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Special Consideration in cardiac rehabilitation program
for patients with CHF
Submitted to: Dr. Jamal Moiz
submitted by: Sumaiya shams
MPT (cardio)
JMI
Chronic heart failure: (CHF) is a condition in which the heart can no longer
sufficiently supply the body with the blood needed to maintain homeostasis. it is
a complex clinical syndrome, initiated by inability of the heart to pump blood at a
rate commensurate with the requirement of metabolising tissue.
Common causes of heart failure include
• coronary artery disease,
• myocardial infarction (heart attack),
• high blood pressure,
• atrial fibrillation,
• valvular heart disease,
• excess alcohol use,
• infection, and
• cardiomyopathy of an unknown cause. These cause heart failure by changing
either the structure or the function of the heart(national clinical guideline
centre UK)
Pathophysiology
 Heart failure is caused by any condition which reduces the efficiency of the
heart muscle, through damage or overloading.
 Over time these increases in workload, which are mediated by long-term
activation of neurohormonal systems such as the renin–angiotensin system,
leads to fibrosis, dilation, and structural changes in the shape of the left
ventricle from elliptical to spherical.
 The heart of a person with heart failure may have a reduced force of contraction
due to overloading of the ventricle.
 In a normal heart, increased filling of the ventricle results in increased
contraction force by the Frank–Starling law of the heart, and thus a rise
in cardiac output.
 In heart failure, this mechanism fails, as the ventricle is loaded with blood to
the point where heart muscle contraction becomes less efficient. This is due to
reduced ability to cross-link actin and myosin filaments in over-stretched heart
muscle.
Physiological Consequences of Heart Failure
1. Cardiovascular: Decreased myocardial performance, with subsequent peripheral
vascular constriction to increase venous return (attempting to increase stroke volume
and cardiac output)
2. Pulmonary: Pulmonary edema because of elevated cardiac filling pressures resulting
from poor myocardial performance and fluid overload
3. Renal: Fluid retention resulting from decreased cardiac output
4. Neurohumoral: Increased sympathetic stimulation that eventually desensitizes the
heart to beta-1 adrenergic receptor stimulation, thus decreasing the cardiac inotropic
effect
5. Musculoskeletal: Skeletal muscle wasting and possible skeletal muscle myopathies as
well as osteoporosis resulting from inactivity or other accompanying diseases
6. Hematologic: Possible polycythemia, anemia, and hemostatic abnormalities resulting
from a reduction in oxygen transport, accompanying liver disease, or stagnant blood
flow in the heart chambers caused by poor cardiac contraction
7. Hepatic: Possible cardiac cirrhosis from hypoperfusion resulting from an inadequate
cardiac output or hepatic venous congestion
8. Pancreatic: Possible impaired insulin secretion and impaired glucose intolerance as
well as the source of a possible myocardial depressant factor
9. Nutritional/biochemical: Anorexia that leads to malnutrition (protein, calorie, and
vitamin deficiencies) and cachexia
Clinical Manifestations:
• Shortness of breath (dyspnea)
• Fatigue and weakness
• Swelling (edema) in legs, ankles and feet
• Rapid or irregular heartbeat
• Reduced ability to exercise
• Persistent cough or wheezing with white or pink blood-tinged phlegm
• Increased need to urinate at night
• Swelling of abdomen (ascites)
• Very rapid weight gain from fluid retention
• Lack of appetite and nausea
• Difficulty concentrating or decreased alertness
• Sudden, severe shortness of breath and coughing up pink, foamy mucus
• Chest pain if heart failure is caused by a heart attack
Treatment
1. Pharmacological Management
• Beta-blockers,
• ACE inhibitors,
• glycosides, and
• diuretics are the key medications used for managing congestive heart
failure through regulating renal function and the sympathetic nervous
system
2. Life style modification
3. Implantable devices
4. Surgical therapies
5. Palliative care
Cardiac rehabilitation
Reduced exercise capacity negatively affects the ability of patients with heart
failure (HF) to perform activities required for daily life, further decreasing their
independence and quality of life (QoL). Cardiac rehabilitation (CR) can
effectively improve aerobic fitness and overall health status in patients with HF.
