The Cardiac Cycle, ECG and Oxygen Transport

Physiology — The Cardiac Cycle, ECG and Oxygen Transport, NMC MBBS licence examination syllabus (Nepal Medical Council).

The Cardiac Cycle, the ECG and Oxygen Transport

A patient breathing 30 times a minute with a normal saturation is not reassuring. Understanding why is physiology, not monitoring.

The first physiology chapter covered the equations that explain shock, filtration and feedback. This one covers what the heart is doing beat to beat, what the ECG is actually recording, and how oxygen gets from the air to a cell — including the several situations where the monitor tells you something misleading.

The cardiac cycle: pressure decides everything

The cardiac cycle is usually taught as a sequence to memorise. It does not need to be, because one rule generates all of it:

A valve opens when the pressure behind it exceeds the pressure in front, and closes when that reverses. Valves are passive flaps. They do not decide anything — pressure does.

Work through a beat with only that rule:

The ventricle begins to contract. Pressure inside rises above the atrium, so the atrioventricular valve slams shut — and that closure is the first heart sound. The outflow valve is not yet open because aortic pressure is still higher, so for a moment the ventricle is a sealed box: pressure climbs with no change in volume.
Ventricular pressure exceeds aortic pressure. The outflow valve opens and blood is ejected. Note that the ventricle never empties completely — which is why ejection fraction is a fraction.
The ventricle relaxes and its pressure falls below the aorta. The outflow valve shuts, and that closure is the second heart sound.
Pressure falls below the atrium. The AV valve opens and filling begins, mostly passively.

Why this is worth understanding rather than memorising: it explains murmurs. A sound occurring between the first and second sounds is systolic, so it must involve either blood leaking backwards through an AV valve or forwards through a narrowed outflow valve. The timing localises the lesion without any additional facts.

What the ECG actually records

The most common misconception about the ECG is that it shows the heart contracting. It shows electrical activity only — the signal that instructs contraction, not the contraction itself.

P wave — atrial depolarisation. Absent P waves with an irregular baseline and irregular rhythm suggest atrial fibrillation.
QRS complex — ventricular depolarisation. It is the largest deflection simply because the ventricular muscle mass is largest. A wide QRS means the impulse spread slowly through muscle rather than quickly through the conducting system.
T wave — ventricular repolarisation, which is electrical recovery rather than mechanical relaxation. Tall peaked T waves are the classic early sign of hyperkalaemia.

Atrial repolarisation happens too, but it is buried inside the much larger QRS and is not seen.

💡 The clinical consequence of "electricity, not contraction" is the one that matters in an arrest: a normal-looking ECG in a patient with no pulse is still cardiac arrest. The electrical system can continue producing an orderly trace while the muscle fails to generate any output — pulseless electrical activity. You treat the patient, not the monitor. This is a favourite examination point and a real clinical trap.

No interval durations are given in this chapter, deliberately. They vary with heart rate and with the measurement convention, and the point of learning the ECG is to read the trace in front of you rather than to compare it with a remembered number.

The oxygen dissociation curve

Haemoglobin's affinity for oxygen is not constant — it increases as more oxygen binds. That produces the characteristic S-shaped curve, and the shape does two useful jobs.

The flat upper portion protects loading. Across a wide range of inspired oxygen, saturation stays high. That is why a patient can have significantly impaired gas exchange and still saturate well — and why saturation falls late.

The steep lower portion assists unloading. In tissue, where oxygen levels are low, a small further fall releases a large amount of oxygen. Delivery is therefore concentrated exactly where consumption is highest.

And the curve shifts. Acid, carbon dioxide and heat all move it to the right, which means oxygen is released more readily. Those three are precisely the local conditions of exercising or infected tissue — so the tissue working hardest automatically extracts the most oxygen, with no signalling required. That is an elegant piece of design and a reliable exam question.

Fetal haemoglobin sits to the left of the adult curve — it binds oxygen more avidly. That is how a fetus extracts oxygen from maternal blood across the placenta: at the same oxygen level, fetal haemoglobin takes it and adult haemoglobin gives it up.

When the saturation misleads

Pulse oximetry is one of the most useful bedside tools and one of the most misread. Four situations matter.

Carbon monoxide poisoning. The oximeter measures how much haemoglobin is bound, but cannot distinguish what it is bound to. Carboxyhaemoglobin is read as if it were oxygenated, so the saturation can look normal or high in a severely poisoned patient. Suspect it after smoke exposure or with faulty indoor heating, particularly when several people in one household are unwell together.

Severe anaemia. Saturation is a percentage of the haemoglobin present. If there is very little haemoglobin, every molecule can be fully loaded — 100% saturation — while total oxygen delivery is dangerously low. The first physiology chapter makes the same point from the delivery equation.

Poor perfusion. A cold, shocked or vasoconstricted finger gives an unreliable reading or none, and this happens exactly in the patients who are sickest.

And saturation says nothing about carbon dioxide. A patient who is tiring can maintain saturation while their carbon dioxide climbs — so an exhausted patient with a "normal sats" is not necessarily safe. That is why the respiratory rate and the patient's appearance matter more than the number.

Dead space and the work of breathing

Not all inspired air participates in gas exchange. The volume filling the conducting airways — the dead space — never reaches an alveolus and is exhaled unchanged. It is a roughly fixed volume with every breath, regardless of how big that breath is.

That fixed cost explains why shallow rapid breathing ventilates poorly. If each breath is small, a much greater proportion of it is wasted filling dead space, so the amount reaching the alveoli falls even though the respiratory rate has risen. The exhausted patient breathing fast and shallow is working harder and achieving less — which is why increasing respiratory rate with falling tidal volume is an ominous combination rather than a compensation.

Surfactant reduces surface tension in the alveoli, and its particular value is that it prevents the smallest alveoli from collapsing into larger ones. Without it, each breath requires enormous effort to reopen collapsed lung — which is the central problem of the preterm infant's lung, covered in the neonatal and preterm chapters.

One practical conclusion runs through all of this: the respiratory rate is the single most sensitive vital sign. It rises early in almost every serious deterioration — sepsis, acidosis, heart failure, pain — and it is the observation most often not counted properly.

Putting it together

Valves follow pressure, so the whole cardiac cycle derives from one rule — and the timing of a murmur localises the lesion.
The ECG shows electricity, not contraction, so a normal trace without a pulse is still cardiac arrest.
The curve is flat on top and steep at the bottom — loading is protected, unloading is easy, and saturation falls late.
Acid, carbon dioxide and heat shift it right, so hard-working tissue extracts more oxygen automatically.
Saturation misleads in carbon monoxide poisoning, anaemia and poor perfusion — and says nothing about carbon dioxide.
Shallow rapid breathing wastes more of each breath on dead space, so a rising rate with falling depth is deterioration.

No ECG intervals, saturation targets, partial pressures or lung volumes appear here: intervals vary with rate and convention, targets differ by condition and guideline, and volumes vary with age, sex and height. Read the trace and the patient in front of you.

Syllabus points

Valves follow pressure — deriving the cycle
The two heart sounds; timing localises a murmur
P, QRS and T — electricity, not contraction
Normal trace without a pulse is still arrest
The S-shaped curve: loading protected, unloading easy
Right shift in working tissue; fetal haemoglobin left
When saturation lies — CO, anaemia, perfusion, CO2
Dead space, shallow breathing and surfactant

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