Ace Inhibitors Nursing Considerations

Last updated on May 15th, 2022 at 05:28 pm

Ace Inhibitors Nursing Implications

Ace Inhibitors Nursing Pharmacology

Angiotensin-converting enzyme or ACE inhibitors were initially approved in 1981 for the treatment of intractable hypertension.

They have demonstrated lower morbidity and mortality in patients with congestive heart failure, myocardial infarction, diabetes, chronic renal insufficiency, and atherosclerotic cardiovascular disease.

Angiotensin-converting enzyme inhibitors, or ACE inhibitors, are a class of medications that work by interacting with blood enzymes to widen or dilate blood vessels and lower blood pressure. These medications are used to treat high blood pressure (hypertension), heart disease, and renal damage in diabetics with high blood pressure.

These treatments also help patients who have survived heart attacks live longer and prevent people from dying too soon from heart attacks, high blood pressure, and heart failure. In some cases, ACE inhibitors are used in conjunction with other medications to treat a problem.

Dizziness, headache, cough, rash, and chest pain are some of the most prevalent side effects of ACE Inhibitors, while kidney failure, severe allergic responses, and liver dysfunction or failure are all serious side effects of the medicine.

ACE inhibitors are all the same in the way they work; however, they have different ways of elimination in the body. Prior to taking this medication, check for drug interactions, dosage, and pregnancy and safety information.

Indications of ACE Inhibitors

ACE inhibitors  are used to treat a variety of disorders, including:

• Hypertension or high blood pressure. ACE inhibitors are usually effective at lowering blood pressure. In the treatment of stage 1 hypertension, ACE inhibitors are considered “first-line therapy.” They may also be used to treat hypertension induced by renal artery stenosis, which results in renin-dependent hypertension due to the kidneys’ increased secretion of renin. When angiotensin II production is reduced, arterial and venous dilatation occurs, lowering arterial and venous pressures. ACE inhibitors promote natriuresis and diuresis, which lowers blood volume and cardiac output, and so lowers arterial pressure, by diminishing the effects of angiotensin II on the kidney.

Monotherapy with ACE inhibitors or angiotensin receptor blockers (ARBs) does not work as effectively for African Americans as it does for other races; however, disparities in blood pressure lowering efficacy are erased with proper diuretic dose.

• Heart failure. ACE inhibitors have been shown to be particularly helpful in the treatment of systolic dysfunction-related heart failure (e.g., dilated cardiomyopathy). The following are some of the advantages of ACE inhibition in heart failure:

• Reduced afterload improves ejection fraction and increases ventricular stroke volume.
  • Preload is reduced, resulting in less pulmonary and systemic congestion and edema.
  • Sympathetic activity is reduced, which has been found to be harmful in heart failure.
  • Improving the oxygen supply/demand ratio primarily via lowering demand via afterload and preload decreases.
  • Stops angiotensin II from causing harmful cardiac remodeling.

• Diabetic nephropathy or diabetic kidney disease. These drugs can help keep your kidneys in excellent shape.
• Chronic kidney disease. ACE inhibitors may assist to reduce kidney disease progression.
• After a heart attack or myocardial infarction- They aid in the reduction of deleterious remodeling that happens post-infarction.
• Psychogenic polydipsia. ACE inhibitors can also be used to help persons with schizophrenia who have psychogenic polydipsia reduce their excessive water consumption. Enalapril, when used for this purpose, was found to reduce consumption (as measured by urine output and osmolality) in 60% of people in a double-blind, placebo-controlled trial; other ACE inhibitors have had the same effect.
• After Renal Transplant. ACE Inhibitors have been shown to decrease erythropoietin production, they are commonly used after renal transplant to manage post-transplant erythrocytosis, a condition marked by a persistently high hematocrit greater than 51 percent that develops 8-24 months after successful transplantation.

Contraindications for ACE Inhibitors

Contraindications must be considered before using an ACE Inhibitor in a patient’s treatment. Hyperkalemia (>5.5 mmol/L), renal artery stenosis, pregnancy (ACE or ADEC pregnancy category D), or a previous adverse reaction to an ACE, such as angioedema, are all contraindications to taking an ACE. A novel class of drugs known as Angiotensin-Neprilysin Receptor Inhibitors (ARNI-LCZ696 or EntrestoTM) has just been available as an alternative to ACEIs for patients with heart failure and a lower left ventricular ejection fraction.

