Difficulty: Intermediate | Prerequisites: Blood composition and hemostasis notes (Doc 1 of this series), basic understanding of action potentials and membrane channels.
This unit zooms in on the heart itself, the electrical system that makes it beat, the mechanical cycle of each heartbeat, and the network of vessels that distribute blood to every tissue. You will learn how the heart generates its own rhythm (autorhythmicity), how an EKG traces that electrical activity, how the cardiac cycle translates electrical signals into pressure and volume changes, and how blood pressure and flow are regulated across the vascular system. This builds directly on the blood composition material: the oxygen-carrying blood you studied needs a pump and pipes to reach the tissues. If you are behind, make sure you understand action potentials, membrane ion channels and the basics of smooth and striated muscle before diving in.
The heart beats on its own via autorhythmic cells (the SA node sets the pace). Each cardiac cycle involves atrial and ventricular systole (contraction) and diastole (relaxation), tracked electrically on an EKG as the P wave, QRS complex and T wave. Cardiac output equals stroke volume times heart rate, and blood pressure depends on cardiac output, blood volume and vascular resistance. Blood flows from arteries through capillaries (where exchange occurs) into veins and back to the heart.
Mediastinum
The central compartment of the thoracic cavity where the heart is located. In simple terms, the middle zone of the chest, between the lungs.
Atrioventricular (AV) valves
The right (tricuspid) and left (mitral/bicuspid) valves that sit between the atria and ventricles. They prevent backflow from ventricles into atria during ventricular contraction. Think of them as one-way doors between the upper and lower chambers.
Semilunar (SL) valves
The aortic and pulmonary valves that prevent backflow from the arteries into the ventricles. They open when ventricular pressure exceeds arterial pressure during ejection. Think of them as the exit doors of the ventricles.
Autorhythmic cells (pacemaker cells)
Specialised cardiac muscle cells that spontaneously generate action potentials without external nerve stimulation. They form the conduction system of the heart. In simple terms, the cells that make the heart beat on its own.
SA node (sinoatrial node)
The primary pacemaker of the heart, located in the right atrium. It initiates action potentials at the fastest rate (~60 to 100 bpm), setting the heart's rhythm. Think of it as the conductor of the heart's orchestra.
AV node (atrioventricular node)
The second relay point in the conduction system. It briefly delays the signal (~0.1 s), allowing the atria to finish contracting before the ventricles begin. Can pace at 40 to 60 bpm if the SA node fails. In simple terms, the speed bump that ensures atria empty before ventricles contract.
Bundle of His (AV bundle)
The conduction pathway from the AV node through the interventricular septum. Can pace at 20 to 40 bpm if both the SA and AV nodes fail.
Purkinje fibres
Conduction fibres that spread action potentials across the ventricular walls, ensuring coordinated ventricular contraction from apex upward.
Pacemaker potential (prepotential)
The unstable resting potential of autorhythmic cells (~-60 mV) that gradually drifts toward threshold through slow Na+ leak, then T-type and L-type Ca2+ channel opening, triggering depolarisation. Repolarisation occurs via slow K+ channels. In simple terms, the slow, automatic climb to threshold that fires each heartbeat.
Electrocardiogram (EKG / ECG)
A recording of the heart's electrical activity from the body surface. It does not measure the heart's mechanical contraction directly.
P wave
Represents depolarisation of the atria (triggered by the SA node).
QRS complex
Represents ventricular depolarisation (and atrial repolarisation, which is hidden within it).
T wave
Represents ventricular repolarisation.
Systole / Diastole
Systeme: the contraction phase of a chamber. Diastole: the relaxation phase. Each cardiac cycle = atrial systole/diastole followed by ventricular systole/diastole.
Cardiac output (CO)
The volume of blood ejected by one ventricle per minute. CO (mL/min) = stroke volume (mL/beat) x heart rate (beats/min). A normal resting CO is roughly 5.25 L/min.
Stroke volume (SV)
The amount of blood pumped out of one ventricle per beat. SV = EDV minus ESV. Normal resting SV is about 70 mL.
End diastolic volume (EDV)
The volume of blood in a ventricle at the end of filling (diastole). Approximately 120 mL at rest.
