acid base determination

Acid-Base Determination

Spring Semester, 2006

Nursing 2904Carol Isaac MacKusick, MSN, RN, CNN

Arterial Blood Gases

Technique for ABG Sampling– Allen’s Test

Once arterial site is selected, must test for collateral circulation

Allen test used for radial and ulnar arteries Simultaneously compress the radial and ulnar arteries,

ask client to make fist until hand blanches, ask client to open fist, release pressure from ulnar artery, check for return of pinkness to hand

ABG Technique

Indwelling arterial catheter or arterial puncture If arterial puncture

– Painful to client– Same procedure as catheter except for flushing line– HOLD pressure– Complications: Arterial vessel tears, air embolism,

hemorrhage, arterial obstruction, loss of an extremity, and infection

ABG Technique

Arterial line (a-line)– Used to obtain direct and continuous BP

measurements in critically ill clients and to obtain frequent ABG measurements

– Nursing responsibilities for a-line Setting up the equipment Calibrating equipment to ensure accurate readings Assist physician with procedure of inserting a-line

ABG Technique

A-line Nursing Responsibilities– Secure pressure tubing to prevent dislodgement

and possible exsanguination– Put a pressure bag around the flush solution bag

and inflate to about 300 mmHg to prevent blood from backing up into pressure tubing

– Flush solution may or may not have heparin added

ABG Technique

A-line Nursing Responsibilities– Monitor circulation distal to insertion site– Notify physician of any alteration in circulation– Observe for signs of infection– ABGs and blood samples can be drawn without

pain or discomfort to client– Manual baseline blood pressures should be taken

at least once per shift to correlate with arterial readings

A-Line

Works with stopcocks Discard 3-5 cc’s to clear catheter of any flush

system fluid Obtain 1 cc sample in a heparinized syringe Remove air and place on airtight cap Put on ice to ensure accuracy Flush the line

ABG Interpretation

Look at PaO2

– Reflects 3% of total oxygen in blood– Normal range 80-100 mmHg at sea level; lower at

higher elevations– Normal level for infants breathing room air is 40-

70– Older adults, 80 mmHg – 1 mmHg for every year

over the age of 60

ABG Interpretation

PaO2

– If PaO2 more than lowest level for age, it is normal

– Abnormally low PaO2 = hypoxemia

– At any age, PaO2 lower than 40 mmHg represents a life-threatening situation

ABG Interpretation

Look at pH– Normal 7.35-7.45– Below 7.35 = Acidosis– Higher than 7.45 = Alkalosis

ABG Interpretation

Look at PaCO2

– Indicates whether the client can ventilate well enough to rid the body of waste products from metabolism

– Normal 35-45 mmHg– Less than 35, alkalosis– Greater than 45, acidosis

Less than 35, alkalosis.

Causes: – Alveolar

hyperventilation,– hypoxia, – anxiety, – PE, – pregnancy,

– hyperventilation with mechanical ventilator,

– compensatory mechanism to metabolic acidosis,

– head injury,– fever, – fear, – pain

Greater than 45, acidosis:

– alveolar hypoventilation, – respiratory depression, – oversedation, – drug overdose, – head injury, – decreased ventilation, – respiratory muscle fatigue, – neuromuscular disease,

– mechanical ventilation w/ underventilation,

– altered diffusion / ventilation – perfusion mismatch from pulmonary edema,

– severe atelectasis, – pneumonia, severe

bronchospasm. – Chronic acidosis causes

usually COPD

acute causes:

Respiratory Alkalosis

Clinical Presentation– Cardiovascular

Increased myocardial irritability, palpitationsIncreased HRIncreased sensitivity to digitalis

– RespiratoryRapid, shallow breathingChest tightness and palpitations


Clinical presentation– CNS

Dizziness, lightheadedness, anxiety, panic, tetany, convulsions, difficulty concentrating, blurred vision, numbness and tingling in extremities, hyperactive reflexes

– Diagnostic findings High pH, low PaCO2

Hypokalemia, hypocalcemia


Compensation– Kidneys conserve H and excrete HCO3

– Low HCO3 indicates body’s attempt to compensate

– With partial compensation, pH is elevated– With full compensation, pH returns to normal


