COPD CHF Differential

Jim Upchurch, M.D., NREMTP

Scenario

You are dispatched to a older person with shortness of breath. On arrival you find a 65 year-old female in moderate respiratory distress. She is sitting upright with nasal oxygen prongs in place. The patient reports increasing fatigue and difficulty breathing over the past 2 to 3 days. She gives a history of heart and lung problems. As you obtain vital signs and place the patient on your own oxygen source, your AMPLE history reveals no allergies and a medication list that includes an Atrovent inhaler, Lisinopril, and Digoxin. Past medical history is significant for a myocardial infarct five years ago and a thirty-pack year history of smoking. To tired to cook, her last meal was the previous evening. Vital signs: P 102  BP 100/72  RR 24  O2Sat 88% on 2 liters via nasal cannula.

Your exam reveals jugular venous distention (JVD), a rounded chest with equal rise and no retractions, decreased breath sounds in all lung fields without crackles (rales) or wheeze, regular tachycardia on heart auscultation, soft abdomen on palpation and the presence of lower extremity pitting edema. You suspect your patient has worsening COPD complicated by right ventricular heart failure. Clues for COPD come from the patient presentation (increased dypnea, fatigue), medications (Atrovent, oxygen) and exam (barrel chest, decreased breath sounds). Evidence for right ventricular heart failure includes the presentation (fatigue), medications (Lisinopril, Digoxin) and exam (JVD and peripheral edema).

After increasing the patient’s oxygen flow, you transport her in the position of comfort. The patient feels better after nebulized albuterol and intravenous Lasix. Patient is improved on arrival to the receiving facility.

Epidemiology

The American College of Cardiologist and the American Heart Association have defined heart failure as a “complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.”[1] This applies to both ventricles although heart failure is more common with the left ventricle. Not all patients with heart failure have volume overload, thus the term “congestive heart failure” is reserved for those heart failure patients with evidence of fluid backup or congestion. The single most common cause of heart failure is coronary artery disease [1]. Basically, more people are surviving their heart attacks and later in life developing heart failure due to the previously damaged heart muscle. Other causes of heart failure include hypertension, thyroid disease, heart valve problems, alcohol abuse, and unidentifiable causes. Not surprisingly, heart failure is more common in the elderly. [2] Overall, heart failure is a problem for about 4.8 million Americans, almost evenly split between men and women, and accounts for 962,000 hospital admissions yearly. [2] Diseases of the heart are the number one cause of death in the U.S. Forty percent of these deaths are due to heart failure as a primary cause or as a contributing cause. [1]

Chronic Obstructive Pulmonary Disease (COPD) is a “disease state characterized by air flow limitation that is not fully reversible”.[3] This is in contrast to the reversible airflow restriction characteristic of the asthmatic patient. Further, the airflow limitation in COPD is “both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases.”[3] COPD is the 4th leading cause of death in the U.S. [4] and like heart failure is more common the older one gets. The number one cause of COPD is smoking. Other causes include exposure to air pollution, cystic fibrosis and inherited lung diseases.

Pathophysiology

The human body requires energy to maintain life. Each organ is made up of millions of cells that perform various life support functions. All of these organs and cells have the same basic requirements. They need delivery of oxygen and fuel (such as glucose) in order to produce energy. And they need removal of unwanted energy byproducts like carbon dioxide. It is the team effort provided by the heart and lungs that provides this service to the cells. The lungs provide oxygenation of the blood and the heart pumps that oxygenated blood along with glucose and other nutrients to the cells. The heart then transports the carbon dioxide back from the cells to the lungs where it is disposed. [pic1]This cycle begins when the diaphragm contracts and generates a negative pressure inside the chest cavity that causes the lungs to expand thus drawing in outside air. This air traverses a system of tubes that begins with the trachea and ends where the terminal bronchiole connects to the alveolus or air sac. The oxygen in this inspired air is loaded onto the red blood cells that circulate in the capillaries covering the alveolus. At the same time carbon dioxide moves from the red blood cell into the alveolus. The force that moves the oxygen and carbon dioxide is called diffusion. When the diaphragm relaxes, the negative pressure is decreased inside the chest cavity and the lungs begin to deflate which reverses the airflow. The carbon dioxide laden air in the alveolus now travels to the outside. To keep the red blood cells circulating between the alvoli and the rest of the body cells, the heart uses a two-pump system. The right heart pump sends low oxygen/high carbon dioxide laden blood through the low-pressure vessels of the lungs (pulmonary circulation) and thus to the alveolar capillaries. After traveling through the alveolar capillaries in the lungs, the blood is now high oxygen/low carbon dioxide blood and the left heart pump sends this blood through the high-pressure vessels contained in the rest of the body (systemic circulation).

