Patient with Congestive Heart Failure

longanimous with Congestive Heart FailurePatient S.V. is a 54 years old female. She is a postmenopausal ho engagementwife and her family history is not cosmos recorded. She is a non-smoker and does not drink alcohol at all. She has no-known medicate allergic. The historic medical history showed us that Madam S.V. is having, woebegone arthritis (RA), hypertension (HPT) for 10 years and diabetes mellitus (DM) for 7 years. She was admitted to the hospital on a couple of(prenominal) weeks ago receivable(p) to congestive nubble bereavement.Madam S.V.s drugs history includeT. furosemide40mg odOedema HFT. perindopril4mg odHF HPTT. spironol lay outone25mg odHFT. Losec (Omeprazole)20mg bdDuodenal ulcerationP. Calcium lactate1 puff odCalcium supplementT. Rocatriol0.25mg bdVita minute of arc D supplementT. Metformin500mg bdDMT. vitamin Bc5mg odFolate inadequacyT. Methotrexate20mg/weekRAclinical dataThe abnormal extend of FBC whitethorn imputable to folate deficiency that readyd by side effect of methotrexate. Besides that, long-suffering was having noble neutrophile number for his differential count which is 8.7 k/L (normal mountain range 1.9-8.7 k/L). This whitethorn collect to the long-term use of corticorsteroid. Patients total carbon dioxide in the blood was two times higher than normal range (23-27 Vol%). factor II time and INR of the enduring was low PT =11.1 sec (normal range = 11.9-14.5 sec), INR = 0.82 (normal range 2-4). tho, the reason is unknown.Diagnosiscardiogram and chest X-ray were carried egress and the results showed that long-suffering was having sinus tachycardia and megacardia. Cardiovascular system of unhurried as well had been checked. It found that the affected role was having a 3rd flavour sound. Hence, the forbearing was diagnosed with congestive heart calamity (CHF).Clinical progressDAY 1Patient is admitted to the hospital at 10.30am by ambulance. She is weak but conscious and alert. The tolerant role complains that she is shortness of touch (SOB) and her sleep has been interrupted due to SOB. It tidy sum in addition be considered as paroxysmal nocturnal dyspnoea (PND) which is sudden, serious SOB at darkness that awakes a person from sleep, often coughing and wheezing.At the same time, she also experiences from chest discomfort and swelling leg. Besides that, the patient also shows the symptoms of cushings syndrome much(prenominal)(prenominal)(prenominal) as moonface and hirstuism. The blood pressure (BP) and pulse grade (PR) of Madam S.V. argon found to be quite high as well, which is 118/87mm/Hg and 146b/min respectively.Test ordered include FBC, RP, LFT, ABG, Coagulation foot race, UE, CXR, ECG and random glucose establish.Nebulizer is disposed(p) to patient once she is admitted. She is also on high prevail bury oxygen 15L/min at the same time to ease the worry of SOB. Salfasalazine 1g bd is added to patient. The management plan is to carry protrude lung function runnin g die hard, treat to on the face mask for oxygen supply, revise all test results, limit quiet and continue with old medications.DAY 2Patient hushed complain of minimal SOB and minimal chest ail. Another refreshed complain, headache, has been recorded. Her BP and PR go for been slowly declined but they ar relieve not within the normal range.T. bisoprolol 2.5mg od is added for a better suss out of HPT and HF. Management plan include restrict fluid DAY 3Patient is no longer complaining for allthing. She has no chest pain and SOB whatsoever more than. Her PR has back to normal range. However her BP is still just virtually higher than normal range. Management plan is same as sidereal solar mean solar day 2. Sulphasalazine since the condition of RA is improved.DAY 4Patient is feeling well, well-situated and tolerating orally. Her BP and PR be within the normal range. The management plan is to realize a CRX report, patient abide be discharged if normal result is obt ained and continue old medications.Pharmaceutical care issuesthither are few things destiny to be taken care of in this case. Firstly, the patient is having the line of nausea and vomiting and no action is taken to solve this problem. antiemetic drug (H1 receptor antagonist, cyclizine D2 receptor antagonist, halopiridol) should be given. At the same time, underlying cause of nausea and vomiting has to be identified if possible. This whitethorn ca utilise by side effect of perindopril.Secondly, patient is having cushings syndrome due to long-term economic consumption of steroids for her rheumatoid arthritis. However, on that point is no any record some the steroids intake for patient in clinical notes. Hence, we have to ask GP or patient to make sure that whether she has stopped fetching steroids or still continue with it. harmonise to CSM, long-term corti addresseroids therapy should be withdrew step by step. Abrupt discontinuation of corticosteroids therapy may cause severe symptoms because normal production of steroids by the body has been affected. The panelling may be turn offd rapidly down to physiological drugs (prednisolone 7.5mg daily). Then, the progress of pane reducing lav be slowed