Lawrence P. Cahalin & Lori A. Buck*
INTRODUCTION
Practice Pattern D represents a progression in heart disease beginning with cardiac pump dysfunction, which eventually may progress to cardiac pump failure. It is critically important that a physical therapist be able to distinguish between a person with cardiac pump dysfunction and a person with cardiac pump failure. The inclusion/exclusion criteria of Practice Pattern D list two specific pathologies that may distinguish between cardiac pump dysfunction from cardiac pump failure (ejection fraction <30% and exercise-induced myocardial ischemia) and two specific impairments that may distinguish between cardiac pump dysfunction from cardiac pump failure (hypoadaptive blood pressure response to exercise and achieved MET level during exercise testing).1 These distinguishing characteristics are listed in Box 18-1.
BOX 18-1
Although these tests and measures are available from the patient’s medical history, they may, in fact, be history and not represent current cardiac performance. Similarly, the only aforementioned test providing specific information to distinguish cardiac pump dysfunction from failure is the ejection fraction. Another simple measurement that can be performed by a physical therapist that may provide important information to distinguish cardiac pump dysfunction from failure is observing the blood pressure response during a controlled expiratory maneuver.2–10 This simple test can provide important information about the disablement of heart disease and can provide a basis upon which the physical therapist can determine necessary outcomes, subsequent examinations, and specific treatment methods. The most relevant characteristics of cardiac pump dysfunction and cardiac pump failure will be presented in the following sections beginning with the microanatomy and physiology of both the dysfunctional and the failing cardiac pump, which will be followed by a brief review of the effects of cardiac pump dysfunction and failure on the pulmonary system and skeletal muscles.
MICROANATOMY AND PHYSIOLOGY
Cardiac Pump Dysfunction
The microanatomy and physiology of cardiac pump dysfunction are similar to cardiac pump failure. However, the pathological microanatomy and physiology are less extreme in cardiac pump dysfunction.11 The primary characteristic of cardiac pump dysfunction is cardiac muscle dysfunction which produces a slight to modest cardiac impairment represented by slight to modest reductions in stroke volume, cardiac output, and ejection fraction.11These impairments often produce limitations in functional abilities which lead to some level of disability (Fig. 18-1). Functional abilities and disability are less marked in cardiac pump dysfunction compared to the significant reductions in function and greater levels of disability in cardiac pump failure.11–15 In cardiac pump failure, the cardiac muscle fails to contract or relax adequately and results in marked reductions in stroke volume, cardiac output, and ejection fraction.16,17
FIGURE 18-1 The Nagi Disablement Model applied to the examination component of Practice Pattern D. Items from the Guide are listed underneath the major headings of the Disablement Model. Sections within the examination component of the Guide that each item is categorized are indicated in parentheses: H, History; S, Systems Review; T, Tests and Measures. Evidence-based outcomes are underlined. (Adapted with permission from Gordon J, Quinn L. Guide to Physical Therapist Practice: a critical appraisal. Neurol Rep. 1999;23(3):122-128.)
The effects of cardiac muscle dysfunction or failure on the aforementioned areas of disablement are essentially due to changes in microanatomy and physiology from cardiac muscle damage or specific pathological processes which impair cardiac muscle performance. The specific pathological processes are listed in Box 18-2. Cardiac muscle damage from myocardial infarction is the most common cause of cardiac muscle dysfunction.18 The predominant factors contributing to cardiac muscle dysfunction include myocardial cell death, myocardial scar formation, and subsequent physiologic changes associated with myocardial cell death such as impaired cardiac action potential propagation or cardiac arrhythmias which cause alterations in action potential movement in and around damaged myocardial cells18 (see Chapter 6, Fig. 6-5).
BOX 18-2
*Low-density lipoprotein levels ≥130 mg/dL without CAD. CAD, coronary artery disease. Low-density lipoprotein levels >100 mg/dL with CAD. High-density lipoprotein levels <35 mg/dL.
†Female relative <65 years of age with CAD; male relative <55 years of age with CAD. ‡Female >55 years of age; male >45 years of age.
Myocardial Cell Death
Myocardial cell death is initially characterized by interstitial edema, fatty deposits in muscle fibers, and infiltration of neutrophils and red blood cells. Over the 4 to 6 weeks following infarction, macrophages remove the necrotic muscle fibers until a scar has formed.18
Myocardial Scar Formation
Myocardial scar formation is characterized by a thin layer of connective tissue interspersed with muscle cells. Over time the scar gets stronger, initially in the periphery, and later progressing to its center.18
Pathophysiology of Myocardial Cell Death, Scar Formation, and Myocardial Dysfunction
The pathophysiology of myocardial cell death is associated with the aforementioned changes in myocardial cells and the resultant dysfunction as well as the consequences of cardiac muscle dysfunction.18 The consequences of dysfunctional cardiac muscle include the aforementioned impairments of stroke volume, cardiac output, and ejection fraction as well as elevated pressures within the cardiac chambers, pulmonary artery, and throughout the peripheral and pulmonary vasculature.18 Elevation of the pressure in the pulmonary vasculature past 25 mm Hg often leads to pulmonary congestion, the hallmark of congestive heart failure and cardiac pump failure.16,17 The pathophysiological consequences of cardiac pump failure are described in Table 18-1 and will be discussed further in the following section.
TABLE 18-1 Physiologic Consequences of Congestive Heart Failure
Cardiac Pump Failure
Cardiac failure is often described and defined as a syndrome of signs and symptoms due to the heart’s inability to provide an adequate amount of blood flow to sustain normal organ and physiologic system function.16,17 The signs and symptoms of cardiac failure are listed in Box 18-3; the two most common symptoms are dyspnea and fatigue. The dyspnea and fatigue resulting from cardiac failure are due to the inadequate delivery of blood to the lungs, organs, and periphery as well as to the accumulation of blood in the chambers of the heart. The accumulation of blood in the chambers of the heart increases the pressures within the cardiovascular system both centrally and peripherally. The increase in peripheral arterial pressure (eg, due to increases in the peripheral vascular resistance) further decreases cardiac performance because the blood ejected from the heart must overcome the increased peripheral vascular resistance. Ejecting blood from a failing left ventricle against increased resistance in the peripheral vasculature is difficult because the failing cardiac pump must contract with greater force. Frequently, the failing cardiac pump has no capacity to generate a greater force of contraction, and heart failure worsens.16,17
BOX 18-3
Clinical Manifestations of Congestive Heart Failure
1.Dyspnea and fatigue
2.Tachypnea
3.Paroxysmal nocturnal dyspnea
4.Orthopnea
5.Peripheral edema
6.Cold, pale, and possibly cyanotic extremities
7.Weight gain
8.Hepatomegaly
9.Jugular venous distention
10.Crackles (rales)
11.Tubular breath sounds and consolidation
12.Presence of a third heart sound (S3)
13.Sinus tachycardia
14.Decreased peripheral skeletal muscle strength and endurance
15.Decreased ventilatory muscle strength and endurance
16.Decreased exercise tolerance or physical work capacity
17.Functional limitations (eg, limited walking, stair climbing)
18.Disabilities (eg, difficulty doing things with family or friends and being a burden to family or friends)
Centrally, the accumulation of blood in the chambers of the heart elevates the systolic and diastolic pressures within the (1) chambers of the heart and (2) vasculature within the thorax such as the pulmonary artery and veins, superior and inferior vena cava, and the jugular veins. This increase in pressure within the pulmonary vasculature often produces pulmonary edema.16,17 The pressure within the pulmonary vasculature at which pulmonary edema begins is approximately 25 mm Hg. The aforementioned increase in pressure in the pulmonary vasculature, chambers of the heart, and peripheral vasculature leads to worsening cardiac performance, cardiac failure, and signs and symptoms of cardiac failure.16,17 Therefore, treatment of cardiac failure is often directed toward decreasing the elevated pressures in the aforementioned areas (eg, to unload the heart) and improving the pathophysiological events associated with heart failure. The pathophysiological processes at a microanatomical level will be presented in the following section.
Microanatomy and Pathophysiological Processes of Cardiac Failure
The microanatomical processes associated with cardiac failure are due to apoptosis. Apoptosis is the programmed death of cells, which is often extreme in persons with heart failure. Although heart failure may be due to a variety of causes, apoptosis appears to occur at a greater rate in all persons with heart failure despite the etiology of the heart failure. This suggests that a specific genetic predisposition which aggressively “turns on” myocardial cell death may be present in persons with heart failure.19
The causes of apoptosis are thought to be due to either genetic predisposition from birth (eg, some types of cardiomyopathy) or genetic reprogramming/mutation from specific types of heart disease including hypertension, coronary artery disease, or chronic valvular heart disease.20
Apoptosis from either genetic predisposition or genetic reprogramming/mutation from heart disease will frequently produce a cardiomyopathy. Cardiomyopathy is a disease in which the contraction, relaxation, or both the contraction and the relaxation of myocardial muscle fibers are impaired. These are described in detail in Chapter 6.21
Pulmonary Function in Cardiac Pump Dysfunction and Failure
One of the hallmark signs of heart failure is pulmonary edema, and it is therefore the reason the word “congestive” is often added to heart failure.16 The following review of the pulmonary pathophysiology associated with congestive heart failure (CHF) assists in the understanding of pulmonary edema and particular aspects of the examination of persons with CHF such as the presence of inspiratory rales, tachypnea, and dyspnea.
Pulmonary edema can be cardiogenic (hemodynamic) or noncardiogenic (caused by alterations in the pulmonary capillary membrane) in origin.22 The differential diagnosis can be made by history, physical examination, and laboratory examination, as shown in Box 18-4. Despite the different origins of pulmonary edema, the “sequence of liquid accumulation” is similar for both and appears to consist of three distinct stages that are also described in Box 18-4.22
BOX 18-4
Perhaps the most important principle in treating pulmonary edema is that of “maintaining pulmonary capillary pressures at the lowest possible levels,” because it has been demonstrated that pulmonary edema can be decreased by more than 50% when pulmonary capillary wedge pressures are decreased from 12 to 6 mm Hg.22
The effect of repeated bouts of pulmonary edema (which is common in CHF) upon pulmonary function appears to be profound. In fact, it is believed that more advanced CHF may produce a “global respiratory impairment” that is associated with varying degrees of obstructive and restrictive lung disease.23,24 In fact, several measures of pulmonary function have recently been found to be significantly related to the level of dyspnea of persons with advanced CHF (Table 18-2).25
TABLE 18-2 Relationship Between Pulmonary Function and Symptoms in CHFa
Neurohumoral Consequences of Cardiac Pump Dysfunction and Failure
The neurohumoral system profoundly affects heart function in physiologic (eg, fight-or-flight mechanism) and pathologic states such as cardiac pump failure. In general, the neural effects are much more rapid, whereas humoral effects are slower. This is because the information sent by the autonomic nervous system via efferent nerves travels faster than the information traveling through the vascular system.26
Neurohumoral signals to the heart are perceived, interpreted, and augmented by the transmembrane signal transduction systems in myocardial cells. The primary signaling system in the heart appears to be the receptor-G protein-adenylate cyclase (RGC) complex as it regulates myocardial contractility. Figure 18-2 illustrates the complexity of this system, which consists of (1) membrane receptors; (2) guanine nucleotide-binding regulatory proteins (the G proteins, which transmit stimulatory or inhibitory signals); and (3) adenylate cyclase, which converts adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). Adenylate cyclase is an effector enzyme activated by a receptor agonist, thus enhancing cAMP synthesis. The lower portion of Figure 18-2 shows that increased cAMP synthesis ultimately increases the force of myocardial contraction (the inotropic effect).26
FIGURE 18-2 Neurohumoral system in CHF. The receptor G protein-adenylate cyclase complex and other important receptors, all of which affect the inotropic state of the heart. Gs, G-stimulatory protein; G1, G-inhibitory protein; PDE, phosphodiesterase; IBMX, isobutylmethylxanthine; ATP, adenosine triphosphate; cAMP, cyclic adenosine monophosphate. (Adapted with permission from Cahalin LP. Cardiac muscle dysfunction. In: Hillegass EA, Sadowsky HS, eds. Essentials of Cardiopulmonary Physical Therapy. 2nd ed. Philadelphia, PA: WB Saunders; 2001:139.)
The top portion of Fig. 18-2 shows the receptor agonists responsible for the initial activation of the “receptor-G protein-adenylate cyclase complex.” They include norepinephrine, epinephrine, histamine, vasoactive intestinal peptide, adenosine, and acetylcholine.
