The relationship between cardiac output and posthyperventilation hyperpnoea in patients with essential hypertension

S. Bellofiore, L. S. Malatino, M. A. Sapienza, I. Bellanuova, A. Cataliotti, G. U. Di Maria

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

Posthyperventilation hyperpnoea (PHVH) is the progressive decline in minute ventilation (V'(E)) that follows abrupt cessation of voluntary hyperventilation. It has been hypothesized that the increase in cardiac output (CO) during hyperventilation could contribute to the duration of PHVH. This hypothesis was tested by measuring the duration of PHVH in patients with essential hypertension, in whom the increase in CO as a result of various stimuli is less pronounced. Twenty male hypertensives (mean arterial blood pressure±SEM: 178/107±3/1 mmHg), and 12 age-matched male healthy subjects were studied. The study consisted of three periods: control (5 min), voluntary hyperventilation (2 min), and recovery (3 min). V'(E), CO, end- tidal CO 2 and O 2 tensions were measured, and the time constant (τ) of the V'(E) decay during recovery calculated. The V'(E) decay was faster in hypertensives (τ: 0-8.4 s) than in healthy subjects (τ: 12-59 s; p<0.01). During voluntary hyperventilation, CO increased to a lesser extent in hypertensives (6.8+0.7 L·min -1) than in healthy subjects (12.9±1.1 L·min -1; p<0.01). In hypertensives, changes in CO during voluntary hyperventilation were significantly related to τ (r=0.646; n=20; p=0.002). The less pronounced rise in cardiac output during hyperventilation in hypertensives could account for the shorter duration of posthyperventilation hyperpnoea.

Original languageEnglish (US)
Pages (from-to)1160-1163
Number of pages4
JournalEuropean Respiratory Journal
Volume12
Issue number5
StatePublished - Nov 1998
Externally publishedYes

Fingerprint

Hyperventilation
Cardiac Output
Ventilation
Healthy Volunteers
Essential Hypertension

Keywords

  • Cardiac output
  • Cardiovascular-respiratory interactions
  • Control of breathing
  • Essential hypertension
  • Hyperventilation

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Bellofiore, S., Malatino, L. S., Sapienza, M. A., Bellanuova, I., Cataliotti, A., & Di Maria, G. U. (1998). The relationship between cardiac output and posthyperventilation hyperpnoea in patients with essential hypertension. European Respiratory Journal, 12(5), 1160-1163.

The relationship between cardiac output and posthyperventilation hyperpnoea in patients with essential hypertension. / Bellofiore, S.; Malatino, L. S.; Sapienza, M. A.; Bellanuova, I.; Cataliotti, A.; Di Maria, G. U.

In: European Respiratory Journal, Vol. 12, No. 5, 11.1998, p. 1160-1163.

Research output: Contribution to journalArticle

Bellofiore, S, Malatino, LS, Sapienza, MA, Bellanuova, I, Cataliotti, A & Di Maria, GU 1998, 'The relationship between cardiac output and posthyperventilation hyperpnoea in patients with essential hypertension', European Respiratory Journal, vol. 12, no. 5, pp. 1160-1163.
Bellofiore S, Malatino LS, Sapienza MA, Bellanuova I, Cataliotti A, Di Maria GU. The relationship between cardiac output and posthyperventilation hyperpnoea in patients with essential hypertension. European Respiratory Journal. 1998 Nov;12(5):1160-1163.
Bellofiore, S. ; Malatino, L. S. ; Sapienza, M. A. ; Bellanuova, I. ; Cataliotti, A. ; Di Maria, G. U. / The relationship between cardiac output and posthyperventilation hyperpnoea in patients with essential hypertension. In: European Respiratory Journal. 1998 ; Vol. 12, No. 5. pp. 1160-1163.
@article{94a1616000254d59be4043e916611fec,
title = "The relationship between cardiac output and posthyperventilation hyperpnoea in patients with essential hypertension",
abstract = "Posthyperventilation hyperpnoea (PHVH) is the progressive decline in minute ventilation (V'(E)) that follows abrupt cessation of voluntary hyperventilation. It has been hypothesized that the increase in cardiac output (CO) during hyperventilation could contribute to the duration of PHVH. This hypothesis was tested by measuring the duration of PHVH in patients with essential hypertension, in whom the increase in CO as a result of various stimuli is less pronounced. Twenty male hypertensives (mean arterial blood pressure±SEM: 178/107±3/1 mmHg), and 12 age-matched male healthy subjects were studied. The study consisted of three periods: control (5 min), voluntary hyperventilation (2 min), and recovery (3 min). V'(E), CO, end- tidal CO 2 and O 2 tensions were measured, and the time constant (τ) of the V'(E) decay during recovery calculated. The V'(E) decay was faster in hypertensives (τ: 0-8.4 s) than in healthy subjects (τ: 12-59 s; p<0.01). During voluntary hyperventilation, CO increased to a lesser extent in hypertensives (6.8+0.7 L·min -1) than in healthy subjects (12.9±1.1 L·min -1; p<0.01). In hypertensives, changes in CO during voluntary hyperventilation were significantly related to τ (r=0.646; n=20; p=0.002). The less pronounced rise in cardiac output during hyperventilation in hypertensives could account for the shorter duration of posthyperventilation hyperpnoea.",
keywords = "Cardiac output, Cardiovascular-respiratory interactions, Control of breathing, Essential hypertension, Hyperventilation",
author = "S. Bellofiore and Malatino, {L. S.} and Sapienza, {M. A.} and I. Bellanuova and A. Cataliotti and {Di Maria}, {G. U.}",
year = "1998",
month = "11",
language = "English (US)",
volume = "12",
pages = "1160--1163",
journal = "European Respiratory Journal",
issn = "0903-1936",
publisher = "European Respiratory Society",
number = "5",

