Cardiac asthma | |
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Specialty | Cardiology |
Symptoms | Wheezing, Coughing, shortness of breath |
Duration | Acute or chronic |
Causes | Congestive heart failure |
Diagnostic method | Cardiac workup, lung function testing, imaging |
Differential diagnosis | Bronchial asthma |
Treatment | Improving cardiac function, maintaining blood oxygen saturation levels, stabilizing total body water volume and distribution |
Cardiac asthma is the medical condition of intermittent wheezing, coughing, and shortness of breath that is associated with underlying congestive heart failure (CHF). [1] Symptoms of cardiac asthma are related to the heart's inability to effectively and efficiently pump blood in a CHF patient. [2] This can lead to accumulation of fluid in and around the lungs (pulmonary congestion), disrupting the lung's ability to oxygenate blood.
Cardiac asthma carries similar symptoms to bronchial asthma, but is differentiated by lacking inflammatory origin. [1] [3] Because of the similarity in symptoms, diagnosis of cardiac versus bronchial asthma relies on full cardiac workup and pulmonary function testing. [2] [4]
Treatment is centered on improving cardiac function, maintaining blood oxygen saturation levels, and stabilizing total body water volume and distribution. [1] [4]
The most common findings of cardiac asthma are the presence of wheeze, cough, or shortness of breath (predominantly occurring at night or when lying down) in a patient that possesses signs of congestive heart failure. [4] [5] [6] [7]
Additional findings consist of production of frothy or watery sputum and presence of water in the lungs that can be heard via stethoscope. [8] In severe cases, a patient can experience multiple night time episodes of breathlessness, changes in skin coloration, and episodes of bloody sputum. [1]
The underlying causes for cardiac asthma stem from the eventual back up of fluid into the pulmonary vasculature as a result of the heart's, particularly left sided, inability to effectively and efficiently pump blood. [2] The accumulation of fluid in the heart creates a higher than normal pressure system that places increasing pressure demands on the pulmonary venous system in order for appropriate oxygenation of blood to occur. [4] This results in what is called pulmonary venous hypertension (PVH), and results in distention and recruitment of pulmonary capillaries to help distribute the increased pressure gradient. [2] [4] At the capillary, there is a microvascular barrier that helps regulate fluid status via molecular pressure forces such as forces that push outward from vessels and pressures that pull or attract into vessels. [2] With increasing PVH, pressure outward overcomes pressure inward, and fluid is distributed to the lung interstitium, preserving oxygen exchange at the capillary. [2] Fluid is transported to the hilum and pleural space, and removed via the lymphatic system. [2] [7] At first, the body is capable of handling excess water. Later, the capillary vasculature is overwhelmed by increased pressure and fluid backs up into the alveolar sac, resulting in pulmonary edema and decreased oxygenation capability. [2] Additionally, increased pressure demands on capillary vasculature result in increases in vascular tone to include remodeling of pre-capillary vessels such as medial wall hypertrophic changes. [2] Over time, the remodeling efforts of the vessels can progress to hyperplastic changes of the vessels' wall construction, and results in increased pulmonary vascular resistance. [2]
There is ongoing interest into establishing connections of cardiac asthma to abnormalities in bronchiole anatomy. [1] [4] Current evaluation has proposed multiple mechanisms for increased airway resistance, and focus is on four alternate explanations:
The diagnosis of cardiac asthma is accomplished through workup of congestive heart failure, complete with:
As well as evaluation of lung function via:
Treatment of asthma symptoms in CHF patients is directed towards optimizing the patient's cardiovascular status and correcting potential oxygen deficit. [4] Current recommendations in acute asthma symptoms are utilization of diuretics such as furosemide, venodilators such as nitroglycerin, and morphine. [1] The initial strategy should focus on decreasing patient fluid retention with diuretic therapy, thereby decreasing cardiac preload and overall fluid load in pulmonary circuit (pulmonary congestion). [1] Next, if aggressive diuresis is not adequately correcting symptoms, venodilators can be used to distribute blood and fluid to the venous system, thereby decreasing cardiac preload and left heart pressures contributing to pulmonary congestion. [1] Lastly, morphine can be utilized for assistance in improving ease of breathing through a presumed mechanism similar to venodilation, as well as reducing patient anxiety. [1] Additionally, applications of supplemental oxygen and repositioning to upright or standing positions in events of low blood oxygen saturation and difficulty breathing can be utilized as needed. [1]
Chronic management of cardiac asthma is directed at optimizing therapy of heart failure. Current recommendations can be found at its respective page (congestive heart failure). [1]
There is importance of distinguishing whether asthma is of bronchial or cardiac origin because management of bronchial asthma is primarily centered on utilization of inhalers, such as bronchodilators and corticosteroids. At this point in time, there has been limited evidence of improvement of cardiac asthma symptoms with utilization of inhalers. [1] [4] [5]
Edema, also spelled oedema, and also known as fluid retention, dropsy and hydropsy, is the build-up of fluid in the body's tissue, a type of swelling. Most commonly, the legs or arms are affected. Symptoms may include skin that feels tight, the area feeling heavy, and joint stiffness. Other symptoms depend on the underlying cause.
