"134 Main Street for a patient experiencing trouble breathing," the radio squawks. You and your partner look at each other and say, "Daniel O'Shea!" You know Daniel well, and he generally only calls when he is truly sick.
Daniel is a 57-year-old male who lives with his wife in an area of the country known for deep-fried foods. He has a history of hyperlipidemia, coronary artery disease (CAD), hypertension, atrial fibrillation and emphysema, with a 45-pack/year smoking history. Last year, he suffered an acute myocardial infarction (AMI) that involved the anterolateral wall, and he has not been his active self since.
A look inside Daniel would show left ventricular damage from the AMI; however, the damage occurred long before that event. For years, Daniel's hypertension went untreated, causing the left ventricle to pump harder to overcome afterload and expel blood into the systemic circulation to maintain stroke volume. As pressure overload continued, the ventricle wall became thicker and more muscular (hypertrophic), at the same time becoming stiff and rigid and decreasing in elasticity and overall volume. As cardiac output fell and the baroreceptors recognized a state of low pressure, the adrenal gland released norepinephrine and epinephrine to increase cardiac output by increasing stroke volume and heart rate. Prolonged activation of the sympathetic nervous system, or a sensed drop in renal perfusion pressure, activated the renin-angiotensin-aldosterone system (RAAS). Not only did the RAAS release additional norepinephrine, it also promoted a greater preload and afterload through increasing venous and arterial tone by converting angiotensin I into angiotensin II using angiotensin-converting enzyme (ACE). This vasoconstriction increased preload back to the heart, creating increased stretching of the ventricular walls and a greater contraction (Frank-Starling law). Over time, the ventricle walls became overstretched and weak, like a balloon that is repetitively overinflated and deflated. The overstretching caused excessive myocardial dilation that eventually diminished contractility and stroke volume, as well as the ejection fraction. The increased stress finally took its toll on Daniel last year in the form of an AMI. As the infarct progressed, the heart muscle cells, or cardiomyocytes, lengthened and began to thin. An inflammatory response ensued, the necrotic dead tissue was absorbed and scar tissue formed. The ventricle soon dilated, reshaping itself from elliptical to more spherical and changing its mass, composition, volume and cardiac function. This ventricular remodeling further injured the ventricle, decreased the ejection fraction and lowered the amount of blood available to the system.
Daniel's body again responded to decreased cardiac output by engaging the sympathetic nervous system and RAAS, placing more stress upon his already damaged heart that was now expelling less blood. With a greater amount of blood remaining in the ventricle, hydrostatic pressures increased, leading to venous bed congestion in the tissues and organs located near the affected ventricle. As cardiac output continued to diminish, Daniel's heart rate increased to compensate for decreasing coronary filling times, leading to additional hypoxia and ischemia. This increased workload caused the heart to enlarge even further and increase its oxygen demand, worsened by decreased coronary filling times. Essentially, his body's attempt to compensate for decreased cardiac output was worsening his condition by causing the damaged heart to work harder. It was this repetitive downward spiral of injury, compensation, injury that led to Daniel's current state.
Although it would be nice to have this much information about your patients prior to arriving, that is not always possible. Therefore, when a patient presents with a complaint of "trouble breathing," it is imperative to review the potential causes, or differential diagnoses, which include heart failure, COPD, pneumonia, pulmonary emboli, pneumothorax, anaphylaxis, aspiration and any number of cardiac etiologies like myocardial infarction.
When you arrive, you find Daniel sitting on his couch in a tripod position. From a distance, his color appears dusky, and he does not acknowledge your presence or divert his gaze from the floor. As you get closer, you notice a prolonged expiratory phase as he exhales through pursed and cyanotic lips, but you don't see any retractions or hear wheezing. As you approach and ask, "Daniel, you OK?" he looks up and says wearily, "I...can't...breathe."
Your general impression of Daniel is not good. You realize that his skin color may be the result of hypoxia. The prolonged expiratory phase is his attempt to force out air, more specifically carbon dioxide. Pursed lips are a way of increasing positive end expiratory pressure (PEEP), which in turn helps to keep alveoli open and prevent atelectasis and increase the amount of time oxygen is in contact with the alveolar wall, allowing for greater diffusion.
