Lawrence P. Cahalin & William E. DeTurk
INTRODUCTION
Like the pulmonary system, examination of the cardiac system requires optimal use of auditory, observational, positional, tactile, auscultatory, and medical information. Perturbation of initial examination findings with different body positions or maneuvers may provide important observational, tactile, and auscultatory findings that may yield important information that could (1) direct further examination techniques, (2) direct treatment techniques, and (3) provide important prognostic information. This chapter will review a variety of practical examination techniques and specific maneuvers that may help to direct and predict the effects of examination and treatment techniques. Much of this information is alluded to in the patient note of Box 10-1.
BOX 10-1
Examination Techniques and Specific Methods to Determine the Disablement of Cardiac Disorders and Direct and Predict Physical Therapy: A Patient Case Example*
1.Why are you here today?
2.Have you been diagnosed with a cardiac disorder in the past?
3.Have you had any special tests to examine your heart like an electrocardiogram, stress test, echocardiogram, or cardiac catheterization?
4.Do you experience angina or shortness of breath at rest, only with activity/exercise, or both at rest and with activity/exercise?
5.If you experience angina or become short of breath during activity or exercise, could you please describe the type of activity or exercise, which produces your angina or shortness of breath?
6.Can you describe your angina or shortness of breath? Can you help me understand your angina or shortness of breath by pointing to the numbers 1 through 4 to describe the level of angina you experience at rest and exercise or by pointing to your level of shortness of breath using this 10-point scale or by marking this Visual Analog Scale?
7.Could I feel your pulse to determine your heart rate and the strength of your pulse?
8.Could I place this finger probe on your index finger to obtain an oxygen saturation measurement?
9.Could I place these electrodes on your chest to obtain a simple single-lead electrocardiogram (ECG)?
10.Could I take your blood pressure while you are seated and then compare it to the blood pressure while you are lying down and then standing? I would also like to observe your pulse, oxygen saturation, ECG, and symptoms when you are lying down and standing.
11.Could I listen to your heart and lungs with my stethoscope? While I do this I will concentrate on watching your ECG so that I can identify your heart sounds and any changes in the ECG while you are breathing deeply when listening to your lungs.
12.Could I place one of my hands on your stomach and one hand on your upper chest to determine how you breathe?
13.Could I place my hands on the lowermost ribs on each side of your chest to determine how you breathe?
14.Could I place my hands on your back to determine how you breathe?
15.Could I wrap my tape measure around your chest at several different sites to determine how you breathe?
16.Now that I understand some very basic information about the manner in which you breathe could you please breathe in the manner I instruct you via sounds I make, pressure from my hands, methods I show to you, or different body positions? I will occasionally place my hands on your chest and wrap my tape measure around your chest to determine how you breathe during these simple tests, and I will ask you to identify your level of shortness of breath using the 10-Point Scale or Visual Analog Scale—Is this OK with you?
17.Could I measure the strength of your breathing muscles by having you place this mouthpiece in your mouth and breathe in and out as deeply and as forcefully as you are able?
18.I would like you to now perform the activity or exercise which produces your angina or shortness of breath—Could you please do this now?
19.Thank you for giving me the chance to examine you today. I will call your physician to get some more information about you like the electrocardiogram, echocardiogram, and pulmonary function tests that you said were performed last week as well as the arterial blood gas results, chest X-ray, and exercise test results. In the meantime, I would like you to practice breathing in the manner that we discovered helped you feel less short of breath and produced the best chest wall motion that I felt with my hands and measured with the tape measure. I will see you next week for further examinations and treatments!
*Bolded information identifies important examination procedures for patients with pulmonary disorders.
PHYSICAL THERAPY EXAMINATION
Medical Information and Risk Factor Analysis
The past medical history is very important for the patient with cardiac disease and must be included in the systems review process. This is particularly true of patients with known or suspected cardiac disease. A number of previous medical problems may predispose a person to cardiac disorders. Examples of such previous medical problems are shown in Box 10-2 and include pulmonary disorders, neuromuscular abnormalities, peripheral vascular disease, and treatment of oncologic disorders.
BOX 10-2
Risk Factors for Cardiovascular Disorders
Previous Medical Problems Predisposing a Person to Cardiovascular Disorders
1.Pulmonary disorders
2.Neuromuscular disorders (eg, muscular dystrophy)
3.Past oncologic disorder treated with chemotherapy or radiation therapy
4.Obesity
5.Premature birth with low birth weight
6.Autoimmune dysfunction
7.Vascular dysfunction
8.Bacterial or viral infections (chlamydia pneumonia, porphyromonas gingivalis, cytomegalovirus)
9.Hypothyroidism
10.Endocrine or metabolic disorder
Risk Factors for Cardiovascular Diseases
1.Smoking
2.Occupational exposure to irritants or allergens (eg, carbon monoxide, chemicals)
3.Residing in locations with high levels of air pollution
4.Hypertension
5.Diabetes (types 1 and 2)
6.Hypercholesterolemia
7.Sedentary lifestyle
8.Family history of heart disease
9.High stress (type “A” personality and type “D”)*
10.Age (older age > younger age)
11.Gender (males > females)
12.Altered serum sex hormones
a.Men: low testosterone and DHEA
b.Women: low progesterone and possibly estrogen
13.Elevated serum homocysteine
14.Hyperinsulinemia (insulin resistance)
15.Oxidized LDL cholesterol with hypertriglyceridemia
16.Low serum vitamin D
17.Increased serum iron
18.Inadequate dietary mineral intake
19.Inadequate dietary antioxidant intake
20.Inadequate dietary essential fatty acids intake
*Type “A” personality, time urgency with high stress; type “D” personality, suppression of emotions; DHEA, dehydroepiandrosterone.
The key medical alerts for cardiac diseases are also listed in Box 10-2 and include environmental and self-imposed risks. The Framingham studies continue to identify key risk factors responsible for the development of heart disease, including a variety of blood test results (homocysteine, glucose, insulin sensitivity, lipids, fibrinogen, and many others) as well as many environmental, societal, and personal risk factors. The early studies from Framingham identified cigarette smoking, hypertension, and hyperlipidemia as the three major risk factors of heart disease. Recent Framingham studies have confirmed the importance of these three risk factors as well as of other risk factors significant for heart disease. The key risk factors for heart disease are listed in Box 10-2. A complete discussion of the risk factors for heart disease is provided in Chapter 15.
Two relatively simple and objective methods to examine cardiovascular risk are shown in Box 10-3. These risk-factor profiles examine cardiovascular risk by questioning and measuring particular risk factors and assigning the questions and measurements specific scores. Each of the areas of examination can be scored and the scores for each of the areas can be summed. The total summed scores can then be compared to the risk-factor profile of the study population, and the specific degree of risk can be obtained and used as a reference measurement. The second column of Box 10-3 can be used to examine cardiovascular risk at a subsequent examination session. Examination of the body weight question in Box 10-3 requires the calculation of the ideal body weight, which is described in a later section and can be appreciated in Table 10-4. The CD-ROM accompanying this textbook provides prognostic indices of cardiovascular risk. Please use the CD-ROM at this time to see the tremendous amount of prognostic information provided by inputting several simple measurements and answering several pertinent questions. This tool should be useful in primary, secondary, or tertiary settings and can be used to track patient response to physical therapy.
BOX 10-3*
As with pulmonary disease, listening to the patients, past history and primary complaints is critical in the examination process. In fact, a good history can provide very important information that can be very useful in diagnosing a variety of cardiac disorders. Most cardiac and cardiovascular disorders can be grouped or categorized by specific signs and symptoms. Table 10-1 provides a cursory overview of several such signs and symptoms that are helpful to categorize patients with cardiac and cardiovascular diseases. The importance of good listening as the initial part of the auditory examination cannot be underestimated. The remainder of this chapter should provide a better appreciation for the characteristics of specific cardiac and cardiovascular diseases listed in Table 10-1. Of these particular characteristics, the presence of anginal pain is most important and meaningful.
TABLE 10-1 Particular Patient Characteristics Suggestive of a Cardiovascular Disordera
Angina—Methods to Evaluate Angina from Nonanginal Pain
Angina is often described as “heart pain,” “if an elephant is sitting upon my chest,” “if someone is squeezing my chest,” “substernal burning,” “chest pressure,” or “chest tightness.” It is apparent that many descriptions of angina exist. However, it is almost always due to the same thing—myocardial ischemia. The lack of oxygen to a specific portion of the myocardium is identified by the central nervous system, and sensory fibers in the thoracic vertebrae refer the identified sensation of a lack of oxygen as a noxious stimulant to nerve fibers in the chest and elsewhere. This noxious stimulation is often referred to the anterior upper chest (substernal area, left pectoral area, or even upward into the neck) or possibly to the left arm or shoulder (Fig. 10-1).
FIGURE 10-1 Anginal patterns. (Modified with permission from McArdle W, Katch F, Katch V. Exercise Physiology: Energy, Nutrition, and Human Performance. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2001.)
Methods to differentiate angina from nonanginal pain (ie, musculoskeletal pain) exist and are based on several particular characteristics. If a suspected anginal pain changes (increases or decreases) with breathing, palpation in the painful area, or movement of a joint (ie, shoulder flexion and abduction), it is very likely that the pain is NOT angina. Angina cannot be changed with the aforementioned maneuvers. However, it can be worsened by physical exercise or activity. Therefore, if the suspected anginal pain is unchanged with the previously cited maneuvers and the pain occurred with exertion, this finding MAY BE angina. If the suspected anginal pain is unchanged by these maneuvers, if the pain occurred with exertion, and if the pain decreases or subsides with rest, it is very likely that the pain IS angina. Finally, if the suspected pain decreases or subsides with nitroglycerin, it is even more likely that the pain IS angina. This sequence of tests to differentiate angina from nonanginal pain is listed in Table 10-2. Occasionally, angina is not perceived, despite the fact that a patient may be experiencing myocardial ischemia. The inability to perceive angina when myocardial ischemia is present has been described as silent myocardial ischemia. In such cases, the most common complaint is dyspnea. Dyspnea is occasionally described as an anginal equivalent—meaning that, in certain patients, dyspnea is equivalent to the sensation of angina, which again is most often due to myocardial ischemia. Myocardial ischemia may directly or indirectly produce other symptoms, which will be discussed in the following section.
TABLE 10-2 Methods to Differentiate Angina from Nonanginal Pain
“Other” Symptoms of Heart Disease
Other symptoms of heart disease exist and include dyspnea, fatigue, dizziness, light-headedness, palpitations, and a sense of impending doom (Table 10-1). It is apparent from Table 10-1 that dyspnea is possibly the most common complaint of patients with pulmonary and cardiac disorders. However, the other symptoms listed in Table 10-1 may or may not accompany dyspnea. Often, dyspnea accompanied by one of the other symptoms is suggestive for cardiovascular disease alone or combined cardiovascular and pulmonary disease. However, other measurements besides symptoms are necessary to clearly differentiate dyspnea due to a cardiac origin from a pulmonary origin. These other measurements will be presented later but can be seen in Table 10-14.
Symptom Recognition and Grading
New York Heart Association Classification
The recognition and grading of symptoms were initially described by the New York Heart Association (NYHA) in 1964. This classification schema has been accepted universally and consists of categorizing patients into one of four classes, based on symptoms and the amount of effort required to provoke them (Table 10-3). Patients without symptoms and no limitations in ordinary physical activity are categorized into class I, whereas patients who are unable to perform any physical activity without discomfort are categorized into class IV. Classes II and III are characterized by slight limitation and marked limitation in physical activities due to symptoms, respectively (Table 10-3). The symptoms recognized as limiting physical activity can be due to any of those listed in Table 10-1, but the most common symptoms for cardiovascular disease appear to be angina, dyspnea, and fatigue. The Canadian Heart Association classification and Specific Activity Scale are two additional measures used to recognize and grade symptoms in regard to performance of functional tasks. These measures are also presented in Table 10-3.
TABLE 10-3 Symptom Recognition and Grading
Examinations of Patient Appearance
Specific Patient Characteristics (eg, Skin Color and Body Traits)
As presented in Table 10-1, specific patient characteristics can provide important information about the likelihood or presence of cardiovascular disease. In terms of the likelihood of cardiovascular disease, a simple examination of particular body characteristics can provide helpful information about cardiovascular risk. One such characteristic is the skin color of the peripheral extremities. Pale or cyanotic skin in the legs, feet, arms, and fingers is associated with poor cardiovascular function. Another characteristic is the presence of a diagonal earlobe crease. This phenomenon has been investigated for many years and recently was once again found to be highly predictive of heart disease.1 Many other patient characteristics can provide helpful diagnostic or prognostic information and include cyanosis, an abnormal breathing pattern, a look of apprehension, or a variety of symptoms such as dizziness, light-headedness, palpitations, or even a sense of impending doom as mentioned earlier. This subjective information combined with particular aspects of a patient’s appearance can help to categorize the predominant disorder in need of physical therapy (Table 10-1).
Examination of body type (body habitus or somatotype) can also provide important information about cardiovascular risk. Patients who fall outside the somatotype classification of endomorphs (heavyset), mesomorphs (average body build), or ectomorphs (thinset) appear to have a greater risk for cardiovascular disease followed by endomorphs and mesomorphs. Patients with a pear-shaped body are three times more likely to develop cardiovascular disease. Patients with a greater deposition of abdominal fat also appear to have a greater risk of cardiovascular disease. More specific methods to examine body type and physical characteristics will be presented in the following sections.
Anthropometric Measurements
A variety of anthropometric measurements can be made in subjects suspected to have cardiovascular or pulmonary disease or in subjects with known cardiovascular disease. Likewise, anthropometric measurements can be helpful in predicting the risk of cardiovascular disease. The most common methods to perform anthropometric measurements include body weight, finger pressure on an edematous area, girth measurements, skinfold caliper measurements, calculation of the body mass index (BMI), hydrostatic weighing (underwater weighing), and a variety of quick methods to indirectly measure the percentage of body fat and lean muscle mass (bioimpedance analysis, infrared). Appropriate sites from which to obtain girth measurements are shown in Figs. 10-2A and 10-2B. Each of these methods, the methods to perform them, and the strengths and weakness of each method are presented in Table 10-4. Furthermore, the measurement of waist-to-hip ratio can provide very important information regarding risk of cardiovascular disease. The methods to properly perform the waist-to-hip ratio measurements are shown in Fig. 10-3. Measurement of the waist circumference is made just above the umbilicus while the hip circumference is made near the greater trochanter. The following Web site provides excellent resources for anthropometric measurements: http://www.topendsports.com/testing/anthropometry.htm.
