Heart mechanical activity

The most prominent expression of cardiac activity is the rhythmical contraction of the heart - its pumping action. Less well known is the fact, that this mechanical activity is tightly controlled by an electrical process called excitation. ... 

Analytical models of the heart are a reality. They are based on detailed descriptions of cardiac tissue architecture and anatomy, including the coronary vasculature. In sihco cardiac tissues possess realistic passive mechanical properties, and both electrical and mechanical activity can be simulated with high accuracy. Descriptions of key components of cellular metabolism have been introduced, as have models of drug-receptor interactions. 

Another mechanism to maintain CO when contractility is low is to increase heart rate. This is achieved through sympathetic nervous system (SNS) activation and the agonist effect of norepinephrine on P-adrenergic receptors in the heart. Sympathetic activation also enhances contractility by increasing cytosolic calcium concentrations. SV is relatively fixed in HF, thus HR becomes the major determinant of CO. Although this mechanism increases CO acutely, the chronotropic and inotropic responses to sympathetic activation increase myocardial oxygen demand, worsen underlying ischemia, contribute to proarrhythmia, and further impair both systolic and diastolic function. 

The mechanical activity of the heart (contraction of the atria and ventricles) occurs as a result of the electrical activity of the heart. The heart possesses an intrinsic electrical conduction system (Fig. 6-1). Normal myocardial contraction cannot occur without proper and normal function of the heart s electrical conduction system. Electrical depolarization of the atria results in atrial contraction, and ventricular depolarization is... 

Cardiac glycosides bring about diuresis by increasing both cardiac output and renal blood flow the latter in turn reverses the renal compensatory mechanism activated in congestive heart failure. Consequently, the production of aldosterone is reduced, sodium retention is reversed, and the excretion of edematous fluid is enhanced (Figure 35.5). 

K6. Kersting, F., and Brass, H., The effects of uraemic compounds on oxygen consumption and mechanical activity of isolated guinea pig hearts. Dial., Transplant., Nephron 13, 472-479... 

Lundberg, J.M., Hua, X.-Y. Franco-Cereceda, A. (1984a) Effects of neuropeptide Y (NPY) on mechanical activity and neurotransmission in the heart, vas deferens and urinary bladder of the guinea-pig. Acta Physiol. Scand. 121, 325 332. 

B. Slow Influx. The slow influx of Ca gets triggered off to equalize (balance) the loss besides maintaining a proper relative voltage plateau as shown in Fig. 11.1 (d). In fact, as the Ca entry slows down, the membrane potential becomes low very swiftly to the predepolarization levels (i.e., phase 4). Thus, in the heart muscle the electrical activity is coupled to a mechanical activity by Ca as the potential trigger. 

FIGURE 10.21 Simultaneous registration of (1) heart mechanical pumping activity, (2) heart electrical activity, and (3) lung mechanical ventilation, using only two electrodes. (From Patterson R. 1995. The Biomedical Engineering Handbook. Boca Raton, FL, CRC Press, 3rd edition, pp. 1223-1230.)... 

Quantitative rate data for reactions discussed in this section are given in Tables 3 and 4. The use of the ion [Ru(NH3)6] + as an outer-sphere reductant is much in evidence. The effect of sodium polystyrene sulphonate and sodium polyethylene on the rate of reduction of the series of complexes [Co(en)2(Cl)A] + (A = py, HjO, or NH3), [Co(en)2Cla]+, and [(NH3)6CoBrp+ has been investigated, for comparison with known effects in inner-sphere reactions. Though acceleration factors were found for both mechanisms, activation parameters reveal that for outer-sphere a lowering of Aff and for inner-sphere a more favourable AS are responsible. With [Ru(NH3)b] + in large excess, the consumption of horse heart ferricytochrome c obeys the rate law... 

Thus, Borelli (1608-1679) and his disciples favored the view that the stomach was but a mechanical mill, grinding up its contents into chyme. Mobius denied the existence of gastric acid, and Archibald Pitcairn interpreted all function in terms of mechanical activity, believing the teeth to be scissors, the stomach a fermenting vat, and the lungs and heart to be bellows and a pump, respectively. 

Ji, J., et al.. Ultrasound-targeted transfection of tissue-type plasminogen activator gene carried by albumin nanoparticles to dog myocardium to prevent thrombosis after heart mechanical valve replacement. International Journal of Nanomedicine, 7 2911-2919,2012. 

Electrical depolarization, but no synchronous shortening of myocardial fibers and no mechanical activity or contractions in the heart... 

Although death may be attributable to many tmderlying conditions, the final common pathway remains the cessation of the heart electrical activity. With hospitalized patients, cardiac arrest is usually manifested by ventrieular fibrillation, from which the patient may or may not be resuscitated. Sudden eardiae death, which claims over 350,000 lives annually in the United States, results from abrupt disruption of heart rhythm, also primarily in the form of ventricular fibrillation. Death in those instances is due not to extensive cardiac injury, but rather, to transient triggers that impinge on the electrically unstable heart (65-67). Identification of individuals at risk for sudden cardiac death remains a major objective in cardiology. Similarly, the specific mechanism linking ambient air particle exposure to death is unknown. 

The cardiac effects of the calcium antagonists, ie, slowed rate (negative chronotropy) and decreased contractile force (negative inotropy), are prominent in isolated cardiac preparations. However, in the intact circulation, these effects may be masked by reflex compensatory adjustments to the hypotension that these agents produce. The negative inotropic activity of the calcium antagonists may be a problem in patients having heart failure, where contractility is already depressed, or in patients on concomitant -adrenoceptor blockers where reflex compensatory mechanisms are reduced. 

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