Rehabilitation in Patients with Heart Failure by Dr. Thabet

Medical Rehabilitation in
cardiac patients with HF
Salim Thabet PGY3
Moderator: Dr. Mahazarin Ginwalla
• JD is a 60 y.o male pt. known with
1. HFrEF 35-40% due to ICM
2. CAD s/p MIx2 with PCI
4. Smoker 30PY
5. Dietary non-compliance
Presenting with progressive SOB on exertion of 1wk
associated with orthopnea, PNDs and increase
abdominal girth and LE edema. When not in HF
exac. can usually walk on flat surface with mild SOB
• PE: VS: 120/70 100 SR 25 afebrile
JVD to mandible
S4 heard, no murmurs
+2 LEE
• CXR: Pulmonary edema
• ProBNP=10k, Cr=2 with baseline of 1.2
• Meds:
Lisinopril 20, Metoprolol succinate 100, aspirin
81, atorvastatin 20mg, imdur 30mg and Lasix
• Pt. was diuresed with 40mg Lasix IVP BID with
improvement in symptoms and total I/O -10 lt,
• He was discharged home on Lasix 40 mg BID
(with instructions to increase according to
weight increase), metoprolol succinate 150 mg
and Imdur 60 mg
• Heart failure care path and PCP/Cardiology f/u
• He is readmitted 2 months later with same
Exercise and the body
Exercise physiology
Benefits of exercise
Risks of exercise
Heart failure and the body
Exercise capacity in HF
Skeletal muscle dysfunction
III. Rehabilitation in HF
Effect of exercise in HF
IV. Conclusion and recommendations
V. QI project (HF readmission)
Epidemiology of HF
• Hard to estimate and usually based on symptoms
• 5.1 million in the US in 2006
• Lifetime prevalence 1/5
• Incidence increases with age (8/1,000 50-59yrs
and 66/1000 80-89)
• African Americans 25% more than in whites
Exercise physiology
• Skeletal muscle metabolism can increase up to
50 xs resting rate
• To preserve tissue oxygenation and PH the
heart and lung must react
• Exercise testing yields information on the
response to exercise and can determine
cardiac and pulmonary limitations to exercise
• Physiologic data include:
Oxygen uptake (VO2)
CO2 output
Tidal volume
Minute ventilation (VE)
Pulse oximetry
• In certain situations more extensive
monitoring (arterial or pulmonary artery
• VO2max: symptom-limited max O2 uptake during
incremental bilateral leg exercise
• Used to provide overall assessment of exercise
• Normal VO2 means that no serious pathology
exists in pulmonary, cardiovascular and
neuromuscular systems
• However intra and inter-organ compensation can
yield a normal value
1. Med Sci Sports Exerc 1997; 29:591
2. Am J Noninvas Cardiol 1987; 1:244
• VO2 increases linearly with work
• Slope not affected by age, sex or training
• Shifted leftward in obese (increased O2 uptake
for same workload)
• VO2max = plateau of VO2 vs Work
• Nl VO2max > 20ml/kg/min ( training, age)
• Can be predicted by age, gender, height and lean
Am Rev Respir Dis 1984; 129:S49
Normal VO2 vs. Workload
• Central (not well understood) vs peripheral
• Accumulation of metabolic byproducts (lactate,
Ammonia) and depletion of ATP/glycogen
• Lactate threshold (LT): VO2 at which pyruvate exceeds
the ability of it being metabolized by the Krebs cycle
• LT better predictor of sustained performance than
• At VO2 just below LT exercise can be sustained for long
periods (steady state) ex: UFC fighters
Muscle Nerve 1989; 12:660
Normal lactate vs VO2 in exercise
Effect of exercise on skeletal
• Training capillary density and mitochondria
• Training is associated with less ammonia and
lactate with less fatigue at a set metabolic rate
• LT > 40% VO2max in nl. people, less in pts.