Chronic heart failure (CHF) is highly prevalent in older individuals and a major
cause of morbidity, mortality, hospitalizations and disability. Cardiac
rehabilitation (CR) exercise training and CHF self-care counseling have each
been shown to improve clinical status and clinical outcomes in CHF,
recommended by ACC and AHA.
Beneficial Effects of Exercise in Chronic
Heart Failure (Balady et al., 2007).
• Aerobic training
1. Increased exercise capacity
2. Lower heart rate response to submaximal exercise
3. Improved diastolic function
4. Improved endothelial function
5. Increased skeletal muscle oxidative capacity Enhanced vagal tone and
lower sympathetic tone
6. Reduced inflammatory cytokines
7. Lower all-cause mortality or hospitalization Improved quality of life
Resistance training
1. Increased muscle strength and
2. endurance
Exercise Prescription for Patients With Heart Failure
(AACVPR)
1. Cardiorespiratory endurance
• Description: Dynamic activities involving large muscle groups
• Intensity: 40% to 80% of HRR RPE 11 to 14 (where HRR is not
appropriate)
• Frequency: Minimum of 3 days per week, but preferably on most days of
the week
• Duration: 20 to 60 min/session
2. Resistance training
• Description: 8 to 10 muscle-specific exercises involving resistance bands,
weight machines, handheld weights, or combination; begin with one set of
10 to 15 repetitions
• Intensity: 50% to 70% 1RM for lifts involving the hips and lower body;
40% to 70% 1RM for lifts involving the upper body
• Frequency: 2 or 3 days a week
• Duration: 20 to 30 min/session; contraction should be performed in a
rhythmical manner at a moderate to slow controlled speed
Training protocol in CHF (AACVPR):
1. Modes ( in order of use): cycle ergo meter, walking, stair machine, rowing
machine, calisthenics, resistance exercises
2. Intensity:
 40-70% of VO2 peak
 40-70% of heart rate reserve
 11-13 rating of perceived exertion (borg scale 6-20)
3. Frequency: 3-7 times/week (average 3-5)
4. Duration: 8-52 weeks (average 12)
Indication to stop or modify exercise program in CHF patients
(AACVPR):
1. Excessive exercise – induced fatigue (>14 rating of perceived exertion
on borg scale) or dyspnoea (>40 breaths /min)
2. Weight increase of 1 kg or more body weight within 24 hrs
3. Development of pulmonary rales or gallop rhythm
4. Failure of SBP to increase >10 mm Hg with exercises
5. Development of exercise induced complex ectopy
6. Pulse pressure less than 10 mm Hg
7. Resistant HR 100 bpm or more
Safety, Exercise, and Educational Strategies for Patients With
Heart Failure
Safety
• Uncompensated HF is a contraindication to starting an exercise program; decompensation is reason to
discontinue the exercise program
• A thorough patient assessment should be part of pre exercise assessment of vital signs with each CR/SP
visit
• As part of the initial evaluation, patients should be asked about advance directives; copies of such
decisions should be placed in the patient’s chart
Exercise
• Exercise stress tests should include,where possible, metabolic assessment using a carefully progressing
protocol (e.g., 1 MET per stage)
• Patients are at high risk for ventricular arrhythmias and decompensation
• Exercise protocol: longer warm-up and cool-down; use interval exercise (1-6min) as needed; encourage
weight bearing for ADL
• Use ECG and BP monitoring during exercise, as needed; use subjective RPE and dyspnea scales
• Common side effect: fatigue for rest of the day
• Due to slow progression in exercise program and high-risk nature of patients, the supervised exercise may
need to be extended
Education
• Priority: sign and symptom recognition and response, including fatigue,
weakness, dyspnea, orthopnea, edema, weight gain
• Nutrition consult: low-sodium diet (e.g., 1500 mg), heart-healthy diet
• Drug regimen: medication education and compliance monitoring,
diuretics, digitalis, ACE inhibitors, beta-blockers
• Psychosocial consult for depression symptomatology; HF support group
and individual counseling
• Basic information regarding disease processes.
Contraindication:
Exercise training advisable only in stable chronic heart failure and is
contraindicated in
1. Aortic stenosis
2. Obstructive cardiomyopathy
3. Myocarditis
4. Significant ischemia at low work rate (<2METS)
5. Recent onset atrial fibrillation
6. And probably in the case of of a measured peak oxygen intake less than
8 ml/kg/min).
