Volume Assessment in Heart Failure


Finding
 
Summary LR (95 % CI)

Sensitivity

Specificity

Positive

Negative

Initial clinical judgment

0.61

0.86

4.4 (1.8–10.0)

0.45 (0.28–0.73)

History

Heart failure

0.60

0.90

5.8 (4.1–8.0)

0.45 (0.38–0.53)

Myocardial infarction

0.40

0.87

3.1 (2.0–4.9)

0.69 (0.58–0.82)

Coronary artery disease

0.52

0.70

1.8 (1.1–2.8)

0.68 (0.48–0.96)

Diabetes mellitus

0.28

0.83

1.7 (1.0–2.7)

0.86 (0.73–1.0)

Hypertension

0.60

0.56

1.4 (1.1–1.7)

0.71 (0.55–0.93)

Smoking

0.62

0.27

0.84 (0.58–1.2)

1.4 (0.58–3.8)

COPD

0.34

0.57

0.81 (0.60–1.1)

1.1 (0.95–1.4)

Symptoms

PND

0.41

0.84

2.6 (1.5–4.5)

0.70 (0.54–0.91)

Orthopnea

0.50

0.77

2.2 (1.2–3.9)

0.65 (0.45–0.92)

Edema

0.51

0.76

2.1 (0.92–5.0)

0.64 (0.39–1.1)

Dyspnea on exertion

0.84

0.34

1.3 (1.2–1.4)

0.48 (0.35–0.67)

Cough

0.36

0.61

0.93 (0.70–1.2)

1.0 (0.87–1.3)

Physical examination

Third heart sound

0.13

0.99

11 (4.9–25.0)

0.88 (0.83–0.94)

Abdominojugular reflux

0.24

0.96

6.4 (0.81–51.0)

0.79 (0.62–1.0)

Jugular venous distension

0.39

0.92

5.1 (3.2–7.9)

0.66 (0.57–0.77)

Rales

0.60

0.78

2.8 (1.9–4.1)

0.51 (0.37–0.70)

Any murmur

0.27

0.90

2.6 (1.7–4.1)

0.81 (0.73–0.90)

Lower extremity edema

0.50

0.78

2.3 (1.5–3.7)

0.64 (0.47–0.87)

Valsalva maneuver

0.73

0.65

2.1 (1.0–4.2)

0.41 (0.17–1.0)

SBP < 100 mmHg

0.06

0.97

2.0 (0.60–6.6)

0.97 (0.91–1.0)

Fourth heart sound

0.05

0.97

1.6 (0.47–5.5)

0.98 (0.93–1.0)

SBP > 150 mmHg

0.28

0.73

1.0 (0.69–1.6)

0.99 (0.84–1.2)

Wheezing

0.22

0.58

0.52 (0.38–0.71)

1.3 (1.1–1.7)

Ascites

0.01

0.97

0.33 (0.04–2.9)

1.0 (0.99–1.1)


Abbreviations: LR likelihood ratio, CI confidence interval, PND paroxysmal nocturnal dyspnea, SBP systolic blood pressure, COPD chronic obstructive pulmonary disease



In physical examination teachings, the S3 is highly specific for ventricular dysfunction and elevated left ventricular filling pressures. In fact, the presence of an S3 has the highest positive likelihood ratio (LR 11.0) for volume overload [9]. However, the inter-rater reliability of this physical exam finding is very low [12], and it is often difficult to auscultate in patients with confounding diseases (e.g., COPD and obesity) and in noisy environments such as the emergency department. In fact, the 2009 updated guidelines do not list heart sounds as a method to assess volume status or the diagnosis of heart failure [7].

Another confounding factor to the diagnosis of volume overload may be the presence of hypoperfusion. Although the majority of patients with HF do not present with hypoperfusion, their cardiac function may be severely depressed. Conversely, patients with hypoperfusion may have a concurrent illness, or be suffering from hypovolemia rather than pump failure, or have excessive vasodilation from their heart failure; this must be considered when taking the history. When patients present with more severe volume deficits, orthostatic symptoms and hypotension may suggest hypovolemia and not necessarily hypoperfusion. Orthostatic symptoms may include dizziness upon standing, shortness of breath with exertion or at rest, weakness, malaise, and syncope if the deficit is severe. However, the utility of orthostatic vital signs in the emergency department has been questioned. In a sample of 132 presumed euvolemic patients, 43 % had “positive” orthostatic vital signs [13]. In a comparison of over 200 ill patients and 20 control patients, orthostatic changes in systolic blood pressure and diastolic blood pressure demonstrated no statistically significant association with level of dehydration, and it was impossible to define a group of patients who had a “positive” tilt-table test [14].

The combination of history and physical examination findings may aid the physician in diagnosing volume overload. However, diagnostic imaging, natriuretic peptides, and other noninvasive techniques are also available to address the issue.