These medications also raise circulation bradykinin levels, which are linked to angioedema. As a result, combining ACE and ANRI therapy is not recommended.

Renal failure (serum creatinine >2.5 mg/dL); hyponatremia, especially if less than 130 mmol/L (associated with poorer outcomes); hypovolemia/hypotension less than 90 mmHg; aortic stenosis or LV outflow tract obstruction; or patients who may become pregnant or are breastfeeding are all relative contraindications.

Mechanism of Action of ACE Inhibitors

ACE inhibitors suppress the activity of the renin–angiotensin–aldosterone system (RAAS) as the key etiologic (causative) event in the development of hypertension in persons with diabetes mellitus, as part of the insulin-resistance syndrome, or as a symptom of renal disease.

1. The renin–angiotensin–aldosterone system

The renin–angiotensin–aldosterone system is a key regulator of blood pressure. Hypotension, low distal tubule sodium concentration, decreased blood volume, and increased sympathetic tone are all markers of electrolyte and water imbalance in the body that cause the enzyme renin to be released from the cells of the juxtaglomerular apparatus in the kidney. Renin activates angiotensinogen, a circulating liver-derived prohormone, by proteolytically cleaving all except the first 10 amino acid residues, resulting in angiotensin I. After that, ACE (angiotensin converting enzyme) removes two more residues, transforming angiotensin I to angiotensin II. The pulmonary circulation and the endothelium of many blood arteries contain ACE. Although angiotensin is also particularly good at inducing blood vessels to tighten, the system raises blood pressure by increasing the amount of salt and water the body retains (a potent vasoconstrictor)

2. Effects

ACE inhibitors prevent angiotensin I (ATI) from being converted to angiotensin II (ATII), lowering arteriolar resistance and increasing venous capacity; decreasing cardiac output, cardiac index, stroke work, and volume; lowering resistance in blood arteries in the kidneys; and increasing natriuresis (excretion of sodium in the urine). Renin levels in the blood rise as a result of negative feedback from the conversion of ATI to ATII. For the same reason, ATI rises, while ATII and aldosterone fall. Bradykinin levels rise when ACE inactivation decreases.

Angiotensin II has the following actions under normal circumstances:

• Increased blood pressure and hypertension can be caused by ATII-induced vasoconstriction (narrowing of blood vessels) and vascular smooth muscle hypertrophy (enlargement). Furthermore, restriction of the kidney’s efferent arterioles causes an increase in glomerular perfusion pressure.
• Through stimulation of the proto-oncogenes c-fos, c-jun, c-myc, transforming growth factor beta (TGF-B), fibrogenesis, and apoptosis, it contributes to ventricular remodeling and hypertrophy of the heart (programmed cell death).
• The adrenal cortex is stimulated by ATII to release aldosterone, a hormone that works on kidney tubules, causing sodium and chloride ions to be retained and potassium to be excreted. Because sodium is a “water-holding” ion, water is held as well, resulting in an increase in blood volume and, as a result, an increase in blood pressure.
• The kidneys are likewise stimulated to release vasopressin (antidiuretic hormone, ADH) when the posterior pituitary is stimulated to release it. Na+ levels in the plasma may decline (hyponatremia) if ADH production is excessive in heart failure, and this is a marker of an increased risk of death in heart failure patients.
• A reduction in protein kinase C in the kidneys.

The synthesis of ATII is reduced when an ACE inhibitor is used, which stops aldosterone from being released from the adrenal cortex. The kidney is able to eliminate sodium ions along with obligatory water while retaining potassium ions. This reduces blood volume, resulting in lower blood pressure.

