Setting: emergency department (ED)
CC: “I can’t breathe.”
VS: R: 28 breaths/minute; BP: 150/98 mm Hg; P: 118 beats/minute; T: 97°F
HPI: A 63-year-old woman presents to the ED with shortness of breath that started earlier in the day and worsened over several hours. She says the dyspnea is “like swimming a whole pool underwater.” It is worsened by exertion and relieved by sitting up.
She has a history of hypertension and a myocardial infarction 2 years ago. She takes “a bunch of pills” every day, which she cannot remember the name of. Her physician does not have privileges at your hospital, so the record is not available.
ROS:
No chest pain
No history of valve disease
PE:
Chest: rales 2/3 up bilaterally
Cardiovascular: jugulovenous distention (JVD), an extra sound on auscultation
Extremities: bilateral pitting edema up to the knees
What is the mechanism of the finding on the heart examination?
a. Rapid filling of the ventricle during diastole
b. Rupture of the chordae tendineae
c. Fibrinous exudate in between the heart and the pericardium
d. Aberrant conduction tract at the atrioventricular (AV) node
e. Increased gradient of pressure between the left ventricle (LV) and the aorta
Answer a. Rapid filling of the ventricle during diastole
An S3 gallop is most likely in pulmonary edema from congestive heart failure (CHF). When the mitral valve opens in diastole, the massive fluid overload in the lungs rapidly spills into the ventricle making a “splash” of fluid called an “S3 gallop.”
Rupture of the chordae tendineae (choice b) happens acutely as a complication of myocardial infarction 1 to 2 weeks after the muscle dies and necroses. Fibrinous exudate (choice c) is the cause of a rub in pericarditis. Aberrant conduction (choice d) is from short PR or preexcitation syndromes such as Wolff-Parkinson-White (WPW) syndrome. The ausculatory finding of WPW is a loud S1 from early closure of the mitral valve. Increased gradient of pressure is from aortic stenosis. The stenotic valve blocks flow out, so that in severe disease, the pressure in the LV is 50 to 70 mm Hg greater than what is found in the aorta.
Orthopnea is venous pooling in the chest when lying flat.
Edema is found on examination. What is the mechanism?
a. Decreased hydrostatic pressure of the interstitial fluid
b. Decreased oncotic pressure
c. Alteration of the diffusion coefficient (KF) of the capillary
d. Increased hydrostatic pressure in the peripheral capillaries
e. Increased hydrostatic pressure in the glomerular capillaries
Answer d. Increased hydrostatic pressure in the peripheral capillaries
Peripheral edema of CHF is from back pressure from the heart resulting in increased hydrostatic pressure in peripheral capillaries. Because of gravity, the lowest, or most “dependent” areas of the body have the highest hydrostatic pressure. This increases filtration across the capillary membrane. There is no change in the oncotic pressure in CHF, and the intrinsic nature of the capillary wall, or KF, does not change.
The patient is moved from the stretcher in the triage area of the ED already wearing a face mask for oxygen set at 50% forced inspiratory oxygen (FiO2). The nurses sit her upright.
Initial Orders:
Oxygen
Oximeter continuously
Furosemide and morphine IV
Nitroglycerin (paste cutaneously)
Chest x-ray, electrocardiogram (ECG), arterial blood gas (ABG) analysis
B-type natriuretic peptide (BNP) for equivocal cases when diagnosis is uncertain
As you move the clock forward 15 to 30 minutes, the patient begins to feel better. If a loop diuretic such as furosemide is effective, urine will be made within 30 minutes. If not, give an additional IV dose of a loop diuretic at least every 30 minutes until urine is made. Make sure you repeat vital signs in acutely ill patients every 15 to 30 minutes especially when giving medications that can lower blood pressure (BP) such as diuretics, nitrates, morphine, and angiotensin-converting enzyme (ACE) inhibitors. On a single-best-answer question, never consult a cardiologist for pulmonary edema management. You are expected to manage cases like this on your own. The majority of patients with acute pulmonary edema will respond to preload reduction alone.
Nitrates:
• Mainly venous dilators
• Decrease preload more than afterload
If furosemide is not in the choices, which drug should you choose as an alternative that has the same mechanism of action?
a. Spironolactone
b. Acetazolamide
c. Bumetanide
d. Chlorthalidone
e. Conivaptan
Answer c. Bumetanide
The loop diuretics are furosemide, bumetanide, torsemide, and ethacrynic acid. They inhibit the Na+/K+/2Cl− pump in the thick ascending limb of the loop of Henle. This is the site where 25% of sodium is reabsorbed in the kidney. Spironolactone blocks aldosterone’s effect at the late distal tubule and early collecting duct. Spironolactone and eplerenone specifically block the epithelial sodium channel (ENaC). Acetazolamide inhibits carbonic anhydrase. It is effective at the proximal tubule and is rarely used as a diuretic and never for acute pulmonary edema. Chlorthalidone is a thiazide diuretic inhibiting approximately 6% to 7% of total sodium absorption at the distal tubule. Conivaptan inhibits the V2 receptor of the collecting duct. V2-receptor antagonists are replacing demeclocycline in the treatment of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Conivaptan and tolvaptan exclusively block water reabsorption by blocking antidiuretic hormone (ADH).
