Emergency Admission Is Due To Sob Biology Essay

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Patient, Mr. SA is an 83 years old Malay male with a normal BMI. He was admitted to the hospital for 5 days because of shortness of breath (SOB). The emergency admission is due to SOB and orthopnea at rest for the past 3 days. He was diagnosed with chronic cardiac failure (CCF) 15 years ago, in which he experienced SOB on exertion, and it will be relieved by rest, but it had gradually becoming worst. Occasionally, he will cough with some sputum, but do not have previous pulmonary disease. On admission, he was found to have existing left lower limb cellulitis for the past 1 week, and also urinary incontinence. He have had hypertension for the past 30 years, CCF for 5 years and gout diagnosed recently 2 years ago, and had no history of diabetes, myocardial infarction, stroke or asthma. Mr. SA is a retired, married teacher, who is staying at home with a wife and 4 children. He is a non-smoker and non-alcoholic. He does not have any significant family history. Besides that, he had no known drug allergies and previously was on oral perindopril (4mg od), oral felodipine (10mg od), oral metoprolol (100mg bd), oral furosemide (40mg od) and also oral allupurinol (300mg od). He is currently on:

Drug &route of administration

Dose &frequency of dose

Start date

Stop date


T. Perindropril

4mg od

Day 1

Hypertension, adjunct for CCF

T. Felodipine

10mg od

Day 1


T. Metoprolol

100mg bd

Day 1

Day 4


IV Furosemide

40mg tds

Day 1

Day 4


T. Furosemide

40mg od

Day 5


T. Allupurinol

300mg od

Day 1


IV Flucloxacillin

1g qid

Day 1

Day 4

Bacteria infection

IV Benzylpenicillin

1.2g qid

Day 1

Day 4

Bacteria infection

T. Flucloxacillin

500mg qid

Day 5

Bacteria infection

On admission, patient was well and alert, and was given 2L of 100% O2. He had normal body temperature (370C), pulse rate (65 bpm), respiratory rate (20/min) and oxygen saturation (98%), but had high blood pressure (BP) of 161/99 mmHg. The cardiovascular system showed normal heart found with no murmur, respiratory system showed wheezing and bilateral basal crepitation, abdomen test showed soft, non tender, no masses, no organomegaly, and central nervous system showed grossly intact, patient can move all the 4 limbs, and it was not formally examined. His lower limb was found to have bilateral pedal oedema. Patient was also diagnosed to have left lower limb cellulitis, with warm, erythematous and ulceration (2 x 3 cm) on his left shin. His was also had neurovascular intact.

Various laboratory investigations were tested for this patient. Generally, his BP was fluctuating high over the 5 days of admission. His body temperature, pulse rate and oxygen saturation were within the normal range. Electrocardiogram, blood test (such as full blood count, renal function test, liver function test, blood glucose test, coagulation test and urine & electrolyte test), and blood, culture and sensitivity test were examined as well. His fluid balance chart (I/O chart) showed negative result on the first day but positive result on day 2 (+50), day 3 (+150) and day 4 (+100). Consequently, Mr. SA was diagnosed with heart failure plus cellulitis.

The management plan on admission was to supply patient O2 nasal prong (3L/min), restrict daily fluid to <800cc and monitor the vital sign every 4hrly, oxygen saturation and strict fluid balance charting. IV furosemide (40mg tds), IV flucloxacillin (1g qid) and IV benzylpenicillin (1.2g qid) were prescribed to patient. On day 2, the management plan for the patient was keep in view to stop nasal prong oxygen and examine echocardiogram. On day 3, patient was kept in view to change IV furosemide to the oral form. On day 4, patient found to be unable to walk owing to his leg ulceration. The practitioner planned to stop IV furosemide and IV flucloxacillin, and continued with oral furosemide (40mg od) and oral flucloxacillin (1g qid) respectively. Oxygen saturation monitoring every 4hrly was planned. On the last day, patient felt better with improving cellulitis. He was ambulating with a wheel chair. The plan was then to stop nasal prong oxygen and keep monitoring oxygen saturation every 4hrly. His bladder drainage was stopped as well. Oral form of flucloxacillin will be given for 1 week. Patient was allowed to be discharged and will be followed up at outpatient clinic in 1 month time. He was discharged with oral perindopril (4mg od), oral metoprolol (100mg bd), oral felodipine (10mg od), oral allupurinol (300mg od), oral furosemide (40mg od) and oral flucloxacillin (1g qid for 5 days). As a summary, patient was managed accordingly and all the drugs used are within guideline recommendation.

