Transcript Document

Impaired aerobic
capacity/endurance
Min H. Huang, PT, PhD, NCS
Learning Objectives
• Describe causes and factors contributing to
impaired aerobic capacity in older adults.
• Describes physical therapist patient
management to address decreased
endurance and its impact on function for a
geriatric client.
Reading assignments
• Guccione: Ch 12 (pp.229-233, Box 12-2,
Box 12-3 only)
Cardiovascular functional changes
with age
• Decreases
o
o
o
o
o
Cardiac Output: resting and maximal
Max HR
Resting and maximal stroke volume
Venous Return
Blood Flow
 25% increase in Left Ventricular thickness
 Vessel rigidity
 65 yo has 30-40% of aerobic capacity of young adult
• Increases
o Blood Pressure: both resting & exercise BP
o Cardiac Dysrhythmias
 By 75 yo, <10% of SA node cells
J. Blackwood
Age related changes in the heart
• Increase adipose tissue
• Increase collagen content
• Decrease muscle cells (myocytes)
• Increase cardiomyocyte senescence
• Decrease innervation/nerve conduction tissue
• Decrease sympathetic modulation of HR
 Results in decrease excitability, decrease
cardiac output, venous return and an
INCREASE in dysrhythmias.
Age-dependent changes to cardiovascular
tissues
North B J , and Sinclair D A Circulation Research 2012;110:1097-1108
Age related changes in the heart
• With the walls of the heart becoming less
compliant
o Declines in Left ventricle expansion and
contractility (i.e. reduced end diastole volume)
o Results in decreased ejection fraction (FrankStarling law)
• Increased atrial size correlates to Left
ventricular compliance
increased workload on the atria
hypertrophy of the aorta
Ventricular function curves showing
the Frank–Starling relationship
Hanft 2008.
http://cardiovascres.oxfordjournals.org/content/77/4/627.full.pdf+html
Cardiac hypertrophy
• A reduction in cardiac output due to aging
stimulates the myocardium to compensate by
increasing muscle mass
o short-term enhancement of cardiac output
o long-term impact on cardiac function
• Ventricular hypertrophy results from an
increase in size of individual cardiomyocytes
o physiological and reversible, e.g. exerciseinduced
o pathological and irreversible, i.e. disease-based
Valvular changes with aging
• Age related valvular circumference
o Mitral and Aortic valves have the most issues.
• Thickening and calcification of the cusps and
leaflets
o Lose water content.
• Results in valvular stenosis and mitral valve
insufficiency: heart murmurs
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Aging of the peripheral vasculature
• Arterial thickening and stiffness as well as
dysfunctional endothelium
 Increase systolic pressure, increased risks of
atherosclerosis, HTN, stroke, A-fib, ischemia
 Decrease in elasticity of vessel walls may result
in chronic rigidity or vessel wall diameter
• In venous system: valves become stiff and
incompetent
 Impaired return of blood, may play a role in
phlebitis and thrombus formation
Aging changes in cardiac conduction
• Declines in function and number of
pacemaker cells in SA node
o By age 70 only 10% of the number found in
young adults are present
• Proliferation of fibrous tissue in nerve
conduction system may affect SA function
• Incidence of Sick Sinus Syndrome (SSS)
increases with age
o Bradycardia, SA node arrest, SA exit
conduction block
Age related changes on ECG
• ~50% of older adults
have cardiac
conduction
abnormalities at rest.
• PR and QT intervals
have small increases
• ST segment becomes
flattened
• Amplitude of the T
wave diminishes
Oxygen consumption (V·O2)
• A physiological measure of how much
oxygen the body uses at rest or during
activity
• Increases in proportion to intensity of
exercise/physical activity and will plateau
when maximal ability for oxygen delivery is
reached, which is maximal oxygen
consumption (V·O2 max).
• Maximal oxygen consumption is directly
related to aerobic capacity
Oxygen consumption (V·O2)
Heart rate response to an aerobic
exercise bout and adaptation following
aerobic exercise training
Stroke volume response to an
aerobic exercise bout and adaptation
following aerobic exercise training
Cardiac output response to an
aerobic exercise bout and adaptation
following aerobic exercise training
Arteriovenous oxygen difference (a-vO2diff)
response to an aerobic exercise bout and
adaptation following aerobic exercise training.
Warning signs during PT
• SBP > 180 mmHg and/or DBP > 100 mmHg at rest
• HR >100 bpm at rest (consider HRmax or PRE > 13
with exercise )
• Excessive dyspnea
• Low angina threshold
• Claudication pain =DVT
• Lack of HR or BP response with activity or
excessive response with activity
• Drop of SBP >20mmHg or HR > 10 bpm with
exercise
• Slow recovery from activity (>3-5 min)
STOP PT session immediately
• Complaints of light-headedness, confusion,
dyspnea, or onset of angina
• Syncope or near syncope
• Nausea
• Unusual or severe fatigue
• Staggering or persistent unsteadiness
• Severe claudication or other pain
• Angina
• Abnormal HR or BP response to exercise
Aerobic and Strength training
• Aerobic training allows for improved CV
fitness, decrease in HTN, improves lipid
metabolism, prevents Left ventricular
hypertrophy
• Strength training allows for improvements in
overall strength, muscle mass and quality
J. Blackwood
Guidelines for exercise interventions
with cardiovascular
• Consider: intensity, mode, frequency,
duration, and progression
• Monitor: HR, BP, SaO2, ECG, BORG scale
(RPE), estimated VO2 max, MET levels.
• Be aware of the medication side effects
(orthostatic hypotension, blunted HR) that
can occur with this population
• Refer to ex physiology for reference; Also:
AHA, AACVPR, ACSM
J. Blackwood
Guidelines for exercise interventions
with cardiovascular
• Cardiac clients with L vent dysfunction or
cardiac induced ischemia do not have
improvements in max aerobic capacity, but
do with submax strengthening.
• Poor aerobic capacity: not able to sustain
adequate HR and BP with exercise.
• Make changes in an exercise program with
the geriatric client in response to the CV or
CP signs that occur.
J. Blackwood