End systolic volume (ESV)
The volume of blood remaining in a ventricle after contraction (systole). Approximately 50 mL at rest.
Ejection fraction
The percentage of blood in the ventricle that is ejected with each beat (SV / EDV x 100). Normal left ventricular ejection fraction is 55% or higher; 50% or lower is considered reduced.
Preload
The degree of stretch on cardiac muscle cells just before contraction, determined primarily by venous return. Think of it as how much the heart is "loaded" with blood before it squeezes.
Afterload
The pressure the ventricles must overcome to eject blood, primarily arterial blood pressure pushing on the semilunar valves. Think of it as the resistance the heart pushes against.
Contractility
The inherent strength of contraction at a given muscle length, independent of preload.
Mean arterial pressure (MAP)
The average blood pressure during one cardiac cycle. MAP = diastolic pressure + 1/3 (pulse pressure). It is the driving pressure for blood flow through the systemic circuit.
Vascular resistance
The opposition to blood flow caused by friction between blood and vessel walls. Depends on vessel radius (most important), blood viscosity and vessel length.
The heart sits in the mediastinum (central thoracic cavity).
Valves open and close in response to pressure differences as chambers contract and relax.
AV valves (tricuspid and mitral):
When atrial pressure exceeds ventricular pressure, AV valves open and blood flows into ventricles.
When ventricles contract, rising pressure pushes blood against the valve cusps, closing them.
Papillary muscles contract and chordae tendineae tighten to prevent the valve flaps from everting into the atria.
Semilunar valves (aortic and pulmonary):
Open when ventricular pressure exceeds arterial pressure during ventricular systole.
Close when ventricles relax and pressure drops, causing blood to flow back into the valve cusps.
Contractile cells: Striated fibres organised into sarcomeres. These do the mechanical pumping.
Autorhythmic cells (pacemaker cells): Smaller, fewer contractile fibres, no organised sarcomeres. They spontaneously generate action potentials to drive contraction. The heart can beat even when removed from the body because of these cells.
The conduction system is the route by which action potentials spread through the heart:
SA node (pacemaker): Initiates the impulse at the fastest rate.
AV node: Delays the impulse (~0.1 s) so atria finish emptying. Can pace at 40 to 60 bpm as a backup.
Bundle of His (AV bundle): Carries the impulse through the interventricular septum. Backup rate: 20 to 40 bpm.
Right and left bundle branches: Distribute the impulse down each side of the septum.
Purkinje fibres: Spread the impulse across the ventricular walls for coordinated contraction.
Autorhythmic cells have an unstable resting membrane potential (~-60 mV, compared with -90 mV in contractile cells).
They depolarise gradually toward threshold through slow Na+ leak, then T-type and L-type Ca2+ channels open to produce the action potential.
Repolarisation occurs through slow K+ channel opening.
Contractile cells: Depolarisation from rapid Na+ entry; plateau phase from Ca2+ entry (prevents tetanus); repolarisation from K+ exit. Duration: 250 to 300 ms (30 times longer than skeletal muscle).
Autorhythmic cells: Unstable membrane potential (pacemaker potential); depolarisation driven by Ca2+ channels.
The long absolute refractory period of cardiac muscle prevents summation and tetanus, ensuring the heart relaxes between beats.
The SA node sets the intrinsic rhythm; the nervous system and hormones modulate rate and force but do not set the fundamental beat.
Sympathetic input (cardiac accelerator nerves): Increases rate of SA and AV node depolarisation, raises heart rate, and increases contractility and stroke volume.
Parasympathetic input (vagus nerve): Decreases rate of SA and AV node depolarisation, lowers heart rate.
Input to the cardiovascular centre comes from higher brain centres (cortex, limbic system, hypothalamus) and sensory receptors: proprioceptors (movement), chemoreceptors (blood chemistry), baroreceptors (blood pressure).
P wave: Atrial depolarisation (SA node fires).
QRS complex: Ventricular depolarisation (atrial repolarisation is hidden within it).
T wave: Ventricular repolarisation.
P-Q interval: Time from the start of atrial excitation to the start of ventricular excitation.
S-T segment: Period when the entire ventricular myocardium is depolarised.
