ACE Inhibitors: Drug List, Mechanism of Action, Side Effects
ACE inhibitor pharmacology made easy! Provides a list of example drug names along with their mechanism of action, indications, and side effects such as cough, angioedema, and high potassium or hyperkalemia. Mnemonics included!
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Everything you need to know about ACE inhibitors and Angiotensin II Receptor Blockers (ARBs) in the PDF lectures below :)
What are ACE Inhibitors?
Angiotensin-converting enzyme inhibitors (ACE inhibitors) are a class of medications commonly used as antihypertensive drugs to treat hypertension or high blood pressure.
ACE inhibitors also have indications for various cardiac and renal diseases such as heart failure and diabetic nephropathy.
We will discuss the mechanism of action (MOA) and how ACE inhibitors work to lower blood pressure, along with their other indications, contraindications, and major side effects such as cough, angioedema, and hyperkalemia (high potassium).
A list of example ACE inhibitors will be provided along with an easy trick to remember their drug names.
The renin-angiotensin-aldosterone system will also be reviewed as ACE inhibitors block the normal physiology by inhibiting angiotensin-converting enzyme.
The below “Antihypertensive Chart” was used in a previous EZmed lecture in which ACE inhibitors, angiotensin II receptor blockers (ARBs), alpha blockers, beta blockers, calcium channel blockers, and diuretics were all compared to one another.
Although the chart provided a broad overview of the main antihypertensive drugs, we will now focus solely on the pharmacology of ACE inhibitors.
Let’s get started!
Antihypertensive Drug Chart: Review of the main antihypertensive medications including ACE inhibitors, angiotensin II receptor blockers (ARBs), alpha blockers, beta blockers, calcium channel blockers, and diuretics
How Do ACE Inhibitors Work?
In order to better understand how ACE inhibitors work, we need to know what ACE is.
ACE stands for angiotensin-converting enzyme, which plays an important role in the renin-angiotensin-aldosterone system.
Let’s quickly review the renin-angiotensin-aldosterone system (RAAS) as the mechanism of action for ACE inhibitors will become more clear.
Renin Release
The RAAS is important in regulating blood pressure and blood volume, especially when blood pressure is low.
The kidneys detect whenever there is decreased blood flow or blood volume present, and they panic out of concern they are not being perfused well.
As a result, the kidneys release an enzyme called renin which is the first step of the RAAS.
Specifically it is the juxtaglomerular cells (JG cells) of the kidneys that secrete renin.
You can think of RENin and RENal to help you remember renin is released by the kidneys.
The sympathetic nervous system can activate the JG cells to release renin as well.
The sympathetic nervous system is involved in our fight or flight response.
One of those responses is to increase blood pressure in order to better perfuse vital tissues and organs in a stressful or dangerous situation.
Therefore, it makes sense the sympathetic nervous system can activate the RAAS in order to help increase blood pressure.
Sympathetic catecholamines such as epinephrine and norepinephrine activate beta-1 receptors located on JG cells, thereby causing renin release.
Lastly, decreased sodium levels in the distal tubule of the nephron can also stimulate renin release from the JG cells.
Whenever there is decreased blood pressure or perfusion to the kidneys, then there will be increased sodium and water reabsorption at the proximal tubule of the nephron in order to try to increase blood pressure.
As a result, there will be decreased sodium levels in the distal tubule because much of the sodium has already been reabsorbed back into the bloodstream.
The macula densa cells of the distal tubule detect the decreased sodium levels, and they stimulate the JG cells to release renin in order to increase blood pressure as well.
Renin is released by the kidneys (JG cells) secondary to decreased renal blood flow/perfusion, decreased blood volume, sympathetic activation, or decreased sodium levels in the distal tubule of the nephron.
Angiotensinogen to Angiotensin I
Once renin is released by the kidneys, it converts angiotensinogen into angiotensin I.
Angiotensinogen is a protein produced by the liver.
You can use the “GIN” in angiotensinogen to think of alcohol, and alcohol is metabolized by the liver.
This will help you remember angiotensinogen is produced by the liver.
Renin is an enzyme that cleaves angiotensinogen to form angiotensin I.
Renin is an enzyme that cleaves angiotensinogen to form angiotensin I.
