Respiratory mechanics and monitoring (Proceedings)


Basic lung function is designed to exchange oxygen and carbon dioxide. In order to transfer oxygen from atmospheric air to the blood stream three functions must be in place: ventilation, diffusion, and perfusion. Ventilation is the process of air moving into and out of the lungs.

Basic Respiratory Mechanics

Basic lung function is designed to exchange oxygen and carbon dioxide. In order to transfer oxygen from atmospheric air to the blood stream three functions must be in place: ventilation, diffusion, and perfusion. Ventilation is the process of air moving into and out of the lungs. Diffusion is the movement of gases between the alveoli and the blood in the capillaries. And perfusion occurs when the cardiovascular system pumps blood throughout the lungs. Where these three things meet are the interface of each tiny alveolus that is wrapped with a capillary bed consisting of both pulmonary artery (carrying oxygen deficient blood) and pulmonary vein (carrying newly oxygen rich blood to the heart). It is the surface area of millions of alveoli that allow for the movement of carbon dioxide out of the blood and oxygen into the blood.

Recognizing Respiratory Distress: Respiratory distress/dyspnea, as defined, is observable respiratory difficulty or physically labored breathing clinically evident by an inability to ventilate and/or oxygenate adequately. Normal breathing should appear natural, free, and easy. Inspiration is normally no longer than one second with moderate expansion of the chest and abdomen occurring simultaneously. Exhalation is normally 2-3 seconds and should not be forced in character. Prolonged inspirations may indicate upper airway disease while prolonged exhalations may indicate lower airway disease. Anxiety ridden or exaggerated breathing efforts may indicate obstructed ventilation and hyperventilation respectively. Physical manifestations of respiratory distress can vary widely from tachypnea and loud panting to slow stridorous whistling attempts to breath. Cats may demonstrate dyspnea by open mouth panting while visually they appear fairly non-distressed. All of these presentations demand fast action to deliver supplemental oxygen.

Physical Exam

Gentle handling should be employed in order to decrease anxiety in patients with respiratory distress. Oxygen should be delivered in the least stressful manner possible. Methods of oxygen delivery include; flow by oxygen, oxygen mask, oxygen hood (or e-collar with loose baggy hood), nasal cannulation, oxygen cage, intratracheal catheter, or endotracheal tube. Delivery mode should correlate to the patient's need and should not cause any further anxiety to the patient. Physical examination of the patient can now take place as tolerated by the patient and will include auscultation of upper and lower airways and all lung fields. Cats, however, may require a hands-off approach with oxygen being supplied into an oxygen cage and the physical exam waiting for 5-10 minutes. If the cat's dyspnea is not decreasing in that amount of time some degree of intervention is needed to assess the patient. Appropriate oxygen therapy mode varies depending on the severity of the patient's condition. A patient should never die from respiratory distress. To provide oxygen in times of distress may require sedation (moderate distress) or anesthetic induction (life threatening distress) followed by intubation and positive pressure ventilation. These measures would allow for time to diagnose disease and implement therapeutic measures.

Methods to Assess Oxygenation

Pulse oximetry is a painless, quick, and inexpensive method to measure the percentage of hemoglobin saturated with oxygen (SpO2; units=%) within the blood. It is generally the first objective method of assessing a patient's respiratory status. Pulse oximetry works by spectrophotometry and measures two forms of hemoglobin that circulate in arterial blood; those forms of hemoglobin are oxyhemoglobin (saturated) and deoxyhemoglobin (unsaturated). Carboxyhemoglobin (bound to carbon monoxide), and methemoglobin (oxidized) are two additional forms of hemoglobin that would be measured using a cooximeter. As pulse oximetry does not differentiate carboxyhemoglobin and methemoglobin readings are not considered reliable in patients with smoke inhalation or acetaminophen toxicosis. Pulse oximetry probes transmit wavelengths of red to infrared light waves across vascular beds of tissue and read saturated or unsaturated hemoglobin. The amount of light that is reflected or passed through is evaluated during pulsatile flow. Limitations to pulse oximetry are considerable; tissue perfusion (poor cardiac output or body temperature), icterus, skin pigmentation, skin thickness, mucous membrane dryness, patient movement, and ambient light all may affect readings. Moist mucous membrane areas (tongue, buccal membrane) or thin, light colored, skin areas (point of hock, ear, inter digits) usually work the best. In order to be considered reliable, a pulse oximetry waveform reading should demonstrate an accurate heart rate and stable repeating waveform oscillations. Some units will have a signal strength indicator as a bar graph or indice number. Probe types vary from clip on (gentle clamp) types that transmit light through tissues like the ear, lip, or tongue to reflectance probes that lay against tissue beds such as the inner rectum, prepuce, or under tail base. Be aware that once the probe has been in place for several minutes vascular beds may become compressed and readings may decrease. A normal SpO2 reading for patients breathing room air (21% oxygen) should be at least 96%. Readings of <92% SpO2 require supplemental oxygen delivery and/or ventilatory assistance.

