Renal and Cardiovascular Responses to Acute Hypercapnic Acidosis in Conscious Dogs

Ce, Rose; Walker, BR; Erickson, A. L.; Dl, Kaiser; Rm, Carey; Rj, Anderson

doi:10.1097/00005344-198207000-00021

Cited by 8 publications

(4 citation statements)

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“…The PaC>2 levels in the 70's during control are probably related to the altitude of Denver since we have observed comparable Pao2 values during previous investigations in conscious dogs (Rose et al, 1982). Comparable Pao2 levels during acute hypercapnic acidosis are indirectly related to altitude, since N2 was added to inspired air during acute hypercapnic acidosis to maintain the FEO2 and hence the Pao2 at control levels.…”

Section: Discussionsupporting

confidence: 67%

“…We have previously observed increased mean arterial pressure, heart rate, and cardiac output and diminished systemic vascular resistance during comparable acute hypercapnic acidosis in conscious dogs (Rose et al, 1982). The absence of change of these variables during acute hypercapnic acidosis in the present study may in part be related to cardiac pacing with abrogation of increased heart rate during acute hypercapnic acidosis.…”

Section: Discussionsupporting

confidence: 52%

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Right ventricular performance during increased afterload impaired by hypercapnic acidosis in conscious dogs.

Rose¹,

Benthuysen²,

Jackson³

et al. 1983

Circulation Research

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SUMMARY. Since heart failure may occur in the setting of lung dysfunction and CO2 retention with only modest increases in cardiac work load, we questioned whether myocardial function is impaired by hypercapnic acidosis. To determine the influence of hypercapnic acidosis on right ventricular function, we measured the effects of acute (2 hours) and chronic (2 weeks) hypercapnic acidosis on right ventricular performance during normal and increased right ventricular afterload in five conscious dogs. Systemic hemodynamic and right ventricular functions were unaltered during normal right ventricular afterload by acute hypercapnic acidosis (Paco2 = 49 ± 3 mm Hg, pH = 7.27 ± 0.003). As right ventricular afterload was increased by progressive balloon occlusion of the right ventricular outflow tract during acute hypercapnic acidosis, the rise (slope) in right ventricular enddiastolic pressure was increased 4-fold (P < 0.01) over that observed in normocapnic control. Maximum isovolumic right ventricular dP/dt rose (P < 0.05) comparably with increasing right ventricular afterload during normocapnic control and acute hypercapnic acidosis. Chronic hypercapnic acidosis (Paco2 = 55 ± 2 mm Hg, pH = 7.28 ± 0.01) resulted in systemic vasodilation and increased (P < 0.05) heart rate and cardiac output during normal right ventricular afterload. As right ventricular afterload was increased during chronic hypercapnic acidosis, the rate of rise in right ventricular end-diastolic pressure was 2-fold (P < 0.01) above normocapnic control but maximum isovolumic right ventricular dP/dt was unchanged in contrast to normocapnic control and acute hypercapnic acidosis. Moreover, cardiac output fell and stroke work was unchanged with increasing afterload during chronic hypercapnic acidosis. /?-Adrenergic blockade resulted in an increased (P < 0.01) rate of rise in right ventricular end-diastolic pressure with afterload during normocapnic control and chronic hypercapnic acidosis. We conclude that hypercapnic acidosis results in diminished right ventricular performance during increased right ventricular afterload, evidenced by accentuated rise in right ventricular end-diastolic pressure, and may contribute to the congestive heart failure and edema observed in patients with pulmonary hypertension and CO2 retention.

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Section: Discussionsupporting

confidence: 67%

Section: Discussionsupporting

confidence: 52%

Right ventricular performance during increased afterload impaired by hypercapnic acidosis in conscious dogs.

Rose¹,

Benthuysen²,

Jackson³

et al. 1983

Circulation Research

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show abstract

“…Hypercapnia affects renal blood flow directly and indirectly. Directly, hypercapnia may decrease renal blood flow by stimulating renal vasoconstriction (via norepinephrine release), although the net effects on GFR are conflicting [38, 39]. Indirectly, systemic vasodilation triggered by high pCO 2 may lower effective renal perfusion and activate the renin–angiotensin–aldosterone feedback response.…”

Section: Epidemiology: Aki Ali and Multi-organ Disease Syndromementioning

confidence: 99%

Kidney–lung cross-talk and acute kidney injury

Basu

Wheeler

2013

Pediatr Nephrol

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There is a growing appreciation for the role that acute kidney injury (AKI) plays in the propagation of critical illness. In children, AKI is not only an independent predictor of morbidity and mortality, but is also associated with especially negative outcomes when concurrent with acute lung injury (ALI). Experimental data provide evidence that kidney–lung crosstalk occurs and can be bidirectionally deleterious, although details of the precise molecular mechanisms involved in the AKI–ALI interaction remain incomplete. Clinically, ALI, and the subsequent clinical interventions used to stabilize gas exchange, carry consequences for the homeostasis of kidney function. Meanwhile, AKI negatively affects lung physiology significantly by altering the homeostasis of fluid balance, acid–base balance, and vascular tone. Experimental AKI research supports an “endocrine” role for the kidney, triggering a cascade of extra-renal inflammatory responses affecting lung homeostasis. In this review, we will discuss the pathophysiology of kidney–lung crosstalk, the multiple pathways by which AKI affects kidney–lung homeostasis, and discuss how these phenomena may be unique in critically ill children. Understanding how AKI may affect a “balance of communication” that exists between the kidneys and the lungs is requisite when managing critically ill children, in whom imbalance is the norm.

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“…The PAH extraction values were comparable to those observed in normocapnic animals, thus demonstrating that hypercapnia does not change PAH extraction, and that the drop in C PAH corresponds to a true decrease in RBF. A 10% decrease in PAH extraction was observed by Anderson et al (11,12) during hypercapnic acidosis in dogs, but was apparently not found in other studies ofthe same group (13,14), nor was any change in PAH extraction HEIJDEN AND GUIGNARD during hypercapnia mentioned by Norman et al (7) and by Berns et al (15). This is in agreement with studies using either a sine wave electromagnetic flowmeter (6) or microspheres (4,5) for measuring RBF.…”

Section: Discussionmentioning

confidence: 78%

Effect of Hypercapnic Acidosis on Renal Function in the Newborn Rabbit

Heijden

Guignard

1986

Pediatr Res

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Anaesthetized mechanically ventilated newborn rabbits were exposed to different degrees of hypercapnia. One hour of normocapnia was used as a control period. Renal function studies demonstrated an increase in renal vascular resistance with a concomitant decrease in effective renal plasma flow in all hypercapnic animals, combined with a less pronounced decrease in glomerular filtration rate. Filtration fraction rose significantly. A decrease in systemic blood pressure was only observed when the PaCO2 exceeded 100 mm Hg combined with an arterial pH below or equal to 7.10. We conclude that normoxemic hypercapnia in the newborn rabbit leads to an increase in renal vascular resistance and suggest that the renal vasoconstriction predominates at the level of the efferent arteriole.

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Renal and Cardiovascular Responses to Acute Hypercapnic Acidosis in Conscious Dogs

Cited by 8 publications

References 0 publications

Right ventricular performance during increased afterload impaired by hypercapnic acidosis in conscious dogs.

Right ventricular performance during increased afterload impaired by hypercapnic acidosis in conscious dogs.

Kidney–lung cross-talk and acute kidney injury

Effect of Hypercapnic Acidosis on Renal Function in the Newborn Rabbit

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