Physical Inactivity

Physical inactivity accounts for 250,000 deaths annually. More than 60% of adults in the United States do not participate in regular physical activity. Single women, the elderly, the less educated, the less affluent, African Americans, and Hispanics are more likely to be inactive.²¹⁶ The American College of Sports Medicine recommends at least 30 minutes of moderate-intensity physical activity on most days of the week, approximating to 600 to 1200 calories expended per week through exercise. Total energy expenditure, rather than duration or type of activity, has the greatest influence on the development of CAD. Higher levels of energy expenditure predict significantly lower CAD risk.¹²¹

Physical activity improves other modifiable risk factors for CAD (Box 33-2). Physical activity also reduces the incidence of CAD^25,120 and associated morbidity.²¹⁶ A study of more than 40,000 men in the United States shows that a healthy lifestyle might prevent a majority of coronary heart disease events.⁴⁵ The protective effect is maintained only with lifelong exercise.¹⁶³ Physical activity and exercise in adults without HD is extremely safe, with the risk for a cardiac event ranging between 1 in 400,000 and 1 in 800,000 hours of exercise. The risk for an event is significantly lower among regular exercisers.⁶⁴ In a study of more than 6200 men, exercise capacity was found to be a more powerful predictor of mortality than other established risk factors for CVD.¹⁵² A cohort of more than 5700 women followed up over 8 years determined that the same applies to women.⁸⁶

Hypertension

Normal blood pressure and hypertension are classified in Table 33-1.

Table 33-1 Classification of Hypertension

Approximately one billion people worldwide have hypertension, and 7.1 million die annually of its complications. Hypertension is the most significant risk factor for death worldwide.²⁵¹ It affects mostly elderly people,³⁸ and the incidence increases with age.²²⁵ Nearly 25% of adults in the United States have hypertension that requires treatment.⁹⁰ Despite intensive education campaigns, however, 30% of people with hypertension do not know they have it. Hypertension is suboptimally controlled with medication in 25% of patients, and 11% are not medicated. Only one third of patients with hypertension have their blood pressure controlled with medication,⁴⁴ and many elderly patients are not treated to an optimal level.²⁴ Recent public health programs have improved awareness of and treatment rates for hypertension.

Risk for MI and death increase as blood pressure rises above 115/75 mm Hg.¹²⁵ The presence of other CAD risk factors compounds the risk from hypertension.⁷ It is significant that a blood pressure reduction of 5 mm Hg produces a 9% reduction in mortality from CAD.²³⁸

Management of hypertension requires lifestyle modifications, including increased physical activity and dietary changes²³⁸ for weight management, as well as restriction of sodium and alcohol intake. Among other benefits, high-intensity interval walking might be protective against age-associated increases in blood pressure.¹⁵⁶

In an extensive review of the evidence for prescribing exercise as therapy in chronic disease, strong evidence was found for the positive effects of training on the pathogenesis, symptoms specific to the diagnosis, physical fitness and strength, and quality of life (QOL) in hypertension.¹⁶⁶ Lifestyle modification without medication is recommended in stage 1 hypertension for 12 months in those with no other risk factors, or 6 months in people with other risk factors. It can lower systolic blood pressure (SBP) between 3.7 and 4.3 mm Hg.¹⁰ Medications are recommended for stage 2 hypertension, or when lifestyle modifications do not normalize blood pressure.

Smoking

Cigarette smoking is the leading preventable cause of illness and premature death in the United States. More than a third of all smoking-related deaths are caused by CVD,⁴² and up to 30% of all CAD deaths in the United States annually are attributable to smoking.²¹⁵ Patients who continue to smoke after CABG have increased morbidity and mortality compared with those who stop smoking.¹⁰² Financial costs are also significant, with more than $157 billion annually in medical care and lost productivity.⁴²

Prevention of smoking and smoking cessation are essential. With education, fewer youths are starting to smoke, and since 1965 smoking rates have dropped 40% in American adults. Of the 45% of patients who stop smoking spontaneously after a coronary event, 70% relapse within 1 year.¹⁷⁶ A nicotine withdrawal syndrome is responsible for the significant difficulty most people have in quitting smoking.⁶ The benefits of smoking cessation are significant. The risk for developing CAD is reduced by 50% within 1 year, and there is a substantial decrease in CAD mortality.^79,184,192 Mortality rates by 3 to 5 years after MI are reduced by 50%,²⁴⁸ and sudden cardiac deaths are also reduced.⁷⁶ A combination of behavioral support, nicotine replacement, and bupropion provides the highest success rates for smoking cessation, approaching 20%.¹⁷³

