Physiology, Cardiac Index


Article Author:
Nishil Patel


Article Editor:
Amgad Makaryus


Editors In Chief:
Michael Firstenberg
Lawrence Greiten


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Avais Raja
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Carrie Smith
Abdul Waheed
Khalid Alsayouri
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James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
4/5/2019 10:39:08 AM

Introduction

The human heart is one of the most studied and vital organs to life. There are many ways to describe the status of the heart’s function and health. One of the measures of the function used most by clinicians is the cardiac index. The cardiac index relies on another important parameter, the cardiac output, and turns it into a normalized form which accounts for the body size of the patient. For example, the cardiac output of a person who weighs 120 pounds would be expectedly different from a person who weighs 220 pounds. For this reason, a simple cardiac output alone cannot be a reliable indicator of cardiac performance. Calculating a cardiac index solves this problem.[1][2][3]

Cellular

Cardiac output (CO) can be further broken down as the product of stroke volume (SV), which is the blood volume ejected by one heartbeat, and heart rate (HR), which is the number of heartbeats per minute. Specifically, this is a measure of left ventricular output and a clinical indicator of left ventricular function. Conditions that increase heart rate or stroke volume then directly affect cardiac output. At the cellular level, increases of sympathetic tone or myocardial stretch increase cardiac output, albeit by slightly different mechanisms. Sympathetic fibers directly influence the adrenal medulla which then releases catecholamines, norepinephrine, and epinephrine. These circulating catecholamines then work their way to the receptors in the heart resulting increases in both contractility and rate.[3][2]

Discrete increases in the stretch of the myocardium, or increases in pre-load, also increase cardiac output 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 placed on the heart while in diastole, or its filling cycle. Specifically, stretching the muscle fibers increases troponin’s affinity for Ca2+ and decreases the space between thick and thin filaments of the cardiac muscle – ultimately leading to an increase in the number of cross-bridges which can form. [4][5]

Another variable that can have a profound effect on 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. 

Organ Systems Involved

  • Primary organ
    • The heart
  • Secondary organs
    • The autonomic nervous system

Function

The function of the cardiac index is to create a normalized value for the cardiac function, which effectively correctS for the patient’s body size. The units for the cardiac index are (Liters/minute)/(body surface area) measured in meters squared (m^2). 

The goal of the heart is to keep blood circulating at an appropriate volume to meet the current metabolic demand of the body. In a healthy 70 kg, male patient the cardiac output should be 4.0 - 8.0 Liters/minute. This value accounts for both resting states with very low cardiac demand on the 4.0 end and high demand states such as strenuous exercise on the 8.0 side. 

The normal value for the cardiac index should be between 2.5L/min/m^2 - 4.0L/min/m^2. With a value under 2.0 highly suspicious for cardiogenic shock.[6]

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 best suit the patient's needs. They range from non-invasive imaging techniques to highly invasive pressure readings. It bears mentioning that although non-invasive procedures are available and can provide a more accurate value, there is limited evidence that the benefits of value outweigh the risks and complications of the 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.[7][8]

Cardiac Output

Non-invasive 

  • 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 

Invasive

  • The 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 and subsequently calculated
    • Benefits: highly accurate
    • Drawbacks: invasive, time-consuming 

Body Surface Area

While there are an array of methods for calculating the BSA, the most common 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 the 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.[9]

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.[10]

  • 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 cardiac index comes from the fact that it is a measure of cardiac function that can be normalized for the patient's body habitus, which 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, treatment options and educate patients on prognosis given these objective parameters. 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. 


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Physiology, Cardiac Index - Questions

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Which of the following parameters is directly used to calculate cardiac index?



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A 72-year-old male patient is being evaluated by the cardiology team for surgical clearance. The surgeon asks basic questions as to how the patient is feeling if he is able to walk up a flight of stairs and if he has experienced any chest pain. Based on the patient’s answers, the provider is unclear whether or not the patient should go to surgery and orders objective testing. He explains to the family that if the results of the echocardiogram show a normal cardiac index, he will clear him for surgery. Which of the following is a normal cardiac index value of an adult?



