William E. DeTurk & Lawrence P. Cahalin
INTRODUCTION
The reader may recall that Chapters 9 and 10 presented information on pulmonary and cardiac evaluations. This information included tests and measures appropriate for diagnosis and measurement of cardiac and pulmonary status. Heart rate and blood pressure (BP) determination as well as pulse oximetry and evaluation of ventilatory muscle function were also included. Chapter 11 introduced electrocardiography, which provided another important measurement tool. However, knowledge of examination, instrumentation, and procedures is only part of the picture: During an exercise session, the clinician must also interpret these data and decide what to do with the information once it is acquired. Use of this information may be confined to deciding whether or not to stop exercise. Certainly this would be an appropriate first consideration. Just as important is the synthesis of this information with therapeutic interventions that optimizes outcomes. Examination and intervention are thus dynamic processes that are not only restricted to the therapist–patient relationship. Appropriate documentation and consultation may also bring in other members of the multidisciplinary team—the nurse, cardiologist, and social worker, for example. A physical therapy program that utilizes ongoing continuous evaluation, blended with treatment, and integrated with documentation that incorporates other members of the health care team would appear to optimize results. Indeed, such an approach is of benefit in at least three ways: (1) It enhances the physical therapist’s ability to develop an effective exercise prescription, (2) it provides the referral source with information elicited during an exercise state; information that might not be otherwise available, and (3) it ultimately benefits the patient, the recipient of the combined care of both the physical therapist and the other members of the health care team.
This chapter* has two sections. The first portion will present pathophysiological processes that limit exercise capacity. These processes will be summarized in two cardiopulmonary hypothesis–oriented algorithms—one for patients with cardiovascular disease and the other for patients with pulmonary disease. These can be used to direct the physical therapist’s actions by assignment of exercise response into categories subsumed under them. The second part of the chapter will apply the algorithms to two case studies of patients with cardiopulmonary disease. In this way, the chapter will provide a systematic approach to patient management during an exercise session and will highlight hypothesis testing as a means of identifying impairments and functional limitations in patients who are limited by cardiovascular or pulmonary disease. This chapter will also prepare the reader for subsequent discussion of patient management strategies for an overall plan of care, found in the six preferred practice pattern chapters.
This chapter will serve to reinforce an important point: Ongoing, systematic examination and evaluation during treatment may be important determinants for an overall plan of care. Practical tips on how to make accurate measurements and how to document the findings are also included.
HYPOTHESIS TESTING AND THE ALGORITHMS
As discussed in Chapter 2, a diagnosis of “ischemic heart disease” or “chronic obstructive pulmonary disease” does not provide specific information about the nature of the disablement as it relates to the status and location of the impairment. Neither do such diagnoses guide the practitioner toward specific treatment interventions. The exercise response categories found in the hypothesis-oriented algorithms in this chapter are designed to be used during individual treatment sessions. They include sets of questions that are appropriate to each of the categories. A positive response to any given question assists the therapist in “ruling in” the patient to that category and is part of a general hypothesis-testing approach that is integral to the proper use of the algorithms. In this chapter, hypothesis testing is defined as an approach to patient care whereby the therapist applies the algorithm to the patient through the formulation of questions about findings that, when answered, either supports or refutes the inclusion of the finding in the appropriate exercise response category. Hypothesis testing may begin at the level of subjective complaints of chest pain or shortness of breath (SOB) during exercise, for example. It may continue as additional information is gathered through the use of an electrocardiogram (ECG) telemeter or pulse oximeter. Hypothesis testing culminates in the synthesis of all the obtained data, at which point the therapist places the patient in the most appropriate exercise response category and reaches conclusions about the feasibility of exercise continuance. Along the way, additional information is obtained as regards the location of impairments and the nature of the functional limitations. This information is then used to direct subsequent treatment. Hypothesis testing may be used to direct a total plan of care. However, the hypothesis testing that drives the algorithms in this chapter is part of a dynamic, ongoing process that occurs during an exercise session.
EXERCISE DOSAGE
It is not uncommon for the physical therapist to receive referrals for patients who are in need of “exercise conditioning” or “endurance training.” These patients may or may not be patients whose primary diagnosis is cardiac or pulmonary disease; however, all should undergo some sort of an initial exercise test. This need not be a formal treadmill protocol with cardiologists in attendance. It can be, and often is, performed by the physical therapist and may consist of climbing up flights of stairs, walking down the hall, or exercising with an arm-crank ergometer. Although not traditionally interpreted as an exercise test, examination of the cardiovascular and pulmonary responses during bouts of physical exertion yields information that may be just as important as traditional exercise testing.
CLINICAL CORRELATE
The concept of both exercise testing and training, however, is that exercise should be treated like a drug: A measured “dose” should be administered to the patient, and future “doses” should be based on the patient’s response to exercise.
It is important to quantify the amount of exercise that a patient is given. This can be expressed in a number of ways. It may be simply the total distance walked, usually coupled with the time it takes. It may be the workload, for example, watts on a cycle ergometer, and the time spent exercising. The data obtained during such testing should include heart rate (HR) and systolic blood pressure (SBP), which, when multiplied, is expressed as the rate–pressure product (RPP). The RPP is highly correlated with both myocardial oxygen consumption, systemic oxygen consumption, and cardiac output. Measurement of HR and BP at rest, peak exercise, and at periodic points along the way (depending on the patient) will help ensure patient safety and be used later to write the exercise prescription. Use of pulse oximetry, the dyspnea index (DI), and measurement of respiratory rate may be important additions to HR and BP when monitoring patients with pulmonary disease.
Information obtained from the exercise evaluation can be used to place the patient into any or multiple categories of exercise intolerance that may be subsequently used to direct treatment interventions. For patients with cardiac disease, these categories include arrhythmia, ischemia, cardiovascular pump failure, and cardiovascular pump dysfunction. For pulmonary disease, these categories include poor oxygenation, ventilatory pump dysfunction, ventilatory pump failure, and pulmonary hypertension.
EXERCISE LIMITATIONS IN CARDIAC DISEASE
Arrhythmia
It is not uncommon to find that a patient’s pulse is irregular prior to exercise. Some therapists may dismiss this finding as unimportant, and place the patient in an unmonitored exercise program, thereby exposing the patient to unnecessary risk. Other therapists may be tempted to make a guess as to the origin of the “skipped beats.” This temptation should be resisted. The most common arrhythmias include premature atrial complexes (PACs), premature ventricular complexes (PVCs), and atrial fibrillation. There is no way of knowing the true cause of the irregularity—unless the patient is hooked up to an ECG machine. Many therapists do not have access to an ECG telemeter (a device consisting of a radiotransmitter and an oscilloscope that enables one to look at the ECG complexes). However, most therapists can borrow a standard 12-lead unit with a paper printout. What is seen may very well determine how the patient is treated. In general, PACs are not as significant as PVCs: Loss of adequate filling and contraction of the atria are not as hemodynamically disruptive as premature contractions within the ventricles. Occasional isolated PACs present no particular problem to the patient—unless those PACs are hemodynamically compromising. Patients can present with very rapid (200–300 beats per minute [bpm]) atrial arrhythmias that produce reduction of forward blood flow and decreased BP. Symptoms of dizziness, light-headedness, or even syncope can result. Physical therapists should check with the patient for the presence of symptoms when irregular pulse rhythms are palpated. In order to maximize accuracy, physical therapists should measure the HR for 1 full minute by palpating the peripheral pulse. Electrocardiography/radiotelemetry should be utilized, when available, to determine the exact type of arrhythmia.
