Need help to reply three post.

DO NOT JUST REPEAT SAME INFORMATION, DO NOT JUST SAY I AGREE OR THINGS LIKE THAT. YOU NEED TO ADD NEW INFORMATION TO DISCUSSION.

1- Each reply should be at least 200 words.

2- One scholarly reference ( NO MAYO CLINIC/ AHA)

3- APA style needs to be followed.

4- Each response should have reference at the end

5- Reference should be within last 5 years

Need help to reply three post.

DO NOT JUST REPEAT SAME INFORMATION, DO NOT JUST SAY I AGREE OR THINGS LIKE THAT. YOU NEED TO ADD NEW INFORMATION TO DISCUSSION.

1-

Each reply should be at least 200 words.

2- One scholarly reference ( NO MAYO CLINIC/ AHA)

3- APA style needs to be followed.

4- Each response should have reference at the end

5- Reference should be within last 5 years

DQ1

Amiodarone is considered the most effective antiarrhythmic drug available today for the treatment of atrial fibrillation and ventricular arrhythmias (Srinivasan, Ahmad, Bhindi & Allahwala, 2019). Amiodarone is a potassium channel blocker and is able to prolong the cardiac action potential by slowing conduction and refractory periods of the SA and AV nodes, bundles of His, and Purkinje fibers (Srinivasan et al., 2019). This blocking of the potassium channel and slowing down conduction give Amiodarone its anti-arrhythmic properties and show its effective use in atrial fibrillation and ventricular tachycardia (Srinivasan et al., 2019).

With amiodarone’s anti-arrhythmic properties and its incredible effectiveness, it has become the number one choice for rhythm control in patients who experience atrial fibrillation and ventricular tachycardia (Vamos & Hohnloser, 2016). When compared to other anti-arrhythmic medications, amiodarone has the greatest potential of maintaining sinus rhythm once the patient converts (Vamos & Hohnloser, 2016). When a patient is experiencing an arrhythmia, the first step would be to obtain an EKG to confirm the type of rhythm, if it is atrial fibrillation or ventricular tachycardia then amiodarone would be indicated (Vamos & Hohnloser, 2016).

Monitoring of amiodarone consists of measuring the patient’s heart rate to ensure that there are no signs of bradyarrhythmias that are caused by overdosing of amiodarone (Srinivasan et al., 2019). An ECG should be measured as well due to amiodarone prolonging the QT interval and can interact with other drugs causing the same issue, possibly leading to an R on T phenomenon (Srinivasan et al., 2019).

As food interactions are concerned, patients need to avoid drinking grapefruit juice as it inhibits CYP3A4 which is also the enzyme responsible for metabolizing amiodarone leading to elevated serum levels (Srinivasan et al., 2019). Absorption of amiodarone is variable when following oral administration, and IV administration leads to 100% bioavailability (Srinivasan et al., 2019). Amiodarone has a half-life of 60-90 days when taken chronically by the oral route due to the body storing amiodarone in adipose tissue (Srinivasan et al., 2019).

References

:

Srinivasan, M., Ahmad, L., Bhindi, R., & Allahwala, U. (2019). Amiodarone in the aged. Australian Prescriber, 42(5), 158–162. https://doi-org.lopes.idm.oclc.org/10.18773/austprescr.2019.051

Vamos, M., & Hohnloser, S. H. (2016). Amiodarone and dronedarone: An update. Trends in Cardiovascular Medicine, 26(7), 597–602.

https://doi-org.lopes.idm.oclc.org/10.1016/j.tcm.2016.03.014

DQ-2

For this question, I selected Levophed or norepinephrine.

In the ICU setting, we receiving a lot of patients who have a variety of emergency medical issues present. Most of the time in the ICU I work it we see patients who are undergoing septic shock. Other diseases that can induce symptomatic hypotension are drug overdose, sepsis, hypovolemia, and hypovolemic shock, and hypotension with the use of sedation for mechanical ventilator management (Cheung et al., 2015). Levophed is used as a first-line vasoconstrictor and is administered via IV for its quick effect on the body (Cheung et al., 2015). Levophed is also the first line choice due to its fewer adverse side effects when compared to other vasoconstrictors like dopamine (Cheung et al., 2015).

Levophed’s mechanism of action is that it stimulates alpha 1 and 2 adrenergic receptors causing blood vessel constriction (Cheung et al., 2015). This constriction occurs systemically (Cheung et al., 2015). The constriction of the vessels increases blood pressure by decreasing the intra-vessel diameter (Cheung et al., 2015). Levophed also acts on beta 1 adrenergic receptors causing an increase in cardiac output and heart rate (Cheung et al., 2015). The vasoconstriction also reduces blood supply regardless of blood demand and causes increased heart and decreased blood supply to the kidneys as well (Cheung et al., 2015).

