1
Cardiopulmonary Function

E. Christopher Orton

A major function of the cardiopulmonary system is to deliver oxygen to tissues and eliminate carbon dioxide generated by tissue metabolism. To accomplish these functions, the respiratory and cardiovascular systems must act in close concert. Compromise of either system—or both systems—can adversely affect the outcome of animals undergoing thoracic surgery. The ability to quickly assess cardiopulmonary function and pinpoint the cause and severity of problems is firmly grounded in an understanding of cardiopulmonary physiology and pathophysiology. This ability is a core skill for those who undertake interventions in the thorax.

The Oxygen Pathway

The oxygen pathway is a clinically useful concept that provides a logical framework for evaluation and correction of disturbances in the cardiopulmonary system (Figure 1.1). It considers the transport of oxygen as a sequential, step-by-step process beginning with atmospheric oxygen and ending with oxygen delivery to tissues. Each step in the pathway is critically important and must be assessed independently to assure adequate overall cardiopulmonary function. The steps of the oxygen pathway can be viewed as a clinical checklist for monitoring cardiopulmonary function in animals before, during, and after thoracic surgery. Steps in the pathway include ventilation, pulmonary gas exchange, hemoglobin saturation, hemoglobin concentration, oxygen content, cardiac output, and oxygen delivery.

Figure 1.1 Oxygen Pathway

Ventilation

Ventilation is the mechanical process that causes air (a mixture of gases) to flow into and out of the lungs. Not all gas flow (L/min) into the respiratory system reaches areas of gas exchange; consequently, total ventilation or minute volume (VT) is divided between alveolar ventilation (VA), where gas exchange occurs, and dead space ventilation (VD).

Anatomic dead space ventilation includes gas flow to anatomic areas not normally involved in gas exchange. Physiologic dead space includes anatomic dead space, as well as flow to alveoli that are ventilated but not receiving pulmonary blood flow. While anatomic dead space remains constant, physiologic dead space changes depending on the number of functioning alveoli. Furthermore, the ratio of VD to VA changes with the respiratory rate and tidal volume and cannot be easily determined clinically. For example, an animal that is panting increases VT and VD several-fold without necessarily changing VA. Thus, the adequacy of VA cannot be determined by just measuring VT.

Carbon Dioxide Tension

The primary drive for alveolar ventilation is arterial carbon dioxide tension (PaCO2). Under physiologic conditions, the central respiratory center drives VA to keep PaCO2 at about 40 mm Hg, regardless of the total amount of carbon dioxide produced (VCO2) based on the size, metabolism, and activity level of the patient. This relationship of PaCO2, VA, and VCO2 is described by Equation 1.2, where K is a conversion constant:

By definition, hypoventilation is present when VA fails to match VCO2, and as a result, PaCO2 increases (i.e., > 40 mm Hg for animals at sea level). Conversely, hyperventilation is present when VA exceeds what is necessary to eliminate VCO2 causing PaCO2 to decrease (i.e., < 40 mm Hg at sea level). Thus, in the clinical setting, adequacy of ventilation is determined by PaCO2 from a blood gas analysis. If PaCO2 is normal based on the regional normal value, then ventilation to the gas exchange regions of the lung is considered adequate. (Note: The regional normal value of PaCO2 is altitude dependent because animals that reside at higher altitudes increase relative VA to compensate for lower inspired oxygen tension.)

Alveolar Gas Equation

Because arterial oxygen tension (PaO2) cannot be higher than alveolar oxygen tension (PAO2), PAO2 is critically important to all subsequent steps in the oxygen pathway. PAO2 is not measured clinically, but can be estimated from the alveolar gas equation:

From above equation, it is apparent that PAO2 is a function of the inspired oxygen tension (PIO2), PaCO2 (and thereby VA), and the respiratory exchange ratio (R). The respiratory exchange ratio is the ratio of oxygen consumption (VO2) to VCO2. The respiratory exchange ratio can be determined by indirect calorimetry, but this is not routinely done in the clinical setting. In a study of dogs evaluated by indirect calorimetry, R was found to be 0.76 in postoperative or post-trauma dogs compared to an R of 0.84 in normal dogs [1]. For purposes of the above calculation, R is generally assumed to be 0.8. The PIO2 is determined by the fraction of inspired oxygen (FIO2, 0.21 in ambient air), barometric pressure (PB, 760 mm Hg at sea level), and the vapor pressure of water (PH2O, 47 mm Hg at 100% saturation and body temperature):