Evaluating the Significance of PVCs
PVCs are quite common in the setting of coronary artery disease and require further discussion. They are characterized by complexes that are usually wide, bizarre looking, and premature. PVCs originate from an ectopic focus (or multiple foci) within the ventricles (see Chapter 11). Like PACs, these complexes do not necessarily present a problem: PVCs are present in roughly half of healthy normal adults. In this population, PVCs may present themselves during times of emotional stress, upon lying down at night, or after caffeine ingestion. Occasional PVCs in a normal population are usually well tolerated because the myocardium is healthy and nonischemic. The significance of PVCs in patients with heart disease is more ominous. The myocardium from which these PVCs arise is oxygen deprived. These PVCs occur as a result of spontaneous depolarization of irritable foci, through either reentry or blocked conduction1 (see Chapter 11). The following are key concepts in understanding the significance of PVCs:
1.PVCs can present a problem to the patient for two reasons. When they occur as a run of PVCs at a rapid rate (ventricular tachycardia, or VT), they can be hemodynamically compromising. This rhythm can also degenerate into a lethal arrhythmia (ventricular fibrillation) that is difficult to terminate.
2.The significance of PVCs is based on the company they keep. Healthy, normal hearts can tolerate an occasional PVC very well without sacrifice of forward blood flow or degeneration into ventricular fibrillation. PVCs in the presence of ischemic heart disease, however, take on added significance, and some physicians might treat frequent PVCs in this latter group with anti-ischemic or antiarrhythmic drugs.1
The first appearance of PVCs may be at rest, when the patient is first connected to the ECG machine or radiotelemeter. The question that may be asked by the physical therapist when confronted by PVCs at rest is as follows: What happens to them during exercise? It is an important question and one that the physical therapist is in perhaps a unique position to answer. There are three possibilities:
1.The PVCs decrease with exercise. This is a good response to exercise. It indicates that the PVCs get suppressed by a higher-order pacemaker (overdrive suppression) as physical activity (and HR) increases.
2.The PVCs increase with exercise. This is a less desirable response, as it indicates that the PVCs may be ischemic in origin. Normally quiescent foci become irritable and fire as myocardial O2 demand outstrips the supply of oxygen available to it.
3.There are PVCs at rest and with exercise that do not change during exercise. The most that can be said about these PVCs is that they are unrelated to exercise.
To document this response, resting PVC activity should be quantified and qualified. The clinician should take a moment to examine the resting rhythm. The number of PVCs per minute should be counted. The characteristics of the waveforms should then be evaluated. PVCs may be unifocal or multifocal, or interpolated, or appear as an R-on-T phenomenon. They may occur in a regularly recurring pattern, for example, trigeminy, bigeminy, or PVC pairs. Categorization of PVC activity will help to determine their overall significance. Multifocal complexes are more significant than unifocal complexes; R-on-T phenomenon can predispose to ventricular tachycardia; closely coupled (eg, paired) PVCs are more significant than distant (eg, trigeminal) PVCs2 (see Fig. 12-1).
FIGURE 12-1 Examples of PVC morphologies. (A) Multifocal PVCs; (B) interpolated PVC; (C) R-on-T PVC; (D) bigeminal PVCs; (E) PVC couplets; (F) ventricular tachycardia. (Reprinted from DeTurk WE. Exercise and the intolerant heart. Clin Manag. 1992;12(1):67-73, with permission of the American Physical Therapy Association. Guide to Physical Therapist Practice. 2nd ed. Phys Ther. 2001 Jan;81(1):9-746.)
Following the evaluation of resting PVC activity, the physical therapist may elect to evaluate PVC behavior during exercise. As the patient begins to exercise, there may be an increase in ectopic activity, another ectopic focus may manifest itself and the form of the PVC may change, or the PVCs may become coupled closer together. Once it is clearly established that PVC activity does increase, exercise should be terminated. Document these findings, and refer the patient back to the physician or other referral source on the same day. It should be noted that there may be diurnal variability to PVC frequency; therefore, the time of the day of the treatment session and the relationship of the session to the last meal should also be noted. It is important not to draw hasty conclusions about the importance of PVC activity. However, it should be noted that PVCs in the setting of an acute myocardial infarction (MI) are always significant. The physician may follow up the findings obtained during the treatment session with 24-hour ECG Holter monitoring.
Ventricular tachycardia deserves special mention. This is defined as three or more consecutive PVCs that occur at a rate of at least 100 bpm. Its appearance at rest or during exercise is a contraindication to further effort. It is important to document the number of complexes in the run, calculate the rate at which the complexes occur, and notify the referral source. The patient should be observed for further arrhythmias and seen by a physician as soon as possible.
In general, the therapist’s response to ventricular ectopy is a function of two factors. The therapist’s experience in cardiopulmonary physical therapy and their own “comfort level” should be taken into account. Recent graduates, more so than therapists with more experience, tend to be more hesitant in working with patients having ventricular ectopy, and this is appropriate. The work setting is an important factor also. Hospital-based therapists working with a crash cart down the hall and an arrest team close by can evaluate and treat patients more aggressively than those who are employed by an outpatient clinic in a shopping plaza. In both settings, however, the question remains the same: What happens to PVCs during exercise?
Palpitations
Many patients with arrhythmia may complain of skipped beats or “fluttering” of the heart. Therapists should pursue description of this symptom. By inquiring whether the palpitations are rapid, forceful, or irregular in nature, the therapist may gain some insight into their origin. Rapid palpitations are often associated with supraventricular arrhythmias, forceful with exercise, and irregular with ventricular ectopy. These descriptions should be followed up with an ECG evaluation.
CLINICAL CORRELATE
More important is the question of whether the patient’s complaints of palpitations are producing symptoms of light-headedness, dizziness, or syncope. This is a potentially life-threatening problem that must be treated.
Palpitations producing symptoms should be followed up with a formal evaluation, which usually includes Holter monitoring, graded exercise testing or electrophysiologic testing.
Ischemia
Myocardial ischemia occurs when the demand for oxygen by cardiac muscle outstrips the supply of oxygen available to it. This situation frequently arises during exercise with the onset of chest pain or angina. It is usually relieved by rest. There are electrocardiographic changes as well, typically presenting as a downward shift in the position of the ST segment (see Chapters 6 and 11).
Myocardial ischemia produces classic symptoms that can be obtained through a comprehensive patient history. It is typically described as crushing or squeezing in quality and is either precordial or substernal in location. It comes on with exercise and is relieved by rest. There are wide variations in this presentation; the discomfort may go up into the jaw, neck, back, or down to one or both arms; the “chest pain” may present as SOB, particularly among the elderly (see Chapter 6 and the CD-ROM representation for that chapter).
It should be noted that other pathologies may present with similar symptoms. Gastrointestinal disturbances can radiate pain into the chest; musculoskeletal problems (eg, arthritis) can involve pain in the costochondral or sternoclavicular joints. These symptoms, although coming on with exercise, are related to the mechanics of heavy breathing and can be elicited through palpation of the chest wall, thus ruling out chest pain of cardiac origin. Because so many things produce chest pain, it is helpful to know the typical presentation of angina and differential maneuvers that the therapist can perform to rule out other causes. An examination of the patient via electrocardiography can provide additional information and “cinch” the clinical impression.
Various bipolar lead systems have been described.3 Placement of the positive electrode over the apex of the heart and the negative electrode over the sternum, right shoulder, or on the back under the inferior angle of the right scapula usually provide adequate waveform differentiation and maximum sensitivity to changes in the ST segment.
Most facilities recognize a 1.0 mm (0.1 mV) of horizontal or downsloping depression of the ST segment as a criterion for a positive exercise test indicative of myocardial ischemia.4 Upsloping ST-segment depression is usually considered positive when it exceeds 1.5 mm. The measurement is made as shown in Fig. 12-2.
