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Arterial catheters and blood gases: What do all these numbers mean? (Proceedings)

Article

The use of arterial blood gas analysis has become commonplace in many veterinary practices for the assessment both qualitative and quantitative assessment of metabolic and respiratory acid-base problems, including the interrelationships between ventilation, oxygenation, and metabolic conditions.

The use of arterial blood gas analysis has become commonplace in many veterinary practices for the assessment both qualitative and quantitative assessment of metabolic and respiratory acid-base problems, including the interrelationships between ventilation, oxygenation, and metabolic conditions. Blood gas analysis is a useful adjunct to clinical patient assessment in determining appropriate therapy for specific and complex conditions. There are two reliable means to procure an arterial sample, whether by a one time draw or by placement of an arterial catheter either can get you the necessary sample. The placement of arterial catheters, once learned, is a useful, invaluable skill for veterinary technicians to possess.

The advantage of analyzing arterial over venous blood samples is that you can access both gas exchange and metabolic status. When using venous samples the data is only reliable for metabolic status. The more clinical applications for blood gas analysis would be ventilation status and acid-base status by differentiating hypo-ventilation from other causes of hypoxemia, helping to determine the need for supportive therapy and to monitor the response to therapy.

Sample drawing technique

Most times a one or three milliliter heparinized syringe is used along with a 25ga. needle. Artery location is up to the person drawing the sample but commonly used sites are the femoral artery, the dorsal pedal artery and the lateral coccygeal artery (tail). NOTE: When "sticking" an awake patient a moderate amount of discomfort and pain are felt by the patient, to avoid this you can apply 4% lidocaine crème to the area, wait a few minutes and proceed as the area will be effectively numb. Once a site is chosen the artery should be palpated. It is best to secure the artery between two fingers and advance the needle into the artery. Arteries are thick walled and loosely attached to the adjacent tissues; therefore the needle must be place above the artery and advance with a short, jabbing motion to achieve entry. Many times arteries will constrict as you attempt to enter them, hence some training is involved before you become proficient at this skill. Once in the artery, many times the plunger on the syringe will pulse back and fill the syringe. The sample should be a brighter red (than venous samples) unless the patient is extremely compromised.

After removing the needle from the site, pressure should be applied to the site for 5 minutes to prevent the formation of a hematoma. Any air that is entrapped in the sample syringe should be immediately removed, the syringe should be capped with a rubber stopper (needle discarded) to prevent false readings due to room air exposure. If the sample is not to be immediately analyzed it should be place on ice.

Placement of arterial catheters

As stated, once a technician becomes proficient at placing arterial catheters, their use can be invaluable. The most common site for an arterial catheter is the dorsal pedal artery as it allows mobility in the awake patient. Although this site is at times difficult for catheter placement in short legged animals as you tend to hit the carpal joint with the catheter and are unable to feed it past that point. Typically, a smaller arterial than venous catheter is placed with 22-20 gauge catheters being the most commonly used. With larger patients 2 inch catheters give you more stability in transport. However, it is not always possible due to disease progression causing contracted arteries. Other common places are the lateral coccygeal (tail) artery for either awake or anesthetized patients or the lingual artery as a last resort in anesthetized patients. Caution should be used when placing tail catheters for contamination from feces. Femoral catheter placement, while not impossible, causes it's own set of problems if the catheter becomes dislodged as bleeding from this site is a bigger issue than the other sites. Caution should be used when dealing with any arterial catheter and the real possibility of significant blood loss via disconnection.

Monitoring blood pressure

Placement of an arterial catheter will allow us to most accurately monitor blood pressure. This is the most precise form of BP monitoring as it measures beat-by-beat inside of the artery as opposed to non-invasive devices which tend to give non-reliable readings through fur and tissue. The values that are collected via this method are: systolic pressure defined as the peak pressure in the arteries, which occurs near the beginning of the cardiac cycle, the diastolic pressure is the lowest pressure (at the resting phase of the cardiac cycle), the mean arterial pressure (MAP) and the pulse pressure which reflects the difference between the maximum and minimum pressures measured. The main concern of these 4 measurements in clinical practice is the MAP or mean arterial pressure which in small animals should be between 60-70 mmHg in order to profuse the bodies organs sufficiently.

