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Physiology, Afterload Reduction

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Author: [Philip LaCombe](/content/point-of-care/17279#/ ""/index.html)Author: [Muhammad Ali Tariq](/content/point-of-care/17279#/ ""/index.html)Editor: [Sarah L. Lappin](/content/point-of-care/17279#/ ""/index.html)Updated: 4/24/2023 12:27:30 PM

Introduction

The systolic performance of the heart is determined by 3 factors: preload, afterload, and contractility. The direct relationship between preload and cardiac output was formulated in the early 1900s based on the work of Otto Frank and Ernest Starling. It led to the well-known Frank-Starling curves. Gordon et al. helped elucidate the underlying mechanism of this phenomenon in their 1966 experiments on sarcomere length-tension relationships. During this same period, extensive research demonstrated an inverse relationship between afterload and systolic performance, a relationship now widely accepted. This means that cardiac output decreases as afterload increases, and vice versa. Despite this simple concept, there has been substantial controversy over the best way to represent cardiac afterload.

The afterload of any contracting muscle is defined as the total force opposing sarcomere shortening, minus the stretching force present before contraction. Applying this definition to the heart, afterload can be most easily described as the "load" against which the heart ejects blood. The load on individual fibers can be expressed as left ventricular wall stress, which is proportional to [(left ventricular pressure x left ventricular radius)/ left ventricular wall thickness], or [(P x r)/h]. However, the true equation is complex because it depends on the shape of the cardiac chamber, which is affected by several factors that are changing over time. Therefore, afterload cannot be represented by a single numerical value or described only in terms of pressure. Arterial pressure (diastolic, mean, or systolic) is frequently used as a surrogate measure, but perhaps the best available techniques involve measuring systemic arterial resistance by various invasive and noninvasive methods. Several mathematical models have been developed using arterial impedance and pressure-flow relationships to better characterize afterload, but they are complex and less commonly used in practice. The inverse relationship between afterload and cardiac output is important in understanding the pathophysiology and treatment of several diseases, including aortic stenosis, systemic hypertension, and congestive heart failure. [[1]](/content/point-of-care/17279#ref_30757937 ""/index.html) [[2]](/content/point-of-care/17279#ref_30370283 ""/index.html) [[3]](/content/point-of-care/17279#ref_29478124 ""/index.html)

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Function

Afterload is the pressure the heart must generate to eject blood during ventricular contraction. This is recorded as the heart's systolic pressure. Changes in afterload affect stroke volume, end-systolic volume, end-diastolic volume, and left ventricular end-diastolic pressure. Afterload increases due to increased systemic vascular resistance and aortic pressure. An increase in afterload decreases stroke volume and increases end-systolic volume. This also indirectly affects cardiac output due to reduced stroke volume. A Frank-Starling curve gives a relationship between stroke volume and left ventricular end-diastolic pressure. Pressure-volume loops illustrate the effects of afterload on end-systolic and end-diastolic volumes. [[4]](/content/point-of-care/17279#ref_32059631 ""/index.html) [[5]](/content/point-of-care/17279#ref_32280417 ""/index.html)

Mechanism

The relationship between afterload and cardiac output is somewhat intuitive, as one would expect the flow to increase as the load against which the heart contracts decreases. Several researchers during the 1960s and 1970s sought to develop this understanding at the cellular level. Experiments by Sonnenblick on isolated cat papillary muscle strips demonstrated that the extent and velocity of muscle shortening decrease as the load on the muscle is increased. A major limitation of this study was its basic design, which employed isolated muscle strips. Monroe and French overcame this by using isolated whole-preparation dog hearts to show an inverse relationship between peak aortic flow and arterial impedance. Ross et al. took this 1 step further and examined the effects of changing left ventricular afterload in anesthetized dogs by injecting or withdrawing blood from the aorta between systolic contractions. They reported findings similar to those of previous studies, providing further support for an inverse relationship between afterload and cardiac output due to alterations in sarcomere shortening. Figure 1 is a graphic representation of the effect of increases or decreases in afterload on cardiac output, illustrated by shifting the baseline Frank-Starling curve downward or upward, respectively. [[6]](/content/point-of-care/17279#ref_29189934 ""/index.html) [[7]](/content/point-of-care/17279#ref_29154423 ""/index.html) [[8]](/content/point-of-care/17279#ref_29077636 ""/index.html)

