Contraction systolic

Cardiac function may be evaluated by the determination of left (or right) ventricular ejection fraction (VEF). In this procedure, regions of interest are defined at the end diastolic and end systolic phases of heart beat. The ejection fraction is defined as the ratio of tracer (blood) in the heart in the contracted (systolic) versus the relaxed (diastolic) phases of the heart cycle with appropriate corrections for decay and gamma camera dead time. The value obtained provides a measure of the ability of the heart to pump blood through the lungs (RVEF) or the body (LVEF). A criticism of Ir-191m for this application has been that the half-life (4.96s) is too short to allow effective visualization and quantitation of left ventricular function in adults, particularly those with delayed transit times. A recent... 

Heart failure can result from any disorder that affects the ability of the heart to contract (systolic function) and/or relax (diastolic dysfunction) common causes of heart failure are shown in Table 14—1 Systolic heart failure is the classic, more familiar form of the disorder, but current estimates suggest that 20% to 50% of patients with heart failure have preserved left ventricular systolic function and suffer from diastolic dysfunction. In contrast to systolic heart failure that is usually caused by previous myocardial infarction (Ml), patients with diastolic heart failure typically are elderly, female, and have hypertension and diabetes. However, systolic and diastolic dysfunction frequently coexist. The common cardiovascular diseases such as MI and hypertension can cause both systolic and diastolic dysfunction thus many patients have heart failure as a result of reduced myocardial contractility and abnormal ventricular filling. 

Investigations of the heartbeat have revealed that the heart may occur in two fundamental states the state of decontraction (diastole) and the state of contraction (systole). Responding to an electrochemical stimulation, each fibre of the cardiac muscle rapidly contracts, remaining in this state momentarily, followed by a rapid return to the state of decontraction. 

Myeloproliferative disorder A group of diseases of the bone marrow in which excess cells, usually lymphocytes, are produced. Myelosuppression A condition in which bone marrow activity is decreased, resulting in fewer red blood cells, white blood cells, and platelets. Myelosuppression is a side effect of some cancer treatments. Myocardial contractility The force of contraction of the heart during systole. 

Systolic dysfunction An abnormal contraction of the ventricles during... 

Systole, in which the chambers contract and eject the blood... 

Ventricular contraction. This process occurs during ventricular systole. When the ventricular myocardium begins to contract and squeeze down on the blood within the chamber, the pressure increases rapidly. In fact, ven-... 

Another noteworthy anatomical feature of the arteries is the presence of elastic connective tissue. When the heart contracts and ejects the blood, a portion of the stroke volume flows toward the capillaries. However, much of the stroke volume ejected during systole is retained in the distensible arteries. When the heart relaxes, the arteries recoil and exert pressure on the blood within them, forcing this "stored" blood to flow forward. In this way, a steady flow of blood toward the capillaries is maintained throughout the entire cardiac cycle. 

Heart sounds Sound Si occurs at the beginning of systole as the mitral and tricuspid valves close S2 occurs at the beginning of diastole as the aortic and pulmonary valves close. These points should be in line with the beginning of electrical depolarization (QRS) and the end of repolarization (T), respectively, on the ECG trace. The duration of Si matches the duration of isovolumic contraction (IVC) and that of S2 matches that of isovolumic relaxation (IVR). Mark the vertical lines on the plot to demonstrate this fact. 

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. 

The percentage of ventricular volume that is ejected from the ventricle during systolic contraction (°/o)... 

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). 

The decreased work capacity of the in-farcted myocardium leads to a reduction in stroke volume (SV) and hence cardiac output (CO). The fall in blood pressure (RR) triggers reflex activation of the sympathetic system. The resultant stimulation of cardiac 3-adreno-ceptors elicits an increase in both heart rate and force of systolic contraction, which, in conjunction with an a-adren-oceptor-mediated increase in peripheral resistance, leads to a compensatory rise in blood pressure. In ATP-depleted cells in the infarct border zone, resting membrane potential declines with a concomitant increase in excitability that may be further exacerbated by activation of p-adrenoceptors. Together, both processes promote the risk of fatal ventricular arrhythmias. As a consequence of local ischemia, extracellular concentrations of H+ and K+ rise in the affected region, leading to excitation of nociceptive nerve fibers. The resultant sensation of pain, typically experienced by the patient as annihilating, reinforces sympathetic activation. 

The main property of cardiac glycosides is their selective action on the heart, the main effect of which is the strengthening of systole, which creates a more economic condition for heart work strong systolic contractions change into periods of rest (diastole), which facilitate restoration of energetic resources of the myocardium. 

Diastolic BP (DBP), which measures the pressure in the arteries when the heart is at rest, was largely unaffected by the intervention. Systolic BP (SBP), or the maximum pressure exerted when the heart contracts, did change in response to CCM supplementation in most children. The data specifically showed that over 12 weeks, children in the lowest quartile of baseline daily Ca intake (150- < 347 mg/1000 kcal) were affected most significantly by CCM supplementation in terms of a reduction in systolic BP (effect estimate -3.5 mm Hg), whereas children in the highest quartile of baseline daily Ca intake (514- < 882 mg/1000 kcal) demonstrated no appreciable reduction in systolic BP due to CCM supplementation. Children in quartiles two and three of the baseline Ca intake benefited from a CCM-induced reduction in SBP with the effect estimated to be -2.8 mm Hg and -1.3 mm Hg, respectively. The overall trend for the estimated effect of Ca intake on BP across quartiles was highly significant p = 0.009). 

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