Effect of lactic acidosis on canine hemodynamics and left ventricular function

1990 ◽  
Vol 258 (4) ◽  
pp. H1193-H1199 ◽  
Author(s):  
K. Teplinsky ◽  
M. O'Toole ◽  
M. Olman ◽  
K. R. Walley ◽  
L. D. Wood
Keyword(s):  
Cardiac Output ◽  
Lactic Acidosis ◽  
Stroke Volume ◽  
Venous Return ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Right Atrial ◽  
Lactic Acidemia

Hypoperfusion states cause lactic acidosis, and the acidemia further reduces the inadequate cardiac output. Conceivably, the adverse effect of lactic acidemia on cardiac output is due to depressed contractility demonstrated in isolated myocardium. Alternatively, factors governing venous return cause a relative hypovolemic state and/or acidemic pulmonary vasoconstriction-induced right ventricular dysfunction. We reasoned that examination of left ventricular pressure-volume relationships at end systole and end diastole would determine which of these potential mechanisms accounted for reduced cardiac output during progressive lactic acidosis in anesthetized, mechanically ventilated dogs. Left ventricular (LV) volume was estimated from two pairs of epicardial ultrasonic crystals placed in the anterior-posterior and longitudinal planes, and LV pressure was obtained rom a catheter-tipped transducer. During progressive acidemia induced by a continuous intravenous infusion of 0.5 N lactic acid, cardiac output, stroke volume, and mean systemic arterial pressure fell significantly while mean pulmonary artery pressure and right atrial pressure increased significantly. These variables did not change with time in control (no-acid infusion) dogs. Lactic acidemia caused a 40% reduction in stroke volume, which could be attributed to depressed LV contractility, characterized by a decrease in maximum dP/dt as well as a fall in slope (Emax) with no change in volume intercept (Vo) of the left ventricular pressure-volume relationship at end systole. Neither the measured left ventricular end-diastolic pressure nor the estimated left ventricular end-diastolic volume (LVEDV) decreased with acidemia, suggesting that the reduced venous return did not result from relative hypovolemia. However, acidemic pulmonary hypertension may have interfered with the expected response to myocardial depression, which is an increase in LVEDV.

scholarly journals Pharmacodynamics and Pharmacokinetics of Injectable Pimobendan and Its Metabolite, O-Desmethyl-Pimobendan, in Healthy Dogs

2021 ◽  
Vol 8 ◽  
Author(s):  
Poonavit Pichayapaiboon ◽  
Lalida Tantisuwat ◽  
Pakit Boonpala ◽  
Nakkawee Saengklub ◽  
Tussapon Boonyarattanasoonthorn ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Maximum Rate ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Cardiac Contraction ◽  
Ventricular Pressure ◽  
Right Atrial ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial

Objectives: This study was designed to thoroughly evaluate the effects of bolus pimobendan at a dose of 0.15 mg/kg on cardiac functions, hemodynamics, and electrocardiographic parameters together with the pharmacokinetic profile of pimobendan and its active metabolite, o-desmethyl-pimobendan (ODMP), in anesthetized dogs.Methods: Nine beagle dogs were anesthetized and instrumented to obtain left ventricular pressures, aortic pressures, cardiac outputs, right atrial pressures, pulmonary arterial pressures, pulmonary capillary wedge pressures, electrocardiograms. After baseline data were collected, dogs were given a single bolus of pimobendan, and the pharmacodynamic parameters were obtained at 10, 20, 30, 60, and 120 min. Meanwhile, the venous blood was collected at baseline and 2, 5, 10, 20, 30, 60, 120, 180, 360, and 1,440 min after administration for the determination of pharmacokinetic parameters.Results: Compared with baseline measurements, the left ventricular inotropic indices significantly increased in response to intravenous pimobendan, as inferred from the maximum rate of rise in the left ventricular pressure and the contractility index. Conversely, the left ventricular lusitropic parameters significantly decreased, as inferred from the maximum rate of fall in the left ventricular pressure and the left ventricular relaxation time constant. Significant increases were also noted in cardiac output and systolic blood pressure. Decreases were observed in the systemic vascular resistance, pulmonary vascular resistance, left ventricular end-diastolic pressure, pulmonary capillary wedge pressure, right atrial pressure, and pulmonary arterial pressure. The heart rate increased, but the PQ interval decreased. There was no arrhythmia during the observed period (2 h). The mean maximum plasma concentration (in μg/L) for ODMP was 30.0 ± 8.8. Pimobendan exerted large volume of distribution ~9 L/kg.Conclusions: Intravenous pimobendan at the recommended dose for dogs increased cardiac contraction and cardiac output, accelerated cardiac relaxation but decreased both vascular resistances. These mechanisms support the use of injectable pimobendan in acute heart failure.

