Part 3: Cardiac Electrophysiology & Hemodynamics

Cardiac Electrical System

The heart is unique among muscles — it generates its own rhythmic electrical impulses without any external nervous input. Cut every nerve to the heart, and it still beats. This property, called automaticity, arises from specialised pacemaker cells that spontaneously depolarise, setting the tempo for the entire organ. Understanding the cardiac electrical system is the gateway to interpreting ECGs, diagnosing arrhythmias, and managing life-threatening cardiac emergencies.

Pacemaker vs Contractile Cells

The heart contains two fundamentally different cell types, each with a distinct electrophysiology:

Conduction Pathway (SA → AV → His-Purkinje)

The cardiac impulse follows a precise anatomical route, ensuring coordinated contraction:

1. SA Node (sinoatrial) — the primary pacemaker at the junction of the superior vena cava and right atrium. Intrinsic rate: 60–100 bpm
2. Atrial Conduction — impulse spreads through atrial myocardium and three internodal pathways (anterior/Bachmann's, middle/Wenckebach, posterior/Thorel)
3. AV Node (atrioventricular) — located in the interatrial septum near the coronary sinus. Intrinsic rate: 40–60 bpm. Introduces a critical 0.1-second delay allowing atrial contraction to complete before ventricular filling
4. Bundle of His — penetrates the fibrous skeleton separating atria from ventricles (the only electrical connection)
5. Bundle Branches — right and left (the left further divides into anterior and posterior fascicles)
6. Purkinje Fibres — fastest conducting tissue in the heart (2–4 m/s), ensuring near-simultaneous ventricular depolarisation from apex to base. Intrinsic rate: 20–40 bpm

Cardiac Action Potentials

Ventricular contractile cells exhibit a distinctive five-phase action potential that lasts 250–300 ms — about 100 times longer than a skeletal muscle action potential:

The prolonged plateau (Phase 2) is critically important — it creates a long effective refractory period (ERP) that prevents tetanic contraction of the heart. Unlike skeletal muscle, which can sustain contraction, the heart must relax between beats to refill with blood.

import numpy as np
import matplotlib.pyplot as plt

# Simulate ventricular action potential (simplified 5-phase model)
time = np.linspace(0, 400, 1000)  # milliseconds
vm = np.zeros_like(time)

# Phase 4: resting (-90 mV)
vm[:] = -90

# Phase 0: rapid depolarisation (0-2 ms)
phase0 = (time >= 10) & (time < 12)
vm[phase0] = np.linspace(-90, 20, phase0.sum())

# Phase 1: early repolarisation (2-5 ms)
phase1 = (time >= 12) & (time < 15)
vm[phase1] = np.linspace(20, 0, phase1.sum())

# Phase 2: plateau (5-200 ms)
phase2 = (time >= 15) & (time < 210)
vm[phase2] = np.linspace(0, -10, phase2.sum())

# Phase 3: repolarisation (200-300 ms)
phase3 = (time >= 210) & (time < 310)
vm[phase3] = np.linspace(-10, -90, phase3.sum())

plt.figure(figsize=(10, 5))
plt.plot(time, vm, 'r-', linewidth=2)
plt.xlabel('Time (ms)')
plt.ylabel('Membrane Potential (mV)')
plt.title('Ventricular Cardiomyocyte Action Potential')

# Annotate phases
plt.annotate('Phase 0\n(Na⁺ in)', xy=(11, 10), fontsize=8, ha='center')
plt.annotate('Phase 1', xy=(13, 10), fontsize=8, ha='center')
plt.annotate('Phase 2 (Plateau)\nCa²⁺ in = K⁺ out', xy=(110, 5), fontsize=8, ha='center')
plt.annotate('Phase 3\n(K⁺ out)', xy=(260, -50), fontsize=8, ha='center')
plt.annotate('Phase 4\n(Resting)', xy=(360, -85), fontsize=8, ha='center')
plt.grid(True, alpha=0.3)
plt.tight_layout()
plt.show()

ECG Interpretation Basics

The electrocardiogram (ECG/EKG) records the heart's electrical activity from the body surface. Willem Einthoven invented the string galvanometer in 1903 and won the Nobel Prize in 1924 for this work. The standard 12-lead ECG provides 12 different "views" of the heart's electrical activity.

Systematic ECG Reading Approach

Always follow a methodical approach — never rely on pattern recognition alone:

1. Rate — 300 ÷ (number of large boxes between R-R) or count R waves in 6 seconds × 10
2. Rhythm — regular or irregular? P wave before every QRS?
3. Axis — normal (–30° to +90°), left deviation, right deviation
4. Intervals — PR, QRS, QT durations
5. Morphology — P wave, QRS, ST segment, T wave abnormalities

Mechanical Function

Electrical events drive mechanical events — the heart is ultimately a pump. Every beat propels approximately 70 mL of blood (the stroke volume) into the circulation. At 72 beats per minute, that's over 5 litres per minute at rest and up to 25 L/min during maximal exercise. Understanding the mechanical function of the heart is essential for managing heart failure, valvular disease, and cardiogenic shock.

