Cardiac asthma

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Cardiac asthma
Purposediagnosis of congestive heart failure

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.

Contents

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]

Signs and symptoms

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]

Pathophysiology

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:

Diagnosis

The diagnosis of cardiac asthma is accomplished through workup of congestive heart failure, complete with:

As well as evaluation of lung function via:

Management

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]

See also

Related Research Articles

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<span class="mw-page-title-main">Respiratory failure</span> Inadequate gas exchange by the respiratory system

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 mental status due to ischemia in the brain.

<span class="mw-page-title-main">Shortness of breath</span> Feeling of difficulty breathing

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<span class="mw-page-title-main">Heart failure</span> Failure of the heart to provide sufficient blood flow

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<span class="mw-page-title-main">Pulmonary edema</span> Fluid accumulation in the tissue and air spaces of the lungs

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 dyspnea which can progress to hypoxemia and respiratory failure. Pulmonary edema has multiple causes and is traditionally classified as cardiogenic or noncardiogenic.

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<span class="mw-page-title-main">Pulmonary artery</span> Artery in pulmonary circulation carrying deoxygenated blood from heart to lungs

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.

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<span class="mw-page-title-main">Cardiac catheterization</span> Insertion of a catheter into a chamber or vessel of the heart

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<span class="mw-page-title-main">Hypoxemia</span> Abnormally low level of oxygen in the blood

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<span class="mw-page-title-main">Respiratory disease</span> Disease of the respiratory system

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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):

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.

<span class="mw-page-title-main">Transfusion-associated circulatory overload</span> Medical condition

In transfusion medicine, transfusion-associated circulatory overload is a transfusion reaction resulting in signs or symptoms of excess fluid in the circulatory system (hypervolemia) within 12 hours after transfusion. The symptoms of TACO can include shortness of breath (dyspnea), low blood oxygen levels (hypoxemia), leg swelling, high blood pressure (hypertension), and a high heart rate (tachycardia).

<span class="mw-page-title-main">Acute decompensated heart failure</span> Medical condition

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.

<span class="mw-page-title-main">Pathophysiology of heart failure</span>

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:

<span class="mw-page-title-main">Ventilation–perfusion coupling</span> Relationship between respiratory and cardiovascular processes

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.

References

  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 Litzinger MH, Aluyen JK, Cereceres R, Feik AN, Iltis KE, Perez CR, Horne KE, Litzinger M (February 20, 2013). "Cardiac Asthma: Not Your Typical Asthma". www.uspharmacist.com. Retrieved 2022-03-08.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 Buckner, Kern (1 February 2013). "Cardiac Asthma". Immunology and Allergy Clinics of North America. 33 (1): 35–44. doi:10.1016/j.iac.2012.10.012. PMID   23337063.
  3. ↑ "What causes cardiac asthma?". Mayo Clinic.
  4. 1 2 3 4 5 6 7 8 9 10 11 Tanabe, Tsuyoshi; Rozycki, Henry J; Kanoh, Soichiro; Rubin, Bruce K (December 2012). "Cardiac asthma: new insights into an old disease". Expert Review of Respiratory Medicine. 6 (6): 705–714. doi:10.1586/ers.12.67. PMID   23234454. S2CID   207223314.
  5. 1 2 Jorge, Stéphane; Becquemin, Marie-Hélène; Delerme, Samuel; Bennaceur, Mohamed; Isnard, Richard; Achkar, Rony; Riou, Bruno; Boddaert, Jacques; Ray, Patrick (2007-05-14). "Cardiac asthma in elderly patients: incidence, clinical presentation and outcome". BMC Cardiovascular Disorders. 7 (1): 16. doi: 10.1186/1471-2261-7-16 . ISSN   1471-2261. PMC   1878501 . PMID   17498318.
  6. ↑ Keet, Corinne A.; McCormack, Meredith (September 2016). "Cardiac Asthma: An Old Term That May Have New Meaning?". The Journal of Allergy and Clinical Immunology: In Practice. 4 (5): 924–925. doi:10.1016/j.jaip.2016.04.023. PMID   27587322.
  7. 1 2 3 4 5 Wolf, P. S. (October 1976). "Cardiac asthma--its origin, recognition and management". Annals of Allergy. 37 (4): 250–254. ISSN   0003-4738. PMID   824980.
  8. ↑ Jorge, Stéphane; Becquemin, Marie-Hélène; Delerme, Samuel; Bennaceur, Mohamed; Isnard, Richard; Achkar, Rony; Riou, Bruno; Boddaert, Jacques; Ray, Patrick (2007-05-14). "Cardiac asthma in elderly patients: incidence, clinical presentation and outcome". BMC Cardiovascular Disorders. 7 (1): 16. doi: 10.1186/1471-2261-7-16 . ISSN   1471-2261. PMC   1878501 . PMID   17498318.
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