We can classify the severity of respiratory complaints as distress, failure or respiratory arrest. To determine which state a patient is in, we look at how well he is ventilating and oxygenating. We see that Daniel has positioned himself in a tripod position, which helps to expand his chest and shows that he has muscle tone. His focused gaze is initially disturbing, but the fact that he looks up when you approach shows that he is alert. Daniel's respiratory distress shows that oxygenated blood is getting to his brain and carbon dioxide is being removed. If his compensatory mechanisms fail, Daniel will begin to retain carbon dioxide, initially become confused, then progress to lethargy and unresponsiveness as he goes into respiratory failure. If Daniel progresses to this state of decompensation, you will need to provide positive pressure ventilation (PPV) immediately.
Assessment of the airway shows that it is open, but you must still assess patency. You don't observe any drooling or frothy sputum that would indicate excessive fluid in the airway, and, when you ask him to swallow, he does, demonstrating that he is able to maintain his own airway at this time and therefore does not require additional management.
A normal ratio of inspiratory to expiratory time is 1:2; Daniel's ratio is about 1:4, with a brief resting phase between breaths. You lift his shirt to look for retractions and do not see any. You listen to his lungs, starting in the posterior bases and working toward the apices. As you listen bilaterally, you notice little to no air movement in the bases, but the higher you go, the lungs sound less dim and you begin to hear faint wheezes along with fine crackles, or rales. These crackles are the result of the small airways opening against fluid and are often heard in the late inspiratory phase in the lower, or dependent, lung fields. Hearing these sounds high and bilaterally in the lung fields raises concern that there may be a great volume of fluid in his lungs. If Daniel had called earlier, you may have heard inspiratory and expiratory wheezing as increased hydrostatic pressures in the alveolar capillaries forced fluid into lung parenchyma, narrowing the airways. This in turn causes the wheezing known as cardiac asthma, which has a different pathology from asthma and COPD. You place a pulse oximeter on Daniel's finger and obtain an oxygenation reading of 87%. To validate the abnormal reading, you try the other hand and get a similar reading. Noting that Daniel is moderately hypoxic, you have your partner place a non-rebreather mask at 15 liters per minute as you assess Daniel's radial pulse, which is rapid and irregular. You try to remember if he has a history of atrial fibrillation, at the same time wondering if the irregularity is the result of premature ventricular contractions (PVCs) that often manifest in hypoxic states. The tachycardia also concerns you, as this may be the result of hypoxia or early shock, or may be the causative factor of Daniel's dyspnea. As you assess his pulse, you make note of his skin color, condition and temperature. You are relieved that it is dry and warm, but are a bit concerned about the circumoral cyanosis. Moist skin would concern you, as this may be an early sign of shock; hot skin may indicate infection.
Seeing that Daniel is in respiratory distress, you must now weigh the efficacy of providing treatment on scene versus providing immediate transport. Unlike basic providers, paramedics are more apt to initiate certain treatment modalities before transport while "always working toward the door."
As you work, your partner is gathering Daniel's medical history from his wife. He tells you that Daniel has no known allergies to sulfa drugs, latex or food products. Assessing his medications allows you insight into his medical history. As your partner gathers and records Daniel's medications, his wife confirms that he is compliant with all of them, which include nitroglycerin for occasional bouts of angina, metoprolol for hypertension, warfarin for atrial fibrillation, and albuterol with ipratropium bromide for COPD. She tells you that Daniel had a heart attack last year, but he was never implanted with a pacemaker or defibrillator. He has no history of diabetes, but has been diagnosed with peripheral vascular disease ,and hyperlipidemia that is being treated through diet. She also tells your partner that he has been eating well but is stubborn and still puts salt on everything he eats, despite doctor's orders.
You ask Daniel about his present complaint, with some help from his wife due to his dyspneic state. Knowing there are numerous causes of dyspnea, you use the mnemonic HAPISOCS (see Table 1) to help focus your questions. You first ask Daniel if he has a history of pulmonary disease besides COPD. He says the last time you picked him up he was diagnosed with pneumonia, but denies any history of heart failure or pulmonary embolism.
