Mild hypothermia induces incomplete left ventricular relaxation despite spontaneous bradycardia in pigs

Standard

Mild hypothermia induces incomplete left ventricular relaxation despite spontaneous bradycardia in pigs. / Schwarzl, M; Alogna, A; Zirngast, B; Steendijk, P; Verderber, J; Zweiker, D; Huber, S; Maechler, H; Pieske, B M; Post, H.

In: ACTA PHYSIOL, Vol. 213, No. 3, 03.2015, p. 653-663.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Schwarzl, M, Alogna, A, Zirngast, B, Steendijk, P, Verderber, J, Zweiker, D, Huber, S, Maechler, H, Pieske, BM & Post, H 2015, 'Mild hypothermia induces incomplete left ventricular relaxation despite spontaneous bradycardia in pigs', ACTA PHYSIOL, vol. 213, no. 3, pp. 653-663. https://doi.org/10.1111/apha.12439

APA

Schwarzl, M., Alogna, A., Zirngast, B., Steendijk, P., Verderber, J., Zweiker, D., Huber, S., Maechler, H., Pieske, B. M., & Post, H. (2015). Mild hypothermia induces incomplete left ventricular relaxation despite spontaneous bradycardia in pigs. ACTA PHYSIOL, 213(3), 653-663. https://doi.org/10.1111/apha.12439

Vancouver

Schwarzl M, Alogna A, Zirngast B, Steendijk P, Verderber J, Zweiker D et al. Mild hypothermia induces incomplete left ventricular relaxation despite spontaneous bradycardia in pigs. ACTA PHYSIOL. 2015 Mar;213(3):653-663. https://doi.org/10.1111/apha.12439

Bibtex

@article{b867f5bcb5d84c5baafae218639bb5b6,
title = "Mild hypothermia induces incomplete left ventricular relaxation despite spontaneous bradycardia in pigs",
abstract = "AIM: Mild hypothermia (MH) decreases left ventricular (LV) end-diastolic capacitance. We sought to clarify whether this results from incomplete relaxation.METHODS: Ten anaesthetized pigs were cooled from normothermia (NT, 38 °C) to MH (33 °C). LV end-diastolic pressure (LVPed), volume (LVVed) and pressure-volume relationships (EDPVRs) were determined during stepwise right atrial pacing. LV capacitance (i.e. LVVed at LVPed of 10 mmHg, LV VPed10) was derived from the EDPVR. Pacing-induced changes of diastolic indices (LVPed, LVVed and LV VPed10) were analysed as a function of (i) heart rate and (ii) the ratio between diastolic time interval (t-dia) and LV isovolumic relaxation constant τ, which was calculated using a logistic fit (τL ) and monoexponential fit with zero asymptote (τZ ) and nonzero asymptote (τNZ ).RESULTS: Mild hypothermia decreased heart rate (85 ± 4 to 68 ± 3 bpm), increased τL (22 ± 1 to 57 ± 4 ms), τZ (26 ± 2 to 56 ± 5 ms) and τNZ (41 ± 1 to 96 ± 5 ms), decreased t-dia/τ ratios, and shifted the EDPVR leftwards compared to NT (all P < 0.05). During NT, pacing at ≥140 bpm shifted the EDPVR progressively leftwards. During MH, relationships between diastolic indices and heart rate were shifted towards lower heart rates compared to NT. However, relationships between diastolic indices and t-dia/τ during NT and MH were superimposable.CONCLUSION: We conclude that the loss of LV end-diastolic capacitance during MH can be explained at least in part by slowed LV relaxation. MH thereby is an example of incomplete LV relaxation at a spontaneous low heart rate. Caution may be advised, when heart rate is increased in patients treated with MH.",
keywords = "Animals, Bradycardia/diagnosis, Cardiac Pacing, Artificial, Diastole, Heart Rate, Hypothermia, Induced/adverse effects, Stroke Volume, Swine, Time Factors, Ventricular Dysfunction, Left/diagnosis, Ventricular Function, Left, Ventricular Pressure",
author = "M Schwarzl and A Alogna and B Zirngast and P Steendijk and J Verderber and D Zweiker and S Huber and H Maechler and Pieske, {B M} and H Post",
note = "{\textcopyright} 2014 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.",
year = "2015",
month = mar,
doi = "10.1111/apha.12439",
language = "English",
volume = "213",
pages = "653--663",
journal = "ACTA PHYSIOL",
issn = "1748-1708",
publisher = "Wiley-Blackwell",
number = "3",

}

RIS

TY - JOUR

T1 - Mild hypothermia induces incomplete left ventricular relaxation despite spontaneous bradycardia in pigs

AU - Schwarzl, M

AU - Alogna, A

AU - Zirngast, B

AU - Steendijk, P

AU - Verderber, J

AU - Zweiker, D

AU - Huber, S

AU - Maechler, H

AU - Pieske, B M

AU - Post, H

N1 - © 2014 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.

