Acute effects of moderate heart failure
When cardiac output is temporarily reduced, many rapid circulatory reflexes are activated. The most well-known reflex is the pressure receptor reflex, which is activated when atrial pressure changes.
If the heart is suddenly severely damaged, such as a heart attack, the heart's ability to pump blood decreases immediately. Consequently, (1) decreased cardiac output and (2) venous blood stasis, leading to increased venous pressure.
Progressive changes in the heart's pumping efficiency at different stages after an acute myocardial infarction are shown in the figure. The top curve shows the normal cardiac output.
Figure. Progressive change in cardiac output after acute myocardial infarction. Both cardiac output and right atrial pressure gradually change from point A to point D (illustrated by the black line) over a period of seconds, minutes, days and weeks.
Point A in this curve is the starting point, showing a normal resting cardiac output of 5 L / min and a right atrial pressure of 0 mmHg. Immediately after heart damage, the cardiac output curve descends rapidly to the lowest line below the graph. Within seconds, a new cyclic state was established at point B, showing that cardiac output decreased to only 2 L / min, only 2/5 of normal, while left atrial pressure increased. 4 mmHg due to stagnation of venous blood in the left atrium. Cardiac output is reduced enough to sustain life for a few hours, but it is often accompanied by dizziness. Fortunately, this acute phase usually lasts only a few seconds due to the presence of sympathetic reflexes to compensate, to a great extent.
Compensation in sympathetic-induced acute heart failure. When cardiac output is temporarily reduced, many rapid circulatory reflexes are activated. The best-known reflex is the pressure receptor reflex, which is activated when the atrial pressure changes. Chemical reflexes, the central nervous system's anaemia response, and even those originating in the damaged heart also contribute to sympathetic activation. The sympathetic system is strongly stimulated for a few seconds, and the parasympathetic signals to the heart are suppressed at the same time. The sympathetic system is strongly stimulated and has a strong effect on the heart and peripheral vessels. If all the ventricular damage is diffuse but still functioning, sympathetic stimulation increases muscle damage. If one part of the muscle loses its function and the other remains normal, the healing muscle will be strongly stimulated by sympathomimetics, thus partially compensating for the loss of muscle function.
Therefore, the heart beats harder due to sympathetic stimulation. This effect is shown in the figure, showing a 2-fold increase in cardiac output after sympathetic compensation.
Sympathomimetic stimulation also increases venous blood flow to the heart by increasing vascular tone, especially veins, increasing systemic filling pressure from 12-14 mmHg, almost 100% above normal. Increased filling pressure significantly increases the amount of blood flowing from the veins to the heart.
Because of this, the damaged heart becomes stronger with more blood expelled than usual, and atrial pressure is still increasing, helping the heart to still pump enough blood. Thus, in the figure, the new cyclic state is represented at point C, showing the cardiac output of 4.2 L / min and atrial pressure of 5 mmHg. The sympathetic reflex maximizes for 30 seconds. As a result, a person with a moderate sudden heart attack may experience only a heart attack and dizziness for a few seconds. Immediately afterwards, with the help of sympathetic reflex compensation, the same amount of the heart may be sufficient to support it.