Cardiovascular System Notes: Conduction Pathways, ECG, Output, and Pathologies

The cardiac conduction system contains specialised myocytes (muscle cells that transduce contractile impulses).
The Sinoatrial (SA) node is located in the right atrium and acts as the pacemaker, initiating the heartbeat and setting the pace of the heart rate.

Step 1: SA node initiates the electrical signal in the wall of the right atrium.
Step 2: Internodal tract transmits the signal through the walls of the right atrium, allowing propagation toward the left atrium.
Step 3: Atrioventricular (AV) node sits between the atria and ventricles and slows the conducting impulse as it passes through the tough connective tissue in the interventricular septum.
Step 4: AV bundle (bundle of His) delays the signal to allow the atrium to contract prior to the ventricles, promoting blood flow from the atria to the ventricles.
Step 5: Bundle branches (left and right) split to carry the signal to both sides of the heart, reaching the left and right ventricular walls.
Step 6: Purkinje fibers terminate within cardiac tissue at the apex and spread the signal through the ventricular walls and papillary muscles; this is the endpoint of the conduction pathway and precedes ventricular contraction followed by relaxation and the next heartbeat.

A heartbeat at 60 beats per minute results in a signal pathway that completes about once per second:
- Each cycle involves all six steps, leading to one contraction-relaxation sequence per beat.

An ECG records electrical activity by placing skin electrodes; it detects voltage changes and records them on a chart.
The ECG trace shows waves corresponding to phases of the heartbeat:
- P wave: atrial depolarization and atrial contraction; a relatively small change in voltage potential.
- QRS complex: ventricular depolarization (contraction) and, momentarily, atrial repolarization (which occurs as ventricles depolarize but is masked by the larger ventricular signal).
- T wave: ventricular repolarization (ventricular relaxation).
The sequence is often described in order: P wave (atria depolarize), QRS complex (ventricles depolarize and atria repolarize), T wave (ventricles repolarize).

SA node initiates the signal.
P wave corresponds to atrial depolarization and atrial contraction.
Atria fully depolarize (P wave completes).
QRS complex occurs: ventricular depolarization; atria repolarize during this time.
Atria return to a relaxed repolarized state while ventricles remain depolarized.
T wave appears: ventricles repolarize and prepare for the next beat; voltage returns to baseline.

P wave = atrial depolarization.
QRS complex = ventricular depolarization (and atrial repolarization).
T wave = ventricular repolarization.
Waveforms are measured in time intervals (milliseconds) on the ECG; a common example interval useful for assessment is around $0.12 ext{ s} ext{ to } 0.20 ext{ s}$ (12–20 ms is a typical reference range for certain intervals, depending on the specific segment).
These time intervals serve as reference ranges to identify abnormalities if the signal timing is abnormal, which can indicate heart pathologies.

P wave: depolarisation of the atria, triggering atrial contraction.
QRS complex: depolarisation of the ventricles (and repolarisation of the atria).
T wave: repolarisation of the ventricles (ventricular relaxation) in preparation for the next heartbeat.
Initial resting state: heart wall is relaxed and no action potentials are being generated.
Early P wave: initiation of the heartbeat with atrial depolarization.
Completion of P wave: atria fully depolarized.
QRS: ventricles depolarize; atria repolarize.
Post-QRS: ventricles fully depolarized; atria repolarization completes, and the ECG baselines.
T wave: ventricles repolarize; baseline is restored.

The chart can show multiple parameters at the same time scale, including ECG, heart sounds, ventricular volume, aortic blood flow, and pressure.
The first heart sound (S1) occurs during systole; it is typically louder when the QRS complex occurs (ventricular contraction and blood rushing as valves close).
The second heart sound (S2) occurs during diastole; marks the end of systole and the heart preparing for filling.
Pressure dynamics: pressure is greatest when the left ventricle ejects blood through the open aortic valve (high pressure in the aorta during systole).
As the mitral valve opens and blood fills the atria, pressure in the chambers decreases.

Cardiac output (CO) is defined as:
- $CO = SV \times HR$
Resting values (typical example):
- Stroke volume (SV) ≈ 70 mL/beat
- Heart rate (HR) ≈ 70 beats/min
- Therefore, CO ≈ 5 L/min (≈ 5000 mL/min)
Distribution of resting blood flow (per minute) to tissues (approximate):
- Brain: ≈ 700 mL/min
- Coronary circulation: ≈ 225 mL/min
- Kidneys: ≈ 1000 mL/min
- Gut: ≈ 1250 mL/min
- Skeletal muscle: ≈ 1450 mL/min
- Skin: ≈ 375 mL/min

Light exercise: CO increases; main changes involve skeletal muscle blood flow increasing; brain blood flow remains essentially constant; heart rate increases slightly; skin blood flow increases due to thermoregulation (vasodilation for cooling).
Strenuous exercise: Skeletal muscle takes up a larger proportion of blood flow; heart rate and CO increase; skin blood flow remains elevated for cooling.
Maximal exercise: Skeletal muscle receives a very large proportion of total CO; skin perfusion decreases relative to muscle demand to accommodate the high muscle blood flow.

Atrial fibrillation: an irregular, often rapid heart rhythm that reduces the heart’s ability to pump blood effectively; increases the risk of blood clots forming in the atria.
Ventricular fibrillation: disordered electrical activity causing the ventricles to quiver instead of contracting normally; if not treated, the heart stops pumping blood, leading to collapse and cardiac arrest.

Real-world relevance and connections:

The conduction system ensures the heart beats in a coordinated, sequential manner, enabling efficient filling and ejection of blood.
ECG is a primary non-invasive diagnostic tool for assessing rhythm, conduction blocks, and timing abnormalities that can indicate pathologies.
Cardiac output reflects overall perfusion to tissues; its regulation is essential during rest and exercise to meet changing tissue demands.
Understanding the distribution of blood flow at rest and during exercise helps explain symptoms and performance in health and disease (e.g., during exercise, skeletal muscle demand rises, influencing CO distribution and thermoregulation).
Pathologies like atrial and ventricular fibrillation have immediate clinical significance due to their impact on cardiac output and risk of clot formation or arrest, underscoring the need for rapid recognition and treatment.