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Diagnosis and Therapy of Heart Failure

Congestive heart failure is a clinical syndrome resulting from a primary abnormality in the function of the heart as a pump, and its diagnosis and therapy depend on an understanding of the underlying pathophysiology. This pathophysiology involves a wide variety of initial cardiac events as well as vascular and neurohumoral compensatory responses that contribute not only to the clinical syndrome, but also to its progression and premature mortality.

Primary cardiac overloads (e.g., hypertension or valve disease, like mitral insufficiency or stenosis, aortic stenosis or insufficiency, see definitions hypertension, mitral valve, aortic stenosis, aortic insufficiency) or loss of myocardium (e.g., myocardial infarction, heart attack, see definition myocardial infarction) elicite adaptive myocardial (heart muscle) changes including hypertrophy (enlargement of muscle cells) and ventricular chamber dilation. These adaptations may result in myocardial dysfunction that, if extensive enough, produces ventricular dysfunction, which ultimately eventuates in the syndrome of congestive heart failure.

Thus, etiology of the heart disease forms only one part of the physiologic derangement. The evaluation and treatment of the overt clinical syndrome involves consideration of not only the initial cause of the cardiac dysfunction but also the evolving compensatory process.

Terminology to be used below

1. Left ventricular dysfunction: an abnormality of systolic (contraction phase of the heart beat) or diastolic (relaxation phase when the ventricle refills) performance of the left ventricle such that either the contractile force is impaired and ventricular emptying reduced or the diastolic relaxation and filling are impaired, or both.

a. Systolic dysfunction: an impairment of the contraction of the left ventricle such that the stroke volume (SV, the amount of blood pumped out per heart beat) is reduced for any given end-diastolic volume (amount of blood remaining after contraction) or filling pressure. In general, the end-diastolic volume is increased significantly while the stroke volume is reduced. This may involve either or both ventricles.

b. Diastolic dysfunction: a state in which ventricular filling rate and the extent of filling is associated with an inappropriate rise in ventricular diastolic pressure (pressure after contraction ends). Normal systolic emptying (EF or ejection fraction)) may be maintained.

2. Heart failure: a clinical syndrome in which symptoms are associated with abnormalities in systolic or diastolic function. These symptoms may include fatigue, exercise limitation, dyspnea (shortness of breath) on exertion, orthopnea (shortness of breath relieved by sitting up), or paroxysmal nocturnal dyspnea(sudden shortness of breath at night).

3. Congestive heart failure: a clinical syndrome in which symptoms of cardiac dysfunction as noted under heart failure are accompanied by signs or symptoms of congestion, including peripheral edema (ankle swelling) or pulmonary congestion (rales in the lungs).

4. Impedance: the total force opposing left ventricular ejection of blood out through the aortic valve and composed primarily of arterial wall compliance, arteriolar resistance, and inertance.

5. Systemic vascular resistance: the calculation resulting from the division of the mean systemic arterial pressure, minus the mean systemic venous pressure, by the cardiac output (amount of blood pumped out per minute) and representing the sum of the resistance to flow of all parallel vascular channels in the systemic circulatory system.

6. Ventricle remodeling: an adaptive process which the ventricle is reshaped by structural changes resulting in increased chamber volume and increased myocardial mass. This involves myocyte (heart muscle cell) hypertrophy with cell widening and elongation as well as myocyte rearrangements in the ventricular wall. Interstitial growth (in between the myocytes) also is characteristic of the process.

Etiology of Heart Failure

In general, heart failure begins with either abnormality of coronary blood flow (ischemia and infarction, see definition of coronary atherosclerosis, angina and myocardial infarction in this web site), ventricular overloads whether from pressure (systemic arterial hypertension, aortic stenosis) or volume (mitral regurgitation or congenital shunt lesions, see definition congenital heart disease), or unexplained myocyte loss and depression (cardiomyopathies, viral myocarditis, toxins; see definition cardiomyopathies). It may also evolve from incessant arrhythmias (sustained tachycardia). Less commonly, the syndrome of congestive failure can result from external factors that limit ventricular filling (constrictive pericarditis). See definitions respectively on this web site.

Ischemic Heart Disease

Both systolic and diastolic dysfunction are early manifestations of myocardial ischemia, since even modest reductions of blood flow may deprive the myocardium of adequate nutrition for generation of muscle contraction and muscle relaxation.

