Congestive Heart Failure: Diagnosis, Pathophysiology ...

1 Congestive Heart failure : Diagnosis, Pathophysiology ,Therapy, and Implications for Respiratory CareMichael S Figueroa MD and Jay I Peters MD FAARCI ntroductionPathophysiology of Congestive Heart FailureEvaluation of the Patient With Congestive Heart FailureTherapy for Congestive Heart FailurePulmonary Complications of Congestive Heart FailureExacerbations of Heart failure : Use of CPAP and NPPVS ummaryCongestive Heart failure (CHF) is a common clinical disorder that results in pulmonary vascularcongestion and reduced cardiac output. CHF should be considered in the differential diagnosis ofany adult patient who presents with dyspnea and/or respiratory failure . The diagnosis of heartfailure is often determined by a careful history and physical examination and characteristic chest-radiograph findings. The measurement of serum brain natriuretic peptide and echocardiographyhave substantially improved the accuracy of diagnosis. Therapy for CHF is directed at restoringnormal cardiopulmonary physiology and reducing the hyperadrenergic state.

2 The cornerstone oftreatment is a combination of an angiotensin-converting-enzyme inhibitor and slow titration of a blocker. Patients with CHF are prone to pulmonary complications, including obstructive sleepapnea, pulmonary edema, and pleural effusions. Continuous positive airway pressure and nonin-vasive positive-pressure ventilation benefit patients in CHF words: Heart failure ,diastolic dysfunction, systolic dysfunction, obstructive sleep apnea, Cheyne-Stokes respiration, respira-tory failure , noninvasive ventilation. [Respir Care 2006;51(4):403 412. 2006 Daedalus Enterprises]IntroductionCongestive Heart failure (CHF) is a complex clinicalsyndrome that can result from any functional or structuralcardiac disorder that impairs the ventricle s ability to fillwith or eject blood. Since there is no definitive diagnostictest for Heart failure , it remains a clinical diagnosis that islargely based on a careful history and physical examina-tion and supported by ancillary tests such as chest radio-graph, electrocardiogram, and echocardiography.

3 Heartfailure is a common disease, affecting approximately 5million people in the United States, and it occurs predom-inately in the elderly, with almost 80% of cases occurringin patients over the age of magnitude of theproblem cannot be precisely assessed, because reliable pop-ulation-based data on the prevalence, incidence, and prog-nosis are lacking. Nevertheless, several studies have foundthat CHF is associated with a 2-year mortality rate ofapproximately 45 50%, which approaches that of , from a societal perspective, car-Michael S Figueroa MD and Jay I Peters MD FAARC are affiliated withthe Division of Pulmonary and Critical Care Medicine, The University ofTexas Health Science Center, San Antonio, S Figueroa MD presented a version of this paper at the 21stannual New Horizons symposium at the 51st International RespiratoryCongress of the American Association for Respiratory Care, held De-cember 3 6, 2005, in San Antonio, : Michael S Figueroa MD, Division of Pulmonary andCritical Care Medicine, University of Texas Health Science Center, 7704 Merton Minter Boulevard, 111E, San Antonio TX 78229.

4 APRIL2006 VOL51 NO4403ing for patients with CHF accounts for 2 3% of the federalhealth-care budget. The estimated direct and indirect costof CHF in the United States in 2005 was $ are 2 mechanisms of reduced cardiac output andheart failure : systolic dysfunction and diastolic dysfunc-tion. The most common causes of systolic dysfunction(defined by a left-ventricular ejection fraction of 50%)are ischemic Heart disease, idiopathic dilated cardiomyop - athy , hypertension, and valvular Heart disease. Diastolicdysfunction (defined as dysfunction of left-ventricular fill-ing with preserved systolic function) may occur in up to40 50% of patients with Heart failure , it is more prevalentin women, and it increases in frequency with each decadeof life. Diastolic dysfunction can occur in many of thesame conditions that lead to systolic dysfunction. The mostcommon causes are hypertension, ischemic Heart disease, hypertrophic cardiomyopathy , and restrictive cardiomyop - athy .

5 Many patients who have symptoms suggestive ofheart failure (shortness of breath, peripheral edema, par-oxysmal nocturnal dyspnea) but also have preserved left-ventricular function may not have diastolic dysfunction;instead, their symptoms are caused by other etiologies,such as lung disease, obesity, or occult coronary article will review the Pathophysiology , diag-nosis, and treatment of CHF, with specific discussion ofthe pulmonary manifestations and their treatment, includ-ing noninvasive positive-pressure ventilation (NPPV) of Congestive Heart FailureThe syndrome of CHF arises as a consequence of anabnormality in cardiac structure, function, rhythm, or con-duction. In developed countries, ventricular dysfunctionaccounts for the majority of cases and results mainly frommyocardial infarction (systolic dysfunction), hypertension(diastolic and systolic dysfunction), or in many cases valve disease, idiopathic cardiomyopathy ,and alcoholic cardiomyopathy are also major causes ofheart failure .

