Effects of vasopressin on left anterior descending coronary artery blood flow during extremely low cardiac output

Resuscitation ◽  
2004 ◽  
Vol 62 (2) ◽  
pp. 229-235 ◽  
Author(s):  
Viktoria D Mayr ◽  
Volker Wenzel ◽  
Tilko Müller ◽  
Herwig Antretter ◽  
Klaus Rheinberger ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Coronary Artery ◽  
Artery Blood Flow ◽  
Low Cardiac Output

scholarly journals To Balloon or Not to Balloon? The Effects of an Intra-Aortic Balloon-Pump on Coronary Artery Flow during Extracorporeal Circulation Simulating Normal and Low Cardiac Output Syndromes

2021 ◽  
Vol 10 (22) ◽  
pp. 5333
Author(s):  
Philippe Reymond ◽  
Karim Bendjelid ◽  
Raphaël Giraud ◽  
Gérald Richard ◽  
Nicolas Murith ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Coronary Artery ◽  
Coronary Blood Flow ◽  
Low Cardiac Output ◽  
Coronary Artery Flow ◽  
Artery Flow

ECMO is the most frequently used mechanical support for patients suffering from low cardiac output syndrome. Combining IABP with ECMO is believed to increase coronary artery blood flow, decrease high afterload, and restore systemic pulsatile flow conditions. This study evaluates that combined effect on coronary artery flow during various load conditions using an in vitro circuit. In doing so, different clinical scenarios were simulated, such as normal cardiac output and moderate-to-severe heart failure. In the heart failure scenarios, we used peripheral ECMO support to compensate for the lowered cardiac output value and reach a default normal value. The increase in coronary blood flow using the combined IABP-ECMO setup was more noticeable in low heart rate conditions. At baseline, intermediate and severe LV failure levels, adding IABP increased coronary mean flow by 16%, 7.5%, and 3.4% (HR 60 bpm) and by 6%, 4.5%, and 2.5% (HR 100 bpm) respectively. Based on our in vitro study results, combining ECMO and IABP in a heart failure setup further improves coronary blood flow. This effect was more pronounced at a lower heart rate and decreased with heart failure, which might positively impact recovery from cardiac failure.

scholarly journals Sevoflurane provides better haemodynamic stability than propofol during right ventricular ischaemia–reperfusion

2019 ◽  
Vol 30 (1) ◽  
pp. 129-135
Author(s):  
Pernille Haraldsen ◽  
Doris Cunha-Goncalves ◽  
Carsten Metzsch ◽  
Lars Algotsson ◽  
Sandra Lindstedt ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Coronary Artery ◽  
Right Ventricular ◽  
Vascular Resistance ◽  
Right Coronary Artery ◽  
Stroke Work ◽  
Artery Blood Flow ◽  
Ischaemia Reperfusion ◽  
Haemodynamic Stability

Abstract OBJECTIVES To assess whether sevoflurane provides better haemodynamic stability than propofol in acute right ventricular (RV) ischaemia–reperfusion. METHODS Open-chest pigs (mean ± standard deviation, 68.8 ± 4.2 kg) anaesthetized with sevoflurane (n = 6) or propofol (n = 6) underwent 60 min of RV free wall ischaemia and 150 min of reperfusion. Haemodynamic parameters and blood flow in the 3 major coronary arteries were continuously monitored. Biomarkers of cardiac ischaemia were analysed. RESULTS Mean arterial pressure and stroke volume decreased, whereas pulmonary vascular resistance increased equally in both groups. Heart rate increased 7.5% with propofol (P < 0.05) and 17% with sevoflurane (P < 0.05). At reperfusion, left atrial pressure and systemic vascular resistance decreased with sevoflurane. While RV stroke work (mmHg·ml) and cardiac output (l·min−1) decreased in the propofol group (4.2 ± 1.2 to 2.9 ± 1.7 and 2.65 ± 0.44 to 2.28 ± 0.56, respectively, P < 0.05 both), they recovered to baseline levels in the sevoflurane group (4.1 ± 1.5 to 4.0 ± 1.5 and 2.77 ± 0.6 to 2.6 ± 0.5, respectively, P > 0.05). Circumflex and left anterior descending coronary artery blood flow decreased in both groups. Right coronary artery blood flow (ml·min−1) decreased with propofol (38 ± 9 to 28 ± 9, P < 0.05), but not with sevoflurane (28 ± 11 to 28 ± 17, P > 0.05). Biomarkers of cardiac ischaemia increased in both groups. CONCLUSIONS Compared to propofol, sevoflurane-anaesthetized pigs showed higher RV stroke work, cardiac output and right coronary artery blood flow during reperfusion. These findings warrant a clinical trial of sevoflurane in RV ischaemia in humans.

Control of Blood Pressure and the Distribution of Blood Flow

1991 ◽  
Vol 7 (S1) ◽  
pp. 79-84 ◽  
Author(s):  
Hans T. Versmold
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Systemic Blood Pressure ◽  
Adrenergic Innervation ◽  
Systemic Blood ◽  
Low Cardiac Output ◽  
Neurohumoral Control ◽  
The Brain

Systemic blood pressure (BP) is the product of cardiac output and total peripheral resistance. Cardiac output is controlled by the heart rate, myocardial contractility, preload, and afterload. Vascular resistance (vascular hindrance × viscosity) is under local autoregulation and general neurohumoral control through sympathetic adrenergic innervation and circulating catecholamines. Sympathetic innovation predominates in organs receivingflowin excess of their metabolic demands (skin, splanchnic organs, kidney), while innervation is poor and autoregulation predominates in the brain and heart. The distribution of blood flow depends on the relative resistances of the organ circulations. During stress (hypoxia, low cardiac output), a raise in adrenergic tone and in circulating catecholamines leads to preferential vasoconstriction in highly innervated organs, so that blood flow is directed to the brain and heart. Catecholamines also control the levels of the vasoconstrictors renin, angiotensin II, and vasopressin. These general principles also apply to the neonate.

