The Ellestad Protocol

2018 ◽  
pp. 149-159
Author(s):  
Myrvin H. Ellestad ◽  
Gregory S. Thomas
Keyword(s):  
Perceived Exertion ◽  
Diastolic Pressure ◽  
Oxygen Demand ◽  
Left Ventricular ◽  
Myocardial Oxygen Demand ◽  
Warm Up ◽  
Case Examples ◽  
St Segment ◽  
Patient Preparation ◽  
Electrocardiogram Ecg

The chapter The Ellestad Protocol reviews the performance of a maximal exercise test from start to finish using the Ellestad protocol as an example. Patient preparation should include caffeine avoidance should a vasodilator myocardial perfusion imaging (MPI) test be necessary secondary to inadequate exercise. A light meal prior to exercise testing is acceptable. The Bruce and Ellestad protocols both begin with a stage each investigator regarded as a warm-up, 3 minutes of exercise at 1.7 mph at a 10% grade. With two minute stages, primarily of increasing grade, the Ellestad protocol is completed approximately one minute earlier than the Bruce protocol. The use of the Borg scale of perceived exertion is helpful in determining a patient’s effort. If ancillary MPI is not being performed, an abrupt stop for a motion-free electrocardiogram (ECG) and then immediately placing the patient supine or semi-supine increases pre-load and, via the law of Laplace, increases left ventricular end-diastolic pressure, myocardial oxygen demand and thus ischemia. ST segment depression is observed earlier in recovery than if a cool-down walk is performed. Case examples are provided.

scholarly journals Levosimendan treatment of severe acute congestive heart failure refractory to dobutamine/milrinone in children

2011 ◽  
Vol 68 (11) ◽  
pp. 979-984
Author(s):  
Sergej Prijic ◽  
Sanja Rakic ◽  
Ljubica Nikolic ◽  
Bosiljka Jovicic ◽  
Mila Stajevic ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Myocardial Contractility ◽  
Severe Heart Failure ◽  
Oxygen Demand ◽  
Left Ventricular ◽  
Myocardial Oxygen Demand ◽  
Univentricular Heart ◽  
Dilatative Cardiomyopathy ◽  
Hemodynamic Improvement

Introduction. Levosimendan is a novel positive inotropic agent which, improves myocardial contractility through its calcium-sensitizing action, without causing an increase in myocardial oxygen demand. Also, by opening ATP-sensitive potassium channels, it causes vasodilatation with the reduction in both afterload and preload. Because of the long halflife, its effects last for up 7 to 9 days after 24-hour infusion. Case report. We presented three patients 2, 15 and 17 years old. All the patients had severe acute deterioration of the previously diagnosed chronic heart failure (dilatative cardiomyopathy; univentricular heart with bidirectional Glenn anastomosis and restrictive bulboventricular foramen; bacterial endocarditis on artificial aortic valve with severe stenosis and regurgitation). Signs and symptoms of severe heart failure, cardiomegaly (cardio-thoracic index 0.65) and left ventricular dilatation (end-diastolic diameter z-score 2.6; 4.1 and 4.0) were confirmed on admission. Also, myocardial contractility was poor with ejection fraction (EF - 27%, 25%, 35%), fractional shortening (FS - 13%, 11%, 15%) and stroke volume (SV - 40, 60, 72 mL/m2). The treatment with standard intravenous inotropic agents resulted in no improvement but in clinical deterioration. Thus, standard intravenous inotropic support was stopped and levosimendan treatment was introduced. All the patients received a continuous 24-h infusion 0.1 ?g/kg/min of levosimendan. In a single patient an initial loading dose of 11 ?g/kg over 10 min was administrated, too. Levosimendan treatment resulted in both clinical and echocardiography improvement with the improved EF (42%, 34%, 44%), FS (21%, 16%, 22%) and SV (59, 82, 93 mL/m2). Hemodynamic improvement was registered too, with the reduction in heart rate in all the treated patients from 134-138 bpm before, to less than 120 bpm after the treatment. These parameters were followed by the normalization of lactate levels. Nevertheless, left ventricular end-diastolic diameter did not change after the levosimendan treatment. Conclusion. Our initial experience demonstrates that administration of levosimendan in patients with severe chronic heart failure not responsive to standard intravenous inotropic treatment might result in a significant clinical and hemodynamic improvement and that, in selected patients, it might be life saving. According to our best knowledge patients presented are the first pediatric patients treated with levosimendan in our country.

