In: Nursing
Explain the relationship between CO/CI, SVR and its effect on kidney perfusion, specifically addressing the RAAS system.
CO- Cardiac output :
A healthy heart with a normal cardiac output pumps about 5 to 6 liters of blood every minute when a person is resting.
The cardiac index is frequently measured and used in both intensive care medicine and cardiac intensive care. The CI is a useful marker of how well the heart is functioning as a pump by directly correlating the volume of blood pumped by the heart with an individual's body surface area.
SVR- systemic vascular resistance
Systemic vascular resistance (SVR) refers to the resistance to blood flow offered by all of the systemic vasculature, excluding the pulmonary vasculature. This is sometimes referred as total peripheral resistance (TPR).
◾️Systemic vascular resistance (SVR) reflects changes in the arterioles, which can affect emptying of the left ventricle. For example, if the blood vessels tighten or constrict, SVR increases, resulting in diminished ventricular compliance, reduced stroke volume and ultimately a drop in cardiac output.
◾️increased SVR can be caused by vasoconstrictors, hypovolemia, or late septic shock. A decreased SVR can be caused by early septic shock, vasodilators, morphine, nitrates, or hypercarbia.
Peripheral resistance is determined by three factors:
Signs and symptoms - Cardiogenic Shock
The Renin-Angiotensin-Aldosterone System (RAAS) is a hormone system within the body that is essential for the regulation of blood pressure and fluid balance. The system is mainly comprised of the three hormones, they are
◾️renin
◾️angiotensin
◾️aldosterone.
Renin splits angiotensinogen, a large protein secreted from the liver that circulates in the bloodstream into pieces. One piece is angiotensin I. Angiotensin I, which is relatively inactive, is split into pieces by angiotensin converting enzyme (ACE), found in high levels in the lung.
The renin-angiotensin system or RAS regulates blood pressure and fluid balance in the body. When blood volume or sodium levels in the body are low, or blood potassium is high, cells in the kidney release the enzyme, renin. Renin converts angiotensinogen, which is produced in the liver, to the hormone angiotensin I.
Function
The RAAS functions to elevate blood volume and arterial tone in a prolonged manner. It does this by increasing sodium reabsorption, water reabsorption, and vascular tone.
In summary, the renin-angiotensin-aldosterone system (RAAS) is a critical regulator of blood pressure (blood volume & electrolyte balance) as well as vascular tone & resistance. Normally, renin is secreted if blood pressure is too low thus activating angiotensin II to increase blood pressure and vascular resistance.
◾️When angiotensin II or aldosterone levels are inappropriately elevated, the antinatriuretic effects of these hormones shift pressure natriuresis to higher levels, thereby necessitating increased blood pressure to maintain sodium balance.
the symptoms of too much aldosteron
◾️Psychological stress also activates the sympathetic-adrenomedullary system which stimulates rennin release leading to increases in angiotensin II and aldosterone secretion. Aldosterone activates MR which in turn may lead to vascular injury and inflammation, and ultimately heart disease, renal disease, and stroke