While pulse oximetry is generally the first tool used to assess a patient; arterial blood gas analysis is considered the gold standard in evaluating a patient's ability to oxygenate and ventilate. Arterial blood gas analysis measures the lung's ability to diffuse oxygen into arterial capillary blood (oxygenation) while extracting CO2 from venous capillaries (ventilatory efficiency). Because it also measures PaCO2 (partial pressure of carbon dioxide in arterial blood) it can be used to evaluate for evidence of hypoventilation whereas pulse oximetry only addresses oxygenation status. Blood gas analysis is considered a standard of care now that the units have become more affordable (I-Stat®I-Stat Corporation, East Windsor, NJ: and IRMA SL®Diametrics Medical, St. Paul, MN). Blood gas analysis works by measuring the partial pressure of oxygen (PaO2; units=mmHg) and carbon dioxide (PaCO2; units=mmHg) dissolved in the plasma. It does this by using electrodes to compare a known electrolyte solution to the blood sample across a semi-permeable membrane (permeable to CO2 and 02). Obtaining blood gas samples does require practice and causes some stress to the patient. Measures should be taken to minimize stress because anxiety and struggling will alter results (hyperventilation). Potential sites for sampling are the dorsal pedal, femoral, and auricular arteries. Any artery punctured must be held off for 10 minutes or bandaged to control hemorrhage and preserve the artery. Using the dorsal pedal artery will require less manipulation of patient position , as compared to the femoral artery and is more easily bandaged. Anatomical proximity of the femoral artery and vein makes the possibility of obtaining a venous or mixed venous/arterial sample greater when using the femoral artery. Placement of an arterial catheter will facilitate repeated sampling and serial monitoring. Obtaining arterial gas samples from cats requires extensive experience and is usually not tolerated by a non-anesthetized patient.

Relationship between PaO2 and oxygen saturation: Pulse oximetry measures the percentage hemoglobin saturated with oxygen while PaO2 represents the partial pressure of oxygen gas dissolved in arterial blood. These two measurements relate to each other in a sigmoid relationship called the oxyhemoglobin dissociation curve. The relatively flat area of the curve represents a small change of approximately 10% saturation while reflecting a potential drop in PaO2 of up to 40mmHg. What this means to patients is a smaller change in pulse oximetry percent that would correlate to a significant decrease in PaO2. In example, a pulse oximetry reading of 90% roughly equals a PaO2 of 60mmHg, which would qualify a patient as hypoxemic. When analyzing an arterial blood gas, a current patient body temperature should be programmed into the analyzer due to the fact that hypothermia shifts the oxyhemoglobin dissociation curve to the left. Hypothermia (left shift of dissociation curve) results in a decrease in oxygen release from hemoglobin and therefore decreased amounts of oxygen available for tissue pickup. A decrease in pH and PaCO2 will also occur with hypothermia. The reverse is true of changes due to hyperthermia. Details of normal and abnormal PaO2 and PaCO2 results and the steps to evaluate an arterial blood gas will follow.

Hypoxemia: Normal PaO2 is 80-100mmHg for patients breathing room air. Hypoxemia is defined as PaO2<80mmHg; with less than 60mmHg PaO2 requiring oxygen supplementation and/or ventilatory assistance. Causes of hypoxemia include:

     • Decreased oxygen concentration of inspired air (high altitude)

     • Hypoventilation (decreased volumes or movement of air into lungs)

     • Venous admixture resulting from shunt, V/Q (ventilation/perfusion) mismatch, diffusion

     • impairment

Shunting occurs whenever blood passes from the right side of the heart to the left side of the heart without passing through a functional alveoli and receiving oxygenation. Many times these are anatomic conditions such as right to left cardiac anomalies or intrapulmonary defects. An example would be a ventricular septal defect as part of Tetralogy of Fallot or large atelectic lung areas respectively. Regardless of cause, venous blood is returned to the arterial circulation without oxygenation resulting in a decrease of PaO2. V/Q mismatch occurs whenever the rate at which the supply of oxygen into the alveoli and the blood perfusion to the alveoli are not approximately equal as would be in normal function. Lower airway disorders such as bronchospasm or pulmonary edema and pulmonary perfusion disturbances such as pulmonary thromboembolism are possible causes of V/Q mismatch. Diffusion impairment may occur when severe disease provides a barrier to the diffusion of oxygen into arterial capillary blood. An example of diffusion impairment would be pulmonary fibrosis and it is not well recognized in veterinary medicine.

