Hemodynamic determinants of the maximal rate of rise of left ventricular pressure

Wallace, Andrew G.; Skinner, N.Sheldon; Mitchell, Jere H.

doi:10.1152/ajplegacy.1963.205.1.30

Cited by 309 publications

(130 citation statements)

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“…However, dP/dt max reflects both the contractile state of the LV and the loading conditions under which the LV is functioning. 34 Heart rate and LV end-systolic pressure were similar in the paced and unpaced states ( Table 2). The observed increase in LV dP/dt max may be explained by an increase in LV preload via the mechanisms described earlier or by an increase in intrinsic LV contractile function, as exemplified by cases 10 and 13 ( Figure 5A and 5B).…”

Section: Bleasdale Et Al LV Pacing Reduces Ventricular Interactionmentioning

confidence: 83%

Left Ventricular Pacing Minimizes Diastolic Ventricular Interaction, Allowing Improved Preload-Dependent Systolic Performance

et al. 2004

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Background-Left ventricular (LV) pacing improves hemodynamics in patients with heart failure. We hypothesized that at least part of this benefit occurs by minimization of external constraint to LV filling from ventricular interaction. Methods and Results-We present median values (interquartile ranges) for 13 heart failure patients with LV pacing systems implanted for New York Heart Association class III/IV limitation. We used the conductance catheter method to measure LV pressure and volume simultaneously. External constraint was measured from the end-diastolic pressure-volume relation recorded during inferior vena caval occlusion, during LV pacing, and while pacing was suspended. External constraint to LV filling was reduced by 3.0 (4.6 to 0.6) mm Hg from 4.8 (0.6 to 7.5) mm Hg (PϽ0.01) in response to LV pacing; effective filling pressure (LV end-diastolic pressure minus external constraint) increased by 4.0 (2.2 to 5.8) mm Hg from 17.7 (13.3 to 22.6; PϽ0.01). LV end-diastolic volume increased by 10 (3 to 11) mL from 238 (169 to 295) mL (Pϭ0.01), whereas LV end-systolic volume did not change significantly (Ϫ1 [Ϫ2 to 3] mL from 180 [124 to 236] mL, Pϭ0.97), which resulted in an increase in stroke volume of 11 (5 to 13) mL from 49 (38 to 59) mL (PϽ0.01). LV stroke work increased by 720 (550 to 1180) mL ⅐ mm Hg from 3400 (2110 to 4480) mL ⅐ mm Hg (Pϭ0.01), and maximum dP/dt increased by 120 (2 to 161) mm Hg/s from 635 (521 to 767) mm Hg/s (Pϭ0.03). Conclusions-This study suggests a potentially important mechanism by which LV pacing may produce hemodynamic benefit. LV pacing minimizes external constraint to LV filling, resulting in an increase in effective filling pressure; the consequent increase in LV end-diastolic volume increases stroke volume via the Starling mechanism. (Circulation.

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Section: Bleasdale Et Al LV Pacing Reduces Ventricular Interactionmentioning

confidence: 83%

Left Ventricular Pacing Minimizes Diastolic Ventricular Interaction, Allowing Improved Preload-Dependent Systolic Performance

et al. 2004

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“…566 *.U".L rate of rise of the left ventricular pressure pulse (dp /dt), as suggested by Hamacher (1960Hamacher ( , 1963 and by Benfey, Greeff & Heeg (1967). The validity of this method has been reviewed by Gleason & Braunwald (1962), Wallace, Skinner & Mitchell (1963) and by Schaper, Lewi & Jageneau (1965). Provided LVEDP is adequately monitored, dp/dt max is a useful index of cardiac contractility which can be used in closed-chest, spontaneously breathing, preparations.…”

Section: Discussionmentioning

confidence: 99%

The effect of catecholamine infusions on myocardial blood flow, metabolic heat production and on general haemodynamics, before and after alprenolol (H56/28), in anaesthetized cats

