Discussion Questions: Heart Failure
•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%.
Systolic heart failure is when the left ventricles of the heart cannot contract completely. The heart is unable to generate adequate cardiac output for perfusion. According to McCance, K. L., & Huether, S. E., systolic heart failure is heart failure with reduced ejection fraction (HRrEF) with an ejection fraction of less than 40% along with the inability of the heart to adequately produce cardiac output to perfuse vital tissues, (2019). The heart cannot pump forcefully enough to move blood throughout the body.
In diastolic heart failure, the left ventricles can no longer relax between heartbeats because the tissues have become stiff. Diastolic heart failure is defined as pulmonary congestion even though a patient may have a normal stroke volume and cardiac output, (McCance, K. L., & Huether, S. E., 2019). Diastolic heart failure is heart failure with preserved ejection fraction (HFpEF). When the heart cannot fully relax, the heart will not be able to fill up properly with blood before the next contraction.
In this case study, the patient is in systolic heart failure. In heart failure, a person’s heart is unable to generate adequate cardiac output by not being able to fill properly, or pump effectively. In this case study, we see that the patient’s ejection fraction is 25% which means the patient’s heart has the inability to provide adequate cardiac output to perfuse vital tissues, (McCance, K. L., & Huether, S. E., 2019).
Myocardial infarction is the most common cause of decreased contractility. This patient had a silent MI that caused his heart tissues to stiffen resulting in the heart to not fill properly.
Dyspnea is having difficulty breathing, and dyspnea on exertion is caused by failure of the left ventricular output to rise during exercise resulting in an increase of pulmonary venous pressure. This means the blood is back flowing into the lungs causing interstitial pulmonary edema, (McCance, K. L., & Huether, S. E., 2019). Since the heart cannot pump out enough blood from the lungs, pressure in the heart builds up
and pushes the extra fluid into the lungs’ alveoli making it difficult for the patient to breathe on exertion. This symptom also goes hand-in-hand with orthopnea. When the patient is laying down, this causes blood from the patient’s legs to flow back to the heart
and lungs. The heart is now working against gravity which increases pressure in the blood vessels of his lungs. The extra fluid in the lungs makes it difficult to breathe and usually patients will feel better when sitting propped up on a few pillows.
Jugular vein distention is a manifestation of abnormal right heart mechanics, most likely caused by elevated pulmonary pressure from left heart failure. This distention usually implies fluid overload. Just like how the blood cannot be moved out of
the lungs adequately, this also affects the right side of the heart including the superior vena cava, (McCance, K. L., & Huether, S. E., 2019). When the left ventricle is unable to pump adequately, fluid is then backed up into the lungs. Eventually this pressure will then weaken the right ventricle causing the distention of the jugular vein.
Pitting edema is when excess fluid builds up in the body causing it to swell. It usually occurs in the feet, ankles, and legs. Heart failure is one of causes for edema because as cardiac output begins to decline, renal perfusion diminishes that activates the Renin-Angiotensin-Aldosterone System (RAAS), (McCance, K. L., & Huether, S. E.,
2019). RAAS is a hormone system that regulates blood pressure and fluid balance. If the kidneys are not getting enough perfusion due to blood loss, dehydration, or ventricular pump failure the kidneys will then compensate for that loss by initiating a vasoconstrictor response and stimulate aldosterone synthesis by the adrenal gland, (Maron, B. A., & Leopold, J. A., 2016 ). Aldosterone acts on the renal tubules to initiate sodium and water retention to increase circulating blood volume and blood pressure.
Additionally, baroreceptors in the central circulation detect the decrease in perfusion and stimulate the sympathetic nervous system to further vasoconstric and to cause the hypothalamus to produce antidiuretic hormone, (McCance, K. L., & Huether, S. E., 2019). The increase of fluid, vasoconstriction, combined with the limit of sodium and water excretion forces the fluid to move extracellularly, causing pitting edema. If someone were to have real blood loss or experiencing dehydration, then activating RAAS would be beneficial. When it comes to patients with heart failure, RAAS creates a
vicious cycle of increasing preload and afterload. This makes the heart work even harder when it already has a decrease in contractility thus worsening of left heart failure, (McCance, K. L., & Huether, S. E., 2019).
The 3rd heart sound is also called the S3 or ventricular gallop. During the early diastolic phase, the atrial contracts to push blood into the ventricles. If there is volume overload, more blood pushes into the ventricles which causes a sudden opening of the mitral valve, (McCance, K. L., & Huether, S. E., 2019). In this case, with an ejection fraction of 25%, the heart cannot handle the increase of preload in between contractions, there is not enough contractility for blood to move adequately. When the mitral valves are forced open this causes the tensing of the chordae tendineae. This tensing of the chordae tendineae is what you hear in a 3rd heart sound, or in S3.
References
Maron, B. A., & Leopold, J. A. (2016). The Role of the Renin-Angiotensin-Aldosterone System in the Pathobiology of Pulmonary Arterial Hypertension. Pulmonary Circulation,
4(2), 200–210. https://doi.org/10.1086/675984
McCance, K. L., & Huether, S. E. (2019). In Pathophysiology: the biologic basis for disease in adults and children (8th ed.). Elsevier Health Sciences.
Describe the process or formation of pitting edema due to heart failure?
