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Medical Rehabilitation in cardiac patients with HF

Medical Rehabilitation in cardiac patients with HF. Salim Thabet PGY3 Moderator: Dr. Mahazarin Ginwalla. Case. JD is a 60 y.o male pt. known with HFrEF 35-40% due to ICM CAD s/p MIx2 with PCI HTN/DLD Smoker 30PY Dietary non-compliance

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Medical Rehabilitation in cardiac patients with HF

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  1. Medical Rehabilitation in cardiac patients with HF Salim Thabet PGY3 Moderator: Dr. MahazarinGinwalla

  2. Case • JD is a 60 y.o male pt. known with • HFrEF 35-40% due to ICM • CAD s/p MIx2 with PCI • HTN/DLD • Smoker 30PY • 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

  3. PE: VS: 120/70 100 SR 25 afebrile JVD to mandible S4 heard, no murmurs Crackles +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 40mg

  4. 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 150mg and Imdur 60 mg • Heart failure care path and PCP/Cardiology f/u • He is readmitted 2 months later with same symptoms

  5. Outline • Exercise and the body • Exercise physiology • Benefits of exercise • Risks of exercise • Heart failure and the body • Exercise capacity in HF • Skeletal muscle dysfunction • Rehabilitation in HF • Safety • Effect of exercise in HF • Readmission • Morbidity/Mortality • Psychosocial/Economic • Conclusion and recommendations • QI project (HF readmission)

  6. 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

  7. 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

  8. Physiologic data include: • Oxygen uptake (VO2) • CO2 output • Tidal volume • Minute ventilation (VE) • ECG • Pulse oximetry • In certain situations more extensive monitoring (arterial or pulmonary artery catheterization)

  9. VO2max: symptom-limited max O2 uptake during incremental bilateral leg exercise • Used to provide overall assessment of exercise capacity • 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 Med Sci Sports Exerc 1997; 29:591 Am J NoninvasCardiol 1987; 1:244

  10. VO2 increases linearly with work (slope=10ml/min) • 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 weight Am Rev RespirDis 1984; 129:S49

  11. Normal VO2 vs. Workload VO2maxx

  12. Fatigue • 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 VO2max • At VO2 just below LT exercise can be sustained for long periods (steady state) ex: UFC fighters Muscle Nerve 1989; 12:660

  13. Normal lactate vs VO2 in exercise

  14. Effect of exercise on skeletal muscles • Training capillary density and mitochondria • Training is associated with less ammonia and lactate with less fatigue at a set metabolic rate (VO2) • LT > 40% VO2max in nl. people, less in pts. with CVD and more in athletes Sports Sci Exchange 1995; 8:1

  15. Circulation • Fick equation: VO2 = CO x (CaO2 – CvO2) • 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 Heart Lungs Tissue metabolism

  16. 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

  17. Acidosis O2 extraction also by shifting oxyhemoglobin dissociation curve to the right

  18. Blood flow distribution with exercise

  19. 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

  20. 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 acidosis)

  21. Summary • Intense exercise 15 xs O2 uptake, by 10 xs VE, 5 xs CO & 3 xs VO2 • Microvascular adaptation to increase O2 delivery to the muscles • 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

  22. 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

  23. 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

  24. Effect of physical activity level on life expectancy at age 50 • Framingham Heart Study

  25. Benefits of regular physical activity

  26. Biologic mechanisms for benefit of exercise

  27. 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

  28. 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

  29. 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

  30. Examples of moderate physical activity • Moderate amount of physical activity uses roughly 150 Cal/day or 1000 Cal/wk

  31. 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 • Ventilatorythreshold (VT) or anaerobic threshold:when VE increases disproportionately to VO2 seen at 60-70% VO2max

  32. 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 inexpensive) • 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)

  33. 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

  34. Impaired hemodynamic response to exercise in CHF

  35. By definition HF is a high chatecholamine state which will lead to down regulation of beta receptors and desensitization • 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

  36. Skeletal muscle dysfunction • Acute and chronic (more important) hypoperfusion • 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

  37. Oxidative stress in the muscles with production of ROS has been implicated in pathophysiology of HF • 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

  38. 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

  39. Left ventricular dysfunction Skeletal muscle dysfunction in HF Increased vascular resistance Decreased perfusion Decreased activity Catabolic factors Insulin resistance Muscle fatigue Muscle wasting Decreased aerobic capacity Sympathetic activation Respiratory muscle changes Baroreflexdownregulation Ergoreflex activation Fatigue Breathlessness Increased VE/VCO2

  40. 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

  41. 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

  42. Peak VO2 and survival

  43. Limitations • 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.

  44. Additional predictors • The value of peak VO2 can be enhanced by: • 3 yr survival of pts with VO2< 14 unable to reach a SBP of 120mm Hg was 55% vs 83% • Ability to have a CO (by invasive techniques) adequate with exercise had better prognosis

  45. Peak VO2 + BP predict outcome in CHF

  46. VT or AT < 11 mL/Kg/min in a study was more predictive of 6 mo mortality than VO2 • Another non invasive test is dobutamine stress echocardiography, with increase in LVED diam. and wall stress indicating higher mortality • VE/VCO2 slope (>34 bad) is easier to obtain and better predictor than VO2max, NYHA class and LVEF • Another parameter is O2 uptake efficiency slope (OUES) derived from VO2 and VE • Peak stroke work index (> 30gm/m2 good) by Swan-Ganz is most predictive of prognosis

  47. Ventilatory response to exercise predicts survival

  48. Stroke work index and survival

  49. Recommendations • 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

  50. 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

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