FIGURE 12-2 Measurement of ST segment changes as a criterion for a positive ECG stress test indicative of myocardial ischemia. (Reprinted from DeTurk WE. Exercise and the intolerant heart. Clin Manag. 1992;12(1):67-73, with permission of the American Physical Therapy Association. Guide to Physical Therapist Practice. 2nd ed. Phys Ther. 2001 Jan;81(1):9-746.)
In addition to quantifying the amount of ST-segment depression that occurs during exercise, the response should be qualified. The shape of the ST segment is as important as the amount of depression. Three morphologies of ST segments have been described: horizontal, upsloping, and downsloping (Fig. 12-3). In general, downsloping ST-segment depression is more significant than horizontal ST-segment depression; similarly, upsloping ST-segment depression is less significant than horizontal ST-segment depression. ST-segment elevation that occurs during exercise (a rare finding) could signify coronary artery spasm and/or transmural ischemia and should prompt immediate termination of exercise (see Chapter 6).
FIGURE 12-3 Diagnostic shapes of ST segments. (Reprinted from DeTurk WE. Exercise and the intolerant heart. Clin Manag. 1992;12(1):67-73, with permission of the American Physical Therapy Association. Guide to Physical Therapist Practice. 2nd ed. Phys Ther. 2001 Jan;81(1):9-746.)
There is a moderate relationship between the time spent in exercise and the severity of ischemic heart disease.5,6 Patients who experience ST-segment depression early in an exercise test tend to have more severe ischemic heart disease than patients who become ischemic later in the exercise test, as measured by the number of coronary vessel involvement via angiography. Physical therapists encountering this situation should treat these patients conservatively. Additionally, patients who become ischemic during exercise may remain ischemic for a protracted period of time in the postexercise recovery period. It may take many minutes before myocardial blood flow is fully restored. Therefore, the time of recovery from ST-segment depression should also be noted. These patients need more conservative management, as they tend to demonstrate more advanced disease.6,7
CLINICAL CORRELATE
If the patient develops chest discomfort during exercise, it is important that exercise be terminated at once if other possible causes of the chest discomfort have already been ruled out.
The patient should be positioned in a semifowlers or seated position if such positions are tolerated without light-headedness. A supine body position should be avoided, as this position will enhance venous return, which is likely to increase the work of the heart, thereby increasing myocardial ischemia. The level of exertion that provokes symptoms is called the anginal threshold. The workload and/or HR at which the patient becomes symptomatic should be noted. This is important to the physical therapist because this information can be used to formulate a safe exercise program. The physical therapist may also decide to teach the patient how to take his or her own pulse and then instruct the patient not to exceed the HR at which myocardial ischemia becomes manifest. Documentation of the anginal threshold is also useful to the referral source who may want to prescribe, or adjust, cardiac medications to enhance the patient’s tolerance to exercise.
Documentation
If the patient is monitored via electrocardiography, it is important to obtain a paper printout at both rest and peak exercise. Therapists should measure the amount of ST-segment depression, characterize the morphology, note the HR and BP, and state what the patient was doing. For example:
Ms. R terminated treadmill walking because of the onset of chest pain and 1.5 mm of downsloping ST-segment depression in the lateral precordial leads. Peak exercise HR was 134 bpm and BP was 158/84 mm Hg.
Cardiovascular Pump Failure
The third category, which may be responsible for intolerance to exercise, is cardiovascular pump failure, which is combined with cardiovascular pump dysfunction to form the Guide’s preferred Practice Pattern 6D.8 In the setting of the acute response to exercise, cardiovascular pump dysfunction is often a sequela to cardiovascular pump failure. Therefore, heart failure will be discussed separately from dysfunction.
Cardiovascular pump failure may be abbreviated to pump failure and is also known as heart failure (HF). Many therapists associate SOB with this pathology, but SOB alone is not a very specific finding, because SOB can also be due to pulmonary dysfunction, physical inactivity, or even anxiety. Additional information is required to rule out the other causes and to rule in pump failure.
It is important to obtain a good patient history. The therapist may ask, “Do you ever get unusual SOB?” If the answer is yes, the response may be quantified by asking “How many blocks/stairs can you walk before you have to stop because of SOB?” Responses limited to a description of SOB may be of little help, because patient responses vary widely, from “air hunger” to panting. It is helpful to ascertain the presence of SOB at rest, using the methods described in Chapter 9. Ask about the number of pillows the patient slept on at night, and whether, if those pillows were removed, the patient would then get SOB. The presence of paroxysmal nocturnal dyspnea (PND) should also be ascertained. The patient goes to sleep without symptoms but wakes up several hours later acutely short of breath and has to sit up for relief. The feeling subsides and the patient returns to bed. This scenario is typical of patients with paroxysmal nocturnal dyspnea and is most likely associated with pump failure.
Common causes of cardiovascular pump failure include MI, cardiomyopathy, and valvular heart disease. It is useful to differentiate between left-sided and right-sided pump failure. In left-sided failure, the left side of the heart cannot pump out all the blood that is delivered to it by the right side. The pressure builds up in the left ventricle and is reflected backward, up through the left atrium and into the lungs. The lungs become wet, stiff, soggy, and difficult to move, hence, the feeling of SOB. In patients with heart disease, right-sided failure is usually the result of left-sided failure. The pressure, due to a restriction in forward flow, now passes through the lungs and gets reflected through the right ventricle and right atrium and into the venous circulatory system. However, patients with pulmonary disease can have pump failure confined to the right side.
Signs and Symptoms of Cardiovascular Pump Failure
Patients can present in chronic pump failure at rest or can develop transient pump failure during exercise. Before proceeding with exercise, it is important to check for signs and symptoms of left-sided pump failure at rest. Patients with pump failure at rest should not be exercised and should be tested only in a safe, well-equipped setting with appropriate medical backup. The objective of a resting pump failure evaluation is to verify its absence at rest and then to identify the point during exercise at which the patient goes into failure.
The therapist should listen to the heart sounds with a stethoscope, at rest, and immediately following exercise. One of the hallmarks of cardiovascular pump failure is the presence of an S3 heart sound. It is a very low-pitched sound, heard best with the bell of the stethoscope placed lightly on the chest wall over the apex of the heart. S3 follows close on the heels of the second heart sound. It is, at best, difficult to hear, but its presence is highly significant. The lungs should be auscultated for the presence of crackles. These adventitious sounds are discrete, popping sounds that are heard primarily during inspiration. Unlike pulmonary crackles, they do not clear with a cough. Crackles, like the S3 heart sound, can be absent at rest but come on during exercise, indicating that the workload is too strenuous and producing transient pump failure. The therapist’s clinical response is similar to that of arrhythmia and ischemia: Mark the onset of these signs by noting the workload, HR, and BP, and then stop exercise and adjust the exercise regimen accordingly.
CLINICAL CORRELATE
It is important to avoid placement of a patient with cardiovascular pump failure in supine during recovery; this will increase the volume of blood that the heart has to pump out and exacerbate the patient’s symptoms. Rather, the patient’s upper chest and head can be propped up with pillows, or the head of the bed can be cranked up, or the patient can be seated in a chair.
Cardiovascular pump failure will be discussed in greater detail in Chapter 18.
Cardiovascular Pump Dysfunction
The fourth classification of exercise intolerance is specific to patients with overt, manifest heart disease, usually those patients recovering from MI. The term dysfunction refers to residual mechanical pathology as the result of myocardial necrosis or ischemia. Radionuclide imaging recognizes three kinds of pump dysfunction: left ventricular (LV) wall hypokinesis, akinesis, and dyskinesis. Normal myocardial fibers contract together in a spiral, corkscrew fashion around a given volume of blood to effect systolic ejection. Damaged myocardium contracts only slightly (hypokinesis), fails to contract (akinesis), or balloons out the other way (dyskinesis). This latter category represents ventricular wall aneurysm.