CHF is the result of a ventricle that is unable to function normally. When any type of pump fails, the substance being pumped backs up. For the right ventricle, blood will accumulate in the systemic venous circulation but spare the pulmonary venous circulation.[pic2] This can result in distended jugular veins (JVD), an enlarged liver from venous congestion and dependent edema from fluid leaking out of the over-loaded, over-pressurized capillaries. However, as long as the left ventricle is not affected, blood will not build up in the lungs. When the left ventricle fails and causes congestion, the lungs are the first regions affected by the fluid overload. The alveoli become ‘wet’ and crackles (rales) can be heard on auscultation. [pic3] If the congestion progresses, then the systemic circulation may become overloaded and the signs of right ventricular failure may appear as noted above.

COPD includes emphysema, chronic bronchitis, or most commonly a combination of both. Emphysema is the result of damaged alveoli that are unable to perform normal oxygen/carbon dioxide exchange. The emphysema patient can get outside air to the alveoli without problem but has difficulty getting oxygen across the alveolus into the capillary. The patient compensates in several ways. The respiratory rate increases. Breathing is accomplished through pursed lips in an attempt to increase the pressure in the alveolus to push oxygen into the capillaries. The number of circulating red blood cells increases in response to the chronically low oxygen level (polycythemia). Because of these compensating factors, the emphysema patient can generally maintain near normal oxygen levels and prevent increased carbon dioxide levels. This avoids the development of cyanosis and indeed the patient may appear pink in color. All of these efforts are fueled by a high consumption of calories and the patient is typically thin as a result. This combination produces the classic ‘Pink Puffer’ description used for the pure emphysematous patient.

When the primary problem is chronic bronchitis, the diameter of the bronchi and bronchioles is decreased due to swelling and increased mucous production. The alveoli are not affected. This results in decreased air exchange between the normally functioning alveoli and the outside air supply. The alveoli are thus under ventilated in the chronic bronchitis patient in contrast to the emphysema patient’s drive to over ventilate the alveoli. Thus carbon dioxide is increased and oxygen decreased in the alveolus and subsequently in the circulation of the chronic bronchitic. The patient tries to compensate with an increase in red blood cell production, which results in polycythemia also seen with the emphysema patient. However instead of a pink color, a bluish color (cyanosis) occurs due to the decreased oxygen level and increased carbon dioxide level in these red blood cells. These patients tend to be inactive and overweight. This combination produces the classic ‘Blue Bloater’ description of the individual with pure chronic bronchitis. It is important to recall that the majority of patients with COPD suffer from a combination of emphysema and chronic bronchitis. [pic4] When you mix the ‘Pink Puffer’ and the ‘Blue Bloater’ you may get the ‘Purple Person’, which is often the COPD patient’s initial appearance on your arrival.

One must always think in terms of the heart/lung system when approaching the CHF or COPD patient. Problems with one part of the system can adversely affect the function of other parts, even when the other parts are functioning normally. For example, the most common cause of right ventricular heart failure is left ventricular heart failure. This makes sense if you think about the increased pressure on the right ventricle if the left ventricle is unable to pump effectively and blood backs up into the right ventricle. COPD can also cause right heart failure. The pressure in the pulmonary circulation can increase because of changes in the pulmonary vessels caused by COPD. This is called pulmonary hypertension and causes the right heart to pump against a higher pressure than normal. Other lung diseases can cause pulmonary hypertension such as pulmonary emboli and pulmonary fibrosis. Over a period of time the pulmonary hypertension can lead to right ventricular heart failure. When pulmonary hypertension causes right heart failure it is called Cor Pulmonale. [5]Although left ventricular failure does not cause COPD, it can worsen the oxygen/carbon dioxide exchange if fluid backs up into the lungs and collects in the alveolus. This congestion makes it harder for oxygen and carbon dioxide to move back and forth between the alveolus and the capillary. [pic] .

