by Walid Hammad – USA
An ambulance crew rushes into your emergency department (ED) with a 56-year-old man. He is severely short of breath, sitting upright on the stretcher, using his accessory respiratory muscles, and gasping for air. You find that he is diaphoretic, tachypneic, and in severe respiratory distress. You ask him, “What’s going on?” He replies: “I…can’t…(pauses and inhales a shallow breath)…breathe!”
The paramedics inform you that they received a call from the patient’s wife about 6:30 that morning, saying that her husband was short of breath and sweaty and that he had vomited once. The wife told them that she and her husband had returned from a long trip the night before and that her husband had not taken his “water pills” because he did not want to stop for frequent restrooms breaks during their drive. When they got home, he still did not take his pills because he wanted to sleep through the night. His breathing problems woke him during the night, and he tried to get more comfortable by adding pillows under his head to the point that he was almost sitting up in bed.
You thank the paramedics and turn back to the patient, who now looks even worse. He is more short of breath, and you sense that he is getting tired, about to give up. He looks like he is about to collapse. What is your next step?
Critical Bedside Actions and General Approach
The first step in managing such a patient, as for most ED patients, is measuring vital signs. This information will help you identify a part of the pathology. For example, if the patient is hypertensive, he could be in acute heart failure; on the other hand, if the patient is hypotensive, he could be in shock. Similarly, if the patient is tachycardic, his symptoms could be caused by the very fast heart rate; conversely, if he is bradycardic, he could have symptomatic bradycardia. The vital signs will guide your treatment options. When you examine the patient described in this case report, you find his blood pressure (BP) to be 265/145 mm Hg, his heart rate (HR) to be 138 beats/min, his respiratory rate at almost 40 breaths/min, and his pulse oximetry reading is 92% on 4 liters of oxygen delivered by nasal cannula. (Note: A patient who is severely short of breath might be breathing through his or her mouth, so a nasal cannula may not be of great benefit; in these patients, the use of a face mask might be prudent.)
This patient’s clinical presentation and vital signs represent a clinical pattern of acute heart failure (AHF) with severe acute pulmonary edema (APE) secondary to acute left ventricular failure (LVF). The LVF and subsequent pulmonary edema are secondary to any or a combination of (1) an increased preload, (2) a decreased left ventricular ejection fraction, or (3) an extremely elevated blood pressure.
On the other hand, a patient who presents with the same clinical picture but with a low BP instead of a high one could have APE or acute LVF secondary to cardiogenic shock. In this scenario, your treatment choices will change, and your strategy will be directly opposite that for a patient with elevated BP. It is crucial to make this distinction early because the administration of vasodilators in high doses to a patient in cardiogenic shock could have a devastating outcome.
The second step in management is the clinical examination. In a patient with AHF with consequential severe APE, the clinical picture might resemble severe Stage D congestive heart failure (CHF), but with a swifter, more acute onset. Generally, the patient is in moderate to severe distress, is uncomfortable, and is usually diaphoretic, with jugular venous distention (JVD) and bilateral rales on lung examination. Depending on how long the patient has been in severe CHF, the rales might be basal initially but then heard in all lung fields, up to the apices, in late stages or even audible without a stethoscope.
Hepatic engorgement, a positive abdominojugular test, and bilateral lower extremity edema are signs of chronic CHF and might not have developed yet in a patient with acute left heart failure. These signs start to manifest when the pulmonary arterial wedge pressure increases. Think about the pathology: the heart (the pump or engine), specifically the left ventricle, is unable to pump the blood against the overwhelming resistance generated by the increased systemic vascular resistance (SVR) that is generating an extremely high BP in the aorta. With such elevated BP, the left ventricle is unable to offload the suitable amount of blood with each stroke, i.e., stroke volume (SV) is decreased, leading to a decrease in cardiac output (CO). With time, if the preload does not decrease and the afterload continues to increase, the blood will back up behind the left ventricles (in the lungs), causing the lungs to become engorged with accumulated blood and thus increasing transudation of protein-poor fluid into the interstitial space and the alveoli. This cascade compromises the air exchange mechanisms, causing the patient to manifest signs and symptoms of respiratory failure, presenting clinically as tachypnea and hypoxia.
