In: Nursing
ACE Inhibitors tend to cause a dry, persistent cough in some patients.
When this occurs a physician may switch the patient to an Angiotensine Receptor II antagonist.
Reason
ACE, angiotensin-converting enzyme, converts Angiotensin I to Angiotensin II.
Angiotensin II is a potent vasoconstrictor and triggers the release of Aldosterone.
Aldosterone helps the kidneys to keep water and sodium but excrete potassium.
ACE inhobitors
ACE Inhibitors prevent the conversion of Angiotensin I to Angiotensin II.
ACE Inhibitors block the role of angiotensin II and the blood vessels dilates and result in decreased systemic vascular resistance and blood pressure. It also causes kidneys to excrete water and sodium but keeps potassium.
ACE also inactivates bradykinin by breaking it down. Bradykinin is an inflammatory substance. However, when a patient takes an ACE Inhibitor it will prevent this inactivation process and cause bradykinin levels to increase.
Bradykinin leads to a dry, persistent cough in some patients. However, this doesn’t occur with Angiotebsin Receptor Blockers II because these medications do not inhibit Angiotenin Converting Enzyme and bradykinin gets inactivated.
Angiotensin II receptor type 1 sites
Angiotensin II receptor type I sites are responsible for vasoconstriction and triggering the release of aldosterone by the adrenal cortex, which increases the blood volume. This causes the kidneys to keep sodium and water but excrete potassium.
Angiotensin II Receptor Antagonists
Angiotensin II receptor type 1 antagonists/ blockers are cardiac medications that lower the blood pressure by preventing the activation of angiotensin II type 1 receptors.This will prevent angiotensin II from binding to these receptors site. Since Angiotensin Receptor II Antagonists block the activation of these receptor sites, it will cause the opposite effects. That is dilate blood vessels and results in decreased systemic vascular resistance and blood pressure. It also decreases the recreation of aldosterone.
Q)What type of lab work should be checked when patients take the above medications and why?How often should lab work be checked?
DRUG INDUSED HYPERKALEMIA.
Angiotensin II Receptor Antagonists also deecreases the secretion of aldosterone so there is no increase in blood volume but actually a decrease in blood volume because the kidneys will excrete sodium and water but keep potassium.
So monitor for HYPERKALEMIA while administering Angiotensin II Receptor Antagonists.
Nornal: 3.5-5 mEq/L
Therefore, people on Angiotensin II Receptor antagonists should regularly have blood tests to measure potassium levels. Because Hyperkalemia results in ECG changes, confusion, irregular heartbeat, nervousness, numbness or tingling in hands, feet or lips, shortness of breath or difficulty breathing, and weakness or heaviness in legs.
BUN, creatinine
This drug causes a decrease in glomerular filtration rate (GFR) and decease renal blood flow. In severe heart failure patients monitor BUN, creatinine, and urine out put also for any signs of renal impairment as these patients are dependent on the Renin-Angiotensin-Aldosterone System for maintaining cardiac output with the compromised cardiovascular system