Atrial Fibrillation Treatment & Management
Pulmonary Edema
Pulmonary edema causes accumulation of fluid in the lungs leading to shortness of breath and coughing of blood. Although it is commonly caused due to congestive heart failure, there might be other reasons that increase your risk of suffering from this lung condition. Our expert Dr Manisha Mendiratta,Consultant Respiratory Medicine, Saroj Super Speciality Hospital, New Delhi lends some significant inputs on this topic.
CausesPulmonary oedema is the abnormal build-up of fluid in the air sacs of the lungs because of disorders such as –
Dr Manisha explains, 'Patients suffering from heart problems or heart failure are at an increased risk of pulmonary edema. However, it does not mean that every case of pulmonary edema is due to heart problems.' Here are some of the common risk factors that make you susceptible to this lung condition -
Read about Hyperventilation — causes, symptoms, treatment and prevention. SymptomsThe common signs and symptoms of pulmonary edema which might experience, if suffering from the condition are -
DiagnosisPulmonary edema is diagnosed based on symptoms (like shortness of breath, coughing up blood and chest pain) and physical examination. Test done used to diagnosed pulmonary edema may include –
Chest X-ray: Chest X-ray is a simple, useful imaging test for diagnosing a lot of heart conditions like congestive heart failure, enlargement of the heart, heart infections and lung problems.
Blood test: It is mainly recommended to check oxygen levels in the blood and thus, determine the efficiency of lung and heart function.
ECG or echocardiography: It helps in the diagnosis of an underlying heart disease thereby aiding in the treatment option. Here are 8 tests that can tell if you have heart disease.
Pulse oximetry: A procedure used to measure blood levels of oxygen (or oxygen saturation in the blood); this test helps in the diagnosis of pulmonary oedema and also aids in the determination of the cause of the condition.
Pulmonary artery catheterization: In this procedure, a catheter is inserted into a pulmonary artery to determine the severity of heart disease or any inflammation of the organ.
Here's everything you should know about Lung Function Tests (LFTs).
TreatmentThe conventional measures used to treat pulmonary edema include –
Medications: The drugs that are normally prescribed for people suffering from this condition include diuretics (to remove excess fluid from the body). Also, medicines that improve heart functioning by controlling heartbeat, relieving pressure and strengthening heart muscle are also recommended.
Ventilation: In cases of emergency, oxygen is supplied to the heart and lungs through a face mask or with the help of a breathing tube attached to the ventilator (a breathing machine).
Other effective treatment options that are currently gaining significance include use of liposomes. According to Dr Manisha'Use of liposomal drugs or delivery of drugs through liposomes is one of the most advanced treatment option that is been used to treat pulmonary oedema in recent times. Liposomes are microscopic phospholipids bubbles with a bilayered membrane structure that are targeted to delivery drugs to the affected area'.
Read about Tara asana — a asana to strengthen your lungs.
PrognosisAlthough the prognosis of this condition is dependent on the cause, in most cases it gets better in quick time. In some case, you might need to use a breathing machine for a long time for effective results. If left untreated, pulmonary edema can be life-threatening.
PreventionPulmonary edema is not always preventable, but there are few measures that can help you to reduce the risk of suffering from this condition. Here are few tips from our expert Dr Manisha -
The content has been verified by Dr Manisha Mendiratta,Consultant Respiratory Medicine, Saroj Super Speciality Hospital, New Delhi.
More From Pulmonary EdemaRestrictive Cardiomyopathy
A restrictive cardiomyopathy results in severe diastolic congestive heart failure with intact systolic function.
This is due to significantly impaired left ventricular relaxation, which results in increased cardiac pressure and clinical manifestations of congestive heart failure.
Etiology Causes of restrictive cardiomyopathies include:Restrictive cardiomyopathy manifests as congestive heart failure. This will result in low cardiac output symptoms and transmission of the increased left-sided cardiac pressures into the lungs causing pulmonary edema and a sense of dyspnea. With physical exertion the heart demands increased cardiac output that cannot be satisfied in states of heart failure, and thus left heart pressures increase significantly causing this transient pulmonary edema.
As those increased pressures from the left heart affect the right ventricle, right heart failure can ensue. The most common cause of right heart failure is left heart failure.Right heart failure symptoms include lower-extremity-dependant edema. When the legs are elevated at night, the fluid redistributes centrally causing pulmonary edema resulting in orthopnea (dyspnea while laying flat) or paroxysmal nocturnal dyspnea (PND). Hepatic congestion can occur causing right upper quadrant abdominal pain.
Symptoms related to low cardiac output include fatigue, weakness and, in extreme cases, cardiac cachexia can occur.
Physical Examination DiagnosisDiagnosis can be made via echocardiography and, in some cases, cardiac biopsy. Echocardiography will reveal normal left ventricular systolic function with significant diastolic impairment, frequently grade III or grade IV diastolic dysfunction (see image below).
