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Disorders of Ventilation University of San Francisco Dr. M. Maag ©2003 Margaret Maag Class 10 Objectives Upon completion of this lesson, the student will be able to • design nursing interventions for patients presenting with atelectasis, pneumonia, TB, COPD, SARS • recognize clinical manifestations of respiratory disease for different age groups. • predict major symptoms seen in patients experiencing respiratory difficulty. • analyze arterial blood gases associated with various respiratory disorders. Respiratory Failure • Dynamics: alveolar hypoventialtion, V/Q disequilibrium, decreased FiO2 & inadequate exchange of gases between alveoli & blood • Results in hypoxia, hypercapnia, and acidosis • Work of breathing becomes difficult, exhaustion occurs, and there is no energy to breathe. • Risk factors: pneumonia, Hantavirus, sepsis, atelectasis, bronchospasms, CHF – atelectasis: areas of the lung where alveoli are collapsed (alveoli are airless & no gas exchange) Respiratory Failure Failure of Oxygenation: Etiology • “Hypoxemia” = reduced PaO2 concentrations – PaO2 < 80 mm Hg (Horne & Derrico, 1999) – Hypoventilation can reduce the PaO2 & PAO2 – Factors leading to hypoventilation are drugs (opiods), neurological disorders (e.g. IICP) & COPD • Ventialtion/ Perfusion Mismatching: V/Q ratio – Perfusion exceeds ventilation at the lung base • 4:5 = 0.8 = normal V/Q – “In respiratory failure, the V/Q mismatching is the most common cause of hypoxemia” (Hartshorn, 1997, p. 325) Respiratory Failure Clinical S & S • Severe dyspnea (difficulty breathing) – > RR & HR – use of accessory muscles of ventilation • Cyanosis: indicative of unoxygenated hemoglobin – check nailbeds & mucous membranes • Clubbing: check fingers and toes • Multi-organ failure leading to death • Tx: O2 & ventilation support See p. 1108 of McCance Pulmonary Embolism Image borrowed from http://www.benlovejoy.com/pulmonary_embolism_main.html Pulmonary Embolism Image borrowed from the online NHS encyclopedia Pulmonary Embolism: “PE” A complication of a venous thromboembolism – d/t immobility or leg injuries – The most common preventable cause of hospital deaths – 60-80% of fatal PE cases are not suspected • S&S – – – – – – Pleuritic chest pain (> with inspiration) Dyspnea: check ABGs tachycardia Dry cough & low grade fever Hemoptysis & syncope Abnormal ECG (up to 85% of PE patients) Pulmonary Embolism: “PE” • A common and challenging diagnosis – Diagnostic procedures: • • • • Presenting symptoms assessed by medical team Pulmonary angiography: ? Accuracy V-P lung scan: not real definitive CT angiography: accurate non-invasive tool – Can diagnose other intrathorasic disease as well • MRI, Echocardiography, CT angiography & venography • Treatment – Anticoagulation: heparin drip then coumadin – Streptokinase – Surgery Chronic Obstructive Pulmonary Disease (COPD) • Refers to 3 diseases: – Chronic bronchitis – Emphysema – Asthma • Causes obstruction of airflow into the lungs Chronic Bronchitis Pathophysiology • Bronchial inflammation with hypertrophy and hypersecretion of the bronchial mucous glands • Pulmonary “fibrosis” (scarring) occurs due to inflammatory response, leading to “stenosis” of airway passages and airway obstruction • Causes: inhalation of chemical or physical irritants – tobacco smoke, smog, occupational hazards – viral or bacterial infections Chronic Bronchitis • Clinical Sx: – productive cough is the earliest symptom – chronic productive cough for 3 months each year for 2 consecutive years (excluding other causes) – > Work of breathing (WOB) to overcome obstruction • > PaCO2 with < PaO2 – stimulus to breathe is low level of oxygen – breathlessness, rhonchi, cyanosis, increased susceptibility to infections – cor pulmonale: right-sided heart failure due to pulmonary hypertension; pulmonary edema occurs – “Blue Bloater:” appearance of arterial blood is poor Chronic Bronchitis • Tx: – – – – – – – Cigarette smoking cessation programs Prophylactic antibiotic treatment Bronchodilators