Echocardiography in the assessment of shock

Harish Mallapura Maheshwarappa

Director – Institute of Critical Care Medicine, Kauvery Hospitals, Marathahalli

Introduction

Echocardiography has evolved to become a crucial noninvasive imaging modality in the critically ill patients. Its portability, safety, and widespread availability allow for the rapid diagnosis of life-threatening cardiac problems and rapid exclusion of cardiac disease in critically ill patients. These benefits encourage the use of 2D Echo in ICU on routine day-to-day basis.

Indications for Transthoracic Echocardiography in Critical Care

1. Hemodynamics

Left ventricular function

Regional wall motion abnormalities
Global dysfunction
Transient dysfunction (sepsis, ischemic/catecholamine stunning)

Right ventricular function

Hypotension

Pericardial effusion/tamponade

Assess volume status

Outflow tract obstruction and valvular stenosis/insufficiency.

2.Hypoxia

Right ventricular function
Right ventricular pressure
Intracardiac/extracardiac shunting
Pulmonary embolus

3. Infections

Bacterial endocarditis

4. Trauma

Blunt thoracic trauma
Penetrating thoracic trauma

5. General

Assess proximal ascending aorta—dissection, hematoma
Source of murmur
Source of embolus
Procedural guidance (especially pericardiocentesis).

6. Indications for Transesophageal Echocardiography in Critical Care

Inadequate or non-diagnostic transthoracic echocardiographic images.
Evaluate suspected aortic dissection or trauma.
Evaluate prosthetic valves, especially mitral.
Investigate persistent hypoxemia.
Detect presence of valvular vegetations.
Identify complications of infective endocarditis:

Abscesses
Leaflet perforation
Pseudoaneurysm formation
Fistulas

7. Identify cardiac source of systemic embolus:

Thrombus in left atrium and left atrial appendage
Patent foramen ovale/atrial septal aneurysm
Atheromatous debris of the aorta

8. Identify pulmonary embolus in transit

9. Characterize intracardiac shunts:

Atrial septal defect (ASD)
Ventricular septal defect (VSD)
Anomalous pulmonary venous connections

10. Guide invasive procedures:

Shunt closure
Percutaneous balloon valvuloplasty

Diagnostic echocardiography

Clinical findings	Cardiac Cause	2D echo findings
Low CO unresponsive to inotropes	Valvular disease	Any severe stenotic or regurgitate lesion
	Intrinsic cardiac disease	HOCM/LVH with LVOTO Large VSD/ASD Severe LV/RV dysfunction
	Extrinsic cardiac disease	Cardiac Tamponade Pericardial effusion Pericardial disease

Clinical findings	Cardiac Cause	2D echo findings
Oliguria	Underfilling	Low trans mitral/tricuspid velocities Small ventricular volumes Apposition of LV papillary muscles in systole
	Intrinsic cardiac disease	Poor LV function, severe AS
	Pericardial disease: Pericardial	Pericardial effusion, pericardial tamponade, pericardial constriction

Clinical findings	Cardiac Cause	2D echo findings
Increased filling pressures (left-sided)	Impaired LV	Increased E > A ratio, short IVRT
Increased filling pressures (left-sided)	MV disease	Significant MS or MR
Increased filling pressures (right- sided)	Secondary to left-sided disease	Significant AS, AR, MS, MR/LV disease
	Impaired RV	Reduced TAPSE
	TR	Annular dilatation or endocarditis

Clinical findings	Cardiac Cause	2D echo findings
Sepsis/SIRS	LV/RV dysfunction	Ventricular dilatation, systolic/diastolic dysfunction
	Source of sepsis	Masked endocarditis
Endocarditis:	Native/prosthetic valve pacemaker wires extracardiac ‘endocarditis’	Vegetations paraprosthetic leaks aortic root abscess
Pulmonary hypertension	Acute PE	Dilated RV, severe TR
	Post-pneumonectomy	Displaced heart, increased pulmonary acceleration time
	Mitral valve disease	Significant MS or MR