with CVD and more in athletes
Sports Sci Exchange 1995; 8:1
• Fick equation: VO2 = CO x (CaO2 – CvO2)
Tissue metabolism
• CO due to HR (autonomic changes) and SV (increased
contractility and LVEDV 20-40%)
• Training results in lower resting HR
• LVEDP up to 20 mm Hg & filling is limited by
pericardium (CO + VO2 inc. with pericardiectomy)
• CO limits VO2max in healthy adults with training CO
can up to 5 xs resting value
Systemic circulation
• Balance bet muscle chemoreflex and arterial
baroreceptors results in net in SBP whereas DBP
remains near resting value
• Rise in SBP is much less than what is expected by
rise in CO reflecting in SVR
PH &PO2, K+, adenosine & NO causes local
muscle vasodilatation whereas sympathetic
arterial vasoconstriction directs flow to muscles
• NO activity is increased with training
• Acidosis O2 extraction also by shifting
oxyhemoglobin dissociation curve to the right
Rest (% total)
Maximal exercise (% total)
Skeletal muscle
Other organs
Blood flow distribution with exercise
Pulmonary circulation/Ventilation
• PAP rarely exceeds 30 mm Hg at peak exercise in
normal individuals
• This is done by PVR by passive dilation and due to
NO effect
• Minute ventilation (VE) rises due increase RR
• TV increase in hyperbolic relation with exercise
• Training decreases VE for any given VO2
CO2 and O2
• Blood flow is directed more to the lung apices which are
more ventilated
• Improved distribution of blood flow increases diffusing
surface area
• More CO2 is produced but CO2 elimination becomes much
more efficient (high TV and VE)
• PAO2 = PiO2 – (PACO2/RER)
• Net effect: PaO2 remains near resting value, PvO2
decreases and PaCO2 decreases (compensated metabolic
• Intense exercise
CO & 3 xs VO2
15 xs O2 uptake, by 10 xs VE, 5 xs
• Microvascular adaptation to increase O2 delivery to the
• Link bet. cardiopulmonary adaptation & changes in
muscle metabolism not well understood
• Max CO is what limits aerobic exercise capacity
• Training enhances every step from lung to mitochondria
Observational studies
Study of 5,159 men aged 40-49 yrs followed for 19 yrs showed less CHD in
people who perform any physical activity vs inactive
Additional years gained after adoption of certain lifestyle change in 10,269
Harvard alumni from 1977 to 1985
• Moderately vigorous exercise was associated with 23 %
decrease in mortality than less exercise
Effect of physical activity level on life expectancy at age 50
• Framingham Heart Study
Reduces the risk of dying prematurely
Reduces the risk of dying from heart disease
Reduces the risk of stroke
Reduces the risk of developing diabetes
Reduces the risk of developing high blood pressure
Helps reduce blood pressure in people who already have high blood pressure
Reduces the risk of colon, prostate and breast cancer
Reduces feelings of depression and anxiety/Delays Alzheimer’s disease
Helps control weight
Helps build and maintain healthy bones, muscles and joints
Helps older adults become stronger and better able to move about without falling
Promotes psychological well-being and helps with smoking cessation
Decreases healthcare costs (estimated at $4,950/life saved in US)
Benefits of regular physical activity
Antiatherogenic effects
Reduction of adiposity, particularly in those with excess upper body and abdominal fat
Reduction of elevated blood pressure
Reduction of elevated plasma TG (and associated small dense LDL particles)
Increase in HDL cholesterol levels
Important in insulin sensitivity and glucose use and reduction in risk of type 2 diabetes
Antithrombotic effects
Endothelial function alteration
Autonomic functional changes
Anti-ischemic effects (promotes atheroprotective and decreases atherogenic cytokines)
Antiarrhythmic effect
Biologic mechanisms for benefit of exercise
Risks in normal individuals
• Musculoskeletal injury is the most common
⁻ Acute strains, tears, inflammation, chronic strain,
stress fractures, traumatic fractures, nerve palsies,
tendonitis and bursitis
• Secondary to overuse and can be preventable
• More serious but less common include:
⁻ Arrhythmias, SCD, MI, LVH, rhabdomyolysis,
bronchoconstriction and heat-related problems.
• More common in who do not exercise regularly &
suddenly decide to do heavy exercise
How much exercise?
