ARTERIAL BLOOD GAS LECTURE

1. Normal ABG values:

A. pH: 7.35-7.45B. PaCO2: 35-45C. PaO2: 80-100 mgD. HCO3: 22-26E. O2 Saturation: 95-100%F. Base excess or deficit: + or – 3 mEq/LG. Anion Gap: < 12 mEq

2. pH: Must be maintained between a very narrow range. This is done by increasing/decreasing acids and bases as needed.

Decreased pH: acidosis

Increased pH: alkalosis

a. Acids: are molecules that can release hydrogen ions. There are two groups of acids:

1. Carbonic acid (H2CO3): the most important acid in the body and is equal to CO2. It is a weak acid that leaves the body through respirations. Increased RR = decreased CO2. Decreased RR = increased CO2.

2. Noncarbonic/fixed/inorganic acids: are not eliminated by the lungs but are buffered by body proteins or extracellular buffers such as bicarb (HCO3). They are then excreted by the kidneys. Examples include:

a. HCL: Hydrochloric acid: Strong acidb. H2PO4: Phosphoric acid: weakc. Sulfuric acidd. Lactic acid: formed by the incomplete oxidation of

glucosee. Ketoacids: formed by the incomplete oxidation of fats

b. Bases: are molecules that can accept or combine with H+ ions. The most important base is HCO3 (Bicarb).

1. HCO3: weak2. NH3: ammonia: weak3. Hydroxides: strong. This is not found in the body unless

there are many antacids consumed.

c. How we maintain acid-base balance:

1. Respirations: Blow off CO2 to remove acids. Works within 1-2 minutes of decrease in pH.

2. Proteins: The largest buffer system in the body. In acidosis, calcium will jump off albumin (increasing serum Ca) and allow H+ to bind with albumin to correct (Increase) the pH.

3. Bicarbonate: can combine with an acid to make it weaker or with a base to make it stronger.

4. Potassium-Hydrogen exchange: In acidosis, hydrogen will move into the cell and potassium will move out of the cell causing an increase in pH and potassium. In alkalosis: hydrogen will move out of the cell and potassium into the cell thus decreasing the pH and potassium levels.

5. Renal Control mechanisms: The kidneys will excrete acid or alkaline urine depending on what the body needs to rid itself of. It has several mechanisms to perform this task:

a. Acidosis: H+ will be excreted and HCO3 will be held

onto. (proximal tubule)

b. Phosphate buffer system. Excessive acidosis will result in PO4 (Phosphate) combining with H+ to form H2PO4 which is then excreted in the urine.

c. Ammonia buffer system: H= combines with ammonia (NH3) to form Ammonium ion (NH4). NH4 combines

with Chloride to form ammonium chloride which is then excreted in the urine.

d. Hydrogen-potassium exchange in the urine. Acidosis: excrete hydrogen and hold onto potassium. Alkalosis: excrete potassium and hold onto hydrogen.

e. Aldosterone: increased aldosterone causes sodium to be reabsorbed by the kidneys and potassium & hydrogen to be excreted. This causes metabolic alkalosis and hypokalemia. Decreased aldosterone causes the opposite. Potassium and hydrogen are retained and metabolic alkalosis occurs.

3. PaCO2: This is the respiratory component. CO2 makes carbonic acid. The more CO2 you have the more acidic your blood. High CO2 levels are called hypercapnea and are compatible with respiratory acidosis.

a. Hypercapnea: CO2 > 45. Causes include:

1. Impaired respiratory center: Drug OD, head injury2. Pulmonary conditions: Bronchitis, pneumonia, p.

edema, respiratory distress syndrome3. Chest wall abnormalities: Paralysis of respiratory

muscles, chest injuries, deformities, obesity4. Other: Paralytic drugs, air high in CO2 content

S/S:

1. H/A, weakness, confusion, tremor, paralysis, stupor, coma

2. Acidic urine (It takes at least one day for the kidneys to compensate and increase the bicarb level to compensate for the high CO2 content in the blood)

3. Cerebral artery vasodilatation: Increased ICP, papilledema if severe

4. Warm, flushed skin, weakness, tachycardia if less severe due to peripheral vasodilatation.

5. Hypercapnea in the lungs results in pulmonary vascular vasoconstriction (increased PHPT).

Treatment of Hypercapnea:

