Which is first: HF or HTN?

[HighB]

How to differentiate between:
1. Hypertension causing hypertrophy and eventual heart failure and congestion
and
2. congestive heart failure for another reason causing decreased renal blood flow and increased RAAS leading to HTN?

I came by a Q in UW (qid: 1532) where they show a patient presenting with CHF and HTN and ask about angiotensin II levels in his pulmonary veins.

The answer was increased, because the patient has scenario number 2.

What if it was scenario number 1 where he has essential hypertension and decreased RAAS? Wouldn't the presentation still be the same?

Thank you.

---

Members don't see this ad.

 

[chromuffin]

How to differentiate between:
1. Hypertension causing hypertrophy and eventual heart failure and congestion
and
2. congestive heart failure for another reason causing decreased renal blood flow and increased RAAS leading to HTN?

I came by a Q in UW (qid: 1532) where they show a patient presenting with CHF and HTN and ask about angiotensin II levels in his pulmonary veins.

The answer was increased, because the patient has scenario number 2.

What if it was scenario number 1 where he has essential hypertension and decreased RAAS? Wouldn't the presentation still be the same?

Thank you.

I remember this question. I think the question is getting at the fact that ACE is in the lung. Correct me if I'm wrong but it was asking you to compare between he pulmonary artery and pulmonary vein. So Ang II is higher in the pulmonary vein.

To get at your question, I don't think it's possible to distinguish the two solely on presentation. The only likely way to figure this out is to know the patient's PMH. If they have a history of HTN, family Hx of primary HTN, risk factors, viral infections, etc. Some patients get HF from HTN and some get it from cardiomyopathy.

 

[HighB]

Thank you for your answer.

Correct me if I'm wrong but it was asking you to compare between he pulmonary artery and pulmonary vein. So Ang II is higher in the pulmonary vein.

You are correct about this.

I don't think it's possible to distinguish the two solely on presentation. The only likely way to figure this out is to know the patient's PMH. If they have a history of HTN, family Hx of primary HTN, risk factors, viral infections, etc. Some patients get HF from HTN and some get it from cardiomyopathy.

Presentation:
63 yo; progressive dyspnea over 3 weeks; history of HTN, dyslipidemia; BP 158/89; distended jugular vein, bilateral lower extremity pitting edema.

I though of it this way: since he has PMH for HTN and dyslipidemia, then this BP is basically due to a primary cause and this would decrease the activity of the RAAs.

The answer was this way: since he has HF, CO is decreased and RBF is then decreased leading to increased activity of the RAAs (increased Ang II in the pulmonary vein).

Is there something I'm missing that makes my rationale wrong?

 

[chromuffin]

Thank you for your answer.



You are correct about this.




Presentation:
63 yo; progressive dyspnea over 3 weeks; history of HTN, dyslipidemia; BP 158/89; distended jugular vein, bilateral lower extremity pitting edema.

I though of it this way: since he has PMH for HTN and dyslipidemia, then this BP is basically due to a primary cause and this would decrease the activity of the RAAs.

The answer was this way: since he has HF, CO is decreased and RBF is then decreased leading to increased activity of the RAAs (increased Ang II in the pulmonary vein).

Is there something I'm missing that makes my rationale wrong?

I mean I think it doesn't matter how he got the CHF. The patient is decompensating with his heart failure. The distended neck vessels tell you he has left heart dysfunction. So then you know there is pulmonary edema. Lower edema tells you right heart failure.

If you think about it like this. He has poor lipid control so he's gonna have to have atherosclerosis. The atherosclerosis likely leads to renal stenosis. This leads to decreased RBF to the JGA, causing increased renin---> increased Ang II.

The question was basically just setting you up to see where ACE was located.

 

[HighB]

I mean I think it doesn't matter how he got the CHF. The patient is decompensating with his heart failure. The distended neck vessels tell you he has left heart dysfunction. So then you know there is pulmonary edema. Lower edema tells you right heart failure.

If you think about it like this. He has poor lipid control so he's gonna have to have atherosclerosis. The atherosclerosis likely leads to renal stenosis. This leads to decreased RBF to the JGA, causing increased renin---> increased Ang II.

The question was basically just setting you up to see where ACE was located.

Thank you again