Dyslipidemia

Dyslipidemia is defined in Table 33-2.¹⁵³

Table 33-2 Classification of Dyslipidemia

About 105 million adults in the United States have total cholesterol levels of 200 mg/dL or higher, and 50% have a low-density lipoprotein (LDL) level of 130 mg/dL or higher. Up to 40% of white men have a high-density lipoprotein (HDL) level below 40 mg/dL. A raised LDL level over 100 mg/dL is an independent risk factor for CAD²⁴⁵ and predicts risk for recurrent events in preexisting CAD.²⁵⁰ Reducing the LDL level is associated with fewer CAD events.³³ Elevated triglyceride levels are also correlated with CAD.¹⁴ A low HDL level is an independent risk factor for CAD, reversed by raising HDL.²⁴⁵ Although genetics is the main factor, 50% of HDL levels are accounted for by overweight, inactivity, smoking, and diabetes.

Achievement of optimal lipid levels is initially done by lifestyle modification, including dietary changes, increased physical activity, and weight loss. Aerobic exercise, including the use of a bicycle ergometer,⁵⁰ and strength training can lower LDL and triglyceride levels, raise the HDL level, and reduce the risk for CAD. This benefit is maintained as long as exercise is ongoing.²¹² The effects of therapeutic exercise on the pathogenesis of dyslipidemia, as well as on specific symptoms of the condition, physical fitness, and strength are supported by strong evidence.¹⁶⁶

Reduction of LDL levels through dietary changes reduces CAD incidence. Plant stanols and sterols, and soluble fibers including oats, barley, and psyllium can lower LDL levels.⁷⁸ Dietary guidelines for lipid management are summarized in Table 33-3. Medications, including statins,¹⁸⁸ are also effective in reducing total cholesterol, LDL, and triglyceride levels, and increasing HDL levels, as well as reducing the risk for developing CAD and recurrent events.¹⁸⁴

Table 33-3 Dietary Guidelines for Lipid Management

Overweight and Obesity

More than 60% of American adults are overweight, defined as a body mass index greater than 25 kg/m². Approximately 30% of all white and African American men, and 50% of African American women are obese (body mass index >30 kg/m²). Increasing numbers of children are overweight. Currently 22% of African American children are overweight.¹⁹⁶ Childhood obesity is linked to a greater risk for adult mortality from CVD.

Overweight is associated with 300,000 deaths annually from all causes.⁴ Obesity is also related to increased morbidity and poorer QOL.^65,67 Overweight contributes to hypertension, dyslipidemia, diabetes, and the metabolic syndrome. A 10-lb weight gain increases the risk for CVD and mortality.¹³⁴ Conversely, a weight loss of 10% reduces risk factors for CAD.¹⁵⁴ Direct economic costs of obesity-related CAD, diabetes, and hypertension approach $43 billion. Indirect costs total $31 billion, approximately 9.4% of the U.S. health care expenditure.⁴⁸ Strong evidence for the positive effect of training has been established on pathogenesis, diagnosis-specific symptoms, physical fitness and strength, and QOL in obesity.¹⁶⁶

Diabetes

A fasting blood glucose level greater than 125 mg/dL defines diabetes. A normal fasting blood glucose level is less than 110 mg/dL, and a level between 110 and 125 mg/dL is considered an impaired fasting glucose level.⁶⁰ About 17 million people in the United States and 5% of all adults have diabetes, and 14.5 million have impaired fasting glucose levels. There are 800,000 new cases of type 2 diabetes diagnosed annually. One third of all people with diabetes are undiagnosed and untreated.⁹⁵ African Americans and Hispanic Americans have twice the incidence of diabetes as that of white persons.¹⁹³ The prevalence of diabetes in the United States is currently 7%, and increasing in parallel with increasing rates of obesity and physical inactivity.⁹⁴

Impaired fasting glucose²²⁹ and diabetes increase the incidence of and mortality from CAD.³⁹ In 65% of patients with diabetes, mortality is due to CAD.⁷³ CAD can go undetected because myocardial ischemia is often silent in people with diabetes as a result of autonomic dysfunction.²⁴⁷ Adequate diabetic control in patients with CAD reduces the incidence of MI, decreases the need for cardiac interventions and surgery, improves QOL, and extends survival.¹⁹⁰ Dietary modification for weight loss and increased physical activity are first-line therapy for hyperglycemia. Strong evidence supports the prescription of therapeutic exercise in type 2 diabetes, improving outcome on pathogenesis, symptoms specific to the diagnosis, physical fitness and strength, as well as QOL.¹⁶⁶ The addition of oral medications or injectable insulin might be needed to optimize control.

