Geriatrics Flashcards
(92 cards)
“Older adults” or “elderly” = ____.
persons 65 years or older
Aging is not synonymous with ____.
poor physiologic function.
Chronological age versus biological
Chronologic age (age in years since birth), is often used in clinical practice.
Biologic age also known as functional status
Chronologic age alone is no longer a reliable indicator of morbidity or of mortality.
MAP and PP calculations
MAP = SBP + 2 X DBP divided by 3
PP=SBP-DBP
The cardiovascular system is less _____ with advancing age.
Less Compliant CV system (heart/vessels/autonomic nervous system) less compliant- widen pulse pressure (higher sbp,lower dbp)
The decreased cardiac compliance increases ___ which ___.
Increases SBP which increases afterload—->LVH—->prolong LV ejection times—>late diastolic filling—>diastolic dysfunction.
The less compliant cardiovascular system results in increased dependence on ____.
atrial contraction “atrial kick” for optimal filling
Age related changes to autonomic nervous system
decrease responsiveness to adrenergic receptor stimuliation which decreases HR variability to respond to hypotension, hypovolemia, hypoxemia.
Age related changes to the conduction system
1.Calcification w/ fewer SA nodal cells
- predisposes the elderly to atrial fibrillation, sick sinus syndrome, first- and second-degree heart blocks, and arrhythmias.
- PPM/ICDs
- Calcification also w/ heart valves (primarily aortic and mitral).
* valvular stenosis or regurgitation. - Baroreceptors (aortic arch, carotid sinuses) are less sensitive in response to BP change which causes increased episodes of hypotension
Myocardium changes
less sensitive to b-adrenergic modulation results in lower HR, lower cardiac dilation at the end of diastole and systole).
Decreased CO & SV is related to _____.
decreased conduction velocity and reduction in venous blood flow.
What is the most common cardiac complication and the leading cause of death post op?
MI
Most common CV diseases in older adults
HTN, HLD, CAD, CHF
Mechanism and consequences of myocardial hypertrophy
Mechanism: Apoptotic cells are not replaced and there is compensatory hypertrophy of existing cells; reflected waves during late systole creates strain on myocardium leading to hypertrophy
Consequences: Increased ventricular stiffness, prolonged contraction and delayed relaxation
Anesthetic implications of myocardial hypertrophy
Failure to maintain preload leads to an exaggerated decrease in CO; excessive volume more easily increases filling pressures to congestive failure levels; dependence on sinus rhythm and low/normal HR
Mechanism and Consequences of myocardial stiffening
Mechanism: Increased interstitial fibrosis; amyloid deposition
Consequences: Ventricular filling dependent upon atrial pressure
Mechanism and Consequences of Reduced LV relaxation
Mechanism: Impaired calcium homeostasis; reduced B-receptor responsiveness; early reflected wave
Consequeces: Diastolic dysfunction
Mechanism and Consequences of Reduced beta receptor responsiveness
Mechanism: Diminished coupling of beta receptor to intracellular adenylate cyclase activity; decreased density of beta receptors
Consequence: Increased circulating catecholamines; limited increase in HR and contractility in response to endogenous and exogenous catecholamines; impaired baroreflex control of BP
Anesthetic implications of reduced beta receptor responsiveness
Hypotension from anesthetic blunting of sympathetic tone; altered reactivity to vasoactive drugs; increased dependence on Frank-Starling mechanism to maintain CO; labile BP, more hypotension
Mechanism & Consequences of Conduction system abnormalities
Mechanism: Apoptosis; fibrosis; fatty infiltration; and calcification of pacemaker and His-Bundle cells
Consequences: Conduction block; sick sinus syndrome; AF; decreased contribution of atrial contraction to diastolic volume
Anesthetic Implication of Conduction System Abnormalities
Severe bradycardia with potent opioids; decreased CO from decrease in end-diastolic volume
Mechanism and Consequence of stiff arteries
Mechanism: Loss of elastin, increased collagen, glycosylation cross-linking of collagen
Consequences:
1) Systolic hypertension
2) Arrival of reflected pressure wave during end-ejection leads to myocardial hypertrophy and impaired disatolic relaxation
Mechanism & Consequences of Stiff Veins
Mechanism: Loss of elastin; increased collagen; glycosylation cross-linking of collagen
Consequence: Decreased buffering of changes in blood volume impairs ability to maintain atrial pressure
Anesthetic implications for stiff arteries
Labile BP; diatolic dysfunction; sensitive to volume status