Side Effects of ACE Inhibitors

• Dry and irritating cough. One of the most prevalent side effects documented in people on ACE inhibitors is constipation. The accumulation of inflammatory chemicals such as bradykinin and substance P, whose release is promoted by ACE inhibitors, causes it. Dry coughs affect about one out of every ten individuals on ACE inhibitors, and it might take up to 12 weeks for the cough to go away once the medicine is stopped. Because this effect happens with all ACE medications, switching to a different type of ACE inhibitor is unlikely to help.
• Dizziness and lightheadedness. Because ACE inhibitors only provide minor blood pressure reductions for most individuals, light-headedness and dizziness are rarely noticed. These effects are particularly pronounced in hypotensive patients (very low blood pressure). Because hypotension is common in individuals with heart failure, caution is advised while starting or changing ACE inhibitors in these patients.
• Hyperkalemia or elevated potassium levels in the blood. Aldosterone is a hormone that controls potassium excretion in the kidneys through urine. ACE inhibitors suppress aldosterone levels, allowing potassium to be retained in the kidneys and circulation.
• Angioedema or swelling under the skin. Angioedema is the most serious side effect of ACE inhibitors, affecting 0.1-0.2 percent of individuals. Angioedema is characterized by airway swelling and blockage caused by the accumulation of fluid (and bradykinin). The severity of the illness is determined by the affected area. Angioedema is a condition that causes transient swelling of the lips, tongue, and mouth. Patients may have difficulty breathing in extreme situations where the upper airway and larynx are impacted, and emergency care may be required. Patients who develop angioedema while using an ACE inhibitor should stop taking it and avoid taking any other ACE inhibitors in the future.
• Dysgeusia or an abnormal taste in the mouth. Dysgeusia is a typical ACE inhibitor adverse effect. The presence of a sulfhydryl component is typically linked with a metallic taste. These side effects, on the other hand, tend to fade away with continued use.
• Renal dysfunction. Patients with significant bilateral renal artery stenosis who start on an ACE inhibitor frequently develop renal insufficiency. Because ACE medications block efferent renal arteriolar vasoconstriction, which lowers the kidney’s filtration rate, this problem arises. The effects of the medicine can be reversed if you stop using it.

Adverse Reactions to ACE Inhibitors

Although ACE inhibitors are generally well tolerated, the following are some adverse effects that have been reported:

• Vomiting and diarrhea– vomiting and diarrhea may lead to dehydration in severe cases and can lead to hypotension or dangerously low blood pressure.
• Fatigue
• Headaches
• Fainting
• Weakness
• Sexual dysfunction

ACE Inhibitors Overdose

Only a few cases of ACE inhibitor overdose have been reported. Hypotension, which can be severe, hyperkalemia, hyponatremia, and renal impairment with metabolic acidosis are the most common symptoms.

Treatment should be symptomatic and supportive, with normal saline volume expansion to correct hypotension and enhance renal function, and stomach lavage followed by activated charcoal and a cathartic to prevent additional drug absorption. Hemodialysis is known to remove captopril, enalapril, lisinopril, and perindopril.

Interactions of Ace Inhibitors with other drugs

ACE inhibitors have few important interactions with other drugs,

• Potassium Supplements. Because ACE inhibitors can raise potassium levels in the blood, using potassium supplements, salt substitutes (which typically contain potassium), or other medications that raise potassium levels in the body can lead to high blood potassium levels.
• Lithium. ACE inhibitors also may increase the blood concentration of lithium which may lead to an increase in side effects from lithium.
• Non- steroidal anti-inflammatory drugs (NSAIDs). Other nonsteroidal anti-inflammatory drugs have been reported to reduce the blood pressure-lowering effects of ACE Inhibitors
• Diuretics. When patients using diuretics start taking ACE inhibitors, their blood pressure may drop too low. Preventing excessive blood pressure decrease may require stopping the diuretic or increasing salt consumption before starting the ACE inhibitor. If the diuretic cannot be stopped, close supervision for at least two hours after starting ACE inhibitors and until blood pressure is stable is recommended.
• Angiotensin receptor blockers (ARBs). ACE inhibitors and ARBs should never be taken together since they raise the risk of hypotension, hyperkalemia, and renal impairment.
• Other blood pressure medications. Ace inhibitors should not be used with another kind of blood pressure medication, because this increases the risk of renal failure, extremely low blood pressure, and hyperkalemia.
• Hypoglycemic medications. Controlling blood pressure and blood glucose levels are essential for avoiding diabetic nephropathy and its consequences. Because ACE inhibitors are known to minimize the risk of developing end-stage renal disease, they are rarely used for diabetic nephropathy patients.

