansion of lung after large pleural effusion evacuated


Clinical manifestations l.jpg

Clinical manifestations

  • Increasing respiratory distress—central cyanosis,dyspnea, air hunger

  • Anxiety and agitation

  • Frothy, blood tinged sputum

  • LOC changes

  • Crackles in lungs

  • Chest xray reveals increased interstitial markings

  • Pulse oximetry falls

  • ABG reveals hypoxemia


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Management

  • Treating underlying condition

  • Ventricular dysfunction-- inotropes, vasodilators, intra-aortic balloon pump

  • May need ventilator assist

  • Morphine one of drugs of choice


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Acute respiratory failure

  • Results when supply of oxygen cannot keep up with rate of oxygen consumption and carbon dioxide production at cellular level

  • Defined as decrease of arteriolar oxygen tension less than 50 mm Hg and an increase in arteriolar carbon dioxide > 50 mm Hg and pH < 7.35

  • Can have co-existent acute and chronic respiratory failure—chronic being COPD or neuromuscular diseases then superimposed heart failure, resp. infection, etc.


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Pathophysiology

  • Four classifications

  • Decreased respiratory drive—Ex. brainstem injury, sedation

  • Dysfunction of the chest wall—Ex. myasthenia gravis, muscular dystrophy, polio

  • Dysfunction of the parenchyma—pleural effusion, hemothorax, pneumothorax, obstruction

  • Other—Ex. Post-op combination of anesthesia, sedatives, analgesics, pain may severely depress respirations


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Clincal manifestations

  • Restlessness

  • Fatigue

  • Dyspnea

  • Air hunger

  • Tachycardia

  • Increased BP

  • LOC changes

  • Cyanosis

  • diaphoresis


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managment

  • Aim is to correct underlying cause

  • Nurse assists in intubation

  • Ongoing respiratory monitoring

  • Prevent complications

  • Communication and support

  • education


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Acute respiratory distress syndrome

  • Sudden and progressive pulmonary edema, increasing bilateral infiltrates, hypoxemia refractory to oxygen supplementation and reduced lung compliance

  • S/S occur in absence of left-sided heart failure

  • Most often require mechanical ventilation

  • Multicausality

  • Mortality rate is 50-60%

  • Major cause of death is nonpulmonary multiple system organ failure, possibly w/sepsis


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Etiologic factors r/t ARDS

  • Aspiration

  • Drug ingestion and overdose

  • Massive transfusions, cardiopulmonary bypass, DIC

  • Prolonged inhalation of high %O2, smoke or corrosives

  • Metabolic disorders—e.g. pancreatitis

  • Shock

  • Trauma

  • Major surgery

  • Fat or air embolism

  • Systemic sepsis

  • Localized infection


Pathophysiology32 l.jpg

Pathophysiology

  • Secondary to an inflammatory trigger, release of cellular and chemical mediators>>>injury to alveolar capillary membrane

  • Leads to leakage of fluid into alveolar interstitium causing pulmonary edema, damage to pneumocytes, microatelectasis

  • V/Q mismatch—alveolar collapse r/t inflammatory infiltrate and surfactant dysfunction

  • Fibrosing alveolitis, “stiff lungs”, creates shunting

  • Severe hypoxemia ensues


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Clinical manifestations

  • Rapid onset of dyspnea that usually occurs 12-48 hours after initiating event

  • Arterial hypoxemia that does not respond to O2

  • Chest xray reveals bilateral infiltrates resembling cardiogenic pulmonary edema


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Assessment and diagnostic findings

  • Presents with intercostal retractions and crackles

  • Based on criteria:

  • History of systemic or pulmonary risk factors

  • Acute onset of respiratory distress

  • Bilateral pulmonary infiltrates

  • Absence of left heart failure


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Medical management

  • ID underlying cause

  • Intubation

  • Ventilator support

  • Circulatory support

  • Nutritional support

  • PEEP—improves oxygenation by preventing alveolar collapse; use allows lower FiO2 (sometimes)