Patient Assessment

History

In general, the CHF or COPD patient you will be called to assess and treat will be aware of their diagnosis. Your call to assistance is often because things have gotten worse. These patients may present with similar complaints. Dyspnea, fatigue and productive cough are common symptoms for both COPD and CHF. Dyspnea is defined by the American Thoracic Society as a “subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity.”[6]  Can’t catch your breath? Feel short of breath? Hard to breath? Most of us have experienced dyspnea, fortunately it is generally not frequent or persistent. For the patient with CHF or COPD, dyspnea is a common companion. Early in the disease process it may appear only with exertion. As each disease progresses dyspnea may begin to appear with little or no exertion, or show up suddenly during sleep (paroxysmal nocturnal dyspnea). As with any symptom, it is important to determine your patient’s baseline experience. It is significant if your patient with COPD or CHF generally experiences dyspnea climbing a few stairs, but over the past day or two has dyspnea at rest. The change may be secondary to worsening of their primary disease or due to an acute complicating problem such as infection or ischemia. Ask the patient if they have experienced this change in the past? You may luck out if your patient reports that the last time she felt this way was when her home oxygen supply ran low! Fatigue is common to both COPD and CHF and like dyspnea, it generally worsens with disease progression. Once again it is important to determine the baseline level of fatigue and any current changes and previous causes for increasing fatigue. Coughing is a shared characteristic of both diseases but for different reasons. The COPD patient can over produce mucous in the bronchi and bronchioles. This results in a cough that produces thick, sticky sputum. An increase in the amount of usual daily sputum production may signal a complication such as infection. The CHF patient may produce a frothy, blood tinged sputum if the pulmonary vascular congestion caused by the left heart failure produces enough pressure to force fluid and red blood cells from the capillaries into the alveoli (air sacs).

When CHF patients assume the supine position, as when sleeping, the edema fluid partially returns to the capillaries. This fluid is circulated to the lungs and kidneys causing increase dyspnea when lying down (orthopnea) and the need to urinate during the night (nocturia).  Many patients with CHF sleep on several pillows or even in a chair to prevent orthopnea. A patient who reports a need to use more pillows than usual or a move from the bed to a chair to get relief is reporting a worsening condition. Weight gain is another indicator that the congestion is getting worse. CHF patients should record their weight on a regular basis. If not you will have to depend on their estimate of any recent weight gain. In contrast, the COPD patient tends to experience weight loss in response to the increase calories required for breathing.

The patient with CHF will likely be on medications such as beta blockers (metoprolol) and angiotensin converting enzyme (ACE) inhibitors (Lisinopril). These medications are utilized to break the cycle of sympathetic stimulation and vasoconstriction induced by the failing heart in the body’s attempt to maintain an adequate blood pressure. This normal body response to inadequate tissue perfusion, makes the failing heart work harder and actually worsens the heart failure. If the patient is fluid overloaded, then the patient may be taking a diuretic such as furosemide (Lasix). The CHF patient already on several medications but still suffering from poor pump function may be placed on digitalis (Digoxin) in an attempt to improve pumping. Digitalis is used much less frequently than in the past. The COPD patient may have one or more multidose inhalers for bronchodilation such as albuterol (Ventolin, Proventil), ipratropium (Atrovent) or a combination of both (Combivent). The patient may also have a steroid inhaler. In addition oral steroids and antibiotics are frequently prescribed for the COPD patient. Physical Exam