High-Intensity Interval Training in Patients With Heart Failure With
Reduced Ejection Fraction
Impact factor – 23.60
journal- Circulation, is a scientific journal published by Lippincott Williams &
Wilkins for the American Heart Association.
Indexing- pubmed, web of science, scopus
Author- Ellingsen., et al, 2017
Design: Randomized controlled trial.
Setting: Cardiac rehabilitation center.
Purpose- to test the hypothesis that HIIT ( high-intensity interval training ) is
superior to MCT(moderate continuous training ) with regard to improvement
of left ventricular dimensions and exercise capacity.
Clinical Assessments- Screening procedures and clinical assessments before and
after exercise interventions were performed. Briefly, medical history,
anthropometrics, physical examination including fasting blood sampling,
quality-of-life questionnaires, echocardiography were performed.
Cardiopulmonary exercise testing was performed with standard equipment for
indirect calorimetry in an incremental protocol until exhaustion on either a
treadmill or a bicycle ergometer, depending on exercise training equipment.
Interventions: 261 patients with left ventricular ejection fraction ≤35% and
New York Heart Association class II to III were randomly assigned to HIIT at
90% to 95% of maximal heart rate, MCT at 60% to 70% of maximal heart rate,
or recommendation of regular exercise (RRE). Thereafter, patients were
encouraged to continue exercising on their own. Clinical assessments were
performed at baseline, after the intervention, and at follow-up after 52 weeks.
Primary end point was a between-group comparison of change in left ventricular
end-diastolic diameter from baseline to 12 weeks.
Results- Groups did not differ in age (median, 60 years), sex (19% women),
ischemic pathogenesis (59%), or medication. Change in left ventricular end-
diastolic diameter from baseline to 12 weeks was not different between HIIT and
MCT (P=0.45); left ventricular end-diastolic diameter changes compared with RRE
were −2.8 mm (−5.2 to −0.4 mm; P=0.02) in HIIT and −1.2 mm (−3.6 to 1.2
mm; P=0.34) in MCT. There was also no difference between HIIT and MCT in
peak oxygen uptake (P=0.70), but both were superior to RRE. However, none of
these changes was maintained at follow-up after 52 weeks. Serious adverse events
were not statistically different during supervised intervention or at follow-up at 52
weeks (HIIT, 39%; MCT, 25%; RRE, 34%; P=0.16). Training records showed that
51% of patients exercised below prescribed target during supervised HIIT and 80%
above target in MCT
Conclusions- This study did not confirm the hypothesis that a 12-week
program of supervised HIIT was superior to MCT in reducing left ventricular
remodeling in patients with stable heart failure. None of the interventions led
to deterioration of cardiac function compared with RRE, and both exercise
programs increased aerobic capacity. However, these positive changes were
smaller than expected and were not maintained at follow-up after 52 weeks.
Numeric differences in readmissions for worsening of heart failure suggested a
favor of MCT relative to HIIT and RRE, but the study was not powered to
assess safety. Training records showed that exercise intensities >90% of
maximal heart rate were not achieved in a significant proportion of the
patients.
Limitations-
1. Even after several measures were taken to ensure quality and consistency,
including supervised training sessions based on heart rate monitoring, the
differences in training intensity between HIIT and MCT were less than
intended and partly overlapped which was an unexpected finding.
2. exercise intensities were not regularly adapted to improvements in
exercise capacity and to worsening of symptoms or changes of
medication.
3. questionnaires were of limited value for assessing physical activity
outside supervised sessions and recommend accelerometer recordings,
particularly in the unsupervised follow-up period.
4. women were not focused because only 19% of the patients in this study
were women. this sex bias was unintended and constitutes a limitation of
the generalization of the results.
Future consideration
1. further studies are needed to define the role of HIIT as an alternative
exercise modality in patients with heart failure with reduced ejection
fraction.
2. exercise intensities should be regularly adapted to improvements in
exercise capacity and to worsening of symptoms or changes of
medication. Repeated assessment of maximal heart rate and more
emphasis on adjusting workload according to perceived level of effort
might also be helpful.
