Differential Diagnosis
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In cases where the clinical presentation is similar- a simple hemodynamic challenge such as PLR may assist in the diagnosis by providing insight into the heart’s responsiveness to fluids.
Shock Etiologies
Shock presents two separate challenges:
- First, differentiating between types of shock is critical (e.g. septic, hypovolemic, cardiogenic, neurogenic) but may be very challenging.
- Second, refining decisions on fluids and drugs requires continuous feedback on fluid responsiveness as well as response to medication such as pressors or cardiac agonists that may be used in some shock patients (Drug titration).
During most types of shock (but not in many septic shock cases), by increasing vascular tone Baroreceptor-mediated vascular compensation can sustain a constant blood pressure in a patient losing as much as 20% of blood volume before being associated with a drop in mean arterial pressure (MAP) (reference 1).
Monitoring only BP does not provide any lead time warning, nor does it enable differential diagnosis between hypovolemic shock, septic shock and cardiogenic shock.
With NICOM monitoring of cardiac output (CO) and total peripheral resistance (TPR) enables early detection of impending hemodynamic collapse and combined with a simple bedside hemodynamic challenge such as passive leg raising or response to 250 ml fluid bolus provides an insight as to the shock etiology.
See figure 1 for a sample differential diagnosis empowered by knowledge of CO and related hemodynamics.
Shortness of Breath
Shortness of breath is a common symptom in ED, ICU, and perioperatively. Differentiating between shortness of breath due to Chronic Obstructive Pulmonary Disease (COPD) to pulmonary congestion due the Heart Failure (CHF) or other causes is a clinical challenge.
A recent trial demonstrated figure2 that a response to Hemodynamic challenges with NICOM might serve as a diagnostic tool to differentiate between COPD and CHF (reference 2; see also figure 2). In acute decompensated heart failure the heart operates on the flat portion of the starling curve implying that there is no cardiac reserve to propel the additional preload forward and hence no increase in cardiac output following the hemodynamic challenge, whereas in Dyspnea due to COPD the response to the hemodynamic challenge is expected to be positive as the heart is functioning on the ascending limb of starling curve, where the increase in preload causes an increase in cardiac output.
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References:
<p>1. Arterial and Plethysmographic Waveform Analysis in Anesthetized Patients with Hypovolemia; R. Pizov,M.D et al, Anesthesiology 2010;113:83–91</p>
<p>2. Engineer RS, Benoit JL, Hicks CW, et al. Hemodynamic changes as a diagnostic tool in acute heart failure—a pilot study. Am J Emerg Med. 2010 Oct 26</p>
Fig 1. Differential Diagnosis Table click to enlarge
Fig 2. Adapted from: Benoit J. et al. Hemodynamic changes as a diagnostic tool for acute heart failure. Academic emergency medicine. 2009; 16(s1):S11 click to enlarge
References
1. Arterial and Plethysmographic Waveform Analysis in Anesthetized Patients with Hypovolemia; R. Pizov,M.D et al, Anesthesiology 2010;113:83–91
2. Engineer RS, Benoit JL, Hicks CW, et al. Hemodynamic changes as a diagnostic tool in acute heart failure—a pilot study. Am J Emerg Med. 2010 Oct 26