effect of aging on cardio-pulmonary system
DESCRIPTION
The PPT presents in brief the importance and effect of age on cardio-pulmonary systemTRANSCRIPT
Effect of aging in CARDIO-PULMONARY
SYSTEMKrishna priya
?
PHYSIOTHERAPY - AGING
Physiological changes Exercise prescription Exercise response Factors affecting aging – biological and
psychological factors, disuse, disease etc…….
SAFETY OF THE CLIENT DURING REHABILITATION
ANATOMICAL - Increase in heart weight Decrease in myocardial cells and
enlargement of remaining cells
Cardio-vascular system
Increased left ventricular thickness Increase in left atrial size Reduced elastin and increased collagen in
the intimal layer of the heart and blood vessel walls and calcification stiffness
Decreased aortic distensibility
Stiffness increase in systolic blood pressure
Decreased distensibility increased load on LV
AT RESTDiastolic propertiesEDV in cardiac cycle - Sufficient venous return Relaxation of ventricles Duration of atrial contraction Inspite of the stiffness if the walls, LA increase
in size maintains EDV
Relation between anatomical and physiological changes
Increase in iso-volumic myocardial relaxation Decrease in ventricular filling rate in early
diastole Over all increased diastole of
ventricles DURING ACTIVITY OR MINIMAL EXERCISE EDV index increases Ventricular filling rate decreases due to
prolonged relaxation time and ventricular stiffness
AT RESTSystolic properties End systolic volume Stroke volume same Ejection fractionDURING ACTIVITY OR MINIMAL EXERCISE End systolic volume Ejection fraction Myo-cardial contractility
Causes – Decreased response to B-adrenergics Systolic BP Ventricular wall changesAEROBIC CAPACITY VO2 max As age VO2 max 0.4-0.5 ml/kg/min/yr – male 0.2-0.35 ml/kg/min/yr – female 10% per decade
VO2 max inversely proportional to body weight and physical inactivity
Causes – Maximum HR CO and SV A-V O2 difference OTHER CHANGES Reduced baro receptor and cardio pulmonary
reflexes Reduced A-V dilatation Postural hypotension
Diastole – Left ventricular wall thickness Left ventricular filling rate End diastolic volume Systole – Myocardial contractility End diastolic volume Ejection fraction
Effect of aging
Arterial wall thickness Systolic blood pressure Diastolic blood pressure Orthostatic tolerance Arterial and venous dilation Vasoconstriction
same
Cause peripheral effects not central HR max cannot be changed so SV, CO, VO2
max cannot be altered significantly Extraction of O2 by peripheral skeletal
musculature A-V O2 difference
VO2 max increases
EDV at rest and exercise Peak rate of ventricular filling
Effect of exercise training on CVS
6 months – avg- 30 min, 3 times/week, 4-6 months – increased VO2 max by 14%
Active / sedentary – VO2 max reduces (5%) (10%)Poor improvements in Less initial VO2 max Increased age Short sessions of exercises Short over all duration of the study period
Study –60-82 yrs, intensive endurance training,
Increase in EDV and peak ventricular filling rates
Causes Increased uptake of Ca Reduced relaxation time Increased fatty acid oxidation and
cytochrome C oxidase levels
Systolic performance Increased exercise stroke volume, Increased ejection fraction, on
exercise End systolic volume decrease
Very old age, estrogen deficient women – no changes on exercise training
Improvement in postural hypotension – blood flow to peripherally active muscles from inactive limbs and viscera
Reduce systolic and diastolic BP Reduce age related baro-reflex sensitivity Alters ANS and its control on resting HR Increase para-sympathetic activity and
attenuates sympathetic activity
Long term aerobic training - Decrease symp + at given work rate Decrease exe HR Decrease BP
Diastole – on exercise Left ventricular wall thickness
Left ventricular filling rate End diastolic volume Systole – Myocardial contractility End diastolic volume Ejection fraction
Effect of exercise training
Arterial wall thickness ? Systolic blood pressure Diastolic blood pressure / Orthostatic tolerance ? Arterial and venous dilation ? Vasoconstriction Central venous pressure
?
PULMONARY SYSTEM
Anatomical changes – (thoracic cage, lungs, diaphragm) decreased – Calcification of costal cartilage with sternum Degenerative changes in thoracic spine and rib
articulations Kyphosis Reduced intervertebral spaces, Wedge shaped Increases AP diameter
Resp muscles in mechanically disadvantageous position
Decreased force generation
Loss of elastic fibres in alveolar ducts Loss and destruction of supporting structures
of lung parenchyma Pre-mature closure of airways
Hyper-inflation Elastic recoil chest wall compliance Progressive decrease in respiratory muscle
strength (mild)
Compliance – lung and chest wall Decrease in chest wall complian-ce is more than lung compliance
Decrease in Alveolar – capillary surface area Alveolar surface area Total surface area of lung parenchyma Pulmonary blood flow volume
Reduced diffusion Increased dead space ventilation V/Q mis-match
Reduced elastic recoil – reduced exp flow + narrowing of airways
Reduced FEV1 Reduced closing volumes, increased FRC and
RV
Reduced FVC and flow rates Increased FRC TV decreases
Minute ventilation –RR*vol of air inhaled in 1 breath
Increase in RR, inspite of TV inspiration Diaphragm – change in muscle type –
reduced type 1 muscle fibres
Easy fatigue during increased load on RSIncreased WOB
Immunological changes – BAL – broncho alveolar lavage Increased neutrophils; IgA, IgM, Reduced macrophages Antigens toxin production
Increased T lymphocytesIncreased neutrophilsRelease of super-oxide
Persistent low grade inflammation
Damage to lung matrix
Impaired gaseous exchange ELF- epithelial lining fluid – rich in anti-
oxidantsAging – reduced ELF
Increased susceptibility to env toxins
25-35/40 yrs (plateau)
Growth and maturation declines
0-20 yrs
Pulmonary changes also depend on -nutrition / dietlife style – sedentary/active, smokinginfections, environmentimmune system
Chest wall stiffness Elastic recoil Alveolar capillary surface area Forced expiratory flow Total residual volume Forced vital capacity P I max and P E max V/Q matching Pa O2 Oxygen saturation Pulmonary vascular resistance
Effect of aging
Expiratory flow limitation Minute ventilation Work of breathing Resp muscle O2 consumption Pulmonary artery pressure
DURING ACTIVITY OR MINIMAL EXERCISE Expiratory flow limitation due to narrow air
ways Increase in minute volume, minimal increase
in TV, more in RR, shortness of breath Increased WOB to meet O2 demands via
alveolar ventilation, diffusion Exe – stiff alveolar walls – reduced elastic
recoil- increase pressure development by insp and exp muscles – increased WOB – increased O2 consumption by resp muscles (10-12% of total body O2 consumption)
Sub-maximal exe – aerobic training – MV Walking, 70 yr, 12 week sub-maximal aerobic
exe, 7.7% in MV Reduced breathlessness Low exertion Use of low % of max ventilatory capacity
during exercise (reduced WOB)
Effect of exercise training
Maximal exercise – 5 days/ week, 78% HR max Same case 14% in max MV Improved MV in terms of TV not RR
aging on exercise
Expiratory flow limitation Minute ventilation
S M Work of breathing Resp muscle O2 consumption Arterial hypoxemia Pulmonary artery pressure Pulmonary wedge pressure
Effect of exercise training
Thank You