Cardiac function curves

It is this reduction in preload that, in some cases, is beneficial to patients experiencing heart failure or hypertension. Unlike a healthy heart, a failing heart is unable to pump all of the blood returned to it. Instead, the blood dams up and overfills the chambers of the heart. This results in congestion and increased pressures in the heart and venous system and the formation of peripheral edema. Because the failing heart is operating on the flat portion of a depressed cardiac function curve (see Figure 14.2), treatment with diuretics will relieve the congestion and edema, but have little effect on stroke volume and cardiac output. 

Hypertension (blood pressure >140/90 mmHg) may be caused by an elevation in cardiac output or excessive vasoconstriction. Diuretics are used in these patients to reduce cardiac output. Assume that the hearts of these individuals are operating on the ascending portion of the cardiac function curve. As the plasma volume is reduced in response to treatment with diuretic drugs, venous return and preload are reduced, as are ventricular filling and stroke volume, and cardiac output, thus bringing blood pressure back within the normal range. 

Much of the criticism of the interpretation of Starling s original measured input-output relations was resolved by the introduction of a family of cardiac function curves [74], which accommodated neural and metabolic stimulation of the heart. Such influences manifest themselves in graphs of input (preload)-output (stroke volume, stroke work, etc.) as counter clockwise rotation (steeper) and stretch along the output (vertical) axis. Alteration in parameter c in Equation 18.1 and Equation 18.2 carries major responsibility for these modifications. In addition, it has recently been found that the cardiac function curve can be shifted along the horizontal (preload) axis [75]. This shift is effected by changes in air pressure, pe, external to the cardiac chambers, such as caused by the respiratory system, or by CPR, and modifies Equation 18.2 by approximation to... 

In accordance with Starling s law of the heart, cardiac output is intimately dependent on In our simplified model, we have let = P. In the discussion to follow, graphs of cardiac output as a function of P (Figure 4) will be called cardiac function curves . Extrinsic regulatory influences may be expressed as shifts in such curves (Guyton et ai, 1973 Levy, 1979 Berne and Levy, 1981). 

In addition, it has recently been found that the cardiac function curve can be shifted along the horizontal (preload) axis (Noordergraaf 2010). This shift is effected by changes in air pressure, p, external to the cardiac chambers, such as caused by the respiratory system, or by CPR, and modifies Equation 27.2 by approximation to... 

Ventricular function curve The graph that relates cardiac output, stroke volume, etc, to filling pressure or end-diastolic fiber length also known as the Prank-Starling curve... 

A graph of P plotted as a function of Q (Figure 4) has been termed a vascular function curve (Levy, 1979 Berne and Levy, 1981). From eq. 5, it is evident that the slope of the relationship between P and Q depends only on R, C and C . Changes in flow have an inverse effect on P, i.e., as 0 is increased, there will be a proportionate decrease in P. There is a limit to the reduction of P that can be produced by an increase in 0, however. At some critical maximum value of 0, sufficient fluid will be translocated from the venous to the arterial side of the circuit such that P, will drop below the ambient pressure. In a system of distensible tubes, the venous system will be collapsed by this negative transmural pressure (P minus ambient pressure). This will, of course, limit the maximum value of cardiac output regardless of the capabilities of the pump. 

Figure 4. Hypothetical cardiac and vascular function curves. (From Berne and Levy.)...

The administration of bicarbonate is to be used with cautioa The indiscriminate use of bicarbonate is particularly dangerous in resuscitation of patients with metabolic acidosis as a concomitant of hypovolaemic shock lactic acid itself is innocuous and is readily removed by the liver as soon as the perfusion of the tissues is re-established. If administration of bicarbonate causes alkalosis and shifts the oxygen dissociation curve to the left, there is interference with oxygen unloading at the cellular level in tissues which are already hypoxic. Treatment of metabolic acidosis by bicarbonate therapy is reserved for situations in which partial correction of the pH is needed to restore cardiac function, which is depressed by acidaemia as described in Chapter 4. 

Ventricular function (Frank-Starling) curves, which plot any function of preload versus any function of cardiac work, reveal that compensatory mechanisms in untreated heart failure (mostly deleterious) may shift such curves upward and to the left. Compensation in heart failure is offset by specific drugs that can ... 

Figure 13-2. Ventricular function (Frank-Starling) curves. The abscissa can be any measure of preload—fiber length, filling pressure, pulmonary capillary wedge pressure, etc. The ordinate is a measure of useful external cardiac work—stroke volume, cardiac output, etc. In congestive heart failure, output is reduced at all fiber lengths and the heart expands because ejection fraction is decreased. As a result, the heart moves from point A to point B. Compensatory sympathetic discharge or effective treatment allows the heart to eject more blood, and the heart moves to point C on the middle curve.

Figure 110.3 Survival curves in euthyroid cardiac patients and in cardiac patients with subclinical hypothyroidism. Kaplan-Meier survival curves of cardiac patients with normal thyroid function and of cardiac patients with low-T3 syndrome. Events considered cardiac and overall death. Modified from lervasi et al., (2007). Reprinted with permission.

Figure 8.18 shows computed initial muscle shortening velocity plotted as a function of isotonic load, which resembles Hill s hyperbolic force-length relation for tetanized skeletal muscle. This curve closely resembles the experimental E — v curves of Brady from cardiac twitch contractions [43]. 

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