Heart failure: Renal fluid retention causes peripheral oedema
Reduced cardiac output usually reduces glomerular pressure due to decreased arterial blood pressure and arteriole contraction resulting from sympathomimetic enhancement.
After day one, either generalized heart failure or right ventricular heart failure, peripheral oedema begins to occur primarily due to renal fluid retention. Hypertensive fluid retention fills the system on average, leading to increased blood flow to the heart. The right atrial pressure increases and the arterial blood pressure returns to normal. Consequently, capillary blood pressure is also significantly increased, leading to a loss of fluid in the tissue and the development of severe oedema.
Reduced urine output in heart failure
1. Reduce glomerular filtration pressure. A decrease in cardiac output usually reduces glomerular pressure due to (1) a decrease in arterial blood pressure and (2) a contraction of the arterioles due to sympathomimetic enhancement. Consequently, except for the slightest degree of heart failure, a decrease in glomerular filtration pressure, and a decrease in glomerular filtration rate, often leads to a decrease in urine output. A decrease in cardiac output by about half can lead to complete anuria.
2. Activates the renin-angiotensin system and reduces the renal tubular reabsorption of salt and water. Reducing blood through the kidneys cause an increase in renin secretion in the kidney, leading to an increase in angiotensin II production. Angiotensin II has a direct effect on the renal arterioles to reduce renal blood flow, reduce the capillary pressure around the renal tubules, increase the reabsorption of both saline and water. This is because the excretion of water and salt in the urine drops sharply, and the amount of salt and water is concentrated in the blood and interstitial fluid everywhere in the body.
3. Increased secretion of aldosterone. In the chronic stage of heart failure, large amounts of aldosterone are secreted in the adrenal cortex. This is mainly due to the effect of angiotensin II to stimulate the secretion of aldosterone in the renal cortex. However, some increased aldosterone secretion is usually caused by hyperkalaemia. Hyperkalaemia often stimulates aldosterone secretion and increased K levels in response to decreased renal function in patients with heart failure. Increasing aldosterone intake increases renal tubular Na reabsorption. This increase in reabsorption leads to a secondary increase in water reabsorption for two reasons: first, Na is reabsorbed, it reduces the osmotic pressure in the tubule but increases the osmotic pressure in the interstitial fluid, this change in osmotic pressure causes water to travel from the lumen into the bloodstream. Second, Na is reabsorbed and the anion associated with Na, mainly Cl-, increases extracellular fluid osmolality pressure everywhere in the body, leading to the release of antidiuretic hormone by the hypothalamus-pituitary system. The anti-diuretic hormone ADH further increases tubular water reabsorption
4. Activate the sympathetic system. Heart failure activates the sympathetic system, has many effects that lead to the kidneys keeping fluid and salt: (a) contracting the incoming arterioles, reducing the glomerular filtration factor (b) stimulating tubular reabsorption by stimulating activates the alpha-adrenergic receptor on renal tubular endothelial cells (c) stimulates the release of renin and angiotensin II increases renal tubular reabsorption and (d) stimulates ADH to release in the posterior pituitary lobe, increases water reabsorption.
The role of the ANP in delaying the decompensation process. ANPs are hormones released in the atrial wall when they are dilated. Since heart failure mostly increases left and right atrial pressure causing the atrial wall to dilate, circulating ANP levels increase 5-10 times in severe heart failure. ANP has a direct effect on the kidneys to increase the excretion of salt and water. Therefore, ANP plays a natural role in preventing symptoms of severe congestion in heart failure.
Acute pulmonary oedema in end-stage heart failure - another pathological spiral
A common cause of death is acute pulmonary oedema in patients who have had long-term heart failure. When acute pulmonary oedema occurs, it usually begins with a temporary increase in heart load, for example as a result of exertion or increased emotion or too cold. Acute pulmonary oedema is thought to result from the following twists:
1. Temporarily increase the already weak left ventricular load. Due to the limited ability to pump blood in the left heart, blood begins to accumulate in the lungs.
2. Increased blood to the lungs increases pulmonary capillary pressure, and a small amount of fluid begins to seep into the lung and alveolar tissue.
3. Increased fluid in the lungs reduces oxygenation in the blood.
4. Reducing oxygen in the blood leads to weakness of the heart muscle and also causes peripheral vasodilation.
5. Peripheral vasodilation increases venous blood flow from the peripheral circulation.
6. Increasing the amount of venous blood poured increases blood stasis in the lungs, leading to more fluid permeability, reduced arterial oxygen saturation, more venous blood. Thus, this helix is established after critical points, which will last until the patient dies without prompt treatment. Strong therapies that can reverse course and save the patient's life include:
a. Place Garo in both legs and arms to squeeze the veins and reduce the burden on the heart
b. Use of a fast-acting diuretic, for example, furosemide, causes a rapid decrease in the amount of fluid in the blood.
c. Allow the patient to breathe pure oxygen to avoid hypoxaturation, heart failure, and vasodilation.
d. Administer drugs that act on the heart, eg digitalis, to strengthen the heart muscle.
The spiral of pulmonary oedema can accelerate death within 20 minutes to 1 hour. That's why any trick that wants to be successful needs to be established immediately.