Patients in the early recovery period of MI are subject to LV pump dysfunction. One clinical reflection of LV pump dysfunction is the presence of an S3 heart sound, described previously. Three other clinical findings should be of interest to physical therapists because they can be exercise related. The first of these is the appearance of ST-segment elevation at rest on ECG in leads with a significant Q wave. When present, it may represent the residual effects of the MI (eg, aneurysm) and should be noted as such. This finding should not be confused with ST-segment elevation during exercise in non–Q-wave leads, which represents a markedly positive test for ischemic heart disease, because of coronary artery vasospasm (see Chapter 6).
The second finding is the murmur of mitral regurgitation, appreciated during auscultation of the heart. It is an adventitious, blowing type of sound that occurs between S1 and S2. It is relatively high pitched and therefore heard best with the diaphragm of the stethoscope applied to the apical area of the heart. In the setting of MI, it frequently represents papillary muscle dysfunction. In this latter case, the murmur is invariably associated with an S4 heart sound and often with a loud S1.
ST-segment elevations and murmurs may be absent at rest. The physical therapist who can detect these findings during exercise and report their presence to the physician or other referral source is making a substantial contribution to the care and well-being of the patient.
The third finding is more problematic because it requires not only accurate assessment but also immediate response. This is a fall in SBP during exercise. Although both diastolic and SBPs are important when making a resting determination of the presence of hypertension, during exercise the SBP assumes preeminence. This is because the SBP more accurately reflects the functional state of the left ventricle.
When a patient first begins to exercise, there may be an early, transient drop in SBP. This is most likely due to regional changes in blood distribution (shunt); as exercise continues, pressure will usually rise. One should be particularly concerned when an increase in exercise workload fails to elicit a normal SBP response (usually 10–20 mm Hg per stage), or if there is a fall in SBP during moderate exercise. Absence of a rise in SBP during exercise, or a “flat response,” may also signify evolving cardiovascular pump dysfunction.
When the patient complains of dizziness during exercise, the therapist should protect the patient from injury and document the findings. Instruct the patient to tell you if these symptoms become more severe; then immediately take the BP again. If SBP is dropping, continue to monitor and check with the patient and take serial BPs until a definite, inexorable trend has been established. Then stop exercise and place the patient supine.
The previous protocol requires that the therapist become proficient in taking rapid, accurate SBPs. This can be done with practice. The benefits in doing so can be significant: The patient is not “undertreated,” useful information about exercise-induced cardiac function is obtained, and patient safety is assured.
Accurate measurement of diastolic blood pressure (DBP) can be problematic during exercise. During strenuous exercise, the “thump” representing DBP frequently becomes audible “all the way down” the column of mercury and thus loses significance. In this situation, the therapist should use the fourth Karotkoff sound as the measure of DBP. Documentation of this event in the following manner communicates to the reader that the fifth sound was heard all the way down the column of mercury:
Blood pressure on treadmill at 3 mph, 5% grade = 168/85/0.
Elevation of DBP during exercise is a pathologic finding and probably reflects evolving stiffness of the myocardium as a result of ischemia. An elevation in DBP coupled with a fall in SBP with increasing exercise causes a narrowing of pulse pressure and is particularly ominous. If allowed to continue, the patient could lose consciousness. Once again, the physical therapist must protect the patient from injury by terminating exercise and document the findings (see Chapter 10).
Four categories of cardiac effort intolerance have been identified, consisting of arrhythmia, ischemia, cardiovascular pump failure, and cardiovascular pump dysfunction. Figure 12-4 summarizes these response categories as a hypothesis-oriented algorithm that can be used to classify patients with cardiac disease into categories which then may be used to direct treatment.
FIGURE 12-4 Hypothesis-oriented algorithm describing an evaluation approach for classifying patients with cardiovascular disease through the collection of data obtained during exercise. (Modified from DeTurk WE. Exercise and the intolerant heart, part 2. Clin Manag. 1992;12(2):32-39, with permission of the American Physical Therapy Association. Guide to Physical Therapist Practice. 2nd ed. Phys Ther. 2001 Jan;81(1):9-746.)
EXERCISE LIMITATIONS IN PULMONARY DISEASE
Four categories of exercise intolerance will now be presented that are appropriate to patients with pulmonary disease. These categories consist of poor oxygenation, ventilatory pump dysfunction, ventilatory pump failure, and pulmonary hypertension. These response categories are summarized in Fig. 12-5 as a hypothesis-oriented algorithm. Like the cardiac algorithm, this figure subsumes signs and symptoms of pulmonary decompensation under their appropriate headings.
FIGURE 12-5 Hypothesis-oriented algorithm describing an evaluation approach for classifying patients with pulmonary disease through the collection of data obtained during exercise. (Modified from DeTurk WE. Exercise and the intolerant heart, part 2. Clin Manag. 1992;12(2):32-39, with permission of the American Physical Therapy Association. Guide to Physical Therapist Practice. 2nd ed. Phys Ther. 2001 Jan;81(1):9-746.)
The reader may note that SOB is a symptom that is shared by all four categories and, therefore, is of little value in differentiating one response category from the other, or even pulmonary disease from cardiac disease. Nevertheless, the hallmark of pulmonary disease is SOB. This abnormality may be present at rest; however, it may become more pronounced during exercise. Similarly, the decrease in oxygen saturation (SaO2) and resultant cyanosis are shared by all four response categories. Clearly, the best discriminators between categories are those unique to them: retained secretions for poor oxygenation, accessory muscle use and costal retractions for ventilatory pump dysfunction, paradoxical breathing for ventilatory pump failure, and the abrupt onset of symptoms and reduction in oxygen saturation found in patients with pulmonary hypertension.
As noted previously, the decrease in SaO2 and cyanosis are global symptoms of pulmonary disease. Use of a pulse oximeter can be particularly helpful in evaluating the pulmonary system’s ability to transfer oxygen to the blood and then to peripheral tissues. This device consists of a small, portable control unit that is battery powered and a finger sensor connected to the control unit by a cable. The oximeter determines SaO2 by passing two wavelengths of light, one red and one infrared, through the finger to a photodetector. The intensity of the light sources and the differential absorption of light of arterial and venous blood allows calculation of saturation of oxygen on the hemoglobin molecule.9 The accuracy of this device depends on adequate perfusion of the selected finger, the absence of nail polish, and absence of motion artifact. Although determination of SaO2 can be accomplished during exercise, it is recommended that the actual measurement take place immediately after the patient stops exercise in order to minimize faulty readings.
Loss of peripheral oxygen saturation is usually accompanied by increasing cyanosis. This cyanosis may be particularly evident in the fingernail beds and the lips. Indeed, one of the first clinical signs that herald the onset of oxygen desaturation occurs during exercise when the lips take on a “dusky” color. Oxygen desaturation, cyanosis, and SOB are typical findings that cause early termination of exercise among patients with pulmonary disease.
Poor Oxygenation
This response category is related to preferred Practice Pattern 6C: Impaired Ventilation, Respiration/Gas Exchange, and Aerobic Capacity Associated with Airway Clearance Dysfunction. The site of the lesion could be anywhere within the alveolar–pulmonary capillary unit. For example, it could appear on the alveolar side as excessive mucus that impedes gas exchange. It could appear on the interstitial side as a pneumoconiosis, or it could appear more globally as pneumonia. Any or all of these pathologies can account for the findings that are subsumed under poor oxygenation that limit exercise capacity—SOB, retained secretions, decreased SaO2, and cyanosis.