In humans the induction of ischemia, through either decreased coronary blood flow or increased oxygen need not met by increased blood flow, results in a rapid loss of contraction in the region involved. If blood flow is restored to the region before necrosis ensues, contractile activity does not return for hours or even days.

This persistent loss of contractile activity for hours or days despite return of blood flow and the absence of necrosis is termed "stunning" and may contribute to ventricular dysfunction and symptoms of heart failure. Severe stunning may also produce persistent segmental dilatation of the ventricle by damaging connective tissue connections between cells, a form of remodeling.

Another concept, "hibernating" myocardium, refers to myocardium with a contractile dysfunction resulting from a chronic inadequacy of blood flow without histologic evidence of myocardial infarction (see magnetic resonance definition on this web site, and figures 122, 123, 124, 125).

Myocardial infarction results in a loss of functioning myocardium in the region served by the occluded coronary vessel. If the loss of coronary flow is incomplete perhaps due to collateral blood flow, only a subendocaridal infarction (occurring just under the inner lining of the ventricle and not extending through the entire wall to the outer surface of the heart) may result. Nevertheless, this leaves a larger load for the myocardium remaining in the region.

The scar resulting from myocardial infarction may further contribute to left ventricular dysfunction by restricting filling or by creating an aneurysm (see definition myocardial infarction and aneursym on this web site). With large infarctions, compensatory ventricular dilation occurs and reactive hypertrophy occurs in the remaining well-perfused myocardium. With large increases in diastolic filling pressure, "myocyte slippage" occurs and leads to further loads on the ventricular wall. These compensation processes of myocyte hypertrophy, dilatation, and changes in wall conformation comprise ventricular remodeling.

Mitral regurgitation may also develop, secondary to either left ventricular dilatation or papillary muscle (cardiac muscle bundles, which connect to the mitral or tricuspid valve through chordae tendonae) dysfunction (see definition on this website, figure 104b).

Thus, although the regional dysfunction or scar formation association with coronary artery disease initially is confined to an area in the distribution of the involved coronary artery, this process often progresses to a dilated ventricle with global impairment of contractile function (hypokinesis). This chamber enlargement, or ventricular remodeling, may occur over days, weeks, months, or years and eventuate in a marked impairment of systolic function. In other instances, however, the regional dysfunction may persist and the ventricle may remain normal in size for many years.

Hypertrophy is an almost invariable accompaniment of the remodeling process in patients with primary ischemic disease of the myocardium. This hypertrophy may, in part, represent a reactive process to normalize wall stress induced by dilatation of the chamber dimension. Neurohumoral factors may also contribute to the ventricular hypertrophy.

With these considerations in mind, therapy of ischemic processes is directed both to the ischemic event as well as to the ventricular remodeling it induces.

Nonischemic Disease

In a patient with epicardial coronary arteries that angiographically appear to be normal or nearly normal and with no other apparent disease, a dilated, poorly contracting left ventricle is usually diagnosed as idiopathic dilated cardiomyopathy (figure 43b). Nonetheless, even in this clinical situation ischemia cannot be excluded as an important etiologic factor. Small vessel disease that can influence regional or global perfusion may not be demonstrable by angiographic techniques.

A primary disease affecting the myocyte and its contractile process appears to be the cause of most cases of idiopathic dilated cardiomyopathy (see Definition Cardiomyopathy on this web site, and figure126). In general, idiopathic dilated cardiomyopathy is characterized by focal, diffuse myocyte loss, replacement fibrosis (scar like tissue), and reactive hypertrophy of the remaining myocytes.

A variety of etiologic agents has been implicated, and the process can be multifactorial. In most instances the etiology of cardiomyopathy or heart muscle disease of unknown cause cannot be determined by histological examination. Aside from systemic arterial hypertension and coronary artery atherosclerosis, viruses, alcohol, and diabetes may represent the most prevalent factors contributing to heart muscle dysfunction in North America. Diabetes may also be associated with large and small vessel obstructive disease.

Due to increasingly effective therapy for hypertension, the incidence of hypertension as a primary cause of heart failure has been greatly reduced, but remains an important cofactor in heart failure from other etiologies.


Ventricular Function

The myocardial abnormalities described above ultimately result in hemodynamic derangement of ventricular function. As capacity for force development and shortening by the ventricular wall is lost, a compensatory increase in diastolic ventricular volume occurs. Thus, stroke volume is only maintained by an increase in diastolic volume and pressure.

