effect of aging on cardio-pulmonary system

Effect of aging in CARDIO-PULMONARY

SYSTEMKrishna priya

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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

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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

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