Priority nursing diagnoses– Sensory perceptual alterations R/T neurological

deficits– Altered thought processes R/T altered cerebral

functioning– Ineffective breathing pattern R/T hyperventilation– Risk for injury R/T weakness, seizures


Management– Treat underlying cause– Rebreathe CO2 using a rebreather mask or paper

bag– Give oxygen if hypoxic– Medicate as needed with antianxiety drugs


Planning and Implementation– Provide support and reassurance– Monitor VS and ABGs– Assist client to breathe slowly– Provide paper bag or rebreather mask– Protect from injury– Administer antianxiety medications and monitor

response

ABG Interpretation

Look at PaCO2

– > 45 is acidosis– Acute ventilatory failure results when PaCO2

exceeds 50 mmHg & pH < 7.30– Chronic ventilatory failure when PaCO2 >50 and

pH > 7.30

Respiratory Acidosis

Clinical presentation– Cardiovascular

Hypotension Delayed cardiac conduction that can lead to heart block,

peaked T waves, prolonged PR intervals, and widened QRS complexes

Peripheral vasodilation with thready, weak pulse Tachycardia Warm, flushed skin


Clinical Presentation– Respiratory

Dyspnea, may have hypoventilation with hypoxia

– CNS Headache, seizures, altered mental status, papilledema,

muscle twitching, decreased LOC, drowsiness -> coma

– Diagnostics Decreased pH, elevated PaCO2

Hyperkalemia


Compensation– Increased rate and depth of respirations to blow

off CO2

– Kidneys eliminate H ions and retain HCO3

– HCO3 levels rise when body attempts to compensate

– With partial compensation, pH remains decreased– With full compensation, pH returns to normal


Priority Nursing Diagnoses– Ineffective breathing pattern R/T hypoventilation– Impaired gas exchange R/T alveolar

hypoventilation– Sensory-perceptual alterations R/T acid-base

alterations– Anxiety R/T breathlessness– Risk for injury R/T decreased LOC– Risk for decreased CO R/T dysrhythmias


Management– Treatment directed at underlying cause and

improving ventilation– Implement pulmonary hygiene measures– Provide adequate fluid intake– Administer supplemental oxygen cautiously in

client with chronic respiratory acidosis– Mechanical ventilation if necessary


Planning and Implementation– Assess respiratory rate and depth– Monitor for complications and response to tx– Assess for tachycardia and irregularities– Assess LOC– Monitor ECG for dysrhythmias– Monitor serum electrolytes and ABGs– Administer oxygen as indicated and ordered


Planning and Implementation– Administer medications as ordered and indicated

Bronchodilators to decrease bronchospasm Antibiotics to treat infections Respiratory agents to decrease viscosity of secretions Anticoagulants and thrombolytics to prevent or treat PE

– Provide good oral hygiene frequently– Maintain safe positioning


Planning and Implementation– Keep a calm, quiet environment– Assess for cyanosis– Orient confused client frequently– Position to facilitate maximum lung expansion– Provide adequate fluid intake

ABG Interpretation

Look at HCO3 level– Reflects kidney function– Normal 22-26 mEq/L– < 22, Metabolic Acidosis– > 26, Metabolic Alkalosis– Causes: Ketoacidosis, lactic acidosis, CKD,

diarrhea, severe infection, fever, trauma, starvation, laxative abuse

Metabolic Acidosis

Clinical presentation– Cardiovascular

Hypotension, dysrhythmias, peripheral vasodilation, cold, clammy skin

– Respiratory Deep, rapid, Kussmaul’s respirations

– CNS Drowsiness, coma, HA, confusion, lethargy, weakness

Metabolic Acidosis

Clinical presentation– GI

N, V, diarrhea, abdominal pain

Diagnostics– pH low, HCO3 low, hyperkalemia– ECG changes related to high potassium levels

Tall, tented T waves

– Increased anion gap calculations– Base excess decreases

Metabolic Acidosis

Compensation– Lungs eliminate CO2

– Kidneys conserve HCO3

– Urine pH less than 6– PaCO2 decreases with compensation

– pH returns to normal with full compensation

Metabolic Acidosis

Priority Nursing Diagnoses– Decreased CO R/T dysrhythmias or FVD– Risk for sensory/perceptual alterations– Risk for injury– Risk for FVD