down. The patient is hirudism which is one of the symptoms of cushings syndrome. This problem preserve be overcome by local measures such as shaving, or depilation such as using wax or scan (eg eflornithine).The dose of T.folate for patient which is 5mg once daily is indicated for manipulation of megaloblastic anemia. However, the FBC test result does not show any symptoms of megaloblastic anemia. The dose of T.folate should be 5mg once daily if it is indicated for folate deficiency induced by mehtotrexate. simple eye film should be carried out to make sure that whether the patient is having megaloblastic anemia or not. FBC, serum folate and serum B12 are authorized indicator of folate status. Real indication of T.folate has to be clarified with mend forrader dispense the drug.Oedema problem never been improved since the day patient been admitted into the hospital. Restrict fluid intake and strict I/O charting is carried out. However, patient is not compliance to it. Some simple self-care techniques can be taught to patient to reduce the build up of fluid. Counsel the patient about the importance of following Strict I/O chart. Dose of furosemide can be increase if oedema doesnt improve.The blood pressure of patient is still not stable yet. Patient has to be counseled to improve her fast and mannerstyle. It is also necessary to monitor BP of patient regularly. Increasing dose of -blocker can be considered if BP is not reducing. However, due to its negative inotropic effect, -blocker should be started in rattling low dose and increase gradually.Lastly, upon discharge, check off all appropriate medications are prescribed and patient is counseled suitably. We have to tell patient that Perindopril is added in and ensure patien ts compliance with medication. Patient should be told to avoid alcohol and cranberry juice and confab GP if anything goes wrong.Disease overviewIncidenceHeart hardship (HF) affects 0.3-2% of general population. In 2001, officially there are 11500 deaths are recorded in the UK due to HF. The incidence graze increase by double each cristal from age 45. It affects 3-5% of those over 65 years and 8-16% of those over 75 years. The Rotterdam adopt shows that prevalence is higher in men compared to women.PathophysiologyHeart failure can be defined as inability of the heart to supply capable blood flow to meet the bodys needs. HF can result from any disorder that reduces ventricular filling (diastolic disfunction) and myocardial contractility (systolic disfunction). The leading causes of HF are coronary artery infirmity and HPT. As cardiac function decreases after(prenominal) myocardiac injury, the heart relies on few compensatory mechanisms. Although those compensatory mechanisms c an initially plead the cardiac function, they are responsible for HF symptoms and contribute to disease progression. An initiating til nowt such as acute MI can cause the HF pass on becomes a systemic disease whose progression is largely mediated by neurohormones and autocrine/paracrine factors such as agiotensin II, norepinephrine, aldosterone, natriuretic peptides, and so on. Some drugs may incense HF due to their inotropic, cardiotoxic and sodium-/water- retention properties.DiagnosisA complete history, natural examination and appropriate lab testing are essential in initial evaluation of patients suspected from having HF. The signs and symptoms are the key for early detection. Breathlessness, angina, endure and wheeze are special K signs and symptoms. Patient complains that she is having SOB and PND.Electrocardiogram (ECG) and B-type natriuretic peptides (BNP) are essential tests for e actually patient with suspected HF. ECG is carried out once the patient is admitted int o the hospital. Madam S.V. was detected to have sinus tachycardia by ECG which is one for the common ECG abnormalities in HF. Others common ECG abnormalities include sinus bradycardia, a discharge fibrillation, ventricular arrhythmias and so on. Plasma BNP is not measured in this case.Chest X-ray (CXR) is also an essential constituent of diagnostic work-out in HF. It is very useful for detection of cardiomegaly, pulmonary over-crowding and pleural fluid accumulation. It also demonstrates the presence of any pulmonary disease or infection that provide lead to dyspnoea. Via CXR, patient is detected from having cardiomegaly which is also one of the abnormalities for HF.Echocardiography (ECHO) should be performed shortly if one or somewhat(prenominal) ECG and BNP get an abnormal result. ECHO is widely available and untroubled and provides essential information on aetiology of HF. However, ECHO is not carried out in this case. Some other tests such as FBC, RP, LFT, ABG, UE and rando m glucose test have been carried out to exclude others possible conditions.Pharmacology basis of drug therapyDiureticsThe most important function of diuretic drug is to act by decreasing Na+ resorption. Diuretic drugs can forbid Na+ reabsorption by actions on different transport mechanism, which are located at different sites in nephron. All diuretics are acting on the phenobarbital surface of the nephron. They are protein bound in blood and