Because SOB is such an important marker of pulmonary dysfunction, its quantification deserves comment. The 0 to 10 category ratio scale used by Borg10 has particular utility, as it relates to the immediate ventilatory response to exercise.11 The DI has also been used to document the degree of SOB obtained during exercise. Both of these scales are described in Chapter 9. The DI is the ratio of the ventilation obtained during exercise (numerator) to the maximal voluntary ventilation (MVV, denominator). The ventilation during exercise is measured via closed-circuit gas analysis. The maximal voluntary ventilation is obtained by multiplying the forced expiratory value in the first second of expiration (FEV1), in liters, by 35. DIs around 0.70 reflect a normal balance between ventilatory demand and ventilatory capacity. DIs greater than or equal to 1.0 are associated with pulmonary disease.12 Either scale may be administered as a pretest to subjects about to undergo exercise. Subjects are then retested using the same scale immediately following exercise. Pretest data are then compared to posttest data in order to measure the effect of exercise on pulmonary function.
The singular finding that differentiates poor oxygenation from the other three response categories is the presence of retained secretions. Indeed, retained secretions alone can cause the other three and thus limit exercise performance.
Disease entities like cystic fibrosis and chronic bronchitis are characterized by copious mucus production. These individuals may possess a strong cough, but the thickness and tenaciousness of the mucus make the cough ineffective in raising secretions. Patients with an ineffective cough are thus doubly jeopardized, in that the excessive mucous production is not matched by an optimal secretion clearance mechanism. Thus, the presence of an ineffective cough may contribute to poor oxygenation.
Many patients who are limited in their exercise capacity because of poor oxygenation respond well to supplemental oxygen. These patients have a relatively intact pulmonary anatomy that allows the increased oxygen to reach the pulmonary artery circulation for subsequent distribution to working skeletal muscle. Those who fail to respond to supplemental oxygen do so because scarring or fibrosis at the level of the alveolar–pulmonary capillary unit does not allow adequate oxygen transfer. Supplemental oxygen may be administered both at rest and during exercise. Highly portable liquid oxygen units deliver oxygen to the patient via nasal cannula and are well tolerated for even 24-hour use.
Secretion clearance techniques include postural drainage with percussion and vibration as well as a myriad of cough facilitation techniques. These interventions may be provided routinely or prior to exercise. Aerobic endurance activities like cycle ergometry or treadmill walking have been used to enhance the removal of secretions by lowering the threshold for spontaneous cough (see Chapter 17).
Ventilatory Pump Dysfunction
This exercise response category is related to preferred Practice Pattern 6E: Impaired Ventilation and Respiration/Gas Exchange Associated with Ventilatory Pump Dysfunction or Failure. Patients with ventilatory pump dysfunction may be placed on a continuum with those demonstrating ventilatory pump failure. The difference between categories is one of degree or advancement of the disease. The hypothesis-oriented algorithm presented in Fig. 12-5separates dysfunction from failure because there are clinical findings that may be used to differentiate them and each calls for a somewhat different set of treatment interventions. Ventilatory pump dysfunction is typically a precursor of pump failure and is characterized by the increased reliance on accessory muscle use and the presence of costal retractions. Depending on the severity of the disease, the potential for the diaphragm to descend during inspiration may or may not be present. Patients with advanced ventilatory pump dysfunction typically present with hyperinflated lung fields that flatten the diaphragm and restrict further descent during inspiration. This finding will negatively influence the patient’s exercise capacity. It is this phenomenon that is reflected in this chapter’s algorithm. A more detailed algorithm reflecting breathing patterns obtained at rest among patients with lung disease can be found in Fig. 20-3.
Patients with ventilatory pump dysfunction may be comfortable at rest, with only a slight decrease in oxygen saturation, and may show only mild accessory muscle use. However, during exercise the patient may complain of increasing SOB. If not already present at rest, this symptom will usually be accompanied by the appearance of costal retractions, a further decrease in oxygen saturation, and concomitant cyanosis. Physical therapists should be attentive to the onset of these findings and terminate exercise when they become prohibitive to further exercise.
Immediately upon exercise termination the patient should be placed supine with the head of the bed gatched up, or the patient may be placed in the seated position with his or her arms supported. The flat-lying position places the ventilatory muscles at a mechanical disadvantage and contributes to SOB and should be avoided. Supplemental oxygen administered immediately following exercise usually restores oxygen saturation levels quickly and relieves SOB. Oxygen use during exercise may also be beneficial. As before, the workload and/or HR at which ventilatory pump dysfunction becomes apparent should be noted. Subsequent exercise “doses” should be administered at an intensity below the threshold that evokes symptoms. Most facilities recognize an oxygen desaturation level less than 85% to 90% as a criterion for exercise discontinuance.
Ventilatory Pump Failure
Like ventilatory pump dysfunction, this exercise response category is related to preferred Practice Pattern 6E: Impaired Ventilation and Respiration/Gas Exchange Associated with Ventilatory Pump Dysfunction or Failure. Ventilatory pump failure may be thought of as the advancement of ventilatory pump dysfunction, as the accessory muscles of ventilation and the diaphragm continue to weaken, which in turn cause further declines in oxygen saturation. It is not surprising that exercise tolerance in these individuals tends to be less than that for those in ventilatory pump dysfunction.
The algorithm in Fig. 12-5 contains signs and symptoms that are found in patients with ventilatory pump failure. The finding that helps to differentiate dysfunction from failure is paradoxical breathing. The reader may recall that, in patients with chronic lung disease, the shortened muscle fibers of the diaphragm and its flattened position prevent the generation of enough negative pressure required to adequately ventilate the lungs. Because the diaphragm has become ineffective, contraction of the muscles of the upper chest must provide the negative pressure to draw air into the lungs. In doing so, the upper chest sucks the abdominal area inward, while the upper chest moves outwardduring inspiration. This is termed paradoxical breathing. This breathing pattern is characteristic of ventilatory pump failure. Ventilatory failure is usually accompanied by deterioration in arterial blood gases, most notably an increase in carbon dioxide and a fall in oxygen tensions.
Paradoxical breathing may be improved by leaning the seated patient forward in a chair or by applying an abdominal binder. If the paradox resolves, the patient may be a candidate for exercise training, and hence appears in this chapter’s hypothesis-oriented algorithm (Fig. 12-5). If paradoxical breathing continues in spite of the forward lean posture, the patient’s level of function is quite low and may require mechanical ventilation. See Chapter 20, Fig. 20-3, which presents an algorithm that provides analysis of this breathing pattern in a resting patient.
Paradoxical breathing may be absent at rest but becomes manifested during exercise. It may also be present at rest and increase in severity with exercise. As before, the workload and/or HR at which ventilatory pump dysfunction becomes apparent should be noted. Future exercise training sessions should occur at an intensity somewhat below the onset of symptoms.
Pulmonary Hypertension
The fourth category of pulmonary intolerance to exercise is pulmonary hypertension. This pathology is not found as a preferred practice pattern per se. However, it is actually a common element in both ventilatory pump dysfunction and failure. Indeed, most patients with chronic obstructive lung disease develop pulmonary hypertension as their disease progresses. It is represented in the hypothesis-oriented algorithm in Fig. 12-5 because, although it may be occult at rest, it will become manifested during exercise.
