Bunnany Chhun Pekar, PhD, APRN, CRNA
Congestive heart failure is a common inpatient and outpatient medical problem. Identifying the correct causes and types is therefore crucial to good medical decision-making. This discussion will focus on identifying the type of heart failure your patient has, and also good management strategies.
Types of Heart Failure
Structural or functional defects in cardiac muscle are the usual causes of Heart failure (HF). This results in impairment of ventricular filling of blood. As a result, the heart can no longer pump blood to the rest of the body as it is either too weak or not elastic enough. There are many ways to classify heart failure: systolic versus diastolic, right versus left sided HF, low output versus high output HF just to name a few.
When describing the heart’s ability to contract or fill, a patient could have either systolic, diastolic HF, or both. Heart failure encompasses patients who have both preserved ejection fraction (EF > 50% (HFpEF)) and reduced ejection fraction (EF< 40%). In systolic HF, the heart is not able to maintain its ejection fraction, and is classified as HF with reduced EF (HFrEF), typically when the LVEF is around 40%. When the heart Is able to pump, but It Is unable to relax prior to the next cardiac cycle, diastolic heart failure ensues. This results in less blood entering the ventricle and less stroke volume being ejected out.
Heart Failure Considerations
When a patient suffers from both systolic and diastolic HF, management can be even more challenging. A patient may not know that they have HF as functional limitation. In fact, they may not become compromised until their EF is reduced to about 40%. Acute decompensated heart failure (ADHF) may be the first presentation of the patient’s heart failure or more generally a decompensation of chronic heart failure. Comorbidities such as HTN, ischemic and nonischemic cardiomyopathy, arrhythmias, peripartum cardiomyopathy, congenital heart disease, and valvular dysfunctions can lead to systolic HF. On the other hand, advancing age, DM, obesity in addition to long standing uncontrolled HTN and CAD can lead to diastolic HF.
Low Output Vs. High Output
Most patients who suffer from systolic HF have low output HF, in that their cardiac output (and cardiac index) is low but they have elevated systemic vascular resistance. In contrast, high output heart failure (HOHF) is characterized by decreased systemic vascular resistance. This can be secondary to underlying conditions such as morbid obesity, thyroid storm, cirrhosis or AV shunt resulting in a compensatory increase in ejection fraction as well as retention of salt and water. Once the underlying condition is treated, HOHF improves or resolves.
Left and Right Heart Failure
HF often affects the left side, the right side of the heart, or both. In left sided HF, the LV can no longer pump enough blood to the rest of the body. As a result, blood backs up in the lungs causing dyspnea or coughing. This mechanism represents the most common type of heart failure. The usual causes of this condition include CAD, valvular disease, and also arrhythmias.
In right sided HF, the RV is too weak to pump enough blood to the lungs. This results in blood backing up in the veinous return system. The increased pressure in the veins lead to edema of surrounding tissue such as in the legs, abdomen, genitalia, or in the neck which present as jugular venous distention. Right sided HF is caused by advanced left sided heart failure or from conditions that also cause high pressure in the lungs (pulmonary hypertension). These conditions include COPD, acute pulmonary embolus, or chronic thromboembolic pulmonary hypertension. Unfortunately, some patients develop biventricular HF, causing symptoms of both left and right sided HF such as dyspnea and generalized edema.
Heart Failure Epidemiology
6.5 million Americans are diagnosed with HF and 5-55% have an approximate 5-year mortality. Overall, 2-3% of the population is effected, most commonly the elderly. However, due to the projected increase in elderly population, the number of heart failure cases will continue to rise. There are approximately three million office visits per year with HF as the primary health issue. In 2013, 5.1 million patients with HF had a direct cost of care around 32 billion dollars. By 2030, this number is projected to triple.
Most of the time, heart failure is a slow potentially progressing disease (except in the case of acute MI or massive PE) where a patient may have a condition, such as uncontrolled HTN, that would place him/her at risk for the development of heart failure if untreated. The American College of Cardiology and the American Heart Association (ACC/AHA) have therefore developed the A-D staging system to classify heart failure based on risk for HF or the presence of structural heart disease:
A: high risk for HR, but no structural heart disease or symptoms of HF
B: Presence of structural heart disease but no symptoms of HF
C: Presence of structural heart disease and symptoms of HF
D: Presence of refractory HF requiring specialized interventions
A person may be able to compensate for the weakening heart until compensatory mechanisms fail and symptoms such as shortness of breath, fatigue, decrease exercise tolerance occur. The New York Heart Association (NYHA) classification categorizes a heart failure on a I-IV scale based on the presence of limitations on physical activity:
A person with advanced heart failure would be classified as stage D, according to the ACC/AHA but their NYHA classification can vary day to day depending on how they feel (symptom management). However, from clinical observation and experience in managing HF patients, most advance HF patients tend to have marked limitations in their physical activity or experience SOB even at rest (Class III-IV), especially in the presence of other comorbidities. These two classifications complement one another and help guide nonpharmacologic and pharmacologic interventions.
A patient with HF would usually also have an associated diagnosis of congestive heart failure (CHF). Fortunately however, with medical and dietary adherence, most HF symptoms are manageable. These patients are therefore considered to have chronic compensated CHF. Some patients experience a sudden deterioration of CHF or a new onset of severe CHF due to an acute cardiac condition such as an MI or a massive PE. This defines decompensated HF (ADHF) and accounts for 80% of hospitalizations related to HF.
