Physical Examination and Radiographic Studies
On physical examination in a spontaneously breathing patient, one can often recognize diaphragm dysfunction by reduced auscultation of breath sounds on the side of the dysfunction. Even with diaphragm paresis in the absence of true paralysis, one can generally hear reduced breath sounds. When diaphragm elevation is marked in the setting of paralysis, there are often nearly absent breath sounds at the base on the involved side.
Auscultation, however, provides on a very crude estimate of diaphragm dysfunction, and there are of course many other disease processes that can cause reduced breath sounds from which diaphragm dysfunction must be distinguished. In clinical practice, then, the main means of establishing diaphragm dysfunction in spontaneously breathing patients (i.e., nonventilated patients) are (1) the position of the diaphragm on radiographic examinations and (2) diaphragm fluoroscopy.
Essentially any study that images the chest and upper abdomen can suggest the possibility of diaphragm dysfunction by demonstrating elevation of the diaphragm above its normal position. It is important to remember, however, that different radiographic studies are performed with the patient in different body positions, and that the dysfunctional diaphragm will move to markedly different apparent degrees of elevation depending upon the body position of the patient. For example, a patient with diaphragm paralysis will usually demonstrate far less elevation of the involved side of the diaphragm on a PA and lateral chest radiogram (which is obtained with a patient standing upright) than on the scout films from a computed tomogram (CT) of the chest (which is obtained with the patient fully supine) (Fig. 148-5). I suspect that many dyspneic patients have been misdiagnosed to have normal diaphragm function on the basis of PA/lateral chest radiogram showing near-normal diaphragm position.
PA upright chest radiogram and computed tomogram of the same preoperative patient with a paralyzed right hemidiaphragm. Note that the diaphragm nearly reaches the carina on the CT taken in a supine position, whereas on the upright radiogram the elevation is far less impressive.
Diaphragm fluoroscopy (often termed the “sniff test”) examines the movement of the diaphragm in real time as the patient is asked to breathe deeply. A diaphragm that is paretic but not paralyzed may show some, but a reduced degree of, descent with deep inspiration, or it may show no motion at all. A fully paralyzed diaphragm will generally show paradoxical elevation during inspiration. This is because the involved side of the diaphragm not only fails to contract and thus fails to descend, but also actually rises in response to the increased negative pressure created in the ipsilateral pleural space as a result of contraction of the uninvolved, fully contractile, contralateral side of the diaphragm. When the intact side of the diaphragm contracts, it conveys a strong negative pressure to its ipsilateral pleural space, which is then conveyed to a lesser degree through the mediastinal structures to the contralateral pleural space, which will therefore result in mild paradoxical elevation of the paralyzed diaphragm.
It is important to remember that there are degrees of diaphragm dysfunction, any of which may cause a patient to be dyspneic, and which may result in less than classic findings on fluoroscopy. In fact, a patient may be dyspneic when the diaphragm is elevated but fully contractile (termed an eventration). In this situation, the phrenic nerve may be fully intact, but a structural weakness of the diaphragm muscle leads it to assume a more elevated position. An eventrated diaphragm may descend nearly normally on diaphragm fluoroscopy, but more commonly it appears to descend incompletely, or there may be portions of the diaphragm that descend normally while others do not. Some portions may actually show paradoxical motion. With an eventration, even though the diaphragm may descend, thereby reducing intrapleural pressure and causing inspiration as in normal diaphragm function, if the muscle is significantly elevated it may cause atelectasis of the lung, ventilation/perfusion mismatch, and shunting, which may themselves be causes of dyspnea.
Changes in diaphragmatic electrical activity reflect various aspects of diaphragm contraction. Although perhaps less clinically useful than measurement of maximal inspiratory pressure (MIP) (see below), the “compound motor action potential” (electromyography [EMG] signal) measured at the skin level does correlate with force of contraction. Other information, for example, on whether the diaphragm is fatiguing, can also be learned from more detailed evaluation of the EMG signal characteristics. Phrenic nerve conduction time can be measured with electrodes placed over the rib cage and stimulation of the nerve in the neck. Although not a primary mode of evaluating diaphragm paralysis – a diagnosis which is more easily established by fluoroscopy – nerve conduction time can be useful in the evaluation of phrenic nerve dysfunction when the diagnosis is in doubt.
Maximal Inspiratory Pressure
The most commonly used and clinically useful means of measuring the overall strength of diaphragm contraction are measurements of the maximal amount of negative inspiratory pressure that can be created by a patient at the level of the mouth. Although rarely ordered preoperatively in the evaluation of surgical patients, most pulmonary function laboratories are equipped to measure the MIP. This is done by having the patient inspire maximally from residual volume against an obstructed mouthpiece with only a small leak. It has been suggested that in cardiac surgery, preoperative MIP and MEP are associated with the need for prolonged postoperative ventilation.8 To my knowledge, a study of whether preoperative MIP is an independent determinant of postoperative pulmonary complications in general thoracic surgical patients has never been carried out.
In the intensive care unit, MIP is commonly used as one of the determinants of whether a ventilated patient is “ready to wean.” There are a number of studies that correlate successful weaning with higher levels of inspiratory pressure that are able to be generated. A MIP of less than 30-cm water is generally considered insufficient to support successful weaning. However, more complex formulas combining MIP, respiratory load, and/or minute ventilation have also been proposed to predict successful weaning.9
Although used primarily in research applications, the force of diaphragmatic contraction can be more precisely measured by measuring the transdiaphragmatic pressure (Pdi) that is generated and plugging this into a formula that allows calculation of the force of contraction. The Pdi is measured by placing a catheter perorally that has both intraesophageal and intragastric balloons that can measure the intrathoracic and intraabdominal pressures, respectively. The difference between intrathoracic and intraabdominal pressures is the Pdi. Pdimax can be measured while having awake patients inspire maximally against a nearly occluded mouthpiece, or while maximally stimulating the phrenic nerves in the neck in sedated, intubated patients.
Since a variety of factors affect the force of contraction from breath to breath, clearly the more objective measure of diaphragm function is the Pdimax measured during maximal bilateral phrenic nerve stimulation. Since this value is designed to measure the force the diaphragm can create when all of its muscle fibers are maximally recruited, it is a measure that is relatively reproducible and can be used to follow diaphragm function over time far more precisely than with measures such as MIP.