Heart and vessels

David C. Poole , Howard H. Erickson , in Equine Sports Medicine and Surgery (Second Edition), 2014

Stroke volume

Stroke volume refers to the volume of blood ejected per beat from the left or right ventricle and increases from approximately 1000 mL (2–2.5 mL/kg) at rest up to 1700 mL (3–4 mL/kg) or higher at maximal exercise ( Table 31.6). 12,60,61,63,73 If a maximum heart rate of 225 beats/min is assumed for Secretariat, his stroke volume would have been well in excess of 2000 mL/beat. Typically, stroke volume increases sharply at exercise onset up to around 40%

consequent to increased blood volume, venous return, and filling pressures according to the Frank–Starling mechanism. 30,77 What is particularly remarkable is that ventricular filling (and thus stroke volume) does not appear to be compromised at maximal exercise despite heart rates of 4 beats/s.

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The Cardiac Function Curve

Joseph Feher , in Quantitative Human Physiology (Second Edition), 2012

Abstract

Stroke volume is defined as end-diastolic volume minus end-systolic volume; cardiac output is the stroke volume times the heart rate. The left ventricular pressure–volume loop is drawn and the work of the heart is considered as the area within the loop. Total cardiac work, however, includes the kinetic work, PV work, and gravitational work. The stretch of the heart caused by the preload determines the stroke volume. This becomes the Frank–Starling Law of the Heart. The plot of cardiac output against right atrial pressure is considered to be the cardiac function curve. The effect of afterload and preload on the PV loop is considered. The effect of sympathetic stimulation on the left ventricular pressures and the PV loop is shown. Experimental determination of cardiac output by Fick's principle and the indicator dilution method are discussed.

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The cardiovascular system

Edward M. Dzialowski , Dane A. Crossley , in Sturkie's Avian Physiology (Seventh Edition), 2022

18.5.3.2.3.2 Role of stroke volume in control of CO

Stroke volume, like heart rate, is dependent upon factors intrinsic and extrinsic to the heart. As all myocytes within the heart contract during each beat, the primary intrinsic factors which determine stroke volume are the inherent contractile properties of each muscle fiber and the resting lengths of all the fibers. The amount of force developed during contraction by a cardiac muscle fiber at a specified precontraction length is properly termed "contractility," but this term has also been used more loosely to describe the collective contractile properties of all muscle fibers associated with one chamber of the heart. A major problem in quantifying contractility is that the force developed by a single cardiac muscle fiber is difficult to measure in working hearts. Consequently, a number of indirect indices have been developed to estimate this variable. These include measuring cardiac outflow volume over time to calculate stroke volume; recording the ventricular peak systolic pressure developed against a fixed afterload or into a constant arterial pressure; and measuring the rate of rise of ventricular pressure during systole. The major assumption in all of these methods is that the measured variable reflects the contractility of all muscle fibers integrated over the dimensions of the whole chamber. However, the variety of indices of contractility used by investigators under different experimental conditions has made it difficult to compare estimates across studies. The direct measurement of volume flow from the ventricle would appear to give the most reliable index of cardiac contractility, being independent of the complicating effects of changing arterial or ventricular pressures. This measurement is also among the most difficult to make, requiring highly invasive procedures to place the appropriate instrumentation.

By analogy with the contraction of skeletal muscle, the amount of force developed by a contracting cardiac muscle fiber depends upon its precontraction length ("preload"). This principle was first applied to the heart by Otto Frank (summarized in Rushmer, 1976), who showed that, within limits, the greater the preload on ventricular muscle in diastole, the more tension was developed during the next systole. This length–tension relationship was further investigated by Ernest Starling and co-workers, who demonstrated that the amount of blood ejected by the left ventricle during systole was proportional to the volume of blood in the ventricle at the end of the diastolic filling phase of the cardiac cycle. These concepts have been combined into the Frank–Starling relationship to describe the intrinsic responses of ventricular stroke volume to changes in cardiac venous return, expressed graphically in Figure 18.30. Elevated contractility of each muscle fiber in the ventricle is evoked by increasing the preload on all of the fibers by increasing the volume of blood filling the ventricle before each beat; this is reflected in an overall increase in ventricular stroke volume. The curve designated A in Figure 18.30 is termed a ventricular function curve. The relationship embodied in this curve demonstrates an autoregulatory feature of cardiac function known as heterometric regulation: a change in the resting fiber length (heterometry) results in a change in contractility in the same direction. This regulatory mechanism is an intrinsic property of cardiac muscle. The consequence of this mechanism for the overall function of the heart is that, if all other conditions remain constant, CO will be determined by venous return. An increase in venous return to the left ventricle via the left atrium will result in greater end-diastolic stretch of the ventricle walls and an increase in stroke volume at the next beat; conversely, stroke volume will be reduced if cardiac return falls. In short, the heart "pumps what it gets" if all other factors are unchanging.

