Effects of contrast media on pulmonary hemodynamics: comparison of ionic and non-ionic agents.

Peck, Wallace W.; Slutsky, R A; Hackney, David B.; Mancini, G.B.John; Higgins, Charles B.

doi:10.1148/radiology.149.2.6622678

Cited by 34 publications

(10 citation statements)

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“…As such, the difference in perfusion values between normal subjects and those with PPH may have been overestimated. Secondly, radiographical contrast agents, even nonionic media, are known to have mild vasodilatory properties [23,24]. The relative importance of this effect in the increase in perfusion seen with the addition of adenosine in patients with PPH is difficult to quantify, but in previous work, where subjects have been studied under the same conditions on two occasions, the effects seem to be minimal [4].…”

Section: Discussionmentioning

confidence: 99%

Quantifying pulmonary perfusion in primary pulmonary hypertension using electron-beam computed tomography

Jones

Hansell²,

Evans

2004

Eur Respir J

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Traditionally, a gravitational distribution of pulmonary perfusion has been described in normal subjects. How this may vary in patients with primary pulmonary hypertension (PPH), which is characterised by vascular obstruction due to intimal thickening, smooth muscle cell proliferation and episodes of thrombosis in small and medium sized pulmonary arteries, is unclear. In this study the potential of electronbeam computed tomography in quantifying the distribution of pulmonary perfusion in patients with PPH was investigated.Contrast-enhanced sections were obtained during inspiration in the supine position at baseline and during administration of the vasodilator adenosine in five healthy subjects and five patients with PPH. Under each experimental condition, regions of interest were placed along the nondependent-to-dependent axis and values for relative perfusion derived.In healthy individuals, a marked nondependent-to-dependent gradient in perfusion was observed. By contrast, in PPH, perfusion values were significantly lower and were uniform across the lung section, although the administration of adenosine resulted in increased perfusion in all regions of interest.Electron-beam computed tomography provides physiological and structural information about the pulmonary circulation in subjects with pulmonary vascular disease. Traditionally, a gravitational distribution of pulmonary perfusion has been described in normal subjects, determined by the interrelationship between hydrostatic, alveolar and interstitial pressures [1,2]. More recently, animal studies, employing techniques with high spatial resolution, have suggested that the influence of gravity is less important than the structure of the pulmonary vascular tree in determining regional blood flow in the lungs [3]. Similar findings in humans have been confirmed by a study employing electronbeam computed tomography (EBCT) to quantify regional pulmonary perfusion [4]. EBCT allows the fast (millisecond) acquisition of the data necessary for cardiac imaging. Pulmonary regional blood flow can be calculated by applying an appropriate model to changes in lung density detected, following the passage of contrast. EBCT has been used previously in both animal and clinical studies of perfusion [5][6][7], the results obtained showed a good correlation with those found from microsphere-based investigations.Primary pulmonary hypertension (PPH) is characterised by the restriction of the pulmonary vascular bed, secondary to a combination of intimal thickening, vascular smooth muscle cell proliferation and episodes of thrombosis, in small-and medium-sized arteries. Studies of pulmonary perfusion patterns in PPH, excluding those aimed at differentiating between PPH and chronic thromboembolic disease, are scarce. However, investigations using computed tomography (CT) have shown that patients with systemic sclerosis and secondary pulmonary hypertension have a reduced density gradient between the dependent and nondependent parts of the lung, compared with similar patients ...

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Section: Discussionmentioning

confidence: 99%

Quantifying pulmonary perfusion in primary pulmonary hypertension using electron-beam computed tomography

Jones

Hansell²,

Evans

2004

Eur Respir J

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“…Thus, the indicator must mix completely with blood, should be as near as possible a bolus and must not itself influence flow. Others have shown that radiographic contrast material may influence regional pulmonary blood flow [20,21], although comparison of the results from repeated measurements in the current study made before and after each intervention (hypoxia, hypoxia plus NO) would effectively control for such variability.…”

Section: Discussionmentioning

confidence: 87%

Pulmonary perfusion quantified by electron-beam computed tomography: effects of hypoxia and inhaled NO