Figure 18-2 does not reveal the degree of influence each receptor agonist has on cardiac function. In general, the most influential receptor agonists are the sympathetic neurotransmitters norepinephrine and epinephrine, as they relay excitatory autonomic nervous system stimuli to both postsynaptic α- and β-adrenergic receptors in the myocardium. Inhibitory autonomic nervous system stimuli are transmitted by the parasympathetic nervous system via the vagus nerve and the neurotransmitter acetylcholine.26
β2-receptor stimulation promotes vasodilation of the capillary beds and muscle relaxation in the bronchial tracts, whereas β1-adrenergic receptor stimulation increases heart rate and myocardial force of contraction.26The stimulation of α1-adrenergic receptors appears to activate the phosphoinositide transmembrane signaling system,27,28 which increases phosphodiesterase and activates protein kinase, thus marginally increasing the inotropic effect.29 Conversely, stimulation of α2-adrenergic receptors activates the G-inhibitory protein and inhibits adenylate cyclase, which decreases the inotropic effect.30
The activation of adenylate cyclase (and subsequent increase in myocardial force of contraction) is, unfortunately, poorly understood but has been observed to be decreased in patients with CHF. This is the result of “a paradoxical diminution in the function of the RGC complex,”26 which alters the receptor–effector coupling and “limits the ability of both endogenous and exogenous adrenergic agonists to augment cardiac contractility.” The inability of endogenous (produced in the body) or exogenous (medications) adrenergic agonists to increase the force of myocardial contraction is frequently seen in patients with CHF.26–32
The abnormal RGC complex function in CHF appears to be associated with the insensitivity of the failing heart to b-adrenergic stimulation. This insensitivity to b-adrenergic stimulation is apparently the result of a decrease in β1-adrenergic receptor density and is very important because the heart contains a ratio of 3.3 to 1.0 β1- to β2-adrenergic receptors.26 In CHF, the ratio decreases to approximately 1.5 to 1.0, producing a 62% decrease in the β1-adrenergic receptors. This marked decrease in β1-adrenergic receptors decreases the ability of the heart to respond to increased b-adrenergic stimulation and results in a less than optimal increase in heart rate and myocardial force of contraction.26
Skeletal Muscle in Cardiac Pump Dysfunction and Failure
No specific skeletal muscle abnormalities have been observed in patients with cardiac pump dysfunction. However, inactivity due to coronary artery disease or inactivity alone is associated with skeletal muscle weakness, decreased endurance, and atrophy.33
The skeletal muscle of persons with heart failure appears to be markedly impaired in the areas of strength, endurance, mitochondrial function, and energy production.34–45 These impairments of skeletal muscle have been hypothesized to be due to marked neurohumoral activation associated with heart failure, deconditioning associated with heart failure, or the presence of a myopathic process that is not limited to only cardiac muscle, but to all muscles. Studies of patients with CHF with and without cardiomyopathy have identified several important characteristics of skeletal muscles in CHF.
Skeletal Muscle Activity in CHF Without Cardiomyopathy
Results of a study by Shafiq et al. revealed no abnormalities in the skeletal muscles of normal subjects. In patients with CHF but without cardiomyopathy there was a decrease in the average diameters of the type I and type II fibers and in the patients with CHF and cardiomyopathy three distinct skeletal muscle abnormalities were observed including selective atrophy of type II fibers, pronounced nonselective myopathy and hypotrophy of type I fibers.34
Lipkin et al. studied nine patients with CHF of whom three had a dilated cardiomyopathy, five had coronary artery disease, and one had a previous aortic valve surgery for aortic regurgitation. The results of the study by Lipkin et al. revealed low maximal oxygen consumption (11.7 mL/kg/min) and isometric maximal voluntary contraction of the quadriceps (only 55% of the predicted value for weight), increased intracellular acid phosphatase activity in six subjects, increased intracellular lipid accumulation in four subjects, and atrophy of type I and type II muscle fibers in four subjects.35 In conclusion, the previous results and the results of a nuclear magnetic resonance spectroscopy study have shown that skeletal muscle fatigue in patients with CHF is associated with intracellular acidosis and phosphocreatinine depletion,36 which if prolonged may predispose to myopathic processes.
CLINICAL CORRELATE
In view of this, physical therapists should utilize appropriate modes of exercise and exercise prescriptions that minimize intracellular acidosis and phosphocreatinine depletion. This can often be accomplished by beginning with low-level exercise and gradually progressing to higher levels of exercise based on objective signs and symptoms. Activation of the short-term energy system (glycolysis) should be minimized, and exercises utilizing the long-term aerobic energy system (citric acid cycle) will decrease the likelihood of this phenomenon (see Chapter 3).
Skeletal Muscle Activity in CHF with Cardiomyopathy
Skeletal muscle activity is apparently impaired by chronic CHF as well as cardiomyopathy. Skeletal muscle abnormalities due to dilated37–39 and hypertrophic40–44 cardiomyopathies have previously been reported and have consistently revealed type I and type II fiber atrophy.37–44
Caforio et al. studied 11 patients with dilated cardiomyopathy and eight patients with hypertrophic cardiomyopathy via neuromuscular and electromyographic analysis of the right biceps brachii muscle during a maximal voluntary contraction.45 Six of the 19 patients underwent muscle biopsy of the right biceps brachii, and three underwent biopsy of the deltoid muscle with light and electron microscopy analysis.
Results of the neuromuscular assessment were relatively insignificant, except that (1) all symptomatic patients with dilated and one with hypertrophic cardiomyopathy demonstrated a slight hyposthenia in the girdles or proximal limbs, and (2) none of the patients had muscular hypotrophy. Electromyography revealed abnormalities typical of myogenic myopathy in nine patients (five dilated and four hypertrophic), but none showed signs of neurogenic alteration (ie, a reduction of nerve conduction velocities or increase in single motor unit potential duration).45
Muscle biopsies consistently detected pathologic changes (primarily mitochondrial abnormalities) in the type I (slow twitch) fibers in all nine patients from whom a biopsy was obtained, eight of which demonstrated increases of atrophy factors. No alteration of type II fibers was observed in any patient.45
Although echocardiographic and hemodynamic indices of ventricular function were similar in patients with and without EMG abnormalities, patients in functional class III were slightly, but not statistically, more likely to have EMG abnormalities.45
Caforio et al. believe the findings from this study support the hypothesis that skeletal myopathic changes, which are occasionally observed in patients with cardiomyopathy, are of a primary rather than a secondary nature.45 It is likely that both chronic CHF and cardiomyopathy have profound effects on skeletal muscle activity that have been observed to reduce isometric muscle strength by nearly 50%. This reduction may be due to specific changes in skeletal muscle metabolism that produce fatigue at lower absolute workloads, hence limiting maximal exercise capacity in patients with chronic CHF.35 The physical therapist must therefore examine and address many characteristics of the skeletal muscles of persons with CHF and determine how the pathologies and impairments of skeletal muscles impact upon functional abilities and disabilities.
CASE STUDY: A GUIDE AND EVIDENCE-BASED EXAMPLE
Inclusion and Exclusion Criteria for Practice Pattern D
Practice Pattern D describes the generally accepted elements of the management that physical therapists provide to patients who have impaired aerobic capacity associated with cardiovascular pump dysfunction or failure.1 The specific characteristics of the patient/client diagnostic groups for each of the two subgroups of Practice Pattern D are listed in Box 18-1. The inclusion and exclusion criteria for each of the two subgroups in Practice Pattern D are also presented in Box 18-1.
The case chosen to illustrate the physical therapy management of a patient fitting the diagnostic classification of Practice Pattern D is George, a 41-year-old man who suffered a small uncomplicated myocardial infarction (MI) in 1995 at the age of 35 years. He subsequently underwent coronary artery bypass grafting (CABG) 2 months later for recurrent angina. He fit the broad diagnostic classification for Practice Pattern D, Impaired Aerobic Capacity/Endurance Associated with Cardiovascular Pump Dysfunction or Failure. More specifically, his examination findings of having suffered a small uncomplicated MI, having an ejection fraction (EF) of 50%, and having a mild impairment in aerobic capacity of six metabolic equivalents (METs) are common to patients/clients with cardiovascular pump dysfunction. Six years later, George suffered a second massive anterior wall myocardial infarction complicated by congestive heart failure. The progression of his disease resulted in severe impairments, functional limitations, and disabilities consistent with cardiovascular pump failure. He had an abnormal heart rate response to increased oxygen demand, a left ventricular ejection fraction of 25%, a functional capacity of far less than four METs, and a symptomatic response to increased oxygen demand. He also demonstrated an abnormal phase 2 arterial blood pressure response (eg, the blood pressure was maintained) during a controlled expiratory maneuver, which prior to the massive anterior wall myocardial infarction was normal (eg, phase 2 arterial blood pressure decreasing during a controlled expiratory maneuver). This patient met the criteria for a patient/client with cardiovascular pump failure because of the (1) massive anterior wall myocardial infarction which reduced the ejection fraction and produced an abnormal heart rate, functional capacity, and symptoms during increased oxygen demand and (2) abnormal phase 2 arterial blood pressure response during a controlled expiratory maneuver.
The Disablement of Cardiac Pump Dysfunction and Cardiac Pump Failure
The disablement of the patient in this case involved both cardiac pump dysfunction and failure. The active pathology illustrated in the case study is coronary artery disease with subsequent myocardial infarction. The patient had impairments in aerobic capacity, muscle performance, ventilation, respiration and circulation. Functional limitations in self-care, bed mobility, transfers, and gait were noted. He was disabled in that he was unable to work or perform usual household chores/duties, and his family and social relationships were interrupted. These aspects of disablement are shown in Figure 18-1.
Risk Factors
Risk Factors for Developing Coronary Artery Disease
Coronary artery disease is the most common cause of cardiac pump dysfunction and failure (eg, CHF) and is true for this case study.15 Risk factors associated with the development of coronary atherosclerosis46,47 are listed in Box 18-2 and are discussed in detail in Chapters 6 and 15. Identifying risk factors is important in order to assign appropriate risk for recurrent events and therapeutic interventions. A patient at high risk for developing coronary artery disease will be more aggressively managed in those areas of greatest risk. Identifying key risk factors specific to the individual will help the health care professional select the most appropriate interventions. For example, a patient with a past MI and risk factor of inactivity alone can be best managed by prescribing physical exercise alone, whereas another patient with a past MI and risk factors of inactivity, hypertension, elevated lipids, and cigarette smoking is likely in need of an exercise prescription as well as management of lipids, hypertension, and cigarette smoking.
The major risk factors for developing coronary atherosclerosis are dyslipidemia, hypertension, diabetes mellitus, and tobacco use.46 This patient’s major risk factors were dyslipidemia (elevated low-density lipoproteins) and hypertension. He did not have diabetes mellitus nor did he use tobacco. His other risk factors included a family history of heart disease (mother, brother, and sister); age and gender (63-year-old man); and psychological factors (stressful job, history of anxiety for which he takes Xanax, rare bouts of intense anger). Though he did not participate in regular aerobic exercise, he had a physically active work environment (owner of a building supply company) and enjoyed yardwork during leisure time. He was overweight but not obese (height 5 ft 6 in., weight 75.2 kg, body mass index [BMI] 27.6 kg/m2). Premorbid hemostatic factors and serum homocysteine and C-reactive protein levels were not available. He reported alcohol consumption of 2 beers/wk. In summary, this patient had multiple risk factors for developing coronary atherosclerosis, which put him at high risk for a recurrent event.
Risk Factors for Developing Cardiomyopathy and Cardiac Pump Failure
A multitude of inflammatory, metabolic, toxic, infiltrative, fibroplastic, hematological, hypersensitivity, genetic, miscellaneous acquired, and physical agent–related factors have been associated with the development of cardiomyopathy.21 This patient did not have any of these conditions, confirming that coronary atherosclerosis with subsequent myocardial infarctions was the active pathology responsible for his cardiomyopathy and cardiac pump failure.
Examination Techniques
History
Through a careful review of the medical record, consultation with other members of the health care team, and interview of the patient and support system, the physical therapist obtained a detailed history of George’s past and current health status. The information obtained indicated that the patient/client would benefit from physical therapy.
George was married for 18 years and had a 15-year-old daughter who was in highschool. He owned a building supply company. He lived with his family in a two-story private home.
His general health status had been relatively good since his coronary artery bypass graft (CABG) surgery and was limited only by rare episodes of angina, panic attacks, and bouts of anger. He did not smoke or use recreational drugs, and he only drank approximately 2 beers/wk. He worked full-time until this admission, and in his leisure time, he enjoyed yardwork and outings with family and friends. Prior to this admission, George was independent in both activities of daily living (ADL) and instrumental activities of daily living (IADL). His family history was positive for heart disease. The past medical history was significant only for the cardiac issues described in detail in the following section.
In July of 1995, George suffered an inferior MI. This was followed 2 months later by CABG of saphenous vein grafts to the left anterior descending artery, left circumflex artery, and right coronary artery because of recurrent angina. He subsequently returned to full activities including work. He was maintained on cardizem, a calcium channel blocker for its antianginal and antihypertensive properties; mevacor, a statin drug for its lipid-lowering effects; Xanax, a benzodiazepine used for the treatment of anxiety and panic attacks; and, sublingual nitroglycerin (SLNTG), a nitrate used for rare angina. At this time the patient entered a local outpatient multidisciplinary cardiac rehabilitation program. A complete examination including risk-factor analysis and a maximal exercise tolerance test was performed (see Chapter 10 and the CD-ROM for risk-factor analyses and exercise test methods). He also underwent arterial blood pressure measurement during a controlled expiratory maneuver and was found to have a normal response. The patient subsequently participated in an individually tailored rehabilitation program consisting of education, exercise training, and stress management.
Six years later on October 24, 2001, while working in his yard, George developed sudden onset of chest pain, nausea, and diaphoresis. It was the worst pain he had ever felt. He took two SLNTGs without relief and went to the emergency room of the local community hospital. He arrived in the emergency room within 1 hour of onset of chest pain.