Figure 18.30. Idealized graphical representation of the Frank–Starling relationship for cardiac ventricular muscle. (A) Intrinsic ventricular function curve depicting the relationship between end-diastolic volume (representing degree of stretch of muscle fibers) and stroke volume (index of contractility) in the absence of extrinsic influences. The curve peaks and begins to decline at high end-diastolic volumes because resting sarcomere length is maximal here. (B and C) Factors extrinsic to the heart which alter inotropic function of cardiac muscle reset the ventricular function curve to operate over different ranges of stroke volume, independent of end-diastolic volume or initial fiber length. (B) Elevated cardiac sympathetic drive or circulating catecholamines have positive inotropic effects, resetting the curve toward higher stroke volumes. (C) Elevated vagal drive has negative inotropic effects, resetting the curve toward lower stroke volumes. Points 1 through 5 are the operating points assumed for the text discussion of the effects of extrinsic factors on ventricular function.

Cardiac contractility is influenced by extrinsic factors in addition to the intrinsic Frank–Starling mechanism. Circulating hormones such as EPI and the autonomic neurotransmitters NE and ACh (see Sections 18.5.3.1 and 18.5.3.2) directly affects the contractility of cardiac muscle fibers. These extrinsic factors are superimposed on the intrinsic autoregulatory factors governing stroke volume and can shift the whole ventricular function curve (curve A in Figure 18.30) toward higher (curve B) or lower (curve C) stroke volumes at the same resting muscle fiber length or degree of ventricular filling. This type of regulation of stroke volume is referred to as homeometric regulation to emphasize the fact that changes in contractility can occur independent of resting fiber length. An increase in sympathetic drive to the heart or an increase in the level of circulating catecholamines will increase ventricular inotropic function homeometrically; thus a greater stroke volume will result from the same degree of cardiac filling, as indicated in Figure 18.30 by the arrow from point 1 on curve A to point 2 on curve B. Another way to consider this is that after such a shift in the curve a much smaller end-diastolic volume will give the same stroke volume (arrow from point 1 to point 3). On the other hand, elevated vagal drive to the heart of birds can decrease the contractility of ventricular muscle and will shift the ventricular function curve toward a lower stroke volume (curve C in Figure 18.30). At the new operating point, the same degree of preload will result in a lower stroke volume (arrow from point 1 to point 4); alternatively, a much larger end-diastolic volume will be required to maintain the same stroke volume (arrow from point 1 to point 5).

The arterial pressure against which the ventricle pumps ("afterload") is a major extrinsic factor in determining the magnitude of stroke volume. The pressure generated during the isometric phase of ventricular contraction is a function of the contractility of the muscle fibers, and when chamber pressure exceeds that in the aorta the valves open and blood is ejected from the ventricle during the isotonic phase. If the preload on the ventricle is increased by elevating the arterial blood pressure without a change in contractility or end diastolic volume, stroke volume of subsequent beats will be reduced because more energy will be required to raise chamber pressure above the new level of arterial pressure. Initially, this will leave a larger fraction of the previous end-diastolic volume still in the chamber at the end of systole, resulting in an increased level of resting tension on the muscle fibers during the next filling phase. This increased tension, according to the Frank–Starling mechanism, will quickly result in increased contractility during subsequent beats, restoring stroke volume by heterometric regulation in the face of the increased arterial pressure.

