Posts Tagged ‘heart failure’

I am unable to answer this question confidently even after spending 25 years in the specialty of cardiology. I thought, the answer was yes. Reality is definitely different. Such is the complexity in the biology of the fluid and circulatory systems. The heart’s function doesn’t seem to end with just pumping 6 liters of blood every minute, ultimately, it has to handle a huge load of water as well with delicate coordination with the kidney. (ANP,& RASS feedback). It is fascinating to note, that the heart transforms into a powerful endocrine organ as and when it is necessary.

Read further, with a caution: (There is no specific physiological /molecular answer attempted)

About 28 of the 42 liters of fluid in the body are inside the 100 trillion cells and are collectively called the intracellular fluid. Thus, the intracellular fluid constitutes about 40 percent of the total body weight in an “average” person. Still, cells are somehow protected from the edema creating hemodynamic force until the very late stages. Fortunately, the Interstitium is the place all excess fluid stagnates. This is a great biological adoption. The simplest explanation is (Na /K+pump never sleeps  ) Bi-directional osmotic forces keep the cell dry even in adverse cellular milieu. Can’t imagine the implications, if every cell begins to swell in early heart failure. Still, it does happen to some degree I guess. We never quantified this.( Andrew Boyle,et al  Myocellular and Interstitial Edema and Circulating Volume Expansion as a Cause of Morbidity and Mortality in Heart Failure)


What happens to massive Intra cellular compartment size in HF? If renal perfusion is compromised (As one would expect in any significant heart failure) How does it affect this fluid distribution over that of heart failure? If the lymphatics’ final destination is the right heart how does this interfere with interstitial space clearance?

Practical implications

Though local factors operate, edema* in heart failure is a reflection of a more serious systemic plumbing issue. Even, subclinical fluid collection can interfere with cell function and contribute to unexplained fatigue which is an early sign of heart failure. No doubt, NYHA  gave much importance to this non-specific symptom in heart failure. Further, Individual organ functions may react in a different fashion with respect to water logging.Hepatic, portal splanchnic congestion directly affect GI function and intermediate energy metabolism.

.(*HF with zero edema so-called dry CHF  is a bigger mystery, is discussed elsewhere on this site)

When does the cardiac failure become a disorder of sodium & water metabolism 

Though the heart is a mechanistic pump when it fails it soon becomes a neuro-metabolic-endocrine problem. We are not clear whether heart failure retains sodium and water equally?  In renal failure-free water, accumulation is less than sodium. What happens in cardio-renal syndrome. These have practical implications as both hyponatremia and hypernatremia can be a feature with water content modulating it.(Now the term dysnatermia is more often used)

If RASS is activated net gain in sodium is expected. It doesn’t really happen. (Even with secondary hyperaldosteronism  sodium knows how to escape from the kidney). Vasopressin antagonist was considered a new innovation for hyponatremia associated with HF. To know the current role of V2 receptor antagonists Tolvapan, read here. 

Can we get rid of this excess water by any other means 

We do have powerful diuretics. It can unload the heart rapidly but can be harmful due to intracellular dehydration and electrolyte imbalance. When I asked an experienced Nephrology colleague  “Does excessive diuretics deplete ICF or ECF space? and how to quantify? , he was honest enough to accept, that it is primarily guesswork in a given patient and clinical assessment is supreme.

It is understood now, that there is a role for ultrafiltration of pure water in refractory hydrophilia. Bart B.A  (RAPID-CHF) trial. J Am Coll Cardiol. 2005; 462043-2046

Imaging subclinical edema in heart failure 

How to catch Heart failure early before clinical edema ? NT pro-BNP is a good option (>400pg/l) but physiologists armed with new generation imaging are working on how and where the fluid is accumulating in early heart failure. Nailfold video capillaroscopy (NVC) and confocal laser scanning microscopy (CLSM).  Wish, these modalities are really useful and do not end up as fancy tools and hike up the heart failure treatment costs. 


