RT 126
CHRONIC BRONCHITIS

 

Chronic Bronchitis is a disease that is diagnosed on the basis of the symptoms: a daily, productive cough for at least 3 consecutive months for 2 years in a row. Most frequently it is the result of tobacco smoke exposure. While our textbooks identify Chronic Bronchitis and Emphysema as distinct disorders, most patients have a combination of both, with very few patients that fit only in one disorder.

CHANGES IN VITAL SIGNS

Vital sign changes are most frequently related to hypoxemia for which the body tries to compensate by increasing cardiac output / perfusion, thus heart rate and blood pressure are usually increased. Respiratory rate, when stable, may show a slow rate with a prolonged expiratory phase, or will increase as a result of hypoxemia, and hypercapnia when in acute failure.

CHANGES IN PHYSICAL APPEARANCE

Obstructive disorders result in the patient being unable to exhale and thus traps air in the distal regions of the lung, so even though they are hyperaerated, they are extremely underventilated! If you take in a deep breath, only exhale a third of the volume, and then try to breath in and out at that level you will get a little idea of how uncomfortable it is to try to breath like that! Therefore chronic bronchitis patients have to work hard to try and get air out past obstruction, while struggling to get a little bit of fresh air in, resulting in signs of increased work of breathing. This would include the fixation of the shoulder girdle by resting their arms on a bed side table, or bracing on the bed-rails - creating a tripod that stabilizes the shoulders and allows the sternocleidomastoid muscles to lift the upper rib cage in an attempt to bring air into lungs that are over distended. Then, when they exhale they will purse-lip breathe - blow out through pursed lips - which helps generate a positive back pressure in the airways that stents the airway open and allows more air to be exhaled before their collapse. Pursed-lip breathing prolongs the expiratory phase.

Air-trapping keeps the chest cage in an expanded condition and results in the barrel-chest appearance.

Signs of right-heart failure are most common in end-stage COPD patients.

CHANGES IN COUGH AND SPUTUM PRODUCTION

Secretion retention is a result of destruction of the normal muco-ciliary escalator. Cough therefore is the primary defense mechanism that a COPD patient has to clear secretions from their lungs. Morning productive coughing (frequently experienced by smokers before they are ever diagnosed with a chronic lung disease) is a result of the lack of normal airway clearance combined with positional changes that cause the secretions to move and trigger the cough reflex. This loss of the normal protective mechanism also predisposes the patient to lung infections as the mucus in the airways has all the ideal nutrients for bacterial growth. Sputum will become thicker, more yellow or green as a result of infection.

CHANGES IN PULMONARY FUNCTION VALUES

The primary dysfunction of hyperinflation results in an increase in the residual volume (air that cannot be exhaled from the lungs even after a forced effort), which results in the overall increase in FRC. Increased residual volume means there is less effective air exhange.

PFT.JPG

Forced expiratory manuevers accentuate the collapse of the airways, therefore the patient will have a very prolonged expiratory phase, not uncommon to exceed 6 seconds. While they may be able to eventually exhale a relatively normal VC - the time parameters of 1, 2 or 3 seconds will show greatly reduced volumes at those times in comparison to a normal person without obstruction. Airway collapse also limits exhaled flow rates so those parameters will also be reduced.

 

PFT1.jpg

 

PFT2.jpg

 

PFT3.jpg

 

PFT4.jpg

 

PFT5.jpg

 

PFT6.jpg

CHANGES IN HEMATOLOGY / ELECTROLYTES

Increases in RBC, hematocrit, and hemoglobin values are common due to chronic hypoxia stimulating RBC production. Chloride ion is excreted to facilitate retention of bicarbonate ion to balance retained CO2 and decreased pH - therefore patients may be hypochloremic.

CHANGES IN OXYGENATION INDICES

Oxygenation Saturation and Content-Based Indices

These values assess the transport and utilization of oxygen at the tissues, and are ways of quantifying whether or not the patient's tissue oxygenation needs are being met.

Most Common Oxygenation–Saturation and Content-Based Indices

Total oxygen delivery

Arterial-venous oxygen content difference

Oxygen consumption

Oxygen extraction ratio

Mixed venous oxygen saturation

Pulmonary shunting

Total Oxygen Delivery

DO2 = QT x (CaO2 x 10)

For example, if a patient has a cardiac output of 4 L/min and a CaO2 of 15 vol%, what is the DO2?