Clinical findings	Cardiac Cause	2D echo findings
Failure to wean from ventilator	Intrinsic cardiac disease	Ischaemia severe MR HOCM LV/RV dysfunction
CVA/embolic event	Intracardiac thrombus	LA appendage RA apical LV thrombus Endocarditis
Cyanosis	Intracardiac shunting	Positive contrast study

Ventricular function Assessment

Left ventricle Systolic Function:

Techniques exist to assess LV function

Measurement of dimensions and volumes in two/three dimensions
Wall thickness and motion
Assessment of filling patterns
Measurement of myocardial deformation.

All these measures are variably load and inotropy-dependent; therefore measured values should be interpreted cautiously in the critically ill. LV contractility has depended upon linear measurement of changes in LV internal dimensions (fractional shortening, FS)

Differences between systolic and diastolic areas/volumes in the minor axis (ejection fraction, EF). Normal values of FS/EF are unknown for the critically ill patient population. Measured values should be interpreted with caution in the critically ill.

Regional functional abnormalities:

Myocardial thinning (normal 6–12 mm). Abnormal motion (hypokinesis/akinesis/dyskinesis)

ICU echocardiogram should be interpreted in the context of the level of inotropic support, and where abnormalities in contractility conform to known coronary artery territories, ischemia/infarction should be suspected.

The longitudinal axis (LAX) function has three components:

Amplitude
Velocity
Timing

Measured using M-mode (mitral annular plane systolic excursion, MAPSE) (Normal 10-12 mm). Velocities of this motion assessed using tissue Doppler imaging (TDI).

LV diastolic function:

Derived measures of diastolic function

Isovolumic relaxation time (IVRT, normal 70–110 ms)
Ratio of peak velocities (E/A, normal 0.75 – 1.40)
E-wave deceleration time (normal 160 – 240 ms)

Normal values are age, inotropy, and filling dependent, as well as varying with pathology, interpretation in critically ill patients.

(A) – Pulsed Doppler echocardiographic recording of mitral inflow velocity

(B) – Tissue Doppler imaging of the septal or medial mitral annulus velocity

(C) – IVRT

Color M-mode

Colour flow propagation velocity (CFPV), as determined by color M-mode Doppler

Measurement to diagnose LV diastolic dysfunction (Vp < 50 cm/s indicating diastolic disease.

Tissue Doppler imaging (TDI)

Tissue Doppler imaging (TDI) of the myocardium at the base of the heart may assist in the diagnosis. Here early myocardial tissue velocities (E′)

Providing a measure of myocardial relaxation:

E′ of ≥10 cm/s is normal relaxation,
<10 cm/s is impaired
<5 cm/s is severely impaired.

Normal TDI velocity

RV systolic function:

RV is exquisitely sensitive to increases in afterload and reduction in coronary perfusion

In the ICU, RV dysfunction is due to:

Secondary to pulmonary disease
Mechanical ventilation
LV dysfunction

A range of techniques is used to assess RV function, including M-mode, PW Doppler, and TDI. Measurement of the longitudinal annular movement of the RV free wall using M-mode (tricuspid annular plane systolic excursion, TAPSE) correlates well.

Normal TAPSE is 2 cm, falling after cardiac surgery to 1.5 cm. Any reduction in TAPSE in the setting of pulmonary hypertension indicates significant RV dysfunction. Amplitude of <1 cm implies severe impairment. RV diastolic function measurement on same principles of LV diastolic dysfunction; but its often unreliable in critical care setting.

Positive-pressure ventilation may abolish this pulmonary arterial diastolic wave, making the diagnosis more challenging. Confounding factors include the presence of LV restriction, elevation of pulmonary arterial diastolic pressures, tachycardia and requirement for high ventilatory pressures.

Pericardial Disease

Pericardial effusion and cardiac tamponade can be easily diagnosed in critically ill patients who are oligouric and having low CO even with inotropes.

