I think alot of people might have over emphasized how important ANP and BNP really are, yes it is important to know these peptides get secreted by the atrial/ventricular myocardium during heart failure. However their overall effectiveness in treating heart failure is zilch, a preceptor told me that if ANP and BNP were so useful in natriuresis then why do we give diuretics? It's because RAAS overpowers this system hence causing negative effects and the endless loop of heart failure. AKA why we give ACE inhibitors.

Knowing that ANP gets neutralized by the RAAS system, we can shift our focus back to heart failure in this patient, where cardiac output is decreased, leading to ADH secretion and finally dilutional hyponatremia.

I also thought the same as @bubbles, but now trying to "justify" this tricky NBME question: I think this revolves on the fact that the patient has a HIGH blood pressure meaning we should focus on an answer that explains both increased BP and Hypovolemia (i.e: increased ADH which vasoconstricts and also absorbs free-water, both of which increase BP and cause hypovolemia).

Maybe if this patient were decompensated with LOW BP, one could think more about ANP.

I still think this question is TOO tricky.

From UpToDate: PATHOGENESIS

Like most other causes of hyponatremia, heart failure impairs the ability to excrete ingested water by increasing antidiuretic hormone levels. When cardiac output and systemic blood pressure are reduced, "hypovolemic" hormones, such as renin (with a subsequent increase in angiotensin II formation), antidiuretic hormone (ADH), and norepinephrine, respond [1-3]. Although edematous patients with heart failure have increased plasma and extracellular fluid volumes, the body perceives volume depletion (reduced effective arterial blood volume) since the low cardiac output decreases the pressure perfusing the baroreceptors in the carotid sinus and the renal afferent arteriole. The degree of neurohumoral activation is generally related to the severity of cardiac dysfunction, as assessed by left ventricular ejection fraction or functional class [2]. The neurohumoral changes limit both sodium and water excretion in an attempt to return perfusion pressure to normal. ADH release directly enhances water reabsorption in the collecting tubules, whereas angiotensin II and norepinephrine limit distal water delivery (and thereby water excretion) by lowering the glomerular filtration rate (due to a marked reduction in renal perfusion) and by increasing proximal sodium and water reabsorption [4]. In addition, both the low cardiac output and high angiotensin II levels are potent stimuli to thirst, leading to enhanced water intake.

https://www.uptodate.com/contents/hyponatremia-in-patients-with-heart-failure#H2

This question confused me a lot because so many questions have drilled me on the importance of the ANP escape mechanism in times of fluid overload (as in CHF).

I thought ANP was a huge player in the loss of Na in circumstances of volume overload as in this patient (which is why you see euvolemic hypOnatremia in patients with SIADH or overactivity of the RAAS as in CHF).

Why is ADH now being named as the responsible agent?

CHF patients often display signs and symptoms of increased vasopressin secretion.

Here we go:

• decreased LV contractility (bilateral crackles)
• decreased cardiac output
• activate RAAS → ADH
• increase sympathetic activity → more RAAS → more ADH

https://www.ncbi.nlm.nih.gov/pubmed/7058822

"syndrome of "dilutional hypo-osmolality" in severe congestive heart failure may be caused by an inappropriately high ADH secretion in which the osmoreceptor system is dominated by nonosmolar stimuli"

Hyponatremia from Heartfailure pt.

It should be approached from Heart faiure.

HF-> RAAs -> excessive Aldosterone, ADH; ANP escape faiure, like secondary hyperaldosteronism; Hyponatremia

https://www.wjgnet.com/1949-8462/full/v5/i9/WJC-5-317-g001.htm

Decompensated HF. Lack of blood flow due to failing heart -> lower BP -> increased ADH to increase blood pressure back to stable level. In DHF, ADH outpaces homeostasis of counteracting ANP & BNP. Thus, the term "decompensated". Associated with shortness of breath, edema (often of lungs).

This vicious cycle continues as body prioritizes adequate BP for survival, but it comes at the expense of overworked heart that must work harder and harder, ultimately exacerbating the heart failure condition.

Always know this Hypo or hypernatremia is because of change in the volume, this patient is going through heart failure, renal perfusion has gone down that leads to release of ADH cos of osmoreceptors stimulation. Now high ADH will reabsorb more free water that will lead to hyponatremia. So hyponatremia is almost always related to high ADH. I know few of you will think but RAAS system is activated too but that abosrb Na along with water but ADH just free water.

i kinda of feel "odd" asking this question : but the patient had an MI 6 months ago, so why would it be unlikely that he was told to "restrict salt, restrict fluids (water) " ??

Guess what i'm asking is : what makes choice E such an unlikely choice (JVD, bi-basilar crackles, peripheral edema) ?

& @meningitis : his bp is 135/82 mmHg ... why is that "HIGH" ??

Firstly, I chose ADH. When I thought twice in review, I picked crossed ADH and picked ANP. My logic to cross ADH: 1. The main inducer of ADH are Osm and BP/vlomue. THis pt, Osm obviously not high, Bp obviously not low. So, nonsense in increased ADH. 2.You may see AngII also induces ADH. But it seems to be a minor inducer. Meanwhile, if it is exactly high AngII→ high ADH. Then, Aldo must be high as well, and High Aldo →Salt preserving→ HOW CAN serum Sodium be LOW? "Low Cardiac output→ High RASS (AngII Aldo ADH)" pathway is WATER-SODIUM retention. NOT pure WATER retention Please correct me