Q-T interval: From the beginning of ventricular depolarisation through ventricular repolarisation.
Arrhythmias: Irregular heart rhythms from defects in the conduction system.
Fibrillation: Rapid, irregular contractions; the heart cannot pump effectively. Treatment: defibrillation (electrical reset).
Extrasystole (premature contraction): An ectopic focus fires before the SA node, often triggered by excess caffeine or nicotine.
Tachycardia: Heart rate above 100 bpm; persistent tachycardia may lead to fibrillation.
Bradycardia: Heart rate below 60 bpm. May indicate inadequate circulation in non-athletes, or may be a normal result of endurance training.
One cardiac cycle = contraction (systole) and relaxation (diastole) of both atria, followed by systole and diastole of both ventricles.
Five phases:
Late diastole: All chambers relaxed; ventricles fill passively (80% of filling occurs here).
Atrial systole: Atria contract (P wave), pushing the remaining 20% of blood into ventricles. The volume in each ventricle at this point = end diastolic volume (EDV, ~120 mL).
Isovolumetric contraction: Ventricles begin contracting; AV valves close (first heart sound, "lub") but SL valves are not yet open. All valves closed, volume constant.
Ventricular ejection: Ventricular pressure exceeds arterial pressure; SL valves open and blood is ejected.
Isovolumetric relaxation: Ventricles relax; SL valves close (second heart sound, "dup") as blood briefly flows back against them. The volume remaining = end systolic volume (ESV, ~50 mL). The dicrotic notch on a pressure tracing marks the brief pressure rise from aortic valve closure.
First sound (S1, "lub"): Closing of AV valves at the start of ventricular systole.
Second sound (S2, "dup"): Closing of SL valves at the start of ventricular diastole.
The mitral valve closes slightly before the tricuspid; the aortic closes slightly before the pulmonary.
Heart murmurs are abnormal sounds caused by turbulent blood flow, often through narrowed or leaky valves.
CO (mL/min) = SV (mL/beat) x HR (beats/min)
Also: CO = MAP / resistance
Three factors regulate SV:
Preload: The degree of stretch on the heart muscle before contraction. Determined mainly by venous return. More blood returning to the heart stretches the ventricle further, producing a stronger contraction (Frank-Starling law).
Afterload: The pressure the ventricle must overcome to eject blood, primarily arterial blood pressure. Higher afterload means the ventricle works harder and ESV increases.
Contractility: The strength of contraction independent of stretch. Enhanced by sympathetic stimulation and certain hormones.
Key formulas:
SV = EDV minus ESV
Normal SV = 120 mL minus 50 mL = 70 mL/beat
Ejection fraction = (SV / EDV) x 100. Normal LV ejection fraction: 55% or higher.
Arteries: Carry blood away from the heart. Thick, elastic walls absorb the pulsatile pressure from ventricular ejection. Smooth muscle in the tunica media allows diameter regulation.
Arterioles: Smallest arterial branches; primary site of resistance regulation.
Capillaries: Smallest vessels, composed of a single endothelial cell layer and basement membrane. Site of nutrient and waste exchange between blood and tissues.
Venules: Collect blood from capillaries; drain into veins.
Veins: Return blood to the heart. Thinner tunica interna and media, thicker tunica externa compared with arteries. Less elastic tissue and smooth muscle. Contain valves that prevent backflow.
Blood flow path: arteries, arterioles, capillaries, venules, veins.
Most blood vessels have three layers:
Tunica interna (intima): Innermost, lines the lumen. Endothelial cells.
Tunica media: Middle layer of smooth muscle and elastic fibres.
Tunica externa (adventitia): Outermost connective tissue layer.
Continuous capillaries (most common): Tiny pores, limited passage. Found in muscle, skin, lungs. Ions remain in blood.
Fenestrated capillaries: Larger pores, more filtration. Found in kidneys (filtration), endocrine glands (hormone absorption).
Sinusoid capillaries: Very leaky, large gaps. Found in the liver (allows passage of large molecules and recycled RBC components), also in spleen and bone marrow.
Substances cross capillary walls by three mechanisms:
Diffusion: O2, CO2, glucose, amino acids and some hormones cross via simple diffusion.
