scholarly journals Novel Porcine Model of Acute Severe Cardiogenic Shock Developed by Upper-Body Hypoxia

2016 ◽  
pp. 711-715 ◽  
Author(s):  
P. OSTADAL ◽  
M. MLCEK ◽  
S. STRUNINA ◽  
M. HRACHOVINA ◽  
A. KRUGER ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Cardiogenic Shock ◽  
Acute Heart Failure ◽  
Porcine Model ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Upper Body ◽  
Large Animal ◽  
Myocardial Hypoxia

Despite the urgent need for experimental research in the field of acute heart failure and, particularly cardiogenic shock, currently there are only limited options in large animal models enabling research using devices applied to human subjects. The majority of available models are either associated with an unacceptably high rate of acute mortality or are incapable of developing sufficient severity of acute heart failure. The objective of our research was to develop a novel large animal model of acute severe cardiogenic shock. Advanced left ventricular dysfunction was induced by global myocardial hypoxia by perfusing the upper body (including coronary arteries) with deoxygenated venous blood. The model was tested in 12 pigs: cardiogenic shock with signs of tissue hypoxia developed in all animals with no acute mortality. Cardiac output decreased from a mean (± SD) of 6.61±1.14 l/min to 2.75±0.63 l/min, stroke volume from 79.7±9.8 ml to 25.3±7.8 ml and left ventricular ejection fraction from 61.2±4.3 % to 17.7±4.8 % (P≤0.001 for all comparisons). In conclusion, the porcine model of acute cardiogenic shock developed in the present study may provide a basis for studying severe left ventricular dysfunction, low cardiac output and hypotension in large animals. The global myocardial hypoxia responsible for the decrease in cardiac contractility was not associated with acute death in this model.

Hemodynamic changes before acute heart failure episodes in patients with advanced systolic left ventricular dysfunction

2008 ◽  
Vol 9 (8) ◽  
pp. 799-804 ◽  
Author(s):  
Stefano Ghio ◽  
Alessandra Serio ◽  
Maurizio Mangiavacchi ◽  
Barbro Kjellström ◽  
Sergio Valsecchi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Hemodynamic Changes

Adrenomedullin-epinephrine cotreatment enhances cardiac output and left ventricular function by energetically neutral mechanisms

2012 ◽  
Vol 302 (8) ◽  
pp. H1584-H1590
Author(s):  
Thor Allan Stenberg ◽  
Anders Benjamin Kildal ◽  
Ole-Jakob How ◽  
Truls Myrmel
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Acute Heart Failure ◽  
Coronary Blood Flow ◽  
Drug Effects ◽  
Left Ventricular ◽  
Experimental Myocardial Infarction ◽  
Energetic Cost ◽  
Lv Function

Adrenomedullin (AM) used therapeutically reduces mortality in the acute phase of experimental myocardial infarction. However, AM is potentially deleterious in acute heart failure as it is vasodilative and inotropically neutral. AM and epinephrine (EPI) are cosecreted from chromaffin cells, indicating a physiological interaction. We assessed the hemodynamic and energetic profile of AM-EPI cotreatment, exploring whether drug interaction improves cardiac function. Left ventricular (LV) mechanoenergetics were evaluated in 14 open-chest pigs using pressure-volume analysis and the pressure-volume area-myocardial O2 consumption (PVA-MV˙o2) framework. AM (15 ng·kg−1·min−1, n = 8) or saline (controls, n = 6) was infused for 120 min. Subsequently, a concurrent infusion of EPI (50 ng·kg−1·min−1) was added in both groups (AM-EPI vs. EPI). AM increased cardiac output (CO) and coronary blood flow by 20 ± 10% and 39 ± 14% (means ± SD, P < 0.05 vs. baseline), whereas controls were unaffected. AM-EPI increased CO and coronary blood flow by 55 ± 17% and 75 ± 16% ( P < 0.05, AM-EPI interaction) compared with 13 ± 12% ( P < 0.05 vs. baseline) and 18 ± 31% ( P = not significant) with EPI. LV systolic capacitance decreased by −37 ± 22% and peak positive derivative of LV pressure (dP/d tmax) increased by 32 ± 7% with AM-EPI ( P < 0.05, AM-EPI interaction), whereas no significant effects were observed with EPI. Mean arterial pressure was maintained by AM-EPI and tended to decrease with EPI (+2 ± 13% vs. −11 ± 10%, P = not significant). PVA-MV˙o2 relationships were unaffected by all treatments. In conclusion, AM-EPI cotreatment has an inodilator profile with CO and LV function augmented beyond individual drug effects and is not associated with relative increases in energetic cost. This can possibly take the inodilator treatment strategy beyond hemodynamic goals and exploit the cardioprotective effects of AM in acute heart failure.