The First 5 to 10 Minutes
The main pathology in AHF is the extremely high SVR in the heart, so the treatment modalities should focus on decreasing the resistance, i.e., decreasing the blood pressure (afterload) or decreasing preload. The mean arterial pressure (MAP) can be used as a treatment guideline. It is determined by the cardiac output (CO) and SVR: MAP=CO x SVR. Note that about 50% of patients presenting with APE are euvolemic rather than hypervolemic and that the treatment options should focus on volume redistribution rather than volume removal.
Since you do not want to decrease CO in a patient who is barely perfusing because of the elevated BP, your best bet is to work on decreasing preload and/or SVR and thus decrease the MAP. This can be achieved by several means. However, in this scenario, in which the patient is extremely ill and needs the MAP to be dropped quickly, we head directly to the rapid-onset options—nitro derivatives (fast-acting nitroglycerin derivatives) and BIPAP or CPAP.
- Acute Kidney Injury
- Acute Respiratory Distress Syndrome
- Bacterial Pneumonia
- Cardiogenic Pulmonary Edema (secondary to cardiogenic shock)
- Chronic Obstructive Pulmonary Disease (COPD)
- Cirrhosis of the liver
- Community-Acquired Pneumonia
- Goodpasture Syndrome
- Idiopathic Pulmonary Fibrosis
- Interstitial (nonidiopathic) Pulmonary Fibrosis
- Myocardial Infarction
- Nephrotic Syndrome
- Neurogenic Pulmonary Edema
- Pulmonary Embolism
- Respiratory Failure
- Venous Insufficiency
- Viral Pneumonia
History and Physical Examination Hints
- JVD might be present, indicating increased central venous pressure (CVP) resulting from pulmonary edema and increased right ventricular pressures.
- An extremely elevated BP in a previously relatively healthy patient presenting with APE points to acute heart failure.
- Bilateral pulmonary rales are typical of APE but not specific. Rales on only one side could suggest other causes such as pneumonia or emphysema (dry crackles).
- APE can also present as bilateral wheezing (cardiac asthma); however, this presentation should not be confused with the wheezing associated with pure reactive airway disease or asthma.
- If the patient presents with altered mental status or has an abnormal neurologic exam, the APE might be neurogenic pulmonary edema.
- If the patient is receiving dialysis or has nephrotic syndrome, cirrhosis, or other causes of volume overload, the backbone of treatment will be diuresis rather than redistribution (preload or afterload reduction).
- If lung sounds are unequal, the patient might have a spontaneous pneumothorax. If the patient is as sick as the one in our scenario, he or she could be experiencing cardiac tamponade (pay attention to the position of the trachea).
Emergency Diagnostic Tests and Interpretation
- By placing the head of the stretcher at a 45-degree angle, you should be able to assess the patient for JVD.
- An electrocardiogram (ECG) might show sinus tachycardia, atrial fibrillation, or another arrhythmia (tachycardia or bradycardia), suggesting the reason for a decrease in cardiac output (CO=HR X SV). The ECG could also reveal a left ventricular strain pattern.
- With proper training, emergency physicians can reliably obtain the following information with an ultrasound examination performed at the bedside:
- Complete Blood Count (CBC): May show an elevated white blood cell (WBC) count, which may indicate an infectious cause rather than a cardiac cause. However, stress in itself can induce hypoxia and shortness of breath, which can cause margination of WBCs, leading to an elevated WBC count. A patient with severe chronic obstructive pulmonary disease (COPD) or Goodpasture syndrome is likely to be taking corticosteroids, which can raise the WBC count.
- Comprehensive Metabolic Panel (CMP): May indicate renal failure if the SVR is so high that it is causing severe spasm in the renal artery and thus impairing kidney function, especially if the patient has other comorbidities that predispose him/her to kidney injury. The patient might be alkalotic in response to tachypnea, which presents as low CO2. He may also present with acidosis due to elevated lactate levels resulting from tissue hypoxia. Liver function test results could be elevated, especially if the patient has long-standing CHF that is causing hepatic engorgement.
