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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