Anti-inflammatory medications Expectorants & hydration O2 therapy Vaccine against pneumococcal pneumonia Emphysema • A nonreversible obstructive disease characterized by the destruction of alveolar walls & connective tissue • Terminal airways collapse during expiration & secretions are retained – < forced expiratory volume (FVE) • Causes: – inhalation of physical or chemical irritants • (almost always cigarette smoke) – genetic: very rare Emphysema • Clinical Sx: – – – – tachypnea caused by hypoxia & hypercapnia barrel chest configuration non-productive cough pursed-lip breathing • use of accesory muscles to aid in exhalation – respiratory acidosis – “Pink Puffers” Emphysema • Tx: – stop smoking and live in clean air – relaxation and energy conservation – breathing techniques to reduce air trapping – bronchodilators, antibiotics, hydration, – chest physiotherapy, – O2 therapy to assist with ADLs • Prognosis: – poor for those who continue to smoke Asthma • Intermittent airway obstruction due to bronchospasm, bronchial edema, and > mucus secretions. • Hyper-responsiveness of the airways after exposure to one or more irritating stimuli. • Immunologic (Allergic, Extrinsic) – usually occurs in children – follows other allergic disorders (e.g.eczema) – IgE levels are elevated • Nonimmunologic (Nonallergic,Intrinsic) – usually does not occur until adulthood – associated with recurrnet upper RTI – IgE levels are not generally elevated Asthma Pathophysiology Episode may be triggered by – physical exertion – change in temperature and humidity – emotional stress: PNS constricts broncioles – Animal dander – Strong fumes • Mast cells degranulate releasing histamine, SRSA, and ECF-A “Status Asthmaticus:” • A life-threatening condition: – prolonged bronchiolar spasm that can’t be reversed with medications – WOB greatly increased O2 demand increases – can’t meet the high O2 demands needed to inspire and expire during prolonged bronchiolar spasm, bronchiolar edema, and thick mucous. – Client is exhausted with effort to breathe • respiratory acidosis • respiratory failure • death can occur Asthma • Clinical S & S: – tachypnea (>RR) – wheezing – coughing at night – hyperventilate – < PaCO2 – >WOB – anxiety – dyspnea • Tx:is based on staging – mild to severe • Prevent exposure to allergens • Avoid cigarette smoke • Inhalation of steroids • Oral use of steroids • Bronchodilators • Relaxation techniques Pneumonia • Inflammation of the respiratory unit tissue caused by a microorganism that is inhaled, circulated, or aspirated • Common bacterial agents: – gram positive: strep pneumonia, mycoplamsa, staph aureas – gram negative: E. coli, proteus, P. aeruginosa • Non-bacterial agents: – pneumocystis carinii, fungi, viruses, Legionella • Clinical Sx: fever, chills,productive or dry cough, malaise, pleural pain, dyspnea, hemoptysis, leukocytosis • Tx: rest, hydration, decongestants, cough suppressants, antibiotics for bacterial, Vitamin C Tuberculosis • A communicable infection of lung tissue – Mycobacterium tuberculosis – Lower respiratory tract infection • Inhalation of droplets: colonizes respiratory bronchioles or alveoli • Risk factors: living in close quarters, immigrants, HIV, malnourished, homeless in shelters • Primary: overt disease occurring within 2 yrs.after infection • Reactivation: disease that occurs later Tuberculosis • Patho: tubercles are formed in the lung • Primary: first TB infection – About 5% or Americans infected with TB develop active clinical disease – A CMI reaction occurs and sensitized T cells develop • Positive skin test indicates a CMI reaction and previous exposure to the bacillus – Sputum culture will reveal the bacillus of an active tuberculosis – Chest x-ray demonstrates current or previous tubercle formation Tuberculosis • Clinical manifestations of active disease: – fevers (afternoon), malaise, night sweats, anorexia, productive purulent cough with chest pain • Prevention: education & screening to < risk of infection and transmission • Tx: of active disease – INH, Rifampin, and other non-resistant