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Ventilation-perfusion mismatch

Patients with an oxygen saturation less than 90% (less than 95% in children, pregnant women, and patients with co-existing heart disease) should receive oxygen with the dose adjusted to keep oxygen saturation above these levels.3,12,40 Hypoxemia usually results from a ventilation/perfusion mismatch, and low oxygen levels (less than 30% of the fraction of inspired air) administered by nasal cannula or facemask are sufficient to reverse hypoxemia in most patients. [Pg.225]

Ventilation-perfusion mismatch leads to hypoxemia. Reduced ventilation caused by obstructed airflow or reduced perfusion caused by obstructed blood flow leads to impaired gas exchange. Interestingly, each of these conditions is minimized by local control mechanisms that attempt to match airflow and blood flow in a given lung unit. [Pg.263]

Cyanide toxicity, overshoot hypotension, and myocardial ischaemia. Hypoxia caused by increased ventilation-perfusion mismatch due to pulmonary vasodilatation and inhibition of hypoxic pulmonary vasoconstriction. Rebound hypertension after discontinuation of SNP infusion. [Pg.147]

Calcium channel blockers with vasodilator effects, such as nifedipine, nicardipine, and nimodipine, will potentiate the effect of vasodilator effects of, e.g. halothane or isoflurane, potentiating any hypotension. This is especially obvious in hypertensive patients and when combined with similarly acting agents, such as sodium nitroprusside or nitroglycerin. Similarly, they also enhance the tendency of volatile anaesthetics to reduce hypoxic pulmonary vasoconstriction, which might exacerbate ventilation/perfusion mismatching during anaesthesia. [Pg.276]

Copper iron sulfide dust explosion 1 miner died within minutes. The other 2 experienced intense bunting of eyes, nose, and throat dyspnea diffuse pircoedial and retro sternal chest pain nausea, vomiting urinary incontinence. 3 wk after the exposure, the workers had severe airway obstruction, hypoxemia, markedly decreased exercise tolerance, ventilation-perfusion mismatch, evidence of active inflammation (positive gallium scar)... [Pg.283]

Q7 If the embolus is quite large and obstructs a significant area of the pulmonary circulation, the affected area of lung will be underperfused or non-perfused. The area may continue to be ventilated for some time, causing a ventilation-perfusion mismatch, which leads to poor gas exchange and abnormal blood gas tensions. The lung volume in the affected area decreases, and this decrease in size can sometimes be seen on a chest X-ray. After some hours, surfactant production declines in the non-perfused area of lung and the alveoli collapse. [Pg.256]

Basoglu T, Erkan L, Canbaz F, Bernay I, Onen T, Sahin M, Furtun F, Yalin T. Transient reverse ventilation-perfusion mismatch in acute pulmonary nitrofurantoin reaction. Ann Nucl Med 1997 ll(3) 271-4. [Pg.2546]

The PO2 in arterial blood, however, is further reduced by venous admixture (shunt), the addition of mixed venous blood from the pulmonary artery, which has a POj of -5.3 kPa (40 mm Hg). Together, the diffusional barrier, ventilation-perfusion mismatches, and the shunt fraction are the major causes of the alveolar-to-arterial oxygen gradient, which is normally 1.3-1.6 kPa (10-12 mm Hg) when air is breathed and 4.0-6.6 kPa (30-50 mm Hg) when 100% oxygen is breathed. [Pg.253]

Nitroprusside can worsen hypoxemia in patients with chronic obstructive pulmonary disease because the drug interferes with hypoxic pulmonary vasoconstriction and thereby promotes ventilation/perfusion mismatch. [Pg.559]


See other pages where Ventilation-perfusion mismatch is mentioned: [Pg.474]    [Pg.127]    [Pg.67]    [Pg.246]    [Pg.2542]    [Pg.516]    [Pg.519]    [Pg.567]    [Pg.346]    [Pg.170]    [Pg.1148]    [Pg.458]    [Pg.468]    [Pg.376]    [Pg.66]    [Pg.73]    [Pg.76]    [Pg.106]    [Pg.27]    [Pg.28]    [Pg.372]    [Pg.446]    [Pg.664]   
See also in sourсe #XX -- [ Pg.127 ]




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