How does chf affect the respiratory system

However, to limit radiation only one CT image was taken per treatment condition. We chose to measure at TLC to maximize the size of the airways and the ability of the software to properly segment the airway structures Brown et al.

Third, the resolution of the CT scanning may not be sufficient to detect changes at smaller airway generations. At generation 6, the diameter of the airway is approximately 2 pixels, making the measurement of airway area and luminal area susceptible to partial volume effects. Nevertheless, this study has characterized the more proximal airways that tend to be cartilaginous, which are still an important determinant of maximal air flow Coxson et al.

Finally, the sensitivity of the automatic airway segmentation algorithm may not properly segment all possible airways. While the automatic segmentation algorithm has been well validated on healthy individuals, it may occasionally miss airway segments or, alternatively, segment nonairway structures, leading to large standard deviations in the measurement of airway area and wall thickness.

In order to account for these potential occurrences, we have been careful to visually validate the automatic segmentation to remove significant deviations from structures of interest. The heart and lungs are intimately linked and during the development and progression of the HF syndrome the pulmonary system undergoes significant changes that in turn contribute to the pathophysiology of the disease through alterations in lung function, breathing pattern, respiratory gas exchange, and ultimately symptomatology.

This study examined the structure—function relationships of the pulmonary system in HF patients and the influence of an acutely inhaled ADRB2 agonist; known to dilate airways and stimulate extravascular lung fluid clearance. However, airway wall thicknesses and airway luminal areas were maintained relative to healthy controls in the large airways studied, despite significant reductions in pulmonary function.

An acutely nebulized ADRB2 agonist caused significant clearance of EVLW, but did not change airway wall thickness or luminal area in the large generations, suggesting the importance of lung fluid in stable HF patients, and the possibility of ADRB2 agonists as a treatment in improving lung air flows and volumes and clearing EVLW. Chase S. Impact of chronic systolic heart failure on lung structure—function relationships in large airways. Physiol Rep , 4 13 , , e, doi: National Center for Biotechnology Information , U.

Journal List Physiol Rep v. Physiol Rep. Published online Jul Steven C. Chase , 1 Courtney M. Wheatley , 1 Lyle J. Olson , 1 Kenneth C. Beck , 1 Robert J. Wentz , 1 Eric M. Snyder , 1 Bryan J.

Taylor , 1 and Bruce D. Johnson 1. Courtney M. Lyle J. Kenneth C. Robert J. Eric M. Bryan J. Bruce D. Author information Article notes Copyright and License information Disclaimer. Corresponding author. Physiological Reports published by Wiley Periodicals, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

This article has been cited by other articles in PMC. Abstract Heart failure HF is often associated with pulmonary congestion, reduced lung function, abnormal gas exchange, and dyspnea.

Keywords: Airway walls, airways, congestion, CT , edema. Introduction The heart and lungs are intimately linked, with the disease pathophysiology of one organ system often influencing the other. Overview of experimental procedures Experimental procedures were conducted on a single visit day. Table 1 Participant characteristics in heart failure and control subjects. Open in a separate window. Figure 1. Table 2 Baseline values and percent change after albuterol for quantitative CT indices.

FWHM, full width half max. Figure 2. Figure 3. Pulmonary function Pulmonary function characteristics are shown in Figure 4 for both groups. Figure 4. Structure—function relationships Linear regression was performed to assess the relationship between airway area and CT quantitative indices and lung function.

Table 3 Pearson correlation coefficients r for airway area versus pulmonary function at baseline. Effects of an ADRB2 agonist on lung structure and function After ADRB2 agonist administration, the CT attenuation distributions for both groups shifted significantly to the left and were narrower relative to baseline Fig.

Figure 5. Table 4 Pearson correlation coefficients r for change in quantitative CT indices at baseline versus change after albuterol for both groups. Discussion In this study, we examined measures of lung congestion, airway structure and the relationship between airway structure and lung function in HF patients and in control subjects. Extravascular lung water Extravascular lung water EVLW is known to alter lung mechanics and could contribute to the loss of function in HF, but it is difficult to quantitatively measure in vivo Grossman et al.

Airway wall thickness and luminal area Numerous studies have attempted to understand the factors that contribute to loss of pulmonary function in HF. Airway structure and lung function Pulmonary function exhibited both restrictive and obstructive changes in HF patients in this study Fig.

