High-output heart failure
High-output heart failure happens when the amount of blood pumped out is more than typical and the heart is unable to keep up. This can occur in overload situations such as blood or serum infusions, kidney diseases, chronic severe anemia, beriberi (vitamin B1/thiamine deficiency), hyperthyroidism, cirrhosis, Pagets disease, multiple myeloma, arteriovenous fistulae, or arteriovenous malformations. Acute decompensation
Chronic stable heart failure may easily decompensate. This most commonly results from a concurrent illness (such as myocardial infarction (a heart attack) or pneumonia), abnormal heart rhythms, uncontrolled hypertension, or a persons failure to maintain a fluid restriction, diet, or medication.Other factors that may worsen CHF include: anemia, hyperthyroidism, excessive fluid or salt intake, and medication such as NSAIDs and thiazolidinediones. NSAIDs increase the risk twofold. Medications
A number of medications may cause or worsen the disease. This includes NSAIDs, COX-2 inhibitors, a number of anesthetic agents such as ketamine, thiazolidinediones, some cancer medications, several antiarrhythmic medications, pregabalin, alpha-2 adrenergic receptor agonists, minoxidil, itraconazole, cilostazol, anagrelide, stimulants (e.g., methylphenidate), tricyclic antidepressants, lithium, antipsychotics, dopamine agonists, TNF inhibitors, calcium channel blockers (especially verapamil and diltiazem), salbutamol, and tamsulosin.By inhibiting the formation of prostaglandins, NSAIDs may exacerbate heart failure through several mechanisms, including promotion of fluid retention, increasing blood pressure, and decreasing a persons response to diuretic medications. Similarly, the ACC/AHA recommends against the use of COX-2 inhibitor medications in people with heart failure.
The role of the heart in fluid retention began to be better appreciated, as dropsy of the chest (fluid accumulation in and round the lungs causing shortage of breath) became more familiar and the current concept of heart failure, which brings together swelling and shortage of breath due to fluid retention, began to be accepted, in the 17th and especially in the 18th century: Richard Lower linked dyspnea and foot swelling in 1679, and Giovanni Maria Lancisi connected jugular vein distention with right ventricular failure in 1728. Dropsy attributable to other causes, e.g. kidney failure, was differentiated in the 19th century. The stethoscope, invented by René Laennec in 1819, x-rays, discovered by Wilhelm Röntgen in 1895, and electrocardiography, described by Willem Einthoven in 1903, facilitated the investigation of heart failure. 19th century also saw experimental and conceptual advances in the physiology of heart contraction, which led to the formulation of the Frank-Starling law of the heart (named after physiologists Otto Frank and Ernest Starling, a remarkable advance in understanding mechanisms of heart failure.One of the earliest treatments of heart failure, relief of swelling by bloodletting with various methods, including leeches, continued through the centuries. Along with bloodletting, Jean-Baptiste de Sénac in 1749 recommended opiates for acute shortage of breath due to heart failure. In 1785, William Withering described the therapeutic uses of the foxglove genus of plants in the treatment of edema; their extract contains cardiac glycosides, including digoxin, still used today in the treatment of heart failure.