Angiotensin I to Angiotensin II
Angiotensin II is the active peptide hormone we need, not angiotensin I.
Angiotensin I is simply the inactive precursor for angiotensin II, so we need to convert the inactive form into the active one.
We accomplish this through another enzyme called angiotensin-converting enzyme (ACE), which is primarily located in the endothelium of blood vessels in the lungs.
You can associate ACE with AIR, and this will help you remember ACE is primarily found in the lungs.
As the name suggests, angiotensin-converting enzyme converts angiotensin I into angiotensin II.
Angiotensin II has multiple effects on the body to increase blood pressure.
Remember we said the RAAS is activated by decreased renal perfusion, so it makes sense the goal of the RAAS is to increase blood pressure in order to better perfuse the kidneys.
Angiotensin-converting enzyme (ACE) converts angiotensin I into angiotensin II. Angiotensin II has multiple effects on the body to increase blood pressure.
What is the Role of Angiotensin II?
Now that we know how angiotensin II is produced by the RAAS, let’s review the effects angiotensin II has on the body.
Understanding angiotensin II will help us figure out how ACE inhibitors work.
Angiotensin II has several mechanisms to increase blood pressure:
Vasoconstriction
Sodium/Water Reabsorption
Aldosterone Release
Antidiuretic Hormone Release
Sympathetic Augmentation/Adrenal Medulla Stimulation
Blood Pressure Equation
Here is a quick reminder of the blood pressure equation as its variables will be referenced below when discussing the effects of angiotensin II.
BP = Blood Pressure; CO = Cardiac Output; SVR = Systemic Vascular Resistance; HR = Heart Rate; SV = Stroke Volume
1. Vasoconstriction
First, angiotensin II is a potent vasoconstrictor.
There are angiotensin II receptors located on the smooth muscle cells of blood vessels.
Just so you are aware, there are 2 main types of angiotensin II receptors - type I (AT1) and type 2 (AT2).
It is mainly type 1 we are referring to as we discuss the angiotensin II receptors.
When angiotensin II binds to these receptors, it causes vascular smooth muscle contraction.
Vascular smooth muscle contraction leads to increased vasoconstriction.
If we reduce the diameter of a blood vessel, then systemic vascular resistance increases.
Systemic vascular resistance (SVR) is also known as total peripheral resistance (TPR).
As we can see from the blood pressure equation above, increasing SVR will increase blood pressure.
Angiotensin II is a potent vasoconstrictor. It binds to angiotensin II receptors on blood vessels leading to smooth muscle contraction, vasoconstriction, increased systemic vascular resistance (SVR), and increased blood pressure (BP).
2. Sodium/Water Reabsorption
Angiotensin II also affects the kidneys.
First, it can directly stimulate sodium and water reabsorption at the proximal tubule of the nephron.
If we reabsorb sodium and water from the kidney back into the bloodstream, then blood volume will increase.
An increase in blood volume will increase stroke volume, which will increase cardiac output.
As we can see from the blood pressure equation above, an increase in stroke volume will increase blood pressure.
Angiotensin II stimulates sodium and water reabsorption in the proximal tubule of the nephron. This increases blood volume (BV), stroke volume (SV), cardiac output, and blood pressure (BP).
3. Aldosterone Release
Angiotensin II can also stimulate the release of aldosterone from the adrenal cortex.
Aldosterone is a hormone that primarily acts on the distal tubule of the nephron to increase sodium and water reabsorption.
This will then have the same downstream effects of increasing blood volume, stroke volume, and blood pressure that we saw before.
Aldosterone also increases potassium excretion in the urine, which will become important when we talk about the side effects and contraindications of ACE inhibitors.
Angiotensin II stimulates aldosterone release from the adrenal cortex. Aldosterone increases sodium and water reabsorption in the distal tubule of the nephron, as well as increases potassium (K) excretion in the urine.
4. Antidiuretic Hormone Release
Angiotensin II also stimulates the release of antidiuretic hormone from the posterior pituitary gland.
Antidiuretic hormone (ADH) is also known as vasopressin.
ADH acts on the collecting duct of the nephron to facilitate water reabsorption.
As we saw above, water reabsorption will increase blood volume, which will increase stroke volume, which will increase blood pressure.
There are also vasopressin receptors located on the smooth muscle cells of blood vessels.