reach the vasiform fluid by secretion into proximal convoluted tubule utilizing the organic pungent transport mechanism. They are mostly use to ascendancy symptoms of breathlessness and fluid retention. However, they do not alter disease progression or aspirate survival. Thus they are not considered mandatory therapy for patients without fluid retention.Loop diuretics for exemplification furosemide is most widely used if compared to other thiazide. It produces diuresis with NaCl loss. It also has vasodilative action which is let unacco mpanied mediated via prostaglandin. This will increase blood flow in the medulla and hence contributes to their natriuretic effect. Unlike thiazides, circle diuretics principal(prenominal)tain their forte in the presence of impaired nephritic function, although higher doses may be necessary. Thizide diuretics are relatively weak diuretics and used alone infrequently in HF. However, thiazide like metolazone can be used in the combination with loop diuretic to promote effective diuresis.Angiotensin-Converting Enzyme Inhibitors (ACEIs)ACE is binding to the plasm membrane and can also exist as a disintegrable enzyme. The ACEIs act by substrate competition by binding in the Leu-His binding pocket on ACE. Thus, action of angiotensin-I is inhibited. They also decrease the assimilation of angiotensin II and aldosterone and attenuating many of their deleterious make, including reducing ventricular remodelling, myocardial fibrosis, vasoconstriction and sodium and water retention. In a ddition, they also very helpful in reducing blood pressure due to arterial vasodilation. However, they will inhibit the breakdown of bradykinin which contributes to strong hypotensive action and cough.There are soon 11 ACEIs available for clinical use with similar structure and properties, including captopril, enalapril, lisinopril and others. ACEIs are indicated in all browses I to IV of heart failure which stated in NYHA. Potassium sparing diuretics should be stopped before starting ACEI. ACEIs may increase the venture of renal failure in patient with high dose diuretics, elderly, those with existing renal dysfunction and patients with grade IV HF. Hence regular renal function observe is infallible once patient has stabilized on drug.-blockers-blockers can be either selective for 1-adrenoceptor which is cardioselective such as atenolol, bisoprolol and metoprolol or non-selective which can act on both 1-and 2-adrenocepors such as propranolol and timolol. Blockade of 1-receptor s will decrease rate and force of contraction of heart. Meanwhile, 2-adrnoceptor blockade inhibits adrenaline-induced vasodilatation mediated by these receptors. Via these mechanisms, heart rate and cardiac output can be bring down. Beneficial effect of -blockers may result from antiarrhythmic effects, slowing ventricular remodelling, decrease myocyte death, up(a) LV systolic function, decreasing heart rate, and ventricular wall stress.The use of -blockers is not suitable for patients who have unstable HF. Patients should receive a -blocker even if symptoms are mild or well controlled with ACEI and diuretic therapy. Because of negative inotropic effects of -blockers, they should be started in very low doses with slow upward dose titration to avoid any symptomatic worsening. -blockers may worsen HF in the short term, but if use with caution they may be very useful in preventing long-term alloy.Aldosterone antagonistsAldosterone antagonists such as spironolactone and eplerenone al so can be called as potassium sparing diuretics. They act on aldosterone-sensitive portion of nephron (last part of distal convoluted tubule and first part of collecting tubule. They block the mineralcorticoid receptor and inhibit Na+ reabsoption and K+ excretion.spironolactone can be added to ACEI, diuretic and digoxin to improve morbidity and death rate rate in patient with severe HF. Eplerenone is more specific compared to spirinolactone as inhibitor of aldosterone receptors and has been shown to reduce morbidity and mortality in patient with left ventricular dysfunction post-MI. However, the diuretic effects of aldosterone antagonists are minimal. Combination of aldosterone antagonist with thiazide or loop diuretics will potentiate the effect of thiazide or loop diuretics. This is a more effective alternative compared to potassium supplement.Angiotensin receptor blockers ( arbitrageurs) and DigoxinARBs may be used as an alternative to ACEIs (eg losartan) when patient is intole rant to ACEIs or may be used as adjunct therapy (eg valsartan and cadesartan) in patient who remains symptomatic despite the dose of ACE and -blockers have been optimised. However, ARB is not given to the patient since she is well endured to ACEIs.Digoxin is one of the main drugs for HF treatment. However, digoxin is not recommended in this case. Digoxin can only been given if patients HF is worsening or patient is having atrial fibrillation at the same time. Hence, it is reasonable to exclude digoxin from treatment in this case. express for treatment of the conditionsDiureticsDiuretic is a very important drug for heart failure treatment especially for symptoms of fluid retention. A meta-analysis which includes 18 randomized controlled trials (RCT), n=982, had been carried out to discipline the role of diuretics (loop diuretics and thiazides) in patient with congestive heart failure (CHF). 