Moreover, the relation of stroke volume to end-diastolic pressure is not only depressed but flattened at higher filling pressure. Should marked ventricular hypertrophy without myocyte loss occur, such as with systemic arterial hypertension, prolonged systole, and delayed or incomplete diastolic relaxation of the ventricle, along with thicker ventricular wall, may elevate the end-diastolic filling pressures even with normal volumes, and the end-diastolic pressure be actually less than expected for the increase in volume.

In the early stages of left ventricular dysfunction, the hemodynamic abnormalities may be confined to exercise, when the increase in stroke volume demanded by exercise may be inadequate and/or accompanied by an abnormally brisk increase in left ventricular filling pressure. The left ventricle normally is capable of adjusting its work output to match an increasing aortic impedance over a wide physiological range.

The dysfunctional left ventricle loses this ability and its performance becomes progressively more impaired as the impedance is increased. Thus, the failing left ventricle becomes very sensitive to impedance or afterload and, becomes quite insensitive to preload. This important physiological shift from a preload-dependent and afterload-independent ventricle in the normal individual to a preload-independent and afterload-dependent ventricle in the setting of heart failure has important therapeutic implications.

In most patients with heart failure some degree of diastolic dysfunction accompanies systolic dysfunction. The left ventricular diastolic dysfunction, or reduced diastolic ventricular compliance, implies that the left ventricular is stiffer than normal and therefore responds to a small increment in volume with a prominent increase in diastolic filling pressure that is transmitted backward into the pulmonary vasculature, leading ultimately to pulmonary congestion rales,and dyspnea..

Neurohormonal Activation

Neurohormonal systems are activated in the setting of left ventricular dysfunction (regardless of etiology) with decreased cardiac output and consequently arterial underfilling and activation of baroreceptors in the aortic arch, carotid sinus, and left ventricle (figure151). These baroreceptors stimulate vasomotor regulatory centers in the medulla, which activate the sympathetic nervous system(see definition autonomic nervous system), arginine-vasopressin system, and renin-angiotensin-aldosterone system.

Activation of the sympathetic nervous system is manifested by elevated plasma norepinephrine levels, increased spillover into the bloodstream of norepinephrine released into the synaptic cleft, and evidence for increased sympathetic nerve traffic (increases in heart rate, myocardial contractility, peripheral vasoconstriction).

The renin-angiotensin system activated in heart failure, presumably through intrarenal mechanisms stimulated by changes either in pressure or changes in sodium load in the macula densa, leads to sodium and water retention.

Peripheral Vasculature

An increase in systemic vascular resistance and a reduction of arterial and venous compliance are hallmarks of the syndrome of heart failure.

Clinical Manifestation of Heart Failure

The four major clinical manifestations of heart failure are left ventricular dysfunction, exercise intolerance, congestion or edema, and ventricular arrhythmias.

Chronic heart failure symptoms can be divided into four classes according to the New York Heart Association (NYHA) as follows:

Class1: Symptoms cause no limitation of physical activity. Ordinary physical activity does not lead to undue fatigue, or dyspnea.

Class2: Symptoms cause slight limitation of physical activity.Patient is comfortable at rest, but ordinary physical activity results in fatigue, palpitations,or dyspnea.

Class3: Symptoms cause marked limitation of physical activity. Patient is comfortable at rest, but even slight physical activity causes fatigue ,palpitations, or dyspnea.

Class4: Symptoms of cardiac insufficiency are present at rest, and discomfort is increased with any physical activity.

Clinical Diagnosis (see other related sections on this website for history, physical diagnosis, and laboratory tests)


1. The first responsibility of treatment is to correct or stabilize any primary abnormality or overload that can be identified. Thus, ischemia is controlled by medical or surgical intervention, hypertension is rigorously treated, and primary valve abnormalities are evaluated for the possibility of repair. ( see other related sections of this website)

2. Nonpharmacologic Therapy

A. Salt restriction B. Weight loss C. Restriction of dietary saturated fat and cholesterol D. No smoking E. Exercise prescription

3. Pharmacologic Therapy

A. Diuretics

B. Vasodilator Drugs (to relax the systemic vasculature and/or reduce venous tone)
i. Nitrate (isosorbide)
ii. Hydralazine (Especially when added to a regimen of digoxin and diuretic therapy)
iii. Ace inhibitors (captopril, enalapril)

C. Inotropic Drugs (positive ones which increase the contractile force of the myocardium)
i. digitalis glycosides (i.e.digoxin)

D. Neurohormonal Inhibition

i. Ace inhibitors inhibit the conversion of angiotensin1 to angiotensin 2(A2) through angiotensin-converting enzyme(ACE) causing a reduction in circulating and tissue levels of angiotensin11 and a reduction in norepinephrine (through down-regulation of the sympathetic nervous system see definition autonomic nervous system), subsequent reduction in aldosterone leading to decrease in sodium and fluid retention, possble inhibition of myocardial hypertrophy and remodeling and vascular hypertrophy, reduction of resistance to left ventricular outflow through vasodilation.

