Physiology, Pathophysiology, and Anesthetic Management of Patients with Respiratory Disease

McDonell, Wayne N.; Kerr, Carolyn L.

doi:10.1002/9781119421375.ch27

Cited by 29 publications

(68 citation statements)

References 212 publications

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“…A reason for hypercapnia may be The value of pCO 2 increased in spontaneously breathing dogs anesthetized with isoflurane and the increase depends on the dose of isoflurane. The lowest increase of pCO 2 was noted with methoxyflurane and enflurane anaesthesia and in dogs in comparison to other species (McDONELL and KERR, 2007).…”

Section: Discussionmentioning

confidence: 99%

Acid-base balance during volatile and total intravenous anaesthesia in dogs

Capak

Filipović-Genter

Nesek-Adam³

et al. 2017

Vet.arhiv

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The aim of this study was to compare the effects of two different anesthetic techniques on the acid base balance in bitches. Research was carried out on 20 bitches randomly divided into two groups. In group A general anaesthesia was induced by intravenous application of ketamine and diazepam, and maintained with an additional intravenous bolus of ketamine. In group B a combination of propofol and ketamine was used for induction of anaestesia. General anaesthesia was maintained with N 2 O and O 2 in a range of 1:1 in combination with 2% isoflurane. Animals in both groups were kept on spontaneous ventilation. Arterial blood for blood gas analysis was taken at two time points (3 and 45 min. after induction of anaesthesia, respectively). Group A had a significantly (P<0.05) higher pH value than Group B at 45 min. The pCO 2 was significantly (P<0.05) lower in group A than in group B at 3 and 45 min, respectively. There was also a significant difference in values of pO 2 between the groups at 3 and 45 min. The pO 2 was lower in group A than in group B. Group B had a significantly (P<0.05) higher HCO 3 -value than Group A at 45 min. Volatile anaesthesia minimally disturbs acid-base balance, and oxygen access capability is better.

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Section: Discussionmentioning

confidence: 99%

Acid-base balance during volatile and total intravenous anaesthesia in dogs

Capak

Filipović-Genter

Nesek-Adam³

et al. 2017

Vet.arhiv

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“…The P (a-ET) CO 2 was divided by P a CO 2 and denoted as an estimate of alveolar dead space, and called alveolar dead space fraction [VDalv frac = P (a-ET) CO 2 /P a CO 2 ] ( 4 ). The concept of using P a CO 2 and P ET CO 2 to estimate “dead space” was adapted in equine anesthesia over 40 years ago ( 5 , 6 ) and has been used extensively ever since to estimate “dead space” in many animal species ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

Physiologic Factors Influencing the Arterial-To-End-Tidal CO2 Difference and the Alveolar Dead Space Fraction in Spontaneously Breathing Anesthetised Horses

et al. 2018

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The arterial to end-tidal CO2 difference (P(a-ET)CO2) and alveolar dead space fraction (VDalvfrac = P(a-ET)CO2/PaCO2), are used to estimate Enghoff’s “pulmonary dead space” (V/QEng), a factor which is also influenced by venous admixture and other pulmonary perfusion abnormalities and thus is not just a measure of dead space as the name suggests. The aim of this experimental study was to evaluate which factors influence these CO2 indices in anesthetized spontaneously breathing horses. Six healthy adult horses were anesthetized in dorsal recumbency breathing spontaneously for 3 h. Data to calculate the CO2 indices (response variables) and dead space variables were measured every 30 min. Bohr’s physiological and alveolar dead space variables, cardiac output (CO), mean pulmonary pressure (MPP), venous admixture (Q˙s/Q˙t), airway dead space, tidal volume, oxygen consumption, and slope III of the volumetric capnogram were evaluated (explanatory variables). Univariate Pearson correlation was first explored for both CO2 indices before V/QEng and the explanatory variables with rho were reported. Multiple linear regression analysis was performed on P(a-ET)CO2 and VDalvfrac assessing which explanatory variables best explained the variance in each response. The simplest, best-fit model was selected based on the maximum adjusted R2 and smallest Mallow’s p (Cp). The R2 of the selected model, representing how much of the variance in the response could be explained by the selected variables, was reported. The highest correlation was found with the alveolar part of V/QEng to alveolar tidal volume ratio for both, P(a-ET)CO2 (r = 0.899) and VDalvfrac (r = 0.938). Venous admixture and CO best explained P(a-ET)CO2 (R2 = 0.752; Cp = 4.372) and VDalvfrac (R2 = 0.711; Cp = 9.915). Adding MPP (P(a-ET)CO2) and airway dead space (VDalvfrac) to the models improved them only marginally. No “real” dead space variables from Bohr’s equation contributed to the explanation of the variance of the two CO2 indices. P(a-ET)CO2 and VDalvfrac were closely associated with the alveolar part of V/QEng and as such, were also influenced by variables representing a dysfunctional pulmonary perfusion. Neither P(a-ET)CO2 nor VDalvfrac should be considered pulmonary dead space, but used as global indices of V/Q mismatching under the described conditions.