Tests and Measures
The electrocardiogram showed ST-segment elevation in leads V2 through V4. He was given tissue plasminogen activator (tPA), a thrombolytic agent; heparin, an anticoagulant; lopressor, a b-blocker to decrease the demand for oxygen; and aspirin, a platelet inhibitor and anti-inflammatory agent. The creatine phosphokinase (CPK) peaked at 2,900 (reference range = 37–200) with a myocardial band fraction of 14%, which was diagnostic for a myocardial infarction. The following day the patient became progressively cold, clammy, and hypotensive. A chest radiograph showed moderate pulmonary vascular congestion and bilateral pleural effusions. He developed cardiogenic shock for which an intra-aortic balloon pump (IABP) was placed, and intravenous dobutamine, a positive inotropic medication, was started. The lopressor was held because it would lower the blood pressure further. The patient was then transferred to the university medical center for further management.
At the university medical center George underwent a cardiac catheterization, which showed occluded grafts to the left anterior descending artery and left circumflex artery. The graft to the right coronary artery was patent. An echocardiogram showed akinesis of the entire anterior wall, septum, and apex; basal and posterior areas were hypokinetic. The left ventricular ejection fraction (LVEF) was severely depressed at 25%. A 24-hour thallium scan was performed to search for areas of hibernating myocardium, which could have benefited from coronary revascularization. Unfortunately there was no viability in any of the infarcted areas. Therefore it was decided that CABG surgery would not yield therapeutic gain. Based on the LVEF of 25% his prognosis was poor with a 40% to 60% 1 year mortality rate.48 Because of the poor prognosis, the patient was referred for a cardiac transplantation evaluation.
On October 30, 6 days after admission, the intra-aortic balloon pump was discontinued. He continued to undergo therapeutic diuresis with careful observation of hemodynamic measures through a Swan–Ganz catheter (see Chapter 19).
George was referred to physical therapy upon IABP removal. The physical therapy tests and measures are detailed at the end of this section and in Box 18-5. Although the patient had a Swan–Ganz catheter, he was still able to actively participate in formal exercise training, which was initiated with breathing exercises and progressed to inspiratory, and expiratory muscle training and cycle ergometry. In fact, the Swan–Ganz catheter enabled more specific exercise to be provided with a better understanding of the effects of exercise on the cardiovascular system. Before, during, and after all breathing and cycling exercises the mean arterial pressure, pulmonary artery pressure, and occasionally the pulmonary artery wedge pressure could be examined with the information provided by the Swan–Ganz catheter. This information was combined and evaluated with the more traditional exercise measurements of electrocardiography and oxygen saturation. Appropriate changes were then made in the patient’s exercise prescription.
BOX 18-5
On November 7, eight days after admission, the Swan–Ganz catheter was removed and the patient was transferred from the intensive care unit (ICU) to the cardiac telemetry floor. More aggressive cardiac rehabilitation was instituted upon transfer out of the ICU. His medications upon transfer included Dobutamine, for inotropic support; Dopamine, for increased renal perfusion; Digoxin, for inotropic support; Lasix, for diuresis; and, Vasotec, for afterload reduction. His laboratory values upon transfer to the floor include hemoglobin (Hgb) 10.2 g/dL, hematocrit (Hct) 30.1%, blood urea nitrogen (BUN) 30 g/dL, and creatine (Cr) 1.3 g/dL. On the floor the patient’s activities were increased, but he consistently complained of increased dyspnea and fatigue. In addition, the patient’s blood pressure continued to decrease with increasing exercise until the patient lost consciousness during hallway ambulation. At this time the patient was transferred back to the cardiac care unit (CCU) because of hypotension despite the addition of the inotropic drug Dobutamine, which was administered intravenously. Another inotropic agent, Milrinone, was added; however, he continued to be hemodynamically unstable despite a maximal medical regimen. Therefore the patient was evaluated for left ventricular assist device (LVAD) implantation. Because the patient remained hypotensive even at rest (despite maximal inotropic therapy) and had other specific indications for LVAD implantation (Table 18-3), an LVAD was implanted on December 7.
TABLE 18-3 Indications for LVAD Placement
Physical therapy reexamination of the patient following LVAD implantation is outlined in Box 18-6. As suggested by the literature, this patient’s initial physical therapy goals were directed toward preventing the ill effects of immobility while he required multiple vasopressive agents for hemodynamic stability.49–52 Specific interventions included airway clearance techniques, upright positioning, active range of motion exercises and bedside functional training activities. When he consistently demonstrated appropriate responses to sitting out of bed and all prohibitive lines (Swan–Ganz catheter, femoral arterial line, or CVVHD) had been removed, the treatment was progressed to training in LVAD battery management and gait training. Methods for the early mobilization of a patient on LVAD support are suggested in Box 18-7.50 Once the patient gained independence in ambulation on level surfaces, the treatment was advanced to aerobic conditioning on a treadmill in a gymnasium setting.>49–51 The physical therapist used the Borg Scale of Perceived Exertion (see Chapter 9) to guide the intensity of the exercise aiming for a grade of 11 to 13 on the 6 to 20 scale.49–51 Selected treatment sessions following LVAD implantation are presented in Box 18-8. A cycle ergometer was also used by ensuring that the exit site for the LVAD drive line was not too low to inhibit the hip flexion necessary for cycling (Fig. 18-3). Resistive exercise for the upper extremities was purposefully omitted to ensure adequate sternal healing.
BOX 18-6
BOX 18-7
Mobilizing a Patient on LVAD Support
1.Note resting supine HR, BP, LVAD rate, flow, and volumes
2.Note all drips, lines, and tubes
3.In general, treatment would be held for:
a.LVAD rate < 50 bpm
b.LVAD volumes < 30 mL
c.LVAD flows < 3.0 L/min
d.Systolic BP < 80 mm Hg
e.Heart rate > 150 bpm
f.Sustained ventricular tachycardia or ventricular fibrillation
4.Assist patient supine to sitting, being certain not to kink or apply torque to the drive line
5.Dangle legs 3 to 5 minutes
6.Assess for orthostasis using parameters listed in number 1 and note any signs or symptoms of intolerance
7.Proceed to LE AROM exercises or;
8.Prepare to ambulate (Heartmate VE LVAD) Attach fully charged batteries one at a time. Apply holster and insert batteries. Clip controller to waist belt or holster (procedure must be reviewed with the LVAD coordinator)
9.Assist patient sitting to standing and begin ambulation as quickly as possible to prevent orthostasis. It is highly recommended to have the assistance of another health care worker when ambulating for the first time. There is a high incidence of orthostasis due to prolonged bed rest, and the sequelae of falling include LVAD dislodgement and hemorrhage.
10.Reassess: BP, LVAD rate, HR (if telemetry available), symptoms
Adapted with permission from Humphrey R, Buck L, Cahalin L, et al. Physical therapy assessment and intervention for patients with left ventricular assist devices. Cardiopulmonary Phys Ther. 1998;9(2):3-7.
BOX 18-8
FIGURE 18-3 Arterial blood pressure response to the valsalva maneuver. (A) Normal response. (B) Abnormal response.
Systems Review
The systems review (limited examination) in this case study was normal except for the cardiopulmonary impairments in aerobic capacity, ventilation, and respiration as expected from the history.
Physical Therapy Tests and Measures
Arousal, attention, and cognition—Measures of arousal, attention, and cognition are important to evaluate in order to determine the patient’s ability to participate in the plan of care and to adhere to safety precautions. This patient was alert and oriented to person and place. On questions relating to time, he was accurate to the month and year. He followed commands tentatively and appeared anxious and fearful.
Aerobic capacity and endurance—The initial examination of aerobic capacity and endurance began with observation of the patient. On observation the patient was found to be diaphoretic at rest, reclining in the bed. Cardiac auscultation revealed a normal first heart sound (S1) and second heart sound (S2) and presence of third heart sound (S3) and fourth heart sound (S4), frequently referred to as a summation gallop. The S3 was heard because of a noncompliant left ventricle.53–55 It is a classic sign of congestive heart failure.56 The “(S4) is heard when augmented atrial contraction generates presystolic ventricular distension.”57 Auscultation of the lungs revealed bibasilar crackles, a common finding in CHF due to pulmonary edema and fluid overload.
Changes in body position and exercise tolerance were initially assessed at the bedside. Heart rate, blood pressure, and oxygen saturation levels were measured with changes from supine to sitting and standing; and, with gentle active range of motion exercises. The results are listed in Box 18-5 and 18-6. Resting tachycardia consistent with cardiac pump failure and deconditioning was found. Mild orthostatic changes were noted. There was an appropriate increase in heart rate and blood pressure to low-level exercise.
The patient also underwent measurement of the arterial blood pressure during a controlled expiratory maneuver, which revealed an arterial blood pressure that remained elevated throughout the maneuver (Fig. 18-3). This abnormal response to the valsalva maneuver indicated that the cardiac pump was failing.
A 6-minute walk test was performed several days after cardiovascular stability was observed and revealed poor exercise tolerance and aerobic capacity/endurance. The results of the 6-minute walk test are shown in Table 18-4. The information obtained from the 6-minute walk test was used to establish a baseline from which to evaluate progress over time and to prescribe exercise and functional training.58 More recently the 6-minute walk test has been shown to predict mortality in patients with heart failure and to predict aerobic capacity.59,60 Aerobic capacity and endurance were measured to assess the patient’s ability to tolerate increased activity and the subsequent increase in demand for oxygen.
TABLE 18-4 Six-Minute Walk Test Results, 11/10/2001
Anthropometric characteristics—An examination of the extremities showed 31 bipedal edema. The fluid overload of congestive heart failure frequently accumulates in the extracellular spaces of the dependent parts of the body, usually the lower extremities. The pitting edema scale may help measurements to be more objective so that change can be followed over time (see Chapter 10).
Assistive and adaptive devices—An occupational therapy consultation was obtained in order to evaluate the patient for assistive devices which would decrease his energy cost of performing simple ADL. Because of the prolonged stay in intensive care, patient’s fearfulness, and orthostatic responses; the therapist anticipated that the patient would eventually need an assistive device for ambulation. A rolling walker may require less energy than a standard walker and therefore would be helpful for the patient with heart failure.
Gait, locomotion, and balance—Static standing balance at the bedside required contact guard. Dynamic standing balance tested upon transfer to the chair required minimal assistance. Gait was not assessed at this time because of hypotension in standing; and, because of the risk of dislodging the Swan–Ganz catheter.
Integumentary integrity—The integumentary system was intact. The patient was at high risk for skin breakdown due to his impaired mobility and poor nutritional intake. Frequent reexamination was performed before and after each treatment session.
Muscle performance—A gross assessment of peripheral muscle strength was performed through observation of active limb movement against gravity. Manual resistance was not given because of his severely compromised pump function.
Range of motion—A standard physical therapy range of motion assessment was performed revealing significant limitation in hamstring length only with a straight leg test bilaterally of approximately 0 degree to 40 degrees.
Self-care—Moving from supine to sitting required moderate assistance. Static short sitting balance (at edge of bed) required close supervision to contact guard. Stand pivot transfer from the bed to the chair required minimal assistance. Bathing, grooming, and toilet needs also required minimal assistance by patient and nursing report.
Ventilation and respiration—Many of the tests and measures presented earlier provided information about ventilation and respiration. An additional area worthy of examination was cough. The patient was observed to have a strong cough, which was sufficient to clear his airway. He produced 2 cc of pink frothy sputum, a classic finding in congestive heart failure.61
Evaluation, Diagnosis, and Prognosis
George is a 41-year-old man with primary impairments in aerobic capacity and endurance associated with cardiovascular pump failure. Additionally he has secondary impairments in range of motion, muscle strength, self-care, and gait and balance. Short-term goals to be achieved within two to three sessions include (1) the patient will be independent in diaphragmatic breathing and cough, (2) the patient will require supervision and verbal cues for gentle active range of motion exercises, (3) the patient will move from supine to sitting with minimal assistance, (4) the patient will require close supervision only for static sitting balance, and (5) the patient will require contact guarding/minimal assistance for stand pivot transfers. Long-term goals to be achieved over 8 to 16 weeks include the following: (1) patient will be independent in self-care; (2) patient will be independent in ambulation on level surfaces and one to two flights of stairs; (3) patient will demonstrate maximal strength and aerobic capacity within the constraints of his disease, impairments, functional limitations, and disability. Goals were progressed as they were achieved or as external constraints were removed allowing greater freedom of movement (ie, the Swan–Ganz catheter removal will allow ambulation). Goals remained unchanged or were decreased when signs or symptoms of intolerance to exercise or instability were observed. Medical instability occasionally increased the duration of care by causing a pause in the provision of physical therapy. The frequency of intervention was daily until the patient became independent in ambulation after which the frequency of intervention was progressively decreased until all goals were achieved.
Results of the initial and subsequent physical therapy examinations provided important diagnostic and prognostic information. The key examination findings in this case include the poor ejection fraction, maintenance of the blood pressure response during a controlled expiratory maneuver (rather than the normal decrease in blood pressure during the maneuver), poor 6-minute walk test distance ambulated, and abnormal cardiorespiratory responses during the 6-minute walk test and during attempts to increase exercises and activities of daily living. Specific characteristics of cardiac pump dysfunction and failure can be extremely useful in the diagnosis and prognosis of patients with cardiovascular disease. A complete description of the rationale and cause of many of the characteristic signs and symptoms of cardiac pump dysfunction and failure are presented in the following sections.
