ABSTRACT physical examination. Heart failure can be


failure is a condition of the heart that fail to function to maintain the
cardiac output. It can be caused by many factors that can be arise from the
heart itself. This is a report of 59 years old gentleman who had been diagnosed
with decompensated congestive cardiac failure. This case emphasizes and focuses
on the management of decompensated congestive cardiac failure.

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failure is a clinical syndrome that arise from the abnormalities of the cardiac
structure or function that contribute to impairment of ventricular filling or
ejection of blood and failure to maintain adequate cardiac output. In Malaysia,
the prevalence of the patient with congestive cardiac failure is high in the
patient age of 65 and above which is 100 in 1000 populations. The most common
cause of heart failure are coronary artery disease and hypertension which
accounts for almost 70% of all cases. There are other causes of heart failure
such as dilated cardiomyopathy, diabetes cardiomyopathy and congenital heart
disease. Heart failure is clinically diagnosed by careful history and physical
examination. Heart failure can be decompensated by several factors such as
non-compliance to medications and uncontrolled hypertension.


A 59-year
old Malay gentleman, non-smoker and teetotaler underlying with Diabetes
Mellitus and hypertension for 10 years and history of right lower limb
cellulitis in 2014 and peptic ulcer disease 1 month ago presented with
shortness of breath 3 days prior to admission and bilateral leg swelling 2
weeks prior to admission associated with orthopnea, paroxysmal nocturnal dyspnea,
cough and loss of appetite. Shortness of breath was sudden in onset and he had
limited distance to walk (50 metres). Bilateral leg swelling was gradual in
onset and worsened by walking. He needed 3 to 4 pillows to sleep but currently
he cannot lie down to sleep. The cough was intermittent and non-productive
cough. Otherwise, there was no fever, no runny nose, no chest pain, no
palpitation, no calf pain and no urinary tract infection symptoms.

He had
diabetes mellitus for 10 years on metformin 2g and subcutaneous mixtard 38units/32
units BD with complication of hypertrophic cardiomyopathy. He had admission due
to right lower limb cellulitis on 2014 and completed IV Unasyn(ampicillin and
sulbactam) for 1 week.  He also had
hypertension for 10 years on amlodipine 100mg OD and aspirin(currently stopped
aspirin after he had been diagnosed to have peptic ulcer disease) and
hypercholesterolemia for 8 years on tab simvastatin 20mg ON. He claimed he was
compliance to the medications. He was diagnosed to have peptic ulcer disease 1
month ago as he had passing out fresh melena but no hematemesis. Oesophagogastroduodenoscopy
(OGDS) was done and showed 2 ulcers seen at prepylorus, both Forest 3 ulcer
near incisura 1 cm deep, another ulcer superficial 0.5cm. Multiple ulcers at D1
and D2. He was on tab esomeprazole 40mg OD and loratadine 10mg OD.

Upon arrival
at emergency department, he was alert, conscious and mild tachypneic with
respiratory rate of 22 breaths per minute and SpO2 of 100% under face mask. His
blood pressure was 145/80 mmHg, pulse rate was 92 beats per minute and
temperature was 37°C. On general examination, the
peripheries were warm. Lung examinations revealed reduced chest expansion,
resonance in percussion and reduced breath sound bilaterally with bibasal crepitations.
On cardiovascular examination, the apex beat was displaced at 6th
intercostal space at anterior axillary line and dual rhythm no murmur. On
abdominal examination, the abdomen was grossly distended with no organomegaly
and positive shifting dullness but negative fluid thrill. On leg examination, the
right leg was warmer compared to left leg. There was tenderness over the right
leg. The skin was dry, hyperpigmented and erythematous at the right leg. There
was leg edema until the knee on both sides but no sacral edema. The central
nervous system examination showed no significant finding. Blood investigations
were done and showed anemia of 9.7g/dL and high creatinine level of 130µmol/L. Others were within the normal value. Arterial blood
gas showed partially compensated respiratory acidosis with low pH of 7.27, high
pCO2 of 55mmHg, high pO2 of 211mmHg and high bicarbonate of 25mmol/L. Chest
X-ray showed blunted costophrenic angle bilaterally, increase haziness at the
lower zone bilaterally, increase pulmonary vascular marking and increase
cardiothoracic ratio indicate cardiomegaly.