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A 32-year-old female of Northern European decent comes to the emergency room with palpitations, tachycardia, and dizziness. Her father died of a heart attack when he was 50, and she is worried that she might be having one as well. Her EKG, echocardiogram, and chest x-ray showed no acute cardiopulmonary findings. She tells you that she has been worked up for “neurological problems” in the past and that she recalls her neurologist saying that her MRI showed “multiple plaques.” She cannot remember any more details as she is very anxious, you reassure her that she is not having a heart attack and that she most likely experienced an episode of autonomic instability secondary to her neurological condition, which temporarily lowered her cardiac output and caused her to faint. Which of the following cranial nerves (CN) has a direct effect on lowering the cardiac index?



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A 19-year-old female recently started a new exercise training program with the goal of competing in a bodybuilding competition. She comes to her provider to ensure that she is healthy enough to undertake this new goal. She has a past medical history of postural orthostatic tachycardia syndrome, and her provider warns her changing her body composition too quickly might put a lot of demand on her heart. In her case, an increase in which one of her body's parameters will result in a sub-optimal cardiac index reading?



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Physiology, Cardiac Index - References

References

Reynolds HR,Hochman JS, Cardiogenic shock: current concepts and improving outcomes. Circulation. 2008 Feb 5;     [PubMed]
Kovacs G,Avian A,Olschewski A,Olschewski H, Zero reference level for right heart catheterisation. The European respiratory journal. 2013 Dec;     [PubMed]
Swan HJ,Ganz W,Forrester J,Marcus H,Diamond G,Chonette D, Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter. The New England journal of medicine. 1970 Aug 27;     [PubMed]
Arnsdorf MF, The cellular basis of cardiac arrhythmias. A matrical perspective. Annals of the New York Academy of Sciences. 1990;     [PubMed]
Thygesen K,Alpert JS,Jaffe AS,Chaitman BR,Bax JJ,Morrow DA,White HD, Fourth Universal Definition of Myocardial Infarction (2018). Journal of the American College of Cardiology. 2018 Oct 30;     [PubMed]
Reddy YNV,Melenovsky V,Redfield MM,Nishimura RA,Borlaug BA, High-Output Heart Failure: A 15-Year Experience. Journal of the American College of Cardiology. 2016 Aug 2;     [PubMed]
Nishimura RA,Otto CM,Bonow RO,Carabello BA,Erwin JP 3rd,Guyton RA,O'Gara PT,Ruiz CE,Skubas NJ,Sorajja P,Sundt TM 3rd,Thomas JD, 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Journal of the American College of Cardiology. 2014 Jun 10;     [PubMed]
Godley RW,Green D,Dillon JC,Rogers EW,Feigenbaum H,Weyman AE, Reliability of two-dimensional echocardiography in assessing the severity of valvular aortic stenosis. Chest. 1981 Jun;     [PubMed]
Jaffe AS,Vasile VC,Milone M,Saenger AK,Olson KN,Apple FS, Diseased skeletal muscle: a noncardiac source of increased circulating concentrations of cardiac troponin T. Journal of the American College of Cardiology. 2011 Oct 18;     [PubMed]
Yancy CW,Jessup M,Bozkurt B,Butler J,Casey DE Jr,Drazner MH,Fonarow GC,Geraci SA,Horwich T,Januzzi JL,Johnson MR,Kasper EK,Levy WC,Masoudi FA,McBride PE,McMurray JJ,Mitchell JE,Peterson PN,Riegel B,Sam F,Stevenson LW,Tang WH,Tsai EJ,Wilkoff BL, 2013 ACCF/AHA guideline for the management of heart failure: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. 2013 Oct 15;     [PubMed]

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