Cardiac Cycle Phases

The cardiac cycle describes the sequence of pressure and volume changes during one complete heartbeat (~0.8 s at 75 bpm). Think of it as a precisely choreographed four-act play:

Stroke Volume & Cardiac Output

Two fundamental equations define cardiac pump function:

Frank-Starling Mechanism

Otto Frank (1895) and Ernest Starling (1914) independently discovered the most elegant self-regulatory mechanism of the heart:

Molecular Mechanism: Increased stretch brings actin and myosin filaments to a more optimal overlap position and increases troponin C sensitivity to calcium (length-dependent activation). At the organ level, stretching the right atrial wall also triggers the Bainbridge reflex — increased heart rate in response to increased venous return.

import numpy as np
import matplotlib.pyplot as plt

# Frank-Starling curve simulation
edv = np.linspace(50, 200, 100)  # End-diastolic volume (mL)

# Normal curve (sigmoidal function)
sv_normal = 90 / (1 + np.exp(-0.05 * (edv - 120))) + 20
# Enhanced contractility (e.g., sympathetic stimulation)
sv_enhanced = 110 / (1 + np.exp(-0.05 * (edv - 110))) + 25
# Depressed contractility (e.g., heart failure)
sv_depressed = 60 / (1 + np.exp(-0.05 * (edv - 140))) + 15

plt.figure(figsize=(10, 6))
plt.plot(edv, sv_normal, 'b-', linewidth=2, label='Normal')
plt.plot(edv, sv_enhanced, 'g--', linewidth=2, label='Enhanced (Sympathetic)')
plt.plot(edv, sv_depressed, 'r:', linewidth=2, label='Depressed (Heart Failure)')
plt.xlabel('End-Diastolic Volume / Preload (mL)')
plt.ylabel('Stroke Volume (mL)')
plt.title('Frank-Starling Curves')
plt.legend()
plt.grid(True, alpha=0.3)
plt.annotate('Normal operating\npoint', xy=(120, 78), fontsize=9,
            arrowprops=dict(arrowstyle='->', color='blue'),
            xytext=(140, 60))
plt.tight_layout()
plt.show()

Preload, Afterload & Contractility

The three determinants of stroke volume can be remembered from the perspective of the ventricle:

Hemodynamics

Hemodynamics is the physics of blood flow — how pressure, flow, and resistance interact throughout the vascular system. Just as Ohm's law governs electrical circuits (V = IR), an analogous relationship governs the circulation: ΔP = Q × R (pressure gradient = flow × resistance). This section applies fluid physics to the living circulation.

Blood Pressure Determinants

Blood pressure is determined by two fundamental variables:

Flow, Resistance & Compliance

Three interdependent concepts govern haemodynamics:

• Flow (Q) = ΔP / R (analogous to Ohm's law: I = V / R)
• Resistance (R) — opposition to flow; primarily determined by arteriolar diameter. Arterioles are the "resistance vessels" and the major site for blood pressure regulation
• Compliance (C) = ΔV / ΔP — the ability of a vessel to stretch. Veins have high compliance (capacitance vessels holding ~65% of blood volume). Arteries have lower compliance but higher elastic recoil (Windkessel function)

Poiseuille's Law

Jean Léonard Marie Poiseuille (1838) derived the mathematical relationship between flow and vessel dimensions:

import numpy as np
import matplotlib.pyplot as plt

# Poiseuille's Law: demonstrate r^4 relationship
radius_fraction = np.linspace(0.3, 1.5, 100)  # Fraction of normal radius
flow_fraction = radius_fraction ** 4  # Flow relative to normal

plt.figure(figsize=(10, 6))
plt.plot(radius_fraction * 100, flow_fraction * 100, 'b-', linewidth=2)
plt.axhline(y=100, color='gray', linestyle='--', alpha=0.5, label='Normal flow')
plt.axvline(x=100, color='gray', linestyle='--', alpha=0.5, label='Normal radius')

# Mark clinically relevant points
plt.plot(50, (0.5**4)*100, 'ro', markersize=10)
plt.annotate('50% stenosis\n→ 94% flow reduction!', xy=(50, (0.5**4)*100),
            xytext=(60, 20), fontsize=9,
            arrowprops=dict(arrowstyle='->', color='red'))

plt.plot(70, (0.7**4)*100, 'o', color='orange', markersize=10)
plt.annotate('30% stenosis\n→ 76% flow reduction', xy=(70, (0.7**4)*100),
            xytext=(75, 40), fontsize=9,
            arrowprops=dict(arrowstyle='->', color='orange'))

plt.xlabel('Vessel Radius (% of normal)')
plt.ylabel('Blood Flow (% of normal)')
plt.title("Poiseuille's Law: Flow ∝ Radius⁴")
plt.legend()
plt.grid(True, alpha=0.3)
plt.tight_layout()
plt.show()

Microcirculation & Capillary Exchange

Capillaries are the functional unit of the circulation — where the actual business of gas exchange, nutrient delivery, and waste removal occurs. There are approximately 10 billion capillaries with a total surface area of ~500 m².