Intra-aortic balloon counterpulsation in the ICU

2016 ◽  
Author(s):  
Alain Combes ◽  
Nicolas Bréchot
Keyword(s):  
Insertion Site ◽  
Oxygen Demand ◽  
Left Ventricular ◽  
Myocardial Oxygen Demand ◽  
Ventricular Afterload ◽  
Retroperitoneal Haemorrhage ◽  
Computer Controlled ◽  
Intra Aortic Balloon Counterpulsation ◽  
Critical Ischaemia ◽  
Balloon Counterpulsation

The intra-aortic balloon pump (IABP) is a mechanical device consisting of a cylindrical polyethylene balloon that sits in the aorta, approximately 2 cm from the left subclavian artery. A computer-controlled console linked to either an electrocardiogramor a pressure transducer inflates the balloon with helium during diastole (counterpulsation) and actively deflates in systole. This results in an increase in coronary artery blood flow and cardiac output, and reduced left ventricular afterload. These actions combine to decrease myocardial oxygen demand and increase supply. Major complications include bleeding at the insertion site and retroperitoneal haemorrhage, critical ischaemia of the catheterized leg, catheter infection, and stroke. IABP duration usually varies from 48 to 72 hours. Weaning from IABP is not well defined; the most common approach is to reduce cycling of inflation to 1:2 or 1:4 for 15 minutes to several hours before device removal.

Unstable angina: The significance of ST segment elevation or depression in patients without evidence of increased myocardial oxygen demand

1986 ◽  
Vol 112 (3) ◽  
pp. 463-467 ◽  
Author(s):  
Samuel Sclarovsky ◽  
Ehud Davidson ◽  
Boris Strasberg ◽  
Ruben F Lewin ◽  
Alexander Arditti ◽  
...  
Keyword(s):  
Unstable Angina ◽  
Oxygen Demand ◽  
Myocardial Oxygen Demand ◽  
St Segment Elevation ◽  
St Segment

Sex differences in noninvasive estimates of left ventricular pressure energetics but not myocardial oxygen demand in young adults

2014 ◽  
Vol 8 (4) ◽  
pp. 197 ◽  
Author(s):  
William E. Hughes ◽  
Nicole L. Spartano ◽  
Wesley K. Lefferts ◽  
Jaqueline A. Augustine ◽  
Kevin S. Heffernan
Keyword(s):  
Young Adults ◽  
Sex Differences ◽  
Oxygen Demand ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Myocardial Oxygen Demand

scholarly journals Repetitive Myocardial Infarctions Secondary to Delirium Tremens

2014 ◽  
Vol 2014 ◽  
pp. 1-3
Author(s):  
David Schwartzberg ◽  
Adam Shiroff
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Alcohol Withdrawal ◽  
Delirium Tremens ◽  
Oxygen Demand ◽  
Myocardial Infarctions ◽  
Myocardial Oxygen Demand ◽  
Significant Morbidity ◽  
St Segment ◽  
Patients Experience

Delirium tremens develops in a minority of patients undergoing acute alcohol withdrawal; however, that minority is vulnerable to significant morbidity and mortality. Historically, benzodiazepines are given intravenously to control withdrawal symptoms, although occasionally a more substantial medication is needed to prevent the devastating effects of delirium tremens, that is, propofol. We report a trauma patient who required propofol sedation for delirium tremens that was refractory to benzodiazepine treatment. Extubed prematurely, he suffered a non-ST segment myocardial infarction followed by an ST segment myocardial infarction requiring multiple interventions by cardiology. We hypothesize that his myocardial ischemia was secondary to an increased myocardial oxygen demand that occurred during his stress-induced catecholamine surge during the time he was undertreated for delirium tremens. This advocates for the use of propofol for refractory benzodiazepine treatment of delirium tremens and adds to the literature on the instability patients experience during withdrawal.

fMLP provokes coronary vasoconstriction and myocardial ischemia in rabbits

1988 ◽  
Vol 254 (3) ◽  
pp. H481-H486 ◽  
Author(s):  
M. N. Gillespie ◽  
D. C. Booth ◽  
B. J. Friedman ◽  
M. R. Cunningham ◽  
M. Jay ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Inflammatory Cell ◽  
Coronary Spasm ◽  
Inflammatory Cells ◽  
Left Ventricular ◽  
Ecg Changes ◽  
St Segment ◽  
Perfusion Defects ◽  
The Right ◽  
Electrocardiogram Ecg