Respiratory failure results from inadequate gas exchange by the respiratory system, meaning that the arterial oxygen, carbon dioxide, or both cannot be kept at normal levels. A drop in the oxygen carried in the blood is known as hypoxemia; a rise in arterial carbon dioxide levels is called hypercapnia. Respiratory failure is classified as either Type 1 or Type 2, based on whether there is a high carbon dioxide level, and can be acute or chronic. In clinical trials, the definition of respiratory failure usually includes increased respiratory rate, abnormal blood gases, and evidence of increased work of breathing. Respiratory failure causes an altered state of consciousness due to ischemia in the brain.
Shortness of breath (SOB), known as dyspnea or dyspnoea, is an uncomfortable feeling of not being able to breathe well enough. The American Thoracic Society defines it as "a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity", and recommends evaluating dyspnea by assessing the intensity of its distinct sensations, the degree of distress and discomfort involved, and its burden or impact on the patient's activities of daily living. Distinct sensations include effort/work to breathe, chest tightness or pain, and "air hunger". The tripod position is often assumed to be a sign.
Heart failure (HF), also known as congestive heart failure (CHF), is a syndrome caused by an impairment in the heart's ability to fill with and pump blood.
Pulmonary edema, also known as pulmonary congestion, is excessive fluid accumulation in the tissue or air spaces of the lungs. This leads to impaired gas exchange, most often leading to shortness of breath (dyspnea) which can progress to hypoxemia and respiratory failure. Pulmonary edema has multiple causes and is traditionally classified as cardiogenic or noncardiogenic.
A pulmonary artery is an artery in the pulmonary circulation that carries deoxygenated blood from the right side of the heart to the lungs. The largest pulmonary artery is the main pulmonary artery or pulmonary trunk from the heart, and the smallest ones are the arterioles, which lead to the capillaries that surround the pulmonary alveoli.
Mitral stenosis is a valvular heart disease characterized by the narrowing of the opening of the mitral valve of the heart. It is almost always caused by rheumatic valvular heart disease. Normally, the mitral valve is about 5 cm2 during diastole. Any decrease in area below 2 cm2 causes mitral stenosis. Early diagnosis of mitral stenosis in pregnancy is very important as the heart cannot tolerate increased cardiac output demand as in the case of exercise and pregnancy. Atrial fibrillation is a common complication of resulting left atrial enlargement, which can lead to systemic thromboembolic complications such as stroke.
Hypoxemia is an abnormally low level of oxygen in the blood. More specifically, it is oxygen deficiency in arterial blood. Hypoxemia is usually caused by pulmonary disease. Sometimes the concentration of oxygen in the air is decreased leading to hypoxemia.
Respiratory diseases, or lung diseases, are pathological conditions affecting the organs and tissues that make gas exchange difficult in air-breathing animals. They include conditions of the respiratory tract including the trachea, bronchi, bronchioles, alveoli, pleurae, pleural cavity, the nerves and muscles of respiration. Respiratory diseases range from mild and self-limiting, such as the common cold, influenza, and pharyngitis to life-threatening diseases such as bacterial pneumonia, pulmonary embolism, tuberculosis, acute asthma, lung cancer, and severe acute respiratory syndromes, such as COVID-19. Respiratory diseases can be classified in many different ways, including by the organ or tissue involved, by the type and pattern of associated signs and symptoms, or by the cause of the disease.
Hypervolemia, also known as fluid overload, is the medical condition where there is too much fluid in the blood. The opposite condition is hypovolemia, which is too little fluid volume in the blood. Fluid volume excess in the intravascular compartment occurs due to an increase in total body sodium content and a consequent increase in extracellular body water. The mechanism usually stems from compromised regulatory mechanisms for sodium handling as seen in congestive heart failure (CHF), kidney failure, and liver failure. It may also be caused by excessive intake of sodium from foods, intravenous (IV) solutions and blood transfusions, medications, or diagnostic contrast dyes. Treatment typically includes administration of diuretics and limit the intake of water, fluids, sodium, and salt.