Next you ask what activity he was doing when he began having trouble breathing and how rapidly it came on. He answers, "Nothing...I was...just sitting...here..." This concerns you. A patient with a sudden onset of dyspnea while resting may rapidly deteriorate and require more assertive airway and ventilatory management, such as in a heart failure patient with acute pulmonary edema (APE), compared with a patient who had a gradual onset of trouble breathing as seen in pneumonia. It is also worthwhile to determine if Daniel becomes fatigued with activity and which activities exacerbate those complaints, such as climbing stairs or simply moving about a room. Dyspnea on exertion (DOE) demonstrates that the patient is unable to meet the metabolic or oxygen demands of the body, either as a result of impaired cardiac output or decreased diffusion at the alveoli.
You ask Daniel to take a deep breath, and he denies any pain on inspiration, which may be common with conditions like trauma, cardiac infections, pleurisy and costochondritis.
At this point, you think Daniel may be in heart failure, but with his recent history, you are also concerned that the causative factor of dyspnea may be pneumonia. Since the treatment modalities between these two disease states are different, you ask about signs of infection, such as night sweats, fever or chills, all of which he denies.
Knowing that a history of smoking is a risk factor for many cardiac and pulmonary diseases, you ask if he is a smoker, which he denies, but when you arrived, you noticed a faint odor of cigarette smoke in the air. His wife admits to occasionally having a cigarette, but only in the kitchen. Knowing Daniel has a history of COPD, you ask if he ever smoked and how many packs a day. He tells you he smoked about a pack-and-a-half a day for 30 years. Using the formula (number of packs per day times number of years smoked), you document that Daniel is a 45 pack year smoker, which puts him at risk for cardiopulmonary dysfunction and could cause him to rapidly deteriorate, as he may not be able to tolerate periods of hypoxia or APE.
Conditions like heart failure and pneumonia that lead to an accumulation of fluid or mucus within the lungs may make it difficult for some patients to lie flat. Determining if the patient has orthopnea, or positional dyspnea, may alert you to impairment of alveolar diffusion. Daniel tells you that he normally sleeps with one pillow, but since being diagnosed with pneumonia, he has to use three or four pillows and has even spent nights in a recliner.
Determining if Daniel has a cough may also help form your differential diagnosis. Daniel says he has had a cough, but denies that it produces any sputum. He tells you that during his bout of pneumonia he was coughing up thick, greenish-yellow sputum.
Supplemental questions may help you work through various differential diagnoses. Since Daniel previously mentioned having orthopnea, you wonder if he has pneumonia again, or if he is actually in moderate heart failure. Asking Daniel if he wakes at night short of breath, known as paroxysmal nocturnal dyspnea (PND), or has frequent nocturia, demonstrates that fluid returns to the lung fields and kidneys when he lies down.
Knowing of his pre-existing pulmonary history, you evaluate today's complaint against previous episodes. When you ask if his trouble breathing today is different from previous complaints, such as when he calls you for COPD, he nods and says it is more like the last time he had pneumonia. You determine his perceived severity by using the 0 to 10 scale to rate how this episode compares to his previous experience. He wearily rates it as an 8. He says he has never been intubated.
Concerned that an AMI may be causing APE, you ask Daniel if he is having any chest pain or discomfort, which he denies. If he admitted to having pain or discomfort, you would use the standard mnemonic OPQRST to delve further into this complaint.
You perform a physical assessment, starting at the head. You see that the conjunctiva is moist, showing that he is hydrated, but also pale, demonstrating that perfusion may be compromised. You also notice a slight cyanotic tinge that coincides with the low pulse ox reading. You move to the neck and notice that, despite being upright, there is significant jugular venous pressure, demonstrating that there is a measurable amount of pressure within the right atria. You plan on reassessing this once Daniel is on the stretcher and you can place him into a 45° angle, if he allows it.
During the initial assessment, you briefly listened to Daniel's lung sounds. This time you listen more intently and confirm that the sounds are dim in the bases with fine crackles in the apices, and are truly bilateral in origin. As you listen to Daniel's lungs, your partner asks who his doctor is and you hear him answer clearly, "Doctor...Johnson." The fact that his response is so clear, when it should have been muffled, demonstrates that Daniel may have fluid from heart failure or consolidation from pneumonia. You place your stethoscope over Daniel's heart and hear the S1 and S2 heart sounds followed by the S3, with a cadence like "Ken-tuck-y," signifying atrioventricular regurgitation. The S3 sound is heard in a large number of patients over age 40 who have an ejection fraction of 30% or less.