Transcytosis: Large, lipid-insoluble molecules (e.g. insulin) cross in vesicles (endocytosis on one side, exocytosis on the other).
Bulk flow: Large-scale movement of fluid driven by pressure gradients. More important for regulating relative volumes of blood and interstitial fluid than for solute exchange.
Filtration (at the arterial end): Pressure-driven movement of fluid and solutes out of capillaries into interstitial fluid. Promoted by blood hydrostatic pressure (BHP) and interstitial fluid osmotic pressure (IFOP).
Reabsorption (at the venous end): Pressure-driven movement of fluid back into capillaries. Promoted by blood colloid osmotic pressure (BCOP) and interstitial fluid hydrostatic pressure (IFHP).
Blood flow is the volume of blood flowing through a tissue per unit time (mL/min).
Flow is directly proportional to the pressure gradient and inversely proportional to resistance.
Resistance depends on vessel radius (most significant factor), blood viscosity and vessel length.
Vasoconstriction: Decreased vessel radius, increased resistance, decreased flow.
Vasodilation: Increased vessel radius, decreased resistance, increased flow.
A small change in radius produces a large change in resistance (fourth-power relationship).
Generated by ventricular contraction.
Determined by cardiac output, blood volume and vascular resistance.
Systolic pressure: Peak pressure during ventricular systole. Normal: < 120 mmHg.
Diastolic pressure: Lowest pressure during ventricular diastole. Normal: < 80 mmHg.
Pulse pressure = systolic minus diastolic pressure.
MAP = diastolic + 1/3 (pulse pressure).
Measured using a sphygmomanometer and auscultation of Korotkoff sounds over the brachial artery.
The volume of blood flowing back to the heart through systemic veins, driven by the pressure gradient created by left ventricular contraction.
Increased venous return leads to greater preload, greater stroke volume and greater cardiac output.
Assisted by: venous valves (prevent backflow in low-pressure vessels), the respiratory pump (thoracic pressure changes during breathing), and the skeletal muscle pump (muscle contraction squeezes veins, pushing blood toward the heart).
At rest, the largest proportion of blood resides in the systemic veins and venules, which serve as blood reservoirs.
Systemic circulation: Left ventricle to body tissues and back to right atrium.
Pulmonary circulation: Right ventricle to lungs and back to left atrium.
Hepatic portal circulation: Carries nutrient-rich blood from the digestive tract through the liver before returning to the heart.
Students often think the EKG directly measures the heart's mechanical contraction. It records electrical activity only. The P wave, QRS complex and T wave represent depolarisation and repolarisation events, not the physical squeezing of chambers.
Students sometimes assume the SA node needs signals from the brain to fire. The SA node is intrinsically autorhythmic. The nervous system modulates rate and force but does not initiate the beat.
Students frequently mix up the first and second heart sounds. S1 ("lub") is the closing of AV valves at the start of ventricular systole. S2 ("dup") is the closing of SL valves at the start of ventricular diastole. Both sounds come from valve closure, not valve opening.
Students sometimes believe arteries always have higher pressure than veins everywhere in the body. In pulmonary circulation, pressures are much lower than in the systemic circuit, though the direction rules still apply (pulmonary arteries carry blood away from the heart to the lungs).
⚠️ Be able to trace the conduction pathway: SA node, AV node, Bundle of His, bundle branches, Purkinje fibres.
⚠️ Know what each EKG wave represents (P = atrial depolarisation, QRS = ventricular depolarisation, T = ventricular repolarisation).
⚠️ Understand the five phases of the cardiac cycle and which valves are open or closed during each.
⚠️ Know the formulas: CO = SV x HR; SV = EDV minus ESV; MAP = diastolic + 1/3 (pulse pressure).
⚠️ Distinguish preload, afterload and contractility and their effects on stroke volume.
⚠️ Understand how vessel radius affects resistance (small radius change = large resistance change).
⚠️ Know the three mechanisms assisting venous return (valves, respiratory pump, skeletal muscle pump).
⚠️ Distinguish continuous, fenestrated and sinusoid capillaries by structure and location.
