Pressure aortic

Dopamine should generally be avoided in decompensated HF, but its pharmacologic actions may be preferable to dobutamine or milrinone in patients with marked systemic hypotension or cardiogenic shock in the face of elevated ventricular filling pressures, where dopamine in doses greater than 5 mcg/kg/min may be necessary to raise central aortic pressure. 

Left Ventricle (LV) A simple inverted U curve is drawn that has its baseline between 0 and 5 mmHg and its peak at 120 mmHg. During diastole, its pressure must be less than that of the CVP to enable forward flow. It only increases above CVP during systole. The curve between points A and B demonstrates why the initial contraction is isovolumic. The LV pressure is greater than CVP so the mitral valve must be closed, but it is less than aortic pressure so the aortic valve must also be closed. The same is true of the curve between points C and D with regards to IVR. 

B End of IVC. The LV pressure rises above aortic pressure. Aortic valve opens and blood flows into the circulation. 

C Start of IVR. The LV pressure falls below aortic pressure and the aortic valve closes (S2). 

Telgmann, R., Harb, B. A., Ozcelik, C., et al. (2007) The G-231A polymorphism in the endothelin-A receptor gene is associated with lower aortic pressure in patients with dilated cardiomyopathy. Am. J. Hypertens. 20, 32-37. 

Factors determining oxygen demand. The heart muscle cell consumes the most energy to generate contractile force. O2 demand rises with an increase in (1) heart rate, (2) contraction velocity, (3) systolic wall tension ( afterload ). The latter depends on ventricular volume and the systolic pressure needed to empty the ventricle. As peripheral resistance increases, aortic pressure rises, hence the resistance against which ventricular blood is ejected. O2 demand is lowered by 3-blockers and Ca-antago-nists, as well as by nitrates (p. 308). 

Several studies have indicated that n-butane sensitizes the myocardium to epinephrine-induced cardiac arrhythmias. In anesthetized dogs, 5000 ppm caused hemodynamic changes such as decreases in cardiac output, left ventricular pressure, and stroke volume, myocardial contractility, and aortic pressure. Exposure of dogs to 1-20% butane for periods of 2 minutes to 2 hours hypersen-... 

Arteriolar and venous tone (smooth muscle tension) both play a role in determining myocardial wall stress (Table 12-1). Arteriolar tone directly controls peripheral vascular resistance and thus arterial blood pressure. In systole, intraventricular pressure must exceed aortic pressure to eject blood arterial blood pressure thus determines the systolic wall stress in an important way. Venous tone determines the capacity of the venous circulation and controls the amount of blood sequestered in the venous system versus the amount returned to the heart. Venous tone thereby determines the diastolic wall stress. 

Manganism, the result of overexposure to manganese, primarily affects the brain [23]. Severe psychiatric symptoms including hyperirritability, violent acts, and hallucinations are characteristic of manganism. These symptoms manifest themselves due to the ability of manganese(II) to cross the blood-brain barrier [24]. Manganese(II) ions also interfere with the calcium channels of cardiac cells, which leads to decreased ability of the heart muscle to contract [25]. This results in a decrease in heart rate, an increase in aortic pressure and ventricular fibrillation [25,26]. Manganese has been found to interfere with DNA replication and has been shown to increase the occurrence of cancer [27]. 

If the gradient is indeed confirmed, a 6 or 7Fr sheath is placed in the left coronary artery from the contralateral femoral artery, in order to reliably assess the ascending aortic pressure even in the presence of intracoronary wires and a balloon inside it (Fig. 2),... 

The hemodynamic and ECG parameters include systolic, diastolic and mean aortic pressure, peak systolic and end-diastolic left ventricular pressure, LV dP/dt max and dP/dt min, heart rate PQ-, QRS- and QT intervals. NOTOCORD-software (or equivalent) is used for acquisition of data whereas EXCEL (or equivalent) is used for data analysis. Data are summarized at predefined time points by calculating median values+ SD. Whereas all physiological parameters are routinely averaged over predefined time intervals, it has been proposed that for the ECG only a few beats... 

In central circulatory failure (cardiogenic shock, e.g. after myocardial infarction) the cardiac output and blood pressure are low due to pump failure myocardial perfusion is dependent on aortic pressure. Venous return (central venous pressure) is normal or high. The low blood pressure may trigger the sympathoadrenal mechanisms of peripheral circulatory failure summarised below. 