Limitations There are four major limitations of this study. Conclusion The heart and lungs are intimately linked and during the development and progression of the HF syndrome the pulmonary system undergoes significant changes that in turn contribute to the pathophysiology of the disease through alterations in lung function, breathing pattern, respiratory gas exchange, and ultimately symptomatology.

Conflict of Interest None declared. Notes Chase S. References Agostoni, P. Heart J. Quantitative CT indexes in idiopathic pulmonary fibrosis: relationship with physiologic impairment. Radiology — Airway edema potentiates airway reactivity. Multiple breath helium dilution measurement of lung volumes in adults.

Congestive heart failure that leads to pulmonary edema may be caused by: Heart attack, or any disease of the heart that weakens or stiffens the heart muscle cardiomyopathy Leaking or narrowed heart valves mitral or aortic valves Sudden, severe high blood pressure hypertension Pulmonary edema may also be caused by: Certain medicines High altitude exposure Kidney failure Narrowed arteries that bring blood to the kidneys Lung damage caused by poisonous gas or severe infection Major injury.

Symptoms of pulmonary edema may include: Coughing up blood or bloody froth Difficulty breathing when lying down orthopnea Feeling of "air hunger" or "drowning" This feeling is called "paroxysmal nocturnal dyspnea" if it causes you to wake up 1 to 2 hours after falling asleep and struggle to catch your breath. Grunting, gurgling, or wheezing sounds with breathing Problems speaking in full sentences because of shortness of breath Other symptoms may include: Anxiety or restlessness Decrease in level of alertness Leg or abdominal swelling Pale skin Sweating excessive.

Exams and Tests. The health care provider will perform a thorough physical exam. The provider will listen to your lungs and heart with a stethoscope to check for: Abnormal heart sounds Crackles in your lungs, called rales Increased heart rate tachycardia Rapid breathing tachypnea Other things that may be seen during the exam include: Leg or abdominal swelling Abnormalities of your neck veins which can show that there is too much fluid in your body Pale or blue skin color pallor or cyanosis Possible tests include: Blood chemistries Blood oxygen levels oximetry or arterial blood gases Chest x-ray Complete blood count CBC Echocardiogram ultrasound of the heart to see if there are problems with the heart muscle Electrocardiogram ECG to look for signs of a heart attack or problems with the heart rhythm.

Oxygen is given through a face mask or tiny plastic tubes are placed in the nose. A breathing tube may be placed into the windpipe trachea so you can be connected to a breathing machine ventilator if you cannot breathe well on your own. Medicines that may be used include: Diuretics that remove excess fluid from the body Medicines that strengthen the heart muscle, control the heartbeat, or relieve pressure on the heart Other medicines when heart failure is not the cause of the pulmonary edema.

Outlook Prognosis. When to Contact a Medical Professional. Alternative Names. Lung congestion; Lung water; Pulmonary congestion; Heart failure - pulmonary edema. Lungs Respiratory system. Time-consuming placement of pulmonary artery catheters has not been shown to prolong survival, even in the coronary care unit and, thus far, has not been well studied in the ED setting.

Cardiac catheterization may be necessary for a complete evaluation, treatment and assessment of prognosis. In patients refractory to medical therapy or with evidence of cardiogenic shock, cardiac catheterization, angioplasty, coronary bypass, or intra-aortic balloon pump IABP may be helpful.

Cardiac monitoring and continuous pulse oximetry must also be utilized, and intravenous IV access obtained.

To reduce venous return, the head of the bed should be elevated. Patients may be most comfortable in a sitting position with their legs dangling over the side of the bed, which allows for reduced venous return and decreased preload. Therapy generally starts with nitrates and diuretics if patients are hemodynamically stable. Many other treatment modalities may play some role in acute management. If possible, the underlying cause should be treated as well. This is particularly true for patients with known diastolic dysfunction who respond best to reductions in blood pressure rather than to diuretics, nitrates, and inotropic agents.

Contributing factors must be eliminated where possible, and fluid and sodium restricted. Recent data comparing nasal CPAP therapy with facemask ventilation therapy has demonstrated a decreased need for intubation rates when these modalities are used.

BiPAP and CPAP are contraindicated in the presence of acute facial trauma, the absence of an intact airway, and in patients with an altered mental status or who are uncooperative.