The metabolic syndrome (see following discussion) is a combination of insulin resistance with dyslipidemia, hypertension, and a prothrombotic state.⁸¹ This syndrome can precede the development of overt diabetes.

Metabolic Syndrome

Key components of the metabolic syndrome are noted in Box 33-3. Three or more of components 1 through 5 must be present for diagnosis.¹⁵³ Approximately 47 million people in the United States have metabolic syndrome. Prevalence increases with age. It is noted in nearly 45% of people older than 60 years and in one third of overweight or obese people.⁶⁶ Metabolic syndrome is an independent risk factor for CAD⁸⁹ and predisposes to diabetes and increased mortality.¹¹⁶ Treatment focuses on management of underlying risk factors including overweight, physical inactivity, and poor diet. Medications for dyslipidemia, hypertension, hyperglycemia, and thrombosis are considered to optimize control. There is strong evidence that in the metabolic syndrome, the pathogenesis of insulin resistance, specific symptoms, physical fitness, strength, and QOL are all affected by exercise.¹⁶⁶

Emerging Risk Factors

Other emerging factors associated with CAD risk are summarized in Table 33-4.

Table 33-4 Emerging Risk Factors for the Development of Coronary Artery Disease

Nonmodifiable Risk Factors

The risk for CAD increases with age, and men have higher rates of CAD at any age than those of women. Women lag about 10 to 15 years behind men in the incidence of CAD.²⁴⁵ A previous personal history of CAD, peripheral vascular disease (PVD), and CVD increases the chance of a future cardiac event. Family history also correlates with risk for CAD, although the influence of genetic predisposition is not easily separated from environmental factors and learned behaviors.¹⁸⁷ Men and postmenopausal women are more likely to develop CAD, as are many minorities, partly because of higher rates of hypertension, obesity, and diabetes in these populations.

Energy Substrates

Energy substrates are the fuels used in metabolic pathways (Table 33-5).

Table 33-5 Substrates Used in Metabolic Pathways

Carbohydrates and fats are the primary sources of metabolic fuel. Protein and amino acids are used as an energy source only with severe caloric deprivation, starvation dieting, or “overexercising.” Oxygen is required to maximize energy production from carbohydrates and fats. At intense external “work rates,” the body’s physiologic mechanisms cannot provide oxygen at the rate it is required by the metabolizing tissues. Aerobic pathways are limited, and anaerobic pathways take over.

Muscles store energy in the form of ATP and phosphocreatine in sufficient quantities to support short bursts (10 seconds) of intense activity. Use of stored ATP and phosphocreatine is considered anaerobic metabolism. After burst activity, restoration of these stores occurs through aerobic pathways. The production of pyruvate from any substrate does not require oxygen and is also considered anaerobic metabolism. Transport of pyruvate into the mitochondria is oxygen dependent. The anaerobic conversion of pyruvate to lactic acid by lactate dehydrogenase also occurs, but has a very limited capacity to produce ATP. The accumulation of lactic acid is associated with impairment of cellular metabolic pathways, muscle soreness, fatigue, significant respiratory stimulation, and a “forced” decrement or cessation of exercise. Cardiac arrhythmias are more likely to occur under anaerobic conditions.

To limit lactic acid accumulation, at least two mechanisms exist to increase its degradation. First is the Cori cycle, where lactate is transported to the liver, converted back into pyruvate and then into glucose, and released for further muscle metabolism. Second are buffering systems that are important in the energy process. With the production of lactic acid the pH of the local milieu is lowered, activating buffering mechanisms. Sodium bicarbonate (NaHCO₃) is the most abundant and active buffering system for lactic acid, with the production of sodium lactate and carbonic acid (H₂CO₃):

Carbonic acid is rapidly converted to water (H₂O) and carbon dioxide (CO₂):

Sodium lactate is converted back to lactic acid and then to pyruvate when aerobic conditions are restored.