Characteristics of cardiac pump dysfunction—Cardiac pump dysfunction is commonly associated with several characteristic signs and symptoms which are thoroughly described in Chapters 6 and 10 and briefly described in the following:
•Ejection fraction greater than 30% to 40%
•Angina and anginal equivalents and myocardial ischemia
•Cardiac arrhythmias
•Myocardial infarction
•Hypertension
•Decrease in the systolic blood pressure during a controlled expiratory maneuver
•Mild-to-moderate decrease in exercise tolerance and functional abilities
•Disability
•Decreased quality of life
Laboratory findings of cardiac pump dysfunction—The laboratory finding of cardiac pump dysfunction is ventriculographic evidence (via radiologic or echocardiographic methods) of a cardiac ejection fraction above a threshold level of approximately 30% to 40%. It has been accepted that an ejection fraction greater than 40% is associated with adequate cardiac performance.62
Angina and anginal equivalents and myocardial ischemia—Angina is well described in Chapter 10 and can be summarized as the discomfort of myocardial ischemia which may occur in the chest, left arm, neck, back, jaw, teeth, or ears and is frequently described as a heaviness, pressure, or squeezing sensation brought on by exercise, eating a large meal, or emotional excitement or stress. An anginal equivalent is another symptom of myocardial ischemia that is frequently represented by dyspnea and fatigue. The myocardial ischemia producing angina may subsequently result in cardiac pump dysfunction due to inadequate oxygen supply to the heart (the demand for oxygen is greater than the supply). The lack of adequate oxygenation to the heart can also be observed in the electrocardiogram and is often associated with ST-segment depression and cardiac arrhythmias.62
Cardiac arrhythmias—Cardiac arrhythmias may produce cardiac pump dysfunction and are most likely due to myocardial ischemia, electrolyte imbalance, autonomic nervous system abnormalities. Though usually not life threatening, arrhythmias often need to be controlled with medication, and/or a pacemaker or pacemaker/defibrillator in order to optimize myocardial function through proper atrioventricular conduction.62
Myocardial infarction—Myocardial infarction is the most common cause of cardiac pump dysfunction. It is the result of a sustained inadequate supply of oxygen to meet the demands of the myocardium because of (1) coronary artery smooth muscle spasm, or (2) a sudden thrombotic occlusion at the site of a previously atherosclerotic coronary artery culminating in regional myocardial cell necrosis and the associated impairment of cardiac pump dysfunction.62
Hypertension—Hypertension is thoroughly discussed in Chapters 6, 10, and 15 and can be summarized as an arterial blood pressure observed in repeated examinations to be greater than 140/90 mmHg.63 Chronic uncontrolled hypertension places excessive strain on the left ventricle. Initially the ventricle hypertrophies concentrically as a compensation to overcome the afterload. It also stiffens causing systolic and/or diastolic dysfunction. Eventually, the left ventricle will weaken and dilate resulting in CHF. Additionally, hypertension increases the likelihood of coronary atherosclerosis and myocardial infarction.
Mild-to-moderate decrease in exercise tolerance and functional abilities—The exercise tolerance and functional abilities of patients with cardiac pump dysfunction are mildly to moderately decreased compared to the more significant reduction in exercise tolerance and function of patients with cardiac pump failure. The reduction in exercise and functional abilities of patients with cardiac pump dysfunction are often due to limited cardiac performance from myocardial ischemia and associated angina, myocardial infarction, and cardiac arrhythmias. The patient with cardiac pump failure has greater limitations in cardiac performance yielding a much greater decrease in exercise tolerance and functional abilities.62
Disability and decreased quality of life—Disability and quality of life are mildly to modestly affected in patients with cardiac pump dysfunction. Numerous instruments have been used to measure disability and quality of life in patients with cardiac pump dysfunction and include both general and disease-specific instruments. Several examples of general instruments include the Medical Outcomes Study Short Form (SF-36), Sickness Impact Profile, and the DUKE Health Profiles. Several examples of disease-specific instruments include the Quality of Life After Myocardial Infarction, Outcomes Institute Angina Type Specification, and Ferrans and Powers Quality of Life Index-Cardiac Version.64 Chapter 10 provides a brief summary of several of the aforementioned instruments.
Characteristics of cardiac pump failure—Cardiac pump failure is commonly associated with several characteristic signs and symptoms which are thoroughly described in Chapter 10 and briefly described here:
•Chest X-ray evidence of pulmonary edema
•Ejection fraction less than 30% to 40%
•Dyspnea and fatigue
•Tachypnea
•Paroxysmal nocturnal dyspnea
•Orthopnea
•Abnormal breathing patterns
•Peripheral edema
•Cold, pale, and possibly cyanotic extremities
•Weight gain
•Hepatomegaly
•Jugular venous distention
•Crackles (rales)
•Tubular breath sounds and consolidation
•Presence of an S3 heart sound
•Sinus tachycardia
•Maintenance of the systolic blood pressure during a controlled expiratory maneuver
•Markedly decreased exercise tolerance (functional abilities) and peak oxygen consumption
•Decrease in systolic blood pressure and increase in diastolic blood pressure during incremental exercise
•Disability
•Markedly decreased quality of life
Laboratory findings of cardiac pump failure—Laboratory findings of cardiac pump failure include radiologic and ventriculographic evidence of pulmonary edema and a cardiac ejection fraction below a threshold level of 30% to 40%; elevated urine-specific gravity, blood urea nitrogen (BUN), and creatinine levels; decreased erythrocyte sedimentation rates (because of decreased fibrinogen concentrations resulting from impaired fibrinogen synthesis); and occasionally reduced partial pressure of oxygen, arterial (PaO2)), and oxygen saturation levels and elevated partial pressure of carbon dioxide, arterial (PaCO2)) and liver enzyme (eg, serum glutamic-oxaloacetic transaminase [SGOT], alkaline phosphatase) levels; and abnormal serum electrolytes during rigid sodium restriction and diuretic therapy.16,17
Radiologic evidence of CHF is dependent on the size and shape of the cardiac silhouette as well as on the presence of interstitial, perivascular, and alveolar edema (evaluating fluid in the lungs).16 Interstitial, perivascular, and alveolar edemas are the radiologic hallmarks of CHF. The other traditional hallmark of cardiac pump failure is a cardiac ejection fraction below the threshold level of approximately 30% to 40%. It has been accepted that an ejection fraction (measured via radiography or echocardiography) less than 40% is associated with inadequate cardiac performance.16,17,62
Symptoms of cardiac pump failure—Dyspnea: It is often described as breathlessness or air hunger and is probably the most common finding associated with CHF. It is frequently the result of (1) poor gas transport because of acute and chronic pulmonary edema, (2) abdominal ascites from peripheral edema and the potential limitation in diaphragmatic descent, and (3) ventilatory muscle weakness all of which may contribute to an inadequate oxygen supply.16,17,22–25 Inadequate oxygen supply either at rest or during exercise will increase the respiratory rate and tidal volume and frequently produces easily provoked dyspnea or, in severe cases of CHF, dyspnea at rest.16
Paroxysmal nocturnal dyspnea and orthopnea—Sudden shortness of breath awakening a patient with CHF from sleep (eg, nocturnal) is often referred to as paroxysmal nocturnal dyspnea (PND).16 The supine body position assumed during sleep increases venous return to an overloaded cardiac pump which worsens cardiac performance and increases pulmonary edema. In fact, patients with CHF who become dyspneic in the supine position are described as suffering from orthopnea, which can be improved by assuming a more upright body position. Often patients with CHF, PND, and orthopnea will use many pillows to attain a more upright position and sleep more comfortably. The severity of CHF and orthopnea (and essentially cardiac pump failure) can be roughly estimated by determining the number of pillows needed to improve orthopnea and sleep. Four-pillow orthopnea (or more) would suggest more severe pump failure than two-pillow orthopnea. Patients with frequent PND and orthopnea will often place the head of the bed on blocks or sleep in a reclining chair rather than on a bed.16
Signs associated with cardiac pump failure—Abnormal breathing patterns: Rapid and shallow breathing at rest which worsens with exercise is common in patients with CHF. A clinical finding observed in many patients with CHF is extreme dyspnea with quick and shallow breaths after a change in position, most frequently from sitting to standing. This response appears to be associated with orthostatic hypotension and tachycardia and is most profound in patients with more severe CHF. Measuring blood pressure and heart rate while timing the duration of dyspnea may be useful to document progress or deterioration in patient status. Cheyne–Stokes breathing is also frequently associated with CHF and is characterized by waxing and waning depths of respiration with recurring periods of apnea.16
Crackles (rales)—Pulmonary crackles are abnormal breath sounds that were formerly referred to as rales. Crackles are heard during inspiration due to alveolar opening in the presence of pulmonary edema and are considered a hallmark sign (although nonspecific) of CHF. The sound of crackles is identical to that of hair near the ears being rubbed between the thumb and index finger. Crackles are frequently heard at both lung bases in individuals with CHF but may extend upward depending on the patient’s position, the severity of CHF, or both. The importance of the presence and magnitude of rales was first addressed in 1967 and provided data for the Killip and Kimball classification of patients with acute myocardial infarction.65 Individuals with rales extending more than 50% of the lung fields have been observed to have a far poorer prognosis.65
Abnormal heart sounds—The normal heart sounds include the S1 and S2. S1 represents closure of the mitral and tricuspid valves, and S2 represents closure of the aortic and pulmonic valves (see Chapter 10 for a more complete description of examining heart sounds). The most common abnormal heart sounds are S3 and S4. S3 occurs early in diastole (immediately after S2) as blood begins to rapidly fill a stiff, noncompliant ventricle. S4 occurs late in diastole (immediately before S1) as the final filling of a ventricle is assisted by an exaggerated atrial kick to complete ventricular filling. Note that S3 may be normal in children, young adults, and pregnancy. The presence of an S3 is considered the hallmark of CHF.56,57 An S4 is commonly heard in patients with hypertension, left ventricular hypertrophy, increased left ventricular end-diastolic pressure, pulmonary hypertension, and pulmonic stenosis, all of whom need assistance (via an atrial “kick”) with the final filling of the ventricles. Auscultation of the heart may also reveal adventitious (additional) sounds, most frequently murmurs. They not only are common in patients with cardiac pump failure but also appear to be of great clinical significance by identifying CHF patients most responsive to medical therapy or patients with papillary muscle ischemia.56,57
Peripheral edema—Peripheral edema frequently accompanies CHF, but may, in some clinical situations, be absent when, in fact, a patient has significant CHF.16 The failing pumping ability of the heart provides an inadequate amount of blood to peripheral tissues and central organs. As a result, the body senses a decreased volume of blood, which promotes a decrease in fluid excretion with subsequent fluid retention.
Increased fluid retention further loads the heart and makes the work of the heart greater which further decreases its pumping ability. Retained fluid commonly accumulates bilaterally in the dependent extracellular spaces of the periphery such as the ankles, pretibial areas, as well as sacral and abdominal areas (see Chapter 10 for examination of peripheral edema).16
Jugular venous distention—Jugular venous distention (JVD) may also accompany CHF. It may occur as fluid is retained and the heart’s ability to pump is further compromised; the retained fluid increases the filling pressures of the cardiac chambers and results in pulmonary edema and less forward venous flow. Slowed or stagnant venous flow will distend the jugular veins and produce the characteristic JVD of CHF (see Chapter 10 for the examination and a photo of JVD).16
Weight gain—As fluid is retained, total body fluid volume increases as does total body weight. Fluctuations of a few pounds from day to day are usually considered normal, but increases of several pounds per day (>3 lb) are suggestive of CHF.16 Body weight should always be measured from the same scale at approximately the same time of day with similar clothing before exercise is started.
Maintenance of the systolic blood pressure during a controlled expiratory maneuver—The systolic blood pressure response during a controlled expiratory maneuver has an extensive evidence base indicating the important role it has in examining persons with heart disease.2>–10 It has been very useful in determining the presence or absence of heart failure. A systolic blood pressure that is well maintained is associated with cardiac pump failure, whereas a systolic blood that decreases during a controlled expiratory maneuver is associated with cardiac pump dysfunction or normal cardiac performance. Other tests and measures must be used to distinguish between cardiac pump dysfunction and normal cardiac performance including the cardiac ejection fraction and exercise test results. See Chapter 10 and the CD-ROM for a complete description of the methods used to perform and interpret the blood pressure response to a controlled expiratory maneuver.
Cold, pale, and possible cyanotic extremities—The extremities of persons with cardiac pump failure may occasionally be cold, pale, and cyanotic. This abnormal sensation and appearance are due to the increased sympathetic nervous system activation of CHF which increases peripheral vascular vasoconstriction and decreases peripheral blood flow.66,67
Sinus tachycardia—Persons with cardiac pump failure may also experience sinus tachycardia or other tachyarrhythmias because of increased sympathetic nervous system stimulation.16 The sinus tachycardia or tachyarrthymias attempt to improve physiologic function by increasing cardiac output. Unfortunately, this makes the work of the heart greater, which further impairs its ability to pump.