These goals may need to be modified for some patients. Use of diuretics, nitrates, analgesics, and inotropic agents are indicated for the treatment of CHF and pulmonary edema. Calcium channel blockers, such as nifedipine and nondihydropyridines, increase mortality and increase incidence of recurrent CHF with chronic use.

Conflicting evidence currently exists in favor as well as against the use of calcium channel blockers in the acute setting - at this time is limited to acute use in patients with diastolic dysfunction and heart failure, a condition not easily determined in the emergency department ED.

First-line therapy generally includes a loop diuretic such as furosemide, which will inhibit sodium chloride reabsorption in the ascending loop of Henle. Loop diuretics should be administere IV, since this allows for both superior potency and higher peak concentration despite increased incidence of side-effects, particularly ototoxicity.

Higher doses and more rapid redosing may be appropriate for the patient in severe distress. Metolazone and chlorothiazide have been used as adjunctive therapy in patients initially refractory to furosemide.

Nitrates reduce myocardial oxygen demand by lowering preload and afterload. Nitoglycerin is particularly useful in the patient who presents with acute pulmonary edema with a systolic blood pressure of at least mmHg. However, oral nitrates, due to delayed absorption, have little role in the acute presentations of CHF.

Morphine IV is an excellent adjunct in acute therapy. In addition to being both an anxiolytic and an analgesic, its most important effect is venodilation, which reduces preload.

Morphine also causes arterial dilatation, which reduces systemic vascular resistance SVR and increases cardiac output. Narcan can also reverse the effects of morphine. However, some evidence indicates that morphine use in acute pulmonary edema may increase the intubation rate. Angiotensin converting enzyme ACE inhibitors, such as SL captopril or IV enalapril, may rapidly reverse hemodynamic instability and symptoms, possibly avoiding an otherwise imminent intubation.

Haude compared 25mg of SL captopril with 0. Annane gave 1mg of IV enalapril to 20 patients presenting with acute class III and class IV CHF over two hours and demonstrated rapid hemodynamic improvement with no significant adverse effects on cardiac output or hepatosplanchnic measurements.

Captopril may play a unique role in sustaining patients with renal failure and concomitant acute CHF while awaiting definitive therapy with dialysis. Since the information on this subject is still controversial and limited to small studies, their routine use cannot be recommended at this time. ACE inhibitors remain a promising area in need of further study.

Beta-blockers, possibly by restoring beta-1 receptor activity or via prevention of catecholamine activity, appear to be cardioprotective in patients with depressed left ventricular function. Beta-blockers, particularly carvedilol, have been shown to improve symptoms in patients with moderate-to-severe heart failure.

The role of beta-blockers in the acute setting, however, is currently unclear - use should be limited until hemodynamic studies indicate that further deterioration will not occur. Because differentiating CHF and asthma exacerbations is often difficult, treating both with the shotgun approach often is employed, particularly as both may cause bronchospasm. Aerosolized beta-2 agonists, which are the more selective of beta-agonists, decrease tachycardia, dysrhythmias, and cardiac work while transiently enhancing cardiac function.

Terbutaline has been shown to be successful in this setting, as well as albuterol, isoetharine, and bitolterol. Roles of theophyline and aminophylline in the acute setting must be limited. They are positive inotropic agents mediated by an increase in catecholamines, and they dilate coronaries and exert mild diuretic effects.

Nevertheless, they can exacerbate dysrhythmias by increasing cardiac work. Steroids, IV or oral PO , have been shown to worsen pre-existing heart failure due to systemic sodium retention and volume expansion, hypokalemia, and occasional hypertension.

Inhaled steroids, due to their lack of systemic side-effects, may be a reasonable option in this confusing patient presentation. However, given their delayed onset of action, they remain an area in need of further study. Human B-type natriuretic peptides such as Nesiritide may decrease hospital length of stay by up to four days. BNP binds to particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells.

Binding to the receptor causes increase in cyclic GMP, which serves as second messenger to dilate veins and arteries. BNP reduces pulmonary capillary wedge pressure and improves dyspnea in patients with acutely decompensated CHF. Nesirtitide may affect renal function in patients whose renal function may depend on activity of renin-angiotensin-aldosterone system; it may cause hypotension, ventricular tachycardia, non-sustained VT, headache, abdominal pain, back pain, insomnia, anxiety, angina pectoris, nausea, and vomiting.

Digoxin has no role in the emergency management of CHF due to delayed absorption and diminished efficacy at times of increased sympathetic tone.