Cardiac output (CO) represents the volume of blood the heart pumps into the circulatory system each minute. It is calculated by multiplying the heart rate (beats per minute) by the stroke volume (volume of blood ejected per beat). Reduced cardiac output occurs when the heart’s pumping action is insufficient to supply the body’s tissues with necessary oxygen and nutrients. This state prevents the delivery of blood flow matched to the body’s metabolic demands, which compromises organ function.
The Core Factors Affecting Output
Cardiac output is determined by four physiological components: heart rate, contractility, preload, and afterload. Impairment of any of these factors can reduce the volume of blood pumped per minute. Heart rate relates to the speed of the heart’s rhythm. If the rate is too fast or too slow, it compromises output because a very fast rate does not allow enough time for the ventricles to fill completely, decreasing stroke volume.
Contractility is the intrinsic force with which the ventricular muscle fibers contract. A weaker contraction means less blood is ejected with each beat. Preload refers to the volume of blood returning to and filling the heart before contraction, stretching the ventricular muscle fibers. While increasing preload generally increases stroke volume, excessive volume can lead to muscle overstretching and reduced efficiency.
Afterload is the total resistance the ventricles must overcome to eject blood into the circulatory system. This resistance is largely determined by systemic blood pressure and the tone of the arterial blood vessels. High afterload, such as that caused by severe hypertension, forces the heart to work harder to push blood out. This ultimately decreases stroke volume and can exhaust the heart muscle.
Common Underlying Causes
Underlying diseases that damage the heart muscle or disrupt its function cause reduced cardiac output. Coronary artery disease is a frequent cause, as narrowed arteries lead to myocardial ischemia, damaging the heart muscle and reducing contractility. An acute myocardial infarction (heart attack) causes the irreversible loss of viable muscle tissue, permanently weakening the heart’s pumping force.
Disorders of the heart’s electrical system, known as severe arrhythmias, significantly impair output by altering heart rate and coordinated contraction. Conditions like rapid atrial fibrillation or extreme bradycardia (slow heart rate) prevent adequate ventricular filling or ejection. Valvular heart disease, involving stiffening (stenosis) or leaking (regurgitation) of the heart valves, also directly affects stroke volume. For example, a stenotic aortic valve increases afterload, while a regurgitant valve reduces effective forward flow.
Chronic, uncontrolled hypertension is a major contributor because it persistently increases afterload. This prolonged stress forces the heart to pump against high resistance, causing the muscle to thicken. This thickening can stiffen the ventricle and impair filling, leading to reduced efficiency. Additionally, conditions affecting the sac around the heart, such as pericardial tamponade, restrict the heart’s ability to fill by physically compressing the chambers, severely limiting preload.
Recognizing the Symptoms
Symptoms of reduced cardiac output result directly from inadequate tissue perfusion, meaning the body’s tissues are not receiving enough oxygenated blood. Profound fatigue and generalized weakness are common complaints, especially during physical activity. The body attempts to compensate by redirecting blood flow away from non-essential areas, such as the limbs, to prioritize the brain and heart.
This redistribution causes the skin to appear pale and the extremities to feel cool or clammy. Reduced blood flow to the brain (cerebral hypoperfusion) can manifest as dizziness, lightheadedness, or altered mental status, including confusion. The kidneys are sensitive to blood flow and often respond by significantly reducing urine output.
Fluid retention is a hallmark symptom, resulting from the body retaining sodium and water to compensate for low output. This fluid often backs up into the lungs, causing shortness of breath, particularly when lying flat (orthopnea). Fluid accumulation also manifests as peripheral edema, which is visible swelling, most commonly in the legs, ankles, and feet.
Treatment and Management Strategies
Treatment focuses on correcting the underlying cause of reduced cardiac output. Medical therapy often begins with diuretics, which manage fluid volume and reduce preload by increasing the excretion of sodium and water. This action alleviates symptoms like pulmonary congestion and edema.
Vasodilator medications relax the smooth muscle in blood vessel walls, decreasing systemic vascular resistance (afterload). By reducing afterload, the heart pumps less forcefully, allowing for improved forward blood flow and increased stroke volume. If contractility is severely impaired, positive inotropic drugs, such as dobutamine, may be used temporarily to directly increase the force of the heart’s contraction.
Lifestyle and Interventions
Lifestyle modifications are integral to long-term management, including strict monitoring of fluid intake and adherence to a low-sodium diet to control fluid retention. For patients with irregular heart rhythms, advanced interventions may be necessary to regulate heart rate. These include a pacemaker or an implantable cardioverter-defibrillator. In cases of severe structural damage, surgical repair of defective heart valves or the implantation of mechanical devices, such as a left ventricular assist device, may be required to mechanically support the failing heart.