Detection of a spike in CO₂ production (CO₂) with a metabolic gas analysis identifies the transition from aerobic to predominantly anaerobic metabolism. During exercise testing the intensity of exercise when CO₂ exceeds oxygen consumption (O₂) is considered the anaerobic threshold. Anaerobic threshold is one of the key determinants of functional and exercise performance. Because patients with HD do not feel well under anaerobic conditions, exercise intensities should be set below anaerobic threshold.

Oxygen Consumption

O₂ is measured using a metabolic cart, and is the volume of oxygen consumed at any level of activity. Under controlled conditions, at rest, an average 70-kg man consumes 3.5 mL of oxygen per minute for every kilogram of body weight. The unit of oxygen consumption at resting, or “basal metabolic rate,” is referred to as one metabolic equivalent (1 MET). Any increment in activity will produce greater oxygen consumption, or METs. Many tables exist of the MET level equivalent for varying intensities of exercise and different activities, such as in Table 33-6.

Table 33-6 The Metabolic Equivalent Energy Expenditure of Varying Intensity Activities

For any given level of aerobic training, as exercise intensity increases past a critical point, the ability of physiologic systems to provide oxygen is outstripped by the body’s oxygen requirements. This represents anaerobic threshold, and using metabolic gas analysis, no further increase in O₂ is seen (Figure 33-1). A rate of maximal O₂ has been reached (O_2max, or aerobic capacity). If further exercise is done after this point, anaerobic mechanisms produce the energy required. Because of lactic acid accumulation, only a short duration of further exercise is possible.

FIGURE 33-1 Relationship between oxygen consumption and intensity of work being performed.

The Fick Equation

Complex multicellular organisms use organ systems to transport oxygen from the atmosphere to the site of energy production. The efficiency of these systems at any given level of aerobic fitness determines the O_2max and the maximal functional capacity. The Fick equation links the significant organ systems involved in the transportation of oxygen—lungs, cardiovascular, and muscle—and is the central theme underlying the enhanced function achieved with aerobic exercise training:

Cardiac output at any degree of aerobic training is a product of the heart rate (HR) and stroke volume (SV; the volume of blood expelled by the left ventricle during one contraction). The major determinant of SV is the diastolic filling volume. However, diastolic filling volume decreases as HR increases. With slow HR at low exercise intensities, cardiac output initially increases because of increased SV, but at higher intensity levels it increases because of increased HR.⁶³

The relationship of exercise intensity to cardiac output is essentially linear (Figure 33-2). HR also increases in a linear relationship to exercise intensity (Figure 33-3).

FIGURE 33-2 Relationship between cardiac output and oxygen consumption.

FIGURE 33-3 Relationship between heart rate and oxygen consumption.

Maximal HR is physiologically determined by a person’s age, and is estimated by subtracting age in years from 220. However, this estimation is never used to determine training HR in CR.

The arteriovenous oxygen difference reflects the ability of the muscle to extract oxygen from the blood for use with muscle metabolism and energy production. Determinants include the pulmonary, hematopoietic, vascular, and muscular systems (Box 33-4).

Myocardial Oxygen Consumption

Myocardial oxygen consumption (MO₂) increases in a linear fashion with increasing exercise intensity. In a normal heart the supply of blood and oxygen matches the MO₂. The major determinant of myocardial blood flow is the diameter of the coronary arteries, which normally dilate to increase capacity as myocardial oxygen demand increases. In coronary arteries affected by atherosclerosis, a point is reached where the supply can no longer be increased, and further demand produces a relative lack of myocardial oxygen, or ischemia or angina. The exercise intensity when this point is reached is considered the ischemic or anginal threshold (Figure 33-7).

FIGURE 33-7 Relationship between myocardial oxygen demand and total body oxygen consumption.

Ischemia is noted on an electrocardiogram (ECG) as ST-segment depression, on echocardiography as wall motion abnormalities, and on nuclear imaging as reversible perfusion deficits. Ischemia can be present before the symptom of angina is perceived, and is a more sensitive indicator of myocardial hypoperfusion than angina. Without CAD, the ischemic threshold is not reached, and O_2max determines maximum MO₂. Patients with CAD have narrowed arteries that do not dilate with exercise. Myocardial blood flow is significantly reduced, and at low levels of exercise the MO₂ overcomes supply, and the ischemic threshold is subsequently low.