Future of Cardiac Hydraulics management.
1. Afterload reduction, 2. Preload optimization, and 3.Inotropics. We have been playing with these three famous principles in heart failure treatment for quite some time. We must admit, nothing really worked to our expectations. “Total body water management” is a new hope. It will revolve around a mechanical fluid management system as this overview from circulation tantalizingly discuss. DRI2P2S  (Circulation heart failure 2020)

Final message 

Edema in HF is primarily extracellular and interstitial until the end stage. Fortunately, the ionic and osmotic forces along with capillary hemodynamic forces keep the excess fluid within a safer interstitial compartment. However, we must realize each organ swells in a different manner depending upon cell membrane responsiveness to neural and humoral factors. The mechanism and content of edema fluids are different in heart vs kidney failure. It is also true, that every cardiac failure patient has a renal component and vice versa.

That’s it. I know it was a superficial attempt to understand water distribution in HF. Someone needs to break the complete truth about H2O metabolism in cardiac failure.

Postamble & a Non-academic trail

 Should we really bother to know where does fluid accumulate in HF ?  In a pragmatic sense the answer is “No” Let it accumulate anywhere, just push inj. Lasix, or if refractory add Metolazone and Torsemide, (I need to rush to the cath lab for the next angioplasty for that angina-free RCA stenosis, you know !)


This 37-page landmark review about fluid dynamics will help you find many queries raised here. (Tough read though)




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The long standing controversy about diastolic heart failure is settled !

The perception that diastolic heart failure ( Now renamed as heart failure with preserved EF ) is less dangerous than systolic HF has been exposed by this land mark study by Owan TE, in 2006 (nejm) But unfortunately this information is not yet fully disseminated among the physician community. Hence this post, with due acknowledgment to NEJM & Owan et all.

Experts from the article

“The nosology of heart failure has been the
subject of much current debate, and some extreme
positions have been taken. The observation
that 22 to 29 percent of patients with diastolic
heart failure die within one year of hospital
discharge, and 65 percent die within five years,
is a reminder that we are facing a lethal condition,
regardless of its name. Owan et al. also
show that, in recent years, there has been little
improvement in survival rate among patients with
diastolic heart failure, in contrast to the improvement
in survival rate over time among patients
with systolic heart failure”

Have a look at the survival curve below, almost similar , surprise surprise ! DHF survival is not only worse ( in many ), than systolic CHF and further they respond poorly to treatment, compared to conventional systolic CHF .

Click below for the link to full text article

Short abstract :

Trends in prevalence and outcome of heart failure with preserved ejection fraction.

Cardiorenal Research Laboratory, Mayo Clinic College of Medicine, Rochester, Minn 55905, USA.

BACKGROUND: The prevalence of heart failure with preserved ejection fraction may be changing as a result of changes in population demographics and in the prevalence and treatment of risk factors for heart failure. Changes in the prevalence of heart failure with preserved ejection fraction may contribute to changes in the natural history of heart failure. We performed a study to define secular trends in the prevalence of heart failure with preserved ejection fraction among patients at a single institution over a 15-year period. METHODS: We studied all consecutive patients hospitalized with decompensated heart failure at Mayo Clinic Hospitals in Olmsted County, Minnesota, from 1987 through 2001. We classified patients as having either preserved or reduced ejection fraction. The patients were also classified as community patients (Olmsted County residents) or referral patients. Secular trends in the type of heart failure, associated cardiovascular disease, and survival were defined. RESULTS: A total of 6076 patients with heart failure were discharged over the 15-year period; data on ejection fraction were available for 4596 of these patients (76 percent). Of these, 53 percent had a reduced ejection fraction and 47 percent had a preserved ejection fraction. The proportion of patients with the diagnosis of heart failure with preserved ejection fraction increased over time and was significantly higher among community patients than among referral patients (55 percent vs. 45 percent). The prevalence rates of hypertension, atrial fibrillation, and diabetes among patients with heart failure increased significantly over time. Survival was slightly better among patients with preserved ejection fraction (adjusted hazard ratio for death, 0.96; P=0.01). Survival improved over time for those with reduced ejection fraction but not for those with preserved ejection fraction. CONCLUSIONS: The prevalence of heart failure with preserved ejection fraction increased over a 15-year period, while the rate of death from this disorder remained unchanged. These trends underscore the importance of this growing public health problem. Copyright 2006 Massachusetts Medical Society.

Other interesting article

Heart failure with preserved ejection fraction: dangerous, elusive, and difficult.

Eur Heart J. 2008 Feb;29(3):339-47. Nielsen OW, Køber L, Torp-Pedersen C.

BMJ editorail 2009


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