Electrophysiology & Vascular Biomechanics Georgia Institute of Technology In-Vivo Experimental Study

Non-Invasive Cardiovascular Hemodynamics & Electromechanical Profiling

A synchronized dual-channel investigation coupling thoracic Lead II electrocardiography (ECG) with digital infrared photoplethysmography (PPG). Quantified electromechanical pre-ejection latency, autonomic vasomotor thermoregulation, and age-dependent arterial stiffening across lifespan cohorts (ages 9–86) using pulse contour analysis and the Moens-Korteweg hydrodynamic formulation.

Lead Investigator: Álvaro García Casas Affiliation: Georgia Institute of Technology

iWorx TA-ROAM PPG-320 Plethysmograph ECG Lead II Pulse Wave Velocity LabScribe Matplotlib

Young Adult Baseline (SI)

5.61 m/s

Optimal Clinical Reference (5–6 m/s)

Late-Life Arterial Stiffness

12.80 m/s

+128% vs young baseline (86-yr subject)

Electromechanical Latency

244 ms

R-wave to distal finger pulse peak

Cold Vasoconstriction Response

-92.6%

Pulse amplitude drop (1.604 → 0.119 mV)

Synchronized Bio-Signal Monitor (ECG Lead II + Peripheral PPG)

Real-time visualization of myocardial electrical depolarization synchronized with digital infrared volumetric pulse arrival.

CH1: ECG Lead II (Thoracic ROAM) • 1.0 mV/div CH2: Digital Volume Pulse (PPG-320) • 0.5 V/div

RR Period: 845 ms R-to-Pulse Delay: 244 ms HR: 71 bpm

[BASELINE NORM]: Physiological resting state. R-R = 897 ms (71 bpm). Normal ventricular depolarization initiates myocardial contraction; the systolic arterial pulse arrives at the distal phalanx ~244 ms later. Dicrotic notch clearly distinguished during aortic valve closure.

Phase 1 • Bioinstrumentation Architecture

Data Acquisition (DAQ) & Sensor Telemetry

Biopotential recording in physiology labs is frequently contaminated by skeletal muscle motion artifacts and 60 Hz power-line interference. The experimental setup utilized the wireless iWorx TA-ROAM telemetry biopotential unit docked on an iWorx TA acquisition chassis, combined with an infrared transmission plethysmograph (PPG-320) on the finger.

Electrode Configuration (Modified Lead II)

3-lead thoracic montage: Infraclavicular $(-)$, Left lower rib $(+)$, Sternal ground.

1. Thoracic Vector Orientation

The positive lead $(+)$ was placed on the left anterior chest below the pectoralis major and the negative lead $(-)$ at the right subclavicular fossa. This approximates the anatomical mean electrical axis of ventricular depolarization (Einthoven Lead II), maximizing the signal-to-noise ratio of the R-wave peak.

2. Optical Photoplethysmography (PPG-320)

Fastened with velcro to the volar aspect of the distal segment of the left middle finger. It illuminates dermal capillary beds with near-infrared light and detects transmitted photodiode current, registering local blood volume expansions synchronously with central aortic ejections.

3. Signal Conditioning & Pre-Processing

Hardware bandpass filtering (0.05 Hz high-pass to eliminate respiration baseline wander, 100 Hz low-pass to eliminate high-frequency EMG noise) with an active 60 Hz notch filter. A continuous mathematical pulse integral transform was applied in LabScribe to reconstruct smooth pressure-analog volume pulses.

Phase 2 • Autonomic Physiology

Vasomotor Autonomic Reactivity: Thermal Stress Profiling

To characterize autonomic vascular regulation, the subject's left forearm was subjected to targeted acute localized cooling (ice water cold pressor) followed by rewarming and localized hyperthermia (heat pack). Pulse contour and propagation timing were logged continuously.

Experimental Thermal Response Dataset (Subject 1: 20-yr Young Adult)

Empirical DAQ Telemetry

Condition	R-R Interval	Heart Rate	R-Pulse Latency	Systolic Amplitude	Physiological Mechanism
Pre-Test Baseline	0.860 s	71 bpm	0.170 s	1.604 mV	Normothermic baseline
Cold Pressor (1 min)	0.865 s	68 bpm	0.275 s	0.119 mV	Sympathetic vasoconstriction
Cold Pressor (2 min)	0.790 s	77 bpm	0.260 s	0.184 mV	Sustained thermal defense
Rewarming (1 min)	0.815 s	75 bpm	0.235 s	1.330 mV	Reactive hyperemic rebound
Rewarming (2 min)	0.855 s	71 bpm	0.195 s	1.560 mV	Hemodynamic stabilization
Local Heat (2 min)	0.698 s	86 bpm	0.145 s	1.950 mV	Arteriolar vasodilation

Key Finding: Localized hypothermia induced profound peripheral vasoconstriction, dropping pulse amplitude by 92.6% (1.604 mV → 0.119 mV) and increasing transit latency from 0.170 s to 0.275 s due to increased vascular resistance. Rewarming produced reactive hyperemic vasodilation, while direct heating expanded vascular cross-section, accelerating propagation (latency dropped to 0.145 s) and elevating pulse amplitude to 1.950 mV.