The muscle group performing the exercise also influences MO₂. MO₂ is greater for the same exercise intensity performed by the upper limbs as compared with the lower limbs. MO₂ is also greater at higher exercise intensities of upright (treadmill) compared with supine (reclining bike) exercise. Exercises with a significant isometric component (rowing machine) generate a higher MO₂ compared with the same intensity of exercise without the isometric component (such as with the step machine).

Measurements of myocardial blood flow and MO₂ are only possible with invasive techniques and are not clinically applicable. An estimation of MO₂ can be made from the product of HR and SBP, or the double product (DP):

This equation is useful in clinical situations in which ischemia is noted or angina is experienced. If the SBP and HR are recorded when ischemia or angina is noted, the DP can be calculated at the ischemic threshold. Future exercise should be completed at a HR at least 10 beats below this point.

Exercise training does not affect the ischemic threshold. Only catheter-based coronary interventions or CABG will alter the anatomy of the coronary arteries and enhance blood flow. Combined intensive programs of lifestyle changes, very-low-fat vegetarian diets, aerobic exercise, stress management, smoking cessation, and group psychologic support have also produced significant regression of coronary atherosclerosis compared with control subjects, with a significant decline in cardiac events.¹⁶²

MO₂ after an aerobic training program is lower at rest and submaximal levels of exercise intensity. This is clinically relevant for patients with CAD, who will be able to perform activities at a greater intensity after an aerobic training program before reaching ischemic threshold as compared with before training. For the same intensity of activity performed after training, a lower MO₂ is achieved, providing a wider margin of safety for those with CAD (Figure 33-8).

FIGURE 33-8 Effect of training on the relationship between myocardial oxygen demand and total body oxygen consumption.

History

The initial evaluation of the patient referred for CR includes a thorough history and physical examination, as well as a review of the available laboratory and physiologic testing data.

The history is the initiation of the physician-patient relationship that nurtures the patient’s trust in the physician and promotes adherence with the CR prescription. A patient’s trust in the physiatrist’s therapeutic recommendations is essential for compliance with a heart-healthy lifestyle. Specific questions identify key areas that influence the CR prescription. Nonsolicited information from the patient can provide insight into emotional concerns, as well as disability and handicap. Some patients overlook symptoms that, in hindsight, were cardiac related. Failure to recognize and report cardiac symptoms is a significant challenge in HD management. A syndrome of overcompensation is typical after a cardiac event, with hypervigilance, anxiety, and overreporting of trivial symptoms. Correlation of these symptoms with physiologic and ECG data during CR helps allay fears and refocus on potential significant symptoms. Education and counseling are beneficial.

Cardiac causes of chest pain must be differentiated from noncardiac causes (Table 33-7). Besides chest pain, cardinal symptoms likely to materialize in CR, such as palpitations, dyspnea, edema, cough, and dizziness, are important to evaluate. For their significance, relevant textbooks in cardiology are recommended. It is also important to note that deconditioning, depression, medications including β-blockers, and poor sleep are common noncardiac causes of fatigue. Patient education that cardiac fatigue worsens with further rest and improves with physical exertion is important for compliance with exercise recommendations.

Table 33-7 Cardiac Versus Noncardiac Causes of Chest Pain

Physical Examination

The physiatric examination before CR includes all organ systems that influence the rehabilitation process. Particular attention should be paid to the following.

Pulse rhythm and rate are important. A normal sinus rhythm is a regular pulse between 60 and 100 beats/min with a P wave preceding every QRS complex on the ECG. Bradycardia is a rate less than 60 beats/min. It can be physiologic in athletes because of increased vagal tone to the heart, and can be pharmacologic as a result of medications including β-blockers. It can also be pathologic, as in sick sinus syndrome, heart block, and junctional or ventricular escape rhythms. Tachycardia, a rate above 100 beats/min, is normal only after exertion. Other causes include pain, dehydration, anemia, CHF, hypotension, and hyperthyroidism.Fear and anxiety can also play a role during CR in a patient who is unfamiliar with the rehabilitation process. Medication (β-blocker and calcium channel blocker) noncompliance can produce rebound tachycardia.

Sinus arrhythmia is a normal physiologic variant in which the HR increases with inspiration and slows with expiration. An irregularly irregular HR can indicate atrial fibrillation. Atrial flutter, premature atrial contractions, premature ventricular contractions, and second-degree heart block can also produce an irregular pulse.