- Pro-BNP: The b-type natriuretic protein (BNP) concentration will be elevated in a patient with acute heart failure, but usually the values are not very high. Be careful: pro-BNP could also be elevated in patients with large pulmonary embolisms that are causing right ventricular strain. Cardiac enzymes might be slightly elevated due to the myocardial strain; significantly elevated numbers warrant consideration of Acute MI.
A chest x-ray (obviously a portable frontal view in our patient) would show pulmonary congestion, with cephalization of the pulmonary vessels, Kerley B lines, peribronchial cuffing with air bronchograms, a “bat wing” pattern, and possibly, though not always, an increase in cardiac shadow size. Note that not all these findings may be present on the chest x-ray.
Emergency Treatment Options
- If the patient is lying down flat, move him/her into a sitting position, which should lessen the pooling of blood in the lungs and allow the utilization of the superior lung fields for aeration and gas exchange.
- Place the patient on supplemental oxygen.
- Obtain intravenous access quickly.
Non-invasive positive pressure ventilation (NIPPV)
NIPPV for cardiogenic pulmonary edema is an effective and safe modality in adult patients with APE. There is a potential benefit of NIPPV in reducing mortality.
- Nitro derivatives: Nitrogen inhibits the motor function of the smooth muscles in the systemic vasculature, leading to vasodilation and a decrease in SVR.
- Nitroglycerin: Reduces preload.
- Nitroglycerin has been found to be safe for use in patients with acute heart failure and improves short-term outcomes in EDs and ED-like settings.
- Nitroglycerin is a rapid-onset, short-acting smooth muscle relaxant that reduces preload through venous dilation and, in high doses, reduces afterload through arteriolar dilation.
- Sublingual tablets dissolve under the tongue and are manufactured in 400-mcg minitablets. After you have confirmed the diagnosis by exam and the monitor is indicating a high blood pressure, place one, two, or even more tablets under the patient’s tongue (up to one tablet per minute).
- Nitroglycerin might cause hypotension, which is usually temporary and associated with overall clinical improvement. However, the persistence of the hypotension after the nitroglycerin is stopped might indicate a right ventricular malfunction, e.g., right ventricular MI or volume depletion.
- Intravenous nitroglycerin can be administered, starting as a drip at 0.5‒0.7 mcg/kg/min and then increased by 10‒20 mcg/min q3-5 minutes up to 200 mcg/min. The BP must be monitored closely during administration.
- Transdermal nitroglycerin (1‒5 cm) can be applied to the chest wall.
- Pediatric dosing: 0.25‒5 mcg/kg/min IV, to a maximum dose of 20 mcg/kg/min
- Safety profile
- Class C in pregnancy
- Safety during lactation is unknown
- Nitroprusside: Reduces afterload.
- Is a more potent arteriolar vasodilator than nitroglycerin
- Poses the potential for thiocyanate toxicity
- If further afterload reduction is needed after administration of nitroglycerin, a nitroprusside drip can be started.
- Dosage: 0.3–10 mcg/kg/min
- Pediatric dosing: 0.25‒4 mcg/kg/min to a maximum dose of 10 mcg/kg/min
- Safety profile
- Class C in pregnancy
- Possibly unsafe during lactation
- Nitroglycerin: Reduces preload.
- Has not been found to increase or decrease the rate of hospitalization or death. It might have a negative effect, causing hypotension. Its use in acute heart failure is still being investigated.
- Dosing: 0.01 mcg/kg/min IV to a maximum of 0.03 mcg/kg/min
- Safety profile
- Class C in pregnancy
- Safety during lactation is unknown
- Loop diuretics: Reduces preload.
- Loop diuretics may be the first line of treatment for chronic heart failure. However, Cotter and colleagues found that for patients with acute heart failure accompanied by severe pulmonary edema and respiratory distress, high-dose nitro derivatives combined with a small dose of furosemide were more effective than high-dose furosemide with a small dose of nitro derivatives. IV dosing of diuretics, especially in large doses, is more helpful than the oral route; diuresis will begin within 15 to 20 minutes after administration.
