Introduction

The human heart is among life's most studied and vital organs, with numerous methods to delineate its function and health status. One such measure of heart function is the cardiac index, which relies on another important parameter—cardiac output. This output converts to a normalized value that accounts for the patient's body size.

For example, the cardiac output of an individual with a body weight of 120 pounds (54 kg) may contrast with that of a person with a body weight of 220 pounds (100 kg). Hence, cardiac output alone cannot be a reliable indicator in gauging cardiac performance. Calculating the cardiac index helps solve this problem.

The equation for the cardiac index is mentioned below and is denoted in units of (L/min) / (m²):

Cardiac index = cardiac output / body surface area (BSA) = (heart rate x stroke volume) / BSA

Cellular Level

Cardiac output (CO) is further broken down as the product of stroke volume (SV), which is the blood volume ejected by a heartbeat, and heart rate (HR), which is the number of heartbeats per minute. Specifically, this metric measures left ventricular output and is a clinical indicator of left ventricular function. Therefore, conditions that affect heart rate or stroke volume directly affect cardiac output. Heart rate is influenced by multiple factors, including neuronal and hormonal input (eg, norepinephrine, epinephrine, acetylcholine, and thyroid hormones), ion concentrations (eg, Ca²⁺ and K⁺), body temperature, chemoreception (ie, blood oxygen levels, blood CO₂ levels, and pH), and drugs (eg, β-blockers, muscarinic antagonists, and digitalis). Stroke volume is affected by 3 variables—contractility, afterload, and preload. A useful mnemonic is stroke volume coronary arterial pressure (CAP) for stroke volume affected by contractility, afterload, and preload.[1]

At the cellular level, alterations in autonomic nerve activity or myocardial stretch affect cardiac output, albeit by slightly different mechanisms. To increase the heart rate, the autonomic nervous system increases sympathetic innervation and reduces vagal tone to the sinoatrial node.[2] In addition, sympathetic fibers directly influence the adrenal medulla, prompting the release of catecholamines, predominantly epinephrine, and norepinephrine. These neuronal and hormonal catecholamines influence β1-adrenergic receptors of the heart, leading to increased contractility and heart rate.[3][4]

Discrete increases in the stretch of the myocardium, or increases in preload, also increase cardiac output by augmenting the relationship between myofibril and Ca²⁺ binding. The term "preload" derives from the temporal association with the myocardium being "pre" contraction, representing the load on the heart during diastole or the filling cycle. Specifically, stretching the muscle fibers is believed to increase troponin's affinity for calcium and decrease the space between thick and thin filaments of the cardiac muscle, increasing cross-bridges. This elevation in stroke volume consequently boosts cardiac output. However, the precise underlying mechanism remains a subject of ongoing debate.[5][6][7]

Another variable with a profound impact on cardiac output is "afterload," aptly named due to its temporal relationship with the heartbeat. Afterload refers to the load or resistance against which the heart must pump, or conversely, the pressure in the aorta that the heart needs to overcome to eject left ventricular volume, or preload. Clinical scenarios characterized by increased afterload include hypertension and aortic valve stenosis. An elevation in afterload leads to a reduction in stroke volume, whereas an increase in contractility or preload results in an augmented stroke volume.[8]

Organ Systems Involved

The organ systems that are involved include:

• Primary system: This comprises the cardiovascular system.

• Secondary systems: This comprises the autonomic nervous system, the endocrine system, and the vascular system.