Chronic cardiac failure is defined by SIGN 95 as a complex clinical syndrome which is caused by any structural/functional cardiac/non-cardiac disorder that will affect the heart's ability to respond to physiological demands for the augmented cardiac output. Over the last decade, CCF was the most significant public health problem among cardiovascular diseases. The hospital admissions for CCF has rises >3-fold over the last 15 years. Heart failure causes more than 200,000 patients deaths each year. In Scotland, it leads to almost 11,000 deaths per year, in which approximately 1/5 deaths in men, 1/6 deaths in women. HF is caused by ischemic heart disease, heart attack, cardiomyopathy, and conditions that overwork the heart (such as hypertensive, diabetes). These disorders will generate viable myocardium loss, mechanical stresses that elevate heart's loading conditions, or a combination of these mechanisms. It is vital to clarify these mechanisms because each mechanism will respond differently to therapeutic approaches.

The risk factors for CCF include lack of exercise, obese, high fat and cholesterol diet with nutrient deficiencies (vitamin B1), smoking and past history of CHD, myocardial infarction, angina. CCF occurred with symptoms of fatigue, SOB, peripheral oedema and enlarged heart. It can be diagnosed by imaging (X-ray), electrocardiogram, echocardiogram (indicates heart failure causes), blood tests, angiography and fluid balance monitoring.3

Figure 1: Heart Failure X-ray

X-ray showed enlarged cardiac silhouette. (circle)

Given that mortality and disability are characteristics of CCF, the severity of CCF is thus affected by the degree of death risk and functional disability. The degree of functional impairment can be measured by questioning or exercise testing. Therefore, disease severity can be estimated by two different classifications.3 The first approach, New York Heart Association (NYHA) classification, categorize heart disease as stated in table 1.

Table 1: New York Heart Association (NHYA) classification.6

Class I

No limitation in exercise tolerance.

No symptoms found during daily activities.

Class II

Mild limitation in exercise tolerance.

Symptoms induced by daily ordinary activity.

Class III

Moderate limitation in exercise tolerance.

Symptoms induced by less than daily ordinary activity.

Class IV

Severe limitation in exercise tolerance.

Symptoms present even at rest.

The second approach, Weber Classification of Exercise Tolerance, classify heart disease by measuring oxygen consumption throughout a standardized bicycle or treadmill test, as stated in table 2.

Table 2: Weber Classification of Exercise Tolerance.7

Class A

Maximum consumption of oxygen

= >20mL/min/kg

Class B

Maximum consumption of oxygen

= 16-20 mL/min/kg

Class C

Maximum consumption of oxygen

= 10-15 mL/min/kg

Class D

Maximum consumption of oxygen

= <10 mL/min/kg

The pharmacologic therapy of CCF is targeted as a combination of preventive and symptomatic relieved strategy. The major drugs used are summarized in table 3. Patients with left ventricular systolic dysfunction should start with therapy of ACE inhibitor, beta blocker (and diuretic in most cases), except contraindicated. For patients who are still symptomatic, candesartan may be considered to be added. If HF progresses to class IV, spironolactone should then be added. At the same time, candesartan should be stopped due to the common side effects on kidney and potassium function when consuming three drugs together to block renin-angiotensin system.1

Table 3: Drugs used according to NYHA class.1

Class I

ACE inhibitor, beta-blocker

Class II-III

ACE inhibitor, beta-blocker, candesartan (initiation after specialist advice)

Class III-IV

ACE inhibitor, beta-blocker, spironolactone (initiation after specialist advice)

The pharmacological therapies for CCF according to SIGN 95 are listed in table 4.1

Table 4: Pharmacological therapies (SIGN 95)1

ACE Inhibitors


Angiotensin Receptor Blockers

Aldosterone Antagonists



As for the patient in this case, ACE inhibitor, beta blocker and diuretic were prescribed. Angiotensin Converting Enzyme inhibitor, perindopril was given to this patient. As mentioned in its name, it acts by blocking angiotensin converting enzyme, thus inhibiting the conversion of angiotensin I to angiotensin II, which causes vasoconstriction that leads to high BP. The decreased BP will make the heart works lesser to pump blood around the whole body. Therefore, it is used to recover heart failure symptoms, in which heart not pumping well, and also improve survival after heart attack. Perindopril is long-acting with elimination half-life of 27-60hrs.