• Gold sodium aurothiomalate. When gold sodium aurothiomalate injection used in the treatment of rheumatoid arthritis, is combined with ACE inhibitors, nitritoid reactions symptoms include facial flushing, nausea, vomiting and low blood pressure may occur.

Precautions when taking ACE Inhibitors

Although ACE inhibitors are effective in the treatment of a variety of disorders, the medication is not suggested for patients who have had a severe reaction in the past.

Patients with a history of angioedema or hypersensitivity to this class of medications should avoid taking ACE inhibitors. Angioedema (severe airway swelling) is a symptom of ACE inhibitor hypersensitivity responses, which can be life-threatening if the respiratory pathways are compromised.

Ace Inhibitors Nursing Considerations for patients

• Instruct the patient that ACE inhibitors should be taken one hour before meals on an empty stomach.
• Advise the patient to strictly follow the advice of the healthcare provider for how often to take the medicine, the prescribed number of dosages to be taken each day, the period between doses, and the length of time the medication should be taken will all be determined by the type of ACE inhibitor recommended as well as the patient’s medical condition.
• Educate the patient that when taking ACE inhibitors, avoid using salt substitutes. Potassium is present in salt alternatives, and ACE inhibitors induce the body to retain potassium. Discuss with the patient the importance of learning how to read food labels to select foods that are low in sodium and potassium and if possible, it is best to consult with a dietitian to assist in making the best food choices.
• Advise the patient to avoid over-the-counter nonsteroidal anti-inflammatory medications (NSAIDs). Explain to the patient that NSAIDs causes the body to retain sodium and water, and minimize the effect of an ACE inhibitor, It is best to consult with the healthcare provider before taking any anti-inflammatory medications.
• Monitor the patient’s blood pressure and kidney function regularly, as advised by the healthcare provider, while taking ACE Inhibitors.
• Instruct the patient to never stop taking the medication without discussing the concern to the healthcare provider, even if the patient is feeling that the medicine is not working. If the patient is taking ACE inhibitors for heart failure, discuss with the patient that the heart failure symptoms may not improve right away. However, long-term use of ACE inhibitors helps manage chronic heart failure and reduces the risk that the condition will become worse.
• Document any unfavorable reaction of the patient to any ACE inhibitors, to avoid future exposure to the medication.
• Women of childbearing age should be advised not to get pregnant due to an increased risk of malformations and birth defects that can be caused by ACEI use.
• Pregnant patients should be advised not to take an ACE inhibitor because it lowers blood pressure and may cause kidney failure or high potassium levels in the blood.
• Instruct the patient that when starting the medication, it is important to foresee potential complications and inform the patient to improve compliance and decrease anxiety associated with the introduction of a new medicine.
• Advise the patient to report any untoward reaction to the medication.
• If the patient has developed a cough while taking the medication, Assess the cause, duration and characteristic of the patient’s cough and advise the patient to seek consultation.

Nursing Care Plan for Patients on ACE inhibitors

• Possible Ace Inhibitors Nursing Diagnoses
  • Risk for Impaired Renal Perfusion related to the mechanism of action of ACE inhibitors
  • Risk for Electrolyte Imbalance (Hyperkalemia) related to side effect of ACE inhibitors
  • Fatigue related to side effect of ACE inhibitors
  • Deficient Knowledge related to ACE inhibitors

Nursing Assessment

Nursing Planning and Intervention

Nursing Evaluation

Nursing References

Ackley, B. J., Ladwig, G. B., Makic, M. B., Martinez-Kratz, M. R., & Zanotti, M. (2020). Nursing diagnoses handbook: An evidence-based guide to planning care. St. Louis, MO: Elsevier.  Buy on Amazon

Gulanick, M., & Myers, J. L. (2022). Nursing care plans: Diagnoses, interventions, & outcomes. St. Louis, MO: Elsevier. Buy on Amazon

Ignatavicius, D. D., Workman, M. L., Rebar, C. R., & Heimgartner, N. M. (2018). Medical-surgical nursing: Concepts for interprofessional collaborative care. St. Louis, MO: Elsevier.  Buy on Amazon

Silvestri, L. A. (2020). Saunders comprehensive review for the NCLEX-RN examination. St. Louis, MO: Elsevier.  Buy on Amazon

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