Recent pathological studies of coronary arteries from humans with suspected coronary spasm have revealed an augmented intramural burden of inflammatory cells. To test the hypothesis that inappropriate activation of inflammatory cells participates in the evolution of coronary vasospasm, the present experiments employed a newly developed coronary arteriographic technique for use in pentobarbital-anesthetized rabbits to evaluate the coronary vasomotor actions of the nonselective inflammatory cell stimulant, N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP). In 10 of 10 animals, selective left intracoronary injection of 200 ng fMLP evoked profound left coronary narrowing accompanied in all cases by ST segment deviation and dysrhythmias. Thallium-201 scintigraphy demonstrated hypoperfusion of the left ventricular free wall and septum supplied by the spastic coronary artery. The fMLP-induced epicardial vaso-constriction, ischemic electrocardiogram (ECG) changes, and thallium perfusion defects were reversed by intravenous nitroglycerin. Neither the right coronary artery nor its distribution were influenced by left coronary injection of fMLP. Additional experiments in isolated, salt solution-perfused rabbit hearts demonstrated that fMLP failed to exert direct coronary vasoconstrictor effects. These observations indicate that the non-selective inflammatory cell stimulant, fMLP, provokes arteriographically demonstrable coronary spasm with attendant myocardial hypoperfusion and ischemic ECG changes in anesthetized rabbits. Such a model may be useful in exploring the dynamic role of inflammatory cells in development of coronary spasm.

Hemodynamic and Pressor Responses to Combination of Yoga and Blood Flow Restriction

2020 ◽  
Author(s):  
Savannah V. Wooten ◽  
Sten Stray-Gundersen ◽  
Hirofumi Tanaka
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Perceived Exertion ◽  
Oxygen Demand ◽  
Blood Flow Restriction ◽  
Rating Of Perceived Exertion ◽  
Myocardial Oxygen Demand ◽  
Flow Restriction ◽  
Pressor Responses ◽  
The Impact

AbstractA combination of yoga and blood flow restriction, each of which elicits marked pressor responses, may further increase blood pressure and myocardial oxygen demand. To determine the impact of a combination of yoga and blood flow restriction on hemodynamic responses, twenty young healthy participants performed 20 yoga poses with/without blood flow restriction bands placed on both legs. At baseline, there were no significant differences in any of the variables between the blood flow restriction and non-blood flow restriction conditions. Blood pressure and heart rate increased in response to the various yoga poses (p<0.01) but were not different between the blood flow restriction and non-blood flow restriction conditions. Rate-pressure products, an index of myocardial oxygen demand, increased significantly during yoga exercises with no significant differences between the two conditions. Rating of perceived exertion was not different between the conditions. Blood lactate concentration was significantly greater after performing yoga with blood flow restriction bands (p=0.007). Cardio-ankle vascular index, an index of arterial stiffness, decreased similarly after yoga exercise in both conditions while flow-mediated dilation remained unchanged. In conclusion, the use of lower body blood flow restriction bands in combination with yoga did not result in additive or synergistic hemodynamic and pressor responses.

Impaired subendocardial function in tachycardia-induced cardiac failure

1995 ◽  
Vol 268 (5) ◽  
pp. H1788-H1794 ◽  
Author(s):  
I. J. LeGrice ◽  
Y. Takayama ◽  
J. W. Holmes ◽  
J. W. Covell
Keyword(s):  
Heart Failure ◽  
Diastolic Pressure ◽  
Substantial Reduction ◽  
Median Sternotomy ◽  
Vena Cava ◽  
Oxygen Demand ◽  
Experimental Models ◽  
Left Ventricular ◽  
Miniature Swine ◽  
Reduced Ejection Fraction

Chronic rapid ventricular pacing (CRVP) in many experimental models induces ventricular dilatation, reduced ejection fraction, and symptomatic congestive heart failure. We have investigated transmural mechanical function in the left ventricular (LV) wall of five Hanford miniature swine before and after CRVP-induced failure. Three columns of radiopaque markers 1 mm in diameter were implanted in the anterior LV wall through a median sternotomy. A pair of LV pacing wires were sutured into the myocardium, a pneumatic cuff was placed around the inferior vena cava (IVC), and two fluid-filled Silastic catheters were implanted into the LV apex. Two weeks after surgery, the pigs were suspended awake in a sling, and markers were tracked with biplane cineradiography. The hearts were paced for 3 wk (225-240 beats/min), and the study was repeated with the pacemaker off. Saline infusion and IVC occlusion were used to vary LV end-diastolic pressure (EDP) so control-to-failure comparisons could be made at matched LV EDPs. End-systolic strains in the circumferential (E11), longitudinal (E22), and transmural (E33) directions were quantified using finite element methods. There was a significant reduction in E11 and E33 for the subendocardium: in E11, from -0.27 to -0.18; in E33, from 0.83 to 0.46. There were no significant changes in subendocardial E22 or in any of the outer wall normal strains. These results indicate that CRVP causes substantial reduction of subendocardial, but not subepicardial, function; taken together with previous data indicating subendocardial hypoperfusion, these results support the contention that an imbalance between blood flow and oxygen demand plays a role in the etiology of heart failure in this model.

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