  • With peep, use low tidal volume

  • Hemodynamic monitoring


Management of the patient with ards l.jpg

Management of the patient with ards

  • Many therapies under investigation including: neutrophil inhibitors, pulmonary specific vasodilators, surfactant replacement therapy, antisepsis agents (Xigris), antioxidant therapy, steroids

  • Nutritional support ensuring caloric intake of 35-45 kcal/kg per day


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Nursing management

  • Implementing medical plan of care

  • May perform prone positioning

  • Closely monitor for deteriorating status

  • Rest

  • Treat anxiety

  • Sedatives

  • Neuromuscular blocking agents such as Pavulon, Norcuron (vecuronium), Tracrium (atracurium), and Zemuron (rocuronium)---requires continuous close monitoring

  • Eye care


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Pulmonary embolism

  • Obstruction of the pulmonary artery or one of its branches by a thrombus

  • Often associated with trauma, major surgery, pregnancy, heart failure, age greater than 50, hypercoagulable states, prolonged immobility


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Risk factors for pulmonary embolus

  • Venous stasis—prolonged immobilization, prolonged periods of sitting, varicose veins, spinal cord injury

  • Hypercoagulability-injury, tumor (pancreatic, gastrointestinal, genitourinary, breast, lung), increased platelet count (splenectomy, polycythemia)

  • Certain disease states—heart disease, trauma, postop/postpartum, diabetes mellitus, COPD

  • Other—obesity, pregnancy, oral contraceptive use, constrictive clothing, hx of DVT or PE


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Pathophysiology

  • Caused by blood clot; other emboli such as air, fat, amniotic fluid, septic

  • Often originate in long veins or pelvis

  • Also may originate in atria

  • With occlusion, substances are released from clot resulting in constriction of regional blood vessels and bronchioles>>>results in increased pulmonary vascular resistance

  • This in turn increases work load of right heart>>>can result in right heart failure, decrease in systemic blood pressure and development of shock


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Clinical manifestations

  • s/s dependent on size of thrombus

  • Dyspnea

  • Tachypnea

  • Chest pain possibly imitating angina or MI

  • Anxiety, fever, tachycardia, apprehension, cough, diaphoresis, hemoptysis and syncope


Assessment and diagnostic findings42 l.jpg

Assessment and diagnostic findings

  • Varied symptoms depending on size of thrombus and area(s) involved

  • Chest xray (excludes other causes)

  • ECG (T wave changes may be seen)

  • peripheral vascular studies, ABGs, V/Q scans

  • Spiral CT

  • D-dimer

  • Pulmonary angiogram—best method of diagnosis but may not be feasible


Prevention l.jpg

Prevention

  • Leg exercises

  • Early ambulation

  • Elastic stockings/compression stockings

  • Anticoagulants—low dose heparin before surgery but not in those undergoing major orthopedic surgery, radical prostatectomy, surgery on the eye or brain. May use low molecular wt. heparin


Medical and surgical management l.jpg

Medical and surgical management

  • improve respiratory status—oxygen, other adjuncts

  • Anticoagulation—heparin, maintaining APTT 1.5-2 times normal level; coumadin to maintain INR 2.0-2.5. Refludan (lepirudin) direct thrombin inhibitors for those unable to take heparin

  • Thrombolytic therapy--

  • Surgical intervention—surgical embolectomy, patient will be placed on bypass machine, high intraoperative mortality rate


Surgical management cont l.jpg

Surgical management cont.

  • Transvenous catheter embolectomy using a vacuum-cupped catheter

  • Pulverizing catheters in conjunction with inferior vena cava filters

  • Transvenous filters—Greenfield or umbrella. Placed in inferior vena cava. Anticoagulation continued.


