Mechanisms of hypoxemia and hypocapnia in pulmonary embolism.

Santolicandro, A.; Prediletto, Renato; Fornai, E.; Formichi, Bruno; Begliomini, E; Giannella-Neto, Antonio; Giuntini, C.

doi:10.1164/ajrccm.152.1.7599843

Cited by 73 publications

(57 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Anatomically, blood fl ow was diverted to the less embolized regions, while in contrary, the regions distal to the heavily embolized regions received less blood fl ow. Our data were compatible with those from Santolicandro et al who pioneered in this fi eld using the multiple inert gas elimination technique (MIGET) and showed the importance and varying extent of V/Q mismatch after APTE, at the time of diagnosis among patients and during their subsequent recovery (Santolicandro et al 1995).…”

Section: Introductionsupporting

confidence: 92%

The Unpredictable Effect of Changing Cardiac Output on Hypoxemia after Acute Pulmonary Thromboembolism

Tsang

Lamm

Neradilek³

et al. 2008

Clinical medicine. Circulatory, respiratory and pulmonary medic

View full text Add to dashboard Cite

Previous studies reported that the degree of hypoxemia following acute pulmonary thromboembolism (APTE) was highly variable and that its mechanism was mainly due to the creation of many high and low ventilation/perfusion (V/Q) units, as a result of the heterogeneous regional blood fl ow (Q) caused by embolic obstruction. We studied the effect of changing cardiac output (Q t ) on gas exchange after APTE in 5 embolized piglets (23 ± 3 Kg), using Dobutamine intermittently at approximately 20 µg/kg/min for 120 minutes. The distribution of ventilation (V) and perfusion (Q) at various times was mapped using fl uorescent microspheres in 941 ± 60 lung regions. After APTE, increase in Q t by Dobutamine improved venous oxygen tension (PvO 2 ) but arterial PaO 2 did not change consistently. On the other hand, cluster analysis showed that the V/Q ratio of most lung regions was lowered due to increases in Q at the same time. We concluded that the effect of changing cardiac output on gas exchange following APTE was affected by the simultaneous and varying balance between the changing V/Q mismatch and the concomitantly changing PvO 2 , which might explain the unpredictability of PaO 2 in the clinical setting.

show abstract

Section: Introductionsupporting

confidence: 92%

The Unpredictable Effect of Changing Cardiac Output on Hypoxemia after Acute Pulmonary Thromboembolism

Tsang

Lamm

Neradilek³

et al. 2008

Clinical medicine. Circulatory, respiratory and pulmonary medic

View full text Add to dashboard Cite

show abstract

“…Some hypotheses are suggested, aiming to explain hypoxemia during PE. Santolicandro et al [14] declare that one of the causes may be the inadequate ventilation/perfusion ratio (V A /Q), which leads to a reduction in PvO 2 ; hypothesis also defended by D'Alonzo et al [15].…”

Section: Discussionmentioning

confidence: 99%

Embolia pulmonar quase fatal, um modelo experimental

Pereira¹,

Moreira²,

Paschoal³

et al. 2011

Rev Bras Cir Cardiovasc

View full text Add to dashboard Cite

Embolia pulmonar quase fatal, um modelo experimental: variáveis hemodinâmicas, gasométricas e capnográficasNear-fatal pulmonary embolism in an experimental model: hemodynamic, gasometric and capnographic variables Abstract Introduction: Experimental studies on pulmonary embolism (PE) are usually performed under mechanical ventilation. Most patients with suspicion of PE enter the Emergency Services in spontaneous breathing and environmental air. Thus, under these conditions, measurements of hemodynamic, gasometric and capnographic variables contribute largely to a more specific comprehension of cardiopulmonary and gasometric alterations in the acute phase of the disease. Studies which evaluated animals under conditions are lacking.Objective: This study aimed to submit animals under spontaneous ventilation and without supplemental oxygen to PE.Methods: PE was induced in six pigs using autologous blood clots, and cardiorespiratory and gasometric records were performed before and after PE. The values of "near fatal" mean pulmonary arterial pressure (MPAP) were previously determined.Results Conclusion: In this model, the near fatal MPAP was from 2 to 2.5 times the basal MPAP; and the capnographic variables, associated with arterial and venous gasometry, showed effective in discriminating an acute obstructive profile.Descriptors: Pulmonary embolism. Hypertension, pulmonary. Capnography. Models, animal. Swine. ResumoIntrodução: Estudos experimentais de embolia pulmonar (EP) são habitualmente realizados sob ventilação mecânica. A maioria dos pacientes com suspeita de EP adentra os Serviços de Emergência em respiração espontânea e em ar ambiente. Assim, medidas das variáveis hemodinâmicas, gasométricas e capnográficas, nessas condições, em muito Universitária "Zeferino Vaz"

show abstract

“…The new onset of hypocarbia resulting from hyperventilation, is another possible manifestation of PE. 9 Also, hyponatremia, representing high antidiuretic hormone levels (ADH) may have been induced by the hypotension of PE. Hypotension is a powerful stimulus to ADH secretion and can over-ride osmolality as a control for its secretion, particularly in tetraplegic patients.…”

Section: Pulmonary Hypertension and Pulmonary Embolimentioning

confidence: 99%

Recurrent pulmonary embolism and pulmonary hypertension in chronic tetraplegia

Frisbie

Sharma

Brahma³

et al. 2005

Spinal Cord

View full text Add to dashboard Cite

Study design: Case report. Objective: To describe an unusual case of progressive pulmonary hypertension due to recurrent pulmonary embolism in a chronically paralyzed spinal cord injury patient. Setting: Veterans Administration Hospital, West Roxbury, MA, USA. Subject: A 57-year-old man, tetraplegic, sensory incomplete and motor complete for 30 years due to a diving accident, complained of lightheadedness and shortness of breath intermittently for 7 years. Examination during the latest episode revealed anxiety, confusion, respirations 28 per min, blood pressure 80/60 mmHg, and arterial pH 7.41, P CO 2 28 mmHg, P O 2 95 mmHg on 2 l of oxygen. A chest film 2 weeks earlier had revealed a right-sided cutoff of pulmonary vasculature; the current film showed right-sided pleural effusion. Review of EKGs showed a trend of increasing right axis deviation with recovery and recurrences during the previous 9 years and a current incomplete right bundle branch block with clockwise rotation and inverted T waves in V1-4. Computerized tomography with contrast material revealed small pulmonary emboli, but only in retrospect. The patient died shortly after scanning. Autopsy: The pulmonary arteries were free of thromboemboli on gross examination but medium and small-sized arteries were constricted or obliterated with thrombotic material microscopically. The estimated ages of the thromboemboli ranged from days to years. The right ventricle was hypertrophied; the coronary arteries were patent. Conclusion: Recurrent pulmonary emboli resulted in chronic pulmonary hypertension and eventual death in a patient with chronic tetraplegia.Spinal Cord (2005) 43, 625-630.

show abstract

Mechanisms of hypoxemia and hypocapnia in pulmonary embolism.

Cited by 73 publications

References 29 publications

The Unpredictable Effect of Changing Cardiac Output on Hypoxemia after Acute Pulmonary Thromboembolism

The Unpredictable Effect of Changing Cardiac Output on Hypoxemia after Acute Pulmonary Thromboembolism

Embolia pulmonar quase fatal, um modelo experimental

Recurrent pulmonary embolism and pulmonary hypertension in chronic tetraplegia

Contact Info

Product

Resources

About