FIGURE 10-2 Methods to measure limb girth. (A) midcalf and (B) midforearm.
FIGURE 10-3 Methods to measure the waist-to-hip ratio.
TABLE 10-4 Common Methods to Perform Anthropometric Measurements
The calculations of ideal body weight and BMI are also described in Table 10-4. In brief, ideal body weight can be calculated by determining body height and frame size (small, medium, large) and assigning a certain amount of weight for body height and frame size (Table 10-4). The BMI is simply the quotient of body weight in kilograms and the square of height in meters (BMI = kg/[m]2). The BMI is quite easy to calculate, but a very useful Web site (http://www.nhlbisupport.com/bmi/) provides rapid conversions from English to metric and provides helpful information about individual results. An overview of normal (normal BMI is considered to be between 20 and 25) and abnormal values is provided and methods to improve abnormal results are suggested. Figure 10-4 shows several sites for skinfold caliper measurements.
FIGURE 10-4 Sites for the measurement of body fat and lean body mass using skinfold calipers.
Jugular Venous Distension
Jugular venous distension (JVD) is simply the filling of the jugular vein(s) with excessive fluid such that they become visibly distended. The etiology of JVD is varied, but it is often due to right-sided heart failure. Figure 10-5 shows a patient with right-sided heart failure and visible JVD. It is easily seen in this patient and can be documented by simply indicating that the jugular veins were markedly distended bilaterally. However, not all patients demonstrate such extreme JVD as that shown in Fig. 10-5. Patients with suspected JVD can actually be placed semisupine (lying on a table at a 45-degree angle). This position is the standard initial reference position to measure for JVD. After assuming this body position, the patient is slowly brought to a more upright position, and the angle of the table and the patient’s neck are observed for signs of JVD. If JVD is observed, the position of the table and the magnitude of JVD should be measured. The position of the table can be easily read off of the goniometer-like device providing the exact angle of the table. The magnitude of JVD is measured with the base of a small metric ruler placed at the sternal angle of Louis and aligned cranially alongside the jugular vein. The movement of the pulse of JVD can then be measured in centimeters and documented. Observation of an increase or decrease in the pulse of JVD can then be tracked and provides important information about the status of the cardiovascular system. Figure 10-6 provides an overview of the methods to measure JVD.
FIGURE 10-5 Patient demonstrating signs and symptoms of right-sided heart failure. Copyright (2004) Icon Learning Systems, LLC. A subsidiary of MediMedia, Inc. US. All rights reserved. (Reprinted with permission from The CIBA Collection of Medical Illustrations, by Frank H. Netter, MD.)
FIGURE 10-6 Measurement of jugular venous distension. (Reproduced, with permission, from McPhee SJ. Pathophysiology of Disease: An Introduction to Clinical Medicine, 6th ed. New York: McGraw-Hill, 2010:265.)
From Fig. 10-6, it is apparent that more detailed measurements can be obtained by rotating the head slightly away from the vein being examined, and at the point of elevation of the bed at which distention is first observed, pressure should be applied to the external jugular vein just above and parallel to the clavicle for approximately 10 to 20 seconds. This amount of time should allow the lower part of the vein to fill, and after removing the finger that was occluding the vein, the height of the distended fluid column within the vein will rise and can then be measured. Normally, the level is less than 3 to 5 cm above the sternal angle of Louis. In summary, the highest point of visible pulsation is determined as the trunk and head are elevated and the vertical distance between this level and the level of the sternal angle of Louis is recorded as shown in Fig. 10-6.
Evaluation of the jugular waveforms can also be performed in this position, but catheterization of the pulmonary artery for assessment of pulmonary arterial pressures and waveforms (via Swan–Ganz monitoring) provides the greatest amount of information. A tremendous amount of information can be projected to a hemodynamic monitor, where the pulmonary artery pressure and waveforms can be examined. A variety of different waveforms may be identified by this invasive method of monitoring, but a thorough noninvasive examination of the jugular neck veins for particular pulsatile waveforms may allude to specific cardiac disorders. Several examples of this are the wave of venous distention from right atrial systole (that occurs just before the first heart sound [S1]) and the v wave that is frequently associated with a regurgitant tricuspid valve.
Although the assessment of hemodynamic function via Swan–Ganz monitoring is considered an advanced skill, it is relatively simple to interpret the typical intensive care unit (ICU) monitor and thus obtain important hemodynamic information to examine and treat patients in the ICU. Perhaps one of the most important measurements from such monitoring is identifying the pulmonary artery pressure waveform and digital display of the systolic, diastolic, and mean pulmonary artery pressures. A mean pulmonary artery pressure greater than 25 mm Hg is the threshold level that is used to define pulmonary hypertension. This is a very important measurement, because pulmonary hypertension is associated with a variety of life-threatening pathophysiologic phenomena (hypoxia, cardiac arrhythmias, and pulmonary abnormalities).
Palpation of the Radial Pulse
Palpation of the radial pulse can provide important information about the status of the cardiovascular system. The radial pulse is the preferred pulse to palpate because of the possibility of excessive vagal stimulation from excessive palpation (actually searching or massaging) of the carotid artery. Such excessive vagal stimulation may significantly decrease the heart rate and induce a hypotensive vagal eposide. The correct method to palpate the radial artery is to place the index finger lightly on the subject’s radial artery just below the thumb on either wrist. The pulse should be examined in both wrists in similar locations.
Much of the information obtained from the palpation of the radial pulse is listed in Table 10-5 and includes the rate of the pulse (the heart rate by counting the number of beats per minute), regularity or lack of regularity of the pulse, strength of the pulse, palpable turbulence, relationship of the pulse to a continuous electrocardiographic tracing and heart sounds, and the relationship of the pulse to the breathing cycle. Palpation of the pulse can provide an enormous amount of information about normal and abnormal physiologic phenomenon. Of particular importance is learning to get the “feel” of the cardiac cycle and determining the heart rate.
TABLE 10-5 Information Obtained from Palpation of the Radial Pulsea
Feeling the Cardiac Cycle and Determining the Heart Rate
Palpation of the radial pulse allows for a quick examination of the contraction and relaxation characteristics of the heart. The contraction of the heart is associated with the blood being ejected from the heart into the peripheral vasculature yielding an arterial pulse. The relaxation of the heart is that period of time between palpated arterial pulses and is called diastole. Palpation of the arterial pulse identifies systole, whereas the absence of a pulse identifies diastole. Palpation of the radial pulse, therefore, yields very specific information about the cardiac cycle and can provide information about the actual heart rate and other important findings (Table 10-5).
The method to determine the heart rate from the radial pulse basically involves counting the number of palpated pulses in 1 minute. In addition to determining the heart rate, it is critically important to palpate for differences in the strength and regularity of the pulses at rest during the breathing cycle (examining the strength and regularity of the pulses during inspiration and during expiration), during different body positions, and during physical activity or exercise. Differences in these parameters during the aforementioned perturbations can identify normal or abnormal physiologic function (Table 10-5). One particular palpable parameter is the presence of excessive turbulence in an artery. Turbulent blood flow can be easily palpated by applying light pressure on a suspected artery and feeling for the turbulent blood flow. Turbulent blood flow in an artery is referred to as a thrill. The presence of a thrill is often associated with different types of heart disease, which produce an abnormal degree of turbulent blood flow because of hyperdynamic circulations or abnormal valvular function. Finally, it is also important to examine the pulse and the relationship of the pulse to other cardiovascular examinations such as auscultation of the heart, a continuous electrocardiogram, or even while taking the blood pressure. The examination of the pulse as it pertains to the electrocardiogram will be discussed in Chapter 11. The examination of the pulse as it pertains to the blood pressure and auscultation of the heart will be discussed in the following sections.
Blood Pressure Examination
Measurement of Systolic Blood Pressure
Arterial blood pressure can be measured in a variety of methods, but the standard examination of arterial blood pressure utilizes a sphygmomanometer (either aneroid or a mercury column) and blood pressure cuff, which occludes blood flow (by filling the cuff with air) at the site the blood pressure cuff is inflated (Fig. 10-7). The occlusion of blood flow at a particular site of the body is identical to a tourniquet. Arterial blood flow is stopped at the site of the blood pressure cuff. When the air filling the cuff is slowly released from the cuff, the stopped blood will forcefully flow past the blood pressure cuff when the arterial blood pressure is greater than the pressure in the blood pressure cuff. The forceful and rapid flow of blood past the site of cuff occlusion produces turbulence and yields the sounds heard with a stethoscope (often referred to as Korotkoff sounds). The Korotkoff sounds and the manner that they are used to measure blood pressure are described in Table 10-6. Using the methods described in Table 10-6 should provide accurate and reliable measurements of the systolic and diastolic blood pressure using a sphygmomanometer. Figure 10-7 graphically portrays the previously cited methods and changes when measuring arterial blood pressure.
FIGURE 10-7 Measurement of blood pressure with the resultant arterial pressure waveform.
TABLE 10-6 Measurement of Blood Pressure
The relationship of the pulse to blood pressure is that the pulse will be absent when the blood pressure cuff is inflated. In fact, this relationship is very important because it is the method used to determine the maximal cuff inflation pressure needed to measure the blood pressure (Table 10-6) and because it can provide an indirect measurement of the systolic blood pressure when a stethoscope is unavailable. Inflating a blood pressure cuff at the brachial artery will stop blood flow distal to the brachial artery. Thus, the radial pulse will be absent—no pulse will be palpated due to the occluded blood flow at the brachial artery. As air is slowly released from the blood pressure cuff, there will be a time when the pressure within the artery exceeds that in the cuff. When this occurs, blood will flow past the brachial artery and can be palpated in the radial artery. The initial pulse that is palpated after such an occlusion is essentially the systolic blood pressure. Observing a mercury column or aneroid sphygmomanometer as air is being released from the blood pressure cuff and identifying the point on the sphygmomanometer that the radial pulse is palpated provide an indirect estimate of the systolic blood pressure. Auscultation of the turbulent blood flowing past the deflating blood pressure cuff is the preferred method to measure arterial blood pressure.
Measurement of Diastolic Blood Pressure
The measurement of arterial blood pressure involves the pressure not only during systole but also during diastole. As inferred from Table 10-6, the measurement of the diastolic blood pressure is made using one of two different criteria. The main two criteria are the absence of sound during the release of air from the blood pressure cuff and the muffling of sound during the release of pressure from the cuff. As previously mentioned, diastole is that period of time when there is no palpated pulse and essentially represents the resting phase of the heart. During this resting phase of the heart, the ventricles are filling with blood, which will subsequently be ejected during the next systolic period. The pressure within the cardiovascular system can be identified by the point at which blood flow traveling through the arteries produces less turbulence such that sound is no longer heard with the stethoscope.
As mentioned previously, the relationship of the pulse to the blood pressure is that the pulse will be absent when the blood pressure cuff is inflated and felt when the blood pressure cuff is deflated to a level that is less than the pressure within the artery. The pulse first palpated after the cuff is deflated is an indirect estimate of the systolic blood pressure. Unfortunately, no indirect relationship can be obtained for the diastolic blood pressure. Its measurement is dependent on the absence (essentially, the last sound heard) or muffling of sound as air is released from the blood pressure cuff. In view of this, the practice of listening to the Korotkoff sounds and using the methods described in Table 10-6 and shown in Fig. 10-7 is essential to obtain valid and reliable measurements of both systolic and diastolic blood pressure.
Measurement of Systolic and Diastolic Blood Pressure
Systolic and diastolic blood pressures provide important information to detect, categorize, and treat hypertension. The American Heart Association and American College of Cardiology (AHA/ACC) have developed strict guidelines to classify blood pressure. These stages are shown in Table 10-7 and consist of optimal, normal, and hypertensive classifications.2 Both systolic and diastolic blood pressures are important and can contribute to a diagnosis of hypertension separately or in combination (Table 10-7). This table also lists particular treatment strategies according to the hypertension classification consisting of lifestyle modification and drug treatment.
TABLE 10-7 Classification of Systolic and Diastolic Blood Pressure and Recommended Treatments
Another important aspect of measuring the systolic and diastolic blood pressure is calculating the pulse pressure. The pulse pressure is the difference between the systolic and the diastolic blood pressure and is considered the force or pressure responsible for the perfusion of organs and tissues. Therefore, it is preferable to have a wide pulse pressure like 50 mm Hg compared to a narrow pulse pressure like 10 mm Hg. It can be assumed that the wider the pulse pressure, the better organs and tissues are perfused, whereas the more narrow the pulse pressure, the poorer organs and tissues are perfused.
The examination of blood pressure described previously pertains to adults. Examination of blood pressure in children and adolescents is performed using methods similar to those described in Table 10-6, but the categorization and classification of hypertension are different. Appendix 1 of this chapter shows the expected systolic and diastolic blood pressures of children, adolescents, and young adults at specific ages (above which a child, adolescent, or young adult would be recognized to have hypertension). See the CD-Rom activity for Chapter 5 to review and practice taking blood pressures.
MEASUREMENT OF THE SYSTOLIC BLOOD PRESSURE AND PULSE DURING BREATHING AND SIMPLE PERTURBATIONS OF THE BREATHING CYCLE
As previously suggested, it is important to examine the pulse and blood pressure during the breathing cycle. This is because the examination of the systolic blood pressure and pulse during breathing can provide important diagnostic and prognostic information about cardiovascular performance. For example, an alternating strong and weak pulse can identify severely depressed cardiac function. Such an alternating strong then weak pulse has been referred to as pulsus alternans and has been specifically described as a mechanical alteration of the femoral or radial pulse characterized by a regular rhythm and alternating strong and weak pulses. If such an alternating pulse is suspected, the suggested method to further examine the pulse is to use light pressure on the radial artery (as one would obtain the radial pulse) with the patient’s breath held in midexpiration (to avoid the superimposition of respiratory variation on the amplitude of the pulse previously mentioned). If during midexpiration breathholding the pulse is observed to alternate from strong to weak, the patient is identified to have pulsus alternans, which is associated with cardiac pump failure.
