Assignment: Week 2 Pathophysiology of Heart Failure

 Assignment: Week 2 Pathophysiology of Heart Failure

Purpose
The purpose of the graded collaborative discussions is to engage faculty and students in an interactive dialogue to assist the student in organizing, integrating, applying, and critically appraising knowledge regarding advanced nursing practice. Scholarly information obtained from credible sources as well as professional communication are required. Application of information to professional experiences promotes the analysis and use of principles, knowledge, and information learned and related to real-life professional situations. Meaningful dialogue among faculty and students fosters the development of a learning community as ideas, perspectives, and knowledge are shared.

BUY A CUSTOM PAPER HERE ON; Assignment: Week 2 Pathophysiology of Heart Failure

Activity Learning Outcomes
Through this discussion, the student will demonstrate the ability to:
1. Explain the pathophysiology of heart failure by analyzing a patient\’s symptoms. (CO1)
2. Differentiate between systolic and diastolic heart failure. (CO1)
3. Explain the significance of physical exam and diagnostic findings in the diagnosis of heart failure. (CO4)
Requirements:
1. Read the case study below.
2. In your initial discussion post, answer the questions related to the case scenario and support your response with at least one evidence-based reference by Wed., 11:59 pm MT.
3. Provides a minimum of two responses weekly on separate days; e.g., replies to a post from a peer; AND faculty member’s question; OR two peers if no faculty question using appropriate resources, before Sun., 11:59 pm MT.
Case Scenario:
A 72-year-old male presents to the primary care office with shortness of breath, leg swelling, and fatigue. He reports that he stopped engaging in his daily walk with friends three weeks ago because of shortness of breath that became worse with activity. He decided to come to the office today because he is now propping up on at least 3 pillows at night to sleep. He tells the NP that he sometimes sleeps better in his recliner chair. PMH includes hypertension, hyperlipidemia and Type 2 diabetes.
Physical Exam:
BP 106/74 mmHg, Heart rate 110 beats per minute (bpm)
HEENT: Unremarkable
Lungs: Fine inspiratory crackles bilateral bases
Cardiac: S1 and S2 regular, rate and rhythm; presence of 3rd heart sound; jugular venous distention. Bilateral pretibial and ankle 2+pitting edema noted
ECG: Sinus rhythm at 110 bpm
Echocardiogram: decreased wall motion of the anterior wall of the heart and an ejection fraction of 25%
Diagnosis: Heart failure, secondary to silent MI
Discussion Questions:
• Differentiate between systolic and diastolic heart failure.
• State whether the patient is in systolic or diastolic heart failure.
• Explain the pathophysiology associated with each of the following symptoms: dyspnea on exertion, pitting edema, jugular vein distention, and orthopnea.
• Explain the significance of the presence of a 3rd heart sound and ejection fraction of 25%.

 Assignment: Week 2 Pathophysiology of Heart Failure Sample

Nurse practitioners have the mandate, knowledge, and skills to diagnose and manage patient conditions. They must analyze patient presentations and assessment results to diagnose and manage a patient appropriately. Differentiating closely related conditions requires knowledge of the two and the ability to integrate assessment results. An accurate diagnosis promotes faster patient recovery and eliminates the delays that occur when patients are wrongly diagnosed hence delayed treatment. This essay analyses a case study that diagnoses the patient and explains the difference and the significance of the review of symptoms, patient history, and physical assessment results.

ORDER A PLAGIARISM-FREE PAPER HERE ON; Assignment: Week 2 Pathophysiology of Heart Failure

Differences Between Systolic and Diastolic Heart Failure.

Systolic and diastolic heart failure can occur on either side of the heart. Systolic heart failure occurs when the left ventricle is weak and flabby; hence it cannot contract effectively. Systolic heart failure presents with decreased blood supply to the body and organs and retention of fluid in the lung or body tissues because the blood cannot be effectively pumped out of the heart, and thus, inflow is limited (Cross et al., 2019). In diastolic heart failure, the ventricles cannot relax effectively and thus fail to fill up adequately. The ventricle pump is adequate; hence ejection fraction is not affected like in systolic heart failure. Diastolic heart failure results from disorders such as the growth of fibrous tissues in the ventricle following myocardial infarction and other fibrous tissues forming conditions that prevent the heart from contracting adequately (Plitt et al., 2018).

Patients Condition

The patient in this case study has systolic heart failure secondary to myocardial infarction. The patient presents with respiratory presentations and other clinical symptoms typical of systolic heart failure.