A recent study has shown that enalapril therapy (an angiotensin-converting-enzyme inhibitor) is associated with a significant reduction in the risk of hospitalizationfor heart failure among white patients with left ventricular dysfunction, but not not among similar black patients. This difference may be related to the lower plasma renin levels and endogenous nitric acid levels in black patients as well as to under lying genetic determinants of drug response.

Reference: Exner,D.V.,et. als.,Lesser Response To Angiotensin-Converting-Enzyme Inhibitor Therapy In Blcak As Compared With White Patients With Left Ventricular Dysfunction,N.Engl.J.Med.,Vol.344,No.18,May3,20011351-57.

ii. Ace2 receptor blockers (ie, losartan) block A2 from all pathways at the receptor level, producing vasodilation and inhibiting muscle cell proliferation. But these agents are to be used only if the ACE inhibitors can not be tolerated due to side effects such as cough, since a recent study showed no statistical difference in mortality rates between the captopril and the losartan groups.

iii. Beta blockers improve left ventricular function,symptoms and functional class, and prolong survival in patients with CHF due to left ventricular dysfunction.

Currently, carvedilol,metoprolol,and bisoprolol are proven therapies. Carvedilol in addition has alpha-receptor-blocking effects, which theoretically gives more complete sympathetic blockade.

It has been shown that one year of treatment with carvedilol in dialysis patients with congestive heart failure (CHF) and dilated cardiomyocardiopathy (DCM) reduced LV volumes and improved LV function and clinical status.

Beta blockers modify the dysregulated cytokine network (interleukin-10, tumor necrosis factor-alpha (TNF-alpha), and soluble TNF receptors (sTNF-R-1 and R2) in dilated cardiomyopathy and may be responsible for the efficacy of therapuetic drugs for heart failure.

A recent study showed that the benefit of carvedilol was apparent and of similar magnitude in both black and nonblack patients with heart failure.

Reference:Yancy,C.W.,Et.Als.Race and the Response to Adrenergic Blockage with Carvedilol in Patients with Chronic Heart Failure,N.Engl.J.Med.,Vol.344.No.18,May 3,2001,1358-65.

Also, another recently reported study reveals that carvedilol's benefit extends to patients in severe heart failure with regards to morbidity and mortality.

Reference:Packer,M. and others,Effect of Carvedilol on Survival in Severe Chronic Heart Failure,N.Engl.J.Med.,Vol.344,No.22,May31,2001,1651-1658.

On the other hand, another study published in the same journal at the same time indicate that in a group of patients with NYHA class111 and 1V treatment with bucindolol(a beta-blocker) resulted in no significant overall survival benefit. But there was a benefit in nonblack patients.

One possible reason for the difference between the two preceding studies may be due to the different pharmacologic properties of bucindolol, a nonselective beta-blocking agent with unique sympatholytic activity due to its strong B2-adrenergic blockade and only weak alpha-1-blocking properties.

Reference:The Bata-Blocker Evaluation of Survival Trial Investigators, A Trial of the Beta-Blocker Bucindolol in Patients with Advanced Chronic Heart Failure,N.Engl.J.Med.,Vol.344,No.22,May31,2001,1659-1667.

But it has been pointed out that the most advanced forms of heart failure (not extremely severe) patients were excluded in the first referred to study above and an improvement was observed in nonblack patients. It is important to remember that these drugs must be administered and the dose escalated slowly in patients with heart failure, especially those in whom the condition is severe.

Indications for beta-blockers:

1. Treat all patients who have NYHA class2 or 3 symptoms.

2. Consider therapy for patients with NYHA class1 or 4 symptoms.

3. Use agents that have proved beneficial in major mortality trials (see above second paragraph).

4. Before adding beta- blocker therapy, make sure patient is stable and on standard heart failure treatment (eg, ACE inhibitor, diuretic, digoxin).

