![]() Fatigue from increased respiratory effort leads to shallow respiration, which leads to CO2 retention, or hypercapnea. Īs heart failure worsens, less surface area of the lungs is available for oxygenation and ventilation. If a heart failure patient has a normal to low ETCO2, and a normal to high blood pressure, this indicates that they are compensating for their respiratory distress and that perfusion is adequate. The sympathetic response from heart failure also initially causes hypertension. To compensate for increased work of breathing from heart failure, the patient may initially hyperventilate and blow off excess CO2, which would cause hypocapnea, ETCO2 less than 35 mm Hg. They key is to understand how blood pressure relates to capnography to assess respiration and perfusion. Normal ETCO2 is between 35 and 45 mm Hg.īecause heart failure affects circulation and ventilation, either aspect may cause an abnormal ETCO2 reading. The amount of exhaled carbon dioxide, the ETCO2, at the end of exhalation depends on the amount of blood circulated to the lungs, as well as how well CO2 moves through the lower airways. Capnography and blood pressure help identify the severity of respiratory and circulatory compromise from heart failure. Gradual onset of cough productive of clear or dark sputum, sharp chest pain that increases with fever and dehydration are additional signs and symptoms of pneumonia. As you collect the patient’s history listen for complaints of chest discomfort suggestive of ischemia and a productive cough of frothy white or pink sputum,Ĭrackles from pneumonia are localized to the area affected by infection, and are usually unilateral. The onset of heart failure may be sudden or gradual, and patient may report a history of difficulty lying flat or waking up short of breath.ĭuring the physical exam look for signs of heart failure like pale and diaphoretic skin, jugular venous distention and dependent edema. As heart failure worsens crackles can be heard in the middle and upper lung fields. A through history and physical exam is needed to differentiate heart failure from pneumonia.Ĭrackles from heart failure are usually bilateral and begin in the lower lung fields. CO2 diffuses well across fluid in the lungs from pulmonary edema, and the capnography waveform will have a normal rectangular shape, even if the patient is wheezing or has diminished breath sounds.Ī word of caution: pneumonia can also cause patients to have crackles on auscultation and a rectangular shaped waveform on the capnogram, as well as low pulse oximetry. ![]() A normal capnography waveform is a crisp, rectangular shape, but in patients with bronchospasm it has a slurred upstroke, or “shark fin” appearance. While the presentations can be similar, difficulty breathing from heart failure requires a much different treatment plan than for asthma and COPD.Ĭapnography can be used to differentiate pulmonary edema from bronchospasm, which is especially useful in patients who have a history of both heart failure and COPD or asthma. Wheezes from heart failure are caused by fluid obstructing the lower airways, or a cardiac wheeze, which is a different mechanism than wheezing from bronchoconstriction caused by asthma or COPD. ![]() Pulmonary edema causes crackles or rales, wheezing or diminished breath sounds which can be heard on auscultation over the affected area of the lungs. Capnography can help identify heart failure from other causes of respiratory distress. If the pump problem is not corrected, heart failure patients are at risk both respiratory failure and circulatory collapse. Patients in cardiogenic shock present with pulmonary edema and hypotension, often along with altered mental status or unconsciousness. Cardiogenic shock occurs when these compensatory mechanisms have failed and the heart cannot meet the body’s metabolic demands. Increased preload, afterload, and heart rate in heart failure add stress to heart muscle that is already weak, which worsens pulmonary edema and myocardial damage. The result is increased pressure that the left ventricle must pump against (afterload), and more blood returned to the heart to be circulated (preload). The body releases epinephrine and norepinephrine to compensate, which increases heart rate and constricts blood vessels.ĭecreased perfusion to the kidneys also triggers the release of renin, angiotensin and aldosterone, which causes fluid retention as well as vasoconstriction. On the other side of the left ventricle in heart failure, less oxygenated blood is circulated to vital organs. Pulmonary edema, the fluid accumulating in the lungs, obstructs the lower airways and causes alveoli to collapse, which impairs oxygenation and ventilation and increases work of breathing. Failure of the left ventricle causes blood to accumulate in the pulmonary vasculature, which increases pressure in pulmonary veins and pushes fluid into the lungs.
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