Congestive Heart Failure and Noninvasive Positive Pressure Ventilation

Patients with heart failure account for 12--15 million doctor office visits each year and 300,000 deaths.¹ There are many predisposing factors to heart failure, several of which--such as diabetes and sleep apnea--are on the increase. Not only is the death toll from heart failure appalling, but also the economic costs strain our healthcare delivery systems. Approximately 5% of the total United States healthcare budget is spent on heart failure.¹ Heart failure (DRG#127) is the most common diagnostic Medicare group.¹ Since many of these admissions come through the emergency department after being transported to the hospital by ambulance, EMS providers play a central role in the recognition of heart failure and early initiation of the most important lifesaving modality available to heart failure patients in transport: oxygen.

A recent article summarized the problem as follows: "Heart failure, a disease of epidemic proportions, has a tremendous clinical and financial impact on the U.S. healthcare system. With more than five million Americans diagnosed with heart failure and a five-year mortality approaching 50%, it is the most common cause of hospitalization in patients older than 65 years and is the single most expensive diagnosis in the U.S. healthcare system. Because the average U.S. hospital loses more than $1,000 per heart failure admission, effective therapies that decrease length of stay, reduce hospital costs and prevent 30-day readmissions are needed."²

Heart failure patients constitute a major economic burden to hospitals. If a patient in heart failure receives therapy, like early application of continuous positive airway pressure (CPAP), the possibility of an intensive care unit (ICU) stay on a ventilator and the associated cost is greatly reduced. Thus, EMS plays a critical role in the management of these patients, because the sooner proper treatment is initiated, the higher the chances that the patient will avoid an ICU admission.³

Congestive Heart Failure
(Right and Left Ventricular)

Congestive heart failure (CHF) is not identified as a disease; rather, it is referred to as a condition. Simply put, ventricular failure occurs when the amount of blood entering the ventricle is more than the ventricle can pump out (backward failure), or when the ventricle is damaged to the degree that it cannot deliver enough blood to meet the body's metabolic needs (forward failure). Right and left ventricular failure is merely noting which ventricle has failed.

When the right ventricle fails, the neck veins become distended; blood backs up in the liver, resulting in chronic passive congestion of the liver (CPC); and ankle edema occurs, because this part of the anatomy is so gravity-dependent. When this constellation of findings occurs, the patient is diagnosed as having "cor pulmonale." Cor pulmonale is seen in patients with advanced lung disease, such as chronic obstructive pulmonary disease (COPD).

As COPD advances past the early stages of airway inflammation and narrowing (remodeling), there is an eventual loss of lung capillary bed surface area. Hypoxemia now becomes almost continuous. These changes cause a marked increase in pulmonary artery pressure, higher than the right ventricle is capable of pumping against. If not treated, pulmonary hypertension will cause the right ventricle to fail. Another group of chronic lung diseases that have as their end result pulmonary hypertension is pulmonary (or interstitial) fibrosis. These disorders will also cause pulmonary artery hypertension and cor pulmonale.

The term congestive heart failure refers to failure of the left ventricle. When the left ventricle fails, blood congests in the lungs (pulmonary edema). If allowed to continue, this congestion will eventually cause the right ventricle to fail, the liver to develop CPC and ankle edema to appear. The causes for left ventricular failure are many. Coronary artery disease is the most common cause. Abnormal rhythms, incompetent or narrowed heart valves, toxic damage to the ventricular muscles (alcohol and certain antitumor drugs) and viral infections are other causes of heart muscle damage leading to ventricular failure.

When the left ventricle fails, needed nutrients such as oxygen, glucose, fatty acids and proteins are in short supply to the body's cells. All organs of the body need these nutrients in order to be healthy enough to perform their specific tasks. Equally important, the waste products of metabolism (CO2 and urea to name two) are no longer eliminated efficiently. As these toxins accumulate, they poison the body, which leads to death if not interrupted.