Significance of the Presence Of a 3rd Heart Sound and Ejection Fraction Of 25%

In systolic heart failure, the ventricles do not contract adequately despite the ventricle filling adequately. Katz (2018) notes that poor ventricular contraction produces little force, and only a small volume of blood is pumped out of the heart. The decreased contraction strength accounts for the 25% ejection fraction. The heart tries to compensate for the decreased cardiac output by increasing the heartbeat rate. The decreased blood pump force causes the auricles to overflow, and the ventricles fill with pressure (ventricular filling pressure), producing the S3 sound or murmur (Murphy et al., 2020). The sound is more prominent in left-sided systolic heart failure. S4 can be auscultated in individuals with diastolic heart failure. S4, also atrial gallop, occurs when the auricle force blood into the ventricle with relaxing problems. S3 and decreased ejection fraction are thus typical of systolic heart failure.

Pathophysiology Associated with Dyspnea on Exertion, Pitting Edema, Jugular Vein Distention, and Orthopnea

Systolic heart failure means that blood is not circulating as it should be hence hypoxia. The ventricles are weak and do not pump blood as required. Blood flow into the auricle is also interfered with overflow and is thus retained in the respective tissues, depending on the side of the heart affected (Katz, 2018). Fluid can accumulate in the lungs of the rest of the body tissues. On the right side, the blood accumulates in tissues hence fluid retention in the tissues hence pitting edema. Pitting edema occurs when tissues swell after the accumulation of fluids. The tissue contents can be displaced when pressure is applied because the water is in the interstitial spaces and intravascular compartment instead of fluid accumulation in the cells hence pitting edema.

Unlike other tissues, blood accumulation in the brain is highly regulated, and blood flow resistance causes blood accumulation in the veins. The most remarkable vein is the jugular vein which is stretched by the high blood volume and markedly distended. Most of the other significant veins are not visible. Palacio et al. (2020) note that jugular vein distension is a hallmark and distinguishing heart failure symptom. With left-sided systolic heart failure, the left ventricle does not supply enough blood to the tissues hence hypoxia. Due to the decreased blood supply to the tissues, the Sino atria node stimulates the heart to increase its pace, causing tachycardia and ventricular hypertrophy. The action causes fatigue. Fatigue, hypoxia, and lung tissue involvement are responsible for orthopnea and dyspnea on exertion (Palacio et al., 2020). Heart failure produces symptoms that could be mistaken for respiratory conditions without a good assessment.

Hypoxia and decreased blood supply to the kidneys stimulate it to increase fluid retention. People experience dyspnea on exertion, and activity is highly decreased. A severe disease could lead to syncope and death due to decreased blood supply to the brain. Cross et al. (2020) note that blood accumulates in the lung vessels due to the decreased pumping, and fluid retained in the tissue accumulates in the alveoli hence the crackles and other respiratory symptoms. The condition can be adequately managed, but an accurate diagnosis using additional tests such as EKG and cardiac troponins is vital.

Conclusion

Heart failure is a group of conditions categorized into right or left-sided heart failure or diastolic heart failure. Diastolic and systolic heart failure are distinguished by presenting symptoms such as the presence of S3 and S4 and changes in the ejection fractures. Other organ systems’ structural and physiological changes and involvement are responsible for the presenting symptoms. An understanding of the pathophysiology of heart failure helps the healthcare provider understand the presentation.

 References

Cross, T. J., Kim, C. H., Johnson, B. D., & Lalande, S. (2020). The interactions between respiratory and cardiovascular systems in systolic heart failure. Journal of Applied Physiology, 128(1), 214-224. https://doi.org/10.1152/japplphysiol.00113.2019

Katz, S. D. (2018). Pathophysiology of chronic systolic heart failure. A view from the periphery. Annals of the American Thoracic Society, 15(Supplement 1), S38-S41. https://doi.org/10.1513/AnnalsATS.201710-789KV

Murphy, S. P., Ibrahim, N. E., & Januzzi, J. L. (2020). Heart failure with reduced ejection fraction: a review. JAMA, 324(5), 488-504. https://doi.org/10.1001/jama.2020.10262

Palacio, A., Machuca, M., Tamariz, L., Team, G., Ropero, G., Vallejo, C., Rendon, L., & Palacio, A. (2020). Physical signs and symptoms predict diastolic and systolic function in heart failure patients. Journal of the American College of Cardiology, 75(11_Supplement_1), 1027-1027. https://doi.org/10.1016/S0735-1097(20)31654-5

Plitt, G. D., Spring, J. T., Moulton, M. J., & Agrawal, D. K. (2018). Mechanisms, diagnosis, and treatment of heart failure with preserved ejection fraction and diastolic dysfunction. Expert Review Of Cardiovascular Therapy, 16(8), 579-589. https://doi.org/10.1080/14779072.2018.1497485