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Medical Rehabilitation in cardiac patients with HF Salim Thabet PGY3 Moderator: Dr. Mahazarin Ginwalla.

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Presentation on theme: "Medical Rehabilitation in cardiac patients with HF Salim Thabet PGY3 Moderator: Dr. Mahazarin Ginwalla."— Presentation transcript:

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

2 Case JD is a 60 y.o male pt. known with 1.HFrEF 35-40% due to ICM 2.CAD s/p MIx2 with PCI 3.HTN/DLD 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

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

5 Outline I.Exercise and the body A.Exercise physiology B.Benefits of exercise C.Risks of exercise II.Heart failure and the body A.Exercise capacity in HF B.Skeletal muscle dysfunction III.Rehabilitation in HF A.Safety B.Effect of exercise in HF 1.Readmission 2.Morbidity/Mortality 3.Psychosocial/Economic IV.Conclusion and recommendations V.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: 1.Oxygen uptake (VO2) 2.CO2 output 3.Tidal volume 4.Minute ventilation (VE) 5.ECG 6.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 1.Med Sci Sports Exerc 1997; 29:591 2.Am J Noninvas Cardiol 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 Respir Dis 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 Maximal exercise (% total)Rest (% total) 124Splanchnic 8821Skeletal muscle 119Kidneys 313Brain 28Skin 43Heart 110Other organs

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 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 Observational studies

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 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)

26 Biologic mechanisms for benefit of exercise 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

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 Ventilatory threshold (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 Skeletal muscle dysfunction in HF Left ventricular dysfunction Decreased perfusion Decreased activity Catabolic factors Insulin resistance Increased vascular resistance Sympathetic activation Baroreflex downregulation Ergoreflex activation Increased VE/VCO2 Breathlessness Respiratory muscle changes Fatigue Muscle fatigue Muscle wasting Decreased aerobic capacity

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: 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

45 Peak VO2 + BP predict outcome in CHF

46 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 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

51 Plot of individual values of anaerobic threshold pre and post-training

52 No relationship bet. LVEF and peak exercise performance 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 dysfunction

53 Ejection fraction vs peak VO2 in HF Ejection fraction Peak VO2 (mL/Kg/min

54 SM theory of HF Inactivity leads to muscle atrophy In HF high energy phosphates are used inefficiently Lactic acid accumulates more rapidly contributing to fatigue and limited exercise capacity Respiratory muscles are involved which adds to dyspnea

55 Skeletal muscle hypothesis of HF LV dysfunction Reduced peripheral blood flow Increased ergoreceptor activity Increased ventilation Dyspnea Skeletal and respiratory Catabolic state TNF, insulin resistance, malnutrition, inactivity Muscle fatigue Sympatho-excitation Vagal-withdrawal Vasoconstriction Increased afterload

56 Effect of exercise in HF No benefit at all in acute setting In compensated HF it has the following benefits: 1.Improves diastolic function with increase in peak early diastolic filling rate both at rest and during exercise which enhances peak VO2 and CO

57 2.Improves SM energetics allowing pts. To perform same work at lower HR, rate-pressure product and VE 3.Symptomatic improvement in dyspnea and fatigue 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

58 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

59 Effect on mortality and morbidityResponse to exercise trainingOrgan system/Tissue Peak VO2 survival hospitalization in cardiac output; in peak VO2; reverse chronotropic incompetence; regional blood flow Improve central transport and regional blood flow HRV arrhythmia survival hospitaliz. plasma NE survival HRV; plasma NE (rest)Autonomic nervous system Change in muscle composition QOL hospitalization aerobic enzymes; mitochondria size/density; capillary density; relative type 1 fibers Skeletal muscle Coronary blood flow survival Ischemia and MI hospitaliz. vascular reactivityPeripheral vasculature Potential mechanism of how exercise training improves survival

60 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 hemodynamics Type of exercise training may be imp (interval vs continuous)

61 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

62 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 & jogging)

63 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

64 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%)

65 HF ACTION study 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

66 Cost-effectiveness 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

67 Recommendations 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

68 QI project

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