A pulmonary shunt is the passage of deoxygenated blood from the right side of the heart to the left without participation in gas exchange in the pulmonary capillaries. It is a pathological condition that results when the alveoli of parts of the lungs are perfused with blood as normal, but ventilation fails to supply the perfused region. In other words, the ventilation/perfusion ratio of those areas is zero.
The zones of the lung divide the lung into four vertical regions, based upon the relationship between the pressure in the alveoli (PA), in the arteries (Pa), in the veins (Pv) and the pulmonary interstitial pressure (Pi):
Paroxysmal nocturnal dyspnea or paroxysmal nocturnal dyspnoea (PND) is an attack of severe shortness of breath and coughing that generally occurs at night. It usually awakens the person from sleep, and may be quite frightening. PND, as well as simple orthopnea, may be relieved by sitting upright at the side of the bed with legs dangling, as symptoms typically occur when the person is recumbent, or lying down.
Obstructive shock is one of the four types of shock, caused by a physical obstruction in the flow of blood. Obstruction can occur at the level of the great vessels or the heart itself. Causes include pulmonary embolism, cardiac tamponade, and tension pneumothorax. These are all life-threatening. Symptoms may include shortness of breath, weakness, or altered mental status. Low blood pressure and tachycardia are often seen in shock. Other symptoms depend on the underlying cause.
Acute decompensated heart failure (ADHF) is a sudden worsening of the signs and symptoms of heart failure, which typically includes difficulty breathing (dyspnea), leg or feet swelling, and fatigue. ADHF is a common and potentially serious cause of acute respiratory distress. The condition is caused by severe congestion of multiple organs by fluid that is inadequately circulated by the failing heart. An attack of decompensation can be caused by underlying medical illness, such as myocardial infarction, an abnormal heart rhythm, infection, or thyroid disease.
Swimming induced pulmonary edema (SIPE), also known as immersion pulmonary edema, is a life threatening condition that occurs when fluids from the blood leak abnormally from the small vessels of the lung (pulmonary capillaries) into the airspaces (alveoli).
The main pathophysiology of heart failure is a reduction in the efficiency of the heart muscle, through damage or overloading. As such, it can be caused by a wide number of conditions, including myocardial infarction, hypertension and cardiac amyloidosis. Over time these increases in workload will produce changes to the heart itself:
Ventilation–perfusion coupling is the relationship between ventilation and perfusion processes, which take place in the respiratory system and the cardiovascular system. Ventilation is the movement of gas during breathing, and perfusion is the process of pulmonary blood circulation, which delivers oxygen to body tissues. Anatomically, the lung structure, alveolar organization, and alveolar capillaries contribute to the physiological mechanism of ventilation and perfusion. Ventilation–perfusion coupling maintains a constant ventilation/perfusion ratio near 0.8 on average, while the regional variation exists within the lungs due to gravity. When the ratio gets above or below 0.8, it is considered abnormal ventilation-perfusion coupling, also known as a ventilation–perfusion mismatch. Lung diseases, cardiac shunts, and smoking can cause a ventilation-perfusion mismatch that results in significant symptoms and diseases, which can be treated through treatments like bronchodilators and oxygen therapy.
Negative-pressure pulmonary edema (NPPE), also known as Postobstructive Pulmonary Edema, is a clinical phenomenon that results from the generation of large negative pressures in the airways during attempted inspiration against some form of obstruction of the upper airways. The most common reported cause of NPPE reported in adults is laryngospasm, while the most implicated causes in children are infectious croup and epiglottitis. The large negative pressures created in the airways by inhalation against an upper airway obstruction can lead to fluid being drawn from blood vessels supplying the lungs into the alveoli, causing pulmonary edema and impaired ability for oxygen exchange (hypoxemia). The main treatment for NPPE is supportive care in an intensive care unit and can be fatal without intervention.
Pulmonary Arterial Hypertension (PAH) is a syndrome in which the blood pressure in the pulmonary arteries and pulmonary arterioles is elevated. This pre-capillary pulmonary artery pressure being elevated is essential, and by definition a mean pulmonary artery pressure greater than 20 mmHg as measured by a right heart catheterization is required for the diagnosis. This pre-capillary pulmonary hypertension is confirmed with measuring pulmonary vascular resistance being greater than 3 Woods Units. A pulmonary artery wedge pressure being less than 15 mmHg excludes post-capillary bed pulmonary hypertension. Pulmonary arterial hypertension is a subgroup of pulmonary hypertension and is categorized as World Health Organization as group 1. PAH is further subdivided into various categories based on the cause, including idiopathic, heritable, drug and toxin induced, PAH associated with specific diseases, PAH that is responsive to vasodilators, PAH with venous or capillary involvement, and persistent PAH in the newborn period.