Approach to shock (echocardiography)
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An organized approach to shock is critical in the management of these often very sick patients. Shock - of any form - manifests as inadequate tissue perfusion, the end-point of which is multisystem organ failure and death.
Clinical signs of shock, which may not always be accompanied by hypotension, include:
cool, mottled extremities
decreased urine output
Common pathophysiological mechanisms, and common etiologies, which result in shock include 6:
left ventricular dysfunction
An immediate differential diagnosis may be formed by the assessment of preload dependence (i.e. fluid responsiveness) and the measurement of cardiac output. Subsequent division of shock etiologies may then be possible based on cardiac output; separation of states associated with a low cardiac output (cardiogenic, hypovolemic, obstructive) and those which are associated with a preserved, or inappropriately high, cardiac output (distributive/vasoplegic shock).
The presence or absence of central venous plethora is also a crucial component of the clinical exam; echocardiographic correlates of high central venous pressures combined with shock and/or hypotension is immediately suggestive of cardiogenic or obstructive shock. The presence or absence of pulmonary edema, readily assessed with ultrasonography, is another crucial element of the clinical picture, as its presence would highly suggest the former (cardiogenic shock), and its absence should prompt a search for evidence of the latter (obstructive).
An initial basic goal-directed examination is performed in order to determine the most prudent resuscitative measures, which may be followed by more advanced examinations. Parameters assessed include:
left ventricular function
right ventricular function
presence or absence of pericardial fluid
However, advanced techniques involving the use of modalities such as spectral and tissue Doppler allow for more accurate hemodynamic assessments 5.
Assessment of preload dependence
Using a physical maneuver that increases preload, such as passive leg raise, or administration of intravenous fluids, one may observe the effect on cardiac output or stroke volume. Fluid responsiveness is deemed present if there is >10-15% increase in cardiac output or stroke volume in response to an increase in preload; this also defines a state of preload dependence 5. This so called dynamic assessment of fluid responsiveness is preferred over a so called static assessment of fluid responsiveness.
In the absence of preload dependence, the next step is to document the presence or absence of reduced cardiac output.
Assessment of cardiac output
Calculation of stroke volume using a combination of pulsed wave Doppler and B-mode measurements is possible as follows 2:
measurement of the left ventricular outflow tract from the transthoracic parasternal long axis view
free aortic cusp excursion should be observed to screen for aortic stenosis
measurement should occur when aortic valve cusps are fully open in mid-systole
visualization of the left ventricular outflow tract (apical 5-chamber view)
placement of a pulsed wave Doppler gate in the LVOT
the spectral envelope may be traced to obtain a velocity-time integral
represents systolic displacement of a column of blood, measured in centimeters (stroke distance)
calculation of stroke volume and clinical integration
assuming the LVOT is cylindrical, the volume would be equal to:
π x radius2 x height
the diameter of the LVOT, as previously measured, can be halved to obtain the radius, and the VTI can be used as the height of the column of blood displaced
Stroke volume can then be calculated and used to derive the cardiac output if the heart rate is known, using the equation:
cardiac output (CO) = stroke volume (SV) x heart rate (HR)
Cardiac output, when corrected for body surface area, is reported as a cardiac index (CO/BSA) with a normal range between 2.5-4.0 L/min/m2.
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