Coronary Artery Vasomotion and Post-Stenotic Coronary Artery Blood Flow after Intracoronary Lacidipine in Patients with Ischaemic Heart Disease

Drugs ◽  
1999 ◽  
Vol 57 (Supplement 1) ◽  
pp. 19-26
Author(s):  
Corrado Vassanelli ◽  
Giuliana Menegatti ◽  
Alberto Marini ◽  
Federico Beltrame ◽  
Jonata Molinari ◽  
...  
Keyword(s):  
Blood Flow ◽  
Heart Disease ◽  
Coronary Artery ◽  
Ischaemic Heart Disease ◽  
Artery Blood Flow

Circulatory and renal control by prostaglandins and renin in low cardiac output in dogs

1989 ◽  
Vol 256 (4) ◽  
pp. H1079-H1086 ◽  
Author(s):  
G. A. Riegger ◽  
D. Elsner ◽  
E. P. Kromer
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Glomerular Filtration Rate ◽  
Renal Blood Flow ◽  
Plasma Levels ◽  
Filtration Rate ◽  
Sympathetic Nerve Activity ◽  
Peripheral Vascular ◽  
Nerve Activity ◽  
Low Cardiac Output

Changes of neurohumoral factors including vasodilatory prostaglandins (PGs) were investigated in an experimental model of moderate low-cardiac-output status induced by rapid right ventricular pacing (240 beats/min). After 7 days of pacing, we studied the response of renal, hormonal, and hemodynamic parameters to cyclooxygenase inhibition by indomethacin and the effects of the renin system by converting-enzyme blockade in addition to the inhibition of PG synthesis. Lowering cardiac output increased plasma levels of norepinephrine and atrial natriuretic peptide. Plasma renin concentration was suppressed, despite a fall in cardiac output and blood pressure and a stimulation of sympathetic nerve activity. Urinary excretion of PGE2 was increased (P less than 0.04); plasma levels of PGE2 and 6-keto-PGF1 alpha were unchanged as measured in blood from the renal vein, pulmonary artery, and aorta. During low cardiac output, we found a significant decrease of glomerular filtration rate, whereas renal blood flow and renal and peripheral vascular resistances were unchanged. Administration of indomethacin decreased plasma and urinary PGs significantly, markedly reduced renal blood flow, and increased renal vascular resistance without affecting peripheral vascular resistance. The additional blockade of the renin-angiotensin system by captopril showed mainly a vasodilator effect on peripheral arterial resistance vessels, resulting in an increase of cardiac output. Our results suggest that, in moderate low-cardiac-output status, renal blood flow is maintained by renal vasodilator PGs, which counterbalance vasoconstrictor mechanisms like the activated sympathetic nerve activity. We indirectly showed the importance of angiotensin II in preserving glomerular filtration rate, which declines when renin secretion is suppressed, as it may be the case in moderate heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Tracheal blood flow during spontaneous and mechanical ventilation of dry gases in sheep

1990 ◽  
Vol 69 (3) ◽  
pp. 1117-1122 ◽  
Author(s):  
D. A. White ◽  
G. H. Parsons
Keyword(s):  
Mechanical Ventilation ◽  
Blood Flow ◽  
Cardiac Output ◽  
Left Atrial ◽  
Bronchial Artery ◽  
Minute Ventilation ◽  
Fold Increase ◽  
Artery Blood Flow ◽  
The Common ◽  
Spontaneously Breathing

Tracheal blood flow increases greater than twofold in response to eucapnic hyperventilation of dry gas in anesthetized sheep. To determine whether this occurs at normal minute ventilation, we studied sheep in which tracheal blood flow was measured in response to humid and dry gas ventilation while 1) awake and spontaneously breathing and 2) anesthetized and intubated during isocapnic mechanical ventilation. In additional sheep, three tracheal mucosal temperatures were measured during humid and dry gas mechanical ventilation to measure airway tissue cooling. Tracheal blood flow was determined by use of a left atrial injection of 15-microns-diam radiolabeled microspheres. Previously implanted flow probes on the pulmonary artery and the common bronchial artery allowed continuous recording of cardiac output and bronchial blood flow. Tracheal blood flow in awake spontaneously breathing sheep was 10.8 +/- 5.6 (SD) ml.min-1.100 g wet wt-1 while humid gas was breathed, and it was unchanged with dry gas. In contrast, isocapnic ventilation of intubated animals with dry gas resulted in a 10-fold increase in blood flow to the most proximal two-ring tracheal segment compared with that seen while humid gases were spontaneously ventilated [101 +/- 75 vs. 11 +/- 6 (SD) ml.min-1.100 g-1, P less than 0.05]. Despite a 10-fold increase in proximal tracheal blood flow, there was no response in distal tracheal and bronchial blood flow, as indicated by no change in the common bronchial artery blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

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