Activation of these receptors by ADH/vasopressin will cause vascular smooth muscle contraction.
As we saw above, vascular smooth muscle contraction leads to increased vasoconstriction, increased SVR, and increased blood pressure.
Angiotensin II stimulates antidiuretic hormone (ADH)/vasopressin release from the posterior pituitary gland. ADH increases water reabsorption in the collecting duct of the nephron, and it also binds to vasopressin receptors on blood vessels causing smooth muscle contraction and vasoconstriction.
5. Sympathetic Augmentation/Adrenal Medulla Stimulation
As mentioned above, the sympathetic nervous system can help activate the RAAS by stimulating JG cells to release renin.
Angiotensin II can then go back and affect the sympathetic nervous system by augmenting sympathetic outflow centrally.
Angiotensin II can also stimulate the adrenal medulla to secrete epinephrine and norepinephrine, which are the main catecholamines of the sympathetic nervous system.
So we can see how the effects of angiotensin II connect together, and how angiotensin II has multiple mechanisms to increase blood pressure.
Angiotensin II augments sympathetic outflow centrally and stimulates the adrenal medulla to release epinephrine and norepinephrine.
What is the Mechanism of Action of ACE Inhibitors?
Now that we understand the RAAS and the effects of angiotensin II, let’s review how ACE inhibitors work.
As the name suggests, ACE inhibitors inhibit angiotensin-converting enzyme (ACE).
We now know ACE plays an important role in converting angiotensin I into angiotensin II.
If we inhibit ACE, then there will be decreased angiotensin II production.
The decrease in angiotensin II levels will lead to a decrease in blood pressure.
ACE inhibitors inhibit ACE from converting angiotensin I into angiotensin II. Decreased angiotensin II levels will decrease blood pressure (BP).
What Are the Effects of ACE Inhibitors?
The decrease in angiotensin II levels from ACE inhibitors will have multiple effects on the body.
Simply put, all of the angiotensin II effects we saw above will be inhibited or reduced by ACE inhibitors.
Knowing these effects will help us understand the indications for ACE inhibitors.
Decreased Vasoconstriction
Decreased Sodium/Water Reabsorption
Decreased Aldosterone Release
Decreased Antidiuretic Hormone Release
Decreased Sympathetic Augmentation/Adrenal Medulla Stimulation
1. Decreased Vasoconstriction
Angiotensin II normally binds to angiotensin II receptors on blood vessels, which causes smooth muscle contraction and vasoconstriction.
With decreased levels of angiotensin II from ACE inhibitors, we will have less vascular smooth muscle contraction and less vasoconstriction.
Less vasoconstriction means the blood vessels have a larger diameter, which will decrease systemic vascular resistance.
Decreased systemic vascular resistance leads to a decrease in blood pressure.
Decreased angiotensin II levels from ACE inhibitors results in decreased smooth muscle contraction, decreased vasoconstriction, decreased systemic vascular resistance (SVR), and decreased blood pressure (BP).
2. Decreased Sodium/Water Reabsorption
Normally angiotensin II increases sodium and water reabsorption in the proximal tubule of the nephron.
Decreased angiotensin II levels from ACE inhibitors means less sodium and water reabsorption, which will decrease blood volume, which will decrease stroke volume, which will decrease blood pressure.
Decreased angiotensin II levels from ACE inhibitors results in decreased sodium and water reabsorption in the proximal tubule of the nephron. This decreases blood volume (BV), stroke volume (SV), and blood pressure (BP).
3. Decreased Aldosterone Release
We also know angiotensin II stimulates aldosterone secretion from the adrenal cortex.
Decreased angiotensin II levels from ACE inhibitors means less aldosterone release, which means less sodium and water reabsorption in the distal tubule of the nephron.
This too will decrease blood volume, stroke volume, and blood pressure.
Remember we also said aldosterone increases potassium excretion in the urine.
With less aldosterone, there will be less potassium excretion which means more potassium in the serum.
This will become important in a bit when we talk about the side effects and contraindications of ACE inhibitors.
Decreased levels of angiotensin II from ACE inhibitors results in decreased aldosterone release. This will decrease sodium and water reabsorption in the distal tubule of the nephron, which will decrease blood volume (BV), stroke volume (SV), and blood pressure (BP). Decreased aldosterone also leads to decreased potassium (K) excretion in the urine.
