Cardiac output is one of the most powerful bedside concepts in cardiology and critical care. It connects physiology, echocardiography, and real-time clinical decision-making, especially in unstable patients where numbers matter less than trends and response to intervention.
Cardiac output is the volume of blood pumped by the heart per minute. It reflects how effectively the heart meets the metabolic demands of the body. In simple terms, it answers a crucial question: is tissue perfusion adequate?
The physiological relationship is straightforward.
Cardiac Output = Stroke Volume × Heart Rate
What makes this concept clinically rich is how stroke volume is derived and how dynamically it changes with preload, afterload, and contractility.
Echocardiographic calculation of cardiac output relies on left ventricular outflow tract (LVOT) measurements. The LVOT is treated as a circular conduit through which blood exits the left ventricle.
First, the LVOT diameter is measured in the parasternal long-axis view during mid-systole. This is the most error-prone step, because the diameter is squared in the formula, so small inaccuracies lead to large errors in calculated output.
LVOT area = Ο × (LVOT diameter ÷ 2)²
Next, pulsed-wave Doppler is placed just proximal to the aortic valve in the apical five-chamber or long-axis view to obtain the LVOT velocity time integral (VTI). VTI represents the distance a column of blood travels during one systolic ejection.
Stroke Volume = LVOT area × LVOT VTI
Cardiac Output = Stroke Volume × Heart Rate
Among these variables, LVOT VTI is the most reproducible and clinically useful. While LVOT diameter is usually constant in an individual patient, VTI changes beat-to-beat with loading conditions and contractility. This makes VTI an excellent marker to track hemodynamic response.
Normal LVOT VTI is approximately 18–22 cm. Values below this suggest low forward flow, while higher values suggest high output states, keeping heart rate and body size in mind.
Case example 1: Undifferentiated shock in the emergency department
A 58-year-old man presents with hypotension, tachycardia, and altered sensorium. Blood pressure is 80/50 mmHg, heart rate 120/min. Clinical examination is inconclusive. Lung fields are clear, JVP is difficult to assess.
Bedside echocardiography shows a non-dilated left ventricle with preserved systolic function. LVOT diameter is measured once. LVOT VTI is only 12 cm, suggesting low stroke volume. Inferior vena cava is collapsible.
A passive leg raise is performed for 60 seconds. Repeat LVOT VTI increases to 14 cm, a rise of more than 15 percent. This confirms volume responsiveness. A cautious fluid bolus is given. Blood pressure improves and mental status clears.
In this case, LVOT VTI guided fluid therapy more safely than static measures like central venous pressure.
Case example 2: Septic shock in the ICU
A 42-year-old woman with pneumonia is on norepinephrine for septic shock. Blood pressure is maintained, but lactate remains elevated.
Baseline LVOT VTI is 19 cm, within normal range, but heart rate is 130/min, resulting in a high calculated cardiac output. Despite adequate global output, tissue hypoperfusion persists.
This highlights an important principle: normal or high cardiac output does not exclude shock. In distributive shock, maldistribution of flow and impaired oxygen extraction are dominant. Increasing fluids further would be inappropriate. Vasopressor optimization and source control become priorities.
Case example 3: Acute decompensated heart failure
A 65-year-old man with dilated cardiomyopathy presents with dyspnea and hypotension. Echocardiography shows severely reduced ejection fraction. LVOT VTI is 9 cm, indicating critically low forward flow.
After low-dose inotrope initiation, repeat VTI increases to 13 cm with improvement in urine output and mentation. This objective improvement supports continuation of inotropic support while planning definitive therapy.
Volume responsiveness and passive leg raise
Passive leg raise acts as a reversible internal fluid challenge, transferring approximately 300 ml of venous blood from the lower limbs to the central circulation. The response should be assessed within 30–90 seconds.
A patient is considered volume responsive if:
– Stroke volume or cardiac output increases by more than 15 percent
– LVOT VTI increases by more than 12–15 percent
This dynamic assessment is superior to static indices because it tests the heart’s ability to utilize additional preload without actually giving fluids.
Clinical interpretation pearls
LVOT VTI is more useful than calculated cardiac output for trending.
Always interpret values in clinical context, including heart rate, body size, and rhythm.
A low VTI with normal blood pressure may still indicate early shock.
A normal or high cardiac output does not guarantee adequate tissue perfusion.
Common pitfalls
Inaccurate LVOT diameter measurement leading to false calculations.
Incorrect Doppler sample position causing under- or overestimation of VTI.
Ignoring rhythm irregularity, especially in atrial fibrillation, where averaging multiple beats is essential.
Take-home message
Cardiac output assessment using echocardiography transforms abstract physiology into bedside decision-making. LVOT VTI, in particular, is a powerful, reproducible, and dynamic parameter that helps clinicians decide when to give fluids, when to stop, and when to escalate therapy. When integrated with clinical judgment, it improves precision, safety, and outcomes in critically ill cardiac and non-cardiac patients.
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