ABG...EASY AS...

1,2,3
NORMAL VALUES & DEFINITIONS
NAME pH DEFINITION Refers to hydrogen ion (H+) levels, hence the H in pH. H+ levels are important because a lack of (deficit) or too much (excess) will tell you if the patient is acidotic or alkolotic. One confusing point about pH is that it is an INVERSE ratio, which means that the more H+ present, the lower the pH and vice versa. Can give away a H+ or can separate (dissociate) hydrogen from its ion, so the hydrogen is not positive and therefore no longer an acid. Acids are end products of metabolism and must be buffered or excreted to achieve a normal pH Unlike Acids, bases can accept a H+ and bond with hydrogen. They are all negative and like to buffer body acids. VALUE 7.35 - 7.45

3 STEPS TO ABG INTERPRETATION

1. What is the pH? Is it alkolotic (57.45) or acidotic (67.35)? 2. Whats happening with the respiratory system (CO2) and the metabolic systems (HCO3-)? If the problem is in the lungs (respiratory) the CO2 will be heading in the opposite direction of the pH. For example: respiratory acidosis: The pH will be low - 6pH 7.22 and the CO2 will be high - 5CO2 55mmhg If the problem is metabolic the HCO3 will head in the same direction as the pH For example: metabolic alkalosis: The pH will be high - 57.55 and the HCO3- will also be high HCO3- 535mmol/L. Note: an easy way to remember for a Metabolic problem, think M as in the pH will head in the saMe direction as the HCO3-. For respiratory the pH will head in the Opposite direction as the CO2. 3. Is there any (if any) compensation occurring? No compensation: pH remains abnormal, and the other value (where the problem isnt occurring, i.e. CO2 or HCO3-) will remain normal or has made no attempt to help normalise the pH. For example: in uncompensated metabolic acidosis: pH 67.23, HCO3- 6 15mmol/L, and the CO2 will be normal at 40mmHg. Partial compensation pH is still abnormal, and the other value is abnormal in an attempt to help normalise the pH. For example: in partially compensated respiratory alkolosis: pH 57.62, CO2 627 and the HCO3- will be abnormal at 617mmol/L Full compensation The pH is normal, as the other value is abnormal and has been successful in normalising the pH. For example: Fully compensated metabolic acidosis pH 7.38, HCO3- 615mmol/L and the CO2 630mmHg 6

Acid

20 parts base / 1 part acid

Base

WHAT CAUSES THESE CHANGES?

METABOLIC ACIDOSIS Can be caused by either an increase in circulating acids and or a loss of base (HCO3-). These include: Renal failure (unable to excrete acids or H+) Lactic acidosis (increase in circulating acids) Keto - acidosis (increase in circulating acids) Diarrhoea (HCO3- loss) METABOLIC ALKOLOSIS Can be caused by an increase in HCO3- or loss of metabolic acids. These include: Prolonged vomiting (acid loss) GI suctioning (acid loss) Hypokalaemia (H+ (an acid) excreted to maintain electrolyte balance) RESPIRATORY ACIDOSIS Caused by increased CO2 levels which is then converted to an acid (H+) as the body tries compensate by excreting acids via the kidneys. These include: Hypoventilation: - sedatives/sedation/opiates Depression of respiratory centre in brain stem via trauma Pneumonia Pulmonary oedema Asthma RESPIRATORY ALKALOSIS Caused by a hyperventilation, the body getting rid of too much CO2, for example: Anxiety Hypoxaemia (caused by heart failure)

Base excess / Base deficit

Represents an increase or decrease in the -2 to +2mmol/L amount of base compared with the amount of acids present Concentration of hydrogen carbonate in blood. Used to determine along with pH and CO2 source of acid base imbalance. 22-26mmol/L

HCO3-

pCO2

Carbon dioxide partial pressure (tension). 35-45 mmhg Reflects alveolar ventilation as it diffuses across the alveolar capillary membrane and blown off.

paO2

Arterial oxygen tension. In other words 75-100mmhg how well the lungs are able to pick up oxygen, i.e. supply, but not demand (this is shown in a mixed venous gas, discussed later). Lactate When cells no longer have enough O2 for 0.5 - 2.0mmol/L (Lactic Acid) normal aerobic metabolism (cell hypoxia) Anaerobic metabolism takes over resulting in lactate production, leading to lactic acidosis Hb Amount of haemoglobin in blood possibly 135 - 180g/L 7 (Haemoglobin) capable of carrying oxygen.

