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Acute Changes in Left Ventricular Mechanics During Voluntary Apnea
Author(s) -
Sutterfield Shelbi L,
Smith Joshua R,
Baumfalk Dryden R,
Didier Kaylin D,
Ade Carl J
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.843.16
Subject(s) - medicine , cardiology , blood pressure , apnea , heart rate , myocardial infarction , diastole , stroke volume , anesthesia
Obstructive sleep apnea (OSA) is characterized by intermittent apneic events and is associated with hypertension, sudden cardiac death, and acute cardiac infarction. During an apneic event asphyxia‐induced increases in sympathetic nerve activity result in subsequent increases in arterial blood pressure and systemic vascular resistance. However, it is currently unknown how cardiac mechanics are acutely impacted by these systemic responses to an apneic event. Therefore, the purpose of the present study was to evaluate changes in left ventricular systolic and diastolic function during voluntary apnea. We hypothesized that during voluntary apnea left ventricular systolic and diastolic function would be compromised in parallel with increases in arterial blood pressure and myocardial work. Methods 9 healthy men (23 ± 3 yrs) were recruited for the study. Subjects performed multiple voluntary breath holds at functional residual capacity with 3–5 minutes in between. Beat‐by‐beat blood pressure, heart rate and stroke volume were measured continuously. End‐tidal CO 2 was measured at end‐apnea. Tissue Doppler echocardiography was used to measure tissue velocities, and myocardial deformation via strain (S), and strain rate (SR) at the mid‐interventricular septum across 3 continuous cardiac cycles at baseline and end‐apnea. Results Systolic blood pressure (Δ13.8 ± 8.4 mmHg, p<0.01), mean arterial pressure (Δ12.4 ± 7.0 mmHg, p<0.01), and rate pressure product (Δ8.4 ± 5.6 mmHg × bpm 10 −2 , p<0.01) significantly increased with apnea, but not stroke volume (Δ3.3 ± 8.1 ml, p=0.26). Peak longitudinal systolic (Δ −0.56 ± 0.69 cm s −1 , p=0.04) and early LV filling (Δ −2.32 ± 2.04 cm s −1 , p<0.01) myocardial velocities were significantly decreased during the apnea. Longitudinal Systolic S (Δ −2.17 ± 2.36%, p=0.02) and SR (Δ −0.20 ± 0.29 1/s, p=0.07) were significantly decreased during the apnea. Early LV filling SR was not different compared to baseline with apnea (p=0.41). Conclusion Consistent with our hypotheses, left ventricular deformation was significantly impaired with voluntary apnea. These data suggest that the systemic increases in arterial pressure during voluntary apnea have an adverse effect on left ventricular systolic mechanics.