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ACE inhibitors are a class of drugs that act to reduce systemic vascular resistance. They are prescribed for patients suffering from hypertension, heart failure or chronic renal disease due to this.
ACE inhibitors are contraindicated in patients with:
This is a rare but severe airway swelling due to the accumulation of fluid and bradykinin which results from their first dose of an ACE inhibitor. This could be life-threatening if the upper airway and larynx are affected as cases of acute respiratory distress may result.
Patients who show hypersensitivity should avoid all ACE inhibitors.
This therapy consists of three components - a diuretic, an ACE inhibitor and Non-steroidal anti-inflammatory drugs (NSAIDs). Diuretics can reduce plasma volume which results in a decreased inflow to the glomerulus. NSAIDs inhibit prostaglandins and bradykinin, thereby causing vasoconstriction of the afferent renal arteriole and hampering the ability of the kidney to regulate (increase) glomerular blood flow.
Ordinarily, the kidney can address this via the renin-angiotensin system; it constricts the efferent renal arteriole to increase glomerular filtration pressure and promoting the retention of water and sodium.
However, when ACE inhibitors are administered as part of triple therapy, the kidney cannot use its normal compensatory mechanisms and the person may suffer an acute reduction in glomerular filtration. This is because ACE inhibitors inhibit the renal arteriolar vasoconstriction which lowers glomerular filtration pressure.
Together, these result in an increased risk of acute kidney injury.
These people might suffer from further deterioration of renal function therefore they need to have their renal function evaluated prior to the initiation of ACE inhibitor therapy. Following this, a reduced dose of the drug and close, regular monitoring might be suggested.
ACE inhibitors should be used with caution in patients who are:
These individuals are volume depleted and their doctor is likely to monitor them quite closely because the first doses can cause rapid hypotension in these patients; treatment should therefore be initiated with very low doses.
Glycemic control can also induce a sustained osmotic diuresis and, in the process, produce significant enough decrease in volume to also exacerbate an ACE inhibitor's effect on blood pressure.
ACE inhibitors are not recommended in women who are in their second or third trimester of pregnancy. At this stage, the fetal kidney is newly-formed and highly susceptible to hemodynamic fluctuations. ACE inhibitors will interrupt the fetal renin-angiotensin system and maternal hypotension and/or a decrease in fetal-placental blood flow will result in fetal ischemia. These lead to fetal renal failure and specific abnormalities (limb deformities, cranial ossification deficits) many of which are a consequence of a reduction in amniotic fluid volume.
Potassium supplementation should be used with caution and under medical supervision because ACE inhibitors already elevate potassium levels (Hyperkalemia). In actual fact, ACE inhibitors will raise the serum potassium level in practically all patients however to a degree that is clinically undetectable and never even approaches a significant enough level for the patient to be diagnosed with hyperkalemia.