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Cardiovascular and Pulmonary Changes in the Geriatric Patient

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Title: Cardiovascular and Pulmonary Changes in the Geriatric Patient


1
Cardiovascular and Pulmonary Changes in the
Geriatric Patient
  • Tim Sauvage, MS, CRNA, ARNP

2
Cardiovascular
  • Increase in afterload
  • Buildup of plaque ? radius
  • Left ventricle works harder to empty
  • Takes more time to empty the left ventricle
  • Decrease in arterial compliance and increased
    impedance to left ventricular output

3
  • Increases circulation time
  • It takes longer for the blood to circulate
  • Onset of intravenous medication is delayed
  • Decrease/reduced myocardial pump function,
    reduced cardial output

4
  • All increase in the elderly
  • Conduction fibrosis
  • Incidence of dysrhythmia
  • SA node cell loss
  • Conduction system fibrosis and loss of SA nodal
    cells will increase the incidence of
    dysrthythmias
  • SA nodal cells do not replicate as when they were
    young
  • Vagal tone a decrease sensitivity of
    adrenergetic receptors leads to decreases in
    heart rate.

5
  • Increase in left ventricular wall tension
  • Due to the chronic increase in afterload in the
    elderly
  • Remember the left ventricle will pump against
    the afterload
  • Walls stay tense longer
  • Stiff
  • balloon

6
  • Increase in systolic blood pressure
  • Usually seen with increased arterial pulse
    pressure caused by gradual increases in large
    artery stiffness
  • Arteries are less compliant more like PVC pipe
  • As the SV leaves the L.V., it does so as one
    volume and the energy is absorbed into the
    arterial wall by dilation.

7
  • Increase in cardiac workload
  • A reduction in arterial compliance results in
    increases in afterload, systolic pressure, and
    left ventricular hypertrophy
  • Stiff vessels will increase after L hypertrophy
    stretch of muscle fibers

8
  • Increase in peripheral vascular resistance
  • The reduction in arterial compliance caused by
    fibrosis of the tunica media layer of the vessel.

9
  • Decrease in cardiac reserve
  • Manifested as exaggerated drops in blood pressure

10
  • Decrease in resting heart rate
  • Due to an increase in vagal tone and normal aging
    loss of one beat per minute for each year over 50
    years.
  • Can the elderly compensate for decreases in BP
  • Decrease in heart rate?
  • What about Beta blockers?

11
  • Decrease in stroke volume
  • A decreased myocardial pump function leads to
    decreased stroke volume and decreased cardial
    output.
  • Ask about BP, HR, and volume

12
  • Decrease in left ventricular compliance
  • Based on stiffer myocardial fibers and
    replacement of these fibers with non-muscle
    connective tissue.
  • Stiff, not as flexible
  • Not as good a pump
  • Stiff seal in H2O pump

13
  • Decrease in barorecpetor function
  • Due to decreased sensitivity of stretch receptors

14
  • Decrease perfusion to vital organs
  • Organs with a major blood supply, atrophy as you
    age and this results in less blood pumped to
    them.
  • There is a general loss of tissue mass in many
    organs

15
  • Decrease in maximum cardiac output
  • Due to increase in afterload (pressure)

16
  • Decrease in arterial compliance
  • Based on stiffening of the walls of the vessel
  • Less expandable
  • Like PVC pipe

17
Geriatric Ventilation
  • As we have completed the cardiac section, lets
    look at aspects of the cardiac that may follow
    through to respiratory.
  • The area I see is the carotid bodies decreased
    sensitivity and the conduction fibrosis.
  • The replication of receptor (sensory, chemo,
    pressure, stretch) are not nearly as functional
    or selectively sensitive as they were years ago.