DO2  = QT x (CaO2 x 10)

  = 4 L/min x (15 ml/100 ml x 10)

  = 600 ml O2/min

Normally, about 1000 ml/min

Decreases if the following occur:

Low PaO2

Low SaO2

Low Hb

Low cardiac output (perfusion inadequate to meet tissue metabolic needs)

Increases if the following occur:

Increased PaO2

Increased SaO2

Increased Hb

Increased cardiac output

Arterial-Venous Oxygen Content Difference

*also referred to as the a-vDO2

For example, if a patient's CaO2 is 15 vol% and the CvO2 is 8 vol%, what is the C(a-v)O2?

C(a-v)O2 = CaO2 – CvO2

  = 15 vol% – 8 vol%

  =  7 vol%

          Normally, 5 vol%  

Increases (which means the tissues are pulling off larger amounts of oxygen) may be caused by:

Decreased cardiac output

Exercise

Seizures

Hyperthermia

Decreases (which means the tissues are using less oxygen) may be caused by:

Increased cardiac output

Skeletal relaxation

Peripheral shunting

Cyanide

Hypothermia

Oxygen Consumption

For example, if a patient has a cardiac output of 4 L/min and a C(a-v)O2 of 6 vol%, what is the total amount of oxygen consumed by the tissue cells in 1 minute?

VO2 = QT [C(a-v)O2] x 10

  = 4 L/min x 6 vol% x 10

  = 240 ml O2/min

Normal is 250 ml O2/min

Increases in consumption can occur with:

Seizures

Exercise

Hyperthermia

Body size

Decreases in consumption can occur with:

Skeletal muscle relaxation

Peripheral shunting

Certain poisons (e.g., cyanide)

Hypothermia

Oxygen Extraction Ratio

For example, if a patient's CaO2 is 15 vol% and the CvO2 is 10 vol%, what is O2ER?

  = 15 vol% – 10 vol%

             15 vol%

  = 5 vol%

     15 vol%

  = 0.33

      Normal is 0.25 or, when expressed as a percentage, 25%

Increases:

Decreased cardiac output

Periods of increased O2 consumption

Exercise, seizures, hyperthermia

Anemia

Decreased arterial oxygenation

↓Hb, ↓PaO2

Decreases:

Increased cardiac output

Skeletal muscle relaxation

Peripheral shunting

Certain poisons (e.g., cyanide)

Hypothermia

Increased arterial oxygenation

↑Hb, ↑PaO2

Mixed Venous Oxygen Saturation

Signals changes in the:

C(a-v)O2

VO2

O2ER

    Normally about 75%

Decreases:

Decreased cardiac output

Exercise

Seizures

Hyperthermia

Increases:

Increased cardiac output

Skeletal muscle relaxation

Peripheral shunting

Certain poisons (e.g., cyanide)

Hypothermia

Pulmonary Shunting

 

Qs = CcO2 – CaO2

QT    CcO2 – CvO2

 

CHANGES IN ARTERIAL BLOOD GAS VALUES

MILD TO MODERATE CHRONIC BRONCHITIS

CONDITION: Acute Alveolar Hyperventilation

Acute Alveolar Hyperventilation is ventilation in excess of needs and the blood gas values would show the following:

pH > 7.45

PaCO2 < 35

HCO3 slightly low

 

DISORDER

CAUSE

SIGNS 

TREATMENT 

ACUTE RESPIRATORY ALKALOSIS

 

ANXIETY

SHOCK

SEPSIS

HYPOXEMIA

 

PARESTHESIA

HYPERACTIVE REFLEXES

LIGHT HEADEDNESS

DIZZINESS

 

TREAT CAUSE

REBREATHE CO2

OXYGEN

 

 

We can use the formulas given on the previous page to determine if the following blood gas changes are appropriate for acute alveolar hyperventilation / respiratory alkalosis

Blood Gas Example:

pH    7.53

PaCO 28 mm Hg

HCO3   20 mEq/L

RULE: Each 1 mm Hg ↓ in PaCO2 should give 0.01 ↑ in pH

When the PaCO2 < 40 mmHg the expected pH = 7.40 + (40 mm Hg – measured PaCO2)0.01

Expected pH = 7.40 + (40 – 28)0.01

      = 7.40 + .12

         = 7.52

Expected change matches actual. This indicates that the changes in the blood gas would be primarily due to PaCO2 and therefore would be an acute respiratory or ventilatory disturbance.

