In geriatric anesthesia, echocardiography is not merely a cardiac assessment—it is a systemic physiologic mirror that reflects the functional interdependence of the heart, brain, and vasculature.
In a 90-year-old woman with dementia scheduled for proximal femoral nailing (PFN) under general anesthesia, the preoperative echocardiogram appears deceptively “normal”:
LVEF ≈ 60 %
Grade I diastolic dysfunction (DD)
Mild aortic regurgitation (AR)
Trivial mitral and tricuspid regurgitation
Calcific aortic valve and mitral annular calcification (MAC)
IVC ≈ 19 mm with normal collapsibility
While these findings suggest preserved cardiac mechanics, they collectively reveal an age-fragile cardiovascular system: a ventricle with impaired relaxation, arteries that have lost elasticity, and a brain that has lost buffering capacity.
Thus, anesthesiologists must interpret this echo as a tri-systemic story of aging—where every cardiac observation has vascular and cerebral implications. The goal is to predict instability, not just respond to it.
The echo does not report just cardiac function; it narrates the functional synchrony (or loss thereof) among three organ systems that regulate perfusion.
Key Point:
When the heart loses compliance, the brain loses buffering.
Every intraoperative blood pressure fluctuation now directly alters cerebral perfusion.
The anesthesiologist’s task is not only to maintain cardiac stability but to preserve synchronized perfusion across all three systems.
Age-related fibrosis, cross-linked collagen, and reduced calcium reuptake cause impaired LV relaxation.
Grade I DD indicates the heart fills slowly, relying heavily on atrial contraction and diastolic time.
When combined with mild AR, LVEDP rises further, narrowing coronary perfusion pressure.
Clinical translation:
Avoid tachycardia (< 90 bpm) to preserve diastolic filling.
Avoid bradycardia (< 65 bpm) to prevent regurgitant overload.
Maintain sinus rhythm—loss of atrial contraction can drop cardiac output by 30–40 %.
Use invasive arterial monitoring to maintain MAP ≥ 70 mmHg and DBP ≥ 60 mmHg.
Echo findings of calcific AV and MAC reveal systemic arteriosclerosis. Arteries lose Windkessel elasticity, leading to widened pulse pressure and dampened baroreflexes.
These structural changes mean that induction agents (propofol, volatile anesthetics) cause exaggerated hypotension, while vasopressors evoke unpredictable hypertensive surges.
Anesthetic management:
Induce slowly (propofol ≤ 1 mg/kg over 60 s).
Prime with norepinephrine 0.02 µg/kg/min prior to induction.
Avoid phenylephrine boluses (pure α-agonism increases afterload).
Maintain steady-state anesthesia (sevoflurane 0.8–1.0 MAC).
The same oxidative stress and amyloid accumulation that stiffen cardiac and vascular tissue also damage cerebral microcirculation.
Autoregulation curve flattens—cerebral blood flow becomes directly dependent on systemic...
