Acute Heart Failure and Pulmonary Edema

This syndrome is seen in patients with an established diagnosis of HF who develop increasing signs or symptoms of decompensation after a period of relative stability.

Progressive dyspnea is the most common complaint of patients, along with lower extremity edema, epigastric tenderness, or abdominal fullness.

An elevated jugular venous pressure, positive hepatojugular reflux test, and a tender, enlarged liver are frequent findings.

Rales and wheezing may be heard with significant pulmonary congestion, but the absence of rales does not imply that the pulmonary venous pressures are not elevated.

Diminished air entry at the lung bases is usually caused by a pleural effusion, which is often more frequent on the right.

Leg edema is frequently evident in both legs, particularly in the pretibial region and ankles in ambulatory patients.

The cardiac examination may be entirely normal in patients with heart failure with preserved LVEF, whereas many patients with advanced LV systolic dysfunction (LVSD) exhibit a third heart sound and a laterally displaced point of maximal impulse.

A murmur of mitral regurgitation is often audible when the LV is markedly enlarged, whereas a tricuspid regurgitation murmur is present when the right ventricle (RV) is volume or pressure overloaded.

The syndrome of ADHF is characterized by the rapid onset of symptoms or signs of HF.

This phenotype is more common in females and the systolic BP on admission usually exceeds 180 mm Hg.

There is usually predominant pulmonary congestion and minimal weight gain prior to admission.

Virtually all patients have a preserved LVEF.

Severe pulmonary edema is seen in less than 3% of all patients admitted with ADHF.

Patients typically experience a sudden and overwhelming sensation of suffocation and air hunger accompanied by extreme anxiety, cough, expectoration of a pink frothy liquid, and a sensation of drowning.

The patient sits bolt upright, is unable to speak in full sentences owing to a marked respiratory rate, and may also thrash about.

An ominous sign is obtundation, which may be a sign of severe hypoxemia.

Sweating is profuse, and the skin tends to be cool, ashen, and cyanotic.

The oxygen saturation is usually less than 90% on room air before treatment.

Auscultation of the lung usually reveals coarse airway sounds bilaterally with rhonchi, wheezes, and moist fine crepitant rales that are detected first at the lung bases, but then extend upward to the apices as the lung edema worsens.

Cardiac auscultation may be difficult in the acute situation, but third and fourth heart sounds may be present.

Systolic BP is less than 90 mm Hg in approximately 8% of patients with acute decompensated HF.

Low-output HF is characterized by symptoms and signs that are related to decreased end-organ perfusion.

A typical patient with this clinical syndrome has severe LVSD and usually presents with symptoms of fatigue, altered mental status, or signs of organ hypoperfusion.

The patient may present with tachypnea at rest, tachycardia, and a cold and cyanotic periphery.

The degree of peripheral hypoperfusion may be so advanced that the skin over the lower extremities is mottled and cool.

Occasionally, the clinician may detect pulsus alternans —when a strong or normal pulse alternates with a weak pulse during normal sinus rhythm, a sign of severe LVSD.

The phenotype is uncommon and generally presents with warm extremities, pulmonary congestion, tachycardia, and a wide pulse pressure.

Underlying conditions include anemia, thyrotoxicosis, advanced liver failure, and Paget disease.

This syndrome occurs commonly in patients with severe isolated tricuspid regurgitation, RV dysfunction, chronic lung disease, or long-standing pulmonary hypertension.

These patients present with signs and symptoms of right-sided volume overload.

Arterial underfilling is sensed by mechanoreceptors in the LV, carotid sinus, aortic arch, and renal afferent arterioles, caused by a decrease in systemic arterial pressure, stroke volume, renal perfusion, or peripheral vascular resistance.

This leads to an increase in sympathetic outflow from the central nervous system, activation of the renin-angiotensin-aldosterone system, and the nonosmotic release of arginine vasopressin, as well as the stimulation of thirst.

These factors—together with increased release of vasoconstrictors, such as endothelin and vasopressin, and resistance to endogenous natriuretic peptides—contribute to sodium and water retention leading to decompensation of HF.

The flux of fluid out of any vascular bed results from the sum of forces promoting extravasation of fluid from the capillary lumen versus forces acting to retain intravascular fluid.

Under normal conditions, the sum of the forces is slightly positive, producing a small vascular fluid flux into the precapillary interstitium of the lung that is drained as lymph into the systemic veins.

Because the intravascular pressure in the pulmonary capillaries is always higher than plasma osmotic pressure, transcapillary fluid flux out of the pulmonary capillary is continuous.

When the interstitial fluid exceeds the interstitial space capacity, fluid floods into the alveoli.

The interstitial space is drained by a rich bed of lymphatics and pulmonary lymph flow may increase threefold before fluid extravasates into the alveolar airspaces.

Table 7.2 lists the causes of pulmonary edema based on the initiating mechanism.

Pulmonary edema occurs if the pulmonary capillary pressure exceeds the plasma colloid osmotic (oncotic) pressure, which is approximately 28 mm Hg in humans.

The normal pulmonary capillary wedge pressure is approximately 8 mm Hg, which allows a margin of safety of about 20 mm Hg.

Although pulmonary capillary pressure must be abnormally high to increase the flow of the interstitial fluid, these pressures may not correlate with the severity of pulmonary edema when edema is clearly present.

Pressures may return to normal when there is still considerable pulmonary edema because of the time required for removal of interstitial and pulmonary edema.