PY - 2015/3

Y1 - 2015/3

N2 - AIM: Mild hypothermia (MH) decreases left ventricular (LV) end-diastolic capacitance. We sought to clarify whether this results from incomplete relaxation.METHODS: Ten anaesthetized pigs were cooled from normothermia (NT, 38 °C) to MH (33 °C). LV end-diastolic pressure (LVPed), volume (LVVed) and pressure-volume relationships (EDPVRs) were determined during stepwise right atrial pacing. LV capacitance (i.e. LVVed at LVPed of 10 mmHg, LV VPed10) was derived from the EDPVR. Pacing-induced changes of diastolic indices (LVPed, LVVed and LV VPed10) were analysed as a function of (i) heart rate and (ii) the ratio between diastolic time interval (t-dia) and LV isovolumic relaxation constant τ, which was calculated using a logistic fit (τL ) and monoexponential fit with zero asymptote (τZ ) and nonzero asymptote (τNZ ).RESULTS: Mild hypothermia decreased heart rate (85 ± 4 to 68 ± 3 bpm), increased τL (22 ± 1 to 57 ± 4 ms), τZ (26 ± 2 to 56 ± 5 ms) and τNZ (41 ± 1 to 96 ± 5 ms), decreased t-dia/τ ratios, and shifted the EDPVR leftwards compared to NT (all P < 0.05). During NT, pacing at ≥140 bpm shifted the EDPVR progressively leftwards. During MH, relationships between diastolic indices and heart rate were shifted towards lower heart rates compared to NT. However, relationships between diastolic indices and t-dia/τ during NT and MH were superimposable.CONCLUSION: We conclude that the loss of LV end-diastolic capacitance during MH can be explained at least in part by slowed LV relaxation. MH thereby is an example of incomplete LV relaxation at a spontaneous low heart rate. Caution may be advised, when heart rate is increased in patients treated with MH.

AB - AIM: Mild hypothermia (MH) decreases left ventricular (LV) end-diastolic capacitance. We sought to clarify whether this results from incomplete relaxation.METHODS: Ten anaesthetized pigs were cooled from normothermia (NT, 38 °C) to MH (33 °C). LV end-diastolic pressure (LVPed), volume (LVVed) and pressure-volume relationships (EDPVRs) were determined during stepwise right atrial pacing. LV capacitance (i.e. LVVed at LVPed of 10 mmHg, LV VPed10) was derived from the EDPVR. Pacing-induced changes of diastolic indices (LVPed, LVVed and LV VPed10) were analysed as a function of (i) heart rate and (ii) the ratio between diastolic time interval (t-dia) and LV isovolumic relaxation constant τ, which was calculated using a logistic fit (τL ) and monoexponential fit with zero asymptote (τZ ) and nonzero asymptote (τNZ ).RESULTS: Mild hypothermia decreased heart rate (85 ± 4 to 68 ± 3 bpm), increased τL (22 ± 1 to 57 ± 4 ms), τZ (26 ± 2 to 56 ± 5 ms) and τNZ (41 ± 1 to 96 ± 5 ms), decreased t-dia/τ ratios, and shifted the EDPVR leftwards compared to NT (all P < 0.05). During NT, pacing at ≥140 bpm shifted the EDPVR progressively leftwards. During MH, relationships between diastolic indices and heart rate were shifted towards lower heart rates compared to NT. However, relationships between diastolic indices and t-dia/τ during NT and MH were superimposable.CONCLUSION: We conclude that the loss of LV end-diastolic capacitance during MH can be explained at least in part by slowed LV relaxation. MH thereby is an example of incomplete LV relaxation at a spontaneous low heart rate. Caution may be advised, when heart rate is increased in patients treated with MH.

KW - Animals

KW - Bradycardia/diagnosis

KW - Cardiac Pacing, Artificial

KW - Diastole

KW - Heart Rate

KW - Hypothermia, Induced/adverse effects

KW - Stroke Volume

KW - Swine

KW - Time Factors

KW - Ventricular Dysfunction, Left/diagnosis

KW - Ventricular Function, Left

KW - Ventricular Pressure

U2 - 10.1111/apha.12439

DO - 10.1111/apha.12439

M3 - SCORING: Journal article

C2 - 25515791

VL - 213

SP - 653

EP - 663

JO - ACTA PHYSIOL

JF - ACTA PHYSIOL

SN - 1748-1708

IS - 3

ER -