Hemodynamics & Heart Function Simulator Interactive Clinical Tool

Hemodynamics & Heart Function Simulator : An interactive clinical heart function and hemodynamics simulator. Adjust heart rate, stroke volume, and blood pressure to visualize cardiovascular metrics and an active ECG in real time.

Hemodynamics & Heart Function Simulator | Interactive Clinical Tool
Interactive Cardiovascular Lab

Hemodynamics & Heart Simulator

Manipulate physiological parameters in real-time. Witness synchronized chamber contractions, live clinical calculations, and an active ECG waveform tracer.

Clinical Controls

Heart Rate (BPM) 72
Bradycardia (30) Normal (60-100) Tachycardia (200)
Stroke Volume (SV) 70 mL
Low Ejection (20) Athletic Normal (70-120) Max Reserve (160)
Systolic Pressure (SBP) 120 mmHg
Hypotension (70) Ideal (120) Severe Crisis (220)
Diastolic Pressure (DBP) 80 mmHg
Low Resistance (40) Ideal (80) Severe (140)
Hemodynamics Classification Calculating…
Body Surface Area (BSA): 1.83 m²
Dynamic Simulator Active Beating
RA LA RV LV
DIASTOLE (RELAXATION)
Real-Time ECG Trace Interval: ~830ms
Lead II
P Wave: Atrial Depol. QRS: Ventricular Depol. T Wave: Repol.

Hemodynamics Dashboard

Cardiac Output (CO) Total blood ejected / min
5.0 L/min
Cardiac Index (CI) Output indexed to BSA
2.7 L/min/m²
Vascular Resistance (SVR) Arterial constriction load
1488 dynes·s/cm⁵
Mean Arterial (MAP) Average organ perfusion
93 mmHg
Calculations follow standard clinical formulas: $CO = (HR \times SV) / 1000$; Body Surface Area (BSA) uses the Mosteller formula: $\sqrt{\frac{H \times W}{3600}}$. MAP is estimated as $DBP + \frac{1}{3}(SBP – DBP)$. SVR is computed as $\frac{(MAP – CVP) \times 80}{CO}$ (assuming typical CVP = 4 mmHg).

Understanding Cardiac Mechanics & Hemodynamics

The cardiovascular system acts as a sophisticated, dynamic fluid circuit. The heart serves as a dual-pump engine generating flow, while systemic arteries provide resistive pathways that control the pressure supplied to tissues.

The Cardiac Cycle and the Wiggers Phenomenon

The mechanical action of the heart progresses through two primary phases: Systole (contraction and active blood ejection) and Diastole (relaxation and ventricles refilling).

During atrial diastole, passive venous blood flows from the vena cava and pulmonary veins into the Right Atrium (RA) and Left Atrium (LA). The electrical pacemaker, the **Sinoatrial (SA) Node**, initiates depolarization (seen as the **P wave** on an ECG), sending waves across the atria causing atrial contraction to finish ventricular filling.

Depolarization reaches the **Atrioventricular (AV) Node**, traveling down the Bundle of His and Purkinje fibers to trigger rapid, coordinated ventricular contraction (the **QRS complex**). Ventricular systole rapidly increases internal pressures, locking shut the tricuspid and mitral valves to prevent backflow, forcing open the aortic and pulmonary valves to expel blood.

Key Clinical Equations Explained

  • Cardiac Output (CO) $$CO = \frac{\text{Heart Rate (HR)} \times \text{Stroke Volume (SV)}}{1000}$$ The absolute volume of blood delivered to the systemic circulation each minute. Normal resting range is roughly 4.0 to 8.0 L/min.
  • Cardiac Index (CI) $$CI = \frac{CO}{\text{Body Surface Area (BSA)}}$$ Adjusts Cardiac Output for different body frames. Normal clinical values range from 2.5 to 4.2 L/min/m². Values below 2.0 indicate high cardiogenic hypoperfusion risk.
  • Systemic Vascular Resistance (SVR) $$SVR = \frac{(MAP – CVP) \times 80}{CO}$$ Calculates total resistance presented by the arterial tree. Normal resistance is 800–1200 dynes·s/cm⁵. Elevated values point to systemic vasoconstriction, while low values indicate shock or systemic vasodilation.

Frequently Asked Questions (Cardiology Lab)

1. What is the significance of the Mean Arterial Pressure (MAP)?
Mean Arterial Pressure (MAP) represents the average pressure driving blood into body organs throughout an entire cardiac cycle. Because the heart spends two-thirds of the cycle in diastole, MAP is heavily weighted towards diastolic blood pressure. In clinical settings, a MAP greater than **65 mmHg** is typically required to maintain adequate organ perfusion (especially for vital organs like kidneys and brain).
2. How does physical training alter resting heart rate and stroke volume?
Aerobic conditioning causes physiological hypertrophy of the left ventricle (athletic remodeling). This increases the heart’s ventricular volume and contractility, leading to a much higher **Stroke Volume (SV)** at rest (e.g., 100–110 mL instead of the normal 70 mL). Consequently, to maintain a normal resting Cardiac Output of ~5 L/min, the resting heart rate adapts downward (often below 50 BPM, known as physiological bradycardia).
3. What goes wrong during cardiogenic shock?
In cardiogenic shock, the heart’s primary pumping mechanism is severely impaired (often due to acute myocardial infarction or heart failure), dropping **Stroke Volume** drastically (e.g., to 20-30 mL). Despite a compensatory sympathetic increase in Heart Rate (tachycardia), the overall Cardiac Output is insufficient, lowering blood pressure and resulting in life-threatening organ hypoperfusion.
4. What do different parts of the ECG wave trace signify?
An electrocardiogram detects systemic surface electrical fields generated by myocardial cell action potentials:
  • P Wave: Atrial depolarization, triggering atrial systole (contraction).
  • QRS Complex: Massive electrical depolarization wave passing down ventricular walls, triggering ventricular systole. Atrial repolarization is buried inside this complex.
  • T Wave: Ventricular repolarization, resetting myocytes for the next cycle (diastole).

Related Tags & Subjects:

#Hemodynamics Simulator #CardiacOutput #ECGTraceSimulator #VascularResistance #ClinicalPhysiology #WiggersDiagram