Sources and References

Primary texts — Hall and Hall, Guyton and Hall Textbook of Medical Physiology, 14th ed. (Elsevier). Enderle and Bronzino, Introduction to Biomedical Engineering, 3rd ed. (Academic Press).

Supplementary texts — Boron and Boulpaep, Medical Physiology, 3rd ed. (Elsevier). Kandel et al., Principles of Neural Science, 6th ed. (McGraw-Hill). Nordin and Frankel, Basic Biomechanics of the Musculoskeletal System, 4th ed. (Lippincott).

Online resources — MIT OCW HST.542J Quantitative Physiology and 2.782J Design of Medical Devices. PhysioNet open-access cardiac signal databases. NIH Bioengineering and Research Methods open resources. ISO 14971 application of risk management to medical devices.

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Chapter 1: The Engineered View of Physiology

1.1 Body as a System of Systems

For the biomedical engineer, physiology is a hierarchy of interacting regulated systems: mechanical (musculoskeletal), electrical (nervous, cardiac), fluidic (cardiovascular, respiratory), chemical (endocrine, metabolic). Each subsystem maintains homeostasis around a regulated variable through negative feedback — arterial pressure, blood glucose, core temperature — and each can be represented by block diagrams amenable to the same tools used for engineered controls.

1.2 Design-Driven Physiology

Devices that interact with the body must respect the body’s mechanical compliance, electrical impedance, chemical chemistry, and biological response. A device’s “specification” is the physiology it must measure, replace, or augment. This chapter orients the subsequent treatment: each system is presented with the quantitative models and interfaces that directly support device design.

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Chapter 2: The Musculoskeletal System

2.1 Bone Mechanics

Cortical bone has longitudinal modulus ≈ 17 GPa, ultimate tensile strength ≈ 130 MPa, and is anisotropic and viscoelastic. Trabecular bone modulus depends on apparent density \( \rho \) via \( E \propto \rho^{n} \) with \( n \approx 2\text{–}3 \). Wolff’s law — bone adapts its architecture to mechanical loading — drives the design of porous implants that mimic native stiffness to minimize stress shielding.

2.2 Joints and Articular Cartilage

Synovial joints combine low-friction articular cartilage (µ ≈ 0.001–0.01) with synovial fluid acting as a boundary and hydrodynamic lubricant. Cartilage is a biphasic tissue of proteoglycan-rich matrix and interstitial water; its response to load follows poroelastic mechanics:

\[ \sigma = -p \mathbf{I} + 2\mu \mathbf{\varepsilon} + \lambda \mathrm{tr}(\mathbf{\varepsilon}) \mathbf{I}, \qquad \mathbf{v} = -k \nabla p . \]

2.3 Muscle Mechanics

Skeletal muscle force depends on length and velocity. The Hill model combines a contractile element in parallel with passive elasticity:

\[ (F + a)(v + b) = (F_0 + a)\,b . \]

Force–length relationships peak at an optimum sarcomere length near 2.6 µm in human muscle. EMG signals, recorded in BME 294, report the motor-unit firing pattern that generates these forces.

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Chapter 3: The Nervous System

3.1 The Neuron as an Electrical Element

The resting membrane potential of ≈ −70 mV arises from selective permeability governed by the Goldman–Hodgkin–Katz equation

\[ V_m = \frac{RT}{F} \ln\!\left(\frac{P_K[\mathrm{K^+}]_o + P_{Na}[\mathrm{Na^+}]_o + P_{Cl}[\mathrm{Cl^-}]_i}{P_K[\mathrm{K^+}]_i + P_{Na}[\mathrm{Na^+}]_i + P_{Cl}[\mathrm{Cl^-}]_o}\right) . \]

Action potentials arise from the Hodgkin–Huxley gating dynamics; conduction velocity in myelinated fibres scales linearly with diameter, in unmyelinated fibres as the square root.

3.2 Synaptic Transmission and Networks

Chemical synapses convert presynaptic spikes to neurotransmitter release, ionotropic or metabotropic receptor activation, and postsynaptic potentials. Spatial and temporal summation at the axon hillock decides whether a new action potential fires. Networks of sensory, interneuron, and motor populations implement reflexes, central pattern generators, and higher processing.