Based on
history of patients, physical examinations and investigations that were done,
this patient was treated as decompensated congestive cardiac failure. He was
treated pharmacologically and non-pharmacologically. Pharmacologically by given
IV Lasix 40mg stat and reduced to 4mg BD, IVi glyceryltrinitate 4mcg, tab
simvastatin 20mg ON and continue old medication. Non-pharmacologically by giving
oxygen 10L/min via face mask, restriction of fluid of 500cc/day and strict
input output chart.












            Heart failure is a clinical syndrome that arise from
the abnormalities of the cardiac structure or function that contribute to
impairment of ventricular filling or ejection of blood and failure to maintain
adequate output. Prevalence of heart failure in Malaysia varies between 3 to 20
per 1000 populations although it is higher in persons over the age of 65 years
old which is 100 per 1000 population.

Patients with heart failure usually come with typical signs
and symptoms such as breathlessness, ankle swelling, fatigue, elevated jugular
venous pressure, ankle edema, bibasal crepitations and displaced apex beat.  In this patient, he had all the typical signs
and symptoms that mention above except elevated jugular venous pressure.

            Identifying the underlying disease
and the precipitating factors is a must as heart failure cannot come alone.
There are several causes of heart failure such as coronary artery disease, hypertension,
dilated cardiomyopathy, valvular heart disease, diabetic cardiomyopathy and
constrictive pericarditis. This patient is underlying with hypertension and
diabetes mellitus that can be the cause of heart failure. On echocardiography,
it has shown that there is hypertrophic cardiomyopathy which may be secondary
to diabetes mellitus. Hypertrophic cardiomyopathy may also lead to heart

            Heart failure is a clinical
diagnosis which we can diagnose by a careful history and physical examination.
For this patient, he came with breathlessness and bilateral leg swelling
associated with orthopnea, paroxysmal nocturnal dyspnea(PND) and reduced effort
tolerance. These are the characteristic symptoms of heart failure. Signs of
heart failure which is more specific are an elevated jugular venous pressure, 3rd
heart sound and laterally displaced apical impulse in the presence of a cardiac
murmur. Other signs that support the diagnosis of heart failure are peripheral
edema, tachycardia, narrow pulse pressure, bibasal crepitations hepatomegaly
and ascites. This patient has majority of the signs and symptoms that can lead
to a diagnosis of heart failure such as orthopnea, PND, peripheral edema and
bibasal crepitations.

            Acute heart failure can be described
as rapid onset or rapid worsening of the signs and symptoms of heart failure.
The progressively worsening can be within hours to several days which depend on
the cause of the heart failure. There are factors that lead to decompensated
heart failure such as non-compliance to medications, excessive salt and fluid intake,
inappropriate medications such as NSAIDs and COX-2 inhibitors, infections,
acute coronary syndrome, fluid overload, suboptimal treatment, uncontrolled
hypertension and alcohol consumptions.

            The management of acute heart
failure is as follow: Give oxygen, frusemide, nitrate and morphine sulphate.
The aim of the oxygen therapy is to achieve SpO2>95% to maximize tissue
oxygenation and to prevent end organ failure. Frusemide is given intravenously
40-100mg. Frusemide should be administered by giving loading dose first and
then continuous infusion as it had been showed that this method can produce
greater effect of diuresis and weight reduction. Nitrates is considered if
SBP>100mmHg and administered intravenously. The patient with nitrates should
be monitored their blood pressure as nitrates can cause hypotension due to
vasodilatation. Hypotension usually occurs with combination of diuretic therapy
and nitrates. The combination of low dose frusemide and nitrates has greater
effect when compared to high dose frusemide. Nitrates is contraindicated for
the patient with severe valvular stenosis. Morphine sulphate is administered to
reduce pulmonary venous congestion although it had only minimal effect of
venodilation and reduce anxiety. Antiemetics should be given if the patient is
on morphine sulphate as the side effect of morphine is vomiting. As for this
patient, he was given oxygen 10L/min, IVi GTN 4mcg and IV frusemide 40mg.

            As this patient has hypertension, he
had been prescribed aspirin to reduce major cardiovascular events such as
myocardial infarction and ischemic cerebrovascular accidents.  However, the risk of getting upper
gastrointestinal bleeding is high in patient who are taking aspirin. In this
patient, he was diagnosed to have peptic ulcer disease 1 month ago maybe due to
regular use of aspirin. So, currently he had to stop taking aspirin to reduce
the gastrointestinal bleeding. He was treated by taking esomeprazole which is
proton pump inhibitor that inhibit hydrogen-potassium ATPase pump and reduce
gastric acid secretion. He was also given loratadine, H1-antihistamine which
reduce the production of gastric acid in the stomach.