Clinical Assessment and Diagnosis

Precipitating Factors

It is important for the clinician to identify the cause(s) of AHF in order to maximize treatment efficacy and reduce future disease exacerbations. Cardiovascular, metabolic, and lifestyle factors can all precipitate AHF. The most common precipitating factors for acute decompensation and how they contribute pathophysiologically are listed in Table 6-3.

Laboratory Assessment

Routine laboratory testing of patients with AHF includes electrolytes and blood glucose, as well as serum creatinine and blood urea nitrogen to assess renal function. CBC count is measured to determine if anemia or infection is present. Creatine kinase and/ or troponin concentrations are used to diagnose ischemia, and hepatic transaminases are measured to assess hepatic congestion. Thyroid function tests are measured to assess hyperthyroidism or hypothyroidism as causes of AHF. A urinalysis is obtained in patients with an unknown history of renal disease to rule out nephrotic syndrome. Lastly, a toxicology screen is obtained in patients in whom use of illicit drugs is suspected.

Assays measuring BNP and its degradation product NTproBNP are being used with greater frequency in clinical practice.10 BNP is synthesized, stored, and released from the ventricles in response to increased ventricular filling pressures. Hence, plasma levels of BNP can be used as a marker for volume overload. The most widely accepted indication for BNP measurement is as an adjunctive aid for diagnosing a cardiac etiology for dyspnea.10

The current values for ruling out a cardiac etiology for dyspnea are a BNP less than 100 pg/mL (100 ng/L or 28.9 pmol/L) or an NT-proBNP less than 300 pg/mL (300 ng/L or 35.4 pmol/L). BNP measurements require cautious interpretation, as numerous conditions can also elevate BNP concentrations. These include older age, renal dysfunction, pulmonary embolism, and chronic pulmonary disease. Nesiritide, a recombinant BNP drug, has an identical structure to native BNP and will interfere with the commercial BNP assay, resulting in a falsely elevated level. Therefore, blood for BNP determination should be obtained 2 hours after the end of a nesiritide infusion, or alternatively the NT-proBNP assay should be utilized.

Other diagnostic tests should also be obtained in order to help determine precipitating factors (chest radiograph) and to evaluate cardiac function (ECG).

Invasive hemodynamic monitoring in patients with HF entails placement of a right heart or pulmonary artery catheter (PAC). The catheter is inserted percutaneously through a central vein and advanced through the right side of the heart to the pulmonary artery. Inflation of a balloon proximal to the end port allows the catheter to "wedge," yielding the PCWP, which estimates pressures in the left ventricle during diastole. Additionally, CO can be estimated and SVR calculated (Table 6-8).

There are no universally accepted guidelines dictating when invasive monitoring in HF is required. The use of a PAC remains an essential component of management and monitoring of patients in cardiogenic shock; however, the use of inotropic agents does not mandate invasive monitoring. Invasive hemodynamic monitoring is most commonly used to aid in the assessment of hemodynamics when there is disagreement between signs and symptoms and clinical response. In addition, invasive monitoring is helpful in guiding ongoing therapy for AHF. Invasive monitoring offers the advantage of immediate hemodynamic assessment of an intervention, allowing for prompt adjustments. Risks with PACs include infection, bleeding, thrombosis, catheter malfunction, and ventricular ectopy.

Table 6-8 Hemodynamic Monitoring: Normal Values

Hemodynamic Variable

Normal Value

Central venous (right atrial) pressure,

Less than 5 rim Hg

mean

Right ventricular pressure

25/0 mm Hg

Pulmonary artery pressure

25/10 mm Hg

Pulmonary artery pressure, mean

Less than IS mm Hg

Pulmonary artery occlusion pressure.

Less than 12 mm Hg

mean

Systemic arterial pressure

120/80 mm Hg

Mean arterial pressure

90-120 mm Hg

CI

2.S-4.2 L/mtn/im'

SV index

30-65 mL/beat/m-'

SVR

900-1,400 dyns-nr5

Pu I rnona r y va sc i. la r resistance

150-250 dyns-nr5

Arterial oxygen content

20 mL/dL

Mixed venous oxygen content

IS mL/dL

Arteriovenous oxygen content difference

3-5 mL/dL

CI, cardiac index: SV, stroke volume; SVR, systemic vasculai resistance.

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