4. Decreased Antidiuretic Hormone Release
We also know angiotensin II increases the release of antidiuretic hormone (ADH) from the posterior pituitary gland.
With lower levels of angiotensin II from ACE inhibitors, we will have less ADH release.
As a result, there will be less water reabsorption in the collecting duct of the nephron, which will lead to decreased blood volume, stroke volume, and blood pressure.
With lower levels of ADH (also known as vasopressin), there will also be less binding to vasopressin receptors on blood vessels.
This will lead to decreased smooth muscle contraction, decreased vasoconstriction, decreased systemic vascular resistance, and decreased blood pressure.
Decreased levels of angiotensin II from ACE inhibitors results in decreased antidiuretic hormone (ADH)/vasopressin release. This will decrease water reabsorption in the collecting duct of the nephron, which will decrease blood volume (BV), stroke volume (SV), and blood pressure (BP). It also leads to decreased binding of vasopressin to blood vessels, causing decreased smooth muscle contraction and decreased vasoconstriction.
5. Decreased Sympathetic Augmentation/Adrenal Medulla Stimulation
We also know angiotensin II augments sympathetic outflow centrally and stimulates the adrenal medulla to secrete epinephrine and norepinephrine.
Lower levels of angiotensin II from ACE inhibitors will decrease sympathetic outflow augmentation and decrease the stimulation of the adrenal medulla.
Decreased levels of angiotensin II from ACE inhibitors will decrease sympathetic outflow augmentation, as well as decrease stimulation of the adrenal medulla.
ACE Inhibitor Mnemonic
The main effects of ACE inhibitors can be remembered using the mnemonic “ACE”.
A
ACE inhibitors decrease the levels of angiotensin II, aldosterone, and antidiuretic hormone (ADH), all of which can be remembered using the letter “A”.
C
ACE inhibitors decrease vasoconstriction, which can be remembered using the letter “C” for constriction.
E
ACE inhibitors decrease endovascular/intravascular volume, which can be remembered using the letter “E” for endovascular volume.
Use the mnemonic “ACE” to remember the effects of ACE inhibitors in reducing levels of (A) angiotensin II, aldosterone, and antidiuretic hormone; in reducing (C) constriction of blood vessels; and in reducing (E) endovascular/intravascular volume.
ACE Inhibitor Examples
Let’s take a look at some example ACE inhibitor medications.
The easy way to remember ACE inhibitors is their drug names usually end with the suffix “pril”.
Examples include lisinopril, enalapril, captopril, quinapril, and benazepril.
ACE Inhibitor List of Example Medications: ACE inhibitor drug names usually end in “pril”.
ACE Inhibitor Indications
Now that we understand the mechanism of action of ACE inhibitors, let’s go over their indications.
ACE inhibitors have 2 major effects on the body as we saw above:
They decrease vasoconstriction by decreasing angiotensin II and ADH levels.
They decrease sodium/water reabsorption by decreasing angiotensin II, ADH, and aldosterone levels.
Decreased vasoconstriction and decreased sodium/water reabsorption are 2 of the main underlying mechanisms in which ACE inhibitors treat various conditions.
ACE inhibitors can be used in:
Hypertension
Heart Failure
Coronary Artery Disease/Post-Myocardial Infarction
Cardiac Remodeling
Renal Disease
ACE inhibitors have 2 main effects on the body: decreased vasoconstriction and decreased sodium/water reabsorption in the kidney.
1. Hypertension
We know decreasing vasoconstriction will decrease systemic vascular resistance (SVR).
We also know decreasing sodium/water reabsorption will decrease blood volume, which will decrease stroke volume, which will decrease cardiac output (CO).
Remember our equation for blood pressure was CO x SVR, with cardiac output equaling heart rate x stroke volume.
So it should be no surprise that if we decrease systemic vascular resistance and cardiac output, then we will decrease blood pressure.
This is why ACE inhibitors can be used to treat hypertension (high blood pressure).
ACE inhibitors can be used to treat hypertension as they decrease systemic vascular resistance (SVR) and cardiac output (CO).
2. Heart Failure
ACE inhibitors are also indicated for heart failure as they can decrease afterload and preload.