Decreased exercise tolerance, low peak oxygen consumption, and abnormal blood pressure responses to exercise—The exercise tolerance of patients with CHF is significantly less than that of normal subjects and patients with cardiac pump dysfunction.68–74 The substantial decrease in exercise tolerance of persons with cardiac pump failure is due to the numerous pathophysiologies and subsequent signs and symptoms of CHF, as well as the constraints of the Fick equation (oxygen consumption per unit time [
O2] =cardiac output 3 arteriovenous oxygen difference). Oxygen supply is limited by a poor cardiac output and an inadequate arteriovenous oxygen difference because of poor delivery of blood to exercising muscle and the possible myopathic changes in the skeletal muscles of patients with CHF. During exercise, a poor cardiac output may be manifested by a decrease in systolic blood pressure and subsequent increase in diastolic blood pressure, whereas an inadequate arteriovenous oxygen difference is manifested by a narrow arteriovenous oxygen difference (limited capacity to widen) and low peak oxygen consumption (see Chapter 10). In fact, patients with CHF often have peak oxygen consumption levels in the range of 10 to 20 mL/kg/min (approximately 3–6 METs). Peak oxygen consumption less than 10 to 14 mL/kg/min is often used as a threshold level range to list patients for cardiac transplantation.74
Such a low level of peak oxygen consumption was apparent in the preexercise training exercise test results of the case study patient. Peak oxygen consumption was observed to be substantially greater after LVAD implantation and physical therapy. Measurement of the ventilatory threshold (VT) and the change in oxygen consumption to change in work rate above the anaerobic threshold also appear to be useful and relatively reliable when examining exercise tolerance in patients with CHF.68–73 The effects of LVAD implantation and physical therapy on these parameters are also apparent in that the VT moved to the right, yielding increased aerobic capacity and improved cardiorespiratory function of the patient presented in the case. Finally, it is apparent that as individuals at rest become short of breath, retain fluid, develop peripheral and pulmonary edema, gain weight, and develop a faster resting heart rate, their ability to exercise is dramatically decreased.
Disability and decreased quality of life—In the past several years much research has been performed in the area of quality of life in CHF.75–90 Early attempts to measure quality of life used instruments that were limited, such as dyspnea indices and exercise tolerance tests. More comprehensive instruments have been designed and consist primarily of questionnaires that measure specific attributes of life such as socioeconomic, psychologic, and physical functioning (see Chapter 10). Several such instruments include the Minnesota Living with Heart Failure Questionnaire, Chronic Heart Failure Questionnaire, and the Kansas City Heart Failure Questionnaire. These instruments have consistently found significantly greater disablement and poorer quality of life in patients with cardiac pump failure compared to patients with cardiac pump dysfunction and normal individuals.75–90
Intervention Techniques
Medical Interventions for Cardiac Pump Dysfunction
The medical interventions for cardiac pump dysfunction include several of the interventions presented for the acute treatment of a myocardial infarction presented in Chapter 6. The acute treatment of a myocardial infarction via PTCA with or without stenting is used not only for an acute myocardial infarction but also for patients with chronic coronary artery disease and coronary occlusion in need of reduction.91 Although this is the current standard of care for coronary artery disease, increasing evidence suggests that pharmacologic treatment may be just as effective as these more invasive and costly interventions.92 Many of the pharmacologic interventions that have the potential to manage coronary artery disease are listed in Table 18-5.
TABLE 18-5 Medical Interventions for Cardiac Pump Dysfunction and Failure
Table 18-5 also lists other medical interventions that all have the potential to (1) decrease the work of the heart, (2) decrease the amount of blockage in a coronary artery, or (3) provide new “plumbing” to the myocardium of a person with cardiac pump dysfunction. It is important to note that pharmacologic agents combined with optimal cardiac rehabilitation services have the potential to decrease the work of the heart and blockage in a coronary artery as well as improve myocardial blood flow.93–95
The first goals of medical treatment of persons with cardiac muscle dysfunction are to decrease the work of the heart and to decrease the amount of blockage in a coronary artery. Pharmacologic agents accomplish the aforementioned goals by decreasing the preload, afterload, and heart rate. In view of this, b-adrenergic blockers are a class of drugs frequently used to treat patients with coronary artery disease due to the reduction in both afterload and heart rate (see Chapter 8 for more information regarding b-adrenergic blockers). If this and other forms of medical treatment are ineffective in controlling the signs and symptoms of coronary artery disease, many patients undergo PTCA with and without stenting and experience results that are somewhat inconclusive.91,92 These results are shown in Table 18-6.92
TABLE 18-6 Invasive Versus Noninvasive Treatment of Stable CAD
Medical Interventions for Cardiac Pump Failure
The medical interventions for cardiac pump failure are also listed in Table 18-5 and have the potential to either (1) decrease venous return and decrease the work of the heart or (2) improve the work of the heart.96 The methods to attain these goals are quite different from one intervention to another as is evident in Table 18-5. However, all of the medical interventions listed for the treatment of cardiac pump failure in Table 18-5 decrease the work of the heart and improve the work of the heart.
Utilization of Specific Tests and Measures to Direct Therapeutic Intervention
The medical treatment of patients with heart disease is based on the results of numerous tests and measures of which the preceding signs and symptoms of cardiac pump dysfunction and failure are instrumental in prescribing physical therapy.57 Each of these tests and measures are thoroughly discussed in Chapter 10, but the method to use the results of these tests and measurements to direct and provide physical therapy will be discussed here.
CLINICAL CORRELATE
The most useful measurements to categorize patients with cardiac pump dysfunction or failure and provide physical therapy appear to be ejection fraction, electrocardiographic signs of myocardial ischemia, blood pressure monitoring during exercise, estimated or measured MET level achieved during an exercise test, and the blood pressure response to a controlled expiratory maneuver.2–10,57
The blood pressure response to a controlled expiratory maneuver (Fig. 18-3) may also be valuable when providing specific interventions to patients with cardiac pump dysfunction and failure. Recently, the medical treatment of persons with heart failure has been directed by evaluating the arterial blood pressure response during a controlled expiratory maneuver.2–10 A patient with a blood pressure response like that in Figure 18-3 (indicating a failing cardiovascular pump) would receive medical treatments like digoxin, diuretics, and afterload reducers to improve the cardiac pump by (1) decreasing the venous return and fluid volume and (2) improving the force of myocardial contraction. These effects appear to improve cardiovascular and functional performance of patients with CHF and even improve the arterial blood pressure response during a controlled expiratory maneuver (yielding a more normal response similar to that in Figure 18-3A).2–10
Therefore, initial measurement of blood pressure during a controlled expiratory maneuver may be the most clinically efficacious method to categorize a patient with a failing cardiac pump or a dysfunctional cardiac pump (see Chapter 10 and Fig. 18-3) from which a hypothesis-oriented algorithm can be developed (Fig. 18-4). Maintenance of the systolic blood pressure during a controlled expiratory maneuver (Fig. 18-4) indicates that the cardiac pump is failing and prefers to have less venous return. A decrease in systolic blood pressure during a controlled expiratory maneuver indicates that the cardiac pump is either normal or dysfunctional and prefers to have an increased venous return.
FIGURE 18-4 A hypothesis-oriented algorithm for the use of the controlled expiratory maneuver. IMT, inspiratory muscle trainer; EMT, expiratory muscle trainer.
Other specific tests and measures that would categorize a patient with cardiac pump dysfunction include an ejection fraction between 30% and 50%, exercise-induced myocardial ischemia, a functional capacity of less than or equal to 5 or 6 METs with a history of heart disease, a hypertensive blood pressure response, nonmalignant arrhythmias, and dyspnea and fatigue with a history of heart disease.57
Other tests and measures that would categorize a patient as having cardiac pump failure include an ejection fraction of less than 30%, complex ventricular arrhythmias, falling systolic blood pressure response to increased oxygen demand, functional capacity of less than or equal to 4 or 5 METs, marked exercise-induced myocardial ischemia, and marked dyspnea and fatigue in a person with evidence of a failing cardiac pump.57
Physical therapy intervention should incorporate methods of treatment that mimic the traditional medical therapy for persons with cardiac pump failure and dysfunction while increasing strength, endurance, and functional abilities. Utilization of body positions that decrease venous return and maximize ventilatory strategies are keys to improving the impairments, functional limitations, and disabilities associated with cardiac pump failure (associated with a well-maintained blood pressure during a controlled expiratory maneuver). Likewise, breathing exercises and possibly noninvasive positive-pressure ventilation at rest and during exercise may improve the disablement of cardiac pump failure.25,97–103 Conversely, a decrease in blood pressure during a controlled expiratory maneuver indicates that the heart can very likely tolerate substantial increases in venous return from supine body positions, physical exercise, and other modalities or physical therapy treatments that may increase venous return (eg, aquatic physical therapy in cold or lukewarm water).
The interventions for the patient with cardiac pump dysfunction are very similar to those for the patient with cardiac pump failure, but subtle differences in the application and progression of treatments exist (Fig. 18-4). The examination and treatment differences between these patients are shown in the decision tree for a patient categorized with a dysfunctional or failing cardiovascular pump.
CLINICAL CORRELATE
Patients with cardiac pump failure have been observed to train more effectively with one-legged cycling than with two-legged cycling (indicating that the patient with cardiac pump failure prefers to have a limited venous return).104
Conversely, patients with cardiac pump dysfunction or clients who have been identified as healthy with normal cardiac pump performance favor an increase in venous return which could be accomplished via two-legged cycling or a variety of other modes of exercise at higher exercise intensities.79,105,106
Although patients with cardiac pump dysfunction can tolerate daily, high-intensity exercise reasonably well, the patient with cardiac pump failure is likely to train most effectively at lower exercise intensities, less often.107–109
CLINICAL CORRELATE
The frequency of exercise for a patient with cardiac pump failure may be best if prescribed every second or third day based on observations that patients with cardiac pump failure experience diastolic cardiac dysfunction for 24 hours or more after a single symptom-limited exercise test.109
However, there is little consensus regarding the intensity or duration of rehabilitative treatment for a person with a failing or dysfunctional cardiac pump.108
Although the medical management of persons with cardiovascular pump dysfunction and failure is similar with respect to the fundamental basis of treatment (eg, to decrease the workload imposed on the heart often by decreasing venous return) particular results of different tests and measures can more clearly direct physical therapy. Some of the additional tests and measures include the observation of a decrease in the cardiac output and systolic blood pressure during exercise, an elevated resting heart rate, electrocardiographic evidence of myocardial ischemia or cardiac arrhythmias, and a low level of peak oxygen consumption (Table 18-7).75,88,90,106,110–115 Utilization of the test results in Table 18-7 can better direct the specific intervention, frequency of intervention, and outcomes for a patient with cardiovascular pump dysfunction and failure.
TABLE 18-7 Possible Predictors of Success or Failure of Patients with Cardiac Pump Dysfunction in Cardiac Rehabilitationaa
The specific interventions for patients with specific threshold behaviors suffering from cardiovascular pump dysfunction and failure outlined in the branching diagram of Fig. 18-4 are based on peer-reviewed published research.2–10,75,88,90,106,110–166 The initial branching is dependent on the arterial blood pressure response to a controlled expiratory maneuver and the remaining branches are dependent on many of the threshold behaviors listed in Box 18-1 and Table 18-7.2–10,75,88,90,106,110–166 Subtle adjustments in the exercise prescription of patients with cardiac pump dysfunction and failure may improve the outcomes of patients in both subgroups. The methods to provide these subtle adjustments in the exercise prescription will be discussed in the following sections.
Exercise Training: Management of Pathology, Impairments, Functional Abilities, Disability, and Quality of Life in Persons with Cardiac Pump Dysfunction
The results of numerous studies of persons with cardiac pump dysfunction reveal the important role of exercise training in improving the pathology, impairments, functional abilities, disability, and quality of life. Perhaps the most important evidence documenting the role of exercise training and cardiac rehabilitation for patients with cardiac pump dysfunction are the results of several meta-analyses of exercise training in patients with coronary artery disease and the United States Cardiac Rehabilitation Guidelines (USCRG) document.93,116–118 The USCRG outlined and categorized the strength of the evidence for cardiac rehabilitation on the disablement of patients with cardiac pump dysfunction. The strength of the evidence for many domains of disablement was determined from the available literature and was based on the lettering criteria cited in the following and is shown in Box 18-9.93
BOX 18-9
•A = Scientific evidence provided by well-designed, well-conducted, controlled trials (randomized and nonrandomized) with statistically significant results that consistently support the guideline recommendation.
•B = Scientific evidence provided by observational studies or by controlled trials with less consistent results to support the guideline recommendation.
•C = Expert opinion that supports the guideline recommendation because the available scientific evidence did not present consistent results, or controlled trials were lacking.
Exercise Training: Management of Pathology, Impairments, Functional Abilities, Disability, and Quality of life in Persons with Cardiac Pump Failure
Historically, physical activity was restricted in persons with CHF. Patients were commonly confined to their homes and were restricted from cardiac rehabilitation. Even today, cardiac rehabilitation for patients with CHF is not reimbursed, yet it is these patients who may benefit the most from cardiac rehabilitation.93 The following section will provide evidence of the important role exercise training and physical therapy have for patients with CHF.
A significant literature exists regarding the efficacy of cardiac rehabilitation in patients with NYHA class II–III heart failure.75–90,119–152 The major areas which will be discussed in this section include the muscle hypothesis of chronic heart failure, aerobic exercise training (inpatient exercise, home exercise, and rehabilitation center exercise programs), strength training, breathing exercises, left ventricular assist device care, and heart failure clinic care for patients with heart failure. Tables 18-8 through 18-12 show the studies that have been performed in each of the previously cited areas.