Function

The function of the cardiac index is to create a normalized value for the cardiac function, adjusting for the patient's body size. The heart's objective is to maintain blood circulation at an adequate volume to fulfill the body's current metabolic demands. Cardiac output varies depending on body size and activity level. Generally, the cardiac output at rest falls within a range of 4 to 8 L/min, averaging around 5 L/min. During intense physical activity, elite athletes can achieve cardiac outputs as high as approximately 40 L/min. The normal cardiac index value should range between 2.5 and 4 L/min/m². A value less than 2 should raise suspicion for cardiogenic shock, which is characterized by <2.2 L/min/m² with support or <1.8 L/min/m² without support.[9][10]

Related Testing

Clinicians have a few options for assessing the cardiac index at their disposal. Depending on the specific circumstances, necessity, and severity of the patient's condition, a clinician can select from a range of options to best meet the patient's requirements. These options range from noninvasive imaging techniques to highly invasive pressure readings. Noninvasive procedures are readily accessible and can provide accurate values, with limited evidence suggesting that their benefits outweigh the risks and complications associated with invasive procedures. Furthermore, considering the absence of a gold standard for measuring cardiac output and, consequently, cardiac index, caution is recommended when selecting appropriate tests. This decision should involve careful consideration of testing motives, goals, and the patient's condition.[11][12]

Cardiac Output

Noninvasive imaging techniques: These techniques are listed below.

• Doppler ultrasound: Using a specialized probe, an ultrasound machine gauges the Doppler shift in returning ultrasound waves to determine blood flow rate and volume, thereby assessing the cardiac index. The benefits of Doppler ultrasound include its affordability, fast results, and noninvasive nature. However, its drawback lies in its high dependency on operator proficiency.

• Echocardiogram: The echocardiogram uses 2-dimensional ultrasound in conjunction with Doppler shift measurements to analyze blood flow rate and volume. The benefits of this method include being noninvasive and accurate when performed by trained professionals. However, its drawbacks include high cost and a significant reliance on operator skills.

• Modified CO₂ Fick method: This method applies the Fick principle and measures changes in CO₂ elimination and end-tidal CO₂, indicative of atrial CO₂. The advantages of this method include being noninvasive, offering comparable accuracy to invasive methods. However, it is limited to patients under mechanical ventilation and lacks measurement of preload indexes, similar to other noninvasive techniques.

• Cardiac Magnetic Resonance Imaging (MRI): A cardiac MRI offers a comprehensive evaluation of cardiovascular diseases, including cardiomyopathy, ischemic heart disease, congenital anomalies, valvular disorders, and pericardial diseases. This imaging modality uses high-definition flow imaging to precisely quantify blood flow and velocities across chambers, valves, and shunts. Besides diagnosing cardiac conditions, cardiac MRI accurately assesses left ventricular function and cardiac output/index.[13]

Invasive techniques: These techniques are listed below.

• The oxygen Fick method: This method uses the Fick equation (VO₂) / (CaO₂₋CvO₂) to calculate the cardiac output numerically. The individual variables in the equation are measured via invasive procedures, typically pulmonary artery catheterization (PAC), and then calculated subsequently. Although this method boasts exceptional precision in cardiac output calculation, it is invasive and carries risks of infection, arrhythmias, and pulmonary artery disruption. This is also a time-consuming method.

• Lithium dilution cardiac output (LiDCO): This technique measures cardiac output by utilizing a specialized sensor connected to an existing arterial line, central line, or peripheral venous line. Following the placement of the line, intravenous injection of lithium chloride ensues, and a lithium-sensitive electrode generates a lithium dilution curve for deriving cardiac output. Multiple studies indicate the necessity of averaging three lithium dilution measurements for accurate cardiac output assessment.[14][15]

FloTrac

The FloTrac is a minimally invasive device used in an acute care setting. The device utilizes arterial line waveform analysis to continuously monitor various hemodynamic parameters, updating every 20 seconds. These parameters include cardiac output (CO)/cardiac index (CI), stroke volume (SV), stroke volume variation (SVV), and systemic vascular resistance (SVR). This device utilizes a specialized sensor that attaches to an inserted arterial line to obtain pressure readings. Although the FloTrac device offers a valuable means of assessing real-time hemodynamic status in critically ill patients post-therapeutic interventions or clinical course changes, reliance on its data has drawbacks. For instance, it proves inaccurate in patients with advanced liver disease, septic shock, and conditions causing decreased vascular tone.[16] Similarly, its accuracy diminishes in patients with low cardiac output (cardiac index <2.2 L/min/m²), as a low cardiac output state can lead to a high systemic vascular resistance index, resulting in inaccuracies in pressure readings.[17]

Body Surface Area

Among the various methods available for calculating the BSA, the Mosteller formula is frequently utilized, which is expressed as:

BSA = The square root of (bodyweight [kg[ x height [cm] / [3600]).