Beta blocker given is metoprolol. It acts by decreasing sympathetic actions, portion of involuntary nervous system, by inhibiting beta receptors on sympathetic nerves (responsible for increased heart rate). Thus, heart rate will be reduced. It decreases contraction force of heart muscle as well and therefore blood pressure is reduced. Through these reductions, the oxygen need by heart muscle will also be decreased. Metoprolol has a plasma half-life of 3-7hrs.

Furosemide (diuretic) was prescribed to the patient. It acts by inhibiting Na-K-2Cl co-transporter in the thick ascending limb of loop of Henle, thereby retains chloride, sodium, potassium, and hydrogen ions intraluminally, which will then lost in urine. It has a plasma half-life of 1.5hrs and duration of action is 4-6hrs.

According to Klein L et al., the basic CHF treatment are ACE inhibitors and β-blockers (carvedilol, metoprolol, bisoprolol), with diuretics for fluid balance management. The therapies prescribed for patient in this case are as recommended. Spironolactone is for patients having NYHA class III-IV symptoms even with maximal treatment of ACE inhibitors, β-blockers, diuretics, and digoxin. That is why this patient does not need spironolactone yet. The therapy approach recommended is similar as SIGN 95 and NYHA.1

As suggested, ACE inhibitor, perindopril, the choice of drug in chronic cardiac failure was prescribed.1 According to Edmund H et al., ACE inhibitors are successful in decreasing CHF patients' mortality. In a worldwide review, perindopril once daily dosing had been proved to be helpful in CHF patients of all severities. It also has the advantages of having low risk of hypotension during the first-dose, no undesired effects on normotensive patients' BP, improving arterial compliance, reversing left ventricular hypertrophy, well tolerated and has no major effects on heart rate, plasma lipid, or renal function. Moreover, it has no momentous drug interactions, with digoxin for example, which is possibly also taken by CHF patients.

From another study, Lau CP et al., perindopril and captopril were compared in terms of hemodynamic changes and tolerability in the body after an Acute Myocardial Infarction (AMI). 212 patients were randomized to take perindopril (n=110) or captopril (n=102) within 72hr after AMI. Although perindopril was in higher Killip class, and perindopril treated patients after initial dose had higher minimal systolic and diastolic BP, but they was found to have low minimal BP much later (3.6 ± 0.2 versus 2.7 ± 0.1 hr; p <0.001), with lower occurrence of persistent hypotension (5% versus 16%; p <0.01) when compared to captopril. Furthermore, 97% and 82% patients reached target doses of perindopril and captopril respectively (p <0.01). These results were showed to have significant difference. It was also found that there were no differences in the revascularization requirement and mortality rates after 6 months of treatment among perindopril and captopril treated patients. Thus, perindopril proved to tolerate better in short-term, cause less hemodynamic changes and withdrawals in comparison to captopril.

Flammang D et al. studied the short-term and long-term hemodynamic efficacy of perindopril in severe chronic CHF patients. 15 patients (12 men, 3 women) were given oral perindopril (4 mg od) for 3 months. In this study, hemodynamic improved similarly at day 2 and 3 months. Cardiac index increased 21% (p < 0.05) at second day and 37% (p < 0.001) at 3 months, whereas pulmonary capillary wedge pressure, mean arterial pressure reduced 54% and 21% respectively (p < 0.01) at second day, with 41% and 19% respectively (p < 0.01) at 3 months. These results showed significant difference. Besides that, heart rate or plasma creatinine concentration did not change much and no adverse effects were detected. Hence, perindopril again proved to have valuable short-term hemodynamic efficacy.

