The Effect of Hypocapnia on Arterial Blood Pressure

Burnum, John F.; Hickam, John B.; McIntosh, Henry D.

doi:10.1161/01.cir.9.1.89

Cited by 114 publications

(58 citation statements)

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“…On the contrary, hypercapnia causes an increase in peripheral resistance and a decrease in CVR. 17,28 Similar to our findings, these systemic changes are hardly seen because of the buffering effect of the systemic baroreflex. However, in patients with severe autonomic failure, hyperventilation-induced hypocapnia causes a devastating decrease in BP and fainting.…”

Section: Lavi Et Al Nitric Oxide and Cerebral Blood Flowsupporting

confidence: 91%

Role of Nitric Oxide in the Regulation of Cerebral Blood Flow in Humans

et al. 2003

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Background-From animal studies it emerged that nitric oxide is important for the modulation of CO 2 -mediated cerebral blood flow (CBF chemoregulation) but not for the pressor-dependent mechanism (mechanoregulation). This hypothesis was tested in 18 healthy subjects. Methods and Results-Peak velocity (PV), diastolic velocity (DV), and mean velocity (MV) were measured by transcranial Doppler of the middle cerebral artery. Chemoregulation was assessed during normocapnia, hypocapnia, and after inhaled mixture of 95% O 2 ϩ5% CO 2 . Mechanoregulation was evaluated by incremental doses of phenylephrine. Measurements were repeated during infusion of sodium nitroprusside (SNP). Regional cerebrovascular resistance (CVR) was calculated as mean blood pressure (BP)/MV. SNP infusion decreased mean BP by 7 mm Hg and CVR decreased from 1.38Ϯ0.08 to 1.29Ϯ0.09 mm Hg/cm ⅐ s Ϫ1 ; Pϭ0.01, resulting in unaffected CBF. Phenylephrine (25 to 250 g) caused a similar increase in BP in a dose-response fashion before and during SNP infusion. Despite the increments in BP and CVR, CBF remained unaffected. During hyperventilation (end-tidal CO 2 Ϸ24 mm Hg), CVR increased by 75Ϯ3% and PV and DV decreased by 27Ϯ2% and 43Ϯ2%, respectively (PϽ0.001 for all). SNP infusion blunted the vasoconstrictive effect of hypocapnia; CVR increased only by 57Ϯ5%, and PV and DV decreased by 23Ϯ2% and 35Ϯ3%, respectively, (PϽ0.05 for all). Similarly, SNP augmented the vasodilatory effect of hypercapnia. Conclusions-Exogenous nitric oxide donor affects the basal cerebral vascular tone without affecting the CBF mechanoregulation. However, it selectively affects only the chemoregulatory mechanism (CO 2 -dependent). Thus, the CO 2 -NO axis is a cardinal pathway for CBF regulation in humans.

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Section: Lavi Et Al Nitric Oxide and Cerebral Blood Flowsupporting

confidence: 91%

Role of Nitric Oxide in the Regulation of Cerebral Blood Flow in Humans

et al. 2003

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“…The effects of uncontrolled spontaneous hyperventilation are primarily the result of hypocapnia causing respiratory alkalosis19; these effects substantially resolve when CO 2 is normalized 8, 43. Because CO 2 is lipid soluble, alkalotic changes distribute across cell membranes and the blood‐brain barrier.…”

Section: Discussionmentioning

confidence: 99%

“…Dyspnea, hyperventilation, and hypocapnia have been reported in association with POTS and also in other forms of OI, including neurogenic orthostatic hypotension and vasovagal syncope 6, 7, 8. Circulatory collapse9 and milder perturbations, such as induction of hypotension in healthy volunteers, result in hyperventilation and hypocapnia 10, 11.…”

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confidence: 99%

Postural Hyperventilation as a Cause of Postural Tachycardia Syndrome: Increased Systemic Vascular Resistance and Decreased Cardiac Output When Upright in All Postural Tachycardia Syndrome Variants