1. Improve ventilation2. Intubate and ventilate3. Pulmonary toilet4. Tx the cause (ie: hold sedation)

b. Hypocapnea: PaCO2 < 35. Associated with respiratory alkalosis and can occur suddenly without compensation. Caused by hyperventilating. Causes include:

1. Anxiety2. Panic attacks3. Fever4. O2 deficiency5. Early salicylate toxicity6. Encephalitis7. Anesthesia8. Treatment for IICP9. Metabolic acidosis (compensatory)

Signs and symptoms include:

1. Light-headedness2. Dizziness3. Tingling & Numbness of the fingers and toes,

seizures4. Sweating5. Palpitations6. Air hunger, dyspnea7. Possible Chvostek and trousseaus if calcium drops8. Tetany and convulsions (Hypocalcemia)

Tx:

1. Rebreathe air from a paper bag or cupped hands2. Calm the patient

4. PaO2: An indirect measure of the oxygen content of arterial blood. PaO2 is a measure of the tension (pressure) of oxygen dissolved in the plasma. This pressure determines the force of O2 to diffuse across the pulmonary alveoli membrane. It is decreased in:

a. O2 diffusion difficulties: pneumonia, shock lung, CHF

b. Premature mixing of venous blood with arterial blood:

c. Under ventilated and overperfused pulmonary alveoli: Pickwickian syndrome, obese patients who cannot breathe properly when in the supine position or patients with significant atelectasis.

5.HCO3: Bicarb is the metabolic component. Bicarb = base, so the more bicarb the more Alkalotic the patient.

a. Bicarb > 26 is compatible with metabolic alkalosis. Causes:

10.Excessive alkali: ingestion of NaHCO3, TPN with acetate, IVF with lactate, citrate in blood transfusions.

11.Loss of H-: vomiting, GI suction, binge-purge, hypokalemia, diuretics, hyperaldosteronism

Signs and symptoms of metabolic alkalosis: Asymptomatic or s/s volume depletion or hypokalemia. There rarely are CNS s/s Because HCO3 ions enter the CSF more slowly than H+ ions.

1. Mental confusion2. Hyperactive reflexes3. Tetany4. Hypoventilation (Compensatory)

Treatment:

Treat the cause (give Cl-, K, antiemetics, etc)

c. Bicarb < 22 is compatible with metabolic acidosis. Causes include:

1. Lactic acidosis: MI, shock, seizures, cardiac arrest where tissues to continue to metabolize without O2 and the byproduct is lactic acid.

2. Ketoacidosis: uncontrolled DM, fasting, low carbohydrate diets, excessive ETOH, vomiting and dehydration.

3. Salicylate toxicity: ASA OD4. Methanol/Ethylene glycol toxicity: AKA wood

alcohol. Can be absorbed through the skin, GI tract or lungs. As little as 30cc can be fatal. Causes metabolic acidosis, severe optic nerve and CNS toxicity. Organ damage occurs after 24 hours when it converts to formaldehyde and formic acid. Ethylene is a component of antifreeze and solvents. Lethal dose is about 100 cc. Converts to oxalic and lactic acid.

5. Decreased renal function. CRF is the most common cause of chronic metabolic acidosis because it interferes with H+ secretion and HCO3 retention.

6. Increased HCO3 loss: loss of GI secretions which are high in HCO3 such as occurs with severe diarrhea, small bowel-pancreatic or biliary fistula drainage, ileostomy drainage and intestinal suctioning.

7. Hyperchloremic acidosis: When Cl- ions are increased then HCO3 ions are decreased causing a metabolic acidosis. Causes include chloride containing meds such as ammonium chloride or hyperal.

Signs and symptoms of metabolic acidosis: Will see s/s of the causal disorder:

1. Weakness, fatigue, malaise, h/a2. anorexia, n/v, abd pain3. Decreased LOC, stupor, coma4. Skin dry, warm, flushed5. Cardiac irritability, decreased contractility,

decreased Cardiac output with pH < 7.06. Increased RR (compensatory)7. Acidic urine

6. Base excess or deficit. Base deficit (-) indicates metabolic acidosis. Base excess (+) indicates metabolic alkalosis or compensation to a prolonged respiratory acidosis. This number is calculated by the pH, PCO2, and the Hct. It represents the amount of buffers in the blood including HCO3, proteins and phosphate.