antibiotics Lung Cancer • Defined as a malignant neoplasm arising in the epithelial lining of the respiratory tract or any lung tissue • Four types: – squamous cell: 30 % bronchogenic cancers – adenocarcinoma: 35-40% of all bronchogenic cancers • arises from the glands of the lungs – small cell (“oat cell”): 25% of all lung cancers – large-cell undifferentiated: 10-15% of all lung cancers • rapid metastasis; comfort measures • Local tumor growth is invasive & erodes blood vessels and adjacent structures Lung Cancer The most common fatal malignancy in the US for both males and females (2000) 156,900 people will die d/t this disease (2000) many are minorities: black men have > incidence • Primary risk factor is tobacco – Women have a higher risk of lung cancer from smoking then men. Why? – Air pollution, asbestos, chemicals, and dusts • Clinical Sx: persistent cough, hemoptysis, recurring lower respiratory tract infection, respiratory failure Pulmonary edema • Third spacing in the interstitial spaces around the alveoli • Conditions associated with pulmonary edema – Cardiogenic • MI, shock related to cardiac failure, hypertension – Noncardiogenic • septic shock, aspiration pneumonia, fat emboli, burns • Gas exchange is compromised – hypoxemia occurs when alveolar-capillary membrane is impaired • Clinical Sx: > WOB, dyspnea, pink frothy sputum, chest x-ray shows “whiteout” ARDS • A widespread breakdown of the alveolar and/or capillary membranes • Patho: injury to lung results in hypoperfusion which damages the alveolar epithelium – > mediators of inflammatory response causes injury – > Permeability of alveolar capillary membrane – > edema leads to a < production of surfactant – A major cause of severe respiratory failure in clients with previously healthy lungs • Risk factors: – Elderly and severe infections: > mortality rate – occurs after major pulmonary,cardiovascular, or systemic insult ARDS • Clinical Sx: – – – – – Rapid, shallow breathing Respiratory alkalosis Dyspnea Refractory hypoxemia Diffuse alveolar infiltrates • Tx: prevention of trauma to body – diuretics, digoxin, anti-inflammatory medications, O2 & ventilator therapy SARS Epidemic • Etiology – Thought to be caused by a coronavirus – animal host: masked palm civet, raccoon dog, ferret badger – First known case in Guangdong, China 11/02 • High percentage of victims were caterers in Southern China – 22 countries, but China, Hong Kong, Canada reports the most cases • WHO reported 8,200 cases as of May 30, 2003 – 700 deaths • http://www.nytimes.com/pages/multimedia/index.html • http://www.cdc.gov/ncidod/sars/qa/illness.htm - 2 Developmental differences • CHILDREN: < surfactant until 28 weeks gestation • lung tissue develops until ~ 8 years old • airways are small • muscles underdeveloped • > exposure • < immune system • nasal breathers until 2 months • ELDERLY: < muscle mass makes > WOB • < immunity • > risk for pneumonia • > malnourisment • pathology may place patient at risk for aspiration References • Corwin, E.J.(2000).Handbook of pathophysiology. Baltimore: Lippincott. • Hansen, M. (1998). Pathophysiology: Foundations of disease and clinical intervention. Philadelphia: Saunders. • Hartshorn, J. C., Sole, M. L., & Lamborn, M. L. (1997).Introduction to critical care nursing. Philadelphia: Saunders. • Horne, C., & Derrico, D. (1999). Mastering ABGs. The art of arterial blood gas measurement. American Journal of Nursing, 8:26-32. • http://www.pathoplus.com • Huether, S. E., & McCance, K. L. (2002). Pathophysiology. St. Louis: Mosby. • Ryu, J.H., Swensen, J., Olson, EJ, & Pellikka, A. (2001). Diagnosis of pulmonary embolism with use of computed tomographic angiography. Mayo Clin Proc.,76, 59-65. Acid – Base Pure Water: H H O 55 M + H H O H -7 + 1 x 10 M O H 1 x 10-7 M pH = log 1 + = -log[H+] [H ] pH = 7 [neutral] Highly Acidic Highly Basic 1 M pH = 0 1 x 10-14 M pH = 14 1 x 10-14 M 1M Buffer Systems [Base] pH = pK + log [Acid] • pH dominated by pK • Small changes in the concentration ratio of the acid and the base have a small effect on pH • Biological