Sphygmomanometry can more readily recognize this phenomenon, which commonly demonstrates ≥20 mm Hg alternating systolic blood pressure. Characteristically, if pulsus alternans exists, a 20 mm Hg or greater decrease in systolic blood pressure occurs during breath holding because of increased resistance to left ventricular ejection. It should be noted that a difference exists between pulsus alternans and pulsus paradoxus, the latter of which is characterized by a marked reduction of both systolic blood pressure (− 20 mm Hg) and strength of the arterial pulse during inspiration. Pulsus paradoxus can also be detected by sphygmomanometry and is occasionally seen in cardiac pump failure. However, it is associated more frequently with cardiac tamponade and constrictive pericarditis primarily due to increased venous return and right heart volume, which bulges the interventricular septum into the left ventricle, thus decreasing the amount of blood present in the left ventricle and the amount of blood ejected from it (because of a decreased left ventricular volume and opposition to stroke volume from the bulging septum).
Finally, the integrity of the autonomic nervous system can be examined by measuring the pulse or an electrocardiogram before and after 1 minute of deep breathing at a rate of approximately 6 breaths per minute. While seated, the resting pulse should be obtained after which a subject is asked to breathe deeply and slowly. The patient should be encouraged to breathe at a respiratory rate of approximately 6 breaths per minute. After breathing in this manner for approximately 1 minute, the pulse should again be measured. Normally, the pulse should decrease by approximately 15 to 20 beats per minute with deep, slow breathing. If the pulse rate decreases less than 15 to 20 beats from the resting pulse before deep, slow breathing, it is suggestive that an autonomic nervous system disturbance exists.3 A more rigorous perturbation of breathing with measurement of pulse and blood pressure has been found to be highly predictive of cardiovascular function and will be discussed later in this chapter.
MEASUREMENT OF THE SYSTOLIC AND DIASTOLIC BLOOD PRESSURE AND PULSE IN DIFFERENT BODY POSITIONS—SUPINE VERSUS STANDING
The examination of heart rate and arterial blood pressure before, during, and after a change in body position is clinically useful because it can (1) alert a clinician to the status of the cardiovascular system, (2) enable the cardiovascular system to be perturbated to determine the health of the cardiovascular system, and (3) help the clinician to predict the likelihood of cardiovascular pathology developing in the future. Each of these areas will be discussed in the following section. It is clinically important to evaluate the changes in both systolic and diastolic blood pressure as well as the subsequent change in pulse during body position changes. Of particular importance is the understanding that arterial blood pressure is the product of cardiac output and total peripheral resistance (BP = cardiac output × TPR). It is also important to make several rather broad assumptions about the previous equation to enhance one’s understanding of blood pressure and the changes accompanying positional change. First, although BP in this equation defines overall arterial blood pressure, it is possibly easier to understand the physiology of blood pressure by assuming that BP (in the previous equation) is equivalent to the systolic blood pressure. Second, although TPR in this equation defines overall total peripheral resistance, it is likely easier to more thoroughly understand the influence of positional changes on blood pressure by assuming that TPR (again, in the previous equation) is equivalent to the diastolic blood pressure. The reason for this latter assumption is that the changes in diastolic blood pressure appear to be quite reflective of the changes occurring in the peripheral vasculature (either peripheral vascular constriction or relaxation). These two assumptions and the rationale for them will become more apparent in the following sections. Also, utilization of Table 10-8 should enable a better appreciation for the previous assumptions and examinations described in the following section.
TABLE 10-8 Heart Rate and Blood Pressure Measurements: A Data Sheet
EXAMINATION OF THE PULSE AND ARTERIAL BLOOD PRESSURE WITH BODY POSITION CHANGE TO DETERMINE THE STATUS OF THE CARDIOVASCULAR SYSTEM
The status of the cardiovascular system can be easily determined by examining the change in heart rate and blood pressure while changing the position of the body from supine to standing and vice versa.
CLINICAL CORRELATE
The observation of a reduction in both the systolic and diastolic blood pressure upon standing suggests that the cardiovascular system may be impaired and is unable to produce the necessary peripheral vascular constriction needed to increase venous return and subsequently maintain or increase the systolic blood pressure.
Although venous pooling may be responsible for a decrease in venous return when standing from a supine or seated position, the forward movement of blood back to the heart can only occur with an increase in peripheral vascular constriction or, essentially, with an increase in diastolic blood pressure. When such an increase in peripheral vascular constriction is delayed or does not occur, the compensatory response of the cardiovascular system is to increase the heart rate in hope of increasing the cardiac output (because cardiac output is the product of heart rate and stroke volume; cardiac output = HR × stroke volume; see Chapter 5).
In fact, observation of a decrease in systolic and diastolic blood pressure without a subsequent increase in heart rate when changing body position from supine to standing is considered a positive sign for autonomic nervous system dysfunction.4,5 Several studies have examined the heart rate and systolic and diastolic blood pressure responses to body position change and observed that subjects with a significant decrease in both systolic and diastolic blood pressure (greater than 20–30 mm Hg) and an unchanged heart rate suffered from autonomic nervous system dysfunction that was often the result of diabetes.
EXAMINATION OF THE PULSE AND ARTERIAL BLOOD PRESSURE WITH BODY POSITION CHANGE TO DETERMINE THE HEALTH OF THE CARDIOVASCULAR SYSTEM
The health of the cardiovascular system can also be determined by examining the change in heart rate and arterial blood pressure while changing the body position from supine to standing and vice versa. A cardiovascular system that responds rapidly to body position change is likely in a better state of health than a cardiovascular system that responds sluggishly. This is apparent from the previous section. However, one patient population who seems to be a contradiction to this phenomenon is the extremely well-conditioned athlete. Subjects who are well conditioned have been observed to have greater parasympathetic versus sympathetic nervous system activity. The parasympathetic predominance of a well-trained athlete may limit or delay the heart rate response and peripheral vascular constriction needed when moving from a supine to standing position. Therefore, the time that it takes for the heart rate and blood pressure to increase in an athlete is delayed and is similar to the response of a person who has an unhealthy cardiovascular system. Methods to differentiate the delayed cardiovascular response of persons with a healthy versus unhealthy cardiovascular system can be done with several simple questions. Questions about activity and exercise habits as well as past medical history should enable a quick differentiation of a healthy versus unhealthy cardiovascular system based on a delayed cardiovascular response to body position change. Insufficient data exist to identify a normal time period for the cardiovascular system to respond to body position change. However, it has been suggested that a pulse rate taken approximately 30 seconds after standing which is less or greater than a pulse rate taken immediately after standing is indicative of autonomic nervous system dysfunction. This measurement of pulse rate at approximately 30 seconds after standing (or the 30th pulse beat or ECG complex after standing) compared to the pulse rate immediately after standing (or the 15th pulse beat or ECG complex after standing) has been referred to as the “30:15” ratio.6 The 30:15 ratio reflects the change in heart rate at approximately 30 seconds compared to that at approximately 15 seconds after moving from supine to standing. A heart rate that is unchanged would yield a 30:15 ratio of 1, whereas a heart rate that decreases after 30 seconds of standing would be less than 1.0. Both an unchanged or decreased heart rate after standing for 30 seconds (compared to the heart rate at 15 seconds) is suggestive of autonomic dysfunction. This phenomenon has been observed primarily in persons with diabetes but likely has direct application in the examination of persons with known or suspected cardiovascular disease. Additionally, a sluggish or hypoadaptive (less than normal) heart rate and blood pressure response during a change in body position from supine to standing should be considered abnormal and suggestive of an unhealthy cardiovascular system. Conversely, a more adaptive rapid increase in heart rate and blood pressure after moving from a supine to standing position (approximately 30 seconds) is likely associated with a healthier cardiovascular system which should probably respond favorably to increased functional tasks and therapeutic exercise which will be discussed in a subsequent section.
EXAMINATION OF THE PULSE AND ARTERIAL BLOOD PRESSURE WITH BODY POSITION CHANGE TO DETERMINE THE PRESENCE OR LIKELIHOOD OF CARDIOVASCULAR PATHOLOGY DEVELOPING IN THE FUTURE
The presence or likelihood of future development of cardiovascular pathology has been found to be related to the heart rate and blood pressure response during a change in body position from supine to standing. Nardo et al.7observed in 13,340 men and women aged 45 to 65 years that the mean change in systolic blood pressure from supine to standing was a very slight decrease of approximately 0.5 mm Hg. Unfortunately, no data were provided on the diastolic blood pressure response from supine to standing. However, it is likely that the diastolic blood pressure increased to prevent a more substantial decrease in the systolic blood pressure.
Several important findings were observed in this study of one of the largest cohorts to date including mean positional changes in systolic blood pressure of white and black men and women as well as analyses of the systolic response to cardiovascular morbidity, sociodemographic factors, and cigarette smoking. Table 10-9 presents the mean positional changes in systolic blood pressure of black and white men and women. It is apparent that black men were the only subset to have an increase in the mean systolic blood pressure when moving from supine to stand.
TABLE 10-9 Mean Change in Systolic Blood Pressure of Black and White Men and Women
The change in systolic blood pressure during the aforementioned positional change was also categorized into deciles and the top and bottom 30% of the distribution were compared with the individuals in the middle 40% of the distribution. It is important to note that a larger proportion of the participants in the top 30% of the distribution (having an increase in systolic blood pressure when standing) were black, had a mean seated blood pressure that was greater, and had a predicted risk of developing coronary heart disease after 8 years that was greater than the middle 40% or bottom 30% of the distribution.
EXAMINATION OF THE PULSE AND ARTERIAL BLOOD PRESSURE DURING FUNCTIONAL TASKS AND EXERCISE
The examination of the pulse and arterial blood pressure during functional tasks is occasionally performed by physical therapists, but not to the extent that these measurements are used to determine the exercise prescription or functional exercise training session. Application of the examination processes described previously during functional or exercise training can provide an indirect measurement of cardiovascular function, which is frequently the primary system affected in many patients seen by a physical therapist (eg, neurological disorders from stroke, heart diseases, pulmonary diseases, or endocrine/metabolic disorders). Frequent monitoring of the heart rate and blood pressure may be the best way to examine the safety of exercise and help to establish guidelines and procedures for functional or exercise training. The heart rate and blood pressure responses during exercise and functional training can determine the mode, intensity, duration, and frequency of functional and exercise training as well as determine the need to terminate or continue training. For example, a patient with a recent coronary artery bypass graft surgery seen for progressive exercise and functional training may be limited to several minutes of hallway ambulation due to an abnormally high heart rate and low systolic blood pressure. The abnormally high heart rate and low systolic blood pressure may or may not be accompanied with symptoms of dizziness or light-headedness which would also alert a clinician to modify or terminate training, but often the subjective complaints of dizziness or light-headedness are too late and results in a syncopal or near syncopal episode.
Observation of specific changes in the diastolic blood pressure can also be valuable. The diastolic blood pressure should decrease or remain unchanged during functional or exercise training. If the diastolic blood pressure is observed to increase during increased activity, it is a strong indication that the cardiovascular system is dysfunctional. An increase in the diastolic blood pressure of 10 mm Hg or more is an indication to modify or terminate functional or exercise training. Likewise, an increase in the diastolic blood pressure when the diastolic blood pressure should be decreased (or low) is a strong indicator of cardiovascular dysfunction. An example of this is when the diastolic blood pressure is higher in the supine position compared to the standing position. Such a finding is highly suggestive of a failing cardiovascular (rather than dysfunctional) system. In fact, it is well documented that increased diastolic blood pressure in the supine position (which should promote peripheral vascular dilation) after a maximal exercise test (when the peripheral vasculature is maximally dilated) is highly predictive of ischemic heart disease. In this scenario, ischemic heart disease decreases the pumping ability of the heart (because of myocardial ischemia from maximal exercise) making it difficult for the heart to eject blood from the left ventricle (resulting in elevated left ventricular filling pressures and volume) that is worsened in the supine position (because of increased venous return). Thus, a decreased volume of blood is ejected into the periphery. To compensate for this, the body attempts to return more blood back to the heart (interpreting that the decreased ejection of blood is due to inadequate blood volume and that there is a need for greater venous return). The body subsequently increases venous return by increasing the peripheral vascular resistance (resulting in an increased diastolic blood pressure). The body’s assumption that an increase in venous return will improve cardiovascular function is incorrect and only worsens cardiac pumping leading to further increases in the diastolic blood pressure and subsequent decreases in systolic blood pressure as cardiac pumping continues to fail. Therefore, examination of the pulse and systolic and diastolic blood pressure at rest and during exercise can provide very important diagnostic, prognostic, and therapeutic information.
Auscultation of the Heart
Auscultation of the heart is considered an advanced skill, but listening for several select heart sounds can provide important diagnostic, prognostic, and therapeutic information. The sounds that are likely most important to recognize when auscultating the heart are the first heart sound (S1) and second heart sound (S2), the third heart sound (S3) and fourth heart sound (S4), and a loud S2. These sounds will be presented in the following section.
Proper Use of the Stethoscope
As discussed in Chapter 9, the stethoscope frequently consists of a diaphragm and bell as shown in Fig. 9-1 and should have many of the characteristics that are listed in Box 9-3. The presence of a diaphragm and bell is critically important when auscultating the heart. Similarly, correct insertion of the ear-pieces into the ears (with the earpieces pointing to the patient we want to examine) is possibly more important when auscultating the heart because a proper fit will improve the identification and differentiation of the high- and low-frequency sounds of the heart. Optimal auscultation of the heart can be accomplished by using the helpful hints listed in Box 9-3.
From Box 9-3 it is apparent that the bell is used extensively when auscultating the heart. The bell is used with light pressure and identifies low-frequency sounds such as the Korotkoff sounds when measuring blood pressure or when listening for abnormal heart sounds (eg, the S3 and S4).
Method of Auscultating the Heart
The method of auscultating the heart is similar to that when auscultating the lungs and requires proper use of the stethoscope as well as the correct placement of the diaphragm and bell of the stethoscope on the chest (Box 10-4). A logical and systematic sequence of placing the diaphragm and bell on the chest is necessary. The standard sites used for auscultation of the heart are shown in Fig. 10-8. It is apparent from Fig. 10-8 that there are six to eight sites on the anterior chest that are used for diaphragm and bell placement. The axillary area can also be used (often just the left, but the right may also be examined for particular heart sounds). Placement of the diaphragm and bell of the stethoscope in these areas in a systematic manner and comparing the sounds heard in the different areas can provide much information about the physiologic and mechanical events occurring within the cardiac chambers. Referring to Fig. 10-9 will be helpful in understanding what chambers of the heart are being auscultated and what mechanical events are likely taking place underneath the sites where the diaphragm or bell is placed on the chest. A review of laboratory exercises 2 and 3 may also be helpful. See Appendix 1.
