Physiology, Cardiac Preload


Article Author:
Erin O'Keefe


Article Editor:
Paramvir Singh


Editors In Chief:
Jesse Cole


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
4/26/2019 11:36:40 PM

Introduction

Also termed left ventricular end-diastolic pressure (LVEDP), preload is a measure of the degree of the ventricular stretch when the heart is at the end of diastole. Preload, in addition to afterload and contractility, is one of the three main factors that directly influence stroke volume (SV), the amount of blood pumped out of the heart in one cardiac cycle.[1] Affected by changes in venous tone and circulating blood volume, changes in preload directly affect stroke volume, therefore influencing cardiac output and the overall function of the heart. A thorough understanding of preload, what affects it, and how pharmacological treatments can manipulate preload is essential to understanding overall cardiac physiology.[2]

Cellular

On a cellular level, preload is related to the intrinsic properties of the actin and myosin filaments that make up the myocardial muscle. Preload determines the resting length of the cardiac muscle fibers at a given LVEDP.  Initially, when preload increases, the starting length of the muscle fibers also increases, consequentially the resting tension increases. However, the amount the muscle fibers shorten during contraction also increases correspondingly. As a result, the final length of the muscle fibers does not change dramatically.[2]

Mechanism

The effects of isolated changes in preload are best demonstrated on the pressure-volume (P-V) loop, which relates ventricular volume to the pressure inside the ventricle throughout the cardiac cycle. The P-V loop plots volume along the x-axis and pressure on the y-axis. The area of the loop is equal to the stroke volume, which refers to the amount of blood pumped out of the left ventricle in one cardiac cycle. This number is calculated as the end diastolic volume (EDV), point B, minus the end systolic volume (ESV), point A, on the graph. The effects of intramyocardial and extra myocardial events can be plotted on the P-V loop. Changes in preload are visible as movements along the line showing the end diastolic P-V relationship as shown. If afterload and contractility are held constant, an increase in preload will result in a rightward shift along this line. As a result, the EDV increases, and thus the stroke volume increases. Also, as EDV increases, the proportion of blood ejected by the heart also increases slightly; this is the ejection fraction (EF) calculated by the equation: (EDV-ESV)/EDV. The reverse is also true. A decrease in preload will result in a leftward shift down the end diastolic P-V line, and thus a decrease in EDV, stroke volume, and a slight decrease in ejection fraction.[3]

What the P-V loop doesn’t account for are the neurohormonal and reflex responses that can affect preload. For example, the activation of beta-Adrenergic receptors leads to an increase in renin and antidiuretic hormone. Consequently, there is an increase in preload via salt and water retention. Further, stimulation of beta1-adrenergic receptors specifically, increases both the inotropy and lusitropy of the heart, which results in a shift of the end diastolic P-V curve down and to the right, as the time the heart spends in diastole decreases. The sympathetic stimulation of the alpha-1 receptors in the veins causes vasoconstriction and forces more of the blood in the veins to return to the heart, increasing preload. Additionally, the release of angiotensin II stimulates the release of aldosterone from the adrenal cortex; this causes additional sodium and water retention.[3]

Related Testing

Cardiac preload can be estimated by measuring the pulmonary capillary wedge pressure (PCW) using a catheter.[1] By advancing a catheter into the right or left pulmonary artery, the catheter will be fed into the smaller pulmonary artery branches and block blood flow briefly. This blockage creates a stagnant area of blood flow between the catheter tip and the pulmonary venous system which feeds into the left atrium. Thus, the pressure recorded from the catheter in this placement gives an estimate of the pressure of the left atrium known as the PCW. In a healthy heart, since the left atrium and left ventricle share a similar pressure during diastole, as blood flows freely across the mitral valve from the LA to the LV, the PCW can also be used to estimate the LV diastolic pressure; this is a measurement of preload.[4]

Pathophysiology

As demonstrated by the pressure-volume loops, left ventricular myocardial function is determined by the combination of preload, afterload, and contractility. Thus, changes in preload are associated with a myriad of different clinical scenarios.[3]

Increases in preload, as demonstrated through an elevated PCW, are seen in several conditions such as heart failure, mitral stenosis, and mitral regurgitation. At higher preloads, the heart also has an increased oxygen demand, further debilitating the already diseased heart.  In the case of heart failure, eventually the heart cannot keep up with the increased load, and deleterious ventricular remodeling and loss of function ensue.[2]

Abnormally low preload is associated with several related pathologies including distributive and hypovolemic shock. For example, in the beginning, phases of sepsis, a hypovolemic state, induced by the capillary leak and low vascular resistance, can lead to low preload and afterload. A similar response occurs in the setting of hemorrhage. Severe blood loss leads to a decrease in circulating blood volume and consequently decreases the amount of blood returning to the heart, which accounts for the reduction in stroke work and cardiac output seen in this setting.[5]

Clinical Significance

A variety of commonly used medications affect cardiac preload. These are some of the first-line treatments for heart failure, myocardial ischemia, and hypertension. Drugs that decrease preload and the mechanism by which they work are detailed below[1][6][7][8][9][8][7][6][1]:

  • Angiotensin-converting enzyme (ACE) inhibitors – interrupts the RAAS system
  • Angiotensin receptor blockers (ARBs) - interrupts the RAAS system
  • Nitrates – causes nitric oxide-induced vasodilation
  • Diuretics – promotes the elimination of salt and water resulting in a decreased overall intravascular volume
  • Calcium Channel Blockers – blocks calcium-induced vasoconstriction and decreases cardiac contractility

