Topic 5-6 Discussion

Q-1

Chief complaints: Chest pain.

HPI:- Mrs. Rosetti, a 78-year-old male with PMH HTN, angina for years, and hyperlipidemia is c/o of Intermittent chest and left arm pain for several years with exertion and past 3 days on awakening and several times a day even at rest, worst with activity and better with rest or nitro pills. The pain is burning or a hot sensation in the left side of the chest radiating to the left arm with numbness or tingling sensation in the left arm and hands. Recently for 3 days, pain is getting more often and lasting longer, and rest is not relieving pain.

Family history: - Parents died at a younger age at an unknown cause, sisters 2 died with TB, 3 brothers died at age 60-90 age, and no one in the family had a stroke, diabetes pr cancer.

Social and personal history: - Retired and living with wife, 3 children grown up and moved out, one daughter lives close by, no major stress in the day-to-day life. Diet and extra weight may be contributed to it. drink 2 beers a week, occasional soda, trying to cut down salt and cholesterol, Not exercise, work around the house,

Immunization history: - Not taking any shots, The other surgical histories.

Home medications: - No medication allergy, Taking Procardia XL 60 mg q day for blood pressure, Isordil Tembids 40 mg tid for CP, Nitro PRN.

Physical exam: - 5’4’’, 198 lbs., BMI-34, BP140/70, HR-112, TEM-97.2, RESP-20, RHYTHM -Regular, No JVD, No tenderness. No palpitation or irregularity was noted, urinary frequency and hesitancy were reported.

Diagnostic tests: - EKG Sinus rhythm without any ST changes with PACs.

CXR: - with costophrenic angle on right not visible,

Lab tests: CBC and chemistry unremarkable, Lipid Panel-Cholesterol 283, VLDL-44. LDL-191, HDL-48, Triglyceride, 220 mg/dL, TSH-1.9. Trop-0.3 ng/dl.

Stress Thallium Myocardial Scan: -There is marked ischemia at the lateral wall extending to the diaphragmatic wall with prominent reversibility at rest. Mild reversible ischemia is seen at the anterior wall and apex. The perfused portion of the myocardium is the septum. EKG 5 years ago showed inferior and lateral changes on exercise to stage 2 of the Bruce protocol and was treated medically.

Carotid Angiogram: - Normal vascular anatomy, with no evidence of stenosis, aneurysm, or other arteriovenous malformation.

Based on your initial patient consultation, provide three differential diagnoses.

My three differential diagnoses will be

1. NSTEMI (non-ST elevation myocardial infarction) with acute coronary syndrome

2. Hypertension

3. Hyperlipidemia

Describe the patient's workup and treatment plan.

1. NSTEMI with acute coronary artery syndrome

The EKG tracing is not clear enough to me to read maybe a possible ST elevation in V1, V2, and V3 leads (arterio-septal wall). sinus rhythm with PACs with or without ST changes. The stress test is positive with marked ischemia at the lateral wall extending to the diaphragmatic was with prominent reversibility at rest which explains the patient is getting symptom relief at rest, mild ischemia at the anterior wall and apex. He has positive risk factors of HTN, ischemic heart disease with anginal episodes and hyperlipidemia, and being overweight with a BMI of 34.

Treatment plan

· Admit the patient to a telemetry unit with cardiac monitoring for new heart block development with strict bed rest and keep NPO for possible cardiac catheterization.

· EKG now to confirm any ST changes and repeat in 1 hour after.

· Institute MONA treatment, morphine to control chest pain as well as it helps to relax vascular smooth muscles, oxygen to keep saturation above 92%, nitroglycerin sublingual up to 3 tablets if not taken before and 325 mg PO aspirin and continue home Isordil Tembids 40 mg tid for CP.

· His workup was showed with negative troponin, will repeat serial cardiac enzymes 6 hours apart x 3 since the patient has positive symptoms

· Consult cardiology for cardiac catheterization and possible intervention.

· Lovenox 30mg SQ loading dose and 1mg/kg q 12H and monitor therapeutic coagulation values (Larson, German, Shatzel, & DeLoughery, 2019).

· Continue medical management for hypertension and start aggressive statin therapy for hyperlipidemia.

 

1. Hypertension: -  Known history of HTN on medications, Patient’s Bp 140/70 and tachycardia 112.

Treatment plan

· Will continue home medication Procardia XL 60 mg PO Q Day which is a calcium channel blocker extended-release, a peripheral arterial vasodilator, and acts on vascular smooth muscles. The new JNC-8 guideline for hypertension for patients over 60 years or older is the target BP is 150/90 (Fernandes, & Rikkert, 2019).

· -1.5 gm sodium-restricted diet, and a DASH dietary pattern which is a Diet rich in fruits, vegetables, whole grains, and low-fat dairy products with reduced content of saturated and total fat and a diet rich in potassium (Bakris, Ali, & Parati, 2019).

· encourage physical activity as possible if chest pain-free.

