Respiratory Acid Base Disorders

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• Blood Gases
• Respiratory Acidosis
• Management of Respiratory Acidosis
• Respiratory Alkalosis
• Management of Respiratory Alkalosis
• Additional Information 

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Interpreting ABG's

• Evaluate the pH

• Evaluate ventilation

• Evaluate metabolic processes

• Determine the primary and the compensating disorder.

• Evaluate oxygenation

• Normal P02 range is 80 to 100
• Mild hypoxemia is 60 to 80
• Moderate hypoxemia is 40 to 60
• Severe hypoxemia is < 40
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        Pathophysiology                                           Clinical Manifestations
 

Sudden elevated  PaCO2	Increased pulse  Increased respiratory rate  Increased B/P  Mental cloudiness  Feeling of fullness in the head
Severe respiratory acidosis     Leads to  increased intracranial pressure	Papilledema  Dilated conjunctiva blood vessels
Severe respiratory acidosis      Hydrogen concentrations overcome compensatory mechanism and moves into cells causing potassium to move out	Hyperkalemia
Chronic respiratory acidosis	Weakness  Dull headache  Symptoms of underlying disease

When PaCO2 is chronically > 50 mmHg,  hypoxemia becomes the major drive for respiration.  Administer 02 with caution because this could lead to CO2 narcosis.

When compensation has fully occurred (renal retention of bicarbonate) the arterial pH may be within the lower limits of normal.
                                    pH - 7.35
                                    PaCO2 - 42 or 45

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MANAGEMENT OF RESPIRATORY ACIDOSIS

• Goal is to improve ventilation
• Intervention is based on cause
• Bronchodialators to decrease bronchial spasm
• Antibiotics to treat respiratory infection
• Pulmonary hygiene to promote mucous drainage
• Adequate hydration (2 to 3 liters per day) to liquefy secretions
• Oxygen therapy to reduce the work of breathing
• Semi-fowler's position to increase lung expansion


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RESPIRATORY ALKALOSIS (Carbonic Acid Deficit)

    Etiology
        Clinical disorder in which the arterial pH is > 7.45 and the PaCO2 is< 35 or 38.
    Always due to hyperventilation.  Anxiety, aspirin intoxication and excessive ventilation
    causes excess "blowing off" of CO2 and results in a decrease in plasma carbonic acid
    content.  Chronic alkalosis is due to hepatic insufficiency, cerebral tumors or any state
    leads to chronic hypocapnea or increased serum bicarbonate.

   Pathophysiology                                             Clinical Manifestations
 

Vasoconstriction                                     Decrease cerebral blood flow	Lightheadedness  Inability to concentrate  Possible loss of consciousness
Decrease calcium ionization	Numbness and tingling
Potassium ions reentering the cell due to hydrogen ions being pulled out	Hypokalemia

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 MANAGEMENT OF RESPIRATORY ALKALOSIS

• Goal is to improve breathing pattern
• Management is aimed at cause
• Breath slower into paper bag to rebreath carbon dioxide
• Administer sedatives to reduce anxiety and slow respiration rate


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ADDITIONAL INFORMATION

    See the following WEB sites

Evaluation of Blood Gases	http://www.aacb.asn.au/educ/noel/bgas/tsld001.htm
Physical Examination of the Chest	http://www.medinfo.ufl.edu/year1/bcs/clist/chest.html
Respiratory Disease and Asthma Resources	http://www.pharminfo.com/disease/respir/#dis
Basic Lung Sounds	http://www.wices.com/iceslung.htm

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developed by Nancy Torre

last updated 07/26/00

email comments to nancy.torre@jcjc.cc.ms.us