Jones¹,

Hansell²,

Evans³

2003

Eur Respir J

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Patients with acute lung injury may benefit from the manipulation of pulmonary blood flow using inhaled nitric oxide (iNO) to optimise ventilation/perfusion matching. Current techniques for studying changes in regional pulmonary perfusion are difficult to apply clinically. This study therefore investigated the potential of electronbeam computed tomography (EBCT) to quantify the effects of hypoxia and iNO on regional pulmonary perfusion in five healthy subjects.Contrast-enhanced sections were obtained sequentially under conditions of normoxia, hypoxia (fractional concentration of oxygen in inspired gas (FI,O 2 ) 0.12) and hypoxia, with iNO (14.8 parts per million (ppm)) administered during inspiration in the supine position. Regions of interest were placed along the nondependent to dependent axis and values for relative perfusion derived.Under normoxic conditions a vertical gradient of perfusion existed, which became less apparent due to increased perfusion in nondependent regions after the induction of hypoxia (FI,O 2 0.12). Under physiological circumstances, the distribution of pulmonary blood flow is regulated by a local action of alveolar oxygen tension on precapillary pulmonary vessels. Thus, the reflex of hypoxic pulmonary vasoconstriction (HPV) ensures that blood flow is diverted away from areas of damaged lung, thereby preserving the matching of ventilation (V9) and perfusion (Q9) [1,2]. In contrast, patients with acute lung injury (ALI) demonstrate diminished HPV leading to adverse changes in V9/Q9 matching, manifesting clinically as refractory hypoxaemia [3]. The favourable manipulation of V9/Q9 therefore assumes considerable therapeutic significance. In this context, nitric oxide (NO), an endothelially derived vasodilator that modulates vascular tone in health and disease [4], has been demonstrated to be a selective pulmonary vasodilator when administered by inhalation both in experimental animals [5,6] and humans [7], improving physiological variables (specifically pulmonary artery pressure (Ppa) and arterial oxygen tension) in patients with ALI [4]. The effects of NO on HPV in terms of the modulation of changes in regional pulmonary blood flow induced by hypoxaemia are, however, unknown.Although techniques for studying regional pulmonary perfusion have been difficult to apply clinically, a gravitational distribution of pulmonary perfusion has been described in normal subjects, determined by the interrelationship between hydrostatic, alveolar and interstitial pressures [8,9]. Moreover, animal studies employing high spatial-resolution techniques suggest that the influence of gravity is less important than the structure of the pulmonary vascular tree in determining regional blood flow in the lung [10,11]. The authors have recently employed electron-beam computed tomography (EBCT) to quantify regional pulmonary perfusion in normal subjects placed in the supine and prone positions, demonstrating that a gravitational gradient of pulmonary perfusion existed in both supine and prone positions [12]....

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“…An increase in pulmonary artery pressure has been reported following the intravascular injection of contrast media (Frisinger et al 1965;Almen et al 1980;Mills et al 1980;Peck et al 1983;Schrader et al 1987;Nicod et al 1987;Rees et al 1988;Tajima et al 1994;Pitton et al 1996;Sunnegardh et al 1990;Sorenson et al 1994). This sudden increase in pulmonary artery pressure is thought to contribute to the morbidity and mortality associated with pulmonary angiography, particularly in patients with pulmonary hypertension (Schrader et al 1987;Nicod et al 1987;Rees et al 1988;Tajima et al 1994;Pitton et al 1996).…”

Section: Effects Of Contrast Media On Pulmonary Circulationmentioning

confidence: 98%

“…This sudden increase in pulmonary artery pressure is thought to contribute to the morbidity and mortality associated with pulmonary angiography, particularly in patients with pulmonary hypertension (Schrader et al 1987;Nicod et al 1987;Rees et al 1988;Tajima et al 1994;Pitton et al 1996). There are conflicting reports in the literature about the mechanisms responsible for these effects (Almen et al 1980;Peck et al 1983;Schrader et al 1984Schrader et al , 1987Rees et al 1988;Sunnegardh et al 1990;Sorenson et al 1994;Kuhtz-Buschbeck et al 1997;Emery et al 2001). Some studies showed that the rise in pulmonary artery pressure is secondary to an increase in pulmonary vascular resistance (PVR) (Schrader et al 1984;Emery et al 2001), whereas others indicated that it is due to an increase in cardiac output associated with a decrease in pulmonary vascular resistance (Almen et al 1980;Sunnegardh et al 1990;Sorenson et al 1994;Kuhtz-Buschbeck et al 1997).…”

Section: Effects Of Contrast Media On Pulmonary Circulationmentioning

confidence: 99%

“…In the studies that suggested a fall in the vascular resistance, the PVR was not directly measured and was calculated from the formula PVR = (pulmonary artery pressure-pulmonary venous pressure)/cardiac output. The increase in cardiac output was attributed to reduced peripheral vascular resistance of the systemic circulation caused by contrast medium-induced vasodilatation (Almen et al 1980;Peck et al 1983;Schrader et al 1987;Sunnegardh et al 1990;Sorenson et al 1994;Kuhtz-Buschbeck et al 1997). The fall in PVR could be due to an increase in the capacity of the pulmonary vascular bed by recruitment of closed vessels and active vasodilatation of pulmonary arteries (Emery et al 2001).…”

Section: Effects Of Contrast Media On Pulmonary Circulationmentioning

confidence: 99%

See 1 more Smart Citation

Pulmonary Effects of Iodine-Based Contrast Media

Morcos

2014

Medical Radiology

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Effects of contrast media on pulmonary hemodynamics: comparison of ionic and non-ionic agents.

Cited by 34 publications

References 0 publications

Quantifying pulmonary perfusion in primary pulmonary hypertension using electron-beam computed tomography

Quantifying pulmonary perfusion in primary pulmonary hypertension using electron-beam computed tomography

Pulmonary perfusion quantified by electron-beam computed tomography: effects of hypoxia and inhaled NO

Pulmonary Effects of Iodine-Based Contrast Media

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