Patients with chronic bronchitis and emphysema typically demonstrate chronic hypercapnia and hypoxia. Hypoxic pulmonary vasoconstriction causes chronically elevated pulmonary artery pressures—the hallmark of pulmonary hypertension. Right ventricular hypertrophy and some degree of right heart failure are commonly observed with pulmonary hypertension. Right ventricular hypertrophy develops over time as a compensatory mechanism in response to scarring and disruption of the pulmonary capillary bed, which creates a chronically high afterload against which the right ventricle must pump. These limitations may reach critical mass during exercise, as the demand for oxygen by metabolically active (skeletal muscle) tissues outstrips the pulmonary system’s ability to load oxygen. Therefore, a patient with pulmonary hypertension may experience a sudden decrease in exercise capacity, which is caused by a cascade of events. (1) Increasing hypoxia during exercise causes increasing pulmonary vasoconstriction. (2) As pulmonary vascular resistance increases, right ventricular stroke volume decreases. (3) A reduction in blood volume from the right side of the heart causes a reduction in oxygenated blood volume to the left side of the heart. (4) This causes a reduction in left side of the heart’s cardiac output. (5) BP falls and the patient becomes dizzy and lightheaded.
If exercise is allowed to continue, the patient will likely lose consciousness. The physical therapist must accurately and rapidly evaluate the situation, collect useful data, and protect the patient from injury. Exercise should be terminated immediately. The patient may be seated if BP can be maintained, or he or she may be placed supine with the head and upper trunk propped up with pillows. The workload and/or HR at which pulmonary hypertension becomes apparent should be noted. An exercise prescription should be developed that emphasizes steady-state, aerobic activities at an intensity below the symptom threshold.13 The use of low-flow supplemental oxygen may significantly improve exercise tolerance.
SUMMARY
Four categories of effort intolerance for patients with cardiovascular disease have been identified: arrhythmia, ischemia, cardiovascular pump failure, and cardiovascular pump dysfunction. Similarly, patients with pulmonary disease may be limited by poor oxygenation, ventilatory pump dysfunction, ventilatory pump failure, or pulmonary hypertension. Categorization of exercise intolerance is appropriate for patients with documented cardiac or pulmonary disease, but it is also useful for patients at risk for their presence: the elderly, or those with multiple risk factors for cardiopulmonary disease, for example. Figures 12-4 and 12-5 summarize the evaluation approach for classifying patients into categories that then may be used to direct procedural interventions.
The following are three closing thoughts on cardiopulmonary evaluation obtained from the patient’s acute response to exercise:
1.Physical therapists should be alert to the presence of other, more general signs of effort intolerance that may appear during therapeutic intervention. Some patients may demonstrate unusual pallor or diaphoresis, for example. The therapist should take note of the onset of these signs and make an assessment of the appropriateness of that response given the workload. Other patients may adopt a dull, fixed stare as exercise progresses, or fail to initiate conversation or respond to questions. Although admittedly these responses are “soft” data, they may be the earliest, and most important, indication of effort intolerance. They should be followed up with an evaluation to determine their etiology. With or without the other objective parameters discussed previously, these observations must not be ignored. Appropriate clinical responses include cautious continuance of exercise or its termination. It should be noted that these general signs of effort intolerance may be due to metabolic problems, pain (eg, visceral, orthopedic, neurologic), or comorbid disease (eg, cancer, multiple sclerosis).
2.Proper exercise evaluation and subsequent training challenge the cardiovascular and pulmonary systems with a progression of workloads applied over time, which should be both quantified and qualified by the physical therapist. Patient safety should be ensured through the use of the monitoring techniques outlined previously. The patient should not be encouraged to continue exercise in order to provoke symptoms; provocative testing should be performed only in an exercise laboratory with emergency equipment and personnel close by.
3.As the hypothesis-oriented algorithms demonstrate, the clinical evaluation of a patient’s cardiovascular and pulmonary status should not rest on one or two isolated findings; all the available data should be examined and a clinical impression should be developed out of that total.
CASE STUDIES
The following case studies will use the system for evaluation and classification of patient intolerance to exercise, as just described, and place this system in the context of a comprehensive cardiopulmonary rehabilitation service. Two patients referred to physical therapy will be described—one for “early mobilization cardiac rehabilitation” and the other for “pulmonary rehabilitation and evaluation for supplemental oxygen.”
Case Study
John Speed is a 57-year-old advertising executive who was admitted to the emergency department of a local community hospital on January 28, 2001, at 3:00 in the morning following 1½ hours of severe, unremitting precordial chest pressure. He was admitted to the cardiac intensive care unit (CICU) to rule out an MI. Data collected during the initial examination of Mr. Speed while in the CICU are summarized in Box 12-1.
BOX 12-1
Mr. Speed ruled in for an inferior wall MI. His 36-hour course in the CICU was unremarkable, and he was subsequently transferred to a private room, at which time he was referred to physical therapy for “cardiac rehabilitation.”
Magda Nuchal, PT, was assigned to the patient on day 2 post-MI. She reviewed the chart. She noted that the patient’s course in the CICU was characterized by the absence of ongoing chest pain, arrhythmia, or CHF. She examined the latest ECG and noted the presence of significant Q waves in leads II, III, and aVF indicative of a full-thickness inferior wall MI. She also noted that the patient had been placed on β-blockade and was anxious to begin physical therapy. After introducing herself to the patient, she began her physical assessment of Mr. Speed by obtaining resting baseline data (Table 12-1). These data show no evidence of ischemia, CHF, or LV dysfunction at rest, but do not preclude the onset of these findings with exercise. Magda palpated a slow, irregular pulse that she thought could be indicative of either atrial or ventricular arrhythmia. She decided to connect the patient to a portable ECG radiotelemeter to assess the origin of the skipped beats. She placed the negative electrode over the patient’s sternum and the positive one just under the patient’s left nipple. Figure 12-6 illustrates what Magda saw. The rhythm strip shows multifocal PVCs at an intrinsic HR of 60 bpm. These resting PVCs are worrisome for three reasons. (1) They probably originate from two areas within the ventricles and thus increase the likelihood of becoming more frequent. (2) They were absent during the patient’s CICU stay. (3) They occur in the presence of known ischemic heart disease.
FIGURE 12-6 Mr. Speed: Telemetered ECG rhythm strip obtained at rest.
TABLE 12-1 Mr. Speed: Results of the Preexercise Resting Examination
Her initial resting evaluation now complete, Magda formulated two questions to be answered by the patient’s response to exercise: “What happens to the PVCs during exercise?” and “Is occult myocardial ischemia present?”
Comment
It should be noted that the patient is in the early recovery period of an MI and as such is vulnerable to reinfarction, or extension, or in some cases myocardial rupture. This situation does not preclude mild exercise, but cardiovascular training at high levels is a contraindication. Exercise prescription during this period is characterized by the administration of a known “dose” of exercise that is usually identified by the HR and SBP response to that exercise and expressed as the RPP. Future doses are based on the patient’s response to the prior session. Early mobilization exercises tend to be dynamic as opposed to static and progress from a low level to a moderate level, compatible with most activities of daily living by the time of hospital discharge to the home. There is no “exercise test” per se at the beginning of an early mobilization rehabilitation program; each exercise session becomes, in effect, a “mini-stress test.”
Progressive Exercise Sessions
Magda began her initial exercise session with some low-level calisthenics designed to provoke a modest increase in HR, generally no more than 10 bpm above the resting level. The patient remained connected to a radiotelemeter throughout the exercise session. She noted that the PVC frequency stayed about the same during exercise and thus appeared to be unrelated to mild levels of exertion. She also noted that the ST segment did not change its position with the exercise, and the patient did not complain of any chest discomfort, indicating an absence of myocardial ischemia.
Over the next few days, Mr. Speed increased his activities, from bed level through self-care activities to ambulation down the hall and back. He was taken off β-blockade. His PVCs went away. As the time of hospital discharge approached, the patient was able to walk 200 ft down the hall and back fairly rapidly, at a HR not exceeding 98 bpm and a SBP of 134 mm Hg (RPP of 13.1 x 103) without any signs or symptoms of effort intolerance.