In many species of birds, CO is adjusted to match perfusion requirements of the tissues in a variety of conditions, such as during exercise, hypoxia, or submersion (see Section 18.6). These adjustments appear to be made primarily through alterations in heart rate with stroke volume remaining relatively unchanged. Changes in CO during exercise are driven by increased heart rate in ducks (Bech and Nomoto, 1982; Kiley et al., 1985), geese (Fedde et al., 1989), and turkeys (Boulianne et al., 1993a,b). However, in the emu (Grubb et al., 1983) and the chicken (Barnas et al., 1985), stroke volume may increase by up to 100% during exercise, contributing significantly to elevated CO. Reflex changes in CO mediated by systemic arterial baroreceptor input also appear to operate via alterations in heart rate, leaving stroke volume relatively unchanged (Section 18.5.4.2). In summary, during exercise, hypoxia, or submersion, birds display significant changes in heart rate, arterial blood pressure, and venous return from the resting condition. In the transition from the resting condition to these altered states, stroke volume also varies. However, in most of the species examined so far, stroke volume returns to values close to those at rest after a short period of initial adjustment. This indicates that intrinsic autoregulation of CO has the potential to play an important role in the maintenance of stroke volume in the face of largescale circulatory adjustments.

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Diseases of the Cardiovascular System

In Veterinary Medicine (Eleventh Edition), 2017

Cardiac Reserve and Stroke Volume

Stroke volume is variable and depends on the amount of shortening that the myocardial fibers can attain when working against arterial pressure. It is determined by the interplay of four factors:

•

Ventricular distending or filling pressure (preload)

•

Contractility of the myocardium (inotropic state)

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The tension that the ventricular myocardium must develop during contraction and early ejection (afterload)

•

The sequence of atrial and ventricular depolarization

An increase in ventricular distending pressure (end-diastolic pressure or volume) will increase ventricular end-diastolic fiber length, which, by the Frank–Starling mechanism and stretch-dependent calcium sensitization, will result in increased stroke work and a larger stroke volume. Ventricular distending pressure is influenced by atrial contraction and is greatly augmented by increased venous return associated with exercise and increased sympathetic activity. Contractility is most influenced by adrenergic activity and circulating catecholamines. An increase in stroke volume is achieved primarily by an increase in the ejection fraction and a reduction in the end-systolic volume but can also be achieved by a decrease in afterload, which is primarily a function of aortic or pulmonary impedance (the resistance and reactance of the vasculature to ejection).

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Cardiac responses to exercise and training

David L Evans , Lesley E Young , in Cardiology of the Horse (Second Edition), 2010

Stroke volume and cardiac output

Stroke volume in the resting horse is approximately 800–900 mL, or about 2–2.5 mL/kg. 42 , 43 Stroke volume increases by about 20–50% in the transition from rest to submaximal exercise. 7,46,52,53 It does not change as intensity of exercise increases from approximately 40%

to 100%
, despite the limited time available for ventricular filling at high heart rates during exercise. 54 Stroke volumes of 2.4 mL/kg (1250 mL) 54 and 3.8 ± 0.4 mL/kg (approximately 1700 mL) 55 have been reported in fit Thoroughbreds during treadmill exercise at
. This large difference could reflect biological variation, or differences in the method of measuring oxygen uptake during the exercise test.

Values reported for cardiac output in fit Thoroughbreds during treadmill exercise at

are 534 ± 54 mL/kg/minute (277 L/minute) 54 and 789 ± 102 mL/kg/minute (355 L/minute). 55

During tethered swimming at low work loads, stroke volume decreased from 2.06 mL/kg at rest to about 1.5 mL/kg. This response may be related to decreased venous return secondary to the alterations to breathing pattern during swimming. 6

During prolonged exercise cardiac output is decreased in dehydrated horses, and this limits thermoregulation. 22 In an experiment in which horses were exercised for 40 minutes while euhydrated, or dehydrated by either withdrawal of water (DDH) or administration of furosemide (FDH), cardiac output was significantly lower in FDH (144.1 ± 8.0 L/minute) and in DDH (156.6 ± 6.9 L/minute) than in euhydrated horses (173.1 ± 6.2 L/minute) after 30 minutes of exercise (see Fig. 3.5). Dehydration resulted in higher temperatures in the middle gluteal muscle and pulmonary artery during exercise, but temperatures in the superficial thoracic vein and at subcutaneous sites on the neck and back were not significantly different. Sweating rates were also similar in control and dehydrated horses, and it was concluded that the impairment of thermoregulation was primarily due to decreased transfer of heat from core to periphery.