TABLE 18-8 Aerobic Exercise Training Studies in Patients with Heart Failure
The muscle hypothesis of chronic heart failure—is shown in Figure 18-5 and presents the interrelated manifestations of chronic heart failure.153–156 Central to this conceptual model is the role of skeletal muscle. It is hypothesized that a reduction in peripheral blood flow to skeletal muscle contributes substantially to the vicious cycle of heart failure resulting in skeletal muscle catabolism, myopathy, increased ventilation, increased dyspnea and fatigue, sympathetic nervous system activation, vagal nervous system withdrawal, vascular constriction, and poorer left ventricular function.153–156 It is important to note that vascular constriction (and the resultant increase in afterload) not only produces poorer left ventricular function, but also further diminishes peripheral blood flow to skeletal muscle. In fact, each of the above manifestations is intimately interrelated with the capacity to substantially worsen cardiovascular pump function if not managed and or treated. Properly prescribed exercise is a key modality that has been suggested to manage and improve many of the manifestations of chronic heart failure shown in Figure 18-5.153–156 The following sections will provide the rationale and methods that support the favorable role of exercise in addressing almost all of the manifestations of chronic heart failure.
FIGURE 18-5 The muscle hypothesis of chronic heart failure. (Used with permission from Piepoli M, Clark A,
Inpatient care—Several inpatient studies of aerobic exercise have been performed and have affirmed the safety of inpatient aerobic exercise training and significant improvements in many areas of disablement including symptoms, heart rate, exercise tolerance via exercise test or 6-minute walk test, and peak oxygen consumption.80,119–122 The exercise training programs in these studies consisted of flexibility exercises, cycle ergometry, and treadmill ambulation for an average of 30 minutes total, 3 to 5 days/wk for 2 to 4 weeks duration at 50% to 70% of peak cycle ergometry work rate and a mean of 2.4 mph on the treadmill.
Home care—Aerobic exercise training in the home of heart failure patients has been performed safely in seven separate studies in which significant improvements have been observed in many areas of disablement including symptoms, heart rate, blood pressure, exercise tolerance via exercise test, and peak oxygen consumption.75,77,89,121–124 One recent study demonstrated improved quality of life in patients with heart failure who exercised at home.75The exercise training programs in these studies consisted of cycle ergometry or walking for an average of 20 to 60 minutes, 3 to 7 days/wk for 2 to 6 months duration at 50% to 80% of peak heart rate or oxygen consumption.
Rehabilitation center care—The majority of studies investigating aerobic exercise training have been performed in supervised rehabilitation centers. These studies have consistently shown that aerobic exercise training can be performed safely with significant improvements in many areas of disablement including symptoms, heart rate, blood pressure, exercise tolerance via exercise test or 6-minute walk test, peak oxygen consumption, and recently, quality of life.75,76,78–88,90,106,110–122,125–152 The exercise training programs in these studies consisted of a variety of modes of exercise (however, cycling was the most frequent mode) for 20 to 60 minutes, 3 to 7 days/wk for 1 to 57 months duration at 40% to 90% of peak heart rate or oxygen consumption.
The results of the multicenter HF-Action trial of cardiac rehabilitation in persons with heart failure demonstrated nonsignificant effects of cardiac rehabilitation on all-cause mortality, cardiovascular mortality, cardiovascular hospitalization, or heart failure hospitalization. However, analyses adjusted for baseline characteristics found that patients with heart failure undergoing cardiac rehabilitation had significantly improved all-cause mortality or hospitalization, cardiovascular mortality or cardiovascular hospitalization, and cardiovascular mortality or heart failure hospitalization.151 Additional analyses demonstrated that heart failure patients undergoing cardiac rehabilitation had significantly greater self-reported health status that persisted after the rehabilitation program.152
Strength training—A number of studies have been published investigating the clinical efficacy of strength training in patients with heart failure (Table 18-9).157–164 This literature suggests that strength training may be an important mode of exercise training that is safe and effective in patients with heart failure. Circuit strength training combined with aerobic exercise appears to improve peripheral muscle strength and endurance, exercise tolerance, cardiorespiratory function, and symptoms. The strength training performed in these studies was administered to major muscle groups at 60% to 80% of maximum voluntary contraction or of the 10-repetition method (10-RM) for 2 to 6 months.
TABLE 18-9 Strength Training Studies in Patients with Heart Failure
The number of repetitions and strength training session durations were slowly progressed and varied among studies. No major complications were observed in the studies.
The manner by which the above strength training studies are related to the muscle hypothesis of chronic heart failure is also shown in Table 18-9. It is important to note that almost every domain of the muscle hypothesis of chronic heart failure was favorably affected by resistance training or a combination of resistance training and aerobic exercise.164
Breathing exercises—An increasing number of studies have investigated the effects of breathing exercises on the clinical manifestations of heart failure (Table 18-10).25,165–171 Five of the six studies utilized a threshold inspiratory muscle training device which consisted of a portable handheld device through which a patient would inspire only when they overcame the threshold resistance (provided via a calibrated spring) of the device. Such a Thresholdinspiratory muscle trainer is shown in Figure 18-6. Inspiratory muscle training was performed daily for an average of 15 to 30 minutes at 15% to 60% of maximal inspiratory mouth pressure for 2 to 3 months.167–171
TABLE 18-10 Breathing Exercise Studies in Patients with Heart Failure
FIGURE 18-6 A Threshold inspiratory muscle trainer.
One additional study investigated the acute and chronic effects of slowing the respiratory rate via yoga breathing. Threshold inspiratory muscle training appears to consistently improve ventilatory muscle strength and endurance and dyspnea. Yoga breathing appears to have both acute and chronic benefits including improved oxygen saturation, exercise tolerance, cardiorespiratory function, and dyspnea.
Left ventricular assist devices—Left ventricular assist devices are becoming more commonplace, yet have received very little clinical rehabilitative investigation (Table 18-11).49,50,172–175 Exercise training of patients with LVADs appears to be safe, but requires gradual progressive mobilization which can lead to treadmill or cycling exercise. Treadmill or cycle ergometry exercise often begins after patients become independent with hallway ambulation. Specific criteria for mobilization and progression of a patient with heart failure and LVAD will be provided in the following section. Mobilization and progression of such patients has been observed to improve functional status and exercise tolerance and to optimize recovery before heart transplantation.
TABLE 18-11 Aerobic Exercise and Strength Training Studies in Patients with Heart Failure and Left Ventricular Assist Device
Heart failure clinics—Table 18-12 also includes a number of studies that have investigated the usefulness of heart failure clinics.76,176–190 Heart failure clinics provide comprehensive heart failure management, frequently through a physician and nurse team. The team often follows specific patient care pathways, which ensure timely performance of specific tests and measures as well as allocation of a variety of services. Heart failure clinics are becoming more popular due to favorable economic and patient outcomes including a reduction in hospital admissions, readmissions, days, and costs as well as an improvement in quality of life and morbidity.
TABLE 18-12 Studies of Structured Heart Failure Clinics
Specific Methods of Exercise Training for Patients with Cardiac Pump Dysfunction and Failure
Boxes 18-10 and 18-11 provide an overview of several important aspects of exercise training in patients with cardiac pump dysfunction and failure. As previously mentioned, patients with cardiac pump dysfunction can tolerate an increase in venous return relatively well and can exercise at a greater intensity, duration, and frequency while utilizing a greater number of modalities and body positions than can the patient with cardiac pump failure. The exercise prescription for a patient with cardiac pump dysfunction should be developed from exercise test results when available and should likely follow the methods outlined in Box 18-10.64,93
BOX 18-10
Exercise Training Methods for Patients with Cardiac Pump Dysfunction
1.Perform an exercise test or utilize recent exercise test results.
2.Determine whether the cardiovascular and pulmonary responses during the exercise test are adaptive.
3.If exercise test results are adaptive without signs or symptoms of myocardial ischemia or cardiac arrhythmias, the exercise prescription should be developed via one of several methods including:
a.Karvonen method
b.60% to 85% of peak heart rate or peak oxygen consumption
c.Rate of perceived exertion corresponding to optimal training heart rate or level of oxygen consumption
d.Heart rate or rate of perceived exertion just below the ventilatory threshold/anaerobic threshold
4.If exercise test results are not adaptive and show signs or symptoms of myocardial ischemia or cardiac arrhythmias, the exercise prescription should be developed via one of several methods including:
a.Ischemic threshold via heart rate
b.Ischemic threshold via rate pressure product (double product)
c.Ischemic threshold via electrocardiographic evidence of myocardial ischemia or cardiac arrhythmias
d.Heart rate or rate of perceived exertion just below the threshold for maladaptive cardiovascular or pulmonary exercise test results
5.Perform physical exercise using the most appropriate mode, duration, frequency, and duration based on exercise test results, the blood pressure response during a controlled expiratory maneuver, and patient goals/enjoyment.
6.Begin with gentle stretching and aerobic exercise and progress to a greater exercise duration and intensity as exercise training is continued.
7.Set realistic goals for exercise with a range of 20 to 45 minutes of exercise duration, at a frequency of 3–5 ×/wk, and at an appropriate training intensity based on numbers 3 and 4.
8.Monitor patient during exercise using the methods described in Chapter 10 and determine the frequency of monitoring during an exercise training session based on the exercise test results, blood pressure response during a controlled expiratory maneuver, and patient signs/symptoms.
9.Reexamine the patient during each exercise session using the methods described in Chapter 10.
10.Perform a second exercise test after 1 to 3 months of exercise training to establish safety of progressive exercise training and develop a new exercise prescription.
BOX 18-11
Criteria for the Initiation and Progression of Exercise Training in Patients with Cardiac Pump Failure
I.Relative criteria necessary for the initiation of an aerobic exercise training program—Compensated heart failure:
1.Ability to speak without signs or symptoms of dyspnea (able to speak comfortably with an RR <30 breaths/min)
2.Moderate fatigue
3.Crackles present in <1/2 of the lungs
4.Resting heart rate <120 bpm
5.Cardiac index ≥2.0 L/min/m2 (for invasively monitored patients)
6.Central venous pressure <12 mm Hg (for invasively monitored patients)
II.Relative criteria indicating a need to modify or terminate exercise training
(a)Marked dyspnea or fatigue (eg, Borg rating > 3/10)
(b)Respiratory rate >40 breaths/min during exercise
(c)Development of S3 or pulmonary crackles
(d)Increase in pulmonary crackles
(e)Significant increase in the intensity of the second component of the second heart sound (P2)
(f)Poor pulse pressure (<10 mm Hg difference between the systolic and diastolic blood pressures)
(g)Decrease in heart rate or blood pressure of >10 bpm or mm Hg, respectively, during continuous (steady-state) or progressive (increasing workloads) exercise
(h)Increased supraventricular or ventricular ectopy
(i)Increase of >10 mm Hg in the mean pulmonary artery pressure (for invasively monitored patients)
(j)Increase or decrease of >6 mm Hg in the central venous pressure (for invasively monitored patients)
(k)Diaphoresis, pallor, or confusion
Adapted with permission from Cahalin LP. Heart failure. Phys Ther. 1996;76:529.
In contrast to the patient with cardiac pump dysfunction, the patient with cardiac pump failure cannot tolerate a substantial increase in venous return. Therefore, the exercise prescription should be developed with this in mind (Box 18-11) and should be provided at a lesser intensity, duration, and frequency with a thorough appreciation for body position (and the effect of body position on venous return) and patient signs and symptoms (requiring more thorough monitoring). Of primary concern for the patient with cardiac pump failure is the degree of heart failure and whether it is compensated or decompensated.16,191 Several clinical findings appear to be suggestive of decompensated heart failure (Box 18-11), and identification of one or more of these findings may be sufficient to terminate exercise training until heart failure has become compensated.16,191 Clinical findings suggesting modification or termination of exercise training are also listed in Box 18-11 and include marked dyspnea and fatigue, a fall in systolic blood pressure response during progressive exercise, and development of a S3 or crackles in a patient who did not demonstrate these signs prior to exercise.16,191
Table 18-13 provides a structured approach to the rehabilitation of patients with heart failure in a variety of settings such as those who are hospitalized, seen in the home, or attending a rehabilitation center.182 Patients who are debilitated may require a more gradual exercise progression (gradual activity protocol), whereas patients who are less debilitated may progress more rapidly through a rehabilitation program (standard activity protocol). The progression of the patient through either activity protocol or in any setting is based on the initial patient status and subsequent responses to exercise and other components of the cardiac rehabilitation program that have been identified as necessary.191
TABLE 18-13 Two Different Methods of Activity Progression in Patients with Heart Failurea
For most patients, ambulation may be the most effective and functional mode of exercise to administer and prescribe, beginning with frequent short walks and progressing to less frequent, longer bouts of exercise. Occasionally, patients may be so deconditioned that gentle strengthening exercises, restorator cycling, or ventilatory muscle training is the preferred mode of exercise conditioning. As strength and endurance improve, patients can be progressed to upright cycle ergometry or ambulating with a rolling walker.