· Consult a dietician for active weight reduction management. Ideal body weight is the best goal but ≥1 kg reduction in body weight for most adults who are overweight (Bakris, Ali, & Parati, 2019).

 

1. Hyperlipidemia - The patient’s lipid panel showed high cholesterol with high LDL and HDL and triglyceride (Cholesterol 283, VLDL-44. LDL-191, HDL-48, Triglyceride, 220 mg/dL). The patient is also overweight with a BMI of 34.

Treatment plan

· Start Statin therapy Atorvastatin 80 mg PO q hs. Studies showed moderate-intensity and high-intensity statin therapy has shown benefits in reducing the risk of atherosclerotic cardiovascular disease in both primary and secondary prevention (Adhyaru, & Jacobson, 2018).

· Aggressive weight reduction therapy by consulting dietician.

· Encourage physical activity as tolerated

· Follow up for lipid panel and LFT in 3 months and further review and report any increasing muscle aches. Although hepatotoxicity has been a concern when using statin therapy, data suggest that statins are safe and that levels of liver enzymes do not need to be checked routinely (Adhyaru, & Jacobson, 2018).

· Prophylactic thromboembolism interventions such as pneumatic compression devices and chemical prophylaxis with a loading dose of Plavix and 75 mg PO after the procedure up to 6 months for patients who had a drug illuding stent placed (Larson, German, Shatzel, & DeLoughery, 2019).

After reviewing the patient's workup, discuss the final diagnosis.

My final diagnosis for this patient is  NSTEMI with the acute coronary syndrome.  Antiplatelet and anticoagulant therapies are mainstays of treatment in NSTEMI with the acute coronary syndrome to slow or stabilize thrombus growth and reduce myocardial damage (Larson, German, Shatzel, & DeLoughery, 2019).  Having an established diagnosis of hypertension and ischemic heart disease with intermittent anginal episodes,  elevated BMI and another lifestyle risk such as poor diet and exercise and moderate alcohol use all contributes high risk for cardiovascular events for this patient. The plan is to continue medical therapy for hypertension control (keep BP under 150/90) with calcium channel blocker, statin therapy for hyperlipidemia, Aspirin, antiplatelet agents (Plavix) if any metallic stent or drug illuding stents are placed as PCI, and weight reduction and a planned exercise program will be an ideal therapy for this patient.

Discuss potential ongoing problems for which you should monitor .

This patient is at high risk for CVS events such as thromboembolism, MI, stroke, patient needs to be educated and counseled regarding this high risk of these complications and counseling regarding prevention and management. The strict medical management by continuing medications such as antihypertensives, statin therapy, aspirin, Plavix and its benefits. The side effects to be discussed in detail such as muscle aches, elevated liver enzymes with statin therapy, heart failure symptoms with beta-blockers or calcium channel blockers, bleeding risk to watch for with aspirin and Plavix. Follow-up appointments, blood tests, and review of management are also an important part of disease management.

Support your answer with two or three peer-reviewed resources.

Reference.

Adhyaru, B. B., & Jacobson, T. A. (2018). Safety and efficacy of statin therapy. Nature Reviews Cardiology, 15(12), 757-769. Retrieved from https://www.nature.com/articles/s41569-018-0098-5

Larson, E. A., German, D. M., Shatzel, J., & DeLoughery, T. G. (2019). Anticoagulation in the cardiac patient: A concise review. European journal of hematology, 102(1), 3-19. Retrieved from https://onlinelibrary.wiley.com/doi/full/10.1111/ejh.13171

Fernandes, M., & Rikkert, M. G. O. (2019). The new US and European guidelines in hypertension: A multi-dimensional analysis. Contemporary clinical trials, 81, 44-54. Retrieved from https://www.sciencedirect.com/science/article/pii/S1551714418307195

Bakris, G., Ali, W., & Parati, G. (2019). ACC/AHA versus ESC/ESH on hypertension guidelines: JACC guideline comparison. Journal of the American College of Cardiology, 73(23), 3018-3026. Retrieved from https://www.jacc.org/doi/full/10.1016/j.jacc.2019.03.507

Q-2

Cardiac Output

There are multiple factors that contribute to cardiac output such as; the heart can only pump out what comes back to it so, cardiac compliance, capacitance, stressed volume, and overall resistance to flow are important factors (Magder, 2016);(Nordmeyer et al., 2021). You can get the current cardiac output information as a number following the formula: Cardiac Output = (Stroke Volume X Heart Rate)/ 1000, and it falls within a normal range of 4-8 L per minute (Magder, 2016);(Nordmeyer et al., 2021).

Low Cardiac Output occurs when there is a decrease in perfusion from myocardial dysfunction, and the imbalance attributes to an overall metabolic acidosis (Yuichi et al., 2021). Metabolic acidosis also then increases the demand for oxygen due to the previous lack of perfusion, creating a cycling effect that worsens over time (Yuichi et al., 2021). This disease process closely resembles heart failure in its pathophysiology leading to some common differential diagnoses (Yuichi et al., 2021). Some differentials that contribute to low cardiac output include cardiogenic shock, hypovolemic shock, septic shock, and tachycardia arrhythmias (Yuichi et al., 2021). The decrease in cardiac output can be imagined by a decrease in cardiac return due to vasodilation from another underlying etiology (Yuichi et al., 2021).