On day 4 post-MI, Magda decided to simulate the patient’s home environment by allowing him to walk up and down a flight of stairs followed by ambulation down the hospital corridor. After climbing the flight of stairs, Mr. Speed complained of mild chest pain and palpitations. Magda terminated exercise immediately but was able to get a peak exercise paper printout from the telemeter before doing so (Fig. 12-7). Magda took an immediate postexercise BP measurement and listened to the heart and lungs. The patient was placed in a wheelchair and taken back to his room. His chest pain subsided after approximately 2 minutes. Magda paged the physician and wrote the following note in the patient’s chart:
FIGURE 12-7 Mr. Speed: Telemetered ECG rhythm strip obtained during ambulation.
Progress note: Day 4 post-MI. The patient experienced mild precordial chest pressure and palpitations after walking up and down a flight of stairs, associated with 1.5 mm of horizontal ST-segment depression in lead CM5 via telemeter. Maximum HR was 140 bpm and BP was 148/80 mm Hg. No arrhythmia, S3, S4, murmur, or crackles before, during, or after exercise. Pain subsided with rest within 2 minutes. See attached ECG telemeter strip.
Ischemia at a Distance
The rhythm strip (Fig. 12-7) documents for the health care team the inappropriately high HR during exercise off beta-blockade and the exercise-induced ischemic event. This is a significant finding. Mr. Speed suffered an inferior wall MI as evidenced by significant Q waves in leads II, III, and aVF. This usually results from occlusion of the right coronary artery. The ST-segment depression in lead CM5 implicates high lateral wall ischemia that is supplied by branches of the left coronary artery. The patient is at risk for an ischemic event from another, distant source, frequently the left circumflex artery. The physical therapist responded appropriately by not only terminating exercise immediately but also correctly documenting and reporting her findings to the physician. She protected the patient from potential injury at home by identifying a problem while the patient was still in the hospital.
Postscript
Mr. Speed was kept in the hospital by his physician and referred to the cardiac catheterization laboratory for coronary angiography. The results of that test showed a totally occluded right coronary artery and a 90% lesion of the circumflex artery. The ejection fraction was 45%. The patient subsequently underwent coronary artery bypass grafting of the circumflex artery, thus saving the lateral wall of the heart. He was placed back on beta-blockade and enjoyed an uneventful postoperative hospital course. (Magda married the attending physician.)
Case Study
Charlene Posey is a 51-year-old retired laboratory technician with a 66 pack year smoking history, which she discontinued 13 years ago. She was diagnosed with chronic bronchitis and emphysema 2 years ago. Her chief complaint has been exertional SOB and early onset of fatigue. Until recently these symptoms were predictable and relatively stable, until the afternoon of August 16, 2000, when she developed an acute attack of SOB while pulling weeds in the garden in her backyard. Her local physician had prescribed Atrovent (ipratropium) to be taken as needed for relief of SOB due to bronchospasm. Usually two metered doses were sufficient, but this time it took four. This event caused Ms. Posey to call her physician. The physician scheduled her for pulmonary function testing. This procedure revealed further deterioration in her pulmonary status. He recommended that the patient enroll in the pulmonary rehabilitation program at the local community hospital and be evaluated for supplemental oxygen use.
One week later Ms. Posey was referred to outpatient physical therapy for endurance training. In order to substantiate the medical diagnosis, Walt Early, the physical therapist, scheduled her for a maximum symptom-limited exercise test to be performed by the Division of Pulmonary Medicine. Recognizing her severe exercise limitations, this laboratory chose a bicycle ergometer exercise test protocol. This protocol is characterized by 2-minute stages and small increments in exercise intensity between stages. It is designed to increase both the HR and systemic O2 transport mechanism slowly up to a maximum exercise level. Testing is terminated if the patient demonstrates early signs and symptoms of exercise intolerance. Otherwise, the test is terminated when the patient reaches 90% of their age-related maximum heart rate (ARMHR). This HR is calculated by the following revised formula (see Chapter 3):
ARMHR = 208 – 2 0.7 × age.
Ms. Posey was 51 at the time of her test; her ARMHR was thus 172 bpm. The goal of testing was to increase the subject’s HR up to the onset of signs and symptoms of exercise intolerance or 90% of 172 bpm, whichever came first.
The test was performed on September 1, 2000. Expired gas analysis was performed using a closed-circuit metabolic cart. Ms. Posey’s performance is presented as a formal report (see Box 12-2).
BOX 12-2
MS. Posey: Report of the Results of the Community Hospital Protocol Bicycle Ergometer Exercise Test
The patient exercised for 4.0 minutes, 2.0 minutes into stage II of the Community Hospital protocol bicycle ergometer exercise test. She achieved a maximum HR of 140 bpm with an SBP of 112 mm Hg and SaO2 of 80%. Exercise was terminated because of the onset of shortness of breath and dizziness, coupled with a fall in blood pressure and oxygen saturation. There was no anginal pain, no change in the position of the ST segments, and no ectopic activity. Immediately following exercise, physical examination revealed an increase in both peripheral cyanosis and crackles in the lung bases. Functional aerobic capacity, as measured by closed-circuit gas analysis, was 4.0 MET, less than that predicted for sedentary women of this age. Results of this test suggest a diagnosis of pulmonary hypertension secondary to chronic obstructive lung disease.
Comment
Ms. Posey’s tests did not perform well. The exercise test results in Box 12-2 confirm the reduced functional capacity (4 MET) that accounts for the patient’s complaint of early fatigue. The test suggests that, although there are no symptoms of pulmonary decompensation at rest, the patient is limited by pulmonary hypertension during exercise. This is evidenced by increasing SOB, coupled with sudden decreases in both oxygen saturation and SBP, that was accompanied by feelings of light-headedness. The SOB, although a nonspecific finding by itself, takes on added significance when coupled with the other data. Taken together, these data confirmed a diagnosis of exercise-limiting pulmonary hypertension.
Before pulmonary rehabilitation could begin, the patient was referred back to the physician for medical management. The physician suspected that there was an exercise-induced bronchospastic component to her disease. She was placed on Proventil (albuterol) tablets for the prevention of bronchospasm and Flovent inhalation aerosol to use as an anti-inflammatory. She was referred back to pulmonary rehabilitation almost 2 weeks later, with a request to begin exercise trials using supplemental oxygen.
A Dilemma
Walt Early was faced with a dilemma. Initially, Ms. Posey received a maximum symptom-limited exercise test for the purpose of rendering a diagnosis, while on Atrovent. However, before Walt could develop an exercise program, her medications had been expanded to include Proventil and Flovent. This change made the bicycle ergometer exercise test no longer useful in developing an exercise prescription. Additionally, Walt noted that the diagnosis of pulmonary hypertension was based on an exercise test characterized by increasing levels of physical exertion on a bicycle. Walt wondered what her tolerance to exercise would be if the workload was maintained at one level of intensity. Finally, Walt also questioned the validity of applying a bicycle ergometer test to a patient whose goal was to resume walking with her friends. Because of the change in medications, and the inappropriateness of the bicycle test for the purpose of developing an exercise prescription, Walt decided to conduct his own exercise test.
Walt chose the 6-minute walk test. He felt that this test would have more functional relevance to Ms. Posey, as much of her time is spent in walking. This test is different from the bicycle ergometer exercise test. In the 6-minute walk test, the patient walks down a corridor or other flat area, where distance is mapped out, for a period of 6 minutes. The patients are instructed to cover as much ground as possible during this time. The patients are allowed to stop walking if they have to rest, but then must resume walking if they are still within the 6-minute period. Ambulation down a corridor represents a relatively constant workload; the intensity of effort is based on how fast the patient chooses to walk and is thus controlled by the patient (see Chapter 10).
