Through this discussion, the student will demonstrate the ability to:
Explain the pathophysiology of heart failure by analyzing a patient’s symptoms. (CO1)
Differentiate between systolic and diastolic heart failure. (CO1)
Explain the significance of physical exam and diagnostic findings in the diagnosis of heart failure. (CO4)
Read the case study below.
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.
Respond to at least one peer and all faculty questions directed at you, using appropriate resources, before Sun., 11:59 pm MT.
- 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)
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
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.
here is the first response neededChristian Laine5:31pmSep 7 at 5:31pmManage Discussion EntrySystolic and Diastolic Heart Failure Systolic and diastolic heart failure are both due to dysfunctions of the left ventricle. Systolic and diastolic heart failure can occur individually or together (McCance & Huether, 2019). Systolic heart failure is heart failure with a reduced ejection fraction of less than forty percent and the inability of the heart to generate adequate cardiac output. Signs and symptoms of systolic heart failure include: dyspnea, orthopnea, cough of frothy sputum, decreased urine output, and edema. On physical examination the patient usually has pulmonary edema (cyanosis, inspiratory crackles, pleural effusions), hypotension or hypertension, an S3 gallop, and chest x-ray showing pulmonary congestion with cardiomegaly (McCance & Huether, 2019). Diastolic heart failure is heart failure with a preserved ejection fraction and can involve pulmonary congestion. In diastolic heart failure there is a decreased compliance of the left ventricle and abnormal diastolic relaxation (McCance & Huether, 2019). Signs and symptoms of diastolic heart failure include dyspnea on exertion and fatigue. If symptoms are severe then a physical exam may show some pulmonary edema such as inspiratory crackles and pleural effusions. Physical findings also include S4 gallop, chest x-ray showing pulmonary congestion without cardiomegaly and electrocardiography showing left ventricular hypertrophy (McCance & Huether, 2019). Case Study Patient The subjective and objective findings lead to a diagnosis of systolic heart failure. The patient’s subjective symptoms were shortness of breath worsening with activity and propping himself up at night to be able to sleep/ breath (orthopnea). The physical findings include inspiratory crackles in bilateral bases, bilateral pretibial and ankle 2+ pitting edema, and S3 heart sound. All of these findings are positive signs of systolic heart failure, however the number one telling sign that the patient is in systolic heart failure is that his ejection fraction is 25%. Pathophysiology of Symptoms Dyspnea on Exertion Dyspnea on exertion is caused by failure of the left ventricular output to rise during exercise, resulting in an increase in pulmonary venous pressure. Pitting Edema The two basic steps involved in edema formation are alterations in the capillary hemodynamics that favors the leakage of fluid from the vascular compartment into the interstitium and renal retention of sodium and water by the kidneys via the renin-angiotensin-aldosterone system as a compensatory mechanism (Goyle et al., 2022). Any obstruction or expansion in plasma volume leads to an increase in the hydrostatic pressure that predisposes to edema. Jugular Vein Distention When right heart failure occurs in the absence of left heart failure, it is caused most commonly by pulmonary hypertension resulting from diffuse hypoxic pulmonary disease. This in turn will cause diastolic and systolic deterioration and will dilate and fail. When this happens, pressure will rise in the systemic venous circulation, resulting in jugular venous distention. (McCance & Huether, 2019). Orthopnea The clinical manifestations of systolic heart failure are the result of pulmonary vascular congestion and inadequate perfusion of the systemic circulation (McCance & Huether, 2019). Orthopnea occurs during heart failure when an individual is recumbent, which causes the abdominal contents to exert pressure on the diaphragm and decreases the efficiency of the respiratory muscles (McCance & Huether, 2019). Significance of S3 Heart Sound and Ejection Fraction The third heart sound is the initial clue suggesting left heart failure and is associated with a low ejection fraction, restrictive diastolic filling, and cardiovascular mortality (Shono et al., 2019). A S3 heart sound reflects rapid left ventricular distention along with an increased atrioventricular flow. Meaning that the ventricles are dysfunctioning and there is volume overload. The ejection fraction is the amount of blood the left ventricle pumps out with each beat. An amount of sixty percent means that sixty percent of the total amount of blood is pushed out through the left ventricle with each heartbeat. A normal ejection fraction may be between fifty and seventy percent (American Heart Association, 2017). The ejection fraction is increased by factors that increase contractility. A decrease in ejection fraction may indicate ventricular failure (McCance & Huether, 2019). Therefore, an ejection fraction of 25% means that the heart is poorly pumping and less oxygen rich blood is pumping throughout the body. As stated above, an ejection fraction less than forty percent is indicative of systolic heart failure. ReferencesEjection Fraction Heart Failure Measurement. (2017). American Heart Association. https://www.heart.org/en/health-topics/heart-failure/diagnosing-heart-failure/ejection-fraction-heart-failure-measurement (Links to an external site.)Goyal, A., Cusick, A., Bhutta, B. (2022) Peripheral Edema. StatPearls https://www.ncbi.nlm.nih.gov/books/NBK554452/ (Links to an external site.) McCance, K.L. & Huether, S.E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Elsevier Health Sciences.Shono, A., Mori, S., Yatomi, A., Kamio, T., Sakai, J., Soga, F., Tanaka, H., Hirata, K. (2019). Ultimate Third Heart Sound. Intern Med. https://doi:10.2169/internalmedicine.2731-19