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“…As the FiO 2 was the same for both groups, this difference occurred due to V/Q changes (Cortopassi et al, 2002) occurring in PG impairing gas exchange. This hypothesis can be confirmed by values of PA-aO 2 (Table 2), which provide a convenient and practical measure of the relative efficiency of gas exchange (McDonell and Kerr, 2007). In TG, PA-aO 2 was lower than in PG, in which high values of this parameter occurred mainly due to V/Q and diffusion impairment (Levistzky, 2004).…”

Section: Resultsmentioning

confidence: 54%

“…According to Hirota et al (2002) and Hashimoto et al (2000), when PH is induced by serotonin, the bronchial cross-sectional area (BCA) decreases by 50% and Raw increases as described by the Hagen-Poiseuille law (McDonell and Kerr, 2007). Therefore, the BCA should be decreased in this study, because the protocol used to induce PH was the same cited by these authors.…”

Section: Resultsmentioning

confidence: 99%

Cardiopulmonary parameters in propofol- or thiopental-anesthetized dogs induced to pulmonary hypertension by serotonin

Lopes¹,

Nunes²,

Paula³

et al. 2015

Arq. Bras. Med. Vet. Zootec.

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Cardiopulmonary parameters in propofol-or thiopental-anesthetized dogs induced to pulmonary hypertension by serotonin ABSTRACTThe cardiopulmonary changes in propofol-or thiopental-anesthetized dogs induced to pulmonary hypertension (PH) were evaluated. Twenty adult animals were randomly assigned to two groups: propofol group (PG) and thiopental group (TG). In PG, propofol was used for induction (80.03mg.kg -1 ) and anesthesia maintenance (0.8mg.kg -1 .minute -1 ), while, in TG, thiopental was used (22±2.92mg.kg -1 ; 0.5mg.kg -1 .minute -1 , respectively). Mechanical ventilation using time cycle was started. PH was induced by administration of serotonin (5HT) (10µg.kg -1 and 1mg.kg -1 .hour -1 ) through a thermodilution catheter positioned in the pulmonary artery. The measurements were performed before administration of 5HT (T0), after 30 minutes (T30), then at 15-minute intervals (T45, T60, T75 and T90). No differences between groups were registered for systolic (sPAP) and mean pulmonary arterial pressure (mPAP), mean arterial pressure (MAP), total peripheral resistance index (TPRI) and pulmonary vascular resistance index (PVRI). In PG, sPAP and mPAP increased from T30. While in TG, sPAP and mPAP increased from T75. In PG, heart rate (HR) increased from T30, in which PG was higher than TG. The TPRI values decreased from T30 in PG, and in TG, at T45, T60 and T90. In PG, at T0, PVRI was lower than at other times. In PG, arterial partial pressures of oxygen (PaO 2 ) decreased from T60 and alveolar-arterial oxygen gradient (PA-aO 2 ) increased at T60. In TG, at T0 PaO 2 was higher than at T30, T45, T60 and T90, while PA-aO 2 at T0 was lower than at T90. From T30 to T90, TG showed higher PaO 2 means and lower arterial partial pressures of carbon dioxide (PaCO 2 ) values when compared to PG. In PG, from T30, PaCO 2 increased, while in TG this parameter was stable. In conclusion, thiopental anesthesia attenuated the cardiopulmonary changes resulting from serotonin-induced PH, probably by attenuation of vasoconstriction and bronchoconstriction.

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Physiology, Pathophysiology, and Anesthetic Management of Patients with Respiratory Disease

Cited by 29 publications

References 212 publications

Acid-base balance during volatile and total intravenous anaesthesia in dogs

Acid-base balance during volatile and total intravenous anaesthesia in dogs

Physiologic Factors Influencing the Arterial-To-End-Tidal CO2 Difference and the Alveolar Dead Space Fraction in Spontaneously Breathing Anesthetised Horses

Cardiopulmonary parameters in propofol- or thiopental-anesthetized dogs induced to pulmonary hypertension by serotonin

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