These drugs have utility in cases such as the acute management of heart failure where the goal is to reduce the volume of blood the failing heart has to pump. By decreasing the volume overload experienced by the patient, using one or more of the above-listed medications, symptoms such as dyspnea and edema can improve rapidly. Long term, use of ACE Inhibitors or ARBs has been shown to lower mortality in chronic heart failure patients by decreasing the amount of filling pressure in the heart and downregulating the compensatory neurohormonal stimulation [6].  In the treatment of myocardial ischemia, nitrates are used to decrease the amount of blood returning to the left ventricle, preload, by causing venous dilation. As a result, the oxygen demand of the heart decreases. This process is crucial in the treatment of ischemia.[9] A third clinical scenario in which drugs may be used to decrease preload is in the treatment of hypertension. Specifically, one of the most effective IV medications for the treatment of hypertensive emergencies is sodium nitroprusside.[7]

In addition, several non-pathological states may result in increased preload.[3] These include:

  • Pregnancy
  • Exercise
  • Excessive sodium intake
  • IV fluid

Finally, manipulations in preload, using several bedside maneuvers, may be useful in diagnosing murmurs associated with several different conditions. For example, rapid squatting causes an increased volume in the LV at the end of diastole. This increase in preload increases the intensity of murmurs such as aortic stenosis, mitral regurgitation, and ventricular septal defect. A later onset, signified by a click, will be heard in mitral valve prolapse. In contrast, maneuvers that decrease preload, such as the Valsalva maneuver or standing up, increase the intensity of hypertrophic cardiomyopathy and cause an earlier onset in the click heard in mitral valve prolapse.[10]


  • Image 9930 Not availableImage 9930 Not available
    Image courtesy S Bhimji MD
Attributed To: Image courtesy S Bhimji MD

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Physiology, Cardiac Preload - Questions

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A patient presents to the clinic with an acute exacerbation of heart failure after claiming he ran out of his medication for the past two weeks. The patient is having difficulty understanding why taking his medication is crucial, and explains he thinks it's ok to "skip a few days here and there." To encourage him to get back on track, he is educated as to the mechanism by which his heart "doesn't work as well." What is the consequence of decreased left atrial function in this patient with chronic heart failure?



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Which of the following is the main determinant of myocardial fiber length?



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A patient presents with chest pain radiating to her back and skin cool to the touch. She is hypotensive, her heart rate is 110 bpm, and respirations 22 breaths per minute. Her neck veins look distended. Echocardiogram confirms the suspicion of cardiac tamponade. What determinate of preload is decreased in this scenario?



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A catheter is advanced into the pulmonary artery and fed into the smaller pulmonary artery branches, occluding blood flow distal to the tip of the catheter. The pulmonary capillary wedge pressure, an estimate of the left atrial pressure, is measured. In a normal heart, this pressure is approximately equivalent to the left ventricular end diastolic pressure. A change in which of the following would not be affected by a change in the pressure being measured in this procedure?



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A patient comes into the emergency department with a blood pressure of 190/130 mmHg. The provider immediately gives a medication to decrease the patient's blood pressure. Which medication, properly matched to its mechanism, could be used in this scenario?



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After complaining of severe chest pain during practice, a young high school athlete undergoes screening for heart disease and is found to have an abnormally thick myocardium, especially of the septum, thereby restricting his left ventricular outflow tract. The intensity of the noise of this murmur may be increased by which of the following maneuvers?



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Physiology, Cardiac Preload - References

References

Fukuta H,Little WC, The cardiac cycle and the physiologic basis of left ventricular contraction, ejection, relaxation, and filling. Heart failure clinics. 2008 Jan;     [PubMed]
Sheth PJ,Danton GH,Siegel Y,Kardon RE,Infante JC Jr,Ghersin E,Fishman JE, Cardiac Physiology for Radiologists: Review of Relevant Physiology for Interpretation of Cardiac MR Imaging and CT. Radiographics : a review publication of the Radiological Society of North America, Inc. 2015 Sep-Oct;     [PubMed]
Villars PS,Hamlin SK,Shaw AD,Kanusky JT, Role of diastole in left ventricular function, I: Biochemical and biomechanical events. American journal of critical care : an official publication, American Association of Critical-Care Nurses. 2004 Sep;     [PubMed]
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Kreimeier U, Pathophysiology of fluid imbalance. Critical care (London, England). 2000;     [PubMed]
Miller AJ,Arnold AC, The renin-angiotensin system in cardiovascular autonomic control: recent developments and clinical implications. Clinical autonomic research : official journal of the Clinical Autonomic Research Society. 2018 Nov 9;     [PubMed]
Walter U,Waldmann R,Nieberding M, Intracellular mechanism of action of vasodilators. European heart journal. 1988 Jun;     [PubMed]
Oh GC,Lee HY,Chung WJ,Youn HJ,Cho EJ,Sung KC,Chae SC,Yoo BS,Park CG,Hong SJ,Kim YK,Hong TJ,Choi DJ,Hyun MS,Ha JW,Kim YJ,Ahn Y,Cho MC,Kim SG,Shin J,Park S,Sohn IS,Kim CJ, Comparison of effects between calcium channel blocker and diuretics in combination with angiotensin II receptor blocker on 24-h central blood pressure and vascular hemodynamic parameters in hypertensive patients: study design for a multicenter, double-blinded, active-controlled, phase 4, randomized trial. Clinical hypertension. 2017;     [PubMed]
Lu L,Liu M,Sun R,Zheng Y,Zhang P, Myocardial Infarction: Symptoms and Treatments. Cell biochemistry and biophysics. 2015 Jul;     [PubMed]
Frank JE,Jacobe KM, Evaluation and management of heart murmurs in children. American family physician. 2011 Oct 1;     [PubMed]

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