Objective. Students will describe the phases of the cardiac cycle in sequence, explain the pressure changes that open and close each valve, and define stroke volume and cardiac output in measurable terms.
This lesson, its worked examples and its practice questions has not yet been verified by a licensed clinician in the field or by a certification or approval body. It is a study draft and may contain errors. Do not use it to make decisions about any patient or medication. Always follow your instructor, your supervising professional, and current official references and regulations.
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Every heartbeat is the result of a precisely timed sequence of electrical and mechanical events. As an EKG technician, you record the electrical side of this cycle. Understanding the mechanical side — what the heart is actually doing with pressure and blood volume at each moment — helps you connect the waves on a tracing to real events inside the heart.
Systole is the phase of contraction. During systole, the ventricles squeeze and eject blood into the great vessels. Pressure inside the ventricles rises sharply.
Diastole is the phase of relaxation. During diastole, the ventricles refill with blood from the atria. Pressure inside the ventricles falls and remains relatively low.
These two phases alternate continuously. At a normal resting heart rate, diastole is longer than systole, which gives the heart time to fill adequately before the next contraction.
A useful tool for visualizing these events together is the Wiggers diagram, a graph that plots pressure changes in the aorta, left ventricle, and left atrium over time, alongside ventricular volume and the ECG waveform.
The left ventricular cycle proceeds through the following key phases:
1. Late diastole (ventricular filling): The mitral valve is open. Blood flows passively from the left atrium into the left ventricle. Ventricular volume rises to its maximum — the end-diastolic volume (EDV). Atrial contraction (corresponding to the P wave on the EKG) adds a final boost of blood into the ventricle.
2. Isovolumetric contraction: The ventricle begins to contract after electrical depolarization (QRS complex). Ventricular pressure rises rapidly. Both the mitral valve and aortic valve are closed — no blood leaves or enters — so volume stays constant. This phase ends when ventricular pressure exceeds aortic pressure.
3. Ventricular ejection: Rising ventricular pressure forces the aortic valve open. Blood is ejected into the aorta. Ventricular volume falls to its minimum — the end-systolic volume (ESV). The T wave on the EKG corresponds to ventricular repolarization during this period.
4. Isovolumetric relaxation: The ventricle begins to relax. Ventricular pressure falls below aortic pressure, so the aortic valve closes (producing the dicrotic notch visible on the aortic pressure curve). The mitral valve has not yet opened. Again, both valves are closed and volume is constant.
5. Ventricular filling (diastole again): When ventricular pressure falls below atrial pressure, the mitral valve opens and filling begins once more, starting the cycle over.
The same sequence occurs on the right side of the heart through the tricuspid and pulmonic valves, at lower pressures.
Cardiac valves are passive structures — they open and close in response to pressure gradients, not muscles pulling on them.
Remember this principle: blood flows from high pressure to low pressure, and valves simply follow.
Stroke volume (SV) is the volume of blood ejected by one ventricle in a single beat. It equals the difference between end-diastolic volume and end-systolic volume:
> SV = EDV − ESV
A typical resting stroke volume is approximately 70 mL, though normal ranges vary by individual.
Cardiac output (CO) is the total volume of blood pumped by one ventricle per minute:
> CO = Heart Rate (HR) × Stroke Volume (SV)
At rest, a heart rate of 72 beats per minute and a stroke volume of 70 mL yields a cardiac output of about 5,040 mL/min (roughly 5 liters per minute) — close to the total blood volume circulating each minute.
As an EKG technician, the recording you produce directly reflects heart rate. You measure the rate from the tracing; you do not directly measure stroke volume or cardiac output. However, knowing how heart rate affects the cycle is clinically important.
When heart rate is very high — for example, 140 bpm as seen in certain tachycardias — the time spent in diastole shortens significantly. Because diastole is when the ventricle fills, a shortened diastole means less filling time, a lower end-diastolic volume, and therefore a lower stroke volume. If stroke volume drops enough, cardiac output may fall even though heart rate has risen. This is why very fast heart rates can reduce, rather than maintain, effective circulation.
Recognizing an abnormally fast rate on a tracing and reporting it promptly to the supervising clinician is part of your scope of practice and supports patient safety.
Scope of practice for EKG technicians does not include diagnosing arrhythmias or making treatment decisions. Your role is to obtain a high-quality tracing and report significant findings — such as an unexpectedly rapid or irregular rate — to the nurse or physician immediately. Never delay alerting a clinician when a tracing shows an acutely abnormal rate or rhythm.
Answer each question, then check it. Nothing is recorded; this is your own practice.
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