Cardiac pump

Inadequate diuretic therapy Ineffective cardiac pump function... 

The cardiac pump theory states that the active compression of the heart between the sternum and vertebrae creates an artificial systole in which intraventricular pressure increases, the atrioventricular valves... 

The electrical impulse for contraction (propagated action potential p. 136) originates in pacemaker cells of the sinoatrial node and spreads through the atria, atrioventricular (AV) node, and adjoining parts of the His-Purkinje fiber system to the ventricles (A). Irregularities of heart rhythm can interfere dangerously with cardiac pumping func-tioa... 

Since approximately 130 mL of plasma water is filtered across the porous glomerular capillary membranes each minute (190 L/day), the kidney is admirably suited for its role in drug excretion. As the ultrafiltrate is formed, any drug that is free in the plasma water, that is, not bound to plasma proteins or the formed elements in the blood (e.g., red blood cells), will be filtered as a result of the driving force provided by cardiac pumping. 

Cardiac phospholamban (cardiac pump regulator) AIRRAST Intracellular [Ca2+]... 

An arrhythmia can be broadly defined as any significant deviation from normal cardiac rhythm.6 Various problems in the origination and conduction of electrical activity in the heart can lead to distinct types of arrhythmias. If untreated, disturbances in normal cardiac rhythm result in impaired cardiac pumping ability, and certain arrhythmias are associated with cerebrovascular accidents, cardiac failure, and other sequelae that can be fatal.1,2 16 Fortunately, a variety of drugs are available to help establish and maintain normal cardiac rhythm. 

Decreased cardiac performance. Any number of factors that affect cardiac pumping ability may be responsible for initiating a change in myocardial performance. Factors such as ischemic heart disease, myocardial infarction, valve dysfunction, and hypertension may all compromise the heart s pumping ability.29 53 71 Also, cardiomyopathy may result from other diseases and infections.13... 

Neurohumoral compensations. The body responds to the decreased cardiac pumping ability in a number of ways. In the early stages of failure, cardiac output decreases, and the delivery of oxygen and nutrients to tissues and organs is diminished. To compensate for this initial... 

Likewise, heart failure is not always associated with systolic dysfunction and an obvious decline in cardiac pumping ability. In approximately half the cases of symptomatic heart failure, systolic function and cardiac output may appear normal when the patient is at rest.53,63 In this type of heart failure, cardiac function is impaired because the left ventricle is stiff and unable to relax during the filling phase, resulting in increased pressures at the end of diastole.31 This condition is often described as diastolic heart failure, but it is also identified by other names such as heart failure with preserved left ventricular... 

It is well documented that coordinated myocyte handling of Ca2+ is essential for efficient excitation-contraction coupling in the heart. Since cardiac pump is able to alter its function in response to any requirement in the body and the regulation of contractile function of individual myocytes obtained by modulation of intracellular Ca2+ signaling, the characteristics of regulation induced by adrenergic stimulations are very important for maintaining the normal heart function in humans. 

The cardiac pump theory states that the active compression of the heart between the sternum and vertebrae creates an artificial systole in which intraventricular pressure increases, the atrioventricular valves close, the aortic valve opens, and blood is forced out of the ventricles. When ventricular compression ends, the decline in intraventricular pressure causes the mitral and tricuspid valves to open, and ventricular fining begins. 

It has been postulated that cardiac pump function can be reduced by binding of free calcium to albumin (6). 

Although thromboprophylaxis of microvascular anastomoses seems advisable theoretically, there is little clinical evidence to support the use of dextran for this purpose. The pulmonary edema in these cases was thought to be non-cardiogenic, similar to that caused by heroin, methadone, propoxyphene, and salicylates, due to a direct adverse effect on the pulmonary vasculature, rather than anaphylaxis, cardiac pump failure, or volume overload. 

The clinical manifestations of heart failure vary considerably and depend on many factors, including the (1) clinical characteristics of the patient, (2) extent and rate at which the heart s performance becomes abnormal, (3) etiology of the heart disease, (4) concomitant co-morbidities, and (5) distribution of the abnormal cardiac function. The severity of impairment can range from mild-— manifested clinically only during stress—to advanced, in which cardiac pump function is unable to sustain life without external support. 

R.J. Solaro, Integration of myofilament response to Ca2+ with cardiac pump regulation and pump dynamics, Am J Physiol 277(6 Pt 2), S155-63 (1999). 