Clinical Significance

Conditions in which there are chronic elevations in afterload, such as aortic stenosis and systemic hypertension, generate a cascade of adaptive responses, which can be both beneficial and ultimately detrimental. Initially, cardiac output is maintained through various regulatory mediators that increase inotropy. However, the ventricle responds to chronic elevations in afterload with concentric hypertrophy, leading to increased wall thickness and decreased chamber diameter. This reduces internal wall stress at the expense of ventricular compliance, leading to diastolic dysfunction (heart failure with preserved ejection fraction), which can further deteriorate into systolic dysfunction (heart failure with reduced ejection fraction). [[9]](/content/point-of-care/17279#ref_29047083 ""/index.html) [[10]](/content/point-of-care/17279#ref_29056408 ""/index.html)

Afterload reduction agents are an essential component in treating congestive heart failure with reduced ejection fraction, as these patients have elevated systemic resistance due to the neurohormonal response to the decreased cardiac output. They are also frequently used in the management of systemic hypertension. These drugs typically act by dilating the arterial system, thereby reducing the total load on the contracting heart and improving systolic performance. Arterial dilators fall under the broader category of vasodilators, which include arterial, venous, and mixed-acting drugs. Venous dilators reduce preload by increasing blood pooling in the highly compliant venous system and are an important part of the treatment of angina. The preload-reducing properties of venodilators lead to decreased cardiac output and arterial pressure. Most drugs have mixed arterial and venous action, and the relative balance between these determines the effect on cardiac output. [[11]](/content/point-of-care/17279#ref_26463987 ""/index.html)

Several classes of vasodilators are frequently used in practice and deserve a brief mention of their mechanism:

  1. Ace Inhibitors are one of the first-line medications for managing hypertension and improving mortality in congestive heart failure with reduced ejection fraction. Their exact mechanism in CHF is considered complex, but it is accepted that they inhibit the formation of angiotensin II, thereby decreasing vascular tone and improving systolic function. ACE inhibitors also prevent the formation of aldosterone, mediated by angiotensin II, thereby decreasing preload by reducing sodium and water reabsorption.
  2. Nitroglycerin, isosorbide dinitrate/ mononitrate, and sodium nitroprusside belong to a subclass of vasodilators known as nitrodilators that work by increasing nitric oxide within the vascular smooth muscle and play a pivotal role in the management of angina and myocardial infarction. Nitric oxide activates guanylyl cyclase, leading to cGMP formation, which induces vascular relaxation through several mechanisms: decreasing intracellular calcium, activating potassium channels, inducing hyperpolarization, and activating cGMP-dependent protein kinase, which activates myosin light chain phosphatase. Nitroglycerin and isosorbide dinitrate/mononitrate are considered organic nitrates because enzymatic conversion is required to generate nitric oxide, and they act primarily on the venous system to reduce preload with limited arterial dilation. Sodium nitroprusside is slightly different in that it releases nitric oxide without undergoing enzymatic conversion. It acts primarily on the arterial resistance vessels, which provide useful afterload-reducing properties in hypertensive emergencies and severe heart failure. [[12]](/content/point-of-care/17279#ref_32303182 ""/index.html)
  3. Hydralazine provides powerful afterload-reducing properties and is thought to act solely as an arterial dilator through direct action on the vascular endothelium, leading to nitric oxide generation. The full mechanism of hydralazine is complex and not completely understood.
  4. Sympatholytics include alpha-1-selective (prazosin) and non-selective alpha-blockers (phenoxybenzamine), which are used to manage primary hypertension or a hypertensive emergency secondary to pheochromocytoma, respectively. Sympatholytics reduce afterload by inhibiting norepinephrine binding to post-junctional alpha receptors, preventing smooth muscle contraction. The effect is more significant on the arterial system, but they also have some venodilating properties.
  5. Dihydropyridine calcium channel blockers also affect the peripheral vessels. They act by inhibiting the movement of calcium ions into the vascular smooth muscle cells. This has a vasodilatory effect on the vessels, leading to decreased systemic vascular resistance. [[13]](/content/point-of-care/17279#ref_32323339 ""/index.html)