Afterload
Another way to think of systemic vascular resistance is afterload.
Afterload is the amount of resistance the heart must overcome in order to pump blood forward into the vasculature.
So if we decrease systemic vascular resistance using ACE inhibitors, then afterload decreases because the heart does not have to work as hard to pump blood forward.
Preload
Similarly, another way to think of blood volume is preload.
Preload is the amount of stretch on the heart before contraction, which is influenced by the volume of blood returning to the heart.
So if we decrease blood volume using ACE inhibitors, then preload decreases because there is less venous pressure and blood return to the heart.
Furthermore, vasodilation from ACE inhibitors can dilate the veins. This can further reduce preload by decreasing venous pressure and blood return to the heart.
Afterload and Preload
By collectively reducing afterload and preload with ACE inhibitors, we decrease the amount of stress and work on the heart.
This will also decrease the oxygen demand on the heart.
As a result, ACE inhibitors can be used in heart failure when the heart is already weak and will perform better under less stress.
Decreasing the afterload helps improve ejection fraction in heart failure because there is less resistance the heart must overcome.
Reducing preload can help decrease the pulmonary/systemic congestion and edema seen in heart failure because there is less venous pressure.
ACE inhibitors can be used in heart failure as they decrease afterload, preload, and overall oxygen demand/stress on the heart. Reducing afterload can improve the ejection fraction (EF) of the heart, and reducing preload can decrease edema.
3. Coronary Artery Disease/Post-Myocardial Infarction
Reducing afterload and preload decreases the oxygen demand on the heart as we saw above.
This is not only beneficial in heart failure, but also in coronary artery disease (CAD) or after a myocardial infarction (MI) when it is important to limit the oxygen demand and stress on the heart.
As a result, ACE inhibitors are commonly indicated in CAD or after an MI.
ACE inhibitors can be used in coronary artery disease (CAD) or after a myocardial infarction (MI) as they decrease afterload, preload, and overall oxygen demand/stress on the heart.
4. Cardiac Remodeling
Chronic hypertension, heart failure, coronary artery disease, or a recent myocardial infarction can all lead to changes in the size and shape of the heart, called cardiac remodeling.
Cardiac remodeling can result in decreased pumping function of the heart.
ACE inhibitors can prevent cardiac remodeling by decreasing afterload, preload, and overall stress on the heart.
ACE inhibitors can decrease the cardiac remodeling that can occur from chronic hypertension, heart failure, coronary artery disease (CAD), or a recent myocardial infarction (MI).
5. Renal Disease
Finally, ACE inhibitors can be used to reduce the progression of renal disease from chronic diabetes or hypertension, called diabetic nephropathy and hypertensive nephropathy.
Chronic hypertension and diabetes can progressively damage the kidney leading to proteinuria, worsening renal function, and development of chronic kidney disease.
Inhibiting the renin-angiotensin-aldosterone system with ACE inhibitors has been shown to protect the kidneys and slow the progression of renal disease.
ACE inhibitors can be used to decrease the progression of renal disease by inhibiting the renin-angiotensin-aldosterone system.
ACE Inhibitor Side Effects
Now that we know the indications for ACE inhibitors, let’s review their side effects.
You can use the mnemonic “CAPTOPRIL” (which is a type of ACE inhibitor) to remember the main side effects.
“CAPTOPRIL” stands for cough, angioedema, pregnancy problems, taste changes, other (rash and fatigue), proteinuria, renal insufficiency, increased potassium, and low blood pressure.
ACE Inhibitor Side Effects: Use the mnemonic “CAPTOPRIL”.
Cough and Angioedema
Cough and angioedema are mainly caused by increased bradykinin levels.
Bradykinin is a peptide with a couple effects on the body.
First, it can cause bronchoconstriction in the lungs which can lead to a cough.
Second, bradykinin is involved in inflammation.
It causes vasodilation and increased vascular permeability which will increase edema.
It also causes increased pain perception.
So how do ACE inhibitors play a role?
Angiotensin-converting enzyme (ACE) normally degrades bradykinin, which would lead to a decrease in bradykinin levels.
This makes sense as the goal of the RAAS is to increase blood pressure, and bradykinin causes vasodilation which would be counterproductive.
If we block ACE with an ACE inhibitor, then we will have less bradykinin degradation which will result in higher levels of bradykinin.