The left and right atrium may be markedly enlarged and a pericardial effusion may be present. The myocardium itself may exhibit a "starry-sky" or a "speckled" appearance if amyloid cardiomyopathy is the etiology. Pulmonary hypertension is commonly present due to the left heart failure.
Amyloid protein deposition can be seen as apple green birefringence upon microscopic examination. Iron deposition can be detected by biopsy, as well.
TreatmentTreatment is aimed at the primary etiology, if possible; however, no specific therapy exists to improve outcomes in regard to the congestive heart failure that manifests. Diuretics are used to relieve symptoms of dyspnea from volume overload. Beta-blockers and ACE inhibitors have not been extensively studied in this setting and are not commonly used. Heart-liver transplantation is used for amyloid cardiomyopathy with a transthyretin component since this form of amyloid protein is produced in the liver.
Chronic Heart Failure - Heart Failure With Preserved Ejection Fraction Topic Review
IntroductionChronic heart failure occurs when either the left ventricle, the right ventricle, or both require elevated filling pressures to maintain cardiac output. Heart failure is a syndrome, not a specific disease, and occurs as a final common pathway in multiple disease states.
Heart failure (HF) can be due to the following:
The section presents a review of diastolic congestive heart failure, commonly called HFpEF. Reviews of systolic congestive HF, or HFrEF, valvular heart disease, pulmonary hypertension and right HF, and high output HF are discussed elsewhere.
Pathophysiology –HFpEFLeft ventricular diastolic dysfunction is manifest when increased filling pressure (ie, left atrial, pulmonary capillary wedge and pulmonary artery diastolic pressures) is required in order to maintain cardiac output. HFpEF connotes diastolic dysfunction despite a normal ejection fraction. Diastolic dysfunction also occurs frequently in patients with HFrEF. [Hurst's The Heart Section 11:13a,14a-b,15a]
Although the renin-angiotensin-aldosterone system is activated in HFpEF, it is not as prominent as with systolic HF, and cardiac remodelling is less marked.
The figure below shows a schematic of the negative neurohormonal feedback mechanisms that become active in worsening HF:
Etiology –HFpEFSome of the underlying causes of HFpEF are listed below:
Hypertension may cause left ventricular hypertrophy (LVH) and impaired relaxation. Over time, this condition progresses, resulting in higher degrees of diastolic dysfunction, low cardiac output and symptoms of congestive HF.
Restrictive cardiomyopathies frequently involve myocardial infiltration — amyloid deposition, for instance. This results in diastolic relaxation abnormalities and, eventually, the syndrome of HFpEF.
Obstruction to LV outflow leads to left ventricular hypertrophy and diastolic dysfunction. Sustained tachycardia, such as unrecognized and uncontrolled atrial fibrillation with a rapid ventricular response, may occasionally result in HFpEF symptoms. However, more commonly, tachycardia-induced cardiomyopathy results in reduced ejection fraction.
The aging process of the heart is not well understood, but fibrotic changes in the myocardium typically occur with advanced age. This results in relaxation abnormalities that are often present by the age of 60. This can progress in the elderly, causing significant diastolic impairment and HFpEF.
Symptoms –HFpEFThe symptoms of HF include fatigue, exercise intolerance, dyspnea and eventually edema. The symptoms are similar regardless of the etiology of the heart disease, and reflect either impaired cardiac output or fluid retention. Symptoms are important in differentiating left ventricular failure from right ventricular failure.
Early in the course of left ventricular failure, the compensated right heart generates elevated pulmonary artery and wedge pressures that may result in dyspnea, pulmonary congestion or pulmonary edema.
As HF progresses, chronic elevation of pulmonary pressures lead to the development of right ventricular failure. The negative feedback mechanisms outline above result in fluid retention and systemic venous congestion.
Right HF symptoms include lower extremity-dependent edema. When the legs are elevated at night, reabsorption of extracellular fluid increases right heart preload, the fluid redistributes centrally and may cause pulmonary congestion with orthopnea (dyspnea while laying flat) or paroxysmal nocturnal dyspnea (PND). Systemic venous congestion may also lead to hepatic congestion with right upper quadrant abdominal pain.
Symptoms related to low cardiac output include fatigue, exercise intolerance and weakness. In extreme cases, cardiac cachexia can occur.
