We have touched on multiple aspects of CHF in several blogs this year, including discussions of how it occurs—whether in the setting of systolic dysfunction or diastolic dysfunction—what its manifestations are, how it is treated, and most recently a look at cardiomyopathies and how they cause CHF. All of these aspects of CHF have one thing in common—the heart isn’t doing what it should be doing, either because it is too large, too thick, too stiff, or too weak. But there are times when CHF occurs with the heart essentially being an innocent bystander—in these situations, the heart is pumping out an elevated amount of blood. We call these states high-output heart failure.
High-output failure generally occurs when the body’s need for blood flow is abnormally elevated and the heart is stimulated to pump more in order to augment that increased demand. As with other situations where the organs and tissues aren’t getting enough blood flow, fluid retention occurs in an effort to help the heart pump harder, at the expense of increased pressures in the heart and lungs, leading to the types of symptoms we’ve discussed previously—shortness of breath and swelling.
I’ll touch on several causes of high-output failure—many have in common that the condition directly or indirectly leads to vasodilation (dilation of the arteries) or shunting (bypassing of blood flow before it reaches the capillary bed, which is where oxygen and nutrients are exchanged with individual cells in the body’s tissues). Vasodilation causes a drop in peripheral vascular resistance, the resistance against which the heart pumps. With this lower resistance, the cardiac output rises. Shunting also leads to a drop in vascular resistance, as well as causing the affected tissues to send signals to the body that the blood flow isn’t adequate.
Anemia is perhaps the most common cause of high-output failure. With anemia, the blood can’t carry as much oxygen to the organs due to the low hemoglobin levels that define anemia (hemoglobin is the protein in red blood cells that is the carrier of oxygen). With the body’s tissues not receiving enough oxygen, they send signals to the blood vessels to vasodilate, the kidneys to retain fluid, and the heart to pump harder and faster, all in order to provide better blood flow and make up for the oxygen deficit. The vasodilation leads to a high-output state and the fluid retention leads to symptoms of heart failure.
Pregnancy is another common high-output state. In this situation, the mother has a whole new being that needs blood flow, so the heart is again stimulated to pump out more. Furthermore, new blood vessels that form in the placenta lower the overall vascular resistance. On top of that, signals are generated during pregnancy that cause the blood vessels to dilate.
Sepsis (infection in the bloodstream) and liver disease both cause the blood vessels to dilate—sepsis due to toxins that dilate the blood vessels and liver disease because normal liver function is necessary to metabolize (remove) naturally occurring vascular dilating molecules. Furthermore, toxins that build up in each of these conditions often lead the body’s tissues to be unable to properly absorb nutrients from the bloodstream, creating a shunting effect.
Abnormal connections between arteries and veins, called AV (arteriovenous) fistulas, can cause high-output heart failure. They can occur via trauma, where a knife or bullet wound pierces an artery and vein and they heal with a hole connecting them. It can occur surgically in the case of AV fistulas that are created in patients with kidney failure who need hemodialysis. And sometimes they occur spontaneously in various organs, for instance the GI tract.
Paget’s disease is a bone disorder that leads to abnormally fast and often disordered turnover of bone tissue. It is associated with formation of extra blood vessels, which can cause both a drop in vascular resistance, as well as AV shunting. Thiamine deficiency, also called beriberi, can create a high-output state through arterial vasodilation. Heart failure occurs also due to the inability of the heart to fully utilize energy.
Finally, a look at hyperthyroidism, which can cause both high-output heart failure, and later normal or low-output failure. Hyperthyroidism is a state of heightened stimulation by thyroid hormones, which enhances the effects of adrenaline. The heart rate increases, leading to a high-output state. The body’s metabolism is revved up, so fuel is burned more quickly, which leads to the heart being stimulated to pump out more. The failure occurs when the heart can’t keep up with this need and fluid starts to be retained. Furthermore, over time the heart can be weakened by the constant stimulation and develops systolic dysfunction with a decrease in cardiac output.
All of these conditions are treatable, once they are recognized, so high-output failure usually has a happy ending. But the doctor has to keep these entities in mind so that the proper therapy can be provided, allowing the patient to turn “failure” into “success!”
Greg Koshkarian, MD, FACC