Levophed is indicated in patients who are experiencing symptomatic hypotension from a variety of disease processes (Duclos et al., 2019) (Cheung et al., 2015). The advantages of Levophed are that it is fast-acting and provides a systemic response and an overall increase in blood pressure (Duclos et al., 2019). Some disadvantages of Levophed include the increased cardiac oxygen demand not being met and could trigger a cardiac arrhythmia (Duclos et al., 2019). Another disadvantage comes from its potent vasoconstriction abilities (Duclos et al., 2019). Levophed causes such potent vasoconstriction that in the smaller vessels such as in the hands and toes, blood supply becomes very limited and almost cut off and the patient’s skin will begin to mottle (Duclos et al., 2019). This has coined the phrase “Levophed leaves them dead” because their skin begins to show signs of mottling and discoloration and they look like they have expired.

In the past, cultural and ethnic differences come into play when the family is first seeing the use of the medication and some side effects such as mottling. After careful explanation and expressing that the patient needs this medication to keep their blood pressure in good ranges to sustain life, most if not all family agrees with the usage of Levophed.

References:

Cheung, W. K., Chau, L. S., Laurinda Mak, I. I., Wong, M. Y., Wong, S. L., & Yee Tiwari, A. F. (2015). Clinical management for patients admitted to a critical care unit with severe sepsis or septic shock. Intensive and Critical Care Nursing, 31(6), 359–365. https://doi-org.lopes.idm.oclc.org/10.1016/j.iccn.2015.04.005

Duclos, G., Baumstarck, K., Dünser, M., Zieleskiewicz, L., & Leone, M. (2019). Effects of the discontinuation sequence of norepinephrine and vasopressin on hypotension incidence in patients with septic shock: A meta-analysis. Heart & Lung, 48(6), 560–565.

https://doi-org.lopes.idm.oclc.org/10.1016/j.hrtlng.2019.05.007

DQ-3

There are many drugs that affect the cardiovascular and renal systems, but one class of medications that has an effect on both systems is the angiotensin-converting enzyme inhibitors (ACEIs). ACEIs reduce the production of angiotensin II and aldosterone in the renin-angiotensin-aldosterone system (RAAS), which not only aids in lowering blood pressure but also helps with the adverse effects of diabetes on the kidneys (Robinson, 2016, p. 295). They also improve oxygenation and reduce cardiac remodeling after a heart attack or during heart failure (Robinson, 2016, p. 295). One such drug within this class of medications is Lisinopril. Lisinopril works by binding with and inhibiting the action of ACE, which block the conversion of angiotensin I to II, and reduces the secretion of aldosterone from angiotensin II activity (Lisinopril, 2020, para 1). In doing so it prevents vasoconstriction and increases sodium and water excretion from the kidneys, which both aid in reducing blood pressure. In patients with proteinuria, from diabetes related kidney disease, Lisinopril helps slow the progression of the disease state. It aids in reducing efferent arteriolar resistance in the glomeruli, reduces capillary pressure inside the glomeruli, stops hypertrophy of the glomeruli, and reduces the declining glomerular filtration rates (Robinson, 2016, p. 296). Contraindications for the use of Lisinopril include angioedema, pregnancy, and renal artery stenosis (Robinson, 2016, p. 297). Renal artery stenosis requires increased vascular pressure, and when reduced it can further damage renal arteries and reduce perfusion within the kidneys. In patients with hyperkalemia the use of Lisinopril should be withheld because this medication can worsen the electrolyte imbalance. Lisinopril is contraindicated in pregnancy because of the injury and death risk of the developing fetus from direct actions on the RAAS (Lisinopril, 2020, para 63). Angioedema can be life threatening due to airway constriction, and ACEIs can cause this phenomenon because of the bradykinin activity of inhibiting ACE (Robinson, 2016, p. 297). Drug interactions with Lisinopril include other antihypertensives due to their hypotensive effect, potassium supplements or potassium sparring diuretics due to the risk of hyperkalemia, and concurrent use of Lithium because of increased risk of Lithium toxicity (Robinson, 2016, p. 303). Other interactions include using Lisinopril with antidiabetic agents and with renal impairment due to hypoglycemia, and use with nonsteroidal anti-inflammatories due to the decreased efficiency of Lisinopril for hypertension management (Lisinopril, 2020, para 130). Dosage recommendations included starting at a low dose and also stopping diuretics for a few days to allow rehydration and prevents drastic declines in blood pressure (Robinson, 2016, p. 304). Switching to thiazide diuretics is also recommended if able due to the risk of hyperkalemia with other diuretics in combination with ACEIs (Robinson, 2016, p. 304). Increment increases within the first couple weeks, starting with a low dose, until target blood pressure is achieved is recommended. Monitoring includes blood pressure and pulse before initiating therapy and with dose changes, weight measurements, renal function labs, and potassium levels (Robinson, 2016, p. 307). If kidney function is too high then reducing the dose is recommended. Complete blood counts should also be monitored due to the risk of neutropenia from kidney disease, and if the neutrophil count is lower than 1,000/mm³ therapy should be stopped (Robinson, 2016, p. 308).

References

Lisinopril. (2020). Retrieved from the National Center for Biotechnology Information website: https://pubchem.ncbi.nlm.nih.gov/compound/Lisinopril

Robinson, M. V. (2016). Drugs affecting the cardiovascular and renal systems. In T. M. Woo & M. V. Robinson (Eds.), Pharmacotherapeutics for advanced practice nurse prescribers (pp. 3-10). Philadelphia, PA: F. A. Davis Company.