Fig. 14.1
Transthoracic echocardiography. Left: parasternal long axis view (1, IVSd; 2, LVEDD; 3, PWd). Right: apical four-chamber view
The diagnosis of heart failure with preserved systolic function was made, and the patient was treated with bumetanide 2 × 1 mg and spironolactone 25 mg and lost more than 6 kg of fluid. He was discharged in NYHA II–III and referred to cardiac rehabilitation.
During the initial visit at the beginning of cardiac rehabilitation, the patient was depressed and anxious, and he worried a lot about his future and the future of his family and his work. He was working full time as a technical engineer before he was admitted for heart failure. His work required moderate physical activity. An exercise test showed a VO2 max of 15 ml/kg/min (55 % pred), with a heart rate staying at around 50–55/min up to maximal exercise. A rehabilitation program was started, consisting of 45-min moderate continuous exercise training sessions between the patient’s 1st and 2nd ventilatory threshold for 3 times a week, as well as psychological counselling.
After 3 months of training, the patient remained dyspneic, and his control cardiopulmonary exercise test showed an increase of VO2 max to only 16.5 ml/kg/min (Table 14.1).
Table 14.1
Maximal cardiopulmonary exercise test results before and after cardiac rehabilitation
Before rehabilitation | After rehabilitation | |
|---|---|---|
Heart rate max | 55/min (33 % pred) | 59/min (36 % pred) |
Load max | 80 watt | 90 watt |
VO2 max | 15 ml/kg/min (55 % pred) | 16.5 ml/kg/min (61 % pred) |
RER max | 1.22 | 1.26 |
Anaerobic threshold | 50 watt | 60 watt |
VE/VCO2 slope | 38 | 38 |
Breathing reserve | 58 % | 60 % |
Question
What are possible reasons for the lack of influence of rehabilitation on his feeling of dyspnea:
- 1.
Hyperventilation
- 2.
Lack of muscle mass or muscular strength
- 3.
Pulmonary hypertension
- 4.
Chronotropic incompetence
Answer
All four possible explanations may play a role in limiting exercise capacity after rehabilitation in this patient:
Anxiety and hyperventilation are frequently found in patients with heart failure: a possible clue to this problem is often found when patients do not support the face mask of the ergospirometry. A history of claustrophobia is also often present in these patients. Psychological counselling and breathing control exercises can reduce the anxiety and increase the feeling of control for the patient
Peripheral muscle atrophy is very common in heart failure, due to disuse, but also to the inflammatory state that often accompanies this pathology. Exercise tolerance and quality of life in heart failure patients are more related to peripheral muscle function than to ejection fraction. Testing and training of the large muscle groups is more and more standard in rehabilitation programs for severe heart failure.
Respiratory muscle weakness is often present in heart failure and after cardiac surgery. Strength training of the respiratory muscles (inspiratory muscle strength training) was shown to be almost as efficient as endurance training in increasing exercise capacity in severe heart failure.
The pulmonary artery pressure was slightly elevated at rest, but it is well known that exercise can increase the pulmonary artery pressure importantly in these patients. A sign suggesting that pulmonary hypertension may play a role is the evolution of the VE/VCO2 slope, which in this patient was increased to 38. Exercise echocardiography may allow quantification of the pulmonary artery pressures and confirm exercise-induced pulmonary hypertension, thereby explaining part of the patient’s symptoms. Prior research indicates exercise training to be effective in improving pulmonary hypertension patients’ exercise capacity, functional class, and quality of life [1]. However, more clinical trials and research are required to assess the effects of different types of exercise programs (including aerobic exercise training, resistance training, inspiratory muscle training, or a combination).
Chronotropic incompetence, especially in patients with a relatively fixed cardiac output due to the presence of two artificial valves, may also play a role in his dyspnea. In the patient presented in this case, the CPET was maximal during both tests (RER max of 1.22 and 1.26, respectively); however, heart rate max < 85 % pred for age (220 – age = 220–55 = 165; 165 × 85 % = 140) confirms the presence of chronotropic incompetence in the absence of bradycardia-inducing therapy.