Hello Dr. Holsey,
•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%.
Systolic heart failure is when the left ventricles of the heart cannot contract completely. The heart is unable to generate adequate cardiac output for perfusion. According to McCance, K. L., & Huether, S. E., systolic heart failure is heart failure with reduced ejection fraction (HRrEF) with an ejection fraction of less than 40% along with the inability of the heart to adequately produce cardiac output to perfuse vital tissues, (2019). The heart cannot pump forcefully enough to move blood throughout the body.
In diastolic heart failure, the left ventricles can no longer relax between heartbeats because the tissues have become stiff. Diastolic heart failure is defined as pulmonary congestion even though a patient may have a normal stroke volume and cardiac output, (McCance, K. L., & Huether, S. E., 2019). Diastolic heart failure is heart failure with preserved ejection fraction (HFpEF). When the heart cannot fully relax, the heart will not be able to fill up properly with blood before the next contraction.
In this case study, the patient is in systolic heart failure. In heart failure, a person’s heart is unable to generate adequate cardiac output by not being able to fill properly, or pump effectively. In this case study, we see that the patient’s ejection fraction is 25% which means the patient’s heart has the inability to provide adequate cardiac output to perfuse vital tissues, (McCance, K. L., & Huether, S. E., 2019).
Myocardial infarction is the most common cause of decreased contractility. This patient had a silent MI that caused his heart tissues to stiffen resulting in the heart to not fill properly.
Dyspnea is having difficulty breathing, and dyspnea on exertion is caused by failure of the left ventricular output to rise during exercise resulting in an increase of pulmonary venous pressure. This means the blood is back flowing into the lungs causing interstitial pulmonary edema, (McCance, K. L., & Huether, S. E., 2019). Since the heart cannot pump out enough blood from the lungs, pressure in the heart builds up
and pushes the extra fluid into the lungs’ alveoli making it difficult for the patient to breathe on exertion. This symptom also goes hand-in-hand with orthopnea. When the patient is laying down, this causes blood from the patient’s legs to flow back to the heart
and lungs. The heart is now working against gravity which increases pressure in the blood vessels of his lungs. The extra fluid in the lungs makes it difficult to breathe and usually patients will feel better when sitting propped up on a few pillows.
Jugular vein distention is a manifestation of abnormal right heart mechanics, most likely caused by elevated pulmonary pressure from left heart failure. This distention usually implies fluid overload. Just like how the blood cannot be moved out of
the lungs adequately, this also affects the right side of the heart including the superior vena cava, (McCance, K. L., & Huether, S. E., 2019). When the left ventricle is unable to pump adequately, fluid is then backed up into the lungs. Eventually this pressure will then weaken the right ventricle causing the distention of the jugular vein.
Pitting edema is when excess fluid builds up in the body causing it to swell. It usually occurs in the feet, ankles, and legs. Heart failure is one of causes for edema because as cardiac output begins to decline, renal perfusion diminishes that activates the Renin-Angiotensin-Aldosterone System (RAAS), (McCance, K. L., & Huether, S. E.,
2019). RAAS is a hormone system that regulates blood pressure and fluid balance. If the kidneys are not getting enough perfusion due to blood loss, dehydration, or ventricular pump failure the kidneys will then compensate for that loss by initiating a vasoconstrictor response and stimulate aldosterone synthesis by the adrenal gland, (Maron, B. A., & Leopold, J. A., 2016 ). Aldosterone acts on the renal tubules to initiate sodium and water retention to increase circulating blood volume and blood pressure.
Additionally, baroreceptors in the central circulation detect the decrease in perfusion and stimulate the sympathetic nervous system to further vasoconstric and to cause the hypothalamus to produce antidiuretic hormone, (McCance, K. L., & Huether, S. E., 2019). The increase of fluid, vasoconstriction, combined with the limit of sodium and water excretion forces the fluid to move extracellularly, causing pitting edema. If someone were to have real blood loss or experiencing dehydration, then activating RAAS would be beneficial. When it comes to patients with heart failure, RAAS creates a
vicious cycle of increasing preload and afterload. This makes the heart work even harder when it already has a decrease in contractility thus worsening of left heart failure, (McCance, K. L., & Huether, S. E., 2019).
The 3rd heart sound is also called the S3 or ventricular gallop. During the early diastolic phase, the atrial contracts to push blood into the ventricles. If there is volume overload, more blood pushes into the ventricles which causes a sudden opening of the mitral valve, (McCance, K. L., & Huether, S. E., 2019). In this case, with an ejection fraction of 25%, the heart cannot handle the increase of preload in between contractions, there is not enough contractility for blood to move adequately. When the mitral valves are forced open this causes the tensing of the chordae tendineae. This tensing of the chordae tendineae is what you hear in a 3rd heart sound, or in S3.
References
Maron, B. A., & Leopold, J. A. (2016). The Role of the Renin-Angiotensin-Aldosterone System in the Pathobiology of Pulmonary Arterial Hypertension. Pulmonary Circulation,
4(2), 200–210. https://doi.org/10.1086/675984
McCance, K. L., & Huether, S. E. (2019). In Pathophysiology: the biologic basis for disease in adults and children (8th ed.). Elsevier Health Sciences.
Describe the process or formation of pitting edema due to heart failure?
Hello Dr. Holsey,