3. in future studies, women should be a focus because only 19% of the
patients in this study were women.
THANK YOU!
Seminar 1

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Seminar 1

  • 1. Special Consideration in cardiac rehabilitation program for patients with CHF Submitted to: Dr. Jamal Moiz submitted by: Sumaiya shams MPT (cardio) JMI
  • 2. Chronic heart failure: (CHF) is a condition in which the heart can no longer sufficiently supply the body with the blood needed to maintain homeostasis. it is a complex clinical syndrome, initiated by inability of the heart to pump blood at a rate commensurate with the requirement of metabolising tissue. Common causes of heart failure include • coronary artery disease, • myocardial infarction (heart attack), • high blood pressure, • atrial fibrillation, • valvular heart disease, • excess alcohol use, • infection, and • cardiomyopathy of an unknown cause. These cause heart failure by changing either the structure or the function of the heart(national clinical guideline centre UK)
  • 3. Pathophysiology  Heart failure is caused by any condition which reduces the efficiency of the heart muscle, through damage or overloading.  Over time these increases in workload, which are mediated by long-term activation of neurohormonal systems such as the renin–angiotensin system, leads to fibrosis, dilation, and structural changes in the shape of the left ventricle from elliptical to spherical.  The heart of a person with heart failure may have a reduced force of contraction due to overloading of the ventricle.  In a normal heart, increased filling of the ventricle results in increased contraction force by the Frank–Starling law of the heart, and thus a rise in cardiac output.  In heart failure, this mechanism fails, as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient. This is due to reduced ability to cross-link actin and myosin filaments in over-stretched heart muscle.
  • 4. Physiological Consequences of Heart Failure 1. Cardiovascular: Decreased myocardial performance, with subsequent peripheral vascular constriction to increase venous return (attempting to increase stroke volume and cardiac output) 2. Pulmonary: Pulmonary edema because of elevated cardiac filling pressures resulting from poor myocardial performance and fluid overload 3. Renal: Fluid retention resulting from decreased cardiac output 4. Neurohumoral: Increased sympathetic stimulation that eventually desensitizes the heart to beta-1 adrenergic receptor stimulation, thus decreasing the cardiac inotropic effect 5. Musculoskeletal: Skeletal muscle wasting and possible skeletal muscle myopathies as well as osteoporosis resulting from inactivity or other accompanying diseases 6. Hematologic: Possible polycythemia, anemia, and hemostatic abnormalities resulting from a reduction in oxygen transport, accompanying liver disease, or stagnant blood flow in the heart chambers caused by poor cardiac contraction 7. Hepatic: Possible cardiac cirrhosis from hypoperfusion resulting from an inadequate cardiac output or hepatic venous congestion 8. Pancreatic: Possible impaired insulin secretion and impaired glucose intolerance as well as the source of a possible myocardial depressant factor 9. Nutritional/biochemical: Anorexia that leads to malnutrition (protein, calorie, and vitamin deficiencies) and cachexia
  • 5. Clinical Manifestations: • Shortness of breath (dyspnea) • Fatigue and weakness • Swelling (edema) in legs, ankles and feet • Rapid or irregular heartbeat • Reduced ability to exercise • Persistent cough or wheezing with white or pink blood-tinged phlegm • Increased need to urinate at night • Swelling of abdomen (ascites) • Very rapid weight gain from fluid retention • Lack of appetite and nausea • Difficulty concentrating or decreased alertness • Sudden, severe shortness of breath and coughing up pink, foamy mucus • Chest pain if heart failure is caused by a heart attack
  • 6. Treatment 1. Pharmacological Management • Beta-blockers, • ACE inhibitors, • glycosides, and • diuretics are the key medications used for managing congestive heart failure through regulating renal function and the sympathetic nervous system 2. Life style modification 3. Implantable devices 4. Surgical therapies 5. Palliative care
  • 7. Cardiac rehabilitation Reduced exercise capacity negatively affects the ability of patients with heart failure (HF) to perform activities required for daily life, further decreasing their independence and quality of life (QoL). Cardiac rehabilitation (CR) can effectively improve aerobic fitness and overall health status in patients with HF. Chronic heart failure (CHF) is highly prevalent in older individuals and a major cause of morbidity, mortality, hospitalizations and disability. Cardiac rehabilitation (CR) exercise training and CHF self-care counseling have each been shown to improve clinical status and clinical outcomes in CHF, recommended by ACC and AHA.