RULE: Each 5 mm Hg ↓ in PaCO2 should ↓ HCO3 by 1 mEq

Expected HCO3 = 22 – (12/5)

                           = 22 – 2.4

    = 19.6

Verifying that the changes in bicarb are tied to the changes in PaCO2 and not due to renal compensation by elimination of bicarb. 

SEVERE CHRONIC BRONCHITIS

CONDITION: Chronic Ventilatory Failure

pH  IN NORMAL RANGE BUT ON ACID SIDE OF 7.40 (7.35 - 7.39)

PaCO2 > 45

HCO3 significantly increased

Would be identified as a fully compensated respiratory acidosis

DISORDER

CAUSE

SIGNS 

TREATMENT

CHRONIC RESPIRATORY ACIDOSIS

COPD

PROLONGED EXPIRATION

ACCESSORY MUSCLE USE

NONE

 

We can evaluate the following for compensation by looking at the expected pH in relation to the measured PaCO2

Blood Gas Example

pH    7.38

PaCO2  66 mm Hg

HCO3   35 mEq/L

RULE: Each 1 mm Hg in ↑PaCO2 should give 0.006 ↓ in pH

When the PaCO2 is > 40, the expected pH = 7.40 - (measured PaCO2– 40 mm Hg)0.006

Expected pH = 7.40 - (66 – 40)0.006

         = 7.40 - .156

         = 7.24

This indicates that there is compensation as the pH of 7.38 is not as low as expected.

RULE: Each 10 mm Hg ↑ in PaCO2 should ↑ HCO3 by 1 mEq

Expected HCO3 = 24 + (26/10)

                           = 24 + 2.6

  = 26.6

Indicates that the elevated HCO3 is higher than expected and is the result of renal retention.

ACUTE CONDITIONS SUPERIMPOSED ON CHRONIC VENTILATORY FAILURE

CONDITION:Acute Alveolar Hyperventilation on Chronic Ventilatory Failure

pH > 7.45

PaCO2 > 45

HCO3 significantly increased

Can be confused with partially compensated metabolic alkalosis where the elevated PaCO2 would be related due to hypoventilation, not hyperventilation that has actually caused a much higher initial PaCO2 to be reduced.

Assess oxygenated status – usually have significant hypoxemia (not present with metabolic disturbances)

Blood Gas Example:

pH    7.55

PaCO2  62 mm Hg

HCO3   38 mEq/L

PaO2    51 mm Hg

RULE: Each 1 mm Hg in ↑PaCO2 should give 0.006 ↓ in pH

Expected pH = 7.40 - (measured PaCO2– 40 mm Hg)0.006

Expected pH = 7.40 - (62 – 40)0.006

         = 7.40 - 0.132

         = 7.268

Indicates that measured pH not as low as would be expected based on PaCO2

RULE: Each 10 mm Hg ↑ in PaCO2 should ↑ HCO3 by 1 mEq

Expected HCO3 = 24 + (22/10)

                           = 24 + 2.2

    = 26.2

Indicates additional bicarb retention by the kidneys.

Moderate hypoxemia of 51 mm Hg indicates this is a ventilatory problem. Patient's with chronic ventilatory failure will increase respiratory rate in response to decrease in PaO2. The patient has a chronically elevated CO2 that is higher than the 62 mmHg on the blood gas - but has blown off some of it in an effort to improve oxygenation. The renal system being a slow response system is not able to eliminate the HCO3 that had been retained as compensation, causing the patient's blood pH to swing from less than 7.4 to 7.55.

Another way to differentiate between a ventilatory problem and a partially compensated metabolic alkalosis to to calculate the P(A-a)O2. A wide gradient that would be evident in a patient with acute alveolar hyperventilation superimposed on chronic ventilatory failure, is not normally present in hypoventilation associated with a partially compensated metabolic alkalosis.

Also, look at the clinical presentation of the patient: What is their respiratory rate? What is their work of breathing? In acute alveolar hyperventilation superimposed on chronic failure the respiratory rate should be increased and the patient should be working hard to breathe. In partially compensated metabolic alkalosis the respiratory rate should be decreased.

