Physiology, Cardiac Index

Cellular Level

Cardiac output (CO) is further determined by 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. Conditions that affect heart rate or SV 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). SV is affected by 3 variables—contractility, afterload, and preload.[1]

At the cellular level, autonomic nerve activity or myocardial stretch alterations affect cardiac output by slightly different mechanisms. To increase the heart rate, the autonomic nervous system increases sympathetic innervation and reduces vagal tone to the sinoatrial node. 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.[2][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 SV boosts cardiac output. However, the precise underlying mechanism remains a subject of ongoing debate.[5][6][7]

Another variable that profoundly impacts cardiac output is afterload, aptly named due to the 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 reduces SV, whereas an increase in contractility or preload results in an augmented SV.[8]

Organ Systems Involved

The organ systems 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 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, 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. 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. Considering the lack of a gold standard for measuring cardiac output and index, caution is recommended when selecting tests. This decision should involve consideration of testing motives, goals, and the patient's condition.[11][12]

Cardiac Output

Noninvasive imaging techniques

• Doppler ultrasound: Using a specialized probe, an ultrasound machine gauges the Doppler shift in returning ultrasound waves to determine blood flow rate and volume and assess the cardiac index. The benefits of Doppler ultrasound include affordability, fast results, and noninvasive nature. However, the drawback lies in the high dependency on operator proficiency.
• Echocardiogram: The echocardiogram uses 2-dimensional ultrasound and Doppler shift measurements to analyze blood flow rate and volume. This method is noninvasive and accurate when performed by trained professionals. However, the drawbacks include high cost and 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 main advantage is providing comparable accuracy to invasive methods. However, the method 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 quantify blood flow and velocities across chambers, valves, and shunts. Besides diagnosing cardiac conditions, cardiac MRI accurately assesses left ventricular function and cardiac output or index.[13]

Invasive techniques

• The oxygen Fick method: This method uses the Fick equation (VO₂)/(CaO₂₋CvO₂) to calculate the cardiac output numerically. The individual variables, typically pulmonary artery catheterization (PAC), are measured via invasive procedures. Although providing exceptional precision, the method is invasive, time-consuming, and carries risks of infection, arrhythmias, and pulmonary artery disruption.
• Lithium dilution cardiac output: 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 3 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 monitor hemodynamic parameters, updating every 20 seconds. These parameters include CO/cardiac index, SV, stroke volume variation, 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 data has drawbacks. For instance, readings are inaccurate in patients with advanced liver disease, septic shock, and conditions causing decreased vascular tone. Similarly, 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.[16][17]

Body Surface Area

Among the methods available for calculating the body surface area (BSA), the Mosteller formula is frequently utilized, which is expressed as:

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

The average BSA for adult men is 1.9 and 1.6 for women. Smartphone applications can calculate BSA for patients; however, caution must be exercised to select the appropriate equation for the clinical encounter 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.

• 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, resulting 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 [19]

Clinical Significance

The clinical significance of the cardiac index arises from the measurement of cardiac function normalized to the patient's body habitus. Considering the diverse body types, clinicians can gain crucial insights into 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. The cardiac index provides a comprehensive understanding of how the heart functions relative to the body rather than in isolation.[20]

The cardiac index is a hemodynamic measurement to evaluate the different forms of shock and 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

A decrease in cardiac index is expected in cardiogenic, obstructive, and hypovolemic shock. In contrast, an 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] 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]