BOX 10-4
Methods of Auscultation of the Heart
1.Identify a reference point in the cardiac cycle:
a.Listen for the difference in the time interval between S1 and S2 (shorter duration) and S2 and S1 (longer duration).
b.Palpate the pulse—the sound heard at or near the time the radial pulse is palpated is the S2.
c.Observe the ECG—the sound heard at the time the R wave is displayed is the S1.
2.Use the stethoscope properly:
a.Diaphragm—designed to identify high-frequency sounds and should be used with firm pressure.
b.Bell—designed to identify low-frequency sounds and should be used with light pressure. However, firm pressure applied to the bell of the stethoscope transforms the bell into a diaphragm. Alternating light and firm pressure to the bell of the diaphragm can help to differentiate normal from abnormal heart sounds.
3.Auscultate with a “systematic standard” utilizing different chest wall locations and body positions (ie, left side-lying, sitting, squatting, and standing):
a.Aortic area = second ICS, right sternal border—S2 is best heard in this area.
b.Pulmonic area = second ICS, left sternal border—pulmonic valve closure (P2) of the second heart sound is best heard in this area.
c.Tricuspid area = fifth ICS, right sternal border—tricuspid valve closure (T2) of the first heart sound is best heard in this area.
d.Mitral area = fifth ICS, midclavicular line near the left nipple—mitral valve closure (M1) of the first heart sound is best heard in this area.
FIGURE 10-8 Cardiac auscultatory areas. (Used with permission from Hillegass E, Sadowsky S. Essentials of Cardiopulmonary Physical Therapy. 2nd ed. Philadelphia, PA: WB Saunders; 2001:124.)
FIGURE 10-9 Procedure for performing and recording the ankle–brachial index.
Sounds Heard During Auscultation of the Heart—Heart Sounds
The sounds heard during auscultation of the heart can be cursorily summarized as being one of five possible sounds. These sounds include the normal S1 and S2, the abnormal S3 and S4, and adventitious heart sounds such as murmurs, clicks, and snaps. The different types of heart sounds and the different characteristic qualities of each of the sounds are listed in Box 10-5 and Tables 10-10 through 10-13. Subtle, yet specific characteristics may accompany the presence of a heart sound in a specific area that allows for specific diagnostic, prognostic, and therapeutic information to be obtained. These specific characteristics enable the clinician to better understand the pathological processes and the need for further examination and subsequent treatment. A summary of different heart sounds heard when auscultating the heart of individuals with known or suspected cardiac pathologies are listed in Table 10-11, and specific methods to differentiate the various types of heart sounds are provided in Table 10-12.
BOX 10-5
Normal and Abnormal Heart Sounds
Normal Heart Sounds
First heart sound (S1)—due to closure of the mitral (M1) and tricuspid (T1) valves—that is heard as a high-frequency sound.
Second heart sound (S2)—due to closure of the aortic (A1) and pulmonic (P2) valves—that is heard as a high-frequency sound.
Abnormal Heart Sounds
Third heart sound (S3)—due to poor ventricular compliance and subsequent turbulence—that is heard as a low-frequency sound in early diastole.
Fourth heart sound (S4)—due to an exaggerated atrial contraction and subsequent turbulence—that is heard as a low-frequency sound in late diastole.
Ejection sound—due to the forceful and rapid ejection of blood, often past an obstruction—that is heard as a harsh higher-frequency sound most often during systole.
Systolic click—due to a prolapsed mitral or tricuspid valve that falls backward into the atria with regurgitant blood flowing forcefully past the prolapsing valve causing turbulence—that is heard as single or multiple “clicking” sounds during systole.
Opening snap—due to the forceful opening of a stenotic mitral valve—that is heard as a harsh “snapping” sound in early diastole.
Pericardial friction rub—due to increased pericardial fluid in the pericardial sac—that impairs filling of the ventricles during diastole and during which the filling ventricles “rub” against the engorged pericardial sac producing a “leathery to squeaky-door” sound during diastole. A pericardial friction rub can also be heard in systole with marked pericardial inflammation or fluid.
Heart murmurs—due to rapid and forceful blood flow or blood flowing past a site of stenosis or regurgitation, all of which produce turbulence—that is heard as a “swishing” sound in systole, diastole, or both systole and diastole.
TABLE 10-10 Systolic and Diastolic Murmurs
TABLE 10-11 Heart Sounds and Physical Examination Findings Associated with Specific Diseases
TABLE 10-12 Distinguishing Characteristics of Heart Soundsa
TABLE 10-13 Potential Indirect Measures of Cardiac Function
The bell of the stethoscope is used when attempting to distinguish abnormal from normal heart sounds. S3 and S4 are abnormal heart sounds that occur because of elevated filling pressures. The elevated filling pressure of the left ventricle (with elevated left ventricular volume) causes blood entering the left ventricle in early diastole to produce a low-frequency sound of turbulence (S3, which results from blood entering a high-pressure and high-volume system). The same elevated ventricular filling pressure causes the atria to contract forcefully near the end of diastole to complete ventricular filling. The forceful contraction of the atria sends a final surge of blood into the ventricles to complete ventricular filling, but if the pressure and volume in the ventricle are elevated, turbulence is produced yielding a low-frequency sound in late diastole (the S4). Auscultatory areas for the appreciation of abnormal heart sounds are shown in Fig. 10-8.
Potential Indirect Measures of Cardiac Function
A number of potential indirect measures of cardiac function exist, which can help to categorize and treat patients with cardiac and cardiovascular disease (Table 10-13). Some of these measurements are more sensitive and specific to cardiac function than others, but combining measurements may be helpful to better understand the degree of cardiac and cardiovascular dysfunction or failure. The majority of these measurements will assist in the differentiation of a failing versus normal or dysfunctional cardiac pump. The following section will provide the rationale for these measurements as potential measures of cardiac function.
Symptoms and Functional Classification
Symptoms and functional classification using one or more classification methods (eg, NYHA classes I–IV as shown in Table 10-4) can provide an indirect measure of cardiac function. Patients with greater symptoms and lower levels of function have been repeatedly observed to suffer from poorer cardiac function (refs of GSHFA). Similarly, paroxysmal nocturnal dyspnea (PND) and orthopnea are two symptoms that are commonly associated with poorer cardiac function.
Cold, Pale, and Possibly Cyanotic Extremities
Individuals with cold, pale, and possibly cyanotic extremities may suffer from cardiovascular dysfunction or failure, which is frequently due to the profound sympathetic nervous system activation associated with cardiac dysfunction and failure. Peripheral vascular constriction in the extremities is likely more common in patients with cardiac pump failure and can be a potential sign of poor cardiac function. However, other disorders such as peripheral vascular disease can produce similar findings, which decrease the specificity of this measure as a true measure of cardiac function.
Jugular Venous Distension and Peripheral Edema
Jugular venous distension and peripheral edema are indirect measures of cardiac function because they represent the end result of poor cardiac function. Good cardiac function is associated with a jugular venous measurement of 3 to 5 cm above the sternal angle of Louis and an absence of peripheral edema (at least due to a cardiac origin). The greater that the JVD is above 5 cm from the sternal angle, the poorer the cardiac pumping ability and the greater the venous congestion (which may or may not be associated with peripheral edema). Therefore, JVD is more specific for poor cardiac function, whereas peripheral edema is associated with poor cardiac performance but is less specific due to the many etiologies of peripheral edema.
Heart Sounds
Heart sounds are another indirect measure of cardiac function.
CLINICAL CORRELATE
The presence of a third heart sound (S3) has been considered a hallmark for heart failure and as such identifies a poor cardiac pump.
Furthermore, an S4 appears to be commonly associated with myocardial infarction (MI) and hypertension, which provide it a certain degree of predictive ability for MI and hypertension. The presence of a combined S3 and S4 is suggestive of a poor cardiac pump, and a loud S2 is suggestive of pulmonary hypertension (which would be associated with either the potential or the presence of a poor cardiac pump).
Pulse
As previously discussed, much of the information obtained from the palpation of the radial pulse is listed in Table 10-5 and includes the rate of the pulse (the heart rate by counting the number of beats per minute), regularity or lack of regularity of the pulse, strength of the pulse, palpable turbulence, relationship of the pulse to a continuous electrocardiographic tracing and heart sounds, and the relationship of the pulse to the breathing cycle. Palpation of the pulse can provide an enormous amount of information about normal and abnormal physiologic phenomena. A pulse that is relatively regular with a normal rate, strength, relationship to heart sounds, electrocardiogram, and breathing cycle and absence of turbulence is a pulse that is likely associated with a good cardiovascular system and normal cardiac pump. However, a pulse that is accompanied by palpable turbulence or lacking one or more of the previously cited normal characteristics is a pulse that is likely associated with a dysfunctional or failing cardiac pump. For example, if during midexpiration breath holding the pulse is observed to alternate from strong to weak, the patient is identified to have pulsus alternans, which is associated with cardiac pump failure. Furthermore, a decrease in the strength of the pulse during inspiration may be associated with pulsus paradoxus, which is also associated with cardiac pump failure.
Electrocardiography
Electrocardiography will be discussed in detail in the following chapter, but several electrocardiographic (ECG) measurements have been found to be associated with cardiovascular function and cardiac performance and include the presence of an irregular ECG rhythm, unchanged R-R wave interval, Q waves, lack of R waves, where R waves should be present, ST-T wave abnormalities such as ST-T wave depression or elevation, prolonged PR, QRS, and QT intervals, excessive voltage, and single-chamber pacer spikes. All of these ECG findings are associated with poorer cardiac and cardiovascular function. More specific ECG findings and the methods to examine them are described in Chapter 11.
Blood Pressure
As previously presented, the systolic and diastolic blood pressures can provide important information to detect, categorize, and treat hypertension (Table 10-7). The American Heart Association and American College of Cardiology guidelines to classify blood pressure were developed to detect, categorize, and treat blood pressure that is observed to be too high. Minimal data exist for blood pressure that is too low, but poor cardiac pumping may eventually progress to low systolic blood pressure and higher diastolic blood pressure (thus decreasing the pulse pressure). It is generally assumed that a patient’s systolic blood pressure can be as low as they can tolerate—once a patient becomes symptomatic (eg, dizziness, light-headedness, dyspnea, fatigue) due to a low blood pressure, attempts should be made to increase the systolic blood pressure. Often this is done by decreasing the dosage or timing of antihypertensive drugs. However, if after decreasing the dosage or frequency of antihypertensive drugs, the systolic blood pressure and pulse pressure are abnormally low and producing symptoms, it may be that the cardiac pump is failing and unable to maintain adequate cardiac output (remember BP = cardiac output × TPR).
Blood Pressure During the Breathing Cycle
As previously discussed, blood pressure changes during the breathing cycle may be suggestive of cardiac dysfunction or failure. In fact, the palpated pulsus alternans associated with cardiac failure that was presented earlier can also be measured via sphygmomanometry. If pulsus alternans exists, a 20 mm Hg or greater decrease in systolic blood pressure will occur during breath holding because of increased resistance to left ventricular ejection. Likewise, a marked reduction in the systolic blood pressure of 20 mm Hg or more during inspiration is associated with pulsus paradoxus, which is also associated with cardiac pump failure.
Pulse and Blood Pressure During Positional Change
Methods to examine the status of the cardiovascular system via pulse rate and blood pressure response while changing the position of the body from supine to standing and vice versa were presented earlier. It is important to remember that an observation of a reduction in both the systolic and the diastolic blood pressure upon standing without subsequent increase in pulse rate suggests that the cardiovascular system may be impaired and is unable to produce the necessary (1) peripheral vascular constriction needed to increase venous return or (2) chronotropic response. Without peripheral vascular constriction to increase venous return and without an increase in pulse rate to compensate for the reduction in venous return, symptoms of dizziness, light-headedness, and even syncope or near-syncope may occur. Such findings are often the result of overmedication with antihypertensive drugs (in particular large doses of α-blockers), but if antihypertensive drugs are not a possible cause, autonomic nervous system dysfunction and a poor cardiac pump are the most likely culprits.
Pulse and Blood Pressure During the Valsalva Maneuver
Examination of the pulse and blood pressure response to the Valsalva maneuver has been studied extensively and has been found to reliably distinguish between a failing and a dysfunctional cardiac pump with a high degree of sensitivity and specificity. It is important to understand the physiologic changes accompanying the Valsalva maneuver, which can be appreciated by viewing Box 9-4, which displays the biomechanics of breathing. It is helpful to view this table, because the changes taking place within the intrathoracic area during the Valsalva are opposite those occurring during normal breathing (which as shown in Table 9-11 are associated with a decrease in intrathoracic pressure). During a Valsalva maneuver, the intrathoracic pressure is increased. This increase in intrathoracic pressure produces an opposite reaction to venous return. It is seen in Box 9-4 that the decrease in intrathoracic pressure facilitates inspiration and venous return (increasing venous return because blood at the superior and inferior vena cava sense a low-pressure area within the thorax to which it will readily move). The opposite is true of the Valsalva maneuver. The increased intrathoracic pressure from the Valsalva decreases venous return because the movement of blood from the vena cava now encounters a high-pressure system, which makes the movement of blood into the thorax less facilitated (decreasing the venous return).
The decrease in venous return and subsequent physiologic changes accompanying the Valsalva maneuver can be appreciated in Fig. 10-10. Figure 10-10A shows the normal pulse and arterial blood pressure response to the Valsalva via an arterial line tracing. The blood pressure is observed to increase initially (stage I), but after it peaks, it drops precipitously to a rather stable level (stage II). After the Valsalva has been held for approximately 10 seconds, it is released (and subjects inspire) and a characteristic negative spike is observed which represents a slight decrease in arterial pressure (stage III). This slight decrease in arterial pressure is the result of inspiration and the development of negative pressure within the thorax. During inspiration the venous return is facilitated (or increased; see Box 9-4), which increases diastolic filling and results in an improved stroke volume and an increase in blood pressure (stage IV) with subsequent reduction in pulse. (This also should be apparent in the tracing of Fig. 10-10A as each spike represents a pulse and the distance between these spikes is greater indicating a lower pulse.)