Monitoring PaO2 and PaCO2

PaO2 is more appropriately the partial pressure of oxygen. When looking for "normal" values one must consider whether the patient is breathing room air, in which the normal values are between 70-100 mm Hg, or on 100% O2, in which the normals would be in the range of 400-500 mm Hg. However, many factors can cause decreases in this value such as shunting, V/Q mismatch or diffusion impairment. At times the terms hypoxemia and hypoxia are used interchangeably, in actuality a distinction can be made in that hypoxemia refers only to situations in which there is low oxygen content in the blood. As opposed to hypoxia which more broadly refers to impaired oxygen delivery which takes into account cardiac output, perfusion and oxygen extraction by the tissues. With that being said there are five primary causes for hypoxemia in animals: shunting, V/Q mismatch, hypoventilation, diffusion impairment and low inspired oxygen concentration.

PaCO2 is more appropriately the partial pressure of carbon dioxide. Normal values range from 35-55 mm Hg. PaCO2 is used most commonly in evaluating ventilation. Acceptable PaCO2 under anesthesia is between 30-60 mm Hg. Possible causes of hypercapnia include: hypoventilation secondary due to central nervous system depression caused by anesthetic agents, respiratory muscle weakness secondary to use of neuromuscular blocking agents or hypokalemia, intrinsic pulmonary disease, rebreathing, exhausted soda sorb, excessive dead space, malignant hyperthermia, airway obstruction, restriction of lung expansion, All of these can also cause decreased PaO2. Although hypocapnia is less common it is still seen. The usual case for hypocapnia is hyperventilation due to things like light plane of anesthesia, over aggressive ventilation and the like. Although usually well tolerated the concern with values under 20-25 mm Hg are decreased cerebral blood flow and oxygen delivery to the brain.

Monitoring PH

Any physiologic event that changes pH is called a primary disorder, this will stimulate a compensatory response to restore pH. Normal values are 7.36-7.44. Anything above is considered alkalodic and anything below is considered acidodic. Many situations can cause alkalosis or acidosis. There are two distinct types, respiratory and metabolic. Common causes of respiratory alkalosis include: pulmonary disease, hyperventilation secondary to pain, fear or anxiety, gram-negative sepsis, CNS disorders (neurogenic hyperventilation), exogenous drug administration, overzealous ventilator therapy. Common causes of respiratory acidosis include: respiratory center depression from drugs, large airway obstruction, intrinsic pulmonary and small airway diseases, cardiopulmonary arrest, CNS trauma, brain lesions or respiratory embarrassment (pneumothorax, pulmonary edema, airway obstruction, restricted chest movement). Common causes of metabolic alkalosis include: secondary to vomiting (loss of H+ in stomach- pyloric obstruction), hyperadrenocorticism, exogenous steroid therapy, K+ depleting diuretic therapy leading to hypokalemia and contraction alkalosis, bicarbonate therapy. Lastly, common causes for metabolic acidosis include: DKA, renal insufficiency, lactic acid production (shock, sepsis, pancreatitis, hypoxemia), exogenous toxins (ethylene glycol, salicytic acid), diarrhea (HGE, parvo).

Putting it all together

  • Step #1- pH < 7.36 = an acidemia

o > 7.44 = an alkalemia

  • Step #2- Look at the PACO2. If it is increased or decreased then a respiratory component exists.

  • PaCO2 < 36 = respiratory alkalosis

  • > 44 = respiratory acidosis

  • Step #3- Look at the bicarb (HCO3-), if it is increased or decreased, then a metabolic component exists.

  • HCO3- < 20 = metabolic acidosis

  • > 28 = metabolic alkalosis

  • Step #4- Find out which one is the primary cause of the shift in pH. In simple acid-base disturbances the primary disorder is the component that has changed in the same manner as the pH.

For example:

  • in pH + ↓ in HCO3- → primary metabolic acidosis

  • in pH + ↑ in pCO2 → primary respiratory acidosis

  • in pH + ↑ in pCO2 + ↓ in HCO3- → mixed acidosis

  • Step #5- Is there a compensatory response? A compensatory response will cause the component to move in the opposite manner of the pH. This is the body's way of trying to correct the problem by compensating for the disturbance.

A compensatory response to an acidemia would be an increase in HCO3- or a decrease in pCO2. Likewise, a compensatory response to an alkalemia would be a decrease in HCO3- or an increase in pCO2.

  • ↓ pH + ↓ HCO3- + ↓ in pCO2 = primary metabolic acidosis with respiratory compensation.

  • ↓ pH + ↑ HCO3- + ↑ pCO2 = primary respiratory acidosis with metabolic compensation.

  • ↑ pH + ↑ HCO3- + ↓ pCO2 = primary metabolic alkalosis with respiratory compensation.

