Gastrointestinal distress such as bloating or indigestion, along with muscular imbalances and poor posture, can also irritate the vagus nerve causing palpitations)
Sympathetic overdrive (panic disorder, low blood sugar, hypoxia, antihistamines (levocetirizine), low red blood cell count, heart failure, mitral valve prolapse). Hyperdynamic circulation (valvular incompetence, thyrotoxicosis, hypercapnia, high body temperature, low red blood cell count, pregnancy). Abnormal heart rhythms (ectopic beat, premature atrial contraction, junctional escape beat, premature ventricular contraction, atrial fibrillation, supraventricular tachycardia, ventricular tachycardia, ventricular fibrillation, heart block).Palpitations can occur during times of catecholamine excess, such as during exercise or at times of stress. The cause of the palpitations during these conditions is often a sustained supraventricular tachycardia or ventricular tachyarrhythmia. Supraventricular tachycardias can also be induced at the termination of exercise when the withdrawal of catecholamines is coupled with a surge in the vagal tone. Palpitations secondary to catecholamine excess may also occur during emotionally startling experiences, especially in patients with a long QT syndrome. Psychiatric problems
Anxiety and stress elevate the bodys level of cortisol and adrenaline, which in turn can interfere with the normal functioning of the parasympathetic nervous system resulting in overstimulation of the vagus nerve. Vagus nerve induced palpitation is felt as a thud, a hollow fluttery sensation, or a skipped beat, depending on at what point during the hearts normal rhythm the vagus nerve fires. In many cases, the anxiety and panic of experiencing palpitations cause a patient to experience further anxiety and increased vagus nerve stimulation.
In such conditions, heme along with globin chains can be released from further oxidization of met-hemoglobin (ferric Hb). In which, the free heme can then accelerate tissue damage by promoting peroxidative reactions and activation of inflammatory cascades. At this time, hemopexin, another plasma glycoprotein come to bind with heme with its privilege of high heme affinity, forming a complex of heme-hemopexin, which is non-toxic, and travel together to a receptor on hepatocytes and macrophages within the spleen, liver and bone marrow. (Note that the "free hemoglobin-haptoglobin" complex is taken up by hepatocytes and, to the lesser extent, macrophages.) Thereafter, these complexes will undergo the metabolic mechanisms like extravascular hemolysis.Nevertheless, if the binding capacities of haptoglobin and hemopexin are saturated, the remaining "free hemoglobin" in the plasma will be oxidized to met-hemoglobin eventually, and then further disassociates into free heme and others. At this stage, the "free heme" will bind to albumin, forming met-hemalbumin. As to the remaining unbound (met)hemoglobin is filtered into the primary urine and re-absorbed via proximal tubules of the kidney. In proximal tubules, the iron is extracted and stored as hemosiderin. (Long-term hemoglobinuria is associated with substantial deposition of hemosiderin in proximal tubule (excessive accumulation of hemosiderin in proximal tubule), Fanconi syndrome (damaged renal re-absorption capability of small molecules which give rises to hyper-aminoaciduria, glycosuria, hyperphosphaturia, and bicarbonate and dehydration), and chronic kidney failure.)