Chronic elevations in left atrial pressure are associated with hypertrophy in the lymphatics, which then clear greater quantities of capillary filtrate during acute increases in pulmonary capillary pressure.

The removal of edema fluid from the alveolar and interstitial compartments of the lung depends on active transport of sodium and chloride across the alveolar epithelial barrier.

Reabsorption of these electrolytes is mediated by the epithelial ion channels located on the apical membrane of alveolar epithelial type I and type II cells and distal airway epithelia.

Water follows passively, probably through aquaporins that are found predominantly on alveolar epithelial type I cells.

The relationship between pressure and volume throughout the cardiac cycle can be presented as a pressure-volume (PV) loop ( Fig. 7.1 ).

The PV loop can provide a simple, but comprehensive, description of LV pump function as it encapsulates the systolic and diastolic functions of the heart.

Because these loops also circumscribe end-systolic volume (ESV) and end-diastolic volumes (EDV), the stroke volume (SV) and EF can be derived.

The bottom limb of the loop, also termed” diastolic pressure-volume curve,” describes LV diastolic compliance.

Progressive increases in systolic pressure produce a nearly linear increase in ESV.

By matching the end-systolic pressure (ESP) and volume coordinates from multiple, variably loaded beats, a near-linear relationship is established.

The slope of this relationship (E _max ), determined by altering load, reflects LV contractility (see Fig. 7.1 ).

A positive inotropic intervention is associated with an increased ESP and SV and a decreased EDV.

This results in an increased E _max and a shift of the PV relationship to the left ( Fig. 7.2A ).

Conversely, a negative inotropic intervention decreases ESP and SV and increases EDV.

This results in a decrease in E _max and a shift of the PV relationship to the right (see Fig. 7.2B ).

In the intact human heart, an increase in systolic pressure is associated with an increase in ESV and, if the LV fails to dilate, stroke volume decreases ( Fig. 7.3A ).

An increase in preload is accompanied by an increase in SV and a modest increase in ESP (see Fig. 7.3B ).

Acute and chronic changes in the PV relationship in the failing heart depend on the underlying myocardial structure and function, the type and extent of injury, and the severity and nature of the hemodynamic load.

Chamber stiffness is determined by analyzing the curvilinear diastolic PV relationships ( Fig. 7.4 ).

The slope of the tangent (dP/dV) to this curvilinear relationship defines the chamber stiffness at a given filling pressure.

An increase in dP/dV owing to an increase in volume, shown in Fig. 7.4 (A → B), has been called a “preload-dependent change in stiffness.”

When the pressure-volume relationship shifts to the left (A → C), the tangent is steeper at the same diastolic pressure.

The latter may be caused by an increase in myocardial mass or intrinsic myocardial stiffness or by changes in several extramyocardial factors.

Chamber stiffness of the LV is determined by static factors (e.g., chamber volume, wall mass, stiffness of the wall) and dynamic factors (e.g., pericardium, RV, myocardial relaxation, erectile effects of the coronary vasculature).

Most acute alterations in LV chamber stiffness result from a preload-dependent increase in chamber stiffness, a shift to a different PV curve, or a combination of the two.

All can result in elevated left atrial pressure, pulmonary venous hypertension, and the signs and symptoms of ADHF.

During the early phase of myocardial infarction or with acute ischemia, reduced ventricular ejection increases ESV (residual volume) and, together with reduced LV compliance, leads to rapid increases in LV filling pressures.

It is thought that lusitropic dysfunction associated with ischemia is the result of an increase in stiffness in the ischemic myocardial segment (possibly caused by slowing and incompleteness of the relaxation process) and dilation of the nonischemic segment, causing a preload-dependent increase in chamber stiffness.

The increase in LV filling pressure that occurs with acute infarction or ischemia is caused by the combination of a preload-dependent increase in chamber stiffness and a leftward shift of the diastolic PV curve.

Increased diastolic pressures after an acute ischemic insult may also result from the redistribution of blood from the periphery to the central blood pool.

The effects of these changes on the PV relationship are shown in Figure 7.5A .

In acute volume overload, as seen in patients with sudden and severe valvular regurgitation or after ischemic ventricular septal rupture, the LV dilates, causing the ventricle to operate on the steeper portion of the pressure-volume curve.

Consequently, small increments in volume result in a marked increase in filling pressures.

The effects of these changes on the PV relationship are shown in Figure 7.5B .

The lusitropic abnormalities of LV hypertrophy secondary to aortic stenosis, severe hypertension, or hypertrophic cardiomyopathy are caused by abnormalities of the static and dynamic determinants of chamber stiffness.

Increased passive stiffness of the hypertrophied heart results in part from the increased myocardial mass and the low volume-to-mass ratio; abnormal intrinsic myocardial stiffness also may contribute to increased chamber stiffness.

Abnormalities of myocardial relaxation further impair filling in the hypertrophied heart.

The effects of these changes on the pressure-volume relationship are shown in Figure 7.5C .

Chronic HF is characterized by a compressed PV.

This compressed loop, characterized by a decrease in ESP and an increase in end diastolic pressure (EDP), means that the work of the failing heart is reduced while maintaining a near-normal SV.

Comparable to the changes with ischemia, the elevated filling pressures in HF are caused by a combination of a preload-dependent increase in chamber stiffness (i.e., the LV operates at higher end-diastolic volumes to optimize the Starling relationship) and a preload-independent increase in chamber stiffness (see Fig. 7.5D ).

Several steps are necessary for a comprehensive evaluation of a patient with ADHF.