here is the second one :)Elena TimoftiYesterdaySep 6 at 8:03pmManage Discussion EntryHeart failure is defined as an inability of the heart to efficiently generate an adequate cardiac output and/or maintain a normal diastolic filling pressure (McCance & Huether, 2019). The left ventricular failure, or congestive heart failure, has two main types: the systolic heart failure, when ejection fraction of left ventricle is lower than 40%, and diastolic heart failure, when the ejection fraction is preserved.The main risk factors of the systolic heart failure include ischemic heart disease, hypertension, obesity, diabetes, renal failure, and valvular heart disease (McCance & Huether, 2019). In contrast, diastolic heart failure is usually caused by ventricular remodeling as a result of hypertension-induced hypertrophy or myocardial ischemia.In systolic heart failure, the stroke volume is decreased, which leads to a compromised perfusion of organs and tissues. The stroke volume may be affected by decreased myocardial contractility, increased preload, and afterload. The abnormal contractility is usually related to ventricular remodeling due to myocardial infarctions, myocarditis, or cardiomyopathies, and represents structural changes in myocardial calls and intracellular structure, resulting in progressive contractile dysfunction. Increased plasma volume and residual blood in the left ventricle after inefficient systole cause increased left ventricular end-diastolic volume (LVEDV) and ventricular dilation. Increased peripheral vascular resistance due to hypertension, or valvular heart disease may lead to increased afterload, increasing workload for the left ventricle and oxygen demand of the heart muscle. The increased afterload is also promoting hypertrophy and myocardial remodeling, further compromising heart contractility. The ineffective tissue perfusion activates the renin-angiotensin-aldosterone cascade and sympathetic nervous system, resulting in vasoconstriction, increase in heart rate and blood pressure, sodium and water retention, cardiac hypertrophy, dysrhythmias, and myocardial remodeling (McCance & Huether, 2019).The diastolic heart failure is characterized by decreased left ventricle compliance and abnormal diastolic relaxation (lusitropy), related to myocardial structure changes, such as alterations of collagen, myocyte skeleton, calcium transport, and endothelial dysfunction. The decreased ventricular compliance and lusitropy cause the resistance to the blood flow filling left ventricle during diastole and leads to the increased left ventricle end-diastolic pressure (LVEDDP), while the LVEDV remains normal. The increased pressure promotes atrial hypertrophy and enlargement, as well as a consequent increases in pressure within pulmonary circulation, causing pulmonary hypertension, pulmonary edema, and even right ventricular failure (McCance & Huether, 2019).In the presented case study, the patient is in systolic heart failure, which is evidenced by recent MI, decreased EF 25%, typical clinical presentation, and objective findings.Subjective findingsDyspnea on exertion is caused by inadequate perfusion and general hypoxia as a result of decreased stroke volume due to compromised contractility (recent MI). In addition, dyspnea is related to pulmonary congestion and fluid accumulation in lungs. Also, increased respiration may be explained as a compensatory mechanism for mild acidosis that develops in hypoxic conditions.Pitting edema develops as result of sodium and water retention due to RAAS system activation, increased blood volume, and high venous capillary pressure. There factors promote fluid extravasation and edema formation. By gravity, edema develops in the dependent parts of the body (Harjola et al., 2017).Jugular vein distention reflects the increased pressure and blood volume in right side of the heart, which is characteristic for right-sided failure.Orthopnea is related to pulmonary congestion and fluid accumulation in lungs in the recumbent position.Objective findingsThe ejection fraction of 25% is an essential component of the systolic heart failure diagnosis since it confirms the inadequate stroke volume of the heart.The 3rd heart sound is also a typical sign of the systolic heart failure. S3 stems from left ventricular wall disfunction or overload in the early rapid filling phase.ReferencesHarjola, Mullens, W., Banaszewski, M., Bauersachs, J., Brunner-La Rocca, H.-P., Chioncel, O., Collins, S. P., Doehner, W., Filippatos, G. S., Flammer, A. J., Fuhrmann, V., Lainscak, M., Lassus, J., Legrand, M., Masip, J., Mueller, C., Papp, Z., Parissis, J., Platz, E., Mebazaa, A. (2017). Organ dysfunction, injury and failure in acute heart failure: from pathophysiology to diagnosis and management. A review on behalf of the Acute Heart Failure Committee of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC). European Journal of Heart Failure, 19(7), 821836. https://doi.org/10.1002/ejhf.872 (Links to an external site.)McCance, K.L. & Huether, S.E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Elsevier Health Sciences.