CONDITION: Acute Ventilatory Failure on Chronic Ventilatory Failure

pH < 7.35 but not as low as would be expected

PaCO2 significantly > 45

HCO3 increased

Blood Gas Example

pH    7.23

PaCO2  107 mm Hg

HCO3   41 mEq/L

PaO  38 mm Hg

RULE: Each 1 mm Hg in ↑PaCO2 should give 0.006 ↓ in pH

Expected pH = 7.40 - (measured PaCO2– 40 mm Hg)0.006

Expected pH = 7.40 - (107 – 40)0.006

         = 7.40 - .402

         = 6.998

 Shows that pH change not as severe as it would be if there was no compensation

RULE: Each 10 mm Hg ↑ in PaCO2 should ↑ HCO3 by 1 mEq

Expected HCO3 = 24 + (67/10)

                           = 24 + 6.7

  = 30.7

 

CHANGES IN CARDIAC INDICES / HEMODYNAMICS

Changes are evident in the parameters that reflect the work of the right heart due to the resistence of blood flow through the pulmonary vascular system. Left heart parameters are within normal ranges. (Note Table 6.3 below)

 

(Des Jardins, Terry. Clinical Manifestations and Assessment of Respiratory Disease, 5th Edition. C.V. Mosby, 112005.).

 

 

TABLE 6-1 Hemodynamic Values Measured Directly

(Des Jardins, Terry. Clinical Manifestations and Assessment of Respiratory Disease, 5th Edition. C.V. Mosby, 112005.).

 

 

TABLE 6-2 Hemodynamic Values Calculated from Direct Hemodynamic Measurements

(Des Jardins, Terry. Clinical Manifestations and Assessment of Respiratory Disease, 5th Edition. C.V. Mosby, 112005.).

 

 

TABLE 6-3 Hemodynamic Changes Commonly Seen in Respiratory Diseases

(Des Jardins, Terry. Clinical Manifestations and Assessment of Respiratory Disease, 5th Edition. C.V. Mosby, 112005.).

 

PROBLEMS AND PROTOCOLS

The primary disorders for patients presenting to the hospital with exacerbation of chronic bronchitis are hypoxemia and excessive bronchial secretions. Therefore the protocols that should be immediately implemented would be the oxygen therapy and bronchopulmonary hygiene protocols - with the type and frequency dependent on the severity of the patient's presentation. The inflammatory response triggered by infection indicates the application of bronchodilators (with anticholinergics, or a combination of beta adrenergic and anticholinergic, often being more effective) and the delivery of an aerosolized anti-inflammatory (corticosteroid).

Infections can result in pneumonia and consolidation - which would indicate the need for hyperinflation protocol implementation.

Identification of Severity

The evidence based guideline from the American College of Chest Physicians is the standard for differentiation between mild, moderate, and severe exacerbations, and selection of relevant treatment.

Patient's are assessed for the diagnostic criteria of:

If one of the diagnostic criteria above is present the patient is evaluated for the presence of the following symptoms, if one is present this is identified as a mild exacerbation, with treatment with inhaled bronchodilators:

If two of the diagnostic criteria above are present this is identified as a moderate exacerbation with treatment with inhaled bronchodilators plus the addition of systemic corticosteroids, oxygen therapy as needed, and non-invasive positive pressure ventilation as needed.

If three of the diagnostic criteria above are present this is identified as severe exacerbation, with the addition of antibiotics to the treatments given for moderate exacerbation.

 

Staging of COPD is also based on pulmonary function as given in Table 11-2

 

TABLE 11-2 Therapy at Each Stage of COPD (GOLD)

(Des Jardins, Terry. Clinical Manifestations and Assessment of Respiratory Disease, 5th Edition. C.V. Mosby, 112005.).

 

Beneficial Therapy


Note that in the management of mild to severe exacerbations of COPD (including Chronic Bronchitis and Emphysema) that chest physiotherapy, and mucolytics are not given as treatment options. This seems contradictory to the bronchopulmonary hygiene protocol indicated by excessive secretions. This does not mean that all bronchopulmonary hygiene treatments should not be used. CPT is very stressful to a patient who is hypoxic and hyperinflated - and is much like trying to pound ketchup out of a small bottle neck - and usually not worth the stress. Flutter valve, increased humidification (both systemic with increased oral intake of fluids, and inhaled with bland aerosol therapy), and supported deep breathing exercises with controlled cough will facilitate secretion clearance. Mucolytics may be ineffective on the type of secretions, can cause airway irritation and bronchospasm, and in general have not been proven effective in controlled studies.