acute heart failure | SYMPTOMS, TREATMENT

 

acute heart failure | SYMPTOMS, TREATMENT

Severe heart failure is widely described as a rapid onset of new or worse HF symptoms and symptoms [8]. It is usually a life-threatening condition, requiring hospitalization, and emergency treatment aimed primarily at treating fluid overload and hemodynamic congestion. This umbrella term includes first-time patients with common symptoms and signs of heart failure (de novo AHF) and those with complications of their pre-existing cardiomyopathy (severe heart failure).

De novo AHF occurs when there is a sudden increase in intracardiac filling pressure and / or myocardial dysfunction that can lead to a reduction in peripheral function and pulmonary edema. The most common aetiology is cardiac ischemia when the (sub) -total coronary occlusion leads to a reduction in contraction in the myocardium released by the affected coronary artery. In this case, management focuses not only on haemodynamic reduction but also on recurrence with the aim of restoring myocardial contractile function.

Abnormal exposure to AHF is one of the many non-ischemic myocardial infarction. These include early onset of myocardial dysfunction with inflammatory bowel disease (e.g. cardiomyopathy), toxic stigma (e.g. drug-induced cardiomyopathy) and unexplained environmental shocks such as peripartum cardiomyopathy. Admission to the hospital with AHF may announce a diagnosis of CHF as these severe lesions may have long-term sequelae in myocardial function. Equally, patients may present with AHF in the context of chronic myocardial dysfunction such as tachycardia-induced arrhythmogenic cardiomyopathy, Takotsubo cardiomyopathy caused by human disease and those related to endocrine disease such as hypermetabolic conditions in the thyroid storm. The treatment of these causes is aimed not only at reducing haemodynamic relaxation during induction induction but also on respecting and correcting the underlying stigma.

In addition to myocardial dysfunction, AHF can be overcome by valvular dysfunction. This usually occurs in the ischemic context (damage to the lower valvular tissue) leading to severe mitral recovery but can also occur without ischemia per se as is the case with non-infectious and non-infectious endocarditis. Extra-cardiac pathologies can also reduce AHF as is the case with pulmonary embolism or pericardial effusion causing tamponade, both of which reduce LV discharge and thus reduce borderline tilt.

De novo AHF can therefore be reduced by many causes, not just pump failure, which are symptoms present with decreased perfusion pressure and pulmonary edema. Management aims to support, either medically or mechanically, haemodynamic relaxation and correction of the underlying cause.

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Minor Heart Failure

Most patients presenting with AHF do so in the form of pre-existing cardiomyopathy, a condition described as severe heart failure (ADHF). There are several significant differences between this group of patients and those presenting with de novo AHF which influences how haemodynamic tests are assessed and how the condition is managed.

Unlike de novo AHF, patients with ADHF often present with signs and symptoms of congestion and fluid retention (weight gain, exertional dyspnoea, orthopnoea, dependent edema) rather than with pulmonary edema or cardiogenic shocks indicating dysfunction. of LV systolic. This is the result of chronic, often poorly regulated, neuro-humoral compression methods that work to maintain a haemodynamic state despite the active LV. Depreciation occurs when balance tips are used for overload as compensation methods prove to be insufficient or fail all together. This is evidenced by data from the IMPACT-HF book showing that acute coronary heart disease is taking a hidden course and patients arriving at the hospital in extremes following reported symptoms of congestion before being admitted for days or weeks [9]