On average, the BSA for adult men is 1.9, while for adult women, it is 1.6. Presently, smartphone applications are capable of calculating BSA for patients; however, caution must be exercised to select the appropriate equation for the given situation and patient.[18] 

Pathophysiology

The pathophysiology of cardiac index primarily stems from dysfunctions within the heart, which can be categorized into systolic and diastolic dysfunctions.[19]

• Systolic dysfunctions: Systolic dysfunctions, characterized by a failure to pump effectively, can arise from various conditions, including
  • High blood pressure (high afterload)
  • Cardiomyopathy 
  • Coronary artery disease 
  • Heart valve disease 
  • Other structural diseases, whether congenital or otherwise 

• Diastolic dysfunctions: Diastolic dysfunctions, characterized by an inability to fill properly, typically result in secondary effects of other diseases, including
  • Hypertrophy 
  • Sequelae of complications associated with diabetes, hypertension, obesity, and physical inactivity
  • Other structural conditions, whether congenital or otherwise

Clinical Significance

The clinical significance of the cardiac index arises from its measurement of cardiac function normalized to the patient's body habitus. Considering the diverse body types, clinicians can gain crucial insights into the patient's heart function. This understanding is pivotal as clinicians often need to make medication and treatment decisions and educate patients on prognosis based on these objective parameters. For example, bedside echocardiogram monitoring in patients with septic shock can inform the tailored administration of vasopressors and dilators.[20] The strength of the cardiac index lies in its ability to provide a comprehensive understanding of how the heart functions relative to the body rather than in isolation.

The cardiac index is a hemodynamic measurement used to evaluate the different forms of shock, which are circulatory disorders that lead to poor tissue perfusion. The 4 forms of shock are listed below.

• Cardiogenic: This shock stems from underlying heart dysfunction, such as myocardial infarction, arrhythmias, heart failure, cardiomyopathy, myocarditis, or severe mitral or aortic regurgitation.
  • Cardiac index in cardiogenic shock: Decreased
  • SVR in cardiogenic shock: Increased

• Obstructive: This shock occurs due to obstruction of the heart or the great vessels, as seen in conditions such as cardiac tamponade, massive pulmonary embolism, or tension pneumothorax.
  • Cardiac index in obstructive shock: Decreased
  • SVR in obstructive shock: Decreased

• Hypovolemic: This shock results from a loss of intravascular blood volume, which can occur due to hemorrhage or non-hemorrhagic fluid loss, such as diarrhea, vomiting, burns, third spacing, diuresis, or adrenal insufficiency.
  • Cardiac index in hypovolemic shock: Decreased
  • SVR in hypovolemic shock: Increased

• Distributive: This shock arises from the redistribution of body fluid, often due to vasodilation with or without capillary leakage, such as septic or anaphylactic shock. 
  • Cardiac index in distributive shock: Increased
  • SVR in distributive shock: Decreased

One would anticipate a decrease in cardiac index in cardiogenic, obstructive, and hypovolemic shock. In contrast, a normal increase in cardiac index in septic and anaphylactic shock is expected.[21]

Numerous studies have linked cardiac index to overall health. For instance, findings from the Framingham Heart Study revealed that individuals with a low cardiac index faced a heightened risk of developing dementia.[22] Additionally, another study examining cardiac index among organ donors identified a lower likelihood of 1-year mortality in recipients of hearts from donors with a higher cardiac index (>3.7 L/min/m²).[23]