FIGURE 10-10 Arterial blood pressure response to the Valsalva maneuver. (A) Normal response. (B) Abnormal response.
Figure 10-10B shows an abnormal pulse and arterial blood pressure response to the Valsalva maneuver. The initial increase in blood pressure seen in the normal response of Fig. 10-10A remains elevated and does not decrease during stages II or III as seen normally. In fact, when the Valsalva is terminated, the blood pressure returns to the pre-Valsalva level. Additionally, the pulse rate (or pressure spikes from the arterial line) does not change in Fig. 10-10B. The graphic depiction in Fig. 10-10B is a classic arterial blood pressure response associated with cardiac pump failure. Identification of such a response is highly suggestive of cardiac pump failure.
The methods to measure the blood pressure and pulse during the Valsalva maneuver are shown in Box 10-6. Adhering to these methods should enable accurate and safe measurements of the pulse and blood pressure during the Valsalva maneuver. It is important to note that no complications have been reported in more than 50 studies of the Valsalva maneuver with more than 5,000 patients being examined. Nonetheless, the term Valsalva has a bad connotation and as such we have referred to this examination technique as a controlled expiratory maneuver, because the methods described in the literature and in Box 10-6 are best represented (and possibly better accepted) by a controlled expiratory maneuver during which one exhales through a blood pressure manometer. The methods to perform and interpret the controlled expiratory maneuver are also described on the CD-ROM included with this textbook.
BOX 10-6
Methods to Measure Blood Pressure and Pulse During the Valsalva Maneuver
1.Obtain the resting systolic blood pressure.
2.Inflate the blood pressure cuff approximately 30 to 40 mm Hg above the resting systolic blood pressure. Immediately before the Valsalva maneuver, inflate the sphygmomanometer cuff pressure approximately 30 to 40 mm Hg above the resting systolic blood pressure.
3.Valsalva maneuver: Forceful exhalation into a mouthpiece connected to an aneroid sphygmomanometer with sufficient strength to maintain the pressure steadily at approximately 40 mm Hg for approximately 10 seconds (see CD-ROM).
4.Listen for the Korotkoff sounds at the higher blood pressure cuff pressure. The systolic blood pressure should be greater during phase 1 of the Valsalva maneuver and should normally decrease approximately 10 to 20 mm Hg during phase 2 of the Valsalva maneuver (because of a decrease in venous return from the increase in intrathoracic pressure during the Valsalva maneuver). This can be heard by closing the sphygmomanometer valve to release air when the first Korotkoff sound is heard. In the normal person or person with dyspnea due to pulmonary disease, the following Korotkoff sounds will fade and eventually disappear because of the decrease in systolic blood pressure due to the decreased venous return from the increased intrathoracic pressure. In the person with dyspnea due to cardiac muscle dysfunction the Korotkoff sounds following the first Korotkoff sound will not fade and will not disappear because the systolic blood pressure does not decrease during phase 2 of the Valsalva maneuver, because the elevated end-diastolic volume and pressure of CHF find the 10-second decrease in venous return favorable.
Blood Pressure During Supine to Standing
The aforementioned changes in systolic blood pressure during the Valsalva maneuver may also be apparent during a simple change in body position from supine to standing. As previously discussed in this chapter, body position change can produce dramatic changes in the cardiovascular system. Likewise, the observed response of the cardiovascular system to positional change can identify present or future cardiovascular and cardiac disorders. Because of this, it may also be possible to identify current cardiovascular function by examining the changes in systolic and diastolic blood pressure during a position change from supine to standing.
Like the Valsalva maneuver, a position change from supine to standing produces a reduction in venous return. The specific changes in the systolic and diastolic blood pressure can provide important indirect information about cardiac and cardiovascular function. The decrease in venous return accompanying a change in position from supine to standing can possibly provide information that is similar to that obtained during the Valsalva maneuver; understanding whether the cardiac pump is normal, dysfunctional, or failing. Normally, the diastolic blood pressure will be lower in the supine position (compared to that in the standing position) because of the positional related increase in venous return and subsequent decrease in peripheral vascular constriction (remember, BP = cardiac output × TPR). However, if the diastolic blood pressure is observed to be higher in the supine position compared to that in the standing position, it is likely that the heart is failing and prefers to have a decreased venous return. A change in body position from supine to standing should normally cause the diastolic blood pressure to increase to maintain the systolic and mean arterial blood pressures. A diastolic blood pressure that decreases with standing and is associated with a systolic blood pressure that is similar to that observed in supine is indicative of a heart that has a poor pumping capacity and pumps better with less of a venous return (such as that when standing). Therefore, signs of a failing cardiac pump are (1) a higher diastolic blood pressure in a supine position compared to that in a standing position, (2) a lower diastolic blood pressure standing compared to that when supine, and (3) maintenance of the systolic blood pressure (despite a lower diastolic blood pressure in standing compared to that when supine). Signs of a more normal cardiac pump are (1) a lower diastolic blood pressure in supine compared to that when standing, (2) a higher diastolic blood pressure standing compared to that when supine, and (3) maintenance of the systolic blood pressure as a result of the higher diastolic blood pressure in standing compared to that when supine. These characteristics are shown in Box 10-7.
BOX 10-7
Methods to Distinguish a Normal from Abnormal Cardiovascular System Using the Supine to Standing Test
Method to perform test
1.Measure supine systolic and diastolic blood pressure (patient should lie supine for 5 minutes) and record (see Box 10-4).
2.Measure standing systolic and diastolic blood pressure (immediately upon standing)* and record (see Box 10-4).
Method to distinguish a normal from an abnormal response
Normal response
1.A lower diastolic blood pressure in supine compared to standing
2.A higher diastolic blood pressure standing compared to supine
3.Maintenance of the systolic blood pressure as a result of the higher diastolic blood pressure in standing compared to supine.
Abnormal response
1.A higher diastolic blood pressure in supine compared to standing
2.A lower diastolic blood pressure standing compared to supine
3.Maintenance of the systolic blood pressure (despite a lower diastolic blood pressure in standing compared to supine).
*The blood pressure cuff and stethoscope should be in place and immediately ready to use when the patient initially stands (the cuff of the sphygmomanometer should be inflated when the patient initially stands).
Differentiation of Dyspnea due to a Cardiac Origin from Pulmonary Origin
Dyspnea is possibly the most common complaint of patients. It may be due to a variety of disorders, but the two major categories producing dyspnea are of cardiac and pulmonary origins. A variety of examination techniques may provide important information to differentiate dyspnea of a cardiac origin from that of a pulmonary origin (Table 10-14). The etiology of dyspnea is important to know so that optimal treatment interventions can be allocated. Often, the etiology of dyspnea is apparent from the patient history. The patient history can help to differentiate the shortness of breath of pulmonary disease from heart disease and the shortness of breath of congestive heart failure versus anginal equivalents such as that in patients with diabetes mellitus. Table 10-14 presents the distinguishing characteristics of shortness of breath in pulmonary and cardiac disease. The three main categories represent the past history, symptoms, and signs. The information important in the category of patient history includes a past history of (1) congestive heart failure (CHF), (2) cardiac disease (or risk factors for cardiac disease/dyspnea), (3) combined coronary artery disease and diabetes mellitus (diabetes may impair the sensation of angina to be perceived), or (4) pulmonary disease (or risk factors for pulmonary disease/dyspnea).
TABLE 10-14 Differential Diagnosis of Dyspnea: Cardiac or Pulmonary Origin?
The methods used to evaluate dyspnea in patients with known or suspected pulmonary disorders (Chapter 9) can also be used for patients with known or suspected cardiac disease. Tables 9-2 and 9-3 show several different methods that can help to measure and quantify dyspnea. However, often other important tests and measurements are necessary to fully understand the true etiology and treatment of dyspnea. Several such measurements are described in Table 10-14. The differentiating signs include the appearance, heart rate, blood pressure, pulse pressure, respiratory rate, oxygen saturation level, and the blood pressure response during the Valsalva maneuver. The distinguishing characteristics of each of these measurements are described in Table 10-14. These characteristics are broad generalizations that can be cautiously applied to both resting and exercising conditions.
Of these characteristics, the heart rate and blood pressure observations may be the most confusing and in greatest need of clarification. Persons with known cardiac disease who experience dyspnea will likely have a poorer stroke volume than patients with pulmonary disease (because of damaged myocardium from myocardial infarction [MI]). Because of this, the patient with cardiac disease must increase the resting and exercise heart rate to maintain an optimal cardiac output. Therefore, the heart rate of a patient with cardiac disease may be greater than that of a patient with pulmonary disease. However, a patient with pulmonary disease may suffer from poor oxygenation and may need to increase the resting and exercise heart rate to maintain optimal oxygenation. Therefore, the heart rate category of Table 10-14 is less specific in distinguishing cardiac from pulmonary dyspnea. The systolic blood pressure may be only slightly better at distinguishing cardiac from pulmonary dyspnea. As shown in Table 10-14, the systolic blood pressure of a patient with dyspnea due to a cardiac disorder is likely to be lower than the systolic pressure of a patient with dyspnea due to a pulmonary disorder. The lower systolic blood pressure of the patient with a cardiac disorder appears to be the result again of damaged myocardium, which in the long term reduces the overall cardiac output and responsiveness of the autonomic nervous system (resulting in a reduced cardiac output and total peripheral resistance). Reducing both cardiac output and total peripheral resistance will subsequently decrease the arterial blood pressure because BP = cardiac output × TPR (yielding a lower systolic blood pressure at rest and during exercise in a patient with dyspnea due to a cardiac origin). A quick glance at Table 10-14 also reveals that the diastolic blood pressure does not distinguish cardiac from pulmonary dyspnea, but the pulse pressure appears to be a distinguishable characteristic (being lower in a patient with dyspnea due to a cardiac origin) that is modestly supported in the literature.
Patients suffering from shortness of breath due to heart disease will likely have congestive heart failure or anginal equivalents represented as shortness of breath. The differentiation of dyspnea between heart and lung disease as well as the primary cause of shortness of breath in heart disease (anginal equivalent vs CHF) are relatively simple. However, it may be difficult to distinguish the shortness of breath of pulmonary disease from cardiac disease because of combined heart and lung disease, a poor medical history or similar signs, symptoms, and risk factors for cardiac and pulmonary disease. Another method to examine shortness of breath is by performing the Valsalva maneuver. The Valsalva maneuver has been observed to differentiate the shortness of breath of heart disease from that of pulmonary disease. In this case, it may be helpful to perform a controlled Valsalva maneuver and evaluate the arterial blood pressure response and pulse during the Valsalva.
CLINICAL CORRELATE
A blood pressure and pulse response similar to that in Fig. 10-10A is indicative of dyspnea due to a pulmonary origin. A blood pressure response like that in Fig. 10-10B is indicative of dyspnea due to a cardiac origin of congestive heart failure.
MEDICAL EXAMINATIONS USED BY PHYSICAL THERAPISTS
This section will briefly review the medical examinations that are used by physical therapists. They will include the traditional tests of cardiovascular and cardiac function as well as other less traditional measurements of cardiac function. Table 10-15 provides an overview of the different methods of examination (and treatment) that may be employed in heart diseases. A categorization of the nine most common forms of heart disease and methods to examine them are provided in Table 10-15.
TABLE 10-15 Methods to Examine and Manage Heart Disease
Examination of Cardiac Function
Standard Measurements of Cardiac Function
The standard measurements of cardiac function, perfusion, and viability, as well as the strengths and weaknesses of each method, are listed in Table 10-16. Each method will also be presented in the following sections.
TABLE 10-16 Direct Measures of Cardiac Function: Methods, Strengths, and Weaknesses
Cardiac catheterization—Cardiac catheterization is considered the gold standard to examine cardiac function, blockage in coronary arteries, and the status of cardiac valves and structures. It is an invasive technique that requires a small incision in the femoral artery through which a catheter is introduced and carefully moved through the femoral artery to the common iliac and then to the descending aorta. From here the catheter is progressed to the ascending aorta and then positioned at the base of the coronary sinus where radioactive dye is injected into the coronary arteries after which radiographic films are made of the dye in the coronary arteries. These films are often referred to as angiograms. Areas of blockage can be readily observed, and decisions can then be made on the type of intervention (angioplasty, bypass surgery, or medicine). Repeat catheterizations are often done to examine the efficacy of an intervention. Cardiac catheterization may be immediately performed after an angioplasty or weeks to months after bypass surgery or medical therapy. Ventricular performance can also be examined as measurements of the dye injected into the ventricles are made during systole and diastole that are then used to calculate the ejection fraction and wall motion abnormalities.
Figures 10-11A to 10-11D show the catheter and other equipment needed for the cardiac catheterization. It also shows the progression of a cardiac catheterization from the initial incision to the final injection of dye into the coronary arteries. Dye can also be injected into the left ventricle and examination of the radiographic films can provide fairly accurate measurements of stroke volume, cardiac output, and ejection fraction. In addition to the visual information from a catheterization, information about the pressures within the cardiac chambers can be obtained from a pressure transducer positioned at the tip of the catheter. Figures 10-11E show the pressure data from a catheterization that can then be compared to the normal (ie, expected) values within the cardiac chambers (the normal values for the cardiac chambers are also shown in Fig. 10-11E).
FIGURE 10-11 (A–E) Cardiac catheterization. (A–D) The procedure. (E) The formal report.
Several drawbacks to cardiac catheterization exist and include in some an allergic reaction to the radioactive dye, a high cost (approximately $3,000.00), and the fact that it is an invasive technique which carries a potential risk of complications (eg, stroke, MI, death) in 1 out of every 10,000 individuals. However, specialized centers where catheterizations are frequently performed have lower complication rates.
Finally, another indirect measure of cardiac function can be obtained at the same time a catheterization is performed. This indirect measure is a biopsy of the endocardium of the left or right ventricle. Biopsy of the ventricular endocardium can provide important information related to myocardial cell structure (to diagnose particular types of cardiomyopathy), presence of myocarditis, or myocardial rejection in patients with cardiac transplantation.
