Cardiogenic Pulmonary Edema

Description

Cardiogenic pulmonary edema (CPE) is the accumulation of fluid with a low protein content in the lung interstitium and alveoli. It results from the left ventricular (LV) output being lower than pulmonary and left atrial venous return.
CPE is the end-result of several different pathological processes that cause increased hydrostatic pressure. Alternatively, increased permeability is seen more commonly with primary pulmonary processes such as acute respiratory distress syndrome or acute lung injury (noncardiogenic pulmonary edema).
Analogy: The heart functions like a dam, and the lungs are the banks along the river. When the dam does not let the water through, the river rises, backs up, and overflows onto the banks. In CPE, the heart pump malfunctions and thus causes backup and overflow leading to edema in the lungs.

Epidemiology

Incidence

Difficult to assess exact incidence; however, pulmonary edema occurs in 1–2% of the general population.

Prevalence

CHF, a major cause of CPE, affects nearly 5 million Americans.

Mortality

In-hospital mortality: 15–20%
CPE resulting from an acute myocardial infarction (MI) has a 40% mortality; this can reach 80% when the patient is hypotensive.

Etiology/Risk Factors

Acute MI (1)
Severe myocardial ischemia
Cardiomyopathies (low ejection fraction)
LV volume overload
LV outflow obstruction (aortic stenosis)
Diastolic dysfunction
Acute mitral regurgitation
Left atrial myxoma
Atrial fibrillation, due to low LV filling

Physiology/Pathophysiology

LV pump dysfunction increases left atrial volume and pressure that transmits to the pulmonary vasculature. The increased hydrostatic pressures initially cause dilation and recruitment of pulmonary vessels, followed by extravasation into the interstitial space, and entry into alveoli. This manifests as follows:
- Decreased pulmonary compliance
- Atelectasis and decreased functional residual capacity; results in V/Q mismatching and increased Alveolar-artery (A-a) gradient
- Increased work of breathing

Prevantative Measures

Ischemia and infarction
- Increase myocardial oxygen supply
  - Increase the FIO₂
  - Increase hemoglobin levels (if appropriate)
  - Increase diastolic perfusion pressure
  - Decrease heart rate (increases diastolic perfusion time)
  - Avoid hyperventilation (which can cause vasospasm of the coronary arteries)
- Decrease myocardial oxygen demand
  - Decrease heart rate (as appropriate)
  - Decrease contractility (as appropriate)
  - Decrease preload (as appropriate)
  - Decrease afterload (as appropriate
  - Maintain sinus rhythm (if possible)
- Cardiac catheterization and percutaneous intervention
- Emergency coronary artery bypass surgery
Hypertensive emergency. Aggressively treat BP to decrease myocardial wall tension (and decrease oxygen consumption). Insert invasive monitors as needed
Diastolic dysfunction. Avoid volume overload, increase lusitropy (myocardial relaxation), maintain sinus rhythm (atrial kick is important for adequate end diastolic volumes)
Systolic dysfunction. Avoid volume overload, promote afterload reduction
Aortic stenosis. Maintain normal sinus rhythm, slow heart rate, adequate diastolic perfusion pressures, and volume status (preload dependent)
Mitral stenosis. Maintain normal sinus rhythm, slow heart rate, avoid volume overload.
Atrial fibrillation. Convert to a sinus rhythm if possible; if not, maintain rate control.

Diagnosis ⬆ ⬇

Under general anesthesia, the intraoperative diagnosis may be difficult; many signs and symptoms will be masked or are nonspecific.
- There is usually a history of an acute cardiac or coronary event prior to its onset, or conversely volume overload in the setting of baseline cardiac dysfunction.
- Hypoxia and desaturation can result from atelectasis. Auscultation can reveal crackles, rales, wheezing, and murmurs.
- Arterial blood gas measurements can reveal an increased A-a gradient.
- Increased sympathetic tone can result in tachycardia and hypertension. However, in the setting of severe LV dysfunction, hypotension may be present.
- S3 gallop or jugular venous distention may be observed.
- Pink, frothy sputum in the endotracheal tube or laryngeal mask airway may be seen.
Invasive monitoring
- PCWP is useful in differentiating causes of pulmonary edema, as CPE will usually have a PCWP >18 mm Hg, pulmonary edema from other causes typically has a PCWP <18 mm Hg.
- Transesophageal echocardiogram (TEE) is useful when a patient is under anesthesia to help determine if the cause of pulmonary edema is from a cardiac cause. Ventricular dysfunctions (wall motion, ejection fraction), ventricular pathology (stenosis, regurgitation), and volume status can be determined.