• 1 MET = 3.5 mL O2/kg/min consumption (seated adult)
• Based on physical fitness BP reduction, HDL elevation, O2
consumption and weight reduction data; CDC, AHA and
Surgeon General recommend 30-60 min moderate intensity
exercise (3-6 METs) 4-6 xs/wk
• Pts. should move gradually from sedentary life style to
moderate intensity exercise
• Brisk walking, active yard work, dancing, bicycling, jogging
and other leisure sports work
• Indicators of adequate exercise include
breathlessness, fatigue and sweating
• Strength-developing exercise 2-3 xs a wk add to
benefits of endurance-type activities
• Importance of warm up is controversial
• Cool-down for 5 min after exercise is important
for lactic acid removal from muscles, slow return
from vasodilation and gradual return of blood to
other parts
Examples of moderate physical activity
• Moderate amount of physical activity uses roughly
150 Cal/day or 1000 Cal/wk
HF and exercise capacity
• Limitations of exercise capacity is one of the
main manifestations of HF
• Varies with severity of disease and correlates
with survival
• Ventilatory threshold (VT) or anaerobic
threshold: when VE increases
disproportionately to VO2 seen at 60-70%
• VT is a reflection of lactic acid production by muscles
• If a patient fatigues before reaching VT, it means that
the cause in noncardiac
• 6 min walk test has also been used (simple and
• Measures distance covered in 6 min on a flat surface
and correlates well with VO2max and outcome
(distinguish better bet. NYHA class 3 &4 than 1 & 2)
Cardiac dysfunction
• CO might be nl at rest but unable to increase
adequately with even mild exertion
• Decreased CO would lead to less perfusion of
muscles, early anaerobic metabolism, fatigue
and eventual wasting
• HF patients are not able to attain VO2max and
peak VO2 is used instead
Impaired hemodynamic response to exercise in CHF
• By definition HF is a high chatecholamine state which
will lead to down regulation of beta receptors and
• Starling mechanism is altered due to DHF and possible
pericardial constraint with inability to increase SV
• With exercise PCWP is significantly increased which
causes more lung congestion
• With time PAP will rise and will contribute to decrease
in CO
• Mitral regurgitation complicates the picture
Skeletal muscle dysfunction
• Acute and chronic (more important)
• Apoptosis is seen in SM of HF pts. correlating
with exercise limitation and muscle wasting
• Capillary density is decreased in HF which
means less oxidative capacity
• Oxidative stress in the muscles with production of
ROS has been implicated in pathophysiology of
• Muscle fiber type changes to more fatigable
• Intrinsic SM metabolic defects (lower PH, less PCr,
reduced mitochondrial size and function)
• leading to less efficient use of energy and rapid
accumulation of lactic acid
Functional abnormalities
• SM ergo and metaboreceptors are enhanced in
HF resulting in increased ventilation and
sensation of dyspnea with exercise
• Increased sympathetic tone with decreased
effective renal perfusion (more Na and H2O)
• Inducible NO synthase increases with decrease in
CK needed in energy transfer from mit. to cytosol
Left ventricular
Increased vascular
Catabolic factors
Insulin resistance
Muscle fatigue
Muscle wasting
aerobic capacity
muscle changes
Skeletal muscle dysfunction in HF
Pulmonary dysfunction
• Respiratory muscle dysfunction is part of
general myopathy in HF (fatigue and dyspnea)
• Diaphragm on the contrary shows increase in
slow high endurance fibers (increased work)
• Impaired pulmonary diffusion with increase in
VE due to ventilation/ perfusion mismatch
severity of which is related to degree of HF
Peak VO2 and prognosis
• Most objective of functional capacity in HF
• Important predictor for transplant
• Peak VO2 ≤10-12 & no malignancy/advanced
lung ds were accepted for transplant
• Survival varied with peak VO2
Peak VO2 and survival
• Data was published before era of B-blockers
• PVD, muscular deconditioning, arthritis,
angina pectoris and low motivation can
terminate the test prematurly
• Peak VO2 less useful in women than men but
prognosis is better; a better variable would be
% predicted VO2 for age and wt.
Additional predictors
• The value of peak VO2 can be enhanced by:
1. 3 yr survival of pts with VO2< 14 unable to
reach a SBP of 120mm Hg was 55% vs 83%
2. Ability to have a CO (by invasive techniques)
adequate with exercise had better prognosis
Peak VO2 + BP predict outcome in CHF
3. VT or AT < 11 mL/Kg/min in a study was more
predictive of 6 mo mortality than VO2
4. Another non invasive test is dobutamine stress
echocardiography, with increase in LVED diam. and
wall stress indicating higher mortality
5. VE/VCO2 slope (>34 bad) is easier to obtain and
better predictor than VO2max, NYHA class and LVEF
6. Another parameter is O2 uptake efficiency slope
(OUES) derived from VO2 and VE
7. Peak stroke work index (> 30gm/m2 good) by SwanGanz is most predictive of prognosis
Ventilatory response to exercise predicts survival
Stroke work index and survival
• 2009 ACC/AHA class 1 recommendation to the
use of exercise testing and ventilation gas
analysis before transplantation
• Peak VO2 should be interpreted in the context
