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PY5.1-16 | Cardiovascular Physiology — Glossary

Automaticity
The ability of cardiac muscle cells (especially SA node) to generate spontaneous action potentials without external neural input.
Cardiac cycle
The complete sequence of events from the beginning of one heartbeat to the beginning of the next, lasting ~0.8 seconds at rest (75 bpm).
Cardiac output (CO)
The volume of blood pumped by each ventricle per minute; CO = Heart Rate x Stroke Volume. Normal: ~5 L/min at rest.
Stroke volume (SV)
The volume of blood ejected by each ventricle per beat. Normal: ~70 mL. Determined by preload, afterload, and contractility.
Frank-Starling mechanism
The intrinsic ability of the heart to increase its force of contraction when ventricular filling (preload) increases — the heart pumps whatever volume it receives.
Preload
The degree of stretch of ventricular muscle fibres at end-diastole, determined by venous return and end-diastolic volume.
Afterload
The resistance the ventricle must overcome to eject blood; primarily determined by aortic pressure and total peripheral resistance.
Ejection fraction (EF)
The percentage of end-diastolic volume ejected per beat (SV/EDV x 100). Normal: 55-70%. Reduced in systolic heart failure.
Mean arterial pressure (MAP)
The average arterial pressure during one cardiac cycle. MAP = DBP + 1/3(Pulse Pressure). Must remain >60 mmHg for organ perfusion.
Baroreceptor reflex
The primary short-term blood pressure regulatory mechanism using stretch receptors in the carotid sinus and aortic arch to modulate autonomic output.
Functional syncytium
A group of cardiac muscle cells that behave as a single coordinated unit due to electrical coupling through gap junctions at intercalated discs.
Refractory period
The time during which cardiac muscle cannot be re-excited (~250 ms), preventing tetanus. Caused by the prolonged plateau (Phase 2) of the cardiac action potential.
Starling forces
The four pressures governing capillary fluid exchange: capillary hydrostatic, interstitial hydrostatic, plasma oncotic, and interstitial oncotic pressure.
Total peripheral resistance (TPR)
The total resistance to blood flow offered by the systemic vasculature, primarily determined by arteriolar diameter. BP = CO x TPR.
Renin-angiotensin-aldosterone system (RAAS)
A hormonal cascade (renin → angiotensin I → angiotensin II → aldosterone) that raises blood pressure through vasoconstriction and sodium/water retention.
Pulse pressure
The difference between systolic and diastolic blood pressure (SBP - DBP). Normal: ~40 mmHg. Reflects stroke volume and arterial compliance.
Jugular venous pressure (JVP)
The pressure in the internal jugular vein, reflecting right atrial pressure. Measured at 45 degrees; normal < 3-4 cm above sternal angle.
Inotropic effect
A change in the force of cardiac muscle contraction. Positive inotropes (sympathetic stimulation, digoxin) increase force; negative inotropes decrease it.
Chronotropic effect
A change in heart rate. Positive chronotropes (sympathetic stimulation) increase HR; negative chronotropes (vagal stimulation) decrease HR.
Shock
A state of inadequate tissue perfusion leading to cellular hypoxia and organ dysfunction. Classified as hypovolaemic, cardiogenic, distributive, or obstructive.
Heart failure
A clinical syndrome where the heart cannot pump sufficient blood to meet the body's metabolic demands, or can do so only at elevated filling pressures.
Pacemaker potential
The spontaneous Phase 4 depolarisation in SA and AV node cells, driven by the funny current (If), that brings the cell to threshold without external stimulation.
Electrocardiogram (ECG)
A surface recording of the electrical activity of the heart. Standard 12-lead ECG shows atrial depolarisation (P wave), ventricular depolarisation (QRS), and repolarisation (T wave).
Autoregulation
The intrinsic ability of an organ to maintain constant blood flow despite changes in perfusion pressure, particularly important in cerebral and renal circulations.
Orthostatic hypotension
A drop in SBP >20 mmHg or DBP >10 mmHg within 3 minutes of standing, caused by failure of compensatory mechanisms (baroreceptor reflex, venoconstriction).