  • 8. Beneficial Effects of Exercise in Chronic Heart Failure (Balady et al., 2007). • Aerobic training 1. Increased exercise capacity 2. Lower heart rate response to submaximal exercise 3. Improved diastolic function 4. Improved endothelial function 5. Increased skeletal muscle oxidative capacity Enhanced vagal tone and lower sympathetic tone 6. Reduced inflammatory cytokines 7. Lower all-cause mortality or hospitalization Improved quality of life Resistance training 1. Increased muscle strength and 2. endurance
  • 9. Exercise Prescription for Patients With Heart Failure (AACVPR) 1. Cardiorespiratory endurance • Description: Dynamic activities involving large muscle groups • Intensity: 40% to 80% of HRR RPE 11 to 14 (where HRR is not appropriate) • Frequency: Minimum of 3 days per week, but preferably on most days of the week • Duration: 20 to 60 min/session 2. Resistance training • Description: 8 to 10 muscle-specific exercises involving resistance bands, weight machines, handheld weights, or combination; begin with one set of 10 to 15 repetitions • Intensity: 50% to 70% 1RM for lifts involving the hips and lower body; 40% to 70% 1RM for lifts involving the upper body • Frequency: 2 or 3 days a week • Duration: 20 to 30 min/session; contraction should be performed in a rhythmical manner at a moderate to slow controlled speed
  • 10. Training protocol in CHF (AACVPR): 1. Modes ( in order of use): cycle ergo meter, walking, stair machine, rowing machine, calisthenics, resistance exercises 2. Intensity:  40-70% of VO2 peak  40-70% of heart rate reserve  11-13 rating of perceived exertion (borg scale 6-20) 3. Frequency: 3-7 times/week (average 3-5) 4. Duration: 8-52 weeks (average 12)
  • 11. Indication to stop or modify exercise program in CHF patients (AACVPR): 1. Excessive exercise – induced fatigue (>14 rating of perceived exertion on borg scale) or dyspnoea (>40 breaths /min) 2. Weight increase of 1 kg or more body weight within 24 hrs 3. Development of pulmonary rales or gallop rhythm 4. Failure of SBP to increase >10 mm Hg with exercises 5. Development of exercise induced complex ectopy 6. Pulse pressure less than 10 mm Hg 7. Resistant HR 100 bpm or more
  • 12. Safety, Exercise, and Educational Strategies for Patients With Heart Failure Safety • Uncompensated HF is a contraindication to starting an exercise program; decompensation is reason to discontinue the exercise program • A thorough patient assessment should be part of pre exercise assessment of vital signs with each CR/SP visit • As part of the initial evaluation, patients should be asked about advance directives; copies of such decisions should be placed in the patient’s chart Exercise • Exercise stress tests should include,where possible, metabolic assessment using a carefully progressing protocol (e.g., 1 MET per stage) • Patients are at high risk for ventricular arrhythmias and decompensation • Exercise protocol: longer warm-up and cool-down; use interval exercise (1-6min) as needed; encourage weight bearing for ADL • Use ECG and BP monitoring during exercise, as needed; use subjective RPE and dyspnea scales • Common side effect: fatigue for rest of the day • Due to slow progression in exercise program and high-risk nature of patients, the supervised exercise may need to be extended
  • 13. Education • Priority: sign and symptom recognition and response, including fatigue, weakness, dyspnea, orthopnea, edema, weight gain • Nutrition consult: low-sodium diet (e.g., 1500 mg), heart-healthy diet • Drug regimen: medication education and compliance monitoring, diuretics, digitalis, ACE inhibitors, beta-blockers • Psychosocial consult for depression symptomatology; HF support group and individual counseling • Basic information regarding disease processes.
  • 14. Contraindication: Exercise training advisable only in stable chronic heart failure and is contraindicated in 1. Aortic stenosis 2. Obstructive cardiomyopathy 3. Myocarditis 4. Significant ischemia at low work rate (<2METS) 5. Recent onset atrial fibrillation 6. And probably in the case of of a measured peak oxygen intake less than 8 ml/kg/min).
