Heart failure is not a specific disease, but a clinical syndrome characterized by dyspnea, activity intolerance, and fluid overload adversely affecting patients' functional status and quality of life. Dyspnea and activity intolerance are the two most common symptoms of heart failure, while manifestations of fluid overload, such as edema and jugular venous distention, are the most common signs. This clinical syndrome occurs as a consequence of structural or functional (or both) cardiac abnormalities that impair cardiac pumping or filling.
Heart failure is a clinical syndrome that commonly is the final manifestation of cardiac risk factors (e.g., untreated hypertension) and cardiac diseases or events (e.g., acute myocardial infarction [MI]). Patients with heart failure commonly report very poor quality of life because heart failure has a negative impact on all aspects of life, particularly symptom burden and ability to perform usual activities. Heart failure has an impact on quality of life comparable to, or worse than, that seen in other serious chronic conditions.
Given the enormous personal, social, and economic burdens of heart failure, preventing it from occurring in the first place is a major priority that all healthcare providers must embrace. Once heart failure develops, prevention of both rehospitalization and progression of heart failure becomes a major priority.
Heart failure is a response to cardiac dysfunction, a condition in which the heart cannot pump blood at a volume required to meet the body’s needs. Any condition that impairs the ability of the ventricles to fill or eject blood can cause heart failure. CAD with resultant necrotic damage to the left ventricle is the underlying cause of heart failure in most patients. Other major conditions that lead to heart failure include valvular dysfunction, infection (myocarditis or endocarditis), cardiomyopathy, and uncontrolled hypertension. Hypertension is the precursor of heart failure in men and women.
When the heart begins to fail and the cardiac output is no longer sufficient to meet the metabolic needs of tissues, the body activates several major compensatory mechanisms:
The sympathetic nervous system
The sympathetic nervous system compensates for low cardiac output by increasing heart rate and blood pressure. Levels of circulating catecholamines are increased, resulting in peripheral vasoconstriction and causing the shunting of blood from nonvital organs to vital organs. This mechanism, although initially helpful, may become a negative factor if elevation of heart rate increases myocardial oxygen demand while shortening the amount of time for diastolic filling and coronary artery perfusion.
The Renin-angiotension-aldosterone system
Activation of the RAAS in heart failure promotes fluid retention. A physiologic chain of events is then set in motion that leads to volume overload. To break the RAAS cycle of fluid retention in heart failure, medications are prescribed to interrupt the steps.
Ventricular Hypertrophy
This is the final compensatory mechanism. Because myocardial hypertrophy increases the force of contraction, hypertrophy helps the ventricle overcome an increase in afterload. When this mechanism is no longer efficient for the ventricle, it will remodel by dilation.
Ventricular Remodeling
In this final stage of heart failure, the shape of the ventricle is changed, or is remodeled, to resemble a round bowl. A dilated ventricle has poor contractility and is enlarged without hypertrophy.
All patients do not have the same type of heart failure. The type of heart failure/classification is based upon either the area of the heart affected or the type of dysfunction that occurs.
Left Ventricular Failure: is a disturbance of the contracile function of the left ventricle; resulting in low cardiac output. As a result, the arterial bed vasoconstricts, increasing afterload (systemic vascular resistance). This then, creates congestion and edema in the pulmonary circulation and alveoli. Patients with LV failure are often diagnosed when they present with one or more of the following:
Clinical Manifestations of LV Failure
Signs
Symptoms
Right Ventricular Failure: is a disturbance of the contractile function of the right ventricle. While this type of heart failure may result from an acute condition such as a pulmonary embolus, it can be caused by LV failure.
Clinical Manifestations of RV Failure
Signs
Symptoms
Systolic dysfunction: the type of failure associated with the decreased contractility during systole, lessens the quantity of blood that can be ejected from the heart (decreased cardiac output).
Diastolic dysfunction: normally caused by LV dysfunction, this is when the heart muscle is unable to relax, stretch or filling during diastole.
The treatment of heart failure is based upon the stage of heart failure they are exhibiting.
The patient is at risk for heart failure but without structural heart disease or symptoms of heart failure. These are patients diagnosed with hypertension, diabetes or metabolic syndrome, atherosclerosis, peripheral vascular disease and/or obesity.
The management for patients with stage A heart failure involves the treatment of risk factors for heart failure and its precursors. For example:
The patient has structural heart disease without heart failure symptoms. These are patients who may have previous myocardial infarction, left ventricular hypertrophy and low ejection fractions.
The management for patients with stage B heart failure involves all those in stage A, as well as the introduction of beta blockers unless contraindicated.
The patient has structure heart disease with prior or current heart failure symptoms such as; shortness of breath, fatigue or activity intolerance.
The management for patients with stage C heart failure involves all those in stages A and B, as well as:
The patient has refractory heart failure that requires specialized interventions because they are experiencing symptoms at rest despite optimal therapy.
These interventions include:
Put the following events that are the consequences of heart failure in sequence.