True or False: The QRS complex on an EKG represents atrial depolarisation. (False, it represents ventricular depolarisation.)
Fill in the blank: Cardiac output equals ______ multiplied by ______. (Stroke volume multiplied by heart rate.)
True or False: During isovolumetric contraction, both AV and SL valves are closed. (True.)
Fill in the blank: The three factors regulating stroke volume are ______, ______ and ______. (Preload, afterload, contractility.)
True or False: Veins have thicker tunica media and more smooth muscle than arteries. (False, arteries have thicker tunica media and more smooth muscle.)
Q: Trace the path of an electrical impulse through the heart's conduction system.
A: SA node (initiates impulse), AV node (delays briefly), Bundle of His, right and left bundle branches, Purkinje fibres (spread impulse across ventricular walls).
Q: During which phase of the cardiac cycle does the first heart sound occur, and what causes it?
A: The first heart sound (S1, "lub") occurs at the start of ventricular systole, caused by the closure of the AV valves (tricuspid and mitral) when ventricular pressure exceeds atrial pressure.
Q: Calculate stroke volume and ejection fraction given EDV of 130 mL and ESV of 60 mL.
A: SV = 130 minus 60 = 70 mL. Ejection fraction = 70 / 130 x 100 = approximately 54%. This would be borderline low (normal is 55% or higher).
Q: Explain how increased venous return affects cardiac output.
A: Increased venous return increases preload (greater stretch of ventricular muscle). By the Frank-Starling mechanism, this increases stroke volume. Since CO = SV x HR, an increase in SV raises cardiac output (assuming heart rate stays constant).
Q: Why does vasoconstriction increase blood pressure?
A: Vasoconstriction decreases vessel radius, which dramatically increases vascular resistance (fourth-power relationship). Since blood pressure is determined by cardiac output and vascular resistance, increased resistance raises BP.
Q: Name and compare the three types of capillaries.
A: Continuous (most common, tiny pores, limited permeability, e.g. muscle and skin), fenestrated (larger pores, more filtration, e.g. kidneys and endocrine glands), sinusoid (very leaky with large gaps, allows passage of large molecules, e.g. liver, spleen, bone marrow).
The cardiac output and blood pressure material connects directly to the renal system (the kidneys regulate blood volume and therefore BP) and to the autonomic nervous system (sympathetic and parasympathetic regulation of heart rate). The conduction system and EKG content is foundational for understanding cardiac pharmacology (drugs that target ion channels, beta-blockers, calcium channel blockers). Capillary exchange ties into the respiratory unit (gas exchange at pulmonary capillaries) and fluid balance/oedema in pathophysiology.
Heart, mediastinum, cardiac muscle, contractile cells, autorhythmic cells, pacemaker cells, SA node, sinoatrial node, AV node, atrioventricular node, Bundle of His, AV bundle, Purkinje fibres, pacemaker potential, prepotential, depolarisation, repolarisation, action potential, plateau phase, refractory period, EKG, ECG, electrocardiogram, P wave, QRS complex, T wave, P-Q interval, S-T segment, Q-T interval, cardiac cycle, systole, diastole, isovolumetric contraction, isovolumetric relaxation, ventricular ejection, heart sounds, S1, S2, lub-dup, heart murmur, cardiac output, stroke volume, heart rate, EDV, ESV, ejection fraction, preload, afterload, contractility, Frank-Starling law, venous return, sympathetic, parasympathetic, vagus nerve, baroreceptor, chemoreceptor, arrhythmia, fibrillation, tachycardia, bradycardia, extrasystole, defibrillation, arteries, arterioles, capillaries, venules, veins, tunica interna, tunica media, tunica externa, continuous capillaries, fenestrated capillaries, sinusoid capillaries, diffusion, transcytosis, bulk flow, filtration, reabsorption, blood hydrostatic pressure, blood colloid osmotic pressure, blood flow, resistance, vasoconstriction, vasodilation, blood pressure, systolic pressure, diastolic pressure, pulse pressure, MAP, mean arterial pressure, sphygmomanometer, Korotkoff sounds, venous valves, respiratory pump, skeletal muscle pump, systemic circulation, pulmonary circulation, hepatic portal circulation