3.3 Imaging and Interfacing

EEG (scalp µV-scale), ECoG, local field potentials, and intracortical microelectrodes form a hierarchy of invasiveness vs spatial resolution. Device design trades charge-injection limits (Shannon criterion \( k = \log(Q) + \log(Q/A) \) ≤ 1.7 for safe stimulation), foreign-body response, and long-term recording stability.

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Chapter 4: The Cardiovascular System

4.1 Hemodynamics

Mean arterial pressure satisfies

\[ \mathrm{MAP} = \mathrm{CO} \times \mathrm{SVR} , \]

with cardiac output \( \mathrm{CO} = \mathrm{HR} \times \mathrm{SV} \). In rigid tubes, Poiseuille’s law gives flow

\[ Q = \frac{\pi \Delta P r^4}{8 \mu L} , \]

explaining the dominance of small arteries in vascular resistance. Elastic arteries act as Windkessel capacitors, smoothing pulsatile flow into steady perfusion of capillaries.

4.2 The Electrocardiogram

The cardiac electrical cycle — SA node, atrial depolarization, AV delay, ventricular depolarization, repolarization — projects onto the body surface as the 12-lead ECG. Einthoven’s triangle and the dipole model explain lead vectors. Device design for arrhythmia detection exploits QRS morphology and R-R variability.

4.3 Device Interfaces

Pacemakers deliver charge-balanced pulses (typically 0.5–5 V, 0.25–1 ms, 60–80 bpm). Defibrillators deliver biphasic shocks tuned to damage thresholds. Left-ventricular assist devices generate rotary flow; their design balances flow rate, shear-induced hemolysis (\( \tau > 150\) Pa over ms scales), and thrombogenicity.

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Chapter 5: Pathology and Medical Device Design

5.1 Disease as Perturbed Homeostasis

Pathology is best understood as the failure or mis-regulation of normal control systems. Diabetes is a failure of glucose regulation; heart failure, of cardiac output regulation; COPD, of gas exchange. Devices replace, augment, or monitor these control loops.

5.2 Diagnostic Devices

Imaging (X-ray, CT, MRI, US), biosignal monitors (ECG, EEG, pulse oximetry), and in-vitro diagnostics measure state variables of the body’s systems. Each modality resolves different physical quantities at different spatial/temporal scales; selection follows clinical question, risk profile, and cost.

5.3 Assistive and Therapeutic Devices

Cochlear implants bypass damaged hair cells by direct auditory-nerve stimulation. Orthoses and prostheses restore musculoskeletal function; their design requires anatomical anchoring, user-specific fit, and dynamic response matching. Drug-delivery devices — infusion pumps, inhalers, transdermal patches — match pharmacokinetics to therapeutic windows.

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Chapter 6: The Respiratory System and Integrative Perspectives

6.1 Ventilation and Gas Exchange

Tidal volume \( V_T \) and respiratory rate set minute ventilation. Alveolar gas exchange is described by the alveolar gas equation

\[ P_{A,O_2} = P_{I,O_2} - \frac{P_{A,CO_2}}{R} , \]

with respiratory quotient \( R \approx 0.8 \). Airway resistance rises sharply in asthma and COPD; mechanical ventilators must adjust flow, pressure, and timing to avoid barotrauma while ensuring gas exchange.

6.2 Oxygen Transport

Oxygen dissociation from hemoglobin follows the sigmoidal curve fit by the Hill equation

\[ S_{O_2} = \frac{[P_{O_2}]^n}{P_{50}^n + [P_{O_2}]^n} , \]

with \( n \approx 2.7 \) and \( P_{50} \approx 26 \) mmHg. Shifts from CO₂, pH, temperature, and 2,3-BPG (Bohr effect) tune delivery to metabolic demand.

6.3 Integration

The musculoskeletal, nervous, cardiovascular, and respiratory systems are coupled. Exercise raises cardiac output, respiratory drive, and skeletal muscle metabolism simultaneously, coordinated by the autonomic nervous system. Device design must respect these couplings: a pacemaker that fixes rate irrespective of metabolic demand is inferior to a rate-responsive design that senses activity.