}

TY - JOUR

T1 - The relationship between cardiac output and posthyperventilation hyperpnoea in patients with essential hypertension

AU - Bellofiore, S.

AU - Malatino, L. S.

AU - Sapienza, M. A.

AU - Bellanuova, I.

AU - Cataliotti, A.

AU - Di Maria, G. U.

PY - 1998/11

Y1 - 1998/11

N2 - Posthyperventilation hyperpnoea (PHVH) is the progressive decline in minute ventilation (V'(E)) that follows abrupt cessation of voluntary hyperventilation. It has been hypothesized that the increase in cardiac output (CO) during hyperventilation could contribute to the duration of PHVH. This hypothesis was tested by measuring the duration of PHVH in patients with essential hypertension, in whom the increase in CO as a result of various stimuli is less pronounced. Twenty male hypertensives (mean arterial blood pressure±SEM: 178/107±3/1 mmHg), and 12 age-matched male healthy subjects were studied. The study consisted of three periods: control (5 min), voluntary hyperventilation (2 min), and recovery (3 min). V'(E), CO, end- tidal CO 2 and O 2 tensions were measured, and the time constant (τ) of the V'(E) decay during recovery calculated. The V'(E) decay was faster in hypertensives (τ: 0-8.4 s) than in healthy subjects (τ: 12-59 s; p<0.01). During voluntary hyperventilation, CO increased to a lesser extent in hypertensives (6.8+0.7 L·min -1) than in healthy subjects (12.9±1.1 L·min -1; p<0.01). In hypertensives, changes in CO during voluntary hyperventilation were significantly related to τ (r=0.646; n=20; p=0.002). The less pronounced rise in cardiac output during hyperventilation in hypertensives could account for the shorter duration of posthyperventilation hyperpnoea.

AB - Posthyperventilation hyperpnoea (PHVH) is the progressive decline in minute ventilation (V'(E)) that follows abrupt cessation of voluntary hyperventilation. It has been hypothesized that the increase in cardiac output (CO) during hyperventilation could contribute to the duration of PHVH. This hypothesis was tested by measuring the duration of PHVH in patients with essential hypertension, in whom the increase in CO as a result of various stimuli is less pronounced. Twenty male hypertensives (mean arterial blood pressure±SEM: 178/107±3/1 mmHg), and 12 age-matched male healthy subjects were studied. The study consisted of three periods: control (5 min), voluntary hyperventilation (2 min), and recovery (3 min). V'(E), CO, end- tidal CO 2 and O 2 tensions were measured, and the time constant (τ) of the V'(E) decay during recovery calculated. The V'(E) decay was faster in hypertensives (τ: 0-8.4 s) than in healthy subjects (τ: 12-59 s; p<0.01). During voluntary hyperventilation, CO increased to a lesser extent in hypertensives (6.8+0.7 L·min -1) than in healthy subjects (12.9±1.1 L·min -1; p<0.01). In hypertensives, changes in CO during voluntary hyperventilation were significantly related to τ (r=0.646; n=20; p=0.002). The less pronounced rise in cardiac output during hyperventilation in hypertensives could account for the shorter duration of posthyperventilation hyperpnoea.

KW - Cardiac output

KW - Cardiovascular-respiratory interactions

KW - Control of breathing

KW - Essential hypertension

KW - Hyperventilation

UR - http://www.scopus.com/inward/record.url?scp=0031787569&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031787569&partnerID=8YFLogxK

M3 - Article

VL - 12

SP - 1160

EP - 1163

JO - European Respiratory Journal

JF - European Respiratory Journal

SN - 0903-1936

IS - 5

ER -