Thus, the PIO2 of room air at sea level is approximately 150 mm of Hg. From the above equation, it can be seen that either barometric pressure or FIO2 can alter PIO2, and, in turn, the PAO2. Substantial change in barometric pressure is most likely to result from residence at altitude, whereas FIO2 is altered clinically by administration of supplemental oxygen. Increasing FIO2 to 40% nearly doubles PIO2 and increases PAO2 without changing VA.

Alveolar ventilation is the other major determinant of PAO2. The alveolar gas equation predicts that an animal breathing room air at sea level with a PaCO2 of 40 mm Hg would have a PAO2 of approximately 100 mm Hg:

A rule of thumb, for every 1 mm Hg elevation in PaCO2, there will be approximately a 1.25 mm Hg decrease in PAO2 (and PaO2).

Hypoventilation

Adequate ventilation requires central respiratory centers, spinal pathways, peripheral respiratory nerves, primary respiratory muscles, pleural-pulmonary coupling, and pulmonary mechanics to be intact or normal. Hypoventilation occurs when any component of this pathway is disrupted or abnormal. Important causes of hypoventilation include depression or injury of the central respiratory center, injury or disease of the neuromuscular apparatus of ventilation, disruption of pleural-pulmonary coupling (e.g., pneumothorax), and/or abnormal pulmonary mechanics that increase the work of respiration to levels that cannot be sustained by the patient. The major determinants of respiratory work are airway resistance and lung compliance. Obstructive airway disorders or restrictive lung conditions, or both, increase respiratory work leading to hypoventilation when they are severe.

Breathing Patterns

Clinical assessment of ventilation should include observation of breathing. The first indication that a patient is hypoventilating may come from the simple observation that ventilatory excursions are poor. Information about abnormal pulmonary mechanics is gained from observation of the pattern of breathing. Animals adopt a respiratory rate and pattern that minimizes respiratory work. Normal breathing balances the major elastic force of lung compliance with the major viscous force of airway resistance. Elastic forces in the lung are minimized by a rapid and shallow breathing pattern, whereas resistance forces in the lung are minimized by a slow and deep breathing pattern (Figure 1.2). Thus, animals with restrictive lung diseases (e.g., pulmonary edema, interstitial pneumonia, pulmonary fibrosis, pleural effusion) will adopt a rapid and shallow breathing pattern, whereas animals with airway obstruction (e.g., laryngeal paralysis, bronchoconstriction) will tend to adopt a slow and deep pattern of breathing. Obstructive breathing patterns can be further assessed by observing of the phase of respiration that produces the most ventilatory effort. Upper airway obstruction causes an exaggerated effort during inspiration, whereas lower airway obstruction causes an exaggerated effort during expiration.

Figure 1.2 Work of Breathing

Tidal Volume and Minute Volume

Total ventilation can be measured directly with a respirometer attached to an endotracheal tube or tight-fitting mask. Tidal volume is the volume (mL) of gas expired during each breath and is normally at least 10 mL/kg of body weight. Minute volume (VT) is the total volume of gas expired each minute (L/min). If tidal volume or minute volume are low, there is a good possibility that ventilation is inadequate. However, because VT includes both VD and VA, measurement of a normal tidal volume or minute volume does not assure that VA is adequate.

Arterial Carbon Dioxide Tension

Ultimately, clinical assessment of alveolar ventilation is based on the PaCO2. By definition, a patient is hypoventilating when hypercapnia (increased PaCO2) present. The most direct method of assessing PaCO2 is by arterial blood gas analysis. Alveolar ventilation should be considered inadequate when the PaCO2 is > 45 mm Hg for patients at or near sea level. Hypoventilation causes both hypoxemia and respiratory acidosis. Administration of supplemental oxygen (i.e., increasing the FIO2) corrects hypoxemia caused by hypoventilation by increasing the PIO2 and PAO2 (see the...