The first case study of this chapter outlines the development of a model of left ventricular pumping. The model is devised from canine experiments and represents the left ventricle as a time, volume, and outflow-dependent pressure generator. In the course of model development, a new analytical method of measuring ventricular elastance emerges, with the potential of clarifying issues with previous elastance measurements. One application is a slight model expansion to study the cardiac pump theory of cardiopulmonary resuscitation (CPR). 

The main results of this predictive study are twofold. First, the normal circulation, including the mitral and aortic valves, can effectively circulate blood (with a reduced stroke volume) via external compression. This result supports the cardiac pump theory proposed by Kouwenhoven et al. [16]. Second, if the valves are removed or made incompetent no significant net flow is circulated, for either the normally beating ventricle, or the asystolic ventricle subjected to external compressions. The small (8 ml/sec) net outflow... 

The energy requirement of cardiac muscle fibers and the useful work they can generate are of considerable interest [Starling and Visscher, 1926 Robardet al., 1959 Li, 1983 Liao etal., 2003], They define the mechanical efficiency of the cardiac pump. In hemodynamic terms, the efficiency of the heart is defined as the ratio of external mechanical work (EW) to myocardial oxygen consumption (MVO2) ... 

Gradually, divergent opinions appeared as to the mechanism by which blood was actually pumped. Two schools of thought developed. The cardiac pump theory [12] suggested that pumping was achieved by direct compression of the heart, despite doubts expressed about the ability of the heart to function as a unidirectional pump under CCCR conditions as early as 1961 [18], Weale, in his letter to the... 

The cardiac pump theory advocates that there is (direct) pressure on the ventricles. This is supported by indications that compression depth is related to output, that cardiac (or more specifically ventricular) deformation is related to stroke volume, that the duration of compression has no effect, and that an increased compression rate will increase flow [17]. In the original manuscripts, as well as over time, 1.5 to 2 in. (4 to 5 cm) has been maintained as standard. Forward flow of blood is assumed to be caused by competent atrioventricular valves and sufficient competence of the aortic and pulmonary valves to avoid regurgitation during CPR diastole. Implicitly, ventricular filling is essential and artificial systole must be sufficiently frequent to generate acceptable flow, as stroke volumes may be relatively small compared to the normal 60 to 100 ml per beat at ejection fractions of 40 to 75%. Mitral valve closure during CPR systole is deemed essential for the cardiac pump theory to work. 

Much of the research and development in CPR has followed the line of thinking set out by Kouwenhoven in 1960. In the following section the emphasis is shifted to evaluation of a widely accepted aspect, which was not properly scrutinized before, namely the sternum depression depth, discussed in Section 18.2.3, earher. Additional information is needed to verify whether depression depth may or may not be a factor in the poor outcome after sudden cardiac death. This threshold, conceptually, apphes to the cardiac pump theory. 

Returning to CPR, the second term on the right in Equation 18.5 is now the application of external pressure, either directly as in the cardiac pump theory, or via general intrathoracic pressure increase as in the thoracic pump theory. 

There has been no lack of efforts to improve outcome. In an attempt to achieve better understanding [83 ], literal Kouwenhoven adherents believe in what became known as the cardiac pump theory, while other investigators prefer the thoracic pump theory, since they believe that alterations in intrathoracic pressure prevail. A wide variety in adjuvant techniques — most but not all of them paralleling either of the two theories — was conceived and developed. Thus far, little of this effort has borne fruit convincingly. 

Sudden cardiac death (SCD) is defined as abrupt loss of consciousness caused by failure of cardiac pumping function, generally because of an electrical problem. In certain cases, cardiac activity ceases completely because cardiac electrical impulse generation fails (bradycardic sudden death). Most commonly, however, cardiac electrical activity is present, but is either too rapid for effective mechanical response or too disorganized for coordinated mechanical response (tachycardic sudden death). Despite the term, resuscitation from SCD is possible, but lack of prompt treatment is almost invariably fatal. SCD is responsible for at least 160,000 deaths each year in the United States alone [4]. 

Burch GE, Ray CT, Cronvich JA (1952) Certain mechanical pecularities of the human cardiac pump in normal and diseased states. Circ 5 504-513... 

The mechanical reliability of PAEK has led to their use in a variety of devices. For example, they are being evaluated in applications such as heart valves [19] and by Impella AG as rotors for bi-ventricular, intra-cardiac pump systems which can be inserted into the heart to replace heart-lung machines. PAEK also find applications as housings for implantable medical devices such as heart pacemakers [20, 21]. 

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