Beat-to-Beat Analysis of Left Ventricular Pressure-Volume Relation and Stroke Volume by Conductance Catheter and Aortic Modelflow in Cardiomyoplasty Patients

Circulation ◽  
1995 ◽  
Vol 91 (7) ◽  
pp. 2010-2017 ◽  
Author(s):  
J.J. Schreuder ◽  
F.H. van der Veen ◽  
E.T. van der Velde ◽  
F. Delahaye ◽  
O. Alfieri ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Conductance Catheter ◽  
Volume Relation

scholarly journals Possible mechanism of the cardio-renal protective effects of AVE-0991, a non-peptide Mas-receptor agonist, in diabetic rats

2012 ◽  
Vol 13 (3) ◽  
pp. 334-340 ◽  
Author(s):  
Kulwinder Singh ◽  
Kuldeepak Sharma ◽  
Manjeet Singh ◽  
PL Sharma
Keyword(s):  
Blood Pressure ◽  
Receptor Agonist ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Protective Effects ◽  
Mas Receptor ◽  
Arterial Blood

Hypothesis: This study was designed to investigate the cardio-renal protective effect of AVE-0991, a non-peptide Mas-receptor agonist, and A-779, a Mas-receptor antagonist, in diabetic rats. Materials and methods: Wistar rats treated with streptozotocin (50 mg/kg, i.p., once), developed diabetes mellitus after 1 week. After 8 weeks, myocardial functions were assessed by measuring left ventricular developed pressure (LVDP), rate of left ventricular pressure development (d p/d tmax), rate of left ventricular pressure decay (d p/d tmin) and left ventricular end diastolic pressure (LVEDP) on an isolated Langendorff’s heart preparation. Further, mean arterial blood pressure (MABP) was measured by using the tail-cuff method. Assessment of renal functions and lipid profile was carried out using a spectrophotometer. Results: The administration of streptozotocin to rats produced persistent hyperglycaemia, dyslipidaemia and hypertension which consequently produced cardiac and renal dysfunction in 8 weeks. AVE0991 treatment produced cardio-renal protective effects, as evidenced by a significant increase in LVDP, d p/d tmax, d p/d tmin and a significant decrease in LVEDP, BUN, and protein urea. Further, AVE-0991 treatment for the first time has been shown to reduce dyslipidaemia and produced antihyperglycaemic activity in streptozotocin-treated rats. However, MABP and creatinine clearance remained unaffected with AVE-0991 treatment. Conclusions: AVE-0991 produced cardio-renal protection possibly by improving glucose and lipid metabolism in diabetic rats, independent of its blood pressure lowering action.

Left Heart Bypass in the Pig with a Centrifugal Pump Using Cannulae Prepared for Percutaneous Placement

1998 ◽  
Vol 21 (5) ◽  
pp. 285-290 ◽  
Author(s):  
B.H. Walpoth ◽  
V. Mehan ◽  
R. Rogulenko ◽  
B. Aeschbacher ◽  
G. Vucic ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Cardiogenic Shock ◽  
Centrifugal Pump ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Left Heart ◽  
Mean Flow ◽  
Left Heart Bypass ◽  
Heart Bypass