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The Cardiac Function Curve

Joseph Feher , in Quantitative Human Physiology, 2012

•

Define the stroke volume

•

Calculate the cardiac output from the stroke volume and heart rate

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List the determinants of the stroke volume

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On a PV diagram, identify: ventricular filling, isovolumetric contraction, ejection, isovolumetric relaxation

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List three components of cardiac work

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Describe the Frank–Starling Law of the Heart

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Define central venous pressure, preload, and afterload

•

Draw a normal, resting cardiac function curve

•

Describe what happens to stroke volume when preload is increased at constant afterload

•

Describe what happens to stroke volume when afterload is increased at constant preload

•

Describe Fick's method for estimating cardiac output

•

Describe the indicator dilution method for estimating cardiac output

•

Describe the effect of positive inotropic agents on the cardiac function curve

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Exercise and the Cardiovascular System

H.K. Hammond , in Reference Module in Biomedical Sciences, 2014

Stroke Volume

Although SV increases during upright dynamic exercise (it changes minimally if at all during swimming), its contribution to increases in CO at peak effort is relatively small. Table 1 illustrates that most of the increases in CO stems from a 2.4-fold increase in HR, with a relatively small increase (1.3-fold) in SV. It is difficult to measure SV directly in human subjects at rest, and even harder during exercise, so typically this is a calculated measure, based on CO and HR. Although HR can be precisely measured, measures of CO typically have coefficients of variation of 15% in healthy subjects, so value shown for basal SV in Table 1 (73 ml) translates to a range from 64 to 84 ml. Alterations in SV of 24 ml, the difference between basal and peak exercise in Table 1, are barely outside experimental error. To determine rigorously whether such a small change predominantly reflects in increased left ventricular (LV) end-diastolic volume (EDV) (Starling effect) or a reduction in LV end-systolic volume (ESV) (an inotropic effect) is an irresolvable matter in humans. Although magnetic resonance imaging and computed tomography have enabled resolution of relatively small changes in LV volume in human subjects, their application to upright dynamic exercise is limited. Suffice it to say that during peak exercise, increased HR is the primary means by which CO increases, and HR increases in SV are less important.

Studies using ultrasonic micrometers to measure LV volumes during maximal upright dynamic exercise in dogs confirm that increases in LV EDV during dynamic exercise are a minor contributor to increasing CO during peak effort (Vatner et al., 1972). The difficulty in demonstrating that the Starling effect is a dominant factor in the exercise response is also reported in clinical studies (Stratton et al., 1994).

HR also rises linearly with work rate and plateaus briefly right before exhaustion. Therefore, it can be used as an objective assessment of effort intensity. There is a decline in maximal HR with age, i.e., it falls about 10 beats min− 1 per decade. A useful formula provides an estimate of maximal HR:

Maximal HR = 220−age

For example, a 40-year-old subject would be predicted to attain a maximal exercise HR of 180 beats min− 1. Although more complex formulas may provide somewhat better estimates, the standard error of the estimate of these formulas is ±15 beats min− 1, providing rough but useful guidelines. Barring primary abnormalities in cardiac conduction system function or pharmacological agents that influence HR, the value of HR at maximal effort should be close to the one predicted by formula. The individual also provides a subjective assessment of whether they feel they are approaching maximal effort.

HR alone, however, is an inadequate means to increase CO. For example, a doubling of HR by atrial pacing in a supine nonexercising subject results in a halving of SV and no change in CO. A case can be made that the force–frequency effect may provide a small increase in CO in this setting, but it would be small, of the order of a 10% increase. While it is true that patients with third degree AV block with extremely low HR (<40 beats min− 1) may have increased CO with increased HR, this does not apply when basal HR is in the physiologically normal range and is then doubled by pacing. The dependence of CO on venous return is at play here, and doubling the HR by atrial pacing does not provide a means of increasing venous return, hence the fall in SV (Figure 3). In contrast, having a subject double his/her resting HR by running on a treadmill would more than double CO – SV would be maintained and likely increased somewhat (Table 1) due to increased inotropy associated with increased sympathetic activation.

Figure 3. The effect of atrial pacing in conscious resting dogs demonstrates a progressive reduction in left ventricular (LV) diameter, and hence LV volume, with increasing heart rate (HR). Increasing HR alone, without a means of increasing venous return and preload, is an ineffective means of increasing cardiac output.

 Modified from Rushmer, R.F., 1976. Cardiovascular Dynamics. W.B. Saunders Co., Philadelphia, pp. 70–112.