As for the beta blocker, metoprolol was prescribed for this patient. In Groenning BA et al., the effects on left ventricular size and function of beta-blockade in CHF patients were examined. 41 patients were tested. The LV end-diastolic volume (150 ml/m2 to 126 ml/m2) and LV end-systolic volume (107 ml/m2 to 81 ml/m2) are reduced, while LV ejection fraction rose in patients taking metoprolol (29% to 37%). All these readings showed significant difference. Placebo group on the other hand had no significant changes. Metoprolol hence revealed to have antiremodeling effects on LV. As a result, it causes notable decrease in HF patients' mortality, as suggested in MERIT-Heart Failure trial.

However, carvedilol was found to act more effectively when compared to metoprolol in a few recent studies. The effects of metoprolol and carvedilol were compared in Torp-Pedersen C et al. 3029 patients were investigated. In carvedilol treated patients, these incidences were decreased more significantly - cardiovascular death (P=0.0004), sudden deaths, deaths due to circulatory failure or stroke, and fatal or nonfatal AMI (P=0.03). Carvedilol is thus found to act better than metoprolol.

Another recent study Delea TE et al. also recommends carvedilol instead of metoprolol. COMET (Carvedilol or Metoprolol European Trial) verified that carvedilol improves survival rate in HF patients compared to metoprolol tartrate as well. In the study, two groups of 887 patients were given carvedilol and metoprolol tartrate. Carvedilol was found to diminish all-cause mortality and hospitalization risks more. It also had a lower inpatient care expected cost (US$10,509 lesser). It is therefore proved that carvedilol increases survival rate and minimizes cost for HF patient care. To summarize, carvedilol is cost effective.

The diuretics prescribed for this patient is furosemide. A meta analysis of several randomized controlled trials supported the diuretics roles in HF. This analysis had summarise all the evidence from the current randomised controlled trials for diuretics in CHF patients. Diuretics showed to reduce risk of disease worsening and perk up exercise capacity as compared with control. Small studies also illustrate that diuretics minimise death and HF worsening risks in the investigation with placebo.

A study, Muller K et al. had demonstrated that torasemide had better improvement in primary care CHF patients compared to furosemide. Torasemide tends to improve patients significantly (P=0.014), has higher tolerability (P=0.0001) and daily restrictions enhancement (P=0.0002), and significantly lowers miction frequency (P<0.001) and urination urgency (P<0.0001). Thus, torasemide improve quality of life greater than furosemide. Nevertheless, an investigation of pharmacoeconomic between torsemide (torasemide) and furosemide in Noe LL et al. had been done. 240 patients were randomized for the two drugs. Torsemide treated patients were showed to have higher drug-acquisition costs ($121.01 versus $42.95; P < 0.0001) but identical CHF/CV-related medical costs as furosemide ($1520.07 versus $1503.26; P = 0.975). As a result, torasemide is not cost effective.

According to another study, Parker JO et al., duration of exercise increased drastically when comparing to placebo group for furosemide treated (1.2 min, P < 0.035) and ibopamine treated HF patients (1.3 min, P < 0.025). Both medications do not affect patients' quality of life and have only mild side effects. This concluded that both drugs are effective in CHF therapy. Consequently, furosemide is proved to be effective and appropriate in treating CCF.

For the patient in this case, he seems to be well managed, well-tolerated and well-controlled by the drug therapy prescribed, which include perindopril (ACE inhibitor), metoprolol (beta blocker) and furosemide (diuretic). These drugs are all within guideline recommendation.1 Regarding the evidence found, perindopril, an ACE inhibitor has no major side effects and is effective and appropriate for treating chronic cardiac failure patients, as what had been done for this patient. After evaluating all the evidence, I suggest to change the beta blocker, metoprolol to carvedilol, which appears to be cheaper and acts better against HF (cost effective). Furosemide is still a better choice for CCF treatment, since torasemide is not cost effective and furosemide had been proved to be effective in treating CHF patients. The exacerbation of CCF that causes hospital admission of this patient might be due to the effectiveness of metoprolol and also the cellulitis infection. Therefore, metoprolol should be suggested to be replaced by carvedilol. Patient should also be counseled to be compliant with the drugs prescribed and modify his diet and lifestyle to improve the quality of life. Regular review of the risk factors and the patient's medication should also be done.