Chest Radiography


Chest radiographs may aid in the diagnosis of volume overload or may help guide the differential diagnosis of the acutely dyspneic patient in the emergency department. In the presence of heart failure, one may find pulmonary venous congestion, cardiomegaly, and interstitial edema. However, the absence of radiography findings does not exclude heart failure [7]. Collins et al. found that up to 20 % of patients who were eventually diagnosed with heart failure had negative chest radiographs at the time of evaluation in the emergency department [15]. Furthermore, in late-stage heart failure patients, chest radiography has unreliable sensitivity, specificity, and predictive value for identifying individuals with high PCWP.


Natriuretic Peptides


The natriuretic peptides (NP) are hemodynamically active neurohormones that are released into the bloodstream when there is increased myocardial pressure and stretching, so that they can enable vasodilation and natriuresis. It is released as a prohormone and cleaved into the biologically active BNP and NT-proBNP. Assays for BNP and its synthetic by-product NT-proBNP are commercially available.

Compared with BNP, NT-proBNP has a longer plasma half-life [16]. There is ample evidence that both BNP and NT-proBNP are useful in diagnosing and predicting prognosis in heart failure, including the Breathing Not Properly Multinational Trial (BNP Trial) [17], the Rapid Emergency Department Heart Failure Outpatient Trial (REDHOT) [18], PRIDE (pro-BNP Investigation of Dyspnea in the Emergency Department) [16], and the ESCAPE (Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness) Trial [19]. These molecules behave similarly and are elevated in the setting of heart failure. These studies demonstrated that BNP and NT-proBNP are useful in the diagnosis and risk stratification of patients with heart failure.

Furthermore, the natriuretic peptides also provide an overall assessment of volume status. In studies of patients on hemodialysis, plasma BNP levels before and after hemodialysis correlate with the degree of body fluid and volume retention [20, 21] and with inferior vena cava diameter measurements that are reflective of hydration status.

However, because the NPs can be elevated with any type of myocardial stress, independent of volume status (e.g., myocardial infarction, pulmonary embolus), physician judgment must also be used. Both BNP and NT-proBNP interpretation must be used carefully in obese individuals [22], older patients, and those with renal disease or on hemodialysis [21]; all these factors affect the sensitivity and specificity of the test. Knowledge of the patient’s baseline levels and any associated change may also be useful.

For more detailed information regarding the diagnostic and prognostic utility of natriuretic peptides, please refer to Chap. 12.


Phonocardiography


Auscultation of an S3 heart sound is difficult in the emergency department setting, and as mentioned previously, interobserver concordance is low [23]. Phonoelectrocardiographic devices have been developed in order to improve detection of abnormal heart sounds, specifically an S3 or S4. The Audicor system is an acoustic cardiogram that collects both sound and electrical data. Earlier studies showed that it has increased the likelihood of the diagnosis of HF and left ventricular dysfunction [24, 25]. However, in a multinational study of over 990 patients, although the system was specific for the diagnosis of acute decompensated heart failure and affected physician confidence, its lack of sensitivity did not improve diagnostic rates [26]. Furthermore, the test did not have any independent prognostic information.


Ultrasonography


Ultrasound has become increasingly available at the bedside. It has been shown to be useful in a myriad of conditions and has been helpful in the assessment of volume status in the critically ill patient [27] including septic shock and trauma [28].

The inferior vena cava diameter (IVCd) has been shown to indicate volume status and blood loss. In a study of 31 healthy male volunteers who were donating 450 ml of blood, IVCd measured both during inspiration (IVCi) and during expiration (IVCe) showed a decrease of 5 mm after blood loss [29]. The wide variation between individuals of IVC diameter makes isolated measurements difficult to interpret for volume status (Fig. 10.1).

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Fig. 10.1
Over 75 % collapse of IVC, seen on long axis view (Image reproduced with the permission of Dr Alfred Cheng)

Studies have addressed using respiratory variation in IVCd as a marker for the diagnosis of HF. IVCd is dynamic and changes with changes in intrathoracic pressure. During inspiration, intrathoracic pressure decreases thereby increasing venous return and causing distention of the IVC. During expiration, an increase in intrathoracic pressure causes a collapse of the IVC [27, 29]. A measurement for this variation in IVC diameter is the IVC collapse index (IVC-CI). The IVC-CI is equal to the difference between the IVCDe and the IVC diameter in inspiration (IVCi) divided by the IVCe. Absolute values for a normal IVC-CI do not exist; however, the IVC-CI in normal healthy subjects is typically between 0.25 and 0.75 (see Fig. 10.1). In HF, volume overload dilates the IVC to the point that decreased intrathoracic pressure does not change the resulting diameter and thus the IVC-CI remains close to 1 (Fig. 10.2). In patients who are intubated, a similar measure can be used known as distensibility index (dIVC), which instead uses the maximum and minimum diameter of the IVC rather than the IVCi and IVCe. dIVC is equal to the (maximum diameter – minimum diameter)/minimum diameter. If the value is greater than 18 %, it suggests the patient is fluid responsive and may not be volume overloaded [30, 31].
Jul 1, 2017 | Posted by in CARDIOLOGY | Comments Off on Volume Assessment in Heart Failure

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