The symptoms of left ventricular failure include shortness of breath, heart palpitations, fatigue, increased urination at night (nocturia) and the need to sleep sitting up (orthopnea).

Physical findings in patients with left ventricular failure include crackles in the lungs on auscultation, ankle edema, distended neck veins, heart murmurs and abnormal rhythms and sounds (third heart sound--S3). All of these findings are a direct result of blood backing up in the chamber of the left ventricle and causing congestion in every part of the vascular system carrying blood to the left ventricle. As many of these physical findings are gravity-dependent, they are found early in the lower extremities.

Other methods of diagnosing heart failure include the chest radiograph, electrocardiogram and a new blood test called the brain natriuretic peptide (BNP). BNP is a peptide which naturally occurs in heart muscle (myocardium) and is excreted into blood in increased amounts when myocardium is stretched. The more the myocardium is stretched, as in congestive heart failure, the higher the level of BNP. This new test allows the clinician to differentiate between respiratory failure due to CHF or other causes such as COPD.

Noninvasive Positive-Pressure Ventilation

Noninvasive positive-pressure ventilation (NPPV) has become increasingly important in the management of respiratory insufficiency and respiratory failure. Patients using NPPV modes must be able to breathe spontaneously. There are three basic iterations of NPPV available. The earliest method was called intermittent positive-pressure breathing (IPPB). IPPB requires the end-expired pressure to return to zero after the patient has finished a respiratory cycle. A respiratory cycle has two phases: inspiratory and expiratory. The inspiratory pressure level must be set high enough to deliver an adequate volume of air or oxygen (tidal volume) to the patient before the device cycles off. These devices were classified as pressure-cycled ventilators. IPPB is rarely used anymore.

The second mode is bi-level positive airway pressure (BiPAP). With BiPAP, the inspiratory phase of the respiratory cycle (IPAP) is set higher than the expiratory phase (EPAP). A common setting would be IPAP of 12 cm and EPAP of 6 cm. At no time does the airway pressure return to zero. These devices have gained widespread acceptance in hospitals and are frequently used to ventilate patients without having to intubate.

The third mode is continuous positive airway pressure ventilation (CPAP). In this mode, the patient breathes through a pressurized circuit against a threshold resistor that keeps the airway pressure at a preset level. To qualify as CPAP, both the inspiratory and expiratory pressures must be the same. CPAP is known to lessen dyspnea by improving the pathophysiology of heart failure in two general areas: pulmonary mechanics and hemodynamics.

CPAP improves pulmonary mechanics by recruiting micro-atalectatic (collapsed and airless) alveoli and improving the ability of oxygen to diffuse from the alveoli onto red blood cells. Pulmonary recruitment is a phenomenon that occurs in the lung when pressure is applied to the airways in such a way as to open up unused or collapsed alveolar segments not participating in gas exchange.

CPAP is frequently described as being able to stent or stretch the airways open. This allows for deeper penetration into the alveolar region of the lung by each breath, and this stenting holds the airways open longer during exhalation. There is a subsequent decrease in work of breathing, due to an increase in lung compliance and lessening of auto-PEEP. Auto-PEEP is the abnormal residual pressure above atmospheric pressure that is trapped in the distal airways and alveoli at the end of exhalation.

Distribution of ventilation improves, as does secretion removal.⁴ Both ventilation (CO2 removal) and oxygenation (increased SaO2 and PaO2) are improved as a result.

Hemodynamics are improved by reducing pre- and afterload. When speaking in terms of the heart muscle, preload is the stretch on the ventricular muscle fibers before the next contraction occurs. Preload is created by the volume of blood left in the ventricle after the chamber has contracted and relaxed (end-diastolic volume). As the ventricle fails, the end-diastolic volume increases, and the cardiac muscles stretch as a result. The more they stretch, the more forcefully they are able to contract (Starling's law), until a physiological limit is reached. When that limit is exceeded, the ventricle is now in failure. Factors that influence preload include the degree of stiffness of the ventricular wall (compliance), changes in circulating blood distribution and volume and the ability for the atria to contract normally.⁵

