Medical Inspection – Health Blog

Presentation of a clinical case

A 48-year-old businessman presented himself at our Stone Centre 6 years ago, subsequent to a recent recurring episode of right kidney colic followed by the expulsion of a calcium ox- alate stone with traces of calcium phosphate. The medical history of the patient revealed a pneumonia in his youth, cured without repercussions, a duodenal ulcer treated with ranitidine and antacids, and a history of bilateral kidney stones, with at least 5 episodes in 13 years, one of which was treated with ESWL for left ureteral stone. In that occasion a pyelography was performed and was found to be normal ex­cept for hydronephrosis due to the stone which was later bro­ken up. We care about you health mycanadianhealthcare com

He had not been referred to a specialized Centre for stone dis­ease and the only advice given had been to eliminate milk, yo­ghurt and cheese from his diet and to drink plenty. The patient had only partially followed these instructions due to problems connected with his intense and stressful lifestyle. On occasions when his arterial blood pressure had been mea­sured it had, he reported, been “a little” high, but no provisions were then taken.

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Nitroprusside is frequently employed to lower blood pressure in a variety of situations where precise control over systemic hemodynamics is imperative. In the normal lung, this vasodilator does not produce any significant change in gas exchange. In contrast, a significant deterioration in gas exchange is produced when the drug is infused during pulmonary edema in experimental animals. Pulmonary edema is associ­ated with an increase in lung segments with low V/Q ratios using the inert gas technique. After vasodila­tor therapy, a further increase in perfusion of lung segments with low V/Q ratios in association with a decrease in arterial Pa0₂ and no change in cardiac output suggests inhibition of hypoxic vasoconstriction.

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There are a group of diverse, unrelated clinical states where alteration of the normal AHPR is ob­served, but the mechanisms remain unclear. The influence of lung inflation on the response is contro­versial. An increase in lung inflation is associated with a decrease in the magnitude of the response. Pul­monary hypertension and elevations of left atrial pressure blunt the AHPR, which may help, in part, to explain the V/Q abnormalities and hypoxemia associated with congestive heart failure, mitral steno­sis, and volume overload.

Alteration of the response occurs in some patients with pulmonary disease. A recent report of variability of the response in patients with COPD illustrates this point. Approximately 50 percent of the patients were nonresponders or poor responders in this series. An attenuation of hypoxic vasoconstriction in COPD is also suspected based upon the findings of maintained perfusion of nonventilated areas of lung in cases of suspected pulmonary embolism. Reports of the presence of marked ventilation/perfusion abnor­malities in the lungs of some, but not all, asthmatic patients with equivalent degrees of airway obstruction suggest variability of the AHPR in this patient popu­lation as well. These scattered observations do not answer the question of whether the alteration of the response preceded the onset of symptoms, or is an integral part of the disease in some patients.

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The pathophysiologic role of the AHPR in patients with acute cor pulmonale presenting with right ven­tricular failure, increased right ventricular afterload, and an elevated pulmonary vascular resistance is well known. A more controversial subject is whether hypoxic vasoconstriction is a stimulus for the vascular changes that occur during chronic hypoxic exposure. Chronic hypoxia is associated with well-documented morphologic changes of the pulmonary vasculature consisting of an increased muscularization of the pulmonary arteries, most prominently the small arte­rioles. Most of the evidence to date suggests that elevation in pulmonary artery pressure and vascular resistance alone are not the initiating events in the morphologic changes seen in the pulmonary circula­tion after chronic hypoxic exposure, although this remains a controversial point.

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The clinical implications of alterations of the AHPR are not widely appreciated. Our discussion of modifi­cation of the normal response will be arbitrarily divided into three areas: loss of the response in lung injury states; alteration of the response after chronic hypoxic exposure; and the alteration of the response in a diverse set of clinical conditions. Clinical condi­tions associated with alterations of the AHPR are in Table 3.

Loss of the Response in Lung Injury States

Pulmonary hypertension frequently accompanies the increase in vascular permeability in the adult respiratory distress syndrome. The pulmonary hy­pertension is the result of a combination of factors: vascular obstruction, obliteration, and vasoconstric­tion. The vasoconstrictive element in ARDS may represent a basic alteration of pulmonary vasoreac- tivity. In the presence of acute lung injury, even in the absence of pulmonary hypertension, blunting of hy­poxic pulmonary vasoconstriction may produce a mal­distribution of ventilation relative to perfusion, an increase in shunting, and an exacerbation of arterial hypoxemia.

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Direct effects of hypoxia on the vasculature are often discussed using a three-part model: sensor, transducer, and effector. The key questions for the oxygen sensor are its location and what specific cell or cell organelle plays this role. The likely site for the sensor is the precapillary arteriole, but the specific identity of the sensor cell(s) is still an open question. The location of the endothelial cell, the evidence that a normally functioning endothelium may be required for hypoxic vasoconstriction and endothelial produc­tion of relaxing and constricting factors strengthens the case that this cell may act as an oxygen sensor. Biochemical candidates for the sensor include: the mitochondrial oxidative phosphorylation system and cytochrome.

The pulmonary vascular smooth muscle cell is the effector cell. If the vascular smooth muscle cell is not also the sensor cell, a key unresolved issue is the form of communication, or signal transduction, between the sensor and effector cells. Undefined signals from other lung cells to the effector cell may be important in the cascade of events leading to contraction.

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Mechanism

Two main hypotheses underlie most investigations of the mechanism of the AHPR. The first is that the response is dependent on the release of a vasoactive mediator from some site within the lung. The opposing view states that acute hypoxia elicits vasoconstriction via a direct effect on pulmonary vascular smooth muscle without the involvement of a mediator.

Mediator Hypothesis

The mediator hypothesis is derived from work with isolated pulmonary artery segments in which the AHPR appeared to be dependent upon the presence of parenchyma attached to the vessels, since the response could not be elicited with isolated vessels alone. Data gathered in pursuit of this question occupied a central position in research involving the pulmonary circulation for many years.

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