John is an 82 year old gentleman who lives alone in sheltered accommodation. John’s son and daughter live close and take it in turns to visit daily. John is an ex-smoker who gave up 20 years ago, has long standing hypertension and is overweight having a BMI of 30 kg/m.
John was diagnosed with heart failure a year ago after being hospitalised three times in the space of four months. Stewart (2004) feels that a diagnoses of heart failure is problematic in older patients as their symptoms can often mimic other …show more content…
These changes alter the vascular media, thereby causing arterial stiffening (McCance & Huether 20029).
John’s arteries and arterioles will have become less elastic and stiff due to his age, this means they can not relax as quickly during the rhythmic pumping of the heart.
When the heart is damaged, the body will compensate by using three compensatory mechanisms to help increase cardiac output and venous return. These are increased sympathetic activity (ref10), renal retension of fluid and increased stretch of the heart muscle.
These three compensatory mechanisms result in increased heart rate. Increased contractility and basoconstriction?
Sign (2007) state that there are 3 main goals of pharmacological management in heart failure, these being relieving symptoms, avoiding hospital admissions and to increase life expectancy.
John was taking Candesartain 16 mg daily. This is a Angiostensin receptor blocker (ARB’s). This drug is one of two ARB’s licensed for use in heart failure in the UK. Candesartain is a neurohormonal antagonist and acts in the same way as an ACE inhibitor; by inhabiting angiotensin I Convertina to angiotensin II. When discussing his medication, I asked John about his Candesartan as I was wondering why he was taking this and not an ACE inhibitor. John confirmed what I was thinking, he confirmed that he was originally commenced on Ramipril, but before he could reach the