Hemorrhagic hypotension




By Justin Schwartz, MBS 2019, Geisinger Commonwealth School of Medicine

Mentor: David Averill, PhD


All of us have suffered from an injury resulting in bleeding, whether it has been miniscule as in a scathed knee, or severe from a traumatic incidence such as a car accident. Our first instinct is always to apply pressure and stop the bleed, but what happens if the bleeding simply cannot be stopped? What happens if your body begins to lose so much blood that it begins shutting down? This is what we call Hemorrhagic Shock, and this is what we will be discussing today.

Your arteries function to carry “fresh” blood containing oxygen and nutrients from your heart to your tissues, while your veins carry the “used” blood containing waste products back to the heart. If you lose a significant amount of blood then you will no longer be able to bring adequate oxygen to the tissues. Your tissues operate just like you do. Imagine you were scuba diving and there was a leak in your oxygen tank. You start to lose oxygen and you can no longer breathe. If we do not restore this oxygen quickly and stop the leak, you will die. This is the exact same premise behind restoring blood flow to your tissues. Without restoring the blood flow, your tissues will not receive adequate oxygen, and they will die.

Luckily for us, our body has mechanisms to restore blood pressure on its own. There is a system called the Renin-Angiotensin-Aldosterone System (RAAS) that has many parts that work in concert to restore blood pressure. The Renin-Angiotensin-Aldosterone System is a system comprised of many hormones that work together to restore blood pressure, and consequently blood flow to your tissues. Remember our goal is to restore blood flow so that your tissues can get oxygen and not die! When your body begins to lose all of this blood you have special cells in the kidney, Juxtaglomerular cells, which sense the decreased blood pressure and release a hormone called renin. Renin is important because it converts Angiotensinogen from the Liver into Angiotensin I. Angiotensin I can then get converted into Angiotensin II by ACE in the lungs that function in many ways to increase blood pressure. I know that was a mouth full, but let us discuss why this is so important.

The main player here is Angiotensin II, which acts as a true leader and not only has roles of its own to increase blood pressure but also delegates responsibility to other organs to help increase blood pressure as well. Angiotensin II acts directly on blood vessels and decreases their diameter, causing an increased blood pressure. Angiotensin II also acts on the adrenal cortex and tells it to secrete the hormone Aldosterone. Aldosterone functions in the kidney to reabsorb salt and water instead of urinating these out. This reabsorption increases the amount of fluid that remains in the body and therefore increases the blood pressure. Angiotensin II also communicates all the way up to your hypothalamus in the brain and tells it to create and release the hormone ADH, or Anti-Diuretic Hormone, which also acts on a specific area of the kidney to increase water reabsorption, and therefore helps restore blood pressure as well.

Unfortunately, the Renin-Angiotensin-Aldosterone system has its limitations and sometimes the bleeding is so severe that your body cannot compensate. We just learned that the RAAS works on the kidney to reabsorb salt and water to increase body fluid and consequently blood pressure, but what happens if the kidney fails? At high levels of Angiotensin II, the artery that brings blood to the kidney actually squeezes and stops the blood flow to the kidney, this begins a state we refer to as Acute Renal Failure.

It is important to remember that the renal system functions to keep toxic materials from building up in your body by allowing you to pee them out, but what happens if the kidney fails and you can no longer urinate out these toxic materials? The buildup of acidic materials in the blood can lead to a state called metabolic acidosis that can be life-threatening.

In order to provide the best patient outcomes, it is important for practitioners to treat the health problem that may cause metabolic acidosis before it occurs. In the early stages, therapy will be directed towards restoring oxygen to the tissues to prevent tissue death, as well as any possible surgical interventions to stop the bleeding if necessary. This can be done by restoring lost blood volume with fresh frozen plasma that not only restores blood volume, and consequently blood pressure, but also effectively replaces the hemoglobin content of the blood so that you can get optimal delivery of oxygen to the tissues. If the amount of blood loss is too severe and irreversible acute kidney failure occurs, dialysis treatment may be needed. Dialysis treatment utilizes a machine that pumps your blood out of the body and cleans out all of the toxic materials and then proceeds to pump the clean blood back in.

Hemorrhagic hypotension resulting in acute renal failure is associated with a significantly increased risk of death in hospitalized individuals, especially those admitted to ICU, where in-hospital mortality rates exceed 50%. Therefore, it is important for clinicians to be able to effectively identify that shock is present, determine the type of shock, and restore oxygen delivery to the tissues such as the kidneys to prevent acute renal failure from occurring and effectively improve patient outcomes.

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