Stewart

Pianosi

Shaban

et al. 2018

JAHA

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BackgroundPostural tachycardia syndrome (POTS) is a heterogeneous condition. We stratified patients previously evaluated for POTS on the basis of supine resting cardiac output (CO) or with the complaint of platypnea or “shortness of breath” during orthostasis. We hypothesize that postural hyperventilation is one cause of POTS and that hyperventilation‐associated POTS occurs when initial reduction in CO is sufficiently large. We also propose that circulatory abnormalities normalize with restoration of CO 2.Methods and ResultsFifty‐eight enrollees with POTS were compared with 16 healthy volunteer controls. Low CO in POTS was defined by a resting supine CO <4 L/min. Patients with shortness of breath had hyperventilation with end tidal CO 2 <30 Torr during head‐up tilt table testing. There were no differences in height or weight between control patients and patients with POTS or differences between the POTS groups. Beat‐to‐beat blood pressure was measured by photoplethysmography, and CO was measured by ModelFlow. Systemic vascular resistance was defined as mean arterial blood pressure/CO. End tidal CO 2 and cerebral blood flow velocity of the middle cerebral artery were only reduced during head‐up tilt in the hyperventilation group, whereas blood pressure was increased compared with control. We corrected the reduced end tidal CO 2 in hyperventilation by addition of exogenous CO 2 into a rebreathing apparatus. With added CO 2, heart rate, blood pressure, CO, and systemic vascular resistance in hyperventilation became similar to control.ConclusionsWe conclude that all POTS is related to decreased CO, decreased central blood volume, and increased systemic vascular resistance and that a variant of POTS is consequent to postural hyperventilation.

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“…They also are of recognized importance in the control of general circulatory homeostasis; for example, systemic hypertension accompanies acutely induced hypercapnia (2,3), and hypotension the hypocapnia of hyperventilation (4). Furthermore, disorders of acid-base equilibrium occur in pathologic states with sufficient frequency to merit consideration of the role of blood pH and CO2 tension in control of the circulation burdened by disease such as the acidosis of uremia and diabetic coma or the alkalosis of vomiting.…”

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confidence: 99%

General and Regional Circulatory Responses to Change in Blood Ph and Carbon Dioxide Tension*

Richardson¹,

Wasserman²,

Patterson³

1961

J. Clin. Invest.

120

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The pH and the carbon dioxide tension of the blood flowing through a tissue are commonly thought to be major factors in the local control of regional blood flow, for instance in the vasodilation in exercising muscle (1). They also are of recognized importance in the control of general circulatory homeostasis; for example, systemic hypertension accompanies acutely induced hypercapnia (2, 3), and hypotension the hypocapnia of hyperventilation (4). Furthermore, disorders of acid-base equilibrium occur in pathologic states with sufficient frequency to merit consideration of the role of blood pH and CO2 tension in control of the circulation burdened by disease such as the acidosis of uremia and diabetic coma or the alkalosis of vomiting.With these considerations in mind, the present studies were undertaken in healthy humans to determine the effects of variation in blood pH and CO2 tension (Pco2) on cardiac output and on the flow of blood through extremity musculature. In an attempt to separate direct effects of change in pH or Pco0 on blood vessels themselves from those mediated by the nervous system, sympathetic impulses to the extremity were blocked with phenoxybenzamine (Dibenzyline 1) administered intraarterially to the extremity under study. METHODSThe subjects studied were healthy male volunteers and one male with essential hypertension. Their ages ranged from 22 to 46 years. Most had participated repeatedly in similar studies in the same laboratory and were, therefore, relaxed and at ease.Acidemia was induced by intravenous infusion of 500 to 800 ml of 0.2 M lactic acid or 0.17 M ammonium chlo-*

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The Effect of Hypocapnia on Arterial Blood Pressure

Cited by 114 publications

References 0 publications

Role of Nitric Oxide in the Regulation of Cerebral Blood Flow in Humans

Role of Nitric Oxide in the Regulation of Cerebral Blood Flow in Humans

Postural Hyperventilation as a Cause of Postural Tachycardia Syndrome: Increased Systemic Vascular Resistance and Decreased Cardiac Output When Upright in All Postural Tachycardia Syndrome Variants

General and Regional Circulatory Responses to Change in Blood Ph and Carbon Dioxide Tension*

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