7.Anion gap: Compares the amount of positive ions (Cations Na+) with the amount of negative ions (anions such as Cl- and HCO3-). There appear to be more positive cations than negative anions, because some of the negative anions are not measured.

The difference between the number of cations (+) and anions (-) is called the anion gap.

The gap of unmeasured anions includes sulfates, phosphates and organic acids.

A normal anion gap is < 12 mEq

The anion gap is helpful in determining how much of an acidotic state the client has and if it is improving or worsening. The higher the gap, the worse the metabolic acidosis.

8. Directions for interpreting ABG’s:

Normal values: pH = 7.35-7.45

PaCO2 = 35-45

HCO3 = 22 – 26

1. Look at your pH first. Is the patient normal, acidotic or Alkalotic?

2. Look at your PaCOs (acid). Is it normal, high or low. High would be compatible with acidosis. Low with alkalosis. The PaCO2 will go in the opposite direction of the pH if the problem is respiratory.

3. Look at your HCO3 (base). Is it normal, high or low. If it is high it is compatible with alkalosis, if it is low it is compatible with acidosis. The HCO3 will go in the same direction as the pH if the problem is metabolic.

4. ROME: Respiratory opposite the pH, Metabolic equal (same) direction as the pH.

9. Explain the difference between an uncompensated, partially compensated and compensated acid base imbalance.

When a problem originally happens, it is uncompensated. For example: A COPD patient retains CO2 and develops a respiratory acidosis:

pH = 7.32 PaCO2 = 48 HCO3 = 24. Only the pH & paCO2 are abnormal.

The kidneys will begin to excrete H+ and hold onto bicarb in an attempt to compensate causing a partially compensated ABG:

pH = 7.34, PaCO2 = 48, HCO3 = 28 All are abnormal

Eventually the kidneys will be successful in holding on to the “right” amount of bicarb = compensated abg’s:

pH = 7.36, PaCO2 = 48, HCO3 = 32 pH is normal, PaCO2 & HCO3 are abnormal.

How do I know which one caused the problem. The body will not overcorrect the acid-base imbalance, which means the pH will be closest to the problem. A pH of 7.36 is closest to acidosis, right? So, to create an acidosis, you need either more acid (CO2) than usual or less base (HCO3) than usual. The abg’s above have more acid and more base. Only more acid can cause a acidosis. So this is a compensated respiratory acidosis.

Case Study 1: Mr. J is a 65 y/o male with a long history of chronic bronchitis and a 3 pack a day smoking habit for 50 years. He is taken to radiology and is returned to the room. You are checking on him when you find him obtunded and difficult to rouse. His respirations are 6 per minute and you note his oxygen has been turned up to 6 liters (Orders read 2 l/m). The following are the results from his ABGs:

pH= 7.29, PaCO2 = 90, PaO2 = 150, HCO3 = 24, O2 = 98%

1. Respiratory Acidosis

2. O2 is set too high, he has lost his hypoxic drive. Therefore he is hypoventilating and retaining CO2

3. A person’s O2 level does not need to be higher than 100. High O2 levels can be toxic to the lungs

4. Chronic hypoxia is interpreted by the kidneys as anemia and they secrete erythropoietin to produce more RBC’s. With higher RBC to Oxygen ratio, the O2 saturation will decrease.

5. ROME means that a respiratory acid base imbalance goes in the opposite direction as the pH and a metabolic imbalance goes in the same (equal) direction as the pH.