Nursing management46 l.jpg

Nursing Management

  • ID risk factors

  • Prevent thrombus formation by ambulating patients, turning, applying pneumatic stockings, avoiding prolonged sitting, being vigilant about central venous catheter removal

  • Perform thorough history

  • Frequent physical assessment

  • Monitoring thrombolytic and anticoagulant tx

  • Managing pain

  • teaching


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Case studies #1

  • Mr. Embry is a 63 yo male who underwent colon resection for polyps three days ago. Today he c/o SOB, BP dropped to 60/40 and spiked a fever of 101.8. Patient became confused and agitated. ABGs 7.3—46—22—70. He is emergently intubated and taken to the ICU.

  • In ICU patient is placed on ventilator with following settings: fiO2 90%, SIMV 6 TV 800ml. Patient is given fluid bolus of 500ml. Started on dopamine at 3-5mcg/kg/min. Started on Vancomycin empirically and Swan-Ganz catheter is inserted. His PCWP is 12.


Case study 1 l.jpg

Case study 1

  • Following day patient has BP of 135/70 on dopamine drip of 7mcg. Has been started on TPN and is receiving MS for comfort. ABGs are as follows: 7.35—46.1—HCO3 25—pO2 55. Patient’s FiO2 is increased from 90 to 100%, tidal volume is 800mL, SIMV is now 10. PEEP of 5 cm of H2O is added. Two hours after vent settings ABGs are: 7.42—46.2—28.9—75 .

  • Now fifth postop day, peep is increased to 10 cm h20. ABGs are 7.43—46.2—30.5—86.8. Patient condition continues to improve. Gradually patient is weaned from ventilator. Ten days postop, patient is extubated and placed on nasal cannula.


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Case Study 1

  • What is the patient’s condition?

  • What was the precipitating insult?

  • How is the diagnosis made?

  • What are some medical complications associated with this patient’s diagnosis.

  • What lab findings are diagnostic?

  • What radiologic findings will be seen?

  • What is the principal treatment.

  • Name some pharmacologic therapies.

  • Why might hemodynamic monitoring be indicated?


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Case Study 2

  • Sandra Brown is a 35 year female who presents for an elective cholecystectomy. She is married, has two children. Is on no medications except OrthoTricyclen. She has a 10 pack year history of smoking.

  • Her preop data include: BP 140/80, HR 88, RR 22, Temp 97.9, Hgb 15 g/dl, Hct 39%, RBCs 5.1, WBCs 6000, PT 13.2 sec, PTT 35 sec., normal ECG, Cxray and UA


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Case Study 2

  • Mrs. Brown tolerated the surgery w/o complications and was admitted to the step-down unit. VSS. NG in place. Demerol and Vistaril are given IM q3-4h prn for pain. Encouraged to get OOB and sit in chair but tolerates only for 15 min.

  • Postop Day 2—VSS but with low grade temp of 100. NG out. Started on clear liquids. Labs wnl except H&H of 10.8 and 35%. When encouraged to get OOB, patient refuses as “hurts too much”.


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Case Study cont.

  • Postop Day 3—patient becomes restless and apprehensive. C/o SOB, chest pain that worsens with inspiration and right calf pain. Has crackles in LLL, labored respirations and diaphoresis. Right calf is war, tender and erythematous. BP is now 160/90, HR 124, RR 36 bpm, Temp 100.1.

  • Placed on O2 at 4L, MD called, stat ABGs obtained, 12 lead ECG and chest xray obtained.

  • ABGs are 7.52—27—pO2 is 78. Cxray reveals bibasilar atelectasis, ECG reveals Stach.


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Case study 2

  • Heparin bolus of 10,000 U is administered. VQ scan revealed perfusion defects of left lung. Patient is transferred to ICU.

    What is your diagnosis?

    Next day respiratory status worsens requiring intubation. Swan-Ganz catheter is inserted.


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Case Study 2

  • What are risk factors for Mrs. Brown?

  • What diagnostic tests may be used in the diagnosis of PE?

  • What are some treatments for treating this condition?

  • How can the nurse prevent this condition?


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