Cardiovascular atlas ↗SA-node impulse
Pacemaker cells initiate atrial depolarization; autonomic input changes firing rate.
CARDIOVASCULAR / BLOOD FLOW
An electrical wave
becomes forward flow.
Follow one heartbeat from pacemaker activation through filling, valve motion, pressure generation, ejection, tissue exchange, and venous return. Rate alone never describes pump performance: rhythm, preload, contractility, afterload, and valves all matter.
12-STAGE CLOSED LOOP
Fill. Activate.
Eject. Return.
The right and left heart work in series. The same blood volume must traverse the pulmonary and systemic circuits over time, although beat-to-beat filling and ejection can differ.
Atrial activation
Electrical spread coordinates atrial contraction and adds the final portion of ventricular filling.
AV-node delay
A short conduction delay allows ventricular filling to finish before ventricular activation.
His–Purkinje spread
Rapid conduction synchronizes ventricular depolarization from apex toward outflow tracts.
End-diastolic filling
Venous return, relaxation, compliance, atrial pressure, and valve opening determine preload.
Isovolumetric contraction
Ventricular pressure rises after mitral and tricuspid closure while all valves are briefly closed.
Ventricular ejection
Pulmonary and aortic valves open when ventricular pressure exceeds arterial pressure.
Relaxation and valve reset
Semilunar valves close, ventricular pressure falls, and atrioventricular valves reopen for the next fill.
Cardiac output
Heart rate × stroke volume gives output; ejection fraction is a different measure and can be preserved despite impaired filling.
Pulmonary circuit
The right ventricle sends blood through low-resistance lung vessels for gas exchange.
Systemic exchange
The left ventricle supplies organ arteries; arterioles distribute flow and capillaries exchange oxygen, fuels, signals, and waste.
Venous return
Blood volume, venous tone, breathing, valves, and skeletal-muscle pumping return blood to the right atrium.
CONTROL & FAILURE MODES
One loop,
several control knobs.
Each modifier acts at a different point; the same cardiac output can arise from different combinations of rate and stroke volume.
Rate and contractility
Sympathetic activity tends to raise rate and contractility; parasympathetic vagal activity primarily slows nodal firing and conduction.
Filling before contraction
Volume and venous return shape end-diastolic stretch. Too little limits output; excessive filling pressure promotes congestion.
Resistance to ejection
Arterial pressure and outflow obstruction alter the work required to eject blood.
Timing and synchrony
Atrial fibrillation, conduction block, or ventricular arrhythmia can disrupt coordinated filling or ejection.
Contractility and relaxation
Ischemia, cardiomyopathy, inflammation, and metabolic stress can impair force generation or relaxation.
Direction without obstruction
Stenosis raises pressure load; regurgitation sends part of stroke volume backward.
Core sources: NHLBI: How the Heart Works ↗ · NHLBI: How the Heart Beats ↗
Educational use only. New chest pressure, severe breathlessness, fainting, or collapse requires urgent professional assessment.