Additional features: swinging heart, pseudo systolic anterior motion of the MV demonstration of fixed, dilated caval veins.

Cardiac Tamponade on echo:

RV early-diastolic collapse [Mild increase in filling pressure]
RA late-diastolic collapse [Moderate increase in filling Pressure]
LA late-diastolic collapse [Moderate increase in filling Pressure]
LV early-diastolic collapse [Severe increase in filling Pressure].

Hemodynamic on Echo in ICU

It is possible to calculate blood flow at several levels in the heart and aorta using Doppler echocardiography.

Measurements of flow useful in the ICU setting to derive:

LV stroke volume, cardiac output, regurgitant volumes of MR and AR, flow across an ASD or VSD, valve areas (by continuity principle)
Response to therapeutic measures such as intravenous administration of inotropic drugs or the effect of an intra-aortic balloon pump on systemic output.
PW Doppler calculates stroke volume as the product of the cross-sectional area (cm2) of the LVOT and the TVI (cm).

Cardiac output: Stroke Volume X Heart Rate.

LA pressure (LAP) estimation

Combining transmitral Doppler (blood velocities) with TDI (tissue velocities) has been shown to improve the correlation with LAP.

Here, the ratio E/E′ is calculated:

Ratio <10 corresponding to LAP < 15 mmHg (2 kPa)
Ratio >15 corresponding to LAP > 18 mmHg (2.4 kPa)

Correlation between 11–14 is poor, additional parameters should be used, generally in combination.

Pulmonary Art Systolic Pressure

Peak PA systolic pressure is calculated from the peak Doppler velocity (v) of TR by CW.

RV pressure = 4 × (peak TR velocity)2
RV pressure + Estimated RA Pressure = PA systolic pressure.

RA pressure Estimation:

Normal variation or collapse of the IVC with breathing (>50%) implies normal RA pressure (0-5 mm Hg).
Partial collapse (<50%) is generally estimated at 5 to 10 mm Hg
No (or only minimal) change in IVC diameter implies an RA pressure of 15 mm Hg or more.
When available, RA pressure can be obtained directly from a central venous pressure tracing, which is more accurate. Care is needed in severe RV dysfunction, as PASP may be significantly underestimated by this technique. In the absence of TR, the pulmonary regurgitation (PR) trace can be interrogated to estimate PA diastolic pressure.

Volume responsiveness

Echocardiography allows assessment of the patient’s volume status, complementary to invasive hemodynamic measurements.

Echocardiographic volume status assessment:

Static values (single-measure dimensions and flows)
Dynamic indices (variation in flows and dimensions after dynamic maneuvers).

Static parameters

Estimation of preload- and volume- -responsiveness using static measurements is generally unreliable in ICU due to changes in the hemodynamics of critically ill patients.

LAP does not correlate with volume responsiveness, but demonstration of abnormally high pressures with a restrictive filling pattern should signal caution in volume resuscitation.

Indicators of Severe Hypovolemia in the Critically Ill

Hyperkinetic LV (in the presence of a normal RV) with end-systolic cavity obliteration

LV end-diastolic area <5.5 cm2/m2 BSA

Small IVC (<10 mm) with inspiratory collapse (spontaneously breathing patients)

Small IVC at end-expiration with variable respiratory change (mechanically ventilated patients).

Dynamic parameters

Passive leg raising has been proposed to predict fluid responsiveness in spontaneously breathing patients. Sensitivity and specificity are relatively low. Confounding factors (intra-abdominal pressure, hypovolemia, arrhythmia) probably limit its usefulness in the ICU population.

Respiratory variations in VTI may be used as an index of fluid responsiveness. Respiratory variation in SVC and IVC dimensions have been proposed to predict fluid responsiveness. An IVC distensibility index (maximum–minimum/minimum) >18% (12% normalized to mean value) has been suggested to predict a significant increase in SV in response to fluid challenge.

In contrast, a high SVC collapsibility index (maximum– minimum/maximum) >36% predicts a positive response to volume expansion (≥15% increase in SV) with sensitivity 90% and specificity 100%.

