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 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

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

PULMONARY TUBERCULOSIS

Reactivation allows release of cheesy material into bronchi

Bacteria then become airborne resulting in spread of the disease

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

SIGNS AND SYMPTOMS OF TUBERCULOSIS

Fever Cough Night sweats Fatigue Weight loss Extrapulmonary much more common in

those with AIDS

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

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

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

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

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.

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)

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

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

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

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

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

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.

CLINCAL MANIFESTATIONS

s/s r/t underlying disease Severity r/t size of effusion, speed of

formation and underlying lung disease

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.

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

NURSING MANAGEMENT

Implement medical regimen Prepare patient for thoracentesis Label specimens Prepare chest tube and water seal system Monitor drainage Pain management Education

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

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

MANAGEMENT

Treating underlying condition Ventricular dysfunction-- inotropes,

vasodilators, intra-aortic balloon pump May need ventilator assist Morphine one of drugs of choice

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.

PATHOPHYSIOLOGY

Four classifications1. Decreased respiratory drive—Ex. brainstem

injury, sedation2. Dysfunction of the chest wall—Ex.

myasthenia gravis, muscular dystrophy, polio3. Dysfunction of the parenchyma—pleural

effusion, hemothorax, pneumothorax, obstruction

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

CLINCAL MANIFESTATIONS

Restlessness Fatigue Dyspnea Air hunger Tachycardia Increased BP LOC changes Cyanosis diaphoresis

MANAGMENT

Aim is to correct underlying cause Nurse assists in intubation Ongoing respiratory monitoring Prevent complications Communication and support education

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

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

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

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

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

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

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

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

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

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

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

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 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

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

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.

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 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

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 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.

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?

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

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”.

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.

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.

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?