TREATMENT GOALS/GUIDELINES
As with both acidosis and alkolosis, there needs to be a diagnosis of why the patients acid base status is such. Treatment is then aimed at stabilising the initial/presenting problem as well the acid-base status. However, general guidelines include correcting the fluid balance and electrolyte status. Continuous regular ABG monitoring and recording for trends. Possible dialysis to remove excess lactate, manipulation of ventilation settings to adjust CO2 levels, but always maintaining tissue perfusion. Depending on severity of HCO3- levels and pH - possible sodium bicarbonate infusion (this is controversial however). Of course any of the adjustments made should only be done with an order from a medical officer, and must go through the intensive care team before any changes to treatments are applied. 4

MIXED VENOUS BLOOD GAS VALUES

NAME pH HCO3pCO2 paO2 sO2 VALUE 7.33 - 7.44 24-28mmol/L 41-57 mmhg 35-40mmhg 70 - 75%

Superior Vena Cava

OXYHAEMOGLOBIN DISSOCATION CURVE (ODC)

What is it and why is it important? The ODC looks at the relationship between oxygen tension (pressure) and oxygen saturation. It helps us better understand how our blood interacts with oxygen, i.e. how and why it picks up and lets oxygen go. The S shape tells us that after an amount of oxygen has accumulated in the blood, there isnt room for any more, no matter how much oxygen you throw at the haemoglobin molecule, it wont change Affinity basically means how much we (or blood) are attracted to someone (oxygen). The ODC shows us what changes the affinity of blood for oxygen. RIGHT SHIFT (ACIDOSIS) Shift of the curve to right decreases affinity - meaning that the Hb isnt very attracted to oxygen, and when it does pick up oxygen, it lets it go very quickly. Increased temperature and CO2 help this right shift. LEFT SHIFT (ALKALOSIS) Shift of the curve to the left increases affinity - meaning that the Hb is very attracted (oh la la) to oxygen and when oxygen is picked up, the Hb has a hard time letting it go at the cellular level. Decreased temperature and CO2 help the curve move to the left. 2

Pulmonary Artery

Mixed venous gases measures oxygen left in the blood as it returns to the heart (right side) after it has been pumped around the body supplying cells with oxygen. The body normally extracts 25% of available oxygen and leaves 75% in reserve in times of stress or illness.4 The heart above shows where our subclavian central lines sits - in the superior vena cava, it is here we can take venous blood gases. Samples from the pulmonary artery are however, more accurate and can only be performed if the patient has a PA catheter.