Starling Forces (Capillary Exchange)

Ernest Starling (the same Starling of the heart law) described the forces governing fluid movement across capillary walls:

Cardiovascular Regulation

The cardiovascular system maintains blood pressure and organ perfusion through a layered hierarchy of control mechanisms — ranging from rapid neural reflexes (seconds) through hormonal responses (minutes to hours) to long-term renal mechanisms (hours to days). This redundancy ensures survival even when one regulatory pathway fails.

Baroreceptors & Chemoreceptors

Baroreceptors are stretch-sensitive mechanoreceptors located in the carotid sinus and aortic arch. They provide the fastest blood pressure regulation — the baroreceptor reflex corrects acute changes within seconds:

Chemoreceptors — peripheral (carotid body, aortic body) and central (medulla) — detect PaO₂, PaCO₂, and pH changes. Hypoxia and hypercapnia trigger sympathetic-mediated vasoconstriction and tachycardia alongside increased ventilation.

Autonomic Control

The heart receives dual innervation — parasympathetic (vagus nerve) and sympathetic (cardiac accelerator nerves from T1-T5):

Hormonal Influences (RAAS, ANP)

Hormonal regulation provides medium- to long-term blood pressure control:

Renin-Angiotensin-Aldosterone System (RAAS)

1. Trigger: Low renal perfusion pressure, low Na⁺ at macula densa, or sympathetic stimulation → juxtaglomerular cells release renin
2. Renin cleaves angiotensinogen (liver) → angiotensin I
3. ACE (pulmonary endothelium) converts angiotensin I → angiotensin II
4. Angiotensin II effects:
   • Potent arteriolar vasoconstriction → ↑ SVR → ↑ BP
   • Stimulates aldosterone release (adrenal cortex) → Na⁺/H₂O retention → ↑ blood volume
   • Stimulates ADH release (posterior pituitary) → water retention
   • Stimulates thirst centre (hypothalamus)
   • Promotes cardiac and vascular remodelling (hypertrophy, fibrosis)

Counter-Regulatory Hormones

Advanced Topics

This section integrates electrical and mechanical cardiovascular physiology into clinical pathophysiology — understanding what happens when the system fails. These are the highest-yield topics for clinical medicine and critical care.

Shock Physiology

Shock is defined as inadequate tissue perfusion leading to cellular hypoxia and organ dysfunction. It is not synonymous with low blood pressure — compensatory mechanisms may maintain BP initially while tissues are already oxygen-starved.

Heart Failure Mechanisms

Heart failure (HF) occurs when the heart cannot meet the body's metabolic demands at normal filling pressures. It is classified by ejection fraction:

Coronary Circulation Regulation

The heart receives its own blood supply through coronary arteries — and has uniquely demanding requirements:

• High oxygen extraction: The heart extracts ~70–80% of delivered O₂ (vs ~25% for most tissues). It cannot significantly increase extraction further — increased demand can only be met by increasing coronary blood flow
• Flow occurs mainly in diastole: Left ventricular contraction compresses intramural coronary vessels; most LCA flow occurs during diastole (this is why tachycardia is dangerous in coronary disease — it shortens diastole)
• Metabolic autoregulation: Adenosine (produced from ATP breakdown during increased work) is the primary local vasodilator; NO, K⁺, CO₂, and H⁺ also contribute

Interactive Tool

Use this Cardiac Cycle Analyser to document the hemodynamic parameters of any cardiac condition. Enter your data and download a professional report in Word, Excel, or PDF format.

Conclusion & Next Steps

In this article, we explored the heart as both an electrical and mechanical organ. We traced the cardiac impulse from the SA node through the His-Purkinje system, understood the ionic basis of cardiac action potentials, and learned systematic ECG interpretation. We then connected electrical events to mechanical function — the cardiac cycle, Frank-Starling mechanism, and the three determinants of stroke volume (preload, afterload, contractility).

The hemodynamics section revealed how the circulation obeys physical laws (Poiseuille, Starling forces) while being exquisitely regulated by neural reflexes (baroreceptors), hormonal systems (RAAS, natriuretic peptides), and local metabolic factors. Finally, we applied these principles to clinical pathophysiology — shock classification and heart failure mechanisms.

The cardiovascular system doesn't work in isolation. It is intimately linked with the respiratory system — pulmonary blood flow, gas exchange, and the oxygen-haemoglobin relationship are the critical next step in understanding how the body delivers oxygen to every cell.