Acute effects of moderate heart failure

2021-04-29 02:43 PM

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.



Pathophysiology of cardiogenic shock

Urine formation: Reabsorbed glomerular filtration

Air in and out of the lungs: pressure causes the movement of air

Mechanism of urine concentration: osmotic pressure changes in different segments of the renal tubule

Absorption and excretion of potassium through the kidneys

Nephron: The functional unit of the kidney

Estimated renal plasma flow: PAH clearance

Prothrombin activation: initiates blood clotting

Pulmonary capillary dynamics: capillary fluid exchange and pulmonary interstitial fluid dynamics

Graphical analysis of high-volume heart failure

Red blood cells: differentiation and synthesis

Calculate the glomerular filtration rate (GFR): the forces that cause the filtration process

Ammonia buffering system: excretes excess H + and creates new HCO3

Concentrated urine formation: urea contributes to increased osmotic pressure in the renal medullary

Reduced sodium chloride, dilates arterioles, increases Renin release.

Extracellular fluid distribution between interstitial space and blood vessels

The proximal tubule reabsorption: active and passive reabsorption

Pathophysiology of fever

Origin of lymphocytes: the body's resistance to infection

Acidosis causes a decrease in HCO3- / H + in renal tubular fluid: compensation mechanism of the kidney

The endocrine regulates tubular reabsorption

Sodium channel blockers: decrease the reabsorption of sodium in the manifold

Self-regulation of glomerular filtration rate and renal blood flow

Physiological anatomy of the kidneys and urinary system

The myogenic mechanism itself regulates renal blood flow and glomerular filtration rate