Oxygen consumption. Oxygen consumption (VO2) is measured in ml kg− 1 min− 1. The normal basal VO2 is 3.5 ml kg− 1 min− 1, and is referred to as 1 MET (metabolic equivalent of task) in many exercise laboratories. This is a useful index that enables one to refer to multiples of basal VO2. The VO2 at peak effort (VO2max) is a reliable and reproducible measure of aerobic fitness.

There is a 10 ml kg− 1 min− 1 decay in VO2max with each decade in life. A useful formula to predict VO2max (in METS) is

Maximal METS = 15−(age/10).

For example, a sedentary but otherwise healthy 40-year-old should be able to achieve 15−(40/10) = 11 METS at peak dynamic effort. Since 1 MET = 3.5 ml kg− 1 min− 1, this would be 11 (3.5) = 39 ml kg− 1 min− 1. By comparison, a 20-year-old sedentary subject would be anticipated to attain 2 METS more (two decades younger) or an additional 7 ml kg− 1 min− 1 for a total of 46 ml kg− 1 min− 1. If one would collect expired air on such an individual, the actual measure of VO2 would be near this value, and, for research purposes actual measurement of VO2 is preferred. However, in clinical settings, one can calculate METS based on treadmill grade and speed and estimate a subject's aerobic fitness on the basis of maximal work rate achieved. We will later examine the effects of chronic sustained dynamic exercise (training), where the hallmark of a training effect is increased VO2max. A normal (not genetically gifted) subject should be able to increase his/her VO2max by about 25% – for our 40-year-old subject with a pretraining VO2max of 39 ml kg− 1 min− 1, this would mean attaining a VO2max after training of 49 ml kg− 1 min− 1 – superior to a sedentary subject who is 20 years younger.

In contrast, the typical 40-year-old 70 kg patient with well-treated congestive heart failure, who normally would have a VO2max of 39 ml kg− 1 min− 1, would likely attain less than 50% of this value – around 20 ml kg− 1 min− 1. The primary problem would be a marked diminution in maximal CO; HR and AVO2D would be similar at peak effort. For example, using the Fick equation and assuming an AVO2D of 16 ml dl− 1, the CO associated with a VO2max of 20 ml kg− 1 min− 1in such a subject would be 8.8 l min− 1 (Figure 4), 50% of that anticipated in a normal subject of the same age and weight (Table 1). Nowhere are the physiological principles of exercise more relevant than in managing patients with cardiovascular diseases.

Figure 4. Use of Fick equation to calculate cardiac output (CO) from measured oxygen consumption (VO2) and oxygen extraction (AVO2D). Since the AVO2D at maximal effort is relatively fixed (16 ml dl− 1), VO2 is a direct correlate of CO. In clinical settings, this is quite useful, because VO2 and work rate are tightly coupled, and, therefore, maximal treadmill performance provides information about maximal heart function.

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DESIGN AND PHYSIOLOGY OF THE HEART | Cardiac Cellular Length–Tension Relationship

H.A. Shiels , in Encyclopedia of Fish Physiology, 2011

Abstract

Fish use stroke volume to adjust cardiac output. Changes in stroke volume stretch the chambers of the fish heart and invoke the Frank–Starling mechanism. This mechanism ensures the heart contracts more forcefully when it is filled with larger volumes of blood, thus propelling the blood into the circulation. Stretch of the whole heart is transduced to the individual cardiac myocytes and their composite myofilaments. Cellular stretching results in an increase in cellular contractile force due to changes in myofilament overlap and to length-dependent increases in myofilament Ca sensitivity. Fish myofilaments are more sensitive to Ca than mammalian myofilaments and demonstrate a greater length dependence of this Ca sensitivity. This property allows fish myocytes to beat forcefully at the long sarcomere lengths required to volume-modulate cardiac output of the whole heart.

