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Posts Tagged ‘cardiac failure’

Edema is considered the cardinal feature of cardiac failure for decades. It is one of the minor criteria of  the Framingham protocol  to diagnose cardiac failure.

The mechanism of edema in cardiac failure is multifactorial . The major mechanism attributed is raised venous pressure. This is transmitted backwards into the circulation and resultant increase in hydrostatic pressure in the venous end of capillaries results  in edema .

Even though this is considered as the  dominant mechanism for decades , it may not be true. Apparent reduction in cardiac output (Effective circulatory volume) and resultant reduction in renal blood flow triggers renal ischemic response and RASS activation (Rennin angiotensin aldosterone system). This is a powerful stimulus for sodium and water retention . This could be the major mechanism of cardiac edema. While there is clearcut explanation for the mechanism of edema in cardiac failure the explanation for lack of edema in many is not available in literature.

Does the activation of neuroendocrine happen in every one with cardiac failure ?

We think so ! but it may not be. Further,  activation of RASS trigger a counter hormone  response mediated by atrial natriuretic peptide  that promotes active water loss  from  the distal tublues which could prevent edema formation in many. So there is a distinct group of patients with cardiac failure who rarely develop edema .

In which type of cardiac failure edema is common and gross?

  • Predominatly right sided failure.
  • Corpulmonale
  • Tricuspid valve disese
  • Constrictive pericarditis

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The debate of rate control verses rhythm control in atrial fibrillation  goes on and on. The AFFIRM, RACE,PIAF, STAF the HOT CAFE all went against sinus rhythm in the last 10 years . This was one of the settled contoversies in cardiology . The conclusion was ventricular  rate control was no way inferior to rhythm control in patients with SHT, CAD population .This made the electrophyiologists wonder how can a natural rhythm fare bad ! . But the findings  were consistent .Rhythm control neither improved the quality of life nor  it reduced the incidence of stroke. The later finding was very surprising but the explanation was convincing as stroke in elderly was more related to SHT, CAD, DM etc than  AF itself. The source of emboli in ischemic stroke could come any where distal to LA .The big assumtion that all strokes in elderly  should come from LA appendage or the body  of LA was  premature and  wrong. What prevented stroke in AF was not restoration of SR but administration of oral anticoagulants with adequate INR.(2-3)

Having failed to document superiority in elderly  population   , the  logic machine  strongly suggested restoring SR  in patients with CHF,  will atleast provide hemodynamic and also survival  benefit .

And thus came the AF-CHF trial  published in NEJM 2008

Alas !  AF-CHF  also found there is no useful purpose of restoring sinus rhythm in patients  with atrial fibrillation and cardiac failure. In fact patients in SR fared little worse !

 Why . . .  why . . . why ?

Should we ask the seemingly absurd question !

Is sinus rhythm poorly tolerated by cardiac failure  patients ?

It is some times possible atrial fibrillation by itself could be a mechanism to amplify the  cardiac reserve by which it provides a  relatively high ventricular rate to improve the cardiac index  . Even though the optimal ventricular rate in AF is around 80-90 at times of need it has to increase to 120-130. Patients in class 3 CHF and AF often achieve this in times of demand .This is not possible in patients who are getting rhythm control drugs and further patients in SR can  not increase the HR suddenly from 80 -130  .

So is this a  wild imagination !   AF could be a safety valve mechanism in CHF to increase the HR . Where the atria come to the rescue of ventricle like a rate adaptive pacemaker .

The other logical* ! argument is that  there  is nothing wrong with restoring  SR , but the  methods to achieve and  maintain SR  is too cumbersome and results in adverse outcome .The currently available  drugs are too toxic for the purpose  .

If we have a simple and safe way to restore SR in these patients it should always be superior to AF .

But it is a well  known fact  that , whatever be the rhythm or rate the ultimate outcome will be dictated by the LV function, mitral valve function etc.

 Read abstract of AF-CHF

Rhythm Control versus Rate Control for Atrial Fibrillation and Heart Failure

Denis Roy, M.D., Mario Talajic, M.D., Stanley Nattel, M.D., ., for the Atrial Fibrillation and Congestive Heart Failure Investigators

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Rhythm Control versus Rate Control for Atrial Fibrillation and Heart Failure

Denis Roy, M.D., Mario Talajic, M.D., Stanley Nattel, M.D.,  the Atrial Fibrillation and Congestive Heart Failure Investigators* –>ABSTRACT

Background It is common practice to restore and maintain sinus rhythm in patients with atrial fibrillation and heart failure. This approach is based in part on data indicating that atrial fibrillation is a predictor of death in patients with heart failure and suggesting that the suppression of atrial fibrillation may favorably affect the outcome. However, the benefits and risks of this approach have not been adequately studied. Methods We conducted a multicenter, randomized trial comparing the maintenance of sinus rhythm (rhythm control) with control of the ventricular rate (rate control) in patients with a left ventricular ejection fraction of 35% or less, symptoms of congestive heart failure, and a history of atrial fibrillation. The primary outcome was the time to death from cardiovascular causes.
Results A total of 1376 patients were enrolled (682 in the rhythm-control group and 694 in the rate-control group) and were followed for a mean of 37 months. Of these patients, 182 (27%) in the rhythm-control group died from cardiovascular causes, as compared with 175 (25%) in the rate-control group (hazard ratio in the rhythm-control group, 1.06; 95% confidence interval, 0.86 to 1.30; P=0.59 by the log-rank test). Secondary outcomes were similar in the two groups, including death from any cause (32% in the rhythm-control group and 33% in the rate-control group), stroke (3% and 4%, respectively), worsening heart failure (28% and 31%), and the composite of death from cardiovascular causes, stroke, or worsening heart failure (43% and 46%). There were also no significant differences favoring either strategy in any predefined subgroup.
Conclusions In patients with atrial fibrillation and congestive heart failure, a routine strategy of rhythm control does not reduce the rate of death from cardiovascular causes, as compared with a rate-control strategy.
 
 

 

 

 

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

 

 

 

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Orthopnea is a classical sign of established CHF.

While paroxysmal nocturnal dyspnea is an early sign of cardiac failure,orthopnea is a late manifestation of cardiac failure .This symptom was mainly attributed to volume displacement from systemic venous to pulmonary circulation when the patient goes to recumbent posture.The exact mechanism of this has been speculative. Now with liberal usage of bedside echocardiography, we have found out there is postural variation in the diastolic function of the failing left venticle.

Many patients develop a restrictive ventricular filling pattern in recumbent posture (Grade 3 diastolic dysfunction). While sitting up some of them revert to normal or downgrade to grade 1 diastolic dysfunctionThis observation proves another fact that every patient with severe systolic dysfunction also has significant diastolic dysfunction at some point in their course of illness.

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Heart is a muscular pump .But it contains more of  non muscular cells than contractile cells.

The average human heart which weighs 300 -400 grams . Contrary  to the popular perception heart is not purely a muscular organ. In fact myocytes constitutes only 30% of heart mass. Rest formed by

1.Fibroblasts

2.Endothelial cells

3.Purkinje cells

4.Interstitial cells

5.Collagen

6.Fibrous skeleton

7.Extracellualr matrix.

Why is this important to recognise ?

Cardiac failure is not synonymous with myocardial failure .

Many times cardiac failure is due to supporting structure failure like in connective tissue disorders.

Exceesive fibroblast proliferation and resulting in fibrosis of heart.

Cardiac interstitial failure is new emerging clincal entity.

In future individual cell based therapy will aim  at replacing specific cells that are defective or depleting.

 

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