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Heart failure, ejection fractions, hypertensive emergency, and more are topics for discussion at one hospital

Association of Clinical Documentation Improvement Specialists, January 8, 2008

Send us your areas of concern, subjects to address in this column

by Cesar M. Limjoco, MD, and Robert S. Gold, MD

For this month's column, we've asked one of our client hospitals to provide us with some topics that they'd like us to clarify. The following is a summary of our discussions with that hospital.

Causes of heart failure

Our client hospital wanted to know whether mitral valve insufficiency and aortic valve stenosis (code 396.2) are always the cause of heart failure. Category 396, Diseases of mitral and aortic valves, has an "includes note" that states "involvement of both mitral and aortic valves, whether specified as rheumatic or not."

The rationale behind this is that most cases of combined involvement of mitral and aortic disease are due to rheumatic heart disease. However, if the valves occur singly, or the involvement is minimal, you cannot assume that heart failure is rheumatic in nature. The physician needs to document the significance of the valvular disease and clarify whether he or she knows that the heart failure is due to something entirely different and that the minimal valvular disease has absolutely nothing to do with the patient's chronic heart failure condition. All other valvular diseases-whether they occur singly or in combination-should not be coded to rheumatic unless the physician indicates it.

Echocardiograms and ejection fractions

Another client asked about echocardiograms and ejection fractions. Heart failure usually refers to the left side of the heart. A patient can experience right heart failure due to chronic lung disease or ischemia of the right side of the heart. However, in accordance with core measures, we will concentrate on left heart failure, which encompasses systolic and diastolic heart failure.

Systolic heart failure occurs when the heart muscle contracts with too little force, causing less oxygen-rich blood to be pumped through the body (contracting function). Diastolic heart failure occurs when the heart contracts normally, but the ventricle walls don't relax enough to let the chamber fill as it should. The result is that the heart has less blood to pump out (filling function). A patient can also experience a combination of systolic and diastolic failure.

When the left ventricle contracts-forcing blood out into the body-physicians refer to this as an "ejection" because it is ejecting the blood out into the aorta and then into the arteries throughout the body. Because the left ventricle is the one that pushes blood throughout your body, that is how left heart function is measured. That's the ejection phase. The fraction phase refers to the fact that the left ventricle never quite manages to pump out all the blood inside of it. There's always a little left behind (around 30%) that remains to wait for the next contraction. The amount that your left ventricle pumps out per beat is called the "ejection fraction." It's X% (the fraction or portion pumped out) of the total amount of blood in the ventricle per heart beat. The normal ejection fraction is between 55% and 70%.

Ejection fractions of 40% and below are indicative of systolic left ventricular heart failure. Heart failure medications (e.g., cardiac glycosides) improve the ejection fraction. Diastolic left ventricular failure may have normal ejection fractions because the ejection fraction measures the contracting function of the left ventricle. Cardiac catheterization remains the gold standard for demonstrating impaired relaxation and filling because it provides direct measurement of ventricular diastolic pressure.

The patient's specific type of heart failure-acute, chronic, or acute on chronic-depends on whether the patient is currently symptomatic (in which case the heart failure is acute), has a history of heart failure in the past but is not currently symptomatic (in which case the patient's heart failure is chronic, or stable), or is both currently symptomatic and has a history of heart failure (in which case is the heart failure is acute on chronic).

Acute (and acute on chronic) systolic/diastolic heart failures have more severity of illness and risk of morbidity/mortality. A patient with chronic (stable) heart failure may respond to therapy and, therefore, may not be symptomatic at the current time because he or she has shown improvement in cardiac function from the time when he or she experienced acute failure.

Brain natriuretic peptide

Another topic that came up was brain natriuretic peptide (BNP). Produced by the heart, this hormone indicates how well the heart is working. Normally, only a low amount of BNP is found in the blood. However, if the heart has to work harder and the right atrium becomes stretched over a long period of time-such as from heart failure-the heart will release more BNP, and the blood level of BNP will rise. BNP is secreted as a response to volume expansion, pressure overload, and resultant increased wall tension. BNP encourages the kidneys to respond to too much volume in the circulation by urinating out additional sodium, which automatically takes additional water along with it. When treatment for heart failure is working, BNP levels drop.

BNP levels increase with age and are higher in women. Tests conducted on women aged 75 years or older can yield false positives. Increased BNP levels are also seen in kidney disease/dialysis, myocardial infarction, pulmonary hypertension, pulmonary embolism, and in patients who take heart drugs (e.g., cardiac glycosides and diuretics).

Troponin I

Another client asked about which the client hospital inquired was Troponin I, a protein that becomes elevated during a myocardial injury. For example, damaged myocardial cells release Troponin I as a result of an acute myocardial infarction. Troponin I is elevated in cardiac amyloidosis, cardiac contusion, cardiac surgery (e.g., a heart transplant), cardiac defibrillation, cardiomyopathies, heart failure, and supraventricular tachycardia. Troponin I levels may also be elevated with acute or chronic conditions, such as myocarditis (heart inflammation), severe infections, kidney disease, dermatomyositis, polymyositis, pulmonary hypertension, chemotherapy, pulmonary embolism, subarachnoid hemorrhage, scorpion venom, stroke, and heavy exercise (e.g., running a marathon).

D-dimer

D-dimer-a blood test that indicates hypercoagulability in the blood-frequently comes up. The test detects an elevation in deep vein thrombosis/thrombophlebitis, pulmonary embolism, acute myocardial infarction, strokes, disseminated intravascular coagulation, and recent surgery, trauma, or infection when hypercoagulability is present. Elevated levels are also seen with liver disease, pregnancy, eclampsia, heart disease, and some cancers.

Hypertensive urgency vs. emergency

Another topic that came up was hypertensive urgency. It's important to distinguish this condition from hypertensive emergency. Urgency is defined as severely elevated blood pressure (i.e., systolic > 220 mmHg or diastolic > 120 mmHg) with no evidence of target organ damage. Hypertensive emergency is a condition in which elevated blood pressure results in target organ damage. The systems that are primarily involved include the central nervous system, the cardiovascular system, and the kidneys. Hypertensive emergencies require immediate therapy to decrease blood pressure within minutes to hours.

In contrast, no evidence suggests a benefit from rapidly reducing blood pressure in patients with hypertensive urgency. In fact, such aggressive therapy may harm the patient, resulting in cardiac, renal, or cerebral hypoperfusion (decrease in blood flow to these organs).

There are two types of hypertensive emergencies:

1. Accelerated hypertension (HTN)-A significant increase over baseline blood pressure that is associated with target organ damage. There is usually vascular damage, such as flame-shaped hemorrhages or soft exudates on funduscopic examination; however, there is no papilledema.

2. Malignant HTN-The same findings as accelerated, plus papilledema on funduscopic examination.

Editor's note: Limjoco is vice president of clinical operations of DCBA, Inc., a consulting firm that provides physician-to-physician programs in clinical documentation improvement. The goals are data accuracy, profile management, and compliance, either in the inpatient or outpatient arenas. He can be reached by phone at 770/216-9691 or by e-mail at drlimjoco@DCBAInc.com.

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