- The dose in emergency circumstances can be up to 2.5 times the patient’s regular dose. If the patient is loop diuretic naïve; give 40 mg IV of furosemide or the equivalent of another loop diuretic.
- Check the safety profile for each individual medication that is considered or administered.
- Severe left ventricular dysfunction or acute valvular problems may cause hypotension in some patients. Therefore, using the above agents can be harmful to these patients. Therefore, inotropic medications such as dopamine and dobutamine can be inevitable to preserve normal blood pressure.
Please read RUSH protocol chapter and watch its’ videos to learn more about US evaluation of pulmonary edema.
- All patients who present to an ED with acute heart failure and severe pulmonary edema should be admitted to either an intensive care unit or an intermediate care unit based on the institution’s ability to handle the necessary therapeutic modalities, especially drips and noninvasive positive-pressure ventilation (NIPPV).
- Some patients might be stable enough on a telemetry floor/ward, especially patients who had resolved symptoms and findings.
- Risk-stratifying patients with acute failure in the ED is difficult and requires additional investigation.
References and Further Reading
- Ewy GA. The abdominojugular test: technique and hemodynamic correlates. Ann Intern Med. 1988;109(6):456‒460. Erratum in: Ann Intern Med. 1988;109(12):997.
- Nemeth J. Acute decompensated heart failure. CMAJ. 2007 Jul 17;177(2):175; author reply 175-6
- Labovitz AJ, Noble VE, Bierig M, et al. Focused cardiac ultrasound in the emergent setting: a consensus statement of the American Society of Echocardiography and American College of Emergency Physicians. J Am Soc Echocardiogr. 2010;23(12):1225‒1230.
- Jones AE, Tayal VS, Kline JA. Focused training of emergency medicine residents in goal-directed echocardiography: a prospective study. Acad Emerg Med. 2003;10(10):1054‒1058.
- Alexander P, Alkhawam L, Curry J, et al. Lack of evidence for intravenous vasodilators in ED patients with acute heart failure: a systematic review. Am J Emerg Med. 2015;33(2):133‒141.
- Daiber A, Münzel T. Organic nitrate therapy, nitrate tolerance, and nitrate-induced endothelial dysfunction: emphasis on redox biology and oxidative stress. Antioxid Redox Signal. 2015;23(11):899‒942.
- Den Uil CA, Brugts JJ. Impact of intravenous nitroglycerin in the management of acute decompensated heart failure. Curr Heart Fail Rep. 2015;12(1):87‒93.
- O’Connor CM, Starling RC, Hernandez AF, et al. Effect of nesiritide in patients with acute decompensated heart failure. N Engl J Med. 2011;365(1):32‒43.
- Cotter G, Metzkor E, Kaluski E, et al. Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema. Lancet. 1998;351(9100):389‒393.
- Elker GM, Lee KL, Bull DA, et al.; NHLBI Heart Failure Clinical Research Network. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med. 2011;364(9):797‒805.
- Auble TE, Hsieh M, McCausland JB, Yealy DM. Comparison of four clinical prediction rules for estimating risk in heart failure. Ann Emerg Med. 2007;50(2):127‒135, 135.e1-2.
- Vital FMR, Ladeira MT, Atallah ÁN. Non-invasive positive pressure ventilation (CPAP or bilevel NPPV) for cardiogenic pulmonary oedema. Cochrane Database of Systematic Reviews 2013, Issue 5. Art. No.: CD005351. DOI: 10.1002/14651858.CD005351.pub3
Additional References and Links To More Information
- National Clinical Guideline Centre (UK). Acute Heart Failure: Diagnosing and Managing Acute Heart Failure in Adults. London: National Institute for Health and Care Excellence (UK); 2014 Oct.
- Silvers SM, Howell JM, Kosowsky JM, et al.; American College of Emergency Physicians. Clinical policy: Critical issues in the evaluation and management of adult patients presenting to the emergency department with acute heart failure syndromes. Ann Emerg Med. 2007;49(5):627‒669. Erratum in: Ann Emerg Med. 2010;55(1):16.
- Yancy CW, Jessup M, Bozkurt B, et al.; American College of Cardiology Foundation; American Heart Association Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013;62(16):e147‒239.