systolic and diastolic heart failure

First peer response

….. Please respond to these 2 post and not the samples…..

Professor and class,


Differentiate between systolic and diastolic heart failure

Zhang et al (2019) describe heart failure as the heart’s inability to transport enough blood to meet the body’s demand at normal filling pressures resulting in a complex and severe disease syndrome. Systolic heart failure is referred to as heart failure with reduced ejection fraction HFrEF. This occurs when the heart’s ejection fraction pumps below 45% ( McCance & Huether, 2019). According to Zhang et al (2019), HFrEF results from cell death due to lack of oxygen and nutrients to the cell as well as the build up of metabolites from cell processes. Diastolic heart failure HFpEF occurs due to fibrosis and decreased ventricular compliance along with ventricular relaxation ( Zhang et al 20219). Heart failure with preserved ejection fraction is pulmonary congestion in the presence of a normal stroke volume and normal cardiac output (McCance & Huether, 2019). The American Heart Association, in an article written by Pfeffer et al (2019) defined HFpEF as those individuals who have heart failure with an ejection fraction in the midrange of 40% but below 50% ( Pfeffer et al., 2019).

State whether the patient is in systolic or diastolic heart failure

I believe that the patient is in systolic heart failure HFrEF because of the result of his echocardiogram showing an ejection fraction of 25%. Moreover, the patient has two other medical history that puts him at risk for this type of heart failure; hypertension and type 2 diabetes. He also has a new diagnosis of MI which is the most common cause of decreased contractility ( McCance & Huether, 2019). Furthermore, individuals with HFrEF or systolic heart failure will present with crackles, dyspnea and S3 gallop ( McCance & Huether, 2019).

Explain the pathophysiology associated with each of the following symptoms: dyspnea on exertion, pitting edema, jugular vein distention, and orthopnea.

As a result of the decrease in contractility due to presence of MI, an inflammatory response results from the release of neurohumoral activation (McCance & Huether, 2019). The neurohumoral activation releases a cascade of sympathetic nervous system (SNS) and renin angiotensin aldosterone system (RAAS). The kidneys retain sodium and water (McCance & Huether, 2019). The combined activation of the system leads to ventricular remodeling which further weakens the heart’s ability to maintain adequate contractility (McCance & Huether, 2019). As a result, stroke volume decreases while there is an increase in left ventricular end-diastolic volume (LVEDV), leading to an increase in preload (McCance& Huether, 2019). The combination of increase in preload and the heart’s inability to contract effectively, diminishes the supply to the kidneys exacerbating the RAAS and SNS response (McCance & Huether, 2019). The increasing preload results in a lack of adequate blood supply to the body and diminished oxygen which leads to dyspnea on exertion. Pitting edema results as part of the cascade of hormone release. Arginine vasopressin causes both peripheral vasoconstriction and retention of renal fluid resulting in edema (McCance & Huether, 2019). The inadequate pumping action of the heart results in low blood pressure, forcing the heart to pump harder to meet demand as evidenced by distended jugular distension and a low BP of 106/74 and an elevated HR 110 bpm. Decreased contractility of the heart leads to peripheral vascular resistance associated with vaso-congestion (McCance & Huether, 2019), this action is evidenced by fluid build up in the lower extremities of heart failure patients. When patients with heart failure attempt to lie down, the accumulated fluid in the legs returns into circulation thereby resulting in overload and shortness of breath.

Explain the significance of the presence of a 3rd heart sound and ejection fraction of 25%.

The 3rd heart sound, ventricular gallop, occurs after S2 when the atrioventricular valves open and blood flows rapidly from the atria into the left ventricle (Higgins, 2019). Calcium transport into, out of and into the myocytes is impaired due to changes in the intracellular transport mechanisms. This causes a decrease in myocardial contractility and the heart resulting in a decreased ejection fraction ( McCance & Huether, 2019). A patient with decreased ejection fraction will be very weak and fatigued from lack of oxygen perfusion. They often present with limited activity tolerance.

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