scholarly journals Acute Heart Failure Exacerbation with Cardiogenic Shock and Elevated Systemic Vascular Resistance Treated with a Combination of Nicardipine and Dobutamine Therapy

2017 ◽  
Vol 2017 ◽  
pp. 1-2
Author(s):  
Lydia E. Issac ◽  
Setri Fugar ◽  
Naser Yamani ◽  
Burhan Mohamedali
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Cardiogenic Shock ◽  
Acute Heart Failure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Severe Hypertension ◽  
Subsequent Recovery ◽  
History Of ◽  
Heart Failure Exacerbation

Acute heart failure is a common reason for hospital admission and is usually caused by decreased cardiac output either as a result of an intrinsic cardiac issue or as a result of severe hypertension with elevated afterload. We present a patient with a history of HFrEF who presented with acute heart failure, found to have hypotension requiring Dobutamine support and an elevated systemic vascular resistance requiring Nicardipine drip, with subsequent recovery of cardiac function.

Intra-Aortic Balloon Pumping in Acute Decompensated Heart Failure With Hypoperfusion: From Pathophysiology to Clinical Practice

2021 ◽  
Author(s):  
Luca Baldetti ◽  
Matteo Pagnesi ◽  
Mario Gramegna ◽  
Alessandro Belletti ◽  
Alessandro Beneduce ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Cardiac Output ◽  
Cardiogenic Shock ◽  
Acute Decompensated Heart Failure ◽  
Therapeutic Option ◽  
Decompensated Heart Failure ◽  
Left Ventricular ◽  
Ventricular Afterload ◽  
Clinical Scenarios

Trials on intra-aortic balloon pump (IABP) use in cardiogenic shock related to acute myocardial infarction have shown disappointing results. The role of IABP in cardiogenic shock treatment remains unclear, and new (potentially more potent) mechanical circulatory supports with arguably larger device profile are emerging. A reappraisal of the physiological premises of intra-aortic counterpulsation may underpin the rationale to maintain IABP as a valuable therapeutic option for patients with acute decompensated heart failure and tissue hypoperfusion. Several pathophysiological features differ between myocardial infarction- and acute decompensated heart failure–related hypoperfusion, encompassing cardiogenic shock severity, filling status, systemic vascular resistances rise, and adaptation to chronic (if preexisting) left ventricular dysfunction. IABP combines a more substantial effect on left ventricular afterload with a modest increase in cardiac output and would therefore be most suitable in clinical scenarios characterized by a disproportionate increase in afterload without profound hemodynamic compromise. The acute decompensated heart failure syndrome is characterized by exquisite afterload-sensitivity of cardiac output and may be an ideal setting for counterpulsation. Several hemodynamic variables have been shown to predict response to IABP within this scenario, potentially guiding appropriate patient selection. Finally, acute decompensated heart failure with hypoperfusion may frequently represent an end stage in the heart failure history: IABP may provide sufficient hemodynamic support and prompt end-organ function recovery in view of more definitive heart replacement therapies while preserving ambulation when used with a transaxillary approach.

Pathophysiology and clinical assessment of the cardiovascular system (including pulmonary artery catheter)

2015 ◽  
Author(s):  
Romain Barthélémy ◽  
Etienne Gayat ◽  
Alexandre Mebazaa
Keyword(s):  
Heart Failure ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Artery Catheter ◽  
Acute Heart Failure ◽  
Ventricular Dysfunction ◽  
Systolic Dysfunction ◽  
Right Ventricular Dysfunction ◽  
Left Ventricular ◽  
Haemodynamic Instability

Haemodynamic instability in acute cardiac care may be related to various mechanisms, including hypovolaemia and heart and/or vascular dysfunction. Although acute heart failure patients are often admitted for dyspnoea, many mechanisms can be involved, including left ventricular diastolic and/or systolic dysfunction and/or right ventricular dysfunction. Many epidemiological studies show that clinical signs at admission, morbidity, and mortality differ between the main scenarios of acute heart failure: left ventricular diastolic dysfunction, left ventricular systolic dysfunction, right ventricular dysfunction, and cardiogenic shock. Although echocardiography often helps to assess the mechanism of cardiac dysfunction, it cannot be considered as a monitoring tool. In some cases (in particular, in cases of refractory shock secondary to both vascular and heart dysfunction or in cases of refractory haemodynamic instability associated with severe hypoxaemia), pulmonary artery catheter can help to assess and monitor cardiovascular status and to evaluate response to treatments. Last, macro- and microvascular dysfunctions are also important determinants of haemodynamic instability.