There is a theoretical contraindication to nicorandil in patients with cardiogenic shock, acute left ventricular failure with low fiUing pressure, and hypotension. A sublingual dose of 20 mg in patients with coronary artery disease and normal left ventricular function was associated with a 12% fall in left ventricular end-systolic pressure, a 3% fall in left ventricular end-diastolic pressure, accentuated diastohc filhng, a 13% reduction in mean aortic pressure, and a reduced cardiac output at rest (9,30). However, cardiac output may be augmented by up to 60% in patients with congestive cardiac failure or... 

Propane has been shown to have adverse effects on the cardiovascular system in the primate, dog, cat, and mouse. Guinea pigs exposed to 2.2-5.5% of the gas showed sniffing and chewing movements. In dogs, 1% caused hemodynamic changes, whereas 3.3% produced decreases in aortic pressure, stroke volume, and cardiac output and an increase in pulmonary resistance. Ten percent propane in the mouse and 15% in the dog did not produce arrhythmia but did produce weak cardiac sensitization. 

The effects of berbamine of the isolated and perfused working heart of the guinea pig was studied. The alkaloid was observed to depress the function of the isolated working heart in a dose-dependent manner. The alkaloid (3 mol/l) decreased the left ventricular pressure, aortic pressure -dP/dtmax, aortic blood flow and coronary blood flow, and increased left ventricular end-diastolic pressure. At a concentration of 100 mol/l, ventricular asystole was produced, but there was no influence on atrial contraction. Berbamine was also observed to antagonize epinephrine-induced arrhythmias [202]. 

Blood flow to the coronary arteries arises from orifices located immediately distal to the aorta valve. Perfusion pressure is equal to the difference between the aortic pressure at an instantaneous point in time minus the intramyocardial pressure. Coronary vascular resistance is influenced by phasic systolic compression of the vascular bed. The driving force for perfusion therefore is not constant throughout the cardiac cycle. Opening of the aortic valve also may lead to a Venturi effect, which can slightly decrease perfusion pressure. If perfusion pressure is elevated for a period of time, coronary vascular resistance declines, and blood flow increases however, continued perfusion pressure increases lead, within limits, to a return of coronary blood flow back toward baseline levels through autoregulation. 

Neural components that participate in the regulation of coronary blood flow include the sympathetic nervous system, the parasympathetic nervous system, coronary reflexes, and possibly, central control of coronary blood flow. Within the sympathetic system, stimulation of the stellate ganglion elicits coronary vasodilation, which is associated with tachycardia and enhanced contractility. This indirect coronary vasodilation is secondary to increased MVO2 related to increased heart rate, contractihty, and aortic pressure and occurs following stellate stimulation. The direct effect of the sympathetic system is a 1-mediated vasoconstriction at rest and during exercise. Other receptor types, 2 and have little influence on tone, whereas /32-stimulation produces a modest vasodUatory effect. Although coronary atherosclerosis may decrease blood flow secondary to obstruction, severe coronary atherosclerosis and obstruction also may increase the sensitivity of coronary arteries to the effects of aj-stimulation and vasoconstriction. 

The prototypic percutaneous aortic valve was implanted in a 57-year-old male with calcified critical aortic stenosis who failed previous balloon valvuloplasty and was in cardiogenic shock as well as leg ischemia at the time of procedure. Following the procedure, the aortic pressure rose from a 70 mmHg systolic to 120 mm Hg with the aortic valve gradient decreased from 30 to 6 mm Hg. The calculated valve... 

FIGURE 8.5 Ventricular and root aortic pressures (solid curves, left ordinate) and ventricular outflow (dashed curve, right ordinate) computed using the model of Equation 8.8 for a normal canine left ventricle pumping into a normal arterial circulation. The topmost solid curve corresponds to a clamped aorta (isovolumic). This ventricle has initial volume of 45 ml and pumps out 30 ml, for an ejection fraction of 66%, about normal. 

FIGURE 8.8 The ejection effect, showing that early during blood ejection (systole) the heart generates somewhat less pressure than expected, denoted deactivation (down arrows). Later in systole, the heart generates greater pressure, denoted hyperactivation. Curves 1 and 2 are ventricular pressures for initial and ejected volumes, respectively. Curve 3 is the measured ejecting pressure curve. Curve 4 is root aortic pressure. 

FIGURE 8.21 Premature ventricular contraction following ultrasound irradiation, during diastole, of the in vivo frog heart. The top trace is aortic pressure and below is the EGG. A lithotripter pulse of 20 MPa, 5 msec duration, is delivered at the vertical arrow. (Adapted from Dalecki, D., Raeman, C.H., Child, S.Z., and Carstensen, E.L. 1997. Ultrasound Med. BioL 23 275-285.)... 

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