Echocardiography—Echocardiography is fast becoming one of the most common examinations of persons with known or suspected cardiopulmonary disorders. It involves placing a handheld transducer that emits sound waves through the chest wall to the heart. Sound waves introduced to the heart bounce back to the transducer and produce images that often look similar to the structures underlying the transducer. The extensive amount of information that can be obtained noninvasively via echocardiography is exceptional. In fact, today’s technology has improved the acquisition, processing, and analysis of data obtained from echocardiography and novel modes of echocardiographic imaging (ie, transesophageal [TEE]) appears to provide information about the patency (openness) of the coronary arteries that is similar to that obtained from cardiac catheterization. Nonetheless, perhaps the major variables obtained from echocardiography are the stroke volume, cardiac output, and ejection fraction both at rest and during exercise. Exercise echocardiography is becoming a common technique to diagnose and prognosticate persons with suspected and known heart disease. Different methods used in echocardiography include Doppler, color flow Doppler, two-dimensional (2-D), M-mode, and TEE echocardiography.
Swan–Ganz catheterization—Swan–Ganz catheterization was first introduced by the doctors Swan and Ganz in the 1960s. They developed a special balloon flotation catheter that currently provides much of the data that are projected to an ICU monitor such as the pulmonary artery pressure and pulmonary capillary wedge pressure. The procedure used for Swan–Ganz catheterization includes a small incision in the jugular artery through which a catheter is introduced and progressed to the common carotid and then to the superior vena cava. The catheter is then progressed into the right atrium past the tricuspid valve and into the right ventricle. From here the catheter is moved into the pulmonary artery and the balloon tip is allowed to float and essentially wedge itself into the pulmonary capillaries (thus providing a pulmonary capillary wedge pressure).
The information obtained from Swan–Ganz catheterization is pressure and temperature related. The key pressure variables are those mentioned previously (eg, pulmonary artery and pulmonary capillary wedge pressures), and oximetry and the key temperature variable is the cardiac output. The temperature probe of the Swan–Ganz catheter is used to measure the time it takes for a known amount of cold injectate (between 0°C and 5°C) to move within the cardiovascular system, yielding the thermodilution measurement of cardiac output. Dye is also used to measure the cardiac output and requires a spectrophotometer to examine the dye dilution to measure cardiac output. All of the data obtained via Swan–Ganz catheterization provide direct information relevant to cardiac function.
Arterial line—An arterial line is simply an indwelling catheter with a pressure transducer attached to the end of a catheter. It is commonly placed at the radial artery and is used primarily to (1) measure the arterial pressure and (2) as a site to obtain frequent arterial blood gases. Therefore, the arterial line indirectly measures cardiac performance via the blood pressure and blood gas information. The arterial line travels from the arm of the patient to a monitor where the arterial blood pressure waveform and digital readout are displayed. Often, the noninvasive automatic blood pressure is digitally displayed just above or below the arterial blood pressure on the standard ICU monitor. The proximity of one to the other is a check mechanism for the clinician. Both the arterial line and noninvasive automatic blood pressures should be similar. If a discrepancy exists, it is an indication that a potential problem may exist (eg, arterial line displacement or automatic blood pressure cuff unattached).
Central venous pressure—The central venous pressure (CVP) is obtained via a catheter introduced at a vein and advanced to the inferior or superior vena cava or right atrium. It reflects right-sided heart function and is frequently used to examine blood volume, vascular tone, and venous return. The differences between the CVP and the arterial line include the initial access via a vein versus artery and more detailed information regarding cardiac function than that obtained from the arterial line alone.
Cardiac enzymes—Cardiac enzymes can provide a measurement of cardiac function by identifying the presence of myocardial damage. Myocardial damage and cardiac function examined by cardiac enzymes alone, however, are somewhat incomplete. However, it is generally accepted that a large release of cardiac enzymes from necrotic myocardial fibrils can indirectly identify the degree of cardiac dysfunction that is likely to be associated with myocardial damage. A minimal release of cardiac enzymes is usually suggestive of a small myocardial infarction and less cardiac dysfunction.
The cardiac enzymes commonly measured when myocardial damage is suspected are listed in Table 10-17. Of these, the most specific enzymes for myocardial tissue are the myocardial band of creatine kinase (CK-MB) and troponin T. Levels that are observed to be greater than the accepted normal range are indicative of myocardial damage. Furthermore, a cardiac enzyme level that is markedly elevated is associated with a greater degree of myocardial damage and dysfunction, whereas a minimal elevation is associated with a slight degree of myocardial damage and dysfunction. This is an important characteristic and is best seen in the enzyme troponin-t, which has been observed to be elevated in not only myocardial infarction but also the failing cardiac pump. Despite this apparent degree of nonspecificity, troponin-t is perhaps one of the most sensitive and specific markers of myocardial infarction and cardiac pump failure. Patients with myocardial infarction will have markedly elevated levels that will decrease within 7 to 14 days, whereas the less elevated level of troponin-t of cardiac failure will not subside and will enzymatically profile a failing cardiac pump. It is apparent that each enzyme is released from the dying cardiac tissue at different times and with different durations to reach peak concentration and reabsorption (uptake) of the released enzymes. Therefore, identification of the time post injury and the relationship of time post injury to the observed cardiac enzymes should further improve the examination of cardiac function via cardiac enzymes.
TABLE 10-17 Cardiac Enzymes Associated with Myocardial Injury and Infarction
Atrial Natriuretic Peptide and Brain Natriuretic Peptide
Atrial natriuretic peptide (ANP) is a regulatory hormone that is released from the atrial myocytes when atrial volume and pressure are elevated. It is the body’s initial attempt to decrease excess fluid volume via natriuresis (excretion of sodium) and diuresis (excretion of water). ANP also suppresses the secretion of renal renin and aldosterone that increases the excretion of electrolytes and water and subsequently decreases fluid volume and blood pressure. Elevated levels of ANP are associated with cardiac pump failure and increased morbidity and mortality rates.8,9 Brain natriuretic peptide (BNP) also reflects increased pressure within the cardiovascular system (commonly due to a poor cardiac pump) and is released from the brain when cardiovascular pressures and volumes are elevated. The specific values of pressure or volume that cause ANP and BNP to be released are unknown, but the release often suggests poor cardiac function.
Radiologic Evidence (eg, Heart Size, Pulmonary Edema)
Indirect measures of cardiac function can be obtained from radiographic methods such as a chest radiograph. Evidence of poor cardiac function can be ascertained when the chest radiograph shows (1) a dilated heart, (2) pulmonary edema, (3) increased size of the pulmonary artery, and (4) other findings suggestive of abnormal structural or compensatory abnormalities. For example, the poor cardiac function responsible for coronary heart failure (CHF) can be appreciated via radiography by the size and shape of the cardiac silhouette as well as via the presence of interstitial, perivascular, and alveolar edema (evaluating fluid in the lungs). Interstitial, perivascular, and alveolar edema are the radiologic hallmarks of CHF, but the size and shape of the cardiac silhouette provide evidence about the etiology of the pulmonary edema. A review of the radiologic examination process described in Chapter 9 will enable a better understanding of the previous information.
Examination of Cardiac Perfusion
Examination of cardiac perfusion is often used to assist in the diagnosis, prognosis, and understanding of the effectiveness of treatment of heart disease. The examination of cardiac perfusion is essentially the measurement of blood flow to myocardial tissue. Perhaps the best example of this is thallium scanning immediately after exercise and then several hours after exercise. Thallium-201 is often used in conjunction with an exercise test, and at peak exercise it is injected intravenously. Areas of the heart receiving less blood flow are identified by either decreased areas of thallium uptake that become reperfused or areas of thallium uptake that remain underperfused long after exercise has ended. The former scenario is associated with myocardial ischemia, whereas the latter is associated with a past myocardial infarction.
Areas of the heart with coronary blockage may be observed to receive less blood flow at peak exercise because of the greater work of the heart (due to higher heart rates and blood pressures which increase the myocardial oxygen demand). As the work of the heart decreases after exercise, the areas of the heart observed to have diminished blood flow at peak exercise now have a return of blood flow to the areas observed to be deficit of blood flow at peak exercise. These changes are reflected in the absence of thallium uptake at peak exercise and in the presence of thallium uptake after resting. This scenario is associated with myocardial ischemia and blockage in the coronary arteries. These thallium findings are often referred to as signs of reversible ischemia. A sign of irreversible ischemia (where thallium uptake is diminished at peak exercise and long after exercise testing; thallium is not absorbed after exercise or at peak exercise) is indicative of a past myocardial infarction. Irreversible ischemia is actually somewhat of a misnomer because the area showing this finding is not really ischemic; it is dead. It is an area where blood flow no longer travels (often because of a complete obstruction of a coronary artery). Such areas are often referred to as fixed defects where the lack of thallium uptake is consistent immediately after exercise and hours after exercise.
Cardiac perfusion measurements such as those mentioned here can be performed with other radioisotopes such as technetium, and they can be performed with pharmacologic methods to increase the work of the heart. Patients unable to exercise (ie, patients with severe orthopedic or peripheral vascular disorders) are often provided drugs such as persantine, adenosine, or dobutamine to increase the work of the heart. The same procedures described previously can be employed at peak pharmacologic effect and several hours after the peak pharmacologic effect. In this manner, areas of reversible or irreversible ischemia can be examined.
Examination of Cardiac Viability
Cardiac viability is essentially the examination of the heart’s metabolism. It is an examination of life or death in particular regions of the heart. In fact, examination of cardiac viability has gained new importance since the discovery of stunned or hibernating areas of myocardium associated with myocardial injury and the development of newer therapeutic interventions for heart disease (eg, feasibility of angioplasty and thrombolytic therapy based on salvageable tissue). Several different techniques are used to examine the viability of cardiac tissue, but all appear to incorporate positron-emitting tomography (PET). PET acquires information related to tissue metabolism. The main methods of PET include perfusion-FDG metabolism imaging, [11C-] acetate oxidative metabolism scanning, and technetium-99M-pyrophosphate scanning. The strengths and weakness of each method are presented in Table 10-16.
Examination of Cardiovascular Function and Risk
Examination of the peripheral cardiovascular system is not dissimilar to that for central cardiac function. In fact, many of the same methods and principles apply to both central and peripheral examination of the cardiovascular system. The following sections will describe some of the similarities and differences and will present several other examination techniques that may be quite useful to the physical therapist attempting to diagnose, categorize, and treat patients with peripheral vascular disease.
Arterial and Venous Angiography
Arterial and venous angiography are simply angiograms of the arterial and venous systems in the periphery compared to the central angiograms of the heart discussed previously. The same radioactive dye injected into the coronary arteries is injected into the peripheral arteries and veins, and a radiograph of the dye within the vessels provides a radiograph similar to that of the coronary arteries. The same concerns with angiography of the heart exist with peripheral angiography and include the invasive nature of the procedure and the potential for infection as well as the possibility of an allergic reaction to the radioactive dye.
Doppler Ultrasound
Doppler ultrasound is also used to examine cardiovascular function. It utilizes the same methodology and principles used to examine cardiac function via echocardiography. Sound waves are directed to areas suspected of being blocked, and the underlying structures can be visualized by the reflected sound wave. Evidence of blockage can be quantified and results of therapeutic interventions can be reexamined. Another benefit of ultrasound is the clinical utility of the auditory aspect of the circulation as it flows past a Doppler transducer. Blood flow can be heard and visualized by the interruption of sound waves from the transducer. In fact, Doppler velocimetry uses the methods and principles described previously to identify pulses that are difficult to palpate and is helpful in the bedside diagnosis of peripheral vascular disease.
Peripheral Limb Pressure Measurements
Peripheral limb pressure measurements can be made with a standard sphygmomanometer cuff (by inflating the cuff 20 to 40 mm Hg above the systolic blood pressure at a number of sites such as the thigh, knee, calf, and ankle) or via special plethysmographic pressure cuffs at the thigh and ankle. The actual blood pressure measurements are obtained with the sphygmomanometer cuff (possibly using a Doppler device), and a pulse volume recording is made with the special plethysmographic pressure cuffs at the thigh and ankle. The pulse volume recording can be examined for signs of peripheral artery disease that may include an absent waveform in severe complete or near-complete occlusion of the peripheral arteries of the legs or simply minor alterations in the rapid systolic upstroke and downstroke of the pulse volume recording.
Ankle–Brachial Index
Although the ankle–brachial index (ABI) is relatively easy to perform and analyze, it is only seldom performed by physical therapists. The methods to perform and analyze the ABI are provided in Fig. 10-9 and simply consist of measuring the systolic blood pressure in the arms and ankles and developing a ratio of the highest ankle pressure and the highest arm pressure (highest ankle systolic BP/highest arm systolic BP), bilaterally. It is important to note that an ABI above 0.90 is normal, whereas an index less than 0.40 is associated with severe arterial obstruction.
Systolic Blood Pressure Response After Exercise
The systolic blood pressure response to exercise can also be used to diagnose peripheral artery disease. Observation of a decrease in ankle systolic blood pressure after exercise is strongly related to peripheral artery disease.
Venous Filling Time and Rubor Dependency Tests
Body position and cardiovascular response to change in body position can help to diagnose and categorize patients with known or suspected peripheral vascular disease. For both the venous filling time and rubor dependency tests, patients are positioned supine on a table with the legs elevated to approximately 45 degrees. After several minutes with the legs in this position they are brought down to rest on the table in a dependent position, which should promote increased blood flow back to the legs. Patients with peripheral artery disease will be observed to have a deep red color in the feet (the “rubor” of the rubor dependency test) and delayed filling (>15 seconds) of the veins.
Homan’s Sign and Trendelenburg Test of Venous Insufficiency
Homan’s sign is simply a test for deep vein thrombophlebitis and consists of squeezing the gastrocnemius muscle while the foot is dorsiflexed. Elicitation of pain in the gastrocnemius strongly suggests thrombophlebitis. A positive Homan’s sign with signs of thrombophlebitis (rubor, warmth, and swelling) confirms thrombophlebitis but requires further examination via Doppler ultrasound, plethysmographic pressure recordings, venograms (dye injected into the venous system), and possibly immediate treatment.
The Trendelenburg test is a test to examine the valvular competence of the venous system. It requires the patient to lie supine with the legs elevated to 45 to 90 degrees. After lying in this position for several minutes, a tourniquet is placed around the thigh to occlude venous flow. The patient then stands and the time for venous filling is measured. Venous filling should normally occur within 30 seconds, and filling taking longer than this is associated with venous insufficiency. Furthermore, filling of the superficial veins within or after 30 seconds suggests that the veins are incompetent, whereas further filling of the superficial veins after the tourniquet is removed suggests that the valves of the saphenous veins are incompetent.