Comment
Walt’s dilemma and his resolution to the problem are not atypical in cardiopulmonary rehabilitation settings. Stress tests ordered for the purpose of rendering a medical diagnosis or clearing the patient for cardiovascular training frequently reveal residual pathology that require medical intervention, but may be inappropriate for use in developing an exercise program. The patient who comes back to physical therapy after alterations in cardiopulmonary medication is not the same patient who left. Fiscal restraints or full laboratory appointment schedules make it impractical to formally test repeat patients in the same circumstances with the same protocol. The physical therapist must utilize the resources available within his or her department without sacrificing patient safety. The 6-minute walk test is a test that meets these criteria. It is safe, economical, and requires only a measured corridor and a stopwatch. It also matches the type of activity that Ms. Posey engages in on a daily basis—and the workload is relatively constant.
After introducing himself to the patient and conducting an initial interview, Walt proceeded to perform a physical examination. He then connected Ms. Posey to an ECG telemeter and collected pretest resting baseline data (Table 12-2). He also connected her to a pulse oximeter. The abnormal DI and the decreased oxygen saturation values suggest some nonspecific pulmonary decompensation at rest. However, although the physical examination, ECG, and pulse oximeter data show no evidence of ventilatory pump dysfunction, ventilatory pump failure, or pulmonary hypertension at rest, they do not preclude the onset of these findings with exercise.
TABLE 12-2 Ms. Posey: Results of the First 6-Minute Walk Test
The results of Ms. Posey’s 6-minute walk test are also shown in Table 12-2. Ms. Posey covered 500 ft in 6.0 minutes with 4 rest stops. At the end of 6 minutes, she was markedly short of breath but maintained her BP and had no complaints of dizziness. Her oxygen saturation dropped to 84%. Ms. Posey was placed supine on a treatment table, and her head and chest were propped up with four pillows. She was given supplemental O2 at 2.0 L/min. These signs and symptoms resolved after approximately 5 minutes of rest. Her O2 saturation normalized within 2 minutes. The patient felt exhausted following the test and further evaluation was deferred until the next treatment session.
Walt evaluated the findings and recognized that the patient was experiencing some of the findings obtained during the bicycle ergometer test, but that, while the bicycle test elicited symptomatic hypotension, the 6-minute walk test did not. The bicycle test brought the patient up to a maximal level of exertion as measured by the HR response. The 6-minute walk test was a submaximal test that allowed the patient to walk at their own, self-selected pace at a relatively constant workload. Use of the walk test is consistent with literature that suggests that steady-state aerobic exercise may be of benefit in patients with pulmonary hypertension.13 Walt documented his findings in the chart and sent the patient back to the referring physician. Two weeks later, Ms. Posey returned to the Pulmonary Rehabilitation Program for her second visit. The patient reported feeling unusually fatigued for the rest of the afternoon and evening, following her initial visit but felt “back to normal” at present.
This time Walt decided to repeat the same test using supplemental oxygen. Walt proceeded to administer the second 6-minute walk test in the same way as he had administered the first. However, this time Ms. Posey wore a nasal cannula connected to an E cylinder supplemental O2 source set at 2 L/min (see Fig. 12-8). A physical therapy aide trundled the unit behind Ms. Posey as she walked down the hall and progressed through the test. The results of this test are shown in Table 12-3. This second test is notable for the increase in distance ambulated, combined with a higher oxygen saturation both pre- and postexercise, a lower DI, and a lower HR response.
TABLE 12-3 Ms. Posey: Results of the Second 6-Minute Walk Testa
FIGURE 12-8 Ms. Posey: Just before her second 6-minute walk test. Note the presence of the pulse oximeter, oxygen tank, nasal cannula, and ECG telemeter. (Courtesy of Dr. W. E. DeTurk.)
The beneficial effect of oxygen on cardiac function in the second test is apparent both at rest and during exercise when compared to the first test. The patient was able to walk for a longer period of time with fewer rest periods. Most importantly, SBP was maintained and Ms. Posey was less symptomatic. The beneficial effect of oxygen therapy is due to its direct action on pulmonary vasculature causing decreased pulmonary vascular resistance and enhanced arterial oxygen content, providing more oxygen to the heart, brain, and other organs. This also indicates that, with supplemental oxygen, the heart does not have to work hard to supply blood to working skeletal muscles during the 6-minute walk test.
The Exercise Prescription
Ms. Posey began exercise training on the treadmill with 2.0 L of supplemental oxygen soon after her second exercise test. There were five components to her exercise prescription.14 (1) The intensity of exercise was determined as a percentage of the maximum HR attained on the second 6-minute walk exercise test, while Ms. Posey was on low-flow oxygen. Walt found, through trial and error, that Ms. Posey could comfortably sustain an HR that was 75% of 128 bpm, or 96 bpm. (2) The total duration of training at this intensity was approximately 20 minutes. However, Ms. Posey could not sustain 20 minutes of continuous exercise; therefore, she trained for 4 minutes in the training window and rested for 2 minutes, and then repeated this sequence 5 times for a total of 20 minutes in the training window. The training period was preceded by 5 minutes of stretching and calisthenic warm-up exercises and concluded with 5 minutes of slower walking. (3) The frequency of training was three times a week. Ms. Posey was able to undergo training as an outpatient for a period of 10 weeks. (4) The modality of choice was the treadmill, set at 1.2 mph at a 0% grade. (5) This last component of the exercise prescription took into consideration the patient’s goals and level of motivation; both Walter and the patient felt that cardiovascular training should be geared toward return to household activities such as gardening and recreational walking with her friends.
Postscript
Eleven weeks later, Walt assessed the results of the patient’s training program with another 6-minute walk test, again with supplemental O2 set at 2.0 L/min (see Table 12-4). This test showed a reduction in both the patient’s resting HR and the HR immediately following completion of the test. Ms. Posey was able to increase her ambulation distance to 1,060 ft. These data demonstrate successful acquisition of a cardiopulmonary training effect. The use of oxygen combined with a program of aerobic endurance exercise training were key elements in her rehabilitation.
TABLE 12-4 Ms. Posey: Results of the Third 6-MinuteWalk Test After a 9-Week Aerobic Endurance Training Programa
Upon discharge from the Pulmonary Rehabilitation Program, Ms. Posey was prescribed very high dose calcium channel blockade15 and continuous supplemental oxygen to be used during the day. She was outfitted with a nasal cannula and a highly portable liquid O2 system that was attached to a belt that she wore around her waist. Ms. Posey feels that the combination of pulmonary rehabilitation and supplemental O2 have given her a new lease on life. She has rejoined the walking club with her friends and continues to pull weeds in her garden.
CLOSING
This chapter has summarized some of the examination tools and techniques found in the pulmonary and cardiac evaluation chapters and in the electrocardiography chapter. It has structured these tools and techniques to form an evaluation approach for classifying patients into categories that are summarized as hypothesis-oriented algorithms in Figs. 12-4 and 12-5. This classification system was applied to two case studies. An ongoing evaluation approach that is applied during a therapeutic intervention session that utilizes such a classification system will direct the therapist to respond in ways that are appropriate for optimum patient management. Additionally, an understanding of this process will provide the reader with a proper background with which to appreciate the complexity inherent in monitoring patient progress, not only during a treatment session but also over the course of a total plan of care.
Management plans for patients exemplifying the Cardiopulmonary Preferred Practice Patterns will be covered in detail in Chapters 15 through 22.
Heads Up!
This chapter includes a CD-ROM activity.
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