5. Start beta-blocker theray at low dosage (eg,carvedilol, 3.125 mg PO bid; metoprolol CR/XL, 12.5 mg PO qd; bisoprolol, 1.25 mg PO qd)

6. Increase dosages at 2 to 3 wk intervals, as tolerated to target levels established in major mortality trails (eg, carvedilol, 25-50 mg PO bid; metoprolol CR/XL, 200 mg PO qd; bisoprolol, 10 mg PO qd)

7. Tell Patients, Side effects may occur early in therapy but do not preclude long-term use. Symptomatic improvement may not be noticed for 2 to 3 months. Treatment may reduce risk of disease progression, even if symptoms do not improve.

Contraindications to beta-blocker therapy for CHF: signs of clinically unstable heart failure in the previous 2 weeks: a). increase in body weight, b). increase in diuretic dose, c). need for intravenous diuretic ot inotrpic ageents, d). need for hospitalization for cardiac symptoms, 4). presence of episodic worsening of CHF symptoms, e). bronchial asthma or emphysema sensitive to beta agonists, f). bradycardia (heart rate<60beats perminute, g). hypotension (systolic blood pressure<100mmHg), h). second or third degree heart block.

iv. Aldosterone antagonists such as spironolactone should be considered in all patients with severe symptomatic heart failure in the absence of significant renal insufficiency or hyperkalemia.

v. Preliminary data suggest that endothelin receptor antagonists, vasopeptidase inhibitors, and synthetic natriuretic peptides may represent the next wave of CHF treatment options.

Reference:Cice,Gennaro,MD and others.Dilated Cardiomyopathy in Dialysis Patient-Beneficial Effects of Carvedilol:A Double-Blind, Placebo-Controlled,Trial,Jacc,,vol.37,no2,2001 February 2001:398-406

Reference:Packer,M. and others,for the US Carvediol Heart FAILURE STUDY STUDY GROUP.The effect of carvedilol on morbidity and mortality in patients with chronic heart failure,NEJM 1996;334:1349-55.

Ohtsuzki,T. MD,and others,Effect of Beta-blockers on Circulating Levels of Inflammatory and Antiflammatory Cytokines in Patients with Dilated Cardoimyopathy,JACC,VOL37,nO.2,2001 PP.412-417.

Ward,R.P. and Anderson,A.S.,Slowing the progression of CHF,Postgraduate M ed.,Vol.109,No.3,March2001,36-45.

Garg, Ravi M.D. and Sorrentino, Matthew MD, Postgraduate Medicine Vol 109/ No 3./ March 2001 pg 49-56

E. Antiarrhythmic Therapy (may shorten life expectancy and hence are used with caution during symptomatic ventricular arrhythmias in view of the risk. In such patients other pharmacologic agents (? like amiodarone) or implantible defibrillators may be more effective therapy. See definition ventricular tachycardia on this web site).

F. Anticoagulant Therapy (to reduce the risk of systemic embolization in patients with atrial fibrillation, but it is not indicated in patients who are fairly active and have not had a previous episode of embolization).

G. Biventricular Pacing in Patients with Severe Congestive Heart Failure due to Idiopahitic or Ischemic Heart Left Ventricular Systolic Dysfunction with Intraventricular conduction delay (QRS complex duration, see figure 94 re normal EKG) of more than 150ms. (over 100ms is abnormal) and without a standard indication for insertion of a pacemaker (see definition bradycardia management).

This procedure of atriobiventricular pacing has been shown to significantly improve exercise tolerance, symptoms, and the quality of life in these patients and is associated with a reduced number of hospitalizations for decompensated heart failure.

It involves the implantation of all leads transvenously. The atrial lead is placed high in the right atrium. The left ventricular lead is placed in a tributary of the coronary sinus, according to a previously described method (figure 149). Specially designed electrodes are used. A venogram helps to optimize the position of the leads (figure 150). The target area was preferably the lateral wall, midway between base and apex, but other lateral or posterior sites were also acceptable. The great cardiac vein or the mid cardiac is used only when other sites were not accessible. The right ventricular lead was positioned as far as possible from the the left ventricular lead.

The pacemakers were triple-output devices that made use of standard dual-chamber technology, with built-in adapters to synchronize the pacing of the two ventricles.