You move Daniel to the stretcher, expose and assess his abdomen, which is soft and non-tender, and continue your assessment looking for fluid (ascites), which is indicative of heart failure. Your partner places his forearm down the midline of Daniel's abdomen and gently presses. You then place your hands on the right and left lateral aspects of his abdomen and quickly press toward the midline with your right hand. You do not observe or feel any wave transmission toward your left hand, signifying no fluid. If there had been fluid, it would have felt like pressing down on a waterbed. You also reach around Daniel's sides and lower back looking for sacral edema, but do not find any.
You pull up his pajama legs and pull off his socks, which leave an indentation. You press firmly into his foot with your thumb and let go, also leaving an indentation. You do the same farther up his leg and note pitting edema to about four inches above his ankles on both legs. There is no redness or drainage and no pain, nor are the legs excessively warm, decreasing the likelihood that the edema is a result of a DVT or cellulitis.
As you perform your assessment, your partner begins taking vital signs. Daniel's blood pressure is 188/110, leading you to think you heard fluid in his lungs, as that pressure is high enough to force fluid from the capillaries into the alveoli. Although his pressure is high, you are slightly relieved, because you know that pulmonary edema can also occur with low pressures, signifying poor cardiac output and cardiogenic shock.
Your partner reports that Daniel's radial pulse is 118, irregular and slightly weak, which is opposite of what you would expect with such high blood pressure. You conclude that Daniel may have had a catecholamine release that shunted the majority of his blood volume to central circulation. You also note that when Daniel takes a deep breath, there is no paradoxical pulse, which is commonly seen with such conditions as COPD, asthma and pneumothoraces, and demonstrates an increased pressure within the thoracic cavity that leads to decreased cardiac output during inhalation, when intrathoracic pressure naturally increases.
Daniel's ventilatory rate is 32 and labored, which is better than a slow rate, as bradypnea is an ominous sign of respiratory failure and impending respiratory arrest. His tachypnea is a response to both hypoxia and hypercarbia. The earlier pulse oximeter reading of 87% helps confirm moderate hypoxia, but since he was placed on oxygen, saturation has improved to 92%. You place Daniel on waveform capnography and note a fairly normal-appearing waveform (Figure 1) without a slurring of the upstroke that is indicative of bronchospastic diseases such as COPD and asthma. The capnometer shows an end-tidal reading of 40 mmHg. Typically, readings between 35–45 mmHg are considered normal; however, Daniel's respiratory rate of 32 is most likely a compensatory mechanism to hypercarbia and he may still have an underlying acidosis. Trending his waveform and numbers will be important, as the end-tidal numbers will increase with decreasing ventilations as he begins to enter respiratory failure.
Your partner is on the ball and has performed a 12-lead echocardiogram. You see right away that the irregularity you felt was the result of an occasional unifocal premature ventricular contraction (PVC), a common occurrence in patients suffering from heart failure, and you note that Daniel is tachycardic at a rate of 115. Every QRS has a preceding upright P-wave that is about 0.16 seconds off of the QRS. There is a discernable Q-wave noted, but overall the QRS appears tight and without any ST-segment elevation in any of the leads.
Earlier, we talked about ventricular hypertrophy, and this may be evident in the leads that overlie the affected ventricle. In Daniel's case, you notice that the R-wave is extremely tall in V5 (or may be seen in V6), exceeding 25mm in height and showing that the left ventricle is hypertrophic. You could also reach the same conclusion if the S-wave was noticeably deep (>25mm) in V1 or V2. Seeing this, it would not have surprised you to see ST-segment depression or T-wave inversion in those leads, evidence of strain on the ventricle.
You have now gathered a good history and performed a thorough physical exam. You know that Daniel is having issues with oxygenation and ventilation as shown by his presentation and vital signs. You sit back for a second, looking at your tools, and start to work through the differential diagnoses that you came up with earlier, eliminating the easy ones such as aspiration, anaphylaxis, pneumothorax and pulmonary embolism (see Table II on page 42). Considering that Daniel denied fever and chills and has an oral temperature of 98.6 degrees Fahrenheit greatly reduces the possibility of pneumonia. You are now down to three possible causes: COPD, heart failure or myocardial infarction.
You strongly consider an exacerbation of COPD by Daniel's presentation and the faint wheezes heard earlier. However, you remember fine crackles in addition to wheezes, and the waveform capnogram showed no slurring of the upstroke or shark fin appearances. You also recall the pitting pedal edema and his cardiac history and realize that treating him for COPD before considering that his distress may be the result of cardiac dysfunction may be detrimental.
