A sudden worsening of heart failure, known as an exacerbation, usually occurs when some change places an increased demand on the weakened heart, which can't compensate by beating harder or faster. Heart failure exacerbations can be life-threatening, so it's important to recognize the signs of an exacerbation and know what to do.
Causes of Decompensated Heart Failure:
Chronic stable heart failure may easily decompensate. This most commonly results from an intercurrent illness (such as pneumonia), myocardial infarction (a heart attack), abnormal heart rhythms, uncontrolled hypertension, or a patient's failure to maintain a fluid restriction, diet, or medication. Other well recognized factors that may worsen CHF include the following: anemia and hyperthyroidism which place additional strain on the heart muscle, excessive fluid or salt intake, and medication that causes fluid retention such as NSAIDs and thiazolidinediones. NSAIDs in general increase the risk twofold.
Heart failure is a multisystem syndrome characterized by abnormalities in cardiac and skeletal muscle and renal function, stimulation of the sympathetic nervous system and a complex pattern of neurohormonal changes. The deterioration in heart failure is not only associated with hemodynamic changes such as increased right and left ventricular filling pressures and reduced cardiac output, but are also associated with increases in inflammatory cytokines such as tumour necrosis factor-alpha and interleukin (IL)-1beta, IL-6, IL-18; and inflammatory chemokines such as monocyte chemoattractant peptide-1, IL-8 and macrophage inflammatory protein-1 alpha. Thus, therapies should target not only improvement in hemodynamic alterations, but also have beneficial effects on the pathophysiological processes that contribute to the acute hemodynamic decompensation and progression of heart failure.
So the mechanisms underlying the progression of heart failure can be categorized as:
Recognizing Heart Failure:
The signs and symptoms of AHF can include dyspnea on exertion (DOE), orthopnea, paroxysmal nocturnal dyspnea (PND), fatigue, edema, weight gain, positive jugular venous distention (JVD), rales, pulmonary edema, tachycardia, ventricular filling murmur (S3), cool extremities, or poor urine output. The Framingham Heart Failure criteria were developed as a tool to diagnose HF. These criteria can be applied to both acute and chronic HF.
The goals of therapy for acutely decompensated heart failure include treating the underlying precipitating factor, to improve symptoms and stabilize the hemodynamic situation. Short-term improvements must be balanced against the risk of long-term myocardial damage. Treatment of AHF is based on the presence of pulmonary congestion (volume overload) and the patient’s cardiac output (i.e., “cold and wet” versus “warm and dry”). Treatment choices include diuretic therapy, vasodilators, inotropic medications, natriuretic peptides, and calcium sensitizers.
1. Allen LA, O’Connor CM. Management of acute decompensated heart failure. CMAJ. 2007;176:797-805.
2. McKee PA, Castelli WP, McNamara PM, Kannel WB. The natural history of congestive heart failure: the Framingham study. N Engl J Med. 1971;285:1441-1446.
3. Tsuyuki RT, Shibata MC, Nilsson C, Hervas-Malo M. Contemporary burden of illness of congestive heart failure in Canada. Can J Cardiol. 2003;19:436–8. [PubMed]
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