Article Figures & Data
Figures
- Figure 1
Pathophysiology of arteriovenous high-output heart failure. Creation of arteriovenous access, with mixing of arterial and venous blood, leads to increased shunting into the lower-resistance venous system, resulting in decreased cardiac afterload and increased venous return. These changes impact the right and left ventricles, contributing to the development of high-output heart failure.
LV = left ventricle; RV = right ventricle
- Figure 2
Algorithm for evaluating arteriovenous (AV) access–associated high-output heart failure (HOHF). The evaluation process begins with a high clinical suspicion. Initial assessment is with noninvasive modalities, followed by invasive diagnostic techniques if noninvasive methods are inconclusive or to confirm the diagnosis definitively.
Qa = vascular access blood flow; RSVP = right ventricular systolic pressure
Tables
Cause Mechanism Obesity Vasoactive adipokines released from visceral adipose tissue lead to peripheral vasodilation, decreased systemic vascular resistance, and increased cardiac output
Paracrine release of fatty acids from ectopic adipose tissue can result in direct lipotoxicity-mediated alterations in myocardial metabolism, leading to negative cardiac remodeling5End-stage liver disease (cirrhosis) Systemic circulation of vasodilators from increased portal pressures results in splanchnic vasodilation and overall decreased systemic vascular resistance and increased cardiac output8 Arteriovenous shunting Connection to the lower-resistance venous system decreases both afterload and systemic vascular resistance while increasing venous return to the right and left ventricle, leading to increased cardiac output7 Hypercapnic lung disease (chronic obstructive pulmonary disease, connective tissue disease, bronchiectasis) Long-standing hypercapnia-induced peripheral vasodilation results in decreased systemic vascular resistance, leading to increased cardiac output7 Sepsis (acute and long-standing) Interleukin 1, interleukin 6, and tumor necrosis factor–induced endocapillary leak and peripheral vasodilation decrease systemic vascular resistance, leading to increased cardiac output9 Anemia (severe) Increased renal nitric oxide production leads to peripheral vasodilation, lower systemic vascular resistance, and increased cardiac output9 Hyperthyroidism Increased thyroid hormone production causes increased cardiac contractility, increased heart rate, and decreased systemic vascular resistance, leading to increased cardiac output10 Pregnancy Peripartum increased stroke volume, chronotropy, and increased endothelial synthesis of vasodilating prostaglandins result in decreased systemic vascular resistance and increased cardiac output11 Vitamin B1 deficiency, beriberi Vitamin B1 is a necessary cofactor for aerobic metabolism; severe deficiency results in a switch to anaerobic metabolism, leading to a buildup of pyruvate and lactic acid, causing systemic vasodilation, decreased systemic vascular resistance, and increased cardiac output9 Myeloproliferative disease Poorly understood; proposed mechanisms include myeloproliferative neoplasm causing increased metabolism by malignant cells, extramedullary hematopoiesis, or anemia12
In this issue
Jump to section
Related Articles
Cited By...
- No citing articles found.