(Chorum 7336MSP,ELA Medical,Montroube,France, and InSync 8040,Medtronic, Minneapolis).
Reference:Cazeau,S. and Others,Effects of Multisite Biventricular Pacing in Patients with Heart Failure and Intraventricular Conduction Delay,NEJ of M.ed.,March22,2001,No.12 V.344.pp873-880.
Reference:Dauber,J.C.,and Others,Permanent Left Ventricular Pacing With Transvenous Leads Inserted Into The Coronary Veins,Pacing Clin.Electrophysiol.1998;21;239-245

4. Invasive Approaches

A. Coronary Reperfusion,especially if there is the occurence of repeated episodes of acute left heart failure associated with pulmonary edema even in the absence of chest pain and dietary salt indiscretions (suggesting "flash" or acute ischemic left ventricular diastolic dysfunction. Coronary angography may be indicated. See coronary angiography definition on this web site).

If ischemia is obvious, the presence of left ventricular dysfunction is not a deterrent to coronary revascularization.

B. Valvular Heart Disease (surgery for functional valvular regurgitation due to left ventricular heart failure is not very effective and very risky).

C. Reduction ventriculoplasty involves excising the part of the left ventricular muscle which is dyskinetic, resulting in an increase in the contracting myocardium that maintains cardiac output (figure 151b). It offers a potential solution to a subset of patients with end stage heart failure.

D. Transmyocardial laser revascularization may be used in patients deemed ineligible for bypass surgery or any percutaneous intervention. It involves using a laser instrument to drill holes into the myocardium, which sets up an inflammatory reaction around the area, to neovascularization to increase the blood supply to the ischemic area.

E. Procedures to assist or replace heart function:
1) intra-aortic balloon pump (figure 152),
2) permanent implantable balloon pump (figure 153),
3) total artificial heart (figure 154).

F. Heart Transplantation (most effective therapy for severe heart failure, figure 155).

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Reference:Cohen,J. and Sonnenblick,E.H., Diagnosis and Therapy of Heart Failure, Hurst's THE HEART,8th Edition ,pp.557-571

Reference:Jayakar,D.V.,Surgical treatment of CHF,Postgraduate Med. vol.109/n.3,March2001,61-69




There are numerous respiratory complications of obesity, including an increased breathing workload,respiratory muscle inefficiency,decreased functional reserve capacity and expiratory reserve volume ,and closure of peripheral lung units.These complications often result in a ventilation-perfusion mismatch,especially in the supine position.Obesity is a classic

cause of alveolar hypoventilation. Historically, the obesity-hypoventilation syndrome has been described as the "pickwickian" syndrome, and obstructive apnea was first observed in patients with severe obesity. Sleep apnea is defined as repeated episodes of obstructive apnea and hypopnea during sleep, together with daytime somnolence and/or altered cardiopulmonary function. The prevalence of sleep-disordered breathing and sleep disturbances rises dramatically in obese subjects and obesity is by far the most important modifiable risk factor in sleep-disordered breathing.It has been estimated that 40 million Americans suffer from sleep disorders and that the vast majority of these patients remain

Despite careful screening by history and physical examination, sleep apnea is revealed only by polysomnography in most patients. Although, some clinical features could be useful in screening for sleep apnea, the diagnostic accuracy is inadequate.
Patients with sleep apnea have an increased risk of diurnal hypertension, nocturnal dysrhythmias, pulmonary hypertension, right and left ventricular failure, myocardial infarction, stroke, and mortality. The prevalence of pulmonary hypertension in subjects with obstructive sleep apnea is 15 to 20 percent; however, pulmonary hypertension rarely is observed in the absence of daytime hypoxemia. According to Kessler and colleagues the extent of pulmonary hypertension in patients with obstructive sleep apnea is generally mild to moderate (pulmonary artery pressures ranging between 20 and 35 mmHg) and does not necessitate specific treatment.

Although there is a link between sleep apnea and systemic hypertension, the association of obesity with both disorders confounds the relationship. A physician who evaluates an obese patient who has been referred for hypertension should address related symptoms such as habitual snoring, nocturnal gasping or choking, witnessed episodes of apnea, and daytime sleepiness. It is important to remember, however, that the clinical and ECG signs of cor pulmonale appear later than do those of pulmonary hypertension (assessed by right heart catheterization). Numerous treatments are available for sleep apnea, but weight loss in obese patients should always be advocated.

Severe untreated sleep-disordered breathing can further impair LV function,leading to arterial oxyhemoglobin desaturation and arrhythmias.Central sleep apnea may occur in as many as 40% of patients with heart failure,and 10% suffer from obstructive sleep apnea.Obstructive sleep apnea increases afterload and heart rate during sleep but is responsive to continuous positive airway pressure.