It is important to consider a cardiac cause like supraventricular tachycardia or an AMI for his acute pulmonary edema. During assessment, you discovered that although Daniel was tachycardic, the rate was not high enough to be worrisome. He also had no complaints of chest pain or other symptoms of cardiac ischemia, nor did his ECG show any ST-segment changes. Typically, if an infarction is severe enough to cause pulmonary edema, there will be associated hypotension or some sign or symptom indicative of myocardial infarction. However, this is a moot point now. The treatment for heart failure runs similar to acute coronary syndrome. With his dyspneic state, cardiac demand may exceed its capacity and potentially induce an acute coronary syndrome. By looking at Daniel's physical exam, ECG and vital signs, and considering his history of present illness and past medical history, you deduce that he is most likely experiencing heart failure.
You begin to consider different treatment modalities, but realize you should focus upon those that will improve ventilation and oxygenation. Secondary treatment should look at decreasing Daniel's preload and afterload and allowing the heart not to work as hard, thus decreasing oxygen demand and finally interrupting the compensatory mechanisms to give his heart a rest.
Daniel is already on oxygen, but his saturation still shows mild hypoxia and he looks as though he is getting tired, a sign that he may need help with ventilation. Today, there are two types of ventilation: invasive and non-invasive. Invasive ventilation refers to endotracheal intubation, generally reserved for those patients in or near the late stages of respiratory failure or arrest, and which may not be possible without rapid sequence induction. Considering the potential risks of oral trauma, misplacement, barotrauma and ventilator-associated pneumonia, this skill should be avoided unless the patient absolutely requires it. Alternatively, non-invasive positive support ventilation (NIPSV) has not only become a standard in treating patients with pulmonary edema, but has been demonstrated to be highly effective in treatment of moderate to severe pulmonary edema.1 The most common form of NIPSV in EMS is continuous positive airway pressure, or CPAP, which provides a constant flow of oxygen during inspiration and exhalation. This keeps the smaller airways open and increases alveolar pressure, which, in turn, keeps fluid out and alveoli open. This decreases the work of breathing, as the airways do not have to be reopened with each breath, and allows more time for oxygen to be in contact with the alveoli and increases diffusion. CPAP also increases intrathoracic cavity pressure, especially around the left ventricle, making it easier to move blood out of the heart. You explain to Daniel that you are about to put a mask on his face that may seem awkward but will help him breathe easier. He nods, but you know you may have to coach him through it.
You recognize an increased sympathetic tone, as evidenced by Daniel's high blood pressure and pulse, and realize that to help reduce myocardial workload you will need to reduce preload and afterload. After ensuring that Daniel is not taking any medications for erectile dysfunction, you decide that administering a nitrate to reduce preload would be best, as they are effective vasodilators but short-acting if his blood pressure drops. Ideally, you would start him on intravenous nitroglycerin at 60 to 100 micrograms a minute, but all you have is sublingual nitroglycerin. Figuring that the sublingual route of administration has about a 75% absorption rate of nitroglycerin, meaning the patient will receive approximately 300 of the 400 microgram dose, or 60 micrograms a minute,2 and that his systolic blood pressure (SBP) is above 180 mmHg, you are more assertive and give him three 0.4 milligram doses of sublingual nitroglycerin equaling 180mcg/min. If SBP is between 140-180 mmHg, you would give two doses, or 120 mcg/min; if he were normotensive with a SBP between 90-140 mmHg, you would stay with the single dose.3 Knowing that the half-life of nitrates is short, you make a mental note to continually recheck Daniel's blood pressure every five minutes, administering additional nitroglycerin as needed. You decline using nitroglycerin paste, knowing that the rate of absorption for topical nitroglycerin is erratic and unpredictable, but you will keep it handy in case Daniel is not able to tolerate the sublinguals with CPAP.3
Recalling the pathophysiology of heart failure and the circular pathway of the disease, you know that you must interrupt the compensatory mechanism of vasoconstriction to decrease afterload and lower the pressure the left ventricle has to pump against. Remembering that angiotensin II is the culprit of this, you wish to administer an ACE inhibitor. The base-station physician reminds you to ensure Daniel has no history of allergies to ACE inhibitors nor any history of renal failure or aortic stenosis, and to double-check that the nitroglycerin has not caused him to become hypotensive, or even borderline hypotensive. Daniel denies any of those histories. His blood pressure is now 146/94, and the physician suggests a single dose of 1.25 mg of enalaprilat (IV form of enalapril) intravenously over five minutes. You tell her you do not carry that drug but do have a 25 mg tablet of captopril, which she tells you to wet with sterile water and place under Daniel's tongue. She reminds you to keep a close eye on his blood pressure and watch for any signs of angioedema, a common life-threatening side effect with ACE inhibitors.