Catecholamines (Norepinephrine and Epinephrine)
The measurement of catecholamines can provide an indirect measurement of cardiovascular function. The release of norepinephrine and epinephrine is stimulated by cardiovascular stress (ie, often due to the so-called fight or flight response). In cardiovascular and cardiac disease, these catecholamines are released to compensate for impaired cardiac and cardiovascular function. The measurement of catecholamines can be easily performed with a sample of blood that can provide accurate measures of sympathetic nervous system activity.
Lipids
The examination of lipids is routinely done in subjects with suspected and known heart disease. It has also become a common screening tool to predict the likelihood of cardiovascular disease. Lipid tests have become almost as commonplace as having blood pressure measured. The lipids that appear to be most important to examine include the total cholesterol, low-density lipoprotein, high-density lipoprotein, apolipoproteins, and triglycerides. The specific lipids, normal values, and rationale for these lipids contributing to cardiovascular disease are provided in Table 10-18.
TABLE 10-18 Examination of Lipids
EXERCISE TESTING
Exercise testing is an important method to examine the cardiovascular, pulmonary, and muscular systems. Perhaps the best example of this is Fig. 10-12, which was first introduced by Wasserman and Whipp in 1975. Figure 10-12shows the relationship of these systems and the potential methods to distinguish a disorder in 1 system from the others. In brief, the three major wheels shown in this Figure represent the interrelatedness among the muscular, cardiovascular, and pulmonary systems. Defects in one or more of these major “wheeled” systems may produce observable signs and symptoms that may be best observed during a controlled bout of exercise—during an exercise test. Furthermore, defects in one or more of the cogs in one or more of the wheels may also produce observable signs and symptoms that may best be observed during exercise testing (Fig. 10-12). Defects in one system may produce defects in another. The observation of particular signs and symptoms during exercise testing combined with other tests and measures can provide a wealth of information about the cardiac, pulmonary, and muscular systems.
FIGURE 10-12 The interrelationship among cardiac, pulmonary, and muscular systems.
The following sections will attempt to briefly distinguish cardiac dysfunction and failure from pulmonary, vascular, and muscular dysfunctions and failures. Furthermore, they will also attempt to outline the pertinent information that can be obtained from an exercise test. The primary reason patients with known or suspected heart disease undergo an exercise test is to examine the electrocardiogram for signs of myocardial ischemia. Although this is the primary reason for the administration of an exercise test, much more important information can be obtained from a properly performed exercise test. Diagnostic and prognostic information can be obtained from exercise testing with and without electrocardiographic interpretation and analyses. The goals of this section are to review the methods and results of exercise testing in patients with known or suspected heart disease and to highlight the diagnostic and prognostic information obtained from an exercise test. The methods of electrocardiographic interpretation and analysis will be presented in the following chapter.
Traditional Exercise Testing
Exercise testing in the United States has undergone a significant history. A variety of modes to exercise patients and protocols to follow when performing an exercise test have been used over the years. The first mode of exercise used in exercise testing was the step test from which other similar and more sophisticated methods were employed. Today in the United States, the most common mode of exercise to administer an exercise test is the treadmill ergometer (or simply, the motorized treadmill). The most common protocol is likely the Bruce, which was first introduced in 1973 by Robert Bruce. Table 10-19 provides a historical perspective of exercise testing in the United States. It is striking how the development of particular modes, methods, and protocols were dependent on the initial work of Master, in 1920, who introduced the first exercise test, the step test.
TABLE 10-19 History of Exercise Testing
Step Tests
Step tests were the first mode to administer exercise to subjects with known or suspected heart disease. The first step test appears to have been developed by Leo Master and resulted in the Master’s 2-Step Test. However, Master developed the step test from reports by his contemporaries who had subjects ascend a certain number of steps in a specific time period. A brief description of the step tests will be presented below with the equipment, methods, and use of results.
Master’s 2-Step Test—Master’s 2-Step Test is a step test that was developed to quickly examine large groups of subjects for health screening. The 2-Step Test is simply a test in which subjects ascend and descend two steps in synchrony with a metronome. Figure 9-13 in Chapter 9 shows the procedure used to perform the Master 2-Step Test and the need for specially constructed steps (with specified dimensions for height and width) to standardize the test. It was developed as a tool to first predict oxygen consumption, but with the clinical use of electrocardiography in the 1950s it quickly became the mode by which patients were exercised to achieve higher heart rates and blood pressures to attempt to diagnose heart disease. Figure 10-13 describes the method used to interpret the step test results and includes measuring the heart rate after the step test and estimating the maximal oxygen consumption. The first such report of using the Master’s 2-Step Test to diagnose heart disease was published in the 1950s. From this point on, exercise testing underwent tremendous growth.
FIGURE 10-13 Nomogram utilizing measurement of heart rate and the results of the step test to predict oxygen consumption. (Used with permission from Robergs R, Roberts S. Exercise, Physiology: Exercise, Performance and Clinical Applications. The McGraw-Hill Companies; 1997.)
1-Step Test—The 1-Step Test was developed from the Master’s 2-Step Test and appears to have developed because the 2-Step Test was too time consuming. The procedure consists of 1 step that is ascended and descended in such a way that the subject initially steps onto the step with right foot and then brings the left foot onto the step. The right foot is then removed from the step and placed on the floor that is followed by the left foot. The stepping sequence begins again, but the left foot is initially placed on the step followed by the right foot. This reciprocal sequence of right foot up followed by left foot, right foot down followed by left foot, left foot up followed by right foot, and left foot down followed by right foot down is done in synchrony with a metronome. The heart rate at the end of the step test was then used to estimate oxygen consumption (Fig. 10–13).
Climbing-Step Test—The Climbing-Step Test was an extension of the aforementioned step tests and appears to have been developed to again decrease the time required of 1- and 2-step tests. The Climbing-Step Test was developed by the German physician Kaltenbach, who found the standard step tests too time consuming. Therefore, he added a component of arm exercise to increase the heart rate and blood pressure response. This method of testing was done primarily to diagnose heart disease and examine the electrocardiogram for evidence of myocardial ischemia. The Climbing-Step Test also utilized standardized steps and arm heights, which were used in the manner shown in Fig. 9-13 in Chapter 9. The results of the Climbing-Step Test were then used to estimate fitness level, oxygen consumption, and presence or absence of heart disease.
Cycle Ergometry Tests
Shortly after step tests became an accepted method to diagnose heart disease, European physiologists began studying the physiologic response to cycle ergometry. The most prolific and noteworthy investigator of the exercise response to cycling was Per Olif Astrand. Astrand standardized cycle ergometry testing and developed normal values that could be estimated based on a given level of work. These standardized estimated values for healthy individuals are still in use today. A number of cycling protocols exist, but the most common appear to be the Astrand–Rhyming protocol, the YMCA protocol, and ramping protocols.
Treadmill Tests
As European and American physicians and physiologists continued to use cycling ergometry exercise tests and step tests to diagnose heart disease, the treadmill ergometer was fast becoming a mode of exercise that no longer was limited to specialized laboratories. Physicians in the United States began using the treadmill ergometer almost exclusively after the seminal work of Robert Bruce was published in April of 1973. Robert Bruce was the co-director of cardiology at the University of Washington in Seattle, Washington. He had experimented with treadmill testing for approximately 10 years during which time he gathered extensive data and examined the cardiorespiratory response to treadmill exercise in healthy persons and patients with heart disease. In 1973, he published the article Maximal Oxygen Intake and Nomographic Assessment of Functional Aerobic Impairment in Cardiovascular Disease in the American Heart Journal. This paper described the Bruce exercise testing protocol, which is still likely the most popular protocol for testing patients with known or suspected heart disease. The reasons it likely remains the most popular treadmill protocol even today are because it (1) is dynamic exercise of large muscle groups using a functional task (walking and running if necessary), (2) begins with relative submaximal exertion and provides progressive increments of work until exhaustion, (3) is safe and relatively acceptable to patients, (4) requires minimal time to perform (perhaps this is one of the most important reasons), and (5) has established normal standard values of oxygen consumption and functional impairment based on the duration of exercise. These same reasons were given as rationale for the development of this protocol by Dr. Bruce at the time of the 1973 publication in the American Heart Journal.
Bruce protocol—The Bruce protocol is a relatively straightforward exercise testing protocol consisting of 3-minute intervals of incremental workloads beginning with a speed of 1.7 mph and a 10% grade and progressing to increased tread-mill speeds and grades every 3 minutes until exhaustion or a predetermined endpoint is attained. The Bruce treadmill exercise testing protocol is shown in Table 10-20. Corresponding to this protocol are the data shown in Fig. 10-14, which show the cardiorespiratory response of normal men and women and cardiac men. It is clear from this figure that there is a relatively linear response to oxygen consumption using the Bruce protocol. This figure also shows the slight differences in submaximal and maximal oxygen consumption among normal men and women and cardiac men. In fact, close examination of Fig. 10-14 reveals that women without heart disease who exercised more than 10 minutes were observed to have a higher level of oxygen consumption than men without heart disease. This is typically not the case (men usually have a higher level of peak oxygen consumption), but Bruce suggested that the reason for this finding in his study was the fact that the women were well-trained athletes.
TABLE 10-20 A Comparison of The Bruce and Naughton Exercise Test Protocols
FIGURE 10-14 Aerobic requirements for multistage treadmill exercise stress test (submaximal only). (Modified with permission from Bruce RA, Kusumi F, Hosmer D. Maximal oxygen intake and nomographic assessment of functional aerobic impairment in cardiovascular disease. Am Heart J. 1973;85(4):546-560.)
Other important results of this study are shown in Table 10-20 and Fig. 10-15. Table 10-20 provides a simple equation to estimate maximal oxygen consumption based on the amount of time completed during the Bruce protocol. Maximal oxygen consumption 
O2max for healthy men and women was estimated with the following equation: O2max = 6.70 − 2.82 (gender factor of 1 for men and 2 for women) + 0.056 (time completed during the Bruce protocol in seconds). Maximal oxygen consumption for cardiac men was estimated with the following equation O2max = 10.5 + 0.035 (time completed during the Bruce protocol in seconds). Figure 10-15 shows three nomograms developed with the data from this study by Bruce. The three nomograms allow for the prediction of the functional aerobic impairment (FAI), which is defined as the difference between the predicted and the measured maximal oxygen consumption divided by the predicted oxygen consumption (FAI = predicated O2max − measured O2max/predicated O2max). Using a ruler, the FAI can be determined by placing 1 end of the ruler at the point representing age (on the A axis) and the other end of the ruler on the point representing the duration of exercise (in minutes) on the Bruce protocol (on the B axis). The FAI is then evaluated based on the activity level of the individual that can be interpreted as either sedentary or active. No specific definition of either sedentary or active was described by Bruce, so this parameter is left to the interpretation of the examiner. The range for FAI using these nomograms is between −20% and +70%. An FAI of −20% is associated with no FAI (actually, no FAI is measured at 0%, and −20% represents a person with an aerobic capacity above the normal standard), whereas an FAI of +70% represents a person with significantly impaired aerobic capacity.
FIGURE 10-15 Bruce nomograms of functional aerobic impairment (FAI) for (A) men, (B) women, and (C) cardiac men. (Reprinted with permission from Bruce RA, Kusumi F, Hosmer D. Maximal oxygen uptake and nomographic assessment of functional aerobic impairment in cardiovascular disease. Am Heart J. 1973;85:545.)
The results of the 1973 Bruce article provided a standardized format for exercise testing of healthy men and women and for men with cardiac disease. He did not study women with cardiac disease and subsequently was unable to provide data to estimate oxygen consumption of FAI of women with heart disease. Overall, the Bruce exercise testing protocol was observed to be acceptable for many patients. However, the rather large and rapid workload increments of the Bruce protocol were found to be less acceptable by patients who were debilitated. Additionally, the amount of useful information was limited because the muscular systems of the debilitated patients fatigued before the cardiac, pulmonary, or cardiovascular systems were taxed, thus yielding little useful information about these other systems (which likely was the reason for the test). Therefore, exercise testing protocols with more gradual and lower increments of work were developed. One such protocol was the Naughton.
Naughton protocol—The Naughton protocol is a lower-level exercise testing protocol developed by John Naughton. It is somewhat difficult to find the actual first description of the complete Naughton protocol, but the protocol as performed today is also outlined in Table 10-20. It should be apparent from Table 10-20 that the gradual workload increments of the Naughton protocol are preferred by patients who are debilitated. For this reason and because of perhaps a greater linearity in cardiorespiratory response during the Naughton protocol, it is the exercise testing protocol most often used in patients who are debilitated such as those with heart failure.
Distinguishing Characteristics From Exercise Test Results
Earlier in this section it was suggested that a distinction between or among the cardiac, pulmonary, and muscular systems could be made using exercise test results. This section will describe several important distinguishing characteristics based on information provided in Chapter 3 and presented earlier in this chapter. Of major importance is once again appreciating the Fick equation (O2 = heart rate × stroke volume × arteriovenous oxygen difference). This equation and several other variables will be used to distinguish between and among cardiac and pulmonary disease, cardiac and cardiovascular disease, cardiac and muscular disease, pulmonary and muscular disease, cardiovascular and muscular disease, and cardiovascular and pulmonary disease.
Distinction Between Cardiac and Pulmonary Disease
The distinction between cardiac and pulmonary disease may be the simplest of all the distinctions listed previously. This is because a distinction can be made by examining the heart rate alone during standardized exercise testing. Figure 10-16A shows the relationship of the heart rate and oxygen consumption during exercise testing in octogenarians, normal subjects, and patients with cardiac and respiratory diseases. It should be clear that the heart rate response of the cardiac patients is much greater at lower workloads than that of the patients with respiratory disease and the other two groups (octogenarians and normal subjects). The reason that this was observed is due to the Fick equation (O2 = heart rate × stroke volume × arteriovenous oxygen difference). Because patients with cardiac disease have a reduced stroke volume during exercise (because of myocardial ischemia or infarction), the heart rate must be greater to maintain cardiac output and the work performance. This particular finding is also shown in Fig. 10-16B, where the oxygen pulse (milliliters of oxygen consumed per heart rate) is lower in the patients with cardiac disease compared to that in the other groups. The oxygen pulse is generally accepted as an indirect measure of stroke volume and in keeping with the common finding of a reduced stroke volume with heart disease, the oxygen pulse is also observed to be lower in heart disease than in pulmonary disease in the other groups shown in Fig. 10-16. Other distinguishing characteristics are presented in Table 10-21.