ALKALOSIS

ACIDOSIS

OTHER VALUES OFTEN OVERLOOKED

Anion gap - This value is used in metablic acidosis to find the cause. It reflects unmeasured anions (negatively charged ions) such as proteins, sulfates, phosphates etc. The equation to find the anion gap is (Na + K+) - (cl + [HCO3-]) a high value can be caused by keto or lactic acidosis, or renal failure. Low values may indicate hyponatremia or decreased plasma protiens. 10-20mmol/L OXYGEN STATUS p50a - oxygen tension at 50% saturation on ODC. This is used to reflect affinity of Hb for oxygen. 25-29mmhg FMetHb - This is the fraction of methaemoglobin. Think of methaemoglobin like haemoglobin, but we carry less than 1% of it in our blood. As it is unable to combine with oxygen and it also decreases the oxygen carrying capacity of blood. Exposure to certain drugs and chemicals can dangerously elevate levels. 0.2-0.6% FCOHb - Fraction of carboxyhaemoglobin. Much similar to FMetHb in its actions. Affinity of Hb for carbon monoxide is 200 times greater than that of oxygen and impairs oxygen transport and release (ODC shift to left, alkolosis). This level can be high in heavy smokers. 0.0-8.0% Fshunte - Relative physiological shunt. Basically the amount of venous (de-oxygenated) blood that did not receive oxygen whilst travelling through the lungs. This can be caused by atelectasis, a pulmonary embolism (PE), mucous plugs and pulmonary oedema, all of which reduces oxygen transport into the blood. 1.0-10% FO2Hb - fraction of oxyhaemoglobin. This measures just how much blood (Hb) is carrying oxygen compared to the total amount of Hb capable of carrying. Similar to your SO2, however FCOHb and FMetHb are not included as they are not capable of carrying oxygen. 94-98% Hct - Hematocrit. This shows us how much red blood cells there are in a sample of blood - i.e. how watered down (or not) blood is. 36-44%7
REFERENCE LIST 1. Coleman, n. and Houston, L. 1998 Demystifying acid-base regulation Australian nursing Journal 5, 8, 23-26 2. Dickson, S. 1995 Understanding the Oxyhemoglobin Dissociation Curve. Critical care Nurse 15, 10, 54-58. 3. Minor, J. and George, E. 2008 Using mixed venous oxygen saturation to improve patient assessments. Nursing2008 56, 1, 1-3. 4. McCance, K. and Heuther, S. 1998 Pathophysiology, 3rd edn, Mosby, St. Louis, Missouri. 5. Pruitt, W. 2004 Interpreting Arterial blood gases: Easy as ABC. Nursing2004 34, 2, 50-53. 6. Tastota, F. 1994 Assessing A.B.G.s: Maintaining the delicate balance. Nursing94 24, 5, 34-44. 7. The Blood Gas Handbook, 2005. Radiometer Medical ApS RadiometerCopenhagen, Bronshoj. 8. Wikipedia contributors, 2008 Pulmonary artery. n.p. Available URL: www.wikipedia.org/w/index.php?title=Pulmonary artery&oldid=183841779 <Accessed 2008 February 2> 9. Wikipedia contributors, 2008 Oxygen-haemoglobin dissociation curve. n.p. Available URL: wikipedia.org/w/index.php?title=Oxygen-haemoglobin dissociation curve&oldid=187503438 <Accessed 2008 February 2>

Hb

O2

O2

Hb

BICARBONATE/CARBONIC (HCO3-/H2CO3) BUFFERING SYSTEM

H2O + CO2 n H2CO3 nH+ + HCO3 The H2O and CO2 is regulated via the lungs and HCO3- and H+ via the kidneys. An increase in one value can shift the equation and helps maintain equilibrium. A problem in either the lungs or kidneys or both can throw this equation out of whack, resulting in an acid base imbalance. Other buffers include protein and phosphate buffers.

This is the most active buffering system. Needs good renal function (HCO3- regulation) Converts H+ (hydrogen) to H2CO3 (carbonic acid) which is then able to be blown off via the lungs as CO2.

RESPIRATORY REGULATION OF ACID BASE BALANCE

Eliminates volatile acids (CO2) Works within minutes Dependent on HCO3- stores and adequate gas exchange CO2 diffuses passively into the cerebrospinal fluid and the medulla controls rate and depth of respiration Eliminates fixed acids (harder to remove than volatile) H+ Regulates HCO3- depending on need Controls phosphate and ammonia buffer systems Bicarbonate/carbonic acid system can only work if bicarbonate stores are replaced by the kidneys.1 Works slowly, from hours to days

RENAL REGULATION OF ACID BASE BALANCE

Author: Amy ODonnell Date: 9th February, 2008