Your partner now hands you two medications: furosemide and morphine. You explain that although furosemide is still commonly used in heart failure for patients with fluid overload and would have been a consideration if Daniel were already on a loop diuretic, it is not appropriate at this stage of treatment. Daniel's pulmonary edema was most likely due to increased hydrostatic pressure, which in turn caused misdistribution of fluid, and the diuretic might make him dehydrated and hypokalemic. Morphine has been completely removed from the heart failure algorithm, as it has been shown to increase morbidity and mortality. It was once thought to cause vasodilatation through the release of histamine, which it does, but it also releases catecholamines that could cause an increase in heart rate and oxygen demand and worsen the patient's condition. Others would use morphine to help reduce anxiety, but other drugs, such as benzodiazepines, are more appropriate.
During transport, you continue to monitor Daniel's vital signs every five minutes and watch for signs of respiratory failure and hypoperfusion. You talk with him, watching his anxiety level and level of consciousness, looking for the infamous head bob, bradypnea and hypoventilation often associated with respiratory acidosis and impending respiratory failure. His breathing now appears less labored, as evidenced by an increase in the number of words he can say, good eye contact and appropriate interaction with you. His blood pressure and other vital signs remain stable throughout transport to a cardiac care center with advanced treatment abilities to support his cardiovascular system if needed.
Three days later, Daniel is discharged home with a new diagnosis of heart failure. An ACE inhibitor and beta-blocker have been added to his prescription list, as well as a diet that calls for much less sodium. He will follow up with his cardiologist and be monitored for electrical and mechanical changes that may warrant the need for an implanted pacemaker/defibrillator.
There are many potential pathologies that cause a patient to have a complaint of shortness of breath and it may not always be easy to differentiate between heart failure, COPD/asthma and pneumonia. Misdiagnosis of heart failure is common and inappropriate treatment may be harmful.2 It has been shown that 25% of patients given furosemide developed significant electrolyte imbalances and hypotension requiring fluid boluses; adding morphine increased mortality by 22% compared to 2% with only nitroglycerin.2 If you have any question about the diagnosis, it would be appropriate to treat your patient with bronchodilators, nitroglycerin and NIPSV, avoiding morphine and furosemide.2 Remember that heart failure might be the result of an AMI, so it is important to consider aspirin as well.
1. Bledsoe BE. Mastering CHF: Current strategies for the prehospital care of congestive heart failure. JEMS. 34(2),2009.
2. Mattu A. Cardiac Update (Audio podcast EM2321). San Francisco: Audio Digest Emergency Medicine 23(21), 2006. www.audio-digest.org.
3. Bledsoe BE, Porter RS, Cherry RA. Cardiology. In Paramedic Care: Principles and Practice Vol. 3, pp. 202-206, 2001. Upper Saddle River, NJ: Prentice-Hall.
Aehlert B. Cardiac emergencies. In Comprehensive Pediatric Emergency Care, pp. 307-308. St. Louis: Mosby, 2005.
Aufderheide T, Brady W, Gibler W. Acute ischemic coronary syndromes. In J. A. Marx, R. S. Hockenberger & R. M. Walls (Eds.), Rosen's Emergency Medicine: Concepts and Clinical Practice 5th ed., Vol. 2, p. 1017. St. Louis: Mosby, 2002.
Ballew CC, Reigle J. Mechanisms and management of ventricular dysrhythmias in heart failure. AACN Clinical Issues: Advanced Practice in Acute and Critical Care 9(2):208-224, 1998.
Blum K. (2005). Heart failure. In P. A Morton, D. K. Fontaine, C. M. Hudak, & B. M. Gallo (Eds.), Critical Care Nursing, A Holistic Approach, 8th ed., pp. 393-421. Philadelphia: Lippincott Williams & Wilkins, 2005.