Pathophysiology and clinical assessment of the cardiovascular system (including pulmonary artery catheterization)

2021 ◽  
pp. 115-126
Author(s):  
Alessandro Sionis ◽  
Etienne Gayat ◽  
Alexandre Mebazaa
Keyword(s):  
Heart Failure ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Cardiovascular System ◽  
Acute Heart Failure ◽  
Ventricular Dysfunction ◽  
Systolic Dysfunction ◽  
Right Ventricular Dysfunction ◽  
Left Ventricular ◽  
Ventricular Diastolic Dysfunction

The underlying pathophysiological derangements of the cardiovascular system in many medical conditions are often complex. Acute circulatory dysfunction can be related broadly to a cardiogenic cause leading to acute heart failure or be secondary to hypovolaemia or vascular dysfunction (e.g. sepsis). Different mechanisms may be involved, including left ventricular diastolic and/or systolic dysfunction and/or right ventricular dysfunction. Many aspects of left ventricular function are explained by considering ventricular pressure–volume characteristics. Epidemiological studies show that clinical signs at admission, morbidity, and mortality differ between the main scenarios of acute heart failure: left ventricular diastolic dysfunction, left ventricular systolic dysfunction, right ventricular dysfunction, and cardiogenic shock. Although echocardiography is usually the first investigation used to assess the mechanism of cardiac dysfunction, in selected cases (in particular, in cases of refractory shock secondary to both vascular and heart dysfunction or in cases of refractory haemodynamic instability associated with severe hypoxaemia), the pulmonary artery catheter can help to assess and monitor the cardiovascular status and evaluate response to treatments.

Development of Acute Ischemic Heart Failure in Sheep

2000 ◽  
Vol 23 (5) ◽  
pp. 325-330 ◽  
Author(s):  
D. Mihaylov ◽  
H. Reintke ◽  
P. Blanksma ◽  
E.D. De Jong ◽  
J. Elstrodt ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Diastolic Pressure ◽  
Heart Function ◽  
Circulatory System ◽  
Left Ventricular ◽  
Fine Tuning ◽  
Large Animal Model ◽  
Large Animal ◽  
Failure Conditions

The goal of the present study was to develop a large animal model of acute ischemic left ventricular heart failure (LVHF) that can be used to assess the influence of the PUCA pump on the heart and circulatory system under realistic conditions. We tested the hypothesis that mild stenosis of the coronary artery in combination with mild ventricular pacing induces an acute heart failure condition, whereas the separate phenomena themselves do not lead to impaired heart function. Mean aortic pressure (AoP), left ventricular end-diastolic pressure (LVEDP), stroke volume (SV) and myocardial systolic shortening (MSS) were compared 30 minutes after a pacemaker (PM) induced tachycardia in anaesthetized sheep (n=3) without and with ± 50% stenosis of the proximal LCx. All parameters measured restored to basic levels when stenosis was absent. When the LCx was partially occluded, mild PM-induced tachycardia resulted in decreased AoP (P=0.045) as well as in decreased SV (P=0.048); the LVEDP remained high (P=0.002). Also the recovery of MSS was impaired when stenosis was present (P=0.002). These values indicate that acute heart failure conditions were present. The technique used proved to be safe and allowd fine-tuning of the demand ischemia by adapting heart frequency to the required heart failure conditions. The model can be used to study the effect of LV mechanical support during acute heart failure conditions.

scholarly journals Acute Heart Failure Triggered by Coronary Spasm With Transient Left Ventricular Dysfunction

2017 ◽  
Vol 58 (2) ◽  
pp. 286-289
Author(s):  
Yusuke Adachi ◽  
Kenichi Sakakura ◽  
Tatsuro Ibe ◽  
Nanae Yoshida ◽  
Hiroshi Wada ◽  
...  
Keyword(s):  
Heart Failure ◽  
Acute Heart Failure ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Coronary Spasm ◽  
Left Ventricular
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