Systole contraction

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

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. 

Crude leaf preparations of Digitalis have been in medical use since 1785. Pure cardiac glycosides are now available. These preparations in injectable tinctures or powdered leaf tablets are used extensively for the treatment of congestive heart failure. They increase the force of the heart muscle and the power of systolic contraction, apparently by inhibiting the active transport of K and Na ions through cell membranes. 

All cardiac glycosides have qualitatively the same effect. Primarily the systolic contraction of the heart muscle is strengthened. The mode of action of the cardiac glycosides, which is not known in all details, depends on rhythmic intracellular liberation of calcium-ions by inhibition of the calciumion outflow and an increase in the inflow of calcium-ions into the cell. This takes place by inhibition of Na+/K-r-activating membrane-ATP-ase. (Digitalis receptor). The concentration of Na+ is increased and that of K-r is decreased intracellularly. In this way the myosin-ATP-ase is activated with improved use of ATP, which gives increased power of contraction by facilitated reaction between actin and myosin. 

Stroke volume - volume of blood ejected by the left ventricle in one contraction Supplementary prescriber - prescribing in partnership with an independent prescriber Suppressor oncogene - alternative to tumour suppressor gene Systole - contraction phase of heart beat... 

A decrease is associated with decreased cardiac function, reflecting reduced systolic contraction. 

An increase is associated with deficits in contractibility or high afterload, a relatively shortened period of systolic contraction. 

Cardiac glycosides increase the force and speed of systolic contraction. In the failing heart they cause a more complete emptying of ventricles and shortening in length of systole. The heart has more time to rest between contractions. Increased cardiac output causes a lower heart rate and increases renal excretion. As to the pharmacology of digoxin itself, four main actions occur ... 

There is continuous pressure in arteries to propel blood through them. The level of blood pressure fluctuates during each cardiac cycle. Pressure is highest during systole (contraction) when blood is ejected from the left ventricle into the aorta this pressure is labeled SBP. Pressure is lowest during diastole (relaxation) and labeled... 

In Figure 7.14, again 3 denotes the compression fingers made with IPMNCs, 5 is the heart itself, 4 depicts an encapsulated enclosure filled with water to create a soft cushion for the compression fingers, 4d s are IPMNC based sensors cilia to continuously monitor the compression forces applied to the heart and 3e and 3f are the associated wiring and electronics. Note that, assisting or soft compression of the left ventricle of a weak heart will produce more internal pressure to pump more blood in synchrony with the natural systolic contraction of the ventricle. Additionally, the proposed system will also provide... 

Relaxation of the cardiac muscle requires uncoupling of the crossbridges that generated the force for the prior systolic contraction. At the level of the molecular motors (sarcomeres), this requires adenosine triphosphate (ATP) so that the molecules involved in a crossbridge interaction return to their deactivated, or off conformation. Additional ATP is required at sarcoplasmic reticulum (SR) membrane sites so that the pumps that sequester calcium back into the SR can operate. The sliding filament-based... 

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