FIGURE 10-16 Wasserman and Whip plots of the (A) relationships of heart rate and (B) oxygen pulse to oxygen consumption. (Used with permission from Wasserman K, Whipp B. Exercise physiology in health and disease. Am Rev Respir Dis. 1975;112(2):219-249.)
TABLE 10-21 Distinguishing Characteristics Among Cardiac, Pulmonary, Cardiovascular, and Muscular Diseases Using Exercise Test Resultsa,b
Distinction Between Cardiac and Cardiovascular Disease
The distinction between cardiac and cardiovascular disease is difficult because both often accompany each other. However, depending on the type of cardiovascular disease, particular signs or symptoms may be present that can help to distinguish cardiac from cardiovascular disease. Several signs and symptoms suggestive of cardiovascular disease include attainment of only low levels of exercise and work due to intermittent claudication in the calf musculature, a hypertensive blood pressure response, attainment of a low peak heart rate, an attenuated or blunted heart rate response, and a decreased systolic blood pressure in the lower extremities after exercise. This last finding of a decreased systolic blood pressure at the ankle after exercise and several other findings consistent with cardiovascular disease (eg, a low ankle–brachial index, delayed venous filling time, and a positive rubor dependency test) can be found in several earlier sections of this chapter. Other distinguishing characteristics are shown in Table 10-21.
Distinction Between Cardiac and Muscular Disease
The distinction between cardiac and muscular disease is not that dissimilar from the distinction discussed for cardiac and cardiovascular disease. The characteristics of muscular disease would be associated with many of the same signs during exercise testing (low levels of exercise and work due to muscular fatigue, attainment of a low peak heart rate, or an attenuated or blunted heart rate response). Other characteristics are presented in Table 10-21.
Distinction Between Pulmonary and Muscular Disease
The distinction between pulmonary and muscular disease is difficult because many of the signs and symptoms of pulmonary disease are the same as those of muscular disease. Several possible distinguishing characteristics are signs of arterial desaturation with pulmonary disease. However, abnormal biomechanics of breathing, low attainment of exercise duration and workload, rapid respiratory rates, and low levels of oxygen consumption are seen in both patients. Table 10-21 provides several other potential characteristics of distinction.
Distinction Between Cardiovascular and Muscular Disease
The distinction between cardiovascular and muscular disease is also difficult, and in fact cardiovascular disease may produce several forms of muscular disease. Low levels of attained exercise and work are observed in both patients, and similar lower heart rates and respiratory rates may be observed. However, a hypertensive blood pressure response is more likely in cardiovascular disease. Cardiovascular disease may also produce the distinguishing characteristics listed previously (intermittent claudication in the calf musculature, a decreased systolic blood pressure in the lower extremities after exercise, a low ankle–brachial index, delayed venous filling time, and a positive rubor dependency test). Again, the specific methods to perform these examinations can be found in the previous sections, and other possible distinguishing characteristics are shown in Table 10-21.
Distinction Between Cardiovascular and Pulmonary Disease
The distinction between cardiovascular and pulmonary disease can be made using the findings discussed previously, including the signs and symptoms associated with cardiovascular disease (a hypertensive blood pressure response, intermittent claudication in the calf musculature, a decreased systolic blood pressure in the lower extremities after exercise, a low ankle–brachial index, delayed venous filling time, and a positive rubor dependency test) and the signs and symptoms associated with pulmonary disease (arterial desaturation, abnormal bio-mechanics of breathing, and rapid respiratory rates). However, attainment of low exercise duration and low workload as well as low levels of oxygen consumption is seen in both patients.
Issues of Sensitivity and Specificity Regarding ECG-Monitored Exercise Tests
With any diagnostic test, the following questions arise and must be resolved: How well does the test identify those patients with disease (sensitivity); and how well does the test identify those patients without disease (specificity)? In order to answer these questions, test results must be compared to some sort of a benchmark or gold standard. In the case of diagnostic stress tests, that benchmark is coronary angiography, which allows direct visualization of the coronary anatomy and exposes lesions of atherosclerosis which is the etiology of coronary artery disease. Coronary angiography is both risky and costly: Clearly, it is to both the patient’s and the clinician’s advantage to substitute (whenever possible) coronary angiography for a test that possesses both good sensitivity and good specificity. An ECG-monitored stress test is noninvasive, relatively inexpensive, and easy to administer. The hallmark of myocardial ischemia is depression of the ST segment that comes on with exercise and resolves with rest. Use of ECG monitoring during exercise testing maximizes both sensitivity and specificity when the ECG criterion for a positive test is established at 1.0 mm of ST-segment depression.
In order to understand the clinical implications of sensitivity and specificity, we will consider two scenarios:
1.Let us arbitrarily set the ECG diagnostic criterion at 0.5 mm of ST-segment depression. It should be obvious that setting the criterion at such a low level will cause a lot of subjects to rule in for coronary disease. However, if they subsequently undergo coronary angiography, very few of these subjects will show evidence of coronary artery disease. This is an example of a test with very high sensitivity.
2.Now let us arbitrarily set the ECG diagnostic criterion at 2.0 mm of ST-segment depression. It should be obvious that setting the criterion at such a high level will cause very few subjects to rule in for coronary disease. However, if they subsequently undergo coronary angiography, almost all of these subjects will show evidence of coronary artery disease. This is an example of a test with very high specificity.
Clearly, sensitivity and specificity are reciprocal to each other and, within any given test, need to be balanced so that the test accurately identifies not only those individuals who have the disease, but also those people who do not.
It turns out that sensitivity and specificity are maximized when the ECG criterion is set at 1.0 mm of ST-segment depression. Indeed, when data from multiple studies are pooled, meta-analysis of noninvasive ECG exercise testing demonstrates a sensitivity of 68% and a specificity of 77%.10
Walk Tests
Walk tests have also been used in patients with heart disease. They have been used extensively in the examination of patients with heart failure. The same methods described in Chapter 9 can be used when performing a walk test in a patient with heart disease. The 6-minute walk test appears to provide information about the functional status, exercise tolerance, oxygen consumption, and survival of persons with cardiac pump failure. Although the exercise performed during the 6-minute walk test is considered submaximal, it nonetheless closely approximates the maximal exercise of persons with cardiac pump failure and is correlated to peak oxygen consumption (Fig. 10-17A). Additionally, information obtained from the 6-minute walk test has been used to predict peak oxygen consumption and survival in persons with advanced heart failure awaiting cardiac transplantation (Box 10-8). Patients unable to ambulate greater than 300 m during the 6-minute walk test appear to have poorer survival (Fig. 10-17B).
FIGURE 10-17 The relationship between the 6-minute walk test distance ambulated to (A) peak oxygen consumption and (B) survival. (Reprinted with permission from Cahalin LP, Mathier MA, Semigran MJ, Dec GW, DiSalvo TG. The six-minute walk test predicts peak oxygen uptake and survival in patients with advanced heart failure. Chest. 1996;110:325-332.)
BOX 10-8
Prediction Equations for Peak Oxygen Consumption and expected 6-Minute Walk Test Distance Ambulated in Persons with Cardiac Pump Failure
Prediction equations for peak oxygen consumption in patients with heart failure using 6-minute walk test results
1.Distance
Peak 
2 = 0.03 × distance (m) + 3.98
r = 0.64; r2 = 0.42; P < 0.0001; SEE = 3.32*
2.Distance + age + weight + height + RPP
Peak 2 = 0.02 × distance (m) − 0.191 × age (y) − 0.07 × weight (kg) + 0.09 × height (cm) + 0.26 × RPP (× 10−3) + 2.45
r = 0.81; r2 = 0.65; P < 0.0001; SEE = 2.68
3.Distance + age + weight + height + RPP + FEV1 + FVC
Peak 2 = 0.02 × distance (m) − 0.14 × age (y) − 0.07 × weight (kg) + 0.03 × height (cm) + 0.23 × RPP (× 10−3) + 0.10 × FEV1 (1) + 1.19 × FVC (1) + 7.77
r = 0.83; r2 = 0.69; P < 0.0001; SEE = 2.59
4.Distance + age + weight + height + RPP + LVEF + PAP + CI
Peak 2 = 0.02 × distance (m) − 0.15 × age (y) − 0.05 × weight (kg) + 0.04 × height (cm) + 0.17 × RPP (× 10−3) + 0.03 × EF (%) − 0.04 × PAP (mm Hg) + 0.31 × CI (mL/min/m2) + 8.43
r = 0.85; r2 = 0.72; P = 0.0001; SEE = 2.06
Prediction equation to determine the expected 6-minute walk test distance ambulated by heart failure patients
SMWT (m) = (gender [1 = male, 0 = female] × 89) − (age [y] × 3) − (HFdur [y] × 7.3) + 401
r2 = 0.34; P < 0.0001
*r, correlation coefficient; r2, coefficient of determination; SEE, standard error of the estimate; 2max, maximal oxygen consumption; RPP, rate–pressure product; LVEF, left ventricular ejection fraction; PAP, pulmonary artery pressure; CI, cardiac index; HFdur, heart failure duration.
Finally, the equations provided in Box 10-8 can be used to estimate peak oxygen consumption of patients with heart failure who are being examined for possible heart transplantation and who have undergone a 6-minute walk test. However, the predicted values of peak oxygen consumption have a relatively high standard error of the estimate (approximately 2.0–3.0 mL/kg/min). Nonetheless, the ability to predict peak oxygen consumption from the 6-minute walk test can be helpful in categorizing and possibly treating patients with heart failure. Finally, we have developed a prediction equation to determine the normal or expected 6-minute walk test distance ambulated by heart failure patients. This equation is also shown in Box 10-8.
EXAMINATION OF OUTCOMES AND QUALITY OF LIFE IN HEART DISEASE
Table 10-22 provides an overview of many instruments that can be used to measure outcomes and quality of life in cardiac disease. The general health status questionnaires that can be used in patients with cardiac disease are the same general health questionnaires previously presented in Chapter 9 Table 9-16. The disease-specific questionnaires commonly used in persons suffering from heart disease are outlined in Table 10-22. Likewise, the strengths and weaknesses of the different instruments are also presented in Box 10-8 and Table 10-22.11,12 The most frequently used instruments used to evaluate the quality of life of persons with heart disease appear to be the general heart disease and the Minnesota Living with Heart Failure Questionnaire. The MOSSF-36 appears to be one of the most useful tools to examine general perceived health status (MOSSF-36) of patients with heart disease. The MOSSF-36 is shown in Fig. 9-14A to 9-14C, Chapter 9. The MLWHFQ is a 21-item questionnaire that evaluates socioeconomic, psychologic, and physical characteristics of patients with heart failure by using a Likert scale of 0 to 5. A score of 0 indicates that a patient has not been affected by heart failure within the past month, whereas a score of 5 indicates that the patient has been “very much” affected by heart failure within the past month. The higher the total score from the 21 questions, the poorer the quality of life. The worst quality of life would be associated with a total score of 105 (the maximum score of 5 on each of the 21 questions).
TABLE 10-22 Quality of Life and Health-Related Instruments Specific for Cardiac Disease
Finally, Box 10-9 shows the relationships among the MLWHFQ and several other instruments used to examine the health status of persons with cardiac pump failure. It is important to note that of these instruments the 6-minute walk test was consistently found to be modestly correlated to other measures of health status and quality of life. This is an important characteristic in an examination tool and makes the 6-minute walk test an important test for persons with heart failure and possibly other cardiac diseases.
BOX 10-9
SUMMARY
The majority of the methods of examination presented in this chapter, like those presented in the pulmonary examination chapter, have focused on those that can be allocated by a physical therapist. The traditional medical tests and measures for a patient with cardiac disorders have also been presented, but the focus of these tests and measures has been on the clinical application for the patient being examined and treated by a physical therapist. A number of data sheets have also been incorporated into the tables of this chapter and an initial patient note has been provided in Appendix 1 of this textbook. The key tests and measures presented in this chapter include examining the (1) appearance of the patient, (2) feel of the pulse, (3) resting systolic and diastolic blood pressures, (4) systolic and diastolic blood pressures’ response to a variety of perturbations, (5) heart sounds via auscultation, (6) specific signs and symptoms of cardiac and cardiovascular diseases, (7) direct and indirect measurements of cardiac and cardiovascular function, (8) exercise and functional abilities via exercise testing, and (9) outcome measures and quality of life of patients with known or suspected cardiac disorders. Of all these examinations, observing the signs and symptoms of cardiac and cardiovascular disease may be the most clinically useful for the physical therapist. Of the signs presented in this chapter, the manner in which the systolic and diastolic blood pressures respond to a variety of perturbations may be the most simple and informative in terms of examining the status of the cardiac and cardiovascular system. Furthermore, the arterial blood pressure response to the Valsalva maneuver appears to have the strongest supportive literature supporting its role in distinguishing a normal from failing cardiac pump. This simple test will be the basis for the hypothesis-oriented algorithm presented in Chapter 17. The information gained from this and other examinations presented in this chapter can then be used to allocate treatment interventions and determine appropriate outcome measures and effects on quality of life. The results of these examinations have been used to allocate further examinations and treatments based on previously published literature. Again, such evidence-based examination is needed in physical therapy.
APPENDIX 1
I.Expected systolic and diastolic blood pressures of children, adolescents, and young adults at specific ages (above which a child, adolescent, or young adult would be recognized to have hypertension).
II.Suggested laboratory exercises for cardiac examination
Laboratory Exercise 1—Evaluating Risk Factors for Heart Disease Risk-Factor Profiles
Laboratory Exercise 2—Effects of Body Position Change on Heart Rate and Blood Pressure
Laboratory Exercise 3—Effects of the Valsalva Maneuver on Heart Rate and Blood Pressure
Laboratory Exercise 4—Electrocardiography Practice
Laboratory Exercise 5—Auscultation of the Heart Practice
Laboratory Exercise 6—Echocardiography and Other Medical Tests Review via CD-ROM, World Wide Web, and Video
Laboratory Exercise 7—Exercise Testing Practice
Laboratory Exercise 8—Quality of Life Examination
Heads Up!
This chapter includes a CD-ROM activity.
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