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Ayurvedic Treatment For Heart Valve Problems

The valves have very important role and these valves prevent back flow of blood during pumping of heart. When these valves are not fully functional or there is stenosis in valves then back flow of blood occurs results in insufficient blood supply to different body parts and to heart itself.

The only permanent and complete treatment available for stenosed mitral valves is surgical repair or replacement of valves. So we recommend you to consult your cardiologist for appropriate treatment. Till you are waiting for operation take package for heart problems to strengthen your heart and increasing functional cardiac output. Take low salt and low fat diet. Increase water intake.

Valves of heart are very necessary to keep the blood pumping function of heart going smoothly. These valves prevent back flow of blood while heart muscles contract and forces blood to pass in major blood vessels of body. So healthy valve function is necessary and if valves are not working efficiently, we recommend you to please go for valve replacement by surgery.

This is very important for the life of patient. Medicines have very little role let for this patient. He should undergo heart surgery first and then look for the treatment of paralysis. Paralysis can be cured with ayurvedic medicines and panchkarma therapy. Divya vrihat vata chintamani rasa is very effective in paralysis problem. But the emergency is for heart problem, so go for the treatment of heart problem first.

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Chronic heart failure in outpatients Management – general measures

The cause of heart failure must be established and remediablecauses sought and treated. These might include thereplacement or repair of valves, stripping of the pericardiumin constriction, or the closure of significant intracardiacshunts.

The overall aim of treatment in chronic (non-surgical)heart failure is to relieve symptoms, to improve quality oflife and functional capacity, and lastly to improve longevity.The general measures should include stopping smoking,reducing alcohol intake, fluid restriction, and possiblyregular exercise training.

Bed rest is helpful only in acute myocardial infarction,active myocarditis, infective endocarditis and intractablecongestion unresponsive to conventional doses of diuretics. The disadvantages of bed rest (skeletaland myocardial deconditioning, muscular atrophy andweakness, bedsores, deep vein thrombosis, autonomicmaladjustment) outweigh the benefits. Patients who areasymptomatic at rest should be encouraged to mobilize assoon as possible, as exercise rehabilitation may improvefunctional capacity even in severe chronic heart failure.

Drug therapy to improve prognosis is now possible, and(3-blockers, ACE inhibitors, spironolactone and nitratehydralazinecombinations are the most effective, althoughthe prolongation of survival only averages 6 months. About 20-50% of patients in heart failure die suddenly. No antiarrhythmicagent has been shown to be effective in reducingthis incidence, although the use of amiodarone appearspromising. Patients with life-threatening arrhythmia mayneed AICD.

This class of drug is still the first-line treatment for symptomaticcongestive cardiac failure because it is the mosteffective at relieving the symptoms of congestion, therebyproducing the greatest impact on quality of life. They areall natriuretic and aquauretic; some of them conserve K+and Mg2+, whereas others induce losses. Injudicious use ofdiuretics may lead to severe electrolyte imbalance (resultingin arrhythmias and sudden death) and hypovolaemia(resulting in tissue hypoperfusion and renal failure).

These are used principally to treat hypertension, but mayoccasionally have a role in controlling mild oedema and,when added to loop diuretics, may induce a diuresis whenresistance to loop diuretics has arisen. Hypokalaemia andhyperuricaemia are two of the more commonly encounteredproblems with these drugs. To combat the former,combination with potassium-sparing agents is advised.Metolazone is a curious thiazide-like diuretic with a verypowerful ability to induce diuresis when combined withloop agents in patients with renal impairment or resistanceto loop diuretics. However, it is also remarkably potentin inducing electrolyte disturbances, and the most difficultone to correct is severe hyponatraemia. It should thereforebe used sparingly, and stopped before hyponatraemiaoccurs.Bendroflumethiazide(bendrofluazide)HydrochlorothiazideMetolazone2.5-5.0mg per day25-100 mg per day5-10 mg per day