Brashers VL. Alterations of cardiovascular function. In S. E Huether & K. L. McCance (Eds.). Understanding Pathophysiology, 3rd ed., pp. 684-688. St. Louis: Mosby, 2004.
Cardiovascular emergencies. In R. S. Holleran (Ed.), Air & Surface Transport: Principles and Practice, 3rd ed., pp. 379-389. St. Louis: Mosby, 2003.
Cohn JN, Ferrari R, Sharpe N. Cardiac Remodeling-Concepts and Clinical Implications. A Consensus Paper from an International Forum on Cardiac Remodeling. J Am Coll Cardiol 35(3):569-582, 2000.
Corey E. Improving CHF Care: A New Algorithm for Prehospital Care. JEMS 32(4): 68-75, 2007.
Delgado RM III, Willerson JT. Pathophysiology of heart failure. Texas Heart Institute Journal 26(1):28-33, 1999.
Ellis KM. Hypertrophy. In EKG Plain and Simple: From Rhythm Strips to 12-Leads, pp. 425-432. Upper Saddle River, NJ: Prentice-Hall, 2002.
Falk JL, O'Brien JF, Shesser R. Heart Failure. In J. A. Marx, R. S. Hockenberger & R. M. Walls (Eds.). Rosen's Emergency Medicine: Concepts and Clinical Practice, 5th ed., Vol. 2, pp. 1110-1128. St. Louis: Mosby, 2002.
Hunt SA, et al. ACC/AHA 2005 Guidelines Update for the Diagnosis and Management of Chronic Heart Failure in the Adult. Circulation 112, pp. 154-235, 2005.
Jackson G, Gibbs CR, Davies MK, Lip GY. ABCs of Heart Failure: Pathophysiology. BMJ 320:167-170, 2000.
Mattera CJ. Heart failure and pulmonary edema: Understanding and correcting problems with the body's amazing pump. JEMS 25(5):36-47, 2000.
Miller GT, Garcia TB. Too much fluid, not enough oxygen? JEMS 31(11):36-40, 2006.
Upchurch J. COPD vs. CHF: Use history and physical exam clues to differentiate and treat two significant medical emergencies. JEMS 27(9): 82-94, 2002.
Kyle David Bates, MS, NREMT-P, CCEMT-P, FP-C, is a paramedic with the Town of Tonawanda (NY) Emergency Medical Unit. Contact him at www.KyleDavid Bates.com.
Table 1: HAPISOCS Mnemonic
History of pulmonary disease
There are both pulmonary and non-pulmonary causes for dyspnea. Heart failure may fall into both categories and should be assessed as such.
Activity at onset
Acute dyspnea occurring at rest may progress quickly, requiring more assertive airway management. Heart failure patients may experience rapid onset of respiratory distress as a result of APE from acute left ventricular dysfunction or may have more of a gradual onset from general fluid overload.
Pain upon inspiration
Patients with heart failure typically do not have pain on inspiration, although they may have cardiac chest pain. Treat accordingly, watching for cardiogenic shock.
"Is it pneumonia or heart failure?" Both may present similarly but often it comes down to whether the patient has been experiencing any signs of infection. Patients presenting with night sweats, chills, fever and a productive cough of yellow or greenish sputum may lead the paramedic toward a field diagnosis of pneumonia.
Nicotine causes a release of catecholamines, increasing heart rate, blood pressure, venous constriction, cardiac workload and oxygen demand, which are causative factors of heart failure.
When a patient with heart failure lies down, fluid returns to the pulmonary capillaries, decreasing the ability to diffuse gases. Similarly, a patient with a respiratory infection lying down allows the mucus to spread out into more of the lung fields, decreasing the surface area for gas exchange as well.
Patients suffering from respiratory infections may have a thick productive cough of yellow, yellowish-green or green sputum. Heart failure patients may start out with a dry cough, but as pulmonary vascular congestion worsens and the hydrostatic pressures increase red blood cells, fluid is forced into the alveoli, producing pink, frothy sputum. If the capillaries have yet to break or there is only fluid being forced into the alveoli, the sputum will be white and frothy.
These are questions that help focus the assessment, such as if the dyspnea has changed in intensity, history of intubation or CPAP use, and rating it 0–10.
Table II: Differential Diagnosis
Unilateral or bilateral crackles or wheezing, RLL most common