Feasibility of preclinical cardiac output and systemic vascular resistance in HEMS in thoracic pain—the ultrasonic cardiac output monitor

2006 ◽  
Vol 25 (6) ◽  
pp. 270-275 ◽  
Author(s):  
K. Knobloch ◽  
V. Hubrich ◽  
P. Rohmann ◽  
M. Lupkemann ◽  
T. Gerich ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Thoracic Pain ◽  
Cardiac Output Monitor

scholarly journals Hemodynamic abnormalities during muscle metaboreflex activation in patients with type 2 diabetes mellitus

2019 ◽  
Vol 126 (2) ◽  
pp. 444-453 ◽  
Author(s):  
Silvana Roberto ◽  
Raffaele Milia ◽  
Azzurra Doneddu ◽  
Virginia Pinna ◽  
Girolamo Palazzolo ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Blood Pressure ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Blood Pressure Response ◽  
Pressure Response

Metaboreflex is a reflex triggered during exercise or postexercise muscle ischemia (PEMI) by metaboreceptor stimulation. Typical features of metaboreflex are increased cardiac output (CO) and blood pressure. Patients suffering from metabolic syndrome display hemodynamic abnormalities, with an exaggerated systemic vascular resistance (SVR) and reduced CO response during PEMI-induced metaboreflex. Whether patients with type 2 diabetes mellitus (DM2) have similar hemodynamic abnormalities is unknown. Here we contrast the hemodynamic response to PEMI in 14 patients suffering from DM2 (age 62.7 ± 8.3 yr) and in 15 age-matched controls (CTLs). All participants underwent a control exercise recovery reference test and a PEMI test to obtain the metaboreflex response. Central hemodynamics were evaluated by unbiased operator-independent impedance cardiography. Although the blood pressure response to PEMI was not significantly different between the groups, we found that the SVR and CO responses were reversed in patients with DM2 as compared with the CTLs (SVR: 392.5 ± 549.6 and −14.8 ± 258.9 dyn·s−1·cm−5; CO: −0.25 ± 0.63 and 0.46 ± 0.50 l/m, respectively, in DM2 and in CTL groups, respectively; P < 0.05 for both). Of note, stroke volume (SV) increased during PEMI in the CTL group only. Failure to increase SV and CO was the consequence of reduced venous return, impaired cardiac performance, and augmented afterload in patients with DM2. We conclude that patients with DM2 have an exaggerated vasoconstriction in response to metaboreflex activation not accompanied by a concomitant increase in heart performance. Therefore, in these patients, blood pressure response to the metaboreflex relies more on SVR increases rather than on increases in SV and CO. NEW & NOTEWORTHY The main new finding of the present investigation is that subjects with type 2 diabetes mellitus have an exaggerated vasoconstriction in response to metaboreflex activation. In these patients, blood pressure response to the metaboreflex relies more on systemic vascular resistance than on cardiac output increments.

The effect of Trendelenburg and modified trendelenburg positions on cardiac output, blood pressure, and oxygenation: a preliminary study

1994 ◽  
Vol 3 (5) ◽  
pp. 382-386 ◽  
Author(s):  
CL Ostrow ◽  
E Hupp ◽  
D Topjian
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Critically Ill ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Critically Ill Patients ◽  
Hemodynamic Parameters ◽  
Trendelenburg Position ◽  
Dependent Variables ◽  
Preliminary Study

BACKGROUND: Although we have insufficient knowledge about the effects of Trendelenburg positions on various hemodynamic parameters, these positions are frequently used to influence cardiac output and blood pressure in critically ill patients. OBJECTIVES: To determine the effect of Trendelenburg and modified Trendelenburg positions on five dependent variables: cardiac output, cardiac index, mean arterial pressure, systemic vascular resistance, and oxygenation in critically ill patients. METHODS: In this preliminary study subjects were 23 cardiac surgery patients (mean age, 55; SD, 8.09) who had a pulmonary artery catheter for cardiac output determination and who were clinically stable, normovolemic and normotensive. Baseline measurements of the dependent variables were taken in the supine position. Patients were then placed in 10 degrees Trendelenburg or 30 degrees modified Trendelenburg position. The dependent variables were measured after 10 minutes in each position. A 2-period, 2-treatment crossover design with a preliminary baseline measurement was used. RESULTS: Five subjects were unable to tolerate Trendelenburg position because of nausea or pain in the sternal incision. In the 18 who were able to tolerate both position changes, no statistically significant changes were found in the five dependent variables. Changes in systemic vascular resistance over time approached statistical significance and warrant further study. CONCLUSIONS: This preliminary study does not provide support for Trendelenburg positions as a means to influence hemodynamic parameters such as cardiac output and blood pressure in normovolemic and normotensive patients.

L-propionylcarnitine increases postischemic blood flow but does not affect recovery of energy charge

1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Contractile Function ◽  
Energy Charge ◽  
Left Ventricular ◽  
Arterial Blood

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.

scholarly journals Augmentation of Electrocardiographic QRS R-Amplitude Precedes Radiocontrast-Induced Hypotension during Mobile Computed Tomography Scanning

2019 ◽  
Vol 8 (4) ◽  
pp. 505
Author(s):  
Hye-Mee Kwon ◽  
Sung-Hoon Kim ◽  
Hee-Sun Park ◽  
Yong-Seok Park ◽  
Young-Jin Moon ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Cardiac Output ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Adverse Reactions ◽  
Artery Aneurysm ◽  
Ct Scanning ◽  
Hemodynamic Changes ◽  
Computed Tomography Scanning ◽  
Mobile Ct