18
Peripheral Chemo Receptors
  • Are found in the carotid bodies and the aortic
    bodies
  • They respond to decreased PaO2 (lt 60 mmHg) most
    responsive
  • Increased hydrogen ion concentration (decreased
    arterial blood pH)
  • Increased PaCO2

19
Changes in the PAO2-PaO2 gradient with age
  • PAO2 PaO2 0.21 x (age 2.5)
  • Normal PAO2 PaO2 gradient
  • gt 5-15 mmHg (breathing room air)
  • Based on the above formula
  • 20 yr old 4.4
  • 30 yr old 6.5
  • 40 yr old 8.5
  • 50 yr old 10.5
  • 60 yr old 12.5
  • 70 yr old 14.5
  • 80 yr old 16.5
  • ? These numbers tell us that as we get older, our
    PAO2 PaO2 gradient gets larger numerically and
    falls out of range when you reach 80 years old.

20
Spirometry Normal
21
Flow Volume Loops
  • Normal

22
  • Flow-volume loops associated with restrictive and
    obstructive disease
  • With restrictive lung disease, the flow-volume
    loop still looks like an upside-down baby ice
    cream cone however, lung volumes are smaller
    remember that the lungs are restricted-smaller
    volumes. With obstructive lung disease, one side
    of the upside down ice cream cone appears caved
    in (the loop looks like a baby carriage without
    wheels) also, lung volumes are greater

23
Closing Volume
  • As airways begin to close, the volume that can be
    exhaled is the closing volume

24
Closing Capacity
  • This is the closing volume plus the residual
    volume

25
  • Point
  • As you age (60yrs), there is a constant change
    taking place. The closing volume of the older
    patient increased from the younger person. It
    increased enough to be part of the tidal volume.
  • Residual volume increased in the older person
  • Closing capacity increased in the older person
  • CC CV RV each increased

26
OR.
27
Respiratory
  • Increased risk of pulmonary complications
  • Aspiration pneumonia is common and life
    threatening due to a decrease in protective
    laryngeal reflexes with age
  • Also, the decreased ability to cough adds to
    increased pulmonary complications

28
  • Increased risk of aspiration
  • Due to vocal cord stimulation being elevated,
    thus putting the patient at risk for aspiration

29
  • Increased incidence of airway obstruction
  • Decreased sensitivity of the need to clear
    secretions, food, etc.
  • The decrease in laryngeal reflexes compunds the
    problem

30
  • Increase work of breathing
  • Skeletal calcification and increased airway
    resistance increase the work of breathing.
  • Predisposed to acute postoperative ventilatory
    failure

31
  • Increased potential for hypoxia
  • Decreased elasticity of lung tissue which reduces
    alveolar surface area and decrease the efficieny
    of gas exchange
  • Airway collapse and a decrease in normal oxygen
    tension
  • V/Q mismatch, increase in pre-oxygenation time

32
  • Increase in alveolar compliance
  • Absorption of connective tissue
  • Loss of protective netting to limit the expansion
    of alveoli

33
  • Increase in FRC
  • Failure to hold alveoli open (lungs)

34
  • Increased closing capacity
  • Caused by airway collapse and the distribution of
    tidal volumes to areas of the lung that are less
    perfused

35
  • Tissue elasticity decreases
  • Some muscle is replaced with adipose tissue and
    less elastic components

36
  • Alveolar surface area decreases
  • Alveolar wall tissue decreases
  • Loss of recoil
  • Less airway patency

37
  • Chest wall compliance decreases
  • Cartilage and connective tissue become stiffer
  • Increased stiffness of thoracic cage
  • Restricted chest expansion

38
  • Response to hypoxia decreases
  • Sensitivity of receptors is less

39
  • Cervical spine mobility decreases
  • Chest wall non-compliant
  • Arthritis
  • Decrease in muscle stretch and elasticity

40
  • Lung recoil decreases
  • Chest wall rigidity

41
  • Ability to meet heavy loads decreases

42
  • Ability to cough decreases
  • Decreased muscle strength
  • Takes more stimulation to cough

43
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