Acid base imbalance pH CO2 or HCO3Respiratory acidosis Decreased Increased CO2Respiratory alkalosis Increased Decreased CO2Metabolic acidosis Decreased Decreased HCO3Metabolic alkalosis Increased Increased HCO3

6. Other conditions which can cause respiratory acidosis include:

A. Impaired respiratory center: OD, head injury

B. Pulmonary conditions: Asthma, emphysema, bronchitis, pneumonia, pulmonary edema, ARDS

C. Chest wall abnormalities: paralysis, trauma, deformities, obesity

D. Paralytic drugsE. Air high in CO2F. Sleep apnea

7. Signs and symptoms of Respiratory acidosis include:

a. headache, weakness, confusion, tremor, paralysis, lethargy, stupor or coma

b. Acidic urine (will take one day to produce)

c. Cerebral artery vasodilatation (increased ICP, papilledema) d. Warm, flushed skin; tachycardia

CASE STUDY 2: There has been a school bus accident. A 7 year old boy c/o lightheadedness, numbness and tingling in his fingers and toes. His arterial blood gases are:

pH: 7.55 PaCO2 = 28 PaO2 = 100 HCO3 = 25 O2 Sat = 100%

1. This patient has Respiratory alkalosis.

2. The patient has hyperventilated due to fear and anxiety and “Blown off” their CO2.

3. Signs and symptoms of hypocapnea are:

a. Light-headedness, dizziness b. Tingling and numbness of the fingers and toes c. Sweating and palpitations d. Air hunger, dyspnea e. Chvostek and Trousseaus f. Tetany and convulsions

4. Slow down the patient’s breathing, have them re-breathe CO2 from a bag.

5. Other conditions which can cause this problem include: panic attacks, fever, Oxygen deficiency, early salicylate toxicity, encephalitis, anesthesia, and treatment for IICP.

6.Respiratory alkalosis causes the body to hold onto hydrogen ions to correct the pH. The amount of ionized calcium decreases and the patient experiences numbness, tingling, etc.

CASE STUDY 3: Mrs K is a 46 y/o female s/p abdominal surgery. She has a nasogastric tube (NGT) to low-intermittent suction and is draining about 700 cc of gastric secretions every 12 hours. She has the following ABG results and potassium level.

pH = 7.55 PaCO2 = 48 PaO2 = 100 HCO3 = 34 O2 Sat = 100% K = 2.8

1. Metabolic equal means that the pH and the HCO3 go in the same direction if the problem is metabolic in nature.

2. This patient has metabolic alkalosis because their HCL acid is removed by naso-gastric suctioning.

3. GI suctioning

4. Causes include excessive gain of alkali: ingestion of NaHCO3, hyperalimentation with acetate, IVF with lactate, Citrate in blood transfusions or d/t loss of H- ions such as occurs with vomiting, GI suction, binge-purge, hypokalemia, diuretics, hyperaldosteronism

5. Signs and symptoms of metabolic alkalosis include: May be asymptomatic or have s/s volume depletion or hypokalemia, mental confusion, hyperactive reflexes, tetany, hypoventilation (compensatory). Death occurs if > 7.55

6. Decreased hydrogen ions leads to hyperkalemia. Why? The body holds onto hydrogen and rids itself or binds with potassium in an effort to lower the pH and return it to WNL.7. Treatment includes treating the cause, replacing chloride and potassium, antiemetics and stop antacids.

CASE STUDY 4:

Mr. P has suffered a cardio-pulmonary arrest. He was “down” for 3 minutes before CPR was initiated. He has now been intubated and given 100% oxygen via an ambu bag when you obtain the following ABG’s:

pH = 7.28 PaCO2 = 32 PaO2 = 76 HCO3 = 16 O2Sat = 100%

1. This condition is known as metabolic acidosis

2. This condition can occur either d/t the following:

a. Lactic acidosis (anaerobic metabolism of glucose without O2) b. Ketoacidosis: burning fats instead of carbs c. Salicylate toxicity d. Decreased renal function* (the most common cause for this condition e. Methanol/ethylene glycol toxicity f. Hyperchloremic acidosis g. HCO3 loss with severe diarrhea, intestinal suctioning/drainage

3. His CO2 is low because they have been hyperventilating him with 100 % via ambu bag.

4. A venous CO2 is an indirect measurement of arterial HCO3. It is drawn much more frequently than arterial blood gases and can therefore alert you to acid-base imbalances.

5. Signs and symptoms of metabolic acidosis include: weakness, fatigue, malaise, h/a, anorexia, n/v, abd pain, decreased LOC, stupor, coma, skin dry, warm, flushed, cardiac irritability, decreased contractility, decreased CO.

6. The patient will increase their respiratory rate if at all possible to blow off CO2 and correct the acidosis.

Case studies and quiz are under: Case studies: acid-base lecture