Introduction

The human heart is one of life's most studied and vital organs, and there are many ways to describe its function and health status. One measure of heart function is the cardiac index. The cardiac index relies on another important parameter, cardiac output, which converts to a normalized value that accounts for the patient's body size. For example, the cardiac output of a person weighing 120 (54 kg) pounds might differ from a person weighing 220 pounds (100 kg). For this reason, cardiac output alone cannot be a reliable indicator of cardiac performance. Calculating a cardiac index helps solve this problem. The equation for the cardiac index is below with units of (Liters/minute)/(meter^2).[1][2][3]

• Cardiac Index = Cardiac Output / Body Surface Area (BSA) = (Heart Rate * Stroke Volume) / BSA

Cellular Level

Cardiac output (CO) can be further broken down as the product of stroke volume (SV), which is the blood volume ejected by 1 heartbeat, and heart rate (HR), which is the number of heartbeats per minute. Specifically, this 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, thyroid hormones), ion concentrations (eg, Ca2+, K+), body temperature, chemoreception (ie, blood oxygen levels, blood CO2 levels, and pH), and drugs (eg, beta-blockers, muscarinic antagonists, digitalis), among others. Stroke volume is affected by 3 variables: contractility, afterload, and preload (remember the mnemonic SV CAP for Stroke Volume affected by Contractility, Afterload, and Preload).[4]

At the cellular level, autonomic nerve activity or myocardial stretch changes affect cardiac output, albeit by slightly different mechanisms. To increase the heart rate, the autonomic nervous system increases sympathetic innervation and decreases vagal tone to the sinoatrial node. Sympathetic fibers also directly influence the adrenal medulla, releasing the catecholamines epinephrine (mostly) and norepinephrine. These neuronal and hormonal catecholamines influence B1-adrenergic receptors of the heart, leading to an increase in both contractility and heart rate.[2][3][5]

Discrete increases in the stretch of the myocardium, or increases in pre-load, also increase cardiac output by augmenting the myofibril - Ca2+ binding relationship. The term pre-load comes from the temporal relationship of being "pre" contraction of the myocardium. That is the load on the heart while in diastole, or its filling cycle. Specifically, stretching the muscle fibers is believed to increase troponin’s affinity for Ca2+ and decrease the space between thick and thin filaments of the cardiac muscle – ultimately leading to an increase in the number of cross-bridges that can form. This increases stroke volume and, hence, cardiac output. The exact underlying mechanism is still a topic of debate.[6][7][8]

Another variable that can profoundly affect cardiac output is the afterload, which is aptly named due to its temporal relationship with the heartbeat. Afterload then can be described as the load against which the heart must pump, or put another way, the pressure in the aorta that the heart must overcome to eject its left ventricular volume or preload. Clinical scenarios where afterload is increased include hypertension and aortic valve stenosis. An increase in afterload results in decreased stroke volume (in contrast, an increase in contractility or preload results in increased stroke volume).[9]

Organ Systems Involved

Primary organ

• The heart

Secondary organs

• The autonomic nervous system
• The endocrine system
• The vascular system

Function

The function of the cardiac index is to create a normalized value for the cardiac function, which effectively corrects the patient’s body size. The goal of the heart is to keep blood circulating at an appropriate volume to meet the current metabolic demands of the body. The cardiac output varies by body size and activity level. Generally, a normal range for cardiac output at rest is between 4.0 - 8.0 L/min, with an average of 5 L/min. During exercise, elite athletes can reach a cardiac output as high as ~40 L/min. The normal value for the cardiac index should be between 2.5 - 4.0 L/min/m^2. A value under 2.0 should raise suspicion for cardiogenic shock (characterized by <2.2 L/min/m2 with support or <1.8 L/min/m2 without support).[1][10][11]

Related Testing

The clinician has a few options for testing for the cardiac index at his or her disposal. Given the specific circumstances, necessity, and acuity of the patient's medical picture, the provider can choose from this battery of options to suit the patient's needs best. They range from non-invasive imaging techniques to highly invasive pressure readings. It bears mentioning that although noninvasive procedures are available and can provide an accurate value, there is limited evidence that the benefits of value outweigh the risks and complications of invasive procedures. Furthermore, given that there is no gold standard for measuring cardiac output and, by proxy, cardiac index, caution should be taken to pick the appropriate tests after weighing the motives for testing, goals of testing, and patient condition.[12][13]