Parratt

Wadsworth

1970

British J Pharmacology

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Summary1. In cats anaesthetized with pentobarbitone sodium, infusions of adrenaline, noradrenaline (05 ,ug/kg per min) and isoprenaline (025 ,ug/kg per min) increased myocardial blood flow, myocardial heat production, left ventricular systolic and end-diastolic pressures, left ventricular +ve and -ve dpidt max, and calculated cardiac output, effort and oxygen consumption. These effects (apart from the effect of noradrenaline on left ventricular systolic pressure) were markedly reduced by previous administration of alprenolol (05 or 1-0 mg/kg). 2. Infusions of adrenaline and noradrenaline increased arterial diastolic blood pressure and isoprenaline reduced it. After alprenolol the effects of adrenaline and noradrenaline were potentiated and that of isoprenaline abolished; in some experiments isoprenaline increased arterial diastolic pressure after alprenolol. Alprenolol did not influence the increases in arterial systolic pressure which followed the administration of adrenaline and noradrenaline. 3. Isoprenaline-induced tachycardia was markedly reduced and adrenaline tachycardia was converted to bradycardia after alprenolol. The bradycardia which occurred during noradrenaline infusions was unaffected. 4. After blockade by alprenolol, recovery of the effects of isoprenaline on left ventricular dp/dt and on heart rate occurred more quickly than recovery of the effects on arterial diastolic pressure. This suggests that alprenolol has a greater affinity for 32-than for /3-adrenoceptors. 5. Intravenous administration of acetylcholine decreased arterial blood pressure, left ventricular pressure and +ve and -ve dp/dt max. During recovery from these effects there was a marked increase in +ve dp/dt max. which was absent after the administration of alprenolol (05 mg/kg). Because this dose of alprenolol is thus able to block the effects of reflex sympathetic cardiac nerve stimulation but does not completely antagonize the effects of exogenous adrenaline on dp/dt, it is suggested that alprenolol may have some adrenergic neurone blocking activity. 6. Increases in liver and myocardial blood flow and heat production produced by noradrenaline, adrenaline and isoprenaline were reduced after alprenolol. 7. Isoprenaline reduced air-way resistance and this effect was abolished by alprenolol; increases in air-way resistance produced by adrenaline and noradrenaline were augmented. All three amines inhibited intestinal smooth

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“…If the peripheral venous responses observed were sufficiently generalized to lead to an increase in venous return and end-diastolic pressure, an autoregulatory positive inotropic response in the heart (Wallace, Skinner & Mitchell, 1963) could also have contributed to the blood pressure rise. It appears then that the only changes observed which are definitely both primary and the result of a spinal reflex are venoconstriction and a decreased skin and muscle blood flow.…”

Section: Cardiovascular Changes In Muscle Spasms 391mentioning

confidence: 99%

Cardiovascular changes associated with skeletal muscle spasm in tetraplegic man

Corbett¹,

Frankel²,

Harris³

1971

The Journal of Physiology

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SUMMARY1. A study has been made of the effect of spontaneous and induced muscle spasms on blood pressure, heart rate, hand blood flow, calf blood flow and occluded vein pressure in the hand and foot in non-bedridden patients with chronic, closed, complete, localized transaction of the cervical spinal cord.2. Both types of spasm produced a similar response consisting of an increase in blood pressure and occluded vein pressure and a decrease in heart rate and hand and calf blood flow. The changes commenced within 2-3 see and usually reached maxima in 20-30 sec. On some occasions there was a temporary initial increase in heart rate and calf blood flow.3. The changes occurred independently of changes in bladder pressure. 4. It is concluded that the changes in peripheral blood vessels result from a spinal sympathetic reflex to somatic afferents associated with muscular contraction.

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Hemodynamic determinants of the maximal rate of rise of left ventricular pressure

Cited by 309 publications

References 1 publication

Left Ventricular Pacing Minimizes Diastolic Ventricular Interaction, Allowing Improved Preload-Dependent Systolic Performance

Left Ventricular Pacing Minimizes Diastolic Ventricular Interaction, Allowing Improved Preload-Dependent Systolic Performance

The effect of catecholamine infusions on myocardial blood flow, metabolic heat production and on general haemodynamics, before and after alprenolol (H56/28), in anaesthetized cats

Cardiovascular changes associated with skeletal muscle spasm in tetraplegic man

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