| Congestive Heart Failure (CHF) | | Counselor, Congestive Heart Failure is a failure of the pumping function of the heart that results in the failure to maintain blood circulation to other parts of the body. If the heart is not functioning to pump the blood adequately, pressures in the heart increase and blood leaks out of pulmonary capillaries into the alveoli causing pulmonary edema which leads to respiratory failure. The significance of this condition is that the estimated annual cost of CHF in the U.S. is $60 billion. More than 1 million hospital admissions per year are attributed to the primary diagnosis of acute exacerbation of CHF. We value all your comments, so, if you have a suggestion for a newsletter subject but haven't submitted it yet, or if you have already submitted one but think of another, please take a minute to let us know by clicking on your "Reply" button and dropping us a note. To learn more about AMFS, Inc., the organization run by Physicians and Attorneys that provides medical experts and case review services nationwide, and has produced the following informational newsletter to aid you in understanding complex medical issues, please click here - www.medicalexperts.com. |
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|  Pathophysiology: Anything that causes a cardiomyopathy (damaged heart tissue) can lead to CHF. The list is long but includes congestive cardiomyopathy (viral, alcoholic, idiopathic), restrictive cardiomyopathy (amyloidosis, sarcoidosis, hemachromatosis), ischemic cardiomyopathy from an acute myocardial infarction, and hypertrophic cardiomyopathy (Idiopathic hypertrophic subaortic stenosis--occur in young athletes). The other causes of CHF include pericarditis, endocarditis, myocarditis, pulmonary emboli, long standing hypertension, valvular disease, and high output states (hyperthyroid, vitamin B1 deficiency-Beri-Beri, anemia), cocaine, long standing diabetes, drug-induced cardiomyopathy (adriamycin), cor pulmonale, various cancer syndromes (carcinoid, multiple myeloma), Paget's disease, and polycythemia vera. With a decrease in systolic and diastolic function there is a decrease in heart stroke volume. This results in a compensatory sympathetic response designed to increase peripheral vascular resistance so as to maintain perfusion, which in turn promotes myocardial hypertrophy and cardiac enlargement. The heart gets bigger but less functional. Echocardiogram reveals global hypokinesis of the heart and decreased ejection fraction. If the precipitating cause is not corrected, the condition is progressive and irreversible. |
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| Frequency, Morbidity, Mortality: 2% of the population is affected, and this is twice the number seen 15 years earlier. It is the most frequent cause of hospitalization in patients older than 65 years. Morbidity and mortality rates are high, with an estimated 5 year mortality rate of 50%, despite recent advances in treatment. CHF patients die from sudden lethal arrhythmia's, respiratory failure from pulmonary edema, myocardial infarctions from severe hypoxia, and toxic medication reactions because of progressive liver and kidney disease with resulting impaired medication metabolism. |
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| | History: The telltale story given by the patient is increasing swelling in their legs, increasing exertional shortness of breath (dyspnea on exertion), difficulty lying flat (orthopnea), sudden breathlessness upon wakening (paroxysmal nocturnal dyspnea), cough with frothy or pinkish sputum, anxiety, dyspnea at rest, increasing weakness and dizziness. All of this in a patient with a history of CHF indicates an acute exacerbation of the condition. |
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| | Physical: The classical findings include peripheral edema (in the lower legs), jugular venous distention, tachycardia (rapid heart rate), tachypnea (rapid breathing), hypertension, and congested lungs (rales and rhonchi and wheezes). These are the typical findings in left ventricular heart failure. In right ventricular heart failure classical findings also include ascites (free fluid in the abdomen from liver abnormalities and long standing hypertension), hepatomegaly, and hepatojugular reflux. |
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| | Laboratory Studies: An important diagnostic tool is the Beta Natriuretic Peptide (BNP). An elevated BNP can confirm the diagnosis of CHF over other acute pulmonary processes such as asthma or an acute exacerbation of COPD (chronic obstructive pulmonary disease). Cardiac isoenzymes should be run to rule out myocardial infarction, liver enzymes should be checked, arterial blood gases can evaluate hypoxemia, ventilation/ perfusion mismatches seen with pulmonary emboli, and various types of acidosis. Electrolytes should be checked because they are frequently abnormal secondary to long standing diuretic use. A chest x-ray should always be obtained. CHF has a classic pattern on x-ray (enlarged heart, various amounts of pulmonary edema and pleural effusions). Echocardiograms will establish left and right ventricular function, chamber size, wall thickness, and wall motion abnormalities. A MUGA scan (multiple gated acquisition) is a reliable study to determine global heart function. Of course, an electrocardiogram should always be performed. |
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| | Procedures: Often a Swan-Ganz catheter is inserted into the pulmonary artery to measure pulmonary capillary wedge pressure. The degree of CHF can be assessed by measuring these pressures. A PCWP greater than 18mm Hg is indicative of acutely decompensated heart failure. Levels above 30mm Hg are sufficient to produce pulmonary edema. Cardiogenic shock is defined as severe hypotension caused by a severe depression in myocardial function. This occurs when systolic blood pressure is less than 80 mm Hg and the PCWP is greater than 18mm Hg. The mortality rate for cardiogenic shock is 50-90%. CHF can be staged in 4 different classes according to severity, with Class I being most mild, and Class IV being most advanced. In severe cases of CHF, an intraaortic balloon pump (IABP) might be necessary for optimal hemodynamic support. |
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| | Treatment: Patients should be placed on high flow 100% oxygen. O2 saturation should be monitored by pulse oximetry, IV access should be established. A cardiac monitor should be placed. Venous return (preload reduction) should be reduced by elevating the head of the bed, and by giving nitrates and diuretics. Both fluids and sodium should be restricted as well and this will assist in preload reduction. In severe cases IV nitroglycerin and nitroprusside (nipride) can be given. The goal of pharmacotherapy is to achieve a PCWP of 15-18 mm Hg, a cardiac index >2.2 L/min, and a stable blood pressure. This is done by using diuretics, nitrates, analgesics and inotropic agents (pressors). The typical medications are Lasix (diuretic), Nitroglycerine, Morphine, and Dopamine or Dobutamine (pressors). Digoxin (an oral inotropic agent), although not appropriate for emergency use, is used for chronic CHF. The same applies to ACE inhibitors which are combined pre and afterload reducers. Patients should have their sodium intake (causes fluid retention) restricted. |
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| | Medical/Legal Concerns: The following is a list of potential failings: Failure to distinguish CHF from other pulmonary diseases, failure to rapidly treat, failure to rapidly diagnose and treat coronary syndromes that produced the CHF (the most common cause of CHF is coronary artery disease), failure to rapidly treat cardiac arrhythmias, failure to rapidly treat pulmonary edema and hypoxia and acidosis, failure to institute aggressive critical care support and intervention in those patients who are hemodynamically unstable. |
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