Cardiac Output

Noninvasive 

• Doppler ultrasound 
  • Uses an ultrasound machine with a special probe that measures the Doppler shift in the returning ultrasound waves to decipher the blood flow rate and volume, both of which lead to the cardiac index
  • Benefits: relatively cheap, fast results, and non-invasive
  • Drawbacks: highly operator dependent
• Echocardiogram 
  • Uses two-dimensional ultrasound paired with Doppler shift measurements to elucidate blood flow rate and volume
  • Benefits: non-invasive, accurate (if properly trained)
  • Drawbacks: expensive, highly operator dependent
• Modified carbon dioxide Fick method
  • Utilizes the Fick principle and measures changes in CO2 elimination and end-tidal CO2 (which is a measure of atrial CO2)
  • Benefits: non-invasive, comparable accuracy to invasive methods
  • Drawbacks: can only be utilized in patients receiving mechanical ventilation and, like the other noninvasive techniques, does not provide a measurement of preload indexes
• Other noninvasive methods: cardiac magnetic resonance

Invasive

• 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 through invasive testing, commonly pulmonary artery catheterization (PAC), and subsequently calculated
  • Benefits: highly accurate
  • Drawbacks: invasive (risking infection, arrhythmias, and pulmonary artery disruption), time-consuming [14] 
• Other invasive methods: lithium dilution

BSA

While there are an array of methods for calculating the BSA, a commonly used method is the Mosteller formula where BSA = The square root of [bodyweight (kg) x height (cm) / (3600)]. The average BSA for an adult male is 1.9 and for an adult female, 1.6. Today, a cellular phone application can be used to calculate the body surface area for a patient; however, caution must be taken to ensure the correct equation is selected for the situation and patient.[15]

Pathophysiology

The pathophysiology behind cardiac index is rooted mainly in dysfunctions of the heart. These dysfunctions can be further broken down into systolic and diastolic dysfunctions.[16]

• Systolic dysfunctions (failure to pump)
  • High blood pressure (high afterload)
  • Cardiomyopathy 
  • Coronary artery disease 
  • Heart valve disease 
  • Other structural diseases, congenital or otherwise 
• Diastolic dysfunctions (inability to fill, usually secondary to other diseases)
  • Hypertrophy 
  • Sequelae of diabetes, hypertension, obesity, and inactivity
  • Other structural diseases, congenital or otherwise

Clinical Significance

The clinical significance of the cardiac index comes from the fact that it measures cardiac function that can be normalized for the patient's body habitus. This means that the clinician can gain critical insight into the patient's heart function given the variations in body type. Often, physicians need to make decisions on medications and treatment options and educate patients on prognosis given these objective parameters. For example, bedside echocardiogram monitoring in patients with septic shock can help guide the administration of vasopressors and dilators to certain patients.[17] The cardiac index's strength is that it is a number that includes a more detailed picture of how the heart is functioning relative to the body and not independently.

The cardiac index is a hemodynamic measurement used to help evaluate the different forms of shock (circulatory disorders that lead to poor tissue perfusion). There are four main forms of shock:

• Cardiogenic: Underlying heart dysfunction (eg, as a result of myocardial infarction, arrhythmias, heart failure, cardiomyopathy, myocarditis, or severe mitral/aortic regurgitation)
• Obstructive: Obstruction of the heart or its great vessels (eg, as a result of cardiac tamponade, massive pulmonary embolism, or tension pneumothorax)
• Hypovolemic: Loss of intravascular blood volume (eg, as a result of hemorrhage or non-hemorrhagic fluid loss [diarrhea, vomiting, burns, third spacing, diuresis, adrenal insufficiency])
• Distributive: Redistribution of body fluid due to vasodilation with/without capillary leakage (eg, septic or anaphylactic shock) 

One would expect a decrease in cardiac index in cardiogenic, obstructive, and hypovolemic shock. In contrast, there is usually a normal increase in cardiac index in septic and anaphylactic shock.[18]