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It is almost always necessary to add these agents tothe treatment of patients taking diuretics alone. ACEinhibitors usually diminish the need for potassium-sparingagents and when used in this combination close monitoringof serum potassium (aimed between 4.5 and 5.5mmol/L)is essential because severe hyperkalaemia may occur.Spironolactone, an aldosterone receptor antagonist,at a dose of 25 ing/day, has been shown to be safe andextend the lives of patients with heart failure treated withloop diuretics and ACEI. Its antiandrogenic effects (e.g.gynaecomastia) may not be tolerated by some malepatients, in which case amiloride may be used instead.AmilorideSpironolactoneTriamterene5-20mg/day25-200 mg/day50-250 mg/day

These are the cornerstone of diuretic therapy in all but themildest degrees of heart failure. They share with thiazidesthe tendency to produce metabolic disturbance and needthe addition of potassium-sparing agents to avoid thesepitfalls.BumetanideFurosemide (frusemide)Torasemidel-10mg/day40-1000 mg/day2.5-40 mg/day

, incorporating fixed doses ofpotassium-sparing agents, are very widely prescribed. Itis accepted that combinations of diuretic with potassiumsupplements are likely to be less effective at maintainingpotassium homeostasis, and unhelpful for magnesiumhomeostasis.Coamilofruse 1-2 tablets/ furosemide (frusemide)(Frumil) dayFrusene 1-240 + amiloride 5furosemide (frusemide)40 + triamterene 50Dyazide 1-2 triamterene 50 +hydrochlorothiazide 25

Vasodilator drugs are used to decrease both preload andafterload. Excessive preload reduction may result in lossof Starling’s effect and compromise ventricular output.Excessive afterload reduction can cause hypotension,reduce coronary perfusion, and exacerbate myocardialischaemia and cerebral hypoperfusion, leading to dizzinessand syncope.

ACE inhibitors are the vasodilators of first choice in thetreatment of chronic moderate and severe heart failure.There are many ACE inhibitors available:Captopril 6.25-50 mg t.d.s. Short-actingEnalapril 2.5-20mg b.d.Lisinopril 5-40mg o.d.Perindopril 2-4 mg o.d.Ramipril 1.25-5 mg b.d.Intermediate durationof actionLong duration of actionLong-acting, least firstdosehypotensionLong-acting

It is still unclear whether the different properties exhibitedby the different types make any significant difference totheir clinical efficacy.• Up to 10% of all patients do not tolerate ACE inhibitortherapy owing to unacceptable coughing.• First-dose hypotension at the start of ACE inhibitortherapy can occur unexpectedly in patients with chronicheart failure, especially in those with unsuspected renalartery stenosis. Certain precautions should be heeded.

• The most problematic adverse effect is impairment ofrenal function. In a significant minority inhibition ofangiotensin-induced constriction of the efferent glomerulararteriole and overall renal function is affected.Rising creatinine (>200 mol/L) is a reason to withdrawthis therapy.

In patients with heart failure secondary to coronary heartdisease nitrates have a distinct role, particularly as ACEinhibitors do not have any specific antianginal activity.Long-acting nitrates are used, leaving a 6-8-hour nitratefreeperiod to avoid tolerance to the haemodynamic effectsof nitrates.

With indication for use in heart failure, p-blockers can nowbe claimed to be a ubiquitous cardiological drug. Trial datahave shown that they can improve the prognosis, in termsof survival and hospitalization. There are no conclusivedata to show that they improve functional capacity orquality of life. Clinician concerns (which led to these drugsbeing previously categorized as contraindicated for use inheart failure) are still valid, as inappropriate use in somepatients may precipitate exacerbation of heart failure. Itis therefore vital that -blockers should be introduced bytrained personnel, starting with the lowest doses, whichmay be increased very gradually if tolerated.

is a non-cardioselective -blocker with ocreceptorblocking activity, which produces vasodilatation.It was the first to be reported to provide remarkable496 survival improvements in heart failure.

These drugs often have to be used in heart failure patients.Most intravenous antiarrhythmic agents are cardiodepressantto varying degrees. The most negatively inotropic arep-blockers, verapamil and disopyramide, and these are generallyavoided in severe heart failure. In therapeutic dosesthe following intravenous agents exert little negativeinotropism, and may be used in heart failure: lidocaine (lignocaine),mexiletine and procainamide. Orally, amiodarone,digoxin, mexiletine and procainamide are virtuallydevoid of negative inotropic effects.