Decreased cardiac output is a synonymous term used for heart failure or heart insufficiency. In patients suffering from decreased cardiac output or heart failure, the amount of blood that vessels „offer” to the tissues is not enough for the metabolic demands. Decreased cardiac output means that heart can’t function at its proper parameters, even if the heart muscle labor increases and all types of compensating mechanisms are used.
How can doctors tell us if we have a decreased cardiac output?
Decreased cardiac output determines a diminished ejection fraction (a smaller amount of blood is delivered to the aorta and its branches) and can be discovered when your doctor performs an echocardiography. Measuring the ejection fraction periodically will offer information about the heart failure evolution, but is not always correlated with the severity of symptoms. For example, there are patients with severe decreased cardiac output (about 24%) that still can perform common activities without having shortness of breath, chest pain, palpitations or getting tired, while other patients with a higher ejection fraction (and therefore a higher cardiac output) have all the symptoms listed above.
Decreased cardiac output- clinical case report:
After the theoretical part of this article listed above is time to
pass to a more practical part, in order to understand what the decreased
cardiac output manifestations are and how it can affect people life and
daily activities.Next we will present a case of a 63 years old patient suffering from heart failure, with a decreased cardiac output, so we can have a better image of how life is for a person diagnosed with this disorder.
Case report:
A 63-year-old Caucasian man had a 40 years medical history of diabetes, treated with glyburide 10 mg twice/day. He was also known with coronary heart disease and heart failure (left ventricular ejection fraction 25% determined by echocardiogram, NYHA class II-III), hypercholesterolemia, and chronic renal insufficiency (serum creatinine 1.4-1.8 mg/dl). His drug therapy included aspirin 325 mg/day, digoxin 0.125 mg/day, simvastatin 20 mg at bedtime, metoprolol 50 mg twice/day, and nitroglycerin 0.4 mg sublingually as needed. At that clinic visit, the patient had no other complaints and his heart failure appeared stable. Nine days later he came to the clinic with an increase in weight of 3.6 kg (baseline weight 78.6 kg) complaining of shortness of breath. Physical examination revealed bibasilar rales (pulmonary sounds heard during breathing which may indicate infection, pulmonary edema, allergy or bleeding etc.), +S3 gallop (abnormal sound heart during heart auscultation, which indicates heart failure), and increased jugular venous distention (JVD-because right heart has a decreased function, blood will flow back into the veins that bring it into the heart chambers), but no lower extremity edema. Again, he reported adherence to drug therapy and no dietary indiscretions. After treatment adjustment he was released from the hospital, but returned 2 weeks later reporting that his weight increased, and legs edema occurred, while his wife confirmed he had a high sodium intake. Chest radiograph was consistent with pulmonary edema. Fluids were immediately restricted, and the patient was given bumetanide 5 mg intravenously twice/day. By hospital day 2 the patient had lost 4.1 kg by diuresis and on hospital day 5 his heart failure was stable.
In conclusion, decreased cardiac output is the main manifestation of heart failure and has a great impact in patients’ life (as we saw in the case above).