of age, lifestyle, goals and current treatment
Rehabilitation in HF
• Old recommendation was to decrease activity
in HF (1970s)
• Now well known that inactivity increases
symptoms of HF
• Exercise training HF patients improves
symptoms, exercise tolerance, quality of life
and may impact outcome
Plot of individual values of anaerobic threshold pre and post-training
• No relationship bet. LVEF and peak exercise
• Treatment with Inotropes, and vasodilators
such as ACEI, nitrates and hydralazine did not
acutely improve exercise tolerance
• There must be other reasons than just cardiac
Peak VO2 (mL/Kg/min
Ejection fraction
Ejection fraction vs peak VO2 in HF
SM theory of HF
• Inactivity leads to muscle atrophy
• In HF high energy phosphates are used
• Lactic acid accumulates more rapidly contributing
to fatigue and limited exercise capacity
• Respiratory muscles are involved which adds to
LV dysfunction
Increased afterload
Reduced peripheral
blood flow
TNF, insulin resistance,
malnutrition, inactivity
Catabolic state
Skeletal and respiratory
ergoreceptor activity
Increased ventilation
Skeletal muscle hypothesis of HF
Muscle fatigue
Effect of exercise in HF
• No benefit at all in acute setting
• In compensated HF it has the following
1. Improves diastolic function with increase in
peak early diastolic filling rate both at rest
and during exercise which enhances peak
VO2 and CO
2. Improves SM energetics allowing pts. To
perform same work at lower HR, rate-pressure
product and VE
3. Symptomatic improvement in dyspnea and
4. Reduces sympathetic tone and increases vagal
tone at rest with resultant decrease in SVR and
improved CO
5. Reduces resting levels of angiotensin,
aldosterone, ADH and BNP
6. Improves endothelial function with more NO
production and AC mediated vasodilation
7. Reduction of TNFa, IL6 and their receptors is
addition to apoptotic mediators (Fas and FasL)
• Nothing predicts outcome of exercise training
in HF pts. except in pts. with hibernating
cardiomyopathy who always benefit
Organ system/Tissue
Response to exercise training
Improve central
transport and regional
blood flow
in cardiac output; in peak VO2;
reverse chronotropic
incompetence; regional blood
Autonomic nervous
HRV; plasma NE (rest)
Effect on mortality and morbidity
Peak VO2
plasma NE
Skeletal muscle
Peripheral vasculature
aerobic enzymes; mitochondria
size/density; capillary density;
relative type 1 fibers
vascular reactivity
Change in muscle composition
Coronary blood flow
Ischemia and MI
Potential mechanism of how exercise training improves survival
Effect on hemodynamics
• In a meta-analysis of RCTs of exercise in HF
aerobic training was associated with sig.
improvement in LVEF, EDV and ESV
• May be due to decreased SVR
• Also BNP is reduced meaning improved
• Type of exercise training may be imp (interval vs
Effect on functional capacity
• Different studies have shown sig improvement in
exercise time, peak VO2 and NYHA class after 1-6 mo
of exercise training
• This means that pts. can participate in their daily
activities more easily and comfortably
• In a review aerobic plus strength training was not more
effective in terms of VO2max
• Some evidence that strength training might actually
obliterate benefits gained by aerobic exercise
• High intensity interval aerobic exercise up to 95%
peak HR was associated with better outcome
concerning remodeling and improvement in
VO2max than moderate continuous exercise
training up to 70% peak HR
• Since HF pts. rarely exert themselves to maximal
capacity, a more important result was reported in a
study which showed a 25% increase in VT and 52%
increase in submaximal exercise time after 4-6
months 3-5 hrs/wk training (walking, biking &
Other benefits reported
• Sig. increase in 6 min walk distance (mean of
41 m in 2003 Cochrane review)
• 16-52% reduction of resting catecholamines
indicating better hemodynamics
demonstrated also by better heart rate
variability and lower resting HR
Effect on outcome
• Meta-analysis of 9 RCT (801 pts.)
• Supervised exercise for at least 8wks to at
least 60% peak HR or 50% peak VO2
• Average 2 yr F/U showed sig. reduced
mortality (22 vs 26%) and combined end
points of death or hospitalization (32 vs 43%)
• Most previous studies are small and single center
• Meta-analyses are retrospective & prone to error
• Negative trials are less likely to be published
• Necessitated RCT: HF ACTION study which enrolled
2,331 pts. in the US and Canada to see if exercise
training will reduce mortality and hospitalization in
NYHA 2-4 HF pts (95% NYHA 2-3)
• Modest but significant improvement in all-cause
mortality and hospitalizations
• Assessed over 14 mo training period in pts with
stable HF
• 1.82 yrs/person increase in life expectancy over
15.5 yrs
• Cost of $1,773/ life-yr saved
• HF ACTION compared hospitalization costs vs cost
of exercise training
• Medical costs were lower with exercise training
• ACC/AHA 2009 update of 2005 Class 1
recommendation to cardiac rehabilitation in
NYHA 2&3 with no advanced arrhythmias and
other limitations
• Benefits are seen in high or low levels of
training and as early as 3 wks
• Not enough data to recommend it for NYHA 4
QI project

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