Arrhythmias are significant if they result in symptoms or signs of ischemia or low SBP. Appropriate treatment must be instituted rapidly to prevent MI or syncope. When there are no hemodynamic consequences, arrhythmias can be considered more benign. A wide complex tachycardia on ECG indicates a more malignant ventricular complex arrhythmia.

Blood pressure normally is 120/70 mm Hg. Hypertension is defined by a blood pressure greater than 140/90 mm Hg. In those patients with significant vasculopathy, recording blood pressure from both arms can result in significantly different values because of subclavian artery stenosis. Coarctation of the aorta produces similar findings. A “low” blood pressure at rest (i.e., 90/60 mm Hg) that is asymptomatic and that increases with walking and exercise is normal and acceptable. Any blood pressure associated with dizziness or fatigue, or that drops on standing or exercise is abnormal. Deconditioning, dehydration, anemia, and medications are reversible causes of hypotension. Testing for orthostatic hypotension is important. Pulsus paradoxus, which is a fall in SBP greater than 10 mm Hg with inspiration, can indicate pericardial effusion and tamponade requiring urgent surgical evaluation.

A resting blood pressure greater than 200/110 mm Hg is a contraindication to exercise. Many patients, however, present for exercise with an elevated blood pressure maintained by anxiety. A patient with an asymptomatic elevated blood pressure might be allowed to start CR under close observation, realizing that the pressure most likely will fall toward normal as anxiety dissipates with the onset of exercise.

Heart and lungs are an important part of the physical examination. Auscultation of the heart should correlate with the history of HD. New and unexpected or changed murmurs require further evaluation with echocardiography before the patient can be cleared for exercise. A harsh ejection systolic murmur heard over the aortic region can suggest critical aortic stenosis, a contraindication to CR. Pericardial rubs after heart surgery are suggestive of pericarditis, the treatment of which includes antiinflammatory medication. Diminished breath sounds in the lung bases are suggestive of pleural effusions. Wheezes, rales, and rhonchi are suggestive of interstitial edema, pulmonary congestion, and retained secretions or mucus. An oxygen saturation below 90% on pulse oximetry requires supplemental oxygen and treatment of the causative cardiopulmonary pathology. Coexistent lung disease, asthma, and chronic obstructive pulmonary disease require appropriate treatment.

Limb examination is also helpful, especially when there is bilateral, symmetric lower limb edema that implies fluid retention. In this case fluid and sodium restriction and diuretic therapy should be considered. Daily weight gain supports a diagnosis of CHF. Asymmetric lower extremity edema often occurs in the limb where vein grafts were removed. Local cellulitis and deep venous thrombosis should be considered, especially when there is unilateral upper limb swelling.

Peripheral pulses should be examined. Carotid bruits and diminished or absent lower extremity pulses indicate widespread vasculopathy. Skin integrity of the feet can be impaired, producing ulceration and gangrene (see Chapter 56). Lower limb amputation requires special consideration when planning CR.

Musculoskeletal examination is needed to detect generalized or focal muscle atrophy and weakness, significant arthritic conditions, and postoperative myofascial findings (most commonly in the shoulders) and sternal pain (costochondritis). If not successfully treated, these conditions can require modification of the CR program.

Neurologic examination is important because cerebrovascular disease is often associated with CAD. Preexisting or perioperative strokes are not uncommon, especially with atrial fibrillation. Evaluation for focal sensory and motor deficits is essential. Gait and balance disorders also influence planning of the CR program. Peripheral neuropathy is also frequently present in patients with diabetes.

Cognitive examination is helpful, because atherosclerosis underlies CAD, CVD, and some dementias. Post-MI or post-CABG confusion can be caused by preexisting dementia or indicate a new cerebral event. Anesthesia, hypoxia, and medications can result in significant temporary orpermanent cognitive deficits, with safety and dependency issues. “Pump head” is a slang term for an acute confusional state after cardiopulmonary bypass used for cardiac surgeries. Some patients who go through surgery “off pump” also experience confusional states. A fluctuating cognitive state after a cardiac event or surgery is consistent with a toxic encephalopathy. This usually resolves over days to weeks. Magnetic resonance imaging (MRI) of the brain can also reveal a “shower” of cerebral emboli, originating from an aortic atheroma or the left ventricle during surgery. Recovery is usually complete. Monitoring for safe use of exercise equipment is necessary during CR in cognitively impaired patients.