Afterload is the sum of the external forces that oppose blood being ejected out of the ventricle. There are two main components of afterload: tension in the ventricular wall and peripheral resistance (impedance). Factors that oppose ventricular emptying include ventricular distention, increased intraventricular pressure, a thin ventricular wall, negative intrathoracic pressure and peripheral resistance caused by the arterial tree.⁵

CHF and CPAP

CPAP is believed to support the heart in failure by increasing intrathoracic pressure. This causes an increase in cardiac output by decreasing the pressure gradient across the ventricular wall (transmural ventricular pressure or afterload). This in turn allows the left ventricular end-diastolic volume to decrease, thereby reducing afterload. As a result, left ventricular ejection fraction is increased, muscle strength improves, and blood pressure and pulse rate decrease. Overnight plasma and urinary norepinephrine levels fall. Since there is less stretching of the myocardial muscles, the blood natriuretic peptide level falls.⁵

Studies show that CPAP is therapeutic when applied to patients in CHF.6 CPAP has also been shown to reduce the need for heart failure patients to be intubated and placed on a ventilator.^3,7--9

Conclusion

Heart failure is a serious medical condition that is on the increase. The sooner a patient is diagnosed with CHF and treatment started, the better the patient's chance for survival, especially when the CHF has occurred acutely.10 CPAP is a critical prehospital therapy that will lead to improved patient outcomes.¹¹ EMS providers have been successfully trained to initiate NPPV modes safely so as to improve survival of the patients committed to their care during transport.¹² If CPAP is applied to these patients, there is evidence that these patients will avoid more potentially dangerous interventions, and their hospital stays will be shorter.

References

1. ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult. A Report of the American College of Cardiology/American Heart Association task force on Practice Guidelines (Committee to Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure).
2. Peacock WF, et al. Management of acute heart failure in the emergency department. Congestive Heart Failure Suppl 1:3--18, 2003.
3. Kosowsky JM, et al. Prehospital use of continuous positive airway pressure (CPAP) for presumed pulmonary edema: A preliminary case series. Prehosp Emerg Care 5:190--196, 2001.
4. Scanlan C, Wilkins R, Stoller J. Egan's Fundamentals of Respiratory Care, 7th Edition. Mosby, 1999.
5. Wilkins R, Sheldon R, Krider S. Clinical Assessments in Respiratory Care, 5th Edition. Elsevier Mosby, 2005.
6. Midelton G, Frishman W, Passo S. Congestive heart failure and continuous positive airway pressure therapy: Support of a new modality for improving the prognosis and survival of patients with advanced congestive heart failure. Heart Dis 4(2):102--109, Mar--Apr 2002.
7. Lin M, Yang YF, Chiang HT, et al. Reappraisal of continuous positive airway pressure therapy in acute cardiogenic pulmonary edema. Short-term results and long-term follow up. Chest 107:1379--1386, 1995.
8. Hastings D, et al. A supportive adjunct for congestive heart failure in the prehospital setting. J Emerg Med Serv 23(9):58--65, 1998.
9. Bersten AD, Holt AW, Vedig AE, et al. Treatment of severe cardiogenic pulmonary edema with continuous positive airway pressure delivered by face mask. Dis Manage Health Outcomes 1:75--83, 1997.
10. Gardtman M, Waagstein I, Karlsson T, Herlitz J. Has an intensified treatment in the ambulance of patients with acute severe left heart failure improved the outcome? Europ J Emerg Med 7(1): 5--24, Mar 2000.
11. Kosowsky JM, Storrow AB, Carleton SC. Continuous and bilevel positive airway pressure in the treatment of acute cardiogenic pulmonary edema. Am J Emerg Med 18(1):91--95, Jan 2000.
12. Craven R, Singletary N, et al. Use of bilevel positive airway pressure in out-of-hospital patients. Acad Emerg Med 7(9):1065--1068, Sep 2000.