Hypercarbia: Normal canine PaCO2 is 35-45mmHg; feline normal may be slightly lower. PaCO2 reflects the difference between alveolar minute ventilation and metabolic CO2 production. Hypercarbia is defined as PaCO2 levels >45mmHg and results from disorders that affect the mechanical ability to move air into the lungs (alveolar hypoventilation). Hypoventilation will often manifest as increased PaCO2 levels accompanied by decreased PaO2 levels. Supplemental oxygen delivery alone will increase PaO2 levels but will not decrease PaCO2 levels as it does not necessarily provide an increase in alveolar minute ventilation. If hypoventilation is clinically evident, measures must be taken to improve the ventilatory status by either resolving the cause of hypoventilation or beginning positive pressure ventilation if treatment will require some length of time to resolve. Some of the more common causes of hypercarbia include:

     • Airway obstruction (laryngeal paralysis, occluded endotracheal tube)

     • Central neurologic disease or anesthesia (decrease in central respiratory drive)

     • High cervical spinal cord injury or dysfunction

     • Flail chest

     • Respiratory muscle dysfunction or neuromuscular disease (Polyradiculoneuritis or

     • neuromuscular blocking agents)

Interpretation of Respiratory Function (calculating A-a gradients) of ABG's: The first step in evaluating the respiratory components of a patient's sample is to verify if the sample was indeed an arterial sample. This is especially important because ventilatory function cannot be evaluated from venous blood. If the hemoglobin saturation (SpO2) is >85% the sample is most often assumed arterial. Saturations less than 75% are most likely venous samples and values between 75-85 are a gray zone and can depend on the severity of pulmonary disease. Certain circumstances may account for very low saturations. A mixed arterial/venous sample, high altitude, or significant lung disease may be responsible. Once a sample has been identified as arterial the next step is taken to quantify respiratory function. Calculation of the alveolar (PaO2)-arterial (PaO2) oxygen gradient, commonly referred to as the A-a gradient, gives an estimate of the effectiveness of gas transfer while accounting for the extent of ventilation. A-a gradients are based on theory that the majority of oxygen that enters the lungs should pass into arterial circulation. As lung function decreases the oxygen gradient (difference) between the alveoli and the arterial capillaries increases. At sea level, patients with normal lung function breathing room air (21% oxygen) will have an A-a gradient ranging from 0-10. Values of 10-20 may be considered mild pulmonary dysfunction and values > 20 would be considered moderate pulmonary dysfunction. Patients exhibiting A-a gradients of >30 would require careful assessment of ventilation to determine if mechanical ventilation is required. A-a gradients should only be evaluated for patients breathing room air and a reasonably accurate barometric pressure should be determined. Calculating an A-a gradient is as follows:

PaO2 = (barometric pressure – water vapor pressure) x FIO2 – 1.2 x PaCO2

A-a gradient = PaO2 – PaO2

PaO2 (partial pressure of alveolar oxygen) is calculated using the factors; barometric pressure at sea level is 760mmHg; water vapor pressure is 47mmHg; FIO2 is fractional inspired oxygen concentration (21%); 1.2 is the respiratory quotient (value ranges from .8 – 1.2). PaCO2 and PaO2 (partial pressure of arterial gases) are obtained from the arterial blood gas sample. Another approach to calculating A-a gradient is a more simplified equation that can only be used when at sea level. At sea level, water vapor pressure (roughly 50) is subtracted from barometric pressure (760) then multiplied by inspired room air oxygen concentration (21%). This gives a PaO2 value of 150. Equation form this would look like (760-50) x .21 = 150. This simplified formula provides a constant value of PaO2 as long as a patient is breathing room air at sea level. Putting in the respiratory quotient and the values from the arterial blood gas gives a simplified A-a gradient calculation of:

A-a gradient = [150 – PaCO2(1.1)] – PaO2

Again A-a gradients are not accurate when a patient is receiving supplemental oxygen. PaO2/FIO2 ratio is a calculation used for patients receiving supplemental oxygen. A general rule of thumb is that the PaO2 should equal roughly 5x the inspired oxygen concentration. PaO2/FIO2 ratio would be helpful for patients maintained on a ventilator or anesthetized patients. In normal lung function PaO2/FIO2 ratio is nearly 500mmHg and values below 200 indicate severe venous admixture. Calculating PaO2/FIO2 ratio of patients receiving nasal or mask oxygen is not practical since the inspired oxygen concentration would be difficult to determine. This usually warrants taking the patient off oxygen for 5-10 minutes in order to calculate an A-a gradient on room air. Serial monitoring of A-a gradients on room air will give the clinician objective information on a patients progress.

References available on request

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