Although intravenous administration of contrast media may trigger a variety of adverse reactions, sedated patients undergoing computed tomography (CT) scanning usually are not able to report their symptoms, which may delay detection of adverse reactions. Furthermore, changes in vital signs cannot be typically measured during mobile CT scanning, which worsens the situation. We aimed to characterize contrast-related hemodynamic changes that occur during mobile CT scanning and predict sudden hypotension based on subtle but robust changes in the electrocardiogram (ECG). We analyzed the digitized hemodynamic data of 20 consecutive patients who underwent clipping of a cerebral artery aneurysm and contrast-enhanced CT scanning following the surgical procedure. Hemodynamic variables, including ECG findings, invasive blood pressure (BP), pulse oximetry results, capnography findings, cardiac output, and systemic vascular resistance, were monitored simultaneously. We measured morphological changes in ECG-derived parameters, including the R–R interval, ST height, and QRS R-amplitude, on a beat-to-beat basis, and evaluated the correlation between those parameters and hemodynamic changes. After the radiocontrast injection, systolic BP decreased by a median 53 mmHg from baseline and spontaneously recovered after 63 ± 19 s. An increase in QRS R-amplitude (median 0.43 mV) occurred 25 ± 10 s before hypotension developed. The receiver operating characteristic curve showed that a 16% increase in QRS R-amplitude can predict a decrease in systolic BP of >25% (area under the curve 0.852). Increased cardiac output (median delta 2.7 L/min from baseline) and decreased systemic vascular resistance (median delta 857 dyn·s/cm5 from baseline) were also observed during hypotension. During mobile CT scanning, profound but transient hypotension can be observed, associated with decreased vascular resistance. Augmentation of QRS R-amplitude from an ECG represents a sensitive surrogate for onset of a hypotensive episode after contrast injection, thereby serving as a simple and continuous noninvasive hemodynamic monitoring tool.

Rho kinase and Ca2+ entry mediate increased pulmonary and systemic vascular resistance in l-NAME-treated rats

2007 ◽  
Vol 293 (5) ◽  
pp. L1306-L1313 ◽  
Author(s):  
Jasdeep S. Dhaliwal ◽  
David B. Casey ◽  
Anthony J. Greco ◽  
Adeleke M. Badejo ◽  
Thomas B. Gallen ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Rho Kinase ◽  
Systemic Arterial Pressure ◽  
Intravenous Injections ◽  
Pulmonary Arterial ◽  
Dose Dependent

The small GTP-binding protein and its downstream effector Rho kinase play an important role in the regulation of vasoconstrictor tone. Rho kinase activation maintains increased pulmonary vascular tone and mediates the vasoconstrictor response to nitric oxide (NO) synthesis inhibition in chronically hypoxic rats and in the ovine fetal lung. However, the role of Rho kinase in mediating pulmonary vasoconstriction after NO synthesis inhibition has not been examined in the intact rat. To address this question, cardiovascular responses to the Rho kinase inhibitor fasudil were studied at baseline and after administration of an NO synthesis inhibitor. In the intact rat, intravenous injections of fasudil cause dose-dependent decreases in systemic arterial pressure, small decreases in pulmonary arterial pressure, and increases in cardiac output. l-NAME caused a significant increase in pulmonary and systemic arterial pressures and a decrease in cardiac output. The intravenous injections of fasudil after l-NAME caused dose-dependent decreases in pulmonary and systemic arterial pressure and increases in cardiac output, and the percent decreases in pulmonary arterial pressure in response to the lower doses of fasudil were greater than decreases in systemic arterial pressure. The Ca++ entry blocker isradipine also decreased pulmonary and systemic arterial pressure in l-NAME-treated rats. Infusion of sodium nitroprusside restored pulmonary arterial pressure to baseline values after administration of l-NAME. These data provide evidence in support of the hypothesis that increases in pulmonary and systemic vascular resistance following l-NAME treatment are mediated by Rho kinase and Ca++ entry through L-type channels, and that responses to l-NAME can be reversed by an NO donor.

Prevention of fatal hemorrhagic shock in dog by pretreatment with chronic high-salt diet

1985 ◽  
Vol 249 (3) ◽  
pp. H577-H584
Author(s):  
A. P. Rocchini ◽  
K. P. Gallagher ◽  
M. J. Botham ◽  
J. H. Lemmer ◽  
C. A. Szpunar ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Sodium Chloride ◽  
Hemorrhagic Shock ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Blood Flows

The ability of a chronic high-salt diet to prevent fatal hemorrhagic shock was examined in 36 mongrel dogs. Twenty-one dogs received a dietary supplement of 9 g sodium chloride/day for 6 wk, and 15 dogs received the same basic diet for 6 wk but without the sodium chloride supplement. Hemorrhagic shock was induced in all dogs by bleeding into an overhanging sealed reservoir. After 3 h of shock, salt-pretreated dogs had a lower systemic vascular resistance of 0.70 +/- 0.02 versus 1.44 +/- 0.04 mmHg X ml-1 X min X kg (P less than 0.01) and a higher cardiac output of 53 +/- 3 versus 26 +/- 3 ml X min-1 X kg-1 (P less than 0.01) than was observed in controls. At 2.5 h of shock, the salt-pretreated dogs also experienced an increase in gastrointestinal (P less than 0.01), hepatic arterial, (P less than 0.05), kidney (P less than 0.05), brain (P less than 0.01), and heart blood flows (P less than 0.001) compared with 0.5 h of shock, whereas the control dogs experienced no increased flow during this same period. We also observed that after 3 h of hypotension there was a significantly smaller increase in plasma renin activity in the salt-pretreated dogs. Administration of 0.1 U X kg-1 X min-1 of hog renin eliminated the differences in systemic vascular resistance, cardiac output, and survival in five salt-pretreated dogs.

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