When the ambulance is called, the COPD and CHF patient often present with a poor general impression. They may need to sit upright or in a tripod position just to breath. Tachycardia and tachypnea are common to both, as well as decreased oxygen saturation. They may need to rely on accessory muscle use and/or diaphragmatic breathing (belly breathing). The CHF patient may have signs of fluid overload in the pulmonary and/or systemic circulation. Auscultation of fine crackles or rales in the lungs in the CHF patient is an indication of pulmonary fluid overload. These crackles follow the fluid. If the patient is sitting, the crackles will be heard in the lower lung fields, but may also be heard higher on the chest depending on the severity of congestion. The supine patient will have more diffuse crackles on auscultation as the fluid layers out. Not all crackles (rales) are from CHF. Pneumonia can produce crackles (usually localized) as can pulmonary fibrosis (usually diffuse). Systemic congestion is represented on physical exam by JVD, dependent edema, and/or a palpable liver edge. On the monitor, atrial fibrillation is frequently associated with the CHF patient.

The COPD patient may present with pursed lip breathing to help keep the alvoli open and functioning. This method of providing positive end expiratory pressure (PEEP) is sometimes referred to as self-PEEP. Expiration is often prolonged in the COPD patient due to the narrowing of the bronchi and bronchioles from edema and mucus. The patient’s chest can take on a rounded or barrel shape in an attempt to maximize air movement. Breath sounds may be diminished and wheezing present. On the monitor, multifocal atrial tachycardia is frequently associated with COPD.

EMS Assessment and Management

The initial assessment and management for both COPD and CHF focus on the same primary problems: lack of oxygen delivery to the cells and inadequate disposal of carbon dioxide from the cells. Ensure your patient has a patent airway and is ventilating adequately with sufficient supplemental oxygen. The decision to continue further treatment at the scene or initiate immediate transport and continue treatment in route will depend on your determination of the need for priority transport. According to your local protocols, various medications may be helpful. The CHF patient can benefit from a decrease in blood return to the heart (preload) and a decrease in the pressure it must pump against (afterload). Nitroglycerine and morphine produce venous and arterial dilation that can provide a decrease in both preload and afterload. Additionally, morphine is effective in alleviating the symptom of dyspnea if it persists despite adequate oxygenation and ventilation. Furosemide (Lasix) is rapidly acting diuretic, which helps the kidneys excrete water from the systemic circulation thus decreasing preload. In addition it causes vasodilation that may help decrease preload and afterload.

Recall that COPD is defined as airflow restriction that is not fully reversible, which implies there exists a potentially reversible component. The patient may benefit significantly from reversing any existing bronchospasm. Beta 2 agonist and parasympatholytic (anticholinergic) medication produce bronchodilation when inhaled via a nebulizer or multidose inhaler. Beta 2 agonists such as albuterol (Ventolin, Proventil) attach to the sympathetic beta 2 receptors in the lungs and stimulate smooth muscle relaxation that results in bronchodilation. Parasympatholytic medication such as ipratropium (Atrovent) blocks the parasympathetic receptor which then produces smooth muscle relaxation and thus bronchodilation. Since these medications use different receptor sites to produce bronchodilation, combination therapy is generally more effective. Because of this, albutrol and ipratropium are available together in a single multidose inhaler (Combivent). 

The peak expiratory flow meter can be a useful prehospital tool. Peak expiratory flow is an individual’s maximal forced expiration. It can help differentiate COPD from CHF, as a low reading is consistent with COPD but not CHF.[7] In addition, by taking a baseline reading, you can objectively measure any improvement in airflow after treatment or any changes during prolonged transport. To obtain an accurate measurement, the patient must be alert and cooperative.[pic4]

Through out your patient contact, be vigilant for patient deterioration. The patient may require ventilatory assistance via bag valve mask or tracheal tube. Notify the receiving medical facility of any change in condition.

Hospital Care

On arrival to the receiving medical facility, your prehospital treatments have laid the foundation for the continuing care to come.

For the CHF patient, additional diuretics, nitroglycerine and morphine can be administered. Support for the pumping action of the heart via ionotropic agents such as dopamine and/or dobutamine may be necessary.

For the COPD patient, inhaled medication can be readministered and dosages adjusted. Intravenous antibiotics and steroids may be indicated. Aminophylline may be considered but its routine use is not supported.  Patients with COPD and CHF will benefit from further diagnostic procedures such as chest radiograph, ECG, arterial blood gas analysis, cardiac markers and various other blood tests.