Prerequisite for interpreting dynamic volume responsiveness:

Sinus rhythm
Fully mechanically ventilated, with no spontaneous breathing effort.
Further, the effects of lung protective ventilatory strategies may lead to false-negative values.

Echocardiography in specific scenarios

ICU echocardiographer must know the potential pitfalls and coexisting pathologies in order to make a relevant assessment.

Myocardial ischaemia/infarction

Echocardiography is included in the universal definition of myocardial infarction (MI), and suspicion of a mechanical complication of MI is a class IA indication for echocardiography.
Extent of infarction/ischaemia should be demonstrated and complications (MR, ventricular septal rupture (VSR)/cardiac rupture/RV infarction) actively excluded.

Acute cor pulmonale

Sudden severe increase in RV afterload resulting in acute RV dilatation and failure.
Major causes: acute pulmonary embolism and ARDS.

Pulmonary embolism (PE)

Echocardiography provides only indirect signs of PE

Pulmonary hypertension
Signs of RV systolic (septal dyskinesia) & diastolic overload
RV-free wall hypokinesia
Moderate-severe TR.
Pre-existing pulmonary hypertension is suggested by RV hypertrophy and PASP > 60 mmHg.

Hypoxemia

Diagnosis and management of hypoxemic patients on the ICU. Establishing the differential diagnosis (cardiogenic vs non-cardiac). Assessment of secondary effects of pulmonary pathology on cardiac performance.
Diagnosis of a low CO state and/or diagnosis of anatomical shunt (intracardiac or intrapulmonary). Many ICU factors increase right-sided pressures, leading to right–left intracardiac shunting across an atrial septal defect/patent foramen ovale.
Intrapulmonary shunts are independent of right-sided pressure, and have been described in ARDS, pneumonia, thoracic trauma and hepatic cirrhosis. Diagnosis depends on a positive agitated saline contrast study.

Weaning from Mechanical Ventilation

Discontinuation of positive-pressure ventilation increases LV afterload and preload, and significantly increases the rate–pressure product.
In patients with cardiac disease; mismatch of the dynamic changes leads: increased work, leading to rising LAP, pulmonary edema, and/or RV dysfunction.
A baseline echocardiogram should be performed at the start of the weaning trial, and evidence of inotropy, lusitropy, chronotropy (negative/positive), preload and afterload mismatch should be actively sought.
Evidence of increasing LAP, myocardial ischaemia, decrease in LV/RV global function and/or worsening atrioventricular valvular regurgitation suggests a cardiac contribution to failure to wean.

Sepsis Syndromes

Echocardiography plays a key role in the management of the septic ICU patient by guiding haemodynamic management and excluding cardiac causes for sepsis.
Sepsis-related LV dysfunction is well recognised, with global and regional wall motion abnormalities. RV dysfunction develops either in isolation or associated with LV dysfunction.
Echocardiography may reveal a cardiac source of sepsis related to either native/prosthetic valve infection or indwelling catheters/implanted devices.
The diagnosis of endocarditis is made based on a well-established set of diagnostic criteria, of which echocardiography is one of the major factors.
Three echocardiographic findings are important:
Mobile echo-dense mass(es) attached to valvular/mural endocardium/implanted material
Fistulae/abscess formation, and/or new disruption/dehiscence of a prosthetic valve.
TOE has a higher sensitivity and specificity, and is mandated where prosthetic valve endocarditis is suspected, to identify major complications and guide surgical planning.

Chest trauma

A good comprehensive study should be performed to diagnose/exclude:
Pericardial/pleural collections
Aortic and mitral valve disruption
Aortic disruption
VSR
Coronary artery disruption (ischemia and/or fistulae)
Myocardial contusion.

Dr. Harish Mallapura Maheshwarappa

Director – Institute of Critical Care Medicine

Echocardiography in the assessment of shock

Echocardiography in the assessment of shock

Harish Mallapura Maheshwarappa

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