After a second dose of furosemide, the patient fails to produce urine in significant amount and her shortness of breath worsens. Her respiratory rate increases from 26 to 36 breaths/minute. Her BNP level is markedly elevated, but it is of marginal value in a person who comes in with an obvious presentation of pulmonary edema.
Which test will make the most difference in the management of acute pulmonary edema?
a. BNP
b. Chest x-ray
c. ABG
d. ECG
e. Echocardiogram
Answer d. ECG
If the ECG shows an arrhythmia such as ventricular tachycardia (VT) or atrial fibrillation (AFib) or flutter, you may be able to quickly restore cardiac output by performing immediate synchronized cardioversion. In a healthy person, atrial systole provides only a small amount to the overall LV filling and cardiac output, on the order of 10% to 15%. In a person with dilated cardiomyopathy or valve disease, atrial systole or “kick” is essential to providing a much greater percentage, such as 30% to 50%. With cardiomyopathy, AFib can propel the patient into flash pulmonary edema. Echocardiography does not change acute management. It is essential to long-term treatment to know if there is systolic or diastolic dysfunction, but this has no effect on acute pulmonary edema management.
You move the clock forward 10 to 20 minutes, and the results of the test are automatically sent to you. You will receive the notice, “report available.”
ECG: Sinus tachycardia
ABG: pH 7.48; partial pressure of carbon dioxide (PCO2) 28 mm Hg; partial pressure of oxygen (PO2) 58 mm Hg on 50% face mask
Chest x-ray: Pulmonary vascular congestion, cardiac enlargement, and pleural effusion
Pleural effusion in CHF is from increased pulmonary capillary hydrostatic pressure. The mechanism is the same as in peripheral edema (Figure 1-1).
Figure 1-1. Pulmonary edema. Note indistinct vasculature, perihilar opacities, and peripheral interstitial reticular opacities. Although this is an anteroposterior film, making cardiac size more difficult to assess, the cardiac silhouette still appears enlarged. (Reproduced with permission from Loscalzo J. Harrison’s Pulmonary and Critical Care Medicine, 2nd ed. New York: McGraw-Hill Education; 2013.)
Atrial stretch creates BNP production. BNP excretes water and salt through the kidney.
Additional doses of diuretic and morphine are given. IV nitroglycerin is given with no effect. As you move the clock forward, oxygen saturation on 50% or 100% face mask hovers near 90%. Always recheck vital signs every 15 to 30 minutes in patients as unstable as this. On the computer-based case simulation (CCS), you should order a consultation with cardiology and critical care on a patient not responding to preload reduction. Consultants on CCS will never give specific treatment or testing advice.
Maximum Preload Treatment + Persistent Hypoxia = Intensive Care Unit Placement
Morphine works by dilating pulmonary veins and decreasing hydrostatic pressure in capillaries.
What is the mechanism of the medication you should try next?
a. Dilation of afferent arteriole of glomerulus
b. Beta-hydroxy-beta-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibition
c. Vasoconstriction of arterioles
d. Positive inotrope and vasodilation
e. Venodilation
Answer d. Positive inotrope and vasodilation
Dobutamine acts as both a positive inotrope, increasing contractility, and as a peripheral vasodilator. This allows greater forward flow of blood. Dopamine will increase contractility but is a vasoconstrictor on peripheral vessels. Dopamine increases afterload.
The patient in placed on dobutamine and transferred to the intensive care unit (ICU). Many patients in these circumstances are intubated for mechanical ventilation. If your case describes a failure to improve with dobutamine or the phosphodiesterase inhibitors milrinone or inamrinone, then intubation is correct. Continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) can be tried to keep the patient from being intubated. Ventilators have frequent complications with pneumonia, and CPAP or BiPAP can save a person from this complication.
On Step 3 CCS, it is unlikely to combine the details of acute pulmonary edema management with long-term treatment issues such as ACE inhibitors, angiotensin receptor blockers (ARBs), beta-blockers, spironolactone, and digoxin. These issues are addressed in separate cases.
The final point of management addressed is why a patient develops acute pulmonary edema. Less than 0.1% of patients with CHF are admitted in this condition. If someone presents with acute pulmonary edema, the most likely precipitants of decompensation are
Nonadherence to medication
Ischemia
Arrhythmia
Infection
If you see patients who are taking their medications but still develop pulmonary edema, the most important first step is to exclude arrhythmia. If there are no arrhythmias, you must exclude ischemia as a cause of decompensation. People do not develop pulmonary edema for no reason. Exclude coronary artery disease when you have no clear reason for the acute episode of pulmonary edema.
Pulmonary Edema Precipitants
• Ischemia
• Arrhythmia
• Infection
• Nonadherence to medications