  • 15. High-Intensity Interval Training in Patients With Heart Failure With Reduced Ejection Fraction Impact factor – 23.60 journal- Circulation, is a scientific journal published by Lippincott Williams & Wilkins for the American Heart Association. Indexing- pubmed, web of science, scopus Author- Ellingsen., et al, 2017 Design: Randomized controlled trial. Setting: Cardiac rehabilitation center. Purpose- to test the hypothesis that HIIT ( high-intensity interval training ) is superior to MCT(moderate continuous training ) with regard to improvement of left ventricular dimensions and exercise capacity.
  • 16. Clinical Assessments- Screening procedures and clinical assessments before and after exercise interventions were performed. Briefly, medical history, anthropometrics, physical examination including fasting blood sampling, quality-of-life questionnaires, echocardiography were performed. Cardiopulmonary exercise testing was performed with standard equipment for indirect calorimetry in an incremental protocol until exhaustion on either a treadmill or a bicycle ergometer, depending on exercise training equipment. Interventions: 261 patients with left ventricular ejection fraction ≤35% and New York Heart Association class II to III were randomly assigned to HIIT at 90% to 95% of maximal heart rate, MCT at 60% to 70% of maximal heart rate, or recommendation of regular exercise (RRE). Thereafter, patients were encouraged to continue exercising on their own. Clinical assessments were performed at baseline, after the intervention, and at follow-up after 52 weeks. Primary end point was a between-group comparison of change in left ventricular end-diastolic diameter from baseline to 12 weeks.
  • 17. Results- Groups did not differ in age (median, 60 years), sex (19% women), ischemic pathogenesis (59%), or medication. Change in left ventricular end- diastolic diameter from baseline to 12 weeks was not different between HIIT and MCT (P=0.45); left ventricular end-diastolic diameter changes compared with RRE were −2.8 mm (−5.2 to −0.4 mm; P=0.02) in HIIT and −1.2 mm (−3.6 to 1.2 mm; P=0.34) in MCT. There was also no difference between HIIT and MCT in peak oxygen uptake (P=0.70), but both were superior to RRE. However, none of these changes was maintained at follow-up after 52 weeks. Serious adverse events were not statistically different during supervised intervention or at follow-up at 52 weeks (HIIT, 39%; MCT, 25%; RRE, 34%; P=0.16). Training records showed that 51% of patients exercised below prescribed target during supervised HIIT and 80% above target in MCT
  • 18. Conclusions- This study did not confirm the hypothesis that a 12-week program of supervised HIIT was superior to MCT in reducing left ventricular remodeling in patients with stable heart failure. None of the interventions led to deterioration of cardiac function compared with RRE, and both exercise programs increased aerobic capacity. However, these positive changes were smaller than expected and were not maintained at follow-up after 52 weeks. Numeric differences in readmissions for worsening of heart failure suggested a favor of MCT relative to HIIT and RRE, but the study was not powered to assess safety. Training records showed that exercise intensities >90% of maximal heart rate were not achieved in a significant proportion of the patients.
  • 19. Limitations- 1. Even after several measures were taken to ensure quality and consistency, including supervised training sessions based on heart rate monitoring, the differences in training intensity between HIIT and MCT were less than intended and partly overlapped which was an unexpected finding. 2. exercise intensities were not regularly adapted to improvements in exercise capacity and to worsening of symptoms or changes of medication. 3. questionnaires were of limited value for assessing physical activity outside supervised sessions and recommend accelerometer recordings, particularly in the unsupervised follow-up period. 4. women were not focused because only 19% of the patients in this study were women. this sex bias was unintended and constitutes a limitation of the generalization of the results.
  • 20. Future consideration 1. further studies are needed to define the role of HIIT as an alternative exercise modality in patients with heart failure with reduced ejection fraction. 2. exercise intensities should be regularly adapted to improvements in exercise capacity and to worsening of symptoms or changes of medication. Repeated assessment of maximal heart rate and more emphasis on adjusting workload according to perceived level of effort might also be helpful. 3. in future studies, women should be a focus because only 19% of the patients in this study were women.