Differential Diagnosis

Aspiration
Pulmonary embolism
Sepsis
Anaphylaxis
Acute asthma exacerbation
Chronic obstructive pulmonary disease
Pneumonia
Pneumothorax
Acute respiratory distress syndrome

Treatment ⬆ ⬇

Should be aimed at the underlying cause while supporting cardiac pump function (2).
Preload reduction decreases the volume that the heart needs to pump forward; akin to decreasing the river flow to the dam.
- Venodilators. Nitroglycerin is fast acting and easily titratable (increases capacitance, does not decrease intravascular volume).
- Diuretics. Loop diuretics such as furosemide reduce intravascular volume, but require ~20 minutes for onset. In the setting of poor renal perfusion, it may be even longer.
- Hemodialysis may be necessary in the setting of renal failure and volume overload.
Afterload reduction improves forward flow (stroke volume and hence cardiac output) for a given contractility; it decreases wall tension and myocardial oxygen demand. This is accomplished via vasodilators (3).
- Nitroprusside is a potent arterial dilator and easily titratable (4).
- Intravenous calcium channel blockers may also be utilized.
- Volatile anesthetics
Inotropic support should be considered when CPE is refractory to preload and afterload reduction, or when hypotension prevents the use of these strategies. Improved pump function allows improved management of venous return and forward flow with resultant:
- Decreases in LV end-diastolic pressure (LVEDP) and volume; results in decreased wall tension (decreased radius, as per LaPlace's Law).
- Improvement in coronary perfusion during diastole (CPP = MAP–LVEDP)
- Improvement in cerebral and systemic perfusion
- However, this comes at the cost of increased myocardial oxygen consumption secondary to enhancing the contractile state.
Inotropic agents include the following:
- Dobutamine is a -1 agonist; it causes a mild reduction in afterload that helps to increase cardiac output.
- Milrinone is a phosphodiesterase inhibitor, which increases inotropy and decreases both SVR and PVR (5).
- Dopamine has and alpha effects depending on the dosage. At high doses, it can cause tachycardia and has arrhythmogenic potential.
- Norepinephrine is a potent alpha-1 agonist with some activity. It is typically reserved for patients with refractory hypotension as it tends to cause a much greater increase in afterload than the other inotropes.
Oxygenation
- Increase the FiO₂
- Increase hemoglobin levels with packed red blood cell transfusion, if appropriate
- PEEP should be optimized in an attempt to keep the SpO₂ >90%

Follow-Up ⬆ ⬇

Treatment of the underlying cause should be the initial step in managing these patients once they are stabilized.
Any arrhythmias must be corrected.
If CPE is caused by an acute valvular dysfunction, emergent valve surgery is required.
CPE from an acute MI typically requires either aggressive medical management, percutaneous intervention, or bypass surgery
Left ventricular assist device (LVAD) or heart transplants may be warranted.

References ⬆ ⬇

LeConte P , Coutant V , Nguyen JM , et al. Prognostic factors in acute cardiogenic pulmonary edema. Am J Emerg Med. 1999;17(4):329–332.
Mattu A , Martinez JP , Kelly BS. Modern management of cardiogenic pulmonary edema. Emerg Med Clin North Am. 2005;23(4):1105–1025.
Annane D , Bellissant E , Pussard E. Placebo-controlled, randomized, double-blind study of intravenous enalaprilat efficacy and safety in acute cardiogenic pulmonary edema. Circulation. 1996;94(6):1316–1324.
Dupuis J. Nitrates in congestive heart failure. Cardiovasc Drugs Ther. 1994;8(3):501–507.
Karlsberg RP , DeWood MA , DeMaria AN. Comparative efficacy of short-term intravenous infusions of milrinone and dobutamine in acute congestive heart failure following acute myocardial infarction. Milrinone-Dobutamine Study Group. Clin Cardiol. 1996;19(1):21–30.
Gropper MA , Wiener-Kronish JP , Hashimoto S. Acute cardiogenic pulmonary edema. Clin Chest Med. 1994;15(3):501–515.
Teerlink JR. Overview of randomized clinical trials in acute heart failure syndromes. Am J Cardiol. 2005;96(6A):59G–67G.

section name header

Basics ⬇

Incidence

Prevalence

Mortality

Diagnosis ⬆ ⬇

Treatment ⬆ ⬇

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