How can catecholamines decrease CO after hemorrhage?

[pulshuvud]

Hi folks,

I have a question regarding the effects of catecholamines on cardiac output. My professor in physiology has stated that chatecholamines, when administered to patients suffering from severe hemorrhage can cause a decrease in cardiac output. Why is this? My intuition says that an infusion of chatecholamines will have the same effect as sympathetic stimulation by the vagus nerve, i.e. increase contractility of the cardiac muscles and thus increase cardiac output. Am I missing something here?

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[popopopop]

If you don't stop the bleeding, a faster heart rate will simply make you lose blood faster. That's what I'm getting by his/her statement. There just wouldn't be any volume left very quickly, hence why we push fluids fast.

 

[comed]

Hi folks,

I have a question regarding the effects of catecholamines on cardiac output. My professor in physiology has stated that chatecholamines, when administered to patients suffering from severe hemorrhage can cause a decrease in cardiac output. Why is this? My intuition says that an infusion of chatecholamines will have the same effect as sympathetic stimulation by the vagus nerve, i.e. increase contractility of the cardiac muscles and thus increase cardiac output. Am I missing something here?

Maybe it's because catecholamines increase HR (by mimicing sympathetic stimulation). Since the heart is racing so fast, it won't be effectively pumping a lot of blood, thereby decreasing cardiac output. Kinda like tachycardia, perhaps? Not really sure.

 

[jeep1010]

I think its because a faster heart rate implies a smaller stroke volume (as you are giving less time for the blood to fill) and therefore because CO = HR x SV you have a smaller CO with a smaller SV?

 

[andelJ94]

was his on an MCAT test you took? seems way too vague to be a valid Q unless they gave you more info.

On the one hand, catecholamines will raise HR and could lead to faster bleeding. On the other hand, too high a HR could result in very low stroke volume and thus, less blood loss, though that would cause reduced blood flow everywhere, right?

 

[Thoth]

I think it's secondary to vasoconstriction.

 

[SergeantBuzzKill]

Vasoconstriction of the blood vessels would presumably cause an increase in the resistance of the system. This, in turn, would cause the heart to work against a larger afterload and therefore cause a decrease in CO


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[andelJ94]

Vasoconstriction of the blood vessels would presumably cause an increase in the resistance of the system. This, in turn, would cause the heart to work against a larger afterload and therefore cause a decrease in CO


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Thanks! So the catecholamines make your heart beat faster with greater force and narrow the blood vessels, causing a rise in blood pressure. Still don't think this is a valid MCAT Q, more like a med school question.

 

[FCMike11]

Thanks! So the catecholamines make your heart beat faster with greater force and narrow the blood vessels, causing a rise in blood pressure. Still don't think this is a valid MCAT Q, more like a med school question.

Catecholamines increase arterial muscle vasoconstriction, increasing SVR. Increasing SVR increases afterload thus decreasing CO. Generally, CO and SVR will have inverse relationship.

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[Newtonian21]

Hi folks,

I have a question regarding the effects of catecholamines on cardiac output. My professor in physiology has stated that chatecholamines, when administered to patients suffering from severe hemorrhage can cause a decrease in cardiac output. Why is this? My intuition says that an infusion of chatecholamines will have the same effect as sympathetic stimulation by the vagus nerve, i.e. increase contractility of the cardiac muscles and thus increase cardiac output. Am I missing something here?

This basic physiology. But you might not get it at this stage. I am an ICU RN and a prospective med student. It's easy. During hemorrhage a patient is losing blood, and there will be a decrease in system volume. A decrease in systemic volume leads to an increase in heart rate as the heart tries to compensate for hypotension resulting from blood loss. During hypotension, there's a decrease in systemic vascular resistance. Simply put, hemorrhage leads to hypotension which results in tachycardia. The heart is already beating faster, you do not want to let it beat even faster during this time. Tachycardia or fast heart rate leads to loss of atrial kick due to inadequate filling time, and this further results in decreased cardiac output. You do not want to give load a patient with catecholamines during hemorrhage, all you need is crystalloids like lactated ringers or saline solution then transfuse blood based on hemoglobin level. You will see that tachycardia will resolve once there's a enough volume.

 

[Thoth]

This basic physiology. But you might not get it at this stage. I am an ICU RN and a prospective med student. It's easy. During hemorrhage a patient is losing blood, and there will be a decrease in system volume. A decrease in systemic volume leads to an increase in heart rate as the heart tries to compensate for hypotension resulting from blood loss. During hypotension, there's a decrease in systemic vascular resistance. Simply put, hemorrhage leads to hypotension which results in tachycardia. The heart is already beating faster, you do not want to let it beat even faster during this time. Tachycardia or fast heart rate leads to loss of atrial kick due to inadequate filling time, and this further results in decreased cardiac output. You do not want to give load a patient with catecholamines during hemorrhage, all you need is crystalloids like lactated ringers or saline solution then transfuse blood based on hemoglobin level. You will see that tachycardia will resolve once there's a enough volume.

You're not wrong, persay, but that's not really the question. It's more of a theoretical question. Fluid resuscitation is the #1 way to raise pressures, which is why it's a huge part of the Surviving Sepsis campaign, but there's also a reason why we keep phenyl sticks in our ED - a little bump to help keep the CO down while waiting for the NS or massive transfusion to kick in can be helpful.

Edit: My credentials: ER pharmacist.

 

[Newtonian21]

You're not wrong, persay, but that's not really the question. It's more of a theoretical question. Fluid resuscitation is the #1 way to raise pressures, which is why it's a huge part of the Surviving Sepsis campaign, but there's also a reason why we keep phenyl sticks in our ED - a little bump to help keep the CO down while waiting for the NS or massive transfusion to kick in can be helpful.

Edit: My credentials: ER pharmacist.

I get where you're coming from phenylephrine standpoint but we're talking about volume loss I don't know what else you want the heart to do when you have no volume. Neo is a peripheral vasoconstrictor correct me if I'm wrong. I get you're trying to prevent vasodilation. But Neo alone won't help Sir. Fluid resuscitation alone can solve the problem from hemorrhage