This can cause increased cough and increased edema, known as angioedema.
Angiotensin-converting enzyme (ACE) normally degrades bradykinin. ACE inhibitors block ACE (red “x”) leading to less bradykinin degradation and increased bradykinin levels. This can cause a cough, as well as increased vasodilation/vascular permeability resulting in edema/angioedema.
Pregnancy Problems
ACE inhibitors have also been shown to be teratogenic and should be avoided during pregnancy.
Taste Changes and Other
ACE inhibitors can also lead to side effects such as taste changes, rash, and fatigue.
Proteinuria and Renal Insufficiency
The proteinuria and renal insufficiency in the mnemonic reference the acute kidney injury that can occur, especially when first starting an ACE inhibitor.
We said earlier that ACE inhibitors are renal-protective and slow the progression of renal disease.
However, if a patient already has an underlying condition causing poor renal perfusion such as chronic kidney disease, polycystic kidney disease, or renal artery stenosis, then ACE inhibitors could be detrimental by decreasing renal perfusion even more.
Therefore, it is important to monitor renal function closely when first starting an ACE inhibitor, especially if an underlying kidney disease is already present.
ACE inhibitors can lead to kidney injury, especially in the presence of underlying renal disease and poor renal perfusion at baseline. ACE inhibitors can decrease the already poor renal perfusion even more.
Increased Potassium (Hyperkalemia)
The next side effect is hyperkalemia (increased potassium levels).
Remember we said angiotensin II stimulates aldosterone release, and aldosterone increases potassium excretion in the urine.
This means there will be lower levels of potassium in the blood.
If we decrease aldosterone secretion using an ACE inhibitor, then there will be less potassium excreted in the urine which will mean more potassium in the blood.
Hyperkalemia may be present as a result.
Aldosterone increases potassium excretion in the urine. ACE inhibitors decrease aldosterone release (red “x”) which will result in decreased potassium excretion in the urine and increased potassium levels in the blood (hyperkalemia).
Low Blood Pressure (Hypotension)
Another side effect of ACE inhibitors is hypotension, which makes sense as the goal of ACE inhibitors is to decrease blood pressure.
This is especially true if someone is already taking multiple medications for their hypertension.
ACE Inhibitor Contraindications
Let’s wrap this up with contraindications of ACE inhibitors, most of which can be pieced together from the side effects and pathophysiology already discussed.
ACE inhibitor contraindications include angioedema, anaphylaxis, pregnancy, and bilateral renal artery stenosis. Use with caution in hyperkalemia or when taking other antihypertensive medications.
Angioedema/Anaphylaxis
If a patient has a prior history of angioedema or anaphylaxis from an ACE inhibitor, then ACE inhibitors should be avoided.
There is also a form of hereditary angioedema in which patients are deficient in C1 esterase inhibitor.
C1 esterase inhibitor normally inhibits bradykinin production.
So if there is a deficiency in C1 esterase inhibitor, then there will be less inhibition of bradykinin production.
This can lead to increased bradykinin levels which can predispose a patient to developing angioedema.
Therefore, ACE inhibitors should be avoided in this patient population.
Pregnancy
As mentioned above, ACE inhibitors can be teratogenic and should be avoided during pregnancy.
Bilateral Renal Artery Stenosis
We also mentioned ACE inhibitors can lead to worsening renal function in a patient with underlying kidney disease and poor renal perfusion at baseline.
This is particularly true in patients with bilateral renal artery stenosis, in which perfusion to the kidneys is already limited.
Giving an ACE inhibitor to a patient with bilateral renal artery stenosis could decrease what little perfusion to the kidneys they already have, and could make their renal function worse.
Caution and close monitoring should also be used in anyone with underlying chronic kidney disease (CKD).
Hyperkalemia
Another contraindication, or at least a relative one in some circumstances, is hyperkalemia.
This is particularly true if the patient is taking other medications that can raise potassium levels, or they have a diet rich in potassium, or have any other risk factors for developing hyperkalemia.
As we know from above, ACE inhibitors can cause hyperkalemia by decreasing aldosterone levels.
Antihypertensives
Although not a major contraindication, be mindful if the patient is already taking other antihypertensive medications as adding an ACE inhibitor could cause hypotension.
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