Because dyspnea is the most common complaint of patients with CHF, the level of dyspnea or Borg rating of perceived exertion appears to be an acceptable method to prescribe an exercise program.182 This is supported by the observation that these subjective indices correlate well with training heart rate ranges in this patient population. Therefore, a basic guideline of increasing the exercise intensity to a level that produces a moderate degree of dyspnea (conversing with modest difficulty, ability to count to 5 without taking a breath, or a Borg rating of 3/10) may be the simplest and most effective method to prescribe exercise for patients with CHF. It also appears to be the most effective method to progress a patient’s exercise prescription. The exercise prescription can be progressed when (1) the cardiopulmonary response to exercise is adaptive and (2) workloads which previously produced moderate dyspnea (eg, Borg rating of 3/10) produce mild dyspnea (eg, Borg rating of ≤2/10).191
Ventricular Assist Devices
Patients with end-stage heart failure who are refractory to maximal inotropic therapy may benefit from a ventricular assist device. Currently there are two intracorporeal devices operated by battery packs, which are approved by the United States Food and Drug Administration (USFDA) for use as a bridge to transplantation and/or a bridge to recovery of function. Thoratec, Inc. (Heartmate VE, Fig. 18-7A) and Novacor (Oakland, CA) have developed these portable devices allowing the patient mobility not afforded by earlier generations of assist devices with the potential for discharge home.192–195 Additionally, the USFDA has recently approved the Heartmate V.E LVAD as a destination therapy in those patients who are not candidates for heart transplantation following successful outcomes in a multicenter study.186 Physical therapy has been shown to be safe and effective at helping these patients to regain independence in ADL and gait; and to maximize strength, flexibility, and endurance while awaiting transplantation.49 The reexamination of the case study following LVAD implantation is presented in Box 18-6. Clinical trials are currently in progress to evaluate the Novacor LVAD as a destination therapy.
FIGURE 18-7 Diagram of LVAD types with photo of treadmill and cycle exercise. (A) Schematic representation of the HeartMate VE LVAD; (B) schematic representation of the Novacor N100PC LVAS; (C) photo of George with HeartMate VE LVAD performing treadmill exercise; (D) Photo of George with HeartMate VE LVAD performing bicycle exercise.
As more and more patients are being discharged home following LVAD implantation to wait until a donor heart becomes available, more attention needs to be given to discharge planning. Adequate social support and home environment must be considered. It is the LVAD nurse coordinator’s responsibility to perform the final safety check-out of the patient and family in performing LVAD emergency procedures. It is the physical therapist’s responsibility to provide the patient and family with verbal and written instructions for a home exercise program. Those who have had a complicated hospital course and who are very weak and debilitated may benefit from transfer to an inpatient rehabilitation center prior to discharge home. In the rare case in which the patient is not independent in their ADL or in ambulation prior to discharge home but has the potential to make progress, home physical therapy would be warranted. Finally, contact information regarding local outpatient cardiac rehabilitation facilities should be provided to the patient prior to discharge home. A nurse coordinator may provide on-site training (device management and emergency procedures) to staff at a local cardiac rehabilitation facility prior to their accepting this type of patient.51
The right ventricular assist device (RVAD) and bi-ventricular assist device (BiVAD) have been utilized clinically, but minimal research has investigated the best methods to provide exercise to patients provided an RVAD or BiVAD. The available data suggest that the LVAD provides better hemodynamic support and exercise tolerance than the BiVAD. However, more research in this area is needed. Nonetheless, the rehabilitation of patients with an RVAD or BiVAD appears to be similar to that provided to patients with an LVAD.
Allocation of Services in Cardiac Rehabilitation for Persons with Cardiac Pump Dysfunction and Failure
The allocation of appropriate services for patients with cardiac pump dysfunction and failure participating in cardiac rehabilitation can be performed via a detailed history, results of medical and psychological tests, and results from disease specific and general health status questionnaires.16,106,111–118,196 Exercise test results often provide important information about the severity of heart failure, safety of exercise training, and exercise prescription. Patients with a peak oxygen consumption of less than 10 to 14 mL/kg/min appear to have a poorer prognosis and are often considered candidates for cardiac transplantation. However, these same patients may benefit from closely monitored and gradually progressed cardiac rehabilitation. Exercise test results can also provide (1) some indication of the potential for complications during exercise training based on the comprehensive examination of the cardiorespiratory response (eg, peak oxygen consumption, heart rate and blood pressure response, electrocardiogram, and symptoms) and (2) patient-specific exercise training parameters.16,106,111–118,196
Additional data may be helpful in allocating cardiac rehabilitation as recently presented for the long-term clinical management of patients with coronary artery disease (Table 18-14).196 As shown in Table 18-14, important patient data and critical threshold levels may help to stratify and subsequently allocate cardiac rehabilitation. The patient data include traditional risk factors as well as other factors that may influence the risk for the progression of atherosclerosis.
TABLE 18-14 Allocation of Cardiac Rehabilitation Based on Risk Stratification
Examination of the results of a general health status questionnaire (eg, SF-36) or a disease-specific questionnaire like the Minnesota Living with Heart Failure Questionnaire or the Chronic Heart Failure Questionnaire can also provide important information about the domain of disablement most affected by heart disease for patients with cardiac pump dysfunction and failure. These instruments can also address the specific areas in need of direct medical, physical, educational, psychological, social, occupational, and nutritional interventions.64 Cardiac rehabilitation provided in this manner will likely address the specific disablement of each patient and provide cost-effective and comprehensive care.
Monitoring and Reexamination
Monitoring persons with cardiac pump dysfunction and failure is dependent on the past history as well as on the findings from specific physical therapy tests and measures. These include symptoms, heart rate and blood pressure at rest and during exercise, heart rate and blood pressure during the valsalva maneuver, and exercise test results (eg, exercise duration, peak workload, peak oxygen consumption, and electrocardiographic findings such as ST-segment depression). Specific medical tests and measurements (eg, ejection fraction) can also provide important information about patient monitoring and reexamination.16,64,106,111–118
Monitoring of persons with cardiac pump failure and LVAD support requires constant monitoring of the patient’s response to physical therapy intervention in order to ensure safety and to evaluate effectiveness of the intervention. Heart rate and rhythm (via telemetry), blood pressure, oxygen saturation, LVAD rate (pulse), stroke volume, and flow, and the patient’s symptoms are monitored with position change and with exercise.49–52 Once the patient is transferred from alternating current to battery operation of the LVAD, the power base display of device rate, volume, and flow is no longer available. The rate of the device can still be ascertained by counting the pulse. Rhythm would be monitored in patients with known or suspected arrhythmia. Blood pressure and symptoms would continue to be watched. Treatment would be terminated for LVAD rate <50 bpm, LVAD volume <30 mL, LVAD flows <3.0 L/min, symptomatic drop in blood pressure of more than 10 mm Hg, heart rate <150 bpm, or sustained ventricular tachycardia or ventricular fibrillation.49–51
Allocation of Services for Persons After Cardiac Transplantation
The care provided to persons before cardiac transplantation is identical to that provided to persons with cardiac pump failure. However, after cardiac transplantation several important issues must be considered including the effects of cardiac denervation on heart rate, immunosuppression on skeletal muscle, and marked deconditioning on the progression of therapeutic exercise.197–199
Table 18-15 provides an overview of the possible outcomes after cardiac transplantation. Cardiac denervation produces a blunted heart rate during exercise and a slower decrease in heart rate after exercise, which reinforces the importance of a proper warm-up and cool-down period after exercise for patients after a cardiac transplant. Immunosuppressive drugs are provided to patients after a cardiac transplant to prevent the body from rejecting the transplanted heart. However, immunosuppressive drugs weaken the immune system making infection and the development of malignancies a potential problem. Furthermore, immunosuppressive drugs have been associated with the development of skeletal muscle myopathies making the rehabilitation of cardiac transplant recipients challenging. Finally, almost all cardiac transplant recipients have suffered from chronic heart failure and the marked deconditioning associated with chronic heart failure. Despite these issues, favorable outcomes are associated with cardiac transplantation and it has been shown that properly prescribed exercise can facilitate the favorable outcomes.197–199
TABLE 18-15 Possible Outcomes After Cardiac Transplantion
Because of the above possible adverse outcomes after cardiac transplantation, cardiac transplant recipients demonstrate a very different physiologic profile from age- and gender-matched healthy subjects which is shown in Table 18-17. The major differences include the higher resting heart rate and lower peak exercise heart rate, higher resting systolic and diastolic blood pressure, higher resting cardiac output, and lower lean body mass, peak power, and peak oxygen consumption.197–199
TABLE 18-17 Differences in the Physiologic Profile of Cardiac Transplant Recipients Compared to Healthy Subjects
However, properly prescribed exercise can improve many of the less than favorable outcomes after cardiac transplantation and make the cardiac transplant recipient more physiologically similar to healthy individuals. The potential for change is shown in Table 18-18 with substantial improvement likely in peak power, peak ventilation, and peak oxygen consumption.197–199
TABLE 18-18 Training Adaptations in Cardiac Transplant Recipients
Finally, the methods to develop the favorable exercise training adaptations shown in Table 18-18 can be appreciated by examining the exercise training methods outlined in Table 18-19. Gradual increases in strengthening as well as functional and exercise training before and after transplantation are likely to safely promote training adaptations. Breathing exercises may also be of benefit and prescription of exercise using rating of perceived exertion as opposed to heart rate is preferred because of the blunted heart rate from cardiac denervation.197–199
TABLE 18-19 Exercise Training Before and After Cardiac Transplantationa
Outcomes—Utilization of Threshold Behaviors for Improvements in Exercise and Functional Abilities as a Result of Aerobic Exercise Training
A review of the outcomes listed in the Guide for patients with cardiovascular pump dysfunction and failure in Practice Pattern D reveals a lack of specificity.1 Despite the fact that the medical management of persons with cardiovascular pump dysfunction and failure is similar (eg, the fundamental basis of treatment which is to decrease the workload imposed on the heart and to decrease venous return) the specific outcomes are likely to be different and should be based on the results of specific tests and measures. Several such results of specific tests and measures include the observation of a decrease in cardiac output during exercise, an elevated resting heart rate, and low level of peak oxygen consumption. Identification of particular responses of key tests and measures can provide important prognostic information regarding the likelihood of success or failure of aerobic exercise training. Understanding the likelihood for success or failure during specific therapeutic interventions can better direct specific patient outcomes. The specific signs and symptoms of cardiac pump dysfunction and failure listed in Table 18-7 provide important outcome and prognostic information. The results of these tests and measures can provide an evidence base for goal-setting and patient outcomes.16,106,111–118,196
Important outcomes for physical therapy and potential goals for patients with cardiac pump dysfunction and failure are listed in Table 18-16. The key areas of disablement in cardiac pump dysfunction and failure are listed in this table, from which the specific results of tests and measures of persons with cardiac pump dysfunction and failure can be compared. The list of key disablements are supported by a substantial literature which has identified important patient characteristics associated with heart disease and successful outcomes.200–205 The results of these specific tests and measures within their respective domains of disablement are described in the following sections.
TABLE 18-16 The Primary Domains of Disablement in Cardiac Pump Dysfunction and Failure
Pathology concept—etiology of heart failure—The etiology of CHF is often due to either an ischemic cardiomyopathy or an idiopathic cardiomyopathy. Persons with CHF due to an ischemic cardiomyopathy have a poorer prognosis and exercise tolerance than do patients with an idiopathic cardiomyopathy.206 The presence of myocardial ischemia in a patient with depressed myocardial performance appears to predispose a patient to poorer exercise tolerance and prognosis.111 Poor prognosis and exercise intolerance (a health outcome and impairment measure, respectively) are therefore negative outcomes that may be expected in patients with CHF due to an ischemic cardiomyopathy. The use of pathological information such as this may alert a therapist to provide more frequent monitoring and a more gradual progression in exercise for a patient with an ischemic cardiomyopathy.
Impairment concept—peak oxygen consumption and oxygen consumption at the ventilatory threshold—A great deal of investigation has been done on measuring exercise tolerance, functional capacity, and survival in persons with heart disease.68,69,71–75,207–212 Peak oxygen consumption measurements have traditionally been used to categorize persons with heart disease, and numerous studies have shown that persons with lower levels of peak oxygen consumption have poorer exercise tolerance, functional capacity, and survival than persons with greater levels of peak oxygen consumption.68,69,71–75,207–212
It has been observed that a peak oxygen consumption and oxygen consumption at the ventilatory threshold have been identified as important threshold behaviors.73–75,106
CLINICAL CORRELATE
A peak oxygen consumption greater than 10 mL/kg/min and oxygen consumption at the ventilatory threshold less than 12 mL/kg/min appear to be associated with successful rehabilitation.73–75,106
These values likely represent a moderate degree of CHF (patients who are not severly deconditioned or suffering from decompensated CHF). If patients had more severe CHF they would have lower levels of peak oxygen consumption (less than 10 mL/kg/min) and higher levels of oxygen consumption at the ventilatory threshold (greater than 12 mL/kg/min).
CLINICAL CORRELATE
Patients with a peak oxygen uptake and lower oxygen consumption at the ventilatory threshold appear to be best suited for aerobic exercise training and most likely to develop training adaptations.
Similar findings have recently been observed by Belardinelli et al.75
Impairment concept—reduced cardiac output during exercise—A reduction in the cardiac output during exercise is indicative of poor myocardial function that will unlikely improve with chronic aerobic exercise training.107,116
CLINICAL CORRELATE
Patients presenting with such a reduction in cardiac output during exercise may be best suited for gentle to moderate strength training of the peripheral musculature and the muscles of breathing as well as for energy conservation techniques and patient education regarding signs/symptoms of CHF, work/hobby habits, and diet. Single-legged cycling or other exercise may also be indicated.104
Impairment concept—resting heart rate and heart rate change during exercise—A resting heart rate of less than 90 bpm and a change in heart rate during exercise testing that is greater than 50 bpm appear to be associated with successful rehabilitation of persons with CHF.106,110,116,118 These findings are likely due to a healthier person with CHF and a better preserved stroke volume which would provide an adequate cardiac output at rest and during exercise with lower heart rates. Patients with a resting heart rate greater than 90 bpm and a change in heart rate during exercise testing that is less than 50 bpm will have less cardiac reserve for aerobic exercise training and therefore may predispose such patients to less exercise tolerance and earlier dyspnea, fatigue, and myocardial ischemia if coronary artery disease exists. Similar findings have recently been observed by Belardinelli et al.75 These patients may benefit from the same interventions that were described previously for patients with a reduction in cardiac output during exercise.