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The Cardiovascular System

Erika J. Eliason , Katja Anttila , in Fish Physiology, 2017

1.4.1 Acute Responses

Cardiac stroke volume ( V S, volume of blood pumped per heart beat) is much less responsive to changes in temperature in comparison with f H. Resting V S has been reported to be insensitive to acute temperature increases in several fish species (Fig. 2): lingcod (Stevens et al., 1972); rainbow trout (Gamperl et al., 2011; Petersen et al., 2011); Chinook salmon (Clark et al., 2008); sockeye salmon (Steinhausen et al., 2008); Atlantic salmon and Arctic char (Penney et al., 2014); spiny dogfish (Sandblom et al., 2009); European sea bass (Wang et al., 2014); and European perch (Ekström et al., 2016a). However, studies have also reported moderate decreases in resting V S with warming temperatures: P. bernacchii (Axelsson et al., 1992); P. borchgrevinki (Franklin et al., 2007); M. scorpioides and M. scorpius (Gräns et al., 2013); Asian swamp eel (Lefevre et al., 2016); rainbow trout (Brodeur et al., 2001; Sandblom and Axelsson, 2007); sockeye salmon (Eliason et al., 2013); and European perch (Sandblom et al., 2016a). Finally, one study with rainbow trout found a minor, but significant, increase in resting V S (by 14%) during an acute temperature increase (Keen and Gamperl, 2012), and both Gollock et al. (2006) and Ekström et al. (2014) found no change in resting V S during acute warming until fish approached their CT max; at which time V S increased significantly, concomitant with a reduction in f H. Collectively, these studies show that that V S does not normally increase greatly with an acute increase in temperature.

Fewer studies have assessed the effects of acute increases in temperature on V S in swimming fish. Steinhausen et al. (2008) found that V S was maintained during an acute temperature increase in sockeye salmon swum at 75% of their maximum swimming speed. Similarly, V S was maintained after exhaustive exercise (i.e., a chase) across a 10°C temperature range in three species of Arctic fish (G. tricuspis, M. scorpioides, and M. scorpius) (Franklin et al., 2013). In contrast, V S decreased at high temperatures in continuously swimming yellowfin tuna, maximally swum pink salmon and sockeye salmon, and following exhaustive exercise in P. borchgrevinki and European perch (Clark et al., 2011; Eliason et al., 2013; Franklin et al., 2007; Korsmeyer et al., 1997; Sandblom et al., 2016a) (Figs. 2 and 3). Scope for V S was also unaffected by an acute temperature increase in sockeye salmon swum at 75% of their maximum (Steinhausen et al., 2008), but clearly declined at elevated temperatures when this species was swum maximally (Eliason et al., 2013 and Figs. 2 and 3). Acute temperature effects on the scope for V S also differed with acclimation temperature in P. borchgrevinki (Franklin et al., 2007). The scope for V S decreased with acute temperature increases in fish acclimated to −   1°C, while it remained unchanged in fish acclimated to 4°C (note: the scope for V S was zero at all test temperatures for 4°C acclimated fish) (Franklin et al., 2007).

Given that V S can increase more than two-fold during aerobic exercise (e.g., Eliason et al., 2013; Fig. 2), it is curious why V S does not generally increase with warming. This could be due to limitations in filling time, filling pressure, and/or contractility (Sandblom and Axelsson, 2007). Studies have repeatedly shown that as contraction frequency increases, the force of contraction decreases (termed the negative force–frequency relationship), and this is exacerbated with acute temperature increases (Shiels et al., 2002). As a result, the heart may not empty as much during contraction (Gamperl, 2011). Another strong possibility is that the heart is unable to increase its blood volume during diastole (i.e., end-diastolic volume), which would limit V S. As f H increases, filling time decreases (e.g., Sandblom and Axelsson, 2007), and this would limit the capacity of the heart to fill. In addition, V S is inextricably linked with cardiac filling pressure in fishes. A mere 0.02   kPa increase in filling pressure can double V S (Farrell et al., 2009). If cardiac filling pressure becomes compromised at warm temperatures, or cannot increase to compensate for the decrease in filling time, V S would suffer. However, this does not appear to be the case for most species studied to date. Concurrent with a decrease in V S, central venous blood pressure (P CV) was stable, venous capacitance decreased, and mean circulatory filling pressure increased during an acute moderate temperature increase from 10 to 16°C in resting rainbow trout (Sandblom and Axelsson, 2007). Similarly, central venous blood pressure was maintained and the mean circulatory filling pressure increased (but V S did not change) in resting dogfish acutely warmed from 10 to 16°C (Sandblom et al., 2009). Furthermore, P CV actually increased, while V S was maintained, as temperatures approached upper critical temperatures in resting Chinook salmon (Clark et al., 2008). These studies suggest that cardiac filling pressure is not compromised, or increases, when fishes are exposed to acute increases in temperature.