8 trials were placebo-controlled and another 10 were comparison surrounded by diuretics an d other drugs such as ACEIs, digoxin and ibopamine. The results had shown that diuretics reduce the risk of deterioration of disease and mortality compared to placebo group. When compared to active controls, diuretics also showed significant improvement in patients exercise capacity. The beneficial effects of diuretics are further supported by Cochrane database which also indicated that diuretics cause significant simplification rate and improvement in patients morbidity.Another study also proved that the withdrawal of furosemide will cause increase in volume load and right ventricular pressure. There will lead to deterioration of CHF which include impaired type of life, weight gain and walking distance lessen. Higher dose of furosemide will have more desirable effects such as increasing general well-being and reducing symptoms of disease. However, the inappropriate high dose of furosemide will lead to hypotension. The risk of hypotension will be increased if patient on ACEIs or vasodilators at the same time with diuretics. According to NICE guidelines, low dose should be prescribed for the initiation of therapy and titrated up gibe to patients condition.Furosemide is the most commonly used loop diuretic. However, some patients are more responsive to other loop diuretic such as torasemide. This may due to its longer duration of action and high absorption. Some pharmaco scotch analyses also proved that torsemide reduces hospitalisation for patient with CHF. Hence, general treatment costs are rock-bottom although torasemide is more expensive than furosemide. Patients that treated with torasemide have improved their quality of life. The data also suggest torasemide to be used as first-line treatment for patients with CHF and for those who are not response to furosemide.Besides that, according to a double-blind study, n= 1663, additional of aldosterone antagonist, spironolactone with furosemide had importantly reduced mortality and morbidity rate of patient s with severe HF Hence from the evidences in a higher place, we can conclude that furosemide 40mg od is rationale to be given to patient to treat the symptoms of her CHF.Angiotensin-Converting Enzyme Inhibitors (ACEIs)The patient is taking perindopril 4mg od for her HF. A clinical trial has been carried out to compare the effectiveness between ACEIs and placebo in patients with symptomatic CHF. The overall results showed the significant reduction in total rate of mortality and risk hospitalisation.The benefits of ACEIs are further supported by five long-term disarrange trials which had recruited 12763 patients with heart failure or left-ventricular systolic dysfunction (LVSD) to compare the effectiveness between ACEIs and placebo. Results showed that mortality rate has been reduced by 23%, readmission rate of heart failure reduced by 35% and re-infarction rate had been reduced by 26% for the patients who assessed ACEIs compared to placebo group. The benefits of ACEIs were observed at the beginning of therapy and it persisted long term.In SOLVD investigation, n=4228, ACEIs (enalapril) reduced the rate of hospitalisations and also incidence of heart failure in patients with reduced left ventricular riddance fractions compared to placebo group. Some randomize controlled trials proved that ACEIs also improve the exercise capacity and quality of life in majority of the patients. Not all the patients with heart failure due to left-ventricular systolic dysfunction experienced the improvement of exercise capacity. However, ACEIs alone is not enough for the treatment of heart failure with pulmonary oedema. Diuretic is requisite to maintain sodium balance and prevent any fluid retention. ACEIs are more often to be prescribed compared to vasodilators and angiotensin receptor blockers due to more evidence supports.ACEIs will cause hyperkalaemia, cough and deterioration of renal function. Hence, renal function and serum potassium level need to be checked before the tr eatment is initiated. The SOLVD data, a randomised, double-blind and placebo controlled trial with 3379 patients, proved that enalapril caused 33% increased in deterioration of renal function compared to control group (P = 0.03). There is another study (n=191) showed that 44% of patients taking ACEIs suffered from unyielding cough compared to controls which is only 11.1% (PThe studies above showed that ACEIs are rationale to be used as first-line treatment HF.