Impairment concept—peak systolic blood pressure—A peak exercise systolic blood pressure that is greater than 10 mmHg from the resting blood pressure appears to be associated with successful rehabilitation.116 A peak systolic blood pressure which is unable to increase greater than 10 mmHg likely identifies a poor level of myocardial performance. Systolic blood pressure characteristically rises with progressive incremental exercise, but in a patient with a poor cardiac pump, the rise may be less than 10 mmHg from the resting level or the systolic blood pressure may rise, but precipitously fall to a level that is less than 10 mmHg above the resting systolic blood pressure at peak exercise. Patients presenting with a peak systolic blood pressure that is less than 10 mmHg above the resting systolic blood pressure may benefit from the same interventions listed previously for patients with a reduction in cardiac output during exercise.
Impairment concept—pulse pressure—A pulse pressure (the difference between the systolic and diastolic blood pressures) greater than 10 mmHg is likely to be associated with successful rehabilitation.110,116 The greater the pulse pressure, the greater will be the perfusion pressure to vital organs and to peripheral musculature and tissues. Improved perfusion to organs and peripheral tissues and musculature will likely yield greater exercise tolerance and an improved exercise response due to maintenance of organ function (including the heart), adequate blood flow to exercising muscles, and cooling of the body during exercise. A smaller pulse pressure reflects not only poorer myocardial performance and an inability to increase the systolic blood pressure but also increased peripheral vascular constriction that may be associated with an increase in diastolic blood pressure. Thus, a narrowing of the pulse pressure may ensue in a person with CHF who has poor myocardial performance and increased peripheral vascular resistance because of worsening blood flow to the periphery and to vital organs. Patients presenting with a narrow pulse pressure less than 10 mmHg during exercise testing should likely be prescribed very low-level strength training to the peripheral musculature and the muscles of breathing as well as energy conservation techniques and patient education.
Functional abilities/disability/quality-of-life concepts—6-minute walk test distance ambulated—Results of the 6-minute walk test (a functional performance measure) have recently been shown to be helpful in estimating peak oxygen consumption (an impairment measure) and survival (an important measurement of health outcome) in persons with heart failure.60 The distance ambulated during the 6-minute walk test was significantly related to the measured peak oxygen consumption during cycle ergometry exercise testing. The distance ambulated during the 6-minute walk test can be used to estimate peak oxygen consumption via a number of prediction equations (see Chapter 10).60
Another important finding from the results of the 6-minute walk test is that patients walking less than 300 m (approximately 1,000 ft) appear to have a poorer survival.60 This has been observed in a relatively large number of studies of persons with heart failure. Observation of such poor exercise tolerance and functional ability provides a threshold behavior level which may be useful for the medical management of patients with heart failure and in directing physical therapy intervention. Heart failure patients ambulating less than 300 m are frequently provided more extensive and structured physical therapy interventions than patients ambulating greater than 300 m.
Overall disablement—Minnesota Living With Heart Failure Questionnaire (MLWHFQ)—A total score of 50 or greater on the MLWHFQ appears to be associated with greater potential for successful rehabilitation.116 The greater the score on the MLWHFQ, the greater the functional limitation and disability and the poorer the quality of life (see Chapter 10). A total score of 50 or greater may be a threshold level below which disablement is less likely to change, but above which (because of greater disability and functional limitation) disablement may be more prone to improve.
Outcomes—utilization of threshold behaviors for improvements of symptoms and ventilatory muscle strength as a result of ventilatory muscle training—Impairment Concept—Ventilatory Muscle Strength and Dyspnea: A previous study investigating the effects of inspiratory muscle training on ventilatory muscle strength and symptoms of persons with heart failure can be used to show a more specific application of a threshold behavior to direct physical therapy intervention.25,213,214 It was observed that ventilatory muscle strength and symptoms (eg, dyspnea) improved significantly after an 8-week period of inspiratory muscle training.25,213,214 Univariate and multivariate regression analyses revealed that the percent change in dyspnea at rest and during exercise was significantly related to the pulmonary artery pressure, right ventricular ejection fraction, and left ventricular end-diastolic volume of the heart failure patients.214
CLINICAL CORRELATE
It appears that patients with heart failure will benefit from inspiratory muscle training when they have (1) a poor right ventricular ejection fraction (less than 45% = a threshold behavior level), (2) elevated pulmonary artery pressure (greater than 20 mm Hg = a threshold behavior level), and (3) elevated left ventricular enddiastolic volume (greater than 150 mL = a threshold behavior level).
Patients with one or more of these particular threshold behaviors are likely to succeed with inspiratory muscle training performed in the manner described in this research study.213,214 In fact, from these preliminary data, it may even be possible to predict the degree of improvement in dyspnea from inspiratory muscle training. The use of such threshold behaviors, therefore, may enable the prediction of physical therapy intervention outcomes in much the same way that the degree of success with medical intervention is predicted.
Outcomes—utilization of threshold behaviors for improvements in exercise and functional abilities as a result of aerobic and strength training in patients with cardiac pump failure and left ventricular assist devices—Extraindividual concept: Many extraindividual concepts appear to be related to the improvements in exercise and functional abilities of persons with LVAD and include the possible constraints of the LVAD, the possible contribution of the native heart to cardiac output during exercise, the duration post-LVAD implantation when exercise training is performed, and whether or not exercise training was performed as well as the potential role training adaptations may have on cardiorespiratory performance after LVAD implantation.215 O2peak and V.E have been observed to be significantly greater in LVAD patients than in patients with CHF, and a trend for greater .E/O2 has been observed in LVAD patients. The available literature of exercise for LVAD patients is limited, but the results of a recent research synthesis reveal that (1) many issues involving the possible constraints and benefits of the LVAD need further investigation, (2) persons with LVAD have greater O2peak and V.E than persons with end-stage CHF, (3) LVAD patients appear to have greater levels of O2peak, V.E, and V.E/O2 when exercise is performed, and (4) more substantial improvements in O2peak, V.E, and V.E/O2 appear to occur later, rather than earlier, after LVAD implantation.215 These are important issues, because an improvement in O2peak and V.E due to LVAD implantation will likely yield greater functional abilities in persons with end-stage CHF. Knowledge of the expected timeline of these improvements can help to develop realistic and comprehensive patient goals, exercise prescriptions, and discharge plans. Physical therapists examining and treating patients with end-stage CHF should appreciate and further examine the safety and possible role of LVAD combined with exercise to improve the disablement of end-stage CHF.
It is presumed that all acute LVAD patients will benefit from airway clearance techniques, deep breathing, splinted coughing, positioning (1/–splinting), and range-of-motion exercises until they are able to be mobilized as dictated by their hemodynamic stability and by their external supports (ie, CVVHD). Instruction in LVAD management, bed mobility, transfers, and gait is indicated until the patient is independent in these activities or until it is determined that they have reached a plateau in their progress toward these goals. It seems logical that all LVAD patients would benefit from specific and individualized strengthening and aerobic training until they are independent in their training program or in their physiologic and functional adaptations to training plateau. A plateau in exercise duration, symptom relief, 6-minute walk distance, or O2peak is examples whichever comes first. It is likely that the same threshold behaviors that have been established in patients/clients with cardiovascular pump dysfunction/failure (distance walked in 6 minutes and MIP) may hold true in patients/clients following LVAD implantation and warrant clinical investigation. Additional behaviors, which may prove to be valuable markers, include peripheral muscle strength, vital capacity, and maximal or submaximal O2 as well as LVAD type and the period of time since LVAD implantation. Further research may validate these threshold behaviors.215
Criteria for Discharge
The criteria for discharge of persons with cardiac pump dysfunction, cardiac pump failure, and cardiac pump failure with LVAD have not been established. The criteria for discharge are dependent on the attainment of the anticipated goals and outcomes. Anticipated goals and outcomes will be based on the initial and subsequent results of specific tests and measures such as exercise testing, functional activities, questionnaires, and patient symptoms. Further investigation of the specific tests and measures and the level of improvement needed to ensure safe and optimal function after discharge from physical therapy is needed. Medical deterioration from compensated to uncompensated CHF would also warrant discharge from physical therapy until the patient is stabilized.
NAGI MODEL
Gordon and Quinn suggest organizing the physical therapy examination according to the expanded version of the Nagi model of disablement as described by Verbrugge and Jette.216,217 Figure 18-1 demonstrates how this model can be applied to the examination component of a patient with cardiac pump dysfunction and failure (Practice Pattern D). The evidence-based outcomes to date for physical therapy interventions in these practice patterns are underlined.
THE LIMITS OF OUR KNOWLEDGE
Cardiac Pump Dysfunction and Failure
The rehabilitation of persons with cardiac pump dysfunction and failure has evolved tremendously. Substantial evidence exists for the rehabilitation of persons with cardiac pump dysfunction, and more evidence is becoming available for the rehabilitation of persons with cardiac pump failure. Although the knowledge of rehabilitation of persons with cardiac pump dysfunction is extensive, much is unknown about the rehabilitation of persons with cardiac pump failure.
The future rehabilitation of persons with heart failure will likely utilize the results of exercise training trials to develop prediction equations to determine the degree of success or failure with specific modes of exercise. Specific patient populations with CHF will likely be observed to improve a specific amount in particular areas of disablement from physical therapy and other rehabilitation interventions. The percentage of improvement in aerobic exercise capacity and other areas of disablement will likely be accurately predicted once specific baseline threshold behaviors are identified. Such an evolution in the rehabilitative care of persons with CHF is in keeping with the medical management of many diseases.
Patients with CHF not presenting with particular threshold behaviors of success may still be successful with rehabilitation efforts, and patients presenting with particular evidence-based threshold behaviors may not necessarily respond favorably to rehabilitation. Threshold behaviors can only provide us with some degree of likelihood for success or failure during rehabilitative care. In fact, a recent European multicenter study of exercise training in CHF found no significant correlations between baseline patient characteristics and successful rehabilitation.88 Threshold behaviors may better direct our treatment and allow us to treat the most important concept of disablement that will most likely improve a patient’s functional abilities and quality of life. They may provide physical therapists with very specific evidence-based practice.
The specific intervention provided to a patient with CHF will be based on the patient’s primary need and will likely result in very specific educational and therapeutic programs aimed at the area of disablement most affected. Methods to identify the areas of disablement most affected by CHF should include specific tests and measures such as the 6-minute walk test or other functional tests and measures. General and specific questionnaires of a patient’s perceived health status such as the Medical Outcomes Study SF-36 and the MLWHFQ, respectively, may also be helpful in identifying the areas of disablement in need of intervention.218 Provision of therapeutic exercise will likely be much more specific using not only aerobic exercise training but also strength training to peripheral skeletal muscles. Improving the strength and endurance of the breathing muscles via inspiratory muscle training may also prove to be helpful for patients with CHF by directing intervention at the two main complaints of persons with CHF—dyspnea and fatigue.25 Aerobic exercise will likely continue to be prescribed using symptom scores of dyspnea and fatigue (Borg rating of perceived exertion score of 3–4/10 or 12–14/20), but may include other objective indices (in combination with symptom scores or separate) such as heart rate, systolic and diastolic blood pressures at rest and during exercise, pulse pressures, rate–pressure product, ventilatory threshold, oxygen consumption, or even lactate levels. However, much more research is needed to identify the specific exercise prescription most effective for patients with cardiac pump failure. Such specific allocation of an exercise prescription directed at the primary areas of disablement and utilizing specific threshold behaviors will likely result in optimal physical therapy. However, future investigation is needed in all of the aforementioned areas to expand our knowledge base and improve the care provided to patients with cardiac pump dysfunction and failure.
Left Ventricular Assist Devices
Exercise training following LVAD implantation is safe and increases the duration and intensity of submaximal exercise.49 Patients following LVAD implantation have an improved O2peak.219
We do not know which impairments keep these patients from regaining normal exercise capacity. It has been suggested that persistent right ventricular failure and chronic peripheral changes may be the limiting factors.220 Can specific exercise conditioning in patients following LVAD placement reverse the peripheral skeletal muscle and vascular changes that occur in congestive heart failure, thus further improving their exercise capacity? It has also been hypothesized that the presence of the rather large LVAD pump in the abdomen below the left hemidiaphragm may cause a restrictive lung dysfunction preventing the LVAD patient from achieving a greater exercise capacity.173–175Further defining the causes for peak exercise deficits may help to develop more specific interventions that will in turn improve exercise performance and thereby reverse the functional limitations and disability imposed by the device and the underlying pathology.
We also have not established threshold behaviors for determining which LVAD patient will benefit most from a specific intervention. Furthermore, investigation of right ventricular and biventricular assist devices is needed to facilitate the rehabilitation of this increasing patient population.221 This information would enable us to quickly identify patients at risk for a poor outcome and respond by delivering the appropriate therapy. Additionally, these threshold behaviors could be used to justify insurance reimbursement. Administratively these markers may help us to ensure that physical therapy services are being utilized in an appropriate and efficient manner.
Heads Up!
This Chapter includes a CD-ROM activity.
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