Competitive inhibition of angiotensin converting enzyme leads to decreased angiotensin II production and its effects.

Competitive inhibition of angiotensin converting enzyme leads to decreased angiotensin II production and its effects.

Competitive inhibition of angiotensin converting enzyme leads to decreased angiotensin II production and its effects.

CVS
- TPR and Afterload is decreased to a greater extent than preload, and this may result in improved CO in heart failure patients.
- HR is usually unchanged and baroreceptor reflexes also
unchanged.

Renal
- the impairment of Ang-II means that the body is less able to respond to a drop in renal perfusion and this may precipitate failure.

Metabolic
– Accumulation of K+ may occur due to decreased aldosterone.

CVS
- TPR and Afterload is decreased to a greater extent than preload, and this may result in improved CO in heart failure patients.
- HR is usually unchanged and baroreceptor reflexes also
unchanged.

Renal
- the impairment of Ang-II means that the body is less able to respond to a drop in renal perfusion and this may precipitate failure.

Metabolic
– Accumulation of K+ may occur due to decreased aldosterone.

CVS
- TPR and Afterload is decreased to a greater extent than preload, and this may result in improved CO in heart failure patients.
- HR is usually unchanged and baroreceptor reflexes also
unchanged.

Renal
- the impairment of Ang-II means that the body is less able to respond to a drop in renal perfusion and this may precipitate failure.

Metabolic
– Accumulation of K+ may occur due to decreased aldosterone.

PO. rapidly absorbed, BA: 60-70%

PO. absorbed variably. BA: 30%

PO. 50–60% is absorbed. BA: 30%

25%

25%

75%

2 L/kg

1.7 L/kg

0.1 L/kg

oxidised in the liver and converted to sulphides

not metabolised

Hepatic to the active form, ramiprilat

urine both as active metabolites and unchanged

urine unchanged

Urine (60%) and feces (40%) as parent drug & metab

2-4 hours

12 hours

triphasic elimination profile of the active metabolite ramiprilat with T1/2 1-2 hrs, 13-17hrs and >50hrs.

A dry cough may occur especially in patients with pre-existing lung disease.
Caution should be exercised in patients on potassium sparing medications. NSAIDs may precipitate renal failure.

A dry cough may occur especially in patients with pre-existing lung disease.
Caution should be exercised in patients on potassium sparing medications. NSAIDs may precipitate renal failure.

A dry cough may occur especially in patients with pre-existing lung disease.
Caution should be exercised in patients on potassium sparing medications. NSAIDs may precipitate renal failure.

ACE inhibitor

ACE inhibitor

ACE inhibitor

used for management of hypertension, LV dysfunction post-myocardial infarction and in the setting of heart failure. Its use has been shown to decrease progression of heart failure (disease modifying)

used for management of hypertension, LV dysfunction post myocardial infarction and in the setting of heart failure.
Its use has been shown to decrease progression of heart failure (disease modifying).

used for management of hypertension, LV
dysfunction post myocardial infarction and in the setting of heart failure. Its use has been shown to ↓progression of heart failure (disease modifying).

active drug converted to active metabolites. It is a competitive ACE inhibitor

Active drug that is not metabolised and is excreted directly into urine. It is a competitive ACE inhibitor

prodrug requiring hepatic activation to ramiprilat.
Ramiprilat is a competitive ACE inhibitor

Level 3

Level 3

Level 3

moderately potent

highly potent

potent

oral formulation presented as white tablets in dosage ranging from
12.5mg to 50mg

oral formulation presented as white tablets in dosage ranging from 5mg
to 20mg tablets.

oral formulation presented as tablets or capsules in dosage ranging from
1.25mg to 10mg

PO: doses commenced at 6.25mg TDS and uptitrated

PO: doses commenced at 6.25mg TDS and uptitrated

PO: doses commenced at 2.5 mg Daily and uptitrated