Phase 3 • Hemodynamic Biomechanics

Arterial Aging: Stiffness Index (SI) & Moens-Korteweg Modeling

Arterial compliance ($\Delta V / \Delta P$) acts as a hydraulic buffer (Windkessel effect), converting pulsatile left ventricular outflow into steady capillary perfusion. With aging, elastic fiber fragmentation and advanced glycation end-product (AGE) cross-linking of collagen elevate vessel wall stiffness. We quantified these alterations across four age groups using digital volume pulse contour analysis.

Stiffness Index (SI)

SI = Height (m) / ΔT_refl (s)

Estimates large artery pulse wave velocity by normalizing subject height over the transit time between forward and reflected waves.

Reflection Index (RI)

RI = (A_diastolic / A_systolic) × 100%

Measures peripheral vascular tone. High RI indicates marked peripheral vasoconstriction; low RI reflects vascular relaxation.

Rate Pressure Product (RPP)

RPP = Heart Rate × Systolic BP

Direct index of myocardial oxygen consumption (MVO₂) and cardiac workload under differing vascular afterload.

• Critical Engineering Insight: Why R-Pulse Interval ≠ Pure Pulse Wave Velocity (PWV)

Although the ECG R-wave marks ventricular depolarization and the PPG wave detects peripheral pulse arrival, their difference (R-Pulse interval) cannot be used directly as PWV. The interval incorporates the pre-ejection period (PEP, 50–80 ms) — the isovolumetric contraction time required for intraventricular pressure to exceed aortic pressure before the aortic valve leaflets open. True PWV requires differential measurement between two arterial transit points ($\Delta D / \Delta t$) or pulse contour reflection time analysis.

Cross-Sectional Lifespan Dataset & Cardiovascular Indices

JNC VI Classification

Cohort Subject	Age	Height	Stiffness Index (SI)	Reflection Index (RI)	Blood Pressure	Heart Rate	RPP Workload	BP Status
Subject 1 (Young Adult)	20	1.56 m	5.61 m/s	38.63%	95.8 / 60.9	69 bpm	6,608	Optimal
Subject 2 (Pediatric Female)	9	1.27 m	7.74 m/s	33.68%	82.5 / 60.0	77 bpm	6,349	Hypotensive
Subject 3 (Middle-Aged Male)	52	1.85 m	7.81 m/s	15.08%	115.7 / 73.6	65 bpm	7,519	Optimal
Subject 4 (Geriatric Male)	86	1.83 m	12.80 m/s	38.42%	130.8 / 82.8	64 bpm	8,370	Prehypertensive

Phase 4 • Quantitative Evidence

Experimental Figures & Matplotlib Analytics

Publication-ready figures generated from lab data illustrating the biophysical relationships between vascular stiffness, age progression, and myocardial demand.

Figure 1: Stiffness and Reflection Indices by Subject

Figure 1 • Discrete Cohort Comparison

Stiffness Index (A) vs. Reflection Index (B)

SI demonstrates a pronounced upward trajectory with chronological age (5.61 m/s → 12.80 m/s), whereas RI exhibits non-monotonic behavior, highlighting that structural wall stiffness and real-time vasomotor tone are physiologically decoupled.

Clinical Takeaway: Baseline vascular compliance degrades over 128% between young adulthood and the 9th decade.

Figure 2: Arterial Stiffness as a Function of Age

Figure 2 • Clinical Reference Calibration

Arterial Stiffness Trajectory Across Lifespan

Continuous age trajectory mapping across subjects aged 9 to 86 years. The green shaded region depicts the clinical reference interval for healthy young adults (5–6 m/s, Millasseau et al. 2002).

Notice the accelerated compliance loss beyond the 5th decade, where medial elastin fragmentation and collagen glycation substantially accelerate large artery pulse wave velocity.

Moens-Korteweg Formulation: PWV = √((E · h) / (2r · ρ)), directly linking Young's modulus (E) with observed propagation velocity.

Figure 3: Rate Pressure Product and Pulse Pressure

Figure 3 • Hemodynamic Workload

Myocardial Workload & Pulse Pressure Escalation

Panel (A) confirms that the 86-year-old heart bears the heaviest workload (RPP = 8,370), driven by elevated systolic pressure against an unyielding aorta.

Panel (B) reveals pulse pressure widening (22.5 → 47.95 mmHg) resulting directly from lost aortic Windkessel damping.

RPP = HR × SBP • JNC VI Standards

Conclusions & Translational Impact

Clinical Significance in Preventative Cardiology

Early Vascular Aging (EVA) Detection

Digital pulse contour analysis is non-invasive, low-cost, and easily reproducible. It detects microstructural arterial remodeling long before overt hypertension or atherosclerotic plaques appear on ultrasound.

Decoupled Vasomotor Tone

Proved empirically that Reflection Index (RI) does not follow chronological age monotonically, as peripheral resistance is modulated dynamically by autonomic sympathetic tone and aerobic fitness level.

Wearable Point-of-Care Translation

Demonstrated that synchronizing optical PPG with single-lead biopotentials provides a viable framework for continuous, cuffless cardiovascular monitoring in modern smart wearables.

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