6 Heart failure often occurs in elderly patientswho have multiple comorbid conditions (eg, angina, hy-pertension, diabetes, and chronic lung disease). Some com-mon comorbidities such as renal dysfunction are multifac-torial (decreased perfusion or volume depletion fromoverdiuresis), whereas others (eg, anemia, depression, dis-orders of breathing, and cachexia) are poorly indicates not only an inability of the Heart to main-tain adequate oxygen delivery; it is also a systemic re-sponse attempting to compensate for the inadequacy. Thedeterminants of cardiac output include Heart rate and strokevolume (Fig. 1). The stroke volume is further determinedby the preload (the volume that enters the left ventricle),contractility, and afterload (the impedance of the flow fromthe left ventricle). These variables are important in under-standing the pathophysiologic consequences of Heart fail-ure and the potential treatments.

7 Furthermore, an appreci-ation of cardiopulmonary interactions is important in ourunderstanding of Heart failure . In the simplest terms, theheart can be viewed as a dynamic pump. It is not onlydependent on its inherent properties, but also on what ispumped in and what it must pump against. The preloadcharacterizes the volume that the pump is given to sendforward, the contractility characterizes the pump, and theafterload determines what the Heart must work preload is often expressed as the end-diastolic pres-sure/volume of the left ventricle and is clinically assessedby measuring the right atrial pressure. However, the pre-load is not only dependent on intravascular volume; it isalso influenced by any restriction to ventricular the Heart resides in the thoracic cavity, an increasedpositive pleural pressure (as seen with dynamic hyperin-flation in chronic obstructive pulmonary disease or asthma)can reduce right-atrial pressure (which equals central ve-nous pressure minus pleural pressure) and thus reduce ven-tricular filling.

8 The cardiac pump is a muscle and willrespond to the volume it is given with a determined volume increases, so will the amount pumped out in anormal physiologic state, to a determined plateau; thisrelationship is described by the Frank-Starling law (Figs. 2and 3).5A concept that is often poorly understood is the diastolicfunction of the Heart . Diastolic function is determined by2 factors: the elasticity or distensibility of the left ventri-cle, which is a passive phenomenon, and the process ofmyocardial relaxation, which is an active process that re-quires metabolic of the myocardiumoccurs in early diastole, and the untwisting of the leftventricle is an active process that produces a suction effectthat augments left-ventricular filling. Loss of normal left-ventricular distensibility or relaxation by either structuralchanges (eg, left-ventricular hypertrophy) or functionalchanges (eg, ischemia) impairs ventricular filling (preload).

9 The exercise intolerance seen with diastolic dysfunctionlargely results from the impairment of ventricular filling,Fig. 1. Determinants of cardiac : Diagnosis, Pathophysiology ,THERAPY,ANDIM PLICATIONS FORRESPIRATORYCARE404 RESPIRATORYCARE APRIL2006 VOL51 NO4which elevates left-atrial pressure and pulmonary venouspressure and causes pulmonary ,inadequate cardiac output during exercise results in poorperfusion of skeletal muscles, especially the leg musclesand the accessory muscles of second variable of stroke volume is cardiac con-tractility, which represents the muscular pumping of theheart and is commonly expressed as the ejection on autonomic input, the Heart will respond to thesame preload with different stroke volumes, depending oninherent characteristics of the Heart . A Heart with normalsystolic function will maintain an ejection fraction of over50 55%. A previous myocardial infarction may result innonfunctioning myocardium that will impair recent concept is that ischemic myocardial tissue can benonfunctioning (hibernating) but revitalized by surgical ormedical therapy directed at ischemic Heart of myocardial systolic function include phar-macologic agents (calcium-channel blockers), hypoxemia,and severe final determinant of stroke volume is afterload.

10 Inbasic terms, afterload is the load that the pump has to workagainst, which is usually clinically estimated by the meanarterial pressure. The normal cardiac output is relativelyinsensitive to afterload up to 140 mm Hg. However, theafterload represents not only the vascular resistance butalso the wall tension and intrathoracic pressure that themyocardium must work against. Together, these 3 vari-ables are impaired in the patient with failing Heart in CHF can be best evaluated with theabove variables considered together. If cardiac output falls,either the Heart rate or stroke volume must change in orderto maintain perfusion. If stroke volume cannot be main-tained, then Heart rate must increase to maintain cardiacoutput. However, the Pathophysiology behind CHF in-cludes not only a structural abnormality; it also includesthe cardiovascular response to poor perfusion with theactivation of the neurohumoral of therenin-angiotensin system attempts to increase preload bystimulating retention of salt and water, increasing vaso-constriction (and, thus, afterload), and augmenting cardiaccontractility.