Metabolic Acidosis

Management– Treat underlying problem– Provide hydration to restore water, nutrients,

electrolytes– Administer IV alkalotic solution (NaHCO3 or

sodium lactate) may be indicated – Mechanical ventilation if necessary

Metabolic Acidosis

Planning and Implementation– Monitor ABGs– Monitor I&O– Measure daily weights– Assess VS, especially respirations– Assess LOC– Assess GI function

Metabolic Acidosis

Planning and Implementation– Monitor ECG for conduction problems– Monitor serum electrolytes– Protect from injury– Administer medications and fluids as needed

ABG Interpretation

Look at HCO3 level– If > 26, metabolic alkalosis– Causes: Fluid loss from UGI tract, diuretic

therapy, severe hypokalemia, alkali administration or steroid therapy, excessive ingestion of bicarbonate-based antacids, binge – purge syndrome

Metabolic Alkalosis

Clinical Presentation– Cardiovascular

Tachycardia, dysrhythmias, hypertension, atrial tachycardia, PVCs

– Respiratory Hypoventilation, respiratory failure

– CNS Dizziness, irritability, nervousness, confusion, tremors,

muscle cramps, hyperreflexia, tetany, paresthesias, seizures

Metabolic Alkalosis

Clinical presentation– GI

Anorexia, N, V, paralytic ileus

Diagnostics– High pH and HCO3, hypokalemia, hypocalcemia,

hyponatremia, hypochloremia– Base excess increases

Metabolic Alkalosis

Compensation– Lungs retain CO2; and kidneys conserve H and

excrete HCO3

– PaCO2 increases with compensation

– Urine pH greater than 6– pH returns to normal with full compensation

Metabolic Alkalosis

Priority Nursing Diagnoses– FVD R/T excessive GI losses– Decreased Cardiac Output R/T FVD and

conduction problems secondary to hypokalemia and alkalosis

– Knowledge deficit R/T appropriate use of K-wasting diuretics and antacids

– Risk for impaired gas exchange– Risk for injury R/T hypotension

Metabolic Alkalosis

Management– Treat underlying cause– Provide sufficient chloride to enhance renal

absorption of Na and excretion of HCO3

– Restore fluid balance

Metabolic Alkalosis

Planning and Implementation– Assess LOC– Assess VS, especially respirations– Administer medication and IV fluids as indicated

NS based IV fluid replacement Potassium supplementation if hypokalemic Histamine-2 receptor antagonists (Tagamet, Zantac) to

reduce production of H ions and loss of H ions from GI drainage

Correct other electrolyte imbalances

Metabolic Alkalosis

Planning and Implementation– Monitor I&O– Monitor response to therapy– Protect from injury– Monitor ECG for conduction abnormalities– Monitor ABGs– Monitor serum electrolytes

ABG Interpretation

Look back at pH– If abnormal, the PaCO2 or HCO3 level will be

abnormal = Uncompensated– Abnormal pH, PaCO2, and HCO3 = Partially

compensated– Normal pH, abnormal PaCO2 and HCO3 =

Compensated Primary disorder is the abnormality that caused the pH

to shift initially. Look to see on which side of 7.4 is pH

ABG Interpretation

O2 saturation– Measurement of amount of oxygen bound to

available hemoglobin– Assessed through ABGs (SaO2) or noninvasively

through pulse oximetry (SpO2)

– Normal 93-97%– Must evaluate the hemoglobin level

ABG Interpretation

O2 Content– Measures total amount of oxygen carried in the

blood, including the amount dissolved in plasma and the amount bound to hemoglobin

– Normal is 20 ml per 100 ml blood

ABG Interpretation

Base Excess or Base Deficit– Non-respiratory contribution to acid-base balance– Normal -2 to +2 mEq/L– Below -2, base deficit, metabolic acidosis– Above +2, base excess, metabolic alkalosis

Mixed Acid-Base Disturbances

Occurs when two or more independent acid-base disorders occur at the same time

Example: Client with metabolic acidosis from acute renal failure may also have a very slow respiratory rate and retain CO2 -> respiratory acidosis

Mixed

Mixed acidosis– pH 7.25, PaCO2 56, PaO2 80, HCO3 15

– Acute pulmonary edema, cardiac arrest

Mixed alkalosis– pH 7.55, PaCO2 26, PaO2 80, HCO3 28

– Postoperative clients with severe hemorrhage, massive transfusions, excessive NG drainage

acid base determination

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