systems are typically highly buffered around neutral pH Carbonic Acid - Bicarbonate CO2 + H2O CO32- H2CO3 H+ + HCO32 H+ + pK = 6.1 pK = 10.2 [HCO3-] [Base] pH = pK + log [Acid] pH = 7.4 = 6.1 + log pH = 6.1 + log 24 mEq/L 0.03 x PCO2 [H2CO3] = 6.1 + 1.3 Partial Gas Pressures Air (at sea level) Blood (Humans) Total: 760 mmHg pO2 (21%) 160 mmHg 80 mmHg pCO2 (<1%) < 7 mmHg 40 mmHg System greatly favors absorption of oxygen and elimination of carbon dioxide Arterial Blood Gas Interpretation • ABGs reflect oxygenation, adequacy of gas exchange in the lungs, and acid-base balance – PaO2: partial pressure of oxygen dissolved in arterial blood – SaO2 reflects oxygen saturation of hemoglobin • Oxygen is carried from alveoli into the plasma • ~ 3% is dissolved in plasma • 97% attached to Hgb • PaO2: 80-100 mm Hg at sea level Arterial Blood Gas Interpretation • • • • PaO2 < 80 mm Hg = hypoxemia PaO2 < 60 mm Hg may be seen in COPD PaO2 < 40 mm Hg is life threatening S & S of hypoxemia: pallor, dyspnea, use of accessory muscles, anxiety, tachypnea • Hypoxia is decreased oxygen at the tissue level – SaO2: amount of oxygen bound to Hgb • normal saturation is defined as 93 - 100% Arterial Blood Gas Interpretation • pH: negative log of H+ concentration • In blood: –Normal range: 7.35 - 7.45 –Acidosis = pH less than 7.35 –Alkalosis = pH greater than 7.45 –A pH < 7.0 or > 7.8 can cause death Arterial Blood Gas Interpretation • PaCO2: partial pressure of carbon dioxide dissolved in the arterial plasma – normal: 35 - 45 mm Hg – is regulated in the lungs – A primary respiratory problem is when PaCO2 is: – > 45 mm Hg = respiratory acidosis – < 35 mm Hg = respiratory alkalosis – HCO3 is normal (22 - 26 mEq/L) Arterial Blood Gas Interpretation • HCO3 (bicarbonate) normal is: 22 -26 mEq/L • A primary metabolic or renal disorder is when the HCO3 is less than 22 (acidosis) or greater than 26 (alkalosis) – PaCo2 is normal Arterial Blood Gas Interpretation • Compensation: – body attempts to recover from primary problem and return to homeostasis – Primary metabolic acidosis can cause the patient to breathe faster to compensate (blow off CO2) by creating a respiratory alkalosis state – This would be labeled as: Metabolic acidosis with a compensatory respiratory alkalosis – pH 7.30; PaCO2 28; & HCO3 15 • Are PaCo2 & HCO3 below normal? Yes, compensation Metabolic Acidosis • Risk factors: >ingestion of acids or < production of HCO3 • Etiology: lactic acidosis, ketoacidosis, uremic acidosis • Patho:compensatory hyperventilation – hyperkalemia: shift of acid to ICF – <pH, <HCO3, PaCo2 normal; or low if compensation is occurring – cardiac dysrhythmias & CNS dysfunction – headache, diarrhea, tremors Metabolic Alkalosis • Risk factors: hypovolemia, excess aldosterone, iatrogenic base administration • Etiology: acid loss or base gain – renal excretion of HCO3 will fix the problem – prolonged vomiting (loss of HCL) • Patho: respiratory compensation is limited – hypokalemia: Loop diuretics? NGT? Diarrhea? cardiac dysrhythmias; seizures; confusion; muscle twitching, agitation – > pH; >HCO3; normal PaCo2 or elevated if compensation occurs Respiratory Acidosis • Risk factors: excess of acid in body fluids • Etiology: due to hypoventialtion; COPD; Cystic Fibrosis; airway obstruction; spinal cord injury; CVA; depressant drugs; inadequate mechanical ventilation • Patho: hypercapnia; CO2 diffuses easily across biological membranes • Clinical: <pH; >PaCo2; HCO3 is normal or > in renal compensation – vasodilatation; cardiac arrhythmias, tachycardia, somnolence, decreased ventilation Respiratory Alkalosis • Risk factors: relative excess of base in body fluids secondary to > ventilatory elimination of CO2; pneumonia; ARDS; shock; severe anemia • Etiology: hypoxemia (<PaO2) causing rate & depth of ventilation to increase in an attempt to raise CO2 • Patho: buffer response is to shift acid from ICF to the blood by moving HCO3 into the cells in exchange of chloride – >pH; <PaC02; HCO3 normal or low due to compensation – nausea, vomiting, tingling of fingers