Acute Decompensated Heart Failure
ADHF is a syndrome where the patient experiences worsening fatigue, dyspnea, cough, or edema that also results from deteriorating heart function. They may also have associated chest pain as the symptoms become more severe. Conversely, this usually leads to a hospital admission or unscheduled medical intervention. The primary reasons for hospital admission are non-adherence to their medication regimen or dietary restrictions, uncontrolled HTN, ACS/ischemia, dysrhythmias, or COPD exacerbation.
Shortness of breath is the cardinal symptom of heart failure. At first, exertion triggers dyspnea. Cardiac output must be increased is to provide oxygen to active muscles. As heart failure progresses, less stress triggers dyspnea. Fluid shifts occur when the patient lies flat and dyspnea worsens. This leads to orthopnea. In Its final stages, shortness of breath is seen at rest. This is when the CO can no longer keep up with the demands.
Other conditions such as COPD, PE, or Pneumonia can also cause shortness of breath. It is crucial to make the correct diagnosis as these patients can deteriorate rapidly. Below is a table of some laboratory workup and tests that can help make the diagnosis of ADHF or congestive heart failure:
Testing for CHF
|Vital signs||A must for all patients and compare to their NL VS|
|CBC||Anemia may cause or exacerbate HF Leukocytosis may point to an infection which may worsen HF|
|CMP||Check for electrolytes, LFTs may be abnl with congestive hepatomegaly and cardiac cirrhosis, low albumin can lead to further edema|
|FSBS/HbA1C||DMs are at high risk for the development of CAD and HF|
|Iron study||Low Fe may be assoc. w/ poor cardiac fxn|
|TSH||Thyrotoxicosis can lead to high output HF|
|BNP/NT-proBNP||Establishes dx of HF when symptoms are ambiguous/confounding comorbidities are present (NT-proBNP better at detecting HF than BNP due to chemically more stable in circulating blood and is a sensitive marker even in early cardiac decompensation)|
|EKG||May help ID cause of HF from an electrical standpoint|
|CXR||Help assess heart size, pulmonary congestion, r/o or r/i pulmonary causes of dyspnea, assess positioning implanted cardiac devices. Important to note that about 1/5 of HF pts have a NL CXR|
|Cardiac enzymes (serial)||If ischemia is suspected as cause of HF|
|ABG||Not helpful unless severe HF and presenting with hypoxemia not responsive to oxygen therapy or presenting with comorbid conditions|
|TTE||Help establish type of heart failure and etiology (EF, valvular abnormalities)|
Liver Function Test Pearls
Abnormal Liver function tests are detected in about 75% of acute HF patients. These are closely related to the severity of disease and clinical findings. Patients with bilateral and right sided acute HF can also have cholestatic type (Tbili, GGT, alkaline phosphatase) liver dysfunction. This is also usually seen in patients with moderate-to-severe tricuspid insufficiency. As a result, a patient with left sided acute HF and hypotension (SBP <100 mm Hg) will have transaminase elevation. Likewise, all liver function tests except for alkaline phosphatase may be abnormal in patients with advanced HF (NYHA functional class III -IV). Liver dysfunction almost always recovers after treatment. However, most of these patients are on many medications or have comorbid conditions that could negatively affect their liver function. For this reason, we advise repeating CMP/LFT testing.
Cardiac Biomarker Pearls
Obtain myocardial injury biomarkers if suspected ACS as the cause of ADHF. However, elevation of these biomarkers alone does not confirm presence of myocardial infarction. On the other hand, cardiac biomarkers can be elevated without myocardial infarction. This is a poor prognostic sign. Likewise Increases in troponin with ischemic symptoms or EKG changes suggest Acute Coronary Syndrome.
Brain Natriuretic Peptide (BNP)
Depending on institution, BNP or NT-proBNP is utilized as a cardiac biomarker that assist in the diagnosis of HF. In response to myocardial wall stretch, pre-BNP is synthesized to pro-BNP, which is further processed to the biologically inactive NT-proBNP and the biologically active BNP. Both are elevated in HF, thus are useful adjuncts to clinical evaluation of HF. The concentration of NT-proBNP is much higher thus have a higher cut-off point. However, for most institutions, the accepted rule out cut-points for acute HF for BNP is 100 pg/mL and for NT-proBNP is 300 pg/mL. Remember that elevated BNPs could also be presented in conditions such as: renal failure, PE, pulmonary HTN, and chronic hypoxia. In contrast, obesity and overweight individuals have relatively lower BNPs. NT-proBNP levels are less affected by obesity.
In summary, Americans who are older than 40 years old have a 20% lifetime risk for the development of HF. HF is a serious disease because of its significant impact on morbidity and mortality. Unfortunately, HF will continue to be one of the top diseases that providers will encounter due to the increased in aging population. The pathophysiology of HF explains why a patient with ADHF will likely present with dyspnea. However, dyspnea is a common presentation of other conditions such as COPD, asthma, PE. Therefore, It is important to be able to differentiate ADHF from other diseases with like presentation.
The above table provides suggestions for initial laboratory/test workup that will help with making the diagnosis. It is not meant to be a complete list but will provide enough information to rule in or rule out ADHF. If a patient is found to be in ADHF, it would be wise to obtain expert consultation from our cardiology colleagues to help manage such a complicated disease with diverse causes. While the initial goal is symptom relief such as the administration of a diuretic to help with fluid overload, it is more about mitigating future admissions for ADHF and interventions to slow the progression of HF which ultimately improve quality of life.
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