A rapid and efficient circulatory support system may save a patient in cardiogenic shock. Left heart bypass with percutaneous and trans-septal placement of the aspiration cannula simplifies the circuit and eliminates the need for an oxygenator. In this pre-clinical study we assessed left heart bypass support with a centrifugal pump using new cannulae prepared for percutaneous placement (14 F arterial catheter and 16 F left atrial aspiration line) in 5 anaesthetized pigs. Animals were supported for two hours at a mean flow of 3.2 l/min (4,033 rpm), a mean haematocrit of 29% and low heparinisation (ACT double baseline). Hemodynamic measurements and blood samples were taken at baseline (A), 10 minutes (B), one hour (C) and 2 hours (D) on support. Results show maintenance of hemodynamic parameters throughout the 2 hour support period. Only systolic arterial and left ventricular pressure decreased by 12% and 20% respectively from baseline to the end of the support period with a 13% increase in cardiac output. When the pump was turned on (0–3 l/min) there was usually a decrease in heart rate, systolic pressure and left ventricular pressure, with unchanged cardiac output (non failing model). Potassium increased from 3.9 to 4.2 mmol/l (ns), and plasma hemoglobin from 6.0 to 18.2 mg/dl (p<0.05). Thrombocytes decreased from 187 to 155 109/1 (ns). In conclusion, this preclinical study demonstrated the feasibility of an efficient left heart bypass of short duration with a centrifugal pump using cannulae prepared for percutaneous placement. Left heart bypass was well tolerated hemodynamically and no significant laboratory change occurred within the two hours of support. This opens several possibilities for the short term support of patients in cardiogenic shock and eventually also for patients submitted to minimally invasive cardiac surgery.

scholarly journals Autocorrelation Patterns in the Left-Ventricular Pressure Course of Isolated Working Hearts at Sinus Rhythm

2016 ◽  
Vol 8 ◽  
Author(s):  
Stefan F. J. Langer
Keyword(s):  
Sinus Rhythm ◽  
Small Animal ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Right Atrial ◽  
Random Fluctuation ◽  
Contractile Reserve ◽  
Random Component ◽  
Hemodynamic Parameters

<pre class="western">Background Observations of short term uniformity or microrhythmical undulation in ventricular pressure courses at sinus rhythm are lacking but necessary to describe cardiac status. The present investigation aims for (a) detecting repetitive similarity patterns in ventricular pressure at isolated sinus rhythm, (b) tagging hemodynamic parameters which contribute most to dissimilarity, and (c) for a stochastical characterisation of the random component in mutual similarity. Methods Left-ventricular pressure curves from isolated working small animal hearts, at sinus rhythm and electrical stimulation, are analysed by autocorrelation. Results Ventricular pressure courses consistently reach their peak coefficient of autocorrelation either at one-beat lag (monorhythm) or at two-beat lag (duorhythm). Replacing sinus rhythm with strictly even electrical right-atrial stimulation provokes more duorhythms to occur (Langer paradox). Duorhythms become scarcer at hypothermia and high cardiac output. Repetition of very similarly shaped beats accords with an exponential law. Variability of twelve hemodynamic parameters, regarding microrhythm, is given as a Table. Conclusions (a) Incidence of alternating patterns (duorhythms) suggests the presence of effective heterometric autoregulation (Frank-Starling law). Consequently, a pacing test may assess contractile reserve in certain conditions. Higher multi-beat patterns occur by chance at isolated sinus rhythm. (b) Interbeat variability of relevant hemodynamic parameters complies with the initial conclusion. Statistical pooling of data from consecutive beats seems permissible; pooling alterant beats separately will do better. (c) Random fluctuation is a constituent part of medium-term ventricular pressure course. Mutually very similar beats occur stochastically by a Poisson process with fade-out. Deviations accord with the presence of mono- or duorhythms.</pre>

Hemodynamic determinants of the maximal rate of rise of left ventricular pressure

1963 ◽  
Vol 205 (1) ◽  
pp. 30-36 ◽  
Author(s):  
Andrew G. Wallace ◽  
N. Sheldon Skinner ◽  
Jere H. Mitchell
Keyword(s):  
Heart Rate ◽  
Diastolic Pressure ◽  
Complex Function ◽  
Left Ventricular Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Maximal Rate ◽  
Pressure Development ◽  
Ventricular Activation