Systemic vascular resistance (R sys) has been shown to decrease when fish are exposed to acute increases in temperature (Clark et al., 2008; Gamperl et al., 2011; Mendonça and Gamperl, 2010; Sandblom et al., 2009). In contrast, Sandblom and Axelsson (2007) reported no change in R sys during acute warming in rainbow trout, though they only tested the fish across a moderate temperature range close to the species' optimum (10–16°C). Similarly, vascular resistance did not change in the Antarctic fish P. bernacchii during acute warming from 0 to 5°C (Axelsson et al., 1992). A reduction in R sys with acute warming has been speculated to be associated with increased tissue perfusion to reduce diffusion distances, and thus, enhance tissue oxygen delivery (Clark et al., 2008). However, since the increase in Q̇ typically outpaces the reduction in R sys with warming, the heart must generate greater blood pressures to distribute blood to the tissues (Gamperl, 2011). This could further hinder the ability of the heart to increase or maintain V S at high frequencies, especially given the well-documented negative force–frequency relationship (Shiels et al., 2002).

Numerous extrinsic factors (e.g., hormones, paracrine factors) also control the strength and rate of cardiac contraction (e.g., see Chapter 4, Volume 36A: Farrell and Smith, 2017; Chapter 5, Volume 36A: Imbrogno and Cerra, 2017), and autonomic nervous control is influenced by temperature (see Sections 1.3.1 and 1.6). Alterations in both these influences on cardiac function could lead to negative ionotropic effects, and thus, prevent V S from increasing. On the other hand, cardiac contractility could become compromised at high temperature for many of the same reasons outlined earlier (e.g., the noxious hyperkalemic, acidotic, and/or hypoxic venous blood environment, or a limitation in energy metabolism in the heart (see Sections 1.3.1, 1.7, and 1.9.1; and Chapter 6, Volume 36A: Rodnick and Gesser, 2017).

Notably, elevated temperature, per se, does not limit the ability of the heart to increase V S at rest (Gamperl et al., 2011). When resting rainbow trout were acutely warmed to 24°C after zatebradine administration to pharmacologically reduce f H by 50%, routine Q̇ was maintained by a doubling of V S (Gamperl et al., 2011). Similarly, zatebradine injection in resting rainbow trout prior to a CT max test significantly reduced f H but Q̇ remained comparable to control levels via an increase in V S (Keen and Gamperl, 2012). As such, it is possible that central control mechanisms favor an increase in f H over an increase in V S with acute temperature increases (Gamperl, 2011). While the mechanisms preventing V S from increasing during warming may not be resolved (see Keen and Gamperl, 2012), the outcome is that V S does not compensate for the commonly observed plateau in maximum f H at high temperature, and thus, cardiac performance has been observed to deteriorate in fish swimming at temperatures approaching upper critical limits (see Section 2.2 and Fig. 3).

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Aortic Regurgitation

Steven McGee MD , in Evidence-Based Physical Diagnosis (Fourth Edition), 2018

C Abnormal Pulsations of Other Structures: The Aortic Regurgitation Eponyms

The large stroke volume and aortic runoff of aortic regurgitation may induce pulsations in other parts of the body, which has generated many eponyms of what is fundamentally a single physical finding (the number of eponyms for aortic regurgitation rivals those of some neurologic reflexes). 1,14-17 These various bobbings include the following: (1) an abnormally conspicuous capillary pulsation, best elicited by blanching a portion of the nail and then observing the pulsating border between the white and red color (Quincke capillary pulsations, described in 1868, although Heinrich Quincke should be known instead for inventing the lumbar puncture); (2) an anterior-posterior bobbing of the head, synchronous with the arterial pulsations (de Musset sign, named after the French poet Alfred de Musset, who was afflicted with aortic regurgitation); 18 (3) alternate blanching and flushing of the forehead and face (lighthouse sign); (4) pulsations of organs or their parts, including the uvula (Müller sign, 1899), retinal arteries (Becker sign), larynx (Oliver-Cardarelli sign), spleen (Sailer sign, 1928), 19 and cervix (Dennison sign). 20 †

In many of the original descriptions of these eponymous findings, the sign was presented simply as an interesting observation, not one of particular diagnostic value. Excellent videos of patients with bounding carotids, 21 Quincke pulse, 22 and Müller sign 23 are available.

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