Continuous positive airway pressure (CPAP) and noninvasive positive pressure ventilation (NPPV) can be effective in preventing the need for tracheal intubation and mechanical ventilation in the COPD and CHF patient with respiratory compromise.[8] CPAP is not a ventilating device, but because of its ability to maintain a positive airway pressure during inspiration and expiration, CHF patients with pulmonary edema and COPD patients with worsening respiratory status may improve. This can ‘buy’ time for the current therapeutic interventions to become maximally effective and potentially prevent the need for ventilator use. Should mechanical ventilation become necessary, NPPV can be effective for the CHF and the COPD patient and prevent the need for invasive mechanical ventilation via a tracheal tube and the associated complications such as tracheal damage and pneumonia. Both CPAP and NPPV require a tight fitting nasal or face mask and a machine to generate the positive pressure or provide mechanical ventilation. [pic5] CPAP and NPPV are not commonly available in the field but may be available in your receiving medical facility.

Summary

Treatment advances have evolved for the patient with heart failure that alter the progression of the disease and positively impacts the patient’s ability to function and survive. Unfortunately this is not the case for the patient with chronic obstructive pulmonary disease. Current treatments for COPD have been successful in alleviating symptoms and improving activity, however have not been effective in halting  progression of the disease. COPD is predicted to move from the fourth leading cause of death to the third leading cause of death in the future. CHF and COPD are on the increase. You will have increasing opportunities to care for these patients. As an EMT, you can have a positive impact on the patient’s outcome by providing field assessment and treatment based on a thorough understanding of both disease processes.

 

References

1.         Hunt, S.A., Baker, D. B., Chin, M. H., et. al., ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult. 2001, American College of Cardiology and the American Heart Association. http://www.americanheart.org/presenter.jhtml?identifier=11841

2.            American Heart Association, 2002 Heart and Stroke Statistical Update. 2001, American Heart Association: Dallas, Texas.

3.            Pauwels, R., Anthonisen, N., Bailey, W.C., et al, Global Initiative for Chronic Obstructive Lung Disease. 2001, National Heart, Lung, and Blood Institute and the World Health Organization. http://www.goldcopd.com

4.            National Center for Health Statistics, National Vital Statistics Report. National Center for Health Statistics, 2001. 49(12): p. 5.

5.         Beers, M.H., Berkow, R., ed. Merck Manual. 17 ed. 1999, Merck & Company, Inc.: Whitehouse Station, NJ.

6.            American Thoracic Society, Dyspnea mechanisms, assessment, and management: a consensus statement. American Journal of Respiratory and Critical Care Medicine, 1998. 159(1): p. 321-340.

7.         Ailani, R.K., Ravakhah, K., DiBiovine, B., et al, Dyspnea differentiation index, a new method for the rapid separation of cardiac vs pulmonary dyspnea. Chest, 1999. 116: p. 1100-1104.

8.         Mehta, S., Hill, N.S., Noninvasive ventilation. American Journal of Respiratory and Critical Care Medicine, 2001. 163: p. 540-577.

 

Tables

Signs

Signs

CHF

COPD

Tripod or upright position

+

+

Tachycardia

+

+

Tachypnea

+

+

Accessory muscle use

+

+

Decreases oxygen saturation

+

+

JVD

+

_

Auscultation of bilateral dependent crackles (rales)

+

_

Weight gain

+

_

Weight loss

_

+

Auscultation of decreased breath sounds         

_

+

Chest diameter increase

_

+

Pursed lip breathing

_

+

Prolonged expiratory phase

_

+

Low peak flow

_

+

 

Symptoms

Symptoms

CHF

COPD

Dyspnea

+

+

Fatigue

+

+

Cough

+

+

Orthopnea

+

_

PND

+

_

Dependent edema

+

_

Nocturia

+

_

 

 

 

 

 

 

 

Medication

Medication

CHF

COPD

Oxygen

+

+

Diuretic

+

_

ACE Inhibitor

+

_

Beta blocker

+

_

Digitalis

+

_

Beta 2 agonist

_

+

Ipratropium

_

+

Steroids

_

+