  • ↑ pH + ↓ HCO3- + ↓ pCO2 = primary respiratory alkalosis with metabolic compensation.

Treating respiratory acidosis

The number one priority for treatment of respiratory acidosis is to ensure adequate oxygenation and to provide adequate alveolar ventilation. In acute hypoventilation like airway obstruction or cardiopulmonary arrest, hypoxemia is an immediate threat to life. Most commonly, patients die from hypoxemia before hypercapnia becomes severe. Abrupt interruption of breathing is fatal within 4 minutes, whereas severe hypercapnia would take 10-15 minutes to develop in such a setting. Many times small animals come in that have been chronically ill and hence have a steady but chronic state (2-5 days) and so their blood gases reflect an adaptation to chronic hypercapnia. However, if these chronic respiratory acidotic patients decompensate acutely, life-threatening consequences can occur and lead to sudden death. Many times these are the patients that require mechanical or assisted ventilation in order to give the medical team time to correct the underlying issue(s). It would be fair to say that a quick diagnosis and elimination of the underlying cause of alveolar hypoventilation is the most effective treatment for respiratory acidosis. Airway obstruction should be identified and promptly relieved, whereas medications that depress ventilation should be discontinued if at all possible. Pleurocentesis should be performed to remove fluid or air when pleural effusion or pneumothorax is present. Although at times it is not possible to remove the underlying cause of hypoventilation (e.g., chronic pulmonary disease), appropriate treatment of the primary disease should still be initiated along with supportive therapeutic measures. Since the primary goal is remove the CO2, again mechanical ventilation is often the necessary choice.

Quick reference chart to changes in PaCO2 and PH

Treating respiratory alkalosis

Treatment should be directed towards relieving the underlying cause of the hypocapnia; no other treatment is effective. Respiratory alkalosis severe enough to cause significant clinical consequences for the animal is uncommon. Hypocapnia itself is not a major threat to the well being of the patient. Thus, the underlying disease responsible for hypocapnia should receive primary therapeutic attention.

Treating metabolic acidosis

The number one priority for treatment of metabolic acidosis is the prompt diagnosis of the underlying cause of the acid-base disorder and initiation of appropriate treatment. At times the underlying disease cannot be corrected and alkali therapy becomes a probability. Severe alkalosis may cause life-threatening cardiovascular complications. It is at these times (pH <7.1-7.2) that treatment with Sodium Bicarbonate would be justifiable to reduce life-threatening hemodynamic complications.

Treating metabolic alkalosis

Again the most common cause of metabolic alkalosis in small animal practices are either vomiting or by administration of diuretics. It is most commonly recognized as a decrease in hydrogen ion concentration which leads to increased bicarbonate and carbon dioxide concentrations. Metabolic alkalosis patients are usually divided into two groups. One group has ECFV (extracellular fluid volume) depletion and an ardent renal retention of sodium and chloride. These types of patients respond well to chloride administration. Group two has normal or increased ECFV and all sodium chloride that is taken in is secreted in the urine. These patients do not respond to chloride treatment. Fortunately, chloride resistant metabolic alkalosis is rare in dogs and cats. The primary cause is hyperaldosteronism and hyperadrenocorticism. Again, treatment of the underlying disease is the key to treating metabolic acid-base disorders.

Conclusion

In conclusion, veterinary technicians have a great deal in which they can do to aid in the diagnosis, monitoring and treatment of acid-base disorders, blood gas collection and blood pressure monitoring.

References

1. Clinical Tech Small Animal Practice. 1999 Nov, 14(4): 227-30.

2. Respiratory monitoring: arterial blood gas analysis, pulse oximetry, and end-tidal carbon dioxide analysis. Proulx J.

3. Greene S, Veterinary Anesthesia and Pain Management Secrets, Hanley & Belfus, Inc; 2002;15-18.

4. Nelson R. et al. Small Animal Internal Medicine, Mosby; 1998: 278-282.

5. ACVIM Proceedings CLINICAL APPROACH TO RESPIRATORY ACID-BASE DISORDERS Helio Autran de Morais, DVM, PhD, DACVIM (Internal Medicine and Cardiology) and Rebecca A. Johnson, DVM, PhD, DACVA

6. Cohen JJ and Kassirer JP: Acid-base. Boston, Little, Brown & Co., pp. 307-348, 1982.

7. DiBartola SP:Fluid, Electrolyte and Acid-Base Disorders in Small Animal Practice.. Philadelphia, WB Saunders Co., pp.268-269,277-278. 2006.

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