Stroke volume preload

Increased preload (through Optimize stroke volume via Pulmonary and systemic congestion... 

Practitioners must have a good understanding of cardiovascular physiology to diagnose, treat, and monitor circulatory problems in critically ill patients. Eugene Braunwald, a renowned cardiologist, described the interrelationships between the major hemodynamic variables (Fig. 10-1).1 These variables include arterial blood pressure, cardiac output (CO), systemic vascular resistance (SVR), heart rate (HR), stroke volume (SV), left ventricular size, afterload, myocardial contractility, and preload. While an oversim-... 

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. 

As cardiac function decreases after myocardial injury, the heart relies on the following compensatory mechanisms (1) tachycardia and increased contractility through sympathetic nervous system activation (2) the Frank-Starling mechanism, whereby increased preload increases stroke volume (3) vasoconstriction and (4) ventricular hypertrophy and remodeling. Although these compensatory mechanisms initially maintain cardiac function, they are responsible for the symptoms of HF and contribute to disease progression. 

Nitrates (e.g., ISDN) and hydralazine were combined originally in the treatment of HF because of their complementary hemodynamic actions. Nitrates are primarily venodilators, producing reductions in preload. Hydralazine is a direct vasodilator that acts predominantly on arterial smooth muscle to reduce systemic vascular resistance (SVR) and increase stroke volume and cardiac output. Evidence also suggests that the combination may provide additional benefits by interfering with the biochemical processes associated with HF progression. 

During IV administration, milrinone increases stroke volume (and cardiac output) with little change in heart rate. It also decreases PAOP by venodilation and thus is particularly useful in patients with a low cardiac index and an elevated LV filling pressure. However, this decrease in preload can be hazardous for patients without excessive filling pressure, leading to a decrease in cardiac index. 

Stroke volume is itself dependent on the prevailing preload, afferload and contractility. 

Mechanism of Action Adirect-acting inotropic agent acting primarily on beta,-adrenergic receptors. Therapeutic Effect Decreases preload and afterload, and enhances myocardial contractility, stroke volume, and cardiac output. Improves renal blood flow and urine output. 

Both large arteries and veins relax in response to GTN. But in small doses, marked venorelaxation is seen leading to reduced preload. This causes decrease in stroke volume which is compensated with reflex tachycardia. 

The three factors that regulate the stroke volume are preload, afterload and contractility ... 

The workload of the heart is modified by using medication that increases or decreases preload and afterload, thereby adjusting stroke volume and cardiac output. Vasodilators decrease the preload and afterload, resulting in a decrease in blood pressure (arterial pressure) and cardiac output. Vasopressors increase the preload and afterload, causing in an increase in blood pressure cardiac output. 

Heart rate is controlled by the autonomic nervous system. Stroke volume, or the volume of blood ejected during systole, depends on preload, afterload, and contractility. As defined by the Frank-Starling mechanism, the ability of the heart to alter the force of contraction... 

Heart Four-chamber dilation atrophic degeneration with necrosis and fibrosis myofibrillar disruption QT prolongation, low voltage, bradycardia decreased cardiac output, stroke volume, and contractility preload intolerance diminished responsiveness to drugs... 

PHARMACOLOGICAL EFFECTS In younger patients with uncomplicated essential hypertension, methyldopa reduces vascular resistance without much change in cardiac output or heart rate. In older patients, cardiac output may be decreased as a result of decreased heart rate and stroke volume secondary to relaxation of veins and reduced preload. The fall in arterial pressure is maximal 6-8 hours after an oral or intravenous dose. Although the decrease in supine blood pressure is less than that in the upright position, symptomatic orthostatic hypotension is less common... 

In patients with elevated systemic vascular resistance and normal-to-elevated systemic blood pressure, afterload reduction with nitroprusside is logical it should be emphasized that nitroprus-side also increases venous capacitance, thereby also decreasing preload. In the context of myocardial dysfunction, afterload reduction will typically lead to improved forward cardiac output. Nitroprusside may also be effective when the systemic vascular resistance is elevated and systemic blood pressure is reduced the caveat in this more complex hemodynamic setting is that the load reduction produced by nitroprusside must be counterbalanced by an increase in stroke volume. This derivative increase in stroke volume may not occur in the patient with advanced heart failure rather, the result will be a further reduction in mean arterial pressure and the potential risk of peripheral organ hypoperfusion. An alternative approach would be the use of an inotropic-dilator drug such as milrinone, which will provide both preload and afterload reduction its concurrent positive inotropic effect may offset the reduction in mean arterial pressure that can occur from vasodilation alone. 

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.

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... 

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