-blockers-blockers should be included in the treatment of HF even though the patient is already well controlled by diuretics and ACEIs. The European Journal of Heart Failure suggested that -blockers should be prescribed to all patients with stable HF and when left-ventricular ejection fraction 40%. A lot of meta-analyses showed that -blockers race a role in increasing life expectancy in patients with HF due to LVSD.In a meta-analysis which includes 21 trials (n= 5894), -blockers showed a significantly reduction of overall a nd cardiovascular mortality by 34-39%in patients with severe HF. Another meta-analysis of 16 clinical studies also showed the reduction of 24% for patients who were taking -blockers for their HF treatment rather than placebo. An interesting meta-analysis had been carried out to test the readiness of -blockers in the patients with diabetes mellitus (DM) and CHF. The result of this meta-analysis showed that -blockers had reduced the mortality rate of patient with DM and CHF. However, the reduction was not significant (P=0.11) compared to CHF patients without DM.Most of the survival benefits for patient with NYHA twelvemonth II and III are well documented. There is a meta-analysis had turn out that -blockers are having the same improvement of survival rate among the patients with severe HF compared to patients with NYHA class II and III. However, further studies need to be carried out to pronounce overall benefits versus risks of treatment in NYHA class IV. There are common chord main studies, n9000, had been carried out to compare the efficacy between -blockers (bisoprolol, metoprolol succinate CR, carvedilol) and placebo. Almost 90% of patients involve in there three randomised trials were on ACEIs or ARB. Most of them also took diuretics and digoxin. All trials showed the improvement of mortality rate (RRR= 34%), risk of hospitalisation (RRR= 28-36%) and self-reported well being. So far, there are no significant differences between selective and non-selective -blockers and those with or without vasodilating properties.In one randomised controlled trial (COMET), n=3029, carvedilol was used to compared with the efficacy and clinical outcome of metoprolol tartate. The result has shown that carvedilol reduced the mortality rate significantly among the patients compared to short-acting metoprolol tartate (P=0.0017). However, there is no any clinical trial about comparison between carvedilol and long-acting metoprolol succinate. There is little economic evidenc e can be found for -blockers. NICE guidelines suggested that -blockers are cost effective due to reduction of hospitalisation rate.Bisoprolol 2.5mg od had been added to the patient on second day since patient was admitted. The evidences above do support that the usage of -blocker should be included in patient with HF.Aldosterone antagonistsSpironolactone is the most common aldosterone antagonist used in treatment of HF. In a double-blind study (RALES), 1663 patients with severe HF (NYHA class III and IV), left ventricular ejection fraction 35% and being treated with diuretics, ACEIs or digoxin were recruited to test the effectiveness of spironolactone on their morbidity and mortality. The result showed 30% reduction in mortality rate and 35% reduction of frequency of hospitalisation compared to placebo group. Addition of spironolactone to ACEIs, diuretics or digoxin had reduced the mortality rate in patients with severe HF. Additional of spironolactone may lead to hyperkalaemia. Ho wever the problem of hyperkalaemia can be solved by closing monitoring the potassium level of patients. Another study also showed that spironolactone reduced 30% mortality rate in patients with HF when it has been added to -blockers and digoxin.A selective aldosterone antagonist, eplerenone, has fewer side effects compared to spironolactone. A randomised controlled trial (EPHESUS), n=6633, proved that morbidity and mortality rate among patients with left ventricular dysfunction after acute myocardial infarction had been reduced with the addition of eplerenone compared to placebo group. There is no relevant economic evidence of aldosterone antagonist. Eplerenone is mostly used when patients cannot tolerate with spironolactone.Hence, spironolactone 25mg od is appropriate to used as adjunct to diuretics, ACEIs or maybe -blockers for patient in this case. Since the patient does not suffer any side-effects from spironolactone, it is not necessary to change to eplerenone.ConclusionAs a co nclusion, patients CHF has been appropriately treated by following the guidelines and also supported by many of clinical studies. From the clinical process, we can see that the condition of patient was gradually improved day by day. A -blocker, bisoprolol was added in the second day in order to achieve a better control of patients HF and also HPT. According to guidelines, the dose of bisoprolol should be initiated with 1.25mg, not 2.5mg. The potassium levels need to be monitored regularly due to the concomitant use of perindopril and spironolactone which may cause hyperkalaemia. ARB and digoxin are not prescribed to the patient because she is well tolerated with ACEIs and she does not have AF. Other treatment for HF such as vasodilators (hydrazine and ISDN) will only be considered when all of the treatment options above have failed to this patient. Non pharmacological treatment such as life-style modification, florid diet, restrict fluid intake and salt intake also play a very imp ortant in controlling patients HF and HPT for long-term.