Clinical Classification –HFpEFTwo HF classification systems are widely used: the New York Heart Association (NYHA) functional classification and the American College of Cardiology and American Heart Association (ACC/AHA) staging system. [Heidenreich 2022;10a(e905)]
The NYHA system categorizes patients into one of four classes based on a health care professional's subjective assessment of the patient's symptoms:
Class I: No symptoms of HFClass II: Symptoms of HF with moderate exertion, such as walking two blocks or climbing two flights of stairsClass III: Symptoms of HF with minimal exertion such as walking one block or one flight of stairs, but no symptoms at restClass IV: Symptoms of HF at rest
The ACC/AHA staging categorizes patients into one of four stages on the basis of risk factors, cardiac structural abnormalities associated with HF and the presence of symptoms of HF: [Heidenreich 2022:10a]
Stage A: At high risk for HF but without symptoms, structural heart disease or cardiac biomarkers of stretch or injuryStage B: Pre-HF, defined as no signs or symptoms of HF but evidence of one of the following: structural heart disease, evidence of increased filling pressures or risk factors plus increased levels of BNPs or persistently elevated cardiac troponinStage C: Structural heart disease with prior or current symptoms of HFStage D: Marked HF symptoms that interfere with daily life and with recurrent hospitalizations despite attempts to optimize guideline-directed medical therapy (GDMT)
In addition to focusing on different classificatory parameters, the NYHA functional classification differs from the ACC/AHA heart failure staging in that NYHA allows movement from any one class to another while the ACC/AHA system only allows unidirectional progression of stages (A→B→C→D). [Heidenreich 2022:10a]
Diagnosis –HFpEFIn general, diagnosis of HF is initially based on clinical findings on history and physical examination. However, in recent years, 2D and Doppler echocardiography has become the standard laboratory method to confirm the clinical diagnosis and assess cardiac structure and function. [Metra 2017:3d]
There are four grades of echocardiographic diastolic dysfunction, as described below. Clinical manifestations of congestive HF may occur once grade II diastolic dysfunction is present, but not in the presence of grade I diastolic dysfunction (impaired relaxation).
Grade I (impaired relaxation): The E-wave velocity is reduced, resulting in E/A reversal (ratio < 1). The left atrial pressures are normal. The deceleration time of the E wave is prolonged, measuring greater than 200 milliseconds. The e/e' ratio measured by tissue Doppler is normal.
Grade II (pseudonormal): This is pathological finding characterized by elevated left atrial pressures. The E/A ratio is normal (0.8-1.5), and the deceleration time is normal (160-200 ms), but the e/e' ratio is elevated. The E/A ratio will be less than 1 with Valsalva. A major clue to the presence of grade II diastolic dysfunction vs. Normal diastolic function is the presence of structural heart disease such as left atrial enlargement, left ventricular hypertrophy or systolic dysfunction. If significant structural heart disease is present, and the E/A ratio as well as the deceleration time appear normal, suspect a pseudonormal pattern. Valsalva distinguishes pseudonormal from normal as well as the e/e' ratio. Diuresis can frequently reduce the left atrial pressure, relieving symptoms of HF and returning the hemodynamics to those of grade I diastolic dysfunction.
Grade III (reversible restrictive): This pathological finding is characterized by significantly elevated left atrial pressures. Also known as a "restrictive filling pattern," the E/A ratio is greater than 2, the deceleration time is less than 160 ms and the e/e' ratio is elevated. The E/A ratio changes to less than 1 with Valsalva. Diuresis can frequently reduce the left atrial pressure, relieving symptoms of HF and returning the hemodynamics to those of grade I diastolic dysfunction.
Grade IV (fixed restrictive): This finding is characterized by severely elevated left atrial pressures and indicates a poor prognosis. The E/A ratio is greater than 2, the deceleration time is low and the e/e' ratio is elevated. The major difference distinguishing grade III from grade IV diastolic dysfunction is the lack of E/A reversal with the Valsalva maneuver (no effect will be seen with Valsalva). Diuresis will not have a major effect on the left atrial pressures, and clinical HF is likely established. Grade IV diastolic dysfunction is present only in very advanced HF and frequently seen in end-stage restrictive cardiomyopathies such as amyloid cardiomyopathy.
Treatment –HFpEFUntil recently, prospective randomized controlled interventional trials in HFpEF populations did not a firm evidence base for therapy, and therapy was thus aimed at symptom relief and management of comorbidities. However, recent trials showed effectiveness of several agents in the HFpEF population, and based on those, the 2022 ACC/AHA/Heart Failure Society of America guideline for the management of HF makes several recommendations: [Heidenreich 2022:55b]
The guideline states that routine use of nitrates or phosphodiesterase-5 inhibitors to increase activity or quality of life is ineffective.
The guideline also states that patients with HFpEF and hypertension should have antihypertensive medications titrated to attain guideline-recommended blood pressure targets (Class I, level of evidence C) and that management of atrial fibrillation can be useful to improve symptoms in patients with HFpEF (Class IIa, level of evidence C).
As in patients with HFrEF, in patients with HFpEF, diuretics are recommended to reduce congestion and improve symptoms (Class I, level of evidence B). [Heidenreich 2022:56a]
References:
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