High Cardiac Output is also a type of failure of the heart's normal function and can be categorized into two separate categories of an increase in demand for blood from an increase in metabolism, or there is a bypass of the arteriolar and capillary bed causing an increased flow into venous circulation from lack of resistance leading to increased oxygen demand (Harada et al., 2019). Metabolism etiologies can arise from hyperthyroidism, hypercontractility, tachycardia, and volume overload (Harada et al., 2019). There have been some links established from myeloproliferative disorders due to an increase in cellular metabolism and higher cell turnover rates (Harada et al., 2019). Myocardial etiologies arise from hyperthyroidism, sepsis, severe thiamine deficiency, and chronic lung disease (Harada et al., 2019).

Overall, low output and high output are usually responses by the heart from an underlying etiology that starts the initial issue. There can be compensations mechanisms that then develop such as cardiomyopathy in low cardiac output, but this in itself creates new issues in the future such as a decreasing ejection fracture from cardiomyopathy (Nordmeyer et al., 2019). Overall, the patient can exhibit signs and symptoms of low and high cardiac output, and the overall treatment is supportive with a focus on the underlying etiology (Nordmeyer et al., 2019).

References:

Harada, T., Obokata, M., Kurosawa, K., Sorimachi, H., Yoshida, K., Ishida, H., Ito, K., Ogawa, T., Ando, Y., Kurabayashi, M., & Negishi, K. (2019). Relationships of high cardiac output with ventricular morphology, myocardial energetics, and energy costs in hemodialysis patients with preserved ejection fraction. The International Journal of Cardiovascular Imaging, 35(3), 469–479.  https://doi-org.lopes.idm.oclc.org/10.1007/s10554-018-1472-4 Nordmeyer, S., Lee, C. B., Goubergrits, L., Knosalla, C., Berger, F., Falk, V., Ghorbani, N., Hireche-Chikaoui, H., Zhu, M., Kelle, S., Kuehne, T., & Kelm, M. (2021). Circulatory efficiency in patients with severe aortic valve stenosis before and after aortic valve replacement. Journal of Cardiovascular Magnetic Resonance (BioMed Central), 23(1), 1–14. Magder S. (2016). Volume and its relationship to cardiac output and venous return. Critical care (London, England), 20(1), 271.  https://doi.org/10.1186/s13054-016-1438-7 Yuichi, B, Toru, K., Yuri, O., Tatsuya, N., Naohito, Y., & Hiroaki, K. (2021). What is low cardiac output syndrome? A report of two cases. Critical Care & Shock, 24(3), 135–142.

Q-3

Pulmonary catheter is characterized as a catheter that is located in the heart. It measures the cardiac output or the cardiac index. It is consisting odd a proximal injectate lumen port, a PA distal port, a thermistor connector and a balloon- inflation port with valve (p. Mc Vay, 2017, p. 609). It can measure the pulmonary artery wedge pressure or the pulmonary capillary wedge pressure. The normal pulmonary artery pressure is 15-25 mmHg. The normal PA pressures can be elevated in patients who have PA hypertension, pulmonary disease, mitral valve disease, LV failure, atrial or ventricular left to right shunt, pulmonary emboli and hypervolemia (Mc Vay, 2017, p. 609). According to Mc Vay (2017), patients who have a low PA pressure are those who have low volume and low pulmonary vascular resistance or vasodilation. In my practice as a nurse, I have limited encounter with PA catheter and sure need to learn more on how to manage patients with Pulmonary catheter. I do remember watching an intensivist putting a pulmonary catheter in the unit and how they are looking to the different waveforms that represent the right atrium and pulmonary artery occlusion pressures with the continuous ECG and PA monitoring. The three waves that the physician look for is the a, c and v waves. The a waves is referred as the atrial contraction, the c waves reflects the closure of the atrioventricular valve and the v waves is defined as the reflection of the passive filling of the atria during ventricular systole(Mc Vay, 2017, p. 609).

The normal PAOP is 6-15 mmHg with a mean of 9 mmHg. For example, patients who have an elevated a wave in the PAOP waveform can happen in patients with mitral valve stenosis, acute LV ischemia, infarction, LV failure and AV dissociation (Mc Vay, 2017, p. 611). On the other hand, patients with pulmonic or tricuspid val;ve stenosis, RV ischemia or infarction, RV failure, PA hypertension and AV dissociation will show an elevated a waves in the central venous pressure (Mc Vay, 2017, p. 611).

Reference:

Mc Vay, R (2017). Pulmonary artery catheter insertion and pressure monitoring. D.L. Wiegand. AACN Procedure Manual for High Acuity, progressive and critical care (7th ed p. 609-629).