The maximal rate of left ventricular pressure development (max. dp/dt) was measured in an areflexic preparation which permitted independent control of stroke volume, heart rate, and aortic pressure. Max. dp/dt increased as a result of elevating ventricular end-diastolic pressure. Elevating mean aortic pressure and increasing heart rate each resulted in a higher max. dp/dt without a change in ventricular end-diastolic pressure. Aortic diastolic pressure was shown to influence max. dp/dt in the absence of changes in ventricular end-diastolic pressure or contractility. Increasing contractility increased max. dp/dt while changing the manner of ventricular activation decreased max. dp/dt. These findings demonstrate that changes in max. dp/dt can and frequently do reflect changes in myocardial contractility. These data also indicate that max. dp/dt is a complex function, subject not only to extrinsically induced changes in contractility, but also to ventricular end-diastolic pressure, aortic diastolic pressure, the manner of ventricular activation, and intrinsic adjustments of contractility.

Impaired early and intact late diastolic function in stunned myocardium induced by demand ischemia

1993 ◽  
Vol 264 (3) ◽  
pp. H739-H746 ◽  
Author(s):  
S. Miyazaki ◽  
Y. Goto ◽  
H. Nonogi ◽  
Y. Kawase ◽  
K. Haze ◽  
...  
Keyword(s):  
Diastolic Function ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Stunned Myocardium ◽  
Segment Length ◽  
Short Axis ◽  
The Mean

Changes in left ventricular diastolic properties of pacing-induced stunned myocardium were examined in 10 anesthetized dogs instrumented with a micromanometer for left ventricular pressure and sonomicrometers for left ventricular short axis, anterior and posterior segment lengths, and posterior wall thickness. After the creation of a critical stenosis on a carotid-circumflex coronary artery bypass, left ventricular pressure and dimensions were recorded simultaneously during temporary superior and inferior vena caval occlusion to allow for the construction of end-diastolic pressure-segment length curves. After 15 min of high-frequency pacing (190–220 beats/min), measurements were repeated and compared with those before pacing. The mean lengthening rate of each dimension during the first half of diastole was calculated as an index of early diastolic function. Three minutes after the end of pacing, coronary blood flow and perfusion pressure were unchanged, whereas systolic function of the posterior wall was depressed, indicating stunning of the posterior myocardium. The time constant of left ventricular pressure decay was prolonged by 14%. The mean lengthening rate during the first half of diastole decreased by 50% in the left ventricular internal short axis and by 119% in the posterior segment. Despite the significant impairment of early diastolic function, the regional end-diastolic pressure-segment length relation of the posterior wall was unchanged. Thus, in contrast to the results reported for pacing-induced ischemia that were measured immediately after pacing, the distensibility of the left ventricular wall in stunned myocardium induced by pacing was unchanged despite depressed early diastolic function.

scholarly journals Maximum heart rate does not limit cardiac output at rest or during exercise in the American alligator (Alligator mississippiensis)

2018 ◽  
Vol 315 (2) ◽  
pp. R296-R302 ◽  
Author(s):  
William Joyce ◽  
Ruth M. Elsey ◽  
Tobias Wang ◽  
Dane A. Crossley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Venous Return ◽  
Reciprocal Relationship ◽  
Alligator Mississippiensis ◽  
Right Atrial ◽  
Atrial Pacing ◽  
American Alligator ◽  
Maximum Heart Rate

In most vertebrates, increases in cardiac output result from increases in heart rate (fH) with little or no change in stroke volume (Vs), and maximum cardiac output (Q̇) is typically attained at or close to maximum fH. We therefore tested the hypothesis that increasing maximum fH may increase maximum Q̇. To this end, we investigated the effects of elevating fH with right atrial pacing on Q̇ in the American alligator ( Alligator mississippiensis) at rest and while swimming. During normal swimming, Q̇ increased entirely by virtue of a tachycardia (29 ± 1 to 40 ± 3 beats/min), whereas Vs remained stable. In both resting and swimming alligators, increasing fH with right atrial pacing resulted in a parallel decline in Vs that resulted in an unchanged cardiac output. In swimming animals, this reciprocal relationship extended to supraphysiological fH (up to ~72 beats/min), which suggests that maximum fH does not limit maximum cardiac output and that fH changes are secondary to the peripheral factors (for example vascular capacitance) that determine venous return at rest and during exercise.

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