Media

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Frank-Starling Curve. Contributed by P LaCombe, MD

References

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Jain P, Hayward CS. Afterload Sensitivity of Continuous-Flow Left Ventricular Assist Devices and Abolition of Frank-Starling Forces Under Strain. Circulation. Heart failure. 2020 Feb:13(2):e006787. doi: 10.1161/CIRCHEARTFAILURE.119.006787. Epub 2020 Feb 14 [PubMed PMID: 32059631]

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Salgado BC, Bhimaraj A. Physiological Concepts of Cardiogenic Shock Using Pressure-Volume Loop Simulations: A Case-Based Review. Methodist DeBakey cardiovascular journal. 2020 Jan-Mar:16(1):43-49. doi: 10.14797/mdcj-16-1-43. Epub [PubMed PMID: 32280417]

Level 3 (low-level) evidence

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Avendaño-Pérez L, Soto ME, Ávila-Vanzzini N, Bracamontes-Castelo G, Ruán-Díaz JC, Alexanderson-Rosas E, Espinola-Zavaleta N. Mechanical deformation in adult patients with unrepaired aortic coarctation. The international journal of cardiovascular imaging. 2018 May:34(5):735-741. doi: 10.1007/s10554-017-1286-9. Epub 2017 Nov 30 [PubMed PMID: 29189934]

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Schotola H, Sossalla ST, Renner A, Gummert J, Danner BC, Schott P, Toischer K. The contractile adaption to preload depends on the amount of afterload. ESC heart failure. 2017 Nov:4(4):468-478. doi: 10.1002/ehf2.12164. Epub 2017 Apr 19 [PubMed PMID: 29154423]

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Howden EJ, Carrick-Ranson G, Sarma S, Hieda M, Fujimoto N, Levine BD. Effects of Sedentary Aging and Lifelong Exercise on Left Ventricular Systolic Function. Medicine and science in sports and exercise. 2018 Mar:50(3):494-501. doi: 10.1249/MSS.0000000000001464. Epub [PubMed PMID: 29077636]

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Jernigan NL, Resta TC, Gonzalez Bosc LV. Altered Redox Balance in the Development of Chronic Hypoxia-induced Pulmonary Hypertension. Advances in experimental medicine and biology. 2017:967():83-103. doi: 10.1007/978-3-319-63245-2_7. Epub [PubMed PMID: 29047083]

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Negishi K, Borowski AG, Popović ZB, Greenberg NL, Martin DS, Bungo MW, Levine BD, Thomas JD. Effect of Gravitational Gradients on Cardiac Filling and Performance. Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography. 2017 Dec:30(12):1180-1188. doi: 10.1016/j.echo.2017.08.005. Epub 2017 Oct 19 [PubMed PMID: 29056408]

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Mills KI, Costello JM, Almodovar MC. A Review of Systemic Vasodilators in Low Cardiac Output Syndrome Following Pediatric Cardiac Surgery. Current vascular pharmacology. 2016:14(1):29-36 [PubMed PMID: 26463987]

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Zayed M, Nassar H, Hasanin A, Saleh AH, Hassan P, Saad D, Mahmoud S, Abo Bakr G, Fouad E, Saleh N, Ismail M, El-Hadi H. Effects of nitroglycerin versus labetalol on peripheral perfusion during deliberate hypotension for sinus endoscopic surgery: a randomized, controlled, double-blinded trial. BMC anesthesiology. 2020 Apr 17:20(1):85. doi: 10.1186/s12871-020-01006-w. Epub 2020 Apr 17 [PubMed PMID: 32303182]

Level 1 (high-level) evidence

[13]

Naseratun N, Kobara M, Watanabe Y, Toba H, Nakata T. Comparison of effects of L/N-type and L-type calcium channel blockers on post-infarct cardiac remodelling in spontaneously hypertensive rats. Clinical and experimental pharmacology & physiology. 2020 Sep:47(9):1545-1553. doi: 10.1111/1440-1681.13329. Epub 2020 May 25 [PubMed PMID: 32323339]

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